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204 Chapter 18 Diagnostic algorithms for acute deep venous thrombosis and pulmonary embolism
https://t.me/med1917
population as a complication of contemporary health care.
The majority of VTE episodes (85%) occurred in the hospital setting. One-third of the cases were associated with a
central venous catheter.
Children less commonly develop diseases causing damage to vessel endothelium (i.e., diabetes mellitus, dyslipidemias, and hypertension). Children are less frequently
exposed to acquired risk factors. Compared to adults, children have lower plasma concentrations of all vitamin K–
dependent clotting factors and almost all contact factors, as
well as reduced ability to generate thrombin. The capacity
to inhibit thrombin is enhanced throughout childhood due
to increased plasma concentrations of thrombin inhibitor
alpha-2-macroglobulin.
113
Presentation is variable depending on the degree of
vessel occlusion and location. Duplex ultrasonography
remains the preferred initial diagnostic test in most children with suspected venous thrombosis. CTPA is the imaging modality of choice for children with suspected PE.
Clinical tools commonly used in adult patients to assess
the pretest probability of PE (i.e., Wells score and D-dimer
measurements) do not appear to perform well in children.
The majority of PEs in children are nonmassive.
114
18.2.13 DVT/PE in COVID-19
COVID-19 may present with a broad spectrum of clinical
cardiac symptoms. Dyspnea and chest pain may be caused
by noncardiac and/or cardiac causes. Acute cor pulmonale
may be precipitated by acute PE or acute respiratory distress syndrome (ARDS) in patients with COVID-19. VTE is
common in acutely ill patients with COVID-19. Biomarkers
include cardiac troponin and natriuretic peptide (BNP and
N-terminal pro–BMP [NT–proBNP]) and are commonly
elevated among hospitalized patients with COVID-19 and
are associated with an increased risk of mortality. Myocarditis may also result in abnormalities of biomarkers, as well
as abnormalities on both the ECG and echocardiogram.
In patients with COVID-19, the traditional risk factors of PE are absent and the incidence of DVT is lower.
COVID-19 patients showed signicantly higher lymphocyte counts, lactate dehydrogenase, lactic acid, and
D-dimer levels. COVID patients had PEs of smaller size
(12.39% versus 25.5% main pulmonary artery, 29.8%
versus 37.1% lobar, 44.7% versus 29.5% segmental, and
13.2% versus 7.9% subsegmental respectively: p < 0.001,
less right ventricular risk categories were independently
associated with in-hospital mortality in COVID patients.
The usual tools for risk stratication of PE are valid
in COVID patients. In a study of COVID patients and
non-COVID patients with Pes, higher sPESI scores and
the intermediate and high risk of PE are associated with
higher mortality risk. Autopsy studies in some individuals
who have died of COVID-19 have demonstrated microvascular thrombosis in the lungs.
115
The guidance from the American Society of Hematology regarding the diagnosis of PE in COVID patients
includes the following:
A normal D-dimer (unusual in critically ill individuals
•
with COVID-19) is sufcient to exclude the diagnosis
of PE if the pretest probability for PE is low or moderate but is less helpful in those with a high pretest
probability.
An increase in D-dimer is not specic for VTE and is not
•
sufcient to make the diagnosis.
In patients with suspected PE due to unexplained hypo-
•
tension, tachycardia, worsening respiratory status, and/
or risk factors for thrombosis, CTPA is the preferred test
to conrm or exclude the diagnosis.
116
Guidelines 18.0 of the American Venous Forum on diagnostic algorithms for acute deep venous thrombosis and
pulmonary embolism
No. Guideline Grade of
18.1 In symptomatic outpatients with suspected acute deep venous thrombosis (DVT),
we recommend to obtain rst a clinical score and D-dimer level to select patients
for further diagnostic studies.
18.2 D-dimer levels are inaccurate for diagnosing DVT in several clinical conditions,
including recent surgery, pregnancy, malignancy, infection, elevated bilirubin,
trauma, and heparin use. In these situations, alternative diagnostic modalities are
recommended.
