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230 Diagnostic algorithms for acute deep venous thrombosis and pulmonary embolism
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perfusion imaging, there is a subsequent increase in sensitivity rivaling that of 16-MDCT angiography.90 e current role for MRI/MRA is as a backup when conventional
diagnostic methods are unavailable or contraindicated
due to dye allergy, renal insuciency, or concerns about
radiation exposure.
59,88,89
MRI may also prove to be valuable in the follow-up of acute PE in order to determine
thrombus age.
91
Notably, recent studies have questioned the traditional
thinking that gadolinium was less nephrotoxic than iodinated contrast. In fact, at angiographic concentrations, gadolinium has demonstrated equal or greater renal cell toxicity
than iodinated contrast.32 ere is also mounting evidence
that gadolinium administration may play a signicant role
in the development of nephrogenic systemic brosis.
33–35
18.2.9 Other studies
Other modalities have been studied with the intention of
using them for the diagnosis of PE, with varying levels of
success. Although electrocardiogram (ECG) changes may
be present, they are neither sensitive nor specic for PE.92
e changes may, however, indicate a way of stratifying risk,
since patients with acute major PE and ECG changes have
worse outcomes than those without the changes.93 Likewise,
although arterial blood gas changes may be present, they are
non-specic and therefore of limited diagnostic utility in
the workup of PE.94 Lastly, although chest radiographs are
routinely ordered in those experiencing respiratory distress,
the results are most oen normal, even in the presence of
PE. Chest radiographs may be useful for determining which
patients should undergo s-CT versus VP scintigraphy, since
abnormal chest radiographs increase the likelihood of indeterminate-probability VP scans.
Once a PE has been conrmed, algorithms now exist to
help risk-stratify patients into treatment groups, and/or testing groups for further evaluation. e process of patient risk
stratication helps identify patients who will do well with
standard therapy and who are likely to need more aggressive
treatment. is also helps determine resource utilization.
Some patients with small, incidental pulmonary emboli and
some segmental pulmonary emboli are now being treated
as outpatients, while other patients may require immediate
interventional therapy, either operative or lytic. Two dierent scoring systems have been used to predict the severity of
PE. ese include the Pulmonary Embolism Severity Index
(PESI) score and the Geneva score (Table 18.4).
In validation studies, a PESI score of less than 66 predicts a 30-day mortality rate of less than 3%.98 Studies have
recently been completed of large multinational randomized
trials comparing outcomes and costs for inpatient management versus immediate discharge from ambulatory centers
when patients had a PE diagnosed and a PESI score of less
than 66 (Figures 18.8 through 18.11).
e use of ECG, biomarkers, echocardiography, and CT
pulmonary angiogram ndings can be combined to predict mortality in those with and without right ventricular
95
96,97
98,99
Table 18.4 Two scoring systems to predict the severity of
pulmonary embolism
PESI score
Age, per year Number of years
Male gender 10
Cancer 30
Heart failure 10
Chronic lung disease 10
Pulse >110 beats/minute 20
Systolic blood pressure <100 mmHg 30
Respiratory rate >29 breaths/minute 20
Temperature <36°C 20
Altered mental status 60
SaO
Low-risk score <66
High-risk score >125
Geneva score
Cancer 2
Heart failure 1
Prior deep venous thrombosis 1
Systolic blood pressure <100 mmHg 2
PaO
Concomitant deep venous thrombosis 1
Low-risk score <3
High-risk score >2
Source: From Kline JA, Miller DW. J Natl Compr Canc Netw
Note: PaO2: arterial partial pressure of oxygen; PESI: Pulmonary
96
<90% 20
2
97
<8 kPa 1
2
2011;9(7):800–10. With permission.
Embolism Severity Index; SaO2: percentage of oxygen saturation of arterial blood.
Points assigned
of life
Warning: Not for diagnostic use
Figure 18.8 Right ventricular shift into the left ventricle.
18.2 Pulmonary embolism 231
https://t.me/med1917
Warning: Not for diagnostic use
Figure 18.9 Bowing of septum into the left ventricle.
Warning: Not for diagnostic use
Figure 18.11 Central saddle embolus.
Warning: Not for diagnostic use
Figure 18.10 Proximal pulmonary emboli.
dysfunction. For patients with right ventricular dysfunction, mortality is 15%; for those without, mortality is 5%.
If there is elevated troponin, the mortality rate is greater
than 43%, while those without have less than 15% mortality.
In those with an elevated brain natriuretic peptide (BNP),
the mortality risk is 47%, but less than 13% in those who
lack elevated BNP. For those with an elevated n-terminal
prohormone of BNP (proBNP), mortality is 32%; if it is not
elevated, mortality is less than 5%.
98
Experts can then bundle this stratication data in order
to categorize patients into risk categories and thus determine dierent treatment and monitoring needs (Table 18.5).
