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280 Treatment algorithms for acute venous thromboembolism
Algorithm for diagnosing pulmonary embolism
https://t.me/med1917
Suspected acute DVT
Calculate pretest clinical probability
Low/moderate probability
High probability
Negative
No
treatment
Negative
treatment
No
D-dimer
Positive/indeterminate
Positive
Treatment
Venous US
Negative
No
treatment
Indeterminate
MRI/CV
Positive
Treatment
Negative Po sitiveIndeterminate
Serial US
5–7 days
Negative
No
Treatment
treatment
Positive
Venous US
Treatment
Negative
No
treatment
MRI/CV
Positive
Treatment
Algorithm for diagnosing DVT
Figure 22.2 Algorithm for diagnostic workup of suspected DVT. Note that the pre-test probability can be calculated utiliz-
ing the Well’s score (described in the text). In patients for whom the D-dimer is likely to be elevated from other sources
(recent surgery or trauma), it is reasonable to proceed directly to ultrasound, even with low suspicion. CV: contrast venography; DVT: deep vein thrombosis; MRI: magnetic resonance imaging; US: ultrasound.
Suspected acute PE
Calculate assessment/probability
Low probability
D-dimer
Negative
No
treatment
Negative NegativePositive Po sitive
No
treatment
Repeat CT angio or CTV/CTA if poor quality
If CT angio only, US or MRV
Pulmonary scintigraphy
Digital subtraction angiography
Serial ultrasound
CT angio vs.
CTV/CTA
Segmental or
subsegmental
Moderate probality
D-dimer
Negative
No
treatment
Main or
lobar PE
Treat
PositivePositive
CT angio vs.
CTV/CTA
No
treatment
Option if CT angio only,
US or MRV
Treat
High probability
CT angio vs. CTV/CTA
Negative
Repeat if poor quality
If CTA only, US or
MRI venography
Pulmonary
scintigraphy
Digital subtraction
angiography
Serial US
Positive
Treat
Figure 22.3 Algorithm for diagnostic workup of suspected PE. CT: computed tomography; CTA: CT angiogram; CTV: CT
venogram; MRI: magnetic resonance imaging; MRV: magnetic resonance venography; PE: pulmonary embolism; US: ultra-
3
sound. (Adapted with permission from Stein PD etal.; PIOPED II Investigators. Radiology 20 07;242(1):15–21.
)
Conrmed diagnosis of
antagonist for 3 months
Management of iliofemoral DVT
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DVT
22.5 Treatment of iliofemoral DVT 281
Uncomplicated DVT case:
start anticoagulation
DVT without comorbid
risk factors
Start vitamin K antagonist
with LMWH, discontinue
LMWH when stable INR
(2.0–3.0) is reached
For spontaneous DVT
continue vitamin K
antagonist for 3–6 months
Contraindication to or
failure of anticoagulation
Consider IVC lterLMWH
Start anticoagulation
when safe to do so
DVT during pregnancy
Continue LMWH until 24 h
prior to delivery
Continue anticoagulation
for a minimum of 6 weeks
For DVT caused by
reversible risk factor
continue vitamin K
Limb threatening DVT or
proximal DVT < 14 days,
good functional status,
long life expectancy
Catheter directed
thrombolysis (CDT)
followed by
anticoagulation
Cancer related DVT
Anticoagulation with
LMWH for 6 months,
extend anticoagulation
until malignancy cured
For DVT cases at high risk
of recurrence, consider
extended duration
anticoagulation at INR 2–3
Figure 22.4 Management of acute DVT as recommended by ACCP guidelines, does not include management of new oral anti-
coagulants. Of note, some of the new oral anticoagulants do not require a LMWH bridge, and are not monitored with INRs.
CDT: catheter-directed thrombolysis; DVT: deep vein thrombosis; INR: international normalized ratio; IVC: inferior vena cava;
LMWH: low-molecular-weight heparin.