18.3 We recommend to repeat duplex scan or alternative imaging modality in the follow-up of patients with negative duplex studies and high clinical suspicion of DVT.1(strong)
18.4 We suggest that a combination of clinical probability score and D-dimer level has
similar utility in the diagnosis of DVT to a computed tomography scan.
18.5 We suggest judicious use of gadolinium in patients with renal insufciency because of the risk of nephrogenic systemic brosis.
recommendation
1
(strong)
1
(strong)
2
(weak)
2
(weak)
Quality of
evidence
B
(moderate)
B
(moderate)
B
(moderate)
B
(moderate)
C
(low to very low)
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https://t.me/med1917
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patients with low-risk pulmonary embolism suitable for outpatient treatment
using the Pulmonary Embolism Severity
Index (PESI). Ir J Med Sci 2013;182:
291–295.
100. Carpenter C.R., Keim S.M., Seupaul
R.A., and Pines J.M. Best evidence in
emergency medicine investigator group.
Differentiating low-risk and no-risk PE
patients: The PERC score. J Emerg Med
2009;36:317–322.
101. Paiva L.V., Providencia R.C., Barra
S.N., Faustino A.C., Botelho A.M.,
and Marques A.L. Cardiovascular risk
assessment of pulmonary embolism with
the GRACE risk score. Am J Cardiol
2013;111:425–431.
102. Becattini C., Casazza F., Forgione C.,
etal. Acute pulmonary embolism:
External validation of an integrated
risk stratication model. Chest
2013;144:1539–1545.
103. Kohn C.G., Mearns E.S., Parker M.W.,
Hernandez A.V., and Coleman C.I.
Prognostic accuracy of clinical prediction rules for early post-pulmonary
embolism all-cause mortality: Abivariate
meta-analysis. Chest 2015;147:
1043–1062.
104. Costantino G., and Furlan R. Syncope
risk stratication in the emergency
department. Cardiol Clin 2013;31:27–38.
105. Yoo H.H., Queluz T.H., and El Dib R.
Outpatient versus inpatient treatment of acute pulmonary embolism
(Review). Cochrane Database Syst Rev
2014;11:CD010019.
106. Zondag W., Vingerhoets L.M., Durian
M.F., etal. Hestia Study Investigators.
Hestia criteria can safely select patients
with pulmonary embolism for outpatient treatment irrespective of right
ventricular function. J Thromb Haemost
2013;11:686–692.
107. Clark D.C. III., McGifn D.C., Dell’Italia
L.J., and Ahmed M.I. Submassive
pulmonary embolism: Where’s the
tipping point? Circulation
2013;127:2458–2464.
108. Erkens P.M., Gandara E., Wells P.S.,
etal. Does the pulmonary embolism
severity index accurately identify low
risk patients for outpatient treatment?
Thromb Res 2012;129:710–714.
★109. Vinson D.R., Zehtabchi S., and Yealy
D.M. Can selected patients with newly
diagnosed pulmonary embolism be
safely treated without hospitalization?
Asystematic review. Ann Emerg Med
2012;60:651–662.
110. Penaloza A., Roy P.M., and Kline J. Risk
stratication and treatment strategy of
pulmonary embolism. Curr Opin Crit
Care 2012;18:318–325.
111. Chartier L., Bera J., Delomez M., etal.
Free-Floating Thrombi in the right heart:
Diagnosis, management, and prognostic indexes in 38 consecutive patients.
Circulation 1999;99(21):2779–2783.
112. Sabbagh E., Elzanaty A., Alhourani O.,
etal. “Clot in transit”: Percutaneous or
surgical approach? Cath Lab Digest 2020.
113. Biss T.T., Brandao L.R., Kahr, etal. Clinical features and outcome of pulmonary
embolism in children. Br J Haematol
2008;142:808.
