Acute Subdural Hematoma

Our Specialists for Acute Subdural Hematoma

Acute subdural hematoma is one of the highest-stakes operations in neurosurgery, and outcomes depend on experienced trauma neurosurgeons who can move fast without cutting corners. At UChicago, these patients are managed by fellowship-trained neurotrauma specialists around the clock.

Paramita Das, M.D., M.S.

Director, Neurotrauma; Director, Neurosurgical Trauma Fellowship

Dr. Das is Director of Neurotrauma at UChicago's Level 1 Trauma Center and directs the Neurosurgical Trauma Fellowship, one of only a few dedicated neurosurgical trauma fellowships in the country. She manages both head trauma and acute spine pathology and has been named to the Bucksbaum-Siegler Institute for Clinical Excellence. She trained at the University of Minnesota for residency and completed a skull base fellowship at Cleveland Clinic. Dr. Das is the Director of Surgical Neurotrauma at UChicago and directs the Neurosurgical Trauma Fellowship, making her the senior surgeon most likely to take your acute SDH to the OR in the middle of the night. Her academic work focuses on outcomes after severe traumatic brain injury and biomarkers of injury severity.

P. B. Raksin, M.D.

Associate Program Director, Neurological Surgery Residency

Dr. Raksin is an Associate Professor of Neurological Surgery and serves as Associate Program Director of the UChicago Neurological Surgery residency program. She is a senior clinician within the department and contributes broadly to resident education and general neurosurgical care. Dr. Raksin brings decades of experience in emergency cranial trauma surgery, including large-flap craniotomies and decompressive craniectomies for acute subdural hematomas. If you arrive at UChicago with an operative acute SDH, she is one of the senior surgeons on the trauma rotation making the craniotomy-versus-craniectomy call in real time.

What Is an Acute Subdural Hematoma?

An acute subdural hematoma (SDH) is a collection of blood that forms between the brain and the dura, the tough leathery membrane that lines the inside of the skull. In the acute form, the blood is fresh — usually less than 72 hours old — and it comes from bridging veins or small arteries that tore when the head was struck with force.

Acute SDH is almost always caused by severe head trauma: a fall from height, a motor vehicle collision, an assault, or a high-impact sports injury. In older adults, especially those on blood thinners, even a ground-level fall can be enough. Because the skull is a closed box, a rapidly expanding clot pushes on the brain from the outside and can shift it off midline within minutes to hours.

What makes acute SDH so dangerous isn't just the clot itself — it's the underlying brain injury. The same force that tore the vein often bruised the brain beneath it (a contusion) and set off swelling that keeps building for days after the bleed stops. That's why two patients with the same size clot on CT can have very different outcomes.

Roughly 10-30% of patients with severe traumatic brain injury have an acute SDH, and historically the reported mortality has ranged from about 40% to 60% in comatose patients. Modern trauma systems, faster CT scanning, and protocol-driven surgery have improved these numbers, but acute SDH remains one of the most lethal injuries in neurosurgery.

What Does It Look Like?

Acute SDH almost always follows a clear-cut injury, but the symptoms can evolve over minutes to hours as the clot expands. A person may initially seem "okay" after the trauma and then deteriorate — the so-called lucid interval.

Early signs right after the injury

• Loss of consciousness at the time of impact
• Severe headache
• Confusion or not knowing where they are
• Nausea and vomiting
• Slurred speech

Signs that the clot is getting worse

• Increasing drowsiness or becoming harder to wake up
• One pupil becoming larger than the other (a "blown pupil")
• Weakness on one side of the body
• Seizures
• Slow heart rate with high blood pressure (a late sign of rising pressure in the skull)
• Unresponsiveness and abnormal posturing

Any of these warning signs after a head injury is a 911-level emergency. Get to the nearest trauma center as fast as possible.

How Is It Diagnosed?

Diagnosis of acute SDH happens in the emergency department and is usually fast — minutes, not hours.

Non-contrast head CT

The first and most important test is a non-contrast CT scan of the head. Acute blood shows up as a bright white, crescent-shaped collection that hugs the curve of the brain. The radiologist and neurosurgeon will measure two key numbers on that CT:

• Clot thickness — the maximum width of the blood collection
• Midline shift — how far the brain has been pushed from its normal center position

These numbers directly drive the decision to operate. Current surgical guidelines recommend evacuation of any acute SDH more than 10 mm thick or causing more than 5 mm of midline shift, regardless of the patient's GCS score. Smaller clots are also operated on urgently if the patient's exam is worsening, if the GCS drops by 2 or more points, if a pupil becomes unreactive, or if ICP is persistently above 20 mm Hg.

Neurologic exam and GCS

Alongside the scan, the team performs a focused neurologic exam. The Glasgow Coma Scale (GCS) — a 3 to 15 score based on eye opening, verbal response, and motor response — is a powerful prognostic marker. Pupil size and reactivity are checked repeatedly; a fixed and dilated pupil suggests the brain is being pushed into the tentorium (a process called uncal herniation) and turns the operation into a true race against the clock.

Whole-body trauma workup

Because acute SDH is almost always part of a severe polytrauma, the patient also gets a rapid trauma survey: cervical spine imaging, chest and abdominal CT, and labs including a coagulation panel. If they're on blood thinners, reversal agents are given immediately.

