eMedicine Specialties > Pediatrics: General Medicine > Gastroenterology

Cyclic Vomiting Syndrome: Treatment & Medication

Author: Thangam Venkatesan, MBBS, Assistant Professor, Department of Internal Medicine, Division of Gastroenterology and Hepatology, Medical College of Wisconsin
Coauthor(s): B UK Li, MD, Professor of Pediatrics, Division of Gastroenterology, Hepatology and Nutrition, Director, Pediatric Fellowships and Gastroenterology Fellowship, Medical Director, Functional Gastrointestinal Disorders and Cyclic Vomiting Program, Medical College of Wisconsin; Attending Gastroenterologist, Children's Hospital of Wisconsin; Seth Marcus, MD, Fellow, Department of Pediatric Gastroenterology, Hepatology and Nutrition, Children's Memorial Hospital, Northwestern University; Shikha Sundaram, MD, Fellow, Department of Gastroenterology, Hepatology and Nutrition, Children's Memorial Hospital of Chicago and Northwestern University; Abhilasha Pandey, MBBS, Froedtert Hospital, Medical College of Wisconsin
Contributor Information and Disclosures

Updated: Oct 29, 2009

Treatment

Medical Care

In the absence of known pathophysiology, treatment of cyclic vomiting syndrome (CVS) remains empiric.17,45 The following 5 management strategies are used for cyclic vomiting syndrome: avoidance of triggers, prophylactic pharmacotherapy, abortive therapy, supportive care during acute episodes, and family support.28

Pharmacologic therapy is used to prevent episodes of vomiting or to decrease their frequency. Other medications may be used to abort or attenuate episodes once they begin. Preventive medications are normally used in patients with more than a single episode of cyclic vomiting syndrome per month. The mainstays of prophylactic therapy include cyproheptadine, amitriptyline, propranolol, phenobarbital, and erythromycin. If abortive therapy fails, supportive combinations such as ondansetron plus lorazepam or chlorpromazine plus diphenhydramine may attenuate an attack of cyclic vomiting in progress.

In some instances, avoiding identified dietary triggers, such as chocolate, cheese, and monosodium glutamate (MSG) can prevent episodes without the use of medication.28 If psychological stressors trigger episodes, stress management techniques or benzodiazepine anxiolytics (lorazepam or diazepam) may help to abort attacks in the early stages. However, avoiding common triggers such as car rides and infection may be impractical or impossible. Interestingly, a 70% decrease in frequency of episodes (placebo effect) upon consultation and lifestyle changes without drug therapy has been noted.10

Daily prophylactic pharmacotherapy may be used to prevent episodes that occur more than once per month or if they are extremely severe and disabling (eg, lasting ³ 3 d).46,47 Most of these drugs are non-GI medications, such as antimigraine agents, anticonvulsants, neuroleptics, and prokinetic drugs. A family history positive for migraines predicts a high response rate (80%) to antimigraine medications; therefore, these agents are a logical first choice.28

In an open-label experience, with efficacy defined as greater than 50% reduction in episode frequency or severity, propranolol, cyproheptadine, and amitriptyline were effective 57%, 39%, and 67% of the time, respectively.34,48 The NASPGHAN guidelines recommend cyproheptadine as first-line therapy in children younger than 5 years. However, cyproheptadine can cause substantial weight gain because of an increase in appetite. Amitriptyline is the first-line choice in children older than 5 years and adolescents.28 Phenobarbital demonstrated a 79% success rate in one open-label trial in children who did not have EEG changes.49 Erythromycin, a gastric prokinetic agent, demonstrated a 75% success rate in one open-label study.50

Winner et al reported a significant reduction (>75%) in days with migraine headaches in patients receiving topiramate compared with placebo.51 Topiramate is currently used anecdotally in patients with cyclic vomiting syndrome. Another small therapeutic trial using L-carnitine reported reduced episode frequency and neurologic symptoms in patients with cyclic vomiting syndrome.52

