Acute and chronic subdural haematoma

01Core principlesThe concepts and mechanisms needed to understand the subject.

Subdural blood lies between dura and arachnoid. In acute traumatic SDH, high-energy acceleration, deceleration or impact tears bridging veins or cortical vessels and often injures brain directly. The collection spreads along the convexity, producing a crescentic CT appearance that may cross sutures but is constrained by the falx and tentorium. Outcome depends on both the clot and associated contusion, oedema, hypoxia and hypotension, so removing the haematoma cannot reverse every component of injury.

Chronic SDH is a different biological process. After minor or unremembered trauma, a collection becomes enclosed by membranes with fragile neovasculature, inflammation, fibrinolysis and recurrent microbleeding. Cerebral atrophy creates a larger subdural space, helping explain the association with older age, frailty, alcohol excess and antithrombotic use. Symptoms evolve over days to weeks and may mimic stroke, dementia or delirium. Bilateral disease can compress the brain without producing a dramatic unilateral shift.

The management evidence and urgency must remain separate. Acute traumatic surgical thresholds come from the BTF focal mass-lesion guideline. Chronic SDH care is addressed by a 2024 UK multidisciplinary consensus guideline, which explicitly excludes acute SDH and emphasises function, frailty, shared decision-making, perioperative optimisation and rehabilitation. Antithrombotic decisions require named-drug and jurisdiction-specific guidance, with early specialist escalation instead of a universal reversal prescription.

Key points

Acute SDH is usually traumatic fresh blood between dura and arachnoid, often with severe underlying brain injury; chronic SDH is an organised collection of fluid and blood products, commonly affecting older, frail and antithrombotic-exposed people.
On CT, acute blood is usually a hyperdense crescent that can cross sutures but is limited by dural reflections; chronic collections are often hypodense or mixed-density and may be bilateral. Density alone does not date every component reliably.
For acute traumatic SDH, BTF recommends evacuation when thickness exceeds 10 mm or midline shift exceeds 5 mm regardless of GCS, and also identifies deterioration, pupillary abnormality or ICP above 20 mmHg in selected comatose patients with smaller scans.
For chronic SDH, the 2024 UK multidisciplinary guideline recommends urgent neurosurgical referral, consideration of surgery for symptomatic disease and for large-volume mass effect even with few symptoms; burr-hole drainage with a temporary drain is usual first-line surgery.
Corticosteroids should not treat symptomatic chronic SDH. The same guideline found insufficient evidence for routine tranexamic acid, statins, ACE inhibitors or middle meningeal artery embolisation outside research at publication.
Antithrombotic interruption, reversal and restart are individualised by agent, bleeding/surgical urgency and thrombosis risk; do not transfer a spontaneous-ICH drug rule or one UK nation’s availability assumption into this combined topic.

02Mechanisms and patternsImportant relationships and how to distinguish them.

Identify acute traumatic physiologyRed flag

Reconstruct injury timing and energy, initial consciousness, subsequent GCS change, vomiting, seizure and extracranial bleeding. Acute SDH may coexist with skull fracture, contusions and diffuse axonal injury, making the neurological state worse than clot size alone predicts.

Recognise chronic evolution

Ask about progressively worsening headache, speech disturbance, gait instability, falls, focal weakness, confusion and reduced consciousness over days to weeks. Arrange urgent non-contrast CT and urgent neurosurgical referral when new or progressive symptoms suggest chronic SDH, and record the exact anticoagulant or antiplatelet, indication, dose and last administration, renal function and relevant haemostatic results without delaying imaging or referral.

Detect herniationRed flag

New anisocoria, impaired pupil response, unilateral weakness, posturing, a rapidly falling motor score or abnormal breathing requires immediate emergency treatment. This applies to acute SDH and to a chronic collection that rebleeds or expands.

Assess frailty and competing illness

In chronic SDH, measure frailty with a validated tool and assess delirium, comorbidity, functional reserve, goals and treatment wishes. Frailty informs optimisation and recovery planning; it must not become an automatic reason to withhold specialist assessment.

