M a s s i v e G a s t ro i n t e s t i n a l

Hemorrhage
a, b
Katrina D’Amore, DO, MPH *, Anand Swaminathan, MD, MPH

KEYWORDS
 Gastrointestinal hemorrhage  Resuscitation  Massive hemorrhage
 Massive transfusion  Thromboelastography  Anticoagulant reversal

KEY POINTS
 Massive gastrointestinal hemorrhage requires aggressive resuscitation with prompt trans-
fusion of blood products and initiation of a massive transfusion protocol if clinical insta-
bility does not improve.
 Successful resuscitation begins with the placement of reliable, large-bore, peripheral
intravenous or intraosseous access.
 Reversal of anticoagulant medications is a critical component in the management of pa-
tients with massive gastrointestinal hemorrhage. Using thromboelastography or rotational
thromboelastometry can guide transfusion strategies specific to the patient’s unique
needs.
 Consider delayed sequence intubation; bed-up head-elevated positioning; reduced dose
of the sedative; increased dose of the paralytic; and the SALAD (suction-assisted laryn-
goscopy for airway decontamination) technique to intubate the patient and minimize
aspiration.
 Consult gastroenterology, interventional radiology, and acute care emergency surgery
early in the patient’s resuscitation for definitive source control.

INTRODUCTION

Massive gastrointestinal (GI) hemorrhage is a life-threatening condition that requires

prompt recognition and skilled resuscitation to increase the chance of good out-
comes. Although no consensus definition exists, any gastrointestinal bleeding (GIB)
that results in hemodynamic instability, signs of poor perfusion (eg, altered mental sta-
tus, syncope, pallor), transfusion of more than 2 units of packed red blood cells
(pRBCs) during the initial resuscitation, or the presence of bleeding that is overt and
rapid can be considered massive.1 Although the mortality of all patients with a GIB
ranges from 3% to 14%, the mortality from massive hemorrhage is much higher.2 Suc-
cessful resuscitation of massive GIB (MGIB) involves prompt establishment of reliable

a
Department of Emergency Medicine, Good Samaritan Hospital Medical Center, 1000 Mon-
tauk Highway, West Islip, NY 11795, USA; b St. Joseph’s University Medical Center, 703 Main
Street, Paterson, NJ 07503, USA
* Corresponding author.
E-mail address: [email protected]

Emerg Med Clin N Am 38 (2020) 871–889

https://doi.org/10.1016/j.emc.2020.06.008 emed.theclinics.com
0733-8627/20/ª 2020 Elsevier Inc. All rights reserved.
872 D’Amore & Swaminathan

vascular access, transfusion of appropriate blood products, reversal of coagulopa-

thies, early involvement of consultants, and, in many cases, definitive airway
management.

DOES THIS PATIENT HAVE A MASSIVE GASTROINTESTINAL HEMORRHAGE?

MGIB describes patients with severe bleeding who require emergency intervention in
order to prevent mortality and limit morbidity.3 Patients with clinically obvious MGIB
include those with overt hematemesis, brisk hematochezia, or hemodynamic insta-
bility (eg, hypotension) in the setting of bleeding. When significant hemorrhage leads
to poor perfusion, organs such as the skin and distal extremities manifest distinct
signs and symptoms. Physical examination signs of poorly perfused organs are
markers of circulatory shock and impending organ failure. These signs are listed in
Box 1.4
Several findings from the history and physical examination have been shown to pre-
dict the need for immediate intervention in patients with an upper GI bleed (UGIB).
MGIB is more likely if the patient reports a history of cirrhosis or malignancy (Likeli-
hood Ratio (LR), 3.7; 95% confidence interval [CI], 1.6–8.8) or syncope (LR, 3.0;
95% CI, 1.7–5.4).3 Clinical signs of MGIB include tachycardia (LR, 4.9; 95% CI, 3.2–
7.6) and a nasogastric lavage that shows red blood (LR, 3.1; 95% CI, 1.2–14.0).3 A
normal heart rate (LR, 0.34; 95% CI, 0.22–0.53) was the most predictive clinical factor
of a nonsevere UGIB.3 However, tachycardia may not be present if the patient is taking
a b-blocker or calcium channel blocker medication. b-Blocker medication use is
particularly common in patients with advanced cirrhosis, because they are first-line
therapy in the treatment of portal hypertension. Similar factors (tachycardia, syncope,
hemodynamic instability) have also been shown to predict MGIB in the setting of a
lower GI bleed (LGIB).5 Additional characteristics of severe LGIB include active
bleeding per rectum during the initial evaluation, a nontender abdominal examination,
history of aspirin use, and more than 2 comorbid conditions.6,7 Comorbidities such as
renal failure, liver failure, and malignancy are considered higher risk. Regardless of the
patient’s initial presentation and vital sign measurements, all patients with signs and

