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UPPER GASTROITESTINAL BLEEDING
PRESENTER: NEGESU G(EMCCR1)
MODERATOR: DR.IBSA (EMCCR3)
1
OUTLINE
ī‚§ Introduction
ī‚§ Approach of patient with UGI bleeding
ī‚§ Cause of upper GI bleeding and Its management
ī‚§ Disposition
ī‚§ Reference
2
INTRODUCTION
GASTROINTESTINAL BLEEDING (GIB)
ī‚§ are defined based on their location relative to the ligament of Treitz in the terminal
duodenum, so esophagus, stomach, and duodenum origin bleeds are upper and all
others are lower.
ī‚§ Upper gastrointestinal bleeding is any GI bleeding originating proximal to the
ligament of Treitz.
ī‚§ Upper GI (UGI) bleeding is more common than lower GI (LGI) bleeding (2x)
3
Contâ€Ļ
ī‚§ Patients with acute UGIB commonly present may present in five
ways:
ī‚§ Hematemesis is vomitus of red blood or "coffee-grounds" material.
ī‚§ Melena is black, tarry, foul-smelling stool.
ī‚§ Hematochezia is the passage of bright red or maroon blood from
the rectum.
ī‚§ Occult GI Bleeding (GIB) may be identified in the absence of overt
bleeding by a fecal occult blood test or the presence of Iron
Deficiency.
ī‚§ Finally, patients may present only with symptoms of blood loss or
anemia such as Lightheadedness, Syncope, Angina, or Dyspnea.
4
Contâ€Ļ
ī‚§ UGIB may be a life-threatening emergency and requires prompt evaluation,
diagnosis, stabilization, and therapeutic measures in a rapid fashion.
ī‚§ The initial evaluation of patients with involves an assessment of hemodynamic
stability and resuscitation if necessary.
ī‚§ Diagnostic studies (usually endoscopy) follow, with the goals of diagnosis, and
when possible, treatment of the specific disorder
ī‚§ Management depends on the location and severity of the source and the
methodical identification of these.
5
Contâ€Ļ
ī‚§ The mortality rate for patients <60 years in the absence of major concurrent
illness is <1%.
ī‚§ Outcomes are dependent upon time to diagnosis and appropriate management.
ī‚§ Independent predictors of rebleeding and death in patients hospitalized with
UGIB include
ī‚§ Increasing Age,
ī‚§ Comorbidities, and
ī‚§ Hemodynamic Compromise (Tachycardia or Hypotension).
6
contâ€Ļ
ī‚§ UGIB can be classified into several broad categories based on anatomic and
pathophysiologic factors.
ī‚§ From a pathophysiologic perspective,
ī‚§ ulcerative and erosive lesions (gastric or duodenal ulcers, esophagitis, and gastritis) .
ī‚§ vascular lesions (varices, angiodysplasia),
ī‚§ mass lesions (adenocarcinoma, polyps), or
ī‚§ traumatic lesions (Mallory-Weiss tear).
7
Contâ€Ļ
ī‚§ The source of bleeding cannot be identified in 10 to 15 percent of patients with
UGIB, probably because the culprit lesion is either
ī‚§ difficult to identify (such as a Dieulafoy's lesion),
ī‚§ obscured by retained blood clot at endoscopy, or because the culprit lesion healed
by the time endoscopy was performed.
8
Contâ€Ļ
ī‚§ The most common causes of UGIB include the following (in approximate
descending order of frequency):
ī‚§ Gastric and/or duodenal ulcers
ī‚§ Severe or erosive gastritis/duodenitis
ī‚§ Severe or erosive esophagitis
ī‚§ Esophagogastric varices
ī‚§ Portal hypertensive gastropathy
ī‚§ Angiodysplasia (also known as vascular ectasia)
ī‚§ Mallory-Weiss syndrome
ī‚§ Mass lesions (polyps/cancers)
ī‚§ No lesion identified (10 to 15 percent of patients)
9
Contâ€Ļ
ī‚§ Other less common causes of UGIB include:
ī‚§ Dieulafoy's lesion
ī‚§ Gastric antral vascular ectasia
ī‚§ Hemobilia
ī‚§ Aortoenteric fistula
ī‚§ Cameron lesions
ī‚§ Ectopic varices
ī‚§ Iatrogenic bleeding after endoscopic
10
11
Approach of patient with UGI bleeding
Initial Assessment
ī‚§ initial evaluation begins with a prompt assessment of hemodynamic
instability and aggressive resuscitation.
ī‚§ Delays in resuscitation lead to delays in therapeutic interventions, and
thus increased morbidity.
ī‚§ The first priority in managing UGIB is to stabilize and resuscitate the
patient.
ī‚§ Briefly, the examiner must rapidly assess the airway, breathing, and
circulation and be prepared to institute critical care measures such as
intubation, insertion of large bore intravenous lines, and goal directed
resuscitation.
12
Contâ€Ļ
ī‚§ Key steps in the management of any patient with GI hemorrhage include the
following:
ī‚§ Resuscitation; correction of coagulopathy, thrombocytopenia, if present.
ī‚§ Diagnosis and treatment- medical, endoscopic, or invasive radiologic or
surgical intervention, if indicated
ī‚§ Chief complaint GI bleed
ī‚§ Triage, vital sign assessment
ī‚§ Stable or unstable?
13
Contâ€Ļ
ī‚§ Triage
ī‚§ All patients with hemodynamic instability or active bleeding (manifested by
hematemesis, bright red blood per nasogastric tube, or hematochezia) .
ī‚§ should be admitted to an intensive care unit for resuscitation and close
observation with automated BP monitoring, ECG monitoring, and pulse oximetry.
14
CONTâ€Ļ
ī‚§ Unstable patient : -Abnormal vital signs, Shock
ī‚§ Resuscitate: Two large-bore Ivs, Crystalloid infusion, Consider transfusion
ī‚§ Massive upper GIB
ī‚§ Airway management- Intubate as needed to protect airway
from aspiration of hematemesis.
ī‚§ Emergent GI consult with ED endoscopy to identify and stabilize bleed.
15
Contâ€Ļ
ī‚§ Objectives of treatment
ī‚§ Hemodynamic restoration
ī‚§ Arresting or decreasing bleeding
ī‚§ Preventing recurrence of bleeding
16
RESUSCITATION
General support —
ī‚§ Maintain the air way
ī‚§ Elective endotracheal intubation in patients with ongoing hematemesis or
altered respiratory or mental status may facilitate endoscopy and decrease
the risk of aspiration.
ī‚§ Patients should receive supplemental oxygen by nasal cannula and
ī‚§ should receive nothing per mouth.
ī‚§ Establish two large bore IV lines (16 gauge).
ī‚§ For patients who are hemodynamically unstable treat initially with rapid,
bolus infusions of isotonic crystalloid.
17
Hemodynamic Resuscitation
Fluid resuscitation:
ī‚§ Adequate resuscitation and hemodynamic stabilization is essential prior to
endoscopy to minimize treatment-associated complications.
ī‚§ Administration of a 1 L bolus of crystalloid fluid should then ensue, unless
contraindicated by a medical comorbidity.
ī‚§ If hemodynamics has not improved, this bolus should be repeated.
ī‚§ The rate of fluid resuscitation will in part depend on whether the patient is
hemodynamically unstable.
ī‚§ Patients at risk of fluid overload may require intensive monitoring.
18
Contâ€Ļ
Blood product transfusions
ī‚§ Provide transfusion if either of the following is present
o Hemodynamic instability (hypotension) is present.
o Hemoglobin <9 g/dL in high-risk patients (e.g. elderly, CAD)
o Hemoglobin <7 g/dL (70 g/L) in low-risk patients
ī‚§ Patients with active bleeding and hypovolemia may require blood transfusion
despite an apparently normal hemoglobin.
