A 65-year-old female was admitted to our hospital in February 2023 due to “persistent headache for six months” and CTA revealed multiple intracranial aneurysms. Subsequently, a digital subtraction angiography (DSA) was performed to identify an aneurysm at the terminal bifurcation of the left middle cerebral artery (M1 segment), left posterior communicating artery aneurysm, left ophthalmic artery aneurysm, right posterior communicating artery aneurysm, and right ophthalmic artery aneurysm. During the injection of Iohexol, a rash appeared on the skin, which quickly resolved with antiallergic treatment. The patient reported no discomfort upon discharge. In April 2023, the patient returned for treatment of the right posterior communicating artery aneurysm and ophthalmic artery aneurysm. And no hypersensitivity reaction occurred with iodixanol injection during the operation. A month ago, she was readmitted for reexamination of the embolization status of the aneurysms. During the cerebral angiography procedure, approximately 25 mL of iodixanol (Yangtze River pharmaceutical group, Batch No: 23070461) was injected through a 5F Pigtail catheter for angiography of aortic arch. After completing the aortic arch angiography, a 5F VER 135° single-curve catheter was used for cervical-vertebral angiography. Approximately 3 mins after the injection of iodixanol into the ascending aorta through the 5F single-curve catheter via the femoral artery sheath, the patient experienced dizziness, increased heart rate (HR 120 bpm), followed by hypotension (BP 90/43 mm Hg), a sudden drop-in heart rate (HR 68 bpm), and SpO2 decreased to 92%. Intravenous dexamethasone (10 mg) was immediately administered for antiallergic treatment, oxygen therapy via a mask for oxygen-inhalation, accelerated fluid infusion and other anti-shock treatment measures. However, the patient subsequently experienced tics of the limbs, foaming in the mouth and unresponsiveness, emergency administration of intravenous diazepam (5 mg) for sedation, and aspiration of sputum to maintain airway patency. At this point, the blood pressure continued to drop to 53/29 mm Hg, and no SpO2 reading was detected. Intravenous drip saline was accelerated, and dopamine 20 mg was administered to increase the blood pressure. Endotracheal intubation and mechanical ventilation were initiated to assist breathing. After ~3 mins, no blood pressure readings were obtained, and intermittent intravenous boluses of epinephrine (1 mg) were administered immediately to raise the blood pressure (total of 4 mg). The blood pressure gradually recovered to 126/90 mm Hg, and SpO2 gradually increased to 95%. However, the patient had a Glasgow Coma Scale (GCS) score of 3, bilateral dilated pupils with a diameter of approximately 5 mm, no light responsiveness, and no reaction to painful stimuli was observed. The patient was urgently transferred to the NICU for further monitoring and treatment. The patient remained in a deep coma state with bilateral fixed dilated pupils measuring approximately 5 mm. Spontaneous breathing was not observed, and cardiopulmonary resuscitation was initiated to actively revive the patient’s heartbeat. However, there was still no spontaneous breathing observed (the concentration of K+ dropped to 2.8 mol/L). After continuing with antiallergic, anti-shock, and correction of internal environmental disturbances, the patient was transferred to the Intensive Care Unit (ICU) for further treatment. After being transfer to the ICU, the patient remained in a deep coma state with bilateral dilated pupils measuring approximately 3.5 mm. She had a delayed response to light reflex and shallow breathing. The patient was supported with ventilator (FiO2, 90%) to maintain SpO2 above 90%. Blood pressure and heart rate were relatively stable after intravenous of norepinephrine (10 mg) and epinephrine (2 mg), with HR was 102 bpm and BP was 108/63 mm Hg. Continuous mild hypothermic brain protection therapy was administered. The patient experienced extensive subcutaneous bleeding in the lower limbs, coarse breath sounds in the lungs, dull heart sounds in the apex, absent bowel sounds, low muscle tone in the limbs, and no lower limb edema. Analysis of arterial gas indicated: pH 7.38, PCO2 20.63 mmHg, PO2 86.71 mmHg, K+ 5.04 mmol/L, Na+ 155 mmol/L, Ca2+ 0.84 mmol/L, Lac 17.60 mmol/L. Coagulation tests showed: INR 1.75, PT 19.40 s, Fbg 0.78 g/L, TT 87.60 s, APTT 55.90 s (Key values of coagulation tests can be found in ). The patient had abnormal coagulation function and received plasma to correct coagulation, the posterior pituitary (36U/50 mL) and carbazochrome sodium sulfonate (80 mg/250 mL) for hemostasis, omeprazole (80 mg/250 mL) to suppress acid, antiallergic and anti-shock treatment, and correction of internal environment disturbances. Laboratory evaluations revealed the white blood cell count of 19.01×10^9/L, with 94.9% being neutrophils, and TNT-HSST was 2210.00 ng/L (Changes in white blood cells and neutrophil percentages can be found in ). The alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) levels were 317 U/L (normal 7~40 U/L), 562 U/L (normal 13~35 U/L), and 1788 U/L (normal 109~245 U/L), respectively. IL-6 was 9168.38 pg/mL and procalcitonin (PCT) level was 49.71 ng/mL, prompting timely continuous renal replacement therapy (CRRT). Afterwards, the patient’s condition deteriorated further (PH 6.9, K+ 6.72 mmol/L, AST 953 U/L, ALT 1580 U/L, SCR 350 μmol/L), with loss of light reflex and no response to painful stimuli in the limbs. And the patient’s severe metabolic acidosis, persistent hyperlactacidemia, and severe internal environmental disturbances could not be corrected, leading to continuous deterioration (key indicators of blood gas analysis, electrolyte levels, and liver and kidney function tests are shown in ). Finally, the patient was declared dead due to rescue invalid as a result of anaphylactic shock, disseminated intravascular coagulation, and multiple organ dysfunction.