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Defecation-induced bronchospasm
The Journal of Emergency Medicine, Vol. 18, No. 2, pp. 195–197, 2000 Copyright © 2000 Elsevier Science Inc. Printed in the USA. All rights reserved 0736-4679/00 $–see front matter
PII S0736-4679(99)00193-6
Clinical Communications
DEFECATION-INDUCED BRONCHOSPASM Lorca Rossman,
MD
Department of Emergency Medicine, Alameda County Medical Center, Highland Campus, Oakland, California Reprint Address: Lorca Rossman, MD, Department of Emergency Medicine, Alameda County Medical Center, Highland Campus, 1411 East 31st Street, Oakland, CA 94602
e Abstract—Acute asthma exacerbations are common. Patients with asthma experience symptoms in response to a wide variety of stimuli, and identifying the precipitating cause may be useful in guiding treatment and preventing future attacks. A case of asthma exacerbation occurring during multiple defecations is reported. Abnormal parasympathetic tone has been implicated in the pathogenesis of certain types of asthma, and defecation can be associated with increased parasympathetic tone. This patient’s pattern of defecation-related asthma exacerbations responded to prophylactic anticholinergic medication. © 2000 Elsevier Science Inc.
her prophylactic medication. It is postulated that the exacerbations were the result of increased parasympathetic activity during defecation.
CASE REPORT A 26-year-old woman with a history of asthma presented to the emergency department (ED) with severe shortness of breath. She had self-administered three nebulized albuterol treatments and taken 10 mg prednisone before calling 911. She was noted by the paramedics to be unable to speak and to have marked intercostal retractions. En route, she received three more nebulized albuterol treatments and 0.3 mg of epinephrine subcutaneously, with significant improvement. She stated that her symptoms had begun suddenly an hour before while having a bowel movement. She denied recent illness, exposure to allergens, or exercise. The patient’s history was significant for asthma since childhood, with three visits to this emergency department and one admission for defecation-related asthma exacerbation in the last year. She had been intubated for asthma once four years before admission but did not know what triggered that attack. She denied other medical problems. Her only reported allergy was to penicillin. Her usual medications included albuterol metered-dose inhalers (MDIs) four times a day, ipratropium MDIs every morning, and a triamcinolone MDI irregularly. She saw her primary physician rarely and received most of her medica-
e Keywords—asthma; bronchospasm; defecation; anticholinergic; ipratropium
INTRODUCTION In certain patterns of asthma, particularly cold-, sleep-, and exercise-induced asthma, exacerbations appear to be related to abnormal parasympathetic tone (1–5). Vagal manifestations of defecation are well described, including bradycardia and defecation syncope (6). Although defecation is associated with increased parasympathetic activity, it has not been previously identified as a trigger for asthma exacerbations. The case of a 26-year-old asthmatic with recurrent asthma exacerbations temporally related to defecation is reported. She was treated with prophylactic anticholinergic medication before bowel movements with resolution of her symptoms. She subsequently returned with another severe exacerbation on an occasion when she had skipped
RECEIVED: 6 January 1999; FINAL ACCEPTED: 21 June 1999
SUBMISSION RECEIVED:
21 May 1999;
195
196
L. Rossman
tions through the ED. She smoked one-half pack of cigarettes daily and denied any illicit substance use. On examination, vital signs were: temperature 37.1°C (98.8° F), heart rate 146 beats per minute, blood pressure 156/98 mmHg, and respirations 32 breaths per minute. Pulse-oximetry revealed 100% oxygen saturation on high-flow oxygen by mask. The patient appeared to be in mild respiratory distress and was speaking in short sentences. She was not cyanotic and had no nasal flaring or intercostal retractions. The lungs had diffuse wheezes and good air movement, with equal breath sounds bilaterally and a prolonged expiratory phase. The heart was regular, tachycardic, and without murmur. The rest of the physical examination was normal. Peak expiratory flow rate (PEFR) was 120 liters per second; she reported her baseline PEFR to be 200. The patient was placed on continuous nebulized albuterol and ipratropium and received 125 mg methylprednisolone i.v. She continued to improve clinically, and oxygen and nebulized treatments were discontinued after 1 h. At this time, the PEFR was 250 liters per second, and she was able to speak in extended sentences. After a period of observation, she was discharged with a 5-day course of prednisone, an epinephrine auto-injector (Epi-Pen娂), and instructions to use her ipratropium inhaler before bowel movements. The patient returned to the ED by ambulance with severe respiratory distress 10 weeks later. She stated that she had been regularly using the ipratropium inhaler before and after bowel movements and had had no problems with her asthma during that time. On the day of her return visit, she did not use the inhaler and experienced a rapid onset of wheezing and shortness of breath during defecation. In the ED, she responded well to nebulized albuterol and ipratropium and was discharged home breathing comfortably.