Box 1
Signs of poor perfusion

 Altered or decreased mental status

 Decreased peripheral pulses
 Delayed capillary refill
 Skin pallor or mottling, most commonly around the knees and fingers (limited utility in
darker complexions)
 Cold skin
 Low peripheral oxygen saturation
 Decreased mean arterial pressure
 Increased lactate level

Data from Hasanin A, Mukhtar A, Nassar H. Perfusion indices revisited. Journal of Intensive
Care. 2017;5(1). https://doi.org/10.1186/s40560-017-0220-5.
 Massive Gastrointestinal Hemorrhage 873

symptoms of GIB should be taken seriously and prompt treatment initiated. The po-
tential for rapid decompensation among GIB patients is high.
Shock index (SI) is defined as the heart rate divided by systolic blood pressure and
can be used as an indicator of impending hemodynamic instability or collapse.8 An SI
greater than 0.7 is considered abnormal. An abnormal SI in the presence of bleeding
indicates considerable hypovolemia and, possibly, occult shock. An SI greater than
0.9 portends a poorer prognosis, and an SI greater than 1.0 indicates the need for a
massive transfusion (MT).8,9 Calculation of the SI can aid in the recognition of critical
illness before a patient becomes overtly hypotensive and can prompt more aggressive
evaluation and treatment.10,11

IDENTIFYING THE LOCATION OF HEMORRHAGE

MGIB can result from both upper and lower GI sources (Tables 1 and 2).12 It is impor-
tant to differentiate between upper and lower sources of GIB, because this affects the
type of diagnostic studies and consultants needed for definitive source control. In he-
modynamically unstable patients, an UGIB is more likely. Although UGIB carries a
higher mortality, recent data show that the prevalence of hospitalizations and inpatient
death from LGIB are approaching those seen in UGIB.13
UGIB occurs at locations proximal to the ligament of Treitz, a suspensory ligament
located at the duodenojejunal flexure (Fig. 1). Massive UGIB can present in several
ways: hematemesis, melena, or hematochezia. Hematemesis can occur as either
bright red blood or so-called coffee-ground emesis, which gains its appearance
from gastric acids converting hemoglobin to the brown-pigmented hematin. Melena
occurs when hemoglobin undergoes digestion by intestinal enzymes and endogenous
gastrointestinal flora. UGIB that presents as hematochezia results from a brisk bleed
that passes rapidly through the small and large intestines and encounters little diges-
tion. One in 10 patients presenting with hematochezia are bleeding from an upper GI
source.14
LGIB originates anywhere distal to the ligament of Treitz and typically presents with
hematochezia, with or without associated clots. LGIB rarely presents with melena,
although it can occur with very proximal lower sources that undergo some intestinal
digestion. Up to 80% of LGIB stops spontaneously.15

Table 1
Common causes of massive upper gastrointestinal bleed

Frequency
Cause (%)
Peptic ulcer disease 55–74
Varices 5–14
Esophageal and gastric
Portal hypertensive
gastropathy
Hemorrhagic gastritis 11–15
Vascular lesions 2–3
Malignancy 2–5
Aortoenteric fistula <1

Data from Lee E, Laberge J. Differential Diagnosis of Gastrointestinal Bleeding. Techniques in

vascular and interventional radiology. 2004;7: 112-22. https://doi.org/10.1053/j.tvir.2004.12.001.
874 D’Amore & Swaminathan

Table 2
Common causes of massive lower gastrointestinal bleed

Prevalence
Cause (%)
Diverticular disease 5–42
Colitis
Ischemic 6–18
Infectious 3–29
Radiation related 1–3
Vascular lesions 0–3
Malignancy 3–11
Rectal varices 1–8
Inflammatory bowel disease 2–4

Data from Lee E, Laberge J. Differential Diagnosis of Gastrointestinal Bleeding. Techniques in

vascular and interventional radiology. 2004;7: 112-22. https://doi.org/10.1053/j.tvir.2004.12.001.

