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

In adults supplemental parenteral nutrition (PN) is advisable in burns over 40% especially when weight loss exceeds 10% of body weight. In children with smaller reserves and higher requirement of proteins and energy no rigid scheme for parenteral supplementation is used at our unit. In a young infant it may be added already at a 20-30% deep burn, especially with connected gastrointestinal tract problems, infection etc. Metabolic and protein requirements are estimated 50-100% in addition to their normal needs. Hypertonic glucose (gradually increased from 20-40%), covered with insulin in the early phase, is used as source of carbohydrates. L-amino acid mixture containing the "pediatric essential amino acids" histidine and cysteine is given as a nitrogen source. 20% Intralipid is given in a gradually increased amount of 2-4 g/kg per day to provide calories and essential fatty acids. Among electrolytes K, Ca, P and Mg must be added. Increased amounts of vitamin C and folate are needed by burned children. Vitamin E is also required during prolonged lipid administration. Trace elements (Zn. Fe, etc.) are supplied orally or i.v. with special solutions or fresh plasma infusions. Our experience with parenteral nutrition in severely burned children will be presented. There were no severe metabolic side-effects but sepsis represented the major problem. The concomitant heat preservation by warming the room and use of infra-red heaters is emphasized.
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PMID:Parenteral nutrition in severely burned children. 10 12

A randomized, double-blind study to determine the effect of intramuscular vitamin E on mortality and intracranial hemorrhage (ICH) was performed. One hundred forty-nine neonates with birth weights less than or equal to 1000 g and less than or equal to 24 hours of age were grouped by weight (501 to 750 g and 751 to 1000 g) and randomized to treatment or control. The treatment group received intramuscular injections of vitamin E (dl-alpha-tocopherol) on days 1, 2, 4, and 6 of life. The control group received intramuscular injections of placebo on the same schedule. All neonates initially received oral vitamin E (100 mg/kg/day dl-alpha-tocopheryl acetate), which was subsequently adjusted to keep serum levels at 0.5 to 3.5 mg/dL. Ultrasonographic examinations of the head were performed as possible on days 1, 5 to 7, and 12 to 14. Hemorrhage was defined as mild if less than or equal to grade II ICH, or severe if grade III or IV. No significant differences in neonatal or total hospital mortality between groups were found. However, all ICH, as well as severe ICH, were significantly less in the vitamin E-treated 501 to 750-g subgroup (all ICH: 60% vs 29%; severe ICH: 32% vs 4%). When survivors were analyzed separately, a significant decrease in severe ICH was seen in the vitamin E-treated neonates (25% vs 5%). Necrotizing enterocolitis and sepsis did not occur more frequently in the neonates treated with intramuscular injections of vitamin E. Other than two cases of mild induration at injection sites, no deleterious side effects of treatment were identified. Vitamin E may have a role in the prevention of severe ICH in premature neonates weighing between 501 and 750 g.
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PMID:Effect of intramuscular vitamin E on mortality and intracranial hemorrhage in neonates of 1000 grams or less. 217 50

The effect of acute endotoxin-induced septic shock on myocardium oxidative stress after low or high vitamin C and/or E dietary supplementation was studied in guinea pigs, laboratory animals which, like human, do not have capacity for ascorbate synthesis. Neither the antioxidant enzymes or GSH were modified by endotoxin and vitamin treatments. Vitamin E showed a strong capacity to protect the myocardium against both enzymatic and non-enzymatic lipid peroxidation even in the presence of endotoxin. Vitamin C supplementation increased heart ascorbate whereas endotoxic shock totally depleted the heart ascorbate of vitamin C supplemented animals without changing vitamin E. Endotoxin significantly increased myocardium uric acid, a marker of ischemia induced oxidative stress, in animals fed with low vitamin C levels. This increase was totally prevented in vitamin C supplemented, but not in vitamin E supplemented animals. Strongly depressed levels of plasma vitamin C have been recently described in sepsis in human patients. The results suggest that ascorbate is a primary antioxidant target in the heart of endotoxin treated mammals lacking the capacity to synthesize ascorbate and that ascorbate can have a protective value against endotoxin-induced free radical damage in the myocardium. Implications of these results for the possible preventive role of vitamin C in humans during sepsis are discussed.
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PMID:Endotoxin depletes ascorbate in the guinea pig heart. Protective effects of vitamins C and E against oxidative stress. 876 Oct 15

