UGI Bleed
Obie M. Powell, M.D.
Joseph A. Iocono, M.D.
Department of Surgery
University of Kentucky
Mr. Mellenna
57 year-old white male with recent history of
dark stools presents to the emergency room
complaining of a two hour history of vomiting
blood and feeling faint.
On presentation the patient is pale and lethargic
complaining of abdominal pain.
History
What other points of the history do
you want to know?
History, Mr. Mellenna
Consider the Following
Characterization of
symptoms
Temporal sequence
Alleviating /
Exacerbating factors:
Pertinent PMH, ROS,
MEDS.
Relevant family hx.
Associated signs and
symptoms
Characterization of Symptoms
Un-relenting nausea with associated burning
epigastric discomfort
Pain is steady and rates it as a 5 on a scale of 110.
Temporal Sequence
Dark stools off and on for approximately 6 months.
Often has some mild epigastric pain to which he pays
little attention. This pain has been occurring for the
same duration.
Today he has been feeling “light headed” for about 3-4
hours, and has been throwing up blood for 2 hours.
Alleviating / Exacerbating Factors
Standing erect worsens his light headedness and laying
down improves it.
Nothing improves the pain or nausea
In the past eating food sometimes relieved his
abdominal pain.
PMH
The patients past history is significant for
 HTN
 MI 3 years prior treated with angioplasty
and stenting.
 COPD
 Osteoarthritis
 No prior abdominal surgery
PMH
Medications
 ASA - supposed to be on it but it bothers his
stomach
 Metoprolol 50mg po BID
 Simvastatin 10mg po daily
 Ibuprofen 400mg po QID prn, none in past 2
weeks
NKDA
Family/Social History
Family History
 Non-contributory
Social History
 Married
 Computer programmer
 ETOH- 6 pack per week
ROS
As in HPI.
The patient denies chest pain, shortness of breath,
fever, chills, anorexia, and dysuria
ROS should emphasize further characterization of
the active disease process AND risk factors that may
complicate surgery such as active infection, active
CAD, poor exercise tolerance
What is your Differential
Diagnosis?
Differential Diagnosis
Consider the following
Esophageal varices
Vascular malformations
Gastric varices
Nose bleed
Erosive gastritis
Aorto-enteric fistula
Mallory Weiss tear
Gastric ulcer
Reflux esophagitis
Duodenal ulcer
Gastric malignancy
Physical Exam
What are you looking for?
Physical Exam
What to look for
 Vital signs: instability, respiratory distress, beware
of beta blockade
 Overall appearance: signs of anemia, dehydration
 Abdominal exam: probe for peritonitis
 Rectal exam: mandatory. Look for perianal causes
of bleeding.
Physical Exam, Mr. Mellenna
Vital signs: Temp. 97.8, Pulse 90, BP 95/63
Resp. 30
Patient is alert and oriented. Pale skin and dry
mucous membranes.
During your examination the patient has a large
maroon bowel movement
Physical Exam
 Head is atraumatic /
normocephalic, eyes sunken,
pale conjunctiva
 Neck- No lymphadenopathy,
flat neck veins.
 Oropharynx - dried blood, no
active bleeding, dry mucus
membranes.
 CV- Regular rate and rhythm, no
murmur, rubs, or gallops
 Chest- Mild tachypnea,
respirations are clear bilaterally no
rales, rhonchi, or wheezes
 Abdomen is scaphoid, soft,
mildly tender in midepigastrum. Bowel sounds are
present and hyperactive.
 Extremities show no clubbing,
cyanosis, or edema.
 Rectal exam shows gross blood,
enlarged smooth prostate, no
palpable masses, no
hemmorhoids or other peri-anal
disease
Would you like to revise your initial
differential diagnosis?
What Labs do you need ?
Laboratory studies:
What is necessary?
Type and Cross
CBC: Do you expect anemia?
CMP: evaluate for hepatic dysfunction and renal
compromise
Coags: active hemorrhage can cause
coagulopathy and requires aggressive
replacement
ABG: probe for acidosis
Laboratory Values
10.2
11
144
31.1
140
LFTs: Normal
55
108
4.3
ABG: 7.23 | 28 | 80 | 18 | -5
PT: 18 (1.5) PTT: 36
110
20
1.1
What do you think about the labs?