DISCUSSION Cardiovascular changes associated with defecation are well described (6). The term defecation syncope has been used to describe a transient loss of consciousness during or immediately after bowel movement (6). The presumed mechanism of this syndrome is a sudden fall in arterial
blood pressure resulting from a vagally mediated decrease in heart rate. Rectal stimulation has been used successfully as a “vagal-maneuver” in the treatment of PSVT to slow conduction through the AV node (7). This patient had a history of asthma exacerbations beginning during bowel movements. It seems possible that these exacerbations resulted from a reflexive vagal discharge similar to that occurring in defecation syncope, and her syndrome might appropriately be termed defecation-induced bronchospasm. Autonomic control of the airways is complex and relies primarily upon -2-adrenergic and muscarinic receptors (8). Muscarinic M3 receptors occur in bronchial smooth muscle and cause bronchoconstriction in response to vagal stimulation (9 –11). Abnormal parasympathetic tone may be involved in the pathogenesis of asthma. Asthmatics have increased sinus dysrhythmia (variation in beat-to-beat heart rate with the respiratory cycle) compared with controls, as well as more pronounced bradycardic responses to Valsalva maneuver; both are markers of vagal activity (12–14). Because of the heightened parasympathetic tone in asthmatics and evidence that vagal efferent activity can cause bronchospasm, anticholinergics have been used in the treatment of asthma. Initial enthusiasm for the use of atropine in treating asthma was dampened by the presence of significant systemic side effects. Nonetheless, cholinergic stimulation is probably important to varying degrees in certain subpopulations of asthmatics. In particular, vagal tone appears to play an important role in patients with cold-, sleep-, and exercise-induced asthma, and there is evidence that such patients may benefit from anticholinergic medications (1–5,15,16). This case emphasizes the importance of identifying triggers for patients who present with asthma exacerbations. At the time of discharge, the patient was prescribed an inhaled anticholinergic agent, ipratropium, for use before bowel movements with the hope of preventing recurrence of her attacks. She reported good compliance with this medication and had no asthma exacerbations while using it. The reoccurrence of a severe asthma exacerbation on an occasion when she did not use her ipratropium supports the hypothesis that the bronchospasm was mediated by a parasympathetic reflex that was preventable by cholinergic blockade.
REFERENCES 1. Nolte D, Berger D. On vagal bronchoconstriction in asthmatic patients by nasal irritation. Eur J Respir Dis Suppl 1983;128: 110 –5. 2. Sheppard D, Epstein J, Holtzman M, Nadel JA, Boushey HA. Dose-dependent inhibition of cold air-induced bronchoconstriction by atropine. J Appl Physiol 1982;53:169 –74. 3. van Aalderen WM, Meijer GG, Oosterhoff Y, Bron AO. Epidemi-
ology and the concept of underlying mechanisms of nocturnal asthma. Respir Med 1993;87(Suppl B):37–9. 4. Martin R. Nocturnal asthma: circadian rhythms and therapeutic interventions. Am Rev Respir Dis 1993;147:S25– 8. 5. Finnerty JP, Holgate ST. The contribution of histamine release and vagal reflexes, alone and in combination, to exercise-induced asthma. (See comments.) Eur Respir J 1993;6:1132–7.
