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Biomedical subjects

W G Rector

Publications and source records attributed to W G Rector.

53 records · Page 3Linked to original sources
PubMed1985

Membranous obstruction of the inferior vena cava in the United States.

The pathogenesis of membranous obstruction of the inferior vena cava (MOVC) is unclear. Although the lesion is rare in the United States compared to Japan, India, and black South Africa, it has been responsible for 23% of cases of hepatic outflow obstruction we have encountered in the ethnically heterogeneous indigent population of Los Angeles. Most patients with MOVC are male. In contrast, recent series of patients with Budd-Chiari Syndrome (BCS) have demonstrated a female predominance. Compared to BCS without involvement of the inferior vena cava (IVC), patients with MOVC have more chronic symptoms. Large truncal collaterals, particularly on the back, strongly suggest MOVC. In patients without this sign, a high index of diagnostic suspicion is required. Chronic hepatitis B infection occurs with increased frequency in these patients. Chest radiograph may show an enlarged azygous shadow. Liver-spleen scan is not helpful, and the liver biopsy is frequently nondiagnostic. A useful screening procedure for hepatic outflow block is transhepatic portal pressure measurement demonstrating aberrant hepatic veins with pressures higher than in the portal vein and, occasionally, hepatofugal portal flow. Transcardiac membranotomy appears to be symptomatically effective in patients with MOVC and at least one patent hepatic vein. It is not known whether this operation will prolong life and prevent the development of hepatocellular cancer, which may occur in up to 48% of these patients. The correct therapeutic approach has not been established for those patients whose lesion is not amenable to surgery because of extensive IVC occlusion or absence of patent hepatic veins.

Adult↗
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

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

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

The significance of bloody ascites in patients with cirrhosis.

Five percent of cirrhotic patients with ascites in our unit have grossly bloody fluid. Eleven of 32 randomly selected retrospective patients had hepatocellular carcinoma, one tuberculous peritonitis, seven prior trauma, and in 13 the bloody ascites was apparently spontaneous. Five prospectively encountered patients brought the number of cases of spontaneous bloody ascites available for review to 18. Three of these had sudden large intraperitoneal hemorrhages, and bloody ascites in the remaining 15 was incidentally noted at routine diagnostic paracentesis. Bleeding in the former three patients was from a retroperitoneal vein, spontaneous splenic rupture, and an unknown site, respectively. All patients required laparotomy and two died. Ascites red cells in the latter 15 patients may have been from a slowly leaking collateral vein or a hepatic lymphatic and required no treatment. However, the prognosis of these patients was significantly poorer than that of a control group of patients with similar liver tests and clear ascites.

Adult↗
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

Spontaneous chylous ascites of cirrhosis.

The spontaneous development of chylous ascites in patients with cirrhosis is documented, but its clinical features are not well defined. The incidence of this complication of chronic liver disease was 0.5% in ascitic patients in our liver unit. These patients were older than a control group with nonchylous cirrhotic ascites and, despite better liver tests, appeared to have a higher diuretic requirement. Several had disabling, recurrent spontaneous encephalopathy. The mechanism of chylous ascites in cirrhosis is probably portal hypertension causing lymphatic rupture; however, the fact that serum-to-ascites albumin gradients were similar in the two groups, indicating similar degrees of portal hypertension, suggests that other factors also play a role. Spontaneous transformation of previously clear ascites appeared to be associated with a poor prognosis. In contrast, the appearance of chylous ascites de novo in a cirrhotic patient appeared to have a more favorable outcome. Conservative management is recommended for most patients, as the degree of their liver disease appears to be the most important factor determining prognosis.

Adult↗
PubMed1984

Direct transhepatic assessment of hepatic vein pressure and direction of flow using a thin needle in patients with cirrhosis and Budd-Chiari syndrome. An effective alternative to hepatic vein catheterization.

