Deep and superficial venous system

Venous Thromboembolism
Deep Venous Thrombosis
and Pulmonary Embolism

Venous disease
Veins
Tunica media

Intima

Adventitia
Internal
elastic membrane

Telangiectasis

Varicose veins

Oedema

Lipodermatosclerosis

Venous
leg ulcer

Varicose vein
What Is DVT?
Membrane adhesion Molecule expression
(ICAM-1, E-selectin,)

Venous valve

Venous wall
remodeling

Pressure and shear stress

induced gene expression
(TNF, IL-1, )

DVT is a blood clot

that forms in a vein
deep in the body
Most often occurs in
the deep veins of the
legs, either above the
knee or below it
The blood clot or part of it can break free (called
emboli) and become lodged in the blood vessels of
the lung, causing PE

Thrombophlebitis
Formation of a venous clot depends on the
presence of of at least of one of Virchows triad
factors
-venous stasis
-injury to vessel wall
-hypercoagulable state

Malignancy
Surgery
Trauma
Pregnancy
Oral contraceptives or
hormonal therapy
Immobilization
Inherited
thrombophillia

Annual incidence of venous

thromboembolism (VTE) is 1/1000
DVT accounts for over one half of VTE
Carefully evaluated, up to 80% of patients
with VTE have one or more risk factors
Majority of lower extremity DVT arise from
calf veins but ~20% begin in proximal veins
About 20% of calf-limited DVTs will
propagate proximally

Absolute Risk of DVT

DVT VTE Risk Factors

DVT Epidemiology and Etiology

Patient Group

Presence of venous
catheter
Congestive failure
Antiphospholipid
antibody syndrome
Hyperviscosity
Nephrotic syndrome
Inflammatory bowel
disease

DVT Prevalence, %

Medical patients
General surgery
Major gynecologic surgery
Major urologic surgery
Neurosurgery
Stroke
Hip or knee arthroplasty,
hip fracture surgery
Major trauma
Spinal cord injury
Critical care patients

10 20
15 40
15 40
15 40
15 40
20 50
40 60
40 80
60 80
10 80

Pathophysiology
Thrombi usually form at the venous cusps of
deep veins where altered or static blood flow
causes clot formation
Alternatively,
clots form from
intimal defects
Clots are
composed from
fibrin, red cells and
platelets and cause
partial/complete
obstruction of vein

Pathophysiology
Postphlebitic syndrome (PPS) may
develop after the resolution of a DVT
PPS is due to valvular incompetence,
persistent outflow obstruction and
abnormal microcirculation.

Superficial Thrombophlebitis
Thrombosis can occur in any superficial vein
primarily the saphenous vein and its tributaries
Local pain, redness, and tenderness are
characteristic findings.
Mild cases can be treated with warm compresses,
analgesia and elastic supports
Severe cases can be debilitating and should be
managed by bed rest, elevation of extremity,
support stockings, and analgesia.
Antibiotics and anticoagulants are useful in septic
thrombophlebitis

DVT Clinical Presentation

Classically = calf pain, tenderness, swelling,
redness and Homans sign
Overall sens/spec = 3-91%
Up to 50% have none of these

Wells developed and tested a clinical

prediction model for DVT

Superficial Thrombophlebitis
Incidence of DVT from extension of a
superficial clot is 3%.
Most clots in great saphenous vein will
extend into a deep vein system in a week or
so thus a follow-up US is guaranteed
Definite treatment is ligation and excision of
affected vein.

Physical examination
Homans test: Dorsiflexion of foot elicits pain
in posterior calf. However, it must be noted
that it is of little diagnostic value and is
theoretically dangerous because of the
possibility of dislodgement of loose clot.
Pratts sign: Squeezing of posterior calf elicits
pain.

Wells PS, Anderson DR, Bormanis J, et al. Value of assessment of pretest

probability of deep-vein thrombosis in clinical management. Lancet 1997;350
(9094):1795-8.

