INTRODUCTION — Epidural hematoma (EDH), also known as extradural hematoma, is a hemorrhage into the space between the dura and the overlying calvarium. It is almost exclusively caused by trauma. The morbidity and mortality result from mass effect on the brain as the hematoma expands and strips the dura away from the skull. EDH in children requires special knowledge of location and clinical presentation. Prompt diagnosis and neurosurgical consultation is critical to the successful management of EDH.
This topic discusses the clinical features, diagnosis, and management of EDH in children. Epidemiology, anatomy, and pathophysiology of EDH in children as well as EDH in adults are presented separately. (See "Intracranial epidural hematoma in children: Epidemiology, anatomy, and pathophysiology" and "Intracranial epidural hematoma in adults".)
CLINICAL FEATURES — A rapid overview provides the clinical features, diagnostic evaluation, and emergent management for epidural hematomas in children (table 1).
Concerning history — Historical features that identify an increased risk of EDH include the following:
●High risk trauma mechanism – A high risk trauma mechanism, such as fall from a significant height (>10 feet or two to three times the child’s height), any mechanism involving a motor vehicle, or direct blow to the temporal or occipital region should raise concern for EDH, even in initially well-appearing children. Of note, even relatively minor mechanisms of head injury in young infants 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, or loss of consciousness are associated with EDH and other intracranial injuries.
●Classic presentation – Although less commonly seen in children, 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 an abrupt onset of coma. (See 'Temporal skull injury with a lucid interval' below.)
●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. Observational studies suggest that the frequency of serious traumatic brain injury, including EDH may not be more common after minor head trauma in children with bleeding disorders when compared to normal children. (See "Minor blunt head trauma in infants and young 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 [1].
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 nonspecific. Furthermore, EDH may occur in infants younger than three months of age, even with relatively minor mechanisms of injury.
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 'Common findings' and "Minor blunt head trauma in infants and young children (<2 years): Clinical features and evaluation", section on 'Approach' and "Minor blunt head trauma in children (≥2 years): Clinical features and evaluation", section on 'Common findings'.)
Similarly, a subgaleal hematoma may result from decompression of an EDH through an associated skull fracture [2,3].
Other signs include [4,5]:
●Irritability
●Anemia
●Cephalohematoma
●Vomiting
●A bulging anterior fontanelle
●Lethargy
●Coma
●Seizures
Seizures and hypotonia are frequent presenting signs in neonates [6].
Associated fever or hemorrhagic shock has been described in up to 10 percent of infants with EDH [4].
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 are late findings often associated with rapid neurologic deterioration and poor outcomes despite rapid intervention [5,7,8].
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) (table 2). 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.
●Severe signs and symptoms – Children with large hematomas often are comatose (GCS ≤8 or rapidly changing level of consciousness). These patients warrant urgent surgical 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.
Temporal skull injury with a lucid interval — 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). After this, as the blood accumulates in the epidural space and compresses the brain, the child rapidly deteriorates. However, this type of history is variably present in children (37 to 67 percent of patients) and often absent in infants [6,9-14]. 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. (See 'Definitive management' below and 'Outcomes' below.)
Occipital injury — EDH in the posterior fossa deserves separate discussion because of a significant potential for sudden clinical decompensation with few warning signs (image 1 and image 2).
EDH is located in the posterior fossa in 3 to 17 percent of pediatric cases [4,7,9,10,13]. Falls onto the occipital region of the head account for most of these injuries. Occipital bone fractures are present in 78 to 90 percent of cases [4,15]. These fractures often cross a dural sinus, resulting in venous hemorrhage and delayed symptoms.
Children commonly present with an initial loss of consciousness, headache, and vomiting. Less commonly, there may be dizziness, stiff neck, or pyramidal or cerebellar signs (eg, dysmetria, ataxia, Romberg sign, or pronator drift). Children may have a subacute onset of symptoms up to a few days after minor occipital trauma [8,15,16].
Despite a relatively benign presentation, these children can deteriorate rapidly with lethal outcomes caused by compression of the brainstem or by hydrocephalus secondary to fourth ventricular obstruction [13]. The limited spatial capacity of the posterior fossa and its vital contents provide the substrate for such grave consequences when an EDH causes mass effect in this region.
ANCILLARY STUDIES — Imaging of the head is essential to rapidly make the diagnosis of epidural hematoma (EDH). (See 'Diagnosis' below.) In most centers, computed tomography is the study of choice, but rapid magnetic resonance imaging (MRI) will also accurately detect the blood clot, although is less likely to demonstrate a fracture.
Other studies (eg, cervical spine imaging and laboratory testing) may be necessary as adjuncts for management of associated trauma or in preparation for operative management.
Laboratory studies — The usefulness and need for initial laboratory studies varies according to the severity of the head trauma and whether additional injuries are suspected.
