Intracranial epidural hematoma in children

INTRODUCTION — This topic discusses the clinical features, diagnosis, and management of epidural hematoma (EDH) in children. The evaluation and treatment of severe traumatic brain injury and increased intracranial pressure in children is provided separately:

●(See "Severe traumatic brain injury (TBI) in children: Initial evaluation and management".)

●(See "Elevated intracranial pressure (ICP) in children: Clinical manifestations and diagnosis" and "Elevated intracranial pressure (ICP) in children: Management".)

DEFINITION — Epidural hematoma, also known as extradural hematoma, is a hemorrhage into the space between the dura and the overlying calvarium. It is almost exclusively the result of trauma.

EPIDEMIOLOGY — Epidural hematoma (EDH) occurs infrequently among the large population of infants and children seen in emergency departments and physician offices for head trauma but is present in about 1 to 3 percent of pediatric closed head injury admissions [1,2]. There is a strong gender difference, with a 2 to 2.5:1 male predominance [2-5]. Single-center cohorts suggest that the etiology varies by age:

●EDH occurs rarely in neonates and is associated with delivery by forceps or vacuum extraction [6].

●In infancy and the intermediate childhood years, low velocity impact (such as falls) comprise the most common mechanism of injury although motor vehicle collisions are also an important etiology [7-9]. However, falls less than 5 feet (1.5 m) may infrequently result in EDH in this age group [8]. EDH may also occur in patients with clotting factor deficiencies after minor head trauma [10]. Although intentional head injury in young children and infants typically causes subdural hematomas, child abuse accounts for 6 to 18 percent of EDH in case series [7,11]. (See "Child abuse: Epidemiology, mechanisms, and types of abusive head trauma in infants and children", section on 'Epidural hemorrhage' and "Intracranial subdural hematoma in children: Epidemiology, anatomy, and pathophysiology".)

●In older children and adolescents, motor vehicle collisions (MVCs) are the most common mechanisms of injury followed by falls. Assaults are an uncommon mechanism [2,3,9,12].

Acute intracranial EDH without a history of trauma is rare. Potential etiologies include [13-16]:

●Middle ear and sinus infection [13]

●Complication of neurosurgical procedures, such as ventricular shunt placement or craniotomy [14,17,18]

●Coagulopathy [19-21]

●Invasive skull tumors, such as Langerhans cell histiocytosis or solid tumor metastasis to the skull [15]

●Sickle cell anemia with skull infarction [16,22,23]

ANATOMY — During direct impact, the skull is deflected inward and the dura is stripped from the undersurface of the bone where blood can accumulate from disrupted arteries and/or veins. Because the dura is less adherent to the skull in the center of the bone plate than near the suture lines, an epidural hematoma (EDH) generally does not cross suture lines of the skull (image 1).

●Location of hematoma — The most common location of EDH in children is temporoparietal but frontal EDH is also frequent [9]. Relative to adolescents and adults, there is a decreased incidence of purely temporal EDH because the middle meningeal artery is not indented into the temporal bone as deeply in younger children [2,24,25]. Posterior fossa EDH is rare in children and is associated with occipital skull fractures in proximity to dural sinuses [2]. (See 'Posterior fossa epidural hematoma' below.)

●Blood vessel injury — In older children and adolescents, hemorrhage most commonly arises from lacerated branches of meningeal arteries that are injured by fractured bone edges. In infants and young children, hemorrhage more often follows disruption of emissary venous channels in the bone, large venous sinuses in the dura, or from multiple bleeding sources on the dural surface [26]. Infants and young children have a higher frequency of venous EDH due to the abundance of dural and diploic vasculature in areas of rapid bone growth [2,27].

●Associated injuries — Children with an EDH frequently have an associated skull fracture [2-4,24,27-29]. The associated fractures are almost always linear and usually cross either middle meningeal arterial branches or a dural venous sinus. Often, blood collects on either side of the bone adjacent to the fracture. Thus, subgaleal hematoma is frequently present in association with EDH and fracture as a result of bone bleeding and direct soft tissue injury from impact.

Children with EDH also appear to have fewer concomitant intracranial injuries (ICI) than adults [26,29]. This may, in part, explain improved outcomes following EDH in children [29]. When EDH coexists with another brain injury in children, the other brain injury is typically diffuse cerebral edema rather than hemorrhagic cerebral contusion [26]. (See 'Outcomes' below.)

PATHOPHYSIOLOGY — Arterial and, less commonly, venous bleeding into an intracranial EDH in children can displace brain parenchyma, cerebrospinal fluid (CSF) leak, and ultimately compromise blood vessels. If the epidural hematoma continues to increase in size, then increased intracranial pressure (ICP) and death due to brain herniation occurs. (See "Elevated intracranial pressure (ICP) in children: Clinical manifestations and diagnosis", section on 'Physiology' and "Elevated intracranial pressure (ICP) in children: Clinical manifestations and diagnosis", section on 'Brain herniation syndromes'.)

