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Management of Life-Threatening Bradycardia in Spinal Cord Injury
Metal fatigue and an intrinsic metal defect were suggested as the cause of the breakage of the forceps. 1 •3 The real cause of the breakage remains to be determined. The breakage of the grasping forceps and the wire cytology brush was also reported. 5 •6 We recommend that the magnetic extractor be kept on hand at any institution where bronchoscopic examination is performed. It is also useful to retrieve other metallic foreign bodies. REFERENCES
1 Fulkerson WJ. Fiberoptic bronchoscopy. N Eng! J Med 1984; 311:511-15 2 Malilc SK, Behera D. Breakage of alligator biopsy furceps: an unusual complication during fiberoptic bronchoscopy. Chest 1984; 85:837-38 3 Masa-Jimenez JF, Verea-Hernando HR, Martin-Egana MT, Fontan-Bueso J. Breakage of alligator furceps in transbronchial biopsy. Chest 1985; 88:156 4 Herf SM, Suratt PM, Arora NS. Deaths and complications associated with transbronchial lung biopsy. Am Rev Respir Dis 1977; 115:708-11 5 Sanders DM. Needle in a haystack. Chest 1983; 83:935-36 6 Olesen LL, Thorshauge H, Nielsen BA. Breakage of the wire cytology brush during fiberoptic bronchoscopy. Chest 1987; 92:188
Management of Life-Threatening Bradycardia in Spinal Cord Injury Antoine G. Abd, M.D.;* and Norma M. T. Braun, M.D., F.C.C.P.t
A 19-year-old man with SCI at C5 suffered recurrent lifethreatening bradycardia and asystole. ~ detail his course, which included continual movement in a motion bed and propantheline-bromide (Pro-Banthine) therapy, over 3~ months. Possible cawes of bradycardia and autonomic dysfunction in this setting are discussed.
(Cheat 1989;95:701-0!)
B
radycardia and asystolic cardiac arrest are potentially preventable complications in SCI. Those with lesions above T6 exhibit exaggerated autonomic responses after innocuous stimuli, including bradycardia and cardiac arrest. Because of the scarcity of reports in the American literature, we detail the course of a 19-year-old man with SCI at C5, who suffered recurrent life-threatening bradycardia and asystole. We discuss the hypotheses for the pathogenesis of the bradyarrhythmias and autonomic dysfunction and describe their management. CASE REPORT A 19-year-old man was admitted to the ICU in coma with multiple traumas following a suicide attempt. He sustained a compression fracture of C6 and dislocation of C5, and had flaccid thorax, abdomen, and extremities, absent deep tendon and bulbocavernosus *Fellow, I?ivision of Pulmonary Diseases, Department of Medicine, St. Lukes-Roosevelt Hospital Center, New York. tAssociate Professor of Clinical Medicine, Columbia University, College
10025
reflexes, and a negative Babinski reflex. His Glasgow coma scale response was 6. 1 His chest x-ray film was normal. He was intubated to receive respiratory support. Analysis of his arterial blood gases on 35 percent Flo1 , respiratory rate 14, and tidal volume 800 ml, were: pH, 7.41; PaC01 , 26 mm Hg; Pa01 , 124 mm Hg; and bicarbonate, 16 mEq/L. His vital signs included blood pressure of 100160 mm Hg, a regular pulse of 75 to 80 beats/min, and a respiratory rate of 18 breaths/min. While he had spontaneous breathing, weaning from mechanical ventilation was unsuccessful owing to ineffectual inspiratory efforts with paradoxic chest wall movements. On day 17 he had + 1 reflexes in the extremities, and tracheostomy and posterior cervical fusion were done. A new right upper lobe infiltrate was noted; his WBC count was 14.2 x 1()3 cu mm. He began receiving therapy with cefutan and gentamicin and had gradual clearing. His heart rate declined to between 65 and 70 beats/min, with bradycardia occurring during suctioning and when moving the patient. Occasionally, the heart rate would fall unpredictably to 10 beats/ min. On one such occasion, he became hypotensive with decreased mental responsiveness. He began receiving atropine, 0.4 mg subcutaneously every 6 h, which controlled the bradycardia. A motion bed was introduced that moved the patient side to side, slowly and continuously, 15-16 times per hour. During this time, he was weaned from mechanical ventilation and atropine therapy. He was transferred to floor care with a normal mental