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Peripancreatic fluid collections are among the common post pancreas transplant complications, which are mainly due to leakage from the anastomosis site to bowel and graft pancreatitis. Differentiation between these two entities is important because they are treated differently. In this case, secretin stimulated magnetic resonance cholangiopancreatography revealed gradual intraperitoneal fluid collection and accumulation of fluid in small bowel excluded leakage from the anastomosis of the pancreas to bowel and changed the management from surgery to medical treatment.

Background: The majority of patients with end-stage renal disease are dependent on hemodialysis. Significant stenosis or occlusion of the subclavian vein is known to occur in 20% to 50% of patients who have had central venous catheters inserted into the subclavian vein or the internal jugular vein. Surgical bypass of the obstructed venous segment proximal to a functioning dialysis access site is an established treatment to relieve symptoms and salvage the functional dialysis access., Study Design: A retrospective review of all subclavian venous bypass procedures performed at St Louis University Hospital from May 1987 to May 2000 was undertaken. Twelve procedures were performed during this time. The mean age of the patient was 55.5 years (range 17 to 72 years). There were 11 men and 1 woman. Before surgical bypass, all patients underwent bilateral venograms to evaluate their central venous systems., Results: An extraanatomic surgical bypass was performed in all patients. Patients were followed for a mean of 16 months (range 1 to 79 months). At 1 month, 100% of hemodialysis access sites remained functional. At 1 year, 80%; 2 years, 60%; and 3 years, 25% of the salvaged arteriovenous hemodialysis access sites provided for functional dialysis. One patient required thrombectomy of the bypass graft at 14 months., Conclusions: Surgical bypass of an occluded or stenotic subclavian vein segment is successful in providing both symptomatic relief and salvage of a functioning dialysis access in the hemodialysis patient population. Study of the central venous system is essential in selecting an appropriate bypass procedure in individual patients.

Over the last decade a large number of patients with portal vein thrombosis have undergone successful liver transplantation. In most of these patients, simple modifications in vascular reconstruction techniques are adequate. However, anastomosis of the donor portal vein may not be possible in the presence of extensive portal and superior mesenteric venous thrombosis and in the absence of any other large tributary of the portal venous system. Cavoportal hemitransposition has been described as a salvage technique under these circumstances. We report a 43-year-old patient who underwent such a procedure and remains well 1 year later. We review the literature and discuss the implications of cavoportal hemitransposition.

Two patients with successful combined cardio-renal transplantation (CCRT) using allografts from the same donor are reported. Both patients underwent staged procedure with hearts being transplanted first followed by kidneys. One patient suffered simultaneous acute rejection of both allografts, indeed a very rare event, which was successfully treated with pulse steroids. Because of the successful patient and graft outcomes, we propose that staged CCRT offers a reasonable therapeutic option for patients with co-existing, irreversible cardiorenal failure.

Stenting of the biliary tract is performed for a variety of benign and malignant disorders. Although uncommon, proximal and distal migration of these stents is known to occur. We report a case of jejunal perforation from a distally migrated biliary stent.

Spontaneous rupture of the liver has been described in association with many benign and malignant conditions. We report, to our knowledge, the first case of spontaneous rupture of the liver upon revascularization, requiring total hepatectomy and portocaval shunt, followed by successful retransplantation. Routine pathological examination of the explanted liver failed to reveal the etiology of the rupture. However, electron microscopy demonstrated abnormal collagen in the hepatic arterial wall compatible with a collagen disorder such as Ehlers-Danlos type IV disease. We conclude that the donor liver had a previously undiagnosed collagen disorder. Review of the literature does not preclude the use of livers from donors with a history of connective tissue disorders. Based on our experience one should exercise caution when using livers from such donors. With a history of connective tissue disorder in an immediate family member, further tests should be performed in the donor to rule out a subclinical connective tissue disorder. In addition, a review of all patients reported thus far to have undergone total hepatectomy and portocaval shunt, followed by liver transplantation as a two-stage procedure is presented.

We report a young male patient who developed spontaneous renal allograft rupture 7 days after cadaveric renal transplant, complicated by delayed graft function, without evidence of rejection on allograft biopsy., (Copyright 2000 S. Karger AG, Basel)

Ischemia reperfusion injury (IRI) contributes significantly to posttransplant graft dysfunction. An emphasis, therefore, has been directed toward the identification of novel renoprotective agents. In this study, the renoprotective effect of tetrodotoxin (TTX) alone, or in combination with a thromboxane synthetase inhibitor (OKY-046), was investigated in a 60-min warm ischemia, 72-h reperfusion, IRI rodent model. Unilateral nephrectomized rats were treated with the test vehicle alone, 1, 2, or 4 microgram/kg of TTX or 2 mg/kg of OKY-046 intravenously, either 15 min pre- or postischemia, or 2 microgram/kg TTX administered simultaneously with OKY-046 (2 mg/kg), following the ischemic interval. Baseline, 24, and 72 h mean plasma creatinine (Cr) and urea nitrogen (BUN) were compared. Maximal renoprotection was demonstrated by significantly improved 72-h Cr and BUN levels with the 2 microgram/kg of TTX or with 2 mg/kg of OKY-046, each administered after ischemia (ischemic control Cr = 8. 01 +/- 1.07 mg/dl vs TTX = 3.84 +/- 0.80 mg/dl, P = 0.008; vs OKY-046 = 4.0 +/- 1.5, P + 0.008; ischemic control BUN = 241.3 mg/dl +/- 32.8 vs TTX = 85.7 mg/dl +/- 18.7, P < 0.008; vs OKY-046 = 52.6 +/- 22.5, P = 0.008). The combination therapy utilizing TTX with OKY-046 resulted in reduced animal survival, demonstrating no renoprotection as measured with the biochemical parameters. These results support the renoprotective effects of TTX in a severe, rodent IRI model. The exact mechanism of action, as well as the therapeutic potential of TTX in preservation/transplantation, warrants further study., (Copyright 1999 Academic Press.)

