acute gi bleeding
DESCRIPTION
ACUTE GI BLEEDINGTRANSCRIPT
1
Prepared by
OUTLINE2
Introduction
Definition
Epidemology
classificationCause and risk factors
Aproach to patients with acute GI bleeding
Management
Introduction
3Figure 23.2
The principal function
of GIT is to provide the
body with a continuous
supply of nutrients, water
and electrolytes.
Introduction….
Histology of the Alimentary Canal
4
From esophagus to the anal canal the walls of the GIT
have the same four layers
From the lumen outward they are the
1. Mucosa,
2. Submucosa,
3. Muscularis externa, and
4. Serosa
Each layer has a predominant tissue type and a
specific digestive function
Introduction…Blood Supply to Digestive System
5
The blood vessels of the GI-system are part of a more extensive system called the splanchric circulation.
splanchnic BF =1000 ml/min
It includes the blood flow through the GIT itself plus through the spleen, pancreas and the liver.
All of the blood that courses through the gut, spleen and pancreas then flows immediately into the liver by way of the portal vein.
In the liver, blood passes through million of liver sinusoids and finally leaver the liver by way of the hepatic veins that empty into the inferior venacava of the general circulation.
Blood Supply to GIT (cont’d)
6
Gastrointestinal Bleeding:7
Bleeding from the gastrointestinal (GI) tract may present in five ways.
Hematemesis is vomitus of red blood or "coffee-grounds" material.
Melena is black, tarry, foul-smelling stool.
Hematochezia is the passage of bright red or maroon blood from the rectum.
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.
Finally, patients may present only with symptoms of blood loss or anemia such as lightheadedness, syncope, angina, or dyspnea.
Classification of GI Bleeding8
UGIB blood loss proximal to ligament of
Treitz(DJ flexure)
LGIBblood loss distal to ligament of Treitz
(DJ flexure)
Ligament of treize….
Upper GI bleeding 4x more common
than lower GI bleeding
Suspencery ligament of doudenum
or ligament of tertz9
UGIB10
Upper GI bleeding refers to bleeding from
oesophagus, stomach, duodenum.
Can be:
Variceal bleeding
Non-variceal bleeding
Sources of Gastrointestinal
Bleeding11
Upper Gastrointestinal Sources of Bleeding
The annual incidence of hospital admissions for upper GIB (UGIB) in the United States and Europe is 0.1%, with a mortality rate of 5–10%.
Patients rarely die from exsanguination; rather, they die due to decompensation from other underlying illnesses.
The mortality rate for patients <60 years in the absence of major concurrent illness is <1%.
Independent predictors of rebleeding and death in patients hospitalized with UGIB include increasing age, comorbidities, and hemodynamic compromise (tachycardia or hypotension).
Sources of bleeding in patients hospitalized for upper gi
bleeding
12
Sources of Bleeding Proportion of Patients, %
Ulcers 31–67
Varices 6–39
Mallory-Weiss tears 2–8
Gastroduodenal erosions 2–18
Erosive esophagitis 1–13
Neoplasm 2–8
Vascular ectasias 0–6
13
Peptic ulcers are the most common cause of
UGIB, accounting for up to 50% of cases; an
increasing proportion is due to nonsteroidal anti-
inflammatory drugs (NSAIDs), with the prevalence
of Helicobacter pylori decreasing.
Mallory-Weiss tears account for 5–10% of cases.
The proportion of patients bleeding from varices
varies widely from 5 to 40%, depending on the
population.
Hemorrhagic or erosive gastropathy (e.g., due to
NSAIDs or alcohol) and erosive esophagitis often
cause mild UGIB, but major bleeding is rare.
14
PUD (DU & GU)
Are break in the gastric or duodenal mucosa
that arises when the normal factors are impaired
or overwhelmed by acid or pepsin
Erosive Gastritis
Because this process is superficial, it is a relatively
unusual cause of severe gastrointestinal bleeding (<
5% of cases).
MW TEAR (LACERATION)
15
Classically, Mallory-Weiss tears are mucosal lacerations at the GEJ or in the cardia of the stomach
associated with repeated retching or vomiting
another important cause of nonvariceal UGIB.
acute UGIB secondary to Mallory-Weiss tears bleeding episodes are self-limited.
ESOPHAGITIS16
Is a common medical condition,
usually caused by gastroesophageal reflux.
Less frequent causes include
infectious esophagitis (in patients whoare immunocompromised),
radiation esophagitis, and
esophagitis from direct erosive effects of medication or corrosiveagents.
VASCULAR ECTASIAS17
Vascular ectasias, also referred to as “angiomas,” “arteriovenousmalformations,” and “angiodysplasia,” are another source of acute and chronic nonvariceal UGIB
Abnormal communication
The severity of bleeding can also range from trivial to severe
Vascular ectasias are associated with chronic renal insufficiency or failure; valvular heart disease, specifically aortic stenosis; and congestive heart failure.
