bubble_chart Overview

Typical acute epidural hematomas are commonly seen in young and middle-aged males with linear skull fractures, most frequently occurring in the frontotemporal and parietotemporal regions. This is related to the presence of arteries and veins in the meninges of the temporal region, which are prone to being torn by fractures.

bubble_chart Pathological Changes

Rapidly developing epidural hematomas are often caused by arterial injuries, leading to a swift increase in the hematoma size, which can result in brain herniation within hours, posing a life-threatening risk to the patient. If the bleeding originates from veins, such as the meningeal veins, diploic veins, or venous sinuses, the progression of the condition is somewhat slower, potentially presenting as subacute or chronic. Acute epidural hematomas are less common in the occipital region due to the tight adherence of the dura mater to the occipital bone and the typically venous nature of the bleeding. Research indicates that a force of at least 35 grams is required to separate the dura mater from the skull. However, in some cases, fracture lines crossing the superior sagittal sinus or transverse sinus can lead to large epidural hematomas straddling the sinus. The continuous expansion of such hematomas is often due to new rebleeding after the dura mater is stripped from the inner table of the skull, rather than solely from venous pressure. The size of the hematoma is closely related to the severity of the condition; the larger the hematoma, the more severe the condition. However, the rate of bleeding is more critical, as small but rapidly expanding hematomas can cause early symptoms of brain compression, while slowly bleeding hematomas may take days or even weeks to manifest increased intracranial pressure. Acute hematomas located on the convexity of the hemisphere often push the brain tissue inward and downward, causing the medial temporal lobe, including the hippocampus and uncus, to herniate below the tentorial edge, compressing the cerebral peduncle, oculomotor nerve, posterior cerebral artery, and affecting the drainage of the pontine veins and superior petrosal sinus, a condition known as tentorial herniation. Chronic epidural hematomas typically show signs of organization within 6 to 9 days, with fibrous cells growing from the dura mater and a thin layer of granulation tissue encapsulating and adhering to the dura mater and skull. Small hematomas may completely organize, while larger ones may become cystic, containing brownish bloody fluid.

bubble_chart Clinical Manifestations

The clinical manifestations of epidural hematoma can vary depending on the rate of bleeding, the location of the hematoma, and the age of the patient. However, from a clinical perspective, there are certain patterns and commonalities, namely unconsciousness─lucid interval─recurrent unconsciousness. Taking acute supratentorial epidural hematoma as an example, the following is an overview:

1. Altered consciousness: Due to varying degrees of primary brain injury, the changes in consciousness in these patients can present in three different scenarios: ① Mild primary brain injury, with no initial unconsciousness after the injury, but progressive intracranial pressure increase and altered consciousness occurring after the formation of the intracranial hematoma. These patients are prone to misdiagnosis. ② Slightly more severe primary brain injury, with grade I unconsciousness after the injury, followed by complete lucidity or improvement in consciousness, but soon falling back into unconsciousness. These patients are considered typical cases and are easily diagnosed. ③ Severe primary brain injury, with persistent unconsciousness after the injury and progressive deepening of unconsciousness. The signs of intracranial hematoma are often masked by primary brain contusion or brainstem injury, making misdiagnosis more likely.

2. Increased intracranial pressure: As intracranial pressure increases, patients often experience headaches, worsening vomiting, restlessness, and the classic Cushing's response, including elevated blood pressure, increased pulse pressure, rising body temperature, and slowed heart rate and respiration. When exhaustion sets in, blood pressure drops, the pulse becomes weak, and respiration is suppressed.

3. Neurological signs: In simple epidural hematoma, neurological signs of impairment are less common in the early stages. Only when the hematoma compresses functional areas of the brain do corresponding positive signs appear. If symptoms and signs such as deviation of the mouth, hemiplegia, or aphasia appear immediately after the injury, they should be attributed to primary brain injury. When the hematoma continues to grow and causes uncal herniation, the patient will not only experience deepening altered consciousness and disordered vital signs but also develop classic signs such as ipsilateral pupillary dilation and contralateral limb hemiplegia. Occasionally, due to rapid hematoma development, early brainstem distortion, displacement, and impingement on the contralateral tentorial notch may cause atypical signs: contralateral pupillary dilation and contralateral hemiplegia; ipsilateral pupillary dilation and ipsilateral hemiplegia; or contralateral pupillary dilation and ipsilateral hemiplegia. Immediate auxiliary examination is required for localization.

bubble_chart Diagnosis

Early diagnosis of acute epidural hematoma above the tentorium should be determined before the signs of temporal lobe herniation, rather than after the deepening of unconsciousness and pupil dilation. Therefore, clinical observation is crucial. When a patient experiences worsening headache and vomiting, restlessness, elevated blood pressure, increased pulse pressure difference, and/or new signs, intracranial hematoma should be highly suspected. Immediate necessary imaging examinations should be conducted, including X-ray skull radiographs, A-mode ultrasound, cerebral angiography, or CT scans.

bubble_chart Treatment Measures

The treatment of acute epidural hematoma generally involves surgical intervention upon diagnosis to evacuate the hematoma and relieve intracranial pressure (hydrocephalus). Postoperative non-surgical treatment is administered based on the patient's condition. Generally, if there are no other severe complications and the primary brain injury is mild, the prognosis is favorable. The mortality rate ranges between 10-25%, with significant variations across different regions or institutions. In fact, the primary cause of death in these patients is not the hematoma itself but secondary brainstem damage caused by brain herniation. Therefore, early diagnosis and timely intervention are crucial to effectively reduce mortality.

