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

Severe malaria is a major cause of infant and childhood death in the tropics. Effective management relies on rapid diagnosis, prompt administration of parenteral schizonticidal antimalarial drugs, careful fluid balance, prevention of convulsions and early recognition of complications such as hypoglycemia, metabolic acidosis, anemia, pulmonary edema, renal failure, bleeding and supervening bacterial sepsis. The mortality of treated cerebral malaria remains 20%. New, more rapidly acting antimalarials and earlier referral of children with complicated infections should reduce this unacceptable death rate.
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PMID:Management of severe malarial infection. 268 Sep 36

The authors describe a term female, asphyxiated, small for gestational age (SGA) infant with documented hyperinsulinism and hypoglycemia occurring at approximately 45 hours of age. The hypoglycemia was refractory to a high rate glucose infusion and steroid administration but responded to diazoxide. The subsequent hospital course was complicated by right-sided heart failure and sepsis. With the onset of sepsis, a transient hyperglycemia was noted that required intermittent insulin therapy for 10 days. Hypoglycemia and hyperinsulinism reemerged and responded to diazoxide therapy. An attempt to discontinue diazoxide at age 6 months was aborted at 2 weeks when hyperinsulinism and hypoglycemia recurred. The infant required diazoxide for 7 more months, then she recovered without having any sequelae. The review of this uncommon hypoglycemia etiology in an SGA and asphyxiated infant and the merits of long-term diazoxide treatment are discussed.
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PMID:Prolonged hyperinsulinism and hypoglycemia. In an asphyxiated, small for gestation infant. Case management and literature review. 268 73

In a prospective study of all patients with Pseudomonas pseudomallei infections admitted to a large provincial hospital in northeastern Thailand, 63 cases of septicemic melioidosis and 206 patients with other community-acquired septicemias were documented during a 1-y period. Apart from P. pseudomallei, the spectrum of bacteria isolated from blood cultures and the overall mortality (32%) were similar to those previously reported elsewhere. Death from septicemia was associated with failure to develop a leukocytosis or pyrexia over 38 degrees C, azotemia, hypoglycemia, and jaundice. Septicemic melioidosis presented mainly in the rainy season, occurred predominantly in rice farmers or their families, and was significantly associated with preexisting diabetes mellitus or renal failure (P = .03). Blood-borne pneumonia and visceral abscesses were common and the mortality was high (68%; P less than .001). The response to appropriate treatment was slow (median fever clearance time 5.5 d) and the median duration of hospital stay was 4 w. Septicemic melioidosis is a major cause of morbidity and mortality in northeast Thailand.
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PMID:Melioidosis: a major cause of community-acquired septicemia in northeastern Thailand. 270 42

Gram-negative septicemia/endotoxemia remains a serious clinical disorder that is often complicated by disseminated intravascular coagulation (DIC). Plasma antithrombin-III (AT-III) levels usually decrease during gram-negative septicemia/endotoxemia, and even moderate decreases in this major inhibitor of the coagulation system are associated with serious DIC. We demonstrated in an earlier study that prophylactic treatment of rats with 250 U/kg of AT-III followed by endotoxin challenge markedly attenuates DIC, indices of organ damage, and metabolic dysfunction. The present study was to determine whether treatment with 250 U/kg AT-III 1 hr after endotoxin challenge would be similarly efficacious. Rats treated with 250 U/kg of AT-III inactivated by human sputum elastase (ATX) served as protein controls. Blood samples for analysis were obtained 4 hr after AT-III or ATX treatment (5 hr after endotoxin challenge). Rats in the ATX treatment group exhibited abnormalities characteristic of endotoxemia, i.e., decreased fibrinogen levels and platelet counts, increases in prothrombin time and activated partial thromboplastin time, elevated serum glutamic oxaloacetic transaminase (SGOT) and alkaline phosphatase (AKP), and hypoglycemia. Treatment with AT-III markedly and significantly (P less than .05) attenuated all of these abnormalities, although survival was not increased. This study strongly suggests that supplementation of plasma AT-III is efficacious after the development of sepsis, although not as efficacious as prophylactic treatment.
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PMID:Antithrombin-III treatment limits disseminated intravascular coagulation in endotoxemia. 273 21

