The forces of labor and delivery occasionally cause physical injury to the infant. The incidence of neonatal injury from difficult or traumatic deliveries is decreasing due to increasing use of cesarean section in place of difficult versions, vacuum extractions, or mid- or high-forceps deliveries.
A traumatic delivery is anticipated when the mother has small pelvic measurements, when the infant seems large for gestational age (often the case with diabetic mothers), or when there is a breech or other abnormal presentation, especially in a primipara. In such situations, labor and the fetal condition should be monitored closely. If fetal distress is detected, the mother should be positioned on her side and given O2. If fetal distress persists, an immediate cesarean section should be done.
Head molding is common in vaginal delivery due to the high pressure exerted by uterine contractions on the infant's malleable cranium as it passes through the birth canal. This molding rarely causes problems or requires treatment.
Caput succedaneum is edema of the presenting portion of the scalp. It occurs when the area is forced against the uterine cervix. Subgaleal hemorrhage results from greater trauma and is characterized by a boggy feeling over the entire scalp, including the temporal regions. Treatment is not required.
Cephalhematoma, or hemorrhage beneath the periosteum, can be differentiated from subgaleal hemorrhage because it is sharply limited to the area overlying a single bone, the periosteum being adherent at the sutures. Cephalhematomas are commonly unilateral and parietal. In a small percentage, there is a linear fracture of the underlying bone. Treatment is not required, but anemia or hyperbilirubinemia may result.
Depressed skull fractures are uncommon. Most result from forceps pressure or rarely from the head resting on a bony prominence in utero. Infants with depressed skull fractures or other head trauma may also have subdural bleeding, subarachnoid hemorrhage, or contusion or laceration of the brain itself (see Perinatal Problems: Intracranial Hemorrhage). Depressed skull fractures cause a palpable (and sometimes visible) step-off deformity, which must be differentiated from the palpable elevated periosteal rim occurring with cephalhematomas. CT is done to confirm the diagnosis and rule out complications. Neurosurgical elevation may be needed.
Cranial Nerve Injury
The facial nerve is injured most often. Although frequently attributed to forceps pressure, most injuries probably result from pressure on the nerve in utero, which may be due to fetal positioning (eg, from the head lying against the shoulder, the sacral promontory, or a uterine fibroid).
Facial nerve injury usually occurs at or distal to its exit from the stylomastoid foramen and results in facial asymmetry, especially during crying. Identifying which side of the face is affected can be confusing, but the facial muscles on the side of the nerve injury cannot move. Injury can also occur to individual branches of the nerve, most often the mandibular. Another cause of facial asymmetry is mandibular asymmetry resulting from intrauterine pressure; in this case, muscle innervation is intact and both sides of the face can move. In mandibular asymmetry, the maxillary and the mandibular occlusal surfaces are not parallel, which differentiates it from a facial nerve injury.
Testing or treatment is not needed for peripheral facial nerve injuries or mandibular asymmetry. They usually resolve by age 2 to 3 mo.
Brachial Plexus Injuries
Brachial plexus injuries follow stretching caused by shoulder dystocia, breech extraction, or hyperabduction of the neck in cephalic presentations. Injuries can be due to simple stretching, hemorrhage within a nerve, tearing of the nerve or root, or avulsion of the roots with accompanying cervical cord injury. Associated injuries (eg, fractures of the clavicle or humerus or subluxations of the shoulder or cervical spine) may occur.
Injuries of the upper brachial plexus (C5 to C6) affect muscles around the shoulder and elbow, whereas lesions of the lower plexus (C7 to C8 and T1) primarily affect muscles of the forearm and hand. The site and type of nerve root injury determine the prognosis.
Erb's palsy is an upper brachial plexus injury causing adduction and internal rotation of the shoulder with pronation of the forearm. Ipsilateral paralysis of the diaphragm is common. Treatment includes protecting the shoulder from excessive motion by immobilizing the arm across the upper abdomen and preventing contractures by passive range-of-motion exercises to involved joints done gently every day starting at 1 wk of age.
Klumpke's palsy is a lower plexus injury resulting in paralysis of the hand and wrist, often with ipsilateral Horner's syndrome (miosis, ptosis, facial anhidrosis). Passive range-of-motion exercises are the only treatment needed.
