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

The case studies of four patients with post-transplantation calcinosis are presented. Three of the four patients died of inanition and sepsis secondary to infection of extensive soft tissue ulcers and diffuse cutaneous vascular calcification with gangrene. The fourth patient survived following removal of all four parathyroid glands and autografting of approximately one-half of one gland. Common to the patients was secondary hyperparathyroidism, elevated mean serum calcium levels after transplantation, and radiographic evidence of small and medium vessel calcification. No other differences could be found between these patients and other patients with post-transplantation hyperparathyroidism without calcinosis. In the face of apparently minor complaints of lower extremity discomfort, elevated parathyroid hormone levels (PTH) and positive xerography may indicate subtotal parathyroidectomy regardless of the serum calcium level.
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PMID:Lethal post-transplantation calcinosis. 37 90

On March 26, 1970, a 33-year-old male suffered intestinal infarction which required total enterectomy and duodeno-transverse colostomy. Nutrition was maintained in the hospital by daily parenteral feeding for 2 months postoperatively, after which parenteral feedings were decreased and stopped for long periods. Various oral dietary regimens failed to provide adequate nutrition, and the patient lost 40 kg and became severely malnourished during the next 13 months. In June 1971, supplemental home parenteral nutrition (PN) via an arteriovenous fistula was instituted on a 3 or 4 nights per week basis. The patient's weight and strength increased markedly after institution of the home supplemental PN program. The first fistula became occluded after 9.5 months of home PN use and subsequent successive fistulae have remained patent for 31.3, 8.8, and 5.5 months of use. The patient prepares his own PN fluids at home, using a commercial device for filling plastic intravenous fluid bags. Although several different types of fluid have been used, the current mixture of 25% glucose and 2.75% amino acids with added vitamins, potassium, calcium, magnesium, and insulin plus simultaneously administered lipid emulsion has proven most effective. Only when the patient's low fat, low oxalate diet is supplemented with this parenteral mixture 4 nights each week is he in positive nitrogen, phosphorus, and magnesium balance. However, his negative calcium balance is only partially corrected. There has been no sepsis, embolism, or fistula infection during 5 years of home PN.
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PMID:Parenteral nutrition at home for 5 years via arteriovenous fistulae. Supplemental intravenous feedings for a patient with severe short bowel syndrome. 40 51

A 52-year-old man with mild diabetes and acute stem cell leukaemia developed an orbitofacial mucormycosis. Cultures showed the fungus to be Rhizopus oryzae. Vigorous treatment with amphotericin B and other bactericidal and bacteriostatic antibiotics for a concurrent sepsis failed to suppress the infections, and the patient died. On post-mortem examination characteristic haematoxylin-staining, broad, aseptate fungal hyphae were found in the right eye, orbit, and lung. A striking and unusual feature of this case is the presence of brightly birefringent crystals within the severely degenerated eye. These were found by histochemical staining and x-ray diffraction studies to be calcium salts of fatty acids, apparently liberated from necrotic adipose tissue of the orbit.
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PMID:Orbitofacial mucormycosis with unusual pathological features. 50 83

In conclusion, patients on chronic maintenance dialysis have an increased incidence of death from cardiovascular disease. Hypertension plays a major role, and these patients must be carefully monitored for complete control of blood pressure. Adequacy of ultrafiltration to maintain normal extracellular volume is an essential part of the dialytic treatment. Hypertensive patients should be screened for excessive renin secretion because of its possible role in unresponsive hypertension in patients on dialysis. Nephrectomy should be used when necessary, where dialysis and antihypertensive medication have not adequately controlled blood pressure. Patients must be monitored for the presence of pericardial disease to avoid subsequent pericardial effusion and the development of constrictive pericarditis with its adverse effect on myocardial function. When constrictive pericarditis is present, it obviously should be relieved by appropriate surgery. Efforts should be made to minimize cardiac output in hemodialysis patients. Whether or not routine transfusions to maintain a higher hematocrit are indicated is a question that cannot yet be answered. However, patients with marginal cardiovascular function who are accepted on hemodialysis and must have an arteriovenous shunt should be supported in any manner to minimize an increase in cardiac output. Early and aggressive treatment of known episodes of sepsis is important in the elimination of valvular endocarditis in this patient population. Perhaps one of the finer indicators of adequacy of hemodialysis will be K rate and peak immunoreactive insulin levels. Continued abnormality of these parameters may contribute to cardiovascular disease. Clearly, further study of the effect of abnormal carbohydrate metabolism on lipid metabolism is in order. Serum triglyceride, serum cholesterol and lipid electrophoretic pattern should be followed to evaluate the beneficial effects of drug therapy and changes in dialytic technique on the development of cardiovascular disease. Careful monitoring of calcium, phosphorus, bone films and parathyroid hormone levels is indicated to assess parathyroid status. The use of aluminum binders and parathyroidectomy to prevent vascular and myocardial calcification is important in the therapy of these patients. The use of cardiac catheterization, coronary artery arteriography, and possibly cardiac vascular repair, should be considered in the chronic hemodialysis patient with coronary artery disease if he is otherwise well. Adequacy of hemodialysis perhaps can be evaluated through its effect on all of the above parameters. Whether or not changes in artificial kidney treatments can correct the final vascular disease remains to be seen.
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PMID:Cardiovascular disease in uremic patients on hemodialysis. 109 1

