UMLS:C0036690 - FACTA Search

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

Pulmonary failure is almost always present in the early or late phase of multiple organ failure (MOF). Acute lung failure (ALF) is a uniquely constant response to direct or indirect insults to the lung. Increased pulmonary microvascular permeability (PMVP) is associated with the onset of lung permeability edema, the hallmark of ALF. The sequence of PMVP and the development of ALF caused by direct insults are studied. METHODS. A series of 255 trauma patients admitted to our intensive care unit (ICU) from 1987 to 1988 were enrolled in this prospective study. ALF was defined as stage III of the Posttraumatic Pulmonary Insufficiency Score; sepsis syndrome, according to Montgomery; organ failure, as stage II of the MOF score, and MOF was recorded when at least two organs had failed. Thoracic injury and aspiration were expected as direct, sepsis and shock alone as indirect insults to the lung. A computerized large field of view gamma camera was used to measure PMVP simultaneously over both lungs by means of 113mIn-transferrin and 99mTc-erythrocytes. The pulmonary microvascular permeability index (PMVPI; %/h) was used to quantify PMVP in the dynamic scintigraphic measurement. RESULTS. Of the 255 trauma patients (ISS = 33.9 +/- 18.7), 21% (52) patients (ISS = 41 +/- 17.8) developed ALF. 50 (or 96%) of the ALF patients developed MOF in addition, and 27 (72%) of the patients with directly induced ALF developed sepsis syndrome later. Direct lung injury was present in 77% (37) of the patients with posttraumatic ALF. Thoracic injury was the main cause of ALF: 58% (30) of 52 patients with ALF had a thoracic injury, which was true of only 30% of the non-ALF group (P less than 0.05). 33 (or 89%) of the ALF patients with direct injury developed ALF less than 72 h after injury (early ALF), and only 11% (4) later than 72 h after injury (late ALF). Indirect injury of the lung was present in 22% (12) of the patients with posttraumatic ALF. Indirectly induced ALF occurred in less than 72 h in 36% (4) and more than 72 h after injury in 64% (7) trauma patients. PMVP was determined in 21 of the 30 patients with thoracic injury. Initial evaluation of these patients with direct induced ALF showed significantly elevated (P less than 0.01) PMVP for the traumatized (PMVPI = 10.8 +/- 5.1%/h) but normal values for the nontraumatized lung (PMVPI = 3.9 +/- 3.4%/h), whereas 4 days later the PMVP increased significantly (P less than 0.05) on the primarily healthy side (PMVPI = 8.0 +/- 5.0%/h) while remaining elevated for the traumatized lung (PMVPI = 10.9 +/- 6.0%/h). In the control group the PMVPI was 2.6 +/- 2.8%/h for the right and 2.0 +/- 2.8%/h for the left lung. Similar values were found in mechanically ventilated ICU patients without ALF. DISCUSSION. Direct injury seems to be the dominant mechanism for early manifestation (less than 72 h) of posttraumatic ALF. The thoracic trauma seems to damage the pulmonary endothelium directly, thus increasing PMVP in a circumscribed region. An overwhelming inflammatory response may cause the later increase in PMVP in the primarily healthy lung areas.
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PMID:[Acute lung failure following thoracic trauma]. 227 73

In a series of 56 patients (24 uncomplicated postoperative and 32 septic patients), neopterin and elastase alpha 1 protease inhibitor complex (E-alpha 1 PI) plasma levels were measured daily. The clinical course of each patient was evaluated with the Multiple Organ Failure (MOF) score according to Goris. Neopterin could differentiate between septic and nonseptic patients (p less than .001), and E-alpha 1 PI between septic nonsurvivors and nonseptic patients only (p less than .01). In septic patients, acute pulmonary insufficiency was indicated by elevated E-alpha 1 PI values (greater than or equal to 400 micrograms/L) 1 day before mechanical ventilation was performed with a sensitivity of 81% and a specificity of 82%. Defining a patient with MOF whose score was greater than or equal to 5 as a high-risk septic patient, a comparison neopterin greater than or equal to 40 nmol/L and E-alpha 1 PI greater than or equal to 400 micrograms/L, measured 1 day before the evaluation of an MOF score of greater than or equal to 5 yielded a sensitivity of 91% and a specificity of 99% when patients fulfilled both criteria. We conclude that neopterin and E-alpha 1 PI might be useful parameters for the diagnosis of septicemia and monitoring of the clinical course in septic patients. Moreover, they might indicate the possible central role of macrophage and PMN activation in the development of MOF.
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PMID:Relationship between neopterin and granulocyte elastase plasma levels and the severity of multiple organ failure. 278 90

