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

Splenectomized subjects show a higher incidence of myocardial ischemia and of Overwhelming Post-Splenectomy Infection (OPSI). It is doubtful that implanted splenic tissue guarantees an adequate protection from OPSI. The histological characteristics and the capacity of protection from OPSI of two models of omental autoimplantation of splenic tissue in rats were examined. The implanted splenic tissue offers a significant protection from pneumococcal sepsis, even though there is no relation between implant architecture and survival rate.
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PMID:Omental autoimplantation of splenic tissue and intravenous pneumococcal challenge. A comparative study in rats. 262 85

The characteristic hemodynamic profile of human septic shock consists of a normal or elevated cardiac index and a decreased systemic vascular resistance index. When a patient with septic shock has a low cardiac index, concomitant hypovolemia is usually present. Within 48 hours of the onset of septic shock, most patients develop marked dilatation of both ventricles, depressed ejection fractions, and alterations of the Frank-Starling and diastolic pressure-volume relationships; stroke volume typically is well maintained. In surviving patients, cardiac function returns to normal within 10 days. An identical sequence of hemodynamic abnormalities occurs in an experimental canine model of sepsis that employs intraperitoneal implantation of infected fibrin clots. This myocardial dysfunction is not due to global myocardial ischemia; instead, there appear to be one or more circulating myocardial depressant substances. The chemical nature of these circulation mediators is under intensive investigation clinically, in vitro, and in the canine model.
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PMID:Myocardial dysfunction in sepsis. 264 29

Cardiac metastases are often clinically inapparent but have important prognostic significance. A total of 1046 consecutive autopsies performed between 1981 and 1983 were reviewed, and 210 patients with both premortem and autopsy diagnoses of cancer were found, in whom a recent (less than 3 months before death) ECG was available. Of these patients, 47 had cardiac metastases (group I) and 163 did not (group II). In group I, 19 patients had new ECG changes suggestive of myocardial ischemia or injury, including either diffuse T wave inversion (10%), segmental (ECG pattern suggestive of a specific coronary distribution) T wave inversion (80%), or ST elevation (10%). None of these patients had symptoms suggestive of myocardial ischemia. In group II, six patients had ECG changes suggestive of myocardial ischemia or injury: four patients with preterminal sepsis, one with myocardial infarction, and one with aspergillus nodules within the myocardium. New atrial arrhythmias (seven patients) and low voltage (10 patients) were found with greater frequency in group I patients (p less than 0.0005 and p less than 0.00001, respectively, vs group II). Patients with normal ECGs were unlikely to have cardiac metastases; however, the finding of nonspecific ST-T wave changes was not helpful in differentiating the two groups. In clinically stable patients with cancer and no cardiac symptoms suggestive of ischemia, any new ECG change should raise the suspicion of cardiac metastases. The ECG finding of myocardial ischemia or injury has high specificity (96%, p less than 0.000001) for cardiac metastases.
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PMID:Electrocardiographic markers of cardiac metastasis. 378 78

In spite of all the scientific and technical advances in recent years, shock that is not rapidly correctable with fluid can have a morbidity rate exceeding 80%. Consequently awareness of such precipitating factors as sepsis and early diagnosis and treatment are essential. Treatment should be rapid and should follow a previously outlined protocol. Such protocols should include correction of the precipitating problem and aggressive resuscitation to assure adequate ventilation and oxygenation of the blood and optimal oxygen delivery to the tissues. Fluid and blood should be given as needed until filling pressures begin to rise rapidly with further fluid infusion. With hemorrhagic shock in previously healthy individuals, a hemoglobin level of 10.0 g/dL is usually adequate. In older, septic, or cardiogenic shock patients, a hemoglobin level of 12.5 to 14.0 may be preferable. If an optimal preload does not increase cardiac output to normal or higher levels, inotropic agents should be used. If shock still persists, one must be sure that the arterial pH is not excessively high or low. Glucocorticoids may then be given in low dose (200 mg hydrocortisone) in case some degree of adrenal insufficiency is present. They can also be given in high doses (equivalent to 150 mg/kg hydrocortisone) early in septic shock primarily to prevent excess complement activation and to preserve membrane integrity. Vasopressors may occasionally be required if there is excessive vasodilation, especially if there is persistent hypotension in the presence of high-grade coronary or cerebral artery stenosis. Vasodilators may be used to try to correct myocardial ischemia (nitroglycerin), excessive preload (nitroglycerin), or excessive afterload (nitroprusside or hydralazine). Combinations of vasodilators and inotropic agents may be required in some patients with high systemic vascular resistance and persistently low cardiac outputs. Mechanical assist with IABP can be of great value in persistent cardiogenic shock. Diuretics may occasionally help prevent renal failure in patients who are persistently oliguric after blood flow and pressure are restored. Heparin is occasionally of value if DIC develops with no concomitant fibrinolysis. Antibiotics are important in septic shock and may also be important if persistent shock has reduced gastrointestinal mucosal integrity so that bacteria and bacterial products can enter the portal system.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Science and shock: a clinical perspective. 389 56

