In a patient with Child‑Pugh cirrhosis who suddenly develops an acute stroke with right upper‑motor‑neuron facial palsy and right hemiplegia, how should the acute management be approached?

Acute Stroke Management in Child-Pugh Cirrhosis

In a cirrhotic patient presenting with acute stroke (right UMN facial palsy and right hemiplegia), immediately pursue standard acute stroke protocols—including urgent neuroimaging to differentiate ischemic from hemorrhagic stroke—because cirrhosis does not confer "auto-anticoagulation" and these patients face both thrombotic and bleeding risks in a rebalanced hemostatic state. 1

Immediate Assessment and Neuroimaging

• Obtain non-contrast head CT or MRI within minutes of presentation to distinguish ischemic stroke from intracranial hemorrhage, as management pathways diverge completely based on this finding. 1
• The elevated INR in cirrhosis reflects reduced procoagulant factor synthesis but is counterbalanced by reduced anticoagulant protein synthesis, creating a prothrombotic state rather than natural anticoagulation. 1, 2
• Cirrhosis significantly increases the risk of subarachnoid hemorrhage (HR 2.36; 95% CI 1.80–3.09) and intracranial hemorrhage (HR 1.48; 95% CI 1.06–2.05), making hemorrhagic stroke exclusion critical before any intervention. 3

Management of Ischemic Stroke in Cirrhosis

Thrombolysis Considerations

• Standard IV thrombolysis (alteplase) eligibility criteria apply, but the elevated baseline INR in cirrhosis complicates interpretation: the INR does not reflect true anticoagulation status, yet most stroke protocols exclude patients with INR >1.7. 1, 2
• Check platelet count immediately: full therapeutic anticoagulation and thrombolysis can proceed safely at platelet counts ≥50 × 10⁹/L without platelet transfusion support. 1, 4
• For platelet counts 40–50 × 10⁹/L, consider platelet support during the initial 30 days if thrombolysis is administered. 2

Anticoagulation for Secondary Stroke Prevention

• For Child-Pugh A or B cirrhosis with atrial fibrillation (a common stroke mechanism), initiate standard-dose DOACs (apixaban, dabigatran, or edoxaban) as first-line therapy after the acute phase, as they demonstrate superior safety versus warfarin with lower major bleeding (HR 0.63; 95% CI 0.43–0.93) and intracranial hemorrhage (HR 0.49; 95% CI 0.40–0.59). 1, 2
• Apixaban shows particularly favorable outcomes with reduced major bleeding versus warfarin (HR 0.43; 95% CI 0.30–0.63) and lower all-cause mortality. 2
• For Child-Pugh C cirrhosis, use low-molecular-weight heparin (LMWH) alone or as a bridge to warfarin if baseline INR is normal, as DOACs should be avoided due to altered pharmacokinetics and unpredictable anticoagulant effects. 1, 5

Pre-Anticoagulation Safety Measures

• Screen for esophageal varices with upper endoscopy before initiating anticoagulation and ensure adequate variceal prophylaxis (beta-blockers or endoscopic band ligation) is in place. 5, 2
• Do not withhold anticoagulation for moderate thrombocytopenia (platelet count >50 × 10⁹/L). 2

Management of Hemorrhagic Stroke in Cirrhosis

• If imaging reveals intracranial hemorrhage, immediately reverse any anticoagulation and hold all antiplatelet agents. 1
• Platelet transfusion thresholds for neurosurgical intervention: transfuse to achieve platelet count ≥100 × 10⁹/L before any neurosurgical procedure. 4
• For platelet counts <50 × 10⁹/L with active CNS bleeding, combine platelet transfusion with intravenous immunoglobulin (IVIg 0.8–1 g/kg single dose) to rapidly increase platelet count. 4

Differential Diagnosis: Hepatic Encephalopathy Mimicking Stroke

• Consider hepatic encephalopathy (HE) as a stroke mimic, especially if the patient has fluctuating consciousness, flapping tremor, or speech disturbance beyond aphasia. 6
• HE can present with focal neurologic signs (including hemiparesis and sensory disturbances) that resolve once HE is controlled, particularly in patients with pre-existing silent ischemia. 6
• All cirrhotic patients admitted to ICU with neurologic symptoms have at least one precipitating factor for HE (infection 64%, acute kidney injury 63%, drugs 41%, GI bleeding 36%), and 82% have multiple concomitant precipitating factors. 7
• Obtain electroencephalography and serum ammonia level to differentiate HE from acute stroke if clinical features are atypical or if the patient has known cirrhosis with recent decompensation. 6

Critical Pitfalls to Avoid

• Do not assume elevated INR indicates "auto-anticoagulation": the elevated INR in cirrhosis reflects reduced procoagulant factor synthesis but is counterbalanced by reduced anticoagulant protein synthesis, creating a rebalanced but prothrombotic state. 1, 2
• Do not withhold standard acute stroke protocols solely because of cirrhosis: these patients require the same urgent neuroimaging and stroke team activation as non-cirrhotic patients. 1
• Do not use standard DOAC dosing in Child-Pugh C cirrhosis: altered pharmacokinetics unpredictably increase bleeding risk. 5
• Do not overlook hepatic encephalopathy as a stroke mimic: focal neurologic signs can resolve with HE treatment alone, avoiding unnecessary thrombolysis or anticoagulation. 6