Atlas of Neonatal Pathology
Marta Ježová, Josef Feit
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+ Neonatal pathology
+ Basic terms and classification of newborn infants
+ The Apgar score
+ Classification of newborn infants by weight and gestation
+ Pathology of gestation length
+ Prematurity
+ Postmaturity (Clifford syndrome)
+ Growth and developement
+ Intrauterine growth retardation (IUGR), small for gestational age infant (SGA)
+ Large for gestational age infant (LGA)
+ Physical maturity
+ Pathology of prematurity
+ Gross appearance of premature infant
+ Difficulties in maintaining homeostasis
+ Thermoregulation
+ Hypoglycemia
+ Hyperbilirubinemia
+ Fluids and electrolytes
+ Apnea of prematurity
+ Anemia of prematurity
+ Hyaline membrane disease (HMD)
+ Necrotizing enterocolitis (NEC)
+ Intraventricular hemorrhage (IVH)
+ Periventricular leukomalacia (PVL)
+ Patent ductus arteriosus (PDA)
+ Iatrogenic diseases and damage
+ Respiratory system
+ Injuries caused by endotracheal intubation
+ Pulmonary air leak
+ Bronchopulmonary dysplasia (BPD)
+ Retinopathy of prematurity (ROP)
+ Cardiovascular system
+ Total parenteral nutrition associated hepatic damage
+ Infections
+ Viability, survivability and long term sequelae of prematurity
+ Viability
+ Survivability in prematurity
+ Severe long term sequelae in babies born prematurely
+ Birth asphyxia
+ Hypoxic-ischemic encephalopathy (HIE)
+ Meconium aspiration syndrome (MAS)
+ Persistent pulmonary hypertension of the newborn (persistent fetal circulation)
+ Birth trauma
+ Extracranial lesions
+ Soft tissus injuries
+ Intraabdominal injuries
+ Peripheral and cranial nerve injuries
+ Bone injuries
+ Cranial trauma
+ Perinatal infection
+ Intrauterine infections (TORCH group)
+ Sepsis neonatorum
+ Blenorrhea neonatorum
+ HIV infection
+ Stillbirth and perinatal mortality
+ Stillbirth
+ Perinatal mortality
+ Neonatal pathology nonrelated to prematurity, birth asphyxia or infection
+ Congenital anomalies in liveborn infants
+ Kernicterus
+ Hemorrhagic disease of the newborn
+ Spontenous gastric perforation in a neonate
Birth asphyxia

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.


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 0 – 3 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: oligo-anuria, 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

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


  • congestion, swelling
  • typical patterns of hypoxic-ischemic encephalopathy are evident if the infant survives for 24 – 48 hours or more.


  • acute congestion of the medulla
  • acute tubular necrosis

Hemorrhagic lesions

  • massive pulmonary hemorrhage
  • adrenal hemorrhage seen particularly in breech delivery