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Biomedical subjects

A E Gimson

Publications and source records attributed to A E Gimson.

At least 19 recordsLinked to original sources
PubMed1992

Effects of vasopressor agents and epoprostenol on systemic hemodynamics and oxygen transport in fulminant hepatic failure.

Hypotension is a serious complication in patients with fulminant hepatic failure, because it is associated with tissue hypoxia and a further compromise to end-organ function. In this study we investigated the effects of epinephrine and norepinephrine on hemodynamics and oxygen transport variables in 30 patients with fulminant hepatic failure. All had a mean arterial pressure of less than 60 mm Hg, despite adequate intravascular filling pressures. Both epinephrine (n = 15) and norepinephrine (n = 15) improved mean arterial pressure (p less than 0.001 epinephrine and norepinephrine), although this was not associated with a rise in oxygen delivery. Oxygen consumption fell (p less than 0.05 epinephrine, p less than 0.001 norepinephrine) because of a lower oxygen extraction ratio (p less than 0.01 epinephrine and norepinephrine). The addition of epoprostenol, a microcirculatory vasodilator, in 10 patients from each group led to an increase in oxygen consumption (p less than 0.001 epinephrine and norepinephrine) because of a rise in oxygen delivery (p less than 0.05 epinephrine, p less than 0.01 norepinephrine) and oxygen extraction ratio (p less than 0.01 epinephrine, p less than 0.001 norepinephrine), without a fall in mean arterial pressure. The fall in oxygen consumption after the institution of vasopressor therapy could exacerbate tissue hypoxia and thus contribute to further organ damage in an already susceptible patient. In patients with fulminant hepatic failure who are given vasopressor support, the addition of epoprostenol may prevent the development of tissue hypoxia.

Adolescent↗
PubMed1991

Liver transplantation after paracetamol overdose.

OBJECTIVE: To evaluate the role of liver transplantation after paracetamol overdose. DESIGN: Prospective study of consecutive candidates for transplantation and performance of transplantation over 18 months. SETTING: Liver unit, King's College Hospital, London. MAIN OUTCOME MEASURES: Fulfilment of indicators of poor prognosis, selection for transplantation, transplantation, survival. RESULTS: 30 of 37 patients considered to have a reasonable prognosis with intensive medical care survived. Of 14 of 29 patients considered to have a very poor prognosis and registered for urgent liver transplantation, six received liver transplants, four of whom survived, while seven died and one survived without a transplant. Three of 15 patients with poor prognostic indicators but not selected for transplantation survived. CONCLUSION: Liver transplantation will have a definite but limited role in the management of fulminant hepatic failure induced by paracetamol.

Acetaminophen↗
PubMed1991

Improvement by acetylcysteine of hemodynamics and oxygen transport in fulminant hepatic failure.

BACKGROUND: When administered early after an overdose of acetaminophen, intravenous acetylcysteine prevents hepatic necrosis by replenishing reduced stores of glutathione. How acetylcysteine improves the survival of patients with established liver damage induced by acetaminophen, however, is unknown. This study was undertaken to determine whether the beneficial effect of acetylcysteine under such circumstances could be due to enhancement of oxygen delivery and consumption. METHODS: We studied the effect of acetylcysteine on systemic hemodynamics and oxygen transport in 12 patients with acetaminophen-induced fulminant hepatic failure and 8 patients with acute liver failure from other causes. The acetylcysteine was given in a dose of 150 mg per kilogram of body weight in 250 ml of 5 percent dextrose over a period of 15 minutes and then in a dose of 50 mg per kilogram in 500 ml of 5 percent dextrose over a period of 4 hours; measurements were made before treatment began and after 30 minutes of the regimen. RESULTS: In the patients with acetaminophen-induced liver failure, the infusion of acetylcysteine resulted in an increase in mean oxygen delivery from 856 to 975 ml per minute per square meter of body-surface area (P = 0.0036), due to an increase in the cardiac index from 5.6 to 6.7 liters per minute per square meter (P = 0.0021). Mean arterial pressure rose from 88 to 95 mm Hg (P = 0.0054) despite a decrease in systemic vascular resistance from 1296 to 1113 dyn.sec.cm-5 per square meter (P = 0.027). There was an increase in oxygen consumption from 127 to 184 ml per minute per square meter (P = 0.0007) associated with an increase in the oxygen-extraction ratio from 16 to 21 percent (P = 0.022). The effects in the patients with acute liver failure from other causes were similar. CONCLUSIONS: The increase in oxygen delivery and consumption in response to acetylcysteine may account for its beneficial effect on survival in patients with fulminant hepatic failure induced by acetaminophen.

