Pre-Res Case Presentation: Jo Anne N. Ramos, MD

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Pre-Res Case Presentation

Jo Anne N. Ramos, MD

Upper GI Bleeding in A Chronic NSAID user

GOOD AFTERNOON!

Objectives
To present a case of a male patient who came in

with pallor and a history of melena.


To discuss the different differential diagnosis,

pathopyhsiology, and treatment of UGIB secondary to Chronic NSAID use.

Objectives
To review the journals regarding the

correlation of NSAID use with the development of a Peptic Ulcer Disease.

General Data
E.M.
56 year-old

Male
Mulawin Lane, Old Cabalan, Olongapo City

First admission

Chief Complaint

LIGHTHEADEDNESS/PALLOR

History of Present Illness


4 years PTA (+) epigastric pain characterized as burning, non-radiating, grade 5/10,during the night(1am)

relieved by food intake


No nausea, vomiting noted. No consult done.

History of Present Illness


2 months PTA
(+) epigastric pain, with the same character radiating to the LUQ, associated with 2-3 episodes of black, foul smelling stools no medications were taken or consult done

History of Present Illness


4 days PTA

(+) 3 episodes of black tarry, foul smelling


stools, assoc. with lightheadedness and pallor No medications taken or consult done.

1 day PTA
consult with private MD, given Multivitamins and PPI (Omeprazole 40mg/tab OD) and CBC requested. No follow-up was done.

History of Present Illness


Few hours PTA

(+) lightheadedness, (+) pallor, (+) black tarry stool, (-) hematochezia
sought consult and subsequently admitted

Past Medical History


Hypertensive x 3 years, Metropolol 50mg/tab OD

Arthritis for 4 years, Diclofenac Na, 3-4x as needed for knee

pains
(-) DM (-) Allergies/Asthma/PTB (-) Previous blood transfusion, surgery, or hospitalizations

Family History
(+) Hypertension- maternal side

(+) CVD- maternal side


(-) DM (-) CA (-) Asthma (-) Kidney dse

Personal/Social History
Unemployed at the moment

Heavy alcohol drinker (3-4x of drinking session/week),

Emperador brandy, consumes 3 bottles, with 3-5 drinking companions


39 pack years

Review Of Systems
No weight loss, (+) easy fatiguability, no loss of appetite No jaundice, no abnormal pigmentation of the skin No headache, no colds, no throat pain No palpitation, no chest pain, no paroxysmal nocturnal dyspnea, no

orthopnea
No cough, no difficulty of breathing No changes in bowel habits, (+) melena, (-) diarrhea, (-) hematochezia,(-

) hematemesis, no nausea/vomiting, (-) tenesmus


No dysuria, no hematuria, no flank pain

Review of Systems
No polyuria, polydipsia, polyphagia

No unusual bruising, no cheilosis, no koilonychia, (+) reduced

exercise capacity

Physical Examination
Patient is conscious, coherent, pale, lying comfortably on bed
Vital Signs: BP 100/70 CAR 109 RR 24 T 36.8 Pale palpebral conjunctiva, (-) nasoaural discharge, (-)

tonsillopharyngeal congestion, (-) CLAD


C/L: Symmetrical chest expansion, (-) retractions, no blanching visible

superficial veins, no gynecomastia, clear breath sound,


Adynamic precordium, tachycardic and regular rhythm, (-) murmur

Cont.

Flat,no caput medusae ,normoactive bowel sounds, soft, no

organomegaly non-tender, non-distended, tympanitic on percussion


DRE: (-) mass, (-) skin tag, good sphinteric tone, partially

filled rectal vault, (-) tenderness, (+) black stool on examining finger
Extremities are grossly normal, no edema, no clubbing, no

palmar erythema, with full and equal peripheral pulses,

Salient Features
56 year-old
Male Hypertensive

Dizziness

Osteorthritis 4-yr use of

Diclofenac

Heavy alcohol drinker

Epigastric pain
Melena Pallor

Differential Diagnosis

Characteristic of GI bleeding
Hematemesis Coffee-ground emesis Hematochezia

Melena

Common Causes of GI Bleeding


Peptic Ulcer Disease
Esophagitis Varices Vascular lesions Diverticula Hemmorrhoids Fissures

Inflammatory Bowel Disease

Inflammatory Bowel Disease


UC: diarrhea, rectal bleeding, tenesmus,

passage of mucus, and crampy abdominal pain.


CD: chronic history of recurrent episodes of RLQ

pain and diarrhea

Fissures and Hemmorrhoids do not

causes melena

Diverticula
True and false (pseudodiverticula)bleeding,

hematochezia due to an eroded nutrient artery


Diverticulitis: fever, anorexia, LLQ pain and diarrhea

Vascular lesion (Intestinal Ischemia)


Risk factors: atrial fibrillation, recent myocardial infarction,

valvular heart disease, and recent cardiac or vascular catheterization.


