Nausea and Vomiting

Educational Objectives

The goal of this program is to improve the management of nausea and vomiting and gastroparesis. After hearing and assimilating this program, the clinician will be better able to:

1. Identify the cause of nausea and vomiting.

2. Evaluate and treat patients with nausea and vomiting.

3. Explain the pathophysiology of gastric neuromuscular disorders.

Summary

Case example 1: 18-yr-old man with intermittent nausea for several years; nausea worsened and became constant after he started college; vomiting intermittent (3-4 times/day); loss of appetite and early satiety reported; patient denied heartburn and regurgitation, but had lost weight; endoscopy showed some retained food in stomach; gastric-emptying study (GES) normal; metoclopramide (Reglan) not beneficial; fasting cortisol and celiac panel negative; patient taking medications for pulmonary symptoms and anxiety; patient has history of irritable bowel syndrome (IBS); denies smoking and consumption of alcohol; review of systems positive for back pain, dizziness, headaches, anxiety, and depression; weight 130 lb; physical examination within normal limits

Causes of chronic nausea: determine whether nausea associated with pain syndrome; anatomic — obstruction; peptic disease; peritoneal irritation; carcinoma — gastric; ovarian; hypernephroma; paraneoplastic syndrome; metabolic or hormonal — diabetes; uremia; Addison disease; hypercalcemia; pregnancy; drugs; postoperative — vagotomy; partial gastrectomy; fundoplication; other causes — chronic mesenteric ischemia (rare); neuromuscular disorders of stomach and gastrointestinal (GI) tract (including headaches); psychiatric or psychologic disorders related to eating (may have component of nausea)

Evaluation: history, physical examination, and laboratory testing; most patients placed on empiric trial of proton pump inhibitors (PPIs), antinauseant, antiemetic, or prokinetic drugs (if stomach motility problem suspected); endoscopy — used to detect inflammation (eg, esophagitis, gastritis) in lining of mucosa possibly requiring additional therapy; normal ≈80% of time; if normal, consider gastric neuromuscular abnormalities

Gastric rhythm: pacemaker region located between fundus and body of stomach; electrical frequency circles stomach and migrates to pylorus at rate of 3 cycles/min (cpm; frequency for most efficient mixing and emptying of food); pacemaker cells known as interstitial cells of Cajal (ICC) allow signal to circle and propagate every 20 sec; enteric nerves add acetylcholine to contract stomach, or nitric oxide to relax stomach, especially in response to meals; autonomic nervous system (ANS), central nervous system (CNS), and hormones involved; neuromuscular events required for proper mixing and emptying of food complex and coordinated; electrogastrography (EGG) — records electrical activity and calculates rhythm (cpm); provocative test requiring ingestion of 750 mL of water over 5 min; normal range 2.5 to 3.7 cpm

Rhythm shift: onset of nausea may be due to shift in electrical rhythm (ie, from eurhythmia to dysrhythmia [tachygastria and bradygastria]); study looking at nausea during pregnancy found that electrical rhythm correlated with occurrence of nausea; rotating drum used to create illusion of motion to induce nausea while electrical rhythm recorded (individuals begin to experience nausea related to motion as rhythm shifts); migraine may have central influence that moves downward; motion sickness mostly visual stimulation but affects stomach; other GI inputs also affect stomach; dynamic interaction exists between stomach, ANS, brain, and perception

Differential diagnosis: chronic idiopathic nausea — bothersome nausea occurring several times per week; not usually associated with vomiting; no sign of abnormalities on upper endoscopy or metabolic disease that explain nausea; functional vomiting — vomiting occurs ≥1 time/wk; individuals do not have eating disorder, rumination (effortless regurgitation of food), self-induced vomiting, chronic cannabinoid use, CNS problems, or metabolic disease; cannabinoid hyperemesis — patient history of long-term cannabis use necessary for diagnosis; nausea and vomiting severe; resolves with cessation of cannabis; symptoms relieved with hot shower; mechanism unknown; sometimes associated with pain; usually occurs in individuals <50 yr of age; symptoms include weight loss and morning nausea; bowel habits normal; laboratory tests normal; cyclic vomiting syndrome — stereotypic episodes of vomiting that begin acutely and last 3 to 5 days; resolves suddenly; associated with personal or family history of migraines; possibly migraine with interaction between CNS and stomach; most common in children and adolescents

Gastric neuromuscular evaluation: performed in patients who have unexplained nausea and vomiting and normal findings on endoscopy, computed tomography, and brain imaging; study — workup included GES and EGG in response to water challenge; ≈50% of participants had delayed gastric emptying and 80% had dysrhythmia; 20% with delayed gastric emptying had normal rhythm, which suggested pyloric dysfunction (pyloric stenosis or pylorospasm); 60% with normal gastric emptying had dysrhythmia only; remaining group had normal gastric emptying and normal rhythm (problem may not involve stomach)

Treatment: metoclopramide — effective short-term treatment for nausea (improves rhythm and emptying); side-effects (eg, tardive dyskinesia) associated with long-term use; 5-hydroxytryptamine (HT)4 agonist and dopamine (D)2 antagonist; other side effects include Parkinson-like symptoms and depression; 25% to 40% of patients have difficulty tolerating side effects; prescribe 10 mg 4 times daily and taper to 5 mg or less; erythromycin — motilin agonist (allows stomach to contract with increased force); low doses recommended; domperidone — peripheral D2 antagonist (not available in United States); diet — patients with frequent dehydration advised to replenish with liquids containing salt and potassium (eg, “sports drinks” and bouillon); patients can then progress to soups (easy for stomach to mix and empty); nonspecific drug treatments — include ondansetron (Zofran, Zuplenz), granisetron patch, mirtazapine (Remeron), dronabinol (Marinol; cannabinoid receptor agonist), and lorazepam (Ativan; beneficial for anxiety associated with chronic nausea)