Oxidative stress during sepsis induces tissue damage, leading to organ dysfunction and high mortality. The antioxidant effects of vitamin E have been reported in several diseases, but not in sepsis. Statins have cholesterol-independent anti-inflammatory effects that are related to a decrease of isoprenoid proteins and oxidative stress. Therefore, we evaluated superoxide anion (O2- degree) production and ex vivo effects of vitamin E and simvastatin in sepsis. Fourteen healthy volunteers, 14 intensive care unit (ICU) nonseptic, and 14 ICU patients with sepsis were included in this prospective study. Plasma cholesterol, triglyceride, and vitamin E levels were determined by routine laboratory tests. Superoxide anion production was measured in the venous blood by chemiluminescence technique after phorbol myristate acetate stimulation. Effects of vitamin E and simvastatin on O2- degree production was investigated ex vivo. Luminescence was indexed to the leukocyte count. We also investigated the in vitro effect of simvastatin on translocation of NADPH oxidase p21 Rac2 subunit in THP-1 monocytic cell line. The ratio of vitamin E/cholesterol + triglycerides was significantly decreased in septic as compared with nonseptic patients and volunteers. The O2- degree production was significantly higher in the group of septic patients than in the others, regardless of the polymorphonuclear leukocyte count. Vitamin E and simvastatin induced ex vivo an inhibition of O2- degree production of 20% and 40% respectively. In vitro, simvastatin inhibited phorbol myristate acetate-induced- O2- degree production by monocytes through NADPH oxidase inactivation. We conclude that sepsis is associated with a significant decrease in vitamin E and an overproduction of O2- degree. Vitamin E and simvastatin lessen this phenomenon through NADPH oxidase inactivation.
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PMID:Superoxide anion overproduction in sepsis: effects of vitamin e and simvastatin. 1520 99

There are many risk factors contributing to retinopathy of prematurity (ROP). Some are still controversial, including the use of glucocorticoid and intraventricular hemorrhage. Hence, a retrospective study was performed to evaluate the association between the suspected risk factors and ROP in a medical center in southern Taiwan. One hundred fifty-nine infants with birth body weight < 1600 g admitted to our neonatal intensive care unit before the 29th day of life were enrolled into this study. Clinical data were analyzed by means of logistic regression. The prevalence of ROP in all infants (birthweight < 1600 g) is 36.48% (58 of 159) and 59.46% (22 of 37) in extremely low birthweight infants (birthweight < or = 1000 g). One infant with gestational age 32 weeks and birthweight 1420 g developed stage III ROP. Logistic regression revealed six factors to be significant variables. Birthweight < or = 1000 g, intraventricular hemorrhage, sepsis, and use of glucocorticoid or dopamine were risk factors associated with higher incidence of ROP. Supplementation of vitamin E was shown to relate to lower incidence of ROP. This study confirms several risk factors recognized in previous statistical analyses. Sepsis is the most significant factor contributing to ROP. Vitamin E was proven to be effective in prophylaxis of development of ROP. The possibility of development of ROP could not be excluded in infants with gestational age > 32 weeks.
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PMID:Risk factors of retinopathy of prematurity in premature infants weighing less than 1600 g. 1573 92

Mr. Richard Clarke presents in this Journal his arguments against continued application of hyperbaric oxygen (HBO2) therapy to the pre-extraction neoadjuvant treatment or the treatment of frank mandibular ORN. In the same article he advocates a promising renewed interest in HBO2 as a radiosensitizer. Arguments against HBO2 prior to extractions are based on several papers which consistently include low-risk patients. The just-released HOPON trial reports a negative pre-extraction outcome for HBO2, but patients were enrolled with radiation doses as low as 50Gy. For advanced mandibular necrosis (Marx Stage III) requiring resection, fibular free flap reconstruction is advocated. A high complication rate with free flaps is acknowledged but the magnitude of these complications is not discussed. A cost savings for this procedure is suggested, but no mention is made of the typical cost of the procedure ($90,000) or the requirement of a typical one-week hospital stay, including an initial one or two days in the ICU. Nor is mention made of the very low rate of subsequent dental rehabilitation. The success reported by Delainian, et al. employing pentoxifylline, Vitamin E and sometimes a bisphosphonate is equated to the four decades of HBO2 success with the Marx protocol for Stage I and II ORN. In the phase II trial by Delainian (not randomized) six of her 54 patients died secondary to sepsis, and she graded patients as complete responders if 5mm or less bone was exposed. Even at entry patients had an average of only 1.7 cm exposed bone and treatment was prolonged (16 + or -9 months). Any cost comparison studies will have to account for the indirect expenses of this prolonged treatment including lost productivity.
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PMID:Hyperbaric oxygen is still needed in the management and prevention of mandibular necrosis: a response to Mr. Richard Clarke. 3150 95