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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty consecutive patients with severe sepsis were randomized to fluid challenge with 5% albumin or 10% low MW hydroxyethyl starch (pentastarch) solutions. Fluid challenge was administered iv as 250 ml of test colloid every 15 min until the pulmonary artery wedge pressure (WP) was greater than or equal to 15 mm Hg or a maximum dose of 2000 ml was infused. Hemodynamic, respiratory, and coagulation profiles were measured before and after fluid infusion. The amount of colloid required to achieve a WP of 15 mm Hg was comparable between groups. Both colloid infusions resulted in similar increases in cardiac output, stroke output, and stroke work. The effect of fluid infusion with pentastarch on coagulation was not significantly different from albumin, although pentastarch was associated with a 45% decrease in factor VIII:c. We conclude that pentastarch is equivalent to albumin for fluid resuscitation of patients with severe sepsis.
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PMID:Effects of pentastarch and albumin infusion on cardiorespiratory function and coagulation in patients with severe sepsis and systemic hypoperfusion. 246 47

Although adequate volume resuscitation has decreased mortality from hemorrhagic shock, recovery in many patients is complicated by sepsis. To determine whether a subject debilitated by hemorrhagic shock would exhibit greater cardiocirculatory dysfunction when challenged with sepsis, ten dogs (Group I) were hemorrhaged to a mean arterial blood pressure of 30 mm Hg. After 2 hours of hypotension, shed blood and lactated Ringer's solution (50 ml/kg) were given, and the dogs were observed for 3 to 6 days. Ten dogs were sham hemorrhage and served as controls (Group II). On the experimental day, all cardiovascular and hemodynamic parameters were measured in both groups of animals before endotoxin challenge. There was no significant difference in cardiac output, stroke volume, stroke work, +dP/dt max, myocardial blood flow, myocardial oxygen metabolism, or acid-base balance in the two groups. Compared to sham-hemorrhaged dogs, resuscitated shock dogs had a significantly lower mean arterial blood pressure (127 +/- 7 vs. 110 +/- 6 mm Hg; p less than 0.05), and heart rate was significantly higher (86 +/- 6 vs. 109 +/- 7 beats/minute; p less than 0.05). Furthermore, maximal rate of left ventricular pressure fall (-dP/dT max) was significantly lower in the animals previously hemorrhaged, suggesting a persistent defect in left ventricular relaxation. Blood glucose and insulin levels were significantly elevated in the resuscitated shocked dogs, likely due to increased circulating catecholamine concentrations and enhanced glycogenolysis. Endotoxin shock caused significant hypotension, acidosis, and impaired regional perfusion in all dogs. In addition, cardiac output, stroke volume, dP/dT, and left ventricular end-diastolic pressure fell and hyperglycemia and hyperinsulinemia occurred in all dogs after endotoxin injection.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The cardiocirculatory and metabolic effects of endotoxin challenge after canine resuscitated hemorrhagic shock. 256 78

105 patients with acute calculous cholangitis who did not respond to conservative management underwent urgent endoscopic drainage of the biliary system at a mean of 1.5 days after admission. Treatment was successful in 102 (97%) patients. 3 of the patients in whom drainage was not successful underwent emergency surgery, with 1 death. 3 patients died of uncontrolled sepsis despite successful endoscopic drainage. 1 patient died of a stroke. The overall mortality was 4.7%. Among those in shock 2 out of 4 drained after 72 h died, compared with 3 out of 38 drained before 72 h. There were no deaths in the group without shock irrespective of the timing of drainage.
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PMID:Urgent endoscopic drainage for acute suppurative cholangitis. 256 34

A young woman presented with a 4-month history of retinal and vertebrobasilar ischemia. Angiography demonstrated narrowing of major branches of the aortic arch. Intractable, severe retroorbital pain of the right eye developed after a middle cerebral artery stroke. During 4 weeks of aggressive immunosuppressive therapy including IV high dose bolus corticosteroids and pulse cyclophosphamide, her neurologic deficit improved transiently, but her retroorbital pain persisted. She died of staphylococcal sepsis and pneumonia. An autopsy demonstrated thrombotic or fibrous occlusion, with minimal inflammation, of extracranial arteries.
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PMID:Takayasu arteritis presenting as retinal and vertebrobasilar ischemia. 257 Jan 49

