Version May 2024
INTRODUCTION — Subdural hematoma (SDH) forms when there is hemorrhage into the potential space between the dura and the arachnoid membranes. SDH in children differs significantly from SDH in adults because inflicted head injury is a common etiology, especially in pediatric patients under two years of age [1]. In contrast to epidural hematoma (EDH), indications for operative management of SDH are less clear, and surgery is less likely to prevent morbidity and mortality. (See "Intracranial subdural hematoma in children: Clinical features, evaluation, and management" and "Intracranial epidural hematoma in children".)
This review will discuss the epidemiology, anatomy, and pathophysiology of subdural hematoma in children. The clinical features, evaluation, and management of SDH in children and SDH in adults are discussed separately. (See "Intracranial subdural hematoma in children: Clinical features, evaluation, and management" and "Subdural hematoma in adults: Etiology, clinical features, and diagnosis" and "Subdural hematoma in adults: Management and prognosis".)
A rapid overview summarizes the important clinical features and initial management of SDH in children (table 1).
EPIDEMIOLOGY — The etiology of SDH in children varies by age. SDH occurs most frequently in infants and toddlers less than two years of age.
Neonates — SDH may occur in up to 8 percent of term deliveries and appears to be associated with delivery by vacuum extraction or forceps [2]. These hematomas are typically small and usually resolve within four weeks. They are usually asymptomatic.
Infants and toddlers — The incidence of SDH in young children under two years of age approaches 13 cases per 100,000 child-years with a higher incidence in infants (≤1 year of age) [3,4]. Inflicted head trauma accounts for the majority of SDH found in these children. (See "Child abuse: Epidemiology, mechanisms, and types of abusive head trauma in infants and children".)
Older children and adolescents — Motor vehicle collision or other forms of major unintentional head trauma cause most traumatic brain injury, including SDH, in older children and adolescents [5].
ANATOMY — Subdural hematoma (SDH) occurs in the potential space between the dura and the arachnoid. Under normal conditions, the subdural region does not exist as a separate layer, unlike the subarachnoid space [6].
Site of hemorrhage — There are two major sources of bleeding in patients with SDH: bridging blood vessels that cross the subdural space and cerebral cortical hemorrhage caused by direct brain trauma [7]. (See 'Pathophysiology' below.)
Subdural hematoma location — SDH can appear in any intracranial location. Chronic hematomas in the higher convexities are associated with brain sag as gravity assists the brain separating from the dura. SDH associated with severe head injury is often located along the convexities of the frontal, parietal, and temporal lobes where tearing of bridging vessels and traumatic impact between the brain and the skull occurs. SDH seen in the interhemispheric space or posterior fossa highly suggests inflicted injury, as do hematomas in multiple sites. (See "Child abuse: Evaluation and diagnosis of abusive head trauma in infants and children".)
Subdural and epidural hematoma anatomic comparison — Key differences between SDH and epidural hematoma (EDH) are readily demonstrated by unenhanced head CT or by pathologic specimens. EDH, which is located in the potential space between dura and skull, does not cross the tight dural attachments at the cranial sutures. Consequentially, EDH characteristically has a lens-shaped, convex appearance and is limited in scope (image 1). SDH can cross cranial suture margins but is limited by internal dural attachments, such as the falx and tentorium, and therefore typically appears as a crescent-shaped or concave extra-axial lesion (image 2).
PATHOPHYSIOLOGY
Blood vessel injury — In the setting of closed head injury, rotational force can produce injury to veins, arteries, or brain parenchyma, resulting in subdural hematoma (SDH), epidural hematoma (EDH), or coup-countercoup contusions [8]. In young children with inflicted head injury, vigorous shaking, with or without a direct blow, causes shearing of white upon gray matter and disruption of bridging vessels caused by violent movement of the brain within the skull [9].
Venous hemorrhage — Acute SDH is usually caused by tearing of the bridging veins that drain from the surface of the brain to the dural sinuses [10]. Rupture of these vessels allows for bleeding into the space between the arachnoid membranes and dura through which the vessels traverse. Venous bleeding is usually arrested by the rising intracranial pressure or direct compression by the clot itself.
Arterial hemorrhage — Arterial rupture can also result in SDH, and this source accounts for approximately 20 to 30 percent of adult SDH cases. Most arterial SDHs arise from injuries to small cortical arteries of <1 mm diameter. In adults, both arterial and venous SDHs have generally similar postmortem characteristics, although SDHs caused by arterial rupture are predominately located in the temporoparietal region, while those caused by bridging vein rupture are predominately frontoparietal. (See "Subdural hematoma in adults: Etiology, clinical features, and diagnosis", section on 'Pathophysiology and etiology'.)
