Brain death in a septic patient: possible relationship with posterior reversible encephalopathy syndrome?

A 41-year-old man with a previous kidney transplant was referred for arterial hypertension and acute renal failure. Initial neurological examination was normal. Laboratory data showed a high serum cyclosporine A concentration. A few hours later, he developed generalised tonic-clonic seizures. The brain computed tomogram was not remarkable, but Glasgow Coma Scale score remained at 8. Mechanical ventilation was required for rapidly progressive hypoxaemia related to Staphylococcus aureus pneumonia and septicaemia. Noradrenaline infusion was needed for only nine hours, with no major drop in mean arterial blood pressure. On day three his Glasgow Coma Scale score was 3/15, with fixed dilated pupils. The brain computed tomogram revealed bilateral hypodense lesions in the posterior areas together with cerebral oedema and the patient was subsequently declared brain dead. We discuss the possibility of a posterior reversible encephalopathy syndrome, likely triggered by a gram-positive septicaemia in addition to other risk factors.

[Acute methanol intoxication: physiopathology, prognosis and treatment]. / Intoxication aiguë par le méthanol: physiopathologie, pronostic et traitement.

Acute methanol poisoning is still complicated by a poor vital or visual prognosis. The pathophysiology of methanol poisoning is not yet fully understood. It appears that the major toxic effects are related to the main metabolite of methanol, formic acid. The central nervous system and the visual pathway are the main targets of methanol poisoning. When irreversible brain lesions occur, the diagnosis of brain death can be made. Other organs, like the pancreas or the kidney, may also be damaged according to the severity of metabolic acidosis; however, the toxic manifestations are in this case mostly reversible. The historical treatment of methanol poisoning relies on ethanol administration. However, ethanol therapy has numerous side effects and a new antidote, fomepizole, that was previously approved for the treatment of ethylene glycol poisoning, appears effective, safe and easy to use. Hemodialysis remains effective for the removal of both methanol and formic acid.

Hypokalaemia related to acute chloroquine ingestion.

Large doses of chloroquine can cause poisoning. Our aim was to determine the possible relation between the plasma potassium concentration on admission with the severity of acute chloroquine poisoning and to assess the mechanism of chloroquine-induced hypokalaemia. We conducted a retrospective study of 191 consecutive cases. The main data included the occurrence of vomiting before admission, plasma, and urinary potassium concentration at admission, whole blood chloroquine concentration on admission, haemodynamic parameters and ECG, administration of catecholamines and outcome. Mean blood chloroquine level was 20.1 mumol/L (SD 14.3) (therapeutic level < or = 6 mumol/L). Mean plasma potassium concentration was 3.0 mmol/L (0.8) and was lower in the subjects who died than in those who survived (p = 0.0003). Plasma potassium varied directly with the systolic blood pressure and inversely with the QRS and QT. Plasma potassium varied inversely with the blood chloroquine (p = 0.0001; tau = -0.42). Acute chloroquine intoxication is responsible for a hypokalaemia which correlates with the gravity of the intoxication and may be due to a transport-dependent mechanism. Plasma potassium concentrations should be carefully observed, particularly among patients who also receive catecholamine infusions. We should keep in mind, however, that overzealous repletion invokes the risk of subsequent hyperkalaemia and thus should be avoided.