ABSTRACT
A case of venous air embolism occurring during liver resection is reported. Diagnosis was made early from the continuous recording of pulmonary artery pressure. The aetiology was neither surgical nor an obvious disconnection of a venous line. It was caused by a blockage of the blood filter, resulting in subambient pressure between the filter and a peristaltic pump, leading to aspiration of numerous small air bubbles. The clinical course after replacement of the defective material was uneventful, except for transient postoperative pulmonary oedema.
Subject(s)
Blood Transfusion/instrumentation , Embolism, Air/etiology , Hepatectomy , Adult , Blood Pressure Determination , Embolism, Air/diagnosis , Female , Hemorrhage/complications , Humans , Intraoperative Complications/diagnosis , Intraoperative Complications/etiology , Monitoring, Physiologic , Pulmonary ArteryABSTRACT
The acid-base disorders after hepatic vascular exclusion (HVE) were studied in 30 major liver resections. HVE included portal triad clamping and occlusion of the inferior vena cava below and above the liver, without venous shunt nor cooling. Clamping of the supra-coeliac abdominal aorta (AoC) was associated with HVE in 12 patients. HVE lasted 18 to 65 min (mean 37 min). Liver ischemia and splanchnic blood pooling resulted in metabolic acidosis and hyperlactatemia. In order to prevent his acidosis, prophylactic administration of NaHCO23 was used during the first 19 cases. This induced significant metabolic alkalosis during HVE and the early postoperative period; increasing experience made us reduce the amount of NaHCO3. After the release of the clamps, Paco2 increased 25% following HVE without AoC (p less than 0.001) and 53% following HVE with AoC (p less than 0.001). In an attempt to distinguish between the effects of the metabolic acidosis and the rise of Paco2 in the fall of pH which occurred after removal of the clamps, NAaHCO3 was deliberately not given in the last 11 patients. Acidosis appeared to be greater with AoC than without and mainly related to the rise of Paco2. A fall of Paco2 to its initial value was always followed by the return of pH to the normal range. This study demonstrated the human ability to correct spontaneously the acidosis which followed HVE. The need for NaHCO3 after HVE reflected a poor hemodynamic state after major liver resection rather than a metabolic consequence of hepatic ischaemia.
