Acute Pulmonary Embolism

Suree Sompradeekul, MD, FCCP

Div of Respiratory Diseases & Tuberculosis
Dept of Medicine, Siriraj Hospital
 Step 1

Symptoms & Signs

and/or
Clinical predictions rules
 Clinical characteristics of patients with suspected
PE in the emergency department
(adapted from Pollack et al. 2011)

Feature PE confirmed PE not confirmed

(n= 1880) (n= 528)
Dyspnea 50% 51%
Pleuritic chest pain 39% 28%
Cough 23% 23%
Substernal chest pain 15% 17%
Fever 10% 10%
Haemoptysis 8% 4%
Syncope* 6% 6%
Unilateral leg pain 6% 5%
Sign of DVT (unilateral extremity 24% 18%
swelling)

Hypotension***
 Signs in acute pulmonary
embolism
Signs Frequency (%)
Tachycardia 70
Crackles or crepitations 51
Right sided S4 30
Loud P2 23
Fever (T<38.9 C) 14
Circulatory collapse 8
 Predisposing factors

• Fracture (hip or leg) •Previous VTE

• Hip or knee replacement •Thrombophilia
• Major general surgery or •Central venous lines
trauma
• Chemotherapy
• Chronic heart or
• Postpartum /
respiratory failure
antepartum
• Malignancy
• Increasing age
• Oral contraceptive
• Obesity
therapy
• Varicose veins
• Paralytic stroke / spinal
cord injury • Bed rest > 3 days
• Immobility due to sitting
 Risk assessment tools in
surgical patients : Caprini

HIGH risk
• Orthopedic surgery
• Orthopedic injury
Lower risk
• Malignancy
• Spinal injury
• Central venous line
• Stroke
• Surgery open/laparoscopic
• age >75
• Varicosities
• h/O VTE
• Pregnancy/postpartum
• FHx VTE
• IBD
• Hypercoagulable
disorder

Consider prophylaxis
 Clinical prediction rules for PE
Items Clinical decision rule points
Wells rule Original version Simplified version
Previous PE for DVT 1.5 1
Heart rate > 100 b.p.m. 1.5 1
Surgery or immobilization within the 1.5 1
past four weeks
Haemoptysis 1 1
Active cancer 1 1
Clinical signs of DVT 3 1
Alternative diagnosis less likely than 3 1
PE
Clinical probability
Three-level score
Low 0-1 N/A
Intermediate 2-6 N/A
High >7 N/A
Two-level score
PE unlikely 0-4 0-1
PE likely >5 >2
 Clinical prediction rules for PE
Items Clinical decision rule points
Revised Geneva score Original version Simplified version
Previous PE or DVT 3 1
Heart rate
75-94 b.p.m. 3 1
> 95 b.p.m. 5 2
Surgery or fracture within the past month 2 1
Haemoptysis 2 1
Active cancer 2 1
Unilateral lower limb pain 3 1
Pain on lower limb deep venous palpation and 4 1
unilateral oedema
Age > 65 years 1 1
Clinical probability
Three-level score
Low 0-3 0-1
Intermediate 4-10 2-4
High >11 >5
Two-level score
PE unlikely 0-5 0-2
PE likely >6 >3
 Step 2

• CXR

• EKG sinus tachycardia, no signs

of CAD
• +/- ABG hypoxia with acute
respiratory alkalosis
7T
 Step 3

Confirmation
 Suspected acute PE: step1+2

Shock or hypotensions?

Yes No

High-riskb Not high-riskb

PE = pulmonary embolism.
aDefined as systolic blood pressure <90 mmHg, or a systolic pressure drop by >40 mmHg,

for > 15 minutes, if not caused by new-onset arrhythmia, hypovolaemia, or sepsis.

bBased on the estimated PE-related in-hospital or 30-day mortality.
 Suspected acute PE: step1+2

Shock or hypotensions?

Yes

High-riskb = Massive PE

PE = pulmonary embolism.
aDefined as systolic blood pressure <90 mmHg, or a systolic pressure drop by >40 mmHg,

for > 15 minutes, if not caused by new-onset arrhythmia, hypovolemia, or sepsis.

bBased on the estimated PE-related in-hospital or 30-day mortality.
 Massive PE
Pulmonary embolism with hemodynamic
instability usually associated with large
emboli
(Systolic BP < 90 mmHg or decreased >
40 mmHg for > 15mmmm
min)
mm
Associated with high mortality
 CAMI
Suspected PE with shock or hypotension

IV heparin
CT angiography immediately available

Noa Yes

O
Echocardiography

RV overloadb
CT angiography

O
available
No Yes and
CT angiography
patient stabilized

No other test availableb

or patient unstable positive negative

Search for other causes PE-specific treatment: Search for other causes
of hemodynamic instability Primary reperfusionc of haemodynamic instability
 Suspected acute PE

Shock or hypotensions?

