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Uncomplicated hypertensive crisis:
Hypertensive emergency:
intense headaches, nausea/vomitting, confusion, seizures, coma in the event of hypertensive
encephalopathy;
dyspnoea, chest pain in the event of heart failure or cardiac ischaemia;
rapid and/or irregular heart rate in the event of heart failure;
anuria, oliguria in the event of renal impairment.
History and clinical examination should look for: 
medications being taken that can cause or aggravate HBP; a
focal neurological sign(s) suggestive of stroke;
comorbidities and risk factors: heart failure, diabetes, renal impairment; excessive smoking or consumption of
alcohol, excess weight (BMI ≥ 25), etc.
Blood test: ionogram (particularly serum potassium levels), serum creatinine.


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alcohol, excess weight (BMI ≥ 25), etc.
Blood test: ionogram (particularly serum potassium levels), serum creatinine. 
Other necessary laboratory tests according to comorbidities (e.g. diabetes).


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Long-term treatment
Lifestyle and dietary advice
Recommended for all hypertensive patients:
Pharmacological treatment 
Start with a monotherapy. One of four classes of antihypertensive drugs can be chosen as ﬁrst line treatment,
according to the patient’s characteristics (e.g. age, contra-indications, etc.). For information:  
ECG and echocardiogram to look for signs of heart failure, coronary disease, or arrhythmia.
The goal of treatment is to lower BP. Target BP are:
SBP < 140 and/or DBP < 90
SBP < 140 and/or DBP < 80 in diabetic patients
SBP < 150 and/or DBP < 90 in patients aged > 80 years
In patients with mild HBP (SBP ≥ 140 and/or DBP ≥ 90) without associated cardiovascular disorders or stroke or
diabetes, start with lifestyle and dietary advice.


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diabetes, start with lifestyle and dietary advice. 
Pharmacological treatment is indicated in the following cases:
SBP ≥ 160 and/or DBP ≥ 100;
HBP associated with cardiovascular disorder, stroke or diabetes;
HBP not controlled by lifestyle and dietary changes alone.
Reduce calorie and salt intake.
Regular physical activity.
Weight loss if BMI ≥ 25.
Stop smoking and alcohol consumption.


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 In patients with no comorbidity start with a thiazide diuretic and check BP after 4 weeks of treatment. 
If the treatment has been correctly taken but there is no improvement after 4 weeks, add a second antihypertensive
drug.
After 4 weeks of bitherapy, reevaluate. If the patient’s BP remains too high, consider triple-therapy. In diabetic patients, if there is no improvement after 4 weeks of AEC inhibitor treatment taken correctly, add a calcium
channel blocker. In patients with a cardiac disorder (heart failure or coronary heart disease), bitherapy is usually necessary from the start
(AEC inhibitor + beta-blocker).
Surveillance and monitoring
Laboratory surveillance
According to treatment (diuretic, AEC inhibitor, etc.): ionogram and serum creatinine every 6 to 12 months.


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Laboratory surveillance
According to treatment (diuretic, AEC inhibitor, etc.): ionogram and serum creatinine every 6 to 12 months.
Clinical monitoring
Patient education
Patient with no comorbidities Patient with comorbidities
Thiazide diuretic After a stroke: thiazide diuretic
Patient > 65 years: thiazide diuretic or calcium
channel blocker 
Diabetic patient:
angiotensin converting enzyme (ACE) inhibitor
or beta blocker if concomitant cardiovascular disorder
Patient with black skin: thiazide diuretic or calcium
channel blocker (avoid ACE inhibitors)
Renal impairment: ACE inhibitor
Thiazide diuretic:
hydrochlorothiazide PO: 12.5 to 25 mg once daily in the morning (max. 25 mg daily)
 
Angiotensin converting enzyme inhibitor:


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Thiazide diuretic:
hydrochlorothiazide PO: 12.5 to 25 mg once daily in the morning (max. 25 mg daily)
 
Angiotensin converting enzyme inhibitor:
enalapril PO: start with 5 mg once daily. Gradually increase, every 1 to 2 weeks, according to BP, up to 10 to 20 mg
once daily (max. 40 mg daily).
In elderly patients or patients taking a diuretic or patients with renal impairment: start with 2.5 mg once daily.
 
Calcium channel blocker:
amlodipine PO: 5 mg once daily. Increase to 10 mg once daily if necessary (max. 10 mg daily). 
In elderly patients or patients with hepatic impairment: start with 2.5 mg once daily.
 
Beta-blocker:  (contra-indicated in patients with asthma)
bisoprolol PO: 5 to 10 mg once daily in the morning
Do not stop treatment abruptly (risk of malaise, angina).


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bisoprolol PO: 5 to 10 mg once daily in the morning
Do not stop treatment abruptly (risk of malaise, angina).
Consultations every 3 months (BP, weight), then every 6 months, then individualised frequency of consultations
depending on the patient's characteristics.
Management of comorbidities (e.g. diabetes).


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Treatment of hypertensive crisis
Uncomplicated hypertensive crisis 
Most frequent. Reassure the patient and prescribe rest. Check BP a few days later to start or adapt treatment.
Hypertensive emergency
Treat in an intensive care unit.
The aim is to reduce BP by 10 to 15% within the ﬁrst hour and to not reduce it more than 25% during the ﬁrst 24
hours. 
labetalol IV (contra-indicated in patients with asthma :
20 mg over at least 1 minute. Administer another dose after 10 minutes if BP has not decreased. If necessary, 40
mg doses are administered every 10 minutes until hypertension is controlled (max. 300 mg total dose).
 
References
Lifestyle and dietary advice.


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mg doses are administered every 10 minutes until hypertension is controlled (max. 300 mg total dose).
 
References
Lifestyle and dietary advice.
Treatment observance: do not stop treatment abruptly, particularly if taking beta blockers (risk of malaise, angina).
Consultation in the event of epistaxis, tinnitus, eye ﬂoaters; adverse effects of treatment (e.g. cough with AEC
inhibitors, erectile dysfunction with beta blockers, oedema with calcium channel blockers).
Hypertensive encephalopathy: 
 b 
Stroke: do not try to decrease BP during the ﬁrst 3 days unless SBP is ≥ 220 and/or DBP ≥ 120 (in this event
administer labetalol). 
Acute pulmonary oedema: see Acute heart failure.
Footnotes


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administer labetalol). 
Acute pulmonary oedema: see Acute heart failure.
Footnotes
(a) Consider secondary hypertension caused by medications being taken, mainly NSAID, corticosteroids, opioids, oralestroprogestogens, etc. Treatment, in this event, consists in stopping or replacing the causative drug.
(b) In patient with asthma, hydralazine IV: 5 to 10 mg diluted in 10 ml of 0,9% sodium chloride administered by slow IV, to berepeated after 20 to 30 minutes if necessary.
1. World Health Organization. Media center. High blood pressure: a public health problem, 2018.http://www.emro.who.int/media/world-health-day/public-health-problem-factsheet-2013.html [Accessed 12 September2018]


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Heart failure in adults
 
 
Heart failure (HF) is deﬁned as the inability of the heart to maintain adequate cardiac output. 
It is a serious condition, particularly frequent in people over 70 years. 
There are two types:
 
 
 
chronic HF: gradual onset of signs of HF;
acute HF: sudden onset of life-threatening HF (cardiogenic acute pulmonary oedema or shock), in most cases in
patients with known cardiopathy.
Chronic heart failure
Acute heart failure (acute pulmonary oedema)


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Chronic heart failure
Clinical features
Fatigue  and/or progressive onset of dyspnoea, occurs on exertion and then at rest, accentuated by the decubitus
position, preventing the patient from lying down; peripheral oedema.
Oedema of the lower limbs, hepatomegaly, jugular vein distention, hepatojugular reﬂux; ascites in advanced stages.
Left and right-sided signs; right-sided signs are often the most prominent. 
Evaluate severity of HF : 
Identify causative or aggravating factors:
Paraclinical investigations
Treatment
Lifestyle and dietary advice
Left-sided HF (left ventricle failure; most frequent form)
Right-sided HF (right ventricle failure)
Global HF (failure of both ventricles)
 [1]


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Left-sided HF (left ventricle failure; most frequent form)
Right-sided HF (right ventricle failure)
Global HF (failure of both ventricles)
 [1] 
Class I No limitation of physical activity. No symptoms during ordinary physical activity.
Class II Slight limitation of physical activity. Comfortable at rest. Ordinary physical activity results in fatigue,
palpitation, dyspnoea.
Class III Marked limitation of physical activity. Comfortable at rest. Less than ordinary activity causes fatigue,
palpitation, or dyspnoea.
Class IV Unable to carry on any physical activity without discomfort. Symptoms of heart failure at rest.
Coronary or valvular heart disease, hypertension, viral or toxic cardiopathy, pericarditis.


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Coronary or valvular heart disease, hypertension, viral or toxic cardiopathy, pericarditis.
Anaemia, American trypanosomiasis, rheumatic fever, diabetes, thyroid disorder, drug/alcohol addiction.
Cardiac ultrasound: if available, method of choice to conﬁrm cardiopathy.
Electrocardiogram (ECG): can diagnose left ventricular cardiomyopathy (left ventricular hypertrophy and/or left
bundle branch block) or arrhythmia and particularly atrial ﬁbrillation (AF or Aﬁb) or signs of myocardial ischemia or
infarction.
Chest x-ray: can exclude lung disease in patients with dyspnoea or can show cardiomegaly or pleural effusion (often
bilateral) and alveolar-interstitial syndrome.
Blood test: full blood count, ionogram, serum creatinine.


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bilateral) and alveolar-interstitial syndrome.
Blood test: full blood count, ionogram, serum creatinine.
Other necessary laboratory tests according to comorbidities (e.g. diabetes, thyroid disorder).
Reduce salt intake to limit ﬂuid retention.
Normal ﬂuid intake except in cases of very severe oedema.
Stop smoking.
Physical activity adapted to the patient’s capacity.


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Treatment of ﬂuid retention
furosemide PO: start with 20 mg once daily; increase if necessary, according to clinical response (certain patients
need doses of 80 mg 1 to 2 times daily) then reduce once oedema decrease (20 to 40 mg once daily). The reabsorption of oedema can sometimes be slow, taking up to 2 to 3 weeks.
The gradual worsening of HF may require an increase in dosage. Lifelong treatment with diuretics is not always
necessary.  In the event of resistant oedema, add hydrochlorothiazide PO (25 mg 1 to 2 times daily for a few days) but only in
hospital settings and monitoring renal function.
Long-term (lifelong) treatment
Other treatments
Weight loss if BMI ≥ 25.


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hospital settings and monitoring renal function.
Long-term (lifelong) treatment
Other treatments
Weight loss if BMI ≥ 25.
ACE inhibitors are the ﬁrst line treatment. Start with low doses, especially in patients with hypotension, renal
impairment, hyponatraemia. 
While increasing the dose monitor: drug tolerance (dry cough), blood pressure (the systolic BP should remain above
> 90 mmHg), serum potassium and creatinine levels.
In patients taking diuretics, reduce the dose of the diuretic if possible while introducing ACE inhibitors (risk of
hypotension if the patient is on high doses of diuretics).
enalapril PO:
Week 1: 2.5 mg once daily for 3 days then 5 mg once daily 
Week 2: 10 mg once daily for 3 days then 20 mg once daily


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enalapril PO:
Week 1: 2.5 mg once daily for 3 days then 5 mg once daily 
Week 2: 10 mg once daily for 3 days then 20 mg once daily
The effective dose is usually 20 mg once daily (or 10 mg 2 times daily). Doses of 10 mg daily are sometimes
enough; conversely, doses of 40 mg daily (maximum) are sometimes necessary.
Once the patient has been stable for at least 2 weeks taking ACE inhibitors and in the absence of any contra-
indications (asthma, hypotension, bradycardia, conduction disorders, particularly atrio-ventricular heart blocks), add
a beta blocker.
bisoprolol PO: start with a low dose and gradually increase as long as the drug is well tolerated (monitor for signs
of worsening HF, blood pressure, heart rate).
Week 1: 1.25 mg once daily 
Week 2: 2.5 mg once daily


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of worsening HF, blood pressure, heart rate).
Week 1: 1.25 mg once daily 
Week 2: 2.5 mg once daily
Week 3: 3.75 mg once daily
Weeks 4 to 8: 5 mg once daily
If insufﬁcient:
Weeks 9 to 12: 7.5 mg once daily
As from week 13: 10 mg once daily (max. 10 mg daily)
In the event of temporarily worsening HF, hypotension or bradycardia, readjust doses of associated treatments and
reduce the dose of bisoprolol or gradually stop treatment (stopping abruptly can lead to acute deterioration of the
patient’s condition). Once the patient is stabilized, re-increase/recommence bisoprolol.
Antagonist of aldosterone: only if serum potassium levels and ECG can be monitored (risk of severe hyperkalaemia),


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Antagonist of aldosterone: only if serum potassium levels and ECG can be monitored (risk of severe hyperkalaemia),
add spironolactone PO (25 mg once daily) to long-term treatment, particularly in cases of severe HF (Classes III
and IV).
Nitrates: can be used in left-sided or global HF in patients with intolerance to ACE inhibitors (cough is not tolerated,
renal impairment, severe hypotension).
isosorbide dinitrate PO: start with 5 to 40 mg 2 to 3 times daily and increase up to the effective dose, usually 15
to 120 mg daily.


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Treatment of causative or aggravating factors
According to the cause.
Surveillance and monitoring
Laboratory surveillance 
According to treatment (ACE, diuretic, etc.).
Clinical monitoring
Patient education
 
References
Digitalis glycosides: administer with caution, in intensive care unit (the therapeutic dose is close to the toxic dose),
only in patients with AF with rapid ventricular response conﬁrmed by ECG: no visible P waves, irregularly irregular
QRS complex (120-160).
Once stabilised, consultations once a month for the ﬁrst 6 months, then individualised frequency of consultations
depending on the patient's characteristics.
Routine consultations: weight curve, BP, progress of signs (dyspnoea, oedema, etc.).
Monitoring of comorbidities and causative or aggravating.


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Routine consultations: weight curve, BP, progress of signs (dyspnoea, oedema, etc.).
Monitoring of comorbidities and causative or aggravating.
Lifestyle and dietary measures (diet, weight control, physical activity adapted to the patient’s capacity, etc.).
Warning signs (shortness of breath or oedema of the lower limbs, serious adverse effects of treatment) and
management (timely/urgent medical consultation).
1. Chop WM, Jr. Extending the New York Heart Association classiﬁcation system. JAMA. 1985;254:505.


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Acute heart failure (acute pulmonary oedema)
Last updated: April 2021
 
Clinical features
 Signs of severity:
Paraclinical investigations
Diagnosis is mainly clinical.
 If available:
Treatment
Systolic blood pressure is < 90 mmHg
See Shock, Chapter 1.
Systolic blood pressure is ≥ 90 mmHg
Sudden onset or exacerbation of dyspnoea
Fatigue, increased time to recover after exercise
Bilateral peripheral oedema
Cold extremities
Elevated jugular venous pressure
On auscultation: bilateral pulmonary crepitations and/or extra heart sound (gallop rhythm)
Severe respiratory distress (intercostal retractions, nasal ﬂaring, see-saw breathing, SpO < 90%,
etc.), cyanosis, profuse sweating, confusion
2
Systolic blood pressure < 90 mmHg (cardiogenic shock)


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etc.), cyanosis, profuse sweating, confusion
2
Systolic blood pressure < 90 mmHg (cardiogenic shock) 
Rapid and excessive increase in arterial blood pressure (hypertensive emergency)
Heart rate (HR) > 130/minute or < 40/minute
Respiratory rate (RR) > 30/minute or < 12/minute 
Chest pain if underlying cardiac ischemia
ECG: look for signs of myocardial ischemia or arrhythmia.
Chest x-ray: signs vary depending on the severity of pulmonary oedema. In early stage, dilation of vessels in upper
lobes then perihilar haze and thickening of septa. In advanced stage, prominent opacities in hilar and perihilar regions
and pleural effusion. Can exclude other lung disease, such as pulmonary infection.
POCUS : a


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and pleural effusion. Can exclude other lung disease, such as pulmonary infection.
POCUS : a 
Perform 12-zone lung exam to evaluate for signs of bilateral pulmonary oedema and/or pleural effusions.
Perform 5-view cardiac exam to evaluate for signs of acute volume overload and/or decreased cardiac
function.
Monitoring: full blood count, electrolytes, serum creatinine; cardiac troponins if available.
 [1] [2]
The patient must be hospitalised.
Place patient in semi-seated position, legs down.
In patients with SpO < 90%, administer oxygen with a mask at the necessary ﬂow rate to maintain SpO ≥ 95%. If
pulse oximetry is not available, administer oxygen at a ﬂow rate of 6 to 10 litres/minute to patients with signs of
2 2


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isosorbide dinitrate sublingual (5 mg tablet)
 5 mg per dose; if necessary up to 2 doses taken 10 minutes apart
or
isosorbide dinitrate IV (10 ml ampoule, 1 mg/ml)
 2 mg (= 2 ml) by slow IV injection (over 2 minutes) then if necessary 2 to 10 mg/hour by continuous      infusion with
an electric syringe pump
or 
glyceryl trinitrate sublingual (0.5 mg tablet)
0.5 mg per dose; if necessary up to 3 doses taken 5 minutes apart
 Subsequent treatment depends on the underlying pathology (chronic heart failure, hypertension, acute coronary
syndrome, etc.).
References
hypoxia.
Insert an IV line.
If there are signs of volume overload (and/or in case of hypertensive emergency): furosemide IV, 40 to 80 mg, may


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hypoxia.
Insert an IV line.
If there are signs of volume overload (and/or in case of hypertensive emergency): furosemide IV, 40 to 80 mg, may
be repeated if necessary according to urine output, signs of respiratory distress and SpO. If the patient was
already taking furosemide at doses of > 40 mg, administer pre-existing dose by IV route.
2
Add a short-acting nitrate (vasodilator) if systolic blood pressure is > 100 mmHg. The aim is to gradually lower
systolic blood pressure to near-baseline value. If the patient’s baseline value is unknown, for information, lower
systolic blood pressure to 120-150 mmHg and the diastolic pressure to under 110 mmHg.
Non-invasive ventilation using continuous positive airway pressure (CPAP) is recommended in patients with


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Non-invasive ventilation using continuous positive airway pressure (CPAP) is recommended in patients with
persistent hypoxaemia, unless contraindicated (e.g. impaired consciousness) and on condition that appropriate
monitoring is available.
Monitoring: HR, RR, BP, SpO, mental status, urine output.2
Footnotes
(a) POCUS should only be performed and interpreted by trained clinicians.


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Monitoring: HR, RR, BP, SpO, mental status, urine output.2
Footnotes
(a) POCUS should only be performed and interpreted by trained clinicians.
1. Ponikowski P et al. 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure: The Task Forcefor the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC). Developedwith the special contribution of the Heart Failure Association (HFA) of the ESC. Eur J Heart Fail. 2016;18(8):891-975.https://academic.oup.com/eurheartj/article/37/27/2129/1748921 [Accessed 23 March 2021]


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2. Ezekowitz, Justin A. et al. 2017 Comprehensive Update of the Canadian Cardiovascular Society Guidelines for theManagement of Heart Failure. Can J Cardiol 2017;33:1342-1433.https://www.onlinecjc.ca/action/showPdf?pii=S0828-282X%2817%2930973-X [Accessed 23 March 2021]


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Endemic goitre and iodine deﬁciency
Goitre is an enlargement of the thyroid gland. Endemic goitre occurs in iodine-deﬁcient areas. Goitre can also be
caused or aggravated by the regular consumption of goitrogens such as manioc, cabbage, turnips, millet etc. Goitre is an adaptive process: iodine is essential for the production of thyroid hormones; iodine deﬁciency impairs
thyroid hormone synthesis; to compensate, the thyroid gland increases in volume. Thyroid function usually remains
normal. As well as the development of goitre, iodine deﬁciency in pregnant women has serious consequences for the child
(foetal and perinatal mortality, physical and mental retardation, cretinism). These risks must be prevented by providing
iodine supplementation in iodinedeﬁcient areas.


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iodine supplementation in iodinedeﬁcient areas.
Clinical features
Prevention and treatment
The objective of prevention is to reduce the consequences of iodine deﬁciency in neonates and children. Supplying
iodised salt through national programmes is the recommended method of prevention. For prevention in populations living in iodine deﬁcient areas where iodised salt is not available and for curative
treatment of patients with goitre: use iodised oil, according to national protocols. For information (according to the
WHO): 
 Curative and preventive single-doses are the same. Oral treatment is preferred. The target populations are pregnant


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WHO): 
 Curative and preventive single-doses are the same. Oral treatment is preferred. The target populations are pregnant
and breastfeeding women, women of childbearing age and children. In children, goitre disappears after several months. It disappears more slowly (or never) in adults despite restoration of
normal thyroid function in 2 weeks. Surgery is only indicated for patients with local mechanical dysfunction.
The WHO proposes a simpliﬁed classiﬁcation based on the signiﬁcance of goitre:
Group 0: normal thyroid, no palpable or visible goitre
Group 1: enlarged thyroid, palpable but not visible when the neck is in the normal position
Group 2: thyroid clearly visible when the neck is in the normal position


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Group 2: thyroid clearly visible when the neck is in the normal position
Possible mechanical complications (rare): compression, deviation of the trachea or of the oesophagus.
Population
Iodised oil PO
once yearly 
(190 mg capsule)
Children under 1 year 1 capsule
Children from 1 to < 6 years 2 capsules
Children from 6 to 15 years 3 capsules
Pregnant or lactating women
or women of childbearing age 2 capsules


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Appendix 1. Normal daily maintenance IV ﬂuidsin children > 1 month
Last updated: January 2021
 
Indications
Basic hydration needs for patients unable to drink sufﬁciently. After 48 hours, it is essential to provide nutrition to the
patient orally or by nasogastric tube and to gradually reduce IV ﬂuids.  This protocol should not be used for surgical or burns patients, those with renal, cardiac disease or diabetic
ketoacidosis.
Fluid to be administered
The ﬂuid of choice in children is Ringer lactate-Glucose 5% (RL-G5%). Use a premixed solution if available. If not,
add 50 ml of G50% to 500 ml of RL or 100 ml of G50% to 1000 ml of RL. If RL is not available, use 0.9% sodium


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add 50 ml of G50% to 500 ml of RL or 100 ml of G50% to 1000 ml of RL. If RL is not available, use 0.9% sodium
chloride instead. For ease of prescription and administration, the daily volumes and rates in drops per minute have been rounded off. 
 a  
 
 
Weight Volume
/24 hours
Rate
(paediatric infusion set 1 ml = 60 drops)
 (*) 
3 to < 4 kg 350 ml/24 h 15 drops/min
4 to < 5 kg 450 ml/24 h 19 drops/min
5 to < 6 kg 550 ml/24 h 23 drops/min
6 to < 7 kg 650 ml/24 h 27 drops/min
7 to < 8 kg 750 ml/24 h 31 drops/min
8 to < 9 kg 850 ml/24 h 35 drops/min
9 to < 11 kg 950 ml/24 h 40 drops/min
11 to < 14 kg 1100 ml/24 h 46 drops/min
14 to < 16 kg 1200 ml/24 h 50 drops/min
16 to < 18 kg 1300 ml/24 h 54 drops/min
18 to < 20 kg 1400 ml/24 h 58 drops/min


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Weight Volume 
/24 hours
Rate
(paediatric infusion set
1 ml = 60 drops)
 (*) Rate 
(standard infusion set 
1 ml = 20 drops)
20 to < 22 kg 1500 ml/24 h 63 drops/min 21 drops/min
22 to < 26 kg 1600 ml/24 h 67 drops/min 22 drops/min
26 to < 30 kg 1700 ml/24 h 71 drops/min 24 drops/min
30 to < 35 kg 1800 ml/24 h 75 drops/min 25 drops/min
≥ 35 kg 2000 ml/24 h 83 drops/min 28 drops/min
(*) In a paediatric infusion set, the number of drops per minute is equal to the number of ml per hour.For example: 15 drops/min = 15 ml/hour
Footnotes


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Footnotes
(a) Daily needs are calculated according the following formula:Children 0-10 kg: 100 ml/kg per dayChildren 11-20 kg: 1000 ml + (50 ml/kg for every kg over 10 kg) per dayChildren > 20 kg: 1500 ml + (20-25 ml/kg for every kg over 20 kg) per dayAdults: 2 litres per day


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Main references
 
Websites consulted between June 2019 and December 2022
British National Formulary (BNF) and British National Formulary for Children (BNFc)
MedicinesComplete Martindale. The Complete Drug Reference
MedicinesComplete UpToDate. Evidence-based clinical decision support resource BMJ Group. BMJ Best Practice. La revue Prescrire Centre belge d’information pharmacothérapeutique (CBIP)
http://www.cbip.be/fr/start Centers for Disease Control and Prevention
http://www.cdc.gov/DiseasesConditions/ Cochrane Library World Health Organization
http://www.who.int/publications/en/


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1
Chapter 1
INTRODUCTION TO RATIONAL USE OF MEDICINES
Rational Useof Medicines requires that patients receive medications appropriate to their
clinical needs, in doses that meet their own individual requirements, for an adequate period of
time, and at affordable cost to them and the community (WHO , 1985). In other words,
rational use means ‘prescribing right medicines, in adequate dose for the sufficient duration
and appropriate to the clinical needs of the patient at lowest cost’. M edicine useis a complex
cyclical process and in the clinical context, rational drug use implies correct drug, appropriate
indication and selection with respect to efficacy, safety, suitability for the patient and cost.
The concept of Rational Useof Medicinesis age old; however, it has attained more


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The concept of Rational Useof Medicinesis age old; however, it has attained more
significanceand momentum in terms of medical and socioeconomic aspects recently. Three
tools have been identified to implementRational Use of Medicineseffectively. These include
Essential Medicines List, Standard Treatment Guidelines andDrug Formulary. To be
meaningful, all three tools should work in concert and subjectforperiodic review and update.
I. The concept of Essential Medicines
EssentialM edicines(EM) are those that satisfy the health care needs of the majority of
the population and therefore should be available at all times in appropriate amounts and in
appropriate dosage forms.Following the concept of EM, WHO published the first


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appropriate dosage forms.Following the concept of EM, WHO published the first
Essential Medicine List (EML) in 1977, which has been updated successively every 5
year in view of changing world scenario about the medical needs and availability of new
and better drugs.The selection of these medicines is based on public health relevance,
evidence of efficacy and safety and comparative cost-effectiveness. Thesepriority
medicines should be available at each functioning health care facilitywith assured quality
and adequate information at a price the individual and the community can afford.
The selection of essential medicines depends upon level of health care facility, adequate
data on the efficacy, safety, suitability and comparative cost effectiveness of available


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data on the efficacy, safety, suitability and comparative cost effectiveness of available
treatments. In addition, stability of the product, need for special diagnostic or treatment
facilities and pharmacokinetic properties are also considered. Most essential medicines
are formulatedas single compound. However, fixed dose combinations are selected only
when it has proven pharmacokinetic and/or pharmacodynamic advantages over single
compound administered separately. While comparing the costof medicines among the
alternative treatments, the cost of total treatment and not the unit cost is considered. Other
factors taken into account include pattern of diseases, treatment facilities, training and
experience of the available personnel, financial resources etc.


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experience of the available personnel, financial resources etc.
Advantages of Essential Medicines
The implementation of the concept of EM has several logistic and prescribing advantages.
For example better management of medicines i.e. easier procurement, storage,


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2
distribution, more manageable stock, better qualityassurance, easier dispensing, less
fragmentation of budget  with improve drug availability. Moreover,prescribing improves
due to focused training and drug information, better recognition of adverse drug reactions,
drug interactions and focused educationefforts. The list ofEM closely relates to
treatment guidelines for clinical diseases andisalso used for the procurement and supply
of medicines in public sector, schemes for reimburses medicines costs and local medicine
production.
Its implementation is intended to be flexible and adaptable to different situations; which
medicines are regarded as essential remains a national responsibility.
II.Standard Treatment Guidelines


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medicines are regarded as essential remains a national responsibility.
II.Standard Treatment Guidelines
Standard TreatmentG uidelines (STGs), treatment protocols, and prescribing policies are
defined assystematically developed statements designed to assist prescribers in making
decisions about the appropriate treatment and health care for specific clinical problem.
These guidelines usually reflect the consensus on the optimal treatment options within a
health facility or system. In fact, they represent one of the approaches to promote
therapeutically effective and economically efficient use of medicines.
STGs list the preferred pharmacological and non-pharmacological treatment for common
health problems experienced by people in a specific health system. The pharmacological


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health problems experienced by people in a specific health system. The pharmacological
treatment should include the name, dosage form, strength, average dose (pediatric and
adult), number of doses per day, and duration of treatment. Other information on
diagnosis and advice to the patient may also be included. The most common diseases and
serious medical conditions that have high morbidity and mortality rate are selected.
Treatment guidelines must have the most up-to-date and evidence based information to
determine appropriate treatment options by expert authors and reviewers. Effective
implementation, however, is perhaps the greatest challenge in introducing STGs. When
implemented effectively, it offers several advantages to patients, health care providers,


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implemented effectively, it offers several advantages to patients, health care providers,
supply management personnel and policy makers as follows:
Patients,
 Most cost-effective optimal therapy is provided.
 Better compliance through consistency among prescribers.
 Improvement in availability of drugs.
 Overall better quality of care.
Health care providers,
 Provides standardized guidance to practitioners
 Quality of care standard-based on expert consensus and basis for monitoring
 Utilizes only formulary or essential medicines, so the health care system needs to
provideonly the medicines in theSTGs .
Supply managers,
 Identification of medicines to be available for the most commonly treated problems.


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3
 Facilitation of prepackaging of course-of-therapy quantities of commonly prescribed
items.
 Medicine demand more predictable, so forecasting more reliable
Health care policy makers,
 Provides focus therapeutic integration of special programs (diarrhea disease control,
acute respiratory infection)
 Provides a system for controlling cost by using funds more efficiently
STGs also have certain drawbacks. Establishing, developing and implementation of STGs
isa difficult, lengthy and time consuming process. Moreover, it needs to be updated
regularly to reflect changes in treatment strategies. If a regular schedule for updating the
STGs is not followed, they lose credibility and become obsolete. The extent of


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STGs is not followed, they lose credibility and become obsolete. The extent of
information to be provided in each medical condition is often a difficult decision.
However, the STG manual should be concise and small enough to carry it easily.
Key features of asuccessful STG manual
Simplicity- The numb er of health problem is limited to commonly observed conditions.
Each clinical condition list a few salient features with clear and concise information on
pharmacological and non-pharmacological treatment.
Credibility- Guidelines developed by the most respectedexperienced cliniciansin the
country and revisionis based on actual experience.
Treatment standards for all levels of health care facility- Health care providers use the


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country and revisionis based on actual experience.
Treatment standards for all levels of health care facility- Health care providers use the
same standard treatment; however,the referral criterion differs. While the first choice
treatment for a patient depends upon the patient’s diagnosis and condition and not on the
prescriber.
Medicine supply based on standards- The supply of medicines must match with the
standard treatment and list of essentialmedicines.
Regular updating- A ny change in the therapeutic options, bacterial resistance pattern
should be incorporated in the revised version to reflect current recommendations.
User friendly- The STGs should be published as small, durable pocket manualwhich
make itconvenient to carry and use.
III.Drug Formulary


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User friendly- The STGs should be published as small, durable pocket manualwhich
make itconvenient to carry and use.
III.Drug Formulary
A formulary is a compendium of practical drug information for clinical practice adapted
for use at a particularhealth care facility. It is a ready reference to key information on the
selection, prescribing, dispensing and administration of medicines. Although the concept
of formulary is old, a drug formulary is considered an essential element in achieving
rational prescribing in addition to controllingthe costs. The task of development of a
formulary in a hospital is usually undertaken by Drugs and Therapeutics Committee with
a multidisciplinary membership of doctors, pharmacists, nurses and administrative staff.


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4
The consultants place a request for inclusion of medicines along with its dosage
formulations to Drugs and Therapeutics Committee. The committee mayaccept the
request andinclude it in formularyorrejectand suggest an alternative with information to
the prescriber. The committee then monitors the impact, cost and benefits of various
med icines in the health care facility. Depending on the outcome,theuse of medicine is
extended or curtailed. Formularies have significant advantages for patients care.
However, the introduction of formularies may cause friction sinceit may beviewed as a
m ajor threat to their clinical freedom. Effective multidisciplinary working methods and


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m ajor threat to their clinical freedom. Effective multidisciplinary working methods and
consultation is needed to overcome this attitude. Potential advantages and disadvantages
of drug formularies are as follows:
Advantages
 Reduces range of products to bepurchased / stored / distributed
 Encourages generic prescribing
 Lowers drug costs
 Improved knowledge of a limited number of medicines
 Improves drug safety
 Improves patient care
 Provides opportunity for  multidisciplinary work
Disadvantages
 Restricts prescribing choice
 Reduces treatment options
 Inhibits introduction of new products
 Restricts research efforts
IV.Rational Approach To Therapeutics
Medicinesshould only be prescribed when necessary, and the benefit of administering the


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IV.Rational Approach To Therapeutics
Medicinesshould only be prescribed when necessary, and the benefit of administering the
medicine should be considered in relation to the risks involved. Bad prescribing habits
lead to ineffective and unsafe treatment, exacerbation or prolongation of illness, distress
and harm to the patient, and higher cost.The Guideto Good Prescribing;WHO; 1994,
providesmedical undergraduates with important tools for training in the process of
rational prescribing.
The following steps will help to remind prescribers of the rational approach to
therapeutics.
1. Define the patient’s problem
Whenever possible, making the right diagnosis is based on integrating many pieces of
information: the complaint as described by the patient; a detailed history; physical


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information: the complaint as described by the patient; a detailed history; physical
examination; laboratory tests; X-rays and other investigations. This will help in rational
prescribing, always bearing in mindthat disease are evolutionary process.


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5
2. Specify the therapeutic objective
Doctors must clearly state their therapeutic objectives based on the pathophysiology
underlying the clinical situation. Very often physicians must select more than one
therapeuticgoal for each patient.
3. Selecting therapeutic strategies
The selected strategy should bediscussedwith the patient.The selected treatment can be
non-pharmacological and/or pharmacological; it also needs to take into account the total
cost of all therapeutic options.
a. Non -pharmacological treatment
The patient does not always need amedicinefor treatment of the condition. Very often,
health problems can be resolved by a change in life style, dietary habits,use of


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health problems can be resolved by a change in life style, dietary habits,use of
physiotherapy or exercise, provision of adequate psychological support and other non-
pharmacological treatments; they have the same importance as a prescription drug and
instructions must be written, explained and monitored in the same way.
b. Pharmacological treatment
Selecting the correct group of drugs
Knowledge about the pathophysiology involved in the clinical situation of each patient
and the pharmacodynamics of the chosen group of drugs, are two of the fundamental
principles for rational therapeutics.
Selecting the drug from the chosen group
The selection process must consider benefit/risk/cost information. This step is based on


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Selecting the drug from the chosen group
The selection process must consider benefit/risk/cost information. This step is based on
evidence about maximal clinical benefits of the drug for a given indication (efficacy) with
minimum production of adverse effects (safety).
It must be remembered that eachdrug has adverse effects and it is estimated that up to
10% of hospital admissions in industrialized countries are due to adverse effects. Not all
drug-induced injury can be prevented but much of it is caused by inappropriate selection
of drugs.
In cost comparisons between drugs, the cost of total treatment and not only the unit cost
of the drug must be considered.
Verifying the suitability of the chosen pharmaceutical treatment of each patient


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of the drug must be considered.
Verifying the suitability of the chosen pharmaceutical treatment of each patient
The prescriber must checksuitability of the chosen active substance, its dosage form,
dosage schedule and duration of treatment are suitable for each patient. Drug treatment
should be individualized to the needs of each patient.
Prescription writing
The prescription is the link between the prescriber, the pharmacist(or dispenser) and the
patient so it is important for successful management of presenting medical condition. The
item is covered in more detail in the following section.
Giving information, instructions and warnings
This step is important to ensure patient adherence and is covered in detail in the following
section.


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Introduction to Rational Use of Medicines
6
Monitoring treatment
Evaluation of the follow up and the outcome of treatmentprovides information whether
the patient’s problem is solved or to reformulate , ifnecessary. This step gives riseto
important information about the effectsand adverse effectsof medicines,contributing to
the evidence ofknowledge, necessaryto promote the rational useof drugs.
V. Adverse Drug E ffects andDrug Interactions
Adverse drug reactions
An adverse drug reaction (ADR) may be defined as ‘ A response to a drug which is
noxious, unintended and occurs at doses normally used for prophylaxis, diagnosis or
therapyof disease, or for the modification of physiological function’ . ADRs are therefore


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therapyof disease, or for the modification of physiological function’ . ADRs are therefore
unwanted or unintendedeffects of a medicine, including idiosyncratic effects, which
occur during its proper use.
An adverse drug event (ADE) is defined as‘Any untoward medical occurrence that may
present during treatment with a medicine but which does not necessarily have acausal
relationship with this treatment’.
Two types of ADRs and their differentiating characteristicshave been identified.The
common , predictable, dose relatedreactionwith low mortality is type ‘A’ ADR. For
example,anticholinergic effect oftricyclic antidepressants anddigoxintoxicity. ADRs
may also be unrelatedto the known pharmacological action of a drug. These are


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may also be unrelatedto the known pharmacological action of a drug. These are
uncommon, non-dose related bizarre ‘B’ type reactions , for example,anaphylaxis with
penicillins, malignant hyperthermia with halothane.
Thalidomide marked the first recognized public health disaster related to the
introduction of a new drug. It is now recognized that clinical trials, however through,
cannot be guaranteed to detect all adverse effects likely to be caused by a drug. Health
workers are thus encouraged to record and reportto their national pharmacovigilance
centre any unexpected adverse effects with any drug to achieve faster recognition of
serious related problems.The Central Drugs Standard Control Organization(CDSCO),


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serious related problems.The Central Drugs Standard Control Organization(CDSCO),
Director General of Health Services under the influence of Ministry of Health & Family
Welfare, has initiated a nationwide Pharmacovigilance programme for protecting the
health of the patients by assuring drug safety.
The specific aims and objectives of the National Pharmacovigilance Programme are:
 To monitor ADRs in Indian population.
 To create awareness amongst health care professionals about the importance of  ADR
reporting in India
 To ensure that the benefits of use of medicine outweighs the risks andthus safeguard
the health of the Indian population
 To generate independent, evidence based recommendations on the safety of medicines


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Introduction to Rational Use of Medicines
7
 To encourage safe, rational and cost effective use of medicines.
Under the National Coordinating Center, several ADR monitoring centers operates to
detect ADEs. These ADR monitoring centers are located at MCI approved medical
colleges and hospitals, private hospitals, public health programmes, and autonomous
institutions such as Indian Council of Medical Research etc. The ADRmonitoring centers
record and analyze the ADEs and submit them to the National Coordinating center via
online reporting system known as Vigiflow.
Spontaneous reporting
Spontaneous reporting is the reporting of ADRs by healthcare professionals (and in some
countries consumers) to identify and report any suspected adverse drug reaction to a


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countries consumers) to identify and report any suspected adverse drug reaction to a
pharmacovigilance center and/or to the manufacturer. It is one of the important methods
of collecting information about ADRs.
All suspected adverse reactions, known orunknown, serious or otherwise should be
reported. It is important to report even minor reactions of new drugs. For established
drugs, the reporting of serious ADRs is important. An increased frequency of a known
ADR to a drug is also important.
Adverse drug reactions may be reported or notified to the nearest ADR monitoring centre
under the National Pharmacovigilance Program. The Department of Pharmacology, B. J.
Medical College is one of the approved ADR monitoring center in Gujarat state. The


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Medical College is one of the approved ADR monitoring center in Gujarat state. The
ADRs can be reported by the forms available at the department.Reporting is the process
of providing ADR information by filling in the ADR form appropriately giving details of
the clinical case as well as the ADR( Appendix– I).
Major factors predisposing to adversedrug effects
It is well known that different patients often respond differently to a given treatment
regimen. For example, patients taking combinations of drugs known to interact, only a
small number show any clinical evidence of interactions. In addition to the
pharmaceutical properties of drug therefore, there are characteristics of the patient which
predispose to ADRs.


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pharmaceutical properties of drug therefore, there are characteristics of the patient which
predispose to ADRs.
Extremes of age:The very old and the very young are more susceptible to ADRs. Drugs
which commonly cause problems in the elderly include hypnotics, diuretics, non-steroidal
anti-inflammatory drugs, antihypertensives, psychotropics and digoxin.
All children and particularly neonates, differfrom adults in their response to drugs. Some
drugs are likely to cause problems in neonates (for example morphine), but are generally
tolerated in children. Other drugs (for example valproic acid) are associated with
increased risk of ADRs in children of all ages. Other drugs associated with problems in
children include chloramphenicol (G rey baby syndrome), antiarrhythmics (worsening of


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children include chloramphenicol (G rey baby syndrome), antiarrhythmics (worsening of
arrhythmias), acetylsalicylic acid (Reye syndrome).
Intercurrent illness: If besides the condition being treated, the patient suffers from
another disease, such as kidney, liver or heart disease, special precautions maybe


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Introduction to Rational Use of Medicines
8
necessary to prevent ADRs. The genetic make-up of the individual patient may also
predispose to ADRs.
Drug interactions: May occur between drugs which compete for the same receptor or act
on the same physiological system. They may also occur indirectlywhen a drug-induced
disease or a change in fluid or electrolyte balance alters the response to another drug.
Incompatibilities between drugs and intravenous fluids
Drugs should not be added to blood, amino acid solutions or fat emulsions. Certain drugs,
wh en added to intravenous fluids, may be inactivated by pH changes, by precipitation or
chemical reaction. Benzylpenicillin and ampicillin lose potency after 6-8 hours if added


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chemical reaction. Benzylpenicillin and ampicillin lose potency after 6-8 hours if added
to dextrose solutions, due to the acidity of the solutions. Some drugs bind to plastic
containers and tubing, for example diazepam and insulin. Aminoglycosides are
incompatible with penicillins and heparin. Hydrocortisone is incompatible with heparin,
tetracycline and chloramphenicol.
Adverse effects caused by traditional medicines
Patients who have been or are taking traditional herbal remedies may develop ADRs. It is
not always easy to identify the responsible plant or plant constituent. Refer to the drug
and toxicology information service if available or to suitable literature.
The effect of food on drug absorption


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and toxicology information service if available or to suitable literature.
The effect of food on drug absorption
Food delays gastric emptying and reduces the rate of absorption of many drugs; the total
amount of drug absorbed may or may not be reduced. However, some drugs are
preferably taken with food, either to increase absorption or to decrease the irritant effect
on the stomach.
VI.Prescription writing
A prescription is an instruction from a prescriber to a dispenser. Every country has its
own standards for the minimum information required for a prescription, and its own laws
and regulations to define which drugs require a prescription and who is entitled to write it.
Many countries have separate regulations for prescriptions for controlled drugs such as


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Many countries have separate regulations for prescriptions for controlled drugs such as
opioid analgesics.The following guidelines will help to ensure that prescriptions are
correctly interpreted and leave no doubt the intension of the prescriber. The guidelines are
relevant for primary care prescribing; they may, however, be adapted for use in hospitals
or other specialist units.
Prescription form
The most important requirement is that the prescription beclear and legibleand indicate
precisely what should be given. The local languagemay be preferred.
The following details should be shown on the form:
 The prescriber’s name, address and telephone number. This will allo w either the
patient or the dispenser to contact the prescriber for any clarification or potential


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patient or the dispenser to contact the prescriber for any clarification or potential
problem with the prescription.


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Introduction to Rational Use of Medicines
9
 Date of the prescription. In many countries the validity of a prescription has no time
limit, but in some countries pharmacists do not dispense drugs on prescriptions older
than 3 to 6 months.
 Name, form and strength of the drug. The International Non-proprietary Name of the
drug should always be used. If there is a specific reason to prescribe a special brand,
the trade name canbe added. Generic substitution is allowed in some countries. The
pharmaceutical form (for example ‘tablet’, ‘oral solution’, ‘eye ointment’) should also
be stated.
 The strength of the drug should be stated in standard units using abbreviations that are
consistent with the System International (SI). ‘Microgram’ and ‘nanogram’ should


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consistent with the System International (SI). ‘Microgram’ and ‘nanogram’ should
not, however, be abbreviated. Also, ‘units’ should not be abbreviated. Avoid decimals
whenever possible. If unavoidable, a zero should be written in front of the decimal
point.
 Specific areas for filling in details about the patient including name, address and age.
Directions
Directions specifying the route, dose and frequency should be clear and explicit; use of
phrases such as ‘take as directed’ or ‘take as before’ should be avoided.
For preparations which are to be taken on an ‘as required’ basis, the minimum dose
interval should be stated together with, where relevant, the maximum daily dose. It is
good practice to qualify such prescriptions with the purpose of the medication(for


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good practice to qualify such prescriptions with the purpose of the medication(for
example ‘every 6 hours as required for pain’, ‘at night as required to sleep’).
It is good practice to explain the directions to the patient; these directions will then be
reinforced by the label on the medicinal product and possibly by appropriate counseling
by the dispenser. It may be worthwhile giving a written note for complicated regimens
although it must be borne in mind that the patient may lose the separate note.
Quantity to be dispensed
The quantity of the medicinal product to be supplied should be stated such that it is not
confused with either the strength of the product or the dosage directions.
Alternatively, the length of the treatment course may be stated (for example ‘for 5 days’).


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Alternatively, the length of the treatment course may be stated (for example ‘for 5 days’).
Wherever possible, the quantity should be adjusted to match the pack sizes available.
For liquid preparations the quantity should be stated in milliliters (abbreviated as ‘ml’) or
litres (preferably not abbreviated since the letter ‘l’ could be confused with the figure ‘1’).
Narcotics and controlled substances
The prescribing of a medicinal product that is liable to abuse requires special attention
and may be subject to specific statutory requirements. Practitioners may need to be
authorized to prescribe controlled substances; in such cases it might be necessaryto
indicate details of authority on the prescription.


