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. 2023 Jan 4;16:1070357. doi: 10.3389/fncel.2022.1070357

Contrast-induced encephalopathy and permanent neurological deficit following cerebral angiography: A case report and review of the literature

Yujing Zhang 1,2,†, Jiancheng Zhang 1,2,†, Shiying Yuan 1,2,*, Huaqing Shu 1,2,*
PMCID: PMC9847581  PMID: 36687520

Abstract

Contrast-induced encephalopathy (CIE) is an uncommon complication associated with contrast exposure during angiographic procedures that is usually transient but occasionally leads to permanent complications or death. Due to the low incidence of CIE, there are still insufficient reports. This study was used to summarize the clinical features of CIE through a case report and systematic review. We summarized and reviewed 127 patients with CIE, and we found that the total incidence of CIE between men and women had no difference (49.61 and 50.39%, respectively), but the average age in female patients with CIE was older than that in male patients (62.19 and 58.77 years, respectively). Interestingly, the incidence of female patients with CIE in the poor prognosis group was significantly higher than that in the good prognosis group (62.50 and 36.51%, respectively), and the average age of these female patients in the poor prognosis group was younger than that in the good prognosis group (61.39 and 62.82 years, respectively). The contrast medium types were mainly nonionic (79.69 and 73.02%, respectively) and low-osmolar (54.69 and 71.43%, respectively) in both groups. Importantly, the total contrast media administrated in patients with poor prognoses was greater than that administrated in patients with good prognoses (198.07 and 188.60 ml, respectively). In addition, comorbidities in both groups included hypertension (55.91%), diabetes mellitus (20.47%), previous contrast history (15.75%), renal impairment (11.81%), and hyperlipidemia (3.15%). The percentage of patients with cerebral angiography was significantly higher in the poor prognosis group than that in the good prognosis group (37.50 and 9.52%, respectively), whereas the percentage of patients with coronary angiography in both groups had the opposite results (35.94 and 77.78%, respectively). In conclusion, CIE may not always have a benign outcome and can cause permanent deficits. Female gender, younger age, the higher dose of contrast medium, and the procedure of cerebral angiography may be related to the patient’s poor prognosis.

Keywords: cerebral angiography, contrast-induced encephalopathy, neurological deficit, prognosis, risk factor

Introduction

Contrast-induced encephalopathy (CIE) is an uncommon complication associated with intravenous or intra-arterial exposure to iodinated contrast media during angiographic procedures. The incidence of CIE ranges between 0.3 and 4.0% (de Bono, 1993; Potsi et al., 2012; Liu et al., 2020). Since the first description in 1970, the clinical features of CIE have included headache, memory loss, confusion, visual and speech impairment, seizures, hemiparesis, and even coma. The underlying mechanisms and causes of iodine-based CIE remain unclear. Studies suggest that this may be related to transient blood–brain barrier (BBB) breakdown and increased permeability, which may subsequently contribute to extravasation of contrast medium into the central nervous system, resulting in cerebral edema and altered neuronal excitability (Dangas et al., 2001; Babalova et al., 2021). In addition, some high concentrations of contrast media may cause the clumping of red blood cells and, consequently, occlusion of arterial branches, which may play a role in permanent neurological deficits (Cristaldi et al., 2021). Most patients with CIE have a good prognosis and resolve quickly within 1–2 days (Spina et al., 2017). A minority (approximately 15% of CIE) may develop permanent neurological deficits or fatal cerebral edema (Hamra et al., 2017; Donepudi and Trottier, 2018; Zhao et al., 2019). However, the development of an evidence-based consensus on CIE has been hindered by the low incidence of CIE. Although the current literature on CIE is extensive, only case reports in the literature describe CIE and further analyses on the risk factors of CIE prognosis have been rarely performed. Here, we provided a case report as a reference and summarized existing reports about CIE, aiming to explore pathogenesis, risk factors, diagnosis, treatment strategy, and future exploration direction of the disease.

Case report

A 51-year-old woman was admitted to our hospital with a suspected intracranial aneurysm. The patient had a history of hypertension. On admission, a physical examination showed no signs of neurological deficits. Cerebral angiography was urgently performed through the right femoral approach. The procedure lasted for 60 min. A total of 50 ml iodixanol (Jiangsu Hengrui Pharmaceutical Co., Ltd., China), an iso-osmolar non-ionic dimeric hydrophilic contrast medium, was injected. Notably, 1% lignocaine was administered for local anesthesia prior to cerebral angiography. This was the patient’s first exposure to a contrast medium, and no obvious aneurysm or vascular malformation was found.

Approximately 5 h after surgical completion, the patient developed a decrease in the upper and lower extremity motor strength, and the pupils were symmetric and reactive. The left muscle strength was grade 2, and the right muscle strength was grade 3. An emergency brain computed tomography (CT) scan was requested and revealed the diffuse contrast enhancement in brain sulci, fissures, cisterns, third ventricle, fourth ventricle, and subarachnoid space with mild global brain edema, and softening foci in the left basal ganglia-insular area (Figures 1A,B). On the second day, the patient’s clinical symptoms further deteriorated and the upper and lower muscle strength was grade 0 with positive pathological signs. Brain CT was reviewed and showed diffuse enhancement disappeared, but the brain parenchyma was diffusely swollen and the lateral ventricles were slightly more compressed than that in the previous scan (Figures 1C,D). A diagnosis of CIE was suspected given the worsening of the clinical manifestations and symptoms compatible with higher functional impairment following the administration of the contrast medium.

FIGURE 1.

FIGURE 1

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Contrast-induced encephalopathy in brain computed tomography (CT) scans. (A,B) Emergency brain CT 5 h after the procedure showed diffuse contrast enhancement in the brain parenchyma and subarachnoid space with mild global brain edema and the softening foci in the left basal ganglia-insular area. (C,D) Brain CT 2 days after the procedure indicated diffuse enhancement disappeared, and the brain parenchyma was diffusely swollen and the lateral ventricle was slightly more compressed.

