Mandeep Walia

Current perspectives of enteric fever: a hospital-based study from India

Abstract The last two decades have seen a change in the pattern of enteric fever with the emergence of multidrug-resistant strains (MDRS), particularly strains resistant to nalidixic acid. Aim: The aim of the study was to undertake a retrospective analysis of blood culture-confirmed cases of enteric fever diagnosed at Safdarjang Hospital, New Delhi, India from January 2001 to December 2003. Methods: The epidemiological details, clinical features, treatment outcome and antimicrobial resistance patterns were studied. Results: Of 377 blood culture-positive cases, 80.6% were Salmonella typhi and 19.4% Salmonella paratyphi A; 21.7% were children aged under 5 years and 6.1% were under 2 years. A significant decline in MDRS was observed, from 21.9% in 2001 to 12.4% in 2003 (p=0.04). There was a significant increase in nalidixic acid-resistant Salmonella (NARS) from 56.9% in 2001 to 88.9% in 2003 (p=0.0001). Complete resistance to ciprofloxacin (MIC>4 μg/ml) was detected in only two isolates, both Salmonella paratyphi A. Minimal inhibitory concentrations (MICs) of ciprofloxacin for NARS were increased (0.125–0.5 μg/ml) but were within National Committee for Clinical Laboratory Standards susceptibility ranges. NARS had a significantly longer fever defervescence time (7.7 vs 4.7 days, p<0.001) and hospital stay (12.1 vs 8.2 days, p<0.001), and higher rates of complications (55.5% vs 24.0%, p=0.014) and mortality than nalidixic acid-sensitive Salmonella (NASS). The rate of isolation of MDRS was higher in NARS than NASS (18.8% vs 7.3%, p=0.013). Conclusion: The high rate of occurrence of enteric fever in children <5 years and also of infections caused by Salmonella paratyphi A in India calls for critical re-assessment of vaccination strategy. Nalidixic acid resistance and rising MICs of fluoroquinolones in Salmonella spp pose a new global threat requiring debate on the optimum treatment of enteric fever.

Montelukast in pediatric asthma management

Leukotriene modifiers (receptor antagonist and biosynthesis inhibitor) represent the first mediator specific therapeutic option for asthma. Montelukast, a leukotriene receptor antagonist is the only such agent approved for use in pediatric patients. Montelukast modifies action of leukotrienes, which are the most potent bronchoconstrictors, by blocking Cysteinyl leukotriene receptors. Systemic drug like mountelukast can reach lower airways and improves the peripheral functions which play a crucial role in the evolution of asthma. Review of existing literature showed that montelukast compared to placebo has proven clinical efficacy in better control of day time asthma symptoms, percentage of symptom free days, need for rescue drugs and improvement in FEV1. Studies also demonstrated improvement in airway inflammation as indicated by reduction in fractional exhaled nitric oxide, a marker of inflammation. Studies comparing low dose inhaled corticosteroids (ICS) with montelukast are limited in children and conclude that it is not superior to ICS. For moderate to severe persistent asthma, montelukast has been compared with long acting beta agonists (LABA) as an add-on therapy to ICS, montelukast was less efficacious and less cost-effective. It has beneficial effects in exercise induced asthma and aspirin-sensitive asthma. Montelukast has onset of action within one hour. Patient satisfaction and compliance was better with montelukast than inhaled anti-inflammatory agents due to oral, once a day administration. The recommended doses of montelukast in asthma arechildren 1–5 years: 4 mg chewable tablet, children 6–14 years: 5mg chewable tablet, adults: 10 mg tablet; administered once daily. The drug is well tolerated. Based on the presently available data montelukast may be an alternative treatment for mild persistent asthma as monotherapy where ICS cannot be administered. It is also an alternative to LABA as an add-on therapy to ICS for moderate to severe persistent asthma. The other indications for use of montelukast include: allergic rhinitis, exercise induced bronchoconstriction and aspirin-induced asthma.

Congenital Langerhans cell histiocytosis: the self-healing variety.

Congenital self-healing Langerhans cell histiocytosis (CSHLCH) is a rare variant of Langerhans cell histiocytosis, presenting at birth or in the neonatal period with cutaneous lesions that involute spontaneously. Affected infants are otherwise well with no systemic illness. A case of CSHLCH, probably the first case report from India, is described. The patient presented on the third day of life with multiple papulonodular lesions over the body, with no systemic involvement. The lesions spontaneously regressed by 6 months of age, with no evidence of relapse at 1 year of age. Although CSHLCH is a benign and self-limited condition, long-term follow-up for evidence of relapse is emphasized.

