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interventions.6 We are reporting in this case a patientin whom a trial of ATT for 2 months failed to improve symptoms of the patient resulting in the need for more invasive procedures. Endoscopic management may be done using over the scope clips or stents. In this case a self-expanding partially covered metal stent was placed at the level of the fistulous opening and achieved a closure of the fistulous opening. Chauhan et al have described the use of covered stent for rapid closure of TEF with a reported closure in 89% of patients (range of 67% to 100%.). Uncovered metal stents were found to result in tissue ingrowth causing dysphagia.7,8

Stent placement is associated with complications including displacement and impaction. The optimal time to remove an esophageal stent has no consensus, though esophageal healing usually occurs within 4 weeks of stent placement.8 Prolonged stent placement causes inflammation and complications including epidural abscess, aorto-esophageal fistula and stent impaction. In this patient stent was left in situ for 12 weeks which resulted in tissue ingrowth leading to dysphagia. This case report also demonstrates the surgical approaches that can be considered in a patient. The repair of the TEF can be done by primary closure, use of body tissues 9 or use of prosthetic materials such as Dacron or PTFE to buttress the fistulous opening. In this patient a rim of the native esophagus was left behind at the fistulous opening in the right bronchus. In conclusion the management of acquired TEF/BEF has multiple modalities that has tobe tailor made in accordance with the patients’ nutritional status, size of the defect, facilities available. Use of endoscopic methods should be done keeping in mind the possible complications that may follow.

REFERENCES

1. Burt M, Diehl W, Martini N, Bains MS, Ginsberg RJ, McCormack PM, Rusch VW. Malignant esophagorespiratory fistula: management options and survival. AnnThorac Surg. 1991:1222-9.

2. Sersar SI, Maghrabi LA. Respiratory-digestive tract fistula: two-center retrospective observational study. Asian Cardiovascular and Thoracic Annals. 2018 ;26:218-23.

3. Devarbhavi HC, Alvares JF, Radhikadevi M. Esophageal tuberculosis associated with esophagotracheal or esophagomediastinal fistula: report of 10 cases.

GastrointestEndosc. 2003;57:588-92.4. Udwadia ZF, Mehra C. Tuberculosis in India. BMJ. 2015

Mar 23;350:h1080.5. Macchiarini P, Delamare N, Beuzeboc P, et

al.Tracheoesophageal fistula caused by mycobacterial tuberculosis adenopathy. Ann Thorac Surg. 1993;55(6):1561-3.

6. Narayanan S, Shiji PV, KA AM, Udayabhaskaran V. Tuberculosis presenting as bronchoesophageal fistula. IDCases. 2017:19-21.

7. Chauhan SS, Long JD. Management of Tracheoesophageal Fistulas in Adults. Curr Treat Options Gastroenterol. 2004;7(1):31-40.

8. van Heel NC, Haringsma J, Spaander MC, Bruno MJ, Kuipers EJ. Short-term esophageal stenting in the management of benign perforations. Am J Gastroenterol. 2010 ;105(7):1515-20.

9. Bertheuil N, Cusumano C, Meal C, Harnoy Y, Watier E, Meunier B. Skin Perforator Flap Pedicled by Intercostal Muscle for Repair of a Tracheobronchoesophageal Fistula. Ann Thorac Surg. 2017 ;103(6):e571-e573.

Sandheep Janardhanan Mary George

Benoy Sebastian Sunil Mathai

Department of Gastroenterology, Medical Trust Hospital, Cochin, India.

Corresponding Author: Dr Sandheep Janardhanan Email: sandheepjanardhanan47@gmail.com

Maltoma Causing Massive Upper Gastrointestinal (GI) Bleed: A Rare Presentation

Massive upper Gastrointestinal (GI) bleed is a life threatening medical emergency that can cause significant mortality and needs urgent intervention. Most common cause of upper GI bleed are peptic ulcer disease, varices, Mallory Weiss tear, vascular malformations etc.

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Gastric Mucosa associated Lymphoid Tissue (MALToma), a type of Non Hodgkin Lymphomas (NHL) are uncommon cause of gastric neoplasm even though stomach is the most common extranodal site of involvement in lymphoma. Also, upper GI bleed is a rare presentation in MALT lymphoma. Here, we present a case of MALT lymphoma presenting as massive upper GI bleed.