Portal pressure can be accurately measured transhepatically with a Chiba needle. Since 1980, we have used transhepatic hepatic vein pressures as our zero reference for transhepatic portal pressure measurements. To validate the latter technique, we performed hepatic vein catheterization and transhepatic hepatic vein puncture in 11 patients undergoing portal pressure measurement. Transhepatic hepatic vein puncture was simple, providing pressures as reproducible as those obtained by hepatic vein and inferior vena cava catheterization. These pressures were minimally higher than simultaneous free hepatic vein and inferior vena caval pressures, possibly reflecting the more proximal location of the small hepatic vein radicles often entered by this technique. Transhepatic hepatic vein puncture is an accurate way to determine hepatic vein pressure and, combined with transhepatic portal vein pressure measurement, completely obviates the need for venous catheterization for portal pressure determination. Transhepatic hepatic vein pressure was also measured in 3 patients with Budd-Chiari syndrome. In these patients, transhepatic hepatic vein pressure was elevated and equaled or exceeded portal vein pressure. Abnormal venous collaterals were identified in all patients. Transhepatic portal pressure studies are also an appropriate way to evaluate patients suspected of having hepatic outflow obstruction.

Blood Pressure Determination↗
PubMed1982

Nonketotic hyperglycemia appearing as choreoathetosis or ballism.

A number of focal neurologic abnormalities may accompany severe, nonketotic hyperglycemia, but extrapyramidal movement disorders have not previously been described. We evaluated the conditions of three patients with marked hyperglycemia in whom hemichorea or ballism developed that resolved completely with normalization of the blood glucose level. Potential pathogenetic mechanisms include relative dopaminergic hypersensitivity, impaired synthesis of acetylcholine or gamma-aminobutyric acid, or an undefined effect of hyperosmolarity, perhaps unmasking a previously subclinical lesion of the basal ganglia. Serum glucose level should be determined in anyone with the new onset of choreoathetosis or ballism, as hyperglycemia is a rapidly reversible cause of these conditions.

Aged↗
PubMed1981

Fever, shock and chills in gram-negative bacillemia: clinical correlations in 100 cases.

Patterns of fever, shock, and chills in 100 episodes of febrile, Gram-negative bacillemia were retrospectively analyzed to determine features predictive of the site of infection, organism, and prognosis. Pneumonias most often produced morning temperature rises, whereas infections in other sites were usually associated with an afternoon or evening peak. Peritonitis (usually due to Bacteroides fragilis) tended to cause an indolent temperature rise (over a day or more), whereas pyelonephritis and cholangitis typically produced an abrupt "spike." Relatively low fevers characterized Enterobacter pneumonias while very high fevers were noted in Pseudomonas aeruginosa infections in patients with leukemia. Chills occurred with unusually high frequency in cholangitis and in Klebsiella bacteremia. Patients going into shock had higher fevers than those who did not. More importantly, the development of shock was shown to be related to severity of underlying disease. Shock never developed if the disease was not serious, unless the bacteremia was caused by instrumentation, but occurred in 73% of patients with leukemia or lymphoma. The clinical setting, pattern of fever, and presence or absence of a chill can in many cases usefully guide diagnosis and therapy in patients with Gram-negative bacillemia.

Adult↗
PubMedDate not supplied

Tubular dysfunction in the deeply jaundiced patient with hepatorenal syndrome.

We examined beta 2-microglobulin (B2MG) excretion, an index of tubular function, in patients with hepatorenal syndrome, in whom tubular function is generally regarded as normal. Urine B2MG was significantly higher in these patients than in control patients with normal serum creatinine concentration. Patients with high urine B2MG concentration had markedly higher serum bilirubin than did patients with normal values (31 +/- 3 vs. 10 +/- 8 mg%, p less than 0.001), whereas prothrombin activity, serum albumin and serum B2MG concentration were similar. A "threshold" serum bilirubin concentration of about 23 mg% differentiated patients with normal and high urine B2MG values. Renal morphology at autopsy was unremarkable in both groups. Tubular dysfunction, manifested by increased urinary excretion of B2MG, occurs in patients with hepatorenal syndrome and deep jaundice. This measurement cannot, therefore, be used to make a diagnosis of acute tubular injury, as due to aminoglycosides, in such patients.

Bilirubin↗
PubMedDate not supplied

Hepatofugal portal flow in cirrhosis: observations on hepatic hemodynamics and the nature of the arterioportal communications.

