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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 5-year-old boy had a 10-month remission of acute lymphocytic leukemia (ALL) after chemotherapy. Re-induction chemotherapy was performed for relapse of ALL. Thereafter, he suffered from an episode of neutropenic fever with pneumonia. One week following control of the condition with antibiotics, a 1 x 1-cm, red, painful nodule appeared on the left thigh, which was initially suspected to be Pseudomonas infection. Parenteral ceftazidime and amikacin were administered, but persistent high fever, mild cough, and a few painful erythematous papulonodules on the face and lower extremities appeared several days later (Fig. 1). These lesions increased insidiously in diameter up to 2-5 cm with central necrosis. Hemogram showed neutropenia with a shift to the left [white blood cell (WBC) count, 2.1 x 10(9)/L; neutrophil count, 0.21 x 10(9)/L]. A skin biopsy showed heavy growth of hyaline branching septate hyphae in the deep dermis and subcutis, together with fat necrosis (Fig. 2). Invasion of molds into vessels and sweat glands was also seen. A culture from a lesion yielded Fusarium moniliforme, but no fungi were isolated from blood specimens. Only mild infiltrations on bilateral lower lung fields were detected by chest roentgenography. The skin lesions gradually healed and the fever subsided 2 weeks after the initiation of therapy with amphotericin B 30 mg and itraconazole 200 mg daily. Meanwhile, relapse of leukemia was detected by hemogram showing atypical leukocytosis (WBC count of 24,400 x 10(9)/L, with blast cells representing 78%). A course of chemotherapy with cytarabine, mitoxantrone, and VP-16 was prescribed, subsequently resulting in neutropenia (WBC count, < 0.1 x 10(9)/L; neutrophil count, 0/L) and spiking fever. Although the aforementioned antifungal therapy was continued, the centers of the originally healed lesions turned dusky red, swollen, necrotic, and ulcerative. There were more than 10 such ecthymiform lesions. After administration for 22 days, itraconazole was discontinued because of no appreciable effects. Granulocyte colony-stimulating factor (G-CSF) salvage was used, and the neutropenia gradually subsided 20 days later. In addition, the ecthymiform lesions gradually resolved. Amphotericin B was discontinued 1 week following neutrophil recovery. The patient died of Acinetobacter baumannii and Stenotrophomonas maltophilia sepsis 8 months later.
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PMID:Disseminated cutaneous Fusarium moniliforme infections in a leukemic child. 1747 77

Parenteral nutrition is a life-saving therapy in patients with intestinal failure. One of the major causes of morbidity and mortality in patients receiving long-term total parenteral nutrition (TPN) is liver disease. Early on, there is steatosis, which can evolve to steatohepatitis and eventually to cholestasis of varying severity. The etiology of parenteral nutrition related liver disease is multifactorial. Provision of excess calories in the TPN solution, along with lipids administered >1 g/kg are thought to increase the risk of parenteral nutrition related liver disease. Other factors such as nutrient deficiencies and nutrient toxicities may also play a role in the pathogenesis of liver disease, along with sepsis and the lack of enteral stimulation. Non-pharmacological management strategies for TPN-related liver disease include enteral stimulation, optimal TPN composition, and avoidance of excess carbohydrate and lipid calories. Pharmacological therapy with ursodeoxycholic acid and antibiotic therapy to reduce the risk of bacterial translocation and sepsis should be considered. Early referral for transplantation should be considered in patients with evidence of portal hypertension. This review focuses on the clinical aspects, pathogenesis, and management strategies of parenteral nutrition-related liver disease in adult patients.
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PMID:Parenteral nutrition related hepato-biliary disease in adults. 1762 78

The application of covered metallic stents in the treatment of benign strictures and perforations is still in the early stages, because their removal is difficult and may cause tissue proliferation. The therapeutic effect and the efficiency of a new method for the extraction of a removable metallic stent were examined in three patients treated for oesophageal perforation. Two of the three patients were dilated with a balloon catheter because of corrosive oesophageal stenosis, and the oesophagus was perforated. In one patient mediastinal drainage, and jejunostomy and in the other primary suturing and drainage were performed. Sepsis and mediastinitis developed due to the oesophageal perforation and the fistula caused by the mediastinal drain in the first patient, and the insufficiency of the suture in the second patient. The oesophageal defects were sealed on day 8 and 10 after the perforation, and surgery by a covered stent. In the third patient, the oesophageal rupture caused by the dilatation and the attempt to stent a malignant obstruction was sealed with a covered stent within 2 hours. Parenteral nutrition and broad-spectrum antibiotic therapy were started. Three days after the interventions, swallowing tests with water-soluble contrast medium (Gastrografin) did not reveal any extravasations. Feeding via a nasogastric tube, and later oral feeding was started. After transient mediastinal drainage, the stents were removed on day 35 and 74 after implantation. Both openings healed completely. Restenoses above the stents were dilated again. The rupture of the malignant oesophagus in the third patient, following early, permanent stenting, healed without drainage and with no complications. Even with mediastinitis and concomitant sepsis, large oesophageal perforations can be treated successfully with removable, covered metallic stents and adequate mediastinal drainage.
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PMID:[Treatment of large, esophageal perforations and mediastinitis with a covered, removable metallic endoprosthesis and mediastinal drainage]. 1770 89

