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270 Endovascular and surgical management of acute pulmonary embolism
P
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AngioVac
cannula
Filter
ump
Venous
cannula
Figure 21.4 AngioVac setup for venous thrombectomy. Jugular access is obtained and the blood drawn through the spe-
cially designed filter via a centrifugal pump that returns the blood to the femoral vein through a standard venous cannula.
are under 200 mg/dL, the dose should be reduced or the
infusion stopped. In a meta-analysis of CDT series, the
frequency of success was higher if at least 80% of patients
received locally delivered thrombolytic therapy during the
procedure (91.2% vs. 82.8%, P = 0.01) or for an extended
period of time (89.2% vs. 84.2%, P = 0.045). However, the
included studies were quite heterogeneous, making a denitive benet of catheter-directed thrombolytic treatment
over other CDTs dicult to prove.
11
To improve delivery of tPA to the pulmonary vasculature and decrease tPA infusions times (and subsequently
tPA doses), ultrasound-assisted thrombolysis (USAT) for
the treatment of massive and submassive PE may be used.
Currently, the EkoSonic Endovascular System (EKOS Corp.,
Bothwell, WA) is the only USAT device that is approved for
use in the United States. e use of ultrasound energy results
in reversible disaggregation of non-cross-linked brin bers
and opens up sites for tPA binding in order to facilitate drug
eect. Additionally, ultrasound pressure waves may increase
20
thrombus penetration by acoustic streaming.
is can be
done unilaterally or bilaterally, the latter of which is more
common. e USAT catheter is 6-Fr compatible; however,
if bilateral treatment is planned, a 10-Fr femoral venous
sheath is necessary. e pulmonary vasculature is selected
Figure 21.5 AngioVac in the right main pulmonary artery
P
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via a right jugular approach.
21.6 Catheter-directed thrombolysis 271
using standard techniques. Once wire access to the lobar
branches is obtained, the infusion catheter is advanced over
the wire and the ultrasound core is inserted that delivers
high-frequency (2.2 GHz), low energy (0.5 W per transducer) ultrasound waves.
20
e ULTIMA trial is the only randomized trial of
treatment with USAT to date.21 is trial randomized 59
patients with intermediate-risk PE (RV/LV ratio ≥1.0) to
heparin therapy or heparin plus USAT with the EkoSonic
Endovascular System to deliver either unilateral or bilateral tPA at 1 mg/hour for 15 hours. e primary endpoint
was the RV/LV ratio change from baseline to 24 hours aer
treatment. In the USAT group, placement of the catheter
was successful in 100% of patients (87% received bilateral
catheter placement). ere was a signicant dierence in the
RV/LV ratio for the USAT group (1.28 ± 0.19 to 0.99 ± 0.17
[P < 0.001] vs. heparin 1.2 ± 0.14 to 1.17 ± 0.2 [P = 0. 31]).
e mean RV/LV ratio dierence was 0.3 ± 0.2 for USAT
compared to 0.03 ± 0.16 for the heparin group (P < 0. 0 01).
However, these dierences were not signicant at 90 days.
Most RV hemodynamics were signicantly improved at 24
hours with USAT compared to heparin treatment. Mean
hospital stay was not dierent. At 90 days, mortality was
AngioVac
cannula
Filter
ump
Arterial
cannula
Oxygenator
Venous
cannula
Figure 21.6 AngioVac set up with extracorporeal membrane oxygenation.
Pump
272 Endovascular and surgical management of acute pulmonary embolism
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Overal l, these studies demonstrate the feasibilit y of USAT
for the treatment of intermediate-risk PE. However, there
are no randomized trials of USAT compared to standard
catheter-directed thrombolytic infusion. Additionally, the
endpoints for these studies are usually markers of cardiac
and pulmonary hemodynamics. ey represent surrogate
endpoints without clear correlation to long-term outcomes.
ere has been no long-term mortality or morbidity benet
demonstrated with many of these techniques to date, which
would support changing current guidelines for treatment
in submassive PE. Further eorts are necessary to delineate
the patients who will receive the most benet from these
techniques.
21.7 SURGICAL PULMONARY
Surgical pulmonary embolectomy (SPE) remains a viable
and eective means of treating massive acute PE, as well
as submassive acute PE with adverse prognosis, when
thrombolysis is contraindicated. ese are oen best performed in centers with experience in these procedures,
as candidates for this procedure are inherently unstable.
