Transcript Upper and Lower Gastrointestinal Bleeding

Upper and Lower Gastrointestinal
Bleeding
Thomas A Kintanar, MD
FAAFP/ABFM
Learning Objectives
At the end of this session, participants will be able to:
1. Identify the symptoms and possible underlying causes of upper
and lower GI
bleeds.
2. Perform tests to determine the site of an upper or lower GI bleed
and
recommend further testing or treatment as necessary to discover
underlying conditions responsible for bleeds.
3. Determine the location of severe or acute GI bleeds while
keeping the patient stable, and treat the patient in a timely
manner to avoid excessive blood loss and/or shock.
Definition
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Gastrointestinal (GI)
bleeding refers to any
bleeding that starts in the
gastrointestinal tract
Divided into upper GI
bleeding, which includes the
esophagus, stomach, and
duodenum
Lower GI bleeding includes
much of the small intestine,
large intestine or bowels,
rectum, and anus
Acute vs occult or obscure
GI Bleeding
Upper
Lower
Acute versus occult
Or obscure
Acute vs Chronic Upper or Lower?
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Signs and symptoms of bleeding in the upper or lower digestive
tract depend on the site and severity
Can include bright red blood in vomit, black or tarry stool, or
bloody stool.
Signs of acute bleeding may include weakness, dizziness,
shortness of breath,abdominal pain and cramping, and/or
diarrhea
Acute GI bleeding can be life threatening and may cause a
person to go into shock, hospitalization is often required.
Chronic bleeding may be accompanied by fatigue, lethargy, and
shortness of breath and can also lead to anemia
Major Presenting Factors of Upper GI
Bleed
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Hematemesis (either red blood or
coffee-ground emesis) suggests
bleeding proximal to the ligament of
Treitz
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The majority of melena (black, tarry
stool) originates proximal to the
ligament of Treitz (90 percent)
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It may also originate from the small
bowel or right colon [3]. Melena may
be seen with variable degrees of
blood loss, being seen with as little as
50ml of blood
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Hematochezia (red or maroon blood in
the stool) may occur in cases of upper
GI bleeding although seen in lower GI
bleeds more commonly
Sudden, severe bleeding is
called acute bleeding. If
acute bleeding occurs,
symptoms may include
 weakness
 dizziness or faintness
 shortness of breath
 crampy abdominal pain
 diarrhea
 paleness
Major Causes of Upper GI Bleed:
Ulcers
Peptic ulcer disease
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Idiopathic
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Drug induced: Aspirin
Nonsteroidal
antiinflammatory drugs
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Infectious: Helicobacter
pylori, Cytomegalovirus,
Herpes simplex virus
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Stress-induced ulcer
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Zollinger Ellison syndrome
Portal hypertension: Varices
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Esophageal varices
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Gastric varices
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Duodenal varices
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Portal hypertensive gastropathy
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Cirrhosis the most common cause
of these anomalies
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In a series of 1000 patients at the
UCLA and West Los Angeles
Veterans Administration Medical
Centers found that esophagogastric
varices were the second most
common cause of UGI bleeding,
accounting for 14 percent of
episodes
Gastritis
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NSAIDs and other
drugs
Infections
Crohn's disease
Illness and injuries
Esophagitis
Esophagitis
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Peptic
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Infectious: Candida
albicans, Herpes simplex
virus, Cytomegalovirus,
Miscellaneous
Pill-induced :Alendronate
Tetracycline Quinidine
Potassium chloride Aspirin
Nonsteroidal
antiinflammatory drugs
Benign tumors and Cancer
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Adenomas and other
benign tumors
Gastric or Esophageal
cancer
Other Causes of Upper GI Bleed
Arterial, venous, or other vascular
malformations
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Idiopathic angiomas
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Osler-Weber-Rendu syndrome
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Dieulafoy's lesion
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Watermelon stomach (gastric
antral vascular ectasia)
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Radiation-induced
telangiectasia
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Blue rubber bleb nevus
syndrome
Traumatic or post-surgical
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Mallory-Weiss tear
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Foreign body ingestion
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Post-surgical anastamosis
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Aortoenteric fistula
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Post gastric/duodenal
polypectomy
Other Causes of Upper GI Bleed:
Tumors
Benign
Miscellaneous
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Leiomyoma
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Hemobilia
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Lipoma
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Hemosuccus pancreaticus
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Polyp (hyperplastic, adenomatous,
hamartomatous)
Malignant
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Adenocarcinoma
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Mesenchymal neoplasm
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Lymphoma
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Kaposi's sarcoma
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Carcinoid
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Melanoma
Metastatic tumor
Major causes of Lower GI tract
Bleeding
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Diverticulosis — 5 to 42
percent
Ischemia — 6 to 18 percent
Anorectal (hemorrhoids,
anal fissures, rectal ulcers)
— 6 to 16 percent
Neoplasia (polyps and
cancers) —3 to 11 percent
Angiodysplasia — 0 to 3
percent
Postpolypectomy — 0 to 13
percent
–
–
–
–
–
–
Inflammatory bowel
disease — 2 to 4 percent
Radiation colitis — 1 to 3
percent
Other colitis (infectious,
antibiotic associated,
colitis of unclear etiology)
— 3 to 29 percent
Small bowel/upper GI
bleed — 3 to 13 percent
Other causes — 1 to 9
percent
Unknown cause — 6 to 23
percent
Major Presenting Factors and
Symptoms of Lower GI Bleed
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Black or tarry stool
Dark blood mixed with
stool
Stool mixed or coated
with bright red blood
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Diverticular disease. This disease is
caused by diverticula—pouches in the
colon wall.
