SummaryAlphaxalone-alphadolone (Althesin), diluted and administered as a controlled infusion, was used as a sedative for 30 patients in an intensive therapy unit. This technique allowed rapid and accurate control of the level of sedation. It had three particularly useful applications: it provided "light sleep," allowed rapid variation in the level of sedation, and enabled repeated assessment of the central nervous system. Sedation was satisfactory for 86% of the total time, and no serious complications were attributed to the use of the drug. Furthermore, though alphaxalone-alphadolone was given for periods up to 20 days there was no evidence of tachyphylaxis or delay in recovery time.

Advanced liver disease with portal hypertension may be associated with pulmonary hypertension. A review of 1,205 consecutive liver transplant patients was made to assess the incidence and severity of pulmonary hypertension in patients with end-stage liver disease. Postoperative data were reviewed to determine if outcome was influenced and, in patients with severe pulmonary hypertension, whether pulmonary hypertension was reversed after transplantation. The hemodynamic data of 5 patients who were found to have severe pulmonary hypertension before transplantation and did not receive transplants were also reviewed. The incidence of pulmonary hypertension in the patients who received transplants was 8.5% (n ‫؍‬ 102; mean pulmonary artery pressure, G25 mmHg). The incidence of mild pulmonary hypertension was 6.72% (n ‫؍‬ 81; systolic pulmonary artery pressure, 30 to 44 mmHg); that of moderate pulmonary hypertension was 1.16% (n ‫؍‬ 14; systolic pulmonary artery pressure, 45 to 59 mmHg); and that of severe pulmonary hypertension was 0.58% (n ‫؍‬ 7; systolic pulmonary artery pressure, G60 mmHg). Mild and moderate pulmonary hypertension did not influence the outcome of the procedure. Severe pulmonary hypertension was associated with mortality rates of 42% at 9 months posttransplantation and 71% at 36 months posttransplantation. Only 2 of 7 patients with severe pulmonary hypertension have survived liver transplantation with a good quality of life. The remaining 5 patients continued to deteriorate with progressive right heart failure with no evidence of amelioration of the pulmonary hypertension. This experience supports the view that in most patients who have severe pulmonary hypertension associated with advanced liver disease, it is caused by fixed pathological changes in the pulmonary vasculature, is not reversible with liver transplantation, and is associated with a very high perioperative mortality rate. Copyright 1997 by the American Association for the Study of Liver DiseasesA review of perioperative data was undertaken to establish the incidence of pulmonary hypertension in the first 1,205 consecutive orthotopic liver transplant (OLT) patients at Baylor University Medical Center (BUMC) and to elucidate whether the presence of pulmonary hypertension influenced the clinical outcome. Mild to moderate pulmonary hypertension has not been reported to contribute to mortality after transplant or to influence the clinical outcome. 1-3 On the other hand, severe primary pulmonary hypertension carries a significant perioperative risk and in many cases limits the quality of postoperative survival. 4 All records of OLT patients with severe pulmonary hypertension were studied in detail in an attempt to establish criteria for likely success of OLT in these patients. Patients and MethodsWe have defined pulmonary hypertension as a mean pulmonary artery pressure of 25 mmHg or greater and a pulmonary vascular resistance (PVR) of greater than 120 dyne · s Ϫ1 · cm Ϫ5 . 3 Pulmonary hypertension was then arbitrarily divided into three gro...

that 32 out of our 33 patients had developed thrombocytopenia before any other drug was given. The one patient who had a haemorrhage on the fifth day of treatment received Darafan on Day 0, and even he had had thrombocytopenia on admission. Therefore, it is concluded that drugs played no part in the pathogenesis of thrombocytopenia in these patients. ConclusionThrombocytopenia is the rule in the acute attack of malaria, and it is not associated with depletion of other coagulation factors in the mild case. We suggest that the platelets are removed at an excessive rate from the circulating blood, probably by the reticuloendothelial system, and that they are in some way altered immunologically, which assists in their removal.It must be realized that thrombocytopenia can occur in malaria in the absence of intravascular coagulation, and that heparin should be withheld in such cases until other evidence is produced of disordered coagulation, when its use might then be justified.

SummaryFull clinical and laboratory details of 203 patients with postoperative jaundice were submitted to a panel of hepatologists. All patients whose jaundice may have had an identifiable cause were excluded, which left 76 patients with unexplained hepatitis following halothane anaesthesia (UHFH). Hepatitis in 95°o of these cases followed multiple exposure to halothane, with repeated exposure within four weeks in 551)O of cases. Twenty-nine patients were obese, 52 were aged 41-70, and 53 were women. Thirteen patients died in acute hepatic failure. Rapid onset of jaundice after anaesthesia, male sex, and obesity in either sex were poor prognostic signs. Of the clinical stigmata of hypersensitivity, only eosinophilia was impressive. The UHFH group had a much greater incidence of liver kidney microsomal (LKM) and thyroid antibodies and autoimmune complement fixation than those patients whose jaundice related to identifiable factors. Thirteen of the 19 patients with LKM antibodies also had thyroid antibodies. In six patients retested two to three years later LKM antibodies had disappeared, although thyroid antibodies persisted.Rapidly repeated exposure to halothane may cause hepatitis, but such a complication is probably rare. Possibly obese women with a tendency to organ-specific autoimmunity may be more at risk. Nevertheless, the comparative risks of rapidly repeated halothane or non-

arterial line in selected cases, but in our opinion it is neither necessary nor justifiable to insert routinely intra-arterial lines in all patients admitted to a general medical intensive care unit.Flexibility is the essence of modular monitoring apparatus. It allows the clinician to decide which physiological variables he wishes to monitor, and he should never regard such a system as a "panindicator" unit. Therefore each separate system must be reliable in its own right, and reliability in the clinical environment can be assessed only by intensive study in a clinical situation. The technique we used seems to give a useful indication of whether a particular system is suitable for routine clinical use. Moreover, we would suggest that to be of value in hospital conditions an automatic monitor needs to be at least 90% reliable.We would like to acknowledge the unstinted co-operation of the nursing staff of Starling Ward; Mr. A.