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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sepsis and septic shock are complicated by a number of hemodynamic and metabolic aberrations. These include catecholamine refractoriness and altered glucose metabolism. Recently, a nonshock rat model of continuous endotoxin infusion via an implanted osmotic pump was developed that reproduces some of the metabolic and cardiovascular findings of human sepsis. By using this model, we have found a decreased number of hepatic plasma membrane alpha 1-adrenergic and [Arg8]vasopressin receptors in rats continuously infused with endotoxin. There was a significant decrease in [3H]prazosin (35 +/- 7%) and [3H] [Arg8]vasopressin (43 +/- 8%) receptors after 30 h of continuous endotoxin infusion with no change in affinity. The ability of norepinephrine to form the high-affinity complex with alpha 1-adrenergic receptors was not altered after chronic endotoxin infusion. The results are consistent with the concept that alterations in receptor number might underlie certain of the metabolic consequences of chronic sepsis.
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PMID:Altered hepatic vasopressin and alpha 1-adrenergic receptors after chronic endotoxin infusion. 303 72

Our results reviewed here may be summarized as follows: 1. Continuous endotoxemia significantly interferes with Ca2+-dependent information flow in the liver. 2. The subcellular sites where these molecular lesions can be localized include: a.) the plasma membrane-there are effects at the level of alpha 1-adrenergic and vasopressin binding, and also in the coupling of receptor activation to inositol lipid metabolism in terms of PIP2 degradation and resynthesis b.) the endoplasmic reticulum in terms of Ca2+ release and PI synthesis. Another one of the sequelae of Ca2+-associated receptor activation, namely, cytosolic ionized Ca2+ concentration is also affected. 3. Finally, in addition to seeing the impact of acute or continuous endotoxemia at the level of receptor activation and signal generation, we can also document alterations in the expression of physiologic function subserved by these Ca2+- and inositol lipid-associated signaling processes--i.e. in glycogen phosphorylase activity-being consistent with the above described changes. In conclusion, we state that a causal link is shown between receptor binding, agonist-induced phosphoinositide hydrolysis, intracellular Ca2+ mobilization and activation of phosphorylase a in the liver, suggesting that these alterations may underlie some of the metabolic consequences of chronic sepsis.
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PMID:Perturbation of transmembrane signaling mechanisms in acute and chronic endotoxemia. 303 27

Massive arterial hemorrhage from multiple sites caused by tissue injury and infection following severe pancreatitis occurred in 12 patients, who were treated with the combination of angiographic embolization techniques and surgery; five survived. Complete hemostasis was obtained in eight of 12 patients who underwent primary angiographic therapy. Bleeding was temporarily controlled in two patients, who then underwent directed surgical ligation of the bleeding vessel under more favorable conditions. In two patients, bleeding was not controlled. The use of permanent occluding materials, particularly bucrylate, resulted in the highest success rate. When the bleeding artery could not be individually catheterized for safe occlusion, balloon occlusion or vasopressin infusion stabilized the patient's condition, with a decrease in the rate of bleeding prior to subsequent surgical therapy. Inadequate control of further tissue necrosis and sepsis was the cause of death in five of the seven patients who died. The other two patients died of recurrent hemorrhage despite attempts at both arteriographic occlusion and surgical ligation.
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PMID:Massive arterial hemorrhage in patients with pancreatitis. Complementary roles of surgery and transcatheter occlusive techniques. 348 20

Rats were treated with Escherichia coli endotoxin (ET) either acutely or chronically or rendered septic by cecal ligation and puncture. At 6 h after ET injection, at various intervals of continuous ET infusion, and at 17-18 h after the onset of peritonitis, animals were killed and hepatocytes were isolated. Cytosolic [Ca2+] ([Ca2+]c) was measured by quin 2 during the resting state and after stimulation with epinephrine and vasopressin. Basal and epinephrine-, vasopressin- and glucagon-stimulated glycogen phosphorylase activity were also determined. In hepatocytes from acutely ET-treated rats, resting levels of [Ca2+]c were decreased 46% from 245.8 +/- 11.0 to 131.0 +/- 8.5 nM (n = 4-6, P less than 0.05). In septic rats a 39.5% decrease was noted [i.e., from 154.0 +/- 17.7 (n = 4, sham) to 93.3 +/- 91 nM (n = 5, septic, P less than 0.05)]. These decreased [Ca2+]c levels were associated with changes of glycogen phosphorylase activity in a manner suggesting a cause and effect relationship; e.g., acute ET treatment resulted in greater than 80% depression of phosphorylase a activity, whereas sepsis induced a 58% decrease in the activity of this enzyme. In ET-infused rats the resting level of [Ca2+]c and its response to hormonal stimulation were not different from hepatocytes of saline-infused rats, although glycogen phosphorylase activity was less responsive to these hormones. The effect on the enzyme's response to Ca2+-mobilizing hormones was more marked than to glucagon. This is consistent with the concept that information flow in the Ca2+-messenger system is a site of metabolic lesions produced by endotoxicosis and sepsis.
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PMID:Rat liver free cytosolic Ca2+ and glycogen phosphorylase in endotoxicosis and sepsis. 353 41

