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

Postoperative acute renal failure, especially associated with oliguria, carries a high rate of mortality and morbidity. This complication can frequently be avoided if physicians are knowledgeable about preventable or modifiable risk factors. Patients who have underlying renal disease, sepsis, volume depletion or other conditions associated with renal hypoperfusion, or who have severe liver disease, are at particular risk. Exposure to nephrotoxic agents and wide fluctuations of intravascular volume are key conditions that can usually be minimized. Managing patients with chronic advanced renal failure (creatinine clearance 10 to 25 ml per minute) requires close interaction between the internists, anesthesiologists and surgeons. Understanding associated metabolic and organ system disorders is necessary to prevent complications and preserve remaining renal function. Chronic renal failure should not be a contraindication to an elective or emergent surgical procedure.
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PMID:Preserving renal function in surgical patients. 357 22

An enhanced frequency and morbidity of urinary tract infections (UTI) have been observed in association with alcoholism and liver disease. The causes of these phenomena may relate, in part, to the defects in humoral and cellular immune mechanisms that occur in alcoholism. Urinary catheterization is the most common cause of UTI in hospitalized alcoholics. The severity of the sequelae of UTI in alcoholism is demonstrated by the unusually frequent occurrence of renal papillary necrosis (RPN) in conjunction with pyelonephritis in these patients. Indeed, in over 90% of the reported cases of RPN occurring with alcoholism or liver disease, pyelonephritis has been a contributing factor. The proclivity to medullary ischemia and RPN in this patient group may be, at least in part, a result of interstitial renal edema secondary both to infection and the effect of ethanol per se and to renal arterial vasoconstriction that occurs in cirrhosis. The frequency with which death due to sepsis or renal failure occurs in association with UTI in alcoholics obliges the physician to exercise caution in the prevention and treatment of UTI in these patients.
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PMID:Urinary tract infections and renal papillary necrosis in alcoholism. 370 22

Kingella kingae is a rare human pathogen. Most reported infections are in children and involve endocardium, vascular space, and skeletal tissues. We report herein two cases of K. kingae infection recently seen in adults. Kingella kingae caused acute meningitis in a patient with sickle cell anemia and in the second patient with alcoholic liver disease, sepsis with a petechial rash. The clinical presentation due to K. kingae closely resembled that caused by related Neisseria genus.
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PMID:Manifestations of Kingella kingae infections in adults: resemblance to neisserial infections. 370 97

Gamma-aminobutyric acid (GABA) is a potent amino acid neurotransmitter that suppresses normal neuronal activity in the central nervous system. Recently it has been suggested that GABA may play an important role in the pathogenesis of hepatic encephalopathy. In the present study GABA production by 8 common bacterial pathogens was measured during mid-log, stationary and mid-death phases of growth. All bacteria produced some GABA (range: 160-50 250 pmole/ml) with the majority of GABA production occurring during the mid-death phase of growth. These results suggest that the depressed levels of consciousness seen in patients with overwhelming sepsis or advanced liver disease and extraintestinal infection may in part be secondary to increased bacterial GABA production.
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PMID:Gamma-aminobutyric acid (GABA) production by eight common bacterial pathogens. 377 73

Sepsis, peritonitis, and gastroenteritis developed in a 45-yr-old homosexual man 1 day after ingestion of raw oysters. The patient had chronic active hepatitis and cirrhosis with hepatitis B virus and delta-infection. He also had persistent generalized lymphadenopathy associated with HTLV-III antibody positivity. Vibrio vulnificus was isolated from the patient's blood and peritoneal fluid as well as from the same batch of oysters at the restaurant where the patient had visited. To our knowledge, this is the first report relating direct microbiologic and clinical evidence that the infection is acquired through the gastrointestinal tract by consuming raw seafood containing the pathogen. This is also the first reported case of peritonitis associated with sepsis and gastroenteritis from this organism. Patients with liver disease and other immunocompromised states should be warned about such life-threatening infections and complications associated with the consumption of raw oysters or other undercooked seafoods.
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PMID:Vibrio vulnificus infection after raw oyster ingestion in a patient with liver disease and acquired immune deficiency syndrome-related complex. 381

We analyzed the clinical data and liver histology for iron overload in 74 renal allograft recipients. Twenty of the 74 patients had histological evidence of hemosiderosis. Four patients had hemochromatosis. Of the 2 noninvasive diagnostic tests the serum ferritin level was more reliable than percent saturation of transferrin in predicting the histological diagnosis of hemosiderosis. Of the 20 patients with hemosiderosis 14 died either from liver failure or concomitant sepsis. Female patients and those who received long-term dialysis had higher susceptibility for developing hemosiderosis. Of the 6 patients treated with phlebotomies, the response was good in 4 and incomplete in 2. Hemosiderosis and hemochromatosis should be considered in the differential diagnosis of posttransplant liver disease. Intermittent phlebotomies if carried out early may prevent the progression of hemosiderosis to micronodular cirrhosis.
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PMID:Hemosiderosis and hemochromatosis in renal transplant recipients. Clinical and pathological features, diagnostic correlations, predisposing factors, and treatment. 390 17