114. Biss T.T., Brandao L.R., Kahr W.H.,
etal. Clinical probability score and
D-dimer estimation lack utility in
the diagnosis of childhood pulmonary embolism. J Thromb Haemost
2009;7:1633.
115. Franco-Moreno A., Brown-Lavalle D.,
Campos-Arenas M., etal. acute phase
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center study. BMC Pul Med 2023.
doi: 10.1186/S12890-02302323-9.
116. https:www.hematology.org/covid-19/
covid-19-and-pulmonary–embolism
(Accessed on April24, 2020).
18
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CHAPTER
19
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Medical treatment of acute deep vein
thrombosis and pulmonary embolism
Henry Han and Geoffrey D. Barnes
19.1 INTRODUCTION
Anticoagulation is the mainstay of treatment for acute
venous thromboembolic (VTE) disease, which comprises
deep venous thrombosis (DVT) and pulmonary embolism (PE). Early and rapid initiation of anticoagulation
is critically important once VTE is diagnosed, as this has
been shown to improve outcomes and reduce the risk of
life-threatening embolization. With the advent and availability of direct oral anticoagulants (DOACs), the landscape of treatment for VTE has evolved signicantly in
favor of easier administration, reduced bleeding events, and
enhanced safety prole. While most patients can be treated
with anticoagulation alone, a select group of patients at
higher risk for complications may require interventional
therapies beyond just anticoagulation. This chapter will
review the approach to anticoagulation for acute VTE and
discuss when interventional therapies beyond anticoagulation may be appropriate.
19.2 OVERVIEW OF ANTICOAGULANT
OPTIONS
Over the past decade, the growth in the number of anticoagulant options facilitates new treatment paradigms
and personalized treatment strategies. These include both
parenteral and oral anticoagulant medications. The two
parenteral anticoagulants commonly used for VTE include
unfractionated heparin (UFH) and low-molecular-weight
heparin (LMWH). For patients with heparin-induced
thrombocytopenia (HIT), options include argatroban,
bivalirudin, and fondaparinux. Oral anticoagulant options
include vitamin K antagonists (VKAs) and the DOACs,
which include both factor Xa inhibitors and direct thrombin inhibitors (Table19.1).
19.2.1 Parenteral anticoagulants
19.2.1.1 Unfractionated heparin
UFH binds to antithrombin and inhibits several key clotting factors, primarily thrombin (factor IIa) and factor Xa.
UFH is a titratable intravenous infusion with a half-life of
approximately 30 minutes. For that reason, it is a good
option for situations that may require rapid cessation or
reversal due to procedural timing or increased risk of bleeding. Furthermore, elimination occurs through both hepatic
and renal means, which means that UFH is the preferred
parenteral option for those with severe renal failure (CrCl
<30 mL/min). However, it can take several (up to 12) hours
to reach therapeutic levels and requires careful monitoring to maintain the therapeutic range. As such, it requires
hospitalization and close nursing care to safely administer.
19.2.1.2 Low-molecular-weight heparin
LMWH primarily inhibits factor Xa and has a more predictable pharmacokinetic property compared to UFH.
LMWH can be used in the acute phase of anticoagulation
treatment for VTE. It has a quick onset of action, achieving
target levels of anticoagulation within 2–3hours. And it
has been shown to be safe for patients undergoing catheter-based procedures.
UFH for many patients with acute VTE. As opposed to
continuous IV infusion with UFH, LMWH can be given as
subcutaneous injections, which can be used in both inpatient and outpatient settings. LMWH is dosed based on
weight and can be split up in two subcutaneous injections
daily. One disadvantage is that it is given as subcutaneous injections, which may not be the preferred route of
administration for some patients. Furthermore, LMWH is
primary excreted through the kidneys and should be used
with caution in patients with severe or end-stage renal disease.
