DISPOSITION

� Admission

A patient requiring anticoagulation therapy with heparin is

usually admitted to the hospital for coadministration with

warfarin. This is to prevent the hypercoagulable state that

occurs in the early phase of warfarin treatment. Patients with

a supratherapeutic INR and bleeding require admission.

Patients with a supratherapeutic INR who have a poor social

situation or are at risk of falling should also be admitted.

� Discharge

A patient with no other admission indications who requires

anticoagulation may be discharged with warfarin and a

7 -day course of LMWH injections. Close follow-up should

be arranged within 24-48 hours, and the patient must be

ds to antithrombin III, resulting in

inhibition of thrombin and coagulation factors II, IX, X,

XI, and XII. LMWH is prepared from unfractionated

• When the international normal ized ratio (INR) is

supratherapeutic in a patient who is not bleeding, a cau ­

tious approach to vitamin K administration is important.

Administering excess vitamin K may overcorrect the INR,

leaving the patient refractory to further anticoagulation.

heparin and includes only short chains. LMWH binds to

antithrombin III but inhibits only factor X. LMWH is

advantageous because it has a more predictable dose

response and greater bioavailability. Heparin-induced

thrombocytopenia (HIT) is due to immunoglobulin G (IgG)

antibody that binds platelets and results in their activation,

creating both thrombocytopenia and thrombosis. Typically,

the onset of HIT is generally 5-12 days after onset of

therapy. The incidence of HIT is 1-3% in patients treated

with unfractionated heparin, but is much less common in

patients taking LMWH.

Warfarin inhibits the cofactor of vitamin K, which normally allows for the production of anticoagulants (protein C

and S) and coagulants (factors II, VII, IX, and X). Because

protein C has a half-life that is much shorter than the halflife of factors II, VII, IX, and X, a hypercoagulable state is

seen first, necessitating the coadministration of unfractionated or LMWH until warfarin has reached its full anticoagulant potential after 5 days. Dabigatran etexilate directly and

competitively binds to free and clot-bound thrombin, which

prevents further clot formation.

CLINICAL PRESENTATION

..... History

Consider the reason the patient has presented to the ED as

it relates to their anticoagulant use.

308

ANTICOAGU LANT THERAPY AND ITS COMPLICATIONS

Gastrointestinal ( GI) bleeding is a common complication

and may not be noticed by the patient; therefore, inquire

about blood in the stool or melena. Any history of trauma,

especially head trauma, should be taken very seriously in

the patient on anticoagulant medications. Intracranial

bleeding is the most common fatal bleeding complication

related to anticoagulation therapy.

If a bleeding complication is occurring, make sure to

have investigated why the patient is taking anticoagulant

therapy. Patients who have had a recent VTE or a prosthetic

heart valve have a greater need for anticoagulation than a

patient with isolated AF. This information is extremely useful when there is a severe bleeding complication that

requires reversal of anticoagulation.

Consider coadministration of additional medications

to patients already taking warfarin that will either increase

or decrease the anticoagulant effects. Medications that

increase the international normalized ratio (INR) include

several antibiotics, nonsteroidal anti-inflammatory drugs,

prednisone, cimetidine, amiodarone, and propanolol. A

decrease in INR is induced by carbamazepine, barbiturates,

haloperidol, and ranitidine. Additionally, several herbal

medications may also increase or decrease the INR.

Lastly, assess for risk factors that increase the patient's

chance of bleeding. For patients on warfarin, risk factors

include INR >4.0, age >75 years, prior history of GI bleed,

hypertension, cerebrovascular disease, renal insufficiency,

alcoholism, and known malignancy. Risk factors for bleeding

in patients on heparin or LMWHs include increasing dose,

degree of elevation of partial thromboplastin time (PTT),

recent surgery or trauma, renal failure, use of another anticoagulant (aspirin, glycoprotein inhibitor), and age >70 years.

..... Physical Examination

Abnormal vital sign that suggest hypovolemia and shock

should be addressed immediately in a patient with a bleed ­

ing complication. Look for any evidence of head trauma.

