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conditions that might falsely elevate D-dimer
levels, according to the diagnosis guidelines created
by the American College of Chest Physicians
(ACCP), patients with low pre-test probability
should undergo initial testing with a moderately
or highly sensitive D-dimer or proximal CUS. If
these tests are negative, no further testing is
required. However, if a D-dimer is positive further
confirmation should be done with a whole leg
ultrasound. For patients with a high pre-test probability whole leg US should be the preferred initial
diagnostic modality.
15
In recent years treatment of DVT has become
increasingly aggressive, with initiation of anticoagulation in the ED considered paramount in
halting thrombus progression. The standard
treatment regimen for DVT in patients who are
not at a high risk of bleeding has changed over the
last several years as a new class of medications, the
non-vitamin K oral anticoagulants (NOACs),
have made their way onto the market. Currently
available medications in the United States include
apixaban (Eliquis®) dabigatran (Pradaxa®), rivaroxaban (Xarelto®) and edoxaban (Savaysa®),
with others on the horizon.
These medications have revolutionized the
treatment of VTE. Apixaban, edoxaban and rivaroxaban are orally absorbed direct Factor Xa inhibitors with rapid onset and relatively short half-lives.
Dabigatran is a direct Thrombin inhibitor that also
exhibits a short half-life. (See Table 31.1.) The
benefits of these medications over other treatment
regimens are that they do not require significant
anticoagulation monitoring, are taken orally, and
are associated with similar efficacy and a lower
risk of major bleeding and intracranial hemorrhage when compared to treatment with enoxaparin plus a vitamin K antagonist (VKA) such as
warfarin.
16,17
Drawbacks to the use of the Factor Xa inhibitors are that there is currently no reversal agent,
other than time, and they are not currently recommended for pregnant women, breastfeeding
women, and patients on strong CYP3A inhibitors
or inducers. They are currently contraindicated if
a patient has hepatic disease associated with coagulopathy, clinically relevant bleeding or if they
have significant renal disease.
Reversal agents are expected to be available
soon for the Factor Xa inhibitors. A reversal agent
for dabigatran was recently approved in the
United States. Due to the lower risk of major
bleeding and in particular intracranial bleeding,
the NOACs are quickly becoming the therapy
of choice for VTE. Eliminating the need for frequent blood draws and the NOAC’s ability to be
taken orally make them significant options for
treatment of these conditions. Renal function
should be monitored in these medications as their
bleeding risk can change if creatinine clearance
decreases. The nuances of each of these medi cations are beyond the scope of this chapter but are
important information for prescribing physicians
to be awa re of.
18,19,20,21
Another treatment option available consists
of administration of a “bridging” anticoagulant
(intravenous unfractionated heparin), or a lowmolecular-weight heparin (LMWH such as enoxaparin) with a continued course of warfarin. The
advantages of LMWH over unfractionated heparin include once or twice daily injections without
the need for monitoring, a long half-life, and a
lower risk of major hemorrhage.
22
This again
allows the patient to be treated as an outpatient
without the need for hospitalization.
With both forms of acceptable outpatient
treatment, enoxaparin/warfarin or the NOACs,
the duration will depend on the risk of thrombus
recurrence. Three months is the initial recommended time of therapy followed by reassessment of future risk. In some cases of increased
risk such as recurrent VTE, significant thrombophilia or cancer, lifelong therapy may be recommended. Treatment of VTE using NOACs has
become common and acceptable practice since
their emergence on the market. With either
drug regimen (enoxaparin/warfarin or NOACs),
the patient has the benefit of being treated at
home, which has be en shown in studies to not
only be cost-effective, but these patients also
exhibit greater activity levels, higher levels of
social functioning, and better treatment satisfaction scores.
23
Table 31.1 Half Lives of Factor X A and Direct Thrombin
Inhibitors
Apixaban: 12–15 hours
Edoxaban: 9–14 hours
Rivaroxaban: 5–9 hours, longer in > 60 y.o.:
11–13 hours
Dabigatran: 12–17 hours, increases to 27.2
hours with severe renal dysfunction
Deep Vein Thrombosis (DVT)
035
20:59:08
Management
The Observation Unit (OU) can serve as a valuable tool in the diagnosis and management of
DVT in a select group of patients. In hospitals
where diagnostic modalities are not readily available at all times, the OU is an efficient place
to complete testing as well as further observe
patients for the progression of symptoms. To this
end, patients are continually monitored by pulse
oximeter while in the OU looking for signs of a
large pulmonary embolus and decompensation.
