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Biomedical subjects

J T Fulenwider

Publications and source records attributed to J T Fulenwider.

36 records · Page 2Linked to original sources
PubMed1981

Hemodynamics of LeVeen shunt pulmonary edema.

In order to characterize the circulatory changes which may lead to pulmonary edema following the surgical placement of a LeVeen peritoneovenous shunt, intraoperative hemodynamic studies were performed on five consecutive patients without clinical evidence of cardiac disease undergoing shunt insertion. Within 30 minutes after opening the peritoneovenous shunt, there was a marked increase in pulmonary capillary wedge pressure, cardiac output, and stroke work index, and a sharp decline in both pulmonary and systemic vascular resistances. In three patients, pulmonary edema did not occur; in one patient, pulmonary edema occurred transiently but responded to furosemide administration. In these four patients, systemic vascular resistance continued to drop over the ensuing hours and the elevated pulmonary capillary wedge pressure also decreased appropriately with furosemide. The fifth patient developed persistent pulmonary edema. In this subject, systemic vascular resistance continued to rise and the elevated pulmonary capillary wedge pressure did not respond to intravenous furosemide. This study suggests that uncomplicated LeVeen peritoneovenous shunt insertion may result in a drop in systemic vascular resistance which lowers left ventricular afterload, and, thus, may protect most patients from pulmonary edema. In contrast, a continued rise in systemic vascular resistance and afterload may contribute to pulmonary edema refractory to diuretic therapy and should probably be treated with a parenteral afterload-reducing agent.

Ascites↗
PubMed1981

Accelerated fibrinogen and platelet destruction after peritoneovenous shunting.

Peritoneovenous shunting with the LeVeen valve is generally recognized as an effective procedure for the treatment of intractable ascites and renal failure associated with severe liver disease. We recently observed a generalized hemorrhagic diathesis in patients receiving these valves. To investigate the mechanism of this hemorrhagic complication, we prospectively performed kinetic studies with 51Cr-labelled platelets and 125I-labelled fibrinogen in ten patients. When results of studies before and after valve insertion were compared, the following reductions were noted: fibrinogen concentration, 55%; the fibrinogen survival, 49%; the platelet count, 55% and the platelet survival, 35%. No endotoxin was detectable in ascitic fluid preoperatively, and there was no apparent relationship between ascitic fluid cell counts and changes in fibrinogen and platelet survival. Until the component or components of ascitic fluid responsible for accelerated consumption can be identified and steps are taken to modify the rates of platelet and fibrinogen consumption, it would seem prudent to select patients for surgery conservatively.

Ascites↗
PubMed1980

Endotoxemia of cirrhosis: an observation not substantiated.

Physiologic similarities between cirrhotic and septic patients have implicated systemic endotoxemia as a possible mediator of the hemodynamic, neurologic, and hematologic complications observed in patients with cirrhosis of the liver. The recently reported high prevalence of endotoxin in ascites, as well as in portal and systemic plasma, has further incriminated endotoxin of gut origin as the responsible agent. Limulus amebocyte lysate tests were performed upon peripheral plasma of 38 cirrhotic patients; portal plasma and ascites were assayed in 14 and 11 of these patients, respectively. No endotoxin was detectable. We believe that the ubiquity of endotoxin, with the attendant opportunities for specimen contamination, is the most likely explanation for the recently reported high prevalence of endotoxin in the plasma and ascites of cirrhotic patients.

Adult↗
PubMed1979

Portal pseudoperfusion: an angiographic illusion.