Varices
18
There is communication between the intra-abdominal
splanchnic circulation and the systemic venous circulation
through the esophagus.
When portal venous blood flow into the liver is impeded by
cirrhosis or other causes, the resultant portal hypertension
induces the formation of collateral bypass channels.
The increased pressure in the esophageal plexus produces
dilated tortuous vessels called varices.
Variceal rupture produces massive hemorrhage into the lumen.
produce no symptoms until they rupture
LGIB19
Lower GI bleed refers to bleeding arising distal to
the ligament of Treitz (DJ flexure)
Although this includes jejunum and ileum bleeding
from these sites is rare.
Vast majority of lower GI bleeding arises from
colon/rectum/anus
over 90% of cases arise from the colon
CAUSES OF Acute LGIBMajorcauses
Diverticulosis(40%)
Colitis
IBD
Ischemia
Infection
Angiodysplasia
(avm)(30%)
Neoplasia
Anorectal
Hemorrhoids
Fissure
20
Causes...21
Causes of Colon
bleeding
Causes of
Rectal bleeding
Causes of Anal
bleeding
Diverticular
Disease
Polyps Haemorrhoids
Polyps Malignancy Fissure
Malignancy Proctitis Malignancy
Colitis
IBD22
Chronic inflammation of the colon.
ulcerative colitis & Crohn disease
is characterized by severe inflammation and
ulceration of the colon and rectum
Patients with inflammatory bowel disease
(especially ulcerative colitis) often have
diarrhea with variable amounts of
hematochezia
23
Hematemesis indicates an upper GI source of bleeding (above the ligament of Treitz).
Melena indicates that blood has been present in the GI tract for at least 14 h (and as long as 3–5 days).
The more proximal the bleeding site, the more likely melena will occur.
Hematochezia usually represents a lower GI source of bleeding, although an upper GI lesion may bleed so briskly that blood does not remain in the bowel long enough for melena to develop.
When hematochezia is the presenting symptom of UGIB, it is associated with hemodynamic instability and dropping hemoglobin.
Differentiation of Upper from Lower Gib
24
Bleeding lesions of the small bowel may present as melena or hematochezia.
Other clues to UGIB include hyperactive bowel sounds and an elevated blood urea nitrogen level (due to volume depletion and blood proteins absorbed in the small intestine).
A nonbloody nasogastric aspirate may be seen in up to 18% of patients with UGIB—usually from a duodenal source.
Even a bile-stained appearance does not exclude a bleeding postpyloric lesion because reports of bile in the aspirate are incorrect in 50% of cases.
Testing of aspirates that are not grossly bloody for occult blood is not useful.
25
Obscure GIB is defined as persistent or recurrent
bleeding for which no source has been identified
by routine endoscopic and contrast x-ray studies;
it may be overt (melena, hematochezia) or occult
(iron-deficiency anemia).
Current guidelines suggest angiography as the
initial test for massive obscure bleeding, and
video capsule endoscopy, which allows
examination of the entire small intestine, for all
others.
GIB of Obscure Origin
26
Push enteroscopy, with a specially designed enteroscope or a pediatric colonoscope to inspect the entire duodenum and part of the jejunum, also may be considered as an initial evaluation.
A systematic review of 14 trials comparing push enteroscopy to capsule revealed "clinically significant findings" in 26% and 56% of patients, respectively.
However, in contrast to enteroscopy, lack of control of the capsule prevents its manipulation and full visualization of the intestine; in addition, tissue cannot be sampled and therapy cannot be applied.
Clinical Presantation :
27
Hematemesis
Melena
Hematochezia
Syncope
Dyspepsia
Epigastric pain
Heartburn
Diffuse abdominal pain
Dysphagia
Weight loss
Jaundice
Approach to the Patient:
Gastrointestinal Bleeding28
History
Physical examination
Lab investigation
APROACH TO PATIENT………….. Con’t
29
History:
• Abdominal pain
• Haematamesis
• Haematochezia
• Melaena
• Features of blood loss: shock, syncope, anemia
• Features of underlying cause: dyspepsia, jaundice, weight loss
30
o Drug history: NSAIDs, Aspirin, anticoagulants,
o History of epistaxis or hemoptysis to rule out the GI
source of bleeding.
o Past medical :previous episodes of upper
gastrointestinal bleedin; coronary artery disease;
chronic renal or liver disease;
o Past surgical: previous abdominal surgery
Approach
Cont…..31
Physical Examination :
• General examination and systemic examinations
• VITALS:
Pulse = Feable pulse
BP = Orthostatic Hypotension
• SIGNS of shock:
Cold extremeties, Tachycardia, Hypotension
Chest pain, Confusion, Delirium, Oliguria, and etc.
