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Biomedical subjects

C Andrus

Publications and source records attributed to C Andrus.

9 recordsLinked to original sources
PubMed2001

Faulty design resulting in temporary pacemaker failure.

A 77-year-old man became asystolic 3 days after aortic valve replacement and coronary artery bypass surgery. A dual-chamber temporary pacemaker generator was turned on but failed to discharge; instead, an obscure error message appeared on the liquid crystal display of the pacemaker. The intensive-care nurses and physicians were unable to activate the pacemaker. We describe the pacemaker design that led to this instance of pacemaker failure. This case is important because it illustrates how a medical equipment design flaw can turn a human error into a potentially catastrophic event.

Aged↗
PubMed1992

Staging laparoscopic pelvic lymph node dissection: comparison of results with open pelvic lymphadenectomy.

A total of 24 men scheduled for radical prostatectomy was alternately designated to undergo either a modified open (12 men) or laparoscopic (12 men) lymphadenectomy. Both groups were similar in regard to age and clinical stage. Tumor grade and serum prostate specific antigen level for each group are reported. Nodal metastases were found in 1 patient in the open and 3 in the endoscopic group. The average total number of lymph nodes retrieved by open dissection was 11 +/- 5.7, which was not statistically different from the average number of 10.7 +/- 5.7 obtained laparoscopically. No statistically significant variance in the number of nodes harvested in regard to site of dissection was observed. In the 9 men who underwent radical prostatectomy after laparoscopic dissection no additional lymphatic tissue was obtained from the surgical margins. No morbidity related to either procedure occurred. The data suggest that laparoscopic pelvic lymphadenectomy offers a reliable and minimally invasive alternative to open node dissection in selected patients.

Aged↗
PubMed1991

Intracranial pressure: dynamics and nursing management.

Patients suffering from traumatic or nontraumatic cerebral injury often develop intracranial hypertension. Accurate monitoring and prompt management are necessary to prevent deleterious and sometimes fatal effects of intracranial hypertension. This article reviews dynamics of intracranial pressure as well as compensatory and autoregulatory mechanisms. Essential management principles focusing upon prevention are presented to promote thorough and adequate nursing care for patients at risk for intracranial hypertension.

Cerebral Ventricles↗
PubMed1991

The effect of cholecystokinin-receptor antagonists on cholecystokinin-stimulated bile flow in dogs.

Cholecystokinin is a choleretic in dogs. Some of the effects of cholecystokinin in stimulating bile flow in dogs are produced by cholecystokinin stimulating the release of other choleretic hormones such as insulin and glucagon. The purpose of this study was to determine the effects of cholecystokinin receptor antagonists on canine hepatic bile flow and insulin and glucagon release from the pancreas. Cholecystokinin octapeptide (CCK-8) and intraduodenal fat were administered to dogs that had undergone cholecystectomy with chronic biliary fistulas with and without the administration of cholecystokinin receptor antagonists. Bile secretion and systemic venous insulin, glucagon, and cholecystokinin levels were measured. The cholecystokinin receptor antagonists benzotript and CR 1409 had no effect on bile flow or hormone levels when administered without cholecystokinin, whereas proglumide produced a large increase in bile flow without altering hormone levels. The response produced by proglumide may be the result of an osmotic effect produced by the substance being secreted in bile and its stimulating bile salt secretion in bile. CCK-8 and intraduodenal fat increased bile flow, bile chloride secretion, and cholecystokinin, insulin, and glucagon concentrations in venous blood. The cholecystokinin receptor antagonists benzotript and CR 1409 significantly decreased the bile flow and insulin and glucagon changes produced by exogenous CCK-8. The effect of intraduodenal fat on bile flow was not inhibited by the cholecystokinin receptor antagonists, whereas the increased insulin and glucagon levels were decreased significantly. Intraduodenal fat may release other choleretic hormones not affected by cholecystokinin receptor antagonists. The choleresis produced by exogenous CCK-8 is inhibited by cholecystokinin receptor antagonists, perhaps by inhibiting the release of the choleretic hormones insulin and glucagon.

Animals↗
PubMed1987

Pancreatitis after biliary tract surgery.