Rickets: A cause of delayed walking in toddlers

ObjectiveChildren with complaints of not able to walk were investigated for rickets by appropriate history, clinical examination, serum biochemistry and radiology.MethodsChildren more than 1 yr were included. Each child was evaluated keeping in mind the possible causes of delayed walking. Also each child was thoroughly examined and diagnosed by combination of clinical, radiological, biochemical findings and response to treatment.ResultsOut of forty-two non-walkers during the study period, 25 patients turned out to be affected by nutritional rickets (60%). On follow-up at 3 weeks of treatment, all 25 patients (100%) showed radiological and biochemical response. Five patients were lost to follow-up after 3 weeks of treatment. Seventeen patients started walking within 3 months of treatment. Two patients did not start walking even after complete biochemical and radiological resolution. Radiological resolution, with limiting factor being the healing of lower end of ulna, averaged 5 months.ConclusionThe study reveals that majority of ricketic non-walkers start walking within 2 to 5 months of appropriate treatment.

Swyer-James-Macleod syndrome in a 10-year-old boy misdiagnosed as asthma

The boy was admitted with complaints of frequent cough, whitish expectoration, fever and dyspnea since 2 years of age. Since the last 5 years his dyspnea had significantly worsened during exertion. There was no personal or family history of asthma. He was diagnosed with asthma elsewhere and was variably treated for asthma without much relief to his symptoms, patient was born at term at home. At three days of age, he was admitted for ten days at a neonatal intensive care unit for pneumonia. There was no history suggestive of foreign body aspiration. He did not report recurrent infections involving other systems, coughing with food or change of body posture. His weight was 19.7Kg and height 130 cm and vital signs were within normal limits. ABG at room air showed PaO2 74mmHg, PaCO2 38mmHg, pH 7.38 and SpO2 96%. Chest examination revealed flattening of left side with reduced movements on respiration. Coarse crackles were auscultated in left infrascapular area.

Potassium Depletion Myopathy Following Acute Gastroenteritis

To the Editor: Severe hypokalemia following acute diarrhea can cause persistent muscle weakness and raised muscle enzymes. We report a case of hypokalemic myopathy following an episode of acute gastroenteritis. A 2-y-old girl was referred to us for non-improvement of muscle-weakness following an acute episode of waterydiarrhea. While recovering from diarrhea, parents noticed that child was not able to bear weight or stand properly; not able to feed herself; and also developed head drop. The musclepower was grade II/V in lower-limbs and III/V in upperlimbs with diminished deep tendon jerks (DTR’s). Serum biochemistry showed sodium 159 meq/L, potassium 2.3 meq/L, calcium 8.8 mg %, phosphorus 3.9 mg % and alkaline phosphatase (ALP) 134U/L. Electrocardiogram showed depressed T-waves with normal rhythm suggestive of hypokalemia. Her muscle enzymes were significantly elevated; serum creatinine phosphokinase (CPK) 87,534U/L and lactate dehydrogenase (LDH) 2153 U/L. Child was managed for hypokalemia and her subsequent potassium records gradually improved and normalized. Because of persistent muscle weakness and significantly elevated muscle enzymes; diagnosis of hypokalemic myopathy was made. Child was discharged after a week of admission, while her muscle weakness was improving. At 3-wk follow-up, there was no residual weakness and serum potassium (3.8 mEq/L) and muscle enzymes (CPK 203 U/L) were normal. Severe hypokalemiamay lead tomore severemuscle injury and can have prolonged muscular weakness [1]. Possible explanations for persistent weakness are muscle injury, muscle necrosis and myopathy; suggested by significantly elevated muscle enzyme [2]. Literature review shows many reports of patients with severe hypokalemia and persistent muscle weakness [3–5]. Muscle biopsy may show muscle necrosis and large doses of potassium can reverse clinical signs and muscle enzymes to normal range [1]. Although, muscle biopsy was not done in our case, but presence of severe hypokalemia, elevated muscle enzymes, gradual reversal of muscle weakness after potassium correction lead us to conclude that hypokalemia was responsible for proximal myopathy. It’s more commonly reported with chronic diseases, but can occur even after an episode of acute gastroenteritis as happened in our case. The onset of weakens is usually not abrupt and large doses of potassium are required to reverse the symptoms in such cases. This reversible illness can be treated, if correct diagnosis is made promptly.