Case Report

A 57 year old gentleman presented to our emergency with three to four episodes of hematemesis and melena of one day duration associated with syncope but without

any abdominal pain. He was taking medications for Type 2 Diabetes and Hypertension (Insulin, metformin, glimeperide and amlodipine). There was no history of alcohol usage, smoking, NSAID intake, previous ulcer disease etc. Pertinent clinical examination revealed pallor, tachycardia, hypotension and no stigmata of chronic liver disease. Abdominal examination revealed epigastric tenderness, but no organomegaly and per rectal examination showed maelenic stool. Baseline investigations confirmed pallor, (Hb-6.2mg/dl and PCV-32), since Glasgow Blatchford score was 20, he was admitted in ICU, stabilized with crystalloids, blood transfusion and pantoprazole infusion

Figure 1: First endoscopic view of the lesion.

Figure 2: CECT abdomen showing gastric wall thickening and perigastric lymph nodes.

Figure 3: First Endoscopic ultrasound (EUS) showing prominent perigastriclymphnode.

Figure 4: Histology of EUS guided lymph node biopsy showing reactive lymphocytosis.

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and was taken up for esophagogastroduoenoscopy (EGD) six hours later. Endoscopy revealed erythematous shallow ulcers in the antrum and body with ragged edges and active ooze. Endoscopic hemostasis was achieved after mucosal epinephrine injection and biopsy was taken from involved areas few days later, since malignancy was suspected and CECT abdomen showed stomach wall thickening and multiple perigastriclymphnodes (10mm). However biopsy report was inconclusive. An endoscopic

ultrasound guided lymph node biopsy was taken, reported as reactive lymphadenopathy. Since there was a diagnostic dilemma, we proceded with deeper biopsy using Endoscopic mucosal resection (EMR) knife from edge of involved area. Biopsy revealed lymphoblastic infiltration suggestive of chronic gastritis associated with presence of Helicobacter pylori. Hence in view of suspicion of lymphoma, Immunohistochemical (IHC) workup was done, which was positive for CD20, BCL2 and CD43 and non-reactive to cyclin D and CD6. Post procedure he did not have any bleed, hemoglobin improved (Hb-10.2), He was commenced on triple therapy for Helicobactor pylori eradication (twice

Figure 5: Low power view of gastric tissue showing chronic gastritis (Stain-Hemotoxylin & Eosin).

Figure 6: High power view of gastric tissue showing chronic Hpylori gastritis with lymphoplasmocytic infiltrate.

Figure 7: Immunohistochemical(IHC)work up positive for CD20, BCL2 and CD43, non-reactive to cyclin D, CD6.

Figure 8: Follow up endoscopy shows healed lesion.

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daily triple drug combination of pantoprazole 40 mg, amoxicillin 1000 mg and clarithromycin 500 mg for two weeks. A follow up endoscopy showed normal stomach mucosa, normal histology and no lymph nodes on follow up endosonography. His hemodynamics and baseline blood parameters remained stable. He was reviewed three months later, was asymptomatic and was doing well.

Discussion

Stomach is the most common site of extranodal Non Hodgkins lymphoma (NHL). Even though, the most common of primary GI lymphoma, MALT lymphoma is rare (1-6%). Chronic H Pylori infection is associated with ninety percent of MALTomas.1,2 Even then, the incidence of MALT lymphomas presenting as life threatening GI bleed is very rare.3,5

In our case, early endoscopy and hemostasis was achieved within six hours of the bleed, which has been cited by previous studies as game changer in non variceal bleed.5.6 The diagnosis of our patient was established by repeat deeper biopsy and histopathological examination including Immunohistochemical examination (IHC) after initial result was inconclusive. Our primary diagnosis was gastric adenocarcinoma considering into account patients age, commoner presentation and constitutional symptoms. The importance of H. pylori eradication is the cornerstone in management of MALT lymphoma, taking into account the recent guidelines which advocate, H. pylori eradication itself can be curative in 75% in localized disease as ours, Even in advanced disease or non responsive cases, has to be combined with chemo/radiotherapy (Figure 10)7. The eradication therapy has benefit in survival with one and five year survival rates of 90.3% and 76.2%.8,9,10

To summarize, gastric MALTymphoma is an uncommon GI neoplasm, and even rarer cause of upper GI bleed. References

1. Roberts D, Hopkins M, Miller S, Schafer W. Gastric MALT lymphoma in the absence of Helicobacter pylori infection

presenting as an upper gastrointestinal hemorrhage. South Med J. 2006 ;99(10):1134-6.

