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T B Reynolds

Publications and source records attributed to T B Reynolds.

At least 55 records · Page 3Linked to original sources
PubMed1985

Risk factors for haemorrhage from oesophageal varices and acute gastric erosions.

Rupture, versus erosion, is the most likely cause of variceal bleeding. The risk of rupture appears to be enhanced in large varices and varices with reddish discoloration. Incompetent perforating veins connecting varices to deeper venous systems may also be important in the pathogenesis of this event. Perhaps one-third of patients with large varices will bleed from them over a period of one to two years. Portal hypertension cannot be used to predict the future risk of bleeding among groups of patients. Nevertheless, it is possible that increases or decreases in portal pressure in individual patients may alter their bleeding risk. We and others have observed portal pressure as low as 10 mmHg in patients with clear-cut, recurrent variceal bleeding. Portal hypertension probably predisposes to gastric mucosal injury by enhancing, by an undefined mechanism, back-diffusion of acid. Consequently, haemorrhagic gastritis is more common in patients with portal hypertension than those without. Whether haemorrhagic gastritis is a more severe lesion in patients with portal hypertension is unclear.

Acute Disease↗
PubMed1984

Impaired renal acidification in alcoholic liver disease.

The prevalence of impaired renal acidification in alcoholic liver disease and its relationship to clinical and biochemical features were evaluated during a one-year period in a 60-bed liver unit. No cases of overt renal tubular acidosis (RTA) were found; all of 12 patients with low serum bicarbonate values and normal anion gap proved to have chronic respiratory alkalosis. However, there was a 57% prevalence of incomplete distal RTA in 42 patients who were tested with an acid load. Subjects with RTA had higher serum bilirubin levels (5.3 +/- 6.1 v 2.1 +/- 2.7 mg/dL) and lower prothrombin times (45% +/- 22% v 64% +/- 20%). Urinary pH correlated directly with serum bilirubin levels (r = +.38) and inversely with prothrombin times (r = -.46). The frequency of ascites and encephalopathy did not differ notably between the two groups of patients. No pathogenetic relation was observed with avid sodium retention, decreased excretion of nonreabsorbable anions, and elevated urinary excretion of bile acids. Therefore, we conclude that impaired renal acidification in alcoholic liver disease may be a sign of liver cell failure since it is more frequently observed in patients with a greater degree of liver dysfunction.

Acid-Base Equilibrium↗
PubMed1984

Superiority of the serum-ascites albumin difference over the ascites total protein concentration in separation of "transudative" and "exudative" ascites.

The serum-ascites albumin difference, an index of the serum-ascites oncotic pressure difference, correlates directly with the pressure gradient between the portal capillaries and the peritoneal cavity. This test was compared with the ascites total protein concentration in the separation of "transudative" and "exudative" ascites. The serum-ascites albumin difference was large in patients with transudative ascites (1.6 +/- 0.5 g/dl) and small in patients with exudative ascites (0.6 +/- 0.4 g/dl, p less than 0.001) and provided significantly better discrimination of these categories than did the ascites total protein concentration. The serum-ascites albumin difference was especially useful in the separation of cardiac ascites, which usually has a high total protein concentration, from high protein exudative ascites. The serum-ascites albumin difference did not provide perfect discrimination of any category, however; in patients with mixed causes of ascites, this difference tended to be large, resembling ordinary transudative ascites, a potential source of diagnostic error. Nevertheless, the serum-ascites albumin difference has superior discriminatory power and should replace the ascites total protein concentration in the routine diagnostic examination of ascites.

Ascites↗
PubMed1984

Idiopathic fatty liver of pregnancy: findings in ten cases.

Ten cases of fatty liver of pregnancy are reported from a large metropolitan medical center for the period 1972 to 1982. Compared to earlier reports, a marked decrease in both maternal and fetal mortality was noted (1 mother died and 2 of 12 infants were stillborn). Eight other cases obtained from liver biopsies referred from other hospitals were also reviewed and combined mortality data were similar. Since delivery was spontaneous in 8 of our 10 patients, the lower mortality cannot be attributed to early delivery. Instead, we ascribe it to improved supportive therapy with transfusions, clotting factors, antibiotics, glucose and monitoring. Also, earlier reports emphasized autopsy material. The incidence of FLP was 1 per 13,328 deliveries in a predominantly Hispanic population. Our review yielded new data concerning presenting signs and symptoms, laboratory features including serial clotting screens documenting disseminated intravascular coagulation (DIC), obstetric and perinatal information as well as maternal follow-up.

Adolescent↗
PubMed1984

Fulminant hepatic and renal failure complicating Wilson's disease.

