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• W2016021893 abstract "This report describes a patient who experienced cardiopulmonary arrest caused by severe hypoglycemia and malnutrition, which was successfully treated with percutaneous cardiopulmonary support (PCPS) and intra-aortic balloon pumping (IABP).A 33-year-old female with anorexia nervosa (AN) was transferred to the emergency center because of a loss of consciousness. On admission, she was extremely emaciated, hypotensive, and hypoglycemic (10 mg/dl). A chest X-ray showed butterfly shadow. Echocardiography showed severe hypokinesis of left ventricular wall motion. On the 3rd hospital day, she experienced cardiac arrest. Myocardial dysfunction caused by malnutrition was suspected, and therefore both PCPS and IABP were administered for circulatory support and myocardial protection. Thereafter, cardiac function gradually recovered and she was later weaned from PCPS and IABP on the 9th and the 10th hospital day, respectively. She was discharged from the intensive care unit on the 43rd hospital day with normal cardiac function. Her neurological outcome after 6 months as evaluated by the Glasgow Outcome Scale was considered to be good recovery.Cardiomyopathy in AN patients is reversible ventricular dysfunction, and circulation assisting devices are considered for the treatment of cardiogenic shock. This report describes a patient who experienced cardiopulmonary arrest caused by severe hypoglycemia and malnutrition, which was successfully treated with percutaneous cardiopulmonary support (PCPS) and intra-aortic balloon pumping (IABP). A 33-year-old female with anorexia nervosa (AN) was transferred to the emergency center because of a loss of consciousness. On admission, she was extremely emaciated, hypotensive, and hypoglycemic (10 mg/dl). A chest X-ray showed butterfly shadow. Echocardiography showed severe hypokinesis of left ventricular wall motion. On the 3rd hospital day, she experienced cardiac arrest. Myocardial dysfunction caused by malnutrition was suspected, and therefore both PCPS and IABP were administered for circulatory support and myocardial protection. Thereafter, cardiac function gradually recovered and she was later weaned from PCPS and IABP on the 9th and the 10th hospital day, respectively. She was discharged from the intensive care unit on the 43rd hospital day with normal cardiac function. Her neurological outcome after 6 months as evaluated by the Glasgow Outcome Scale was considered to be good recovery. Cardiomyopathy in AN patients is reversible ventricular dysfunction, and circulation assisting devices are considered for the treatment of cardiogenic shock. Anorexia nervosa (AN) is an eating disorder with a significant risk of sudden death due to severe cardiac complications [1Birmingham C.L. Su J. Hlynsky J.A. Goldner E.M. Gao M. The mortality rate from anorexia nervosa.Int J Eat Disord. 2005; 38: 143-146Crossref PubMed Scopus (236) Google Scholar, 2Neumarker K.J. Mortality and sudden death in anorexia nervosa.Int J Eat Disord. 1997; 21: 205-212Crossref PubMed Scopus (168) Google Scholar]. In AN patients, cardiovascular abnormalities such as bradycardia, hypotension, mitral valve prolapse, and arrhythmias due to hypokalemia or hypomagnesaemia are often found [[3]Thurston J. Marks P. Electrocardiographic abnormalities in patients with anorexia nervosa.Br Heart J. 1974; 36: 719-723Crossref PubMed Scopus (66) Google Scholar]. However, the left ventricular function is generally normal [[4]Swenne I. Heart risk associated with weight loss in anorexia nervosa and eating disorders: electrocardiographic changes during the early phase of refeeding.Acta Paediatr. 2000; 89: 447-452Crossref PubMed Scopus (42) Google Scholar]. This report describes a case of a temporary and reversible myocardial dysfunction with cardiopulmonary arrest (CPA) caused by severe hypoglycemia and malnutrition, which was successfully treated using percutaneous cardiopulmonary support (PCPS) and intra-aortic balloon pumping (IABP). A 33-year-old female, who had been suffering from AN for several years, was transferred to our emergency center because of a loss of consciousness. On admission, her vital signs were Glasgow Coma Scale 5 (E1 V1 M3), systolic blood pressure of 70 mmHg, heart rate of 70 beats/min, body temperature of 33.8 °C, and respiratory rate of 20 breaths/min. Her height, body weight, and body mass index were 150 cm, 20 kg, and 8.9, respectively. Laboratory data showed hypoglycemia (blood glucose, 10 mg/dl), hypoproteinemia (total protein, 5.0 g/dl; albumin, 2.9 g/dl), an