To minimize perioperative cardiac events, we utilize a screening protocol consisting of intravenous dipyridamole thallium-201 myocardial imaging (DPT), with the selective use of coronary angiography based on the presence of reversible defect(s) on DPT test. A retrospective study was performed to determine the prognostic value of this protocol and to identify any clinical parameters predictive of an abnormal DPT test. To accomplish this, a detailed chart analysis of 176 consecutive kidney (n = 89) and kidney-pancreas (n = 87) transplant recipients who had undergone pretransplant DPT testing was performed. The results of the DPT test were interpreted as normal in 111, fixed defect in 15, and reversible defect(s) in 50 patients. Forty-two of the 50 patients with reversible defect(s) underwent coronary angiography. Twelve of the 27 patients with significant coronary artery disease (CAD, > 50% stenosis in one or more coronary arteries) underwent pretransplant revascularization and the remaining 15 were treated medically. Cardiac events (documented acute myocardial infarction or sudden cardiac death) within 6 wk of transplant were stratified by the results of this protocol. Also, various clinical parameters were compared between patients with normal and abnormal (fixed and reversible defect) DPT tests. Only one of the 111 (0.9%) transplant recipients with a normal DPT test had a perioperative cardiac event. None of the 15 (0%) patients with a fixed defect and none of the 15 (0%) patients with reversible defect(s), but a nonsignificant (< 50% narrowing) coronary angiogram, had a perioperative cardiac event. Three of the 27 (11.1%) patients with reversible defect(s) and significant disease on coronary angiography, who had undergone pre-transplant revascularization or were managed medically, had a perioperative coronary event. Of 14 recipients parameters analyzed, age > 50 yr was the only variable predictive of an abnormal DPT test. We conclude that the incidence of perioperative cardiac events in patients with a normal or fixed defect, or reversible defect(s) but a nonsignificant (< 50% narrowing) coronary angiogram is very low, indicating the high correlation of these findings on DPT and an uneventful (cardiac) post-transplant course. The incidence of perioperative cardiac complications amongst the high-risk transplant recipients with reversible defect(s) and significant CAD on coronary angiogram may be minimized by appropriate preoperative medical management or revascularization. None of the clinical variables except age > 50 yr was predictive of an abnormal DPT test.

This study was designed to investigate a possible mechanism of action by which octreotide acetate causes insulin suppression in the denervated pancreas. Canine tissue slices were placed in a pH-adjusted medium with varying concentrations of glucose and octreotide acetate: Experiment 1, 30 min in basal medium with 0.6 mg/ml glucose; Experiment 2, addition of 6.0 mg/ml glucose; Experiment 3, addition of 4 microg octreotide acetate/70 ml (comparable to 100 microg/25 kg body weight); Experiment 4, addition of 16 microg octreotide acetate/70 ml; Experiment 5, incubation with 6.0 mg glucose/ml and 4 microg octreotide acetate/70 ml; Experiment 6, incubation with 6.0 mg glucose/ml and 16 microg octreotide acetate/70 ml; Experiment 7, preincubation with 4 microg octreotide acetate/70 ml, then with 6.0 mg glucose/ml; and Experiment 8, preincubation with 16 microg octreotide acetate/70 ml, then with 6.0 mg glucose/ml. Medium levels of insulin, glucagon, and amylase were collected at intervals during the incubation periods. There was an appropriate increase in the rate of insulin release to glucose stimulation in the high-glucose (6.0 mg/ml) group. There was no significant inhibition of basal or glucose-stimulated insulin release with either simultaneous or pretreatment of the canine pancreatic tissue slices with either concentration of octreotide acetate. These studies support an indirect mechanism by which octreotide acetate exerts its inhibitory effect on endocrine and exocrine function in the canine pancreas transplant model.

Free radical mediated lipid peroxidation (LPO) has been implicated in the pathogenesis of ischemic-reperfusion injury (IRI). To address the renoprotective effect(s) of LPO inhibition, the efficacy of the 21 aminosteroid U74389G was evaluated in three IRI models. In Model 1 51 unilateral nephrectomized rats that underwent 60 min of warm ischemia followed by a 72-hr reperfusion interval were treated with the test vehicle only, or 3, 6, or 12 mg/kg of U74389G intravenously, 5 min pre- or postischemia. In Model 2 Sprague-Dawley rats underwent sham operation (n=9), or 45 min of warm ischemia and 10 min of reperfusion with U74389G (6 mg/kg; n=10) or test vehicle only (n=10) administered intravenously over 10 min beginning 5 min prior to clamp release. After reperfusion, LPO was determined by assay of snap frozen tissue for thiobarbituric acid (TBA) concentrations (nmol/g tissue weight). In Model 3 domestic lean maid pigs (14-18 kg) underwent left nephrectomy with 30 min of warm ischemia, Collins C-4 flush, and 24 hr of cold storage preservation. Heterotopic autotransplantation and immediate contralateral nephrectomy was then performed in Group A-nonischemic controls (n=4), Group B-ischemic controls (n=5), and Group C-U74389G (6 mg/kg) administered preischemia and at autotransplantation (n=5). In Model 1 maximal renoprotection was demonstrated with the 6 mg/kg dose of U74389G administered after ischemia (ischemic control 72-hr serum creatinine (Cr) = 8.01+/-1.1 mg% vs. 3.32+/-0.96 mg%; ischemic control creatinine clearance = 0.069+/-0.03 ml/min vs. 0.206+/-0.04 ml/min; P<0.05). In Model 2 TBA levels were significantly lower in U74389G treated animals (88.5+/-10.0 vs. ischemic controls = 296.8+/-81.4; P=0.02). In Model 3 graft survivals were 100%, 0%, and 60% respectively. Peak Cr and BUN (mg%) were significantly greater in Group C vs. Group A, (Group A Cr = 8.59+/-0.63 vs. Group C = 12.8+/-1.01; Group A BUN = 64.1+/-2.73 vs. Group C = 104.9+/-12.21)--however, by day 10, thee were no significant differences in renal function: (Group A Cr = 2.15+/-0.3 vs. Group C = 2.10+/-0.06; Group A BUN = 27.0+/-6.0 vs. Group C = 31.1+/-6.4). These results support the beneficial effects of LPO inhibitors in models of ischemia-reperfusion, as well as preservation/transplantation, and suggest that this renoprotection correlates with decreased membrane lipid peroxidation.