We report a case of fatal fulminant liver failure complicating Wilson's disease that is unique in several respects. The illness supervened after several years of medical noncompliance in a patient who had been previously diagnosed and successfully treated with penicillamine. Re-institution of penicillamine therapy 2 weeks prior to the fulminant decompensation failed to prevent it. Renal failure in this patient was apparently secondary to rhabdomyolysis. Addition of penicillamine to a peritoneal dialysis solution allowed chelation and removal of over 14 mg per day of copper but without apparent benefit. Exchange transfusion and high dose dexamethasone therapy (24 mg/day) were equally ineffective in reversing the liver failure. Other reported cases have also been fatal. The best treatment for fulminant Wilson's disease is prevention by diagnosis in a pre-symptomatic stage and institution of carefully supervised life-long therapy with penicillamine.

Acute Kidney Injury↗
PubMed1984

Propranolol in the treatment of cirrhotic ascites.

Propranolol hydrochloride is reported to lower portal pressure and inhibit renin secretion in patients with chronic liver disease, actions that might lessen the tendency to ascites formation. We compared the effect of diuretics with that of the same dose of diuretics plus propranolol on natriuresis, urine output, and daily weight loss in 13 hospitalized patients with stable chronic liver disease, sodium retention, and ascites. The propranolol hydrochloride dose was 20 to 160 mg four times a day, titrated to reduce resting pulse by 25% or systolic BP 10 mm Hg. Diuretics given were furosemide, 80 to 160 mg, and triamterene, 100 or 200 mg/day. Periods of time when each regimen was received ranged from one to four days. Creatinine excretion documented complete urine collections. Compared with diuretics alone, diuretics plus propranolol substantially reduced resting pulse, systolic BP, and urine sodium excretion, although not creatinine clearance. This antinatriuretic effect may limit the proposed usefulness of propranolol for prevention of variceal bleeding in patients with cirrhosis and ascites.

Ascites↗
PubMed1984

Mechanism for the abnormal liver scan in acute alcoholic liver injury.

The mechanism of liver scan abnormality was investigated in patients with acute alcoholic liver injury evaluated shortly after admission (18 patients) with repeat examination 1 month later (14 patients). Indocyanine green (ICG) and Tc99 sulfur colloid extraction ratios (ERICG and ERSC), elimination rate constants (KICG and KSC), total body clearance (TBCICG and TBCSC), and hepatic clearance of sulfur colloid (HCSC) were determined from sequential blood samples obtained at the time of hepatic vein catheterization after the intravenous injection of ICG and Tc99 sulfur colloid. Liver size and sulfur colloid redistribution expressed as a scan score (SS) and redistribution ratio (RR) were assessed from an external scan immediately after the procedure. Improvement in hepatic tests and function was noted between the first and second study. At both the first and second study, the SS (or RR) correlated with the hepatic removal of sulfur colloid (ERSC; r = -0.59; p less than 0.001; HCSC: r = -0.56; p = 0.003) and ICG (ERICG: r = -0.85; p less than 0.001; KICG: r = -0.83; p less than 0.001). ERSC correlated with ERICG (r = 0.76; p less than 0.007) and both correlated with SS and RR consistent with intrahepatic shunting as the mechanism of decreased hepatic clearance and of sulfur colloid redistribution. However, the systemic clearance of sulfur colloid (KSC) did not correlate with redistribution (SS: r = -0.25; NS) at either study period or to ICG clearance (r = 0.23; p = NS) in the first period. The KSC/KICG ratio in both study periods correlated with serum bilirubin (r = 0.83; p less than 0.001 and r = 0.73; p less than 0.001), but was significantly higher in the first period (3.37 +/- 2.37 versus 2.00 +/- 0.75; p less than 0.01). This lack of correlation between intrahepatic shunting and systemic clearance of sulfur colloid is consistent with an increase in the nonhepatic clearance of sulfur colloid in patients with alcoholic liver injury and deep jaundice. A decrease in liver size between the first and second study correlated inversely with change in portal pressure (r = -0.67; p = 0.004) and SS (r = -0.49; p = 0.038) and directly with change in KICG (r = 0.48; p = 0.04). By virtue of these relationships, redistribution of Tc99 sulfur colloid by liver scan may have prognostic significance in patients with alcoholic liver disease.

Acute Disease↗
PubMed1984

A new method for the measurement of intrahepatic shunts.