ī‚§ It is particularly important to avoid overtransfusion in patients with suspected
variceal bleeding, as it can precipitate worsening of the bleeding.
19
Contâ€Ļ
ī‚§ Thrombocytopenia -
ī‚§ Patients with active bleeding and a low platelet count (<50,000/microL) should
be transfused with platelets.
ī‚§ To perform an upper endoscopy if the platelet count is >20,000/microL,
though if the patient is suspected to have active bleeding, we attempt to raise
the platelet count to >50,000/microL prior to endoscopy.
20
Contâ€Ļ
ī‚§ Coagulopathy —correction of coagulopathy
ī‚§ Patients with a coagulopathy that is not due to cirrhosis and with a prolonged
prothrombin time with INR >2.0 should generally be transfused with FFP.
ī‚§ More rapid reversal of anticoagulation can be achieved if needed by the use
of prothrombin complex concentrate infusions and is the preferred
approach for patients with serious/life-threatening bleeding.
ī‚§ Low dose vitamin K should be considered for hemodynamically unstable
patients who are taking a vitamin K antagonist.
ī‚§ A unit of FFP should also be given after every four units of PRBC because
packed red blood cells do not contain coagulation factors.
21
Contâ€Ļ
History
ī‚§ the diagnosis of the location of the hemorrhage becomes the priority.
ī‚§ Ask about hematemesis, coffee-ground emesis, or melena.
ī‚§ The history should involve inquiring about prior gastrointestinal bleeds, since up to
60 % of UGIB are from the same lesion previously identified.
ī‚§ as well as alcohol use, liver disease or presence of varices,
ī‚§ history of ulcers or symptoms related to them, history of vascular
anomalies, prior surgeries or interventions.
ī‚§ Symptoms that suggest the bleeding is severe include orthostatic dizziness,
confusion, angina, severe palpitations, and cold/clammy extremities.
22
Contâ€Ļ
ī‚§ Symptoms related to the underlying cause
ī‚§ Peptic ulcer – Upper abdominal pain
ī‚§ Esophageal ulcer – Odynophagia, gastroesophageal reflux, dysphagia
ī‚§ Mallory-Weiss tear – Emesis, retching, or coughing prior to hematemesis
ī‚§ Variceal hemorrhage or portal hypertensive gastropathy: Jaundice,
abdominal distention (ascites)
ī‚§ Malignancy – Dysphagia, early satiety, involuntary weight loss, cachexia
23
Contâ€Ļ
ī‚§ Past medical history —
ī‚§ prior episodes of UGIB, since up to 60% of patients with a history of an
upper GI bleed are bleeding from the same lesion.
ī‚§ Potential bleeding sources suggested by a patient's past medical history
include:
ī‚§ Varices or portal hypertensive gastropathy in a patient with a history of
liver disease or alcohol abuse
ī‚§ Aorto-enteric fistula in a patient with a history of an abdominal aortic
aneurysm or an aortic graft
ī‚§ Angiodysplasia in a patient with renal disease, aortic stenosis, or
hereditary hemorrhagic telangiectasia
24
Contâ€Ļ
ī‚§ Medication history:
ī‚§ Predispose to peptic ulcer formation, such as aspirin and other NSAIDs.
ī‚§ Are associated with pill esophagitis.
ī‚§ Promote bleeding, such as antiplatelet agents.
ī‚§ Have been associated with GI bleeding, including SSRI, calcium channel
blockers, and aldosterone antagonists
ī‚§ May alter the clinical presentation, such as bismuth, charcoal, and iron,
which can turn the stool black
25
Contâ€Ļ
ī‚§ Comorbid illnesses may influence patient management:
ī‚§ Make patients more susceptible to adverse effects of anemia (eg,
coronary artery disease, pulmonary disease).
ī‚§ Predispose patients to volume overload in the setting of vigorous fluid
resuscitation or blood transfusions (eg, renal disease, heart failure). Such
patients may need more invasive monitoring during resuscitation.
ī‚§ Result in bleeding that is more difficult to control (eg, coagulopathies,
thrombocytopenia, significant hepatic dysfunction). Such patients may
need transfusions of prothrombin complex concentrate, fresh frozen
plasma, or platelets.
ī‚§ Predispose to aspiration of GI contents into the lungs (eg, dementia,
hepatic encephalopathy). Endotracheal intubation should be considered in
such patients.
26
PHYSICAL EXAMINATION
ī‚§ Focuses on the following two elements:
ī‚§ The hemodynamic status of the patient and the degree of anemia
o Blood pressure: check for supine BP. If supine BP is normal check for
postural hypotension ( supine, followed by measurement after 3 minutes of
standing
o Pulse rate: assess for resting tachycardia
o Degree of pallor
ī‚§ Signs of the underlying cause
o Signs of CLD or portal hypertension indicating the possibility of bleeding
varices: Ascites, splenomegaly, encephalopathy.
o Other site bleeding: platelet related disorders or coagulopathies
27
Contâ€Ļ
ī‚§ is a key component of the assessment of hemodynamic stability.
ī‚§ Signs of hypovolemia include :
ī‚§ Mild to moderate hypovolemia (less than 15 percent of blood volume lost) –
Resting tachycardia.
ī‚§ Blood volume loss of at least 15 percent – Orthostatic hypotension (a decrease
in the systolic blood pressure of more than 20 mmHg and/or an increase in
heart rate of 20 beats per minute when moving from recumbency to standing).
ī‚§ Blood volume loss of at least 40 percent – Supine hypotension.
28
Contâ€Ļ
ī‚§ Vital sign
ī‚§ hypotension/ normotensive
ī‚§ tachycardia / bradycardia
ī‚§ tachypnea
ī‚§ HEENT-
ī‚§ ear, nose, and throat examination can reveal an occult bleeding source that
has resulted in swallowed blood and subsequent coffee-ground emesis
ī‚§ pale conjunctiva , jaundice
ī‚§ LGS- gynecomastia , testicular atrophy ,parotid gland enlargement
29
Contâ€Ļ
ī‚§ RS - may be in respiratory distres-anemia,hypotension
ī‚§ Abdominal examination :
ī‚§ may disclose tenderness, masses, ascites, or organomegaly.
ī‚§ rectal examination- to detect the presence of blood and its appearance,
whether bright red, maroon, or melanotic
30
Contâ€Ļ
ī‚§ Skin –
ī‚§ Cool, clammy skin- is an obvious sign of shock.
ī‚§ Spider angiomas, palmar erythema, jaundice, and gynecomastia suggest
liver disease.
ī‚§ Petechiae and purpura suggest an underlying coagulopathy.
ī‚§ Nervous system-altered mentation ,asterixes
31
LABORATARY
ī‚§ Blood group & Rh with cross match
ī‚§ CBC with RBC indices
ī‚§ Coagulation profile
ī‚§ BUN & Cr BUN/Cr>30 or urea/Cr>100
ī‚§ Liver function test
ī‚§ RBS
ī‚§ Electrolyte
ī‚§ ECG , cardiac marker
ī‚§ Barium swallow
ī‚§ Lactate level
32
ī‚§ NASOGASTRIC LAVAGE
ī‚§ Nasogastric intubation and aspiration are diagnostically useful.
ī‚§ In patients without a history of hematemesis, a positive aspirate provides
strong evidence for an upper GI source of bleeding.
ī‚§ High-risk lesions are more likely in patients with bloody aspirates.
ī‚§ Visual inspection of the aspirate to identify bloody, maroon, or coffee-
ground material verifies upper GI bleeding.
ī‚§ Early nasogastric lavage is associated with decreased time to endoscopy.
33
DIAGNOSTIC STUDIES
ī‚§ Upper endoscopy-
ī‚§ is the diagnostic modality of choice for acute upper GI bleeding.
