Caput succedaneum, a common finding in the newborn, involves soft tissue swelling of the presenting part of the head in a vertex (head first) delivery. The scalp edema consists of serum, blood, or both and may have ecchymosis, petechiae, or purpura. Caput succedaneum may occur after spontaneous delivery due to pressure of the fetal head against the uterine wall, the cervix, or the vaginal wall or after use of a vacuum extractor. The scalp edema may cross over suture lines and does not continue to increase in size after delivery. This injury heals in hours to days and rarely has complications. Nursing care involves parent education about the cause of the tissue swelling and/or discoloration (Cavaliere and Sansouci 2014).

Cephalohematoma is a subperiosteal collection of blood secondary to the rupture of blood vessels between the skull and the periosteum. It is typically over the parietal bone, and is usually unilateral, but can occur bilaterally. Cephalohematoma occurs most often in infants after a prolonged, difficult, or forceps-assisted delivery. The characteristic finding is a firm, tense mass that does not cross the suture lines. It may enlarge slightly by 2–3 days of age and takes weeks to months to resolve, occasionally with residual calcification. The calcified “lump” gradually subsides as bones grow and reshape. Approximately 10–25% of cephalohematomas have an underlying linear skull fracture (Parsons et al. 2016). Rarely, the cephalohematoma may contain enough blood to affect hematocrit and bilirubin levels. Nursing care involves monitoring and parent teaching about the expected time course for resolution. Anemic infants should also be evaluated for symptoms of intracranial hemorrhage. Generally, there are no long-term sequelae from a cephalohematoma.

Subgaleal hemorrhage is the most serious extracranial hemorrhage in newborns, though it occurs much less frequently than caput succedaneum and cephalohematoma. Blood collects below the epicranial aponeurosis, which is a tough layer of dense fibrous tissue that covers the upper part of the cranium, and may spread beneath the entire scalp and down the subcutaneous tissue in the neck. There is a strong association between vacuum extraction and forceps-assisted delivery and subgaleal hemorrhage (Swanson et al. 2012). The hemorrhage may be from suture diastasis, linear skull fracture, or fragmentation of the superior margin of the parietal bone. Subgaleal hemorrhage presents as a firm fluctuant mass, crosses suture lines, and may increase in size after birth. Blood loss can be significant, possibly 260–280 ml, exceeding the total blood volume of a full-term infant (Colditz et al. 2015; Ditzenberger and Blackburn 2014). This volume loss into the large potential space between the galea aponeurotica and the periosteum of the skull can necessitate urgent blood transfusion and may contribute to hyperbilirubinemia (Colditz et al. 2015; Ditzenberger and Blackburn 2014). Early detection of this clinical emergency is vital, and the nurse should maintain a high level of suspicion for this injury after a difficult delivery. Nursing interventions include serial measurements of head circumference, inspection of the back of the head and neck for increasing edema, and observation of the ears being pushed forward and lateral. The nurse should also monitor for changes in LOC and decrease in hematocrit along with signs of hypovolemic shock (Barkovich and Raybaud 2012; Schierholz and Walker 2014). Parent teaching includes preparing them for the swelling and discoloration of the face, head, and neck and emotional support. Lesser lesions resolve in 2–3 weeks, while moderate to severe lesions may require intensive care, and up to 25% of these babies may die (Colditz et al. 2015).

Skull fractures, both depressed and linear, are occasionally seen in the newborn. The fetal skull is flexible, malleable, and poorly ossified when compared to the adult skull and thus is often able to tolerate mechanical stressors relatively well. Skull fractures can occur in utero, during labor, with forceps delivery (Fig. 8.5), or during a prolonged or difficult labor. The fetal skull can be compressed against the maternal ischial spines, sacral promontory, or symphysis pubis. Cerebral injury should be suspected when neurologic signs are apparent and there is a history of a difficult delivery. While neonatal skull fractures are generally diagnosed with skull x-rays, skull films are challenging to interpret in neonates, as they have widened sutures and decreased bone mineralization (Merhar et al. 2016). Low-dose CT scan may be a better first line of imaging, as it can be accomplished quickly without the need for sedation, and used to identify space-occupying hematomas and injury to the underlying brain (Fig. 8.5).