The patient routinely received fluids to accelerate the excretion of contrast medium, 1,000 mg of intravenous methylprednisolone once daily for 2 days to mitigate inflammation, 250 ml of mannitol every 8 h to dehydrate and reduce intracranial pressure, 10 mg of nimodipine once daily to prevent vasospasm, 120 mg of sodium valproate once daily to prevent epilepsy, as well as strengthen nutrition to improve clinical symptoms. Furthermore, lumbar cistern drainage was performed to reduce intracranial pressure, and cerebrospinal fluid (CSF) was clear with increased white blood cell count and glucose level and decreased chloride level. In the following hours, the patient experienced further deterioration in mental status and fell into a coma with respiratory insufficiency. Therefore, the patient was transferred to the intensive care unit (ICU) where she underwent tracheal intubation with ventilator-assisted breathing, dehydration, anti-epileptic therapy, body temperature and blood pressure control, and close neurological observation.

On the second day after being admitted to the ICU, the patient regained consciousness, but her motor deficit was unchanged. A neurological examination showed muscle weakness in the upper and lower limbs and sensory loss below the T2 sensory level, which may be related to spinal cord edema. Considering that the patient was temporarily unable to remove the tracheal tube, a tracheotomy was performed 4 days later. A magnetic resonance imaging (MRI) performed at 2 weeks revealed a diffuse hyperintense signal on FLAIR sequences in the cervical cord, which may be consistent with the patient’s motor deficits and sensory disturbances, as well as a softening foci formation in the left basal ganglia-insular area (Figure 2). Dramatically, the patient suffered from a lung infection during hospitalization and was eventually discharged from the neurosurgery ward to another hospital for hyperbaric oxygen therapy after 20 days. A telephone follow-up after 2 months revealed that the patient’s persistent neurological deficits had not improved.

FIGURE 2.

FIGURE 2

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The brain and cervical spine magnetic resonance imaging (MRI) performed at 2 weeks. (A,B) Brain MRI showed the left basal ganglia-insular softening foci in T1 (A) and T2 (B) weighted image. (C–E) Cervical spine MRI showed diffuse hyperintense signal in the cervical cord in T2-weighted image (D) and fluid-attenuated inversion recovery (FLAIR) images (E), and normal findings were observed in T1-weighted image (C).

Literature review

In searching for the keywords “Contrast-induced encephalopathy” and “Angiography” in PubMed, 95 relevant articles were found. A total of 54 papers were selected after screening abstracts and titles. After reading through the whole paper, the reviews, editorial, and duplicate cases were excluded, and 40 papers were left. However, four of them were excluded because it was defined as allergic reactions, vasospasm, and posterior reversible encephalopathy syndrome, and complete data were not available in the other six papers. Finally, we accurately summarized 30 papers (Leong and Fanning, 2012; Yan and Ramanathan, 2013; Kocabay et al., 2014; Nagamine et al., 2014; Hamra et al., 2017; Park et al., 2017; Spina et al., 2017; Dattani et al., 2018; Heemelaar et al., 2018; Hirata et al., 2018; Kahyaoğlu et al., 2018; Tong et al., 2018; Renault and Rouchet, 2019; Riahi et al., 2019; Şimşek et al., 2019; Zhao et al., 2019, 2021; Fernando et al., 2020; Harada et al., 2020; Lei et al., 2020; Liu et al., 2020; Andone et al., 2021; Cristaldi et al., 2021; García-Pérez et al., 2021; Kamimura et al., 2021; Li et al., 2021; Vigano et al., 2021; Yao et al., 2021; Zhang et al., 2021; Rashid et al., 2022). A total of 127 patients were enrolled. Figure 3 shows the screening process. Table 1 shows the basic information of 31 studies (including our case).

FIGURE 3.

FIGURE 3

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Screening process.

TABLE 1.

Basic information of all patients.

