Also known as traumatic subdural hydroma, it occurs when the brain tissue moves violently within the cranial cavity during a craniocerebral injury, causing the arachnoid membrane to tear. Cerebrospinal fluid then flows through the rupture into the subdural space between the dura mater and arachnoid membrane, accumulating there. The incidence rate is 1.16% of craniocerebral injuries, accounting for approximately 10% of traumatic intracranial hematomas.

bubble_chart Pathogenesis

The mechanism is due to the perforation in the arachnoid membrane acting like a one-way valve, allowing cerebrospinal fluid to continuously flow out during the patient's straining, breath-holding, coughing, or other forceful actions, but preventing it from returning to the subarachnoid space. This eventually leads to the formation of a hygroma-like fluid accumulation in the subdural space, resulting in local brain compression and progressive intracranial hypertension.

bubble_chart Clinical Manifestations

The clinical manifestations of subdural fluid accumulation closely resemble those of subdural hematoma, also categorized into acute, subacute, and chronic forms, making preoperative differentiation difficult. Its clinical features include mild or moderate closed head injury, often with relatively minor primary brain injury, followed by progressively worsening headaches, vomiting, and signs of increased intracranial pressure such as papilledema. The disease course is mostly subacute or chronic, occasionally presenting acutely. In severe cases, it may lead to uncal herniation, with approximately 30.4% of patients exhibiting unilateral pupillary dilation, and about half showing progressive deterioration of consciousness and positive pyramidal signs. The volume of subdural fluid typically ranges from 50 to 60 ml, but can reach up to 150 ml in some cases. In terms of characteristics, acute cases often present with bloody cerebrospinal fluid, which later turns into clear yellow fluid with slightly elevated protein content.

The definitive diagnosis of this disease relies on special examinations, such as CT or MRI. Sometimes, even with CT scans, it may be confused with isodense or hypodense subdural hematomas. However, on MRI images, the signal of the effusion is similar to that of cerebrospinal fluid, while the signal of the hematoma is stronger. Especially in T₂-weighted images, hematomas consistently show high-intensity signals, which can aid in differentiation.

bubble_chart Treatment Measures

The treatment of fluid accumulation generally involves burr hole drainage, where a drainage tube is placed at the lowest point of the fluid cavity and connected to an external closed drainage bag (or bottle) to prevent pneumocephalus. Within 48–72 hours post-surgery, once the fluid cavity has significantly reduced but before cerebral edema has fully subsided, the drainage tube is removed to prevent recurrence. For chronic fluid accumulation, strong dehydrating agents may be minimized or avoided postoperatively to allow the brain tissue to expand and better close the fluid cavity. The patient should lie flat or in a head-down position on the affected side to promote brain tissue repositioning. If necessary, 20–40 ml of saline can be slowly injected via lumbar puncture to aid in closing the residual cavity. For a few recurrent cases that are difficult to cure, craniotomy with bone flap or bone window may be performed to remove the fluid, widely incise the thickened cyst wall to communicate with the subarachnoid space, or place a tube to connect the fluid-filled cyst with the basal cisterns. If needed, the bone flap can be removed to allow scalp collapse and reduce the residual cavity. Postoperatively, saline or filtered air can be injected via lumbar puncture to increase intracranial pressure, or intravenous fluid intake can be increased, or blood pressure can be appropriately elevated. Additionally, calcium channel blockers may be administered to reduce cerebrovascular resistance, thereby improving cerebral perfusion and promoting brain expansion.

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Patients with subdural fluid accumulation generally have milder primary brain injuries. If treated promptly and appropriately, the outcomes are usually favorable. However, if the primary brain injury is severe and/or accompanied by intracranial hematoma, the prognosis is poorer, with a mortality rate ranging from 9.7% to 12.5%.