New focal deficit 3 days after a fall on warfarin

The presentation fits an acute stroke syndrome, but the preceding head trauma and anticoagulation force you to consider intracranial hemorrhage first:

• Subdural hematoma - classic in elderly patients, may present subacutely (3 days) with fluctuating confusion and focal deficit; anticoagulation increases risk and progression.
• Intraparenchymal or epidural hemorrhage - less likely without a lucid interval but possible.
• Ischemic stroke - still very possible given atrial fibrillation (cardioembolic risk); fluctuating deficits can reflect stuttering embolism or evolving stroke.
• TIA, seizure with postictal deficit, hypoglycemia (glucose 132 makes it unlikely), toxic/metabolic encephalopathy from anticoagulant effect.

Because the treatments diverge completely, emergent non-contrast head CT is the first step, with INR and coagulation studies drawn simultaneously. You cannot give thrombolysis or reverse anticoagulation until imaging clarifies the diagnosis.

Priorities, in order:

1. Airway/breathing/circulation and neuroprotection - avoid hypoxia and hypotension; elevate head of bed; treat pain and agitation; keep glucose and temperature normal. Anticipate herniation if mass effect progresses.
2. Reverse anticoagulation immediately - do not wait for the INR result to start. Give vitamin K (phytonadione) IV plus a four-factor prothrombin complex concentrate (PCC); if unavailable, consider three-factor PCC with fresh frozen plasma. PCC works within minutes and is preferred over FFP for speed and volume. Recheck INR frequently and redose as needed.
3. Urgent neurosurgical consultation for possible decompression/evacuation, especially with deterioration; also consider ICP-lowering measures.
4. Blood pressure control - modest, controlled lowering per hemorrhage protocols, avoiding abrupt drops that compromise perfusion.
5. Stop warfarin, hold antithrombotics, admit to a stroke/ICU unit, and address reversal of any residual anticoagulant effect before any procedure.

Reasoning: in anticoagulation-associated ICH, time to reversal correlates with hematoma expansion and outcome, so reversal is simultaneous with, not after, imaging confirmation.

This is a genuine equipoise question and should be individualized:

• Stroke risk without anticoagulation - her CHA2DS2-VASc score is high (age, hypertension, prior event), so the absolute stroke risk is substantial.
• Recurrence risk of ICH - depends on hemorrhage location (lobar vs deep), age, hypertension control, cerebral amyloid angiopathy suspicion, and whether the initial bleed was anticoagulation-related and reversible.
• Timing - observational data suggest restarting after roughly 4–8 weeks for deep hemorrhages and longer (weeks to months) for lobar hemorrhages; earlier restart raises rebleeding risk, later restart raises ischemic risk.
• Agent choice - a direct oral anticoagulant (e.g., apixaban) is often favored over warfarin for lower ICH risk, though evidence in prior-ICH populations is evolving; left atrial appendage occlusion is an alternative when anticoagulation is deemed prohibitive.
• Modifiable risks - strict BP control, fall prevention, avoiding NSAIDs/antiplatelets, alcohol moderation.

Framing: the decision is a shared one weighing a high ischemic stroke risk against a meaningful but quantifiable rebleeding risk; document the discussion and revisit as her risk profile changes.