Dural traction — Low cerebrospinal fluid (CSF) pressure (intracranial hypotension) is another mechanism that can result in SDH. Intracranial hypotension is typically caused by a spontaneous or iatrogenic cerebrospinal fluid leak, as may occur following ventricular peritoneal shunting for hydrocephalus in children [11]. As the cerebrospinal fluid pressure decreases, there is a reduction in the buoyancy of the brain, causing traction on the anchoring and supporting structures, including the dura. Traction on bridging veins can cause tearing and rupture of these vessels, while intracranial hypotension itself leads to engorgement of cerebral veins and subsequent leakage of fluid into the subdural space. (See "Spontaneous intracranial hypotension: Pathophysiology, clinical features, and diagnosis".)
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) [12]:
●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 [13,14]. 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 [12,14-17]. With an expanding SDH, CSF, intracranial venous blood, and then brain parenchyma are displaced. If the SDH continues to increase in size, then death due to brain herniation through the foramen magnum ensues. (See "Elevated intracranial pressure (ICP) in children: Clinical manifestations and diagnosis".)
This pathophysiology does not necessarily apply in young children because the sutures of the skull remain open until approximately 18 months of age. As a result, they tend to tolerate an expanding SDH better than older children or adults. There may also be age dependent responses to the SDH with younger brains being somewhat resistant to injury from the hematoma alone, but susceptible to other insults [18]. (See "Trauma management: Overview of unique pediatric considerations", section on 'Brain'.)
Because of the capacity for large volume intracranial bleeding, young infants may become anemic from hemorrhage in addition to showing objective signs of increased ICP (eg, altered mental status, seizures, pupillary changes, vomiting).
Type of injury — The source of bleeding and amount of associated brain injury correlate with the type of head trauma that produces a SDH.
Severe head injury — After severe head injury (eg, motor vehicle collision), hemorrhage arises from bridging vessels and an extensively damaged cerebral cortex. The subdural may be very small on radiographic imaging, but accompanies clinical and radiographic signs of severe diffuse brain injury. In this setting, the expected morbidity and mortality is higher than for patients with SDH and minor head injury, even though the size of the hematoma in children with minor head injury is often larger. (See 'Minor head injury' below.)
SDH after major trauma typically has a worse prognosis than EDH because of the associated extensive brain damage [19]. Although EDH can cause rapid deterioration if not detected and treated, EDH is typically associated with little to no direct brain injury. (See "Intracranial epidural hematoma in children".)
Inflicted head injury (shaken baby syndrome) — In addition to SDH, acceleration-deceleration forces cause diffuse brain injury in victims of shaken baby syndrome. The susceptibility of infants to shaking injury arises from the relatively large size of the head, the weakness of the cervical musculature, softness of the skull, and high water content of the brain caused by incomplete myelination. The role of a direct blow as a major cause of injury in shaken babies is controversial. Associated injuries include retinal hemorrhage and fractures of the skull and skeleton. (See "Child abuse: Epidemiology, mechanisms, and types of abusive head trauma in infants and children", section on 'Mechanisms of injury' and "Physical child abuse: Diagnostic evaluation and management".)
In victims of inflicted head trauma, hypoxic-ischemic injury frequently accompanies severe brain injury and hemorrhage because appropriate medical care is not immediately sought by the perpetrator.
Minor head injury — Rupture of blood vessels (generally veins) crossing the subdural space is the prime source of hemorrhage following minor head injury. The SDH in this instance can become large, with few clinical findings because the hematoma typically accumulates slowly and without serious direct brain injury. Patient susceptibility to hematoma formation is common. Predisposing factors include:
●Dural traction or brain sag (eg, treated hydrocephalic patients or those with brain atrophy) [11]
●Subdural hygroma or chronic subdural effusion occurring after an acute SDH or meningitis [4,20-22]
●Enlargement of the subarachnoid spaces (eg, benign extra-axial fluid of infancy) (image 3) [23-25]
●Bleeding tendency (eg, thrombocytopenia, hemophilia, patients receiving anticoagulants, such as aspirin or Coumadin) [9]
●Osteogenesis imperfecta [26]
●Glutaric aciduria, type 1 [27,28]
●Rupture of an arachnoid cyst resulting in intracystic hemorrhage and subdural hematoma [29-33]
At times the distinction between posttraumatic SDH and enlargement of the subarachnoid space is difficult. Radiographic imaging can assist in making this important determination [21]. (See "Intracranial subdural hematoma in children: Clinical features, evaluation, and management", section on 'Radiographic imaging'.)
