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Gastrointestinal hemorrhage

- Diagnosis
- Assesment
- Treatment

Dr. Ruxandra Oprita

Presentation of a patient with GI bleeding:
hematemesis / melena/ hematochezia
anemic syndrome: pallor, headache,
angina, dyspneaHematemesis Melena Hematochezia Esophagus

Upper GI bleeding
proximal to the ligament of

Lower GI bleeding from

a site distal to the ligament
of Treitz
Hematemesis = vomiting red, fresh blood or darker ("coffee
grounds" - digested under the action of hydrochloric acid)
Melena = black stools (black/ crude oil, as a result of Hb decay
to hematin), shiny, soft, with a specific odor.
- in UGIB, rarely LGIB(small intestine + proximal colon)
Hematochezia = stool with red-cherry coloured blood, clots;
- in HDI, rarely seen in a severe UGIB

hematemesis melena

Upper GI bleeding
History of liver disease or
1. Initial evaluation : alcohol abuse Varices
History Renal disease, aortic stenosis
Symptom assessment
History of Helicobacter pylori,
Physical examination nonsteroidal anti-inflammatory
drug (NSAIDs) use- Peptic
Lab tests (CBC, BUN, ulcer disease
Nasogastric lavage
Controversial red blood Epigastric or right upper quadrant
cells - Assessment of pain - Peptic ulcer
Confirms an hemodynamic stability
upper GI source Odynophagia, gastroesophageal
Facilitates Microcytic Examination of the
reflux, dysphagia - Esophageal ulcer

endoscopy red blood stool color Emesis, retching - Mallory-Weiss

cells - tear
Presence of rebound
chronic Jaundice, weakness - Variceal
tenderness or
bleeding involuntary guarding - Hemorrhage
perforation Dysphagia, early satiety, involuntary
weight loss - Malignancy
Clinical manifestations:
Pay attention to:
intense feeling of thirst;
cold extremities;
profuse sweating; SHOCK
shortness of breath;
severe paleness.

The appearance of blood loss can be predictive of the

severity: - Hematemesis with red, fresh blood
- Hematochezia originating from upper GI
Evaluation of arterial blood
pressure and heart rate
the highest value for evaluating patients with GI
reflects the amount and the speed of blood loss
from the gut + the compensatory activity of the
cardiovascular system.

Blood volume SBP < 100

> 20%
40% HR > 100 bpm

Blood volume
> 40%
Hematocrit determination
severity of an episode of GI bleeding can not be
estimated immediately after bleeding by Ht or Hb values
because the blood loss consists of figurative elements
and plasma.
Ht / Hb decrease begins with the restoration of plasma V;
24-72 hours are required to complete the process -> Hb
underestimates the severity of the haemorrhage in the
early days.
patient follow-up: clinical (!), TA, AV, stool, Hb.
Laboratory tests

blood samples collected as quickly as possible;

complete blood count: Ht, Hb, platelets, white
blood cells (leukocytosis = normal
posthemorrhagic phenomenon)
INR, PT = coagulopathy, liver failure,
anticoagulant therapy.
urea, creatinine, electrolyte status, ABG( arterial
blood gas).
Evaluation and resuscitation of
the patient with GI bleeding
!! CRITICAL STAGE = fast resuscitation and
hemodynamic stabilization before any diagnostic
or therapeutic procedures
Hemodynamically unstable patient:
- Two large peripheral venous lines;
- Oxygen;
- Infusion: sodium chloride, Ringer's,
- Blood transfusion (Target Hb = 7g / dl)
- Coagulopathy -> Fresh frozen plasma (FFP)
Nasogastric tube