Somatostatin and its analogue, octreotide acetate (Sandostatin), have been demonstrated to suppress exocrine secretion in a denervated canine pancreatic autograft model. To help define this inhibitory mechanism, the effect of these agents on cholecystokinin (CCK)-stimulated acinar cell secretion was evaluated. In vitro assessment evaluated the effect of somatostatin on octapeptide (OP)-CCK-stimulated amylase release of pancreatic tissue slices. In vivo assessment employed animals with pancreatic autografts and pancreaticocystostomies, evaluating the effect of a bolus intravenous injection of 100 micrograms of octreotide acetate on the basal and OP-CCK-stimulated (125 ng/kg/h) secretion of urinary (autograft) amylase and bicarbonate. Incubation of tissue slices with 0.16, 0.24, or 0.32 microgram/ml somatostatin had no significant effect on in vitro OP-CCK-simulated amylase release. Intravenous octreotide acetate resulted in a significant decrease in the basal rate of amylase secretion but had no significant effect on OP-CCK-stimulated autograft amylase or bicarbonate release. These studies demonstrate that octreotide acetate has an in vivo inhibitory effect on basal amylase release of pancreatic autografts but cannot counteract maximal stimulation with exogenous OP-CCK. Also, somatostatin does not inhibit OP-CCK-stimulated acinar cell secretion of pancreatic tissue slices. These results indicate that the exocrine inhibition produced by somatostatin analogues in the grafted pancreas occurs via an indirect mechanism.

This study was designed to determine the effect of a potent cholecystokinin antagonist, L-364,718, on canine pancreatic endocrine function following partial pancreatectomy. Plasma glucose, insulin, and glucagon were determined over a 2-hr interval following an intravenous bolus of 0.5 g/kg glucose in a 50% solution. The following groups were established: normal animals (group A, n = 5), normal animals pretreated with 20 nmole/kg L-364,178 (group B, n = 5), partially pancreatectomized animals (group C, n = 5), and partially pancreatectomized animals pretreated with 20 nmole/kg L-364,178 (group D, n = 5). In contrast to animals with an intact pancreas, pretreatment with L-364,718 following partial pancreatectomy resulted in a significant decrease in peak insulin (group C = 132.8 +/- 13.0 microU/ml vs Group D = 90.4 +/- 16.1 microU/ml, P < 0.05) and the basal-to-peak insulin difference (group C = 111.9 +/- 11.5 microU/ml vs group D = 77.5 +/- 16.6 microU/ml, P < 0.05). Despite this, the rate of glucose utilization (K value) was significantly increased in the partially pancreatectomized animals given the antagonist (group C = -1.22 +/- 0.22%/min vs group D = -2.79 +/- 0.427%/min) and there were no significant differences in basal or peak glucose when comparing the groups given L-364,718 with the groups given placebo (group A vs B and group C vs D). Thus, the CCK antagonist L-364,718 significantly decreases peak insulin in partially pancreatectomized animals but not in nonoperative control animals. There is a paradoxical increase in the rate of glucose utilization but no effect on glucose homeostasis. The effect of this antagonist in other models of reduced islet cell reserve (i.e., pancreas transplantation) remains to be determined.

Blindness is an extremely rare complication of cyclosporine neurotoxicity. In all 10 cases in the literature, this form of blindness is completely reversible with the reduction or withdrawal of cyclosporine. We describe the first case of sudden, complete, and permanent blindness within 36 h after administration of intravenous cyclosporine in a kidney-pancreas transplant recipient.

Combined kidney-pancreas transplantation is an effective surgical therapy for end-stage renal failure secondary to type I diabetes mellitus. However, obstructive pancreatitis and pancreaticocutaneous fistula remain significant postoperative complications unique to extraperitoneal segmental pancreatic transplantation. We present our experience with 13 patients (7 with obstructive pancreatitis and 6 with pancreaticocutaneous fistulae) after segmental extraperitoneal pancreatic transplantation, who subsequently underwent intraperitoneal reconstruction of the pancreaticocystostomy. This reconstruction was successful in 11 of 13 (85%) patients with minimal morbidity and no mortality. This intraperitoneal approach to reconstruction of the pancreaticocystostomy after segmental extraperitoneal pancreatic transplantation is a safe and effective means of graft salvage and this technique has not been described in the literature.