Study Number Gender/Age (year) Procedure Risk factor Previous angio-
graphy		 Contrast medium Contrast medium class Volume (ml) Presentation Neuroimaging Symptom duration Complete resolution
Andone et al., 2021 1 M/70 Diagnostic coronary angiography HT, DM No Ioversol Non-ionic, monomer, low osmolar 100 Headache, behavioral changes and aggressive tendencies CT: a mild hyper-density in the frontal lobes;
MRI: normal		 72 h Yes
Dattani et al., 2018 2 M/76 Coronary angiography HT, DM No Iohexol Non-ionic, monomer,
low osmolar		 120 Confused and aggressive, expressing verbal profanities CT: normal 9 days Yes
3 M/65 Diagnostic coronary angiography Previous CIE, HT, Dyslipidaemia, Smoking. Yes Iopromide Non-ionic, monomer,
low osmolar		 110 Global aphasia, bilateral limb weakness CT and MRI: normal; 24 h Yes
4 M/49 Coronary angiography – – Iopromide Non-ionic, monomer,
low osmolar		 205 Confusion, decreased GCS – 12 h Yes
5 M/32 Coronary angiography – – Iopromide Non-ionic, monomer,
low osmolar		 100 Cortical blindness CT: normal 24 h Yes
6 F/39 Coronary angiography – No Iopamidol Non-ionic,monomer, low osmolar 100 Cortical blindness CT: normal 1 h Yes
7 M/74 Coronary angiography + aortogram HT, Obse No Iomeprol Non-ionic, monomer,
low osmolar		 320 Cortical blindness CT: normal 24 h Yes
8 M/73 Coronary angiography + PCI Sleep apnea, Hypoventilation, Obese – None reported N/A 240 Cortical blindness CT: normal 7 h Yes
9 M/53 Coronary angiography – – Ioversol Non-ionic, monomer,
low osmolar		 100 Cortical blindness, catatonia – 12 h Yes
10 M/45 Coronary angiography + PCI HT No Ioversol Non-ionic, monomer,
low osmolar		 167 Cortical blindness – 24 h Yes
11 M/59 Coronary angiography + PCI HT No Ioversol Non-ionic, monomer,
low osmolar		 220 Cortical blindness – 12 h Yes
12 M/68 Coronary angiography + PCI HT No Ioversol Non-ionic, monomer,
low osmolar		 262 Homonymous hemianopia – 15 min Yes
13 M/55 Coronary angiography – Yes Diatrizoate Ionic, monomer,
high osmolar		 280 Cortical blindness CT: both occipital lobes enhancement 24 h Yes
14 M/61 Coronary angiography – Yes Diatrizoate Ionic, monomer,
high osmolar		 145 Cortical blindness CT: normal 36 h Yes
15 M/44 Coronary angiography – No Diatrizoate Ionic, monomer,
high osmolar		 50 Cortical blindness No brain CT 12 h Yes
Kamimura et al., 2021 16 F/70 Diagnostic erebral angiography Not reported No Iopamidol Non-ionic, monomer,
low osmolar		 43 Confusion and generalized tonic-clonic seizures CT: high-density signaling in the cortex;
MRI: high signal intensity in temporal lobe		 24 h Yes
17 M/71 Cerebral angiography Not reported No Iohexol Non-ionic, monomer,
low osmolar		 46 Cortical blindness, confusion, and Ophthalomoplegia No brain CT 10 days N/A
18 F/68 Cerebral angiography Not reported No Iohexol Non-ionic, monomer,
low osmolar		 24 Cortical blindness, confusion, and amnesia No brain CT 6 days N/A
19 F/71 Cerebral angiography HT, Transient ischemic attack No Iopromide Non-ionic, monomer,
low osmolar		 25 Confusion, disorientation, and hemiparesis CT: edema, right diffuse cortical hyperattenuation 24 h Yes
Fernando et al., 2020 20 F/52 Coronary angiography HT N/A Iopromide Non-ionic, monomer,
low osmolar		 130 Left sided hemiparesis, disorientation, and decreased GCS CT: cortical and subarachnoid
hyper-densities		 5day Yes
Cristaldi et al., 2021 21 F/54 Cerebral angiography HT,
Cerebral ischemia		 N/A Iobitridol Non-ionic, monomer,
low osmolar		 Not reported Severe right hemiparesis and complete aphasia CT: edema, abnormal subarachnoid contrast enhancement zone >6 months No
22 M/10 Angiocardio-
graphy		 Fallot’s tetralogy Not stated Urografin
76%		 Ionic, monomer,
high osmolar		 76 Apnoea and cardiac arrest No CT brain (autopsy showed brain edema) During Death
23 F/7 Aortography HT No Renografin
76%		 Ionic, monomer,
high osmolar		 340 Seizures CT: contrast enhancement of cortex, basal ganglia and thalamus During Death
24 M/68 Bypass graft angiography HT, DM Yes Iohexol Non-ionic, monomer,
low osmolar		 180 Confusion, amnesia, aphasia, cortical blindness CT: contrast enhancement of occipital lobes, temporal lobes, thalami During No
25 F/73 Coronary angiography HT No Iohexol Non-ionic, monomer,
low osmolar		 1150 Seizures, gait instability, postural tremor, dysphasia CT: abnormal signal in bilateral frontal and occipital During No
26 F/62 Cerebral angiography None reported No Not specified Non-ionic 297 Confusion, cortical blindness CT: abnormal signal in bilateral occipital, basal ganglia, frontal During No
27 M/41 Cerebral angiography None reported Yes Not specified Non-ionic 225 Bilateral visual loss, agitation CT: right parietal abnormal signal 3 h No
28 F/54 Cerebral angiography None reported Yes Not specified Non-ionic 62 Cortical blindness with only light perception MRI: bilateral occipital 1 months Yes
29 M/46 Cerebral angiography None reported Yes Not specified Non-ionic 225 Right homonymous hemianopia CT and MRI: normal 1 months Yes
30 M/47 Cerebral angiography None reported No Not specified Non-ionic 384 Right homonymous hemianopia CT: normal 7 days Yes
31 F/67 Coronary angiography Angina, DM, HT – Iodixanol Non-ionic, dimer,
iso-osmolal		 Not reported Gradually GCS 3 N/A During Yes
32 F/71 Cerebral angiography HT, hyperlipidemia, Angina – Iopamidol Non-ionic, monomer,
low osmolar		 110 Dizziness, nausea, vomiting; then respiratory distress, deep coma, GCS 3 CT: cerebral edema 56 days Death
33 F/51 Carotid artery angioplasty HT, DM,
Coronary artery disease		 – Iohexol Non-ionic, monomer,
low osmolar		 Not reported Seizures, unconsciousness N/A During Death
Spina et al., 2017 34 F/44 Diagnostic coronary angiography + PCI End-stage kidney disease, HT, DM – Iohexol Non-ionic, monomer,
low osmolar		 190 Left-sided weakness, seizure activity CT: contrast enhancement of right cerebral hemisphere 72 h Yes
35 M/69 Diagnostic coronary angiography + PCI HT, DM – Not reported N/A N/A Aphasia, left-sided hemiparesis CT: contrast enhancement of right cerebral hemisphere 12 h Yes
36 F/63 Diagnostic coronary angiography HT, DM – Iopramide Non-ionic, low osmolar 250 Cortical blindness CT: contrast enhancement of occipital lobes; MRI: normal 72 h Yes
37 F/60 Diagnostic coronary angiography HT – Not reported N/A N/A Abrupt decrease in GCS score to 6/15 CT: cerebral edema confined to the right cerebral hemisphere;
