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Appendix > Acute GI Hemorrhage > Flashcards

Acute GI Hemorrhage Flashcards

1
Q

What % of pts hospitalized for bleeding require an operation?

A

5-10 % of pts

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2
Q

Most pts with an acute GI bleed will what?

A

stop bleeding spontaneously

15% of cases, the bleeding will persist

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3
Q

Mortality from acute GI bleed?

A

> 5%

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4
Q

Bleeding can occur anywhere along the GI tract and is classified based on its location relative to the;

A

ligament of treitz

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5
Q

Most cases of acute bleeding originate where?

A

proximal to the ligament of Treitz (>80%)

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6
Q

Upper GI hemorrhage, bleeding proximal to the ligament of treitz, accounts for > 80% of cases of GI hemorrhage, what are most common?

A

PUD

variceal bleeding

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7
Q

Most lower GI bleeding, distal to the ligament of treitz, is from ?

A

the colon

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8
Q

Most lower GI bleeding is from the colon, with common causes being?

A

diverticula

angiodysplasias

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9
Q

Most lower GI bleeding comes from colon, what % comes from the small bowel?

A

5%

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10
Q

What is obscure vs occult bleeding?

A

obscure—> hemorrhage that recurs or persists after negative endoscopy

occult—> not apparent to pts until they present with symptoms of anemia

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11
Q

Initial approach to a pt with GI hemorrhage?

A

airway and breathing take first priority

then we focus on pt’s hemodynamics

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12
Q

The severity of bleeding can be based on clinical parameters, what do we see with hemorrhagic shock?

A

SBP < 90
cool clammy extremities
obtundant
agitated

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13
Q

In regards to GI bleeding, what signs do we see with 20-40% blood loss?

A

HR >100 beats/min

decreased pulse pressure

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14
Q

Hemodynamic signs of bleeding are less reliable in which pts?

A

elderly

pts taking beta-blockers

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15
Q

What is the BLEED scoring system for GI hemorrhage?

A

it’s a model that predicts risk of recurrent hemorrhage

need for surgical intervention or even death

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16
Q

What 5 criteria do we take into account with BLEED model?

A 
ongoing bleeding
SBP < 100 mmHg
PT > 1.2x normal
AMS
comorbid conditions requiring ICU admission

if any of these criteria present, model predicts 3 fold increase in recurrent hemorrhage, need for surgery, death

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17
Q

Leading cause of morbidity and mortality in pts with acute GI bleeding?

A

multiorgan failure due to inadequate initial resuscitation

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18
Q

How do we resuscitate a pt with acute GI bleeding?

A

intubate and ventilate if concern for resp compromise

two large bore IVs placed

unstable pts give 2L bolus of LR

send labs

insert Foley

triple lumen, A-line if needed, ICU admission if needed

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19
Q

In pts that receive >10 U of blood, what else should they receive empirically?

A

FFP
platelets
calcium

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20
Q

What are the most common manifestations of acute hemorrhage?

A

hematemesis
melena
hematochezia

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21
Q

Hematemesis is vomiting blood usually caused by ?

A

bleeding from upper GI tract

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22
Q

What’s melena?

A

passage of dark, tarry stools

** usually indicative of bleeding from upper GI
hbg degraded to hematin by stomach acid

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23
Q

What hematochezia?

A

bright red blood per rectum

usually lower GI source
upper GI bleeds can produce hematochezia if large or brisk enough

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24
Q

Older pts tend to bleed from what?

A

angiodysplasia
cancer
diverticula
ischemic colitis

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25
Q

Younger pts tend to bleed from?

A

peptic ulcers
varices
Meckel’s

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26
Q

Why do we place an NG tube in a pt suspected of acute GI hemorrhage?

A

although melena usually an upper GI problem, it can be from colon and small bowel

although hematochezia is a lower GI problem, it can be caused by upper GI bleed

NG tube helps lavage the stomach and see what kind of contents are inside

can help see rate of bleeding, helps remove old blood from stomach

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27
Q

If we have an NGT in place and aspirate shows red blood or coffee ground fluid, what does this mean?

A

we have an upper GI bleed

** return of bile from NGT shows that duodenum has been sampled and can rule out an upper GI source in most cases

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28
Q

NGT aspirate is helpful most of the time, regardless these pts should still have what done?

A

upper endoscopy

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29
Q

When do we perform an endoscopy, time-wise?

A

should be performed within 24 hrs

proven to reduce transfusion requirements, resource use, and hospital stay

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30
Q

EGD in the emergent/urgent setting is associated with what?

A

reduced accuracy
poor visualization
increased complication rate

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31
Q

Morbidity and mortality increases significantly in pts who have losts how many units?

