BackgroundDengue fever is an endemic illness in the tropics with early and post infectious complications affecting multiple systems. Though neurological sequelae including mononeuropathy, encephalopathy, transverse myelitis, polyradiculopathy, Guillain-Barre syndrome , optic neuropathy and oculomotor neuropathy have been reported in medical literature, the abducens nerve despite its notoriety in cranial neuropathies in a multitude of condition due to its long intracranial course had not been to date reported to manifest with lateral rectus paralysis following dengue.Case presentationA previously well 29 year old male with serologically confirmed dengue hemorrhagic fever developed symptomatic right lateral rectus palsy during the critical phase of the illness, which persisted into convalescence and post convalescence with proven deficit on Hess screen. Alternate etiologies were excluded by imaging, serology and electrophysiology.ConclusionsThe authors detail the first reported case of abducens nerve palsy complicating dengue fever in a previously healthy male from Sri Lanka. In a tropical country with endemic dengue infections, dengue related abducens neuropathy may be considered as a differential diagnosis in cases of acquired lateral rectus palsy after dengue fever.

We read with interest the article by Mumtaz et al. [1] on the role of oral N-acetylcysteine (NAC) in adults with nonacetaminophen-induced acute liver failure. We agree that their findings are of particular relevance to many developing countries, where liver transplantation is neither available nor affordable. There has been another recent study in which intravenous NAC has been shown to improve transplant-free survival in early-stage non-acetaminophen-induced acute liver failure in adults [2]. We report our initial experience in treating acute liver failure caused by dengue infection with NAC. Use of NAC in this situation has not been previously described.Sri Lanka is experiencing its worst-ever dengue epidemic yet, with more than 250,000 reported cases and more than 250 deaths, mainly adults, since January 2009. Severe hepatic and cardiac complications and a higher than usual mortality have been notable features of this epidemic. Mild-moderate elevations in serum aminotransferase levels are very common in dengue, but acute liver failure can also occur [3] and has a poor outcome, with case fatality rates of up to 50% in children [4]. There is little information on the management of dengue-associated acute liver failure. There are isolated reports of rapid improvement in the biochemical profile and encephalopathy with molecular adsorbent recirculating system [5]. Liver transplantation is difficult because of hemodynamic instability, bleeding manifestations, and organ dysfunction caused by the infection itself, and may not be a treatment option in most countries where dengue is prevalent.We retrospectively analyzed the outcome of eight consecutive adult patients (5 men and 3 women; age range, 28-64 years) presenting during the current epidemic with serologically confirmed dengue-associated acute liver failure. In addition to other supportive management [6,7], they received NAC 150 mg/kg loading dose by intravenous administration over 15 min followed by 12.5 mg/kg/h for 4 h and then 6.25 mg/kg/h for up to 72 h. Two patients had dengue hemorrhagic fever [6], six had dengue shock syndrome [6], seven had pleural effusions, and five had ascites. Five patients had early-stage pretreatment hepatic encephalopathy (coma grades I-II), and three had advanced encephalopathy (coma grades III-IV). Time from disease onset to appearance of encephalopathy was 5-8 days. Worst recorded pretreatment value ranges for the eight patients were as follows: platelet count = 6,000-30,000/mm 3 ; international normalized ratio = 1.6-3.2; serum bilirubin = 2.7-12.2 mg/dL; alanine aminotransferase = 4,070-19,800 IU/L; aspartate aminotransferase = 4,455-26,500 IU/L; serum albumin = 2.7-3.9 g/dL; serum globulin = 3.1-3.9 g/dL; and serum creatinine = 0.7-2.5 mg/dL. None had taken acetaminophen more than the prescribed therapeutic dose, used hepatotoxic drugs, or had a history of alcohol abuse. Serology was negative for hepatitis A, B, C, and E, leptospira, and rickettsiae. All patients underwent computerized tomography of the brain to exclude intr...

IntroductionSystemic lupus erythematosus is a disease which may initially present with varying symptoms, most commonly a photosensitive rash and arthritis. Protein losing enteropathy is a recognized but rare presenting manifestation. Diagnosing protein losing enteropathy in resource limited centres is challenging but possible through the exclusion of other possible causes of hypoalbunaemia.Case PresentationWe report a case of protein losing gastroenteropathy secondary to intestinal lymphangiectasia as the initial manifestation of systemic lupus erythematosus in a 57 year old Sri Lankan (South Asian) male patient. The diagnosis was made by the exclusion of other causes of hypoalbuminaemia as the gold standard investigations for protein losing enteropathy were not available at this centre.ConclusionsProtein losing enteropathy is a diagnosis of exclusion in resource limited centres in the world. Systemic lupus erythematosus should be considered in the differential diagnosis of protein losing enteropathy. Intestinal lymphangiectasia should also be recognized as a possible pathophysiological mechanism.

ObjectivesTo study the safety of low dose subcutaneous adrenaline given as prophylaxis against acute adverse reactions to anti-venom serum (AVS) in patients bitten by snakes. MethodsPatients admitted with snakebite envenoming who satisfied inclusion criteria were given 0.25 ml of 1:1000 adrenaline subcutaneously immediately before administration of AVS. They were observed for adverse effects, and pulse and blood pressure (BP) were monitored.Results 51 patients [35 males, mean age 34.8 years (SD 14)] were included in the study. Adverse reactions to AVS occurred in 15 (29.4%) patients. There was one death from suspected cerebral haemorrhage, and 3 (5.9%) patients developed small haematomas at the subcutaneous injection site. There were no significant changes in mean pulse or BP following administration of subcutaneous adrenaline.Conclusions Low dose subcutaneous adrenaline did not cause significant changes in pulse rate or BP. Although the death was unlikely to be directly related to subcutaneous adrenaline, we suggest further studies on the safety of this prophylactic treatment before its routine use.

BackgroundDengue is considered one of the most common mosquito borne illnesses in the world. Although its clinical course is usually uneventful, complications have rarely been known to arise. These include neurological manifestations such as neuropathies.Case presentationWe report a middle aged patient from urban Sri Lanka who developed diaphragmatic paralysis secondary to phrenic neuropathy a month after recovering from dengue fever. He was managed conservatively and made a full recovery subsequently.ConclusionIsolated phrenic nerve palsy causing diaphragmatic paralysis should be considered a recognized complication of Dengue fever. A patient usually gains full recovery with conservative management.