bubble_chart Overview

The incidence of acute (within 3 days) subdural hematoma is the highest, accounting for 70%, while subacute (4-21 days) cases account for about 5%. The causative factors and sources of bleeding are essentially the same for both, and both commonly occur in the frontotemporal-parietal region. The speed of clinical progression varies depending on the severity of the primary brain injury, the amount of bleeding, and individual compensatory capacity.

bubble_chart Pathological Changes

Both acute and subacute subdural hematomas are caused by bleeding from ruptured cortical vessels due to cerebral contusion and laceration, thus both are classified as complex subdural hematomas. The only difference lies in the slight variation in the speed of disease progression. The causative factors and injury pathology are also similar: in acceleration injuries, cerebral contusion and hematoma often occur on the same side, whereas deceleration injuries typically result in contrecoup cerebral contusion and bleeding on the opposite side. A blow to one side of the occiput consistently leads to a complex subdural hematoma in the anterior part of the contralateral frontal or temporal lobe, sometimes accompanied by an intracerebral hematoma. A midline occipital impact tends to cause bilateral hematomas in the frontal poles and temporal tips. Lateral head trauma may produce a complex subdural hematoma on the injured side, i.e., a subdural-intracerebral hematoma. When the head is struck or falls laterally, the ipsilateral side often develops a complex subdural hematoma or epidural hematoma, while the contralateral side may exhibit a simple and/or complex subdural hematoma. Additionally, frontal trauma, whether from a direct blow or impact, usually results in hematomas in the frontal region and rarely in the occipital area. In elderly individuals, such trauma frequently causes unilateral or bilateral simple subdural hematomas.

bubble_chart Clinical Manifestations

In acute cases, most are compound subdural hematomas, so the clinical manifestations closely resemble cerebral contusion and laceration, with the difference being that the progressive increase in intracranial pressure is more pronounced, exceeding the degree and speed of cerebral edema following general brain injury. The patient's post-injury disturbance of consciousness is more prominent, often presenting as persistent unconsciousness with progressive deterioration, and there is rarely an intermediate lucid interval. Even if the degree of consciousness impairment temporarily improves to grade I, it is short-lived, and as cerebral herniation develops, the patient quickly falls into deep unconsciousness. In subacute cases, because the primary cerebral contusion and laceration are less severe and the bleeding rate is slightly slower, the process from hematoma formation to brain compression is somewhat prolonged, allowing the compensatory capacity of the intracranial volume to come into play. Therefore, there is often an intermediate lucid interval, though the degree of mental recovery is not as distinct and clear as in epidural hematomas.

Symptoms of increased intracranial pressure: In acute cases, the main manifestations are deepening disturbance of consciousness and prominent changes in vital signs, along with earlier signs of tentorial herniation. In subacute cases, symptoms often include worsening headache, vomiting, restlessness, and progressive deterioration of consciousness, leading to unconsciousness once cerebral herniation occurs.

Focal signs: In the early post-injury period, certain brain functional areas may be affected by cerebral contusion and laceration, resulting in corresponding signs such as hemiplegia, aphasia, or epilepsy. If new signs appear during observation that were not present in the early post-injury period or if pre-existing positive signs significantly worsen, the possibility of an intracranial secondary hematoma should be considered.

bubble_chart Diagnosis

After craniocerebral injury, if the primary unconsciousness lasts for a prolonged period or overlaps with secondary consciousness disorders, manifesting as progressively deepening unconsciousness accompanied by signs of brain compression and increased intracranial pressure—especially when focal signs are present—acute subdural hematoma should be highly suspected. If the condition develops more slowly over 4–12 days, with an intermediate period of improved consciousness followed by worsening, along with fundus edema and symptoms of increased intracranial pressure, it often indicates a subacute subdural hematoma. Diagnostic auxiliary examinations should be performed promptly without delay, avoiding waiting for typical signs of brain herniation such as pupillary dilation, contralateral hemiplegia, deepening unconsciousness, and life-sign disturbances, which may worsen the condition. If necessary, exploratory drilling can be conducted directly. Additionally, the diagnosis of acute subdural hematoma in children and the elderly should account for their distinct clinical features. In children, symptoms of brain compression appear earlier and are more severe. Even with mild cerebral contusion, brain edema or swelling can be pronounced, often leading to neurological deficits and frequent seizures, with a poorer prognosis compared to adults. In the elderly, due to vascular sclerosis, brain atrophy, and greater brain mobility, even minor head injuries can cause severe damage. Acute subdural hematomas in this group are often contrecoup and compound, frequently accompanied by intracerebral hematomas. Although brain edema is less severe than in younger individuals, tissue repair is slower, complications are more common, and mortality is higher.

