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Takotsubo cardiomyopathy associated with sepsis in type 2 diabetes mellitus
230 [7] Moin M, Kersten RC, Bernardini F, Kulwin D, Biddinger PW, Ernst RJ, et al. Spontaneous hemorrhage in an intraorbital arteriovenous malformation. Ophthalmology 2000;107(12):2215 - 9. [8] Wright JE, Sullivan TJ, Garner A, Wulc AE, Moseley IF. Orbital venous anomalies. Ophthalmology 1997;104(6):905 - 13. [9] Sullivan TJ, Wright JE. Non-traumatic orbital hemorrhage. Clin Exp Ophthalmol 2000;28(1):26 - 31. [10] Rahman I, Ataullah S. Retrobulbar hemorrhage after sub-Tenon’s anesthesia. J Cataract Refract Surg 2004;30(12):2636 - 7. [11] Gilhotra JS, McNab AA, McKelvie P, OTDonnell BA. Late orbital hemorrhage around alloplastic orbital floor implants: a case series and review. Clin Exp Ophthalmol 2002;30(5):352 - 5. [12] Cates CA, Hodgkins PR, Morris RJ. Slipped medial rectus muscle secondary to orbital hemorrhage following strabismus surgery. J Pediatr Ophthalmol Strabismus 2000;37(6):361 - 2. [13] Kallio H, Paloheimo M, Maunuksela EL. Haemorrhage and risk factors associated with retrobulbar/peribulbar block: a prospective study in 1383 patients. Br J Anaesth 2000;85(5):708 - 11. [14] Oruc S, Sener EC, Akman A, Sanac AS. Bilateral orbital hemorrhage induced by labor. Eur J Ophthalmol 2001;11(1):77 - 9. [15] Boyer MM, Lucarelli MJ. Valsalva-induced subperiorbital hemorrhage during migraine. Arch Ophthalmol 1998;116(1):106 - 7.
Takotsubo cardiomyopathy associated with sepsis in type 2 diabetes mellitus Takotsubo cardiomyopathy (TC)—ampullar cardiomyopathy—is a novel cardiac syndrome that has acute onset of chest pain, electrocardiographic change, and minimal elevation of
Case Reports cardiac enzymes resembling acute myocardial infarction without any evidence of myocardial ischemia or injury. Its characteristic image in angiography is a transient left ventricular (LV) apical ballooning having the appearance of takotsubo, Japanese for octopus trap [1-3]. We report here a rare case of a 69-year-old woman with type 2 diabetes mellitus (DM) who exhibited myocardial depression with the typical wall motion abnormality seen in TC during a period of sepsis. The patient was admitted because of high fever and appetite loss. Laboratory investigations showed a white blood cell count of 16 100 per microliter, C-reactive protein of 26.9 mg/dL, platelet cell count of 12.3 104 per microliter, and fibrin/fibrinogen degradation product of 19.9 lg/mL. Her HbA1c was 6.5%. Her urine analysis revealed severe leukocyturia and hematuria. Abdominal computed tomography scan showed left hydronephrosis with ureteral stone. Our diagnosis was sepsis with disseminated intravascular coagulation (DIC) from pyelonephritis, and intravenous antibiotic and anticoagulant therapy was started immediately. Klebsiella pneumoniae was detected in cultures from both blood and urine. On the second day, she had acute onset of chest discomfort with fever. Electrocardiography revealed sinus tachycardia with ST-segment elevation in leads V1 to V6 (Fig. 1), and echocardiography showed apical dyskinesis and basal hyperkinesis, with overall LV systolic function being severely impaired with an ejection fraction of 20% (Fig. 2). A
Fig. 1 Time course of electrocardiograms. A, Twelve-lead electrocardiogram obtained on admission. B, Twelve-lead electrocardiogram obtained next day after admission (onset) revealed ST-segment elevation in leads V1 to V6. C, Twelve-lead electrocardiogram obtained 7 days later revealed diffuse T-wave inversion. D, Twelve-lead electrocardiogram obtained 24 days later revealed increased T-wave inversion.