A

if they have lost > 6 units

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32
Q

Are most GI hemorrhage upper or lower?

A

upper

>80% occur proximal to the ligament of Treitz

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33
Q

More than 80% of acute GI hemorrhages occur where?

A

proximal to ligament of Treitz (upper)

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34
Q

Causes of upper GI bleeding?

A

non-variceal sources (80%) ** PUD most commonly

variceal sources

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35
Q

This is the foundation for diagnosis and management of an upper GI bleed:

A

upper endoscopy

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36
Q

In general what % of pts undergoing an upper GI endoscopy will require intervention?

A

20-35% need intervention

5-10 % need surgery

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37
Q

In what % of pts with upper GI hemorrhage, is EGD not able to localize source of bleeding because of excessive blood impairing visualization of mucosal surface?

A

1-2%

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38
Q

How can we improve visualization of upper GI with EGD?

A

flush stomach w/NS

IV erythromycin to promote gastric emptying

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39
Q

PUD accounts for majority of UGI bleed, what % of cases?

A

40%

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40
Q

In pts with PUD what’s the most frequent cause of death and most frequent indication for operation?

A

bleeding

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41
Q

Why do we see bleeding with PUD?

A

peptic acid erodes mucosal surface

major bleeding seen when erodes into artery (gastroduodenal or left gastric arteries)

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42
Q

Pts with evidence of GI bleed should receive endoscopy within 24 hrs, whole waiting this they should be on?

A

PPI

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43
Q

What’s the Forrest classification system?

A

developed to assess risks based on endoscopic findings for GI bleed

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44
Q

Which pts under Forest classification system do we initiate endoscopic therapy?

A

IA; active pulsatile bleeding (have high rebleed risk)
IB: active, non-pulsatile bleed (high rebleed risk)
IIA: non-bleeding visible vessel (high rebleed risk)
IIB: adherent clot–> remove clot and evaluate ulcer base, clean base or black spot not treated

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45
Q

What are some meds that are ulcerogenic?

A

NSAIDs

SSRIs

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46
Q

Once a bleeding ulcer has been identified, how do we tackle the bleeder endoscopically?

A

epi inj
heater probes
coagulation
clips

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47
Q

Epi injections as an endoscopic tool to prevent bleeding?

A

1:10,000 to all 4 quadrants of the lesion

> 13 cc of epi is assc/w better hemostasis

    • epi inj alone assc w high rebleed rate
    • epi + thermal energy control 90% of PUD bleeding
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48
Q

After 1st endoscopic attempt at controlling bleeding, pt rebeleeds, what do we do?

A

endoscopy again

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49
Q

After a 1st endoscopic attempt at controlling bleeding, the pt bleeds again, thus a 2nd attempt at endoscopic control is warranted, what % of bleeders are controlled with this second attempt?

A

75%

***25% will need surgery

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50
Q

At the time of endoscopy, Forrest classification is most important indicator of rebleeding risk, but ulcer size and location also important;

A

ulcers > 2 cm
posterior duodenal ulcers
gastric ulcers

**have higher risk of re-bleed

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51
Q

What blood transfusion requirements necessitate surgical intervention?

A

ongoing blood transfusion requirement > 6 units in older pts

8-10 units in younger pts

52
Q

What are the indications for surgery in someone with GI hemorrhage?

A

hemodynamic instability despite resuscitation (>6 U)

2 failed endoscopic attempts

shock due to recurrent hemorrhage

continued slow bleed with transfusion requirement > 3 U a day

53
Q

If bleeding is from duodenal ulcer, mostly are found in duodenal bulb, how do we tackle it surgically?

A

expose via longitudinal duodenotomy

bleeding can be controlled with pressure then suture ligation w/non-absorbable suture

54
Q

Most frequently used operation for a bleeding duodenal ulcer?

A

pyloroplasty with truncal vagotomy

55
Q

For gastric ulcer bleeding, why is gastric ulcer resection generally indicated?

A

10% risk of malignancy

56
Q

For bleeding gastric ulcers, operation we normally perform?

A

simple excision assc with 20% rebleed so distal gastrectomy performed

57
Q

These are mucosal and submucosal tears that occur near the GE junction:

A

Mallory-Weiss tears

seen in pts after intense retching

can occur in pts w/repeated emesis

58
Q

MOA that causes Mallory-Weiss tears?

A

forced abdominal contractions against an unrelaxed cardia

get mucosal laceration of cardia due to increased gastric pressure

59
Q

Mallory-Weiss tears account for what % of upper GI bleeding?

A

5-10

60
Q

How do we diagnose Mallory-Weiss tears?

