GI bleed Flashcards by Monica Palumbo

upper GI tract is

proximal to the ligament of trietz

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ligament of Trietz

a fold of peritoneum that attaches the duodenojejunal flexure to the retroperitoneum
can be used as a landmark to distinguish the upper and lower GI tracts

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lower Gi tract is

distal to the ileocecal valve

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upper GI bleeding is bleeding from

eosophagus, stomach, duodenum (proximal to the ligament of trietz)

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Lower GI bleeding is bleeding from

colon or rectum

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small bowel bleeding is bleeding from

a source between the ligament of treitz and the ileocecal valve

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overt GI bleeding

Gi bleeding that is visible in the form of hematemesis, melon, or hematochezia (including intermittant scant hematochezia)

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causes of upper Gi bleeding

peptic ulcer disease (20-50% of cases)
eosophagitis
erosive gastritis and/or duodenitis
varices eg. gastric or eosophageal varicies
gastric astral vascular ectasia
dieulafoy lesion
angioma
telangiectasias
angiodysplasia
eosophageal cancer
gastric cancer
mallory weiss syndrome
hiatal hernias
boerhaave syndrome
foreign body ingestion
following open or endoscopic surgery
portal hypertensive gastropathy
coagulopathies

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causes of LGIB

diverticular bleeding
colitis
proctitis
ulcers
haemorrhoids
intenstinal ischaemia
arteriovenous malformation
colorectal varices
colorectal cancer
anal cancer
colonic polyps
lower abdominal trauma
anorectal trauma
following open or endoscopic surgery
anal fissures
meckel’s diverticulum
etiology of lower GI bleeding in children
coagulopathies

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risk factors for GI bleeding

NSAID use
antithrombotic use eg. antiplatelet therapy, anticoagulants
history of prior GI bleeding
older age

specifically for upper GI bleeding: H pylori infection, renal failure, especially in the first year of haemodialysis

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coffee ground appearance of hematemesis

caused by coagulation and the presence of hematin, a dark pigment that forms when heme is oxidised by gastric acid in the stomach
most commonly caused by UGIB

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melena

black tarry stool with strong offensive odour
caused by the presence of hemetin, a dark pigment formed by the oxidation of heme
in UGIB, heme is oxidised by gastric acid, in LGIB, it is oxidised by intestinal bacteria

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hematochezia

passage of blood through the anus with or without stool
maroon, jelly like traces of blood indicate colonic bleeding
streaks of fresh blood indcate rectal bleeding

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approach for initial management

obtain IV access for possible fluid resus and blood transfusion: two large bore peripheral IV catheters
order nill per mouth status
A-E assessment
consider intubation to protect the airway in patients with altered mental state or severe ongoing hematemesis
immediate hemodynamic support with management of haemorrhagic shock
consider anticoagulation reversal

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immediate hemodynamic support should consist of

IV fluid resus with crystalloids
blood transfusion

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blood transfusion for stable patients

follow a restrictive transfusion strategy
packed red blood cell transfusion if Hb is <7
a higher threshold may be considered in patients with preexisting cardiovascular disease or delays in endoscopy

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empiric pharmacotherapeutic treatment for UGIB

prior to Endoscopy: consider erythromycin to improve visualization during EGD
benefit of preprocedural PPIs is unclear
if oesophageal variceal bleeding is suspected: start vasoactive therapy with octreotide or vasopressin and start antibiotic prophylaxis with caeftriaxone

elevated BUN/Creatinine ratio in upper GI bleed

may be a sign of severe UGIB and is especially relevant in patients who present with an unknown source of bleeding eg. unstable patients with hematochezia).
BUN is elevated in UGIB due to intestinal absorption and metabolism of hemoglobin as well as decreased urea secondary to hypovolaemia

issues on medical history suggesting UGIB

history of UGIB
known potential source of UGIB
- history of PUD
- hepatic cirrhosis, portal hypertension

issues on medical history suggesting LGIB

history of LGIB
known potential source of LGIB
- diverticulitis
- colonic angiodysplaasia
- recent polypectomy