Once a DVT has been diagnose d the OU can serve
as a place to initiate therapy, educate the patient
about the disease and the risks and specifics of
the medication regimen. In addition, a review
of insurance and reimbursement issues can be
done and the patient can be prepared for outpatient treatment and safe follow-up. While institutions do send a patient with the diagnoses of
DVT directly home from the ED, this does
require a significant upfront amount of resources.
Many busy EDs will not have adequate time to
educate patients about their condition, the
nuances of their medications, their bleeding risk
and appropriate follow-up care. This is important
in the safe care and treatment of patients. The OU
can be the ideal place to accomplish all that is
required to safely send the patient home thoroughly educated and prepared for outpatient
treatment, without the added days and cost of an
inpatient stay. Outpatient therapy consists of
treatment with a NOAC (apixaban or rivaroxaban), LMWH with warfarin, or LMWH followed
by a NOAC (dabigatran or edoxaban) depending
on the individual patient factors and physician
choice.
If there is concern for a hereditary clotting
disorder, the patient can have a hypercoagulability panel ordered before anticoagulation is undertaken (see Table 31.2). This may be important in
idiopathic DVTs as results may have important
implications to the patient and other family
members regarding length of therapy and other
hereditary/familial conditions. These laboratory
tests do not have to be resulted during the OU
stay, but should be drawn before initiation of
therapy or delayed until after the patient is no
longer on therapy.
Dosing of each individual medication will not
be discussed in this chapter but should be
reviewed and confirmed prior to discharge. The
importance of consistently taking anticoagulants
on a set schedule should be impressed upon the
patient. When LMWH (enoxaparin) and warfarin
are being used, close follow-up of the Prothrombin
time (PT) and International Normalized Ratio
(INR) by an anticoagulation management service
or the private physician is required until the
INR has become adequate, between 2.0 and 3.0.
Enoxaparin should be continued for a minimum
of 5 days and until the INR reaches therapeutic
range; warfarin is then continued for the duration
of therapy, at least 3 months. Similarly, if edoxaban
or dabigatran are used the patient must be treated
with LMWH (enoxaparin) injections for 5 days
before initiation of oral therapy.
In the OU the chosen medicati on is started
after appropriate contraindications are assessed.
The patient can be given educational material
about their disease and medication. If enoxaparin
is necessary then the patient can be directed on
how to give a subcutaneous injection by trained
staff. If a VKA will be used, the patient can be
given a prepared manual on the necessary lifestyle
changes regarding the diet restrictions that treatment with warfarin requires.
The OU can serve an important role in educating VTE patients regarding the disease and
the risks and safety precautions that anticoagulant therapy entails. Educational videos can be
useful in this aspect. Patients can be given the
opportunity to ask questions and develop a level
of comfort with their illness and treatment.
Patients using injections should be able to
show proficiency using the injectables before
discharge.
Table 31.2 OU Hypercoagulability Screen
Protein C
Protein S
AntiThrombin III Antibody
Factor VIII Activity
Hexagonal Phase Phospholipids
Factor V Genotyping
Prothrombin Genotyping
Antiphospholipid Antibody Panel
Homocysteine
Activated Protein C Resistance
Carol Lynn Clark and Michelle A. Wiener
035
20:59:08
The patient then can be discharged home with
prescriptions for the appropriate medication with
appropriate follow-up. If a patient is on enoxaparin/ warfarin, serial PT/INRs must be tracked
every few days with warfarin dosing adjustments
until the INR is between 2.0 and 3.0. The initiation
of follow-up lab draws should be arranged before
discharge. Serial complete blood counts should
be followed after discharge as well, ensuring there
are no undetected thrombocytopenias or bleeding
complications that develop. If a patient is on a
NOAC, it is recommended that complete blood
counts, platelets and renal function be followed
after discharge. Outpatient follow-up may be
arranged with the patient’s private physician, an
anticoagulation management service or a combination of the two. Outpatient follow-up should be
confirmed before the patient is discharged from
the OU.