In adults few studies are available; in one study, the overall treatment response in 24 adult patients receiving amitriptyline (1 mg/kg/day) for at least 3 months indicated that 93% had decreased symptoms and 26% achieved full remission.53

In a study of 132 patients with cyclic vomiting syndrome who had been monitored for 4 years, 17 subjects were identified as nonresponders to therapy with tricyclic antidepressants.41 When compared with responders, the nonresponders were significantly more likely to have a history of migraine (p <0.05), coexisting psychological disorders (p <0.05), chronic marijuana use (p <0.05), and reliance on narcotics for pain control between cyclic vomiting syndrome episodes (p <0.05). These findings favor a multidisciplinary approach to these patients, with aggressive treatment of other comorbid illnesses. 

In another study, 20 adult patients with cyclic vomiting syndrome received zonisamide (median dose, 400 mg/d) or levetiracetam (median dose, 1000 mg/d) because tricyclic antidepressants alone were unsatisfactory as maintenance medications. At least moderate clinical response was reported in 15 subjects (75%), and 4 of these (20%) reported symptomatic remission during 9.5 ± 1.8 months of follow-up. Newer antiepileptic agents appeared beneficial as maintenance medications for nearly three fourths of adults with cyclic vomiting syndrome.54

Abortive agents may be taken at the onset of an attack to stop progression when prophylactic medication fails or is not taken because of the sporadic and infrequent occurrence of cyclic vomiting episodes (<1/mo). These antinausea and antimigraine agents are best administered nasally, rectally, or parenterally because they are not usually tolerated by mouth during intractable emesis.43 Sumatriptan, a 5-hydroxytryptamine receptor 1B/1D (5-HT1B/1D) agonist used off-label, has a 46% efficacy rate when administered either intranasally or subcutaneously. The subcutaneous route has fallen out of favor because of a severe associated burning sensation in the chest and neck.55

Ondansetron, a 5-hydroxytryptamine receptor 3 (5-HT3) antagonist, is a potent and effective antiemetic that acts on the chemoreceptor zone in the brainstem. In cyclic vomiting syndrome, it is more effective at a higher dose of 0.3-0.4 mg/kg every 6 hours and is rendered more effective in severe episodes with use of a benzodiazepine or diphenhydramine as an adjunctive antinausea agent.1 High-dose intravenous ondansetron has a 59% efficacy rate and ameliorates episodes more often than it aborts episodes. Aprepitant, a promising tachykinin (NK-1)-receptor antagonist, is used for chemotherapy-induced emesis and could have benefit in cyclic vomiting syndrome.43

When both prophylactic and abortive therapy fail, supportive care becomes an essential aspect of treatment during acute episodes. Intravenous glucose-containing fluids may diminish the severity of episodes by as much as 42%.43 Glucose may be the active ingredient by truncating the ketosis. However, the abdominal pain may be severe enough to require nonsteroid anti-inflammatory drugs (NSAIDs) or narcotics once a surgical abdomen has been excluded. Sedatives such as diphenhydramine, lorazepam, and chlorpromazine have been administered to permit sleep and to provide temporary respite from unrelenting nausea.43 The combined use of lorazepam and ondansetron appears to be more effective than ondansetron alone.

Families are also encouraged to contact the Cyclic Vomiting Syndrome Association, which is an international voluntary organization that serves the needs of patients in the United States and Canada, for ongoing support and information.

Medication

Antiemetic agents

The CNS vomiting center (VC) may be stimulated directly by GI irritation, motion sickness, or vestibular neuritis. Increased activity of central neurotransmitters, such as dopamine in the chemoreceptor trigger zone (CTZ) or acetylcholine in the VC, appear to be major mediators of vomiting. An emetogenic episode may initiate the release of serotonin (5-HT) from enterochromaffin cells in the GI tract. 5-HT then binds to 5-HT3 receptors that stimulate vagal neurons that transmit signals to the VC, resulting in nausea and vomiting. Pharmacologic agents are directed to the particular etiology or mechanism that stimulates the vomiting response.