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authorized to prescribe controlled substances; in such cases it might be necessaryto
indicate details of authority on the prescription.
In particular, the strength, directions and the quantity of the controlled substance to be
dispensed should be stated clearly, with all quantities written in words as well as in


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Introduction to Rational Use of Medicines
10
figures to prevent alteration. Other details such as patient particulars and date should also
be filled in carefully to avoid alteration.
References
1. The Guide to Good Prescribing;Geneva: WHO; 1994
2. WH0 Model Formulary 2008.
3. www.cdsco.nic.in/pharmacovigilance.htm


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11
Chapter 2
COMMON CONDITIONS
FEVER
A body temperature greater than 37.7°C is defined as fever. Fever may be continuous,
intermittent or remittent.
Investigations
A meticulous history of chronology of symptoms, any associated focal symptom(s), exposure to
infectious agents and occupational history may be useful. A thorough physical examination
repeated on a regular basis may provide potentially diagnostic clues.
 If there are no clinical clues, the tests include a complete haemogram with ESR, smear for
malaria parasite, blood culture, Widal test andurine analysis including urine culture.
 If the febrile illness is prolonged to more than 2 weeks, anX -ray chest is indicated even in
the absence of respiratory symptoms. Any abnormal fluid collection should besampled.
Treatment


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the absence of respiratory symptoms. Any abnormal fluid collection should besampled.
Treatment
Routine use of antipyretics in low-grade fever is not justified. This may mask important clinical
indications. However, in acute febrile illnesses suggestive of viral or bacterial cause, fever
should be treated.
Non pharmacological treatment
Hydrotherapy and rest
Pharmacological treatment
Non -specific
 Tab. paracetamol 500-1000 mg 6-8 hourly. Or Tab. ibuprofen 400-600 mg 8 hourly.
Specific
 Antibiotics/antimalarials depending upon the cause suggested by clinical andlaboratory
evaluation.
Outcome
In most cases of fever, patient may either recover spontaneously or a diagnosis is reached after
repeated clinical evaluation and investigations. If no diagnosis is reached in up to 3 weeks,


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repeated clinical evaluation and investigations. If no diagnosis is reached in up to 3 weeks,
patient is said to be having feverof unknown origin (FUO) and should be managed accordingly.
Patient education
 Self medication should be avoided.
 Antibiotics should be taken only on advice of a physician.
 Avoid covering the patient having high fever with blanket etc.
 Plenty of fluids should be taken. Stay in cool environment. Cold sponging of face and limbs
shouldbe done repeatedly.


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Common Conditions
12
 Common causes include
- Infections, particularly extrapulmonary tuberculosis, typical and atypical mycobacterial
infections,Pneumocystis cariniipneumonia, toxoplasmosis, lymphoma etc. In neutropenic
patients, gram negative bacterial, staphylococcal and fungal infections are important causes.
- Neoplastic conditions
- Noninfectious inflammatory causes collagen vascular diseases, drug fevers
 Prolonged unexplained fever, often with no localizing clue on history, physical examination
and basic laboratory investigations.
References
1. Alterations in Body Temperature. In: Harrison's Principles of Internal Medicine. Kasper DL, Braunwald E,
Fauci AS et al (eds), 16th Edition, 2005, McGraw Hill Company Inc., New York, pp 104-25.


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Fauci AS et al (eds), 16th Edition, 2005, McGraw Hill Company Inc., New York, pp 104-25.
2. Physiological Changes in Infected Patients. In: Oxford Textbook of Medicine. Warrell DA, Cox TM, Firth
JD, Benz EJ Jr (eds), 4th Edition, 2003. Oxford University Press, 1289-92.
FEVER OF UNKNOWN ORIGIN (FUO)
FUO is defined as thepresence of fever of 38.3°C or more recorded on several occasions,
evolving for at least 3 weeks with no diagnosis reached even after one week of relevant and
intelligent investigations. FUO is usually an uncommon presentation of common diseases.
Salient features
Investigations
 A detailed clinical history, repeated physical examination to provide potentially
diagnostic clues (PDC).
 No single algorithmic approach to diagnosis can be recommended for all patients of FUO


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diagnostic clues (PDC).
 No single algorithmic approach to diagnosis can be recommended for all patients of FUO
and diagnostic approach needs to beindividualized.
 A complete haemogram including peripheral blood smear for malaria parasite, serum
biochemistry particularly liver function tests, a tuberculin test and an X-ray of chest
should be done in every patient with prolonged fever.
 Other investigations which are often helpful include tests related to collagen vascular
diseases, an ultrasonographyto localize intra-abdominal foci of infections and a contrast
enhanced computed tomography (CECT) of chest and abdomen in detecting mediastinal
lymph nodes and parenchymal lung abnormalities not seen on conventional chest X-ray.


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lymph nodes and parenchymal lung abnormalities not seen on conventional chest X-ray.
 Further, diagnostic approach should take into consideration the PDCs from the evaluation
of history, results of repeated physical examination, basic investigations and any
investigations done prior to this episode. If any abnormal or doubtful lesion is detected
FNAC/biopsy should be obtained.
Treatment
Sometimes evaluation may need discontinuation of all drugs being taken by the patient to rule
out drug fever as the cause of FUO.
Symptomatic treatment for fever(for details see section on fever)


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Common Conditions
13
 Major criteria are pancarditis,polyarthritis,chorea,erythema marginatumand subcutaneous
nodule.
 Minor criteria arearthralgia,fever,raised PR interval.
 Cold sponging may be done if fever produces discomfort. The emphasis in patients with
classic FUO is on continued observation and examination.
 (Caution: Avoid 'shotgun' trials. Empirical therapies consisting of therapeutic trials
commonly used in patients with FUO are: antibiotics, anti-tubercular treatment (ATT)
and corticosteroids).
 The ability of glucocorticoids and NSAIDs to mask fever while permitting the spread of
infection dictates thattheir use should be avoided unless infection has been largely ruled
out.
 If on the basis of clinical evaluation and inability to reach a definitive diagnosis, a


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out.
 If on the basis of clinical evaluation and inability to reach a definitive diagnosis, a
therapeutic trial is started, the following principles must be kept in mind:
- Give only one setof trial at a given time
- The doses of drugs and period of therapeutic trial must be adequate-
- The patient must be followed closely for response
Patient education
 Self medication should be avoided.
 Antibiotics should be taken only on advice of a physician.
 Plenty of fluids should be taken. Stay in a cool environment.
ACUTE RHEUMATIC FEVER
Rheumatic fever is due to an autoimmune reaction to group streptococci and involves many
organs, primarily the heart, the joints and the central nervous system.
Salientfeatures
Non pharmacological treatment


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organs, primarily the heart, the joints and the central nervous system.
Salientfeatures
Non pharmacological treatment
 Bed rest for two weeks followed by gradual ambulation
Pharmacological treatment
 Tab.  penicillin V 500 mg BD  for 10 days or Inj. benzathine penicillin G- 1.2 million
units in single does orTab. erythromycin 250 mg QID for 10 days– if patient is allergic
to penicillin.
 For secondary prophylaxis for rheumatic fever, giveInj. benzathine penicillin 1.2 million
units every 3 weeks or Tab. penicillin V 250 mg BD daily or Tab. erythromycin 250 mg
twice daily.
 Duration of prophylaxisis given in Table 1.


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Common Conditions
14
Table 1. Duration of secondary prophylaxis in acute rheumatic fever
Category of Patient Duration of Prophylaxis
Rheumatic fever without carditis For 5 years after the last attack or 21 years of
age (whichever islonger).
Rheumatic fever with carditis but no
residual valvular disease
For 10 years after the last attack, or 21 years of
age (whichever is longer).
Rheumatic fever with persistent valvular
disease, evident clinically or on
echocardiography
For 10 yearsafter the last attack, or 40 years of
age (whichever is longer). Sometimes lifelong
prophylaxismay be required.
 Arthritis:Tab. aspirin 2 g QID in adults and 80-100 mg/kg/day in children till symptoms
persist or Tab. naproxen: 10-20 mg/kg/day can alsobe used.


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 Arthritis:Tab. aspirin 2 g QID in adults and 80-100 mg/kg/day in children till symptoms
persist or Tab. naproxen: 10-20 mg/kg/day can alsobe used.
 Carditis: Tab. prednisolone 1-2 mg/kg/day can be used for short periods or up to a
maximum of 3 weeks.
 Chorea: It occursas a long term sequelae (3-6 months). Carbamazepine or sodium
valproate is preferred to haloperidol(0.05 mg/kg/day) to reducethe abnormal movements
but response may take up to 2 weeks. Treatment should continue up to 1-2 weeks after
symptoms subside.
ANAEMIA
Anaemia is defined as a low haemoglobin level (less than 13.5 g/dl in males and less than
13.5 gm/dl in females).The common causes of anaemia in Indiaincludes,reduced production


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13.5 gm/dl in females).The common causes of anaemia in Indiaincludes,reduced production
due to deficiency of iron, folic acid, rarely vitamin B12, or an ineffective erythropoiesis
secondary to many causes (anaemia of chronic disease, secondary to infections and
inflammation, endocrinal disorders, primary bone marrow disorders like infiltration or
hypoplasia),  blood loss (whichalso leads to iron deficiency) and increased destruction of
RBCs (haemolysis due to many causes of which thalassaemia is the commonest).


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Common Conditions
15
Salientfeatures
Pharmacological treatment
Iron deficiency anaemia
 Treat the underlying cause: menorrhagia in women, gastrointestinal blood loss in all age
groups including hookworm infestation, dietary deficiency, rarely malabsorption.
 Tab. ferrous sulfate 200 mg 3 times a day.
 Reduce the dose as haemoglobin rises to over 10 g/dl. Once haemoglobin is normal,
continue with 1 tablet daily for at least three months.
 Other preparations of iron are not superior, but they can be tried ifpatient does not find
ferrous sulfate suitable. These include ferrous fumarate and ferrous gluconate. The rate of
rise of haemoglobin should be 1 g/dl per week.
 If this does not occur, consider ongoing blood loss, noncompliance,and associated


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rise of haemoglobin should be 1 g/dl per week.
 If this does not occur, consider ongoing blood loss, noncompliance,and associated
haemoglobinopathy like thalassaemia carrier status, malabsorption, or an incorrect
diagnosis.
 Parenteral iron does not lead to a faster rise in haemoglobin. It is indicated in the
following situations: (i)m alabsorption of iron, (ii)intolerance of oral iron, (iii)in late
pregnancy to ensure that foetal stores of iron are replenished rapidly, (iv)if ongoing
blood loss exceeds the capacity to absorb oral iron(like in inoperable malignancy) and(v)
in noncompliant patient. There is danger of anaphylactoid reactions;hence facilities to
manage these should be readily available.
Folic acid deficiency


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manage these should be readily available.
Folic acid deficiency
 Treat the cause: Dietary deficiency, increased requirement as in pregnancy and children,
haemolytic anaemia.
 Tab. folic acid 5 mg daily. This dose is adequate even in malabsorption syndrome.
Vitamin B12 deficiency
 Tiredness, weakness and lack of desire to work.
 Nails and tongue look pale. Severe anaemia produces general pallor and swelling of feet.
 Most aetiologies may be determined on the basis of MCV performed in an accurate cell
counter as follows:
 Low MCV -Iron deficiency or haemoglobfnopathy like thalassaemia.
 High MCV - Folic acid or B12 deficiency. Less commonly alcohol intake, liver disease,
haemolysis and hypothyroidism.
 Normal MCV - Anaemia of chronic disease, primary bone marrow disorders, renal


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haemolysis and hypothyroidism.
 Normal MCV - Anaemia of chronic disease, primary bone marrow disorders, renal
failure, haemolysis.
 In case of associated leucocyte and platelet abnormalities or if anaemia does not respond
to therapy in 4 weeks despite correcting the apparent cause, a bone marrow examination
by aspiration/biopsy should be performed.


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Common Conditions
16
 The onset of fever is typically gradual, continuous (temperature upto 40º C)
constitutional symptoms such as malaise, anorexia, lethargy, headache.
 Constipation or diarrhea (pea-soup stools) which may be associated with abdominal
pain and tenderness.
 Hepatomegaly and splenomegaly may be observed.
 Complications such as hepatitis, meningitis, pneumonitis and myocarditis can occur
after the first week.
 Treat the cause: Dietary deficiency in vegetarians, pernicious anaemia. Although
uncommon, it is also under diagnosed due to lack of facilities.
 Tab. vitamin B complex, as in haematinic tablets. Or Inj. B12 1000 mcg IM, one injection
on alternate days for total 5 injections, then once a week for 5 weeks, then once in 3 to 6


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on alternate days for total 5 injections, then once a week for 5 weeks, then once in 3 to 6
months will be adequate for most patients.
Patient education
 Educate the patient about preventive measures for worm infestation.
 Inform about importance of taking adequate food with green leafy vegetables to meet the
nutritional requirement.
 Cooking food in iron utensils may increase iron content in the diet.
 Instruct the patient to take iron tablets after food; iron tablets sometimes produce stomach
upset.
 Inform the patient that the stools could turn black during iron therapy
 Reduce the dose of iron if it produces stomachache, diarrhoea or constipation.
 Explain that the response to iron therapy is gradual and it takes weeks or months for


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 Explain that the response to iron therapy is gradual and it takes weeks or months for
blood to become normal. Continue iron tablets for six months.
 Keep iron tablets out of the reach of children. They may swallow the tablets as candies
causing adverse reactions including death.
TYPHOID FEVER
It is caused bySalmonella typhiand Salmonella paratyphi.Salmonella typhicauses a variety
of illnesses including asymptomaticcarrier state, gastro-enteritis andenteric fever.
Salient features
Investigations
 Diagnosis is suggested by
- Rising of O antibodies (W idal test) and
- Confirmed by isolation of organism in blood, bone marrow, urine or stool
Pharmacological treatment
 Most patients with uncomplicated enteric fever can be managed at home with oral
antibiotics and antipyretics.


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Common Conditions
17
 Patients with persistent vomiting, diarrhea, and/or abdominal distension should be
hospitalized and given supportive therapy as well as a parenteral third-generation
cephalosporin or fluoroquinolone, depending on the susceptibility profile(Table 2).
 Therapy should be administered for at least 10 days or for 5 days after feverresolution.
Table 2. Dosage schedule of antibiotics in treatment of typhoid fever
Indication Agent Dosage (Route) Duration, Days
Empirical
Treatment
Ceftriaxonea 1-2 g/d IV 7–14
Fully
Susceptible
Ciprofloxacinb (first line)500 mg BD (PO) or 400
mg BD (IV)
5–7
Amoxicillin (second line)1 g TDS (PO) or 2 g QID
(IV)
14
Chloramphenicol 25 mg/kg TDS (PO or IV) 14–21
Trimethoprim-
sulfamethoxazole
160/800 mg BD (PO) 7–14


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(IV)
14
Chloramphenicol 25 mg/kg TDS (PO or IV) 14–21
Trimethoprim-
sulfamethoxazole
160/800 mg BD (PO) 7–14
Ciprofloxacin 500 mg BD (PO) or 400
mg BD (IV)
5–7
Multidrug-
Resistant
Ceftriaxone 2–3 g/day (IV) 7–14
Azithromycin 1 g/day (PO)c 5
Ceftriaxone 2–3 g/d (IV) 7–14
Azithromycin 1 g/d (PO) 5
Nalidixic Acid–
Resistant
High-dose ciprofloxacin750 mg bid (PO) or 400
mg q8h (IV)
10–14
aOr another third-generation cephalosporin [e.g., cefotaxime, 2 g TDS (IV); or cefixime, 400 mg
bid (PO)].
bOr ofloxacin 400 mg bid (PO) for 2–5 days.
cOr 1 g on day 1 followed by 500 mg/day PO for 6 days.
 The 1–5% of patients who develop chronic carriage ofSalmonellacan be treated for 4–6
weeks with an appropriate oral antibiotic.


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 The 1–5% of patients who develop chronic carriage ofSalmonellacan be treated for 4–6
weeks with an appropriate oral antibiotic.
 Treatment with oral amoxicillin,cotrimoxazole, ciprofloxacin, or norfloxacin is 80%
effective in eradicating chronic carriage of susceptible organisms.
 However, in cases of anatomic abnormality (e.g., biliary or kidney stones), eradication
often requires both antibiotic therapy and surgical correction.


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Common Conditions
18
 It is an acute and chronic illness characterized by paroxysms of fever, chills, sweats,
fatigue, anemia and splenomegaly.P. falciparummalaria (severe and complicated
malaria) is associated in varying degrees with the following clinical signs.
 Symptoms of cerebral malariaincludemental clouding,coma, convulsions,delirium
and occasionally localizing signs, hyperpyrexia (more than 40.5ºC), haemolysis,
oliguria,anuria,pulmonary edemaand macroscopic haemoglobinuria.
MALARIA
Parastitic infection due to protozoa of genusPlasmodium transmitted by the female anopheles
mosquito. There are four plasmodia species:Plasmodium falciparum, Plasmodium vivax,
Plasmodium malaria, Plasmodium ovale.
Salient features
Investigations


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Plasmodium malaria, Plasmodium ovale.
Salient features
Investigations
Diagnosis is made by presence of protozoa in the blood in thick and thin smear slides (thick
smear for easy detection of parasite and thin smear for identification of species).
Note: That blood films may be negative even in a severe attack because of parasites in the
deep capillaries.
Pharmacological treatment(Figure 1, 2 and 3)
Figure1. Treatment where microscopy result is available within 24 hours


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Common Conditions
19
Figure 2. Treatment where microscopy result is not available within 24 hours and
monovalent RDT is used
Figure3. Treatment where microscopy result is not available within 24 hours and
bivalent RDT is used


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Common Conditions
20
Treatment ofP.vivaxm alaria
 Tab. chloroquine:25 mg/kg body weight divided over three days i.e.
 10 mg/kg on day 1
 10 mg/kg on day 2
 5 mg/kg on day 3
 Tab. primaquine:0.25 mg/kg body weight daily for 14 days.
 Primaquine is contraindicated in infants, pregnant women and individuals with G6PD
deficiency.14 day regimen of primaquine should be given under supervision.
Treatment ofP.falciparumm alaria
 Artemisinin based Combination Therapy (ACT-SP) – Tab.artesunate 4 mg/kgbody weight
daily for 3 days plussulfadoxine (25 mg/kg body weight)- pyrimethamine (1.25 mg/kg
body weight) on first day.
 Tab.primaquine:0.75 mg/kg body weight on day 2
Treatment of mixed infections(P.vivax+ P.falciparum)cases


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body weight) on first day.
 Tab.primaquine:0.75 mg/kg body weight on day 2
Treatment of mixed infections(P.vivax+ P.falciparum)cases
All mixed infections should be treated with full course of ACT andprimaquine 0.25 mg per
kg body weight daily for 14 days(Table 3).
Table 3. Dosage schedule for treatment of mixed infection(P.vivax+ P.falciparum)
Age
Day 1 Day 2 Day 3 Days 4-14
AS
(50 mg)
SP
(500 mg +
25 mg)
PQ
(2.5 mg)
AS tablet
(50 mg)
PQ
(2.5 mg)
AS tablet
(50 mg)
PQ
(2.5 mg)
PQ
(2.5 mg)
Less than 1 yr 1/2 1/2 0 1/2 0 1/2 0 0
1-4 years 1 1 1 1 1 1 1 1
5-8 years 2 1 .5 2 2 2 2 2 2
9-14 years 3 2 4 3 4 3 4 4
15 yrs or more 4 3 6 4 6 4 6 6
AS – artesunate, SP– sulfadoxine-pyrimethamine, PQ-primaquine


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Common Conditions
21
T reatment of complicated or severe malaria (Table 4)
Table 4. Treatment of severe and complicated malaria
Initial parenteral treatment for at least 48hrs.
Choose any one of the following
Follow-up treatment, when patient
can take oral medications following
parenteral  treatment
Quinine:20mg quinine salt/kg body weight
on admission (IV infusion or divided IMinjection)
followed by maintenance dose of 10 mg/kg 8 hourly;
infusion rate should notexceed 5 mg/kg per hour.
Loading dose of20mg/kg should not be given, if the
patienthas already received quinine.
Quinine10 mg/kg three times a day
plusdoxycycline 100 mg once a day
orclindamycin in pregnant women
and childrenunder 8 years of age, to
complete 7 days oftreatment.
Artesunate:2.4 mg/kgIV or IM given onadmission,


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orclindamycin in pregnant women
and childrenunder 8 years of age, to
complete 7 days oftreatment.
Artesunate:2.4 mg/kgIV or IM given onadmission,
then at 12 h and 24 h, thenonce a day or
Artemether: 3.2 mg/kgIM given onadmission then
1.6 mg/kg per dayor
Arteether:150 mg dailyIM for 3 days inadults only
(not recommended for children).
Treat with: ACT-SP for 3days + PQ
single dose on second day to
complete 7 days of treatment.
Note: The parenteral treatment in severe malaria cases should be given for minimum of 24 hours once started
(irrespective of the patient's ability to tolerate oral medication earlier than 24 hours).
Chemoprophylaxis of malaria
Short term chemoprophylaxis (up to 6 weeks)
Doxycycline: 100 mg once daily for adults and 1.5 mg/kg once daily for children


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Short term chemoprophylaxis (up to 6 weeks)
Doxycycline: 100 mg once daily for adults and 1.5 mg/kg once daily for children
(contraindicated in children below 8 years). The drug should be started 2 days before travel
and continued for 4 weeks after leaving the malarious area.
Chemoprophylaxis for longer stay (more than 6 weeks)
Mefloquine:250 mg weekly for adults and should be administered two weeks before, during
and four weeks after exposure.
DENGUE
Dengue is the mostimportant emerging tropical viral disease of human beings in the world
today.  All four dengue virus (Dengue 1, 2, 3 and 4) infections maybe asymptomatic, may
lead todengue fever (DF),dengue hemorrhagic fever (DHF)or when associated withplasma
leakage may lead to hypovolemic shock and dengue shock syndrome (DSS).


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Common Conditions
22
Salient features
Dengue hemorrhagic fever(DHF) ,if one or more of the following are present
 Positive tourniquet test
 Petechiae, purpura or ecchymosis
 Bleeding from mucosa
 Haematemesis, melena
 Thrombocytopenia (platelets 100,000cells/mm 3 or less) and evidence of plasma leakage.
Dengue shock syndrome (DSS)
 All the above criteria of DHF plus signs of circulatory failure.
Notes: The tourniquet test is performedby inflating a blood pressure cuff to mid way
betweenthe systolic and diastolic pressure.
Non pharmacological treatment
 Bed rest is advisable during the acute phase.
 Use cold sponging to keep temperature below 39ºC
Pharmacological treatment
 Management ofdengue fever is symptomatic and supportive


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 Use cold sponging to keep temperature below 39ºC
Pharmacological treatment
 Management ofdengue fever is symptomatic and supportive
 Antipyretics may be used to lower the body temperature. Aspirin/NSAIDs likeibuprofen
etc should be avoided since it may cause gastritis, vomiting, acidosisand platelet
dysfunction.
 Paracetamol is preferablein the doses as follows:1-2 years: 60–120 mg/doses,3-6 years:
120 mg/dose,7-12 years: 240 mg/dose,Adult : 500mg/dose
Note: In children the dose is calculated as per 10mg/kgbody w eight per dose which can
be repeated at the interval of 6hrs.
 Oral fluid and electrolyte therapy are recommended for patients with excessivesweating
or vomiting.
 Patients should be monitored in DHF endemic area until they become afebrilefor one


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or vomiting.
 Patients should be monitored in DHF endemic area until they become afebrilefor one
day without the use of antipyretics and after platelet and haematocrit determinations are
stable, platelet count is more than 50,000/mm 3.
Management of Dengue Hemorrhagic Fever (Febrile Phase)
 The management of febrile phase is similar to that of DF.
 Paracetamol isrecommended to keep the temperature below 39O C. Copious amount of
fluidshould be given orally, to the extent the patient tolerates, oral hydration solution
(ORS), such as those used for the treatment of diarrhoeal diseases and/or fruitjuices are
preferable to plain water
 Dengue fever is an acute febrile illness of 2-7 days with two or more of the following


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preferable to plain water
 Dengue fever is an acute febrile illness of 2-7 days with two or more of the following
manifestations. Headache, retro orbital pain, myalgia, arthralgia, rash.
 Hemorrhagic manifestation (petechiae and positivetourniquet test) and Leucopenia


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Common Conditions
23
 IV fluid may be administered if the patient isvomiting persistently or refusing to feed.
 Patients should be closely monitored for the initial signs of shock. The criticalperiod is
during the transition from the febrile to the afebrile stage and usuallyoccurs after the
third day of illness.
 Serial haematocrit determinations are essentialguide for treatment, since they reflect the
degree of plasma leakage and need forintravenous administration of fluids.
 Haematocrit should be determined daily fromthe third day until the temperature has
remained normal for one or two days. Ifhaematocrit determination is not possible,
haemoglobin determination may becarried out as an alternative.
 The details of IV treatment when required for patientsare given inFigure 4.


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haemoglobin determination may becarried out as an alternative.
 The details of IV treatment when required for patientsare given inFigure 4.
Figure 4. Treatment algorithm of dengue


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Common Conditions
24
Management of DHF Grade I and Grade II:
 Any person who has dengue fever with thrombocytopenia and haemoconcentrationand
presents with abdominal pain, black tarry stools, epistaxis, bleeding from thegums and
infection etc needs to be hospitalized.
 All these patients should beobserved for signs of shock. The critical period for
development of shock istransition from febrile to abferile phase of illness, which usually
occurs after third day of illness.
 A rise of haemoconcentration indicates need for IV fluid therapy. Ifdespite the treatment,
the patient develops fall in BP, decrease in urine output orother features of shock, the
management for Grade III/IV DHF/DSS should beinstituted.


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the patient develops fall in BP, decrease in urine output orother features of shock, the
management for Grade III/IV DHF/DSS should beinstituted.
 Oral rehydration should be given along with antipyretics likeparacetamol sponging,etc.
as described above.
 The detailed treatment for patient with DHF Grade Iand II is given atFigure 5. Common
signs of complications are observed during the afebrile phase of DHF.Immediately after
hospitalization, the haematocrit, platelet count and vital signsshould be examined to
assess the patient’s condition and intravenous fluid therapy should be started. The patient
requires regular and sustained monitoring.
Figure 5. Volume replacement flow chart for patients with dengue haemorrhagic fever
grade I and II


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Common Conditions
25
Fluid requirement
 The volume of fluid required to be replaced should be just sufficient to maintaineffective
circulation during the period of plasma leakage. To ensure adequate fluidreplacement
and avoid over-fluid infusion, the rate of intravenous fluid should beadjusted throughout
the 24 to 48 hour period of plasma leakage by periodichaematocritdeterminations and
assessment of vital signs.
 The required regimen of fluid should be calculated on the basis of body weightand
charted on a 1-3 hourly basis, or more frequently in the case of shock. Theflow of fluid
and the time of infusion are dependent on the severity ofDHF. The schedule given below
is a guidelineand calculatedfor moderate dehydration of about 6% deficit(plus
maintenance)(Table 5).


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is a guidelineand calculatedfor moderate dehydration of about 6% deficit(plus
maintenance)(Table 5).
Table 5. Fluid requirement as per body weight of the patient
Weight on
admission (kg)
Fluid requirement/kg body
weight/day (ml/kg)
<7 220
7-11 165
12-18 130
>18 90
 In older children who weigh more than 40 kg, the volume needed for 24 hoursshould be
calculated as twice that required for maintenance (using the Holidayand Segar formula).
The maintenance fluid should be calculated as follows:
Table 6. Maintenance fluid requirement according to Holiday and Segar formula
Body weight in kg Maintenance volume for 24 hours
<10kg
10-20kg
>20kg
100 ml / kg
1000+50 ml / kg
1500+20 ml / kg
For a child weighing 40 kgs, the maintenance is: 1500 + (20x20) = 1900 ml. Thismeans that


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10-20kg
>20kg
100 ml / kg
1000+50 ml / kg
1500+20 ml / kg
For a child weighing 40 kgs, the maintenance is: 1500 + (20x20) = 1900 ml. Thismeans that
the child requires 3800 ml IV fluid during 24 hours.
Indications of red cell transfusion
 Loss of blood(overt blood)-10% or more of total blood volume
 Preferably whole blood/ component to be used
 Refractory shock despite adequate fluid administration and declininghaematocrit-
replacement volume should be 10 ml/kg body wt at a time andcoagulogram should be
done.


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Common Conditions
26
 Acute self limiting illness Incubation period is of 2 to 4 days. Abrupt onset presenting
as fever with severe joint pain
 After 1– 4 days, fever subsides, there will be a afebrileperiod 3 days, fever returnswith
an itching maculopapular rash on trunk and extensor surfaces of limbs.
 Afteranother3-6 days fever subsides and there is complete recovery.
 Cripping arthropathycan occur intermittently for upto 4 months, in somecases even
upto 5 years.
 If fluid overload is present,PCV is to be given
Indications of platelet transfusion
 In general there is no need to give prophylactic platelets even atlessthan 20,000
cells/mm 3.
 Prophylacticplatelet transfusion may be given at level ofless than 10,000 cells/mm 3 in
absence of bleeding manifestations.


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cells/mm 3.
 Prophylacticplatelet transfusion may be given at level ofless than 10,000 cells/mm 3 in
absence of bleeding manifestations.
 Prolonged shock; with coagulopathy and abnormal coagulogram.
 In case ofsystemic massive bleeding, platelet transfusion may be needed in addition to
red cell transfusion.
CHIKUNGUNYA
Chikungunya is caused by an alpha virus closely related to O’ nyong – nyong virus.The main
vector isAedes aegyptimosquito.
Salient features
Non pharmacological treatment
 Mild exercises and physiotherapy may be suggested in recovering persons.
 Exposure to warm environment may be suggested
 Non weight bearing exercises
 Surgery in severely damaged joints
Pharmacological treatment
 Acute stage of illness


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 Non weight bearing exercises
 Surgery in severely damaged joints
Pharmacological treatment
 Acute stage of illness
 Treat symptomatically (Tab. paracetamol 1gm 3-4 times a day for fever, headache and
pain.)
 Avoid aspirin and steroid becauseof risk of GI side effects and Reye’s syndrome with
aspirin.
 Tab. hydroxychloroquinine 200mg orally once daily or Tab. chloroquinine phosphate
300mg per day for aperiod of 4 weeks in cases where arthralgia is refractory to other
drugs.
 Sideeffects of hydroxychloroquinine includeretinal damageand elevated liver enzymes.


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Common Conditions
27
Pulmonary tuberculosis(PTB): The most common symptom of PTB is a persistent cough
of two weeks or more, with or without expectoration.It may be accompanied by one or
more of the following symptoms,
 Fever, night sweats, weightloss
 Chest pain, hemoptysis, shortness of breath, tiredness and loss of appetite
Such patients should be selected and subjected for sputum examination. This enhances the
chances of detection of the bacilli in the smear microscopy.
Extra pulmonary tuberculosis: A person with extra-pulmonary TB may have symptoms
related to the organs affected along with constitutional symptoms stated above.
 Enlarged cervical lymph nodes with or without discharging sinuses (TB Lymphadenitis)
 Chest pain with or withoutdyspnoea in pleural TB


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 Enlarged cervical lymph nodes with or without discharging sinuses (TB Lymphadenitis)
 Chest pain with or withoutdyspnoea in pleural TB
 Pain and swelling of the joints in bone tuberculosis (fever, backache, deformity in spinal
TB).
 Signs of raised intra-cranial tension like irritability, headache, vomiting, fever, stiffness
of the neck and mental confusion in TBmeningitis
 Painless haematuria or sterile pyuria in renal tuberculosis and, infertility in genito-
urinary TB.
TUBERCULOSIS
Salient features
Investigations
 Pulmonary TB in adults (Figure6)
- Sputum smear microscopy
- Chest x-ray
- Sputum culture and drug sensitivity testing(DST) for diagnosis of Drug Resistant TB.
- Newer rapid diagnostic tools for detection of multidrug resistant(MDR) TB .


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- Newer rapid diagnostic tools for detection of multidrug resistant(MDR) TB .
- Newer tools under evaluation for diagnosis of MDR/XDR TB


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Common Conditions
28
Figure6. Algorithm for diagnosis of pulmonary tuberculosis
 Paediatric TB patients (Figure 7)
- In all children with presumptive intra-thoracic TB, microbiological confirmation
should be sought through examination of respiratory specimens (like sputumby
expectoration, gastric aspirate, induced sputum, bronchio-alveolar lavage or any other
appropriate specimen) with diagnostic test like smear microscopy or rapid molecular
test or culture.
- In the event of negative or unavailable microbiological results,a diagnosis of
probable TB in children should be based on the presence of abnormalities consistent
with TB on radiography, a history of exposure to an infectious case, evidence of TB
infection and clinical findings suggestive of TB.


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with TB on radiography, a history of exposure to an infectious case, evidence of TB
infection and clinical findings suggestive of TB.
- For children with presumptive extra-pulmonary TB, appropriate specimens from the
presumed sites of involvement should be obtained for microscopy, culture and DST,
rapid molecular test and histopathological examination.


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Common Conditions
29
Figure7. Diagnostic algorithm for pediatric pulmonary tuberculosis
 Extra-pulmonary TB
- Demonstration of AFB bacilli in a smear from extra pulmonary site is often difficult
because of low bacillary load. The clinical features pertaining to the system affected
should be considered in the diagnosis of extra pulmonary tuberculosis.
- However, the following are some of the special investigations which are helpful in
diagnosing extra pulmonary tuberculosis. These may be radiological, cytological /
pathological, biochemical and immunological (Figure8).
(a)Fine Needle Aspirations Cytology and direct smear examination
(b)Excision / Biopsy of specimen for histopathological examination
(c)Fluid for cytology , biochemical analysis and smear examination


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(b)Excision / Biopsy of specimen for histopathological examination
(c)Fluid for cytology , biochemical analysis and smear examination
(d)X -ray of the involved region
(e)Ultrasonography for abdominal tuberculosis
(f)Culture forMycobacterium tuberculosis
(g)Computerized tomography (CT) and  magnetic resonance imaging (MRI)


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Common Conditions
30
Figure8. Diagnostic algorithm for TB lymphadenitis
 Diagnosis of Pleural TB
- Tubercularpleural effusion is consideredas extra pulmonary tuberculosis. TB
Patients presenting with chest pain with or without difficulty in breathing for more
than two weeks should be referred for chest radiograph.
- In pleural effusion, chest X-ray features may include obliteration of costophrenic
angle and varying degree of effusion.
- Biochemical and cytological analysis of the aspirated pleura fluid will help in
confirming the diagnosis. Pleural fluid is generally an exudate with mainly
lymphocytes and few mesothelial cells.
- Pleural biopsy is confirmatory in a high proportion of patients.
Pharmacological treatment


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lymphocytes and few mesothelial cells.
- Pleural biopsy is confirmatory in a high proportion of patients.
Pharmacological treatment
Revised National Tuberculosis Control Programme (RNTCP) uses short course
chemotherapy given intermittently- thrice weekly underDirect Observationfor both
pulmonary and extrapulmonary tuberculosis patients.
Treatment regimens
For the purpose of treatment regimen to be used, TB patients are classified into two groups,
namely, “New” or “Previously Treated”, based on the history of previous treatment.


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Common Conditions
31
 Regimen for New cases : This regimen is prescribed to all new pulmonary (smear
positive and negative) and extra pulmonarytuberculosis.The regimen is2H 3R 3Z3 E 3 / 4
H 3R 3.
 Regimen for Previously Treated cases: This regimen is prescribed for TB patients who
have had more than onemonth anti-tuberculosis treatment previously. These patients are
at a higher risk of having drug resistance. Hence, 5 drugs are prescribed in the intensive
phase and the total duration of treatment is 8 months. Relapses, treatment after Default,
Failures and Others are treated with this regimen.The regimen is2S3H 3R3Z3 E3 / 1H3R3Z3
E3 / 5 H3R3 E3. The table below indicates the treatment regimen, type of patients and
regimens prescribed(Table 6).


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E3 / 5 H3R3 E3. The table below indicates the treatment regimen, type of patients and
regimens prescribed(Table 6).
Table 6. Treatment regimens recommended by RNTCP for treatment of Tuberculosis
Treatment
groups
Type of patient Regimen1
Intensive
Phase (IP)
Continuation
Phase (CP)
New* Sputum smear-positive
Sputum smear-negative
Extra-pulmonary
Others
2H 3R 3Z3E3 4H 3R 3
Previously
Treated**
Smear-positive relapse
Smear-positive failure
Smear-positive treatment after default
Others1
2H 3R 3Z3E3S3
/ 1H3R 3Z3E3
5H 3R 3E3
* New includes former categories I and III
** Previously treated is former category II.
1 -In rare and exceptional cases, patients who are sputum smear-negative or who have extra-
pulmonary disease can have recurrence or non-response. This diagnosis in all such cases


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pulmonary disease can have recurrence or non-response. This diagnosis in all such cases
should always be made by an MO and should be supported by culture or histological
evidence of current, active TB. In these cases, the patient shouldbe typed as ‘Others’ and
given treatment regimen for previously treated
 The number before the letters refers to the number of months of treatment. The subscript
after the letters refers to the number of doses per week.
 The dosage strengths are as follows: isoniazid (H) 600 mg, rifampicin (R) 450 mg,
pyrazinamide (Z) 1500 mg, ethambutol (E) 1200 mg, streptomycin (S) 750 mg.
 Patients who weigh 60 kg or more receive additional rifampicin 150 mg.
 Patients more than 50 years old receive streptomycin 500 mg.Patients who weigh less


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 Patients more than 50 years old receive streptomycin 500 mg.Patients who weigh less
than 30kg, receive drugs as per paediatric weight band boxes according to body weight
(Table 7).


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Common Conditions
32
Table 7. Drug dosages for adults in the blister packs
Drugs Dose
(thrice a week)
Number of tablets in blister
pack
Isoniazid (H) 600mg 2 x 300 mg
Rifampicin     (R) 450mg 1 x 450 mg
Pyrazinamide (Z) 1500mg 2 x 750 mg
Ethambutol     (E) 1200mg 2 x 600 mg
Streptomycin  (S) 0.75g -
 Treatment of Pediatric TB(Table 8, 9 and 10, Figure 9)
Pediatric cases are to be treated under RNTCP with the same thrice weekly short course
chemotherapy regimens (“New” or “Previously treated”) given under Directly Observed
Treatment Short Course (DOTS) as for adult patients.  They are to be registered in the
respective RNTCP TB Register. Pediatric patient-wise boxes are available with different
dosages under two weight bands for children weighing 6 to 10 kgand 11 to 17 kg.


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dosages under two weight bands for children weighing 6 to 10 kgand 11 to 17 kg.
Wherever possible, before a child is started on the “Previously Treated” regimen, she/he
should be examined by a pediatrician or TB expert.
Table 8. Pediatric patient wise boxes (PWB) with dosages
IP – Intensive phase,CP – Continuation phase
Table 9. Pediatric patient wise boxes (PWB) for new cases according to weight band
Weight band
For New cases Prolongation of IP
IP CP
6-10 Kg PC 13 PC 15
11-17 Kg PC 14 PC 16
18-25 Kg PC 13 + PC 14 PC 15 + PC16
26-30 kg* PC 14 x 2 PC 16 x 2
* For children weighing >30 kgs, adult PWB are tobe used
IP – Intensive phase,CP – Continuation phase
DRUGS
Product code(PC) -13 Product code(PC) -14 PC -15 PC -16
IP
24 blisters
CP
18 blisters
IP
24 blisters
CP


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DRUGS
Product code(PC) -13 Product code(PC) -14 PC -15 PC -16
IP
24 blisters
CP
18 blisters
IP
24 blisters
CP
18 blister 12 blisters 12 blisters
Isoniazid 75 mg 75 mg 150 mg 150 mg
Prolongation
of IP for PC
13
Prolongation
of IP for PC
14
Rifampicin 75 mg 75 mg 150 mg 150 mg
Pyrazinamide 250 mg 500 mg
Ethambutol 200 mg 400 mg


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Common Conditions
33
Table 10. Pediatric patient wise boxes for previously treated cases according to weight
band
Weight For previously treated cases Prolongation
of IPIP (Intensive phase) CP (Continuation phase)
6-10 Kg
(PC 13+ PC15)
+
(24 vialsInj sm*)
(PC 13 + 54 Tab E 200 mg)
+
(PC 15 without Z)
PC 15
11-17 Kg
(PC 14 + PC16)
+
(24 vialsInj sm*)
(PC 14 + 54 E  400 mg)
+
(PC 16 without Z)
PC 16
18-25 Kg
(PC 13 + PC 14 + PC 15
+ PC 16)
+
(24 vialsInj sm*)
(PC 13 + PC14 + 54 Tab E 600 mg)
+
(PC 15+ PC 16 without Z)
PC 15 + PC
16
26-30 kg
(PC 14 x 2)+ (PC 16 x 2)
+
(24 vialsInj sm*)
(PC 14 x 2+ 54 Tab E 800 mg)
+
(PC 16 x 2 without Z)
PC 16 x 2
* Injection streptomycin 15mg/kg body weight
Figure 9.Clinical monitoring of children with Tuberculosis


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Common Conditions
34
Non DOTS (ND) treatment regimen under RNTCP
In rare and exceptional situations, non-DOTS treatment (with a self-administered non-
rifampicin containing regimen) may be needed in a few TB cases. Examples include:
- Those with adverse reactions to rifampicin and / or pyrazinamide
- “New” patients who refuse DOTS despite all efforts
This is a treatment regimen of 12-month duration comprising 2 months of SHE and10
months of HE (2SHE / 10HE).Dosages administered perday in the regimen are:
Isoniazid - 300 mg
Ethambutol - 800 mg
Streptomycin - 750 mg (500 mg for those >50 years of age)
Those who weigh lessthan 30 kgreceive dosages calculated as per body-weight.
 Drug resistant tuberculosis (MDR/XDR-TB)


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Those who weigh lessthan 30 kgreceive dosages calculated as per body-weight.
 Drug resistant tuberculosis (MDR/XDR-TB)
MDR TB suspect: A patient suspected of drug-resistant tuberculosis, based on RNTCP
criteria for submission of specimens for drug-susceptibility testing.
MDR TB suspect criteria
Criteria A
- All failures of new TB cases
- Smear positive previously treated cases who remain smear positive at 4th month
onwards
- All pulmonary TB caseswho are contacts of known MDR TB case
Criteria B(in addition to Criteria A)
- All smear positive previously treated pulmonary TB cases at diagnosis
- Any smear positive follow up result in new or previously treated cases
Criteria C(in addition to Criteria B)
- All smear negative previously treated pulmonary TB cases at diagnosis,


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Criteria C(in addition to Criteria B)
- All smear negative previously treated pulmonary TB cases at diagnosis,
- HIV TB co-infected cases at diagnosis
In other words, for districts implementing MDR Suspect Criteria B, any smear-positive
diagnostic (except in a new patient) or any smear-positive follow-up result, should prompt a
referral for DST.
MDR -TB case: A TB patient whose sputum is culture positive forMycobacterium
tuberculosisand is resistantin-vitroto isoniazid and rifampicin with or without other anti-
tubercular drugs based on DST results from an RNTCP-certified culture and DST laboratory
Extensive Drug Resistant Tuberculosis(XDR TB) case: An MDR TB case whose
recovered M. tuberculosisisolate is resistant to at leastisoniazid, rifampicin, a


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recovered M. tuberculosisisolate is resistant to at leastisoniazid, rifampicin, a
fluoroquinolone (ofloxacin, levofloxacin, or moxifloxacin) and a second-line injectable anti-
TB drug (kanamycin, amikacin, or capreomycin) at a RNTCP-certified culture and DST
laboratory. A patient is confirmed to have MDR or XDR TB only when the results are from a
RNTCP quality-assured culture and DST Laboratory and by a RNTCP-endorsed testing
method mentioned as below:


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Common Conditions
35
Choice of Diagnostic Technology
Currently, the programme is scaling up the laboratory capacity of various cultureand DST
laboratories at state level IRLs and other laboratories. The choice of technology to be used for
diagnosis of MDR TB has been determined as per recommendations of the National
Laboratory Committee. Thus, for DST at certified laboratory,wherever available Molecular
DST (e.g. Line Probe Assay (LPA)) is preferred diagnostic methodbecause of the rapid and
highly-accurate rifampicin results, followed in preference by Liquid C-DST and then Solid
C -DST.
MDR Diagnostic Technology Choice
First Molecular DST (e.g. LPA DST)
Second               Liquid culture isolation and LPA DST
Third                 Solid culture isolation and LPA DST


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Second               Liquid culture isolation and LPA DST
Third                 Solid culture isolation and LPA DST
Fourth                Liquid culture isolation and Liquid DST
Fifth                   Solid cultureisolation and DST
Similarly for follow up cultures, wherever available, liquid culture will be preferred over
solid culture. However, this will be liquid cultures for at least the crucial months of follow-up
(IP-3, 4, 5, 6 and CP-18, 21, 24) and over andbeyond this, it will be determined by the
workload of individual laboratories.
Table 11. Grouping anti-TB agents (first line and second line drugs)
Grouping Drugs
Group 1: First-line oral anti-TB
agents
Isoniazid (H); Rifampicin (R); Ethambutol (E);
Pyrazinamide(Z)
Group 2: Injectable anti-TB
agents


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Group 1: First-line oral anti-TB
agents
Isoniazid (H); Rifampicin (R); Ethambutol (E);
Pyrazinamide(Z)
Group 2: Injectable anti-TB
agents
Streptomycin (S); Kanamycin (Km); Amikacin (Am);
Capreomycin (Cm); Viomycin (Vm).
Group 3: Fluoroquinolones
Ciprofloxacin (Cfx); Ofloxacin (Ofx); Levofloxacin
(Lvx);
Moxifloxacin (Mfx); Gatifloxacin (Gfx)
Group 4: Oral second-line anti-
TB agents
Ethionamide (Eto); Prothionamide (Pto); Cycloserine
(Cs);
Terizadone (Trd); para-aminosalicylic acid (PAS)
Group 5: Agents with unclear
efficacy (not recommended by
WHO for routine use in MDR-TB
patients)
Clofazimine (Cfz); Linezolid (Lzd); Amoxicillin/
Clavulanate
(Amx/Clv); thioacetazone (Thz); imipenem/cilastatin
(Ipm /Cln);
high-dose isoniazid (high-dose H); Clarithromycin (Clr)


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Clavulanate
(Amx/Clv); thioacetazone (Thz); imipenem/cilastatin
(Ipm /Cln);
high-dose isoniazid (high-dose H); Clarithromycin (Clr)
- All drugs should be given in a single daily dosage under directly observed treatment (DOT)
by a DOT Provider. All patients will receive drugs under direct observation on 6 days of the


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Common Conditions
36
week. On Sunday, the oral drugs will be administered unsupervised whereas injection
kanamycin will be omitted.
- If intolerance occurs to the drugs, ethionamide, cycloserine and PAS may be split into two
dosages and the morning dose administered under DOT. The evening dose will be self-
administered. The empty blister packs of the self-administered doses will be checked the next
morning during DOT.
- Pyridoxine should be administered to all patients on an RNTCP Category IV regimen.
Drug dosages for MDR-TB cases are base on the weight bands as shown in below(Table 12).
 Treatment of MDR TB (Category IV regimen)
- RNTCP will be using a standardised treatmenttegimen (Cat IV) for the treatment of
MDR -TB cases (and those with rifampicin resistance) under the programme.


