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Download Nausea, Vomiting, and Indigestion
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Nausea is the subjective feeling of a need to vomit. Vomiting (emesis) is the oral expulsion of gastrointestinal contents resulting from contractions of gut and thoracoabdominal wall musculature. Vomiting is contrasted with regurgitation, the effortless passage of gastric contents into the mouth. Indigestion is a nonspecific term that encompasses a variety of upper abdominal complaints including nausea, vomiting, heartburn, regurgitation, and dyspepsia (the presence of symptoms thought to originate in the gastroduodenal region). Some individuals with dyspepsia report predominantly : epigastric burning, gnawing discomfort, or pain. Others with dyspepsia experience a constellation of symptoms including : postprandial fullness, early satiety (an inability to complete a meal due to premature fullness), bloating, eructation (belching), anorexia. • MECHANISMS Vomiting is coordinated by the brain stem is effected by responses in the gut, pharynx, and thoracoabdominal wall. The mechanisms underlying nausea are poorly understood likely involve the cerebral cortex, because nausea requires conscious perception. This is supported by electroencephalographic studies showing activation of temporofrontal regions during nausea. MECHANISMS Coordination of emesis Brain stem nuclei-including the nucleus tractus solitarius; dorsal vagal and phrenic nuclei; medullary nuclei that regulate respiration; and nuclei that control pharyngeal, facial, and tongue movements coordinate the initiation of emesis. Neurotransmitters involved in this coordination are uncertain, but neurokinin NKI, serotonin 5-HT3, and vasopressin pathways may participate. MECHANISMS Coordination of emesis Somatic and visceral muscles exhibit stereotypic responses during emesis. Inspiratory thoracic and abdominal wall muscles contract, producing high intrathoracic and intraabdominal pressures that facilitate expulsion of gastric contents. The gastric cardia herniates across the diaphragm and the larynx moves upward to promote oral propulsion of the vomitus. MECHANISMS Activators of emesis Emetic stimuli act at several sites. Emesis provoked by unpleasant thoughts or smells originates in the cerebral cortex, whereas cranial nerves mediate vomiting after gag reflex activation. MECHANISMS Activators of emesis Motion sickness and inner ear disorders act on the labyrinthine apparatus. whereas gastric irritants and cytotoxic agents such as cisplatin stimulate gastroduodenal vagal afferent nerves. Nongastric visceral afferents are activated by intestinal and colonic obstruction and mesenteric ischemia. The area postrema, a medullary nucleus, responds to bloodborne emetic stimuli and is termed the chemoreceptor trigger zone. Many emetogenic drugs act on the area postrema, as do bacterial toxins and metabolic factors produced during uremia, hypoxia, and ketoacidosis. Neurotransmitters that mediate induction of vomiting are selective for these anatomic sites. Labyrinthine disorders stimulate vestibular muscarinic MI and histaminergic HI receptors. whereas vagal afferent stimuli activate serotonin 5-HT3 receptors. The area postrema is richly served by nerves acting on 5-HT3, MI, HI‘ and dopamine D, subtypes. Transmitters in the cerebral cortex are poorly understood, although cannabinoid CBI pathways may participate. Optimal pharmacologic therapy of vomiting requires understanding of these path ways. Intraperitoneal disorders Visceral obstruction and inflammation of hollow and solid viscera may produce vomiting. Gastric obstruction results from ulcer disease and malignancy. small-bowel and colonic obstruction occur because of adhesions, benign or malignant tumors, volvulus, intussusception, or inflammatory diseases such as Crohn's disease. The superior mesenteric artery syndrome, occurring after weight loss or prolonged bed rest, results when the duodenum is compressed by the overlying superior mesenteric artery. Intraperitoneal disorders Abdominal irradiation impairs intestinal motor function and induces strictures. Biliary colic causes nausea via action on visceral afferent nerves. Vomiting with pancreatitis, cholecystitis, and appendicitis is due to visceral irritation and induction of ileus. Enteric infections with viruses or bacteria such as Staphylococcus aureus and Bacillus cereus commonly cause vomiting, especially in children. Opportunistic infections such as cytomegalovirus