elevation of hepatic enzymes (aspartate aminotransferase, 1875 IU/l; alanine aminotransferase, 3063 IU/l; lactate dehydrogenase, 782 IU/l), and bleeding tendency (prothrombin time-international normalized ratio, 2.88). Creatine kinase was elevated mildly (156 IU/l), but troponin T-test was negative. Free triiodothyronine level was 1.3 pg/ml and free thyroxine level was 1.3 ng/dl. Chest X-ray (Fig. 1) showed butterfly shadow. An electrocardiogram (ECG) demonstrated abnormal Q waves in V3, V4, and V5 (Fig. 2A ). An echocardiogram showed severe left ventricular dysfunction with an ejection fraction (EF) of 10% (Fig. 2C). The head computed tomography (CT) scan showed no abnormal lesion such as hemorrhage or stroke.Figure 2Electrocardiogram (ECG) and echocardiogram on admission and on the 43rd hospital day. (A) ECG on admission; abnormal Q waves in V3, V4, and V5 were demonstrated. (B) ECG on the 43rd hospital day; abnormal Q waves in V3, V4, and V5 normalized. (C) Echocardiogram on admission; it showed severe left ventricular dysfunction with an ejection fraction (EF) of 10%. (D) Echocardiogram on the 43rd hospital day; cardiac function improved to EF of 40%. LVDd, left ventricular internal dimension in diastole; LVDs, left ventricular internal dimension in systole; IVS, interventricular septum; PW, left ventricular posterior wall thickness.View Large Image Figure ViewerDownload (PPT) She was diagnosed to have cardiogenic shock and was therefore intubated and mechanically ventilated, because she did not regain consciousness in spite of treatment for hypoglycemia. Low-dose dobutamine (2 μg/(kg min)) was administered to improve the low EF. To prevent refeeding syndrome, potassium phosphate was administered and her calorie intake was a maximum of 480 kcal/day until the 5th hospital day and thereafter it was increased gradually. Her clinical course in the intensive care unit (ICU) is shown in Fig. 3. On the 3rd hospital day, she abruptly developed CPA. Bradycardia (heart rate, 45 beats/min) was shown on the ECG monitor. Cardiopulmonary resuscitation with the use of epinephrine was immediately performed, but spontaneous circulation could not be established. An echocardiogram revealed almost total akinesis of the whole left ventricular wall. Therefore, PCPS and IABP were induced and maintained. The continuous administration of dobutamine was discontinued for myocardial protection. To protect the patient's neurological function, her deep body temperature was maintained at less than 37.0 °C. After the start of PCPS and IABP, her hemodynamics gradually improved and the systolic blood pressure exceeded more than 90 mmHg. Her cardiac function thereafter recovered gradually, and the EF recovered to 25% on the 9th hospital day (Fig. 3). She was thereafter weaned from PCPS on the 9th hospital day and weaned from IABP on the 10th hospital day. She was extubated on the 15th hospital day, because she regained consciousness. She was discharged from the ICU on the 43rd hospital day with normalized ECG (Fig. 2B) and an improved EF (Fig. 2D). After discharge from the ICU, she had no cardiac events and was discharged from the hospital on the 78th hospital day. Her neurological outcome after 6 months, as evaluated by the Glasgow Outcome Scale, was good recovery. AN is a psychiatric disease with a high mortality and it is often associated with cardiovascular abnormalities including sudden death [1Birmingham C.L. Su J. Hlynsky J.A. Goldner E.M. Gao M. The mortality rate from anorexia nervosa.Int J Eat Disord. 2005; 38: 143-146Crossref PubMed Scopus (236) Google Scholar, 2Neumarker K.J. Mortality and sudden death in anorexia nervosa.Int J Eat Disord. 1997; 21: 205-212Crossref PubMed Scopus (168) Google Scholar]. The sudden death is often caused by arrhythmias and acute heart failure [1Birmingham C.L. Su J. Hlynsky J.A. Goldner E.M. Gao M. The mortality rate from anorexia nervosa.Int J Eat Disord. 2005; 38: 143-146Crossref PubMed Scopus (236) Google Scholar, 2Neumarker K.J. Mortality and sudden death in anorexia nervosa.Int J Eat Disord. 