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MDR -TB cases (and those with rifampicin resistance) under the programme.
- Cat IV regimen comprises of 6 drugs(Table 11)kanamycin, high dose levofloxacin,
ethionamide,pyrazinamide, ethambutol and cycloserine during6-9 months of the intensive
phase (IP) and 4 drugs- high dose levofloxacin, ethionamide, ethambutol and cycloserine
during the 18 months of the continuation phase (CP).
- P-aminosalicylic acid (PAS) is included in the regimen as a substitute drug in case of
intolerance i.e. severe ADR leading to discontinuation of drug to any of the drug in the Cat
IV regimen.
- For management of patients with Km mono resistance, the committee recommended
replacement of Km with capreomycin, If Km is intolerant, substitute amikacin (AK) if
possible, or PAS if injectable agent not feasible.


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replacement of Km with capreomycin, If Km is intolerant, substitute amikacin (AK) if
possible, or PAS if injectable agent not feasible.
 Drug dosages and administration
Table 12. Dosage and weight band recommendationsof second line drugs
S.No Drugs 16-25 Kgs 26-45 Kgs 46-70 Kgs
1
2
3
4
5
6
7
8
Kanamycin
Levofloxacin (High Dose)
Ethionamide
Ethambutol
Pyrazinamide
Cycloserine
PAS (80% Bioavailability)1
Pyridoxine
500 mg
250 mg
375 mg
400 mg
500 mg
250 mg
5 gm
50 mg
500 mg
750 mg
500 mg
800 mg
1250 mg
500 mg
10 gm
100mg
750 mg
1000 mg
750 mg
1200 mg
1500 mg
750 mg
12 gm
100mg
1 In case of PAS with 60% bioavailability the dose will be increased to 7 gm (16-25 Kg); 14
gm (26-45 Kg) and 16 gm (> 45 Kg)
- If a patient gains 5 kgor more in weight during treatment and crosses the weight-band


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gm (26-45 Kg) and 16 gm (> 45 Kg)
- If a patient gains 5 kgor more in weight during treatment and crosses the weight-band
range, the DOTS–Plus site committeemay consider moving the patient to the higher
weight-band drug dosages.


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Common Conditions
37
- Similarly if a patient loses 5 kgs or more in weight during treatment and crosses the
weight band the DOTS Plus site committee may consider moving the patient to the lower
weight band.
- The new higher/lower dosages are provided whenever the patient is due for the next
supply of drugs in the normal course of treatment and not as soon as change of weight is
noted.
- The dosages of 2nd line drugs for MDR TB cases in paediatric age group weighing< 16
kg as per the Table 13.
Table 13. Dosage of 2nd line drugs for treatment of pediatric MDR TB cases
Drug Daily Dose– mg/kg body weight
Kanamycin 15-30
Levofloxacin 7.5-10
Ethionamide 15-20
Cycloserine 15-20
PAS 150
Ethambutol 25
Pyrazinamide 30-40


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Drug Daily Dose– mg/kg body weight
Kanamycin 15-30
Levofloxacin 7.5-10
Ethionamide 15-20
Cycloserine 15-20
PAS 150
Ethambutol 25
Pyrazinamide 30-40
- The dosages for higher weight patients include use additional dosages of some 2nd line
drugs for MDR TB cases in patients weighing > 70 kg taking the dosage to kanamycin (1
gm), ethionamide (1 gm), cycloserine (1 gm), ethambutol (1.6 gm) and pyrazinamide (2
gm). All these are well within the maximum permissible dosage for each drug as per the
WHO guidelines.
 Treatment of XDR-TB (C ategory V)
All XDR -TB patients who are considered for category V regimen, will be screened by the
DOTS -Plus  committee and if found suitable will be referred to a thoracic surgeon for


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DOTS -Plus  committee and if found suitable will be referred to a thoracic surgeon for
consideration of surgery to improve the treatment outcomes. Identification must be done for
the site (tertiary centres) with such surgical facilities.
XDR Regimen (Table 14)
6-12 months Cm, PAS, Mfx, High dose‐H, Cfz, Lzd, Amx/Clv
18 months PAS, Mfx, High dose‐H, Cfz, Lzd, Amx/Clv
- The Category V treatment regimen consists of 7 drugs, with 2 reserve/substitute drugs.
The dosage of the drugs would vary as per the weight of the patient(≤ 45Kg or > 45Kg).
All drugs are to be given on a daily basis. Injections of capreomycin will be given for 6
days/week (not on Sundays).


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Common Conditions
38
- All morning doses are to be supervised by the DOT Provider except on Sundays. After
taking DOT for morning doses onSaturday, next day medicines would be given to the
patient to be taken at home on Sunday.
- Empty blisters of medicines taken unsupervised in evening and on Sundays are to be
collected by DOT Provider.
- The change from IP to CP will be done only after achievement of culture conversion i.e.
2 consecutive negative cultures taken at least one month apart. In case of delay in culture
conversion, the IP can be extended from6 months up to a maximum of 12 months. In
case of extension, the DOTS– Plus site Committee, which will beresponsible for
initiating and monitoring the Category V regimen, can decide on administering


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initiating and monitoring the Category V regimen, can decide on administering
capreomycin injection intermittently (3 times/week) for the months 7 to 12.
Table 14. Drugs and Dosages for management of XDR TB
Drugs Dosage/day
< 45 Kgs > 45 Kgs
Inj. Capreomycin (Cm) 750 mg 1000 mg
PAS 10 gm 12 gm
Moxifloxacin (Mfx) 400 mg 400 mg
High dose INH (High dose-H) 600 mg 900 mg
Clofazimine (Cfz) 200 mg 200 mg
Linezolid (Lzd) 600 mg 600 mg
Amox iclav(Amx/Clv) 875/125 mg BD 875/125 mg BD
Pyridoxine 100 mg 100 mg
Reserve/Substitute drugs
Clarithromycin (Clr) 500 mg BD 500 mg BD
Thiacetazone (Thz)# 150 mg 150 mg
# Depending on availability, not to be given to HIV positive cases
The reserve/substitute drugs would be usedin the following conditions:


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# Depending on availability, not to be given to HIV positive cases
The reserve/substitute drugs would be usedin the following conditions:
- In case the patient was on PAS in Category IV, PAS will be replaced with one of
the reserve drugs in the Category V regimen
- If the patient is unable to tolerate one or more of the drugs
- If the patient is found to be resistant to capreomycin
 HIV co-infection with TB
- TB patients living with HIV should receive the same duration of TB treatment with
daily regimen as HIV negative TB patients.
- Antiretroviral therapy (ART) must be offered to all patients with HIV and TB as well
as drug-resistant TB requiring second-line anti-TB drugs, irrespective of CD4 cell-
count, as early as possible (within the first 8 weeks) following initiation of anti-TB


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count, as early as possible (within the first 8 weeks) following initiation of anti-TB
treatment. Appropriate arrangements for access to antiretroviral drugs should be made


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Common Conditions
39
for patients. However, initiation of treatment for TB should not be delayed. Patients
with TB and HIV infection should also receive co-trimoxazole as prophylaxis for
other infections.
- People living with HIV should be screened for TB using four symptom complex
(current cough or, fever or weight loss or night sweats) at HIV care settings and those
with any of these symptoms should be evaluated for ruling out active TB. Such
patients in whom active TB is ruled out, Isoniazid Preventive Therapy (IPT) in the
dosage of10 mg/Kg body weight should be offered to them for 6 months.
 Adherence
- Supervision and support should be individualized.
- Ensuring Adherence in M/XDR TB patients: Patient support systems, including direct


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 Adherence
- Supervision and support should be individualized.
- Ensuring Adherence in M/XDR TB patients: Patient support systems, including direct
observation of treatment, are required to ensure adherence. It should be ensured that
the patient consumes all the dosages of the drugs.
- Trained treatment supporter for treatment adherence: Such measures may include
identification and training of a treatment supporter (for TB and, if appropriate, for
HIV, diabetes mellitus etc.) who is acceptable, accessible and accountable to the
patient and to the health system.
- Information Communication Technology to promote treatment literacy and
adherence: Optimal use of Information Communication Technology (ICT) should be
done to promote treatment literacy and adherence


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adherence: Optimal use of Information Communication Technology (ICT) should be
done to promote treatment literacy and adherence
Other important points to remember
 Public Health Responsibility- Any practitioner treating a TB patient is assuming an
important public health responsibility to prevent ongoing transmission of the infection
and the development of drug resistance. To fulfill this responsibility the practitioner must
not only prescribe an appropriate regimen, but also utilize local public health services /
community health services, and other agencies including NGOs whennecessary, to assess
the adherence of the patient and to address poor adherence when it occurs.
 Maintain Records for all TB patients:A written record of all medications given,


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 Maintain Records for all TB patients:A written record of all medications given,
microbiological response and adverse reactions should be maintained for all patients.
Every patient’s clinical outcome should be recorded in the case register and available for
public health monitoring.
 Notification of TB Cases: All health establishments must report all TB cases and their
treatment outcomes to public health authorities (District Nodal Officer for Notification).
Proper feedback need to be ensured to all health care providers who refer cases to public
health system on the outcome of the patients which they had referred.
 Contact Investigation:
All providers of care for patients with TB should ensure all household contacts (including


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 Contact Investigation:
All providers of care for patients with TB should ensure all household contacts (including
children) and other persons who are in close contact with TB patients are screened for TB
as per defined diagnostic standards.


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Common Conditions
40
In case of pediatric TB patients, reverse contact tracing for search of any active TB case in
the household of the child must be undertaken.
The highest priority contacts of known TB cases for intensive case finding (such as are:
- Persons with symptoms suggestive of TB
- Children aged <6 years
- Known or suspected immune-compromised patient, particularly HIV infection.
- Diabetes Mellitus
- Other higher risks including pregnancy, mental disorders, smokers and alcoholics etc.
- Patients with DR-TB - In case of contact with a DR-TB index case, close clinical
mo nitoring should be provided, as there is no evidence that treatment of latent
infection with available drugs is presently effective
Follow up
Follow up smear and culture schedule during treatment


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infection with available drugs is presently effective
Follow up
Follow up smear and culture schedule during treatment
- For follow up examination two sputum specimens will be collected and examined by
smear and culture at least 30 days apart from the 3rd to 7th month of treatment (i.e. at
the end of the months 3, 4, 5, 6 and 7) and at 3-monthly intervals from the 9th month
onwards till the completion of treatment (i.e. at the end ofthe months 9, 12, 15, 18, 21
and 24).
- The two specimens for smear and culture at the RNTCP accredited lab (one early
morning and one supervised spot) will be collected and transported from the
respective DTC to the RNTCP accredited laboratory.
- If any ofthe cultures in the last three quarters becomes positive, it will be followed up


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respective DTC to the RNTCP accredited laboratory.
- If any ofthe cultures in the last three quarters becomes positive, it will be followed up
by monthly cultures in the following 3 months.
Table 15. Common adverse effects of 2nd line drugs and management strategies
Adverse effects Suspected agent(s) Suggested management strategies
Gastrointestinal
Nausea and
vomiting
PAS, isoniazid, moxifloxacin
linezolid, clofazamine
amoxyclav, alarithromycin
thioacetazone
 Assess for dehydration; initiate rehydration
if indicated
 Initiate anti-emetic therapy
 Discontinue suspected agent if this can be
done without compromising regimen–
rarely necessary
Gastritis
PAS, moxifloxacin
isoniazid, linezolid
amoxiclav, clarithromycin
thioacetazone
 H2 -blockers, proton-pump inhibitors, or
antacids


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Gastritis
PAS, moxifloxacin
isoniazid, linezolid
amoxiclav, clarithromycin
thioacetazone
 H2 -blockers, proton-pump inhibitors, or
antacids
 Stop suspected agent(s) for short periods of
time (e.g., one to seven days)
 Lower dose of suspected agent, if this can
be done without compromising regimen
 Discontinue suspected agent if this can be
done without compromising regimen
Hepatitis Isoniazid, PAS, moxifloxacin
linezolid
 Stop all therapy pending resolution of
hepatitis


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Common Conditions
41
 Eliminate other potential causes of hepatitis
 Consider suspending most likely agent
permanently. Reintroduce remaining drugs,
one at a time with the most hepatotoxic
agents last, while monitoring liver function
Cutan eous and hypersensitivity reactions
HypersensitivityPAS, linezolid,
clarithromycin
 Withhold all drugs and treat
symptomatically with antihistamines/
steroids till the reaction subsides.
 Identify offending drug in severe forms
 Attempt desensitization ofthe offending
drug
 Discontinue suspected agent and substitute
with the reserve drug
Cutaneous Linezolid,
clofazamine
 Treat symptomatically with antihistamines
till the reaction subsides.
 Patient should be counseled on the skin
discoloration with long term use of
clofazamine
Psychiatric


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till the reaction subsides.
 Patient should be counseled on the skin
discoloration with long term use of
clofazamine
Psychiatric
Depression
Socio-economic
circumstances,
chronic disease,
moxifloxcin,
isoniazid
 Improve socioeconomic conditions
 Group or individual counseling
 Initiate antidepressant therapy
 Lower dose of suspected agent if this canbe
done without compromising the regimen
 Discontinue suspected agent if this can be
done without compromising regimen
Neurological
Peripheral
neuropathy
Isoniazid, linezolid
 Increase pyridoxine to maximum daily dose
(200 mg per day)
 Initiate therapywith tricyclic
antidepressants such as amitriptyline. Non-
steroidal anti-inflammatory drugs or
acetaminophen may help alleviate
symptoms
 Lower dose of suspected agent, if this can


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steroidal anti-inflammatory drugs or
acetaminophen may help alleviate
symptoms
 Lower dose of suspected agent, if this can
be done without compromising regimen
 Discontinue suspected agent if this can be
done without compromising regimen
Convulsions Isoniazid, moxifloxacin,
linezolid
 Suspend suspected agent pending resolution
of convulsions
 Initiate anticonvulsant therapy (e.g.
phenytoin, valproic acid)
 Increase pyridoxine to maximum daily dose
(200 mg per day).
 Restart suspected agent or reinitiate
suspected agent at lower dose, if essential to
the regimen


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Common Conditions
42
 Discontinue suspected agent if this can be
done without compromising regimen
Hearing loss Capreomycin
clarithromycin
 Document hearing loss and compare with
baseline audiometry if available
 Change parenteral treatment to
capreomycin if patient has documented
susceptibility to capreomycin
 Increase frequency and/or lower dose of
suspected agent if this can be done without
compromising the regimen(consider
administration three times per week)
 Discontinue suspected agent if this can be
done without compromising the regimen
Ocular Linezolid In consultation with the ophthalmologist
Musculoskeletal
Arthralgia Moxifloxacin
 Initiate therapy with non-steroidal anti-
inflammatory drugs.
 Lower dose of suspected agent, if this can
be done without compromising regimen.


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 Initiate therapy with non-steroidal anti-
inflammatory drugs.
 Lower dose of suspected agent, if this can
be done without compromising regimen.
 Discontinue suspected agent if this can be
done without compromising regimen
Musculoskeletal Moxifloxacin In consultation with the orthopedician
Haematological
Haematalogic Capreomycin, PAS,
linezolid, clarithromycin
Monitor for anemia, bleeding tendency and cell
counts
Renal
Renal toxicity
Capreomycin
linezolid
clarithromycin
 Discontinue suspected agent
 Consider using capreomycin if an
aminoglycoside had been the prior
injectable in regimen
 Consider dosing 2 to 3 times a week if drug
is essential to the regimen and patient can
tolerate (close monitoring of creatinine)
 Adjust all TB medications according to the
creatinine clearance


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tolerate (close monitoring of creatinine)
 Adjust all TB medications according to the
creatinine clearance
Met abolic and Electrolytes
Metabolic and
electrolyte
Capreomycin, linezolid
moxifloxacin
Periodic monitoring of serum electrolytes and
blood sugar
Endocrine
Thyroid
dysfunction PAS Supplement with thyroxine
Cardiovascular
QT prolongation Moxifloxacin, clarithromycin  Monitor for QT prolongation, monitor
platelet count, bleeding tendencies


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Common Conditions
43
 Chemoprophylaxis of contacts of MDR-TB cases
Among contacts of patients with MDR-TB, the use of isoniazid may reasonably be
questioned. Although alternative prophylaxis treatments have been suggested, there is no
consensus regarding the choice of the drug(s) and the duration of treatment. Prompt
treatment of MDR-TB is the most effective way of preventing the spread of infection to
others. The following measures should be taken to prevent spread of MDR-TB infection:
- Early diagnosis and appropriate treatment of MDR-TB cases;
- Screening of contacts as per RNTCP guidelines
- Further research into effective and non-toxic chemoprophylaxis in areas of high
MDR -TB prevalence.
Patient education


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- Further research into effective and non-toxic chemoprophylaxis in areas of high
MDR -TB prevalence.
Patient education
- Providing counseling and health education to the MDR-TB patient and their family
members about the disease and about the necessity of taking regular and adequate
treatment is of utmost importance.
- Health education and counseling is provided to all patients and family members at
different levels of health care, right from one at the periphery to those at the DOTS-Plus
site facility. It is started at the initial point of contact and carried on a continuous basis at
all visits by the patientto a health facility. The counseling and motivation is required to
be done not only of the patient but also of the family members.
EPILEPSY


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be done not only of the patient but also of the family members.
EPILEPSY
A seizureis a paroxysmal event due to abnormal excessive or synchronous neuronal activity
in the brain.Epilepsydescribes a condition in which a person hasrecurrentseizures due to a
chronic, underlying process.
Classification of Seizures
 Generalized seizures
Tonic clonic, clonic, tonic, absence (typical/ atypical), atonic and myoclonic
May be focal, generalized, or unclearepileptic spasms
 Focal seizures(can be further described as having motor, sensory, autonomic, cognitive,
or other features)with andwithout dyscognitivefeatures
Investigations
It should be made sure that the patient had a seizure and other differentials should be ruled


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Investigations
It should be made sure that the patient had a seizure and other differentials should be ruled
out.  In the patient with prior seizures or a known history of epilepsy, the evaluation is
directed toward (1) underlying cause and precipitating factors (2) adequacy of current
therapy.
Pharmacological treatment
 Treatment of underlying conditions
- Metabolic imbalancessuch as abnormal serum electrolytes and glucose, medications
(theophylline), illicit drug use (e.g., cocaine),structural CNS lesion such as a brain
tumor, vascular malformation, or brain abscess.


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Common Conditions
44
 Av oidance ofprecipitating factors like sleep deprivation, alcohol, bright light, etc.
 Antiepilepticdrug therapy mainstay of treatment for most patients with epilepsy.
Table 16.Selection of antiepileptic drugsaccording to classification of epilepsy
Gene ralized tonic
clonic seizures Focal seizures Typical absence
seizures
Atypical absence,
myoclonic and atonic
seizures
First line drugs
Valproic acid Lamotrigine Valproic acid Valproic acid
Lamotrigine Capbamazepine Ethosuximide Lamotrigine
Topiramate O xcarbazepine Topiramate
Phenytoin
Levetiracetam
Alternatives
Zonisamide Topiramate Lamotrigine Clonazepam
Phenytoin Zonisamide Clonazepam Felbamate
Capbamazepine Valproic acid
Oxcarbazepine Tiagabine
Phenobarbitone Gabapentin
Primidone Lacosamide


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Phenytoin Zonisamide Clonazepam Felbamate
Capbamazepine Valproic acid
Oxcarbazepine Tiagabine
Phenobarbitone Gabapentin
Primidone Lacosamide
Felbamate Phenobarbitone
Primidone
Felbamate
Pregnancy
 Most women with epilepsy who become pregnant will have an uncomplicated gestation
and deliver a normal baby. Since the potential harm of uncontrolled convulsive seizures
on the mother and fetus is considered greater than the teratogenic effects of antiepileptic
drugs, it is currently recommended that pregnant women be maintained on effective drug
therapy. Patients should take folic acid(1–4 mg/d), to prevent development ofneural tube
defects.
Contraception
 Drugs such as carbamazepine, phenytoin, phenobarbital, and topiramate can significantly


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defects.
Contraception
 Drugs such as carbamazepine, phenytoin, phenobarbital, and topiramate can significantly
decrease the efficacy of oral contraceptives via enzyme induction and other mechanisms.
Patients should be advised to consider alternative forms of contraception.


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Common Conditions
45
STATUS EPILEPTICUS
Status epilepticus refers to continuous seizures or repetitive, discrete seizures with impaired
consciousness in the interictal period. The duration of seizure activity sufficient to meet the
definitionof status epilepticus has traditionally been specified as 15–30 minutes.The
treatment plan for an adult with status epilepticus is as in Figure 10.
Figure 10. Treatment algorithm for generalized tonic clonic status epilepticus in adults


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Common Conditions
46
 Burning micturition, urinary frequency, flank pain, fever
 Predisposing factors are diabetes mellitus, large prostate, and circumcision.
 Common organisms areE.coli, Pseudomonas, Klebsiella.
URINARY TRACT INFECTION
Urinary tract infections include infection of any part of urinary tract from kidneys to urethra.
It can be caused by unhygenic lifestyle, sexually transmitted, per urethral catheterization,
renal calculus disease and vesicoureteric reflux.
Salient features
Investigations
 TC with DC,X -ray KUB ,USG -KUB ,Urine (routine and microbiological examination)
 Urine culture and sensitivityto be done if bacterial colony count is more than1000.
Non pharmacologicaltreatment
Plenty of fluids orally, maintain hygiene
Pharmacologicaltreatment


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Non pharmacologicaltreatment
Plenty of fluids orally, maintain hygiene
Pharmacologicaltreatment
 Tab.ciprofloxacin 500 mg twice a day for five days.
 In resistance cases 3rd generation cephalosporins (cefixime) followed by antibiotics as per
culture and sensitivity report.
 If fever then Tab. paracetamol 500 mgthrice a day for three days.


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47
Chapter 3
EMERGENCY CONDITIONS
CARDIOPULMONARY RESU SCITATION
Cardiopulmonary resuscitation (CPR) consists of a series of maneuvers by which oxygenated
blood supply to brain and vital organs is maintained during cardiopulmonary arrest (CPA) i.e.
cessationof respiration and circulation. In children, CPA is not sudden but end result of long
period of hypoxaemia secondary to inadequate ventilation, oxygenation or circulation. Therefore,
prompt management of these is essential to prevent CPA, the outcome of which is poor.
Diagnosis of cardiopulmonary and cardiac arrest
1. Absence of pulse in major arteries (carotid or femoral in older children and
femoral or brachial in infants as carotid is difficult to palpate due to short neck).
2. Absence of heart sounds on auscultation.


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femoral or brachial in infants as carotid is difficult to palpate due to short neck).
2. Absence of heart sounds on auscultation.
3. Asystole /ventricular fibrillation on ECG.
Respiratory arrest
Absence of respiration on examination (absent chest movements), listening (absent air flow on
bringing ears in front of mouth) and feeling (absent air flow on keeping hands in frontof mouth
or nose).
Levels of CPR
Basic life support (BLS):The elements of CPR areprovided without additional equipment.
Skill and speed are most essential.
Advanced cardiac life support (ACLS):Use of equipment and drugs for assisting ventilation
orcirculation.
Primary survey to assess the patient's condition:
 Tap the patient on the shoulder and ask, "Are you all right?"


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orcirculation.
Primary survey to assess the patient's condition:
 Tap the patient on the shoulder and ask, "Are you all right?"
 If the patient does not respond, call for help.
 Give 2 minutes (5 cycles) of CPR before leaving patient to call for help.
 Check forpulse or any other signs of life;begin CPR, 30 compressions to 2 respirations
(push hard and fast--100/minuteand release chest completely).
 Open airway and check for breathing. Give 2 breaths that make the chest rise.
 Start an IV line.
 Begin oxygen.
 Attach a monitor
 Intravenous / Intra osseous (IO) access is a priority over advanced airway management. If an
advanced airway is placed, change to continuous chest compressions without pauses for
breaths. Give 8 to 10 breaths per minute and check rhythm every2 minutes.


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Emergency Conditions
48
CHART
SIMPLIFIED ADULT BLS
Source 2010 American Heart Association  Guidelines


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Emergency Conditions
49
ADULT BLS HEALTHCARE PROVIDERS
Source 2010 American Heart Association   Guidelines


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Emergency Conditions
50
AHA ACLS ADULT CARDIAC ARREST ALGORITHM
Source 2010 American Heart Association   Guidelines


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Emergency Conditions
51
AHA ACLS ADULT CARDIAC ARREST ALGORITHM
Source 2010 American Heart Association   Guidelines


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Emergency Conditions
52
ANAPHYLAXIS
It is a generalized hypersensitivity reaction characterized by hypotension, peripheral
circulatory collapse and respiratory difficulty in the form of stridor and dyspnoea.
Anaphylaxis can be due to food, inhaled/ingested allergens or drugs. Symptoms occur
instantaneously or within a few minutes following exposure to the offending agent.
Anaphylaxis to oral drugs may take 1-2 hours, but in many patients it can be instantaneous. A
severe anaphylactoid reaction is a life-threatening emergency. Effective treatment depends on
prompt diagnosis and rapid supplementation of appropriate therapy.
Clinical criteria for diagnosis
Anaphylaxis is highly likely when any one of the following three criteria is fulfilled:


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Clinical criteria for diagnosis
Anaphylaxis is highly likely when any one of the following three criteria is fulfilled:
1. Acute onset of an illness (minutes to several hours) with involvement of the skin, mucosal
tissue, or both (e.g., generalized urticaria, itching or flushing, swollen lips/tongue/uvula)
with one of the following,
 Respiratory compromise (e.g., dyspnoea, wheeze-bronchospasm, stridor, reduced
peak expiratoryflow (PEF),hypoxemia)
 Reduced blood pressure or associated symptoms of end-organ dysfunction (e.g.
hypotonia, collapse, syncope, incontinence)
 Involvement of the skin-mucosal tissue
 Persistent gastrointestinal symptoms (e.g., crampingabdominal pain, vomiting) or
2. R educed blood pressure after exposure to known allergen,


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 Persistent gastrointestinal symptoms (e.g., crampingabdominal pain, vomiting) or
2. R educed blood pressure after exposure to known allergen,
 Infants and children- low systolic blood pressure (age-specific) or greater than 30%
decrease in systolic blood pressure
 Adults- systolic blood pressure of less than 90 mm Hg or greater than 30% decrease
from baseline


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Emergency Conditions
53
Skin, subcutaneous tissue, and mucosa
 Flushing, itching, urticaria (hives), angioedema, morbilliform rash, piloerection
 Periorbital itching, erythema and edema, conjunctival erythema, tearing
 Itching of lips, tongue, palate, and external auditory canals; and swelling of lips, tongue,
and uvula
 Itching of genitalia, palms, and soles
Respiratory
 Nasal itching, congestion, rhinorrhea, sneezing
 Throat itching and tightness, dysphonia, hoarseness, stridor, dry staccato cough
 Lower airways: increased respiratory rate, shortness of breath, chest tightness, deep cough,
wheezing/bronchospasm, decreased peak expiratory flow
 Cyanosis,respiratory arrest
Gastrointestinal
 Abdominal pain, nausea, vomiting (stringy mucus), diarrhea, dysphagia
Cardiovascular system


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 Cyanosis,respiratory arrest
Gastrointestinal
 Abdominal pain, nausea, vomiting (stringy mucus), diarrhea, dysphagia
Cardiovascular system
 Chest pain
 Tachycardia, bradycardia (less common), other arrhythmias, palpitations
 Hypotension, feeling faint, urinary orfecal incontinence, shock
 Cardiac arrest
Central nervous system
 Aura of impending doom, uneasiness (in infants and children, sudden behavioral change,
e.g. irritability, cessation of play, clinging to parent); throbbing
 H eadache (pre-epinephrine), alteredmental status, dizziness, confusion, tunnel vision
Salient features
Non pharmacological treatment
 Remove exposure to trigger if possible (discontinue intravenous diagnostic or therapeutic


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Salient features
Non pharmacological treatment
 Remove exposure to trigger if possible (discontinue intravenous diagnostic or therapeutic
agent that seems to triggering symptoms). Place the patient supine and elevate the
extremities.
 Ob serve vital signs frequently and if possible, monitor electrocardiogram and pulse
oximetry.
 For severe anaphylaxis with shock, initial management should be directed at the ABC of
resuscitation, namely maintenance of adequate airway- suction, breathing, and
circulation. If working alone, call for assistance.
Pharmacological treatment
 Inj. adrenaline 1:1000 (1mg/ml), 0.01 ml/kg (maximum 0.3 ml in children and 0.5 ml in
adults) IM (mid anterolateral aspect of thigh). If necessary, dose can be repeated every15
minutes.


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Emergency Conditions
54
 If the anaphylaxis is due to an allergen extract or to a hymenoptera sting intoan
extremity, half the dose of adrenaline can be infiltrated locally, subcutaneously after
dilution with 2 ml saline.
 High flow oxygen (4-6 lit/min by face mask ororopharyngeal airway).
 Establish two wide bore intravenous lines. Commence rapid fluid resuscitation with Inj.
NS (0.9% normal saline) at rate of 5-10 ml/kg in 5 to 10 minutes. One to two litres of
fluid bolus can be given.
 Intubate and commence intermittent positive pressure ventilation if severe laryngeal
obstruction, bronchospasm, circulatory shock or coma.
 If no response to the initial intramuscular dose of adrenaline, administer adrenaline 5


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obstruction, bronchospasm, circulatory shock or coma.
 If no response to the initial intramuscular dose of adrenaline, administer adrenaline 5
mcg/kg slowly in to the intravenous line. Repeat at 5 minutes intervals depending on
response. If the patient remains in shock, start an adrenaline infusion (preferably via a
central venous line), commencingat0.1 mcg/kg/min in children and 0.2 mcg/kg/min in
adults with titration required to restore blood pressure. Large doses of adrenaline may
be needed.
 Commence cardiopulmonary resuscitation, if necessary.
 If the only manifestation of anaphylaxis is urticaria or angioedema, initial IM dose of
adrenaline should be given in addition to antagonists. If no other manifestation, patient


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adrenaline should be given in addition to antagonists. If no other manifestation, patient
can be kept under observation for at least 12 hours and then discharged.
Additional measures
 IV infusion of chlorpheniramine 10 mg (adult), 2.5-5 mg (child) or diphenhydramine 25-
50 mg (adult) (1 mg/kg, maximum 50 mg [child]).
 Inj. salbutamolsolution, 2.5to 5mg/3 mlgiven by nebulizer and face mask.
 IV hydrocortisone infusion 200 mg (adult), maximum 100 mg (child); or
methylprednisolone 50-100 mg (adult); 1 mg/kg, maximum 50 mg (child).
Supportive treatment
All patients with severe anaphylactic reaction must be hospitalized. Patients who remain
clinically unstable after initial resuscitation should be admitted tointensivecare unit (ICU).


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clinically unstable after initial resuscitation should be admitted tointensivecare unit (ICU).
Patientsrespondingto the initial treatmentshould be observed forpossible late reaction.
Patient education
To check and look for the cause (food, drugsetc.) and to avoid it in future
ACUTE AIRWAY OBSTRUCTION
The cause of acute airway obstruction can be underlying malignancy, abscess, laryngeal cyst
or laryngocele. It is necessary to assess the severity of the condition before initiating the
treatment.
Emergency treatment
 Head extension with lower jaw thrust forward
 Suctioning for clearing secretions


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Emergency Conditions
55
 Ventilatory mask with 100% oxygen
 Endotracheal intubation or tracheostomy
In stable patient
 Plain X-ray neck
 Fibre optic endoscopy / micro-laryngoscopy / bronchoscopy to find out the cause
Treatment guidelines
Assess Severity of airway
Portableradiographic ultrasonography
ECG m onitoringand supplemental oxygen
Pulse oximetry,blood pressure
Cricothyrotomy Tracheostomy
Emergency intubation
STRIDOR
Stridor is noisy, harsh and difficult breathing due to obstruction of the airway. It is classified
inspiratory, expiratory and biphasic type. Inspiratory stridor occurs due to an obstruction at or
above the level of vocal cords. Expiratory stridor is due to obstruction at bronchiolar level


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above the level of vocal cords. Expiratory stridor is due to obstruction at bronchiolar level
such as bronchial asthma while biphasic stridor occurs in tracheal and subglottic stenosis. In
children the stridor of laryngo-tracheo-bronchitis has a crowing quality and is called ‘Croup’.
Salient features
Pharmacologicaltreatment
 Humidified oxygen
 Inj. hydrocortisone 100 mgIV stat and can be repeated as required.
 Inj. ampicillin 500mgQID IV/for5-7 days
 Inj. adrenaline 0.2-0.5mg subcutaneously if necessary.
• Restlessness, anxiety and distress, labored/ noisy breathing, predominantly on
inspiration
• Difficulty in swallowing and speaking
• In children: cyanosis, chest retraction, tachypnea, altered level of consciousness,
feeding difficulties


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Emergency Conditions
56
SHOCK
Shock is defined as a circulatory insufficiency that creates an imbalance between tissue
oxygen supply and demand.
Classification and causes of shock
1. Haemorrhagic shock
 Traumatic– blunt or penetrating injury, fractures of long bones and pelvis
 Non -traumatic- GI bleeds (e.g. peptic ulcer, gastric mucosalerosions, oesophageal
varices, typhoid bleeds,disseminatedintravascular coagulation (DIC),aortic
dissection, rupture of aneurysmof a large vessel
2. Hypovolaemic shock
 Fluid loss from vomiting and/or diarrhoea e.g.in cholera, other GI infections
 Fluid loss in diabetes mellitus, adrenal insufficiency, excessive sweating, exfoliative
dermatitis, diabetes insipidus, reaccumulation of ascites after tapping


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dermatitis, diabetes insipidus, reaccumulation of ascites after tapping
 Sequestration of fluid e.g. in intestinal obstruction, pancreatitis, burns, crush injuries
3. Cardiogenic shock
 Acute myocardial infarction
 Cardiomyopathy, cardiac arrhythmias
 Mechanical causes e.g. valvular disease, outflow tract obstruction, ruptured
ventricular septum
4. Distributive or vasogenic (relative hypovolaemia)
 Septic shock; toxic shock syndrome
 Anaphylactic
 Neurogenic
Shock is a progressive disorder, if untreated can lead to severe haemodynamic and metabolic
deterioration causing multi-organ failure. Stages of shock can be arbitrarily classified as:
 Early compensated shock-Vital organ function is maintained by intrinsic compensatory


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 Early compensated shock-Vital organ function is maintained by intrinsic compensatory
mechanisms. Blood pressure is usually normal, there is increasing tachycardia and
hypotension. The skin is cold and clammy, increased capillary refill time (>3 sec). If there
is delay in treatment it may-lead to decompensated shock.
 Decompensated shock - There is fall in blood pressure and cardiac output. Features of
peripheral poor perfusion are compounded with manifestations of vital organ impairment.
Patient may have alteration of mentation (impaired cerebral perfusion), oliguria (renal
hypoperfusion) and myocardial ischaemia (coronary flow impairment). Patient has
acrocyanosis, cold and damp extremities and a pale look. If untreated, progress to
irreversible state of shock.


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acrocyanosis, cold and damp extremities and a pale look. If untreated, progress to
irreversible state of shock.
 Irreversibleshock is a term applied to the clinical situation in which even
haemodynamic correction does not halt the progressive organ failure.


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Emergency Conditions
57
 Tachycardia, blood pressure may be normal or elevated due to compensatory
mechanisms, later falls as cardiovascular compensation fails. Neck veins may be
distended or flattened, depending on the etiology of shock. Decreased coronary
perfusion pressures can lead to ischemia, decreased ventricular compliance, and
increased left ventricular diastolic pressure and pulmonary edema.
 Tachypnea, increased minute ventilation, and increased dead space are common.
Bronchospasm, hypocapnia with progression to respiratory failure, and adult
respiratory distress syndrome can be seen.
 Skin pale, dusky, clammy skin with cyanosis, sweating, altered temperature, and
decreased capillary refill, oliguria.
Salient features
Treatment
 Start oxygen 4-6 L/min


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decreased capillary refill, oliguria.
Salient features
Treatment
 Start oxygen 4-6 L/min
 Airway control, endotracheal intubation
 Adequate venous access. Large-bore peripheral intravenous catheters for adequate fluid
resuscitation.Central venous accessmay be necessary for monitoring and employing
pulmonary artery catheters, venous pacemakers, and long-term vasopressor therapy.
 Volume replacement. Isotonic, intravenous crystalloid fluids (0.9%NaCl, Ringer’s
lactate) are preferred for the initial resuscitation phase. Initial bolus volume is 20 to 40
m l/kg over 10 to 20 min (rapid infusion). Colloids (dextran, hetastarch, etc.) can be used
till blood is available.
 Blood is the ideal resuscitative fluid for hemorrhagic shock or in the presence of


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till blood is available.
 Blood is the ideal resuscitative fluid for hemorrhagic shock or in the presence of
significant anemia. Fully cross-matched blood is preferred, but if more rapidintervention
is required, type specific or type O negative blood may be employed. The decision to use
platelets or fresh frozen plasma (FFP) should be based on evidence of impaired
hemostasis and on frequent monitoring of coagulation parameters. Plateletsare generally
given if there is ongoing hemorrhage and the platelet count is 50,000 or less; FFP is
indicated if the prothrombin time is prolonged more than 1.5 times.
 Vasopressors should be used if there is persistent hypotension after adequate volume
resuscitation. Inj. dobutamine 2.0 to 20.0 µg/kg/min for systolic BP over 100 mmHg,


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resuscitation. Inj. dobutamine 2.0 to 20.0 µg/kg/min for systolic BP over 100 mmHg,
dopamine 2.5 to 20.0 µg/kg/min for systolic BP 70 to 100 mmHg, andInj.norepinephrine
0.5 to 30.0 µg/min for systolic BP under 70 mmHg.
 Acidosis should be treated with adequate ventilation and fluid resuscitation. Use of
sodium bicarbonate (1 meq/kg) is controversial. If it is used, it is given only in the setting
of severe acidosis refractory to ventilation and fluid resuscitation.
 Early surgical or medical consultation for admission or transfer as indicated.


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Emergency Conditions
58
Monitoring
Special care in ICUshould be takenby careful and continuous monitoring of BP, pulse rate
and respiratory rate, urine output and mental status frequently. Sedated patients should be
allowed to awaken ("drugholiday") daily to assess their neurologic status and to shorten
duration of ventilator support.
Management guidelines for common causes of shock
Hemorrhagic Shock
 Ensure adequate ventilation/oxygenation
 Provide immediate control of hemorrhage (e.g., traction for long bone fractures, direct
pressure)
 Initiate judicious infusion of isotonic crystalloid solution (10–20 ml /kg) or colloid
solution
 With evidence of poor organ perfusion and 30-minute anticipated delay to hemorrhage
control, begin packed red blood cell (PRBC) infusion (5–10 ml/kg)


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control, begin packed red blood cell (PRBC) infusion (5–10 ml/kg)
 Treat coincident dysrhythmias (e.g., atrial fibrillation with synchronized cardioversion)
Cardiogenic Shock
 Ameliorate increased work of breathing; provide oxygen and positive end-expiratory
pressure (PEEP) for pulmonaryedema
 Begin vasopressor or inotropic support; Inj. norepinephine (0.5 µg/min) and Inj.
dobutamine (5 µg/kg/min)
 Seek to reverse the insult (e.g., initiate thrombolysis, arrange percutaneous transluminal
angioplasty)
 Consider intra-aortic balloon pump counterpulsation for refractory shock
Septic Shock
 Ensure adequate oxygenation
 Administer 20 ml/kg of crystalloid (0.9% normal saline or RL) or 5 ml/kg of colloid


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Septic Shock
 Ensure adequate oxygenation
 Administer 20 ml/kg of crystalloid (0.9% normal saline or RL) or 5 ml/kg of colloid
(hemaccel or hetastarch), and titrate infusion to adequate central venous pressure and
urine output
 Begin antimicrobial therapy; attempt surgical drainage or débridement
 Begin packedRBC infusion for hemoglobin < 8 g/dL
 If volume restoration fails to improve organ perfusion, begin vasopressor support; initial
choice includes dopamine infusion at 5–15 µg/kg/min
FLUID AND ELECTROLYTE IMBALANCE AND REPLACEMENT (IN ADULTS)


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59
Disturbances in fluid and electrolyte balance occur in a wide spectrum of diseases such as
following burns, trauma and major surgery. The conventional and easy method of evaluating
disturbances in fluid and electrolyte balance is the frequent measurement of the concentration
of serum electrolytes. It is crucial to remember that intracellular and extracellular electrolytes
are normally constant, and that major shifts in and out of 'compartments' can occur in disease
with minimal changes in serum electrolyte. Compositional changes also involve disturbances
in acid-base balance.
I. Volume deficit
 Obvious causes
Vomiting, diarrhoea, intestinal fistulae, nasogastric suction, fluid loss following burns,


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in acid-base balance.
I. Volume deficit
 Obvious causes
Vomiting, diarrhoea, intestinal fistulae, nasogastric suction, fluid loss following burns,
sequestration of fluid in soft tissue injuries and infections, diuretics, renal disease/adrenal
insufficiency
 Less obvious causes
Inadequate fluid intake, fluid loss through excessive sweating as in high fever, hot humid
temperature, haemodialysis, haemofiltration fromsurgical incisions and tetanus
Treatment
The first principle is to restore circulating volume through infusion of intravenous fluids.
Once this is satisfactorily achieved, disturbances in electrolytes and acid-base balance if
present need to be rectified. Various fluids used for volume replacement are given below:
Replacement fluids


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present need to be rectified. Various fluids used for volume replacement are given below:
Replacement fluids
 Replacement fluids are used to replace abnormal loss of blood, plasma or other
extracellular fluids as first line treatment for hypovolemia in:
- Patients with established hypovolemia e.g. haemorrhagic shock.
- Maintenance of normovolaemia in patients with ongoing fluid losses e.g. surgical
blood loss.
 Intravenous replacement fluids are the first line of treatment for hypovolemia.
 Crystalloid maintenance fluids, which contain dextrose, are not suitable for use as
replacement fluids. However, crystalloid solutions with a similar concentration of
sodium to plasma (normal saline or balanced salt) solutions (Ringer's lactate or


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sodium to plasma (normal saline or balanced salt) solutions (Ringer's lactate or
Hartmann's solutions) are effective as replacement fluids. These should be available in
all hospitals where intravenous replacement fluids are used. Crystalloids should be
infused in a volume at least three times the volume lost in order to correct hypovolemia.
 All colloid solutions (albumins, dextran, gelatins and hydroxyethyl starch solutions) are
replacement fluids. However, they have not been shown to be superior to crystalloids in
resuscitation.Colloid solutions should be infused in a volume equal to the blood
volume deficit.
 Plasma should never be used as a replacement fluid.
 Plain water should never be infused intravenously as it can cause haemolysis.


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Emergency Conditions
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 In addition to the intravenous route, the intraosseous, oral, rectal or subcutaneous routes
can be used for the administration of fluids, blood and certain drugs. However, with the
exception of intraosseous route, other routes are generally unsuitable in severely
hypovolemic patients.
 Rectal fluids are administered through a plastic or rubber enema tube which is inserted
into the rectumand connected to a bag or bottle of fluid. A safe and effective solution
for a rectal rehydration is 1 liter of clean drinking water with teaspoon of table salt.
 Subcutaneous fluidscan be used when other route of administration of fluids are
unavailable.A cannula or needle is inserted into the subcutaneous tissue (the abdominal


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unavailable.A cannula or needle is inserted into the subcutaneous tissue (the abdominal
wall is a preferred site) and sterile fluids are administered in a conventional manner. Do
not give dextrose-containing solutions subcutaneously as they can cause sloughing of
tissues.
 Oral and nasogastric fluids: Oral rehydration can often be used in mildly hypovolemic
patients if the oral route is not contraindicated. Do not use if:
- The patient is unconscious.
- The patient has gastrointestinal lesions or reduced gut motility e.g. obstruction.
- General anaesthesia and surgery is planned imminently.
WHO/UNICEF formula for oral rehydration fluid:
Dissolve in one litre of drinkable water
Sodium chloride 2.6 g/L
Trisodium citrate, dihydrate 2.9 g/L
Potassium chloride 1.5 g/L


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Dissolve in one litre of drinkable water
Sodium chloride 2.6 g/L
Trisodium citrate, dihydrate 2.9 g/L
Potassium chloride 1.5 g/L
Glucose anhydrous 13.5 g/L
Resulting concentrations
Na 75 mmol/L, CI65 mmol/L, K 20 mmol/L, Glucose anhydrous75 mmol/ L, Citrate 10
mmol/L, total osmolarity 245 mmol/L.
Maintenance fluids
Maintenance fluids are used to replace the normal physiological loss that occurs through skin,
lung, faeces and urine. Since a considerable proportion of the loss is water, maintenance
fluids are mainly composed of water in the form of a dextrose solution. Some electrolytes
may also be included in these solutions.
Before giving any intravenous infusion:
 Check that the seal of the infusion fluid bottle or bag is not broken.
 Check the expiry date.