EMERGENCY DEPARTMENT RESUSCITATION OF THE PATIENT WITH MASSIVE

GASTROINTESTINAL BLEED
Vascular Access
Effective resuscitation of a patient with MGIB begins with the urgent placement of reli-
able and appropriate intravenous (IV) or intraosseous (IO) access, so that additional
therapies can be given rapidly and safely. The rate of flow through IV or IO catheters
can be described by Poiseuille’s law, which states that the larger the diameter and the
shorter the length, the faster the flow through the catheter will be. Maximal flow rates
have been determined for a variety of IV and IO catheters.16 Table 3 summarizes the
gravity and pressure bag flow rates of commonly used catheters. Application of a
pressure bag, a decrease in the length or an increase in the diameter of the catheter,
increases the flow rate.16 Two large-bore (14-gauge to 18-gauge) peripheral IV cath-
eters are ideal for resuscitating patients with MGIB, because these patients often
require large-volume transfusions.17 Importantly, the largest port of a central venous

Fig. 1. Suspensory muscle of the duodenum/ligament of Treitz at the duodenojejunal

flexure.
 Massive Gastrointestinal Hemorrhage 875

Table 3
Flow rates of commonly used intravenous and intraosseous catheters

Timeb Timeb to
Pressure to Infuse
Gravity Bag Infuse 1 L of
Flow Flow 1 L of 0.9% NS
Ratea Ratea 0.9% Under
(mL/ (mL/ NS Pressure
Catheter Size min) min) (min) (min)
14 G, 50 mm 236 384 4 3
16 G, 50 mm 154 334 7 3
18 G, 45 mm 98 153 10 7
Humeral IO 82 148 12 7
16 G port, 69 116 15 9
central line 34 cm
Tibial IO 68 204 15 5
20 G, 33 mm 64 105 16 10
22 G, 25 mm 35 71 29 14
18 G port, 30 79 33 13
central line 35 cm

Abbreviations: IO, intraosseous; NS, normal saline.

a
Rounded to the nearest 1 mL/min.
b
Rounded to the nearest minute.
Data from Reddick AD, Ronald J, Morrison WG. Intravenous fluid resuscitation: was Poiseuille
right? Emergency Medicine Journal. 2010;28(3):201-202. https://doi.org/10.1136/emj.2009.
083485; and Ngo AS, Oh JJ, Chen Y, Yong D, Ong ME. Intraosseous vascular access in adults using
the EZ-IO in an emergency department. Int J Emerg Med. 2009;2(3):155–160. Published 2009 Aug
11. https://doi.org/10.1007/s12245-009-0116-9

catheter has a slow flow rate caused mostly by its long length (>33 cm). Therefore,
these are often inadequate for efficient resuscitation of patients with MGIB. Patients
with a history of diabetes mellitus, IV drug abuse, sickle cell disease, end-stage renal
disease, and obesity have been shown to be challenging to obtain emergent periph-
eral vascular access.18 Ultrasonography guidance may aid in placement of IV cathe-
ters in these patients.
If reliable IV access proves difficult to quickly obtain, a humeral or tibial IO catheter
should be inserted.19 Modern IO devices allow rapid insertion (average insertion time
of 4 seconds) and are safe options for infusing blood products and most medica-
tions.19,20 IO marrow aspirate can also be used to obtain point-of-care hemoglobin,
hematocrit, blood urea nitrogen, creatinine, and glucose values. IO values for these
laboratory studies have all shown good correlation with serum samples.21
Although a humeral IO catheter can infuse 1 L of 0.9% normal saline (NS) faster than
a tibial IO catheter (12 vs 14 minutes), the application of a pressure bag has been
shown to produce the opposite result, with 1 L of 0.9% NS administered in 5 minutes
via the tibial route compared with 7 minutes via the humeral route.19 A tibial IO catheter
should be placed 2 finger widths below the patella and 1 to 2 cm medial to the tibial
tuberosity (Fig. 2). A humeral IO catheter is placed on the most prominent aspect of
the greater tuberosity with the patient’s hand on the abdomen or the humerus in an
internally rotated position (Fig. 3).
876 D’Amore & Swaminathan

Fig. 2. Tibial IO placement landmark.

Fig. 3. Humeral IO placement landmark.