Depressed skull fractures may occur after forceps delivery but are occasionally observed after a spontaneous vaginal or cesarean delivery (Parsons et al. 2016). A birth-related depressed skull fracture is a visible and palpable dent in the skull, usually over the right parietal bone, which does not cross suture lines. This type of depressed skull fracture may be referred to as a “ping-pong” lesion, as it resembles a dent in a ping-pong ball (Fig. 8.6). There may be no other symptoms unless there is an underlying cerebral contusion or hemorrhage. Depressed skull fractures that are small or treated early have a good prognosis. The uncomplicated depressed fracture can be manually elevated if it does not resolve spontaneously in the first few days of life (Parsons et al. 2016). Manual elevation becomes more difficult later on. Methods to elevate the fracture include gentle pressure or use of a breast pump or vacuum extractor. As recently demonstrated, elevation can be accomplished by use of a pediatric CPR mask and negative pressure from a 50 mL syringe (Lopez-Elizalde et al. 2013). Surgical intervention is necessary when the depressed fracture cannot be elevated manually, when bone fragments are in the cerebrum, if neurologic deficits exist, or if intracranial pressure is increased. If there is CSF leakage, antibiotics may be prescribed for prophylaxis. Some infants will require treatment for shock and hemorrhage.

Linear skull fractures usually occur in the frontal and parietal bones and are often associated with extracranial hemorrhage, such as cephalohematoma. They are typically asymptomatic. The exact incidence is unknown as routine x-rays in otherwise healthy newborns are uncommon. Linear fractures are rarely complicated by intracranial hemorrhage (Ditzenberger and Blackburn 2014). Linear skull fractures in infants may spontaneously heal in 6 months with no sequelae (Barkovich and Raybaud 2012), unless a dural tear allows the leptomeninges to protrude into the fracture site (i.e., growing fracture of childhood). A cyst may form and grow, causing the fracture to enlarge. Leptomeningeal cyst is rare, occurring in less than 1% of linear fractures in children under age 3 years (Greenberg 2016). Larger fractures have a greater risk of sequelae, especially if treatment is delayed. Sequelae are related to the cerebral injury, from either dural hemorrhage or hypoxic event, or both, not from the fracture itself (Ditzenberger and Blackburn 2014).

Nursing interventions for neonatal skull fractures include supportive care and monitoring of the infant for signs of neurologic dysfunction, such as increased ICP from hemorrhage, seizures, apnea, and meningitis. If there is a depressed fracture, parents may be concerned about brain damage and their infant’s appearance. Parents should be educated to observe their infant for and report signs of increased ICP, which would include irritability, poor feeding, vomiting, and hypersomnolence. Parents should also report a growing bulge at the fracture site, which could indicate a growing fracture. The fracture site should be examined at each newborn visit.

Intracranial hemorrhage may occur in the neonate secondary to trauma or hypoxia in the perinatal period (epidural hemorrhage (EDH), primary subarachnoid hemorrhage (SAH), subdural hemorrhage (SDH), intracerebellar hemorrhage) or due to immature structures and hemodynamics in the premature infant (periventricular/intraventricular hemorrhage (P/IVH)), especially those under 32-week gestational age at birth. The pathophysiology of P/IVH involves disruption to the autoregulation of CBF, which is affected by hypoxia and acidosis, leaving the germinal matrix area vulnerable to systemic blood pressure changes. Systemic blood pressure changes may be caused by handling, suctioning, positive-pressure ventilation, hypercapnia, and rapid volume expansion (Ditzenberger and Blackburn 2014).

EDH is a rare occurrence and may be associated with cephalohematoma. An EDH in the newborn is a blood collection above the dura mater and below the periosteum. Most cases are associated with a linear skull fracture. Nearly all affected infants have a history of difficult delivery. Signs of increased ICP, including a bulging fontanel, may be apparent within the first hours of life. An emergent CT scan should be performed, and surgical evacuation may be required, depending on the size of the EDH and the associated symptoms of increased ICP. Aspiration of any accompanying cephalohematoma has been reported as a means of reducing the epidural lesion (Smets and Vanhauwaert 2010). Significant untreated lesions may result in death within 48 h.