To assess for anemia or coagulopathy and to prepare for potential surgery, blood studies are warranted in patients with severe head trauma as indicated by altered mental status, focal neurologic examination, or other physical findings of increased intracranial hypertension (eg, vomiting or headache) as follows:
●Complete blood count with platelets
●Prothrombin time (PT)
●Partial thromboplastin time (PTT)
●International normalized ratio (INR)
●Type and cross
Other studies (eg, AST, ALT, and urinalysis) are also typically obtained in patients with multiple trauma, depending upon specific findings. (See "Severe traumatic brain injury (TBI) in children: Initial evaluation and management", section on 'Laboratory studies'.)
Patients with isolated head trauma and a normal mental status (GCS 15) typically do not need initial laboratory studies even though they may have features, such as mechanism of injury, history of loss of consciousness, or findings of a skull fracture that warrant neuroimaging. (See "Minor blunt head trauma in infants and young children (<2 years): Clinical features and evaluation", section on 'Neuroimaging' and "Minor blunt head trauma in children (≥2 years): Clinical features and evaluation", section on 'Neuroimaging'.)
Lumbar puncture is contraindicated in cases where a space occupying lesion such as EDH is suspected, due to the risk of herniation [17].
Radiographic imaging — Because EDH is potentially life-threatening, The clinician needs to make an early radiographic diagnosis, followed by prompt surgical treatment, if needed.
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 plain radiography or CT of the cervical spine as part of their evaluation (table 3). 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 emergent surgical evacuation is anticipated. (See 'Operative treatment' below.)
Cervical spine immobilization should be maintained throughout emergent 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 until awake and without neck pain. (See 'Initial assessment and treatment' below.)
The evaluation of cervical spine injuries in children and adolescents is discussed in greater detail separately. (See "Evaluation and acute management of cervical spine injuries in children and adolescents", section on 'Cervical spine imaging'.)
Computed tomography (CT) — Head CT is indicated in children with a head injury and signs suggesting an EDH. (See 'Clinical features' above.)
Head CT is the mainstay of diagnostic imaging 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 primarily due to the rapidity of diagnosis [9,10,18,19]. (See 'Operative treatment' below and 'Outcomes' below.)
The characteristic appearance of an EDH is a biconvex or lentiform mass that displaces the brain away from the calvarium (image 3 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.
The hypodense areas (or "swirl sign") typically represents active bleeding or unclotted blood and should not be misinterpreted as chronic blood [20]. A swirl sign usually provides evidence for a rapidly expanding hematoma that requires prompt surgical evacuation.
Other important findings seen in association with EDH include:
●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
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 a 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 [21]. MRI is especially useful in the diagnosis EDH at the vertex [22].
The MRI signal appearance of EDH and subdural hematoma evolves over time in a manner similar to that observed in parenchymal hematoma [23]:
●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.
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 3 and image 4 and image 5). An EDH generally does not cross suture lines of the skull. (See 'Computed tomography (CT)' above.)
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, 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.)
INITIAL MANAGEMENT — A rapid overview provides the clinical features, diagnostic evaluation, and emergent management for epidural hematomas in children (table 1).
Initial assessment and treatment — The order of priority in the initial assessment and treatment of the injured child suspected with possible EDH is the same as for any trauma patient (table 4). (See "Trauma management: Approach to the unstable child", section on 'Primary survey'.)
●A - Airway maintenance with cervical spine protection
●B - Breathing and ventilation
●C - Circulation with hemorrhage control
●D - Disability (evaluation of neurologic status)
●E - Exposure (complete visualization)/environmental control (prevention of hypothermia)
A rapid neurologic examination should focus on mental status using an age appropriate GCS (table 2), pupillary findings, cranial nerves, motor function, and cerebellar findings. 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.
●The clinician should provide supplemental oxygen to keep saturation above 95 percent.
●Cervical spine immobilization should be maintained throughout emergent 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 until awake and without neck pain. (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, or severe neurologic findings (GCS ≤8, pupillary abnormalities, neurologic deficit, or rapidly declining mental status) require early rapid sequence endotracheal intubation using measures to prevent increased ICP (table 5).
Aggressive hyperventilation (PaCO2 <30 mmHg) may cause cerebral ischemia as the result of decreased cerebral blood flow. Consequently, PaCO2 should be maintained between 35 and 40 mmHg unless there are signs of impending herniation. (See "Elevated intracranial pressure (ICP) in children: Management", section on 'Breathing' and "Severe traumatic brain injury (TBI) in children: Initial evaluation and management", section on 'Rapid sequence intubation'.)
●Patients with hypotension require rapid fluid resuscitation to maintain cerebral perfusion. (See "Trauma management: Approach to the unstable child", section on 'Circulation'.)
