INTRODUCTION — This topic discusses epidemiology, anatomy, and pathophysiology of EDH in children. Clinical features, evaluation, and management of EDH are presented separately. (See "Intracranial epidural hematoma in children: Clinical features, diagnosis, and management" and "Intracranial epidural hematoma in adults".)
DEFINITION — 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 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 [1-4]. There is a strong gender difference, with a 2 to 2.5:1 male predominance [4-6]. The etiology varies by age:
●EDH occurs rarely in neonates and is associated with delivery by forceps or vacuum extraction [7].
●In infancy and the intermediate childhood years, low velocity impact (such as falls) comprise the most common mechanism of injury [8-10]. Even falls less than 5 feet (1.5 m) may rarely result in EDH in this age group [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 [9,11]. (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 the adolescent years, motor vehicle collisions (MVCs) are the primary cause of EDH [4,5].
ANATOMY — During direct impact, the skull is deflected inward and the dura is stripped from the undersurface of the bone where blood can accumulate. Epidural hematoma (EDH) generally does not cross suture lines of the skull (image 1). This is because the dura is less adherent to the skull in the center of the bone plate where bone resorption and remodeling takes place and it is more adherent at the suture lines where osteoblastic activity is the highest.
Location of hematoma — The most common locations of EDH in children are frontal, parietooccipital, and posterior fossa. Compared with their adult counterparts, children differ in the distribution of the location of EDH in the following ways:
●There is a decreased incidence of purely temporal EDH because the middle meningeal artery is not indented into the temporal bone as frequently as it is in adults [4,12,13].
●There is an increased incidence of posterior fossa EDH in children associated with occipital skull fractures in proximity to dural sinuses [4].
The source of hemorrhage in posterior fossa EDH is usually venous and slower to accumulate compared with arterial hemorrhages. 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 (image 2 and image 3). (See "Intracranial epidural hematoma in children: Clinical features, diagnosis, and management", section on 'Posterior fossa epidural hematoma' and "Intracranial epidural hematoma in children: Clinical features, diagnosis, and management", section on 'Occipital injury'.)
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 [14]. 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 [4,15].
Associated abnormalities — Although fracture is a marker of EDH in infants under one to two years of age, skull fractures are associated with EDH less often in children than in adults, occurring in 40 to 80 percent in case series of pediatric patients [4-6,8,12,15-17].
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.
Based on observational studies, children with EDH also have fewer concomitant intracranial injuries (ICI) than adults [14,17]. This may, in part, explain improved outcomes following EDH in children [17]. When EDH coexists with another ICI in children, it typically takes the form of diffuse cerebral edema rather than hemorrhagic cerebral contusion often seen in adults [14]. (See "Intracranial epidural hematoma in children: Clinical features, diagnosis, and management", section on 'Outcomes'.)
PATHOPHYSIOLOGY
Increased intracranial pressure (ICP) — In children with closed sutures, the intracranial compartment is protected by the skull, a rigid structure with a fixed internal volume. The intracranial contents include (by volume) [18]:
●Brain parenchyma – 80 percent
●Cerebrospinal fluid (CSF) – 10 percent
●Blood – 10 percent
ICP is a function of the volume and compliance of each component of the intracranial compartment, an interrelationship recognized over 150 years ago and known as the Monro-Kellie doctrine [19,20]. Because the overall volume of the cranial vault cannot change in children with closed sutures, an increase in the volume of one component, or the presence of pathologic components, necessitates the displacement of other structures, an increase in ICP, or both [18,20-23]. With an expanding epidural hematoma, CSF, intracranial venous blood, and then brain parenchyma are displaced. If the epidural hematoma continues to increase in size, then death due to brain herniation can occur. (See "Elevated intracranial pressure (ICP) in children: Clinical manifestations and diagnosis".)
This pathophysiology does not necessarily apply in infants and young children because the intracranial compartment can expand at the sutures of the skull if they are open. In addition, young children have larger subarachnoid and extracellular spaces than adults. As a result, they tend to tolerate an expanding epidural hematoma (EDH) better than older children or adults. An associated fracture or subgaleal hematoma may also allow an EDH to decompress to extracranial spaces. (See "Trauma management: Unique pediatric considerations", section on 'Brain'.)
Because of the capacity for large volume intracranial bleeding, young infants occasionally become anemic from hemorrhage before showing objective signs of increased intracranial pressure (eg, altered mental status, seizures, pupillary changes, vomiting) [9]. As an example, pallor was a clinical sign noted upon admission in 30 of 31 patients in one series [9]. (See "Intracranial epidural hematoma in children: Clinical features, diagnosis, and management", section on 'Clinical features'.)
Delayed epidural hematoma — 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 [24-27]. 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 [26,28,29], 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 allow for timely surgical intervention. (See "Intracranial epidural hematoma in children: Clinical features, diagnosis, and management", section on 'Operative treatment'.)
Spontaneous epidural hematoma — Spontaneous acute EDH is rare. Potential etiologies in children include [30-33]:
●Middle ear and sinus infection [30]
●Complication of neurosurgical procedures, such as ventricular shunt placement or craniotomy [31,34,35]
●Minor head trauma in children with coagulopathy (eg, hemophilia, thrombocytopenia) [30]
●Invasive skull tumors, such as Langerhans cell histiocytosis or solid tumor metastasis to the skull [32]
●Sickle cell anemia with skull infarction [33]
SUMMARY
●Definition – Epidural hematoma (EDH) is a potentially life-threatening hemorrhage in the space between the dura and the overlying calvarium that usually results from trauma. (See 'Definition' above.)
●Etiology – In infancy and the intermediate childhood years, low velocity impact (such as falls) is the most common mechanism of injury for intracranial EDH. Even falls less than 5 feet (1.5 m) may rarely result in EDH. In adolescents, motor vehicle collisions account for most EDH. (See 'Epidemiology' above.)
●Anatomy – During direct impact, the skull is deflected inward and the dura is stripped from the undersurface of the bone where blood can accumulate. EDH generally does not cross suture lines of the skull (image 1). (See 'Anatomy' above.)
Infants and young children have a higher frequency of venous than arterial EDH. In older children and adolescents, bleeding typically arises from the middle meningeal artery in association with a temporal skull fracture. (See 'Blood vessel injury' above.)
●Associated injuries – EDH in children frequently occurs without an associated skull fracture compared to adults. Children with EDH also have fewer concomitant intracranial injuries than adults. (See 'Associated abnormalities' above.)
●Pathophysiology – An expanding EDH causes increased intracranial pressure in children and may result in death due to brain herniation without prompt intervention. (See 'Increased intracranial pressure (ICP)' above and "Elevated intracranial pressure (ICP) in children: Clinical manifestations and diagnosis".)
The impact of increased intracranial pressure (ICP) may be blunted in children with open sutures and larger subarachnoid and extracellular spaces. (See 'Increased intracranial pressure (ICP)' above.)
