.A. Figure 74-2. Eva l uating the cornea l surface using a

narrow beam at a 45-degree angle. The curved beam

represents the reflection of l ight off the cornea . When

the cornea is in focus, protein deposits are freq uently

visual ized on its surface.

of fluorescein uptake (green fluorescence) that suggest corneal or conjunctival epithelial injury. Running or oozing of

the fluorescein (Seidel sign) is caused by aqueous humor

leaking from a full-thickness penetration of the cornea.

Evaluating the anterior chamber for cell and flare is the

third part of the examination. The slit height should be

decreased and the slit width increased to create a short,

wide beam of white light. Swing the light source temporally, aiming the beam of light nasally through the anterior

CHAPTER 74

.&. Figure 74-3. The appearance of the light when

eva l uating for cell and flare.

chamber at the height of the pupil (Figure 74-3 ). Push the

microscope forward until the patient's iris is in sharp

focus, then move back slightly until the iris is out of

focus-but not so far that the cornea comes into focus.

The focal plane is now between the iris and cornea, in the

anterior chamber. Using the pupil as a dark backdrop,

watch for any material reflecting the light. Flare is caused

by protein in the anterior chamber and creates a smoky

appearance in the beam of light (a common analogy is

"headlights in fog:') Cells will look like "dust particles in a

sunbeam." The presence of either signifies inflammation

of the anterior chamber. Use of dilating drops can cause

cells to be present and applanation tonometry can cause

flare, so slit lamp examination should be performed

before these other tests.

If a foreign body (FB) is identified during the examination, first attempt to wash it out using saline. If this is not

successful, it can be removed using a burr drill or a 25- or

27 -gauge needle. Anesthetize the patient's eye using proparacaine or tetracaine. Be sure the patient's head is stabilized by full contact with the forehead brace and chin rest.

Stabilize your hand on the patient's cheek or forehead so

the removal device will track any movements the patient

may make. Keep the removal device tangent to the surface

of the patient's cornea. Guide it to the cornea under direct

vision, switching to the eyepieces once the removal device

is in view. If using a burr drill, press the side of the burr

against the FB. When activated, the drill will "fling" the FB

out of the cornea. If using a needle, place it on a small

syringe (eg, insulin syringe) to provide better control.

Guide the needle to the FB and use a scooping or flicking

motion to pull the FB out of the cornea. Always move

tangential to the globe.

COMPLICATIONS

When using the slit lamp and syringe/needle to remove an

FB, careless attempts at removal or patient movement may

result in penetration through the cornea. Additionally, in

the setting of ocular trauma, avoid placing pressure on the

eye when the possibility of a globe rupture exists. Excessive

pressure may cause the intraocular contents to be extruded.

Suggested Reading

Knoop K, Dennis W, Hedges ]. Ophthalmologic procedures. In:

Roberts ]R, Hedges JR Roberts: Clinical Procedures in Emergency

Medicine. 5th ed. St. Louis, MO: Saunders, 2009, pp. l l4 1-l l 77.

Walker RA, Adhikari S. Eye emergencies. 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. 1517-1 549.

Red Eye

Craig H uston, MD

Key Points

• Always begin with visual acuity, the vital sign of the eye.

• The patient should be instructed to remove contact lens and

not to put them back in until the symptoms have resolved.

• The presence of pain and the relief of pain with insti llation of anesthetic agents are helpful in determining the

cause of red eye.

INTRODUCTION

Eye complaints account for 3% of all emergency department (ED) visits. Red eye is a common complaint, and

although most cases are benign, self-limited conditions,

some may be vision-threatening. Conjunctivitis is the most

common cause of a red eye, but other frequent problems

include subconjunctival hemorrhage, corneal injuries

(abrasions, keratitis, and foreign bodies), and acute uveitis.

Conjunctivitis may be viral, bacterial, or allergic. Viruses

are the most frequent cause, especially adenovirus. The most

common bacterial pathogens are Staphylococcus aureus,

Streptococcus pneumoniae, and Haemophilus influenzae.

Chlamydia trachomatis or Neisseria gonorrhea are unusual,

butimportantcauses of conjunctivitis. Allergic conjunctivitis

is due to recurrent seasonal inflammation from allergen

exposure. About 15% of the population will experience

allergic conjunctivitis at one time in their life.

Subconjunctival hemorrhage is blood between the

conjunctiva and sclera that results from a ruptured con ­

junctival blood vessel. Subconjunctival hemorrhage is

caused by direct trauma or indirect injury. Although it may

be alarming to the patient, it is usually a benign process

that occurs with a sudden increase in pressure from sneez ­

ing, coughing, straining, or vomiting. If atraumatic, the

etiology is usually hypertension or spontaneous rupture.

• Follow a systematic approach to the physical examination:

visua l acuity, lids and lashes, conjunctiva, sclera, cornea,

pupil examination, and anterior chamber.

• Never prescribe topical steroids without consulting with

an ophthalmologist.

Corneal injury is common because the epithelium is

thin and easily damaged. Corneal abrasions are particularly

common, representing 10% of all ED visits for eye complaints. The cornea is resistant to infection, but when

injured, a potential portal to bacteria is created. Viral infections that cause injury to the cornea include herpes simplex

and varicella (ie, herpes zoster ophthalmicus). Contact lens

use may predispose the patient to keratitis or a corneal ulcer

due to gram-negative bacteria.

 

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.

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

knowledgeable about self-inj ecting. Patients with

supratherapeutic INR without bleeding are frequently safe

to discharge if they are not at increased risk of falling.