Auxiliary examinations primarily rely on CT scans, which can assess both cerebral contusion and the presence of subdural hematomas. Skull X-rays reveal fractures in about half of patients, though these are less significant for localization compared to epidural hematomas and serve mainly as references for injury mechanisms. Magnetic resonance imaging (MRI) not only directly visualizes the extent and severity of injury but also excels in detecting hematomas during the CT isodense phase, as methemoglobin released after erythrocyte lysis produces high signals in both T1 and T2 sequences. Additionally, cerebral ultrasonography or angiography can aid in lateralization or localization of subdural hematomas (Table 1).

Table 1 Clinical Features of Acute Epidural Hematoma and Acute Subdural Hematoma

bubble_chart Treatment Measures

Acute subdural hematoma progresses rapidly and severely, especially in extremely urgent cases, with a mortality rate as high as 50–80%. Once diagnosed, immediate action is imperative, and surgical treatment should be performed as soon as possible, without delay. In cases of subacute subdural hematoma, some patients with milder primary brain injuries and slower progression may achieve successful non-surgical treatment under strict intracranial pressure monitoring or dynamic CT observation. However, if the condition worsens during treatment, surgical intervention should be promptly adopted. Any hesitation or delay is extremely dangerous.

1) **Surgical Treatment**: The choice of surgical method depends on the patient's condition. Commonly used surgical techniques include the following three: ① **Drilling, Irrigation, and Drainage**: Based on the location of the hematoma shown by CT, drilling and drainage are performed. If it is an emergency exploratory drilling due to insufficient preoperative localization, the positioning should be determined based on the injury mechanism, impact point, and the patient’s clinical manifestations, followed by sequential drilling. For contrecoup injuries, drilling should first be performed in the anterior temporal region, followed by the frontal and then the parietal regions. For direct impact injuries, drilling should first be done at the impact site, followed by the contrecoup site. After identifying the hematoma, the drilling hole should be slightly enlarged to facilitate irrigation and hematoma removal. If the hematoma is liquid and there is no active bleeding, 1–2 additional drilling holes can be made in the thicker parts of the hematoma, followed by catheter irrigation between the holes to remove most of the hematoma. If intracranial hypertension is relieved and cerebral pulsation is good, the surgery can be terminated. A drainage tube is left in place at a low position for continuous drainage for 24–48 hours, and the scalp is sutured in layers. For pediatric acute subdural hematoma with an open fontanelle, repeated aspiration via the anterior fontanelle can gradually remove the hematoma. If the hematoma is solid, drilling and drainage or craniotomy for hematoma removal is required. ② **Craniotomy with Bone Window or Bone Flap**: This is suitable for patients with clearly localized hematomas; those in whom exploratory drilling reveals a clotted hematoma that is difficult to flush out; those with continuous fresh bleeding during irrigation and drainage; or those in whom intracranial pressure rises again after hematoma removal. In such cases, the drilling hole should be immediately expanded into a bone window or a bone flap craniotomy should be performed. Under good exposure, the hematoma and crushed or necrotic brain tissue should be thoroughly removed, and hemostasis should be ensured. If necessary, brain puncture should be performed to remove intracerebral hematomas, along with ventricular drainage or basal cistern drainage. After surgery, the dura mater and scalp layers are sutured as usual, with an external rubber drainage tube left in place for 24–48 hours. If intracranial pressure improves initially but then rises again after hematoma removal, exploratory drilling should be performed at possible sites of multiple intracranial hematomas, especially in the frontal and temporal bases or deep brain regions. Intraoperative B-mode ultrasound or brain scanning may be used if necessary. If no other hematomas are found, subtemporal decompression or decompressive craniectomy can be performed, along with ventricular drainage and/or tentorium cerebelli incision and basal cistern drainage. If doubts remain, CT scanning or cerebral angiography should be conducted to rule out residual or delayed hematomas. ③ **Subtemporal Decompression or Decompressive Craniectomy**: In cases of acute subdural hematoma with severe cerebral contusion, edema, or concurrent brain swelling, even after thorough removal of the hematoma and necrotic brain tissue, intracranial pressure may remain uncontrolled, and the brain may continue to bulge. In such cases, subtemporal decompression or decompressive craniectomy is necessary. If required, the affected frontal and temporal poles may be resected as internal decompression measures before closing the cranial cavity.

