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

Sepsis is associated with profound catabolism and hypermetabolism that complicate provision of nutritional support. These metabolic changes are caused by inflammatory mediators involved in the septic process and cannot be reversed by nutritional means. High protein isocaloric nutritional regimens are recommended if possible, in association with aggressive measures to control the sepsis. However, nutritional therapy and its complications may also affect the incidence and course of sepsis. Hyperglycemia and conventional intravenous fat emulsions have been shown to increase susceptibility to infection. Enteral nutrition is associated with fewer infectious complications than parenteral nutrition, at least in severely injured patients. Recently nutritional formulations have been introduced that contain novel substrates that enhance various aspects of immunity. Several studies have suggested that this immunonutrition reduces infection risk in the critically ill, and preliminary findings suggest it may even have an effect on survival in sepsis.
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PMID:How to feed patients with sepsis. 1132 8

Because of several factors, including a change in the hormonal behavior, the postoperative period is at high risk for the diabetic patient to present a metabolic complication. On the other hand, a diabetic metabolic disorder may be secondary and reveal a severe underlying complication (sepsis...). Ketoacidosis is the consequence of an absolute or relative lack of insulin and occurs mainly in insulin dependent diabetic patients. Its incidence should be very low during the postoperative period since insulin protocols are systematically used. The main clinical and biological signs are a polypnea, signs of dehydration, an hyperglycemia associated with a high anion gap metabolic acidosis and the presence of ketoacids in the urine. Its treatment is mainly based on an active rehydration and an insulin and potassium supply. Sodium bicarbonate should not be used systematically any more, even during severe acidosis. Hyperosmolar non ketotic states affects insulin nondependent and older diabetic patients for the most part and occurs under similar conditions than ketoacidosis, revealing most of the time a severe underlying complication. Clinical and biological manifestations include a severe dehydration, alterations in consciousness and a major hyperglycemia associated to a moderate or mild metabolic acidosis. Its main treatment is an active rehydration and insulin plus potassium in a second time. Hypoglycemia is usually the consequence of a mistake in the diabetes care and in the insulin management. Every sickness or consciousness disorder occurring in a diabetic patient treated with insulin should lead to perform a blood glucose measurement. In case of severe manifestations, glucose should be administered in emergency, orally if the patient is conscious or intravenously if he is not. Lactic acidosis occurring during the postoperative period in a diabetic patient is usually non specific of diabetic disease and reflects the existence of an underlying complication (sepsis, hemorrhage, hypoxia,...), as it would in an non diabetic patient. Lactic acidosis due to a treatment with metformin is now very rare and occurs almost only in patients having a contraindication to the use of metformin.
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PMID:Acute postoperative metabolic complications of diabetes. 1137 21

Diabetes mellitus carries a great burden on healthcare costs due to its growing population and high co-morbidity. This adverse effect sustains even when patients develop end-stage renal disease (ESRD). We here present data showing the effect of diabetes on economic costs in dialysis therapy in Taiwan. As of the end of 1997, we have 22,027 ESRD patients with a prevalence and incidence rate of 1013 and 253 per million populations, respectively. Diabetic nephropathy is the second most common cause of the underlying renal diseases, but accounts for 24.8% of the prevalent patients and 35.9% of the incident cases. The diabetic patients engendered 11.8% more expense for care of dialysis than the non-diabetic patients (US $26,988 vs. US $24,146 per patient-year). Higher inpatient cost mainly account for the difference. As compared to non-diabetic patients, the diabetic patients had 3.5 times more inpatients costs (US $1325 vs. US $4677 per patient-year), and higher proportion of inpatient-to-annualized cost ratio (5.5 vs. 17.3%) resulting from their more frequent hospitalization (0.59 vs. 1.13 times per patient-year) and longer hospital stay (6.7 vs. 18.9 days per patient-year). The major causes responsible for a more frequent hospitalization were cardiovascular disease, poorly controlled hyperglycemia, sepsis and failure of vascular access. The annualized costs for care of dialysis patients in Taiwan, including inpatient and outpatient costs, averaged US $25,576 per patient-year. This value is approximately half of that in most of the western countries and Japan. Thus, a more cost-effective way to achieve savings is to reduce the high incidence rate of dialysis population and to maximize the quality of dialysis treatment for avoiding hospitalization. Recent studies had shown that tight blood pressure control, intensive glycemic control, and use of angiotensin converting enzyme inhibitors in diabetic patients significantly reduced not only the rate of progressive renal failure, but also substantially reduced the cost of complications and led to higher cost effectiveness. Once diabetic patients reach stage of ESRD, an optimized pre-ESRD care and consideration of kidney transplantation are essential in terms of better patient survival and cost savings.
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PMID:The impact of diabetes on economic costs in dialysis patients: experiences in Taiwan. 1158 Sep 69