Much confusion regarding the hemodynamics following interposition mesosystemic shunts prevails. Many authorities have claimed that portal venous perfusion continues following interposition mesocaval shunts. In 1971, a prospective, randomized trial comparing the distal splenorenal shunt with a variety of interposition mesosystemic shunts (primarily mesocaval or mesorenal) was begun. Visceral angiography was utilized to assess the early and late postoperative hemodynamic changes following both selective and nonselective shunts. None of the patients with patent interposition shunts retained portal perfusion present preoperatively. Searching for an explanation for this hemodynamic discrepancy, we examined two patients of the randomized trial angiographically. Both patients had excellent portal perfusion preoperatively, yet following interposition shunting (one mesocaval and one splenocaval), neither maintained portal perfusion of the liver. Celiac artery injections produced opacification of the entire splenoportal axis; however, it is shown that such portal venous opacification occurred in a retrograde direction by selective hepatic arterial injections demonstrating hepatofugal portal venous flow. Additionally, two nonrandomized patients received interposition mesorenal shunts and exemplify this phenomenon, entitled "portal pseudoperfusion". The explanation for conflicting literature reports lies in the misinterpretation of venous phase celiac and non-selective SMA arteriography in determining the direction of portal flow. A narrative of preoperative and postoperative angiograms of four patients will clarify the mechanism of "portal pseudoperfusion" and demonstrate that interposition shunts totally siphon portal venous perfusion. Clues to the detection and techniques to avoid this phenomenon will be presented.

Adult↗
PubMed1979

Tyramine kinetics and metabolism in cirrhosis.

Hypertyraminemia is common in hepatic cirrhosis and correlates in severity with encephalopathy. The mechanism of cirrhotic hypertyraminemia has not been established. The alternative possibilities are increased production from tyrosine and impaired degradation by monoamine oxidase. This investigation determined the pharmacokinetics of tyramine after an intravenous bolus injections of [3H]-tyramine (180--200 muCi 12 Ci/mmol sp act) in 13 cirrhotics and 9 controls. In normals, [3H]tyramine levels initially declined rapidly (alpha-phase) followed by a slower decline (beta-phase) with an average t 1/2 of 20.8 min. Average normal metabolic clearance rate and production rate were 13.2 liters/min and 15.4 microgram/min, respectively. In cirrhotic patients, the plasma disappearance curve for [3H]tyramine was qualitatively similar to that of the control subjects with no apparent different in beta-t 1/2 (17.2 min). The hypertyraminemia of cirrhosis resulted primarily from overproduction of tyramine, as the production rate (32.0 microgram/min) in these patients was significantly greater (P less than 0.05) than in controls, whereas the metabolic clearance rate remained normal (average 12.2 liters/min). A difference in ratio of tyramine metabolic products was noted as well. Cirrhotics had a high ratio of plasma 4-hydroxyphenylethanol:4-hydroxyphenylacetic acid (60:40 vs. 30:70) as compared with normals. Although the tyramine clearance rates are similar in normals and cirrhotics, different mechanisms may be responsible for catabolism.

Adult↗
PubMed1979

Hyperalimentation in alcoholic hepatitis.

Enteral hyperalimentation in four patients with severe alcoholic hepatitis and anorexia increased spontaneous food intake, increased their nitrogen balance and the patients improved clinically. Seven patients with alcoholic hepatitis, who were clinically ill and able to eat only 410-1,100 calories per day, were given a 900 mosM/l. parenteral "hyperalimentation" solution by a peripheral vein (P-900). The intravenous nutrition provided daily 51.6-77.4 gm. amino acids in addition to oral intake. All patients improved. None developed detectable encephalopathy after 16-42 days of P-900 therapy. Five additional patients had ascites and alcoholic hepatitis. The daily infusion of 2,000 ml. P-900 was not associated with hyponatremia, renal failure or encephalopathy in four of these five patients who improved and continued their diuresis. P-900 therapy was discontinued in one because of progressive hyponatremia. The observations indicate that over and above the maximum tolerable oral nutrition, intravenous nutrition can be effectively utilized by clinically ill, jaundiced patients with alcoholic hepatitis without precipitating encephalopathy or interference with standard therapy of ascites.

Hepatitis, Alcoholic↗
PubMed1979

Tyrosine metabolism in cirrhosis.

