Abstract
Troponin I is a biomarker for cardiac injury in children. The role of troponin I in neonatal Hypoxic–Ischemic encephalopathy (HIE) may have valuable clinical implications. Troponin I levels were measured within 6 h of birth to determine their relationship to HIE stage, short-term cardiac functional outcomes, and neurodevelopmental outcomes at 1 year. Seventy-three patients were divided into two groups: mild HIE and moderate to severe HIE. Troponin I levels within 6 h of birth were obtained in 61 patients, and were significantly higher in patients with moderate to severe HIE than in patients with mild HIE (Mann–Whitney U test, U = 146, p = 0.001). A troponin I cut-off level of ≥60 pg/mL predicted moderate to severe HIE with a specificity of 81.1% and a negative prediction rate of 76.9%. A troponin I cut-off level of ≥180 pg/mL was significantly (χ2 (1, n = 61) = 33.1, p = 0.001, odds ratio 96.8) related with hypotension during first admission and significantly (χ2 (1, n = 61) = 5.3, p = 0.021, odds ratio 4.53) related with abnormal neurodevelopmental outcomes at 1 year. Early troponin I level may be a useful biomarker for predicting moderate to severe HIE, and initialization of hypothermia therapy.
Highlights
Birth asphyxia is a physiological disorder in newborn infants resulting from a prolonged or profound mismatch between oxygen demand and oxygen delivery [1]
We investigated the comorbidities of lung and cardiac disorders in neonatal hypoxic–ischemic encephalopathy (HIE) treated with hypothermia therapy and the biomarkers related to the cardiopulmonary system and neurodevelopmental outcomes
This study found that creatine phosphokinase (CK) and creatine kinaseMb (CKMB) were not useful biomarkers of neonatal HIE staging
Summary
Birth asphyxia is a physiological disorder in newborn infants resulting from a prolonged or profound mismatch between oxygen demand and oxygen delivery [1]. Birth asphyxia is a major cause of long-term severe sequelae in children and neonatal deaths [2,3,4,5]. Birth asphyxia ranges from mild to severe. When it is moderate or severe, it can cause irreversible cerebral cell damage and death, leading to hypoxic–ischemic encephalopathy (HIE) [5,6,7]. HIE can cause disorders of multiple organs, including the brain, heart, liver, kidney, and hemopoietic system, and it may lead to an altered conscious state, autonomic instability, absence of primitive reflexes, seizures, decreased cardiac output, impairment of liver and renal function, and even death. HIE is a critical and common etiology of neonatal death and neurodevelopmental consequences [5,6]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