Nursing care involves prompt recognition and reporting, timely preparation and transport for CT scan, transfer to the appropriate facility, and preparation for surgery. Postoperative nursing care includes supportive care for oxygenation, ventilation, thermoregulation, fluids and nutrition, pain management, and monitoring of neurologic signs. Parents will need support and teaching to understand their infant’s condition and participate in the treatment plan. Complications range from none to permanent neurologic deficits and/or seizures.

Primary SAH is the most common intracranial hemorrhage in the neonate. SAH is more common in the premature infant but also occurs in full-term infants. Primary SAH consists of venous bleeding into the subarachnoid space, unlike SAH in older children and adults, which is usually the result of arterial bleeding. The cerebral convexities, especially in the posterior fossa, are the usual sites for SAH in the neonate (Parsons et al. 2016).

Trauma causing increased intravascular pressure and capillary rupture is associated with SAH in the full-term infant. Asphyxia may cause SAH in the premature infant. Risk factors for SAH include birth trauma, prolonged labor, difficult delivery, fetal distress, and perinatal asphyxia.

The most common presentation of SAH is the asymptomatic premature infant with a minor SAH. The SAH is discovered incidentally with a bloody lumbar puncture during a sepsis work-up or cerebral ultrasound to rule out intraventricular hemorrhage. SAH can also present in a full-term or preterm infant as seizures or apnea at 2–3 days of age. Between seizures, the infant appears healthy. Rarely, infants with a massive SAH associated with birth trauma and severe asphyxia have a rapid and fatal course (Ditzenberger and Blackburn 2014).

Ultrasonography or CT is useful to confirm the diagnosis of SAH. If the infant has seizures, other causes of seizures must be eliminated. Blood in the CSF on lumbar puncture may be from SAH or from a bloody tap. Although rare, a severe, acute SAH may require a craniotomy. Infants with minor or asymptomatic SAH survive and generally have good developmental outcomes. Up to half of infants with symptomatic SAH, with sustained traumatic and hypoxic injury, have neurologic sequelae. Occasionally, SAH results in hydrocephalus due to CSF obstruction at the level of the arachnoid villi. Periodic cerebral ultrasound evaluation for ventricular size may be indicated. Nursing care involves assessment for seizures and other neurologic signs. Parents will need support and teaching about SAH, so they can understand the needs of their infant.

SDH is not unusual after vaginal delivery. Small posterior fossa subdural hematomas are common after uncomplicated vaginal deliveries (Barkovich and Raybaud 2012). The most likely site for hemorrhage is over the cerebral hemispheres. Significant bleeding over the posterior fossa causes compression of the brainstem, as do dural tears near the great vein of Galen. SDH affects full-term infants more often than preterm infants, usually as a result of precipitous, prolonged, or difficult delivery, use of forceps, cephalopelvic disproportion, breech delivery, or a large infant (Parsons et al. 2016).

Excessive head molding results in stretching of the falx (folds of dura mater that separate the two cerebral hemispheres and the two cerebellar hemispheres) and tentorium (dura mater between the cerebrum and cerebellum), and venous sinuses, with tearing of the vein of Galen or cerebral or cerebellar veins (Lynam and Verklan 2015). As with SAH, SDH diagnosis depends upon the history and presentation of the infant. If seizures are present, other causes must be excluded. SDH can occur along with SAH; cephalohematoma; subgaleal, subconjunctival, and retinal hemorrhages; skull fractures; and brachial plexus and facial palsies. MRI or CT will help to confirm the diagnosis, while ultrasound is less reliable.

