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The files of patients who underwent emergency endoscopy in a 2-yr period (January 1985 to January 1987) in the Heinz-Kalk Hospital were analyzed to establish the frequency, significance and therapy of the Mallory-Weiss syndrome associated with portal hypertension, an association observed in 55 of 339 patients (16.2%). Portal hypertension was caused by cirrhosis in 53 patients and by a prehepatic block in two patients. For 21 of these patients (37%) with portal hypertension, Mallory-Weiss syndrome was the first bleeding manifestation. They numbered 6.2% of the whole population. In the remaining 34 patients (63%) sclerotherapy treatment had been previously performed. No lesions that suggested peptic esophagitis were seen in these 55 patients, although in 25 of them (45.4%) a gastroesophageal reflux was observed. The frequency of bleeding from a Mallory-Weiss tear was significantly higher in patients with advanced liver disease, particularly with Child-Pugh classifications C and B. In patients with prehepatic block, a hemorrhage from a Mallory-Weiss tear may occur, but the frequency is significantly lower than it is in patients with cirrhosis. The bleeding tear was treated by transendoscopic esophageal and cardial wall sclerosis (paravariceal technique) and was, in all cases, successfully controlled. Mallory-Weiss syndrome is observed more frequently in patients with portal hypertension and cirrhosis. Gastroesophageal reflux apparently does not play a major role in the pathogenesis of this syndrome. It may simply be the manifestation of an abnormal gastroesophageal function. Mallory-Weiss syndrome can also be observed as a cause of rebleeding in patients treated with chronic sclerotherapy. Paravariceal endoscopic sclerotherapy is apparently the treatment of first choice to stop hemorrhage.
The files of patients who underwent emergency endoscopy in a 2-yr period (January 1985 to January 1987) in the Heinz-Kalk Hospital were analyzed to establish the frequency, significance and therapy of the Mallory-Weiss syndrome associated with portal hypertension, an association observed in 55 of 339 patients (16.2%). Portal hypertension was caused by cirrhosis in 53 patients and by a prehepatic block in two patients. For 21 of these patients (37%) with portal hypertension, Mallory-Weiss syndrome was the first bleeding manifestation. They numbered 6.2% of the whole population. In the remaining 34 patients (63%) sclerotherapy treatment had been previously performed. No lesions that suggested peptic esophagitis were seen in these 55 patients, although in 25 of them (45.4%) a gastroesophageal reflux was observed. The frequency of bleeding from a Mallory-Weiss tear was significantly higher in patients with advanced liver disease, particularly with Child-Pugh classifications C and B. In patients with prehepatic block, a hemorrhage from a Mallory-Weiss tear may occur, but the frequency is significantly lower than it is in patients with cirrhosis. The bleeding tear was treated by transendoscopic esophageal and cardial wall sclerosis (paravariceal technique) and was, in all cases, successfully controlled. Mallory-Weiss syndrome is observed more frequently in patients with portal hypertension and cirrhosis. Gastroesophageal reflux apparently does not play a major role in the pathogenesis of this syndrome. It may simply be the manifestation of an abnormal gastroesophageal function. Mallory-Weiss syndrome can also be observed as a cause of rebleeding in patients treated with chronic sclerotherapy. Paravariceal endoscopic sclerotherapy is apparently the treatment of first choice to stop hemorrhage.
The Mallory-Weiss syndrome is a relatively infrequent cause of digestive tract bleeding and most cases have been described in alcoholics. Nonoperative management is frequently successful. We present here a case of sudden onset of wretching and vomiting after IV infusion of cis-platinum for recurrent carcinoma of the uterine cervix in which the patient had profuse hematemesis secondary to three posterior gastroesophageal tears requiring operative intervention after failure of nonsurgical management. This is an unusual complication of antineoplastic chemotherapy and its prevention is emphasize in this paper.
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