With proper nursing care and procedures, small hospitals in rural areas of developing countries can provide good neonatal care and achieve perinatal mortality rates comparable to those found at teaching hospitals. The 1st ingredient of adequate neonatology is the establishment of proper regimens for feeding, observation, and resuscitation of newborns. Even in areas where the majority of births take place at home, good neonatal care is possible as long as local risk factors are identified, all newborns are screened for these factors, and at-risk infants are referred for treatment. Factors that place infants at risk include birthweight under 2 kg or above 4 kg, delivery before 34 weeks' gestation, respiratory distress, severe birth asphyxia or trauma, jaundice, prolonged rupture of the membranes, infant not sucking or febrile, convulsions, congenital malformations, and maternal disease. 4 areas require special knowledge on the part of health personnel: the asphyxiated infant, hypothermia, hypoglycemia, and neonatal sepsis. Health workers must be familiar with proper resuscitation techniques, especially avoidance of excessive suctioning of the pharynx, and be alert to signs of hypoxic ischemic encephalopathy. Premature, small, asphyxiated, and sick infants are at greatest risk of hypothermia, a condition that can be prevented by drying and wrapping newborns immediately. Providers should be alert to signs of hypoglycemia in infants of diabetic mothers, large-for-gestational-age babies, the low- birthweight infant, and sick babies. To prevent sudden infant deaths, all sick newborns should be treated for neonatal sepsis.
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PMID:Neonatology in the developing world. Part 1. 277 46

The response of the sympathoadrenal system to hypoglycaemia of different etiology was studied in seven infants, aged 10-189 days. Five infants had hyperinsulinism secondary to nesidioblastosis or to a beta-cell adenoma of the pancreas, one infant had neonatal sepsis due to staphylococcal infection and one infant congenital growth hormone (HGH) and adrenocorticotropic hormone (ACTH) deficiency. In babies with hyperinsulinism, plasma noradrenaline increased from 0.29 +/- 0.03 to 0.61 +/- 0.09 ng/ml (P less than 0.01), whereas adrenaline increased only in three, but did not change in two babies. Increases in heart rate and blood pressure paralleled these changes. In hypoglycaemia due to congenital sepsis, noradrenaline increased from 0.39 to 1.64 ng/ml and adrenaline from 0.05 to 0.86 ng/ml. This was associated with marked haemodynamic changes. In congenital HGH and ACTH deficiency, the low basal plasma levels of noradrenaline (0.12 ng/ml) and adrenaline (0.01 ng/ml) remained unchanged in response to hypoglycaemia. Heart rate and blood pressure were unaffected. The sympathoadrenal system was activated by hypoglycaemia in all infants except in congenital HGH and ACTH deficiency. In contrast to adults, noradrenaline was the preferentially released catecholamine, suggesting an involvement of noradrenaline in glucose counter regulation in infancy.
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PMID:Sympatho-adrenal response to hypoglycaemia in infants. 285 Sep 15

Catecholamine therapy is often ineffective in reversing the peripheral vasodilatation and hypotension of septic shock. This suggests that catecholamines might not be able to activate alpha 1-adrenergic receptors to cause vasoconstriction. Despite elevations in endogenous catecholamines, hypoglycemia is also a complication of human sepsis, suggesting that among many other causes, hepatic alpha 1-receptors might be altered. To better understand the pathophysiologic basis for this pharmacologic dilemma, we studied the effect of experimental sepsis on alpha 1-adrenergic receptors in hepatic tissue, a rich source of alpha 1-receptors, from septic and control Sprague-Dawley rats. alpha 1-adrenergic receptors were measured with [3H]-prazosin and data analyzed by a computerized nonlinear least-square regression algorithm. Twenty-four hours following cecal ligation with puncture, a decreased number of alpha 1-adrenergic receptors was noted in crude and purified plasma membrane fractions (23 and 40% reductions respectively) from septic animals. No changes in either agonist or antagonist affinity for receptors from septic animals were noted. These data indicate that the catecholamine refractoriness seen in septic shock may be a result of alterations in alpha 1-adrenergic receptor number or receptor-effector coupling.
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PMID:Hepatic alpha 1-adrenergic receptor alteration in a rat model of chronic sepsis. 301 54