Clinical signs are related to the site and severity of the bleeding. Infants with minor hemorrhage will either be asymptomatic or have minor neurological signs, such as irritability and hyperalertness. If the posterior fossa SDH is small, there may be no signs for 3–4 days. As the subdural clot enlarges, signs of increased ICP appear and the infant’s condition deteriorates. With more significant hemorrhage, the infant may demonstrate seizures in the first 2–3 days of life. These seizures are usually focal, and other neurologic signs may or may not be present, such as hemiparesis, unequal or sluggish pupils, full or tense fontanel, bradycardia, and irregular respirations. Infants with significant posterior fossa SDH have abnormal neurologic signs from birth, including stupor or coma, eye deviation, asymmetric pupil size, altered pupillary reaction to light, tachypnea, bradycardia, and opisthotonos (prolonged, sustained posture with leg extension, trunk arching, and variable arm posture, often extended). As the clot enlarges, there is rapid deterioration with signs of shock in minutes to hours. The infant becomes comatose, with fixed, dilated pupils, altered respirations and heart rate, and finally respiratory arrest.

A subset of infants have no or nonspecific signs in the neonatal period, but then present at 4 weeks to 6 months of age with increasing head size as a result of continued hematoma formation, poor feeding, failure to thrive, altered LOC, and, occasionally, with seizures due to chronic subdural effusion.

Care is primarily supportive, including oxygenation and perfusion, thermal management, and fluids and nutrition. Surgical evacuation of bleeding over the temporal convexity associated with increased ICP may be necessary for infants unable to be stabilized neurologically. Massive posterior fossa hemorrhage requires neurosurgical intervention. Infants at risk for SDH should be monitored for 4–6 months for head size, growth, feeding, activity, LOC, and seizure activity. Aside from supportive nursing care, nurses provide parents education about the cause and prognosis for their infant. Referral to early intervention services is recommended at discharge.

Prognosis varies with the size and severity of the hemorrhage. Infants with SDH, who are asymptomatic or have transient seizures in the neonatal period, do well if there is no associated cerebral injury. Minor posterior fossa hemorrhages rarely have clinical significance (Barkovich and Raybaud 2012). Early diagnosis of large posterior fossa hemorrhage with MRI and CT has improved the outcome for those infants. Most infants with massive bleeding over the tentorium or falx cerebri near the great vein of Galen die. Those who survive usually have hydrocephalus and neurologic sequelae.

Intracerebellar hemorrhage is more common in preterm than full-term infants. Although rare, it is generally associated with hypoxia in the preterm infant and associated with trauma in the full-term infant.

Intracerebellar hemorrhage may be caused by intravascular factors (vitamin K deficiency, thrombocytopenia), vascular factors (damage due to hypoxia, followed by hypertensive spikes, e.g., from too rapid intravenous colloid infusion), and extravascular factors (mechanical deformation of the occiput during forceps or breech delivery in the full-term infant, compression of the compliant skull during caregiving, or the use of constrictive bands around the head, especially in the preterm infant) (Lynam and Verklan 2015). Intracerebellar hemorrhage may be a primary bleed or extension of a hemorrhage into the cerebellum.

Infants with intracerebellar hemorrhage either present critically ill from birth, with apnea, a declining hematocrit, and death within 24–36 h, or present less ill with symptoms developing at up to 2–3 weeks of age. Clinical signs include apnea, bradycardia, hoarse or high-pitched cry, eye deviations, facial paralysis, opisthotonos or intermittent tonic extension of the limbs, seizures, vomiting, hypotonia, diminished or absent Moro reflex, and hydrocephalus (Ditzenberger and Blackburn 2014).

Cranial ultrasound and/or CT scan is used for diagnosis. Lack of echogenicity of the cerebellum may be an important finding (Lynam and Verklan 2015). Intracerebellar hemorrhage is frequently diagnosed at autopsy. Treatment is primarily supportive. Surgery may be indicated, including hematoma evacuation or ventriculoperitoneal shunt for hydrocephalus. Nursing care involves supportive care for the infant and care and comfort for the parents/family, including referral for early intervention services after discharge. Prognosis is poor in preterm infant survivors. Full-term infants have more favorable outcomes, but generally with subsequent neurologic deficits, especially motor and variable involvement of intellect.

