How can I recognize vasospasm in patients after subarachnoid hemorrhage, cardiac catheterisation, drug‑induced coronary spasm, or traumatic limb injury?

Recognizing Vasospasm After Subarachnoid Hemorrhage

The first objective sign of symptomatic vasospasm is the development of a new focal neurological deficit that cannot be explained by hydrocephalus or rebleeding, typically occurring 3-5 days after the initial hemorrhage with peak incidence at 5-14 days. 1, 2

Clinical Recognition

Timing and Presentation

• Vasospasm typically begins 3-5 days after SAH, reaches maximum severity at 5-14 days, and gradually resolves over 2-4 weeks. 1, 2
• New focal deficits (motor weakness, aphasia, neglect) are the hallmark clinical sign in patients with adequate neurological examination. 1, 2
• Unexplained increases in mean arterial pressure may occur as cerebral autoregulation attempts to compensate for reduced perfusion. 1
• In comatose or poor-grade patients, maintain a higher index of suspicion since symptomatic vasospasm can occur without obvious clinical changes—even subtle examination changes warrant investigation. 1, 3

Critical Pitfall

Do not wait for dramatic neurological deterioration in sedated or poor-grade patients. Delayed cerebral ischemia (DCI) can progress to infarction without overt symptoms in approximately 50% of patients with angiographic vasospasm. 1, 2

Diagnostic Monitoring Strategies

Transcranial Doppler (TCD) Ultrasound

• TCD monitoring is reasonable for detecting vasospasm and predicting DCI (Class IIa, Level B-NR). 1
• Use Lindegaard ratios (cerebral vessel velocity/extracranial ICA velocity) rather than absolute velocities, as absolute values can be misleading during hypertensive therapy. 1, 2, 3
• Lindegaard ratios of 5-6 indicate severe vasospasm requiring treatment based on clinical context. 1, 2
• Limitation: TCD is operator-dependent with variable sensitivity/specificity, requiring institutional quality control and threshold establishment. 1

CT Angiography (CTA)

• CTA is useful for detecting vasospasm and predicting DCI (Class IIa, Level B-NR), with 91% sensitivity for central vasospasm when symptoms develop. 1
• CTA has 90% diagnostic accuracy with only 5% false-positive rate compared to conventional angiography. 1
• CTA is particularly valuable when TCD readings become elevated and neurological examination is limited. 1
• Accuracy diminishes in distal vascular territories (78-81% for distal vessels versus 96-100% for proximal vessels). 1, 4

CT Perfusion (CTP)

• CTP can detect vasospasm and predict DCI (Class IIa, Level B-NR), with 74% sensitivity and 93% specificity in meta-analysis. 1
• CTP provides information about small-vessel perfusion, complementing CTA's evaluation of large vessels. 1
• Important caveat: CTP-guided therapy does not improve clinical outcomes compared to treating all patients without imaging guidance. 1, 2

Continuous EEG (cEEG) Monitoring

• In high-grade SAH patients, cEEG monitoring is useful to predict DCI (Class IIa, Level B-NR). 1
• EEG alarms occur in 96.2% of patients with subsequent DCI (median 1.9-day latency before clinical DCI). 1
• Late-onset epileptiform abnormalities have the highest predictive value among EEG alarm subtypes. 1

Invasive Neuromonitoring

• Brain tissue oxygen (PbtO2), lactate/pyruvate ratio, and glutamate monitoring may be considered in high-grade SAH (Class IIb, Level B-NR). 1
• Major limitation: these provide only regional information, so probe placement in the highest-risk territory is critical. 1

Conventional Angiography

• Digital subtraction angiography remains the reference standard for definitive vasospasm diagnosis, especially when endovascular treatment is being considered. 1
• Angiographic vasospasm occurs in 30-70% of patients, but only 50% develop clinical symptoms. 1, 2

Recommended Monitoring Algorithm

For alert patients with good neurological examination:

• Serial neurological examinations every 2-4 hours
• TCD monitoring with Lindegaard ratios
• CTA if TCD shows concerning trends or new deficits develop 1

For poor-grade or comatose patients:

• Continuous EEG monitoring 1
• Daily TCD with Lindegaard ratios 1, 3
• Consider invasive neuromonitoring (PbtO2, microdialysis) 1
• Low threshold for CTA/CTP when subtle examination changes occur 1

Key Clinical Context

Despite maximal therapy, 15-20% of patients suffer stroke or die from vasospasm, accounting for nearly 50% of deaths in patients surviving to treatment. 1, 2 DCI can occur without angiographic vasospasm in 3% of patients, and conversely, severe vasospasm may not produce symptoms in 50% of cases. 1, 2 This underscores why clinical vigilance combined with multimodal monitoring is essential rather than relying on any single diagnostic modality.