Contralateral subdural effusion related to decompressive craniectomy performed in patients with severe traumatic brain injury
Section snippets
Patients and methods
From 2004 to 2008, 123 patients, 18 years of age or older, were retrospectively identified as having undergone DC for refractory IICP with or without removal of a blood clot or contused brain after severe TBI at E-Da Hospital (Kaohsiung, Taiwan).
All patients were admitted to intensive care unit (ICU) and managed according to a protocol that was consistent with the international guidelines for severe TBI.14 Severe TBI was defined as a Glasgow Coma Scale (GCS) score of 8 or less following
Results
All the nine patients were male with an age of 41 ± 13 years (mean ± SD) (range, 28–63 years). The injury mechanism was a motor vehicle accident (MVA) in six and a fall in three patients. The time interval from DC to contralateral subdural effusion was 23 ± 11 days (mean ± SD) (range, 8–39 days).
The clinical manifestations of contralateral subdural effusion were deterioration of consciousness, pupil dilation, muscle power weakness, headache and IICP. The average midline shift on CT scan of these
Illustrative case report
A 29-year-old man was brought to the emergency department of E-Da Hospital because he was a victim of an MVA. On arrival, he was in a deep coma (GCS 4), and his left pupil was dilated and not reactive to light. The initial brain CT scan revealed acute subdural haematoma and contusion haemorrhage in the left fronto-temporo-parietal region, with midline structures deviating to the right (Fig. 1). Emergency left fronto-temporo-parietal decompressive craniectomy and evacuation of the subdural
Discussion
Several possible mechanisms could be responsible for the development of contralateral subdural effusions. Rapid reduction in intracranial pressure as well as outward herniation after decompression may incite a pressure gradient between the two hemispheres and lead to the enlargement of the contralateral subdural space and the accumulation of effusion, especially when, initially, there is a possible rupture in the arachnoid layer after head trauma.12, 13, 16 Rupture of the arachnoid layer
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Cited by (15)
Effects of Cranioplasty on Contralateral Subdural Effusion After Decompressive Craniectomy: A Literature Review
2022, World NeurosurgeryCitation Excerpt :Contralateral subdural effusion (CSE) is defined as a new subdural effusion (SE) on the opposite side of the decompressive craniectomy (DC) and has the same computed tomography density as cerebrospinal fluid (CSF).1,2 Cases diagnosed with CSE after decompressive craniectomy (CSEDC) are rarely reported.3-5 Although many theories have been proposed to explain the development of CSE, the pathogenesis by which it develops remains somewhat obscure.
Contralateral subdural effusion after decompressive craniectomy: What is the optimal treatment?
2021, Clinical Neurology and NeurosurgeryCitation Excerpt :The best treatment of CSEDC has yet to be determined. Currently, treatment options include: conservative treatment, compression bandaging, burr hole drainage, Ommaya catheter drainage, subdural-peritoneal shunting, ventriculo-peritoneal shunting, lumbo-peritoneal shunting, cranioplasty, and combination of them [1–6,10–13,16,18]. Conservative treatment is recommended when the CSEDC does not cause clinical deterioration and without significant mass effect on CT scan.
Factors involved in the development of subdural hygroma after decompressive craniectomy for traumatic brain injury. A systematic review and meta-analysis
2020, Journal of Clinical NeuroscienceCitation Excerpt :This data might be related to an adjunctive brain damage due to the compression by SDG [15]. Thus it is crucial to rapidly recognize and treat this condition [15]. Our study has some limitations including the limited literature on SDG.