Sublingual or neck hematomas are airway emergencies,

especially if they are expanding. During the cardiovascular

exam, listen for murmurs or an irregular heart rhythm that

suggests AF. Tenderness during the abdominal exam may

suggest intraperitoneal hemorrhage. A rectal examination

is indicated to diagnose GI bleeding. Conduct a thorough

skin assessment because patients recently started on warfarin may develop warfarin skin necrosis due to capillary

thrombosis in the subcutaneous tissues. Patients with HIT

may also develop similar skin lesions. Ecchymosis and

hematomas should be noted.

DIAGNOSTIC STUDIES

...,_. Laboratory

General laboratory studies include a complete blood count

(to detect anemia and thrombocytopenia) and a

prothrombin time, INR, and PTT. In addition, get a basic

metabolic panel to assess renal function.

..... Imaging

Lower the threshold to obtain an imaging study in patients

on anticoagulant medications. Any patient taking oral

anticoagulation therapy who suffers minor or major head

trauma with or without a headache should have a head

computed tomography ( CT) scan to rule out intracranial

hemorrhage.

MEDICAL DECISION MAKING

History, physical examination, and laboratory studies may

be sufficient to arrive at a diagnosis of an anticoagulation

complication. However, when indicated, intracranial,

splenic, liver or retroperitoneal bleeding should be ruled

out with CT. If skin lesions are noted, consider the diagnosis of warfarin skin necrosis or HIT.

TREATMENT

For patients starting on heparin therapy due to VTE disorders, the therapy begins with an 80 IU /kg bolus followed by

continuous infusion of 18 IU/kg/hr. For patients receiving

treatment for acute coronary syndrome or on fibrinolytic

therapy or a glycoprotein inhibitor, the dose is reduced

60 IU/kg bolus, 12 IU/kg/hr infusion. PTT is measured

6 hours after initiation of the bolus, with a goal of 1.5-2.5 times

normal. When clinically significant bleeding is present, stop

the heparin infusion. Anticoagulation lasts up to 3 hours

after the infusion is stopped. If major bleeding occurs,

administer protamine (1 mg/100 IU heparin) intravenously (IV), given slowly over 5-10 minutes to a maximum

dose of 50 mg.

 

XI, and XII. LMWH is prepared from unfractionated

• When the international normal ized ratio (INR) is

supratherapeutic in a patient who is not bleeding, a cau ­

tious approach to vitamin K administration is important.

Administering excess vitamin K may overcorrect the INR,

leaving the patient refractory to further anticoagulation.

heparin and includes only short chains. LMWH binds to

antithrombin III but inhibits only factor X. LMWH is

advantageous because it has a more predictable dose

response and greater bioavailability. Heparin-induced

thrombocytopenia (HIT) is due to immunoglobulin G (IgG)

antibody that binds platelets and results in their activation,

creating both thrombocytopenia and thrombosis. Typically,

the onset of HIT is generally 5-12 days after onset of

therapy. The incidence of HIT is 1-3% in patients treated

with unfractionated heparin, but is much less common in

patients taking LMWH.

Warfarin inhibits the cofactor of vitamin K, which normally allows for the production of anticoagulants (protein C

and S) and coagulants (factors II, VII, IX, and X). Because

protein C has a half-life that is much shorter than the halflife of factors II, VII, IX, and X, a hypercoagulable state is

seen first, necessitating the coadministration of unfractionated or LMWH until warfarin has reached its full anticoagulant potential after 5 days. Dabigatran etexilate directly and

competitively binds to free and clot-bound thrombin, which

prevents further clot formation.

CLINICAL PRESENTATION

..... History

Consider the reason the patient has presented to the ED as

it relates to their anticoagulant use.

308

ANTICOAGU LANT THERAPY AND ITS COMPLICATIONS

Gastrointestinal ( GI) bleeding is a common complication

and may not be noticed by the patient; therefore, inquire

about blood in the stool or melena. Any history of trauma,

especially head trauma, should be taken very seriously in

the patient on anticoagulant medications. Intracranial

bleeding is the most common fatal bleeding complication

related to anticoagulation therapy.