Presentation: severe acute nonremitting abdominal pain,

nausea and vomiting, transient diarrhea, bloody stools.

Esophageal Varices
Increased resistance to portal flow leads to a dilated veins.

There is only a small amount of bleeding, the only symptom may be

dark or black streaks in the stools.


PE will reveal:
Melena Low BP Tachycardia Signs of chronic liver disease

NONVARICEAL BLEEDING Clinical Indicators Absence of liver dse History of peptic ulcers History of H. pylori History of retching/vomiting NSAID/Aspirin use Chronic renal dse Valvular Heart dse History of hereditary hemorrhagic telangiectasia

VARICEAL BLEEDING Cinical Indicators History of varices/variceal bleeding Spider angiomata Caput medusa Ascites Splenomegaly Hepatic encephalopathy Pancytopenia, low albumin

Esophagitis
Chronic intake of NSAID

S/S:
Odynophagia/dysphaghia Pyrosis

Stomatitis
Feeling of something stuck on the throat Nausea/Vomiting

Admitting Diagnosis
Upper GI Bleeding prob. Secondary to BPUD vs. NSAID-induced gastropathy Anemia Secondary

T/C Gouty Arthtritis

Diet: NPO, insert NGT Diagnostics: CBC, ABO typing, Na, K, BUN, SGPT/SGOT, Bleeding profile, Urinalysis, Blood Uric A, Chest Xray, 12-lead ECG IVF: PNSS 1L x 80 cc/hr

Admitting Orders

Therapeutics: Sucralfate 1 gm/tab, 1 tab now then QID Omeprazole 40mg/IV now then 40mg/IV OD Tranexamic Acid 1 g,/IV now

Diagnostics
Exam Blood type/Rh Hemoglobin Hematocrit Result B+ 44 0.14 0.85 0.14 0.01 Ref. Value -------140-180 0.40-0.50 0.30-0.70 0.20-0.40 0.01-0.05 Exam APTT PROTIME % Activity Result 27.3 sec 10.1 sec 145.6% Ref. Value 28-42 10-13.6 70-130

WBC Count
Neutrophils Lymphocytes Eosinophils

20.22 x 109 5.0-10 x 109

INR
MCHC RDW BUA

0.85
31 0.195 0.640 0.200-0.400

Platelet
MCH MCV

274 x 10 9
23.8 76.8

150-350
28-32 82-96

Cholesterol
Triglycerides HDL LDL

4.26
1.53 1.35 2.21

3.1-5.6
0.34-2.28 1.42-6.42 3.9-4.9

Diagnostics

Result Sodium Potassium SGPT SGOT 131.7 3.89 24 14

Reference Value 135-145 3.5-5.5 5-35 8-40

Diagnostics
Light yellow Clear 1.010

Macroscopic Analysis Urinalysis


RBC 0.5 / uL WBC 0.30/ uL

Acidic
Negative for Glucose, Protein

Microscopic Analysis

EC 02 / uL Bacteria none

Chest Xray
Clear lung fields Normal Heart Size Atherosclerotic Aorta Diaphragms and bony thoracic cage are intact

Course in the Ward

Order:
Secure and transfuse 4U PRBC properly typed and crossmatched, each

unit to run for 4-6 h with 6 h interval each.

Course in the Ward


Day 1 of Hospitalization:

S> (-) BM, (-) melena, (-) dizziness


O> Vital Signs: BP130/80, CR 85, RR 20, T 36.8

Patient is pale looking with pale palpebral conjunctiva,

oral mucosa and palms, no coffee ground appearance per NGT, chest/lungs findings are normal, abdominal findings are normal

Course in the Ward


A> S/P BT 2U PRBC,

Patient appears hemodynamically stable

but still with pallor

Course in the Wards


P> Maintain patient on NPO
Facilitate blood transfusion Advised for esophagogastroduodenoscopy Monitor vital signs and watch out for signs of

hypotension Cont. Sucralfate 1gm/tab QID, Omeprazole 40mg/IV OD, Tranexamic Acid 500 mg/IV q6

Course in the Ward


Day 2 of hospitalization

S> S/P BT 4U PRBC (-) dizziness, (-) lightheadedness, (-) BM

since admission, (-) allergic reactions


O> (+) less pallor with light pink palpebral conjunctiva, no

coffee ground material per NGT


A> Patient is asymptomatic and appears to tolerate the

medications given. He shows improvement from anemia with no other signs and symptoms of continuous GI bleeding. He is hemodynamically stable.