The operative management of stress ulcer in children is controversial. Between the years 1969 and 1981, ten children were operated on at the Babies Hospital for stress ulcer. Their illnesses included connective tissue disorders (3), sepsis (2), Reye's syndrome (1), hemolytic uremic syndrome (1), leukemia (1), closed head injury (1), and renal failure (1). In those with bleeding (8), aggressive conventional medical management was attempted prior to operation. Four children also received intravenous cimetidine. Four patients underwent embolization of a feeding artery and/or selective vasopressin infusion. In those patients who perforated (2), operation was performed after a brief period of resuscitation. Ten patients underwent 11 operations. In those who bled, multiple ulcerations were the most common finding. Operative procedures consisted of partial gastrectomy and vagotomy (4), partial gastrectomy alone (2), and vagotomy and pyloroplasty (2). One child who underwent vagotomy and pyloroplasty required partial gastrectomy for recurrent bleeding. Of the two children who perforated, one was managed by plication and the other by partial gastrectomy. There were two deaths (20%), both occurring in patients who had undergone gastrectomy. One survivor has mild dumping. This experience suggests that in children (1) stress ulcers are commonly multiple when associated with major medical illnesses; (2) partial gastrectomy with or without vagotomy affords maximum protection against recurrent bleeding; (3) lesser procedures are effective for solitary bleeding duodenal ulcers or perforation; and (4) selective arterial embolization or vasopressin infusion are unreliable methods for controlling bleeding.
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PMID:Operative management of stress ulcers in children. 709 47

Gallbladder and extrahepatic bile duct operations merit special consideration in cirrhotic patients. During the past 15 years at Strong Memorial Hospital, 33 cirrhotic patients have undergone cholecystectomy or an operation for bile duct obstruction. Of the 21 patients with cirrhosis subjected to cholecystectomy for cholecystitis and cholelithiasis, nine had uncomplicated courses. Included in this group was one patient in whom the intrahepatic portion of the gallbladder was deliberately not resected. The other 12 patients (57%) had excessive intraoperative bleeding and required transfusion of three or more units of blood. One patient required additional exploratory surgery and antifibrinolytic therapy to control bleeding. In an additional group, only one of seven patients whose gallbladder was removed during a portal decompressive procedure bled excessively from the liver bed. A third group of five patients, including four with secondary biliary cirrhosis who underwent operations on the bile duct for obstruction, had massive intraoperative bleeding (greater than 5 U). Four of the five exsanguinated, and the remaining patient died of sepsis. A more conservative approach toward elective cholecystectomy in the cirrhotic patient is indicated. If an operation is performed, increased bleeding should be anticipated; extensive intrahepatic dissection should be avoided. Intraoperative infusion of vasopressin and an antifibrinolytic agent should be considered.
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PMID:Biliary tract surgery and cirrhosis: a critical combination. 728 Sep 97

