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

Most techniques described in animal models of pancreatic transplantation use either segmental or autotransplants. We employ a technique of pancreaticoduodenal allotransplantation in the dog that closely resembles the operation used in humans. The arterial supply of the entire pancreatic graft is preserved by procuring a Carrel patch of aorta encompassing the origin of the celiac and the superior mesenteric arteries. Splenic, inferior pancreaticoduodenal, and superior pancreaticoduodenal arteries remain intact with the graft. Venous drainage is through a short segment of portal vein. A 6-cm cuff of duodenum is taken with the head of the pancreas. Engraftment proceeds by placing the allograft within the peritoneal cavity of the recipient. End-to-side vascular anastomoses are constructed to distal aorta and inferior vena cava. The duodenal cuff is anastomosed to the dome of the bladder for drainage and analysis of exocrine secretions and to provide a port of entry for cystoscopically directed needle biopsy. A total pancreatectomy is performed to induce a state of diabetes. The average operating time is 5 h. Twenty-two dogs have undergone allotransplantation using this technique. Six dogs had no complications and were sacrificed after meeting criteria of their study protocol. There were three technical failures, two arterial thromboses and one exsanguination, yielding an 86% rate of successful engraftment. Three other dogs died of intussusception and three dogs died of sepsis, one secondary to wound dehiscence and one due to inadvertent common bile duct ligation during pancreatectomy. Wound problems, four dehiscences and two superficial infections, occurred only in immunosuppressed dogs.
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PMID:Canine pancreaticoduodenal allotransplantation with cystoduodenostomy: an animal model with clinical application. 248 44

126 cases of sepsis were retrospectively studied in an Internal Medicine Department, giving special attention to the clinical evolution. 67 males and 59 females with a median age of 65 years old were discovered. 92% had one or more diseases, mainly COLD (30%) and diabetes mellitus (28%). The septic sources were urinary (37%) and respiratory (31%). 84% of the germs were gram (-), mainly E. Coli and Proteus sp. A mortality rate of 36% was found, the primary rates being: eighth decade (52%), patients with neoplastic disease (46%), biliary tract diseases (64%), endocarditis (66%), infection by Serratia (60%), Pseudomonas (50%), shock (55%) and DIC (50%). These last two complications were analysed and found to be the more frequent (35% and 6.3% respectively), also being those with higher mortality rate. Finally, the prognostic factors are established based on the results obtained.
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PMID:[Sepsis: clinical course study of 126 patients in an internal medicine department]. 249 19

Causes of death were analyzed for 63 diabetic patients treated with hemodialysis. In all cases, autopsy-based death certificates were evaluated. The causes of death were compared during the periods 1969 through 1979 versus 1980 through 1987, and the causes of death in patients who died after less than 18 months versus those who died greater than 18 months after starting hemodialysis treatment. Our population of decreased diabetics had a mean age of 41.8 years, with a mean of 23.4 years of diabetes duration. The mean age at manifestation of diabetes was 18.2 years. Cardiac failure has been shown to be the most prevalent cause of death (55.6%), while sepsis accounted for 20.6% of the deaths. In both the period from 1969 through 1979 and that from 1980 through 1987, cardiac failure was identified as the commonest cause of death, with an equal proportion of septic causes (i.e., 20% versus 21.05%). When comparing causes of death among diabetics on hemodialysis for less than 18 months versus those receiving greater than 18 months of treatment, cardiac failure was responsible for 54% versus 61.5% of deaths. Septic causes were found to be more prevalent after a longer duration of treatment (i.e., 30.8%). Therefore, it is concluded that to prevent cardiac deaths, blood pressure control has to be as tight as possible in patients with diabetic kidney disease. To prevent late-occurring septic deaths, good nutritional status in patients undergoing hemodialysis seems to be of importance. The prevention of macroangiopathy in diabetes represents a major medical problem that needs to be solved.
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PMID:Causes of death in insulin-dependent diabetic patients treated with hemodialysis. 252 60

