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Thoracic Spinal Cord Ischemia Following Acute Myocardial Infarction and Cardiac Arrest in a Young Male
CASE REPORT
Case Report
Thoracic Spinal Cord Ischemia Following Acute Myocardial Infarction and Cardiac Arrest in a Young Male O. Akbar Ali, MBBS a , A. Aggarwal, MBBS, FRACP b , G. Thanakrishnan, MBBS, FRACP c and H.C. Lowe, PhD, FRACP a,∗ a
Department of Cardiology, Concord Repatriation General Hospital, Sydney, NSW 2139, Australia b Department of Neurology, Concord Repatriation General Hospital, Sydney, NSW, Australia c Department of Intensive Care, Concord Repatriation General Hospital, Sydney, NSW, Australia Available online 2 June 2005
In an era of percutaneous stenting for acute myocardial infarction (AMI), a case of thoracic spinal cord ischemia following AMI and cardiac arrest is presented, to highlight and discuss this rare but debilitating condition, well-documented within the neurological literature, but rarely encountered in cardiovascular practice. (Heart Lung and Circulation 2006;15:53–55) © 2005 Australasian Society of Cardiac and Thoracic Surgeons and the Cardiac Society of Australia and New Zealand. Published by Elsevier Inc. All rights reserved. Keywords. Myocardial infarction; Coronary intervention
Introduction
W
ith an increasing preference for percutaneous treatment of acute myocardial infarction (AMI) with excellent angiographic and clinical outcomes often occurring, a case of thoracic spinal cord ischemia following AMI and cardiac arrest is presented, to highlight and discuss this rare but debilitating condition, well-documented within the neurological literature, but rarely encountered in cardiovascular practice.
Case Report A 24-year-old male was admitted to our institution having collapsed shortly after playing soccer. He had been previously well, except for two episodes of syncope in the three months prior. He smoked a packet of cigarettes per day. Immediately following the collapse, bystander cardiopulmonary resuscitation was commenced. On ambulance arrival, he was found to be in ventricular fibrillation, which required four d.c. cardioversions to achieve sinus rhythm. An acceptable cardiac output was then achieved, with the time from collapse to restoration of sinus rhythm estimated at 29 min. He was then intubated, ventilated and brought to the emergency department. Initial ECG suggested anterior myocardial infarction, and he was promptly taken to the cardiac catheterisation laboratory. His blood pressure was 90/60 mmHg ∗ Corresponding author. Tel.: +61 2 9767 6296; fax: +61 2 9767 6994. E-mail address: [email protected] (H.C. Lowe).
and his heart rate was 110 bpm. There was no evidence of pulmonary congestion. Coronary angiography revealed a single, proximal left anterior descending (LAD) artery coronary artery lesion, which appeared thrombusladen (Fig. 1A, thrombotic lesion marked by arrow). Flow in the distal LAD was also reduced, assessed at TIMI 0–11 (Fig. 1A). The lesion was promptly stented with a 4.5 mm × 18 mm Ultra stent (Guidant Corp, USA), though with no improvement in distal flow (Fig. 1B, poor distal flow marked by arrow). A bolus and infusion of abciximab (Lilly, USA) was given in addition to the aspirin, clopidogrel and heparin already administered. A 34 cm intraaortic balloon pump (IABP) was placed uneventfully and the patient was transferred to the intensive care unit (ICU). Echocardiography immediately after the intervention suggested anterior, apical and inferior akinesis. The IABP was removed the following day, with the blood pressure maintained at 120/70 without support. The ICU course was complicated by aspiration pneumonia, gramnegative septicaemia and delirium. Total Creatinine Kinase peaked at 5545 U/L and troponin T at 7.2 g/L. Beta blockade, ACE inhibition and statin therapy were started, and the patient transferred to the coronary care unit. On Day 6, he was unable to stand unaided or walk without assistance, when he first attempted to get out of bed. Neurological examination revealed bilateral pyramidal lower limb weakness of Medical Research Council (MRC) grade 4, absent lower limb deep tendon reflexes and a sensory level to touch and pain to T4-5. Posterior columns (vibration and proprioception) were preserved.
© 2005 Australasian Society of Cardiac and Thoracic Surgeons and the Cardiac Society of Australia and New Zealand. Published by Elsevier Inc. All rights reserved.