How Is It Treated?

Resuscitation comes first

Before any operation, the trauma team stabilizes the airway, breathing, and circulation. A comatose patient is intubated. Blood pressure is kept up to preserve brain perfusion. If the patient is on warfarin, a direct oral anticoagulant, or antiplatelet drugs, reversal is started immediately — prothrombin complex concentrate, platelets, or specific antidotes depending on the drug. Seizure prophylaxis is given.

Emergency craniotomy

The standard operation for an acute SDH that meets surgical criteria is a large trauma craniotomy. The surgeon makes a big curved incision behind the hairline, removes a sizeable piece of bone (the bone flap), opens the dura, and evacuates the clot. The source of bleeding is identified and controlled, and the dura is closed. The bone flap is replaced and secured with small plates and screws.

The goal is not only to remove the clot but to stop the pressure from pushing the brain off midline. Every minute matters: the landmark Seelig study from 1981 showed that comatose patients operated on within 4 hours of injury had dramatically lower mortality (30%) than those operated on later (90%), and although modern systems have tempered those numbers, early decompression is still the single most actionable factor in outcome.

Decompressive craniectomy

In a decompressive craniectomy, the bone flap is removed and left off at the end of the case. The dura is opened widely and closed with a patch that gives the swollen brain room to expand outward instead of being crushed against the skull. The patient wears a helmet until the bone is replaced in a second operation (cranioplasty) weeks to months later.

Historically, surgeons reached for a craniectomy whenever the brain looked "tight" or swollen at the time of surgery. The RESCUE-ASDH trial, published in the New England Journal of Medicine in 2023, randomized 450 adults undergoing surgery for acute SDH to craniotomy vs. decompressive craniectomy. At 12 months, disability and quality-of-life outcomes were similar between the two approaches. Craniectomy patients had fewer follow-on operations to control pressure but more wound complications. The takeaway: both operations are reasonable, and the choice comes down to surgeon judgment, brain swelling at the time of surgery, and whether the bone can be safely replaced.

ICP monitoring and neurocritical care

After surgery, patients go to the neuro-ICU, usually with an intracranial pressure (ICP) monitor — a thin probe placed in the brain that gives continuous pressure readings. The Brain Trauma Foundation guidelines recommend monitoring ICP in patients with severe TBI and an abnormal CT. When ICP rises, the team escalates through a tiered protocol: head-of-bed elevation, sedation, osmotic therapy (hypertonic saline or mannitol), CSF drainage, controlled hyperventilation, cooling, and, if refractory, a second decompressive craniectomy (the RESCUEicp protocol).

Rehabilitation

Recovery from acute SDH is measured in months, not days. Patients typically move from the ICU to a neurosurgical floor, then to an inpatient rehabilitation hospital for physical, occupational, and speech therapy. Ongoing follow-up includes cognitive assessment, seizure monitoring, and eventual cranioplasty for those who had a craniectomy.

What Are the Outcomes?

Outcomes after acute SDH are driven by a handful of factors that are set before the patient ever reaches the operating room: age, GCS at presentation, pupillary response, and the presence of underlying brain injury. How quickly the clot is removed and how well the ICU team controls swelling afterward are the things that can still be influenced.

Mortality by GCS and age

Across modern cohorts, mortality after surgical acute SDH ranges widely depending on who is being operated on. The Austrian multicenter study by Leitgeb and colleagues, which followed severe TBI patients with acute SDH, gives a useful picture:

These ranges come from surgical series — patients who were deemed candidates for operation. Adding fixed/dilated pupils, significant underlying contusion, or pre-injury anticoagulation pushes mortality substantially higher within each GCS band.

Functional outcomes

Mortality is only part of the story. Among survivors, many have meaningful recoveries — returning home, regaining independence, and in some cases returning to work. Younger patients and those with higher admission GCS generally do best. In the RESCUE-ASDH trial, at 12 months, roughly 30-40% of surgical patients achieved "upper good recovery" or "lower good recovery" on the extended Glasgow Outcome Scale, while about 30% had died and the remainder fell into the severely or moderately disabled range.

Decompressive craniectomy vs. craniotomy

For years it was unclear whether more aggressive surgery — taking the bone off and leaving it off — improved outcomes for acute SDH. RESCUE-ASDH answered this prospectively. Among 450 patients randomized to craniotomy or decompressive craniectomy:

• 12-month mortality was 30.2% in the craniotomy group vs. 32.2% in the craniectomy group (no significant difference)
• Disability and quality of life at 12 months were similar between groups
• Additional cranial surgery within 2 weeks was needed in 14.6% of craniotomy patients vs. 6.9% of craniectomy patients
• Wound complications occurred in 3.9% of craniotomy patients vs. 12.2% of craniectomy patients

The observational CENTER-TBI cohort reached a similar conclusion: centers that favored decompressive craniectomy did not achieve better functional outcomes than centers that favored craniotomy. In other words, both operations work — what matters is that an experienced trauma neurosurgeon is making a fast, judgment-driven call in the OR based on what the brain is doing at the moment of decompression.

That judgment is the single biggest reason the identity of the surgical team matters. Acute SDH is one of the operations where having a fellowship-trained neurotrauma surgeon in the room changes what is possible.

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