The pathophysiology of ischemia-reperfusion renal injury is mediated, in part, by the generation of the vasoconstricting prostanoid thromboxane A2 (TXA2). This study was undertaken to evaluate the renoprotective effects, as well as the optimal timing and dosage, of a selective thromboxane synthetase inhibitor, OKY-046, in a unilateral nephrectomized, 60 min ischemia, 72 hr reperfusion, rodent model. Forty-one rats were subjected to right nephrectomy only (group A), or right nephrectomy with 60 min of left renal ischemia and treatment with inactive vehicle only (group B), or 2 mg/kg or 4 mg/kg of OKY-046 administered intravenously before (groups C and D) or after (groups E and F) pedicle clamping. Outcome variables included animal survival; change in kidney weight; 0, 24, and 72 hr plasma creatinine (CR); urea nitrogen (BUN); thromboxane B2 (TXB2) and 6-keto prostaglandin F(1alpha) (6 kPGF(2alpha)) levels; creatinine clearance (CRCL); and histologic evidence of renal injury. Animal survival and postperfusion kidney weight were not significantly different among the groups. However, renal functional parameters were significantly improved with the 2 mg/kg dose of OKY-046 administered after renal ischemia. (group B 72 hr Cr= 8.01 +/- 1.1 mg% vs. group E=3.99 +/- 1.5 mg%, and group B 72 hr BUN=241.3 +/- 32.8 mg% vs. group E=52.6 +/- 22.5 mg%). The CRCL was also improved in group E vs. group B, although these results did not reach statistical significance (group B=0.069 ml/min vs. group E=0.194 ml/ min). The 24 hr TXB2 levels were significantly increased in group B (0 hr=754.1 +/- 219.4 pg/ml vs. 24 hr=2055.9 +/- 550.0 pg/ml), and pre- or posttreatment with OKY-046 abrogated this increase (group C 0 hr=517.1 +/- 80.9 pg/ml vs. 24 hr=384.7 +/- 251.5 pg/ml, and group E 0 hr=781.6 +/- 390.4 pg/ml vs. 24 hr=183.0 +/- 81.4 pg/ml). The 24 hr 6 kPGF(1alpha) levels decreased in all groups, whereas 72 hr 6 kPGF(1alpha) levels increased above baseline in groups A, C, and E, but not in group B. These data demonstrate the beneficial effects of thromboxane A2 synthesis inhibition in the setting of ischemia-reperfusion injury and suggest that this renoprotection correlates with late vasodilatory prostanoid synthesis.

This study evaluated the effect of the cholecystokinin antagonist L-364,718 on exocrine secretion in canine pancreatic autografts with pancreaticocystostomies. Urinary (autograft) amylase (U/min) and bicarbonate (mmole/min) secretion, over a 6 hr interval, were determined in the basal state (Group A), after a bolus injection of 20 nmoles/kg of L-364,718 (Group B), during a continuous cholecystokinin octapeptide (OP-CCK) infusion at 125 ng/kg/hr either alone (Group C), with a bolus injection of 20 nmoles/kg (Group D), or 30 nmoles/kg (Group E), of L-364,718 1 hr before initiating OP-CCK, or 20 nmoles/kg of L-364,718 1 hr after initiating OP-CCK (Group F). L-364,718 had no effect on basal or OP-CCK-stimulated secretion of bicarbonate. Basal amylase secretion was decreased 1 hr after L-364,718 and remained significantly lower than controls throughout the study interval. When compared to Group C (280.3 +/- 48.6), OP-CCK-stimulated amylase secretion was significantly lower for the first hour after L-364,718 in both Group D (157 +/- 46.7) and Group E (31.9 +/- 11.6). In Group E, 2, 3, and 4 hr post-L-364,718 amylase releases were 60.2 +/- 19.7, 77.7 +/- 25.1, and 87.2 +/- 28.3 compared to 335.5 +/- 85.9, 291.0 +/- 21.8, and 289.9 +/- 45.7 in Group C indicating a sustained significant inhibition of stimulated autograft amylase secretion with the higher L-364,718 dosage. In Group F, no significant change in amylase secretion was demonstrated, indicating that L-364,718 must be administered prior to CCK stimulation to be effective. These studies demonstrate that L-364,718 has a dose dependent, inhibitory effect on basal, and OP-CCK-stimulated amylase secretion in a denervated autograft model. The therapeutic potential of L-364,718 and other CCK receptor antagonists in pancreatic transplantation warrants further study.

A retrospective chart analysis of 200 consecutive, cyclosporine-treated, renal allograft recipients, transplanted between January 1988 and June 1992, was conducted to determine the incidence of and the etiologic variables for post-transplant hypercholesterolemia. In addition, the effectiveness of dietary intervention alone or in combination with gemfibrozil (600 mg b.i.d.), in post-transplant hypercholesterolemia was evaluated. Hypercholesterolemia (> or = 240 mg/dl on two separate determinations, while on maintenance immunosuppression) was present in 138 patients (Group A-69%). When compared to the remaining 62 patients without hypercholesterolemia (Group B-31%), there were no differences in mean age, body weight at transplantation, race, incidence of overt diabetes, systolic and diastolic blood pressure, or serial serum creatinine, albumin, and cyclosporine levels between these groups. Post-transplant hypercholesterolemia was significantly more prevalent in females, in recipients with higher baseline serum total cholesterol levels (mean +/- SEM, Group A = 229.0 +/- 5.0 vs. Group B = 192.0 +/- 6.1 mg/dl, p < 0.001), and in recipients with an elevated fasting blood glucose at 1 year post-transplant (Group A = 150.5 +/- 10.5 vs. Group B = 105.2 +/- 10.7 mg/dl, p < 0.05). In all patients with hypercholesterolemia, a hypocaloric low fat and low cholesterol (< 300 mg/day) diet was initiated at a mean of 0.59 +/- 0.06 years after transplantation with grading of dietary compliance at each follow-up visit (Grade 1, < 300 mg cholesterol; Grade 2, 300-500 mg cholesterol; Grade 3, > 500 mg cholesterol intake in 24 hours).(ABSTRACT TRUNCATED AT 250 WORDS)

