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

Profound hypothermia (core temperature of less than 28 degrees C) is a life threatening state and a medical emergency associated with a high mortality rate. The prognosis depends on underlying diseases, advanced or very early age, the duration prior to treatment, the degree of hemodynamic deterioration, and especially, the methods of treatment, including active external or internal rewarming. This is a case study of an 80-year-old female patient with severe accidental hypothermia (core temperature 27 degrees C). She was found in her home lying immobile on the cold floor after a fall. The patient was in a profound coma with cardiocirculatory collapse, and the medical staff treating her was inclined to pronounce her deceased. On her arrival at the hospital, she was resuscitated, put on a respirator and actively warmed. Very severe metabolic disorders were found, including a marked metabolic acidosis composed of diabetic ketoacidosis (she had suffered from insulin treated type 2 diabetes mellitus) and lactic acidosis with a very high anion gap (42) and a hyperosmotic state (blood glucose 1202 mg/dl). There were pathognomonic electrocardiographic abnormalities, J-wave of Osborn and prolonged repolarization. Slow atrial fibrillation with a ventricular response of 30 bpm followed by a nodal rhythm of 12 bpm and reversible cardiac arrest were recorded. The pulse and blood pressure were unobtainable. Despite the successful resuscitation and hemodynamic and cognitive improvement, rhabdomyolysis (CKP 6580 u/L), renal failure and hepatic damage developed. She was extubated and treated with intravenous fluids containing dopamine, bicarbonate, insulin and antibiotics. Her medical condition gradually improved, and she was discharged clear minded, functioning very well and independent. Renal and liver tests returned eventually to normal limits. Progressive bradycardia, hypotension and death due to ventricular fibrillation or asystole commonly occur during severe hypothermia. Respiratory and metabolic, sometimes lactic, acidosis, lethargy and coma, hypercoagulopathy, hyperosmolar state, acute pancreatitis and renal and hepatic failure are frequent complications of hypothermia. Underlying predisposing causes of hypothermia are diabetic ketoacidosis, cerebrovascular disease, mental retardation, hypothyroidism, pituitary and adrenal insufficiency, malnutrition, acute alcoholism, liver damage, hypoglycemia, sepsis, hypothalamic dysfunction, sepsis and polypharmacy, and especially, the use of sedative and narcotic drugs. Our case demonstrates once again that CPR once begun should continue until the successful rewarming because "no one is dead until warm and dead".
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PMID:[Severe accidental hypothermia in an elderly woman]. 1175 73

Adequate adrenocortical function is essential to survive critical illness. Most critically ill patients display an elevated plasma cortisol level, reflecting activation of the pituitary-adrenal axis, which is considered to be a homeostatic adaptation. In the setting of critical illness, the failure of an appropriate neuroendocrine response can lead to the picture of vasopressor-dependent refractory hypotension. This state of relative or functional adrenal insufficiency is characterized by an inadequate production of cortisol in relation to an increased demand during periods of severe stress, particularly prolonged critical illness such as multi-organ failure. This clinical entity, however, lacks clear-cut diagnostic criteria. What are the appropriate cortisol concentrations in the critically ill? Should base-line and adrenocorticotropic hormone-stimulated cortisol concentrations be assessed? The classical adrenocorticotropic hormone stimulation test is often used, but there are problems with interpreting its results. Other diagnostic tools, such as the low-dose adrenocorticotropic hormone test and relative eosinophilia, are promising but also lack proper criteria. A prompt response to hydrocortisone treatment is a major clue to the diagnosis. Recent studies with stress doses of hydrocortisone in sepsis and septic shock have shown a marked haemodynamic improvement, but whether patients with relative adrenal dysfunction benefit most from this treatment and whether there is definitely an effect on outcome is still undecided.
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PMID:Relative adrenal failure in intensive care: an identifiable problem requiring treatment? 1180 May 21

In general, a rule for corticosteroids in preventing or relieving the acute respiratory distress syndrome (ARDS) has yet to be established, although these drugs are indicated for conditions such as Pneumocystis carinii pneumonia. High-dose corticosteroids have not been shown to reduce mortality through their anti-inflammatory properties when given early to patients with sepsis, septic shock, or ARDS. Corticosteroids have been shown, however, to reduce mortality in patients with late ARDS only in one small, inconclusive study. More recent investigators have focused on the usefulness of low-dose corticosteroids in reducing mortality in patients with sepsis or septic shock who may have relative adrenal insufficiency, but these studies also are inconclusive, and it is unclear that low-dose corticosteroids affect the development of ARDS in these patients.
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PMID:Corticosteroids in ARDS. An evidence-based review. 1191 Jul 34

