NEUROIMAGING
Contrast-induced encephalopathy (CIE)
Created 08/12/2021, last revision 01/01/2023
- contrast-induced encephalopathy (CIE) is a rare neurological complication that occurs during or after the use of a contrast medium in various angiographic procedures
- coronary angiography, diagnostic cerebral DSA, CAS, EVT in acute stroke patients (Chu, 2020)
- reported with the use of different contrast agents, but the hyperosmolar ones pose a higher risk (up to 4%)
- transient symptoms
- incidence 0.1-3% (Chu, 2020)
- good prognosis, spontaneous regression of symptoms (within 15 min – 5 days)
Etiopathogenesis of contrast-induced encephalopathy
- provoked by the intraarterial application of iodinated contrast agent
- not reported after IV administration
- the exact mechanism is not clear – probably, a combination of HEB disruption and direct neurotoxicity from the contrast medium results in altered neuronal excitability and dysfunction (Leong, 2012) (Yu, 2011)
- occipital lobes have increased HEB permeability; therefore, changes are most common here [Muruve, 1996]
- predisposing factors:
- hypertension
- nephropathy with reduced contrast agent clearance
- impaired cerebral autoregulation
- a large amount of contrast agent (usually > 100 ml)
- application into the vertebrobasilar territory (selective DSA)
- history of stroke (the previous stroke could disrupt the blood-brain barrier in the same or adjacent vascular territory, which facilitates leakage of the contrast medium into the broader cerebral territory and causes tissue reaction and cerebral edema)
Clinical presentation
- development during the endovascular procedure or within a few hours following intraarterial contrast agent administration
- focal symptoms or encephalopathy
- headache
- cortical blindness [Studdard, 1981]
- hemiparesis
- aphasia
- confusion
- epileptic seizures
- altered level of consciousness (LOC)
- transient global amnesia
- CIE should be suspected in acute stroke patients with clinical worsening, contrast staining, and edematous changes observed on imaging after EVT (particularly in patients with renal dysfunction or a history of stroke)
- regression occurs within 24h or a few days
Diagnostic evaluation
- NCCT+CTA/MRI+MRA to rule out thromboembolism or bleeding (especially after EVT in acute stroke patients)
- NCCT
- normal
- cortical or subcortical enhancement due to contrast leakage
- vasogenic edema with potential mass effect
- dual-energy CT can help to differentiate contrast staining from hemorrhage
- MRI shows cortical hyperintensities in T2, FLAIR, and DWI, but ADC is negative! (differentiation from ischemia)
- GRE or SWI can distinguish subtle hemorrhages from contrast staining
Differential diagnosis
- hemorrhagic transformation of ischemia or recurrent thromboembolism in acute stroke patients treated with EVT
- hyperperfusion syndrome / reperfusion syndrome
- subarachnoid hemorrhage
Management
- hydration with crystalloids
- symptomatic treatment (e.g., antiepileptic drugs, anxiety control, blood pressure control)
- there is a probable effect of corticosteroids [Chisci, 2011]
Prognosis
- complete recovery usually occurs within a few days
- permanent neurological deficits are uncommon