Birth Injuries

Etiology

Serum or blood or both accumulate above the periosteum in the presenting part during labor. This extravasation results from the higher pressure of the uterus or vaginal wall on those areas of the fetal head that border the caput. Thus, in a left occiput transverse presentation, the caput succedaneum occurs over the upper and posterior aspect of the right parietal bone; in a right-sided presentation, it occurs over the corresponding area of the left parietal bone.

Clinical Manifestations

The soft swelling is usually a few millimeters thick and may be associated with overlying petechiae, purpura, or ecchymoses. Because of the location external to the periosteum, a caput succedaneum may extend across the midline of the skull and across suture lines. After an especially difficult labor, an extensive caput may obscure various sutures and fontanelles.

Differential Diagnosis

Occasionally, a caput succedaneum may be difficult to distinguish from a cephalhematoma, particularly when the latter occurs bilaterally. Careful palpation usually indicates whether the bleeding is external to the periosteum (caput) or beneath the periosteum (cephalhematoma). Iatrogenic encephalocele is an infrequent complication of vacuum extraction delivery and may present like a caput succedaneum initially. Imaging should be considered in every child with a large caput succedaneum that does not diminish in 48-72 hours or with enlargement of the swelling more than 24 hours after delivery, especially when there are neurologic deficits and hemodynamic instability.

Treatment

Usually no specific treatment is indicated. Rarely, a hemorrhagic caput may result in shock and require blood transfusion.

Prognosis

A caput succedaneum usually resolves within several days.

Etiology

A cephalhematoma is caused during labor or delivery by a rupture of diploic blood vessels that traverse from skull to periosteum. Repeated buffeting of the fetal skull against the maternal pelvis during a prolonged or difficult labor and mechanical trauma caused by use of forceps and vacuum suction devices in delivery have been implicated. Petrikovsky and associates described seven infants in whom cephalhematoma or caput succedaneum was identified prenatally before onset of labor. Occurrence of premature rupture of membranes in five of the pregnancies suggests an etiology of fetal head compression by the uterine wall, resulting from oligohydramnios subsequent to the ruptured membranes.

Clinical Manifestations

The bleeding is sharply limited by periosteal attachments to the surface of one cranial bone; there is no extension across suture lines. The bleeding usually occurs over one or both parietal bones. Less often, it involves the occipital bones and, very rarely, the frontal bones. The overlying scalp is not discolored. Because subperiosteal bleeding is slow, the swelling may not be apparent for several hours or days after birth. The swelling is often larger on the second or third day, when sharply demarcated boundaries are palpable. The cephalhematoma may feel fluctuant and often is bordered by a slightly elevated ridge of organizing tissue that gives the false sensation of a central bony depression. It may be associated with an underlying linear, nondepressed skull fracture in a small percentage of infants.

Radiographic Manifestations

Radiographic manifestations vary with the age of the cephalhematoma. During the first 2 weeks, bloody fluid results in a shadow of water density. At the end of the second week, bone begins to form under the elevated pericranium at the margins of the hematoma; the entire lesion is progressively overlaid with a complete shell of bone.

Differential Diagnosis

Cephalhematoma must be distinguished from other birth complications such as subgaleal hematoma, caput succedaneum, vacuum caput, leptomeningeal cyst, or congenital anomalies such as meningoceles. It may be differentiated from caput succedaneum by (1) its sharp periosteal limitations to one bone, (2) the absence of overlying discoloration, (3) the later initial appearance of the swelling, and (4) the longer time before resolution. Cranial meningocele is differentiated from cephalhematoma by pulsations, an increase in pressure during crying, and the demonstration of a bony defect on a radiograph. An occipital cephalhematoma may be confused initially with an occipital meningocele and with cranium bifidum because all occupy the midline position.