2. Bestari MB, Palungkun IG, Hernowo BS, Abdurachman SA, Nugraha ES. Low-Stage Gastric MALT Lymphoma Causing Life-Threatening Upper Gastrointestinal Bleeding. Case Rep Gastroenterol. 2019 25;13(3):376-384.

3. Juárez-Salcedo LM, Sokol L, Chavez JC, Dalia S. Primary Gastric Lymphoma, Epidemiology, Clinical Diagnosis, and Treatment. Cancer Contr. 2018;25((1)):1073274818778256.

4. Misra SP, Misra V, Dwivedi M. Low grade B cell gastric mucosa associated lymphoma presenting as upper gastrointestinal bleeding from non-healing stomal ulcers Postgraduate Medical Journal 2005;81:135-137.

5. Chang Y, Huang M, Shih H, et al. Gastric MALT lymphoma

Figure 9: Follow up EUS shows resolved perigastric lymphadenopathy.

Figure 10: Algorithm for management of MALT lymphoma.

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presented with primary perforation in an adolescent: a case report. BMC Pediatr 2019; 19 :63.

7. Kumar PS, Vinod P, Sudhanwa P et.al. A bleeding gastric lesion: MALToma. Int J Health Sci Res. 2019; 9(5):456-458.

8. Eva Zálabská 1 , Lucie Bareková, Darko Klobuča Gastric MALT Lymphoma - A Case Report] KlinMikrobiolInfekc Lek . 2011 Jun;17(3):89-91.

9. Caletti G, Togliani T, FusaroliP, et al. Consecutive regression of concurrent laryngeal and gastric MALT lymphoma after anti-Helicobacter pylori therapy. Gastroenterology. 2003;124(2):537-43.

10. G. Pinotti, E. Zucca, E. Roggero, A. et al. Clinical features, treatment and outcome in a series of 93 patients with low-grade gastric MALT lymphoma.Leuk Lymphoma. 1997;26: 527-537.

Syed ShafiqHarshad Devarbhavi

Mallikarjun Patil

Department of Medical Gastroenterology, St. John’s Medical College Hospital, Sarjapur Road, Bengaluru-560034, India.

Corresponding Author: Dr Syed ShafiqEmail: syed.dr.s@gmail.com

Chronic Gastric Volvulus: A Rare Cause of Chronic Iron Deficiency Anemia

Gastric volvulus as a clinical entity was first described by Berti in 1866 during an autopsy on a female patient.1

Gastric volvulus occurs when the stomach rotates more than 180 degrees either along its longitudinal (organoaxial)or transverse (mesenteroaxial) axis. Acute gastric volvulus, characterised by Borchardt’s triad of acute epigastric pain, retching with inability to vomit, and difficulty to pass a nasogastric tube, can lead to

strangulation of the stomach with resultant perforation and septic shock and requires urgent surgical attention.2,3 On the other hand, chronic gastric volvulus presents with vague symptoms such as episodic upper abdominal pain, bloating, hiccups, and/or chronic anemia.

Case Report

A 67-year-old male patient with no significant past medical history was referred to us as part of evaluation for his anemia. The patient on further probing gave history of recurrent, self-limiting, spasmodic, on-and-off upper abdominal pain which was unrelated to meals and was nonradiating. He had no other associated symptoms during these pain episodes. Physical examination was non-contributory except for mild pallor. Laboratory evaluation showed a haemoglobin and haematocrit of 7.60 and 23 with a platelet count of 4,26,000. His iron studies pointed towards iron-deficiency anemia with a ferritin level low at 6.1 (21.81 to 274.6 ng/mL). Stool for fecal occult blood was positive. He was subjected to esophagogastroduodenoscopy which revealed severe, Los Angeles grade D reflux esophagitis. Upon entering the stomach, the gastric folds appeared “twisted and turned” and there was difficulty negotiating through the antrum and pylorus indicative of an organoaxial gastric volvulus (Figure 1). The diagnosis was further confirmed with barium study which demonstrated type 4 hiatus hernia with intrathoracic stomach and associated organoaxial gastric volvulus with no evidence of obstruction noted on the study (Figure 2). Since the patient only had on and off pain which did not limit his day-to-day activities, he was

Figure 1 (A): Esophagogastroduodenoscopy showing severe reflux esophagitis; (B): Stomach showing “twisted” gastric folds; (C): Retroflexion view demonstrating the huge hiatus hernia.

A B C