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

The effects of intermittent and continuous positive-pressure ventilation (IPPV and CPPV) instituted prophylactically were evaluated in a porcine model of endotoxin-induced pulmonary and cardiovascular failure. Pigs under ketamine anaesthesia were infused i.v. with E. coli endotoxin over 6 h. Twenty animals, breathing air spontaneously, received endotoxin without treatment. Fifteen animals were treated prophylactically with IPPV (normoventilation with air). Nine animals received prophylactic treatment with CPPV (positive end-expiratory pressure 0.8 kPa (8 cmH2O). Endotoxin infusion in spontaneously breathing animals caused profound deterioration of pulmonary gas exchange, a marked rise in pulmonary vascular resistance (PVR) and a moderate increase in extravascular lung water (EVLW). Cardiac output (Qt) and O2 delivery decreased considerably. Metabolic acidosis indicated oxygen deficit. Eleven of 20 animals died during the observation period. IPPV improved arterial oxygenation during endotoxin infusion, and the increase in EVLW tended to be lower. The alterations in pulmonary haemodynamics, Qt and O2 delivery, were of the same magnitude as in spontaneously breathing animals. Survival was improved. CPPV fully prevented the deterioration in pulmonary gas exchange and the development of pulmonary oedema. There was an accentuated increase in PVR. Qt and O2 delivery decreased markedly and a severe metabolic acidosis developed. All animals treated with CPPV died during the observation period. These results indicate that prophylactic IPPV and CPPV may counteract the development of sepsis-induced lung insufficiency in man. However, it must be emphasized that adequate cardiovascular support is essential in optimizing the treatment.
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PMID:Intermittent and continuous positive-pressure ventilation in the prophylaxis of endotoxin-induced lung insufficiency. A study in pigs. 354 98

During approximately a 9-year period, 37 severe preeclamptic-eclamptic patients had pulmonary edema for an incidence of 2.9%. The incidence was significantly higher in older patients (p less than 0.0001) and in multigravid patients (p less than 0.05). Eleven (30%) had antepartum edema with 10 (90%) of the 11 having preexisting chronic hypertension. Twenty-six (70%) had postpartum edema with an average onset of 71 hours post partum. The majority of these patients had excessive colloid and crystalloid infusions for various medical, surgical, and obstetric complications. There were four maternal deaths and morbidity was significant. Eighteen patients had disseminated intravascular coagulopathy, 17 had sepsis, 12 had abruptio placentae, 10 had acute renal failure, six had hypertensive crisis, five had cardiopulmonary arrest, two had rupture of the liver, and two had ischemic cerebral damage. The overall perinatal mortality was 530/1000 and neonatal morbidity was significant. Pulmonary edema is infrequent in severe preeclampsia-eclampsia without associated medical, surgical and obstetric complications. The occurrence of pulmonary edema in such patients is associated with high maternal and perinatal mortality and morbidity.
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PMID:Pulmonary edema in severe preeclampsia-eclampsia: analysis of thirty-seven consecutive cases. 357 33

To evaluate the significance of lung granulocytes in the adult respiratory distress syndrome (ARDS), 12 ARDS patients were studied with bronchoalveolar lavage (BAL) within 4-12 hours after clinical diagnosis of the syndrome. The specificity of pulmonary granulocytes in ARDS was investigated in comparison with five patients requiring ventilator treatment for cardiogenic pulmonary oedema and 17 normal patients about to undergo cholecystectomy. The percentage of granulocytes among recovered BAL cells was significantly higher in ARDS (77 +/- 18, M +/- SD) than in the cardiac (7 +/- 4) or the normal (1.5 +/- 1.0) group. In serial BAL (48-hour intervals) in five ARDS patients, significant reduction of granulocytes 86 +/- 11----32 +/- 10%) accompanied clinical improvement. The percentage of granulocyte in BAL correlated significantly and inversely with the PaO2/FiO2 ratio (r = -0.98), and in ARDS it was significantly higher after septic than after traumatic shock (89 +/- 14 vs. 55 +/- 12). Myeloperoxidase, a specific constituent of neutrophils, was significantly and inversely correlated with PaO2/FiO2 ratio (r = -0.62). The findings suggest a role for activated granulocytes in the lung, with release of tissue-damaging substances, in initial ARDS pathogenesis, notably when the syndrome is sepsis-induced.
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PMID:Pathophysiologic significance of lung granulocytes in human adult respiratory distress syndrome induced by septic or traumatic shock. 363 May 24