Pulmonary insufficiency is a major cause for mortality and morbidity following shock and sepsis. We studied the effect of hemorrhagic shock and retransfusion on endotoxin-induced lung dysfunction. Eighteen unanesthetized sheep with chronic lung lymph fistulae were divided into 3 groups. In Group I (n = 5) hemorrhagic shock of 50 torr was induced by arterial bleeding. Shed blood was retransfused after 4 h, and the animals were observed for 5 h. In Group II (n = 7) 1 microgramg/kg E. coli endotoxin was injected intravenously, and the animals were observed for 5 h. In Group III (n = 6) hemorrhagic shock was induced similarly to Group I. After 2 h of hypotension, E. coli endotoxin was injected similarly to Group II. Blood was retransfused after 4 h. During hemorrhagic shock arterial oxygen tension (PaO2) increased from 78.0 to 94.0 torr (P less than 0.005), lymph flow (QL) decreased from 7.2 to 5.2 ml/h (P less than 0.05) and lymph protein clearance (L/P.QL) from 4.6 to 3.3 ml/h (P less than 0.05). Calculated pulmonary microvascular pressure (Pmv) decreased from 11.1 to 7.0 torr (P less than 0.05). Plasma TXB2 increased from 197 to 967 pg/ml (P less than 0.05) and lymph TXB2 from 272 to 833 pg/ml (P less than 0.05). Endotoxin infusion was followed by a fall in WBC to 2,900/microliters (P less than 0.001), rise in pulmonary artery pressure (Ppl) from 17.5 to 49.7 torr (P less than 0.005), and Pmv from 12.1 to 23.7 torr (P less than 0.01). PaO2 decreased from 78.0 to 61.0 torr (P less than 0.01), QL increased to 36.9 ml/h (P less than 0.001), and L/P.QL to 24.3 ml/h (P less than 0.001). Plasma TXB2 increased to 7,600 pg/ml (P less than 0.005) and 6-Keto PGF1 alpha to 1,519 pg/ml (P less than 0.01). Infusion of endotoxin during hemorrhagic shock was followed by a comparable fall in WBC, pulmonary hypertensive response and hypoxemia, while Pmv increased only to 19.2 torr which was significantly lower than Group II (P less than 0.05). The rise in QL to 17.4 and L/P.QL to 10.6 ml/h in response to endotoxin was also significantly lower than Group II (P less than 0.05 and P less than 0.05, respectively). Plasma and lymph TXB2 and 6-Keto PGF1 alpha were unchanged. It is concluded that hemorrhagic shock reduced endotoxin-induced pulmonary microvascular pressure, pulmonary lymph production and protein flux, while the fall in WBC, early pulmonary hypertensive phase, hypoxemia, and prostanoid production were not altered by the hypotensive insult.
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PMID:Effect of hemorrhagic hypotension on endotoxin-induced lung injury in awake sheep. 291 72

Intestinal stenosis or stricture occurs in approximately one third of medically treated infants surviving the acute phase of necrotizing enterocolitis (NEC). Identification of these lesions by the use of routine contrast enemas has been advocated as a means of decreasing potential morbidity from delayed diagnosis. However, the significant incidence of spontaneous resolution and reluctance to submit asymptomatic infants to contrast enema have led recent researchers to reserve these studies for patients developing symptoms of obstruction during a period of close observation. From July 1984 to July 1986, symptomatic strictures developed in five infants (15%) responding to medical management at our institution. Contrast enemas were not routinely performed and four (80%) of these patients presented with life-threatening sepsis or perforation associated with intestinal obstruction. Two infants developed complete colonic obstruction 4 and 6 weeks after discharge from the Intensive Care Nursery, having initially tolerated oral feedings. Both infants were critically ill due to perforation or sepsis and underwent emergency colostomy at community hospitals. Two other infants developed abdominal distension with sepsis and cardiopulmonary decompensation while remaining hospitalized for prematurity and pulmonary insufficiency. These patients became symptomatic 5 and 7 weeks after cautious refeeding while closely monitored in the Intensive Care Nursery. The occurrence of such life-threatening complications suggests that clinical observation alone is not adequate in the management of many of these infants. Contrast enemas should be performed to identify those patients at risk of such potential morbidity or mortality, especially those infants not residing near pediatric surgical facilities.
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PMID:Post-necrotizing enterocolitis strictures presenting with sepsis or perforation: risk of clinical observation. 304 59

