IMAGING METHODS

Contrast-induced encephalopathy (CIE)

Created 08/12/2021, last revision 17/09/2022

  • 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)

Etiopathognesis of contrast-induced encephalopathy

  • provoked by the intraarterial application of iodinated contrast agent
    • not reported after I.V. 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
  • 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 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 possible 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 MR-SWI can differentiate contrast staining from subtle hemorrhage

Differential diagnosis

  • hemorrhagic transformation of ischemia or recurrent thromboembolism in acute stroke patients treated with EVT
  • hyperperfusion syndrome  or 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 not common