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Biomedical subjects

A M Freedman

Publications and source records attributed to A M Freedman.

At least 19 recordsLinked to original sources
PubMed1999

The psychiatrist's dilemma: a conflict of roles in legal executions.

In the United States, a critical controversy is taking place in regard to psychiatrists' and other physicians' participation in legal executions. Under pressure from the criminal justice system and legislatures to expedite executions, some forensic psychiatrists have succeeded in loosening traditional prohibitions against such participation. Further, there has been a weakening of the prohibition against treatment designed to facilitate immediate execution of those condemned to death. The rationale offered for these departures from current psychiatric ethical codes is the novel notion that when a psychiatrist acts in the court or criminal justice situation, that individual is no longer a psychiatrist and is not bound by psychiatric ethics. Rather, the forensic psychiatrist, termed a 'forensicist', serves as an assistant in the 'administration of justice' or 'an agent of the State' and thus works in a different ethical framework from the ordinary psychiatrist. This justification has similarities to the rationale offered by physicians involved in human experiments and other criminal acts in Nazi Germany, as well as psychiatrists in the former Soviet Union who explained their involvement in psychiatric abuse as a result of being agents of the State and thus not responsible for carrying out orders. Clearly, this controversy could be eliminated by a campaign for the abolition of capital punishment, characterised by the American Psychiatric Association as 'anachronistic, brutalizing [and] ineffective'. Such a campaign should serve as a call for psychiatrists and other physicians to join in the struggle to uphold ethical and moral principles.

Capital Punishment↗
PubMed1997

Transjugular intrahepatic portosystemic shunts compared with endoscopic sclerotherapy for the prevention of recurrent variceal hemorrhage. A randomized, controlled trial.

BACKGROUND: Transjugular intrahepatic portosystemic shunts (TIPS) have widened the use of portal decompression as therapy for variceal hemorrhage. However, no controlled studies have examined the efficacy of TIPS compared with that of other treatments. OBJECTIVE: To compare the efficacy and safety of TIPS with those of endoscopic sclerotherapy for the prevention of recurrent variceal hemorrhage. DESIGN: Randomized, controlled trial. SETTING: Tertiary-care academic medical center. PATIENTS: 100 patients with cirrhosis were evaluated a mean of approximately 10 days after an episode of acute variceal bleeding; 20 patients were excluded because of portal venous thrombosis (n = 6), hepatoma (n = 3), florid alcoholic hepatitis (n = 6), and refusal to give consent (n = 5). INTERVENTIONS: TIPS (n = 41) or sclerotherapy (n = 39). The latter was performed by freehand injections of 5% Na morrhuate at 2- to 3-week intervals. Recurrent variceal hemorrhage was managed by sclerotherapy followed by angiographic assessment of TIPS and dilatation of the stents (TIPS group) or crossover to TIPS (sclerotherapy group). MEASUREMENTS: Rebleeding and survival were the primary end points. Complications and rates of rehospitalization were secondary end points. RESULTS: During a mean follow-up of approximately 1000 days, recurrent gastrointestinal bleeding resulted from variceal hemorrhage (9 patients in the TIPS group and 8 in the sclerotherapy group), portal gastropathy (1 patient in each group), and gastric lipoma (0 and 1 patients, respectively). A higher mortality rate was seen with TIPS (P = 0.03). Death resulted from variceal bleeding (5 patients in the TIPS group and 3 in the sclerotherapy group), sepsis (3 and 2 patients, respectively), liver failure (2 patients in each group), hepatoma (1 and 0 patients, respectively), and hemoperitoneum (1 and 0 patients, respectively). Encephalopathy was the most common complication in the TIPS group (n = 12), and pain developing after sclerotherapy was the most common in the sclerotherapy group (n = 10). The two groups had similar rates of rehospitalization. CONCLUSIONS: Endoscopic sclerotherapy and TIPS are equivalent with respect to rebleeding developing over the long term. However, sclerotherapy may be superior to TIPS with respect to survival.

