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Cyclic vomiting syndrome

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]

Overview

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Cyclic vomiting syndrome (US English) or cyclical vomiting syndrome (UK English) (CVS) is a condition whose symptoms are recurring attacks of intense nausea, vomiting and sometimes abdominal pain and/or headaches or migraines. CVS can affect both children and adults. It was first described in the 19th century with one of the earliest references being that of Samuel Gee in 1882. Onset of the condition is possible at any age but is seen to occur more often in a young age. Why anyone develops it is not clear since it is of unknown etiology. There is a strong suggestion of maternal inheritance. A background of migraines could also be the cause of Cyclic Vomiting Syndrome[1].

References

  1. ↑ Fleisher DR, Gornowicz B, Adams K, Burch R, Feldman EJ (2005). “Cyclic Vomiting Syndrome in 41 adults: the illness, the patients, and problems of management”. BMC Med. 3: 20. doi:10.1186/1741-7015-3-20. PMC 1326207. PMID 16368014.


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Historical Perspective

Historical Perspective

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References


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Pathophysiology

Pathophysiology

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Causes

Causes

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Differentiating Cyclic Vomiting Syndrome from other Diseases

Differentiating Cyclic Vomiting Syndrome from other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2]

Overview

Cyclic vomiting syndrome should be differentiated from other diseases presenting as chronic nausea and vomiting. The differentials include gastroparesis, anorexia nervosa, bulimia nervosa, rumination syndrome, pancreatitis, functional dyspepsia and gastric outlet obstruction.

Differentiating Cyclic Vomiting Syndrome From other Diseases

Cyclic vomiting syndrome should be differentiated from other diseases that cause chronic nausea and vomiting. The differentials include the following:[1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32]

Disorder Clinical features Laboratory findings
Chronic nausea Vomiting Diarrhea Retching Lethargy Social withdrawal Photophobia Epigastric pain/burning Lanugo hair Hypogonadism Russel’s sign Body mass index (normal range: 18.5 to 24.9) Complete blood count (CBC) Electrolyte imabalance Lipase and amylase levels Gastric scintigraphy Ambulatory esophageal pH and impedance testing
Gastroparesis ✔ ✔ (within 1 hour of eating) – ✔ ✔ – – ✔ – – – ↓ ✔
  • Normal (maybe elevated if chronic renal failure is the cause of gastroparesis- usually less than threefold)
  • Periodic measurement of radiolabeled solid meal:  
    • Grade 1 (mild), 11%-20% retention at 4 h
    • Grade 2 (moderate), 21%-35% retention at 4 h
    • Grade 3 (severe), 36%-50% retention at 4 h
    • Grade 4 (very severe), > 50% retention at 4 h
  • Impedance testing (antroduodenal manometery): Loss of normal fasting migratory motor complexes (MMCs) and reduced postprandial antral contractions and, in some cases pylorospasm
Anorexia nervosa ✔ ✔ ✔ – ✔ ✔ – – ✔ ✔ – ↓ ✔
  • Increased
Bulimia nervosa ✔ ✔ ✔ ✔ ✔ ✔ – – – ✔ ✔ Normal ✔
  • Increased
Rumination syndrome ✔ ✔ (Regurgitation more common- within minutes of meal intake) ✔ – ✔ ✔ ✔ ✔ – – – ↓
  • Normal
 ✔
  • Normal
  • Esophageal pH: Fall in esophageal pH immediately after reguritation (occurs while patient is awake and erect; this is in contrast to GERD, where reflux occurs diurnally and supine position)
Functional dyspepsia ✔ ✔ ✔ ✔ – – – – – – – Normal
  • Normal
 ✔
  • Esophageal pH: May be decreased if patient develops reflux
Cyclic vomiting syndrome ✔ ✔ – ✔ ✔ – – – – – – ↓ ✔
  • Rapid or normal
  • Esophageal pH: Decreased
Pancreatitis ✔ ✔ ✔ ✔ ✔ – – ✔ – – – Normal ✔
  • Increased
  • Not indicated
  • Esophageal pH: Normal
Gastric outlet obstruction ✔ ✔ (within 1 hour of eating) – – – – – ✔ – – – ↓ ✔
  • Esophageal pH: Increased
  • Esophageal manometery:   High manoraetric score