If a bleeding complication is occurring, make sure to

have investigated why the patient is taking anticoagulant

therapy. Patients who have had a recent VTE or a prosthetic

heart valve have a greater need for anticoagulation than a

patient with isolated AF. This information is extremely useful when there is a severe bleeding complication that

requires reversal of anticoagulation.

Consider coadministration of additional medications

to patients already taking warfarin that will either increase

or decrease the anticoagulant effects. Medications that

increase the international normalized ratio (INR) include

several antibiotics, nonsteroidal anti-inflammatory drugs,

prednisone, cimetidine, amiodarone, and propanolol. A

decrease in INR is induced by carbamazepine, barbiturates,

haloperidol, and ranitidine. Additionally, several herbal

medications may also increase or decrease the INR.

Lastly, assess for risk factors that increase the patient's

chance of bleeding. For patients on warfarin, risk factors

include INR >4.0, age >75 years, prior history of GI bleed,

hypertension, cerebrovascular disease, renal insufficiency,

alcoholism, and known malignancy. Risk factors for bleeding

in patients on heparin or LMWHs include increasing dose,

degree of elevation of partial thromboplastin time (PTT),

recent surgery or trauma, renal failure, use of another anticoagulant (aspirin, glycoprotein inhibitor), and age >70 years.

..... Physical Examination

Abnormal vital sign that suggest hypovolemia and shock

should be addressed immediately in a patient with a bleed ­

ing complication. Look for any evidence of head trauma.

Sublingual or neck hematomas are airway emergencies,

especially if they are expanding. During the cardiovascular

exam, listen for murmurs or an irregular heart rhythm that

suggests AF. Tenderness during the abdominal exam may

suggest intraperitoneal hemorrhage. A rectal examination

is indicated to diagnose GI bleeding. Conduct a thorough

skin assessment because patients recently started on warfarin may develop warfarin skin necrosis due to capillary

thrombosis in the subcutaneous tissues. Patients with HIT

may also develop similar skin lesions. Ecchymosis and

hematomas should be noted.

DIAGNOSTIC STUDIES

...,_. Laboratory

General laboratory studies include a complete blood count

(to detect anemia and thrombocytopenia) and a

prothrombin time, INR, and PTT. In addition, get a basic

metabolic panel to assess renal function.

..... Imaging

Lower the threshold to obtain an imaging study in patients

on anticoagulant medications. Any patient taking oral

anticoagulation therapy who suffers minor or major head

trauma with or without a headache should have a head

computed tomography ( CT) scan to rule out intracranial

hemorrhage.

MEDICAL DECISION MAKING

History, physical examination, and laboratory studies may

be sufficient to arrive at a diagnosis of an anticoagulation

complication. However, when indicated, intracranial,

splenic, liver or retroperitoneal bleeding should be ruled

out with CT. If skin lesions are noted, consider the diagnosis of warfarin skin necrosis or HIT.

TREATMENT

For patients starting on heparin therapy due to VTE disorders, the therapy begins with an 80 IU /kg bolus followed by

continuous infusion of 18 IU/kg/hr. For patients receiving

treatment for acute coronary syndrome or on fibrinolytic

therapy or a glycoprotein inhibitor, the dose is reduced

60 IU/kg bolus, 12 IU/kg/hr infusion. PTT is measured

6 hours after initiation of the bolus, with a goal of 1.5-2.5 times

normal. When clinically significant bleeding is present, stop

the heparin infusion. Anticoagulation lasts up to 3 hours

after the infusion is stopped. If major bleeding occurs,

administer protamine (1 mg/100 IU heparin) intravenously (IV), given slowly over 5-10 minutes to a maximum

dose of 50 mg.

