Dysphagia

DYSPHAGIA

Dysphagia is difficulty moving food or liquid through the mouth, pharynx, and

esophagus. The pt senses swallowed material sticking along the path. Odynophagia

is pain on swallowing. Globus pharyngeus is the sensation of a lump

lodged in the throat, but swallowing is unaffected.

PATHOPHYSIOLOGY Dysphagia is caused by two main mechanisms:

mechanical obstruction or motor dysfunction. Mechanical causes of dysphagia

can be luminal (e.g., large food bolus, foreign body), intrinsic to the esophagus

(e.g., inflammation, webs and rings, strictures, tumors), or extrinsic to the esophagus (e.g., cervical spondylitis, enlarged thyroid or mediastinal mass, vascular compression). The motor function abnormalities that cause dysphagia may be related to defects in initiating the swallowing reflex (e.g., tongue paralysis, lack of saliva, lesions affecting sensory components of cranial nerves X and XI),

disorders of the pharyngeal and esophageal striated muscle (e.g., muscle disorders

such as polymyositis and dermatomyositis, neurologic lesions such as

myasthenia gravis, polio, or amyotrophic lateral sclerosis), and disorders of the

esophageal smooth muscle (e.g., achalasia, scleroderma, myotonic dystrophy).

Approach to the Patient

History can provide a presumptive diagnosis in about 80% of pts. Difficulty

only with solids implies mechanical dysphagia. Difficulty with both solids and

liquids may occur late in the course of mechanical dysphagia but is an early

sign of motor dysphagia. Pts can sometimes pinpoint the site of food sticking.

Weight loss out of proportion to the degree of dysphagia may be a sign of

underlying malignancy. Hoarseness may be related to involvement of the larynx

in the primary disease process (e.g., neuromuscular disorders), neoplastic disruption of the recurrent laryngeal nerve, or laryngitis from gastroesophageal

reflux.

Physical exam may reveal signs of skeletal muscle, neurologic, or oropharyngeal

diseases. Neck exam can reveal masses impinging on the esophagus.

Skin changes might suggest the systemic nature of the underlying disease (e.g.,

scleroderma).

Dysphagia is nearly always a symptom of organic disease rather than a

functional complaint. If oropharyngeal dysphagia is suspected, videofluoroscopy

of swallowing may be diagnostic. Mechanical dysphagia can be evaluated

by barium swallow and esophagogastroscopy with endoscopic biopsy. Barium

swallow and esophageal motility studies can show the presence of motor

dysphagia.

OROPHARYNGEAL DYSPHAGIA Pt has difficulty initiating the swallow;

food sticks at the level of the suprasternal notch; nasopharyngeal regurgitation

and aspiration may be present.

Causes include: for solids only, carcinoma, aberrant vessel, congenital or

acquired web (Plummer-Vinson syndrome in iron deficiency), cervical osteophyte;

for solids and liquids, cricopharyngeal bar (e.g., hypertensive or hypotensive

upper esophageal sphincter), Zenker’s diverticulum (outpouching in the

posterior midline at the intersection of the pharynx and the cricopharyngeus

muscle), myasthenia gravis, glucocorticoid myopathy, hyperthyroidism, hypothyroidism, myotonic dystrophy, amyotrophic lateral sclerosis, multiple sclerosis, Parkinson’s disease, stroke, and bulbar and pseudobulbar palsy.

ESOPHAGEAL DYSPHAGIA Food sticks in the mid or lower sternal

area; can be associated with regurgitation, aspiration, odynophagia. Causes include: for solids only, lower esophageal ring (Schatzki’s ring, symptoms are

usually intermittent), peptic stricture (heartburn accompanies this), carcinoma,

lye stricture; for solids and liquids, diffuse esophageal spasm (occurs with chest

pain and is intermittent), scleroderma (progressive and occurs with heartburn),

achalasia (progressive and occurs without heartburn).

NONCARDIAC CHEST PAIN

Thirty percent of pts presenting with chest pain have an esophageal source rather

than angina. History and physical exam often cannot distinguish cardiac from

noncardiac pain. Exclude cardiac disease first. Causes include: gastroesophageal

reflux disease, esophageal motility disorders, peptic ulcer disease, gallstones,

psychiatric disease (anxiety, panic attacks, depression).

Evaluation Consider a trial of antireflux therapy (omeprazole); if no response,

24-h ambulatory luminal pH monitoring; if negative, esophageal manometry

may show motor disorder. Trial of imipramine, 50 mg PO qhs, may

be worthwhile. Consider psychiatric evaluation in selected cases.

ESOPHAGEAL MOTILITY DISORDERS

Pts may have a spectrum of manometric findings ranging from nonspecific abnormalities to defined clinical entities.

ACHALASIA Motor obstruction caused by hypertensive lower esophageal

sphincter (LES), incomplete relaxation of LES, or loss of peristalsis in

smooth-muscle portion of esophagus. Causes include: primary (idiopathic) or

secondary due to Chagas’ disease, lymphoma, carcinoma, chronic idiopathic

intestinal pseudoobstruction, ischemia, neurotropic viruses, drugs, toxins, radiation

therapy, postvagotomy.

Evaluation Chest x-ray shows absence of gastric air bubble. Barium swallow

shows dilated esophagus with distal beaklike narrowing and air-fluid level.

