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

We describe here four cases of disseminated strongyloidiasis. In Okinawa, it has been reported that about 10% of the residents are infected with Strongyloides stercoralis, but disseminated cases are rare. Detailed histopathological examination revealed that the present four cases could clearly be separated into two groups, two acute cases and two subacute cases. The acute cases died rapidly due to extensive diffuse intra-alveolar haemorrhage in both lungs. However, there were no inflammatory infiltrates, abscesses or granulomas in the lungs. Worms were demonstrated in the alveolar spaces. No extensive bleeding was observed in any organs except the lungs. The acute cases could be diagnosed as severe diffuse intra-alveolar haemorrhage syndrome, but deposition of immune complex (parasite antigen and immunoglobulins) and complement C3c was not demonstrated in the alveolar wall and small vessels of the lung. The subacute cases exhibited no such extensive haemorrhage, but scattered microabscesses were found with sepsis. During the migration of the worms from the colon, enteric bacteria entered the circulation in the two subacute cases. The acute cases received steroid therapy before the dissemination of the worms, but the two subacute cases did not. Steroids might have influenced the Strongyloides stercoralis dissemination and/or the course of the disease.
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PMID:Extensive intra-alveolar haemorrhage caused by disseminated strongyloidiasis. 951 96

Steroids have been used in the treatment of infants with chronic lung disease (CLD) for over a decade. Some studies have reported beneficial effects from long, tapering 42-day course of dexamethasone. Short term regimens have also shown beneficial effects on ventilator dependent infants with CLD. Although steroid therapy has been successful in infants with established CLD, more recently, dexamethasone therapy is being initiated in infants with RDS considered to be at risk for developing CLD. Some of the initial studies reported higher rates of infection, but more recent prospective data have not shown an increased incidence of sepsis in patients treated with steroids. Presently, early steroid therapy appears to be beneficial to minimize lung injury in infants treated with surfactant.
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PMID:Dexamethasone therapy in chronic lung disease. 1082 66

Crohn's disease often involves the stomach, yet a permanent enterocutaneous fistula does not usually occur, after a percutaneous endoscopic gastrostomy is removed from a patient with Crohn's disease. This is because the factors that are related to the non-closure of a fistula are absent or have been treated (distal bowel obstruction, abdominal sepsis, undernutrition, poor gastric blood supply or abnormal serum levels of C-reactive protein and albumin). Gastric involvement in patients with Crohn's disease is common. Enterocutaneous fistulas from the stomach are rare. Percutaneous endoscopic gastrostomy (PEG) insertion and subsequent removal rarely cause problems in patients with Crohn's disease. Endoscopic removal of a PEG is advised in patients with Crohn's disease. Steroids may delay gastric adhesion to the anterior abdominal wall.
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PMID:Gastrostomy placement in patients with Crohn's disease. 1105 51

The optimal therapy for the treatment of sepsis and septic shock remains controversial. Many protocols are followed, using different strategies for initial resuscitation, cardiovascular monitoring, hemodynamic intervention, and eradication of infection. Overall, an aggressive approach to the management of cardiovascular dysfunction in septic shock is warranted. Initially, large volume fluid resuscitation is instituted. Our first choice of resuscitation fluid is 0.9% normal saline. Invasive hemodynamic monitoring using a flotation pulmonary artery catheter as well as invasive arterial blood pressure monitoring is a necessity in the hemodynamic management of septic shock. If the patient remains hypotensive (mean arterial pressure < 65 mm Hg) after adequate volume resuscitation has been established (pulmonary capillary wedge pressure 12 to 15 mm Hg), then vasopressor agents must be instituted. Our first choice is usually dopamine. In patients who remain hypotensive after maximal doses of dopamine are reached, norepinephrine is added. If these agents generate excessive tachycardia or if tachyarrhythmias develop, phenylephrine can be substituted or added. Inotropic agents are useful if the patient demonstrates hypotension with a low cardiac output state. Dobutamine is the agent of choice. We initiate broad-spectrum empiric antibiotics at presentation, modifying the exact regimen based on 1) site of infection; 2) prevailing organisms and antibiotic resistance patterns in the patient's environment; and 3) other specific risk factors (immunosuppression, chronic disease, exposure and vaccination history, invasive medical devices). When appropriate, aggressive surgical debridement is pursued. Currently, there are no clinical data to support the use of antagonists for sepsis mediators, although various clinical trials remain underway. Steroids are contraindicated except for adrenal replacement therapy.
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PMID:Cardiovascular Dysfunction in Sepsis and Septic Shock. 1109 49

