Obscure G I BLEED

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A CONCEALED INVADER Dr Murali Krishna MD DM

Transcript of Obscure G I BLEED

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A CONCEALED INVADER Dr Murali Krishna MD DM

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Panelists

Dr Rakesh Kochar DM Dr Naresh Bhat DM Dr T G Balachander MS, MCH Dr M Hariharan DM Dr R Ravi Kumar MD

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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.

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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.

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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

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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

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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.

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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.

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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

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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.

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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

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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.

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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.

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Steroids were started for the vasculitis.

Anticoagulants were titrated to adjust INR between 2-3.

Nutritional supplements were given.

Patient was later discharged asymtomatic.

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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

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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

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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

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Presentation

GI involvement - 14 to 65% of patients with PANGastrointestinal 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, Le Thi Huong Du, Godeau P, Jais P, Wechsler BSO Br J Rheumatol. 1988;27(4):258.

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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

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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.

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 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.

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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

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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

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Poor prognostic factors are proteinuria, renal insufficiency, cardiomyopathy, severe GI 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

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Thank you