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18, NAUSEA, VOMITING, AND ,INDIGESTION

18 NAUSEA, VOMITING, AND INDIGESTION
Harrison’s Manual of Medicine

18

NAUSEA, VOMITING, AND INDIGESTION

Nausea and Vomiting

Pathophysiology

Etiology

Evaluation

Complications
Indigestion

Pathophysiology

Natural History

Evaluation
Bibliography

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 18-1).

Table 18-1 Causes of Nausea and Vomiting

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 also may be helpful: vertigo and tinnitus in Ménière’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, 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, a serotonin receptor blocker, and glucocorticoids are used for treating nausea and vomiting associated with cancer chemotherapy. 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 patients with dyspeptic symptoms. However, peptic ulcer disease from either Helicobacter pylori infection or ingestion of NSAIDs is present 15% of cases.
In most cases, the esophagus is not damaged, but 5% of patients 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, 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. Patients 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. 148. Cisapride can stimulate gastric emptying. Omeprazole plus cisapride is a rational combination.
Surgical techniques (Nissan fundoplication, Belsey procedure) can be used in the rare patients who are refractory to medical management. Clinical trials have not documented the superiority of one over another.

Bibliography

For a more detailed discussion, see Hasler WL: Nausea, Vomiting, and Indigestion, Chap. 41, p. 236, in HPIM-15.

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