Case Reports
231 several circulating cytokines such as tumor necrosis factor a and interleukin-1b might be involved. Myocardial depression according to sepsis is presented by biventricular dilation and depression of the ejection fraction [9,10]. In the present case, echocardiography revealed no biventricular dilation, but it did show apical dyskinesis and basal hyperkinesis, as well as depression of the ejection fraction as seen in TC. Takotsubo cardiomyopathy may coexist in the condition, which is known as myocardial depression during sepsis. The prognosis of TC is generally thought to be good, although there have been a few severe cases that needed hemodynamics stabilization with vasopressor agents and/or intra-aortic balloon counterpulsation [2,4,11]. Prompt diagnosis and careful management of fluid balance and heart function succeeded in normalizing the marked initial impairment in LV contractility. Takotsubo cardiomyopathy should be considered within the differential diagnosis of acute coronary syndrome, one of the severe complications of type 2 DM.
Fig. 2 Subcostal long-axis (4-chamber) view obtained next day after admission (onset), showing apical dyskinesis and basal hyperkinesis. LA indicates left atrium.
chest x-ray showed cardiomegaly and pulmonary edema. Blood examinations revealed an increment of creatine phosphokinase and the presence of troponin in serum, suggesting the onset of anterior myocardial infarction. Emergency cardiac catheterization was performed, showing a distinctive ballooning appearance of the apical LV with no significant stenosis in the coronary. Based on these findings, we reached a diagnosis of TC. Her heart failure gradually recovered, with improvement of infection and DIC. Electrocardiography revealed normalization of the elevated ST segment and inversion of T wave on the seventh day (Fig. 1). Echocardiography on the 24th day showed improvement of impaired regional wall motion. The precise etiology of TC is still obscure, although its onset is typically triggered by acute medical illness or intense emotional or physical stress [4,5]. Several mechanisms have been proposed that may result in transient LV apical ballooning, including multivessel epicardial spasm [6], coronary microvascular dysfunction [7], and catecholamine-mediated neurogenic stunning [8]. In the present case, diffuse coronary microvascular dysfunction due to type 2 DM might be associated with and may play a pathogenic role in the syndrome. In addition, DIC might have complicated the microvascular disturbance. It was reported that myocardial depression can be demonstrated in most patients with sepsis [9,10], in which
Sawako Ohigashi-Suzuki Yasushi Saito Ichiro Tatsuno Department of Clinical Cell Biology Chiba University Graduate School of Medicine Chiba University Hospital Chiba, Japan Department of Clinical Endocrinology and Metabolism Chiba University Hospital Chiba, Japan E-mail address: [email protected] doi:10.1016/j.ajem.2006.11.003
References [1] Kurisu S, Sato H, Kawagoe T, et al. Tako-tsubo–like left ventricular dysfunction with ST-segment elevation: a novel cardiac syndrome mimicking acute myocardial infarction. Am Heart J 2002;143:448 - 55. [2] Tsuchihashi K, Ueshima K, Uchida T, et al. Transient left ventricular apical ballooning without coronary artery stenosis: a novel heart syndrome mimicking acute myocardial infarction. Angina Pectoris– Myocardial Infarction Investigations in Japan. J Am Coll Cardiol 2001;38:11 - 8. [3] Abe Y, Kondo M, Matsuoka R, et al. Assessment of clinical features in transient left ventricular apical ballooning. J Am Coll Cardiol 2003; 41:737 - 42. [4] Sharkey SW, Lesser JR, Zenovich AG, et al. Acute and reversible cardiomyopathy provoked by stress in women from the United States. Circulation 2005;111:472 - 9. [5] Wittstein IS, Thiemann DR, Lima JA, et al. Neurohumoral features of myocardial stunning due to sudden emotional stress. N Engl J Med 2005;352:539 - 48. [6] Dote K, Sato H, Tateishi H, et al. Myocardial stunning due to simultaneous multivessel coronary spasms: a review of 5 cases. J Cardiol 1991;21:203 - 14. [7] Kurisu S, Inoue I, Kawagoe T, et al. Left ventricular apical thrombus formation in a patient with suspected tako-tsubo–like left ventricular dysfunction. Circ J 2003;67:556 - 8.
