Birth asphyxia

Definition : Birth asphyxia is a condition of impaired gas exchange occuring during labor leading to progressive hypoxia associated with carbon dioxide retention and significant metabolic acidosis. The word is derived from Greek meaning stopping of the pulse. Birth asphyxia is an important cause of perinatal mortality and neurological morbidity. Etiology:

During normal labor uterine contractions compress uterine blood vessels, resulting in intermittent interruption to blood flow into the placenta. There is no oxygen delivery to the fetus at the height of conctractions with subsequent restoring of oxygen delivery between contractions when the uterus is relaxed. There is only a slight fall in blood pH in a normal labor with a healthy fetus and placenta. On the other hand all abnormalities in the mother, placenta or fetus which prevent such succesful adaptation to the effects of uterine contractions or factors that prolonge labor result in intrapartum fetal hypoxemia. The fetus is equipped with wide range of adaptive mechanisms so moderate degree of hypoxemia is tolerated for some time. If the condition persists, the switching to anaerobic metabolism results in increasing production of lactate, acidosis and asphyxia. Prolonged periods of low oxygen concentration and acidosis have adverse effects on the fetal circulation, intrauterine fetal breathing, the brain, kidneys and other organs. Unless immediate delivery the result is irreversible organ damage to susceptible organs and ultimately cardiac arrest and intrapartum death. Causes of birth asphyxia

All the conditions which predispose to intrauterine hypoxia (fetal distress) prior to the onset of contractions may increase the asphyxial stress during labor. Maternal maternal shock, cardiac arrest or grand mal fits, preeclampsia, pregnancy cholestasis, severe anemia, smoking, compression of the aorta by the gravid uterus, chronic renal failure and heart disease, administration of anesthetics, sedative and hypotensive drugs to the mother during labor, prolonged gestation, uterine rupture Placental diseases of the placenta are frequently an extension of maternal disease. Infarcts, abnormal villous maturation, placenta praevia, placental abruption, widespread vilitis, massive perivillous fibrin deposition, villous oedema, thrombotic occlusion of fetal chorionic vessels Umbilical cord abnormal cord lenght, entaglements around fetal body and nuchal cords (only a cord tightly around the neck more than once is a risk factor), true knots, umbilical cord prolaps or compression, funisitis, umbilical vessels thrombosis, velamentous cord insertion, acute fetal blood loss with rupture of vasa previa Fetal conditions fetal size (large fetus/small growth-retarded fetus), malpresentation, fetal malformations, chronic fetal anemia and cardiac failure from any cause Mechanical factors excessive uterine contractions, prolonged labor, pelvic abnormalities Clinical signs:

Signs of fetal hypoxia before and during delivery fetal heart rate abnormalities, decreased or stopped fetal movements, thick amniotic fluid contaminated by meconium. Fetal heart rate monitoring using cardiotocography can detect hypoxic episodes well before the developement of asphyxia. Essential criteria for birth asphyxia after delivery

 prolonged metabolic or mixed acidemia (pH 7,0) on an umbilical cord arterial blood sample persistence of an Apgar score 03 for more than 5 minutes clinical neurological manifestations e.g. seizures, hypotonia, coma or hypoxic-ischemic encephalopathy in the immediate neonatal period clinical evidence of multiorgan system dysfunction in the immediate neonatal period: oligoanuria, congestive heart failure not related to structural disease, shock, persistent fetal circulation, meconium aspiration syndrome, ventilatory dependence or requirement of increased oxygen in more than 24 hours, elevated transaminasis, DIC, necrotising enterocolitis perinatal asphyxia is an extention for asphyxia occuring in the perinatal period that means antepartum, intrapartum and postpartum in the first few hours of life. Antepartum and intrapartum events are responsible for 90% of cases. Macroscopic appearance: Asphyxial lesions at autopsy congested internal organs small hemorrhages over the thymus, lungs and heart (epicardial hemorrhage), engorgement of the cerebral veins these signs are seen in the immediate post asphyxial period and are exaggerated in infants who die as a result of placental abruption

Lungs An episode of hypoxia and acidosis induces intrauterine breathing movements. The period of respiratory effort ends in deep sighing breaths and terminal apnea. The deep breaths result in masses of epithelial squames and amniotic debris being aspirated into the bronchi, bronchioli and acini. These may be visible for many weeks. intense congestion of alveoalar capillaries meconium aspiration

Brain

congestion, swelling typical patterns of hypoxic-ischemic encephalopathy are evident if the infant survives for 2448 hours or more.

Kidneys acute congestion of the medulla acute tubular necrosis Hemorrhagic lesions massive pulmonary hemorrhage adrenal hemorrhage seen particularly in breech delivery

Systemic consequences of asphyxia Perinatal asphyxia leads to muti-organ dysfunction. Virtually any organ can be effected. And care in the nursery should be oriented to determining the presence or the absence of dysfunction of the critical organ systems.. Many of these complications are potentially fatal. In term infants with asphyxia, renal, CNS, cardiac and lung dysfunction occur in 50%, 28%, 25% and 25% cases, respectively6. The extent of organ system dysfunction determines the early outcome of an asphyxiated neonate Metabolic involvement may include hypocalcemia, hyponatremia (as a result of SIADH or direct renal injury), and alterations in glucose metabolism. There may be haematological alterations (thrombocytopenia and DIC) Hypoxic ischemic encephalopathy (HIE) refers to the CNS dysfunction associated with perinatal asphyxia. HIE is of foremost concern in an asphyxiated neonate because of its

potential to cause serious long-term neuromotor sequelae among survivors

Hypoxic-ischemic encephalopathy (HIE)

