Loughlin Ch.J., Koufman J. Paroxysmal Laryngospasm Secondary to Gastroesophageal Reflux. Laryngoscope. 1996 Dec;106(12 Pt 1):1502-5.

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Авторы: Loughlin Ch.J.  / Koufman J.A.

Paroxysmal Laryngospasm Secondary to Gastroesophageal Reflux

Christopher J. Loughlin, MD, and Jamie Koufman, MD, FACS.


Over a two-year period (1992-1994), 12 consecutive adult patients with paroxysmal laryngospasm were prospectively studied. All had had other symptoms of gastroesophageal reflux (GER); however, only 4 (33%) experienced symptoms of heartburn. Each patient underwent fiberoptic laryngeal examination, barium swallow/ esophagography, and ambulatory 24-hour double-probe pH monitoring (pH-metry).

Eleven of the 12 patients (92%) had evidence of GER on examination, and 10 (83%) had abnormal pH-metry, including 3 who demonstrated pharyngeal reflux while having normal total acid exposure times in the esophageal probe. All of the patients responded to antireflux treatment, using dietary/lifestyle modifications and omeprazole, with complete cessation of the laryngospastic episodes.

This study documents the role of GER in the etiology of paroxysmal laryngospasm, it highlights the advantages of double-probe pH-metry in diagnosing this extraesophageal manifestation of GER, and it demonstrates that antireflux therapy with omeprazole is effective in controlling GER-induced laryngospasm.


Patients with gastroesophageal reflux (GER) are commonly encountered in otolaryngology (ORL); however, most ORL patients do not have complaints of heartburn.1 Instead, ORL patients complain of symptoms related to the reflux of gastric contents into the upper aerodigestive tract. Therefore, this type of GER appears to be different than that seen by gastroenterologists, and it may be more precisely termed gastropharyngeal reflux.

GER is believed to be an important contributing factor in the etiology of many inflammatory and neoplastic laryngopharyngeal disorders.1-6 Its most common symptoms are hoarseness, globus pharyngeus, dysphagia, aspiration, chronic cough, and throat clearing.1 Laryngospasm is uncommon, but is a highly significant and distressing symptom of patients with GER.6-8

Laryngospasm is defined as a sudden, prolonged, forceful apposition of the vocal cords, and it is believed to be the result of a laryngeal reflex-response to noxious stimuli. The reflex arc, as described by Suzuki and Sasaki, consists of an afferent limb carried by the stimulated superior laryngeal nerve (SLN) and an efferent limb carried by the recurrent laryngeal nerve (RLN).9 They showed that electrical stimulation of the SLN produces repetitive excitatory "after discharges" of the RLN, which in turn causes prolonged adduction of the vocal folds by stimulation of the thyroarytenoid and lateral cricoarytenoid muscles and inhibition of the posterior cricoarytenoid muscle9

In humans, GER-induced laryngospasm was first described by Chodosh in 1977.7 It has since been reported by others,1,6-14 and studies using animal models have implicated acid contact with the endolaryngeal mucosa as a cause of both laryngospasm and reflex central apnea.15-17 In addition, it has been postulated that GER may be a cause of sudden infant death syndrome (SIDS) in children.8,15-19

Bortolotti reported two adult patients with recurrent episodes of sudden upper airway obstruction followed by choking.6 Twenty-four-hour double-probe pH monitoring (pH-metry) confirmed a diagnosis of GER, and antireflux treatment with famotidine, metoclopramide, antacids, and dietary/lifestyle modifications resulted in the cessation of the laryngospastic episodes in both patients over a period of six months. Campbell et al. reported six patients with laryngospasm. On the basis of history and barium esophagography, they considered GER to be contributory in two of the patients, and "non-specific laryngeal irritation" to be contributory in the other four.10

At the Center for Voice Disorders of Wake Forest University, we have seen an increasing number of patients whose chief complaint was episodic, sudden upper airway obstruction associated with stridor and "choking spells" (laryngospasm). In some patients, the episodes were related to eating, and in some they awoke the patient from sound sleep. For diagnostic purposes, most of the patients could mimic their stridor, and in most cases, it was consistent with that of acute laryngospasm.