No

Not high-riskb

PE = pulmonary embolism.
aDefined as systolic blood pressure <90 mmHg, or a systolic pressure drop by >40 mmHg,

for > 15 minutes, if not caused by new-onset arrhythmia, hypovolemia, or sepsis.

bBased on the estimated PE-related in-hospital or 30-day mortality.
 Suspected PE without shock or hypotension

Assess clinical probability of PE

Clinical judgment or prediction rulea

Low/intermediate clinical probability

or PE unlikely

D-dimer

negative positive

CT angiography

no PE PE confirmedc

No treatmentb Treatmentb
 Recommendations for diagnosis
Recommendations Class Level

Suspected PE without shock or hypotension

The use of validated criteria for diagnosing PE is recommended. I B

Clinical evaluation
It is recommended that the diagnostic strategy be based on I A
clinical probability assessed either by clinical judgement or a
validated prediction rule.
D-dimer

Plasma D-dimer measurement in outpatients/emergency I A

department patients with low or intermediate clinical probability, or
PE-unlikely, to reduce the need for unnecessary imaging and
irradiation, preferably using a highly sensitive assay.
In low clinical probability or PE-unlikely patients, normal D-dimer I A
level using either a highly or moderately sensitive assay excludes
PE.
Further testing may be considered in intermediate probability IIb C
patients with a negative moderately sensitive assay
D-dimer measurement is not recommended in patients with III B
high clinical probability, as a normal result does not safely
exclude PE, even when using a highly sensitive assay.
 D-dimer
• Use in outpatient, ER setting
• In low to moderate clinical probability
• Level < 0.5mg/L (highly sensitive enzyme-
mmmm
linked immunosorbent assay) – sensitivity
96-98% R/O venous thromboembolism
(high negative predictive value)
D diner so 5 Riv TEToi
mm

Konstantinides S. N Engl J Med 2008;359:2804-13.

Tapson VF. N Engl J Med2008;358:1037-52
 D-dimer
• Not to be used in patients with high clinical
probability and not be used as a PE
screening test
• Careful interpretation in
– Patients with symptoms lasting > 14 days
– Receiving therapeutic heparin or oral
anticoagulant Rx

0
– Elevated in hospitalized patients, infection,
inflammation, cancer, surgery and trauma,
extensive burn or bruises, ischemic heart
disease, stroke, peripheral artery disease,
ruptured aneurysm, aortic dissection,
pregnancy, aging
Suspected PE without shock or hypotension

Assess clinical probability of PE

Clinical judgment or prediction rulea

High clinical probabiltiy

or PE likely

LMWH
(heparin)

CT angiography

no PE PE confirmedc

No treatmentb Treatmentb
or investigate further
 Suspected PE without shock or hypotension

Assess clinical probability of PE

Clinical judgment or prediction rulea

Low/intermediate clinical probability High clinical probabiltiy

or PE unlikely or PE likely

8
D-dimer
LMWH
(heparin)
negative positive

CT angiography CT angiography

no PE PE confirmed no PE PE confirmed

No treatmentb Treatmentb No treatmentb Treatmentb

or investigate further
 Step 3
Confirmation
SHOCK Normotension
mm mm

•CTA •D-dimer
•Echo •CTA
•(Pulmonary •V/Q
angiography) •MRI
•(Pulmonary
angiography)
Computerized tomography of
chest with angiography
(CT angiography)
Ventilation / Perfusion
Lung scan
(V/Q lung scan)
Pulmonary angiography
Acute PE
 Recommendations for diagnosis
Recommendations Classa Levelb
Suspected PE without shock or hypotension
Lower-limb CUS
Lower-limb CUS in search of DVT may be considered IIb B
in selected patients with suspected PE, to obviate the
need for further imaging tests if the result is positive.

