Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Esophageal Spasm Workup

  • Author: Ahmad Malas, MD; Chief Editor: BS Anand, MD  more...
 
Updated: Jun 24, 2015
 

Laboratory Studies

Laboratory evaluation usually does not aid in the diagnosis if the patient history and physical examination findings are unremarkable for other diseases mentioned in the differential diagnosis. All differentials mentioned can present with esophageal dysmotility.

The diagnostic modalities of choice are barium swallow and esophageal manometry.

Blood glucose and hemoglobin A1C levels should be checked to rule out diabetes. However, patients can have esophageal spasm and diabetes concomitantly.

The findings discovered by monitoring a patient's pH can demonstrate reflux, which can present with somewhat similar symptoms. In fact, gastroesophageal reflux is thought by some to trigger esophageal spasm.

Next

Imaging Studies

Barium swallow

Barium swallow or esophagram is the best imaging study to aid in the diagnosis of esophageal spasm by evaluating for nonpropulsive contractions in the esophagus.

Diffuse esophageal spasm has a characteristic appearance of multiple simultaneous contractions causing a corkscrew appearance with segmentation (see the image below).

Barium swallow demonstrates diffuse uncoordinated Barium swallow demonstrates diffuse uncoordinated contractions of the esophagus in a patient with diffuse esophageal spasm.

Unlike in diffuse esophageal spasm, the barium swallow findings for nutcracker esophagus are not specific and can present minimal findings.

CT scanning

Nino-Murcia and colleagues demonstrated thickening of the esophagus with CT scan studies in patients with esophageal spasm.[9] Muscular hypertrophy has been documented in some patients with diffuse esophageal spasm and nutcracker esophagus. The hypertrophy of the muscle wall is the cause of the increased thickness that is observed on CT scan images. The normal thickness of the esophagus is less than 3 mm.

Many other disease processes, including malignancy, cause thickening of the esophagus that can be seen radiographically. Thus, thickening of the esophagus seen on CT scan images should prompt further workup. Even in patients with symptoms consistent with esophageal spasm, thickening seen on CT scan images should not be dismissed as muscular hypertrophy secondary to the esophageal spasms without further investigation.

Ultrasonography

Catheter-based high-frequency intraluminal ultrasound imaging assesses both the sensory function and the motor function of the esophagus.[10]  This imaging modality may be useful to differentiate diffuse esophageal spasm, nutcracker esophagus, and achalasia.

Previous
Next

Other Tests

Manometry

Two recent advances have revolutionized the performance of clinical esophageal manometry: practical high-resolution manometric (HRM) systems and the development of sophisticated algorithms to display the expanded manometric dataset as esophageal pressure topographic plots.[11]

Two strengths of esophageal pressure topographic plots compared with conventional manometric recordings are the ability to delineate the spatial limits, vigor, and integrity of individual contractile segments along the esophagus and to distinguish between loci of compartmentalized intraesophageal pressurization and rapidly propagated contractions.[11] See the image below.

High-resolution manometric display of a normal eso High-resolution manometric display of a normal esophageal swallow using esophageal pressure topography. Image courtesy of Wikimedia Commons.

Manometry is the best modality to help diagnose diffuse esophageal spasm. Findings include aperistalsis in greater than 30% of wet swallows, 20% of contractions being simultaneous, amplitudes greater than 30 mm Hg in the distal three fifths of the esophagus, and, rarely, repetitive contractions or lower esophageal sphincter (LES) dysfunction. Vigorous achalasia can easily be confused with diffuse esophageal spasm.[3]

Diffuse esophageal spasm, when defined by premature contractions measured with distal latency, describes a more clinically homogeneous entity than when defined by contractile front velocity.[12]

The classic definition is more than 2 uncoordinated contractions during 10 consecutive wet swallows (≥20% simultaneous esophageal contractions during standardized stationary motility testing). At least one peristaltic contraction must be present. Artificial neural networks may be useful in the recognition and objective classification of primary esophageal motor disorders investigated with stationary esophageal manometry recordings.[13]

Herbella et al conducted a study in patients with manometric patterns of diffuse esophageal spasm and nutcracker esophagus to determine whether symptoms alone can distinguish primary esophageal motility disorder from gastroesophageal reflux disease, a secondary esophageal motility disorder, and the value of ambulatory pH monitoring.[14] Of 180 patients with manometric criteria for nutcracker esophagus, 124 (69%) had gastroesophageal reflux that was detected with ambulatory pH monitoring. Of 56 patients with primary esophageal motility disorder, 31 (55%) were taking proton pump inhibitors.[14] No difference in chest pain prevalence was noted between the groups, but those with primary esophageal motility disorder had greater chest pain symptom severity, whereas patients in the gastroesophageal reflux group had a higher prevalence and severity of heartburn.[14]

Of the 121 patients with manometric criteria for diffuse esophageal spasm, 73 (60%) demonstrated gastroesophageal reflux by ambulatory pH monitoring.[14] Of the 48 patients with primary esophageal motility disorder, 39 (81%) were on proton pump inhibitors. The group with primary esophageal motility had a higher prevalence of dysphagia disorder relative to the gastroesophageal reflux group.

