PubMed Health⌕ Search

Biomedical subjects

G D Burtch

Publications and source records attributed to G D Burtch.

13 recordsLinked to original sources
PubMed1992

Biochemical and histopathological correlation in liver transplant: the first 180 days.

It is not known whether the histopathology of the liver allograft can be predicted from biochemical measurements in serum with the same confidence as in the native liver. To answer this question we compared the histopathological diagnoses in 170 biopsy specimens from 70 adult transplant recipients obtained during the first 180 days, with the concentrations of the serum bilirubin and the activities of AST, ALT and alkaline phosphatase measured at the same time. The most frequent diagnosis was cholestasis (n = 45), which was mild, moderate or severe and which may have been complicated by rejection (n = 28) or ischemia (n = 14). Hepatitis (n = 14), ischemia with rejection (n = 6) and spotty focal necrosis (n = 6) were diagnosed less frequently. Fifteen biopsy specimens were reported as histopathologically normal. In general, biochemical measurements discriminated poorly between different histopathological diagnoses. The histopathologically normal liver often showed an abnormal pattern of enzymes and an increase in the serum bilirubin level. As a result histopathologically normal biopsy specimens were indistinguishable biochemically from those with hepatitis. When two pathological conditions were found to coexist (e.g., cholestasis with either rejection or ischemic necrosis, or ischemic necrosis with rejection), the effect on the serum biochemistry was usually not additive and in some instances returned the biochemical abnormalities toward normal. With the exception of the serum bilirubin level, which increased with the severity of uncomplicated cholestasis, we could not identify a specific pattern of biochemical changes corresponding to a given histopathological diagnosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Obesity and renal transplantation.

In this study, we examined the influence of pre-existing obesity (weight more than 120 per cent of ideal body weight) on outcome after renal transplantation. Among 263 cyclosporine-treated recipients of renal allografts, 223 (85 per cent) were nonobese and 40 (15 per cent) were obese prior to transplantation. Obese and nonobese recipients were similar with regard to age, sex, renal diagnosis, history of prior transplant, donor source, pretransplant blood pressure, pretransplant antihypertensive agents, diabetic recipients with insulin requirements more than 40 units per day and pretransplant serum cholesterol. Duration of hospitalization was similar (26 +/- 25 versus 25 +/- 14 days; p = NS). There was a significantly higher incidence of wound infections in obese recipients (17.5 versus 6.3 per cent; p = 0.036); other complications occurred with similar incidence. Preoperative per cent of ideal body weight correlated with post-transplant weight gain during the first post-transplant year (p = 0.00002). After one year, obese recipients had gained 14.2 +/- 2.2 kilograms compared with 8.9 +/- 0.6 kilograms for nonobese patients (p = 0.002). Mean doses of prednisone, azathioprine and cyclosporine were similar at three, six and 12 months post-transplant. There were no differences in blood cyclosporine, serum cholesterol or blood glucose levels at any time. Blood pressure measurements were similar throughout the first post-transplant year. There was no difference in the incidence or number of rejection episodes. Actuarial patient survival rate for nonobese patients was 93 per cent at three years. For obese patients, three year actuarial patient survival rate was 90.5 per cent (p = NS). Actuarial graft survival rate among nonobese patients was 71.8 per cent at three years. For obese patients, three year actuarial graft survival rate was 64.5 per cent (p = NS). In conclusion, obese patients with end stage renal disease are good candidates for renal transplantation. Obesity does not seem to constitute a major risk factor, the most notable adverse outcomes being an increased incidence of wound infection and continued weight gain through the first post-transplant year.

Actuarial Analysis↗
PubMed1990

The production of tumor necrosis factor alpha and the development of a pulmonary capillary injury following hepatic ischemia/reperfusion.

The large mass of fixed macrophages resident in the liver make it a potentially rich source of cytokines. We have previously demonstrated that an isolated and severe ischemia/reperfusion injury to the liver results in cytokine release, specifically tumor necrosis factor alpha, and that TNF is then involved in the development of pulmonary pathology. This study was designed to determine the kinetics of TNF release following varying periods of hepatic ischemia and to further investigate the acute lung injury that follows. Suprahepatic blood samples were obtained at serial time points following a 45-, 60-, 75-, or 90-min ischemic insult to a segment of the rat liver with subsequent reperfusion. Using a bioassay based on the WEHI 164 cell line, plasma TNF levels were measured in all experimental animals; sham-operated control animals had undetectable levels. Changes in pulmonary capillary permeability were then measured using a standard 125I-labeled albumin washout technique following a 90-min ischemic insult with subsequent reperfusion. A significant increase in the mean permeability index was observed 9 to 12 hr following hepatic reperfusion (.601 +/- 102 as compared with .114 +/- .085 in sham-operated controls, P less than 0.005). Animals treated with anti-TNF antiserum prior to the induction of hepatic ischemia had a significantly reduced pulmonary capillary leak compared to animals pretreated with rabbit serum without TNF-blocking properties (.184 +/- .029 versus .694 +/- 052 for the control serum, P less than 0.005). TNF release follows both moderate and severe ischemic injury to the liver and the results reported here implicate TNF as an important mediator of increased pulmonary capillary permeability. These experiments confirm previous histologic studies that demonstrated pulmonary edema and intra-alveolar hemorrhage following hepatic ischemia/reperfusion, with subsequent blockade of the histologic injury by pretreatment with anti-TNF antiserum.

