Gastrointestinal Disorders
INTRODUCTION
The GI tract, also known as the alimentary canal, is a long, hollow, musculomembranous tube consisting of glands and accessory organs (salivary glands, liver, gallbladder, and pancreas). (See Reviewing GI anatomy and physiology. See also Histology of the GI tract, page 216.) The GI tract breaks down food—carbohydrates, fats, and proteins—into molecules small enough to permeate cell membranes, thus providing cells with the necessary energy to function properly; it prepares food for cellular absorption by altering its physical and chemical composition. (See Primary source of digestive hormones, page 217.) Consequently, a malfunction along the GI tract can produce far-reaching metabolic effects, eventually threatening life itself. The GI tract is an unsterile system filled with bacteria and other flora; these organisms can cause superinfection from antibiotic therapy or they can infect other systems when a GI organ ruptures. A common indication of GI problems is referred pain, which makes diagnosis especially difficult.
Reviewing GI anatomy and physiology
The GI tract includes the mouth, pharynx, esophagus, stomach (fundus, body, and antrum), small intestine (duodenum, jejunum, and ileum), and large intestine (cecum, colon, rectum, and anal canal).
Digestion begins in the mouth through chewing and through the action of an enzyme secreted in saliva—ptyalin (amylase)—which breaks down starch. Digestion continues in the stomach, where the lining secretes gastric juice that contains hydrochloric acid and the enzymes pepsin (begins protein digestion), lipase (speeds hydrolysis of emulsified fats) and, in infants, rennin (curdles milk).
Through a churning motion, the stomach breaks food into tiny particles, mixes them with gastric juice, and pushes the mass toward the pylorus. The liquid portion (chyme) enters the duodenum in small amounts; any solid material remains in the stomach until it liquefies (usually from 1 to 6 hours). The stomach also produces an intrinsic factor necessary for the absorption of vitamin B12. Although limited amounts of water, alcohol, and some drugs are absorbed in the stomach, chyme passes unabsorbed into the duodenum.
Small intestine’s role
Most digestion and absorption occur in the small intestine, where the surface area is increased by millions of villi in the mucous membrane lining. For digestion, the small intestine relies on a vast array of enzymes produced by the pancreas or by the intestinal lining itself. Pancreatic enzymes include trypsin, which digests protein to amino acids; lipase, which digests fat to fatty acids and glycerol; and amylase, which digests starches to sugars. Intestinal enzymes include erepsin, which digests protein to amino acids; lactase, maltase, and sucrase, which digest complex sugars such as glucose, fructose, and galactose; and enterokinase, which activates trypsin.
In addition, bile, secreted by the liver and stored in the gallbladder, helps neutralize stomach acid and aids the small intestine to emulsify and absorb fats and fat-soluble vitamins.
Final stages
By the time ingested material reaches the ileocecal valve (where the small intestine joins the large intestine), all its nutritional value has been absorbed through the villi of the small intestine into the bloodstream.
The large intestine, so named because it’s larger in diameter than the small intestine, absorbs water from the digestive material before passing it on for elimination. Rectal distention by feces stimulates the defecation reflex, which, when assisted by voluntary sphincter relaxation, permits defecation.
Throughout the GI tract, peristalsis (a coordinated, rhythmic contraction of smooth muscle) propels ingested material along; sphincters prevent its reflux.
ACCURATE ASSESSMENT VITAL
Your assessment of the patient with suspected GI disease must begin with a careful history that includes occupation, family history, and recent travel. The medical history should include previous hospital admissions; surgical procedures (including recent tooth extraction); family history of ulcers, colitis, liver disease, or cancer; and current medications, whether prescribed, over-the-counter, or herbal remedies, with particular attention to aspirin, steroids, and anticoagulants. In addition, assess for food or drug allergies.
Histology of the GI tract
The GI tract consists of four tissue layers whose structure varies in different organs:
Mucous membrane—innermost layer; secretes gastric juice, protects the tract, and absorbs nutrients
Submucosa—connective tissue that contains the major blood vessels and nerves
External muscle coat (muscularis externa)— double layer of smooth-muscle fibers; inner circular and outer longitudinal layers propel gastric contents downward by peristalsis
Fibroserous coat (serosa)—outermost protective layer of connective tissue; forms the peritoneum, which is the largest serous membrane of the body. The peritoneum’s parietal layer covers the walls of the abdominal cavity. An extension of the parietal peritoneum, called the mesentery, anchors the small intestine to the abdominal wall. The visceral layer drapes most of the abdominal organs, covering the upper surface of the pelvic organs.
Have the patient describe his chief complaint in his own words. Does he have abdominal pain, indigestion, heartburn, or rectal bleeding? How long has he had it? What relieves these symptoms or makes them worse? Has he experienced nosebleeds or difficulty in swallowing recently? Has he had recent weight loss or gain? Is he on a special diet? Does he drink alcoholic beverages or smoke? If yes to either, how much and how often? Ask about bowel habits. Does he regularly use laxatives or enemas? If he experiences nausea and vomiting, what does the vomitus look like? Does changing his position relieve nausea?
Next, try to define and locate any pain. Ask the patient to describe the pain. Is it dull, sharp, burning, aching, spasmodic, or intermittent? Where is it located? Does it radiate? How long does it last? When does it occur? What triggers it? What relieves it?
VISUAL ASSESSMENT
Observe how the patient looks, and note appropriateness of behavior. Changes in fluid and electrolyte balance, severe infection, drug toxicity, and hepatic disease may cause abnormal behavior. Your visual examination should check:
Skin—loss of turgor, jaundice, cyanosis, pallor, diaphoresis, petechiae, bruises, edema, and texture (dry or oily)
Head—color of sclerae, sunken eyes, dentures, caries, lesions, tongue (color, swelling, dryness), and breath odor
Chest—shape (asymmetrical, barrel, or sunken)
Lungs—rate, rhythm, and quality of respirations
Abdomen—size and shape (distention, contour, visible masses, and protrusions), abdominal scars or fistulae, excessive skin folds (may indicate wasting), and abnormal respiratory movements (inflammation of diaphragm)
AUSCULTATION, PALPATION, AND PERCUSSION
Auscultation provides helpful clues to GI abnormalities and should always be performed before palpation and percussion to avoid altering the assessment. For example, absence of bowel sounds over the area to the lower right of the umbilicus may indicate peritonitis. High-pitched sounds that coincide with colicky pain may indicate small-bowel obstruction. Less intense, low-pitched rumbling noises may accompany minor irritation.
Palpating the abdomen after auscultation helps detect tenderness, muscle guarding, and abdominal masses. Watch for muscle tone (boardlike rigidity points to peritonitis or hemorrhage; transient rigidity suggests severe pain) and tenderness (rebound tenderness may indicate peritoneal inflammation).
Percussion helps detect air, fluid, and solid matter in the abdominal region.
DIAGNOSTIC TESTS
After physical assessment, several tests can identify GI malfunction.
A barium or gastrografin swallow is used primarily to examine the esophagus. Gastrografin may be used instead of barium. Like barium, gastrografin facilitates X-ray imaging. However, if gastrografin escapes from the GI tract, it’s absorbed by the surrounding tissue, whereas escaped barium isn’t absorbed and can cause complications.
In an upper GI series, swallowed barium sulfate travels through the esophagus, stomach, and duodenum to reveal abnormalities. The barium outlines stomach walls and delineates ulcer craters and defects.