or herpes simplex virus induce emesis in immunocompromised individuals. Intraperitoneal disorders Disordered gut sensorimotor function commonly causes nausea and vomiting. Gastroparesis is defined as a delay in gastric emptying of food and occurs: after vagotomy, with pancreatic adenocarcinoma, with mesenteric vascular insufficiency, in systemic diseases such as diabetes, scleroderma, and amyloidosis. Intraperitoneal disorders Patients with gastroesophageal reflux may report nausea and vomiting, as do some individuals with irritable bowel syndrome (IBS). Intraperitoneal disorders Other functional disorders without organic abnormalities have been characterized in adults. Chronic idiopathic nausea is defined as nausea without vomiting occurring several times weekly. whereas functional vomiting is defined as one or more vomiting episodes weekly in the absence of an eating disorder or psychiatric disease. Intraperitoneal disorders Cyclic vomiting syndrome is a rare disorder of unknown etiology that produces periodic discrete episodes of relentless nausea and vomiting. The syndrome shows a strong association with migraine headaches, suggesting that some cases may be migraine variants. Cyclic vomiting is most common in children, although adult cases have been described in association with rapid gastric emptying and with chronic cannabis use. Extraperitoneal disorders Myocardial infarction and congestive heart failure Postoperative emesis occurs after 25% of surgeries, most commonly laparotomy and orthopedic surgery, and is more prevalent in women. Increased intracranial pressure from tumors, bleeding, abscess, or obstruction to cerebrospinal fluid outflow Motion sickness, labyrinthitis, and Meniere's disease evoke emesis via labyrinthine pathways. psychiatric illnesses including anorexia nervosa, bulimia nervosa, anxiety, and depression Medications and metabolic disorders Drugs evoke vomiting by action on the stomach (analgesics, erythromycin) area postrema (digoxin, opiates, anti- Parkinsonian drugs). Emetogenic agents include antibiotics, cardiac antiarrhythmics, antihypertensives, oral hypoglycemics, and contraceptives. Cancer chemotherapy Medications and metabolic disorders Pregnancy is the most prevalent endocrinologic cause of nausea, which affects 70% of women in the first trimester. Hyperemesis gravidarum is a severe form of nausea of pregnancy that can produce significant fluid loss and electrolyte disturbances. Uremia, ketoacidosis, and adrenal insufficiency, as well as parathyroid and thyroid disease, are other metabolic causes of emesis. Circulating toxins evoke emesis via effects on the area postrema. Endogenous toxins are generated in fulminant liver failure exogenous enterotoxins may be produced by enteric bacterial infection. Ethanol intoxication is a common toxic etiology of nausea and vomiting. HISTORY AND PHYSICAL EXAMINATION The history helps define the etiology of unexplained nausea and vomiting. Drugs, toxins, and gastrointestinal infections commonly cause acute symptoms, whereas established illnesses evoke chronic complaints. Pyloric obstruction and gastroparesis produce vomiting within one hour of eating, whereas emesis from intestinal obstruction occurs later. HISTORY AND PHYSICAL EXAMINATION Hematemesis raises suspicion of an ulcer, malignancy, or Mallory- Weiss tear, feculent emesis is noted with distal intestinal or colonic obstruction. Bilious vomiting excludes gastric obstruction, emesis of undigested food is consistent with a Zenker's diverticulum or achalasia. HISTORY AND PHYSICAL EXAMINATION Relief of abdominal pain by emesis characterizes intestinal obstruction. vomiting has no effect on pancreatitis or cholecystitis pain. Pronounced weight loss raises concern about malignancy or obstruction. Fevers suggest inflammation. an intracranial source is considered if there are headaches or visual field changes. Vertigo or tinnitus indicates labyrinthine disease. HISTORY AND PHYSICAL EXAMINATION The physical examination complements information from the history. Orthostatic hypotension and reduced skin turgor indicate intravascular fluid loss. Pulmonary abnormalities raise concern for aspiration of vomitus. Abdominal auscultation may reveal absent bowel sounds with ileus. HISTORY AND PHYSICAL EXAMINATION High-pitched rushes suggest bowel obstruction, a succussion splash upon abrupt lateral movement of the patient is found with gastroparesis or pyloric obstruction. Tenderness or involuntary guarding raises suspicion of inflammation. fecal blood