Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma kallikrein releases bradykinin when activated by gram-negative septicemia or irreversible hemorrhagic shock. Pancreatitis releases glandular kallikrein causing hypotension and increased vascular permeability. Bradykinin in the brain produces hypertension. Renal kallikrein is released by high arterial pressure, vasodilators, low doses of noradrenaline, angiotensin II, mineralocorticoids and rapid volume expansion. It has a biphasic relation to sodium excretion. In essential hypertension, kallikrein release into the blood and urine is low and facilitates hypertension. High renin in Bartter's syndrome is balanced by high PGE and kallikrein without hypertension.
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PMID:Kallikrein, kininogen and kinins in control of blood pressure. 37 13

Alterations occur in human muscle electrolyte and water composition in response to infection. There appear to be at least two basic mechanisms; the first is an exchange of sodium for potassium without alteration in water content of muscle. The second is an increase in cellular Na and water without a loss of K on a dry weight basis. In a series of studies in monkeys, Salmonella typhimurium sepsis was induced as an experimental model. Both patterns of muscle response to infection were detected. Electron probe microanalysis revealed that the loss of K concentration was due to an accumulation of intracellular saline which dilute the K content. The mechanism of this is unclear; however, a concomitant increase in undertermined osmoles in the serum suggests that there may be an increase in organic osmoles within the cell which leads to the dilution of intracellular K concentration.
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PMID:Sequential changes in body composition during infection: electron probe study IV. 40 71

Septic thrombosis of central veins is rarely diagnosed during life and nearly always proves fatal. We have recently successfully treated a patient with a 75% body surface burn in whom septic thrombosis of the inferior vena cava developed associated with high-grade candidemia as a complication of parenteral nutrition. Signs of venous thrombosis and candidemia persisted after catheter removal. Prompt and intensive therapy with amphotericin B, monitored by fungicidal assays of serum, resulted in cure. Generous hydration and directed supplementation of sodium bicarbonate permitted us to administer a large total dose of amphotericin over a relatively brief period of time with no nephrototoxic effect whatsoever. Septic central venous thrombosis mandates a pharmacologic approach to therapy similar to that used for infective endocarditis, with the addition of anticoagulation. Should sepsis prove refractory to this program of it pulmonary embolization occurs, operative intervention is indicated despite the high risks involved.
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PMID:Management of septic thrombosis of the inferior vena cava caused by Candida. 41

The reported complication rate from T-tube infusion of sodium cholate for dissolution of retained biliary stones is low. Among 84 patients reported in the English-language literature, and 10 additional cases of our own, there have been no deaths, an incidence of liver enzyme elevation in 7%, fever in 5%, cholangitis in 2%, and pancreatitis in 2%. Recently, we have infused 100mM sodium cholate at 30 cc/hr into patients through transhepatic biliary stents in an effort to rid the intrahepatic biliary tree of retained stones and biliary sludge. Appropriate precautions were taken to prevent increased biliary pressures by the insetion of a 30 cm manometer into the perfusion system. During four transhepatic infusions in three patients, all experienced nausea and vomiting, and two of the three patients developed diarrhea and abdominal pain. Liver enzymes became elevated during all four infusions, and two of the three patients became septic and died shortly after their infusions. Experimental work in animals suggests that intrahepatic sodium cholate infusion results in injury to the ductal epithelium and predisposes patients to bactermia and sepsis. Even though T-tube infusion of sodium cholate into the common bile duct is well tolerated, direct infusion into the intrahepatic biliary tree through a transhepatic tube is not and carries a high risk of sepsis and death.
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PMID:Sodium cholate dissolution of retained biliary stones: mortality rate following intrahepatic infusion. 43 6

The clinical course of 11 patients with neonatal group D streptococcal septicemia is reviewed. Two of the infants died and hydrocephalus developed in one. Group D Streptococcus, both enterococci and nonenterococci, should be considered pathogenic in the neonate until proved otherwise. The antibiotics of choice for treating such infections in the newborn are ampicillin sodium and either kanamycin sulfate or gentamicin sulfate.
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PMID:Group D streptococcal septicemia in the neonate. 43 74