status. The tracheostomy was allowed to close, and he was returned to an ordinary bed. Two months later, while on standard floor care, he was noted to be bradycardic after a seizure. He was returned to the ICU, where two additional episodes of bradycardia occurred during suctioning and without apparent external stimuli. Hypoxemia was not documented befure these episodes. He was reintubated and given atropine but continued to have intermittent severe bradycardia. Atropine dosage was increased to 0.6 mg every 4 h, but it failed to inhibit these episodes. lsoproterenol1:200 (Isuprel) drip at 0.25 JJ.g/ min was substituted and then increased to 0.5 JJ.g/min, with poor control of the bradycardia. Cardiac pacemaker implantation was considered but deferred because of pneumonia and two large infected decubitus ulcers over the buttocks and scapula. Two weeks later, lsuprel was still needed, causing excessive perspiration, which limited skin care. Furthermore, bradycardia control was not achieved. The motion bed therapy was resumed, and propantheline (Pro-Banthine), 30 mg every 4 h, added. This successfully controlled the bradycardia without Isuprel. Therapy with Pro-Banthine induced gastric atony, which was incompletely alleviated with metoclopramide. Gastrostomy placement with sustained feedings helped. The decubitus ulcers necessitated a diverting colostomy and skin grafting to heal. A gradual, monitored decrease of the Pro-Banthine dosage from 30 mg to 15 mg every 4 h, then to every 6 h, was cautiously done. As the patients status improved and spasticity developed, the motion bed therapy was discontinued. Pro-Banthine dosage was decreased further to 15 mg every 8 h, then to 15 mg every 12 h, then to 15 mg nightly, and finally was successfully discontinued after a total course of 3lh months. The patient had no further bradyarrhythmias over the next two weeks, when be was transferred to a rehabilitation center. DISCUSSION
There are no reports to our knowledge in the American literature detailing the management of cardiac arrhythmias in SCI. The frequency of death from this complication is unknown. While the spinal shock syndrome includes reflex depression and vasomotor instability, the most threatening aspect of this dysfunction is bradycardia, occasionally progressing to heart block. Kewalramani• reported that the earliest onset of autonomic CHEST 195 I 3 I MARCH, 1989
701
dysfunction was four weeks after SCI; most occurred between three and four months. In one patient it was first recorded 13 years after SCI. The delay between trauma and syndrome expression has been attributed to denervation hypersensitivity or to sprouting of ascending fibers forming abnormal synapses. 2 About 30 percent of all tetraplegics and about 80 percent of those with cervical or high thoracic lesions experienced autonomic dysfunction, of which the most frequent was paroxysmal hypertension. Bradycardia was seen in about 8 to 10 percent of these patients and hypotension in 10 percent. 2 Cardiac manifestations reported included premature atrial and ventricular contractions and heart block of varying degrees. Even in the absence of intrinsic cardiac disease, blood flow redistribution contributed to cardiac silhouette enlargement but did not explain the arrhythmias. Mathias3 described four tetraplegic males receiving mechanical ventilation who developed bradycardia progressing to cardiac asystole in two, following tracheal suctioning or change in position. In one patient, cardiac arrest occurred during suctioning 44 days after SCI. Three of four patients had collapsed lobes on chest roentgenogram but had no evidence of hypoxemia. The bradycardia may have been due to the combined effect of hypoxemia during suctioning and unopposed vagal reflex due to absent sympathetic activity. The resolution of the bradycardia after various combinations of atropine, ephedrine, or Pro-Banthine and oxygen gave support to that speculation. 3 Plasma and urinary catecholamine levels have been variable and thus do not explain these events. 