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

The ventilatory response in acute lactic acidosis was assessed in 39 patients. In 18 patients, the acidosis was associated with phenformin ingestion and in 21, with other causes such as shock and sepsis, but not pulmonary edema. Arterial blood CO2 tensions and plasma bicarbonate concentrations were compared to those previously found in patients with uncomplicated diabetic ketoacidosis. In most of the lactic acidosis patients, arterial blood CO2 fell within the 95% confidence band calculated from the data in the ketoacidotic patients. Only 1 lactic acidotic patient had a triflingly lower CO2 tension. Shock was present in 8 of the 9 lactic acidotic patients whose CO2 tensions were more than 2 torr above the 95% confidence band.
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PMID:Ventilatory response in patients with acute lactic acidosis. 680 Jul 2

Previous investigations have demonstrated impairment of hepatic gluconeogenic activity during both hypovolemia and sepsis, but the mechanisms responsible remain unclear. The present study was designed to determine the influence of lack of oxygen on gluconeogenesis independent of humoral factors, products of ischemic peripheral tissues or pH changes. Livers obtained from Sprague-Dawley rats fasted 24 hours were perfused with Krebs-Henseleit buffer containing 5 mM lactate for 30 minutes. In the control group (n = 8) perfusion was continued; in others, anoxia was induced by perfusing with buffer equilibrated with 95% N2 and 5% CO2 for periods of 15, 30, or 60 minutes (n = 4, 5, and 5, respectively). The initial conditions were then reinstituted for an additional 45 minutes. Anoxia caused hepatic release of K+, indicative of disordered hepatic cellular ionic gradients and an abrupt cessation of gluconeogenesis. Reoxygenation partially reversed these alterations but some impairment of gluconeogenesis persisted and the degree of uptake of K+ from the perfusion media was decreased as the duration of anoxia increased. The degree of restoration of gluconeogenesis after a period of anoxia was closely associated with restoration of cellular uptake of K+. By comparison, livers taken from hypovolemic animals maintained at a mean arterial blood pressure of 40 mm Hg until the beginning of the decompensatory stage of shock exhibited a gluconeogenic capacity of only 41% of control animals and was comparable to the compromise induced by between 30 and 60 minutes of anoxia. These results suggest that the abilities to restore hepatic electrolyte balance and gluconeogenesis after oxygen deprivation are affected in parallel and may reflect a common dependence on the restoration of ATP stores after the insult.
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PMID:Effect of hemorrhage and anoxia on hepatic gluconeogenesis and potassium balance in the rat. 684 34

The course of the illness of a 56 year old female patient is reported, who is still surviving one and a half years after developing advanced, presumably progressive, so called "shock-lung syndrome". Following two episodes of hemorrhagic shock due to intestinal hemorrhage and post-operative secondary hemorrhage, interstitial lung edema developed, which was resistant to therapy. During the following weeks this was followed by bronchopneumonia with symptoms of sepsis persisting over several weeks. Between the third and seventh week of artificial ventilation X-ray of the lungs showed significant progressive changes of the interstitial tissues. This correlated with a progressive deterioration in gas exchange for O2 and CO2, which reached its peak in the seventh week with a paO2 of 71 mm Hg at a FIO2 = 1 and a paCO2 of 68 mm Hg at a minute volume of 15,51. The compliance of lung and thorax was severely reduced at 19 m1/cm H2O. At this apparently unfavourable time the patient was weaned off the respirator, and subsequently, over a period of three weeks, from oxygen insufflation. After eleven weeks of therapy, transfer to the medical ward was possible, with discharge from the hospital following three weeks later. The lung function tests at the time of discharge revealed a high grade reduction of all lung volumes and capacities without a significant obstructive component. The findings have shown a definite improvement during the following one and a half years. In retrospect the polypragmatic intensive therapy measures do not allow valid generalised therapeutic guidelines to be derived. We conclude, however, from this single observation, that therapeutic nihilism is not justified even in a progressive shock-lung syndrome which appears clinically and radiologically to be at an "irreversible" end stage.
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PMID:[Pulmonary fibrosis following ARDS. Case report of successful intensive therapy (author's transl)]. 711 41

Endotoxinaemia stimulates the generation of cysteinyl leukotrienes (LT), potent mediators of inflammation which are preferentially eliminated into the bile. Nitric oxide (NO) is a mediator molecule that has a possible protective role in liver injury. As sepsis and shock often lead to the development of hypoxic regions in the liver, the influence of hypoxia on the metabolism of cysteinyl leukotrienes and the hepatic production of NO were investigated in the isolated perfused rat liver. Livers were perfused in a non-recirculating haemoglobin-free system from the portal to the caval vein. Perfusion medium was equilibrated with 95% O2/5% CO2. In hypoxia experiments, gassing was changed to 95% N2/5% CO2 for 20 min. Tritiated leukotrienes were infused to the portal vein and metabolites in effluent and bile were measured by HPLC. Hypoxia did not influence the uptake of 3H-LTC4 and 3H-LTE4 but biliary elimination was reduced by 50-60% compared to normoxic control experiments. In hypoxia, the metabolite pattern in bile was also significantly changed with a decrease of omega-oxidation products. Following reoxygenation larger amounts of leukotrienes were excreted from the liver into the bile. To induce NO synthase in the liver, rats were injected intraperitoneally with endotoxin 6 hours before livers were isolated for perfusion. In contrast to nontreated livers, nitrite and nitrate, the oxidation products of NO, were detectable in the effluent perfusate. Basal NO2(-)+NO3- release was 5.3 (1.2) nmol/g liver/min. NO2(-)+NO3- release was stimulated by L-arginine infusion, whereas hypoxia resulted in an almost complete inhibition.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effect of hypoxia on nitric oxide formation and leukotriene metabolism in the perfused rat liver]. 751 4