ī‚§ has a high sensitivity and specificity for locating and identifying bleeding
lesions in the upper GI tract.
ī‚§ Therapeutic endoscopy can achieve acute haemostasis and prevent
recurrent bleeding in most patients.
ī‚§ Early endoscopy (within 24 hours) is recommended for most patients with
acute upper GI bleeding.
ī‚§ For patients with suspected variceal bleeding, we perform endoscopy within
12 hours of presentation.
34
Contâ€Ļ
ī‚§ capsule endoscopy for patients who have presented to the emergency
department with suspected upper GI bleeding.
ī‚§ colonoscopy is generally required for patients with hematochezia and a negative
upper endoscopy unless an alternative source for the bleeding has been
identified.
35
36
1. Peptic ulcer disease
ī‚§ Gastroduodenal ulcers are a common cause of UGIB.
ī‚§ The four major risk factors for bleeding peptic ulcers are as follows :
ī‚§ H. pylori infection , NSAIDs ,Physiologic stress ,Excess gastric acid
ī‚§ Reduction or elimination of these risk factors reduces ulcer
recurrence and rebleeding rates.
ī‚§ H. pylori – infects the superficial gastric mucosa and disrupts the
mucous layer, making the mucosa more susceptible to acid damage.
ī‚§ The chronic inflammation induced by H. pylori upsets gastric
secretory physiology to varying degrees and leads to chronic gastritis
that, in most individuals, is asymptomatic and does not progress.
37
Contâ€Ļ
ī‚§ NSAIDs –
ī‚§ Including low-dose aspirin, commonly predispose to ulceration in the GI tract.
ī‚§ NSAID-induced injury results from both local effects and systemic
prostaglandin inhibition.
ī‚§ The majority of these ulcers are asymptomatic and uncomplicated.
ī‚§ However, older adults with a prior history of bleeding ulcer disease are at
increased risk for recurrent ulcers and complications .
ī‚§ NSAIDs have also been implicated as an important factor for nonhealing ulcers.
38
Contâ€Ļ
ī‚§ Stress –
ī‚§ Stress-related ulcers are a common cause of acute UGIB in patients who are
hospitalized for life-threatening nonbleeding illnesses.
ī‚§ Patients with these secondary episodes of bleeding have a higher mortality than
those admitted to the hospital with primary UGIB.
ī‚§ The risk of stress ulcer bleeding is increased in patients with respiratory failure and
those with a coagulopathy.
ī‚§ The psychologic stress that is commonly associated with life events and/or
psychological factors has not clearly been associated with gastroduodenal ulcer
disease, and acid reduction therapy is not routinely indicated in this situation.
39
Contâ€Ļ
ī‚§ Gastric acid –
ī‚§ Gastric acid and pepsin are essential cofactors in the pathogenesis of peptic
ulcers.
ī‚§ Impairment of mucosal integrity by factors such as H. pylori, NSAIDs, or
physiologic stress leads to increased cell membrane permeability to back
diffusion of hydrogen ions, resulting in intramural acidosis, cell death, and
ulceration.
ī‚§ Rarely, hyperacidity is the sole cause of peptic ulceration, as in patients with
Zollinger-Ellison syndrome.
ī‚§ Control of gastric acidity is considered an essential therapeutic maneuver in
patients with active UGIB.
40
Contâ€Ļ
ī‚§ In addition to clinical features, characteristics of an ulcer at endoscopy provide
important prognostic information.
ī‚§ One-third of patients with active bleeding or a nonbleeding visible vessel have
further bleeding that requires urgent surgery if they are treated conservatively.
ī‚§ These patients clearly benefit from endoscopic therapy with
ī‚§ Bipolar Electrocoagulation; Heater Probe;
ī‚§ Injection Therapy (e.g., absolute alcohol, 1:10,000 epinephrine); and/or
ī‚§ Clips -With reductions in Bleeding, Hospital Stay, Mortality Rate, and
Costs.
41
Contâ€Ļ
ī‚§ In contrast, patients with clean-based ulcers have rates of recurrent bleeding
approaching zero.
ī‚§ If there is no other reason for hospitalization, such patients may be discharged
on the first hospital day, following stabilization.
ī‚§ Patients without clean-based ulcers should usually remain in the hospital for
three days because most episodes of recurrent bleeding occur within three days.
ī‚§ A high-dose, constant-infusion IV proton pump inhibitor (PPI) (e.g., Omeprazole
80-mg bolus and 8-mg/h infusion),
ī‚§ Designed to sustain intragastric pH > 6 and enhance clot stability,
ī‚§ Decreases further bleeding and mortality in patients with high-risk ulcers
(Active Bleeding, Nonbleeding Visible Vessel, Adherent Clot) when given
after endoscopic therapy.
42
Contâ€Ļ
ī‚§ Approximately one-third of patients with bleeding ulcers will rebleed within the
next 1–2 years if no preventive strategies are employed.
ī‚§ Prevention of recurrent bleeding focuses on the three main factors in ulcer
pathogenesis,
ī‚§ H. pylori,
ī‚§ NSAIDs, and
ī‚§ Acid.
ī‚§ Eradication of H. pylori in patients with bleeding ulcers decreases rates of
rebleeding to <5%.
43
Contâ€Ļ
ī‚§ If a bleeding ulcer develops in a patient taking NSAIDs, the NSAIDs should
be discontinued, if possible.
ī‚§ If NSAIDs must be continued or reinstituted, a cyclooxygenase 2 (COX-2)
selective inhibitor (Coxib) plus a PPI should be used.
ī‚§ PPI co-therapy alone or a coxib alone is associated with an annual rebleeding
rate of appx10% in patients with a recent bleeding ulcer,
ī‚§ While combination of a coxib and PPI provides a further significant
decrease in recurrent ulcer bleeding.
ī‚§ Patients with cardiovascular disease who develop bleeding ulcers while
taking low-dose aspirin should restart aspirin as soon as possible after their
bleeding episode (e.g., <7 days).
44
Contâ€Ļ
ī‚§ Surgical intervention is usually reserved for cases in which other
interventions have failed to control the bleeding due to PUD.
ī‚§ Patients requiring surgery are typically critically ill and other methods have
failed and are therefore associated with a higher rate of mortality.
45
2. EROSIVE DISEASE
ī‚§ Erosions are endoscopically visualized breaks which are confined to the
mucosa and do not cause major bleeding due to the absence of arteries and
veins in the mucosa.
ī‚§ These are mucosal lesions and, thus, do not cause major bleeding.
ī‚§ Erosions in the esophagus, stomach, or duodenum commonly cause mild
UGIB,
ī‚§ with erosive gastritis and duodenitis accounting for perhaps ~10–15%
ī‚§ erosive esophagitis (primarily due to gastroesophageal reflux disease)
~1–10% of UGIB hospitalizations.
46
Contâ€Ļ
ī‚§ The most important cause of gastric and duodenal erosions is NSAID use:
~50% of patients who chronically ingest NSAIDs may have gastric
erosions.
ī‚§ Other potential causes of gastric erosions include alcohol intake, H. pylori
infection, and stress related mucosal injury
47
Contâ€Ļ
ī‚§ Stress-related gastric mucosal injury occurs only in extremely sickpatients,
ī‚§ serious trauma,
ī‚§ Major surgery,
ī‚§ burns covering more than one-third of the body surface area,
ī‚§ major intracranial disease, or severe medical illness (i.e., ventilator dependence,
coagulopathy).
ī‚§ Severe bleeding should not develop unless ulceration occurs.
ī‚§ The mortality rate in these patients is high because of their serious underlying illnesses.
48
Contâ€Ļ
ī‚§ Pharmacologic prophylaxis for bleeding may be considered in the
high-risk patients.
ī‚§ Bleeding from gastritis or duodenitis is typically self-limited.
