Risk of strut fracture of Björk-Shiley convexo-concave valves.
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Biomedical subjects
Publications and source records attributed to J G Chandler.
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Congenital anomalies of the alimentary tract can evade detection into adulthood because they cause only moderate symptoms or they escape purview of a prepared observer. In other instances, evolution or copathogenesis may need to occur before the lesions become manifest. We have managed 17 of these patients presenting at ages 23 to 71 years. The median duration of symptoms was 5 years, ranging from 1 months to 23 years. Defects of foregut embryogenesis predominated (71%). We were able to establish the correct diagnosis before operating on nine patients, but three had already had a previous celiotomy for the same problem so a truly preoperative diagnosis was possible in only six (35%). The literature validates the dominance of foregut anomalies in adults. There is no older age limit that would exclude consideration of these lesions. Endoscopy, computerized tomography, and ultrasonography have greatly facilitated recognition, but our experience suggests that the principal obstacle to timely diagnosis is the reluctance to consider a congenital cause for an adult's symptoms.
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The distal splenorenal shunt is less likely to provoke encephalopathy than conventional shunting procedures, and it may offer a survival advantage for certain cirrhotic individuals, presumably because of its selective nature. This study suggests that the distal splenorenal shunt, even with exceptional efforts to achieve portomesenteric-gastrosplenic (PM-GS) disconnection, is not nearly as selective as it originally was assumed to be. In 11 patients intraoperative pressure determinations showed a significant decrease in portal pressure after end-to-side distal splenorenal anastomosis and no restoration of portal pressure after PM-GS disconnection. Measurements of flow through the shunt were comparable to those reported for portacaval shunts, and shunt flow was not decreased significantly by PM-GS disconnection. Postoperative angiography showed some PM-GS collateral in 17 of 18 patients, and later angiographic studies showed a tendency for progressive collateral development and consequent loss of hepatopetal portal perfusion. The advantages of the distal splenorenal shunt must accrue from gradual, as opposed to abrupt, portal deprivation, rather than from lasting selectivity.
Eleven patients underwent jejunoileal bypass for morbid obesity. Serial intestinal biopsies were obtained prior to, and at timed intervals following, operation in both fasted and fat-fed states. Villus height increased asymptotically, reaching a plateau one year after operation, with an increase of 80 per cent in mean villus length. The postbypass body weight reached a plateau at 63.9 per cent of initial body weight and correlated linearly with villus height following an asymptotic curvilinear course. The time required to attain 90 per cent of total body weight loss was 15.9 months. A study of intestinal fat absorption at both the light microscopic and ultrastructural levels showed that the enlarged villi are lined along the entire villus by functionally mature epithelium capable of transporting lipid. Villus hypertrophy is an important mechanism in the plateauing of weight loss after jejunoileal bypass for morbid obesity.
Pancreatic trauma, regardless of etiology, has been consistently associated with a mortality of 20 percent and enormous morbidity. Twenty-five pancreatic injuries, including four solitary wounds of the pancreas, were analyzed to determine why pancreatic trauma should have such an adverse prognosis. Eleven patients were victims of blunt trauma and fourteen sustained gunshot wounds. There were no stab wounds. The important determinants of mortality were associated injuries to major vessels, wounds of the head of the gland, and failure to adequately control leaking exocrine secretion. All four deaths were directly related to massive hemorrhage; in two instances leakage of pancreatic juice was also implicated. With the exception of benign solitary blunt wounds of the pancreas to the body of the gland immediately ventral to the spinal column, an injury of the pancreas is evidence that the abdomen has been subjected to severe trauma, which predisposes the patient to a high mortality and morbidity. The pancreatic injury, interacting with other abdominal injuries, is likely to be a cause of significant mortality and to result in complications that will prolong the patient's hospitalization.
The consequences of occlusion of a major upper extremity vein were evaluated in eight patients with effort thrombosis, ten with thrombosis secondary to intimal injury, six with extrinsic compression, and one hypercoagulable patient, all of whom were followed for an average of 4 years. Twenty-two patients had venography, which confirmed the diagnosis but often failed to define the proximal extent of obstruction. Thirteen patients had noninvasive hemodynamic studies which did not corroborate chronic morbidity, but which were valuable in assessing the effect os specific therapy. Twelve patients were treated with anticoagulants, and six had operative removal or bypass of the obstruction. Three patients had pulmonary emboli; two embolized while on anticoagulants and both died. Swelling, pain, prominent veins, and easy fatigability of the affected extremity were the late sequelae of occlusion. Chronic morbidity was more dependent on etiology than on initial treatment. Thrombosis secondary to intimal injury caused no persistent symptoms, whether treated with anticoagulants or not. Effort thrombosis was intermediate: three fourths complained that their affected arm tired easily and half had prominent veins or persistent swelling. All of those with obstruction secondary to extrinsic compression had easy fatigability. The majority also had concomitant swelling, pain, and prominent collaterals. Operative treatment produced objective improvement in venous outflow but often was unsuccessful in relieving symptoms, particularly in patients with obstruction from extrinsic compression.
The characteristics of hepatocyte intramitochondrial filaments (IMF's) were studied in 16 patients undergoing jejunal ileal bypass for morbid obesity. At the time of bypass, all of the liver biopsies showed varying degrees of steatosis and IMF's were present in 13 of the 16 operative specimens. The IMF's were most prominent in the periportal cells, whereas the intracellular lipid was concentrated in centrilobular cells. Midzonal hepatocytes were intermediate in both respects. The IMF'S were more abundant in biopsies showing moderate steatosis than in those with marked lipid accumulation in which the IMF's were limited to hepatocytes in juxtaposition to portal triads. The IMF's appeared to originate from mitochondrial cristae. When steatosis resolved 12 to 18 months after intestinal bypass the prevalence of IMF's diminished also. It is hypothesized that the presence of IMF's is ultrastructural evidence of an adaption to an altered metabolic environment which resolves when the inciting influence is removed.
