Mitchell C. Sokolosky
DYSPHAGIA
PATHOPHYSIOLOGY
Dysphagia is defined as difficulty in swallowing.
Most patients will have an identifiable, organic process causing their symptoms.
Dysphagia can be grouped into two broad classification schemes: (1) transfer dysphagia (difficulty in initiating swallowing) and (2) transport dysphagia (feeling of food getting “stuck”).
CLINICAL FEATURES
Historical information is the key to the diagnosis of dysphagia.
Transport dysphagia that is present for solids only generally suggests a mechanical or obstructive process.
Motility disorders typically cause transport dysphagia for solids and liquids.
A poorly chewed meat bolus may obstruct the esophagus and be the presenting sign for a variety of underlying esophageal pathologies.
Physical examination of patients with dysphagia should focus on the head and neck and the neurologic examination. Unfortunately, the examination is often normal.
The patient should be watched taking a sip of water.
DIAGNOSIS AND DIFFERENTIAL
The diagnosis of the underlying pathology of dys-phagia is most often made outside the emergency department (ED).
Initial evaluation may include anteroposterior (AP) and lateral neck and chest radiographs.
Barium swallow is usually the first test for patients with transport dysphagia.
Direct laryngoscopy can be used to identify structural lesions.
Oropharyngeal dysphagia is best worked up using videoesophagography.
Structural or obstructive causes of dysphagia include neoplasms (squamous cell carcinoma is most common), esophageal strictures and webs, Schatzki ring, and diverticula.
Motor lesions causing dysphagia include neuromuscu-lar disorders (cerebrovascular accident [CVA] is most common), achalasia, and diffuse esophageal spasm.
EMERGENCY DEPARTMENT CARE AND DISPOSITION
Protection of the airway and breathing is vital since aspiration is a major concern with most causes of dysphagia.
Most causes of dysphagia can be further evaluated and managed in the outpatient setting.
Many of the structural lesions will ultimately require dilatation as definitive therapy.
CHEST PAIN OF ESOPHAGEAL ORIGIN
EPIDEMIOLOGY
The incidence of esophageal disease in patients with chest pain and normal coronary arteries ranges from 20% to 60%.
Gastroesophageal reflux disease (GERD) affects up to 20% of the US population, with higher rates in elderly populations.
PATHOPHYSIOLOGY
Reflux of gastric contents into the esophagus causes a wide array of symptoms and long-term effects.
Transient relaxation of the lower esophageal sphincter (LES) complex (with normal tone in between periods of relaxation) is the primary mechanism causing reflux.
Hiatal hernia, prolonged gastric emptying, agents that decrease LES pressure, and impaired esophageal motility predispose to reflux.
Inflammatory esophagitis can be caused by GERD and medications. Patients with immunosuppression can develop infectious esophagitis.
Esophageal dysmotility is the excessive, uncoordinated contraction of esophageal smooth muscle.
CLINICAL FEATURES
Heartburn is the classic symptom of GERD, and chest discomfort may be the sole manifestation of the disease.
The association of pain with meals, postural changes in pain, and relief of symptoms with antacids are more consistent with GERD.
Less obvious presentations of GERD also occur such as pulmonary symptoms, especially asthma exacerbations, and multiple ear/nose/throat symptoms.
GERD has also been implicated in the etiology of dental erosion, vocal cord ulcers and granulomas, laryngitis with hoarseness, chronic sinusitis, and chronic cough.
Over time, GERD can cause complications such as strictures, inflammatory esophagitis, and Barrett’s esophagus (a premalignant condition).
Esophagitis can cause prolonged periods of chest pain and almost always causes odynophagia as well.
Esophageal dysmotility often presents with chest pain, onset usually in fifth decade.
DIAGNOSIS AND DIFFERENTIAL
Diagnosis is often made by history and favorable response to antacid treatment.
Unfortunately, like cardiac pain, esophageal pain may be squeezing, be pressure-like, and include a history of onset with exertion and rest. Both types of pain may be accompanied by diaphoresis, pallor, radiation, and nausea and vomiting.
EMERGENCY DEPARTMENT CARE AND DISPOSITION
Comprehensive treatment of reflux disease involves decreasing acid production in the stomach, enhancing upper tract motility, and eliminating risk factors for the disease.
Mild disease is often treated empirically with an H2 blocker or proton pump inhibitor. A prokinetic drug may also greatly decrease symptoms.
Patients should avoid agents that exacerbate GERD (ethanol, caffeine, nicotine, chocolate, fatty foods), sleep with the head of the bed elevated 30 degrees, and avoid eating within 3 hours of going to bed at night.
Pain from spasm may respond to nitroglycerin. Calcium channel blockers and anticholinergic agents can also be employed.
ESOPHAGEAL PERFORATION
EPIDEMIOLOGY
Perforation of the esophagus is associated with a high mortality rate regardless of the underlying cause.
PATHOPHYSIOLOGY
Iatrogenic injury is the most common cause of esophageal perforation.
Other causes include Boerhaave’s syndrome (up to 15%), trauma (10%), and foreign body ingestion.
Boerhaave’s syndrome is a full-thickness perforation of the esophagus after a sudden rise in intraesophageal pressure, often due to forceful emesis. Alcohol consumption is frequently an antecedent to this syndrome.
CLINICAL FEATURES
Pain is classically described as acute, severe, unrelenting, and diffuse, and is reported in the chest, neck, and abdomen.
Pain can radiate to the back and shoulders, or back pain may be the predominant symptom.
Swallowing often exacerbates pain.
Physical exam varies with the severity of the rupture and the elapsed time between the rupture and presentation.
Tachycardia and tachypnea are common.
