eMedicine Specialties > Pediatrics: General Medicine > Gastroenterology

Cyclic Vomiting Syndrome

Author: Thangam Venkatesan, MBBS, Assistant Professor, Department of Internal Medicine, Division of Gastroenterology and Hepatology, Medical College of Wisconsin
Coauthor(s): B U K 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
Contributor Information and Disclosures

Updated: Nov 19, 2008

Introduction

Background

Cyclic vomiting syndrome (CVS) is a chronic functional disorder of unknown etiology that is characterized by paroxysmal, recurrent episodes of vomiting and was first described in children by Samuel Gee in 1882. Although this was initially thought to occur mostly in children, it is being recognized with increasing frequency in adults. Although the pathophysiology is unknown, various mechanisms such as corticotropin-releasing factor (CRF) and a heightened sympathetic response may play a role. Recent data also suggest a strong genetic component, with evidence of mitochondrial heteroplasmies that predispose to cyclic vomiting syndrome and other related disorders, such as migraine and chronic fatigue syndrome.

Pathophysiology

The etiology, pathophysiology, and target organ in cyclic vomiting syndrome remain unknown. Over the last decade, studies have proposed several potential brain-gut mechanisms. Migraine-related mechanisms have been proposed, and patients with cyclic vomiting syndrome have a significantly higher prevalence of family members with migraine headaches (82% vs 14% of control subjects with a chronic vomiting pattern). Furthermore, 28% of patients with cyclic vomiting syndrome whose vomiting subsequently resolved developed migraine headaches. Finally, 80% of affected patients with family histories positive for migraine respond to antimigraine therapy.1

Mitochondrial DNA mutations may be involved in the pathogenesis of cyclic vomiting syndrome. Boles et al have demonstrated that, among children with cyclic vomiting syndrome and neuromuscular disease, 86% have a history of migraines on the matrilineal side. Boles and colleagues also reported a large mitochondrial DNA deletion in a single child with cyclic vomiting syndrome and have identified additional mutations concentrated in the D-loop, a hypervariable locus of the control region, in other children with cyclic vomiting syndrome.2

Children with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke (MELAS) syndrome are known to have both severe migraines and episodic vomiting, as in cyclic vomiting syndrome.3 Several children with cyclic vomiting syndrome, including 4 members of an Italian family, have recently been reported to have various mitochondrial mutations.4,5

Sympathetic hyperresponsivity and autonomic dysfunction also appear to contribute to the pathogenesis of cyclic vomiting syndrome.6 Many associated symptoms, such as pallor, flushing, fever, lethargy, salivation, and diarrhea, are mediated by the autonomic nervous system.7,8,9  

Several studies support altered autonomic function in cyclic vomiting syndrome. Rashed et al (1999)10 and To et al (1999)11 demonstrated a heightened sympathetic cardiovascular tone in patients with cyclic vomiting syndrome. Kasawinah et al (2003) reported the successful use of dexmedetomidine, an alpha-2 adrenergic agonist, to treat cyclic vomiting syndrome.12 In a small study involving 6 children with cyclic vomiting syndrome, all patients had sympathetic autonomic dysfunction, affecting mainly the vasomotor and sudomotor systems. Symptoms developed during tilt testing in half of these patients, suggesting that these findings may play a role in the pathophysiology of this disorder.13

The stress response, mediated by the hypothalamic-pituitary-adrenal (HPA) axis, can also potentially induce episodes of cyclic vomiting syndrome. Infectious, psychological, and physical stressors are known triggers of episodes.14,15,16,17,18 Sato et al documented increased levels of adrenocorticotropic hormone (ACTH) and cortisol, associated with extreme lethargy and hypertension, before the onset of vomiting.19,20,21,22  Furthermore, Taché (1999) has definitively shown that central CRF induces gastric stasis, emesis, or both in animals.23  Therefore, CRF may be a potential brain-gut mediator of cyclic vomiting syndrome that directly connects stress and vomiting.24 If this theory holds true, CRF receptor antagonists currently in development could theoretically ablate the vomiting by blocking the CRF receptor's vagally mediated actions.25

How these pathways fit together is still unclear. Li and Misiewicz have proposed that heightened neuronal excitability due to enhanced membrane ion permeability (ion channelopathy), mitochondrial energy deficits (due to dysfunction), or hormonal state (eg, menstrual periods) may be present.1 Both physical (infection) and psychologic stressors (excitement) can initiate a known cascade that releases hypothalamic CRF, the suspected neuroendocrine trigger, resulting in vomiting. Altered brainstem regulation of these autonomic signals may be the necessary abnormality that allows the dysautonomia to feed forward and become self-sustained for days on end.

