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

Two patients developed local gangrene after subcutaneous infiltration of vasopressin (Pitressin, Parke, Davis & Company, Detroit, Mich.) utilized for the control of bleeding from esophageal varices. In the 1st patient, ischemic gangrene resulted in transmetatarsal amputation and also necessitated skin grafts on the forearm. The 2nd patient developed gangrene and clostridial sepsis and expired. The effects of systemically administered Pitressin are reviewed and suggestion to prevent local necrosis are presented.
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PMID:Local gangrene: a complication of peripheral Pitressin therapy for bleeding esophageal varices. 30 80

Eighty four cases of meningococcal infections are reviewed. Fifty seven cases presented themselfs as meningococcal meningitis, twelve cases as sepsis with moderate hypotension and 15 cases were sepsis with septic shock. A brief course of the disease, shock, echymosis, absence of meningeal signs, leucopenia and intravascular coagulation were findings more frequent in the group of patients with hiperacute sepsis, whereas other signs as fever, headaches, vomiting and petechiae were present with equal frequency in the three groups. N. meningitis was isolated in 73% of the cases. Shock (18.85%) and intravascular coagulation (12%) were the complications more frequently found, followed by convulsions (4.81%), arthritis (4.81%), skin necrosis (4.81%), subdural efusion (3.57%), cerebral palsy (3.40%), thrombophlebitis (1.20%), recurrence (1.20%), inapropiate antidiuretic hormone secretion (1.20%) and subaracnoideal hemorrage (1.20%). The overall mortality was 10.70% and 60% of the patients which initially presented with shock and intravascular coagulation died. Autopsy findings included wide spred hemorragic lesions and intravascular thrombi in skin, mucous membranes and viscera. Adrenal hemorrhage was present in five of the six cases studied.
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PMID:[Incidence, clinical, forms and complications of meningococcal infections (author's transl)]. 41 52

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

Since Shumway carried out the first successful heart-lung transplant (HLT) in Stanford in 1981, HLT has become a new therapeutic means for patients with end-stage pulmonary disease or arterial hypertension. However, it is still rarely carried out because of a lack of donors and the complexity of the surgery and postoperative course. This review described the criteria for proper donor and recipient selection, as well as the anaesthetic and postoperative management of HLT patients at Marie Lannelongue Hospital. The lack of suitable organ grafts results, at least in part, from improper donor management. Pulmonary oedema by fluid overloading and excessive haemodilution should be carefully prevented. Low doses of catecholamines and vasopressin maintain circulatory stability and convenient organ function. The indications for HLT (primary pulmonary hypertension, Eisenmenger's complex, and end-stage bronchopulmonary disease) are all characterized by severe pulmonary hypertension, hypoxaemia and cardiac failure. Careful anaesthetic induction is required to avoid circulatory collapse. Cardiopulmonary bypass (CPB) should be started early, so that mediastinal dissection may be carried out in satisfactory haemodynamic conditions. After unclamping the aorta, circulatory support with fluid and catecholamine infusion is often required. High inspired oxygen fraction and end-expiratory positive pressure may be required because of reperfusion pulmonary oedema. Blood transfusion is often needed as there are major blood losses due to dissection of the posterior mediastinum during CPB. Postoperative catecholamine administration is prolonged over several days. Negative fluid balance is often necessary to reduce pulmonary oedema. Improvement in surgical technique, early extubation, and late prescription of steroids have reduced the incidence of tracheal complications. Acute renal failure often occurs as a result of prolonged CPB, hypovolaemia, drug nephrotoxicity and sepsis. Bacterial complications (pneumonia, mediastinitis) are the main causes of early death. After the 15th postoperative day, opportunistic infections and allograft rejection are the main complications. Since 1981, major advances in HLT recipient management resulted in improved survival rates (70-80% at 1 year, and 60-70% at 2 years for the best teams). Despite the complexity of management, and the longterm threat of obliterative bronchiolitis, HLT is, at present time, the only possibility for these young patients to recover a normal quality of life.
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PMID:[Anesthesia and intensive care for heart-lung transplantation]. 205 32