Patients at low risk for PE may require heparin anticoagulation with either low-molecular-weight or unfractionated
heparin. Patients at low risk for PE can be admitted to an
unmonitored bed, and some of these patients may be discharged directly to home.
100 –109
Patients with moderate-risk PE should be hospitalized
with telemetry monitoring and initial heparinization. Any
patient with degradation or development of new or worsening signs should undergo repeat biomarker testing and
echocardiography. e risk should be re-evaluated.
Patients with more severe and moderate pulmonary
emboli or submassive pulmonary emboli may require more
aggressive care and monitoring, with consideration of brinolytic therapy (Figure 18.12). e treatment of submassive
embolism remains one of the most controversial subjects,
and is currently the subject of much ongoing research.
110
High-risk patients may also be reported as severe, and
major pulmonary emboli may occur in association with
hypotension, and may require heparin anticoagulation,
intensive care unit monitoring, and treatment escalation.
e most common relative contraindications for brinolytic therapy include age over 80 years, advanced directives,
a “do not resuscitate” order, trauma associated with syncope
or seizure-like presentation, anemia or thrombocytopenia,
current menstruation, recent childbirth, a remote or vague
history of stroke, gastrointestinal bleeding, and metastatic
carcinoma.
232 Diagnostic algorithms for acute deep venous thrombosis and pulmonary embolism
UI
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Table 18.5 Criteria for categorizing patients with acute pulmonary embolism and associated treatment options
Category Definition Recommended treatment options
Low risk Systolic blood pressure >90 mmHg at all times and all of the
following:
• Shock index <1
• SaO
almost always >94%
2
• Normal electrocardiogram (or Daniel score <3)
• Normal troponin and BNP or proBNP
• PESI score <66
Moderate risk Systolic blood pressure >90 mmHg at all times and any one of
the following:
• Shock index ≥1 at any time
• SaO
persistently <94%
2
• Begin low-molecular-weight
heparin
• Optional admission to
unmonitored regular bed
• Consider outpatient treatment if
adequate compliance and
follow-up can be assured
• Begin heparin treatment
• Fibrinolytics in the minority of
cases
• Admission to a telemetry bed
• Electrocardiogram showing any signs of pulmonary
hypertension (tachycardia, S1Q3T3, or incomplete RBBB)
• Elevated troponin or BNP or proBNP
• PESI score >65
• Echocardiography with any degree of right ventricular
hypokinesis
More severe
(submassive)
moderate risk
Appearance of at least moderate distress and:
• Shock index >1 and severe right ventricular hypokinesis on
echocardiography
• Worsening electrocardiogram, such as S1Q3T3 and a new
incomplete RBBB, or progression of incomplete to complete
RBBB, or development of T-wave inversion in V1–V3
High risk (major) Any systolic blood pressure <90 mmHg or <20 mmHg below
documented baseline and appearance of distress
Any persistent systolic blood pressure <90 mmHg regardless of
appearance
• Begin heparin treatment
• Fibrinolytic treatment in most
patients without contraindications
in the emergency department
• Admission to a step-down or
intensive care unit
• Begin heparin treatment
• Fibrinolytic treatment in the
emergency department in all
patients without contraindications
• Admission to intensive care unit
Note: BNP: brain natriuretic peptide; PESI: Pulmonary Embolism Severity Index; proBNP: prohormone of brain natriuretic peptide; RBBB:
right bundle branch block; SaO2: percentage of oxygen saturation of arterial blood.
Hemodynamic
Clinical exam
Biomarkers
Echocardiography
or CT
Risk stratification
Treatment
Location
Normotensive
PESI < 85 PESI ≥ 85
BNP – and
tropo –
Low
LMWH or Fx LMWH or Fx
New anticoagulants ?
Outpatient early
discharged
Intermediate
less-severe
Hospitalization IC
BNP + or
tropo +
No RV
dilatationRVdilatation
Intermediate
more-severe
UFH
Hypotension
shock
High
Thrombolysis
CU
Figure 18.12 Algorithm management in risk stratification and treatment strategy for patients with acute pulmonary embo-
lism. BNP: brain natriuretic peptide; Fx: fondaparinux; ICU: intensive care unit; LMWH: low molecular weight heparin; PESI:
Pulmonary Embolism Severity Index; RV: right ventricle; tropo: troponin; UFH: unfractionated heparin. (From Penaloza A,
Roy PM, Kline J. Curr Opin Crit Care 2012;18:318–25.)
References 233
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18.2.10 Algorithm use for DVT and PE
include consideration of diagnostic uncertainty and patient
anxiety while waiting for a denitive diagnosis. Clinician and
e use of algorithms seeks to separate patients into risk
groups for testing and evaluation while not missing any sig-
patient acceptance are required to use an algorithm, and the
algorithm should utilize tests that are widely available.
nicant pathologies. e algorithms only apply to symptomatic outpatients, using exclusion criteria to increase sensitivity
ACKNOWLEDGMENTS
and specicity. ey have not been validated for inpatients or
asymptomatic patients. Algorithms perform dierently in different populations and when used by dierent care providers.