Corticosteroids were proposed to treat patients with severe sepsis as early as 1940. A summary of all available randomized controlled trials performed between 1966 and 1993 was provided in two systematic review that recommended to abandon the use of high dose coricosteroids to treat patients with severe infection. Nonetheless, a doubt still persist regarding the efficacy of a strategy of replacement therapy in cathecolamines-dependent shock. This strategy relies mainly on the concept that septic shock may be complicated by 1) an occult adrenal insufficiency, 2) a glucocorticoid peripheral resistance syndrome. Some studies demonstrated the effect of replacement therapy with hydrocortisone on the sistemic inflammatory response and on the cardiovascular function during sepsis. The effect of this therapy on survival to septic shock is controversial both in recent and old studies. Finally a recently completed multicenter, placebo controlled, randomized, double-blind study has evaluated the efficacy and tolerance of a replacement therapy with a combination of hydrocortisone (50 mg intravenous bolus four times per day) and fludrocortisone (50 g orally once a day) given for 7 days. This study included 300 catecholamines- and ventilator-dependent septic shock. The authors found a significant reduction in 28-day mortality in patient with occult renal insufficiency. In sum, short course with high doses of corticosteroids should not be given in severe sepsis, except for specific entitles like severe typhoid fever, pneumocystis carinii pneumonia in AIDS or bacterial meningitis in children. The rational for a replacement therapy with hydrocortisone in catecholamines-dependent septic shock grows stronger.
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PMID:Resurrection of steroids for sepsis resuscitation. 1202 69

An analysis of beta thalassemia major patients seen at Hospital Juan P. Garrahan was carried out in order to determine the characteristics and outcome of the population. From August 1987 to July 2000, 45 patients were admitted (27 males-18 females). The most common beta globin gene defects were C-39 (30.7%); IVS-I nt 110 (20%); IVS-I nt 6 (13.3%); IVS-I nt 1(4%). alpha globin genes were normal in 42 patients, 1 patient had triplicate and cuadriplicate alpha globin genes and 2 patients were not analyzed. Six patients of 5 families were heterozygous for -158G gamma mutation. Allogeneic stem cell transplantation was performed in 7 patients, with an identical sibling. Transfusion-related infections and alloantibodies were detected in 6.7% patients. Growth assessment showed no significant difference in the stature of girls compared to the reference population, but 5 boys had short stature. There is a tendency to short trunk. Growth velocity was normal at prepubertal age. No X-ray lesions related to desferrioxamine were observed. Delayed puberty and hypogonadotropic hypogonadism were found in 35.7% and abnormalities in GH/IGF-I axis in 12.5% of the patients. Impaired glucose tolerance was found in 2 patients. No patient developed diabetes mellitus, thyroid or adrenal insufficiency. One patient had cardiac complications. Forty-two patients are alive and 3 died (cardiac failure 1, central nervous system bleeding 1, sepsis 1). We conclude that beta thalassemia major, originated mainly from Italian immigrants, has a cumbersome treatment and is severely hindered by the lack of adequate economic resources in our patients.
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PMID:[Beta thalassemia major in Argentina]. 1203 33

Sepsis and acute lung injury (ALI) or acute respiratory distress syndrome (ARDS) are associated with high mortality rates despite recent therapeutic advances. Both disease states involve uncontrolled host defense responses that lead to inflammation, endothelial damage, enhanced coagulation, diminished fibrinolysis and fibroproliferation to produce microthrombi, and relative adrenal insufficiency. Corticosteroids inhibit the host defense response and may offer an inexpensive therapeutic option. Results of several randomized, double-blind studies demonstrated no survival benefit and higher secondary infection rates when supraphysiologic doses of corticosteroids were administered for less than 24 hours. Recently, the emphasis of research for corticosteroid therapy has involved adrenocortical replacement dosage regimens administered for several days to weeks, with doses corresponding to the stress level of the disease. Stress-dose therapy with hydrocortisone in patients with septic shock who require vasopressor support, especially if adrenal insufficiency is present, accelerates hemodynamic stability and reduces mortality. The frequency of gastrointestinal hemorrhage was higher with corticosteroid therapy than with placebo, but the occurrence of secondary infections was similar to that of placebo. The only randomized, double-blind study that evaluated stress-dose methylprednisolone therapy for ARDS was terminated early after only 24 patients were enrolled because therapy with methylprednisolone was associated with enhanced survival despite higher secondary infection rates. A multicenter study investigating stress-dose methylprednisolone for ARDS is under way and should provide valuable information. Sufficient data support stress-dose hydrocortisone therapy for vasopressor-dependent septic shock. Stress-dose methylprednisolone therapy for ALI-ARDS requires further study but may be warranted in cases of refractory infection-induced ARDS when impending mortality is likely.
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PMID:Stress-dose corticosteroid therapy for sepsis and acute lung injury or acute respiratory distress syndrome in critically ill adults. 1222 50