A small-bowel series, an extension of the upper GI series, visualizes barium flowing through the small intestine to the ileocecal valve.
A barium enema (lower GI series) allows X-ray visualization of the colon.
A stool specimen is useful to detect suspected GI bleeding, infection, or malabsorption as well as the presence of parasites. Guaiac test
for occult blood, microscopic stool examination for ova and parasites, and tests for fat require several specimens.
In esophagogastroduodenoscopy, insertion of a fiber-optic scope allows direct visual inspection of the esophagus, stomach, and duodenum. These structures are examined for varices, tumors, inflammation, hernias, polyps, ulcers, and obstruction.
Proctosigmoidoscopy permits inspection of the rectum and distal sigmoid colon; colonoscopy is used for inspection of the descending, transverse, and ascending colon. These tests help visualize tumors, polyps, hemorrhoids, or ulcers.
Gastric analysis examines gastric secretions for the presence of high levels of gastrin and the amount of acid produced.
Endoscopic retrograde cholangiopancreatography (ERCP) directly visualizes the esophagus, stomach, proximal duodenum, and fluoroscopically visualizes the pancreatic, hepatic, and biliary ducts. This test can help visualize duct obstruction, benign structures, cysts, anatomic variations, and malignant tumors. ERCP can be used to relieve or remove obstructions of the biliary tree.
INTUBATION
Certain GI disorders require nasogastric (NG) intubation to empty the stomach and intestine, to aid diagnosis and treatment, to decompress obstructed areas, to detect and treat GI bleeding, and to administer medications or feedings. Tubes generally inserted through the nose are the short NG tubes (the Levin, the Salem Sump, and the specialized Sengstaken-Blakemore) and the long intestinal tubes (Cantor and Miller-Abbott). The larger Ewald tube is usually inserted orally.
When caring for the patient with a tube:
Explain the procedure before intubation.
Maintain accurate intake and output records. Measure gastric drainage every 8 hours; record the amount, color, odor, and consistency. When irrigating the tube, note the amount of saline solution instilled and aspirated. Check for fluid and electrolyte imbalances.
Provide good oral and nasal care. Brush the patient’s teeth frequently and provide mouthwash. Make sure that the tube is secure, but isn’t causing pressure on the nostrils. Change the tape to the nose every 24 hours. Gently wash the area around the tube, and apply a water-soluble lubricant to soften
crusts. These measures help prevent sore throat and nose, dry lips, nasal excoriation, and parotitis.
Ensure maximum patient comfort. After insertion of a long intestinal tube, instruct the patient to turn from side to side to facilitate its passage through the GI tract. Note the tube’s progress. Never attach an intestinal tube to a patient’s gown, bed linens, side rails of the bed, and so forth.
With both types of tubes, tell the patient to expect a feeling of dryness or a lump in the throat; if he’s allowed, suggest that he chew gum or eat hard candy to relieve discomfort.
Always keep scissors taped to the wall near the bed when the patient has a Sengstaken-Blakemore tube in place. If the tube should dislodge and obstruct the bronchus, cut the lumen to the balloons immediately. Sometimes the tube is taped to the face piece of a football helmet worn by the patient to prevent the tube from dislodging and to put traction on the tube.
After removing the tube from a patient with GI bleeding, watch for signs and symptoms of recurrent bleeding, such as hematemesis, decreased hemoglobin level, pallor, chills, diaphoresis, hypotension, and rapid pulse.
Provide emotional support because the patient may panic at the sight of a tube. A calm, reassuring manner can help minimize his fear.
MOUTH AND ESOPHAGUS
Stomatitis and other oral infections
Stomatitis is an inflammation of the oral mucosa that may extend to the buccal mucosa, lips, and palate. It’s a common infection that may occur alone or as part of a systemic disease. There are two main types: acute herpetic stomatitis and aphthous stomatitis. Acute herpetic stomatitis is usually self-limiting; however, it may be severe and, in neonates, may be generalized and potentially fatal. Aphthous stomatitis, also known as canker sores, usually heals spontaneously, without a scar, in 10 to 14 days. It may be an extra-intestinal symptom of irritable bowel disease. Other oral infections include gingivitis, candidiasis, glossitis, periodontitis, and Vincent’s angina. (See Types of oral infections.)
CAUSES AND INCIDENCE
Acute herpetic stomatitis results from the herpes simplex virus. It’s common in children ages 1 to 3. The cause of aphthous stomatitis is unknown, but predisposing factors include stress, fatigue, anxiety, febrile states, trauma, and solar overexposure. This type is common in young and teenage girls.
COMPLICATIONS
Nutritional deficiencies
Esophagitis
Sepsis
SIGNS AND SYMPTOMS
Acute herpetic stomatitis begins suddenly with mouth pain, malaise, lethargy, anorexia, irritability, and fever, which may persist for 1 to 2 weeks. Gums are swollen and bleed easily, and the mucous membrane is extremely tender.
Papulovesicular ulcers appear in the mouth and throat and eventually become punched-out lesions with reddened areolae. Submaxillary lymphadenitis is common. Pain usually disappears 2 to 4 days before healing of ulcers is complete. If the child with stomatitis sucks his thumb, these lesions spread to the hand.
A patient with aphthous stomatitis typically reports burning, tingling, and slight swelling of the mucous membrane. Single or multiple shallow ulcers with whitish centers and red borders appear and heal at one site and then reappear at another. (See Looking at aphthous stomatitis, page 220.)
DIAGNOSIS
Diagnosis is based on the physical examination; in Vincent’s angina, a smear of ulcer exudate allows for identification of the causative organism.
TREATMENT
For acute herpetic stomatitis, treatment is conservative. For local symptoms, supportive measures include warm salt-water mouth rinses (antiseptic mouthwashes are contraindicated because they are irritating) and a topical anesthetic to relieve mouth ulcer pain. Topical antihistamines, antacids, or corticosteroids may also be recommended. Supplementary treatment includes a bland or liquid diet and, in severe cases, I.V. fluids and bed rest.
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For aphthous stomatitis, primary treatment is application of a topical anesthetic. Effective long-term treatment requires alleviation or prevention of precipitating factors. Aphthous stomatitis that is associated with irritable bowel disease improves with treatment and improvement of the underlying bowel disease.
Gastroesophageal reflux
Gastroesophageal reflux, also called gastroesophageal reflux disease (GERD), is the backflow of gastric or duodenal contents, or both, into the esophagus and past the lower esophageal sphincter (LES) without associated belching or vomiting. Reflux may cause symptoms or pathologic changes. Persistent reflux may cause reflux esophagitis (inflammation of the esophageal mucosa). Prognosis varies with the underlying cause.
CAUSES AND INCIDENCE
The function of the LES—a high-pressure area in the lower esophagus, just above the stomach—is to prevent gastric contents from backing up into the esophagus. Normally, the LES creates pressure, closing the lower end of the esophagus, but relaxes after each swallow to allow food into the stomach. Reflux occurs when LES pressure is deficient or when pressure within the stomach exceeds LES pressure. (See Influences on LES pressure.)
Studies have shown that a patient with symptom-producing reflux can’t swallow often enough to create sufficient peristaltic amplitude to clear gastric acid from the lower esophagus. This results in prolonged periods of acidity in the esophagus when reflux occurs.