The complex pathophysiology of adult respiratory distress syndrome (ARDS) makes preventive and therapeutic concepts difficult. Ample experimental evidence indicates that ARDS can be prevented by blocking systemic inflammatory agents. Clinically, only heparin, for inhibition of coagulation phenomena, is presently used among this array of approaches. Corticosteroids have not proven to be beneficial in ARDS. Alternative antiinflammatory agents are being proposed and are under current clinical investigation (e.g. indomethacin, acetylcysteine, alpha 1-proteinase inhibitor, antitumor necrosis factor, interleukin 1 receptor antagonist, platelet-activating factor antagonists). Symptomatic therapeutic strategies in early ARDS include selective pulmonary vasodilation (preferably by inhaled vasorelaxant agents) and optimal fluid balance. Transbronchial surfactant application, presently tested in pilot studies, may be available for ARDS patients in the near future and may have acute beneficial effects on gas exchange, pulmonary mechanics, and lung hemodynamics; its impact on survival cannot be predicted at the present time. Strong efforts should be taken to reduce secondary nosocomial pneumonia in ARDS patients and thus avoid the vicious circle of pneumonia, sepsis from lung infection, and perpetuation of multiple organ dysfunction syndrome. Optimal respirator therapy should be directed to ameliorate gas-exchange conditions acutely but at the same time should aim at minimizing potentially aggravating side effects of artificial ventilation (barotrauma, O2 toxicity). Several new techniques of mechanical ventilation and the concept of permissive hypercapnia address these aspects. Approaches with extracorporeal CO2 removal and oxygenation are being used in specialized centers.
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PMID:Prevention and therapy of the adult respiratory distress syndrome. 761 57

Earlier observations had indicated profound increases in the carbon dioxide tension of the myocardium, gastric wall, liver parenchyma, and renal cortex in the setting of extreme low-flow states of cardiac arrest and resuscitation, hemorrhagic shock, and anaphylactic shock. In venous blood draining the intestines, kidneys, and pelvic viscera, significant increases in PCO2 have also been observed during septic shock. In the present study, we investigated hepatic, renal, and cerebral cortical tissue carbon dioxide tension during intra-abdominal sepsis and shock in Sprague-Dawley rats. Peritonitis was induced by cecal ligation and fecal spillage. Over an interval of 320 +/- 60 minutes, we measured progressive reduction in mean aortic pressure from 152 +/- 11 mm Hg to 25 +/- 8 mm Hg and a decline in cardiac index from 492 +/- 75 ml/kg/min to 169 +/- 57 ml/kg/min. These hemodynamic deficits were accompanied by increases in liver tissue PCO2, from 58 +/- 4 mm Hg to 110 +/- 27 mm Hg (p = 0.006), in renal tissue PCO2, from 38 +/- 7 mm Hg to 115 +/- 24 mm Hg (p < 0.001), and in cerebral cortical tissue CO2, from 59 +/- 6 mm Hg to 108 +/- 16 mm Hg (p = 0.001). Arterial blood lactate content increased from 0.8 to 5.26 +/- 0.2 mmol/L (p = 0.001). Increases in blood lactate content preceded the changes in tissue PCO2 in each of these organs. These studies demonstrate that tissue hypercarbia is a more general phenomenon of low flow states, including that of circulatory shock associated with septic peritonitis.
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PMID:Hepatic, renal, and cerebral tissue hypercarbia during sepsis and shock in rats. 770

Animal study results have suggested a role in sepsis for human interleukin for DA1.a cells/leukemia inhibitory factor (HILDA/LIF). HILDA/LIF and interleukin-6 (IL-6) levels were prospectively studied by serial ELISAs in 34 septic patients. HILDA/LIF was detected in 11 of 34 patients at plasma levels of 100-37,000 pg/mL. Peak HILDA/LIF levels correlated with increased temperature and creatinine and IL-6 and with decreased arterial CO2 (P < .05). Multivariate analysis showed that shock and decreased arterial CO2 accounted for 75% of peak HILDA/LIF plasma variations (R2 = .753). Fatal outcome was most often associated with detectable HILDA/LIF (> 56 pg/mL) and peak IL-6 plasma levels > 850 pg/mL (sensitivity, 83%; specificity, 87%), but both (at respective levels of > 480 and > 850 pg/mL) were associated with fatal outcome. HILDA/LIF was detected in septic patients exhibiting shock, and its levels correlated with higher mortality and shorter survival.
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PMID:Increased plasma levels of human interleukin for DA1.a cells/leukemia inhibitory factor in sepsis correlate with shock and poor prognosis. 779 71