Sepsis may cause not only failure of parenchymal organs but can also cause damage to peripheral nerves and skeletal muscles. It is now recognized that sepsis-mediated disorders of the peripheral nerves and the muscle, called critical illness polyneuropathy (CIP) and critical illness myopathy, are responsible for weakness and muscle atrophy occurring de novo in intensively treated patients. CIP represents an acute axonal neuropathy that develops during treatment of severely ill patients and remits spontaneously, once the critical condition is under control. The course is monophasic and self-limiting. Among the critical illness myopathies, three main types have been identified: a non-necrotizing "cachectic" myopathy (critical illness myopathy in the strict sense), a myopathy with selective loss of myosin filaments ("thick filament myopathy") and an acute necrotizing myopathy of intensive care. Clinical manifestations of both critical illness myopathies and CIP include delayed weaning from the respirator, muscle weakness, and prolonging of the mobilization phase. The pathogenesis of these neuromuscular complications of sepsis is not understood in detail but most authors assume that the inflammatory factors that mediate systemic inflammatory response and multiple organ failure are closely involved. In thick filament myopathy and acute necrotizing myopathy, administration of steroids and neuromuscular blocking agents may act as triggers. Specific therapies have not been discovered. Stabilization of the underlying critical condition and elimination of sepsis appear to be of major importance. Steroids and muscle relaxants should be avoided or administered at the lowest dose possible.
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PMID:Neurological complications of sepsis: critical illness polyneuropathy and myopathy. 1175 54

Toxic epidermal necrolysis syndrome is an uncommon, acute, life-threatening, medication-induced disorder with a reported mortality rate of 20 to 60 percent. Different variables have been identified as risk factors. The extent to which these variables, when combined, affect the mortality and outcome in toxic epidermal necrolysis syndrome patients has not yet been reliably defined. Because of the high mortality rate, the logistic analysis of studied variables was performed to see whether a prognostic algorithm could be developed to aid the management of these patients. Thus, a retrospective review of 56 consecutive toxic epidermal necrolysis syndrome patients treated over a period of 13 years was undertaken in the authors' burn center. The demographics included age, sex, race, and total body surface area involved. The other variables studied were comorbidities, sepsis, steroid administration, and the interval between onset of rash and burn center admission. Data were subjected to Fisher's exact test and logistic analysis. Thirty-six patients (64.3 percent) were alive and 20 (35.7 percent) died. Univariate analysis indicated that the male/female ratio was 12:24 for survivors and 9:11 for nonsurvivors (p = 0.4). The white/nonwhite ratio was 80 percent for survivors and 54 percent for nonsurvivors (p = 0.58). The median age was 48.4 +/- 22.8 years (survivors, 41.7 +/- 22.0; nonsurvivors, 60.5 +/- 19.5; p = 0.002). Total body surface area involvement for survivors was 56.9 +/- 32 and 77.7 +/- 21 for nonsurvivors (p = 0.005). The presence of one or more comorbidities between the two groups differed (53 percent survivors and 90 percent nonsurvivors, p = 0.007), indicating eight times higher odds of dying in their presence. The average time between the onset of symptoms and admission to the burn unit was 5.25 +/- 3.4 days for survivors and 7.15 +/- 4.5 days for nonsurvivors (p = 0.08). The presence of sepsis (19.4 percent survivors, 95 percent nonsurvivors, p < 0.001) decreased odds for survival by a factor of 79. Steroids given as a single dose or multiple doses before the patient's transfer to the burn unit were not significantly associated with death (44 percent survivors, 65 percent nonsurvivors, p = 0.14). A multivariate logistic regression model yielded odds ratios of 1.11 (95 percent confidence interval, 1.03 to 1.19) for age in years, 304 (95 percent confidence interval, 8.83 to 10,400) for the presence of sepsis, and 1.03 (95 percent confidence interval, 0.99 to 1.08) for body surface area in percent. All those entering the burn unit with sepsis died. Equivalently, no survivors had sepsis before admission to the burn unit, whereas 55 percent of nonsurvivors had sepsis before admission and 40 percent developed sepsis after admission. When investigating the effect of age and sepsis, no patients over age 60 ever having sepsis survived, whereas all those who were under 60 and without sepsis survived. Likewise, all patients whose age was over 60 and whose total body surface area involved was over 60 percent died. The main factors contributing to the mortality from toxic epidermal necrolysis syndrome, when considering covariates separately, are the presence of sepsis at any time (odds ratio, 79), the presence of comorbidities (odds ratio, 8.05), age, and total body surface area, whereas multivariate models suggested age (odds ratio per year of additional age, 1.11), total body surface area (odds ratio per additional percent of body surface area, 1.03), and the presence of sepsis (odds ratio, 304). By using the actual coefficients in the logistic model, the log odds that the patient will die as the result of his or her condition can be summarized in the following formula: -11.5 + (10 percent of the patient's age + 3 percent of total body surface area + 5.75 if sepsis is present). The awareness of the importance of these covariates, and their early recognition as risk factors, should offer a focused approach to the patients' management and improve their outcome.
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PMID:Outcome of patients with toxic epidermal necrolysis syndrome revisited. 1217 37

