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 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The most common complication of chronic pancreatitis is pain, which in many cases seems related to pancreatic ductal obstruction with ductal hypertension. Longitudinal pancreaticojejunostomy is indicated in patients with a dilated (larger than 7 mm) duct and pain that requires narcotic analgesics for relief. Chronic pseudocysts may be corrected surgically without the usual 6-week wait, and asymptomatic pseudocysts less than 4 cm in diameter may not require surgery at all. The relative efficacy and risks of percutaneous drainage of pseudocysts versus the standard surgical approaches need to be studied. Pancreatic fistulas may be external or internal, where pancreatic ascites or hydrothorax can be the clinical manifestation. The pharmacologic suppression of pancreatic secretion (e.g., with somatostatin) may be useful in their management, but surgery may be required. Pancreatic resection or internal drainage is usually effective. Persistent jaundice should be relieved surgically by choledochoduodenostomy to avoid the development of secondary biliary cirrhosis. Obstruction at various levels of the gastrointestinal tract (duodenum, small bowel, colon) may require bypass (gastrojejunostomy) or resection. Hemorrhage from major arteries is an infrequent but often lethal complication of chronic pancreatitis, especially associated with pseudocysts. Angiography is invaluable for diagnosis and occasionally for treatment (embolization). Surgery is preferred in good-risk patients, with suture ligation (resection) of the bleeding source. Chronic pancreatitis is the most common cause of splenic vein thrombosis. The resultant hemorrhage from gastric varices is managed effectively by splenectomy.
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PMID:Complications of chronic pancreatitis. 265 60

Approximately 32% of the rats used as animal models showed an elevated heart weight/body weight ratio (0.432[SEM 0.022] g.100 g-1 compared to 0.293[0.009] g.100 g-1 for sham-operated rats), a hydrothorax, pulmonary and liver congestion, and specific histological changes 82-93 weeks after surgically induced aortic constriction. The histological changes were comparable to those observed in hearts of people suffering from long term hypertension. Cardiac failure was also confirmed by depressed contractility as measured by maximum and minimum dP/dt (first derivative of left ventricular pressure), which were 4604(346) and 3627(526) mm Hg.sec-1, respectively, compared with 9165(745) and 5835(268) mm Hg.sec-1 respectively in rats that did not develop left ventricular hypertrophy and failure (CLIP rats). Systolic and left ventricular blood pressures measured under anaesthesia were also decreased: 71.6(5.0) and 88.1(6.3) mm Hg respectively in rats with congestive heart failure, compared with 83.6(2.4) and 109.5(3.6) mm Hg in CLIP rats. Except for a prolonged mean PQ interval associated with a lower heart rate and for a slightly shorter QRS interval in the conscious state, the electrocardiograms of rats with congestive heart failure did not show any major abnormalities specific to ventricular hypertrophy and/or failure. This model could be useful for studying the pathology and adaptative mechanisms in compensated pressure overload induced congestive heart failure as well as in studies comparing pathological changes and means of treatment of congestive heart failure with different aetiologies encountered in the human population.
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PMID:A pressure overload model of congestive heart failure in rats. 259 Sep 29

Of 582 patients who underwent percutaneous nephrolithotomy, 4% had complications. The most common complications were fever (23%) and bleeding necessitating transfusion (12%). Extravasation was seen in 7% of patients and transient ureteral obstruction in 6%. Other complications included pneumothorax or hydrothorax, pneumonia/atelectasis, paralytic ileus, nephrostomy-tube dislodgment or urine drainage from the flank lasting more than 1 week, significant infection, urinoma formation, renal pelvic laceration, ureteral avulsion, ureteropelvic or ureteral stricture, bowel injury, or escape of stone fragments into the retroperitoneum. Seven patients (1%) required immediate surgery: four to repair renal pelvic lacerations, one to repair a ureteral avulsion, and two to control bleeding after nephrostomy-tube removal when embolization failed. Four patients required delayed surgery for ureteral or ureteropelvic junction strictures, which may have been caused by a tissue reaction to the stones rather than by the procedure itself. There were two deaths--one from respiratory failure in a patient with severe interstitial pulmonary fibrosis and chronic renal failure and the other from myocardial infarction in an obese diabetic patient with hypertension.
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PMID:Complications of percutaneous nephrolithotomy. 349 9

