Cyclic Vomiting Syndrome 

  • Author: Thangam Venkatesan, MBBS; Chief Editor: Carmen Cuffari, MD   more...
 
Updated: Apr 23, 2010
 

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. 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.

Cyclic versus chronic temporal patterns of recurrent vomiting is shown in the image below.

Cyclic versus chronic temporal patterns of recurreCyclic versus chronic temporal patterns of recurrent vomiting. The number of emeses is plotted over a 2-month period. The chronic pattern, represented by a thin dashed line, has low grade on nearly a daily basis (eg, gastroesophageal reflux). The cyclic pattern, represented by a heavy solid line, involves high-intensity episodes intermittently once every several weeks (eg, cyclic vomiting syndrome).
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Pathophysiology

The etiology and pathophysiology in cyclic vomiting syndrome are not 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, 2]

Mitochondrial DNA (mtDNA) 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.[3]

In children with cyclic vomiting syndrome, two mtDNA polymorphisms (16519T and 3010A) are expressed with a high degree of frequency and may serve as a surrogate marker for predisposition to the disease. The mtDNA polymorphism, 16519T, was found to be 6 times more common in pediatric cyclic vomiting syndrome than in control populations.[4] Another common mtDNA polymorphism, 3010A, was noted to increase the odds ratio for developing cyclic vomiting syndrome in subjects with 16519T as much as 17 times. These mtDNA polymorphisms may account for the clustering of functional conditions and symptoms in the same individuals and families. Unlike pediatric cyclic vomiting syndrome, adult-onset cyclic vomiting syndrome is not associated with these mtDNA polymorphisms, suggesting a degree of genetic distinction.

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.[5] Several children with cyclic vomiting syndrome, including 4 members of an Italian family, have been reported to have various mitochondrial mutations.[6, 7]

Sympathetic hyperresponsivity and autonomic dysfunction also appear to contribute to the pathogenesis of cyclic vomiting syndrome.[8] Many associated symptoms, such as pallor, flushing, fever, lethargy, salivation, and diarrhea, are mediated by the autonomic nervous system.[9, 10, 11]

Several studies support altered autonomic function in cyclic vomiting syndrome. Rashed et al[12] and To et al[13] demonstrated a heightened sympathetic cardiovascular tone in patients with cyclic vomiting syndrome. Kasawinah et al reported the successful use of dexmedetomidine, an alpha-2 adrenergic agonist, to treat cyclic vomiting syndrome.[14] 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.[15]

To evaluate this association with autonomic dysfunction, a cross-sectional study using the Ohio dysautonomia (ODYSA) questionnaire was administered to 21 patients with cyclic vomiting syndrome (3 children) and 46 patients with migraines.[16] Both the cyclic vomiting syndrome and the migraine groups had similar comorbid conditions, with fibromyalgia noted in 38% of subjects with cyclic vomiting syndrome, orthostatic intolerance noted in 47% of subjects with cyclic vomiting syndrome, functional dyspepsia in 9.5% of subjects with cyclic vomiting syndrome, and complex regional pain syndrome in 24% of subjects with cyclic vomiting syndrome. The limitation of this study was the findings were not corroborated with either a physical examination or standard autonomic function test findings. However, the findings of orthostatic intolerance are of clinical significance because the use of pharmacological therapy such as fludrocortisone and beta blockers may be considered in these patients.

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.[17, 18, 19, 20, 21] Sato et al documented increased levels of adrenocorticotropic hormone (ACTH) and cortisol, associated with extreme lethargy and hypertension, before the onset of vomiting.[22, 23, 24, 25] Furthermore, Taché has definitively shown that central CRF induces gastric stasis, emesis, or both in animals.[26] Therefore, CRF may be a potential brain-gut mediator of cyclic vomiting syndrome that directly connects stress and vomiting.[27] 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.[28]

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.

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Epidemiology

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%.[29]

International

Limited epidemiologic data by Cullen and MacDonald estimate the prevalence of periodic vomiting in western Australia to be 2.3%.[9] Similarly, Abu-Arafeh and Russell observed a prevalence of 1.9% in school-aged children in Aberdeen, Scotland.[30] 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. This incidence is comparable to other major GI diseases of childhood (eg, Crohn disease) in Ireland.[31, 32]

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.[29]

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.[11] 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 ED visits, and the diagnosis is often unrecognized.[33]

Table 1. Characteristics of Emergency Department Visits in Patients With Cyclic Vomiting Syndrome (Open Table in a new window)

CharacteristicAdults



(n = 104)



Children



(n = 147)



Number of ED visits per patient with cyclic vomiting syndrome (Median)15 (range, 1-200)10 (range, 1-175)
Number of ED visits prior to a diagnosis of cyclic vomiting syndrome (Median)7 (Range, 1-150)5 (Range, 0-65)
Diagnosis not made in the ED89 (93%)119 (93%)
Diagnosis not recognized in the ED in patients with an established diagnosis of cyclic vomiting syndrome84 (88%)97 (80%)
Number of different ED 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.[11]

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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.

Specialty Editor Board

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.

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Pharmacy Editor, eMedicine

Disclosure: Nothing to disclose.

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.

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: Curemark, LLC Consulting fee Board membership; Centocor, Inc. Grant/research funds Independent contractor; Johnson & Johnson, 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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Cyclic versus chronic temporal patterns of recurrent vomiting. The number of emeses is plotted over a 2-month period. The chronic pattern, represented by a thin dashed line, has low grade on nearly a daily basis (eg, gastroesophageal reflux). The cyclic pattern, represented by a heavy solid line, involves high-intensity episodes intermittently once every several weeks (eg, cyclic vomiting syndrome).
Table 1. Characteristics of Emergency Department Visits in Patients With Cyclic Vomiting Syndrome
CharacteristicAdults



(n = 104)



Children



(n = 147)



Number of ED visits per patient with cyclic vomiting syndrome (Median)15 (range, 1-200)10 (range, 1-175)
Number of ED visits prior to a diagnosis of cyclic vomiting syndrome (Median)7 (Range, 1-150)5 (Range, 0-65)
Diagnosis not made in the ED89 (93%)119 (93%)
Diagnosis not recognized in the ED in patients with an established diagnosis of cyclic vomiting syndrome84 (88%)97 (80%)
Number of different ED visited (Mean ± standard deviation)4.69 ± 4.722.6 ± 2.42
Table 2. Clinical Features in Adults and Children with Cyclic Vomiting Syndrome[39]
Feature 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 conditionsAnxietyNot 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 painAbdominal pain, diarrhea
Neurologic SymptomsHeadache, photophobia, phonophobia, abdominal painIrritable, confused
Natural history≥ 28% progress to migraineNot reported
Family history82%57%
ComplicationsDehydration, esophagitisDehydration, esophagitis, laparotomy (18%)
Morbidity14-25 d of missed school/year32% completely disabled
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