Historically, SPE was reserved for massive PE with hemodynamic instability and when standard treatment had
failed, or thrombolytics were contraindicated, as a last-line
eort. It is not unexpected that those selected for treatment
Figure 21.7 Bilateral placement of EKOS catheters into
the right and left pulmonary arteries.
not dierent and no major bleeding occurred. Four minor
bleeding events occurred with USAT and one occurred in
the heparin-only group.
21
In several larger retrospective series (Table 21.2), USAT
had simi lar eects on RV/LV ratio improvement. Engelberger
etal. reported on 52 patients with intermediate- and highrisk PE. e RV/LV ratio decreased from 1.42 ± 0.21 to
1.06 ± 0.23 aer 24 hours (P < 0.001). e greatest benet
appeared to be in high-risk patients. Complications included
a 3.8% mortality rate, major bleeding in 3.8% of patients, and
22
minor bleeding in 21% of patients.
Additionally, Kennedy
etal. reported on 60 patients treated with USAT. All patients
had successful catheter placement. Complete thrombolysis
occurred in 57% of cases and PA pressures decreased significantly. eir series reported a 5% mortality rate.23 McCabe
etal. reported on 53 patients with similar improvements in
RV/LV ratio, PA pressures, and a 9.4% bleeding rate.24 Other
series that have been reviewed have shown that USAT can
be performed with bleeding rates of 2%–20% and low morta l ity.20 Finally, in the only report to compare USAT to standard catheter-directed thrombolytic treatment, Lin et al.
reported more complete thrombolysis, shorter infusion
times (17.4 ± 5.2 vs. 25.3 ± 7.3 (h), P = 0.03), lower tPA doses
(17. 2 ± 2.4 vs. 25.4 ± 5.3 (mg), P = 0.03), and lower bleeding
complications (0% vs. 21%, P = 0.02) with USAT compared
to standard catheter-directed thrombolysis.
25
have been reported to have a poor prognosis. However, outcomes of SPE have greatly improved, and may oer benets
over medical therapy or attempts at repeated thrombolytic
treatment.26 In a literature review by Stein etal. of SPE from
1985 to 2005, average mortality declined from 32% to 20%
over this period, although there were slightly fewer patients
with pre-operative cardiac arrest in the latter group (33%
vs. 27%). Not surprisingly, those undergoing surgery with
pre-operative cardiac arrest had a 59% mortality rate compared to 20% for those who did not have a pre-operative
arrest.
More recently, Leacche et al. reported on 47 patients
undergoing emergent SPE at Brigham and Women’s Hospital,
which has taken an aggressive approach to SPE.
(95%) had RV dysfunction by echo, and indications included
a contraindication to anticoagulation (47%), failed medical
treatment (10%), and RV hemodynamic dysfunction (32%).
eir technique includes mandatory transesophageal echocardiogram (TEE) to assess RV function and the presence of
patent foramen ovale (PFO) and atrial septal defects (ASDs;
these would change operative cannulation and myocardial
protective strategies). Aer median sternotomy, patients are
placed in cardiopulmonary bypass with normothermia and
without cardioplegic arrest (unless PFO or ASD is present).
A longitudinal or transverse PA arteriotomy is made and
clots are removed under direct visualization with forceps
and suction. Fogarty catheters are avoided to prevent distal
vessel injury. An inferior vena cava lter is placed at the end
of the case. irty-day mortality occurred in three patients
(6%), of which two had a pre-operative cardiac arrest, and
EMBOLECTOMY
27
28
Nearly all
(1.7%) in
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heparin
1 death
group at
90 days
days
days
discharge
21.7 Surgical pulmonary embolectomy 273
(1) vs. CDT
14.2% (2)
USAT 9.1%
Minor
bleeding Mortality
Major
bleeding
3% heparin
0% 10% USAT,
0.99 ± 0.17
(P < 0.001); heparin
USAT 1.28 ± 0.19 to
Change in RV/LV ratio:
with10 mg tPA)
and heparin versus
heparin therapy
USAT (EkoS
1.17 ± 0.2 (P = 0.31)
1.2 ± 0.14 to
alone
1.70% 1.70% 7% at 90
ND 3.80% 21% 3.8% at 90
USAT with tPA 10 mg
Complete lysis 57%,
per side for 15
hours
USAT with tPA
9.4% overall bleeding 0% at
(1.12 ± 0.3 to
0.98 ± 0.2 [P = 0.03])
near complete lysis
41%, partial lysis 1.7%
and significantly
Reduced RV/LV ratio
35.1 ± 11.1 mg
over 19.6 ± 6 hours
24 ± 9 mg over
15.9 ± 3 hours
USAT with tPA
reduced PA systolic
(51.4 ± 15.5 to
40 ± 10.8) and mean
0% for USAT vs. 21%
pressure (33.8 ± 10.5
to 27 ± 7.6 [P < 0.01])
Urokinase and tPA USAT complete lysis
(n = 3) for CDT
100% vs. CDT 50%.