References

  1. ↑ Parkman HP (2015). “Idiopathic gastroparesis”. Gastroenterol. Clin. North Am. 44 (1): 59–68. doi:10.1016/j.gtc.2014.11.015. PMC 4324534. PMID 25667023.
  2. ↑ Werlin SL, Fish DL (2006). “The spectrum of valproic acid-associated pancreatitis”. Pediatrics. 118 (4): 1660–3. doi:10.1542/peds.2006-1182. PMID 17015559.
  3. ↑ Noddin L, Callahan M, Lacy BE (2005). “Irritable bowel syndrome and functional dyspepsia: different diseases or a single disorder with different manifestations?”. MedGenMed. 7 (3): 17. PMC 1681633. PMID 16369243.
  4. ↑ Gupta R, Kalla M, Gupta JB (2012). “Adult rumination syndrome: Differentiation from psychogenic intractable vomiting”. Indian J Psychiatry. 54 (3): 283–5. doi:10.4103/0019-5545.102434. PMC 3512372. PMID 23226859.
  5. ↑ Sağlam F, Sivrikoz E, Alemdar A, Kamalı S, Arslan U, Güven H (2015). “Bouveret syndrome: A fatal diagnostic dilemma of gastric outlet obstruction”. Ulus Travma Acil Cerrahi Derg. 21 (2): 157–9. PMID 25904280.
  6. ↑ Talley NJ (2011). “Rumination syndrome”. Gastroenterol Hepatol (N Y). 7 (2): 117–8. PMC 3061016. PMID 21475419.
  7. ↑ Tutuian R, Castell DO (2004). “Rumination documented by using combined multichannel intraluminal impedance and manometry”. Clin. Gastroenterol. Hepatol. 2 (4): 340–3. PMID 15067630.
  8. ↑ Kessing BF, Smout AJ, Bredenoord AJ (2014). “Current diagnosis and management of the rumination syndrome”. J. Clin. Gastroenterol. 48 (6): 478–83. doi:10.1097/MCG.0000000000000142. PMID 24921208.
  9. ↑ Parkman HP (2009). “Assessment of gastric emptying and small-bowel motility: scintigraphy, breath tests, manometry, and SmartPill”. Gastrointest. Endosc. Clin. N. Am. 19 (1): 49–55, vi. doi:10.1016/j.giec.2008.12.003. PMID 19232280.
  10. ↑ Waseem S, Moshiree B, Draganov PV (2009). “Gastroparesis: current diagnostic challenges and management considerations”. World J. Gastroenterol. 15 (1): 25–37. PMC 2653292. PMID 19115465.
  11. ↑ Mearin F, Camilleri M, Malagelada JR (1986). “Pyloric dysfunction in diabetics with recurrent nausea and vomiting”. Gastroenterology. 90 (6): 1919–25. PMID 3699409.
  12. ↑ Abell TL, Camilleri M, Donohoe K, Hasler WL, Lin HC, Maurer AH, McCallum RW, Nowak T, Nusynowitz ML, Parkman HP, Shreve P, Szarka LA, Snape WJ, Ziessman HA (2008). “Consensus recommendations for gastric emptying scintigraphy: a joint report of the American Neurogastroenterology and Motility Society and the Society of Nuclear Medicine”. Am. J. Gastroenterol. 103 (3): 753–63. doi:10.1111/j.1572-0241.2007.01636.x. PMID 18028513.
  13. ↑ Jiang CF, Ng KW, Tan SW, Wu CS, Chen HC, Liang CT, Chen YH (2002). “Serum level of amylase and lipase in various stages of chronic renal insufficiency”. Zhonghua Yi Xue Za Zhi (Taipei). 65 (2): 49–54. PMID 12014357.
  14. ↑ Szmukler, G. I.; Young, G. P.; Lichtenstein, M.; Andrews, J. T. (1990). “A serial study of gastric emptying in anorexia nervosa and bulimia”. Australian and New Zealand Journal of Medicine. 20 (3): 220–225. doi:10.1111/j.1445-5994.1990.tb01023.x. ISSN 0004-8291.
  15. ↑ Diamanti A, Bracci F, Gambarara M, Ciofetta GC, Sabbi T, Ponticelli A, Montecchi F, Marinucci S, Bianco G, Castro M (2003). “Gastric electric activity assessed by electrogastrography and gastric emptying scintigraphy in adolescents with eating disorders”. J. Pediatr. Gastroenterol. Nutr. 37 (1): 35–41. PMID 12827003.
