What is DCI (Delayed Cerebral Ischemia) in Neurology?

What is DCI in Neurology?

DCI (Delayed Cerebral Ischemia) is a delayed clinical deterioration occurring after aneurysmal subarachnoid hemorrhage (aSAH), defined as new focal or global neurological deficits or strokes after excluding other identifiable causes, representing a major complication that significantly impacts mortality and functional outcomes. 1

Definition and Nomenclature

The recommended terminology distinguishes between angiographic vasospasm (aVSP) and DCI. 1

• Angiographic vasospasm (aVSP) refers to the transient radiological narrowing of cerebral arteries visible on CT angiography, magnetic resonance angiography, or digital subtraction angiography 1
• DCI specifically describes the delayed clinical deterioration after excluding identifiable causes such as rebleeding, hydrocephalus, seizures, or metabolic derangements 1, 2

This distinction is critical because reducing vasospasm in multiple randomized controlled trials has not improved overall outcomes, indicating that DCI involves more than just arterial narrowing 1, 3

Pathophysiology

DCI has a multifactorial pathophysiology extending beyond simple vasospasm. 3, 4

Key mechanisms include:

• Cerebral vascular dysregulation affecting autoregulation 3
• Microthrombosis in the cerebral microvasculature 3
• Cortical spreading depolarizations propagating across brain tissue 3
• Neuroinflammation mediated by blood products in the subarachnoid space 2, 3
• Early brain injury (EBI) occurring within 72 hours of aSAH, which is now recognized as the main contributor to downstream mechanisms leading to DCI 4

Clinical Presentation and Timing

DCI typically occurs between days 4 and 10 after aSAH, affecting approximately 30% of patients who survive the initial hemorrhage. 2, 5

• The incidence is higher in high-grade patients (WFNS grade 4-5), who represent 40-70% of ruptured aneurysm patients 5
• Diagnosis is particularly challenging in comatose or sedated patients, where clinical examination is limited 5
• Physician disagreement regarding DCI diagnosis is high, which has significant implications for clinical studies and management 1

Diagnostic Approach

By definition, cerebral ischemia should be demonstrable in patients with DCI, though direct measurement is difficult. 1

Surrogate Markers

• Decreased cerebral perfusion to brain tissue that was previously well-perfused serves as the primary surrogate finding 1
• CT perfusion imaging has a pooled sensitivity of 0.84 and specificity of 0.77 for DCI diagnosis based on meta-analysis of 6 studies 1
• Transcranial Doppler ultrasonography, CT angiography, and CT perfusion may identify patients at high risk for developing DCI 2

Risk Prediction

The most important factors contributing to DCI risk are:

• Volume of subarachnoid hemorrhage 1
• Location of blood 1
• Density of blood on CT 1
• Clearance rate of subarachnoid and intraventricular hemorrhage 1

Several CT-based scales are available to estimate DCI risk, though areas of uncertainty remain regarding the magnitude and duration of neurological decline required for diagnosis 1

Clinical Significance

DCI is an independent predictor of unfavorable outcome and represents a significant cause of death and long-term disability after SAH. 1, 2

• Untreated DCI may result in strokes that account for substantial morbidity and mortality 2
• High-grade global cerebral edema after SAH (present in 29% of patients) is an independent predictor of both DCI and unfavorable outcome 1

Management Implications

The delayed onset of DCI permits initiation of prophylactic interventions before its development, though multiple pharmacologic agents (nicardipine, tirilazad, magnesium, simvastatin, clazosentan) have failed to improve outcomes in well-designed randomized controlled trials 1

If DCI develops, rescue therapies include:

• Induced hypertension with or without inotropic support as first-line treatment 1, 2, 6
• Intraarterial vasodilators (particularly calcium channel blockers and milrinone) for refractory cases 6
• Percutaneous transluminal balloon angioplasty for severe proximal vasospasm refractory to medical management 6

The only pharmacologic intervention with proven efficacy is nimodipine, a calcium channel antagonist 3