CUS showing a proximal DVT, further testing should I B

be considered to confirm PE.
If CUS shows only a distal DVT, further testing should IIa B
be considered to confirm PE.
Pulmonary angiography
Pulmonary angiography may be considered in cases IIb C
of discrepancy between clinical evaluation and results
of non-invasive imaging tests.
MRA
MRA should not be used to rule out PE. III A
 Prognosis (1)
Hemodynamic consequences related to
- Size of emboli
- Number of emboli
- Pre-existing cardiac and respiratory status
Mortality of untreated PE is 25-30%
mostly from recurrent PE
Risk of recurrent PE
Highest during the first 4-6 wk
Chest 2002;121:877-905.
 RV hypokinesia

No RV hypokinesia

Time from diagnosis (days)

Goldhaber SZ, et al. Lancet 1999:353;1386-9.

 Prognosis (2)
Adequate anticoagulation treatment
Reduced both fatal and non-fatal
recurrent PE to < 8%
The effective treatment should be started
as quickly as possible in high clinical
suspicious cases
 Mortality rates vs Onset of Rx
20

15.3%
15

Heparin in ED

10 Heparin After Admission

6.7%

4.4%
5
1.4%

0
Hospital Mortality 30-Day Mortality
P = 0.009 P < 0.001
Smith SB, et al. Chest 2010;137:1382-90
Mortality rates vs Time to achieve
a therapeutic aPTT

p = 0.091 p = 0.037
Smith SB, et al. Chest 2010;137:1382-90.
 Prognosis (3)
ICU stay predictive of increased mortality
Elevated Troponin associated with high
risk of short-term death and adverse
outcome of acute PE
Becattini C, et al. Circulation 2007.

D-dimer >5,000 ng/mL (tubidimetric

immunoassay) associated with 2.9 fold
risk of mortality
Grau E, et al. Crit Care Med 2007;35.
Risk stratification
 Risk stratification in non-massive APE
• Clinical scores: simplified PESI
• Imaging findings: echo parameters of RV
dysfunction, MDCT-enlarged right ventricle
• Laboratory markers: BNP, NT-proBNP,
troponin I or T, high-sensitivity troponin T
(hsTnT), heart-type fatty acid-binding protein (H-
FABP), cardiac expression of growth-
differentiation factor-15 (GDF-15)

Combined parameters
 Original and simplified PESI
Parameter Original version Simplified version
Age Age in years 1 point (if age > 80 years)
Male sex + 10 points -
Cancer + 30 points 1 point
Chronic heart failure + 10 points
1 point
Chronic pulmonary disease + 10 points
Pulse rate > 110 b.p.m. + 20 points 1 point
Systolic blood pressure < 100 mmHg + 30 points 1 point
Respiratory rate > 30 breaths per minute + 20 points -
Temperature < 36 oC + 20 points -
Altered mental status + 60 points -
Arterial oxyhaemoglobin saturation < 90% + 20 points 1 point

Risk strataa
Class I : < 65 points 0 points = 30-day mortality risk
very low 30-day mortality risk (0- 1.0% (95% CI 0.0%-2.1%)
1.6%)
Class II: 66-85 points
Low mortality risk (1.7-3.5%)

Class III: 86-105 points > 1 points(s) =30-day mortality

Moderate mortality risk (3.2-7.1%) risk 10.9% (95% CI 8.5-13.2%)
Class IV: 106-125 points
High mortality risk (4.0-11.4%)
Class V: >125 points
Very high mortality risk (10.0-24.5%)
 Imaging for RV dysfunction
• Echocardiographic criteria of RV dysfunction :
RV dilation and/or increased end-diastolic RV-LV
diameter ratio (in most studies, the reported threshold
value was 0.9 or 1.0); hypokinesia of the free RV wall;
increased velocity of the tricuspid regurgitation jet; or
combinations of the above.
• Computed tomographic (CT) angiography (four-
chamber views of the heart) : an increased end-
diastolic RV/LV (left ventricular) diameter ratio (with a
threshold of 0.9 or 1.0).
 Cardiac biomarkers
• Markers of myocardial injury (e.g.elevated
cardiac troponin I or –T, natriuretic peptide
concentrations in plasma - as a result of
(right) ventricular dysfunction

w
 Classification of patients with acute PE
based on early mortality risk
Early mortality risk Risk parameters and scores
Shock or PESI class III-V Signs of RV Cardiac
hypotension or dysfunction laboratory
sPESI > 1a on an imaging biomarkersc
testb
High + (+)d + (+)d
Intermediate- - + Both positive
Intermediate high
Intermediate- - + Either one (or none) positivee
low
Low - - Assessment optional; if
assessed, both negative

Treatment
 Clinical suspicion of PE

Shock / hypotension?