Nasogastric or orogastric lavage is not required in

patients with UGIB for diagnosis, prognosis,
visualization or therapeutic effect.
Endotracheal intubation
to prevent aspiration;
- altered mental status (shock / hepatic
- massive hematemesis;
- variceal haemorrhage.
Prognostic indicators
- age> 60 years;
- shock;
- > 2 comorbidities;
- decrease of> 5 g / dL Hb;
- haematemesis with fresh, bright red blood+
- giant ulcer (> 2cm);
- hemorrhagic relapse (within 72 hours);
- emergency surgery needed;
- etiology: variceal bleeding = highest rate of
mortality and rebleeding.
Differential diagnosis UGIB
Clinical hematemesis / hematochezia
presentation melena
Nasogastric bloody normal
Bowel sounds hyperactive normal
BUN high normal
Major causes of upper GI
Site of bleeding Prevalence
Peptic ulcer disease 30-60%
Esophago-gastic varices 5-30%
Mallory-Weiss syndrome 5-10%
Gastitis 5-10%
Erosive esoghagitis 5-10%
Malignancy 5%
Vascular ectazia 5%
Miscellaneous 5-15%
Peptic ulcer
The most common cause of UGIB;
duodenal ulcer = bleeds 2 x more frequent > UG;
Two important factors :
- Helicobacter pylori
Risk factors associated with NSAIDs ulcer:
age > 65 years;
history of complicated ulcer especially recent
high dose NSAID therapy
previous history of uncomplicated ulcer
concurrent use of aspirin, corticosteroids, anticoagulants

Aspirin + corticosteroids = 10x risk for GI bleeding (little

increased risk when used alone)
Risk of rebleeding
- the risk of rebleeding decreases progressively in the first 3 days
after the initial episode;
Gastric ulcer Forrest I A

Duodenal ulcer Forrest I B

Gastric ulcer Forrest II A

Duodenal ulcer Forrest II B

Duodenal ulcer Forrest II C

Gastric ulcer Forrest III

Pre-endoscopic therapy
intravenous infusion of erythromycin (250 mg ~ 30
min before endoscopy) should be considered to
improve diagnostic yield and decrease the need
for repeat endoscopy.
pre-endoscopic intravenous PPI (80 mg bolus
followed by 8 mg/h infusion) may be considered
to decrease the proportion of patients who have
higher risk stigmata of hemorrhage at endoscopy
and who receive endoscopic therapy. However,
PPIs do not improve clinical outcomes such as
further bleeding, surgery or death.
if endoscopy will be delayed or cannot be
performed, intravenous PPIs is recommended to
reduce further bleeding.
- Patients with UGIB should generally undergo
endoscopy within 24 h of admission

- In patients with higher risk clinical features (e.g.,

tachycardia, hypotension, bloody emesis or
nasogastric aspirate in hospital) endoscopy within
12 h may be considered

- Further analysis found no additional benefit from

very early or urgent (12 hours) endoscopy over
early (12 hours) endoscopy.
Endoscopic therapy for
non-variceal bleeding
Endoscopic therapy should be provided to patients with
active spurting or oozing bleeding or a non-bleeding
visible vessel .

Endoscopic hemostasis techniques

A. thermal methods: mono / bi / multipolar
electrocoagulation, thermocoagulation, laser
coagulation, argon plasma coagulation;
B. injecting various substances: adrenaline, absolute
alcohol, polidocanol, hypertonic saline solution, fibrin,
distilled water, thrombin etc.
C. Mechanical methods: clips.

NB: Epinephrine therapy should not be used alone. If used, it

should be combined with a second modality.
Endoscopic therapy for non-variceal

Ulcer Forrest I B into the duodenal bulb.