Infants and young children have an intracranial compartment that can expand at the sutures of the skull if they are open. In addition, young children have larger subarachnoid and extracellular spaces than older children and adolescents. As a result, they tend to tolerate an expanding epidural hematoma (EDH) better. Because of the capacity to tolerate a larger hematoma volume, young infants occasionally become hypovolemic and hemodynamically unstable with acute bleeding or anemic with chronic bleeding from hemorrhage before showing objective signs of increased intracranial pressure [7].

CLINICAL FEATURES — A rapid overview table provides the clinical features, diagnostic evaluation, and emergency management of epidural hematomas in children (table 1).

Supratentorial epidural hematoma — Supratentorial epidural hematomas include frontal and temporoparietal EDH.

Concerning history — Historical features that identify an increased risk of EDH include the following:

●High-risk trauma mechanism – A high-risk trauma mechanism should raise concern for EDH, even in initially well-appearing children such as:

•Fall from a significant height (>10 feet or two to three times the child's height)

•Any mechanism involving a motor vehicle

•Direct blow to the temporal or occipital region

In young infants, even relatively minor mechanisms of head injury can cause serious traumatic brain injury, including EDH. The evaluation of minor head trauma in such patients is discussed in detail separately. (See "Minor blunt head trauma in infants and young children (<2 years): Clinical features and evaluation", section on 'Approach'.)

●Symptoms of increased intracranial pressure (ICP) – Symptoms of increased ICP including headache, vomiting, seizure, confusion, lethargy, bulging fontanel in infants, loss of consciousness, or signs of impending hernia (table 2) are associated with EDH and other intracranial injuries.

●Classic presentation – The classically described presentation of EDH consists of initial loss of consciousness. Next, the patient has a lucid interval for a period of time that ranges from minutes to hours but is typically four to six hours. This lucid interval is followed by a rapid onset of coma and signs of herniation as the blood accumulates in the epidural space and compresses the brain. However, this type of history is variably present in children (37 to 67 percent of patients) and often absent in infants [3,4,24,27,30-32]. The clinician's goal is to make the diagnosis of EDH before neurologic deterioration in an asymptomatic or mildly affected child to permit timely surgical intervention, if needed.

●Head trauma in a child with a bleeding disorder – Children with a preexisting bleeding disorder (eg, hemophilia) may be at an increased risk of EDH after moderate to severe head trauma. However, after a minor head injury in children with bleeding disorders, EDH may not be more common compared with normal children. (See "Minor blunt head trauma in children (≥2 years): Clinical features and evaluation", section on 'Epidemiology'.)

●Atraumatic epidural hematoma in patients with sickle cell disease – Although rare, epidural hematomas can occur without known head trauma in patients with sickle cell disease. Affected patients may present with pain crisis, headache, evidence of skull infarction, scalp edema, and/or periorbital edema [33].

Findings by age — Physical findings vary by age. However, any altered mental status associated with head injury in a child should raise suspicion for an epidural hematoma. This heightens the significance of a parental complaint that their infant or child is "not acting right".

Infants — Neonates and infants younger than 12 months of age pose a significant challenge to diagnosis of an EDH because the open fontanelles in these patients permit expansion of the skull volume with accumulation of the EDH. Thus, initial findings are frequently nonspecific and may include [34-36]:

●Irritability

●Anemia

●Vomiting

●A bulging anterior fontanelle

●Fever

●Shock due to intracranial and/or subgaleal blood loss

●Lethargy

●Coma

●Seizures

●Hypotonia

A scalp hematoma, especially large or in the temporal or occipital region, provides an important marker of underlying traumatic brain injury, including EDH, in asymptomatic infants younger than 12 months of age. (See "Minor blunt head trauma in infants and young children (<2 years): Clinical features and evaluation", section on 'Scalp hematoma'.)

A cephalohematoma or subgaleal hematoma suggests an underlying fracture and should also raise concern for an EDH. A subgaleal hematoma may result from decompression of an EDH through an associated skull fracture [37,38].

Presentations with coma and signs of impending herniation are described but less common in infants [35,36]. Because of the increased skull capacity due to the open fontanelles, large amounts of intracranial blood can accumulate prior to changes in the neurologic examination. Thus, bradycardia, pupillary changes, and hemiparesis indicating cerebral herniation are late findings often associated with rapid neurologic deterioration and poor outcomes despite rapid intervention [2,35,36,39].

Seizures and hypotonia are potential presenting signs of EDH in neonates with birth trauma [30].

Older children — In older children, an EDH should be suspected if there is a witnessed deterioration in neurologic status at any time after a head injury. Depending upon the severity of traumatic injury, children may present with varying degrees of impaired consciousness and Glasgow Coma Scale (GCS) score (table 3). Clinical findings also depend upon the size and location of the hematoma as follows:

●Mild to moderate signs and symptoms – Patients are often neurologically intact. In these children, common symptoms include headache, vomiting, or irritability [9].

