Operative Neurosurgery

An acute subdural hematoma (SDH) is a rapidly clotting blood collection below the inner layer of the dura but external to the brain and arachnoid membrane.

Subdural hematomas may be mixed in nature, such as when acute bleeding has occurred into a chronic subdural hematoma.

Acute traumatic subdural hematoma

Acute spontaneous subdural hematoma

Delayed Acute Subdural Hematoma.

Infantile acute subdural hematoma.

Interhemispheric acute subdural hematoma.

Clinically evident or subclinical seizures are common manifestation in acute subdural hematoma (aSDH); however, there is a paucity of research investigating the relationship between seizures and aSDH.

Generally, acute subdural hematomas are less than 72 hours old and are hyperdense compared with the brain on computed tomography scans.

Hyperdense enhancing subdural effusion due to contrast extravasation has been recently described as a potential mimicker of acute subdural hematoma following a percutaneous coronary procedure.

Zamora and Lin report on 2 patients who presented with subarachnoid hemorrhage from ruptured cerebral aneurysms and who developed enhancing subdural effusions mimicking acute subdural hematomas after angiography and endovascular coil placement. In 1 case, the subdural effusions completely cleared but recurred after a second angiography. CT attenuation values higher than expected for blood, as well as the evolution of the effusions and density over time, allowed for differentiation of enhancing subdural effusions from acute subdural hematomas ¹⁾.

see Acute subdural hematoma treatment.

Acute subdural hematoma is a serious complication following traumatic brain injury. Large volume hematomas or those with underlying brain injury can cause mass effect, midline shift, and eventually herniation of the brain. Acute subdural hematomas in the young are associated with high-energy trauma and often have underlying contusions, while acute subdural hematomas in the elderly are associated with minor trauma and an absence of underlying contusions, even though the elderly are more likely to be on anticoagulants or anti-platelet therapy. In the young patients with high impact injuries the hematomas tend to be small and the underlying brain injury and swelling is responsible for the increased intracranial pressure and midline shift. In the elderly, the injuries are low impact (e.g fall from standing), the underlying brain is intact, and the volume of the hematoma itself produces symptoms. In addition the use of anticoagulants and antiplatelet agents in the elderly population has been thought to be a poor prognostic indicator and is considered to be responsible for larger hematomas and poor outcome. When managed conservatively, acute subdural hematomas can sometimes progress to chronic subdural hematoma formation, further enlargement, seizures, and progressive midline shift. Another potential difference in the young and the elderly is brain atrophy, which increases the potential space to accommodate a larger hematoma. It is not known if these two groups differ in other ways that might have implications for treatment or prognosis. In this paper, we investigate the clinical course of 80 patients admitted to our institution with acute subdural hematomas, to identify differences in patients above or below the age of 65 years. The natural progression/resolution of acute subdural hematomas was mapped by measuring volume expansion/regression over time. In this retrospective chart review, we investigated clinical baseline metrics and subsequent volumetric expansion outcomes between patients < 65 years old (N=44) and those > 65 years old (N=36). Volume was estimated by the ABC/2 method. We observed a statistically significant difference between groups in use of anticoagulants χ2 =40.305 with p < 0.001, corrective platelet administration χ2 =19.380 with p < 0.001, gender χ2 =14.573 with p < 0.001, and Glasgow Coma Scale with χ2 =23.125 (p=0.026). Overall outcomes were similar in the two groups. Younger patients on average had worse presenting GCS scores, but recovered comparable to older patients. No significant difference in rate of volume expansion, resolution time, or need for surgical treatment was seen between these two groups. We conclude that the initial volume, size, and severity of subdural hematoma determined by the Glasgow Coma Scale score is more likely to predict surgery or future expansion than age of the patient. Patients on oral anti-coagulants that are given appropriate medical reversal agents early do quite well and no impact on the eventual outcome could be demonstrated. Further work is needed to establish better predictors of future volume expansion, and progression to chronic subdural hematoma based on improved severity scales ²⁾.

Among traumatic brain injuries, acute subdural hematoma (aSDH) is considered one of the most devastating still retaining poor surgical outcomes in a considerable percentage of affected patients. However, according to results drawn from published samples of aSDH patients, overall mortality and functional recovery have been progressively ameliorating during the last decades.

The mortality rate is 40% to 60%.

Two further stages, subacute subdural hematoma and chronic subdural hematoma, may develop with untreated acute subdural hematoma (SDH).

Spontaneous rapid resolution of acute subdural hematoma developing secondary to trauma has been reported in the literature, yet it is very rare in pediatric population ³⁾.

ASDH in the elderly is a common and increasing problem, and differs in its pathophysiology from ASDH in younger people. Admitting doctors may have difficulty identifying those elderly patients whose lesions may benefit from surgery.

All patients aged 65 years or greater referred to Salford Royal Foundation Trust with the diagnosis of ASDH between 01/01/2008 and 31/12/2011.

The initial presenting CT brain scans were reviewed. The linear dimensions, degree of midline shift and hematoma volume (using ABC/2 method) of all scans were measured and recorded. All presenting radiology was also assessed by a consultant neurosurgeon blind to clinical and CT scan measurement data and patients were categorised as having “surgical” lesions or not. Receiver operating characteristic (ROC) curves were generated and cut point value for 100% sensitivity and specificity were tabled to assess which combination of scan parameters best predicted a “surgical” ASDH.

212/483 patients were considered to have a 'surgical' lesion. All 'surgical' lesions had a volume of >35ml (range 35-435), maximum thickness of ≥10mm (range 10-49) and 99% had midline shift ≥1mm (range 0-32). The best predictor of a 'surgical' lesion was a combination of maximum haematoma thickness and midline shift which offered 100% (95% CI 98.3-100) sensitivity with 83% (95% CI 77.6-87) specificity.

Surgically relevant cases of ASDH in the elderly can be reliably and objectively identified by two easily performed scan measurements, haematoma thickness and midline shift. If used in routine practice, these measurements could clarify those patients who may need urgent neurosurgical referral and might avoid unnecessary transfer to neurosurgical units in this cohort ⁴⁾.

Cerebral infarction following acute subdural hematoma.

Seizure following acute subdural hematoma.

see Acute subdural hematoma case series.

A 24-year-old female was admitted because of right sided partial seizure and acute or subacute subdural hematoma over the left cerebral convexity. She had no history of recent head trauma but performed headbanging at a punk rock concert at 3 days before admission. Since, she had a previous acute subdural hematoma on the same side after an accidental fall from a baby buggy when she was 11 months old, the present was recurrent subdural hematoma probably due to headbanging.

Headbanging has the hazardous potential to cause a subdural hematoma ⁵⁾.