Upon further inquiry, these patients also complained of many of the other ORL symptoms of GER. Therefore, beginning in 1992, we began to prospectively study a group of such patients using 24-hour double-probe pH-metry and barium swallow/ esophagography as a routine part of each patient's diagnostic evaluation. We hypothesized that GER was the cause of the laryngospasm in these patients, that pH-metry would assist in making this diagnosis, and that antireflux therapy aimed at preventing GER would result in resolution of these patients distressing symptoms. This article reports a prospective study of 12 patients with laryngospasm, and it appears to validate our hypothesis.


From 1992 to 1994, a prospective study was carried out on 12 consecutive adult, nonsmoking patients (age range: 24-79 years) who presented to the Center For Voice Disorders of Wake Forest University with laryngospasm. All patients suffered from recurring episodes of sudden-onset airway obstruction with loud inspiratory stridor, dyspnea, and coughing. These episodes lasted from 30 seconds to 5 minutes. In most cases, no predisposing events could be recalled by the patient.

Most of the episodes of laryngospasm occurred during wakefulness, but every patient reported at least one episode that had awakened them from sound sleep. One patient had required intubation for an episode that had occurred postprandially and worsened over a 20-minute period.

The initial diagnostic evaluation consisted of: (1) a history obtained by the physician and a "reflux data sheet" filled out by the nursing staff during the initial office visit1; (2) a complete head and neck examination; and (3) a transnasal fiberoptic laryngoscopy (TFL) with laryngeal photography.

None of the 12 patients had a history of cardiovascular, neurological, or pulmonary abnormalities. The most common symptoms other than laryngospasm were hoarseness (9/12), dry cough (6/12), and globus pharyngeus (6/12); but only 33% of the patients (4/12) experienced heartburn and/or regurgitation.

Laryngeal examination revealed signs of GER in 11 patients, including laryngeal erythema, Reinke's edema, edematous and erythematous arytenoids and interarytenoid region ("posterior laryngitis"), thick endolaryngeal mucus, and/or vocal process granulomas. One patient had a laryngospastic episode documented on TFL after an episode of regurgitation during examination.

All of the study patients underwent barium swallow/esophagography with videofluoroscopy and 24-hour double-probe pH-metry. The technique of double-probe pH-metry has been reported previously in detail:1,21,22 Briefly, the distal probe is placed 4 cm above the lower esophageal sphincter (LES), and the second probe is placed 1 cm above the upper esophageal sphincter (UES) behind the laryngeal inlet. Manometry is performed prior to positioning of the probes to accurately locate the UES and LES. Normal values for esophageal acid exposure times detected by the distal probe (percent time pH <4) in our laboratory are <8.1 upright, <2.9 supine, and <5.5 total.22 These values are similar to other reported norms.1 Even a single reflux episode detected by the pharyngeal probe is considered indicative of GER. 1

In some cases, thyroid function testing and electrolyte measurements, including calcium and magnesium, were obtained to exclude hypothyroidism, hypomagnesemia, or hypocalcemia as contributing factors to laryngeal edema and/or spasm. In none of our study patients were abnormalities of thyroid function or electrolytes found. In addition, none of the patients had neurological disorders or spasmodic dysphonia prediposing them to laryngospasm.

Once a presumptive diagnosis of laryngospasm due to GER was made, patients were placed on an anti-reflux treatment regimen consisting of dietary and lifestyle modifications,1 plus oral omeprazole 20 mg b.i.d. Three patients who had been taking cimetidine (1200 mg/day) without benefit were converted to omeprazole treatment.

Study patients were followed on a monthly basis for at least 1 year (mean 16 months, range 1.0 to 2.5 years), and the medical therapy was considered to be successful if the patients reported a complete cessation of their laryngospastic episodes.