MRI: normal		 10 days Yes
38 F/76 Diagnostic coronary angiography HT, DM – Ioversol Non-ionic, monomer,
low osmolar		 125 Aphasia, cortical blindness, right sided weakness MRI: hyperintensity in
frontoparietal regions		 48 h Yes
39 F/69 Diagnostic coronary angiography + PCI CKD, DM, Previous
contrast reaction		 Yes Iodixanol Non–ionic, dimer,
iso-osmolal		 320 Partial seizure, homonymous hemianopia, hemisensory loss, hemiparesis CT: cerebral edema 24 h Yes
40 M/64 Diagnostic coronary angiography + PCI HT, DM – Iopromide Non-ionic, monomer,
low osmolar		 160 Confusion, irritability, limb paralysis, aphasia CT: hyperdensity of
sagittal sinus		 28 h Yes
41 M/68 Diagnostic coronary angiography + PCI HT – Iopromide Non-ionic, monomer,
low osmolar		 250 Left lower extremity weakness and sensory loss
 CT: contrast enhancement in
sagittal sinus and
occipital lobe		 12 h Yes
42 M/47 Diagnostic coronary angiography + PCI None reported – Iopromide Non-ionic, monomer,
low osmolar		 150 Confusion, agitation, nausea, headache CT: contrast enhancement in right occipital lobe 8 h Yes
43 M/70 Diagnostic coronary angiography + PCI DM – Iopromide Non-ionic, monomer,
low osmolar		 120 Confusion; nausea CT: contrast enhancement in occipital lobe 12 h Yes
44 F/76 PCI + carotid artery stenting CKD, DM – Iodixanol Non-ionic, dimer,
iso-osmolal		 200 Stupor, aphasia, hemiparesis CT: hyperdensity of cerebral sulci and subarachnoid spaces 48 h Yes
45 F/39 Diagnostic coronary angiography – – Iopamidol Non-ionic, monomer,
low osmolar		 80 Cortical blindness CT and vertebral angiogram: normal 1 h Yes
46 F/70 Diagnostic coronary angiography + PCI – – None reported N/A N/A Left-sided hemiparesis, conjugate gaze deviation to the right CT: hyperdensity of cerebral sulci and right frontal lobe 72 h Yes
47 F/70 Diagnostic coronary angiography + PCI – – Not specified Ionic 1500 Myoclonus CT: hyperdensity of cerebral sulci <1 h Yes
48 F/52 Diagnostic coronary angiography – – Iomeprol Non-ionic, monomer,
low osmolar		 150 Cortical blindness CT: contrast enhancement of occipital lobes 5 h Yes
49 F/70 Diagnostic coronary angiography DM, HT – Iobitridol Non-ionic, monomer,
low osmolar		 75 Cortical blindness CT: contrast enhancement of occipital lobes 72 h Yes
50 M/56 Diagnostic coronary angiography – – Iopromide Non-ionic, monomer,
low osmolar		 135 Confusion, dysarthria, cortical blindness CT: contrast enhancement of right occipital lobe 24 h Yes
51 F/82 Diagnostic coronary angiography + PCI CKD, HT – Iomeprol Non-ionic, monomer,
low osmolar		 500 Aphasia, right-sided hemiparesis CT: hyperdensities filling
the sulci of both cerebral
hemispheres		 40 h Yes
52 M/82 Diagnostic coronary angiography CKD, DM, HT – Iopromide Non-ionic, monomer,
low osmolar		 150 Right-sided hemiparesis, aphasia CT: Left hemisphere cerebral edema and extravascular local contrast media 6 h Yes
53 M/63 Diagnostic coronary angiography + Aortogram – – Iopremol Non-ionic, monomers 450 Amnesia, numbness, right upper extremity numbness CT: contrast enhancement of right occipital lobe 12 h Yes
54 F/63 Diagnostic coronary angiography DM, HT – Iopromide Non-ionic, monomer,
low osmolar		 160 Cortical blindness, right homonymous hemianopia CT and MRI: contrast
enhancement of occipital lobes		 48 h Yes
55 F/52 Diagnostic coronary angiography + PCI HT Yes Ioversol Non-ionic, monomer,
low osmolar		 280 Cortical blindness CT: contrast enhancement of occipital lobes 36 h Yes
56 M/55 Diagnostic coronary angiography – – Iomeprol Non-ionic, monomer,
low osmolar		 280 Cortical blindness CT: contrast enhancement of occipital lobes 5 days Yes
57 M/58 Diagnostic coronary angiography HT – Ioglaxate Ionic, dimer,
low osmolar		 260 Cortical blindness CT: normal 32 h Yes
58 M/64 Diagnostic coronary angiography – – Ioglaxate Ionic, dimer,
low osmolar		 400 Cortical blindness N/A 30 h Yes
59 M/49 Diagnostic coronary angiography CKD, HT – Diatrizoate Ionic, monomer,
high osmolar		 610 Seizures, encephalopathy CT: contrast enhancement of left frontal gyri 4 h Yes
60 M/62 Diagnostic coronary angiography + PCI CKD, HT – Iopamidol Non-ionic, monomer,
low osmolar		 170 Headache, confusion, cortical blindness CT: contrast enhancement of cerebellum, thalamus 12 h Yes
61 M/62 Diagnostic coronary angiography HT – Iopamidol Non-ionic, monomer,
low osmolar		 270 Cortical blindness, loss of coordination right arm CT: contrast enhancement of occipital lobes 72 h Yes
62 F/57 Diagnostic coronary angiography HT, Previous
contrast reaction		 Yes Ioglaxate Ionic, dimer,
low osmolar		 200 Cortical blindness CT: mild attenuation in
occipital poles		 48 h Yes
63 F/52 Diagnostic coronary angiography + aortogram HT – Diatrizoate Ionic, monomer,
high osmolar		 100 Cortical blindness N/A 18 h Yes
Hamra et al., 2017 64 M/62 Coronary angioplasty HT – Iohexol Non-ionic, monomer,
low osmolar		 200 Right-sided homonymous hemianopia CT: contrast enhancement of the venous sinuses and
cerebral arteries		 48 h Yes
Vigano et al., 2021 65 F/56 Cerebral angiography Migraine, Renal colic, Smoking, Previous heroin abuse – Iomeprol Non-ionic, monomer,
low osmolar		 70 Global aphasia and right hemiplegia CT: left cerebral edema 10 days Yes
66 F/74 Abdominal aorta and renal artery angiography + angioplasty Renal impairment; HT No Diatrizoate Ionic, monomer,
high osmolar		 250 Cortical blindness, left hemiparesis CT: bilateral occipital and basal ganglia alterations 4–5 days Yes
67 M/64 Carotid artery and aorta angiography HT No Iothalamate meglumine Ionic, monomer,
high osmolar		 12 Cortical blindness, fluent aphasia CT: left temporo-parieto-occipital alterations 3 days N/A
68 F/71 Spinal angiography – No Ioxaglate Ionic dimer
low osmolar		 360 Right-sided visual neglect and Wernicke’s aphasia CT: bilateral occipital and left parietal lobe alterations 4 days Yes
69 M/82 Carotid artery angiography + stenting HT Yes Ioxaglate Ionic, dimer,
low osmolar		 50 Confusion, left hemiparesis, neglect CT: right frontoparietal cortical enhancement and edema 2 days Yes
70 M/72 Carotid artery angiography + coiling anterior aneurysm – No Iopamidol Non-ionic, monomer,
low osmolar		 260 Right hemiparesis and motor aphasia CT: enhancement throughout the left cerebral cortex and left basal ganglia, diffuse swelling of the left cerebral hemisphere 7 days Yes