Monitoring of urinary enzymuria has been utilized to detect allograft dysfunction after pancreas transplantation with pancreaticocystostomy. In addition, pharmacologic exocrine suppression has been advocated to minimize bicarbonate and protein wasting. Ensuring the validity of these approaches requires controlling both for immunologic alterations in transplant function and for the renal excretion of amylase, bicarbonate, and protein. Toward this end, adult mongrel dogs were divided into two groups. Group A animals underwent distal pancreatectomy alone, and group B animals underwent distal pancreatectomy with autotransplantation and pancreaticocystostomy. In each group, amylase, bicarbonate, and protein output were determined over a 5-hour period in the basal state, during a continuous infusion of octapeptide-cholecystokinin (OP-CCK) at 125 ng/kg/hour, and during a continuous infusion of OP-CCK (125 ng/kg/hour) plus a bolus injection of one clinical unit of secretion per kilogram. Bicarbonate output was not significantly different in the groups with and without autografts. Compared to nonautograft experiments, a statistically significant increase in amylase output was demonstrated in the autograft animals. An increase in protein output was also demonstrated in the autograft experiments, and this increase was statistically significant in the OP-CCK group and the OP-CCK and secretin group. In addition, compared to basal autograft secretion, OP-CCK and OP-CCK plus secretin stimulation resulted in a sustained and significant increase in urinary amylase and protein secretion, indicating preserved sensitivity of the denervated pancreas to exogenous hormones. These results indicate that the canine segmental pancreatic autograft model with pancreaticocystostomy is a suitable model to identify agents associated with exocrine inhibition after transplantation.

The mechanism of regulation of negative feedback inhibition of the exocrine pancreas and its possible role in decreasing the exocrine secretion of the grafted human pancreas is unknown. To evaluate this we studied the effect of oral pancreatic enzymes on the stimulated transplanted pancreatic exocrine secretion in eight patients with allograft pancreaticocystostomies. After an 8-hr fast, all graft exocrine secretions via graft stent, fistula, and urinary anastomosis were collected for a 1-hr basal period. A standard 300-ml Lundh test meal was then ingested, and all exocrine secretions were collected in 30-min intervals for 3 hr. This test was repeated with 6 capsules of pancrelipase (24,000 units of lipase, 120,000 units of amylase, and 150,000 units of protease) given with the Lundh test meal. Stent, urine and fistula volume, amylase, and pH were measured for each collection period. The total 3-hr amylase secreted after the test meal and the test meal plus pancrelipase were compared. The period of peak amylase secretion after the test meal alone was compared with the same period after the test meal plus pancrelipase and the premeal basal period. The total amylase decreased 34% from 5550 +/- 1000 to 3680 +/- 740 IU/3 hr (P < .03) with pancrelipase. The peak amylase secretion decreased 63% from 1520 +/- 271 to 567 +/- 185 IU/30 min (P < .02) with the addition of pancrelipase to the test meal. Pancrelipase eliminated all meal-stimulated amylase secretion with the mean secretion 16% below the basal secretion of 674 +/- 117 IU/30 min. We conclude that pancreatic negative feedback inhibition significantly decreases meal-stimulated and basal exocrine secretion in the transplanted human pancreas.

A total of 17 patients with hydroceles following renal transplantation underwent sclerotherapy with tetracycline hydrochloride (10 ml. of a 5% solution of tetracycline in 1% lidocaine). A successful outcome was obtained in 15 patients (88%). Post-sclerotherapy hydrocelectomy was necessary in 2 patients (12%). No major complications (testicular loss, scrotal abscess or necrosis) occurred in any patient. Pain at injection was the only adverse effect. Tetracycline sclerotherapy for hydroceles appears to be an effective and safe procedure in the renal transplant population. We recommend this procedure as the initial treatment modality for hydroceles in patients with a renal allograft.

The usefulness of real-time sonography, duplex sonography, computed tomography (CT), cystography, diagnostic aspiration, and percutaneous drainage in the diagnosis and treatment of peri-pancreatic-transplant fluid collections was retrospectively assessed in 46 recipients of extraperitoneal pancreatic transplants. Forty-four abnormalities were identified in the extraperitoneal space at sonography, including four pancreatic pseudocysts associated with malfunction of the pancreatic duct, seven abscesses, six hematomas, nine urinomas, six early postoperative fluid collections that spontaneously resolved, six cases of pancreatitis, and six cases of vascular occlusion. Sonography (including pulsed Doppler sonography) was the procedure of choice in detecting fluid collections and diagnosing pancreatitis, rejection, vascular thrombosis, and pancreatic duct malfunction. CT was diagnostic in four of six hematomas; cystography was diagnostic in seven of nine urinomas. Sonographically guided percutaneous intervention enabled three patients to avoid surgery and allowed optimal surgical planning for six patients.