 Massive Gastrointestinal Hemorrhage 877

Transfusion Strategies
The harms of massive bleeding center on end-organ ischemia secondary to
decreased perfusion through a lack of oxygen-carrying red blood cells. Transfusing
pRBCs sustains hemoglobin levels and oxygen delivery to tissues. Because patients
with MGIB can rapidly deteriorate, exsanguination from hematemesis or hematoche-
zia is a real and feared outcome. Early administration of blood products is a corner-
stone of management. Although restrictive transfusion strategies that target a
hemoglobin level of 7 g/dL are recommended for patients with an acute UGIB, patients
with MGIB should be transfused as soon as possible.22–24
Excessive crystalloid infusion should be avoided. Fluid administration may worsen
anemia and coagulation through further dilution. Large volumes of 0.9% NS can
result in a hyperchloremic acidosis and, if not warmed, decrease body temperature
as well.25 Both hypothermia and acidosis have been shown to increase the time to
clot formation and impair hemostasis.26,27 Administration of small volumes of
warmed balanced solutions (eg, Ringer’s lactate, Plasma-lyte) is reasonable to sup-
port mean arterial pressure while waiting for emergency blood products to be
available.
It is important to recall that hemoglobin measurement lags behind the true serum
concentrations and is not reliable in the face of brisk bleeding.28 Initial transfusion of
2 to 4 units of type-O pRBCs should be initiated as soon as MGIB is recognized. All
persons less than the age of 16 years and women of childbearing age should receive
Rh-negative type-O blood. Men and women past childbearing age may receive initial
resuscitation with Rh-positive type-O blood. If there is no significant improvement af-
ter initial pRBC administration, initiate a massive transfusion protocol (MTP). Clinical
stability and signs of end-organ perfusion should guide transfusion.4,29 Avoid hyper-
tension and over-resuscitation, because this can disrupt nascent clots at sites of
bleeding, especially in the setting of variceal bleeding. Permissive hypotension with
a target systolic blood pressure of 90 mm Hg is acceptable.
Platelets are the component of blood responsible for initiating blood clot formation
at sites of endothelial injury. There are no clear guidelines for transfusion of platelets in
patients with MGIB. Expert opinion recommends transfusion of platelets in the face of
thrombocytopenia to a goal of at least 50,000.30–32

Massive Transfusion Protocols

Unstable patients with GIB may require large transfusion volumes. Solely transfusing
erythrocytes can lead to a dilutional coagulopathy and worse outcomes. MTPs have
been designed to mimic replacement of whole blood, providing an equal ratio of red
blood cells, plasma, and platelets.33,34 MT has been defined as administration of
greater than 10 units of pRBC in 24 hours or transfusion of 4 units of pRBC in the first
30 minutes of resuscitation.17,35 The latter definition is more useful to the emergency
department resuscitation of MGIB. Although these protocols have largely been devel-
oped for patients with trauma, the authors believe they can reasonably be extrapo-
lated to the management of other forms of hemorrhagic shock, such as MGIB.
In patients with hemorrhagic trauma, MTPs that use a 1:1:1 ratio of blood products,
compared with isolated erythrocyte transfusion, have shown a decrease in mortality
and total pRBC transfusions.35,36 A combination of MT with thromboelastography
(TEG) or rotational thromboelastometry (ROTEM) further improves survival while
decreasing overall amounts of blood product given in trauma.37 Evidence of benefit
of MTP and TEG/ROTEM in patients with MGIB does not exist, but the benefit can
be extrapolated from the trauma research.35–39 If the initial transfusion of 2 to 4 units
878 D’Amore & Swaminathan

of pRBC is not effective in improving hemodynamic stability, perfusion, or hemostasis,

consider activating an MTP.
Known complications of MT are hypothermia, hypocalcemia, and hyperkalemia.17
Warming blood through a rapid transfuser and keeping the patient covered in warm
blankets can combat hypothermia. Because fractionated blood products are pre-
served with citrate, their administration can cause precipitation with calcium and
resultant hypocalcemia. Monitor calcium levels closely throughout the resuscitation
or consider empiric calcium administration. Potassium levels should be monitored
as well and hyperkalemia treated accordingly. Familiarity and anticipation of these
complications are important during resuscitation.