Deep Vein Thrombosis

Symptomatic DVT will be in popliteal or more
proximal veins more than 80%
Nonextending calf DVT rarely cause PE
Uncommon presentations of DVT include
phlegmasia cerulea dollens and phlegmasia alba
dollens
In phlegmasia cerulea dollens, patients present with
extensive swollen and cyanotic leg due to massive
ileofemoral thrombosis which can lead to venous
gangrene.

Deep Vein Thrombosis

In phlegmasia alba dolens, the leg is white
due to arterial spasm secondary to massive
iliofemoral thrombosis, often mistaken for
arterial occlusion.
PPS can be difficult to differentiate from
recurrent DVT due to pain, swelling and
ulceration of the skin.
Up to to one third of the patients with DVT
can develop PPS.

DVT Wells Score

The following were assigned a point value of 1 if
present:
Entire leg
Cancer
swollen
Paralysis or
Calf > 3cm
plaster
larger than
immobilization
unaffected leg
Bedrest > 3 d or
Pitting edema
surgery in past
greater than
4 wks
unaffected leg
Localized
Collateral
tenderness
superficial
veins
Wells PS, Andersen DR, Bormanis J et al. Lancet. 1997;350:1795-8

Deep Vein ThrombosisDiagnosis

All patients with any signs or symptoms
suggestive DVT should undergo an
objective diagnostic evaluation
Venography was the historical gold
standard for detection of DVT with 100%
sensitivity and specificity but it is invasive
and can cause contrast-related reactions,
phlebitis and DVT (3%).

Deep Vein Thrombosis-Diagnosis

Impedance plethysmography (IP) is portable
and inexpensive but less sensitive than US
IP measures changes in electrical resistance
in response to changes in calf volume due to
obstruction

DVT Wells Score

Alternative diagnosis more likely than DVT = - 2 points
Probability: High ( 3), Moderate (1-2) or Low (0 or
less)
DVT risk: High 75%, Moderate 17%, Low 3%

Wells PS, Andersen DR, Bormanis J et al. Lancet. 1997;350:1795-8

Deep Vein Thrombosis-Diagnosis

Choice of test to identify DVT is ultrasound
Ultrasound has 97% and
94% sensitivity and
specificity respectively for
detecting proximal DVT
Ultrasound is less sensitive
for pelvic DVT and has
sensitivity of 73% for a calf
DVT.

Deep vein thrombosis-Diagnosis

Radioisotopes have been used to diagnose DVT but
are not particularly useful in ED
MRI is being used with increased frequency and can
detect a filling defect in entire extremity (including
calf and pelvic veins)
D-Dimer fragments which are degradation products
of fibrin can be used to as an indicator for the
presence or absence of DVT or PE.
The ELISA based D-Dimer has sensitivity 97 % and
specificity 35%

Deep Vein Thrombosis-Diagnosis

When D-Dimer is less than 500 ng/ml, the
likelihood of DVT is less than 1%.
The latex agglutination assay D-Dimer is less
sensitive than the ELISA essay.
Sepsis, surgery, trauma, hemorrhage,
pregnancy, cardiovascular diseases, collagen
vascular disease, liver disease, cancer are
associated with elevated d-dimer value.

DVT D-Dimer
A positive quantitative
ELISA
Unfortunately a
positive d-dimer is not
helpful diagnostically
An imaging study is
needed

Clinical Approach to Establishing the Diagnosis

VTE Prophylaxis
1
2
3
4

Low dose unfractionated heparin (LDUH)

Low molecular weight heparin (LMWH)
Intermittent pneumatic compression devices (IPC)
Graduated compression stockings (GCS)
5 Factor Xa
Inhibitor
6

Warfarin

VTE Prophylaxis: Grade 1 Recommendations

Surgery

Recommended Prophylaxis

General surgery

Any of the following:

Low-dose unfractionated heparin (LDUH)
Low molecular weight heparin (LMWH)
LDUH or LMWH combined with IPC or
GCS

