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

Replacement of glucose and albumin in ten patients after hepatic lobectomy shows that hypoglycemia and hypoalbuminemia, the two most common consequences of lobectomy in animals, can be prevented in man. Biosynthesis of protein, cholesterol, and prothrombin are reduced temporarily. In patients having emergency lobectomy, the serum bilirubin and glutamic oxaloacetic transaminase concentrations are statistically greater than in patients having elective lobectomy. Serum ammonia is not elevated and bromsulphalein excretion is normal after bilirubin returns to less than 1 mg/100 ml. Lactic dehydrogenase concentrations in serum are increased and fluctuate in the presence of sepsis or respiratory insufficiency: Mean creatine phosphokinase peaks at concentrations higher than those reported in acute myocardial infarction and returns to normal in three days. Compensatory hyperplasia of the residual lobe occurred in all patients.
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PMID:Physiologic consequences of hepatic lobectomy in man. 16 98

The clinical course and causes of death in 132 consecutive patients with fulminant hepatic failure and grade III or IV encephalopathy have been reviewed. 105 patients died and in 96 of these an autopsy examination was performed. In 36 patients there was cerebral oedema and the mean age of this group was significantly younger than the other fatal cases. In 28 patients death was attributed to major haemorrhage which originated in the gastrointestinal tract in 25. The prothrombin time ratio was not significantly greater in patients with major bleeding than in those without but they did have a significantly lower platelet count. Sepsis contributed to death in 12 patients. In 25 patients massive hepatic necrosis only was found at autopsy and death was considered to be due solely to hepatic failure. The degree of hepatocyte loss was assessed in 80 fatal cases by a histological morphometric technique on a needle specimen of liver taken immediately post-mortem. The proportion of the liver volume occupied by hepatocytes (hepatocyte volume fraction, HVF) was greatly reduced in all patients (normal 85+/-SD 5 percent) but the mean value was significantly higher in the patients dying with sepsis, cerebral oedema or haemorrhage than in the group in whom death was attributed solely to hepatic failure. There were ten patients in whom liver function was improving at the time of death which was due to cerebral (9) or haemorrhage (1). These observations suggest that many patients presently dying from fulminant hepatic failure may be expected to survive, once more effective therapy is available for the complications of the illness.
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PMID:Causes of death in fulminant hepatic failure and relationship to quantitative histological assessment of parenchymal damage. 17 38

Plasma levels of antithrombin III, alpha 2-macroglobulin and inter-alpha-trypsin inhibitor, as well as those of various clotting, complement and other plasma factors, were significantly decreased in 18 patients suffering from hyperdynamic septic shock. A similar statistically significant reduction of the concentrations of several plasma factors (prothrombin and antithrombin III, plasminogen and alpha 2-plasmin inhibitor, complement factor C3 and clotting factor XIII) was observed in experimental endotoxaemia. In this model the reduction in the plasma levels of these factors was considerably diminished by the intravenous injection of a granulocytic elastase--cathepsin G inhibitor of lower molecular weight from soybeans. The results of both studies indicate that consumption of plasma factors in the course of Gram-negative sepsis proceeds not only via the classical routes (by activation of the clotting, fibrinolytic and complement cascades by system-specific proteinases such as thrombokinase or the plasminogen activator) but also to an appreciable degree of unspecific degradation of plasma factors by neutral proteinases such as elastase and cathepsin G. The endotoxin-induced release of both sorts of proteinases, the system-specific ones and the unspecific lysosomal proteinases from leucocytes and other cells, is likely to be mainly responsible for the consumption of antithrombin III and alpha-2-macroglobulin via complex formation (followed by elimination of the complexes) and the increased turnover of the inter-alpha-trypsin inhibitor as observed in the clinical study. The therapeutic use of an exogenous elastase--cathepsin G inhibitor in the experimental model was stimulated by the observation that human mucous secretions contain and acid-stable inhibitor of the neutral granulocytic proteinases, called HUSI-I or antileucoproteinase. This inhibitor protects mucous membranes and soluble proteins against proteolytic attack by leucocytic proteinases released in the course of a local inflammatory response. Preliminary results indicate that HUSI-I, which is produced by the epithelial cells of mucous membranes, does not belong to any known structural type of acid-stable proteinase inhibitor. The search for other candidates suitable for medication in humans led to the discovery of a potent elastase--cathepsin G inhibitor, called eglin, in the leech Hirudo medicinalis. This acid-stable inhibitor with a molecular weight close to 8100 has an unusual structural property in that the structure of the molecule is not stabilized by any disulphide bridge.
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PMID:Proteinase inhibitors in severe inflammatory processes (septic shock and experimental endotoxaemia): biochemical, pathophysiological and therapeutic aspects. 39 95

