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Table of Contents
CASE REPORT
Year : 2023  |  Volume : 14  |  Issue : 1  |  Page : 42-44

Intractable vomiting: An interesting case


Department of Internal Medicine. BLK-Max Super Speciality Hospital, New Delhi, India

Date of Submission01-Aug-2022
Date of Decision18-Oct-2022
Date of Acceptance30-Oct-2022
Date of Web Publication31-Jan-2023

Correspondence Address:
Vivek Pal Singh
Department of Internal Medicine. BLK-Max Super Speciality Hospital, PUSA Road, New Delhi
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/injms.injms_98_22

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  Abstract 


Nausea and vomiting constitute one of the most common presenting symptoms in a variety of diseases in clinical practice. Recurrent vomiting can be due to simple gastritis which may lead to dehydration and electrolyte disturbances to threatening intracranial hypertension. Prolonged recurrent vomiting can also lead to malnutrition. Esophageal dysmotility is usually associated with dysphagia but is infrequently associated with recurrent vomiting. We report a case of acute-onset intractable vomiting in a 50-year-old Indian female who presented with severe dehydration and hypernatremia. A timed barium esophagogram revealed dilated esophagus with a rat-tail appearance. Upper gastrointestinal endoscopy revealed dilated esophagus with a tight esophageal-gastric junction. With a diagnosis of achalasia cardia, the patient underwent peroral endoscopic myotomy with complete resolution of symptoms.

Keywords: Achalasia cardia, dehydration, endoscopy, esophagus, hypernatremia


How to cite this article:
Thapliyal K, Garg A, Singh VP. Intractable vomiting: An interesting case. Indian J Med Spec 2023;14:42-4

How to cite this URL:
Thapliyal K, Garg A, Singh VP. Intractable vomiting: An interesting case. Indian J Med Spec [serial online] 2023 [cited 2023 Mar 31];14:42-4. Available from: http://www.ijms.in/text.asp?2023/14/1/42/368627




  Introduction Top


Esophageal dysmotility is a result of disturbances in musculature, structure, swallowing, and contractile mechanisms involving the esophagus. Achalasia cardia first described by Thomas Williams in 1672 is a primary esophageal dysmotility disorder in which there is relaxation failure of the lower esophageal sphincter (LES) thereby, leading to a functional gastroesophageal junction obstruction. Achalasia is considered a very rare disease with an incidence of 10 cases per 100,000 population. The most common age group in which achalasia is reported is 25–60 years.[1] Usually, the presentation is subacute to chronic with symptoms of progressive dysphagia to solid and liquid with regurgitation of saliva and undigested food. Acute-onset intractable vomiting in achalasia cardia is rarely reported.


  Case Report Top


A 50-year-old euglycemic, normotensive Indian female reported to us with complaints of recurrent vomiting for 15 days. There was no history of fever, abdominal pain, diarrhea, constipation, or abdominal distension. There was no headache, visual disturbances, or focal neurological deficits. Drug history was unremarkable except for self-administration of antiemetics and proton-pump inhibitors. The patient also gave a history of retrosternal discomfort after eating solids and liquids. Vomiting occurred within half hour of eating or drinking and consisted of undigested food. There was no hematemesis or melena. She also gave a history of self-induction of vomiting by stimulation of the posterior pharyngeal wall to get rid of continuous retrosternal discomfort which happened after liquid or solid food intake. She also reported weight loss of approximately 3 kg in 15 days.

She was clinically dehydrated with normal vitals. Routine hematology and biochemistry were normal except hypernatremia (serum sodium 156 mEq/L). Medical history was re-evaluated and was found to be negative for the presence of polyuria or polydipsia. Drug history was negative for the use of lithium, diuretics, or laxatives. Fundus examination, chest radiograph, and ultrasound of the whole abdomen were also normal. Urine analysis revealed 1+ ketonuria but there was no evidence of hyperglycemia (starvation ketosis). She was managed with intravenous (IV) fluid replenishment by 5% dextrose solution and IV ondansetron, but vomiting persisted during the hospital stay. Upper gastrointestinal (GI) endoscopy revealed esophageal candidiasis along with a tight gastroesophageal junction with lots of mucoid secretion in the lower part of the esophagus [Figure 1]. The stomach and first part of the duodenum were unremarkable. HIV 1 and 2 were nonreactive and glycosylated hemoglobin was 5.2%. Barium swallow revealed dilated lower two-thirds of the esophagus with sudden tapering giving a rat-tail appearance [Figure 2]. A diagnosis of achalasia cardia was made and the patient underwent peroral endoscopic myotomy (POEM) along with IV fluconazole 200 mg once daily. Post-POEM gastrografin study revealed an opening up of the distal end of the esophagus with smooth passage of contrast from the esophagus to the stomach [Figure 3]. There was complete resolution of symptoms as the patient resumed oral liquids and solid foods gradually and was discharged to home uneventfully.
Figure 1: Upper GI endoscopy showing esophageal candidiasis along with tight gastroesophageal junction (arrow). GI: Gastrointestinal