Yes No
Diagnostic algorithm Diagnostic algorithm

PE confirmed

Assess clinical risk

(PESI )

PE confirmed PESI class III-IV PESI class I-II

Intermediate risk or sPESI > 1 or sPEI=0

Consider further
risk stratification
RV function (echo or CT)a
Laboratory testingb
One positive
Both positive or both negative
High risk Intermediate-high risk Intermediate-low risk Low riskc

Primary A/C; monitoring; Hospitalization; A/Ce Consider early

reperfusion consider rescure discharge and home
reperfusiond treatment, if feasiblef
 Low-molecular-weight heparins and pentasaccharide
(fondaparinux) for the treatment of
pulmonary embolism
Dosage Interval

Enoxaparin 1.0 mg/kg Every 12 hours

or
1.5 mg/kga Once daliya
Tinzaprin 175 U/kg Once daily
Dalteparin 100 IU/kgb Every 12 hoursb
or
200 IU/kgb Once daily
Nadroparinc 86 IU/kg Every 12 hours
or
171 IU/kg Once daily
Fondaparinux 5 mg (body weight < Once daily
50kg);
7.5 mg (body witght 50-
100 kg);
10 mg (body weight >
100 kg)
 Recommendations for acute phase treatment
Recommendations Classa Levelb
PE with shock or hypotension (high-risk)
It is recommended that intravenous
anticoagulation with UFH be initiated without I C
delay in patients with high-risk PE.
Thrombolytic therapy is recommended. I B
Surgical pulmonary embolectomy is
recommended for patients in whom thrombolysis I C
is contraindicated or has failed. or catmindiotic fu
Percutaneous catheter-directed treatment thronbilyticvoid
murmur
should be considered as an alternative to surgical
pulmonary embolectomy for patients in whom IIa C
full-dose systemic thrombolysis is contraindicated
or has failed.
 Recommendations for acute phase treatment
Recommendations Classa Levelb

0
PE without shock or hypotension (Intermediate-or low-risk)
Anticoagulation: combination of parenteral treatment with VKA
Initiation of parenteral anticoagulation is
recommended without delay in patients I C
with high or intermediate clinical probability of PE
while diagnostic work-up is in progress.
LMWH or fondaparinux is the recommended form
of acute phase parenteral anticoagulation for most I A
patients.
In parallel to parenteral anticoagulation, treatment
with a VKA is recommended, targeting an INR of 2.5 I
B
(range 2.0-3.0)
 Recommendations for acute phase treatment
Recommendations Classa Levelb

Anticoagulation: new oral anticoagulants

As an alternative to the combination of parenteral
anticoagulation with a VKA, anticoagulation with rivaroxaban
I B
(15 mg twice daily for 3 weeks, followed by 20 mg once daily) is
recommended.
As an alternative to the combination of parenteral
anticoagulation with a VKA, anticoagulation with apixaban (10
I B
mg twice daily for 7 days, followed by 5 mg twice daily) is
recommended.
As an alternative to VKA treatment, administration of dabigatran
(150 mg twice daily, or 110 mg twice daily for patients 80 years
of age or those under concomitant verapamil treatment ) is I Be
recommended following acute-phase parenteral
anticoagulation.
As an alternative to VKA treatment, administration of edoxaban
is recommended following acute-phase parenteral I B
anticoagulation .
New oral anticoagulants (rivaroxaban, apixaban, dabigatran,
edoxaban) are not recommended in patients with severe renal III A
impairment.
 Warfarin vs New oral anticoagulants
Warfarin Target-specific oral
anticoagulants
Dosing OD OD or BID

Dietary restriction* yes None; rivaroxaban-take with food

Monitoring * PT/INR Not required

Drug interaction Many CYP-3A4 and P-glycoprotein

inhibitors
Time in therapeutic 65% of time use Expected to be superior than
range* warfarin
Reversal agents Vit K, FFP, PCC None, dialysis-dabigatran, PCC