Gastric ADK with oozing bleeding.
Vasoconstriction efects of epinephrine in
Epinephrine is injected into the
the submucosal layer will determinate
submucosal layer
temporary hemostasis.
Thermal therapy with bipolar electrocoagulation or heater probe and injection of
sclerosant (e.g., absolute alcohol) are recommended because they reduce
further bleeding, need for surgery, and mortality

Duodenal ulcer
cauterization with Gold Probe Duodenal ulcer, Forrest II A
Mecanical hemostasis using
metalic clips
Argon plasma
coagulation (APC)

Its efficacy is well documented in

treatment of angiodysplasia, GAVE
syndrome, Dieulafoy's lesions, post-
polypectomy bleeding

NOT RECOMMENDED as a first line

treatment for bleeding ulcers
(produces severe tissue necrosis with
a high risk of perforation)

Consequence of portal

Assessing the risc of bleeding :

- size of varices: large, tortuos varices that
cause significant luminal narrowing (Grade
III/IV) bleed more frequently than small
- colour : blue > white;
- extension: proximal > distal;
- concomitant gastric varices;
- red signs present on the surface (cherry
red spots = spotlights and red lines, diffuse
- Child Pugh score.

Big tortuos esophageal varices

(grade III), with significant narrowing
of the lumen, and with high risc of
Gastric varices with active bleeding

Esophageal varices with cherry

Active variceal bleeding spurting
Variceal bleeding
Usually stops spontaneously -50%.
Mortality rate near 70-80% for those with continued bleeding.

Treatment modalities in variceal bleeding

Primary prophylaxis- pharmacologic approaches (nonselective beta

blockers, nitrates) or endoscopic approaches (prophylactic
Treatment of an active bleed pharmacologic approaches
(vasopressin /terlipressin, somatostatin, octreotide), endoscopic
approaches (endoscopic variceal ligation or endoscopic
sclerotherapy), balloon tamponade or TIPS.
Prevention of rebleeding
Medical management of
variceal bleeding
- Synthetic vasopressin analogue
- first-line pharmacologic agent ;
- Mechanism of action: arterial vasoconstriction in
splanchnic territory to decrease portal hypertension;
- without the cardiovascular adverse effects of
vasopressin (angina, hypertension, peripheral
ischemia etc.);
first administration = during the transport to hospital;
2 mg IV bolus, then 1 mg / 6 hours, for at least 48
Ligation and sclerotherapy = similar efficacy; a lower rate of complications
with variceal ligation but with a higher risk for variceal relapse.
!! If bleeding is not controlled with two successive endoscopic
sessions, another therapeutic method is recommended: balloon tamponade,
TIPS, surgery.

Hemostasis of bleeding Hemostasis of bleeding

esophageal varices with esophageal varices with
endoscopic variceal ligation scleroterapy
Active variceal bleeding spuring.
Banded varix can be seen through
the transparent cap
Used to obtain a temporary Transjugular intrahepatic
hemostasis in patients with failed portosystemic shunt.
standard pharmacologic and
endoscopic treatment Expandable metal stent by an
high risk of rebleeding following interventional radiologist who
deflation of the balloon (30-50%). performs a communication between
Complications: esophageal the right branch of portal vein and the
perforation, aspiration pneumonia. middle hepatic vein.
Complications: 25% hepatic
encephalopathy; 30% stent occlusion.
Gastric varices
- On the lesser curvature: regress
after endoscopic therapy of esophageal
- The greater curvature and fornix:
difficult to obliterate endoscopically

-risk factors for bleeding: similar to

esophageal varices

Endoscopic therapy: sclerotherapy,

ligation, injection of cyanoacrylate

Prevention of rebleeding: TIPS.

Mallory-Weiss syndrome
Characterized by longitudinal
mucosal lacerations in the distal
Usually it occurs after an abundant
lunch, alcohol abuse or during
Treatment : - conservative
pregnancy, preceded by forceful
- rarely endoscopic.

Deep Mallory Weiss tear

on the distal esophagus
Hemorrhagic (Erosive) gastritis
Erosive esophagitis Development of hemorrhagic and
Manifestation of GERD erosive lesions
Characterized by endoscopically NSAIDs, Hp, stress lesions, alcohol
visible breaks in the distal ! the importance of prevention -
esophageal mucosa NSAID-induced gastritis = PPI adm.