A review of anaesthesia for gynaecologic laparoscopic surgery is given. Special criteria are needed for selection of patients, choice of anaesthesia and intraoperative monitoring. The cardiovascular and respiratory system are affected by tension from the pneumoperitoneum, absorption of CO2 and Trendelenburg position. Gas insufflation can provoke venous gas embolism, pneumothorax, pneumomediastinum, pneumopericardium and subcutaneous emphysema. The introduction of laparoscopic instruments may result in unintentional injuries to intra-abdominal organs. The possibility that the procedure may have to be converted to open laparotomy needs to be considered. Bowel burns may result in perforation, peritonitis and sepsis. Laparoscopy is contraindicated in patients with serious cardiac disease, extensive bowel adhesions or intestinal obstruction. General anaesthesia with muscle paralysis, tracheal intubation and controlled ventilation is the preferred technique in these cases. Short acting anaesthetics are preferred in day case laparoscopy. Central neural blockade or infiltration anaesthesia supplemented with sedation and analgetics can be used for short laparoscopic procedures. The electrocardiogram, noninvasive arterial pressure monitor, airway pressure monitor, intra-abdominal pressure monitor, pulse oximeter and CO2 monitor are used routinely. Antiemetics and analgetics may be needed postoperatively.
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PMID:[Anesthesiological aspects of laparoscopy in gynecological surgery]. 799 2

Deep hypothermic circulatory arrest has been widely used as an adjunct for surgery of the aortic arch to protect the brain and other vital organs. We introduced the use of continuous retrograde cerebral perfusion via the superior vena cava during deep hypothermic circulatory arrest in 1987 and have used it in 33 patients. Continuous retrograde cerebral perfusion times ranged from 10 to 89 minutes (mean 40.2 +/- 22.5), and minimal nasopharyngeal temperatures ranged from 14 to 25 degrees C (mean 17.4 +/- 2.0). Two patients with a ruptured aneurysm died during operation due to bleeding and two other patients, with continuous retrograde cerebral perfusion time of 24 and 35 minutes, died 1 month postoperatively due to preoperative liver cirrhosis and sepsis. Two patients suffered from stroke. The remaining 27 patients, including 6 with from 60 to 82 minutes of continuous retrograde cerebral perfusion, had no complications related to continuous retrograde perfusion. During continuous retrograde cerebral perfusion, 66 pairs of blood samples from the perfusate and from the drainage back to the arch vessels were obtained. Analysis of these samples revealed that partial pressure of oxygen, saturation of oxygen, and oxygen content significantly decreased (p < 0.001), and partial pressure of carbon dioxide (CO2) and CO2 content significantly increased (p < 0.001). The nasopharyngeal temperature gradually increased at the rate of 0.01 to 0.03 degree C/min, but was maintained below 20 degrees C. These results reflect the fact that the aerobic metabolism of the brain is maintained during continuous retrograde cerebral perfusion due to oxygen and substrate availability. This technique offers the potential of metabolic support to the brain during deep hypothermic circulatory arrest and prolongs the safe time limits of deep hypothermic circulatory arrest in surgery of the aortic arch.
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PMID:Protective effect of continuous retrograde cerebral perfusion on the brain during deep hypothermic systemic circulatory arrest. 799

Ventilatory pump failure can occur in the setting of severe infection. Recent in vivo studies have shown a significant decrease in diaphragm force production in rats with pneumococcal sepsis and sepsis secondary to Escherichia coli endotoxin. We hypothesized that diaphragm impairment during sepsis may be mediated by a direct effect of tumor necrosis factor-alpha (TNF) or endotoxin. To test this hypothesis we studied the mechanical characteristics of isolated rat diaphragm strips in tissue baths containing rTNF-alpha or endotoxin and compared the results with control strips. The strips were stimulated to contract isometrically in the tissue baths that were aerated with 95% O2-5% CO2. Baseline force-frequency determinations were made at 60 min. Following this, the strips were fatigued over a 4-min period (20 Hz, 0.33-s trains, 1 train/s) and force-frequency relationships determined 30 s, 10 min, and 60 min post-fatigue. There were no significant differences found between control and experimental strips in any aspect of contractile function tested, including force-frequency characteristics, fatiguability, and recovery from fatigue. Using an isolated cell line assay (L929), we found evidence of attenuated cytotoxicity of TNF at 26 degrees C compared with 37 degrees C. Therefore, we repeated the experiments studying the effects of TNF on in vitro muscle at 37 degrees C. We once again found no effect of TNF on contractile function. We conclude that the impairment of diaphragm function during sepsis is not mediated by a direct effect of TNF or endotoxin.
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PMID:Tumor necrosis factor and endotoxin do not directly affect in vitro diaphragm function. 834 89


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