Sodium and water retention is characteristic of edematous disorders including cardiac failure, cirrhosis, nephrotic syndrome, and pregnancy. In recent years, the use of a sensitive radioimmunoassay for plasma vasopressin has implicated the role of nonosmotic vasopressin release in the water retention of these edematous disorders. In experimental studies and studies in man, it has been found that the nonosmotic release of vasopressin is consistently associated with the activation of the sympathetic nervous and renin-angiotensin-aldosterone systems. Moreover, the sympathetic nervous system has been shown to be involved in the nonosmotic release of vasopressin (carotid and aortic baroreceptors) and in the activation of the renin-angiotensin system (renal beta-adrenergic receptors). These findings have led to our proposal that body fluid volume regulation involves the dynamic interaction between cardiac output and peripheral arterial resistance. In this context, neither total extracellular-fluid (ECF) volume nor blood volume are determinants of renal sodium and water excretion. Rather, renal sodium and water retention is initiated by either a fall in cardiac output (e.g. ECF volume depletion, low-output cardiac failure, pericardial tamponade, or hypovolemic nephrotic syndrome) or peripheral arterial vasodilation (e.g. high-output cardiac failure, cirrhosis, pregnancy, sepsis, arteriovenous fistulae, and pharmacologic vasodilators). With a decrease in effective arterial blood volume (EABV). initiated by either a fall in cardiac output or peripheral arterial vasodilation, the acute response involves vasoconstriction mediated by angiotensin, sympathetic mediators, and vasopressin. The slower response to restoring EABV involves vasopressin-mediated water retention and aldosterone-mediated sodium retention. The renal vasoconstriction which accompanies those states that decrease EABV, by either decreasing cardiac output or causing peripheral arterial vasodilation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A unifying hypothesis of sodium and water regulation in health and disease. 210 96

Hyponatraemia associated with sepsis is known to have an increased morbidity and mortality. The cause of this phenomenon is unknown, but may be related to dilution of the extracellular space with retained exogenous fluid. Fluid and ion redistribution across the cell membrane of striated muscle was investigated in an animal sepsis model and compared with sham controls. The objective was to study the effect of different volumes of fluid replacement with either 0.9% saline or 5% dextrose. Significant shifts of sodium, chloride, and water occurred into the cell in all septic animals but not in controls. This trend was exacerbated by the use of dextrose for intravenous replacement even when the estimated normal fluid requirements had not been exceeded. Hyponatraemia and plasma hypoosmolality were induced only in septic animals, which received 100% of their fluid requirements as dextrose. These animals at the same time had significantly reduced extracellular and increased intracellular volumes compared with controls and the septic animals that received saline replacement. It is concluded that the hyponatraemia and plasma hypoosmolality that occurs in these animals is caused by a combination of intracellular shift of sodium and water, and dilution of the extracellular space, probably on the basis of physiological antidiuretic hormone (ADH) secretion. Dextrose (and by implication 4% dextrose/0.18% saline) is inappropriate, potentially dangerous, and should be avoided in these circumstances.
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PMID:Hyponatraemia and intracellular water in sepsis: an experimental comparison of the effect of fluid replacement with either 0.9% saline or 5% dextrose. 232 57

The redistribution of fluid and electrolytes was investigated in a hyperdynamic sepsis animal model using cecal ligation and puncture (CLP) in Wistar rats. Hyponatremia was not observed. There was a significant shift of sodium, chloride, and water from the extracellular into the intracellular space as early as 12 hours following CLP. These data suggest that the mechanism by which hyponatremia occurs in clinical sepsis is not caused by shift of fluid from the intracellular to the extracellular space as proposed by the sick cell theory. This is more likely to result from fluid retention and dilution of the extracellular space possibly on the basis of antidiuretic hormone secretion.
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PMID:Fluid and ion redistribution in skeletal muscle in an animal sepsis model. 235 91