ī‚§ Treatment includes :
ī‚§ removing the causative agent,
ī‚§ Acid suppression with a proton pump inhibitor,
ī‚§ withholding anticoagulants when they may be contributing (if
possible), and,
ī‚§ if bleeding is severe, endoscopic therapy with modalities such as
argon plasma coagulation.
49
3. MALLORY-WEISS TEARS
ī‚§ account for ~2–10% of UGIB hospitalizations.
ī‚§ The classic history is vomiting, retching, or coughing preceding
hematemesis, especially in an alcoholic patient.
ī‚§ Bleeding from these tears, which are usually on the gastric side of the
gastroesophageal junction, stops spontaneously in 80–90% of patients
and recurs in only 0–10%.
ī‚§ Endoscopic therapy is indicated for actively bleeding Mallory-Weiss
tears.
50
Contâ€Ļ
ī‚§ Most tears heal spontaneously.
ī‚§ Endoscopic therapy is the first-line treatment for actively bleeding
lacerations.
ī‚§ Several hemostatic methods have been used to control bleeding, including
injection of epinephrine, thermal coagulation, hemoclip placement, and
endoscopic band ligation.
51
4. VARICES BLEEDING
ī‚§ Variceal disease secondary to cirrhosis and portal hypertension is another
common cause of UGI bleeding.
ī‚§ In patients with cirrhosis, varices form at a rate of 5%-15%/ year and about
50% of people with cirrhosis have varices.
ī‚§ 1/3 of patients with varices will develop a variceal hemorrhage.
ī‚§ The onset of UGIB from varices usually signifies significant portal
hypertension, which is advanced liver disease (Child-Pugh class B or C).
ī‚§ The likelihood of developing a hemorrhage increases with the size of the
varices and worsening portal hypertension.
52
Contâ€Ļ
ī‚§ Particular attention needs to be paid to the correction of coagulopathy
in patients with liver dysfunction.
ī‚§ Mortality secondary to variceal hemorrhage is approximately 20%.
ī‚§ rebreeding within the first six weeks occurs in 30%-40% of cases and
is associated with an increased mortality rate.
53
Contâ€Ļ
ī‚§ Varices may be identified in the esophagus and/or the stomach.
ī‚§ They may also be seen at sites other than the esophagus or stomach, such as the
small bowel (ectopic varices).
ī‚§ Isolated gastric varices can result from segmental portal hypertension due to
splenic vein thrombosis, which results from injury to the splenic vein due to
pancreatitis, pancreatic carcinoma, or trauma in the left upper quadrant.
ī‚§ Risk factors for variceal hemorrhage include increasing severity of liver disease,
increasing Child-Pugh class, variceal size, and the presence of red wale markings
on varices .
54
Contâ€Ļ
ī‚§ When variceal bleeding is suspected, medical therapy should be
initiated immediately and not delayed pending confirmation of a variceal
source.
ī‚§ The goal of pharmacologic therapy is to reduce portal venous blood
flow and thus pressure.
ī‚§ Useful medications include vasopressin, terlipressin, octreotide, and
somatostatin.
ī‚§ These agents are successful at controlling variceal hemorrhage in up to
80% of cases.
55
Contâ€Ļ
ī‚§ Antibiotic therapy (e.g., Ceftriaxone) is also recommended for patients with
cirrhosis presenting with UGIB because antibiotics decrease bacterial
infections and mortality in this population.
ī‚§ Chronic therapy with Beta Blockers plus Endoscopic Ligation is
recommended for prevention of recurrent esophageal variceal bleeding
56
Contâ€Ļ
ī‚§ Endoscopy can be diagnostic and the therapeutic procedure of choice.
ī‚§ Options for endoscopic treatment include band ligation or
sclerotherapy.
ī‚§ Band ligation involves placing a small elastic band around the varices.
ī‚§ Sclerotherapy involves injecting a sclerosant into the vein to cause
thrombosis.
ī‚§ Band ligation and sclerotherapy are both effective at stopping bleeding
about 90% of the time, but the risk of rebreeding may be higher with
sclerotherapy.
57
Contâ€Ļ
ī‚§ Esophageal Tamponade :In patients with uncontrollable after failed
pharmacologic and endoscopic interventions, balloon tamponade remains
a temporary option.
ī‚§ In patients who have persistent or recurrent bleeding despite endoscopic
and medical therapy, more invasive therapy with Transjugular
Intrahepatic Portosystemic Shunt (TIPS) is recommended.
58
5. Upper gastrointestinal tumors
ī‚§ Neoplasms of the upper GI tract account for < 3% of all cases of severe
UGIB.
ī‚§ Bleeding may occur with both benign and malignant lesions.
ī‚§ Bleeding can result from diffuse mucosal ulceration or from erosion into
an underlying vessel.
ī‚§ Virtually any tumor type may bleed, including adenocarcinomas, GI
stromal tumors, lymphomas, and Kaposi sarcomas.
59
Contâ€Ļ
ī‚§ Endoscopic findings suggestive of gastric malignancy include irregular
ulcer margins and an exophytic or fungating ulcerated mass.
ī‚§ Endoscopic biopsy, brushing, or needle aspiration for histologic or
cytologic examination is performed for definitive diagnosis.
ī‚§ Patient have a poor prognosis, and the majority of patients die within 12
months.
ī‚§ Surgical resection for cure or palliation is the treatment of choice.
ī‚§ Medical therapy is most often palliative and consists of chemotherapy
and/or radiation therapy.
60
DISPOSITION
ī‚§ Several risk scoring systems, including the Blatchford and Rockall
scoring systems, can help emergency clinicians stratify UGIB patients
into low- and high-risk groups for adverse outcomes,
ī‚§ with high-risk patients defined as those who require a blood transfusion
or endoscopic or surgical intervention during their admission.
ī‚§ The Blatchford Score was designed to identify patients requiring
intervention based on simple clinical and laboratory findings.
ī‚§ It does not require endoscopy and can be calculated at an early stage of
triage.
ī‚§ Patients with a score of 0 can be safely discharged for outpatient
managemen.
61
Contâ€Ļ
ī‚§ Patients who are not at high risk and are
ī‚§ without comorbid diseases,
ī‚§ have normal vital signs,
ī‚§ normal or trace positive results on stool guaiac testing,
ī‚§ normal hemoglobin and hematocrit levels,
ī‚§ Good support systems,
ī‚§ proper understanding of signs and symptoms of
significant bleeding, and
ī‚§ access to emergent care and 24-hour follow up may be discharged.
62
63
Rockall score for upper gastrointestinal bleeding
64
Blatchford score for gastrointestinal bleeding
65
DISPOSITION AND FOLLOW-UP
ī‚§ Patients with;
ī‚§ significant active GI bleeding,
ī‚§ hemodynamic instability, or
ī‚§ significant comorbid conditions should be admitted to an ICU for monitoring
66
Indication for in patient Mx
ī‚§ At high-risk for recurrent bleeding,
ī‚§ patients with evidence of severe upper gastrointestinal (UGI) bleeding
(hemodynamic instability, blood transfusion requirement), and
ī‚§ patients at increased risk for complications if bleeding recur;
ī‚§ significant coronary artery or cerebrovascular disease,
ī‚§ age over 65 years,
ī‚§ patients taking antiplatelet or anticoagulant medications
67
Out pt Mx
ī‚§ Patients ;
ī‚§ who are otherwise healthy and who are at low risk for recurrent UGIB
ī‚§ allowed to eat and
ī‚§ discharged from the hospital on oral PPI
ī‚§ once the effects of procedural sedation have
ī‚§ worn off,
ī‚§ provided that the patient is reliable and
ī‚§ can promptly get medical care if bleeding recur.
