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

Mechanisms producing hypertriglyceridemia during bacterial sepsis have not been well defined. In this study lipid disposal mechanisms were assessed in 76 infected and 19 control male rhesus monkeys by the ability to dispose of triglycerides after: (1) oral lipid loading; (2) intravenous lipid loading; and (3) by lipolytic enzyme activity tests as measured by postheparin lipolytic activity (PHLA). Studies were performed both before and 48 hr after intravenous inoculation with either Salmonella typhimurium or Diplococcus pneumoniae when illness was uniformly severe and fasting serum triglyceride elevations were increased maximally. S. typhimurium-infected monkeys demonstrated significant fasting hypertriglyceridemia (p is less than 0.001), reduced clearance of orally and intravenously administered lipid and markedly reduced PHLA. During this gram-negative sepsis, mild lethargy, slight diarrhea, and a 2% mortality were observed. During D. pneumoniae sepsis, average fasting triglyceride concentrations were slightly, but not significantly elevated. While oral lipid clearance was impaired, intravenous lipid clearance was unimpaired, and PHLA was slightly reduced. Marked lethargy, agitation, and a 20% mortality were present during this gram-positive infection. Results of this study support the concept that an impairment of lipid disposal mechanisms, particularly during gram-negative sepsis with S. typhimurium, may significantly contribute to the observed hypertriglyceridemia.
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PMID:Defective lipid disposal mechanisms during bacterial infection in rhesus monkeys. 0 48

The prevalence, presentation, and outcome of bacteremia due to Shigella and other gram-negative bacteria were determined by review of records of 2,018 inpatients with shigellosis who had their blood cultured in a Bangladeshi hospital in 1976-1983. Shigella bacteremia occurred in 82 (4.1%) patients; other bacteremia occurred in 102 (5.1%) patients. Patients with shigella sepsis more frequently (P less than .02) manifested severe dehydration, abdominal tenderness or ileus, agitation or lethargy, and leukocytosis than did nonbacteremic controls; they developed more frequently (P less than .05) renal failure (26%), leukemoid reaction (22%), thrombocytopenia (20%), and hemolytic-uremic syndrome (6%). The prevalence of all bacteremia was highest in the first year of life. Protein-energy malnutrition was a strong risk factor for shigella sepsis (P less than .01). The fatality rate in shigella bacteremia (21%) was higher (P less than .005) than in nonbacteremic shigellosis (10%) but lower (P less than .001) than in other bacteremia (51%). At highest risk of death from shigella bacteremia (P less than .01) were patients less than one year old, non-breast-fed, malnourished, and afebrile.
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PMID:Shigella septicemia: prevalence, presentation, risk factors, and outcome. 404 31

Neurological abnormalities including agitation, confusion, disorientation, lethargy, and obtundation are early characteristic findings in patients with sepsis. The etiology of the changes in mental status that occur during severe infection is unknown. We investigated the effects of sepsis on intermediary metabolism and bioenergetics in the brain during normoxia and moderate hypoxia (8% inspired O2 concentration) in rats 36-42 hr following cecal ligation and perforation. The rats were anesthetized with halothane, and brains frozen using the funnel-freezing technique. Perchloric acid extracts of brains were analyzed with fluorometric enzymatic methods and 31P nuclear magnetic resonance spectroscopy. There was no impairment in bioenergetics or intermediary metabolism in septic brain, and sepsis did not compromise the ability of the brain to maintain high-energy phosphates during hypoxia. Hypoxia did cause the brain lactate-to-pyruvate ratio to increase equivalently in both septic and control rats from approximately 9:1 to 20:1 (P < 0.001). We conclude that the neurologic changes which are characteristic of sepsis are unlikely to be due to alterations in cellular energy stores or intermediately metabolism. In addition, there is no evidence that sepsis results in brain cellular hypoxia.
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PMID:Effect of sepsis on brain energy metabolism in normoxic and hypoxic rats. 837 32

Delirium is mental dysfunctions occurring as impaired attentional and memory systems with disturbances of consciousness, affectivity, psychomotor activity and sleep patterns. Numerous factors and underlying diseases may be responsible for these non-specific symptoms. Therefore, a thorough evaluation of preadmission history and current clinical status, supplemented by laboratory and extended technical diagnostic procedures, are always required. If delirium occurs in connection with emergency admission to hospital, an organic disease can most regularly be found. Due to its rapid time of onset and minor side-effects, the intravenous injection of 2.0 g gamma-hydroxybutyric acid is preferred for sedation of extremely agitated patients. Neuroleptic drugs are indicated in psychiatric patients. A central anticholinergic syndrome in the early postoperative period causative of the symptoms of delirium may respond to intravenous injection of physostigmine. Most of the time, however, these acute disturbances of brain function are best treated by correction of homeostatic imbalances, restoration of cardiovascular and respiratory stability and alleviation of pain. Postoperative delirium occurring two or more days later is frequently due to respiratory distress, followed by sepsis, alcohol withdrawal and many other causes including heart failure, exsiccosis and side-effects of drugs. In intensive care patients, delirium may be caused, for example, by withdrawal (alcohol, opioids, benzodiazepines), the onset of sepsis (often venous catheter related), side-effects of drugs, problems of communication, sleep deprivation and others. Treatment should focus on finding the right approach. Personal care should be intensified and include help from family members. Most problems arise from agitated, non-cooperative patients. Treatment with clonidine, gamma-hydroxybutyric acid or neuroleptic drugs like perazin and haloperidol may be required to reduce agitation and the activation of sympathetic influence.
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PMID:[Intensive care of delirium syndromes]. 1266 6

