BackgroundLaparoscopic cholecystectomy is one of the commonest surgical procedures carried out in the world today. Occasionally patients present with undiagnosed situs inversus and acute cholecystitis. We discuss one such case and outline how the diagnosis was made and the pitfalls encountered during surgery and how they were overcome.Case presentationA 32 year old female presented to our department with epigastric pain radiating through to the back. A diagnosis of acute cholecystitis in a patient with situs inversus totalis was made following clinical examination and radiological investigation. Laparoscopic cholecystectomy was subsequently performed and the patient made an uneventful recovery.ConclusionSitus inversus presenting with acute cholecystitis is very rare. The surgeon must appreciate that care should be taken to set up the operating theatre in the mirror image of the normal set-up for cholecystectomy, and that right handed surgeons must modify their technique to adapt to the mirror image anatomy.

A 42-year-old male presented with right-sided weakness, dysphasia and seizures while climbing the French Alps at an approximate altitude of 3,000 m. Imaging studies were consistent with superior sagittal sinus thrombosis with hemorrhage. Laboratory testing for thrombophilic states, 18 days after presentation at our hospital, showed a low protein C level (0.32 U/ml, normal 0.80–1.60 U/ml). A family member was also found to have protein C deficiency without a history of thrombosis. The patient gradually improved and was discharged on warfarin and valproic acid. This is the first reported case of cerebral venous thrombosis in a patient with congenital protein C deficiency who ascended to high altitude. We postulate that the ascent to high altitude represented an additional prothrombotic risk factor to the congenital protein C deficiency leading to cerebral thrombosis.

Recently reported cases of lupus complicated by a thrombotic thrombocytopenic purpura (TTP)-like syndrome suggest a survival benefit to early treatment with plasma exchange. The following is a report of the eighth such case in the last ten years. A 44-year-old lady known for lupus presented with the nephrotic syndrome and a renal biopsy was consistent with class 4G lupus nephritis. She was given high-dose steroids and cytotoxic therapy, but her induction therapy was complicated by the classic pentad of TTP. She was subsequently treated with another course of high-dose steroids, a different cytotoxic agent, and plasma exchange, with clinical resolution shortly thereafter. Similar to seven recently reported cases of microangiopathy in lupus, this lady's TTP-like syndrome improved dramatically after initiation of plasma exchange, despite not having a severely deficient ADAMTS13. This has implications on both current clinical practice and on the pathogenesis of TTP-like syndromes in lupus.

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Presence of active Crohn's disease along with an incidental Meckel's diverticulum or acute appendicitis raises controversies in their surgical management. We discuss the issues in managing patients with two or more of these co-existent pathologies.