71 M/80 Carotid and coronary angiography + stenting HT No Iohexol Non-ionic, monomer,
low osmolar		 250 Right hemiparesis CT: left frontoparietal-occipital cortical enhancement 2 days Yes
72 M/51 Carotid artery angiography + right internal carotid artery HT No Iopromide Non-ionic, monomer,
low osmolar		 300 Gerstmann’s left visual field deficit, hemiparesis, right gaze deviation CT: cortical enhancement and edema in the right cerebral hemisphere 2 days Yes
73 M/69 Coronary angiography + PCI – – Iohexol Non-ionic, monomer,
low osmolar		 100 Stupor, disorientation, left hemiplegia CT: hyperdense lesion in the right frontoparietal region, parietal lobe and basal ganglia 6 h Yes
74 F/73 Aortic angiography + thoracic aortic aneurysm repair Chronic kidney disease; HT Yes Iodixanol Non-ionic, dimer,
iso-osmolal		 248 Seizure and left-sided hemiplegia CT: hyperdensity of the right cortex, subarachnoid space and basal ganglia 7 days N/A
75 F/67 Cerebral angiography HT Yes N/A N/A N/A Right-sided hemiparesis and aphasia CT: cortical edema of the left cerebral hemisphere and contrast medium leakage to the subarachnoid space 24 h N/A
Liu et al., 2020 76 F/84 Coronary angiography HT, Paroxysmal atrial fibrillation, Chronic bronchitis – Iopromide Non-ionic, monomer,
low osmolar		 20 Lost consciousness, and exhibited left limb hemiplegia with muscle strength level 0 and eyes staring to the right, seizure CT: high-density regions in the subarachnoid space 2 months Yes
77 F/57 Diagnostic coronary angiography + PCI CKD, HT, DM – Iodixanol Non-ionic, dimer, iso-osmolal 130 Tonic–clonic seizures CT: right parenchymal edema 72 h Yes
78 M/6 Diagnostic coronary angiography HT, DM – Iohexol Non-ionic, monomer, low osmolar 120 Confused, aggressive, expressing verbal profanities CT: normal 9 days Yes
79 M/62 Diagnostic coronary angiographyc + PCI HT – Iohexol Non-ionic, monomer, low osmolar 300 Right-sided homonymous hemianopia CT: slight enhancement of
the venous sinuses		 48 h Yes
80 M/49 Diagnostic coronary angiography – – Iopromide Non-ionic, monomer,
low osmolar		 205 Confusion, decrease in level of consciousness CT and MRI: normal 12 h Yes
81 M/69 Diagnostic coronary angiography + PCI – – Iohexol Non-ionic, monomer, low osmolar 100 Confusion, headache, vomiting, left hemiplegia, CT: focal hyperdense lesions 6 h Yes
82 M/74 Diagnostic coronary angiography + aortogram – Iomeprol Non-ionic, monomer, low osmolar 320 Cortical blindness CT: normal 24 h Yes
Riahi et al., 2019 83 F/71 Coronary angiography HT, DM – Iodixanol Non-ionic, dimer, iso-osmolal 80 Aphasia, GCS score to 7/15 CT: normal 24 h Yes
Rashid et al., 2022 84 F/76 Coronary angiography DM, HT, Hyperlipidemia, Coronary artery disease – N/A N/A N/A Confusion and aggressive behavior CT and MRI: normal 16 days Yes
Zhang et al., 2021 85 M/42 Coronary angiography – – Iopromide Non-ionic, monomer,
low osmolar		 200 Severe headache, cortical blindness and neuropsychiatric symptom CT: normal 5 days Yes
Park et al., 2017 86 F/58 Cerebral angiography HT, Hypothyroidism, Peripheral artery occlusive disease, Depressive disorder – Iodixanol Non-ionic, dimer, iso-osmolal 220 Tonic-clonic seizure, left hemiparesis involving face, arm and leg(grade 3/5), sensory loss, and left-sided neglect with drowsy mentality CT:sulcal obliteration of right cerebral hemisphere;
MRI: gyral swelling and hyperintensity in the right cerebral hemisphere		 6 days Yes
Kocabay et al., 2014 87 F/58 Diagnostic coronary angiography + PCI HT, Hyperlipidemia – Iopromide Non-ionic, monomer,
low osmolar		 220 Bilateral oculomotor
ophthalmoplegia		 N/A >30 days No
88 M/68 Diagnostic coronary angiography + PCI HT – Iopromide Non-ionic, monomer, low osmolar 250 Monoplegia N/A 12 h Yes
89 M/68 Diagnostic coronary angiography + PCI HT, DM – Iopromide Non-ionic, monomer, low osmolar 180 Unilateral oculomotor
monoplegia		 N/A 1 h Yes
90 M/70 Diagnostic coronary angiography + PCI HT – Iopromide Non-ionic, monomer, low osmolar 130 Cerebellar dysfunction N/A 14 h Yes
Kahyaoğlu et al., 2018 91 M/66 Lower extremity angiography – – Iohexol Non-ionic, monomer, low osmolar Not reported Confusion and cortical blindness, seizure CT: normal 24 h Yes
Zhao et al., 2019 92 F/71 Digital subtraction angiography HT, Hyperlipemia, Angina – Iopamidol Non-ionic, monomer, low osmolar 110 Headache, dizziness, nausea and vomiting, deep coma CT: cerebral edema 56 days Death
Li et al., 2021 93 F/77 Digital subtraction angiography HT, Coronary heart disease Yes Visipaque Non-ionic 200 Right hemiplegia, aphasia, and epilepsy CT: hyperdensity in the left subarachnoid space 6 days Yes
Zhao et al., 2021 94 F/50 Cerebral angiography – – Iopromide Non-ionic, monomer,
low osmolar		 6 Disturbance of consciousness, seizures, frequent blinking, and stiffness CT: normal;
MRI: swelling of the left cerebral cortex		 10 days Yes
Heemelaar et al., 2018 95 F/67 Coronary angiography DM, HT, Adenocarcinoma of the left breast – Iso-osmolar iodinated contrast Iso-osmolar 100 Acute-onset coma and respiratory insufficiency CT: bilateral cerebral edema 23 days Yes
García-Pérez et al., 2021 96 F/61 Diagnostic digital subtraction angiography Migraine – Iodixanol Non-ionic, dimer, iso-osmolar 70 Confused and drowsy, agitated and vomiting MRI: lesions in the cerebellar hemispheres and parieto-occipital lobes; 36–48 h Yes
97 M/22 Diagnostic digital subtraction angiography Left parietooccipital arteriovenous malformation – None reported N/A None reported Disoriented, bilateral amaurosis and presented amnesia CT and MRI: normal 48–72 h Yes
Harada et al., 2020 98 F/72 Coronary angioplasty HT, Hyperlipidemia – Iodinated contrast None reported 210 Left hemiparesis, left sensory and visual hemineglect, and right gaze preference CT: mild cerebral edema 2 days Yes
Renault and Rouchet, 2019 99 M/49 Renal artery angiography Chronic renal failure – Iohexol Non-ionic, monomer, low osmolar Cortical blindness, global amnesia disappeared MRI: normal 6 days Yes
Hirata et al., 2018 100 M/75 Coronary angioplasty DM – None reported N/A None reported No neurological symptoms were observed because the patient was intubated CT: high-density areas in the cortex, putamen, caudate
nucleus and subarachnoid space of the right cerebral hemisphere		 12 days Yes