Monitoring reversal
rFVIIa)
PT/INR
+/- rivaroxaban

E
TT-dabigatran, anti-factor Xa -
apixaban
Effect of comorbid Renal function**
conditions
 Recommendations for acute phase treatment
Recommendations Classa Levelb
Reperfusion treatment
Routine use of primary systemic thrombolysis is not
recommended in patients not suffering from shock or III B
hypotension.
Close monitoring is recommended in patients with
intermediate-high risk PE to permit early detection of
I B
haemodynamic decomposition and timely initiation of
‘rescue’ reperfusion therapy.
Thrombolytic therapy should be considered for patients
with intermediate-high-risk PE and clinical signs of IIa B
haemodynamic decompensation.
Surgical pulmonary embolectomy may be considered in
intermediate-high-risk patients if the anticipated risk IIb C
ob bleeding under thrombolytic treatment is high.
Percutaneous catheter-directed treatment may be
considered in intermediate-high-risk patients if the
IIb B
anticipated risk of bleeding under thrombolytic
treatment is high
 Recommendations for acute phase treatment
Recommendations Classa Levelb
PE without shock or hypotension (Intermediate-or low-risk)
Anticoagulation: combination of parenteral treatment with VKA
Initiation of parenteral anticoagulation is
recommended without delay in patients with high
I C
or intermediate clinical probability of PE while
diagnostic work-up is in progress.
LMWH or fondaparinux is the recommended form
of acute phase parenteral anticoagulation for most I A
patients.
In parallel to parenteral anticoagulation, treatment
with a VKA is recommended, targeting an INR of 2.5 I
B
(range 2.0-3.0)
 Recommendations for acute phase treatment

Recommendations Classa Levelb

Early discharge and home treatment
Patients with acute low-risk PE should be
considered for early discharge and continuation of
IIa B
treatment at home if proper outpatient care and
anticoagulant treatment can be provided.
 Recommendations for duration of anticoagulation
after pulmonary embolism
Recommendations Classa Levelb
For patients with PE secondary to a transient (reversible)
risk factor, oral anticoagulation is recommended for 3 I B
months.
For patients with unprovoked PE, oral anticoagulation is
I A
recommended for at least 3 months.
Extended oral anticoagulation should be considered for
patients with a first episode of unprovoked PE and low IIa B
bleeding risk.
Anticoagulation treatment of indefinite duration is
recommended for patients with a second episode of I B
unprovoked PE.
Rivaroxaban (20 mg once daily), dabigatran (150 mg twice
daily, or 110 mg twice daily for patients 80 years of age or
those under concomitant verapamil treatment) or
apixaban (2.5 mg twice daily) should be considered as an IIa Be
alternative to VKA (except for patients with severe renal
impairment) if extended anticoagulation treatment is
necessary.
 Recommendations for duration of anticoagulation
after pulmonary embolism
Recommendations Classa Levelb
In patients who receive extended anticoagulation,
the risk-benefit ratio of continuing such treatment I C
should be reassessed at regular intervals.
In patients who refuse to take or are unable to
tolerate any form of oral anticoagulants, aspirin may
IIb B
be considered for extended secondary VTE
prophylaxix
In patients with refuse to take or are unable to
tolerate any form of oral anticoagulants, aspirin may
IIa B
be considered for extended secondary VTE
prophylaxis.
For patients with PE and cancer, extended
anticoagulation (beyond the first 3-6 months) should
IIa C
be considered for an indefinite period or until the
cancer is cured.
Inferior vena caval filter
Indication:
Failure of anticoagulation
Contraindicated for anticoagulation
Patients with low cardiopulmonary
reserve (any further emboli would
likely to be fatal)
Complications
Thrombosis at insertion site
Penetration of the vessel wall
Venous insufficiency
 Catheter embolectomy
Interventional thrombus fragmentation with or
without embolectomy
Using device with suction or balloon
embolectomy
 Surgical Embolectomy
In severe hemodynamic instability
Almost certain clinical diagnosis of massive PE
Contraindication to thrombolytic therapy
Close to OR
Others: free-floating thrombi in the Rt atrium or
ventricle, impending paradoxical embolism via PFO
Postoperative period iv heparin can be started
as early as 12 hr postop (closed monitoring)
 Thrombolytics
Agent Regimen

Streptokinase 250,000 U over 30 min, followed by 100,000 U/hr over 12-24 hr

Accelerated regimen: 1.5 million U over 2 hr

Urokinase 4,400 U/kg over 10 min, followed by 4,400 U/kg over 12-24 hr
Accelerated regimen: 3 million U over 2 hr

Alteplase 100 mg over 2 hr

Accelerated regimen: 0.6 mg/kg over 15 min
Reteplase 2 bolus of 10 U, 30 min apart

tenecteplase 30-50 mg over 5-10 sec. adjusted dose by BW

<60 kg, 30 mg
60 - <70 kg, 35 mg
70 - < 80 kg, 40 mg
80 - < 90 kg, 45 mg
90 kg, 50 mg
 Dx & Rx acute PE
Clinical assessment ( Hx & Physical exam →
clinical probability +/- D-dimer )
Initial empirical treatment ASAP
Investigation for diagnosis and Severity
assessment
Additional treatment e.g. thrombolytics in
massive PE
Asymptomatic pulmonary embolism

• “incidental pulmonary embolism”

• Incidence 2.6% in patients with
malignancy (CT for other reasons)
• No evidence that they are harmless – so it
should be treated as symptomatic PE if no
contraindication
 Defect resolved
With heparin treatment :
- 36% by day 5
- 52% by day 14
- 73% by 3 month
- 76% at 1 year
• Most patients (81%) showed complete
resolution of PE on CT angiography after
28 days. PEs resolved faster in the main
and lobar pulmonary arteries than in the
segmental branches.

