Résumé
BACKGROUND: Blunt traumatic cardiac rupture is rare. However, such cardiac ruptures carry a high mortality rate. This study reviews our experience treating blunt traumatic cardiac rupture. METHODS: This retrospective study included 21 patients who experienced blunt traumatic cardiac rupture from 1999 to 2015. Every patient underwent surgery. Several variables were compared between survivors and fatalities. RESULTS: Sixteen of the 21 patients survived, and 5 (24%) died. No instances of intraoperative mortality occurred. The most common cause of injury was a traffic accident (81%). The right atrium was the most common location of injury (43%). Ten of the 21 patients were suspected to have cardiac tamponade. Significant differences were found in preoperative creatine kinase–myocardial band (CK-MB) levels (p=0.042) and platelet counts (p= 0.004) between the survivors and fatalities. The patients who died had higher preoperative Glasgow Coma Scale scores (p=0.007), worse Trauma and Injury Severity Scores (p=0.007), and higher Injury Severity Scores (p=0.004) than those who survived. CONCLUSION: We found that elevated CK-MB levels, a low platelet count, and multi-organ traumatic injury were prognostic factors predicting poor outcomes of blunt cardiac rupture. If a patient with blunt traumatic cardiac rupture has these factors, clinicians should be especially attentive and respond promptly in order to save the patient’s life.
Sujets)
Humains , Accidents de la route , Tamponnade cardiaque , Créatine , Échelle de coma de Glasgow , Atrium du coeur , Lésions traumatiques du coeur , Rupture du coeur , Score de gravité des lésions traumatiques , Mortalité , Numération des plaquettes , Études rétrospectives , Rupture , SurvivantsRésumé
Postpartum aortic intramural hematoma (IMH) is a rare but potentially lethal condition. We report a case of aortic IMH with massive hemothorax in a postpartum woman. The patient was a 31-year-old woman who had delivered twins by cesarean section. Two days after delivery, she complained of sudden-onset dyspnea. Chest computed tomography revealed a massive left hemothorax. Exploratory thoracotomy was performed, and we found a defect measuring approximately 6 mm in the adventitial layer of the thoracic aorta and an IMH. We repaired the defect primarily, and no more bleeding was observed. The patient was discharged on the 19th postoperative day without any complications.
Sujets)
Adulte , Femelle , Humains , Grossesse , Aorte thoracique , Césarienne , Dyspnée , Hématome , Hémorragie , Hémothorax , Période du postpartum , Thoracotomie , Thorax , JumeauxRésumé
Transplant renal artery stenosis (TRAS) is a common surgical complication after kidney transplantation (KTP) and is the cause of allograft dysfunction. TRAS is a potentially curable cause of refractory hypertension and allograft dysfunction which accounts for approximately 1% to 5% of cases of post-transplant hypertension. Acute cellular rejection (ACR) is also common after KTP, which is the main cause of allograft dysfunction. Although the incidence of ACR has declined with the advent of new immunosuppressive drugs, it is still around 15% worldwide. Although each disease is frequently seen individually, seeing both together is rare. A 42-year-old man with end stage renal disease underwent KTP, and the donor was his younger brother. Four months after KTP, his serum creatinine was increased to 2.1 mg/dL, and renal biopsy showed interstitial lymphocytic infiltration and tubulitis. With the diagnosis of acute T-cell mediated rejection, steroid pulsing therapy was started, but it was resisted. Therefore thymoglobulin 60 mg (1 mg/kg/day) was administered for 6 days, but serum creatinine was 1.8 mg/dL. Abdomen magnetic resonance angiography showed TRAS, stenosis at the anastomosis site and lobar artery in the lower pole. Percutaneous transluminal angiography was performed successfully. After balloon angioplasty, the stenotic lesion showed a normal size and blood flow. The patient's renal function returned to normal levels and he is currently being followed up for 9 months.
Sujets)
Adulte , Humains , Abdomen , Allogreffes , Angiographie , Angioplastie par ballonnet , Artères , Biopsie , Sténose pathologique , Créatinine , Diagnostic , Hypertension artérielle , Incidence , Défaillance rénale chronique , Transplantation rénale , Angiographie par résonance magnétique , Occlusion artérielle rénale , Artère rénale , Fratrie , Lymphocytes T , Donneurs de tissus , TransplantationRésumé
Hyperuricemic patients with gouty arthritis or tophi, a serum uric acid concentration of 8.0 mg/dL or higher, and complications should be treated with urate-lowering drugs. Conventionally, allopurinol is used to treat hyperuricemia and gout, but it is necessary to adjust the dosage according to the degree of renal impairment. Uncommonly, allopurinol may have severe or fatal side effects. The non-purine xanthine oxidase inhibitor febuxostat undergoes hepatic metabolism and may require less dose adjustment in association with renal function. It is considered to be an alternative treatment for hyperuricemic patients with chronic kidney disease. Our experience suggests that low-dose febuxostat is a promising alternative to allopurinol for the treatment of gouty arthritis or tophi in peritoneal dialysis patients.
Sujets)
Humains , Allopurinol , Goutte articulaire , Goutte , Hyperuricémie , Défaillance rénale chronique , Métabolisme , Dialyse péritonéale , Dialyse péritonéale continue ambulatoire , Insuffisance rénale chronique , Acide urique , Xanthine oxidase , FébuxostatRésumé
Pneumocystis jirovecii pneumonia (PCP) can be a life-threatening opportunistic infection after kidney transplantation, occurring most frequently in the first 12 months with the symptoms of dyspnea, cough, fever, and hypoxia. Prophylaxis for PCP is usually applied during the first 3 months to 1 year after transplantation, but late onset incidence of PCP can be detected. We report on a patient who developed PCP 9 years after renal transplantation. The patient showed indolent onset of acute respiratory distress and was treated with trimethoprim-sulfamethoxazole and corticosteroid therapy. Previous rescue treatment of acute cellular rejection with ongoing maintenance of an elevated level of immunosuppressants may have predisposed the patient to PCP.