| disease | Subdural Hematoma |
| alias | Chronic Subdural Hematoma |
Chronic subdural hematoma refers to a hematoma that develops symptoms more than three weeks after a head injury, located between the dura mater and arachnoid membrane, and is encapsulated. It commonly occurs in children and the elderly, accounting for 10% of intracranial hematomas and 25% of subdural hematomas, with a bilateral incidence rate as high as 14.8%. The head injury in this condition is usually mild, with an insidious onset and nonspecific clinical manifestations, making it prone to misdiagnosis. The interval between injury and symptom onset typically ranges from 1 to 3 months, though cases as long as 34 years have been reported in the literature.
bubble_chart Etiology
The majority of cases of chronic subdural hematoma have a history of minor head trauma, particularly in the elderly when the force is applied to the forehead or occiput. In such cases, the brain tissue has greater mobility within the cranial cavity, making it most susceptible to tearing the bridging veins that drain from the cerebral surface into the superior sagittal sinus. Other sources of bleeding include damage to venous sinuses, arachnoid granulations, or subdural hygromas. Non-traumatic chronic subdural hematomas are very rare and may be associated with conditions such as arteriovenous malformations, vascular anomalies, or other cerebrovascular diseases. Regarding the expansion of chronic subdural hematomas, many hypotheses have been proposed in the past, such as the high osmotic pressure mechanism within the hematoma cavity, which has since been disproven. Current research suggests that the continuous enlargement of the hematoma is related to factors such as brain atrophy, decreased intracranial pressure, increased venous tension, and coagulation disorders. Electron microscopy observations reveal that the inner membrane of the hematoma consists of collagen fibers without blood vessels, while the outer membrane contains a dense capillary network with large gaps between endothelial cells, an unclear basement membrane structure, and abnormal permeability. Red blood cell fragments, plasma proteins, and platelets can also be observed at the endothelial cell gaps, indicating the presence of hemorrhagic fistula disease. Yamashima et al. (1985) found that, in addition to red blood cells, the outer membrane of the hematoma contains a significant infiltration of eosinophils, which exhibit degranulation during cell division. The granular matrix contains plasminogen, which activates plasmin to promote fibrinolysis and inhibit platelet aggregation, thereby inducing chronic bleeding.
In children, chronic subdural hematomas are often bilateral and commonly caused by birth trauma, though intracranial injuries after birth are less frequent. The highest incidence occurs within the first six months of life and gradually decreases thereafter. However, trauma is not the sole cause; malnutrition, scurvy, intracranial or extracranial infections, children with hemorrhagic diathesis, and even severely dehydrated infants may also develop this condition. The bleeding is usually due to the rupture of bridging veins draining into the superior sagittal sinus. Non-traumatic subdural hematomas may result from systemic diseases or intracranial inflammation altering the permeability of subdural blood vessels.bubble_chart Pathological Changes
The pathogenesis of chronic subdural hematoma primarily involves: mass effect leading to intracranial hypertension, local brain compression, impaired cerebral circulation, brain atrophy and degeneration, with an epilepsy incidence as high as 40%. In long-standing hematomas, the membrane may calcify due to vascular thrombosis, necrosis, and connective tissue degeneration, resulting in prolonged compression of brain tissue, triggering epilepsy, and exacerbating neurological deficits. There have even been reports of recurrent hemorrhage due to rupture of the inner membrane, forming subcortical hematomas.
bubble_chart Clinical Manifestations
The main manifestations include chronic intracranial hypertension, neurological dysfunction, and psychiatric symptoms. Most patients experience headaches, lack of strength, cognitive decline, mild hemiparesis, and fundus edema, with occasional epileptic or apoplexy-like episodes. In the elderly, dementia, psychiatric abnormalities, and positive pyramidal signs are more common, often confused with intracranial tumors or normal-pressure hydrocephalus. Children frequently exhibit drowsiness, enlarged head size, bulging parietal bones, protruding fontanelles, spasms, convulsions, and retinal hemorrhage, closely resembling hydrocephalus. Bender classified the clinical manifestations of chronic subdural hematoma into four grades: Grade I: Clear consciousness, mild headaches, with or without Grade I neurological deficits; Grade II: Disorientation or confusion, accompanied by mild hemiparesis and other neurological deficits; Grade III: Stupor, appropriate response to painful stimuli, severe neurological dysfunction such as hemiplegia; Grade IV: Unconsciousness, no response to painful stimuli, decerebrate or decorticate posturing.
In such patients, the head injury is often minor, and the bleeding is slow. Additionally, the compensatory space in the cranial cavity of elderly individuals is relatively large, leading to an intermediate stage of remission lasting from a few weeks to several months, during which obvious symptoms may be absent. Later, when the hematoma enlarges and causes symptoms of brain compression and increased intracranial pressure, the patient may have already forgotten the history of head trauma or, due to existing psychiatric symptoms, dementia, or impaired comprehension, may be unable to provide a reliable medical history, making misdiagnosis likely. Therefore, when this condition is clinically suspected, auxiliary examinations should be performed as early as possible to confirm the diagnosis. In the past, methods such as cerebral ultrasonography, electroencephalography, isotopic brain scanning, or cerebral angiography were commonly used to assist in diagnosis. In recent years, the use of CT has further improved early diagnostic accuracy, allowing not only estimation of the hematoma's formation time based on its shape but also inference of its age based on density. Generally, the evolution from a crescent-shaped hematoma to a convex one takes about 3 to 8 weeks. The hematoma appears hyperdense at an average age of 3.7 days, hypodense at 6.3 days, and isodense by 8.2 days. However, for patients with no mass effect or bilateral chronic subdural hematomas, delayed scanning after contrast enhancement may be necessary to improve resolution. Additionally, MRI offers further advantages, providing clear image differentiation for hematomas or effusions that appear isodense on CT.