This retrospective study consisted of 500 consecutive renal transplantations performed between September 1977 and September 1981. Preoperatively, congestive heart failure was registered in 262 cases (53.0%) and blood pressure disease in 352 cases (71.3%). The total number of patients with ischaemic heart disease was 22 (4.5%). General anaesthesia was given in 493 and regional anaesthesia in seven cases. In general anaesthesias, tubocurarine was the main relaxant and halothane the main inhalation agent used. Major complications during anaesthesia were blood pressure changes with a higher incidence of hypotension (49.6%) than hypertension (26.8%). Severe cardiac arrhythmias were rare and no intraoperative deaths occurred. One patient was successfully resuscitated in the ICU postoperatively, this being possibly related to hypoventilation caused by prolonged muscular relaxation. Other rare complications included one pneumothorax, one haemo- and hydrothorax, and two large haematomas all caused by preoperative central venous cannulation. In 69 cases (14.0%) additional neostigmine doses and in 34 cases (6.9%) naloxone was given at the end of anaesthesia. Pneumonia during the first postoperative week was recorded in 11 cases (2.2%), and occurred only in patients who received general anaesthesia. One of the three patients who died during the first week developed pneumonia postoperatively.
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PMID:Anaesthesiological complications in renal transplantation: a retrospective study of 500 transplantations. 354 45

Clinical aspects of Continuous Ambulatory Peritoneal Dialysis (CAPD) were studied in the first fifty patients started on CAPD at our hospital. CAPD was found to achieve good control of the uremic symptoms and of the biochemical values studied. Hypertension became less pronounced. The costs were found to be low. Twenty-four diabetic subjects were studied in detail. Intraperitoneal administration of insulin resulted in good metabolic control of the diabetes. The two catheters used for peritoneal access were compared. Because of problems related to the removal of the Toronto Western Hospital catheter it was concluded that the Tenckhoff catheter was to be preferred. Peritonitis was found to be the worst complication. Coagulase negative staphylococci accounted for 57% of the cases. During the study an increasing percentage of infections were caused by bacteria with multiple resistance to antibiotics. Netilmicin, a new aminoglycoside, was evaluated for the treatment of CAPD-related peritonitis. 84% of the cases responded. One of the nineteen patients treated sustained reversible vestibular toxicity. No other side effects were noted. In two patients right-sided hydrothorax was found to be a complication of peritoneal dialysis. In one case it was demonstrated that defects in the right diaphragm was the cause of the complication. In the other CAPD was continued despite the complication.
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PMID:Clinical aspects of continuous ambulatory peritoneal dialysis. 657 82

From January 1990 to December 1994, 24 parturients were diagnosed as having HELLP syndrome alone or combined with preeclampsia/eclampsia among 8,224 patients who were delivered at our institution. They consisted of 14 primiparous and 10 multiparous patients. Mean maternal age was 28.9 +/- 3.3 and gestational age was 34.8 +/- 5.6 weeks. Of 24 parturients, 8 had vaginal delivery and the remaining 16 were delivered by caesarean section. Serious maternal morbidity included eclampsia (n = 3), preeclampsia (n = 18), renal failure (n = 5), hydrothorax (n = 4), and DIC (n = 1). There was no maternal death. There were 3 intrauterine fetal deaths and two neonatal deaths. Perinatal deaths were 2 (0.9%, 2/26). Three caesarean sections were performed under general anesthesia, and 13 under spinal anesthesia. In cases with apparent bleeding tendency, spinal and epidural anesthesia should be avoided. In providing general anesthesia, hypertension should be controlled, and the uterus is preferably dilated before the delivery and contracted there-after.
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PMID:[HELP syndrome and anesthetic management]. 884 89

An 83-yr-old, 44-kg woman with a 2-month history of abdominal distension received diagnostic laparoscopy. Except for chronic treated hypertension, she was healthy. The preoperative chest X-ray demonstrated small pleural effusion occupying the lower left hemithorax, but she did not present with dyspnea or chest pain. After premedication with intravenous ranitidine 50 mg, anesthesia was induced with thiopental 150 mg, vecuronium 7 mg and maintained by 1-2% sevoflurane in 50% N2O/O2. SpO2 decreased after insufflation of CO2, but breath sound was audible on both lungs. At completion of operation, chest X-ray revealed the left hemilateral hydrothorax and 650 ml of pleural fluid was suctioned. Blood gas improved and the tracheal tube was removed. The diagnosis of tuberculous peritonitis was established by the demonstration of granulomas of the peritoneum. We speculated on four reasons for the increased pleural effusion on the left thorax: 1) Increase of systemic and capillary pressure caused by CO2 insufflation. 2) Increase of capillary permeability by tuberculous pleuritis. 3) Decrease of colloid osmotic pressure by hypoalbuminemia. 4) Decreased pleural fluid removal because of venous compression caused by increased intrathoracic pressure. Peritoneal insufflation of CO2 to create the pneumoperitoneum may induce hydrothorax in patients with tuberculous pleuritis.
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PMID:[Hydrothorax during diagnostic laparoscopy]. 1121 54