Miller score not
different
Patient
of
Number
Table 21.2 Prior studies of ultrasound assisted thrombolysis
population Treatment Outcomes
acute PE (RV/
LV≥1)
patients
2014 RCT 59 Intermediate-risk
21
etal.
Study Year Type
Kucher
(38) and
high-risk (14) PE
(48) and
high-risk (12) PE
52 Intermediate-risk
2013 Retrospective
Engelberger
60 Intermediate-risk
review
2013 Retrospective
22
etal.
Kennedy
review
23
etal.
PE
53 Intermediate-risk
review
2015 Retrospective
24
etal.
McCabe
treated with
USAT (11) vs.
25 Massive PE
review
2009 Retrospective
25
Lin etal.
CDT (14)
PA: pulmonary artery; CDT: catheter-directed thrombolysis.
Note: RCT: randomized controlled trial; RV: right ventricle; LV: left ventricle; USAT: ultrasound-assisted thrombolysis; tPA: tissue plasminogen activator; PE: pulmonary embolism; ND: no data;
274 Endovascular and surgical management of acute pulmonary embolism
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two of the three that died needed a RV assist device. Other
complications included two patients requiring reoperation
and two deep sternal wound infections. Median follow-up
was 27 months, and the 1- and 3-year survival rates were
86% (95% CI: 70%–90%) and 83% (95% CI: 66%–92%),
respectively. Most late deaths were due to cancer.28 Based on
these encouraging results, the authors have extended SPE for
submassive PE patients with massive proximal clot burden
and RV dysfunction. is aggressive approach has been replicated by others, with comparable outcomes.
29
Overall, SPE remains a viable and potentially critical
component of comprehensive care in acute PE. Patients
Guidelines 3.5.0 of the American Venous Forum on the endovascular and surgical management of acute pulmonary
embolism
No. Guideline
3.5.1 We recommend therapeutic anticoagulation with subcutaneous
LMWH, subcutaneous fondaparinux, or IV UFH for initial
anticoagulation of acute PE.
3.5.2 Anticoagulation alone is recommended for low-risk PE or
submassive PE with mild RV dysfunction.
3.5.3 Thrombolysis is recommended for massive PE if bleeding risk is
acceptable.
3.5.4 Thrombolysis is suggested for submassive acute PE that is felt to
have poor prognosis if bleeding risk is acceptable.
3.5.5 Catheter thrombectomy, thrombus fragmentation, or surgical
embolectomy is recommended for patients with massive PE
and contraindications for thrombolysis depending on local
expertise.
3.5.6 Catheter thrombectomy, thrombus fragmentation, or surgical
embolectomy is recommended for patients with massive PE
and who remain unstable after thrombolysis if local expertise is
available.
3.5.7 Catheter thrombectomy or surgical embolectomy is suggested for
patients with submassive PE judged to have poor prognosis.
3.5.8 We recommend against catheter thrombectomy or surgical
embolectomy for low-risk PE or submassive PE with minor RV
dysfunction.
Source: Adapted from Jaff MR etal. Circulation 2011;123(16):1788–830.
Note: LMWH: low-molecular-weight heparin; IV: intravenous; UFH: unfractionated heparin; PE: pulmonary embolism; RV: right ventricle.
should be referred before the onset of cardiogenic shock
and have large central thrombus burdens (within the main
trunk or right or le main PA). Surgery can be performed
with normothermia and with or without bypass, aortic cross
clamping, and cardioplegic arrest. Only visualized thrombus is removed and inferior vena cava lters are placed at
case completion due to the risk of recurrent PE.
