eMedicine Specialties > Gastroenterology > Esophagus

Esophageal Spasm: Treatment & Medication

Author: Alan BR Thomson, MD, MSc, PhD, Professor, Department of Medicine, Division of Gastroenterology, University of Alberta Faculty of Medicine
Contributor Information and Disclosures

Updated: Aug 26, 2009

Treatment

Medical Care

Medical and surgical options are available for the treatment of DES and nutcracker esophagus and have been used with moderate success. Each treatment has a high failure rate, which drives the constant search for a better treatment. Medical treatment consists of calcium channel blockers, tricyclic antidepressants, nitrates, botulinum toxin, and dilatation.9 These conditions are usually not progressive but may interfere with the patient's quality of life.

  • Calcium channel blockers can reduce the amplitude of the contractions.
    • In patients with nutcracker esophagus, calcium channel blockers effectively reduce the amplitude of the contractions, but the chest pain may not always be reduced.
    • Traditionally, calcium channel blockers were thought to decrease the contractions. 
  • Nitrates also have been used with some success.
    • The mechanism of action is unknown but may be related to decreasing vasospasm in the brainstem, similar to calcium channel blockers.
    • Some patients benefit from sublingual nitroglycerin for acute symptoms of esophageal spasm. 
  • Tricyclic antidepressants, specifically imipramine, have been shown to decrease chest pain with no apparent cause on angiogram. Studies specifically evaluating nutcracker esophagus are not yet available.
  • Botulinum toxin binds receptors in the nerve endings, thereby decreasing the release of acetylcholine.
    • By endoscopically injecting botulinum toxin above the LES, symptoms may improve.
    • The effect is temporary, and the response decreases with repeated injections.
  • Balloon dilatation is commonly used for achalasia, but it has been used to treat DES and nutcracker esophagus.
    • The studies are small, the relief is not uniform, and symptoms recur.
    • Dilation with mercury-filled bougies has been used in the past.
  • Proton pump inhibitors effectively reduce or alleviate the symptoms of gastroesophageal reflux disease, which may mimic DES. A trial of acid lowering therapy may be undertaken prior to instigating other treatments. Although treatment is often ineffective, the symptoms from DES and nutcracker esophagus usually improve over time.

Surgical Care

For extreme cases, operative treatment usually involves a myotomy. Myotomy relieves symptoms by eliminating the effectiveness of the contractions. Traditionally, a thoracotomy was required to obtain access to the esophagus, but now, a thoracoscopic approach can be used. In rare, recalcitrant cases, esophagectomy can relieve symptoms.

  • Myotomy is effective for treating DES.
    • The myotomy should extend the entire length of the involved segment, which should be determined preoperatively with manometry.
    • Furthermore, the myotomy should extend through the LES to help prevent dysphagia postoperatively by preventing outlet obstruction.
    • Finally, an antireflux procedure should be performed concomitantly, by either a partial wrap or a floppy Nissen.
  • Myotomy should be used with caution in patients with nutcracker esophagus because it may worsen the symptoms.
    • Myotomy reduces the amplitude of the contractions, but this does not consistently improve symptoms, especially if the primary complaint is pain.
    • Furthermore, dysphagia can develop or worsen after myotomy because the effectiveness of the propagative waves is eliminated, leaving gravity to propel food caudally.
  • As a last resort, esophagectomy can be used to relieve symptoms.
    • The esophagus is resected, and the stomach, small intestine, or colon is used to restore the continuity of the GI tract.
    • Morbidity and mortality of esophagectomy are substantial; therefore, this should be performed only after other treatments have been exhausted.

Diet

  • Diet-induced symptoms are patient-specific.
  • Dietary restriction, even to pureed foods, can decrease symptoms temporarily.

Medication

Medical therapy is the first line of treatment for esophageal spasm. Because the etiology is unknown, all medical therapies are directed at symptoms, not etiology. Proton pump inhibitors may be useful if there is associated gastroesophageal reflux disease. Calcium channel blockers and nitrates may decrease pain associated with esophageal spasms. Botulinum toxin decreases acetylcholine available at nerve endings. Imipramine improves pain by an unknown mechanism of action.

Calcium channel blockers

Reduce amplitude of contractions. In nutcracker esophagus, calcium channel blockers effectively reduce amplitude of contractions, but chest pain often is not reduced. Whether calcium channel blockers decrease force of contraction of muscle or decrease underlying stimulus is unknown.


Diltiazem (Cardizem)

FDA-approved for hypertension, vasospastic angina, and chronic stable angina. Decreases calcium ion flux across cell membranes in smooth muscle, thereby relaxing vascular smooth muscle.

Adult

Initial: 120 mg PO qd; titrate to effect without significant adverse effects; optimal dose not known

Pediatric

Not recommended

Beta-blockers are usually well tolerated but can result in hypotension or CH; cimetidine may increase levels by inhibiting P-450 metabolism of diltiazem; may increase carbamazepine, digoxin, cyclosporine, and theophylline levels; when administered with amiodarone, may cause bradycardia and a decrease in cardiac output

Documented hypersensitivity; severe CHF; sick sinus syndrome; acute MI; second- or third-degree AV block; hypotension (<90 mm Hg systolic)

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Hypotension, dizziness, flushing, nausea, and bradycardia/conduction delays; caution in impaired renal or hepatic function; may increase LFT levels; hepatic injury may occur

Nitrates

Like calcium channel blockers, nitrates may decrease the pain associated with esophageal spasm. The mechanism of action is unknown but may be related to decreasing vasospasm in the brainstem, similar to calcium channel blockers, or it may be a direct effect on the myocytes.