  16. ↑ Ferholt J, Provence S (1976). “Diagnosis and treatment of an infant with psychophysiological vomiting”. Psychoanal Study Child. 31: 439–59. PMID 981449.
  17. ↑ Lee H, Rhee PL, Park EH, Kim JH, Son HJ, Kim JJ, Rhee JC (2007). “Clinical outcome of rumination syndrome in adults without psychiatric illness: a prospective study”. J. Gastroenterol. Hepatol. 22 (11): 1741–7. doi:10.1111/j.1440-1746.2006.04617.x. PMID 17914944.
  18. ↑ Koskenpato J, Kairemo K, Korppi-Tommola T, Färkkilä M (1998). “Role of gastric emptying in functional dyspepsia: a scintigraphic study of 94 subjects”. Dig. Dis. Sci. 43 (6): 1154–8. PMID 9635600.
  19. ↑ Urbain JL, Vekemans MC, Parkman H, Van Cauteren J, Mayeur SM, Van den Maegdenbergh V, Charkes ND, Fisher RS, Malmud LS, De Roo M (1995). “Dynamic antral scintigraphy to characterize gastric antral motility in functional dyspepsia”. J. Nucl. Med. 36 (9): 1579–86. PMID 7658213.
  20. ↑ Hejazi RA, Lavenbarg TH, McCallum RW (2010). “Spectrum of gastric emptying patterns in adult patients with cyclic vomiting syndrome”. Neurogastroenterol. Motil. 22 (12): 1298–302, e338. doi:10.1111/j.1365-2982.2010.01584.x. PMID 20723071.
  21. ↑ “Gastric outlet obstruction – an overview | ScienceDirect Topics”.
  22. ↑ Minami H, McCallum RW (1984). “The physiology and pathophysiology of gastric emptying in humans”. Gastroenterology. 86 (6): 1592–610. PMID 6370777.
  23. ↑ Humphries LL, Adams LJ, Eckfeldt JH, Levitt MD, McClain CJ (1987). “Hyperamylasemia in patients with eating disorders”. Ann. Intern. Med. 106 (1): 50–2. PMID 2431640.
  24. ↑ Hempen I, Lehnert P, Fichter M, Teufel J (1989). “[Hyperamylasemia in anorexia nervosa and bulimia nervosa. Indication of a pancreatic disease?]”. Dtsch. Med. Wochenschr. (in German). 114 (49): 1913–6. doi:10.1055/s-2008-1066848. PMID 2480214.
  25. ↑ Okada R, Okada A, Okada T, Okada T, Hamajima N (2009). “Elevated serum lipase levels in patients with dyspepsia of unknown cause in general practice”. Med Princ Pract. 18 (2): 130–6. doi:10.1159/000189811. PMID 19204432.
  26. ↑ Sansone RA, Sansone LA (2012). “Hoarseness: a sign of self-induced vomiting?”. Innov Clin Neurosci. 9 (10): 37–41. PMC 3508961. PMID 23198276.
  27. ↑ Tack J, Caenepeel P, Arts J, Lee KJ, Sifrim D, Janssens J (2005). “Prevalence of acid reflux in functional dyspepsia and its association with symptom profile”. Gut. 54 (10): 1370–6. doi:10.1136/gut.2004.053355. PMC 1774686. PMID 15972301.
  28. ↑ “gut.bmj.com” (PDF).
  29. ↑ Boles RG, Williams JC (1999). “Mitochondrial disease and cyclic vomiting syndrome”. Dig. Dis. Sci. 44 (8 Suppl): 103S–107S. PMID 10490048.
  30. ↑ Ranasinghe WK, Smith M (2013). “Gastric outlet obstruction with an elevated serum pancreatic lipase secondary to an infraumbilical hernia”. Ann R Coll Surg Engl. 95 (7): 122–4. doi:10.1308/003588413X13629960047795. PMID 24112485.
  31. ↑ Ui, Takashi; Shibusawa, Hiroyuki; Tsukui, Hidenori; Sakuma, Kazuya; Takahashi, Shuhei; Lefor, Alan K.; Hosoya, Yoshinori; Sata, Naohiro; Yasuda, Yoshikazu (2015). “Pretreatment of gastric outlet obstruction with pancrelipase: Report of a case”. International Journal of Surgery Case Reports. 12: 87–89. doi:10.1016/j.ijscr.2015.05.023. ISSN 2210-2612.


