Subdural Hematoma (SDH)

Airway - Intubate for a GCS under 8 or a decline of 2 or more points, and keep oxygenation and ventilation tight from that moment. Check that a cervical collar isn't sitting tight enough to obstruct venous drainage — that alone will raise ICP.

Blood pressure — a narrow window - Keep systolic pressure under 140 to 160 mmHg to limit hematoma expansion, but do not let it fall; hypotension against a raised ICP means cerebral hypoperfusion. Have a short-acting antihypertensive and a vasopressor both drawn up, because you will use each.

Ventilation - Avoid hypercapnia, which will trigger an ICP crisis. Hyperventilation is a bridge to the operating room, not a treatment.

Anticoagulation - Many of these patients are anticoagulated or coagulopathic, and reversal is part of the resuscitation, not an afterthought. Agent-specific reversal products and dosing change frequently — confirm against your institution's current protocol and get coagulation studies or a TEG before incision. ⚠ Do not work from memory here.

Be careful with the usual ICP tools - Surgical evacuation and decompression are the most effective way to drop ICP in SDH. External ventricular drainage of CSF can make things worse by further retracting the injured bridging veins, and osmotic agents can add tension on dural vessels and enlarge the hematoma. Standard ICP management is safer once the clot is out.

Head and neck position - Head of bed up, head midline, nothing constricting the neck. Eliminate every source of venous obstruction you can reach.

Baseline neuro exam - Document a detailed neurologic exam and GCS before induction. It is the only reference point you will have on emergence, and a drop of 2 or more GCS points from presentation is itself an operative trigger even for a smaller clot.

Operative thresholds - Acute SDH: open craniotomy for maximum thickness greater than 1 cm or midline shift greater than 0.5 cm. Chronic SDH: clot thickness greater than 10 mm or midline shift greater than 5 mm, and any symptomatic lesion. If no immediate surgery, a repeat noncontrast head CT at 4 hours checks for stability.

Seizure prophylaxis - Levetiracetam, lacosamide, or fosphenytoin. Acute traumatic injury gets 7 days of prophylaxis. Temporal lobe and tentorial lesions are more epileptogenic, so expect the neurosurgeon to want coverage.

Chronic SDH looks like something else - Headache, light-headedness, behavioral change, cognitive impairment, somnolence, gait disturbance, memory problems, seizures. It is a reversible cause of dementia — the elderly patient on your board for burr holes may have been carrying a dementia or stroke diagnosis for weeks.

Where the case happens - Chronic SDH is drained by burr-hole craniotomy, twist-drill craniostomy, or open craniotomy, and middle meningeal artery embolization is used as an adjunct to prevent recurrence. Twist-drill craniostomy can be done at the bedside in the ICU, so plan a non-OR anesthetic with your own airway equipment, suction, and monitoring.

Pediatric SDH - In infants and children, nonaccidental trauma is the typical etiology. Keep suspicion high and document what you see.

A subdural hematoma is blood between the dura and the arachnoid. Acute SDH is traumatic about 70% of the time, from lateral acceleration tearing the bridging veins; on noncontrast CT it is a hyperdense crescent over the convexity, falx, or tentorium that crosses suture lines. The elderly are the classic patient — cerebral atrophy widens the subdural space, puts more tension on the bridging veins, and permits a larger clot and more midline shift before symptoms appear. Mortality climbs sharply past age 60.

Falling ICP is the other mechanism: a CSF leak after lumbar puncture, ventriculostomy, shunt placement, or an over-draining lumbar drain lets the brain settle and stretch the veins. Chronic SDH encapsulates in neomembranes over weeks to months; the membrane is vascular enough to rebleed and secretes antithrombotic and fibrinolytic enzymes, so it expands rather than resorbs.