Birth Asphyxia Year 4 Paediatrics Notes OmpathStudy

Birth Asphyxia Year 4 · Paediatrics Collection: 4TH YEAR ALL NOTES / PAEDS / PAEDS 4.3 / Munge / NEONATOLOGY -- Slide 1 Birth Asphyxia Dr Rose Munge Slide 2 Objectives Definition Epidemiology Pathophysiology Clinical assessment Investigation Treatment Slide 3 Definitions Hypoxia or Anoxia: A partial (hypoxia) or complete (anoxia) lack of oxygen in the brain or blood Asphyxia: The state in which placental or pulmonary gas exchange is compromised or ceases altogether Ischemia: The reduction or cessation of bloodflow to an organ which compromises both oxygen and substrate delivery to the tissue Hypoxic-Ischemic Encephalopathy: Abnormal neurologic behavior in the neonatal period arising as a result of a hypoxic-ischemic event. Slide 4 Definition Note that other systems are affected! Slide 5 Epidemiology Occurs in 1-6 per 1000 live term births in developed countries Number 5 leading cause of under 5 mortality Significant morbidity among survivors In a cohort of school-aged children with a history of moderately severe hypoxic-ischemic encephalopathy, 15-20% had significant learning difficulties, even in the absence of obvious signs of brain injury.\nMore prevalence among term newborns\nNo sex / race predilection Slide 6 Pathophysiology Systemic hypoxia Central (CNS) hypoxemia, hypercapnea, acidosis Redistribution of blood flow: Brain, Heart, Adrenals Catecholamine surge (Increased blood pressure) Ischaemic brain injury Slide 7 Pathophysiology Constant blood flow to the brain is maintained despite fluctuations in systemic BP In adults, range within which autoregulation occurs is 60-100 mean BP. Poorly studied in newborns, but thought to be narrower After decompensation occurs, CBF becomes pressure-passive i.e. autoregulation is lost and cerebral perfusion is depended on systemic BP. Slide 8 Pathophysiology Early changes 0-6 hours Na+ Ca++ Ca++ Na+/K+ Na+ Ca++ Ca++ NMDA Receptor AMPA Receptor Excitatory amino acids: Glutamate Na+ Increased synaptic glutamate Activation of NMDA / AMPA / Kainate post-synaptic receptors Deactivation of Na/K pump Increased intracellular Na Cellular oedema Necrotic cell death Increased intracellular Ca Ca uptake into nucleus Programmed cell death Programmed cell death (apoptosis) H20 H20 Na+ Na+ Slide 9 Pathophysiology Early changes 0-6 hours Reperfusion Na+/K+ O2 COX / XO / LO Improved perfusion Activation of cyclooxygenase, lipoxygenase, xanthine oxidase Generation of reactive oxygen species Lipid peroxidation / DNA damage Cell death Programmed cell death (apoptosis) O2 NMDA Receptor NO peroxynitrite Slide 10 Pathophysiology Late changes: Delayed phase. 6 – 24 hours following injury Mitochondrial dysfuntion Activation of cellular caspaces Programmed cell death Correlated with adverse neurodevelopmental outcomes at 1 year and 4 years after insult Programmed cell death (apoptosis) Mitochondrial dysfunction Inflammatory mediators (cytokines and chemokines) have also been implicated in the pathogenesis of HIE. IL 1-b Slide 11 Aetiology Inadequate perfusion of the maternal side of the placenta (e.g. maternal hypotension) Failure of gas exchange across the placenta (e.g., placental abruption) Interruption of umbilical blood flow (e.g., cord compression) An otherwise compromised fetus who cannot further tolerate the transient, intermittent hypoxia of normal labor (e.g., the anemic or growth-retarded fetus) / failure to inflate the lungs and complete the changes in ventilation and lung perfusion that must occur at birth. Slide 12 Risk factors Slide 13 Clinical Presentation Slide 14 History Profound metabolic or mixed acidemia (pH < 7) in an umbilical artery blood sample, if obtained Persistence of an Apgar score of 0-3 for longer than 5 minutes Neonatal neurologic sequelae (eg, seizures, coma, hypotonia) Multiple organ involvement (eg, kidney, lungs, liver, heart, intestines) AAP / ACOG criteria for asphyxia severe enough to cause neurological injury Slide 15 Physical examination HIE can be divided into Mild, Moderate, and Severe (Sarnat classification) Slide 16 Adapted from Sarnat HB, Sarnat MS: Neonatal encephalopathy following fetal distress. Archives of Neurology 33:696–705, 1975.1 Slide 17 Mild HIE Muscle tone may be slightly increased and deep tendon reflexes may be brisk during the first few days. Transient behavioral abnormalities, such as poor feeding, irritability, or excessive crying or sleepiness, may be observed. The neurologic examination findings normalize by 3-4 days of life. Slide 18 Moderate HIE Lethargic, with significant hypotonia and diminished deep tendon reflexes. The grasping, Moro, and sucking reflexes may be sluggish or absent. Occasional periods of apnea. Seizures may occur within the first 24 hours of life. Full recovery within 1-2 weeks is possible and is associated with a better long-term outcome.\n Note: An initial period of well-being or mild hypoxic-ischemic encephalopathy may be followed by sudden deterioration, suggesting ongoing brain cell dysfunction, inju