Frequency

United States

The true incidence and prevalence of cyclic vomiting syndrome are unknown. In central Ohio, amid a predominantly white population, the prevalence of cyclic vomiting syndrome in children (evaluated by the sole pediatric gastroenterology referral center) was 0.04%.26

International

Limited epidemiologic data by Cullen and MacDonald estimate the prevalence of periodic vomiting in western Australia to be 2.3%.7 Similarly, Abu-Arafeh and Russell observed a prevalence of 1.9% in school-aged children in Aberdeen, Scotland.27 Both of these figures estimate the prevalence in white populations and may not reflect all races or ethnic populations. In a study performed at KEM Hospital in Pune, India, cyclic vomiting syndrome accounted for 0.5% of admissions to pediatric wards during 1998-2000.

In a population based study in Ireland, the incidence of cyclic vomiting syndrome in Ireland was relatively common at 3.15 cases per 100,000 children in 2005 (95% confidence interval[CI],2.19-4.11). This incidence is comparable to other major GI diseases of childhood (eg, Crohn disease) in Ireland.28,29

Mortality/Morbidity

Although patients are well approximately 90% of the time, cyclic vomiting syndrome can be a medically and academically disabling disorder. More than 50% of patients require intravenous fluids, compared with less than 1% of patients with rotavirus gastroenteritis. The average annual cost of testing, treatment, and work absences totals $17,000. Children miss an average of 24 school days per year and often need home tutoring or, occasionally, home schooling. Additionally, because of its frequency during times of excitement, cyclic vomiting syndrome has ruined many birthdays, holidays, and vacations.26

In adults, significant morbidity is associated with this disorder, perhaps due to a lack of awareness and resultant delay in diagnosis. In a study of 41 patients with cyclic vomiting syndrome, Fleisher found that 32% were completely disabled at the time of diagnosis.9 A total of 293 procedures were performed in 41 patients, and none were indicative of organic etiology in these patients. In addition, 17 surgical procedures, including 10 cholecystectomies, appendectomies, exploratory laparotomies, a pyloroplasty, and a hysterectomy, were performed without any therapeutic benefit.

Adults and children with cyclic vomiting syndrome also have multiple emergency department visits, and the diagnosis is often unrecognized.30

Table 1. Emergency Department Visits in Patients With Cyclic Vomiting Syndrome

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Table
 AdultsChildren
Number of emergency department visits (Median)15 (Range, 1-200)10 (Range, 1-175)
Number of emergency department visits prior to diagnosis of cyclic vomiting syndrome (Median)7 (Range, 1- 150)5 (Range, 0-65)
Diagnosis not made in the emergency department94.5%93%
Diagnosis not recognized in the emergency department in patients with an established diagnosis of cyclic vomiting syndrome96.3%82.5%
Number of different emergency departments visited (Mean ± standard deviation)4.69 ± 4.722.6 ± 2.42
 AdultsChildren
Number of emergency department visits (Median)15 (Range, 1-200)10 (Range, 1-175)
Number of emergency department visits prior to diagnosis of cyclic vomiting syndrome (Median)7 (Range, 1- 150)5 (Range, 0-65)
Diagnosis not made in the emergency department94.5%93%
Diagnosis not recognized in the emergency department in patients with an established diagnosis of cyclic vomiting syndrome96.3%82.5%
Number of different emergency departments visited (Mean ± standard deviation)4.69 ± 4.722.6 ± 2.42

Race

Cyclic vomiting syndrome occurs in all races but seems to disproportionately affect whites.

Sex

Females show a slight predominance over males; the female-to-male ratio is 57:43.

Age

The median age at onset is 4.8 years; however, cyclic vomiting syndrome has been observed in infants as young as age 6 days and in adults as old as age 73 years.1 Typical delay in diagnosis from onset of symptoms is 2.7 years.1

In adults, the average age of onset is 21 years and average age of evaluation for recurrent vomiting was 34 years.9

Clinical

History

Cyclic vomiting syndrome (CVS) is characterized by recurrent, discrete, stereotypical episodes of rapid-fire vomiting between varying periods of completely normal health. This on-and-off stereotypic pattern of vomiting is nearly pathognomonic of cyclic vomiting syndrome. Although periods of complete normalcy typically occur between episodes, a pattern of coalescence has been described in many adult patients. Over time, these patients may lose the cyclic pattern of symptoms, and 63% of patients develop interepisodic symptoms (often nausea) between episodes, which is termed coalescence.9

The Rome III diagnostic criteria for cyclic vomiting syndrome in children includes all of the following:

  • Two or more periods of intense nausea and unremitting vomiting or retching, lasting hours to days
  • Return to usual state of health that lasts weeks to months

The cut off of 2 episodes resulted in a significant proportion of misdiagnosis; thus, the guidelines were modified and the criteria as per the North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition (NASPGHAN) are as follows (all criteria must be met):