68
ī‚§ REFERENCES
ī‚§ Tintinalli’s Emergency Medicine
ī‚§ ROSEN’S EMERGENCY MEDICINE
ī‚§ UpToDate 2021
69
THANK YOU
70

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UGIB.pptx

  • 1. UPPER GASTROITESTINAL BLEEDING PRESENTER: NEGESU G(EMCCR1) MODERATOR: DR.IBSA (EMCCR3) 1
  • 2. OUTLINE ī‚§ Introduction ī‚§ Approach of patient with UGI bleeding ī‚§ Cause of upper GI bleeding and Its management ī‚§ Disposition ī‚§ Reference 2
  • 3. INTRODUCTION GASTROINTESTINAL BLEEDING (GIB) ī‚§ are defined based on their location relative to the ligament of Treitz in the terminal duodenum, so esophagus, stomach, and duodenum origin bleeds are upper and all others are lower. ī‚§ Upper gastrointestinal bleeding is any GI bleeding originating proximal to the ligament of Treitz. ī‚§ Upper GI (UGI) bleeding is more common than lower GI (LGI) bleeding (2x) 3
  • 4. Contâ€Ļ ī‚§ Patients with acute UGIB commonly present may present in five ways: ī‚§ Hematemesis is vomitus of red blood or "coffee-grounds" material. ī‚§ Melena is black, tarry, foul-smelling stool. ī‚§ Hematochezia is the passage of bright red or maroon blood from the rectum. ī‚§ Occult GI Bleeding (GIB) may be identified in the absence of overt bleeding by a fecal occult blood test or the presence of Iron Deficiency. ī‚§ Finally, patients may present only with symptoms of blood loss or anemia such as Lightheadedness, Syncope, Angina, or Dyspnea. 4
  • 5. Contâ€Ļ ī‚§ UGIB may be a life-threatening emergency and requires prompt evaluation, diagnosis, stabilization, and therapeutic measures in a rapid fashion. ī‚§ The initial evaluation of patients with involves an assessment of hemodynamic stability and resuscitation if necessary. ī‚§ Diagnostic studies (usually endoscopy) follow, with the goals of diagnosis, and when possible, treatment of the specific disorder ī‚§ Management depends on the location and severity of the source and the methodical identification of these. 5
  • 6. Contâ€Ļ ī‚§ The mortality rate for patients <60 years in the absence of major concurrent illness is <1%. ī‚§ Outcomes are dependent upon time to diagnosis and appropriate management. ī‚§ Independent predictors of rebleeding and death in patients hospitalized with UGIB include ī‚§ Increasing Age, ī‚§ Comorbidities, and ī‚§ Hemodynamic Compromise (Tachycardia or Hypotension). 6
  • 7. contâ€Ļ ī‚§ UGIB can be classified into several broad categories based on anatomic and pathophysiologic factors. ī‚§ From a pathophysiologic perspective, ī‚§ ulcerative and erosive lesions (gastric or duodenal ulcers, esophagitis, and gastritis) . ī‚§ vascular lesions (varices, angiodysplasia), ī‚§ mass lesions (adenocarcinoma, polyps), or ī‚§ traumatic lesions (Mallory-Weiss tear). 7
  • 8. Contâ€Ļ ī‚§ The source of bleeding cannot be identified in 10 to 15 percent of patients with UGIB, probably because the culprit lesion is either ī‚§ difficult to identify (such as a Dieulafoy's lesion), ī‚§ obscured by retained blood clot at endoscopy, or because the culprit lesion healed by the time endoscopy was performed. 8
  • 9. Contâ€Ļ ī‚§ The most common causes of UGIB include the following (in approximate descending order of frequency): ī‚§ Gastric and/or duodenal ulcers ī‚§ Severe or erosive gastritis/duodenitis ī‚§ Severe or erosive esophagitis ī‚§ Esophagogastric varices ī‚§ Portal hypertensive gastropathy ī‚§ Angiodysplasia (also known as vascular ectasia) ī‚§ Mallory-Weiss syndrome ī‚§ Mass lesions (polyps/cancers) ī‚§ No lesion identified (10 to 15 percent of patients) 9
  • 10. Contâ€Ļ ī‚§ Other less common causes of UGIB include: ī‚§ Dieulafoy's lesion ī‚§ Gastric antral vascular ectasia ī‚§ Hemobilia ī‚§ Aortoenteric fistula ī‚§ Cameron lesions ī‚§ Ectopic varices ī‚§ Iatrogenic bleeding after endoscopic 10
  • 11. 11
  • 12. Approach of patient with UGI bleeding Initial Assessment ī‚§ initial evaluation begins with a prompt assessment of hemodynamic instability and aggressive resuscitation. ī‚§ Delays in resuscitation lead to delays in therapeutic interventions, and thus increased morbidity. ī‚§ The first priority in managing UGIB is to stabilize and resuscitate the patient. ī‚§ Briefly, the examiner must rapidly assess the airway, breathing, and circulation and be prepared to institute critical care measures such as intubation, insertion of large bore intravenous lines, and goal directed resuscitation. 12
  • 13. Contâ€Ļ ī‚§ Key steps in the management of any patient with GI hemorrhage include the following: ī‚§ Resuscitation; correction of coagulopathy, thrombocytopenia, if present. ī‚§ Diagnosis and treatment- medical, endoscopic, or invasive radiologic or surgical intervention, if indicated ī‚§ Chief complaint GI bleed ī‚§ Triage, vital sign assessment ī‚§ Stable or unstable? 13
  • 14. Contâ€Ļ ī‚§ Triage ī‚§ All patients with hemodynamic instability or active bleeding (manifested by hematemesis, bright red blood per nasogastric tube, or hematochezia) . ī‚§ should be admitted to an intensive care unit for resuscitation and close observation with automated BP monitoring, ECG monitoring, and pulse oximetry. 14
  • 15. CONTâ€Ļ ī‚§ Unstable patient : -Abnormal vital signs, Shock ī‚§ Resuscitate: Two large-bore Ivs, Crystalloid infusion, Consider transfusion ī‚§ Massive upper GIB ī‚§ Airway management- Intubate as needed to protect airway from aspiration of hematemesis. ī‚§ Emergent GI consult with ED endoscopy to identify and stabilize bleed. 15
  • 16. Contâ€Ļ ī‚§ Objectives of treatment ī‚§ Hemodynamic restoration ī‚§ Arresting or decreasing bleeding ī‚§ Preventing recurrence of bleeding 16
  • 17. RESUSCITATION General support — ī‚§ Maintain the air way ī‚§ Elective endotracheal intubation in patients with ongoing hematemesis or altered respiratory or mental status may facilitate endoscopy and decrease the risk of aspiration. ī‚§ Patients should receive supplemental oxygen by nasal cannula and ī‚§ should receive nothing per mouth. ī‚§ Establish two large bore IV lines (16 gauge). ī‚§ For patients who are hemodynamically unstable treat initially with rapid, bolus infusions of isotonic crystalloid. 17
  • 18. Hemodynamic Resuscitation Fluid resuscitation: ī‚§ Adequate resuscitation and hemodynamic stabilization is essential prior to endoscopy to minimize treatment-associated complications. ī‚§ Administration of a 1 L bolus of crystalloid fluid should then ensue, unless contraindicated by a medical comorbidity. ī‚§ If hemodynamics has not improved, this bolus should be repeated. ī‚§ The rate of fluid resuscitation will in part depend on whether the patient is hemodynamically unstable. ī‚§ Patients at risk of fluid overload may require intensive monitoring. 18
  • 19. Contâ€Ļ Blood product transfusions ī‚§ Provide transfusion if either of the following is present o Hemodynamic instability (hypotension) is present. o Hemoglobin <9 g/dL in high-risk patients (e.g. elderly, CAD) o Hemoglobin <7 g/dL (70 g/L) in low-risk patients ī‚§ Patients with active bleeding and hypovolemia may require blood transfusion despite an apparently normal hemoglobin. ī‚§ It is particularly important to avoid overtransfusion in patients with suspected variceal bleeding, as it can precipitate worsening of the bleeding. 19
