Alcohol withdrawal-induced Takotsubo.

A 57-year-old lady presented to the hospital for an elective right thoracotomy and upper lobectomy after accidental discovery of a right lung spiculated nodule suggestive of malignancy. The patient had a past medical history of hypertension, dyslipidemia, carotid artery stenosis and peripheral arterial occlusive disease. She was a lifelong smoker who quit smoking 6 months earlier. She reported drinking several alcoholic beverages weekly. Preoperative exercise thallium test ruled out reversible ischemia, and echocardiogram revealed normal left ventricular function and valvular apparatus. Shortly after the extubation, the patient developed bradypnea and hypoxia which required re-intubation and transfer to the ICU. In the ICU, the patient was continuously restless necessitating dose escalation of sedating agents. Multiple attempts of weaning the patient off sedation resulted in intense agitation, tachypnea and tachycardia. On further questioning, the husband confirmed that his wife consumed at least two glasses of vodka daily; therefore, the cause of her agitation was suggested to be due to alcohol withdrawal. The patient was maintained on high-dose sedation with midazolam, and fentanyl in addition to dexmedetomidate and continued on ventilation support with failed extubation attempts. On post-operative day 10, after attempting sedation reduction for a trial of weaning, her clinical status worsened. She became severely agitated, tachypnic at 50 breaths/min, tachycardic with a heart rate of 150 beats/ min and clinical examination revealed evidence of acute pulmonary edema. Arterial blood gases revealed hypoxia and hypocapnea, BNP was 816 ng/L (N 0–100), and cardiac enzymes were as follow: CK 3,197 U/L (N 33–211); CKmB 11.3 ng/mL (N 0–5) and troponin 10 ng/mL N (0–0.08). The initial electrocardiogram revealed Q waves and ST segment elevation in V1 and V2 and T wave inversion in the precordial leads from V2 to V6 (Fig. 1a), and the follow up EKG revealed widespread deep T wave inversions and QT prolongation suggestive of Takotsubo Cardiomyopathy (TC) (Fig. 1b). The echocardiogram revealed severe global hypokinesia with an ejection fraction of 25 %. Our main concern was to rule out occlusive coronary artery disease (CAD), so, the patient was sent for emergent coronary angiography. Coronary angiography revealed non-occlusive CAD; however, left ventriculography revealed severe apical hypokinesis with the characteristic ballooning, which is a marker of TC (Fig. 1c–e). The case was complicated by cardiogenic shock requiring norepinephrine, dopamine and an intra-aortic balloon pump until hemodynamic stability was achieved. The patient was discharged from the hospital 3 weeks after surgery. TC is becoming an increasingly recognized clinical disorder first reported in 1990 in the Japanese population by Sato et al. [1]. It accounts for 1–2 % of suspected acute myocardial infarction cases [2] with a specific predilection for postmenopausal females who make up over 90 % of the patients in most series. Several theories have been proposed to explain the transient cardiac dysfunction in TC, of which the most accepted is a catecholamine surge triggered by various emotional or physical stressors. Clinical H. R. Omar (&) H. D. Abdelmalak I. Komorova Internal Medicine Department, Mercy Hospital and Medical Center, 2525 South Michigan Avenue, Chicago, IL 60616, USA e-mail: [email protected]