Immediate anticoagulation Rapid CT scan with contrast
Leg elevation
Long leg compression
Ambulation permitted
Patient physically active
Strategy of thrombus removalEvaluate vena cava
No Ye s
Contraindication to thrombolysis
PM thrombolysis
• Head
• Chest
• Abdomen
• Pelvis
YesNo
Filter for free-
oating thrombus
Venous thrombectomy
and/or
CD thrombolysis
• Correct iliac vein stenosis
• Arteriovenous stula
• Catheter-directed anticoagulation
Anticoagulation
plus
compression
Correct underlying venous lesion
Figure 22.5 Management of acute occlusive proximal DVT. Aggressive therapies should only be considered in individuals
who are mobile, with long life expectancy. CD: catheter-directed; CT: computed tomography; DVT: deep vein thrombosis;
PM: pharmacomechanical.
282 Treatment algorithms for acute venous thromboembolism
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Patients with iliofemoral DVT who are ambulatory
should be considered for thrombus removal (Figure 22.5).
Imaging of the inferior vena cava (IVC) by CT or duplex
imaging is important in order to assess the degree of IVC
involvement. An IVC lter is recommended for patients
with free-oating, non-occlusive IVC thrombus. Aer
the extent of the disease has been established, contraindications to either surgical or catheter-based techniques
should be reviewed. e majority of patients with iliofemoral DVT should be oered thrombus removal via a catheter-directed approach. Patients with occlusive thrombus
of the femoral vein involving the profunda femoris have
obliterated venous drainage from the lower extremity and
oen exhibit severe post-thrombotic morbidity. Although
most patients receiving anticoagulation may be treated
as outpatients, those with common femoral vein and/or
iliac vein occlusion should be hospitalized and undergo a
procedure in order to restore patency and provide unobstructed venous drainage into the IVC from their lower
ex tremit y.
Pulmonary embolism
22.6 TREATMENT OF PE
For acute PE, treatment needs to address: (1) prevention of
new thrombus; (2) clearance of obstructing thrombus from
the pulmonary artery (either rapidly or over time); and
(3) reduction of right ventricular (RV) dysfunction when
present (see Chapter 21). rombolysis is recommended
for patients with low bleeding risk who have massive PE.
In addition, patients with sub-massive PE with new hemodynamic instability, worsening respiratory insuciency,
severe RV dysfunction, or major myocardial necrosis may
be considered for thrombolysis (Figure 22.6). Catheterbased therapy or surgical embolectomy, however, may be
recommended in a number of circumstances. ese include
a contraindication to systemic thrombolysis (recent intracranial hemorrhage or surgery, recent spinal surgery, recent
head trauma, intracranial neoplasm, uncontrolled hypertension, or active or recent bleeding), a signicant risk of
bleeding, or insucient time to allow infusion and the eect
of systemic thrombolytics in the acute setting. Finally, some
Contraindication to
No
Initiate systemic
thrombolysis
[or consider catheter
directed thrombolysis]
Massive PE
thrombolysis?
Consider multidisciplinary
assessment
Yes
Continue anticoagulation
consider:
• Low dose thrombolytic
• Catheter-based therapy
• Surgical embolectomy
Initiate therapeutic
anticoagulation
Yes
Yes
Hypotension?
[SBP<90 mmHg for 15 min]
Submassive PE
with RV strain
[abnormal echo or
High risk features?
No
biomarkers]
Yes
No
No
High risk features with
potential benefit with
thrombolysis
1. Evidence of shock or
respiratory failure
2. Evidence of moderate
to severe RV strain
Low risk PE
Heparin anticoagulation
Figure 22.6 Management of PE, depending on the presentation massive, submassive, or low risk.
22.9 Aspirin for extended VTE treatment 283
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patients will fail to improve despite thrombolytic treatment
and require more aggressive therapy, such as catheter-based
therapy or surgical embolectomy.
