Severe poisoning with naproxen causing coagulopathy.

Non-steroidal anti-inflammatory drugs (NSAIDs) are well known for their most frequent side effects (digestive, renal and metabolic disorders) but are lesser known for other effects, such as coagulation disturbances. In this issue, we report the case of a 58-year-old woman who ingested 26 g of naproxen in a suicidal attempt and developed cardiovascular shock, hypocoagulability and thrombopenia. Her outcome was positive (extubation 3 days after admission [D3], correction of haemostatic disruptions on D5 and of thrombopenia on D6). Naproxen plasma concentration was at a toxic concentration of 1320 mg/L at 6 hours after drug ingestion. Only few cases of hypocoagulopathy are reported with the NSAIDs, and this is the first case that can be attributed to naproxen. A possible explanation of this phenomenon following naproxen ingestion is an inhibition of thromboxane A2, usually attributed to NSAIDs, combined with an inhibition of activation of downstream the cascade.

Zika virus infection.

A 21-year old woman from New-Caledonia had 40 ÌŠC fever with vomiting, arthralgia, myalgia, and measles-like rash. Etiological analyses showed primary infection with Zika virus. Because of severe clinical presentation, she was hospitalized in the intensive care unit of the Brest military Hospital. Zika virus is mainly transmitted by Aedes mosquitoes. If they settle in Metropolitan France, Zika virus might also spread there.

Self-induced drug intoxication in baclofen: of the calm hypotonic coma in the status epilepticus.

Baclofen is an agonist of peripheral and central B gamma-aminobutyric acid receptors, whose activation causes a myorelaxation and a powerfull depression of the central nervous system. Moreover, it has an action against addiction, in reducing craving. Commercialized since 1975 in France, to control muscle spasticity due to medullar affection or multiple sclerosis, it receives a temporary recommendation of use in march 2014, as a last-line adjuvant treatment in alcohol withdrawal. Beyond its therapeutic use, baclofen is involved in many self-induced intoxications. We report the case of a patient who develops, after a massive ingestion of baclofen (supposed dose ingested: 1 200 mg), a hypotonic and calm coma, requiring her admission in our intensive care unit, and then a status epilepticus.

[Prolonged curarisation following succinylcholine injection on butyrylcholinesterase deficiency and potentiated by a lithium treatment: a case report]. / Curarisation prolongée après injection de succinylcholine sur déficit congénital en butyrylcholinestérase et potentialisée par un traitement au lithium: à propos d'un cas.

Succinylcholine is a short-term curare which degradation depends on its quick hydrolysis by butyrylcholinesterase (or pseudocholinesterase). Thus, a butyrycholinesterase deficiency, congenital or acquired, is a cause of a prolonged neuromuscular block. From an autosomal recessive inheritance, genetic deficiency remains the first etiology. The most frequently discussed variant is the atypical variant which caused a 2 hours prolonged curarisation after administration of succinylcholine. We report a patient who had a prolonged curarisation after succinylcholine's injection, due to a congenital butyrylcholinestérase deficiency and contributed by a lithium treatment. Extubation was only possible 7 hours after administration of curare.