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

Each year between 71,000 and 142,000 cases of septic shock are estimated to occur. Shock is a derangement in the homeostatic mechanisms of the body secondary to decreased tissue perfusion. The proper treatment of septic shock is based on complete understanding of the altered physiologic events, and, consequently, adequate therapy for shock should be approached from the standpoint of applied physiology in the clinical setting. Currently, sepsis is seen in the patients suffering multiple trauma or burns, undergoing immunosuppressive therapy for cancer or connective tissue disease, or who have undergone organ transplants. The initial therapy needs to consider carefully whether subtle clinical parameters are consistent with sepsis. Time and effort should be given to the prevention of septic shock. Good drainage procedures, proper nutritional therapy, and hydration needs to be maintained at all times. An early aggressive approach with regard to diagnosis can beneficially influence the outcome of infection by reducing the duration and complexity of therapy. Focus is on bacteriology and antimicrobial therapy, hemodynamic and fluid therapy, metabolic and nutritional aspects, complications, and steroids. 4 major complications of sepsis are abnormalities in the clotting pathway and changes in the renal, pulmonary, and cardiovascular systems. Steroids have been recommended for septic shock, for they are stabilizing to the lysosomal membranes in the splanchnic circulation. Experimentally, this has led to a decreased production of myocardial depressant factor. To use steroids properly large doses should be administered early in the shock state.
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PMID:Therapy for septic shock. 10 43

Due to poor results with conventional operative therapy for diffuse hemorrhagic gastritis (DHG), a prospective evaluation of gastric devascularization was performed on 21 patients. Sepsis, alcoholism, and steroid abuse were the common etiologic factors. In spite of the fact that these were all critically ill patients, all stopped bleeding with this operation and only two rebled (9%). The average operating time was 84 minutes. There were two operative complications and gastric necrosis did not occur. The mortality was high (38%) due to the primary disease. Gastric devascularization is a useful salvage procedure for the patient with DHG because it can be accomplished rapidly, with few complications, has a low rebleed rate, and causes no permanent sequelae. Since this procedure causes severe gastric mucosal ischemia, it casts doubt only on the importance of this mechanism alone as the cause of "stress ulceration."
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PMID:Gastric devascularization: a useful salvage procedure for massive hemorrhagic gastritis. 30 Oct 14

In order to effectively treat shock the physician must understand the physiology of shock. Shock patients may have a low, normal, or high arterial blood pressure, and the blood volume may be below normal, normal, or above normal. Shock is not necessarily accompanied by low arterial pH or low peripheral resistance. Most cases of acute traumatic and hemorrhagic shock show a high arterial pH, partly due to the blowing off of CO2, despite an elevated blood lactic acid level. Most patients also show a very high resistance. A factor that all shock patients have in common is a deficient capillary perfusion, or an insufficient amount of blood flowing through the capillaries. The cornerstone of the treatment of hypovolemic shock is the administration of adequate amounts of the right kinds of intravenous fluids. Focus is on classification of shock (reversible shock, irreversible or fatal shock, hypovolemia), the heart in shock, respiration, drugs (steroids, vasoactive drugs), and disseminated intravascular coagulation. If edema is a problem, diuretics may be helpful. Antibiotics for infection are very important in sepsis and septic shock. Supportive drugs are also important. Steroids and vasoactive drugs have a secondary place in the treatment of shock, and they should be used when these treatments have failed to produce an adequate blood pressure and urinary output.
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PMID:Treatment of shock. 44 80

Sepsis is an unusually common cause of illness and death in RA. All sorts of infections occur, but pyarthrosis produces exceptional problems. Clinically, pyarthrosis, empyema, and purulent pericarditis mimic bland rheumatoid effusions. Aspiration of the attendant effusions is the only reliable diagnostic procedure. Subcutaneous nodules on the sacrum and back are easily overlooked. Necrosis and ulceration of these nodules may provoke septicemia. Those with Felty's syndrome do not uniformly have problems with recurrent infection. Splenectomy may not benefit such patients. The belief that corticosteroids cause increased infections in rheumatoid patients is not totally justifiable at present. Steroids can, however, disguise underlying sepsis and hamper proper diagnosis.
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PMID:Infection in rheumatoid arthritis. 97 60

