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    PULMONARY THROMBOEMBOLISM IN A CHILD AFTER BURN INJURY
    (2020) Dalkıran, Tahir; Güngör, Olcay; Kandur, Yaşar; Dağoğlu, Besra; Acıpayam, Can; Alpcan, Ayşegül; Tursun, Serkan
    Pulmonary embolism is rarely diagnosed in pediatric burnpatients and is often only discovered at autopsy. Herein we wouldlike to present the case of a pediatric patient with pulmonarythromboembolism who was burnt by hot water at home. A 4-yearoldgirl who was treated at an external center for 9 days due tosecond degree burn injuries in both legs. After the discharge shehad suddenly become restless and than gone unconscious. Sincepulmonary thromboembolism was suspected as the cause ofcardiopulmonary arrest, a pulmonary computed tomographyangiogram was taken, which showed a thrombus in the lobar andsegmental branches of the right pulmonary artery supplying theright lower lobe. Enoxaparin sodium treatment (2×1mg/kg) wasinitiated. At day 16, a control computed tomography angiogramshowed that the thrombus in the lobar and segmental branches ofthe pulmonary artery had disappeared. This case report illustratesthe importance of chemoprophylaxis against pulmonaryembolism in both pediatric and adult burn patients. In such cases,especially the severe ones, a sudden deterioration of patient’sclinical status in the form of respiratory distress or failure shouldraise suspicion about the possibility of pulmonary embolism.
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    Thrombotic Microangiopathy in a Severe Pediatric Case of COVID-19
    (Sage Publications Ltd, 2021) Dalkıran, Tahir; Kandur, Yaşar; Kara, Emine Manolya; Dağoğlu, Besra; Taner, Sevgin; Öncü, Doğan
    In this case report, we report a pediatric patient with COVID-19 and atypical hemolytic uremic syndrome (aHUS). A 3-year-old girl with fever and respiratory distress was admitted to the hospital. The patient tested positive for COVID-19 by a PCR test. As her respiratory distress increased and blood gas indicated deep respiratory acidosis on the third day of the pediatric intensive care unit follow-up, the patient was intubated and ventilated. Thorax computerized tomography (CT) showed bilateral effusion and atelectasis. During her follow-up, the pleural effusion resolved but there were marked consolidation areas and ground glass opacities compatible with COVID-19 on the follow-up CT. On the 10th day, she became anuric and developed progressive thrombocytopenia and persistent microangiopathic hemolytic anemia, which were suggestive of HUS given a high creatinine level (1.9 mg/dl), an undetectable haptoglobin level, reticulocytosis (8%), and an LDH level of 2540 U/l. Direct Coombs test returned negative. Examination of a peripheral blood smear revealed schistocytes. Disseminated intravascular coagulation was ruled out by normal INR and PTT. In the light of the available findings, we considered the patient to have thrombotic microangiopathy (TMA) triggered by COVID-19. It was not a TTP-form of TMA but rather an aHUS type, based on an ADAMTS13 activity level >5%. Hence, plasmapheresis was performed with fresh frozen plasma (FFP). After 4 weeks, she became completely asymptomatic, and her hemodynamic parameters normalized. COVID-19 induced uncontrolled complement activation leading to the development of aHUS. Early diagnosis and treatment may reduce morbidity and mortality since its treatment options.