22.7 SUPERFICIAL VENOUS
THROMBOPHLEBITIS
When seeking a diagnosis of DVT, occasionally a patient
with the diagnosis of isolated supercial venous thrombophlebitis (SVT) will be encountered (see Chapter 27) (Figure
22.7). If concurrent DVT exists, the patient should be man-
aged as outlined in Figures 22.4 and 22.5. Patients with
milder forms of isolated SVT are best managed with nonsteroidal anti-inammatory drugs, compression and warm
compresses, and ambulation. ose with moderate disease
should be managed more aggressively with either prophylactic LMWH or fondaparinux (Figure 22.7). is is dened
as SVT located 3 cm distal to the saphenofemoral junction
(SFJ) and at least 5 cm in length. If the patient develops DVT
or PE, therapeutic anticoagulation should be considered
(Figures 22.4 and 22.5). For patients that cannot tolerate
anticoagulation, great saphenous vein (GSV) disconnection
and ligation are appropriate at the SFJ when thrombus burden is moderate. Surgical treatment with GSV ablation and
phlebectomies of the involved branch varicosities should be
considered for patients with symptomatic SVT and evidence
of venous insuciency (conrmed by duplex ultrasound).
However, this is most eectively performed aer the phlebitis
has resolved, usually within 3 to 6 months of the acute event.
clinician should be prepared to encounter the occasional
patient with a severe bleeding complication or who needs
urgent reversal of coagulopathy for emergent surgical intervention or in the setting of major trauma (see
Chapter 19).
e approach for the reversal of the new oral anticoagulants should be determined by the patient’s clinical status
(Figure22.8). In the case of non-urgent reversal, treatment
involves withholding the anticoagulant for 2–4 days. In the
setting of major bleeding, withholding therapy is not sufcient, and additional measures should be taken. Proposed
reversal measures include the administration of activated
charcoal (dabigatran only) in the event of overdose, the
administration of fresh-frozen plasma, and treatment with
activated or inactive four-factor prothrombin complex
concentrates (PCC), recombinant factor VIIa (rFVIIa),
and hemodialysis (for dabigatran only). Taking into consideration the risk of continued bleeding versus the risk of
thrombosis, a sensible approach would be to initiate fourfactor PCC in the case of major bleeding from rivaroxaban
or apixaban, with the initiation of a pro-hemostatic agent
(aPCC [activated PCC] or rFVIIa) if coagulopathy fails
to reverse. In the case of major bleeding from dabigatran,
the data regarding the use of rFVIIa and aPCC are largely
equivocal, likely because activated factor VIIa is a component of aPCC. A reversal agent has now been Food and
Drug Administration approved for dabigatran (idarucizumab), although this is not widely available at all hospitals,
and a number of agents are under development for the antiXa inhibitors.
22.8 SEVERE BLEEDING FROM NOVEL
ANTICOAGULANTS
22.9 ASPIRIN FOR EXTENDED VTE
TREATMENT
With the approval of the direct thrombin inhibitor dabigatran and the direct Xa inhibitors apixaban, rivaroxaban and edoxaban for the treatment of acute DVT, the
Mild
<5 cm of thrombus length
Moderate
At least 3 cm distal to SFJ
At least 5 cm of thrombus length
SVT
Associated venous insufficiency
Associated VTE
or
thrombus <3 cm from
(or involving) the SFJ
Figure 22.7 Management of SVT. GSV: great saphenous vein; LMWH: low-molecular-weight heparin; NSAID: non-steroidal
anti-inflammatory drug; SFJ: saphenofemoral junction; SVT: superficial venous thrombosis; VTE: venous thromboembolism. (Reproduced with permission from Karthanos C et al. Superficial vein thrombosis in patients with varicose veins: Role
of thrombophilia factors, age and body mass. Eur J Vasc Endovasc Surg 2012;43:355–58.