Patient Criteria for OU Treatment
of DVTs
Deep Venous Thrombosis: OU:
Observation Inclusion Criteria
Stable vital signs
No evidence of significant pulmonary
embolus (right heart strain on 2-D
echocardiogram, elevated troponin or
elevated brain natriuretic peptide)
Suspected DVT awaiting ultrasound or
confirmed DVT by ultrasound
Pulse ox greate r than 95% or stable at baseline
No contraindications to outpatient NOAC or
enoxaparin/warfarin therapy
Deep Venous Thrombosis: OU/
Observation Exclusion Criteria
Clinical evidence of hypoxia
Dyspnea at rest
Morbid obesity, weight over 160 kg
Severe uncontrolled hypertension: systolic
blood pressure > 200, diastolic blood pressure
> than 100
History of heparin induced thrombocytopenia
(for enoxaparin/warfarin)
History of allergy to NOACs, heparin,
warfarin, enoxaparin, pork or pork products
(treatment specific)
History of ongoing alcohol or drug abuse
(safety of anticoagulation)
Inability to self or supportively administer
enoxaparin/ warfarin or take NOACs after
discharge
Inability to follow up for laboratory
monitoring (minimal for NOACs)
Personal refusal of pork product
administration, for religious reasons, etc. (for
enoxaparin)
Severe or unexplained anemia
Platelet count < 100,000/mm
3
, history of
severe liver disease, bilirubin > 2.4
History of mechanical prosthetic heart valve
(heparin/ warfarin only indicated treatment)
History of bleeding disorder
History of GI bleeding or recent diagnosis of
peptic ulcer disease (1 month), documented
positive guaiac of stools on current exam
History of recent spinal/or brain surgery
History of indwelling epidural catheter
History of recent lumbar puncture or epidural
History of recent stroke, within 6 weeks
History of intracranial bleed/aneurysm/
arteriovenous malformation
History of DVT development while on
appropriate anticoagulation
Significant renal failure
Patients with multiple comorbidities and
complex cases
Relative Contraindications:
Poor creatinine clearance: Dosing must be
adjusted per particular medication guidelines
Concomitant use of medications may
influence medication choice of therapy
Prescribers should be aware of specifics of
medications and contraindications. These cases
should be discussed with a qualified pharmacist.
Inability to control pain
Discharge Criteria
Stable vital signs
Pain controlled
Follow-up ability/ physician confirmed
Ability to follow protocol confirmed
Appropriate medication arrangements made
and confirmed
Patient competence and knowledge of therapy
assured
Deep Vein Thrombosis (DVT)
035
20:59:08
Outcome
Utilizing careful patient selection and a structured
OU DVT/VTE protocol, treatment of DVT in the
OU can achieve a similar degree of effectiveness
compared to inpatient care while being costeffective and relieving hospital bed shortages.
The educational interventions available in the
OU allow the patient to safely transition to outpatient therapy of DVT with comfort and insight.
The OU allows for faster, safer, and more
cost-effective therapy of DVT than inpatient therapy. As has been shown with several OU therapeutic treatment protocols, this allows for
increased patient satisfaction.
Conclusion
Using a pre-established protocol, the OU can be
an appropriate bed choice for initiation of patient
education and therapy in the treatment of uncomplicated deep venous thrombosis.
References
1. White, R. The epidemiology of
venous thromboembolism.
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2. Beckman MG, Hooper WC,
Critchley SE, et al. Venous
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8. Prandoni P, Lensing AWA,
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9. Prandoni P, Lensing AWA,
Cogo A, et al. The long-term
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et al. Does this patient have
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SM, et al. Diagnosis of DVT:
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16. Prins M, Lensing AW,
Bauersachs R, et al. Oral
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Thromb J. 2013 Sep 20:11(1).
17. Burness CB, Perry C.
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18. Einstein Investigators,
Bauersachs R, Berkowitz SD,
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23. Bossuyt PM, Van den Belt AG,
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Deep Vein Thrombosis (DVT)
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Subpart IVC
Chapter
32
Clinical – Vascular
Acute Pulmonary Embolism (PE)
David G. Paje, MD, FACP, SFHM
Introduction
Acute pulmonary embolism (PE) is a common
cardiovascular emergency that affects hundreds of
thousands of patients every year with a reported
annual incidence of nearly 1 per 1,000 in the United
States.