Yao et al., 2021 101 M/68 Contrast-enhanced chest CT examination Rheumatoid arthritis – Iso-osmolar iodinated contrast Iso-osmolar 70 Lost consciousness and experienced cardiorespiratory arrest CT: abnormal cortical contrast enhancement and cerebral
sulci hyperdensity		 >17days Yes
Leong and Fanning, 2012 102 F/50 Cerebral angiography HT No Iopramide Non-ionic, low osmolar 220 Right hemisyndrome CT: edema in the left cerebral hemisphere During No
103 F/59 Aortic arch angiography Renal impairment; HT Yes Diatrizoate Ionic, monomer,
high osmolar		 150 Cortical blindness; headache, myoclonus or seizure CT: bilateral parieto-occipital contrast enhancement 3 days Yes
104 F/53 Carotid artery angiography Not reported No Diatrizoate
meglumine		 Ionic, monomer,
high osmolar		 60 Partial motor seizure CT: right temporo-parietal contrast enhancement 24 h Yes
105 M/70 Arch, Carotid & Vertebral arteries angiography None reported No Diatrizoate Ionic, monomer,
high osmolar		 72 Cortical blindness CT: bilateral
Occipital hyperdensity		 2 days Yes
106 F/74 Abdominal aorta angiography HT, Renal impairment No Iopamidol Non-ionic, monomer, low osmolar 415 Visuospatial disorder CT: bilateral parieto-occipital hyperdensity 4 days Yes
107 F/74 Diagnostic cerebral angiography HT No Iohexol Non-ionic, monomer, low osmolar None reported Complete bilateral blindness; confusion CT: left parieto-occipital
hyperdensity;
MRI: left occipita hyperdensity		 24 h Yes
108 F/45 Diagnostic cerebral angiography HT No Iohexol Non-ionic, monomer, low osmolar None reported Complete bilateral blindness; confusion CT: normal;
MRI: bilateral occipital hyperdensity		 7 days Yes
109 F/73 Diagnostic cerebral angiography HT No Iohexol Non-ionic, monomer, low osmolar None reported Cortical blindness CT: normal;
MRI: bilateral occipita hyperdensity		 5 days Yes
110 F/70 Coronary artery angiography HT Yes None reported N/A 1500 Seizure CT: hyperdensity of right frontal 24 h Yes
111 M/56 Coronary artery None reported Yes Iohexol 350 Non-ionic, monomer, low osmolar 220 Bilateral cortical blindness CT: high-density areas in the bilateral occipital and
frontal lobes		 4 days Yes
Nagamine et al., 2014 112 F/58 Cerebral angiography Unknown N/A Iohexol Non-ionic, monomer, low osmolar – Agraphia, right hemiparesis N/A >20 days No
Tong et al., 2018 113 F/64 Diagnostic cerebral angiography HT No ioversol Non-ionic, monomer, low osmolar 300 Lateral blindness MRI: normal 6 days Yes
114 M/53 Diagnostic cerebral angiography HT Yes Omnipaque Non-ionic, monomer, high osmolar 155 Lateral blindness CT: bilateral brain edema on frontal and occipital lobe 5 days Yes
115 F/61 Diagnostic cerebral angiography HT – Omnipaque Non-ionic, monomer, high osmolar 10 Lateral blindness MRI: right occipital cerebellar infarction 3 months Yes
116 M/58 Carotid artery + vertebral artery angiography – Yes Iopromide Non-ionic, monomer,
low osmolar		 350 Cortical blindness CT: cortical hyperdensity and vasogenic edema 10 days Yes
117 M/57 Vertebral artery angiography – Yes Omnipaque Non-ionic, monomer, high osmolar 20 Bilateral cortical blindness CT: normal;
MRI: abnormal bilateral parieto-occipital lobes		 24 h Yes
Lei et al., 2020 118 M/76 Coronary angiography HT, DM, Transient ischemic attacks Yes Iodixanol Non-ionic, dimer, iso-osmolar 150 Epileptic seizures N/A 6 months Yes
Yan and Ramanathan, 2013 119 M/63 Cerebral angiogram HT, DM, Rheumatoid arthritis, End-stage renal disease – Iodixano Non-ionic, dimer, iso-osmolar 910 Left-sided blindness and ophthalmoplegia CT: bilateral subarachnoid hyper-attenuation over the cerebral sulci, and diffuse cerebral edema 72 h Yes
120 F/58 Cerebral arteriogram – – Iodixanol Non-ionic, dimer, iso-osmolar 193 Left hemiparesis CT: hyperdensity of right frontoparietal lobe 4 days Yes
121 F/61 Cerebral arteriogram – – Iodixanol Non-ionic, dimer, iso-osmolar 212 Left hemiparesis CT: hyperdensity of right frontoparietal lobe 3 days Yes
122 F/58 Transfemoral cerebral angiography – – Ioversol Non-ionic, monomer, low osmolar N/A Global aphasia,
right sided hemiparesis		 CT: abnormal enhancement in left cerebral cortex and thalamus 3 days Yes
123 F/63 Right middle cerebral angiography – – Iopromide Non-ionic, monomer,
low osmolar		 150 N/A CT: diffuse subarachnoid
hyperdensity		 2 days Yes
124 M/16 Angiography of the circle of Willis – – Iopromide Non-ionic, monomer,
low osmolar		 50 Cortical blindness CT: occipital lobe hyperdensity 24 h Yes
125 F/69 Coronary angioplasty – – Iopamidol 370 Non-ionic, monomer, low osmolar 260 Seizure, right hemiparesis. CT: left cerebral cortex,
left basal ganglia hyperdensity		 18 h Yes
Şimşek et al., 2019 126 M/68 Coronary angiography HT, DM, Coronary artery disease, Severe renal impairment No Iohexol Non-ionic, monomer, low osmolar 230 seizure CT: hyperdense fields at the vertex and at the right frontal lobe 60 h Yes
Our case 127 F/51 Cerebral angiography HT No Iodixanol Non-ionic, dimer, iso-osmolal 50 Dyskinesia, coma CT:the diffuse hyperdensity in brain sulci, fissures, cisterns, third ventricle, fourth ventricle and subarachnoid space, and global brain edema >3 months No
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From the search results, we found that the total incidence of CIE between women and men has no difference. A total of 63/127 (49.61%) patients were women and 64/127 (50.39%) patients were men, and the average age in women was older than that in men (62.19 and 58.77 years, respectively). More importantly, we classified the statistical results according to prognosis, and patients who recovered less than or equal to 48 h were included in the good prognosis group and the remaining patients were included in the poor prognosis group. Eventually, 63 patients were included in the good prognosis group and 64 patients were included in the poor prognosis group, and the results are shown in Table 2. We found that the incidence of female patients with CIE in the poor prognosis group was significantly higher than that in the good prognosis group (62.50 and 36.51%, respectively), and the average age of these female patients in the poor prognosis group was younger than that in the good prognosis group (61.39 and 62.82 years, respectively). Furthermore, the poor prognosis group had a wider age range, ranging from 6 to 84 years.