Laboratory Values Discussion
An elevated BUN to Creatinine ratio can be a sign of
upper GI bleed due to the digestion of blood or
prerenal azotemia.
A patient actively hemorrhaging will show a normal
Hgb/Hct prior to being resuscitated. Chronic bleeding
presents with typical iron deficiency anemia.
What would you do now?
Interventions to consider
ABC’s
 Ensure adequate airway protection and adequate
respirations
 Start 2 large bore IV’s.
 Fluid bolus either NS or LR
Foley Catheter
NG with gastric lavage
STAT Upper endoscopy
Endoscopy
 Upon upper endoscopy the
esophagus appears normal.
 There is a large amount of clot in
the stomach, irrigation reveals
normal appearing mucosa
without signs of ulcer or
gastritis.
 On passing through the pylorus
copious gross blood is
encountered with a actively
bleeding ulcer on the posterior
wall of the duodenum.
What would you do now?
Endoscopy
Attempt at injecting with epinepherine, and
even direct pressure prove unsuccessful with
continued brisk pulsatile bleeding.
Are there any particular endoscopic findings
that suggest a higher risk of failed therapy or rebleeding?
What would you do next?
Repeat Hct is 18
He is actively bleeding in Endoscopy
Surgery for Bleeding Ulcers
Indications
Pre-operative preparation
Operative approach
Relevant Anatomy
Potential complications
Operative Indications
Duodenal ulcers located on the anterior wall
are prone to perforation and present as
peritonitis and free air. Those on the posterior
wall, which is the more common location, lead
to bleeding.
The gastroduodenal artery passes just distal to
the pylorus and posterior to the duodenum. If
it or one of it’s branches are in the ulcer crater
they may erode and result in massive bleeding.
Operative Technique
Patients are explored through an upper midline
incision.
An incision is made in the anterior duodenum
through the pylorus and distal stomach.
The site of bleeding is identified. The bleeding can
then usually be controlled by placing sutures in 3-4
quadrants around the ulcer base.
The gastroduodenal artery may be ligated if
necessary
Operative Technique
Once bleeding has been controlled, the
horizontal opening through the pyloric channel
is closed vertically resulting in a HeinekeMikulicz pyloroplasty.
A truncal vagotomy is then added for long-term
ulcer control. Specimens of both vagal trunks
are sent to Pathology to document the vagotomy
Gastrointestinal Bleeding
Discussion
Gastrointestinal Bleeding
Bleeding can arise anywhere along the GI tract.
Bleeding represents the initial symptom of
gastrointestinal disease in 1/3 of all patients.
The majority of bleeding will stop
spontaneously.
Gastrointestinal Bleeding
Hematemesis- Vomiting of blood. Can be either gross
blood and blood clots representing rapid bleeding or
“coffee-ground” emesis signifying chronic bleeding.
Hematemesis is the result of bleeding from the
oropharynx to the ligament of Treitz.
Melena- Passage of black and tarry stool caused by
digested blood.
Gastrointestinal Bleeding
 Melena is usually the result of severe upper GI
bleeding. Melena without hematemesis is
caused by severe bleeding distal to the ligament
of Treitz.
 Hematochezia- Passage of maroon to red blood
and blood clots.
Gastrointestinal Bleeding
 As little as 50-60 mL of blood in the GI tract
produces melena. Melena can persist from 5-7
days after a 2 unit bleed and stools can remain
occult positive up to 3 weeks.
 With upper GI blood loss blood urea nitrogen
levels may be elevated to 30-50 mg/dL. A
BUN: Creatinine ratio greater than 36:1 likely
represents blood loss from an upper GI source.
Upper Gastrointestinal Bleeding
 Some dependency on socioeconomic factors.
Peptic ulcers are more common in suburban
hospitals, while gastritis and varices are more
common in urban centers. Patients 60 years old
and older represent ~ 60% of patients presenting
with upper GI bleeding with a mortality rate of
20-25%. For younger patients the mortality rate
drops to 4%.
Upper Gastrointestinal Bleeding
 Although elective surgeries for duodenal ulcers
have dropped off significantly due to H2
blockers and proton pump inhibitors, the
number of surgeries for bleeding duodenal
ulcers has remained stable.
 Sudden cessation of H2 blockers or proton
pump inhibitors may result in a rebound
increase in acid secretion resulting in GI
bleeding.
