B. Schneeweiss

Early prediction of individual outcome after cardiopulmonary resuscitation

Prediction of individual outcome after cardiopulmonary resuscitation is of major medical, ethical, and socioeconomic interest but uncertain. We studied the early predictive potency of evoked potential recording after cardiac arrest in 66 resuscitated patients who returned to spontaneous circulation but were unconscious and mechanically ventilated. Detailed long-latency and short-latency sensory evoked potentials were recorded and neurological evaluations were done 4-48 h after admission to intensive care. In all 17 patients with favourable outcome (cerebral performance categories 1 and 2) the cortical evoked potential N70 peak, a reliable measure of cortical function, was detected between 74 and 116 ms. In 49 patients with bad outcome (categories 4 and 5) the N70 peak was absent in 35 or found with a delay between 121 and 171 ms in 14 (p < 0.05 vs favourable outcome). Thus the predictive ability was 100% with cutoff of 118 ms. To confirm reproducibility and validity, repeated tracings, and linked-earlobe referenced techniques were done and gave similar results. Early recording of long-latency evoked potentials after cardiopulmonary resuscitation is highly predictive of outcome.

Improvement of hepatic encephalopathy treated with flumazenil.

The effects of the benzodiazepine antagonist flumazenil were studied in 20 episodes of hepatic encephalopathy (HE) in 17 patients with acute (n = 9) or chronic (n = 8) liver failure who had not responded to conventional therapy. Patients with a history of benzodiazepine intake were excluded. Changes in HE stage, in Glasgow coma scale, and in somatosensory evoked potentials were measured. In 12 of 20 episodes HE stage improved. The response to treatment occurred rapidly (within 3-60 min). In 8 of these 12 episodes HE worsened 0.5-4 h after treatment. In 5 of the 8 episodes that did not respond to flumazenil patients had clinical evidence of brain oedema. Flumazenil may be valuable in the treatment of HE in acute and chronic liver failure.

Energy Metabolism in Acute Hepatic Failure

BACKGROUND Conflicting data are available concerning energy metabolism in liver disease. Changes should be most pronounced in acute hepatic failure in which loss of 85% of liver cell mass is reported. Metabolic rate could be decreased due to impairment in liver mass but may also be increased as a result of systemic-mediator actions. To clarify this issue we studied energy metabolism in acute hepatic failure. METHODS Energy metabolism was evaluated by indirect calorimetry in 12 patients with acute liver failure and 22 sex-, age-, and body size-matched healthy individuals. In controls and 5 patients, studies were performed in the postabsorptive state; the remaining 7 patients received glucose at a rate of 8 mumol/kg body weight.min to prevent hypoglycemia. RESULTS Resting energy expenditure was increased in acute liver failure compared with healthy controls (5.1 +/- 0.14 kJ.min-1 x 1.73 m-2 vs. 3.97 +/- 0.08 kJ.min-1 x 1.73 m-2; mean +/- SEM; P < 0.001). Respiratory quotient and oxidation rates for major fuels were not different between the total patient-group and controls. In patients without glucose supply, energy derived from fat was higher and from carbohydrate lower than in healthy controls and patients with glucose supply. CONCLUSIONS Energy expenditure is increased in acute liver failure. Altered substrate oxidation can be normalized by glucose supply.

Prevention of upper gastrointestinal bleeding in long-term ventilated patients: Sucralfate versus ranitidine

Thirty-two long-term ventilated patients were randomly selected for a study of the efficacy of sucralfate (1 g six times per day via gastric tube) versus ranitidine (six 50-mg to six 100-mg doses per day intravenously) for the prevention of upper gastrointestinal bleeding. The patients of the two treatment groups (each 16) were comparable with respect to diseases precipitating acute respiratory failure and risk factors of bleeding, e.g., renal failure, thrombopenia, coagulopathy, and anticoagulant treatment. Mean duration of mechanical ventilation was 7.4 in sucralfate- and 7.7 days in ranitidine-treated patients. During mechanical ventilation, macroscopically visible bleeding developed in three of the sucralfate-treated (18.7 percent) and seven of the ranitidine-treated (43.7 percent) patients. Until the end of the study, only three of the sucralfate-treated but nine of the ranitidine-treated (56.2 percent) patients bled; the difference between the two treatment groups was at all times significant (p less than 0.05). Packed red blood cells had to be administered to the three bleeding patients in the sucralfate group and to seven bleeding in the ranitidine group. Therefore it seems that sucralfate prevented mostly minor bleeding. The high bleeding rate during ranitidine treatment was presumably due to the high number of pH-nonresponders, as almost 30 percent of the gastric aspirates of this group had a pH less than 5. During treatment no difference was found in positive blood culture specimens and bronchial secretions between the two groups. However, nosocomial pneumonia developed in two ranitidine-treated patients, whereas that complication developed in none of the sucralfate-treated patients. In long-term ventilated patients, sucralfate prevented minor upper gastrointestinal bleeding significantly better than ranitidine. However, this does not imply that major upper gastrointestinal bleeding can be prevented by either sucralfate or ranitidine in these patients.