1
As such, it is now preferred over
19.2.1.3 Argatroban, fondaparinux, and bivalirudin
Argatroban and bivalirudin are both direct thrombin
inhibitors that are given as a continuous IV infusion, based
on activated PTT therapeutic assays. Both of these direct
thrombin inhibitors have Food and Drug Administration
(FDA) label indications for treatment of HIT and can also
be used for patients in whom there is a suspicion for HIT.
Fondaparinux is a subcutaneous option that acts as a factor
Xa inhibitor. While it does not have an FDA label indication
for treatment of HIT, it can be safely used in that clinical
scenario. Other than for patients with HIT, these agents are
rarely used to treat acute VTE in the United States.
DOI: 10.1201/9781003328971-22
209209
210 Chapter 19 Medical treatment of acute deep vein thrombosis and pulmonary embolism
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TABLE 19.1 Anticoagulant characteristics for treatment of venous thromboembolism
Name Mechanism of
action
Warfarin Vitamin K antagonist Parenteral anticoag-
Dabigatran Direct thrombin
inhibitor
Apixaban Factor Xa inhibitor 10 mg twice daily for
Rivaroxaban Factor Xa inhibitor 15 mg twice daily for
Edoxaban Factor Xa inhibitor Parenteral anticoag-
Abbreviations: CrCl, creatinine clearance (measured using Cockcroft–Gault equation).
Initial lead-in
dosing
ulant until INR ≥2.0
Parenteral anticoagulant for 5–10 days
7 days
21 days
ulant for 5–10 days
Dosing (after
lead-in) and regimen
5 mg daily, adjusted
to INR target 2.5
(range 2.0–3.0)
150 mg twice daily 150 mg twice daily Avoid when CrCl ≤30 mL/
5 mg twice daily 2.5 mg or 5 mg twice
20 mg once daily 10 mg or 20 mg once
60 mg once daily 60 mg once daily Avoid CrCl ≤15 mL/
Dosing for
extended treatment
(after initial 3–6
months)
INR target 2.5 (range
2.0–3.0)
daily
daily
Renal dysfunction
None
min
No specic dose change
recommended
Avoid when CrCl ≤15 mL/
min
min, reduce dose to 30
mg once daily for CrCl
≤15–30 mL/min
19.2.2 Oral anticoagulants requiring
parenteral lead-in
19.2.2.1 Warfarin
Warfarin is a VKA that has been widely used for the treatment of VTE for many years. It inhibits the gamma-carboxylation of vitamin K, which is required for hepatic synthesis
It is readily available and is an inexpensive option for nearly
all patients. It is the preferred anticoagulant for patients with
mechanical heart valves, rheumatic mitral valve disease, and
conrmed antiphospholipid syndrome (APS). Warfarin has
a notoriously variable clinical impact both between patients
and within individual patients based on dietary vitamin K
intake, physical activity, and other drug–drug interactions.
As such, laboratory monitoring with the international normalized ratio (INR) of the prothrombin time is necessary to
ensure therapeutic dosing for warfarin. However, warfarin
also has a long effective half-life, estimated at 2–4 days based
on the natural breakdown of various clotting factors. Warfarin does require parenteral lead-in anticoagulation until
the therapeutic INR is achieved.
dosing and several drug and food interactions, clinical trials
comparing warfarin to DOACs have found increased bleeding risk in the warfarin groups.
19.2.2.2 Dabigatran
Dabigatran is a direct thrombin (factor IIa) inhibitor. With
an onset of action of approximately 1–2hours and a halflife of 12–14hours, it is taken twice daily. Like warfarin, it
requires parenteral (typically UFH or LMWH) lead-in for
the rst 5–10 days.
head-to-head after parenteral lead-in in a randomized controlled trial, showing similar efcacy, similar rates of major
bleeding, and reduced rates of nonmajor bleeding.
the highly predictable pharmacokinetics, dabigatran does
not require frequent blood draw monitoring or dose adjustment. Dabigatran is largely excreted through the kidneys,
so its use is not recommended for patients with severe or
2
Dabigatran was compared to VKAs
2
In part due to the variable
3
Given
end-stage renal disease as well as those on dialysis. Dabigatran has not been prospectively studied in patients with
cancer-associated VTE. While dabigatran has been shown
to have increased GI bleeding rates compared to warfarin,
patients have also complained of increased rates of GI distress and dyspepsia in randomized trials versus warfarin. As
a DOAC, cost considerations remain an issue for patients.