Septic shock occurs in 6 % of paediatric cancer patients with neutropenia and fever. The mortality of the septic shock is 40 % in BMT patients and 5 % in others. One third of paediatric ARDS cases affect immunocompromised individuals with a total mortality of 45 % and 80 % after BMT. Septic shock is caused by gram-negative bacteria in more than 75 %. ARDS is due to pneumonia in more than 50 %, sepsis in about 25 %. This article provides the recommendations of the Infectious Diseases Working Party of the German Society for Pediatric Infectious Diseases (DGPI) and the German Society for Pediatric Hematology/Oncology (GPOH) for treatment of septic shock and ARDS. Therapy of septic shock includes early antibiotic therapy and volume expansion (> or = 40 ml/kg initially). Refractory shock requires vasopressors (noradrenaline), followed by a judicious circulatory management. Hydrocortisone is indicated in patients with high probability of adrenal insufficiency. Mainstay of ARDS therapy is ventilation with sufficient end-expiratory pressure (PEEP) to prevent loss of functional residual capacity and with limited tidal volumes (< or = 6 ml/kg) and limited inspiratory pressure (< 35 cm H(2)O) respectively, to minimize ventilator induced lung injury. Volume therapy consists of maintenance of sufficient preload to counteract the impaired venous return, induced by positive pressure ventilation. Diuretics and eventually veno-venous haemofiltration are used to reduce free lung water. Surfactant application may be considered in severe cases. Steroids are indicated in pneumocystis carinii pneumonia and in engraftment pneumonitis.
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PMID:[Management of septic shock and acquired respiratory distress syndrome in pediatric cancer patients]. 1628 59

Calciphylaxis may be considered a small vessel vasculopathy which is generaly associated with end-stage renal disease and hyperparathyroidism. The precise pathogenesis of the disease is not known. It needs sensitizers and challengers to occur. Steroids and immunosuppressive drugs including methotrexate are among those challenger agents. Calciphylaxis in collagen vascular diseases is rare. Only one case in rheumatoid arthritis was recently reported. Here we describe a case of calciphylaxis associated with active rheumatoid arthritis. This patient had active disease despite treatment of steroids and methotrexate for a long time. She died shortly after the diagnosis of calciphylaxis due to sepsis.
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PMID:Development of calciphylaxis after long-term steroid and methotroxate use in a patient with rheumatoid arthritis. 1635 57