2 Normally tracheal suctioning results in increased heart rate because of sympathetic stimulation from the mechanical irritation. In the absence of sympathetic responsiveness, bradycardia and asystole result from uninhibited vasovagal reflexes. Pelvic afferent stimulation causes hypertension in normal persons, but reflex stimulation of aortic and carotid sinus vagally mediated baroreceptors usually offsets any blood pressure rise. When SCI occurs above the splanchnic outflow, interruption of sympathetic pathways leave the vagal reflexes unopposed, leading to bradycardia. Any cutaneous, proprioceptive, or visceral stimulus can be a trigger mechanism. Thus, changes in body position, abdominal visceral distention, or tracheal suctioning can be precipitants. In contrast to previous reports, it is not clear why the bradycardia that had resolved at one point in our patient recurred. Possible explanations include the following: (1) minor or very transient episodes of bradycardia may have gone unnoticed until a seizure occurred; (2) during standard floor care, he developed decubitus ulcers and pneumonia, which could have acted as cutaneous and visceral triggers; and (3) inability reflexly to increase sympathetic activity in response to infrequent postural changes might have led to hypotension. Regularly rendered, frequent postural changes diminish autonomic dysfunction. •.• In the ICU, our patient had been placed on a motion bed, which could have maintained vasomotor tone owing to the continuous gentle stimulation from body position changes. When he was transferred to standard floor care, he was placed on a regular bed, thus losing vasomotor tone again. After the development of spasticity, tone was spontaneously improved. Regular movement with active rehabilitation rendered the motion 702
bed no longer necessary. Although the exact mechanisms of the spinal shock syndrome are not fully understood, maneuvers aimed at reducing precipitants are clearly important. Therapy is lifesaving for the bradyarrhythmias. Some patients respond to oxygen and atropine alone (0.4 to 0.6 mg every 6 h) over several days. Prolonged therapy with Pro-Banthine, up to 50 mg orally every 6 h, may be needed. Occasionally ephedrine (50 mg orally every 6 h) could be added. BladdeNelated triggers can be inhibited by local anesthesia. 2 Colorectal distention should be relieved promptly. While guanethidine has been recommended for the prevention of dysreflexia, it can itself produce hypotension. • There are no clinical or laboratory guidelines for predicting how long therapy is needed. When reflex spinal cord activity returns, pharmacotherapy can be gradually discontinued under close monitoring. Our experience suggests that continued motion bed use may be helpful in decreasing or even inhibiting the occurrence of autonomic dysfunction. Additional studies are needed to confirm this. Spinal shock syndrome can be expected following upper thoracic and cervical cord lesions, and unopposed vagal action leading to bradycardia after various visceral and cutaneous stimuli seems to be the cause. Continuous movement and pharmacologic intervention are lifesaving. The duration of therapy is individually determined. Awareness of this life-threatening manifestation allows institution of therapy that would decrease the likelihood of unexpected death. REFERENCES 1 Becker DP. Head injuries. In: Wyngaarden J, Smith L Jr, eds. Cecil textbook of medicine, 18th ed. Philadelphia: WB Saunders, 1988:2242 2 Kewalramani LS. Autonomic dysrefiexia in traumatic myelopathy. Am J Phys Med 1980; 59:1-21 3 Mathias CJ. Bradycardia and cardiac arrest during tracheal suction: mechanisms in tetraplegic patients. Eur J lntens Care Med 1976; 2:147-56 4 Mathias CR, Frankel HL. Autonomic failure in tetraplegia. In: Bannister R, ed. Autonomic failure. Oxford: Oxford University Press, 1985:453-88 5 Carpendale M. Orthotics. Redford J, ed, 3rd ed. Baltimore: Williams & Wilkins, 1986:518-40
Elicitation of Myocardial Ischemia by Nifedipine in a Case of Coronary Artery Fistula Piero Montorsi, M.D.,* Antonio BartoreUi, M.D.,* and Francesco Garbagnati, M.D.t
A 63-year-old woman had chest pain that worsened when nifedipine was given. She was found to have a right coronaryto-thorax angioma/fistula. Acute nifedipine administration *lstituto di Cardiologia dell'Universita, Centro di Studio Ricerche Cardiovascolari del Consiglio Nazionale delle Ricerche, lstituto "G. Sisini," Fondazione "I. Monzino," Milan, Italy. tlstituto Nazionale dei Tumori, Sezione di Radiologia, Milan. Reprint requests: Dr. Montorsi, lstituto di Cardiologia Universita, Vw lbroa 4, Milan, Italy 20138 Elicitation of Myocardial Ischemia by Nifedipine (Montotsi, Bartorelli, Garbagnati)