Diagnostic and therapeutic angiography has demonstrated an important role in gastrointestinal hemorrhage. During the past 2 years, we performed angiography in the management of 20 patients with uncontrolled gastrointestinal bleeding. Conservative management including medication and transfusion would not appear to suffice in these patients and most patients had been evaluated to have a high operative risk in our series. Ten of the 20 patients had renal dysfunction (creatinine > 1.7 mg/dl) before angiography. The role of angiography in the management of patients with renal dysfunction remains controversial because angiography is likely to produce acute renal failure. We performed angiography to stop bleeding in these patients with renal dysfunction because they could die of blood loss. In our 20 cases, bleeding sites were identified in 14 patients. The detection rate was 70%. Thirteen of the 14 with the use of either vasopressin infusion or arterial embolization showed complete cessation of bleeding in 10 patients. Three cases failed to be controlled. One received an operation after a bleeding site was located by angiography. In our study, sepsis with renal failure was the leading cause of mortality (6 cases). Ten patients with pre-existing renal dysfunction had angiography performed and only one showed abrupt elevation of creatinine levels after angiography. He also developed sepsis. Deterioration of renal function was possibly due to angiography or more likely due to sepsis and hypovolemia. Six patients died of sepsis after angiography although 4 of these patients showed cessation of bleeding. Four cases with pre-existing renal dysfunction and without evidence of infection survived after angiographic management.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Angiography for the management of poorly controlled gastrointestinal hemorrhage--20 cases clinical observation]. 770 50

Torsade de pointes is an unusual life-threatening ventricular arrhythmia that has been associated with vasopressin, neuroleptic drugs, and electrolyte imbalances, including hypokalemia and hypomagnesemia. Over a 9-month period, we observed torsade de pointes in three patients with cirrhosis and bleeding esophageal varices who did not have prior cardiac disease. All had received endoscopic sclerotherapy and continuous infusions of vasopressin and nitroglycerin. For sedation, two patients received haloperidol and one droperidol. In addition, two patients had either hypokalemia or hypomagnesemia. In all three patients, there was prolongation of the electrocardiographic QT interval and a "long-short" initiating sequence followed by ventricular tachycardia with torsade de pointes morphology. All were successfully cardioverted; there was one late death due to aspiration and septicemia. We conclude that cirrhotics with variceal hemorrhage may be at increased risk of developing this arrhythmia in the setting of treatment with vasopressin, sedation with neuroleptic drugs, and electrolyte abnormalities. We urge close monitoring of these patients for cardiac arrhythmia and recommend that neuroleptics be used cautiously, if at all.
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PMID:Torsade de pointes complicating the treatment of bleeding esophageal varices: association with neuroleptics, vasopressin, and electrolyte imbalance. 773 96

Massive hemorrhage from diverticular disease of the colon is a very difficult problem in abdominal emergency surgery. The pathogenesis of bleeding colonic diverticulosis is strictly correlated to the angioarchitecture of the colonic diverticular wall. Here the vasa recta penetrate the colonic wall from the serosa to the submucosa through connective tissue septa. Injurious factors arising from the colonic or diverticular lumen can produce an eccentric damage to the luminal side with intimal thickening, segmental weakening of the artery and its rupture with massive bleeding. Conventional barium enema is not able to show the source of the hemorrhage in the majority of the bleeding patients; colonoscopy, as primary emergency procedure, has significant positive findings in 41.5%-83.7% of patients. Radionuclide bleeding scans have a sensitivity rate of 86%-94%. Emergency arteriography localizes the bleeding source in higher rates ranging from 58% to 86% and is successful after intraarterial infusion of vasopressin or embolization in 47%-92% of patients. Surgical treatment for continued bleeding from diverticular disease is controversy. Segmental resection should be performed on patients with localized bleeding sources (positive arteriogram). Laparotomy, anterograde irrigation and intraoperative colonoscopy are indicated in patients with multiple bleeding sites and negative arteriography. Because the right colon is the most common site of bleeding in same cases is necessary to perform a subtotal colectomy with ileorectal anastomosis. Blind resections particularly in the elderly patients present high rebleeding rate (> 60%) and high mortality (30%) with sepsis accounting for the majority of deaths.
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PMID:[Massive hemorrhage caused by colonic diverticulosis]. 797 52

Sepsis is associated with a generalised membrane dysfunction leading to an increase in intracellular sodium, chloride, and water. The decrease in extracellular water is thought to act as a nonosmotic stimulus to the secretion of antidiuretic hormone. The resultant hyponatraemia is associated with increased surgical morbidity and mortality. Treatment aimed at improving intracellular electrolytes may improve surgical morbidity and mortality. An animal model of peritonitis was used to evaluate the effect of pentoxifylline. Previously, this dimethyl xanthine derivative was shown to stabilise the cell membrane. Administration of pentoxifylline significantly lowered intracellular sodium and chloride, particularly when given after caecal ligation and puncture. This may have clinical implications in the treatment and prevention of hyponatraemia.
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PMID:Pentoxifylline improves intracellular electrolytes in sepsis. 807 26


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