  • At least 5 episodes, or a minimum of 3 over a 6-month period
  • Episodic attacks of intense nausea and vomiting that lasts 1 hour to 10 days, occurring at least one week apart
  • Stereotypical pattern and symptoms in the individual patient
  • Vomiting during episodes occurs at least 4 times an hour for at least one hour
  • A return to baseline health during episodes
  • Not attributed to another disorder
The Rome III criteria for cyclic vomiting syndrome in adults includes the following:
  • Stereotypical episodes of vomiting regarding onset (acute) and duration (>1 wk)
  • Three or more discrete episodes in the prior year
  • Absence of nausea and vomiting between episodes
  • No metabolic, GI, or CNS structural or biochemical disorders

Supportive criteria include history of migraine headaches and family history of migraine headaches.

The vomiting in cyclic vomiting syndrome is typically much more severe and intermittent than is observed in gastroesophageal reflux. When children with cyclic vomiting syndrome were compared with children with chronic vomiting, children with cyclic vomiting syndrome had a much higher peak rate of emeses per hour (12.6 vs 1.9) but far fewer episodes per month (1.5 vs 36).1 A cut-off criterion of at least 4 emeses per hour at peak and fewer than 2 episodes per week was 92% sensitive and 100% specific for the final diagnosis of cyclic vomiting syndrome.31 With a larger cohort, the median peak rate of emeses is still 6 times per hour.15 Only Bacillus cereus food poisoning matches this high intensity of emesis.26 This singularly severe vomiting (so-called cyclic vomiting pattern) typifies patients with cyclic vomiting syndrome and helps point toward a disorder that is localized outside the GI tract.

Persons with the cyclic pattern (high-intensity, low-frequency) tend to have extraintestinal disorders (eg, neurologic, renal, metabolic, endocrine), whereas persons with a chronic vomiting pattern (low-grade, daily) tend to have upper GI injury, such as gastroesophageal reflux and gastritis.26 The emesis is often projectile (48%) and frequently contains bile (81%), mucous (72%), and blood (34%).1 Hematemesis is more often due to retrograde herniation of the gastric cardia through the gastroesophageal junction (ie, prolapse gastropathy) than to a classic Mallory-Weiss tear.32

The "on-off" stereotypical pattern often begins with a half-hour prodrome of nausea and pallor. Vomiting peaks in the first hour and then begins to decline over the ensuing 4-8 hours, lasting a mean of 24 hours (median, 43 h). Episodes commonly occur in the early morning (2-4 am) or upon awakening (6-8 am). The recovery period from the end of vomiting to the point of being able to eat and play lasts a mere 5 hours. Despite the label cyclic, only one half of patients have a stable periodicity; the rest have sporadic intervals.26
 
Besides vomiting, patients may also experience other GI symptoms. Abdominal pain is present in 80% of patients and may initially be severe enough to mimic acute abdomen and result in a laparotomy.15 Patients may also have epigastric pain secondary to peptic injury of the esophagus.

Most patients experience retching (79%) and nausea (82%) and describe the nausea to be the most distressing symptom.1 It is unrelenting, completely unrelieved by vomiting, and disappears only when the child is asleep or the episode is over.

Many of the behavioral symptoms commonly observed in patients with cyclic vomiting syndrome (eg, fetal positioning, social withdrawal, turning off lights and televisions) are attempts to lessen nausea.26

Approximately one third of patients also experience fever, diarrhea, or both, complicating differentiation from gastroenteritis; this is likely due to associated autonomic symptoms. Autonomic symptoms are also common, particularly lethargy (93%) and pallor (91%).1 Lethargy may be profound, and patients may be unable to walk or talk or may appear comatose. Excess salivation (27%) can also be dramatic.1

Many patients with cyclic vomiting syndrome have neurologic symptoms, which supports the relationship between migraines and cyclic vomiting syndrome. Symptoms include headache (42%), photophobia (38%), phonophobia (30%), and vertigo (26%). Because fewer than one half of patients with cyclic vomiting syndrome have classic migraine symptoms, this precludes using the symptoms as diagnostic criteria for a migraine variant.1

Approximately 68% of families are able to identify events that appear to precipitate a patient's episode.7,33,15,18 The most common precipitating event is infection (41%), particularly chronic sinusitis.26  Psychological stresses (34%) and food products, including chocolate, cheese, and monosodium glutamate (MSG), rank close behind chronic sinusitis.26 Positive excitement, such as birthdays, holidays, vacations, and school outings, appear to trigger more episodes than do negative stresses. Others recognize physical exhaustion or lack of sleep (18%), atopic events (13%), motion sickness (9%), and menses (13%) as triggers.26 Many patients experience remission in the summer, when the number of infections and school stressors decline.34

The terms cyclic vomiting syndrome and abdominal migraine have often been used interchangeably because of overlap in clinical criteria. Indeed, the key criteria, except vomiting, in abdominal migraines are identical to those in cyclic vomiting syndrome and include recurrent, stereotypical, and severe episodes of abdominal pain; punctuating well periods; autonomic symptoms (eg, pallor, lethargy); and a family history of migraine headaches. Because 80% of children with cyclic vomiting syndrome have abdominal pain, and 50% of those with abdominal pain vomit, many children can be diagnosed with either cyclic vomiting syndrome or abdominal migraine. When both symptoms occur, the authors use the predominant or most consistent symptom as the primary label.

