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PERINATAL ASPHYXIA Dr.Nadeem-Ur-Rasool DCH Trainee


DEFINITIONS ASPHYXIA :- Lack of Oxygen due to failure of initiation of breathing. HYPOXEMIA :- ↓ Oxygenation of the blood HYPOXIA :- ↓ Oxygen supply to the tissues. HYPERCAPNIA :- Impairment in the exchang of respiratory gases.


Cont…...…. ISCHEMIA :- Decreased blood flow to cells\organs insufficient to maintain their function. PERINATAL ASPHYXIA \ HIE :- Impaired blood gas exchange during intrapartum period.If persists leads to progressive hypoxemia & hypercapnia with metabolic acidosis that may result in ischemic encephalopathy.


Cont……... NEONATAL ENCEPHALOPATHY :- Disturbed neurologic functions …. difficulity in maintaining respiration,hypotonia,altered level of consciousness,reflexes,seizures&poor feeding.Does not imply HIE.HIE is a subset of NE.


PERINATAL ASPHYXIA Criteria required to define an acute intrapartum event include; Evidence of metabolic acidosis in fetal blood. Early onset of severe or moderate NE in infants born at ≥34 wks gestation. Exclusion of other identifiable etiologies……… ..trauma , coagulation disorders , infections or genetic disorders.


CAUSES MATERNAL CAUSES Placental Insuffiency ( hypertension,pr-eclempsia,eclampsia,renal failure) Diabetes Chronic Lung Disease Hypotension Pelvic Abnormality Abnormal myometrial contractility (Obstructed Labor) Use of anaesthetics


Cont…...… FETAL CAUSES Abnormal lie \ presentation Cephalopelvic disproportion Postmaturity Placental infarction Placental seperation Placentitis Antepartum hemorrhage Cord prolapse \ Cord compression


Cont…..….. NEONATAL CAUSES Airway obstruction (mucus plug \ blood clot) Aspiration pneumonia Choanal atresia Diaphragmatic hernia Depressed respiratory center (Prolonged labor \ anaesthetics )


PATHOPHYSIOLOGY Oxygen is essential for normal functioning of body cells \ organs. The Pathology depends upon the organ affected & severity of insult. Organ system involvement is usually * CNS 72% (most frequently involved) * Renal 42% * Cardiac 29% * GIT 29% * Pulmonary 26%


Cont…..…. ↓ Oxygen (Asphyxia) is followed by * Metabolic Acidosis * Hypoglycemia * Hypotension * Alteration in cerebral blood flow


Cont…. ↑ Glycolysis results in ↑ lactate levels High energy phosphate concentrations ↓


Cont…..….. Energy dependent ionic pumps fails resulting in * ↓ in normal intracellular potassium due to leakage. * Influx of sodium,chloride & calcium into cells


Cont…. Membrane depolarization occurs leading to release of the exitotoxic neurotransmitters (glutamate & Aspartate ) which activate N-methyl-D- aspartate receptors which plays a critical role in neuronal demage .


Cont………. Major circulatory changes during asphyxia are: * Loss of cerebrovascular autoregulation (Cerebral blood flow becomes “Pressure Passive”) * Initial increase in CBF (2 nd ry to redistributin of cardiac output , initial systemic HTN, loss of cerebro -vascular auto-regulation , local accumulation of vasodilator factors i.e H*.K*, adenosine,prostaglandin ) ↓


Cont…. * In prolonged asphyxia…. ↓ In cardiac output, hypotension, ↓ CBF. * Post-asphyxia… persistance state of vasoparalysis & cerebral hypremia ……. severity correlates with severity of insult.


Cont………. In CNS decreased cerebral oxygenation & hypo-perfusion in combination with metabolic changes increased capillary permeability resulting in fluid leaks…cerebral edema & cell death. Full term infants show cortical necrosis & para-sagittal ischemic injury resulting in focal & multifocal cortical infarcts producing focal seizures & hemiplegia .


Cont……. In Preterm infants…. Periventricular leukomalacia,basal ganglia demage & IVH occurs. The majority of neuronal disintegration occurs after termination of the asphyxial insult. (due to persistence of abnormal energy metabolism & low ATP levels)


STAGES OF HIE Stage 1 : Hyperalertness,uninhibited Moro & stretch reflexes lasting < 24 hours. Stag 2 : Progressive obtundation,hypotonia , ↓ spontaneous movements with or without seizures. Stage 3 : Stuporous & flaccid with depressed brain stem responces & have seizures.

Multiple Organ Involvement:

Multiple Organ Involvement CVS : shock,hypotension,tricuspid insufficiency,myocardial necrosis,CCF,ventricular dysfunction RENAL : Oliguria \ anuria,acte tubular or cortical necrosis, renal failure. HEPATIC : ↑ ammonia & indirect bilirubin , ↓ clotting factors at 3-4 days of age in mod. To severe asphyxia . ↓


Cont…..…. GIT : Paralytic ileus , NEC. LUNGS : RDS , Pul.Hemorrhage , shock lung , pul.hypertension HAEMATOLOGIC : Thrombocytopenia,DIC . METABOLIC : Acidosis , hypoglycemia , hypocalcemia , hyponatremia ,SIADH.


INCIDENCE Is usually related to gestational age & birth weight . incidence is higher in premature. In developed countries is 1-2 % and in pakistan is 3.3%.


DIAGNOSIS No specific blood test to diagnose perinatal asphyxia. Fetal acidemia …fetal arterial ph <7 Umbilical artery PO 2 levels.( not predictive of adverse outcome) Apgar score… poor tool for assessing asphyxia. FHR


Cont…. EEG CT.. (assessment of diffuse cortical neuronal injury,brain calcifications, haemorrhagic lesions) MRI.. (technique of choice.periventricular white matter injury,arterial infarction,brain malformations,HIE )


MANAGEMENT Prevention….optimal management. Immediate resuscitation. Maintenance of adequate ventilation. Maintenance of adequate Oxygenation.


Cont…. Maintenance of adequate perfusion. Correction of metabolic acidosis. Maintenance of normal serum glucose level. Control of seizures.


Cont….. Prevention of cerebral edema…* fluid restriction, * mannitol (0.5-1g/kg/dose, * avoide steroids. Maintenance of fluid & electrolyte balance.. *Monitor urine output , should be more than 1 ml/kg/hr. * a single dose of theophylline within 1 st h of life in term HIE pts. May improve renal function.


Cont….. Maintenance of thermoneutral environment. Pharmacologic agents. * Mg* * agents to prevent free O 2 redical formation ( allupurinol,inhibitors of nitric oxide production) * Ca* channel blockers All these pharmacological agents remain investigational


Cont…….…. PROGNOSIS Most survivors do not have major sequelae .


Cont…. Long term neurologic sequelae can be predicted on basis of; * severity of the encephalopathy. * presence of neonatal seizures … esp. in 1 st 12h after birth. * an abnormal MRI .. obtained in 1 st 24-72 h. * severity & duration of EEG abnormalities. * microcephaly at 3 months of age or an abnormal neurologic exam at 12 months of age.


Cont….…. Nondisabled survivors of moderate HIE have ; *delayed skills in reading , spelling. *difficulties with attention. * difficulties in short term recall

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