Orthotropic liver transplantation is currently the treatment of choice for fulminant hepatic failure in Western countries. Most hepatologists in Japan also believe in this view.
Liver transplantation, however, is only a symptomatic treatment of liver failure. Fulminant hepatitis, which refers to fulminant hepatic failure, is not a symptom, but a disease entity included in “hepatitis”. Treatment of fulminant hepatitis, therefore, should focus not only on liver failure, but also on the underlying hepatitis. Thus the administration of antivirals and immunosuppressants for viral hepatitis and immunosuppressants for autoimmune and drug-induced hepatitis should be considered.
Using this strategy, we have obtained a survival rate of 23/31 (74.1%) [13/17 (76.4%) for the acute type, and 10/14 (71.4%) for the subacute type] in three and a half years.
We currently attempt to cure all patients with severe hepatitis by predicting fulminant hepatitis and starting treatment for hepatitis.

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It is now widely recognized that surfactant replacement is a potential life-saving therapy in babies with severe respiratory distress syndrome. The most striking acute effects have been obtained with modified natural surfactant preparations containing both surface active lipids and the hydrophobic proteins, surfactant protein B and surfactant protein C. Clinical applications of exogenous surfactant have become increasingly important. Mechanisms of surfactant inactivation have also been studied extensively in recent years. Data from animal experiments as well as clinical pilot studies indicate that the inactivation of surfactant can be overcome by large doses of exogenous surfactant. The resistance of surfactant to inhibition seems to depend on the presence of surfactant protein A. Exogenous surfactants for treatment of patients with acute respiratory distress syndrome and similar conditions must therefore be carefully designed to resist inhibition.

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Our experimental studies indicated that the initial distribution volume of glucose (IDVG) reflects the central extracellular fluid (ECF) volume status including plasma rather than glucose metabolism. The present study was designed to discover whether the IDVG follows the postoperative fluid shift from the peripheral to the central ECF compartment. Five grams of glucose and 25mg of indocyanine green (ICG) were infused simultaneously over 30 seconds through the central venous line in 21 patients following either subtotal esophagectomy or major vascular surgery. A total of 104 daily comparisons between the IDVG and plasma volume determined by the ICG dilution method (PV-ICG) were performed. Two estimates were calculated using a one compartment model utilizing plasma values from 3 to 7 minutes postinfusion for the IDVG, and from 3 to 11 minutes postinfusion for PV-ICG. Two estimates increased on the 3rd postoperative day (P<0.05), even though body weight remained unchanged. A linear correlation was obtained between two estimates (r=0.68, n=104, P<0.001). Our results demonstrate that two estimates followed the fluid shift, and suggest that the IDVG is useful to evaluate central ECF volume status following major surgical procedures.

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We evaluated whether a drug interaction between intravenous nitrates and heparin exists. Study 1: Twelve patients with acute coronary syndrome (acute myocardial infarction 6, unstable angina 6) were enrolled. Intravenous infusion of heparin was started with intravenous nitroglycerin for five hours, followed by intravenous isosorbide dinitrate for the next five hours, and switched back to intravenous nitroglycerin for the final five hours. Study 2: Nine patients with stable effort angina or chest pain syndrome were enrolled. Intravenous infusion of heparin was started alone for twelve hours at least, then intravenous infusion of nitrate was added onto the prior drip infusion of heparin on the second day, and switched back to intravenous infusion of heparin alone on the third day. Activated clotting time (ACT), activated partial thromboplastin time (APTT), and antithrombin III (AT-III) measurements were taken every five hours (Study 1), or at every drug exchange point (Study 2). Nitrates did not induce attenuation in the anticoagulation effect of heparin. Thus there was no interaction between nitroglycerin or isosorbide dinitrate and heparin in the Japanese.

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We reported a case of fulminant rhabdomyolysis with a high fever of more than 40°C which occured 4 days after total removal of a craniopharyngioma. After admission to the ICU, the patient was treated with surface cooling, wash-out therapy and continuous hemodiafiltration, together with the administration of dantrolene, methyl prednisolone, gabexate mesilate and ulinastatin.
The patient became afebrile with this treatment, but multiple organ failure and severe metabolic acidosis led to death on the 2nd ICU day. We suspect that the cause of rhabdomyolysis was hyperthermia caused by the failure of the thermoregulatory center a few days after surgery for craniopharyngioma.

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A 44-year-old man was admitted to the hospital because of gradually worsening dyspnea, fever, cyanosis, jaundice and acute circulatory impairment with atrial fibrillation. The patient had been well until about fifteen years earlier, when tremors and excessive sweating developed. On admission, serum glutamic oxaloacetic transaminase (GOT) and lactate dehydrogenase (LDH) were 11, 454IU·l^-1 and 20, 292IU·l^-1, respectively. Echocardiography documented a mildly dilated ventricle with diffuse hypokinesis and the left ventricular ejection fraction was 0.2. Because of increased thyroid hormones, undetectable thyroid-stimulating hormone and the clinical course, the patient was diagnosed as having a thyrotoxic crisis due to Graves' hyperthyroidism. Plasma exchange was performed to treat the thyrotoxic crisis and hepatic failure. Thyroid hormones and hepatic enzymes normalized. Although total bilirubin increased to 29mg·dl^-1, this parameter also normalized about two months later. We reconfirmed that plasma exchange is very effective in decreasing hyroid hormones to normal levels in hyperthyroidism with congestive heart failure and acute hepatic failure.

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A case of heart failure caused by thiopental sodium in an 18-year-old female was reported. She was admitted to the PICU (Pediatric Intensive Care Unit) because of intractable epilepsy which required mechanical ventilation and continuous intravenous infusion of thiopental sodium. Her cardiac function deteriorated (ejection fraction=48%) even though thiopental was tapered off.
The negative inotropic effect of thiopental induced by drug overdose is well known. In this case serum concentration of thiopental was within normal limits for the entire clinical course. The delayed side effect of thiopental appears to have developed as a result of the peculiar pharmacokinetics of thiopental. The tissue concentration of thiopental presumably increased although serum concentration was within the normal range.
It is important to be aware of the possible side effects of thiopental even when the serum concentration of thiopental is normal. Barbiturate therapy should be initiated in the ICU because of this potentially life-threatening cardiorespiratory complication.

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