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Biomedical subjects

A E Gimson

Publications and source records attributed to A E Gimson.

64 records · Page 4Linked to original sources
PubMed1982

Reticuloendothelial system and hepatocytic function in fulminant hepatic failure.

Kupffer cell and hepatocyte function were studied in 36 patients with fulminant hepatic failure by measurement of clearance of 125I microaggregated albumin (125IMAA) and galactose, respectively. Both were impaired but there was no correlation with final outcome, although on sequential testing 48 hours later, those patients who survived had a significantly greater improvement in Kupffer cell and hepatocyte function. In six other patients with similar hepatocyte dysfunction but no encephalopathy, Kupffer cell function was not significantly different from that of controls. This is additional support for a possible relation between encephalopathy and damage to Kupffer cell function. The latter was also shown to correlate with renal failure; this is consistent with the suggestion that endotoxaemia is important in the pathogenesis of this complication.

Adolescent↗
PubMed1982

Controlled trial of dexamethasone and mannitol for the cerebral oedema of fulminant hepatic failure.

A controlled trial of 44 patients was undertaken to evaluate the use of dexamethasone (32 mg stat, 8 mg qds) in preventing, and intravenous mannitol (1 g/kg) in reversing the cerebral oedema of fulminant hepatic failure. Diagnosis of cerebral oedema was based on intracranial pressure recordings or the presence of defined clinical signs. Cerebral oedema developed in 34 patients with similar frequency in those treated with and without dexamethasone (16 of 21 and 18 of 23 respectively). In those 34 patients episodes of cerebral oedema resolved significantly more frequently in the 17 patients who received mannitol than in the 17 patients who did not (44 of 53 and 16 of 17 respectively, p less than 0.001). Dexamethasone did not affect survival but among patients who developed cerebral oedema those who received mannitol had a significantly better survival than those who did not receive it (47.1% and 5.9% respectively, p 0.008, Fisher's one-tail test).

Adolescent↗
PubMed1981

Factors contributing to mortality in paracetamol-induced hepatic failure.

Fifty patients with fulminant hepatic failure from paracetamol overdose were reviewed retrospectively to determine whether there had been any avoidable delays in treatment with protective agents, or other preventable factors which could contribute to the high mortality. Only nine were admitted to the local hospital early enough (within 12 hours) to benefit from protective agents, and only three of these were treated. Treatment was delayed in two patients while the results of plasma paracetamol concentrations were awaited. Signs of grade 3 hepatic encephalopathy were never found until 72 hours after the overdose, and sudden deterioration in consciousness at an earlier stage was due either to the sedative effects of drugs or to hypoglycaemia, which in one patient went unrecognised for 24 hours. A rapid deterioration in prothrombin time, which became prolonged by at least 25 seconds at 48 hours, preceded the onset of grade 3 encephalopathy, and this is the time at which transfer should be arranged to avoid the danger of brain-stem coning. This occurred more rapidly in those transferred at a later stage of their illness.

Acetaminophen↗
PubMed1980

Prostacyclin to prevent platelet activation during charcoal haemoperfusion in fulminant hepatic failure.

Adverse effects associated with hypotension and the appearance of platelet aggregates in the circulation complicate charcoal haemoperfusion of patients with fulminant hepatic failure. In an attempt to avoid these difficulties the platelet protective effect of prostacyclin (PGI2) given intravenously before and continuously during haemoperfusion was evaluated with an improved charcoal column design. Two of the six patients who underwent haemoperfusion without PGI2 had hypotension, which in one was associated with a striking rise in Swank screen filtration pressure necessitating discontinuation of haemoperfusion after an hour. No platelet losses were observed in the six patients treated with haemoperfusion and PGI2 infusion, and there was significant protection from platelet activation, as assessed by the prevention of release into plasma of the platelet-specific protein beta-thromboglobulin.

Adult↗
PubMedDate not supplied

An assessment of orthotopic liver transplantation in acute liver failure.