The effects of sepsis on the ATP-dependent Ca2+ transport in rat liver plasma membranes were investigated. Sepsis was induced by cecal ligation and puncture (CLP). Control rats were sham-operated. The results show that the ATP-dependent Ca2+ transport by liver plasma membranes was not affected during early sepsis (9 hr after CLP) but was decreased by 30-50% (P < 0.05) during late sepsis (18 hr after CLP). Kinetic analysis of the data indicates that during late sepsis, the Vmax values for ATP and for Ca2+ were decreased by 38.5% (P < 0.05) and 41.8% (P < 0.05), respectively, while the Km values for ATP and Ca2+ remained unchanged. Mg2+ stimulated ATP-dependent Ca2+ transport. The Mg(2+)-stimulated activity was unaffected during early sepsis but was decreased by 34-63% (P < 0.05) during late sepsis. These data demonstrate that ATP-dependent Ca2+ transport in rat liver plasma membranes was impaired during late sepsis and that the impairment is associated with a mechanism not affecting the affinity of the Ca2+ transporter for ATP and Ca2+. Since plasma membrane ATP-dependent Ca2+ transport plays an important role in the regulation of intracellular Ca2+ homeostasis in hepatocytes, an impairment in the ATP-dependent Ca2+ transport by liver plasma membranes during late sepsis may have a pathophysiological significance in contributing to the development of altered hepatic metabolism during septic shock.
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PMID:Calcium transport by rat liver plasma membranes during sepsis. 129 87

Ten patients with calcitriol-resistant rickets caused by a defect in the ligand-binding domain of the vitamin D receptor are described. Eight patients, 1.7 to 13.8 years of age, received high doses of elemental calcium (range, 0.4 to 1.4 gm/m2) through indwelling intracaval catheters for periods of 1.8 to 3.8 years. Two other patients, aged 1.1 and 2.2 years, were given oral calcium therapy as the sole mode of treatment. In five of the intravenously treated patients, oral calcium therapy was initiated after radiologic evidence of healing of the rickets. To maintain normal serum calcium concentration, the patients required daily doses of elemental calcium of 3.5 to 9 gm/m2 body surface area. Clinical improvement was observed within a week of the start of intravenous therapy, with disappearance of bone pain; several of the younger patients started to walk for the first time. Growth velocity increased within 2 to 3 months, from a pretreatment rate of -0.8 to -6.3 standard deviation score (SDS), to a posttreatment rate of +0.1 to +5.1 (SDS). Serum calcium, parathyroid hormone, phosphorus, and alkaline phosphatase values returned to normal within a year. Radiologic signs of healing occurred more rapidly in the intravenous treatment groups and in younger patients. Episodes of septicemia occurred frequently in those receiving parenteral therapy and required replacement of the catheter. We recommend that in the treatment of calcitriol-resistant rickets, oral calcium therapy be started at the youngest possible age, in doses to the limit of intestinal tolerance. When rickets is present, calcium should be infused through a large vessel in doses high enough to produce normocalcemia, normophosphatemia, and suppression of parathyroid hormone. Only after radiologic healing has been observed can oral calcium therapy be introduced.
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PMID:Calcium therapy for calcitriol-resistant rickets. 133 89