4,28
As outcomes with this re-emerging technique have improved,
this remains a viable treatment options for those with massive and submassive PE, making a coordinated multidisciplinary approach to PE critical to tailoring treatment based
on patient factors and institutional expertise.
Grade of
recommendation
(1: strong; 2:
weak)
1 A
1 B
1 B
2 C
1 C
1 C
2 C
2 C
Grade of evidence (A:
high quality; B:
moderate quality; C:
REFERENCES
●
= Key primary paper
★
= Major review article
1. Cushman M, Tsai AW, White RH etal. Deep vein
thrombosis and pulmonary embolism in two cohorts:
The longitudinal investigation of thromboembolism
etiology. Am J Med 20 0 4;117(1):19–25.
2. Lloyd-Jones D, Adams RJ, Brown TM etal. Executive
summary: Heart disease and stroke statistics—2010
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Association. Circulation 2010;121(7):948–54.
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Antithrombotictherapy for VTE disease:
Antithrombotic Therapy and Prevention of
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ChestPhysicians Evidence-Based Clinical
PracticeGuidelines. Chest 2 012;141(2
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4. Jaff MR, McMurtry MS, Archer SL etal. Management
of massive and submassive pulmonary embolism,
iliofemoral deep vein thrombosis, and chronic
thromboembolic pulmonary hypertension: A scientific statement from the American Heart Association.
Circulation 2011;123(16):1788 –830.
★
5. Goldhaber SZ and Elliott CG. Acute pulmonary
embolism: Part I: Epidemiology, pathophysiology,
and diagnosis. Circulation 2003;108(22):2726–9.
6. Elliott CG. Pulmonary physiology during pulmonary
embolism. Chest 1992;101(4 S uppl.):163S–71S.
7. Castillo C and Tapson VF. Right ventricular responses
to massive and submassive pulmonary embolism.
Cardiol Clin 2012;30(2):233–41.
8. Kuo WT. Endovascular therapy for acute pulmonary
embolism. J Vasc Interv Radiol 2012;23(2):167–79.e4;
quiz 179.
9. Provias T, Dudzinski DM, Jaff MR etal. The
Massachusetts General Hospital Pulmonary
Embolism Response Team (MGH PERT): Creation
of a multidisciplinary program to improve care of
patients with massive and submassive pulmonary
embolism. Hosp Pract (1995) 2014;42(1):31–7.
10. Schmitz-Rode T, Janssens U, Duda SH, Erley CM,
and Gunther RW. Massive pulmonary embolism:
Percutaneous emergency treatment by pigtail rotation catheter. J Am Coll Cardiol 2000;36(2):375–80.
★
11. Kuo WT, Gould MK, Louie JD, Rosenberg JK, Sze DY,
Hofmann LV. Catheter-directed therapy for the treatment of massive pulmonary embolism: Systematic
review and meta-analysis of modern techniques.
JVasc Interv Radiol 2009;20(11):1431–40.
12. Kuo WT, van den Bosch MA, Hofmann LV, Louie JD,
Kothary N, and Sze DY. Catheter-directed embolectomy, fragmentation, and thrombolysis for the treatment of massive pulmonary embolism after failure of
systemic thrombolysis. Chest 2008;134(2):250–4.
13. Koning R, Cribier A, Gerber L etal. A new treatment
for severe pulmonary embolism: Percutaneous rheolytic thrombectomy. Circulation 1997;96(8):2498–500.
14. Zeni PT Jr., Blank BG, and Peeler DW. Use of
rheolytic thrombectomy in treatment of acute
massive pulmonary embolism. J Vasc Interv Radiol
20 03;14(12):1511–5.
15. Dwarka D, Schwartz SA, Smyth SH, and O’Brien
MJ. Bradyarrhythmias during use of the AngioJet
system. J Vasc Interv Radiol 2006;17(10):1693– 5.
16. Kucher N, Windecker S, Banz Y etal. Percutaneous
catheter thrombectomy device for acute pulmonary
embolism: In vitro and in vivo testing. Radiology
2005;236(3):852–8.
17. Eid-Lidt G, Gaspar J, Sandoval J etal. Combined
clot fragmentation and aspiration in patients
with acute pulmonary embolism. Chest
2008;134(1):54–60.