  • 20. Contâ€Ļ ī‚§ Thrombocytopenia - ī‚§ Patients with active bleeding and a low platelet count (<50,000/microL) should be transfused with platelets. ī‚§ To perform an upper endoscopy if the platelet count is >20,000/microL, though if the patient is suspected to have active bleeding, we attempt to raise the platelet count to >50,000/microL prior to endoscopy. 20
  • 21. Contâ€Ļ ī‚§ Coagulopathy —correction of coagulopathy ī‚§ Patients with a coagulopathy that is not due to cirrhosis and with a prolonged prothrombin time with INR >2.0 should generally be transfused with FFP. ī‚§ More rapid reversal of anticoagulation can be achieved if needed by the use of prothrombin complex concentrate infusions and is the preferred approach for patients with serious/life-threatening bleeding. ī‚§ Low dose vitamin K should be considered for hemodynamically unstable patients who are taking a vitamin K antagonist. ī‚§ A unit of FFP should also be given after every four units of PRBC because packed red blood cells do not contain coagulation factors. 21
  • 22. Contâ€Ļ History ī‚§ the diagnosis of the location of the hemorrhage becomes the priority. ī‚§ Ask about hematemesis, coffee-ground emesis, or melena. ī‚§ The history should involve inquiring about prior gastrointestinal bleeds, since up to 60 % of UGIB are from the same lesion previously identified. ī‚§ as well as alcohol use, liver disease or presence of varices, ī‚§ history of ulcers or symptoms related to them, history of vascular anomalies, prior surgeries or interventions. ī‚§ Symptoms that suggest the bleeding is severe include orthostatic dizziness, confusion, angina, severe palpitations, and cold/clammy extremities. 22
  • 23. Contâ€Ļ ī‚§ Symptoms related to the underlying cause ī‚§ Peptic ulcer – Upper abdominal pain ī‚§ Esophageal ulcer – Odynophagia, gastroesophageal reflux, dysphagia ī‚§ Mallory-Weiss tear – Emesis, retching, or coughing prior to hematemesis ī‚§ Variceal hemorrhage or portal hypertensive gastropathy: Jaundice, abdominal distention (ascites) ī‚§ Malignancy – Dysphagia, early satiety, involuntary weight loss, cachexia 23
  • 24. Contâ€Ļ ī‚§ Past medical history — ī‚§ prior episodes of UGIB, since up to 60% of patients with a history of an upper GI bleed are bleeding from the same lesion. ī‚§ Potential bleeding sources suggested by a patient's past medical history include: ī‚§ Varices or portal hypertensive gastropathy in a patient with a history of liver disease or alcohol abuse ī‚§ Aorto-enteric fistula in a patient with a history of an abdominal aortic aneurysm or an aortic graft ī‚§ Angiodysplasia in a patient with renal disease, aortic stenosis, or hereditary hemorrhagic telangiectasia 24
  • 25. Contâ€Ļ ī‚§ Medication history: ī‚§ Predispose to peptic ulcer formation, such as aspirin and other NSAIDs. ī‚§ Are associated with pill esophagitis. ī‚§ Promote bleeding, such as antiplatelet agents. ī‚§ Have been associated with GI bleeding, including SSRI, calcium channel blockers, and aldosterone antagonists ī‚§ May alter the clinical presentation, such as bismuth, charcoal, and iron, which can turn the stool black 25
  • 26. Contâ€Ļ ī‚§ Comorbid illnesses may influence patient management: ī‚§ Make patients more susceptible to adverse effects of anemia (eg, coronary artery disease, pulmonary disease). ī‚§ Predispose patients to volume overload in the setting of vigorous fluid resuscitation or blood transfusions (eg, renal disease, heart failure). Such patients may need more invasive monitoring during resuscitation. ī‚§ Result in bleeding that is more difficult to control (eg, coagulopathies, thrombocytopenia, significant hepatic dysfunction). Such patients may need transfusions of prothrombin complex concentrate, fresh frozen plasma, or platelets. ī‚§ Predispose to aspiration of GI contents into the lungs (eg, dementia, hepatic encephalopathy). Endotracheal intubation should be considered in such patients. 26
  • 27. PHYSICAL EXAMINATION ī‚§ Focuses on the following two elements: ī‚§ The hemodynamic status of the patient and the degree of anemia o Blood pressure: check for supine BP. If supine BP is normal check for postural hypotension ( supine, followed by measurement after 3 minutes of standing o Pulse rate: assess for resting tachycardia o Degree of pallor ī‚§ Signs of the underlying cause o Signs of CLD or portal hypertension indicating the possibility of bleeding varices: Ascites, splenomegaly, encephalopathy. o Other site bleeding: platelet related disorders or coagulopathies 27
  • 28. Contâ€Ļ ī‚§ is a key component of the assessment of hemodynamic stability. ī‚§ Signs of hypovolemia include : ī‚§ Mild to moderate hypovolemia (less than 15 percent of blood volume lost) – Resting tachycardia. ī‚§ Blood volume loss of at least 15 percent – Orthostatic hypotension (a decrease in the systolic blood pressure of more than 20 mmHg and/or an increase in heart rate of 20 beats per minute when moving from recumbency to standing). ī‚§ Blood volume loss of at least 40 percent – Supine hypotension. 28
  • 29. Contâ€Ļ ī‚§ Vital sign ī‚§ hypotension/ normotensive ī‚§ tachycardia / bradycardia ī‚§ tachypnea ī‚§ HEENT- ī‚§ ear, nose, and throat examination can reveal an occult bleeding source that has resulted in swallowed blood and subsequent coffee-ground emesis ī‚§ pale conjunctiva , jaundice ī‚§ LGS- gynecomastia , testicular atrophy ,parotid gland enlargement 29
  • 30. Contâ€Ļ ī‚§ RS - may be in respiratory distres-anemia,hypotension ī‚§ Abdominal examination : ī‚§ may disclose tenderness, masses, ascites, or organomegaly. ī‚§ rectal examination- to detect the presence of blood and its appearance, whether bright red, maroon, or melanotic 30
  • 31. Contâ€Ļ ī‚§ Skin – ī‚§ Cool, clammy skin- is an obvious sign of shock. ī‚§ Spider angiomas, palmar erythema, jaundice, and gynecomastia suggest liver disease. ī‚§ Petechiae and purpura suggest an underlying coagulopathy. ī‚§ Nervous system-altered mentation ,asterixes 31
  • 32. LABORATARY ī‚§ Blood group & Rh with cross match ī‚§ CBC with RBC indices ī‚§ Coagulation profile ī‚§ BUN & Cr BUN/Cr>30 or urea/Cr>100 ī‚§ Liver function test ī‚§ RBS ī‚§ Electrolyte ī‚§ ECG , cardiac marker ī‚§ Barium swallow ī‚§ Lactate level 32
  • 33. ī‚§ NASOGASTRIC LAVAGE ī‚§ Nasogastric intubation and aspiration are diagnostically useful. ī‚§ In patients without a history of hematemesis, a positive aspirate provides strong evidence for an upper GI source of bleeding. ī‚§ High-risk lesions are more likely in patients with bloody aspirates. ī‚§ Visual inspection of the aspirate to identify bloody, maroon, or coffee- ground material verifies upper GI bleeding. ī‚§ Early nasogastric lavage is associated with decreased time to endoscopy. 33
  • 34. DIAGNOSTIC STUDIES ī‚§ Upper endoscopy- ī‚§ is the diagnostic modality of choice for acute upper GI bleeding. ī‚§ has a high sensitivity and specificity for locating and identifying bleeding lesions in the upper GI tract. ī‚§ Therapeutic endoscopy can achieve acute haemostasis and prevent recurrent bleeding in most patients. ī‚§ Early endoscopy (within 24 hours) is recommended for most patients with acute upper GI bleeding. ī‚§ For patients with suspected variceal bleeding, we perform endoscopy within 12 hours of presentation. 34
