Contrast-Induced Encephalopathy Following Cerebral Angiography: A Case Report

Asploro Journal of Biomedical and Clinical Case Reports

ISSN: 2582-0370
Article Type: Case Report
DOI: 10.36502/2026/ASJBCCR.6449
Asp Biomed Clin Case Rep. 2026 Jun 04;9(2):102-106

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Shizhu Lin^1iD*
¹Department of Anesthesiology, West China Hospital, Sichuan University, Chengdu, Sichuan, China

Corresponding Author: Shizhu Lin ^ORCiD
Address: Department of Anesthesiology, West China Hospital, Sichuan University, No. 37, Guoxue Valley, Wuhou District, Chengdu 610041, Sichuan Province, China.
Received date: 09 May 2026; Accepted date: 28 May 2026; Published date: 04 June 2026

Citation: Lin S. Contrast-Induced Encephalopathy Following Cerebral Angiography: A Case Report. Asp Biomed Clin Case Rep. 2026 Jun 04;9(2):102-106.

Copyright © 2026 Lin S. This is an open-access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium provided the original work is properly cited.

Keywords: Contrast-Induced Encephalopathy, Cerebral Angiography, Local Anesthesia

Abstract

Background: Contrast-induced encephalopathy is a rare but potentially serious neurological complication that occurs after intra-arterial injection of iodinated contrast media. It may manifest as acute encephalopathy, seizures, cortical blindness, hemiplegia, or other focal neurological deficits.
Case Presentation: A 46-year-old female developed right-sided limb weakness and language dysfunction during transfer after endovascular treatment of an intracranial aneurysm. After comprehensive management, the patient recovered uneventfully and was discharged without residual neurological deficits.
Conclusion: Contrast-induced encephalopathy is a potential complication following cerebral angiography. Anesthesiologists should remain vigilant regarding postoperative neurological events even in procedures performed under local anesthesia and should actively participate in multidisciplinary collaborative management.

Introduction

Contrast-induced encephalopathy (CIE) is a rare but potentially serious neurological complication that occurs following intra-arterial injection of iodinated contrast media, particularly during neurovascular and coronary interventions [1]. Clinically, it may present as acute encephalopathy, seizures, cortical blindness, hemiplegia, or other focal neurological deficits, often mimicking acute cerebrovascular syndromes such as ischemic stroke or subarachnoid hemorrhage [2]. The reported incidence of CIE ranges from 0.3% to 2%, making it an uncommon clinical condition [3].

From a pathophysiological perspective, CIE is associated with direct neurotoxicity, disruption of the blood-brain barrier, and endothelial dysfunction. Hypertension, diabetes mellitus, renal failure, high contrast volume, and male sex have been identified as potential risk factors. In most cases, symptoms resolve spontaneously and completely within 24-72 hours. Repeated administration of contrast agents should be avoided whenever possible. Although CIE is rare and potentially underdiagnosed, and despite its generally favorable prognosis in most patients [4], heightened clinical vigilance remains essential.

Case Presentation

A 46-year-old female patient presented to the hospital for a follow-up examination after undergoing endovascular intervention for an intracranial aneurysm. Four months prior, she had undergone “Pipeline flow diverter implantation + coil embolization + superselective artery angiography + cerebral angiography of the right internal carotid artery C6/C7 segment aneurysm” under general anesthesia. Intraoperative findings included: a right internal carotid artery C6 segment aneurysm measuring approximately 4.11 × 3.04 mm with a neck width of approximately 3.45 mm; a right internal carotid artery C7 segment blister aneurysm measuring approximately 2.28 × 2.26 mm; and a left internal carotid artery C6 segment aneurysm measuring approximately 1.63 × 1.37 mm (Fig-1).

Fig-1

During the current admission, after completing relevant preoperative evaluations, the patient was scheduled to undergo cerebral angiography under local anesthesia. Preoperative diagnoses included: (1) post-embolization follow-up of right internal carotid artery C6/C7 segment aneurysms; (2) left internal carotid artery C6 segment aneurysm; (3) recovery phase of cerebral hemorrhage; and (4) hyperthyroidism.

Routine disinfection, draping, and local anesthesia were performed. After successful puncture of the right femoral artery, a 5F vascular sheath was inserted, and carotid angiography was performed. Findings revealed post-embolization changes of the right internal carotid artery C6/C7 segment aneurysms with a patent parent artery and no evidence of recurrence; a small left internal carotid artery C6 segment aneurysm; and no significant abnormalities in the bilateral anterior cerebral arteries or bilateral middle cerebral arteries. Vertebral artery angiography showed no significant abnormalities in the bilateral vertebral arteries, basilar artery, or bilateral posterior cerebral arteries.

In the parenchymal phase, no abnormal contrast enhancement timing was observed. In the venous phase, all venous sinuses showed unobstructed drainage with no significant abnormalities. At the end of the procedure, compression bandaging was applied to the puncture site.