In septic patients the clinical course of the disease is characterized by high DIT and rT3 serum concentrations as well as a low T3-syndrome. While rT3 is elevated in almost all critically ill patients, the increase in DIT is indicative of severe infection. Prolactin levels are regularly elevated in sepsis although to variable degrees. Catecholamines and vasopressin should be regarded as acute responders. The pattern of cortisol secretion is uncertain. In most situations the secretion appears to be elevated; the circadian rhythm is disturbed.
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PMID:Patterns of endocrine secretion during sepsis. 255 Sep 59

Capsule-deficient Cryptococcus neoformans (CN-CD) infection is very rare. The authors recently experienced the case of CN-CD infection with the complication of the syndrome of inappropriate antidiuretic hormone secretion (SIADH) in a 83 year old woman. She was admitted to our hospital with the complaints of fever and general fatigue on June 10, 1987. At the time of admission, there were no abnormal findings except a mildly lowered consciousness level on physical examination, there were no abnormal neurological finding nor meningeal signs. Laboratory data revealed a mild leukocytosis and hyponatremia. Chest X-P showed a few small nodular shadows scattered in both lungs. Antibiotics therapy was of no help and hyponatremia became worse. Then with the suspicion of SIADH, Demeclocycline was administered and limitation of water intake was decreased and hyponatremia improvement was used. Yeast-like fungi was detected in the venous blood culture and in the cerebrospinal fluid (cell count: 252/3) CN-CD by India-ink preparation and bacteriological nature were determined. We made a diagnosis of sepsis and meningitis by CN-CD accompanied with SIADH. In spite of Miconazole administration intravenously and intrathecally, she died 2 months after admission. The minimal inhibitory concentration (micrograms/ml) of antibiotics against the isolated CN-CD was as follows: Amphotericin B: 0.78, 5-PC: 1.56, Miconazole less than or equal to 0.05, Nystatin: 25, Ketoconazole: 0.78.
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PMID:[A case of sepsis and meningitis due to capsule-deficient Cryptococcus neoformans with SIADH]. 269 39

Sodium and water retention is characteristic of edematous disorders including cardiac failure, cirrhosis, nephrotic syndrome and pregnancy. In recent years the use of a sensitive radioimmunoassay for plasma vasopressin has implicated the role of nonosmotic vasopressin release in the water retention of these edematous disorders. In experimental studies and studies in humans it has been found that the nonosmotic release of vasopressin is consistently associated with activation of the sympathetic nervous and renin-angiotensin-aldosterone systems. Moreover, the sympathetic nervous system has been shown to be involved in the nonosmotic release of vasopressin (carotid and aortic baroreceptors) and activation of the renin-angiotensin system (renal beta-adrenergic receptors). These findings have led to our proposal that body fluid volume regulation involves the dynamic interaction between cardiac output and peripheral arterial resistance. In this context neither total extracellular fluid (ECF) volume nor blood volume are determinants of renal sodium and water excretion. Rather, renal sodium and water retention is initiated by either a fall in cardiac output (e.g. ECF volume depletion, low-output cardiac failure, pericardial tamponade or hypovolemic nephrotic syndrome) or peripheral arterial vasodilation (e.g. high-output cardiac failure, cirrhosis, pregnancy, sepsis, arteriovenous fistulae and pharmacologic vasodilators). With a decrease in effective arterial blood volume (EABV), initiated by either a fall in cardiac output or peripheral arterial vasodilation, the acute response involves vasoconstriction mediated by angiotensin, sympathetic mediators and vasopressin. The slower response to restoring EABV involves vasopressin-mediated water retention and aldosterone-mediated sodium retention. The renal vasoconstriction which accompanies those states that decrease EABV, by either decreasing cardiac output or causing peripheral arterial vasodilation, limits the distal tubular delivery of sodium and water thus maximizing the water-retaining effect of vasopressin and impairing the normal escape from the sodium-retaining effects of aldosterone. The elevated glomerular filtration rate and filtered sodium load in pregnancy allows increased distal sodium and water delivery in spite of a decrease in EABV, thus limiting edema formation during gestation.
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PMID:Pathophysiology of vasopressin in edematous disorders. 269 4


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