Both acute and chronic hepatic insufficiency can result in lactate accumulation and lactic acidosis; data from both types of patients were compared. In the chronic group, an acute precipitating event was identified in seven of nine subjects. Four had sepsis and three had gastrointestinal hemorrhage. In these patients, results from most tests of hepatic function were not altered dramatically. There were no long-term survivors in this group. In contrast, patients with acute hepatic failure had striking alterations in their results of hepatic function tests. Notable prolongation of the prothrombin time was always present initially and antedated other abnormalities of hepatic function. Three of seven patients in this group survived. Hypoglycemia was seen in both groups and in two subjects with acute hepatic insufficiency, glucose administration alone resulted in rapid lowering of lactate levels.
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PMID:Lactic acidosis and liver disease. 50 18

The association of nephrotic syndrome and renal vein thrombosis has been increasingly reported in the literature due to the use of modern complementary explorative techniques. The incidence of renal vein thrombosis in the nephrotic syndrome varies according to the different authors. The pathogenesis of this association has been widely discussed and even though renal vein thrombosis has formerly been considered as one more cause of nephrotic syndrome, there are at present numerous arguments supporting the opposite thesis. A case of nephrotic syndrome and unilateral thrombosis of the renal vein in a patient with primitive extramembranous glomerulonephritis is reported. Blood coagulation studies revealed an initial hyperfibrinogenemia and a persistent decrease of factors V, VII, and X, with low rates of prothrombin. A thrombectomy was carried out, but the patient presented a Gram-negative sepsis without hypotension in the immediate postoperative period. As a consequence an acute renal failure developed and hemodyalisis was necessary for 2 months. The pathogenesis of both conditions are discussed.
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PMID:[Nephrotic syndrome and unilateral thrombosis of the renal vein. Acute renal failure and disturbances of the hemostasis (author's transl)]. 54 30

We have reviewed 53 cases of disseminated intravascular coagulation (DIC) in the newborn, including 29 cases that were confirmed at autopsy. Factors predisposing to DIC included maternal complications (60%), low Apgar scores (30%), hyaline membrane disease (62%), and sepsis (26%). Diagnostic criteria common to autopsy-proved cases included presence of fibrin degradation products, low factor V activity, a prolonged prothrombin time, and a prolonged partial thromboplastin time and/or thrombocytopenia. There appeared to be no difference in coagulation response or in mortality among patients treated with different therapeutic regimens. Survivors were older gestationally, had higher birth weights, and higher Apgar scores.
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PMID:Disseminated intravascular coagulation in the newborn. 76 May 11

This chapter has provided a review of available literature regarding alterations of hemostasis associated with CPB. The primary pathology of altered hemostasis during CPB appears to be two-fold: (1) a functional platelet defect of unclear etiology, which occurs in virtually all patients, and (2) a primary hyperfibino(geno)lytic defect which occurs in the majority of patients undergoing cardiopulmonary bypass. Significant thrombocytopenia does not appear to be a consistent problem, and is probably a function of perfusion technics; this may, however, be an important source of hemorrhage in some instances. Although hyperheparinemia, heparin rebound, and protamine excess have occasionally been incriminated as sources of hemorrhage during CPB, no well documented cases appear in the literature. Likewise, although DIC gained popularity in early reports of CPB hemorrahge, it appears that this syndrome rarely, if ever, arises as a consequence of CPB alone; it can be seen, however, in CPB patients who are provided a triggerin situation for DIC, such as shock, sepsis, or hemolytic transfusion reaction. It is likely that many reported alterations of hemostasis during CPB which were concluded to represent DIC actually were due to hyperfibino(geno)lysis. The key to prevention of CPB hemorrhage rests simply in obtaining an adequate preoperative workup. Of extreme importance is an adequate history with respect to bleeding tendencies in both patient and family; of equal importance is a careful history regarding antiplatelet drugs. A careful physical examination, searching for clues of a real or potential bleeding diathesis, also can often prevent catastrophic cases of CPB hemorrhage. Lastly, an adequate presurgical laboratory screen must be performed; in addition to the usual prothrombin time, partial thromboplastin time, and platelet count, a thrombin time and standardized template bleeding time must be added. The addition of these two simple modalities will insure against significant defects in fibrinogen, the fibrinolytic system, vascular function, and platelet function. When CPB hemorrhage occurs, simple laboratory screening will usually allow for a quick hemostasis evaluation. The parameters recommended in this review will distinguish between surgical and nonsurgical bleeding and should, therefore, allow for a quick decision regarding necessity for reexploration and the adequacy of hemostasis if reexploration is needed. In addition, this screen will distinguish between difficulties with heparin, protamine, and the fibrinolytic system. The vast majority of nonsurgical hemorrhages during CPB is due to a functional platlet defect, primary hyperfibrino(geno)lysis, or a combination of these. The quick administration of platelet concentrates, while awaiting laboratory evaluation, will control or significantly blunt most instances of CPB hemorrhage. If platelets fail to control bleeding, and reasonable laboratory evidence of primary hyperfibrino(geno)lysis is present, antifibrinolytics should then be used...
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PMID:Alterations of hemostasis associated with cardiopulmonary bypass: pathophysiology, prevention, diagnosis, and management. 79 78

