We present the case of a 33-year-old man who presented with ventricular fibrillation and cardiorespiratory arrest after taking ibuprofen.

HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION

Personal history
No known hypertension, diabetes mellitus or dyslipidaemia. Mental and behavioural disorder due to alcohol consumption, in remission. Mixed adaptive distress. Intrinsic rhinitis and bronchial asthma and history of atopy since childhood. Very doubtful drug allergy years ago, she does not remember to which drug, which has not been studied. No previous cardiological history. No chronic treatment.

Current illness
She came to the emergency department with an incised-contuse wound on the right forearm following an accident at work with an iron. The wound was treated locally, requiring suturing and bandaging. Gamma globulin and a first dose of tetanus vaccine were administered. On discharge a series of recommendations were given: treatment with ibuprofen 600 mg every 8 hours for 5-7 days in the presence of pain and amoxicillin-clavulanic acid 500-125 mg every 8 hours for 8 days.
In the evening, the patient, because of severe pain in the forearm, decided to take 1 tablet of ibuprofen. Thirty minutes after taking it, he began to feel nausea, vomiting, sweating and sudden dyspnoea, so his wife called 061. On arrival of the ambulance, the patient was pale and sweaty, suffering cardiorespiratory arrest in their presence, so they started CPR manoeuvres and performed an ECG which showed ventricular fibrillation. The patient was resuscitated for 75 minutes and required 5 defibrillations at 200 J, 450 mg intravenous amiodarone, 12 mg adrenaline, 1 M intravenous bicabonate and orotracheal intubation for mechanical ventilation. Referred to ICU for further care after recovery of pulse.

COMPLEMENTARY TESTS
061 electrocardiogram: ventricular fibrillation.
ICU blood tests: troponin T 21 ng/ml (normal up to 0.05 ng/ml), creatinine 1.47mg/dl, urea 42 mg/dl, sodium 140 mEq/l, potassium 4.1 mEq/l, glycaemia 159 mg/dl. Haemoglobin 17 g/dl, haematocrit 51%, leucocytes 16,000 10e3/ul, platelets 359,000 10e3/ul. PT ratio 1.1 (0.8-1.3), aPTT ratio 2 (0.8-1.3). Arterial blood gases (FiO2: 50 %): pH 7.30, PCO2 41, PO2 201, bicarbonate 19, lactate 4.2.
Electrocardiogram on admission to ICU: sinus rhythm at 78 bpm, PR < 200 ms, electrical axis deviated to the right. Wide QRS with image of complete right bundle branch block with secondary repolarisation alterations.
Chest X-ray in AP: cardiothoracic index not assessable. Free costophrenic and cardiophrenic sinuses. Right hilar slightly congestive. No parenchymal nodules or masses or pleural pathology.
Simple skull CT scan: findings compatible with significant diffuse cerebral oedema.
Echocardiogram: LV neither dilated nor hypertrophic, severe systolic dysfunction, global hypokinesia (probably secondary to stunning) and akinesia in the LAD territory.
Normal valves. No tricuspid insufficiency or indirect data of pulmonary hypertension. Normal atria. Normal RV. Severe systolic dysfunction of probable ischaemic origin in the LAD territory and stunning component.
Cardiac catheterisation: epicardial arteries without angiographically visible lesions.

EVOLUTION
On arrival at the ICU the patient was intubated, comatose with 3 points on the Glasgow scale. Pupils are mydriatic, reactive and symmetrical. The patient remains under hypothermia protocol at 34°C under sedation and connected to invasive mechanical ventilation. Anticoagulated at that time with enoxaparin and double anti-aggregation with ASA and clopidogrel in the presence of clinical suspicion of AMI.
The electrocardiogram showed the patient in sinus rhythm with a right bundle branch block which was not known to be present previously. An urgent CT scan of the brain showed significant cerebral oedema and an echocardiogram showed severe systolic dysfunction, alterations in contractility in the LAD territory and a stunning component. Given the results of the echocardiogram, cardiac catheterisation was performed, showing epicardial coronary arteries without lesions, and intensive care continued in the ICU.
The patient died two days later.
Given the relationship with the intake of NSAIDs and the symptoms suggesting a high probability of anaphylactic shock, the patient was finally classified as probable Kounis syndrome with a fatal outcome.

DIAGNOSIS
Out-of-hospital cardiorespiratory arrest in ventricular fibrillation, resuscitated.
Related to taking ibuprofen in a patient with a previous history of drug allergy and bronchial asthma.
Severe LV systolic dysfunction with segmental alteration in the LAD territory. Coronary arteries without angiographic lesions.
Presumptive diagnosis of Kounis syndrome type I.