Suppression of an adrenocorticotropic hormone (ACTH) response to insulin hypoglycemia has been reported in ACTH-treated adults. There are no guidelines for withdrawal of ACTH treatment in children. After observing suppressed morning cortisol in several children, insulin tolerance tests were performed in five children within 48 hours after tapered withdrawal of ACTH treatment for myoclonic seizures. ACTH response, as determined by cortisol and beta-endorphin radioimmunoassay, was adequate in four of the children. One child showed low basal levels and minimal elevation during hypoglycemia for both beta-endorphin (0 to 3 pg/ml) and cortisol (3.6 to 4.4 micrograms/dL) on initial testing, but normal responses six weeks later. Measurement of beta-endorphin response supported a central basis for suppression in the child, who had had an adrenal hemorrhage during gram-negative sepsis while on ACTH. ACTH release is transiently suppressed in some children after exogenous ACTH treatment. Tapered withdrawal and stress coverage is recommended.
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PMID:Suppressed pituitary ACTH response after ACTH treatment of infantile spasms. 303 33

We describe our experience in the treatment of acute liver failure in 620 patients who developed grade 3 or 4 encephalopathy between 1973 and June 1985. The principal aetiologies were paracetamol-induced hepatic necrosis, viral hepatitis, halothane hepatitis and idiosyncratic drug reactions. Cerebral oedema is a major cause of death in these patients and is most effectively treated with mannitol (20%). Renal failure occurs in between 30% and 75% of cases, depending on aetiology, and is most effectively managed by haemodialysis. Electrolyte and acid-base abnormalities are common. Haemodynamic abnormalities encountered include a high cardiac output, low peripheral vascular resistance, hypotension and venodilatation. Assisted mechanical ventilation is frequently required to treat hypoxia caused by pneumonia, atelectasis, haemorrhage and oedema. A coagulopathy is always present but coagulation factors and platelets are given only when the patient is clinically bleeding. These patients are prone to sepsis and this is a significant cause of death. Hypoglycaemia is common and must be actively and frequently sought. The use of charcoal haemoperfusion has been associated with improved survival, especially when it is started during the grade 3 phase of encephalopathy. Recently survival figures of between 47% and 60% have been achieved for patients with paracetamol-induced liver failure and hepatitis A and B. However the figure for non A non B hepatitis and halothane- and drug-induced liver failure are disappointing at around 15% and liver transplantation is being explored as a treatment option in these patients.
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PMID:Management of acute liver failure. 308 71

The diagnosis of acute viral hepatitis is based on a thorough history (with a detailed review of possible modes of transmission), consistent physical findings (in which stigmata of chronic liver disease are absent), and laboratory tests confirming the presence of acute hepatocyte damage. Specific etiologic entities can be identified by serologic testing. In some cases, infection by more than one hepatitis virus may be revealed. The occurrence of HBV/HDV coinfection may lead to typical, uncomplicated acute hepatitis. In some patients, however, the development of a prolonged prothrombin time and encephalopathy indicates the presence of fulminant disease. The management of patients with such disease usually requires admission to an intensive care unit in order to increase the likelihood that complications will be recognized at an early stage, when intervention might make a difference. Standard interventions include vigorous treatment of hypoglycemia, attention to electrolyte and acid-base disturbances, and antibiotic therapy for bacterial sepsis. Despite aggressive management by experienced teams, fatality rates remain exceedingly high: As many as 75% to 100% of patients with severe encephalopathy die. Liver transplantation has been attempted in a number of cases. Its role remains ambiguous. Survival rates of 50% to 60% have been reported, but selection bias may turn out to have contributed to this apparently favorable outcome. In the patient under discussion, results of a follow-up physical two months after discharge were entirely normal. Liver chemistries were within normal limits, but a test for HBsAg was still positive. During the course of the examination, the patient admitted to having accidentally pricked his skin nearly two months before the onset of his illness while holding a needle that a friend had used for the intravenous injection of heroin. One year later, HBsAg was no longer detectable, but tests for anti-HBc and anti-HBs were both positive. The anti-HBc positivity was attributable to IgG rather than IgG anti-HBc. A test for anti-HDV was negative.
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PMID:Fulminant hepatitis due to HBV/HDV coinfection. 311 12


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