●Severe signs and symptoms – Children with large hematomas often are comatose (GCS ≤8 or rapidly changing level of consciousness). These patients warrant emergency surgical hematoma evacuation.

Lateralizing neurologic signs (eg, anisocoria, hemiparesis, hemiplegia) arising from compression of the third cranial nerve and brainstem may also be present. These findings are indicators of progression to cerebral uncal herniation. The side of the dilated pupil matches the side of the hematoma in roughly 90 percent of cases.

The constellation of systemic hypertension, bradycardia, and respiratory disturbance (Cushing triad) is another late sign associated with cerebral herniation.

Posterior fossa epidural hematoma — Although much less common than a supratentorial EDH, a posterior fossa EDH after occipital trauma has a significant potential for sudden clinical decompensation with few warning signs (image 2 and image 3) [2-4,31,34]. Occipital bone fractures are present in 70 to 90 percent of patients [34,40,41]. These fractures often cross a dural sinus, resulting in venous hemorrhage and are associated with delayed symptoms [41].

As for supratentorial EDH, common clinical features of posterior fossa EDH include initial loss of consciousness, headache, vomiting , and an occipital subgaleal hematoma or cephalhematoma [31,40]. Less common clinical features include [31,40]:

●Dizziness

●Stiff neck

●Pyramidal or cerebellar signs such as dysmetria, ataxia, a present Romberg sign, or pronator drift

Some children may have a subacute onset of symptoms up to a few days after minor occipital trauma [39,40,42]. Coma at presentation is rare.

Despite a normal mental status, these children can deteriorate rapidly with lethal outcomes caused by compression of the brainstem or by hydrocephalus secondary to fourth ventricular obstruction because of the limited capacity of the posterior fossa to accommodate a rapidly expanding hematoma [31,40,42].

DIAGNOSIS — Epidural hematoma (EDH) is diagnosed by the characteristic radiologic findings of a biconvex or lentiform mass that displaces the brain away from the calvarium on computed tomography of the head (image 1 and image 4 and image 5). An EDH generally does not cross suture lines of the skull. (See 'Computed tomography (CT)' below.)

Clinical suspicion — In children, the diagnosis of EDH is suggested by a history of head trauma, especially to the temporal or occipital region, accompanied by loss of consciousness, altered mental status, or signs of increased intracranial pressure (eg, progressively severe headache or vomiting). (See 'Older children' above.)

In infants with open fontanelles, the findings of EDH may be nonspecific and include irritability, pallor, cephalhematoma, fever, and/or subgaleal hematoma. (See 'Infants' above.)

Neuroimaging — Neuroimaging is essential to rapidly make the diagnosis of epidural hematoma (EDH). In most centers, computed tomography is the study of choice, but rapid magnetic resonance imaging (MRI) will also accurately detect the blood clot, although it is less likely to demonstrate a fracture.

Computed tomography (CT) — Head CT is the mainstay of diagnostic imaging for EDH because of the speed with which it can be obtained and interpreted, and the ability to demarcate in detail the extent of the hemorrhage for surgical planning. Mortality following EDH has decreased markedly in the post-CT era versus the pre-CT era because CT permits much more rapid diagnosis [3,4,28,43]. (See 'Outcomes' below.)

●Characteristic appearance – The characteristic appearance of an EDH is a biconvex or lentiform mass that displaces the brain away from the calvarium (image 1 and image 4 and image 5). The EDH generally does not cross suture lines of the skull. The mass is uniformly hyperdense in two thirds of cases while one-third of cases display mixed hyper- and hypodense areas.

●Criteria for surgery – Many neurosurgeons use one or more of the following CT findings as criteria for surgical hematoma evacuation in children with acute EDH:

•Mass effect – Findings of mass effect include [44,45]:

-Midline shift

-Gyral effacement

-Compression of the lateral ventricle on the side of the hematoma

-Compression of the basilar cisterns

-Focal or generalized loss of gray-white differentiation indicating cerebral edema

-Uncal, subfalcine, or transtentorial herniation

-For posterior fossa EDH, hydrocephalus [42]

•Swirl sign – The hypodense areas (or "swirl sign") typically represents active bleeding or unclotted blood and should not be misinterpreted as chronic blood [46]. A swirl sign usually provides evidence for a rapidly expanding hematoma that requires prompt surgical evacuation.

•Temporal lobe location – Arterial expansion of these hematomas can cause compression of the brainstem with abrupt clinical deterioration.

•Large size – The maximal thickness of the EDH and the estimated volume are used to categorize the hematoma. A maximal hematoma thickness >10 mm and an estimated volume ≥15 mL suggest a large EDH in children [45]. However, large, slowly accumulating hematomas (eg, from venous bleeding) may resolve with observation alone. Pediatric neurosurgeons frequently use other factors in addition to size when deciding about surgical hematoma evacuation.

