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

Sepsis and non-septic shock in pregnancy show characteristic modifications which are caused a) by physiologic changes in hemostasis primarily in the third trimester of pregnancy, b) by etiologic distinctions of shock regarded as pregnancy-specific, c) by hemodynamic changes in the circulation during pregnancy, d) by the ability of the healthy, young organism to compensate adequately. In the dead fetus syndrome and in non-septic shock, i.e., in amnionic fluid embolism and in abruptio placentae, the clinical picture is often governed by marked secundary fibrinolysis. Retroplacental hematoma, the characteristic feature of premature placental separation, remains controversial as either the cause or sequela of the hemostatic disorder. Etiologic, pathogenetic, and morphologic similarities exist between septic abortion, chorioamnionitis, and puerperal sepsis, but the varying response of the maternal organism during the course of pregnancy leads to different clinical and morphologic pictures. Due to a decrease in fibrinolytic activity as a consequence of pregnancy, the hypercoagulability state in a septic endotoxic shock predisposes the kidneys to bilateral renal cortical necrosis, principally in the amnion infection syndrome.
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PMID:Shock in pregnancy: pathophysiology and morphologic findings. 39 33

Two groups of patients in whom endotoxemia was suspected were studied with respect to the laboratory data, clinical picture and autopsy findings. The first group showed the signs of gram-negative septicemia (age range 3 to 54 years with burns of 25 to 80% TBSA) and the second group (age range 20 to 76 years with burns not greater than 20% TBSA) showed an unexpected deterioration of the patient's condition. In 15 patients we established the diagnosis of endotoxemia on positive Limulus test as well as on other laboratory examinations and on the clinical signs. Five different forms of endotoxemia were distinguished varying in the evoking circumstance, clinical manifestation and pathological findings at autopsy: (1) the so called laboratory form--all survived; (2) the pulmonary form displaying the most brief and fulminant course--all died; (3) the form of disseminated intravascular coagulopathy; (4) the form of endotoxic shock due to administration of antibiotics; (5) the form of endotoxic shock as terminal stage of protracted gram-negative septicemia--the fatal outcome was inevitable in all cases. The authors stress the importance of minding and preventing all circumstances that might provoke the endotoxic (septic) shock.
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PMID:Clinical forms of endotoxemia in burns. 45 81

Shunting of radionuclide labeled 9 micron diameter microspheres by the systemic circulation, and 6 body regions was measured in two dog shock models: endotoxic shock (1 mg/kg E. Coli endotoxin intravenously) and sepsis and septic shock (5 days after cecal ligation). Mean systemic arterial blood pressure was significantly lower than control in both the endotoxic and septic shock groups. Mean systemic shunting was 7.7% in the control group and 7.3% and 4.3% respectively in the endotoxic and septic shock groups. Regional shunting of the head, heart, and skeletal muscle were not significantly different in the three groups. However, mean shunting in the splanchnic circulation was 36.5% in the septic shock group as compared to 18.6% in the control group (p less than 0.05). Mean kidney shunting in the endotoxic group was 15.1% compared to 4% in the control group (p less than 0.05). During resuscitation with crystalloid, mannitol, blood, and cortiocosteroids mean aterial blood pressure and cardiac index increased but systemic arterial-venous shunting was 3.8 and 4.3% in endotoxic and septic shock respectively. These data show that systemic anatomic arterial-venous shunting is small and not different from control in both dog shock models, and regional arterial-venous shunting is increased only in the splanchnic circulation in the septic model and in the kidney in the endotoxin model.
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PMID:Anatomic arterial-venous shunting in endotoxic and septic shock in dogs. 88 61

4 maternal deaths from abortion that took place during the 6-year period from March 1968 to February 1974 in the University Hospital, Kuala Lumpur are reviewed with focus on the avoidable causes and preventive aspects. The total maternal deaths from all causes for the 1699 admission was 13. The mortality rate from abortion during this period was 0.241/1000 pregnancies. The number of abortion cases admitted into the hospital during the 6-year period increased steadily. Of the 4 abortion deaths, 3 patients admitted to attempts at inducing abortion. 1 patient denied having induced abortion, although her husband felt that it could have occurred. All 4 cases of abortion deaths occurred in patients with septic abortions and were, theoretically, avoidable deaths. It is most important to prevent sepsis in a case of abortion. Patients with endotoxic shock are often given intravenous steroids in pharmacological doses every 4-6 hours.
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PMID:Maternal mortality from septic abortions in University Hospital, Kuala Lumpur from March 1968 to February 1974. 120 33