The aim of this study was to define the enzyme defect responsible for tyrosinemia in cirrhotic patients. The principal hepatic degradation pathway for tyrosine, tyrosine leads to p-hydroxyphenylpyruvic acid equilibrium homogentisic acid leads to CO2 was studied in 18 cirrhotic patients and eight controls. The classic method employed in elucidation of hereditary tyrosinosis was sued. Metabolic intermediates on the pathway were measured in the basal state, and following oral loading doses (50 mg/kg BW) of tyrosine, PHPA, and homogentisic acid. Cirrhotic patients showed a significant increase (p = 0.005) in fasting plasma tyrosine and in basal PHPA excretion and impaired tolerance to all three metabolites when compared to normals. Fifteen of the 18 cirrhotic patients showed tyrosine intolerance which was not accompanied by change in distal metabolites compared to their basal levels. Nevertheless 13 of the 18 did exhibit intolerance of either PHPA or homogentisic acid. We conclude that in contrast to the single complete defect in hereditary disorders of tyrosine metabolism, cirrhotic patients have partial defects at tyrosine transaminase, PHPA oxidase, and homogentisic acid oxidase, the initial step being rate-limiting.

Adult↗
PubMed1978

Splenic artery ligation in distal splenorenal shunts.

Splenic artery ligation, a simple surgical procedure expected to decrease splenic flow and portal pressure in patients with cirrhosis of the liver, was performed concomitantly with a distal splenorenal shunt procedure in six patients and as the main surgical procedure in two patients. Immediate cessation of bleeding was achieved in the four patients in whom the splenic artery was ligated to reduce intraoperative bleeding. However, three of the seven patients with previous gastroesophageal hemorrhage rebled from various postoperatively. Symptoms of splenic infarction were observed in six patients, resulting in thrombosis of the splenic vein and/or of the distal splenorenal shunt in four patients and necessitating splenectomy in one. This incidence of thrombosis of the distal splenorenal shunt is much higher than the overall incidence of 5 per cent observed at our institution. It is thus concluded that the splenic artery should not be ligated in cirrhotic patients with patent distal splenorenal shunts, since splenic arterial collateral vessels have already been reduced by the gastric devascularization, an integral component of the distal splenorenal shunt.

Adolescent↗
PubMed1978

A randomized, controlled trial of the distal splenorenal shunt.

In 1971 a prospective, randomized trial was initiated to determine efficacy of the distal splenorenal shunt in the management of cirrhotic patients who had previously bled from esophageal varices. When entry into the trial was terminated in 1976, 26 patients had received the distal splenorenal shunt (selective) and 29 had undergone a nonselective shunting procedure (18 interposition mesorenal, six interposition mesocaval, and five other nonselective shunts). Three operative deaths occurred in each group. Early postoperative angiography revealed preservation of hepatic portal perfusion in 14 of 16 selective patients (88%), but in only one of 20 nonselective patients (5%; p < .001). Quantitative measures of hepatic function (maximal rate of urea synthesis or MRUS and Child's score) were similar to preoperative values in the selective group but were significantly decreased in nonselective patients on the first postoperative evaluation (p < .001 for MRUS; p < .05 for Child's score). Eighty-seven per cent of selective and 81% of nonselective patients have now been followed for three to six years since surgery. Late postoperative evaluation of 29 survivors (12 selective, 17 nonselective) still shows an advantage to the selective group with respect to MRUS, Child's score, and incidence of hepatopetal portal blood flow, but differences are no longer statistically significant. However, if the seven patients with portal flow (five selective; two nonselective) are compared to the 20 with absent portal flow (seven selective; 13 nonselective), the former group has significantly higher values for MRUS (p < .05) and Child's score (p < .025). No patient with continuing portal perfusion has developed encephalopathy as compared to a 45% incidence of this complication in individuals without portal flow (p < .05). No significant differences between selective and nonselective groups have appeared with respect to total cumulative mortality (ten selective; 38%; eight nonselective, 28%), shunt occlusion (two selective, 10%; five nonselective, 18%), or recurrent variceal hemorrhage (one selective, 4%; two nonselective, 8%). Overall, significantly fewer selective patients have developed postoperative encephalopathy (three selective, 12%; 15 nonselective, 52%; p < .001). Therefore, we conclude that the distal splenorenal shunt, especially when its objective of maintaining hepatic portal perfusion is achieved, results in significantly less morbidity than nonselective shunting procedures.

Alcoholism↗
PubMed1977

Renal decapsulation in the prevention of post-ischemic oliguria.

