The vast majority of traumatic intracerebral hematomas are acute, with a few being subacute. Superficial intracerebral hematomas, especially those located in the frontal and anterior temporal lobes and at the base, often occur alongside cerebral contusions and subdural hematomas, presenting with rapid clinical manifestations. Deep hematomas, mostly within the white matter, result from deep vascular tears caused by brain deformation or shearing forces, leading to hemorrhage. When the bleeding is minor and the hematoma is small, clinical symptoms are relatively mild. Larger hematomas, particularly those near the basal ganglia, thalamus, or ventricular walls, may rupture into the ventricles, causing intraventricular hemorrhage. Such cases are often severe and carry a poor prognosis.

bubble_chart Pathological Changes

Traumatic intracerebral hematomas most commonly occur in the frontal and temporal lobes, accounting for approximately 80% of all cases, often resulting from contrecoup contusions and lacerations. The parietal and occipital lobes are the next most frequent sites, making up about 10%, typically caused by direct impact injuries or depressed fractures. The remaining cases involve hematomas in deeper brain regions, the brainstem, or the cerebellum, which are relatively rare. In the initial stage of hematoma formation, it appears as a simple blood clot. Superficial hematomas are often mixed with surrounding crushed brain tissue, while deeper ones are encircled by compressed, necrotic, and edematous tissue. After about 4–5 days, the hematoma begins to liquefy, turning into brownish old blood, with surrounding glial cell proliferation. At this stage, surgical removal of the hematoma reveals clear boundaries, minimal bleeding, and relative ease of extraction. Subsequently, over 2–3 days, a membrane forms around the hematoma, enclosing yellowish fluid, which gradually transforms into cystic degeneration. Adjacent brain tissue may show hemosiderin deposition, with local gyri appearing flattened, widened, and softened, exhibiting a fluctuant sensation. However, clinical signs of increased intracranial pressure are typically absent by this stage.

The clinical manifestations of intracerebral hematoma depend on its location. Hematomas in the frontal and temporal lobes or at the base of the brain resemble contrecoup contusions and subdural hematomas, often presenting with increased intracranial pressure but few distinct focal symptoms or signs. If the hematoma affects critical functional areas, symptoms such as hemiplegia, aphasia, hemianopia, hemisensory deficits, or focal seizures may occur. Patients with intracerebral hematomas caused by contrecoup contusions typically experience prolonged and progressively worsening impaired consciousness after injury, often without a lucid interval, and their condition deteriorates rapidly, increasing the risk of brain herniation. In contrast, localized hematomas resulting from direct impact injuries or depressed fractures tend to progress more slowly. Besides focal neurological deficits, these patients often exhibit signs of increased intracranial pressure, such as headache, vomiting, and papilledema. Elderly individuals, due to increased vascular fragility, are particularly prone to developing intracerebral hematomas.

bubble_chart Diagnosis

Acute and subacute intracerebral hematomas are similar to subdural hematomas caused by cerebral contusions and lacerations. When patients exhibit progressive intracranial hypertension and signs of brain compression following craniocerebral injury, CT scans or cerebral angiography should be performed immediately for a definitive diagnosis. In emergency situations, based on the analysis of the injury mechanism or using cerebral ultrasound for lateralization, exploratory burr holes should be drilled as soon as possible in the temporal region or suspected areas, along with frontal and temporal lobe punctures, to avoid missing an intracerebral hematoma. Since these hematomas are often compound and multiple, analyzing the injury mechanism to determine the hematoma's location and conducting imaging examinations are crucial. Otherwise, hematomas may be missed during surgery, which should be noted. In the acute phase, over 90% of intracerebral hematomas appear as high-density masses on non-contrast CT scans, surrounded by low-density edema zones. However, within 2 to 4 days, the hematomas may become isodense and easily missed in diagnosis. After 4 weeks, they turn hypodense and become visible again. Additionally, delayed intracerebral hematomas are among the more common types of delayed hematomas, requiring heightened vigilance. Repeat CT scans should be performed if necessary.

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The treatment for acute intracerebral hematoma is the same as that for acute subdural hematoma, both being composite hematomas associated with cerebral contusion and laceration, and the two often coexist. The surgical approach typically involves a bone window or bone flap craniotomy. After evacuating the subdural hematoma and the contused, necrotic brain tissue, the intracerebral hematoma in the frontal and temporal lobes should be explored and removed. If intracranial pressure does not significantly decrease after hematoma evacuation, or if other suspicious findings remain—such as surface contusion, swollen and widened gyri, or palpable fluctuation—puncture should be performed. For cases suspected of ventricular rupture, ventricular puncture and drainage should also be performed. Intraoperative ultrasound may be necessary to rule out deep-seated hematomas. Patients with rapidly progressing conditions have a poorer prognosis, with mortality rates as high as around 50%. For patients with simple intracerebral hematomas and slower progression, such as subacute cases, the decision should be based on the degree of intracranial pressure elevation. If the pressure is progressively worsening and there is a tendency toward herniation, surgical intervention remains advisable. The choice between craniotomy or drilling and irrigation drainage depends on the proportion of liquid components in the hematoma. If solid components dominate, complete surgical evacuation is preferable. A small subset of acute intracerebral hematomas, despite their acute nature, may involve mild contusion, small hematoma volume (less than 30ml), mild clinical symptoms, clear consciousness, stable condition, or intracranial pressure below 3.33 kPa (25 mmHg). In such cases, non-surgical treatment may also be considered. For a few chronic intracerebral hematomas that have already undergone cystic degeneration and exhibit normal intracranial pressure, no special treatment is required. Surgery is generally not considered unless refractory epilepsy is present.