1443-9506/04/$30.00 doi:10.1016/j.hlc.2005.03.021
54
Ali et al. Thoracic spinal cord ischemia following acute myocardial infarction and cardiac arrest in a young male
Heart Lung and Circulation 2006;15:53–55
CASE REPORT
Figure 2. Anterior spinal magnetic resonance angiogram (MRA). The anterior spinal artery – normally present in the midline – is not detected (inferior arrow). An intercostal vessel is also not detected (superior arrow).
Figure 1. Coronary angiography (right anterior oblique view). (A) Initial angiography. Thrombus-laden proximal LAD lesion (marked by arrow). (B) Appearances post stenting. The stented lesion appears satisfactory. There is TIMI 0–1 flow in the distal LAD. (C) Appearances at 10 days. The stented site appears satisfactory. Distal LAD is normal.
There was evidence of cognitive impairment, as he was slow to process information and exhibited short-term memory impairment. On formal mini-mental examination score, he scored 25/30. There was no bowel or bladder dysfunction. Brain and spinal cord magnetic resonance imaging (MRI) were normal, with no evidence of white matter lesions or spinal cord infarction. The anterior spinal artery and an isolated intercostal artery were not visualised on magnetic resonance angiogram (MRA) (Fig. 2). With rehabilitation and physiotherapy, there was considerable improvement in function and mobility, to a point that, at six weeks, the patient was able to walk independently with only mild persistent weakness of hip flexors. His cognition and short-term memory also improved. Echocardiography on Day 2 showed marked improvement in LV function, with normal apical and anterior contractility, though persisting mild inferior hypokinesis. Coronary angiography demonstrated stent patency and TIMI 3 flow1 in the distal LAD at Day 10 (Fig. 1C). An electrophysiological study demonstrated no inducible arrhythmia.
Ali et al. Thoracic spinal cord ischemia following acute myocardial infarction and cardiac arrest in a young male
The overall impression was that of cardiac arrest and hypotension secondary to anterior myocardial infarction, successfully treated with resuscitation, cardioversion, stenting and IABP support, but resulting in anterior spinal cord ischemia and hypoxic encephalopathy.
Discussion Spinal cord ischemia is a rare but clinically and pathologically well-described entity.2–6 It is thought to be a result of reduced perfusion pressure, which may be the result of hypotension in the setting of cardiac arrest.4–6 Classically, it is considered to occur most frequently at the level of T4–T8 due to a relative paucity of vascular supply at this level.2 The anterior spinal artery arises from the vertebral arteries in the foramen magnum. The main feeder vessel to the thoracic spinal cord segment of this artery is the arteria magna of Adamkiewicz, which usually enters the spinal cord between the T5 and T8 segments. Damage, occlusion or hypoperfusion to this vessel may cause ischaemia or infarction of the thoracic spinal cord, usually up to T4, which is the upper extent of this feeder vessel. A small vessel may be particularly sensitive to prolonged hypotension. Spinal cord MRI may be normal, or show diffuse abnormality2 In this case, magnetic resonance angiography did not identify the anterior spinal artery. This vessel may have been small or even absent, but MRA, even using three dimensional reconstructions, is relatively insensitive for its detection.7 The presence or otherwise of the anterior spinal artery by MRA however, is entirely compatible in this case with a clinical diagnosis of spinal cord ischemia. This patient was young, and it is likely that he had absent or reduced cardiac output for up to 29 min. While he was a smoker, there were no other apparent risk factors, and subsequent hematologic screen for procoagulant markers was unremarkable. Neuronal necrosis has been documented in neonates and premature infants suffering hypotensive episodes,4,5 although this has not been shown to be related to age in one large series.2 The influence of age on outcome in this case can be only speculative. Although IABP use has been reported to cause spinal cord necrosis and paraplegia,8 a combined bowel, renal and spinal cord infarction of only 0.1% has been reported in a large series.9 This is thought to be on the basis of widespread cholesterol embolisation leading to anterior spinal arteriole occlusion.10 In this case, IABP positioning was considered optimal, the IABP was in situ overnight
55
only, and there was no evidence of cholesterol embolisation in a low risk individual. Thus, while use of the IABP cannot be completely excluded as cause for the symptoms and signs, this would appear unlikely. This case therefore most likely demonstrates transient spinal cord ischemia secondary to prolonged hypotension associated with anterior myocardial infarction and cardiac arrest; conditions which, while well described, are rarely encountered in cardiovascular medicine. While the cardiovascular outcome was excellent in this high-risk patient, rare and significant neurologic morbidity occurred. With an increasing use of effective percutaneous means of Ml treatment,11 this report emphasises that serious, noncardiac sequelae of cardiac arrest may still occur. HCL holds a Viertel Clinical Investigatorship and receives research support from the NHMRC.