Pancreatitis associated with biliary tract operations continues to be an important clinical problem. The results of biliary tract operations performed on 1256 patients were carefully scrutinized for the presence of postoperative hyperamylasemia and pancreatitis persisting after 48 hours. Patients were evaluated in the context of the presence or absence of preoperative pancreatic dysfunction. Similarly, various operative risk factors were evaluated, including cholangiography, choledocholithiasis, common duct exploration, choledochoscopy, choledochoduodenostomy, and sphincteroplasty. Operative cholangiography did not induce postoperative pancreatitis. The incidence of postoperative pancreatitis following cholecystectomy was 0.6%, which was significantly greater than the incidence following common duct exploration (8.4%). Pancreatitis following biliary tract surgery seemed to be not directly related to the performance of choledochoscopy, sphincteroplasty, or choledochoduodenostomy, as it developed with similar frequency in patients undergoing common duct exploration alone. The timing of operative therapy in patients with biliary tract pancreatitis did not significantly alter the frequency with which pancreatitis persisted in the postoperative period. In 970 patients undergoing cholecystectomy, one patient who had preoperative pancreatitis died of postoperative pancreatitis. Of 286 patients undergoing common duct exploration, seven patients died with pancreatitis. In three of these patients there was no active preoperative pancreatitis, and in one of these patients pancreatitis was the cause of death. Four patients with preoperative pancreatitis eventually died of pancreatitis in the postoperative period. Pancreatitis is an important complication of biliary tract disease and operations, and all efforts should be extended to suppress its occurrence and development.

Amylases↗
PubMed1987

Effects of somatostatin on acute canine experimental pancreatitis.

Somatostatin is an inhibitory hormone that decreases the secretion and end organ response of cholecystokinin (CCK). Inhibition of hormonal stimulation of pancreatic exocrine secretion by somatostatin may improve the course of acute pancreatitis. Anesthetized dogs underwent cholecystectomy and cannulation of the pancreatic duct, thoracic duct, and portal vein. Twenty experiments were performed in random order with 5 dogs in each group. Hourly measurements of lymph flow and portal and thoracic duct amylase were made. Portal blood insulin, glucagon, and CCK concentrations were determined by radioimmunoassay on samples obtained at the beginning and end of the experiments. Pancreatitis was induced by injecting, under constant pressure, 10 ml bile into the pancreatic duct during 1 min. Somatostatin was administered intravenously (20 micrograms/kg/hr). After 5 h, the dogs were killed, pancreas glands removed and weighed and tissue samples obtained for histologic evaluation. There was a significant increase in lymph amylase output and portal venous amylase and CCK concentrations in the dogs with pancreatitis compared to the control dogs. In dogs with pancreatitis, lymphatic amylase secretion and portal CCK concentrations were significantly decreased by somatostatin. Somatostatin did not significantly alter portal amylase concentrations, pancreas gland weights or histologic inflammation when compared to values from dogs with pancreatitis not treated with somatostatin.

Acute Disease↗
PubMed1986

Planned reoperation for generalized intraabdominal infection.

Intraabdominal infection remains a common cause of death in surgical patients. Progress in this area with improved survival rates is difficult to demonstrate despite the use of antibiotics, nutritional support, and aggressive maintenance of function of failed organs. This report documents our experience with planned reoperation to cleanse the abdominal cavity in 77 patients with generalized intraabdominal infection. In 34 of the patients, reoperation to cleanse the abdominal cavity was performed every 24 to 48 hours after the first operation until the abdominal cavity was judged to be clean. Forty-three patients underwent a single operation for intraabdominal contamination and were treated expectantly, only undergoing reoperation for signs of recurrent infection. In all patients, the hole in the intestinal tract was controlled primarily by stoma formation at the initial operation to treat intraabdominal infection. Patients with appendiceal disease were excluded. The severity of illness in the two patient groups was compared by a modified acute physiologic score. Planned reoperation was not associated with improvement in survival when compared with patients managed expectantly. Patients managed by planned reoperation had significantly more laparotomies than patients managed expectantly without improving survival. The results of this study disclosed that empiric reoperation to clean the abdominal cavity in patients with generalized intraabdominal infection produced no improvement in survival when compared with observation and reoperation when indicated.

Abdomen↗