Colitis. Infections, diseases such as
Crohn's disease, lack of blood flow to the
colon, and radiation can cause colitis—
inflammation of the colon.
Hemorrhoids or fissures. Hemorrhoids
are enlarged veins in the anus or rectum
that can rupture and bleed. Fissures, or
ulcers, are cuts or tears in the anal area.
Angiodysplasia. Aging causes
angiodysplasia—abnormalities in the
blood vessels of the intestine.
Polyps or cancer. Benign growths or
polyps in the colon are common and may
lead to cancer. Colorectal cancer is the
third most common cancer in the United
States and often causes occult bleeding
Diverticular disease
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Results from progressive injury
to the artery supplying that
segment
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As diverticulum herniates, the
penetrating vessel responsible
for the wall weakness at that
point becomes draped over the
dome of the diverticulum,
separated from the bowel lumen
only by mucosa
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Vasa recta exposed to injury
along its luminal aspect, leading
to eccentric intimal thickening
and thinning of the media
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Rupture!
Colitis
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Inflammatory: Chron’s/ UC
Infectious: C diff
Collagenous/Lymphocytic:
Colonic Ischemia
Diversion colitis: segment
lacks short chain fa’s
Colonic Ischemia
The Microscopic Colitis’
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Lymphocyctic Colitis
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Main symptom of this disease is chronic
watery diarrhea
Colonoscopy finding normal
Histopathologic findings include an
increased amount of intraepithelial
lymphycytes and other signs of chronic
inflammation
Association between this disease and
celiac disease noteworthy
Limited treatment experience
Sulfasalazine, 5-ASA-preparations and
cortison can be effective, loperamide is
used as symptomatic treatment
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Collagenous colitis
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characterized by a thickened
subepithelial collagenous band in the
colonic mucosa that varies in thickness
from 7 to as much as 100 µm (normal is
1 to 7 µm, with a more prominent band in
the rectum)
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Same colonscopy findings as
Lymphocytic
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May be associated with abnormal
collagen metabolism, Nsaids, bacterial
toxins, diabetes, Other meds ie:
simvastatin, lansoprazole (with
associated linear mucosal defects [58]),
omeprazole, esomeprazole, and
ticlopidine
Hemorrhoids
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External hemorrhoids arise
from the inferior hemorrhoidal
plexus and are located beneath
the dentate line. They are
covered with squamous
epithelium
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Internal hemorrhoids arise from
the superior hemorrhoidal
cushion. Their three primary
locations (left lateral, right
anterior, and right posterior)
correspond to the end branches
of the middle and superior
hemorrhoidal veins
Anal Fissures
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Tear in the lining of the anal
canal distal to the dentate line,
which most commonly occurs in
the posterior midline
Medical therapy
The majority of anal fissures
are caused by local trauma to
the anal canal, such as after
passage of hard stool
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Oral nifedipine
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Oral diltiazem
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Topical diltiazem or
bethanechol
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Surgical Intervention: Lateral
sphincterotomy / Incontinence.
Seen with Crohn's disease,
tuberculosis, and leukemia
Noted cyclic sphincter spasm,
stretching of damaged area,
with slowing of healing,
continued pain and chronicity
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Topical nitroglycerin
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Botulinum toxin
Angiodysplasia
Most common vascular
anomaly in the GI tract
Vascular tumors or angiomas 1
of 3 classifications
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Most prominent feature in
angiodysplasias is the presence
of dilated, tortuous submucosal
veins
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Vascular anomalies associated
with congenital or systemic
diseases 2/3
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Acquired and sporadic lesions
3/3
Small arteriovenous
communications are also
present and are due to
incompetence of the
precapillary sphincter
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Resulting av communications
may be responsible for the
occasional brisk bleeding that
may ensue
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Composed of ectatic, dilated,
thin-walled vessels that are
lined by endothelium alone or
endothelium along with small
amounts of smooth muscle
Angiodysplasia
Polyps
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Hyperplastic Polyps
Adenomatous Polyps
Tubular adenomas
Peutz-Jeghers
Familial Polyposis
Colon Cancer
Clinical Case of Lower GI Bleed:
Bonnie
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78 yo WF widow had 3 month
history of not “feeling like
herself”.
No evidence of abdominal
pain or discomfort
Had culminated in black tarry
and maroon colored stools.
Weakness and inability to
ambulate well prompting her
daughter to transport to rural
hospital ER.
