0413 Massive Upper GI Bleeding.pdf

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UNDERSTANDING AND CARING FOR

CRITICAL ILLNESS IN EMERGENCY MEDICINE

EM Critical Care

Volume 3, Number 2

Authors

Ryan G. K. Mihata, MD, MPH, FACEPAssistant Professor of Emergency Medicine/Critical Care,

Wright State University, Boonshoft School of Medicine,

Dayton, OH

John-Adam Bonk, MDDepartment of Emergency Medicine, Wright State University,Boonshoft School of Medicine, Dayton, OH

Meaghan P. Keville, MDDepartment of Emergency Medicine, Wright State University,Boonshoft School of Medicine, Dayton, OH

Peer Reviewers

Michelle Lin, MDAssociate Professor of Clinical Emergency Medicine,University of California San Francisco; San Francisco

General Hospital and Trauma Center, San Francisco, CA

John L. Westhoff, II, MD, MPH, FACEPDeputy Commander for Clinical Services, U.S. Army Public

Health Command Region-Pacic; Staff Emergency Physician,

U.S. Naval Hospital, Yokosuka, Japan

Guest Editor

Catherine A. Gogela Carlson, MDCritical Care Medicine Fellow, Departments of Critical Care

Medicine and Emergency Medicine, University of PittsburghMedical Center, Pittsburgh, PA

CME Objectives

Upon completion of this article, you should be able to:

1. Describe the differential diagnosis of massive GIbleeding.

2. Discuss the importance of the resuscitation of patients

with massive GI bleeding.

3. List the available medical and surgical therapeutic

options for patients with massive GI bleeding.

4. Apply a standardized approach to the management of

massive GI bleeding.

Prior to beginning this activity, see the back page for facultydisclosures and CME accreditation information.

Resuscitation Of ThePatient With Massive UpperGastrointestinal BleedingAbstract

Managing an unstable patient with massive gastrointestinal bleedingcan be challenging, but effective management can optimize patientoutcomes. These patients require prompt recognition of severe ill-

ness, resuscitation and stabilization, and diagnostic and treatmentmodalities directed at identication and control of the source of bleeding. Multiple consultants (including gastroenterology, generalsurgery, and interventional radiology) are often required, and earlyconsultation of these subspecialists can improve morbidity and mor-tality. Underlying comorbidities add complexity to the managementof the bleeding patient and are associated with increased mortality.Most cases of massive bleeding are due to an upper gastrointestinalsource, and these patients have a higher mortality rate than thosepresenting with lower gastrointestinal bleeding. Common sources ofupper gastrointestinal bleeding include gastric and duodenal ulcers,esophageal and gastric varices, and erosive esophagitis. Dependingon the source of the bleeding, medical and/or surgical treatment mo-

dalities may be required. Utilization of emergent upper endoscopyand other medical therapies as well as transfusion of blood productsare often necessary to ensure optimal patient outcomes. Knowledgeof the emergency procedures and medications available, as well asfamiliarity with the treatment modalities used by consultants, willhelp the emergency physician orchestrate the care necessary to en-sure patient survival.


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EMCC © 2013 2 www.ebmedicine.net • Volume 3, Number 2

searched for guidelines for the acute treatment ofsevere GI bleeding. Table 1 summarizes the currentguidelines related to GI bleeding.3-6 The literaturereview and these guidelines suggest a general con-sensus about the importance of early evaluation andresuscitation in the ED as well as early involvementof appropriate consultants in order to avoid negativeoutcomes in patients with massive GI bleeding.

Etiology And Pathophysiology

The presence of GI bleeding with evidence of hem-orrhagic shock requires prompt identication of the bleeding source. The most common etiologies ofupper GI bleeding include: duodenal ulcers (28%),gastric ulcers (26%), gastritis (13%), varices (12%),and esophagitis (8%).1 GI bleeding due to esopha-geal or gastric varices and peptic ulceration carrythe highest mortality.2 Exclusion of other bleedingsources (such as pulmonary or intranasal sources)is important. As with management of all cases of

undifferentiated hypotension, initiation of resuscita-tion based on hemodynamic decompensation shouldnot be delayed, regardless of the underlying sourceof the bleeding.

Treatment

Stabilization And Monitoring

Initial resuscitation of patients with massive GI bleed-ing involves restoration of intravascular volume inorder to achieve the relative hemodynamic stabilityrequired to proceed with diagnostic and therapeutic

interventions. An initial primary survey to evaluatethe airway, breathing, and circulation should almostalways include endotracheal intubation in order toprotect the patient’s airway in the setting of activehemorrhage and to assist in identifying the bleedingsource and facilitating these additional interventions.Early resuscitation may start with 2 large-bore pe-ripheral intravenous (IV) catheters, but resuscitationof massive hemorrhage may be aided by the use oflarger, introducer-sized central venous catheters thatcan more efciently restore lost intravascular volumeduring hemorrhagic shock.

The importance of early mobilization of special-

ists cannot be overemphasized. In patients withmassive GI bleeding, medical therapy alone isunlikely to be sufcient to achieve hemostasis. Earlymobilization of the available subspecialists expe-dites time to denitive therapy. The lack of availablesubspecialty support should prompt considerationfor transfer to a tertiary care facility that can providethis care. Depending on the underlying cause of the bleeding as well as patient comorbidities, gastroen-terology, general surgery, and interventional radiol-ogy may all play a role in the care of these patients.