We retrospectively evaluated the clinical features and therapeutic outcomes in 13 consecutive patients with the diagnosis of fusiform aneurysm of the vertebrobasilar system. Four patients (31%) presented with compressive symptoms and 10 (77%) with ischemic symptoms; one patient presented with both types of symptoms. No patient presented with rupture of the fusiform aneurysm. Based on the attending physician's choice, treatment included antiplatelet therapy in five patients, anticoagulation in seven, and no medication in one. Five patients died, four treated with antiplatelet agents and one not treated with any medication. The cause of death was progressive brainstem ischemia in three, sepsis in one, and gastrointestinal bleeding in one patient. All seven patients who received anticoagulants were alive, with no recurrence of symptoms or hemorrhagic complications after a mean follow-up period of 18 months. Based on previous and current series, we conclude that rupture of fusiform aneurysms is rare. Our results suggest a more favorable outcome in the management of these aneurysms with anticoagulation therapy to prevent progressive thrombosis and embolization.
Stroke 1989 Dec
PMID:Fusiform aneurysm of the vertebrobasilar arterial system. 259 37

Pierce-Donachy ventricular assist devices (VADs) were used to support 54 patients. None of the 27 patients supported less than 4 days had any visible thrombi in the VAD at explant. Of the 27 patients supported longer than 4 days, nine patients had visible thrombi. In this group of 27 patients, 19 received VAD support pending myocardial recovery, and anticoagulation consisted of dextran (4-15 days) and heparin during the weaning phase (1-2 days). The other eight patients had VADs implanted as bridges to cardiac transplantation. These patients also received dextran postoperatively (1-5 days), but were switched to a regimen of oral warfarin and dipyridamole. Duration of support for the nine patients in whom thrombi were found ranged from 4-27 days (mean, 12 days). The etiology of thrombus was probably related to mechanical problems in four patients, inadequate anticoagulation in two patients, sepsis in two patients, and unknown causes in one patient. Four of these patients suffered cerebral or peripheral injuries, which were probably embolic in two, and possibly embolic in two. One of these four patients survived, and two patients with thrombi but no emboli survived. One patient suffered a stroke, but no evidence of thrombi was found. Our incidence of thrombus with this VAD was 17%. Thrombi were related to inadequate anticoagulation, interrupted flow, or sepsis, but not to duration of support.
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PMID:Thromboembolic complications with the Pierce-Donachy ventricular assist device. 259 50

The characteristic hemodynamic profile of human septic shock consists of a normal or elevated cardiac index and a decreased systemic vascular resistance index. When a patient with septic shock has a low cardiac index, concomitant hypovolemia is usually present. Within 48 hours of the onset of septic shock, most patients develop marked dilatation of both ventricles, depressed ejection fractions, and alterations of the Frank-Starling and diastolic pressure-volume relationships; stroke volume typically is well maintained. In surviving patients, cardiac function returns to normal within 10 days. An identical sequence of hemodynamic abnormalities occurs in an experimental canine model of sepsis that employs intraperitoneal implantation of infected fibrin clots. This myocardial dysfunction is not due to global myocardial ischemia; instead, there appear to be one or more circulating myocardial depressant substances. The chemical nature of these circulation mediators is under intensive investigation clinically, in vitro, and in the canine model.
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PMID:Myocardial dysfunction in sepsis. 264 29

