Cases reported "Endotoxemia"

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1/7. Antibiotic-induced endotoxemia in a patient with endogenous endophthalmitis.

    PURPOSE: The aim of the study is to describe a case of suspected endotoxin-induced uveitis associated with septic endogenous endophthalmitis followed by antibiotic-induced endotoxemia. methods: The human leukocyte antigen (HLA) typing of peripheral leukocytes was studied by lymphocytotoxicity technique. Histological and immunohistochemical studies of paraffin embedded specimen were conducted. RESULTS: Findings of HLA typing revealed positive reaction for B 51, Cw 3, DR 8, DR 11, DQ 3. The vitreous body of an eviscerated eye was occupied by the non-specific granulomatous tissue, composed of fibroblast, plasma cells, and sudan black staining positive foamy cells, including melaniferous phagocytes, identified as CD 68 positive macrophage. CONCLUSION: It is suggested that antibiotic-induced endotoxemia of a patient with septic endogenous endophthalmitis produced endotoxin-induced uveitis under an upregulation of HLA and endotoxin activated macrophages may release cytokines, followed by fibrin formation and subsequent granuloma. ( info)

2/7. Postoperative acute pulmonary thromboembolism in patients with acute necrotizing pancreatitis with special reference to apheresis therapy.

    Eight patients with pancreatic abscesses secondary to acute necrotizing pancreatitis underwent drainage of their abscesses under laparotomy. Two of them died of acute pulmonary thromboembolism (PTE) within 1 week. autopsy revealed a large thrombus at the main trunk of the pulmonary artery and in the left common iliac vein. Femoral catheter insertion/indwelling, immobilization, surgery, increased trypsin/kinin/kallikrein, increased endotoxin, and decreased antithrombin-III (AT-III) were present following drainage of the pancreatic abscesses. With respect to the bedside diagnosis of acute PTE, alveolar-arterial oxygen gradients obtained by blood gas analysis and mean pulmonary artery pressure estimated by pulsed Doppler echocardiography are very useful. In terms of the treatment, attention should be paid to the following to prevent deep venous thrombosis: prophylactic administration of low molecular weight heparin and administration of AT-III (AT-III > or = 80%), use of the subclavian vein whenever possible as blood access for apheresis therapy, as short a compression time as possible after removing the blood access catheter (< or =6 h), and application of intermittent pneumatic compression devices or elastic compression stockings on the lower extremities. ( info)

3/7. endotoxemia causing fetal bradycardia during urosepsis.

    BACKGROUND: Fetal bradycardia is a recognized response to maternal hypothermia associated with hypoglycemia, tocolysis with magnesium sulfate, or urosepsis, and it is thought to be a direct response to the decrease in the maternal core temperature. CASE: A 25-year-old white woman, gravida 1, para 0, at 31 1/7 weeks' gestation was admitted with a diagnosis of pyelonephritis. The baseline fetal heart rate was 120 beats per minute with accelerations. Within 3 hours of admission, the patient became hypothermic (35.1C) and, concomitantly, the fetal heart rate baseline declined to 90 beats per minute with marked variability. Despite sustained maternal hypothermia, the fetal heart rate baseline rose to 120 beats per minute. It was another 6 hours before the patient's temperature rose above 38.5C. Her urine and blood cultures were positive for serratia rubidacea infection. The patient delivered a healthy infant at 39 weeks' gestation. CONCLUSION: Fetal bradycardia in the presence of urosepsis might be due to the release of endotoxin from gram-negative bacteria, triggering production of cardiotoxic cytokines, rather than to maternal hypothermia alone. ( info)

4/7. Nitric-oxide-lowering effect of terlipressin in decompensated cirrhosis: comparison to the molecular adsorbent recirculating system and correlation with clinical status.