The DIC syndrome is the most common cause of an abnormal hemorrhage tendency during pregnancy and the puerperium and reflects systemic activation of the coagulation cascade by circulating thromboplastic material, with secondary activation of the fibrinolytic system. Its presence in a pregnant patient almost invariably is evidence of an underlying obstetric disorder such as abruptio placentae, eclampsia, retention of a dead fetus, amniotic fluid embolism, placental retention or bacterial sepsis. Diagnosis of the DIC syndrome rests on the demonstration of reduced levels of fibrinogen and platelets, prolongation of the thrombin, prothrombin and partial thromboplastin times, and the presence of fibrin/fibrinogen degradation products (FDP) in the serum. Therapy consists of prompt removal of the source of procoagulant material, replacement of depleted clotting factors and, in some cases, anti-coagulation with heparin.
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PMID:Disseminated intravascular coagulation in pregnancy. 91 82

Serial measurements of coagulation activity, platelet counts, and platelet aggregation were done in patients with full-thickness burns involving 25% or more of body surface area to detect specific changes that might correlate with the onset of septicemia. Mean and maximal values for prothrombin time, partial thromboplastin time, thrombin time, activities of factor V and factor VIII, and concentrations of fibrinogen and fibrinogen-related antigens observed in the presence of bacterial septicemia did not differ significantly from those observed in the absence of septicemia. Mean platelet counts were significantly less with sepsis, but values in individual subjects were not indicative of the presence of septicemia. By contrast, platelet aggregation in response to adenosine diphosphate, epinephrine, and collagen always became severely abnormal with the onset of septicemia but not in the absence of sepsis.
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PMID:Platelet aggregation as a sign of septicemia in thermal injury. A prospective study. 94 30

Disseminated intravascular coagulation (DIC) is a syndrome caused by the systemic generation of thrombin. Most cases are due to pathological activation of the intrinsic coagulation systems (e.g. in sepsis), and/or the extrinsic system (e.g. in malignancy and head trauma). Diagnosis is made by finding abnormalities in at least 3 of 4 laboratory values, namely prothrombin time, platelet count, fibrinogen and fibrinogen/fibrin degradation products. The most common clinical manifestation of DIC is bleeding, with thrombosis in less than 10% of acute cases but more frequently encountered in chronic DIC associated with malignancy. Acute DIC must first be treated by specific therapy of the underlying disease and general support measures. If serial clinical and laboratory monitoring improves, no further treatment is required. If severe or life-threatening haemorrhage occurs or a thrombotic event ensues, heparin anticoagulation followed by aggressive replacement with platelets, fresh plasma and possibly cryoprecipitate is indicated. Heparin doses should be 'therapeutic' (i.e. adequate to overcome the coagulant forces that may have produced a relative heparin-resistant state in the blood). Chronic DIC with haemorrhage, or more usually thrombosis, should also be treated with heparin; warfarin is ineffective. If DIC persists because, for example, a tumour does not regress, long term outpatient subcutaneous heparin therapy may be required.
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PMID:Disseminated intravascular coagulation. Approach to treatment. 128 66


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