32
SKIN changes:
Cirrhosis – Palmer erythema, spider nevi
Bleeding disorders – Purpura /Echymosis,
Haemarthrosis, Muscle hematoma.
• Signs of dehydration (dry mucosa, sunken eyes, skin
turgor reduced).
• Signs of a tumour may be present (nodular liver,
abdominal mass, lymphadenopathy, and etc.
• DRE : fresh blood, occult blood, bloody diarrhea
• Respiratory, CVS, CNS For comorbid diseases
Lab Diagnosis :
33
CBC with Platelet Count, and Differential
A complete blood count (CBC) is necessary to assess the level of blood loss.
CBC should be checked frequently(q4-6h) during the first day.
Hemoglobin Value, Type and Crossmatch Blood
The patient should be crossmatched for 2-6 units, based on the rate of active bleeding.
The hemoglobin level should be monitored serially in order to follow the trend.
An unstable Hb level may signify ongoing hemorrhage requiring further intervention.
34
LFT- to detect underlying liver disease
The BUN-to- creatinine ratio increases with
upper gastrointestinal bleeding (UGIB).
A ratio of greater than 36 in a patient without
renal insufficiency is suggestive of UGIB.
The patient's prothrombin time (PT), activated
partial thromboplastin time, should be checked
to document the presence of a coagulopathy
Endoscopy 35
• Initial diagnostic examination for all patients
presumed to have UGIB.
• Endoscopy should be performed immediately
after endotracheal intubation (if indicated),
hemodynamic stabilization, and adequate
monitoring in an intensive care unit (ICU) setting
have been achieved.
36
Endoscopy
Imaging 37
• CHEST X-RAY-Chest radiographs should be
ordered to exclude aspiration pneumonia,
effusion, and esophageal perforation.
• Abdominal X-RAY- erect and supine films should
be ordered to exclude perforated viscous and
ileus.
Angiography
:38
Angiography may be useful if bleeding persists
and endoscopy fails to identify a bleeding site.
Angiography along with transcatheter arterial
embolization (TAE) should be considered for all
patients with a known source of arterial UGIB that
does not respond to endoscopic management,
with active bleeding and a negative endoscopy.
In cases of aortoenteric fistula, angiography
requires active bleeding (1 mL/min) to be
diagnostic.
Nasogastric
Lavage39
A nasogastric tube is an important diagnostic tool.
This procedure may confirm recent bleeding
(coffee ground appearance), possible active
bleeding (red blood in the aspirate that does not
clear), or a lack of blood in the stomach (active
bleeding less likely but does not exclude an upper
GI lesion).
40
41
1. Better visualization during endoscopy
2. Give crude estimation of rapidity of bleeding
3. Prevent the development of Porto systemic
encephalopathy in cirrhosis
4. Increases PH of stomach, and hence, decreases clot
desolation due to gastric acid dilution
5. Tube placement can reduce the patient's need to vomit
During gastric lavage use saline and not use large volume
of to avoid water intoxication.
Gastric lavage should be done in alert and cooperative
patient to avoid bronco-pulmonary aspiration
BENEFITS OF LAVAGE :
Identifies patients at risk of adverse outcome following acute upper GI bleed
Score <3 carries good prognosis
Score >8 carries high risk of mortality
Risk Stratification: Rockall
Score
Variable Score 0 Score 1 Score 2 Score 3
Age <60 60-79 >80 -
Shock Nil HR >100 SBP <100 -
Co-morbidity Nil major - IHD/CCF/major morbidity Renal failure/liver failure
Diagnosis Mallory Weiss tear All other diagnoses GI malignancy -
Endoscopic Findings None - Blood, adherent clot,
spurting vessel
-
Management
43
Priorities are:
1. Stabilize the patient: protect airway,
restore circulation.
2. Identify the source of bleeding.
3. Definitive treatment of the cause.
Takes priority over determining the
diagnosis/cause
ABC (main focus is ‘C’)
Oxygen: 15L Non-rebreath mask
2 large bore cannulae into both ante-cubital
fossae
Take bloods at same time for FBC, U&E,
LFT, Clotting, X match 6Units
Catheterise
Emegency Resuscitation
45
IVF initially then blood as soon as available (depending on urgency: O-, Group specific, fully X-matched)
Monitor response to resuscitation frequently (HR, BP, urine output, level of consciousness, peripheral temperature, CRT)
Stop anti-coagulants and correct any clotting derrangement
NG tube and aspiration (will help differentiate upper from lower GI bleed)
Organise definitive treatment (endoscopic/radiological/surgical)
Emergency resuscitation as already described
Endoscopy
Urgent (within 24hrs) – diagnostic and therepeutic
Treatment administered if active bleeding, visible vessel, adherent blood clot
Treatment options include injection (adrenaline), coagulation, clipping
If re-bleeds then arrange urgent repeat endoscopy.