Traditionally, there has been little role for the use of aspirin
(ASA) in the treatment or prevention of VTE (see Chapter
NSAIDs
Compression
Warm compresses
Fondaparinux 2.5 mg daily
Medical management (as above) and
interval GSV ablation and phlebectomy
Therapeutic anticoagulation
or
LMWH 40 mg daily
4
)
284 Treatment algorithms for acute venous thromboembolism
treatment
Anticoagulation
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Patient assessment:
Name and dose of medication
Timing of last dose
Indication for therapy
Concurrent antiplatelet therapy
Hemodynamic status
Location and source of bleeding
Evaluate renal and hepatic function
CBC and coagulation parameters
Apixaban
Monitoring
parameters:
PT, aPTT, INR,
anti-factor Xa
Supportive measures: treat anemia with packed red blood cells, treat DIC with fresh frozen plasma, consider platelet transfusion if
on concurrent antiplatelet therapy; consider use of desmopressin and antifibrinolytic agents for ongoing hemorrhage.
Reversal agents:
Four factor PCC (50 U/kg)
Activated PCC (80 U/kg)
Rivaroxaban Dabigatran
Monitoring
parameters:
PT, INR,
anti-factor Xa
Reversal agents:
Four factor PCC (50 U/kg)
Activated PCC (80 U/kg)
Reversal agents:
Activated PCC (80 U/kg)
Hemodialysis
Recombinant factor VIIa
Monitoring
parameters:
aPTT, ECT, TCT,
hemoclot assay
Figure 22.8 Reversal of novel anticoagulants. aPTT: activated partial thromboplastin time; CBC: complete blood count
test; DIC: disseminated intravascular coagulation; ECT: ecarin clotting time; INR: international normalized ratio; PCC:
prothrombin complex concentrate; PT: prothrombin time; TCT: thrombin clotting time. (Reproduced with permission from
Knepper J etal. A systematic update on the state of novel anticoagulants and a primer on reversal and bridging. J Vasc
Surg: Venous Lymphat Disord 2013;1(4):418–26.
6
)
19). However, the new INSPIRE trial has reintroduced ASA
as a potentially useful adjunct in patients who are at moder-
VTE
ate risk of recurrent VTE (Figure 22.9). For patients who have
a provoked DVT, 3 months of anticoagulation is adequate.
For those patients with unprovoked (idiopathic) VTE and
Provoked
Unprovoked
a high risk of recurrence, who would normally need longterm or life-long anticoagulation, he or she should remain
on either oral vitamin K antagonist or one of the novel oral
anticoagulants, and not undergo ASA therapy. For patients
3 months
anticoagulation
3–6 months
anticoagulation
with unprovoked VTE and moderate risk of recurrence, the
use of one baby ASA per day, rather than nothing, would be
Low risk Moderate risk High risk
indicated. For patients with an unprovoked VTE and low
risk of recurrence, no further therapy is indicated. e primary challenge faced by clinicians is dierentiating the low-
No further
ASA
risk patient from the moderate-risk patient. Factors that have
been found to be important include male gender, elevated
D-dimer, signicant residual scar tissue, presence of signicant thrombophilia or, importantly, multiple thrombophilia
states, age >65 years, and presence of post- thrombotic syndrome (least important in our opinion). erefore, if the
patient has one or more risk factor for recurrence from this
group, then one baby ASA a day is indicated.
Figure 22.9 Incorporation of ASA into the VTE extended
treatment paradigm. ASA: aspirin; VTE: venous thromboembolism. (Reproduced with permission from Wakefield
TW, Obi A, and Henke PK. An aspirin a day to keep
the clots away: Can aspirin prevent recurrent thrombosis in extended treatment for VTE? Circulation 2014;
130(3):1031–33.
5
)
22.12 Mesenteric venous thrombosis 285
Partial or complete effort
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22.10 CENTRAL VENOUS THROMBOSIS
Acute central venous thrombosis associated with pacemaker
wires, central venous catheters, or dialysis catheters is usually asymptomatic (see Chapter 25). Diagnosis starts with
a clinical examination, followed by a duplex ultrasound
examination. Once the diagnosis of upper extremity DVT
is conrmed, the mainstay of treatment is anticoagulation.
ere is a limited role for thrombectomy or thrombolysis,
except in the setting of phlegmasia, in which the viability of
the limb is jeopardized (Figure 22.10). rombus prevention
is best obtained by placing the catheter tip at the junction
of the right atrium with the superior vena cava. Improving
catheter and wire proles by making them less thrombogenic may also play a role in decreasing central venous
thrombosis.