Treatment

No therapy is indicated for the uncomplicated cephalhematoma, as more than 80% resolve by gradual hemolysis and resorption in 3-4 weeks. When the hematoma does not resolve spontaneously, it may get organized, and calcification may be seen. It may still get absorbed slowly and often disappears over 3-6 months. Persistent calcification that is not resolved by time may be an indication for surgical excision. Rarely, a massive cephalhematoma may result in blood loss severe enough to require transfusion. Significant hyperkalemia and hyperbilirubinemia may result from resolving hematoma, necessitating appropriate treatment. The most common associated complications are skull fracture and intracranial hemorrhage. Linear fractures do not require specific therapy, but radiographs should be taken at 4-6 weeks to ensure closure and exclude formation of leptomeningeal cysts; depressed fractures require immediate neurosurgical consultation. Routine incision or aspiration of a cephalhematoma is contraindicated because of the risk for introducing infection. Rarely, bacterial infections of cephalhematomas occur, usually in association with septicemia and meningitis. Focal infection should be suspected when a sudden enlargement of a static cephalhematoma occurs during the course of a systemic infection, with a relapse of meningitis or sepsis after treatment with antibiotics, or with the development of local signs of infection over the cephalhematoma ( Fig. 29.3 ). Diagnostic aspiration may be indicated. If a local infection is present, surgical drainage and specific antibiotic therapy should be instituted. Osteomyelitis of the underlying skull may be a rare concurrent problem. The diagnosis may be suggested by periosteal elevation and overlying soft tissue swelling on skull radiographs. Additional rare complications that may accompany an infected cephalhematoma and osteomyelitis include venous sinus thrombosis and cerebellar hemorrhage. Magnetic resonance imaging (MRI) may be used to detect these two intracranial complications, whereas computed tomography (CT) is the best imaging modality to identify the permeative bone erosion and destruction of osteomyelitis.

Prognosis

Most cephalhematomas are resorbed within 2 weeks to 3 months, depending on their size. In a few patients, calcium is deposited ( Fig. 29.4 ), causing a bony swelling that may persist for several months and, rarely, up to several years. Radiographic findings persist after the disappearance of clinical signs. The outer table remains thickened as a flat, irregular hyperostosis for several months. Widening of the space between the new shell of bone and the inner table may persist for years; the space originally occupied by the hematoma usually develops into normal diploic bone, but cystlike defects may persist at the sites of the hematoma for months or years. Rarely, a neonatal cephalhematoma may persist into adult life as a symptomless mass, the cephalhematoma deformans of Schüller.

Etiology

The most common predisposing factor is difficult operative vaginal delivery, particularly midforceps delivery and vacuum extraction. The risk for subgaleal hemorrhage may be reduced by use of softer silicone vacuum cups instead of the original rigid metallic ones. The major risk factors include coagulopathies, prematurity, macrosomia, fetal dystocia, precipitous labor, intrapartum hypoxia, male sex, cephalopelvic disproportion, prolonged labor, and nulliparity.

Mechanism of Injury

When vacuum is used, the mechanism of injury is thought to be the vacuum traction pulling the scalp away from stationary bony calvarium, thus avulsing open the subgaleal space and causing the bridging vessels to tear and bleed into the subgaleal space. The loose connective tissue of the subgaleal space is extremely expansive and extends over the entire area of the scalp. The space can accommodate the entire neonatal blood volume (250 mL or more in a term baby), leading to hypovolemic shock, disseminated intravascular coagulation, and multiorgan failure, resulting in death in 25% of the cases.

Clinical Manifestations

Early manifestations may be limited to pallor, hypotonia, and diffuse swelling of the scalp. The development of a fluctuating mass straddling cranial sutures, fontanelles, or both is highly suggestive of the diagnosis. Because blood accumulates beneath the aponeurotic layer, ecchymotic discoloration of the scalp is a later finding. This is often associated with pitting edema and progressive posterior spread toward the neck and lateral spread around the ears, frequently displacing the ears anteriorly ( Fig. 29.6 ). Periorbital swelling and ecchymosis also are commonly observed. Eventually, hypovolemic shock, multiorgan failure, and signs of cerebral irritation develop. Massive lesions can cause extracranial cerebral compression, which may lead to rapid neurologic decompensation. The clinician should be aware of occasional “silent presentation,” in which a fluctuant mass is not apparent initially despite serial clinical examinations. Subgaleal hemorrhage should be considered in infants who show signs of hypoperfusion and falling hematocrit after attempted or successful vacuum delivery even in the absence of a detectable fluctuant mass. Close monitoring is particularly important in those infants who are considered stable enough to allow admission to the normal newborn nursery.

Radiographic Manifestations

Standard radiographs of the skull may identify possible associated fractures. Computed tomography scanning may demonstrate abundant epicranial blood, parieto-occipital bone dehiscence, bone fragmentation, and posterior cerebral interhemispheric densities compatible with subarachnoid hemorrhage.

Differential Diagnosis

In contrast with cephalhematoma, subgaleal hemorrhage is characterized by its more diffuse distribution, more rapid course, significant anemia, signs of central nervous system (CNS) trauma (e.g., hypotonia, lethargy, seizures), and frequent lethal outcome.