Platelet activating factor (PAF) is considered a key mediator in eliciting the immunologic and metabolic consequences of endotoxic shock and sepsis. Release of oxygen-derived radicals is one of the important and relevant actions of PAF. This study examines the direct and priming effects of PAF on superoxide anion release by perfused liver, isolated Kupffer cells and blood neutrophils. One hour after PAF infusion at a dose of 2.2 micrograms/kg body weight a significant amount of superoxide release (0.71 +/- 0.1 nmol/min/g liver) was measured in the perfused liver compared with the control livers (0.2 +/- 0.01). In the in vitro presence of either phorbol ester or opsonized zymosan, superoxide release following PAF treatment in vivo was significantly increased to 1.36 +/- 0.2 and 4.29 +/- 0.36, respectively. The administration of PAF receptor antagonist (SDZ 63-441) almost completely inhibited the release of this radical. Kupffer cells (KC1, KC2, KC3) and blood neutrophils isolated from PAF-treated rats were also primed for increased production when these cells were challenged in vitro by the activator of protein kinase C, opsonin-coated zymosan as well as the chemotactic factors, complement 5a and F-met-leu-phe. PAF added in vitro to the perfused livers, isolated Kupffer cells or neutrophils from normal animals stimulated the release of superoxide with or without the above agonists. The direct stimulatory effect of PAF on superoxide release was inhibited by the PAF receptor antagonist in vitro. The role of PAF in the LPS-induced superoxide release by the perfused liver was also examined by the administration of PAF antagonist in endotoxic rats. The antagonist inhibited the LPS-mediated superoxide release at 1 hr, but not at 3 hr post-treatment. These results indicate that PAF stimulates and primes the hepatic elements to release superoxide. PAF may be an important factor during the early phase of endotoxemia, while other bioactive substances may take over at a later phase. Therefore, PAF is a key mediator that can directly enhance the release of toxic oxygen-derived radicals which may contribute to organ failure during endotoxemia or sepsis.
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PMID:Platelet activating factor stimulates and primes the liver, Kupffer cells and neutrophils to release superoxide anion. 133 36

Tumor necrosis factor alpha (TNF) has been described as a primary mediator of the pathophysiology associated with bacterial sepsis/endotoxemia. We tested the efficacy and possible mechanisms of protection of a monoclonal antibody against TNF (TNF Mab) in a low mortality (29%), endotoxemic baboon model. A number of parameters were monitored at days 0, 1, 2 and 5-7 after challenge with 2 mg E. coli endotoxin/kg. TNF Mab pretreatment (15 mg/kg) prevented the increase in detectable serum TNF and the early perturbations in cardiovascular function which occurred in the control group. Early metabolic dysfunction was delayed in the TNF MAb group and was attenuated thereafter. Dysfunction of the kidney, liver, and coagulation systems and the increased IL-6 levels were significantly attenuated in the TNF MAb group; neutrophil activation was not affected by TNF MAb. No deaths occurred in the TNF MAb group. These results support the hypothesis that TNF plays a central role in the pathophysiology of endotoxic shock.
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PMID:Efficacy of monoclonal antibody against tumor necrosis factor alpha in an endotoxemic baboon model. 142 24

Systemic bacterial infections continue to be a main cause of death in newborns at neonatal intensive care units (NICU), worldwide. Bacteria causing neonatal septicemia are mainly the gram-negative, which possess endotoxin and are responsible for endotoxic shock. However, gram-positive bacteria are also able to induce septic shock, especially in immunocompromised hosts, like the newborns. Diagnosis and treatment of neonatal septic shock are quite difficult. Furthermore, there is not sufficient knowledge about its real frequency in Latin-american countries. The hyperdynamic phase of septic shock in newborns can be short and the hypodynamic phase is rapidly established, which increases the mortality. Since few years ago, some important aspects of physiopathology in septic shock have been studied and, at the same time that our knowledge about immunologic soluble mediators is increasing, new therapeutic modalities have been discovered. Such is the case of the therapeutic potentialities of cytokines, receptor antagonists and monoclonal antibodies, which is very encouraging at the present time.
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PMID:[Septic shock in newborn infants]. 146 77