Herbella et al thus demonstrated that two thirds of patients with a manometric pattern of diffuse esophageal spasm or nutcracker esophagus also had gastroesophageal reflux disease, and symptoms were indistinguishable between primary esophageal motility disorders and gastroesophageal reflux disease. They concluded esophageal manometry and pH monitoring are crucial to distinguish between primary and secondary esophageal motility disorders and to guide appropriate therapy.[14]

Contraction amplitude is normal.

The distal contractile integral (DCI) is the metric used to define the vigor of the contraction. It is the product of the amplitude, duration, and length of the contraction between the proximal and distal trough.

Nutcracker esophagus is defined as a mean DCI greater than 5000 mm Hg/s/cm over 10 swallows using esophageal pressure topography criteria. This occurs in the context of normal propagation and normal esophagogastric junction relaxation.

Jackhammer esophagus is an extreme phenotype of hypertensive contraction characterized by a DCI greater than 8000 mm Hg/s/cm. This phenotype is never found in asymptomatic patients.[15]

The image below depicts a normal manometric tracing. This depiction uses the older system of pressure tracings (conventional manometric recording) without high-resolution esophageal pressure topography.

This is normal esophageal manometry tracing with n This is normal esophageal manometry tracing with normal amplitude of the contractions. The contractions are coordinated because the contractions in the proximal esophagus (top of image) occur before the contractions further distal in the esophagus.

The image below depicts an example of diffuse esophageal spasm.

Esophageal manometry tracing demonstrates diffuse Esophageal manometry tracing demonstrates diffuse esophageal spasm. Note the multiple uncoordinated contractions in the third tracing from the distal esophagus.

Manometry in patients with nutcracker esophagus demonstrates contractions that progress in an orderly manner, but the amplitude of the contraction is excessive. Amplitude greater than 2 standard deviations above the normal value is considered diagnostic for nutcracker esophagus (see the image below).

Esophageal manometry tracing demonstrates nutcrack Esophageal manometry tracing demonstrates nutcracker esophagus. Note the excessive amplitude of the contractions.

A disassociation may exist between symptoms and manometric findings.

Esophageal electrical impedance recordings show abnormal transit in diffuse esophageal spasm.

Esophageal manometry may be combined with multichannel intraluminal impedance to obtain pressure and bolus transit information.[16, 17] About half the patients with diffuse esophageal spasm have normal transit for liquids and fluids, one fourth have abnormal transit for one substance, and one fourth have abnormal transit for both.

Esophageal pH recording and 24-hour ambulatory manometry may improve the detection of esophageal muscle dysfunction.[18] This method shows that in persons presenting with noncardiac chest pain, gastroesophageal reflux symptoms are common and diffuse esophageal spasm is rare.

Previous
Next

Procedures

Esophagogastroduodenoscopy (EGD), or upper endoscopy, can reveal associated disorders such as hiatal hernia, reflux esophagitis, and strictures.

Endoscopy is not useful to help diagnose dysmotility, but it may be helpful to exclude erosive esophagitis or stricture.

Previous
 
 
Contributor Information and Disclosures
Author

Ahmad Malas, MD Fellow, Department of Gastroenterology, Providence Hospital and Medical Centers

Ahmad Malas, MD is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Coauthor(s)

Janice M Fields, MD, FACG, FACP Assistant Professor of Internal Medicine, Oakland University William Beaumont School of Medicine; Consulting Staff, Department of Internal Medicine, Section of Gastroenterology, Providence Hospital, St John Macomb-Oakland Hosptial

Janice M Fields, MD, FACG, FACP is a member of the following medical societies: American College of Gastroenterology, American College of Physicians-American Society of Internal Medicine, American Gastroenterological Association, American Medical Association, American Society for Gastrointestinal Endoscopy, National Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

BS Anand, MD Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine

BS Anand, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Additional Contributors

John Gunn Lee, MD Director of Pancreaticobiliary Service, Associate Professor, Department of Internal Medicine, Division of Gastroenterology, University of California at Irvine School of Medicine

John Gunn Lee, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Acknowledgements

Simmy Bank, MD Chair, Professor, Department of Internal Medicine, Division of Gastroenterology, Long Island Jewish Hospital, Albert Einstein College of Medicine

Disclosure: Nothing to disclose.