Fig. 4. Normal thromboelastogram. MA, maximum amplitude (mm); SP, initial fibrin forma-
tion; R, reaction time (seconds); K, kinetics (seconds); A30/LY30, amplitude/lysis at 30 minutes
after MA (percentage decrease).
 Massive Gastrointestinal Hemorrhage 879

Assessing Coagulation Status

Although traditional coagulation tests such as prothrombin time and activated partial
thromboplastin time evaluate a portion of the coagulation cascade, they do not give
clinicians the entire picture of in vivo coagulation in patients with massive hemorrhage.
Although frequently ordered, the ability of these tests to inform transfusion strategy is
limited. Importantly, an International Normalized Ratio (INR) value should not be inter-
preted as a degree of anticoagulation or bleeding risk unless the patient is taking
warfarin. In patients not taking warfarin, the INR indicates the synthetic function of
the liver, which is responsible for both procoagulant and anticoagulant (AC) protein
production.40
TEG and ROTEM are laboratory blood assays that measure the efficiency of blood
coagulation, clot strength, and fibrinolysis. Through TEG/ROTEM, platelet mapping
displays real-time platelet function and shows the degree to which platelets are
inhibited by aspirin and clopidogrel. Fig. 4 shows a normal thromboelastogram.
Each part of the curve correlates to a specific aspect of either clot formation or disso-
lution. Characteristic changes to the thromboelastogram signal the need for specific
product transfusion, such as cryoprecipitate, platelets, or fresh frozen plasma.41
Much of the literature on the role of TEG/ROTEM in transfusions has been published
in cardiac surgery and trauma. However, its clinical use is expanding and it may be
applicable to patients with MGIB. A Cochrane Review in 2018 evaluated a total of
17 studies of adults and children with bleeding. Despite the totality of evidence being
categorized as lower quality, the use of TEG/ROTEM reduced overall blood product
transfusion with a trend toward improved mortality and reduced hemodialysis-
dependent renal failure.42 There was no significant difference between the need for
surgical reintervention and MT.42 A 2019 randomized controlled trial evaluating the ef-
fect of TEG on outcomes in cirrhotic patients with nonvariceal UGIB similarly found
that patients in the TEG-guided transfusion group received fewer blood product trans-
fusions.43 There was no significant difference in rates of hemorrhage control, rebleed-
ing, or mortality.43 Although more high-quality evidence is needed, there are emerging
data that the use of TEG/ROTEM decreases the amount of blood products transfused
with no resultant increase in mortality.42–44 Because transfusion and overtransfusion
can have deleterious effects and complications, using TEG/ROTEM when available
is advised.
If TEG or ROTEM is not available, a fibrinogen level may be informative and help
guide transfusion. Fibrinogen is a protein abundant in the human body and is con-
verted to fibrin by the enzyme thrombin. Fibrin molecules then polymerize to aid in
forming hemostatic clots. Fibrinogen also actively aids in platelet aggregation. Normal
fibrinogen levels range from 150 to 400 mg/dL. A low fibrinogen level results from
decreased production (liver disease), hemodilution, or consumption.45–47 Cryoprecipi-
tate is a blood product that contains fibrinogen, factor VIII, von Willebrand factor
(vWF), factor XIII, and platelet microparticles. Fibrinogen concentrate is also available
at some institutions. In patients with MGIB and fibrinogen levels less than 100 mg/dL,
consider administration of cryoprecipitate (1 unit/5 kg body weight up to 10 units).

Reversing Anticoagulant and Antiplatelet Medications

A thorough medication history can provide valuable information in controlling hemor-
rhage. An increase in cardiovascular disease coupled with the advent of newer oral
ACs has seen an increase in the overall prevalence of outpatient antiplatelet and AC
(AC) medication use. These medications impair hemostasis and may contribute to
worsening hemorrhage in patients with GIB. The most commonly used oral ACs are
880 D’Amore & Swaminathan

Table 4
Oral anticoagulants and suggested reversal agents

Oral AC Mechanism of Action Reversal and Suggested Dosing

Warfarin Inhibits the production of 50 U/kg PCC plus vitamin K 5–10 mg IV
vitamin K–dependent factors Or
(II, VII, IX, X) 15 mL/kg FFP plus vitamin K 5–10 mg
IV
Rivaroxaban Factor Xa inhibitor 50 U/kg PCC
Apixaban Or
Edoxaban Andexanet alfaa
Betrixaban
Dabigatran Direct thrombin inhibitor Idarucizumab 5 mg IV with option to
repeat the dose once
Or
50 U/kg PCC

