Esophageal spasm is a sudden, painful tightening of your lower esophagus. Your esophagus is the tube that food and liquids pass through from your mouth to your stomach.
The cause of esophageal spasm is not clear. It may be caused by problems with the nerves that control how your esophagus moves when you swallow. Esophageal spasm may be common among family members. Foods that are too hot or too cold may increase how often your esophagus spasms. Spasms may also happen on their own.
You may have any of the following:
You may receive the following tests:
With treatment, your spasms, pain, and trouble swallowing may improve. Ask your caregiver for more information about these and other treatments for esophageal spasms:
Ask for more information about the following:
Contact your caregiver if:
Seek care immediately or call 911 or your local emergency number if:
You have the right to help plan your care. Learn about your health condition and how it may be treated. Discuss treatment options with your caregivers to decide what care you want to receive. You always have the right to refuse treatment. The above information is an educational aid only. It is not intended as medical advice for individual conditions or treatments. Talk to your doctor, nurse or pharmacist before following any medical regimen to see if it is safe and effective for you.
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Sildenafil, a phosphodiesterase inhibitor, is a smooth muscle relaxant that can lower LES pressure and spastic contractions of the esophagus in nutcracker esophagus.
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. [19] 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 diffuse esophageal spasm and nutcracker esophagus. [20] The studies are small, the relief is not uniform, and symptoms recur. Dilation with mercury-filled bougies has been used in the past. [21]
Proton pump inhibitors effectively reduce or alleviate the symptoms of gastroesophageal reflux disease, which may mimic diffuse esophageal spasm. A trial of acid-lowering therapy may be undertaken prior to instituting other treatments. Although treatment is often ineffective, the symptoms from diffuse esophageal spasm and nutcracker esophagus usually improve over time.
Tricyclic antidepressants have produced much success in the treatment of many patients with esophageal motility disorders. Some of these patients may have associated psychiatric illnesses, and concomitant treatment of those conditions concomitantly may improve outcomes.
Diet-induced symptoms are patient-specific. Dietary restriction, even to pureed foods, can decrease symptoms temporarily.
Patients need close follow-up care upon the initiation of therapy or with a change in therapy. Patients should be monitored for improvements in symptoms and for adverse effects of the medications.
Patients in whom medical management fails should be referred to a thoracic surgeon for possible operative intervention.
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 diffuse esophageal spasm. [22] 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 lower esophageal sphincter (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 Nissen fundoplication.
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.
Overall, surgical therapy is reserved for those refractory to medical therapy.
A thoracoscopy with a long myotomy from the arch of the aorta across the LES with an antireflux surgery is a commonly performed procedure in this setting.
What is the role of smooth muscle relaxants in the treatment of diffuse esophageal spasm.
C. Scarpignato, A. Franze (Parma)
Diffuse esophageal spasm (DES) is a motility disorder of the esophagus which usually presents with chest pain, and sometimes dysphagia. Unfortunately, the criteria for diagnosis are not firmly established and the precise definition of the condition has not been generally agreed [1 ]. Ten years ago, spasm was said to be evidenced by esophageal contractions which were of high amplitude and prolonged duration and repetitive in nature [2 ], but it is now argued that none of these features is essential for the diagnosis, and the swallow-induced non propulsive contractions with preservation of some peristalsis should be the core criteria [3 ].
Despite the uncertainty about the definition of esophageal spasm, its clinical features are not in dispute. patients of any age may be affected, and the pain they suffer varies from recurrent retrosternal discomfort to episodes of severe crushing chest pain radiating to the back, neck and arms, accompanied by sweating and a sensation of chocking. Intermittent mild and poorly localized dysphagia may be apparent with both solids and liquids; more prolonged episodes of esophageal obstruction occur in a few patients.
The therapeutic approach to diffuse esophageal spasm should be directed towards its most disturbing symptoms, i.e. chest pain and dysphagia, and should attempt to reduce the abnormal esophageal motility. If pathologic gastroesophageal reflux (GER) has been diagnosed as the underlying problem, a trial of an antireflux regimen is justified. To abolish GER is therefore an additional aim of the medical management.
A synopsis of the available options for the treatment of DES is shown in table 1. Explanation and reassurance are the most important elements in the management of such patients. With the report that their symptoms are not due to cardiac disease, many patients will improve. A further step in the medical approach is obviously drug treatment. Few and sparce published reports have described drug therapy in the management of DES. The discouraging therapeutic response for this disorder has recently been replaced by some hope and promise.
Smooth muscle relaxants are useful because they reduce abnormal esophageal
motility. These drugs include anticholinergics and myolitics, short- and long-acting nitrates, hydralazine and calcium channel blockers (table 1). These last compounds will be discussed below by R.W. McCallum.
Table 1. Synopsis of the therapeutic options in the treatment of DES.
