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Two chronically ill patients with limited nutritional intake during several weeks developed prolonged lactic acidosis. As no other causes of hyperlactaemia could be identified, thiamine deficiency was suspected. Supplementation of 600 mg thiamine resulted in a rapid normalisation of serum lactate levels (in patient 1 from 10.9-2.4 mmol/l; in patient 2 from 11.8-2.0 mmol/l) and acid base status (patient 1: pH from 7.11-7.30, bicarbonate from 8.6–21.2 mmol/l; patient 2: pH from 7.24-7.46, bicarbonate from 16–28 mmol/l; before and after treatment, respectively). Thiamine deficiency was confirmed by the degree of stimulation of erythrocyte transketolase activation by adding thiamine pyrophosphate, evaluated before and after thiamine replacement therapy. Stimulation decreased in patient 1 from 170% to 17% and in patient 2 from 20% to 0%, respectively. In addition to the metabolic derangement right ventricular heart failure was confirmed by echocardiography in both patients and again this was rapidly reversible by thiamine supplementation. We conclude that in malnourished patients unexplained prolonged lactic acidosis may result from thiamine deficiency, which is rapidly reversible by thiamine replacement therapy.

Oxygen consumption was measured simultaneously by the reverse Fick-principle (V02FICK) and by indirect calorimetry ("Metabolic Measurement Cart Horizon") (V02MMC) in 31 critically ill patients; 24 men and 7 women. Seventeen patients were breathing spontaneously, 14 patients were on mechanical ventilation. The fractional inspiratory oxygen concentration (FI02) in ventilated patients ranged from 0.21 to 0.4 (mean 0.302). Total oxygen consumption as measured by indirect calorimetry was 286.7 +/- 59.7 ml/min (mean +/- SD), and measured by reverse Fick-principle 258.9 +/- 52.2 ml/min (mean +/- SD). The coefficient of correlation between the two methods was r = 0.873. The absolute difference of oxygen consumption between reverse Fick-method and indirect calorimetry was 11.3%. Regression analysis according to Theil revealed a similar regression between spontaneously breathing and mechanically ventilated patients for the studied FI02 values below 0.4. It is concluded that indirect calorimetry is a reliable method for measuring oxygen consumption in spontaneously breathing as well as mechanically ventilated critically ill patients.

Endotracheal misdirection of narrow bore nasogastric feeding tubes resulted in perforation of the lung, pneumothorax and hydrothorax in two intensive care patients. Both were intubated with cuffed endotracheal low pressure tubes, one patient was on respirator therapy with neuromuscular relaxation. Feeding tubes were inserted by experienced personnel with the assistance of a steel stylet without difficulties. Aspiration of fluid was misinterpreted as proof of correct positioning, the liquid being however pleural effusion and not gastric juice. Similarly auscultation of gurgling sounds in the upper epigastrium was not a reliable sign of intragastric position. Insertion of nasoenteric feeding tubes may be complicated by perforation of the upper gastrointestinal tract and lung in poorly responsive pateints with cuffed endotracheal devices during neuromuscular blockage. In these patients a laryngoscope and forceps should be used to ensure free passage of the tube into the oesophagus. Rontgenographic confirmation of correct positioning of the tube immediately after insertion is mandatory.