A

diagnosed by history

endoscopy frequently used to confirm diagnosis

**retroflexion maneuver needs to be performed to view area underneath GE junction

61
Q

Most Mallory-Weiss tears occur where ?

A

lesser curve (less common on greater curve)

62
Q

Tx for Mallory-Weiss tears?

A

supportive tx is effective bc 90% of bleeding episodes are self-limited

mucosa often heals within 72 hrs

63
Q

Recurrent bleeding from a Mallory-Weiss tear?

A

uncommon

64
Q

IF conservative tx fails to manage Mallory-Weiss tears, what do we do?

A

endoscopic tx w/injection or electrocautery

angiography used if endoscopy fails

surgery–> high gastrotomy with suture of mucosal tear

65
Q

This is characterized by multiple superficial erosions of entire stomach, commonly the body;

A

stress related gastritis

66
Q

Cause of stress gastritis?

A

combo of pepsin and acid injury in context of ischemia from hypoperfusion states

67
Q

These are solitary lesions due to acid hypersecretion, that appear in pts with severe head injuries:

A

Cushing’s ulcer

68
Q

When stress ulcers are associated with burn’s these ulcers are called?

A

Curling ulcers

69
Q

In the ICU what factors increase risk of hemorrhage from stress gastritis?

A

ventilator dependence > 48 hrs

coagulopathy

70
Q

These are vascular malformations primarily along the lesser curve of stomach, within 6 cm of GE junction;

A

Dieulafoy’s lesions

71
Q

What are Dieulafoy’s lesions?

A

vascular malformations seen along lesser curve

represent rupture of large vessels in gastric submucosa

erosion of gastric mucosa overlying these vessels leads to bleeding

72
Q

Why can bleeding from Dieulafoy’s lesions be massive?

A

due to rupture of large vessels in gastric submucosa (usually 1-3 mm)

73
Q

Tx for Dieulafoy’s lesion?

A

endoscopic control usually successful

if fails angiographic coil embolization may be used

surgery if all fails (endoscopic tattooing helps identify lesion) –> gastrostomy performed, lesion oversewed

if all else fails–> partial gastrectomy

74
Q

What is watermelon stomach?

A

gastric antrum vascular ectasia

75
Q

What is Gastric Antrum Vascular Ectasia?

A

watermelon stomach

dilated venules that appear as linear red streaks meeting on the antrum

76
Q

How do pts with GAVE present?

A

acute severe bleeding is rare

present with chronic anemia, FOBT

77
Q

Tx for GAVE ?

A

endoscopy successful in 90% of pts

if fails–> antrectomy

78
Q

Do malignancies of the upper GI tract present with acute bleeding or other symptoms?

A

assc w/chronic anemia, FOBT

don’t present with episodes of significant hemorrhage

79
Q

What is an aorto-duodenal fistula as cause of massive upper GI bleeding?

A

rare

develop in setting of previous AAA repair
can also be seen in 1% of aortic graft cases

80
Q

Time frame of when aorto-duodenal fistulas present?

A

3 yrs

81
Q

MOA of aorto-duodenal fistula?

A

pseudo-aneurysm at proximal anastomotic suture line

fistulization into overlying duodenum

82
Q

What type of bleeding pattern do we see in someone with an aorto-enteric fistula?

A

sentinel bleed which heralds next massive bleed

83
Q

How do we diagnose aorto-enteric fistula?

A

emergent EGD, bleeding seen in 3/4th part of duodenum

84
Q

Surgical tx for an aorto-enteric fistula?

A

aorta ligated proximal to the graft
graft removed
extra-anatomic bypass
duodenal defect repair primarily

85
Q

This is an unusual cause of upper GI bleed and pts present with hemorrhage, RUQ pain, jaundice;

A

hemobilia

usually due to trauma or instrumentation of biliary tree

86
Q

How do we diagnose and treat hemobilia?

A

angiography

angiographi embolization is preferred tx

87
Q

Bleeding related to portal HTN is a result of?

A

esophageal varices

88
Q

Esophageal varices are common where in the esophagus?

A

distal esophagus

varices seen in 30% of pts with cirrhosis, and of this group 30% will bleed

89
Q

Why do we give pts with variceal bleeding a 7 day course of broad spectrum abx like FQs?

A

will lower the risk of rebleed

90
Q

What is the vasoactive medication of choice for pts with esophageal varices?

A

somatostatins (ocreotide)

** helps buy time for resuscitation

91
Q

Effectiveness of endoscopy in treating esophageal varices?

A

90% are treated effectively

92
Q

Endoscopic therapy of choice for esophageal varices?

A

banding

93
Q

In pts where pharmacologic therapy or endoscopy fails what do we do for varices?