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Figure 2: Barium swallow showing dilated lower two-thirds of the esophagus with a rat-tail appearance (arrow)

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Figure 3: Post-POEM gastrografin study showing opening up of the distal end of the esophagus with smooth passage of contrast from the esophagus to the stomach (arrow). POEM: Peroral endoscopic myotomy

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  Discussion Top


The main pathophysiology of achalasia chardia is a failure of LES to relax and the absence of esophageal peristalsis. LES relaxation and pressure are regulated by excitatory neurotransmitters (acetylcholine, substance P) and inhibitory neurotransmitters (nitric oxide, vasoactive intestinal polypeptide). In achalasia, there is a lack of noncholinergic and nonadrenergic inhibitory ganglionic cells, leading to an imbalance in inhibitory and excitatory neurotransmission, thus resulting in nonrelaxed LES.[1]

Etiologically, achalasia can be either neurogenic in origin or secondary to gastroesophageal reflux disease, viral infections, Chagas disease, or autoimmune phenomenon. Achalasia cardia when associated with isolated glucocorticoid deficiency and alacrimia is known as Allgrove syndrome.[2],[3]

Clinically, achalasia presents with dysphagia, regurgitation, retrosternal pain or discomfort, and rarely vomiting or weight loss. Barium esophagram is the best single diagnostic study once there is clinical suspicion of achalasia cardia. Proximal esophageal dilatation with smooth tapering at the lower end "rat-tail appearance" is characteristic of achalasia. Upper GI endoscopy is a mandatory investigation to rule out pseudoachalasia. Esophageal manometry in a typical case of achalasia reveals increased pressure at the esophageal-gastric (GE) junction which is about twice the normal (40 mmHg) along with incomplete or absent relaxation of the GE junction after swallowing.[3]

The goal of treatment is aimed at symptom management and maintaining nutritional needs. Conventionally, calcium channel blockers and nitrates are used to decrease LES pressure; however, only around 10% of patients benefit from medical management.[4] Other modalities are endoscopic injection of botulinum toxin in LES and esophageal dilatation with pneumatic dilators. Conventional or modified Heller's esophagocardiomyotomy, either open or laparoscopic is considered to be the gold standard to relieve the functional obstruction at the GE junction.

POEM is a relatively new endoscopic procedure. It is a form of natural orifice transluminal endoscopic surgery that is completed by creating a submucosal tunnel in the lower part of the esophagus to reach the inner circular muscle bundles of the LES to perform myotomy while preserving the outer longitudinal muscle bundles. The result is decreased resting pressure of the LES, facilitating the passage of ingested liquid and solid food. The intervention is successful and efficacious for the management of symptoms with a success rate of 82%–100%.[5] Contraindications to the procedure include severe esophagitis, clinically significant coagulation disorder, decompensated/advanced liver cirrhosis, and submucosal fibrosis from prior radiation therapy. A large esophageal diverticulum is a relative contraindication which depends on the location and the extent of the diverticulum. A benefit of having an endoscopic procedure, especially for achalasia cardia, is that there are no incisions in the chest or abdomen, and includes a minimal or sometimes no hospital stay postprocedure.


  Conclusion Top


This case highlights the importance of clinical suspicion of achalasia cardia in a case of acute intractable vomiting. Furthermore, the role of conventional barium esophagram study cannot be understated in such cases where it can be virtually diagnostic. Medical management of achalasia cardia is relatively less successful when compared to surgical management. POEM is a minimally invasive intervention that aims to treat achalasia. It is regarded as the endoscopic equivalent of Heller myotomy. However, this procedure is currently available only at tertiary centers.

Declaration of patient consent

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

Financial support and sponsorship

None.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Susan DL, Hong-Phuc T, Manual E. Intractable nausea and vomiting in an elderly patient. Endoscopy 2014;79:136-9.  Back to cited text no. 1
    
2.
Chatterjee S, Gajbhiye V, De A, Nath S, Ghosh D, Das SK. Achalasia cardia in infants: Report of two cases. J IMA 2013;44:1-5. Available at http://dx.doi.org/10.5915/44-1-9260.  Back to cited text no. 2
    
3.
Howard PJ, Maher L, Pryde A, Cameron EW, Heading RC. Five year prospective study of the incidence, clinical features, and diagnosis of achalasia in Edinburgh. Gut 1992;33:1011-5.  Back to cited text no. 3
    
4.
Cuillière C, Ducrotté P, Zerbib F, Metman EH, de Looze D, Guillemot F, et al. Achalasia: Outcome of patients treated with intrasphincteric injection of botulinum toxin. Gut 1997;41:87-92.  Back to cited text no. 4
    
5.
Ahmed Y, Othman MO. Peroral endoscopic myotomy (POEM) for achalasia. J Thorac Dis 2019;11:S1618-28  Back to cited text no. 5
    


    Figures

  [Figure 1], [Figure 2], [Figure 3]



 

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