[Pathophysiology of post-operative cognitive dysfunction: current hypotheses]. / Physiopathologie de la dysfonction cognitive postopératoire du sujet âgé: hypothèses actuelles.

Post-operative cognitive dysfunction (POCD) has been reported after a variety of surgical procedures. POCD is associated with a decline in performance of activities of daily living of elderly patients and can cause substantial damage to family and/or to social support systems. The incidence of POCD in the first week after surgery is 23% in patients between 60 and 69 years of age and 29% in patients older than 70. Cognitive dysfunction was still present in 14% of patients over 70 at three month after surgery. The risk of POCD increases with age, and the type of surgery is also important since there is very low incidence of POCD after minor surgery. For many years, it has been known that general anaesthesia is associated with persistent changes in gene expression in the brain for at least 72 hours. These observed modifications suggest an interesting hypothesis to explain the side effects of anaesthetic agents on cognitive dysfunction, particularly in the elderly. The inflammatory response to surgery is consistent with the hypothesis that inflammation contributes to cognitive decline in the elderly. Most of the drugs administered during anaesthesia interact with the cerebral cholinergic system, which seems to be impaired with ageing. One can hypothesize that this cholinergic dysfunction is a potent factor in the pathogenesis of POCD. These findings have implications for the information provided before obtaining consent from elderly patients prior to surgery; a careful evaluation of mental status is mandatory for all elderly patients undergoing general anaesthesia. Perioperative physicians should be familiar with the prevention, diagnosis, and management of postoperative cognitive dysfunction.

[Implication of dexamethasone adjunctive therapy after the onset of cerebral vasculitis in Streptococcus pneumoniae meningitis]. / Implication du traitement adjuvant par dexaméthasone dans la survenue d'une artérite septique cérébrale au cours d'une méningite à Streptococcus pneumoniae.

Few adverse effects have been reported with adjunctive dexamethasone treatment in pneumococcal meningitis. Nevertheless, we report a case of cerebral vasculitis. A 49-year-old man was admitted for fever and altered mental status. Lumbar puncture revealed a high inflammatory response and Streptococcus pneumoniae was identified by culture. Antibacterial therapy and adjunctive dexamethasone treatment were initiated as recommended. The immediate outcome was favorable but due to the onset of focal cerebral abnormalities, a CT scan was performed on the ninth day showing cerebral vasculitis. The patient died on the thirteenth day despite antibacterial therapy and resuscitation. In our case, a secondary neurological worsening appeared when adjunctive dexamethasone treatment was stopped suggesting a rebound effect. Observation of similar cases may lead to modifying adjunctive dexamethasone treatment protocol in bacterial meningitis.

[Use of ECMO as a salvage therapy for refractory hypoxia secondary to a Lemierre's syndrome]. / Utilisation de l'ECMO comme technique de sauvetage d'une hypoxémie réfractaire compliquant un syndrome de Lemierre.

We reported the case of a young adult with a Lemierre syndrome, which was complicated by septic shock and ARDS. Because of rapid onset of a life-threatening hypoxemia (PaO(2)/FiO(2)=60) in the course of the ARDS despite mechanical ventilation, ECMO was started with jugular and femoral cannulas, as rescue therapy. Good control of hypoxemia was obtained and ECMO was set up for six days. No significant complication was observed. The course was nevertheless complicated by acute renal failure and a pleural fistula that necessitated separate-lung ventilation during 24 hours. After 48 days left in the ICU, the patient was sent to a rehabilitation unit.