Subdural Haematoma

Subdural Haematoma RECURS ×2 Definition and classification

Subdural haematoma (SDH) is a collection of blood in the subdural space — the potential space between the dura mater and the arachnoid mater.

The dura has two layers — an outer periosteal layer and an inner meningeal layer, separated from the arachnoid by a dural border cell layer. The potential space becomes a real space when the dural border cell layer cleaves away from the meningeal layer, shearing the bridging veins that traverse it to reach the dural venous sinuses.

Classification by time from ictus: acute <3 days (usually post-traumatic), subacute 4–20 days, chronic >20 days. The spectrum is best regarded as a dynamic continuum, not discrete entities.

With ageing, the brain atrophies and pulls away from the skull, placing traction on the meninges and bridging veins. This predisposes to SDH after minimal or unremembered trauma, or even spontaneously.

The incidence of chronic SDH (CSDH) in patients over 80 has risen significantly over the last three decades; by 2030 CSDH is projected to be the commonest cranial neurosurgical disease in the world.

Falls are the commonest mechanism in older adults. A major confounding factor is the widespread use of antiplatelets and anticoagulants for comorbidities.

Acute SDH: signs and symptoms result from an abrupt rise in intracranial pressure with compression of eloquent brain tissue. The two aetiologies are tearing of bridging veins and parenchymal laceration (the latter reflecting severe primary injury).

Chronic SDH: the mechanism is entirely different — it is driven by an inflammatory response provoked by blood haemolysis and its degradation products, with neomembrane formation, fragile leaky neocapillaries fed by the middle meningeal artery, repeated microhaemorrhage and osmotic exudation. CSDH is phenotypically diverse.

Acute SDH: rapid decline in consciousness, headache, vomiting, focal deficit, seizures, anisocoria and herniation signs. Often a lucid interval is absent.

Chronic SDH — the great mimic: headache, cognitive decline, confusion, gait disturbance, falls, hemiparesis, aphasia and seizures. 50–70% of elderly patients present with altered mental status; the course is characteristically fluctuating.

CSDH may masquerade as dementia, stroke, delirium, normal pressure hydrocephalus, parkinsonism or depression — it is a reversible cause of cognitive decline.

Non-contrast CT of the head is the initial method of choice. Acute SDH is a crescent-shaped hyperdensity with a concave inner surface, causing midline shift and ventricular effacement; it crosses suture lines but not the midline.

Subacute SDH becomes isodense with brain (about 1–3 weeks) and is easily missed — look for effaced sulci, a displaced grey–white junction, and asymmetric ventricles. Chronic SDH is hypodense; mixed density indicates re-bleeding.

MRI is most useful for isodense collections, bilateral collections and for chronic intradural haematoma in evolution. Add coagulation screen, platelet count, and anticoagulant drug levels.

Small acute SDH (clot thickness <10 mm) in a neurologically intact patient, with no herniation, no significant midline shift and no raised ICP, is not emergently evacuated. Monitor clinically and repeat the CT at 24 hours (or sooner) if there is concern about expansion or any change in mental status or neurological examination.

Acute symptomatic SDH is a medical emergency — rapid diagnosis, reversal of anticoagulation, and surgical evacuation (craniotomy or decompressive craniectomy) as soon as indicated.

Anticoagulant reversal: vitamin K plus 4-factor prothrombin complex concentrate for warfarin; idarucizumab for dabigatran; andexanet alfa for factor Xa inhibitors. In patients on antiplatelet medication, preoperative platelet transfusion did not reduce reoperation rates; platelet reversal and platelet transfusion are therefore not routinely recommended.

Surgical options are twist-drill craniostomy, burr-hole craniostomy (5–30 mm hole, better visualisation of dura and cortex, usually under general anaesthesia — the standard operation), and craniotomy (large bone flap, direct access to haematoma and membranes; preferred for multiloculated CSDH with significant membranes).

Evidence: no difference in mortality, morbidity, recurrence or cure between burr-hole and twist-drill craniostomy. Open craniotomy as first treatment has more morbidity but lower recurrence.

Strong evidence supports placement of a subdural drain — it significantly lowers recurrence and improves functional outcome without increasing operative complications or mortality. No universal management consensus exists; each case is individualised.

Complications are frequent given age, frailty and comorbidity: wound infection, subdural empyema, tension pneumocephalus, seizure, brain contusion, fresh subdural or extradural haematoma, intracerebral haemorrhage and death.

Recurrence is up to 33% despite gold-standard drainage and irrigation. Risk factors for recurrence: age >70, bilateral CSDH, large haematoma volume, preoperative seizure, postoperative intracranial air, low GCS, and diabetes mellitus.

Medical adjuncts: atorvastatin 20 mg (Jiang et al., JAMA Neurology 2018 RCT) reduced haematoma volume and improved neurological outcome. Dexamethasone has been studied — see updates below.

Endovascular treatment: middle meningeal artery (MMA) embolisation addresses the underlying pathology rather than simply draining blood — by embolising the MMA the blood supply to the pathological membranes is removed, allowing spontaneous resolution.

Mortality for acute SDH is 22–60%, higher in the elderly. Predictors of poor outcome: advanced age, low GCS at presentation, comorbid intracranial and extracranial injury, and anticoagulant use.

Features favouring spontaneous resolution: coma lasting less than 12 hours after injury, absence of cerebral contusion, a thin haematoma with wide distribution, GCS >8, and clinical stability over time.

Prevention: DOACs reduce the risk of intracranial haemorrhage compared with vitamin K antagonists while remaining at least as effective for thromboembolism. Registry data show DOAC-treated patients have lower in-hospital mortality, fewer severe intracranial haemorrhages, less need for operative intervention and less discharge to skilled nursing facilities than warfarin-treated patients. Add falls prevention, medication review, and vision and gait optimisation.