References 1. Chesebro JH, Knatterud G, Roberts R, et al. Thrombolysis in Myocardial Infarction (TIMI) Trial, Phase I: a comparison between intravenous tissue plasminogen activator and intravenous streptokinase: clinical findings through hospital discharge. Circulation 1987;76:142–54. 2. Duggal N, Lach B, et al. Selective vulnerability of the lumbosacral spinal cord after cardiac arrest and hypotension. Stroke 2002;33:116–21. 3. Zang Z-A, Nonaka H, Hatori T. The microvasculature of the spinal cord in the human adult. Neuropathology 1997;17:32–42. 4. Cheshire WP, Santos CC, Massey EW, Howard Jr JF. Spinal Cord infarction: etiology and outcome. Neurology 1996;47:321–30. 5. Gilles FH, Nag D. Vulnerability of human spinal cord in transient cardiac arrest. Neurology 1971;21:833–9. 6. Silver JR, Buxton PH. Spinal stroke. Brain 1971;97:539–50. 7. Pattany PM, Saraf-Lavi E, Bowen BC. MR angiography of the spine and spinal cord. Top Magn Reson Imag 2003;14:444–60. 8. Riggle KP, Oddi MA. Spinal cord necrosis and paraplegia as complications of the intra aortic balloon pump. Crit Care Med 1989;17:475–6. 9. Stone GW, Ohman EM, Miller MF, et al. Contemporary utilization and outcomes of intra- aortic balloon counterpulsation in acute myocardial infarction. The Benchmark Registry. J Am Cardiol 2003;41:1940–5. 10. Harris RE, Reimer KA, Crain BJ, et al. Spinal cord infarction following intraaortic balloon support. Ann Thorac Surg 1986;42:206–7. 11. Stone GW, Grines CL, Cox DA, et al. Comparison of angioplasty with stenting, with or without abciximab, in acute myocardial infarction. N Eng J Med 2002;346:957–66.
CASE REPORT
Heart Lung and Circulation 2006;15:53–55
Case Report
Thoracic Spinal Cord Ischemia Following Acute Myocardial Infarction and Cardiac Arrest in a Young Male O. Akbar Ali, MBBS a , A. Aggarwal, MBBS, FRACP b , G. Thanakrishnan, MBBS, FRACP c and H.C. Lowe, PhD, FRACP a,∗ a
Department of Cardiology, Concord Repatriation General Hospital, Sydney, NSW 2139, Australia b Department of Neurology, Concord Repatriation General Hospital, Sydney, NSW, Australia c Department of Intensive Care, Concord Repatriation General Hospital, Sydney, NSW, Australia Available online 2 June 2005
In an era of percutaneous stenting for acute myocardial infarction (AMI), a case of thoracic spinal cord ischemia following AMI and cardiac arrest is presented, to highlight and discuss this rare but debilitating condition, well-documented within the neurological literature, but rarely encountered in cardiovascular practice. (Heart Lung and Circulation 2006;15:53–55) © 2005 Australasian Society of Cardiac and Thoracic Surgeons and the Cardiac Society of Australia and New Zealand. Published by Elsevier Inc. All rights reserved. Keywords. Myocardial infarction; Coronary intervention
Introduction
W
ith an increasing preference for percutaneous treatment of acute myocardial infarction (AMI) with excellent angiographic and clinical outcomes often occurring, a case of thoracic spinal cord ischemia following AMI and cardiac arrest is presented, to highlight and discuss this rare but debilitating condition, well-documented within the neurological literature, but rarely encountered in cardiovascular practice.
