Environmental

2015

A challenging case of 
chronic diarrhoea

Volume 44, No.1, 2015 Pages 59-62

Ahmad Al-Hindawi

Vinesh Appadurai

Gemma Ingham

Mostafa Seleem

Case

A man, aged 69 years, presented with a 2-year history of diarrhoea, including nocturnal symptoms, faecal incontinence, abdominal pain and weight loss of 22 kg. He had no per-rectal bleeding. His past medical history included chronic obstructive pulmonary disease (COPD), gout, paroxysmal atrial fibrillation, biventricular failure, aneurysmal dilatation of the ascending aorta, chronic renal failure, hypertension, previous excess alcohol intake and previous endoscopic retrograde cholangiopancreatography (ERCP) for choledocholithiasis. His current medications reflected these conditions. He was an ex-smoker and denied current alcohol use.

Abnormal findings on examination were cachexia, hypotension, reduced air entry in both lung bases and moderate bilateral peripheral oedema. The abdominal examination was unremarkable.

Question 1

What are the differential diagnoses?

Question 2

What non-radiological investigations should be considered?

Answer 1

A history of chronic diarrhoea with weight loss and nocturnal symptoms is suggestive of an organic cause. The main differential diagnoses to consider are:

  • malignancy (eg lymphoma, colorectal cancer, pancreatic carcinoma)
  • coeliac disease
  • inflammatory bowel disease
  • thyrotoxicosis
  • pancreatic exocrine insufficiency
  • mesenteric ischaemia
  • drug-induced effects
  • acute infectious causes (these are unlikely)
  • chronic infectious causes (eg tuberculosis and human immunodeficiency virus infection).

Answer 2

Non-radiological investigations to be considered include:

  • full blood evaluation
  • stool examination
  • oesophagogastroduodenoscopy
  • colonoscopy.

Results for this patient are shown in Table 1.

Table 1. Suggested investigations with the results for this case

Blood examination

Investigation

Result

Units

Reference range

Investigation

Result

Units

Reference range

Hb

118

g/L

135–180

Na+

135

mmol/l

135–145

WCC

9.4

x109/L

4.0–11.0

K+

4.4

mmol/l

3.5–4.1

Platelets

501

x109/L

140–400

Urea

8.4

mmol/l

2.9–8.2

MCV

87

fL

80–100

Creatinine

112

µmol/l

64–108

CRP

121

mg/L

<5.0

Ca2+

2.21

mmol/l

2.15–2.55

INR

1.2

 

 

Mg2+

0.65

mmol/l

0.70–1.10

Albumin

20

g/L

35–50

PO43-

0.80

mmol/l

0.81–1.45

Bili (total)

20

µmol/L

<20

Free T4

22

pmol/l

10–23

Bili (conj)

8

µmol/L

<4

TSH

4.1

mIU/L

0.4–4.0

ALP

133

U/L

56–119

 

 

 

 

GGT

18

U/L

<55

Coeliac antibodies

Negative

 

 

ALT

28

U/L

<45

Vasculitis screen

Negative

 

 

AST

44

U/L

<35

Quantiferon assay

Negative

 

 

Vit D

46

nmol/L

50–150

Anti-S. cerevesiae

Negative

 

 

Iron

8

µmol/L

12–31

C-ANCA

Negative

 

 

Transferrin

0.7

g/l

1.6–3.4

P-ANCA

Negative

 

 

Ferritin

199

µg/L

30–300

 

 

 

 

Folate

32.4

nmol/L

>7.0

 

 

 

 

Stool examination

Investigation

Result

Units

Reference range

 

 

 

 

Calprotectin

750

µg/g

<112

 

 

 

 

Clostridium difficile

Negative

 

 

 

 

 

 

MC&S

Negative

 

 

 

 

 

 

Oesophagogastroduodenoscopy

Macroscopic findings consistent with possible coeliac disease and oesophagitis

Helicobacter pylori CLO test:

Negative

 

 

 

 

 

 

Stomach biopsy:

Mild chronic gastritis

 

 

 

 

 

 

Duodenum biopsy:

Mild active duodenitis

 

 

 

 

 

 

Colonoscopy

Reported as normal, but given suboptimal bowel preparation, recommendation to repeat colonoscopy when possible.