Anticholinergics and myolitics
Anticholinergics strongly affect esophageal motility (for review, see [4 ]). Since a cholinergic mechanism seems to be involved in the control of lower esophageal sphincter (LES) pressure, the resting sphincter closure tension in man is reduced by atropine or propantheline. A well conducted study by Fournet and co-workers [5 ] showed that an optimally effective dose (determined according to Sun and Shay) of propantheline, besides decreasing the resting LESP, dramatically lowers the peristaltic wave amplitude in the smooth muscle part of the esophagus. Hongo et al. [6 ] actually reported oral propantheline (15 mg) more effective than nifedipine (20 mg sublingually) in reducing contraction amplitude in the body of the esophagus, an effect which was enhanced by concomitant nifedipine administration.
Anticholinergics could be therefore useful in the treatment of DES. Unfortunately, controlled trials are lacking and their use is restricted to the control of severe acute spasms after parenteral administration. The oral bioavailability of these compounds is indeed very poor.
Myolitics also relax esophageal smooth muscle (figure 1) both, in vitro and in vivo [7 ]. Although theoretically useful, these compounds have not been studied in patients with primary esophageal motor disorders.
Figure 1. Effect of some smooth muscle relaxants on substance P (10пїЅg/ml) induced contractions in isolated rat LES. x = washing and recording stopped for 15 min. P = papaverine ; M = mebeverine ; V = verapamil; N = nifedipine. Doses are in пїЅg/ml, time is min. On the ordinate, tension of the transducer in g.
Nitrates relax smooth muscle through activation of guanylate cyclase and increase of intracellular cyclic GMP content [8 ]. They are generally considered in the context of vasodilatation and their usefulness for the treatment of angina pectoris is unquestionable. However, the pharmacologic action of nitrates on smooth muscle is a non specific one, and these drugs affect all smooth muscle, including that of the gastrointestinal tract. It is important to recognize and understand the basic pharmacologic actions of drugs and avoid exclusive attention to selected uses implied by conventional therapeutic classifications. Thus, although nitrates may be classified as antianginal drugs, relief of chest or back pain by nitroglycerin (TNG) does not always mean that the pain is of cardiac origin, as it might have relieved muscular spasm of the esophagus or biliary tract.
In patients with DES, administration of TNG sublingually is followed by elimination of repetitive contractions after swallows, an effect which is unfortunately short-lasting [9 ]. Reduction in amplitude of esophageal contractions is usually followed by relief of pain [10 ]. Long-acting nitrates (i.e. erythrityl tetranitrate or isosorbide dinitrate) are preferable to prevent major esophageal spasms. After one week treatment on Cardilate®, abnormal esophageal activity is usually controlled
and pain is absent [10 ]. A recent study [11 ], performed in achalasic patients, suggests that transdermal nitroglycerin could be an effective alternative to orally administered long-acting nitrates.
When nitrates are used for long-term therapy, the presence of GER may strongly influence the response. Swamy [10 ] reported that in the patients who had significant reflux associated with spasm, the response to nitroglycerin was unpredictable.
On the contrary, in the patients with DES but without reflux, the response -both clinical and manometric пїЅ was uniformly good (figure 2).
Figure 2. Clinical and manometric response to TNG and long-acting nitrates in DES patients with and without associated GER (drawn from data in Ref. 10).
Hydralazine causes direct relaxation of arteriolar vascular smooth muscle. The mechanism of this effect seems to be similar to that of organic nitrates, in that it appears to involve activation of guanylate cyclase and accumulation of cyclic GMP[12 ]. The drug was tested in patients with painful primary esophageal disorders (EMD), most of whom had DES [13 ]. Compared with isosorbide (20 mg orally), hydralazine (10mg intramuscularly) was significantly more effective in reducing distal esophageal contractions in response to cholinergic stimulation (figure 3). Consequently, the bethanechol-induced pain was relieved in a greater proportion of patients after premedication with hydralazine (60% versus 20%, respectively) [13 ].
Taking into account the favourable results of acute pharmacological studies, long-term therapy with hydralazine (75-200 mg/day orally) was tested in patients with primary EMD [13 ]: all patients placed on oral hydralazine experienced symptom improvement and, in all of them, a significant decrease of amplitude and duration of esophageal contraction could be demonstrated (figure 4).
Figure 3. Distal esophageal contractions in response to subcutaneous bethanechol (55пїЅg/kg) in patients with primary EMD. effect of premedication with isosorbide or hydralazine (drawn from data in Ref. 13).
Figure 4. Effect of hydralazine therapy on esophageal motility in patients with primary EMD. * p < 0.05 ; ** p < 0.005 (drawn from data in Ref. 13).
To summarize, sublingual nitroglycerin can be used to abort the acute attacks of chest pain in patients with DES. Long-acting nitrates are however preferable to prevent major motor spasms. Although several patients have short-term
improvement, within 3 months these drugs usually loose their efficacy because of development of tolerance.
Compared with long-acting nitrates (i.e. isosorbide), hydralazine is more effective in reducing esophageal motor response to bethanechol and to prevent chest pain in response to cholinergic stimulation. Accordingly, long-term hydralazine therapy gives rise to improvement in chest pain and dysphagia, with concomitant decrease of amplitude and duration of esophageal contractions.
It must be emphasized however that, because of their untoward effects, these drugs are not a first choice in the medical treatment of DES.
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