Currently, the treatment opinions for chronic subdural hematoma have largely reached a consensus. Once symptoms of increased intracranial pressure appear, surgical intervention should be performed, with burr hole drainage being the preferred method, yielding satisfactory results. If no other complications arise, the prognosis is generally favorable. Therefore, even for elderly or critically ill patients, every effort should be made to provide treatment, including bedside twist-drill drainage. With timely intervention, the condition can often be stabilized. The main existing issue is the postoperative recurrence rate of hematoma, which remains between 3.7% and 38% (Koga Hisanobu et al., 1983). 1. **Burr Hole or Twist-Drill Irrigation and Drainage**: Based on the location and size of the hematoma, two holes (one high and one low) are selected. Under local anesthesia, a burr hole or twist-drill hole is first made in the anterior portion. Upon entering the hematoma cavity, old blood and brownish fragmented clots will flow out. A silicone tube or No. 8 urinary catheter is then carefully inserted into the cavity, with the length not exceeding half the radius of the hematoma cavity, to further drain the liquid hematoma. Using the same method, another hole is made in the lower (posterior) portion for drainage, and a catheter is inserted. Subsequently, gentle and repeated irrigation with saline is performed through both catheters until the effluent becomes clear. After the procedure, the two drainage tubes are separately brought out through scalp puncture holes and connected to a sterile sealed drainage bag. The higher tube is for air evacuation, while the lower one is for fluid drainage, and both are removed after approximately 3–5 days. Recently, a simple twist-drill irrigation technique has been reported, where the procedure is performed directly at the bedside. Old blood is drained, and saline irrigation is repeated every 3–4 days until the effluent is clear, typically requiring 2–4 sessions. The procedure is continued under CT monitoring until brain compression is relieved and midline structures are restored. 2. **Subdural Puncture via the Anterior Fontanelle Lateral Angle**: For pediatric chronic subdural hematoma with an open anterior fontanelle, subdural puncture and aspiration of accumulated blood can be performed. A muscle needle with a short bevel is used, inserted at a 45-degree angle through the lateral corner of the anterior fontanelle toward the frontal or parietal subdural space. At a depth of 0.5–1.0 cm, brownish fluid can be aspirated, with each session limited to 15–20 ml. If bilateral hematomas are present, alternate punctures should be performed. The aspirated blood typically becomes lighter in color over time, and the hematoma volume decreases accordingly. If fresh blood is aspirated or the hematoma does not shrink, a craniotomy should be considered.
**Craniotomy for Chronic Subdural Hematoma Evacuation**
This method is suitable for chronic subdural hematomas with thickened membranes or calcification. The craniotomy procedure is as described earlier. After elevating the bone flap, a bluish-purple and thickened dura mater is visible. A small incision is made to slowly drain the accumulated blood. Once intracranial pressure is slightly reduced, the dura mater and the underlying outer hematoma membrane are incised in a flap-like manner and reflected together to minimize bleeding. The inner hematoma membrane is usually not adherent to the arachnoid membrane and can be easily separated and excised. However, excessive traction should be avoided to prevent tearing the junction between the inner and outer membranes, which is prone to bleeding. The membrane should be cut approximately 0.5 cm from the edge. After the procedure, hemostasis is ensured, and the dura mater and scalp layers are sutured in layers. A drainage tube is placed in the hematoma cavity for 3–5 days. For bilateral hematomas, staged and separate surgeries are recommended.
**Management of Postoperative Hematoma Recurrence**
Whether treated with burr hole irrigation and drainage or craniotomy, hematoma recurrence remains a concern. Common causes of recurrence include: brain atrophy in elderly patients, making postoperative brain re-expansion difficult; thick and tough hematoma membranes preventing closure of the subdural space; residual blood clots in the hematoma cavity; and fresh bleeding leading to recurrence. Preventive measures include maintaining a head-low position postoperatively, lying on the affected side, increasing fluid intake, avoiding strong dehydrating agents, and supplementing with hypotonic fluids if necessary. For cases with thick or calcified membranes, craniotomy and excision are recommended. If solid clots or fresh bleeding are present, a bone flap or window craniotomy should be performed for thorough evacuation. Postoperatively, the higher drainage tube is used for air evacuation, and the lower one for fluid drainage, both connected to a closed drainage system. Saline can also be injected via lumbar puncture or ventricular access. The absorption of residual fluid and air in the cavity and brain re-expansion may take 10–20 days, so dynamic CT monitoring is essential. If clinical symptoms improve significantly, even if subdural fluid persists, immediate reoperation is unnecessary.
It should be differentiated from the following diseases:
1. Chronic subdural hygroma: Also known as subdural hydroma, it is mostly related to trauma and is extremely similar to chronic subdural hematoma. Some authors even suggest that subdural hygroma is the cause of chronic hematoma (Yamada, 1980). The main differentiation relies on CT or MRI; otherwise, it is difficult to distinguish before surgery.
2. Cerebral hemisphere space-occupying lesions: In addition to hematomas, other space-occupying lesions such as brain tumors, brain abscesses, and granulomas can easily be confused with chronic subdural hematoma. The key differences lie in the absence of a history of head trauma and more obvious localized neurological deficits. Confirmation also requires CT, MRI, or cerebral angiography.
3. Normal pressure hydrocephalus and brain atrophy: These two conditions are similar to each other and also resemble chronic subdural hematoma, all presenting with cognitive decline and/or mental disorders. However, neither of these conditions shows signs of increased intracranial pressure, and imaging examinations reveal ventricular enlargement, widened cisterns, and brain parenchymal atrophy as characteristic features.