Patients suffering severe burns have an accelerated catabolism with a highly negative nitrogen balance that may worsen their prognosis. Somatropin treatment has been shown to improve this balance in different hypercatabolic situations. Moreover, in children with extensive burns it also reduces the healing time of the skin graft donor site and shortens the hospital stay. In the existing literature there are no controlled prospective clinical trials in adult patients that confirm these data. Our aim was to demonstrate the efficacy of recombinant growth hormone (somatropin) in reducing the healing time of the skin graft donor sites and the length of stay in the burn unit in adult patients with severe burns. A randomized, double-blind, placebo-controlled clinical trial was carried out in 24 adult patients with severe burns (more than 40% of the total body surface burned or more than 15% full-thickness burns). Patients received placebo (n = 11) or somatropin (n = 13) at a dosage of 0.15 mg/kg/day divided into two equal doses (every 12 hours) via intramuscular injection. Treatment was initiated the day the first autograft was performed and terminated the day the patient was discharged from the burn unit. The mean number (+/- SD) of skin grafts per patient was similar between the two groups (4.2 +/- 1.8 vs 3.4 +/- 1.8 in the placebo and somatropin groups, respectively). No reduction in the healing time of the skin graft donor site was observed in the somatropin group compared to the placebo group. Likewise, the time admitted to the burn unit was not significantly different, either in the absolute number of days (36.2 +/- 19.7 vs 30.1 +/- 16.8 days in the placebo and somatropin groups, respectively) or in relation to the percentage of the total body surface burned or the body surface with full-thickness burns. Growth hormone and insulin-like growth factor I (IGF-I) levels were three and five times higher, respectively, in the somatropin group than in the placebo group. Ten of the patients treated with somatropin experienced hyperglycemia, and seven of them required insulin treatment. No other adverse side effect was observed. One patient in the placebo group died as a result of sepsis and multiple organ failure. Somatropin, with the treatment regimen and dosage used in these studies, did not reduce the healing time of the skin graft donor sites or the length of hospitalization in the burn unit in adult patients with severe burns.
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PMID:Effects of human recombinant growth hormone on donor-site healing in burned adults. 1189 25

The use of portable blood glucose meters (PBGM) has become common in veterinary medicine as a rapid means of monitoring animals' blood glucose in a variety of medical conditions. These hand-held monitors allow for diagnostic and therapeutic decisions to be made quickly and relatively inexpensively using only a small amount of blood. Both in conditions resulting in hyperglycemia, such as diabetes mellitus, and in those resulting in hypoglycemia, such as sepsis or the presence of an insulinoma, veterinarians have come to rely on PBGM to provide critical information on the status of their animal patients. In particular, PBGM are frequently used to measure individual blood glucose values in an animal over a period to create a blood glucose curve when evaluating the effectiveness of insulin therapy in diabetic dogs and cats.
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PMID:Portable blood glucose meters as a means of monitoring blood glucose concentrations in dogs and cats with diabetes mellitus. 1221 19

From April 1993 to January 2000, 105 patients in the burn intensive care unit (BICU) that developed septicaemia in the course of their treatment were studied retrospectively to investigate as to why only 36 septicaemic patients (34%) developed hypernatremia (serum sodium >150mmol/l). Septicaemic burn patients who developed hypernatremia were found to have a higher incidence of inhalation injury and a larger burn area (TBSA) signifying greater free water losses in the face of increasing fluid requirements. Patients who developed hypernatremia showed a characteristic pattern of septicaemia: early onset, multiple episodes, polymicrobial, need for multiple antibiotics, longer duration and a higher mortality, indicating a more severe degree of sepsis. The level of incapacitation either from the burn itself, mechanical ventilation or from impaired mental status leading to an inadequate free water intake was more in septicaemic patients who developed hypernatremia. Increased urinary free water losses and solute diuresis from hyperglycemia were significant factors in the development of hypernatremia. Patients who were treated with early wound excisions were less prone to develop hypernatremia when compared to those who did not undergo early wound excision. The close association between the onset of hypernatremia and the onset of septicaemia noted in this study suggests the use of hypernatremia as a marker for septicaemia in burn patients. Hypernatremia in a septicaemic burn patient is multi-factorial and a thorough understanding of the underlying factors will help prevent the onset and progress of hypernatremia.
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PMID:Only some septicaemic patients develop hypernatremia in the burn intensive care unit: why? 1222 Sep 11