The delayed onset of anuria/oliguria in acute tubular necrosis has been theorized to represent a complicating compartment syndrome, i.e., parenchymal swelling within an unyielding capsule. To test this proposition, 12 monkeys had suprarenal aortic cross-clamping, followed by unilateral renal decapsulation to create an experimental as well as a control kidney unit in the same animal. Histologic examination uniformly confirmed tubular necrosis at death or sacrifice. Subsequent split renal function studies (creatinine, urea, and free water clearances) indicated significantly greater maintenance of renal function by the decapsulated kidney than by its paired control. Clinical evaluation in 21 hemorrhagic shock patients, with the capsule of one kidney stripped, revealed on follow-up that 15 developed a renal failure consistent with acute tubular necrosis. Although three patients with polyuric failure died before split studies could be run and two others have been too recent for computer analysis to have been completed, nine of the remaining ten had significantly greater renal plasma flows (194 versus 121 ml/min M(2), p < .01) and significantly greater urine flows (.99 versus .18 ml/min M(2), p < .01) on the decapsulated side than on the control, as determined by differential renal scans. No significant difference in these same lateralized renal functions was noted in the tenth patient with renal failure and in the six survivors without renal failure. Renal decapsulation as prophylaxis reduced the anticipated incidence of oliguria/anuria from an expected 75% to 7% (p < .01) in these 21 shock patients. Such data suggest that delayed renal ischemia, possibly based on a compartment syndrome, may be the cause for a progression of acute tubular necrosis from polyuria to oliguria and then to anuria.

Adolescent↗
PubMed1976

Wringer arm injuries.

During a 20-yr period, 483 children 16 yr of age or under were hospitalized for management of a wringer arm injury. Although the majority were indigent, black males, such trauma was frequently sustained by all classes and races as well as by both sexes. Principles of treatment consisted of cleansing the abrasion wound, application of a pressure dressing from axilla to finger tips, elevation, and close observation. With the exception of a destroyed brachial vein in one patien, significant vascular injuries did not occur despite a "medical fixation" on evidences of impaired circulation. Likewise, no fractures were noted even though all patients had x-rays of the full extremity. However, there were six metacarpophalangeal dislocations, five instances of neuropathy, and one traumatic amputation. Major skin sloughs occurred in 18 children, yet only 11 of them required a skin graft.

Accidents, Home↗
PubMedDate not supplied

Descending thoracic aortofemoral-femoral bypass: a remedial alternative for the failed aortobifemoral bypass.

The patient with densely scarred retroperitoneum, multiple previous celiotomies, failed remedial retroperitoneal aortobifemoral graft or multiple extra-anatomic graft failures presenting with limb-threatening ischemia taxes the ingenuity of the most experienced vascular surgeon. Lower extremity revascularization, in these situations, is dependent upon achieving adequate femoral arterial inflow. One remedial alternative method to achieve this goal is the descending thoracic aortofemoral-femoral bypass (DTAF-F). The authors' experience with three recent patients requiring DTAF-F is described, and literature of similar alternative techniques is reviewed.

Aorta, Abdominal↗
PubMedDate not supplied

Deranged tyrosine metabolism in cirrhosis.

In normal individuals, the main route for tyrosine degradation is the hepatic pathway tyrosine→4-hydroxyphenylpyruvic acid→homogentisic acid→CO(2). Quantitatively minor pathways, in large part extrahepatic, are: tyrosine→tyramine→octopamine and tyrosine→dopa→catecholamines.In cirrhosis, the main hepatic pathway is blocked to varying degrees at the first three stages. This appears to be due to lack of activity of the enzymes tyrosine transaminase, PHPA oxidase, and HGA oxidase, the first step being rate limiting. Hypertyrosinemia and tyrosine intolerance result.With the main hepatic pathway partially blocked, an abnormally large amount of tyrosine passes into the normally minor extrahepatic pathway leading to the false neurotransmitters tyramine and octopamine. Overproduction of these amines ensues and they accumulate in the body fluid.The false neurotransmitters can displace catecholamines from their storage sites in the peripheral and central nervous system, and thereby disrupt adrenergic processes in arterioles, kidneys, and brain. Their accumulation in cirrhotic patients may play a role in the pathogenesis of hepatic encephalopathy, hepatorenal syndrome, and hyperdynamic circulation.

4-Hydroxyphenylpyruvate Dioxygenase↗