A 79-year-old male patient was admitted to the Respiratory Department of our hospital on August 15, 2022, because of fever, cough, sputum production and dyspnea after cold. On July 8, 2022, the patient underwent coronary angiography in the Cardiology Department of our hospital due to coronary artery disease, and a stent was implanted in the right coronary artery. The patient regularly took aspirin enteric-coated tablets, clopidogrel bisulfate tablets and atorvastatin calcium tablets. Other past medical conditions included hypertension, atrial fibrillation, and tuberculosis. The patient's allergic history included iodine (allergic reaction was local skin erythema papules) and "cephalosporins" (allergic reaction was urticaria in the limbs), but the patient had been repeatedly infused with cefazoxime, cefpilamine, ceftazidime and other drugs, no allergic reaction occurred. On the morning of August 23, 28 minutes after the injection of cefoperazone-sulbactam, the patient developed numbness in the extremities, chest tightness, palpitations, flushing of the skin in the extremities and body, progressive loss of consciousness, wheezing, sweating, and cyanosis of the lips. The bedside ECG monitor showed: heart rate of 80 beats per minute, with blood pressure and oxygen saturation being undetectable. The respiratory physician considered that the patient had developed severe anaphylactic shock. Then, them immediately stopped the suspicious fluid infusion, opened the airway, administered epinephrine 1 mg (again 1 mg after 5 minutes), with rapid infusion of sodium chloride injection 1,000 ml and methylprednisolone sodium succinate 40 mg. ICU physicians immediately established central venous access and tracheal intubation upon arrival, maintained blood pressure with norepinephrine and epinephrine, and assisted the patient's breathing with an invasive ventilator. The patient was then transferred to the ICU on advanced life support.
Her blood pressure on arrival at the ICU was 92/52 mmHg (at this point the norepinephrine and epinephrine doses were 1.25 and 0.83 mug/kg/min, respectively), but the patient was extremely hemodynamically unstable, and bedside cardiac ultrasound suggested poor cardiac contractile function and left ventricular ejection fraction only 25% (Figure 1). What's worse, the patient's norepinephrine dose was increased to 3.5 mug/kg/min, and ventricular fibrillation occurred frequently. The ICU physician immediately treated the patient with veno-arterial extracorporeal membrane oxygenation (V-A ECMO) and intra-aortic balloon pump (IABP). After admission to ICU, 18-lead electrocardiogram (ECG) showed a new left anterior fascicular block, the ST segment of lead I, aVL, V2-V6 depression 0.1-0.3 mV, and the ST segment of lead II, III, avF, V3R-V5R elevation 0.10-0.20 mV (Figure 2). Serum cardiac troponin I was 22.35 ng/mL (normal range 0-0.05). Upon completion of our consultation with the cardiologist, the patient was considered to have had an acute myocardial infarction, which required urgent percutaneous coronary angiography (the right coronary angiography results 1 months earlier was shown in Figure 3A). The results showed stent shadow in the proximal and middle segments of the right coronary artery, mild intimal hyperplasia in the stent, complete occlusion in the middle, and myocardial infarction (TIMI) flow of grade 0 (Figure 3B). Right coronary artery lesions were pretreated with 2.0 mm x 20 mm pre-dilated balloon and 3.0 mm x 10 mm open balloon, and then percutaneous transluminal coronary angioplasty was performed with 3.5 mm x 30 mm balloon into the stent. Re-angiography showed no stenosis in the right coronary stent and TIMI flow of grade 3 (Figure 3C). The patient was sent back to ICU after completion of surgery. By then, the postoperative ECG showed that ST-segment elevation of lead III and avF was 0.05-0.1 MV (Figure 4). Laboratory tests suggested a serum immunoglobulin E concentration of 290 IU/ml (normal range 0-165). The diagnosis of type III Kounis syndrome with cardiogenic shock was made, and the condition manifested as acute ST-segment elevation myocardial infarction caused by allergic stent thrombosis.
After from percutaneous coronary intervention, the patient continued to receive ECMO combined with IABP, norepinephrine, epinephrine and other drugs. However, the patient's heart function did not recover and he died seven days later. Cause of death: cardiogenic shock.