Mortality of fulminant hepatic failure with standard supportive therapy is high (80 to 85%), but unfortunately most patients present to hospital already in Grade IV encephalopathy with severe liver dysfunction, and many have secondary organ damage. If seen earlier, during Grade III encephalopathy, recent experience with charcoal hemoperfusion can give good results (65% survival). Transplantation has a place in those patients who do not respond, and in cases with early Grade IV encephalopathy. Transplantation should also be considered in patients with subacute hepatic failure in whom mortality is equally high and progression to cirrhosis may occur in those who recover. In both groups, the ability to correct the hemorrhagic diathesis and an adequate supply of donor organs are essential to achievement of a successful transplant at this critical time.

Acute Disease↗
PubMedDate not supplied

Late onset hepatic failure: clinical, serological and histological features.

The clinical, laboratory and histological features of 47 patients with what is defined as late onset hepatic failure are reviewed. Twenty-five of the patients were female and 22 male with a median age of 45 years. Hepatic dysfunction was severe as evidenced by the prolongation of prothrombin time (median = 32 sec, range = 17 to 120 sec). In only four cases was a viral etiology proven (2 hepatitis B, 2 hepatitis A) although the similarity of the clinical features to patients with fulminant viral hepatitis--apart from the longer period of illness prior to the onset of encephalopathy (median = 9 weeks, range = 8 to 24 weeks)--made non-A, non-B infection a possibility in the remainder. There were also similarities to chronic active hepatitis with low titer antibodies to smooth muscle or antinuclear factor in 17% and elevation of the serum IgG in 49%. Liver biopsy in 5 of 8 survivors more than 1 year after initial presentation showed chronic active hepatitis in three. Lobular inflammatory infiltrate, bridging necrosis and multilobular collapse were the features of the acute stage of illness in both the survivors and fatal cases. The patients given corticosteroids did not have a statistically significant improvement in survival, and overall mortality for the series was 81%. Hepatic transplantation, successfully performed in one patient, would appear to offer the best chance of survival for the majority of these patients.

Adolescent↗
PubMedDate not supplied

A randomized trial of vasopressin and vasopressin plus nitroglycerin in the control of acute variceal hemorrhage.

A randomized trial was undertaken to determine efficacy of nitroglycerin when added to a vasopressin infusion in both reducing the complication rate and giving improved control of acute variceal hemorrhage. Seventy-two bleeding episodes in 57 patients were included, with vasopressin being used on 34 occasions and vasopressin plus nitroglycerin on 38 occasions, for an infusion period of 12 hr. At the end of the 12-hr period, hemorrhage had been controlled significantly more frequently in those receiving combined therapy (26 of 38; 68%) than in those given vasopressin alone (15 of 34; 44%, p less than 0.05), although this difference was not statistically significant if those patients in whom therapy was discontinued due to drug complications were excluded from the analysis [hemorrhage controlled in the combined group (68%) and vasopressin alone (48%); chi 2 = 2.4, p greater than 0.05]. Major complications requiring cessation of therapy were significantly less common in those given nitroglycerin--one occasion compared to seven in those given vasopressin alone (p less than 0.02). Thus, the addition of nitroglycerin to a vasopressin infusion results in a lower rate of complications and is more effective in controlling variceal hemorrhage.

Blood Transfusion↗
PubMedDate not supplied

Use of propranolol to reduce the rebleeding rate during injection sclerotherapy prior to variceal obliteration.

In a prospective, randomized controlled trial, 53 patients with variceal hemorrhage from portal hypertension, including 44 with cirrhosis, were allocated, after initial control of the bleeding, to treatment by sclerotherapy alone, or by this together with oral propranolol in a dose sufficient to reduce resting pulse rate by 25% during the period up to the time when varices were obliterated. Eight of the 27 patients undergoing sclerotherapy alone rebled during this period as compared to 7 of the 26 patients in the additional propranolol group (p greater than 0.80), two patients from each group dying from uncontrollable variceal hemorrhage. Propranolol precipitated encephalopathy in one patient and complicated resuscitation following bleeding in a second, and as there was no evidence in this study that use of the drug reduced the frequency or severity of the variceal bleeding, its administration cannot be recommended during the period prior to obliteration of varices by sclerotherapy.

Clinical Trials as Topic↗