Alan BR Thomson, MD Professor of Medicine, Division of Gastroenterology, University of Alberta, Canada

Alan BR Thomson, MD is a member of the following medical societies: Alberta Medical Association, American College of Gastroenterology, American Gastroenterological Association, Canadian Association of Gastroenterology, Canadian Medical Association, College of Physicians and Surgeons of Alberta, and Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

References
  1. Smout AJ. Advances in esophageal motor disorders. Curr Opin Gastroenterol. 2008 Jul. 24(4):485-9. [Medline].

  2. Ferguson TB, Woodbury JD, Roper CL, Burford TH. Giant muscular hypertrophy of the esophagus. Ann Thorac Surg. 1969 Sep. 8(3):209-18. [Medline].

  3. Floch M, et al. Esophageal Motility Disorders. Netter's Gastroenterology. 2nd ed. Philadelphia, Pa: Saunders; 2010. Chapter 14.

  4. Almansa C, Hinder RA, Smith CD, Achem SR. A comprehensive appraisal of the surgical treatment of diffuse esophageal spasm. J Gastrointest Surg. 2008 Jun. 12(6):1133-45. [Medline].

  5. Grubel C, Borovicka J, Schwizer W, Fox M, Hebbard G. Diffuse esophageal spasm. Am J Gastroenterol. 2008 Feb. 103(2):450-7. [Medline].

  6. Almansa C, Achem SR. [Diffuse esophageal spasm (DES). Practical concepts of diagnosis and treatment] [Spanish]. Rev Gastroenterol Mex. 2007 Apr-Jun. 72(2):136-45. [Medline].

  7. Almansa C, Heckman MG, Devault KR, Bouras E, Achem SR. Esophageal spasm: demographic, clinical, radiographic, and manometric features in 108 patients. Dis Esophagus. 2011 Sep 23. [Medline].

  8. Managing diffuse oesophageal spasm. Drug Ther Bull. 2011 May. 49(5):54-7; quiz i-ii. [Medline].

  9. Nino-Murcia M, Stark P, Triadafilopoulos G. Esophageal wall thickening: a CT finding in diffuse esophageal spasm. J Comput Assist Tomogr. 1997 Mar-Apr. 21(2):318-21. [Medline].

  10. Mittal RK. Motor and sensory function of the esophagus: revelations through ultrasound imaging. J Clin Gastroenterol. 2005 Apr. 39(4 Suppl 2):S42-8. [Medline].

  11. Kahrilas PJ, Ghosh SK, Pandolfino JE. Esophageal motility disorders in terms of pressure topography: the Chicago Classification. J Clin Gastroenterol. 2008 May-Jun. 42(5):627-35. [Medline]. [Full Text].

  12. Carlson DA, Pandolfino JE. The Chicago criteria for esophageal motility disorders: what has changed in the past 5 years?. Curr Opin Gastroenterol. 2012 Jul. 28(4):395-402. [Medline].

  13. Pandolfino JE, Fox MR, Bredenoord AJ, Kahrilas PJ. High-resolution manometry in clinical practice: utilizing pressure topography to classify oesophageal motility abnormalities. Neurogastroenterol Motil. 2009 Aug. 21(8):796-806. [Medline].

  14. Herbella FA, Raz DJ, Nipomnick I, Patti MG. Primary versus secondary esophageal motility disorders: diagnosis and implications for treatment. J Laparoendosc Adv Surg Tech A. 2009 Apr. 19(2):195-8. [Medline].

  15. Clarke JO, Pandolfino JE. Esophageal motor disorders: how to bridge the gap between advanced diagnostic tools and paucity of therapeutic modalities?. J Clin Gastroenterol. 2012 Jul. 46(6):442-8. [Medline].

  16. Nguyen NQ, Ching K, Tippett M, Smout AJ, Holloway RH. Impact of nadir lower oesophageal sphincter pressure on bolus clearance assessed by combined manometry and multi-channel intra-luminal impedance measurement. Neurogastroenterol Motil. 2009 Aug 21. [Medline].

  17. Tutuian R, Mainie I, Agrawal A, Gideon RM, Katz PO, Castell DO. Symptom and function heterogenicity among patients with distal esophageal spasm: studies using combined impedance-manometry. Am J Gastroenterol. 2006 Mar. 101(3):464-9. [Medline].

  18. Cameron R, Barclay M, Dobbs B. Ambulatory oesophageal manometry and pH monitoring for investigation of chest pain: a New Zealand experience. N Z Med J. Mar 10, 2006. 119(1230):U1877. [Medline].

  19. Miller LS, Parkman HP, Schiano TD, Cassidy MJ, Ter RB, Dabezies MA, et al. Treatment of symptomatic nonachalasia esophageal motor disorders with botulinum toxin injection at the lower esophageal sphincter. Dig Dis Sci. 1996 Oct. 41(10):2025-31. [Medline].

  20. Irving JD, Owen WJ, Linsell J, McCullagh M, Keightley A, Anggiansah A. Management of diffuse esophageal spasm with balloon dilatation. Gastrointest Radiol. 1992. 17(3):189-92. [Medline].

