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.

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.

BackgroundManaging 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 presentationA 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/ɥl. 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/ɥl and restarted when it recovered above 50,000/ɥl. The patient was off anticoagulation for 10 days.ConclusionsWe 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.

BackgroundSevere 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 presentationWe 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.ConclusionThe 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.

Dengue fever has a wide range of clinical manifestations from asymptomatic disease to complicated dengue haemorrhagic fever and dengue shock syndrome. Bleeding manifestations in dengue is well known but thrombotic events complicating dengue is uncommon. ST elevation myocardial infarction during dengue is rare and poses important management dilemma. At present, there is no consensus on how to manage this situation. We present two patients with dengue fever developing ST elevation myocardial infarction and our experience in the management. We suggest case-based management of acute coronary syndrome in dengue, guided by the degree of thrombocytopaenia and bleeding risk. Further studies are needed to include this into existing dengue management guidelines.