Ten of the 12 patients (83%) had abnormal pH-metry. See Table 1. Of those 10, 7 had abnormal esophageal acid exposures and 5 had pharyngeal acid exposures (range 1-20 exposures, median 3) in a 24-hour period. Three patients with abnormal pharyngeal reflux had normal esophageal acid exposure times. In other words, in 30% of patients with abnormal studies, the diagnosis of GER was made with no abnormality in esophageal exposure to refluxed gastric acid.

Ten patients had abnormalities on barium esophagography, including non-specific dysmotility, a cricopharyngeal bar, diverticula, esophagitis, and hiatal hernia.20 Only three patients had evidence of esophagitis on barium swallow/esophagography.

Within 1 to 4 months of the start of omeprazole treatment, laryngospasm in all 12 of the patients ceased completely. Other symptoms related to GER also declined, with hoarseness and throat clearing the most persistent symptoms. In addition, repeat laryngeal examination revealed that all patients had shown improvement of laryngeal findings within 4 months of the initiation of therapy.

Once patients reported a cessation of laryngospastic episodes, they were followed on less frequent intervals, varying from every 2 to 4 months. After a mean follow-up of 14 months, 8 patients had normal findings on laryngeal examinations; the other 4 had persistence of Reinke's edema.

Within 1 year of their starting omeprazole therapy, 10 patients were switched to the H2-blocker ranitidine, 150 mg orally b.i.d., and 2 patients to cimetidine, 400 mg orally t.i.d. Interestingly, two of the patients taking ranitidine experienced recrudescence of paroxysmal laryngospasm within 6 weeks, and were then restarted on omeprazole, 20 mg orally b.i.d., (again, with eradication of the laryngospasm). Both patients were subsequently referred for Nissen fundoplication, and neither has experienced any laryngospastic episodes since antireflux surgery.


These data suggest that GER may be the most common cause of laryngospasm; however, it is important to note that only one-third of the patients had symptoms of heartburn or regurgitation. This finding is consistent with the findings of others that the manifestations (and possibly the pathogenesis) of "gastropharyngeal reflux" are different from those of reflux esophagitis.1 Heartburn is associated with impaired mucosal protective mechanisms and esophageal mucosal injury, i.e., esophagitis. Since only 3 of our patients had esophagitis on barium esophagography, it is not surprising that most of our patients did not report heartburn.

In the event double-probe pH-metry is not available and/or affordable, a presumptive diagnosis of GER-induced laryngospasm can be made based on a history suggestive of laryngospasm and GER symptoms, and findings suggestive of GER on laryngeal fiberoptic examination. As shown by our results, treatment for GER could be expected to resolve symptoms of laryngospasm within approximately four months. If laryngospasm persists, the diagnosis may need to be rethought, or pH-metry then performed to exclude continued GER.

Even a single GER event may set off a severe laryngospastic episode in susceptible patients. We chose the proton pump inhibitor omeprazole as the primary therapy, over the H2-blockers, due to its effectiveness in arresting gastric acid production when administered in a twice-daily dose. At the time this study was initially performed, omeprazole was the only proton pump inhibitor available for use. Newer proton pump inhibitors currently available may be predicted to have similar efficacy. Once the laryngospasm and GER are controlled with a proton pump inhibitor, we will switch our patients to H2-blocker therapy, as a cost saving measure. If such therapy subsequently fails, we recommend either restarting the proton pump inhibitor or referring for antireflux surgery.


This study presents the largest series to date of patients with GER-induced laryngospasm, their diagnostic workup, and results of treatment for GER.

Double-probe pH-metry appears to be useful in confirming the diagnosis of GER in patients with laryngospasm; all but two of our 12 patients had abnormal pH studies. (Conversely, barium swallow/esophagography appears to be an less sensitive diagnostic test for gastropharyngeal reflux.)

The second (pharyngeal) probe is especially helpful in detecting gastropharyngeal reflux -- three patients with normal esophageal acid exposure times in the esophageal probe had reflux documented by the pharyngeal probe.