Isosorbide dinitrate (Dilatate SR, Isordil)

Approved indication is for angina pectoris. Relaxes vascular smooth muscle by stimulating intracellular cyclic GMP. By decreasing left ventricular pressure and dilating arteries, reduces cardiac oxygen demand.

Adult

5 mg PO ac or 2.5 mg SL pc

Pediatric

Not established

Coadministration with alcohol may cause severe hypotension and cardiovascular collapse; aspirin may increase serum concentrations of isosorbide and actions; coadministration with channel blockers may increase symptomatic orthostatic hypotension (adjust dose of either agent); isosorbide may decrease effects of heparin

Documented hypersensitivity; severe anemia; closed-angle glaucoma; postural hypotension; head trauma; cerebral hemorrhage

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

The most common adverse reactions are hypotension and headache; methemoglobinemia rarely occurs; safety not known with CHF, with acute myocardial infarction, or in mothers who are breastfeeding; tolerance to vascular and antianginal effects of nitrates may develop; minimize tolerance by using smallest effective dose, pulse therapy (intermittent dosing), or by alternating with other coronary vasodilators (take last daily dose of short-acting agent no later than 7 pm); caution with glaucoma

Tricyclic antidepressants

These agents, specifically imipramine, have been shown to decrease chest pain with no apparent cause on angiogram. Studies specifically evaluating nutcracker esophagus are not yet available. The mechanism of action of imipramine is not known.


Imipramine (Tofranil)

Decreases pain in patients with chest pain with no apparent cause on angiogram, which may be esophageal spasm. This is not an FDA-approved use. Mechanism of action is not known. Primary use of imipramine is in the treatment of depression.

Adult

25 mg PO qhs; titrate to effect as tolerated

Pediatric

Not recommended

Metabolized by P450, therefore, caution with other medications metabolized by this system; potentiates effects of alcohol; additive with CNS depressants; may potentiate effect of sympathomimetics, such as nasal decongestants; increases toxicity of sympathomimetic agents, such as isoproterenol and epinephrine by potentiating effects and inhibiting antihypertensive effects of clonidine

Documented hypersensitivity; secreted in breast milk, therefore, should not be used in mothers who are breastfeeding; narrow-angle glaucoma; in acute recovery phase following myocardial infarction; MAOIs or fluoxetine or took them in previous 2 wk

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Caution in cardiovascular disease, increased intraocular pressure, narrow-angle glaucoma, hyperthyroidism, and history of seizure disorder; decrease dose in elderly patients because of increased adverse effects, such as CV arrhythmias, hypotension, hypertension, or CHF; psychiatric confusion; neurologic paresthesias, extrapyramidal symptoms, lower seizure threshold, allergic reactions, hematologic bone marrow suppression, nausea, vomiting, diarrhea, gynecomastia, galactorrhea, and CVA may occur; adverse anticholinergic effects are a concern

Toxins (botulinum toxin)

Binds receptors in nerve endings, decreasing release of acetylcholine. Injecting botulinum toxin endoscopically above the LES improves symptoms of patients with esophageal spasms. However, effect is temporary and response decreases with repeated injections.


Botulinum toxin (BOTOX®)

Treats excessive abnormal contractions associated with blepharospasm. Binds to receptor sites on motor nerve terminals and inhibits release of acetylcholine, which, in turn, inhibits transmission of impulses in neuromuscular tissue.

Adult

Initial dose: 20 U have been used; reexamine patients at 7-14 d to assess for response; increase dose 2-fold over previous dose for patients experiencing incomplete paralysis of target muscle; not to exceed 25 U when administering as single injection or 200 U as cumulative dose in 30-d period; approved for strabismus and blepharospasm

Pediatric

<12 years: Not established
>12 years: Administer as in adults

Aminoglycosides or drugs that interfere with neuromuscular transmission may potentiate effects

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Most adverse reactions are local irritation; systemic reactions are rare; do not exceed recommended dosages and frequencies of administration; presence of antibodies to botulinum toxin type A may reduce effects of therapy

More on Esophageal Spasm

Overview: Esophageal Spasm
Differential Diagnoses & Workup: Esophageal Spasm
Treatment & Medication: Esophageal Spasm
Follow-up: Esophageal Spasm
Multimedia: Esophageal Spasm
References
Further Reading
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Further Reading

Related eMedicine Topics

Clinical Trials

National Guideline Clearinghouse

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Keywords

esophageal spasm, diffuse esophageal spasm, nutcracker esophagus, DES, dysphagia, regurgitation, achalasia, noncardiac chest pain, esophagectomy, globus, gastric reflux, gastric reflux, microvascular compression of Vagus nerve

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Contributor Information and Disclosures

Author

Alan BR Thomson, MD, MSc, PhD, Professor, Department of Medicine, Division of Gastroenterology, University of Alberta Faculty of Medicine
Alan BR Thomson, MD, MSc, PhD is a member of the following medical societies: American Federation for Aging Research, American Federation for Clinical Research, American Gastroenterological Association, American Geriatrics Society, American Physiological Society, Canadian Association of Gastroenterology, Gastroenterology Research Group, New York Academy of Sciences, and Royal Society of Medicine
Disclosure: Nothing to disclose.

Medical Editor

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, and American Society for Gastrointestinal Endoscopy
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

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.

CME Editor

Alex J Mechaber, MD, FACP, Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine
Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine
Disclosure: Nothing to disclose.

Chief Editor

Julian Katz, MD, Clinical Professor of Medicine, Drexel University College of Medicine; Consulting Staff, Department of Medicine, Section of Gastroenterology and Hepatology, Hospital of the Medical College of Pennsylvania
Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law Medicine and Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility
Disclosure: Nothing to disclose.

 
 
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