1) Surgical Treatment: Craniotomy with bone flap or bone window is commonly used to thoroughly remove the hematoma, achieve hemostasis, and perform necessary subdural exploration. This has been a long-standing surgical approach for epidural hematoma. In recent years, with the widespread use of CT scans, the location, size, and extent of brain injury can be precisely determined, allowing dynamic observation of the hematoma. Consequently, some authors have successfully treated epidural hematoma with burr hole drainage. ① Bone Window Craniotomy for Epidural Hematoma Evacuation: This is suitable for critically ill patients with brain herniation who require immediate imaging diagnosis and localization before being rushed to the operating room. Initial burr hole exploration is performed, followed by expansion into a bone window to evacuate the hematoma. The burr hole should first be made near the temporal fracture line on the side of pupillary dilation, where 60-70% of epidural hematomas can be detected. Upon locating the hematoma, the incision is extended as needed, the bone flap is enlarged, and the hematoma is evacuated with careful hemostasis. If the dura remains tense, bulging, or bluish after hematoma removal, it should be incised and explored to avoid missing subdural or intracerebral hematomas. Postoperatively, a rubber drain is placed epidurally, and the scalp is sutured in layers. Cranial bone defects are repaired electively after 2-3 months. ② Bone Flap Craniotomy for Epidural Hematoma Evacuation: This is suitable for cases with clear hematoma localization. Based on imaging results, a bone flap craniotomy is performed. Upon exposing the hematoma, it is not necessary to rush to remove it, as intracranial pressure has already been significantly relieved. To minimize bleeding, the hematoma is gradually dissected from the periphery toward the thickest part near the skull base, often revealing ruptured dural arteries or veins, which are then coagulated or ligated. After hematoma removal, the surgical site is irrigated with saline, and any bleeding points are meticulously identified and controlled to prevent postoperative rebleeding. If the dura is tense or a subdural hematoma is suspected, the dura should be incised and explored, and the bone flap should not be hastily removed for decompression. It is important to note that missed hematomas are a significant cause of postoperative mortality. Postoperatively, the dura is suspended to the edge of the bone window, the bone flap is replaced, the scalp is sutured in layers, and an epidural drain is left in place for 24-48 hours. ③ Burr Hole Drainage for Epidural Hematoma: This is suitable for emergency treatment of hyperacute epidural hematoma to temporarily relieve intracranial pressure (hydrocephalus) and buy time. A burr hole or twist drill hole is made to partially drain the liquid hematoma. This emergency measure has been used for prehospital care or drainage of intracerebral hematomas. Recently, some scholars have applied it to the treatment of acute epidural hematoma, achieving rapid hematoma drainage and patient rescue. The indications include relatively stable condition, hematoma volume of about 30-50ml, clear localization by CT, midline shift of more than 0.5cm, and no ongoing bleeding. The method involves making a burr hole or twist drill hole at the thickest part of the hematoma as shown by CT, then inserting an aspiration needle or a catheter with a wire mesh. After partial blood drainage, urokinase or urokinase plus hyaluronidase is injected to dissolve residual clots, repeated several times, with the catheter left in place for 3-6 days until CT confirms complete hematoma evacuation.

2) Non-Surgical Treatment: Whether or not surgery is performed, timely and appropriate non-surgical treatment is essential for acute epidural hematoma, especially for patients with severe primary brain injury and/or secondary brain damage. This should never be taken lightly.

Conservative treatment of epidural hematoma: suitable for patients with clear consciousness and stable condition; CT examination shows hematoma volume less than 40ml, midline shift not exceeding 1.5cm; no deterioration of consciousness, fundus edema, or new symptoms; not located in the middle or posterior cranial fossa. Treatment measures should include dehydration, hormone therapy, hemostasis, and blood-activating and stasis-resolving medicinal treatments such as Salvia and Sichuan Lovage Rhizome, under close observation of the patient's clinical manifestations. Dynamic monitoring with CT should be utilized to ensure safety.

bubble_chart Differentiation

Differentiation of acute epidural hematoma, cerebral edema, subdural hematoma, and intracerebral hematoma (Table 1).

Table 1: Differentiation Table of Epidural Hematoma, Subdural and Intracerebral Hematoma, and Cerebral Edema