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The afferent loop syndrome.

The afferent loop syndromes result from obstruction to the afferent jejunal loop. Acute ALS results from complete obstruction, usually occurs early after surgery and runs a devastatingly lethal course unless promptly treated by reoperation. In chronic ALS the obstruction is intermittent and produces a clinical syndrome from which a diagnostic histroy can usually be obtained. Although the exact incidence is unknown, it is certainly not rare, especially in antecolic Billroth II gastrectomies. Treatment consists of doing away with the afferent loop. In gastroenterostomy alone takedown of the anastomosis with a Weinberg pyloroplasty is the treatment of choice. The safest and simplest treatment for patients whose original operation was Billroth II gastrectomy is conversion to a Roux-en-Y procedure. In all cases vagotomy should be added unless previously performed. No medical treatment is available and patients with no other contraindication should have revisional surgery if symptoms are clinically significant. Both acute and chronic afferent loop syndromes should be completely prevented by appropriate choice of the initial operative procedure. The vagotomized stomach should be drained by pyloroplasty, not gastrojejunostomy. Vagotomy and antrectomy should be reconstructed with a Billroth I gastroduodenostomy. The Braun enteroanastomosis should be utilized after subtotal gastrectomy for carcinoma. The wider application of parietal cell vagotomy for duodenal ulcer deserves close observation and further consideration.

Acute Disease

[Acute pancreatitis and afferent loop syndrome].

A new case of afferent loop obstruction presenting as acute pancreatitis is described. It is an uncommon manifestation of the afferent loop syndrome: less than 20 cases found in the literature. The diagnosis of afferent loop obstruction should be suspected in any patient with acute pancreatitis and a previous Billroth II gastrectomy. Duodenopancreatic reflux seems to play an important role in the pathogenesis of acute pancreatitis in this situation. The "closed duodenal loop" experimental model of acute pancreatitis simulates quite closely this clinical situation. The physiopathological principles, diagnosis and treatment of this syndrome is reviewed.

Acute Disease

Gastric evacuation and propulsive intestinal motility in acute afferent loop syndrome in the rat.

The acute afferent loop syndrome, i.e. occlusion of the afferent loop after partial gastrectomy by the Billroth II method, was produced in the rat. In a primary session a gastrojejunostomy with division of the pylorus was performed. 2-3 months later the afferent loop was ligated. The gastric evacuation and the propulsive motility of the intestine were studied quantitatively, using an inert radioisotope. Both the gastric evacuation and the propulsive intestinal motility were considerably delayed in ALS, both in relation to the laparotomized controls and in relation to previous findings in mechanical intestinal obstruction and paralytic ileus due to retroperitoneal irritation or bacterial peritonitis.

Acute Disease

Pathophysiology in the acute afferent loop syndrome. A study in rats.

The afferent loop syndrome, i.e. occlusion of an afferent intestinal loop after a Billroth II partial gastrectomy, was induced in rats. After various time intervals the animals were killed and the haematocrit and serum osmolality were determined. The content of the occluded loop was analysed with respect to volume, bacterial flora and osmolality. In some cases a sample of the content was incubated at 37 degrees C and the osmolality determined at regular intervals. Groups of animals were studied in this way after 30 min or 1, 4, 8 or 12 h of occlusion. The haematocrit rose with time after the occlusion. The osmolality of the plasma and of the content of the occluded loop did not increase. The volume of fluid in the occluded loop increased continuously with time--from an average of 0.5 ml in the control cases to 6.1 ml after 12 h of occlusion. Experiments in vitro showed that the initial osmolality of the content of the loop was 300 mOsm. After incubation of the samples this increased by 43 to 146 percent. The bacterial content of the loop, including Clostridium perfringens, increased significantly. The results indicate that a marked breakdown of substances takes place in such an occluded intestinal loop, which increases the osmolality. As a result fluid is immediately attracted to the loop to keep the osmolality constant. A combination of this fluid increase due to osmosis and contractions of the intestinal wall leads to a pressure in the occluded loop which considerably exceeds the pressure in the common bile duct due to secretions from the pancreas and liver.

Acute Disease

[The chronic afferent loop syndrome (author's transl)].

Between 1968 and 1973, 12 patients with a chronic afferent loop syndrome were treated at the University Surgical Hospital in Munich (6 from own hospital and 6 B II resected patients from external hospitals). 11 of them had to undergo reoperation (1 patient refused). X-ray and gastroscopy confirmed the diagnosis of chronic afferent loop syndrome type I in all 12 cases. The obstruction was caused by: adhesion and kinking of the loop (7 cases), too long and mobile loops (6 cases) incorrect anastomosis (3 cases), torsion and stenosis in the mesocolonic slit (2 cases), internal hernia (1 case). 8 patients showed good operative results, in 2 patients symptoms still persist; 1 patient died of sepsis postoperatively.

Adult

Afferent loop syndrome: sonographic findings in seven cases.

We studied the sonographic findings in seven patients in whom afferent loop obstruction was first detected by sonography. All seven subsequently were proved at surgery to have afferent loop syndrome. The causes of the obstruction included internal hernia (n = 3), cancer recurrence (n = 2), marginal ulcer (n = 1), and development of cancer at the anastomosis site (n = 1). In all cases, the dilated afferent loop was seen on sonography as a tubular structure in the upper abdomen crossing transversely over the midline. The distal end of the afferent loop could be traced toward the anastomosis. The probable cause of the syndrome was predicted on the basis of sonography in two of three patients with cancer at the anastomosis. Our experience suggests that afferent loop syndrome can be diagnosed sonographically on the basis of the detection, location, and shape of the dilated afferent loop.

Adult

Acute pancreatitis and hepatic necrosis in the acute afferent loop syndrome. A histopathological study in the rat.

The morphological changes in the liver and pancreas during the first 12 hours in the acute afferent loop syndrome were studied in rats with a Billroth II gastric resection. Two essentially different types of changes were found in the pancreas. One was a coagulative necrosis without an inflammatory reaction, which has been found after instillation of bile, bile salts and the detergent sodium lauryl sulphate into the pancreatic ducts. The other type of pancreatitis was an intense, acute purulent inflammation often with bacteria visible in the histological sections. In the liver, large areas of necrosis were often encountered, sometimes mixed with polymorphonuclear leukocytes and bacteria, in a few cases combined with thrombi in small portal veins. The changes in the pancreas occurred very rapidly; only 4 hours after occlusion of the afferent loop there were signs of pancreatitis in some cases and 12 hours after occlusion there was an acute pancreatitis in all cases.

Acute Disease