Myocardial function with ultrastructure and high energy phosphate levels in dogs was correlated after 24 hours of sepsis using live Klebsiella aerogenes. All animals developed progressive hemodynamic deterioration over a 24 hour period. Mean arterial pressure decreased from 148 +/- 7 mmHg to 85 (P less than 0.01) and cardiac output decreased from 3.43 +/- .31 to 1.6 +/- 0.5 L/min. Left ventricular stroke work decreased from 48.2 +/- 5 to 18.1 +/- 6 gm-meters (P less than 0.001). Systemic and pulmonary vascular resistances were increased at 24 hours (3,538 +/- 27 to 7,404 +/- 1,400 dyne/sec/cm-5 (P less than 0.01), and 185 +/- 20 and 619 +/- 90 dyne/sec/cm-5 (P less than 0.001), respectively. Left ventricular function curves at 24 hours showed a fixed low output. However, myocardial ultrastructure was preserved and high energy phosphate levels remained normal. These observations correlate well with the changes seen clinically in early gram negative sepsis in hypovolemic patients. Thus, this appears to be a suitable model for further investigation of the effects of gram negative sepsis on myocardial performance, ultrastructure, and maintenance of energy stores.
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PMID:Preservation of myocardial ultrastructure after 24 hours of Klebsiella sepsis: histologic, functional, and biochemical correlations. 268 98

Time-related changes in eicosanoid release and hemodynamic parameters were characterized in baboons during the early development of sepsis induced by intravenous (i.v.) infusion of live Escherichia coli (4 x 10(10) organisms/kg) in baboons. Plasma levels of thromboxane B2 (TxB2), a stable metabolite of thromboxane A2 (TxA2), rose rapidly in arterial, venous, and pulmonary arterial blood after infusion of live E. coli, attaining maximal increases at 30 min and returning to control values by 60 min. In contrast, plasma concentrations of 6-keto-PGF1 alpha rose slowly after infusion, reaching peak concentrations at 120 min, then slowly returned to control values between 4 and 5 hr after infusion of live E. coli. Hemodynamic values remained stable during the first 2 hr after infusion, although early changes in cellular energy metabolism and incipient hemodynamic failure were inferred from pyrexia, tachycardia, and metabolic acidosis. At 3 hr, signs of further hemodynamic compromise developed, including increased venous PCO2, reduced pulmonary capillary wedge pressure, and reduced stroke volume, followed by gradual increases in systemic and pulmonary vascular resistance. These factors coincided with progressive reductions in cardiac output and deteriorating circulatory efficiency. The time course of events following infusion of live E. coli indicates that alterations in cellular energy provision occurred early (within 1 hr), whereas central hemodynamic parameters decayed much more slowly. Additionally, TxA2 and PGI2 appear related to the early events in the development of sepsis as their release preceded cardiocirculatory failure.
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PMID:Eicosanoids and the hemodynamic course of live Escherichia coli-induced sepsis in baboons. 268 55

We have reviewed 108 cases of bacterial endocarditis treated surgically since 1968. The mean age of the patients was 47.7 +/- 15.6 years (+/- SD) (range, 14-79 yr). Seventy-seven percent were male. The most common causative organisms were staphylococci (46%), streptococci viridans group (5%), and other streptococci (20%). Forty-five percent, 25%, and 13% of patients had native aortic valve, native mitral valve, or native double valve (AV/MV) involvement, respectively. Eighteen patients had prosthetic valve endocarditis. No patient underwent surgery for tricuspid valve endocarditis. Seventy-three patients were considered to have active endocarditis (AE) (positive blood or tissue cultures and/or annular abscess). The 35 remaining patients had healed endocarditis (HE). Preoperative complications in patients with either AE or HE were stroke (11%, 11%), renal failure (33%, 3%; p less than 0.001), pulmonary edema (83%, 34%; p less than 0.001), anemia (36%, 8%; p less than 0.01), and inotrope dependence (22%, 6%; p less than 0.05). Hospital mortality for native valve AE was 19.5% (11/56), and for healed endocarditis, 5.7% (2/35). Independent predictors of hospital mortality were inotrope dependence (p less than 0.001), annular abscess (p less than 0.01), pulmonary edema (p less than 0.01), and staphylococcal infection (p less than 0.05). The 5-year actuarial survival for operative survivors was 68.4 +/- 7.5% (AE) and 78.3 +/- 9.2% (HE). We conclude that the operative mortality for patients with continuing sepsis is high and that surgery should be undertaken early in staphylococcal endocarditis. If surgery is successful, then the long-term prognosis is good.
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PMID:The surgical treatment of infective endocarditis. 272 63


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