23% of all septic patients develop septic encephalopathy which is associated with an increased mortality rate. Symptoms such as agitation, confusion and disorientation ranging from stupor to coma often develop in early sepsis. Severe hypotension is significantly associated with the development of septic encephalopathy. Several other factors which may play a role are also discussed: effects of inflammatory mediators on the brain, inadequate cerebral perfusion pressure, blood-brain barrier derangements, disturbances of the cerebral microcirculation, cerebral ischemia e.g. due to hypocapnia,metabolic changes, altered amino acid levels, transmitter imbalances, liver insufficiency, multiple organ failure and infections of the CNS, respectively. Compared to patients with an isolated infection,patients in septic shock have increased levels of aromatic amino acids such as phenylalanine and tryptophan in the plasma and brain as well as decreased levels of branched chain amino acids. Patients who died had higher levels of aromatic amino acids than the survivors. The correlation between aromatic amino acids and the APACHE II score was significant. The tryptophan metabolite quinolinic acid which can be synthesized in activated macrophages could act as an excitatory transmitter on the N-methyl-D-aspartate (NMDA) -receptor. Observations from experimental models indicate that activated NMDA receptors activate the neuronal isoform of the NO-synthase and other calcium dependent enzymes. This releases free radicals which may damage the DNA and activate the nuclear enzyme Poly-ADP-ribose-synthetase (PARS), resulting in energy depletion and cell death. Sepsis is the main cause of metabolic encephalopathies in critically ill patients. The differential diagnoses include hepatic, renal,hypoxic-ischemic or cardiovascular encephalopathies as well as encephalopathies,metabolic disorders and organ dysfunctions of other origin. Therapeutic interventions are numerous,however, so far only investigated in few controlled studies. The primary therapeutic goal is to maintain an adequate perfusion pressure and to prevent hypoxia and hypocapnia. Although the infusion of branched chain amino acids is controversial, experimental investigations demonstrated improvements improvements in an animal model with septic encephalopathy. Further investigations with respect to glutamate receptor antagonists, new radical scavengers, NO- and PARS-inhibitors may show whether these substances are suitable for the prophylaxis or early therapy of septic encephalopathy.
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PMID:[Septic encephalopathy. Diagnosis und therapy]. 1275 14

The sepsis is a bacterial invasion of the organism producing many manifestations which are able to amplify themselves. In the United States of America there are 100,000 death per year and the incidence is among 300,000-500,000 cases. The major surgery in the elder (especially if it is in emergency) has a great percental of risk because the preoperative study isn't often complete. Fever, agitation, panting, bullation, abdominal splinting, enteroplegia, are signals of evolving inflammatory situation. Moreover there are disorders of biochemical values: leukocytosis, thrombocytopenia, increased levels of VES, PCR, amylase and biliribinaemia. The more common radiological examinations are the straight radiography of abdomen and horax, abdomen ultrasonography, CT or MRI. In the last years pro-calcitonin, interleukin-6 , C-reactive protein, and nitric oxide from endothelial and muscularis cells have been evaluated as prognostic factors in the septic shock.
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PMID:[Septic shock: surgical and medical problems in the elderly]. 1467 79

Any hospice professional can identify the syndrome known as terminal restlessness, and all would agree that it is extremely distressing to patients as well as their families and caregivers. Often, caregivers cannot ameliorate the anguish many patients experience at life's end. Many clinicians assert that the causes are physical resulting from medication toxicity, organ shutdown and the associated metabolic changes, pain, urinary or fecal retention, dyspnea and related hypoxia, and sepsis. Yet, many also credit psychosocial and spiritual distress as precipitating factors. The purposes of this study were twofold: to compare the perceptions of practicing hospice clinicians with the literature related to terminal restlessness, and to determine if their experience with terminal restlessness agreed with the components of the one established scale for terminal restlessness found in the literature. In general, the study findings corresponded to the literature in regards to frequency, definition, causes, and behavioral manifestations of terminal restlessness. The clinicians in the study supported the impact of psychosocial and spiritual causes of terminal restlessness and defined the phenomenon in terms of time period; emotional, physical, and spiritual distress; changes in consciousness; and increased activity. However, the study did not support the inclusion of impaired consciousness and withdrawal as comprised in the terminal restlessness scale.
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PMID:Terminal restlessness as perceived by hospice professionals. 1608 13

