Nausea, Vomiting, and Indigestion

NAUSEA AND VOMITING

Nausea refers to the imminent desire to vomit and often precedes or accompanies

vomiting. Vomiting refers to the forceful expulsion of gastric contents

through the mouth. Retching refers to labored rhythmic respiratory activity that

precedes emesis. Regurgitation refers to the gentle expulsion of gastric contents

in the absence of nausea and abdominal diaphragmatic muscular contraction.

Rumination refers to the regurgitation,rechewing,and reswallowing of food

from the stomach.

PATHOPHYSIOLOGY Gastric contents are propelled into the esophagus

when there is relaxation of the gastric fundus and gastroesophageal sphincter

followed by a rapid increase in intraabdominal pressure produced by contraction

of the abdominal and diaphragmatic musculature. Increased intrathoracic pressure

results in further movement of the material to the mouth. Reflex elevation

of the soft palate and closure of the glottis protects the nasopharynx and trachea

and completes the act of vomiting. Vomiting is controlled by two brainstem

areas,the vomiting center and chemoreceptor trigger zone. Activation of the

chemoreceptor trigger zone results in impulses to the vomiting center,which

controls the physical act of vomiting.

ETIOLOGY Nausea and vomiting are manifestations of a large number

of disorders (Table 48-1).

EVALUATION The history,including a careful drug history,and the

timing and character of the vomitus can be helpful. For example,vomiting that

occurs predominantly in the morning is often seen in pregnancy,uremia, and

alcoholic gastritis; feculent emesis implies distal intestinal obstruction or gastrocolic fistula; projectile vomiting suggests increased intracranial pressure;

vomiting during or shortly after a meal may be due to psychogenic causes or

peptic ulcer disease. Associated symptoms may also be helpful: vertigo and

tinnitus in Me´nie`re’s disease,relief of abdominal pain with vomiting in peptic

ulcer,and early satiety in gastroparesis. Plain radiographs can suggest diagnoses

such as intestinal obstruction. The upper GI series assesses motility of the proximal

GI tract as well as the mucosa. Other studies may be indicated such as

gastric emptying scans (diabetic gastroparesis) and CT scan of the brain.

COMPLICATIONS Rupture of the esophagus (Boerhaave’s syndrome),

hematemesis from a mucosal tear (Mallory-Weiss syndrome),dehydration, malnutrition, dental caries and erosions,metabolic alkalosis, hypokalemia, and aspiration pneumonitis.

TREATMENT

This should be directed toward correcting the specific cause. The effectiveness

of antiemetic medications depends on etiology of symptoms,pt responsiveness,

and side effects. Antihistamines such as dimenhydrinate and promethazine

hydrochloride are effective for nausea due to inner ear dysfunction.

Anticholinergics such as scopolamine are effective for nausea associated with

motion sickness. Haloperidol and phenothiazine derivatives such as prochlorperazine are often effective in controlling mild nausea and vomiting,but sedation, hypotension, and parkinsonian symptoms are common side effects.

Selective dopamine antagonists such as metoclopramide may be superior to

the phenothiazines in treating severe nausea and vomiting and are particularly

useful in treatment of gastroparesis. Intravenous metoclopramide may be effective

as prophylaxis against nausea when given prior to chemotherapy. Cisapride,

the preferred drug for gastroparesis,exerts peripheral antiemetic effects

but is devoid of the CNS effects of metoclopramide. Ondansetron and

palosetron,serotonin receptor blockers, and glucocorticoids are used for treating

nausea and vomiting associated with cancer chemotherapy. Aprepitant,a

neurokinin receptor blocker,is effective at controlling nausea from highly

emetic drugs like cisplatin. Erythromycin is effective in some pts with gastroparesis.

INDIGESTION

Indigestion is a nonspecific term that encompasses a variety of upper abdominal

complaints including heartburn,regurgitation, and dyspepsia (upper abdominal

discomfort or pain). These symptoms are overwhelmingly due to gastroesophageal

reflux disease (GERD).

PATHOPHYSIOLOGY GERD occurs as a consequence of acid reflux

into the esophagus from the stomach,gastric motor dysfunction, or visceral

afferent hypersensitivity. A wide variety of situations promote GERD: increased gastric contents (from a large meal,gastric stasis,or acid hypersecretion), physical

factors (lying down,bending over),increased pressure on the stomach (tight

clothes,obesity, ascites,pregnancy),loss (usually intermittent) of lower esophageal

sphincter tone (diseases such as scleroderma,smoking, anticholinergics,

calcium antagonists). Hiatal hernia also promotes acid flow into the esophagus.

NATURAL HISTORY Heartburn is reported once monthly by 40% of

Americans and daily by 7%. Functional dyspepsia is defined as _3 months of

dyspepsia without an organic cause. Functional dyspepsia is the cause of symptoms in 60% of pts with dyspeptic symptoms. However,peptic ulcer disease

from either Helicobacter pylori infection or ingestion of NSAIDs is present in

15% of cases.

In most cases,the esophagus is not damaged, but 5% of pts develop esophageal

ulcers and some form strictures. 8–20% develop glandular epithelial cell

metaplasia,termed Barrett’s esophagus,which can progress to adenocarcinoma.

Extraesophageal manifestations include asthma,laryngitis, chronic cough,

aspiration pneumonitis,chronic bronchitis,sleep apnea, dental caries, halitosis,

and hiccups.

EVALUATION The presence of dysphagia,odynophagia, unexplained

weight loss,recurrent vomiting leading to dehydration, occult or gross bleeding,

or a palpable mass or adenopathy are “alarm” signals that demand directed

radiographic,endoscopic, and surgical evaluation. Pts without alarm features

are generally treated empirically. Individuals _45 years can be tested for the

presence of H. pylori. Pts positive for the infection are treated to eradicate the

organism. Pts who fail to respond to H. pylori treatment,those _45 years old,

and those with alarm factors generally undergo upper GI endoscopy.

TREATMENT

Weight reduction; elevation of the head of the bed; and avoidance of large

meals,smoking,caffeine,alcohol,chocolate, fatty food,citrus juices, and

NSAIDs may prevent GERD. Antacids are widely used. Clinical trials suggest

that proton pump inhibitors (omeprazole) are more effective than histamine

receptor blockers (ranitidine) in patients with or without esophageal erosions.

H. pylori eradication regimens are discussed in Chap. 150. Cisapride can

stimulate gastric emptying. Omeprazole plus cisapride is a rational combination.

Surgical techniques (Nissan fundoplication,Belsey procedure) can be used

in the rare pts who are refractory to medical management. Clinical trials have

not documented the superiority of one over another.