1,2
It is a clinical manifestation of venous
thromboembolism (VTE), which is the same disease process that results in deep vein thrombosis
(DVT). In general, PE is a natural sequela of DVT.
Studies show that as much as 70% of patients with
PE are found to have a concomitant DVT in the
lower extremities, specifically in the proximal veins
in two-thirds of cases. Also, among patients with
symptomatic proximal DVT without symptoms of
PE, 40–50% have ventilation-perfusion lung scan
findings that are consistent with a high probability
of PE.
3
The occlusion of the pulmonary arterial bed
that occurs in PE may lead to impairment in
oxygenation as a result of ventilation-perfusion
mismatch, and to more serious hemodynamic
complications arising from an abrupt increase in
pulmonary vascular resistance, including shock
from acute right ventricular failure and sudden
death from electromechanical dissociation. It is
estimated that 11% of patients with acute PE die
within 1 hour of onset,
4
usually even before it is
recognized. However among those who do not die
acutely, the case fatality rates vary depending on
the clinical severity of the thromboembolic
episode.
Patients with severe PE have a high risk of
mortality and are best managed in a critical
care environment. On the other hand, those
with non-high-risk PE are usually admitted to
a general medical unit and they typically stay
for several days. However, various studies
evaluating prognostic models have identified a
group of patients with PE that are appropriate
candidates for initial outpatient therapy; these
patients have a low risk of fatal and nonfatal
adverse outcomes.
5–11
Hence, current published
guidelines recommend outpatient care for
highly selected patients with PE.
12,13
A recent administrative database review found
that the median length of stay (LOS) for patients
hospitalized with PE was 6 days, and the postdischarge mortality rate was 3.3%. But the adjusted
risk of death after discharge was significantly
higher for patients with an LOS of 4 days or less
(OR, 1.55; 95% CI, 1.21–2.00) compared to those
with a LOS of 5 to 6 days,
14
suggesting that patients
with increased risk of complications may have
been inappropriately selected for early discharge.
This highlights the need to apply prognostic
models and to develop explicit decision-support
tools that properly identify patients who may be
discharged early or treated in the outpatient setting. Providing observation services for further risk
stratification and short-term monitoring is a reasonable alternative for non-high-risk PE patients to
identify those who may need further inpatient care
as well as those who may be discharged safely
without the need for hospitalization.
15
Diagnosis
Acute PE is often difficult to recognize and the
diagnosis is sometimes delayed or missed. Its
clinical manifestations may include dyspnea,
chest pain, cough, hemoptysis, syncope, tachypnea, and tachycardia. These signs and symptoms
are nonspecific and unreliable when appraised
separately. However, when these findings are
evaluated together with predisposing factors, the
likelihood of PE can be determined.
Several clinical decision rules (CDR) have been
developed to estimate the probability of PE, which
guides the selection of the appropriate diagnostic
strategy and the subsequent interpretatio n of test
results. The most commonly used and extensively
validated CDR, the Wells rule (Table 32.1), looks
at both clinical findings and risk factors in
036
20:59:16
predicting the presence of PE. It includes one
subjective criterion, the physician’s judgment of
whether an alternative diagnosis is less likely than
PE. Other decision tools, such as the revised
Geneva score, consider only objective variables.
Nevertheless, both Wells and revised Geneva rules
showed similar a ccuracy in assessing the clinical
probability of PE.
16,17
D-dimer is a product of fibrin degradation
and is a highly sensitive laboratory marker for
thrombosis. When the clinical probability is low,
a negativ e D-dimer test reliably excludes PE.
However, when the likelihood of PE is high,
further diagnostic evaluation is required regardless of the D-dimer level. There is a wide variety
of clinical conditions aside from PE that results
in an elevated D-dimer, including advanced age,
inflammation, trauma, recent surgery, malignancy, necrosi s, autoimmune disease, or liver
disease. Therefore, a positive D-dimer result is
not specific for PE and it is not useful as a sole
basis for its diagnosis.
18
Imaging studies are essential in the diagnostic
evaluation of PE and they are particularly indicated if the clinical suspicion is high or if the
D-dimer is elevated.
