Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Five limb extremities gangrene are reported in 54 meningococcemia. Prognosis depends first on early medical treatment. Extremities ischemia require large early aponeurotomy for limb preservation.
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PMID:[Multiple extremities gangrene as complications of meningococcemia (author's transl)]. 54 87

Multiple, irregular ball-and-socket deformities at the ends of long bones were noted in four children several years after they had had meningococcemia. Even though these lesions were clinically unsuspected at the time of the fulminant disease, they were probably the result of ischemia secondary to septic emboli to the epiphyseal vessels, which occurred at the same time as soft-tissue necrosis elsewhere. The individual lesions were radiologically identical to the metaphyseal cupping that has been reported following trauma to the growth plate.
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PMID:Late sequelae of infantile meningococcemia in growing bones of children. 729 46

OBJECTIVE: To investigate the frequency, predisposing factors, clinical presentation, and outcome of abdominal compartment syndrome (ACS) in critically ill pediatric patients. DESIGN: A prospective study over a 5-yr period. SETTING: Pediatric intensive care unit of a tertiary care, university hospital. PATIENTS: All patients admitted to the pediatric intensive care unit were screened for the presence of ACS and were treated with a uniform protocol. ACS was defined as abdominal distention with intra-abdominal pressure (IAP) > 15 mm Hg, accompanied by at least two of the following: oliguria or anuria; respiratory decompensation; hypotension or shock; metabolic acidosis. MEASUREMENTS AND MAIN RESULTS: Of 1762 patients admitted over 5 yrs, ten patients (0.6%) had a total of 15 episodes of ACS. Of 406 trauma cases, three had ACS (0.7%). Three of the ten patients had primary abdominal conditions (mesenteric vein thrombosis, intussusception, enterocolitis), three had abdominal surgery (trauma, Kasai operation, esophageal perforation and peritonitis), three had primary central nervous system involvement, and one had meningococcemia. At laparotomy, bowel ischemia or necrosis was found in four episodes of ACS (27%). Mean IAP at diagnosis of ACS was 23.9 +/- 3.8 (range 17-31) mm Hg. Physiologic parameters were compared during 4 hrs before the development of ACS, during ACS, and after abdominal decompression. Mean arterial pressure, Pao(2), Pao(2)/Fio(2) ratio, and urinary output decreased significantly, whereas Paco(2), peak inspiratory pressures, positive end-expiratory pressures, and base deficit increased significantly after the development of ACS. After decompressive laparotomy, the condition of the patients improved promptly and these variables returned to pre-ACS values. Overall mortality rate in this group was 60%. CONCLUSIONS: Although relatively infrequent compared with adults, ACS occurs in critically ill children. Timely decompression of the abdomen results in uniform improvement, but overall mortality is still high. In contrast with adults, children with ACS have diverse primary diagnoses, with a significant number of primary extra-abdominal-mainly central nervous system-conditions. Ischemia and reperfusion injury appear to be the major mechanisms for development of ACS in children. Clinical presentation is similar to adults, but children may develop ACS at a lower IAP (as low as 16 mm Hg).
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PMID:Abdominal compartment syndrome in children. 1279 89

The local Shwartzman reaction (LSR) is an inflammatory response in the skin that is considered a model for skin necrosis associated with meningococcemia. We tested the hypothesis that ischemia can act as the provocative agent to produce this response. In eight rats, bilateral inferior epigastric flaps were outlined. Within each flap, three injection sites were marked. Site 1 had 0.1 mL of endotoxin injected 24 h before surgery. The other two sites had either endotoxin or saline injected immediately before surgery. Both flaps were raised on their pedicle and one side rendered ischemic for 6 h and then reperfused. Animals were killed either 30 min or 48 h later and the tissue from each site examined. After 48 h of reperfusion, necrosis was grossly visible at the site of 24-h preischemia injection of endotoxin in three of four rats. No abnormalities were present at the other injection sites. Microscopically, all 24-h-delayed injection sites showed hemorrhage into all layers of the skin after both 30 min and 48 h of reperfusion. No hemorrhage was present at the other sites. These findings may serve as a potential model for the skin necrosis seen in meningococcemia.
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PMID:Local Shwartzman reaction in the rat induced by endotoxin and ischemia: potential model for skin necrosis in meningococcemia. 1686 96

Sepsis-induced purpura fulminans is a rare but life-threatening disorder, characterized by hemorrhagic infarction of the skin caused by disseminated intravascular coagulation and dermal vascular thrombosis. The pathogenesis is linked to enhanced expression of the natural procoagulants and depletion of the natural anticoagulant proteins particularly protein C. Meningococcal sepsis is the most common cause, followed by pneumococcal sepsis in adults. The syndrome is associated with more than 50% mortality secondary to multiple organ dysfunction syndrome and is accompanied by long-term morbidity. Necrotic lesions usually progress to distal ischemia, and skin grafting and extremities or limb amputation are often required. Early antibiotic administration and intensive care management according to the recommendations of severe sepsis and shock is crucial for patients' survival. Adjuvant therapies against inflammatory and coagulation cascades and augmenting fibrinolysis are still controversial and need further assessment. Among them activated protein C and supplementation therapy have given promising results.
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PMID:Purpura fulminans in sepsis. 1717 Jun 24

A middle-aged woman presented from an outside hospital with a diagnosis of Neisseria meningitidis and meningococcemia. A nonpalpable purpuric skin rash evolved into multiple wounds, with gradual necrosis of bilateral lower and upper extremities. Throughout the course of hospitalization, the patient developed ventricular tachycardia, normocytic anemia, thrombocytosis, Clostridium difficile infection, depression, and transient right eye blindness. The finding of decreased CH50 in the complement cascade was considered as the potential cause of the meningococcemia. The subsequent ischemia and necrosis of extremities were attributed to the systemic effect and trauma ensuing from N. meningitidis.
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PMID:Disseminated intravascular coagulation, meningococcal infection, and ischemic changes affecting the lower extremities: a case study. 2061 93