A comparison of changes in venous lactate and haematocrit during fluid resuscitation of dengue haemorrhagic fever.

BACKGROUND: Judicious fluid resuscitation and stringent monitoring of clinical parameters improve the outcome of dengue haemorrhagic fever (DHF). The usefulness of serum lactate to monitor adequate fluid therapy has not been adequately explored. METHODS: An observational study was conducted in Sri Lanka, recruiting 162 DHF patients within 12 h of diagnosis of the critical phase. Venous lactate level was measured at each time of performing haematocrit (HCT), using a prevalidated handheld lactate analyser. RESULTS: The median venous lactate level was 1.3 (range 0.3-6) mmol/L in the study population and 154 (95.2%) patients had median lactate levels of <2 mmol/L. The HCT values in the study participants ranged from 28 to 62, with a median value of 43. There was no statistically significant correlation between the lactate and HCT values obtained at the same time. A significant reduction in venous lactate was not observed following the administration of fluid boluses. The expected reduction in HCT was seen following the administration of dextran and crystalloid/dextran combination. The maximum recorded lactate level positively correlated with the duration of hospital stay. CONCLUSIONS: This study concludes that venous lactate is not an appropriate parameter with which to monitor the response to fluid therapy in uncomplicated DHF.

Cerebral Venous Sinus Thrombosis and Hydrocephalus in a Vegan Secondary to Acquired Hyperhomocystinaemia.

Cerebral venous sinus thrombosis associated with acute hydrocephalus and periventricular leukoencephalopathy is a challenging combination, in a critically ill with deteriorating neurology. We report a case of a young man with acute onset neuropsychiatric manifestations, admitted to the intensive care unit. He was found to have widespread cerebral venous sinus thrombosis, hyperintensities in basal ganglia, and acute hydrocephalus in magnetic resonance imaging, necessitating cerebrospinal fluid diversion, by way of an external ventricular drain and therapeutic anticoagulation. He had otherwise normal routine biochemistry, except for macrocytosis, which prompted us to suspect acquired hyperhomocysteinemia secondary to cobalamin and folate deficiency, in the background of him being a vegan. Replacement of vitamin B12, folic acid, pyridoxine along with anticoagulation and control of intracranial pressure with external ventricular drain lead to dramatic improvement of his neurology. Therefore, high index of suspicion is crucial for a better outcome in otherwise irreversible neurological damage in acquired hyperhomocystinaemia.

Cardiogenic Shock due to Kounis Syndrome following Cobra Bite.

Kounis syndrome is associated with mast cell activation resulting in acute coronary syndrome secondary to an allergic insult. Various drugs such as antibiotics, analgesics, and environmental exposures such as bee, wasp sting, and poison ivy are known to induce Kounis syndrome. A 68-year-old man admitted with a cobra bite on both hands to emergency care unit and sustained cardiorespiratory arrest. Electrocardiogram, taken 6 hours after the cardiac arrest, showed ST elevations in leads V2 to V5 suggestive of anterior ST elevation myocardial Infarction (STEMI). Serum Troponin was 10 ng/ml (control= <0.5). Serum IgE levels were significantly high (19155IU/ml, baseline 100). 2-Dimensional echocardiogram showed anterior and apical-septal hypokinesia with left ventricular ejection fraction of 30-35%. Coronary angiogram was normal. He remained hypotensive requiring inotropic and vasopressor support during ICU stay. This was a case of Kounis syndrome leading to cardiogenic shock secondary to Cobra (naja naja) bite. This is the only reported case of cobra bite causing Kounis syndrome and cardiogenic shock. Identification of the cause of myocardial infarction in snake envenomation is useful in the management as some of the drugs like adrenaline, morphine, and beta blockers may worsen the clinical syndrome if it is due to Kounis syndrome.

Posterior Reversible Encephalopathy in a Patient with Severe Leptospirosis Complicated with Pulmonary Haemorrhage, Myocarditis, and Acute Kidney Injury.

Severe leptospirosis (Weil's disease) can give rise to multiorgan failure such as acute renal failure, liver dysfunction, coagulopathy, acute respiratory distress syndrome, pulmonary haemorrhage, and myocarditis. Leptospirosis is a biphasic disease characterised by leptospiraemic phase and immunological phase. Although neurological manifestations are rare in leptospirosis, aseptic meningitis, myeloradiculopathy, transverse myelitis, and cerebellar syndrome are well recognised. We report a rare case of posterior reversible encephalopathy syndrome (PRES) in a patient with severe leptospirosis during recovery phase of the illness.