In the absence of direct toxins, the majority of evidence from animal models suggests that neutrophils (PMN) are necessary for the full expression of the abnormal pulmonary permeability accompanying acute microvascular lung injury. We therefore studied the role of the PMN in the human correlate of this disease, the adult respiratory distress syndrome (ARDS), by assessing the pulmonary retention of infused autologous 111Indium-labeled PMN (PMN-In). We evaluated 79 patients, prospectively categorized as: "active" ARDS (Aa; n = 30), "active" ARDS and concurrent corticosteroid therapy (As; n = 11), "resolving" ARDS (Ar; n = 13), sepsis without pulmonary edema (S; n = 7), and cardiac pulmonary edema (C; n = 18). This clinical separation was confirmed by retrospective analysis of associated measures of hemodynamic and respiratory dysfunction. We found that both analog scintigrams (positive/negative for diffuse pulmonary PMN-In sequestration) and computer-assisted quantitative analysis in 46 patients (T 1/2 of first hour demargination and percentage of peak activity/pixel/second remaining at 17 to 20 h) showed a significant rank order decrease in the pulmonary retention of labeled PMN-In through the Groups Aa----As----S----Ar----C. Our findings recognized aspects of in vivo PMN-In behavior that implied pathophysiologic differences between groups of critically ill patients in either the PMN themselves or in PMN-pulmonary endothelial interaction. This demonstrates the possibility of abnormal in vivo PMN-endothelial interaction in ARDS by virtue of the greater pulmonary localization of PMN in active ARDS versus resolving disease, septic non-ARDS states, and cardiac pulmonary edema.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Abnormal neutrophil-pulmonary interaction in the adult respiratory distress syndrome. Qualitative and quantitative assessment of pulmonary neutrophil kinetics in humans with in vivo 111indium neutrophil scintigraphy. 370 88

In vitro and in vivo studies have suggested that human complement component C5a plays a key role in neutrophil injury in the adult respiratory distress syndrome (ARDS). First, using leukocyte aggregometry, we demonstrated that the addition of a recently developed rabbit anti-human polyclonal antibody to C5a des arg to endotoxin-activated plasma prevented leukocyte aggregation in vitro. We then administered the anti-C5a des arg antibody to septic primates (Macaca fascicularis). Three groups of primates, control, septic, and anti-C5a antibody treated septic, were studied (n = 4 in each group). A 30-min infusion of Escherichia coli (1 X 10(10)/kg) resulted in severe sepsis and ARDS. Primates were killed 4 h after completion of the E. coli infusion. Septic animals not treated with anti-C5a antibody had 75% mortality (3/4), decreased oxygenation, severe pulmonary edema, and profound hypotension. Septic primates treated with anti-C5a antibodies did not die and did not develop decreased oxygenation (P less than 0.05) or increased extravascular lung water (P less than 0.05). They also had a marked recovery in their mean arterial blood pressure (P less than 0.05). This study demonstrates that treatment with rabbit anti-human C5a des arg antibodies attenuates ARDS and some of the systemic manifestations of sepsis in nonhuman primates.
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PMID:Effects of anti-C5a antibodies on the adult respiratory distress syndrome in septic primates. 371 36