Octreotide acetate (Sandostatin), a long-acting somatostatin analogue, has been demonstrated to have an inhibitory effect on exocrine secretion in the neurally intact pancreas. This study was designed to evaluate the effect of this agent on exocrine secretion in the denervated canine pancreas, utilizing animals with pancreatic autografts and functioning pancreaticocystostomies. The rates of secretion of urinary (autograft) amylase (units/min) and bicarbonate (mM/min), over a five-hr interval, were determined in the basal state (group A, n = 10), after a bolus injection of 400 micrograms of Sandostatin (group B, n = 5), after a standard meal (group C, n = 5), or a meal preceded by 400 micrograms of Sandostatin (group D, n = 5). Basal secretion of amylase was decreased for 4 hr following Sandostatin, although this decrease was not significant. Conversely, basal bicarbonate secretion was not inhibited by Sandostatin. When compared with group C (22.4 +/- 3.2), a significant inhibition of meal-stimulated amylase release was demonstrated in group D (5.4 +/- 0.21, P = 0.0006) during the first hour after Sandostatin was given. This inhibition remained significant at 2 hr (group C = 38.5 +/- 5.2 versus group D = 9.4 +/- 0.8; P = 0.0006) and 3 hr (group C = 38.6 +/- 6.3 versus group D = 17.5 +/- 0.9; P = 0.0108) after Sandostatin was given. In addition, meal-stimulated bicarbonate secretion was significantly inhibited for 2 hr following Sandostatin (group C = 0.19 +/- 0.03 versus group D = 0.07 +/- 0.02, P = 0.0096; and group C = 0.23 +/- 0.03 versus group D = 0.10 +/- 0.01, P = 0.0018, respectively). These studies demonstrate that Sandostatin has a profound inhibitory effect on meal-stimulated enzyme and bicarbonate release in a denervated canine autograft model. Although the site of action of this agent remains to be defined, Sandostatin may have therapeutic potential in clinical pancreas transplantation.

The efficacies of two scintigraphic and two sonographic techniques and resultant index values, as markers of renal allograft pathology, were assessed. Index values of 183 combined scintigraphic and sonographic examinations in 47 graft recipients were compared to the pathological diagnosis of transplant biopsies and subsequent clinical outcome. All recipients were studied with baseline imaging techniques postoperatively, again when indicated by predefined clinical criteria, and prior to graft biopsy. The scintigraphic technique involved the calculation of indices of thrombotic activity and cortical graft perfusion. Ultrasound involved determination of the Doppler resistance index of Pourcelot and estimations of graft volume from real time images. A decreased cortical perfusion index was, overall, the most sensitive index of acute or chronic graft pathology, but it lacked specificity. Increased thrombotic and resistance indices were 96% and 86% sensitive for acute vascular rejection and were 82% and 76% specific. Jointly increased thrombotic and resistance indices improved the specificity for acute vascular rejection to 98%. An increase in graft volume of more than 50% over stable values was 100% sensitive and 92% specific for acute interstitial rejection, and 95% specific when paired with a normal thrombotic index. A marked increase in the thrombotic index was 100% sensitive for cyclosporine-induced thrombotic microangiopathy, but only 49% specific. The specificity of a markedly increased thrombotic index for thrombotic microangiopathy improved to 93% when the Doppler resistance index remained normal or was only marginally elevated. None of the scintigraphic or ultrasound indices were helpful for the diagnosis of acute tubular necrosis, chronic rejection, recurrent glomerulopathy, or graft infection.

Patients with diabetes and end-stage renal failure are known to have a high risk for cardiac morbidity and mortality associated with renal transplantation. The most efficient method to determine preoperative cardiac risk has not been established. To determine the effectiveness of intravenous dipyridamole thallium imaging in predicting cardiac events, 40 diabetic renal transplant candidates were studied preoperatively in a prospective trial. The study group consisted of 40 patients whose average age was 42 years (range 27 to 64); 34 (85%) were hypertensive and 21 (53%) were cigarette smokers. Cardiac history included chest pain in 6 patients and prior myocardial infarction in 3 patients. Dipyridamole thallium imaging showed reversible defects in 9 patients, fixed defects in 8 patients and normal scans in 23 patients. Dipyridamole thallium imaging was performed using 0.56 mg/kg of dipyridamole infused intravenously over 4 minutes. Cardiac events occurred only in patients with reversible thallium defects, of which there were 6. Of these 6 patients, 3 had cardiac events before transplantation and 3 had them in the early postoperative phase (within 6 weeks of surgery). Of 21 patients who underwent renal transplantation, 3 had cardiac events within 6 weeks of transplantation. The average duration of follow-up was 11 months (range 1 to 21). Thus, dipyridamole thallium imaging is an effective method of identifying renal transplant candidates likely to develop cardiac complications. Routine coronary angiography may not be necessary to screen all renal transplant candidates for coronary artery disease before surgery.

From April 1975 to September 1980, 16 symptomatic bovine graft aneurysms were identified in 200 grafts used for long-term hemodialysis. Aneurysms occurred in five (3.6%) straight forearm grafts, two (33%) reversed forearm grafts, two (33%) straight thigh grafts, and seven (18.9%) upper arm grafts. Mean blood pressures were similar in the aneurysm and non-aneurysm groups (142/81 vs 153/83 mm Hg). At operation, the aneurysms were determined to be true in three patients and false in 13. Five patients were treated by graft ligation and aneurysm excision and 11 by aneurysm excision and graft revision, with additional graft survivals of one to 25 months. In conclusion, bovine graft aneurysms are usually false and are more frequent in proximal grafts. In the absence of infection, resection is indicated and will result in considerable prolongation of graft survival.