Adult↗
PubMed1997

The natural history of portal hypertension after transjugular intrahepatic portosystemic shunts.

BACKGROUND & AIMS: The effects of transjugular intrahepatic portosystemic shunt (TIPS) on portal hemodynamics, esophageal and gastric varices, and hepatic function have not been fully defined. The aim of this study was to define prospectively the effects of TIPS on portal pressures and flow, variceal resolution, and hepatic function. METHODS: Pressure and flow measurements were made by angiography and Doppler sonography, respectively. Varices were assessed by endoscopy and angiography. Liver functions were evaluated by a battery of tests. RESULTS: In 100 consecutive subjects, mean portosystemic gradient decreased from 24 to 11 mm Hg (means) (P < 0.001) after TIPS. Recurrent portal hypertension caused by stent thrombosis (n = 5), stent retraction (n = 2), and stent stenosis (n = 51) occurred at 6 months but, by year 5, was not present in survivors (n = 0 of 8). Fundic gastric varices failed to resolve in 6 of 12 cases. Systemic venous pressures of >15 mm Hg, stent dysfunction, and continued alcoholism were risk factors for recurrent hemorrhage. Angiography was superior to endoscopy, which was superior to Doppler sonography for detection of recurrent portal hypertension. Progressive liver failure occurred in 8 patients. CONCLUSIONS: Recurrent portal hypertension caused by stent stenosis occurs commonly in the first 2 years after TIPS. Fundic gastric varices often fail to disappear after TIPS. The effects of TIPS on liver function are unpredictable.

Adult↗
PubMed1996

The hematologic consequences of transjugular intrahepatic portosystemic shunts.

Transjugular intrahepatic portosystemic shunts (TIPS) are a recent innovation in the management of portal hypertension. In 1992, we had previously described an instance of severe hemolysis associated with this procedure. This study was undertaken to define and quantify the true incidence of TIPS-associated hemolysis and its clinical spectrum, as well as to test the hypothesis that portal decompression by TIPS would ameliorate hypersplenism in patients with portal hypertension. A total of 60 patients undergoing TIPS for prevention of recurrent variceal hemorrhage (n = 40) or refractory ascites (n = 20) were studied. Forty patients with cirrhosis who were followed concurrently served as controls. At entry, both groups were comparable with the exception of increased ascites in the TIPS group. A total of 7 instances of intravascular hemolysis were identified in 60 TIPS patients, whereas none occurred in controls. Of these, 4 patients were asymptomatic and detected on routine laboratory testing. Hemolysis led to a greater than 4-g/dL decrease in hemoglobin in 2 patients, 2- to 3-g/dL decrease in 2 others and a 3- to 4-gm/dL decrease in 1 patient. Two patients were able to compensate for hemolysis and did not develop anemia. In all but 1 case, the findings of hemolysis subsided by 12 to 15 weeks; in 1 patient, orthotopic liver transplantation was associated with resolution of the hemolysis. Overall, no significant changes in white blood cell or platelet counts were observed in patients undergoing TIPS despite adequate portal decompression. We conclude that TIPS-induced hemolysis occurs in approximately 10% of subjects. However, it is self-limited and rarely requires intervention. Potential mechanisms of such hemolysis are discussed. TIPS is also not recommended as a means of improving platelet counts in patients with severe hypersplenism.

Adult↗
PubMed1996

Transjugular intrahepatic portosystemic shunts for patients with active variceal hemorrhage unresponsive to sclerotherapy.