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Before giving any intravenous infusion:
 Check that the seal of the infusion fluid bottle or bag is not broken.
 Check the expiry date.
 Check that the solution is clear and free from visible particles.
II. Volume excess
Volume excess is often iatrogenic when the fluid intakehas consistently exceeded the
output. Excessive intravenous infusions of saline and blood transfusions are important


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causes of hypervolemia. Renal insufficiency, congestive heart failure, liver disease and
other causes of sodium retention, or excessive sodium administration can all produce
increase in extracellular fluid content and hypervolemia.
Salientfeatures
Treatment
In moderate volume excess, salt restriction, restriction of fluid intake and the use of
frusemide as a diuretic will solve the problem. Fulminant pulmonary oedema secondary to
over hydration from over transfusion of blood or fluids is more appropriately dealt with by
phlebotomy in stages so that pulmonary capillary wedge pressure is reduced below 15 mm
Hg. Rarely ultrafiltration (dialysis) may be required.
References


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Hg. Rarely ultrafiltration (dialysis) may be required.
References
1. Anaesthesia at the District Hospital. In: World Health Organization in collaboration with the World
Federation of Societies of Anesthesiologists, Geneva, 2nd Edition, 2000, WHO.
2. Drugs Used in Anaesthesia. In: WHO Model Prescribing Information, 1989, World Health Organization.
3. Anaesthesia at the District Hospital. In: World Health Organization in collaboration with the World
Federation of Societies of Anesthesiologists, Geneva, 1988, World Health Organization.
SEPTICEMIA
Septicemia is a clinical syndrome caused by invasion of bloodstream by microorganisms.
Gram -negative and gram-positive bacteria account for most common sepsis cases.
Definitions


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Gram -negative and gram-positive bacteria account for most common sepsis cases.
Definitions
 Bacteremia (fungemia): presence of viable bacteria (fungi) in the blood, as evidenced by
positive blood cultures.
 Systemic Inflammatory Response Syndrome (SIRS): at least two of the following
conditions: (1) oral temperature of >38° C or <35° C, (2) respiratory rate of >20
breaths/min or partial pressureof arterial carbon dioxide (PaCO2) of <32 mm Hg, (3)
heart rate of >90 beats/min, (4) leukocyte count of >12,000/dl or <4000/dlor >10%
bands.
 Severe sepsis: sepsis with one or more signs of organ dysfunction, hypoperfusion, or
hypotension, such as metabolic acidosis, alteration in mental status, oliguria, or adult
respiratory distress syndrome.


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hypotension, such as metabolic acidosis, alteration in mental status, oliguria, or adult
respiratory distress syndrome.
 Oedema, ascites, pleural effusion,neck veins full, pulmonary congestion,
hyperdynamic circulation with tachycardia, a warm skin, and a bounding pulse.
 Increase in the systolic pressure and pulse pressure.
 Central venous Pressure (CVP) > 12 mmHg, Pulmonary Capillary Wedge Pressure
(PCWP) > 20 mmHg in the presence of pulmonary oedema.


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 Septic shock: sepsis with hypotension that is unresponsive to fluid resuscitation plus
organ dysfunction or perfusion abnormalities as listed for severe sepsis.
 Multiple Organ Dysfunction Syndrome (MODS): dysfunction of more than one organ,
requiring intervention homeostasis.


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 Fever or hypothermia may be seen in sepsis. Hypothermia is more often seen in patients
at the extremes of age and in immunocompromised patients.
 Other signs include tachycardia, wide pulse pressure, tachypnea,and hypotension.
 Mental status changes ranging from mild disorientation to coma are commonly seen.
 Ophthalmic manifestations include retinal hemorrhages, cotton-wool spots, and
conjunctival petechiae.
 Cardiovascular manifestations initially include vasodilation, resulting in warm
extremities.
 Cardiac output is maintained early in sepsis through a compensatory tachycardia. As
sepsis progresses, hypotension may occur. Patients in septic shock may demonstrate a
diminished response to volume replacement.


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sepsis progresses, hypotension may occur. Patients in septic shock may demonstrate a
diminished response to volume replacement.
 Renal manifestations include azotemia, oliguria, and active urinary sediment due to
acute tubular necrosis.
 Hepatic dysfunction present as cholestatic jaundice, increases in transaminases, alkaline
phosphatase, and S.bilirubin. Painless mucosal erosions may occur in the stomach and
duodenum and cause upper GI bleeds.
 Skin findings include cellulitis, erysipelas, and fasciitis. Hypotension and disseminated
intravascular coagulation (DIC) can also produce skin changes, including acrocyanosis
and necrosis of peripheral tissues.
 Hematologic changes include neutropenia, neutrophilia, thrombocytopenia, and DIC.


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and necrosis of peripheral tissues.
 Hematologic changes include neutropenia, neutrophilia, thrombocytopenia, and DIC.
Thrombocytopenia occurs in over 30 percent of patients with sepsis. DIC is more often
associated with gram-negative sepsis. Decompensated DIC presents with clinical
bleeding and thrombosis. Laboratory studies can show thrombocytopenia, prolonged
prothrombin time (PT) and partial prothromboplastin time (PTT), decreased fibrinogen
level and antithrombin levels, and increased fibrin monomer, fibrin split values,and D-
dimer values.
 Hyperglycemia may be the result of increased catecholamines, cortisol, and glucagon.
Increased insulin resistance, decreased insulin production, and impaired utilization of
insulin may further contribute to hyperglycemia.


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Increased insulin resistance, decreased insulin production, and impaired utilization of
insulin may further contribute to hyperglycemia.
 Arterial bloodgas (ABG) studies in early sepsis may reveal hypoxemia and respiratory
alkalosis. As perfusion worsens and glycolysis increases, a metabolic acidosis results.
Salient features
Non pharmacological treatment
 Aggressive airway management with high-flow oxygen and endotracheal intubation
 Rapid infusion of crystalloid IV fluid (Ringer’s lactate or normal saline) at 500 m l (20
m l/kg in children) every 5 to 10 min; 4 to 6 L (60 ml/kg in children)


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Emergency Conditions
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 Remove source of infection-remove indwellingIV catheters and send the tips for
quantitative culture. Replace urinary drainage catheters if obstructed. Consult the
appropriate specialist for drainage of intra-abdominal, sinus, or soft tissue abscesses.
 Monitor blood pressure, pulse, capillary refill, central venous pressure, pulmonary
capillary wedge pressure, and urine output (>30 ml/h in adults, 1 ml/kg/h in children) to
evaluate therapy. If blood loss is suspected, blood replacement may be necessary
Pharmacological treatment
 Inj. dopamine 5 to 20 µg/kg/min, titrated to response, if hypotension is refractory to IV
fluid.
 If blood pressure remains <70 mmHg despite preceding measures,Inj.norepinephrine 8-


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fluid.
 If blood pressure remains <70 mmHg despite preceding measures,Inj.norepinephrine 8-
12 µg/min loading dose and a 2-4 µg/min infusion to maintain mean arterial blood
pressure of at least 60 mmHg should be started.
 Empiric antibiotic therapy. Dosages should be the maximum allowed and given
intravenously. When source is unknown, therapy should be effective against both gram-
positive and gram-negative organisms.
 In adults, a third-generation cephalosporin (ceftriaxone 1 g IV, cefotaxime 2 g IV, or
ceftazidime 2 g IV) or an antipseudomonal beta lactamase–susceptible penicillin can also
be used. Addition of an aminoglycoside (gentamicin 2 mg/ kg IV, tobramycin 2 mg/kg
IV) to this regimen is recommended.


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be used. Addition of an aminoglycoside (gentamicin 2 mg/ kg IV, tobramycin 2 mg/kg
IV) to this regimen is recommended.
 In immunocompromised adults, ceftazidime 2g IV, imipenem 750 mg IV, or meropenem
1 g IV alone is acceptable. If gram-positive infection is suspected (indwelling catheter or
IV drug use), oxacillin 2 g IV or vancomycin 15 mg/ kg IV should be added. If an
anaerobic source is suspected (intraabdominal, genital tract, odontogenic, and necrotizing
soft tissue infection), metronidazole 7.5 mg/kg IV or clindamycin 900 mg IV should
additionally be administered. IfLegionellais a potential source, erythromycin 500 mg IV
should be added.
 Acidosis to be treated with oxygen, ventilation, and IV fluid replacement. If acidosis is


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should be added.
 Acidosis to be treated with oxygen, ventilation, and IV fluid replacement. If acidosis is
severe, administration of sodium bicarbonate 1 meq/kg IV is acceptable as directed by
ABGs.
 DIC should be treated withfresh-frozen plasma 15 to 20 ml/kg initially to keep PT at 1.5
to2 times normal and treated with platelet infusion to maintain serum concentration of 50
to 100,000.
 Inj.hydrocortisone(100 mg IV)  for adrenal insufficiency
ORGANOPHOSPHOROUS POISONING
Organophosphorous(OP) insecticides are highly lipid soluble and are rapidly absorbed via
dermal, gastrointestinal and respiratory routes. Common agents for OP poisoning are
malathion, parathion, chlorpyrifos, dichlorvos, methylparathionwhich are used as
insecticides.


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Emergency Conditions
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 Clinical features include dyspnoea, tightness around chest, nausea, vomiting, diarrhea,
abdominal pain, excessive sweatingand salivation, miosis, blurred vision, lacrimation,
headache, giddiness, drowsiness, bradycardia, arrhythmias, QT prolongation,
hypotension, fasciculation, muscle weakness, seizures and coma.
 Diagnosis can be confirmed byred blood cell (RBC) cholinesterase and plasma
cholinesterase level which is reduced to 20% of the normal values.
Salient features
Non pharmacological treatment
 Maintain patent airway: oral airway/intubation/mechanical ventilation if required
 Monitor vitals-temperature, pulse, blood pressure, respiratory rate
 Start intravenous line placement: maintenance IV fluids
 Decontamination: remove of all clothes


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 Start intravenous line placement: maintenance IV fluids
 Decontamination: remove of all clothes
 Gastric lavage with activated charcoal and sample collection
 Wash  skin with soap and water
Pharmacological treatment
 Inj. atropine 2 mg IV bolus, repeat every 5-10 minutes until atropinization (pulse
>80/min, pupillary dilation and drying of secretions)followed by atropine IV infusion at
0.02-0.08 mg/kg/min to maintain atropinasation (glycopyrronium can be used in place
atropine to avoid CNS toxicity).
 Inj. pralidoxime IV 30mg/kg immediately followed by 8 mg/kg/hr continued for at least
24 hours. If an infusion cannotbe used, 30 mg/kg every 4 hourly.
 Inj. obidoxime 4 mg/kg bolus initially followed by 0.5 mg/kg/hr infusion Alternatively,4


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 Inj. obidoxime 4 mg/kg bolus initially followed by 0.5 mg/kg/hr infusion Alternatively,4
mg/kg bolus followed by 2 mg/kg every 4 hourly.
 IV crystalloids: normal saline/ringer’s lactate.
 Benzodiazepines: midazolam/lorazepam/diazepam for treatment and prophylaxis of
seizures
KEROSENE AND PETROL POISONING
Salient features
 Most common accidental poisoning in children.
 Inhalational of vapours or pulmonary aspiration can cause toxicity. The lethal dose is 30-100
ml.
 Mild- breathing difficulty, throat pain, nausea / vomiting, vision loss, low blood pressure,
convulsions, headache, weakness, burns / irritation.
 Severe: pulmonary edema, hemoptysis, mental confusion, hallucination, stupor, cyanosis,
convulsions, coma, death (due to ventricular fibrillation / respiratory failure).


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Emergency Conditions
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 Gastric irritation within half an hour of taking the poison.
 Bitter taste, dry mouth and throat, burning pain in the stomach and difficulty in swallowing
and talking.
 Giddiness, ataxia, incoordination of muscles, flushed appearance of the face, dry hot skin,
rise in temperature, diplopia, dilated pupils with loss of accommodation, reddening of the
conjunctiva and drowsiness. Sometimes, an erythematous rash appears all over the body.
 Full, bounding pulse which later becomes weak and irregular.
 Muttering delirium, tries to run away from the bed, picks at bed clothes, tries to pull
imaginary threads from the tips of his fingers and develops dreadful hallucinations of sight
and hearing. The conditionmay pass on to stupor, convulsions, coma and sometimes death


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and hearing. The conditionmay pass on to stupor, convulsions, coma and sometimes death
from respiratory failure.
 Death may occur within 4-24 hours.
Investigations
Chest x ray: perihilar densities, basal pneumonitis, atelectasis, consolidation
Treatment
 Remove all contaminated clothes of the patient
 Flush the skin and oral cavity for at least 15 minutes
 If the chemical is swallowed, immediately give the person water or milk
 If the person breathed in the poison, immediately move him or her to fresh air with patent
airwaywith head low position
 Do not induce emesis
 Put the patient on monitor for vital signs– temperature, pulse, blood pressure, respiratory
rate
 Provide oxygen through nasal cannula or face mask


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rate
 Provide oxygen through nasal cannula or face mask
 Take IV line– start intravenous crystalloids as a supportive therapy
 Patients should be monitored for respiratory complications.
DATURA POISONING
Datura stramonium(thorn apple) grows in India at high altitudes. The seeds and fruits are the
most poisonous parts of the plant with hyoscine, hyoscyamine and traces of atropine,as the
active principles.
Salient features
Non pharmacological treatment
 Stomach wash with 1:10,000 potassium permanganate solution or 5% tannic acid
solution.


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Emergency Conditions
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 Decontamination of the patient must be individualized, based on time since exposure,
type of anticholinergic agent involved, route of exposure, probable amount ingested, and
severity of the clinical condition.
 Early gastric emptying (within 1 hour) may be considered for large ingestions, when an
asymptomatic patient presents immediatelyafter ingestion.
 Measure core body temperature with a flexible rectal probe. Aggressive temperature
reduction with ice water or evaporative cooling with mist and fans should be the first
priority in the severely hyperthermic patient. Antipyretic agents and simple cooling
blankets are ineffective.
Pharmacological treatment
 Benzodiazepines like midazolam or lorazepam can be used to control agitation and
sedation.


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blankets are ineffective.
Pharmacological treatment
 Benzodiazepines like midazolam or lorazepam can be used to control agitation and
sedation.
Inj. midazolam 0.01-0.1 mg/kg IV or Inj. lorazepam 0.05-0.1 mg/kg IV
 In severe poisoning, Inj. physostigmine 1.2 mg IM or IV, to be repeated after half an
hour, if necessary. Watch for side effects (bradycardia, heart block, excessive secretions).
 Inj. diazepam 10 mg IV diluted slowly may be given for convulsions.
ABDOMINAL INJURY
Abdominal injuries arequitecommon in this new eraand it is must for a surgeon to quickly
assess and promptly manage such injuries which can be fatal. They can be broadly classified
as penetrating abdominal injury and blunt abdominal injury.
I. Penetrating abdominal injury


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as penetrating abdominal injury and blunt abdominal injury.
I. Penetrating abdominal injury
 Penetrating abdominal injuriescaused by sharp weapon injury, missile injury/gunshot
injury etc
 History oftime and place of injury,nature of injury,direction of injuring weapon
 Physical examinationassess vitals, assess wound thoroughly, look for peritoneal breach
Investigations
 Generally no investigations are required before proceeding for laparotomy.
 X -rayabdomen standing can be done in cases where peritoneal breach is in doubt
Treatment
 Resuscitate the patient, secure airway, maintain breathing, maintain circulation, arrange
for compatibleblood.
 Emergency exploratory laparotomy and further management according to organ injured.
II.Blunt abdominal injury


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for compatibleblood.
 Emergency exploratory laparotomy and further management according to organ injured.
II.Blunt abdominal injury
Blunt abdominal injuries can be due to assault by blunt objects, road traffic accidents and
falls.
Investigations
 H aemoglobin levels,  hematocrit, X-ray abdomen standing


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Emergency Conditions
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 The common agents causing chemical injuries are alkalis (lime, cement, plasters),
acids, solvents, detergents and irritants. Alkalis tend to penetrate more deeply than
acids, as the latter coagulate surface proteins, forming a protective barrier.
 Symptoms include redness, pain, photophobia, blepharospasm and watering of eyes.
 Corneal epithelial defects ranging from scattered superficial punctate keratopathy
(SPK), to focal epithelial loss, to sloughing of the entire epithelium may occur.
 Focal areas of  conjunctival  chemosis, hyperemia, hemorrhages, or a combination of
these
 Mild eyelid edema, mild anterior chamber (AC) reaction andfirst- and second-degree
burns of the periocular skin.
 USG -abdomen, CECT -abdomen and pelvis.
Treatment


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burns of the periocular skin.
 USG -abdomen, CECT -abdomen and pelvis.
Treatment
 Resuscitate the patient, secure airway, maintain breathing, maintain circulation, arrange
for compatibleblood.
 Temperature, pulse,respiratoryrate,blood pressure (TPRBP) charting, abdominal girth
(AG) charting.
 Management of blunt abdominal trauma depends upon vitals of the patients and organs
involved as per seen in USG- Abdomen and Contrast Enhanced Computed Tomography
(CECT ) abdomen.
 All patients whose vitals are unstableare to be explored. Emergency exploratory
laparotomy and followed by management according to organ involved.
 All patients whose vitals arestable are reviewed by CECT-abdomen and pelvis and
managed according to organs involved and grade of injury.
FOREIGN BODY IN EAR


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managed according to organs involved and grade of injury.
FOREIGN BODY IN EAR
Occasionallya fly or an insect gets trapped in the external canal and cause distress and
discomfort. The foreign body could be animate-insects orinanimate, organic-seeds or
inorganic-stones, beads, cotton buds, match sticks etc.
Treatment
 Insects-immobilized using oil and remove with forceps
 Vegetable foreign bodies– remove with foreign body hook (syringingisnot advisable).
 Non -organic foreign bodies-remove with syringing and foreign body hook.
 Impacted foreign bodies-remove under general anesthesia using the microscope
CHEMICAL INJURIES OF EYE
Salient features
Investigations


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 History: Time of injury? Specific type of chemical? Time between exposure and irrigation
of eyes? Duration and type of irrigation? Was the patient wearing eye protection?
 Slit-lamp examination with fluorescein staining.
 If you suspect an epithelial defect but do not see one with fluorescein staining, repeat the
fluorescein application to the eye. Sometimes the defect is slow to take up the dye. If the
entire epithelium sloughs off, only Bowman membrane remains, which may take up
fluorescein poorly.
 Eyelid eversion to search for foreign bodies.
 Evaluate for conjunctival ulcerations/defects.
 Check the intraocular pressure (IOP). In the presence of a distorted cornea, IOP may be
most accurately measured with atonometer.
Grading of severity


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most accurately measured with atonometer.
Grading of severity
 Grade 1 is characterized by clear cornea (epithelial damage only) and no limbal ischemia
(excellent prognosis).
 Grade 2 shows hazy cornea but with visible iris details and less than one-third of the
limbus being ischemic (good prognosis).
 Grade 3 manifests total loss of corneal epithelium, stromal haze obscuring iris details and
between one-third and half limbal ischemia(guarded prognosis).
 Grade 4 shows opaque cornea and more than half limbal ischemia (very poor prognosis).
Non pharmacological treatment
A. Copious irrigation
 Place an eyelid speculum and instill topical anesthetic.
 Copious irrigation using saline or ringerlactate solution for at least 30 minutes. Tap water


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 Copious irrigation using saline or ringerlactate solution for at least 30 minutes. Tap water
can be used in the absence of these solutions and may be more efficacious in inhibiting
elevated intracameral pH than normal saline for alkali burns.
 Check pH and ifnot neutral, repeat irrigation.
 NEVER use acidic solutions to neutralize alkalis or vice versa.
B. Double-eversion of the upper eyelid:
 It should be performed so that any retained particulate matter trapped in the fornices is
identified and removed with cotton tip applicator.
 Calcium hydroxide particles may be more easily removed with a cotton-tipped applicator
soaked in disodium ethylenediaminetetraacetic acid (EDTA).
C. Debridement: Necrosed area of conjunctiva and cornea should be debrided topromote
healing.


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C. Debridement: Necrosed area of conjunctiva and cornea should be debrided topromote
healing.
D. Hospitalization: It is required for severe injuries to ensure regular eye drop instillation.
Pharmacological treatment
The main aims of treatment of chemical burns are to reduce inflammation, promote epithelial
regeneration and prevent corneal ulceration.


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 Symptoms include foreign body sensation, watering and redness with history of
trauma
 Conjunctival or corneal foreign body with or without rust ring, conjunctival injection,
eyelid edema, mild anterior chamber reaction, and superficial punctuate keraptopathy.
 Steroids
- It reduces inflammation. However, they also impair stromal healing by reducing
collagen synthesis and inhibiting fibroblast migration.
- So topical steroids may be used initially (usually 4–8 times daily, strength depending
on injury severity) but must be tapered off after 7–10 days when sterile corneal
ulceration is most likely to occur.
- Steroids may be replaced by topical NSAIDs, which do not affect keratocyte function.
 Cycloplegiamay improve comfort.


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- Steroids may be replaced by topical NSAIDs, which do not affect keratocyte function.
 Cycloplegiamay improve comfort.
 Topical antibioticdrops are used for prophylaxis of bacterial infection
 Ascorbic acid
Improves wound healing and promotes the synthesis of mature collagen by corneal
fibroblasts. Topical sodium ascorbate 10% is given 2-hourly in addition to a systemic
dose of 1–2 g vitamin C(L-ascorbic acid) QID (not in patients with renal disease).
 Tetracyclinesshould be considered if there is significant corneal melting and can be
administered both topically (tetracycline ointment QID) and systemically (doxycycline
100 mg BD tapering to once daily).
 Symblepharonshould be prevented by lysis of developing adhesions with a sterile glass
rod or damp cotton bud.
Surgical treatment


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 Symblepharonshould be prevented by lysis of developing adhesions with a sterile glass
rod or damp cotton bud.
Surgical treatment
 Earlysurgery may be necessary to promote revascularization of the limbus, restore the
limbal cell population and re-establish the fornices.
 Keratoplasty should be delayed for at least 6 months and preferably longer to allow
maximal resolution of inflammation.
 Keratoprosthesis may be required in very severely damaged eyes because the results of
conventional grafting are poor.
CORNEAL AND CONJUNCTIVAL FOREIGN BODIES IN EYE
Salient features
Investigations
 Determine the mechanism of injury [e.g., metal striking metal, power tools or weed-
whackers may suggest an intraocular foreign body (IOFB)]. Attempt to determine the


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whackers may suggest an intraocular foreign body (IOFB)]. Attempt to determine the
size, weight, velocity, force, and shape of the object. Document visual acuity before any
procedure is performed.


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71
 Examine closely for iris tears and transillumination defects, lens opacities, AC
shallowing, and asymmetrically low IOP.
 If there is no evidence of perforation, evert the eyelids and inspect the fornices for
additional foreign bodies.
 Dilate the eye and examine the posterior segment for a possible intraocular foreign body
 Avoid magnetic resonance imaging (MRI) if there is a history of possible metallic foreign
body.
Treatment
Corneal foreign body
 Apply topical anesthetic (e.g., proparacaine 0.5% eye drops).
 Remove the corneal foreign body with a cotton tip applicator, 26 no needle or fine forceps
at a slit lamp.
 Multiple superficial foreign bodies may be more easily removed by irrigation.


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at a slit lamp.
 Multiple superficial foreign bodies may be more easily removed by irrigation.
 Remove the rust ring as completely as possible on the first attempt. This may require an
ophthalmic drill. It is sometimes safer to leave a deep, central rust ring to allow time for
the rust to migrate to the corneal surface, at which point it can be removed more easily.
 Measure the size of the resultant corneal epithelial defect.
 Treat epithelial defect with antibiotics and carboxy methyl cellulose(CMC) eyedrops, if
necessary pad it.
 Alert the patient to return as soon as possible if there is any worsening of symptoms.
Conjunctival foreign body
 Remove foreign body under topical anesthesia.
- Multiple or looseforeign bodies can often be removed with saline irrigation.


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 Remove foreign body under topical anesthesia.
- Multiple or looseforeign bodies can often be removed with saline irrigation.
- A foreign body can be removed with a cotton-tipped applicator soaked in topical
anesthetic or with fine forceps.
- For deeply embedded foreign bodies, consider pretreatment with a cotton-tipped
applicator soaked in phenylephrine 2.5% to reduce conjunctival bleeding.
- Small, relatively inaccessible, buried subconjunctival foreign bodies may sometimes
be left in the eye without harm unless they are infectious or proinflammatory.
Occasionally, they willsurface with time, at which point they may be removed more
easily.
 Sweep the conjunctival fornices with a glass rod or cotton-tipped applicator soaked with a
topical anesthetic to catch any remaining pieces.


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 Sweep the conjunctival fornices with a glass rod or cotton-tipped applicator soaked with a
topical anesthetic to catch any remaining pieces.
 A topical antibiotic (e.g., bacitracin ointmentBD; trimethoprim/polymyxin B or
moxifloxacin/ciprofloxacin/ofloxacindrops QID) may be used.
 Artificial tears may be given for irritation.
Follow-up


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Emergency Conditions
72
 Corneal foreign body: Follow up as with corneal abrasion. If residual rust ring remains,
reevaluate in 24hours.
 Conjunctival foreign body: Follow up as needed, or in 1 week if residual foreign bodies
were left in the conjunctiva.


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73
 The patient presents with blurred vision, history of blunt trauma and pain in eye.
 Blood orclot or bothcan be observedin theanterior chamber, usually visible without a
slit lamp.
 A total (100%) hyphema may be black or red. When black, it is called an “8 -ball” or
“black ball” hyphema.
 When red, the circulating blood cells may settle with time to become less than a 100%
hyphema.
TRAUMATIC HYPHEMA
Salient features
Investigations
 History of traumatic event including force, velocity, type, and direction of injury should
be taken.
 Use of medications with anticoagulant properties [aspirin, NSAIDs, warfarin  or
clopidogrel], personal or family history of sickle cell disease/trait, symptoms of


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clopidogrel], personal or family history of sickle cell disease/trait, symptoms of
coagulopathy (e.g., bloody nose-blowing, bleeding gums with tooth brushing, easy
bruising)
 Ocular examination, first ruling out a ruptured globe. Document the extent (e.g., measure
the hyphema height) and location of any clot and blood.
 Measure the IOP. Perform a dilated retinal evaluation without scleral depression.
 Co nsider a CT scan of the orbits and brain (axial and coronal views, with 1- to 3-mm
sections through the orbits) when indicated (e.g., suspected orbital fracture or IOFB, loss
of consciousness).
Treatment
 Confine either to bed rest with bathroom privilegesor to limited activity. Elevate head of
bed to allow blood to settle.


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Treatment
 Confine either to bed rest with bathroom privilegesor to limited activity. Elevate head of
bed to allow blood to settle.
 Place a shield (metal or clear plastic) over the involved eye at all times. Do not patch
because this prevents recognition of sudden visual loss in the event of a rebleed.
 Atropine 1% solution BD to TDS or scopolamine 0.25% BD to TDS.
 No aspirin-containing products or NSAIDs.
 Mild analgesics only (e.g., acetaminophen). Avoid sedatives.
 Use topical steroids (e.g., prednisolone acetate 1% four to eight times per day) if any
suggestion of iritis (e.g., photophobia, deep ache, ciliary flush), evidence of lens capsule
rupture, any protein (e.g., fibrin), or definitive white blood cells in anterior


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rupture, any protein (e.g., fibrin), or definitive white blood cells in anterior
chamber. Reduce the frequency of steroids as soon as signs and symptoms resolve to
reduce the likelihood of steroid-induced glaucoma.
 For increased IOP:
- Start with a beta-blocker (e.g., timolol 0.5% or levobunolol 0.5% BD).


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Emergency Conditions
74
- If IOP still high, add topical alpha-agonist (e.g., apraclonidine 0.5%, or brimonidine
0.2% TDS) or topical carbonic anhydrase inhibitor (e.g., dorzolamide 2%, or
brinzolamide 1% TDS). Avoid prostaglandin analogs and miotics (may increase
inflammation). In children under 5, topical alpha-agonists are contraindicated.
- If topical therapy fails, add acetazolamide (500 mg orally, BD foradults, 20
mg/kg/day divided three times per day for children) or mannitol [1 to 2 g/kg
intravenously IV over 45 minutes once a day]. If mannitol is necessary to control the
IOP, surgical evacuation may be imminent.
 If hospitalized, use antiemetics for severe nausea or vomiting [e.g., prochlorperazine 10
mg IM TDS or 25 mg BD].
 Indications for surgical evacuation of hyphema:


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mg IM TDS or 25 mg BD].
 Indications for surgical evacuation of hyphema:
- Corneal stromal blood staining.
- Significant visual deterioration.
- Hyphema that does not decrease to <50% by 8 days [to prevent peripheral anterior
synechiae (PAS)].
- IOP >60 mm Hg for >48 hours, despite maximal medical therapy (to prevent optic
atrophy).
- IOP >25 mm Hg with total hyphema for >5 days (to prevent corneal stromal blood
staining).
Follow up
 The patient should be seen daily for 3 days after initial trauma to check visual acuity,
IOP, and for a slit-lamp examination.
 Look for new bleeding, increased IOP, corneal blood staining, and other intraocular
injuries as the blood clears (e.g., iridodialysis; subluxated, disclocated, orcataractous


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injuries as the blood clears (e.g., iridodialysis; subluxated, disclocated, orcataractous
lens). Hemolysis, which may appear as bright red fluid, should be distinguished from a
rebleed, which forms a new, bright red clot. If the IOP is increased, treat as described
earlier.
 The patient should be instructed to return immediately if asudden increase in pain or
decrease in vision is noted (which may be symptoms of a rebleed or secondary
glaucoma). If a significant rebleed or an intractable IOP increase occurs, the patient
should be hospitalized.
 After the initial close follow-up period, the patient may be maintained on a long-acting
cycloplegic (e.g., atropine 1% solution OD to BD, scopolamine 0.25% OD to BD),


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cycloplegic (e.g., atropine 1% solution OD to BD, scopolamine 0.25% OD to BD),
depending on the severity of the condition. Topical steroids may be tapered as the blood,
fibrin, and white blood cells resolve.
 Glasses or eye shield during the day and eye shield at night. As with any patient,
protective eyewear (polycarbonate or Trivex lenses) should be worn any time a
significant potential for an eye injury exists.
 The patient must refrain from strenuous physical activities (including bearing down or
valsalva maneuvers) for 1 week after the initial injury or rebleed. Normal activities may


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Emergency Conditions
75
be resumed 1 week from the date of injury or rebleed. This period should be extended if
blood remains in the anterior chamber.
 If patient was hospitalized, see 2 to 3 days after discharge. If not hospitalized, see several
days to 1 week after initial daily follow-up period, depending on severity of condition
(amount of blood, potential for IOP increase, other ocular or orbital pathologic
processes).
DOG BITE (RABIES)
Rabies can be transmitted by dog bite or following non-bite exposure to mucous membrane
or an open wound (one that has bled within 24 hours) with saliva. Bites from dogs in
developing countries should always be considered high risk, and prophylaxis should be given
without waiting for test results.
Salient features


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developing countries should always be considered high risk, and prophylaxis should be given
without waiting for test results.
Salient features
Guidelines for Determining Need for Rabies Prophylaxis (Adapted from Human rabies
prevention—United States, 1999. Recommendations of the Advisory Committee on
Immunization Practices)
Animal type & evaluation Post-exposure prophylaxis recommendations
 Dogs, cats, and ferrets Do not start vaccination unless animal develops
(healthy and available for 10-days) clinical signs of rabies during observation
period*
 Rabid or suspected rabid Immediately vaccinate.
 Unknown (escaped) Consult public health officials.
* 10-days observation period, begin postexposure prophylaxis at the first sign of rabies. If the


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 Unknown (escaped) Consult public health officials.
* 10-days observation period, begin postexposure prophylaxis at the first sign of rabies. If the
animal exhibits clinical signs of rabies, it should be euthanized immediately and tested.
Treatmentof dog bite andPost-exposure prophylaxis of rabies
Three steps: wound care, passive immunization, and active immunization.
Immediate measures
 Early treatment is essential (less than 3 hours after the bite/injury occurred).
 Prodromal symptoms- such as headache, malaise, sore throat and fever last about 3-4
days. Pain and tingling at the bitten site.
 Stage of excitation- patient is intolerant to noise, bright light or a cold draught.
Aerophobia may be present. Hydrophobia is a characteristic symptom of rabies.


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Aerophobia may be present. Hydrophobia is a characteristic symptom of rabies.
Examination shows increased reflexes, dilatation of pupils, increased sweating,
lacrimation and salivation. Mental changes include fear of death, anger, irritability and
depression.
 Convulsions may occur resulting in death, paralysis and coma. The total duration of
illness lasts for 2-3 days.


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Emergency Conditions
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 Scrub the wound and its edges with soap and water.
 If the wound is a puncture, swab deeply in the wound and around its edges.
 Follow with application of a virucidal agent: 1% or 2% benzalkonium chlorideor
povidone-iodine andrinse.
 Tetanus prophylaxis should be given as indicated by patient’s current immunization
status.
 Do not suture bite wounds immediately. If suturing is required, hold it for 24-48 hours,
applying minimum number of stitches under the cover of antirabies immunoglobulin
locally.
Non immunized persons
 Human rabies immuno globulin (HRIG)-full dose should be infiltrated around wound(s),
and the  remaining volume should be administered IM at an anatomic site distant from


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and the  remaining volume should be administered IM at an anatomic site distant from
vaccine administration. Do not administer vaccine in the same syringe as HRIG may
partially suppress active production of antibody.
 Vaccine Huma n diploid cell vaccine (HDCV) injected IM (deltoid area), one each on
days 0, 3, 7, 14, and 28.The vaccine should be administered in the deltoid rather than the
gluteal region, to avoid accidental injection into fat, which will prevent antibody
formation.
 Rabies vaccine adsorbed (RVA) and purified chick embryo culture (PCEC) vaccine-
administered for prophylaxisby the intramuscular route and should have antibody titers
checked at 2 to 4 weeks.  It is associated with fewer hypersensitivity reactions in patients


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checked at 2 to 4 weeks.  It is associated with fewer hypersensitivity reactions in patients
receiving boosters and prophylaxis during pregnancy does not increase in fetal wastage,
congenital defects, should not be withheld when indicated.
 Corticosteroids, antimalarials, and other immunosuppressives can interfere with the
development of active immunity and should be withheld during the course of treatment if
possible.
 Patients with a history of hypersensitivity should nevertheless be cautiously given
immunoprophylaxis in a controlled setting, with antihistamines and epinephrine available
Previously immunized persons
 HRIG should not be administered.
 Vaccine HDCV or PCECV 1.0 ml, IM (deltoid area),on days 0 and 3.
References


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Previously immunized persons
 HRIG should not be administered.
 Vaccine HDCV or PCECV 1.0 ml, IM (deltoid area),on days 0 and 3.
References
1. Human rabies prevention—United States, 1999. Recommendations of the Advisory Committee on
Immunization Practices (ACIP).
2. MMWR Morb Mortal Wkly Rep 48:1, 1999.
3. http://www.cdc.gov/rabies/exposure/types.html; 2008.
4. Centers for Disease Control and Prevention: Rabies post-exposure.
5. http://www.cdc.gov/rabies/exposure/postexposure.html; 2008.
6. Rosen’s Textbook of Emergency Medicine, 7th edition


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Emergency Conditions
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SNAKE BITE
India is estimated to have the highest snakebite mortality in the world, with WHO estimates
placing the number of bites at 83,000 per annum with 11000 deaths. Most of the fatalities are
due to the victim not reaching the hospital in time where definite treatment can be
administered.
Snakes inIndia
There are about 236 species of snakes in India, most of which are non-poisonous, however,
there are 13 known species that are poisonous and four of these, namely Indian cobra,
Russell's viper, saw-scaled viper and Indian krait are highly venomous and are believed to be
responsible for mostof the poisonous bites in India
Salient features
Investigations
 Identification of snake, local swelling within few minutes after bite is an important sig of


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Salient features
Investigations
 Identification of snake, local swelling within few minutes after bite is an important sig of
viper envenomization.
 Blood stained sputum and non clotting of blood are diagnostic criteria for Russel viper
and Saw scaled viper poisoning.
 Ptosis and glossopharyngeal palsy are diagnostic criteria for Cobra and Indian Krait
poisoning.
 Investigations include
- 20 minute whole blood clotting test
- Hb/ plateletcount/peripheralsmear/PT/ APTT/ FDP/ D-Dimer
- Urine examination for proteinuria/RBC/ hemoglobinuria/ myoglobinuria
- Serum creatinine/urea/potassium
- Oxygen saturation/ PR/BP/ RR/posturalbloodpressure
- ECG/ X -Ray/ CT/ ultrasound (the use of X-Ray and ultrasoundare of unproven
benefit,       apart from identification of bleeding in viperine bites).


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benefit,       apart from identification of bleeding in viperine bites).
- ELISA to confirm snake species
Treatment
First aid measures (RIGHT approach)
R : reassure patient and control anxiety
I: immobilize bitten part by splinting the limb
 Viper envenomization (haemovasculotoxic): swelling and local pain, tender
enlargement of local lymph nodes, bleeding from any orifice,epistaxis, vomiting,
hypotension, petechiae, purpura, ecchymoses
 Elapid envenomization (neurotoxic): swelling and local pain, local necrosis and
blistering, descending paralysis, ptosis, diplopia, ophthalmoplegia,paralysis of
jaw and tongue, numbness around the lip and mouth, inadequate ventilation,
paradoxical respiration.


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Emergency Conditions
78
G -H: get to hospital-transfer the victim to the nearest treatment facility
T : tell the doctor about any symptoms
Do Not: Apply tourniquet, wash the bite site with soap and any other solution, make cuts or
incision on or near bitten area, apply extreme cold or herbal and folk remedies, suck venom,
give  the victim drink, alcohol or drugs
 Ensure airway, breathing and shock management
 Pain can be relieved with non sedating analgesic-oral paracetamol
 Anti-snake venom (ASV) is the mainstay of treatment. In India polyvalent ASV is
available which is effective against all the four common species.ASV should be
administered only when there are definite signs of envenomation i.e. coagulopathy or
neurotoxicity


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administered only when there are definite signs of envenomation i.e. coagulopathy or
neurotoxicity
 Mild and severe envenomation requires 8 to 10 vials.Each vial is 10ml of reconstituted
ASV. Children should receive the same ASV dosage as adults.ASV should be
administered over 1 hour at constant speed and patient should be closely monitored for 2
hours.
 ASV reactions:Anaphylaxis may be life-threatening.if anaphylaxis is evident, ASV
should be discontinued. Inj. hydrocortisone 100 mg + antihistamine or Inj. adrenaline
subcutaneouslycan be administered for ASV reaction
 Repeat dose of 5-10 vials of ASV i.e. half to one full dose, should continue 6 hourly till
coagulation is restored unless a species is identified against which polyvalent ASV is


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coagulation is restored unless a species is identified against which polyvalent ASV is
ineffective.Only for snakes which inject massive amounts of venom, such as the King
Cobra or Australian elapids, massive doses of 50+ vials are required.
Follow up
A snakebite victim discharged within 24 hrs should be advised to return if there is any
worsening of symptoms or signs such as bleeding, pain or swelling at the site of bite,
difficulty in breathing, altered sensorium etc. Explain about the signs and symptoms of serum
sickness which may manifest after 5-10 days.
INSECT AND ARACHNID BITES
Insect arachnid (spider, scorpion) bites and stings are common and usually cause minor
irritation. However, some stings can be painful and trigger a serious allergic reaction.
Salientfeatures


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irritation. However, some stings can be painful and trigger a serious allergic reaction.
Salientfeatures
 Skin around the bite becomesred, swollen and itchy. The venom from a sting often
causes a swollen, itchy, red mark (a weal) to form on the skin. This can be painful and
itchy for a few days, but is harmless in most cases.They can usually be treated at
home.
 The severity of bites andstings varies depending on the type of insect and sensitivity
of the person. In rare cases, some people can have a serious allergic reaction
(anaphylaxis) to a bite or sting that requires immediate medical treatment.


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Emergency Conditions
79
Non pharmacological treatment
 Remove a sting-by scraping it out with fingernails. Be careful during removing the sting,
prevent further spread the venom into the skin and do not puncture venomous sac.
 Minor bites and stings can be treated by washing theaffected areawith soap and water,
placing a cold compress (a cloth cooled with cold water) over the affected area to reduce
swelling
 Do not scratch thearea becauseit can become infected.
 Wrap an ice pack  in a towel andplace it on the swelling
Pharmacologicaltreatment
If the bite or sting is painful or swollen
 Tab.paracetamoloribuprofen(children under 16 years old should not be given aspirin)
 Apply a spray or cream that contains local anesthetic,antihistamineormild


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 Apply a spray or cream that contains local anesthetic,antihistamineormild
hydrocortisone (1%)on the affected area to prevent itching and swelling
 Tab. cetrizine 10mg once a day and topical administration of calamine lotionto relieve
pruritus
 Systemic corticosteroids may be appropriate if there are severe side-effects.
 Any person who collapses, or complains of wheezing, feeling of anxiety or faintness,
generalized itching, or tightness in the chest within 1 hour of being stung by an insect
should be treated as having anaphylactic shock. Inj. adrenaline1 mg (as hydrogen
tartrate) 0.5-1.0 ml IM injection (1:1000 solution), repeat every 15-20 min if required. All
patients should be observed at least for 24 hours for recurrent anaphylaxis (see section on
anaphylactic shock).


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patients should be observed at least for 24 hours for recurrent anaphylaxis (see section on
anaphylactic shock).
SCORPIONS BITE
 Simple analgesics, such as paracetamol and aspirin, can be given to relieve pain.
However, because of the potential for severe reactions, every effort should be made to get
the patient to a hospital as soon as possible.
 Vasodilators, administered in a hospital setting within 24 hours of the attack, may
attenuate the cardiovascular response and possibly reduce mortality.
 In endemic area, species-specific antiscorpions sera may be available locally and this can
be of value if administered within few hours.
Reference
1. Drugs used in Skin Diseases. In: WHO Model Prescribing Information, 1997, WHO, Geneva.


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80
 Symptoms include fever, night sweats, weight loss, anorexia, cough, dyspnoea,
arthralgia,chest pain.
 Signs are murmur, splenomegaly, clubbing, embolic feature and signs of immune
complex deposition, like Janewaylesions,Roth spots, splinter hemorrhages
Chapter 4
CARDIOVASCULAR DISEASES
INFECTIVE ENDOCARDITIS
It is a microbial infection of endothelial surface of heart. Acute bacterial endocarditis is
caused byS. aureus,group A hemolytic streptococci, pnuemococci or gonococci. Sub acute
bacterial endocarditis is caused by virulentS. Viridansor otherstreptococci.
Salient features
Pharmacological treatment
 Empirical therapy: Pending the availability of diagnostic data, blood culture–negative sub
acute native valveendocarditis is treated either with Inj. ampicillin-sulbactam  12 g every


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acute native valveendocarditis is treated either with Inj. ampicillin-sulbactam  12 g every
24 h or with Inj. ceftriaxone 1 gmOD plus Inj. gentamicin 3 mg/kg QIDIV; Tab.
doxycycline 100 mg twice dailyis added forBartonellacoverage.
 After blood culture report organism specific antibiotic therapy are as underStreptococci:
- Penicillin sensitive: Inj. penicillin G  2–3 M U IV q4h or Inj. ceftriaxone  2 g IVQID
for 2 weeksplusInj. gentamicin 3 mg/kg QID IV or IM, as a single doseor divided
into equal doses TDS for 2 weeks.
- Penicillin resistant: Inj. ceftriaxone 2 g IV QID for 4 weeksplusInj. gentamicin 3
mg/kg QID  IV or IM, as a single dose or divided into equal doses TDS  for 2 weeks
 Enterococci:  Inj. penicillin G 4–5 MU IV every 4 hoursplusInj. gentamicin 1 mg/kg IV


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 Enterococci:  Inj. penicillin G 4–5 MU IV every 4 hoursplusInj. gentamicin 1 mg/kg IV
TDS, both for 4–6 weeks.
 Staphylococci: Inj. nafcillin or oxacillin 2 g IV q4h for 4–6 weeks or Inj. cefazolin 2 g IV
TDS for 4–6 weeks. If methicillin resistant: Inj. vancomycin 15 mg/kg IV 12 hours for 4
to 6 weeks.
 HACEK group : Inj. ceftriaxone 2 gOD  IV for 4 weeks
 Prophylaxisfor infective endocarditis in patients with vulnerable heart valve.Dental
procedures wherein there is manipulation of gingival tissue or peri-apical regions of the
teeth or perforation of the oral mucosa (including surgery on the respiratory track).
Antibiotic regimens for prophylaxis
 Tab. amoxicillin 2 g 1 hour before procedure
 Inability to take oral medication: Inj. ampicillin 2gm IV/IM 1 hour before procedure


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 Tab. amoxicillin 2 g 1 hour before procedure
 Inability to take oral medication: Inj. ampicillin 2gm IV/IM 1 hour before procedure
 Penicillin allergy:  Tab. clarithromycin or azithromycin 500 mg 1 hour before procedure
or Tab. cephalexin 2 gm, 1 hour before procedure or Tab. clindamycin 600 mg 1 hour
before procedure


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Cardiovascular Diseases
81
 May be caused by viruses, bacteria, mycobacteria, connective tissue disorders, uremia,
malignancy, radiation or trauma.
 Pleuritic chest pain which relieves on bending forward breathlessness, tachycardia
 Fever, pleural rub, elevated ESR, irregular pulse, symmetric enlargement of cardiac
silhouette
 Fever, chest pain, basal rales, pedal edema, cardiomegaly, syncope, ventricular
ectopy,
 LVH, raised Jugular Venous Pressure(JVP ), diffuse dyskinetic apex beat, S3,
hepatomegaly, peripheral edema, murmurs of mitral and tricuspid regurgitation
 Penicillin allergy, inability to tolerate oral medication:Inj. cefazolin or ceftriaxone 1 gm
IV/IM,30 min before procedure or clindamycin 600 mg IV/IM, 1 hour beforeprocedure.
ACUTE PERICARDITIS


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IV/IM,30 min before procedure or clindamycin 600 mg IV/IM, 1 hour beforeprocedure.
ACUTE PERICARDITIS
Inflammation of pericardium is called as pericarditis.
Salient features
Pharmacological treatment
 Tab. aspirin 650 mg orally every 3-4 hours or other NSAIDs likeTab. indomethacin 100-
150 mg orally daily in divided dosesare usually effective.
 Tuberculosis pericarditis: Anti tuberculosis  treatment
 Uremic pericarditis: dialysis
 Usually with antibiotics patients have to be carefully observed as they may develop
pericardial effusion. If cardiac tamponade develops, pericardiocentesis must be carried
out at once.
CARDIOMYOPATHY
The cardiomyopathies are a group of diseases that affect the heart mused itself and are not the


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out at once.
CARDIOMYOPATHY
The cardiomyopathies are a group of diseases that affect the heart mused itself and are not the
result of hypertension, congenital or acquired valvular, coronary or pericardial abnormalities.
Salientfeatures
Non pharmacological treatment
 Salt restriction, alcohol discontinuation
Pharmacological treatment
Standard therapy for heart failure with following drugs:
 Diuretics-hydrochlorothiazide 6.25–50 mg  orchlorthalidone 25–50 mg,loop diuretics-
furosemide 40–80 mg, aldosterone antagonists-spironolactone 25–100 mg
 Beta blockers:atenolol 25–100 mg, metoprolol 25–100 mg,  propranolol 40–160 mg
 ACE inhibitors:captopril 25–200 mg,lisinopril 10–40 mg,ramipril 2.5–20 mg


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 Nonspecific symptoms are fatigue, headache, epistaxis.
 Uncontrolled hypertension can lead to target organ damage (TOD) such as coronary
artery disease (CAD), left ventricular hypertrophy (LVH), cerebrovascular accidents
(CVA), transient ischemicattacks (TIA), retinopathy, peripheral vascular diseases
including dissecting aneurysm, renal disease.
 Associated risk factors are- age >55 years in males and>65 years in females, smoking,
diabetesmellitus, microalburninuria or GFR <60 ml/hr, hyperlipidemia, family history,
obesity, sedentary life-style and ethnic group.
 Angiotensin II antagonists:losartan 25–100 mg, valsartan 80–320 mg, candesartan 2–32
mg
 Calcium antagonists:nifedipine (long-acting) 30–60 mg, verapamil (long-acting)120–


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mg
 Calcium antagonists:nifedipine (long-acting) 30–60 mg, verapamil (long-acting)120–
360 mg, diltiazem (long-acting) 180-420 mg
Hypertrophic cardiomyopathy
 β blockers is the first line of drug.
 Calcium channel blockers, especially verapamil, have also been effective in symptomatic
patients. Diuretics for heart failure
 Dual chamber pacing for refractory cases
 Nonsurgical septal ablation with alcohol injectionin septal branches.
Drugs to be avoided
 Calcium channel blockers and NSAIDs – in dilated cardiomyopathy
 Digitalis, Nitrates, Vasodilators, B-agonists- avoided in Hypertrophic obstructive
cardiomyopathy (HOCM)
HYPERTENSION
Usually asymptomatic and discovered on routine measurement of blood pressure. Secondary


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cardiomyopathy (HOCM)
HYPERTENSION
Usually asymptomatic and discovered on routine measurement of blood pressure. Secondary
hypertension (HT) presents as a part of a symptom complex as in acromegaly, Cushing's
disease, renovascular or renal parenchymal disease, connective tissue disorders (SLE,
scleroderma, etc.), or coarctation of aorta.
Salient features
Investigations
Routine laboratory tests recommended before initiating therapy include,
 Electrocardiogram
 Urinalysis;
 Blood glucose and hematocrit; serum potassium, creatinine (or the corresponding
estimated GFR, and calcium;
 Lipid profile (after a 9-12 hour fast) that includes high-density lipoprotein, cholesterol,
low-density lipoprotein cholesterol, and triglycerides.