General surgery with high risk for bleeding

(based on physician-documentation of
bleeding risk)

Any of the following:

Graduated Compression stockings (GCS)
Intermittent pneumatic compression (IPC)

Gynecologic surgery

Any of the following:

Low-dose unfractionated heparin (LDUH)
Low molecular weight heparin (LMWH)
Intermittent pneumatic compression
devices (IPC)
LDUH or LMWH combined with IPC or
GCS

Treatment
Bed rest, leg elevation and elastic stockings
are of unproven benefit in the management
of DVT.
Aggressive anticoagulation will prevent
extension of the clot.
Early ambulation after adequate
anticoagulation is a safe approach
Primary objective of treating DVT is the
prevention of pulmonary embolus

Treatment
Patients with negative ultrasound can safely
have a repeat ultrasound in a week without
anticoagulation
Risk of PE in these patients is near 0% and
risk of forming a DVT is 1%.
Anticoagulation is recommended for
patients with calf DVT who had PE/DVT,
immobile, have hypercoagulable state

Treatment - LMWH
Fondaparinux sodium (Arixtra) - works by
inhibiting factor Xa
Prophylaxis: 2.5 mg SC qd starting 6 h after
surgery for 5-11 d; may administer up to 24
additional days following hip fracture
Treatment:
<50 kg: 5 mg SC qd
50-100 kg: 7.5 mg SC qd
>100 kg: 10 mg SC qd
Initiate warfarin within 72 h and continue
fondaparinux for at least 5 d until oral
anticoagulant effect established (ie, INR 2-3)

Treatment - LMWH
Enoxaparin (Lovenox)
LMWH used in treatment of DVT and PE as well
as DVT prophylaxis.
Enhances inhibition of factor Xa and thrombin by
increasing antithrombin III activity. Slightly affects
thrombin and clotting time and preferentially
increases inhibition of factor Xa.
Average duration of treatment is 7-14 d.

Treatment
Patients with proximal DVT require
anticoagulation
Preferred treatment is LMWH over UFH
because of the ease of administration, more
predictable anticoagulant effect, lack of need
to monitor the anticoagulation effect, lower
incidence of major bleeding and HIT
LMWH has a preferentially inhibitory effect
on factor Xa.

Treatment - LMWH
Dalteparin (Fragmin) - Enhances inhibition of
factor Xa and thrombin by increasing antithrombin
III activity. In addition, preferentially increases
inhibition of factor Xa.
Abdominal surgery: 2500 IU SC qd for 5-10 d
High-risk patients undergoing abdominal surgery:
5000 IU SC qd for 5-10 d
Hip arthroplasty: 2500 IU SC 4-8 h following
surgery, then 5000 IU SC qd for up to 14 d

Treatment
Because of LMWH is cleared by the kidneys, it
should be avoided in outpatients with Cr >2.03
One need not to wait for the creatinine result
before initiating LMWH therapy.
The ability to discharge patients from the ED after
initial dose of LMWH is cost-effective, safe, practical
and acceptable practice as long as there is a secured
24 hr follow up with PCP.

Adult dose - 1 mg/kg SC bid; alternatively,

administer 1.5 mg/kg SC qd

Treatment
Indications for admission include inability to
ambulate, poor social support, unreliable
follow-up, difficulty with education with
drug administration, need for lysis or
invasive therapy, and an alternative serious
diagnosis under investigation or that
requires treatment(arterial ischemia,
cellulitis, pelvic mass)

Treatment
In pregnant pt who cannot have heparin, danaproid
should be used.
It is acceptable to start coumadin and LMWH
simultaneously.
Warfarin interferes with hepatic synthesis of vitamin
Kdependent coagulation factors.
2-10 mg/d PO
Dose must be individualized and adjusted to maintain
INR at 2-3.
Warfarin is contraindicated in pregnancy, active
bleeding, recent major surgery (thoracoabdominal,
nervous system, spine, eye)
LMWH does not interfere with the work up of a
possible hypercoagulable state compared with UFH.

