CIE is a rare adverse effect taking place after procedures applying iodinated contrast media, which is predominantly associated with endovascular intervention or diagnostic imaging directly involving the cerebral circulation [11,12,13,14], and relatively less common during coronary angiography [15,16,17]. Different types (high-/ low-osmolality, ionic or nonionic) and dosages of contrast media can lead to CIE in patients with or without cardiovascular risk factors [5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22,23,24,25,26,27]. CIE has received less attention than other complications caused by contrast media [5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22,23,24,25,26,27]. Furthermore, there is a lack of consensus on the definition of CIE. Currently, the understanding of CIE is that it is an acute reversible encephalopathy induced by contrast media and occurred within minutes to hours after the procedure. The risk factors may include advanced age, male sex, hypertension, renal failure, impaired cerebral autoregulation and transient ischemic attack, but no single factor can explain all cases [7, 16]. In addition, the exact pathophysiology of CIE remains undetermined. Osmotic disruption of the blood–brain barrier, resulting in cerebral edema and neurologic dysfunction is considered to be the likely mechanism, while arterial vasospasm and disruption of the microcirculation of an already impaired cerebral auto-regulatory system is also seemed to lead to this condition [19]. Our patient, a 66-year-old man had a history of hypertension, which may impair cerebral autoregulation and increase the risk of CIE.

Since CIE appears to be in a critical condition after rapid onset, it is challenging to make the diagnosis of CIE prospectively and exclude other neurological complications following cardiac catheterization, including hypoxic-ischemic encephalopathy (HIE) after malignant arrhythmia, hemorrhagic and ischemic stroke, epilepsy, metabolic abnormalities and drug effects [6, 10]. With regards to symptomatology of CIE, transient cortical blindness is the most common manifestation. In addition, other heterogenic symptoms are all reported in previous cases, including focal neurological deficits such as visual disturbances, aphasia, motor and sensory deficits, as well as generalized syndromes such as loss of consciousness and seizures [6, 10]. Neuropathological signs may or may not appear in CIE, which are lack of specific differential diagnostic value. However, detailed past history such as cerebral vascular disease, epilepsy, cardiac arrhythmia, metabolic disease and allergy, is very important in the diagnosis and differential diagnosis when neurologic symptoms appeared following cardiac catheterization. Furthermore, if patients lose consciousness and/or suffer from seizures after cardiac angiography or intervention, cardiogenic shock should be firstly considered. In this condition, a 12-lead ECG and ambulatory ECG monitoring play an important role in differentiating Adams-Stokes syndrome caused by malignant arrhythmia. If new ischemic ST/T changes occurred in ECG, acute coronary syndrome is indicated and emergency coronary angiography should be conducted to evaluate coronary arteries. Moreover, ultrasonic cardiogram and chest X-ray are crucial in differentiating cardiac tamponade as well as acute heart failure. In case unconsciousness and seizures can’t be explained by hypoxic-ischemic encephalopathy following cardiogenic shock, cerebrovascular complications including cerebral ischemia and hemorrhage, which could be identified by brain CT or magnetic resonance imaging (MRI), should be considered then. In few patients with difficulty in differential diagnosis with brain CT or MRI, cerebral angiography can adequately exclude hemorrhagic and ischemic stroke. Patients of epilepsy usually have a history of recurrent seizures. Although metabolic encephalopathy has a low incidence, it should also be thought about in patients with critical metabolic disturbances. Additionally, for patients developing new-onset focal neurologic symptoms, cerebrovascular complications are the most common cause and cerebral imaging is preferred (Fig. 3).

Flow diagram of differential diagnosis and clinical decision making of contrast-induced encephalopathy following cardiac catheterization. ECG: electrocardiogram; eCAG: emergency coronary angiography; ACS: acute coronary syndrome; UCG: ultrasonic cardiogram; HF: heart failure; LVEF: left ventricular ejection fraction; AHF: acute heart failure; CT: computed tomography; MRI: magnetic resonance imagining; CIE: contrast-induced encephalopathy

It has been reported that majority of CIE patients have a good prognosis with neuropathological symptoms, signs and neuroimaging findings complete resolution within 48–72 h [6, 18,19,20]. Thus, if other common neurological complications have been excluded and symptoms of neurological dysfunction fully recover within 72 h, CIE should be taken into account. In addition, although neuroimaging findings in CIE may be normal or mimic cerebral hemorrhage or ischemia, they help in the differential diagnosis. A characteristic finding on non-contrast CT scan of the brain is cortical or subcortical contrast enhancement, with or without cerebrovascular contrast agent retention in corresponding areas [14, 15]. Characteristic findings on MRI of the brain consist of hyperintense signals on T2, DWI and FLAIR modalities in the affected regions.

Due to the low prevalence and varied manifestation, CIE has no formal diagnostic criteria, so does treatment protocol. However, the disorder is self-limiting, treatment is mainly supportive therapy, consisting of intravenous hydration and close observation. Other therapeutic agents used include anticonvulsants, mannitol, corticosteroids, and diuretics, which is focused on complications of CIE rather than the disorder itself [5, 6, 10,11,12,13,14,15,16,17,18,19,20,21,22,23,24,25,26,27].