19.2.2.3 Edoxaban
Edoxaban is a direct factor Xa inhibitor that is taken once
daily. Like dabigatran, it has a relatively short onset of action
and a half-life of 10–14hours and similarly requires 5–10
days of initial parenteral anticoagulant therapy (usually UFH
or LMWH).
2
Given the highly predictable pharmacokinetic
properties, it does not require frequent laboratory monitoring like VKAs. Edoxaban was compared against warfarin in
a head-to-head clinical trial for treatment of acute VTE and
showed similar efcacy with reduced major and clinically relevant nonmajor bleeding.
edoxaban was similarly effective in patients with active cancer and VTE compared to LMWH.
4
Subsequent analysis showed that
5
However, there is a concern about increased GI bleeding, especially among patients
with upper GI cancers. Edoxaban is partially (~27%) cleared
through the renal system and therefore is not recommended
for patients with severe or end-stage renal disease on dialysis.
Additionally, there are no prospective trial data for long-term
treatment of VTE using edoxaban.
19.2.3 Oral anticoagulants without
parenteral lead-in
19.2.3.1 Apixaban
Apixaban is a direct factor Xa inhibitor that is taken twice
daily for treatment of VTE. It does not require parenteral
anticoagulation lead-in.
total daily dose (10 mg twice daily) for the rst 7 days
to halt any active ongoing thrombosis. After the initial 7
days, apixaban is dosed twice daily thereafter at a standard
5 mg, with an option to reduce the dose to 2.5 mg twice
2
Instead, apixaban uses a higher
19.3 Selecting initial medical therapy 211
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daily after the initial 6 months. As with all DOACs, apixaban has a rapid onset of action and a half-life of approximately 12hours. Apixaban is the least renally cleared of all
DOACs, accounting for <25% of all drug metabolism and
elimination. Like the other DOACs, the highly predictable
pharmacokinetic properties and lack of drug–food interactions mean that routine coagulation laboratory monitoring
is not necessary. In a head-to-head comparison for treatment of acute VTE, apixaban was noninferior to VKAs for
recurrent VTE but with signicantly reduced major and
clinically relevant nonmajor bleeding rates.
6
In a randomized trial of patients with cancer-associated VTE, apixaban
had similar efcacy and major bleeding rates as compared
to LMWH.
7
Recent observational studies have found equal
efcacy of apixaban in normal, obese, and severely obese
(body mass index ≥40) patients, suggesting the one-sizets-all dosing is appropriate for nearly all patients with
8
Apixaban can also be used for patients with end-
VTE.
stage renal disease given its relatively low renal clearance.
Important limitations to apixaban use include the need for
twice-daily dosing as well as cost to patients.
19.2.3.2 Rivaroxaban
Rivaroxaban is a direct factor Xa inhibitor with a context-specic dosing regimen. Like apixaban, it does not
require parenteral lead-in therapy.
2
However, to achieve
the higher total daily dose for patients with acute VTE,
rivaroxaban is dosed at 15 mg twice daily for the rst 21
days before returning to the standard 20 mg once-daily
dosing thereafter. After the initial 6 months, there is an
option to reduce the dose to 10 mg daily. Rivaroxaban also
has a rapid onset of action, and its half-life is estimated at
6–7hours. Despite having a shorter half-life than apixaban,
rivaroxaban was tested in all phase 3 clinical trials with a
once-daily dose (except for the initial 3 weeks of acute VTE
treatment) as a way to improve medication compliance.