232 [8] Akashi YJ, Nakazawa K, Sakakibara M, et al. Reversible left ventricular dysfunction btakotsuboQ cardiomyopathy related to catecholamine cardiotoxicity. J Electrocardiol 2002;35:351 - 6. [9] Court O, Kumar A, Parrillo JE, et al. Clinical review: myocardial depression in sepsis and septic shock. Crit Care 2002;6:500 - 8. [10] Grocott-Mason RM, Shah AM. Cardiac dysfunction in sepsis: new theories and clinical implications. Intensive Care Med 1998;24: 286 - 95. [11] Mayer SA, Fink ME, Homma S, et al. Cardiac injury associated with neurogenic pulmonary edema following subarachnoid hemorrhage. Neurology 1994;44:815 - 20.
Uncommon cardiovascular manifestations after a Latrodectus bite Latrodectism is a clinical entity with characteristic symptoms and signs caused by the effect of a spider’s poison on different organs, especially the nervous and cardiovascular system. Acute myocardial damage after envenomation is not common, and cardiac manifestations after a black widow spider bite are rarely observed and their prognostic significance is not known. We report a 22-year-old man with myocardial ischemia caused by the bite of a black widow spider (Latrodectus tredecimguttatus). He had characteristic anxiety, severe hypertension, nausea, vomiting, tremor, generalized pain (especially in the lower extremities), diaphoresis, and rhabdomyolysis. He also had clinical signs of toxic myocarditis with accompanying cTnI elevation and echocardiographic measurements of anteroseptal hypokinesia with depressed left ventricular function. The patient recovered within a week without any sequelae. Clinicians should not overlook the possibility of acute myocardial damage in latrodectism. Spider envenomation is a common medical problem and life-threatening hazard in many countries. Widow spider envenomations generally produce systemic neurologic syndromes without significant local injury. Latrodectism— envenomation by the black widow spider—is a syndrome characterized by approximately 60% of victims developing hypertension and other symptoms including severe muscular pain and stiffness, nausea, vomiting and nausea, diaphoresis, photophobia, and dyspnea. The widow spider, the Latrodectus, is not designed to kill but to immobilize its victim; the female is more dangerous than the male because of its potent neurotoxin and larger size [1,2]. Detailed descriptions of the clinical features of human widow spider bites have been reported [3-7]. Cardiovascular manifestations are rarely observed [8]. Hypertension within the first hours after the bite has been documented in 21% to 31% of patients, accompanied by bradytachycardia [9-11]. The mortality is probably low [1,4] as necropsy studies are very rare; as a result, details of involvement of the cardiovascular system are not available. Cardiac manifestations after a black widow spider bite are rarely observed and their prognostic significance is not known. After a widow spider bite, the mechanism of myocardial damage of those without previous heart disease is not clear [12]. The case of a 22-year-old
Case Reports patient with Latrodectus tredecimguttatus poisoning complicated by myocardial damage is reported. A 22-year-old male farmer was admitted to the ED of the university hospital with complaint of fatigue, pain in the extremities, and swelling on the left eye. Those manifestations emerged after a spider bite at his left shoulder during his work in the farm. He was first admitted to a local community hospital and forwarded to our emergency department after his first treatment. The medical background of the patient and his family was not remarkable. His vital signs were as follows: blood pressure, 200/120 mm Hg; pulse, 77 per minute; respiratory rate, 24 per minute; body temperature, 368C; and O2 saturation, 98%. His physical examination was normal except for a 1 1-mm rash over his left scapular region. He started to experience nausea and vomiting after admission to our department. The culprit spider had been caught and sacrificed by the patient’s relatives who brought it with the patient to the hospital (Fig. 1). After examination, the spider was suspected to be a black widow or a similar species based on the patient’s signs and symptoms such as anxiety, tachycardia, hypertension, generalized sweating that was remarkable on the forehead and face, pain in the extremities, nausea, and vomiting. Samples for the first line laboratory tests were taken and the patient was immediately given treatment. In his first electrocardiogram (ECG), the rhythm was sinus at a rate of 78 per minute and atrial depolarization abnormalities in leads D II, III, and aVF, and depolarization abnormalities in leads V1 and aVL were observed (Fig. 2). Serial ECG recordings revealed a normalization of negative P waves in the inferior leads on the other hand, T-wave inversion in lead V2, and wandering atrial pacemaker activity has developed (Fig. 3). Meperidine was used to stop the continuous pain of the patient, and fluid replacement was continued with close monitoring. The patient was put on 40 lg/min rate of intravenous nitrate upon responsiveness to sublingual
Fig. 1
The venomous black widow spider.