Acetaminophen↗
PubMed1991

Intensive liver care and management of acute hepatic failure.

In describing acute liver failure, the term fulminant hepatic failure (FHF) is used to denote patients with the most rapid progression, normally defined as the onset of encephalopathy within eight weeks of the onset of symptoms. For patients with a slower onset of encephalopathy, ranging from eight weeks to six months after the onset of symptoms, late-onset hepatic failure is the term used to reflect the overlap in clinical features with some patients with FHF. The importance of accurately determining the type of acute liver failure results from increasing evidence of an inverse relationship between the tempo of disease progression and the chances of recovery. Prognosis is also dependent on the underlying etiology. Principles of management are as follows: (1) an accurate recognition of the tempo of the hepatic failure--fulminant, late onset, acute on chronic--and the establishment of a likely etiology; (2) early detection and treatment of complications, particularly metabolic acidosis (early), renal failure, cerebral edema, and infection (late); (3) optimization of conditions for regeneration by maintenance of a near normal metabolic milieu (with removal of toxins by various methods of artificial liver support if necessary); and (4) early consideration of an orthotopic liver transplant for those patients in the poor prognosis group. Variations in the natural history and clinical features of acute liver failure (ALF) have led to a number of different classifications and subgroupings. Knowledge of these is important in relation to the assessment of prognosis and is even more important now that transplantation is a therapeutic option.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetaminophen↗
PubMed1991

Endoscopic sclerotherapy in the management of gastric variceal haemorrhage.

The value of injection sclerotherapy in the management of active gastric variceal bleeding is unclear. A retrospective study was therefore performed of 46 episodes of acute variceal haemorrhage in 41 patients who were treated by endoscopic sclerotherapy. The site of gastric variceal haemorrhage was the lesser curve (Group 1) in 13, within a hiatus hernia (Group 2) in six, and fundal with or without associated oesophageal varices (Type 3) in 22 cases. Haemostasis was achieved by sclerotherapy in 54%, 71.4% and 26%, respectively. After additional measures including balloon tamponade or surgery 85% of the Group 1 cases had stopped bleeding significantly more frequently than was observed in Group 3 (44.4%). More patients in Group 3 died due to uncontrolled bleeding (41%) than in Group I (7.7%). Hospital mortality depended on the severity of the liver disease with 15% of Child's grade A and 56% of grade C cases dying. It is concluded that endoscopic sclerotherapy of gastric varices should be reserved only for lesser curve or hiatal varices and that early surgery (or sclerotherapy using tissue adhesive) be considered for variceal haemorrhage originating from fundal varices.

Esophageal and Gastric Varices↗
PubMed1991

Arterial-venous pH differences and tissue hypoxia in patients with fulminant hepatic failure.

OBJECTIVE: A recent report suggested that, for hypotensive patients, tissue acidemia is best monitored by simultaneous estimates of arterial pH, mixed venous pH, and bicarbonate. This method of detecting tissue acidemia may therefore apply to fulminant hepatic failure patients, who are known to have a high frequency of covert tissue hypoxia. In the present study, both arterial pH and mixed venous pH and bicarbonate were compared in 22 patients with fulminant hepatic failure. Blood samples were drawn from the pulmonary artery and radial artery and this blood was analyzed to determine oxygen delivery and consumption. The arterial pH, mixed venous pH, and bicarbonate were compared using an oxygen flux test to determine the optimal method of demonstrating tissue hypoxia in this group of patients. DESIGN: A prospective study. SETTING: The Liver Unit of our institution. PATIENTS: Patients (n = 22) with fulminant hepatic failure admitted between January 1989 and January 1990. INTERVENTIONS: Patients were studied before and after an infusion of prostacyclin. MEASUREMENTS AND RESULTS: The findings of this study suggest that pH and bicarbonate differences in arterial and mixed venous blood samples were not indicative of tissue hypoxia in patients with fulminant hepatic failure. By contrast, measurement of oxygen consumption after the infusion of prostacyclin, with the demonstrated increase in oxygen uptake, provided a more accurate indication of covert tissue hypoxia. CONCLUSIONS: In critically ill patients with a hyperdynamic circulation, such as those patients with fulminant hepatic failure, an oxygen flux test remains the best method of determining the presence of covert tissue hypoxia.

Acid-Base Equilibrium↗
PubMed1991

Focal nodular hyperplasia of the liver: results of treatment and options in management.