Gentamicin is a commonly used antibiotic in the treatment of gram-negative infections including septicemia and pyelonephritis. Bacterial endotoxin is liberated during antibiotic therapy and may lead to endotoxemic shock. Steroids such as hydrocortisone are generally recommended in the treatment of endotoxemic shock. There are very limited data on the influence of endotoxin or corticosteroids on the pharmacology of antibiotics, especially aminoglycosides, which are nephrotoxic. We studied the influence of both Escherichia coli endotoxin and hydrocortisone succinate on the renal uptake of gentamicin in rats. Animals were injected intravenously with endotoxin (0.25 mg/kg) and/or hydrocortisone (25 mg/kg) plus gentamicin (10 mg/kg). Gentamicin levels in the serum and renal parenchyma as well as renal function and histology were evaluated. Both endotoxin and hydrocortisone given alone increased the concentration of gentamicin in the renal cortex (P less than 0.05). Normal values in serum were observed in all groups at most time intervals. When administered together, endotoxin and hydrocortisone did not potentiate each other. The combination of endotoxin and hydrocortisone gave significantly higher levels of gentamicin than endotoxin or hydrocortisone alone when endotoxin was injected 3 h before hydrocortisone (P less than 0.05). Blood pressure and cardiac frequency were normal when gentamicin was given. Endotoxin alone slightly decreased the glomerular filtration rate, and hydrocortisone alone slightly modified renal plasma flow. The combination of both drugs did not significantly affect renal function. No histological lesion was noted on light microscopy in animals receiving endotoxin. Competitive or synergistic activity of endotoxin, gentamicin, and hydrocortisone at the cellular level, especially on membranes or lysosomes, might explain in part our observation on the renal uptake of gentamicin. By increasing the total amount of drug within the kidney, endotoxin and hydrocortisone might increase the risk of nephrotoxicity associated with aminoglycosides.
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PMID:Influence of hydrocortisone succinate on intrarenal accumulation of gentamicin in endotoxemic rats. 343 28

Steroids and cyclooxygenase inhibitors have been advocated as adjunctive treatment for sepsis. We studied the influences of these treatments on the survival of 98 male Sprague-Dawley rats in which sepsis was induced by cecal ligation and puncture. Rats received one of four treatments: sodium chloride (NaCl); methylprednisolone, 30 mg/kg (MP); ibuprofen, 12.5 mg/kg (I); methylprednisolone, 30 mg/kg, plus ibuprofen, 12.5 mg/kg (MP + I). Cumulative survival statistics were determined daily for 14 days thereafter. Survival was not altered by either MP or I when compared to animals receiving NaCl only. However, the combination of MP + I increased mortality from day 2 through day 14. The authors conclude that (1) MP administration alone does not increase mortality in septic rats; therefore, the results do not support the contention that steroid treatment in the absence of antibiotic therapy may be detrimental; (2) the cyclooxygenase inhibitor I does not improve survival in septic rats; and (3) the combined administration of MP and I increases mortality in septic rats and the possibility that this combination might be harmful in septic patients should be considered also.
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PMID:Methylprednisolone plus ibuprofen increases mortality in septic rats. 650 29

