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

Eighteen of the 71 cases of plague reported in New Mexico from 1980 to 1984 were septicemic. We reviewed these cases to better describe the clinical presentation of this disorder and to identify risk factors for developing septicemic plague. The symptoms (fever, chills, malaise, headache, and gastrointestinal symptoms) and signs (tachycardia, tachypnea, and hypotension) of septicemic plague are similar to those of other forms of gram-negative septicemia. Abdominal pain was reported in nearly half of the cases, and differential white blood cell counts revealed a marked shift to the left. The risk of developing septicemic plague was higher for persons greater than 40 years of age. Because of empirical antibiotic treatment of older persons, deaths from septicemic plague occurred primarily among persons less than 30 years old. Deaths from septicemic plague could be reduced by aggressive antibiotic therapy for patients with a clinical presentation suggesting gram-negative septicemia, especially patients less than 30 years old.
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PMID:Septicemic plague in New Mexico. 379 95

Gelatine capsules containing Escherichia coli and Bacteroides fragilis in a standardized mixture with rat colonic content and barium sulfate were implanted intraabdominally into rats. Capsules of 0.75 g gave approximately 50% mortality whereas 0.35 and 1.10 g caused no or 100% mortality, respectively. In subsequent experiments, using the 0.75 g capsule, all animals became ill with signs of tachypnea, piloerection, low physical activity and hypersecretion of saliva 6-8 h after the implantation. The animals reduced their water and food intake substantially and the body weight decreased. A significant reduction in blood pressure, glucose and leukocyte and platelet counts was found 12 h after challenge. Blood cultures obtained at 12, 24, 48 and 60 h all grew E. coli but none B. fragilis. Succumbed animals revealed diffuse peritonitis with growth of E. coli and B. fragilis at autopsy, whereas surviving animals showed abscess formation at investigation on day 8 after challenge. It was concluded that the model closely resembled intraabdominal abscess formation with sepsis in man.
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PMID:Standardized intraabdominal abscess formation with generalized sepsis: pathophysiology in the rat. 388 37

Bacterial infections are frequent events in premature and newborn infants. The reason is a defective specific and nonspecific defence of bacterial organisms. Some immunoglobulins like IgM and IgA including secretory IgA are absent. Premature infants also show a decreased level of IgG. Cellular immunity is anatomically intact but functionally defective. A number of complement factors are lacking, the activation of the alternative pathway is impaired. Newborn infants with perinatal problems like asphyxia or difficult delivery, show defects of leucocyte function like decreased deformability, defective chemotaxis and defective killing of ingested bacteria. Certain diseases, like hypoxia and malformations of immature organ functions in this age group (decreased acid production in the stomach), facilitate bacterial colonization of surface epithelia and the invasion of tissues. Consequences of these pathogenetic mechanisms are an unimpaired propagation of bacterial organisms into the blood and meninges without localization of the infecting organisms at the entry site. Bacterial meningitis is not considered a separate disease entity but a complication of bacteremia and sepsis. Clinical symptoms are nonspecific at the onset of the infection. Fever is frequently absent; decreased appetite, vomiting, a bloated abdomen, diarrhea, tachycardia, tachypnea are early signs of a bacterial infection, a grey mottled appearance, cyanosis, jaundice, petechiae, apneic spells, seizure activity and a metabolic acidosis are symptoms of advanced infection. Successful treatment at this stage is often not possible. Every sign of a decreased well being of a newborn of premature infant warrants laboratory and bacteriologic work up for septicemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Chemotherapy of severe bacterial infections in pediatrics]. 631 69

For women who are prescreened to be at low risk, the birthing room located in a hospital can provide a home-like environment as well as proximity to the regular obstetrical unit in case of an unforeseen complication. Charts of 356 pairs of infants and mothers who were admitted to birthing rooms at three different hospitals were reviewed. The average age of the mother was 25.9 years. Approximately 20 percent of the women had complications requiring their transfer from the birthing room. Fifteen required a cesarean section. The mean Apgar scores of infants born to all women admitted to the birthing room (including those who were subsequently transferred) were 7.7 at one minute and 8.8 at five minutes. Neonatal complications included meconium aspiration (1), sepsis (1), a question of sepsis (1), congenital heart disease (1), and transient tachypnea of the newborn (1). Four infants and one mother required readmission. Although mothers were prescreened to be at low risk, complications did arise for both mother and infant that made proximity to the regular obstetrical and neonatal units advantageous.
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PMID:Outcomes of three birthing rooms. 684 49