Twenty two patients (19 females) with focal nodular hyperplasia were seen between 1973 and 1989. Five were children, and all the adults were aged under 42 years (median 33 years). Fourteen patients (64%) were symptomatic on presentation. Twelve of the 14 adult women had taken the oral contraceptive pill. Twelve patients, nine of whom were symptomatic, underwent hepatic resection shortly after presentation. There were no deaths or major complications, and all remain well on follow up. Four patients underwent either hepatic artery embolisation or ligation. After an interval of six to 10 years they were asymptomatic and only one has histological evidence of residual focal nodular hyperplasia. Of five patients initially treated conservatively, two were asymptomatic and have remained so for three and 13 years. One of the three symptomatic patients became symptom free after stopping the contraceptive pill. The management of focal nodular hyperplasia requires a flexible approach. Lesions which are asymptomatic can be observed with regular ultrasound and treated if they enlarge or become symptomatic. Symptomatic patients who present while taking the contraceptive pill can also have a trial of conservative treatment. Other symptomatic patients, including those who previously took the pill, are best treated by surgical resection, and, where this is not possible, by embolisation.

Adolescent↗
PubMed1990

A controlled trial of oral propranolol compared with injection sclerotherapy for the long-term management of variceal bleeding.

This trial was carried out to assess the value of propranolol for the prevention of recurrent variceal bleeding in patients with well-compensated cirrhosis. We also compared propranolol therapy to long-term injection sclerotherapy. One hundred and eight patients, in whom the original variceal hemorrhage stopped spontaneously (before diagnostic endoscopy) and without sclerotherapy or surgical intervention, were included. All were Pugh grade A or B; 55% had alcoholic cirrhosis. Patients were chosen randomly to receive oral propranolol (in a dosage to reduce resting pulse rate by 25%) or to undergo long-term injection sclerotherapy. In both groups, episodes of repeat bleeding that did not stop spontaneously were managed with sclerotherapy. Patients considered to have failed propranolol therapy were treated with long-term sclerotherapy. Follow-up ranged from 12 to 64 mo. In the propranolol group, 28 (54%) of the 52 patients had repeat bleeding from varices with a total of 57 episodes; 14 received long-term sclerotherapy. In the sclerotherapy group, 25 (45%) of the 56 patients had repeat bleeding, with a total of 40 episodes (p less than 0.20). On an intention-to-treat basis, the risk of bleeding expressed per patient-month of follow-up was similar for the two groups, at 0.05 and 0.037, respectively. Survival as assessed by cumulative life analysis was also similar, with 55% and 66% alive at 3 yr (p less than 0.40). Stepwise regression analysis of possible factors predicting further bleeding in patients taking propranolol selected only two variables--the pretreatment pulse rate and the extent of pulse-rate reduction in response to propranolol.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1990

Single, total paracentesis for tense ascites: sequential hemodynamic changes and right atrial size.

Hemodynamic changes induced by a single, total paracentesis were evaluated in 21 patients with tense ascites from whom 4 to 16 L of ascites were drained over 2 to 8 hr with no serious complications. At 60 min, compared to baseline, there was an increase in cardiac output (7.7 +/- 0.5 to 8.5 +/- 0.6 L/min, p less than 0.02) and a tendency for right atrial pressure to decrease (9.3 +/- 0.8 to 7.50 +/- 0.8 mm Hg, NS), with no change in pulmonary capillary wedge pressure (10.9 +/- 0.9 to 10.7 +/- 0.9 mm Hg). Between 3 and 12 hr later, there was a drop in right atrial pressure, pulmonary capillary wedge pressure and cardiac output to 5.6 +/- 0.6 (p less than 0.02), 7.2 +/- 0.8 mm Hg (p less than 0.002) and 7.2 +/- 0.6 L/min (NS) respectively, indicative of the development of relative hypovolemia and suggesting that therapeutic plasma expansion is appropriate at this time. Two-dimensional echocardiography before paracentesis (n = 8) showed a reduction in the right to left atrium area ratio as compared with values in patients with minimal ascites (0.54 +/- 0.04 vs 0.82 +/- 0.02, p less than 0.0001). This technique may help in identifying patients with right atrial compression caused by tense ascites.

Adult↗
PubMed1989

Controlled clinical trial of injection sclerotherapy for active variceal bleeding.

In a prospective, randomized clinical trial, immediate injection sclerotherapy was compared with treatment by a combined infusion of vasopressin (0.4 unit per min) and nitroglycerin (40 to 400 micrograms per min) in 50 consecutive patients with 64 episodes of endoscopy-proven variceal hemorrhage. Control of bleeding was assessed over a 12-hr period following entry into the trial. Patients in the vasopressin + nitroglycerin group were then treated by sclerotherapy, as were those in the sclerotherapy group who continued to bleed. At 12 hr, bleeding was controlled in 29 (88%) of the 33 episodes treated by sclerotherapy compared with 20 (65%) of 31 episodes treated by vasopressin + nitroglycerin (p less than 0.05). Recurrence of variceal bleeding occurred at the same frequency (31%). Although admission mortality was less in those initially treated by sclerotherapy compared to those managed by vasopressin + nitroglycerin, this did not reach statistical significance (27 and 39%, respectively, p greater than 0.20). Sclerotherapy carried out as the first treatment of the active variceal hemorrhage proved both safe and effective, even in the presence of major hemorrhage, and as compared to combined vasopressin and nitroglycerin it proved superior.