1 Fulkerson WJ. Fiberoptic bronchoscopy. N Eng! J Med 1984; 311:511-15 2 Malilc SK, Behera D. Breakage of alligator biopsy furceps: an unusual complication during fiberoptic bronchoscopy. Chest 1984; 85:837-38 3 Masa-Jimenez JF, Verea-Hernando HR, Martin-Egana MT, Fontan-Bueso J. Breakage of alligator furceps in transbronchial biopsy. Chest 1985; 88:156 4 Herf SM, Suratt PM, Arora NS. Deaths and complications associated with transbronchial lung biopsy. Am Rev Respir Dis 1977; 115:708-11 5 Sanders DM. Needle in a haystack. Chest 1983; 83:935-36 6 Olesen LL, Thorshauge H, Nielsen BA. Breakage of the wire cytology brush during fiberoptic bronchoscopy. Chest 1987; 92:188
Management of Life-Threatening Bradycardia in Spinal Cord Injury Antoine G. Abd, M.D.;* and Norma M. T. Braun, M.D., F.C.C.P.t
A 19-year-old man with SCI at C5 suffered recurrent lifethreatening bradycardia and asystole. ~ detail his course, which included continual movement in a motion bed and propantheline-bromide (Pro-Banthine) therapy, over 3~ months. Possible cawes of bradycardia and autonomic dysfunction in this setting are discussed.
(Cheat 1989;95:701-0!)
B
radycardia and asystolic cardiac arrest are potentially preventable complications in SCI. Those with lesions above T6 exhibit exaggerated autonomic responses after innocuous stimuli, including bradycardia and cardiac arrest. Because of the scarcity of reports in the American literature, we detail the course of a 19-year-old man with SCI at C5, who suffered recurrent life-threatening bradycardia and asystole. We discuss the hypotheses for the pathogenesis of the bradyarrhythmias and autonomic dysfunction and describe their management. CASE REPORT A 19-year-old man was admitted to the ICU in coma with multiple traumas following a suicide attempt. He sustained a compression fracture of C6 and dislocation of C5, and had flaccid thorax, abdomen, and extremities, absent deep tendon and bulbocavernosus *Fellow, I?ivision of Pulmonary Diseases, Department of Medicine, St. Lukes-Roosevelt Hospital Center, New York. tAssociate Professor of Clinical Medicine, Columbia University, College
10025
reflexes, and a negative Babinski reflex. His Glasgow coma scale response was 6. 1 His chest x-ray film was normal. He was intubated to receive respiratory support. Analysis of his arterial blood gases on 35 percent Flo1 , respiratory rate 14, and tidal volume 800 ml, were: pH, 7.41; PaC01 , 26 mm Hg; Pa01 , 124 mm Hg; and bicarbonate, 16 mEq/L. His vital signs included blood pressure of 100160 mm Hg, a regular pulse of 75 to 80 beats/min, and a respiratory rate of 18 breaths/min. While he had spontaneous breathing, weaning from mechanical ventilation was unsuccessful owing to ineffectual inspiratory efforts with paradoxic chest wall movements. On day 17 he had + 1 reflexes in the extremities, and tracheostomy and posterior cervical fusion were done. A new right upper lobe infiltrate was noted; his WBC count was 14.2 x 1()3 cu mm. He began receiving therapy with cefutan and gentamicin and had gradual clearing. His heart rate declined to between 65 and 70 beats/min, with bradycardia occurring during suctioning and when moving the patient. Occasionally, the heart rate would fall unpredictably to 10 beats/ min. On one such occasion, he became hypotensive with decreased mental responsiveness. He began receiving atropine, 0.4 mg subcutaneously every 6 h, which controlled the bradycardia. A motion bed was introduced that moved the patient side to side, slowly and continuously, 15-16 times per hour. During this time, he was weaned from mechanical ventilation and atropine therapy. He was transferred to floor care with a normal mental status. The tracheostomy was allowed to close, and he was returned to an ordinary bed. Two months later, while on standard floor care, he was noted to be bradycardic after a seizure. He was returned to the ICU, where two additional episodes of bradycardia occurred during suctioning