Rivaroxaban does not require routine coagulation laboratory monitoring given highly predictable pharmacokinetic
properties. In head-to-head prospective trials of patients
with acute VTE, rivaroxaban was noninferior to a VKA for
efcacy, with similar rates of major and clinically relevant
nonmajor bleeding.
9,10
In a small pilot study of patients
with cancer-associated VTE, rivaroxaban had a lower rate
of recurrent VTE at the expense of increased major and
clinically relevant nonmajor bleeding.
11
The majority of the
bleeding events in this smaller pilot randomized trial were
GI bleeding. Rivaroxaban, like apixaban, has been shown
to be reliable for patients across the weight spectrum,
including those with severe obesity.
8
Important disadvantages include cost to patients and mixed observational data
regarding bleeding risk compared to apixaban.
19.3 SELECTING INITIAL MEDICAL
THERAPY
19.3.1 Deep venous thrombosis
For most patients presenting with acute DVT, systemic
anticoagulation alone is sufcient. Preference should be
given for initiation with LMWH if parenteral therapy is
required given its more rapid onset to therapeutic range
compared to UFH; otherwise, DOACs should be considered rst-line therapy.
12,13
DOACs have the convenience
of being dosed orally either once or twice daily and do
not have the frequent lab draws required of VKAs. Additionally, DVTs that are diagnosed in the outpatient setting
can be treated without requiring admission with DOAC
therapies (including their lead-in anticoagulation strategy).
One exception for consideration of escalating therapy is
for phlegmasia cerulea dolens, which is an uncommon
presentation of acute DVT associated with higher morbidity and mortality characterized by marked swelling, pain,
and cyanosis in the affected limb. For phlegmasia cerulea
dolens, UFH should be used, and surgical consultation for
thrombectomy or thrombolysis is warranted given the high
morbidity/mortality.
19.3.2 Pulmonary embolism
As discussed in previous chapters, after diagnosis of PE,
the rst step prior to deciding therapy is risk stratication.
Initial evaluation should pay careful attention to hemodynamics, including hypotension, hypoxia, and tachycardia.
Particularly, if hypotension is noted with PE and felt to
be causing obstructive shock, therapy should be systemic
thrombolysis. Use of the PE Severity Index (PESI)
simplied PESI (sPESI)
15
should be included in this initial
evaluation. Assessment of RV enlargement and function
with cross-sectional imaging or echocardiography, along
with cardiac biomarkers (brain-natriuretic peptide and
troponin), also assist with risk stratication.
Low-risk patients should be assessed if home/outpatient
therapy is acceptable. If this can be done, DOAC therapy
with apixaban or rivaroxaban is recommended since they
do not require parenteral anticoagulation lead-in. If DOAC
is not an option for low-risk PE treatment, LMWH and
warfarin should be second-line therapy.
Intermediate-risk patients may require hospitalization
with monitoring and observation for 24–48hours. Again,
LMWH is the agent of choice for parenteral anticoagulation given its rapid onset of therapeutic effect and lesser
nursing care monitoring as compared to UFH. If stability
is demonstrated, switching after the initial observation
period for treatment with DOAC is recommended.
For patients in the intermediate-to-high-risk group,
LMWH is still the preferred parenteral agent of choice for
initial anticoagulation therapy.
17
Patients who are at high
risk for hemodynamic collapse should be considered for
catheter-based therapies (i.e., catheter-directed thrombolysis, catheter suction thrombectomy). For patients with
hemodynamically unstable, high-risk acute PE, use of UFH
is preferred to allow for exibility in advanced therapy
administration (e.g., systemic thrombolysis, extracorporeal
membrane oxygenation [ECMO] support, surgical thrombectomy). While data in the intermediate-to-high-risk
group are sparse, ongoing studies are being conducted to
elucidate if catheter-based therapies provide additional
morbidity/mortality benet. Patients who demonstrate stability with hemodynamics and vital signs can be switched
to DOAC after 48hours of stability, again with apixaban
and rivaroxaban providing ease of administration without
the need for parenteral lead-in therapy.