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Epidemiology and Demographics

Epidemiology and Demographics

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Epidemiology and Demographics

The prevalence of the condition is not clear. Two published studies on childhood CVS suggest nearly 2% of school age children may have CVS. However, diagnosis is problematic and as knowledge of CVS has increased in recent years more and more cases are emerging. This suggests a tendency for underdiagnosis, and thus the true figure may be higher.

CVS may be related to migraine, CVS sufferers have a much higher number of first degree relatives who have migraine than is the case in the general population. Some CVS sufferers have symptoms similar to abdominal migraine, but in others the relationship is far less strong and they can’t relate to migranous symptoms. Some sufferers obtain some relief from anti-migraine treatments, but they are not universally effective.

The average age at onset is 3-7 years, but CVS has been seen in infants which are as young as 6 days and in adults which are as old as 73 years (Li and Misiewicz, 2003). Typical delay in diagnosis from onset of symptoms is 2.7 – 3 years (Li and Misiewicz, 2003).

Females show a slight predominance over males; the female-to-male ratio is 57:43 (Li and Kagalwalla, 2002). CVS occurs in all races but seems to disproportionately affect whites.

Charitable organizations to support sufferers and their families and to promote knowledge of CVS exist in several countries.

References


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Natural History, Complications and Prognosis

Natural History, Complications and Prognosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Natural History, Complications and Prognosis

There is little hard evidence of death as a result of the condition. However, in severe cases the fluid loss can lead to potentially life-threatening salt imbalances and extremely high blood pressure often develops during an attack. In underdeveloped countries it remains probable that CVS may contribute to mortality. In the developed world with adequate medical interventions most sufferers can be supported during an attack and will recover from the episode. After the average three year duration of Cyclic Vomiting Syndrome, 20 percent of patients were to seen to have developed migraines. Patients seemed to go through three stages: CVS, abdominal migraines which have similar characteristics as CVS then regular migraines.

On average 50% of patients require IV fluids. Whereas rotavirus gastroenteritis has less than 1% which require IV fluids. On average the cost of treatment, testing, work absences and leave per year can total in US dollars $17,000. Most children who have this disorder miss on average 24 school days a year, and will often need tutoring to catch up on their academic studies. The frequency of episodes is higher, for some people, during times of excitement, which often leads to many family events such as holidays, birthdays and vacations being disrupted. For adult sufferers the challenge of maintaining a career or full time employment is considerable. For all sufferers there are associated quality of life issues for not only the sufferer but also for close family members.

References


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Diagnosis

Diagnosis

Diagnostic Criteria | History and Symptoms | Physical Examination | Laboratory Findings | Other Diagnostic Studies

Treatment

Treatment

Medical Therapy | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies

Case Studies

Case Studies

Case #1

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