Initial therapy with twice-daily omeprazole appears to be a highly successful treatment for patients with GER-related laryngospasm.

Nissen fundoplication appears to be an effective treatment alternative in selected patients -- those who fail maintenance medical therapy.


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2. Cherry, J. and Margulies, S.I.: Contact ulcer of the larynx. Laryngoscope 78:1937-1940, 1968.

3. Delahunty, J.E.: Acid laryngitis. J Laryngol Otol 86:335-342, 1972.

4. Ward, P.H. and Hanson, D.G.: Reflux as an etiological factor of carcinoma of the laryngopharynx. Laryngoscope 98:1195-1199, 1988.

5. Morrison, M.D.: Is chronic gastroesophageal reflux a causative factor in glottic carcinoma? Otolaryngol Head Neck Surg 99:370-373, 1988.

6. Bortolotti, M.: Laryngospasm and reflex central apnea caused by aspiration of refluxed gastric contents in adults. Gut 30:233-238, 1989.

7. Chodosh, P.L.: Gastro-esophago-pharyngeal reflux. Laryngoscope 87:1418-1427, 1977.

8. Nielson, D.W., Heldt, G.P. and Tooley, W.H.: Stridor and gastroesophageal reflux in infants. Pediatrics 85:1034-1039, 1990.

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10. Campbell, A.H., Mestitz, H., Pierce, R., et al.: Brief upper airway (laryngeal) dysfunction. Aust NZ J Med 20:663-668, 1990.

11. Sarwar, H. and Sprague, D.H.: Laryngospasm as an early indicator of aspiration. Anesth Analg 57:119-121,1978.

12. Curtis, D.J. and Crain, M.: Aerosol regurgitation as a laryngeal-sensitizing event explaining acute laryngospasm. Dysphagia 2:93-96, 1987.

13. Burton, D.M., Pransky, S.M., Katz, R.M., et al.: Pediatric airway manifestations of gastroesophageal reflux. Ann Otol Rhinol Laryngol 101:742-749, 1992.

14. Overstein, S.R., Overstein, D.M., Whitington, P.F.:Gastroesophageal reflux causing stridor. Chest 84:301-302, 1983.

15. Kovar, I., Selstam, U., Catterton, W.Z., et al.: Laryngeal chemoreflex in newborn lambs: Respiratory and swallowing responses to salts, acids, and sugars. Pediatr Res 13:1144-1149, 1979.

16. Wetmore, R.F.: Effects of acid on the larynx of the maturing rabbit and their possible significance to the sudden infant death syndrome. Laryngoscope 103:1242-1254, 1993.

17. Boggs, D.F. and Bartlett, D., Jr.: Chemical specificity of a laryngeal apneic reflex in puppies. J Appl Physiol: Respirat. Environ. Exercise Physiol.53(2):455-462, 1982.

18. Downing, S.E. and Lee, J.C.: Laryngeal chemosensitivity: A possible mechanism for sudden infant death. Pediatrics 55:640-649, 1975.

19. Bauman, N., Sandler, A.D., Schmidt, C., et al.: Reflex laryngospasm induced by stimulation of distal esophageal afferents. Laryngoscope 104:209-214,1994.

20. Ott, D.J., Cowan, R.J., Gelfand, C.W., et al.: The role of diagnostic imaging in evaluating gastroesophageal reflux disease. Postgrad Radiol 6:3-14, 1986.

21. Johnson, L.F.: 24-hour pH monitoring in the study of gastroesophageal reflux. J Clin Gastroenterol 2:387-399, 1980.

22. Richter, J.E., Bradley, L.A., DeMeester, T.R., et al.: Normal 24-hour ambulatory esophageal pH values:Influence of study center, pH electrode, age, and gender. Dig Dis Sci 37:849-856, 1992.

Paroxysmal Laryngospasm Secondary to Gastroesophageal Reflux

Christopher J. Loughlin, MD, and Jamie Koufman, MD, FACS

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