After transhepatic portal pressure determination, 96 patients were assessed for the presence of intrahepatic shunts by injection of microspheres (25 +/- 5 micron diameter) into the portal vein using RISA-131I as an indicator of dilution. Multiple portal vein injections in each patient allowed blood sampling from the hepatic vein (site 1) and from two inferior vena cava sampling sites (site 2, at the junction of the hepatic vein orifice with the inferior vena cava, and site 3, 2 to 3 cm closer to or within the right atrium). Intrahepatic shunting was calculated from each site: hepatic vein in 57 patients and inferior vena cava, site 2 in 43 patients and site 3 in 77 patients. At least one valid IHS calculation was available in 92 of the patients. Intrahepatic shunting calculated from sequential portal vein injections with sampling from the hepatic vein was highly correlated (r = 0.98, p less than 0.0001, slope = 1.0), with a mean difference of 1.9% +/- 1.9%. There was no significant difference by t test comparison of the mean IHS calculated from sites 1, 2, and 3. The IHShv was correlated with the IHSivc (site 2) (r = 0.79, p less than 0.0001, slope = 1.0) and IHSivc (site 3) (r = 0.82, p less than 0.0001, slope = 2.1). Occasional marked discrepancies were noted between IHS calculated from site 1 or site 2 compared with site 3, and the site 3 calculation was always greater. A shunt index in all patients included shunts calculated from the hepatic vein in 57 patients plus shunt calculation from the inferior vena cava in the remaining patients (site 2 in 26 patients and site 3 in nine). A control group with minimal chronic liver disease (10 patients) had a portal pressure (greater than IVC) of 4.1 +/- 1.4 mm Hg and shunt index of 0.5% +/- 0.6%. The 82 patients with portal hypertension or chronic liver disease had a higher portal pressure, 13.8 +/- 4.6 mm Hg, and a significantly greater shunt index, 13.7% +/- 24.5% (p less than 0.0001) compared with controls. The frequency distribution of IHS in patients with chronic liver disease demonstrated less than 2% IHS in 49% of patients and less than 5% IHS in 63%. The validity of our methods and the implications of the infrequent demonstration of a large IHS are discussed.

Hepatic Veins↗
PubMed1982

Double-blind, controlled trial of propylthiouracil in patients with severe acute alcoholic hepatitis.

Sixty-seven patients entered a double-blind, controlled trial to evaluate the efficacy of propylthiouracil treatment in severe alcoholic hepatitis. Twenty-three percent (7 of 31) given propylthiouracil and 19% (7 of 36) given placebo died during the 6-wk study. Propylthiouracil treatment did not reduce the frequency and incidence of complications in alcoholic hepatitis, but induced hypothyroidism in 4 patients. Treatment produced no beneficial effect on any of the hepatic biochemical tests. We were unable to show any beneficial effect of propylthiouracil treatment on morbidity and mortality in patients with severe acute alcoholic hepatitis.

Adult↗
PubMed1981

Spontaneous portosystemic shunt: relationship to spontaneous encephalopathy and gastrointestinal hemorrhage.

This study examined the effect of large spontaneous portosystemic shunts on the incidence of variceal hemorrhage and hepatic encephalopathy. Twenty cases of chronic liver disease with large spontaneous shunts were compared with a group of patients with liver disease and with Cruveilhier-Baumgarten (C-B) murmurs and with a control group having liver disease and absence of large shunts on angiography. Gastrointestinal hemorrhage was present in similar proportions of patients in the three groups. Hepatic encephalopathy occurred more frequently in the spontaneous shunt group and C-B murmur group. The encephalopathy was spontaneous in 12 of 14 patients with large natural shunts whereas it was precipitated by events such as gastrointestinal bleeding, diuretics, or infection in 14 of 15 of the patients with C-B murmur and five of the seven controls. Therefore, spontaneous portosystemic shunts do not protect against gastrointestinal hemorrhage and are associated with an increased risk of spontaneous hepatic encephalopathy.

Adolescent↗
PubMed1981

Left pleural effusion in patients with chronic liver disease and ascites. Prospective study of 22 cases.

In a prospective study of 22 cases of left pleural effusion in patients with chronic liver disease and ascites, 16 patients underwent thoracentesis, revealing ten transudates, considered to be hepatic hydrothorax, and six exudates, four of which turned out to be due to tuberculosis. Unilateral left pleural effusion is rare in chronic liver disease with ascites, but if present it is associated with a high incidence of pleuropulmonary tuberculosis (18%).

Adult↗
PubMed1981

Results of a 12-year randomized trial of portacaval shunt in patients with alcoholic liver disease and bleeding varices.

During a 7-yr period (1967-1974), 89 patients with alcoholic liver disease and at least one severe upper gastrointestinal hemorrhage thought to be from esophageal varices entered a randomized, controlled trial of medical therapy vs. end-to-side portacaval shunt. Follow-up continued to September, 1979, so that all surviving patients had at least 5 yr observation after randomization. Among 45 patients randomized to surgical therapy, 4 did not receive portacaval shunt, for various reasons. Among shunted patients there were 11 episodes of upper gastrointestinal bleeding, none fatal and none thought to be from esophageal varices. Thirty-seven percent of eligible patients have had moderate or severe hepatic encephalopathy ascribed to the shunt. Of 44 patients randomized to medical therapy, 7 eventually received portacaval shunt after multiple bleeding episodes. Since randomization there have been 190 episodes of bleeding requiring 589 transfusions and resulting in 23 deaths from bleeding or hepatic failure precipitated by bleeding. THere are 12 survivors in the surgically treated group and 8 in the group treated medically. Life-table analysis shows a small increase in survival in the surgically treated group throughout the study, which is not statistically significant. From our data, we could not identify risk factors that would improve the selection of patients for medical or surgical therapy.

Adult↗
PubMed1981

Ascites.

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Ascites↗