A patient with abdominal pain was found to have severe compression of his celiac artery on abdominal angiography. Preoperative evaluation with base line and provocative xylose absorption studies were compatible with decreased intestinal blood flow. Surgical division of the median arcuate ligament corrected the intraoperatively determined pressure gradient. Postoperative studies at three months demonstrate absence of celiac artery compression on angiography and normal provocative xylose absorption studies. This case lends support to the existence of the median arcuate ligament syndrome.

Eight Permcaths were placed into seven patients without other alternative hemodialysis access sites. They lasted from 1-109 treatments. However, recurrent thrombi formed at the tip of two catheters. Although urokinase successfully dissolved the thrombi, recurrence of clot despite anticoagulation therapy led to removal of both catheters. We conclude that the Permcath should be used with caution in patients on hemodialysis who have no alternative vascular access sites because of the risk of thromboembolism. The value of anticoagulants to prevent recurrent thrombi is unclear, because thrombi recurred in both patients despite their use.

Extrathoracic esophagectomy has the potential of improving the results of resectional therapy for carcinoma of the esophagus by eliminating the need for thoracotomy and decreasing postoperative pulmonary complications. This report compares the operative and functional results of blunt extrathoracic esophagectomy and substernal reversed gastric tube reconstruction in patients with esophageal cancer to results in 10 consecutive nonrandomized control patients treated by standard esophagogastrectomy. Extrathoracic esophagectomy was associated with greater pulmonary dysfunction than standard esophagogastrectomy. While there was no significant difference in survival in the two groups, three patients in the standard esophagogastrectomy group (mean survival 9.0 months) and none in the extrathoracic esophagectomy group (mean survival 7.4 months) developed anastomotic recurrence. Extrathoracic esophagectomy evidently does not afford patients with esophageal carcinoma better palliation than standard esophagogastrectomy.

The occurrence of perforated sigmoid diverticulitis in a renal transplant recipient stimulated a review of colorectal complications in renal allograft recipients. One hundred twenty-five renal transplantations were performed in 113 patients between January 1968 and December 1975. Six patients (5%) were identified as having colorectal complications and five of these patients died as a direct result. Chart analysis of these 113 transplant recipients identified 55 patients as having undergone colonic evaluation (contrast enema, postmortem examination), with seven of these 55 (13%) found to have diverticulosis and major colonic complications eventually developing in four of these seven. Since the mortality from the complications of colorectal diseases in immunosuppressed patients is so prohibitive, in patients with diverticulosis and a previous history suggestive of diverticulitis, consideration should be given to exclusion from transplantation or elective segmental colectomy prior to transplantation.

Since elective and emergent nontransplant-related surgical procedures are frequently necessary in renal allograft recipients, it becomes essential to determine the incidence and outcome of these operations in this population. For this reason, a retrospective analysis of 273 consecutive renal transplants performed in 254 patients between January 1978 and November 1985 was accomplished. During this interval, 139 patients underwent 162 nontransplant-related surgical procedures. In the 44 patients who underwent 55 emergent or semiemergent procedures, 8 patients (18 percent) died in the postoperative period. All deaths occurred in patients who underwent major abdominal or thoracic procedures for perforated viscera, gastrointestinal bleeding, or empyema and lung abscess, and all deaths were secondary to sepsis and multiple organ failure. In the survivors of emergent procedures, the mean preoperative and discharge serum creatinine levels were 2.87 mg/dl and 2.82 mg/dl, respectively. In the 95 patients who underwent 107 elective procedures, most of which were performed under general anesthesia, the operative mortality was 4.2 percent. In patients with stable renal allograft function at the time of operation, mean serum creatinine levels preoperatively and at the time of discharge were not significantly different (1.74 mg/dl versus 1.64 mg/dl). In conclusion, emergent operative procedures for intraabdominal or thoracic catastrophes are associated with a high mortality rate in renal allograft recipients. On the other hand, elective surgical procedures can be undertaken with an acceptable mortality rate and no adverse affects on graft function. Of utmost importance in these patients is the close monitoring of the immunosuppressive regimen and the early detection and treatment of potential septic complications.

Operative management provides low risk palliation for symptomatic occlusive disease of the leg. Survival is adversely affected by associated conditions. The rate of limb salvage was 70 per cent at 2 years in patients with gangrene. Bypass grafting did not increase the risk of subsequent amputation (mortality 11 per cent), and therefore primary amputation should be avoided.

This case report presents clinical, scintigraphic, duplex sonographic, and biopsy findings in a 23-year-old female renal allograft (RAG) recipient, who had transplantation for chronic renal failure secondary to hemolytic uremic syndrome (HUS). She demonstrated acute and rapidly progressing RAG failure at 7 weeks after transplantation.

To help determine the etiology of posttransplant aseptic hip necrosis, 11 stable renal allograft recipients (group A) who developed aseptic hip necrosis were compared with 89 patients (group B) without this complication. A comparison of mean age, duration of dialysis, mean daily prednisone dose, and incidence of rejection in the first year following transplant, sex, donor source, incidence of posttransplant parathyroidectomy, and mean serum calcium and alkaline phosphatase levels identified no significant differences between groups A and B. The mean serum creatinine value at three (2.2 +/- 0.31 mg/dL [190 +/- 30 mumol/L] vs 1.9 +/- 0.10 mg/dL [170 +/- 10 mumol/L]) and 12 (2.3 +/- 0.35 mg/dL [200 +/- 30 mumol/L] vs 1.9 +/- 0.10 mg/dL [170 +/- 10 mumol/L]) months and the serum phosphate value at three (3.0 +/- 0.19 mg/dL [0.97 +/- 0.06 mmol/L] vs 2.8 +/- 0.08 mg/dL [0.90 +/- 0.03 mmol/L]) and six (3.2 +/- 0.25 mg/dL [1.03 +/- 0.08 mmol/L] vs 2.9 +/- 0.25 mg/dL [0.94 +/- 0.08 mmol/L]) months were significantly greater in group A. Eight patients in group A underwent 13 total hip replacement an average of 16.5 +/- 3.1 months following transplant without significant complications. In conclusion, posttransplant aseptic hip necrosis occurs frequently, and renal allograft dysfunction may contribute significantly to its pathogenesis. When indicated, total hip replacement is both safe and effective.