ALP, alkaline phosphatase; ALT, alanine aminotransaminase; ANCA, anti-neutrophil cytoplasmic antibodies; ASCA, anti-Saccharomyces cerevisiae antibodies; AST, aspartate aminotransferase; Bili (conj), conjugated bilirubin; Bili (total), total bilirubin; CLO, Campylobacter-like organism; CRP, c-reactive protein; GGT, gamma-glutamyltransferase; Hb, haemoglobin; INR, international normalised ratio; MC&S, microscopy culture and sensitivity; MCV, mean corpuscular volume; TSH, thyroid stimulating hormone; WCC, white cell count

Case continued

The patient underwent suboptimal colonoscopy, which was reported as normal with the caveat that the bowel preparation was inadequate. A plan was put in place to repeat the colonoscopy and take biopsies, but the patient continued to deteriorate and was unable to tolerate the bowel preparation. Radiological investigations were used to assist in developing a working diagnosis. The results were highly suggestive of Crohn’s disease.

Question 3

What radiological investigations would aid in the diagnosis? What features might be seen?

Answer 3

Computed tomography (CT) and magnetic resonance (MR) enterography and enteroclysis are the main imaging modalities that would aid in the diagnosis of Crohn’s disease. CT and MR have equal accuracy, but MR enterography is preferred as radiation exposure is minimised and it is less invasive than enteroclysis.1 The use of plain film imaging is largely unsupported.

There are three diagnostic features of Crohn’s disease identifiable on CT:

  • mural stratification
  • mural hyperenhancement
  • small bowel wall thickening >3mm.

These features are considered good indicators of clinically active disease.2 In addition, MR imaging (MRI) can also identify ulcerations, increased mesenteric vascularity (comb sign), mesenteric inflammation and reactive adenopathy. CT and MRI can also detect extraintestinal manifestations and complications of Crohn’s disease (eg sacroiliitis, fistulae and abscesses).

It should be noted that normal imaging results alone do not sufficiently exclude a diagnosis of Crohn’s disease.

Case continued

The patient’s MR enterography showed numerous thickened hyperenhancing segments of small bowel (Figures 1, 2). The terminal ileum had several mildly narrowed segments with minimally increased enhancement without wall thickening, and mesenteric lymphadenopathy was present. Although these findings were consistent with a working diagnosis of Crohn’s disease, repeat colonoscopy was still planned, when the patient was more stable, to obtain histological evidence to support a definitive diagnosis.

Figure 1. MR enterography T1 weighted vibe post-contrast coronal image 1 demonstrating a significantly thickened, hyperenhancing segment of small bowel (arrows)
Figure 2. MR enterography T1 weighted vibe post-contrast coronal image 2 demonstrating significant lymphadenopathy (block arrows) with multiple thickened, hyperenhancing segments of bowel (thin arrows)

 

Question 4

What are the features of this condition?

Question 5

What management would you follow for this patient?

Answer 4

Crohn’s disease is a chronic inflammatory bowel disorder that may affect any segment of the intestinal tract with a predisposition for the terminal ileum and colon. The hypothesised aetiology of Crohn’s disease is thought to be a consequence of an inappropriate immunological reaction to intestinal bacteria in a genetically susceptible individual.3 The clinical and pathological features of Crohn’s disease are classically compared to ulcerative colitis (Table 2). The clinical course of the disease is relapsing and remitting.

Table 2. Microscopic and macroscopic features of Crohn’s disease and ulcerative colitis

 

Crohn’s disease

Ulcerative colitis

Clinical features

Frank per-rectal blood

+

++

Mucus in stool

+

++

Abdominal pain

++

+

Abdominal mass

+

Perianal manifestations

+

Fistulae

+

Small bowel obstruction

+

Recurrence post surgery

++

ANCA

+

ASCA

+

Pathological features

Location

Terminal ileum 35%
Caecum 30%

Colonic
+/– backwash ileitis

Distribution

Skip lesions

Continuous; distal to proximal

Granulomata

Yes

No

Crypt abscesses

Rare

Common

Cobblestone appearance

Yes

No

Transmural inflammation

Yes

No

ANCA, anti-neutrophil cytoplasmic antibodies; ASCA, anti-Saccharomyces cerevisiae antibodies

