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Explore the definition, causes, and effects of fetal hypoxia-ischemia during childbirth, from maternal disorders to post-birth complications. Discover the pathology, neurology, and clinical manifestations associated with this condition.
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Asphyxia(Hypoxia-Ischemia) Definition: Umbilical artery PH<7 5min apgar <3 Multiple organ dysfunction Hypoxic ischemic encephalopathy
Fetal hypoxia may be caused by various disorders in the mother, including (1)inadequate oxygenation of maternal blood from hypoventilation during anesthesia, cyanotic heart disease, respiratory failure, or carbon monoxide poisoning; (2)low maternal blood pressure from acute blood loss, spinal anesthesia, or compression of the vena cava and aorta by the gravid uterus; (3) inadequate relaxation of the uterus to permit placental filling as a result of uterine tetany caused by the administration of excessive oxytocin; (4)premature separation of the placenta; (5)impedance to the circulation of blood through the umbilical cord as a result of compression or knotting of the cord; and (6)Placental insufficiency from toxemia or postmaturity.
After birth hypoxia may be caused by (1)failure of oxygenation (severe forms of CHD or severe pulmonary disease) (2) anemia severe enough to lower the oxygen content of the blood (severe hemorrhage, hemolytic disease); (3) shock severe enough to interfere with the transport of oxygen to vital organs (from overwhelming sepsis, massive blood loss, and intracranial or adrenal hemorrhage.)
PATHOPHYSIOLOGY Animal studies suggest thathypoxia will not cause lethal brain injury without ischemia. Thetopography of injury typically correlates to areas of decreasedcerebral blood flow. After an episode of hypoxia and ischemia,anaerobic metabolism occurs, which generates increased amountsof lactate and inorganic phosphates. Excitatory and toxic aminoacids, particularly glutamate, accumulate in the damaged tissue.Increased amounts of intracellular Na+ and Ca++ may resultin tissue swelling and cerebral edema. There is also increased productionof free radicals and nitric oxideand free iron in these tissues.
PATHOPHYSIOLOGY Theinitial circulatory response of the fetus is increased shuntingthrough the ductus venosus, ductus arteriosus, and foramenovale, with transient maintenance of perfusion of the brain, heart,and adrenals in preference to the lungs, liver, kidneys, andintestine) Diving reflex). *During prolonged partial asphyxia this redistribution of available cardiac output to more vital organs happens. (Michigan manual of NICU)
PATHOLOGY The pathology of hypoxia-ischemia is dependent on theaffected organ and the severity of the injury. Early congestion,fluid leak from increased capillary permeability, and endothelialcell swelling may then lead to signs of coagulation necrosis andcell death. Congestion and petechiae are seen in the pericardium,pleura, thymus, heart, adrenals, and meninges. Prolongedintrauterine hypoxia may result in inadequate perfusion of theperi ventricular white matter, resulting, in turn, in PVL. Pulmonaryarteriole smooth muscle hyperplasia may develop, whichpredisposes the infant to pulmonary hypertension . If fetal distress produces gasping, the amniotic fluid contents(meconium, squames, lanugo) are aspirated into the tracheaor lungs. The combination of chronic fetal hypoxia and acute hypoxicischemicinjury after birth results in gestational age-specific neuropathology.
NEUROPATHOLOGY Preterm infants Term infants PVL (later, spastic diplegia), status marmoratus of the basal ganglia, and IVH. neuronalnecrosis of the cortex →cortical atrophy and parasagittalischemic injury. Proximal limb weakness Upper extremities affected more than lower extremities.
Clinical manifestations before birth IUGR withincreased vascular resistance may be the 1st indication of fetalhypoxia. During labor, the fetal heart rate slows, and beat-to-beatvariability declines.
prevention Particularly in infants near term, these signs should leadto the administration of highconcentrations of oxygen to themother and immediate delivery to avoid fetal death or CNSdamage.
Clinical manifestations at birth 1-the presence of yellow, meconium-stained amnioticfluid is evidence that fetal distress has occurred. 2-theseinfants are frequently depressed and fail to breathe spontaneously.(Delayed crying). 3-During the ensuing hours, they may remain hypotonicor change from hypotonic tohypertonic, or their tone may appearnormal . 4- low Apgar score and need for CPR at birth. 5- pale – cyanotic 6- seizure during the first 24-48 hr of birth.
Symptoms developover a series of days, making it important to perform serial neurologicalexaminations. During the initial hoursafter an insult, infants have a depressed level of consciousness.Periodic breathing with apnea or bradycardia is present, butcranial nerve functions are often spared with intact pupillaryresponses and spontaneous eye movement. Seizures are commonwith extensive injury. Hypotonia is also common as an earlymanifestation.