Misleading pneumoperitoneum takes one of two forms: true pneymoperitoneum without peritonitis or pneumoperitoneum simulated by adventitious x-ray shadows. In both instances, the roentgenographic appearance of free intraperitoneal air proves to be a specious indication for laparotomy. Twenty-eight per cent of 29 patients with misleading pneumoperitoneum were subjected to operations that, retrospectively, might not seem absolutely necessary. The decisions to operate on patients with pneumoperitoneum without peritonitis were based on the amount of pneumoperitoneum roentgenographically visualized. The instances of pseudopneumoperitoneum had several common features. The diagnosis often was based only on x-ray films of the chest. Compatibility with clinical features was marginal; the radiolucency was often not truly at the apex of the diaphragm. Finally, the x-ray films, interpretation and working conditions frequently were suboptimal.
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There is ample evidence from this retrospective comparison to indicate that emphysematous cholecystitis does merit clinical distinction apart from acute cholecystitis. It is an acute infection of the gallbladder caused by a specific group of bacteria that may be aided by some aspect of local ischemia. Cholelithiasis does not seem to be a major factor in the pathogenesis of emphysematous cholecystitis, and this, in association with some dependence upon ischemia, may account for the predominance of this disease in males rather than females. Gangrene is a common feature of the pathologic process, and thus it is not surprising that the diagnosis of emphysematous cholecystitis implies a risk of gallbladder perforation that is five times that expected from ordinary acute cholecystitis. The key to identifying this disease is the plain abdominal roentgenogram which in most instances will make the diagnosis and provide an impetus for early operative intervention.
The long-term exocrine function of fifty-nine pancreaticoduodenal isografts was evaluated in rats for up to one year post transplantation. At one, three, six, nine, and twelve months after transplantation the grafts were cannulated and the exocrine secretion was collected. The volume, protein content, pH, amylase and trypsin concentrations, and electrolyte composition of the secretion were compared with those obtained from the host pancreas in nineteen control rats. Twenty-four hour secretion studies demonstrated normal basal function of the pancreas transplant when compared with that of the host. Pancreozymin stimulation caused an increase in volume, trypsin concentration, and amylase concentration of the graft pancreas secretion that was similar to those seen in the host. These studies indicate that there is normal exocrine secretion of pancreas transplants in the absence of rejection and that denervation of the gland has little direct effect on over-all pancreatic function.
General recognition of the presence of a specific hepatotrophic factor in portal blood that is necessary for liver regeneration was delayed by two major problems. First, there was a long period of confusion regarding liver atrophy, liver hypertrophy, and cellular hyperplasia. Second, because only exposure to other liver tissue destroys the hepatotrophic activity, all of the studies that were based on bypassing the portal blood into the systemic circulation merely diluted the active substance, which still was available to the hepatocytes by recirculation through the hepatic artery. These problems have been resolved by the development of more sophisticated methods by which to assay liver regeneration and by the introduction of the double liver model to study regeneration. During the time when liver weight alone was used to assess regeneration, the regenerative capacity of the liver was reported to be much greater after portacaval transposition than after end-to-side portacaval shunt, a finding that is inconsistent with current knowledge of the hepatotrophic portal blood factor. To re-evaluate the effect on liver regeneration of providing a compensatory systemic venous inflow after complete portal diversion, 40 partially hepatectomized inbred rats which had previously undergone either a sham operation and end-to-side portacaval shunt or a portacaval transposition were compared on the basis of six separate criteria of regeneration. All of the livers actively regenerated and no significant advantage of providing a substitute systemic venous inflow to the liver could be detected by any of the criteria.
A prospective evaluation of emergency portacaval shunt has been conducted during a 12 year period in 138 unselected, consecutive patients with alcoholic cirrhosis and bleeding esophageal varies. An extensive diagnostic evaluation was completed within seven hours of hospital admission, and the shunt operation was undertaken within a mean of 8.5 hours. Follow-up study was conducted in a special clinic, and the current status of 97.1 per cent of the patients had jaundice, ascites or encephalopathy alone or in combination on admission. Systemic intravenous administration of posterior pituitary extract temporarily controlled the hemorrhage in 94 per cent of the patients, and the emergency portacaval shunt promptly and permanently controlled the varix bleeding in 96 per cent of the patients. Contrary to recent proposals, patients with the highest portal perfusion pressure and, presumably, the largest hepatopetal portal flow had the highest survival rate and those who were presumed from pressure measurements to sustain the smallest portal flow diversion from the shunt had the lowest survival rate. The operative survival rate was 51 per cent, the predicted seven year survival rate for those operated upon seven or more years ago was 42.5 per cent. Encephalopathy requiring dietary protein restriction developed at some time in 17 per cent of the survivors. Sixty per cent of the survivors abstained from alcohol, and 53 per cent resumed gainful employment or full time housekeeping. Preoperative factors that adversely influenced survial rate were ingestion of alcohol within one month of bleeding, ascites, severe muscle-wasting and a small liver. Postoperatively, the single most important factor that compromised long term survival was resumption of alcoholism. In comparisons with our previous prospective studies, emergency portacaval shunt resulted in a significantly greater long term survival rate than did either emergency medical therapy or emergency varix ligation, followed by elective shunt. It is concluded that emergency portacaval shunt is the most effective treatment of bleeding esophageal varices in patients with alcoholic cirrhosis. Criteria for exclusion of those patients who are unlikely to derive long term benefits from portacaval shunt remain to be defined by further studies.
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