Treatment
Thrombolysis for DVT is indicated for
extensive iliofemoral thrombosis and
upper extremity DVT in patients with
low risk for bleeding.

Treatment
If LMWH is contraindicated, use UFH as 80
units/kg bolus and then 18 units/kg/hr
Serious bleeding from LMWH cannot be
completely reversed with protamine which
has been associated with hypotension and
anaphylactoid reactions.
If a patient has contraindication to heparin
like in pt with HIT, you can use a thrombin
inhibitor like lepirudin

Treatment
Initial hematological testing at follow-up
includes factor V leiden, prothrombin
molecular tests, screening for
antiphospholipid anticoagulants and a
fasting homocysteine level.
Upon completion of the anticoagulation ,
further testing includes antithrombin III,
protein C, protein S, and factor VIII level

Thrombolytics
Urokinase - Direct plasminogen activator isolated
from human fetal kidney cells grown in culture. Acts
on endogenous fibrinolytic system and converts
plasminogen to enzyme plasmin. Plasmin degrades
fibrin clots, fibrinogen, and other plasma proteins. It
is nonantigenic but more expensive than
streptokinase, which limits its use. When used for
purely local fibrinolysis, it is administered as local
infusion directly into area of thrombus and with no
bolus.
4400 U/kg IV bolus followed by maintenance
infusion at 4400 U/kg/h for 1-3 d
For regional thrombus-directed therapy, smaller
bolus of 250,000 U IV may be given followed by
infusion at 500-2000 U/kg/h

Thrombolytics
Streptokinase
Acts with plasminogen to convert plasminogen to
plasmin. Plasmin degrades fibrin clots as well as
fibrinogen and other plasma proteins. An increase in
fibrinolytic activity that degrades fibrinogen levels for
24-36 h takes place with IV infusion of
streptokinase.
250,000 U IV bolus followed by an infusion at
100,000 U/h for 1-3 d

Thrombolytics
Alteplase
A tissue plasminogen activator (tPA) produced by
recombinant DNA and used in the management of
acute myocardial infarction, acute ischemic stroke,
and PE.
100 mg IV over 2 h recommended for treatment of
massive PE
For DVT, an infusion of 0.5-1.5 mg/h utilizing
catheter-directed therapy has been used, depending
on local expertise

Treatment
Treatment
Thrombectomy is only indicated with ischemic
leg secondary to a massive venous clot like in
phlegmasia cerulea dolens.
In ED , pt adequately anticoagulated who present
with new thrombus or propagation should
receive LMWH
If the fail LMWH or there is a free-floating
thrombus an IVC should emergently inserted.
IVC filter is indicated for when anticoagulation
therapy is contraindicated, there is embolization of
DVT after 1-2 weeks of anticoagulation

Pelvic Vein Thrombosis

Usually its an extension of a clot from the
femoral vein.
An isolated pelvic vein thrombosis is rare and
can be a complication in the postpartum period,
after pelvic surgery or trauma.
Septic pelvic vein thrombophlebitis is a lifethreatening condition after post-partum
endometritis and is usually diagnosed with CT
or MRI.

Axillary and Subclavian Vein

thrombosis
2-4% of DVTs occur in axillary or
subclavian vein
PE occurs in 5-10% of cases involving
axillary or subclavian DVT

Spontaneous (Primary) ULDVT

Upper vs. Lower DVTs

First described by Paget and

Schroetter - AKA PagetSchroetter syndrome, effort
thrombosis
Compressive anatomy at thoracic
outletcompression of vein b/w
first rib and hypertrophied
scalene or tendons
Can occur after strenuous activity
of arms and shoulders

Virchows triad (venous stasis,

hypercoagulability, endothelial trauma)
UL: Higher venous flow, less stasis,
gravitational effects
Direct endothelial trauma: effort in
primary; iatrogenic in secondary