  21. Winters C, Artnak EJ, Benjamin SB, Castell DO. Esophageal bougienage in symptomatic patients with the nutcracker esophagus. A primary esophageal motility disorder. JAMA. 1984 Jul 20. 252(3):363-6. [Medline].

  22. Salvador R, Costantini M, Rizzetto C, Zaninotto G. Diffuse esophageal spasm: the surgical approach. Dis Esophagus. 2011 Feb 10. [Medline].

  23. Cannon RO 3rd, Quyyumi AA, Mincemoyer R, Stine AM, Gracely RH, Smith WB, et al. Imipramine in patients with chest pain despite normal coronary angiograms. N Engl J Med. 1994 May 19. 330(20):1411-7. [Medline].

  24. Casselbrant A, Edebo A, Wennerblom J, Lonroth H, Helander HF, Vieth M, et al. Actions by angiotensin II on esophageal contractility in humans. Gastroenterology. 2006 Nov. 132(1):249-60. [Medline].

  25. Dogan I, Mittal RK. Esophageal motor disorders: recent advances. Curr Opin Gastroenterol. 2006 Jul. 22(4):417-22. [Medline].

  26. Dogan I, Puckett JL, Padda BS, Mittal RK. Prevalence of increased esophageal muscle thickness in patients with esophageal symptoms. Am J Gastroenterol. 2007 Jan. 102(1):137-45. [Medline].

  27. Drenth JP, Bos LP, Engels LG. Efficacy of diltiazem in the treatment of diffuse oesophageal spasm. Aliment Pharmacol Ther. 1990 Aug. 4(4):411-6. [Medline].

  28. Eslick GD, Coulshed DS, Talley NJ. Diagnosis and treatment of noncardiac chest pain. Nat Clin Pract Gastroenterol Hepatol. 2005 Oct. 2(10):463-472. [Medline].

  29. Feldman M, Friedman L, and Sleisenger M. Sleisenger & Fordtran's Gastrointestinal and Liver Disease: Pathophysiology, Diagnosis, and Management. 7th ed. Philadelphia, Pa: Saunders; 2002. Vol 1:

  30. Lacy BE, Weiser K. Esophageal motility disorders: medical therapy. J Clin Gastroenterol. 2008 May-Jun. 42(5):652-8. [Medline].

  31. Manfrini O, Bazzocchi G, Luati A, Borghi A, Monari P, Bugiardini R. Coronary spasm reflects inputs from adjacent esophageal system. Am J Physiol Heart Circ Physiol. 2006 May. 290(5):H2085-91. [Medline].

  32. Nayar DS, Khandwala F, Achkar E, Shay SS, Richter JE, Falk GW, et al. Esophageal manometry: assessment of interpreter consistency. Clin Gastroenterol Hepatol. 2005 Mar. 3(3):218-24. [Medline].

  33. Rieder F, Cheng L, Harnett KM, Chak A, Cooper GS, Isenberg G, et al. Gastroesophageal reflux disease- associated esophagitis induces endogenous cytokine production leading to motor abnormalities. Gastroenterology. 2007 Jan. 132(1):154-65. [Medline].

  34. Santos R, Haack HG, Maddalena D, Hansen RD, Kellow JE. Evaluation of artificial neural networks in the classification of primary oesophageal dysmotility. Scand J Gastroenterol. 2006 Mar. 41(3):257-63. [Medline].

  35. Spencer HL, Smith L, Riley SA. A questionnaire study to assess long-term outcome in patients with abnormal esophageal manometry. Dysphagia. 2006 Jul. 21(3):149-55. [Medline].

  36. Swamy N. Esophageal spasm: clinical and manometric response to nitroglycerine and long acting nitrites. Gastroenterology. 1977 Jan. 72(1):23-7. [Medline].

  37. Vaezi MF. Review article: the role of pH monitoring in extraoesophageal gastro-oesophageal reflux disease. Aliment Pharmacol Ther. 2006 Mar. 23 Suppl 1:40-9. [Medline].

 
Previous
Next
 
Barium swallow demonstrates diffuse uncoordinated contractions of the esophagus in a patient with diffuse esophageal spasm.
This is normal esophageal manometry tracing with normal amplitude of the contractions. The contractions are coordinated because the contractions in the proximal esophagus (top of image) occur before the contractions further distal in the esophagus.
Esophageal manometry tracing demonstrates diffuse esophageal spasm. Note the multiple uncoordinated contractions in the third tracing from the distal esophagus.
Esophageal manometry tracing demonstrates nutcracker esophagus. Note the excessive amplitude of the contractions.
High-resolution manometric display of a normal esophageal swallow using esophageal pressure topography. Image courtesy of Wikimedia Commons.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.