18. Pasha AK, Elder MD, Khurram D, Snyder BA, and
Movahed MR. Successful management of acute
massive pulmonary embolism using AngioVac
suction catheter technique in a hemodynamically unstable patient. Cardiovasc Revasc Med
2014;15(4):240–3.
●
19. Donaldson CW, Baker JN, Narayan RL etal.
Thrombectomy using suction filtration and
veno-venous bypass: Single center experience
with a novel device. Catheter Cardiovasc Interv
2015;86(2):E81–7.
★
20. Engelberger RP and Kucher N. Ultrasound-assisted
thrombolysis for acute pulmonary embolism: A systematic review. Eur Heart J 2014;35(12):758–64.
●
21. Kucher N, Boekstegers P, Muller OJ etal.
Randomized, controlled trial of ultrasoundassisted catheter-directed thrombolysis for acute
intermediate-risk pulmonary embolism. Circulation
2014;129(4):479–86.
22. Engelberger RP, Moschovitis A, Fahrni J etal.
Fixed low-dose ultrasound-assisted catheterdirected thrombolysis for intermediate and
high-risk pulmonary embolism. Eur Heart J
2015;36(10):597–604.
23. Kennedy RJ, Kenney HH, and Dunfee BL.
Thrombus resolution and hemodynamic recovery using ultrasound-accelerated thrombolysis in
acute pulmonary embolism. J Vasc Interv Radiol
2013;24(6):841–8.
24. McCabe JM, Huang PH, Riedl L, Eisenhauer AC,
and Sobieszczyk P. Usefulness and safety of ultrasound-assisted catheter-directed thrombolysis
for submassive pulmonary emboli. Am J Cardiol
2015;115(6):821– 4.
●
25. Lin PH, Annambhotla S, Bechara CF etal.
Comparison of percutaneous ultrasound-accelerated
thrombolysis versus catheter-directed thrombolysis
in patients with acute massive pulmonary embolism.
Vascular 2009;17(Suppl. 3):S137–47.
26. Meneveau N, Seronde MF, Blonde MC etal.
Management of unsuccessful thrombolysis in
acute massive pulmonary embolism. Chest
20 06;129(4):10 43 – 50.
27. Stein PD, Alnas M, Beemath A, and Patel NR.
Outcome of pulmonary embolectomy. Am J Cardiol
2007;99(3):421–3.
●
28. Leacche M, Unic D, Goldhaber SZ etal. Modern
surgical treatment of massive pulmonary embolism:
Results in 47 consecutive patients after rapid diagnosis and aggressive surgical approach. J Thorac
Cardiovasc Surg 2005;12 9(5):1018–23.
29. Yalamanchili K, Fleisher AG, Lehrman SG etal. Open
pulmonary embolectomy for treatment of major pulmonary embolism. Ann Thorac Surg 2004;77(3):819–
23; discussion 823.
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Treatment algorithms for acute venous
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thromboembolism: Current guidelines
ANDREA T. OBI AND THOMAS W. WAKEFIELD
22
22.1 Introduction 277
22.2 Prophylaxis 277
22.3 Diagnosis 278
22.4 Treatment of DVT 278
22.5 Treatment of iliofemoral DVT 279
22.6 Treatment of PE 282
22.7 Superficial venous thrombophlebitis 283
22.1 INTRODUCTION
Venous thromboembolism (VTE) is a source of major morbidity and mortality. e incidence of VTE exceeds 1/1000,
and there are an estimated 200,000 rst lifetime cases diagnosed in the United States every year. e 7-day mortality
of patients suering from VTE is 25%, with up to a third
of patients with pulmonary embolism (PE) dying suddenly.
VTE is the fourth leading cause of death in Western society
and the third leading cause of cardiovascular death behind
myocardial infarction and stroke. Of those individuals surviving their event, approximately 30% will develop recurrent VTE within 10 years, and greater than 20%–30% will
develop the post-phlebitic syndrome over this time period
(even higher with iliofemoral deep vein thrombosis [DVT]).
VTE is more frequent in the elderly, and the incidence of
thrombosis increases signicantly beyond 60 years of age.
As our population ages, the VTE incidence will increase.