Introduction: Acute and subacute brain injury due to perinatal asphyxia. Etiology:

The fundamental abnormality in HIE is a deficit of oxygen supply. This is due to hypoxemia (diminished amount of oxygen in th blood supply) and ischemia (a diminished amount of blood perfusing the brain). Loss of cerebrovascular autoregulation (the ability of brain vessels to maintain a constant cerebral blood flow in spite of fluctuations in the cerebral perfusion pressure) which occurs in asphyxiated newborns also contributes to the injury. During the perinatal period hypoxemia and/or ischemia result most commonly from asphyxia. Various causes are listed above. Only 10% of cases occur in the early postnatal period with diseases in organs responsible for oxygen delivery. These are pulmonary system diseases (airway obstruction, tracheoesophageal fistula, pneumothorax, pneumonia, hypoplastic lungs, diaphragmatic hernia etc.) and nonpulmonary causes (heart defects, heart failure etc.). There is no single presentation of this disease. Extension and distribution of brain lesions depend upon the maturational stage of the brain and the severity and duration of asphyxial injury. In premature infant the target region for pathologic damage is the periventricular white matter. Anoxic and ischemic damage to the cerebral cortex is characteristic to the term infant. Ischemic damage to the basal ganglia, thalamus and nuclei od midbrain and brain stem may be seen in infants of any gestational age. Clinical signs: Mild HIE irritability, poor feeding, excessive crying or sleepiness muscle tone is normal to slightly increased full recovery within few days Moderate and severe HIE lethargy, stupor or coma irregular heart rate, episodes of apnea poor or absent neonatal reflexes (sucking, swallowing, grasping, Moro) seizures in the first days of life persistent hypotonia

Prognosis

Mortality rate is 5075% in severe HIE. Most deaths occur in the first weeks of life due to multiorgan failure, cardiorespiratory arrest or pneumonia. 80% of infants who survive develop serious complications mental retardation, epilepsy, cerebral palsy or combination of these. Some infants with history of mild to moderate HIE have significant learning disabilities and ADHD in spite of absence of obvious signs of brain injury Cerebral palsy is non-progressive motor deficit sustained in the perinatal period. The neuropathology of cerebral palsy is complex including not only hypoxic-ischemic encephalopathy itn the perinatal period but also malformations, traumatic lesions, infections

and inborn metabolic disordes. The exact time of injury often remains uncertain, probably only 10 25% cases are related to intrapartum asphyxia. Major neuropathological patterns of injury in HIE Selective neuronal necrosis Neuronal necrosis selective to areas with high energy demands (selective vulnerability) Cerebral cortical necrosis may be focal, bilateral, symmetric of diffuse. Neuronal damage is the greatest in the depth of the sulci. Pre- and postcentral gyri, calcarine cortex are often involved. Foci of necrosis in watershed zones of the main cerebral arteries results mainly from hypotension. Hippocampus is also vulnerable to damage. Deep gray matter necrosis predominantly affects the neurons in thalamus and basal ganglia. Damage of the midbrain and brain stem nuclei may be associated Pontosubicular necrosis selective neuronal necrosis affecting the pontine nuclei and subiculum of the hippocampus, rare pattern often coexist with intraventricular hemorrhage or periventricular leukomalacia. Global cerebral necrosis involving much of th cerebral cortex, brain stem and thalamus is seen in cases of severe birth asphyxia with a significant period of cariovascular arrest. Ischemic damage to spinal cord and cerebellum is frequent on these occasions although without cardio-respiratory arrest these areas may remain intact in spite of severe changes in the cerebral hemispheres.

White matter lesions Periventricular leukomalacia common in preterm infants, see section PVL Cerebral white matter gliosis the same period in risk as PVL (2832 weeks), results from preferential injury to oligodendrocyte precursors. Severe damage results in marked decrease in the white matter volume, the corpus callosum is thin. Combined grey and white matter lesions Parasagittal cerebral injury Bilateral necrosis of the cerebral cortex and subjacent white matter in the watershed areas between the three major cerebral arteries maximal over the parasagittal region particularly in the posterior parietal location classic pattern seen in full term infants Focal and multifocal infarcts Infarction with necrosis of grey and white matter in the region of single cerebral artery

Late stages of HIE in survivors Ulegyria narrow and distorted cerebral gyri, often observed in the parasagittal areas. Sclerotic gyri contain few or no neurons being replaced by glial cells. Multifocal cystic encephalopathy sponge-like brain with large septated cavities throught the cortex and white matter of both hemisheres. There is usually relative sparing of temporal lobe, basal ganglia and brain stem. Develops as the result of an hypoxic-ischemic insult near end of gestation or in the early postnatal period. Also occurs in herpes viral infection etc. Status mramoratus marbled appearnace of striatum and/or thalamus, the appearance is caused by neuronal loss, astrogliosis and escessive myelination. This lesion develops up to the postnatal age of 69 months and is associated with complicated labor or acute febrile ilness during the first year of life.

Unifocal pseudocyst Cystic periventricular leukomalacia White matter hypoplasia overall reduction in cerebral white matter volume, hydrocephalus e vacuo and thinning of corpus callosum Porencephaly a pseudocyst which develops as a result of an ischemic brain injury in utero probably dating to the third trimestr, see Atlas of fetal pathology Hydranencephaly/basket brain severe hypoxic-ischemic damage occuring toward the end of second trimestr