Cadaver kidneys from donors who have sustained cardiac standstill are often unsuitable for transplantation due to prolonged warm ischemic time. In an attempt to increase the salvage rate of these kidneys, the efficacy of in situ intra-aortic cold perfusion in producing immediate function of allografted kidneys was assessed in the nonheart beating canine model. In the first experiment, kidneys harvested after cardiac standstill and immediate intra-aortic cold perfusion were demonstrated to function equally as well as kidneys harvested "optimally." In the second experiment, evaluation of intra-aortic cold perfusion on renal core temperature demonstrated rapid cooling of these kidneys to a protective range. Early clinical results in donors whose kidneys were removed after cardiac arrest demonstrate that most of the kidneys allotransplanted after in situ intra-aortic cold perfusion functioned immediately. These preliminary experimental and clinical results demonstrate the effectiveness of in situ intra-aortic cold perfusion. Wider application of this technique to donors with cardiac standstill should increase the available organs for transplantation.

The effect of various nucleotide-enhancing agents on renal function and intracellular nucleotide levels was evaluated in a canine autotransplant model. Thirty-five dogs (18-28 kg) underwent left nephrectomy and 30 min of warm ischemia followed by Collins C-4 flush and 24 hr of cold-storage preservation. Heterotopic autotransplantation and immediate contralateral nephrectomy was then performed. Seven equal groups were evaluated: group A--controls, group B--adenosine pretreatment (1.0 g), group C--dipyridamole pretreatment (10 mg), group D--adenosine (1.0 g), and dipyridamole (10 mg) pretreatment, group E--adenosine (200 mg) and EHNA (2.5 mg/kg) pretreatment, group F--adenosine (200 mg) and EHNA (2.5 mg/kg) in the Collins C-4 flush, and group G--adenosine (200 mg) and EHNA (2.5 mg/kg) at the time of autotransplantation. All kidneys underwent cortical biopsies at the end of preservation and 1 hr after restoration of blood flow for determinations of AMP, ADP, and ATP. In the pretreatment groups (groups B through E) there was 60% graft survival whereas the controls (group A) and the groups treated after ischemia (groups F and G) had 0, 0, and 20% graft survival, respectively. In groups B and E, ATP levels were greater than controls after preservation and 1 hr after restoration of blood flow. Group C AMP and ADP levels and group D energy charge were greater than controls in the post-transplantation biopsies. Administration of adenosine and EHNA after ischemia was not associated with increased intracellular nucleotide levels. One hour post-transplantation biopsies demonstrated greater ability to regenerate cortical nucleotides in the surviving animals but no absolute value could be identified as a predictor of viability. In conclusion, pretreatment with adenosine, dipyridamole, and EHNA alone and in combination is beneficial in ischemically injured kidneys undergoing cold-storage preservation.

Dogs and cats killed by intravenous injection of either 0.3 ml/kg body weight T-61 or 100 mg/kg body weight pentoarbital and necropsied at less than 5 minutes or at 15 minutes after injection did not have gross or microscopic pathological changes. However, dogs and cats killed with T-61 at a dose of 1.0--1.5 ml/kg body weight and necropsied at 15 minutes after injection had significant gross and microscopic pathological lesions. Grossly, the lungs were severely edematous, did not collapse, and were deep red. Microscopically, the lungs had severe pulmonary edema and endothelial necrosis. Endothelial swelling of glomerular tuft vessels was also present. These lung and kidney lesions are classified as an euthanasia artefact.

The effects of ATP-MgCl2 and dipyridamole were evaluated in a canine model. Twenty-five adult mongrel dogs were divided into five equal groups. All dogs underwent left nephrectomy and 30 min of warm ischemia followed by Collins' C-4 flush and 24 hr of cold-storage preservation. Heterotopic autotransplantation and immediate contralateral nephrectomy were then performed. Group A served as controls; Group B was pretreated with intravenous ATP-MgCl2 (2.5 mM); Group C with intravenous dipyridamole (10 mg), and Group D with both ATP-MgCl2 (2.5 mM) and dipyridamole (10 mg). Group E was treated with ATP-MgCl2 (2.5 mM) at the time of transplantation. All kidneys underwent cortical biopsies at the end of preservation and 1 hr after restoration of blood flow for determinations of AMP, ADP, and ATP. In Groups A and E there were no survivors, whereas Groups B, C, and D had 40, 60, and 40% graft survival. In Groups B and D, ATP and energy charge (EC) were greater than that of controls after 24 hr of preservation, with Group D values being significantly greater (P less than 0.01). AMP and ADP levels were significantly greater (P less than 0.02) in Group C when compared to Group A. One hour posttransplantation biopsies demonstrated greater ability to regenerate cortical nucleotides in the surviving animals, but no absolute value could be identified as a predictor of viability. In conclusion, pretreatment with ATP-MgCl2 or dipyridamole maintains intracellular nucleotide levels and has a beneficial effect on graft survival in ischemically injured kidneys undergoing cold-storage preservation.