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Bleeding Duodenal Ulcer in a Healthy Infant Presenting with Rectal Bleeding and Requiring Surgical Treatment

Ramnik Patel¹, Narayanaswamy Bommayya², Muhammad Choudhry³, David Drake¹

¹Department of Paediatric Surgery,Great Ormond Street Children’s Hospital London, United Kingdom

²Department of Paediatric Surgery, Royal Alexandra Children's Hospital, Brighton, United Kingdom

³Department of Paediatric Surgery,Chelsea and West Minister Hospital, London, United Kingdom

 

Correspondence:

Ramnik Patel

Department of Paediatric Urology

University College London Hospitals and

Great Ormond Street Children’s Hospital NHS Foundation Trust

London, United Kingdom

Phone: 00447956896641

Fax: 00441162586089

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Abstract

We wish to report the case of a 12-months-old male infant with bleeding duodenal ulcer who presented with vomiting, diarrhoea and rectal bleeding. The infant required exploratory laparotomy and ligation of bleeding point to control bleeding. The presentation, treatment, and outcome of this case requiring surgery for peptic ulcer disease (PUD) in the post-histamine 2 -blocker era has been highlighted. Rectal bleeding is unusual presenting feature of PUD. The management in an infant with upper gastro-intestinal bleeding is resuscitation and stabilization followed by a diagnostic evaluation. Bleeding duodenal ulcer could be a surgical problem even in the post proton pump inhibitors era and is a now rare scenario in current practice.

Key words: duodenal ulcer, acid peptic disease, gastrointestinal bleeding, infant

 

Introduction

Gastrointestinal bleeding (GIB) is a potentially life threatening paediatric medical emergency requiring an appropriate diagnostic and therapeutic approach [1]. Peptic ulcer disease(PUD) generally presents with upper GIB and rectal bleeding is unusual as initial presentation. Most upper GIB in infants is secondary to drug induced iatrogenic cause [2] and a bleeding duodenal ulcer requiring surgical treatment is exceptional.

Case report

A previously healthy male infant presented to us via his local hospital at a year of age with a five day history of vomiting and diarrhoea and a two-day history of passing blood in stools. He was not on any steroids or non-steroidal anti-inflammatory agents. There was no previous gastro-oesophageal reflux disease. Rota virus gastroenteritis was the provisional diagnosis.

During infancy, he had suffered from eczema and there was a significant family history of atopy and bleeding diathesis. He had a significantly dropped haemoglobin and was referred to us to rule out any underlying surgical cause especially bleeding Meckel’s diverticulum with an ectopic gastric mucosa or an atypical intussusception.

On examination, he was well, active, pale, afebrile and had stable vital signs on observation. Abdominal examination showed soft, non-tender abdomen without any signs of peritonism or a palpable mass. A full blood count, serum albumin, serum gastrin, CRP, total Ig, total IgE, specific IgE, celiac screen, clotting screen and hormone levels failed to show any cause for his symptoms and drop in haemoglobin. Given a history of a bleeding diathesis in the family, a haemophilia and clotting screen were performed and reported as essentially normal.

Ultrasound scans at referring district general hospital and our hospital were normal. He underwent a Tc99 Meckel’s scan that was negative, a laparoscopy failed to show any abnormalities, and an upper gastrointestinal endoscopy showed a minor bleeding from the base of a duodenal ulcer in the first part of duodenum associated with a marked mucosal inflammation. His duodenal biopsies were consistent with inflammation and ulceration of the mucosa and his blood test revealed no antibodies against Helicobacter. Rota virus gastroenteritis, bleeding Meckel’s diverticulum, atypical intussusception, acute gastritis, peptic ulcer, stress ulcer, Helicobacter gastritis and Zollinger-Ellison syndrome well all considered in the differential diagnosis at various stages of management.

He was managed conservatively on admission,required fluid resuscitation and was started on omeprazole intravenous therapy which appeared to help initially and a blood transfusion was given. Unfortunately, his bleeding recommenced after twenty-four hours with a further drop in haemoglobin requiring repeat blood transfusion and was unable to stabilize his haemoglobin and rectal bleeding continued. He underwent an exploratory laparotomy for possible vascular malformation at which a bleeding ulcer in the first part of his duodenum was discovered and its base was over run to achieve haemostasis. Following the above, he made a good recovery, tolerated feeds and was discharged home.