Cyproheptadine (Periactin)

Nonselective antihistamine effective in CVS and for migraines.
Also an appetite stimulant. Therapeutic effects are observed within 1-2 wk. Excellent choice for children <5 y.

Adult

Pediatric

0.3 mg/kg/d PO divided bid/tid

Potentiates effects of CNS depressants; MAOIs may prolong and intensify anticholinergic and sedative effects of antihistamines

Documented hypersensitivity; narrow-angle glaucoma; stenosing peptic ulcer; symptomatic prostatic hypertrophy; bladder neck obstruction; pyloroduodenal obstruction; lower respiratory tract symptoms; overweight children

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution if predisposition to urinary retention, history of bronchial asthma, increased intraocular pressure, hyperthyroidism, cardiovascular disease, or hypertension; may thicken bronchial secretions caused by anticholinergic properties; may inhibit expectoration and sinus drainage; may cause common anticholinergic effects (eg, dizziness, dry mouth, constipation, blurred vision); sedation; substantial weight gain may limit utility


Amitriptyline (Elavil)

TCAs such as amitriptyline are excellent first-line choices in children >5 y. Has anticholinergic and sedating side effects; thus, best administered at bedtime. Cardiac arrhythmia, especially in overdose, has been described; monitoring the QTc interval both before starting and after reaching the target level is advised. Up to 1 mo may be needed to see clinical effects.

Adult

Pediatric

0.3-0.5 mg/kg PO initially; titrate upward by 10 mg/wk to goal dose of 1 mg/kg/d qhs; typical doses are listed below:
<6 years: 10-30 mg/d PO
6-12 years: 30-50 mg/d PO
>12 years: 50-75 mg/d PO

Phenobarbital may decrease effects; coadministration with CYP2D6 enzyme system inhibitors (eg, cimetidine, quinidine) may increase levels; inhibits hypotensive effects of guanethidine; may interact with thyroid medications, alcohol, CNS depressants, barbiturates, and disulfiram

Documented hypersensitivity; MAOIs in past 14 d; history of seizure, cardiac arrhythmia, glaucoma, or urinary retention

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in cardiac conduction disturbances, history of hyperthyroidism, and renal and hepatic impairment


Propranolol (Inderal)

Beta-adrenergic blocker and excellent first-line agent for prophylaxis when used at low doses. Has a 57% efficacy rate, with efficacy defined as 50% reduction in frequency and severity of episodes. Requires 1 wk for efficacy and requires gradual withdrawal over 1 wk. Dose may be monitored by fall in presleep resting pulse from baseline. Decline <15-20 bpm indicates dose may be further increased.

Adult

Pediatric

0.5-1 mg/kg/d PO divided bid/tid; typical dose is 10-20 mg PO bid/tid

Coadministration with aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, or rifampin may decrease propranolol effects; calcium channel blockers, cimetidine, loop diuretics, and MAOIs may increase propranolol toxicity; propranolol may increase toxicity of alpha1-blockers, hydralazine, haloperidol, benzodiazepines, and phenothiazines

Documented hypersensitivity; uncompensated congestive heart failure; bradycardia; cardiogenic shock; AV conduction abnormalities; asthma

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Beta-adrenergic blockade may decrease signs of acute hypoglycemia and hyperthyroidism; abrupt withdrawal may exacerbate symptoms of asthma or hyperthyroidism, including thyroid storm; slowly withdraw and closely monitor; common adverse effects include mild hypotension, bradycardia, and fatigue


Phenobarbital (Luminal)

May be used in patients with or without EEG changes. A 79% response rate has been observed in patients with CVS.