Predisposing factors include:
pyloric surgery (alteration or removal of the pylorus), which allows reflux of bile or pancreatic juice
long-term nasogastric (NG) intubation (more than 4 days)
any agent that lowers LES pressure, such as food, alcohol, cigarettes, anticholinergics (atropine, belladonna, and propantheline), or other drugs (morphine, diazepam, calcium channel blockers, and meperidine)
hiatal hernia with an incompetent sphincter
any condition or position that increases intraabdominal pressure, such as straining, bending, coughing, pregnancy, obesity, and recurrent or persistent vomiting
About 25% to 40% of Americans experience symptomatic GERD at some point in their lives, and 7% to 10% of Americans experience symptoms on a daily basis. True incidence figures may be even higher because many people with GERD take over-the-counter remedies without reporting their symptoms.
Studies show that GERD is common and may be overlooked in infants and children. It can cause repeated vomiting, coughing, and other respiratory problems. An immature digestive system is usually responsible, and most infants grow out of GERD by the time they are age 1.
COMPLICATIONS
Esophageal ulcer
Esophageal stricture
Barrett’s esophagus
Hoarseness
Reflux esophagitis
SIGNS AND SYMPTOMS
GERD doesn’t always cause symptoms, and in patients showing clinical effects, it isn’t always possible to confirm physiologic reflux. The most common feature of GERD is heartburn, which may become more severe with vigorous exercise, bending, or lying down, and may be relieved by antacids or sitting upright. The pain of esophageal spasm resulting from reflux esophagitis tends to be chronic and may mimic angina pectoris, radiating to the neck, jaws, and arms.
Other symptoms include odynophagia, which may be followed by a dull substernal ache
from severe, long-term reflux; dysphagia from esophageal spasm, stricture, or esophagitis; and bleeding (bright red or dark brown). Nocturnal regurgitation can awaken the patient with coughing, choking, and a mouthful of saliva. Reflux may be associated with hiatal hernia. Direct hiatal hernia becomes clinically significant only when reflux is confirmed.
from severe, long-term reflux; dysphagia from esophageal spasm, stricture, or esophagitis; and bleeding (bright red or dark brown). Nocturnal regurgitation can awaken the patient with coughing, choking, and a mouthful of saliva. Reflux may be associated with hiatal hernia. Direct hiatal hernia becomes clinically significant only when reflux is confirmed.
Pulmonary symptoms result from reflux of gastric contents into the throat and subsequent aspiration; they include chronic pulmonary disease or nocturnal wheezing, bronchitis, asthma, morning hoarseness, and cough. In children, other signs consist of failure to thrive and forceful vomiting from esophageal irritation. Such vomiting sometimes causes aspiration pneumonia.
DIAGNOSIS
CONFIRMING DIAGNOSISAfter a careful history and physical examination, tests to confirm GERD include barium swallow fluoroscopy, esophageal pH probe, esophageal manometry, and esophagoscopy In children, barium esophagography under fluoroscopic control can show reflux.
Recurrent reflux after age 6 weeks is abnormal. An acid perfusion (Bernstein) test can show that reflux is the cause of symptoms. Finally, endoscopy and biopsy allow visualization and confirmation of any pathologic changes in the mucosa.
TREATMENT
Promotility agents help increase LES sphincter tone and stimulate upper GI motility. Proton pump inhibitors and histamine-2 (H2) receptor antagonists help reduce gastric acidity. If possible, NG intubation shouldn’t be continued for more than 5 days because the tube interferes with sphincter integrity and allows reflux, especially when the patient lies flat.
PEDIATRIC TIPPositional therapy is especially useful in infants and children who experience GERD without complications. Strategies, such as burping the infant several times during feeding, keeping the infant in an upright position for 30 minutes after feeding, and avoiding feeding 2 to 3 hours before bedtime, may help.
Surgery may be necessary to control severe and refractory symptoms, such as pulmonary aspiration, hemorrhage, obstruction, severe pain, perforation, an incompetent LES, or associated hiatal hernia. Surgical procedures that create an artificial closure at the gastroesophageal junction may be needed in some patients. These include a procedure that invaginates the esophagus into the stomach and
procedures that create a gastric wraparound with or without fixation. The fundoplication procedure can be performed endoscopically.
procedures that create a gastric wraparound with or without fixation. The fundoplication procedure can be performed endoscopically.
PREVENTION Preventing GI refluxChanging his lifestyle will help the patient to prevent GI reflux.
Diet and eating habits
Foods, such as caffeine, chocolate, spicy food, carbonated beverages, orange juice, liquor, wine, and tomato sauce, stimulate the production of acid. Large meals expand the stomach and put pressure on the lower esophageal sphincter (LES). Gravity helps keep the stomach juices from backing up into the esophagus: Don’t allow the patient to lie down for 2 hours after eating. If nighttime heartburn is a concern, raise the head of the bed 6 to 8 inches because a flat position places pressure on the LES.
Weight
Being overweight increases abdominal pressure, which can then push stomach contents up into the esophagus.
Smoking
Nicotine relaxes the esophageal sphincter and stimulates the production of stomach acid. Smoking also may injure the esophagus by causing irritation making it more susceptible to damage from acid reflux. Smoking can decrease gastric motility and reduce the effectiveness of digestion because the stomach takes longer to empty.
Stress
Although stress itself doesn’t cause heartburn, the anxiety that comes along with stress can lead to behaviors that increase the risk of heartburn, such as overeating, drinking, and smoking.
Alcohol
Alcohol can increase the production of stomach acid and can also lower the esophageal sphincter, which allows stomach acids to move up into the esophagus. Alcohol also makes the esophagus more sensitive to stomach acid.
SPECIAL CONSIDERATIONS
Teach the patient what causes reflux, how to avoid reflux with an antireflux regimen (medication, diet, and positional therapy), and what symptoms to watch for and report.
Instruct the patient to avoid circumstances that increase intra-abdominal pressure (such as bending, coughing, vigorous exercise, tight clothing, constipation, and obesity) as well as substances that reduce sphincter control (cigarettes, alcohol, fatty foods, and caffeine).
Advise the patient to sit upright, particularly after meals, and to eat small, frequent meals. Tell him to avoid highly seasoned food, acidic juices, alcoholic drinks, bedtime snacks, and foods high in fat or carbohydrates, which reduce LES pressure. He should eat meals at least 2 to 3 hours before lying down.
Tell the patient to take antacids, as ordered (usually 1 hour before or 3 hours after meals and at bedtime).
Teach the patient correct preparation for diagnostic testing. For example, he shouldn’t eat for 6 to 8 hours before a barium swallow or endoscopy.
After surgery using a thoracic approach, carefully watch and record chest tube drainage and the patient’s respiratory status. If needed, give chest physiotherapy and oxygen. Position the patient with an NG tube in semi-Fowler’s position to help prevent reflux. Offer reassurance and emotional support. (See Preventing GI reflux.)
Tracheoesophageal fistula and esophageal atresia
Tracheoesophageal fistula is a developmental anomaly characterized by an abnormal connection between the trachea and the esophagus. It usually accompanies esophageal atresia, in which the esophagus is closed off at some point. Although these malformations have numerous anatomic variations, the most common, by far, is esophageal atresia with fistula to the distal segment. (See Types of tracheoesophageal anomalies, pages 224 and 225.)
These disorders, two of the most serious surgical emergencies in neonates, require immediate diagnosis and correction. They may coexist with other serious anomalies, such as congenital heart disease, imperforate anus, genitourinary abnormalities, and intestinal atresia.