●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. These treatments are discussed separately. (See "Severe traumatic brain injury (TBI) in children: Initial evaluation and management" and "Elevated intracranial pressure (ICP) in children: Clinical manifestations and diagnosis".)
Neurosurgical consultation — Any child with an EDH and any pediatric trauma patient with a GCS ≤12 (table 2) warrant prompt consultation by a neurosurgeon. When EDH is associated with neurologic decompensation, then rapid evacuation of the hematoma is the primary therapy. (See 'Operative treatment' below.)
DEFINITIVE MANAGEMENT — A rapid overview provides the clinical features, diagnostic evaluation, and emergent management for epidural hematomas in children (table 1).
Operative treatment — In children with acute epidural hematoma (EDH), the decision to perform surgery is primarily based upon physical findings and results of head CT. Rapid evaluation and care by a neurosurgeon are key to optimal outcomes. If there is no neurosurgical coverage at the admitting hospital, the child should be resuscitated and promptly transferred to an appropriate institution. The appropriate teams at the accepting institution, including the trauma and neurosurgical services, should be notified of the acuity of presentation in order to make the appropriate preparations, which may involve the operating room.
Because urgent surgical attention is critical, in remote regions without neurosurgical support, craniotomy by another properly trained practitioner, such as a trauma surgeon, may be reasonable if interhospital transport poses a substantial delay.
Clinical criteria — Based upon observational studies, common physical findings that indicate the need for EDH evacuation include [4,7,18,24-26]:
●Altered mental status, especially rapidly worsening GCS or a GCS ≤8 (table 2) [24,26]
●Signs of increased ICP (eg, vomiting, severe headache, irritability, bradycardia, or hypertension) [7]
●Pupillary abnormalities or focal neurologic findings [25]
●Cerebellar signs (patients with occipital injury) [4,18] (see 'Posterior fossa epidural hematoma' below)
When one or more of these signs are present, the patient should be prepared for an emergent craniotomy. 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 within one to two hours after head trauma. (See "Intracranial epidural hematoma in adults", section on 'Surgical techniques'.)
Radiographic criteria — In addition to the clinical criteria discussed above, the following parameters on head CT suggest the possible need for surgical evacuation [24,27]:
●Temporal location (arterial bleeding can lead to rapid decompensation due to uncal herniation and brainstem compression when the hemorrhage is in the temporal fossa)
●Large size (EDH thickness >10 mm)
●Midline shift
However, decisions regarding the need for surgical evacuation should not be based solely upon radiographic criteria. This is illustrated 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 [28]. 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 'Nonoperative treatment' below.)
Surgical procedure — The surgical management of the epidural hematoma should take precedence over the secondary trauma workup once the primary survey has been performed and the patient stabilized. (See "Trauma management: Approach to the unstable child", section on 'Initial approach'.)
In the operating room, a skin incision is made to permit the removal of a bone flap that overlies the hematoma. The hematoma is evacuated and any visible source of hemorrhage is identified and coagulated. After the hematoma has been removed, the dura is sutured to holes drilled at the periphery of the craniotomy and the center of the bone flap to close the epidural space and prevent the hematoma from reaccumulating. The bone flap is replaced and affixed to the skull with either suture or cranial plates.
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 [6,14].
Burr hole placement was used diagnostically to locate the clot prior to the wide availability of head CT but does not permit full evacuation of the clot, which is generally large and firm. For this reason, in patients with impending herniation, open craniotomy by a surgeon rather than burr hole placement is preferred in situations where neurosurgical care is limited or unavailable and, if possible, should be performed based upon remote consultation with a neurosurgeon. Open craniotomy is necessary to completely evacuate the hematoma [26].
Nonoperative treatment — Based upon small observational studies, we suggest that neurologically intact children with small EDH and no worrisome radiographic features (eg, temporal location) be managed nonoperatively [5-7,24,29]. If at all possible, the decision to manage EDH nonoperatively should be made in conjunction with a neurosurgeon who understands the subtleties that would distinguish the more benign lesion from one that is a surgical emergency. In instances where neurosurgery is not physically available to the managing physician and transport to a higher level of care poses risk to the patient, phone consultation and remote review of the head CT by a neurosurgeon may assist in guiding proper patient disposition.
Children managed nonoperatively should only be observed in a facility where experienced pediatric trained personnel can monitor for neurologic changes. Patients with GCS ≤8 should have continuous intracranial monitoring of ICP during observation (table 2). In addition, 24 hour emergency access to head CT and a properly equipped operating room are essential, because deterioration can occur at any time.
In most cases, it is reasonable to repeat neuroimaging (head CT or rapid magnetic resonance imaging [MRI]) within 24 hours to ensure stable size of the hematoma [30]. When enlargement of the hematoma is of significant concern, the neuroimaging should be repeated within a shorter interval. In addition, if there are any neurologic changes during the course of observation, a head CT should be repeated immediately to look for an enlarging hematoma that needs surgical evacuation.