Clearly, VTE is a problem that is encountered by a wide
variety of patients and providers. is chapter is intended
to guide those involved in patient care by providing direct
access to easy-to-use algorithms for commonly encountered clinical scenarios. Standardized treatment management plans are dened through the algorithms. ese may
decrease practice variation and be useful with inexperienced sta, and may provide some control over risk management. As a word of caution, algorithms sometimes fail to
account for diagnostic uncertainty, unique clinical circumstances, and patient preference/anxiety, and may perform
dierently amongst dierent populations or when used by
22.8 Severe bleeding from novel anticoagulants 283
22.9 Aspirin for extended VTE treatment 283
22.10 Central venous thrombosis 285
22.11 Effort thrombosis 285
22.12 Mesenteric venous thrombosis 285
22.13 IVC filters 286
References 287
dierent care providers. Clinician and patient acceptance
are required in order to use algorithms, and every eort has
been made to ensure that the algorithms listed utilize tests
that are widely available and have been validated for the disease process being evaluated. e following algorithms and
supporting text are obtained from Chapters 18, 19, 20, 21,
23, 24, 25, 26, 27, and 28; key references are as listed at the
conclusion of each chapter.
22.2 PROPHYLAXIS
VTE can be prevented, particularly in the hospitalized
patient (see Chapter 23). Appropriately delivered prophy-
laxis is cost-eective, reduces VTE by 50%–70%, and carries an acceptably low risk of hemorrhage. Without DVT
prophylaxis, VTE rates are high for both surgical and nonsurgical hospitalized patients. Although the incidence of
VTE varies by both patient and procedure, VTE may occur
in up to 20% of surgical patients. As more than 28 million
surgical procedures are performed each year in the United
States, and more than 35 million non-surgical patients are
admitted each year to U.S. hospitals, this is a major health
problem. With the evolution toward expanded outpatient
delivery of medical and surgical services, only the sickest
patients are hospitalized. e thrombotic event rate may
be as high as 16% in these non-surgical patients without
prophylaxis. PE accounts for nearly 10% of all hospital
deaths and is one of the most preventable causes of mortality. PE may occur without prior warning, and sudden
death may be the initial symptom of disease. According to
277
278 Treatment algorithms for acute venous thromboembolism
Venous thromboembolism prevention
*Consider caprini online risk calculator
http://venousdisease.com/caprini-dvt-risk-assessment
IPC- intermittent pneumatic compression pumping
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recent guidelines, low-dose unfractionated heparin, lowmolecular-weight heparin (LMWH), or fondaparinux,
are safe and eective prophylaxis strategies for hospitalized patients with other medical conditions. For bleeding
patients or those who are at low risk of VTE development,
mechanical compression (intermittent pneumatic compression) is indicated (Figure22.1). For patients at moderate and
high risk of VTE, Figure 22.1 provides recommendations
for thromboprophylaxis regimens.
22.3 DIAGNOSIS
e diagnostic workup of a suspected VTE depends on the
degree of clinical suspicion of DVT or PE (see Chapter 18).
Several validated scoring systems exist to aid the clinician
in determining the pre-test probability of such a diagnosis, most notably the Well’s score for DVT (Table 22.1) and
Assess patient and procedure
specific major bleeding risk
Is bleeding risk
high?
PE (Table 22.2) and the Antwerp score for PE (Table 22.3).
Ascore resulting in a low or moderate probability of DVT
or PE should guide the clinician to D-dimer as the initial
“rule-out” test (Figures 22.2 and 22.3). A high probability
should trigger a more aggressive workup with duplex ultrasound (Figure 22.2) if DVT is suspected, or PE protocol
computed tomography (CT) (Figure 22.3) if PE is suspected.
Importantly, modern-day diagnosis should include only
noninvasive testing with a low risk prole. ere is little to
no role for invasive tests, such as lower extremity venography or pulmonary angiography, except under unusual circumstances or when invasive interventions are planned.
22.4 TREATMENT OF DVT
e mainstay of therapy for the diagnosis of acute VTE
is prompt anticoagulation (see Chapter 19). Generally,
Yes
IPC
Very low Low Moderate High
Early
ambulation
No
Assess patient and procedure
specific thrombotic risk*
IPC
LDUFH,
LMWH, or
IPC
LDUFH
LMWH
Combined with
IPC
Very high VTE risk; examples
• Cancer surgery
• Prior surgery related VTE
• Major orthopedic surgery
Yes
Continue pharmacologic
prophylaxis for 4 weeks
Figure 22.1 Practical approach to thromboprophylaxis in the hospitalized patient. IPC: intermittent pneumatic compres-
sion; LDUFH: low-dose unfractionated heparin; LMWH: low-molecular-weight heparin; UFH: unfractionated heparin; VTE:
venous thromboembolism.