Takotsubo cardiomyopathy associated with sepsis in type 2 diabetes mellitus Takotsubo cardiomyopathy (TC)—ampullar cardiomyopathy—is a novel cardiac syndrome that has acute onset of chest pain, electrocardiographic change, and minimal elevation of
Case Reports cardiac enzymes resembling acute myocardial infarction without any evidence of myocardial ischemia or injury. Its characteristic image in angiography is a transient left ventricular (LV) apical ballooning having the appearance of takotsubo, Japanese for octopus trap [1-3]. We report here a rare case of a 69-year-old woman with type 2 diabetes mellitus (DM) who exhibited myocardial depression with the typical wall motion abnormality seen in TC during a period of sepsis. The patient was admitted because of high fever and appetite loss. Laboratory investigations showed a white blood cell count of 16 100 per microliter, C-reactive protein of 26.9 mg/dL, platelet cell count of 12.3 104 per microliter, and fibrin/fibrinogen degradation product of 19.9 lg/mL. Her HbA1c was 6.5%. Her urine analysis revealed severe leukocyturia and hematuria. Abdominal computed tomography scan showed left hydronephrosis with ureteral stone. Our diagnosis was sepsis with disseminated intravascular coagulation (DIC) from pyelonephritis, and intravenous antibiotic and anticoagulant therapy was started immediately. Klebsiella pneumoniae was detected in cultures from both blood and urine. On the second day, she had acute onset of chest discomfort with fever. Electrocardiography revealed sinus tachycardia with ST-segment elevation in leads V1 to V6 (Fig. 1), and echocardiography showed apical dyskinesis and basal hyperkinesis, with overall LV systolic function being severely impaired with an ejection fraction of 20% (Fig. 2). A
Fig. 1 Time course of electrocardiograms. A, Twelve-lead electrocardiogram obtained on admission. B, Twelve-lead electrocardiogram obtained next day after admission (onset) revealed ST-segment elevation in leads V1 to V6. C, Twelve-lead electrocardiogram obtained 7 days later revealed diffuse T-wave inversion. D, Twelve-lead electrocardiogram obtained 24 days later revealed increased T-wave inversion.
Case Reports
231 several circulating cytokines such as tumor necrosis factor a and interleukin-1b might be involved. Myocardial depression according to sepsis is presented by biventricular dilation and depression of the ejection fraction [9,10]. In the present case, echocardiography revealed no biventricular dilation, but it did show apical dyskinesis and basal hyperkinesis, as well as depression of the ejection fraction as seen in TC. Takotsubo cardiomyopathy may coexist in the condition, which is known as myocardial depression during sepsis. The prognosis of TC is generally thought to be good, although there have been a few severe cases that needed hemodynamics stabilization with vasopressor agents and/or intra-aortic balloon counterpulsation [2,4,11]. Prompt diagnosis and careful management of fluid balance and heart function succeeded in normalizing the marked initial impairment in LV contractility. Takotsubo cardiomyopathy should be considered within the differential diagnosis of acute coronary syndrome, one of the severe complications of type 2 DM.