Course in the Ward


P> still for EGD
Maintain on NPO
For repeat CBC

CBC
initial Hgb Hct WBC neutrophils lymphocytes eosinophis platelet 44 0.14 20.22 0.86 0.14 0.01 274 repeat 100 0.30 7.17 0.87 0.12 0.12 256 Ref value 140-180 0.40-0.50 5.0-10.0 0.30-0.70 0.12 0.01-0.06 256

Course in the Ward


Day 3 of hospitalization

S> No subjective complaints; for EGD


O> Less pallor, non tender abdomen A> Patients condition has improved P> Pull out NGT
May have soft diet after EGD

EGD result
ESOPHAGUS GE Junctions CARDIA FUNDUS BODY ANTRUM PYLORUS

NORMAL
Stomach distensible No mass (+) 0.5cm ulcer whitebased at antrum

DUODENAL BULB (+) 1.0 cm ulcer white-based with surrounding inflammation at anterior aspect of duodenal bulb IMPRESSION: Gastric Ulcer; Duodenal Ulcer

Course in the Ward


S> S/P EGD

O>
A> UGIB secondary to Gastric Ulcer and Duodenal Ulcer secondary

to Chronic NSAID Use

P> Diet as tolerated D/C IV Omeprazole and shift to Omeprazole tab Start following medications
Amoxicillin 500mg/tab, 2 tab BID Clarithromycin 500mg/tab, 1 tab BID For 7 days Omeprazole 20 mg/tab 1 tab OD for 2 weeks

Cont.

P> Tramadol + Paracetamol tab, 1 tab PRN for

knee pain
For possible discharge

Course in the Ward


Day 4 of hospitalization

S> (-) dizziness, (-) epigatsric pain, (+) BM, yellowish to brown
O> Less pallor A> Patient improved

P> MGH w/ following medications: Amoxicillin 500mg/tab, 2 tabs BID for 6 more days Clarithromycin 500mg/tab, 1 tab BID for 6 more days Omeprazole 20mg/tab, 1 tab OD for 2 weeks Follow-up at OPD after 1 week.

UGIB secondary to NSAID induced GU and DU Gouty Arthritis


FINAL DIAGNOSIS

Discussion
UGIB secondary to Chronic NSAID use

ACUTE UPPER GI BLEEDING


Common medical emergency Incidence: 100-200 cases per 100,000 population Mortality rate: 6-12%

Bleeding from the upper GI tract is approximately 4 times as common as bleeding from the lower GI tract and is a major cause of morbidity and mortality.

Causes of Acute UGIB


COMMON CAUSES LESS FREQUENT CAUSES RARE CAUSES

1. 2. 3. 4.

Gastric Ulcer Duodenal Ulcer Esophageal varices Mallory Weiss Tear

1. Diuelafoys lesion 2. Vascular ectasia 3. Portal hypertensive gastropathy 4. Gastric varices 5. Neoplasia 6. Esphagitis 7. Gastric erosions

1. 2. 3. 4. 5.

Esophageal Ulcers Erosive duodenitis Aortoenetric fistula Hemobilia Crohns disease

Boonpongmanee S, Fleischer DE, Pezzullo JC, Collier K, Mayoral W, Al-Kawas F, et al. The frequency of peptic ulcer as a cause of upper-GI bleeding is exaggerated. Gastrointest Endosc. Jun 2004;59(7):788-94.

Etiology of Upper GI Bleeding


Peptic ulcer disease
Gastric ulcers
Duodenal ulcers Gastric erosions and gastritis

Esophageal and/or gastric varices Stress ulcers Mallory weiss tear

Esophagitis and esophageal ulcers

Etiology of Upper GI Bleeding


Vascular abnormalities (angiodysplasia, dieulafoy lesion,

telangiectasia)
Portal hypertensive gastropathy Neoplasms, benign or malignant Hemobilia Hemosuccus Aortoenteric fistula

Peptic Ulcer Disease with UGIB


Journal Reviews

Peptic Ulcer Disease and UGIB


Peptic ulcer disease (PUD) remains the most

common cause of UGIB.


In a literature review involving more than 10,000

patients with UGIB, PUD was responsible for 2740% of all bleeding episodes.
Stabile BE, Stamos MJ. Surgical management of gastrointestinal bleeding. Gastroenterol Clin North Am. Mar 2000;29(1):189-222

Peptic Ulcer Disease and UGIB


High-risk patient populations at risk for PUD

include those with a history of alcohol abuse, chronic renal failure, and/or nonsteroidal antiinflammatory drug (NSAID) use.
Cheung FK, Lau JY. Management of massive peptic ulcer bleeding. Gastroenterol Clin North Am. Jun 2009;38(2):231-43

Peptic Ulcer Disease and UGIB


Peptic ulcer disease is strongly associated with

Helicobacter pylori infection.


The organism causes disruption of the mucous

barrier and has a direct inflammatory effect on gastric and duodenal mucosa.
There is an interplay between H. pylori and

NSAIDs in the pathogenesis of PUD.