Defecation-Induced Bronchospasm 6. Goldman JM. Syncope. In: Harwood-Nuss AL, ed. The Clinical Practice of Emergency Medicine, 2nd edn. Philadelphia: Lippincott-Raven; 1996:628 –9. 7. Roberge R, Anderson E, MacMath T, Rudoff J, Luten R. Termination of paroxysmal supraventricular tachycardia by digital rectal massage. Ann Emerg Med 1987;16:1291–3. 8. de Jongste JC, Jongejan RC, Kerrebijn KF. Control of airway caliber by autonomic nerves in asthma and in chronic obstructive pulmonary disease. Am Rev Respir Dis 1991;143:1421– 6. 9. Fryer AD, Jacoby DB. Effect of inflammatory cell mediators on M2 muscarinic receptors in the lungs. Life Sci 1993;52:529 –36. 10. Barnes PJ. Muscarinic receptors in airways: recent developments. J Appl Physiol 1990;68:1777– 85. 11. Barnes PJ. Muscarinic receptor subtypes in airways. Life Sci 1993;52:521–7.
197 12. Kallenbach JM, Webster T, Dowdeswell R, Reinach SG, Millar RN, Zwi S. Reflex heart rate control in asthma. Evidence of parasympathetic overactivity. Chest 1985;87:644 – 8. 13. Gupta S, Dolwani S. A study of autonomic status and its effect on ventilatory functions in bronchial asthma. Indian J Chest Dis Allied Sci 1996;38:147–56. 14. Hashimoto A, Maeda H, Yokoyama M. Augmentation of parasympathetic nerve function in patients with extrinsic bronchial asthma— evaluation by coefficiency of variance of R-R interval with modified long-term ECG monitoring system. Kobe J Med Sci 1996;42:347–59. 15. Coe CI, Barnes PJ. Reduction of nocturnal asthma by an inhaled anticholinergic drug. Chest 1986;90:485– 8. 16. Morrison JF, Pearson SB, Dean HG. Parasympathetic nervous system in nocturnal asthma. BMJ 1988;296:1427–9.
PII S0736-4679(99)00193-6
Clinical Communications
DEFECATION-INDUCED BRONCHOSPASM Lorca Rossman,
MD
Department of Emergency Medicine, Alameda County Medical Center, Highland Campus, Oakland, California Reprint Address: Lorca Rossman, MD, Department of Emergency Medicine, Alameda County Medical Center, Highland Campus, 1411 East 31st Street, Oakland, CA 94602
e Abstract—Acute asthma exacerbations are common. Patients with asthma experience symptoms in response to a wide variety of stimuli, and identifying the precipitating cause may be useful in guiding treatment and preventing future attacks. A case of asthma exacerbation occurring during multiple defecations is reported. Abnormal parasympathetic tone has been implicated in the pathogenesis of certain types of asthma, and defecation can be associated with increased parasympathetic tone. This patient’s pattern of defecation-related asthma exacerbations responded to prophylactic anticholinergic medication. © 2000 Elsevier Science Inc.
her prophylactic medication. It is postulated that the exacerbations were the result of increased parasympathetic activity during defecation.