TABLE 2.

The relationship between prognosis with variable.

≤2 days (n = 63) >2 days (n = 64)
Gender
Female (%) 23 (36.51) 40 (62.50)
Male (%) 40 (63.49) 24 (37.50)
Age (year) 62.82 ± 1.41 61.39 ± 1.45
Contrast types
Non-ionic (%) 46 (73.02) 51 (79.69)
Ionic (%) 12 (19.05) 6 (9.38)
Low-osmolar (%) 45 (71.43) 35 (54.69)
High-osmolar (%) 8 (12.70) 7 (10.94)
Iso-osmolal (%) 4 (6.35) 11 (17.19)
Contrast doses (ml) 188.60 ± 13.99 198.07 ± 14.23
Non-ionic (ml) 193.39 ± 15.59 199.19 ± 14.73
Ionic (ml) 167.70 ± 37.91 235.20 ± 54.49
Low-osmolar (ml) 195.10 ± 16.18 207.83 ± 19.85
High-osmolar (ml) 117.83 ± 35.31 194.20 ± 45.73
Iso-osmolal (ml) 167.50 ± 58.79 152.56 ± 23.40
Comorbidities
Hypertension (%) 32 (50.79) 39 (60.93)
Diabetes mellitus (%) 10 (15.78) 16 (25.00)
History of angiography (%) 9 (14.29) + 1 11 (17.19)
Renal impairment (%) 6 (9.52) 9 (14.06)
Dyslipidaemia (%) 2 (3.17) 3 (4.69)
Angiography types
Coronary angiography (%) 49 (77.78) 23 (35.94)
Cerebral angiography (%) 6 (9.52) 24 (37.50)
Carotid and vertebral angiography (%) 6 (9.52) 4 (6.25)
Abnormal CT or MRI (%) 40 (63.49) 44 (68.75)
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In interventional procedures, the contrast types included non-ionic and ionic, or low-osmolar, high-osmolar, and iso-osmolar in our present study, and we found that both groups were mainly non-ionic (79.69 and 73.02%, respectively) and low-osmolar (54.69 and 71.43%, respectively). Importantly, the total contrast media administrated and the non-ionic, ionic, low-osmolar, or high-osmolar contrast media administrated in patients with poor prognosis were greater than that administrated in patients with good prognosis (198.07 and 188.60 ml, 199.19 and 193.39 ml, 235.20 and 167.70 ml, 207.83 and 195.10 ml, and 194.20 and 117.83 ml, respectively), whereas the iso-osmolar contrast media administrated was lower in patients with poor prognosis compared to patients with good prognosis (152.56 and 167.50, respectively).