Answer 5

The main aim of treatment for Crohn’s disease is to achieve the best possible clinical, biochemical and histological control with the least adverse effects from medication. The development of biological anti-tumour necrosis factor (anti-TNF) agents (eg infliximab and adalimumab) has significantly advanced the treatment of Crohn’s disease and improved the induction and maintenance of clinical remission in patients with moderate-to-severe disease, especially in those who are corticosteroid-dependent.4

Until recently, the step-care approach has been used, but recent evidence has suggested benefits of more aggressive initial treatment:5 an immunomodulator should be introduced early to maintain remission and avoid the need for multiple courses of steroids. Many patients with an exacerbation of Crohn’s disease can be treated on an outpatient basis with oral steroids (to induce remission) and 6-mercaptopurine (6-MP) or azathioprine (to maintain remission).6 If outpatient treatment fails, intravenous hydrocortisone may be required and hospitalisation is warranted.

Note that 5-aminosalicylic acids have no role in the treatment of Crohn’s disease and are no longer recommended.

If medical therapy for active Crohn’s disease fails, surgical resection of the inflamed bowel with restoration of continuity is indicated. Urgent surgery may be required in rare cases of sustained or recurrent haemorrhage, perforation, abscess and toxic megacolon. Partial small bowel obstruction or intra-abdominal abscess may sometimes be treated conservatively if there is no evidence of ischemia.7,8

Nutritional therapy is an important consideration for the treatment of the disease and for any associated malnutrition.9 Issues such as employment difficulties, psychological health, sexual dysfunction, child development and smoking cessation should not be overlooked.10

Key points

  • Chronic diarrhoea with weight loss and nocturnal symptoms should prompt a search for an organic cause.
  • CT and MR enterography and enteroclysis can aid in the diagnosis of Crohn’s disease.
  • Normal imaging results alone do not exclude a diagnosis of Crohn’s disease; conversely, imaging cannot definitively confirm a diagnosis of Crohn’s disease (this requires histological evidence).
  • More aggressive initial treatment may be better than a step-care approach.

Competing interests: None.
Provenance and peer review: Not commissioned, externally peer reviewed.

References

  1. Siddiki H, Fidler J. MR imaging of the small bowel in Crohn’s disease. Eur J Radiol 2009;69:409–17.
  2. Bodily K, Fletcher J, Solem C, et al. Crohn’s disease: mural attenuation and thickness at contrast-enhanced CT enterography – correlation with endoscopic and histologic findings of inflammation. Radiology 2006;238:505–16.
  3. Abraham C, Cho JH. Inflammatory Bowel Disease. N Engl J Med 2009;361;2066–78.
  4. Rubin DT, Panaccione R, Chao J, Robinson AM. A practical, evidence-based guide to the use of adalimumab in Crohn’s disease. Curr Med Res Opin 2011;27:1803–13.
  5. Travis S, Feagan B, Rutgeerts P, van Deventer S. The future of inflammatory bowel disease management: combining progress in trial design with advances in targeted therapy. J Crohn’s Colitis 2012;6:S250–59.
  6. Lichtenstein GR, Abreu MT, Cohen R, Tremaine W. American Gastroenterological Association Institute medical position statement on corticosteroids, immunomodulators and infliximab in inflammatory bowel disease. Gastroenterology 2006;130:935–39.
  7. Kornbluth A, Sachar DB, Salomon P. Crohn’s disease. In: Feldman M, Scharschmidt BF, Sleisenger MH, editors. Sleisenger & Fordtran’s Gastrointestinal and Liver Disease: Pathophysiology, Diagnosis, and Management. Vol 2. 6th edn. Philadelphia: WB Saunders Co,1998, p1708–34.
  8. Robinson M. Optimizing therapy for inflammatory bowel disease. Am J Gastroenterol 1997;92:12–17S.
  9. Borrelli O, Cordischi L, Cirulli M, et al. Polymeric diet alone versus corticosteroids in the treatment of active pediatric Crohn’s disease: a randomized controlled open-label trial. Clin Gastroenterol Hepatol 2006;4:744–53.
  10. Morrison G, Headon B, Gibson P. Update in inflammatory bowel disease. Aust Fam Physician 2009;38:956–61.

Correspondence afp@racgp.org.au

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