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83
 Optional tests include measurement of urinary albumin excretion or albumin/creatinine
ratio. More extensive testing for identifiable causes is not indicated generally unless BP
control is not achieved.
Precautions to be taken while measuring BP
 The auscultatory method of BP measurement with a properly calibrated and validated
instrument should be used. BPshould be measured using an appropriate size cuff in both
upper limbs and at least one lower limb in both supine and erect posture.
 Patient should have been resting for at least 5 minutes and should not have consumed
coffee, smoked during the last 30 minutes before measuring the blood pressure. At least 2
measurements should be made. Systolic BP is the point at which the first of 2 or more


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measurements should be made. Systolic BP is the point at which the first of 2 or more
sounds are heard (phase 1) and diastolic BP is the point before the disappearance of
sounds (phase 5).
Non pharmacologicaltreatment
 Reduce dietary sodium intake to no more than 100 mmol per day (2.4 g sodium or 6 g
sodium chloride).
 Adopt DASH eating plan- diet rich in fruits, vegetables, with low fat dairy products
with a reduced content of saturated and total fat.
 Life-style modification- exercise consisting of vigorous aerobic exercise like brisk
walking, swimming or jogging at least 20 to 30 minutes on most days of the weekwith
the heart rate reaching 65-70% of maximal heart rate.
 Weight control using a combination of dietary and exercise measures to maintainnormal


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the heart rate reaching 65-70% of maximal heart rate.
 Weight control using a combination of dietary and exercise measures to maintainnormal
body weight (body mass index 18.5-24.9 kg nr).
 Moderation of alcohol consumption- limit alcohol to no more than 2 drinks (1 oz or30
ml ethanol; e.g., 24 oz beer, 10 oz wine, or 3 oz 80-proof whiskey) per day in most men
and to no more than 1 drink per day in women and lighter weight persons.
 Cessation of smoking.
 Yoga
Pharmacological treatment
 Pre– hypertension:behavioral modification follow up
Stage 1: thiazide diuretics OR calcium channel blockers   or beta blockers or ACEI
Stage 2: Combination therapy(dosages to be adjusted according to blood pressure
response)
 Diuretics preferred in obese, elderly, CCF


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Stage 2: Combination therapy(dosages to be adjusted according to blood pressure
response)
 Diuretics preferred in obese, elderly, CCF
 Beta blockers in young, coronary artery disease(CAD), vascular headache, atrial
fibrillation
 Calcium channel blockers in  elderly, CAD, ACEI in  diabetic, LVF, young
 Alpha blockers:prostatitism, dyslipidemia
 Alpha methyl dopa-pregnancy


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Dose of commonly usesantihypertensive drugs
 Tab. hydrochlorothiazide 12.5-25 mg OD or BD
 Tab. frusemide 20-40 mg twice day
 Tab. frusemide 20 + spironolactone  50 mg 1-2 times day
 Tab. indapamide 2-5 mg daily
 Tab. atenolol 25-100 mg daily or Tab. metoprolol 25-150 mg BD
 Tab. amlodipine 2.5-20 mg OD or Cap. nifedipine 20-80 mg as sustained release daily
 Tab. enalapril 2.5 mg OD or Tab.  lisinopril 2.5 mg OD or Tab. ramipril1.25-10 mg OD
 Tab. losartan 25-50 mg OD or BD
 Tab. prazosin 1-20 g OD at bed time
 Tab. clonidine 0.05-0.6 mg  BD or Tab. methyldopa 250-1000 mg OD
Accelerated hypertension
Patients presenting with BP 200/140 mmHg or more without papilledema
 Inj. enalapril 1.25-5 mg IV 6 hourly Or Inj. nitroprusside 0.25-1.0 mcg/Kg/min IV


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 Inj. enalapril 1.25-5 mg IV 6 hourly Or Inj. nitroprusside 0.25-1.0 mcg/Kg/min IV
infusion (dose to be titrated with BP, maximum dose for 10 meg only) Or
 Inj. nitroglycerine 5-100mcg/min infusion Or
 Inj. hydralazine 10-20 mg IV or IM, if no response at 20 mg change the drug Or
 Inj. labetalol 20-80 mg IV every 5-10 min up to a total of 300 mg, infusion 0.5-2 mg/min,
oral 100-600 mg 2 times a day. Or
 Inj. phentolamine 5-15 mg IV (especially useful in pheochromocytoma)
Malignant hypertension
 Patients presenting with BP 200/140 mm Hg and evidence of vascular damage like
papilledema, deranged renal function, should be referred to a tertiary care centre.
Resistant hypertension
 Resistant hypertension is the failure to reach goal BP in patients who are adhering to full


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Resistant hypertension
 Resistant hypertension is the failure to reach goal BP in patients who are adhering to full
doses of an appropriate 3-drug regimen that includes a diuretic. Refer these patients to
hypertension specialist.
Follow up
 Regular BP monitoring to ensure optimal or normal BP in young or middleaged or
diabetic subjects (130/80 mm Hg) and at least high normal BP in elderly patients (140/90
mm Hg).
 Monitor all risk factors for coronary artery disease.
 Ensure compliance with life-style modification.
 Assess for complications and target organ damage.
 In accelerated or malignant HT, avoid sudden fall in diastolic BP to below 100 mm Hg


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Cardiovascular Diseases
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 Precordial chest pain due to stress or exertions, palpitation, breathlessnesssymptoms
are typically associated with exertion and emotional upset and are relieved quickly by
rest and/or sublingual nitratesECG shows  ST depression, T wave inversion, LVH.
Hypertension in children and adolescents
 In children and adolescents, hypertension is defined as BP that is, on repeated
measurement, at the 95th percentile or greater adjusted for age, height, and gender. The
fifth Korotkoff sound is used to define diastolic BP.
 Be alert for possibility of identifiable causes of hypertension in younger children (i.e.,
kidney disease, coarctation of aorta).
 Life style interventions are strongly recommended, with pharmacological therapy


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kidney disease, coarctation of aorta).
 Life style interventions are strongly recommended, with pharmacological therapy
instituted for a higher levels of BP or if there is insufficient response to lifestyle
modification.
 Choices of antihypertensive drugs are similar in children and adults, but effective doses
for children are often smaller and should be adjusted carefully.
Patient education
 Explain consequences of uncontrolled HT and the need for the long-term control with
medication.
 Advice regarding control of other risk factors likes diabetes, hyperlipidemia, etc.
 Diuretics should be taken in the morning and if two doses a day are required second dose
should be given before 4 PM.
 Manage target organ damage- referral to a higher centre for CAD (PTCA/ CABG),


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should be given before 4 PM.
 Manage target organ damage- referral to a higher centre for CAD (PTCA/ CABG),
nephropathy (prepare for dialysis or transplant), carotiddoppler to determine presence of
atheroma and possibility of end arterectomy
ANGINA PECTORIS
It is clinically syndrome due to myocardial ischemia, caused by critical obstruction in
coronary arteries due to atherosclerosis, calcific arotic stenosis, or due to spasm or emboli.
Salient features
Non -pharmacological treatment
 Avoid heavy exertion, take rest during acute stage,stop smoking, weight reduction.
Pharmacological treatment
 Tab. isosorbide dinitrate5 mg sublingual during the attack, dose repeated as required or
Tab nitroglycerine 0.3-0.6 mg sublingual


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 Tab. isosorbide dinitrate5 mg sublingual during the attack, dose repeated as required or
Tab nitroglycerine 0.3-0.6 mg sublingual
 If attackoccurs twice in week, chronic prophylaxis is recommendedwith Tab. metoprolol
50 mg BD or Tab.  atenolol 50 mg OD
 If beta blockers are contraindicated or angina persists-Tab. diltiazem -60-120 mg/day
 Tab. aspirin 100-150 mg/ day or Tab. clopidogrel 75 mg/day


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Cardiovascular Diseases
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 Chest pain, breathlessness, perspiration, syncope, tachy or bardycardia, hypo or
hypertension, sudden cardiac arrest, ECG changes showing ischemia or infarction, raised
cardiac markers
MYOCARIDAL INFRACTION
Myocardial Infarction (MI) is due to the formation of occlusive thrombus at the site of
rupture of an atheromatous plaque in a coronary artery.
Salient features
Pharmacological treatment
 Hospitalization and compete immobilization
 Oxygen – 4-6 liters / min
 Oral  uncoated chewable Tab. aspirin– 325 mg
 Tab.  isosorbide dinitrate– 5 mg up to 3 times sublingually
 Tab. atorvastatin– 80 mg
 Tab. clopidogrel– 300 mg
 Inj. morphine sulphate 10 mg or Inj. diamorphine 5 mg IV


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 Tab. atorvastatin– 80 mg
 Tab. clopidogrel– 300 mg
 Inj. morphine sulphate 10 mg or Inj. diamorphine 5 mg IV
 Consider thrombolysis with intravenous streptokinase or alteplase. Thrombolysis to be
done within 30 minsoftime of admission.
 Inj. streptokinase1.5 million units in 100 ml of saline as an intravenous infusion over 1
hour.The drug may cause hypotension, which can be managed with fluids and restricting
the infusion at a slower rate. Or
 Inj. alteplase- rTPA (Recombinant tissue plasminogen activator):  The regimen is given
over 90 minutes (bolus dose of 15 mg followed by 0.75 mg/kg of body weight and then
0.5 mg/kg body weight over 60 minutes)
 Inj. metoprolol 5 mg IV every 2-5 minutes for 3 doses and changed to Tab. metoprolol 50


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0.5 mg/kg body weight over 60 minutes)
 Inj. metoprolol 5 mg IV every 2-5 minutes for 3 doses and changed to Tab. metoprolol 50
mg  every 6 hours for 48 hours, followed by 100 mg every 12 hours.
 Inj. Nitroglycerine IV  0.6– 1.2 mg/hour
 Inj. heparin 200 units/Kg  SC twice daily for 5 days is given in addition to oral aspirin
may prevent reinfarction after successful thrombolysis and reduce the risk of
thromboembolic complications.
 Moni tor ECG, blood pressure and cardiac enzymes
C ontraindications to thrombolytic therapy
 Absolute contraindications are active internal bleeding, previous sub-arachnoid or intra-
cerebral hemorrhage, non hemorrhagic stroke within the last 1 year, uncontrolled
hypertension (systolic > 180mm Hg, diastolic > 110mmHg)


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cerebral hemorrhage, non hemorrhagic stroke within the last 1 year, uncontrolled
hypertension (systolic > 180mm Hg, diastolic > 110mmHg)
 Relative contra-indications are current use of anti-coagulants, recent (< 2 weeks) invasive
surgical procedure, recent prolonged (> 10 min) cardiopulmonary resuscitation, known
bleeding diathesis, pregnancy, hemorrhage prone ophthalmic conditions, active peptic ulcer


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Cardiovascular Diseases
87
 Cough expectoration, breathlessness, pedaledema, hypo or hyper tension, easy fatigability.
 Raised jugular venous pressure, positive abdominojugular reflex, basal rales, pulmonary
edema, orthopnea, paroxysmal nocturnal dyspnea (PND). S3, hepatomegaly, ascites, sinus
tachycardia.Chest X ray shows cardiomegaly, pulmonary congestion.
disease, recent history of severe hypertension.Notes: Streptokinase should not be used, if
given in the preceding 5 days to 2 years because of the risk of allergic reactions.
CONGESTIVE HEART FAILURE (CHF)
CHF is critical syndrome of inadequate cardiac output resulting in fluid retention in the
lungs, abdominal organs and peripheral tissue.
Salient features


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lungs, abdominal organs and peripheral tissue.
Salient features
Patients of heart failure are divided in 4 categories for management(Figure 1).
For category A– No further treatment needed
For category B– Diuretics and vasodilators
For category C– Ionotropic agents
For category L– Fluid challenge can be given
Figure 1. Categories of heart failurefor ease of management
Non pharmacological treatment
 Restrict physical activity, bed rest in propped up position with a back rest. Dietary salt
(sodium) restriction(2– 3 g/day).
 Avoid and discontinue NSAIDs, high dose Beta blockers and calcium channel blocker.
Fluid restriction depending on output and other conditions.
Pharmacologicaltreatment
 Treatment consists of judicious mix of vasodilators, diuretics and inotropic support


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Pharmacologicaltreatment
 Treatment consists of judicious mix of vasodilators, diuretics and inotropic support
 Inj.furosemide 40– 80 mg IV stat every 2 to 3 hours with maximum up to 200 mg/day.
Maintenance dose is 40 mg IV 12 hourly.


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Cardiovascular Diseases
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 Palpitation, breathlessness, syncope, chest pain, “gabharaman”, visual disturbances.
tachy or bradycardia, hypo or hypertension. ECG changes according to type of
arrhythmia
 Tab. spironolactone 25– 200 mg/day or Tab. chlorthiazide 250– 500 mg/day or Tab.
indapamide 2.5– 5 mg/day orTab. benzthiazide 25 mg plus Tab. triamterene 50 mg/day.
 Tab. enalapril 2.5-20 mg/day or Tab. lisinopril 2.5– 10 mg/day
 Tab. isosorbidemononitrate 60 mg/day as slow releasepreparation at night
 Digoxin is indicatedin fast ventricular rate (e.g. atrialfibrillation) and LVEF < 30 %.
Tab. digoxin 0.5 mg first day followed  by 0.25 mg/day 5 days/week
 Tab. carvedilol 3.15– 25 mg per day in one or two divided doses is useful in all


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Tab. digoxin 0.5 mg first day followed  by 0.25 mg/day 5 days/week
 Tab. carvedilol 3.15– 25 mg per day in one or two divided doses is useful in all
symptomatic or asymptomatic heart failure and in case of reduced ejection fraction (40%)
 Inj. heparin 5000 IU 12 hourly SC if patients is bedridden
Monitoring of CHF patient
 Strict intake– output charting
 Daily weight and abdominal girth measurement
 Serum electrolytes and uric acid
ARRHYTHMIAS
Arrhythmias are divided into supraventricular tachycardia, ventricular tachycardia,
bradyarrhythmias
Salient features
SUPRAVENTRICULAR TACHYCARDIA
Pharmacological treatment
 Depends on the hemodynamic status of the patient.
 If he is haemodynamically stable:
- Treatment of acute episode includes vagal maneuvers (carotid sinus massage,valsalva


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 If he is haemodynamically stable:
- Treatment of acute episode includes vagal maneuvers (carotid sinus massage,valsalva
maneuver)
- If the measure fails, AV nodal blocking drugs are tried.Inj. adenosine 6 mg IV bolus
followed by 10 ml saline flush is given.12 mg IV bolus can be repeated if no
response after 2 minutes.Contraindicationsincludesick sinus syndrome or second or
third degree AVblock.
- Inj.metoprolol 5m g IV can be repeated after 5 minutes or
- Inj. verapamil 5-10 mg IV bolus over 2-3 min. can be repeated after 15 minsor Inj.
diltiazem 0.25 mg/kg IV bolus over 2 min. followed by IV infusion at a rate of
10mg/hour.
- If haemodynamically unstable, prompt synchronized direct current (DC).
Cardioversion (using 10 to 100 joules) has to be done.


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Cardiovascular Diseases
89
Maintenance therapy
Once sinus rhythm is established, chronic maintenance therapy includes,
 Tab.  diltiazem 30 mg TDS or Tab. verapamil-40 mg TDS OR
 Tab. metoprolol 25-100 mg BD or Tab.  atenolol 25-100 BD OR
 Tab. digoxin 0.125-0.5 mg OD
Curative therapy
For supraventricular tachycardia involving accessary pathway is radio-frequency ablation.
VENTRICULAR TACHYCARDIA
Runs of three or more consecutive idioventricular beats exceeding a rate of 100 beats per
minute.
Types:
 Sustained– If ventricular tachycardia(VT) persists for > 30 seconds.
 Non -sustained– 3 beats to 30 seconds.
 Monomorphic -Configurations uniform
 Polymorphic– Configuration varies from beat to beat
Pharmacological treatment


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 Monomorphic -Configurations uniform
 Polymorphic– Configuration varies from beat to beat
Pharmacological treatment
1. Patients with nonsustained arrhythmias, without organic cardiac disease are
asymptomatic-need not be treated.
2. Patients with sustained VT in the absence of cardiac disease are symptomatic and require
therapy with  Tab. amiodarone 200-400 mg /day TDS
3. In patients with VT with organic cardiac disease, if haemodynamic instability,
unsynchronized the arrhythmia.
4. If haemodynamically stable, the following drugs can be administered:
5. Inj. lidocaine– 1 mg/kg IV bolus,0.5-1 mg/kg boluses may be repeated at 5 min intervals
followedby 2-4 mg/min maintenance Infusion.
 Inj. amiodarone may be tried.
 If   these drugs fail, over drive padding has to be done.


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followedby 2-4 mg/min maintenance Infusion.
 Inj. amiodarone may be tried.
 If   these drugs fail, over drive padding has to be done.
 To prevent recurrences, sustained VT-ICD implantation is effective.
ATRIAL FIBRILLATION
Common arrhythmia, a variant of supraventricular tachycardia.
Salient features
Pharmacological treatment
Acute atrial fibrillation
 Palpitation, breathlessness, gabharaman, giddiness. Tachycardia, irregularly
irregular pulse, hypotension is commoner than hypertension


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Cardiovascular Diseases
90
 Treat the precipitating factors like thyrotoxicosis
 If the patient is haemodynamically unstable, electrical cardio version using 200 joules is
the treatment of choice.
 If  haemodynamically stable, ventricular rate control is adequate by Tab. metaprolol 25-
100 mg BD
 Tab. warfarin 5 mg OD and dose adjust as per INR
Surgical treatment
 Ablation around pulmonary veins.
BRADYARRHYTHMIAS
Sinus bradycardia– regular heart rate < 60/min.
Types: sinoatrial blockand atrioventricular block
Pharmacological treatment
 Inj.atropine 0.6 mg IV repeated 4-6 hourly orInj. isoproterenol 2-10 mcg/min infusion
Surgical treatment
 Temporary pacemaker
 If needed permanent pacemaker insertion.


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91
 Repeated attacks of headache lasting 4–72 h in patients with a normal physical
examination, no other reasonable causefor the headache, and at least 2 of the
following features
 Unilateral pain, throbbing pain aggravated by movement, moderate or severe intensity
along withone of the following features:
 Nausea/vomiting and orphotophobia and phonophobia
Chapter 5
CENTRAL NERVOUS SYSTEM DISEASES
MIGRAINE
Most often begins at puberty and most affects those aged between 35 and 45 years.
Salient features
N on pharmacological treatment
 Avoidance of factors that triggers a migraine attack and suitable life-style modification.
Pharmacological treatment
 The combination of acetaminophen, aspirin, and caffeine has been use for the treatment of
mild to moderatemigraine.


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Pharmacological treatment
 The combination of acetaminophen, aspirin, and caffeine has been use for the treatment of
mild to moderatemigraine.
 If NSAIDs/analgesicsfail, Tab. sumatriptan 50 mg or 100 mg PO or Tab. zolmitriptan 2.5
mg PO can be used.
 If  early nausea or difficulties taking tablets,zolmitriptan 5 mg nasal spray or  sumatriptan 20
mg nasal spray is used.
 Parenteral administration of drugs such as dihydroergotamine and sumatriptan is used for the
rapid relief of a migraine attack.
 Patients with an increasing frequency of migraine attacks, or with attacks that are either
unresponsive or poorly responsive to abortive treatments, are good candidates for preventive
agents. In general, a preventive medication should be considered in the subset of patients


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agents. In general, a preventive medication should be considered in the subset of patients
with five or more attacks a month. The drugs that have been used for the prophylactic
treatment of migraine include
- Tab. propranolol  40–120 mg BD or Tab. sodium valproate: 400–600 mg BD
- Tab. topiramate :25–200 mg/d OD
Patient education
 Identify the triggers for the migraine attack (lack of sleep, chocolates, wine etc) and avoid
them.


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Central Nervous System Diseases
92
 Episodic TTH attacks usually last a few hours, but can persist for several days.
 This headache is described as pressure or tightness, like a band around the head,
sometimes spreading into or from the neck.
 CH is relatively uncommon, more common in males.Most people developing CH are
in their 20s or older.
 It is characterized by frequent recurring, brief but extremely severe headache
associated with pain around the eye with tearing and redness, the nose runs or is
blocked on the affected side and the eyelid may drop.
TENSION -TYPE HEADACHE (TTH)
TTH often begins during the teenage years.
Salient features
Pharmacological treatment
 The pain of TTH can gen erally be managed with simple analgesics such as
acetaminophen, aspirin, or NSAIDs.


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Pharmacological treatment
 The pain of TTH can gen erally be managed with simple analgesics such as
acetaminophen, aspirin, or NSAIDs.
 Behavioral approaches including relaxation can also be effective.
 For chronic TTH, Tab. amitriptyline 10–75 mg at night time is the only proven treatment
CLUSTER HEADAC HE (CH)
Salient features
Pharmacological treatment
 Cluster headache attacks peak rapidly, and thus a treatment with quick onset is
required.  Many patients with acute cluster headache respond very well to oxygen
inhalation. This should be given as 100% oxygen at 10–12 L/min for 15–20 min.
 Inj.sumatriptan 6 mg SC is rapid in onset and will usually shorten an attack to 10–15
min. Sumatriptan (20 mg) and zolmitriptan (5 mg) nasal sprays are both effective in
acute cluster headache.


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min. Sumatriptan (20 mg) and zolmitriptan (5 mg) nasal sprays are both effective in
acute cluster headache.
Preventive treatments of cluster headache
Short-Term prevention Long -term prevention
 Episodic Cluster Headache  Episodic Cluster Headache  and  Prolonged
Chronic Cluster Headache
 Prednisone 1 mg/kg up to 60 mg daily,
tapering over 21 days
 Methysergide 3–12 mg/d
 Verapamil 160–960 mg/d
 Methysergide 3-12mg.d
 Verapamil 160–960 mg/d
 Greater occipital nerve injection


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Central Nervous System Diseases
93
 Symptoms include weakness, numbness, paresthesia, dysphasia, dysarthria, dysphagia,
dyspraxia, hemianopia, falls, change in personality, ataxia, reduced sensationsand
impaired sensorium.
STROKE
Stroke is the abrupt onset of neurologic deficit that is attributable to a focal vascular cause.
TIA (Transient Ischemic Attacks)requires that all neurologic signs and symptoms resolve
within 24 hours regardless of whether there is imaging evidence of new permanent brain
injury. However, a newly proposed definition classifies those with new brain infarction as
ischemicstrokes regardless of whether symptoms persist.
Salient features
Pharmacological treatment
 Rapid evaluation is necessary for the use of time sensitive treatments such as


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Salient features
Pharmacological treatment
 Rapid evaluation is necessary for the use of time sensitive treatments such as
thrombolysis. Close attention is paid to the ABC’s i.e. Airway, Breathing and Circula tion
of the patient and treat hypoglycemia or hyperglycemia if identified. Once the diagnosis
of stroke is made, a brain imaging study is necessary to determine if the cause of stroke is
ischemia or hemorrhage. CT is useful in identifying early hemorrhagewhile MRI is
useful in identifying early infarct.
 Blood pressure should be lowered if there is malignant hypertension or concomitant
myocardial ischemia or if blood pressure is >185/110 mm Hg and thrombolytic therapy is
anticipated (See section of hypertension)
 Fever is treated with antipyretics and surface cooling.


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anticipated (See section of hypertension)
 Fever is treated with antipyretics and surface cooling.
 Euglycemia is to be maintained.
 Between 5 and 10% of patients develop enough cerebral edema to cause herniation. Other
anti-edema measures such as head elevation, Tab. furosemide 40 mg OD and
hyperventilation are useful.
 Common complications of bedridden patients—infections (pneumonia, urinary, and skin)
and deep venous thrombosis (DVT) with pulmonary embolism are to be prevented.
 Intravenous thrombolysis(Table 1):
 Tab. aspirin 75 mg OD
 Inj.heparin 5000 IU SC
 Proper rehabilitation of the stroke patient includes early physical, occupational, and
speech therapy.
Secondary prevention of stroke and TIA


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 Proper rehabilitation of the stroke patient includes early physical, occupational, and
speech therapy.
Secondary prevention of stroke and TIA
 Control of risk factors such as hypertension, diabetes, dyslipidemia, smoking cessation.
 Tab.aspirin 75-325 mg/day is recommended for stroke prevention.
 Tab. warfarin is useful for stroke prevention with a target INR of 2-3 in patients with
chronic nonvalvular AF as well as untreated rheumatic heart disease with AF.


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Treatment of haemorrhagic stroke
 Inj. mannitol 20% 1g/kg stat followed by 0.5 g/kgIV infusion, Inj. furosemide 40 mg IV
stat, elevation of head end and hyperventilation are useful.
 Antihypertensiveagents are instituted if BP is more than180mmHg systolic or
>130mmHg diastolic. Goalis to keep a mean arterial pressure of less than130mmHg.
 With thrombocytopenia (platelet countless than50,000/µl), transfusion of fresh platelets
is indicated.
 Patients with cerebellar hemorrhages or with depressed mental status and radiographic
evidence of hydrocephalus should undergo urgent neurosurgical evaluation.
 Thrombolytic agents are the mainstay (Table 1).
Table 1. Indications, contraindications and dosage schedule of thrombolytic agents in
stroke


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 Thrombolytic agents are the mainstay (Table 1).
Table 1. Indications, contraindications and dosage schedule of thrombolytic agents in
stroke
Indications Contraindications
 Clinical diagnosis of stroke
 Onset of symptom to drug
administration <3 hours
 CT scan showing no haemorrhage
or edema of >1/3 rd of middle
cerebral artery (MCA) territory
 Age >18 years
 Consent of patient
 Sustained BP >185/110 mm Hg despite
treatment
 Platelets <100,000; HCT <25%; glucose
<50 or >400 mg/dl
 Use of heparin within 48 h and prolonged
PTT, or elevated INR
 Rapidly improving symptoms
 Prior stroke or head injury within 3
months; prior intracranial hemorrhage
 Major surgery in preceding 14 days
 Minor stroke symptoms
 G Ibleeding in preceding 21 days
 Recent myocardial infarction


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 Major surgery in preceding 14 days
 Minor stroke symptoms
 G Ibleeding in preceding 21 days
 Recent myocardial infarction
 Coma or stupor
Administration
 Administer rtPA (recombinant tissue plasminogen activator like alteplase or
tenecteplase) 0.9 mg/kg IV (maximum 90 mg) IV as 10% of total dose by bolus,
followed byremainder of total dose over 1 h
 Frequent cuff blood pressure monitoring
 No other antithrombotic treatment for 24 h
 For decline in neurologic status or uncontrolled blood pressure, stop infusion, give
cryoprecipitate, and reimage brain emergently
 Avoid urethral catheterization for 2 h


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 Presence of Bell’s phenomenon, affection of upper as well as lower part of face, involvement
of taste and lacrimation,
 A bsence of emotional facial movements and absence of other neurological findings favour a
diagnosis of peripheral or LMN facial palsy, the commonest cause being Bell’s palsy.
 Cardinal features include bradykinesia, rest tremor, rigidity, gait disturbance and
postural instability.Other motor features include micrographia, masked facies, reduced
eye blink, soft voice (hypophonia) and dysphagia.
 N on motor features include anosmia, sensory disturbances (e.g., pain), mood disorders
(e.g., depression), sleep disturbances, autonomic disturbances, orthostatic hypotension,


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(e.g., depression), sleep disturbances, autonomic disturbances, orthostatic hypotension,
gastrointestinal disturbances, genitourinal disturbances, sexual dysfunctionand
cognitive impairment/dem entia.
FACIAL PALSY
It can be caused by upper motor neuron (UMN) or lower motor neuron (LMN) lesion.
Salient features
Investigations
 In a typical case, no investigations are required.
 In uncertain cases, it is necessary to getan ESR, blood sugar, workup for sarcoidosis or
MRI scanning maybe indicated. MRI often shows swelling and enhancement of the facial
nerve in idiopathic Bell's palsy.
 Electromyography may aid in diagnosis as well as prognosis
Non -pharmacological treatment
 Use of paper tape to depress the upper eyelid during sleep and prevent corneal drying.


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Non -pharmacological treatment
 Use of paper tape to depress the upper eyelid during sleep and prevent corneal drying.
 Massage of the weakened muscles.
 Splinting of lower part of face to prevent drooping.
 Facial retraining (mime therapy)
Pharmacological treatment
 Tab. prednisone 60-80 mg daily during the first 5 days and then tapered over the next 5
days modestly shortens the recovery period and improves the functional outcome.
 Tab. acyclovir 400 mg five times daily for 10 days in combination with prednisone.
PARKINSON'S DISEASE
Parkinson's disease (PD) is the second commonest neurodegenerative disease.
Salient features
Pharmacological treatment
 Levodopa
- Tab. carbidopa/levodopa (1:4) 10/100mg-25/200mg 4-6 times a day


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 Most common c auses ofdementia are Alzheimer's disease, vascular dementia (multi
in fact/ diffuse whitematter disease (Binswanger's), alcoholism, parkinson’s disease,
drug ormedical intoxication
 Brief screening tools such as the mini-mental status examination (MMSE) help to
confirm the presence of cognitive impairment.
- Adverse effects: Acute side effects include nausea, vomiting, andorthostatic
hypotension.
- Motor complications like wearing-off effect, dyskinesia, on-off phenomenon develop
with long-term therapy.
 Dopamine Agonists-Tab. pramipexole 0.25–1.0 mg TDS, Tab. ropinirole 6–24 mg/d
 Adverse effect: Acute side effects include nausea, vomiting, and orthostatic hypotension,
hallucination.
 MAO -B Inhibitors-Tab. selegiline 5 mg BD


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hallucination.
 MAO -B Inhibitors-Tab. selegiline 5 mg BD
 COMT Inhibitors- Tab. entacapone 200 mg with each levodopa dose or Tab.tolcapone
100–200 mg TDS
 Adverse effects: Primarily dopaminergic (nausea, vomiting, increased dyskinesia). Cases
of fatal hepatic toxicity have been reported with tolcapone.
 Central-acting anticholinergic agents-Tab.trihexyphenidyl 2 mg TDS
 NMDA -receptor antagonist-Tab. amantadine 100-300 mg/day.
DEMENTIA
It is defined as an acquired deterioration in cognitive abilities that impairs the successful
performance of activities of daily living. Memory is the most common cognitive ability lost
with dementia.
Salient features
Pharmacological treatment
 The major goals of dementia management are to treat correctable causes and to provide


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with dementia.
Salient features
Pharmacological treatment
 The major goals of dementia management are to treat correctable causes and to provide
comfort and support to the patient and caregivers.
 Treatment of underlying causes might include thyroid replacement for hypothyroidism;
vitamin therapy for thiamine or B12 deficiency or for elevated serum homocysteine;
antimicrobials for opportunistic infections or antiretroviral for HIV; ventricular shunting
for NPH; or appropriate surgical, radiation, and/or chemotherapeutic treatment for CNS
neoplasm.Drugs used for dementia are listedbelow:


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Table 2. Drugs used in the treatment of dementia
Drug Dose Side effect
Tab.donepezil 10 mg daily nausea, diarrhea, abdominal cramps, altered
sleep with unpleasant or vivid dreams,
bradycardia, muscle cramps
Tab. rivastigmine6 mg twice daily
Tab. galantamine 24 mg daily
Tab. memantine 10 mg twice dailydizziness, confusion, headache, syncopeor
hypotension
GUILLAIN -BARRÉ SYNDROME (GBS)
GBS manifests as a rapidly evolving areflexic motor paralysis with or without sensory
disturbance.
Diagnostic criteriafor GBS
I. Required for Diagnosis
1. Progressive weakness of variable degree from mild paresis to complete paralysis
2. Generalized hypo-or areflexia
II. Supportive of Diagnosis
1. Clinical features


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2. Generalized hypo-or areflexia
II. Supportive of Diagnosis
1. Clinical features
 Symptom progression: Motor weakness rapidlyprogresses initially but ceases by 4
weeks.
 Demonstration of relative limb symmetry regarding paresis.
 Frequent cranial nerve involvement: Facial (cranial nerve VII) 50% and typically bilateral
but asymmetric; occasional involvement of cranial nerves XII,X, and occasionally III,
IV, and VI as well as XI.
 Autonomic dysfunction can include tachycardia, other arrhythmias, postural hypotension,
hypertension, other vasomotor symptoms.
 A preceding gastrointestinal illness (e.g., diarrhea) or upper respiratorytract infection is
common.
2. Cerebrospinal fluid features supporting diagnosis
 Elevated or serial elevation of CSF protein.


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common.
2. Cerebrospinal fluid features supporting diagnosis
 Elevated or serial elevation of CSF protein.
 CSF cell counts are <10 mononuclear cell/mm3.
3. Electrodiagnostic medicine findings supportive of diagnosis
 NCV slowing/conduction block at some time during disease process.
 Distal motor latency increase may reach 3 times normal values.
 F-waves indicate proximal NCV slowing.
III. Findings reducing possibility of diagnosis
1. Asymmetric weakness
2. Failure of bowel/bladder symptoms to resolve


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 Fever with headache, neck stiffness, photophobia, nausea , vomiting and altered mental
status.It is associated with a CNS inflammatory reaction that may result in decreased
consciousness, seizures, raised intracranial pressure (ICP), and stroke.
 Comm on organisms are Streptococcus pneumonia, Haemophilus influenza, Neisseria
meningitides,Listeria monocytogenes, Group B streptococcus, less frequent organism
are Staph. Aureusand coagulase negativeStaphylococcus group A & group B
Streptococcus, enteric gram negativebacilli.
3. Severe bowel/bladder dysfunction at initiation of disease
4. Greater than 50 mononuclear cells/mm3 in CSF
5. Well-demarcated sensory level
IV. Exclusion criteria


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4. Greater than 50 mononuclear cells/mm3 in CSF
5. Well-demarcated sensory level
IV. Exclusion criteria
1. Diagnosis of other causes of acute neuromuscularweakness (e.g., myasthenia gravis,
botulism, poliomyelitis, toxic neuropathy).
2. Abnormal CSF cytology suggesting carcinomatous invasion of the nerve roots
Non pharmacological treatment
 Monitor Airway, Breathing and Circulation. Also includes mechanical ventilator support,
management of autonomic dysfunction and physical therapy.
Pharmacological treatment
 The available treatment modalities are plasma exchange and intravenous immunoglobulin
(IVIG). Both are equally effective. Corticosteroids are notrecommended for treatment of
GBS.
 Plasma exchange:
- The advised regimen of plasma exchange removes a total of 200 to 250 ml/kg of


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GBS.
 Plasma exchange:
- The advised regimen of plasma exchange removes a total of 200 to 250 ml/kg of
plasma in four to six treatments on alternate days, or over a shorter period if there is
no coagulopathy. The replacement fluid is saline combined with 5% albumin.
 IVIG:
- 0.4 g/kg per day for 5 consecutive days
- It is both easier to administer and probably safer because there is no need for large
intravenous access.
- Disadvantage is the higher cost of therapy.
ACUTE BACTERIAL MENIN GITIS
Itis an acute purulent infectionof the meningeswithin the sub-arachnoid space.
Salient features
Investigations
CSF analysis(Table 3)


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Table 3. Cerebrospinal fluid characteristics of different etiologiesof meningitis
Characteristics Normal Bacterial Viral Fungal/TB
Pressure(cmH2O) 5-20 >30 Normal or mildly
increased -
Appearance Normal Turbid Clear Fibrin web
Protein(g/L) 0.18-0.45 >1 <1 0.1-0.5
Glucose(mmol/L) 2.5-3.5 <2.2 Normal 1.6-2.5
Gram Stain Normal 60-90% positive Normal -
Glucose-
CSF: Serum ratio 0.6 <0.4 >0.6 <0.4
WCC <3 >500 <1000 100-500
Others - 90% PMN
Monocytes
10% have>90%PMN
30%have>50%PMN
Monocytes
Pharmacological treatment
Following table shows choice of antibiotic as per patient characteristics and their dose and
frequencyinempiricaltherapy ofbacterialm eningitis andfocal CNSinfections


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frequencyinempiricaltherapy ofbacterialm eningitis andfocal CNSinfections
Table 4. Choice of antibiotics for the treatment of bacterial meningitis as per patient
characteristics
Indication Antibiotic
Preterm infants to infants <1 month Ampicillin + cefotaxime
Infants 1–3 month Ampicillin + cefotaxime or ceftriaxone
Immunocompetent children >3 months and adults <55Cefotaxime, ceftriaxone or cefepime +
vancomycin
Adults >55 and adults of any age with alcoholism or
other debilitating illnesses
Ampicillin + cefotaxime, ceftriaxone or
cefepime + vancomycin
Hospital-acquired meningitis, posttraumatic or post
neurosurgery meningitis, neutropenic patients, or
patients with impaired cell-mediated immunity
Ampicillin + ceftazidime or meropenem
+ vancomycin


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neurosurgery meningitis, neutropenic patients, or
patients with impaired cell-mediated immunity
Ampicillin + ceftazidime or meropenem
+ vancomycin
Antimicrobial Agent Total Daily Dose and Dosing Interval
Ampicillin 12 g/d, every 4 hourly
Cefipime 6 g/d, every 8 hourly
Cefotaxime 12 g/d, every 12 hourly
Ceftriaxone 4 g/d, every 12 hourly
Ceftazidime 6 g/d, every 8 hourly
Gentamicin 7.5 (mg/kg)/d, every 8 hourly


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 Acute or subacute onset of fever, headache,altered consciousness, focal neurological
symptoms
 C ommon cause areHerpes simplexIvirusand Varicella zostervirus.
Meropenem 3 g/d, every 8 hourly
Metronidazole 1500–2000 mg/d, every 6 hourly
Penicillin G 20–24 million U/d, every 4 hourly
Vancomycin 2 g/d, every 12 hourly
 Once culture report comes therapy should be changed accordingly
 Inj. dexamethasone 0.15 mg/kg every 6 hourly IV for 2 days. It should be started shortly
before the antibiotic.
 Emergency treatment of increased ICP includes elevation of the patient's head to 30–45°,
intubation and hyperventilation (PaCO 2 25–30 mm Hg), and Inj. mannitol 20% 1 g/kg stat
followed by 0.5g/kg every 4-6 hourly.


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intubation and hyperventilation (PaCO 2 25–30 mm Hg), and Inj. mannitol 20% 1 g/kg stat
followed by 0.5g/kg every 4-6 hourly.
 A 7 -day course of intravenous antibiotic therapy is adequate for uncomplicated
meningococcal meningitis.
 The index case and all close contacts should receive chemoprophylaxis with a 2-day
regimen of rifampin (600 mg every 12 h for 2 days in adults and 10 mg/kg every 12 h for
2 days in childrenmore than1 yearof age).
 A 2-week course of intravenous antimicrobial therapy is recommended for pneumococcal
meningitis. Meningitis due toL. monocytogenes is treated with ampicillin for at least 3
weeks. Gentamicin is added in critically ill patients (2 mg/kg loading dose, then 7.5
mg/kg per day given every 8 h and adjusted for serum levels and renal function). A 3-


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mg/kg per day given every 8 h and adjusted for serum levels and renal function). A 3-
week course of intravenous antibiotictherapy is recommended for meningitis due to
gram-negative bacilli.
 Tuberculousmeningitisis treatedas per RNTCP protocol.
VIRAL ENCEPHALITIS
In encephalitis the brain parenchyma is also involved. Many patients with encephalitis also
have evidence of associated meningitis (meningoencephalitis).
Salient features
Investigations
C SF analysisasinacute bacterialmeningitis(Table 3)
Pharmacological treatment
 Specific antiviral therapy should be initiated when appropriate.
 Following table shows drugs, dose duration and their common side effects(Table 5).


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Table 5. Dosages and side effects of antivirals in the treatment of viral encephalitis
Drug Dose Duration Etiology Side effect
Acyclovir 10 mg/kg
every 8 hrly
14 to 21
days
HSV,VZV,EBV nausea, vomiting,diarrhea  and
Neurotoxicity (lethargy or
obtundation, disorientation,
confusion, agitation, hallucinations,
tremors, seizures)
Ganciclovir 5mg/kg every
12 hrly,
followed by 5
mg/kg
Indefinite CMV Granulocytopenia and
thrombocytopenia, Gastrointestinal
side effects, including nausea,
vomiting, diarrhea, and abdominal
pain
Ribavirin 15 mg/kg in
divided doses
every 8 hrly
California
encephalitis
(LaCrosse)
virus, severe
adenovirus or
rotavirus
encephalitis.
Hemolysis, nausea, vomiting,
diarrhea, andabdominal pain


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California
encephalitis
(LaCrosse)
virus, severe
adenovirus or
rotavirus
encephalitis.
Hemolysis, nausea, vomiting,
diarrhea, andabdominal pain
 Basic management and supportive therapy should include careful monitoring of ICP, fluid
restriction, avoidance of hypotonic intravenous solutions, and suppression of fever.
 Seizures should be treated with standard anticonvulsant regimens,and prophylactic
therapy should be considered in view of the high frequency of seizures in severe cases of
encephalitis.
NEUROCYSTICERCOSIS
Neurocysticercosis is the most common parasitic disease of the CNS worldwide. Humans
acquire cysticercosis by the ingestion of food contaminated with the eggs of the parasiteT.
solium.
Diagnostic criteria for cysticerosis
Absolute criteria


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solium.
Diagnostic criteria for cysticerosis
Absolute criteria
 Demonstration of cysticercus by histologic or microscopic exam of biopsy material
 Visualization of the parasite in the eye by fundoscopy
 Neuro-radiologic demonstration of cystic lesion containing a characteristic scolex.
Major criteria
 Neuro-radiologic lesions suggestive of neuro-cysticercosis.
 Demonstration of antibodies to cystic in serum.
 Resolution of intracranial cystic lesionsspontaneously or after therapy withalbendazole
or praziquantel alone.


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Minor criteria
 Lesions compatible with neuro-cysticercosis detect by neuro-imagining studies.
 Clinical manifestations suggestive of neuro-cysticercosis.
 Demonstration of antibodies tocysticerd or cycticercal antigen in CSF by ELISA.
 Evidence of cysticercosis outside the central nervous system.
Epidemiologic criteria
 Residence in a cysticercosis endemic area
 Frequent travel to a cysticercosis endemic area
 Household contact with an individual infected withTaenia sodium
Diagnosis is confirmed by either one absolute criteria or a combination to two major criteria
one minor criterion and one epidemiologic criterion.
Investigations
 Enzyme -linked immunoelectrotransfer blot(EITB ) of serum for cysticercal antibodies.
ELISA of serum and CSF


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Investigations
 Enzyme -linked immunoelectrotransfer blot(EITB ) of serum for cysticercal antibodies.
ELISA of serum and CSF
 CT scan shows the cyst and granuloma stages of neuro-cysticercosis. Located in the
cortex or the gray white junction and present as punctuate hyperdense lesion with ring
enhancement with edema around the cyst, associated with the death of the organism.
 MRI use of contrast shows cysticerus death, visibleas enhancement of the cyst wall,
which indicates that the cyst has changed into a granuloma. In addition MRI shows
vasogenic edema around the cyst.
 Soft tissue radiography can be performed to look for extraneural cysts.
 Electro encephalography (EEG): in children with intractable seizures.


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 Soft tissue radiography can be performed to look for extraneural cysts.
 Electro encephalography (EEG): in children with intractable seizures.
 Stoolexamination: Presence of ova may be the sole diagnostic confirmation in children.
Pharmacological treatment
 Treatment with anthelminthic drugs can result in complete resolution or significant
regression 80-90% of patients.
 Tab. praziquantel 5-10 mg/kg single dose can be administered to individuals found to
have T solium tapeworms in their stool.
 Tab. albendazole 400 mg PO BD for 14 days with meals.
 Tab. phenytoin300 mg PO, pediatric dose: 4-8 mg / kg / day PO divided BD / TDSto
prevent seizures.
 To avoid inflammatory response in the CNS, the patient must be started on
anticonvulsants and high dose glucocorticoids.


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prevent seizures.
 To avoid inflammatory response in the CNS, the patient must be started on
anticonvulsants and high dose glucocorticoids.
Surgical treatment
 Reserve neurosurgical intervention for cases of cysts that have failed to resolve with anti-
helminthic treatment and are causing severe neurologic sequelae.
Patient education
 Prolonged freezing or thorough cooking of pork to kill the parasite.