The role of antibiotic therapy in open fractures is secondary to adequate debridement, irrigation, and definitive wound care. Experimental and clinical studies indicate that parenteral administration of appropriate antibiotics within three hours after injury helps to prevent wound sepsis. Intial wound cultures of 158 open fracture wounds revealed bacterial growth in 70.3%. Eighty-six were Gram-positive, 57 were Gram-negative, and 32 yielded mixed bacterial growth. Sensitivity studies of these organisms suggest that cephalothin sodium is the most effective antibiotic for prophylaxis. In a prospective study from 1969 to 1975, treatment of 520 patients was as follows: debridement, copious irrigation, and primary closure for types 1 and 2 fractures and secondary closure for type 3 fractures. No primary internal fixation was done except in vascular injuries. Cultures were taken of all wounds and antibiotics were given before surgery and for three days postoperatively. In type 3 open fractures, severe soft tissue injury, and segmental or traumatic amputation, the infection rate was 9%, compared to a 44% infection rate in the retrospective study from 1955 to 1968.
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PMID:Use of antimicrobials in the management of open fractures. 45 75

Over a period of 2 years, 82 patients out of 2,390 (3.43%) admitted to an intensive care unit developed acute renal failure (ARF). The diagnosis of ARF was based on the usual criteria of oliguria, a rising blood urea nitrogen and creatinine, urine sodium concentration greater than 20 mmol/l and a U/P osmolality ratio less than 1.1. In 9.2% of patients the latter two criteria were misleading. Sepsis was the commonest cause of vasomotor nephropathy but in 20.7% potentially nephrotoxic agents had been administered before development of ARF. Overall mortality was 73.2%, with patients older than 50 years of age having the highest mortality. ARF is associated with prolonged bed occupancy--an average of 59.8 days for the dialysed patients with ARF versus an average length of stay of 8.4 days for the hospital overall.
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PMID:Aetiology, diagnosis, treatment and prognosis of acute renal failure in an intensive care unit. 54 32

30 children suffering from bacterial meningitis and 2 children suffering from septicemia were treated with 6-((R)-2-[3-methylsulfonyl-2-oxo-imidazolidine-1-carboxamido]-2-phenyl-acetmido(-penicillanic acid sodium salt (mezlocillin, Baypen). The daily dose was 250 mg/kg, divided in three portions. Therapy was successful in all patients. Neither signs of toxicity nor side effects of any kind could be found. Mezlocillin concentrations were measured in serum and cerebrospinal fluid (CSF) mainly on days one and six or seven of therapy. Serum concentrations were in the expected range. CSF concentrations depended on the inflammation of the meninges. On the first day of treatment they ranged from 0.5 to 7.2 to 12.0 microgram/ml. After normalisation of CSF no concentrations of mezlocillin were detectable.
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PMID:Treatment of childhood meningitis with mezlocillin. 54 12

Particulate and bacterial contamination of IV fluids and drugs have been implicated in venous thrombosis, infusion phlebitis, suppurative thrombophlebitis, pyrogenic reactions, and systemic sepsis. In a study of the inflammatory potential of the filterable residue of sodium cephalothin, we have found a tissue-specific reaction with venous endothelium but not with cutaneous or subcutaneous tissues. In a controlled animal model, removal of particulates from an infusion by use of a 0.45 micron in-line membrane filter reduces the incidence and severity of infusion phlebitis.
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PMID:Inflammatory potential of foreign particulates in parenteral drugs. 55 45

The morphologic and clinical findings in seven fatal cases of meningococcal septicemia are described and interpreted in light of recent experimental and clinical studies. We include evidence that suggests the disease has two distinct pathogenetic mechanisms. First, a shock-like terminal phase is associated with the development of widespread pulmonary microvascular thrombosis. These thrombi, composed largely of platelets and leukocytes, produce severe cor pulmonale that cannot be prevented with heparin sodium treatment. Meningococcal endotoxin also produces disseminated intravascular coagulation, which includes the rapid consumption of fibrinogen and the formation of fibrin thrombi in adrenal and renal glomerular capillaries, causing hemorrhagic infarction of the adrenal glands and renal cortical necrosis. This secondary phase of the disease can be modified with heparin therapy, but its control does not improve survival because the parenchymal lesions produced are not immediately life threatening.
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PMID:Fatal meningococcal septicemia. 57 4


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