Case Report A 24-year-old male was admitted to our institution having collapsed shortly after playing soccer. He had been previously well, except for two episodes of syncope in the three months prior. He smoked a packet of cigarettes per day. Immediately following the collapse, bystander cardiopulmonary resuscitation was commenced. On ambulance arrival, he was found to be in ventricular fibrillation, which required four d.c. cardioversions to achieve sinus rhythm. An acceptable cardiac output was then achieved, with the time from collapse to restoration of sinus rhythm estimated at 29 min. He was then intubated, ventilated and brought to the emergency department. Initial ECG suggested anterior myocardial infarction, and he was promptly taken to the cardiac catheterisation laboratory. His blood pressure was 90/60 mmHg ∗ Corresponding author. Tel.: +61 2 9767 6296; fax: +61 2 9767 6994. E-mail address: [email protected] (H.C. Lowe).
and his heart rate was 110 bpm. There was no evidence of pulmonary congestion. Coronary angiography revealed a single, proximal left anterior descending (LAD) artery coronary artery lesion, which appeared thrombusladen (Fig. 1A, thrombotic lesion marked by arrow). Flow in the distal LAD was also reduced, assessed at TIMI 0–11 (Fig. 1A). The lesion was promptly stented with a 4.5 mm × 18 mm Ultra stent (Guidant Corp, USA), though with no improvement in distal flow (Fig. 1B, poor distal flow marked by arrow). A bolus and infusion of abciximab (Lilly, USA) was given in addition to the aspirin, clopidogrel and heparin already administered. A 34 cm intraaortic balloon pump (IABP) was placed uneventfully and the patient was transferred to the intensive care unit (ICU). Echocardiography immediately after the intervention suggested anterior, apical and inferior akinesis. The IABP was removed the following day, with the blood pressure maintained at 120/70 without support. The ICU course was complicated by aspiration pneumonia, gramnegative septicaemia and delirium. Total Creatinine Kinase peaked at 5545 U/L and troponin T at 7.2 g/L. Beta blockade, ACE inhibition and statin therapy were started, and the patient transferred to the coronary care unit. On Day 6, he was unable to stand unaided or walk without assistance, when he first attempted to get out of bed. Neurological examination revealed bilateral pyramidal lower limb weakness of Medical Research Council (MRC) grade 4, absent lower limb deep tendon reflexes and a sensory level to touch and pain to T4-5. Posterior columns (vibration and proprioception) were preserved.
© 2005 Australasian Society of Cardiac and Thoracic Surgeons and the Cardiac Society of Australia and New Zealand. Published by Elsevier Inc. All rights reserved.
1443-9506/04/$30.00 doi:10.1016/j.hlc.2005.03.021
54
Ali et al. Thoracic spinal cord ischemia following acute myocardial infarction and cardiac arrest in a young male
Heart Lung and Circulation 2006;15:53–55
CASE REPORT
Figure 2. Anterior spinal magnetic resonance angiogram (MRA). The anterior spinal artery – normally present in the midline – is not detected (inferior arrow). An intercostal vessel is also not detected (superior arrow).
Figure 1. Coronary angiography (right anterior oblique view). (A) Initial angiography. Thrombus-laden proximal LAD lesion (marked by arrow). (B) Appearances post stenting. The stented lesion appears satisfactory. There is TIMI 0–1 flow in the distal LAD. (C) Appearances at 10 days. The stented site appears satisfactory. Distal LAD is normal.
There was evidence of cognitive impairment, as he was slow to process information and exhibited short-term memory impairment. On formal mini-mental examination score, he scored 25/30. There was no bowel or bladder dysfunction. Brain and spinal cord magnetic resonance imaging (MRI) were normal, with no evidence of white matter lesions or spinal cord infarction. The anterior spinal artery and an isolated intercostal artery were not visualised on magnetic resonance angiogram (MRA) (Fig. 2). With rehabilitation and physiotherapy, there was considerable improvement in function and mobility, to a point that, at six weeks, the patient was able to walk independently with only mild persistent weakness of hip flexors. His cognition and short-term memory also improved. Echocardiography on Day 2 showed marked improvement in LV function, with normal apical and anterior contractility, though persisting mild inferior hypokinesis. Coronary angiography demonstrated stent patency and TIMI 3 flow1 in the distal LAD at Day 10 (Fig. 1C). An electrophysiological study demonstrated no inducible arrhythmia.
Ali et al. Thoracic spinal cord ischemia following acute myocardial infarction and cardiac arrest in a young male
The overall impression was that of cardiac arrest and hypotension secondary to anterior myocardial infarction, successfully treated with resuscitation, cardioversion, stenting and IABP support, but resulting in anterior spinal cord ischemia and hypoxic encephalopathy.