CASE REPORT A 26-year-old woman with a history of asthma presented to the emergency department (ED) with severe shortness of breath. She had self-administered three nebulized albuterol treatments and taken 10 mg prednisone before calling 911. She was noted by the paramedics to be unable to speak and to have marked intercostal retractions. En route, she received three more nebulized albuterol treatments and 0.3 mg of epinephrine subcutaneously, with significant improvement. She stated that her symptoms had begun suddenly an hour before while having a bowel movement. She denied recent illness, exposure to allergens, or exercise. The patient’s history was significant for asthma since childhood, with three visits to this emergency department and one admission for defecation-related asthma exacerbation in the last year. She had been intubated for asthma once four years before admission but did not know what triggered that attack. She denied other medical problems. Her only reported allergy was to penicillin. Her usual medications included albuterol metered-dose inhalers (MDIs) four times a day, ipratropium MDIs every morning, and a triamcinolone MDI irregularly. She saw her primary physician rarely and received most of her medica-
e Keywords—asthma; bronchospasm; defecation; anticholinergic; ipratropium
INTRODUCTION In certain patterns of asthma, particularly cold-, sleep-, and exercise-induced asthma, exacerbations appear to be related to abnormal parasympathetic tone (1–5). Vagal manifestations of defecation are well described, including bradycardia and defecation syncope (6). Although defecation is associated with increased parasympathetic activity, it has not been previously identified as a trigger for asthma exacerbations. The case of a 26-year-old asthmatic with recurrent asthma exacerbations temporally related to defecation is reported. She was treated with prophylactic anticholinergic medication before bowel movements with resolution of her symptoms. She subsequently returned with another severe exacerbation on an occasion when she had skipped
RECEIVED: 6 January 1999; FINAL ACCEPTED: 21 June 1999
SUBMISSION RECEIVED:
21 May 1999;
195
196
L. Rossman
tions through the ED. She smoked one-half pack of cigarettes daily and denied any illicit substance use. On examination, vital signs were: temperature 37.1°C (98.8° F), heart rate 146 beats per minute, blood pressure 156/98 mmHg, and respirations 32 breaths per minute. Pulse-oximetry revealed 100% oxygen saturation on high-flow oxygen by mask. The patient appeared to be in mild respiratory distress and was speaking in short sentences. She was not cyanotic and had no nasal flaring or intercostal retractions. The lungs had diffuse wheezes and good air movement, with equal breath sounds bilaterally and a prolonged expiratory phase. The heart was regular, tachycardic, and without murmur. The rest of the physical examination was normal. Peak expiratory flow rate (PEFR) was 120 liters per second; she reported her baseline PEFR to be 200. The patient was placed on continuous nebulized albuterol and ipratropium and received 125 mg methylprednisolone i.v. She continued to improve clinically, and oxygen and nebulized treatments were discontinued after 1 h. At this time, the PEFR was 250 liters per second, and she was able to speak in extended sentences. After a period of observation, she was discharged with a 5-day course of prednisone, an epinephrine auto-injector (Epi-Pen娂), and instructions to use her ipratropium inhaler before bowel movements. The patient returned to the ED by ambulance with severe respiratory distress 10 weeks later. She stated that she had been regularly using the ipratropium inhaler before and after bowel movements and had had no problems with her asthma during that time. On the day of her return visit, she did not use the inhaler and experienced a rapid onset of wheezing and shortness of breath during defecation. In the ED, she responded well to nebulized albuterol and ipratropium and was discharged home breathing comfortably.
DISCUSSION Cardiovascular changes associated with defecation are well described (6). The term defecation syncope has been used to describe a transient loss of consciousness during or immediately after bowel movement (6). The presumed mechanism of this syndrome is a sudden fall in arterial
blood pressure resulting from a vagally mediated decrease in heart rate. Rectal stimulation has been used successfully as a “vagal-maneuver” in the treatment of PSVT to slow conduction through the AV node (7). This patient had a history of asthma exacerbations beginning during bowel movements. It seems possible that these exacerbations resulted from a reflexive vagal discharge similar to that occurring in defecation syncope, and her syndrome might appropriately be termed defecation-induced bronchospasm. Autonomic control of the airways is complex and relies primarily upon -2-adrenergic and muscarinic receptors (8). Muscarinic M3 receptors occur in bronchial smooth muscle and cause bronchoconstriction in response to vagal stimulation (9 –11). Abnormal parasympathetic tone may be involved in the pathogenesis of asthma. Asthmatics have increased sinus dysrhythmia (variation in beat-to-beat heart rate with the respiratory cycle) compared with controls, as well as more pronounced bradycardic responses to Valsalva maneuver; both are markers of vagal activity (12–14). Because of the heightened parasympathetic tone in asthmatics and evidence that vagal efferent activity can cause bronchospasm, anticholinergics have been used in the treatment of asthma. Initial enthusiasm for the use of atropine in treating asthma was dampened by the presence of significant systemic side effects. Nonetheless, cholinergic stimulation is probably important to varying degrees in certain subpopulations of asthmatics. In particular, vagal tone appears to play an important role in patients with cold-, sleep-, and exercise-induced asthma, and there is evidence that such patients may benefit from anticholinergic medications (1–5,15,16). This case emphasizes the importance of identifying triggers for patients who present with asthma exacerbations. At the time of discharge, the patient was prescribed an inhaled anticholinergic agent, ipratropium, for use before bowel movements with the hope of preventing recurrence of her attacks. She reported good compliance with this medication and had no asthma exacerbations while using it. The reoccurrence of a severe asthma exacerbation on an occasion when she did not use her ipratropium supports the hypothesis that the bronchospasm was mediated by a parasympathetic reflex that was preventable by cholinergic blockade.