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 Paraplegia is weakness of both lower limbs and quadriplegia is weakness of all four
limbs. Paraplegia or quadriplegia maybe caused by lesions of cerebrum, spinal cord,
motor roots, peripheral nerves, myoneural junction or muscles. The lesions of the
spinal cord may be compressive or non-compressive.
 Personal hygiene or through washing and avoiding unpeeled fruits and vegetables in
endemic areas.
PARAPLEGIA AND QUADRIPLEGIA
Salient features
Pharmacological treatment
 The treatment depends on the underlying etiology.E.g. compressive myelopathiesusually
require urgent surgical intervention.
 Indications for corticosteroids in paraplegia:neoplastic spinal cord compression,


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require urgent surgical intervention.
 Indications for corticosteroids in paraplegia:neoplastic spinal cord compression,
traumatic spinal cord injuries, acute transverse myelitis, multiple sclerosis, neuromyelitis
optica, sarcoid myelitis, ADEM. The dose is Inj. methylprednisolone 1 g IV for 3-5 days.
Continuation of steroids depends on the underlying cause.
 Fever: The loss of normal thermoregulation and inability to maintain normal body
temperature can produce recurrent fever (quadriplegic fever),although most episodes of
fever are due to infection of the urinary tract, lung, skin, or bone.
 Bladder dysfunction: It generally results from loss of supraspinal innervation of the
detrusor muscle of the bladder wall and the sphincter musculature.


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detrusor muscle of the bladder wall and the sphincter musculature.
- Detrusor spasticity is treated with anticholinergic drugs likeTab. oxybutynin 2.5–5
mg QID or tricyclic antidepressants that have anticholinergic properties, Tab.
imipramine, 25–200 mg/d.
- Failure of the sphincter muscle to relax during bladder emptying (urinary
dyssynergia) may be managed with theadrenergic blocking agent Tab. terazosin
hydrochloride 1–2 mg TDS or QID, with intermittent catheterization, or, if that is not
feasible, by use of a condom catheter in men or a permanent indwelling catheter.
- Bladder areflexia due to acute spinal shock or conus lesions is best treated by
catheterization.
- Surgical options include the creation of an artificial bladder.


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catheterization.
- Surgical options include the creation of an artificial bladder.
 Bowel regimens and disimpaction are necessary in most patients to ensure at least
biweekly evacuation and avoid colonic distention or obstruction.
 During the first 2 weeks, use of calf-compression devices and anticoagulation with Inj.
heparin 5000 U SC every 12 h or Tab.warfarin (INR, 2–3) are recommended. In cases of
persistent paralysis, anticoagulationshould probably be continued for 3 months.
 Prophylaxis against decubitus ulcers: frequent changes in position in a chair or bed, the
use of special mattresses such as water or air beds, and cushioning of areas where


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pressure sores often develop, such as the sacral prominence and heels. Early treatment of
ulcers with careful cleansing, surgical or enzyme debridement of necrotic tissue, and
appropriate dressing and drainage.
 Spasticity: stretching exercises are recommended to maintain mobility of joints. Tab.
baclofen 15–240 mg/d in divided doses is effective. Tab. diazepam 2-4 mg at bed time
acts by a similar mechanism and is useful for leg spasms that interrupt sleep. Tab.
Tizanidine 2–8 mg TDS is another option.
VERTIGO
Vertigo is defined as the hallucination of movement, either of self (subjective) or the
environment (objective). When patient presents with this type of dizziness, the next step is to


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environment (objective). When patient presents with this type of dizziness, the next step is to
determine whether the symptom is central (brain) or peripheral (inner ear, 8th cranial nerve) in
origin(Table 6).
Investigations
Patients are to be subjected to thorough history, clinical examination and various tests such as
head thrust test,head shaking test, Dix Hallpick’s test, calorie test, CT and MRI brain, X-ray
neck,blood sugar andcarotid vertebraldoppler.
Table 6. Features of Peripheral and Central Vertigo
Clinical features Peripheral
(Labyrinth or Vestibular Nerve)
Central (Brainstem
Or   Cerebellum)
Direction of associated
nystagmus
Unidirectional;
fast phase opposite lesion
Bidirectional (direction-
changing) or Unidirectional
Purely horizontal
nystagmus without
torsional component


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fast phase opposite lesion
Bidirectional (direction-
changing) or Unidirectional
Purely horizontal
nystagmus without
torsional component
Uncommon May be present
Purely vertical or purely
torsional nystagmus
Never present May be present
Visual fixation Inhibits nystagmus No inhibition
Tinnitus and/or Deafness Often present Usually absent
Associated central
nervous system
abnormalities
None Extremely common  (e.g.,
diplopia, hiccups, cranial
neuropathies, dysarthria)
Common causes Benign paroxysmal positional
vertigo, labyrinthitis, vestibular
neuritis, Ménière's disease,
labyrinthine ischemia, trauma,
toxin
Vascular, demyelinating,
neoplasm


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Pharmacological treatment
These medications should be reserved for short-term control of active vertigo. They are less
helpful for chronic dizzinessand may hinder central compensation.
 Antihistamines likeTab. meclizine (25–50 mg 3 times daily),Tab. dimenhydrinate (50
mg 1 –2 times daily) andTab. promethazine (25 mg 2–3 times daily,also can be given
rectally and IM)
 BenzodiazepineslikeTab.diazepam (2.5 mg 1–3 times daily) andTab.clonazepam (0.25
mg 1 – 3 times daily.
 Anticholinergicagents like scopolamine transdermal patch (for motion sickness only)
 Physical therapylike repositioningmanoeuvres(for BPPV)
 Diuretics and/or low-sodium (1 g/d) diet(for Ménière's disease)
 Antimigrainous drugs(for vestibular migraine)


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 Diuretics and/or low-sodium (1 g/d) diet(for Ménière's disease)
 Antimigrainous drugs(for vestibular migraine)
 Selective serotonin reuptake inhibitors(for psychosomatic vertigo)
Benign Paroxysmal Positional Vertigo (BPPV)
 A common cause of recurrent vertigo
 Episodes are brief (less than1 min and typically 15–20 s)
 Always provoked by changes in head position relative to gravity, such as lying down,
rolling over in bed, rising from a supine position, and extending the head to look upward.
 With posterior canal BPPV, the nystagmus beats upwardand torsionally
 Horizontal canal BPPV resulting in a horizontal nystagmus
 Superior (also called anterior) canal involvement is rare.
 BPPV is treated with repositioning maneuvers that utilize gravity to remove the otoconia


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 BPPV is treated with repositioning maneuvers that utilize gravity to remove the otoconia
from the semicircular canal.
 For posterior canal BPPV, the Epley maneuver is the most commonly used procedure.
Vestibular Migraine
 Usually part of migraine aura but can occur independently. The duration of vertigo may
be from minutes to hours. Vestibular migraine typically is treatedwith medications that
are used for prophylaxis of migraine headaches.
 Antiemetics may be helpful to relieve symptoms at the time of an attack.(See vomiting
section)
Ménière's Disease
 Attack consists of vertigo, hearing loss, & pain, pressure or fullness in affected ear.
 Diuretics and sodium restriction are the initial treatments.


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 Diuretics and sodium restriction are the initial treatments.
 If attacks persist, injections of gentamicin into the middle ear or full ablative procedures
are required.
 Tab. betahistine 24-48 mg/day relieves pressure from excess fluid. Initial dose 16 mg
TDS initially with maintenance.


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Central Nervous System Diseases
106
Psychosomatic Dizziness/vertigo
 Important role in chronic dizziness
 Dizziness may be a somatic manifestation of a psychiatric condition such as major
depression, anxiety, or panic disorder.
 Thus, treatment with antianxiety medications and cognitive/behavioral therapy may be
helpful.


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107
 Periorbital andgeneralized pitting edema, transudative  pleural effusion, ascites, xanthomata
 Diseases confined to kidney:Min imal change disease, membranous nephropathy, focal
segmental glomerulosclerosis,membranoproliferative GN,mesangioproliferative GN
 Systemic diseases diabetes mellitus, SLE , amyloidosis, H enoch Schonlein purpura,
preeclampsia
 Hereditary diseases like congenital nephritic syndrome and Alports syndrome
Chapter 6
GENITOURINARY DISEASES
NEPHROTIC SYNDROME
Nephrotic syndrome is definedas proteinuria more than 3.5 gm/day in adultsand more than
40mg/m 2/hr in children. Associated features are hypoalbuminemia, hyperlipidemiaand
edema.
Salient features
Investigation
 Urine analysis : Dipstick test for proteinuria
 Urinemicroscopic examination for deposits


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edema.
Salient features
Investigation
 Urine analysis : Dipstick test for proteinuria
 Urinemicroscopic examination for deposits
 24 hrs.urinary protein: more than 3.5 gm/day establishes the diagnosis.
 Renal function tests: Blood urea, Serum creatinine– Usually normal in isolated nephrotic
syndrome.
Indications for renal biopsy in nephroticsyndrome
 Age > 10 yrs.,Micro – hematuria in urine analysis.,No response to steroid therapy in
adequate doses for a period of 4 weeks.,Associated renal failure,Low C3 levels,ANA
positive,Evidence of systemic diseases.
Non pharmacological treatment
 Diet: Protein 0.8g/kg/day and  1 g protein per gm lost in urine, 35 kcals/kg/day
carbohydrates
Pharmacological treatment


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 Diet: Protein 0.8g/kg/day and  1 g protein per gm lost in urine, 35 kcals/kg/day
carbohydrates
Pharmacological treatment
 In children less than 10 yrs., without hematuria, without renal failure, start empirical
steroids viz. Tab. prednisolone 2mg/kg/day for 4weeks, taper over next 4 weeks.
 Tab. atorvastatin 10-20mg/day for hyperlipidemia
 Tab  furosemide  40-80 mg BD
 Tab. enalapril  1.25-5 mg/day
 Treatment of infections
CHRONIC KIDNEY DISEASE
An irreversible, sustainable and usually gradual loss of renalfunction leading to clinical and
laboratory symptom of uraemia. The important underlying diseases arediabetes mellitus,


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Genitourinary Diseases
108
hypertension, chronic glumerulonephritis, chronic pylonephritis, analgesic nephropathy and
polycystic disease.
Salient features
.
Investigations
 High risk-obesity,smoking,diabetes,hypertensionand family history of renal disease.
 Measure BP,Urine for proteinuria, hematuria and other sediments.
 Estimate serum creatinine, screen themat least yearly.
Diagnosis
 Either one of the following establishes the diagnosis;Kidney damage for more than 3
months as defined by any structural or functional abnormalities of the kidney with or
without decreasedglomerular filtration rate(GFR ).Decrease in GFR to < 6.0ml/min for
more than 3 months. The formula for calculation ofGFR = (140– age) x (Wt. in kg) x
(0.85 if female) / (72 x Cr in mg/dl)


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more than 3 months. The formula for calculation ofGFR = (140– age) x (Wt. in kg) x
(0.85 if female) / (72 x Cr in mg/dl)
Staging: Chronickidney disease has been divided into five stages(Table 1).
Table 1. Stages ofchronic kidney disease
Stage Description GFR
(ml/1.73m2/min)
Stage-I Kidney damage with normal or GFR > 90
Stage-II Kidney damage with mild GFR 60 – 89
Stage-III Moderate in GFR 30 – 59
Stage-IV Severe in GFR 15 – 29
Stage-V End stage renal disease < 15
Non pharmacological treatment
 Decrease protein intake to 0.6/kg/day
 Moderates sodium restriction to 60mmol/day
 Phosphate restriction to 1000mg/day
 Obesity: Aim for ideal body mass index of <25
 Cessation of smoking
Pharmacological treatment
Step – 1 Look for clues with respect to etiology:


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 Obesity: Aim for ideal body mass index of <25
 Cessation of smoking
Pharmacological treatment
Step – 1 Look for clues with respect to etiology:
 History of hypertension or diabetes mellitus.
 Symptoms related to lower urinary tract, recent infections.
 Features of connective tissue disease.
 The symptom of uremia developed gradually and late. Fatigue, dyspnoea, anorexia,
vomiting, ankle edema, pruritus, and neuromuscular disturbances.
 Examination shows presence of pallor, nail dystrophy, purpura, hypertension,
cardiomegaly, CHF, features of pulmonary edema, pleural effusion and pericarditis


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Genitourinary Diseases
109
 Past medical record suggestive of proteinuria.
 Pregnancy related problems.
 Past renal evaluation
 Family history of hereditary kidney disease like ADPKD / Alports syndrome.
Step – 2 Reversible factors in CKD
 Obstructive nephropathy, urinary tract infections,extra renal infections
 Nephrotoxic drugs,hypovolemia
 Congestive cardiac failure,pericardial temponade
 Hypokalemia / Hyperuricemia
Step -3
 In patients with proteinuria > 1g/day, BP target is <125/75mmHg
 If proteinuria <1g/day, BP target is <135/85 mmHg
 Tab. frusemide40-160 mg/ day or Tab. amlodipine 5-20 mg/day
 In diabetic nephropathy-Tab. enalapril 1.25-5 mg/day
 If hyperlipidemia– Tab. atorvastatin 10-20 mg/day
 If anemic. Inj. EPO 80-120unit/kg/week  SC


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 If hyperlipidemia– Tab. atorvastatin 10-20 mg/day
 If anemic. Inj. EPO 80-120unit/kg/week  SC
Step – 4 Prevent and treat complications
Malnutrition
 Dietary protein intake of 0.6g/kg body weight/day
 Dietary calorie intake of 30-35 kcal/kg/day
Cardiovascular disease
 C ommonest cause of mortality in CKD patients.Risk for IHD increases by 30% for every
increase in serum creatinine by 0.23mg/dl.
 At least yearly screening for cardiovascular disease should be done.
R enalosteodystrophy
 Target calcium– 8.8 to 9.7mg/dl, Phosphorous– 3.5 to 5.5 mg/dl, Calcium–
Phosphorous product < 55 mg2/dl.
 This is achieved by phosphate restricted diet.Tab. calcium carbonate 1 g/dayand Tab.
vitamin D3-0.25-2 mcg/day
Step – 5 Prepare for renal replacement therapy
 Early referral to Nephrologists


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vitamin D3-0.25-2 mcg/day
Step – 5 Prepare for renal replacement therapy
 Early referral to Nephrologists
 Vaccination- Hepatitis B vaccine 40 micro grams 3 doses 0, 1st and 2nd month
followed by booster dose at 6th months.
 Early creation of arterio-venous fistula when the GFR is <25 ml/minor serum creatinine
> 4.0meg/l.


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Genitourinary Diseases
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ACUTE RENAL FAILURE (ARF)
Acute renal failure is defined as a rapid decline in renal function reflected by GFR over hours
to days as evidenced by raising creatinine values.
Salient features
Etiology
 Pre-renal– 70%
 H ypovolemia – diarrhea, persistant, vomiting, burns, haemorrhage.
 Low cardiac output– CCF
 Systemic vasodilatation– Sepsis, Hepato renal syndrome.
 Drugs – NSAIDs
 Renal-– 25%
 Can occur due to disease process in glomeruli/ tubules / interstitial / vasculature.
 Acute tubular necrosis can occur due to Ischemic kidney injury– can occur with any
cause of pre renal failure if prolonged.
 Nephrotoxic drugs (commonly used) NSAIDs, aminoglycosides, amphotericin-B.
 Post renal– 5%


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cause of pre renal failure if prolonged.
 Nephrotoxic drugs (commonly used) NSAIDs, aminoglycosides, amphotericin-B.
 Post renal– 5%
 Prostatic hyperplasia with obstruction, Renal stone disease, Carcinoma of cervix
Investigations
 Blood : Urea, Creatinine, Serum Electrolytes, Serum Calcium, Serum PO 4, Serum
Albumin
 Urine Analysis
 Pre-renal: occasional hyaline and granular casts.
 Post-renal: Few hyaline casts.
 Proteinuria usually small amounts, WBC’s, epithelial cells, muddy brown appearance.
 Calculate FeNa (Fractional Excretion of Sodium)
 Urine Na x Serum Creatinine x Serum Na x Urine Creatinine x 100
< 1– Pre-renal;> 2– Renal
Pharmacological treatment
 Pre– Renal- Hydration by Inj . normal saline 0.9% , eliminate toxins and  treat
underlying cause


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Pharmacological treatment
 Pre– Renal- Hydration by Inj . normal saline 0.9% , eliminate toxins and  treat
underlying cause
 Renal:  Eliminate toxins,  Nephrology consultation
 Post renal : Relieve obstruction, Urology consultation
 Anorexia, fatigue, mental status changes, nausea/vomiting, pruritus, shortness of breaths
 Signs arepericardialrub,pedal edema,pulmonary rales,raised JVP,seizures. Look for clues
for etiology of renal failure.


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Genitourinary Diseases
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 As serum potassium increases ECG becomes progressively abnormal viz.
 Tenting of T waves.
 Prolonged PR and QRS interval
 Flattened P waves, sine wave and asystole.
 Muscle paralysis can also be a feature of hyperkalemia.
 Indications for Dialysis arehyperkalemia,metabolic Acidosisvolume Overload,
encephalopathy, and pericarditis.
HYPOKALEMIA
Defined as serum potassium <3.5 meq/l.
Salient feature
Non -pharmacological treatment
 Dietary-Potassium rich food in form of fruit juices, banana, coconut water, dryfruits.
Pharmacological treatment
 Urgent treatment is required in rare situations like periodic paralysis, ventricular ectopics
or in the setting of myocardial infarction.


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 Urgent treatment is required in rare situations like periodic paralysis, ventricular ectopics
or in the setting of myocardial infarction.
 IV KCL only required when patient not able to take orallyand Potassium <2.5 mEq/l
 Oral potassium chloride 15ml TDS is usually sufficient if there are no cardiovascular or
neurological emergencies.
HYPERKALEMIA
Hyperkalemia is definedby serum potassium > 5.5meq/l.
Salient features
Pharmacological treatment
 Inj. calcium gluconate 10mlof 10% solution over 10 min. Effect lasts for 30-60 mins.
Repeat hourly.
 Infuse 25% dextrose 100ml + 10 units of regular insulin. The effect lasts for 4-6 hours.
 Salbutamol nebulization 10mg (2-8 times the normal dose).
 Inj. sodium bicarbonate 7.5%   50-100 ml is given bolus i.v. slowly over 10-20 mins


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 Salbutamol nebulization 10mg (2-8 times the normal dose).
 Inj. sodium bicarbonate 7.5%   50-100 ml is given bolus i.v. slowly over 10-20 mins
followed by drip.
 Cation exchange resins- sodium polystyrene sulphonate(Keyxalate), usual dose is 25-30
gm mixed with 100 ml 20% sorbitol 3-4 times daily.
 Note: All three steps are to be combined. All thesecan buy time before patient reaches
the tertiary care center for dialysis.
 It can present with muscular symptoms like flaccid paralysis, cardiovascular
problems like ventricular arrhythmias and renal involvement like polyuria.


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112
 Tiredness, weakness, dry skin, feeling cold, hair loss, difficulty concentrating and poor
memory , constipation, w eight gain with poor appetite, dyspnea, hoarse voice,
m enorrhagia (later oligomenorrhea or amenorrhea), paresthesia, impaired hearing
 Examination shows dry coarse skin; cool peripheral extremities, puffy face, hands, and
feet (myxedema), diffuse alopecia, bradycardia, peripheral edema, delayed tendon
reflex relaxation, carpal tunnel syndrome, serous cavity effusions
Chapter7
ENDOCRIN E DISEASES
HYPOTHYROIDISM
Hypothyroidism may be primary; common causes are autoimmune, iatrogenic due to I131,
antithyroid drugs, lithium treatment, thyroidectomy. It may besecondary to pituitary or
hypothalamic disorders.
Salient features
Investigation:diagnosis is confirmed by


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hypothalamic disorders.
Salient features
Investigation:diagnosis is confirmed by
 Low serum free T3 and T4
 Elevated S. TSH in thyroid types and low in suprathyroid types.
 Thyroid peroxidase (TPO) Anti TPO antibody in autoimmune hypothyroidism.
Pharmacological treatment
 Tab. levothyroxine 50-100 mcg/day. Dose to be adjusted based on TSH level. Measure
TSH level after about 2 months of instituting therapy
 Adjust by 12.5 mcg/day with similar increment every 2-3 months until TSH level is
normalized.
 When full replacement is achieved,follow up measurement at annual intervals and later
by a 2-3 yearly interval.
 Special treatment considerations- A hypothyroid woman should be euthyroid prior to
conception and during early pregnancy. Maintain FT4 0.8 to 1.2.


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 Special treatment considerations- A hypothyroid woman should be euthyroid prior to
conception and during early pregnancy. Maintain FT4 0.8 to 1.2.
 Elderly required lessthyroxine (20%) especially those with CAD, starting dose 12.5
mcg/day with similarincremen t every 2-3 months until TSH level is normalized.
Patient education
 L-thyroxine should be taken as a single daily dose, ideally on awakening, at least 30
minutes before breakfast.
 Fiber andbran products may impair absorption
 Metabolism of L-thyroxine is increased by phenytoin, rifampicin and carbamazepine.
 Explain to the patient that the treatment is lifelong.
 Over treatment may lead to decreased bone mineral density and adverse cardiac
com plications.


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Endocrine Diseases
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 Hyperactivity, irritability, dysphoria, heat intolerance and sweating, palpitations, fatigue and
weakness, weight loss with increased appetite, diarrhea, polyuria, oligomenorrhea, loss of
libido.
 Examinations shows tachycardia; atrial fibrillation in the elderly
 Tremor, goiterw arm, moist skin.Muscle weakness, proximal myopathy, lid retraction or lag
Myxedema coma
Non -pharmacological treatment
 Warm blanket, mechanical ventilation for respiratory failure.
 Correction of metabolic disturbances and treat precipitating factors.
Pharmacological treatment
 Inj. L-thyroxine 500 mcgIV bolus, then 50-100 mcg IV daily.
 If intravenous preparation is not available, the same dose is administered through Ryle’s
tube.


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 If intravenous preparation is not available, the same dose is administered through Ryle’s
tube.
 Once acute phase is over, maintain L-thyroxine as above.
 Inj. hydrocortisone 100 mg IV stat, 25-50 mg 8 hourly.
 Caution: Avoid sedative and anesthetic agents.
HYPERTHYROIDISM
Classically occurs in Grave’s disease, which is characterized by diffuse goitre,
opthalmopathy and dermopathy in varying combinations. Other causes are toxic muti-
nodular goitre and toxic adenomas.
Salient features
Investigations
 Low or undetectable S.TSHand increased S. Free T3 and Free T4.
Pharmacological treatment
Adjunctive treatment
 For adrenergic symptoms, Tab. propranolol 40-120 mg a day.
 Tab. propylthiouracil 100-150 mg every 6-8 hours (Drug of choice for hyperthyroidism in


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 Tab. propylthiouracil 100-150 mg every 6-8 hours (Drug of choice for hyperthyroidism in
pregnancy) orTab. carbimazole 10-20 mg   every 8-12 hours.
 After euthyroid state is achieved in 6-8 weeks once daily dosage.
 Review with serum TSH and FT3 after 3-4 weeks treatment has been initiated.
 Once controlled reduce to the smallest effective dose orcontinue initial dose combined
with L-thyroxin.
 Drugs are given for an average of 2 years.


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Definitive treatment is Surgery/ Ablation of thyroid tissue
 Subtotal thyroidectomy in younger patients in whom antithyroidtherapy has been
unsuccessful and in very large goiters.
 Radioactive iodine (I131) method of choice in elderly, younger patients who have
completed family with recurrent thyrotoxicosis following surgery or when surgery is
refused or contraindicated.
 Caution :  Pregnancy
Op hthalmopathy
 Refer to ophthalmologist.
 Mild cases: diuretic to decrease edema, tinted sunglasses and 1% methyl cellulose eye
drops.
 Refer patients with severe and progressive exopthalmos to an ophthalmologist.
Thyrotoxic crisis or thyroidstorm
 Tab. propylthiouracil 600 mg loading doses, then 200-300 mg every 6 hourly orally or
through Ryle’s tube.


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Thyrotoxic crisis or thyroidstorm
 Tab. propylthiouracil 600 mg loading doses, then 200-300 mg every 6 hourly orally or
through Ryle’s tube.
 Tab. carbimazole 15-25 mg 6 hourly.
 1 hour after the 1stdose of antithyroid drug, saturated solution of potassium iodide (SSKI)
5drops every 6hourly  or
 Lugol’s iodine 10 drops 3 times a day or Sodium iodide 1 g IV slowly
 Tab. propranolol 40-60 mg 4 hourly or 0.5-2.0 mg every 4 hours,
 Inj. dexamethasone 2 mg IV 6 hourly.
 Supportive treatment: Cooling, antipyretics, antibiotics, IV fluids.
 Once euthyroid states are achieved, manage as already outlined.
HYPOCALCEMIA
Caused by hypoparathyrodism, pseudohypoparathyrodism, vitamin D deficiency states,
chronic renal failure, malabsorption syndrome, and hypomagnesemia.
Salient features
.


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chronic renal failure, malabsorption syndrome, and hypomagnesemia.
Salient features
.
Investigation
 Total S.calcium <8.5 mg/dl
 ECG : Prolongation of QTc
 In hypoalbuminemia, add 1 mg/dl of calcium to the estimated level for every 1 gm fall
of albumin below 4 gm/dl ( Correct S. Calcium)
 Treatment depends on the cause, the severity, the presence of symptoms, and how
rapidly the hypocalcemia developed.
 Circumoral paresthesias, muscle cramps, confusion, tetany, convulsion. Positive
chovstek,s sign and trousseau’s sign


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Endocrine Diseases
115
 Fatigue, depression, confusion, anorexia, nausea, vomiting and constipationand
polyurea
 Severe hypocalcemia may result in seizures, tetany, refractory hypotension or
arrhythmias that require a more aggressive approach
Pharmacological treatment
 Severe symptomatic hypocalcaemia: 20 ml of 10% Inj. ca.gluconate solution over 10-
15 mins followed by 60-80ml of 10% solution in 1lt of 5% distilled water (0.5-0.25
mg/kg/hr elemental calcium)
 Caution: Should not be mixed with bicarbonate as it may result in precipitation of
calcium carbonate.
 If associated with hypomagnesemia : Inj. magnesium sulphate 1-2 gm IV day 1
followed by oral magnesium oxide 600-1200 mg 3 times a day to replenish stores.
Asymptomatic hypocalcemia/ maintenance treatment


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followed by oral magnesium oxide 600-1200 mg 3 times a day to replenish stores.
Asymptomatic hypocalcemia/ maintenance treatment
 Treat underlying condition if possible. Long term treatment is required in conditions
such as hypoparathyroidism, pseudohypoparathyroidism and chronic vitamin D
deficiency states.
 Tab. calciumcarbonate (40% elemental ca) 1-2 gm elementalcalciumorally 3 times a
day initially and subsequently maintenance dose of 0.4-1.5 g 3 times a day.
 In CRF , calcium alone gives inadequate results. Correct concomitant hyper-
phosphatemia before instituting following therapy: Vit D 50000 IU/day for 1-2 weeks,
then weekly or bimonthly.
 Calcitriol 0.25 mcg orally daily-more expensive and less toxic.
 Advise low Phosphate diet and Phosphate binding agents.
HYPERCALCEMIA


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 Calcitriol 0.25 mcg orally daily-more expensive and less toxic.
 Advise low Phosphate diet and Phosphate binding agents.
HYPERCALCEMIA
The common causes are hyperparathyroidism and malignancy. Others include excessive
vitaminD action, high bone turnover rate or renal failure. Hypercalcemia is defined as10.5
mEq/L.
Salient features
Investigation
 Symptoms appear when S. Ca >11.5-12.0mg/dl. Severe hypercalcemia >15-18 mg/dl can
result in death.
 ECG : Short QTc and occasionally arrhythmias
Pharmacological treatment
A. Mild
 Rehydration– isotonic saline 2-4 lt/day increase calcium excretion.


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Endocrine Diseases
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 After correcting dehydration administer Inj. frusemide 20-40 mg BD.
 Monitor electrolytes especially potassium and magnesium and replace accordingly.
B. Moderate to severe
 Aggressive preceding approach- isotonic saline 6 lt plus Inj.frusemideup to 100 mg
every 1 to 2 hours.
 Inj. calcitonin 2-8 U/kg IV/SC/IM every 6-12 hr: rapid but mild action.
 Inj. pamindronate 30-90 mg IV infusion in 0.9% saline over 4-24 hrs: response last for
wks OR Tab. alendronate sodium 10 mg orally in the morning with full glass of water at
least 30 mins before any food or drink: remain in upright position for at least 30 mins. OR
Inj. zolendronate 1-4 mg IV in few mins.
 Tab. prednisolone 40-100 mg/day in 4 divided doses. Useful in osteolytic malignancies,


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Inj. zolendronate 1-4 mg IV in few mins.
 Tab. prednisolone 40-100 mg/day in 4 divided doses. Useful in osteolytic malignancies,
Vit. D intoxication and sarcoidosis.
 Tab. phosphorus (sodium and potassium phosphate) 1-1.5 g/day in 4 divided doses for
several days when hypophosphatemia is present.
 Peritoneal/Hemo dialysis with calcium free dialyses is useful especially in cases
complicated by renal failure.
DIABETES MELLITUS
Diabetes mellitus (DM) refers to a group of common metabolic disorders that share the
phenotype of hyperglycemia. Several distinct types of DM are caused by a complex
interaction of genetics and environmental factors.The factors contributing to hyperglycemia
include reduced insulin secretion, decreased glucose utilization, and increased glucose
production.


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include reduced insulin secretion, decreased glucose utilization, and increased glucose
production.
Salient features
Classification
 Polydypsia, polyuria, polyphagia and unexplained weight loss.
 Random blood sugar >200 mg/dl, Fasting plasma glucose >126 mg/dl
 Two hour plasma glucose >200 mg/dl after 75 g glucose load
 Impaired fasting glucose (IFG) 100-125 mg/dl  and impaired glucose tolerance– 2 h
plasma glucose  140-199 mg/dl are considered as pre diabetics.


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Endocrine Diseases
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Non -pharmacologicaltreatment
Caloric requirement for normal weight individual: according to the nature of work
Sedentary Moderate Heavy
Male 1800-2000 1800-2000 2200-3000
Female 1200-1500 1400-1600 1600-2400
 Caloric distribution : Carbohydrate : 45-65%, Protein– 10-35% , 20-35% from fat,
saturated fat <7%, Polyunsaturated fat 10% of Kcal/day
 Exercise: Regular physical exercise for half and one hour (for sedentary workers) is
recommended to have better control of diabetes. At least 150 min/ week of moderate
intensity aerobic physical activity.
Pharmacological treatment
Type 1 DM - Insulin therapy(Table 1)
 Dose of human insulin– 0.5 units/kg/day to 1.0 units/kg/day
 Combination of regular + lente/semilente insulin should be used


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 Dose of human insulin– 0.5 units/kg/day to 1.0 units/kg/day
 Combination of regular + lente/semilente insulin should be used
 One third of the total insulin requirement is given as regular and two third as lente/semi
lente
 One third of the total dose is used before dinner and two third before breakfast
 Insulin is given SC 30-45 min before meals
 Medial aspect of thigh and abdominal wall are generally used for injection.  Rotate
injection site frequently
 Dose, type and timing of insulin is adjusted according preprandialblood sugar levels
 Patient must be trained for administration of SC injections
 Ensure mealsafter injection andexplain features of hypoglycaemia to the patient


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Endocrine Diseases
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Table 1. A list of various insulin preparations
Time of Action
Insulin Preparation Onset, h Peak, h Effective
Duration, h
Short-acting
Aspart <0.25 0.5–1.5 3–4
Glulisine <0.25 0.5–1.5 3–4
Lispro <0.25 0.5–1.5 3–4
Regular 0.5–1 2–3 4–6
Long -acting
Detemir 1–4 — Up to 24
Glargine 1–4 — Up to 24
NPH 1–4 6–10 10–16
Insulin combinations
75/25–75% protamine lispro, 25% lispro<0.25 1.5 h Up to 10–16
70/30–70% protamine aspart, 30% aspart<0.25 1.5 h Up to 10–16
50/50–50% protamine lispro, 50% lispro<0.25 1.5 h Up to 10–16
70/30–70% NPH, 30% regular 0.5–1 Dual 10–16
Type 2 DM (Figure 1)
 If non pharmacological measures not sufficient, oral agents may be used alone and in
combination.
 Level of hyperglycemia influence the initial choice of oral hypoglycaemic agents(Table


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combination.
 Level of hyperglycemia influence the initial choice of oral hypoglycaemic agents(Table
2).
 Therapy can be started with either sulfonylureas or Metformin. Metformin has the
advantage of promoting mild weight loss in obese patients.
 Treatment may be started with any of the following drugs: Tab. glimipride l-8mg/day Or
Tab. glipizide 2.5- 40 mg/day. Or Tab. glipizide extended release 5-10 mg/day Or Tab.
glyburide (glibenclamide) 1.25-20 mg/day. Or Tab. metformin 500 mg once or twice a
day in obese patients and increase the dose to 1000 mg 2 times a day; The dose can be
increased every 2-3 weeks. All drugs should be taken 30-45 min before meals.
 Combination therapy, following combination can be given if inadequate glycaemic


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 Combination therapy, following combination can be given if inadequate glycaemic
control with single oral hypoglycaemic agent: Sulphonylurea + metformin
 Insulin may be required in patients with primary or secondary failure to oral agents; often
as single dose of intermediate acting insulin 0.3-0.4 units/kg/day either before breakfast


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Endocrine Diseases
119
or at bedtime in combination with Tab. metformin. Insulin is also required in situations
like pregnancy, surgery, infection, etc.
Figure1. Algorithm for management of Type 2 DM
T able2. Oral hypoglycaemic drugs with their dose and their common ADRs
Drugs Dose HbA1c
reduction
(%)
Advantages Disadvantages Contraindications
Biguanides
Metformin Initially
500mg OD to
max 2000
mg/d
1-2 Weight
neutral,
Do not cause
hypoglycemia
, inexpensive
Diarrhoea,
nausea, lactic
acidosis
Serum creatinine
>1.5 mg/dl (men)
>1.4 mg/dl
(women), CHF,
radiographic
contrast studies,
seriously ill patients,
acidosis
Insulin secretagogues: Sulfonylureas
Glimepiride
Glipizide
Glyburide
1-8mg/d
5-40mg/d
1.25-20mg/d
1-2 Inexpensive Hypoglycemia,
weight gain
Renal/liver disease


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Glimepiride
Glipizide
Glyburide
1-8mg/d
5-40mg/d
1.25-20mg/d
1-2 Inexpensive Hypoglycemia,
weight gain
Renal/liver disease
Insulin secretagogues: Non-sulfonylureas
Repaglinide 0.5-16mg/d 1-2 Short onset of
action, lower
postprandial
glucose
Hypoglycemia Renal/liver disease
Thiazolidinediones
Pioglitazone15-45 mg/d 0.5-1.4 Lower insulin
requirements
Peripheral
edema, CHF,
CHF, liver disease


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Endocrine Diseases
120
weight gain,
fractures,
macular edema
α -Glucosidase inhibitors
Acarbose
Voglibose
50-100mg
0.2-0.3mg
(per meal)
0.5-0.8 Reduce
postprandial
glycemia
GI flatulence,
liver function
tests
Renal/liver disease
Dipeptidyl peptidase IV inhibitors
Saxagliptin
Sitagliptin
Vildagliptin
2.5-5mg/d
100mg/d
50-100mg/d
0.5-0.8 Do not c ause
hypoglycemia
Reduce dose with
renal disease
Patient education
 Education topics important for optimal diabetes care include self-monitoring of blood
glucose; urine ketone monitoring (type 1 DM); insulin administration; guidelines for
diabetes management during illnesses; prevention and management of hypoglycaemia,
foot and skin care; diabetes management before, during, and after exercise; and risk
factor–modifying activities.


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foot and skin care; diabetes management before, during, and after exercise; and risk
factor–modifying activities.
 Medical nutrition therapy(MNT) is a term used to describe the optimal coordination of
caloric intake with other aspects of diabetes therapy (insulin, exercise, weight loss).
Primary prevention measures of MNT are directed at preventing or delaying the onset of
type 2 DM in high-risk individuals (obese or with prediabetes) by promoting weight
reduction.
 Explain about the warning symptoms and signs of hypoglycaemia and need to take
sweets/candies/drinks in such a situation.
 Regular follow up to monitor BP (quarterly), HbA1C testing (2-4 times/year), eye
examination (annual), foot examination (1-2 times/year by physician; daily by patient);


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examination (annual), foot examination (1-2 times/year by physician; daily by patient);
screening for diabetic nephropathy (annual); lipid profile (annual).


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Endocrine Diseases
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Figure 2. Diabetes algorithm for achieving glycemic control
Abbreviations: MET: Metformin , DPP4: dipeptidyl peptidase-4 inhibitors , TZD:
thiazolidinediones , GLP-1 : glucagon-like peptide-1 , FPG : fasting plasma glucose ,PPG:
post prandial glucose, AGI:alfa glucosidase inhibitors, SU : sulfonylureas
DIABETIC KETOACIDOSIS
Diabetic ketoacidosis is an acute complication of diabetes. It consists of hyperglycemia,
ketosis (positive serum ketones) and metabolic acidosis (with increased anion gap).


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Endocrine Diseases
122
 Nausea, vomiting, abdominal pain, dehydration and altered sensorium.
 DKA results from relative or absolute insulin deficiency combined with counter
regulatory hormone excess (glucagon, catecholamines, cortisol, and growth hormone).
 Precipitating factors for DKA include noncompliance, infection, trauma,infarction,
pregnancy and drug abuse.
Salient features
Diagnosis
 Demonstration of ketones in urine (or elevated levels in blood), hyperglycaemia, low
arterial pH, low bicarbonate (>15 mmol/1) and high anion gap (>15 mmol/1).
Pharmacological treatment
 Admit to hospital; intensive-care setting may be necessary for frequent monitoring or if
pH <7.00 or unconscious. If the patient is vomiting or has altered mental status, a


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pH <7.00 or unconscious. If the patient is vomiting or has altered mental status, a
nasogastric tube should be inserted to prevent aspiration of gastric contents.
 Assess: Serum electrolytes (K+, Na+, Mg2+, Cl–, bicarbonate, phosphate),acid-base
status- pH, HCO3 –, PCO2, β -hydroxybutyrate (orS.acetone),renal function (creatinine,
urine output)
 Replace fluids: 2–3 L of 0.9% saline over first 1–3 hr (15–20 m l/kg per hour);
subsequently, 0.45% saline at 250–500 ml/h; change to 5% glucose and 0.45% saline at
150–250 m l/h when plasma glucose reaches 200 mg/dl. Fluid replacement needs to be
closely monitored in elderly and those with cardiac or renal compromise.
 Administer short-acting insulin: IV (0.1units/kg), then 0.1 units/kg per hour by


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 Administer short-acting insulin: IV (0.1units/kg), then 0.1 units/kg per hour by
continuous IV infusion; increase two- to threefold if no response by 2–4 h. If the initial
serum potassium is <3.3 mEq/L, do not administer insulin until the potassium is
corrected. If the initial serum potassium is >5.2 mEq/L, do not supplement K+ until the
potassium is corrected.
 Assess patient: Initiate appropriate workup for precipitating event (cultures, CXR, ECG).
 Replace K+: 10 meq/h when plasma K+< 5.0–5.2 mEq/L (or 20–30 mEq/L of infusion
fluid), ECG normal, urine flow and normal creatinine documented; administer 40–80
mEq/h when plasma K+< 3.5 mEq/L or if bicarbonate is given. The goal is to maintain the
serum potassium at >3.5 mEq/L.


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mEq/h when plasma K+< 3.5 mEq/L or if bicarbonate is given. The goal is to maintain the
serum potassium at >3.5 mEq/L.
 Bicarbonate replacement: Despite a bicarbonate deficit, bicarbonate replacement is not
usually necessary. However, inthe presence of severe acidosis (arterial pH <6.9), it is
advised to administer bicarbonate [50 mEq/L of sodium bicarbonate in 200 mlof sterile
water with 10 mEq/L KCl per hour for 2 h until the pH is >7.0].
 Phosphate and Magnesium: If the serum phosphate < 1 mg/dl, then phosphate supplement
should be considered and the serum calcium monitored. Hypomagnesemia may develop
during DKA therapy and may also require supplementation.


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Endocrine Diseases
123
 Monitoring: Measure capillary glucose every 1–2 h; measure electrolytes (especially K+,
bicarbonate, phosphate) and anion gap every 4 h for first 24 h. Monitor blood pressure,
pulse, respirations, mental status, fluid intake and output every 1–4 hrs.
 Hyperglycemia usually improves at a rate of 75–100 mg/dl per hour. As ketoacidosis
improves, β-hydroxybutyrate is converted to acetoacetate. Ketone body levels may appear
to increase if measured by laboratory assays that use the nitroprusside reaction, which
only detects acetoacetate and acetone.
 Continue above until patient is stable, glucose goal is 150–250 mg/dl, and acidosis is
resolved. Insulin infusion may be decreased to 0.05–0.1 units/kg per hour.


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resolved. Insulin infusion may be decreased to 0.05–0.1 units/kg per hour.
 Administer long-acting insulin as soon as patient is eating. Allow for overlap in insulin
infusion and SC insulin injection.
Hyperglycemic Hyperosmolar Nonketotic Coma
 It is an acute metabolic derangement whose notable features are marked hyperglycemia,
hyperosmolality (>350 mOsmol/L), and prerenal azotemia.
 In HONC, fluid losses and dehydration are usually more pronounced than in DKA due to
the longer duration of the illness.
 The patients are usually older, more likely to have mental status changes, even with
proper treatment, HHS has a substantially higher mortality rate than DKA.
Chronic Complications of DM
Microvascular
Complications
Treatment


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proper treatment, HHS has a substantially higher mortality rate than DKA.
Chronic Complications of DM
Microvascular
Complications
Treatment
Diabetic Retinopathy Proliferative retinopathy is usually treated with panretinal
laser photocoagulation, whereas macular edema is treated
with focal laser photocoagulation.
 Regular fundus examination is required to monitor the
retinopathy.
Diabetic Nephropathy  Administration of ACE inhibitors or ARBs
 Insulin and other OHA requirement may decrease
 give drugs according to renal clearance
Diabetic Neuropathy  Once fully developed is difficult to treat.
 The following drugs can be tried amitriptylin, pregabalin,
gabapentin, carbamazepine, SSRI
 Can lead to autonomic dysf unction and orthostatic
hypotension.


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gabapentin, carbamazepine, SSRI
 Can lead to autonomic dysf unction and orthostatic
hypotension.
 Foot and joints most be examined for presence of injury.
Diabetic Gastropathy  Smaller, more frequent meals that are easier to digest.
 Dopamin e antagonist’s metoclopramide, 5 –10 mg, and


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Endocrine Diseases
124
domperidone, 10–20 mg, before each meal. Erythromycin
may promote gastric emptying.
 Diabetic diarrhoea treated with loperamide and may respond
to octreotide (50–75 g three times daily, SC).
Diabetic Cystopathy  Timed voiding or self-catheterization, possibly with the
addition of bethanechol.
 Drugs that inhibit type 5 phosphodiesterase are effective for
erectile dysfunction
Macrovascular Complication- Atherosclerotic cardiovascular disease are the common
cause ofdeath in diabetic population
Atherosclerotic CVD are the common cause of death in diabetic population.
Risk factor reduction is important. The important lipid target are as follows
 LDL < 2.6 mmol/l(100 mg/dl);
 HDL >1 mmol/ l(40 mg/dl) in men and >1.3 mmol/l(50 mg/dl) in women; and


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 LDL < 2.6 mmol/l(100 mg/dl);
 HDL >1 mmol/ l(40 mg/dl) in men and >1.3 mmol/l(50 mg/dl) in women; and
 Triglycerides<1.7 mmol/l(150 mg/dl).
If the patient is known to have CHD, an LDL goal of <1.8 mmol/L (70 mg/dl).
GestationalD iabetes
Please refer Obstetrics andG ynecologychapter– Pregnancy with diabetes.


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125
 Recurrent, painful, rounded ulcer with yellowish gray fibrinoid centre.
 Ulcer typically has recurrent appearanceeven after successful treatment
Chapter 8
GASTROINTESTINAL DISEASES
APHTHOUS ULCERS
Salient features
Rule out secondary causes like malabsorption syndrome, inflammatory bowel disease,
Behcet's disease and recurrent trauma from tooth/denture and treat accordingly
Non -pharmacological treatment
Oral hygiene-repeated mouthwash with plain water specially after eating any thing
Pharmacological treatment
 Symptomatic treatment with application of any gel containing local anaesthetic before
taking meals.
 Only in severe cases with large multiple ulcers.
 Pelletshydrocortisone 5mg to be kept on the ulcer and sucked every 4 hours for 3-5 days.


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 Only in severe cases with large multiple ulcers.
 Pelletshydrocortisone 5mg to be kept on the ulcer and sucked every 4 hours for 3-5 days.
Or Tab. prednisolone 0.5 mg/kg/day in a single dose for 3-5 days.
Patient education
 Maintain good oral hygiene.
 Avoid precipitating factors, if any.
 Ensure toothbrush has aligned bristles.
 Avoid chewing betel leaf and other condiments,excessive carbonated drinks and spicy or
sharp/crispy foods.
 Take plenty of green leafy vegetables.
DYSPEPSIA
It is a non-specific group of symptoms related to the upper gastrointestinal tract.  It is also
referred to as non-ulcer dyspepsia / functional dyspepsia.
Salient features
Pharmacological treatment
 Cap. omeprazole 20 mg once a day 45 minutes before breakfast for 4 to 6 weeks or


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Salient features
Pharmacological treatment
 Cap. omeprazole 20 mg once a day 45 minutes before breakfast for 4 to 6 weeks or
 Tab. ranitidine 150 mg twice a day 45 min. before breakfast and dinner for 4 to 6 weeks.
 Antacids 2 to 3 teaspoon or 2 tabs (chewable) when symptomatic despite above
medication.
 For those with dysmotility symptoms,
 Epigastric burning pain, early satiety,post prandial fullness, hiccups, halitosis.