Clinical Trials as Topic↗
PubMed1989

Sucralfate for the prevention of early rebleeding following injection sclerotherapy for esophageal varices.

One hundred eighty patients with variceal bleeding and treated by long-term sclerotherapy were randomized into a prospective randomized controlled clinical trial to assess the efficacy of sucralfate in reducing the frequency of rebleeding from esophageal ulceration prior to variceal obliteration. Overall, 29 (32%) of the 92 patients treated with the addition of sucralfate rebled, compared to 37 (42%) of 88 patients managed by sclerotherapy alone (p less than 0.10), but when patients with well-compensated liver disease were considered, the respective figures were 14 (24%) and 25 (42%)--a statistically significant difference (p less than 0.05). The frequency (approximately 70%), number (per patient) and extent of sclerotherapy-induced esophageal mucosal ulceration were not different for the two groups, although proven rebleeding from the ulceration occurred less frequently in those receiving sucralfate (10 and 20 occasions, respectively, p less than 0.05). Mortality was not different for the two groups. Thus, use of sucralfate will reduce the frequency of rebleeding during long-term treatment by sclerotherapy, although benefit appears to be restricted to well-compensated patients and without an endoscopic overt effect upon esophageal mucosal ulceration.

Combined Modality Therapy↗
PubMed1988

Controlled trials of charcoal hemoperfusion and prognostic factors in fulminant hepatic failure.

One hundred thirty-seven patients with fulminant hepatic failure were entered into two controlled trials of charcoal hemoperfusion carried out concurrently. In trial A, 75 patients with grade 3 encephalopathy were randomized to receive 5 or 10 h of hemoperfusion daily. Overall survival rates for the two groups were similar (51.3% vs. 50.0%) as was the frequency of major complications including cerebral edema and renal failure. In trial B, in which 62 patients with established grade 4 encephalopathy on admission were randomized to a no-perfusion group or to have 10 h of hemoperfusion daily, overall survival rates for the two groups were again similar (39.3% and 34.5%, respectively). There was in both trials a significant relationship between survival and etiology quite independent of the use or duration of hemoperfusion. Thus, percentage survival for the acetaminophen-overdose cases was 52.9%, for hepatitis A 66.7%, for hepatitis B 38.9%, for presumed non-A, non-B hepatitis 20%, and for halothane or drug reaction 12.5%. Within the etiologic subgroups survival was also influenced by the three major complications that developed, being inversely related to their frequency and combination, except in the non-A, non-B hepatitis and halothane or drug reaction subgroups, which had a high mortality throughout. In the latter cases particularly, orthotopic liver transplantation merits early consideration and in the group with better "intrinsic" survival (acetaminophen, hepatitis A and B) intensive management of complications (rather than charcoal hemoperfusion) would appear to be of major importance.

Acetaminophen↗
PubMed1987

Renal function in fulminant hepatic failure: haemodynamics and renal prostaglandins.

Eighteen patients with fulminant liver failure were studied, 10 with normal renal function (group A) and eight with renal failure (group B, plasma creatinine greater than 200 mumol/l). Renal function was assessed by standard clearance techniques and patients in group B had a marked reduction compared with group A in both renal plasma flow and glomerular filtration rate. Raised plasma renin activity was observed in both groups, but levels in group B were significantly higher than in group A. Renal prostacyclin production was estimated by radioimmunoassay (RIA) of 6-keto-prostaglandin F1 alpha in urine, and the excretion rate was markedly increased in group A as compared with nine healthy controls, but was low in group B. The plasma concentrations of 6-keto-prostaglandin F1 alpha and thromboxane B2 were similar in groups A and B and were both significantly higher than in controls. Haemodynamic measurements showed a high cardiac output with low vascular resistance and mean arterial pressure within normal limits in both groups. The pulse pressure, however, was significantly higher in group B than in group A. In conclusion, patients in FHF with renal failure have marked renal vasoconstriction with increased plasma renin activity and reduced renal prostaglandin excretion indicative of an imbalance between vasoactive forces.

6-Ketoprostaglandin F1 alpha↗