Fig. 2 Subcostal long-axis (4-chamber) view obtained next day after admission (onset), showing apical dyskinesis and basal hyperkinesis. LA indicates left atrium.
chest x-ray showed cardiomegaly and pulmonary edema. Blood examinations revealed an increment of creatine phosphokinase and the presence of troponin in serum, suggesting the onset of anterior myocardial infarction. Emergency cardiac catheterization was performed, showing a distinctive ballooning appearance of the apical LV with no significant stenosis in the coronary. Based on these findings, we reached a diagnosis of TC. Her heart failure gradually recovered, with improvement of infection and DIC. Electrocardiography revealed normalization of the elevated ST segment and inversion of T wave on the seventh day (Fig. 1). Echocardiography on the 24th day showed improvement of impaired regional wall motion. The precise etiology of TC is still obscure, although its onset is typically triggered by acute medical illness or intense emotional or physical stress [4,5]. Several mechanisms have been proposed that may result in transient LV apical ballooning, including multivessel epicardial spasm [6], coronary microvascular dysfunction [7], and catecholamine-mediated neurogenic stunning [8]. In the present case, diffuse coronary microvascular dysfunction due to type 2 DM might be associated with and may play a pathogenic role in the syndrome. In addition, DIC might have complicated the microvascular disturbance. It was reported that myocardial depression can be demonstrated in most patients with sepsis [9,10], in which
Sawako Ohigashi-Suzuki Yasushi Saito Ichiro Tatsuno Department of Clinical Cell Biology Chiba University Graduate School of Medicine Chiba University Hospital Chiba, Japan Department of Clinical Endocrinology and Metabolism Chiba University Hospital Chiba, Japan E-mail address: [email protected] doi:10.1016/j.ajem.2006.11.003
References [1] Kurisu S, Sato H, Kawagoe T, et al. Tako-tsubo–like left ventricular dysfunction with ST-segment elevation: a novel cardiac syndrome mimicking acute myocardial infarction. Am Heart J 2002;143:448 - 55. [2] Tsuchihashi K, Ueshima K, Uchida T, et al. Transient left ventricular apical ballooning without coronary artery stenosis: a novel heart syndrome mimicking acute myocardial infarction. Angina Pectoris– Myocardial Infarction Investigations in Japan. J Am Coll Cardiol 2001;38:11 - 8. [3] Abe Y, Kondo M, Matsuoka R, et al. Assessment of clinical features in transient left ventricular apical ballooning. J Am Coll Cardiol 2003; 41:737 - 42. [4] Sharkey SW, Lesser JR, Zenovich AG, et al. Acute and reversible cardiomyopathy provoked by stress in women from the United States. Circulation 2005;111:472 - 9. [5] Wittstein IS, Thiemann DR, Lima JA, et al. Neurohumoral features of myocardial stunning due to sudden emotional stress. N Engl J Med 2005;352:539 - 48. [6] Dote K, Sato H, Tateishi H, et al. Myocardial stunning due to simultaneous multivessel coronary spasms: a review of 5 cases. J Cardiol 1991;21:203 - 14. [7] Kurisu S, Inoue I, Kawagoe T, et al. Left ventricular apical thrombus formation in a patient with suspected tako-tsubo–like left ventricular dysfunction. Circ J 2003;67:556 - 8.
232 [8] Akashi YJ, Nakazawa K, Sakakibara M, et al. Reversible left ventricular dysfunction btakotsuboQ cardiomyopathy related to catecholamine cardiotoxicity. J Electrocardiol 2002;35:351 - 6. [9] Court O, Kumar A, Parrillo JE, et al. Clinical review: myocardial depression in sepsis and septic shock. Crit Care 2002;6:500 - 8. [10] Grocott-Mason RM, Shah AM. Cardiac dysfunction in sepsis: new theories and clinical implications. Intensive Care Med 1998;24: 286 - 95. [11] Mayer SA, Fink ME, Homma S, et al. Cardiac injury associated with neurogenic pulmonary edema following subarachnoid hemorrhage. Neurology 1994;44:815 - 20.