Lipopolysaccharide (LPS) causes the syndrome of septic shock by initiating the release of endogenous mediators such as tumor necrosis factor (TNF) and interleukin-1 (IL-1) from macrophages. Hypotension is one of the important clinical features of septic shock; however, TNF is only hypotensive in high doses. Therefore we have investigated the interactions of low, nonhypotensive doses of LPS, IL-1, and TNF in the restrained unanesthetized rabbit. Combinations of nonhypotensive doses of TNF, IL-1, and LPS produced significant (p less than 0.05) decreases in blood pressure as compared with doses of each of the substances alone. TNF bioactivity in animals that were made hypotensive with combinations of TNF, IL-1, and LPS was lower than in animals that were made hypotensive with TNF alone. This suggests that TNF release that is stimulated by LPS is not the sole cause of the hypotension that is seen in this model of endotoxic shock. In this model, interactions of LPS, IL-1, and TNF occur and may explain hypotension during some episodes of sepsis.
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PMID:Lipopolysaccharide, tumor necrosis factor, and interleukin-1 interact to cause hypotension. 150 Aug 14

Gram-negative sepsis septic shock continues to produce significant mortality and therefore remains a major medical problem. Vasodilators have been studied in the treatment of circulatory shock. However, the effectiveness of calcium channel blockers in the treatment of newborn endotoxic shock has not been well documented. In the present study, diltiazem, a calcium channel blocker, and nitroprusside, a vasodilator, were used for the treatment of endotoxic shock in 10-day-old rats. Mortality rate, hemodynamics, and glucose metabolism were monitored. Diltiazem at a dose of 0.3 mg/kg attenuated the hypotension, bradycardia, hypoglycemia, and lactacidemia in newborn endotoxic shock. Diltiazem treatment resulted in reduced 24-hour mortality. However, 0.6 mg/kg diltiazem enhanced the hypotension, bradycardia, and lactacidemia in endotoxic shock. Nitroprusside blunted the hypoglycemia and decreased the mortality rate among rats with endotoxic shock. Afterload reduction may be responsible for the beneficial effects of 0.3 mg/kg diltiazem and nitroprusside. Diltiazem at a dose of 0.3 mg/kg reduced the lactacidemia of endotoxic shock more than nitroprusside. Therefore the effects of diltiazem may be due not only to afterload reduction but also to inhibition of cellular calcium influx. We conclude that 0.3 mg/kg diltiazem and 1.0 mg/kg nitroprusside are beneficial for the treatment of endotoxic shock in newborn rats.
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PMID:Diltiazem treatment of endotoxic shock in suckling rats. 151 92

There is increasing experimental and clinical evidence that a number of cytokines play a major role in the response to injury and infection and in the development of organ damage in critically ill patients. Tumour necrosis factor (TNF) is now proposed to be a key mediator of organ injury during sepsis. It is elevated early in the course of septic shock and high levels correlate with unfavourable outcome. In animals it can produce the effects of endotoxin. The prophylactic administration of anti-TNF antisera protects mice and rabbits from lethal effects of lipopolysaccharide. Interleukin-1 (IL-1) is an endogenous pyrogen which induces leukocytosis and muscle catabolism. It causes hypotension and tachycardia by reducing smooth muscle contractility. IL-1 receptor blockers have been shown to diminish mortality in experimental endotoxic shock. Interleukin-6 (IL-6) is a pyrogen and lymphocyte activator. It is the major stimulus to acute phase protein production by the liver. A recently described neutrophil-activating peptide (Interleukin-8; IL-8) may be involved in the pathogenesis of ARDS. High blood levels of IL-8 have been found in patients with septic shock. Platelet-derived growth factor (PDGF) has been shown to stimulate TNF production, leukocyte chemotaxis and pulmonary vasoconstriction in response to endotoxin. Other cytokines and growth factors have not yet been studied in critical illness. The cytokine network can be either protective or damaging. Its activation during critical illness triggers complex and still poorly understood interactions. A better comprehension of its role in protection from infection and in the pathogenesis of multiple organ failure may allow therapeutic manipulations aimed at minimising adverse effects while retaining immunological protection.
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PMID:The cytokine network in the critically ill. 152 67


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