Extracorporeal membrane oxygenation (ECMO) has dramatically increased the survival rate of hypoxemic neonates who are unresponsive to maximum conventional medical therapy. Because ECMO involves multiple risks, including ligation of the right common carotid artery and right internal jugular vein, ECMO candidates should be neurologically intact neonates with a high probability of death despite maximum conventional ventilatory support. Currently, criteria based on the calculated alveolar-arterial oxygen gradient (A-aDO2) have replaced the neonatal pulmonary insufficiency index for predicting mortality and, thus, ECMO eligibility. A retrospective review of death prediction for the 26 months prior to the initiation of an ECMO program revealed a sensitivity of 67% and a specificity of 96% using the criterion of a PaO2 of less than 50 mm Hg for four hours. An equivalent A-aDO2 criterion of greater than or equal to 630 for four hours produced a sensitivity of 61% and a specificity of 96%. Prediction of mortality in neonates with sepsis was poor regardless of the criteria used. Excluding the deaths due to sepsis increased the sensitivity to 86% and 79% using criteria based on PaO2 and A-aDO2, respectively. It is concluded that the use of criteria based on PaO2 is equivalent to criteria based on A-aDO2 for predicting mortality. Criteria based on PaO2 may, however, decrease both the false-negative rate (patients with an elevated PCO2) and the false-positive rate (patients with intentionally induced hypocarbia secondary to hyperventilation alkalosis).
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PMID:Extracorporeal membrane oxygenation selection criteria: partial pressure of arterial oxygen versus alveolar-arterial oxygen gradient. 339 89

1. With improvements in treatment of burn shock and wound sepsis, inhalation injury has emerged as the number one cause of fatality in the burn patient; it accounts for 20 to 84 per cent of burn mortality. 2. Only steam is capable of inflicting direct thermal damage; most injury is caused by incomplete products of combustion, the most important being aldehydes. 3. More accurate diagnostic techniques, including fiberoptic bronchoscopy and 133Xe scanning, have been added to the traditional clinical signs of inhalation injury, such as facial burns, singed nasal vibrissae, and closed space injury, and have led to a new estimation of a 30 per cent incidence among patients with major burns. 4. Patients with inhalation injury typically pass through three stages, those of acute pulmonary insufficiency, pulmonary edema, and bronchopneumonia. 5. The major early pathophysiologic changes seen in the lungs of burned patients related to edema. With inhalation injury this is probably mediated by the products of activated neutrophils. Later changes are the result of the reduction of surfactant and thus lung compliance. 6. Treatment consists of intubation at the first hint of respiratory distress; the issue of tracheostomy versus endotracheal intubation has not been scientifically resolved, but most centers employ prolonged nasotracheal intubation. Prophylactic antibiotics or steroids are not of benefit. Further care is only supportive and includes CPAP, PEEP, vigorous pulmonary toilet, humidification of inspired air, and antibiotics for documented infection. 7. Further advances await the development of pharmacologic methods of affecting the lung's response to injury, which includes altered capillary permeability and decreased immune function.
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PMID:Pulmonary injury in burned patients. 391 76

+The results obtained from the study on thermal trauma were summarised on the base of histological, electron microscopic, immunologic and toxicological investigation methods. Shock during burning induces disturbances in the microcirculation. The great clinical significance of the alterations in lungs are stressed upon, manifested in a disorder of blood-gas barrier, permeability of the membranes of capillaries and cells, leading to acute pulmonary insufficiency. One of the probable mechanisms of anemia advancing after burns is described, that is due to the toxic effect of serum. Complement-fixation antibodies are found in the patients with burns, suggesting the involvement of autoimmune mechanisms in the course of the disease. The disturbed microcirculation has an unfavourable effect on the regeneration of wounds, leading to destruction of epithelial regeneration, disturbing the processes of revascularization of skin transplant, having an effect on the immune reactions of organism. Sepsis is discussed, with particular attention paid to that induced by Pseudomonas aeruginosa. In would cachexia some changes in the wounds are pointed to as well as sclerotic and atrophic processes in some internal organs, being usually irreversible. The reversibility if sclerosis in hypertrophic cicatrix and keloid is discussed, stressing on the cellular and extracellular mechanisms, involved in that process.
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PMID:[Current problems in the pathology of burns]. 637 46