Treatment

Prompt restoration of blood volume with fresh frozen plasma or blood is essential. In the presence of continued deterioration, neurosurgery may be considered as a last resort. A bicoronal incision allows for exposure of the subgaleal space. Bipolar cauterization of any bleeding points can then be accomplished, and a drain can be left in the subgaleal space.

Prognosis

Although nearly 25% of infants with subgaleal hemorrhage die, long-term prognosis for survivors is generally good. More experience with aggressive and timely neurosurgical intervention may help to improve outcomes.

Etiology

Skull fractures usually follow a forceps delivery or a prolonged, difficult labor with repeated forceful contact of the fetal skull against the maternal symphysis pubis, sacral promontory, fifth lumbar vertebrae, or ischial spine. They have also been described after vacuum-assisted vaginal delivery. Most of the fractures are linear. Depressed fractures are associated with forceps application. However, they may occur spontaneously after cesarean section or vaginal delivery without forceps. Factors that also have been implicated include pressure on the fetal skull by a maternal bony prominence (e.g., sacral promontory) or uterine fibroid, a fetal hand or foot, or the body part of a twin. Occipital bone fractures usually occur in breech deliveries as a consequence of traction on the hyperextended spine of the infant when the head is fixed in the maternal pelvis.

Clinical Manifestations

Linear fractures over the convexity of the skull frequently are accompanied by soft tissue changes and cephalhematoma. Usually, the infant's behavior is normal unless there is an associated concussion or hemorrhage into the subdural or subarachnoid space. Fractures at the base of the skull with separation of the basal and squamous portions of the occipital bone almost always result in severe hemorrhage caused by disruption of the underlying venous sinuses. The infant may then exhibit shock, neurologic abnormalities, and drainage of bloody cerebrospinal fluid from the ears or nose.

Depressed fractures are visible, palpable indentations in the smooth contour of the skull, similar to dents in a ping-pong ball ( Fig. 29.7 ). The infant may be entirely free of symptoms unless there is an associated intracranial injury.

Radiographic Manifestations

The diagnosis of a simple linear or fissure fracture is seldom made without radiographs in which fractures appear as lines and strips of decreased density. Depressed fractures appear as lines of increased density. On some views, they are manifested by an inward buckling of bone with or without an actual break in continuity. Either type of fracture may be seen on only one view. CT imaging is the optimal diagnostic modality if a skull fracture and possible underlying injury are suspected.

Differential Diagnosis

Occasionally, the fragments of a linear fracture may be widely separated and may simulate an open suture. Conversely, parietal foramina, the interparietal fontanelle, mendosal sutures, and innominate synchondroses may be mistaken for fractures. In addition, normal vascular grooves, “ripple lines” that represent soft tissue folds of the scalp, and lacunar skull may be mistaken for fractures.

Treatment

Uncomplicated linear fractures over the convexity of the skull usually do not require treatment. Fractures at the base of the skull often necessitate blood replacement for severe hemorrhage and shock in addition to other supportive measures. If cerebrospinal fluid rhinorrhea or otorrhea is present, antimicrobial coverage is indicated to prevent secondary infection of the meninges.

Small (<2 cm) “ping-pong” fractures may be observed without surgical treatment. Loeser and associates reported three infants with depressed skull fractures in whom spontaneous elevation of the fractures occurred within 1 day to 3 ½ months of age. Follow-up at 1-2 ½ years revealed normal neurologic development in all three.

Several nonsurgical methods have been described for elevation of depressed skull fractures in certain infants:

• 1.

  A thumb is placed on opposite margins of the depression, and gentle, firm pressure is exerted toward the middle. After several minutes of continuous pressure, the area of depression gradually disappears.

• 2.

  A hand breast pump is applied to the depressed area. Petroleum jelly placed on the pump edges ensures a tighter seal, and gentle suction for several minutes results in elevation of the depressed bone.

• 3.

  A vacuum extractor is placed over the depression and a negative pressure of 0.2-0.5 kg/cm ² is maintained for about 4 minutes.

Because these methods are technically easier and less traumatic, they may be preferable to surgical intervention in a symptom-free infant with an isolated lesion.

Comminuted or large fractures associated with neurologic signs or symptoms should be treated by immediate surgical elevation of the indented segment to prevent underlying cortical injury from pressure. Other indications for surgical elevation include manifestations of cerebrospinal fluid beneath the galea and failure to elevate the fracture by nonsurgical manipulation.

Prognosis

Simple linear fractures usually heal within several months without sequelae.

Basal fractures carry a poor prognosis. When separation of the basal and squamous portions of the occipital bone occurs, the outcome is almost always fatal; surviving infants have an extremely high incidence of neurologic sequelae.