The pediatric skull provides a protective box, which houses the brain. Forces exerted on the skull are absorbed initially in a centrifugal configuration and then directed inward toward the brain. Fractures occur when the skull cannot withstand the force of impact. As mentioned previously, the pediatric skull is thinner and more deformable when compared to the adult skull, which predisposes the child to significant traumatic brain injury with or without the presence of a skull fracture. As summarized by Pinto et al. (2012), the incidence of skull fractures in children with TBI ranges from 2% to 26%. Of these, 75% occur in severe TBI as opposed to less than 10% in mild TBI. Almost half of all intracranial injury occurs without skull fracture. The most common location for pediatric skull fracture is parietal (60–70%), followed by occipital, frontal, and temporal locations. Skull fractures are described as linear, closed/open, depressed, or basilar. The majority of pediatric skull fractures are linear.

The nursing assessment should include inspection and gentle palpation of the scalp to check for findings consistent with a skull fracture. External evidence of skull fracture includes swelling, hematoma, depression of the scalp, laceration with or without hemorrhage or cerebrospinal fluid (CSF) leak, or extruding brain. Basilar skull fractures are identified by external clinical findings. Basilar fracture of the temporal bone results in “Battle’s sign,” which is postauricular ecchymoses and can be associated with CSF leak from the ear (otorrhea). A frontal basilar fracture results in “raccoon eyes,” which is periorbital ecchymoses. CSF leak from the nares (rhinorrhea) can result secondary to frontal basilar fracture. The majority of cerebrospinal fluid leaks resolve within a few days without surgical intervention. Nursing care of the patient with CSF leak includes elevation of the head of the bed, restriction of nose blowing, and reporting of fever or other signs of meningitis. The neurosurgeon may need to place a lumbar drain to allow the leak to seal or perform surgical closure if conservative management is unsuccessful. Check with the neurosurgeon before placement of a nasogastric tube, as a frontal fracture through the cribriform plate can allow placement of the catheter into the brain.

Linear nondepressed skull fractures occur in the calvaria (upper portion of the frontal, parietal, and occipital bones) and heal without intervention (Gaynor et al. 2015). Only 15–30% are associated with intracranial injury (Schutzman and Greenes 2001). Complex fractures – multiple, stellate (multiple linear fractures radiating from the site of impact) (Farlex Medical Dictionary 2012), or crossing a venous sinus – are more often associated with intracranial hemorrhage or injury (Gaynor et al. 2015). Initial management of skull fractures is identification of any serious underlying acute hemorrhage or brain injury. While skull fractures are readily visible on skull radiographs as thin, dark lines, CT is the gold standard to determine if there is any underlying brain injury (Pinto et al. 2012). The middle meningeal artery is housed in a groove of the temporal bone. Laceration by the sharp bony edge of the fracture causes serious life-threatening epidural hematoma formation and need for emergent surgical intervention following temporal bone fracture (Greenberg 2016).

Young children with a diastatic skull fracture (occurring along or widening a cranial suture line) and an underlying dural tear may develop a leptomeningeal cyst or growing fracture of childhood. This is rare, occurring less than 1% of the time in children less than 3 years of age. The opening in the dura allows the cerebrospinal fluid (CSF), dura, and brain to pulse outwardly into the area of the fracture, preventing healing and causing outward eversion or “growth” of the fracture margins. A new soft, pulsatile swelling on the scalp is suspicious for a growing skull fracture and requires imaging with a head CT to assess the fracture and brain MRI to determine the extent of brain changes and dural tear (Pinto et al. 2012). Leptomeningeal cysts require early craniotomy, repair of the torn dura, and cranioplasty, as delayed diagnosis or surgical correction may lead to progressive skull defect and brain damage (Pinto et al. 2012).