Intra-abdominal sepsis was induced in rats by implanting into their abdominal cavities fecal-agar pellets impregnated with Escherichia coli and Bacteroides fragilis. Sham-operated rats received sterile pellets. A group of sterile- and septic-implanted rats was treated intraperitoneally with diltiazem (1.2 mg/kg) 8 h after implantations. Septic- and sterile-implanted rat hepatocytes were loaded with 1) the fluorescent dye indo-1 to quantify hepatocyte basal and vasopressin (100 nM)-elevated cytosolic Ca2+ concentration and 2) 45Ca to quantify Ca2+ flux and cellular content of exchangeable Ca2+. Lipid peroxidation was determined by measuring conjugated dienes (CD) and thiobarbiturate-reactive substances (TBA-RS) in liver homogenates. In septic-implanted rats, the basal cytosolic [Ca2+], cellular exchangeable Ca2+, Ca2+ flux, CD, and TBA-RS were significantly higher than in sterile-implanted rats. Although vasopressin caused a significant elevation in cytosolic [Ca2+] in septic rat hepatocytes, the magnitude of this elevation was significantly smaller than that found in the sterile group. Diltiazem treatment of septic rats significantly decreased basal cytosolic [Ca2+], cellular exchangeable Ca2+ content, Ca2+ flux, CD, and TBA-RS. Also, vasopressin-induced increase in hepatocyte cytosolic [Ca2+] in diltiazem-treated septic rats was significantly greater than that observed in untreated septic rats. Both Ca2+ and membrane lipid alterations were attenuated with diltiazem treatment of septic rats. These results suggest that prevention or attenuation of Ca2+ channel-mediated Ca2+ influx restores both Ca2+ homeostasis and membrane lipid alteration.
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PMID:Ca(2+)-related hepatocellular alterations during intra-abdominal sepsis. 141 41

Pancreatic complications following cardiopulmonary bypass are infrequent but are associated with high mortality. All cases of pancreatic complications following cardiopulmonary bypass from 1972 to 1987 at a single institution were retrospectively reviewed. Of 5621 patients who underwent cardiopulmonary bypass, 25 (0.44%) sustained pancreatic complications. There were 15 cases of acute pancreatitis and 10 cases of pancreatic necrosis, with 11 deaths in the group reviewed, a mortality rate of 44%. Factors that were correlated with mortality associated with pancreatic complications in this study include preoperative hypotension, preoperative use of inotropic agents, and renal failure (preoperative and postoperative). Factors that have been previously associated with mortality from pancreatic complications in other studies, such as fluid sequestration, respiratory failure, sepsis, tachycardia, hypocalcemia, age greater than 55 years, and abnormal laboratory findings, were not found to be significantly associated with mortality in this study. Of the five patients for whom complete data were available, not one patient received greater than 800 mg of calcium per square meter of body surface area in the perioperative period. While the exact mechanism of pancreatic injury remains unclear, based on experimental studies and clinical correlation, it is likely that pancreatic ischemia remains a significant contributing factor. We conclude that no factor specifically associated with cardiopulmonary bypass was correlated significantly with mortality.
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PMID:Pancreatic complications following cardiopulmonary bypass. Factors influencing mortality. 141 91

Calcium is essential for normal cellular function. However, increases in cell calcium are also involved in cellular dysfunction and death by activating destructive enzymatic processes such as proteases, nucleases, and lipases. Since ionized hypocalcemia is common during sepsis, calcium is often administered in an attempt to normalize circulating levels. Previous studies using endotoxin and large amounts of calcium demonstrated increased mortality in calcium-treated animals. This study extends these preliminary data to endogenous sepsis (cecal ligation) and low dose calcium therapy. Sprague Dawley rats (n = 9 per group) had jugular catheters placed and their cecums ligated. They were randomized to an infusion of D5W at 1 ml/hr, calcium chloride at 4 mg/ml/hr (Low Ca), or calcium chloride at 6 mg/ml/hr (High Ca) for 24 hr. An additional group of animals received calcium chloride at 6 mg/ml/hr but had no surgery. Animals were followed for 24 hr survival. A separate group of animals (n = 6 per group) was prepared in a similar manner. Blood was obtained 6 hr following cecal ligation for circulating endotoxin concentrations, and animals were sacrificed. Calcium infusion increased ionized calcium levels slightly (low Ca, 1.12 +/- .06 to 1.21 +/- .09; high Ca, 1.06 +/- .04 to 1.16 +/- .05; P less than 0.05). Survival (24 hr) was 100% in the nonseptic controls and D5W septic animals, 67% in the low Ca septic group, and 44% (P less than 0.05) in the high Ca septic group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Low dose calcium administration increases mortality during septic peritonitis in rats. 142 13

We describe an adult patient who developed persistent hypercalcemia while bedridden for more than three months with pancreatitis and sepsis. On the basis of hypercalciuria, suppressed serum intact PTH, suppressed serum 1,25-dihydroxy vitamin D3 and no clinical evidence of malignancy, the diagnosis of immobilization hypercalcemia was established His hypercalcemia improved during treatment with saline, calcitonin and/or etidronate. With active mobilization and weight-bearing exercises, serum calcium finally normalized. We discuss clinical and laboratory features as well as current modalities of treatment of this rare form of hypercalcemia in adults.
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PMID:Immobilization hypercalcemia in an adult patient with pancreatitis and sepsis: case report. 148 89


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