Deteriorating acute subdural haematoma in an anticoagulated elderly patient
A 68-year-old man with atrial fibrillation taking apixaban 5 mg twice daily falls at home and arrives 90 minutes later. Initial Glasgow Coma Scale (GCS) score is 13 (E3 V4 M6); 40 minutes later it is 11 (E2 V3 M6) and he localizes only on the right. His right pupil is 4 mm and sluggish, the left is 3 mm and reactive. Blood pressure is 168/94 mmHg, heart rate 62/min, and oxygen saturation is 96% on a non-rebreather mask. Non-contrast CT shows a left acute subdural haematoma 12 mm thick with 8 mm midline shift, effaced basal cisterns, and a small frontal contusion. The last apixaban dose was 9 hours ago; serum creatinine is 1.1 mg/dL and anti-Xa activity is elevated. There is no advance care directive, and his wife confirms he was independent at baseline.
1. Outline your first 60 minutes of management, including the order in which you would reverse anticoagulation, control intracranial pressure, and arrange surgery. Justify each priority.
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The priority is to prevent herniation while reversal is arranged; do not wait for full reversal before decompression when the pupil is failing. Airway and physiology first: rapid-sequence intubation with ketamine or etomidate and rocuronium, maintain MAP at least 80 mmHg to preserve cerebral perfusion pressure, elevate the head 30 degrees, and keep the cervical collar loose after imaging. Hyperosmolar therapy: give 3% hypertonic saline 150–250 mL or mannitol 1 g/kg if pupillary asymmetry persists; avoid hypotension. Reverse the anticoagulant in parallel: give 4-factor prothrombin complex concentrate or andexanet alfa where available, plus tranexamic acid 1 g. Platelet transfusion is not routine unless the count is low or the patient is on an antiplatelet agent. Theatre: book urgent craniotomy and haematoma evacuation immediately, because a 12 mm haematoma with 8 mm shift and a sluggish pupil is a surgical emergency. Reversal reduces expansion and operative bleeding but must not delay surgery. Avoid aggressively lowering blood pressure below about 110 mmHg systolic before decompression. Document baseline GCS, pupillary findings, and the time of each intervention.
2. The family asks why you do not simply wait for the anticoagulant effect to wear off before operating. How do you explain the physiological rationale and the haematoma expansion risk?
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Explain that the danger is not only the current clot but continued bleeding into the subdural space, which can increase pressure and cause brainstem compression within hours. Apixaban effect correlates poorly with a single clotting test, and waiting for a normal anti-Xa level may take 24 hours or longer in an elderly patient. During that time, the haematoma can expand, the midline shift can worsen, and a reversible pupillary sign can become a fixed brainstem injury. Reversal with prothrombin complex concentrate or andexanet rapidly improves thrombin generation and allows surgery with a lower risk of uncontrolled bleeding. The small residual risk of thromboembolism from reversal is outweighed by the immediate risk of death or severe disability from herniation. Explain that surgery does not require complete elimination of the drug, only adequate haemostasis, and that the team will continue reversal and monitoring during transfer. Document the discussion with the family and the basis for proceeding urgently.
3. After evacuation, what thresholds would you use for intracranial pressure monitoring, and how would you plan restarting anticoagulation? Address competing stroke and bleeding risks.
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Place an intracranial pressure monitor if the post-operative GCS remains 8 or less, if the CT shows unresolved mass effect, or if the patient cannot be serially examined because of sedation. Target ICP below 22 mmHg and cerebral perfusion pressure 60–70 mmHg, using sedation, normocapnia, normothermia, and hyperosmolar therapy as needed. Repeat CT for any neurological change. Anticoagulation restart: involve cardiology, haematology, and the family. In a patient with atrial fibrillation and a mechanical or high-risk thromboembolic profile, restarting apixaban after documented haemostatic stability at roughly 4–7 days is reasonable; in a lower-risk patient, wait longer and consider left atrial appendage occlusion if recurrent falls are likely. The decision balances recurrent intracranial bleeding against cardioembolic stroke. Use the CHA2DS2-VASc score, renal function, fall risk, and repeat imaging. Do not restart while there is active bleeding or unstable ICP. Address driving, falls prevention, and goals of care before discharge.