We report a case of successful, long-term pleurovenous shunt (PVS) in treating refractory nonmalignant hepatic hydrothorax. An 82-year-old woman with liver cirrhosis, hypertension complicated with chronic renal failure while on hemodialysis, presented with progressive dyspnea in association with a recurrent right-sided pleural effusion, occurring secondary to transdiaphragmatic migration of ascites. The diagnosis was established by a demonstration of (99m)Tc-sulphur colloid sequential scintigraphic scan. Despite repetitive thoracenteses and traditional medical treatment, she suffered dyspnea without relief. Denver peritoneovenous shunt was inserted into the right-sided pleural cavity to drain effusion into the subclavian vein without short- and long-term complications. Manually pumping schedule of 10 min was performed twice daily to remove pleural fluid into the venous circulation for maintaining shunt patency. After 19 months of follow-up, the patient is doing well and PVS remains patent without significant pleural effusion. PVS opens a window of opportunity and offers an alternative procedure with minimal invasiveness for high-risk patients with refractory hepatic hydrothorax. It could be an alternative treatment to other conventional surgical interventions.
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PMID:Pleurovenous shunt in treating refractory nonmalignant hepatic hydrothorax: a case report. 1629 Oct 82

The pseudo- Meigs syndrome is defined as a pelvic tumour, other than the ovarian fibroma complicated with ascites and hydrothorax that can be recovered after the tumour is surgically extirpated. The uterine leiomyoma is an extremely rare cause of this syndrome, only 24 cases have been recorded so far, most of them presenting hydropic degeneration or necrosis. The case exposed by us, a 50- year old obese,with nanism woman, presented clinical, biological and imaging characteristics of the syndrome; moreover, she had arterial high blood pressure for more than five years, fact that didn't need postoperative treatment. She was sent to the ER because she had severe respiratory insufficiency, arterial high blood pressure, tachycardia and, at the clinical examination, she presented massive right hydrothorax, ascites, and pelvic tumour. The biologic explorations (the benign cytology in the pleural liquid and ascites, CA-125 with ten times the normal value) and the imagery completed the picture of a Meigs/ pseudo-Meigs syndrome that implied the laparotomy. The H-P examination and the postoperative evolution confirmed the diagnosis. We presented this case in order to emphasize both its rarity and its real positive and differential diagnosis problems.
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PMID:[Pseudo-Meigs syndrome, a rare variant]. 1675 89

Portal hypertension is the main complication of cirrhosis and is responsible for its most common complications: variceal hemorrhage, ascites, and portosystemic encephalopathy. Portal hypertension is the result of increased intrahepatic resistance and increased portal venous inflow. Vasodilatation (splanchnic and systemic) and the hyperdynamic circulation are hemodynamic abnormalities typical of cirrhosis and portal hypertension. Gastroesophageal varices result almost solely from portal hypertension, although the hyperdynamic circulation contributes to variceal growth and hemorrhage. Ascites results from sinusoidal hypertension and sodium retention, which is in turn secondary to vasodilatation and activation of neurohumoral systems. Hepatic hydrothorax results from the passage of ascites across the diaphragm and into the pleural space. The hepatorenal syndrome represents the result of extreme vasodilatation with an extreme decrease in effective blood volume that leads to maximal activation of vasoconstrictive systems, renal vasoconstriction, and renal failure. Spontaneous bacterial peritonitis is a potentially lethal infection of ascites that occurs in the absence of a local source of infection. Portosystemic encephalopathy is a consequence of both portal hypertension (shunting of blood through portosystemic collaterals) and hepatic insufficiency resulting in the accumulation of neurotoxins in the brain.
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PMID:Portal hypertension. 1703 6


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