Alcohol abuse and dependence, referred to as alcohol-use disorders (AUDs), affect 76.3 million people worldwide and account for 1.8 million deaths per year. AUDs affect 18.3 million Americans (7.3% of the population), and up to 40% of hospitalized patients have AUDs. This review discusses the development and progression of critical illness in patients with AUDs. In contrast to acute intoxication, AUDs have been linked to increased severity of illness in a number of studies. In particular, surgical patients with AUDs experience higher rates of postoperative hemorrhage, cardiac complications, sepsis, and need for repeat surgery. Outcomes from trauma are worse for patients with chronic alcohol abuse, whereas burn patients who are acutely intoxicated may not have worse outcomes. AUDs are linked to not only a higher likelihood of community-acquired pneumonia and sepsis but also a higher severity of illness and higher rates of nosocomial pneumonia and sepsis. The management of sedation in patients with AUDs may be particularly challenging because of the increased need for sedatives and opioids and the difficulty in diagnosing withdrawal syndrome. The health-care provider also must be watchful for the development of dangerous agitation and violence, as these problems are not uncommonly seen in hospital ICUs. Despite studies showing that up to 40% of hospitalized patients have AUDs, relatively few guidelines exist on the specific management of the critically ill patient with AUDs. AUDs are underdiagnosed, and a first step to improving patient outcomes may lie in systematically and accurately identifying AUDs.
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PMID:Alcohol-use disorders in the critically ill patient. 2092 4

Meningococcal infections may develop as episodic or endemic cases particularly among children attending day-care centers, boarding schools or among military personnel. Bivalent (A/C) meningococcal vaccine is applied to all new military stuff since 1993 in Turkey. In this report two cases of meningococcemia and meningitis, developed in two soldiers vaccinated with meningococcal vaccine, were presented. The first case was a 21 years old male patient who was admitted to the emergency service with the complaints of high fever, headache, fatigue and vomiting. He was conscious, cooperative and oriented with normal neurological findings. Maculopapular exanthems were detected at the lower extremities. The patient was hospitalized with the initial diagnosis of sepsis or meningococcemia and empirical treatment was initiated with ceftriaxone and dexamethasone. Cerebrospinal fluid (CSF) examination yielded 10 cells/mm3 (lymphocytes) with normal CSF biochemical parameters. A few hours later skin rashes spread over the body rapidly, the symptoms got worse, confusion, disorientation and disorientation developed, and the patient died due to cardiac and respiratory arrest at the seventh hour of his admission. The second case was also a 21 years old male patient who was admitted to the hospital with the complaints of fever, headache, painful urination, confusion and agitation. He was initially diagnosed as acute bacterial meningitis due to clinical (stiff neck, positive Kernig and Brudzinsky signs) and CSF (8000 cells/mm3; 80% polymorphonuclear leukocytes, increased protein and decreased glucose levels) findings. Empirical antibiotic therapy with ceftriaxone was initiated and continued for 14 days. The patient was discharged with complete cure and no complication was detected in his follow-up visit after two months. The first case had an history of vaccination with bivalent (A/C) meningococcal vaccine three months ago and the second case had been vaccinated one month ago. The bacteria isolated from the blood culture of the first case and the CFS culture of the second case, were identified as Neisseria meningitidis by conventional and API NH system (BioMerieux, France). The isolates were serogrouped as W135 by slide agglutination method (Difco, USA), and both were found to be susceptible to penicillin and ceftriaxone. As far as the last decade's literature and these two cases were considered, it might be concluded that N.meningitidis W135 strains which were not included in the current bivalent meningococcal vaccine, gained endemic potential in Turkey. Since N.meningitidis W135 strains may lead to serious diseases, vaccination of the risk population with the conjugate tetravalent meningococcal vaccine (A/C/Y/W135) should be taken into consideration in Turkey.
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PMID:[Meningococcemia and meningitis due to Neisseria meningitidis W135 developed in two cases vaccinated with bivalent (A/C) meningococcal vaccine]. 2106 98

A 43-year-old white woman presented to the emergency department with confusion, agitation, and progressive dyspnea. Chest x-ray revealed pulmonary edema. Initial diagnostic considerations were pneumonia, pulmonary embolism, sepsis, central nervous system infection, substance toxicity, and heart failure. Her salicylate level was 92.6 mg/dL, and an arterial blood gas revealed a respiratory alkalosis and nonanion gap metabolic acidosis, consistent with salicylate poisoning. Noncardiogenic pulmonary edema is an atypical presentation of salicylate toxicity, and this case highlights the importance of an early toxicology screen to make a time-critical diagnosis and provide specific treatment.
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PMID:Salicylate-induced pulmonary edema--a near-miss diagnosis. 2436 Nov 38


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