Animals↗
PubMed1990

Role of tumor necrosis factor-alpha in the pathophysiologic alterations after hepatic ischemia/reperfusion injury in the rat.

Cytokines are recognized as critical early mediators of organ injury. We attempted to determine whether or not severe hepatic ischemia/reperfusion injury results in tumor necrosis factor-alpha (TNF-alpha) release with subsequent local and systemic tissue injury. After 90 min of lobar hepatic ischemia, TNF was measurable during the reperfusion period in the plasma of all 14 experimental animals, with levels peaking between 9 and 352 pg/ml. Endotoxin was undetectable in the plasma of these animals. Pulmonary injury, as evidenced by a neutrophilic infiltrate, edema and intra-alveolar hemorrhage developed after hepatic reperfusion. The neutrophilic infiltrate was quantitated using a myeloperoxidase (MPO) assay; this demonstrated a significant increase in MPO after only 1 h of reperfusion. Anti-TNF antiserum pretreatment significantly reduced the pulmonary MPO after hepatic reperfusion. After a 12-h reperfusion period, there was histologic evidence of intra-alveolar hemorrhage and pulmonary edema. Morphometric assessment showed that pretreatment with anti-TNF antiserum was able to completely inhibit the development of pulmonary edema. Liver injury was quantitated by measuring serum glutamic pyruvic transaminase which showed peaks at 3 and 24 h. Anti-TNF antiserum pretreatment was able to significantly reduce both of these peak elevations. These data show that hepatic ischemia/reperfusion results in TNF production, and that this TNF is intimately associated with pulmonary and hepatic injury.

Alanine Transaminase↗
PubMed1989

The hepatic artery in liver transplantation.

Hepatic artery complications after liver transplantation are uncommon, but represent an important cause of morbidity and mortality. In addition, these complications tax an already limited supply of donor organs because of the frequent need for retransplantation in this group of patients. In this study, we examined the incidence of hepatic arterial anomalies in donors and recipients of orthotopic liver transplants, focusing on the techniques that are available for hepatic arterial reconstruction and on the occurrence of hepatic arterial complications. A total of 77 liver transplants were carried out in 68 patients. Standard recipient anatomy was present in 60 of 68 patients (88%). Anomalous vessels were identified in eight patients (12%), including six cases of replaced right hepatic artery (9%) and two cases of replaced left hepatic artery (3%). Donor liver arterial anatomy was standard in 62 cases (80%). Anomalous arterial supply was identified in 15 of 77 donor livers (20%), including replaced left hepatic artery in nine (12%) and replaced right hepatic artery in six (8%). A variety of methods were used to manage the anomalous vessels. There was one hepatic artery pseudoaneurysm, three cases of hepatic artery thrombosis (4%), and one patient developed a dissection of the native celiac axis. In primary transplants, utilization of the recipient's proper hepatic artery was associated with a significantly higher risk of hepatic artery thrombosis (P less than 0.04) when compared with the common hepatic artery or the branch patch technique. Use of a Carrel patch on the donor artery was associated with a significantly reduced incidence of hepatic artery thrombosis (P less than 0.0003). For retransplantation, it is recommended that a more proximal recipient anastomotic site be chosen. An innovative method is described that provides increased length of the donor arterial supply without the use of an arterial graft.

Hepatic Artery↗
PubMed1989

Liver transplantation at the University of Michigan.

Liver transplantation is a highly successful therapy for liver diseases that were previously debilitating and often fatal within a few months. One-year actuarial patient survival for our first 162 patients is 74.7%. Our results have improved since the inception of the program despite the fact that the indications have been extended to higher risk patients such as those with fulminating hepatitis or thrombosed portal veins. The prognosis following transplantation for each specific indication needs to be defined, especially for hepatitis, alcoholic cirrhosis and individual cancers. We believe that a more conservative approach to immunosuppression, close attention to intravenous and enteral nutrition, and aggressive treatment of complications (including prompt reoperation when indicated) have been important improvements in our management practices.