Abbreviations: FFP, fresh frozen plasma; PCC, prothrombin complex concentrate (3 or 4 factor).
a
Recommended dosing varies depending on which Xa inhibitor is being reversed as well as the
time since the last dose.
Data from Tomaselli GF, Mahaffey KW, Cuker A, et al. 2017 ACC Expert Consensus Decision
Pathway on Management of Bleeding in Patients on Oral Anticoagulants. Journal of the American
College of Cardiology. 2017;70(24):3042-3067. https://doi.org/10.1016/j.jacc.2017.09.1085; and
Cuker A, Burnett A, Triller D, et al. Reversal of direct oral anticoagulants: Guidance from the Anti-
coagulation Forum. American Journal of Hematology. 2019;94(6):697-709. https://doi.org/10.1002/
ajh.25475

warfarin, dabigatran, and direct oral ACs (DOACs), such as rivaroxaban, apixaban,
and edoxaban.48,49 Importantly, patients with renal dysfunction have decreased
excretion of DOACs and therefore can be expected to have longer half-lives and
higher levels of active drug.50 Dabigatran is the only oral AC amenable to hemodialy-
sis; however, gaining access and initiating dialysis may not be feasible during the initial
resuscitation of patients with MGIB.50
In a recent meta-analysis, DOACs were noted to have significantly lower mortalities
caused by major bleeding compared with warfarin (7% v 11%).51 However, once
bleeding has occurred, the presence of an AC increases morbidity and mortality
and clinicians should consider reversal to aid in achieving hemostasis. Table 4 out-
lines the common oral ACs, their mechanism of action, and recommended reversal
strategies.50,52,53 Although there is no strong clinical evidence to support its routine
use for factor Xa inhibitor reversal, andexanet alfa is recommended when available.52
Antiplatelet agents such as aspirin, clopidogrel, and ticagrelor decrease platelet
function, but they do not affect the overall number of platelets. There are no clear
guidelines for transfusion of platelets in patients with MGIB taking these medications.
Platelet transfusion is not recommended in patients on antiplatelet therapy with
normal platelet counts.32,54 Platelet mapping through a viscoelastic assay, such as
TEG, can provide more information regarding platelet activity and contribution to
clot integrity, thus better informing the need for platelet transfusion.
Patients with MGIB on antiplatelet therapy may benefit from IV desmopressin.55
Desmopressin is thought to increase the levels of factor VIII and vWF and has been
shown to expedite thrombus formation in animal models and decrease pRBC transfu-
sion in cardiac surgery patients.55,56 An IV desmopressin bolus of 0.4 mg/kg is recom-
mended in patients taking antiplatelet therapy and presenting with MGIB.
 Massive Gastrointestinal Hemorrhage 881

Fig. 5. Bed-up head-elevated positioning.

Airway Management
Intubation in the setting of massive UGIB is a critical and challenging task. Although
real-world scenarios are likely to have multiple resuscitative efforts occurring simulta-
neously, securing a definitive airway in the face of massive hematemesis is a high pri-
ority and may be indicated to limit aspiration of blood and other GI contents, protect
the airway in patients with altered mentation, and anticipate the need for emergent
intervention such as endoscopy. Patients with MGIB are often hemodynamically un-
stable and at risk of peri-intubation cardiovascular collapse. Resuscitation should
be initiated before intubation in order to maximize the patient’s physiology and, it is
hoped, prevent peri-intubation cardiovascular collapse.
All of the basic strategies of effective emergency airway management hold true in
the case of MGIB. The following recommendations should be considered when
time, resources, and clinical scenario allow:
1. Preoxygenate the patient: a nonrebreather mask in additional to high-flow nasal
cannula is recommended.57,58 Avoid ventilating with a bag-valve-mask (BVM) de-
vice, because this may lead to further stomach insufflation, vomiting, airway
contamination, and aspiration. If BVM ventilation is necessary, use in conjunction
with a positive end expiratory pressure (PEEP) valve. Aim for a PEEP of less than
20 cm H2O, because this level is unlikely to cause gastric insufflation.59
2. Properly position the patient: elevate the head of the bed to 45 to aid in reducing
the risk of gastric contents filling the hypopharynx and mouth. Keeping the patient
semiupright may also improve preoxygenation by decreasing the collapse of both
upper airway soft tissues and lower airway alveoli. Although the bed-up head-
elevated positioning (Fig. 5) has been shown to improve safe apnea times and
first-pass success and decrease intubation-related complications in the anesthesia
literature, no difference has been found in first-pass success among ED intubations
in limited studies.60–63
3. Consider placement of a nasogastric tube (NGT) before intubation. NGT placement
can empty the stomach and decrease the risk of large-volume aspiration and
airway contamination. If the patient is unable to tolerate NGT placement but it is
determined to be of benefit, ketamine can be used to facilitate placement followed
by intubation (ie, delayed sequence intubation).64
4. Provide proper medication doses: all sedative medications decrease the patient’s
release of catecholamines and decrease sympathetic tone. In hemodynamically
unstable patients, sedative doses should be reduced to minimize this issue.
Although lower doses of sedatives are recommended to facilitate intubation, higher
882 D’Amore & Swaminathan