CAUSES AND INCIDENCE
Tracheoesophageal fistula and esophageal atresia result from failure of the embryonic esophagus and trachea to develop and separate correctly. Respiratory system development begins at about day 26 of gestation. Abnormal development of the septum during this time can lead to tracheoesophageal fistula. The most common abnormality is type C tracheoesophageal fistula with esophageal atresia, in which the upper section of the esophagus terminates in a blind pouch, and the lower section ascends from the stomach and connects with the trachea by a short fistulous tract.
In type A atresia, both esophageal segments are blind pouches, and neither is connected to the airway. In type E (or H-type), tracheoesophageal fistula without atresia, the fistula may occur anywhere between the level of the cricoid cartilage and the midesophagus, but is usually higher in the trachea than in the esophagus. Such a fistula may be as small as a pinpoint. In types B and D, the upper portion of the esophagus opens into the trachea; neonates with this anomaly may experience life-threatening aspiration of saliva or food.
Esophageal atresia occurs in about 1 of every 1,500 to 3,500 live births; about one third of these neonates are born prematurely.
COMPLICATIONS
Recurrent fistulas
Abnormal esophageal motility
Pneumothorax
Esophageal stricture
SIGNS AND SYMPTOMS
A neonate with type C tracheoesophageal fistula with esophageal atresia appears to swallow normally but soon after swallowing coughs, struggles, becomes cyanotic, and stops breathing as he aspirates fluids returning from the blind pouch of the esophagus through his nose and mouth. Stomach distention may cause respiratory distress; air and gastric contents (bile and gastric secretions) may reflux through the fistula into the trachea, resulting in chemical pneumonitis.
An infant with type A esophageal atresia appears normal at birth. The infant swallows normally, but as secretions fill the esophageal sac and overflow into the oropharynx, he develops mucus in the oropharynx and drools excessively. When the infant is fed, regurgitation and respiratory distress follow aspiration. Suctioning the mucus and secretions temporarily relieves these symptoms. Excessive secretions and drooling in the neonate strongly suggest esophageal atresia.
Repeated episodes of pneumonitis, pulmonary infection, and abdominal distention may signal type E (or H-type) tracheoesophageal fistula. When a child with this disorder drinks, he coughs, chokes, and becomes cyanotic. Excessive mucus builds up in the oropharynx. Crying forces air from the trachea into the esophagus, producing abdominal distention. Because such a child may appear normal at birth, this type of tracheoesophageal fistula may be overlooked, and diagnosis may be delayed as long as 1 year.
Type B (proximal fistula) and type D (fistula to both segments) cause immediate aspiration of saliva into the airway and bacterial pneumonitis.
DIAGNOSIS
Respiratory distress and drooling in a neonate suggest tracheoesophageal fistula and esophageal atresia. The following procedures confirm the diagnosis:
A size 10 or 12 French catheter passed through the nose meets an obstruction (esophageal atresia) approximately 4 to 5 (10 to 12.5 cm) distal from the nostrils. Aspirate of gastric contents is less acidic than normal.
Chest X-ray demonstrates the position of the catheter and can also show a dilated, air-filled upper esophageal pouch, pneumonia in the right upper lobe, or bilateral pneumonitis. Both pneumonia and pneumonitis suggest aspiration.
Abdominal X-ray shows gas in the bowel in a distal fistula (type C) but none in a proximal fistula (type B) or in atresia without fistula (type A).
Cinefluorography allows visualization on a fluoroscopic screen. After a size 10 or 12 French catheter is passed through the patient’s nostril into the esophagus, a small amount of contrast medium is instilled to define the tip of the upper pouch and to differentiate between overflow aspiration from a blind end (atresia) and aspiration due to passage of liquid through a tracheoesophageal fistula.
TREATMENT
Tracheoesophageal fistula and esophageal atresia require surgical correction and are usually surgical emergencies. The type and timing of surgical procedure depend on the nature of the anomaly, the patient’s general condition, and the presence of coexisting congenital defects. In premature neonates (nearly 33% of neonates with this anomaly are born prematurely) who are poor surgical risks, correction of combined tracheoesophageal fistula and esophageal atresia is done in two stages: first, gastrostomy (for gastric decompression, prevention of reflux, and
feeding) and closure of the fistula; then, 1 to 2 months later, anastomosis of the esophagus.
feeding) and closure of the fistula; then, 1 to 2 months later, anastomosis of the esophagus.
Types of tracheoesophageal anomalies
Congenital malformations of the esophagus occur in about 1 in 3,500 live births. The American Academy of Pediatrics classifies the anatomic variations of tracheoesophageal anomalies as follows.
Type A (8%): esophageal atresia without fistula
Type B (1%): esophageal atresia with tracheoesophageal fistula to the proximal segment
Type C (84%): esophageal atresia with fistula to the distal segment
Type D (3%): esophageal atresia with fistula to both segments
Type E (or H-Type) (4%): tracheoesophageal fistula without atresia
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Before and after surgery, positioning varies with the physician’s philosophy and the infant’s anatomy: the infant maybe placed supine, with his head low to facilitate drainage, or with his head elevated to prevent aspiration.
The infant should receive I.V. fluids, as necessary, and appropriate antibiotics for superimposed infection.
Postoperative complications after correction of tracheoesophageal fistula include recurrent fistulas, esophageal motility dysfunction, esophageal stricture, recurrent bronchitis, pneumothorax, and failure to thrive. Esophageal motility dysfunction or hiatal hernia may develop after surgery to correct esophageal atresia.
Correction of esophageal atresia alone requires anastomosis of the proximal and distal esophageal segments in one or two stages. Endto-end anastomosis commonly produces postoperative stricture; end-to-side anastomosis is less likely to do so. If the esophageal ends are widely separated, treatment may include a colonic interposition (grafting a piece of the colon) or elongation of the proximal segment of the esophagus by bougienage. About 10 days after surgery, and again 1 and 3 months later, X-rays are required to evaluate the effectiveness of surgical repair.
Postoperative treatment includes placement of a suction catheter in the upper esophageal pouch to control secretions and prevent aspiration, maintaining the infant in an upright position to avoid reflux of gastric juices into the trachea, I.V. fluids (nothing by mouth), gastrostomy to prevent reflux and allow feeding, and appropriate antibiotics for pneumonia.
Postoperative complications may include impaired esophageal motility (in one third of patients), hiatal hernia, and reflux esophagitis.
SPECIAL CONSIDERATIONS
Postoperative care should include the following:
Monitor the infant’s respiratory status. Administer oxygen and perform pulmonary physiotherapy and suctioning, as needed. Provide a humid environment.
Administer antibiotics and parenteral fluids, as ordered. Keep accurate intake and output records.
If the infant has chest tubes postoperatively check them frequently for patency. Maintain proper suction; measure and mark drainage periodically.
Observe carefully for signs of complications.
Maintain gastrostomy tube feedings, as ordered. Such feedings initially consist of dextrose and water (not more than 5% solution); later, add a proprietary formula (first diluted and then full strength). If the infant develops gastric atony, use
an iso-osmolar formula. Oral feedings can usually resume 8 to 10 days postoperatively. If gastrostomy feedings and oral feedings are impossible because of intolerance to them or decreased intestinal motility, the infant requires total parenteral nutrition.
If the infant can safely handle secretions, he may be given a pacifier to satisfy his sucking needs; however, this is done only when he can safely handle secretions because sucking stimulates saliva secretion.
Offer the parents support and guidance in dealing with their infant’s acute illness. Encourage them to participate in the infant’s care and to hold and touch him as much as possible to facilitate bonding.
