Indian Journal of PsychiatryIndian Journal of Psychiatry
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LETTERS TO EDITOR  
Year : 2021  |  Volume : 63  |  Issue : 3  |  Page : 304-306
Cyclical vomiting and clinician's dilemma


1 Department of Psychiatry, Diamond Harbour Medical College, Kolkata, West Bengal, India
2 Mental Health Program, Monash Health, Melbourne, Victoria; Department of Psychiatry, Faculty of Medicine, University of Queensland RCS, Rockhampton, Queensland, Australia

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Date of Submission10-Jun-2020
Date of Decision07-Jul-2020
Date of Acceptance17-Sep-2020
Date of Web Publication17-Jun-2021
 

How to cite this article:
Chatterjee SS, Mitra S. Cyclical vomiting and clinician's dilemma. Indian J Psychiatry 2021;63:304-6

How to cite this URL:
Chatterjee SS, Mitra S. Cyclical vomiting and clinician's dilemma. Indian J Psychiatry [serial online] 2021 [cited 2021 Sep 25];63:304-6. Available from: https://www.indianjpsychiatry.org/text.asp?2021/63/3/304/318729




Sir,

Although cyclical vomiting syndrome (CVS) is a common and long recognized clinical phenomenon, the condition has not been discussed much in medical literature. This ambiguity probably emanates from its position at the interface between psychiatry and internal medicine, and its highly variable presentation often leads to misdiagnosis. In adults, CVS is defined as three or more episodes of intense nausea and vomiting lasting from hours to days, with complete remission in between[1] – resulting in multiple hospital and emergency consultations and admissions.

U, a 24-year-old educated urban male (provided a written informed consent for the purpose of this report), presented to us with bouts of nonbilious, nonsanguineous vomiting recurring every 3–4 weeks for 6 months – at the frequency of 15–20 times a day and lasting for around 2 days. The acts were associated with nausea and were nonprojectile; not associated with fever, headache, visual disturbances, abnormal movements, or posturing. Physical examination and fundoscopy were normal, except for an increased body mass index (27.4 kg/m2). Complete blood count, serum electrolytes, fasting sugar, and renal and liver function tests were unremarkable. Upper gastrointestinal (GI) endoscopy, barium swallow and follow through, and whole abdomen ultrasound did not reveal any significant abnormality. He was subsequently referred to the department of psychiatry for assessment. A detailed session with the patient in the outpatient department (OPD) revealed the presence of an acute stress which preceded most of these attacks: an impending examination, a scheduled job interview, financial worries, or some family altercations. He reported a habit of eating in excess, almost double the amount of what was usual for him, as a way of handling such stresses, and has had this habit since late adolescence. He said that this would have a calming effect on his “nerves.” Over the last few months, he had gradually increased the amount of food he ate because of an escalating severity of stresses in his life. During interview in the OPD, he was fidgety, and affect was anxious. He did not have body image disturbance to qualify for a diagnosis of eating disorders. He scored 24 on Perceived Stress Scale-10, meaning that his perceived stress was “much higher than average.”[2] A session with the parents brought to light a high level of expressed emotion (EE) in the form of over-involvement. No significant family history, substance dependence, or past medical or surgical history was elicited. He reported an unremarkable childhood and developmental history and an anxious personality trait premorbidly. Clinical anxiety was present, but he did not fulfill the criteria for a depressive episode. There was no other diagnosable psychiatric morbidity identified. He was admitted to the inpatient unit for further exploration of symptoms.

While in the hospital, the patient was seen maintaining sick role – including repeated requests for intravenous fluids, which he had learned about from his pervious experiences in the medical wards, despite clear explanations against this. He was started on normal oral feeds.

We envisaged his presentation being a learned pattern of behavior developing on the background of an anxious premorbid personality. A lack of healthy coping skills did not enable him to constructively deal with acute life stresses, leading to initial bouts of vomiting during heightened states of anxiety. Subsequent over-involvement of the family, medical attention, and respite from the acute stresses as a consequence reinforced this behavior, which has since been maintained through escape-avoidance learning. Brief psychotherapy sessions focused on correcting his cognitive distortions and training in relaxation techniques were administered over six daily sessions. Activity schedule was prepared for him to balance his social roles, and a brief psychoeducational session was conducted with his parents, regarding deleterious effects of EE. He was discharged after 7 days. He was better at discharge and is maintaining well for the last 2 months without any medication. We expect a good prognosis for U given initial success in reducing his distress and an intervention based on the above-mentioned formulation.