Discussion Spinal cord ischemia is a rare but clinically and pathologically well-described entity.2–6 It is thought to be a result of reduced perfusion pressure, which may be the result of hypotension in the setting of cardiac arrest.4–6 Classically, it is considered to occur most frequently at the level of T4–T8 due to a relative paucity of vascular supply at this level.2 The anterior spinal artery arises from the vertebral arteries in the foramen magnum. The main feeder vessel to the thoracic spinal cord segment of this artery is the arteria magna of Adamkiewicz, which usually enters the spinal cord between the T5 and T8 segments. Damage, occlusion or hypoperfusion to this vessel may cause ischaemia or infarction of the thoracic spinal cord, usually up to T4, which is the upper extent of this feeder vessel. A small vessel may be particularly sensitive to prolonged hypotension. Spinal cord MRI may be normal, or show diffuse abnormality2 In this case, magnetic resonance angiography did not identify the anterior spinal artery. This vessel may have been small or even absent, but MRA, even using three dimensional reconstructions, is relatively insensitive for its detection.7 The presence or otherwise of the anterior spinal artery by MRA however, is entirely compatible in this case with a clinical diagnosis of spinal cord ischemia. This patient was young, and it is likely that he had absent or reduced cardiac output for up to 29 min. While he was a smoker, there were no other apparent risk factors, and subsequent hematologic screen for procoagulant markers was unremarkable. Neuronal necrosis has been documented in neonates and premature infants suffering hypotensive episodes,4,5 although this has not been shown to be related to age in one large series.2 The influence of age on outcome in this case can be only speculative. Although IABP use has been reported to cause spinal cord necrosis and paraplegia,8 a combined bowel, renal and spinal cord infarction of only 0.1% has been reported in a large series.9 This is thought to be on the basis of widespread cholesterol embolisation leading to anterior spinal arteriole occlusion.10 In this case, IABP positioning was considered optimal, the IABP was in situ overnight
55
only, and there was no evidence of cholesterol embolisation in a low risk individual. Thus, while use of the IABP cannot be completely excluded as cause for the symptoms and signs, this would appear unlikely. This case therefore most likely demonstrates transient spinal cord ischemia secondary to prolonged hypotension associated with anterior myocardial infarction and cardiac arrest; conditions which, while well described, are rarely encountered in cardiovascular medicine. While the cardiovascular outcome was excellent in this high-risk patient, rare and significant neurologic morbidity occurred. With an increasing use of effective percutaneous means of Ml treatment,11 this report emphasises that serious, noncardiac sequelae of cardiac arrest may still occur. HCL holds a Viertel Clinical Investigatorship and receives research support from the NHMRC.
References 1. Chesebro JH, Knatterud G, Roberts R, et al. Thrombolysis in Myocardial Infarction (TIMI) Trial, Phase I: a comparison between intravenous tissue plasminogen activator and intravenous streptokinase: clinical findings through hospital discharge. Circulation 1987;76:142–54. 2. Duggal N, Lach B, et al. Selective vulnerability of the lumbosacral spinal cord after cardiac arrest and hypotension. Stroke 2002;33:116–21. 3. Zang Z-A, Nonaka H, Hatori T. The microvasculature of the spinal cord in the human adult. Neuropathology 1997;17:32–42. 4. Cheshire WP, Santos CC, Massey EW, Howard Jr JF. Spinal Cord infarction: etiology and outcome. Neurology 1996;47:321–30. 5. Gilles FH, Nag D. Vulnerability of human spinal cord in transient cardiac arrest. Neurology 1971;21:833–9. 6. Silver JR, Buxton PH. Spinal stroke. Brain 1971;97:539–50. 7. Pattany PM, Saraf-Lavi E, Bowen BC. MR angiography of the spine and spinal cord. Top Magn Reson Imag 2003;14:444–60. 8. Riggle KP, Oddi MA. Spinal cord necrosis and paraplegia as complications of the intra aortic balloon pump. Crit Care Med 1989;17:475–6. 9. Stone GW, Ohman EM, Miller MF, et al. Contemporary utilization and outcomes of intra- aortic balloon counterpulsation in acute myocardial infarction. The Benchmark Registry. J Am Cardiol 2003;41:1940–5. 10. Harris RE, Reimer KA, Crain BJ, et al. Spinal cord infarction following intraaortic balloon support. Ann Thorac Surg 1986;42:206–7. 11. Stone GW, Grines CL, Cox DA, et al. Comparison of angioplasty with stenting, with or without abciximab, in acute myocardial infarction. N Eng J Med 2002;346:957–66.
CASE REPORT
Heart Lung and Circulation 2006;15:53–55