Stein P, et al. AJR 2010;194(5):1263.

• % Patients with residual pulmonary
thrombi
– 87% at 8 days after diagnosis,
– 68% after 6 weeks,
– 65% after 3 months
– 57% after 6 months
– 52% after 11 months.
• > 50% of patients with PE still have defects 6 M
after Dx, Routine re-imaging after cessation of
anticoagulant therapy in patients with PE to
obtain a new baseline could be considered.
Nijkeuter M, et al. Chest 2006;129(1):192-7
 Estimated radiation absorbed in procedures used for diagnosing PE
(adapted from Bajc et.al. 2009 and Chunilal et.al. 2009).

Test Estimated fetal Estmated maternal

radiation radiation exposure
exposure (mSv) to breast tissue
(mSv)
Chest X-ray < 0.01 0.01
Perfusion lung scan with
technetium-99m labeled albumin
Low dose: 40 MBq 0.11 – 0.20 0.28 – 0.50
High dose: 200 MBq 0.20 – 0.60 1.20
Ventilation lung scan 0.10 – 0.30 < 0.01
Computed tomographic 0.24 – 0.66 10 – 70
angiography
Pulmonary angiography 2.2 - 3.7
 Rx of PE during pregnancy
• UF heparin or weight-adjusted LMWH
• Extreme overweight or renal dysfunction –
monitor anti-Xa activity
• Do not use
– Fondaparinux
– VKA – fetal anormaly, bleeding
– NOACs

heparin IN
greg
 Rx after delivery
• LMWH should be stopped at least 12 h
prior to delivery and restart 12-24 h after
delivery
• Switch to VKA after delivery (OK for breast
feeding mother)
• At least 3 months Rx after delivery
 PE and Cancer
• Risk of VTE 4 x in cancer
– MM : 46 x
– Brain tumor : 20 x
– Pancreatic CA : 16 x
• Common in lung, colon, prostate cancer
• Patients received chemotherapy risk : 6 x
• First 6 weeks after cancer surgery: 90 x
• 4-20 M after cancer surgery: 30 x
 Rx of PE in Cancer
Recommendation Class level
Incidental PE in pt with cancer should e IIa C
managed in the same manner as
symptomatic PE
Negative D-dimer have the same negative Iia B
diagnostic value as in non-cancer patients
Pt with PE and Cancer, weight-adjusted Iia B
SQ LMWH should be considered for the
first 3-6 M
Pt with PE and Cancer, extended IIa C
anticoagulation (beyond first 3-6 M) should
be considered for an indefinite period or
until the cancer is cured
Dx & Rx VTE perioperative aspect
Clinical assessment ( Hx & Physical exam →
clinical probability + addition tests)
Initial empirical treatment ASAP
Investigation for diagnosis and Severity
assessment
Additional treatment in massive PE
Consider risk of bleeding during perioperative
period for Rx
Prophylaxis should be considered
 Previous VTE going to surgery
• Consideration
– Timing of VTE
– ongoing risks for recurrent VTE
– bleeding risk
• High risk group: prefer preop bridging with
LMWH or IV UF heparin - stop 24 hr prior to Sx
and restart 24 hr after Sx
• Low risk group: no need for preop bridging ,
restart Rx 24 hr after Sx
• High bleeding risk: may need preop IVC filter, restart
Rx 48-72 hr after Sx
 Heparin induced
thrombocytopenia (HIT)
HIT more common in UF heparin than LMWH
Presented with rebound or recurrent thrombosis,
not bleeding
Incidence of HIT
- UF heparin up to 5%
- LMWH
8
0-0.9%
Stop heparin when platelet count < 50,000/mm3
or ↓ by 50% or thrombotic event occur
HIT treatment in Thailand

O
Stop heparin or LMWH
Switch to fondaparinux sq once or twice a day

D
Start warfarin when possible (not immediately
after stop heparin)