Gitelman syndrome is a rare autosomal recessive inherited disorder caused by inactivating mutations in the gene for the thiazide-sensitive sodium-chloride cotransporter in the distal renal tubule. The resulting renal potassium and magnesium wasting and decreased calcium excretion are similar to that seen with the use of thiazide diuretics. Treatment is based on potassium and magnesium supplementation, usually combined with spironolactone or a nonsteroidal anti-inflammatory drug [1]. Although often asymptomatic, cramps and muscle weakness can occur and this may affect delivery.A 24-year-old woman with Gitelman syndrome became symptomatic in the second trimester of her first pregnancy when serum potassium and magnesium levels dropped; intravenous supplementation was given (Fig. 1). Assessment in week 38 of pregnancy revealed oligohydramnios, partial placenta previa, and intrauterine growth restriction. A healthy female neonate weighing 3970 g was delivered at 38 weeks by Figure 1 Transthoracic echocardiography in the apical 4-chamber view demonstrating pericardial effusion with clot (arrow). Abbreviations: RV, right ventricle; LV, left ventricle.
Female, 3 month old Yorkshire pigs (n=9, weight ~30kg) were sedated with an intra muscular injection of ketamine (Alfasan, Woerden, Netherlands) and midazolam (Actavis, Hafnarfjordur, Iceland). Throughout the procedure, the pigs were anesthetized using ketamine, midazolam, and sufentanil (Janssen-Cilag, Tilburg, Netherlands). After induction of anesthesia, tracheotomy was performed for intubation and mechanical ventilation. Midline laparotomy was performed, after which the hepatoduodenal ligament was dissected to identify the hepatic artery and portal vein. Before retrieval of the liver, the hepatic artery, portal vein and hepatic veins were clamped for 15 to 45 minutes using vascular type clamps, resulting in a total exclusion of blood flow through the liver, to induce warm ischemic liver injury, mimicking donor warm ischemia in DCD liver donors. After retrieval, the livers were cannulated at the portal vein and hepatic artery, cooled and flushed with 1L of ice-cold preservation fluid (Belzer
Heat stroke is a life-threatening condition characterised by hyperthermia leading to multiple organ dysfunction. Acute liver failure is a rare and potentially fatal consequence of heat stroke. Management of heat stroke is mainly supportive but liver transplantation can be considered as the treatment of acute liver failure in heat stroke. However, literature on liver transplantation as a treatment for acute liver failure in heat stroke is scarce. Until now, no cases of liver transplantation for acute liver failure in non-exertional heat stroke have been reported. Here, we present the first case report of a successful liver transplantation in a patient with acute liver failure caused by non-exertional heat stroke after a sauna visit.
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