Dengue hemorrhagic fever and severe thrombocytopenia in a patient on mandatory anticoagulation: balancing two life threatening conditions: a case report.

BACKGROUND: Managing a severe dengue infection is a challenge specially when complicated by other comorbidities. We report a patient with dengue haemorrhagic fever and spontaneous bleeding who required mandatory anticoagulation for a prosthetic mitral valve replacement. This is the first case report in published literature describing this therapeutic dilemma. CASE PRESENTATION: A fifty one year old Sri Lankan woman was diagnosed with dengue haemorrhagic fever with bleeding manifestations. During the critical phase of her illness, the platelet count dropped to 5,000/É¥l. She was also on warfarin 7 mg daily following a prosthetic mitral valve insertion. In managing the patient, the risk of bleeding had to be balanced against the risk of valve thrombosis without anticoagulation. Warfarin was withheld when the platelet count dropped to 100,000/É¥l and restarted when it recovered above 50,000/É¥l. The patient was off anticoagulation for 10 days. CONCLUSIONS: We managed this patient with close observation and continuous risk benefit assessments of management decisions. However, experience with one patient cannot be generalized to others. Therefore, it is essential that clinicians share their experiences in managing such difficult patients.

Hypokalemic paralysis associated with cystic disease of the kidney: case report.

BACKGROUND: Severe hypokalemia is known to cause muscle paralysis, and renal tubular acidosis is a recognized cause. Cystic disease of the kidney is associated with severe hypokalemia. CASE PRESENTATION: We report a 33-year-old male patient who presented with generalized limb weakness caused by severe hypokalemia due to renal tubular acidosis, who was found to have renal medullary cysts. CONCLUSION: The association of cystic renal disease with hypokalemia, and the possible pathophysiological basis of the development of renal cysts in patients with severe hypokalemia, are discussed.

Very-Long-Chain Acyl-Co-Enzyme A Dehydrogenase Deficiency Presenting as Rhabdomyolysis: First Case Report from Sri Lanka.

BACKGROUND: Rhabdomyolysis can be either inherited or acquired such as in metabolic myopathies. Very-long-chain acyl-CoA dehydrogenase deficiency is a rare fatty acid oxidation disorder which presents with different phenotypes, and the mild adult form can present as intermittent rhabdomyolysis. Here, we present the first adult case of very-long-chain acyl-CoA dehydrogenase deficiency presenting as rhabdomyolysis in a Sri Lankan patient. Case Presentation. A 36-year-old Sri Lankan man who was born to consanguineous parents presented with severe generalized muscle pain, stiffness, and dark-coloured urine for three days following prolonged low-intensity activity. Since fourteen years of age, he has had multiple similar episodes, where one episode was complicated with acute kidney injury. His eldest brother also suffered from the similar episode. Examination revealed only generalized muscle tenderness without any weakness. His creatine phosphokinase level was above 50,000 IU/L, and he had myoglobinuria. Molecular genetic tests confirmed the diagnosis of very-long-chain acyl-CoA dehydrogenase deficiency. Following a successful recovery devoid of complications, he remained asymptomatic with lifestyle adjustments. CONCLUSION: Very-long-chain acyl-CoA dehydrogenase deficiency is a rare inherited cause of metabolic myopathy that gives rise to intermittent rhabdomyolysis in adults. Prompt diagnosis is essential to prevent complications and prevent its recurrence.

Hypothyroidism causing paralytic ileus and acute kidney injury - case report.

We present a patient with severe hypothyroidism complicated by paralytic ileus and acute kidney injury. A 65 year old male patient, diagnosed with hypothyroidism one year ago was transferred to our unit in a state of drowsiness and confusion. He was severely hypothyroid and had paralytic ileus and impaired renal function at the time of transfer. Hypokalaemia was present, and was likely to have contributed to the paralytic ileus and this together with dehydration was likely to have contributed to renal injury. Nonetheless, hypothyroidism is very likely to have been the principal precipitant of both these complications, and both paralytic ileus and acute kidney injury improved with thyroxine replacement. Unfortunately, the patient died unexpectedly eight days after admission to the unit.Hypothyroidism may induce de novo acute kidney injury or it may exacerbate ongoing chronic kidney disease. This rare complication is assumed to be due to the hypodynamic circulatory state created by thyroid hormone deficiency. Paralytic ileus is an even rarer fatal manifestation of hypothyroidism and is thought to be due to an autonomic neuropathy affecting the intestines that is reversible with thyroxine replacement. To our knowledge, both these complications have not been observed in a single patient so far.It is important that clinicians are aware of these rare manifestations of hypothyroidism as in most occasions, thyroxine deficiency may be missed, and treatment can reverse the complications.

Complications and management of acute copper sulphate poisoning; a case discussion.

Copper sulphate ingestion (accidental or deliberate) is a rare form of poisoning usually limited to the Indian subcontinent. Though the rates are on the decline, it is essential that physicians are aware of its lethal complications and management strategies. The main complications of copper sulphate ingestion include intravascular haemolysis, methaemoglobinaemia, acute kidney injury and rhabdomyolysis. The lethal dose can be as small as 10 grams. We have explored the complications of acute copper sulphate poisoning with examples from two case presentations. We also recommend measures for prevention of such events.