REFERENCES 1. Nolte D, Berger D. On vagal bronchoconstriction in asthmatic patients by nasal irritation. Eur J Respir Dis Suppl 1983;128: 110 –5. 2. Sheppard D, Epstein J, Holtzman M, Nadel JA, Boushey HA. Dose-dependent inhibition of cold air-induced bronchoconstriction by atropine. J Appl Physiol 1982;53:169 –74. 3. van Aalderen WM, Meijer GG, Oosterhoff Y, Bron AO. Epidemi-
ology and the concept of underlying mechanisms of nocturnal asthma. Respir Med 1993;87(Suppl B):37–9. 4. Martin R. Nocturnal asthma: circadian rhythms and therapeutic interventions. Am Rev Respir Dis 1993;147:S25– 8. 5. Finnerty JP, Holgate ST. The contribution of histamine release and vagal reflexes, alone and in combination, to exercise-induced asthma. (See comments.) Eur Respir J 1993;6:1132–7.
Defecation-Induced Bronchospasm 6. Goldman JM. Syncope. In: Harwood-Nuss AL, ed. The Clinical Practice of Emergency Medicine, 2nd edn. Philadelphia: Lippincott-Raven; 1996:628 –9. 7. Roberge R, Anderson E, MacMath T, Rudoff J, Luten R. Termination of paroxysmal supraventricular tachycardia by digital rectal massage. Ann Emerg Med 1987;16:1291–3. 8. de Jongste JC, Jongejan RC, Kerrebijn KF. Control of airway caliber by autonomic nerves in asthma and in chronic obstructive pulmonary disease. Am Rev Respir Dis 1991;143:1421– 6. 9. Fryer AD, Jacoby DB. Effect of inflammatory cell mediators on M2 muscarinic receptors in the lungs. Life Sci 1993;52:529 –36. 10. Barnes PJ. Muscarinic receptors in airways: recent developments. J Appl Physiol 1990;68:1777– 85. 11. Barnes PJ. Muscarinic receptor subtypes in airways. Life Sci 1993;52:521–7.
197 12. Kallenbach JM, Webster T, Dowdeswell R, Reinach SG, Millar RN, Zwi S. Reflex heart rate control in asthma. Evidence of parasympathetic overactivity. Chest 1985;87:644 – 8. 13. Gupta S, Dolwani S. A study of autonomic status and its effect on ventilatory functions in bronchial asthma. Indian J Chest Dis Allied Sci 1996;38:147–56. 14. Hashimoto A, Maeda H, Yokoyama M. Augmentation of parasympathetic nerve function in patients with extrinsic bronchial asthma— evaluation by coefficiency of variance of R-R interval with modified long-term ECG monitoring system. Kobe J Med Sci 1996;42:347–59. 15. Coe CI, Barnes PJ. Reduction of nocturnal asthma by an inhaled anticholinergic drug. Chest 1986;90:485– 8. 16. Morrison JF, Pearson SB, Dean HG. Parasympathetic nervous system in nocturnal asthma. BMJ 1988;296:1427–9.