The comorbidities in the present study mainly included hypertension (55.91%), diabetes mellitus (20.47%), previous contrast history (15.75%), renal impairment (11.81%), and hyperlipidemia (3.15%). Although there was no significant difference in comorbidities between the two groups, the percentages of hypertension, diabetes mellitus, previous contrast history, renal impairment, and hyperlipidemia in the poor prognosis group were higher than those in the good prognosis group (60.93 and 50.79%, 25.00 and 15.78%, 17.19 and 4.29%, 14.06 and 9.52%, and 4.69 and 3.17%, respectively). The angiography types, mainly coronary angiography (56.69%), cerebral angiography (23.62%), and carotid and vertebral angiography (7.87%), in both groups, were also analyzed. We found that the percentage of patients with cerebral angiography in the poor prognosis group was significantly higher than that in the good prognosis group (37.50 and 9.52%, respectively), whereas the percentage of patients with coronary angiography in both groups had the opposite results (35.94 and 77.78%, respectively). Moreover, brain CT or MRI abnormalities were found in most patients in both groups (68.83 and 62.00%, respectively).

Discussion

Contrast-induced encephalopathy is a rare and reversible complication that can cause neurotoxicity with a favorable prognosis and resolves within 24–48 h in most cases. Based on previous studies (Yan and Ramanathan, 2013; Spina et al., 2017; Cristaldi et al., 2021), the renal elimination of contrast medium, the regression of cerebral edema, and the recovery of BBB function were assumed to play an important role in the pathophysiology of neurological recovery. Here, we described a case of permanent neurological deficit after cerebral angiography and provided a summary and analysis of a series of CIE cases to explore the probable reasons for permanent neurological deficit. Given that most patients resolved completely within 48 h, we performed a prognostic analysis using 48 h as the node. We found that the total incidence of CIE between female patients and male patients had no difference, but female patients were more likely to have a poor prognosis. In addition, the average age of patients with poor prognoses was younger than that of patients with good prognoses. Surprisingly, no reports are currently available on risk factors associated with prognosis in patients with CIE. Only two reports were found to analyze the relationship between the incidence of CIE and gender or age, and the conclusions of the two reports were inconsistent. One report found that the adverse drug reaction incidence of iodinated contrast medium (e.g., CIE) seemed to be associated with gender, with a significantly higher incidence in female patients than in male patients, and it was also associated with age, with a lower occurrence in older (>44 years) patients compared to younger patients (Jiang et al., 2021). The other report summarized 9 CIE cases in 2013 and proposed that male gender and advanced age are the greatest risk factors for developing CIE. These two reports just provide a reference for us, and further research and a more in-depth analysis are necessary.

Studies showed a correlation between contrast medium dose and CIE (Yu and Dangas, 2011; Vigano et al., 2021), and whether the more contrast medium used is related to the poor prognosis of patients has not been directly reported. Although our study showed that the patients with poor prognosis used more contrast medium among different types of contrast media, including the non-ionic, ionic, low-osmolar, and high-osmolar contrast media, as well as the total contrast media used, the results are not absolute. Because in our reported case and 4 other summarized cases, the patient presented with permanent neurological deficits (more than 10 days) after administrating only a low quantity of contrast medium (no more than 50 ml) for angiography. Among these cases, the contrast medium types included non-ionic, low-osmolar, high- osmolar, and iso-osmolar, suggesting that severe neurotoxic symptoms may occur in response to low doses and different types of contrast agents. A previous study has shown that a 49-year-old man developed CIE and completely resolved within 4 h after receiving 610 ml diatrizoate (an ionic high-osmolar contrast medium) for diagnostic coronary angiography (Muruve and Steinman, 1996), indicating that high-dose contrast media do not cause permanent neurological dysfunction. Therefore, we speculated that, in addition to volume, the poor prognosis is generally related to the route and number of administrated, type of contrast medium, and individual patient characteristics.

Previous research has shown that demographic risk factors for CIE are chronic hypertension, diabetes mellitus, renal insufficiency, and previous reactions to contrast media (Yu and Dangas, 2011; Zhao et al., 2019; Cristaldi et al., 2021). Our study showed that the majority of patients (55.91%) had hypertension, 20.47% had diabetes mellitus, 15.75% had a contrast history, and 11.81% had renal insufficiency. Although there is no statistical difference between the poor prognosis group and the good prognosis group, these risk factors have a higher proportion in patients with poor prognosis, suggesting they may be related to worse prognosis, and further research is needed by increasing the sample size.

For the types of angiographic procedures, the present study showed that the proportion of patients with cerebral angiography was significantly higher in the poor-prognosis group than in the good-prognosis group, whereas patients with coronary angiography had the opposite results. Whether the cerebral angiography procedure itself is more likely to aggravate the prognosis than coronary angiography is unclear. This study demonstrated that 170 ml is recommended as the maximum threshold level of toxicity for coronary angiography procedure, and a smaller volume of contrast media may damage the BBB during selective intracranial injection (Kocabay et al., 2014), suggesting that cerebral angiography may be more likely to damage the BBB than coronary angiography. Furthermore, it is unclear whether procedure-related factors and patient-related factors are involved.

The diagnosis of CIE often requires the exclusion of cerebrovascular accidents such as cerebral hemorrhage and cerebral infarction. Neuroimaging plays an important role in distinguishing CIE from other neurological pathologies such as thromboembolism and hemorrhage following angiography. Our research showed that the most common abnormalities on brain CT included cortical or subcortical contrast enhancement, cerebral edema, focal hyperdense lesions, and hyper-density in the cerebral sulci. MRI abnormalities included hyperintensity on T2, FLAIR, and DWI. This study has suggested that CSF examination is also useful to rule out subarachnoid hemorrhage through the absence of xanthochromia or red blood cells (Shahan et al., 2021). The simultaneous detection of high concentrations of iodinated contrast medium in CSF and serum supports contrast medium extravasation rather than hemorrhage. In addition, the exclusion of contrast allergy or allergic-like reactions is also essential for the diagnosis of CIE. A recent study showed that allergic-like or allergic reactions caused by contrast media are rare, which can be severe or even life-threatening (Fusco et al., 2022). It is important to obtain a history of immediate or delayed reactions to a specific contrast medium, which may contribute to predicting the risk for future reactions. Clinical manifestations such as throat tightness, facial edema, and bronchospasm are helpful in distinguishing.

For the treatment of CIE, most patients with CIE have a good prognosis and a rapid recovery. Therefore, supportive care and observation are generally considered sufficient. Based on the literature summarized in the present study, it is recommended that appropriate hydration, steroids, and mannitol can be given immediately after surgery, and benzodiazepines can be used for epileptic seizures.

Conclusion

A contrast-induced encephalopathy is a form of neurotoxicity caused by contrast media that is usually transient but occasionally leads to permanent complications or death. We summarized a series of cases and found that the female gender, younger age, higher contrast medium dose, and cerebral angiography procedure were associated with poor prognosis in patients with CIE. However, the contrast medium types were not associated with the prognosis. In addition, there was no statistical difference between the poor prognosis group and the good prognosis group; hypertension, diabetes mellitus, renal insufficiency, and previous reactions to contrast media were also important risk factors for CIE. Our case and literature review highlight that CIE may not always have a benign outcome and has the potential to cause permanent neurological dysfunction, even with low-dose contrast media. We should not be overlooked, especially following procedures that use contrast medium.

Author contributions

YZ wrote the manuscript. JZ analyzed the data. HS and SY critically revised and edited the manuscript. All authors discussed the content and read and approved the final version.

Funding

This study was supported by the National Key Research and Development Program of China (2021YFC2501800) and the National Key Research and Development Program of China (2021YFC2501804).

Conflict of interest

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Publisher’s note

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

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