Secondary ULDVT
Central venous catheters
Pacemakers
Higher incidence: Chemotherapy, TPN
via central lines
Improper placement of catheter tip
Incidence varies: 1-4% of all DVTs

Associated Conditions
Presence of a central venous catheter in
(72%)
Infection (28%)
Extrathoracic malignancy (22%)
Thoracic malignancy in (21%)
Renal failure (21%)
Prior lower-extremity deep venous
thrombosis (18%)
Marinella MA, Kathula SK, Markert RJ. Heart Lung. 2000 MarApr;29(2):113-7. Spectrum of upper-extremity deep venous thrombosis in
a community teaching hospital.

Clinical Features

Arm swelling, pain, heaviness

Dilated subcutaneous veins
JVD
Upper limb cyanosis
Can be asymptomatic
DDx: superficial thrombophlebitis

Diagnosis
Duplex ultrasonography

Aggressive diagnosis: digital subtraction

venography, MRV, CTV
Sajid, M, et al. Upper Limb Deep Vein Thrombosis: A Literature
Review to Streamline the Protocol for Management. Acta Haematol
2007; 118.

Treatment Protocol

Treatment
Expectant management
Removal of offending agent
Anticoagulation (standard: heparin x 5-7
days, 3 mos of Coumadin)
Thrombolysis (streptokinase, urokinase,
TPA)
Surgery
SVC filter

SVC Filters

SVC Filters

Ascher, Enrico, Hingorani, Anil, Mazzariol, Fernanda, Jacob, Theresa, Yorkovich, William,
Gade, Prasad
Clinical Experience with Superior Vena Caval Greenfield Filters. Journal of Endovascular
Surgery 1999 6: 365-369

Insertion of SVC Greenfield filters is a safe and

feasible therapy to prevent recurrent
thromboembolism in patients with UEDVT who
are refractory to or inappropriate for
anticoagulation therapy.

Ascher E, Hingorani A, Tsemekhin B, Yorkovich W, Gunduz [Link] learned from a 6-year

clinical experience with superior vena cava Greenfield filters. J Vasc Surg. 2001 Apr;33(4):907

Insertion of SVC-GFs is a safe, efficacious, and

feasible therapy and may prevent reccurent
thromboembolism in patients with UEDVT who are
resistant to anticoagulation or have contraindications
to anticoagulation

PULMONARY EMBOLISM

The American Journal of Medicine, Vol 123, No 5, May 2010

10

PE - PATOPHYSIOLOGY(1)
PE Epidemiology and Etiology
Embolus travels through the heart
and obstructs a blood vessel in the
lung

100-200,000 deaths per year due to

PE
Most PE arise from lower extremity
DVT
In patients with DVT, 40-60% will
have a PE on V/Q scanning

Embolus travels through

the bloodstream to the
heart

Diagnosis crosses most

Specialties
Pulmonary embolus is not a disease.
It is a complication of DVT. Ken
Moser MD

Blood clot forms in a vein and breaks

free from vessel wall

PE - PATOPHYSIOLOGY(3)

DIAGNOSIS

Based on:
Relevant SYMPTOMS & SIGNS
Associated RISK FACTORS
Probability of ALTERNATIVE
Diagnosis
OBJECTIVE Confirmation

Risk factors in those with

Acute DVT / PE

PULMONARY EMBOLISM
What are the risk factors for
pulmonary embolism and or DVT

Risk factor
Age > 40 years

n = 1231

%
88.5

Obesity
Hx venous thromboembolism
Cancer
Bed rest > 5 days
Major Surgery

37.8
26.0
22.3
12.0
11.2

Anderson FA et. Al J Vasc Surg 1992

11

Risk factors in those with

Acute DVT / PE

Risk factors in those with

Acute DVT / PE

Risk factor

Multiple trauma

1.1

CHF

n = 1231

8.2

childbirth

1.1

Varicose veins

5.8

Myocardial infarction

0.7

Fracture hip or leg

3.7

one or more risk factors

96.3

Estrogen

2.0

two or more risk factors

76.0

Stroke

1.8

Three or more risk factors

39.0

Anderson FA et. Al J Vasc Surg 1992

PULMONARY EMBOLISM
90% of clinically important PE results
from leg DVT
96% of patients with DVT or PE have one
or more risk factors
The risk increases in proportion to the #
of risk factors