Define haemostatic exposure

Record anticoagulants, antiplatelets, last doses, indication, previous thrombosis, renal function and relevant laboratory results. Immediate bleeding risk and the hazard of interruption must both enter the decision.

Question causal attribution

If symptoms and imaging do not match, continue the differential. Small chronic collections may be incidental, while infection, electrolyte disorder, medication toxicity, ischaemic stroke and non-convulsive seizure can coexist.

Red flags requiring action

After major trauma, falling GCS, asymmetric pupils, new hemiparesis, posturing or seizure without recovery suggests acute SDH with mass effect and possible herniation.
In an older or frail person, days to weeks of worsening headache, falls, unsteadiness, confusion, speech change or one-sided weakness should prompt consideration of chronic SDH even without remembered trauma.
Sudden decline, a new focal deficit or reduced consciousness in known chronic SDH makes the situation urgent; the word chronic does not mean clinically stable.
Bilateral collections can produce little midline shift despite major brain compression, so apparent symmetry must not be read as low risk.
Exact anticoagulant or antiplatelet, indication, last dose, renal function and haemostatic results are consequential; “on blood thinners” is inadequate for reversal decisions.
An apparently incidental chronic collection does not explain every confusion syndrome: assess infection, metabolic disturbance, medication effects, stroke, seizure and the person’s cognitive baseline.

03Interpreting evidenceInformation, measurements and their limitations.

Reasoning sequence

Consider the information, its meaning and its limitations before deciding what follows.

01
Urgent non-contrast CT head
Why
Differentiate an acute or chronic subdural collection, define mass effect and detect coexisting traumatic lesions.
Interpretation and limitations
Describe side, maximal thickness, density or layering, membranes when visible, midline shift, sulcal and cisternal effacement, ventricular compression, bilateral disease, contusions and fracture. Acute-on-chronic bleeding may be mixed density; bilateral mass effect may occur without large shift.
02
Serial structured neurological observations
Why
Recognise deterioration while awaiting transfer, surgery or repeat imaging.
Interpretation and limitations
Trend GCS components, pupils, limb movement and vital signs against baseline. In acute SDH, a two-point GCS fall from injury to admission is part of the BTF smaller-lesion surgical criterion for comatose patients; any later decline remains clinically urgent.
03
Full blood count, PT, APTT, fibrinogen, renal function and electrolytes
Why
Identify anaemia, thrombocytopenia, conventional coagulopathy, renal impairment and metabolic mimics, and support operative planning.
Interpretation and limitations
The chronic SDH guideline lists this core set plus ECG. Normal PT or APTT may not measure a direct oral anticoagulant accurately; interpret tests with the exact agent and timing.
04
Repeat CT head
Why
Assess expansion after deterioration and support an individual surveillance plan for selected non-operative disease.
Interpretation and limitations
Acute traumatic lesions need serial imaging when observed. For non-operative chronic SDH, evidence does not define one routine interval, so neurosurgery should specify timing case by case. Symptom relapse after discharge requires urgent CT.
05
MRI or vascular imaging in selected atypical cases
Why
Clarify an isodense collection, empyema, tumour, intracranial hypotension or vascular diagnosis when CT and context do not provide an adequate explanation.
Interpretation and limitations
MRI can show membranes and alternative pathology but is not the first test in acute deterioration. Bilateral chronic SDH with suspected CSF leak warrants specialist neuroradiology or subspecialty advice.

04Applied reasoningWorked examples connecting principles to decisions.

01Worked case: compare acute and chronic SDHChoose the acute or chronic pathwayCT shows a subdural collection and the team must decide whether it is an acute traumatic emergency or chronic SDH care problem.