This review presents the rationale for the therapeutic use of antioxidants in treating critically ill patients; it is not a systematic review of the clinical evidence that has been assessed recently by others. Clinical and nonclinical evidence is presented to support the notion that natural antioxidants are of therapeutic value in treating cardiovascular shock. Oxidative stress is a major promoter and mediator of the systemic inflammatory response. The microcirculation is particularly susceptible to oxidative stress that causes hemodynamic instability, leading to multiple organ failure due to systemic inflammatory response syndrome. Vitamin C is the antioxidant used experimentally to demonstrate oxidative stress as a key pathophysiologic factor in septic shock. Pharmacologic studies reveal that vitamin C (as ascorbate), at supraphysiologic doses, significantly affects the bioavailability of nitric oxide during acute inflammation, including inhibiting nitric oxide synthetase induction. Parenteral high-dose vitamin C inhibits endotoxin-induced endothelial dysfunction and vasohyporeactivity in humans and reverses sepsis-induced suppression of microcirculatory control in rodents. In severe burn injury, in both animals and patients, parenteral high-dose vitamin C significantly reduces resuscitation fluid volumes. Therefore, a significant body of pharmacologic evidence and sound preliminary clinical evidence supports the biological feasibility of using the exemplary antioxidant, vitamin C, in the treatment of the critically ill.
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PMID:Antioxidant therapy in critical care--is the microcirculation the primary target? 1771 12

Parenteral nutrition is life saving in patients with intestinal failure but liver dysfunction is commonly encountered, especially in neonates. Although abnormal liver function tests associated with short-term parenteral nutrition are usually benign and transient, liver dysfunction in both children and adults receiving long-term parenteral nutrition can progress to end-stage liver disease and liver failure. The aetiology of parenteral nutrition-associated liver disease is complex and multifactorial, with a range of patient, disease and nutrition-related factors implicated. Sepsis is of particular importance, as is the lack of enteral nutrition and overfeeding with intravenous glucose and/or lipid. Deficiencies of a number of amino acids including choline and taurine have also been implicated. Management of hepatic dysfunction in parenteral nutrition should initially focus on preventing its occurrence. Sepsis should be managed appropriately, enteral nutrition should be encouraged and maximised where possible and parenteral overfeeding should be avoided. Provision of parenteral lipid should be optimised to prevent the adverse effects of both deficiency and excess, and cyclical rather than continuous parenteral feeding should be administered. There is some evidence of benefit in neonates from oral antibiotics to prevent intestinal bacterial overgrowth and from oral ursodeoxycholic acid, but less to support their use in adults. Similarly, data to support widespread use of parenteral choline or taurine supplementation are lacking at present. Ultimately, severe parenteral nutrition-associated liver disease may necessitate referral for small intestine and/or liver transplantation.
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PMID:Managing liver dysfunction in parenteral nutrition. 1796 Dec 74

At the 2007 International Symposium on Intensive Care and Emergency Medicine (ISICEM) in Brussels, a roundtable conference on "Metabolic Support in Sepsis and Multiple Organ Failure" was held. The roundtable was endorsed by the European Society of Intensive Care Medicine, the Society of Critical Care Medicine, the European Society for Clinical Nutrition and Metabolism, and the American Society for Parenteral and Enteral Nutrition. Metabolic support in intensive care has become an exciting topic in recent years, with improved understanding of the effects of compromised mitochondrial function, studies demonstrating outcome benefits of tight glucose control, new insights into the mechanisms behind insulin resistance, recognition of glutamine and antioxidants as key nutrients, and emerging knowledge concerning the interactions between metabolism and endocrinology. Together, these aspects have generated an increased interest in the importance of metabolism in intensive care medicine, reflected in the programs and abstracts at international congresses of the past few years. This roundtable's participants each gave a presentation within their specific area of expertise, and each was followed by general discussion. Discussions became heated as new concepts and ideas were debated. New data will be discussed in this summary which reveals metabolic and nutrition interventions that could lead to major improvements in clinically relevant outcomes.
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PMID:Brussels 2007 roundtable on metabolism in sepsis and multiple organ failure. 1816 40