/
22.5 Treatment of iliofemoral DVT 279
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Table 22.1 Wells etal. clinical model for predicting the
pre-test clinical probability of deep vein thrombosis
a
Clinical characteristic Score
Active cancer (patient receiving treatment for
1
cancer within the previous 6 months or
currently receiving palliative treatment)
Paralysis, paresis, or recent plaster
1
immobilization of the lower extremities
Recently bedridden for 3 days or more or
1
major surgery within the previous 12 weeks
requiring general or regional anesthesia
Localized tenderness along the distribution of
1
the deep venous system
Entire leg swollen 1
Calf swelling at least 3 cm larger than that on
1
the asymptomatic side (measured 10 cm
below tibial tuberosity)
Pitting edema confined to the symptomatic leg 1
Collateral superficial veins (non-varicose) 1
Previously documented deep vein thrombosis 1
Alternative diagnosis at least as likely as deep
−2
vein thrombosis
Source: Reprinted with permission from Wells PS etal. N Engl J
a
Med 2003;349(13):1227–35.
A score of 2 or higher indicates that the probability of deep vein
thrombosis is likely; a score of less than 2 indicates that the
probability of deep vein thrombosis is unlikely. In patients with
symptoms in both legs, the more symptomatic leg is used.
Table 22.2 Wells etal. short clinical score list for
pulmonary embolism
Criteria Score
Clinical signs and symptoms of deep vein
3.0
thrombosis: minimal swelling of the leg
and pain on palpation of the deep leg
veins
Pulmonary embolism more likely than an
3.0
alternative diagnosis
Heart beat frequency >100 beats per minute 1.5
Recent immobilization or surgery within
1.5
<4weeks
Documented history of deep vein
1.5
thrombosis and/or pulmonary embolism
Hemoptysis 1.0
Recent history of malignancy within <6months
1.0
(treatment or palliative treatment)
Clinical score for pulmonary embolism
Low ≤2
Moderate 2.0–6.0
High ≥6
Source: From Michiels JJ et al. Semin Vasc Med 2002;2(4):345–51.
With permission.
Table 22.3 Antwerp clinical score list for pulmonary
embolism
Criteria Score
Age >60 years 0.5
One or more risk factors for venous
1.5
thromboembolism
One or more eliciting circumstances for venous
1.0
thromboembolism
Respiratory signs and symptoms
Dyspnea 1.5
Pleuritic pain 1.0
Non-retrosternal, non-pleural chest pain 1.0
<92% (<3 L O2) 1.0
P
aO2
Hemoptysis 1.0
Pleural rub 1.0
Cardiac and other signs and symptoms
Heart beat frequency >100 beats per minute 1.0
Temperature 37.5°C and 38.6°C 1.0
Chest X-ray: atelectasis and/or unilateral
1.0
diaphragm elevation suspicious for
pulmonary embolism and no other
explanation
Leg symptoms suspicious of deep vein
3.0
thrombosis (swelling, pain, etc.) (clinical
score of Wells etal. for deep vein
thrombosis)
Signs of circulatory and/or respiratory
6.0
insufficiency: 1, 2, or 3
1. Hypotension (systolic <90 mmHg and heart
frequency >100 beats per minute)
2. Respiratory insufficiency (artificial breathing
>3 L O
)
2
3. Recent decompensation cordis right
Clinical score for pulmonary embolism
Low ≤3
Moderate 3.0–6.0
High ≥6
Source: From Michiels JJ etal. Semin Vasc Med 2002;2(4):345–51.
With permission.
LMWH is preferred, although unfractionated heparin
remains an excellent option in patients with renal insuciency or if there is concern regarding bleeding risk, given
its shorter half-life and more reliable reversal with protamine. Figure 22.4 outlines decision making regarding a
variety of commonly encountered comorbid conditions
presenting with DVT, such as pregnancy and cancer.
22.5 TREATMENT OF ILIOFEMORAL DVT
Management following a diagnosis of iliofemoral DVT
(Figure 22.5) is anticoagulation therapy along with leg
elevation and compression; ambulation is encouraged (see
Chapter 19).
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