ANTICOAGU LANT THERAPY AND ITS COMPLICATIONS

SUGGESTED READING

Agena W, Gallus AS, Wittkowsky A, et al. Oral Anticoagulant

Therapy: Antithrombotic Therapy and Prevention ofThrombosis,

9th ed: American Collage of Chest Physicians Evidence-Based

Clinical Practice Guidelines. Chest. 2012;141(Suppl):e44s--e88s.

Garcia DA, Baglin TP, Weitz JI, et al. Parenteral Anticoagulants:

Antithrombotic Therapy and Prevention of Thrombosis, 9th

ed: American Collage of Chest Physicians Evidence-Based

Clinical Practice Guidelines. Chest. 2012;141(Suppl):e24s-e43s.

Slattery DE, Pollack CV. Anticoagulants, antiplatelet agents, and

fibrinolytics. ln: 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, 20 1 1, pp. 1 500-1 507.

S lit Lam p Examination

Douglas S. Franzen, MD

Nathan J. Lewis, MD

Key Points

• Familiarity with the controls is critical to performing a

slit lamp examination.

• When positioning the patient for the exam, make sure

that their forehead is touching the forehead brace and

encourage them to keep it there.

INDICATIONS

The slit lamp is used to evaluate the anterior eye including

the lids, lashes, conjunctiva, cornea, visible sclera, anterior

chamber, iris, and lens for signs of trauma, hemorrhage,

inflammation, or foreign bodies.

CONTRAINDICATIONS

The patient must be cooperative and capable of sitting

upright for the duration of the examination.

EQUIPMENT

In addition to a slit lamp, the examiner will need 2 chairs

or stools, preferably of about equal height. Fluorescein

allows visualization of corneal injury. Other s upplies may

include anesthetic drops and a needle or ophthalmic burr

(for foreign body removal), cotton-tipped applicators (for

lid eversion), and saline (to flush the eyes or lids).

Ideally, one should be familiar with use of the slit lamp

before examining a patient. The slit lamp is a microscope

in which focus is achieved by moving the lenses instead of

the object being examined. The power of the microscope

typically ranges from 1 0-25x (or higher) and is adjusted by

a dial on the housing j ust in front of the eyepieces. The

plane of focus is changed by using the joystick to move the

• When using a slit lamp to remove a corneal foreign body,

first guide the removal device (eg, 25-gauge needle) to the

eye under direct vision, then switch to the magnified view.

• To prevent puncturing the cornea, keep the removal

device tangential to the globe at all times.

microscope toward or away from the patient. The joystick

also moves the microscope left or right. Twisting the

joystick raises or lowers the microscope. If the microscope

does not move when the joystick is moved, you may need

to loosen the locking screw on the microscope base.

The light source is mounted on a swing arm that allows

it to move independently from the microscope. Knowing

how to adjust the multiple controls of the light source is

critical to performing an exam. The power switch activates

the lamp. Many slit lamps also have a rheostat (dimmer),

usually near the power switch or on the base of the

microscope. A selector switch near the base of the bulb

housing allows the examiner to change from white to cobalt

blue light (other options, including green, are usually available). Just below this is a dial to adjust the height of the light

beam. Near the base of the microscope arm is another dial

to adjust the width of the slit. The location of these controls

may vary from lamp to lamp. Figure 74-1 demonstrates

their position on one model.

PROCEDURE

The patient should be seated and the height of the slit lamp

adjusted so the patient can place his or her chin comfortably

on the chinrest and forehead against the forehead brace.

The height of the chinrest should be adjusted so that the

patient's lateral canthus is aligned with the eye level mark

312

SLIT LAMP EXAMINATION

Forehead brace

Chinrest height -1--.....,

adjustment

Figure 74-1. Key components of the slit lamp.

on the chinrest support. The examiner should sit opposite

the patient in a chair or stool of about the same height.

Ask the patient to close his or her eyes. Turn on the lamp

with a white filter and adjust the brightness as needed. Move

the microscope to grossly focus the beam on the patient's

closed lid. Adjust the slit width to make the beam as narrow

as possible without losing brightness. Swing the light source

approximately 45 degrees to your right while leaving the

microscope directly facing the patient. Ask the patient to

open his or her eyes. When you look through the eyepieces,

the image should be very close to focused. Two reflections

will be visible: one that is curved and faint and, to the left of

that, one that is straight and much brighter. The curved

beam is reflecting off of the cornea. Adjust the microscope

so this beam is crisply focused (usually by moving slightly

toward the patient, about 1 mm). Protein deposits are often

visible on the corneal surface when properly focused

(Figure 74-2). Scan the left half of the patient's cornea by

using the joystick. Move in an arc so the plane of focus follows the curve of the patient's cornea--closer to the patient

as you approach the limbus and further from the patient as

you move toward the pupil. Look for any corneal defects or

foreign bodies. Check for ciliary flush (dilated pericorneal

blood vessels, a sign of iridocyclitis) at the edges of the cornea. It may be necessary to have the patient look up, down,

left, and/or right to fully view all parts of the cornea. After

scanning the left half of the cornea, bring the microscope

back to midline, swing the light source 45 degrees to your

left, and examine the right half of the patient's cornea. The

lids and conjunctiva can also be examined using this

method, usually with a wider beam.

After examining the patient with white light, fluorescein

should be instilled. Switch to the cobalt blue filter, widen

the light beam slightly, and repeat the exam. Look for areas

Bulb housing

Filter selector

Slit height

Eyepieces

.. ..

: ��

•

 

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.