Cerebral edema is a life-threatening condition that develops as a result of an inflammatory reaction. Most frequently, this is the consequence of cerebral trauma, massive cerebral infarction, hemorrhages, abscess, tumor, allergy, sepsis, hypoxia, and other toxic or metabolic factors. At present, the following types of cerebral edema are differentiated: the vasogenic cerebral edema resulting from an increased permeability of the endothelium of cerebral capillaries to albumin and other plasma proteins; the cytotoxic cerebral edema resulting from the exhaustion of the energy potential of cell membranes without damage to the barrier; the hydrostatic cerebral edema resulting from disturbance of the autoregulation of cerebral blood circulation; the osmotic cerebral edema resulting from dilution of blood; and the interstitial cerebral edema resulting from acute hydrocephaly. Some authors also differentiate ischemic cerebral edema. At present, when various traumas and traumatic cerebral injuries are frequent causes of death in young people, treatment strategy for cerebral edema is of utmost importance. Monitoring of the patient's condition in the intensive care unit is a necessity. It is important to ensure proper positioning of the patient--the head should be tilted at 30 degrees in order to optimize the cerebral perfusion pressure and control of the increase in intracranial pressure. Hyperventilation should be applied. Controlled hypothermia decreases the rate of metabolism in the brain. Slightly positive fluid balance should be maintained using crystalloid or colloid (hypertonic-hyperoncotic) solutions, at the same time maintaining cerebral perfusion pressure exceeding 70 mmHg. The treatment includes administration of antihypertensive medications, nonsteroidal antiinflammatory drugs, and barbiturates. Steroids decrease the permeability of capillaries and the hemato-encephalic barrier, promoting the movement of Na(+)/K(+) ions and water through the main endothelial membrane, and therefore they are used in the treatment of vasogenic cerebral edema as well as edema caused by a cerebral tumor. Glutamate and N-methyl-D-aspartate receptor antagonists improve cerebral microcirculation and metabolism. Trometamol corrects cerebral acidosis. Extended cerebral edema is treated surgically via a bilateral decompressive craniotomy, sometimes including craniotomy of lateral and posterior fossae. The treatment of cerebral edema is complex, and positive results may be expected only if the diagnosis and the provision of assistance are timely.
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PMID:[Cerebral edema and its treatment]. 1732 53

Acute hypercytokinaemia represents an imbalance of pro-inflammatory and anti-inflammatory cytokines, and is believed to be responsible for the development of acute respiratory distress syndrome and multiple organ failure in severe cases of avian (H5N1) influenza. Although neuraminidase inhibitors are effective in treating avian influenza, especially if given within 48 h of infection, it is harder to prevent the resultant hypercytokinaemia from developing if the patient does not seek timely medical assistance. Steroids have been used for many decades in a wide variety of inflammatory conditions in which hypercytokinaemia plays a role, such as sepsis and viral infections, including severe acquired respiratory syndromes and avian influenza. However, to date, the results have been mixed. Part of the reason for the discrepancies might be the lack of understanding that low doses are required to prevent mortality in cases of adrenal insufficiency. Adrenal insufficiency, as defined in the sepsis/shock literature, is a plasma cortisol rise of at least 9 microg dl(-1) following a 250 microg dose of adrenocorticotropin hormone (ACTH), or reaching a plasma cortisol concentration of >25 microg dl(-1) following a 1-2 microg dose of ACTH. In addition, in the case of hypercytokinaemia induced by potent viruses, such as H5N1, systemic inflammation-induced, acquired glucocorticoid resistance is likely to be present. Adrenal insufficiency can be overcome, however, with prolonged (7-10 or more days) supraphysiological steroid treatment at a sufficiently high dose to address the excess activation of NF-kappaB, but low enough to avoid immune suppression. This is a much lower dose than has been typically used to treat avian influenza patients. Although steroids cannot be used as a monotherapy in the treatment of avian influenza, there might be a potential role for their use as an adjunct treatment to antiviral therapy if appropriate dosages can be determined. In this paper, likely mechanisms of adrenal insufficiency are discussed, drawing from a broad background of literature sources.
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PMID:A rationale for using steroids in the treatment of severe cases of H5N1 avian influenza. 1757 50


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