14
or the
16
19
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For high-risk PE patients who have hemodynamic
instability and evidence of obstructive shock, immediate
thrombolysis should be given.
17
There is strong evidence to
support full-dose thrombolytics (100 mg alteplase); however, if such patients are at high bleeding risk, it is reasonable to consider half-dose thrombolytics. Regardless of
the decision to give thrombolytics, consideration of ECMO
support in capable facilities is warranted prior to other
possible therapies and/or interventional approaches.
19.3.3 Duration of anticoagulation
Primary treatment for acute VTE is 3–6 months from initiation of anticoagulation after diagnosis.
of anticoagulation beyond the initial 3- to 6-month treatment phase should take into account ongoing patient risk
Deep Venous Thrombosis or Pulmonary Embolism
Catheter-associated VTE
(e.g., port or tunneled line)
2,12,13
Continuation
Active cancer or malignancy
Yes
factors (Figure19.1). These risk factors can be divided into
transient and nontransient factors (Table19.2).
19.3.3.1 Transient risk factors
Transient risk factors include both surgical and nonsurgical risk factors. Postprocedural and postsurgical time
period pose an increased risk of VTE in the immediate
period; however, they do not typically factor into increasing risk signicantly for recurrence. Other nonsurgical risk
factors that should be considered include extended travel
(e.g., long-haul driving without stops, air travel >8hours),
pregnancy, acute medical illness such as sepsis/infection
and inammatory conditions, active rheumatologic conditions, use of estrogen-containing hormone therapy, and
pregnancy. Other potentially transient risk factors include
patients who require central venous catheters for intrave-
No
Provoked or known transient risk factors
Yes
No
Previous DVT or PE
Yes
Yes
No
No
High bleeding risk
Yes
Minimum 3
Minimum 3 months
anticoagulation
19.1 Duration of anticoagulation.
Note: VT, venous thromboembolism; DV, deep vein thrombosis; P, pulmonary embolism.
TABLE 19.2 Risk factors for venous thromboembolism recurrence
Nontransient risk factors Transient risk factors
Cancer Surgery/procedure
Previous VTE Trauma
Genetic and acquired thrombophilia Pregnancy
Chronic medical illness such as nephrotic syndrome, vasculitis, inamma-
tory bowel disease
Obesity and metabolic syndrome Estrogen therapy
Advanced age Acute medical illness (e.g., sepsis, infection, inammatory
Chronic heart failure Active rheumatologic conditions
Chronic respiratory failure Acute central venous catheters
Minimum 6 months
anticoagulation
3 months
anticoagulation
Extended
anticoagulation
Extended travel (e.g., air travel >8hours)
conditions)
months
anticoagulation
No
Consider
Extended
anticoagulation
Abbreviations: VT, venous thromboembolism.
19.3 Selecting initial medical therapy 213
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nous access. If a transient risk factor is identied, patients
will often only require initial treatment for 3–6 months,
after which time anticoagulation can be discontinued.
19.3.3.2 Nontransient risk factors
Nontransient risk factors include medical conditions that
are nonmodiable or pose a consistent risk. These include
cancer, obesity and metabolic syndrome, previous thromboembolism, thrombophilia (e.g., protein C or S deciency,
antithrombin III deciency, APS), nephrotic syndrome,
vasculitis, inammatory bowel disease, paroxysmal nocturnal hemoglobinuria, and advanced age, among others.
If present, these factors should be considered in terms of
extending therapy beyond the initial treatment phase of
3–6 months. History of cancer, previous VTE (without
transient risk factors), and thrombophilia pose a higher
risk of recurrence and may benet from extended-phase
treatment beyond the initial 3- to 6-month treatment. Two
of the most common thrombophilia conditions (heterozygous factor V Leiden, heterozygous prothrombin gene
mutation) have shown mixed results regarding their risk
for recurrent VTE.
