Plummer-Vinson syndrome

The article "Anatomy and physiology of the esophagus" is the basis for this AORN Journal independent study. The behavioral objectives and examination for this program were prepared by Helen Starbuck Pashley, RN, MA, CNOR, with consultation from Trish O'Neill, RN, MS, education coordinator, Center for Perioperative Education.

A minimum score of 70% on the multiple-choice examination is necessary to earn two contact hours for this independent study. Participants receive feedback on incorrect answers. Each applicant who successfully completes this study will receive a certificate of completion. The deadline for submitting this study is March 31, 2000.

Send the completed application form, multiple-choice examination, learner evaluation, and appropriate fee to

BEHAVIORAL OBJECTIVES

After reading and studying the article on anatomy and physiology of the esophagus, the nurse will be able to

(1) discuss the risk factors for esophageal cancer,

(2) identify the significant anatomy of the esophagus, and

(3) discuss the physiology of the esophagus.

The earliest accounts of esophageal surgery are found in the document known as the "Smith Surgical Papyrus." This document, unearthed by the American Egyptologist Edwin Smith in 1862, describes a "gaping wound of the throat penetrating the gullet." Cancer of the esophagus was recognized by the Chinese more than 2,000 years ago as a cause of dysphagia. Achalasia was first described by the English anatomist Thomas Willis in 1674. He used a cork-tipped whale bone as an instrument of esophageal dilatation.

Physicians in Germany and Austria contributed significant advances to knowledge about the esophagus and to surgical techniques in the 19th century. In 1868, a German physician, Adolf Kussmaul, hyper-extended a patient's head and neck and passed a lighted tube into the esophagus to diagnose a carcinoma of the thoracic esophagus. Another German surgeon, Friedrich Trendelenburg, introduced endotracheal anesthesia in 1869, and two years later, in 1871, the first successful esophageal resection and reanastamosis was performed on dogs by the Austrian surgeon Theodor Billroth. Vincenz Czerny, another German surgeon, performed the first esophageal resection for cancer in a human in 1877. His patient lived for one year before dying from recurrence of the tumor. In 1913, American surgeon Franz Torek performed the first transthoracic excision of a mid-esophageal carcinoma. His patient was a 67-year-old woman with squamous cell carcinoma of the mid-esophagus. Torek tunneled the cervical esophagus of the patient along her anterior chest wall and formed a cutaneous esophagostomy, which was then connected by a rubber tube to a gastrostomy. The patient lived in good health for 13 years.(1) In Germany, the surgeon E. Heller performed the first esophagomyotomy, to treat achalasia, in 1913. In 1961, Rudolph Nissen, a Swiss surgeon, and later (ie, 1967) English surgeons David B. Skinner and Ronald H. R. Belsey used fundoplication (ie, a reduction in the size of the esophageal hiatus and suturing of the esophagus to the fundus) to create an intraabdominal esophageal valve mechanism to control gastroesophageal reflux.(2) In the ensuing years, many improvements have been made in surgical techniques, anesthesia delivery, diagnostic measures, and in preoperative and postoperative care of patients with esophageal disorders.

EPIDEMIOLOGICAL ASPECTS

Despite the progress in treatment of many esophageal disorders, esophageal cancer is the seventh leading cause of cancer deaths in the world.(3) The most significant risk factors for this malady in the United States are alcohol consumption and cigarette abuse. Associated risk factors for esophageal cancer are disorders of the esophagus such as

* hiatal hernia,

* esophageal stricture,

* gastroesophageal reflux, and

* severe esophagitis.(4)

Cancer of the esophagus is of epidemic proportions in some areas of the world (ie, northeastern Iran, the Transkei of South Africa, the Hunan province of China, and certain areas of Russia, India, the Middle East, and Singapore). In the Hunan province, the prevalence of esophageal carcinoma is 0.9% in people more than 30 years of age. The incidence in humans is matched in the poultry population in the same area. Epidemiological studies suggest that the etiology in both instances is the presence of large amounts of carcinogenic nitrosamines in the soil and contamination of foods by fungi and yeast that produce mutagens.

Drinking "burning hot" tea and chewing tobacco (with or without betel nut) are believed to cause esophageal damage that leads to cancer.(5) Decreased intake of vitamins A, C, E, [B.sub.12], folic acid, riboflavin, and the mineral zinc are also believed to be associated with esophageal cancer.(6) The neuromuscular esophageal disorder termed achalasia (ie, a Greek word meaning failure to relax) is a premalignant lesion that leads to carcinoma in 1% to 10% of people who have had the disease for 15 to 25 years.(7) In Brazil, Chagas' disease, which results from infestation with the parasite Trypanosoma cruzi, affects one of every eight Brazilians, and 5% of these individuals develop motor disorders of the esophagus known as infectious achalasia.(8) Achalasia has also developed after severe emotional and physical trauma and drastic weight reduction in markedly obese people. Because achalasia is incurable and treatment at best is purely palliative, it contributes greatly to morbidity.

