Subdural Hematoma (SDH) — Treatment, ICU Care, and Prognosis

Most families only need the Quick Summary + the First 72 Hours section. Everything else is for deeper understanding.

What Is a Subdural Hematoma (SDH)?

A subdural hematoma is a collection of blood between the dura mater (the brain’s tough protective covering) and the brain surface. The bleeding most often comes from tearing of bridging veins, especially during acceleration–deceleration injuries (falls, car crashes). Sometimes small cortical arteries contribute as well.

The key clinical problem is not “blood itself” — it is pressure:

• SDH can compress the brain, causing midline shift and brainstem compression.
• SDH is frequently accompanied by brain bruising (contusions), DAI and brain swelling, which can further raise intracranial pressure and worsen prognosis.

Image: Presentation of subdural hematoma (SDH) and other types of lesions that may co-occur within Traumatic brain injury (TBI).

Image: Main parts of the brain: the four lobes (frontal, parietal, temporal, and occipital), the cerebellum, and the brainstem.

Mechanism of Injury and External Signs
Acute SDH is most commonly associated with acceleration–deceleration forces (motor vehicle accidents, falls, assaults). Rarely, SDH may arise from impact-dominant mechanisms resembling EDH. These cases may show a short lucid interval and a relatively more favorable course compared with SDH caused by rotational or inertial forces.

SDH Often Comes With Other Lesions (What Changes Prognosis)

An SDH is frequently not “isolated.” Prognosis often depends on what comes with it, such as:

• Brain contusions (which can worsen over 48–72 hours)
• Diffuse axonal injury (DAI) (a common reason for prolonged coma)
• Traumatic subarachnoid hemorrhage (tSAH)
• Intraparenchymal hematoma (traumatic ICH)
• Diffuse brain edema
• Skull fractures
• Intraventricular hemorrhage (IVH) and possible hydrocephalus

In some patients, SDH may also coexist with an epidural hematoma (EDH), reflecting a more complex injury mechanism.

These traumatic lesions are covered on the Traumatic Brain Injury page.

Acute vs Chronic SDH (Key Differences Families Should Know)

Acute Subdural Hematoma (ASDH)

• Happens immediately after trauma (hours to days).
• Blood is usually clotted and spreads over a larger area.
• Often linked to more severe trauma and additional brain damage (contusions, DAI, edema).
• Can cause rapid deterioration and often requires urgent surgery.

Chronic Subdural Hematoma (CSDH)

• Develops over days to weeks, often after minor or forgotten trauma.
• Common in older adults, people with brain atrophy, and patients on anticoagulants/antiplatelets.
• The collection becomes liquefied inside a capsule and slowly enlarges.
• Symptoms are often subtle at first: headache, confusion, imbalance, mild weakness.
• Treatment is often simpler (burr holes with drainage) and prognosis is usually better than severe ASDH.

Clinical Assessment of the Patient With Subdural Hematoma (SDH)

The initial clinical assessment in patients with suspected subdural hematoma (SDH) is a time-critical step performed before CT imaging, in both conscious and unconscious patients. Its goal is to assess the level of consciousness, detect signs of brain compression or herniation, stabilize vital functions, and determine the urgency of imaging and neurosurgical treatment.

The patient is examined for:

• scalp lacerations or bruising,
• skull deformities suggesting fracture,
• bleeding or clear fluid leakage from the nose or ears (possible CSF leak),
• signs of previous head trauma in chronic SDH.

Even subtle external findings can indicate a high-energy mechanism and raise suspicion for associated deep brain injury.

In SDH, clinical findings must always be interpreted together with imaging, because the patient’s neurological status may reflect mass effect, sedation, alcohol or medication effects, systemic instability, or deep brain injury — not just the size of the hematoma itself.

Systemic Stabilization and Associated Injuries
Before neurological findings can be reliably interpreted, basic life functions must be stabilized. Hypoxia (low oxygen levels) and hypotension (low blood pressure) significantly worsen secondary brain injury and are independent predictors of poor outcome in SDH.

The medical team rapidly evaluates and manages:

• airway and breathing (often requiring intubation),
• circulation and blood pressure,
• possible injuries to the cervical spine, chest, abdomen, and long bones.

In many severe SDH cases, neurological assessment evolves over time as systemic instability is corrected.

Level of Consciousness — Glasgow Coma Scale (GCS)
The Glasgow Coma Scale (GCS) remains the standard tool for assessing consciousness in SDH patients. Scores range from 3 (deep coma) to 15 (fully awake).