Case Presentation

You receive a medic call for a 45-year-old male who called911 for massive hematemesis. The medics report that the patient is an alcoholic who has been binge drinking sincelosing his job 1 week ago. He has vomited a large amountof frank blood twice. He is hypotensive, with a MAP of 50mm Hg and a pulse of 128 beats per minute. EMS person-

nel have established a peripheral IV line and are infusingnormal saline as fast as possible; they are 5 minutes out.After you page the gastroenterologist and ask the unit sec-retary to activate your institution’s massive transfusion protocol, you consider the potential causes of massive GIbleeding, the available therapeutic options, and the inter-ventions you should undertake in the next few minutes toimprove this critically ill patient’s chance for survival…

Introduction

Providing optimal care in the emergency depart-ment (ED) for patients with massive gastrointesti-

nal (GI) bleeding requires coordination of multipleconsultants as well as knowledge of both medicaland surgical therapeutic options. For the purposesof this review, massive GI bleeding is dened as bleeding in a patient that has resulted in hemody-namic instability, with signs and symptoms consis-tent with hemorrhagic shock and evidence of eitherhematemesis or hematochezia. In order to provideinitial resuscitation in the ED (either as a bridge tocontinued resuscitation in the intensive care unitor to diagnostic/therapeutic interventions in theoperating room or interventional radiology), emer-gency physicians must be familiar with the widevariety of both diagnostic and therapeutic options aswell as the underlying pathophysiology for massiveGI hemorrhage. The majority (> 75%) of massiveGI bleeding cases are due to an upper GI source.1 Mortality rates for patients with massive GI bleedingrange from 20% to 39%.2 Treatment options dependupon the underlying cause of the bleeding, andearly intervention can mean the difference betweensurvival and death. This issue of EMCC provides anoverview of the current evidence for the treatment ofpatients with massive upper GI bleeding.

Critical Appraisal Of The Literature

A literature search of PubMed, Ovid MEDLINE® , andthe Cochrane Library was performed using the fol-lowing keywords: GI bleeding, severe GI bleeding, upperGI bleeding, and variceal bleeding treatment. The searchfocused only on literature in the English language foradult patients. More than 100 articles were reviewed,which provided the background information and basis for further literature review. Additionally, bothnational and international guidelines as well as theCochrane Database of Systematic Reviews were


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3 EMCC © 2013www.ebmedicine.net • Volume 3, Number 2

In cases of nonvariceal hemorrhage, a bolus of aPPI should be initiated and then followed by acontinuous infusion. This is thought to promoteulcer healing and decrease the rate of rebleeding.7 Additionally, in cases of variceal hemorrhage withsubsequent endoscopic intervention, patients whoare given PPIs intravenously have demonstrated lessrebleeding8 because PPIs work against stomach acidand pepsin, which are thought to destabilize plateletplugs and the hemostatic clot.9-11

Procedural Therapies

Endoscopy

Endoscopy is an important diagnostic and thera-peutic tool for upper GI hemorrhage and should be performed promptly upon patient stabilization.Endoscopy provides denitive therapy in manycases. The gastroenterologist may employ variousendoscopic techniques, including clips, banding,thermocoagulation, or sclerosant injection with orwithout epinephrine. All patients with massive GI

bleeding should be intubated to facilitate endos-copy, control the airway, reduce the risk of aspira-

Patients with massive GI bleeding require con-tinuous cardiac and pulse oximetry monitoring, withfrequent blood pressure checks. Central venous accessmay be required in the ED if the patient has poor pe-ripheral access or if more the rapid infusion of uidsor blood products is needed. Invasive monitoring,including an arterial line, will enable prompt recogni-tion and response to the rapid changes in physiologythat may occur in massive GI hemorrhage.

Initial laboratory values can help guide initialtherapy, but serial coagulation studies in the ED arenot likely to aid in decision making and may be dif-cult to interpret in patients being treated with freshfrozen plasma (FFP), cryoprecipitate, or factor concen-trate. Likewise, an initial D-dimer may offer prognos-tic information, but it should not inuence immediatemanagement in the acute setting.

Regardless of the source of upper GI bleeding,proton-pump inhibitors (PPIs) are typically recom-mended until the etiology of the bleeding can beidentied. While PPIs will not impact the immedi-

ate stabilization of a hemodynamically unstable bleeding patient, their use may improve outcomes.

Table 1. Current Guidelines For Gastrointestinal Bleeding

Organization Topic Type of Guideline Recommendations

American College of

Physicians

Management of patients

with nonvariceal upper

GI bleeding3

Consensus 1. Early evaluation, resuscitation, and risk stratication is recom-

mended.

2. Nasogastric tube placement may have diagnostic value.

3. Transfuse PRBCs to maintain hemoglobin > 7 gm/dL.

4. Correction of coagulopathy is recommended but should not delay

endoscopy.

5. Pre-endoscopic PPIs may be considered.6. Early endoscopy (within 24 h) is recommended.

7. Histamine-2 receptor antagonists are not recommended for patients

with acute bleeding due to a gastric or duodenal ulcer.

8. Somatostatin and octreotide are not routinely recommended for

patients with acute ulcerative bleeding.

Cochrane Library Pharmacologic manage-

ment of patients with GI

bleeding4,5

Systematic review 1. Somatostatin analogues do not reduce mortality in variceal GI

bleeding; however, they may reduce the need for blood transfusion

by 0.5 units.

2. PPI administration prior to endoscopy for upper GI bleeds sig-

nicantly reduces the number of patients with recurrent serious

bleeding and the need for endoscopic intervention, but they have no

effect on the need for surgery or risk of death.

Scottish Intercollegiate

Guidelines Network

Guidelines for initial treat-

ment of patients with

signicant GI bleeding6

Systematic review 1. PRBC transfusion should be considered after loss of 30% of the

circulating blood volume.

2. PPIs should not be used prior to endoscopic diagnosis in patients

presenting with an acute upper GI bleed.

3. Early endoscopic examination should be undertaken within 24 h of

initial presentation, if possible.

4. Pr ior to endoscopic diagnosis, terlipressin (vasopressin analogue)

should be given to patients suspected of variceal hemorrhage.

5. Antibiotic therapy should be initiated in patients with chronic liver

disease who present with acute upper GI bleeding.

6. Balloon tamponade should be considered as a temporizing mea-

sure to gain hemostasis in uncontrolled variceal hemorrhage.

Abbreviations: GI, gastrointestinal; PPI, proton-pump inhibitor; PRBC, packed red blood cell.


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Additional Procedural Therapies

In severe cases of massive GI bleeding, where ur-gent endoscopy is unable to provide a diagnosis ortherapy, urgent or emergent angiography can beperformed to identify the location of the hemorrhage.Angiography is indicated in patients with nonvaricealupper GI bleeding when medical management andendoscopic therapy have failed to control the bleed-ing. Angiographic intervention should be consideredas an alternative to surgery in patients who are highrisk for more invasive surgical intervention.13 Angiog-raphy can detect bleeding at rates of at least 0.5 mL/min with 100% specicity and variable sensitivity(based on the rate).14 During angiography, lesionscan be treated by use of vasopressin or transcatheterembolization.