suggests mucosal injury from ulcer, ischemia, or tumor. Neurologic disease presents with papilledema, visual field loss, or focal neural abnormalities. Neoplasm is suggested by palpation of masses or adenopathy. DIAGNOSTIC TESTING Electrolyte replacement is indicated for hypokalemia or metabolic alkalosis. Detection of iron-deficiency anemia mandates a search for mucosal injury. Pancreaticobiliary disease is indicated by abnormal pancreatic or liver biochemistries. endocrinologic, rheumatologic, or paraneoplastic etiologies are suggested by hormone or serologic abnormalities. If bowel obstruction is suspected, supine and upright abdominal radiographs may show intestinal air-fluid levels with reduced colonic air. Ileus is characterized by diffusely dilated air-filled bowel loops. DIAGNOSTIC TESTING Anatomic studies may be indicated if initial testing is nondiagnostic. Upper endoscopy detects ulcers or malignancy. small-bowel barium radiography diagnoses partial intestinal obstruction. Colonoscopy or contrast enema radiography can detect colonic obstruction. Ultrasound or CT defines intraperitoneal inflammatory processes. CT or MRl of the head can delineate intracranial disease. Advances in CT and MRI enterography have improved definition of bowel inflammation, as in Crohn's disease. Mesenteric angiography, CT, or MRI is useful for suspected ischemia. GENERAL PRINCIPLES Therapy of vomiting is tailored to: correcting medically or surgically remediable abnormalities if possible. Hospitalization is considered for severe dehydration, especially if oral fluid replenishment cannot be sustained. Once oral intake is tolerated, nutrients are restarted with liquids that are low in fat, as lipids delay gastric emptying. ANTIEMETIC MEDICATIONS Antihistamines such as meclizine and dimenhydrinate Anticholinergic drugs like scopolamine act on labyrinthine pathways and are useful in motion sickness and inner ear disorders. ANTIEMETIC MEDICATIONS Dopamine D2 antagonists treat emesis evoked by area postrema stimuli and are useful for medication, toxic, and metabolic etiologies. Dopamine antagonists freely cross the blood-brain barrier and cause anxiety, dystonic reactions, hyperprolactinemic effects ANTIEMETIC MEDICATIONS Serotonin 5-HT3 antagonists such as ondansetron and granisetron exhibit utility in: postoperative vomiting, after radiation therapy, and for preventing cancer chemotherapyinduced emesis. ANTIEMETIC MEDICATIONS Low-dose tricyclic antidepressant agents provide symptomatic benefit in patients with: chronic idiopathic nausea functional vomiting in diabetic patients Other antidepressants such as mirtazapine also may exhibit antiemetic effects. GASTROINTESTINAL MOTOR STIMULANTS Metoclopramide, a combined 5-HT4 agonist and D, antagonist, exhibits efficacy in gastroparesis Erythromycin, a macrolide antibiotic, increases gastroduodenal motility by action on receptors for motilin, an endogenous stimulant of fasting motor activity. Intravenous erythromycin is useful for inpatients with refractory gastroparesis; however, oral forms also have some utility. GASTROINTESTINAL MOTOR STIMULANTS Domperidone, exhibits prokinetic and antiemetic effects but does not cross into most other brain regions; thus, anxiety and dystonic reactions are rare. SELECTED CLINICAL SETTINGS Some cancer chemotherapeutic agents such as cisplatin are intensely emetogenic Given prophylactically, 5-HTJ antagonists prevent chemotherapyinduced acute vomiting in most cases SELECTED CLINICAL SETTINGS Neurokinin NKI antagonists (e.g., aprepitant) exhibit antiemetic and antinausea effects during both the acute and delayed periods after chemotherapy. Cannabinoids such as tetrahydrocannabinol, long advocated for cancer-associated emesis, produce significant side effects and exhibit no more efficacy than antidopaminergic agents. SELECTED CLINICAL SETTINGS The clinician should exercise caution in managing the pregnant patient with nausea. antihistamines such as meclizine and antidopaminergics such as prochlorperazine demonstrate efficacy greater than placebo. Some obstetricians offer alternative therapies such as pyridoxine, or ginger. SELECTED CLINICAL SETTINGS Controlling emesis in cyclic vomiting syndrome is a challenge. In many patients, prophylaxis with tricyclic antidepressants, cyproheptadine, or p-adrenoceptor antagonists can reduce the frequency of attacks. Intravenous 5-HT3 antagonists combined with the sedating effects of a benzodiazepine such as lorazepam are a mainstay of treatment of acute symptom flares.