However, in SDH it is critical to understand that:

• a low GCS may result from mass effect and brain compression,
• but also from sedation, alcohol, drugs, shock, or hypoxia,
• and from diffuse axonal injury (DAI), which may not be visible on early CT.

Therefore, GCS is considered a reliable prognostic indicator only after reversible causes of impaired consciousness have been corrected (sedation, alcohol, drugs, shock, or hypoxia).

Neurological Examination (Pupils and Focal Deficits)
The neurological exam focuses on signs of pressure and lateralization, including:

• pupil size and symmetry (anisocoria or unequal pupils may indicate herniation),
• reaction of pupils to light,
• motor asymmetry (weakness on one side),
• abnormal posturing or loss of brainstem reflexes in severe cases (unusual, rigid body positions or a lack of automatic reactions like blinking and coughing)..

In SDH, pupil changes often reflect acute mass effect and may require immediate surgical action.

Diagnosis of Subdural Hematoma (Imaging Strategy)

CT Scan — The Gold Standard in SDH

Non-contrast brain CT is the first-line and most important diagnostic tool in suspected SDH. It is fast, widely available, and directly guides life-saving decisions.

CT allows assessment of:

• the presence, thickness, and extent of the subdural blood collection,
• whether the hematoma appears acute or chronic based on its density,
• its compressive effect on the brain — including midline shift and signs of increased pressure (such as compressed basal cisterns),
• associated brain injuries (contusions, traumatic subarachnoid hemorrhage, intracerebral or intraventricular bleeding),
• skull fractures.

In acute SDH, CT findings often determine whether urgent surgery is required, sometimes even before clinical deterioration occurs.

Image: Brain CT scans showing SDH and other types of traumatic lesions. On a CT scan, blood usually appears white (hyperdensity).

MRI — Role in Selected SDH Cases

MRI is not a first-line tool in acute unstable patients, but it plays an important role in selected situations:

• prolonged coma unexplained by CT findings,
• suspicion of diffuse axonal injury (DAI),
• detection of ischemic lesions or microhemorrhages not visible on CT.

MRI often explains why a patient does not awaken despite apparently adequate decompression of the SDH.

Importance of Follow-Up Imaging in ICU Patients With SDH

In ICU-treated SDH patients, serial imaging is mandatory. Brain dynamics change rapidly in the first days.

Repeat CT is commonly performed to:

• detect expansion of residual SDH,
• identify new bleeding,
• monitor evolving contusions and edema,
• assess ventricular size and possible hydrocephalus.

Any neurological deterioration, new pupil asymmetry, or unexplained rise in intracranial pressure warrants immediate repeat imaging, regardless of the timing of the last scan.

How Severe Is This SDH? (GCS, Pupils, CT, Midline Shift)

Families often ask: “If the hematoma was removed, why isn’t the patient waking up?”
To understand severity, doctors combine clinical status and CT findings.

Clinical severity (GCS)

The Glasgow Coma Scale (GCS) ranges from 3 to 15:

• 13–15: mild injury (often awake; SDH may still be dangerous if it compresses the brain)
• 9–12: moderate injury (sleepy, confused, slow responses)
• 3–8: severe injury (coma; usually ICU and often ventilator)

Important nuance in SDH:

• A low GCS can be due to mass effect (pressure), but also due to deep brain injury or sedation.
• Prognosis depends on the reason for low responsiveness, not only the number.

Pupils and brainstem warning signs

Pupil findings can be critical:

• One pupil larger (anisocoria) can signal herniation risk from pressure.
• Abnormal brainstem reflexes raise concern for deep injury or critical swelling.

In SDH, the overall pattern often predicts prognosis better than any single measurement.

When Is Surgery Needed for SDH?

Surgery is considered when SDH is compressive or is expected to become compressive quickly.

Doctors typically operate when there is:

• Significant mass effect (pressure), especially with midline shift
• Clinical deterioration (worsening consciousness, focal deficit, pupil changes)
• A large acute SDH even before deterioration if CT predicts high risk
• Failure of conservative monitoring (worsening CT or worsening exam)

Some SDHs can be managed without surgery when:

• The collection is small, not compressive, and the patient is stable
• Serial exams and follow-up CT show no progression

The key concept for families: in SDH, timing is often lifesaving — surgery is sometimes done to prevent further brain injury from brain herniation, not only to “make the patient wake up immediately.”