Corrosive esophagitis and stricture
Corrosive esophagitis is inflammation and damage to the esophagus after ingestion of a caustic chemical. Similar to a burn, this injury may be temporary or may lead to permanent stricture (narrowing or stenosis) of the esophagus that’s correctable only through surgery. Severe injury can quickly lead to esophageal perforation, mediastinitis, and death from infection, shock, and massive hemorrhage (due to aortic perforation).
CAUSES AND INCIDENCE
The most common chemical injury to the esophagus follows the ingestion of lye or other strong alkali; ingestion of strong acids is less common. The type and amount of chemical ingested determine the severity and location of the damage. In children, household chemical ingestion is accidental; in adults, it’s usually a suicide attempt or gesture. The chemical may damage only the mucosa or submucosa or it may damage all layers of the esophagus.
Esophageal tissue damage occurs in three phases: the acute phase, consisting of edema and inflammation; the latent phase, with ulceration, exudation, and tissue sloughing; and the chronic phase, in which there is diffuse scarring.
Gastroesophageal reflux disease accounts for 70% to 80% of all cases of esophageal stricture. Postoperative strictures account for 10% of all cases, and corrosive strictures account for less than 5% of all cases. Peptic strictures are 10 times more common in Whites than in Blacks and Asians and two to three times more common in men than in women.
SIGNS AND SYMPTOMS
Effects vary from none at all to intense pain and edema in the mouth, anterior chest pain, marked salivation, inability to swallow, and tachypnea. Bloody vomitus containing pieces of esophageal tissue signals severe damage. Signs of esophageal perforation and mediastinitis, especially crepitation, indicate destruction of the entire esophagus. Inability to speak implies laryngeal damage.
The acute phase subsides in 3 to 4 days, enabling the patient to eat again. Fever suggests secondary infection. Symptoms of dysphagia return if stricture develops, usually within weeks; rarely, stricture is delayed and develops several years after the injury.
DIAGNOSIS
CONFIRMING DIAGNOSISA history of chemical ingestion and physical examination revealing oropharyngeal burns (including white membranes and edema of the soft palate and uvula) usually confirm the diagnosis
The type and amount of the chemical ingested must be identified; this may be done by examining the container of the ingested material or by calling the poison control center.
Two procedures are helpful in evaluating the severity of the injury:
Endoscopy (in the first 24 hours after ingestion) delineates the extent and location of the esophageal injury and assesses the depth of the burn. This procedure may also be performed a week after ingestion to assess stricture development.
Barium swallow (1 week after ingestion and every 3 weeks thereafter) may identify segmental spasm or fistula, but doesn’t always show mucosal injury.
TREATMENT
Conservative treatment of corrosive esophagitis and stricture includes monitoring the patient’s condition; early endoscopy; administering corticosteroids, such as prednisone and hydrocortisone, to control inflammation and inhibit fibrosis; and using a broad-spectrum antibiotic, such as ampicillin, to protect the corticosteroidimmunosuppressed patient against infection by his own mouth flora.
Treatment may also include bougienage, a procedure in which a slender, flexible, cylindrical instrument called a bougie is passed into the esophagus to dilate it and minimize stricture. Some physicians begin bougienage immediately and continue it regularly to maintain a patent lumen and prevent stricture; others delay it for a week to avoid the risk of esophageal perforation.
Surgery is needed immediately for esophageal perforation or later to correct stricture untreatable with bougienage. Corrective surgery may involve transplanting a piece of the colon to the damaged esophagus. However, even after surgery, stricture may recur at the site of the anastomosis.
Supportive treatment includes I.V. therapy to replace fluids or total parenteral nutrition while the patient can’t swallow, gradually progressing to clear liquids and a soft diet.
SPECIAL CONSIDERATIONS
If you’re the first health care professional to see the patient who has ingested a corrosive chemical, the quality of your emergency care will be critical. To meet this challenge, follow these important guidelines:
Don’t induce vomiting or lavage because this will expose the esophagus and oropharynx to additional injury.
Don’t perform gastric lavage because the corrosive chemical may cause further damage to the mucous membrane of the GI lining.
Provide vigorous support of vital functions, as needed, such as oxygen, mechanical ventilation, administration of I.V. fluids, and treatment for shock, depending on the severity of the injury.
Carefully observe and record intake and output.
Before X-rays and endoscopy, explain the procedure to the patient to lessen anxiety during the tests and to obtain cooperation.
Because the adult who has ingested a corrosive agent has usually done so with suicidal intent, assist him and his family in seeking psychological counseling. Monitor the patient according to facility protocol if the attempt was a suicide.
Provide emotional support for parents whose child has ingested a chemical. They’ll be distraught and may feel guilty about the accident.
Encourage long-term follow-up because of the increased risk of squamous cell carcinoma.
PREVENTIONTell parents to lock accessible cabinets and keep all corrosive agents out of a child’s reach without emphasizing blame
Mallory-Weiss syndrome
Mallory-Weiss syndrome is mild to massive, usually painless bleeding due to a tear in the mucosa or submucosa of the cardia or lower esophagus. Such a tear, usually singular and longitudinal, results from prolonged or forceful vomiting. Sixty percent of these tears involve the
cardia; 15%, the terminal esophagus; and 25%, the region across the esophagogastric junction.
cardia; 15%, the terminal esophagus; and 25%, the region across the esophagogastric junction.
CAUSES AND INCIDENCE
Forceful or prolonged vomiting can cause esophageal tearing when the upper esophageal sphincter fails to relax during vomiting; this lack of sphincter coordination seems more common after excessive alcohol intake. Other factors that can increase intra-abdominal pressure and predispose a person to this type of tear include coughing, straining during bowel movements, traumatic injury, seizures, childbirth, hiatal hernia, esophagitis, gastritis, and atrophic gastric mucosa.
Mallory-Weiss syndrome accounts for 1% to 15% of all cases of upper GI bleeding. It’s two to four times more common in men than in women. There’s no racial predilection. Patients usually present with symptoms during their 40s and 50s, but it can affect people of all ages.
COMPLICATIONS
Hypovolemia (if bleeding is excessive)
Fatal shock
SIGNS AND SYMPTOMS
Mallory-Weiss syndrome typically begins with vomiting of blood or passing large amounts of blood rectally a few hours to several days after forceful vomiting. The bleeding, which may be accompanied by epigastric or back pain, may range from mild to massive, but is usually more profuse than in esophageal rupture. In Mallory-Weiss syndrome, the blood vessels are only partially severed, preventing retraction and closure of the lumen.
ALERTMassive bleeding—most likely when the tear is on the gastric side, near the cardia—may quickly lead to fatal shock.
DIAGNOSIS
CONFIRMING DIAGNOSISFiberoptic endoscopy (esophagogastroduodenoscopy) confirms Mallory-Weiss syndrome by identifying esophageal tears. Recent tears appear as erythematous longitudinal cracks in the mucosa; older tears appear as raised white streaks surrounded by erythema
TREATMENT
Treatment varies with the severity of bleeding. GI bleeding usually stops spontaneously, thereafter requiring supportive measures and careful observation but no definitive treatment. However, if bleeding continues, treatment may include:
proton pump inhibitors or histamine-2 receptor antagonists to help decrease acidity
blood transfusions if blood loss is great
endoscopy with electrocoagulation or heater probe for hemostasis
transcatheter embolization or thrombus formation with an autologous blood clot or other hemostatic material (such as a shredded adsorbable gelatin sponge)
surgery to suture each esophageal laceration
SPECIAL CONSIDERATIONS
Observation is necessary to determine whether bleeding is transitory or ongoing.