RISK FACTORS (uncommon)

Deficiencies Protein C or S
Antithrombin III deficiency
Resistance to protein C activating
Factor V Leiden polymorphism
Homocystinuria
Polycythemia rubra vera
SLE, Bchets, nephrotic syn.

Anderson FA et. Al J Vasc Surg 1992

Proportion of patients clinically

suspected DVT in whom Dx. Was
confirmed increases with the # of risk
factors
# of DVT risk factors
0
1
2
3
4 or more

Confirmed DVT(%)
11%
24%
36%
50%
100%

Arch Surg 1982

PULMONARY EMBOLISM

What are the SYMPTOMS and

SIGNS of Pulmonary embolism?

12

PULMONARY EMBOLISM
SYMPTOMS

Chest Pain

Apprehension

88%

- pleuritic

74%

-non pleuritic

14%

PULMONARY EMBOLISM
SYMPTOMS

Cough
Hemoptysis
Syncope

Dyspnea

59%
53%
30%
13%

85%

PULMONARY EMBOLISM
SIGNS

Tachypnea
Crackles
Tachycardia
Fever
Increased P2
Phlebitis

92%
58%
44%
43%
53%
32%

PE Assign Pretest Probability

PE Assigning Pretest Probability

Single most important step in the

diagnosis of pulmonary embolism
May be done based on clinical
judgment or aided by a clinical
scoring system
Modified Wells Criteria is the most
widely used and studied
Reliably stratifies patients by
likelihood of PE to allow selection of
safe (<2% VTE risk if no
anticoagulation) management
strategy

13

Diagnostic tests in PE

ECG FINDINGS
Sinus Tachycardia
T wave inversion
ST segment depression
Low voltage
L axis
S1 Q3 T3
ST elevation
R Bundle Branch Block

ECG FINDINGS

43%
40%
33%
16%
12%
11%
11%
11%

X-RAY FINDINGS
Diaphragm elevation

41%

Consolidation

40%

Pleural effusion

28%

Distended prox. Pulm art. 23%

X-RAY FINDINGS

Atelectasis

20%

Oligemia

15%

X-RAY FINDINGS

14

X-RAY FINDINGS

X-RAY FINDINGS

P.E.
Hamptons
Hump

DIFFERENTIAL DIAGNOSIS
CHF
Asthma / COPD exacerbation
Pneumothorax
Pneumonia
Shock
Pleural disease
Chest wall Pain

Diagnosis Pulmonary Embolism

P.E.
subsegmental
defect

DIFFERENTIAL DIAGNOSIS

Myocardial infarction
Pericarditis
1 or metastatic ca.
Hyperventilation syndrome
Infradiaphragmatic process
e.g. cholecystitis, splenic infarction

Diagnosis: Objective Confirmation

Documentation of clot in the leg by:

How do you confirm the
diagnosis?

Compression Ultrasound or
Impedance Platysmography or
Intravenous Venogram
1st Test Compr. Ultrasound

15

Diagnosis: Objective
Confirmation

Since the treatment for DVT and PE

is the same, the demonstration of
clot in the leg is sufficient for the
diagnosis of Pulmonary Embolism

Diagnosis: Objective Confirmation

Diagnosis: Objective Confirmation

Pulmonary Angiogram
(GOLD STANDARD)
expensive
Technically more difficult requiring
skilled personnel
More risk for side effects
Not always available