This report studies the principal causes of maternal death at Harare Maternity Hospital. In 1983 the maternal mortality rate for the greater Harare unit was 52/100,000 compared to 11.9/100,000 for England and Wales. Puerperal sepsis, hemorrhage, post-abortal sepsis and hypertensive disease accounted for 78.5% of the deaths. 12 of the deaths were due to puerperal sepsis, 8 of which had normal vaginal delivery and 4 were delivered by Caesarian section. 3 patients died within 48 hours of delivery. Hemorrhage was most commonly a result of ruptured uterus. Avoidable factors were considered present in all cases. Delay in diagnosis, availability of blood or performing laparotomy was evident in 4 of 5 who died from ruptured uterus; 2 were due to pulmonary edema from excessive transfusion, and 2 were attributable to the patient (refusal of transfusion, attempt to self abort.) Post-abortal sepsis occurred in 9 patients, most of whom were septicemic on admission. 8 patients died from hypertensive disease, 7 of which were eclamptic. Reduction in mortality has gone from 34% (1976) to 23.7% (1983) for puerperal sepsis and can be affected by encouraging patients to book for antenatal care. An observed increase in hemorrhagic deaths since 1976 may reflect a decreased staff-patient ratio at Harare Maternity Hospital. Post-abortal sepsis mortality has decreased from 32% (1976) to 17.7% (1983). Reduction in deaths from hypertensive disease necessitates prediction and early detection. Value of a post-mortem exam in all cases of maternal death is stressed.
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PMID:The prevention of maternal deaths: a continuing challenge. 373 Dec 56

Improved survival of patients receiving high-dose steroid therapy in sepsis and adult respiratory distress syndrome (ARDS) has been reported, but such therapy and its benefits remain controversial. Recently research has been directed toward manipulation of the arachidonic acid cascade. Improved survival and hemodynamics with administration of nonsteroidal anti-inflammatory drugs (NSAID) have been reported in animal models of sepsis and ARDS. The purpose of this study was to compare the effects of steroids (methylprednisolone) and NSAID (ibuprofen) in a porcine model of septic ARDS induced by a continuous infusion of live Pseudomonas aeruginosa. Cardiopulmonary parameters were monitored in animals intubated, paralyzed, and ventilated at a 250 ml tidal volume and 0.5 Fio2. Pigs were randomly assigned to one of five groups: groups I and II received respective doses of 12.5 mg/kg ibuprofen and 30 mg/kg methylprednisolone at 20 and 210 minutes after baseline; group III had P. aeruginosa only; groups IV and V received respective doses of ibuprofen and methylprednisolone at 20 and 210 minutes of sepsis. Significant pulmonary edema, increased intrapulmonary shunting, hypoxemia, hemoconcentration, and systemic hypotension occurred with P. aeruginosa infusion. In septic animals treated with ibuprofen normal systemic arterial pressure was maintained, hemoconcentration was decreased, and oxygenation was improved with a significant decrease in shunting and pulmonary edema. Administration of methylprednisolone improved hemoconcentration and cardiac index, but no significant effect on pulmonary edema, intrapulmonary shunting, or oxygenation was observed. The results of this study demonstrated a significant beneficial effect of ibuprofen and we would encourage controlled clinical trials of this drug in the management of sepsis and ARDS. On the other hand, methylprednisolone was found to be relatively ineffective in treatment of circulatory collapse and ARDS associated with sepsis.
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PMID:A critical comparison of the hematologic, cardiovascular, and pulmonary response to steroids and nonsteroidal anti-inflammatory drugs in a model of sepsis and adult respiratory distress syndrome. 376 92

A Denver peritoneovenous (PV) shunt was inserted in 54 consecutive patients for relief of malignant (24 patients) or cirrhotic (30) refractory ascites. The median age of both groups was 58 years, and the most frequent diagnoses were gastrointestinal (15) or ovarian (7) cancers and alcoholic cirrhosis (25). Median survival time was 1.7 and 3.5 months (range, 0.1-15.5 and 0.1-50.5), and the 1-month mortality 42% and 27%, respectively. Postoperative 24-h urinary output increased by 2-31, and the 1-week weight reduction was 8 and 11 kg, respectively, compared with before shunting. Complete shunt failure was encountered early in two patients, due to catheter malposition and clotting. Four more patients experienced transient failure, for an early dysfunction rate of 11%. A shunt-related operative mortality of 6% was caused by pulmonary oedema (two patients) and sepsis (one patient). Shunt malfunction intervened in almost half (6 of 14) of the cancer patients surviving 1 month but was relieved in all but 1. In 3 of 22 cirrhotic 1-month survivors, the Denver shunt had to be removed owing to clotting or sepsis (2 patients) or revised because of blockage. Seven patients with cirrhosis are alive a median of 18 months (range, 2-51) after PV shunt surgery. Side effects were detected in 22 patients (41%): thromboembolism (9 patients), sepsis (7), initially bleeding oesophageal varices (3), DIC syndrome (2), postoperative hepatic coma (2), ascitic leakage (2), and pulmonary oedema (2). Patients with gastrointestinal cancers or severe cardiac disease did not benefit from the procedure. A history of hepatic encephalopathy or a serum bilirubin level above about 100 mumol/l was a bad prognostic sign. We could confirm the reported considerable morbidity and mortality after PV shunting, but also its efficiency in certain cases. Careful patient selection and follow-up study, timing of operation, and adherence to technical details are mandatory to improve the results.
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PMID:Denver peritoneovenous shunting for malignant or cirrhotic ascites. A prospective consecutive series. 380 91