Uncommon cardiovascular manifestations after a Latrodectus bite Latrodectism is a clinical entity with characteristic symptoms and signs caused by the effect of a spider’s poison on different organs, especially the nervous and cardiovascular system. Acute myocardial damage after envenomation is not common, and cardiac manifestations after a black widow spider bite are rarely observed and their prognostic significance is not known. We report a 22-year-old man with myocardial ischemia caused by the bite of a black widow spider (Latrodectus tredecimguttatus). He had characteristic anxiety, severe hypertension, nausea, vomiting, tremor, generalized pain (especially in the lower extremities), diaphoresis, and rhabdomyolysis. He also had clinical signs of toxic myocarditis with accompanying cTnI elevation and echocardiographic measurements of anteroseptal hypokinesia with depressed left ventricular function. The patient recovered within a week without any sequelae. Clinicians should not overlook the possibility of acute myocardial damage in latrodectism. Spider envenomation is a common medical problem and life-threatening hazard in many countries. Widow spider envenomations generally produce systemic neurologic syndromes without significant local injury. Latrodectism— envenomation by the black widow spider—is a syndrome characterized by approximately 60% of victims developing hypertension and other symptoms including severe muscular pain and stiffness, nausea, vomiting and nausea, diaphoresis, photophobia, and dyspnea. The widow spider, the Latrodectus, is not designed to kill but to immobilize its victim; the female is more dangerous than the male because of its potent neurotoxin and larger size [1,2]. Detailed descriptions of the clinical features of human widow spider bites have been reported [3-7]. Cardiovascular manifestations are rarely observed [8]. Hypertension within the first hours after the bite has been documented in 21% to 31% of patients, accompanied by bradytachycardia [9-11]. The mortality is probably low [1,4] as necropsy studies are very rare; as a result, details of involvement of the cardiovascular system are not available. Cardiac manifestations after a black widow spider bite are rarely observed and their prognostic significance is not known. After a widow spider bite, the mechanism of myocardial damage of those without previous heart disease is not clear [12]. The case of a 22-year-old
Case Reports patient with Latrodectus tredecimguttatus poisoning complicated by myocardial damage is reported. A 22-year-old male farmer was admitted to the ED of the university hospital with complaint of fatigue, pain in the extremities, and swelling on the left eye. Those manifestations emerged after a spider bite at his left shoulder during his work in the farm. He was first admitted to a local community hospital and forwarded to our emergency department after his first treatment. The medical background of the patient and his family was not remarkable. His vital signs were as follows: blood pressure, 200/120 mm Hg; pulse, 77 per minute; respiratory rate, 24 per minute; body temperature, 368C; and O2 saturation, 98%. His physical examination was normal except for a 1 1-mm rash over his left scapular region. He started to experience nausea and vomiting after admission to our department. The culprit spider had been caught and sacrificed by the patient’s relatives who brought it with the patient to the hospital (Fig. 1). After examination, the spider was suspected to be a black widow or a similar species based on the patient’s signs and symptoms such as anxiety, tachycardia, hypertension, generalized sweating that was remarkable on the forehead and face, pain in the extremities, nausea, and vomiting. Samples for the first line laboratory tests were taken and the patient was immediately given treatment. In his first electrocardiogram (ECG), the rhythm was sinus at a rate of 78 per minute and atrial depolarization abnormalities in leads D II, III, and aVF, and depolarization abnormalities in leads V1 and aVL were observed (Fig. 2). Serial ECG recordings revealed a normalization of negative P waves in the inferior leads on the other hand, T-wave inversion in lead V2, and wandering atrial pacemaker activity has developed (Fig. 3). Meperidine was used to stop the continuous pain of the patient, and fluid replacement was continued with close monitoring. The patient was put on 40 lg/min rate of intravenous nitrate upon responsiveness to sublingual
Fig. 1
The venomous black widow spider.