Another option for identifying the source of bleeding is radionuclide imaging, which can de-tect bleeding occurring at slower rates than can bedetected by angiography. The primary purpose ofthese studies is to localize the source of the bleed-

ing and to facilitate surgical intervention. An emer-gency surgical consult should be sought in patientswith massive hemorrhage who cannot be stabilizedin the ED, who have contraindications to endos-copy, or who have peritoneal signs on examination(which can occur from a ruptured peptic ulcer).While surgery is typically only considered as a lastresort after medical, endoscopic, and interventionalradiology approaches have been exhausted or arecontraindicated, not all types of bleeding (such asvariceal bleeding) are amenable to surgical interven-tion. Nonetheless, early involvement of surgery andgastroenterology services can facilitate a cooperative

treatment approach and may make surgical inter-vention, if necessary, safer and less emergent.

Pharmacologic Therapies

There are multiple proposed pharmacologic treat-ments for the management of acute upper GI bleed-ing. Understanding the mechanism of action of these

tion, and improve patient safety during treatment.Airway management in severe upper GI bleeds can be technically challenging due to poor visualization.A topic within itself that cannot be covered in this is-sue, extra personnel and airway adjuncts (including2 suction catheters) is advisable for airway manage-ment of this population.

Balloon Tamponade

Balloon tamponade may be required if endoscopy iseither not available or not successful in achieving he-mostasis. Insertion of a balloon tamponade device isa rare but potentially life-saving procedure. It can beused as a temporary rescue device by providers whopractice in a setting where specialty consultation isnot readily available. Use of a balloon-tamponadedevice is associated with a high risk of rebleedingupon balloon deation. Its most lethal complicationis esophageal necrosis and rupture.

There are several different types of commerciallyavailable devices for balloon tamponade. The 3 most

common include the Sengstaken-Blakemore, theMinnesota tube, and the Linton-Nachlas tube.12 (SeeFigure 1.) Each of these tubes varies slightly basedon the number of lumens and balloons. Providersshould be familiar with the specic device used attheir institution. The following is a general guide fortheir use:1. Prior to insertion, secure the airway.2. After applying a lubricant to the tube, insert the

tube through the mouth or nostril to a depth ofat least 50 cm, depending upon the height of thepatient.

3. After evaluation by air injection, conrm place-

ment in the stomach with radiography. (The bal-loon should NOT be inated until its location isveried radiographically so as to avoid potentialcomplications associated with malpositioning ofthe tube.)

4. Inate the gastric balloon (approximately 400-500 mL of air), and clamp the inlet.

5. Retract the tube until resistance is felt (the bal-loon at the gastroesophageal junction). Tensionmust be maintained on the tube in order toproduce the tamponade effect.

6. If gastric balloon tension is not sufcient to stopthe hemorrhage, inate the esophageal balloon

(25-30 mm Hg). This pressure must be checkedfrequently, as overination can lead to esopha-geal necrosis.

It is important to remember that these are tem-porizing devices intended for short-term use and arenot denitive therapy. In some situations, the patientmay need to be transferred to another facility fordenitive care.

Figure 1. Minnesota Tube For BalloonTamponade

Note both the gastric and esophageal balloons. Types of tubes vary

slightly. Be familiar with the type available in your institution.

Image courtesy of Ryan G. K. Mihata, MD


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bleeding from esophageal varices.4 Some data sug-gest that the combination of these medications withupper endoscopy may be benecial.

Given their relatively low-risk side-effect pro-les, the use of these medications can be consideredin patients with acute hemorrhage that is possiblycaused by variceal bleeding.16

Vasopressin

A third class of pharmacologic agents, vasopressinand its analogues, can reduce portal hypertension bycausing systemic and splanchnic vasoconstriction.

Much like somatostatin, the use of vasopressinin the management of upper GI bleeding is contro-versial. The risks (eg, myocardial infarction, arrhyth-mias, mesenteric ischemia, peripheral soft tissue ne-crosis, cardiac arrest) of using this medical therapyare similar to—but usually less severe than—thoseseen with the use of other vasopressor medications.In patients with variceal bleeding, adding nitro-glycerin to vasopressin therapy appears to decrease

systemic complications from the use of vasopressinalone while not affecting the efcacy of the vaso-pressin.17,18 In patients with massive GI bleeding, therisk of systemic vasoconstriction and the potentialfor end-organ ischemia must be weighed againstthe potential benet of splanchnic vasoconstriction,which can help to achieve hemostasis in the actively bleeding patient.

In spite of the potential deleterious effects ofvasopressin, use of vasopressin (or vasopressin plusnitroglycerin) in a patient in extremis due to massiveGI bleeding may be justied.

Blood Product TransfusionThe goal of blood product transfusion for acute bleeding is to replace the blood cells and coagulationfactors that are being lost. Whole blood is a complexheterogeneous solution that serves 3 basic func-tions: (1) to maintain intravascular volume, (2) toprovide oxygen-carrying capacity, and (3) to providethe coagulation factors that are required to reversecoagulopathy and to assist in achieving (and main-taining) hemostasis. The ability to achieve hemostasiscan be complicated by the use of anticoagulation orantiplatelet agents. Because there are inherent risks

involved with transfusing blood products, the risksmust be considered along with the potential benetsfor each individual patient. Goal #1: Provide Intravascular Volume Resuscitation

Prompt volume resuscitation with IV crystalloiduids should be initiated in a bleeding, hypotensivepatient in order to achieve a perfusing mean arterialpressure (MAP) until blood products are available.Given that it lacks oxygen-carrying capacity anddoes not replenish clotting factors, the role of crystal-loid uid for volume resuscitation should ideally

medications can facilitate a deeper understanding ofthe rationale for the existing guidelines for their use.