22.11 EFFORT THROMBOSIS
For patients with thrombosis associated with thoracic outlet obstruction, the best initial procedure (more accurately,
having the best chance of success) is dened by the duration
of symptoms, whereas the subsequent method of thoracic
outlet decompression is dened by the status of the residual vein and symptoms (see Chapter 24). Decompression
should immediately follow thrombolysis (Figure 22.11).
Note that in a patient with chronic thrombus who cannot
be recanalized and is not signicantly symptomatic, rst rib
resection is favored. Discussion is individualized, and the
Central venous thrombosis
diagnosed
Phlegmasia of
upper extremity
thrombosis
Duration of symptoms
More than 14
days
Venography with attempt at wire
passage, but unlikely to be
successful
Remains
completely
occluded
Symptom
status
Severe None or mild
Venous
reconstruction
Anticoagulate for 3 to 6 months, reimage (ultrasound)
Complete
success,
normal vein
First-rib
resection
Less than 14
days
Venography with thrombolysis if
wire passes
Partially open
and/or residual
intrinsic defect
TA first rib
resection
Anticoagulate and observe?
Open, repair, and patch?
Angioplasty (or stent)?
Figure 22.11 Management of venous effort thrombosis,
also known as Page–Schroetter disease.
Clinical suspicion for
mesenteric venous
thrombosis
Confirm diagnosis
with CT angiography*
Bowel infarction, perforation, peritonitis
Yes
Consider
thrombolysis/
thrombectomy
Do not remove
catheter
Central venous
catheter/
dialysis catheter
Is catheter
needed?
Yes
Recommend
anticoagulation
for 3–6 months
No
Pacemaker wires
Do not remove
wires
No
Remove catheter
Figure 22.10 Management of upper extremity deep vein
thrombosis. Note that if the patient is unable to undergo
anticoagulation, consider superior vena cava filter
placement.
No, but patient very
No
Anticoagulation
symptomatic and/or
extensive thrombus
burden
Anticoagulation,
consider CDT if
available
Yes
Anticoagulation,
urgent surgical
referral and bowel
resection
Figure 22.12 Management of mesenteric venous throm-
bosis. Magnetic resonance angiography or ultrasound may
serve as alternative imaging modalities if CT angiography
is not possible. Note that catheter-directed therapies
may be available at select institutions. Only rarely will
thrombus be amenable to operative thrombectomy. CDT:
catheter-directed thrombolysis; CT: computed tomography.
advantages and disadvantages of both resection and leaving
the rib alone are unusually closely discussed.
22.12 MESENTERIC VENOUS
THROMBOSIS
Clinical observations suggest that immediate anticoagulation with heparin for mesenteric venous thrombosis
286 Treatment algorithms for acute venous thromboembolism
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(MVT) early in the course of the disease improves survival,
reduces thrombus propagation, and reduces recurrence (see
Chapter28) (Figure 22.12). Gastrointestinal bleeding is not
necessarily a contraindication to anticoagulant therapy,
whereas the risk of bleeding must be weighed against the
risk of bowel infarction. Observational studies suggest that
chronic anticoagulant use reduces the incidence of recurrent venous thrombosis by a third. In general, anticoagulation should be continued until provoking factors have been
eliminated, if possible. In those patients whose MVT can be
attributed to temporary risk factors, 3 months of anticoagulants is likely to be reasonable. Expert opinion would suggest that antibiotic therapy should be provided for patients
with signs or symptoms of bowel compromise.