Neither Erb's palsy nor Klumpke's palsy usually causes demonstrable sensory loss, which suggests a tear or avulsion. These conditions usually improve rapidly, but deficits can persist. If a significant deficit persists > 3 mo, MRI is done to determine the extent of injury to the plexus, roots, and cervical cord. Surgical exploration and repair have sometimes been helpful.
When the entire brachial plexus is injured, the involved upper extremity cannot move, and sensory loss is usually present. Ipsilateral pyramidal signs indicate spinal cord trauma; an MRI should be done. The involved extremity's subsequent growth may be impaired. The prognosis for recovery is poor. Management may include neurosurgical exploration. Passive range-of-motion exercises can prevent contractures.
Other Peripheral Nerve Injuries
Injuries to other peripheral nerves (eg, the radial, sciatic, obturator) are rare in neonates and are usually not related to labor and delivery. They are usually secondary to a local traumatic event (eg, an injection in or near the sciatic nerve). Treatment includes placing the muscles antagonistic to those paralyzed at rest until recovery. Neurosurgical exploration of the nerve is seldom indicated. In most peripheral nerve injuries, recovery is complete.
Spinal Cord Injury
Spinal cord injury (see also Spinal Trauma: Spinal Cord Injury in Children) is rare and involves variable degrees of cord disruption, often with hemorrhage. Complete disruption of the cord is very rare. Trauma usually occurs in breech deliveries after excess longitudinal traction to the spine. It can also follow hyperextension of the fetal neck in utero (the “flying fetus”). Injury usually affects the lower cervical region (C5 to C7). When the injury is higher, lesions are usually fatal because respiration is completely compromised. Sometimes a click or snap is heard at delivery.
Spinal shock with flaccidity below the level of injury occurs initially. Usually, there is patchy retention of sensation or movement below the lesion. Spasticity develops within days or weeks. Breathing is diaphragmatic because the phrenic nerve remains intact as its origin is higher (at C3 to C5) than the typical cord lesion. When the spinal cord lesion is complete, the intercostal and abdominal muscles become paralyzed and rectal and bladder sphincters cannot develop voluntary control. Sensation and sweating are lost below the involved level, which can cause fluctuations of body temperature with environmental changes.
An MRI of the cervical cord may show the lesion and excludes surgically treatable lesions, such as congenital tumors or hematomas pressing on the cord. The CSF is usually bloody.
With appropriate care, most infants survive for many years. The usual causes of death are recurring pneumonia and progressive loss of renal function. Treatment includes nursing care to prevent skin ulcerations, prompt treatment of urinary and respiratory infections, and regular evaluations to identify obstructive uropathy early.
Hemorrhage in or around the brain can occur in any neonate but is particularly common in those born prematurely; about 20% of premature infants < 1500 g have intracranial hemorrhage. Hypoxia-ischemia, variations in BP, and pressures exerted on the head during labor are major causes. The presence of the germinal matrix (a mass of embryonic cells lying over the caudate nucleus on the lateral wall of the lateral ventricles and present only in the fetus) makes hemorrhage more likely. Risk also is increased by hematologic disorders (eg, vitamin K deficiency, hemophilia, disseminated intravascular coagulation).
Hemorrhage can occur in several CNS spaces. Small hemorrhages in the subarachnoid space, falx, and tentorium are frequent incidental findings at autopsy of neonates that have died from non-CNS causes. Larger hemorrhages in the subarachnoid or subdural space, brain parenchyma, or ventricles are less common but more serious.
Subarachnoid hemorrhage probably is the most common type of intracranial hemorrhage. Neonates may present with apnea, seizures, lethargy, or an abnormal neurologic examination. With large hemorrhages, the associated meningeal inflammation may lead to a communicating hydrocephalus as the infant grows.
Subdural hemorrhage, which is now less common because of improved obstetric techniques, results from tears in the falx, tentorium, or bridging veins. Such tears tend to occur in neonates of primiparas, in large neonates, or after difficult deliveries—conditions that can produce unusual pressures on intracranial vessels. The presenting finding may be seizures; a rapidly enlarging head; or an abnormal neurologic examination with hypotonia, a poor Moro reflex, or extensive retinal hemorrhages.