Repeated bouts of vomiting may be a manifestation of dysfunctions involving brain regions responsible for nausea and/or vomiting. There might be a genetic angle to it as family/personal history of migraine, gastric dysrhythmias, food allergies, or mitochondrial dysfunctions may be found.[3] A diagnosis of CVS is made following the ROME-III criteria,[4] after organic causes have been ruled out.[3] In adults, the average age of onset is around 22 years, with a delay of about 10–20 years in diagnosis,[5],[6] and slightly more common in males. Interestingly, data suggest that CVS symptoms may undergo “kindling,” in that the episode might begin to approximate and eventually fuse into one single cluster, causing confusion with progressive organic etiologies.[6] Psychiatric disorders such as depression and anxiety have been described as comorbidities in CVS, though cause–effect relationship is yet to be clarified. Namin et al.[7] had previously noted 50% self-report of mental stress as a contributory factor and an 86% prevalence of anxiety disorders in a cohort of CVS patients. Furthering this, association with functional bowel disorders has been reported in 10%–30% of patients.[8] Overall, it is possible that psychological stressors alter activation in the hypothalamic–pituitary–adrenal axis, changing gut motility and manifesting as CVS. There are reports of abnormal activation of circuits involving amygdala, anterior cingulate cortex, pontine periaqueductal grey, and locus ceruleus complex in several stress-sensitive functional GI disorders,[9],[10] which further vindicates this relationship.

U's presentation necessitated that we rule out organicity. Once satisfied, we made a diagnosis of CVS as per the ROME-III criteria. He had typical interepisodic remissions, followed by repeated retching-vomiting which gradually subsided – a classical presentation as described by Hejazi and McCallum.[6] Our case illustrates the importance of considering and assessing the role of perceived stress and anxiety, as well as associated cognitive distortions, in CVS. As mentioned earlier, this angle is often ignored in medical clinics given the position of CVS at the interface of medicine and psychiatry. Mr. U had faulty learning and reinforcement of his behavior, using vomiting to escape from immediate stresses with subsequent tangible gains, leading to maintenance; further bolstered by high EE in the family. Our intervention aimed at correcting these distortions and providing the patient with alternatives for managing stress – simultaneously focusing on EE-worked, and the patient could come out of vicious cycle.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understand that name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
   References Top

1.
Kowalczyk M, Parkman H, Ward L. Adult cyclic vomiting syndrome successfully treated with intranasal sumatriptan. J Gen Intern Med 2010;25:88-91.  Back to cited text no. 1
    
2.
Cohen S, Kamarck T, Mermelstein R. A global measure of perceived stress. J Health Soc Behav 1983;24:385-96.  Back to cited text no. 2
    
3.
Abell TL, Adams KA, Boles RG, Bousvaros A, Chong SK, Fleisher DR, et al. Cyclic vomiting syndrome in adults. Neurogastroenterol Motil 2008;20:269-84.  Back to cited text no. 3
    
4.
Tack J, Talley NJ, Camilleri M, Holtmann G, Hu P, Malagelada JR, et al. Functional gastroduodenal disorders. Gastroenterology 2006;130:1466-79.  Back to cited text no. 4
    
5.
Abell TL, Kim CH, Malagelada JR. Idiopathic cyclic nausea and vomiting – A disorder of gastrointestinal motility? Mayo Clinic Proc 1988;63:1169-75.  Back to cited text no. 5
    
6.
Hejazi RA, McCallum RW. Review article: Cyclic vomiting syndrome in adults--Rediscovering and redefining an old entity. Aliment Pharmacol Ther 2011;34:263-73.  Back to cited text no. 6
    
7.
Namin F, Patel J, Lin Z, Sarosiek I, Foran P, Esmaeili P, et al. Clinical, psychiatric and manometric profile of cyclic vomiting syndrome in adults and response to tricyclic therapy. Neurogastroenterol Motil 2007;19:196-202.  Back to cited text no. 7
    
8.
Hejazi RA, Lavenbarg TH, Foran P, McCallum RW. Who are the nonresponders to standard treatment with tricyclic antidepressant agents for cyclic vomiting syndrome in adults? A large single center experience. Aliment Pharmacol Ther 2010;31:295-301.  Back to cited text no. 8
    
9.
Namin F, Patel J, Lin Z, Dusing RW, Foran P, McCallum RW. Recognizing abnormal patterns on PET brain images in adult patients with cyclic vomiting syndrome (CVS). Gastroenterology 2006;125:A124  Back to cited text no. 9
    
10.
Mayer EA, Aziz Q, Coen S, Kern M, Labus JS, Lane R, et al. Brain imaging approaches to the study of functional GI disorders: A Rome Working Team Report. Neurogastroenterol Motil 2009;21:579-96.  Back to cited text no. 10
    

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Correspondence Address:
Sayantanava Mitra
Mental Health Program, Monash Health, Melbourne, Victoria; Department of Psychiatry, Faculty of Medicine, University of Queensland RCS, Rockhampton, Queensland
Australia
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/psychiatry.IndianJPsychiatry_526_20

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