A standardized treatment management plan is also dened
through the algorithms. ese may be useful with inexperienced sta and decrease practice variation, and may provide some control over risk management. Algorithms do not
Guidelines 3.2.0 of the American Venous Forum on diagnostic algorithms for acute deep venous thrombosis
and pulmonary embolism
No. Guideline
3.2.1 In symptomatic outpatients with suspected acute deep
venous thrombosis (DVT), we recommend to obtain first a
clinical score and D-dimer level to select patients for
further diagnostic studies.
3.2.2 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.
3.2.3 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.
3.2.4 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.
3.2.5 We suggest judicious use of Gadolinium in patients with
renal insufficiency because of the risk of nephrogenic
systemic fibrosis.
Ken Zalewski, MHI, TriHealth Imaging PACS/IT Manager,
Good Samaritan TriHealth Hospital, Cincinnati, OH, USA.
e John Cranley Vascular Laboratory, Good Samaritan
TriHealth Hospital, Cincinnati, OH, USA. Angela N Fellner,
PhD, CCRP, Clinical Research Specialist, TriHealth Hatton
Research Institute, Cincinnati, OH, USA.
Grade of evidence
Grade of
recommendation
(1:strong; 2: weak)
1 B
1 B
1 B
2 B
2 C
(A: high quality;
B: moderate quality;
C: low or very low quality)
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Medical treatment of acute deep venous
https://t.me/med1917
thrombosis and pulmonary embolism
ANDREA T. OBI AND THOMAS W. WAKEFIELD
19
19.1 Introduction 239
19.2 Principles of the treatment ofVTE 239
19.3 Standard initial therapy 239
19.4 Duration of therapy 245
19.5 Complications 246
19.1 INTRODUCTION
Despite recent advances in medical and interventional
therapy for venous thromboembolism (VTE), it continues
to be a major cause of in-hospital deaths and emergency
room visits. Historically, VTE was treated with unfractionated heparin (UFH) or low-molecular-weight heparin
(LMWH), commonly as a bridge to anticoagulation with a
vitamin K antagonist (VKA). In the last several years, the
available therapies for the treatment of VTE have broadened to include new classes of oral and injectable anticoagulants, new thrombolysis devices, and new vena cava
lters. roughout this chapter, we provide an overview of
the basic principles of the treatment of VTE, from initial
presentation to determining optimal therapy and duration of anticoagulation to aggressive therapies and special
circumstances.
19.2 PRINCIPLES OF THE TREATMENT
OFVTE
e objectives of treatment in patients with VTE are to
prevent death from pulmonary embolism (PE), to prevent
recurrent VTE, and to prevent the post-thrombotic syndrome (PTS). Traditionally, anticoagulant drugs such as
heparin, LMWH, and warfarin constitute the mainstay
of the initial treatment of venous thrombosis, eectively
decreasing thrombus extension and subsequent embolization. New oral factor Xa inhibitors (rivaroxaban, apixaban, and edoxaban) and a thrombin inhibitor (dabigatran)
have recently been approved for the treatment of VTE. For
19.6 Non-pharmacologic treatments 246
19.7 Aggressive therapies 247
19.8 Special situations 247
19.9 IVC filters 248
References 248
patients with iliofemoral thrombosis, catheter-directed
thrombolysis has been shown to decrease the risk of PTS.
In patients who cannot be anticoagulated, such as those
with intracranial hemorrhage or major trauma, inferior
vena cava (IVC) lters signicantly reduce the risk of death
from PE. e prevention of PTS remains a vexing problem,
with no available medical therapy. Some data suggest that
the use of LMWH, graduated compression stockings, and
restoration of venous ow in massive obstructing iliofemoral thrombosis can decrease the risk of PTS, although none
reliably prevent it.
19.3 STANDARD INITIAL THERAPY
Immediate anticoagulation is paramount in the initial
treatment of the patient presenting with VTE (Figure 19.1).
Systemic anticoagulation decreases thrombus extension,
PE, and recurrence. Failure to achieve therapeutic anticoagulation within 24 hours increases the risk of recurrence.
erefore, it is oen necessary to empirically anticoagulate
the patient with presumed PE while waiting for diagnostic testing. is is infrequently indicated in the patient
with suspected deep venous thrombosis (DVT), as bedside
duplex ultrasound testing is rapid and nearly universally
available. e risks, benets, and costs of anticoagulation
should be weighed carefully against the patient’s clinical probability of having a VTE while waiting for testing.
When using validated clinical prediction scores for estimating risk of DVT or PE,
24 hours for low-risk patients and up to 4 hours for intermediate-risk patients for objective imaging data prior to
1
it is acceptable to wait up to
239
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