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Updated: Jun 11, 2026

A Thrombotic Stroke Model Based On Transient Cerebral Hypoxia-ischemia
Published on: August 18, 2015
Cardiac, lung, and brain thrombosis in a child with obstructive sleep apnea
Shlomo Cohen1, Chaim Springer, Zeev Perles
1Institute of Pulmonology, Hadassah Ein Kerem, Hadassah-Hebrew University Medical Centers, Jerusalem, Israel. shlomoco@hadassah.org.il
Insights
Prolonged obstructive sleep apnea (OSA) in children may lead to a procoagulant state, causing severe cardiovascular issues. Prompt adenotonsillectomy resolved these complications in a young patient.
Area of Science:
- Pediatric Cardiology
- Sleep Medicine
- Hematology
Background:
- Severe obstructive sleep apnea (OSA) in children can lead to significant cardiovascular complications.
- Adenotonsillar hypertrophy is a common cause of pediatric OSA.
Observation:
- A 3-year-old boy with severe OSA presented with respiratory distress, anasarca, right heart failure, and pulmonary hypertension.
- Cardiac and pulmonary artery pathology indicated microemboli, alongside venous sinus thrombosis.
Findings:
- Despite normal thrombophilia screening, the child's condition suggested a procoagulant state linked to prolonged OSA.
- Surgical intervention, including adenotonsillectomy and cardiac lesion excision, led to complete recovery.
Implications:
- This case highlights the potential for prolonged pediatric OSA to induce a procoagulant state, leading to severe cardiovascular morbidity.
- Early diagnosis and treatment of OSA may prevent serious cardiac complications in children.
Abstract:
A 3-year-old boy with failure to thrive and severe adenotonsillar hypertrophy with a clinical presentation of prolonged obstructive sleep apnea (OSA), was referred to the emergency room due to severe respiratory distress and anasarca. Echocardiography revealed right heart failure, a cystic lesion in the right ventricle and severe pulmonary hypertension. D-dimer was elevated but spiral computerized tomography (CT) and lung scan did not show any perfusion defects. Excision of the cardiac lesion during open-heart surgery, lung biopsy, and adenotonsillectomy were performed. Pathological examination showed an intracadiac organized thrombus and eccentric intimal fibrosis of the pulmonary arteries-which is a pathognomonic of pulmonary arterial microemboli. Brain CT revealed vein thrombosis of the left sigmoid sinus. Blood tests for inherited thrombophilia were normal. Today, 5 years after adenotonsillectomy, the child is normally developed, completely asymptomatic, free of any medications, and has a normal echocardiography. This case report may indicate that prolonged OSA can be a procoagulant state which can cause severe cardiovascular morbidity in children.
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