The prognosis for a depressed fracture is usually good when treatment is early and adequate. When therapy is delayed, especially with a large depression, death may occur from pressure on vital areas of the brain. Because the natural history of depressed skull fractures in neonates has not been clearly elucidated, the outcome is uncertain for infants with smaller lesions managed either by simple observation or by surgery after significant delays.

Etiology

Traumatic facial nerve palsy most often follows compression of the peripheral portion of the nerve, either near the stylomastoid foramen through which it emerges or where the nerve traverses the ramus of the mandible. The neonate is vulnerable to these injuries because of the superficial course of the extracranial facial nerves. The nerve may be compressed by forceps, especially when the fetal head has been grasped obliquely. The condition also occurs after spontaneous deliveries in which prolonged pressure was applied by the maternal sacral promontory. Less frequently injury is sustained in utero, often in association with a mandibular deformity, by the persistent position of the fetal foot against the superior ramus of the mandible. An extremely rare cause is the pressure of a uterine tumor on the nerve.

This condition may occur rarely with simultaneous ipsilateral brachial plexus palsy, most likely secondary to compressive forces during delivery. Contributing factors include prolonged second stage of labor and midforceps delivery.

Traumatic facial nerve palsy may follow a contralateral injury to the CNS such as a temporal bone fracture or hemorrhage, tissue destruction, or both to structures within the posterior fossa. This CNS injury is less frequent than peripheral nerve injury.

Clinical Manifestations

Paralysis is usually apparent on the first or second day but may be present at birth. It usually does not increase in severity unless considerable edema occurs over the area of nerve trauma. The type and distribution of paralysis are different in central facial paralysis compared with peripheral paralysis.

Central paralysis is a spastic paralysis limited to the lower half or two-thirds of the contralateral side of the face. The paralyzed side is smooth and full and often appears swollen. The nasolabial fold is obliterated, and the corner of the mouth droops. When the infant cries, the mouth is drawn to the normal side, the wrinkles are deeper on the normal side, and movement of the forehead and eyelid is unaffected. Usually other manifestations of intracranial injury appear, most often a sixth cranial nerve palsy.

Peripheral paralysis is flaccid and, when complete, involves the entire side of the face. When the infant is at rest, the only sign may be a persistently open eyelid on the affected side, caused by paralysis of the orbicular muscle of the eye. With crying, the findings are the same as in a central facial nerve injury, with the addition of a smooth forehead on the involved side. Because the tongue is not involved, feeding is not affected.

A small branch of the nerve may be injured, with involvement of only one group of facial muscles. Paralysis is then limited to the forehead, eyelid, or mouth. Peripheral paralysis caused by nerve injury distal to the geniculate ganglion may be accompanied by a hematotympanum on the same side.

Differential Diagnosis

Central and peripheral facial nerve palsies must be distinguished from nuclear agenesis (Möbius syndrome). The latter frequently results in bilateral facial nerve palsy; the face is expressionless and immobile, suggesting muscle fibrosis. Other cranial nerve palsies and deformities of the ear, palate, tongue, mandible, and other bones may be associated with Möbius syndrome. Congenital absence or hypoplasia of the depressor muscle of the angle of the mouth also may simulate congenital facial palsy and has been associated with an increased incidence of other congenital anomalies.

Treatment

No specific therapy is indicated for most facial palsies. If the paralysis is peripheral and complete, initial treatment should be directed at protecting the cornea with an eye pad and instilling artificial tears every 4 hours. The functional state of the nerve should be followed closely. Falco and colleagues proposed the following comprehensive approach :

• 1.

  Distinguish developmental from acquired lesions on the basis of the birth history and a detailed physical examination. Patients thought to have developmental palsy should be examined with radiologic and electrodiagnostic studies and brainstem-evoked response as appropriate.

• 2.

  Because of the expected 90% likelihood of complete spontaneous recovery, patients should be observed for 1 year before surgical intervention is considered. If recovery is suggested by physical examination or serial electromyography, observation without surgery may be delayed until the second birthday. Infants who require surgery are best treated with decompression or neuroplasty or both.

Prognosis

Most facial palsies resolve spontaneously within several days; total recovery may require several weeks or months. Electrodiagnostic testing is beneficial in predicting recovery; repeatedly normal nerve excitability indicates a good prognosis, but decreased or absent excitability early in the course suggests a poor outlook. The subsequent appearance of muscle fibrillation potentials indicates nerve degeneration. The prognosis in surgically treated infants worsens with increasing age at treatment.