Gastric mucosal barrier: 1.Mucous-bicarbonate layer 2.Surface epithelial layer 3.Microvascular system

Noxious agents: 1.Hydrochloric Acid 2.Pepsin 3.Histamine 4.Bile 5.Pancreatic enzymes 6.Drugs 7.Bacteria

Membrane phospholipids
Phospholipase A2 Stomach Kidney Platelets Endothelium Arachidonic Acid Macrophages Leukocytes Fibroblasts Endothelium

COX-1 housekeeping

COX-2 inflammation

TXA2, PGI2, PGE2, Gastrointestinal mucosal integrity Platelet aggregation Renal function

PGI2, PGE2 Inflammation Mitogenesis Bone formation

Membrane phospholipids

Stomach Endothelium

Arachidonic Acid

Macrophages Leukocytes Fibroblasts Endothelium

COX-1 housekeeping

COX-2 inflammation

Prostaglandin depletion: 1.Inc HCl secretion 2.Dec mucin secretion 3.Dec HCO3 secretion 4.Dec surface active phospholipid 5.Dec epithelial cell proliferation

PGI2, PGE2 Inflammation Mitogenesis Bone formation

Prostaglandin depletion: 1.Inc HCl secretion 2.Dec mucin secretion 3.Dec HCO3 secretion 4.Dec surface active phospholipid 5.Dec epithelial cell proliferation

ULCER HEALING (spontaneous or therapeutic) EROSIONS

EPIGASTRIC PAIN MELENA

Peptic Ulcer Disease and UGIB


Duodenal ulcers are more common than gastric

ulcers, but the incidence of bleeding is identical for both.


In approximately 80% of patients, bleeding

from a peptic ulcer stops spontaneously.


Stabile BE, Stamos MJ. Surgical management of gastrointestinal bleeding. Gastroenterol Clin North Am. Mar 2000;29(1):189-222

Peptic Ulcer Disease and UGIB


The ulcers at highest risk for rebleeding are those that

involve active arterial bleeding or those with a visible, protuberant, nonbleeding vessel in the base of the ulcer.
Despite the dangers associated with a bleeding peptic

ulcer, most patient deaths were not caused by it.


Sung JJ, Tsoi KK, Ma TK, Yung MY, Lau JY, Chiu PW. Causes of mortality in patients with peptic ulcer bleeding: a prospective cohort study of 10,428 cases. Am J Gastroenterol. Jan 2010;105(1):84-9.

Management
Rescusitation Discontinue factors that may propagate further

bleeding
Assess the level of bleeding Etiology of bleeding

Resuscitation

Establish 2 large-bore IVs or central line

Obtain blood for blood typing, CBC, CMP, INR, PTT


Infuse isotonic saline, Ringers lactate, or 5% hetastarch Blood transfusion: O negative if extremely urgent O2 by nasal canula

Discontinue factors that may propagate further bleeding

Discontinue anticoagulants (warfarin, heparin), thrombolytic agents Discontinue antiplatelet agents if possible (aspirin,clopidogrel)

Discontinue antithrombotic agents if possible


Correct prolonged PT/INR with FFP infusions and/or Vitamin K injection

Correct prolonged PTT with protamine infusion if necessary

Level and Etiology of Bleeding

Hematemesis,coffee ground emesis indicate upper GI bleeding Melena usually indicates upper GI bleeding, but can originate more distally

Maroon stool, red blood in the stool typically indicate lower GI bleeding
Any bleeding in the presence of hemodynamic compromise can be upper GI in origin

When is EGD indicated?


The procedure is the best method for examining

the upper GI mucosa.


Compared with upper GI series it is superior for

the detection of ulcers.


Patients must be adequately resuscitated prior

to EGD unless urgent/emergent visualization is needed.

When is EGD indicated?


Recurrent epigastric pain not responsive to therapy

Epigastric pain that is sufficient to wake the patient up.


Weight loss Anorexia Hematemesis Melena

Pharmacologic Treatment:
TRIPLE THERAPY 1. Bismuth subsalicylate 2tabs QID+ Metronidazole 250mg QID+ Tetracycline 500mg QID 2. Ranitidine bismuth citrate 400mg BID + Tetracycline 500mg QID+Clarithromycin/Metronidaz ole 500mg BID 3. Omeprazole 20mg BID + Clarithromycin 500mg BID + Metronidazole 500mg BID or Amoxicillin 1g BID QUADRUPLE THERAPY Omeprazole 20mg (Lansoprazole 30mg) OD Bismuth subsalicylate 2 tab QID Metronnidazole 250mg QID Tetracycline 500mg QID

Center for Disease Control and Prevention, The Key to Cure H. pylori infection and Ulcer, the 2010 update

Thank You!

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