Management of Neurotrauma

Caput Succedaneum

Caput succedaneum is the hemorrhagic edema of the scalp layers above the periosteum caused by head pressure against the birth canal or vacuum extractor. This pressure leads to obstruction of the venous return of the scalp and the consequent extravasation of fluid into the interstitial tissue. This edema of the scalp is usually soft and can cross suture lines of the cranium and the midline.

The management of caput succedaneum is expectant, requiring imaging only in cases of progression of the edema after 24 hours or failure of resolution after 48 to 72 hours. In cases of progression, the diagnosis of caput succedaneum should be questioned. Typical imaging can include a head ultrasound or a rapid sequence magnetic resonance image (MRI) of the head. In most cases, the correct diagnosis can be made by physical examination with determination that the edema (usually pitting) crosses suture lines and/or the midline. Pharmacologic treatment is usually not necessary and the condition usually resolves within a week of birth. Placement of scalp IVs are not contraindicated in cases of isolated caput succedaneum.

Cephalohematoma

A cephalohematoma is a collection of blood between the periosteum and the skull ( Fig. 53.2) . The hematoma is contained to a focal area of the cranium by the periosteal attachments to the sutures of the skull. Cephalohematoma occurs in about 1% to 2 % of all deliveries. The rate is higher with forceps-assisted (5%) and vacuum-assisted (4%) deliveries. Other significant risk factors for cephalohematoma include cephalo-pelvic disproportion, occipital-posterior and occipital-transverse presentations, large size, a primigravida mother, and placement of fetal scalp electrodes. Regardless of the cause, the hematoma is thought to develop from the disruption of emissary or diploic veins as the periosteum is lifted away from the skull when the head of the neonate moves with significant pressure against another surface (e.g., birth canal, forceps).

Management

• 1.

  Diagnosis

  • a.

    Physical examination: The diagnosis should be suspected on physical examination of the head of the neonate. A finding of disproportionate head shape with a nonpedunculated subcutaneous mass that does not cross suture lines or leave pitting edema and is isolated to a region of the calvaria strongly suggests a diagnosis of cephalohematoma. Head circumference measurement and size of the hematoma must be documented and serially measured to establish stability or progression of the hemorrhage. A thorough neurologic examination should always be obtained, looking for associated deficits that can indicate a more serious lesion.

  • b.

    Imaging and laboratory workup: Head ultrasonography can be a practical bedside method to obtain objective measurements of the hematoma; it can also identify associated intracranial hemorrhage such as epidural hematoma. The use of higher-resolution techniques can further delineate the morphologic characteristics and the extent and location of the hematoma(s). The use of limited (rapid sequence T2-HASTE technique) MRI is of particular value in the sense that it provides more detailed images of the brain and scalp without exposing the neonate to ionizing radiation via computerized tomography (CT). In the setting of a cephalohematoma that is rapidly enlarging or larger than 5 cm, laboratory evaluation for coagulopathy, platelet dysfunctions, progressive anemia, or hyperbilirubinemia should be considered with abnormalities corrected accordingly.

• 2.

  Treatment: By the end of the first week of life, the majority of neonates will show signs of dissolution (decreasing size or softening) of the hematoma, and complete resolution can be seen in most cases by the end of the second week without any intervention. Delayed increasing size or appearance of neurologic deficits should trigger neurologic consultation for evaluation.

• 3.

  Complications: The main reported complications of cephalohematoma arise from nonabsorption of the hematoma.

  • a.

    Infection: Several cases of infection of the hematoma have been reported in the literature. In the setting of infection, treatment consists of washout and antibiotic therapy. Of note, in a neonate who meets criteria for sepsis without a known source and a history of cephalohematoma, drainage of the hematoma should be considered to obtain microbiological analysis.

  • b.

    Calcification: Calcification of the residual cephalohematoma (after 4–6 weeks from birth) is part of the expected natural history of these lesions. Significant head deformities can arise in large collections if left untreated, although they often remodel over time ( Fig. 53.3) . In this situation, patients can be referred to a craniofacial surgeon or neurosurgeon for drainage or evaluation for cranioplasty at a later age.

    

Subgaleal Hematoma/Hemorrhage

SGH is an accumulation of blood between the galea aponeurotica (aponeurosis) of the scalp and the periosteum of the skull. SGHs are usually caused by the rupture of emissary veins or arterioles of the scalp during delivery or another traumatic event in a newborn. The peculiarity of this “virtual” space of the scalp is that there is no strong adhesion between the aponeurosis and the pericranium; therefore a significant amount of blood can accumulate (over 250 mL). ^, SGH can represent a significant threat for an actively bleeding neonate, given the small intravascular volume. The incidence of neonatal SGH increases significantly with the use of vacuum devices during delivery, from 0.4 in 1000 vaginal deliveries without the use of vacuum or forceps to 5.9 in 1000 in vacuum-assisted deliveries.

Management

• 1.

  Diagnosis

  • a.

    Neonates diagnosed with SGH the day of admission appear to have better prognosis than those diagnosed the following day. SGH should be suspected on the grounds of examination and characteristics of delivery. Prolonged labor and vacuum extraction should trigger the neonatologist to look for signs of scalp lesions to establish the appropriate diagnosis. Differentiating SGH from cephalohematoma and caput succedaneum can usually be achieved by physical examination. Cephalohematoma, as discussed above, does not cross the midline or suture lines, whereas SGH usually does. In fact, SGH can involve the entire head circumference and it may displace the ear and the skin over the orbital rims. Cephalohematomas are usually tense to palpation and do not change with variations in head position, whereas SGHs palpate as a fluctuant (boggy) mass that can migrate to dependent areas when the position of the neonate is changed. SGH, in comparison to caput succedaneum, usually does not produce scalp pitting edema on palpation and takes longer to resolve than caput succedaneum, which tends to resolve as the swelling starts to dissipate within hours to days.

  • b.

    Head imaging such as head ultrasound and MRI of the brain can be obtained to rule out associated intracranial hemorrhage and pathology. Still, this imaging should not delay other diagnostic tests and measures in the setting of a potentially life-threatening hemorrhage or an unstable neonate. The use of head CT is discouraged given the exposure of the neonate to ionizing radiation and should be avoided if possible, depending on the urgency and medical center capabilities. Close monitoring for signs of hypovolemia, anemia, acidosis, and hyperbilirubinemia should be established, and related laboratory studies including coagulation studies should be obtained at baseline.

• 2.

  Treatment

  • a.

    The mainstay of treatment for patients with SGH is avoidance of complications related to acute blood loss. Patients with suspected SGH or strong risk factors for SGH, such as prolonged vacuum-assisted deliveries, should be closely monitored. In the setting of proven SGH, hourly vital sings, neurologic checks, and recurring examination of the hematoma should be established. Blood transfusions, correction of acidosis, and other supportive measures should be promptly instituted. Surgical intervention is not typically indicated in the setting of isolated SGH. Some practitioners have advocated head wrapping to tamponade the hemorrhage and reduce the subgaleal space, but one must be careful because this can result in elevated intracranial pressure if the head wrap is too tight. Furthermore, the head wrap may make proper examination of the hematoma more difficult. Neurosurgical evaluation can be considered in the setting of an associated intracranial hemorrhage or skull fracture.