Management (Non-variceal)
47
Pharmacology
PPI (infusion) – pH >6 stabilises clots and
reduces risk of re-bleeding following
endoscopic haemostasis
If H pylori positive then for eradication
therapy
Stop
NSAIDs/aspirin/clopidogrel/warfarin/steroids
if safe to do so (risk:benefit analysis)
Surgery Reserved for patients with failed medical management
(ongoing bleeding despite 2x endoscopy)
Nature of operation depends on cause of bleeding (most
commonly performed in context of bleeding peptic ulcer:
DU>GU)
E.g. Under-running of ulcer (bleeding DU), wedge excision
of bleeding lesion (e.g. GU), partial/total gastrectomy
(malignancy)
Management (Non-variceal)
Suspect if upper GI bleed in patient with history of
chronic liver disease/cirrhosis or stigmata on clinical
examination
Liver Cirrhosis results in portal hypertension and
development of porto-systemic anastamosis
(opening or dilatation of pre-existing vascular
channels connecting portal and systemic
circulations)
Variceal Bleeds
50
Sites of porto-systemic anastamosis include:
Oesophagus
(P= eosophageal branch of L gastric v, S= oesophageal branch of azygous v)
Umbilicus
(P= para-umbilical v, S= infeior epigastric v)
Retroperitoneal
(P= right/middle/left colic v, S= renal/supra-renal/gonadalv)
Rectal
(P= superior rectal v, S= middle/inferior rectal v)
Furthermore, clotting derrangement in those with chronic liver disease can worsen bleeding
Emergency resuscitation as already described
Drugs
Somatostatin/octreotide – vasoconstricts splanchniccirculation and reduces pressure in portal system
Terlipressin – vasoconstricts splanchnic circulation and reduces pressure in portal system
Propanolol – used only in context of primary prevention (in those found to have varices to reduce risk of first bleed)
Endoscopy
Band ligation
Injection sclerotherapy
Management of Variceal bleeds
52
Balloon tamponade – sengstaken-blakemore tube
Rarely used now and usually only as temporary measure if failed
endoscopic management
Radiological procedure – used if failed medical/endoscopic Mx
Selective catheterisation and embolisation of vessels feeding the
varices
TIPSS procedure: transjugular intrahepatic porto-systemic shunt
shunt between hepatic vein and portal vein branch to reduce
portal pressure and bleeding from varices): performed if failed
medical and endoscopic management
Can worsen hepatic encephalopathy
Surgical
Surgical porto-systemic shunts (often spleno-renal)
Liver transplantation (patients often given TIPP/surgical shunt
whilst awaiting this)
Sengstaken-Blakemore
Tube
TIPSS
Prognosis closely related to severity of underlying chronic liver disease (Childs-Pugh grading)
Child-Pugh classification grades severity of liver disease into A,B,C based on degree of ascites, encephalopathy, bilirubin, albumin, INR
Mortality 32% Childs A, 46% Childs B, 79% Childs C
Variceal Bleed: Prognosis
Emergency resuscitation as already described
Pharmacological Stop NSAIDS/anti-platelets/anti-coagulants if safe
Endoscopic 15% of patients with severe acute PR bleeding will have an upper
GI source!)
Colonoscopy – diagnostic and therepeutic (injection, diathermy, clipping)
Management-lower GI
BLEEDING
Radiological CT angiogram – diagnostic only (non-invasive)
Determines site and cause of bleeding
Mesenteric Angiogram – diagnostic and therepeutic
(but invasive)
Determines site of bleeding and allows embolisation of
bleeding vessel
Can result in colonic ischaemia
Management
Surgical – Last resort in management as very
difficult to determine bleeding point at
laparotomy Segmental colectomy – where site of bleeding is
known
Subtotal colectomy – where site of bleeding unclear
Beware of small bowel bleeding – always
embarassing when bleeding continues after large
bowel removed!
Management
Resuscitate
Management Flow Chart for
Severe lower GI bleeding
Endoscopy (to exclude upper GI cause for severe PR bleeding)
Colonoscopy (to identify site and cause of
bleeding and to treat bleeding by
injection/diathermy/clipping) – often
unsuccesful as blood obscures views
CT angiogram (to identify
site and cause of
bleeding)
Mesenteric angiogram (to identify
site of bleeding and treat
bleeding by embolisation of
vessel)
Surgery
As 85% of lower GI bleeds will settle
spontaneously the interventions mentioned on
previous slide are reserved for: Severe/Life threatening bleeds
In the 85% where bleeding settles spontaneously
OPD investigation is required to determine
underlying cause: Endoscopy: flexible sigmoidoscopy, colonoscopy
Barium enema
Management
REFERENCE 60
Harrison principles of intrnal medicine 18th edi.
Kumar .clinical medicine 8th edit.
On line search
61
10Q