Box 2
Suction-assisted laryngoscopy for airway decontamination technique

1. Lead with a rigid suction catheter (held in the right hand) and suction any proximal airway
contaminant.
2. Insert the laryngoscope into the midline of the mouth (with left hand).
3. Continue to advance the suction catheter followed by the laryngoscope. The suction
catheter not only clears the airway of any blood, vomitus, or other secretions but also
helps to lift the tongue.
4. Place the laryngoscope in the vallecula and visualize the vocal cords.
5. Move and park the suction catheter at the left corner of the mouth, with the tip of the
catheter in the proximal esophagus. The catheter can then be pinned in place by the
laryngoscope in the left hand, resulting in continuous esophageal suctioning with
endotracheal tube insertion on the right.
6. Advance the endotracheal tube through the vocal cords. Secure and suction the tube.

Data from Suction Assisted Laryngoscopy and Airway Decontamination (SALAD). https://
www.sscor.com/suction-assisted-laryngoscopy-and-airway-decontamination-salad. Accessed
November 30, 2019.

doses of paralytics are needed because the hypotensive state leads to longer cir-
culation time for the paralytic.
5. Use suction-assisted laryngoscopy for airway decontamination (SALAD): SALAD is
a set of actions developed by Dr Jim Ducanto in order to manage grossly contam-
inated airways, and, if used prophylactically, may decrease the risk of contamina-
tion.65 Please refer to the following video for a demonstration of the technique:
https://spaces.hightail.com/receive/V0YyRzYPqP. The steps are summarized in
Box 2.
Balloon Tamponade Devices
Consider placement of a Sengstaken-Blakemore or Minnesota tube if massive UGIB
continues despite aggressive resuscitation and establishment of a definitive airway.
These devices work by applying direct pressure to the mucosal surfaces and, theoret-
ically, the bleeding vessels of the esophagus and stomach through inflation of bal-
loons located on the device. There are risks of gastric and esophageal perforation
or necrosis; however, these devices are potentially lifesaving efforts to tamponade
ongoing hemorrhage in the upper GI tract.66,67 Because the insertion procedure is
infrequently performed, it is recommended to review the steps and equipment before
placement (EM:RAP Productions, Placement of a Blakemore Tube for Bleeding Vari-
ces: https://www.youtube.com/watch?v5NHelCd5Jtp4&t510s).
Medications
In the management of GIB, there are several medications that can be considered after
the initial resuscitation and stabilization. These medications should not be a routine
part of the resuscitative phase of care, because they can be safely administered after
patient stabilization. With the exception of antibiotics for variceal UGIB, none of the
pharmacologic agents have been shown to improve mortality.
Antibiotics
Antibiotics are a crucial medication to administer to patients with massive UGIB with
either variceal bleeding or a history of cirrhosis.68 In these patients, those who survive
 Massive Gastrointestinal Hemorrhage 883

the initial bleeding episode are at risk of developing subsequent bacterial infections
and sepsis. A third-generation cephalosporin, such as ceftriaxone (1 g IV every
24 hours) or cefotaxime (2 g IV every 8 hours), has been shown to decrease the inci-
dence of subsequent infection with a number needed to treat (NNT) of 4 and decrease
mortality with an NNT of 22.68,69 In patients who cannot receive cephalosporins
because of an anaphylactic allergy, a fluoroquinolone can be used (eg, ciprofloxacin
400 mg IV every 12 hours). The increasing prevalence of multidrug-resistant bacteria,
particularly to quinolones, should be noted. The antibiotic should possess activity
against pathogens such as Escherichia coli, Klebsiella species, Pseudomonas spe-
cies, and Enterococcus.70

Octreotide
Octreotide is a somatostatin analogue that acts as a vasoconstrictor on the splanchnic
circulation. This action reduces portal hypertension and, thus, decreases the circula-
tion to esophageal and gastric varices. Decreasing cardiac output to the splanchnic
circulation also shunts blood away from those vessels supplying gastric and duodenal
ulcers. In undifferentiated GIB, octreotide has been shown to decrease initial bleeding,
total transfusion requirements, and the need for surgery. However, it has not been
shown to decrease mortality in undifferentiated patients with GIB.71 Consider a 50-
mg bolus followed by 50-mg/h infusion.