19
Multidetector computed
tomography angiogram (CTA) is currently the
most readily available option. It has excellent test
characteristics; its estimated sensitivity and specificity for the diagnosis of PE are at least 90% and
95%, respectively.
20
It also has the advantage
of providing an alternative or a concomitant diagnosis that may account for the patient’s clinical
presentation. The usual limitation of CTA is the
use of intravenous iodinated contrast, which is an
important concern for patients at high risk for
contrast-induced nephropathy especially those
with underlying renal impairment. Also, in cases
when the CTA is negative but the clinical probability high, further testing is necessary.
Ventilation-perfusion scintigraphy (V/Q scan)
is usually the preferred alternative for patients
who cannot undergo a CTA because of either
renal dysfunction or allergy to iodinated contrast.
V/Q scan results are reported based on criteria
established in the PIOPED
21
trial using four categories: normal or near-normal, low, intermediate
(nondiagnostic), and high probability of PE.
A normal perfusion scan safely rules out PE in
most cases, with a likelihood ratio of 0.10. A high
probability V/Q scan confirms the diagnosis of PE
with a high degree of certainty , especi ally in a
Table 32.1 Wells Rule and Revised Geneva Score
Clinical
Decision
Rule
Clinical Variable Points
Wells
Rule
Clinical signs and symptoms
of DVT (minimum of leg
swelling and pain with
palpation of the deep vein)
3
An alternative diagnosis is
less likely than PE
3
Heart rate greater than 100 1.5
Immobilization or surgery in
the previous 4 week
1.5
Previous DVT/PE 1.5
Hemoptysis 1
Malignancy (on treatment,
treated in the last 6 months
or palliative)
1
Clinical Probability
PE unlikely <
4
PE likely > 4
Revised
Geneva
Score
Age > 65 1
Previous DVT/PE 3
Surgery (under general
anesthesia) or fracture (of
the lower limbs) within 1
month
2
Active malignant condition
(solid or hematologic
malignant condition,
currently active or
considered cured < 1 year)
2
Unilateral lower limb pain 3
Hemoptysis 2
Heart rate 75–94 beats per
minute
3
Heart rate >
95 beats per
minute
5
Pain on lower limb deep
venous palpation and
unilateral edema
4
Clinical Probability
PE unlikely <
5
PE likely > 5
DVT deep vein thrombosis, PE pulmonary embolism
Acute Pulmonary Embolism (PE)
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20:59:16
patient with a high clinical probability. Any other
combination of V/Q scan result and clinical probability is not useful in excluding or establishing
PE, and requires further evaluation.
13
Direct pulmonary angiography has been the
gold standard for the diagnosis of PE. It is an
invasive procedure that involves direct injection
of contrast dye into the pulmonary arteries. With
technological advances in noninvasive alternatives, such as refinement of CT imaging, conventional direct pulmonary angiography is now
rarely performed as an isolated diagnostic procedure. It is best reserved for cases where CT findings
are equivocal.
Finally, compression ultrasonography (CUS) is
another option that may be useful in evaluating
patients with suspected PE. The presence of DVT
in the proximal lower limb, even when asymptomatic, establishes the diagnosis of PE in patients
with high clinical probability and in those with
non-high clinical probability but with positive Ddimer tests (specificity of 99% and likelihood ratio
of 42.2). However, the absence of DVT does not
rule out PE (sensitivity of 39%).
22
Risk Stratification
Once PE is suspected and even while diagnostic
evaluation is still in progress, it is important to
concurrently assess its clinical severity so that
high-risk patients are identified promptly. These
patients are generally hemodynamically unstable
and they require more intensive management,
including more aggressive interventions such as
immediate thrombolysis or surgical embolectomy.
13,23
The European Society of Cardiology
(ESC) guidelines, which recommend a riskstratification approach based on the expected
PE-related early mortality rate (Table 32.2), define
high-risk PE by the presence of shock or systemic
hypotension. It is a distinct clinical entity with an
expected short-term PE-related mortality risk of
more than 15%.
13
Aside from defining high-risk PE, the ESC
guidelines further classify non-high-risk PE
patients as either at intermediate risk (3–15%) or
at low risk (< 1%) of PE-related early mortality.