Abdominal rigidity with hypotension and fever often occur early.
Mediastinal emphysema takes time to develop. It is less commonly detected by examination or radiography in lower esophageal perforation, and its absence does not rule out perforation.
Hammon’s crunch, caused by air in the mediastinum being moved by the beating heart, can sometimes be auscultated.
Pleural effusions develop in half of patients with intrathoracic perforations and are uncommon in cervical perforations.
DIAGNOSIS AND DIFFERENTIAL
Chest radiographs can suggest the diagnosis.
CT of the chest or endoscopy is most often used to confirm the diagnosis; the choice depends upon clinical setting and the local resources available.
Esophageal perforation is often ascribed to acute myo-cardial infarction (MI), pulmonary embolus, peptic ulcer disease, aortic catastrophe, or acute abdomen, resulting in critical delays in diagnosis, the most important factor in determining morbidity and mortality.
EMERGENCY DEPARTMENT CARE AND DISPOSITION
Rapid, aggressive management is key to minimizing the morbidity and mortality associated with esophageal perforation.
In the ED, resuscitation of shock (see Chapter 7) and broad-spectrum parenteral antibiotics should be given to cover both aerobic and anaerobic organisms. Examples include single-drug coverage such as piperacillin-tazobactam3.375 grams IV, or double-drug coverage with cefotaxime 2 grams IV, or ceftriaxone 2 grams IV plus clindamycin 600 milligrams IV or metronidazole 1 gram IV.
Emergent surgical consultation should be obtained as soon as the diagnosis is seriously entertained.
All patients require admission to the hospital.
SWALLOWED FOREIGN BODIES
EPIDEMIOLOGY
Children from 18 to 48 months of age account for 80% of all cases of ingested foreign bodies.
Adult candidates for swallowed foreign bodies are those with esophageal disease, prisoners, and psychiatric patients.
PATHOPHYSIOLOGY
Small objects, such as coins, toys, and crayons, typically lodge in the anatomically narrow proximal esophagus. In adults, most impactions are distal.
In children and adults, once an object has traversed the pylorus, it usually continues through the GI tract and is passed without issue.
Irregular, sharp, wide (>2.5 cm), or long objects (>6 cm) may become lodged distal to the pylorus.
Esophageal impaction can result in airway obstruction, stricture, or perforation.
Esophageal mucosal irritation can be perceived as a foreign body by the patient.
CLINICAL FEATURES
Adults with an esophageal foreign body generally provide unequivocal history. Patients often complain of retrosternal pain, dysphagia, vomiting, choking, and inability to tolerate pooled secretions.
In children, the history can be unclear. Signs and symptoms include refusal or inability to eat, vomiting, gagging and choking, stridor, neck or throat pain, and drooling.
A high degree of suspicion is necessary for unwitnessed ingestions in children, especially in those <2 years of age.
Examination starts with assessment of the airway. Occasionally, a foreign body can be directly visualized in the oropharynx.
DIAGNOSIS AND DIFFERENTIAL
Plain films are used to screen for radiopaque objects. Coins in the esophagus present their circular face on anteroposterior films, as opposed to coins in the trachea, which show that face on lateral films.
Plain films are <50% sensitive for detecting impacted bones, so lack of visualization does not exclude bone impaction. Plain films are often not necessary for patients with food impaction.
Contrast radiographs (barium or meglumine diatri-zoate… Gastrograffin) have low yields; the contrast material can impair endoscopy and present an aspiration risk.
CT scanning is a very high-yield test for esophageal foreign bodies and has replaced the contrast radiographs to evaluate possible nonradiopaque objects.
If endoscopy is clearly indicated, performing advanced imaging studies delays definitive intervention and adds little value to care.
EMERGENCY DEPARTMENT CARE AND DISPOSITION
Patients in extremis or those with pending airway compromise are resuscitated in standard fashion.
Emergent endoscopy is indicated for complete esophageal obstruction due to distal food impaction.
Circumstances warranting urgent endoscopy for esophageal foreign bodies are shown in Table 42-1.
Success rates of glucagon therapy to relax the LES are poor. The use of proteolytic enzymes (meat ten-derizer containing papain) to dissolve a meat bolus is contraindicated.
Very proximally lodged objects may be removed by indirect laryngoscopy or fiber-optic scope.
Coin removal with a Foley catheter is institution dependent. Complications include aspiration, airway compromise, and mucosal laceration.
A button battery lodged in the esophagus is a true emergency requiring prompt removal because of the possibility of perforation.
Sharp objects should be removed by endoscopy while they are in the stomach or duodenum in order to prevent intestinal perforation (up to 35%).
Endoscopy is contraindicated for the removal of ingested narcotic packets ingested by narcotic couriers (body packers) because of the risk of iatrogenic packet rupture. Observation until the packet reaches the rectum is the favored treatment. Whole-bowel irrigation may aid the process.
Consult surgery for worrisome foreign bodies that are in the more distal GI tract or if signs or symptoms of intestinal injury (eg, pain, emesis, fever, GI bleeding) are present.
TABLE 42-1 Circumstances Warranting Urgent Endoscopy for Esophageal Foreign Bodies
Ingestion of sharp or elongated objects (including toothpicks, aluminum soda can tabs)
Ingestion of multiple foreign bodies
Ingestion of button batteries
Evidence of perforation
Coin at the level of the cricopharyngeus muscle in a child
Airway compromise
Presence of a foreign body for >24 h
For further reading in Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7th ed., see Chapter 80, “Esophageal Emergencies, Gastro-esophageal Reflux Disease, and Swallowed Foreign Bodies,” by Moss H. Mendelson.