Subtemporal Decompression: Subtemporal decompression is a traditional surgical procedure used as a decompressive measure following the evacuation of acute cerebral contusion and laceration with subdural hematoma. The decompression area has been expanded, reaching a diameter of 8–10 cm, but should not exceed the coverage area of the temporalis muscle. After fully detaching the temporalis muscle from the skull surface, the squamous part of the temporal bone and adjacent portions of the frontal and parietal bones are removed. The dura mater is then incised in a stellate fashion up to the edge of the bone window. After hemostasis, the temporalis muscle is intermittently sutured, while the temporalis fascia is left unsutured to facilitate decompression. The scalp is closed in layers without drainage. Unilateral decompression is typically performed, though bilateral subtemporal decompression may be performed if necessary.

Decompressive Craniectomy: The so-called decompressive craniectomy involves removing the bone flap, opening the dura mater, and only suturing the scalp to achieve decompression. Typically, unless it is preoperatively decided to perform decompressive craniectomy with the intention of enlarging the bone flap—hence the term large bone flap decompression—it is difficult for the size and location of the bone flap to meet the requirements for decompression. In practice, the decision to perform decompression is often made during the surgery. Therefore, after removing the bone flap, it is often necessary to also excise the squamous part of the temporal bone down to the level of the zygomatic arch and forward to the greater wing of the sphenoid bone behind the orbital process of the frontal bone. This allows the temporal lobe and part of the frontal lobe to protrude outward, alleviating pressure on the brainstem and the vessels of the lateral fissure. However, it must be emphasized that decompressive craniectomy should strictly adhere to indications and not be performed arbitrarily. It is important to note that after large bone flap decompression, adverse consequences such as brain displacement and deformation due to brain herniation, as well as significant disruption of bulk flow in brain tissue, can lead to delayed intracranial hematomas and localized edema in the early stages. This exacerbates brain structural deformation and distortion, increasing neurological deficits. In the late stage [third stage], it can also lead to complications such as brain softening, atrophy, fluid accumulation, porencephaly, hydrocephalus, and epilepsy. The indications for large bone flap decompression include: acute or ultra-acute intracranial hematomas accompanied by severe cerebral contusions and/or edema, preoperative brain herniation, unsatisfactory relief of intracranial hypertension after hematoma evacuation with no other residual hematomas; diffuse brain injury, severe cerebral edema, brain herniation, but no localized large hematoma requiring exclusion; preoperative bilateral dilated pupils and decerebrate rigidity, with intracranial pressure improving to grade I after hematoma evacuation but showing a tendency to rise again shortly thereafter.

Acute subdural hematomas, particularly in elderly patients with contrecoup ultra-acute hematomas, bilateral dilated pupils, and absent light reflexes, where the hematoma is small but the condition is severe, have an extremely poor prognosis.

2) Non-surgical treatment: Whether or not surgery is performed, timely and appropriate non-surgical treatment is essential for acute and subacute subdural hematomas, especially postoperatively for acute hematomas. Although a few acute subdural hematomas may resolve spontaneously, such cases are rare, and one should not rely on chance. In fact, only a small number of subacute subdural hematoma patients, if the primary brain injury is mild and the condition progresses slowly, may be treated non-surgically. The indications are: clear consciousness, stable condition, essentially normal vital signs, and gradually improving symptoms; no localized brain compression causing neurological impairment; CT scans showing no significant compression of the ventricles or cisterns, hematoma volume below 40ml, midline shift not exceeding 10mm; intracranial pressure monitoring below 3.33–4.0kPa (25–30mmHg).