Parenteral nutrition support for burn injury in China began to develop in 1970s along with improvement in burn foundational research of burn injury and the marketing of parenteral nutrition solutions manufactured by Chinese amino acids pharmaceutical industry. Up to 1980s many kinds of parenteral nutrition products were used in clinical therapy, and they were proved to be effective and safe. Meanwhile the guide for parenteral nutrition support of China was drafted to ensure standardized administration. Some problems should be called for attention in present practice of parenteral nutrition support. First, immuno nutrients have been proved to possess synergistic effect on parenteral/enteral nutrition support. But for those critical patients in sepsis/MODS period, more attention should be paid to the use of immuno nutrients in time of administration and optimal dosage because of the complicate physiopathologic reactions. Secondly, the use of growth hormone has been proved to be effective for promoting healing in patients with burn in many cases. However, the indications of growth hormone should be strictly observed and the regime of a low dose and short course should be adopted 7 days after burn for ensuring safety. Thirdly, we should pay attention to the best path of giving nutrition, whether enteral or parenteral. Parenteral nutrition support should be adopted for critical burn patients in early period with intestinal dysfunction, and enteral nutrition support should be used when intestinal functions recover partially. For patients with burn hypermetabolism, the application of enteral and parenteral nutrition support is complimentary, and it is aptly called total nutrition.
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PMID:[Review and prospect of parenteral nutrition support for burn patients in China]. 1910 29

Circulating levels of vitamin C (ascorbate) are low in patients with sepsis. Parenteral administration of ascorbate raises plasma and tissue concentrations of the vitamin and may decrease morbidity. In animal models of sepsis, intravenous ascorbate injection increases survival and protects several microvascular functions, namely, capillary blood flow, microvascular permeability barrier, and arteriolar responsiveness to vasoconstrictors and vasodilators. The effects of parenteral ascorbate on microvascular function are both rapid and persistent. Ascorbate quickly accumulates in microvascular endothelial cells, scavenges reactive oxygen species, and acts through tetrahydrobiopterin to stimulate nitric oxide production by endothelial nitric oxide synthase. A major reason for the long duration of the improvement in microvascular function is that cells retain high levels of ascorbate, which alter redox-sensitive signaling pathways to diminish septic induction of NADPH oxidase and inducible nitric oxide synthase. These observations are consistent with the hypothesis that microvascular function in sepsis may be improved by parenteral administration of ascorbate as an adjuvant therapy.
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PMID:Mechanism of action of vitamin C in sepsis: ascorbate modulates redox signaling in endothelium. 1931 40

Assessment of the severity of acute pancreatitis (AP), together with the patient's nutritional status is crucial in the decision making process that determines the need for artificial nutrition. Both should be done on admission and at frequent intervals thereafter. The indication for nutritional support in AP is actual or anticipated inadequate oral intake for 5-7 days. This period may be shorter in those with pre-existing malnutrition. Substrate metabolism in severe AP is similar to that in severe sepsis or trauma. Parenteral amino acids, glucose and lipid infusion do not affect pancreatic secretion and function. If lipids are administered, serum triglycerides must be monitored regularly. The use of intravenous lipids as part of parenteral nutrition (PN) is safe and feasible when hypertriglyceridemia is avoided. PN is indicated only in those patients who are unable to tolerate targeted requirements by the enteral route. As rates of EN tolerance increase then volumes of PN should be decreased. When PN is administered, particular attention should be given to avoid overfeeding. When PN is indicated, a parenteral glutamine supplementation should be considered. In chronic pancreatitis PN may, on rare occasions, be indicated in patients with gastric outlet obstruction secondary to duodenal stenosis or those with complex fistulation, and in occasional malnourished patients prior to surgery.
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PMID:ESPEN Guidelines on Parenteral Nutrition: pancreas. 1946 71

Acute lung injury (ALI) and sepsis are the major causes of mortality in intensive care units. Lymphocytes apoptosis is a hallmark feature of late detrimental sepsis. Parenteral nutrition in critically ill patients is based on lipid emulsions, but the impact of ALI and lipid emulsions on lymphocytes has not been defined. The effects of intravenously infused conventional soybean oil (SO)-based and new olive oil (OO)-based emulsions on splenic and blood lymphocytes were investigated in a murine model of endotoxin-induced ALI. After LPS challenge and infusion of lipid emulsions, apoptosis of lymphocytes and lung injury were assessed by flow cytometry, Western blot, and histology. Induction of ALI led to a time-dependent decline in splenic and circulating lymphocyte numbers and an increase in apoptosis, with engagement of the extrinsic apoptotic pathway. Both SO- and OO-based emulsions promoted the apoptosis of splenic lymphocytes before induction of ALI. The OO-based emulsions exhibited lower proapoptotic activity than did SO-based emulsions, an observation paralleled by the induction of survival factors. Induction of ALI increased the mortality of mice receiving SO-based emulsions compared with OO-based emulsions and normal saline. Splenic lymphocyte apoptosis is apparent in murine ALI, which may be linked to detrimental outcome. Infusion of lipid emulsions per se provoked splenic lymphocyte apoptosis. Infusion of SO-based emulsions further augmented the apoptosis of splenic and circulating lymphocytes in ALI and led to increased mortality in mice. These findings may be of relevance for patients experiencing ALI that require parenteral nutrition.
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PMID:Induction of lymphocyte apoptosis in a murine model of acute lung injury--modulation by lipid emulsions. 1948 75


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