Endoscopy is done to rule out cancer, particularly in persons _50 years. Manometry shows normal or elevated LESpressure, decreased LES relaxation,

absent peristalsis.

TREATMENT

Pneumatic balloon dilatation is effective in 85%, 3–5% risk of perforation or

bleeding. Injection of botulinum toxin at endoscopy to relax LESis safe and

effective but effects last only about 12 months. Myotomy of LES(Heller

procedure) is effective, but 10–30% of pts develop gastroesophageal reflux.

Nifedipine, 10–20 mg, or isosorbide dinitrate, 5–10 mg SL ac, may avert

need for dilatation or surgery.

SPASTIC DISORDERS Diffuse esophageal spasm involves multiple

spontaneous and swallow-induced contractions of the esophageal body that are

of simultaneous onset, long duration, and recurrent. Causes include: primary

(idiopathic) or secondary due to gastroesophageal reflux disease, emotional

stress, diabetes, alcoholism, neuropathy, radiation therapy, ischemia, or collagen

vascular disease.

An important variant is nutcracker esophagus: high-amplitude (_180

mmHg) peristaltic contractions; particularly associated with chest pain or dysphagia, but correlation between symptoms and manometry is inconsistent. Condition may resolve over time or evolve into diffuse spasm; associated with

increased frequency of depression,anxiety,and somatization.

Evaluation Barium swallow shows corkscrew esophagus,pseudodiverticula,

and diffuse spasm. Manometry shows spasm with multiple simultaneous

esophageal contractions of high amplitude and long duration. In nutcracker

esophagus,the contractions are peristaltic and of high amplitude. If heart disease

has been ruled out,edrophonium,ergonovine, or bethanecol can be used to

provoke spasm.

TREATMENT

Anticholinergics are usually of limited value; nitrates (isosorbide dinitrate,5 –

10 mg PO ac) and calcium antagonists (nifedipine,10 –20 mg PO ac) are

more effective. Those refractory to medical management may benefit from

balloon dilatation. Rare pts require surgical intervention; longitudinal myotomy

of esophageal circular muscle. Treatment of concomitant depression

or other psychological disturbance may help.

SCLERODERMA Atrophy of the esophageal smooth muscle and fibrosis

can make the esophagus aperistaltic and lead to an incompetent LES with attendant

reflux esophagitis and stricture. Treatment of gastroesophageal reflux

disease is discussed in Chap. 48.

ESOPHAGEAL INFLAMMATION

VIRAL ESOPHAGITIS Herpesviruses I and II,varicella-zoster virus,

and CMV can all cause esophagitis; particularly common in immunocompromised

pts (e.g., AIDS). Odynophagia,dysphagia,fever,and bleeding are symptoms

and signs. Diagnosis is made by endoscopy with biopsy,brush cytology, and culture.

TREATMENT

Disease is usually self-limited in the immunocompetent person; viscous lidocaine

can relieve pain; in prolonged cases and in immunocompromised hosts,

herpes and varicella esophagitis are treated with acyclovir,5 –10 mg/kg IV

q8h for 10–14 d,then 200–400 mg PO 5 times a day. CMV is treated with

ganciclovir,5 mg/kg IV q12h, until healing occurs,which may take weeks.

Oral valganciclovir (900 mg bid) is an effective alternative to parenteral treatment.

In nonresponders, foscarnet,60 mg/kg IV q12h for 21 days,may be

effective.

CANDIDA ESOPHAGITIS In immunocompromised hosts,malignancy,

diabetes, hypoparathyroidism,hemoglobinopathy,SLE, corrosive esophageal

injury,candidal esophageal infection may present with odynophagia, dysphagia,

and oral thrush (50%). Diagnosis is made on endoscopy by identifying yellowwhite plaques or nodules on friable red mucosa. Characteristic hyphae are seen on KOH stain. In patients with AIDS,the development of symptoms may

prompt an empirical therapeutic trial.

TREATMENT

Oral nystatin (100,000 U/mL),5 mL q6h,or clotrimazole, 10-mg tablet

sucked q6h,is effective. In immunocompromised host, fluconazole, 100–200

mg PO daily for 1–3 weeks,is treatment of choice; alternatives include itraconazole, 200 mg PO bid,or ketoconazole,200 –400 mg PO daily; long-term

maintenance therapy is often required. Poorly responsive pts may respond to

higher doses of fluconazole (400 mg/d) or to amphotericin,10 –15 mg IV q6h

for a total dose of 300–500 mg.

PILL-RELATED ESOPHAGITIS Doxycycline,tetracycline, aspirin,

NSAIDs,KCl,quinidine, ferrous sulfate, clindamycin, alprenolol, and alendronate

can induce local inflammation in the esophagus. Predisposing factors

include recumbency after swallowing pills with small sips of water,anatomic

factors impinging on the esophagus and slowing transit.

TREATMENT

Withdraw offending drug,use antacids, and dilate any resulting stricture.

OTHER CAUSES OF ESOPHAGITIS IN AIDS Mycobacteria, Cryptosporidium, Pneumocystis carinii,idiopathic esophageal ulcers,giant ulcers

(possible cytopathic effect of HIV) can occur. Ulcers may respond to systemic

glucocorticoids.