What is the appropriate evaluation and management of anisocoria after a head injury?

Anisocoria Post Head Injury: Evaluation and Management

Immediate Assessment Priority

Anisocoria after head injury is a neurological emergency requiring immediate evaluation for intracranial mass lesion, herniation, or brainstem compromise. 1, 2

Critical Initial Evaluation

The initial assessment must focus on three key elements:

• Pupillary examination: Document pupil size in millimeters, reactivity to light, and degree of anisocoria (difference between pupils). 1 This should be performed with both ambient light and after light stimulation, as anisocoria after light stimulation is a stronger predictor of injury severity and outcomes than anisocoria in ambient light. 3

• Glasgow Coma Scale motor response: This is the most critical component of severity assessment, with motor response ≤5 indicating severe injury requiring intensive monitoring. 1, 2

• Associated signs of herniation: Look for bilateral mydriasis, loss of consciousness, posturing, or hemodynamic instability. 1, 2

Immediate Imaging

All patients with anisocoria after head injury require emergent non-contrast head CT to rule out expanding intracranial mass lesion. 1

The CT should specifically evaluate for:

• Compression of basal cisterns (the best radiological sign of intracranial hypertension) 4
• Midline shift >5 mm 4
• Disappearance of cerebral ventricles 4
• Subdural or epidural hematoma thickness >5 mm 1
• Traumatic subarachnoid hemorrhage 4

Understanding the Mechanism

Pupillary dilation after head injury results more commonly from decreased brainstem blood flow and ischemia rather than mechanical compression of the third cranial nerve. 5

Key pathophysiological insights:

• Brainstem blood flow <40 mL/100g/min is significantly associated with pupillary abnormalities and poor outcome. 5
• Patients with bilaterally nonreactive pupils have mean brainstem blood flow of 30.5±16.8 mL/100g/min versus 43.8±18.7 mL/100g/min in those with reactive pupils. 5
• This suggests that rapid restoration of cerebral perfusion pressure may improve prognosis even in patients with dilated pupils. 5

Management Algorithm

Step 1: Stabilization and Monitoring

Maintain systolic blood pressure ≥100 mmHg and cerebral perfusion pressure ≥60 mmHg. 1, 4

• Avoid hypotension (SBP <90 mmHg), which is strongly associated with unfavorable neurological outcome. 1
• Target cerebral perfusion pressure of 60-70 mmHg when ICP monitoring is available. 1, 4
• Maintain normothermia and avoid hypoxia. 2

Step 2: Determine Need for ICP Monitoring

ICP monitoring is indicated if the patient meets any of these criteria: 2, 4

• GCS motor response ≤5 with abnormal CT
• Preoperative anisocoria or bilateral mydriasis
• Preoperative hemodynamic instability
• Severe imaging findings (basal cistern compression, midline shift >5mm, hematoma volume >25mL)
• Inability to perform adequate neurological examination

Use intraparenchymal probes rather than intraventricular drains due to better risk-benefit profile (infection rate 2.5% vs 10%, hemorrhage rate 0-1% vs 2-4%). 2, 4

Step 3: Neurosurgical Consultation

Immediate neurosurgical consultation is required for:

• Symptomatic extradural hematoma at any location 1
• Acute subdural hematoma >5mm thickness with midline shift >5mm 1
• Any patient with anisocoria and declining neurological status 1

Step 4: Serial Monitoring Protocol

For patients not requiring immediate surgery:

• GCS monitoring every 15 minutes for first 2 hours, then hourly for 12 hours 6
• Document individual GCS components (Eye, Motor, Verbal) and pupillary size/reactivity at each evaluation 6
• Repeat head CT at 6-8 hours to assess for hemorrhage expansion, as most expansion occurs within the first 6 hours 6
• Immediate repeat CT if GCS declines by ≥2 points 6

Critical Pitfalls to Avoid

Do not discharge any patient with documented anisocoria after head injury, even with normal neurological examination, as delayed deterioration can occur. 6

Avoid administering long-acting sedatives or paralytics before neurosurgical evaluation, as this masks clinical deterioration. 6

Do not assume anisocoria is always from intracranial pathology—check for pre-existing conditions (artificial eye, physiological anisocoria, prior eye surgery) through corneal reflex testing and manual palpation of the globe. 7

Maintain adequate cerebral perfusion pressure—failure to maintain MAP ≥80 mmHg can worsen brainstem ischemia and pupillary dysfunction. 6, 5

Prognostic Implications

Anisocoria after light stimulation correlates strongly with injury severity and worse outcomes. 3

• Anisocoria after light stimulation is associated with lower discharge GCS scores (OR 0.28,95% CI 0.17-0.45) and worse functional outcomes (OR 0.28,95% CI 0.17-0.47). 3
• Pupillary responsiveness is inversely related to unfavorable outcome at 12 months (p=0.0006). 5
• However, if cerebral perfusion can be rapidly restored, prognosis may improve even with initially dilated pupils. 5