approach to suspected UGIB

if hemodynamically stable
- endoscopy
if endoscopy is not diagnostic
- colonoscopy after bowel prep
- CT abdomen

approach to suspected LGIB if hemodynamically unstable

if hemodynamically unstable: CTA
if CTA identifies source of bleeding,
proceed to catheter angiography or colonoscopy for endoscopic hemostasis

approach to suspected LGIB if hemodynamically stable

non emergency colonoscopy after bowel prep
consider CTA for patients who cannot tolerate bowel prep or if there is high suspicion of active bleeding
tagged RBC scintigraphy may be ordered for patients with ongoing LGIB that can not be loclized with colonoscopy and CTA

obscure Gi bleeding

overt Gi bleeding from an undetermined source that persists of recurs after a negative diagnostic evaluation

approach to suspected small bowel bleeding

evaluate for small bowel bleeding in patients with obscure GI bleeding CTA video capsule endoscopy consider further investigations as necessary - advanced endoscopic evaluation: push enteroscopy, double balloon enteroscopy - radiographic evaluation: CT enter-graphe, tagged RBC scintigraphy, Meckel scan

interventional radiology - catheter angiography

indicated for ongoing severe LGIB in patients with hemodynamic instability refractory to resus identification of an arterial source of UGIB on endoscopy consider in patients with rebleeding despite endoscopic homeostasis techniques: angioembolisation (preferred in faesible), or intraarterial vasopressin (if the source of bleeding is diffuse)

endoscopic hemostasis

preferred intervention for most patients with ongoing bleeding or signs of recent bleeding on endoscopy techniques: thermal coagulation, clip placement, band ligation, injection with epinephrine solution, topical sealants, polypectomy in case of bleeding polyp

surgical hemostasis

may be considered in patients with onogoing Gi bleeding only in the following scenarios - all other therapeutic options have failed - refractory hemodynamic instability techniques: surgical ligation of bleeding vessels, excision of susceptible mucosa, segmental bowel resection

forms of intervention for hemostatic control

- endoscopic hemostasis: preferred method for most patients with ongoing bleeding or signs of recent bleeding on endoscopy - interventional radiology (catheter angiography): consider in patients with ongoing bleeding despite endoscopic hemostass - surgical hemostasis: if all other therapeutic options fail

occult GI bleeding

Gi bleeding that is not visible and can only be detected by faecal occult blood tests or seen on microscopy

management of a positive FOBT

FBC, Fe studies non emergency colonoscopy

what is intermittant scant hematochezia

chronic, intermittant passage of a small amount of bloow from the rectum

eatiology of intermittant scant hematochezia

hemorrhoids, anal fissures colorectal cancer, colon polyps

diagnostics for intermittent scant hematochezia for patients <40

for patients <40 without features of underlying malignancy or IBD, perform DRE and flexible sigmoidoscopy these tests are sufficient to evaluate for haemarhoids and fissures

when is colonoscopy indicated in scant intermittant haamatochezia

non diagnostic sigmoidoscopy age >50 years unexplained red flags for colorectal cancer or IBD eg. weight loss, altered bowel habits, iron deficiency anaemia - other risk factors for colorectal cancer eg. history of colonic polyps or family history of colorectal cancer

differential diagnosis

bleeding from upper respiratory tract eg. nocturnal nosebleeds: blood can be swallowed and vomited or appear as malaena ingestible substances that can darken stool and resemble malaena eg. iron tablets, bismuth preparations certain foods or drinks with red food colouring eg. licorice, soft drinks

complications of GI bleed

haemorrhagic shock hepatic encephalopathy (in patients with liver cirhhosis) aspiration pneumonia

why can GI bleed cause hepatic encephalopathy

hepatic encephalopathy is caused by inadequate elimination of metabolic products by the liver with subsequent accumulation of neurotoxic metabolites e.g ammonia. GI bleeding causes an increased amount of blood to be digested into protein, which increases ammonia concentrations and, subsequently, the risk of heptic encephalopathy

why can GI bleed cause aspiration

commmonly seen in patients with massive UGIB (especially with oesophageal bleeding) and in patients with an aletred mental state eg. dementia, hepatic encephalopathy