Surgical treatment of morbid obesity.
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Biomedical subjects
Publications and source records attributed to H V Villar.
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Twenty-six patients with Hodgkin's disease were restaged both clinically and surgically within 2 months of completing their planned chemotherapy. Six patients (23%) had surgically proven persisting disease. Patients were divided into three groups: group I--eight patients had normal findings at clinical restaging and all were free of disease at surgery; group 2--13 patients had abnormal findings at clinical restaging, but only two (15%) were surgically documented to have persistent disease; and group 3--five patients had incomplete clinical restaging but, because of initial bulky disease, underwent surgical restaging, which showed that four patients had residual disease. The spleen was the site of persisting disease in all six patients with residual disease; four also had para-aortic nodal involvement. All 20 patients in pathologically documented complete remission remain relapse-free, with a mean followup of 26 months. This is significantly better (P less than 0.001) than the 21% relapse rate for 224 comparable patients in complete remission established by clinical but not surgical restaging. It appears that surgical restaging provides useful prognostic and therapeutic information in selected patients with Hodgkin's disease.
Gel fractionation of portal, arterial and peripheral plasma glucagon levels was performed before and after the successful removal of a glucagonoma. A 47 year old woman had symptoms of dermatitis, weight loss, anemia and diabetes mellitus over a 16 year period. Removal of the alpha-cell tumor corrected all of her symptoms. Gel filtration of portal, arterial and peripheral blood showed two peaks of glucagon radioimmunoassay activity, a higher molecular weight glucagon with a molecular weight of 9,000 and a 3,500 dalton glucagon. Five minutes after tumor removal, the higher molecular weight glucagon had disappeared completely from the arterial and peripheral blood but not from the portal vein.
Neurological complications consisting of recent memory loss, visuospatial disorientation, and poor concentration disabled three patients years after a jejunoileal bypass for morbid obesity. The metabolic evaluation and computed tomography gave normal results. The neurological dysfunction cleared completely after reconstitution of normal intestinal anatomy. Neurological recovery was documented by formal neuropsychological testing.
The patterns of fundic and antral motility as well as changes in fundic pressure in response to balloon distention were evaluated in 26 patients before and after gastric partitioning (18 patients) or gastric bypass (8 patients). In addition, the rate of gastric emptying, as measured by the ingestion of 99mTc-tagged chicken liver, was determined after gastric partitioning (12 patients) and bypass (7 patients). A striking alteration in the motility of the fundus occurs after both gastric partitioning and bypass. Normal pressure waves of the fundus disappear with both procedures. Fullness after both operations is secondary to distension of the pouch rather than to an increase in pressure. Changes in antral motility, inhibition, and recovery seem to be neurally mediated. The gastric emptying rate was 6.9% +/0 2.9% per minute after gastric bypass and 1.8% +/- 0.4% per minute after partitioning. Delayed emptying could be an additional benefit of gastric partitioning.
Twelve patients underwent a takedown of the jejunoileal bypass with restoration of normal continuity of the intestine. Specimens were obtained for biopsy from the excluded proximal jejunum and distal ileum as well as the distal in continuity jejunum. Hypertrophy of the mucosa was observed in the in continuity segment, as previously described. Villi of the bypassed jejunum displayed no evidence of hypertrophy or of atrophy and were identical in size to villous measurements prior to creation of the jejunoileal bypass. At the ultrastructural level, absorptive cells of bypassed jejunal segments exhibited normal morphologic characteristics. There was no indication of cellular immaturity above the level of the intestinal crypts. In contrast, villi of bypassed ileum, near the colonic anastomosis, demonstrated hypertrophy, presumably reflecting reflux of luminal material into this segment of bypassed intestine. The results of this investigation support the concept that significant morphologic alterations of the mucosa do not occur in totally bypassed segments of intestine after the jejunoileal bypass procedures with attainment of weight stabilization.
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Surgical procedures involving the parathyroid glands pose special problems. Careful attention to preoperative rehydration, control of hypercalcemia, and evaluation of renal function are mandatory. Intraoperative management is usually uncomplicated. Severe hypocalcemia may complicate the postoperative period, especially if severe bone disease is present.
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Seven patients with acute and progressive abdominal distension secondary to massive cecal and right colon ileus are analyzed. Five had pseudoobstruction of the colon and two had cecal volvulus. Two of the patients with pseudoobstruction and one with cecal volvulus died from preexisting diseases. Pseudoobstruction of the colon is not a rare complication of elderly, sick, bedridden patients. Differential diagnoses include cecal and sigmoid volvulus and acute gastric dilation. Initial conservative therapy is warranted if no peritoneal signs are present. If the cecal diameter is more than 12 cm, colonoscopic decompression with a fiberscope should be attempted. If unsuccessful, tube cecostomy will provide curative, life-saving therapy even if taenia splitting is present. Perforation or widely scattered areas of necrosis make resection mandatory.