Six of 85 patients (7%) with alcoholic liver disease undergoing transhepatic portal pressure measurement had either stagnant (3 patients) or reversed (3 patients) portal blood flow documented by gentle hand injection of 1 to 2 ml of angiographic contrast. Portal blood flow was uniformly hepatopetal in 24 patients with nonalcoholic liver disease. Recurrent spontaneous hepatic encephalopathy and sodium retention occurred in 4 of 6 patients with stagnant or reversed portal flow; gastrointestinal bleeding was not seen. Standard laboratory tests of liver function were widely variable. Net portal pressure was lower in this group than in patients with alcoholic liver disease and forward portal flow (9.2 +/- 2.6 vs. 15.6 +/- 4.1 mm Hg, p less than 0.001). Wedged hepatic vein pressure was 1 to 7 mm Hg higher than portal vein pressure in patients with reversed portal flow. The arterioportal extraction of bile acid was calculated from the difference in concentration between artery and portal vein, and total functional hepatic blood flow was calculated from the hepatic extraction and systemic clearance of indocyanine green. Extraction was 0%, and hepatic blood flow was 0.469 liter per min in a patient with hepatofugal portal flow and recurrent encephalopathy. Extraction was 20%, and hepatic blood flow was 4.014 liters per min in a patient who had never had encephalopathy. These data indicate that arterioportal communications may be sinusoidal or presinusoidal in patients who lose forward portal flow and that the amount of flow in the arterioportal circuit, together with its efficiency, largely determine the clinical outcome.

Collateral Circulation↗
PubMedDate not supplied

Utility and limitations of splanchnic venous ultrasonography in diagnosis of portal hypertension.

The splanchnic venous system was examined by real-time ultrasonography in 46 patients with cirrhosis and documented portal hypertension and in 32 healthy subjects. Patients with portal hypertension had increased diameter of the splanchnic (portal, splenic, and superior mesenteric) veins (76% of patients), attenuation of the normal inspiratory increase in vein size (59%), and demonstrable portasystemic collateral vessels (umbilical or coronary veins or spontaneous splenorenal shunt) (44%). Splanchnic venous dimensions were significantly increased and changed less with respiration in patients with demonstrable portasystemic collaterals as compared to patients without these vessels. Portal pressure correlated only mildly with portal vein diameter (r = 0.30, p less than 0.05). Ultrasound abnormalities are present in a majority of patients with intrahepatic portal hypertension. However, because increased venous diameter and attenuated change in diameter with respiration are less frequent in patients lacking demonstrable portasystemic collaterals, the sensitivity of the test is least in those patients in whom its specificity is also limited.

Humans↗
PubMedDate not supplied

Pica: its frequency and significance in patients with iron-deficiency anemia due to chronic gastrointestinal blood loss.

PURPOSE: Pica, particularly ice-eating (pagophagia), is a recognized symptom of iron deficiency. The value of pica as a clue to the etiology of blood loss has never been studied. PATIENT POPULATION: Fifty-five unselected patients with iron-deficiency anemia due to gastrointestinal blood loss evaluated by a gastroenterology referral service at a city hospital. RESULTS: The patients' mean hematocrit was 26 +/- 15% (SD). Thirty two (58%) had pica, and in 28 (88%) it manifested as pagophagia. Pica was present significantly more often in women (19/32, 68%) than in men (9/23, 39%, p less than 0.05). Pica occurred less frequently in patients with malignancy (2/9 vs. 30/46), but this difference was not significant. CONCLUSION: Pica, a frequent symptom in patients with iron-deficiency anemia due to gastrointestinal blood loss, particularly women, is not of value in predicting the cause of bleeding.

Adult↗
PubMedDate not supplied

Serum magnesium and copper levels in myocardial infarction.

The serum levels and urinary excretion of magnesium and copper were studied in 66 patients with either acute myocardial ischemia or myocardial infarction. Serum for magnesium and copper determinations was obtained daily for three days. The initial serum magnesium levels were normal in patients with ischemia but were low in some patients with myocardial infarction. Patients developing ventricular arrhythmias with myocardial infarction showed the lowest levels of serum magnesium. Copper in the serum appeared elevated in patients developing acute congestive heart failure but the elevation was not statistically significant. These data indicate that a decrease in serum magnesium as evaluated may be associated with ventricular arrhythmias in patients with myocardial infarction; thus continued observations of magnesium levels in the myocardial infarction patient is warranted.

Arrhythmias, Cardiac↗