BACKGROUND & AIMS: Despite urgent sclerotherapy, active variceal hemorrhage has a 70%-90% mortality rate in patients with advanced age, sepsis, renal or pulmonary compromise, tense ascites, or deep coma. The aim of this study was to test the safety and efficacy of transjugular intrahepatic portosystemic shunt (TIPS) performed semiemergently and preceded by stabilization by balloon tamponade in such patients. METHODS: Patients with actively bleeding esophageal or contiguous gastric varices despite sclerotherapy were assessed for risk of dying after emergent portacaval shunt. Those considered to be at high risk were stabilized by balloon tamponade and vasopressin/nitroglycerin and TIPS placed semiurgently within 12 hours. Balloon tamponade and pharmacological therapy were discontinued within 24 hours after TIPS in all cases. RESULTS: Thirty-two patients met entry criteria, and 2 were excluded due to portal vein thrombosis. TIPS was successfully placed in 29 of 30 patients and achieved hemostasis in all. Thirty-day and 6-week survival rates were 63% and 60%, respectively; in those without aspiration, the 6-week survival rate was 90%. After a median follow-up period of 920 days, 46% of the original cohort was alive. Only 2 episodes of early rebleeding and 4 late rebleeds occurred. Eight patients developed encephalopathy. Stent stenosis requiring dilation occurred in 6 of 11 patients within 6 months. CONCLUSIONS: TIPS is highly effective as salvage therapy in high-risk patients with active variceal hemorrhage despite endoscopic sclerotherapy.

Adult↗
PubMed1994

Portosystemic encephalopathy after transjugular intrahepatic portosystemic shunt: results of a prospective controlled study.

Portosystemic encephalopathy is a common complication of surgical portacaval shunts. Recently, transjugular intrahepatic portosystemic shunts have been proposed to produce portal decompression in a manner analogous to a side-to-side portacaval shunt, but with less morbidity. The incidence and clinical spectrum of portosystemic encephalopathy after transjugular intrahepatic portosystemic shunts, however, had not been previously prospectively defined. We therefore prospectively studied portosystemic encephalopathy in 30 patients undergoing transjugular intrahepatic portosystemic shunts and compared these findings with 25 patients concurrently undergoing sclerotherapy (controls). At entry, both study groups were comparable. Portosystemic encephalopathy was assessed by examining and grading mental status, asterixis, plasma ammonia and trail making tests. The portosystemic encephalopathy index was calculated from these parameters. Nine of 30 patients with transjugular intrahepatic portosystemic shunts experienced 24 episodes of acute portosystemic encephalopathy during follow-up; 6 of 9 had a history of portosystemic encephalopathy before transjugular intrahepatic portosystemic shunts and 5 of these 6 patients had Child C cirrhosis. Mental status and asterixis scores as well as portosystemic encephalopathy index worsened significantly in the first month after transjugular intrahepatic portosystemic shunts but showed some improvement thereafter. Increasing age, a medical history of portosystemic encephalopathy and trail scores for part B greater than 100 sec were predictors of portosystemic encephalopathy after transjugular intrahepatic portosystemic shunts. Portosystemic encephalopathy could be managed medically in all but one patient who underwent liver transplant. In contrast, there were no significant changes in mental status, asterixis, ammonia or trail scores over time in sclerotherapy controls. Only six episodes of encephalopathy occurred in endoscopic sclerotherapy patients over the duration of the study. Thus, overall risk of portosystemic encephalopathy after transjugular intrahepatic portosystemic shunts was higher than during sclerotherapy.

Esophageal and Gastric Varices↗
PubMed1993

Complications of transjugular intrahepatic portosystemic shunt: a comprehensive review.

It is generally accepted that the transjugular intrahepatic portosystemic shunt (TIPS) procedure has lower morbidity and mortality rates than those of surgical shunting. Nevertheless, complications occur. The authors have reviewed their experience and that of other institutions in compiling an extensive list of complications. Complications are categorized according to those related to transhepatic needle puncture, transvenous access to the portal vein, portal venous cannulation, the stent, the puncture site, portosystemic shunting, and contrast material. Excluding hepatic encephalopathy and delayed stenosis or occlusion of the shunt, an overall complication rate of less than 10% can be expected for TIPS. The prevalence of aggravated or new cases of encephalopathy is 5%-35%, and over the long term, up to 75% of shunts may undergo stenosis or occlusion. The direct procedural mortality rate is less than 2%, and the 30-day mortality rate ranges from 4% to 45%, depending on several factors. The role to which TIPS is relegated will be influenced by the long-term success rate in the prevention of recurrent variceal hemorrhage.