Sepsis, excessive inflammation, multiple organ failure and weakness prolong the need for intensive care in critically ill patients. Furthermore, the risk of death is high in the prolonged critically ill patient (20% after two weeks and 30% after 3 weeks). In prolonged critical illness, protein hypercatabolism and relative preservation of adipose tissue with fatty infiltration of vital organ systems is present. In view of the crucial role of the hypothalamus-pituitary axis for metabolic homeostasis, we have studied this endocrine organ in the context of critical illness. The initial "adaptive" neuroendocrine response to critical illness illness consists primarily of activated anterior pituitary function. In the chronic phase of critical illness, a uniformly reduced pulsatile secretion of anterior pituitary hormones has been observed, whereby impaired function of target organs. A reduced availability of thyrotropin (TSH)-releasing hormone (TRH), gonadotropin (LH)-releasing hormone (GnRH), the endogenous ligand of the growth hormone (GH)-releasing peptide (GHRP) receptor (ghrelin) and, in very long-stay critically ill men also of GH-releasing hormone (GHRH), inferrentially appears involved. Pulsatile secretion of GH, TSH and LH can be re-amplified by relevant combinations of releasing factors which also substantially increases circulating levels of insulin-like growth factor (IGF)-I, GH-dependent IGF-binding proteins, thyroxine (T4), triiodothyronine (T3) and testosterone. Anabolism is only evoked when GH-secretagogues, TRH and GnRH are administered together whereas the effect of single hormone treatment is minor and accompanied by side effects. A remarkable observation was that a high serum concentration of IGF-binding protein 1 predicts death in the ICU. This observation challenged the classical dogma of adaptive hyperglycemia during critical illness. In a large prospective randomized clinical study (1548 patients), we showed that ICU mortality was reduced by 42% with strict normalization of glycemia using exogenous insulin infusion (N Engl J Med 2001). This was due to prevention of typical ICU complications such as sepsis, multiple organ failure and need for prolonged invasive organ support and intensive care. We conclude that the new concept of reduced stimulation of pituitary function in prolonged critically ill patients opens new therapeutic perspectives to reverse the paradoxical 'wasting syndrome' but that maintenance of strict normoglycemia with insulin is crucial to also increase the chances of survival of these patients.
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PMID:Endocrinology in intensive care medicine: new insights and therapeutic consequences. 1223 41

Intravenous busulfan (i.v. BU) has demonstrated safety when administered at 0.8 mg/kg per dose i.v. every 6 hours x 16 doses. We evaluated the safety and pharmacokinetics (PK) of giving the same total daily i.v. BU dose (3.2 mg/kg) either divided as a twice-daily infusion or as a single infusion to patients undergoing hematopoietic stem cell transplantation (HSCT). Twelve patients with hematologic malignant disease were treated; 7 patients had non-Hodgkin's lymphoma, 4 patients had acute myeloid leukemia, and 1 patient had chronic myelogenous leukemia. The first cohort (group A) received, on the basis of actual body weight, i.v. BU at 1.6 mg/kg per dose over 4 hours every 12 hours for 4 days (day -7 to day -4). The second cohort (group B) received 3.2 mg/kg per dose of i.v. BU (same total dose as group A) as a single infusion over 4 hours daily for 4 days. In both groups the i.v. BU was followed by cyclophosphamide 60 mg/kg daily for 2 days (day -3 and day -2). Blood specimens were collected on the first, fifth, and seventh doses for group A and on the first and fourth doses for group B to determine the disposition of i.v. BU. Peripheral blood stem cells (autologous in 7 cases and HLA-matched allogeneic in 5 cases) were given 2 days after completion of cyclophosphamide administration (day 0), and granulocyte colony-stimulating factor 5 microg/kg was started on the same day. GVHD prophylaxis consisted of tacrolimus plus methotrexate for recipients of allogeneic stem cells. One patient developed presumed fungal pneumonia and died of multisystem organ dysfunction on day +21 before hematologic reconstitution could be evaluated. Another was reported to have sudden death of undetermined cause at home on day 40. The remaining patients had engraftment (absolute neutrophil count >500/microL) at a median of 11 days and sustained platelet counts >20,000/microL at a median of 14 days. Significant regimen-related toxicity (grade III-IV) was limited to hepatic toxicity (2 cases) catheter infection (2 cases), epistaxis (3 cases), diarrhea (1 case), anorexia (1 case), mucositis (1 case), hyperglycemia (1 case), pneumonia (1 case), and sepsis (1). In group B there was 1 case of mild venoocclusive disease, which resolved without sequelae. No central nervous system or pulmonary toxicity was noted. Pharmacokinetic parameters, including clearance, half-life, maximum concentration, and area under the curve, demonstrated that the first dose profile was highly predictive of later dose PK profiles. No accumulation of the drug was noted. The change in dosing schedule did not increase toxicity or end-organ damage despite higher plasma concentration-times. Although further study for long-term efficacy is warranted, i.v. BU can be given safely with reproducible results on a twice-daily divided or single-daily dosing schedule to patients undergoing HSCT.
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PMID:Evaluation of safety and pharmacokinetics of administering intravenous busulfan in a twice-daily or daily schedule to patients with advanced hematologic malignant disease undergoing stem cell transplantation. 1237 50