Magnetic resonance imaging — In the acute setting, an MRI has a limited but increasing role in the diagnosis of an epidural hematoma. It is often less useful in the acute setting due to the time constraints within which important clinical decisions need to be made. However, MRI can be a follow-up study of choice. In some institutions, rapid MRI using a rapid T2 sequence is replacing CT in selected patients to avoid the exposure to radiation associated with CT. The MRI may be useful in monitoring a known epidural hematoma, which is treated non-operatively in a stable patient to ensure no expansion. MRI is also more sensitive than head CT for the detection of small intracranial hemorrhages [47]. MRI is especially useful in the diagnosis EDH at the vertex [48].

The MRI signal appearance of EDH and subdural hematoma evolves over time in a manner similar to that observed in parenchymal hematoma [49]:

●The acute clot is hypointense on T2-weighted images due to the presence of deoxyhemoglobin.

●Over subsequent weeks, deoxyhemoglobin degrades to methemoglobin, which appears bright on both T1- and T2-weighted images.

●At several months, only hemosiderin remains, and the clot again becomes hypointense on the T1-weighted images.

In the rare situation where an EDH arises from a vascular anomaly, cerebral angiography may be an important preoperative study, but this test typically is ordered by the managing neurosurgeon.

Ancillary studies — Other studies are also indicated as adjuncts for management of associated trauma or in preparation for operative management.

Laboratory studies — Blood studies are necessary to identify anemia or coagulopathy in children with EDH and include:

●Complete blood count with platelets

●Prothrombin time (PT)

●Partial thromboplastin time (PTT)

●International normalized ratio (INR)

●Type and cross (patients undergoing emergency surgery) or type and screen (patients receiving nonoperative treatment)

Other studies may also be necessary in children with EDH and multiple trauma, as discussed separately. (See "Severe traumatic brain injury (TBI) in children: Initial evaluation and management", section on 'Laboratory studies'.)

Lumbar puncture is contraindicated in patients in whom a space occupying intracranial lesion such as an EDH is suspected due to the risk of herniation. (See "Lumbar puncture in children", section on 'Contraindications'.)

Cervical spine imaging — Cervical spine injury is also a concern in patients with EDH, especially those with multiple trauma. Most children with EDH meet criteria for screening plain radiography or CT of the cervical spine (table 4). CT of the cervical spine in addition to the head is favored in children with severe head trauma and coma or signs of herniation in whom emergency surgical evacuation is anticipated.

Cervical spine immobilization should be maintained throughout emergency patient care in all patients in whom there is a concern of cervical spine injury. Those patients with altered mental status should continue to be immobilized even if radiographic studies show no bony abnormality. (See 'Initial management' below.)

The evaluation of cervical spine injuries in children and adolescents with reliable (algorithm 1) or unreliable (algorithm 2) physical examinations is discussed in greater detail separately. (See "Evaluation and acute management of cervical spine injuries in children and adolescents", section on 'Cervical spine imaging'.)

INITIAL MANAGEMENT — A rapid overview provides the clinical features, diagnostic evaluation, and emergency management for epidural hematomas in children (table 1). Patients with concerns for significant intracranial injury or increased intracranial pressure (ICP) must be managed appropriately to reduce the likelihood or impact of secondary brain injury from hypoxia, ischemia, and cerebral edema.

Stabilization — The order of priority in the initial assessment and treatment of the injured child with possible EDH is the same as for any trauma patient (table 5) (see "Trauma management: Approach to the unstable child", section on 'Primary survey'):

●Airway with cervical motion restriction – Provide supplemental oxygen to keep oxygen saturation 95 to 99 percent.

Maintain cervical spine motion restriction throughout emergency patient care in all patients in whom there is a concern of cervical spine injury. Patients with altered mental status require cervical spinal motion restriction even if radiographic studies show no bony abnormality. (See 'Cervical spine imaging' above and "Evaluation and acute management of cervical spine injuries in children and adolescents", section on 'Cervical spine imaging'.)

Head-injured patients with compromised airway, inadequate breathing, coma (GCS ≤8 or rapidly declining), or signs of cerebral herniation (table 2) require early rapid sequence endotracheal intubation using measures to prevent increased ICP (table 6). When it does not interfere with emergency airway management, the clinician should perform a brief, focused neurologic examination as described under disability below prior to neuromuscular blockade.

●Breathing – Maintain PaCO₂ between 35 and 40 mm Hg unless signs of cerebral herniation (table 2) unresponsive to osmotic therapy. In all patients, avoid aggressive hyperventilation (PaCO₂ <30 mm Hg) that may cause decreased cerebral perfusion and ischemia. (See "Elevated intracranial pressure (ICP) in children: Management", section on 'Breathing'.)