He was subsequently reviewed in clinic with gastrin levels, thyroid and parathyroid hormone levels as well as calcium and calcitonin levels after discontinuing lansoprazole for 4 days. The levels of these tests were as follows: gastrin (pre and post meal) 27 pmol/l (normal less than 40), gastrin plus sixty minutes 23 pmol/l (normal less than 40), gastrin 61 pmol/l (normal less than 30), free thyroxine 24.1 pmol/l (normal 12 to 222), TSH 1.1 milliunits /l (normal less than 6), BTH 3.5 pmol/l (normal 0.7 to 5.6), calcium 2.46 mmol/l (normal 2.17 to 2.4 4), Calcitonin 8.3 ng/l (normal 0 to 18.9). At follow up, in order to re-assess the intestinal inflammation detected during the previous endoscopic assessment, he underwent an upper and lower endoscopy, which failed to show any macroscopic abnormalities. The histological assessment showed only a mild chronic gastritis. The histology of remaining GI biopsies, including oesophagus, duodenum, terminal ileum and colon were within the normal limit. The celiac screening was negative, as well as immunoglobulin levels, except that the total IgE was just above the normal limit (30.5 kU/L; normal value: 0-23). The haemoglobin level was 11.4.

He continued on lansoprazole treatment for 18 months and remained asymptomatic. However, we suggested weaning him from lansoprazole in two months’ time. For his haemoglobin level, we started iron supplementation for 12 weeks. He has been off Lansoprazole for the past 3 years and iron supplements were stooped after 3 months following satisfactory blood results. He is well, thriving and asymptomatic at 5 years follow-up.

Discussion

Our case exemplifies the fact that the bleeding duodenal ulcer can be a surgical problem and similar incidental cases are reported earlier in the literature with successful outcome [3-6]. PUD remains a condition with high morbidity and mortality in children despite the availability of effective acid-reducing medications [7]. Massive GIB has been reported due to ascariasis infestation in the tropics [8]. The differential diagnosis of GIB in infants is determined by age and severity of bleed. In infants and toddlers mucosal bleed secondary to gastritis and stress ulcers is a common cause [7]. Edwardset al [9] reports a preoperative risk factors or co-morbidities present in 27 of 29 patients and included steroid or non-steroidal anti-inflammatory drug medications.

The fundamental aim in an infant with UGIB is resuscitation and stabilization followed by a diagnostic evaluation. Upper gastrointestinal endoscopy is the most accurate and useful diagnostic tool to evaluate UGIB in children. Preoperative risk factors or co-morbidities may be present in majority of cases and includes steroid or non-steroidal anti-inflammatory drug medications. Effective prophylaxis of children receiving steroids and nonsteroidal anti-inflammatory drugs may play a role in decreasing the risk of PUD. Parenteral vitamin K, proton pump inhibitors, factor VII, tranexamic acid all have been administered empirically in case of a major UGIB [1, 10]. Therapy in patients having mucosal bleed is directed at neutralization and/or prevention of gastric acid release; high dose proton pump inhibitors (pantoprazole) are more efficacious than H2 receptor antagonists for this purpose. Endoscopic control is feasible in mild cases [11].

Indications for operation in PUD in children are bleeding, pneumoperitoneum, peritonitis, and gastric outlet obstruction refractory to medical therapy. For those children with bleeding, majority respond to simple underruning of the bleeding ulcer vessel(s), underruning of the vessel with vagotomy and pyloroplasty or antrectomy are other options in severe or recurrent case [1-6]. Postoperative complications include re-operation for persistent or recurrent ulcer disease and death has been reported following bleeding duodenal ulcers in infancy [12-14]. Our case had a longer term follow up and had no recurrent symptoms so far but these cases are known to have PUD in adult life.

Conclusion

Gastrointestinal bleeding is a potentially life threatening paediatric medical emergency. Rectal bleeding is an unusual presenting feature of peptic ulcer disease. The management in an infant with upper gastro-intestinal bleeding is resuscitation and stabilization followed by a diagnostic evaluation.Effective prophylaxis of infants receiving steroids and non-steroidal anti-inflammatory drugs may help in reducing the risk of bleeding complication of peptic ulcer disease.Bleeding duodenal ulcer could be a surgical problem even in the post proton pump inhibitors era.

Conflict of Interest: None

 

 

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