During sepsis or acute respiratory distress syndrome, the hypothalamic pituitary adrenal axis is rapidly activated through a systemic pathway, i.e. by circulating pro-inflammatory cytokines and through the vagus nerve. Subsequently, the adrenal glands release cortisol, a hormone which will likely counteract the inflammatory process and restore cardiovascular homeostasis. Both experimental models and studies in humans suggest that inadequate hypothalamic pituitary adrenal axis response to stress accounts, at least partly, for the genesis of shock and organ dysfunction in sepsis and acute respiratory distress syndrome. Relative adrenal insufficiency and peripheral glucocorticoid resistance syndrome are the two main features of the inappropriate hormonal response and provide the grounds for cortisol replacement in these diseases. In practice, a high dose of corticosteroids (i.e. one to four boluses of 30 mg/kg of methylprednisolone, or equivalent) had no effects on survival in severe sepsis or acute respiratory distress syndrome. There are at least seven randomised controlled trials reporting the benefits and risks of low dose corticosteroids (i.e. 200 to 300 mg daily of hydrocortisone or equivalent) given for a prolonged period in severe sepsis or in the late phase of acute respiratory distress syndrome. These trials showed consistently that, in these patients, the use of low dose of corticosteroids alleviated inflammation, restored cardiovascular homeostasis, reduced organ dysfunction, improved survival and was safe. Further studies are ongoing to better identify the target population. In the meantime, cortisol replacement (i.e. 200 to 300 mg daily of hydrocortisone or equivalent) should be considered as standard care for these patients.
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PMID:The use of corticosteroids in severe sepsis and acute respiratory distress syndrome. 1255 98

We report on a female infant with disseminated tuberculosis who presented with clinical sepsis and disseminated intravascular coagulation starting at 14 days of age. Parenteral ofloxacin combined with streptomycin were used because the enteral route was not possible and intravenous isoniazid and rifampicin were not available. Rare complications including infection-associated hemophagocytic syndrome, hypercalcemia, and adrenal insufficiency were detected and successfully managed.
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PMID:Neonatal tuberculosis associated with shock, disseminated intravascular coagulation, hemophagocytic syndrome, and hypercalcemia: a case report. 1255 35

Sepsis is an inflammatory syndrome caused by infection. Consequently, anti-inflammatory therapy in sepsis has been a subject of extensive research, and corticosteroids have long been used to treat severe infections. However, studies conducted in the 1980s failed to demonstrate any beneficial effects of high dose, short-term steroid therapy in sepsis and this therapy was therefore abandoned in the last decade. Recently, a new concept has emerged with more promising results--low dose, long-term hydrocortisone therapy- and this approach is now being evaluated in the treatment of septic shock. It is supported by the observation that many sepsis patients have relative adrenal insufficiency. Moreover, the anti-inflammatory effects of steroids and their ability to improve reactivity to catecholamines further contribute to their effects in sepsis. Large randomized clinical trials will be required to determine the exact role of corticosteroids in septic shock.
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PMID:Corticosteroids in sepsis: a new concept for an old drug. 1267 77

Severe sepsis is the leading cause of death among patients in intensive care units. Recombinant activated protein C is the only substance known to directly improve morbidity and mortality. Adrenal insufficiency occurs frequently in patients with sepsis and is associated with poor outcome. Although high-dose glucocorticoids have not positively affected clinical outcome, small trials in which low-dose glucocorticoids were administered to patients with septic shock and relative adrenal insufficiency have shown decreased mortality. The main effect of glucocorticoids in low-doses apparently is exerted through correction of suppression of the hypothalamic-pituitary-adrenal axis. However, the therapeutic benefits of glucocorticoids may be related to their antiinflammatory properties and endogenous catecholamine-enhancing effects.
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PMID:The hypothalamic-pituitary-adrenal axis and low-dose glucocorticoids in the treatment of septic shock. 1268 Apr 81


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