Plummer-Vinson syndrome (ie, cervical dysphagia) occurs in iron deficiency anemia. There is a high incidence of this syndrome in Scandinavia and Great Britain. It is regarded as a premalignant lesion because 10% of patients affected with it develop squamous cell carcinoma of the mouth, throat, or esophagus.(9)

As case finders in the primary care arena, nurses, by virtue of their knowledge base, are able to identify potential causative factors for esophageal carcinoma in the patients they meet. Nurses can teach patients about appropriate nutrition, encourage lifestyle modifications, and make referrals for health counseling and timely medical or surgical interventions.

EMBRYOLOGY OF THE ESOPHAGUS

The esophagus develops at approximately the 20th day of gestation, when septa from the lateral walls of the foregut (ie, the first part of the digestive tube) fuse, separating the trachea from the esophagus. The primitive esophagus is lined with columnar epithelium, but by the seventh gestational week this lining is replaced with ciliated epithelium, which in turn is replaced by stratified squamous epithelium at approximately 20 weeks. The mucous glands form in the esophagus at 16 weeks and the submucous glands at approximately 20 weeks. The muscularis propria (ie, muscular coat) appears at approximately six weeks, and the outer longitudinal coat of muscles develops at nine weeks. The striated muscle in the upper third of the esophagus is not fully formed until 20 weeks.(10)

Developmentally, if incomplete partitioning between the esophagus and trachea occurs, the infant will be born with a tracheo-esophageal fistula or esophageal atresia (ie, esophagus ends in a blind pouch) or both. These conditions constitute surgical emergencies.(11) Cyanotic episodes, copious oral and nasal secretions, and inability to pass a catheter into the stomach suggests these disorders. Inadvertent feeding of such infants results in aspiration, which leads to pneumonia and chemical pneumonitis. Nurses should suspect these disorders in the infant of any woman who experienced polyhydramnious (ie, an excess of amniotic fluid) during the pregnancy.(12) With the sophistication of prenatal care today, the majority of these defects are diagnosed before birth, and some can be fixed via intrauterine surgery during the pregnancy or immediately after birth.

ANATOMY OF THE ESOPHAGUS

The esophagus is a hollow tube approximately 25 cm in length that extends from the pharynx to the stomach. The pharynx is a muscular tube approximately 12 cm long that serves as an entry to the esophagus and respiratory tract.(13) The oropharynx is posterior to the mouth, and the nasopharynx is posterior to the nose. These are separated by the soft palate, which is pulled upward to close the nasopharynx during swallowing.(14) The esophagus consists of three parts: the cervical, thoracic, and abdominal esophagus.

Cervical esophagus. The cervical esophagus lies just left of the midline behind the larynx and trachea. The entry to the cervical esophagus is called the cricopharyngeus muscle or upper esophageal sphincter (UES).

Thoracic esophagus. The upper portion of the thoracic esophagus passes behind the tracheal bifurcation (ie, carina) and left mainstem bronchus. The lower thoracic esophagus runs behind the left atrium. It enters the abdomen through the esophageal hiatus (ie, opening in the diaphragm).

Abdominal esophagus. The abdominal esophagus is an area approximately 2 cm to 4 cm in length. It is also known as the lower esophageal sphincter (LES). It connects the esophagus to the stomach.(15)

There are three areas in the esophagus where the lumen normally narrows (Figure 1). These are in the UES area near the location of the cricoid cartilage in the airway, at the area where the left mainstem bronchus and aortic arch cross the esophagus (these structures compress the esophagus in those areas), and in the area of the LES where the esophagus traverses the diaphragm (ie, the diaphragmatic hiatus).(16) The narrowest point is at the UES. This sphincter measures 14 mm in diameter and is an area of weakness that has the potential for the formation of diverticula (ie, Zenker's diverticula), as well as the potential for perforation during esophagoscopy.(17) The terms oropharyngeal dysphagia and cricopharyngeal dysfunction describe the symptom complex that results in difficulty propelling solids from the oropharynx into the upper esophagus. The cause of this malfunction involves abnormalities of the central and peripheral nervous systems, metabolic and inflammatory myopathy, and other unknown factors.(18) The term globus hystericus (ie, a lump in the throat) is sometimes applied to cervical dysphagia even though it is not always due to nerves; the term should be reserved for those in whom extensive testing shows no evidence of physical disease.(19)

[Figure 1 ILLUSTRATION OMITTED]

The bronchoaortic constriction is 15 mm to 17 mm in diameter. This is a common area for pill-induced strictures. All pills have the potential for injury, but tetracycline, potassium chloride, nonsteroidal anti-inflammatories, and quinidine are pills that are most recognized for causing damage. Nurses need to encourage patients to drink plenty of fluids with pills and to remain upright for 30 to 60 minutes afterward.(20)