    Systemic vasodilatation and arterial hypotension, refractory to adrenergic vasopressors, portend a poor prognosis in patients with decompensated cirrhosis. The production of large amounts of nitric oxide, consequent to endotoxin-induced tumour necrosis factor (TNF)-alpha-mediated upregulation of inducible nitric oxide synthase (iNOS), has been suggested to be central to this phenomenon. Terlipressin has recently been shown in an animal model of cirrhosis to suppress endotoxin-induced TNF-alpha-mediated upregulation of iNOS, thereby preventing overproduction of nitric oxide and restoring normal vascular tone. We present the first evidence that this effect of terlipressin may also occur clinically, in a patient with child-Pugh class C cirrhosis, endotoxaemia, a raised circulating TNF-alpha concentration, and marked systemic vasodilatation with refractory arterial hypotension. Beneficial effects of terlipressin on circulating nitrate and nitrite concentrations, haemodynamic status, plasma renin levels and indocyanine green clearance were comparable to those of the molecular adsorbent recirculating system (mars). Our findings suggest that terlipressin may be the vasopressor agent of choice in patients with decompensated cirrhosis and provide a rationale for combination terlipressin and mars therapy when the therapeutic response to either treatment alone is suboptimal. ( info)

5/7. disseminated intravascular coagulation in an ambulatory young woman.

    We are reporting the case of an ambulatory young woman with a 10-year history of recurrent venous thrombosis who presented to us with diffuse intravascular coagulation (DIC). After excluding the recognized causes of DIC, we examined the possibility that her clinically quiescent ulcerative colitis might be the underlying stimulus. We documented sepsis-range endotoxemia in this patient at a time when she was afebrile and had a normal c-reactive protein level. in vitro her serum upregulated tissue factor in cultured endothelial cells. We postulate that she had become tolerant to the systemic effects of endotoxin leaking from her inflamed colon but that the endotoxin stimulated her endothelium and/or monocytes to produce tissue factor that made her intensely hypercoagulable. Her prothrombotic state may have been compounded by the fact that she was heterozygous for prothrombin G20210A and that her plasma clotting time demonstrated resistance to activated protein c. ( info)

6/7. polymyxin b-immobilized fiber hemoperfusion with low priming volume in an elderly septic shock patient with marked endotoxemia.

    An 84-year-old woman with septic shock caused by pyelonephritis is described herein. She was admitted for severe back pain and high fever. Her white blood cell (WBC) count and c-reactive protein (CRP) and endotoxin levels were elevated at 38,000/microl, 40.0 mg/dl, and 8,400 pg/ml, respectively. Her blood pressure was 80/34 mm Hg. urinalysis revealed occult blood with innumerable WBCs. Plain abdominal radiography showed calcium stones in both kidneys. Septic shock with endotoxemia was diagnosed, and the patient was treated with antibiotics, gamma-globulin, and dopamine. However, her plasma endotoxin level remained high for 3 days. We performed direct hemoperfusion twice using a polymyxin b-immobilized fiber (PMX-F) column with a low priming volume. After PMX-F treatment, the patient's temperature decreased to 36.8 degrees C; her WBC count and CRP level decreased to 9,200/microl and 3.8 mg/dl, respectively. Her plasma endotoxin level decreased to 840 pg/ml after the first treatment and to 188 pg/ml after the second treatment. The next day, her blood endotoxin level further decreased to 32 pg/ml. Her blood pressure increased to 92/60 mm Hg after the first treatment and to 118/76 mm Hg after the second treatment. The patient was discharged on day 26 after admission. Our experience in this case suggests that PMX-F treatment with a low priming volume may be beneficial in elderly patients with septic shock and marked endotoxemia. ( info)

7/7. Endotoxin removal column containing polymyxin b immobilized fiber is useful for the treatment of the patient with vibrio vulnificus septicemia.

    A case of primary septicemia due to vibrio vulnificus infection is reported. The patient was successfully treated with appropriate antibiotic therapy, drainage, and debridement of the necrotic tissues and direct hemoperfusion (DHP) using polymyxin b immobilized fiber (PMX-F). The effectiveness of DHP using PMX-F, which removes endotoxin in the circulating blood for the treatment of septic shock and multiple organ dysfunction occurring due to this fulminant infectious disease, is discussed. ( info)

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