Chronic epidural hematoma is relatively rare, referring to cases occurring more than 2-3 weeks after injury, accounting for 3.5%-3.9% of all epidural hematomas. Since the application of CT, the incidence has increased, with some studies finding it accounts for over one-third of cases (Burres 1979). However, some of these cases may actually be subacute epidural hematomas or even delayed hematomas. Moreover, the diagnostic time criteria for chronic epidural hematoma are not as clearly defined as those for chronic subdural hematoma. Generally, it is believed that hematomas showing calcification 13 days or more after injury can serve as diagnostic evidence for chronic hematoma.

bubble_chart Etiology

The causative factors of chronic epidural hematoma are not significantly different from those of acute cases. The distinction lies in the patient's ability to tolerate the hematoma for an extended period after injury, with clinical symptoms appearing very gradually. This may be related to the size of the hematoma, the rate of its formation, its location, and the compensatory capacity of the patient's cranial cavity. Hence, there is a theory that the bleeding originates from veins. Although venous pressure is low and less likely to strip the dura mater, if the dura mater and skull are already separated at the moment of injury, or if concurrent cerebrospinal fluid fistula disease leads to low intracranial pressure, the mechanism for chronic hematoma formation exists. Additionally, some believe it is caused by the rupture of a pseudoaneurysm in the meningeal artery triggered by trauma (Mercado 1978). The progression of chronic epidural hematoma differs from that of subdural hematoma. Initially, it appears as a blood clot, and in the late stage [third stage], a layer of granulation tissue forms on the local dura mater, which can be detected by CT. Only a few chronic hematomas develop a membrane and central liquefaction, but this process takes a considerable amount of time, approximately five weeks.

This condition is more common in young males, likely because the dura mater's attachment to the skull is less firm compared to women, children, and the elderly, making it easier to detach. The predilection sites are opposite to those of acute epidural hematomas, frequently occurring in the frontal, parietal, and occipital regions, while the temporal area is less affected. The reason is that temporal hematomas are more prone to causing brain herniation, leading to a rapid progression of the disease. The main clinical features include headache, vomiting, and papilledema. Patients may remain in a state of chronic intracranial hypertension for an extended period. Without thorough examination, it is often misdiagnosed as post-traumatic brain syndrome. Only when neurological signs such as impaired consciousness, hemiplegia, abnormal pupils, or ocular signs appear due to increased intracranial pressure does it receive proper attention.

bubble_chart Diagnosis

The diagnosis of chronic epidural hematoma relies on imaging examinations. The vast majority of patients have skull fractures, and the fractures often traverse the vascular grooves or venous sinuses of the dura mater. The typical CT scan findings show a spindle-shaped high-density shadow on the surface of the brain, with smooth boundaries and edges that may be enhanced, occasionally with calcification. On MRI, it appears as a spindle-shaped high-signal area with sharp boundaries on both T₁ and T₂ weighted images.

Delayed epidural hematoma: The concept of delayed hematoma refers to an imaging finding where no significant abnormality is observed on the initial CT scan, but the hematoma is detected upon re-examination hours or even more than ten days later. Hence, it is termed "delayed," not referring to the age of the hematoma or the urgency of the clinical course. Delayed epidural hematomas account for 5–22% of all epidural hematomas and are more common in young males. The pathogenesis may involve a bleeding source in the dura mater during head trauma, which is initially compressed by factors such as post-traumatic cerebral edema, pre-existing hematomas, or other causes of increased intracranial pressure, creating a tamponade effect. However, subsequent interventions such as hyperventilation, aggressive dehydration, cerebrospinal fluid fistula, evacuation of intracranial hematomas, or surgical decompression, or systemic hypotension leading to a rapid decrease in intracranial pressure, may suddenly remove the tamponade effect. This can cause the dura mater to detach from the skull, resulting in a delayed epidural hematoma. Clinically, such patients often experience sudden deterioration or fail to improve despite an initially negative CT scan, necessitating immediate repeat imaging for definitive diagnosis. Once diagnosed, surgical evacuation should be performed as soon as possible. Compared to chronic epidural hematomas, delayed epidural hematomas have a significantly worse prognosis.

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For patients with evident deterioration of their condition, surgical treatment should be performed promptly. Except for a few cases where the hematoma has liquefied and the membrane has not yet calcified, which may be treated with drilling, irrigation, and drainage, the majority of patients require craniotomy with bone flap removal to evacuate the hematoma. This approach ensures adequate exposure and avoids leaving a skull defect. Additionally, it facilitates the identification of bleeding points and hemostatic procedures during surgery. With proper management and the absence of severe complications, the prognosis for such patients is generally favorable. For select patients who are conscious, have mild symptoms, and show no significant brain function impairment, some opt for non-surgical treatment, allowing the hematoma to absorb or organize naturally under CT monitoring.