Enoxaparin is the most commonly prescribed LMWH

in the ED. The most common dosing regimen is 1 mg/kg

subcutaneously every 12 hours. Dosing will need to be

adjusted in morbidly obese patients or those in renal

failure. Protamine (1 mg/1 mg enoxaparin) can be

administered to a maximum dose of 50 mg when r eversal

is indicated, but reversal is not as effective as with unfractionated hepar in. If major or life-threatening bleeds

occur, consider giving blood products such as PRBC and

FFP.

If warfarin therapy is being initiated in the ED, the

usual starting dose is 5 mg by mouth daily. Lower doses are

usually required in the elderly, in patients with liver disease, or those with poor nutrition. The therapeutic range

for the INR depends on the indication. Patients with

mechanical valves are considered therapeutic at INR levels

of 2.5-3.5, whereas other patients ( eg, with AF or VTE) are

therapeutic at INR levels of 2-3 .

Management of bleeding complications or supratherapeutic INR with warfarin is outlined in Figure 73- 1.

CHAPTER 73

No bleeding

Warfa ri n

anticoagu lation

Red uce or omit

next dose of

warfarin

Recheck INR

in 24 hr

Hold warfarin

Recheck INR

in 24 hr

Hold warfarin

Vitamin K 3-5

mg PO

Recheck INR

in 24 hr

Hold warfarin

Vitamin K 10

mg IV Hold warfarin

Vitamin K 10

mg IV

FFP 3-4 units

FFP 3-4 units

• Figure 73-1. Anticoagulant therapy and its compl ications diagnostic algorithm for supratherapeutic INR

from warfarin. FFP, fresh-frozen plasma; INR, international normal ized ratio; IV, intravenous; PO, by mouth.

For reversal, N administration of vitamin K is most rapid,

with onset within 1 -2 hours, compared with 6-10 hours

for oral dosing. Administer N vitamin K over 30 minutes

to minimize the small risk of anaphylaxis. Higher doses

of vitamin K (10 mg) may result in warfarin resistance

(up to 1 week) when it is time to restart anticoagulation

therapy. FFP is used as the flrst-line agent for reversal of

bleeding due to warfarin. The initial dose is 2-4 units.

Consider giving other products such as prothrombin

complex concentrate (PCC) and recombinant factor

VIla.

The oral direct thrombin inhibitor dabigatran is not

routinely started in the ED. However, more patients are

presenting to the ED on dabigatran with bleeding

complications. Currently there is no antidote for the

reversal of bleeding complications associated with its use.

Therefore, clinical management consists of stopping the

medication, and if a major or life-threatening bleed occurs,

consider giving FFP, PRBC, or some in vitro studies suggest

PCC or recombinant factor Vlla.

 

causes of fever during transfusions, including acute

intravascular hemolysis, sepsis, or TRALI. The differential

for hypotension during transfusion includes ongoing

hemorrhage, hemolytic transfusion reaction, anaphylaxis,

sepsis from bacterial contamination, and TRALI. Shortness

of breath is seen in anaphylaxis, hemolytic transfusion

reaction, volume overload, TRALI, and sepsis. Wheezing

may be noted in anaphylaxis, volume overload, or TRALI.

Anaphylaxis is often associated with urticaria (unlike

acute intravascular hemolysis or sepsis) and usually is not

associated with fever. Volume overload or TRALI may

present with isolated shortness of breath, pulmonary

edema, and/or hypoxia without other systemic findings

such as fever or hypotension. A high index of suspicion

and broad differential is required in all cases, particularly

when the patient experiences any new symptom in the

setting of current or recent transfusion.

TREATMENT

When blood products are being transfused, they should be

administered at a slow rate for the first 30 minutes to allow for

early identification of a possible reaction. If a transfusion reaction is suspected, the first step is to immediately STOP the

transfusion. Check the labels on the blood products and

patient, and send blood samples from both the patient and

the blood products to the blood bank for further analysis.

Treatment modalities for each individual type of reaction

follow.

Acute intravascular hemolysis. Stop the transfusion

immediately. Resuscitate volume aggressively with

crystalloid intravenous (IV) fluid. Administer diuretics to

maintain urine output 1-2 mL/kg/hr. Vasopressors should

be initiated if hypotension is refractory to IV fluids. Send

blood and urine specimens to the lab per hospital protocol.