Proton Pump Inhibitors

PPIs, which include omeprazole, pantoprazole, andesomeprazole, are considered to be a mainstay ofearly therapy for acute GI bleeding in the ED. PPIssuppress gastric acid stimulation by inhibiting the pa-rietal cell H+/K+ ATPase (adenosine triphosphatase)pump. One potential benet of the early use of PPIsmay be the reduction of hemorrhage during endos-copy.3,5 Additionally, PPIs may create a more optimalenvironment for the stabilization of blood clots byneutralizing the intraluminal gastric acid that wouldotherwise serve to promote continued bleeding.9

There has been concern about the potentialincreased risk of thrombotic stroke or myocardialinfarction with the addition of PPIs to long-termclopidogrel therapy. Based on cohort studies, a 2009United States Food and Drug Administration warn-ing cited a 50% increased risk of these complications

when PPIs and clopidogrel were taken concurrently.15

However, current data are inconclusive and suggestthat these complications are typically associated withlong-term use of PPIs and clopidogrel. These riskshave not yet been described in the acute, short-termuse of these medications during the stabilization ofpatients with massive GI bleeding. At this time, guidelines continue to encourage theuse of PPIs (either before or immediately followingupper endoscopy) in patients with undifferentiatedupper GI bleeding.3 However, there has not yet beena study showing a statistical improvement in the rateof rebleeding, the need for surgical intervention, or

mortality from their use. Nonetheless, their cost effec-tiveness and excellent safety prole make the benetof giving these agents greater than the potential risks,particularly in high-risk patient populations.

Somatostatin

Somatostatin and its analogues (including octreo-tide and vapreotide) represent another class ofpharmacologic agents that may be used early in themanagement of acute GI bleeding due to a suspect-ed variceal source. Somatostatin (also known as“growth-hormone-inhibiting hormone”) suppressesthe release of GI hormones such as gastrin, chole-

cystokinin, motilin, and secretin. The secondaryeffects of blocking the release of these hormonesinclude a reduction of portal venous blood owdue to splanchnic vasoconstriction and subsequentdecreased GI bleeding.

To date, there are minimal data regarding theuse of somatostatin or its analogues for nonvaricealupper GI bleeding. The data on their use in severevariceal bleeding are also mixed. A Cochrane reviewfound no signicant change in mortality, the rebleed-ing rate, or the number of units of blood transfusedwith the use of somatostatin in patients with acute


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myocardial oxygen delivery.22 However, for patientswith suspected variceal bleeding (even with con-comitant coronary artery disease), consider keepingthe hemoglobin goal to between 7 and 8 gm/dL untilhemostasis is achieved, as the additional blood vol-ume required to achieve this higher target may leadto increased portal pressure and worsening bleedingor rebleeding.

When there is a need for emergent transfusionof PRBCs for acute blood loss anemia with signs ofhypovolemic shock, O-negative PRBCs (or O-positivePRBCs in women past childbearing age and in men)can be given until type-specic crossmatched blood isavailable. For patients requiring massive transfusionof blood products, it is important to remember that thetransfusion will have metabolic complications such asdepletion of intravascular cations due to chelation bythe sodium citrate used to anticoagulate blood compo-nents during storage. Citrate is primarily metabolized by the liver, so in cirrhotic patients receiving massivetransfusion, this effect may be more profound. For

these patients, consider giving calcium replacement(calcium gluconate 1-2 g IV or calcium chloride 0.5-1g IV per 500 mL of transfused blood). Magnesium canalso be affected, and low levels have unwanted sideeffects and should be repleted as necessary, keepingin mind that overly rapid infusion of magnesium canexacerbate hypotension.

Goal #3: Reverse Coagulopathy

Treatment of coagulopathy can be tailored to itslikely or known etiology. Coagulopathy may arisedue to an underlying chronic disorder, but it mayalso be caused by metabolic acidosis due to tissue

hypoxemia in the setting of acute hypotension.To reverse coagulopathy, consider an initial

transfusion of 10 mL/kg of FFP. Prothrombintime (PT)/international normalized ratio (INR),partial thromboplastin time (PTT), platelet count,and brinogen levels can be used to guide patientmanagement. While there are no specic guidelines,keeping the platelet count > 50,000/mm3 , PTT< 60 seconds, and INR < 1.8 is common practice andis recommended by the authors. Because D-dimerlevels have been shown to be inversely related toprognosis in upper GI bleeding, a D-dimer may bedrawn as a prognostic marker, but it has no role in

guiding intervention.23 If available, the thromboelas-tography (TEG) test can evaluate platelet functionand coagulation and may be more efcient to directthe type of transfusion products necessary.

The role of recombinant activated factor VII(rFVIIa) is continuing to evolve. While it may beuseful in certain situations (eg, when a patient ison a direct thrombin inhibitor), it is expensive, itcarries the risk of thromboembolic complications,and studies of its use have had conicting results. Aprospective randomized trial of 245 patients foundno benet with rFVIIa over standard therapy for

be restricted to this early phase of resuscitation in a bleeding patient. In cirrhotic patients with suspectedvariceal hemorrhage, excessive crystalloid resuscita-tion may be particularly harmful due to their suscep-tibility to extravascular uid shifts in the setting ofunderlying low intravascular oncotic pressure.

In patients with massive GI bleeding (especiallythose with hemoglobin < 8.0 gm/dL, coagulopathy,or persistent hypotension despite volume infusion),the use of blood products (such as PRBCs) is im-portant in order to restore hemodynamic stabilityand to achieve hemostasis. However, transfusion ofPRBCs alone is not sufcient because they do notcontain the required coagulation factors. For thisreason, PRBCs should be accompanied by FFP and/or platelets. The military literature on traumatic bloodloss recommends a PRBC:FFP:platelet ratio approach-ing 1:1:1.19,20 Other sources disagree on the exactratio, citing a lack of a specic survival benet to ahigher PRBC to FFP ratio.21 Many large centers havemassive transfusion protocols that allow the rapid

release of blood products in varying ratios. While thesurvival benet remains unclear, most protocols havePRBC:FFP:platelet ratios near 1:1:1. Goal #2: Optimize Oxygen-Carrying Capacity

