What is the best course of management for a non-smoking, non-alcoholic, elderly patient with a history of cardiovascular disease (CVD) and hypertension (HPN), presenting with an acute cerebrovascular infarct in the right middle cerebral artery territory, probably cardioembolic in origin, with a severe neurological deficit, pneumonia, and impaired renal function?

Management of Acute Right MCA Infarct with Severe Neurological Deficit and Complications

This patient requires immediate consideration for decompressive craniectomy given the ASPECTS score of 5, mRS 5, and NIHSS 29, as mortality approaches 78% without surgical intervention in complete MCA territory infarction. 1

Immediate Neurosurgical Evaluation

Decompressive craniectomy should be performed urgently (ideally within 48 hours of stroke onset) for this patient with space-occupying right MCA infarction. 2

Surgical Candidacy Assessment

• The patient meets criteria for decompressive craniectomy: ASPECTS score ≤5 indicates extensive infarction with high risk of malignant edema and herniation 1, 3
• NIHSS 29 and mRS 5 indicate severe deficit, but the guideline explicitly states that carotid revascularization (not craniectomy) is contraindicated when severe disability precludes preservation of useful function 2
• However, for space-occupying MCA infarction specifically, surgery should be considered even with severe deficits to prevent herniation and death 2
• The GCS of 8T (E3VTM5) indicates deteriorating consciousness, a critical sign requiring urgent intervention 4

Surgical Technique Required

• Fronto-parieto-temporo-occipital craniectomy with diameter ≥12 cm extending to the midline 2
• Durotomy with enlargement duroplasty is mandatory 2
• Do not remove ischemic brain tissue 2
• ICP monitor placement is recommended postoperatively 2

Blood Pressure Management

Maintain permissive hypertension with systolic BP target <220 mmHg and diastolic <120 mmHg 5, 4, 6

Critical BP Parameters

• Current BP 140/80 mmHg is appropriate and should NOT be lowered further 5
• Cerebral perfusion pressure (CPP) must be maintained >60 mmHg at all times 2
• Avoid BP reductions >70 mmHg within 1 hour as this causes acute kidney injury and neurological deterioration 5, 6
• The patient's history of prior CVD infarct (left MCA territory) means cerebral autoregulation is impaired bilaterally 6

Antiplatelet and Anticoagulation Strategy

Aspirin should be withheld immediately given the high likelihood of requiring decompressive craniectomy. 2

Specific Recommendations

• Do not administer aspirin or antiplatelet agents when craniectomy is likely 2
• After craniectomy (postoperative day 2), initiate subcutaneous low molecular weight heparin for DVT prophylaxis only after neurosurgical consultation 2
• For cardioembolic stroke prevention long-term, anticoagulation should be started once surgical risk has passed and patient is stable 7, 8
• Given probable cardioembolic etiology, workup for atrial fibrillation with Holter monitoring and echocardiography (TTE/TEE) is essential 7, 8

Infection Management

Continue piperacillin-tazobactam 4.5g IV q6h for hospital-acquired pneumonia as planned. 2

Pulmonary Considerations

• Left lung atelectasis was iatrogenic from malpositioned ETT, now corrected 2
• CXR shows left pneumonia requiring full 7-day antibiotic course 2
• Gram stain showing no organisms does not exclude bacterial pneumonia in intubated patients 2

Ventilator Management

Current ventilator settings are appropriate; proceed with gradual FiO2 weaning as planned. 2

Specific Parameters

• AC mode with TV 360 mL (approximately 5-6 mL/kg for average adult) is lung-protective 2
• Decrease FiO2 by 10% every 2 hours targeting 40% without desaturation 2
• Avoid sedation unless absolutely necessary as this impairs neurological assessment 2
• Attempt weaning from sedation as soon as ICP is controlled post-craniectomy 2

Metabolic and Electrolyte Management

Correct hyponatremia (134.9 mmol/L), hypomagnesemia (0.71 mmol/L), and hypocalcemia (1.06 mmol/L) immediately. 2

Correction Strategy

• Use isotonic fluids only; avoid hypotonic solutions which worsen cerebral edema 2
• Correct magnesium to >0.85 mmol/L to reduce seizure risk 2
• Maintain serum glucose <10 mmol/L but avoid hypoglycemia 2
• Elevated BUN (9.22 mmol/L) with normal creatinine suggests dehydration; correct hypovolemia with isotonic saline 2

Monitoring and Supportive Care

Transfer to neurosurgical ICU with continuous ICP monitoring post-craniectomy. 2, 4

Essential Monitoring

• Neurological examination every 1-2 hours to detect herniation signs 2, 4
• ICP and CPP monitoring continuously post-craniectomy 2
• Repeat CT scan at 24 hours post-surgery or earlier if clinical deterioration 2
• Elevate head of bed 0-30° during periods of increased ICP 2

Temperature and Seizure Management

• Treat hyperthermia aggressively (paracetamol ± metamizol); avoid NSAIDs and opioids 2
• No prophylactic antiepileptics; treat only if seizures occur 2

Nutrition

Initiate enteral nutrition via nasogastric tube within 24-48 hours if no contraindications. 2

• Keep patient NPO until swallowing assessment completed 2
• Early enteral nutrition improves outcomes in critically ill stroke patients 2

Prognosis Discussion

In-hospital mortality for cardioembolic MCA infarction is 27%, rising to 78% with herniation in untreated complete MCA infarction. 8, 1

Realistic Outcome Expectations

• Survivors of decompressive craniectomy for malignant MCA infarction typically have mean Barthel Index 60 (moderate-severe disability) 2
• Early recurrent embolization within 7 days carries 77% mortality 8
• The bilateral MCA disease (acute right + chronic left) significantly worsens functional prognosis 1

Critical Pitfalls to Avoid

• Do not delay neurosurgical consultation; herniation develops predictably over 2-5 days 1
• Do not aggressively lower blood pressure in this patient with bilateral cerebrovascular disease 5, 6
• Do not administer corticosteroids, mannitol, or hypertonic saline as temporizing measures if surgery is planned 2
• Do not start therapeutic anticoagulation during acute phase; this increases hemorrhagic transformation risk 2