Anaphylaxis. Stop the transfusion immediately. Rapidly

resuscitate with crystalloid IV fluids and administer

epinephrine 0.3 mg (1:1,000) subcutaneously (SQ)/intramuscularly (IM), methylprednisolone 125 mg IV, diphen ­

hydramine 50 mg IV, famotidine 20 mg IV, and albuterol

5 mg in 3 mL of saline nebulizer. Repeat epinephrine as

needed, and consider starting an epinephrine drip if

necessary.

Sepsis. Stop the transfusion immediately. Pan-culture

the patient and treat with copious crystalloid IV fluids,

broad-spectrum antibiotics, and vasopressors as needed

for refractory hypotension. Follow the appropriate sepsis

protocol at your institution.

TRALI. Stop the transfusion immediately. Administer

oxygen and gently diurese. Many patients require

noninvasive positive pressure ventilation, and severe

cases may require intubation and mechanical ventilation.

Massive transfusion coagulopathy. Administer FFP

and platelets to reverse coagulopathy and thrombocytopenia. Some hospitals have protocols in massive PRBC

transfusion that include platelets and FFP in fixed ratios.

Treat hypothermia by warming all blood products to room

temperature, coadministration of warm crystalloid IV

fluid, and external rewarming measures such as warming

blankets. Treat hypocalcemia with IV calcium gluconate.

Simple febrile reaction. Stop the transfusion. Treat

with antipyretics such as acetaminophen. Restart the

transfusion only after ruling out acute hemolysis or sepsis

from bacterial contamination.

Urticaria. Treat with an antihistamine such as

diphenhydramine, and consider a short course of steroids

if the rash is severe. The transfusion does not need to be

stopped if isolated urticaria occurs, without fever or

anaphylaxis.

Delayed extravascular hemolysis. Usually no specific

treatment is required; often observed as outpatient.

Graft -versus-host disease. Bone marrowtransplantation

is the only effective treatment. Prevention is the most useful

strategy by transfusing leukocyte-reduced blood in immunocompromised or related recipients.

DISPOSITION

� Admission

Patients with persistent vital sign abnormalities or ongoing

hemorrhage require admission to a monitored setting in a

telemetry or intensive care unit. Additionally, any patients

with findings of intravascular hemolysis, anaphylaxis,

sepsis, TRALI, massive transfusion reactions, or volume

overload should be admitted to a monitored setting.

� Discharge

Although many patients receiving blood transfusions in

the ED already require admission, hemodynamically stable

patients without ongoing hemorrhage may be safely

discharged home in the absence of a transfusion reaction.

Patients who experience a simple febrile reaction or

urticarial rash may require a period of observation, but can

still be discharged safely in most circumstances.

SUGGESTED READING

Coil CJ, Santen SA. Transfusion therapy. In: Tintinalli JE,

Stapczynski JS, Ma OJ, Cline DM, Cydulka RK, Meckler GD.

Tintinalli's Emergency Medicine, A Comprehensive Study Guide.

7th ed. New York, NY: McGraw-Hill, 201 1, pp. 1 493-1 500.

Emery M. and blood components. In: Marx J A, Hockberger RS,

Walls RN. Rosen's Emergency Medicine, Concepts and Clinical

Practice. 7th ed. Philadelphia, PA: Mosby Elsevier, 201 0, pp.

42-46.

Anticoagu lant Therapy

and Its Comp lications

joanne C. Witsil, PharmD

Key Points

• In the anticoagulated patient, have a low threshold to

obta in imaging studies after trauma.

• When initiating warfarin therapy, coadministration with

heparin or low-molecular-weight heparin (3-5 days) is

necessary to avoid a paradoxical hypercoagulable state.