Evaluate the patient’s respiratory status, monitor arterial blood gas values, and administer oxygen as necessary.
Assess the amount of blood lost and record the color, amount, consistency, and frequency of hematemesis and melena.
Draw blood for coagulation studies (prothrombin time, partial thromboplastin time, and platelet count), and type and crossmatch.
Try to keep 3 units of blood available at all times. Insert a 14G to 18G I.V. line, and start an infusion of I.V. solution, as ordered. (If the I.V. infusion is for blood transfusion, use normal saline solution; if the infusion is for fluid replacement, use lactated Ringer’s solution or another appropriate solution, depending on the results of laboratory tests.)
Monitor the patient’s vital signs, central venous pressure, urine output, neurologic status, and overall clinical status.
Explain diagnostic tests to the patient.
Keep the patient warm and maintain a safe environment.
Obtain a detailed history of recent medications taken, dietary habits, and alcohol ingestion.
Administer antiemetics, as ordered, to prevent postoperative retching and vomiting.
Advise the patient to avoid aspirin, alcohol, and other irritating substances.
Esophageal diverticula
Esophageal diverticula are hollow outpouchings of one or more layers of the esophageal wall. They occur in three main areas: just above the upper esophageal sphincter (Zenker’s, or pulsion, diverticulum, the most common type); near the midpoint of the esophagus (traction diverticulum); and just above the lower esophageal sphincter (epiphrenic diverticulum). Generally, esophageal diverticula occur later
in life—although they can affect infants and children—and are three times more common in men than in women. Epiphrenic diverticula usually occur in middle-aged men, whereas Zenker’s diverticula typically affect men older than age 60.
in life—although they can affect infants and children—and are three times more common in men than in women. Epiphrenic diverticula usually occur in middle-aged men, whereas Zenker’s diverticula typically affect men older than age 60.
CAUSES AND INCIDENCE
Esophageal diverticula are due to primary muscular abnormalities that may be congenital or to inflammatory processes adjacent to the esophagus. Zenker’s diverticulum occurs when the pouch results from increased intraesophageal pressure; traction diverticulum occurs when the pouch is pulled out by adjacent inflamed tissue or lymph nodes. Some authorities classify all diverticula as traction diverticula.
Zenker’s diverticulum results from developmental muscular weakness of the posterior pharynx above the border of the cricopharyngeal muscle. The pressure of swallowing aggravates this weakness, as does contraction of the pharynx before relaxation of the sphincter. A midesophageal (traction) diverticulum is a response to scarring and pulling on esophageal walls by an external inflammatory process such as tuberculosis. An epiphrenic diverticulum (rare) is generally right-sided and usually accompanies an esophageal motor disturbance, such as esophageal spasm or achalasia. It’s thought to be caused by traction and pulsation.
Most diverticula occur in middle-aged and elderly patients. Zenker’s diverticula occur most commonly in patients older than age 50 and are especially prevalent in patients in their 70s and 80s.
COMPLICATIONS
Malnutrition
Dehydration
SIGNS AND SYMPTOMS
Midesophageal and epiphrenic diverticula with an associated motor disturbance (achalasia or spasm) seldom produce symptoms, although the patient may experience dysphagia and heartburn. Zenker’s diverticulum, however, produces distinctly staged symptoms, beginning with initial throat irritation followed by dysphagia and near-complete obstruction. In early stages, regurgitation occurs soon after eating; in later stages, regurgitation after eating is delayed and may even occur during sleep, leading to food aspiration and pulmonary infection.
ELDER TIPHoarseness, asthma, andpneu monitis may be the only signs of esophageal diverticula in elderly patients
Other signs and symptoms include noise when liquids are swallowed, chronic cough, hoarseness, a bad taste in the mouth or foul breath and, rarely, bleeding.
DIAGNOSIS
CONFIRMING DIAGNOSISX-rays taken following a barium swallow usually confirm the diagnosis by showing characteristic outpouching.
Esophagoscopy can rule out another lesion; however, the procedure risks rupturing the diverticulum by passing the scope into it rather than into the lumen of the esophagus, a special danger with Zenker’s diverticulum.
TREATMENT
Treatment of Zenker’s diverticulum is usually palliative and includes a bland diet, thorough chewing, and drinking water after eating to flush out the sac. However, severe symptoms or a large diverticulum necessitates surgery to remove the sac or facilitate drainage. An esophagomyotomy may be necessary to prevent recurrence. Endscopic stapling or laser surgery using CO2 microscopy are commonly performed in patients who can’t tolerate traditional surgeries.
A midesophageal diverticulum seldom requires therapy except when esophagitis aggravates the risk of rupture, in which case treatment includes antacids and an antireflux regimen: keeping the head elevated, maintaining an upright position for 2 hours after eating, eating small meals, controlling chronic coughing, and avoiding constrictive clothing.
Epiphrenic diverticulum requires treatment of accompanying motor disorders. Achalasia is treated by repeated dilations of the esophagus; acute spasm is controlled by anticholinergic administration and diverticulum excision; and dysphagia or severe pain are relieved by surgical excision or suspending the diverticulum to promote drainage. Treatment may also include parenteral feeding to improve the patient’s nutritional status.
SPECIAL CONSIDERATIONS
Care includes documenting the patient’s symptoms and nutritional status and educating him about the disorder.
Regularly assess the patient’s nutritional status (weight, calorie intake, and appearance).
If the patient regurgitates food and mucus, protect against aspiration by positioning him carefully (head elevated or turned to one side). To prevent aspiration, tell the patient to empty any visible outpouching in the neck by massage or postural drainage before retiring.
If the patient has dysphagia, record welltolerated foods and what circumstances ease swallowing. Provide a pureed diet, with vitamin or protein supplements, and encourage thorough chewing.
Teach the patient about this disorder. Explain treatment instructions and diagnostic procedures.
Hiatal hernia
Hiatal hernia, also called hiatus hernia, is a defect in the diaphragm that permits a portion of the stomach to pass through the diaphragmatic opening into the chest. Hiatal hernia is the most common problem of the diaphragm affecting the alimentary canal. Two types of hiatal hernia can occur: sliding hernia and paraesophageal hernia. (See Types of hiatal hernia.) In a sliding hernia, the stomach and the gastroesophageal junction slip up into the chest, so the gastroesophageal junction is above the diaphragmatic hiatus. In paraesophageal hernia, a part of the greater curvature of the stomach rolls through the diaphragmatic defect. Treatment can prevent complications such as strangulation of the herniated intrathoracic portion of the stomach.
CAUSES AND INCIDENCE
Hiatal hernia typically results from muscle weakening that’s common with aging and may be secondary to esophageal carcinoma, kyphoscoliosis, trauma, or certain surgical procedures. It may also result from certain diaphragmatic malformations that may cause congenital weakness. Obesity and smoking are common risk factors.
In hiatal hernia, the muscular collar around the esophageal and diaphragmatic junction loosens, permitting the lower portion of the esophagus and the stomach to rise into the chest when intra-abdominal pressure increases (possibly causing gastroesophageal reflux). Such increased intra-abdominal pressure may result from ascites, pregnancy, obesity, constrictive clothing, bending, straining, coughing, Valsalva’s maneuver, or extreme physical exertion.
Sliding hernias are more common than paraesophageal hernias. The incidence of hiatal hernia increases with age (most occur in people older than age 40), and prevalence is higher in women than in men (especially the paraesophageal type). Contributing factors include obesity and trauma.