A murine model was used to test the effects of various therapeutic modalities on the rate of death following intra-abdominal sepsis as produced by cecal ligation and puncture (CLP). There were no deaths among sham-operated control mice after ether anesthesia, whereas CLP produced a mortality rate of 100% by 24 hours. When CLP was followed at 16 hours by excision of the cecum and saline peritoneal lavage (CLPE), the mortality rate was 20% at 24 hours and 60% at 72 hours. The therapeutic modalities consisted of gentamicin (1.5 mg/kg) alone or in combination with methylprednisolone (50 mg/kg) or tuftsin (1 mg/kg) administered before CLP and at 16 and 24 hours after CLP. Separate groups of animals also received only methylprednisolone or tuftsin, a tetrapeptide produced by the spleen. Compared with the mortality rate in the CLPE group, mortality at 24 and 72 hours was decreased for gentamicin alone (0% and 10%, respectively), tuftsin alone (10%, 40%), or the two in combination (0%, 20%). As compared with CLPE, methylprednisolone led to increased mortality rates at 24 and 72 hours (70%, 80%). The data (significant at P less than 0.01, X2 analysis) suggest that gentamicin and tuftsin may improve the rate of early survival after intra-abdominal sepsis in this Model. Steroids do not seem to be beneficial and may, in fact, be harmful.
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PMID:Evaluation of factors affecting mortality rate after sepsis in a murine cecal ligation and puncture model. 687 47

Between 1975 and 1992 450 children with idiopathic thrombocytopenic purpura (ITP) were diagnosed, and of those 100 (22%) developed the chronic form of the disease. Approximately half the patients with chronic ITP presented with mild to moderate hemorrhagic manifestations at the onset of purpura (30 cases) and/or later during the course of the disease (25 cases). The incidence of intracranial hemorrhage was 1%, and the mortality rate due to overwhelming septicemia after splenectomy was also 1%. Overall one-third of the patients received no therapy; two-thirds of them went into spontaneous remission within 8 months to 8 years from the onset of ITP. Steroids given in conventional or high doses (51 cases) achieved a transient (if any) rise in platelet count, but in no case were steroids curative. Remission related to intravenous immune globulin (IVIG) therapy was noticed in 38.5% of the children (10 of 26) after variable courses. The response rate to splenectomy was 95.0%. Ultimately the long-term outcome in children with chronic ITP was as follows: remission, 58 cases (spontaneous, 30; after IVIG therapy, 10; after splenectomy, 18); hemostatic platelet values, 22 cases (spontaneous, 16; after IVIG, 5; after splenectomy, 1). Thirteen children were lost in follow-up, and 7 remain thrombocytopenic but asymptomatic. These data indicate that chronic ITP in childhood runs a benign course in most cases and may remit with or without therapy even several years from onset. Therefore, therapeutic intervention has to be individualized, and splenectomy, which is not always safe, should be reserved for problematic cases that fail to respond to conventional therapeutic modalities.
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PMID:Seventeen years of experience with chronic idiopathic thrombocytopenic purpura in childhood. Is therapy always better? 757 95

Septic shock is currently the most common cause of death in noncoronary intensive care units in the United States. The pathogenesis of sepsis involves a variety of cytokine and noncytokine mediators, which, when activated, can result in a self-perpetuating cascade. This systemic response to infection is a frequent cause of multi-organ system failure and death. Treatment has traditionally focused on antibiotic therapy, but this has not significantly changed patient outcomes. Steroids have been shown to be of little or no value and studies evaluating monoclonal antibodies that target the mediators of the sepsis cascade have not produced promising results.
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PMID:Sepsis: the role of steroids and monoclonal antibodies in treatment. 807 77

In 1994, the National Institutes of Health Consensus Development Conference on Antenatal Steroids recommended corticosteroids between 24 and 30-32 weeks' gestation in pregnancies complicated by preterm premature rupture of membranes (PROM). Since the Consensus Conference, the use of antenatal corticosteroids has increased to approximately 60% of potential treatment candidates. Some of the remaining 40% of pregnant candidates may go untreated because of concern that corticosteroids could increase the risk of neonatal infection. Using decision-analysis techniques, we compared the potential benefit of antenatal corticosteroids in reducing the incidence of severe intraventricular hemorrhage with the potential risk of increasing the rate of neonatal sepsis. Our analysis indicates that the benefit of a small decrease in severe intraventricular hemorrhage outweighs the potential harm of a large increase in the rate of neonatal sepsis. Therefore, we support the Consensus Conference panel's recommendation that antenatal corticosteroids be used in pregnancies complicated by preterm PROM.
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PMID:Antenatal corticosteroids in pregnancies complicated by preterm premature rupture of membranes. 935 78


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