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Gastrointestinal Diseases
126
- Tab. domperidone 10 mg three times a day 30 minutes Before breakfast, lunch and dinner
 Duration: Short courses of therapy (4 to 6 weeks) of the drug may be repeated or long-
term treatment may be continued for up to a year.  Intermittent therapy or biweekly PPI is
also recommended in those requiring long-term treatment
 Anti-H .pyloritreatment is recommended for those on long term NSAIDs or those with
Duodenal / gastric ulcers (complicated e.g. bleeding). Combination of Cap.omeprazole 20
mg twice a day with Cap. amoxicillin 500 mg thrice a day with Tab. metronidazole 400
mg thrice day Followed by Cap. omeprazole 20 mg once a day for three weeks. It is
desirable that the anti-H pylori regimen is taken for at least 14 days.
Patient education


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desirable that the anti-H pylori regimen is taken for at least 14 days.
Patient education
 Avoid excess tea, coffee, fried food items andabstain from alcohol and smoking.
 Avoid unn ecessary NSAIDs: preferparacetamol especially those with ulcer like
symptoms or those with documented duodenal/gastric ulcer.
 Follow meals at regular intervals:4 hourly (including snacks)
 Daily exercise to maintain optimum weight.
PEPTIC ULCER DISEASE
There is ulceration of the gastric or duodenal mucosa due to acid and pepsin.
Salient features
Pharmacological treatment
R ecommended for patients on long term NSAIDs, bleeding peptic ulcer. Preferred two-week
triple therapy (Table1), followed byProton Pump Inhibitor(PPI)for 3 weeks.
Table 1. Preferred regimen for eradication ofH.pylori


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triple therapy (Table1), followed byProton Pump Inhibitor(PPI)for 3 weeks.
Table 1. Preferred regimen for eradication ofH.pylori
Drug Dose(mg) Frequency Duration
Bismuth subsalicylate
Tetracycline
Metronidazole
2 tab
250 mg
500 mg
QID
QID
QID
Two
Week
Bismuth citrate
Amoxicillin
Metronidazole
400 mg
500 mg
500 mg
BD
BD
BD
Two
Week
Omeprazole
Amoxicillin
Clarithromycin
20 mg
1 gm
500 mg
BD
BD
BD
Two
Week
 Heart burn, relation with foods.In advance cases upper abdominal pain, weight loss,
anorexia, cachexia may develop.
 History of NSAIDs or steroid ingestion.
 In case of perforation: severe abdominalpain, guarding, rigidity, shock.


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Gastrointestinal Diseases
127
 A bdominal pain,alternatediarrheaand constipation.
 Abdominal distension, relief of abdominal symptoms with bowel motions, increased
frequency of stool, sense of incomplete evacuation.
 Pencil thin stool, heart burn, bloating, back pain, weakness, faintness, palpitation
Non -Helicobacterpyloripeptic ulcer
 Any PPI for 4 to 6 weeks, 45 minutes before breakfast.
 Tab. ranitidine 150 mg BD OR Tab. famotidine 40 mg OD equally efficacious but takes
longer time for symptom relief.
Patient education
 Stop smoking.
 Curtail alcohol intake.
 Avoid NSAIDs, preferparacetamol.
 Avoid foods which aggravate symptoms; no ride for bland diet or excess milk.
 Meals at regular intervals.
VOMITING


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 Avoid foods which aggravate symptoms; no ride for bland diet or excess milk.
 Meals at regular intervals.
VOMITING
Vomiting is the forceful expulsion of the gastric contents due to contraction of abdominal
musculature and simultaneous relaxation of gastric funds and lower esophageal sphincter.
Pharmacological treatment
 Hospitalize the patientto give intravenous fluids in case of dehydration.  Start oral fluids
as soon as the patient can tolerate.  Appropriate analgesics if patient has severe pain.
 Acute vomiting : Rule out gastric outlet obstruction then Inj. odansetron 8 mg IV repeat 8
hourly if neededor  Inj. metoclopramide 10 mg IM,repeat after 6 hours if needed or Tab.
domperidone 10 mg three times a dayor Tab. metoclopramide 10 mg three times a day


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domperidone 10 mg three times a dayor Tab. metoclopramide 10 mg three times a day
 In pregnancy avoid all drugs, if possible. Tab.  promethazine 25 mg oral/injection is safe
in the first trimester
 If there is history of motion sickness then give Tab. cyclizine 50 mg 3 times daily.
Patient education
 Avoid stale food, cut vegetables, fruits kept in open, drink potable water only.
 Avoid NSAIDS, especially if ulcer symptoms are present.
 Prevent dehydration: Encourage patients to take sips of liquids at short intervals to
prevent dehydration.
 Endoscopy is necessary, if symptom persists.
 Prevent motion sickness by avoiding heavy meal before travel.
IRRITABLE BOWEL SYNDROME (IBS)
A constellation of gastrointestinal symptoms associated with lower bowel symptoms that


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IRRITABLE BOWEL SYNDROME (IBS)
A constellation of gastrointestinal symptoms associated with lower bowel symptoms that
occur in absence of an organic disease.
Salient features


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Gastrointestinal Diseases
128
 Watery profuse loose motions which are unaffected by fasting, nausea and vomiting,
abdominal cramps, dehydration, hypotension
Pharmacological treatment
 Ifpain is predominant: Tab. mebeverine hydrochloride 270 mg three times a day given
for long term or Tab. drotaverine 40 to 80 mg3 times a day
 In those with depressive symptom: Tab. amitriptyline 10 mg HS for 4 to 6 weeks
 In those with diarrheal symptoms Tab. loperamide 2 to 4 mg daily for several days /
weeks depending on the criticalresponse.
 In those with constipation symptoms: Isotonic polyethylene glycol (PEG electrolyte)
solution 125-250 ml. Or Lactulose solution 15 to 20 ml at night
Patient education
 Diet should contain high fiber and supplemented with bulk forming agents such as


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Patient education
 Diet should contain high fiber and supplemented with bulk forming agents such as
isaphghul husk.
 Avoid caffeine and alcohol.
 Avoid milk and other dietary constituents, which worsen the symptoms.
 Psychotherapy may be helpful in selected cases
ACUTE GASTRO ENTERITIS
It is a self-limiting illness characterized by diarrhoea, abdominal cramps, nausea and
vomiting, usually caused by viruses or bacteria(E. coli,V. cholerae, Staph, aureus, Bacillus
cereus,etc). Most of these are noninvasive or toxic diarrhoea. Less commonly patients
present mainly with diarrhoea with passage of mucous and/or blood in stools. This may be
associated with significant systemic symptoms like fever, malaise, etc.
Salient features
Pharmacological treatment(Figure 1)


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associated with significant systemic symptoms like fever, malaise, etc.
Salient features
Pharmacological treatment(Figure 1)
 In acute gastro enteritis the aim is to correct dehydration and electrolyte imbalance.
There is usually no need to investigate for the etiology immediately.
 Further investigations are necessary if there is bloody diarrhea, clinical evidence of
toxicity or prolonged diarrhea.
 Oral rehydration salt (ORS ): given in mild tomoderate dehydration ,75 ml/kg in 4 hours
in case of moderate dehydration
 IV fluid given inpatients with severe dehydration (100 ml/kg). 30 ml/kg to be given in 30
minutes followed by 70 ml/kg in2½ hours
 Tab ciprofloxacin 500 mg two times a day for 3 to 5 days. Indicated only in very ill


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minutes followed by 70 ml/kg in2½ hours
 Tab ciprofloxacin 500 mg two times a day for 3 to 5 days. Indicated only in very ill
patients with systemic symptoms associated with bloody diarrhea
 In amoebic dysentery Tab. metronidazole 400mg three times a day for 5 to 7 days. Oral
Tab. tinidazole 600 mg twice a day for 3 to 5 days.


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Gastrointestinal Diseases
129
 In acute giardiasis Tab. tinidazole 1000 mg single dose or Tab. metronidazole 400 mg
three times a day for 3 days.  Hospitalization is needed when there are clinical signs of
dehydration especially in young children or in the elderly, suspected cholera, immune
suppressed patients and those with severe systemic symptoms.
Patient education
 In the absence of vomiting patient should be asked to take sips of fluid.
 Fluids used at home can be juices, soups and ORS.
 Milk and related products are avoided for at least 2 weeks, because of secondary lactase
deficiency.
Figure 1. Algorithm for the treatment of acutediarrhea
Acute Diarrhea (< 7 days)
Are the following present?
1. Severeillness: T >38.50C, abdominal pain,
bloody diarrhea, >6 stool / 24 hrs,


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Acute Diarrhea (< 7 days)
Are the following present?
1. Severeillness: T >38.50C, abdominal pain,
bloody diarrhea, >6 stool / 24 hrs,
dehydration
2. Immunocompromised patients: AIDS, post
transplantation
3. Elderly patients
No Yes
Symptomatic therapy
Antidiarrheal agents:
Loperamide,
Bismuth Subsalicylate
Send stool for following:
1. Fecal leukocytes
2. Routine stool culture
3. C. difficileassay, if recent
hospitalization of antibiotics
4. Ova and parasitetesting, if:
a. Diarrhea > 10 days
b. Travels to endemic region
c. Community water borne
outbreak
d. HIV infection of men who
have sexwith men
&
Consider empireantibiotic therapy while
awaiting culture, if:
1. Fecal leukocyte positive
2. Bloody diarrhea, fever, abdominal
pain
Illness
resolves
Illness persists
for 7-10 days
or worsens


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130
 Patient may present in acute stage with bloody diarrhoea, may be associated with
systemic symptoms of low to moderate fever, backache, arthralgias.
 The diagnosis is confirmed by sigmoidoscopic examination and mucosal biopsies.
 The disease almost always involves rectum and rest of the colon may be involved to
variable length.
 Ac ute disease is graded as mild (2-4 stool/day), moderate (4-6 stools/day) or severe (> 6
stools/day). During remission patient may be asymptomatic or may have extra-intestinal
symptoms.
ULCERATIVE COLITIS (UC)
Salient features
Non -pharmacological treatment
There is no specific dietary restriction but patient may avoid any food if the patient is
uncomfortable.
Pharmacological treatment


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There is no specific dietary restriction but patient may avoid any food if the patient is
uncomfortable.
Pharmacological treatment
Mild to moderate acute ulcerative colitis (distal/left colonic involvement)
 Tab. sulphasalazine 1 g 3-4 times a day. Or Tab. mesalazine 800 mg 3-4 times a day. Or
Tab. olsalazine 1-3 g/day in divided doses.
 Prednisolone phosphate enema, 20 mgin 100 ml saline 1-2 time a dayor Hydrocortisone
enema 100-125 mg in 100 ml saline 1-2 times a day (to be prepared fresh).
 Or if disease limited to rectum, Hydrocortisone foam 125 mg 1-2 times a day.
Moderate to severe or extensive acute disease
 Start as above.
 Tab. prednisolone 20-60 mg/day in single or divided doses.
Follow-up
If the symptoms do not improve or worsen, patient will need hospitalization.


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 Tab. prednisolone 20-60 mg/day in single or divided doses.
Follow-up
If the symptoms do not improve or worsen, patient will need hospitalization.
Acute severe disease with systemicsym ptoms (requires hospitalization under the care of
specialist)
 Inj. hydrocortisone 100 mg IV 4 times a dayor Inj. dexamethasone 4 mg IV 3-4 times a
day.
 Patient should be kept 'nil by mouth' and should be given adequate intravenous fluids and
electrolytes.
 Blood transfusion to be given as per requirement.
 Patient switched over to oral steroids and aminosalicylates to be started as in I after 5
days when patient is allowed to take orally.
 If patient fails to respond to steroids, refer the patient to gastroenterologist for


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days when patient is allowed to take orally.
 If patient fails to respond to steroids, refer the patient to gastroenterologist for
immunosuppressive therapy or surgery.Once the remission is induced, steroids are
tapered slowly over 4-6 weeks period. For acute attack, there is no use of giving steroids
for more than 12 weeks.


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Gastrointestinal Diseases
131
 Heartburn, regurgitation, anddysphasia. However, a diagnosis of GERDbased on the
presence oftypical symptoms is correct in only 70% of patients.
 In addition to these typical symptoms, abnormal reflux can cause atypical
(extraesophageal) symptoms,such as coughing, chest pain, and wheezing.
 For patients with symptoms and history consistent with uncomplicated GERD, the
diagnosis of GERDmay be assumed and empirical therapy begun. Patients who show
signs of GERD complications or other illness or who do not respond to therapy should be
considered for further diagnostic testing.
Follow-up
 Close clinical/biochemical/radiological monitoring is required for any complications like
toxic megacolon/perforation.
Maintenance of remission


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 Close clinical/biochemical/radiological monitoring is required for any complications like
toxic megacolon/perforation.
Maintenance of remission
 Any of the drugs used in I should be given lifelong.
Patient education
 Patient should be followed up at 6 monthly intervals and maintenance treatment should be
continued.
 In any patient who has disease for more than 10 years, a regular sigmoidoscopy and rectal
biopsy should be done at 6 monthly intervals to look for any dysplasia and total
colonoscopic examination should be done at 2-3 year interval.
 Patient should be explained about chronic nature of the disease and continuation of
maintenance treatment for life long with regular follow-up and risk of colonic cancer after
10 years of onset of disease
GASTROESOPHAGEAL REFLUX DISEASE


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10 years of onset of disease
GASTROESOPHAGEAL REFLUX DISEASE
Gastro esophageal reflux is a normal physiologic phenomenon experienced intermittently by
most people, particularly after a meal. Gastro esophageal reflux disease (GERD) occurs when
the amount of gastric juice that refluxes into the esophagus exceeds the normal limit, causing
symptoms with or without associated esophageal mucosal injury (i.e., esophagitis).
Salient features
Investigations
 Upper GI endoscopy - Endoscopy can help confirm the diagnosis of reflux by
demonstrating complications of reflux (esophagitis, strictures, Barrett oesophagus) and
can help in evaluating the anatomy (e.g., hiatal hernia, masses, strictures)
 Manometry helps surgical planning by determining the lower esophageal sphincter (LES)


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 Manometry helps surgical planning by determining the lower esophageal sphincter (LES)
pressure and identifying any oesophageal motility disorders.
 Optional studies include: 24-hour pH probe test  and  nuclear medicine gastric emptying
study
Treatment


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Gastrointestinal Diseases
132
 Treatment of GERD involves a stepwise approach. The goals are to control symptoms, to
heal esophagitis, and to prevent recurrent esophagitis or other complications.
 The treatment is based on lifestyle modification and control of gastric acid secretion
through medical therapy with antacids or PPIs or surgical treatment with corrective anti
reflux surgery.
Pharmacological treatment
 Omeprazole 40 mg twice day half an hour before meals. Along with domperidone 30 mg
sustained release
 This therapy causes resolution of GERD symptoms at 4 weeks and healing of esophagitis
at 8 weeks so the treatment should be continued up to 8 weeks.
Surgical Treatment
Indications for surgical treatment include the following:


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at 8 weeks so the treatment should be continued up to 8 weeks.
Surgical Treatment
Indications for surgical treatment include the following:
 Patients with symptoms that are not completely controlled by PPI therapy can be
considered for surgery.
 The presence of Barrett esophagus
 The presence of extraesophageal manifestations of GERD may indicate the need for
surgery; these include the following: (1) respiratory manifestations (e.g., cough,
wheezing, aspiration); (2) ear, nose, and throat manifestations (e.g., hoarseness, sore
throat, otitis media); and (3) dental manifestations (e.g., enamel erosion)
 Young patients
 Poor patient compliance with regard to medications
 Postmenopausal women with osteoporosis
 Patients with cardiac conduction defects
 Cost of medical therapy


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 Postmenopausal women with osteoporosis
 Patients with cardiac conduction defects
 Cost of medical therapy
 Types of surgery:Open / Laparoscopic Nissen fundoplication
Patient education
 Lifestyle modifications include the following losing weight (if overweight), avoiding
alcohol, chocolate, citrus juice, and tomato-based products. Recent guidelines also
suggest avoiding peppermint, coffee, and possibly the onion family as well.
 Avoidinglarge meals and waiting 3 hours after a meal before lying down, elevating the
head of the bed 8 inches.Lifestyle modification is as effective as antacid therapy.
UPPER GASTROINTESTINAL BLEEDING
Upper gastrointestinal haemorrhage remains a major medical problem. Causes includes


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UPPER GASTROINTESTINAL BLEEDING
Upper gastrointestinal haemorrhage remains a major medical problem. Causes includes
esophageal, gastric, duodenal ulcer ,erosions of esophageal,  gastric, duodenal,M allory
W eiss tear, oesophageal varices,tumour,vascular lesion, e.g. dieulafoy's diseaseand others
Investigations
 Hb, Abo-Rh, PT,APTT, Upper G.I.Scopy, Ultrasonography
Treatment:Primary and general management includes


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Gastrointestinal Diseases
133
 Epigastric pain, history of alcoholism, gall stone disease, Cholesterol andmetabolic
abnormalities, history of similar complains in family.
 Per abdomen examination- look for tenderness, guarding, rigidity. Look for fever,
tachycardia, tachypnoea,shock.
Pharmacological treatment
 Get wide bore access with IV cannula (16G preferable) for rapid fluid resuscitation,
R yle's tube insertion, catheterization,
 Inj. pantoprazole 40 mg IV 12 hourly, Inj. tranexamic acid  500 mg TDS
 Inj. octreotide 100 mcg IV 6 hourly, banding-in oesophageal varices, gastric balloon of
Sengstaken blackmore tube-in oesophageal varices,
 Injection sclerotherapy-in oesophageal varices, argon diathermy-in pepticulcers, laser-in
peptic ulcers
Surgical treatment


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 Injection sclerotherapy-in oesophageal varices, argon diathermy-in pepticulcers, laser-in
peptic ulcers
Surgical treatment
 Exploratory laprotomy and search for the cause and treat the cause or TIPPS(Tran
jugular intrahepatic portosystemic shunts)-in uncontrolled portal hypertension cases.
ACUTE PANCREATITIS
Acute pancreatitis is the most common pathology of pancreas. It ranges from self limiting
mild pancreatitis to life threatening necrotizing pancreatitis which accounts for 10-20% of
total cases. Causes of acute pancreatitis: alcoholism gall stone disease, hypercholesterolemia
hypercalcemia, hypermagnesemia pancreatic divism, viral infections, familial pancreatitis,
others, idiopathic
Salient features
Investigations


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hypercalcemia, hypermagnesemia pancreatic divism, viral infections, familial pancreatitis,
others, idiopathic
Salient features
Investigations
TC with DC which shows increased with neutrophillia, S.amylase, increased more than 3 fold
normal value, S. lipase (more specific), increased more than 3 fold of normal value, S.
calcium below normal values, USG- Abdomen, shows edema of pancreas, necrosis, CECT-
Abdomen (in unresolving and severe cases), delineates pancreatic anatomy more clearly,
Chest X Ray,to rule out systemic complications likeAcute Respiratory Distress Syndrome
(ARDS )
Prognostic indicators: Ranson's score, Glasgow score, APACHE II score
Non pharmacological treatment
Nil by mouth, nasogastric tube insertion,avoidalcohol
Pharmacological treatment


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Non pharmacological treatment
Nil by mouth, nasogastric tube insertion,avoidalcohol
Pharmacological treatment
 Fluid resuscitation, Correction of electrolyte imbalance
 Inj. diclofenac sodium 75 mg IM 8 hourly and gradually proceeding towards opioid
analogue like  Inj. tramadol  50 mg once day


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Gastrointestinal Diseases
134
 Dull epigastric pain,Weight loss,Malnutrition,Pancreatic diabetes
 History of alcoholism,History of previous attacks of acute pancreatitis.
 Usually non specific,Signs of cachexia and malnutrition
 Inj. pantoprazole 40 mg IV 12 hourly  and  Inj. octreotide100 microgram IV/SC 6 hourly
to 12 hourly till resolution of symptoms
Surgical treatment
 Usually no surgical intervention is required for acute non necrotising pancreatitis.
 Cholecystectomy for gall stone pancreatitis after acute pancreatitis is resolved
Acute necrotising pancreatitis
Non pharmacological treatment
 ICU monitoring, oxygen by mask, nil by mouth, nasogastric tube insertion per urethral
catheterization
Pharmacological treatment
 Fluid resuscitation, correction of electrolyte imbalance


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catheterization
Pharmacological treatment
 Fluid resuscitation, correction of electrolyte imbalance
 Inj.meropenem 1 gm IV 8 hourly
 Inj. diclofenac sodium  75 mg IM 8 hourly
 Inj. pantoprazole 40 mgIV 12 hourly
 Inj. octreotide 100 microgramIV/SC every 6 hourly to 8 hourly
Surgical treatment
 Pancreatic necrosectomy,  distal pancreatectomy ( for disease inbody and tail)
 Cholecystectomy for gall stone pancreatitis after acute pancreatitis is resolved.
CHRONIC PANCREATITIS
Chronic pancreatitis is a disease of pancreas characterized by pancreatic atrophy, fibrosis,
calcification and at times ductal dilatation. It is most commonly caused by repeated alcoholic
pancreatitis.
Salient features
Investigations


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calcification and at times ductal dilatation. It is most commonly caused by repeated alcoholic
pancreatitis.
Salient features
Investigations
S. amylaseand S. Lipase has usually no role. X-ray abdomen, may show calcification in
pancreatic region. USG- Abdomen shows atrophic pancreas with or without foci of
calcification and ductal dilatation.Magnetic Resonance Cholangiopancreatography(MRCP )
gives excellent anatomy of ductal system.Endoscopic Retrograde Cholangiopancreatography
(ERCP ), reserved for chronic pancreatitis due to peri ampullary obstruction
Non -pharmacological treatment
 Avoidance of alcohol, low fat, Low protein diet
Pharmacological treatment
 Enteric coated pancreatic enzymes, for replacement of pancreatic function,


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Gastrointestinal Diseases
135
 Constipation is defined as decrease in frequency and liquidity of stool compared to the
normal pattern in a particular individual.
 Important complaints suggesting constipation include straining at defaecation >25% of
time, lumpy/hard stools, sensation of incomplete evacuation, or less than 3 bowel
actions per week.
 Inj. diclofenac sodium 75 mg IM 8 hourly  and gradually proceedingtowards opioid
analogue like Inj. tramadol  50 mg
 Inj. pantoprazole 40 mg IV 12 hourly
Surgical treatment
 Indicated in severe pain non responding to pharmacological therapy
 Peustaw procedure ( LPJ, Longitudinal Pancreatico-jejunostomy), Frey's procedure( LPJ
with coring out of head ), Duval procedure ( Distal Pancreatico-jejunostomy ), Distal


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with coring out of head ), Duval procedure ( Distal Pancreatico-jejunostomy ), Distal
pancreatectomy, for lesion confined to body and tail,
 Duodenum preserving pancreatic head resection, DPPHR, Beger's procedure, for lesion
confined to head region.Endoscopic stenting, for obstruction in pancreatic duct, coeliac
block, for patients unfit for surgery.
CONSTIPATION
Commonest cause is habitual, the important contributory factors being insufficient dietary
fiber, physical inactivity, suppression of defaecatory urges occurring at inconvenient
moments, prolonged travel etc. Constipation may also occur following an attack of diarrhoea
on the day after taking a purgative; this needs no treatment.The important secondary causes


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on the day after taking a purgative; this needs no treatment.The important secondary causes
may include neurological, hormonal, colonic, malignancy, depression. Secondary causes
should be looked for in case of recent onset or constipation of severe symptoms.
Salient features
Non -pharmacologicaltreatment
 Reassurance-since many patients with normal stools and in pregnancy,imagine that they
are constipated.
 High fiber diet and increased intake of fluid with decrease in consumption of caffeinated
drinks.
 Retraining of bowels (avoiding suppression of urge to defecate, making a regular habit).
 Bulk forming agents like 'isapghula husk' or 'psyllium seeds' also help to relieve mild
constipation.
 Regular physical exercise such as walk for 1/2 to 1 hour daily and abdominal exercises.


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constipation.
 Regular physical exercise such as walk for 1/2 to 1 hour daily and abdominal exercises.
Pharmacologicaltreatment
(Usually required for moderate to severe constipation).
 Lactulose Soln 15-20 ml orally at night. Or Susp. magnesium sulphate 15-20 ml at night.
Or Tab. sodium picosulphate 10 mg at night. Or


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Gastrointestinal Diseases
136
 Abdominal pain in right upper quadrant,fever,history of diarrhea in past 7-10 days.
 Physical examination revelstenderness in right hypochondriac region, Palpable liver
and signs of jaundice.
 Isotonic polyethylene glycol (PEG) electrolyte solution 125-250 ml.
 Any of these may be given 2-4 times a week. Some patients may requiretreatment for
several weeks or months if there is no improvement.
 Tab. mosapride 5 mg 2 or 3 times a day. In some patients may be required for several
weeks.
 Phosphate enemas to be used on as and when required basis in patients having acute
problem with severe constipation or sub-acute intestinal obstruction.
Follow-up
 If patient continues to have severe constipation or symptoms worsen, refer the patient to a


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Follow-up
 If patient continues to have severe constipation or symptoms worsen, refer the patient to a
specialist for investigations to rule out secondary causes.
 Recent unexplained constipation (not acute) in an elderly person whose bowel habits were
always regular should be investigated.
 Acute constipation especially when the patient is vomiting and has not passed even wind
and appears ill, suspect GIT obstruction and refers immediately to a higher centre.
Patient education
 Do not use purgative frequently to treat constipation as it may form a habit.
 Do not use purgatives to treat constipation with fever and following heart attack. A
suppository or simple enema is preferred.
 In pregnancy ispaghula is preferred.
AMOEBIC LIVER ABSCESS


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suppository or simple enema is preferred.
 In pregnancy ispaghula is preferred.
AMOEBIC LIVER ABSCESS
Amoebic liver abscess is most common type of liver abscess in tropical countries. It is caused
by infection byEntamoeba histolyticumthrough feco-oral route which reaches liver via portal
circulation, causing necrosis of liver tissue resulting in what is known as anchovy sauce pus.
Salient features
Investigations
 TC with D increased, PT, APTT: elevated, Liver Function Tests (S. Billirubin, SGPT, and
Albumin).
 Chest X Ray (elevated right diaphragm, rules out perforation). USG Abdomen,  CECT
Abdomen ( if rupture of abscess is suspected extra peritoneal )
 Diagnostic aspiration of abscess  followed by routine microscopic and culture-sensitivity
of pus
Non -pharmacologicaltreatment


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 Diagnostic aspiration of abscess  followed by routine microscopic and culture-sensitivity
of pus
Non -pharmacologicaltreatment
 High glucose diet, Low protein diet


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Gastrointestinal Diseases
137
 Abdominal pain in right upper quadrant (RHC) ,fever,tenderness in RHC.
 Palpable liver and jaundice
Pharmaco logicaltreatment
 Tab. metronidazole 800 mg TDS for 2 weeks followed by Tab. diloxanide furoate 500 mg
BD for 10 days.
 Inj. diclofenac sodium 75 mg IM 8 hourly.
 Inj. pantoprazole 40 mg IV 12 hourly.
 Vit.K injections if PT/APTT is altered.
Surgical treatment
 Amoebic liver abscess usually does not require drainage.Percutaneus aspiration can be
done in abscess having large size (>100 cc).
 Exploratory laparotomy with drainage of abscess is required in suspected ruptured liver
abscess
PYOGENIC LIVER ABCES S
It isthe most common type of liver abscess in western world. It can be caused by ascending


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abscess
PYOGENIC LIVER ABCES S
It isthe most common type of liver abscess in western world. It can be caused by ascending
infection from biliary tract, infection via portal blood supply, hematogenous via hepatic
artery,  direct spread ( gall bladder, duodenum, colon ) or cryptogenic.
Salient features
Investigations
 TC with DC, elevated with neutrophillia, PT, APTT is elevated
 Liver Function Tests (S. bilirubin, SGPT, albumin), Chest X Ray ( elevated right
diaphragm, rules out perforation ),USG Abdomen, CECT Abdomen ( if rupture of
abscessis suspected extra peritoneally).
 Diagnostic aspiration of abscess followed by routine microscopic and culture- sensitivity
of pus
Non -pharmacologicaltreatment
 High glucose diet,  low protein diet
Pharmacological treatment


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of pus
Non -pharmacologicaltreatment
 High glucose diet,  low protein diet
Pharmacological treatment
 Inj. ceftrioxone 1-2 g IV BD
 Inj. diclofenac sodium 75 mg IM 8 hourly
 Inj. pantoprazole 40 mg IV 12 hourly
 Vit.k injections if PT/APTT are altered
Surgicaltreatment
 Percutaneous aspiration can be done in abscess cavity and usually requires 2-3 settings of
aspirations donealternate day.Percutaneus pigtail catheter can be used to avoid repeated
aspirations.Laparoscopic drainage of liver abscess if site of abscess permits.
 Exploratory laparotomy with drainage of abscess is required in suspected ruptured liver
abscess.


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138
 Generalized tetanus starts with trismus or lockjaw followed by rigidity, violent, painful,
generalized muscle spasms and seizures provoked by slightest stimulation. Generalized
muscle spasm may compromise respiration, fever and tachycardia may be present.
 Prognosis and management depends on grade.
C hapter 9
INFECTIONS
TETANUS
It is anacute neurological disorder resulting from contamination of a wound by an obligate
anaerobic organismClostridium tetani.
Salient features
Investigations
 C linical- culture ofC. tetanifrom a wound provides supportive evidence. The few
conditions that mimic generalized tetanus include strychnine poisoning and dystonic
reactions to antidopaminergic drugs. Abdominal muscle rigidity is characteristically


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reactions to antidopaminergic drugs. Abdominal muscle rigidity is characteristically
continuous in tetanus but is episodic in the latter two conditions. Cephalic tetanus can be
confused with other causes of trismus, such as oropharyngeal infection.
 Hypocalcemia and meningoencephalitis are included in the differential diagnosis of
neonatal tetanus.
Grading
 Mild or grade 1– muscle rigidity with few or no spasms.
 Moderate or grade 2-trismus, dysphagia, rigidity and short lasting spasms.
 Severe or grade 3- frequent explosive spasms, autonomic dysfunction particularly
sympathetic over activity may be present.
 Very severe orgrade4-features of grade 3 plus violent autonomic disturbances involving
the CVS – severe hyper or hypotension.
Non -pharmacological treatment


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the CVS – severe hyper or hypotension.
Non -pharmacological treatment
 Admit in a quiet roomorICU with minimum stimulation.
 Protection of airways (intubation/tracheostomy) withor without mechanical ventilation.
Monitorcardiovascular parameters.
 Cleaning/exploration/debridement of wound
 Maintain hydration and enteral/parentral nutrition with high calorie and high protein diet.
Pharmacological treatment
Grade 1
 Tab. diazepam 5-20 mg 3 times a day; slow IV infusion in moderate to severe tetanus; not
exceed a dose of 80-100mg in 24 hours.
 If spasms not controlled, Inj.phenobarbitone 200mg IM every 8-12 hours or Inj.
chlorpromazine 50 mg IM in adults 4 times a day.


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Infections
139
 Rodents are the important reservoirs. Leptospires may enter the host through abrasions in the
skin or intact mucosa, the conjunctive and the liningof oro-and naso-pharynxin contact with
water contaminated withleptospira.
 90% of symptomatic persons have the mild and usual anicteric form of leptospirosis, with or
without meningitis. Severe leptospirosis with profound jaundice– Weil’s syndrome-occurs
in 5 to 10% of patients.The common finding in anicteric leptospirosis is fever with
conjunctival suffusion. Mild jaundice may be present.
 The ideal sedative and muscle relaxant schedulefor each patient should be individualized.
An objective guide to decrease in rigidity is relaxation of abdominal muscles.
Grade 2
 Tracheostomy
Grade 3 and 4
 Ventilatory support


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An objective guide to decrease in rigidity is relaxation of abdominal muscles.
Grade 2
 Tracheostomy
Grade 3 and 4
 Ventilatory support
 Inj.pancuronium 2-4mg or gallamine 20-40mg IV.
 Ifhypotension, give vasopressor support andifhypertension, give antihypertensive.
 For bradyarrythmias,Inj.atropine 0.6-1.2 mg IV.
In addition,give following to all patients;
 Inj. crystalline 2 mega units 6 hourly IV for 10 days or Inj. metronidazole 500mg 8 hourly
or 1gm 12 hourly.Requirement may beaccording totheinfected wound.
 Inj. human tetanus immunoglobulin (TIG) 3000-5000 units IV or IM or Inj. equine
antiserum 10000 units by slow IV injection after sensitivity test when human TIG is not
available.
 Antiserum should be given before local manipulation of the wound.
LEPTOSPIROSIS


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available.
 Antiserum should be given before local manipulation of the wound.
LEPTOSPIROSIS
Leptospirosis is an infectious disease caused by thespirocheteLeptospira.
Salient features
Investigations
 Culture- B lood, CSF and urine is the definite way of confirming the diagnosis of
leptospirosis
 Micro agglutination (MAT )
- Seroconversion / four fold rise in the titera
 ELISA / MSAT
- Positive
Pharmacological treatment
 All clinically suspected leptospirosis patients in endemic area during rainy season should
be given presumptive treatment of leptospirosis andm alaria. Tab. doxycycline 100 mg


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Infections
140
 A symptomatic or have mild diarrhoea;some may have sudden onset of explosive and life-
threatening diarrhoea (cholera gravis). In a non-immune individual, after 24 to 48h
incubation period, characteristicsudden onset of painless wateryvoluminous diarrhoea.
Patients often vomit. In severe cases, volume loss can exceed 250 ml/kg in the first 24 h. If
fluids and electrolytes are not replaced, hypovolemic shock and death may ensue.
 Fever is usually absent. Muscle cramps due to electrolyte disturbances are common. The
stool has a characteristic appearance: a nonbilious, gray, slightly cloudy fluid with flecks of
mucus, no blood, and a somewhat fishy, inoffensive odour,known as "rice-water" stool.


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mucus, no blood, and a somewhat fishy, inoffensive odour,known as "rice-water" stool.
 Clinical symptoms parallel volume contraction: At losses of <5% of normal body weight,
thirst develops; at 5–10%, postural hypotension, weakness, tachycardia, and decreased skin
turgor are documented; and at >10%, oliguria, weak or absent pulses, sunken eyes (and, in
infants, sunken fontanelles), wrinkled ("washerwoman") skin, somnolence, and coma.
 Complications due to volume and electrolyte depletion-renal failure.
twice daily for 7 days and  Tab. chloroquine 600mg (base) stat followed by 600 mg after
24 hours and  300 mg after another 24 hours in malaria endemic areas in adults.
Note: In children less than 6 years 30-50 mg/kg/day of Cap.amoxicillin/ Cap. ampicillin


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Note: In children less than 6 years 30-50 mg/kg/day of Cap.amoxicillin/ Cap. ampicillin
should be given in divided doses 6 hourly for 7 days in place of doxycycline.
Definitive treatment
 Inj. crystalline penicillin 20 lacs IU IV 6 hourlyafter negative test dose (ANTD) for 7
days. For children the dose of crystalline penicillin should be 2-4 lacs IU/kg/day for 7
days.
 For penicillin sensitive patients,Inj.ceftrioxone 1 gm IV. once daily for 7 daysor
Inj.cefotaxime 1 gm. IV. 6 hours daily for 7 days
Symptomatic and supportive treatment
 Care of fluid and electrolyte balance. Hypovolemia and hypotension need prompt
treatment withIV fluids.Patients with oligouria, if prerenal azotemia is suspected,
prompt diuresis should be attempted with fluid therapy.


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treatment withIV fluids.Patients with oligouria, if prerenal azotemia is suspected,
prompt diuresis should be attempted with fluid therapy.
 Headache and myalgiato betreated with analgesic.Fever with antipyretic.
 Restlessness and anxiety with sedatives and anemia with blood transfusion.
 Peritoneal dialysis has been found to be safe, simple and effective procedure for
management of renal failure due to leptospirosis. If there is contraindication to peritoneal
dialysis, hemodialysis can be done.
C HOLERA
It is an acute diarrheal disease thatoccurs in few hours, result in profound, rapidly
progressive dehydration and death.C aused byV. choleraeserogroup O1 or O139—i.e., the
serogroups with epidemic potential.
Salient features


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Infections
141
Investigation
 Identification ofV. choleraein stool examination directly by dark-field microscopy on a
wet mount of fresh stool, and its serotype by immobilization with specific antiserum.
Laboratory isolation of the organism requires the use of a selective medium such as
taurocholate-tellurite-gelatin (TTG) agar or thiosulfate–citrate–bile salts–sucrose (TCBS)
agar.Standard microbiologic biochemical testing forEnterobacteriaceaewill suffice for
identification ofV. cholerae. All vibrios are oxidase-positive.
 A point-of-care antigen-detection cholera dipstick assay is now commercially available
for use in the field or where laboratory facilities are lacking.
Non -pharmacological treatment
 ORS may be made by adding safe water to prepackaged sachets containing salts and


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Non -pharmacological treatment
 ORS may be made by adding safe water to prepackaged sachets containing salts and
sugar or by adding 0.5 teaspoon of table salt (NaCl; 3.5 g) and 4 tablespoons of table
sugar (glucose; 40 g) to 1 L of safe water.
 Potassium intake in bananas or green coconut watershould be encouraged.
Pharmacological treatment
 Euvolemia should first be rapidly restored, and adequate hydration should then be
maintained to replace ongoing fluid losses(Table1& 2).
 WHO recommends "low -osmolarity" ORS for treatment of dehydrating diarrhea. If
available, rice-based ORS is considered superior to standard ORS in the treatment of
cholera. ORS can be administered via a nasogastric tube to individuals who cannot ingest
fluid.


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cholera. ORS can be administered via a nasogastric tube to individuals who cannot ingest
fluid.
 O ptimal managementforsevere dehydration includes the administration of IV fluid and
electrolytes. Ringer's lactate is the best choice among commercial products. It must be
used with additional potassium supplements, preferably given by mouth. The total fluid
deficit in severely dehydrated patients (>10% of body weight) can be replaced safely
within the first 3–6 h of therapy, half within the first hour. Transient muscle cramps and
tetany are common. Thereafter, oral therapy can usually be initiated, with the goal of
maintaining fluid intake equal to fluid output.
 Patients with continued large-volume diarrhea may require prolonged IV treatment to


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maintaining fluid intake equal to fluid output.
 Patients with continued large-volume diarrhea may require prolonged IV treatment to
match gastrointestinal fluid losses. Severe hypokalemia can develop but will respond to
potassium given either IV or orally. In the absence of adequate staff to monitor the
patient's progress, the oral route of rehydration and potassium replacement is safer than
the IV route.
Table 1.Assessing the Degree of Dehydration in Patients with Cholera
Degree of Dehydration Clinical Findings
None or mild, but diarrheaThirst in somecases; <5% loss of total body weight
Moderate Thirst, postural hypotension, weakness, tachycardia,
decreased skin turgor, dry mouth/tongue, no tears; 5–10%
loss of total  body weight


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Severe Unconsciousness, lethargy, or "floppiness"; weak or absent
pulse; inability to drink; sunken eyes (and, in infants,
sunken fontanelles); >10% loss of total body weight
Table 2.Treatment of Cholera, Based on Degree of Dehydration
Degree of Dehydration,
Patient's Age (Weight)
Treatment
None or Mild, but Diarrhea
<2 years 1/4–1/2 cup (50–100 ml) of ORS, to a maximum of 0.5
L/d
2 – 9 years 1/2–1 cup (100–200 ml) of ORS, to a maximum of 1 L/d
More than 10 years As much ORS as desired, to a maximum of 2 L/d
Moderate
<4 months (<5 kg) 200–400 ml of ORS
4–11 months (5–<8 kg) 400–600 ml of ORS
12–23 months (8–<11 kg) 600–800 ml  of ORS
2–4 years (11–<16 kg) 800–1200 ml  of ORS
5–14 years (16–<30 kg) 1200–2200 mlof ORS
15 years (≥30 kg) 2200–4000 ml of ORS
Severe


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2–4 years (11–<16 kg) 800–1200 ml  of ORS
5–14 years (16–<30 kg) 1200–2200 mlof ORS
15 years (≥30 kg) 2200–4000 ml of ORS
Severe
All ages and weights IV fluid replacement with Ringer's lactate (or, if not
available, normal saline): 100 ml/kg in first 3-h period
(or first 6-h period for children <12 months old); start
rapidly,then slow down; total of 200 ml/kg in first 24 h;
continue until patient is awake, can ingest ORS, and no
longer has a weak pulse
 Tab. doxycycline (a single dose of 300 mg) or tetracycline (12.5 mg/kg four times a day
for 3 days) may be effective in adults but is not recommended for children <8 years of
age because of possible deposition in bone and developing teeth. Pregnant women and


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age because of possible deposition in bone and developing teeth. Pregnant women and
children are usually treated with erythromycin or azithromycin (10 mg/kg in children).
INFLUENZA INFECTION
It isa respiratory disease of pigs affecting human beings, caused by types A influenza viruses
with regular outbreaks in pigs.  Source of the virus in swine are avian, human and swine.  All
three viruses re-assort and form a new virus which is a mixture of all three.  At present there
are four types H1N1, H1N2, H3N2 and H3N1.  The present pandemic is by influenza AH1N1
type.


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143
 Symptoms in clude fever, headache, cough, sore throat, rhinorrhea, myalgia, fatigue,
vomiting, or diarrhea.Patients appear flushed and the skin ishot and dry.  Pharynx is normal
despite a severe sore throat.
 There may be mild cervical lymphadenopathy.  Illness generally resolves over 2-5 days and
recovery occurs in 1 week.  Cough may persist 1-3 weeks longer and post influenza asthenia
may persist for several weeks.
 Frank dyspnoea, hyperpnoea, cyanosis, diffuse rales and signs of consolidation are indicative
of pulmonary complications. Symptoms of severe disease may include apnea, tachypnoea,
dyspnoea, cyanosis, dehydration, altered mental status and extreme irritability.
Case Definitions


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dyspnoea, cyanosis, dehydration, altered mental status and extreme irritability.
Case Definitions
 A confirmed case of H1N1 infection is defined as a person with an acute febrile respiratory
illness with laboratory confirmed H1N1 infection at CDC byone or more of the following
tests: realtime RT-PCR, viral culture or four fold increase in H1N1 virus specific neutralizing
antibodies.
 A probable case of H1N1 is a defined as a person with acute respiratory illness who is
positive forinfluenza A but negative to H2 and HB by RT-PCR.
 A suspected case of H1N1 is defined a person with an acute febrile respiratory illness who
has had dose contact with a person who is a swine-origin influenza confirmed case or


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has had dose contact with a person who is a swine-origin influenza confirmed case or
travelled to a community one or more confirmed swine origin influenza cases or resides in a
community where there are one or more confirmed swine origin influenza A(H1N1) cases.
Salient features
Investigations
Upper respiratory specimens, nasopharyngeal swab or wash, nasal, aspirateor tracheal
aspirate should be tested by the state public health laboratory. Real time RT-PCR, viral
cultures are to be performed to confirm the H1N1 infection.
Pharmacological treatment
The guiding principles are:
 Early implementation of infection control precautions to minimize nosocomical /
household spread of disease
 Prompt treatment to prevent severe illness & death.


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household spread of disease
 Prompt treatment to prevent severe illness & death.
 Early identification and follow up of persons at risk.
 Tab. oseltamivir is the recommended drug both for prophylaxis and treatment.Dose for
treatment is as follows:  Byw eight  <15kg 30 mg BD for 5 days , 15-23kg 45 mg BD for
5 days , 24≤ 40kg 60 mg BD for 5 days ,  >40kg 75 mg BD for 5 days
 For infants < 3 months 12 mg BD for 5 days, 3-5 months 20 mg BD for 5 days  6-11
months 25 mg BD for 5 days.If needed dose & duration can be modified as per clinical
condition.


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144
Caution:Oseltamiviris generally well tolerated, gastrointestinal side effects (transient
nausea, vomiting) may increase with increasing dose.
Supportive therapy
 IV fluids, parentral nutrition.
 Oxygen therapy/ ventilatory support.
 Antibiotics for secondary infection.
 Vasopressors for shock.
 Paracetamol or ibuprofen is prescribed for fever, myalgia and headache. Patient is advised
to drink plenty of fluids. Smokers should avoid smoking. For sore throat, short course of
topical decongestants, saline nasal drops, throat lozenges and steam inhalation may be
beneficial.
 Salicylate / aspirin is strictly contra-indicated in any influenza patient due to its potential
to cause Reye’s syndrome.


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beneficial.
 Salicylate / aspirin is strictly contra-indicated in any influenza patient due to its potential
to cause Reye’s syndrome.
 The suspected cases would be constantly monitored forclinical / radiological evidence of
lower respiratory tract infection and for hypoxia (respiratory rate, oxygen saturation, level
of consciousness).
 Patients with signs of tachypnea, dyspnea, respiratory distress and oxygen saturation less
than 90 per cent should be supplemented with oxygen therapy. Types of oxygen devices
depend on the severity of hypoxic conditions which can be started from oxygen cannula,
simple mask, partial re-breathing mask (mask with reservoir bag) and non re-breathing
mask. In children, oxygen hood or head boxes can be used.


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simple mask, partial re-breathing mask (mask with reservoir bag) and non re-breathing
mask. In children, oxygen hood or head boxes can be used.
 Patients with severe pneumonia and acute respiratory failure (SpO2 < 90% and PaO2 <60
mmHg with oxygen therapy) must be supported with mechanical ventilation. Invasive
mechanical ventilation is preferred choice. Non invasive ventilation is an option when
mechanical ventilation is not available. To reduce spread of infectious aerosols, use of
HEPA filters on expiratory ports of the ventilator circuit / high flow oxygen masks is
recommended.
 Maintain hydration,electrolyte balance and nutrition.
 If the laboratory reports are negative, the patient would be discharged after giving full


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 Maintain hydration,electrolyte balance and nutrition.
 If the laboratory reports are negative, the patient would be discharged after giving full
course of oseltamivir. Even if the test results are negative, all cases with strong
epidemiological criteria need to be followedup.
 Immunomodulating drugs have not been found to be beneficial in treatment of ARDS or
sepsis associated multi organ failure. High dose corticosteroids in particular have no
evidence of benefit and there is potential for harm. Low dose corticosteroids(Tab.
hydrocortisone 200-400 mg/ day) may be useful in persisting septic shock (SBP < 90).
 Suspected cases not having pneumonia do not require antibiotic therapy. Antibacterial
agents should be administered, if required, as per locally accepted clinicalpractice


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agents should be administered, if required, as per locally accepted clinicalpractice
guidelines. Patient on mechanical ventilation should be administered antibiotics
prophylactically to prevent hospital associated infections.