The diaphragmatic constriction is the third area of constriction and is 16 mm to 19 mm in diameter. The areas between these areas of constriction have wider diameters and are called the superior and inferior dilations. The superior dilation (ie, the area above the bronchoaortic constriction) has a diameter of 19 mm and that of the inferior dilation (ie, above the diaphragmatic constriction) is 22 mm.(21)

The esophageal wall. The esophagus is a muscular, mucosa-lined tube. It is surrounded by an adventitia (ie, outermost covering of a structure) of fibrous and areolar tissue.(22) Unlike the rest of the gastrointestinal tract, the adventitia of the esophagus lacks an outer serosa (ie, a serous membrane such as the peritoneum or the pleura). This lack of a serosa may contribute to the rapid spread of cancer cells and to the increased potential for leakage after surgery.(23) The adventitia contains collagen and elastic fibers that give strength to the structure.

Beneath the adventitia is a coat of longitudinal muscle over a layer of circular muscle; both layers consist of striated muscle (ie, skeletal or voluntary fibers) in the upper third of the esophagus. The lower two-thirds consists of smooth, nonstriated involuntary fibers. Between these two muscle layers is a network of sympathetic and parasympathetic fibers called the myenteric plexus or Auerbach's plexus. Loss of ganglion cells and neuronal degeneration of this plexus is believed to be a cause of achalasia. In this motility disorder, there is lack of esophageal peristalsis and failure of the LES to relax completely when swallowing.(24) Dysphagia, regurgitation, and weight loss are its main symptoms. A barium swallow used to diagnose achalasia shows a hallmark "bird's beak" taper at the LES.(25) Over months or years, the esophagus enlarges and, in severe cases, it may hold as much as one liter of putrid, infected material that may be aspirated to the lungs.(26)

Underneath the muscle layers of the esophagus lies the submucosa (Figure 2). It contains mucous glands, blood vessels, small amounts of the sympathetic and parasympathetic network known as Meissner's plexus, and an extensive lymphatic network. Beneath the submucosa, forming the lining of the esophagus, is the mucosa. It consists of squamous epithelium except for the distal 1 cm to 2 cm located at the esophageal-gastric junction. At this area, known as the Z-line, the stratified epithelium undergoes a transition to columnar epithelium.(27) Columnar epithelium is the normal lining of the stomach. It is an abnormal finding in the esophagus except for that in this distal area.

[Figure 2 ILLUSTRATION OMITTED]

Mucosa in the distal esophagus (ie, Z-line) is of interest endoscopically. If a segment of salmon-pink, columnar epithelium is found to extend well above the gastroesophageal junction, a diagnosis of Barret's esophagus can be made.(28) The risk of developing adenocarcinoma in the presence of Barrett's epithelium is 1% annually.(29) Nurses can play a significant role in helping detect this disorder by participating in surveillance programs and making referrals of those complaining of pyrosis (ie, heartburn), esophageal reflux, and a change in sensitivity of the mucosa. A history of heartburn that went away may indicate that columnar epithelium is affording "protection" against gastric contents being refluxed into the esophagus. This so-called protection may be the precursor of adenocarcinoma.

Blood supply. The esophagus receives its blood supply from four sources (Figure 3). The cervical esophagus is supplied by branches of the inferior thyroid arteries. The upper portion of the thoracic esophagus is supplied by the bronchial arteries, and its mid-thoracic area is supplied by vessels coming off the thoracic aorta. The lower thoracic esophagus is supplied by branches of the left gastric and inferior phrenic arteries.(30)

[Figure 3 ILLUSTRATION OMITTED]

An extensive submucosal venous plexus connects to peri-esophageal veins. In the neck, these drain into the inferior thyroid veins. In the thorax, they drain into the hemiazygos and azygos veins. The vena caval and portal venous systems are connected through the submucosal plexus. Portal hypertension (ie, portal venous pressure in excess of 20 mm Hg resulting from intrahepatic or extrahepatic portal venous compression or occlusion) can transform these submucosal veins into large varices.(31) Nurses should be mindful that portal hypertension results from disorders such as cirrhosis of the liven Rupture of these varices may occur spontaneously or when there is increased intraabdominal pressure as occurs with vomiting or straining at stool. Such a rupture constitutes a catastrophic event for a patient and carries a first event mortality rate of 40%.(32)

Lymphatic drainage. The esophagus has an extensive lymphatic drainage system, consisting of a lymphatic plexus in the mucosa and another in the muscle layer (Figure 4). The lymph from the upper two-thirds of the esophagus tends to travel upwards and that of the distal esophagus drains down. Because of this pattern of lymph drainage, esophageal carcinoma may metastasize to the internal jugular, paratracheal, subcarinal, lower mediastinal, and left gastric artery lymph nodes and the pulmonary ligaments.(33)

[Figure 4 ILLUSTRATION OMITTED]

Nerve supply. In addition to the intrinsic enervation provided by Auerbach's and Meissner's plexi, the esophagus is also supplied by many branches of the vagus nerve. An example is the recurrent laryngeal nerve, which, if damaged, causes hoarseness and UES dysfunction with aspiration on swallowing. Innervation of the esophagus is also provided by branches from the sympathetic nervous system.(34)

PHYSIOLOGY OF THE ESOPHAGUS

The primary function of the esophagus is to transport ingested material from the pharynx to the stomach.(35) Understanding the swallowing mechanism and testing for intactness of the cranial nerves (CN) involved in this process will help nurses assess a patient's esophageal function correctly and plan for his or her care.