Those with intermediate risk have findings consistent with the presence of right ventricular dysfunction (RVD) and/or myocardial injury.
13
Although there are no universally accepted criteria to determine the presence of RVD in patients
with acute PE, widely available diagnostic tools
include echocardiography, computed tomography, and brain natriuretic peptide (BNP). On
the other hand, myocardial injury in patients with
PE can be detected by elevations in levels of cardiac troponin T or I.
24
Table 32.2 European Society of Cardiology Risk Stratification of Pulmonary Embolism
13
PE-related Early
Mortality Rate
Risk Markers Potential
Treatment
Implications
Clinical (shock
or hypotension)
RV-dysfunction Myocardial
injury
High > 15 % + (+)
a
(+)
a
Thrombolysis
or
embolectomy
Non-high Intermediate 3–15 % + + Hospital
admission
+
+
Low < 1% Early discharge
or home
treatment
a
In the presence of shock or hypotension, it is not necessary to confirm RV-dysfunction or myocardial injury to classify as high risk
of PE-related early mortality.
PE pulmonary embolism, RV right ventricle
Torbicki, A., et al. Guidelines on the diagnosis and management of acute pulmonary embolism: the Task Force for the Diagnosis
and Management of Acute Pulmonary Embolism of the European Society of Cardiology (ESC). Eur Heart J, 2008; 29(18): p. 2281, by
permission of Oxford University Press.
David G. Paje
036
20:59:16
However, these markers of RVD and myocardial injury are actually most useful when
identifying low-risk patients. Normal echocardiographic findings, a bsence of right ventricular
dilatation on CT or low levels of BNP or NTproBNP are all reliable indicators of an excellent
outcome, with a low risk of short-term mortality
or complicated clinical course. Also, a normal
cardiac troponin makes PE-related early mortality very unlikely (negative predictive value,
99–100%), irrespective of method or cutoff value
applied.
13
Nevertheless, to appropriately identify patients
who may safely undergo outpatient treatment, an
ideal prognostic model should not only consider
PE-related early mortality but should also predict
recurrent VTE, major bleeding and all-cause mortality that occur within a short period of time after
PE is diagnosed. These adverse outcomes were
measured as end points in several derivation and
validation studies on clinical models to assess prognosis in patients diagnosed with acute PE.
25–30
Among these models are the Pulmonary Embolism
Severity Index (PESI) and the Geneva risk score
(Table 32.3).
The PESI was developed to stratify patients
treated for PE into five severity classes of increasing risk of mortality within 30 days of hospitalization. The original PESI model includes
11 clinical variables that are routinely available
at the time of presentation. In the derivation
cohort, 59% of patients were classified as intermediate to very high risk (Class III–V) with a 14%
mortality risk, while 41% were thought to be very
low to low risk (Class I and II) with a 2% risk of
death within 30 days.
31
A subsequent prospective
validation study identified 47% of patients as lowrisk (Class I and II) with an overall mortality of
only 1.2% and a PE-specific mortality of 0.7%.
7
In
another validation study, the 90-day mortality in
low-risk patients was 1%, and there were no
recurrent thromboembolic or major bleeding
events.
29
A simplified version of PESI was later
developed to make it easier to calculate, but a
recent comparative analysis showed that the original PESI classified a higher proportion of
patients as low-risk and it had a great er discriminatory power.
32
The Geneva risk score includes six independent predictors of an adverse outcome (i.e., recurrent VTE, major bleeding and death) in patients
with acute PE. In the derivation cohort, 67.2%
were classified as low-risk and 32.8% were highrisk, with rates of adverse outcomes at 90 days of
2.2% and 26.1%, respectively.