Five hundred and thirty-three patients in the Oxford renal unit were reviewed to determine the incidence of infection in one calendar year. There were 310 patients who received dialysis, 53 with acute renal failure and 211 with chronic renal disease. Renal transplant patients were not included in the study. Apart from infections related to dialysis access, patients on maintenance haemodialysis or continuous ambulatory peritoneal dialysis developed few serious infections unless they had another disease causing suppression of immune function. A total of 97 urinary tract infections were seen; in patients with chronic renal disease not receiving dialysis the incidence of urinary tract infection was significantly associated with increasing uraemia, with diabetes, and with treatment with azathioprine or cyclophosphamide. In patients with acute renal failure, Gram-negative septicaemia and fungal infections were important causes of morbidity and mortality, but cardiovascular disease caused 42 per cent of the deaths unlike results from other series where sepsis has been by far the commonest cause of death.
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PMID:Infections in a renal unit. 259 47

Of 400 patients with acute, chronic or chronic relapsing pancreatitis surveyed in the present study, only 54 had had ECG in their files. Among these, 80% showed ECG alterations, mostly sinus tachycardia and diffuse disturbances of ventricular repolarization. The causes of these alterations are, as yet controversial. Some explanations for these alterations are hypovolemia, sepsis and acute inflammatory state. Other important findings in the patients were bundle branch block, not encountered either before the pancreatic crisis or after its resolution, nor was dielectric effect and lesion current observed in either the acute and chronic forms. The possibility of the presence of previous cardiopathy in patients with high alcoholic intake, Chagas' disease, high blood pressure or diabetes, which are quite likely in these patients, should be recalled as important factors: marked electrolytes disorders were not frequent and did not correlate with ECG findings. The aim of this study is to highlight the importance of ECG during systematic search in the follow-up of patients with pancreatitis, in order to better understand associated cardiac disorders and to improve diagnosis, prevention and treatment.
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PMID:[Electrocardiographic changes in pancreatitis]. 260 72

The best definition of risk factors for renal injury, irrespective of the aetiological agent, comes from observations in patients with acute renal failure. From such observations, two subdivisions have evolved, i.e., acute insults and host risk factors. Acute renal insults include: hypertension, sepsis, use of nephrotoxic drugs (e.g., aminoglycoside antibiotics and contrast media), haemoglobinuria or myoglobinuria, liver disease and extracellular volume depletion. Host risk factors include: advanced age, hypertension, gout and hyperuricaemia, diabetes mellitus, chronic renal failure and use of diuretics. Furthermore, the mechanism of acute renal injury can be correlated with different risk factors: for a tubular toxic agent, acting either directly on the cells or haemodynamically, a dose-dependency is characteristic; while for immunologically mediated injury, genetic predisposition is more important. The identification of risk factors for chronic toxic injury is confounded by the possibilities of multiple episodes of subclinical renal injury, the distinct possibility that a major component of the ageing process may be a loss of renal reserve, and a progressive body burden, of, e.g., cadmium, which may deplete intrinsic protective mechanisms. However, clinically relevant risk factors can alert the clinician to exercise additional caution when prescribing medications that are potentially nephrotoxic. Such factors include dehydration, pre-existing renal disease, age, co-existing diseases that cause renal ischaemia, gender, concomitantly administered drugs, and electrolyte abnormalities.
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PMID:Risk factors for toxic nephropathies. 265 33

The pathophysiology and pathologic appearances of adult osteomyelitis are discussed, without reference to childhood hematogenous (metaphyseal) osteomyelitis or chronic osteomyelitis secondary to vascular phenomena such as diabetes or arteriosclerosis. Osteomyelitis as a feature of generalized sepsis in the immunocompromised patient is also excluded. The focus is on infection of the adult skeleton that occasionally arises spontaneously but more commonly presents as a complication of an open fracture or an operative procedure. The special features of adult osteomyelitis that are the result of the infection developing within the confined and rigid structure of the skeleton are highlighted. Lastly, the histopathology of osteomyelitis is examined in an effort to demonstrate the host bone's response to this injury.
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PMID:The pathogenesis of adult osteomyelitis. 265 95