●Circulation with hemorrhage control – Apply manual direct pressure to bleeding sites. Severe bleeding from a large scalp laceration often responds to rapid closure using a figure of eight suture, surgical staples, or scalp clips (Raney clips). A circumferential Penrose drain tourniquet can provide temporary control of scalp bleeding until repair is complete (figure 1). (See "Assessment and management of scalp lacerations", section on 'Techniques' and "Closure of minor skin wounds with staples".)

Obtain intravenous access (two peripheral intravenous catheters at two upper extremity sites. Treat shock with rapid fluid infusion of warmed lactated Ringer's or normal saline. (See "Trauma management: Approach to the unstable child", section on 'Circulation'.)

●Disability – Perform a rapid neurologic examination that includes:

•Age appropriate GCS (table 3)

•Pupillary response to light

•Cranial nerves (gag, corneal, and vestibular reflexes)

•Motor asymmetry

In patients with impending herniation, specific therapies targeted at increased ICP are ideally employed in consultation with a neurosurgeon and include osmotic therapy (hypertonic saline or mannitol) and, if no response, modest hyperventilation (PaCO₂ 30 to 35 mm Hg) (algorithm 3). (See "Elevated intracranial pressure (ICP) in children: Management", section on 'Medical treatment of sustained intracranial hypertension or impending herniation'.)

●Exposure – Perform complete visualization and provide warming or, in patients with fever, acetaminophen and cooling to maintain normothermia (core temperature 36 to 37.5°C [96.8 to 99.5°F]). (See "Elevated intracranial pressure (ICP) in children: Management", section on 'Temperature control'.)

Neurosurgical consultation — Any child with a documented EDH and any pediatric trauma patient with a GCS ≤12 (table 3) require prompt consultation with a neurosurgeon to guide further care and to perform surgical hematoma evacuation when indicated. (See 'Subsequent management' below.)

Interhospital transfer — If there is no neurosurgical coverage at the hospital where the child presents, the managing physician should stabilize and promptly transfer the patient to a level 1 pediatric trauma center or facility with similar neurosurgical capability. The appropriate teams at the accepting institution, including neurosurgical and trauma service attendings, require notification including:

●Mechanism of injury

●Patient condition (vital signs, neurologic examination, and any other pertinent abnormal findings)

●Associated injuries

●Results of head CT as well as any other laboratory studies or imaging that was performed

SUBSEQUENT MANAGEMENT — A neurosurgeon with pediatric expertise should provide subsequent management of children with EDH based upon physical findings and results of head CT.

Patients with neurologic impairment (surgery) — Children with acute EDH and one or more of the following findings require emergency hematoma evacuation [2,8,26,28,34]:

●Altered mental status (especially rapidly worsening GCS score or a GCS score ≤8 (table 3)) due to EDH [8]

●Signs of increased ICP (eg, persistent vomiting, severe headache [irritability in infants], or Cushing triad [bradycardia/tachycardia, respiratory disturbance, and hypertension]) due to hematoma growth [2]

●Signs of brain herniation (eg, pupillary abnormalities, focal neurologic findings, or decorticate or decerebrate posturing) [26]

●Cerebellar signs (patients with occipital injury) [28,34] (see 'Surgical hematoma evacuation' below)

Although not well studied in children, evidence from small observational studies in adults with acute EDH suggests that morbidity and mortality are decreased when surgery is performed as soon as possible in these patients (eg, within one to two hours after head trauma). Although the presenting GCS score is most predictive of surgical outcomes in children, full recovery to baseline after surgery has been described in children with acute epidural hematoma despite low GCS score or advanced signs of cerebral herniation (eg, unresponsive with posturing) at presentation [2,8]. (See "Intracranial epidural hematoma in adults", section on 'Surgical techniques' and 'Outcomes' below.)

The surgical approach is described below. (See 'Surgical hematoma evacuation' below.)

Successful observation with full recovery has also been documented in children who have neurologic deficits or altered mental status at presentation and minimal mass effect on head CT [45,50]. However, this should only be done under the direction of a neurosurgeon in a pediatric intensive care unit.

Neurologically intact patients — In neurologically intact children (ie, nonfocal examination with GCS score 15) with EDH, there are no universally accepted guidelines to indicate when surgical hematoma evacuation versus nonoperative management should occur. Our approach is provided below.

Mass effect or high risk for clinical deterioration (surgery) — For neurologically intact children (ie, nonfocal examination with GCS 15) with an acute EDH, the following neuroimaging findings indicate a mass effect or a high risk for rapid enlargement and clinical deterioration [8,44,51]:

•Any midline shift (image 4)

•Temporal lobe location due to high risk of expansion and brainstem compression

•The "swirl sign" that indicates brisk arterial bleeding (image 1)

•Hydrocephalus in children with posterior fossa EDH

For children with any one of these findings on initial CT, we suggest emergency surgical evacuation. Neurologically intact children with large EDH with mass effect appear to be at greater risk of persistent neurologic deficit or death, as presented below.