The adult respiratory distress syndrome (ARDS) frequently occurs after sepsis and major trauma. Since both sepsis and trauma may cause activation of the complement system, we have infused rabbits with complement-activated plasma (AP) and have studied the effects on leukocyte counts, respiratory rate, PaO2, and lung morphology. Sustained AP infusion caused: (1) early granulocytopenia, (2) progressive hypoxemia and tachypnea, and (3) pulmonary vascular plugging by aggregates of degenerating granulocytes with interstital edema and endothelial injury. These changes were not observed in control animals infused with unactivated plasma or in animals rendered leukopenic with nitrogen mustard. Complement activation in patients with sepsis and trauma may be an etiologic factor in the development of ARDS.
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PMID:Production of acute pulmonary injury by leukocytes and activated complement. 738 23

A major determinant of survival in patients with advanced viral or bacterial infection, or following severe trauma or burns complicated by multiple organ failure, is the combination of clinical signs termed the systemic inflammatory response syndrome (SIRS). SIRS is characterized by hypotension, tachypnea, hypo- or hyperthermia and leukocytosis as well as other clinical signs and symptoms, including a depression in myocardial contractile function. Heart failure complicating systemic sepsis or other causes of SIRS is usually not accompanied by coronary artery ischemia due to hypotension, myocardial necrosis, or marked cardiac interstitial inflammatory infiltrates, and thus the cause of cardiac contractile dysfunction in this syndrome has remained unclear. However, recent evidence has implicated an endogenous nitric oxide (NO) signalling pathway within cardiac myocytes and other cellular constituents of cardiac muscle, including the microvascular endothelium, as a possible contributor to the pathogenesis of heart failure in this syndrome. Cardiac myocytes are now known to express both constitutive NO synthase (cNOS) and inducible NO synthase (iNOS) activities. Activation of cNOS appears to modulate cardiac myocyte responsiveness to muscarinic cholinergic and beta-adrenergic receptor stimulation. Induction of iNOS by soluble inflammatory mediators, including cytokines, causes a marked depression in myocyte contractile responsiveness to beta-adrenergic agonists. Thus, inappropriate activation of cNOS or excessive or prolonged induction of iNOS in the myocardium may contribute to cardiac dysfunction complicating SIRS.
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PMID:Myocardial contractile dysfunction in the systemic inflammatory response syndrome: role of a cytokine-inducible nitric oxide synthase in cardiac myocytes. 753 82

During January 1989-September 1991, in India, neonatologists prescribed assisted ventilation (intermittent positive pressure ventilation [IPPV] and continuous positive airway pressure [CPAP]) for 90 neonates born and treated at a tertiary hospital in Delhi. All neonates requiring more than 168 hours of ventilation received IPPV. The smallest surviving neonate weighed 830 g at birth and was born at 26 weeks' gestation. This neonate received 510 hours of ventilation. One neonate received 48 days of ventilation (gestational age at birth, 28 weeks; birth weight, 800 g). This neonate eventually died due to necrotizing enterocolitis (NEC), bronchopulmonary dysplasia (BPD), and sepsis. This infant was the only infant to develop NEC. A total of two newborns developed BPD. One infant developed retinopathy of prematurity (ROP). Indications for ventilation were hyaline membrane disease (HMD) (45/90), apnea (13/90), and transient tachypnea of the newborn (TTNB) (11/90). Almost all HMD cases who weighed more than 1.5 kg at birth on CPAP survived. CPAP successfully treated all TTNB cases. Nine neonates developed pneumothorax. Three of them survived. 34 neonates developed sepsis, the most common complication. 20 sepsis cases also had underlying pneumonia. Sepsis was responsible for 35% of deaths (14/40). Five infants on IPPV developed persistent pulmonary hypertension (persistent fetal circulation). 35 infants developed infection during ventilation, 34 of whom had a nosocomial infection. The nosocomial infection rate was 37.7%. Nosocomial infection was responsible for 35% of deaths. 12 babies (13%) developed pulmonary air leaks, 50% of whom died. 25 of the 33 infants on CPAP survived. Few CPAP cases developed pulmonary air leak, BPD, and ROP. Six of 22 very low birth weight (VLBW) infants (1 kg) survived. These findings led the researchers to recommend that medical centers with basic facilities for level II care should provide neonatal ventilation. They proposed that ventilation may not be cost effective for VLBW newborns, however.
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PMID:Three-year experience with neonatal ventilation from a tertiary care hospital in Delhi. 788 27