Diabetic ketoacidosis (DKA) and pancreatic pseudocysts are rare complications following treatment of hematological malignancies with L-asparaginase (L-asp). Persistent hyperglycemia with recurrent DKA presenting as a long-term complication of L-asp-induced pancreatitis is even rarer. A 21-year-old man with pre-B-type acute lymphoblastic leukemia (ALL) developed pancreatic pseudocysts, DKA and persistent hyperglycemia after L-asp therapy. The patient was treated with oral hypoglycemic agents (OHA) for sugar control thereafter. Ten months later, another episode of DKA developed during relapsed ALL without having obvious precipitating factors. Insulin was then instituted for control of his blood sugar until death. The leukemic process may play some role in glucose homeostasis and may be considered as a precipitating factor for DKA. The patient finally died of disease progression of ALL and sepsis 2 years after the initial diagnosis of ALL.
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PMID:Diabetic ketoacidosis and persistent hyperglycemia as long-term complications of L-asparaginase-induced pancreatitis. 1243 31

The risk of mortality or significant morbidity is high among critically ill patients who are treated in the intensive care unit (ICU) for > 5 days. These patients are susceptible to sepsis, excessive inflammation, critical illness polyneuropathy, and multiple organ failure, the latter often being the cause of death. Most intensive care patients, even those who did not previously suffer from diabetes, are hyperglycemic, which is presumed to reflect an adaptive development of insulin resistance. In the K.U. Leuven study it was hypothesized that hyperglycemia is not a beneficial adaptation to severe illness but rather predisposes patients to many of the typical intensive care complications--prolonged intensive care dependence and death. The effects of intensive insulin therapy to maintain normoglycemia during critical illness were studied in a large group (N = 1548) of ventilated, surgical ICU patients. An algorithm was proposed for implementing this procedure. The randomly assigned intensive insulin therapy group received insulin infusion tailored to control blood glucose (BG) levels in the range 80-110 mg/dL, whereas the conventional treatment group received insulin only when glucose levels exceeded 200 mg/dL, and in that event were maintained in a target range of 180-200 mg/dL. Intensive insulin therapy induced a 43% reduction of intensive care mortality risk (P = 0.036 after correction for interim analyses) and a 34% reduction of hospital mortality (P = 0.005). A reduced risk of severe infections by 46% (P = 0.003) was associated with a 35% reduction in prolonged (> 10 d) requirement for antibiotic therapy (P < 0.001). In addition, excessive inflammation was prevented. Logistic regression analysis indicated that control of BG levels, rather than insulin administration itself, likely explains the observed clinical benefits. Use of insulin infusion to maintain normoglycemia using a titration algorithm, at least in populations similar to those in the Leuven study, improves outcome. Further data are needed to establish the applicability of this strategy to other patient groups, such as those in a medical ICU and in general hospital care.
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PMID:Insulin therapy for the critically ill patient. 1280 Apr 80


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