Extracorporeal membrane oxygenation in the successful treatment of traumatic adult respiratory distress syndrome: case report and review.

We present the case of a 25-year-old, 28-week pregnant woman with two gunshot wounds to the chest. Extracorporeal membrane oxygenation (ECMO) was begun within 12 hours, despite poor results in prior studies and the need for anticoagulation postoperatively, since oxygenation was rapidly deteriorating despite aggressive treatment. The patient ultimately made a full recovery.

Cardiovascular responses to acute loading with nifedipine alone and nifedipine plus propranolol during inhalation anesthesia in monkeys.

The cardiovascular effects of the administration of nifedipine and nifedipine combined with propranolol were examined in 15 monkeys during 0.75 and 1.25 MAC of anesthesia with isoflurane, enflurane, or halothane. Hemodynamic variables measured included heart rate (HR), mean arterial pressure (MAP), left ventricular end-diastolic pressure (LVEDP), maximum rate of increase of the Left ventricular pressure (max LV dP/dt), and thermodilution cardiac output (CO). The infusion of nifedipine at a rate adequate to produce therapeutic blood levels during 0.75 MAC with each anesthetic decreased MAP and SVR, but had no effect on cardiac index (CI), max LV dP/dt, or HR. Increasing the anesthetic concentration from 0.75 to 1.25 MAC during nifedipine administration decreased HR and MAP in all groups and decreased CI with halothane and enflurane, but not with isoflurane. Addition of propranolol by infusion in amounts adequate to produce 75% beta-adrenergic blockade caused a further depression of CI, max LV dP/dt, HR, and MAP. However, the hemodynamic depression was significantly greater with halothane and enflurane than with isoflurane. Intravenous administration of calcium chloride (10 mg/kg) after calcium channel and beta-adrenergic blockade only partially reversed the hemodynamic depression that occurred with all three anesthetics. It was concluded that acute loading with nifedipine with and without propranolol exerts a greater cardiovascular depressant effect during enflurane or halothane anesthesia than during isoflurane anesthesia. The myocardial depressant effects of nifedipine and propranolol myocardial depressant effects of nifedipine and propranolol may be synergistic with the depressant effects of potent inhalation anesthetics.

Glucose metabolism during liver transplantation in dogs.

Arterial and hepatic venous blood levels of glucose were studied in 12 dogs during orthotopic liver transplantation performed under ketamine anesthesia without exogenous glucose administration. During the early part of surgery, arterial blood glucose levels were stable: 161 +/- 12 mg/dl (mean +/- SEM) after laparotomy and 183 +/- 16 mg/dl 5 min before the anhepatic stage. During the anhepatic stage, arterial blood glucose levels decreased progressively to 135 +/- 9 and 88 +/- 8 mg/dl, 5 min in the anhepatic stage and 5 min before reperfusion of the graft liver, respectively (P less than 0.05). Reperfusion of the graft liver resulted in an increase in arterial glucose levels to 206 +/- 17 and 240 +/- 24 mg/dl, 5 and 30 min after reperfusion, respectively (P less than 0.05). Hepatic venous blood glucose levels increased after reperfusion (405 +/- 37 and 346 +/- 41 mg/dl, 5 and 30 min after reperfusion, respectively) and were significantly higher than in arterial blood (P less than 0.05). Arterial plasma insulin, measured in five animals, did not change significantly during the procedure, whereas plasma glucagon levels, stable during the preanhepatic and anhepatic stages, increased steadily after reperfusion of the graft liver, from 66.1 +/- 14.2 to 108.4 +/- 38.1 pg/ml (P less than 0.05). This study shows that in dogs with ketamine anesthesia mild hypoglycemia occurs during the anhepatic stage of liver transplantation without exogenous glucose administration followed by hyperglycemia on reperfusion of the graft liver, possibly secondary to the release of glucose from the donor liver.

Comparison of the effects of succinylcholine and atracurium on intracranial pressure in monkeys with intracranial hypertension.

The effects of succinylcholine (1.5 mg X kg-1 IV) administered five minutes after a defasciculating dose of curare (0.05 mg X kg-1 IV), were compared with the effects of atracurium (0.5 mg X kg-1 IV) on intracranial pressure (ICP) in 13 cynomolgus monkeys with intracranial hypertension (ICP approximately 25 mmHg). Neither succinylcholine nor atracurium increased ICP during general anaesthesia with 60 per cent N2O/O2, 0.5-1 per cent halothane. During a rapid sequence induction and intubation with thiopentone 5 mg X kg-1 IV, ICP increased equally with intubation following both atracurium (25 +/- 1 to 32 +/- 2 mmHg) and succinylcholine (25 +/- 1 to 31 +/- 2 mmHg) (p less than 0.05). Intubation was also associated with significant increases in PaCO2, CVP and MAP. We conclude that in this primate model of intracranial hypertension, neither atracurium nor succinylcholine (when given following a defasciculating dose of curare) elevates ICP. In terms of the elevation of ICP associated with intubation, atracurium was found to offer no advantage over succinylcholine.

Enflurane-induced grand mal seizures during otic microsurgery.

Abnormal electroencephalographic seizure-like activity and myoclonic movements have been recognized during enflurane anesthesia. This is most commonly seen in the presence of respiratory alkalosis and high concentrations of enflurane. Immediate and delayed postoperative generalized tonic-clonic convulsions have also been reported after enflurane anesthesia. Experimental studies have shown that auditory stimuli could facilitate seizure activity during deep enflurane anesthesia. Here we report a case of intraoperative generalized tonic-clonic convulsion during low concentrations of enflurane without evidence of hyperventilation and the presence of auditory stimulation.