The goal of improving oxygen-carrying capacity bytransfusing PRBCs is to ensure sufcient oxygendelivery to the tissues in order to prevent end-organ ischemia and secondary dysfunction. Clinicalsigns and symptoms of decreased oxygen deliverycan include:• Decreased level of consciousness• Evidence of cardiac ischemia (as shown by elec-

trocardiographic changes or troponin elevation)• Increasing serum lactate• Decreased central venous oxygen saturation

(ScvO2)

The International Consensus guidelines recom-mend maintenance of hemoglobin levels between 7and 8 gm/dL.3 However, there are no randomizedcontrolled trials to suggest an exact hemoglobin goalfor transfusion. Target hemoglobin levels should beindividualized for each patient and should be basedupon the suspected etiology of the bleed (ie, varicealvs nonvariceal hemorrhage) as well as patient comor-

bidities. In the setting of ongoing massive bleeding,the recommended hemoglobin level of 7 to 8 gm/dLshould not be considered to be an endpoint of resus-citation. Instead, a MAP of > 60 mm Hg and evidenceof adequate end-organ perfusion should be the target.

Though the International Consensus guidelinessuggest maintenance of hemoglobin between 7 and8 gm/dL, patients with certain comorbidities mayrequire greater hemoglobin goals. For instance,evidence suggests that patients with suspected activeischemic coronary artery disease may benet froma target hemoglobin closer to 10 gm/dL to support


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rate of 1 mg/min is necessary to achieve a sustainedreversal of the INR; however, it is insufcient whengiven as a single agent, as it has an onset of action of2 to 6 hours and requires up to 24 hours to achieve acomplete response.27 For this reason, FFP must also be administered. Although controversial, rFVIIa can be consid-ered for reversal of effects of warfarin. However,it is expensive, it has minimal proven therapeutic benet for warfarin reversal, it is not FDA ap-proved for this use, and its use may cause thrombotic complications.24-26

Dabigatran: Dabigatran (Pradaxa®) is a directthrombin inhibitor. To quantify the degree ofdabigatran coagulopathy, obtain a PTT andthrombin time (if rapidly available).28 PT/INR is notuseful in assessing dabigatran coagulopathy. ThePTT is only useful to qualitatively assess the degreeof coagulopathy because it lacks sufcient sensitivitywith therapeutic dabigatran levels. A very high PTT

value should be conrmed by another method (eg,thrombin time),28 although this may be impracticalin the emergent setting. Like other anticoagulantmedications, even therapeutic levels may requirereversal in the setting of active bleeding. At this time, an evidence-based reversal strategyfor dabigatran is not available. Many institutionshave a pathway for bleeding patients who are ondabigatran that may inform local practice patterns.Management strategies may range from expectantmanagement to aggressive use of blood products,including FFP and even hemodialysis.

Rivaroxaban: Rivaroxaban (Xarelto®) is a factorXa inhibitor. Administer PCCs for reversal ofrivaroxaban; if PCCs are not available, consideradministration of FFP.29

nonvariceal upper GI bleeding.24 However, a smalluncontrolled study suggested that, in patients withliver disease and an increased INR refractory to FFPtherapy, rFVIIa was effective in stopping bleedingand normalizing the INR.25 Similarly, a study of pa-tients with moderate to severe cirrhosis showed thatadministration of rFVIIa in addition to endoscopichemostatic strategies decreased rebleeding rates.26 Due to the conicting nature of the literature, use ofrFVIIa in patients with massive GI bleeding is notroutinely recommended.

It should be noted that, although the transfu-sion of blood products is indicated in patients withmassive GI bleeding, it is associated with somerisks. The lethal triad of hypothermia, coagulopa-thy, and acidosis must be addressed in order toprevent clinical deterioration. (See Figure 2.) Usewarmed uids, warmed blankets, and other pas-sive external rewarming measures as needed tomaintain normothermia.

Reversal Of Medically Induced Coagulopathy Warfarin: Warfarin (Coumadin® , Jantoven®)inhibits vitamin K-dependent coagulation factorsynthesis. Prothrombin complex concentrates(PCCs) should be the rst-line treatment in apatient who is on warfarin. PCCs do not requirecrossmatch and act more quickly than FFP alone;however, because PCCs in the United States donot contain signicant amounts of factor VII,FFP must also be administered. Dosages areindividually calculated based on weight anddesired factor IX level; 1 unit/kg will increase thefactor IX level approximately 1%.

If PCCs are not available, coagulopathy can bereversed by discontinuing warfarin therapy andadministering vitamin K. Vitamin K at a dose of 5to 10 mg diluted in D5W or D5 saline infused at a

Figure 2. Coagulopathy Chart

Reprinted from: Cherkas D. Traumatic Hemorrhagic Shock: Advances In Fluid Management. Emerg Med Pract. 2011;13(11):1-20.

Copyright © 2011 EB Medicine.

Hemorrhage Tissue damageHypothermia

Fluid replacement ShockAcidosis

Dilution Hypoperfusion

Consumption of platelets and clotting

factorsInammation Hyperbrinolysis

Coagulopathy


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This clinical pathway is intended to supplement, rather than substitute for, professional judgment and may be changed depending upon a patient’s individualneeds. Failure to comply with this pathway does not represent a breach of the standard of care.

Copyright © 2013 EB Medicine. 1-800-249-5770. No part of this publication may be reproduced in any format without written consent of EB Medicine.

Class I

• Always acceptable, safe

• Denitely useful

• Proven in both efcacy andeffectiveness

Level of Evidence:

• One or more large prospective

studies are present (with rare

exceptions)

• High-quality meta-analyses

• Study results consistently posi-

tive and compelling

Class II

• Safe, acceptable

• Probably useful

Level of Evidence:

• Generally higher levels of

evidence

• Non-randomized or retrospec-

tive studies: historic, cohort, or

case control studies

• Less robust randomized con-

trolled trials

• Results consistently positive

Class III

• May be acceptable

• Possibly useful

• Considered optional or alterna-tive treatments

Level of Evidence:

• Generally lower or intermediate

levels of evidence

• Case series, animal studies,

consensus panels

• Occasionally positive results

Indeterminate

• Continuing area of research

• No recommendations until

further research

Level of Evidence:

• Evidence not available

• Higher studies in progress

• Results inconsistent, contradic-

tory

• Results not compelling

Signicantly modied from: The

Emergency Cardiovascular Care

Committees of the American

Heart Association and represen-

tatives from the resuscitation

councils of ILCOR: How to De-

velop Evidence-Based Guidelines

for Emergency Cardiac Care:Quality of Evidence and Classes

of Recommendations; also:

Anonymous. Guidelines for car-

diopulmonary resuscitation and

emergency cardiac care. Emer-

gency Cardiac Care Committee

and Subcommittees, American

Heart Association. Part IX. Ensur-

ing effectiveness of community-

wide emergency cardiac care.