Since 1973, 11 patients have had emergency valve replacement for severe mitral insufficiency and cardiogenic shock within 1 month (mean 10.0 days) of acute myocardial infarction. Mean age was 60 years (range 44 to 71 years). Nine infarcts affected the inferior wall, one patient had a prior myocardial infarction, and only two patients had a history of cardiac symptoms. Ten patients had pulmonary edema, five were oliguric (less than 0.5 ml/kg/hr for 12 hours), four required endotracheal intubation, nine required preoperative intra-aortic balloon support, and three had had a cardiac arrest. Preoperative cardiac index averaged 1.7 L/m2/min even with pharmacologic and circulatory support. Eight patients had cardiac catheterization and nine had echocardiograms. Left ventricular ejection fraction varied from 23% to 83% (mean 51%) and was not prognostic. Five patients had papillary muscle rupture and six patients had papillary muscle dysfunction. The mitral valve was replaced with a mechanical prosthesis in all patients. Five had simultaneous coronary artery bypass grafts. Three of five patients with papillary muscle rupture and two of six with papillary muscle dysfunction survived hospitalization. Two patients could not be weaned from cardiopulmonary bypass, two patients died within 24 hours of low cardiac output, and two patients died 3 weeks postoperatively of acute tubular necrosis and sepsis following prolonged preoperative cardiogenic shock. The interval from onset of shock to operative therapy averaged 1.7 days for survivors versus 9.3 days for nonsurvivors. Although the amount of viable left ventricular mass cannot be measured preoperatively, we recommend early operation, before other organ systems fail, for patients having severe mitral insufficiency and cardiogenic shock within 30 days of acute myocardial infarction.
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PMID:Operation for acute postinfarction mitral insufficiency and cardiogenic shock. 387 81

To study the pathophysiology of early adult respiratory distress syndrome (ARDS) induced by sepsis, spontaneously breathing pigs under ketamine anaesthesia were investigated. Twenty animals were infused i.v. with E. coli endotoxin (10 micrograms . h-1 . kg-1) over 6 h, and ten control animals received physiological saline. In the controls, cardiac output (Qt) and O2 delivery decreased slightly. There were no changes in pulmonary gas exchange, pulmonary haemodynamics or extravascular lung water (EVLW). The polymorphonuclear (PMN) leucocyte count gradually increased, while the platelet count decreased slightly. Endotoxin infusion caused profound deterioration of pulmonary gas exchange, a marked rise in pulmonary vascular resistance (PVR) and a moderate increase in EVLW. The pulmonary dysfunction was not attributable to the pulmonary oedema per se, whereas a "dry" ventilation/perfusion inequality played an important role. The "responders" (peak venous admixture greater than 20%; n = 14) were characterized by higher Qt and lower PVR than the "non-responders". Qt declined progressively, especially in non-survivors. O2 delivery decreased considerably. Metabolic acidosis probably indicated oxygen deficit. Eleven of 20 animals died during the observation period. Mortality was related more to the imbalance between O2 delivery and oxygen demand than to the deterioration in pulmonary gas exchange. The PMN count decreased markedly while the gradual decline in platelet count was similar to that in the controls. Lung microscopy revealed PMN accumulation in the microvasculature, moderate interstitial oedema and microvascular blood stasis. Our porcine model, which closely mimics early ARDS in man, will be useful in further studies of the pathophysiological pathways and the treatment of this syndrome.
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PMID:A porcine model of early adult respiratory distress syndrome induced by endotoxaemia. 390 9


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