For patients with EDH thickness ≥10 mm or computed EDH volume ≥15 mL who are neurologically intact and lack any of the above high-risk features, the optimal approach is uncertain. For such patients, the decision to perform surgery is individualized and made in the context of shared decision-making with the caregivers. Patients with EDH thickness >10 mm or computed EDH volume ≥15 mL are more likely to fail observation. However, some children in this category can be successfully managed nonoperatively. (See 'No mass effect and low risk for clinical deterioration (nonoperative management)' below.)

No mass effect and low risk for clinical deterioration (nonoperative management) — For neurologically intact children with an EDH with no midline shift and without concerning neuroimaging findings such as mass effect, signs of arterial bleeding, or other findings associated with a high risk of clinical deterioration, we suggest nonoperative management [2,8,30,35,45,50-52]. Requirements for nonoperative monitoring include the following:

●Observation must occur under the direction of a neurosurgeon with pediatric expertise and in a level 1 pediatric trauma center or facility with similar capability including 24-hour emergency access to neuroimaging and a properly equipped operating room.

●Monitoring for any signs of neurologic deterioration occurs for at least 24 hours. Children with any neurologic changes during observation require an immediate head CT to look for an enlarging hematoma that requires surgical evacuation.

●Repeat CT scan or MRI is performed to rule out an expanding hematoma [53]. In patients with supratentorial EDH and low concern for progression, the neurosurgeon should repeat neuroimaging (either fast MRI or unenhanced head CT depending upon radiology capability and institutional practice) approximately 12 hours after injury.

When enlargement of the hematoma is of significant concern based upon initial clinical or diagnostic imaging, the repeat neuroimaging should occur within 8 hours after injury. Patients who have an enlarging hematoma on repeat neuroimaging require surgical evacuation.

For children with posterior fossa epidural hematomas without hydrocephalus, the neurosurgical approach is to individualize treatment (operative hematoma evacuation or observation) based upon severity of symptoms and degree of mass effect on imaging. Asymptomatic children who have small posterior fossa epidural hematomas and minimal to no mass effect may also receive nonoperative management with close inpatient observation and serial neuroimaging as for small supratentorial epidural hematomas [40,54-57]. However, evidence is lacking to provide specific CT findings that are associated with successful observation.

Patients who remain asymptomatic without clinical deterioration or progression on neuroimaging for 24 to 48 hours after injury can be safely discharged from the hospital. Prior to discharge, caregivers should receive anticipatory guidance to seek emergency care if the patient develops signs of increased intracranial pressure such as vomiting, progressive headache, or altered mental status. However, in our experience, progression of an epidural hematoma that has been stable on at least two head CT or MRI scans is highly unlikely. Spontaneous resorption of the hematoma after observation usually occurs within one month of diagnosis [2,54].

Limited evidence suggests that an EDH volume <15 mL and no mass effect on initial head CT are associated with successful observation in children [45,50]. For example, in a retrospective cohort of 195 children with acute EDH who were initially observed, 88 percent were managed nonoperatively with uniformly good outcomes, failed observation was associated with larger hematoma size, presence of mass effect, and midline shift [45]. Compared with successful observation, failed observation with delayed surgery was associated with more neurologic deficits (54 versus 23 percent) and higher mortality (5 versus 0 percent). All survivors had a GCS score of 15 at discharge. For children with an acute EDH and GCS score of 15, a prediction rule has been derived and validated from separate cohorts (over 400 total patients) [45,50]. Patients with acute EDH with no neurologic deficit and a head CT showing no mass effect and an estimated EDH volume <15 mL may be successfully observed with a positive predictive value of 98 to 100 percent (lower boundary of CI 92 to 93 percent, prevalence of delayed surgery 12 percent).

By contrast, a separate retrospective study has found that progression during observation requiring surgical evacuation after observation is associated with mass effect (midline shift or ipsilateral basilar cistern or lateral ventricle compression), EDH thickness ≥11 mm, and a digitally computed volume ≥15 mL on initial head CT [51]. However, 8 of 10 patients who underwent delayed surgery in this study had mass effect on the initial CT.

Special circumstances

Late presentation — Most patients diagnosed with EDH >24 hours after head trauma who have a stable neurologic status can be safely monitored without surgical intervention. As an example, in a case series of 13 neurologically intact children with significant EDH, 12 patients were successfully managed nonoperatively despite an average EDH thickness of 19 mm on head CT [52]. All but one of these patients was admitted ≥24 hours after the initial injury, suggesting slow accumulation of the EDH. All patients had full recovery and were normal at follow-up, ranging from four months to >10 years after injury. (See 'No mass effect and low risk for clinical deterioration (nonoperative management)' above.)