In real clinical practice, decisions about surgery are not always identical between neurosurgeons. The same CT scan may be interpreted slightly differently depending on experience, associated injuries, and the expected evolution of brain swelling. This does not mean that one decision is wrong, but that SDH management often involves time-critical judgment where more than one approach may be medically reasonable.

Image: Brain Herniations — An extradural hematoma creates a mass effect, pushing parts of the brain into narrow spaces where they normally do not belong. In these tight areas, the pressure can compromise vital parts of the brain, including the brainstem, which controls breathing and consciousness. Among the different types of herniation, transtentorial (uncal) herniation is the most clinically significant pattern because it is the one most often associated with sudden deterioration.

SDH Surgery Options (Craniotomy vs Decompressive Surgery)

Craniotomy (most common for acute SDH)

A bone flap is opened, the clot is removed, bleeding is controlled, and the bone is usually replaced.

Decompressive craniectomy (selected severe cases)

Sometimes the bone flap is not replaced immediately because severe swelling is expected. This gives the brain room to expand outward instead of compressing the brainstem. The bone flap is stored in a bone bank or under the skin of the patient’s abdomen. Once the patient has stabilized, it is surgically reattached. A decompressive craniectomy may be performed in 15–30% of acute SDH surgeries.

ICP monitor placement, and/or EVD (external ventricular drain) in SDH

ICP monitoring and/or placement of an external ventricular drain (EVD) may be used to monitor and reduce intracranial pressure and to drain cerebrospinal fluid when indicated.

Typical indications include:

• severe traumatic brain lesions with markedly impaired level of consciousness
  (Glasgow Coma Scale 8 or lower),
• acute hydrocephalus caused by intraventricular blood,
• massive intraventricular hemorrhage with impaired or obstructed cerebrospinal fluid circulation,
• the need for deep sedation and mechanical ventilation in patients with traumatic brain lesions on CT that demonstrate extensive mass effect or are at high risk of secondary intracranial pressure elevation.

In clinical practice, the decision to place an ICP monitor or EVD is individualized. It is influenced by the patient’s overall condition, the pattern and evolution of injury, the treating neurosurgeon’s judgment, and the resources and protocols of the treating ICU.

In a small number of highly specialized neurotrauma centers, additional monitoring techniques may be used alongside ICP measurement. These can include brain tissue oxygen monitoring, which measures oxygen levels in brain tissue near the injured area. This type of monitoring is not routine, is available only in selected centers, and is mainly used in complex cases to fine-tune intensive care management.

In many severe SDH cases, surgery is not a single step but part of an ongoing treatment process that includes ICU monitoring, control of brain swelling, and prevention of secondary complications.

Image: Surgical opening of the skull (craniotomy) for removal of hematoma

Why Some Patients Don’t Wake Up After SDH Surgery

This is the most common family question — and the answer is often not one single reason.

1) Sedation and ventilator management can mimic coma

A patient can look “comatose” because medications suppress outward responses. This is especially common in the first 24–72 hours when the ICU team prioritizes stable breathing and ICP control.

2) Diffuse axonal injury (DAI)

DAI is microscopic shearing of nerve fibers caused by rotational forces. These rotational forces typically occur in high-speed traffic accidents, falls from height, assaults, or any injury where the head is suddenly twisted rather than struck straight on. CT can look “not dramatic,” yet coma can be prolonged. Brainstem involvement (severe DAI) is particularly important.

3) Brain swelling and secondary ischemia

Even after the SDH clot is removed, edema can rise for days. Swelling can reduce blood flow and create secondary, stroke-like injury.

4) Residual compression, rebleeding, or expanding contusions

Early repeat CT is often done because:

• residual SDH can remain,
• a new bleed can occur,
• contusions can enlarge during the first 48–72 hours.

5) Hydrocephalus (less common in pure SDH, but possible)

Blood and swelling can disrupt CSF flow, especially when IVH or significant tSAH is present.

6) Systemic problems that damage the brain secondarily

Hypoxia, hypotension, sepsis, severe metabolic imbalance, pulmonary embolism, or organ failure can worsen brain recovery even if surgery was technically perfect.

A key message for families:
Not waking up immediately does not automatically mean “surgery failed.” In SDH, early ICU physiology often determines what the brain can recover.

ICP and Brain Swelling After SDH (ICU Monitoring Explained Simply)

ICP (intracranial pressure) is the pressure inside the skull. High ICP is dangerous because it compresses brain tissue and reduces blood flow.