JAMA. 1992;268(16):2289-2295.

Class Of Evidence Definitions

Each action in the clinical pathways section of EM Critical Care receives a score based on the following denitions.

Clinical Pathway For The Initial Management OfPatients With Massive Upper Gastrointestinal Bleeding

Initial actions: insert 2 large-bore IVs (Class I); establish monitoring

(Class I); provide a PPI bolus & drip (Class I); consider insertion of

a nasogastric tube (Class II); provide a crystalloid bolus (Class II);

and keep the patient warm (Class II)

Are there signs of altered mental status and/or

active hematemesis?

Intubate (Class II)

Transfuse PRBCs, FFP, and platelets (Class II)

Coagulopathy (INR > 1.7

with active bleeding)

Administer:

Octreotide 50-mcg bolus and 50-mcg/h infusion (Class II)

and

Ciprooxacin 400 mg bid (Class I) or ceftriaxone 1g IV qd (Class II)

Anemia

Are there signs or symptoms of shock?

Is there a history of esophageal varices or signs of cirrhosis?

• Perform labs: CBC with differential, BMP, LFTs, PT/PTT, ECG, CXR

• Consider: D-dimer, lactate, ABG

• If hemoglobin < 7.0 gm/dL: transfuse PRBCs (Class II)

• If hemoglobin > 8.0 gm/dL (or with bleeding varices): do not

transfuse PRBCs (Class II)

• Transfuse 2 units FFP (Class II)

• If there is severe liver disease with coagulopathy and refractory

bleeding, consider PCCs or rFVIIa (Class II)

• If the patient is taking warfarin, add vitamin K 10 mg slow IV

push (Class II)

YES

YES

YES

NO

NO

NO

Abbreviations: ABG, arterial blood gas; bid, two times a day; BMP, basic metabolic panel; CBC, complete blood count; CXR, chest x-ray; ECG, elec-

trocardiogram; FFP, fresh frozen plasma; INR, international normalized ratio; IV, intravenous; LFT, liver function test; PCCs, prothrombin complex

concentrates; PPI, proton-pump inhibitor; PRBCs, packed red blood cells; PT, prothrombin time; PTT, partial thromboplastin time; qd, 1 time a day;

rFVIIa, recombinant activated factor VII.


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The foundation of the resuscitation includesinitial management of the airway, breathing, andcirculation. Volume resuscitation requires crystal-loid uids and transfusion of blood products. Earlyconsultation with gastroenterology, interventionalradiology, and general surgery will improve thepatient’s time to denitive care. Endoscopy should beperformed promptly upon stabilization. In additionto volume resuscitation, medical therapies such asPPIs, somatostatin and its analogues, and vasopressinshould be considered either empirically based uponhemodynamic stability of the patient or directed atthe underlying etiology of the bleeding, if known.Surgical intervention may ultimately be necessary ifless-invasive treatments fail or are contraindicated.Depending on the clinical scenario, balloon tampon-ade may be needed as a temporizing and life-sustain-ing measure until the resources required for denitivetherapy become available.

Case Conclusion

The critically ill 45-year-old male patient arrived to yourresuscitation bay with vital signs that were unchanged from the prehospital report. You made a decision to intubatethe patient in order to protect his airway and to facilitateanticipated upper endoscopy. Shortly after intubation,the patient continued to have frank blood coming from hisoropharynx. The nurses established a second large-bore peripheral IV, and emergency release blood was given. Eachlarge-bore peripheral IV had blood infusing, and the initialhemoglobin came back at 5.8 gm/dL. You ordered 4 moreunits of type-specic blood as well as 2 units of FFP and 2single-donor units of platelets, and you subsequently placed

an introducer catheter to expedite large volume infusion ofblood products via a level 1 infuser, which warmed the in-

fusing uid. The gastroenterologist came and performed anendoscopy in the ED, during which he attempted to bandthe large esophageal varices. He was uncertain whether ornot he was able to obtain complete hemostasis during the procedure. The patient initially improved with your re-suscitation but continued to have a MAP in the 50s and a pulse rate in the 120s. You administered an octreotide bolusand infusion as well as a PPI infusion. In consultation with your intensivist team, you started a vasopressin drip witha goal MAP of > 60 mm Hg. This improved not only thevariceal bleeding but also the patient’s hemodynamic stabil-ity. In total, the patient required 4 more units of PRBCsand 2 more units of FFP. He was admitted to the ICU,where the gastroenterologist repeated an endoscopy and found less blood but 2 more bleeding varices, which weresubsequently banded. The patient developed renal failureand liver failure (acute on chronic) with ischemic hepatitissecondary to hemorrhagic shock. He had a prolonged coursein the ICU but eventually improved and was ultimatelydischarged from the hospital.

Unfractionated Heparin: Unfractionated heparin actsat multiple sites in the clotting cascade and serves asa catalyst for clotting factors. Administer protaminesulfate to reverse heparin.

Clopidogrel: Clopidogrel (Plavix®) is a nonreversibleplatelet inhibitor. Empiric transfusion of plateletscan be considered for patients on clopidogrel orother platelet inhibitors (such as aspirin), althoughno randomized controlled trials have demonstrateda favorable impact with this approach.

Special Circumstances

When treating a patient who refuses blood basedon religious beliefs (eg, Jehovah’s Witnesses), itis important to ask the patient or legal guardianwhether they are willing to receive blood prod-ucts. Even though the patient may be a Jehovah’sWitness, it is important to carefully establish anddocument the patient’s current medical wishes. In a

small case study, investigators found a portion of a Jehovah’s Witness congregation who would accept blood transfusions because they disagreed with theofcial doctrine.30 Further, The Watchtower, a legalorganization of the Jehovah’s Witnesses, asserts withrespect to blood transfusion: “Ultimately, you (thepatient or the parent) must decide. Because your (oryour child’s) body, life, ethics, and relationship withGod are involved.”31 Regardless of the patient’s orpower of attorney’s decision, carefully documentconversations about risk and benet as well as thesubsequent management based on that decision.