Upper Gastrointestinal Bleeding
 Nose bleeds- Rarely the cause of major
bleeding. It must be ruled out by a careful
examination of the posterior pharynx to insure
blood is not running down the esophagus,
causing hematemesis .
Upper Gastrointestinal Bleeding
 Esophagitis- Hiatus hernia and reflux
esophagitis are not common causes of upper GI
bleeding. Reflux esophagitis is more likely to
result in chronic occult bleeding usually
associated with grade II-III esophagitis with
friable mucosa. Significant bleeding in this area
is more commonly associated with paraesophageal hernias.
Upper Gastrointestinal Bleeding
 Varices- Bleeding esophageal and gastric
varices in the presence of liver disease account
for about 10% of upper GI bleeds and are life
threatening situations associated with a high
mortality rate. Alcoholism is the most common
cause of portal hypertension but hepatitis B and
C are becoming common causes.
Upper Gastrointestinal Bleeding
 Varices- In pediatric patients 95% of all upper GI
bleeds are caused by variceal hemorrhage, usually as a
consequence of extra hepatic portal venous obstruction.
In patients with cirrhosis and portal hypertension
variceal hemorrhage accounts for 50-75% of all upper
GI bleeds. Variceal hemorrhage is usually precipitated
by ulceration of the varix secondary to reflux
esophagitis or increased pressure within the varix.
Upper Gastrointestinal Bleeding
 Varices- In patients with liver disease bleeding
is precipitated by the inability of the liver to
synthesize clotting factors. Initial therapy
includes sclerotherapy, ligation and vasopressin.
Ligation is as effective as sclerotherapy with
fewer complications. If unsuccessful shunting
or transplant may be necessary.
Upper Gastrointestinal Bleeding
 Mucosal tear (Mallory-Weiss)
 Esophagogastric mucosal tear or Mallory-Weiss tear
account for 5-10% of all upper GI bleeds. Mallory-Weiss
tears present in a classic pattern. Initially the patient has
vomiting without blood. Continued emesis leads to pain
from the tear and eventually the patient develops
hematemesis. 90% of Mallory-Weiss bleeding resolves
spontaneously and require no further therapy.
 If bleeding persists, endoscopic therapy with injection of
vasoconstrictive agents, IV vasopressin or balloon
tamponade with Sengstaken-Blakemoore tube may be
necessary.
Upper Gastrointestinal Bleeding
 Gastritis
• Up to 1/3 of upper GI bleeds are caused by diffuse
gastritis. Erosions are usually multiple and found
primarily in the fundus and body of the stomach. Chronic
slow bleeds are most commonly associated with H. pylori,
while more brisk bleeding is usually a result of ingested
substances harmful to the gastric mucosa such as NSAIDs,
alcohol, steroids, or other drugs.
• Treatment is with vasopressin, iced saline lavage,
sucralfate, H2 blockers, and proton pump inhibitors.
Bleeds refractory to these treatments may require
electrocautery, vagotomy and antrectomy or even total
gastrectomy.
Upper Gastrointestinal Bleeding
 Peptic ulcer
• Most common cause of upper GI bleed, encompassing 1/22/3 of patients. Bleeding is presenting symptom in up to
10% of these patients. Duodenal bleed is four times more
common than gastric ulcer bleed. Duodenal ulcers are
usually posterior and involve branches of the
gastroduodenal artery.
• Benign gastric ulcers bleed more than malignant ulcers.
There will be significant bleeding in 10-15% of peptic
ulcers and surgical intervention is needed in 20% of these
patients
Upper Gastrointestinal Bleeding
 Stress ulcers
• Stress ulcers refer to acute gastroduodenal lesions that
arise after episodes of shock, sepsis, surgery, trauma, burns
(Curling’s ulcer), or intracrainial pathology or surgery
(Cushing’s ulcer). Specific risk factors associated with
these ulcers are, multi system trauma, hypotension,
respiratory failure, sepsis, jaundice, recent surgery and
burns.
• It is believed that stress ulceration is the result of bile
reflux damage to the gastric protective barrier combined
with decreased gastric blood flow secondary to splanchnic
vasoconstriction. Sepsis, coagulopathy, and activation of
cytokines may also play a role in the formation of stress
ulcers.