In SDH patients in ICU, the goals are:

• Maintain oxygenation and blood pressure to protect brain perfusion
• Control swelling and avoid pressure spikes
• Detect deterioration early (neuro exam + monitoring + repeat imaging)

Common measures include:

• Head positioning: The patient’s head is elevated to promote venous drainage and reduce pressure within the skull.
• Sedation and analgesia: Sedation limits agitation, coughing, and blood pressure surges that can worsen ICP and increase the risk of postoperative bleeding.
• Osmotherapy (Mannitol/Saline): Acting like a „chemical sponge,“ these IV fluids draw excess water out of the swollen brain to reduce internal pressure.
• Ventilation management: By precisely adjusting the ventilator (breathing machine), doctors can temporarily shrink the brain’s blood vessels to create more space during pressure emergencies.
• Seizure prevention: Antiepileptic medications are commonly administered during the first 7 days, as seizures are more frequent after SDH and can markedly increase intracranial pressure.
• If needed: ICP monitor and/or EVD (external ventricular drain)
• If swelling is refractory: decompressive craniectomy may be considered

Important note for families:
ICP treatment is not just “numbers.” The ICU team balances ICP with blood pressure to maintain CPP (cerebral perfusion pressure) — the pressure that actually drives blood through the brain.

Image: External ventricular drain (EVD) with ICP monitor

What to Expect in the First 72 Hours After SDH Surgery (Day-by-Day ICU Pattern)

The first 72 hours after acute SDH surgery are often the most unstable. This period is dominated by swelling dynamics, sedation effects, and systemic risks.

Day 0–1 (first 24 hours)

What families commonly see:

• Patient often remains on a ventilator and deeply sedated
• Neurological exam may be limited or intentionally suppressed
• Repeat CT may be done early to confirm decompression and rule out rebleeding
• ICP may fluctuate; the ICU team focuses on stabilization, not “wake-up tests” every hour

What matters most:

• Stable oxygenation and blood pressure
• No signs of herniation (pupils, CT, ICP)
• Early detection of any expanding contusion or residual mass effect

Day 1–2 (24–48 hours)

This is the phase when:

• Brain swelling can increase
• Contusions may enlarge
• Sedation strategy may be adjusted (sometimes briefly lowered for assessment if safe)

What families might misinterpret:

• Lack of eye opening or lack of command following can still be expected
• Motor responses can fluctuate because of sedation, fever, electrolytes, or swelling changes

Day 2–3 (48–72 hours)

This is often the turning point:

• If swelling stabilizes, the ICU team may begin gradual reduction of sedation
• Some patients show subtle improvements (more purposeful movement, better reflexes)
• Others remain unresponsive due to DAI or ongoing edema — which can still evolve over days

What matters most:

• Trend over time: exam + ICP + imaging + systemic status
• Prevention of complications (pneumonia, clots, sepsis), because these can ruin neurological recovery

Bottom line:
In severe SDH, early ICU changes are often slow and non-linear. Families should focus on trends and on whether the brain is protected from secondary injury.

Preventing Systemic Complications in ICU (Pneumonia, Sepsis, Clots, GI Bleeding)

Many late deteriorations in severe neurotrauma occur not from “the SDH itself,” but from systemic complications that secondarily injure the brain.

Key risks include:

• Ventilator-associated pneumonia
• Sepsis and multiorgan failure
• Pulmonary embolism and deep vein thrombosis
• GI bleeding (stress ulcers)
• Electrolyte disturbances, glucose instability
• Pressure sores, constipation, urinary infections

These complications directly worsen brain recovery by causing:

• hypoxia (low oxygen),
• hypotension (low blood pressure),
• inflammation and metabolic stress.

Families often underestimate how central this is. In SDH ICU care, preventing systemic complications is a core neurological strategy.

Early Prognosis in Coma (What Matters Most in SDH)

Prognosis in severe SDH is shaped by:

• preoperative status (especially GCS and pupils),
• CT pattern (midline shift, cisterns, edema, contusions),
• presence of DAI,
• the patient’s age and baseline brain reserve,
• and systemic complications in ICU.

Typical stepwise recovery pattern (when recovery happens)

In patients who improve from deep coma, recovery often follows stages:

1. stabilization of basic brainstem and vital functions
2. defensive limb movements (withdrawal)
3. eye opening and sleep–wake cycles (not always equal to awareness)
4. purposeful movements, following commands
5. speech and higher cognitive recovery

This process can take days to weeks (sometimes longer), and the pace varies greatly.