Adult

Pediatric

2-3 mg/kg PO qhs; may require 2-3 wk to observe effect

May decrease effects of chloramphenicol, digitoxin, corticosteroids, carbamazepine, theophylline, verapamil, metronidazole, and anticoagulants (patients stabilized on anticoagulants may require dosage adjustments if added to or withdrawn from their regimen); coadministration with alcohol may produce additive CNS effects and death; chloramphenicol, valproic acid, and MAOIs may increase phenobarbital toxicity; rifampin may decrease phenobarbital effects; induction of microsomal enzymes may result in decreased effects of oral contraceptives in women (must use additional contraceptive methods to prevent unwanted pregnancy; menstrual irregularities may also occur)

Documented hypersensitivity; severe respiratory disease; acute intermittent porphyria; marked impairment of liver function; nephritic patients

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

In prolonged therapy, evaluate hematopoietic, renal, hepatic, and other organ systems; caution in fever, hyperthyroidism, diabetes mellitus, and severe anemia because adverse reactions can occur; caution in myasthenia gravis and myxedema; long-term use can be associated with cognitive impairment


Erythromycin (E.E.S., Eryc, E-Mycin, Erythrocin)

Gastric prokinetic that stimulates coordinated gastric emptying. A 75% response rate has been demonstrated in patients with CVS.

Adult

Pediatric

20 mg/kg/d PO divided bid/qid

Coadministration may increase toxicity of theophylline, digoxin, carbamazepine, and cyclosporine; may potentiate anticoagulant effects of warfarin; coadministration with lovastatin and simvastatin increases risk of rhabdomyolysis; inhibits CYP3A4; caution with coadministration of isoenzyme substrates

Documented hypersensitivity; hepatic impairment

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in liver disease; estolate formulation may cause cholestatic jaundice; GI adverse effects are common; discontinue use if nausea, vomiting, malaise, abdominal colic, or fever occurs; may cause cramping at higher doses


Ondansetron (Zofran)

This 5-HT3 antagonist directly acts at the CTZ and vagal afferents from the GI tract. Attenuates or occasionally aborts an active episode of CVS. High dose more effective in patients with CVS.

Adult

Pediatric

<3 years: Not established
>3 years: 0.3-0.4 mg/kg/dose IV q6h

CYP450 inducers such as barbiturates, rifampin, carbamazepine, and phenytoin can potentially change half-life and clearance of ondansetron, but dosage adjustment usually not required

Documented hypersensitivity; hepatic impairment

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

May cause constipation or headache


Sumatriptan (Imitrex)

This 5-HT1B/1D agonist may effectively terminate an episode of CVS by constricting cerebral vasculature. High dose more effective in patients with CVS.

Adult

Pediatric

<40 kg: Not established
>40 kg: Up to 20 mg intranasally prn

Toxicity increases when administered concomitantly with ergot-containing drugs, SSRIs, and MAOIs

Documented hypersensitivity; ischemic heart disease; uncontrolled hypertension

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May cause burning sensation of chest or neck (<40% with injectable form, uncommon in nasal form); hypertensive crisis, coronary artery vasospasm, cardiac arrest, peripheral ischemia, and bloody diarrhea may rarely occur


Lorazepam (Ativan)

Because of both their sedative and antinausea properties, sedatives may be helpful. Induce sedation and anxiolysis through central GABA inhibition. Appears synergistic with the antinausea and antiemetic effects of 5-HT3 antagonists. Concomitant sedation and induction of sleep provide sustained relief from intractable nausea.

Adult

Pediatric

0.05-0.1 mg/kg/dose IV q6h prn; not to exceed 4 mg/dose

Toxicity of benzodiazepines in CNS increases when used concurrently with alcohol, phenothiazines, barbiturates, and MAOIs

Documented hypersensitivity; preexisting CNS depression; hypotension; narrow-angle glaucoma

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in renal or hepatic impairment, myasthenia gravis, organic brain syndrome, or Parkinson disease


Diphenhydramine (Benadryl)

For treatment and prophylaxis of vestibular disorders that may cause nausea and vomiting. Provides mild sedation and synergistic antinausea and antiemetic action with 5-HT3 antagonists.