Location of nausea: ask patient to indicate location; of 200 patients, nausea localized in epigastrium in one-third, epigastrium and chest in one-third, periumbilical area in 14%, and substernal area in 12%

Case example 1, continued: 4-hr GES attempted, but patient vomited meal after 1 hr (no result obtained); EGG showed bradygastria, but patient drank adequate volume of water; tilt table test abnormal (blood pressure and pulse rate decreased, and patient developed nausea); patient started on fludrocortisone and advised to increase intake of salt; significant improvement seen after 1 mo (patient able to resume eating and return to school); patient believed to have postural orthostatic tachycardia syndrome with nausea (ANS disorder)

Caveats in differential diagnosis: nausea could be associated with atypical gastroesophageal reflux disease, small-bowel bacterial overgrowth, or IBS; non–GI tract causes — cannabinoid hyperemesis; Addison disease; hypo- or hyperthyroidism; postural orthostatic tachycardia syndrome; temporal lobe seizures; migraines

Readings

Suggested Readings

Bielefeldt K: Factors influencing admission and outcomes in gastroparesis. Neurogastroenterol Motil, 2013 May;25(5):389-98, e294; Broad J et al: Regional- and agonist-dependent facilitation of human neurogastrointestinal functions by motilin receptor agonists. Br J Pharmacol, 2012 Oct;167(4):763-74; Chaudrey KH et al: Idiopathic gastroparesis: case report and literature review of diagnostic and treatment modalities. Am J Ther, 2013 Jan;20(1):111-7; Evans RW, Whyte C: Cyclic vomiting syndrome and abdominal migraine in adults and children. Headache, 2013 Jun;53(6):984-93; Faussone-Pellegrini MS et al: NIDDK Gastroparesis Clinical Research Consortium (GpCRC). Ultrastructural differences between diabetic and idiopathic gastroparesis. J Cell Mol Med, 2012 Jul;16(7):1573-81; Gourcerol G et al: Long term efficacy of gastric electrical stimulation in intractable nausea and vomiting. Dig Liver Dis, 2012 Jul;44(7):563-8; Kloetzer L et al: Motility of the antroduodenum in healthy and gastroparetics characterized by wireless motility capsule. Neurogastroenterol Motil, 2010 May;22(5):527-33, e117; McCallum RW et al: Gastric electrical stimulation improves outcomes of patients with gastroparesis for up to 10 years. Clin Gastroenterol Hepatol, 2011 Apr;9(4):314-319.e1; Morris R, Fisher M: Cannabinoid hyperemesis syndrome: a specific cause of cyclical vomiting. Int J Adolesc Med Health, 2014;26(1):153-6; Nimgaonkar A et al: Gastrointestinal dysmotility. Dig Dis Sci, 2012 May;57(5):1130-3; O’Loughlin PM et al: Pre-operative gastric emptying time correlates with clinical response to gastric electrical stimulation in the treatment of gastroparesis. Surgeon, 2013 Jun;11(3):134-40; Pasricha PJ et al: Characteristics of patients with chronic unexplained nausea and vomiting and normal gastric emptying. Clin Gastroenterol Hepatol, 2011 Jul;9(7):567-76.e1-4; Reddymasu SC et al: Efficacy of gastric electrical stimulation in improving functional vomiting in patients with normal gastric emptying. Dig Dis Sci, 2010 Apr;55(4):983-7.

Disclosures

In adherence to ACCME Standards for Commercial Support, Audio-Digest requires all faculty and members of the planning committee to disclose relevant financial relationships within the past 12 months that might create any personal conflicts of interest. Any identified conflicts were resolved to ensure that this educational activity promotes quality in health care and not a proprietary business or commercial interest. For this program, the following has been disclosed: Dr. Koch is a consultant for GlaxoSmithKline and Targacept, receives grant/research support from COOK Medical, and owns stock in 3CPM Company. The planning committee reported nothing to disclose.

Acknowledgements

Dr. Koch was recorded at the 43rd Annual Emery C. Miller Medical Symposium, held July 28 to August 1, 2014, in Myrtle Beach, SC, and sponsored by Wake Forest School of Medicine. For information about upcoming CME activities presented by Wake Forest School of Medicine, please visit www.wakehealth.edu. The Audio Digest Foundation thanks Dr. Koch and Wake Forest School of Medicine for their cooperation in the production of this program.

CME/CE INFO

Accreditation:

The Audio- Digest Foundation is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.

The Audio- Digest Foundation designates this enduring material for a maximum of 0 AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

Audio Digest Foundation is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center's (ANCC's) Commission on Accreditation. Audio Digest Foundation designates this activity for 0 CE contact hours.

Lecture ID:

IM621201

Expiration:

This CME course qualifies for AMA PRA Category 1 Credits™ for 3 years from the date of publication.

Instructions:

To earn CME/CE credit for this course, you must complete all the following components in the order recommended: (1) Review introductory course content, including Educational Objectives and Faculty/Planner Disclosures; (2) Listen to the audio program and review accompanying learning materials; (3) Complete posttest (only after completing Step 2) and earn a passing score of at least 80%. Taking the course Pretest and completing the Evaluation Survey are strongly recommended (but not mandatory) components of completing this CME/CE course.

Estimated time to complete this CME/CE course:

Approximately 2x the length of the recorded lecture to account for time spent studying accompanying learning materials and completing tests.