Upper Gastrointestinal Bleeding
 Other causes
• Miscellaneous causes may contribute up to 18% of upper
GI bleeds. Gastric neoplasms both malignant and benign
can cause bleeding which is usually mild and chronic.
Dieulafoy’s vascular malformations are dilated arterial
lesions usually amendable to endoscopic injection.
• Aorto-enteric fistulas can present as a herald bleed
followed by a massive bleed in patients with prior aortic
reconstructions. Hematobilia can be found in patients
following hepatic injuries or manipulations.
Upper Gastrointestinal Bleeding
 Management- Complete history with inquiries of
peptic ulcer disease, alcohol use, cirrhosis, heart burn,
reflux, and medications. Exam looking for signs of
cirrhosis including spider angiomata, palmer
erythema, prominent abdominal veins, caput medusa,
and ascites. Examine mucous membranes for
melanin spots associated with Puetz-Jeghers
syndrome. Perform rectal exam and check for occult
blood in the stool.
Upper Gastrointestinal Bleeding
 Management- Fluid resuscitation, foley, nasogastric tube, gastric lavage and arterial line.
 Labs- Complete blood count with platelets,
comprehensive metabolic panel with liver
functions, and coagulation studies. Cross
match for blood transfusion.
Upper Gastrointestinal Bleeding
 Studies/Treatment :
• EGD with sclerotherapy or electrocautery,
tagged red blood cell scan, arteriography with
embolization.
• If esophageal bleeding does not respond to
sclerotherapy, ligation, or intravenous
vasopressin, Sengstaken-Blakemoore tube
should be used.
Upper Gastrointestinal Bleeding
 TIPS- for portal hypertension
• Trans jugular intrahepatic porto-systemic shunt.
Used for bleeding secondary to portal hypertension.
Associated with in hospital mortality rate of 35-56%.
Encephalopathy rate is the same as for patients who
undergo porto-caval shunts. Stenosis or occlusion of
TIPS is up to 50% at one year.
Lower Gastrointestinal Bleeding
 Small Bowel- Small bowel accounts for 10-15% of
all lower GI bleeds. Usually a diagnosis of exclusion.
Seeing blood exiting the ileo-cecal valve accounts for
10% of diagnoses. Causes include, Meckel’s
diverticulum, Crohn’s disease, intussusception,
neoplasm, vascular malformations, intestinal varices,
blood dyscrasias, non-Meckel’s diverticulum,
mesenteric thrombosis, drug reactions, enteric
infections, and polyps.
Lower Gastrointestinal Bleeding
 Colon- Most often related to polyps or
neoplastic disease (occult). Right sided lesions
usually present through anemia and guaiac
positive stools. Larger bleeds can arise from
diverticuli or angiodysplastic lesions on either
the right or left side.
Lower Gastrointestinal Bleeding
 Angiodysplastic lesions have the following
characteristics. They are not congenital or neoplastic
but degenerative. They are not associated with other
vascular lesions. They increase with age. They are
usually small < 5mm. They can be diagnosed by
colonoscopy. 80% of angiodysplastic bleeds will stop
spontaneously and 50% will re- bleed within 3 years.
 Ulcerative colitis- Usually cause chronic bloody
diarrhea, but massive bleeds can occur
Lower Gastrointestinal Bleeding
 Management- Complete H&P. Fluid
resuscitation, foley, naso-gastric tube, gastric
lavage and arterial line.
 Labs- Complete blood count with platelets,
comprehensive metabolic panel with liver
functions, and coagulation studies. Cross
match for blood transfusion.
Lower Gastrointestinal Bleeding
 Studies/Treatment:
• Normalize coagulation. Colonoscopy, tagged
red blood cell scan 91% sensitive and 100%
specific. Angiography with or without coil
embolization.
• Local resection of defined bleeds, otherwise if
bleeding continues and no source can be
identified within the colon, total colectomy is
indicated.
Rectal and Anal Bleeding
 Fresh red blood on the exterior of stool usually
represents hemorrhoids, fissures, or proctitis.
Bleeding that drops into the toilet water is most
likely the result of fissures or hemorrhoids. All
rectal bleeding should be fully investigated with
full H&P, anoscopy / proctoscopy and if
necessary exam under anesthesia.
QUESTIONS ??????
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