EDH may also arise in delayed fashion without being detected on initial imaging studies in about 9 to 10 percent of multiple trauma patients resuscitated from hypovolemic shock or undergoing craniectomy [58-61]. The blood may begin to accumulate well after the initial injury. Delayed hematomas are prone to form if there are measures that decrease intracranial pressure (ICP), such as loss of cerebrospinal fluid through traumatic fistulae or therapeutic external ventricular drainage, surgical evacuation of hematomas at other sites [60,62,63], or pharmacological reduction of ICP. The majority of delayed EDH will arise within 8 to 24 hours, and therefore, repeat imaging within the first day following an injury is likely to detect them and permit timely neurosurgical consultation and management.

SURGICAL HEMATOMA EVACUATION — Surgical evacuation of acute EDH in a critically ill child should take precedence over the secondary trauma workup once the trauma team has performed the primary survey and stabilized the patient. (See "Trauma management: Approach to the unstable child", section on 'Initial approach'.)

In the operating room, the neurosurgeon:

●Makes a skin incision and removes a bone flap over the hematoma.

●Evacuates the hematoma.

●Locates visible bleeding sites and coagulates them.

●Stitches the dura to holes drilled at the periphery of the craniotomy and the center of the bone flap to close the epidural space and prevent recurrent hematoma formation.

●Replaces the bone flap and affixes it to the skull with either suture or cranial plates followed by galea and scalp closure.

Surgical treatment of posterior fossa epidural hematomas involves a suboccipital craniotomy in the region of the fracture with particular attention to avoiding disruption of the venous sinuses, which will lead to massive hemorrhage. Clinical outcomes after surgical evacuation are usually favorable [28,34,40,64]. However, hemorrhage from the venous sinuses remains a significant surgical risk.

In small, observational studies of neonates with EDH, full recovery has also been achieved by aspiration of the hematoma at the bedside without craniectomy followed by medical management [30,32].

In the past, burr hole placement was used diagnostically to locate the clot prior to the wide availability of head CT. However, a burr hole does not permit full evacuation of the clot because the hematoma is usually large and firm. For this reason, in patients with coma or impending herniation, open craniotomy by a neurosurgeon rather than burr hole placement should occur. Burr hole placement under virtual neurosurgical guidance may be indicated as a temporizing measure in settings where neurosurgical care is unavailable until transfer time to definitive care will permit surgical hematoma evacuation [65-68].

FOLLOW-UP AND RECOVERY — All children require follow-up with a neurosurgery with repeat neuroimaging at four to six weeks to ensure that the EDH has resolved. At discharge, caregivers of children managed nonoperatively should be advised to return for emergency evaluation if the child develops signs of increased intracranial pressure such as vomiting, progressive headache, or altered mental status. Children with iron deficiency anemia from blood loss should receive replacement doses of iron. (See "Iron deficiency in infants and children <12 years: Treatment" and "Iron requirements and iron deficiency in adolescents", section on 'Management'.)

Children without neurologic deficits can usually resume school within this timeframe. However, activities must be limited to avoid recurrent head trauma. Children with residual neurologic deficits after epidural hematoma (EDH) evacuation should receive occupational and physical therapy.

After complete resolution of the hematoma, returning to contact sports is at the discretion of the neurosurgeon and depends upon the timing of bone healing at the craniotomy site or, in nonoperative patients, the degree of bone injury. This period varies with the age of the child but typically is about 12 weeks after injury.

OUTCOMES — The frequency of mortality in children with EDH is <6 percent in the post-CT era [3,26,45]. There is a higher mortality in children who present with a lucid interval because this apparent improvement may delay definitive treatment or transfer of the patient. This association emphasizes the importance of prompt transfer of patients if the initial institution does not have appropriate neurosurgical coverage.

Neurologic outcome following prompt surgical evacuation of an epidural hematoma (EDH) is often favorable [69]. Minimizing the time between the onset of impaired consciousness and the evacuation of the hematoma increases the chance for favorable outcomes. Good neurologic recovery after evacuation is associated with a high GCS at presentation and a pure epidural hematoma without associated lesions [70]. In contrast, death or significant disability is associated with a low GCS at presentation, associated intracranial lesions (eg, subdural hematoma), or pupillary changes [2-4,9,71].

Children under the age of five years tend to have lower morbidity and mortality from EDH than older children or adults. This observation may be due to compensatory mechanisms within the brain that permit greater protection against an expanding hematoma; in addition, there is a predominance of low velocity impact falls without associated brain injuries in this age group [4,69].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Pediatric trauma" and "Society guideline links: Increased intracranial pressure and moderate-to-severe traumatic brain injury".)

SUMMARY AND RECOMMENDATIONS

●Rapid overview – A rapid overview provides the clinical features, diagnostic evaluation, and initial management of children with acute epidural hematoma (EDH) (table 1).