After noting that hepatic failure was the leading cause of death in our transplant recipients whose renal allografts had functioned for more than five years, we reviewed retrospectively the post-transplant course of these patients to assess the long-term effect of liver disease in this population. Sufficient data was available to evaluate 184 of 217 long-term survivors (85%). Twenty-six patients (14%) experienced a doubling of SGOT and/or SGPT of greater than six months' duration and were defined as having chronic liver disease. The etiology of chronic liver disease was identified in 14 patients (54%), of whom 11 were HBsAg positive. Evidence of chronic hepatitis developed in only six of 26 patients (22%) during the first four years post transplant. Once enzyme abnormalities occurred, they were unremitting until death or end of the study in 73% of patients. Actuarial survival of patients with chronic liver disease was markedly decreased compared to long-surviving transplanted controls. Ten of the 12 deaths in patients with hepatocellular abnormalities were due to hepatic failure, of which eight occurred in the setting of extrahepatic sepsis. Chronic liver disease is a late complication of transplantation and is associated with significant mortality due to an increased susceptibility to overwhelming sepsis.
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PMID:Liver disease in recipients of long-functioning renal allografts. 391 Sep 17

Despite the fact that the clinical experience with TPN has been gathered from patients of all age groups suffering from a variety of underlying diseases running very different clinical courses and often complicated by a number of septic metabolic and therapeutic problems, certain points can be made with regard to predisposing factors. 1) Prematures and neonates are particularly at risk. 2) Cholestasis occurs earlier and has a greater chance of leading to chronic liver disease in surgical patients. 3) Hepatobiliary abnormalities are more likely to develop after a prolonged period of TPN and are less frequent in patients who are also receiving oral feedings. Definition of the mechanism of hepatobiliary complications remains a problem. Although calcium bilirubinate appears to be responsible for sludge and stones, there is as yet no explanation for the presence of large amounts of indirect-reacting bilirubin in gallbladder and hepatic bile in patients on TPN. The pathogenesis of cholestatic liver disease remains an enigma; the lack of normal gastrointestinal stimuli for bile formation, abnormalities of bile acid metabolism, and sepsis might play roles, but attention has recently been attracted to amino acid toxicity and this possibility deserves further study.
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PMID:Hepatobiliary complications associated with TPN: an enigma. 393 7

Factors associated with prolongation of the prothrombin time were analyzed in 94 patients with intra-abdominal sepsis. Patients were randomized prospectively to receive either the combination of tobramycin and clindamycin (TM/C) or moxalactam (MOX). This paper presents a retrospective review designed to compare the frequency of prolonged clotting times and to analyze predisposing factors. Prothrombin time (PT) prolongation occurred more frequently in patients given moxalactam (19 of 47 patients) than in patients given the combination of tobramycin and clindamycin (9 of 47 patients) (p less than 0.05). Prolongation of the partial thromboplastin time (PTT) occurred in all patients with a prolonged PT. Liver disease, upper gastrointestinal surgery, and use of cimetidine were more frequent in those patients with abnormal PT/PTT values (p less than 0.05). Two moxalactam-treated patients with subsequent PT/PTT prolongation had individual clotting factors assayed before moxalactam treatment and at the time of detection of the abnormal PT. The activity of clotting factors II, VII, VIII, IX, X, and XII was reduced during MOX therapy. Treatment with vitamin K reversed the abnormality. In view of underlying abnormalities and rapid response to parenteral vitamin K, the mechanism is probably an acute vitamin K deficiency superimposed upon chronic vitamin K deficiency. In patients with intra-abdominal infection, those treated with MOX are more likely to develop abnormal PT than those treated with TM/C. Since abnormal PT/PTT was common even in TM/C patients, supplemental vitamin K should be considered for all seriously ill, older patients with abdominal infections.
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PMID:Clinical risk factors for prolonged PT/PTT in abdominal sepsis patients treated with moxalactam or tobramycin plus clindamycin. 396 31

Seven hundred and sixty cardiorespiratory studies, from 151 critically ill or high-risk general surgical patients with extrapulmonary (S) or pulmonary (P) sepsis, cirrhotic liver disease (L), or cardiac failure (C), were analyzed to assess the determinants of a simple, easily obtained measure of respiratory oxygen exchange, the respiratory index (RI). The pattern of cardiorespiratory abnormalities was studied and correlated with the change in RI. The most important relations were with shunt (QS/QT), mixed venous O2 (PvO2), VD, and VE. Higher F1O2 and positive end-expiratory pressure (PEEP) were needed as the RI rose, indicating a greater severity of illness. Regression analysis of all types of critically ill patients and surgical controls showed that QS/QT, PvO2, and F1O2 interacted together to explain most of the variability of the RI. The regressions in each homogeneous patient disease category were all highly significant (p less than .0001) but had somewhat similar coefficients and explained the variability in RI to different degrees. The data suggest that patients with extrapulmonary sepsis or cirrhotic liver disease have an increase in RI (over that in controls) primarily due to a large increase in CI at the high QS/QT caused by the ventilation/perfusion (VA/QT) maldistribution characteristic of these diseases. However, patients with P or C have a disproportionate rise in RI at any given QS/QT compared to that in high-flow states alone, suggesting in P a direct alveolar limitation of oxygen exchange over and above any level of VA/QT mismatching, and suggesting in C a disproportionate decrease in PvO2 that magnifies the QS/QT effect even though VA/QT is more uniform.
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PMID:The physiologic meaning of the respiratory index in various types of critical illness. 407 5


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