There are four stages in the act of swallowing: early oral, late oral, pharyngeal, and esophageal.

Early oral stage. In this stage, food is chewed and lubricated by saliva. The structures involved in this process are the lips, cheeks, and salivary glands, innervated by CN V and VII, and the muscles of mastication, innervated by CN V. Cranial nerves V, VII, and IX supply sensation to the oral cavity.

Late oral stage. In the second stage of swallowing, the food bolus is moved to the oropharynx (innervated by CN IX and X) by the tongue, which is innervated by CN VII, IX, and XII.

Pharyngeal stage. In the third stage, the food bolus is moved to the hypopharynx by reflexes in the larynx, epiglottis, and hypopharynx. Cranial nerves IX and X innervate the hypopharynx.

Esophageal stage. In this stage, food is moved down the esophagus by peristalsis. The autonomic nervous system and CN X provide the innervation for peristalsis in the esophagus.

Nurses should be alert to the many warning signs of patients at risk for aspiration. These include coughing, choking, pocketing of food in the cheeks, and the presence of abnormal oral reflexes such as biting, suckling, chewing, and tongue thrusting.(36) Damage to CN V, IX, and X (eg, after a stroke) can cause paralysis of the swallowing mechanism. Diseases such as poliomyelitis and encephalitis can damage the swallowing center in the brain stem. Myasthenia gravis and botulism poisoning prevent impulse transmission at the myoneural junction, resulting in the inability to swallow. Deep anesthesia also causes serious paralysis of the swallowing mechanism. In patients who have not been NPO before surgery (eg, accident victims), large amounts of emesis may enter the pharynx and trachea, resulting in choking and aspiration.(37)

During the pharyngeal phase of swallowing, a peristaltic wave (ie, primary peristalsis) is created that relaxes the UES and forces the food bolus through it. The UES remains constricted except during swallowing. In this constricted state, air cannot enter the esophagus from the pharynx, and gastroesophageal reflux cannot enter the pharynx. The constricted UES has a mean resting pressure of 20 mm Hg to 60 mm Hg.(38) The peristaltic wave travels down the esophagus at approximately 3 cm to 5 cm/sec and reaches the stomach in five to 10 seconds. If the primary peristaltic wave fails to get the food to the stomach, the distended esophagus initiates another wave known as secondary peristalsis.(39) Gravity and an upright posture facilitate esophageal swallowing, but peristalsis makes it possible (though unusual) to eat and drink even while standing on one's head.(40) Tertiary peristalsis waves are sometimes seen in elderly people and in those with motility disorders. They are nonpropulsive and have no physiological function.(41) They represent uncoordinated contractions of smooth muscle and are responsible for the classic "corkscrew" appearance of esophageal spasm seen on a barium swallow.(42)

The LES allows the ingested food bolus to enter the stomach and prevents gastric contents from refluxing to the esophagus. The title LES is actually a misnomer, in that there is no anatomical circular sphincter muscle in humans or other primates. Despite this lack of a distinct sphincter in humans, manometry has clearly demonstrated an elevated pressure in the distal 3 cm to 5 cm area of the esophagus that guards against reflux. This area is often referred to as the high pressure zone and has a resting pressure of 10 mm to 20 mm Hg.(43) During swallowing, it relaxes to allow the food bolus to enter the stomach. It also has a tendency to relax even if there is no swallowing. Such relaxations are termed "transient lower esophageal sphincter relaxations" and account for the normal physiological reflux that occurs in all normal people. If these relaxations become too frequent, they contribute to reflux disease. The reflux seen in 40% of people results from these relaxations. Postprandial gastric distension is believed to be a cause of these relaxations.(44)

Other conditions known to relax the LES are

* delayed gastric emptying,

* diabetes mellitus,

* vagotomy,

* phlegmon (inflammation) as occurs in pancreatitis, and

* brain stem injury.