●Definition – An intracranial epidural hematoma (EDH) is a potentially life-threatening hemorrhage in the space between the dura and the overlying calvarium that usually results from trauma, although acute intracranial EDH also occurs rarely in children without a history of trauma. Without prompt intervention, an expanding EDH causes increased intracranial pressure and may result in death due to brain herniation. (See 'Anatomy' above and 'Pathophysiology' above.)

●Clinical features – Although variably present in children and frequently absent in infants, the classic presentation of an EDH after a direct blow to the temporal region is characterized by a lucid interval, where a child initially may have a decreased level of consciousness due to the primary brain injury, then returns to normal level of consciousness for several hours (typically four to six hours, although longer lucid periods can be observed). Subsequently, as the blood accumulates in the epidural space and compresses the brain, the child rapidly deteriorates. (See 'Concerning history' above.)

Other findings of EDH in children include (see 'Older children' above and 'Posterior fossa epidural hematoma' above):

•A history of head trauma, especially to the temporal or occipital region

•Loss of consciousness

•Altered mental status

•Signs of increased intracranial pressure (eg, severe headache or vomiting)

•Dizziness, stiff neck or cerebellar signs in children with a posterior fossa epidural hematoma

•Focal neurologic findings or Cushing triad (ie, systemic hypertension, bradycardia, and respiratory disturbance) in patients with cerebral herniation

In neonates and infants with open fontanelles, findings of an EDH are nonspecific or may be absent. The most common findings consist of scalp hematoma, irritability, pallor with anemia, and cephalohematoma. (See 'Infants' above.)

●Diagnosis – The emergency clinician should suspect the diagnosis of EDH in any child with head trauma, especially to the temporal or occipital region, and accompanied by loss of consciousness, altered mental status, or signs of increased intracranial pressure (eg, progressively severe headache or vomiting).

Neuroimaging confirms the diagnosis and provides important information used to decide between surgical or nonoperative management. Head CT is widely available in a timely fashion and most commonly used. The characteristic appearance of EDH on CT is a biconvex or lentiform hyperdense mass that displaces the brain away from the calvarium and does not cross suture lines (image 1 and image 4 and image 5). (See 'Diagnosis' above and 'Computed tomography (CT)' above.)

●Stabilization – The order of priority in the initial assessment and stabilization of the injured child with an EDH is the same as for any trauma patient (table 5 and table 1). (See 'Initial management' above and "Trauma management: Approach to the unstable child", section on 'Primary survey'.)

●Neurosurgical consultation – Any child with an EDH or with a GCS ≤12 (table 3) requires timely consultation and evaluation by a neurosurgeon. Specific therapies targeted at increased ICP and impending herniation (eg, hypertonic saline, mannitol, or modest hyperventilation (algorithm 3)) are ideally employed in consultation with a neurosurgeon. (See 'Neurosurgical consultation' above.)

●Subsequent management – The decision to perform surgical hematoma evacuation is based upon clinical and radiological findings:

•Children with an acute EDH and neurologic impairment such as altered mental status due to the EDH, signs of increased intracranial pressure, pupillary abnormalities, focal neurologic findings, or cerebellar signs require emergency surgical hematoma evacuation. (See 'Patients with neurologic impairment (surgery)' above.)

•For neurologically intact children (ie, nonfocal examination with GCS 15) with an acute EDH, the following neuroimaging findings suggest a mass effect or a high risk for rapid enlargement and clinical deterioration (see 'Mass effect or high risk for clinical deterioration (surgery)' above):

-Any midline shift (image 4)

-Temporal lobe location

-The "swirl sign" (image 1)

-In children with posterior fossa EDH, hydrocephalus

For patients with any one of these findings on initial CT, we suggest emergency surgical evacuation (Grade 2C).

•For neurologically intact children with an acute supratentorial EDH, with no mass effect, and no high risk features described above, we suggest nonoperative management (Grade 2C), Requirements for nonoperative monitoring include the following (see 'No mass effect and low risk for clinical deterioration (nonoperative management)' above):

-Observation must occur under the direction of a neurosurgeon with pediatric expertise and in a level 1 pediatric trauma center or facility with similar capability including 24-hour emergency access to emergency neuroimaging and a properly equipped operating room.

-Monitoring for any signs of neurologic deterioration occurs for at least 24 hours. Children with any neurologic changes during observation require emergency neuroimaging to look for an enlarging hematoma that requires surgical evacuation.

-Repeat CT scan or MRI is performed to rule out an expanding hematoma. Timing and type of repeat neuroimaging (fast MRI versus unenhanced CT) is determined by degree of concern for hematoma enlargement and institutional capability.

Patients who have an enlarging hematoma on repeat head CT require surgical evacuation.

•For patients with a posterior fossa EDH without hydrocephalus, the neurosurgical approach is to individualize treatment (operative hematoma evacuation or observation) based upon severity of symptoms and degree of mass effect on imaging.