Obscure G I BLEED

1. Dr Murali Krishna MD DM

2. Panelists
 Dr Rakesh Kochar DM
 Dr Naresh Bhat DM
 DrT G Balachander MS, MCH
 Dr M Hariharan DM
 Dr R Ravi Kumar MD

3. History
 A 48 year old male, well to do businessman
from Chennai.
 Presented with complaints of fresh bleed per
rectum.
 Massive, painless
 H/o of low grade fever for 3-4 days before 15
days of onset of this bleed.
 History use of NSAIDs frequently.

4. History
 No history of
 Constipation
 Chronic acid peptic complaints
 Use of antiplatelets or anti coagulants
 Diarrhoea/wt. loss/loss of appetite
 Non alcoholic and non smoker.

5.  He was seen in other hospital for this complaints
 There gastroenterologist did gastroscopy and
colonoscopy, normal upper GI study.
 Colonoscopy - altered blood in the entire colon
and terminal ileum.
 They did CT abdomen , cecal bleed with
unidentified cause was found

6.  Later CT angiography was performed and no
active ooze was seen
 Selective gel foam embolisation of the cecal
branch of SMA was performed in view of
continuing bleed.
 When bleeding still persisted he was taken up
for surgery

7.  Intraoperative enteroscopy was performed
and blood in the cecum, but no blood was
seen in the distal ileum.
 Right hemicolectomy was resorted as a
desperate measure to stop bleeding.

8.  Third post op day when the bleed recurred
patient was brought to this hospital
 On interviewing he said he had rumble every time
before he passes blood PR
 Examination
 Palor
 Tachycardia, normal BP
 Systemic examination –
 Operative wounds
 Hurried bowel sounds.

9. Investigations
 CBC
 Hemoglobin - 6.9 gm%
 Neutrophils 82 %
 Lymphocytes 8 %
 Eosinophils 5 %
 Monocytes 5 %
 WBC Count 7.18 10³/mm³
 Platelet -272 10³/mm³
 ESR- 96 mm/hr
 LFT, RFT were normal

10. Course
 Urgent CT angiography was done but was of hardly
any help because of inconclusive findings
 Patient was managed in ICU, PRCs were transfused.
 Capsule endoscopy: No active bleed but altered
blood near the anastomotic site anastomotic ulcer
was seen.
 Remained stable for next 3 days with no fall in Hb.

11.  Stepped down to the ward.
 He was started on liquid diet – tolerated, escalated to semisolids
but ...
 Started having colicky abdominal pain along with obstipation
and abdominal distension
 Examination – BS absent, rest normal
 X- ray abdomen, USG abdomen – Normal
 CECT was done for persistent pain and constipation

14. CECT
 Diffuse submucosal wall edema involving the distal
jejunal and ileal loops causing a target appearance to
the bowel.
 The distal superior mesenteric artery had beading with
one or two small aneurysm in the smaller branches.
 The vasa recta supplying the ileal loops appeared
diffusely narrow.
 Pulmonary thromboembolism involving the basal
lobes.

15. Course
 Multidisciplinary inputs were taken–
pulmonlogist, hematologist and
rheumatologist.
 Anticoagulants started for the PTE
 For vasculitis, complete vasculitis screen was
performed and in absence of any markers and
beading PAN concluded as possible
diagnosis.

16.  Steroids were started for the vasculitis.
 Anticoagulants were titrated to adjust INR
between 2-3.
 Nutritional supplements were given.
 Patient was later discharged asymtomatic.

17. PAN – Poly-Arteritis Nodosa
 Polyarteritis nodosa (PAN) is a systemic
necrotizing vasculitis that typically affects
medium-sized muscular arteries, with
occasional involvement of small muscular
arteries
 Prevalence - range from 2 to 33 per million
Prevalences of polyarteritis nodosa, microscopic polyangiitis, Wegener's
granulomatosis, and Churg-Strauss syndrome in a urban multiethnic population
in 2000 J of Rheumat

18.  Most cases of polyarteritis nodosa (PAN) are
idiopathic but also can be in
 hepatitis B virus (HBV) infection,
 hepatitis C virus (HCV) infection,
 hairy cell leukemia

19. Histolopathology
 Polyarteritis nodosa is characterized by
segmental transmural inflammation of
muscular arteries
 In contrast to some other forms of systemic
vasculitis, PAN does not involve veins

20. Presentation
 GI involvement - 14 to 65% of patients with PAN
Gastrointestinal involvement in polyarteritis nodosa. Ebert EC, Hagspiel KD, Nagar M,
Schlesinger N Clin Gastroenterol Hepatol. 2008;6(9):960
 Abdominal pain – 25 %
 Gastrointestinal bleeding – 7 %
 Peritonitis – 4 %
 Intestinal infarction, pancreatitis, and duodenal
ulcer – 2 % each
 Cholecystitis – 1 %
Clinical findings and prognosis of polyarteritis nodosa and Churg-Strauss angiitis: a study in 165
patients.AUGuillevin L, LeThi Huong Du, Godeau P, Jais P, Wechsler BSO Br J Rheumatol.
1988;27(4):258.

21. Diagnosis
 Arteriography is a primary modality used to
diagnose PAN, being positive in more than
60% of patients
 Saccular aneurysms form in the weakened
portion of the vessel wall.
 Vascular lesions tend to occur at branching
points

22.  CT scan shows bowel wall thickening with the
target sign
 The small intestine is the most commonly
affected part of the GI tract, followed by the
mesentery and colon.

23.  Unlike some other vasculitides PAN is not
associated with antineutrophil cytoplasmic
antibodies (ANCA)
 Tissue biopsy may confirm the diagnosis.
 Common biopsy sites include the sural nerve,
muscle, and skin lesions if present.

24.  Corticosteroids +/-cyclophosphamide, are the
mainstay of treatment for hepatitis B– and C–
negative PAN
 Cyclophosphamide, added particularly in the
presence of severe GI involvement, reduces the
incidence of relapse but does not change the 10-
year survival rate
Fauci, A.S., Katz, P., Haynes, B.F. et al. Cyclophosphamide therapy of severe
systemic necrotizing vasculitis. N Engl J Med. 2009; 301: 235–238

25. Prognosis
 If left untreated, patients with PAN have a
dismal prognosis.
 Corticosteroids and cyclophosphamide have
decreased mortality dramatically
 The 1-year survival rate is 85% with
treatment

26.  Poor prognostic factors are
 proteinuria,
 renal insufficiency,
 cardiomyopathy,
 severeGI manifestations,
 central nervous system involvement
Guillevin, L., Lhote, F., Gayraud, M. et al. Prognostic factors in polyarteritis nodosa
and Churg-Strauss syndrome (A prospective study in 342 patients)
. Medicine. 1996;75: 17–28

27. Thank you