During transfer from the procedure table, the patient reported significant dizziness, followed immediately by slurred speech and right-sided limb weakness. Contrast-induced encephalopathy or stroke could not be ruled out. Therefore, an immediate left femoral artery puncture was performed with insertion of a 5F vascular sheath for angiography, which revealed no significant abnormalities (Fig-2). Intravenous dexamethasone sodium chloride injection and intra-arterial tirofiban were administered. The patient’s language function improved compared with the acute event. Continuous intravenous tirofiban infusion was subsequently administered. At the end of the procedure, compression bandaging was applied to the puncture site, and the patient was returned to the ward in stable condition for monitoring.

Fig-2:

On the first postoperative day, the patient’s general condition was significantly improved compared with the previous day. She responded coherently with clear speech and exhibited normal right-sided limb movement. Vital signs were stable. Pupils were bilaterally equal and round, approximately 3 mm in diameter, with prompt light reflexes. The neck was supple. Muscle strength was normal in all four extremities. Slight oozing was noted at the right groin puncture site without subcutaneous hematoma, and dorsalis pedis artery pulses were normal.

On the second postoperative day, the patient remained in generally good condition with no specific complaints. Vital signs were stable. Pupils were bilaterally equal and round, approximately 3 mm in diameter, with prompt light reflexes. The neck was supple. Muscle strength was normal in all four extremities. Slight oozing persisted at the right groin puncture site without subcutaneous hematoma, and dorsalis pedis artery pulses were normal. The patient was subsequently discharged uneventfully.

Discussion

This case report describes a 46-year-old female patient with a history of post-aneurysm intervention who developed dizziness, slurred speech, and right-sided limb weakness following cerebral angiography performed under local anesthesia. Based on the findings of emergency cerebral angiography and the clinical presentation, contrast-induced encephalopathy (CIE) was considered the most likely diagnosis.

The vast majority of CIE cases reported in the literature occur during neurointerventional procedures performed under general anesthesia or deep sedation, during which patients are unable to report early visual or sensory abnormalities, and the condition is often only detected upon emergence from anesthesia. The distinctive feature of this case is that the procedure was completed under local anesthesia, during which the patient remained awake and communicative throughout. At the time of transfer from the procedure table following angiography, the patient first reported dizziness, slurred speech, and right-sided limb weakness. This real-time symptom reporting in the awake state provides valuable first-hand clinical data regarding the early time window of CIE. Furthermore, local anesthesia eliminated the potential confounding effects of general anesthetics, such as propofol and sevoflurane, on the blood-brain barrier, neuronal excitability, and consciousness, thereby establishing a clearer causal relationship between contrast exposure and the clinical symptoms.

The mechanisms of CIE primarily include contrast-induced disruption of the blood-brain barrier, direct neuronal toxicity, and secondary vasospasm [5]. Under general anesthesia, anesthetic agents may modify the clinical presentation or course of CIE by influencing cerebral blood flow, metabolism, or blood-brain barrier permeability. In the present case, the patient received only local anesthesia, which excluded these confounding factors, suggesting that the clinical manifestations more directly reflected the neurotoxic effects of the contrast agent itself. Thus, this case provides a purer clinical observation of the natural course of CIE.

During cerebral angiography under local anesthesia, the anesthesiologist’s primary responsibilities include maintaining appropriate sedation, ensuring hemodynamic stability, and assisting in the management of intraprocedural complications. In this case, when the patient developed symptoms of CIE post-procedure, including dizziness, slurred speech, and right-sided limb weakness, the anesthesiologist promptly recognized this acute neurological event and assisted the neurointerventionalist in performing a rapid bedside assessment, thereby avoiding misdiagnosis as contrast allergy, over-sedation, or cardiogenic disease. This process highlights that even under local anesthesia, anesthesiologists should maintain a high level of vigilance for postoperative neurological complications.

When altered consciousness or neurological deficits occur following cerebral angiography under local anesthesia, the differential diagnosis is broader than that under general anesthesia [6]. Specific considerations include local anesthetic toxicity, manifesting as perioral numbness, tinnitus, and altered consciousness, as well as over-sedation if midazolam or fentanyl has been administered. In this case, the intraoperative lidocaine dose was 0.1 g, well below the toxic threshold, and the timing of symptom onset did not coincide with the peak concentration of the local anesthetic. Therefore, local anesthetic toxicity could be excluded. After cerebral angiography ruled out cerebral infarction and hemorrhage, combined with the self-limited nature of the symptoms and imaging features, a final diagnosis of CIE was established.

Conclusion

This case report provides a detailed description, from the perspective of an anesthesiologist, of the complete clinical course of contrast-induced encephalopathy following cerebral angiography performed under local anesthesia. The awake state during local anesthesia offers a unique opportunity to observe the natural course of CIE while eliminating the confounding effects of general anesthetics. This case suggests that anesthesiologists should maintain a high level of vigilance for postoperative neurological complications even during procedures performed under local anesthesia and should actively participate in multidisciplinary collaborative management.