Electromechanical dissociation (EMD), defined as electrocardiographically adequate ventricular systolic complexes in the absence of detectable pulse or blood pressure, may occur in the terminal course of patients and is frequently unexplained. The 50 cases in the autopsy files of The Johns Hopkins Hospital in which the patients had died after documented episodes of EMD were reviewed. Four major categories of patients were identified: In 22 of 50 cases (44 per cent) myocardial ischemia appeared to precipitate EMD; in 14 of these 22 cases (64 per cent) myocardial ischemia was global in extent, while in eight (36 per cent) myocardial ischemia was regional, occurring in the distribution of an occluded coronary artery. A subset of ten patients with ischemia had terminal ventricular tachycardia or fibrillation, which was converted to EMD following resuscitation maneuvers. In 12 of 50 cases (24 per cent) systemic shock preceded the development of EMD; in nine of these 12 (75 per cent) hypotension was due to myocardial or arterial rupture, while in three (25 per cent) hypotension was secondary to sepsis. In ten of 50 cases (20 per cent) pulmonary vascular compromise was the apparent cause of EMD. Of these ten cases, eight (80 per cent) were secondary to pulmonary embolization, and two (20 per cent) were due to pneumothorax. In six of 50 cases (12 per cent) the precise cause of EMD could not be determined. The results of this study indicate that in the dying patient with electromechanical dissociation the differential diagnosis should include myocardial ischemia, systemic shock, and pulmonary vascular compromise.
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PMID:Electromechanical dissociation: pathologic explanations in 50 patients. 398 75

To determine the relative importance of multiple interrelated factors that have been considered to contribute to pulmonary infarction, the authors performed a discriminant analysis on consecutively autopsied patients with pulmonary embolism. From the clinic records of 45 individuals, the authors tabulated the underlying illness, history of valvular or ischemic heart disease, right and left ventricular failure, sepsis, shock, malignancy, premortem functional status, and the clinician's suspicion of pulmonary embolism. At postmortem examination, the authors measured and recorded the extent of emphysema, pneumonia, neoplasia, pulmonary vascular atherosclerosis; thickness and dilatation of both cardiac ventricles; the presence of valvular heart disease; the number, diameter, and amount of occlusion of the pulmonary arteries that contained thromboemboli; the extension of the clot, the size of the infarct; the Reid-Index; and the thickness of pulmonary and bronchial arterial wall. The major determinants of infarction were as follows: poor premortem functional status, the number of lobes having emboli, left ventricular failure, and the presence of lung cancer. The authors then tested the equation generated from these patients on 21 additional patients. The discriminant function correctly classified 81% of first group and predicted the occurrence of infarction in new patients with 70% accuracy. The size of the infarct was most correlated with the use of vasodilators and the embolic burden.
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PMID:Factors associated with pulmonary infarction. A discriminant analysis study. 401 73

Monitoring of ventricular function by central venous (CVP) and pulmonary wedge pressures (PCW) was compared with ejection fraction and end-diastolic volume (gated pool scan) in patients resuscitated from hypovolemic and septic shock. Sixteen patients were studied within 24 hours of resuscitation and all showed depressed right ventricular ejection (RVEF) and/or an increased end-diastolic volume (RVEDVI). Group I (eight patients, hypovolemia and sepsis) had low RVEF (mean, 0.30), high RVEDVI (mean 129.2 ml/m2), and nearly normal left ventricular function (LVEF 0.63 and LVEDVI 63.6 ml/m2), compared to angiographic normals (RVEF 0.52, RVEDVI 55.8 ml/m2; nL LVEF 0.59, LVEDVI 52.3 ml/m2). Group II (3 patients, all septic) had better RVEF (mean, 0.54) but high RVEDVI (mean, 121.1 ml/m2) with normal LVEF (mean, 0.67) and high LVEDVI (mean LVEDVI 107.2 ml/m2). Group III consisted of five patients (hypovolemia and sepsis) who had biventricular depression (RVEF 0.25 and LVEF 0.29) and elevated EDVI. The mortality rate for group I (25%) was significantly less than for groups II and III (100% and 80%, respectively), and could be correlated with failure to improve RV function. Follow-up studies in ten patients showed improvement in seven which correlated with increased RVEF and reduced RVEDVI. Comparing survivors to non-survivors showed no predictability on the basis of initial studies but a significantly larger RVEDVI and RV stroke work index in non-survivors' follow-up studies. No correlation could be made with left ventricular performance, and there were no correlations between PCWP and LVEDVI or CVP and RVEDVI. A significant negative correlation was seen between RVEF and pulmonary vascular resistance (r = -0.34, p less than 0.05). Both LVEDVI and RVEDVI were correlated significantly with cardiac index and with each other. RV dysfunction occurs after resuscitation of hypovolemia and sepsis without reliable alteration in filling pressure and is likely related to myocardial ischemia as well as increased pulmonary vascular resistance. Survival seems to depend on improvement in RV performance, which can be measured at the bedside by cardiac scintigraphy.
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PMID:Unsuspected right ventricular dysfunction in shock and sepsis. 661 53