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145
Major signs and symptoms:
 Weight loss (> 10 kg or > 20% of original weight)
 Diarrhoea (> 1 month)
 Fever for more than 1 month
Minor signs:
 Herpes zoster (shingles),Pruritic popular rash.
 Kaposi’s sarcoma
 Persistent generalized lymphadenopathy (PGL)
 Oral candidiasis,Oral hairy leukoplakia
 Persistent painful genital ulceration
 The persistence ofeither Kaposi’s sarcoma or cryptococcal meningitis is sufficient for the
case definition of AIDS.
HIV disease is characterized by three phase.
 Acute primary illness,Asymptomatic chronic illness,Symptomatic chronic illness
HIV AND AIDS
H uman immunodeficiency virus (HIV)infection leads to progressive immunodeficiency and
increased susceptibility to infections, includingtuberculosis.  The rate of disease progression


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increased susceptibility to infections, includingtuberculosis.  The rate of disease progression
is highly variable between individuals, ranging from 6 months to than 20 yrs. The median
time to developAcquired Immunodeficiency Syndrome (AIDS ) after transmissionis 10 yrs
in the absence of Antiretroviral therapy (ART). The case definition of AIDS is fulfilled at
least 2 major signs and at least 1 minor sign are present where HIV testing facilities are not
available.  In children if 2 major and 2 minor signs are present (if no other causes for
immunosuppression)
Salient features
Investigations
 HIV serology
 CD4 + T lymphocytes counts (if available)
 Complete blood count and chemistry of profile andpregnancy test
Supplementary test indicated by history and physicalexamination


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 Complete blood count and chemistry of profile andpregnancy test
Supplementary test indicated by history and physicalexamination
 Chest x-ray
 Urine for routine and microscopic examination
 Hepatitis C Virus IHCV) and Hepatitis B Virus (HBV) serology (depending on test
availability and resources)
Important note: It is most important to confirm the diagnosis of HIV infectionby tests
performed by a trained technician, preferably in a diagnostic laboratory.   The test results
should include the type of test performed to establish the diagnosis based on WHO
guidelines.  In case there is any doubt, the test should be repeated ina standard/referral
laboratory.


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146
WHO Clinical staging of HIV Disease for Adults
Primary HIV Infection
 Asymptomatic
 Acute retroviral syndrome
Clinical stage I
 Asymptomatic
 Persistent generalized lymphadenopathy (PGL)
Clinical Stage 2
 Moderate unexplained weight loss (< 10% of presumed or measured body weight)
 Recurrent respiratory tract infections.
 Sinusitis,Bronchitis, otitis media, pharyngitis
 Herpes zoster, angular cheilitis,recurrent oral ulcerations.
 Papularpruritic eruptions,seborrhoeic dermatitis
 Fungal nail infections of fingers.
Clinical stage 3- Conditions where a presumptive diagnosis can be made on the basis of
clinical signs or simple investigations.
 Severe weight loss (> 10% of presumed or measured body weight)
 Unexplained chronic diarrheafor longer than one month.


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 Severe weight loss (> 10% of presumed or measured body weight)
 Unexplained chronic diarrheafor longer than one month.
 Unexplained persistent fever (intermittent or constant for longer than one month)
 Oral candidiasis,Oral hairy leukoplakia
 Pulmonary tuberculosis (TB), Severe bacterial infections (e.g. pneumonia, emphysema,
pomposities, bone orjoint infection, meningitis, bacteraemia)
 Acute necrotizing ulcerative stomatitis, gingivitis or periodontitis
Clinical stage 4-Conditions where the diagnosis can be made on the basis of clinical signs or
simple investigations.
 HIV wasting syndrome
 Pneumo cystic  pneumonia, recurrent severe or radiological bacterial pneumonia.
 Chronic herpessimplex infection (orolabial, genital or anorectal of more than one
month’s duration)


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 Chronic herpessimplex infection (orolabial, genital or anorectal of more than one
month’s duration)
 Esophageal candidiasis
 Extra-pulmonary tuberculosis including tuberculous lymphadenopathy.
 Kaposi sarcoma
 Central nervous system (CNS) toxoplasmosis
 HIV encephalopathy.
Conditions where confirmatory diagnostic testing is necessary:
 Extra– pulmonary crytococcosis including meningitis.
 Disseminated nontuberculous mycobacterial infection.
 Progressive multifocal leukoencephalopathy (PML)


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147
 Candida of trachea, bronchi or lungs
 Crytosporiodiosis,isosporiasis
 Visceral herpes simplex infection.
 Cytomegalovirus (CMV) infection (retinitis or of an organ other than liver, spleen or
lymph nodes)
 An y disseminated mycosis (e.g. histoplasmosis, coccidiomycosis, penicilliosis)
 Recurrent non-typhoidal salmonella septicaemia
 Cerebral or B-cell Non-Hodgkin lymphoma
 Invasive cervical carcinoma
 Visceral leishmaniasis
Table 3.Initiation of ART in Adults andAdolescents National Guidelines, 2011
Based on WHO Clinical Staging and CD4 Count
WHO Clinical Staging CD4 (cells/cu.mm)
I and II Treat if CD4 Count <350
III and IV Treat irrespective of CD4 Count
Initiation of ART in PLHIV with Pregnancy(Table 4): Same as above.Avoid efavirenz


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III and IV Treat irrespective of CD4 Count
Initiation of ART in PLHIV with Pregnancy(Table 4): Same as above.Avoid efavirenz
during first trimester.Strict Monitoring for Adverse effects of Nevirapine is neededifCD4
count is >250.
Table 4.Initiation of ART in Person living withHIV (PLHIV) with TB Co-infection
Type of Tuberculosis Eligible
Clinical Staging and CD4
Counts
Timing of ART
in relation to start of
TB treatment
Pulmonary TB
(Stage III)
Start ART irrespective of any
clinical stage
and
irrespective of CD4 counts
Start ATT first;
Start ART as soon as
TB treatment is tolerated
after2 wks & before 2mth.
Extra pulmonary TB
(Stage IV)
Table 5.Initiation of ART in PLHIV with Hepatitis B or Hepatitis C Co-infection
Co -infection WHO Clinical Staging CD4 (cells/cu.mm)
HIV -HBV or HIV -HCV


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Co -infection WHO Clinical Staging CD4 (cells/cu.mm)
HIV -HBV or HIV -HCV
co-infection without
evidence of chronic active
Hepatitis
I and II Start ART at CD4 Count <350
III & IV Start ART irrespective
of CD4 Count
HIV -HBV or HIV -HCV
co-infection with
documented evidence of
chronic active Hepatitis
All Clinical stages Start ART Irrespective
of anyCD4 count


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 Sub-acute onset of symptoms over a period of weeks.
 Typically fever, dry cough and progressive difficulty in breathing, also weight loss,night
sweats and fatigue.
Table 6. First line ART Regimens National AIDS Control Organization (NACO )
Guidelines 2009
Regimen National ART Regimen Preference
Regimen I Zidovudine + Lamivudine +
Nevirapine
Preferred regimen
for patients with Hb >9 gm/dl
Regimen I (a) Tenofovir + Lamivudine +
Nevirapine
For patients with Hb <9 gm/dl
Regimen II Zidovudine + Lamivudine +
Efavirenz
Preferred for patients  on anti-
tuberculosis treatment, if Hb >9
gm/dl
Regimen II (a) Tenofovir + Lamivudine +
Efavirenz
For patients on anti-tuberculosis
treatment and Hb <9 gm/dl
Table 7.Second line ART Regimen for Adults and Adolescents in India
Second


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Efavirenz
For patients on anti-tuberculosis
treatment and Hb <9 gm/dl
Table 7.Second line ART Regimen for Adults and Adolescents in India
Second
Line ARVs
Dosage Dosing schedule
TDF + 3TC Fixed dose combination
of TDF 300 mg + 3TC 300 mg
0 –0 –1
(One tablet in the night)
ATV/r
C ap. atazanavir 300 mg 0 –0 –1
(One tablet in the night)
Tab.ritonavir 100 mg 0 –0 –1
(One tablet in the night)
OPPORTUNISTIC INFECTIONS
The common conditions and diseases related to AIDS include tuberculosis,pneumocystis
carinii pneumonia, oesophagea l candidiasis, cryptococcosis, toxoplasmosis,
cryptosporidiosis, cytomegalovirus (CMV), andm ycobacterium avium complex (MAC).
Diagnosis and management of common opportunistic infections is given herewith.
I. PNEUMOCYSTIS CARINII PNEUMONIA (PCP)


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Diagnosis and management of common opportunistic infections is given herewith.
I. PNEUMOCYSTIS CARINII PNEUMONIA (PCP)
PneumocystisCarinii is a fungus that infects the lungs
Salient features
Investigations
 X -ray
 Induced sputum examination or bronchoscopy,CD -4 count <200


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149
 Difficulty in swallowing or retrosternal discomfort.Weight loss is common
 CD4 count < 100
 Usually made directly in presence of oral candidiasis and dysphagia.Endoscopy is indicated
who fail to respond to a clinical trial of appropriate treatment.
 The diagnosis of esophageal candidiasis should be reconsidered if oral candidiasis is not
present.
 Associated fever and oral ulceration are not common.
Pharmacologicaltreatment
 Severe disease – hospitalization, intravenous trimethoprim/sulphamethoxazole
(TMP/SMX) (15mg/kg/day for 21 days), supplemental oxygen for patients with severe
hypoxemia (PaO2 < 70 mmHg breathing room air at rest).Corticosteroids,prednisolone,
40 mg twice daily for 5 days followed by 40 mg once daily for 5 days, followed by 20 mg


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40 mg twice daily for 5 days followed by 40 mg once daily for 5 days, followed by 20 mg
once daily for 11 days.
 For m oderate disease, an oral agent may be used on outpatient basis, although
hospitalization should be considered.While mildcases,oral TMP/SMX can be givenas
above.
Preventive therapy
 Tab. dapsone 100 mg once a day for 21 days– preferred second-line option.
 Tab. clindamycin 450 mg 4 times a day + primaquine 15 mg once daily for 21 days.
 Tab. atovaquone 750 mg once a day for 21 days.
 Inj. pentamidine (intravenous) 3-4 mg/kg/day for 21 days.
II.OESOPHAGEAL CANDIDIASIS
Candidiasis is a fungal infection that frequently occurs in the mouth and vagina.  It is
considered to be an opportunistic infection when it occurs in the oesophagus.
Salient features


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considered to be an opportunistic infection when it occurs in the oesophagus.
Salient features
Pharmacological treatment
 Preventive therapy: not recommended because current drugs effectively treat
(prophylaxis) disease
 Antifungal resistance may develop and drug-drug interactions may occur
 Tab. fluconazole 100-400 mg once a day for 2 weeks is the treatment of choice.
Alternative treatment is Inj. amphotericin B 0.3-0.5 mg/kg/day.
 Maintenance therapy by Tab. fluconazole 50– 100 mg once a day
 Stopping maintenance therapy when there is evidence that patient who achieves CD4
counts > 100 on ART may cease treatment.


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 Headache, nausea, fever, malaise, altered mental status, irritability and seizures, cough, chest
pain, breathlessness
 Presentation:Sub-acute with progressive symptoms over weeks to months or acute with
symptoms over days.
 CD4 count: < 100
 Altered mental state (confusion, unusual behavior),headaches, fever, seizures, paralysis,
coma .
 Presentation: acute to sub acute over days to weeks, CD4 count <100
III.CRYPTOCOCCOSIS
Cryptococcosis is a fungus that is inhaled andcan cause meningitis.
Salient features
Investigations
 Lumbar puncture to test for the presence ofCryptococcusor cryptococcal antigen in
cerebral spinal fluid.  ICP is often raised.
 CSF protein and glucose are generally normal and there may be few white blood cells.
Ph armacological treatment


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 CSF protein and glucose are generally normal and there may be few white blood cells.
Ph armacological treatment
 Inj. amphotericin B 0.5– 0.8 mg/kg/day + flucytosine 100 mg/day 4 times a day for 2
weeks then 8 to 10 weeks.Alternative treatment isliposomal amphotericin.
 Maintenance therapy by  flucanozole 200 mg once a day.Cohort studiessuggest that
maintenance therapy can be ceased in patients with sustained CD4 response to ART (CD4
> 200) for > 3 months
IV.TOXOPLASMOSIS
Toxoplasmosis is a parasite that has a predilection for the brain.
Salient features
Investigations
 Typical appearance on CT or MRI scans.
 Diagnosis is usually presumptive on the basis of appearance on scan.  May show ring
shaped contrast enhancing lesions.
Pharmacological treatment


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 Diagnosis is usually presumptive on the basis of appearance on scan.  May show ring
shaped contrast enhancing lesions.
Pharmacological treatment
 Tab. pyrimethamine 100– 200 mg loading dose and then 50– 75 mg once a day given in
comb ination with sulphadiazine 4– 6 g/day, 4 times a day or  Tab.  clindamycin 2– 4
g/day, 4 times a day for 6– 8 weeks duration depending upon response.If sulphadiazine
is used, Tab. folinic acid 25 mg once a day should be given in the presence of cerebral
edema.


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 Lower abdominal pain. Mild diarrhea develops gradually and may lead to full blown
dysentery. 0-12 stools per day with blood and mucus and little fecal matter.
 Caecal involvement may mimic acute appendicitis. Chronic form i.e. amoebic colitis,
can be confused with inflammatory bowel disease.
 Untreated or incompletely treated intestinal infection may result in amoebic liver
abscess and involvement of other extra intestinal site.
 Acute giardiasis-although diarrhea is common, upper intestinal manifestations such as
abdominal pain, bloating, belching, flatus, nausea and vomiting may predominate.
 Chronic giardiasis– history of one or more episodes of acute diarrhea, increased flatus, loose


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 Chronic giardiasis– history of one or more episodes of acute diarrhea, increased flatus, loose
stools, abdominal distension, borborygmi, eructation of foul tasting gas and passage of foul
smelling flatus, and weight loss.
 Symptoms could be intermittent, recurring and gradually debilitating: severe diseasemay
result in malabsorption, weight loss, growth retardation and dehydration.
 Alternative treatment:pyrimethamine in combination with one of the following: Tab.
azithromycin 1– 15 mg/day or  Tab. atovaquone 3 g/day or Tab. dapsone 100 mg/day or
Tab. clarithromycin 2 g/day
 Maintenance therapy is therapy by Tab.pryimethamine (25 – 75 mg once a day) +
sulphadiazine (50– 100 mg 4 times a day for several days with leucovorin)
AMOEBIASIS (INTESTINAL)


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sulphadiazine (50– 100 mg 4 times a day for several days with leucovorin)
AMOEBIASIS (INTESTINAL)
It is an infection caused by intestinal protozoaEntamoeba histolytica,which usually spreads
by infective cysts in stoolthatcontaminate food and drinking water.
Salient features
Investigations
 D emonstration of cysts and/or trophozoites ofEntamoeba histolyticain the stool.
Pharmacological treatment
 Asymptomatic cyst passers- Tab. diloxanide furoate 500 mg TDS for 10 days
 A cute amoebic dysentery and chronic infection
- Tab. metronidazole 400– 800 mg 8 hourly PO for 10 days. In children 15 mg/kg divided
in three doses for 7 daysor Tab. tinidazole (300 mg, 500 mg and 1 g) 2 g orally as single
dose. In children 50 mg/kg/day inthree divided doses for 10 days


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dose. In children 50 mg/kg/day inthree divided doses for 10 days
- Followed by Tab. diloxanide furoate 500 mg 8 hourly for 10 days
GIARDIASIS
It is an intestinal disease caused by parasiteGiardia lambliathatspreadsby direct faeco-oral
transmission.
Salient features


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152
 Asymptomatic or present with symptoms of anemia (Hypochromic microcytic).
 Pruritic maculopapular dermatitis (ground itch) at site of skin penetration by infective larvae,
serpigenous tracts of subcutaneous migration in previously sensitized host.
 Mild transient pneumonitis because of larvae migration through lungs.
 Intestinal manifestations– epigastric pain often with post-prandial accentuation,
inflammatory diarrhea.
 Major consequences– progressive iron deficiency anemia and hypoproteinemia
Investigations
 D emonstration of cysts and or trophozoites in the stools.
Pharmacological treatment
 Tab. tinidazole 2 g as single dose in adults.  In children 50 mg/kg as a single dose Or


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Pharmacological treatment
 Tab. tinidazole 2 g as single dose in adults.  In children 50 mg/kg as a single dose Or
 Tab. metronidazole 400 mg every TDS for 7 days in adults. In children 15 mg/kg divided
in three doses for 7 days.
Patient education
 Infections spread by ingestion of food or water contaminated with cysts.Properly cooked
food, use of clean drinking water, proper sanitation and good personal hygiene- hand
washing with soap after defecationand before meals may prevent infection.
 Infection can be minimized by avoiding unpeeled fruits and vegetables.
 Side effects are usually mild and transient and include nausea, vomiting, abdominal
discomfort, metallic taste and a disulfiram like reaction, therefore, avoid use of alcohol
during treatment.
HOOKWORM INFESTATION


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discomfort, metallic taste and a disulfiram like reaction, therefore, avoid use of alcohol
during treatment.
HOOKWORM INFESTATION
The majority of worm infestations are asymptomatic Infections causedby A.duodenaleand
N.americanus. The infective larvae penetrate through skin usually the food and travel
through subcutaneous issue to the intestines.  The adult forms live in the jejunum and feed on
blood, thus leading to chronic blood loss and anemia.
Salient features
Pharmacological treatment
 Tab. mebendazole 100mg BD for 3 days in children above 2 years of age.
(Caution: contraindicated in children less than 2 years)or
 Tab.pyrantel pamoate(250mg); once daily for 3 days.
(Caution; not used in children below 1 year of age)


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 Tab.pyrantel pamoate(250mg); once daily for 3 days.
(Caution; not used in children below 1 year of age)
 In children more than 1 year, susp. pyrental palmoate 10mg/kg as a single dose orTab
albendazole 400mg to be given as a single dose.In children between 1-2 years of age
syrup albendazole 200mg as a single dose. In children more than2 years of age syrup
albendazole 400 mg as a single dose.


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153
 Most individuals are asymptomatic.Features of pulmonary involvement because of larval
migration include irritating nonproductive cough, bronchospasm or pneumonitis and burring
substernaldiscomfort aggravated by coughing or deep inspiration, dyspnoea, fever,
eosinophilic pneumonities.
 Small bowel obstruction may get complicated by perforation intussusceptions or volvulus.
 Aberrant migration of a large worm may cause biliary colic, cholangitis, cholecystitis
pancreatic and oral expulsion of the worm.
 Most infestations are asymptomatic.Cardinal symptoms are perianal pruritis, worse at night
due to migration of female worms. Excessive itching can lead to perianal excoriation and
bacterial superinfection.H eavy infection causes abdominal pain and weight loss.


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bacterial superinfection.H eavy infection causes abdominal pain and weight loss.
 Rarely, in female’s vulvovaginitis and pelvic or peritoneal granulomas occur. Eosinophilia.
Patient education
 Hookworm infestation occursthrough skin penetration by the infective larvae.
 The disease can be prevented by use of boots and gloves while working in the fields.
ASCARIASIS (ROUNDWORM INFESTATION)
Ascariasis is caused byAscaris lumbricoides, the largest nematode parasite of humans
reaching up to 40 cm in length.  The worm is located in the large intestine.
Salient features
Pharmacological treatment
 Tab mebendazole 100 mg 12 hourly for 3 days in children above 2 years of age. (Caution:
contraindicated in children < 2 years)


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 Tab mebendazole 100 mg 12 hourly for 3 days in children above 2 years of age. (Caution:
contraindicated in children < 2 years)
 Tab.pyrantel pamoate 11 mg/kg as a single dose or Tab.  albendazole 400 mg as a single
dose. In heavy infestation, however, a 2-3 day course is indicated. (Caution:
contraindicated in pregnancy)
 In children between 1– 2 years of age Syr. albendazole 200 mg asa single dose. In
children more than 2 years, Syr. albendazole 400 mg as a single dose.
Patient education
Proper sanitation and good personal hygiene- hand washing with soap after defecation and
before meals may prevent infection.A void unpeeled fruits and vegetables and use of clean
drinking water.
ENTEROBIASIS
Infection is caused byEnterobius vermicularis(Pin worm). Adult pinworm is around 1 cm


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drinking water.
ENTEROBIASIS
Infection is caused byEnterobius vermicularis(Pin worm). Adult pinworm is around 1 cm
long and dwells in the bowel lumen in the small and large intestine around caecum area.
Salient features


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Infections
154
 In acute presentation episodicattacks of fever with lymphadenitis and lymphangitis.
Occasionally adult worms may be felt subcutaneously.
 Chronic presentation as a case of lymphatic obstruction due to worm or fibrosis causing
massive lower limb oedema, non pitting type, with skin thickening, hydrocele,
chyluria, chylous ascitis,  chylothorax.
Investigations
D emonstration of the ova ofEnterobius vermicularisin perianal swabs or a cellophane tape
should be pressed against perianal skin. In the morning, when the child gets up, eggs stick to
the tape and can be examined under the microscope.
Pha rmacological treatment
 Tab. mebendazole 100 mg as a single dose in adults and children more than 2 years of


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Pha rmacological treatment
 Tab. mebendazole 100 mg as a single dose in adults and children more than 2 years of
age. (Contraindicated in pregnancy and in children below one year of age). Or Tab.
pyrantel pamoate 11 mg/kg body weight as a single dose. Or Tab. albendazole 400 mg as
a single dose.
 Children (1-2 years) Syr. albendazole 200 mg as a single dose; More than 2 years 400 mg
as a single dose.
 Repeat treatment after two weeks.
Assessment of response of worm infestation to therapy
 Repeat stool, perianal swab examination for ova ofEnterobius vermicularis.
 Absolute eosinophil count, haemoglobin and peripheral blood smear examination at
monthly intervals for 3-6 months.
 Serum albumin level in hookworm infection.
Patient education


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monthly intervals for 3-6 months.
 Serum albumin level in hookworm infection.
Patient education
 Treatment of all family members is required to eliminate asymptomatic reservoirs of
potential re infection.
 Proper sanitation and good personal hygiene, hand washing with soap after defecation
and before meals may prevent infection.
 Infection can be minimized by avoidance of unpeeled fruits and vegetables and use of
clean drinking water. Regular washing and disinfection of linen.
FILARIASIS
Filariasis iscaused bywuchereria bancroftiin 90% of cases.Lymphatics are mainly affected,
resulting in gross limb swellings.
Salient features
Investigations: Total and differential count shows eosinophilia. Immature worms
(microfilaria) seen in nocturnal peripheral blood smears.


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Investigations: Total and differential count shows eosinophilia. Immature worms
(microfilaria) seen in nocturnal peripheral blood smears.
Non -pharmacologicaltreatment
 Manual lymphoedema drainage


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Infections
155
 Multilayer lymphoedema bandage
 Compression garments,exercise
 Skin care to prevent athlete foot with 3% benzoic acid, for dry skin paraffin ointment, for
hyperkeratosis 5% salicylic acid,
Pharmacological treatment
Tab.diethylcarbamazine 6mg/kg for 21 days .for acute cases and antipyretics for fever
Surgical treatment
 Bypass procedures
 Omental pedicle
 Nodovenous shunt
 Limb reduction procedures


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156
 Blocked ear andpain
 Tinnitus,reflex cough on manipulation,vertigo
Chapter10
ENT DISEASES
EAR -WAX
External ear wax is the accumulated secretion from ceremonious gland situated in outer part
of meatus may form a solid, often hard mass giving rise to deafness and discomfort in the ear.
Salient features
Investigations
 Otoscopy
 Brownish-black mass in external auditory canal.
Pharmacological treatment
 For severe pain Tab. ibuprofen 400 mg SOS, in children 20 g/kg/day divided into 3 doses.
 Wax softener (turpentine oil- 15%, benzocaine - 2.7%), chlorbutol- 5%,
paradichlorobenzene-2%) 3-4 days before cleaning the ear when the wax is hard.
 Followed by surgical removal (to be carried out by an Otolaryngologist).


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 Followed by surgical removal (to be carried out by an Otolaryngologist).
 Syringing with sterile saline solution at body temperature pushed along the posterior wall
of the meatus to take out the wax. The meatus should be mopped dry after syringing.
(Caution: if there is previous history of ear discharge or perforated drum or instrumental
manipulation with ringprobe, hook or forceps and suction cleaning).
Patient education
 Wax is a normal secretion and provides protection to the ear drum and should be removed
only if it disturbs hearing.
 Avoid cleaning the ear with buds as it can push the wax to the deepercanal.
References
1. Diseases of the External Ear. In: Logan Turner's Diseases of the Nose, Throat and Ear, 10th Edition, pp
265-67.
KERATOSIS OBTURANS


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References
1. Diseases of the External Ear. In: Logan Turner's Diseases of the Nose, Throat and Ear, 10th Edition, pp
265-67.
KERATOSIS OBTURANS
Collection of desquamated epithelium mixed with wax in external auditory canal causing
ballooning of the canal is known as Keratosis obturans.
Salient features
 Difficulty in hearingand severe pain
 Serosanginuous discharge


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 Blocked ear,m ovement of pinna painful
 Severe pain and occasionally discharge
 Regionallymphadenitis
Investigations
Otoscopy- cerumen admixed with desquamated debris, external canal granulations and bone
erosion
Treatment
 Initially soften the mass with sodium bicarbonate ear drops daily for several days
followed by syringing.
 Removal under general anaesthesia using microscope.
FURUNCLE
Furuncle is the infection of the root of a hair follicle caused bystaphylococcus aureusin
cartilaginous external auditory canal.
Salient features
Investigations
 History of recent cold and influenza, sign of middle ear infection
 Otoscopy examination may reveal boils
 Maximum tenderness over tragus and post-auricular lymphadenitis


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 Otoscopy examination may reveal boils
 Maximum tenderness over tragus and post-auricular lymphadenitis
 Obliteration of post aural sulcus with forward displacement of aurical
 Mastoid radiograph show well developed clear cell on affected side
Non -pharmacological treatment
 Local heat
Pharmacological treatment
 10% ichthamol in glycerine wick pack or  antibiotic steroid cream wick pack (polymyxin
B sulphate 500 IU, neomycin sulphate 3400 IU, zinc bacitracin 400 IU, hydrocortisone 10
mg, per g) wick packing to be done on alternate day till swelling subsides followed by/or
 Local ear drops (polymyxin B sulphate 1000 U, neomycin sulphate 3400 U,
hydrocortisone 10 mg/ml).
 Systemic antibacterial like Cap. amoxicillin 500mgTDS 5-7 days or azithromycin 500mg


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hydrocortisone 10 mg/ml).
 Systemic antibacterial like Cap. amoxicillin 500mgTDS 5-7 days or azithromycin 500mg
OD for 3-5 days  antibiotics
 Tab. ibuprofen 400 mg as and when requiredorTab. nimesulide 100 mg twice a day.
 Incision and drainage may be necessary in some cases.
Patient education
 Patients with recurrent boils, diabetes mellitus should be ruled out
 Avoid ear picking.


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 Irritation and itching of ear discharge (thick white debris like.)
 If the discharge isw hitelikeblotting paper– candida, black mass with mycelia–
aspergillus Nigerand pale blue and green– aspergillus fumigatus.
OTOMYC OSIS
Otomycosis is the fungal infection of the ear canal. Secondary growth occurs in patients
using topical antibiotics for otitis externa or middle ear suppuration.
Salient features
Investigations
 Direct otoscopic examination
 Microscopic examination in10% KOH
 Culture in sabourd’s Dextrose agar
Non -pharmacological treatment
 Regular ear toilet-by suction/dry mopping/instrumentation.
Pharmacological treatment
 Topical clotrimazole as 1% powder or liquid 3-4 times a day to be continued for at least
a week after clinical resolution of the infection.


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 Topical clotrimazole as 1% powder or liquid 3-4 times a day to be continued for at least
a week after clinical resolution of the infection.
 Tab. ibuprofen 400 mg as and when required. In children 20 mg/kg/day in 3 divided
doses.
Patient education
 Ear is to be kept dry; entry of water into the ear should be prevented.
References
1. Diseases ofthe External Ear. In: Logan Turner's Diseases of the Nose, Throat and Ear, 10th Edition, pp 274-
75.
2. External Auditory Meatus. In: Scott- Brown's Otolaryngology, JB Booth (ed) Vol 3, 6th Edition, 1997,
Butterworth-Heinemann, pp 3/6/14-15.
MALIGNANT OTI TIS EXTERNA
External otitis in diabetic patients or those who are using immunosuppressive drugs due to
Pseudomonas aeruginosainfection
Salient features
Investigations


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Pseudomonas aeruginosainfection
Salient features
Investigations
 Otoscopy shows external canal inflammation and granulation
 Cranial nerve paralysisor  facial palsy is common
 To exclude diabetes / CT scan temporal bone to rule out osteomyelitis of temporal bone.
 Severe pain andswelling around the ear / facial weakness


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 Pain, feverand ear discharge
 Hearing impairmentand tinnitus
 Symptoms in childrenincludefever, vomiting, diarrhea,sleeplessness, incessant cryand
irritability
Pharmacological treatment
 Topical anti-pseudomonal antibacterials (ciprofloxacin, carbenicillin, amikacin,
tobramycin, ticarcillin, third generation cephalosporins)
 Surgical debridement of devitalised tissue and bone to be done judiciously.
ACUTE SUPPURATIVE OTITIS MEDIA
It is an acute inflammation of middle ear caused by pyogenic organism. It is common in
children, associated with upper respiratory infection and exanthematous fevers.
Salient features
Investigations
 Otoscopy shows congested and bulging tympanic membrane
 Mucopurulent discharge
Non pharmacological treatment


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Salient features
Investigations
 Otoscopy shows congested and bulging tympanic membrane
 Mucopurulent discharge
Non pharmacological treatment
 Steam inhalation and to keep the ear clean in case of pus discharge.
Pharmacological treatment
 Tab. paracetamol 500 mg SOS
 Cap. amoxicillin 250-500 mg 8 hourly for 7 days. In complicated cases and children <2
years duration of treatment 10 days or Cap. cephalexin 250-500 mg 8 hourly. In children
20-40 mg/kg/day in 3 divided doses. Switch antibiotics if no clinical improvement by 3rd
day.
 Xylometazoline HC1 0.1% 1 -2 nasal drops in each nostril 1-2 times daily.
In Children (0.05%) 1-2 nasal drops 1-2 times daily or oxymetazoline 0.05% 1-2 nasal
drops in each nostril 2 times daily. In Children (0.01%) 1-2 drops 2 times daily.


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drops in each nostril 2 times daily. In Children (0.01%) 1-2 drops 2 times daily.
 Refer to an Otolaryngologist if there is intense pain, bulging of the ear drum or persisting
fever despite treatment for myringotomy.
Patient education
 Treat upper respiratory and sinus infections atthe earliest.
References
1. Acute Suppurative Otitis Media and Acute Mastoiditis. In: Scott Brown's Otolaryngology, Vol 3, JB Booth
6th Edition, pp 3/9/1-15.
2. Acute Otitis Media in Adults. In: Logan Turner's Diseases of the Nose, Throat and Ear 10th Edition, pp 280-
81.
3. Diseases of the Middle Ear Cleft. In: A Synopsis of Otolaryngology, 4th Edition, 91-109.


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ENT Diseases
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 Ear discharge-Mucopurulent / intermittent / not foul smelling / profuse / not blood
stained. Associated withupper respiratory tract infection
 Hearing loss (conductive) and Tinnitus
 There are two stages-active and inactive (no discharge, only hearing loss)
 Proteus,Pseudomonas, K lebsiella,E. Coli.,Staphylococcusaureus are the most
common organisms. While anaerobes organisms includeBacteroidesfragilis(most
common) and anaerobicStreptococci.
CHRONIC SUPPURATIVE OTITIS MEDIA
Chronic Suppurative Otitis Media(CSOM)  a long standing infection of middle ear clef,
characterized by ear discharge and permanent perforation of tympanic membrane.It is
classified as tubo tympanic disease (safe ear)and attico-antral disease (unsafe ear).
Salient features
Investigations


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classified as tubo tympanic disease (safe ear)and attico-antral disease (unsafe ear).
Salient features
Investigations
 Otoscopy showsdischarge mucopurulent / mucoid / dry,perforation– central perforation
 Conductive deafness (tuning fork test) (confirm degree and type of hearing loss)
 Middle ear mucosa-normal in quiescent stage, edematous and velvety in active stage
 Examination under microscope,audiogram
 Pus culture and sensitivity
 X -ray mastoids-both ears sclerotic. May be pneumatised with clouding of air cells to
assess co-morbid status
 HRCT temporal bone which help in (1) establishing cholesteatoma (2) operative planning
Non -pharmacological treatment
 Aural toilet by dry mopping orcareful suction.
Pharmacological treatment


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Non -pharmacological treatment
 Aural toilet by dry mopping orcareful suction.
Pharmacological treatment
 Topical antibiotics like ciprofloxacin HC1 0.3% w/v ear drops 2-3 drops 3-4 times daily
 When associated with marked inflammation, addprednisolone 0.5% + chloramphenicol
5% + lignocaine 2% + acetic acid 2% to beused as 3-4 drops 3-4 times daily.
 For profuse mucopurulent discharge and associatedupper respiratory tract infection
(URTI), Cap. amoxicillin 750-1500 mg in 3 divided doses.In children 20-40 mg/kg in 3
divided doses. The choice of antibiotic depends onthe culture and sensitivity report.
Surgical treatment
 O nce the ear is dry and any local nidus of infection has been treated the ear can be taken
up for myringoplasty after assessing the hearing status.
Patient education


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up for myringoplasty after assessing the hearing status.
Patient education
 Avoid water or dust to enter the ear.Explain the patient to take immediate treatment in
case ofURTI. N ot to instill oil if there is a discharge from the ear or if the patient is
known to have perforation of ear drum.


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ENT Diseases
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 Deafness, sensation of fluid, tinnitus.Earache and ear drum appear to be normal,
lusterless retracted or fluid level or air bubbles may be seen behind the drum.
 Headache, nasal obstruction, hawking andpostnasal drip.Fever, malaise,congested
nasal mucosa, pus in the middle meatus and tendersinuses.
References
1. Diseases of the External Ear. In: Logan Turner's Diseases ofthe Nose, Throat and ear 10th Edition, pp 271-
73.
2. Management of Chronic Suppurative Otitis Media. In: Scott Brown's Otolaryngology', JB Boothy (ed), Vol
3, 6th Edition, 1997, pp 3/10/1-11.
SEROUS OTITIS MEDIA
It is characterized by the presence of non-purulent fluid in middle ear cleft which maybe due
toEustachian tube dysfunction, unresolved acute otitis media or viral infection. It is one stage


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toEustachian tube dysfunction, unresolved acute otitis media or viral infection. It is one stage
further then Eustachian tube catarrh where fluid having a consistency of glue collects in the
middle ear producing conductive deafness.
Salient features
Investigations
 Audiogram reveal conductive deafness
 Impedance audiometry show flat type of curve (B curve)
Pharmacological treatment
 Cap. amoxycillin 250 mg with clavulanic acid 375 mg,TDS beforemeals for 21days.
 Tab.pseudoephedrine120 mg 8 hourly. In children 1-2 mg/kg twice daily.
Surgical treatment
 For patients not responding to long term pharmacological measures. This include
myringotomy with or without grommet insertion, adenoidectomy, treatment forsinusitis
and even mastoidotomy in refractory cases.
Patient education


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myringotomy with or without grommet insertion, adenoidectomy, treatment forsinusitis
and even mastoidotomy in refractory cases.
Patient education
 Do not instill oil in the ear.
References
1. Management of Chronic Otitis Media. In: Scott Brown's Otolaryngology, JB Booth (ed), Vol. 3, 6th
Edition, 1997, Butterworth-Heinemann, pp 3/9/1-15.
ACUTE SINUSITIS
Itisinflammation of paranasal sinuses. Acute maxillary sinusitisis the commonest type of
sinusitis while acute ethmoidal sinusitis is more common in infants and children.
Salient features


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ENT Diseases
162
Investigations
 X ray paranasal sinuses– Water’s view -haziness or opacity /fluid level.
 C T-para nasal sinuses in selectedcases where WBC, ESR, Positive blood culture confirm
 Trans illumination test reveal opaque sinuses
Non -pharmacological treatment
 Steam inhalation vianose 2-3 times/dayfor 2-3 days andrest.
Pharmacological treatment
 Tab. paracetamol 500 mg 3-4 times a day for 5days (children 10 kg/dose) or Tab.
ibuprofen 400 mg-600 mg 3 times a day for 5 days (children 10 mg/kg/dose.)
 Cap. amoxicillin 500 mg 8 hourly for 5-7 days(children 50 mg/kg/day).
Sinusitis of dental origin
 Cap. amoxicillin 500 mg 3 times a day for 5-7 days.
 Tab. metronidazole 400 mg 3 times a day for 5-7 days.
 Tab. bromhexine 8 mg 3 times a day for 7 days.


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 Tab. metronidazole 400 mg 3 times a day for 5-7 days.
 Tab. bromhexine 8 mg 3 times a day for 7 days.
If nasal obstruction or rhinorrhoea,
 Normal saline nasal 1-2 drops in each nostril 2-3 times a day.Or ephedrine 0.75% nasal
drops in isotonic saline 1-2 drops in each nostril 2 times a day. In children 0.5% 1-2 drops
in each nostril 2 times daily. Or oxymetazoline HCl 0.05% nasal drops. 1-2 drops in each
nostril 2 times a day. In children 0.025% 1-2 drops in each nostril 2 times daily.
 Xylometazoline 0.1% nasal drops 2-3 drops in each nostril 2-3 times a day. In Children
0.05% 1-2 drops in each nostril 2 times daily.
(Caution:Medicated nasal drops shouldnot be used for more than 7 days).
Improvement is seen in symptoms viz. pain tenderness, nasal obstruction and discharge


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Improvement is seen in symptoms viz. pain tenderness, nasal obstruction and discharge
within 48-72 hours after initiation of therapy. If there is no desirable response patient should
be referred to an Otolaryngologist.
Patient education
 To take full course of systemic antibiotics to avoid the risk of developing antimicrobial
resistance.
 Prolonged use of topical decongestants more than a week to be avoided as it can cause
atrophic rhinitis, anosmia and rhinitis medicamentosa.
References
1. Acute Rhinosinusitis. In: Logan Turner's Diseases of Nose, Throat and Ear. 10th Edition pp 34-6.
EPISTAXIS
Epistaxis is defined as bleeding through the nose. The common cause in children may be due
to nose picking, in adolescents (especially males) due to juvenile nasopharyngeal


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to nose picking, in adolescents (especially males) due to juvenile nasopharyngeal
angiofibroma and hypertension /neoplasm in elderly.


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ENT Diseases
163
 Sneezing, itching, watery nasal discharge and a feeling of nasal obstruction.  It may be
associated with allergic conjunctivitis and bronchial asthma.
 Sneezing, itching watery rhinorrhoea and conjunctivitis areprominent symptoms  in seasonal
allergic rhinitis (SAR/Hay fever) while perennial allergic rhinitis (PAR) due  to long standing
nasal mucosal congestion with purulent nasal dischargeassociated with  nasal blockage, post
nasal discharge and hyposmia.
Investigations
 Baseline investigations including complete hemogram, coagulation profile, blood
grouping and typing
 X rayparanasal sinuses and  CT para nasal sinuses– if necessary
Treatment
 Resuscitative measures if clinical parameters suggestive of hemodynamic compromise
 Cauterization


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Treatment
 Resuscitative measures if clinical parameters suggestive of hemodynamic compromise
 Cauterization
 Anterior and posterior nasal packing
 Surgical– endoscopic cautery and ligation of vessels
Patient education
 Avoid insertingfingers into the nose, especially children.
 As first aid, explain how to pinch the nose tightly and apply ice pack over the nose, while
waiting for proper medical attention.
References
1. Epistaxis. In: Scott Brown's Otolaryngology, IS MacKay and TR Bull (eds) Vd4, 6th Edition, 1997,
London: Buttcrworths. pp 4/18/1-19.
ALLERGIC RHINITIS
Allergic rhinitis is an IgE mediated type I hypersensitivity reaction of mucus membrane of
nasal cavity sometimes affecting paranasal sinuses due to mucosal continuity.
Salient features
Investigations


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nasal cavity sometimes affecting paranasal sinuses due to mucosal continuity.
Salient features
Investigations
 Peripheral blood eosinophilia
 Nasal smear– shows eosinophilia
 X ray nose and para nasal sinuses
 Intranasal provocation test
 Specific IgE antibody test
Non -pharmacologicaltreatment
 Avoid allergens.
Pharmacological treatment
 Tab. cetrizine 10-20 mg in a single daily dose for 7 days In children 5 mg od or


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 Nasal stuffiness, rhinorrhea, sneezing and low grade fever.Nasal obstruction, profuse
mucopurulant secretions
 Sore throat for 1 or 2 days followed by cough and nasal discharge.
 Tab. chlorpheniramine maleate 4 mg 6-8 hourly for 7 days. (Caution: Not recommended
for children under 1 year)  Or
 Tab. pheniramine maleate 25-50 mg 8 hourly for 7 days.In children 0.5mg/kg/day
divided in 3 doses. The duration of treatment may need to be extended depending upon
the response of the patient.
 If nasal obstruction and rhinorrhoea,Normal saline nasal drops 1-2 drops in each nostril 2
times daily or  xylometazoline 0.1% nasal drops 1-2 drops 2-3 times daily for 5-7 days. In
children 0.05% 1-2 drops 2 times daily. or oxymetazoline 0.5% nasal drops 2-3 drops 2-3


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children 0.05% 1-2 drops 2 times daily. or oxymetazoline 0.5% nasal drops 2-3 drops 2-3
times daily for 5-7 days. In children 0.025% 1-2 drops 2 times in each nostril
 If the signs and symptoms are persistent,Betamethasone/ hydrocortisone nasal drops 2-3
times/ day.Beclomethasone inhaler (50 mcg/puff) 2 puffs 12 hourlyor budesonide (50-
100 mcg/puff) 1-2 puffs a day or fluticasone 150 meg/puff 1-2 puffs a day. OrTopical
azelastine intranasal spray 2-3 times a day.
 In case of no response to the above treatment,Tab. prednisolone 5-60 mg/day in3-4
divided doses for 5-7 daysor Tab. dexamethasone 0.5-5.0 mg/day in 3-4 divided doses
for 5-7 days. Or Tab. betamethasone 0.5-5.0 mg/day in 3-4 divided doses for 5-7 days.
Patient education


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for 5-7 days. Or Tab. betamethasone 0.5-5.0 mg/day in 3-4 divided doses for 5-7 days.
Patient education
 This disease is due to hypersensitivity and there is no cure but symptoms can be controlled
effectively by the judicious use of drugs and the patient can lead a normal life.
 Avoid prolong use of topical decongestant nasal drops as it can cause atrophic rhinitis,
anosmia and rhinitis medicamentosa.
 Chlorpheniramine, pheniramine etc. can cause sedation, cognitive impairment. Patient
should avoid tasks requiring alertness and skill. These drugs can also cause dryness of the
mouth and urinary hesitancy.
 Systemic steroids should not be stopped abruptly. Dose to be tapered off before cessation
of therapy.
 Medicated nasal drops should not be used for more than seven days.
References


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of therapy.
 Medicated nasal drops should not be used for more than seven days.
References
1. Mechanism and Treatment of Allergic Rhinitis. In: Scott Brown's Otolaryngology. JB Booth (ed), 6th
Edition, 1997. Butterworth’s-Heinemann, pp 4/6/1-16.
COMMON COLD (CORYZA)
It is one of the most common viral infection affecting upper respiratory tract.
Salient features


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 Sever pain and tenderness over the tip of nose.There may be headache, malaise and
pyrexia.Examination reveals congestion and swelling of vestibule.
Non -pharmacological treatment
 Steam inhalation 2-3 times/day
 For nasal obstruction, saline nasal drops 1-2drops in each nostril 2-3 times daily
Pharmacological treatment
 Tab. chlorpheniramine 4mg 8 hourly for 5-7 days. (in children 0.35mg/kg/day in 3 equal
doses)  or  Tab. pheniramine 25mg 2-3 times daily for 5-7days ( in children 0.5mg/kg/day
divided in equal doses)  or  Tab. cetirizine dihydrochloride 10mg once a day 5-7days (in
children 5mg once per day).
 If patient has malaise and fever,
 Tab. paracetamol 1500mg 3-4 times aday for 2-3 days and then as when required (in
children 40-60mg/kg/day divided in 4 doses)


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 Tab. paracetamol 1500mg 3-4 times aday for 2-3 days and then as when required (in
children 40-60mg/kg/day divided in 4 doses)
If nasal obstruction is severe,
 Ephedrine 0.75% nasal drop,1-2drops in each nostril 3 times a day for 2-3 days or
oxymetazoline HCL 0.05% nasal drops,1-2drops in each nostril 3 times a day for 2-3
days( in children 0.025% nasal drops,1 drop 2 times daily or  xylometazoline 0.1%, 1-
2drops in each nostril 3 times a day for 2-3 days( in children 0.05%, 1-2 drops 2 times
daily)  (Caution: Not recommended in children below 6yrs of age, medicated nasal drops
should not used for more than 7 days)
Patient education
 This is a self-limiting viral infection and usually subsides in one week requiring only
symptomatic relief.
 Antibiotics have no role.


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 This is a self-limiting viral infection and usually subsides in one week requiring only
symptomatic relief.
 Antibiotics have no role.
 Chlorpheniramine and pheniramine can cause sedation and cognitive impairment,
therefore should be avoided for tasks requiring alertness and skill.
 Medicated nasal drops used for longer periods can cause rebound congestion and rhinitis
medicamentosa.
References
1. Acute Rhinosinusitis. In: Logan Turner's Disease of the Nose, Throat and Ear. 10th Edition, PP 34
FURUNCULOSIS OF NOSE (VESTIBULITS)
Furunculosis is acute infection of hair follicle withStaphylococcus aureus.
Salient features
Non -pharmacological treatment
 Local applicationof moist heat will enhance the localization of infection and promote
drainage.


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ENT Diseases
166
 Throat pain, difficulty in swallowing.
 Pyrexia, cervical lymphadenopathy.
 Inflamed tonsils with exudates
Pharmacological treatment
 Cap. amoxicillin 500mg 8hrly for 5-7 days (in children 25-50mg /kg/day in 3 divided
dose)  or Cap. amoxicillin 250/500mg plus clavulanic acid 125mg 8hr for 5-7days
 Tab ibuprofen 400-600mg 3 times in a day for 5 days (In children 10mg/kg/dose orTab
paracetamol 500 mg 6hrly for 2-3days then as and when required till pain and fever
subsides (in children 10mg/kg/dose 6-8hrly).
 Usually improvement in pain,tenderness and inflammation occur within 24-48hr after
imitation of treatment, patient should be monitored regularly. However, if there is flaring


