In June 2010, a 60-year-old male patient presented to clinic for investigation of iron deficiency anaemia and unintentional weight loss. He reported mild heartburn. He had a background medical history of depression, hypertension, hypercholesterolaemia, osteoarthritis, and previous right knee meniscectomy. He admitted to minimal alcohol intake and was an ex-smoker. Regular medications were combination of Lisinopril 20 mg and hydrochlorothiazide 12.5 mg od, Fluoxetine 20 mg od, and Atorvastatin 10 mg od. Relevant laboratory investigations on initial assessment included iron of 4.1 mumol/L (normal 14-31), Hb 9.7 g/dL (normal 13.0-18.0), and transferrin saturation 6.4% (normal 30-40). B12 and folate levels were normal. OGD revealed antral gastritis and full colonoscopy to the caecum was normal. Coeliac antibodies were negative and biopsies confirmed histologically normal colonic and duodenal mucosa with preservation of normal villous architecture. He commenced treatment with oral iron supplementation and was lost to follow up until he was admitted to the hospital with severe abdominal pain in March 2011.
In 2011, bloods showed an elevated white cell count of 16.5 x 109/L (normal 4.0-11.0), neutrophil count of 12.7 x 109/L (normal 2.0-7.5), and a platelet count of 638 x 109/L (normal 150-400). Hb was 13.6 g/dL with normal MCV and MCH values. CRP was 25 mg/dL (normal < 5). Liver enzymes were within normal range with an albumin level of 39 g/L (normal 34-38). He had an acute kidney injury with urea of 16.4 mmol/L (normal 2.1-7.1) and creatinine 144 mumol/L (normal 62-106) on a background of previously normal renal function. PFA showed dilated small bowel loops. See Figure 1.
CT abdomen and pelvis revealed several considerably thickened proximal ileal loops with mildly prominent jejunal loops and small volume ascites suggestive of inflammatory bowel disease. See Figure 2.
His symptoms and blood work settled with conservative management and he was discharged for outpatient follow-up. He continued to take oral iron supplementation.
In April 2012, small bowel follow through showed several dilated jejunal loops measuring up to 6 cm in diameter with regular thickening of the small bowel folds. The terminal ileum was not optimally visualised but appeared normal. Crohn's disease was considered a possible cause of the presentation although the reporting radiologist suggested a differential diagnosis of Whipple's disease or giardiasis. The patient reported vague intermittent abdominal discomfort then but did not commence any treatment.
In July 2013, he proceeded to anterograde double balloon enteroscopy. The procedure was completed successfully to the jejunum and showed that the entire duodenum had duodenitis and definite scalloping of the mucosa. The patient was prescribed a proton pump inhibitor. He was monitored in clinic and continued to report episodic abdominal pain. He was given intravenous iron for persistent iron deficiency anaemia.
Capsule endoscopy was ordered but before this was performed, the patient represented to hospital in May 2014 with a subacute bowel obstruction. He had mildly elevated inflammatory markers (WCC 15.5 Plts 517 CRP 60) and CT abdomen and pelvis noted distal small bowel obstruction.
He settled with conservative management and was labelled with a radiological diagnosis of small bowel Crohn's disease. He commenced on a reducing dose of oral prednisolone and regular Mesalazine 2 g bd. Three months later Azathioprine 50 mg od was introduced to the patient's regimen.
In February 2015, the patient underwent repeat endoscopy as his haemoglobin dropped to 7.9 g/dL. His iron level dropped to 2 mumol/L, transferrin saturations measured 4%, and serum ferritin was 3.8 mug/L (normal 23.0-393.0). OGD showed mild oesophagitis and linear gastritis.
Full colonoscopy to the terminal ileum was entirely normal, with normal colonic and small bowel mucosa on histology. The diagnosis of Crohn's disease was called into question. Mesalazine and Azathioprine were discontinued but the patient experienced a flare of symptom 2 months later and, at his request, his Crohn's medications were reintroduced.
His third admission to hospital occurred in May 2016 when he presented to the emergency department with severe abdominal pain and distension. CT scan noted significant dilatation of small bowel loops with diffuse wall thickening. There was a large amount of free fluid noted in the abdomen and pelvis and free air in the abdomen indicated a bowel perforation. See Figure 3.
He proceeded to laparotomy where he was found to have a large perforated duodenal ulcer involving more than 50% of the circumference of the duodenal wall. Surgeons found also 15 circumferential strictures along the ileum at laparotomy. The strictures were separated by macroscopically normal small bowel giving the pathognomonic appearance of intestinal diaphragm disease. Surgeons, who were unable to photograph the findings, described a "string of sausages" appearance to the bowel. Multiple stricturoplasties were performed.
8 days postoperatively the patient deteriorated due to a leak from the site of previous stricturoplasty and surgical resection of a segment of small bowel was performed with formation of a defunctioning ileostomy. Most of the segments of small bowel with intestinal diaphragms managed by stricturoplasty remained in situ. A 16.5 cm x 5 cm x 4 cm segment of small bowel was sent for pathological examination. There was extensive white exudate present on the external surface. The mucosal surface appeared strictured and flattened with a thickened bowel wall. Histological review of representative sections from the small bowel demonstrated circumferential mucosal ulceration and transmural inflammation. No features of Crohn's disease were identified.
A thorough review of the case uncovered a long-standing history of NSAID use in the past and this confirmed the diagnosis of NSAID-induced diaphragm disease.
The patient admitted to a history of Diclofenac use PRN for 2 years prior to his initial presentation. He took Diclofenac 50 mg intermittently for knee and back pain due to osteoarthritis and stopped taking the drug approximately 3 months before presenting to our services. He was not on a regular proton pump inhibitor (PPI). Although Diclofenac is only available on prescription it did not come to light as part of his medical history. Since the patient had taken it in the past and did not consider it relevant he did not report previous use. After presentation to our services, he did not receive any additional prescriptions for Diclofenac but used over-the-counter ibuprofen intermittently for the next 3 years.
In retrospect, NSAID use accounted for the finding of acute kidney injury in 2011 and gastritis noted at endoscopy. The patient was discharged home one month postoperatively. All Crohn's medications and NSAIDs were discontinued and he remains well.