1First pair time course and physiology with imaging: treat high-energy trauma, fresh hyperdense blood, coma or rapid neurological decline as acute traumatic SDH; recognise days-to-weeks change, frailty and a hypodense or mixed organised collection as chronic SDH, while allowing acute-on-chronic bleeding.
2For either form, escalate falling consciousness, new pupil abnormality or progressive focal deficit immediately; stabilise ABC, involve neurosurgery, make images available and identify antithrombotic exposure without delaying source control.
3For acute traumatic SDH, evacuate lesions over 10 mm thick or with over 5 mm shift, and apply the additional comatose-patient criteria when smaller; if surgery is indicated, perform it as soon as possible.
4For chronic SDH, combine symptoms, mass effect, baseline function, frailty and patient goals; consider surgery for symptomatic disease or a large-volume collection with significant mass effect.
5Verify recovery through serial examination and cause-specific follow-up. Re-open the differential when cognition or focal signs do not improve as expected.

02Chronic SDH surgerySymptomatic chronic collectionAn older or frail patient has symptoms attributable to chronic SDH and the shared neurosurgical decision favours surgery.

1Optimise comorbidities and haemostasis without unsafe delay, involve experienced anaesthesia and geriatric medicine when appropriate, and discuss expected benefits, recurrence and functional recovery.
2Use burr-hole drainage with a temporary subdural or subgaleal drain as first-line surgery where safe; reserve craniotomy for selected cases.
3After surgery, use trained neurosurgical observation, remove the drain through authorised staff usually at 24–48 hours, mobilise as soon as safe and assess rehabilitation needs within 48 hours.

03Non-operative chronic SDHIncidental or minimally symptomatic diseaseNeurosurgery determines that immediate surgery is unlikely to add benefit and the patient is clinically stable.

1Treat competing causes and agree which team coordinates care; individualise anticoagulant interruption and monitoring rather than using trauma alone to decide location.
2Create an explicit clinical and imaging follow-up plan because evidence does not support one routine interval, and provide urgent-return instructions for recurrent headache, weakness, confusion, seizure or reduced consciousness.
3Reassess function, cognition and rehabilitation needs, escalating to urgent repeat CT and neurosurgical discussion if the symptoms relapse or progress.

05Checking understandingVerify the reasoning, revisit uncertainties and apply feedback.

In acute SDH, trend GCS components, pupils, limb response, oxygenation and circulation continuously or at a high-frequency observation schedule agreed with neurosurgery.
In chronic SDH, compare cognition, gait, speech and power with the collateral baseline and screen new postoperative confusion for delirium.
Record anticoagulant interruption, any reversal decision, its responsible specialist and the plan for thromboprophylaxis and long-term restart.
After chronic SDH surgery, monitor drain output and wound through trained staff; obtain postoperative CT for a clinical concern rather than routinely.
Provide a written plan for rehabilitation, medication, driving advice, recurrence symptoms and 24-hour routes to urgent assessment.

06Special situationsVariants, exceptions and circumstances that change the usual approach.

The brain injury differs

Acute SDH often accompanies severe cortical and diffuse injury; chronic SDH is an inflammatory, membrane-lined disease with recurrent microbleeding.

Density is not a clock

Anaemia, mixing, rebleeding and contrast can alter CT density. Use the clinical course and full imaging pattern.

Bilateral can hide shift

Two collections may compress both hemispheres symmetrically, so a small midline shift does not prove low mass effect.

Frailty changes the plan

Baseline function and geriatric needs guide consent, anaesthesia and recovery, but do not replace an assessment of neurological reversibility.

Recurrence needs a route back

Chronic SDH can recur after drainage. A new return of gait, cognitive or focal symptoms requires urgent CT and neurosurgical discussion.

07Common pitfallsFrequent interpretation and management errors.

01
Using acute traumatic SDH surgical thresholds as the sole decision rule for chronic SDH.
02
Calling every low-density subdural collection harmless or every mixed-density collection purely acute.
03
Being reassured by minimal midline shift in a patient with bilateral compression and deteriorating consciousness.
04
Using corticosteroids routinely for symptomatic chronic SDH despite the UK guideline recommendation against them.
05
Prescribing a universal reversal or restart schedule without the exact drug, last dose, renal function, thrombosis indication and current jurisdictional pathway.
06
Failing to investigate competing delirium or stroke when symptoms do not match the collection.

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