Types of hiatal hernia
A hiatal hernia is a displacement of the normal anatomy, as shown in the illustrations below.
 NORMAL STOMACH |
 SLIDING HIATAL HERNIA |
 PARAESOPHAGEAL HERNIA |
COMPLICATIONS
Dysphagia
Gastroesophageal reflux
Barrett’s esophagus
Esophageal adenocarcinoma
SIGNS AND SYMPTOMS
Typically, a paraesophageal hernia produces no symptoms; it’s usually an incidental finding during a barium swallow or when testing for occult blood. Because this type of hernia leaves the closing mechanism of the cardiac sphincter unchanged, it rarely causes acid reflux or reflux esophagitis. Symptoms result from displacement or stretching of the stomach and may include a feeling of fullness in the chest or pain resembling angina pectoris. Even if it produces no symptoms, this type of hernia needs surgical treatment because of the high risk of strangulation that can occur when a large portion of stomach becomes caught above the diaphragm.
A sliding hernia without an incompetent sphincter produces no reflux or symptoms and, consequently, doesn’t require treatment. When a sliding hernia causes symptoms, they are typical of gastric reflux, resulting from the incompetent lower esophageal sphincter (LES), and may include the following:
Pyrosis (heartburn) occurs 1 to 4 hours after eating (especially overeating) and is aggravated by reclining, belching, and increased intraabdominal pressure. It may be accompanied by regurgitation or vomiting.
Retrosternal or substernal chest pain results from reflux of gastric contents, stomach distention, and spasm or altered motor activity. Chest pain usually occurs after meals or at bedtime and is aggravated by reclining, belching, and increased intra-abdominal pressure.
Other common symptoms reflect possible complications:
Dysphagia occurs when the hernia produces esophagitis, esophageal ulceration, or stricture, especially with ingestion of very hot or cold foods, alcoholic beverages, or a large amount of food.
Bleeding may be mild or massive, frank or occult; the source may be esophagitis or erosions of the gastric pouch.
Severe pain and shock result from incarceration, in which a large portion of the stomach is caught above the diaphragm (usually occurs with paraesophageal hernia). Incarceration may lead to perforation of the gastric ulcer and strangulation and gangrene of the herniated portion of the stomach. It requires immediate surgery.
DIAGNOSIS
Diagnosis of hiatal hernia is based on typical clinical features and on the results of these laboratory studies and procedures:
In barium study, hernia may appear as an outpouching containing barium at the lower end of the esophagus. Small hernias, however, are difficult to recognize. This study also shows diaphragmatic abnormalities.
Endoscopy (esophagogastroduodenoscopy) and biopsy differentiate among hiatal hernia, varices, and other small gastroesophageal lesions; identify the mucosal junction and the edge of the diaphragm indenting the esophagus; and can rule out malignancy that otherwise may be difficult to detect.
Esophageal motility studies assess the presence of esophageal motor abnormalities before surgical repair of the hernia.
pH studies assess for reflux of gastric contents.
TREATMENT
The primary goals of treatment are to relieve symptoms by minimizing or correcting the incompetent cardia and to manage and prevent complications. Medical therapy is used first because symptoms usually respond to it and because hiatal hernia tends to recur after surgery. Such therapy attempts to modify or reduce reflux by changing the quantity or quality of refluxed gastric contents, by strengthening the LES muscle pharmacologically, or by decreasing the amount of reflux through gravity. These measures include restricting any activity that raises intra-abdominal pressure (coughing, straining, or bending), giving antiemetics, avoiding constrictive clothing, modifying diet, giving stool softeners or laxatives to prevent straining at stool, and discouraging smoking because it stimulates gastric acid production.
Modifying the diet means eating small, frequent, bland meals at least 2 hours before lying down (no bedtime snack), eating slowly, and avoiding spicy foods, fruit juices, alcoholic beverages, and coffee. Antacids also modify the fluid refluxed into the esophagus and are probably the best treatment for intermittent reflux.
To reduce the amount of reflux, the overweight patient should lose weight to decrease intra-abdominal pressure. Elevating the head of the bed 6” (15 cm) reduces gastric reflux by gravity.
Drug therapy includes antacids to neutralize stomach acid, medications to reduce acid production, and medications to block acid production and to heal the esophagus.
Surgical repair is necessary when symptoms can’t be controlled medically or with the onset of complications, such as stricture, bleeding, pulmonary aspiration, strangulation, or incarceration. Surgery typically involves creating an artificial closing mechanism at the gastroesophageal junction to strengthen the LES’s barrier function. The surgeon may use an abdominal or a thoracic approach, or he may repair the hernia by laparoscopic surgery, which allows for less dependence on a nasogastric (NG) tube and a shorter hospital stay.
SPECIAL CONSIDERATIONS
To enhance compliance with treatment, teach the patient about this disorder. Explain treatments, diagnostic tests, and significant symptoms.
Prepare the patient for diagnostic tests as needed. After endoscopy, watch for signs of perforation (falling blood pressure, rapid pulse, shock, and sudden pain).
If surgery is scheduled, review preoperative and postoperative considerations with the patient.
After surgery, carefully record intake and output, including NG tube and wound drainage.
While the NG tube is in place, provide meticulous mouth and nose care, but don’t manipulate the tube. Give ice chips, if permitted, to moisten oral mucous membranes.
If the surgeon used a thoracic approach, the patient may have chest tubes in place. Carefully observe chest tube drainage and the patient’s respiratory status, and perform pulmonary physiotherapy.
Before discharge, tell the patient what foods he can eat, and recommend small, frequent meals. Warn against activities that cause increased intra-abdominal pressure, and advise a slow return to normal functions (within 6 to 8 weeks).
STOMACH, INTESTINE, AND PANCREAS
Gastritis
Gastritis, an inflammation of the gastric mucosa, may be acute or chronic. Acute gastritis produces mucosal reddening, edema, hemorrhage, and erosion. Chronic gastritis is common among elderly people and people with pernicious anemia. It typically occurs as chronic atrophic gastritis, in which all stomach mucosal layers are inflamed, with reduced numbers of chief and parietal cells. Acute or chronic gastritis can occur at any age.
CAUSES AND INCIDENCE
Acute gastritis has numerous causes, including:
chronic ingestion of (or an allergic reaction to) irritating foods or beverages, such as hot peppers or alcohol
drugs, such as aspirin and other nonsteroidal anti-inflammatory drugs (in large doses), cytotoxic agents, corticosteroids, antimetabolites, phenylbutazone, and indomethacin
ingestion of poisons, especially DDT, ammonia, mercury, carbon tetrachloride, and corrosive substances
endotoxins released from infecting bacteria, such as staphylococci, Escherichia coli, or salmonella
Acute gastritis leading to stress ulcers also may develop in acute illnesses, especially when the patient has had major traumatic injuries; burns; severe infection; hepatic, renal, or respiratory failure; or major surgery.
Chronic gastritis may be associated with peptic ulcer disease or gastrostomy, both of which cause chronic reflux of pancreatic secretions, bile, and bile acids from the duodenum into the stomach. Recurring exposure to irritating substances, such as drugs, alcohol, cigarette smoke, or environmental agents, may also lead to chronic gastritis. Chronic gastritis may occur with pernicious anemia, renal disease, or diabetes mellitus. Pernicious anemia is commonly associated with atrophic gastritis, a chronic inflammation of the stomach resulting from degeneration of the gastric mucosa. In pernicious anemia, the stomach can no longer secrete intrinsic factor, which is needed for vitamin B12 absorption.