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Emergency esophagogastroduodenoscopy has been performed in 192 consecutive patients admitted with massive gastrointestinal bleeding. Accurate endoscopic diagnosis was made in 184 or 96%; 58 patients underwent emergency operations to control bleeding with an overall operative mortality of 26%. Excluding 16 patients who underwent emergency portacaval shunting, the operative mortality was 7%. In 6 patients, the bleeding was controlled by endoscopic electrocoagulation. There were no complications. Emergency endoscopy should be done routinely as the primary diagnostic approach in the diagnosis of upper gastrointestinal bleeding.
In dogs prepared with isolated, innervated antral pouches, intraduodenal perfusion with liver extract at pH 7, with the atrum buffered at pH 7, resulted in a significant release of gastrin selectively from the antrum and from the duodenum. Acidification of the meal to pH 1 abolished both antral and duodenal gastrin release, whereas acidification of the antrum abolished only the antral gastrin response. After antrectomy, liver extract at pH 7 caused a diminished but significant release of duodenal gastrin. These studies provide evidence that an intestinal meal may release (in addition to a specific intestinal phase hormone) gastrin from the intestine, and from antrum, by means of a pH-sensitive mechanism which may involve a humoral agent (enterobombesin?) from the small bowel.
In five awake mongrel dogs, endogenous gastrin was released by continuous irrigation of the antrum with acetylcholine. After 60 minutes of antral perfusion, the entire vascular supply of the antrum was suddenly and totally occluded, and serial samples of peripheral blood were taken for measurement of gastrin. The rate of disappearance of endogenous gastrin was caluclated by standard linear regression analysis; the calculated half-life of endogenous gastrin was 8.62 minutes. Analysis of the data suggests that the disappearance rate of endogenous gastrin could be explained by two distinct half-lives: one of 2.8 minutes (which is similar to the half-time in dogs of both 14- and 17 -amino acid gastrin), and another of 15.4 minutes (which is similar to the half-time of 34 -amino acid gastrin). Physiologically released gastrin is a mixture of three or more molecular forms of gastrin and the half-life of 8.62 minutes probably represents the disappearance half-time of this mixture.
Fourteen dogs received varying doses of antigastrin antibody; after a single dose of 0.07 ml/kg, circulating gastrin levels could not be measured for as long as forty-seven days. Gastric secretion in response to food was not diminished by antigastrin antibody doses as high as 0.07 ml/kg daily for ten days. Larger doses, 0.2 and 0.4 ml/kg, were required to produce a temporary reduction in gastric-stimulated gastric acid secretion. Mucosal levels of gastrin in the antrum, fundus, and duodenum were greatly increased ten days after injection of antigastrin antibody. The therapeutic use of antigastrin antibody to control gastric secretion seems at the present time not feasible because of the scarcity of the antigastrin antibody and because large doses aare required to obtain only a temporary effect.
We have measured serum gastrin and gastric acid secretion in 66 duodenal ulcer patients before and after vagotomy and pyloroplasty (V + P--15 patients), selective proximal vagotomy without drainage (SPV - D--11 patients), and with drainage (SPV + D--19 patients), and vagotomy, antrectomy, and either gastroduodenostomy (V + BI--15 patients) or gastrojejunostomy (V + BII--6 patients). Basal and peak postprandial gastrin levels were increased in postoperative V + P, SPV - D, and SPV + D patients. Basal and peak postprandial levels of gastrin were unchanged after V + BII, indicative of duodenal release of gastrin. Gastrin response to food was abolished in V + BII patients. Acid output was reliably reduced after all five operations; reduction was greatest in patients after antrectomy and least in patients after SPV. No beneficial results were found with drainage in SPV patients. Acid secretion increased with time in SPV patients, especially those with drainage.
Five dogs prepared with Heidenhain pouches received infusions of saline, GIP and VIP before and after a standard meat meal. Blood samples were obtained under basal conditions and at subsequent intervals for measurement of gastrin, insulin, GIP and VIP by radioimmunoassay. GIP and VIP infusions had no effect on basal levels of gastrin. GIP and VIP (in common with secretin and glucagon) were found to suppress food-stimulated release of gastrin and gastrin-stimulated acid secretion from the Heidenhain pouch. Insulin levels were significantly elevated during GIP and VIP infusions. Food released GIP (and perhaps VIP.