Intraventricular and/or intraparenchymal hemorrhage usually occurs during the 1st 3 days of life and is the most serious type of intracranial bleeding. Hemorrhages occur most often in premature infants, are often bilateral, and usually arise in the germinal matrix. Most bleeding episodes are subependymal or intraventricular and involve a small amount of blood. In severe hemorrhage, there may be bleeding into the parenchyma or a cast of the ventricular system with large amounts of blood in the cisterna magna and basal cisterns. Hypoxia-ischemia often precedes intraventricular and subarachnoid bleeding. Hypoxia-ischemia damages the capillary endothelium, impairs cerebral vascular autoregulation, and can increase cerebral blood flow and venous pressure, all of which make hemorrhage more likely. Most intraventricular hemorrhages are asymptomatic, but larger hemorrhages may cause apnea, cyanosis, or sudden collapse.
Intracranial hemorrhage should be suspected in any neonate with apnea, seizures, lethargy, or an abnormal neurologic examination; such infants should have head CT. Although cranial ultrasonography is risk free, requires no sedation, and can readily identify blood within the ventricles or brain substance, CT is more sensitive for thin layers of blood in the subarachnoid or subdural spaces. However, for screening of very premature infants (eg, < 30 wk gestation), some clinicians prefer the logistical simplicity of ultrasonography. If the diagnosis is in doubt, the CSF can be examined for RBCs: it usually contains gross blood. However, some RBCs are often present in the CSF of term neonates. In subdural hemorrhage, transillumination of the skull may reveal the diagnosis after the blood has lysed.
Additionally, clotting studies, a CBC, and metabolic studies to identify other causes of neurologic dysfunction (eg, hypoglycemia, hypocalcemia, electrolyte imbalance) should be done. An EEG may help establish prognosis if the infant survives the acute bleeding episode.
The prognosis for subarachnoid hemorrhage is usually good. The prognosis for subdural hemorrhage is guarded, but some infants do well. Most infants with small intraventricular hemorrhages survive the acute bleeding episode and do well. Infants with large intraventricular hemorrhages have a poor prognosis, especially if the hemorrhage extends into the parenchyma. Preterm infants with a history of severe intraventricular hemorrhage are at risk of developing posthemorrhagic hydrocephalus and must be monitored carefully with serial cranial ultrasound examinations and frequent serial head circumference measurements. Infants with progressive hydrocephalus require neurosurgical evaluation for the placement of a subcutaneous ventricular reservoir (to aspirate CSF) or for the placement of a ventriculoperitoneal shunt. The CSF associated with posthemorrhagic hydrocephalus has a very low glucose concentration known as hypoglycorrhachia. Because many infants will be left with neurologic deficits, careful follow-up and referral for early intervention services are important.
Treatment is mostly supportive unless a hematologic abnormality contributed to the bleeding. All infants should receive vitamin K if not previously given. If deficient, platelets or clotting factors should be given. Subdural hematomas should be managed by a neurosurgeon; evacuation of the hemorrhage may be needed.
Midclavicular fracture, the most common fracture during birth, occurs with shoulder dystocia and with normal, nontraumatic deliveries. Initially, the neonate is irritable and does not move the arm on the involved side either spontaneously or when the Moro reflex is elicited. Most clavicular fractures are greenstick and heal rapidly and uneventfully. A large callus forms at the fracture site within a week, and remodeling is completed within a month. Treatment consists of making a sling by pinning the shirt sleeve of the involved side to the opposite side of the infant's shirt.
The humerus and femur may be fractured in difficult deliveries. Most of these are greenstick, mid-shaft fractures, and excellent remodeling of the bone usually follows, even if moderate angulation occurs initially. A long bone may be fractured through its epiphysis, but prognosis is excellent.
All soft tissues are susceptible to injury during birth if they have been the presenting part or the fulcrum for the forces of uterine contraction. Edema and ecchymosis often follow injury, particularly of the periorbital and facial tissues in face presentations and of the scrotum or labia during breech deliveries. Breakdown of blood within the tissues and conversion of heme to bilirubin result whenever a hematoma develops. This added burden of bilirubin may cause sufficient neonatal hyperbilirubinemia to require phototherapy, and rarely, exchange transfusion (see Metabolic, Electrolyte, and Toxic Disorders in Neonates: Kernicterus). No other treatment is needed.
Last full review/revision March 2007 by James W. Kendig, MD