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Diffuse esophageal spasm is characterized by the occurrence of

normal peristalsis in the upper one-third of the esophagus and intermittent nonperistaltic, simultaneous contractions of the body of the esophagus. Clinical manifestations include intermittent chest pain

with or without eating. Patients will also demonstrate a characterisric

"cork-screw" partern on barium-swallow studies. The etiology is

unknown, and management is directed at smooth muscle relaxation

with pharmacologic agents.'2.",1S

Gastroesophageal Reflux Disease

Gastroesophageal re{lux disease (GERD) is characterized by gastric acid

back flow intO the esophagus as a result of improper lower esophageal

sphincter relaxation. Clinical manifestations include complaints of heartburn (especially with sour or bitter regurgitation), nausea, gagging, cough, or hoarseness. Although the exact etiology of GERD is unknown,

smoking, along with the consumption of fats, alcohol, coffee, or chocolate, has been associated with this inappropriate relaxation. Esophageal and gastric motility disorders may also contribute to GERD. Gastroesophageal reflux is a strong predisposing factOr for developing esoph-

526 AClITE CARE HANDBOOK FOR PHYSICAL THERAPISTS

ageal adenocarcinoma. Depending on the severity of GERD, treatment

can range from either dietary modifications (avoid risk facrors and eat

small, frequent meals in an upright position), antacids, antisecretory

agents, or surgery.12.17,18 However, surgical intervention has nOt shown

positive results in relieving symptoms of GERD.'9

Barrett's Esophagus

Barren's esophagus is a disorder in which columnar epithelium

replaces the normal stratified squamous mucosa of the distal esophagus and is generally associated with chronic GERD. The mechanism of cellular metaplasia is thought to occur from chronic inflammatory

injury from acid and pepsin that refluxes from the stomach into the

distal esophagus.2o Barrett's esophagus is also a strong predisposing

factor for developing esophageal adenocarcinoma, the incidence of

which has risen in the 1990s.'9.2'

Associated signs and symptoms include dysphagia, esophagitis,

ulceration, perforations, strictures, bleeding, or adenocarcinoma.22

Treatment for Barrett's esophagus includes controlling symptoms of

GERD and promising new therapies that include endoscopic ablation

therapy combined with proton pump inhibition (for acid secretion

control). Ablation therapy includes such techniques as photodynamic

therapy, multipolar polar electrocautery, laser therapy, and, most

recently, argon plasma coagulation.2o

Esophageal Varices

Varices are dilated blood vessels in the esophagus caused by portal

hypertension and may result in hemorrhage that necessitates immediate medical and, usually, surgical management. Alcohol abuse is an associated risk factor.23 Refer to Cirrhosis later in this chapter for

more information on portal hypertension and alcoholic cirrhosis.

Esophageal Cancer

A description of esophageal cancers with respecr ro evaluation and management can be found in Cancers in the Body Systems in Chapter 5.

Clinical Tip

Physical therapists should be aware of any positioning precautions for parients wirh esophageal disorders that may

exacerbare their dysphagia or GERD.

GASTROIt-m:SrINAL SYSTE.M

527

Stomach Disorders

Gastrointestinal Hemorrhage

Bleeding in the GI system can occur in either the upper GI system

(upper gastrointestinal bleed [UGIBj) or in the lower GI system (lower

gastrointestinal bleed ILGIB]). A UGIB can result from one or more

of the following: ( I) duodenal u\cers, (2) gastric erosion, (3) gastric

u\cers, (4) esophageal varices, and (5) use of nonsteroidal anti-inflammatory drug medications (NSAlDs). An LGIB can resulr from one or more of the following: (I) inflammatory bowel disease, (2) neoplasms, and (3) anal and rectal lesions (e.g., hemorrhoids).24-26

Gl bleeds can be small and require minimal to no intervention or

very severe and constitute medical emergencies because of hemodynamic instability that can lead to shock. Hemalemesis or dark brown ("coffee-ground") emesis (vomitus), hematochezia (passage of blood

from the rectum), and melella (black, tatry stools) from acid degradation of hemoglobin are the primary clinical manifestations of GI bleeds.

Patients are generally stabilized hemodynamically with intravenous

(i.v.) fluids, blood rransfusions, or both before the cause of bleeding can

be fully delineated. Nasogasrric tubes (see Appendix Table lll-A.6) are

typically used in the stabilization and management of UGIB. Management is targeted at the causative factors that resulred in either UGLB Ot LGI B. Endoscopy, colonoscopy, or sigmoidoscopy can be perfotmed to

help evaluate or treat the source of upper or lower GI hemorrhage.",25,27

Gastritis

Gastritis is the general term used to describe diffuse inflammatory

lesions in the mucosal layer of the stomach. Gasrriris can be classified

as acute, chronic nonerosive, or chronic erosive.

Etiology of aClIte gastritis includes associations with smoking, alcohol abuse, aspirin, NSAlDs, and corticosteroid use, as well as physiologic stress and inrcnse emotional reactions. Clinical manifestations of acute gastritis include nondescript complaints of burning or discomfort

in the stomach. Management of acute gastritis involves removing the

causative risk factors and relieving the mucosal inflammation.IS.28,29

The etiology of chrollic Ilollerosive gastritis has been definitively

linked to Helicobacter pylori bacterial infection, which is thought to

be transmirred by human-to-human contact.IS.28,JO.JI Patients with H.

pylori gasrritis may be asymptomatic until the gastritis leads to gastric

u\ceration, in which case there will be complaints of dull, gnawing

abdominal pain that rypically occurs when the stomach is empty.2S

Management of H. pylori gastritis includes rriple or quadruple antibi-

528 AClITE CARE HANDBOOK FOR PHYSICAL TIIERAI'ISTS

otic therapies, in combination with antacid medication, to eradicate

the bacterial infection. The primary antibiotics used include metronidazole (Flagyl, Protostat) and c1arithromycin (Biaxin) and amoxicillin. Antacid medication can include any one of the following: omeprazole (Prilosec), lansoprazole (Prevacid), and rabeprazole (Aciphex), which is a newer protOn pump inhibitor.28,JO,JI The etiology of chronic erosive gastritis includes NSAJDs and alcohol abuse. Clinical manifestations can range from being asymptomatic to having anorexia nervosa, gastric pain, nausea, and vomiting.

Management of chronic erosive gastritis involves removing the causative risk factOrs and, possibly, antibiotic therapy similar to that used for H. pylori gastritis."

Peptic Ulcer Disease

A peptic ulcer is a loss of the mucosal surface through the muscularis

mucosa of the esophagus, stomach, or duodenum that is at least 5

mm in diameter.32 Peptic ulcers can be classified as acute or chronic.

Acute peptic IIlcers have lesions that involve the full thickness of the

mucosa, whereas chrollic peptic ulcers have lesions of varying depths.

Peptic ulcers occur primarily in rhe stomach or the first part of the

duodenum, or both. IS

Gastric Ulcer

Ulceration in the stomach is characterized by a well-defined perforation in the gastric mucosa that extends into the muscularis mucosa.33