Medications causing LES relaxation include excess estrogen, anticholinergics (eg, atropine), calcium channel blockers, and nitroglycerin.(45) Nurses must anticipate the potential need for antireflux precautions when these states present. Some medications that may be prescribed to decrease the pathology associated with reflux include proton pump inhibitors (eg, omeprazole), histamine receptor antagonists (eg, cimetidine), and prokinetic agents (eg, cisapride). Antacids also may be beneficial adjuncts.(46)

Another disorder in the area of the LES is hiatal hernia. Depending on the type (Figure 5), symptoms vary. For example, Type I hiatal hernia, in which a small amount of the gastric cardia slides into the esophageal hiatus, is a common finding in many adults. It is not of significance unless accompanied by gastric reflux, and the treatment is similar to that for reflux.(47) Type II hiatal hernia, also known as a rolling hernia, is uncommon and represents a tree herniation of the stomach into a peritoneal sac in the mediastinum. Because intrathoracic pressure is less than abdominal pressure, this type of hernia progressively enlarges. The stomach may herniate completely upward to the extent that the pylorus comes to lie near the cardia, and the potential for a gastric volvulus exists. Not all Type II hernias cause symptoms, but gastric strangulation, infarction, bleeding, and respiratory deficiency may occur.(48) If a Type II hernia continues to enlarge, a Type III hernia may occur, in which other organs such as the colon, spleen, pancreas, and small intestine may enter the peritoneal sac.

[Figure 5 ILLUSTRATION OMITTED]

Generally, if the hernia remains in its intraabdominal location there is no reflux or heartburn. When symptoms do occur, the patient complains of fullness after meals, gurgling or splashing noises in the chest, early satiety, and postprandial vomiting. Acute epigastric or chest pain after meals suggests a volvulus. Such may lead to obstruction, strangulation, and death, if not corrected.(49)

Nurses can encourage lifestyle modifications in patients with alterations in the LES, including avoiding foods that decrease LES pressure (eg, chocolate, peppermint, coffee, cola, citrus juice, alcohol, fatty foods). Nurses can educate patients that lying in the left lateral decubitus position is better than lying on the right, that sleeping with the head of the bed elevated decreases nocturnal reflux, and that they should not eat for at least two to three hours before bedtime. They should know that smoking and the use of transdermal nicotine patches also decrease LES pressure and increase reflux.(50)

Nurses can reinforce physician explanations to patients when various diagnostic studies are being performed. Knowledge about the various diagnostic procedures is helpful. For example, vital staining with Lugol's solution (ie, a negative tumor marker) is done via endoscopy to determine if pathologic mucosa exists. This solution stains normal mucosa brown. Barrett's mucosa, early carcinoma, and tissue resulting from esophagitis remain unstained.(51) A gastrointestinal series is used to define the anatomy of the distal esophagus and cardia, and a reflux of barium is almost always associated with reflux disease. Manometry provides information about pressures in the various parts of the esophagus, and a 24-hour pH study is considered the gold standard for defining and quantifying reflux problems.(52)

If pharmacotherapy and lifestyle changes fail to improve symptoms, patients must be carefully assessed to rule out other potential problems before the physician recommends surgery. For example, chest pain caused by reflux may also mimic that of angina pectoris, including radiation of pain to the neck, shoulder, and arms.(53) Figure 6 shows surface areas of referred pain from various visceral areas. The most common procedure for reflux is fundoplication. The ability to perform this procedure laparoscopically has resulted in an increase in the number of patients undergoing it. Eighty four to 89% of patients have good to excellent results with fundoplication; however, it should not be undertaken lightly because the complications can be devastating.

[Figure 6 ILLUSTRATION OMITTED]

Dysphagia, which may be due to edema from the surgery, will disappear as healing takes place, but dysphagia may also be due to a fundoplication that is too tight and that may need dilatation or some form of revision. Recurrent reflux also may occur, but this is usually less than that which existed preoperatively. It usually responds to antacids or acid-blocking agents. The trapping of swallowed air (ie, "gas bloat"), inability to vomit, early satiety, diarrhea, and nausea are other potential complications of fundoplication.(54) Patients should be aware of these possibilities before deciding on surgery. Nurses can remind patients of the importance of remaining still during esophagoscopy if they are minimally sedated.

SUMMARY

A knowledge of the anatomical, physiological, and constitutional aspects of the esophagus in relation to gastrointestinal functioning is important for nurses to provide quality care to patients. The awareness of the aberrations that can occur in the esophagus, the state-of-the-art diagnostic measures, and therapy modalities available (eg, lifestyle changes, pharmacotherapy, surgical interventions, and potential complications) enable nurses to be valuable resources to patients who can become educated consumers and effective participants in their own care.

NOTES

(1.) R B Lee, J I Miller, "Esophagectomy for cancer," Surgical Clinics of North America 77 (October 1997) 1169-1196.

(2.) M B Orringer, "The esophagus: Historical aspects and anatomy," in Textbook of Surgery: The Biological Basis of Modern Surgical Practice, 14th ed, D C Sabiston, Jr, ed (Philadelphia: W B Saunders Co, 1991) 655-659.