and without apparent external stimuli. Hypoxemia was not documented befure these episodes. He was reintubated and given atropine but continued to have intermittent severe bradycardia. Atropine dosage was increased to 0.6 mg every 4 h, but it failed to inhibit these episodes. lsoproterenol1:200 (Isuprel) drip at 0.25 JJ.g/ min was substituted and then increased to 0.5 JJ.g/min, with poor control of the bradycardia. Cardiac pacemaker implantation was considered but deferred because of pneumonia and two large infected decubitus ulcers over the buttocks and scapula. Two weeks later, lsuprel was still needed, causing excessive perspiration, which limited skin care. Furthermore, bradycardia control was not achieved. The motion bed therapy was resumed, and propantheline (Pro-Banthine), 30 mg every 4 h, added. This successfully controlled the bradycardia without Isuprel. Therapy with Pro-Banthine induced gastric atony, which was incompletely alleviated with metoclopramide. Gastrostomy placement with sustained feedings helped. The decubitus ulcers necessitated a diverting colostomy and skin grafting to heal. A gradual, monitored decrease of the Pro-Banthine dosage from 30 mg to 15 mg every 4 h, then to every 6 h, was cautiously done. As the patients status improved and spasticity developed, the motion bed therapy was discontinued. Pro-Banthine dosage was decreased further to 15 mg every 8 h, then to 15 mg every 12 h, then to 15 mg nightly, and finally was successfully discontinued after a total course of 3lh months. The patient had no further bradyarrhythmias over the next two weeks, when be was transferred to a rehabilitation center. DISCUSSION
There are no reports to our knowledge in the American literature detailing the management of cardiac arrhythmias in SCI. The frequency of death from this complication is unknown. While the spinal shock syndrome includes reflex depression and vasomotor instability, the most threatening aspect of this dysfunction is bradycardia, occasionally progressing to heart block. Kewalramani• reported that the earliest onset of autonomic CHEST 195 I 3 I MARCH, 1989
701
dysfunction was four weeks after SCI; most occurred between three and four months. In one patient it was first recorded 13 years after SCI. The delay between trauma and syndrome expression has been attributed to denervation hypersensitivity or to sprouting of ascending fibers forming abnormal synapses. 2 About 30 percent of all tetraplegics and about 80 percent of those with cervical or high thoracic lesions experienced autonomic dysfunction, of which the most frequent was paroxysmal hypertension. Bradycardia was seen in about 8 to 10 percent of these patients and hypotension in 10 percent. 2 Cardiac manifestations reported included premature atrial and ventricular contractions and heart block of varying degrees. Even in the absence of intrinsic cardiac disease, blood flow redistribution contributed to cardiac silhouette enlargement but did not explain the arrhythmias. Mathias3 described four tetraplegic males receiving mechanical ventilation who developed bradycardia progressing to cardiac asystole in two, following tracheal suctioning or change in position. In one patient, cardiac arrest occurred during suctioning 44 days after SCI. Three of four patients had collapsed lobes on chest roentgenogram but had no evidence of hypoxemia. The bradycardia may have been due to the combined effect of hypoxemia during suctioning and unopposed vagal reflex due to absent sympathetic activity. The resolution of the bradycardia after various combinations of atropine, ephedrine, or Pro-Banthine and oxygen gave support to that speculation. 3 Plasma and urinary catecholamine levels have been variable and thus do not explain these events. 