19.3.4 Bleeding risk factors
While most research has focused on estimating VTE recurrence risk, the risk of bleeding while using anticoagulant
therapy is critically important for medical decision making. No formal bleeding risk scores are recommended for
routine clinical practice. However, patients with a history
of bleeding while on anticoagulant therapy and those
with high-risk bleeding factors (e.g., thrombocytopenia,
advanced renal failure, concurrent use of antithrombotic
agents) may benet from shorter courses of anticoagulation to treat VTE.
For patients with an absolute contraindication for anticoagulation, such as those with active bleeding or severe
thrombocytopenia, consideration can be made for IVC
lter placement.
there is a reasonable expectation that the contraindication
to anticoagulation may resolve.
18
Retrievable lters are preferred when
19.3.5 Thrombophilia testing
For the majority of acute VTE patients, thrombophilia testing is generally not warranted, especially in the acute setting, since it will rarely change management.
to this is for APS, for which data support the use of a VKA
over DOAC. Antiphospholipid testing can be considered
for patients who develop thrombosis at a young age, have a
history of arterial and venous thrombosis, or have a history
of pregnancy loss. Acareful evaluation of family history
for thrombosis and other clotting events should be done.
Additionally, thrombophilia testing can be considered for
younger patients (<50years old) without clear VTE risk
factor or provoking factors. Thrombophilia testing may
ultimately be useful in a discussion of longer-term therapy
after acute treatment of VTE, with protein C deciency,
protein S deciency, antithrombin III deciency, and APS
conferring the highest risk for thrombosis.
19
On exception
19.3.6 Cancer screening
It is recommended that all patients have age-appropriate
cancer screening since this would constitute as a persistent
medical risk factor. Cross-sectional imaging for screening
is not recommended to replace guideline-directed cancer
screening modalities (unless the screening recommendation
is CT scan, such as in smokers for lung cancer screening).
19.3.7 Periprocedural management
There are limited data regarding the best way to approach
procedural interruption of anticoagulation in VTE patients.
Most recommendations are extrapolated from studies of
patients with atrial brillation (Table19.3, Figure19.2).
The highest risk period for acute VTE patients occurs
within the rst 1–3 months, and avoiding interruption of
anticoagulation during this initial period is advised whenever possible. If anticoagulation during this period needs to
be interrupted longer than 2–3 days, consider placement of
a temporary IVC lter until anticoagulation can be safely
restarted. Interruption of anticoagulation and the necessity
of bridging has been studied in an atrial brillation population, and though there are certainly differences in this population group compared to VTE patients, the data have not
shown to provide additional benet for bridging parenteral
anticoagulation. Similarly, studies with DOAC interruption
periprocedurally in atrial brillation patients showed comparably low rates of thrombotic events without bridging
anticoagulation.
20,21
19.3.8 Special populations
19.3.8.1 Isolated distal lower extremity DVT
Distal lower extremity DVT is dened as any thrombus
visualized in the deep venous system that is below the knee
(i.e., distal to the popliteal vein). In isolated distal lower
extremity DVT patients without severe symptoms, it is
reasonable to opt for serial imaging with ultrasonography
for observation of progression in lieu of anticoagulation.
If serial ultrasound shows extension of thrombus, particularly toward more proximal veins, then anticoagulation
should be considered. If patients have signicant symptoms, treatment with anticoagulation should be like that
of proximal DVT. Other factors that may suggest a risk
of progression include elevated D-dimer, active cancer, and
previous history of VTE.
19.3.8.2 Upper extremity VTE
Upper extremity VTEs are uncommon and, when found,
are typically associated with a central venous catheter,
thrombophilia, provoking factor or injury, or other structural pathologies such as venous thoracic outlet syndrome.
These patients should all receive anticoagulation for acute
VTE. For those with central venous catheters, anticoagulation should continue so long as the catheter remains in
place. For patients without catheters, evaluation for venous
thoracic outlet syndrome is recommended. Similarly,
thrombophilia workup may be reasonable for non-catheter-related spontaneous upper extremity VTE.
19
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