Between 1975 and 1979 we performed coronary arteriography on 15 patients with end-stage renal failure and clinical evidence of severe ischemic heart disease. One patient died after the procedure of severe pump failure. Ten patients subsequently received coronary-artery bypass grafts, and two of these patients also received mitral-valve replacement. One patient, a diabetic, died of sepsis after surgery. Eight of the nine surviving patients, including the two patients who had undergone mitral-valve replacement, are markedly improved as a result of surgery. Our experience indicates that these patients can undergo angiography and coronary-artery bypass surgery at an increased but acceptable risk, provided dialysis is done before and after cardiac catheterization and surgery to control extracellular volume overload and hyperkalemia. The operation benefits patients with end-stage renal failure and severe ischemic heart disease by relieving angina and improving their level of activity. It is unclear whether survival is improved for these patients.
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PMID:Coronary-artery surgery in patients with end-stage renal disease. 696 31

Inhibitors of nitric oxide (NO) synthesis have been used in the treatment of septic and endotoxic shock. However, several studies question the beneficial effect of inhibiting NO production in sepsis and endotoxemia. We have investigated the effect of inhibition of NO synthesis after endotoxemia in the isolated perfused rat heart. In hearts from endotoxin-treated animals, coronary flow was elevated 64% and oxygen consumption was elevated 20% compared with control hearts. NADH fluorescence imaging was used as an indicator of regional hypoperfusion. A homogeneous low-surface NADH fluorescence, indicative of adequate tissue perfusion, was observed in both control and endotoxin-treated hearts. The increase in coronary flow and oxygen consumption could only partially be prevented by pretreatment of the animals with dexamethasone. Addition of N omega-nitro-L-arginine (NNLA), an inhibitor of NO synthesis, to the perfusion medium eliminated differences in coronary flow and oxygen consumption between normal and endotoxin-treated hearts. However, NADH surface fluorescence images of endotoxin-treated hearts after NNLA revealed areas of high fluorescence, indicating local ischemia, whereas the control hearts remained without signs of ischemia. The ischemic areas were present at various perfusion pressures and disappeared after the infusion of L-arginine, the natural precursor of NO, or the exogenous NO donor sodium nitroprusside. Methylene blue (MB), an inhibitor of soluble guanylate cyclase, the effector enzyme of NO, also eliminated differences in coronary flow and produced similar areas of local myocardial ischemia in endotoxin-treated hearts but not in control hearts.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inhibition of nitric oxide synthesis causes myocardial ischemia in endotoxemic rats. 753 18

A retrospective study of 116 cases of fatal pulmonary thromboembolism, drawn from a total of 11,044 Coroner's autopsies, conducted over a 5-year period, yielded a necropsy prevalence of 1.05%, with an annual incidence varying between 0.78%-1.32%. There was a statistically significant peak monthly incidence of 1.89% in September (P < 0.03), as well as significantly higher rates between April to September as a whole, compared to the rest of the year (P < 0.03). There was a marked preponderance of females (male:female ratio = 0.59) and 48.3% of the subjects were > or = 60 years of age, with a distinct peak (23.3%) in the 8th decade. The prevalence of the common predisposing factors were as follows: surgery 41.4%, trauma 30.2%, sepsis 22.4%, obesity 18.1%, malignancy 10.3% and pregnancy 4.3%. The peak time of death following trauma and/or immobilization was one week. Apparently, a total of 54 subjects (46.6%) were ambulant prior to death, while 29 (25%) did not have any of the common risk factors studied. The prevalence of cigarette smoking and oral contraception could not be ascertained due to inadequate clinical documentation, even among medical inpatients. The majority of deaths (85.3%) occurred in hospitals, of which 44.8% were surgical patients. Pulmonary thromboembolism was apparently not suspected in 77.1% of the 105 patients who died whilst under the care of qualified medical practitioners, there being no significant difference between medical and surgical inpatients. In these cases, death was most often attributed to acute myocardial infarction or ischaemic heart disease. The study also showed a high prevalence of underlying chronic obstructive airways disease (37.1%) and of moderate to severe coronary atheroma (37.9%). The clinico-pathological and medico-legal implications of these findings are discussed.
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PMID:Pulmonary thromboembolism is not uncommon--results and implications of a five-year study of 116 necropsies. 757 14


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