Perinatal Asphyxia PDF

Perinatal asphyxia DR;ZAHRA SALEM Definition Acute or chronic impairment of gas exchange with hypoxia, hypercapnia and acidosis with consequent organ.damage The term Hypoxic Ischemic Injury (HII) has replaced the term of perinatal asphyxia Causes Impairment in oxygenation and perfusion due...

Perinatal asphyxia DR;ZAHRA SALEM Definition Acute or chronic impairment of gas exchange with hypoxia, hypercapnia and acidosis with consequent organ.damage The term Hypoxic Ischemic Injury (HII) has replaced the term of perinatal asphyxia Causes Impairment in oxygenation and perfusion due to o Impaired placental supply due to placental insufficiency, placental abruption and uterine contractions o Impaired umbilical supply due to cord compression/prolapsed or knots o Impaired materno-placental supply due to maternal hypoxia or hypotension o Impaired neonatal supply due to difficult delivery or inadequate resuscitation :o Post-natal causes (uncommon).Severe congenital cyanotic heart diseases - Severe anemia due to severe hemorrhage or severe hemolysis - Clinical picture Depends on duration & severity of asphyxia I. In the fetus :Indicators of fetal hypoxia and distress include Intrauterine growth restriction may indicate -1 chronic hypoxia Umbilical artery Doppler shows absent or -2 even reversed end-diastolic flow suggesting severe fetal circulatory compromise Continuous heart rate recording may reveal -3 a variable or late deceleration pattern (decrease in fetal heart rate beginning at or after the peak of the contraction and returning to baseline only after )the contraction has ended Acidotic scalp or cord pH -4 II. After delivery ,Meconium staining of the newborn -1 amniotic fluid and vernix caseosa Decreased consciousness and -2.failure of spontaneous breathing Low Apgar score with cyanosis and flaccidity -3 III. Later Neurologic and Multi Organ Dysfunction American academy of pediatrics define severe asphyxia as combination of o Low Apgar score < 4 for at least 5 minutes o Umbilical artery pH < 7.00 (if obtained) o Neurological insults e.g. seizures o Multiorgan insults : Cardiac ,pulmonary ,renal or intestinal Hypoxic-ischemic encephalopathy (HIE. Cardiac Heart failure, cardiogenic shock.2 Respiratory Meconium aspiration ,apnea, pulmonary.3 hypertension Renal Oliguria, hematuria, Acute tubular necrosis.4 GIT Necrotizing enterocolitis.5 Hematologic.6 Metabolic.6 ,Hypoglycemia , hypocalcemia ,hypomagnesemia hyponatremia and syndrome of inappropriate secretion of ADH Hypoxic-ischemic encephalopathy (HIE Sarnat and Sarnat clinical grading of HIE Diagnosis There are no specific tests to neither confirm nor exclude a diagnosis of HII Diagnosis is made based on the history, physical and neurological examinations Diagnosis Neuro imaging.1 o Brain MRI Modality of choice for the diagnosis and follow-up of HIE - Early detection of brain edema and brain injury (basal ganglia) - Conventional MRI show changes by the 3rd day - Diffusion Weighted MRI shows changes in the 1st 24 hours - (preferred) o Cranial ultrasonography Less sensitive than MRI (initial scan is negative in up to 50% of - cases) Perform on day 1 then as guided by clinical condition - EEG.2 Both standard EEG and amplitude integrated (aEEG) are used - Detects seizures and evaluate the degree of encephalopathy - Management A. In delivery room Avoid and treat risk factors -1 If fetal distress: provide high flow oxygen & -2 prepare for immediate delivery Neonatal resuscitation according to neonatal -3 life support guidelines Assess severity of encephalopathy -4 B. In NICU Therapeutic Hypothermia.1 Idea: Moderate hypothermia in perinatal asphyxia is neuroprotective :Neuroprotection via o Reduced metabolic rate and energy depletion o Decreased excitatory transmitter release o Reduced apoptosis.o Reduced vascular permeability, and edema Eligibility o 􀂕􀀃􀀖􀀙􀀃􀁚􀁈􀁈􀁎􀁖􀀃􀁊􀁈􀁖􀁗􀁄􀁗􀁌􀁒􀁑 o < 6 hours old o Evidence of moderate to severe encephalopathy (Sarnat) o Evidence of perinatal asphyxia; one of the following 􀀤􀁓􀁊􀁄􀁕􀀃􀂔􀀃􀀘􀀃􀁄􀁗􀀃􀀔􀀓􀀃􀁐􀁌􀁑􀁘􀁗􀁈􀁖 - Continuing resuscitation at 10 minutes - pH < 7.00 in the first hour - Base Excess 􀂔􀀃- 16 in the first hour - Method o Resuscitation as usual o Start selective head cooling or total body )using CoolCap(.cooling (systemic) o Rectal temperature is then.maintained at 34-35°C for 72 hours o Rewarming is carried out gradually, over 6-8 hours IN ICU Supportive care.2 Ventilation o Consider ventilatory support early o Ensure adequate oxygenation; avoid hyperoxia o PaCO2 between 35 - 45 mmHg is neuroprotective o Treat pulmonary hypertension if exist Cardiovascular o Consider invasive blood pressure monitoring o Maintain mean arterial blood pressure above 35-40 mm Hg in term to ensure adequate cerebral perfusion o Consider inotropic support early ; start with dobutamine infusion and add dopamine if required o Fluid boluses if hypovolemic o Monitor Hb% ; acute fall may indicate new intracranial hemorrhage o ECG and Echo if there is concern over poor cardiac function Fluids o Fluid balance based on weight, urine output, serum sodium & renal function o Initially fluid restrict to 60-80 % maintenance and liberalize as urine output improve Neurology o Treat seizures even asymptomatic (i.e., seen only on EEG) o Phenobarbitone is the drug of choice Metabolic o Maintain normoglycemia o Treat hypocalcemia Coagulation o Send coagulation screen; PT, PTT, D-dimer and platelets o Correct any coagulopathy with Vit K ,FFP, cryopreciptate or platelets Feeding o Withhold enteral feeds for the first 3 days o Introduce feeds cautiously when clinical condition has improved o Increase feed volumes slowly o Monitor for necrotizing enterocolitis Withdrawal of care o May be appropriate for severe HIE who have iso electric/burst suppression in EEG and abnormal cerebral blood flow on Doppler o Active treatment should be continued at least for the first 24 hours Prognosis About 20-30% of infants with HIE die in the neonatal period of survivors are left with permanent 50 neurodevelopmental abnormalities (cerebral palsy, mental retardation THAN YOU