Chronic subdural hematoma — Following the initial meningeal trauma and development of SDH, dural collagen synthesis is induced and fibroblasts spread over the inner surface of the dura to form a thick outer membrane [34,35]. Subsequently, a thinner inner membrane develops, resulting in complete encapsulation of the clot. This occurs over a predictable time course of approximately two weeks [35]. This ability to time chronic SDH is often used as forensic evidence that establishes child abuse in cases of inflicted head injury (shaken baby syndrome). (See "Child abuse: Epidemiology, mechanisms, and types of abusive head trauma in infants and children", section on 'Subdural hemorrhage'.)
Over time, a chronic SDH may liquefy, or form a hygroma, and the membranes may calcify [35]. More than one-half of all SDHs liquefy and tend to enlarge as opposed to remaining solid and stable in size [10]. Although the reason for this observation is unknown, a larger initial clot size appears to be related to a greater likelihood of subsequent expansion [36].
At any time, the hematoma may expand secondary to recurrent bleeding ("acute-on-chronic" SDH) or from osmotic draw of water into the hygroma, owing to its high protein content. Cerebral hemisphere lesions and secondary brainstem injury may develop because of the mass effect produced by a large SDH.
Subdural hygroma — Subdural hygromas are thought to develop passively because of traumatic brain injury followed by brain atrophy, dehydration, and/or decreased intracranial pressure. The mechanism of hygroma formation in this setting is related to the separation of the arachnoid layer from the dura, which can occur when a contracting brain pulls the arachnoid along with it while the dura remains adherent to the skull [37].
Most subdural hygromas will resolve with adequate reexpansion of the intracranial contents (eg, hydration). However, some will become chronic [37]. The persistence of hygromas appears to be related to the formation of pseudomembranes (as discussed above) that line the space created between the arachnoid and the dura during the acute phase. These subsequently become vascularized by abnormally permeable capillaries that allow for further accumulation of subdural fluid.
SUMMARY
●The clinical features, evaluation, and management of subdural hematoma (SDH) in children are discussed separately. (See "Intracranial subdural hematoma in children: Clinical features, evaluation, and management".)
●Among children, SDH develops most frequently in infants and toddlers (≤2 years of age). Inflicted head injury (shaken baby syndrome) is the most common cause in this age group. (See 'Epidemiology' above and "Child abuse: Epidemiology, mechanisms, and types of abusive head trauma in infants and children".)
Anatomy
●Subdural hematoma (SDH) occurs in the potential space between the dura and the arachnoid. Bleeding arises from rupture of bridging blood vessels and, when associated with severe head trauma, from an extensively damaged cerebral cortex. (See 'Site of hemorrhage' above.)
●SDH can cross suture margins, but is limited by internal dural attachments such as the falx cerebri and tentorium cerebelli and therefore typically appears as a crescent-shaped or concave extra-axial lesion on unenhanced computed tomography (CT) (image 2). In contrast, epidural hematoma (EDH) crosses internal dural attachments but does not cross suture lines. Thus, EDH characteristically has a lens-shaped, convex appearance on head CT (image 1). (See 'Subdural and epidural hematoma anatomic comparison' above.)
Pathophysiology
●Blood vessel injury in children with SDH following major trauma (inflicted and unintentional) may involve veins or arteries. In young children with inflicted head injury, vigorous shaking, with or without a direct blow, causes extensive bleeding from the brain cortex in addition to bridging vessel rupture during violent movement of the brain within the skull. (See 'Blood vessel injury' above.)
●An expanding SDH causes increased intracranial pressure (ICP) in children with closed sutures and without prompt intervention may result in death due to brain herniation. The impact of increased ICP from SDH may be blunted in young children with open cranial sutures. (See 'Increased intracranial pressure (ICP)' above and "Elevated intracranial pressure (ICP) in children: Clinical manifestations and diagnosis" and "Intracranial subdural hematoma in children: Clinical features, evaluation, and management", section on 'Definitive management'.)
●The type of traumatic brain insult and the associated brain injury largely determine the clinical severity of a SDH. The size of the hematoma is less important. (See 'Type of injury' above.)
●Patients with bleeding tendency, dural traction, enlarged subarachnoid spaces, osteogenesis imperfecta, and glutaric aciduria type I are at increased risk of SDH following minor head injury. (See 'Minor head injury' above.)
●Chronic subdural fluid collections containing clotted blood or proteinaceous fluid commonly develop after a SDH. Membrane formation in chronic SDH predictably occurs two weeks after injury. (See 'Chronic subdural hematoma' above and 'Subdural hygroma' above.)
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