Depressed skull fractures (bone depressed below the inner table of the skull) occur in 7–10% of children with head injury. The depressed fragment can cause hemorrhage secondary to tearing of a venous sinus and injury (contusion) to underlying brain (Pinto et al. 2012). Minimally depressed fractures (less than full thickness of skull), without skin laceration or underlying brain injury, do not require surgery. Nonsurgical management in this case is not associated with increased risk for seizures, neurologic impairment, or cosmetic deformity (Gaynor et al. 2015). In younger children with growing skulls, these fractures tend to remodel to a cosmetically pleasing appearance. Closed, open (compound) depressed skull fractures with skin laceration, dural tear, parenchymal injury, CSF leak, brain extruding through laceration, and focal neurologic deficit require surgical elevation, debridement of pulped brain, evacuation of hemorrhage, and dural repair. The case study in this chapter (see case study and Fig. 8.11a–f) gives an example, including radiographic imaging, of a patient with a depressed skull fracture and severe underlying brain injury.

Ping-pong fractures are a subset of depressed skull fractures which occur in newborns and young infants due to the thin, pliable skull and consist of a greenstick fracture and skull depression which resembles a depression in a ping-pong ball (see Fig. 8.6). Due to rapid skull growth, most ping-pong fractures heal well without surgery and mold to become cosmetically acceptable. Elevation is required for underlying brain injury, parenchymal bone fragments, neurologic deficit, or cosmesis in older infants (Gaynor et al. 2015).

Basilar skull fractures occur in the anterior, middle, or posterior fossa at the base of the skull and frequently extend from temporal bone or from paranasal sinus fractures. They occur in about 6–14% of pediatric traumas, and 80% of those have associated complications (Pinto et al. 2012). Cerebrospinal fluid leak via the ear or nose occurs in about a quarter of basilar skull fractures and most often resolves within a few days. Persistent CSF leak requires surgical closure. Meningitis can occur secondary to CSF leak. The use of antibiotics is controversial and not often recommended due to the risk of selecting out resistant organisms. Structures at the skull base are susceptible to injury and include the carotid artery (dissection), venous sinus, cranial nerves, and the middle ear (Gaynor et al. 2015). Basilar skull fractures may be difficult to see on CT, but findings of pneumocephalus and opacification of the mastoid air cells are suggestive. Plain films and clinical findings such as CSF otorrhea or rhinorrhea, hemotympanum, Battle’s sign, raccoon eyes, and cranial nerve injuries are more sensitive indicators (Greenberg 2016).

Temporal bone fractures are classified as transverse (extending across the petrous portion) or longitudinal (extending lateral to medial). Complications associated with transverse temporal bone fracture include sensorineural hearing loss (CN VIII) and facial nerve dysfunction (CN VII), whereas longitudinal temporal fracture can cause hemotympanum, torn tympanic membrane, CSF leak, and conductive hearing loss secondary due to bony disruption. In most cases, the hearing loss resolves, but it can be permanent. Most basilar skull fractures resolve without surgery (Pinto et al. 2012). Inner ear injury and hearing loss are typically referred to an ENT specialist.

Extra-axial hematomas are those occurring outside the brain itself and are defined by etiology (venous, arterial), location in relationship to the meninges (epidural, subdural, subarachnoid), speed of occurrence, and size. The presentation and acuity level varies based on the child’s age, as well as location and size of the hemorrhage. Rapidly expanding hemorrhage results in an increase in intracranial volume and causes mass effect with shift of the midline brain structures. Mass effect compounded with associated cerebral swelling and injury results in increased ICP. The classic presentation in a child with a rapidly expanding mass lesion is reduced level of consciousness, ipsilateral mydriasis (same-side, fixed, and dilated pupil), and contralateral hemiparesis (opposite-side weakness). Small hemorrhages with minimal or no clinical deterioration may be observed with close monitoring and follow-up imaging. Venous-origin hematomas can present in delayed fashion (Figaji 2015), making serial neurologic assessment and follow-up imaging important in order to catch deterioration early. Hematomas of arterial origin (accumulate rapidly), posterior fossa location (small space, pressure on brainstem, hydrocephalus secondary to occlusion of fourth ventricle), and those that are large or associated with underlying brain swelling are higher risk lesions (Figaji 2015). Large hematomas with significant mass effect, underlying brain injury, and in a deteriorating or comatose patient require emergent craniotomy and surgical decompression.