The principle of iron conservation is the basis of iron metabolism; the normal basal loss of iron from the body is about 1 mg daily in a 70 kg man and 0.8 mg in a 55 kg woman. Iron is lost mainly by the menstrual and gastrointestinal routes. The total iron requirement during pregnancy is 800 mg; in the last month the requirement may amount to 7 to 8 mg/day. Supplementary iron is recommended for many menstruating women, and during the latter part of pregnancy. Correct fetal iron metabolism is ensured by proper maternal iron status, although there are contradictory opinions and findings about the relationship between maternal and fetal iron metabolism. Preterm infants fed on breast milk have a negative iron balance, and require an iron intake of about 0.6 mg/kg/day, and 3.4 mg/1 g haemoglobin, to compensate for intestinal and venesection iron losses, respectively. The absorption of supplementary iron by the preterm infant is a linear function of intake. Preterm infants do not require iron supplements when given repeated blood transfusions. During lactation the total iron losses of the mother are 1 mg/day, and thus no supplementary iron is needed if the iron metabolism has been in balance during the pregnancy. Serum ferritin concentration decreases continuously when iron stores in the body are reduced, and totally empty iron stores are the only known reasons for low serum ferritin concentration. Despite depleted iron stores, serum ferritin concentration can be normal or higher than normal in protein-energy malnutrition, up to 3 months after major surgery, in acute liver damage, in some patients with prolonged hyperglycaemia due to diabetes mellitus, in acute lobar pneumonia, active pulmonary tuberculosis and rheumatoid arthritis on gold therapy, in sepsis secondary to marrow hypoplasia induced by chemotherapy, in heavy drinkers and for a few days after myocardial infarction. In haemochromatosis, iron is deposited in liver (producing fibrosis), pancreas, endocrine glands and heart. The rise in the level of iron in the body is due to increased absorption and/or increased intake. This pathology may occur in transfusions, in alcoholism (especially when alcoholic beverages are contaminated with iron and the diet is low-protein), in several liver diseases, in congenital transferrin deficiency and in idiopathic disease. Patients susceptible to haemochromatosis should receive a low-iron diet. Serum ferritin determination may be helpful in early identification of susceptible members of a family with idiopathic familial haemochromatosis, but transferrin saturation is not a good indicator of either iron depletion or iron overload.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Clinical pharmacokinetics of iron preparations. 267 7

The present study examined whether sepsis exacerbates the diabetes-induced peripheral and hepatic insulin resistance. Vascular catheters were placed in diabetic (70 mg/kg streptozotocin, 4-wk duration) and nondiabetic rats, and sepsis was produced by subcutaneous injections of live Escherichia coli. Basal glucose metabolism was determined with the use of [3-3H]glucose initiated 18 h after the first injection of bacteria. Thereafter, in vivo insulin action was assessed with the use of the euglycemic hyperinsulinemic clamp technique. Sepsis in nondiabetic rats produced a 57% reduction in the maximal responsiveness for the insulin-induced increase in total glucose utilization compared with nondiabetic nonseptic animals. Diabetes alone decreased both insulin sensitivity and responsiveness. When the septic insult was superimposed on the diabetic condition, the maximum responsiveness was unchanged compared with non-septic diabetic rats, but the 50% maximally efficient dose was reduced from 817 to 190 microU/ml, suggesting an improvement in insulin sensitivity. Sepsis did not alter the insulin-induced suppression of hepatic glucose output in either nondiabetic or diabetic animals. Sepsis increased the plasma concentrations of epinephrine, norepinephrine, glucagon, and corticosterone in both nondiabetic and diabetic rats; however, the elevation in catecholamines and glucagon was 65 to 250% greater in the diabetic animals. These results indicate that hypermetabolic sepsis produces peripheral insulin resistance in nondiabetic rats but does not worsen the preexisting insulin resistance in diabetic animals, despite the higher prevailing blood levels of glucagon and catecholamines.
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PMID:Sepsis-induced changes in in vivo insulin action in diabetic rats. 267 27

Postoperative treatment after pancreas surgery is concentrated on the function of the exocrine and endocrine part of the gland. While functional disturbances of the endocrine pancreas may give rise to serious problems associated with diabetes, functional disturbances of the exocrine pancreas are less important. On the other hand, flow disorders of the exocrine pancreas may lead to pancreatitis, fistulas, cysts, and abdominal sepsis. Pancreatic tumours are not infrequently apudomas whose biology has an important bearing on the after-treatment. Thrombophlebitic splenomegaly may lead to portal and possibly to segmental portal hypertension. In this event, a careful follow-up examination will be needed to decide whether further surgery is necessary.
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PMID:[After-care following surgery of the pancreas]. 267 64


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