No Effect of Short-Term Dietary Supplementation of Saturated and Poly- and Monounsaturated Fatty Acids on Insulin Secretion and Sensitivity in Healthy Men

To evaluate the short-term influence of fatty acids with different grades of saturation on insulin secretion and sensitivity, 8 healthy males (age 26 +/- 3.5 years, body mass index 22.4 +/- 1.8 kg/m2) were provided with 800 kcal daily of either carbohydrates (CH; 200 g), or fat (90 g) enriched either with saturated fatty acids (SAFA; 72%) or (omega-6) polyunsaturated fatty acids (PUFA; 60%) or cis-monounsaturated fatty acids (MUFA; 40%; n = 5) in addition to a standard diet (2,000 kcal/ day; 50% CH, 15% protein, and 35% fat; 33% SAFA, MUFA, and PUFA each) for 1 week in a randomized order (washout period 2 weeks). The stimulated insulin secretion was quantified by the frequently sampled intravenous glucose tolerance test (FSIGT; 0.3 g glucose/kg body weight), while the insulin sensitivity was determined by an euglycemic-hyperinsulinemic 5-mU clamp. In parallel, basal and stimulated carbohydrate and fat oxidation rates were estimated by indirect calorimetry. One week of defined fat exposure failed to significantly affect the glucose-induced insulin secretion during FSIGT and insulin-dependent glucose disposal during an euglycemic clamp (M values: CH 9.6 +/- 1.6 mg/kg.min, SAFA 9.7 +/- 2.2, PUFA 9.8 +/- 2.5, and MUFA 11.5 +/- 3.2 mg/kg.min; NS). In addition, oxidation rates for fat and glucose in the postabsorptive state and during hyperinsulinemia did not differ between the different diets. We conclude that short-term (1-week) isocaloric supplementation of a standard diet with fatty acids of varying degree of saturation does not affect either insulin secretion or insulin sensitivity in healthy men, due to the compensatory metabolic capacity of healthy subjects.

Pancreatitis in acute hemolysis

SummaryForty cases of hemolysis (drop of hematocrit > 12%/12 h) were retrospectively analyzed for hyperamylasemia and pancreatic complications. In 15 subjects the serum amylase level was > 360 U/l, i.e., three times the normal range, in ten the amylase level exceeded 900 U/l. Excluding patients in circulatory shock and/or hepatic coma, acute pancreatitis as defined by an elevation of serum amylase and clinical signs (epigastric pain) was present in four, with additional ultrasound findings (pancreatic swelling) and/or laparatomy/postmortem findings in a further six subjects (total ten patients = 25%) with various causes of hemolysis: autoimmune hemolysis 2, microangiopathic hemolytic anemia 2, toxicemia, G-6-PDH deficiency, septic abortion, malaria, Wilsons disease, and hypophosphatemia, one case each. In all subjects acute renal failure and in seven an activation of intravascular coagulation was seen. Three patients died (33% vs 47% of all hyperamylasemic patients and 46% of the whole group), but none of the deaths was attributed to pancreatitis. Pancreatic postmortem findings were diffuse edema and patchy parenchymal necrosis in two cases and petechial bleeding in one case. We conclude that acute pancreatitis is a complication of massive hemolysis, occurring at a prevalence of above 20%. It may progress from diffuse edema and inflammation to focal necrosis, rarely if ever to gross hemorrhage, and does not contribute to the high mortality of massive hemolysis. Back pain in hemolysis might originate from the pancreas rather than from the kidneys.

Short-term energy balance in patients with infections: carbohydrate-based versus fat-based diets.