  • 35. Contâ€Ļ ī‚§ capsule endoscopy for patients who have presented to the emergency department with suspected upper GI bleeding. ī‚§ colonoscopy is generally required for patients with hematochezia and a negative upper endoscopy unless an alternative source for the bleeding has been identified. 35
  • 36. 36
  • 37. 1. Peptic ulcer disease ī‚§ Gastroduodenal ulcers are a common cause of UGIB. ī‚§ The four major risk factors for bleeding peptic ulcers are as follows : ī‚§ H. pylori infection , NSAIDs ,Physiologic stress ,Excess gastric acid ī‚§ Reduction or elimination of these risk factors reduces ulcer recurrence and rebleeding rates. ī‚§ H. pylori – infects the superficial gastric mucosa and disrupts the mucous layer, making the mucosa more susceptible to acid damage. ī‚§ The chronic inflammation induced by H. pylori upsets gastric secretory physiology to varying degrees and leads to chronic gastritis that, in most individuals, is asymptomatic and does not progress. 37
  • 38. Contâ€Ļ ī‚§ NSAIDs – ī‚§ Including low-dose aspirin, commonly predispose to ulceration in the GI tract. ī‚§ NSAID-induced injury results from both local effects and systemic prostaglandin inhibition. ī‚§ The majority of these ulcers are asymptomatic and uncomplicated. ī‚§ However, older adults with a prior history of bleeding ulcer disease are at increased risk for recurrent ulcers and complications . ī‚§ NSAIDs have also been implicated as an important factor for nonhealing ulcers. 38
  • 39. Contâ€Ļ ī‚§ Stress – ī‚§ Stress-related ulcers are a common cause of acute UGIB in patients who are hospitalized for life-threatening nonbleeding illnesses. ī‚§ Patients with these secondary episodes of bleeding have a higher mortality than those admitted to the hospital with primary UGIB. ī‚§ The risk of stress ulcer bleeding is increased in patients with respiratory failure and those with a coagulopathy. ī‚§ The psychologic stress that is commonly associated with life events and/or psychological factors has not clearly been associated with gastroduodenal ulcer disease, and acid reduction therapy is not routinely indicated in this situation. 39
  • 40. Contâ€Ļ ī‚§ Gastric acid – ī‚§ Gastric acid and pepsin are essential cofactors in the pathogenesis of peptic ulcers. ī‚§ Impairment of mucosal integrity by factors such as H. pylori, NSAIDs, or physiologic stress leads to increased cell membrane permeability to back diffusion of hydrogen ions, resulting in intramural acidosis, cell death, and ulceration. ī‚§ Rarely, hyperacidity is the sole cause of peptic ulceration, as in patients with Zollinger-Ellison syndrome. ī‚§ Control of gastric acidity is considered an essential therapeutic maneuver in patients with active UGIB. 40
  • 41. Contâ€Ļ ī‚§ In addition to clinical features, characteristics of an ulcer at endoscopy provide important prognostic information. ī‚§ One-third of patients with active bleeding or a nonbleeding visible vessel have further bleeding that requires urgent surgery if they are treated conservatively. ī‚§ These patients clearly benefit from endoscopic therapy with ī‚§ Bipolar Electrocoagulation; Heater Probe; ī‚§ Injection Therapy (e.g., absolute alcohol, 1:10,000 epinephrine); and/or ī‚§ Clips -With reductions in Bleeding, Hospital Stay, Mortality Rate, and Costs. 41
  • 42. Contâ€Ļ ī‚§ In contrast, patients with clean-based ulcers have rates of recurrent bleeding approaching zero. ī‚§ If there is no other reason for hospitalization, such patients may be discharged on the first hospital day, following stabilization. ī‚§ Patients without clean-based ulcers should usually remain in the hospital for three days because most episodes of recurrent bleeding occur within three days. ī‚§ A high-dose, constant-infusion IV proton pump inhibitor (PPI) (e.g., Omeprazole 80-mg bolus and 8-mg/h infusion), ī‚§ Designed to sustain intragastric pH > 6 and enhance clot stability, ī‚§ Decreases further bleeding and mortality in patients with high-risk ulcers (Active Bleeding, Nonbleeding Visible Vessel, Adherent Clot) when given after endoscopic therapy. 42
  • 43. Contâ€Ļ ī‚§ Approximately one-third of patients with bleeding ulcers will rebleed within the next 1–2 years if no preventive strategies are employed. ī‚§ Prevention of recurrent bleeding focuses on the three main factors in ulcer pathogenesis, ī‚§ H. pylori, ī‚§ NSAIDs, and ī‚§ Acid. ī‚§ Eradication of H. pylori in patients with bleeding ulcers decreases rates of rebleeding to <5%. 43
  • 44. Contâ€Ļ ī‚§ If a bleeding ulcer develops in a patient taking NSAIDs, the NSAIDs should be discontinued, if possible. ī‚§ If NSAIDs must be continued or reinstituted, a cyclooxygenase 2 (COX-2) selective inhibitor (Coxib) plus a PPI should be used. ī‚§ PPI co-therapy alone or a coxib alone is associated with an annual rebleeding rate of appx10% in patients with a recent bleeding ulcer, ī‚§ While combination of a coxib and PPI provides a further significant decrease in recurrent ulcer bleeding. ī‚§ Patients with cardiovascular disease who develop bleeding ulcers while taking low-dose aspirin should restart aspirin as soon as possible after their bleeding episode (e.g., <7 days). 44
  • 45. Contâ€Ļ ī‚§ Surgical intervention is usually reserved for cases in which other interventions have failed to control the bleeding due to PUD. ī‚§ Patients requiring surgery are typically critically ill and other methods have failed and are therefore associated with a higher rate of mortality. 45
  • 46. 2. EROSIVE DISEASE ī‚§ Erosions are endoscopically visualized breaks which are confined to the mucosa and do not cause major bleeding due to the absence of arteries and veins in the mucosa. ī‚§ These are mucosal lesions and, thus, do not cause major bleeding. ī‚§ Erosions in the esophagus, stomach, or duodenum commonly cause mild UGIB, ī‚§ with erosive gastritis and duodenitis accounting for perhaps ~10–15% ī‚§ erosive esophagitis (primarily due to gastroesophageal reflux disease) ~1–10% of UGIB hospitalizations. 46
  • 47. Contâ€Ļ ī‚§ The most important cause of gastric and duodenal erosions is NSAID use: ~50% of patients who chronically ingest NSAIDs may have gastric erosions. ī‚§ Other potential causes of gastric erosions include alcohol intake, H. pylori infection, and stress related mucosal injury 47
  • 48. Contâ€Ļ ī‚§ Stress-related gastric mucosal injury occurs only in extremely sickpatients, ī‚§ serious trauma, ī‚§ Major surgery, ī‚§ burns covering more than one-third of the body surface area, ī‚§ major intracranial disease, or severe medical illness (i.e., ventilator dependence, coagulopathy). ī‚§ Severe bleeding should not develop unless ulceration occurs. ī‚§ The mortality rate in these patients is high because of their serious underlying illnesses. 48
  • 49. Contâ€Ļ ī‚§ Pharmacologic prophylaxis for bleeding may be considered in the high-risk patients. ī‚§ Bleeding from gastritis or duodenitis is typically self-limited. ī‚§ Treatment includes : ī‚§ removing the causative agent, ī‚§ Acid suppression with a proton pump inhibitor, ī‚§ withholding anticoagulants when they may be contributing (if possible), and, ī‚§ if bleeding is severe, endoscopic therapy with modalities such as argon plasma coagulation. 49