Disposition

Most patients who present to the ED with massiveGI bleeding will ultimately require admission to theintensive care unit, although this will depend on thesuccess of early intervention and the clinical stabilityof the patient. Consideration should be made earlyfor involvement of subspecialists. Facilities withoutgastroenterology, general surgery, or interventionalradiology backup should have a rapid interfacilitytransfer protocol in place to expedite patient transferto a facility capable of providing the denitive man-

agement that will be needed after the initial resusci-tation and stabilization.

Summary

The unstable patient with massive upper GI bleed-ing is a high-risk case for the emergency physi-cian, requiring the coordination of resources andconsideration of various treatment modalities.Initial resuscitation efforts should occur concomi-tantly, with diagnostic measures aimed at ndingthe etiology of the bleed.


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Accessed March 1, 2013. (Practice management guideline)7. Chan WH, Khin LW, Chung YF, et al. Randomized controlled

trial of standard versus high-dose intravenous omeprazoleafter endoscopic therapy in high-risk patients with acutepeptic ulcer bleeding. Br J Surg. 2011;98(5):640-644. (Prospec-tive randomized; 122 patients)

8.* Hidaka H, Nakazawa T, Wang G, et al. Long-term admin-istration of PPI reduces treatment failures after esophagealvariceal band ligation: a randomized, controlled trial. JGastroenterol. 2012;47(2):118-126. (Prospective randomized;43 patients)

9. Green FW Jr, Kaplan MM, Curtis LE, et al. Effect of acid andpepsin on blood coagulation and platelet aggregation. A pos-sible contributor prolonged gastroduodenal mucosal hemor-rhage. Gastroenterology. 1978;74(1):38-43. (In vitro study)

10. Berstad A. Does profound acid inhibition improve hae-mostasis in peptic ulcer bleeding? Scand J Gastroenterol.1997;32(4):396–398. (Review article)

11. Vreeburg EM, Levi M, Rauws EA, et al. Enhanced mucosalbrinolytic activity in gastroduodenal ulcer haemorrhageand the benecial effect of acid suppression. Aliment Pharma-col Ther. 2001;15(5):639–646.(Prospective observational; 29patients)

12. Borquez E, Swadron S, Winter M, et al. The unstable patientwith gastrointestinal hemorrhage. In: Emergency DepartmentResuscitation of the Critically Ill. American College of Emer-gency Physicians (Ed), Dallas 2011. (Book chapter)

13. Millward SF. ACR Appropriateness Criteria on treatment ofacute nonvariceal gastrointestinal tract bleeding. J Am CollRadiol. 2008;5(4):550-554. (Consensus statement)

14. Fiorito JJ, Brandt LJ, Kozicky O, et al. The diagnostic yieldof superior mesenteric angiography: correlation with thepattern of gastrointestinal bleeding. Am J Gastroenterol.1989;84(8):878-881. (Retrospective; 58 patients)

15. FDA. Public health advisory: updated safety informationabout a drug interaction between clopidogrel bisulfate (mar-keted as Plavix) and omeprazole (marketed as Prilosec andPrilosec OTC). Available at: http://www.fda.gov/Drugs/DrugSafety/PostmarketDrugSafetyInformationforPatient-sandProviders/DrugSafetyInformationforHeathcareProfes-sionals/PublicHealthAdvisories/ucm190825.htm. AccessedMarch 1, 2013. (FDA public health advisory)

16. Corley DA, Cello JP, Adkisson W, et el. Octreotide for acute

esophageal variceal bleeding: a meta-analysis. Gastroenterol-ogy. 2001;120(4):946-954. (Meta-analysis; 475 patients)

17. Tsai YT, Lay CS, Lai KH, et al. Controlled trial of vasopressinplus nitroglycerin vs. vasopressin alone in the treatment of

bleeding esophageal varices. Hepatology. 1986;6(3):406-409.(Prospective randomized controlled trial; 39 patients)

18. Gimson AE, Westaby D, Hegarty J, et al. A randomized trialof vasopressin and vasopressin plus nitroglycerin in the con-trol of acute variceal hemorrhage. Hepatology. 1986;6(3):410-413. (Prospective randomized trial; 72 bleeding episodes in57 patients)

19. Borgman MA, Spinella PC, Perkins JG, et al. The ratio of blood products transfused affects mortality in patientsreceiving massive transfusions at a combat support hospital.

J Trauma. 2007;63(4):805-813. (Retrospective; 246 patients)20. Perkins JG, Cap AP, Andrew CP, et al. An evaluation of the

impact of apheresis platelets used in the setting of massivelytransfused trauma patients. J Trauma. 2009;66(4 Suppl):S77-S84. (Retrospective; 694 patients)

21. Scalea TM, Bochicchio KM, Lumpkins K, et al. Early aggres-sive use of fresh frozen plasma does not improve outcome incritically injured trauma patients. Ann Surg. 2008;248(4):578-584. (Prospective; 806 patients)

22. Hébert PC, Yetisir E, Transfusion Requirements in Criti-cal Care Investigators for the Canadian Critical Care TrialsGroup, et al. Is a low transfusion threshold safe in criticallyill patients with cardiovascular diseases? Crit Care Med.2001;29(2):227-234. (Prospective randomized; 357 patients)

23. Gutiérrez A, Sánchez-Payá J, Marco P, et al. Prognostic valueof brinolytic tests for hospital outcome in patients withacute upper gastrointestinal hemorrhage. J Clin Gastroenterol.

Must-Do Markers Of Quality Care

• Control the airway by endotracheal intubationprior to endoscopy.

• Establish central venous access after inserting2 large-bore peripheral IVs and utilizing an in-troducer to facilitate high-volume infusions andcentral venous pressure monitoring. Consider

the internal jugular vein as the location for cen-tral line placement in coagulopathic patients dueto vascular compressibility. Line placement withultrasound guidance is the standard of care.