INTRODUCTION

Use of anticoagulation therapy and complications related

to their usage are frequently encountered in the emergency

department (ED). Anticoagulant therapies commonly

seen include heparin, low-molecular-weight heparin

(LMWH), warfarin, and the direct thrombin inhibitor

dabigatran etexilate. These agents are used frequently

in patients with acute coronary syndrome (ACS), venous

thromboembolism (VTE), valve replacement, and atrial

fibrillation (AF). When administered in the appropriate

clinical setting, anticoagulant medications prevent morbidity and mortality. For example, the risk of stroke in

patients with AF and structural heart disease is 5% a year

but is reduced by 70% with the use of chronic oral anticoagulation therapy.

Anticoagulants are not without complications, however. In patients taking warfarin, up to 1 5% will suffer a

bleeding complication, 4.9% will develop a major bleeding

complication, and approximately 1 o/o will develop a fatal

complication annually. The risk of a bleeding complication

from heparin use is approximately 6% and is no different

than the risk of bleeding from LMWH.

Heparin is a mixture of glycosaminoglycan chains of

varying lengths that binds to antithrombin III, resulting in

inhibition of thrombin and coagulation factors II, IX, X,

Infectious complications to transfusion may be

bacterial or viral. Bacterial infections are more common

after platelet transfusion (stored at room temperature)

and longer blood storage times. Organisms are most

commonly skin or gastrointestinal flora. Diagnosis

requires positive cultures from donor and r ecipient blood.

Donor blood is prescreened for human immunodefi ­

ciency virus (HIV), hepatitis B virus (HBV), hepatitis C

virus (HCV), cytomegalovirus ( CMV), human

T-lymphotropic virus (HTLV), West Nile virus (WNV),

and parvovirus; nevertheless, there is a small r isk of transmission of these pathogens (most commonly HCV)

despite screening.

Massive transfusions put the patient at risk for developing coagulopathy, hyperkalemia, lactic acidosis, and hypothermia. Dilutional coagulopathy or thrombocytopenia can occur

when >4 PRBCs are transfused within 1 hour or 10 units

within 12 hours, without the addition of clotting factors or

platelets. Hypocalcemia and metabolic alkalosis may o�cur

due to the effect of citrate. Volume overload from transfusiOns

is more common in the setting of underlying chronic cardiac

or kidney disease as well as plasma transfusion. Patients present with acute pulmonary edema without fever or shock.

Graft-versus-host disease is a rare complication of

transfusion seen in irnmunocompromised or familial

recipients. It is associated with a very high mortality rate.

Donor T lymphocytes attack recipient tissues. This complication is prevented by leukoreduction and irradiation.

Patients may present with fever, rash, pneumonitis, abdominal pain, vomiting, diarrhea, transaminitis, and thrombocytopenia.

The incidence of transfusion-related complications is

highlighted in Table 72- 1.

Acute

Acute hemolysis

Anaphylaxis

Sepsis

TRALI

Simple febrile reaction

Minor allergic

Hepatitis B

Hepatitis C

HIV

Delayed

Incidence

1 in 0.25-1 million

1 in 20,00D-150,000

1 in 5 million

1 in 5,000-10,000

1 in 1 00

1 in 1,000

Incidence

1 in 1 37,000

1 in 1-2 million

1 in 2-3 million

CLINICAL PRESENTATION

� History

Fevers and chills may be seen in acute febrile reactions, acute

intravascular hemolysis, anaphylaxis, sepsis due to bacterial

contamination, or TRALI. Chest pain, shortness of breath,

lightheadedness, or syncope may be seen in the same conditions. Isolated shortness of breath during transfusion is suggestive of volume overload, whereas generalized pruri�us �d

rash (in the absence of other symptoms) suggests urt1car1a.

Risk factors for developing a transfusion-related reaction

include immunocompromised recipients, those requiring

massive transfusion, a history of receiving blood transfusions, preexisting congestive heart failure, or elderly patients.

For example, recipients who are irnmunocompromised are

at increased risk for graft-versus-host disease. Patients

receiving massive transfusions are at significant risk for

hypothermia and coagulopathy. Elderly patients or patients

with congestive heart failure are at risk for pulmonary

edema, particularly when blood products are transfused too

rapidly. Also, patients who have been transfused blood products in the past are at increased risk of having preexisting

antibodies, which may cause a variety of transfusion-related

reactions. See the Introduction for classic presentations.