The following 3 additional criteria help strengthen the diagnosis of cyclic vomiting syndrome:26

  • Negative screening test results to exclude common GI, hepatobiliary, renal, metabolic, and endocrine disorders
  • Subsequent development of migraine headaches
  • A positive response to antimigraine medications

Table 2. Clinical Features in Adults and Children with Cyclic Vomiting Syndrome35

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Table
 ChildrenAdults
Age of Onset4.8 y (Earliest, 6 d) 35 y (Latest, 73 y)
Delay in Diagnosis2.6 y8 y
Female-to-Male Ratio57:4317:24
FrequencyEvery 2-4 wkEvery 3 mo
Duration (Mean)1-2 d (range, 1-10 d)6 d (range, 1-21 d)
Periodicity49%Not reported
Early Morning Onset42%50%
Stereotypical Episodes99%85%
Prodrome72%, 1.5 h93%
SymptomsNausea, anorexia, pallorNausea, epigastric pain
Recovery to Oral Feeding6 h24 h
Relieving FactorsDeep sleepHot bath/shower (56%)
Precipitating FactorsStress (47%), infection (31%)Menses (57%), anxiety
Comorbid conditionsAnxiety Not reported
Interepisodic nausea<6%63%
Coalescence of EpisodesFew50%
Vomiting6/hr at peak, bile (81%)8.5/hr
Systemic SymptomsPallor, salivation, listlessnessIntense thirst (33%)
GI SymptomsAnorexia, nausea, diarrhea, abdominal pain   Abdominal pain, diarrhea
Neurologic SymptomsHeadache, photophobia, phonophobia, abdominal pain
 		Irritable, confused
Natural history³ 28% progress to migraineNot reported
Family history82%57%
ComplicationsDehydration, esophagitisDehydration, esophagitis, laparotomy (18%)
Morbidity14-25 d of missed school/year32% completely disabled
 ChildrenAdults
Age of Onset4.8 y (Earliest, 6 d) 35 y (Latest, 73 y)
Delay in Diagnosis2.6 y8 y
Female-to-Male Ratio57:4317:24
FrequencyEvery 2-4 wkEvery 3 mo
Duration (Mean)1-2 d (range, 1-10 d)6 d (range, 1-21 d)
Periodicity49%Not reported
Early Morning Onset42%50%
Stereotypical Episodes99%85%
Prodrome72%, 1.5 h93%
SymptomsNausea, anorexia, pallorNausea, epigastric pain
Recovery to Oral Feeding6 h24 h
Relieving FactorsDeep sleepHot bath/shower (56%)
Precipitating FactorsStress (47%), infection (31%)Menses (57%), anxiety
Comorbid conditionsAnxiety Not reported
Interepisodic nausea<6%63%
Coalescence of EpisodesFew50%
Vomiting6/hr at peak, bile (81%)8.5/hr
Systemic SymptomsPallor, salivation, listlessnessIntense thirst (33%)
GI SymptomsAnorexia, nausea, diarrhea, abdominal pain   Abdominal pain, diarrhea
Neurologic SymptomsHeadache, photophobia, phonophobia, abdominal pain
 		Irritable, confused
Natural history³ 28% progress to migraineNot reported
Family history82%57%
ComplicationsDehydration, esophagitisDehydration, esophagitis, laparotomy (18%)
Morbidity14-25 d of missed school/year32% completely disabled

More on Cyclic Vomiting Syndrome

Overview: Cyclic Vomiting Syndrome
Differential Diagnoses & Workup: Cyclic Vomiting Syndrome
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, gastritis, hematemesis, prolapse gastropathy, Mallory-Weiss tear, peptic injury, fetal positioning, social withdrawal, turning off lights and televisions, headache, photophobia, phonophobia, vertigo, sinusitis, menses, motion sickness, dehydration, esophagitis, lethargy, nausea

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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 U K 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 U K 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.

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 broker recommendation; Avanir Pharma Stock Investment from broker recommendation

Managing Editor

David A Piccoli, MD, Chief, Division of Gastroenterology and Nutrition, Department of Pediatrics, 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, State University of New York, Downstate Medical Center College of Medicine; Distinguished Lecturer, New York Medical College, School of Public Health
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

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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