Current knowledge about the pathophysiology of septic shock is reviewed, and biotechnology-based therapies under development are discussed. Patients with septic shock begin their clinical course with leukocytosis, fever, tachycardia, tachypnea, and organ hypoperfusion; shock ensues as immunologic and vasoactive mediators produce hypotension. There are many metabolic and cardiovascular responses, and single- or multiple-organ failure is common. Patients may experience adult respiratory distress syndrome. A multitude of endogenous and exogenous factors have been linked to the pathophysiology of sepsis and septic shock, including (1) endotoxin from gram-negative bacteria, (2) peptidoglycan and exotoxins from gram-negative bacteria, (3) endotoxin-binding proteins and receptors, (4) bactericidal proteases, (5) exotoxins from gram-positive bacteria, (6) acute-phase proteins and proteases, (7) cytokines, (8) arachidonic acid metabolites, (9) complement, (10) beta-endorphin, (11) histamine, (12) stimulation of intrinsic and extrinsic coagulation pathways and proteases, and (13) endothelium-derived factors and adhesion molecules. Molecular entities and strategies under development to combat septic shock include monoclonal antibodies to endotoxin, active immunization with lipid-A analogues, bactericidal permeability-increasing protein, interleukin inhibitors, and inhibitors of tumor necrosis factor-alpha. Successful treatment of septic shock will probably require a combination of agents, including antimicrobials. An ideal goal for biotechnology in the area of septic shock is to prevent invading pathogens from overstimulating the host's immune system and to systematically eliminate those pathogens. Biotechnology is opening new avenues to the treatment of septic shock.
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PMID:Pathophysiology of septic shock and implications for therapy. 816 70

Fifteen patients with right-sided infective endocarditis during a 5 year period (1985-1990) were retrospectively reviewed. Isolated tricuspid valve involvement occurred in nine patients. Staphylococcus aureus was the causative organism in seven cases; four were culture negative. The diagnosis was established by two-dimensional echocardiography in 11 patients and at postmortem in the remaining four patients who succumbed shortly after admission. Fever, tachypnoea and pneumonia were universal features. A successful outcome ensued in eight patients with medical therapy alone and in two patients who were submitted to valve replacement. Five patients died, two from uncontrolled infection with repeated pulmonary emboli. Right-sided infective endocarditis should be suspected in any pneumonic illness that complicates post-abortal infection or other inadequately treated sepsis. Two-dimensional echocardiography is important in diagnosis since cardiac signs are minimal at presentation.
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PMID:Right-sided endocarditis in the non-drug addict. 823 4

Adult respiratory distress syndrome (ARDS) is a rare but important complication of blood transfusion because it has a mortality rate of 50-60%. ARDS is characterised by noncardiogenic pulmonary oedema and is often associated with major trauma and/or sepsis. Clinical features include dyspnoea, tachypnoea, chills and extensive crepitations. The pathogenesis has not been elucidated completely and a number of hypotheses have been proposed. Factors which have been implicated include neutrophil sequestration and complement activation, macrophages, metabolites of the arachidonic acid cascade and cytokines, all of which contribute to the amplification of the inflammatory process. In particular, leucoagglutinins have been implicated with blood transfusions. Treatment is generally supportive as specific therapeutic strategies remain largely unproven.
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PMID:Blood transfusion related adult respiratory distress syndrome. 844 6


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