Endovascular therapies may be pursued for selected
patients with acute MVT that is diagnosed early in the course
of the disease before bowel infarction or peritonitis develop
(Figure 22.12). Mechanical thrombectomy may be combined with lytic therapy. e need for surgical intervention
in patients with MVT is not universal and may be necessary
for only a minority. Acute mesenteric ischemia accompanied
by peritonitis or bowel infarction is an accepted indication
for surgical intervention and resection of involved bowel. e
key to successful surgery is to resect sucient bowel to ensure
proper anastomotic healing and halt thrombus propagation,
while preserving as much viable intestine as possible. Oen,
the surgical procedure is staged with a repeat (“second-look”)
laparotomy performed 1 day later. Post-operatively, anticoagulants should be initiated as soon as hemostasis is ensured.
rombectomy remains a potential treatment option for
selected patients, yet must be pursued quickly, as thrombus
maturation (beyond 3 days) reduces its success.
22.13 IVC FILTERS
Vena caval lters provide protection against PE without the
signicant morbidity and mortality associated with a surgical procedure (see Chapter 26). ey should be used in
patients who are at risk of PE, but for whom anticoagulation
is contraindicated, has failed, or is associated with complications (Figure 22.13). IVC lter placement carries low mor-
bidity and mortality. Multiple studies have demonstrated
the ecacy of lters in preventing PE, although these lters
may cause progression/recurrence of DVT, along with IVC
thrombosis. e rates of these complications are device specic. ere has been a recent increase in the placement of
retrievable lters for the prophylaxis of PE in patients with
time-limited contraindications to anticoagulation. e benets with this practice are theoretical and need to be objectively studied. e type of lter used should be tailored to
Venous thromboembolism event
with Indication for IVC filter
(contraindication to anticoagulation,
complication of anticoagulation, or
Contraindication to anticoagulation
Place retrievable IVC filter
Patient can now be safely
anticoagulated?
No
failure of anticoagulation)
permanent?
Yes
YesNo
Place permanent IVC filter
Retrieve IVC filter
Figure 22.13 Algorithm for decision making regarding the type of IVC filter. IVC: inferior vena cava.
Reassess patient in
3 months
22.13 IVC filters 287
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Guidelines 3.6.0 of the American Venous Forum on treatment algorithms for acute deep venous thrombosis
No. Guideline
3.6.1 Low-molecular-weight heparin (LMWH) is now preferred over
standard unfractionated heparin (UFH) for the initial
treatment of deep vein thrombosis (DVT).
3.6.2 The criteria for the discontinuation of oral anticoagulation
include thrombosis risk, residual thrombus burden, and
coagulation system activation (as suggested by D-dimer
measurements).
3.6.3 Heparin-induced thrombocytopenia remains a problem with
all heparin preparations, but is more frequent with UFH
than LMWH. Alternative agents include hirudin, argatroban
and fondaparinux.
3.6.4 The use of strong compression and early ambulation after
DVT treatment can significantly reduce the long-term
morbidity of pain and swelling resulting from the DVT.
each patient. Major eorts toward identifying those patients
3. Stein PD, Woodard PK, Weg JG etal.; PIOPED II
who are at highest risk of signicant PE and so should receive
lters should occur. Eorts must also continue to be directed
toward improving methods of thromboprophylaxis, since no
lter can inuence the development or course of the underly-
4. Karthanos C, Sfyroeras G, Drakou A et al. Superficial
ing thrombosis.
REFERENCES
5. Wakefield TW, Obi A, and Henke PK. An aspirin
1. Wells PS, Anderson DR, Rodger M etal. Evaluation
of D-dimer in the diagnosis of suspected deep-vein
thrombosis. N Engl J Med 2003;349(13):1227–35.
2. Michiels JJ, Berghout A, Schroyens W, De Backer
W, Hoogsteden H, and Pattynama PM. The rehabilitation of clinical assessment for the diagnosis of pulmonary embolism. Semin Vasc Med
2002;2(4):345–51.
6. Knepper J, Horne D, Obi A, and Wakefield
Grade of
recommendation
(1: strong;
2:weak)
1 A
1 A
1 C
1 A
Investigators. Diagnostic pathway in acute pulmonary embolism: Recommendations of the PIOPED II
Investigators. Radiology 2007;242(1):15 –21.
vein thrombosis in patients with varicose veins: Role
of thrombophilia factors, age and body mass. Eur J
Vasc Endovasc Surg 2012;43:355–58.
a day to keep the clots away: Can aspirin prevent
recurrent thrombosis in extended treatment for VTE?
