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

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

We studied pulmonary function in 7 infants age 3-16 months who were dependent upon mechanical ventilation due to bronchopulmonary dysplasia (BPD). Raised lower expiratory airway resistance (RAe), low dynamic lung compliance (CL) and rapid respiratory frequency (f) characterized the breathing pattern in these infants. End-tidal carbon dioxide tension (PECO2) was elevated in spite of abnormally high minute ventilation (VE). One infant died of respiratory failure, 1 died of sepsis and 1 of an occluded tracheostomy after discharge from the hospital. Another infant still requires mechanical ventilation at age 18 months. Recovery from chronic respiratory failure in 4 infants occurred between age 1.2-2.5 years. The infants recovered concomitant with the ability to sustain a high VE in spite of persistently elevated RA and low CL. All of the surviving infants, although developmentally delayed, have the potential for home care with further growth and development.
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PMID:Pulmonary function in chronic respiratory failure of infancy. 741 22

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

Laparoscopy is increasingly used in conditions complicated by peritonitis. A theoretical concern is that carbon dioxide pneumoperitoneum may increase bacteraemia. This study examines the effect of carbon dioxide pneumoperitoneum on bacteraemia, endotoxaemia and physiological correlates of sepsis in an animal model of peritonitis. New Zealand white rabbits were assigned to three groups of six animals. Group 1 received an intraperitoneal inoculation of 10(9) colony-forming units of Escherichia coli followed by a 10-cm midline laparotomy. Group 2 received an identical bacterial inoculum followed by a 12-mmHg carbon dioxide pneumoperitoneum for 1 h. Group 3 received no bacteria but had a 12-mmHg carbon dioxide pneumoperitoneum for 1 h. Groups 1 and 2 had significantly higher levels of bacteraemia (P < 0.01) and endotoxaemia (P < 0.01) accompanied by significantly lower mean arterial pressures (P < 0.05) and higher heart rates (P < 0.05) compared with group 3. After 6 h groups 1 and 2 were significantly hypocarbic (P < 0.01), leucopenic (P < 0.01) and thrombocytopenic (P < 0.01). There was no difference between group 1 and group 2. A carbon dioxide pneumoperitoneum of 12 mmHg does not increase bacteraemia or endotoxaemia, nor does it adversely affect physiological or laboratory correlates of sepsis compared with laparotomy in this animal model of peritonitis.
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PMID:Effect of carbon dioxide pneumoperitoneum on bacteraemia and endotoxaemia in an animal model of peritonitis. 854 57

Impairment of cerebral blood flow (CBF) autoregulation may have serious implications for patients with cirrhosis if arterial hypotension occurs during coma, anesthesia, bleeding, or sepsis. In this study, CBF autoregulation was investigated in patients with cirrhosis with no or mild encephalopathy. Ten patients (median age, 45 years; range, 30 to 61 years) and six healthy volunteers (median age, 30 years; range 21 to 61 years) were included. Catheters were placed in a radial artery and in the internal jugular veins. Baseline CBF was measured using single-photon emission computed tomography (SPECT) with concomitant measurements of cerebral arteriovenous oxygen content differences (AVDO2). CBF autoregulation was evaluated using the AVDO2 method and changes in mean flow velocity in the middle cerebral artery (Vmean) as determined by transcranial Doppler (TCD). Mean arterial pressure (MAP) was increased by 30 mm Hg by intravenous norepinephrine, and subsequently decreased by a combination of lower body negative pressure and ganglion blockade, whereas AVDO2 and Vmean were measured at each 5 mm Hg change in MAP. CBF was 61 (range, 45 to 78) mL 100 g-1 min-1 in patients with cirrhosis and 65 (range < 53 to 88) mL 100 g-1 min-1 in volunteers (not significant [NS]). There were no regional differences in CBF between the two groups. Arterial carbon dioxide tension was 31 (23 to 35) mm Hg in patients with cirrhosis and lower, compared with 36 (range, 34 to 47) mm Hg in the volunteers (P < .01). For evaluation of autoregulation, MAP was raised to 116 (range, 100 to 145) and then decreased to 39 (range, 34 to 50) mm Hg.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cerebral blood flow autoregulation and transcranial Doppler sonography in patients with cirrhosis. 765 76

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

The work of nursing personnel with patients receiving treatment with hyperbaric oxygenation is intended mainly to prepare the patients and provide care and psychological support. Hyperbaric oxygenation as a therapeutic method was included in Cuba's Health System in 1986. Hyperbaric oxygenation is applied in different diseases, both alone and as supportive treatment for clinical or surgical therapy and it is based on the significant increased oxygen dissolved in the plasma when gas pressure is increased to a proper dosage using hyperbaric chambers. Nursing personnel plays a very important role in providing care to patients and the team is in charge of the security measures and techniques. Hyperbaric oxygenation has proved to be effective for the treatment of anaerobic sepsis, intoxication due to carbon monoxide, peritonitis, gastroduodenal ulcers, liver diseases, osteomyelitis, as a support for grafting and transplants and other diseases.
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PMID:[Work of nurses in hyperbaric oxygenation]. 770 13

Recent studies have shown that the veno-arterial gradient for carbon dioxide (dVApCO2) is increased in the case of low cardiac index (CI). In order to further investigate this matter 220 haemodynamic measurements from 34 patients with septic shock and from 28 patients in the post-operative state without sepsis were evaluated. The arteriovenous gradient for pH (dAVpH) was also evaluated. CI was found to be inversely correlated to both dVApCO2 and dAVpH when the two groups of patients were analysed separately (r = -0.76 and r = -0.78, P < 0.001 for the relationship between CI and dVApCO2, r = -0.58 and r = -0.69, P < 0.001 for the relationship between CI and dAVpH). When volume loading over 2h was used to increase CI, 58-66% of the patients in the two groups showed a decline in dVApCO2 > 10% when CI was increased by > 10%. The corresponding values for a reduction in dAVpH > 10% during volume loading was 36-52%. While dAVpH was found to be increased in non-survivors (n = 27) when compared to survivors (0.32 +/- 0.01 vs. 0.24 +/- 0.1, P < 0.05) at the second day in the IUC, dVApCO2 was not a significant predictor of mortality despite the fact that CI was found to be decreased in the non-survivors (3.5 +/- 0.94 vs. 4.3 +/- 1.0 L min-1 m-2, P < 0.01). In conclusion, the veno-arterial carbon dioxide gradient was found to be inversely correlated to cardiac performance in patients both in patients with septic shock and in non-septic post-operative patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Veno-arterial carbon dioxide and pH gradients and survival in critical illness. 778 68

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


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