Adult

Pediatric

Infants: Contraindicated
Children: 1.25 mg/kg/dose PO q6h; not to exceed 300 mg/d

Potentiates effects of CNS depressants; because of alcohol content, do not give syrup form to patients taking medications that can cause disulfiram-like reactions

Documented hypersensitivity; MAOIs; infants

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May exacerbate narrow-angle glaucoma, hyperthyroidism, peptic ulcer, and urinary tract obstruction; xerostomia may occur

More on Cyclic Vomiting Syndrome

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Treatment & Medication: Cyclic Vomiting Syndrome
Follow-up: Cyclic Vomiting Syndrome
Multimedia: Cyclic Vomiting Syndrome
References
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Further Reading

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Keywords

cyclic vomiting syndrome, CVS, vomit, emesis, migraine, syndrome of mitochondrial myopathy, encephalopathy, lactic acidosis, strokelike episodes, MELAS syndrome, abdominal migraine, rotavirus gastroenteritis, gastroesophageal reflux

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Contributor Information and Disclosures

Author

Thangam Venkatesan, MBBS, Assistant Professor, Department of Internal Medicine, Division of Gastroenterology and Hepatology, Medical College of Wisconsin
Thangam Venkatesan, MBBS is a member of the following medical societies: American Gastroenterological Association and Indian Medical Association
Disclosure: Nothing to disclose.

Coauthor(s)

B UK Li, MD, Professor of Pediatrics, Division of Gastroenterology, Hepatology and Nutrition, Director, Pediatric Fellowships and Gastroenterology Fellowship, Medical Director, Functional Gastrointestinal Disorders and Cyclic Vomiting Program, Medical College of Wisconsin; Attending Gastroenterologist, Children's Hospital of Wisconsin
B UK Li, MD is a member of the following medical societies: Alpha Omega Alpha, American Gastroenterological Association, and North American Society for Pediatric Gastroenterology and Nutrition
Disclosure: Nothing to disclose.

Seth Marcus, MD, Fellow, Department of Pediatric Gastroenterology, Hepatology and Nutrition, Children's Memorial Hospital, Northwestern University
Seth Marcus, MD is a member of the following medical societies: American Academy of Pediatrics and North American Society for Pediatric Gastroenterology and Nutrition
Disclosure: Nothing to disclose.

Shikha Sundaram, MD, Fellow, Department of Gastroenterology, Hepatology and Nutrition, Children's Memorial Hospital of Chicago and Northwestern University
Shikha Sundaram, MD is a member of the following medical societies: American Academy of Pediatrics and American Medical Association
Disclosure: Nothing to disclose.

Abhilasha Pandey, MBBS, Froedtert Hospital, Medical College of Wisconsin
Disclosure: Nothing to disclose.

Medical Editor

Jayant Deodhar, MD, Associate Professor in Pediatrics, BJ Medical College, India; Honorary Consultant, Departments of Pediatrics and Neonatology, King Edward Memorial Hospital, India
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

David A Piccoli, MD, Chief of Pediatric Gastroenterology, Hepatology and Nutrition, The Children's Hospital of Philadelphia; Professor, University of Pennsylvania School of Medicine
David A Piccoli, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American Gastroenterological Association, and North American Society for Pediatric Gastroenterology and Nutrition
Disclosure: Nothing to disclose.

CME Editor

Steven M Schwarz, MD, FAAP, FACN, AGAF, Professor of Pediatrics, Children's Hospital at Downstate, SUNY-Downstate Medical Center
Steven M Schwarz, MD, FAAP, FACN, AGAF is a member of the following medical societies: American Academy of Pediatrics, American College of Nutrition, American College of Physician Executives, American Gastroenterological Association, American Pediatric Society, Gastroenterology Research Group, New York Academy of Medicine, North American Society for Pediatric Gastroenterology and Nutrition, and Society for Pediatric Research
Disclosure: TAP Pharmaceuticals Honoraria Speaking and teaching; Curemark, LLC Consulting fee Board membership; Centocor, Inc. Grant/research funds Independent contractor

Chief Editor

Carmen Cuffari, MD, Associate Professor, Department of Pediatrics, Division of Gastroenterology/Nutrition, Johns Hopkins University School of Medicine
Carmen Cuffari, MD is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, North American Society for Pediatric Gastroenterology, Hepatology and Nutrition, and Royal College of Physicians and Surgeons of Canada
Disclosure: Nothing to disclose.

 
 
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