A

Sengstaken-Blakemore tube

has a gastric and esophageal balloon which are both inflated

94
Q

Complications of balloon tamponade therapies?

A

aspiration
esophageal rupture
misplacement

rebleed in 50% of cases

95
Q

For esophageal varices that don’t respond to medicine, endoscopy or baloon tamponade, what do we do?

A

TIPS (required in 10% of pts with varices)

96
Q

Success rate of TIPS in controlling variceal bleeding?

A

95%

97
Q

Rebleeding from TIPS is seen in 20% of pts within what time frame?

A

1st month

98
Q

Lower GI bleeds account for what % of GI bleeds?

A

20 %

seen in older pts

99
Q

LGI bleeds tend to be seen in what patient populations?

A

elderly pts

100
Q

> 95 % of pts with LGIB, the source is the ?

A

colon

101
Q

IN pediatric pts, cause of LGBI?

A

intussussception

102
Q

How does LGIB typically present ?

A

hematochezia

sometimes as melena if bleeding is slow or from a proximal source

103
Q

What makes LGIB more complicated that UGIB?

A

40% of pts with LGIB have more than 1 source of bleeding

25% of pts, the bleeding source is never identified

104
Q

Once resuscitation is initiated in a pt with LGIB, what’s the next step?

A

r/o anorectal bleeding with digital rectal exam, anoscopy or sigmoidoscopy

also need to rule out UGIB by placing NG tube–> if bilious or no blood rules out UGIB source

105
Q

Colonoscopy is considered mainstay in LGIB, and these act as adjuncts:

A

tagged RBC study

angiography

106
Q

RBC tagged scans can detect bleeding as slow as ?

A

0.1 mL/min

difficult to diagnose right sided vs left sided bleeding

107
Q

Selective angiography can detect bleeding as slow as?

A

0.5 cc- 1 cc/min

108
Q

Some complications of angiography?

A

hematoma
arterial thrombosis
contrast reaction
kidney failure

109
Q

MCC of significant LGIB?

A

diverticula

110
Q

MCC of LGIB?

A

diverticula

111
Q

What % of pts with diverticulosis experience bleeding?

A

3-15%

112
Q

What is the cause of LGIB from diverticulosis?

A

bleeding occurs from neck of diverticula

due to bleeding vasa recti as they penetrate the submucosa

113
Q

In terms of diverticulosis, what part of colon do we see bleeding more commonly?

A

diverticula are more common on left colon

but bleeding occurs more often from right colon

  • **75% stop spontaenously
  • **10 % rebleed within 1 year
  • ** 50% rebeleed withn 10 yrs
114
Q

What are angiodysplasias of the intestines?

A

AV malformations

acquired lesions from progressive dilation of normal blood vessels in submucosa of intestine

115
Q

In what age group do we find angiodysplasias?

A

pts > 50

116
Q

These lesions, as sources of LGIB in pts > 50%, are often assc w/ aortic stenosis and renal failure;

A

angiodysplasias

117
Q

Hemorrhage from angiodysplasias tend to occur from right side of colon most often, with what part of colon commonly affected?

A

cecum

118
Q

During colonoscopy these lesions appear as red stellate lesions with a surrounding rim of pale mucosa and can be tx with sclerotherapy or electrocautery;

A

angiodysplasias

119
Q

If angiodysplasias are discovered incidentally what do we do?

A

nothing

if active bleeding can be treated with vasopressin, gelfoam, electrocautery, sclerosing agents, r-hemi as last resort

120
Q

In this source of LGBI, the bleeding is usually painless, intermittent, slow in nature, and often assc with Fe-deficiency anemia;

A

colon ca

121
Q

Hemorrhoids account for what % of acute LGIB?

A

5-10%

122
Q

How do we distinguish bleeding from hemorrhoids vs anal fissure?

A

hemorrhoids as source of LGIB–> usually painless, from internal hemorrhoids, blood on toiler paper

anal fissure—> painful blood on toilet paper

123
Q

Tx for anal fissures?

A

stool bulking agents–psyllium
increased water intake
topical nitroglycerin
diltiazem to relax sphincter

124
Q

UC vs Crohn’s, which one do we see LGIB more often?

A

UC more often (15%)

CD (1%)

125
Q

Tx for c. diff colitis?

A

d/c antibiotics
supportive care
PO/IV flagyl or PO vanco

126
Q

When flex sigmoidoscopy shows bleeding telangiectasias what is on the differential as source of GI bleed?

A

radiation proctitis as source

127
Q

MCC of small intestinal bleeding?

A

angiodysplasias

**commonly in jejunum

Appendix (39 decks)

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