We report here our first experience with the use of a total artificial heart in a human being. The heart was developed at the University of Utah, and the patient was a 61-year-old man with chronic congestive heart failure due to primary cardiomyopathy, who also had chronic obstructive pulmonary disease. Except for dysfunction of the prosthetic mitral valve, which required replacement of the left-heart prosthesis on the 13th postoperative day, the artificial heart functioned well for the entire postoperative course of 112 days. The mean blood pressure was 84 +/- 8 mm Hg, and cardiac output was generally maintained at 6.7 +/- 0.8 liters per minute for the right heart and 7.5 +/- 0.8 for the left, resulting in postoperative diuresis and relief of congestive failure. The postoperative course was complicated by recurrent pulmonary insufficiency, several episodes of acute renal failure, episodes of fever of unidentified cause (necessitating multiple courses of antibiotics), hemorrhagic complications of anticoagulation, and one generalized seizure of uncertain cause. On the 92nd postoperative day, the patient had diarrhea and vomiting, leading to aspiration pneumonia and sepsis. Death occurred on the 112th day, preceded by progressive renal failure and refractory hypotension, despite maintenance of cardiac output. Autopsy revealed extensive pseudomembranous colitis, acute tubular necrosis, peritoneal and pleural effusion, centrilobular emphysema, and chronic bronchitis with fibrosis and bronchiectasis. The artificial heart system was intact and uninvolved by thrombosis or infectious processes. This experience should encourage further clinical trials with the artificial heart, but we emphasize that the procedure is still highly experimental. Further experience, development, and discussion will be required before more general application of the device can be recommended.
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PMID:Clinical use of the total artificial heart. 1476 80

We studied 31 autopsied cases of gestational choriocarcinoma encountered at the Northwestern University Trophoblastic Disease Center in the past two decades to learn if the clinical and morphologic aspects of these cases have been altered by therapy. These cases were analyzed for cause of death, distribution of tumor and histologic patterns in relation to the amount of chemotherapy. Tumor hemorrhage and/or pulmonary insufficiency were the most common causes of death, irrespective of the amount of therapy although other factors including drug toxicity, sepsis, and uremia led to death in six cases. The amount of chemotherapy generally did not affect the number or distribution of metastases. Histologically, nine cases showed extensive or complete necrosis. Eighteen of the remaining tumors had typical biphasic patterns, but four patients who received multiple courses of chemotherapy had atypical patterns with a marked predominance of cytotrophoblast and infiltrative growth. These atypical patterns do not appear to be a direct result of chemotherapy but may represent a more aggressive form of this tumor. This study shows that fatal gestational choriocarcinoma can have a variety of clinicopathologic features which reflect not only the biologic capabilities of the neoplasm but also the effects of chemotherapy and prolonged disease.
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PMID:Fatal gestational choriocarcinoma. Clinicopathologic study of patients treated at a trophoblastic disease center. 711 8

Ordinarily the IUD does not give rise to any unpleasant effects on the woman's organism. But the literature does contain references to peritonitis, sepsis, and even perforation of the uterus. The present case describes an IUD which passed through the uterine tube into the abdominal cavity. The patient, a 28-year old woman, had been fitted with an IUD and a month later came to the clinic with a serious case of nonspecific pneumonia. Soon after she died of cardio-pulmonary insufficiency. At autopsy, in the left uterine tube (in the ampulla) we discovered the IUD threads, while the IUD itself was hanging in the abdominal cavity. We could not find any macro- or micro-pathological changes in the uterus. The reasons might have been connected with the fact that the IUD was inserted 1 month after the woman had a stillbirth. The basic mechanism would be that the IUD was wedged into the isthmus of the uterine tube at the time of insertion and then compressed, thus facilitating its subsequent movement toward the abdominal cavity.
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PMID:[Rare complication of intrauterine contraception]. 728 93

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