(3.) R J Ponec, M B Kimmey, "Endoscopic therapy of esophageal cancer," Surgical Clinics of North America 77 (October 1997) 1197-1217.

(4.) Lee, Miller, "Esophagectomy for cancer," 1174.

(5.) M B Orringer, "The esophagus: Tumors of the esophagus," in Textbook of Surgery: The Biological Basis of Modern Surgical Practice, 14th ed D C Sabiston, Jr, ed (Philadelphia: W B Saunders Co, 1991) 689-700.

(6.) C R Thomas, Jr, "Biology of esophageal cancer and the role of combined modality therapy," Surgical Clinics of North America, 77 (October 1997) 1139-1167.

(7.) M B Orringer, "The esophagus: Disorders of esophageal motility," in Textbook of Surgery: The Biological Basis of Modern Surgical Practice, 14th ed, D C Sabiston, Jr, ed (Philadelphia: W B Saunders Co, 1991) 663-678.

(8.) J G Hunter, W S Richardson, "Surgical management of achalasia," Surgical Clinics of North America 77 (October 1997) 993-1015.

(9.) M B Orringer, "The esophagus: Diverticula and miscellaneous conditions of the esophagus," in Textbook of Surgery: The Biological Basis of Modern Surgical Practice, 14th ed, D C Sabiston, Jr, ed (Philadelphia: W B Saunders Co, 1991) 678-684.

(10.) K J Lewin, H D Appelman, "Normal anatomy, embryology and histology of the esophagus," in Tumors of the Esophagus and Stomach: Atlas of Tumor Pathology (Washington, DC: Armed Forces Institute of Pathology, 1996) 17-29.

(11.) J M Georges, "Gastrointestinal function," in Perspectives on Pathophysiology, ed L E Copstead (Philadelphia: W B Saunders Co, 1995) 701, 702.

(12.) G Danek, "Ingestion, digestion, and elimination: Implications of obstruction and inflammation," in Nursing Care of Children and Families, second ed, S R Mott et al, eds (Redwood City, Calif: Addison-Wesley Nursing, 1990) 1386.

(13.) Georges, "Gastrointestinal function," 702.

(14.) Ibid.

(15.) M G Patti, W Gantert, L W Way, "Surgery of the esophagus: Anatomy and physiology," Surgical Clinics of North America 77 (October 1997) 959-970.

(16.) Ibid.

(17.) Orringer, "The esophagus: Historical aspects and anatomy," 656.

(18.) Orringer, "The esophagus: Disorders of esophageal motility," 663.

(19.) Ibid.

(20.) J M M Wo, J P Waring, "Medical therapy of gastroesophageal reflux and management of esophageal strictures," Surgical Clinics of North America 77 (October 1997) 1041-1062.

(21.) Orringer, "The esophagus: Historical aspects and anatomy," 657-658.

(22) Ibid.

(23.) L M Wilson, "Disorders of the esophagus," in Pathophysiology: Clinical Concepts of Disease Processes, fifth ed, S A Price, L M Wilson, eds (St Louis: Mosby, 1997) 315.

(24.) S S Koshy, T T Nostrant, "Pathophysiology and endoscopic treatment of esophageal motility disorders," Surgical Clinics of North America 77 (October 1997) 971-992.

(25.) Orringer, "The esophagus: disorders of esophageal motility," 667

(26.) V R Lingappa, "Gastrointestinal disease," in Pathophysiology of Disease: An Introduction to Clinical Medicine, second ed, S J McPhee, ed (Stamford, Conn: Appleton & Lange, 1997) 305.

(27.) Orringer, "The esophagus: disorders of esophageal motility," 667.

(28.) C G Bremner, R M Bremner, "Barrett's esophagus," Surgical Clinics of North America 77 (October 1997) 1115-1137.

(29) Ibid, 1123.

(30.) Patti et al, "Surgery of the esophagus: Anatomy and physiology," 960.

(31.) Ibid.

(32.) B L Bullock, "Alterations in gastrointestinal function," in Pathophysiology: Adaptations and Alterations in Functions, fourth ed (Philadelphia: Lippincott, 1996) 784.

(33.) Orringer, "The esophagus: Disorders of esophageal motility," 658.

(34.) Ibid.

(35.) Wilson, "Disorders of the esophagus," 315.

(36.) S E Peck, "Alterations in nutrition: Less than body requirements," in A Guide to Neurological and Neurosurgical Nursing, second ed, M Snyder, ed (Albany, NY: Delmar Publishers, Inc, 1991) 157-159.

(37.) A C Guyton, Textbook of Medical Physiology, eighth ed (Philadelphia: W B Saunders Co, 1991) 736.

(38.) Orringer, "The esophagus: Physiology," in Textbook of Surgery: The Biological Basis of Modern Surgical Practice, 14th ed, D C Sabiston, Jr, ed (Philadelphia: W B Saunders Co, 1991) 660-663.