• Initiate volume resuscitation with crystalloid u-ids and O-negative blood (if available). Switchto type-specic crossmatched blood as soon as it becomes available.

• Consider transfusion of other blood products orinfusions of medications based on the suspectedetiology of the bleed and the patient’s comorbidities.

• Aggressively treat hypothermia and acidosis in

order to facilitate correction of coagulopathy.

References

Evidence-based medicine requires a critical ap-praisal of the literature based upon study methodol-ogy and number of subjects. Not all references areequally robust. The ndings of a large, prospective,randomized, and blinded trial should carry moreweight than a case report.

To help the reader judge the strength of eachreference, pertinent information about the study,such as the type of study and the number of patientsin the study, will be included in bold type followingthe reference, where available. In addition, the mostinformative references cited in this paper, as deter-mined by the authors, will be noted by an asterisk (*)next to the number of the reference.

1. Peura DA, Lanza FL, Gostout CJ, et al. The American Collegeof Gastroenterology Bleeding Registry: preliminary ndings.Am J Gastroenterol. 1997;92(6):924-928. (Retrospective survey;1235 respondents)

2.* Afessa B. Triage of patients with acute gastrointestinal bleed-ing for intensive care unit admission based on risk factorsfor poor outcome. J Clin Gastroenterol. 2000;30(3):281-285.(Prospective; 411 patients)

3.* Barkun AN, Bardou M, Kuipers EJ, et al. Internationalconsensus recommendations on the management of patientswith nonvariceal upper gastrointestinal bleeding. Ann Intern

Med. 2010;152(2):101-113. (Multidisciplinary consensusgroup; 34 experts from 15 countries)

4.* Gotzsche PC, Hrobjartsson A. Somatostatin analogues foracute bleeding esophageal varices. Cochrane Database SystRev. 2008;(3):CD000193. (Systematic literature review)

5. Sreedharan A, Martin J, Leontiadis GI, et al. Proton pumpinhibitor treatment initiated prior to endoscopic diagnosis inupper gastrointestinal bleeding. Cochrane Database Syst Rev.2010;(7):CD005415. (Systematic literature review)

6.* Scottish Intercollegiate Guidelines Network (SIGN). Man-agement of acute upper and lower gastrointestinal bleeding.Available at: http://guideline.gov/content.aspx?id=13167.


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1. The most common cause of massive upper GIbleeding is:

a. Esophageal varices b. Diverticula c. Arteriovenous malformations d. Gastritis e. Gastric and duodenal ulcers

2. In regard to the stabilization and monitoringof patients with massive upper GI bleeding,which of the following is TRUE?

a. PPIs are not recommended. b. Initial and serial coagulation studies should

be used to guide decision making.c. Continuous cardiac and pulse oximetry

monitoring are required.d. Consultation with subspecialists should

be delayed until after stabilization andresuscitation.

3. In regard to the use of angiography in patients

with massive upper GI bleeding, which of thefollowing is TRUE? a. Angiography is highly specic for detection

of bleeding at rates of at least 0.5 mL/min. b. Angiography can detect bleeding at slower

rates than can be detected by radionuclideimaging.

c. Angiography has the disadvantage of beingdiagnostic but not therapeutic.

d. Angiography is contraindicated in patientswith nonvariceal upper GI bleeding.

4. In regard to blood product transfusion for pa-

tients with massive upper GI bleeding, whichof the following is TRUE?a. A hemoglobin level of 7 to 8 gm/dL should

be considered the endpoint of resuscitation. b. The recommended PRBC:FFP:platelet

ratio is 1:2:1.c. Use of crystalloids should ideally be

restricted to the initial phase of resuscitation.d. Calcium gluconate should be administered

to all patients receiving PRBCs.

2001;32(4):315-318. (Prospective; 84 patients)24. Bosch J, Thabut D, European Study Group on rFVIIa in UGI

Haemorrhage, et al. Recombinant factor VIIa for upper gas-trointestinal bleeding in patients with cirrhosis: a random-ized, double-blind trial. Gastroenterology.2004;127(4):1123-1130. (Prospective randomized trial; 245 patients)

25. Ejlersen E, Melsen T, Ingerslev J, et al. Recombinant activatedfactor VII (rFVIIa) acutely normalizes prothrombin time inpatients with cirrhosis during bleeding from oesophagealvarices. Scand J Gastroenterol. 2001;36(10):1081-1085.(Pro-spective observational; 10 patients)

26.* Thabut D, de Franchis R, Bendtsen F, et al. Efcacy of acti-vated recombinant factor VII in cirrhotic patients with uppergastrointestinal bleeding: a randomized placebo-controlleddouble-blind multicenter trial. Gastroenterology.2003;124(4)(Suppl1):A697. (Prospective randomized; 245 patients)

27. Ansell J, Hirsh J, Hylek E, et al. Pharmacology and manage-ment of the vitamin K antagonists: American College ofChest Physicians Evidence-Based Clinical Practice Guide-lines (8th Edition). Chest. Jun 2008;133(6):160S-198S. (Practiceguideline)

28. van Ryn J, Stangier J, Haertter S, et al. Dabigatran etexilate--anovel, reversible, oral direct thrombin inhibitor: interpreta-tion of coagulation assays and reversal of anticoagulantactivity. Thromb Haemost. 2010;103(6):1116-1127. (Literaturereview)

29. Eerenberg ES, Kamphuisen PW, Sijpkens MK, et al. Reversal

of rivaroxaban and dabigatran by prothrombin complexconcentrate. Circulation. 2011;124(14):1573-1579. (Prospectiverandomized; 12 patients)

30. Findley LJ, Redstone PM. Blood transfusion in adult Jehovah’s Witnesses. A case study of one congregation.1982;142(3):606-607. (Retrospective survey; 70 respondents)

31. Watch Tower Bible and Tract Society of Pennsylvania. Howcan blood save your life? Available at: http://www.jw.org/en/publications/books/blood/how-can-blood-save-your-life/. Accessed March 1, 2013. (Website)

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0413 Massive Upper GI Bleeding.pdf