Neonatal hypoxic-ischemic encephalopathy (HIE) occurs when the brain is damaged due to a lack of oxygen before, during, or after birth. It can cause long-term complications such as cerebral palsy, intellectual disability, epilepsy, or death. The document discusses the causes, clinical presentation, treatment, and prognosis of HIE, noting that outcomes depend on the severity of the brain injury and may include permanent neurological deficits or death. Imaging studies and supportive care aim to prevent further brain damage while treatments for seizures and cerebral edema can help reduce complications. Factors like abnormal clinical findings persisting over a week suggest a poor prognosis.

1. Neonatal hypoxic-ischemic encephalopathy (HIE) Xin Yue PEDIATRIC DPT. GENERAL HOSPITAL TIANJIN MEDICAL UNIVERSITY

3. Effects of asphyxia(1) System Effect Central nervous hypoxic-ischemic encephalopathy, system infarction, intracranial hemorrhage, seizures, cerebral edema, hypotonia cardiovascular Myocardial ischemia, poor contractility, cardiac stunning tricuspid insufficiency, hypotension pulmonary pulmonary hypertension, pulmonary hemorrhage, respiratory distress syndrome

4. Effects of asphyxia (2) System Effect necrosis Renal acute tubular or cortical necrosis adrenal adrenal hemorrhage gastrointestinal perforation, ulceration with hemorrhage, necrosis

5. Effects of asphyxia (3) System Effect metabolic inappropriate secretion of antidiuretic hormone, hyponatremia, hypoglycemia , myoglobinuria integument subcutaneous fat necrosis hematology disseminated intravascular coagulation

6. Anoxia is a term used to indicate the consequences of a complete lack of oxygen due to a number of primary causes. Hypoxia refers to an arterial concentration of oxygen that is less than normal. Ischemia refers to blood flow to cells or organs that is insufficient to maintain their normal function.

8. Cerebral palsy and ataxia images

14. Premature separation of the placenta Impedance to the circulation of blood through the umbilical cord: compression or knotting of the cord Uterine vasoconstriction: cocaine Placental insufficiency : toxemia, postmaturity

25. Clinical stages of hypoxic-ischemic encephalopathy in term infants(2) Signs Stage 1 Stage 2 Stage 3 Moro reflex Strong Weak Absent Pupils Mydriasis Miosis Unequal, poor light reflex Seizures None Common Decerebration EEG Normal Low voltage Burst changing to suppression seizure activity to isoelectric

26. Clinical stages of hypoxic-ischemic encephalopathy in term infants(3) Signs Stage 1 Stage 2 Stage 3 Suck reflex Weak Weak or absent Absent Autonomic Generalized Generalized Both systems function sympathetic parasympathetic depressed Heart rate Tachycardia Bradycardia Variable Bronchial and salivary Sparse Profuse Variable secretions poor light reflex Seizures None Common Decerebration EEG Normal Low voltage Burst changing to suppression seizure activity to isoelectric

27. Clinical stages of hypoxic-ischemic encephalopathy in term infants(4) Signs Stage 1 Stage 2 Stage 3 Duration <24hr 24 hr to 14 days Days to weeks Outcome Good Variable Death, severe deficits

39. Keys to be remembered Asphyxia is considered in the presence of The table about effects of asphyxia The definition of anoxia, hypoxia and ischemia The table about the clinical stages of hypoxic-ischemic encephalopathy in term infants Imaging studies and Treatment

40. Thank You ! 5th Mar, 2009