� Physical Examination

During transfusion, patients should be monitored closely

for adverse reactions. New vital sign abnormalities that

develop such as fever, hypotension, tachycardia, or tachypnea are all concerning for possible transfusion reaction.

Even well-appearing patients who develop fever during

transfusion should have the transfusion stopped and be

closely monitored for more serious reactions, as they may

quickly decompensate. In patients with hypotension,

tachycardia, or tachypnea, it is difficult to distinguish

ongoing hemorrhage (the underlying reason for many

transfusions) from potentially life-threatening transfusion

reactions including acute intravascular hemolysis, anaphylaxis, or sepsis. Classically, hypovolemic shock will cause

cool extremities, whereas the shock states seen in acute

intravascular hemolysis, anaphylaxis, or sepsis cause cardiovascular collapse and warm extremities. Patients receiving massive transfusions are at risk of hypothermia, whi�h

also may occur due to sepsis. Wheezing may be noted m

anaphylaxis or pulmonary edema (due to volume overload

or TRALI). Hives or rash is seen in anaphylaxis or urticaria.

Dark pink or brown urine indicate hemoglobinuria after

acute intravascular hemolysis.

DIAGNOSTIC STUDIES

� Laboratory

Laboratory studies are performed to document appropriate

response to transfusion ( eg, rise in hemoglobin) and to aid

in identifying acute intravascular hemolysis, sepsis, or

CHAPTER 72

other symptoms that develop acutely during a transfusion.

Transfusions should always be held pending these results,

and the laboratory should be notified to test samples of

both donor and recipient blood. Most hospitals have

protocols to ensure that the correct blood is transfused to

the correct patient and to manage a possible transfusion reaction.

Basic laboratory tests are generally not helpful in acute

febrile reactions, urticaria, anaphylaxis, TRALI, or volume

overload. Their utility in the ED is in identifying acute

intravascular hemolysis or sepsis. In acute hemolytic

reactions, complete blood count (CBC) may reveal

worsening anemia and schistocytes. Other laboratory

findings include a positive Coombs test, acute renal failure,

DIC, and/or elevated haptoglobin, bilirubin, and lactate

dehydrogenase levels. Hemoglobinuria may be seen on

urinalysis.

If sepsis is suspected, Gram stain and blood cultures

should be ordered. CBC may reveal leukocytosis or

leukopenia; however, sepsis cannot be ruled out definitely

in their absence.

Transfusion

During massive transfusion, dilutional thrombocytopenia or coagulopathy, metabolic acidosis, and hypocalcemia may occur.

..... Imaging

In suspected cases of TRALI or volume overload, a chest

x-ray may demonstrate acute pulmonary edema. In general,

patientswithvolumeoverloadwillhavecardiomegaly,whereas

patients with TRALI will have a normal-heart size. Bedside

ultrasound may help differentiate volume overload from

TRALI. Volume overload is associated with poor cardiac

contractility and inferior vena cava distension, whereas in

TRALI, both of those features would be normal.

MEDICAL DECISION MAKING

Different transfusion reactions present similarly; however,

it is important to differentiate which type of reaction is

occurring to appropriately direct treatment and disposition (Figure 72-1). If there is any suspicion of a transfusion

reaction, the first step is to stop the transfusion.

Sign or symptom

of a transfusion

reaction

Acute hemolytic

reaction

Stop the

transfusion

Fever only

Simple febrile

reaction

Shortness of breath

Pulmonary

edema

TRALI or

fluid

overload

Hypotension,

wheezes,

rash, pruritus

Allergic

reaction

(anaphylaxis)

Figure 72-1. Transfusion reactions diagnostic algorithm.

TRANSFUSION REACTIONS

If the patient experiences a fever with no other signs or

symptoms, a simple febrile reaction is likely. However, it

may be difficult clinically to distinguish between other