A crucial nuance:
Eye opening alone can represent wakefulness without awareness (unresponsive wakefulness/vegetative state). After sedation is withdrawn, most patients open their eyes within days to weeks (often around two weeks), but eye opening alone does not mean regained awareness and may represent wakefulness without awareness (unresponsive wakefulness/vegetative state). Families need clear explanations of what is meaningful and what is not.

In the most severe cases, these injuries can lead to irreversible brainstem failure, which is the key clinical criterion used to diagnose brain death. A clear explanation of what brain death means and how it is clinically confirmed is provided here.

Recovery and Long-Term Prognosis After SDH

What improves most in the first months

Many neurological gains (mobility, attention, speech) occur in the first 3–6 months, but improvement can continue longer with rehabilitation.

Long-term issues after severe SDH

Depending on associated lesions and ICU course, patients may face:

• cognitive and behavioral changes
• motor weakness, balance problems
• post-traumatic epilepsy
• post-traumatic hydrocephalus (in selected cases)
• mood disorders and fatigue
• long-term dependency in daily activities

Levels of recovery (simple framework)

• Good recovery: independent life, possibly minor deficits
• Moderate disability: independent at home, but reduced work capacity
• Severe disability: needs daily assistance
• No meaningful awareness: wakefulness without awareness may persist in some severe cases

Despite modern neurosurgical and ICU care, reported mortality for severe acute subdural hematoma (SDH) remains high, typically ranging from 30–60%, largely driven by the extent of associated brain injury, age, and early systemic complications. Across modern neurotrauma series, approximately 30–50% of survivors of severe acute SDH are left with moderate to severe long-term disability, while a smaller subset (roughly 10–20%) may remain permanently dependent or without meaningful awareness, depending on age, associated brain injury, and ICU course.

SDH in Older Adults and Patients on Blood Thinners

This section matters because SDH is very common in older adults.

Key points:

• Brain atrophy creates more “space,” allowing veins to stretch and tear more easily
• Even minor falls can cause chronic SDH weeks later
• Anticoagulants and antiplatelets can increase bleeding risk and recurrence risk

Since very often these are caused by minor trauma, there are usually no associated brain injuries, and patients typically regain consciousness shortly after the incident. Often, the hematoma does not cause significant pressure and does not require immediate surgery. However, it must be monitored closely because it can develop into a chronic SDH, which can grow over time, put pressure on the brain, and eventually require surgery.

Medico-Legal Questions (When Families Seek a Second Opinion)

During SDH treatment, families often wonder:

• Was surgery indicated and done at the right time?
• Was the ICU plan complete (ICP strategy, repeat imaging, seizure prevention, DVT prevention)?
• Were systemic complications recognized early enough?

If these doubts remain unresolved, they can become long-term sources of distress and sometimes medicolegal disputes. An independent second opinion can clarify whether the care followed standard neurocritical principles and whether any additional steps should be considered.

Glossary — Key Terms (GCS, ICP, EVD, Midline Shift…)

GCS (Glasgow Coma Scale): Scale from 3 to 15 that measures responsiveness (eyes, speech, movement).
ICP (Intracranial Pressure): Pressure inside the skull; high ICP can cause secondary brain injury.
CPP (Cerebral Perfusion Pressure): Pressure driving blood through the brain; depends on blood pressure and ICP.
EVD (External Ventricular Drain): A tube placed into a brain ventricle to drain CSF and monitor ICP.
ICP Monitor: A sensor placed to continuously measure ICP.
Midline Shift: Displacement of brain structures due to pressure; larger shift usually means higher risk.
Mass Effect: Pressure on brain tissue from blood or swelling.
DAI (Diffuse Axonal Injury): Microscopic shearing injury; common cause of prolonged coma.
Herniation: Life-threatening shift of brain tissue that compresses the brainstem.
Sedation: Medications used to reduce agitation, pain, and ICP spikes; can mimic coma.

For more detailed explanations of these terms, visit our Neurosurgery Terms: Patient-Friendly Guides page.

Emergency Red Flags

After head injury or during recovery, urgent in-person evaluation is needed if any of these occur:

• sudden loss of consciousness or worsening responsiveness
• repeated vomiting or rapidly worsening headache
• one pupil larger than the other
• new weakness, numbness, speech difficulty, or seizures
• severe confusion, agitation, unusual behavior
• clear fluid leaking from nose/ear (possible CSF leak)

Additional resources on neurotrauma

Traumatic Brain Injury — TBI

Surgical treatment of brain injuries

Consequences of brain injuries