Circulation 2014; 130(13):1031–33.
TW. Asystematic update on the state of novel
anticoagulants and a primer on reversal and
bridging. J Vasc Surg: Venous Lymphat Disord
2013;1(4):418 – 26.
Grade of evidence
(A:high quality;
B:moderate quality;
C:low or very low quality
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23
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Current recommendations for the prevention of
deep venous thrombosis
ROBERT D. MCBANE AND JOHN A. HEIT
23.1 Introduction 289
23.2 Risk factors for VTE 289
23.3 VTE prophylaxis methods andregimens 292
23.1 INTRODUCTION
Venous thromboembolism (VTE) represents a major cause
of morbidity and mortality in the United States.
incidence of VTE exceeds 1 per 1000, with approximately
201,000 rst life-time cases diagnosed annually in this
country. e 7-day mortality of patients suering a thrombotic event is 25% and up to 35% of patients with pulmonary embolism (PE) die suddenly. VTE is, therefore, the
fourth leading cause of death in Western society, and the
third leading cause of cardiovascular death behind myocardial infarction and stroke. Furthermore, VTE is both
a recurrent disease and a morbid disease. Of those individuals surviving the thrombotic event, 30% will develop
recurrent VTE within 10 years and 20%–30% will develop
the post-phlebitic syndrome over this time period. VTE is
typically a disease of elderly people, with the incidence of
thrombotic events increasing signicantly beyond 60 years
of age (Figure 23.1). As our population ages, the expected
number of VTEs annually will increase. Despite advances
in radiographic detection, expanded knowledge of risk factors, and anticoagulant development, the incidence of VTE
has been relatively constant over the past several decades
(Figure 23.2).
Yet, VTE can be a preventable disease particularly in the
hospitalized patient.4 Appropriately delivered prophylaxis
is cost-eective, reduces VTE rates by 50%–70%, and carries an acceptably low risk of hemorrhage. Without prophylaxis, VTE rates are high for both surgical and non-surgical
hospitalized patients. Although the incidence of VTE varies by both patient- and surgery-specic variables, without
prophylaxis, venous thrombotic events may occur in up to
20% of surgical patients. Underscoring the magnitude of
1–3
e
23.4 Prophylaxis recommendations 296
23.5 Conclusions 301
References 302
this disease is the fact than more than 28 million surgical
procedures are performed each year in the United States.5
Furthermore, more than 35 million non-surgical patients
are admitted each year to U.S. hospitals. PE accounts for
nearly 10% of all hospital deaths and is one of the most
common preventable causes of mortality. Oen, these pulmonary emboli occur without prior warning, and sudden
death may be the initial symptom of disease. With the evolution toward expanded outpatient delivery of medical and
surgical services, only the sickest and frailest of patients
are hospitalized. e thrombotic event rate may be as
highas16% in these non-surgical patients if no prophylaxis
is given.
of death and suering. Providing appropriate VTE prophylaxis is the highest-ranked safety practice for patients who
are at risk. e aims of this chapter are therefore to outline
the risk factors for VTE, review the ecacy and safety of
various prophylactic regimens, and provide recommendations regarding the most suitable prophylaxis based on the
estimated risk.
4,5
In summary, VTE is the most common preventable cause
23.2 RISK FACTORS FOR VTE
A number of patient characteristics have been identied as
independent risk factors for VTE (Box 23.1).3 Increasing age
is a major risk factor for VTE. ere is a direct relationship
with increasing age and the annual incidence of VTE for both
men and women (Figure 23.1). Beyond the h decade of life,
the incidence increases precipitously. Below this age, VTE is
relatively uncommon. PE accounts for an increasing proportion of VTE with increasing age for both genders, which has
important implications for the future of the United States
289
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