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Transient left ventricular systolic dysfunction in a quadriplegic patient
European Journal of Internal Medicine 17 (2006) 221 www.elsevier.com/locate/ejim
Letter to the Editor
Transient left ventricular systolic dysfunction in a quadriplegic patient Beril Cakir * Carolinas Medical Center-University Hospital, Charlotte, NC 28232, U.S.A Received 6 October 2005; received in revised form 27 October 2005; accepted 10 November 2005
Recent developments in the management of spinal cord injury have reduced mortality while prolonging the life span of quadriplegic patients. It is important to remember that even a simple urinary tract infection or constipation can cause fatal outcomes in quadriplegic patients via autonomic dysreflexia. A 40-year-old C3-C4 quadriplegic Caucasian male presented to the emergency room with palpitations. On examination his blood pressure was 211 / 133 mm Hg with a heart rate of 99 beats/min. The patient had no cardiac risk factors and no history of hypertension. Blood work was normal except for leukocytosis (WBC 18,100/mm3). During his hospital stay, the patient’s blood pressure was very labile, ranging from 50 / 30 to 220 / 110 mm Hg. Gross hematuria resolved following bladder irrigations and empiric antibiotic treatment for possible hemorrhagic cystitis. Bowel cleaning was initiated for severe constipation. An echocardiogram revealed severely impaired left ventricular systolic function with an ejection fraction (EF) of 10 – 15%. A repeat echocardiogram on the 3rd day, when he was hemodynamically stable following the above interventions, showed normalization of left ventricular systolic function (EF 55 –60%). The patient was discharged from the hospital in good condition without any further cardiac work-up.
Autonomic dysreflexia can cause life-threatening bouts of hypertension in quadriplegic patients due to excess sympathetic activity reflexly activated by bowel or bladder distension. These patients lack cerebral control of spinal sympathetic reflexes [1]. Although cases of coronary artery disease and cardiac arrhythmias have been reported in this patient population, cardiomyopathy is not frequent. In this patient, impaired left ventricular systolic function was most likely the result of changes in peripheral resistance, venous return, and cardiac output during the course of severe hypertensive and hypotensive episodes due to autonomic dysreflexia. Once the triggering factor for autonomic dysreflexia was treated, the cardiac process improved. Understanding the pathophysiology of autonomic dysreflexia and utilizing basic tests and simple treatment modalities can prevent life-threatening outcomes as well as save quadriplegic patients from undergoing unnecessary procedures. Reference [1] Ziegler MG, Ruiz-Ramon P, Shapiro MH. Abnormal stress responses in patients with diseases affecting the sympathetic nervous system. Psychosom Med 1993;55(4):339 – 46.
* Tel.: +1 704 599 4799; fax: +1 704 376 1939. E-mail address: [email protected]. 0953-6205/$ - see front matter D 2006 European Federation of Internal Medicine. Published by Elsevier B.V. All rights reserved. doi:10.1016/j.ejim.2005.11.005
Letter to the Editor
Transient left ventricular systolic dysfunction in a quadriplegic patient Beril Cakir * Carolinas Medical Center-University Hospital, Charlotte, NC 28232, U.S.A Received 6 October 2005; received in revised form 27 October 2005; accepted 10 November 2005
Recent developments in the management of spinal cord injury have reduced mortality while prolonging the life span of quadriplegic patients. It is important to remember that even a simple urinary tract infection or constipation can cause fatal outcomes in quadriplegic patients via autonomic dysreflexia. A 40-year-old C3-C4 quadriplegic Caucasian male presented to the emergency room with palpitations. On examination his blood pressure was 211 / 133 mm Hg with a heart rate of 99 beats/min. The patient had no cardiac risk factors and no history of hypertension. Blood work was normal except for leukocytosis (WBC 18,100/mm3). During his hospital stay, the patient’s blood pressure was very labile, ranging from 50 / 30 to 220 / 110 mm Hg. Gross hematuria resolved following bladder irrigations and empiric antibiotic treatment for possible hemorrhagic cystitis. Bowel cleaning was initiated for severe constipation. An echocardiogram revealed severely impaired left ventricular systolic function with an ejection fraction (EF) of 10 – 15%. A repeat echocardiogram on the 3rd day, when he was hemodynamically stable following the above interventions, showed normalization of left ventricular systolic function (EF 55 –60%). The patient was discharged from the hospital in good condition without any further cardiac work-up.
Autonomic dysreflexia can cause life-threatening bouts of hypertension in quadriplegic patients due to excess sympathetic activity reflexly activated by bowel or bladder distension. These patients lack cerebral control of spinal sympathetic reflexes [1]. Although cases of coronary artery disease and cardiac arrhythmias have been reported in this patient population, cardiomyopathy is not frequent. In this patient, impaired left ventricular systolic function was most likely the result of changes in peripheral resistance, venous return, and cardiac output during the course of severe hypertensive and hypotensive episodes due to autonomic dysreflexia. Once the triggering factor for autonomic dysreflexia was treated, the cardiac process improved. Understanding the pathophysiology of autonomic dysreflexia and utilizing basic tests and simple treatment modalities can prevent life-threatening outcomes as well as save quadriplegic patients from undergoing unnecessary procedures. Reference [1] Ziegler MG, Ruiz-Ramon P, Shapiro MH. Abnormal stress responses in patients with diseases affecting the sympathetic nervous system. Psychosom Med 1993;55(4):339 – 46.
* Tel.: +1 704 599 4799; fax: +1 704 376 1939. E-mail address: [email protected]. 0953-6205/$ - see front matter D 2006 European Federation of Internal Medicine. Published by Elsevier B.V. All rights reserved. doi:10.1016/j.ejim.2005.11.005