Proton pump inhibitors

Proton pump inhibitors (PPIs) are frequently administered to patients with GIB but
have limited utility in patients with MGIB. PPIs have not shown a significant benefit
in terms of mortality, rebleeding, or need for surgery.72,73 Although PPIs may decrease
the presence of high-risk stigmata (active bleeding, visible vessel, overlying clot) in
peptic ulcer disease, they have little other use in the resuscitation setting.

Tranexamic acid
Tranexamic acid (TXA) acts as a competitive inhibitor and prevents the activation of
plasminogen to plasmin.74 At high concentrations, TXA also directly inhibits plasmin.
This relative decrease in active plasmin reduces the degradation of fibrin clots, fibrin-
ogen, and other plasma proteins. TXA has been widely used in several hemorrhagic
conditions and is often also included in MTPs.75 TXA is inexpensive and generally
well tolerated, with nausea or diarrhea among the commonly reported adverse ef-
fects.75 Studies on the use of TXA in GIB have had inconsistent outcomes with regard
to mortality benefit; however there was no evidence that the use of TXA in patients with
GIB increased the incidence of thromboembolic events and so it has been used for
MGIB.76 The recently published HALT-IT trial has provided more conclusive evidence
of its possible impact on mortality.77 This multicenter, randomized, placebo-controlled
trial demonstrated no difference in five-day mortality due to bleeding in those patients
receiving TXA versus those receiving placebo.77 Additionally, there was a significant
increase in venous thromboembolic events in the TXA treatment group.77 Until further
strong evidence is produced, administering TXA to all-comers with MGIB is not rec-
ommended. However, if TEG/ROTEM is available and demonstrates excessive fibri-
nolysis, then TXA may be indicated.

Source Control
Early consultation with an endoscopist, interventional radiologist, and acute care sur-
geon is paramount to the care of patients with MGIB after initiating the resuscitation
and stabilization.
884 D’Amore & Swaminathan

Upper gastrointestinal source

MGIB is more commonly a result of an upper GI source. Many upper GI sources of
bleeding, such as varices and ulcers, are amenable to endoscopic interventions
such as injection (of a vasoconstricting or sclerosing agent), thermal (through electro-
coagulation), or mechanical therapies (endoscopic clipping or band ligation).78 Endos-
copy within the first 24 hours of hemorrhage has been shown to decrease resource
use and transfusion requirements.79 A recent cohort study showed that patients
who presented with hemodynamic instability from bleeding peptic ulcers experienced
lower in-hospital mortality if they received endoscopic intervention within the first
24 hours.80 With regard to variceal bleeding, the combination of octreotide and endos-
copy was associated with significantly improved initial and 5-day hemostasis rates,
although mortality was not affected.81 The endoscopist ultimately decides on the
timing of endoscopy. Surgical involvement for resection may be necessary when
endoscopic therapies fail to control hemorrhage.
Lower gastrointestinal source
Much of acute massive LGIB is self-limiting with proper medical resuscitation. After
initial stabilization, many patients require computed tomography angiography in or-
der to localize the source of bleeding. Pending this information, interventional radi-
ologists (IRs) should be consulted for possible embolization of amenable vessels.
General surgeons should be consulted as well. In the case of massive LGIB that
is either not amenable to IR intervention or that is continuing in the face of appro-
priate resuscitation, surgical resection may be indicated. With regard to direct visu-
alization, the evidence supporting early colonoscopy for LGIB is mixed and
generally of lower quality; however, a colonoscopy in the first 24 hours is recom-
mended in patients with high-risk features (eg, hemodynamic compromise, older
age, syncope, bright red rectal bleeding) who can undergo appropriate bowel
preparation.82,83 Patients with hemodynamic instability and hematochezia should
prompt suspicion of an upper GI source and thus esophagogastroduodenoscopy
would be warranted.

SUMMARY

MGIB is a condition with high morbidity and mortality that must be recognized
promptly and resuscitated aggressively. The cornerstones of management include
the establishment of large-bore IV access, early transfusion of blood products,
reversal of coagulopathies, as well as the consideration of technology such as TEG/
ROTEM when available. Definitive airway management and early involvement of con-
sultants are also essential to a successful resuscitation.

DISCLOSURE

Dr A. Swaminathan is a deputy editor for EM:RAP and the managing editor of EM Ab-
stracts. Dr K. D’Amore has nothing to disclose.

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