2 Normally tracheal suctioning results in increased heart rate because of sympathetic stimulation from the mechanical irritation. In the absence of sympathetic responsiveness, bradycardia and asystole result from uninhibited vasovagal reflexes. Pelvic afferent stimulation causes hypertension in normal persons, but reflex stimulation of aortic and carotid sinus vagally mediated baroreceptors usually offsets any blood pressure rise. When SCI occurs above the splanchnic outflow, interruption of sympathetic pathways leave the vagal reflexes unopposed, leading to bradycardia. Any cutaneous, proprioceptive, or visceral stimulus can be a trigger mechanism. Thus, changes in body position, abdominal visceral distention, or tracheal suctioning can be precipitants. In contrast to previous reports, it is not clear why the bradycardia that had resolved at one point in our patient recurred. Possible explanations include the following: (1) minor or very transient episodes of bradycardia may have gone unnoticed until a seizure occurred; (2) during standard floor care, he developed decubitus ulcers and pneumonia, which could have acted as cutaneous and visceral triggers; and (3) inability reflexly to increase sympathetic activity in response to infrequent postural changes might have led to hypotension. Regularly rendered, frequent postural changes diminish autonomic dysfunction. •.• In the ICU, our patient had been placed on a motion bed, which could have maintained vasomotor tone owing to the continuous gentle stimulation from body position changes. When he was transferred to standard floor care, he was placed on a regular bed, thus losing vasomotor tone again. After the development of spasticity, tone was spontaneously improved. Regular movement with active rehabilitation rendered the motion 702
bed no longer necessary. Although the exact mechanisms of the spinal shock syndrome are not fully understood, maneuvers aimed at reducing precipitants are clearly important. Therapy is lifesaving for the bradyarrhythmias. Some patients respond to oxygen and atropine alone (0.4 to 0.6 mg every 6 h) over several days. Prolonged therapy with Pro-Banthine, up to 50 mg orally every 6 h, may be needed. Occasionally ephedrine (50 mg orally every 6 h) could be added. BladdeNelated triggers can be inhibited by local anesthesia. 2 Colorectal distention should be relieved promptly. While guanethidine has been recommended for the prevention of dysreflexia, it can itself produce hypotension. • There are no clinical or laboratory guidelines for predicting how long therapy is needed. When reflex spinal cord activity returns, pharmacotherapy can be gradually discontinued under close monitoring. Our experience suggests that continued motion bed use may be helpful in decreasing or even inhibiting the occurrence of autonomic dysfunction. Additional studies are needed to confirm this. Spinal shock syndrome can be expected following upper thoracic and cervical cord lesions, and unopposed vagal action leading to bradycardia after various visceral and cutaneous stimuli seems to be the cause. Continuous movement and pharmacologic intervention are lifesaving. The duration of therapy is individually determined. Awareness of this life-threatening manifestation allows institution of therapy that would decrease the likelihood of unexpected death. REFERENCES 1 Becker DP. Head injuries. In: Wyngaarden J, Smith L Jr, eds. Cecil textbook of medicine, 18th ed. Philadelphia: WB Saunders, 1988:2242 2 Kewalramani LS. Autonomic dysrefiexia in traumatic myelopathy. Am J Phys Med 1980; 59:1-21 3 Mathias CJ. Bradycardia and cardiac arrest during tracheal suction: mechanisms in tetraplegic patients. Eur J lntens Care Med 1976; 2:147-56 4 Mathias CR, Frankel HL. Autonomic failure in tetraplegia. In: Bannister R, ed. Autonomic failure. Oxford: Oxford University Press, 1985:453-88 5 Carpendale M. Orthotics. Redford J, ed, 3rd ed. Baltimore: Williams & Wilkins, 1986:518-40
Elicitation of Myocardial Ischemia by Nifedipine in a Case of Coronary Artery Fistula Piero Montorsi, M.D.,* Antonio BartoreUi, M.D.,* and Francesco Garbagnati, M.D.t
A 63-year-old woman had chest pain that worsened when nifedipine was given. She was found to have a right coronaryto-thorax angioma/fistula. Acute nifedipine administration *lstituto di Cardiologia dell'Universita, Centro di Studio Ricerche Cardiovascolari del Consiglio Nazionale delle Ricerche, lstituto "G. Sisini," Fondazione "I. Monzino," Milan, Italy. tlstituto Nazionale dei Tumori, Sezione di Radiologia, Milan. Reprint requests: Dr. Montorsi, lstituto di Cardiologia Universita, Vw lbroa 4, Milan, Italy 20138 Elicitation of Myocardial Ischemia by Nifedipine (Montotsi, Bartorelli, Garbagnati)