Catheterization, Peripheral↗
PubMed1993

Modulation of cytokines and myocardial lesions by vitamin E and chloroquine in a Mg-deficient rat model.

Antioxidant treatment with alpha-tocopherol did not affect the level of the "inflammatory cytokines" in Mg-deficient animals, although it diminished the extent of the myocardial lesions. In another group of Mg-deficient animals chloroquine treatment diminished significantly the levels of circulating cytokines (interleukin-1, interleukin-6, and tumor necrosis factor-alpha) and also resulted in a major decrease in myocardial lesions. These results raise the question of the role of these inflammatory cytokines in the formation of lesions in Mg-deficient myocardium. Because these cytokines are able to stimulate free radical production in various cell types, we postulate that Mg deficiency involves free radical mechanisms that can be amplified by inflammatory cytokines; whether these cytokines initiate lesion formation is unclear. Although our data do not confirm either possibility, we submit that these results implicate a role for the inflammatory cytokines in the cardiac pathology of Mg deficiency.

Animals↗
PubMed1992

Magnesium-deficiency elevates circulating levels of inflammatory cytokines and endothelin.

We have developed two rodent models of diet-induced magnesium-deficiency in which histologically defined cardiac lesions can be induced within two to three weeks. During the development of these lesions, the magnesium-deficient animals exhibit circulating cytokine levels which are indicative of a generalized inflammatory state. Dramatic elevations of the macrophage-derived cytokines, IL-1, IL-6, and TNF-alpha together with significantly elevated levels of the endothelial cell-derived cytokine, endothelin, were detected in the plasma of these animals. We believe that the pathophysiological effects caused by the action of these cytokines may play a role in the promotion of cardiovascular pathology associated with magnesium deficiency.

Animals↗
PubMed1992

Erythrocytes from magnesium-deficient hamsters display an enhanced susceptibility to oxidative stress.

Previous studies in our laboratory have indicated a role for free radical participation in magnesium deficiency cardiomyopathy. We have demonstrated the ability of various antioxidant drugs and nutrients to protect against magnesium deficiency-induced myocardial injury. In this study, we have examined erythrocytes from normal and magnesium-deficient animals and compared their susceptibility to an in vitro oxidative stress. Syrian male hamsters were placed on either magnesium-deficient or magnesium-supplemented diets. Animals from each group also received vitamin E in doses of 10 and 25 mg as subcutaneous implants. Erythrocytes obtained after 14 days on the diet were exposed to an exogenous hydroxyl (.OH) radical generating system (dihydroxyfumarate not equal to Fe3+ ADP) at 37 degrees C for 20 min. Erythrocyte crenation was observed and quantified by scanning electron microscopy. Lipid peroxidation, hemolysis (%), and intracellular glutathione levels were determined. In addition, serum lipid changes and membrane phospholipids were characterized. Our data demonstrate that erythrocytes from magnesium-deficient animals are more susceptible to free radical injury, supporting our hypothesis that magnesium deficiency reduces the threshold antioxidant capacity.

Adenosine Diphosphate↗
PubMed1992

Antioxidants and the cardiomyopathy of Mg-deficiency.

For several decades the animal models of Mg-deficiency have been studied with particular attention to the cardiomyopathy that develops due to dietary deficiency. In recent years we have studied the effects of nutrients and drugs with antioxidant properties on the development of the cardiomyopathy. We have found that treatment of the Mg-deficient animals with alpha-tocopherol, a naturally-occurring antioxidant, significantly diminishes the number and size of lesions. In addition, treatment with lipophilic drugs with antioxidant properties (probucol, propranolol) or water-soluble drugs that scavenge hydroxyl radicals (captopril, epicaptopril), also provided significant protection. In view of these findings, we suggest that chronic hypomagnesemia results in a pro-inflammatory condition leading to excessive production of oxygen-derived free radicals. Subsequently, the tissue antioxidant capacity is overwhelmed and oxidative tissue destruction results.

Angiotensin-Converting Enzyme Inhibitors↗