Hgb was 6.3 on admission
and was noted to have
normal vital signs except
pulse of 98
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Initial approach included CT
scan which was negative
3 units of PRBC’s given to
bolster Hgb to 10.4
Pt taken to endoscopy suite
by surgeon for upper
endoscopy
Endoscopy negative
Transported to our facility for
completion of workup
Bonnie
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Past history: Hyperlipidemia,
s/p ectopic pregnancy
laparotomy, blepharoplasty,
peripheral neuropathy,
hypovitaminosis D
Family/Soc history: Negative
for Etoh, and smoking.
Widowed
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ROS: fatigue over 2 months
VS: BP 112/55, P 99
PE: Skin: pale. Chest: clear,
CV: RRR no murmur
Data base: hemoccult
positive, Pancytopenia: rbc:
2.76, wbc: 3.3, plates 4.7,
mpv: 7,few atypical lymphs,
rouleaux formation
Patient scheduled for upper
and lower endo.
Hematology consult
obtained
Diagnostic Approach to the Patient
with GI Bleeding
Esophagogastroduodenoscopy inspects
the esophagus, stomach and duodenum.
Tissue can also be biopsied during this
test.
• Colonoscopy. Studies show colonoscopy
can identify definitive bleeding sites in
more than 70 percent of patients with
lower GI bleeding.
• Capsule endoscopy. A small pill containing
a video camera transmits images of the
small intestine.
• Balloon-assisted enteroscopy. A wireless
scope inspects parts of the small
intestine that EGD and colonoscopy can't
reach.
• Endoscopic ultrasound. An ultrasound
probe attached to an endoscope shows
all the layers of tissue in the digestive
tract.
• Endoscopic retrograde
cholangiopancreatography. An X-ray
visualizes the ducts of the liver and pancreas
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CT enterography involves ingestion of a
neutral contrast agent to distend the
small bowel, followed by CT imaging of
the abdomen
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MR enterography an alternative to CT
enterography. It has the advantage of not
using ionizing radiation, which allows for
sequential imaging of the small bowel
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Nuclear GI Bleed Scan a methodology
employing nuclear radioiodide imaging to
identify active hemorrhage
Bonnie
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Colonoscopy to cecum
performed with identification
of blood in rectal vault
Cecal intubation reveals 2
angiodysplastic lesions
which required heater probe
fulguration with copious
irrigation. Procedure lasting
nearly 1 hour 10 minutes
Hemostasis successfully
achieved
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EGD revealed patchy areas
of erythema. Consistent with
gastritis
Appearance very similar to
angiodysplastic lesions seen
in cecum.
Capsule endoscopy
evaluation held pending
consult from hematology.
3 units of PRBC
administered to approximate
nearly normal H/H.
What to Do When the diagnostic
Answer is not clear?
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When the source of bleeding cannot be identified by
endoscopic, radiographic, or nuclear intervention, the patient
may need exploratory laparotomy
In most circumstances this is accompanied by intraoperative
endoscopy, which has a sensitivity of more than 70 percent for
identifying sources of bleeding and limits the extent ofsurgery in
up to 10 percent of cases
When rectal bleeding stops before the source is identified,
evaluation can proceed in the outpatient setting in patients who
remain stable
Repeat endoscopic evaluation may be necessary in certain
cases
Bonnie
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Hematology consult
obtained
Noted increasing protein
count with decreasing
albumin
Hematology notes elevated
protime and lower fibrinogen
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Diagnosis of Waldenstrom’s
macroglobulinemia made
Plans for plasma exchange
and chemotherapy made
Continued melanotic stools
noted but less in volume
than in past few days
Summary
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A Good History and Physical exam always is our
best arsenal piece
The initial clinical presentation gives us the idea of
how urgent the workup must be
The broad range of diagnostic tools aside from the H
and P are elements easily employed or referred out
for further evaluation
Aside from procedural components of workup, the
Family Medicine team is well equipped to work their
patient up to achieve a fairly accurate diagnosis thus
serving our patients best interest
Questions?
Thank You!
References
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1. Gastrointestinal bleeding. MedlinePlus. National Institutes of Health. January
2011. Available at http://www.nlm.nih.gov/medlineplus/ency/article/003133.htm.
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2. Bleeding in the Digestive Tract. National Digestive Diseases Information Clearinghouse.
January 2010. Available at http://digestive.niddk.nih.gov/ddiseases/pubs/bleeding/.
3. Gastrointestinal Bleeding. Mayo Clinic. Accessed August 2011. Available at
http://www.mayoclinic.org/gastrointestinal-bleeding/diagnosis.html.
4. Manning-Dimmitt LL, Dimmitt SG, Wilson GR. Diagnosis of Gastrointestinal Bleeding in
Adults. American Family Physician. American Academy of Family Physicians. April 2005.
Available at http://www.aafp.org/afp/2005/0401/p1339.html.
5. Krumberger JM. How to Manage an Upper GI Bleed. Modern Medicine. March 2005.
Available at
http://www.modernmedicine.com/modernmedicine/article/articleDetail.jsp?id=150046.
6. Barnert J, Messmann H. Diagnosis and management of lower gastrointestinal bleeding.
Nature Reviews. Medscape CME. November 2009. Available at
http://www.nature.com/nrgastro/journal/v6/n11/full/nrgastro.2009.167.html
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