(39.) H C Kutchai, "Section VIII: Gastrointestinal system," in Physiology, third ed, R M Berne, M N Levy, eds (St Louis: Mosby-Year Book, 1993) 630.

(40.) M M McDermot, "Overview of anatomy, physiology, and pathophysiology of the gastrointestinal system," in Adult Nursing in Hospital and Community Settings, L O Burrell, ed (Norwalk, Conn: Appleton & Lange, 1992) 1312.

(41.) Patti et al, "Surgery of the esophagus: Anatomy and physiology," 966.

(42.) Orringer, "The esophagus: Physiology," 661.

(43.) Ibid.

(44.) Patti et al, "Surgery of the esophagus: Anatomy and physiology," 968.

(45.) P E Donohue, "Basic consideration in gastrointestinal reflux disease," Surgical Clinics of North America 77 (October 1997) 1017-1040.

(46.) Wo, Waring, "Medical therapy of gastroesophageal reflux and management of esophageal strictures," 1044-1045.

(47.) D B Skinner, "The esophagus: Perforation of the esophagus: Spontaneous (Boerhaave's syndrome), traumatic, and following esophagoscopy," in Textbook of Surgery: The Biological Basis of Modern Surgical Practice, 14th ed, D C Sabiston, Jr, ed (Philadelphia: W B Saunders Co, 1991) 701-714.

(48.) Ibid.

(49.) Ibid.

(50.) Wo, Waring, "Medical therapy of gastroesophageal reflux and management of esophageal strictures," 1042.

(51.) M B Orringer, "Esophagoscopy," in Textbook of Surgery: The Basis of Modern Surgical Practice, 14th ed, D C Sabiston, Jr, ed (Philadelphia: W B Saunders Co, 1991) 685-689.

(52.) S Horgan, C A Pelligrini, "Surgical treatment of gastroesophageal reflux disease," Surgical Clinics of North America 77 (October 1997) 1063-1082.

(53.) D B Skinner, "The esophagus: Hiatal hernia and gastroesophageal reflux," in Textbook of Surgery: The Biological Basis of Modern Surgical Practice, 14th edition, D C Sabiston, Jr, ed (Philadelphia: W B Saunders Co, 1991) 709.

(54.) R A Hinder et al, "Management of the failed antireflux operation," Surgical Clinics of North America 77 (October 1997) 1083-1098.

Examination

ANATOMY AND PHYSIOLOGY OF THE ESOPHAGUS

1. Despite the progress in treatment of many esophageal disorders, esophageal cancer is the -- leading cause of cancer deaths in the world.

2.The most significant risk factors for this malady in the United States are

3. What are considered associated risk factors for esophageal cancer?

4. Dietary practices such as drinking "burning hot" tea and chewing tobacco with or without betel nut are thought to cause esophageal damage that leads to cancer. What is another dietary influence thought to lead to esophageal cancer?

5. Achalasia, a premalignant neuromuscular disorder, leads to esophageal carcinoma in what percent of people who have this condition for 15 to 25 years?

6. Achalasia can be caused by a parasite (ie, Trypanosoma cruzi); what else is believed to cause achalasia?

7. What syndrome occurs with high incidence in Great Britain and Scandinavia and is associated with a risk of developing squamous cell carcinoma of the mouth, throat, or esophagus?

8. The esophagus develops at approximately the 20th day of gestation, when the septa from the lateral walls of the foregut (ie, the first part of the digestive tube) fuse, separating the trachea from the esophagus.

9. Developmentally, what occurs if incomplete partitioning of the trachea and esophagus takes place?

10. The esophagus is a hollow tube approximately 25 cm in length. What is connected to the esophagus and serves as the entry to the esophagus and the respiratory tract?

11. The esophagus consists of three parts: the cervical, thoracic, and abdominal esophagus.

12. The cervical esophagus lies just left of the midline behind the larynx and trachea. The entry to the cervical esophagus is called what?

13. The upper portion of the thoracic esophagus passes behind the tracheal bifurcation (ie, carina) and the right mainstem bronchus. The lower portion of the thoracic esophagus runs behind the left atrium.

15. What are the three areas in the esophagus where the lumen normally narrows?

16. The UES is an area of weakness and has the potential of developing diverticula, as well as being an area prone to perforation during surgery.

17. The bronchoaortic constriction is a common area for pill-induced strictures, and nurses should encourage patients to take oral medications with plenty of water. What types of medications are most recognized as most likely to damage the esophagus if trapped in this area?

18. The adventitia of the esophagus lacks an outer serosal layer. What does the lack of this layer possibly contribute to?

19. The esophagus receives its blood supply from four sources. What are they?

20. The esophagus has an extensive lymphatic drainage, consisting of a lymphatic plexus in the mucosa and another in the muscle layer.

21. Because of the extensive lymph drainage system, esophageal carcinoma often spreads to the pulmonary ligaments and what other lymph nodes?

