Effect of a low-dose ketamine regimen on pain, mood, cognitive function and memory after major gynaecological surgery: a randomized, double-blind, placebo-controlled trial.

BACKGROUND AND OBJECTIVE: Major gynaecological abdominal surgery is associated with moderate to severe postoperative pain, hyperalgesia and the need for multimodal analgesia to reduce high morphine consumption. A low-dose ketamine regimen appears to prevent postoperative hyperalgesia. We examined the potential beneficial effect of ketamine on postoperative pain management and cognitive function. METHODS: Ninety patients were included in this double-blind, randomized, placebo-controlled study to test the efficacy and adverse effects of ketamine (as an intraoperative bolus of 0.15 mg kg-1, followed postoperatively by ketamine 0.5 mg per morphine 1 mg in a patient-controlled analgesia device). All patients received additionally ketoprofen. The main end-point was morphine consumption over the first 24 h. Secondary efficacy and safety end-points were morphine consumption during the titration period and during the patient-controlled analgesia period (48 h), the number of morphine-related adverse effects and the results of psychometric tests. RESULTS: Ketamine, in combination with morphine and ketoprofen, did not improve postoperative pain scales and did not reduce morphine consumption and the incidence of morphine-related adverse effects. Ketamine did not modify mood, cognitive and memory functioning. CONCLUSION: Adding a low dose of ketamine to an efficacious multimodal analgesic regimen did not improve analgesia after gynaecological surgery. Although this combination appears to be safe, the lack of benefit suggests that a low dose of ketamine should not be used for routine care.

[Non cardiac surgery in patient with coronary stenting: think sirolimus now!]. / Chirurgie générale et endoprothèse coronaire: pensez au sirolimus!

We describe a severe preoperative cardiogenic shock in a patient scheduled for a breast surgery. The cardiogenic shock was in relation with thrombosis of two sirolimus-eluting stents received 3 months ago. A percutaneous transluminal coronary angioplasty was successfully performed. The patient recovered well after a 1-day treatment including intraaortic balloon counter pulsation and dobutamine infusion. We discuss about the ideal timing to plan surgery and how to manage the shift of antiplatelet agents.

Adjunctive analgesia with intravenous propacetamol does not reduce morphine-related adverse effects.

BACKGROUND: Propacetamol is widely used in the management of postoperative pain. It decreases morphine requirements but its effect on the incidence of morphine-related adverse effects remains unknown. METHODS: Patients (550) were randomly assigned to receive propacetamol or a placebo over the first 24 h after operation in a blinded study. Intravenous morphine titration was performed, after which morphine was administered s.c. every 4 h according to their pain score. Pain was assessed using a visual analogue scale (VAS). The primary end-point was the incidence of morphine-related adverse effects. The main secondary end-points were morphine requirements and VAS score. RESULTS: After morphine titration, the VAS score and the number of patients with pain relief did not differ between groups. Morphine requirements were decreased in the propacetamol group (21 vs 14.5 mg, P<0.001) but the incidence of morphine-related adverse effects did not differ between groups (42 vs 46%, not significant). In patients with moderate pain (n=395), morphine requirements decreased by 37% (P<0.001) and the percentage of patients requiring no morphine was greater (21 vs 8%, P=0.002) in the propacetamol group. In patients with severe pain (n=155), morphine requirements decreased by 18% (P=0.04) in the propacetamol group and the number of patients who did not require morphine (3 vs 8%) did not differ significantly. CONCLUSIONS: Although propacetamol induced a small morphine-sparing effect, it did not change the incidence of morphine-related adverse effects in the postoperative period. Moreover, no benefit could be demonstrated in patients with severe postoperative pain.

Use of nitroglycerine to produce controlled decreases in mean arterial pressure to less than 50 mm Hg.

The cardiovascular effects of nitroglycerine (TNG) were studied in 30 patients requiring controlled hypotension for intracranial aneurysm surgery. In patients "resistant" to TNG (n = 9), sodium nitroprusside (SNP) was used to supplement the TNG. With TNG alone at a total dose of 31 mg and a mean hypotension duration of 28 min, mean arterial pressure (MAP) decreased by 43%, from 78.3 to 44.4 mm Hg as a result of decreases in cardiac index (Cl) (18%) and systemic vascular resistances (SVR) (21%). Simultaneously, a moderate increase in (Cao2 - Cvo2) (21%), and a significant increase in plasma renin activity (90%) were observed. In patients "sensitive" to TNG, the MAP decreased by 54%, Cl by 27% and SVR by 35%; HR remained stable. In patients "resistant" to TNG, the decreases in Cl and SVR were less marked: 2% and 22% respectively; the observed increase in HR was 12%. When non-toxic doses of SNP were used (less than 2 micrograms kg-1 min-1), hypotension was caused by decreased SVR (31%) and increased Cl (8%). TNG alone can be used to produce controlled decreases in MAP to around 50 mm Hg, and in patients "resistant" to TNG, SNP can be added to increase the hypotensive effect.

Prediction of cerebral vasospasm value of fibrinogen degradation products (FDP) in the cerebro-spinal fluid (CSF) for prediction of vasospasm following subarachnoid haemorrhage due to a ruptured aneurysm.

In a new treatment regimen with antifibrinolytic drugs in patients with aneurysmal subarachnoid haemorrhages, we have systematically controlled the level of fibrinogen degradation products (FDP) in the cerebrospinal fluid (CSF). The frequency of severe vasospasm with clinical ischaemia has been compared with the patient's initial level of FDP. Fifty patients have been included in this study. (All in Hunt and Hess's grades I or II on their arrival.) Patients with a secondary deterioration unrelated to vasospasm were excluded. The FDP levels were measured in the first three days following the bleeding and we were informed of them at the end of the study. The diagnosis of severe vasospasm was confirmed by arteriography and computed tomography (CT) and it was named "severe" when accompanied with signs of clinical ischaemia. Twenty patients developed a severe vasospasm with clinical ischaemia. In these patients, the mean value of the initial FDP level was between 80 and 320 mcg/ml compared with 20 to 80 mcg/ml for those who had not developed clinical ischaemia (p = 0.0009). Furthermore, two different groups may be discriminated by their initial FDP level: FDP greater than 80 mcg/ml; n = 23, 65% severe vasospasm; FDP less than 80 mcg/ml; n = 27.8% no severe vasospasm (p less than 0.001). These results do not imply a direct role of FDP in pathophysiological mechanisms of vasospasm, but they suggest a relationship between the clot lysis and the appearance of vasospasm with clinical ischaemia. To our knowledge this is the first time that such a predictive role can be attributed to the initial FDP level in the prognosis of vasospasm.