25
In summary, an appropriate risk stratifica-
tion to identify low-risk patients with PE starts
Table 32.3 Pulmonary Embolism Severity Index and
Geneva Risk Score
25,31
Prognostic
Model
Clinical Variable Points
Pulmonary
Embolism
Severity
Index (PESI)
Age Age in
years
Male sex 10
History of cancer 30
History of heart failure 10
History of chronic lung
disease
10
Pulse 110 beats per
minute
20
Systolic blood pressure
< 100 mmHg
30
Respiratory rate
30 breaths per minute
20
Temperature < 36
o
C20
Altered mental status 60
Arterial oxyhemoglobin
saturation (SaO
2
) < 90%
20
The five risk classes based on the
total point score: class I (< 65
points), class II
(66–85 points), class III
(86–105 points), class IV (106–125
points), and class V (> 125 points)
Geneva
Risk Score
History of cancer 2
History of heart failure 1
Previous DVT 1
Concomitant DVT on
ultrasound
1
Systolic blood pressure
< 100 mmHg
2
PaO
2
< 60 mmHg
(or 8 kPa)
1
The two risk classes based on the
total point score: low-risk (≤ 2)
and high-risk ( 3)
DVT deep vein thrombosis
Acute Pulmonary Embolism (PE)
036
20:59:16
with excluding those who are hemodynamically
unstable. Afterwards, predictive models that
incorporate relevant and readily available clinical
data at presentation, such as PESI and Gen eva risk
score, can be applied. Patients categorized as PESI
Class I and II may be discharged early or be
treated completely in the outpatient setting.
33
Those patients with intermediate to very high risk
clinical features (PESI Class III and V) require
further evaluation in the inpatient setting.
Patient Selection
Patients diagnosed with acute pulmonary embolism who are hemodynamically stable may be considered for observation services for short-term
monitoring and further risk stratification to
determine whether they need inpatient care or if
they can be discharged to follow-up for outpatient
treatment. The appropriate patients should be
classified as low-risk based on a validated clinical
prognostic tool, such as PESI.
Another important factor in selecting
patients for observation care is their suitability
for the optimal outpatient treatment regimen.
Currently, the options for immediate anticoagulation for the i nitial treatment of VTE include
rivaroxaban, apixaban and low-molecular-weight
heparin (LMWH) (Table 32.4). Patients who
cannot receive any of these regimens because
of severe renal dysfunction or other nonspecific
patient-related risk factors should be admitted
for intravenous unfractionated heparin (UFH)
therapy.
Observation Care
The goals of observation care for carefully
selected patients with acute PE who are determined to be low-risk for adverse outcomes
include initiation of anticoagulation, short-term
monitoring, and further risk stratification. As
soon as PE is suspected, immediate anticoagulation with an oral or a parenteral agent must be
considered.
34
The appropriate choices for initial
anticoagulant therapy in an observation setting
are rivaroxaban, apixaban, and subcutaneous
LMWH (Table 32.4). Patients should be monitored for the development of any complication
related to treatment or to PE itself, including
allergic reaction, thrombocytopenia, bleeding,
and worsening hypoxemia. While most of the
clinical variables used in risk stratification of
acute PE are readily obtainable at presentation,
imaging modalities, such as echocardiography
and CUS, may have limited availability at some
institutions. A reasonable observation stay
should allow for completion of these tests when
indicated.
Low-risk PE patients may be discharged after
an uneventful observation stay if proper outpatient care and anticoagulant therapy can be provided. For long-term (first 3 months) treatment
of PE, current guidelines prefer rivaroxaban, apixaban, edoxaban or dabigatran over a vitamin
K antagonist (VKA), such as warfarin.
35
Rivarox-
aban
36,37
and apixaban38can be initiated without
the need for a parenteral anticoagulant. Edoxaban
39
and Dabigatran40require 5 to 10 days of
Table 32.4 Initial Anticoagulation Options in Observation
Parenteral Anticoagulant Subcutaneous Dose Comments
Low-molecularweight Heparin
(LMWH)
Enoxaparin 1 mg/kg BID or 1.5 mg/kg
daily
If CrCl < 30 ml/min, reduce dose to 1 mg/kg
daily or consider UFH as an alternative
Dalteparin 100 IU/kg BID or
200 IU/kg daily
Adjust if CrCl < 30 ml/min
Tinzaparin 175 IU/kg daily If CrCl < 30 ml/min, consider UFH as an
alternative
Oral Anticoagulant Oral Dose Comments
Rivaroxaban 15 mg BID for the first 21
days, then 20 mg daily
Should be taken with food Avoid if CrCl
< 30 ml/min
Apixaban 10 mg BID for 7 days,
then 5 mg BID
Avoid if CrCl < 15 ml/min
CrCl creatinine clearance, aPTT activated partial thromboplastin time, BID twice daily, BW body weight
David G. Paje
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