A 45-year-old hypertensive, hypothyroid (on 100 mcg thyroxine) female presented with fever and non-specific joint-ache and body-ache for 2 days, for which she took over the counter analgesic Nimesulide. Following the drug intake, she developed a generalized erythematous maculopapular rash associated with pruritis within 2–3 h, which started on the face and rapidly involved whole body. Within few hours she also developed facial puffiness and oral ulcers. It was associated with gradual development of hoarseness of voice simultaneously. Due to the worsening of symptoms, she visited a local hospital within 4 h of symptom onset. At admission there, she had blood pressure of 90/60 mm hg, heart rate of 112 per min, and temperature of 99°F and saturation of 88% on room air. Clinical Examination showed bilaterally symmetrical non-pitting peri-orbital swelling involving both upper and lower eyelids along with lip swelling and generalized erythema suggestive of angioedema She also had diffuse bilateral wheezing. She did not have any chest pain or shortness of breath. She was stabilized intravenous hydrocortisone 100 mg and diphenhydramine 50 mg and fluids, oxygen supplementation, and referred to our center.
On admission to our center on the same day, her blood pressure of 100/70 mm Hg, pulse rate was 100/minute. According to her attendant peri-orbital and generalized swelling and erythema were improved than before. We continued with steroid, antihistaminic, oxygen and other supportive measures. Routine blood examination revealed hemoglobin of 12.5, total leukoyte count of 8200 with eosinophil of 18%. Urea and creatinine were 98 mg/dL and 2.1 mg/dL most likely suggestive of pre-renal acute kidney injury due to hypotension.
Next day early morning, during ICU stay, her BP fell down to 80/50 for which norepinephrine had to be started. To reveal the cause of hypotension, electrocardiogram (ECG) was done, which showed new onset ST-segment elevation in V2–V6 (Fig. 1A, B). High sensitivity cardiac troponin T (hs-cTnT) and creatine kinase (CK-MB) were elevated to 25.3 ng/ml (normal: 0–0.4 ng/ml) and 254 ng/ml (normal: 0–4.3 ng/ml), respectively. Echocardiography showed regional wall motion abnormalities (RWMA) in left anterior descending (LAD) artery territory with an ejection fraction of 25%. A diagnosis of silent anterior wall myocardial infarction (AWMI) was made and she was started on dual antiplatelets, high-intensity statin, low molecular weight heparin (renal modified dosage) and was taken up for emergency angiography. Coronary angiography showed a complete cut off of the LAD with a heavy thrombotic burden and normal other coronaries (Fig. 2A–D). Percutaneous coronary intervention (PCI) was abandoned in view of high thrombus load and patient was started on Tirofiban infusion to decrease thrombus burden. Plan was to do a check angiography later after Tirofiban infusion. Repeat angiography showed 80% lesion in proximal LAD with some thrombus near it and thrombotic cut off of mid main diagonal branch (D1). Diagnosis of type 2 Kounis syndrome was made in view of allergic manifestations along with presence of ruptured or erosed coronary plague leading to thrombus formation resulting in acute MI. PCI to LAD was done with drug-eluting stent 3.5 × 38 mm and balloon angioplasty (POBA) was done to D1 successfully with thrombolysis in myocardial infarction 3 (TIMI 3) flow (Fig. 2E, F).
She subsequently developed worsening of acute kidney injury with elevated serum creatinine level up to 4 mg/dl most likely due to hypotension, which improved in a week to normal value. Immunological work was sent to rule out connective tissue disorders, which was negative. She improved symptomatically, her rash disappeared, and swelling subsided and was discharged on day ten with precautionary advice against the usage of nimesulide. The patient is under regular follow-up for the last 8 months and her ejection fraction improved to 55%.