Severe confluent erosions Multiple superficial erosions

on the level of eso-gastric with active bleeding
junction (class D Los Angles)
Angiodysplasia Def: rupture of an artery with
Aberrant blood vessels, frequently increased caliber, thick wall and
found in the gastrointestinal (GI) tract. located in the vicinity of the
Associated with: mucosa, ulceration.
- old age; The typical localisation is the
- chronic kidney disease; vertical portion of the lesser
- aortic stenosis; curvature.
- Osler-Weber-Rendu disease;
- radiotherapy. Endoscopic, three aspects:
- active spurting bleeding ;
Treatment: Argon plasma coagulation - protruding vessel bleeding;
(APC) - fresh, adherent clot.
Gastric antral vascular ectasia
Occurs in patients with cirrhosis in context of portal hypertension.
Bleeding is most often chronic .
Primary/metastatic disease
Stromal or mesenchymal neoplasms (gastrointestinal stromal tumors ,

Gastric ADK, infiltrative type, GIST, with its typical presentation,

with low speed difuze bleeding central ulceration, active bleeding (seen
in U-turn)
Lower GI bleeding
Site of bleeding Prevalence

Diverticulosis 35 %

Colitis (infectious, 16 %
IBD 13 %

Neoplasia 10 %

Anorectal (hemorrhoids, 16 %
anal fissures, rectal ulcer)
Angiodysplasia 3%

Radiation colitis 3%

Miscellaneous 4%
A diverticulum is a sac-like protrusion of the colonic wall.

Patients with colonic diverticular bleeding typically present with painless

hematochezia that is self-limited (80% cases).
Surgery for patients requiring more than 4 blood units / 24 h.

optimal diagnostic method in patients with acute

in most patients, LGIB is self-limited, allowing
elective colonoscopy after previous bowel
in patients with active, severe LGIB, visualization of
the colonic mucosa is limited by the presence of
blood; in this case, arteriography should be used
as the diagnostic procedure (which may also be
enteroscopy, capsule endoscopy = when the
bleeding site is not discovered;
Inflammatory Bowel Disease

Ulcerative Colitis Crohns disease

Always involves the Perianal disease
rectum (fistula, abceses)

Continuos , simetrical Aphthous ulcers

Loss of vascular
markings Discontinuous lesions

Granularity of the Involvement of the

mucosa terminal ileum

Crohns disease aphtous

Severe ulcerative colitis

Crohns disease
cobblestone sign
Cecum 37 percent
Ascending colon 17
Transverse colon 7 percent
escending colon 7 percent
Sigmoid colon 18 percent
Rectum 14 percent Angiodysplasia of the

Argon plasma coagulation.

Submucosal injection with a
saline/epinephrine solution.
Mechanical hemostasis.

Transverse colon
Ischemic colitis in the elderly, most commonly
affecting sigmoid, descending colon, splenic flexure;
- Colicky abdominal pain, followed at ~ 24 h by
emission of red blood or bloody diarrhea (minimally);
Radiological exam: "thumb printing"
Dg: colonoscopy with biopsy.
Infectious colitis: C. jejuni, Salmonella, Shigella, CD or
viral = CMV ; fecal culture + antibiotics
Colitis radical: immediately or years after Rx-therapy.
Chronic mild bleeding with iron deficiency anemia.
Dg: patient history + colonoscopy with biopsy.
Treatment: electrocoagulation, APC.
ISCHEMIC COLITIS endoscopic view +
Rx (thumbprinting)
Perianal lesions
- Hemorrhoids;
- anal fissures.

Hemorrhoidal bleeding - painless, source: internal hemorrhoids.

- emission of red, fresh blood that coats the stool or at
the end of defecation, not mixed with the faeces.
- appears after increased consistency of the stools/
difficult defecation.

Fissure - bleeding is often accompanied by anorectal pain.

!! rectal polyps and cancer - patients with a history of LGIB require careful
endoscopic examination of the anal canal, rectum and sigmoid.