Bacterial infection with Helicobacter pylori is a common cause of nonerosive chronic gastritis. About 35% of adults are infected with H. pylori, but the prevalence of H. pylori infection is much higher in minority groups and in immigrants. Children ages 2 to 8 in developing nations acquire the infection at a rate of 10% per year; in the United States, the rate of yearly infection is less than 1 %.
SIGNS AND SYMPTOMS
After exposure to the offending substance, the patient with acute gastritis typically reports a rapid onset of symptoms, such as epigastric discomfort, indigestion, cramping, anorexia, nausea, vomiting, and hematemesis. The symptoms last from a few hours to a few days.
The patient with chronic gastritis may describe similar symptoms or may have only mild epigastric discomfort, or his complaints may be vague, such as an intolerance for spicy or fatty foods or slight pain relieved by eating. The patient with chronic atrophic gastritis may be asymptomatic.
DIAGNOSIS
CONFIRMING DIAGNOSISEsophagogastroduodenoscopy or gastroscopy (with biopsy) confirms gastritis when done before lesions heal (usually within 24 hours). This testis contraindicated after ingestion of a corrosive agent.
Laboratory analyses can detect occult blood in vomitus or stool (or both) if the patient has gastric bleeding. Hemoglobin level and hematocrit are decreased if the patient has developed anemia from bleeding.
TREATMENT
Treatment for gastritis focuses on eliminating the cause; for example, bacterial gastritis is treated with antibiotics, whereas gastritis caused by ingested poison is treated by neutralizing the poison with the appropriate antidote. Proton pump inhibitors or histamine-2 (H2) receptor antagonists may reduce gastric acid production. Many over-the-counter preparations are available. Antacids may be used as buffers.
For critically ill patients, antacids administered hourly, with or without H2-receptor antagonists, may reduce the frequency of gastritis attacks. Some patients also require analgesics. Until healing occurs, patients’ oxygen needs, blood volume, and fluid and electrolyte balance must be monitored.
When gastritis causes massive bleeding, treatment includes blood replacement; iced saline lavage, possibly with norepinephrine; angiography with vasopressin infused in normal saline solution; and, sometimes, surgery.
Vagotomy and pyloroplasty achieve limited success when conservative treatments fail. Rarely, partial or total gastrectomy may be required.
Simply avoiding aspirin and spicy foods may prevent exacerbations of chronic gastritis. If symptoms develop or persist, antacids may be taken. If pernicious anemia is the cause, vitamin B12 may be administered parenterally. A combination of two antibiotics, such as clarithromycin and amoxicillin, is typically given for 14 days to treat H. pylori. Acid-reducing medications may help to enhance the effectiveness of the antibiotics.
SPECIAL CONSIDERATIONS
Patient care includes education and attention to various aspects of nutritional status to control symptoms and prevent their recurrence.
For vomiting, give antiemetics and I.V. fluids, as ordered. Monitor fluid intake and output and electrolyte levels.
Monitor the patient for recurrent symptoms as food is reintroduced; provide a bland diet.
Offer smaller, more frequent meals to reduce irritating gastric secretions. Eliminate foods that cause gastric upset.
Administer proton pump inhibitors, H2-receptor antagonists, and antacids, as ordered.
If pain or nausea interferes with the patient’s appetite, give analgesics or antiemetics 1 hour before meals.
Tell the patient to avoid alcohol, caffeine, and irritating foods such as spicy or highly seasoned foods.
If the patient smokes, refer him to a smokingcessation program.
Urge the patient to seek immediate attention for recurring symptoms, such as hematemesis, nausea, or vomiting.
To prevent exacerbation, urge the patient to take prophylactic medications, as ordered.
PREVENTIONAdvise the patient to take steroids with milk, food, or antacids. Instruct him to take antacids between meals and at bedtime and to avoid aspirin-containing compounds.
Gastroenteritis
A self-limiting disorder, gastroenteritis is characterized by diarrhea, nausea, vomiting, and acute or chronic abdominal cramping. Also called intestinal flu, traveler’s diarrhea, viral enteritis, or food poisoning, it occurs in persons of all ages and is a major cause of morbidity and mortality in underdeveloped nations. In the United States, gastroenteritis ranks second to the common cold as a leading cause of lost work time and fifth as the leading cause of death among young children. It also can be lifethreatening in elderly or debilitated people.
CAUSES AND INCIDENCE
Gastroenteritis has many possible causes, including:
bacteria (responsible for acute food poison ing), such as Staphylococcus aureus, Salmonella,
Shigella, Clostridium botulinum, C. perfringens, and Escherichia coli
amebae, especially Entamoeba histolytica
parasites, such as Ascaris, Enterobius, and Trichinella spiralis
viruses (may be responsible for traveler’s diarrhea) such as adenoviruses, echoviruses, or coxsackieviruses
ingestion of toxins, including plants or toadstools
drug reactions; for example, to antibiotics
enzyme deficiencies
food allergens
The bowel reacts to any of these enterotoxins with hypermotility, producing severe diarrhea and secondary depletion of intracellular fluid. Chronic gastroenteritis is usually the result of another GI disorder such as ulcerative colitis.
Diarrhea accounts for as many as 3% of pediatric office visits and 10% of hospitalizations for patients younger than age 5. Each year, gastroenteritis affects many adults and accounts for 8 million physician visits and 250,000 hospitalizations. Traveler’s diarrhea affects 20% to 25% of people traveling from industrialized countries to developing countries.
COMPLICATIONS
Severe dehydration
Electrolyte loss
Shock
Vascular collapse
Renal failure
SIGNS AND SYMPTOMS
Signs and symptoms vary depending on the pathologic organism and on the level of GI tract involved. However, gastroenteritis in adults is usually an acute, self-limiting, nonfatal disease producing diarrhea, abdominal discomfort (ranging from cramping to pain), nausea, and vomiting. Other possible signs and symptoms include fever, malaise, and borborygmi. In children, the elderly, and the debilitated, gastroenteritis produces the same symptoms, but these patients’ intolerance to electrolyte and fluid losses leads to a higher mortality.
DIAGNOSIS
Patient history can aid in the diagnosis of gastroenteritis. Stool culture (by direct rectal swab) or blood culture identifies the causative bacteria or parasites.
TREATMENT
Treatment is usually supportive and consists of bed rest, nutritional support, and increased fluid intake. When gastroenteritis is severe or affects a young child or an elderly or debilitated person, treatment may necessitate hospitalization, specific antimicrobials, I.V. fluid and electrolyte replacement and, possibly, antiemetics (given orally, I.M., or by rectal suppository).
SPECIAL CONSIDERATIONS
Patient care includes education, administering medications, and assessing symptoms for signs of improvement or worsening.
Administer medications as ordered; correlate dosages, routes, and times appropriately with the patient’s meals and activities (for example, give antiemetics 30 to 60 minutes before meals).
If the patient can eat, replace lost fluids and electrolytes with broth, ginger ale, and lemonade, as tolerated. Vary the diet to make it more enjoyable, and allow some choice of foods. Warn the patient to avoid milk and milk products, which may provoke recurrence.
Record intake and output carefully and obtain serial weight measurements. Watch for signs of dehydration, such as dry skin and mucous membranes, fever, and sunken eyes.
Wash your hands thoroughly after giving care to avoid spreading infection.
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