Seizure • phenobarbital the drug of choice, is given with an intravenous loading dose(20 mg/kg); additional doses of 5-10 mg/kg (up to 40-50 mg/kgtotal) may be needed. • Phenytoin (20 mg/kg loading dose) orlorazepam (0.1 mg/kg) may be needed for refractory seizures. • Phenobarbital levels should be monitored 24 hr after theloadingdose and maintenance therapy(5 mg/kg/24 hr) are begun. • Therapeuticphenobarbital levels are 20-40 μg/ mL .
Other organs: • heart failure and cardiogenicshock, • persistent pulmonary hypertension, • respiratory distresssyndrome, • gastrointestinal perforation, • hematuria, and • Acutetubular necrosis
IMAGING • Ultrasound has limited utility in evaluation ofhypoxic injury in the term infant; it is the preferred modality inevaluation of the preterm infant. • CT scans are helpful in identificationof focal hemorrhagic lesions, diffuse cortical injury, anddamage to the basal ganglia; CT has limited ability to identifycortical injury within the 1st few days of life. • Diffusion-weighedMRI is the preferred imaging modality because of its increasedsensitivity and specificity early in the process and its ability tooutline the topography of the lesion.
PROGNOSIS • The outcome of HIE correlates to the timing andseverity of the insult and ranges from complete recovery to death.The prognosis varies depending on whether the metabolic andcardiopulmonary complications (hypoxia, hypoglycemia, shock)are treated, the infant's gestational age (outcome is poorest if theinfant is preterm), and the severity of the encephalopathy. • Severeencephalopathy, characterized by flaccid coma,apnea, absent oculocephalic reflexes, and refractory seizures, isassociated with a poor prognosis. A low Apgar score at 20 min,absence of spontaneous respirations at 20 min of age, and persistenceof abnormal neurologic signs at 2 wk of age also predictdeath or severe cognitive and motor deficits.
PROGNOSIS • The combined useof an early electroencephalogram (EEG) and MRI is useful in predictingoutcome in term infants with HIE. • Normal MRI and EEGfindings are associated with a good recovery, whereas severe MRIand EEG abnormalities predict a poor outcome. Infants withstage 2 and 3 encephalopathy are at the highest risk for adverseoutcome. • Microcephaly and poor head growth during the 1styear of life also correlate with injury to the basal ganglia andwhite matter and adverse developmental outcome at 12 mo. • Allsurvivors of moderate to severe encephalopathy require comprehensivehigh-risk medical and developmental follow-up ) including BAEPs )Earlyidentification of neurodevelopmental problems allows promptreferral for developmental, rehabilitative, neurologic care, andearly intervention services so that the best possible outcome canbe achieved.
Prognosis • The degree of maturity at birth is an important predictor of mortality in infants asphyxiated at birth. • Metabolic acidosis is a bad prognostic factor as compared with respiratory acidosis. • Extended Apgar score is a reliable predictor of ultimate neurologic morbidity, especially when very low scores are obtained at 20 minutes. • The time from birth until onset of spontaneous, sustained respirations is correlated with long term neurologic function. data suggests that a prolonged delay in the initiation of spontaneous respirations is a reasonable indicator of irreversible brain damage. • For infants with severe HIE the outcome is far worse, varying from a 50% to 100% mortality rate to severe disability with an average incidence of 65% to 75%.
Prognosis Infants may be at higher risk for neurodevelopmental sequelae if: • 1-apgar score ≤3 at≥ 20 minutes • 2- seizures are difficult to control • 3-EEG shows burst suppression pattern • 4-severe, protracted oliguria or renal failure is seen • 5-the infant has an abnormal neurologic examination at≥5days postnatal age( term infants) (Michigan manual of NICU)
Brain death • after neonatal HIE is diagnosed by the clinical findings of coma unresponsive to pain, auditory, or visual stimulation; apnea with PC02 rising from 40 to over 60 mm Hg without ventilatory support; and absent brainstem reflexes (pupil, oculocephalic, oculovestibular, corneal, gag, sucking).These findings must occur in the absence of hypothermia, hypotension, and elevated levels of depressant drugs (phenobarbital). • An absence of cerebral blood flow on radionuclide scans and no electrical activity on EEG (electrocerebral silence) is inconsistently observed in clinically brain-dead neonatal infants. • Persistence of the clinical criteria for 2 days in term and 3 days in preterm infants predicts brain death in most asphyxiated newborns. • Nonetheless, no universal agreement has been reached regarding the definition of neonatal brain death. Consideration of withdrawal of life support should include discussions with the family, the health care team, and, if there is disagreement, an ethics committee.
medical orders for asphyxia 1- NPO (risk of NEC) 2- Restriction of intravenous fluid 3- CBC – Retic – NRBC – Na – K – BUN – Cr – Bs – Ca – P – uric acid – ABG – PT – NH3 – SGOT – SGPT – Alb – Total protein – LP→ (L/P ratio)* 4- Brain sonography – CT scan – MRI 5- EEG / a EEG 6- Local cranial hypothermia – allopurinol - nicardipine – Phenobarbital 7- control for seizure 8- control I/O 9- daily weight 10- control brain edema * lactate/ pyruvate