  • 50. 3. MALLORY-WEISS TEARS ī‚§ account for ~2–10% of UGIB hospitalizations. ī‚§ The classic history is vomiting, retching, or coughing preceding hematemesis, especially in an alcoholic patient. ī‚§ Bleeding from these tears, which are usually on the gastric side of the gastroesophageal junction, stops spontaneously in 80–90% of patients and recurs in only 0–10%. ī‚§ Endoscopic therapy is indicated for actively bleeding Mallory-Weiss tears. 50
  • 51. Contâ€Ļ ī‚§ Most tears heal spontaneously. ī‚§ Endoscopic therapy is the first-line treatment for actively bleeding lacerations. ī‚§ Several hemostatic methods have been used to control bleeding, including injection of epinephrine, thermal coagulation, hemoclip placement, and endoscopic band ligation. 51
  • 52. 4. VARICES BLEEDING ī‚§ Variceal disease secondary to cirrhosis and portal hypertension is another common cause of UGI bleeding. ī‚§ In patients with cirrhosis, varices form at a rate of 5%-15%/ year and about 50% of people with cirrhosis have varices. ī‚§ 1/3 of patients with varices will develop a variceal hemorrhage. ī‚§ The onset of UGIB from varices usually signifies significant portal hypertension, which is advanced liver disease (Child-Pugh class B or C). ī‚§ The likelihood of developing a hemorrhage increases with the size of the varices and worsening portal hypertension. 52
  • 53. Contâ€Ļ ī‚§ Particular attention needs to be paid to the correction of coagulopathy in patients with liver dysfunction. ī‚§ Mortality secondary to variceal hemorrhage is approximately 20%. ī‚§ rebreeding within the first six weeks occurs in 30%-40% of cases and is associated with an increased mortality rate. 53
  • 54. Contâ€Ļ ī‚§ Varices may be identified in the esophagus and/or the stomach. ī‚§ They may also be seen at sites other than the esophagus or stomach, such as the small bowel (ectopic varices). ī‚§ Isolated gastric varices can result from segmental portal hypertension due to splenic vein thrombosis, which results from injury to the splenic vein due to pancreatitis, pancreatic carcinoma, or trauma in the left upper quadrant. ī‚§ Risk factors for variceal hemorrhage include increasing severity of liver disease, increasing Child-Pugh class, variceal size, and the presence of red wale markings on varices . 54
  • 55. Contâ€Ļ ī‚§ When variceal bleeding is suspected, medical therapy should be initiated immediately and not delayed pending confirmation of a variceal source. ī‚§ The goal of pharmacologic therapy is to reduce portal venous blood flow and thus pressure. ī‚§ Useful medications include vasopressin, terlipressin, octreotide, and somatostatin. ī‚§ These agents are successful at controlling variceal hemorrhage in up to 80% of cases. 55
  • 56. Contâ€Ļ ī‚§ Antibiotic therapy (e.g., Ceftriaxone) is also recommended for patients with cirrhosis presenting with UGIB because antibiotics decrease bacterial infections and mortality in this population. ī‚§ Chronic therapy with Beta Blockers plus Endoscopic Ligation is recommended for prevention of recurrent esophageal variceal bleeding 56
  • 57. Contâ€Ļ ī‚§ Endoscopy can be diagnostic and the therapeutic procedure of choice. ī‚§ Options for endoscopic treatment include band ligation or sclerotherapy. ī‚§ Band ligation involves placing a small elastic band around the varices. ī‚§ Sclerotherapy involves injecting a sclerosant into the vein to cause thrombosis. ī‚§ Band ligation and sclerotherapy are both effective at stopping bleeding about 90% of the time, but the risk of rebreeding may be higher with sclerotherapy. 57
  • 58. Contâ€Ļ ī‚§ Esophageal Tamponade :In patients with uncontrollable after failed pharmacologic and endoscopic interventions, balloon tamponade remains a temporary option. ī‚§ In patients who have persistent or recurrent bleeding despite endoscopic and medical therapy, more invasive therapy with Transjugular Intrahepatic Portosystemic Shunt (TIPS) is recommended. 58
  • 59. 5. Upper gastrointestinal tumors ī‚§ Neoplasms of the upper GI tract account for < 3% of all cases of severe UGIB. ī‚§ Bleeding may occur with both benign and malignant lesions. ī‚§ Bleeding can result from diffuse mucosal ulceration or from erosion into an underlying vessel. ī‚§ Virtually any tumor type may bleed, including adenocarcinomas, GI stromal tumors, lymphomas, and Kaposi sarcomas. 59
  • 60. Contâ€Ļ ī‚§ Endoscopic findings suggestive of gastric malignancy include irregular ulcer margins and an exophytic or fungating ulcerated mass. ī‚§ Endoscopic biopsy, brushing, or needle aspiration for histologic or cytologic examination is performed for definitive diagnosis. ī‚§ Patient have a poor prognosis, and the majority of patients die within 12 months. ī‚§ Surgical resection for cure or palliation is the treatment of choice. ī‚§ Medical therapy is most often palliative and consists of chemotherapy and/or radiation therapy. 60
  • 61. DISPOSITION ī‚§ Several risk scoring systems, including the Blatchford and Rockall scoring systems, can help emergency clinicians stratify UGIB patients into low- and high-risk groups for adverse outcomes, ī‚§ with high-risk patients defined as those who require a blood transfusion or endoscopic or surgical intervention during their admission. ī‚§ The Blatchford Score was designed to identify patients requiring intervention based on simple clinical and laboratory findings. ī‚§ It does not require endoscopy and can be calculated at an early stage of triage. ī‚§ Patients with a score of 0 can be safely discharged for outpatient managemen. 61
  • 62. Contâ€Ļ ī‚§ Patients who are not at high risk and are ī‚§ without comorbid diseases, ī‚§ have normal vital signs, ī‚§ normal or trace positive results on stool guaiac testing, ī‚§ normal hemoglobin and hematocrit levels, ī‚§ Good support systems, ī‚§ proper understanding of signs and symptoms of significant bleeding, and ī‚§ access to emergent care and 24-hour follow up may be discharged. 62
  • 63. 63
  • 64. Rockall score for upper gastrointestinal bleeding 64
  • 65. Blatchford score for gastrointestinal bleeding 65
  • 66. DISPOSITION AND FOLLOW-UP ī‚§ Patients with; ī‚§ significant active GI bleeding, ī‚§ hemodynamic instability, or ī‚§ significant comorbid conditions should be admitted to an ICU for monitoring 66
  • 67. Indication for in patient Mx ī‚§ At high-risk for recurrent bleeding, ī‚§ patients with evidence of severe upper gastrointestinal (UGI) bleeding (hemodynamic instability, blood transfusion requirement), and ī‚§ patients at increased risk for complications if bleeding recur; ī‚§ significant coronary artery or cerebrovascular disease, ī‚§ age over 65 years, ī‚§ patients taking antiplatelet or anticoagulant medications 67
  • 68. Out pt Mx ī‚§ Patients ; ī‚§ who are otherwise healthy and who are at low risk for recurrent UGIB ī‚§ allowed to eat and ī‚§ discharged from the hospital on oral PPI ī‚§ once the effects of procedural sedation have ī‚§ worn off, ī‚§ provided that the patient is reliable and ī‚§ can promptly get medical care if bleeding recur. 68
  • 69. ī‚§ REFERENCES ī‚§ Tintinalli’s Emergency Medicine ī‚§ ROSEN’S EMERGENCY MEDICINE ī‚§ UpToDate 2021 69