Asymptomatic patients with small, nonprogressive epidural hematomas on head CT can be safely discharged from the hospital in 24 to 48 hours after injury. Prior to discharge, caregivers should receive anticipatory guidance to emergently seek 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 which has been stable on at least two serial CT scans is highly unlikely.
Spontaneous resorption of the hematoma usually occurs within one month of diagnosis [7,31].
Posterior fossa epidural hematoma — Surgical treatment of posterior fossa epidural hematomas involves a suboccipital craniotomy in the region of the fracture with particular attention toward avoiding disturbance of the venous sinuses, which can be quite menacing. Since the advent of prompt diagnosis with CT scanning, results in children after surgical evacuation are favorable [4,15,18,32]. However, hemorrhage from the venous sinuses remain a significant surgical risk.
In asymptomatic children who have small posterior fossa epidural hematomas with minimal mass effect, it is reasonable for a neurosurgeon to observe closely with serial head CTs as long as the potential for rapid deterioration is appreciated [15,31,33]. (See 'Occipital injury' above.)
FOLLOW-UP AND RECOVERY
Operative patients — Neurosurgical follow-up after evacuation of an epidural hematoma usually involves a delayed head CT in about four to six weeks to ensure that there is no residual or recurrent hemorrhage. Children who have not suffered neurologic deficits can usually resume studies within this timeframe.
Returning to contact sports is at the discretion of the neurosurgeon and depends upon the timing of bone healing at the craniotomy site. This time period varies with the age of the child and extent of injury to the bone from the initial trauma but typically is about 12 weeks after injury.
Children with residual neurologic deficits after epidural hematoma (EDH) evacuation should be referred for occupational and physical therapy.
Children with iron deficiency anemia from blood loss should receive replacement doses of iron (3 mg/kg per day of elemental iron in a single or divided dose for four weeks). (See "Iron deficiency in infants and children <12 years: Screening, prevention, clinical manifestations, and diagnosis".)
Nonoperative patients — Patients with self-limited, stable epidural hematomas that do not warrant surgery are typically reevaluated at four weeks after injury. It is advisable that a repeat image be performed to be certain the hematoma has resolved.
Caregivers of these patients should be advised to return emergently if the child develops signs of increased intracranial pressure such as vomiting, progressive headache, or altered mental status.
Returning to contact sports is at the discretion of the neurosurgeon and depends upon the age of the child and extent of injury to the bone, if any, from the initial trauma.
OUTCOMES — Neurologic outcome following prompt surgical evacuation of an epidural hematoma (EDH) is often favorable [34]. The crucial factor seems to be minimizing the time between the onset of impaired consciousness and the evacuation of the hematoma. Good neurologic recovery after evacuation is associated with a high GCS at presentation and a pure epidural hematoma without associated lesions. In contrast, death or significant disability is associated with a low GCS at presentation, associated intracranial lesions (eg, subdural hematoma), or pupillary changes [7,9,10].
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 allow 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 [10].
The frequency of mortality in children with EDH is 2 to 6 percent in the post-CT era [9,25]. 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.
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".)
SUMMARY AND RECOMMENDATIONS
●Rapid overview – A rapid overview provides the clinical features, diagnostic evaluation, and emergency management for epidural hematomas (EDH) in children (table 1).
●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 'Temporal skull injury with a lucid interval' above.)
Other findings of EDH in children include (see 'Older children' above and 'Occipital injury' 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 clinician's goal is to make the diagnosis of EDH before neurologic deterioration to permit timely surgical intervention, if needed (table 1). Head CT is the mainstay of diagnostic imaging and is indicated in children with a head injury and signs of an EDH. 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 3 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 4 and table 1). (See 'Initial assessment and treatment' 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 2) warrants timely consultation and evaluation by a neurosurgeon. Specific therapies targeted at increased ICP and impending herniation are ideally employed in consultation with a neurosurgeon. (See 'Neurosurgical consultation' above.)
●Definitive management – Children with an acute EDH and altered mental, signs of increased intracranial pressure, pupillary abnormalities, focal neurologic findings, or cerebellar signs require emergency craniotomy and evacuation of the hematoma. Rapid surgical intervention in children with coma or signs of brain herniation is essential for survival. (See 'Operative treatment' above and 'Outcomes' above.)
We suggest that neurologically intact children with small EDH be managed nonoperatively by a neurosurgeon (Grade 2C). Requirements for nonoperative monitoring include the following (see 'Nonoperative treatment' above):
•Observation must occur in a facility where experienced pediatric trained personnel can monitor for neurologic changes.
•24-hour emergency access to a head CT and a properly equipped operating room is assured.
•Monitoring for any signs of neurologic deterioration occurs for at least 24 hours.
•Repeat CT scan or MRI is performed to rule out an expanding hematoma.