22. What are the two plexi that innervate the esophagus in addition to the vagus nerve?

23. In the early oral stage of swallowing, food is chewed and lubricated by saliva. This involves the lips, cheeks, salivary glands, and muscles of mastication. What cranial nerves (CN) innervate these areas and supply sensation to the oral cavity?

24. In the late oral stage, food is moved to the oropharynx by the tongue. What cranial nerves innervate the oropharynx and tongue?

25. In the third stage, food is moved to the hypopharynx by reflexes in the larynx, epiglottis, and hypopharynx. What nerves innervate the hypopharynx?

26. What provides the innervation for the peristalsis that moves food down the esophagus?

27. What are some of the warning signs that a patient is at risk for aspiration?

28. Damage to CN V, IX, and X (eg, after a stroke) can cause paralysis of the swallowing mechanism. What diseases can also affect swallowing and increase a patient's risk for aspiration?

29. Deep anesthesia produces profound paralysis of the swallowing mechanism and can result in emesis, choking, and aspiration.

30. The UES remains constricted except during swallowing. This prevents air from the larynx entering the esophagus and gastroesophageal reflux from entering the pharynx.

31. Peristalsis makes it possible to swallow even while standing on one's head, but what facilitates normal swallowing?

32. Tertiary peristalsis is sometimes seen in the elderly and in patients with motility disorders. These peristaltic waves help these individuals move food through their esophagus.

33. What does the LES do?

34. What are some of the conditions that relax the LES and contribute to reflux?

35. Medications can also cause relaxation of the LES. What are common medications associated with this relaxation?

36. Type I hiatal hemias are common in many adults. This type of hemia results when a large amount of the gastric cardia slides into the esophageal hiatus.

37. Type II hiatal hernia is also known as a rolling hernia and represents a true herniation of the stomach into a peritoneal sac in the mediastinum.

38. Type III hernias may occur in which other organs such as the colon, spleen, pancreas, and small intestine may enter the peritoneal sac.

39. Not all Type II hemias cause symptoms, but what can occur with this type of hernia?

40. Chest pain caused by reflex may mimic what?

Answer Sheet

ANATOMY AND PHYSIOLOGY OF THE ESOPHAGUS

Please fill out the application and answer form below and the evaluation on the back of this page. Tear out the page from the Journal or make photocopies and mail to:

Event #955001 Session #2036

Program offered February 1999.

The deadline for this program is March 31, 2000.

1. Record your identification number in the appropriate section below.

2. Completely darken the space that indicates your answer to the examination starting with question one.

3. A score of 70% correct is required for credit.

4. Record the time required to complete the program --

5. Enclose fee: Members $10; Nonmembers $20.

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Learner Evaluation

ANATOMY AND PHYSIOLOGY OF THE ESOPHAGUS

The following evaluation is used to determine the extent to which this Home Study Program met your learning needs. Rate the following items on a scale of 1 to 5.

OBJECTIVES

To what extent were the following objectives of this home study program achieved?

(1) Discuss the risk factors for esophageal cancer.

(2) Identify the significant anatomy of the esophagus.

(3) Discuss the physiology of the esophagus.

CONTENT

(4) Did this article increase your knowledge of the subject matter?

(5) Was the content clear and organized?

(6) Did this article facilitate learning?

(7) Were your individual objectives met?

(8) Was the content of the article relevant to the objectives?

TEST QUESTIONS/ANSWERS

(9) Were they reflective of the content?

(10) Were they easy to understand?

(11) Did they address important points?

What other topics would you like to see addressed in a future Home Study Program? Would you be interested or do you know someone who would be interested in writing an article on this topic?

Topic(s): --

Author names and addresses: --

AORN is accredited as a provider of continuing education in nursing by the American Nurses Credentialing Center's Commission on Accreditation. AORN recognizes this activity as continuing education for registered nurses. This recognition does not imply that AORN or the American Nurses Credentialing Center's Commission on Accreditation approves or endorses any product included in the activity. AORN maintains the following provider numbers: Alabama ABNP0075, California BRN00667, Florida 27F0177.

AORN is approved as a provider of continuing nursing education by the Kansas Slate Board of Nursing. This course offering is approved for two contact hours. The Kansas State Board of Nursing approved provider number is LTO114-0316.

Professional nurse ore invited to submit manuscripts for the Home Study Program. Manuscripts or queries should be sent to Editor, AORN Journal, 2170 S Parker Rd, Suite 300, Denver, CO 80231-5711. As with all manuscripts sent to the Journal, papers submitted for Home Study Programs should not hove been previously published or submitted simultaneously to any other publication.

Mary Gavaghan, RN, EdD, is an associate professor of nursing at Bloomsburg University, Bloomsburg, Ill.

COPYRIGHT 1999 Association of Operating Room Nurses, Inc.
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