The effects of a carbohydrate-based diet (50% carbohydrate calories, 30% fat calories, 20% protein calories) versus a fat-based diet (28% carbohydrate calories, 55% fat calories, 17% protein calories) on oxidation rates of carbohydrate, fat, and protein were assessed in 12 patients with infections by indirect calorimetry and estimation of urea nitrogen production rate. The diets were given continuously for 18 hours in a randomized cross-over study on 2 consecutive days. Energy supply (kcal/d) was adjusted individually to meet the energy expenditure measured on the preceding day after an overnight fast and was 1,647 +/- 129 (SEM) for the carbohydrate-based diet and 1,655 +/- 131 for the fat-based diet. Oxidation rates (kcal/d) for carbohydrate (carbohydrate-based diet, 525 +/- 70; fat-based diet, 363 +/- 84) were different between the diets (P less than .05), whereas no difference could be found for fat (carbohydrate-based diet, 820 +/- 117; fat-based diet, 968 +/- 136) and protein (carbohydrate-based diet, 252 +/- 29; fat-based diet, 236 +/- 23). However, during carbohydrate-based feeding, carbohydrate balance (288 +/- 93 kcal/d) and fat balance (-327 +/- 107 kcal/d) were significantly different from zero (P less than .05), indicating continuous oxidation of endogenous fat and storage of administered glucose. During the fat-based diet, carbohydrate and fat balances were not different from zero. A correlation between energy and substrate balances was not seen during either diet.(ABSTRACT TRUNCATED AT 250 WORDS)

Fructose-induced hyperlactemia in hyperosmolar syndromes

SummarySevere hyperlactemia of 8.7, 8.6 and 7.9 mmol/l, respectively, developed in three patients with hyperosmolar syndromes (two hypernatremic, 417 and 415 mosmol/kg H2O; one hyperglycemic 437 mosmol/kg H2O) during rehydration treatment with 5% fructose in water (fructose dosage 0.5 g/kg body wt. per hour). After resolution of the electrolyte disturbances, the infusion of fructose at the same dosage increased the plasma lactate concentration in two of the patients to 4.9 and 4.0 mmol/l, indicating near normalization of hepatic lactate utilization. Thus, in addition to peripheral insulin resistance and decreased muscular glucose utilization, the hyperosmolar state is associated with a reduced tolerance to fructose. This is most likely due to an osmolality-dependent impairment of hepatic gluconeogenesis. In rehydration therapy for hyperosmolar syndromes, fructose-containing infusion solutions should no longer be used.

Evoked potentials in severe herpes simplex encephalitis.

Diagnostic and prognostic value of evoked potentials (EP) were studied in 5 patients with severe herpes simplex encephalitis (HSE). Latency of the third negative cortical N70 peak, elicited by median nerve stimulation, was prolonged in 3 survivors with Glasgow coma score of ≤6 (115 vs 71 ms in controls,p<0.05), but normal after improvement of the acute disease, N70 right to left interhemisphere difference was increased initially in the 4 survivors (26 vs 3 ms in controls,p<0.05) indicating focal brain involvement, a crucial finding in HSE. The first cortical N 20 peak was preserved in all survivors even during deep coma where evaluation of brain function is difficult. Auditory brainstem EP were normal in all patients and useful to exclude brainstem death. In severe HSE, somatosensory long-latency EP are an effective monitor of the level of impaired consciousness and can detect brain focal signs. Short-latency N20 components may be predictive of the outcome.

Influence of fluid replacement on extravascular lung water (EVLW) in patients with diabetic ketoacidosis.

Fluid replacement is a major issue in the treatment of patients with diabetic ketoacidosis. During this therapy, development of pulmonary edema has been reported and attributed to an increase in pulmonary microvascular pressure and a decrease in colloid-osmotic pressure (COP). Because clinically apparent pulmonary edema is associated with an increase in extravascular lung water (EVLW) and impairment of pulmonary gas exchange, we studied the effect of fluid replacement on EVLW, COP, pulmonary hemodynamics and gas exchange parameters in 8 patients with diabetic ketoacidosis (blood glucose>300 mg/dl, pH<7.1). EVLW was estimated by the thermal-dye technique. All variables were successively determined upon adminssion (A), after initial fluid replacement (IFR), when glucose had fallen below 180 mg/dl, after 8 h of intravenous glucose treatment (G), and after 24 h of total parenteral nutrition (TPN). Despite a total net fluid intake of 6.0±1.61, a significant decrease (p<0.001) in COP from 29.6±5.5 at A to 18.8±2.2 mmHg after TPE and a significant increase (p<0.001) in PCWP from 4±2 at A to 10±3 mmHg after TPE, EVLW remained almost unchanged. EVLW was 5.1±2.8 at A, 5.3±2.1 after IFR, 4.8±1.4 after G, and 5.3±1.7 ml/kg after TPN. However, PaO2 decreased from 137±17 at A to 87±10 mmHg after TPE (p<0.001), while Qs/Qt increased significantly (p<0.05). The alterations in gas exchange may be indicative of pulmonary dysfunction but as they were not associated with accumulation of EVLW, they may as well reflect the compensation of metabolic derangements in diabetic ketoacidosis.