Adolescent↗
PubMed1989

Bile refeeding after liver transplantation and avoidance of intravenous cyclosporine.

Because absorption of cyclosporine (CyA) given orally immediately after liver transplantation is unreliable, the drug is usually given intravenously until external biliary drainage is discontinued. Intravenous CyA, however, is associated with serious side effects, making its use potentially hazardous. We report the results of a new strategy in which we used oral CyA exclusively and refed bile to enhance oral CyA absorption. Thirty-two liver transplant recipients with indwelling T tubes were studied. All were given sequential quadruple drug immunosuppression with antilymphoblast globulin, azathioprine, and steroids. Oral CyA and refeeding of bile was started when renal function was stable. By the second posttransplant week, satisfactory CyA levels were achieved, and antilymphoblast globulin therapy was stopped. There were significant associations between oral CyA dose and CyA level and between quantity of refed bile and CyA level (p less than 0.001). CyA dose and quantity of bile refed were covariates, however, and in multiple regression analysis, only the quantity of refed bile was significant (p = 0.001). CyA levels did not correlate with rejection. The incidence of rejection was 63%. At a mean follow-up of 9 months, 28/32 (88%) patients were alive, and actuarial 1-year patient survival was 84%. Current graft and renal function are excellent (serum bilirubin, 1.0 +/- 0.1 mg/dl; serum creatinine, 1.2 +/- 0.1 mg/dl). We conclude that intravenous CyA can be avoided in virtually all liver-transplant recipients by administration of oral CyA with bile in the early posttransplant period.

Administration, Oral↗
PubMed1987

Feeding jejunostomy (versus gastrostomy) passes the test of time.

The authors previously reported a higher incidence of early postoperative complications after feeding gastrostomy compared to jejunostomy, prompting the recommendation of jejunostomy for chronic enteral feeding. Long-term follow-up has since been obtained on these 31 patients and an additional 25 patients undergoing surgical feeding procedures. The 26 feeding gastrostomies were 16 Stamm, eight permanent mucosal-lined, and two Witzel. The 30 feeding jejunostomies consisted of 19 Roux-en-Y, nine Stamm, and two Witzel. Patients with gastrostomy have had a mean follow-up of 100 days. Adverse events have occurred in 15/26 (58%), including 9 patients with pulmonary aspiration (35%), two of which were fatal. Twenty-three additional patients have died of underlying diseases. All 11 patients with tube jejunostomy died of underlying diseases within 4 months of surgery. The complication rate was 36%, including pulmonary aspiration in both patients with Witzel jejunostomy. The 19 patients with Roux-en-Y jejunostomy have had mean follow-up of 169 days. Complications have occurred in 9 patients (47%); 16/19 patients (mean age 55 years) have died of underlying disease. The mean age of the patients still alive is 35 years. Feeding jejunostomy has a lower incidence of complications, especially pulmonary aspiration, than gastrostomy. Stamm jejunostomy should be used for enteral feeding in older patients and in patients with short life expectancy. In younger patients requiring lifelong enteral feeding, Roux-en-Y jejunostomy should be used.

Enteral Nutrition↗
PubMed1986

Upper-airway obstruction as a complication of oral anticoagulation therapy.

We treated a patient for warfarin-induced sublingual hematoma causing upper-airway obstruction. This complication of oral anticoagulation therapy is rare; only three other cases have been reported in the English literature. All reported patients developed acute respiratory embarrassment necessitating emergency airway establishment. Sublingual hematomas usually resolve spontaneously, and surgical drainage is rarely necessary.

Airway Obstruction↗
PubMed1985

Feeding gastrostomy. Assistant or assassin?

Following several deaths from pulmonary aspiration in severely ill or chronically debilitated patients receiving nasogastric tube feedings, a study was undertaken to determine the incidence of aspiration pneumonitis in patients with feeding gastrostomies. During a 15-month interval, 22 feeding gastrostomies and nine feeding jejunostomies were performed. In the former group, eight patients experienced aspiration pneumonitis, with two deaths. Six patients with Stamm gastrostomies and two patients with permanent mucosal-lined gastrostomies experienced pulmonary aspiration. In contrast, aspiration pneumonia did not occur in our small series of patients with feeding jejunostomies. The high incidence of pulmonary aspiration in patients with feeding gastrostomies strongly suggests that, for chronic enteral nutrition in patients who are unable to protect their airway, a feeding jejunostomy is preferable to a feeding gastrostomy.

Adult↗