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)

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

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

hemorrhagic transformation of ischemia or recurrent thromboembolism in acute stroke patients treated with EVT
hyperperfusion syndrome / reperfusion syndrome
subarachnoid hemorrhage

hydration with crystalloids
symptomatic treatment (e.g., antiepileptic drugs, anxiety control, blood pressure control)
there is a probable effect of corticosteroids [Chisci, 2011]