Effect of continuous venovenous hemofiltration with dialysis on lactate clearance in critically ill patients.

OBJECTIVE: To evaluate the effect of continuous venovenous hemofiltration with dialysis on lactate elimination by critically ill patients. DESIGN: Prospective, clinical study. SETTING: Surgical intensive care unit of a university hospital. PATIENTS: Ten critically ill patients with acute renal failure and stable blood lactate concentrations. INTERVENTIONS: Two-stage investigation: a) measurement of lactate concentrations in samples of serum and ultradiafiltrate from patients receiving continuous venovenous hemofiltration with dialysis to calculate lactate clearance by the hemofilter; b) evaluation of total plasma lactate clearance by infusing sodium L-lactate (1 mmol/kg of body weight) over 15 mins. MEASUREMENTS AND MAIN RESULTS: Arterial lactate concentration was determined before, during, and after the infusion. Lactate elimination variables were calculated from the plasma curve using model-independent and model-dependent estimates (by software). At the end of the infusion, median blood lactate concentration increased from 1.4 mmol/L (range 0.8 to 2.6) to 4.8 mmol/L (range 2.4 to 5.7) and returned to 1.6 mmol/L (range 0.9 to 3.4) 60 mins later. The median total plasma lactate clearance was 1379 mL/min (range 753.7 to 1880.7) and the median filter lactate clearance was 24.2 mL/min (range 7.1 to 35.6). Thus, filter lactate clearance accounted for < 3% of total lactate clearance. CONCLUSIONS: Continuous venovenous hemofiltration with dialysis cannot mask lactate overproduction, and its blood concentration remains a reliable marker of tissue oxygenation in patients receiving this renal replacement technique.

[Fatal acute liver failure: a rare complication of exertion-induced heat stroke]. / Insuffisance hépatique aiguë mortelle: une complication rare du coup de chaleur d'effort.

Liver injury is a well-known complication of exertional heat stroke. However severe acute irreversible liver dysfunction is rarely associated. Persistent centrolobular hepatocellular necrosis without any regeneration remains very uncommon. We report a case of fatal acute liver failure occurring after exertional heat stroke. Despite the conventional symptomatic treatment, especially active cooling, the patient experienced multiple organ failure with brain death 6 days after his admission. In this case, a chronic treatment with neuroleptic and anticholinergic agents may be considered as a predisposing factor.

Intravenous nicardipine does not alter hepatic blood flow after orthotopic liver transplant.

OBJECTIVE: To evaluate the effects of nicardipine on hepatic blood flow in patients with recent liver transplants. Secondly, to evaluate the liver extraction of nicardipine in order to determine the influence of liver transplantation on its disposition. DESIGN: Prospective self-controlled clinical study. SETTING: University hospital intensive care unit. PATIENTS: Eight patients in the early postoperative period of orthotopic liver transplantation. MEASUREMENTS AND RESULTS: Patients were given 5 mg of i.v. nicardipine. Systemic and splanchnic haemodynamic and metabolic parameters were measured before nicardipine administration (T0) and at 5 min (T1), 30 min (T2), and 120 min (T3) after administration. A catheter was inserted into a hepatic vein to determine the total hepatic blood flow (HBF) and the hepatic extraction coefficient of nicardipine. Nicardipine caused no significant changes in HBF, oxygen delivery, oxygen uptake, hepatic venous oxygen saturation, or the hepatic venous partial pressure of oxygen. Likewise, neither blood lactate concentrations nor arterial and hepatic venous lactate-pyruvate ratios were modified by nicardipine. The hepatic extraction coefficient of nicardipine was approximately 0.70 in the first 3 min after complete infusion, then decreased and remained stable at approximately 0.50, showing a non-linear first-pass metabolism pattern. CONCLUSIONS: Nicardipine administration after liver transplantation appears to have no deleterious effects on HBF. Nicardipine can be classified as a drug of intermediate hepatic extraction coefficient, whose elimination partly depends on hepatic enzyme activity.

Effect of sodium bicarbonate on intracellular pH under different buffering conditions.

Previous in vitro studies have reported a paradoxical exacerbation of intracellular acidosis following bicarbonate therapy due to the generated CO2 entering the cytoplasm. However, these studies were conducted in nonphysiological Hepes-buffered media. We compared the effect of a sodium bicarbonate load on the intracellular pH (pHi) of hepatocytes placed in nonbicarbonate (NBBS) or bicarbonate (BBS) buffering systems. The pHi of isolated rat hepatocytes was measured using the fluorescent pH sensitive dye BCECF and a single-cell imaging technique. Cells were placed in medium buffered with HCO3-/CO2 or Hepes. All media were adjusted to pH 7 with L-lactic acid or HCl. An acute 45 mM sodium bicarbonate load was added to each medium and the changes in pHi were measured every three seconds for 90 seconds. The sodium bicarbonate load caused rapid cytoplasmic acidification of cells in NBBS (N = 50, P < 0.001). In contrast, hepatocytes in BBS underwent a marked increase in pHi (N = 50, P < 0.001) without any initial decrease in pHi. These differences were highly significant for the buffer (P < 0.01), but not for the acid used. We conclude that sodium bicarbonate exacerbates intracellular acidosis only in a NBBS. Hence, in vitro studies reporting a paradoxical intracellular acidosis following bicarbonate therapy cannot be extrapolated to the in vivo buffering conditions, and should not be used to argue against bicarbonate therapy.

Use of i.v. insulin in well-controlled non-insulin-dependent diabetics undergoing major surgery.

We conducted a randomized, prospective study to assess the effect of i.v. insulin on blood glucose control, development of ketone bodies and hormonal changes in 60 well-controlled, non-insulin-dependent diabetics (NIDDM) undergoing major surgery. In group A, patients were given only 0.9% saline; in group B, patients were given insulin as a continuous i.v. infusion (1.25 u. h-1); in group C, patients were given insulin 10 u. i.v. boluses every 2 h. Patients in all three groups were given insulin 5 u. when their intraoperative blood glucose concentration increased to greater than 11.1 mmol litre-1. Blood glucose concentrations were measured every 15 min, from just before induction of anaesthesia to 2 h after surgery. Plasma lactate, pyruvate, ketone body, C-peptide and counter-regulatory hormone concentrations were also measured. Blood glucose concentrations in the three groups did not differ significantly. There was a mild-to-moderate increase in plasma ketone body concentrations in group A, but without any deleterious consequences. Plasma C-peptide concentrations decreased significantly in groups B and C, especially in patients given bolus injections of insulin. Plasma growth hormone concentrations also increased significantly in group B and C patients. This study indicated that the "no insulin--no glucose" regimen was a simple, effective way to control blood glucose in well-controlled NIDDM patients, provided blood glucose was measured frequently and insulin used appropriately.