1997; 21: 205-212Crossref PubMed Scopus (168) Google Scholar]. Malnutrition causes cardiac abnormalities on a cellular level. This leads to diminished protein synthesis, the activation of calcium-dependent proteinases, mitochondrial swelling, a decreased glycogen content, interstitial edema, and myofibrillar atrophy [5Clark A.F. Wildenthal K. Disproportionate reduction of actin synthesis in hearts of starved rats.J Biol Chem. 1986; 261: 168-172Google Scholar, 6Nutter D.O. Murray T.G. Heymsfield S.B. Fuller E.O. The effect of chronic protein-calorie undernutrition in the rat on myocardial function and cardiac function.Circ Res. 1979; 45: 144-152Crossref PubMed Scopus (59) Google Scholar]. These conditions cause a decrease of the contractile force of the ventricle and diastolic compliance [[7]Goldberg S.J. Comerci G.D. Feldman L. Cardiac output and regional myocardial contraction in anorexia nervosa.J Adolesc Health Care. 1988; 9: 15-21Abstract Full Text PDF PubMed Scopus (38) Google Scholar]. Hypoglycemic state induces a high blood level of catecholamine, because the state stimulates the central sympathetic nervous system. An excessive release of catecholamines may cause myocardial damage. A catecholamine surge might cause reversible ventricular dysfunction in patients with subarachnoid hemorrhage, endocrine disorder, and hypoglycemic stress [8Yamaguchi K. Wakatsuki T. Kusunose K. Niki T. Koshiba K. Yamada H. Soeki T. Akaike M. A case of neurogenic myocardial stunning presenting transient left ventricular mid-portion ballooning simulating atypical takotsubo cardiomyopathy.J Cardiol. 2008; 52: 53-58Abstract Full Text Full Text PDF PubMed Scopus (16) Google Scholar, 9de Souza F. Altenburg Odebrecht Curi Gismondi R. Henriques Cunha Neto S. de Mattos M.A. Tako-tsubo-like cardiomyopathy and extra-adrenal pheochromocytoma: case report and literature review.Clin Res Cardiol. 2008; 97: 397-401Crossref PubMed Scopus (22) Google Scholar, 10Ohwada R. Hotta M. Kimura H. Takagi S. Matsuda N. Nomura K. Takano K. Ampulla cardiomyopathy after hypoglycemia in three young female patients with anorexia nervosa.Intern Med. 2005; 44: 228-233Crossref PubMed Scopus (66) Google Scholar]. Catecholamine-mediated myocardial injury is thought to be caused by an elevation of intracellular calcium and possibly oxygen free radicals [[11]Dhalla K.S. Rupp H. Beamish R.E. Dhalla N.S. Mechanisms of alterations in cardiac membrane Ca2+ transport due to excess catecholamines.Cardiovasc Drugs Ther. 1996; 10: 231-238Crossref PubMed Google Scholar]. Histologically, the myocardium shows contraction band necrosis and myocytolysis [[11]Dhalla K.S. Rupp H. Beamish R.E. Dhalla N.S. Mechanisms of alterations in cardiac membrane Ca2+ transport due to excess catecholamines.Cardiovasc Drugs Ther. 1996; 10: 231-238Crossref PubMed Google Scholar]. Ohwada et al. reported a case of ampulla cardiomyopathy in three young female patients with AN [[10]Ohwada R. Hotta M. Kimura H. Takagi S. Matsuda N. Nomura K. Takano K. Ampulla cardiomyopathy after hypoglycemia in three young female patients with anorexia nervosa.Intern Med. 2005; 44: 228-233Crossref PubMed Scopus (66) Google Scholar]. They suggested that excess catecholamine release, possibly induced by hypoglycemia, was the cause of ampulla cardiomyopathy. In the present case, excessive catecholamine release due to persistent hypoglycemia might have caused severe myocardial dysfunction, although ampulla cardiomyopathy could not be diagnosed because coronary angiography was not performed. In the present case, an echocardiogram on admission showed cardiac wall thinning (Fig. 2C), that might have been caused by AN. It was therefore suspected that her heart might be sensitive to catecholamine. Excessive catecholamine released by hypoglycemia might not improve contractile force of the left ventricle but exacerbate cardiac function by increase of myocardial oxygen consumption or vasoconstriction of coronary artery. Thereafter, severe myocardial dysfunction occurred in the present case. Furthermore, the administration of dobutamine (2 μg/(kg min)) might accelerate the myocardial dysfunction and thereby induce cardiac arrest. We considered her myocardial state caused by a catecholamine surge to be temporary and reversible, and a full recovery of the cardiac function was expected following myocardial protective treatment. In addition, myocardial viability was expected because mild elevation of cardiac enzymes was observed including creatinine kinase and negative troponin T. Therefore, when the patient went into cardiac arrest, PCPS and IABP were immediately started. Eventually, her heart recovered and thereafter demonstrated a normal function as expected. The complete recovery of cardiac function suggested that severe myocardial dysfunction with AN might be reversible, so the use of PCPS should be considered to maintain the systemic circulation." @default.
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• W2016021893 title "Complete recovery from severe myocardial dysfunction in a patient with anorexia nervosa" @default.
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