VENTILATION /
PERFUSION SCANS

Normal lung scan means:

no perfusion defects
the perfusion matches
the ventilation scan

VENTILATION /
PERFUSION SCANS

Normal V/Q
Scan

High Probability lung scan

> 1 lung segmental or
greater perfusion defects
with normal ventilation
or > 2 large subsegmental
defects (>75% of a
segment) with normal
ventilation

J. Galvin, M.D. [Link], B.S. The Diagnosis of P. E. Virtual Hospital:[Link]

16

High
Probability
V/Q Scan

CAUSES OF ABNORMAL V/Q SCANS

EXTRA LUMINAL
Tumor
Adenopathy
Vascular structures
REGIONAL HYPOXIC VASOCONSTRICTION
Reactive airways
Mucous plugs or Foreign body
VASCULAR RESISTANCE
CHF
Pneumonia

Advantages of V/Q Lung Scans include:

1. a normal V/Q scan rules out PE

2. the radiation dose is low
3. iodine-based contrast is not used

CAUSES OF ABNORMAL V/Q SCANS

INTRALUMINAL
Clots
Fat emboli
Tumor
Vasculitis
or vascular
stenosis
Parasites
Fungi

VENTILATION /
PERFUSION SCANS

Non-High Probability
Ventilation perfusion defects that
did not qualify as
high or normal

D-dimer

A degradation product of of
crosslinked fibrin
High number of conditions that
activate coagulation & fibrinolysis e.g.
Surgery, inflammation, cancer
trauma.

17

PE Use of D-Dimer
Sensitive assay can exclude PE in low risk
patient
In patients with moderate pretest
probability only rapid quantitative ELISA
can adequately exclude PE
Patients judged to be high risk for PE
would still have a posttest PE probability
of 5-20% even after negative ELISA and
require further testing
Roy PM, Colombet I, Durieux R, et al. Systematic review and meta-analysis of strategies
for the diagnosis of suspected pulmonary embolism. BMJ. 2005;331(7511):259

PE Helical CT (CTA)
Negative CTA could safely exclude PE
in low risk patients
Negative LE US plus negative CTA
could exclude PE in moderate risk
patients

Eng J, Krishnan JA, Segal JB, et al. AJR 2004;183(6):1819-27. Roy PM, Colombet I,
Durieux P, et al. BMJ 2005;331(7511):259.

Role of Spiral CT Scan

PE Helical CT (CTA)

Spiral/Helical CT (SCT)
There are 3 SCT patterns:
1.
No PE seen and an alternate diagnosis
is found. This group does not require any
further investigation for VTE.
2.
Definite PE is detected in a segmental
or larger pulmonary artery.
3.
Patients with normal SCT, technically
inadequate scans, and scans that report
subsegmental PE are all considered
nondiagnostic. Further testing is required in
patients with these SCT patterns.

Easily done non invasive test with few

complications
Requires proper equipment and experienced
readers
Rarely cannot perform e.g. allergy, SVC syn.
Renal insufficiency, Approximately 10-13%
Sensitivity 90%, specificity 95%, with
multidetector CT in experienced hands

Advantages of SCT include:

[Link] to directly visualize emboli

[Link] accuracy for large emboli

(segmental or larger)
[Link] to provide the alternate
diagnosis in patients who dont have PE

18

Limitations of SCT include:

[Link] defects confined to subsegmental
vessels are not diagnostic
[Link] must be given (problematic in
patients with renal insufficiency or a history of
contrast allergy)
3.A normal SCT does not rule-out small PE
[Link] radiation (equivalent to ~500 chest
x-rays)

Venous Imaging in Suspected PE

Since almost all pulmonary emboli arise from DVT, a
useful strategy in some patients with suspected PE is to
look for the presence of DVT using Duplex ultrasound
(DUS).
If the DUS of the proximal veins is positive, the patient
requires treatment (the treatment of proximal DVT and
PE is the same).
If the DUS is negative, the risk of recurrent PE in the
short term is very low.
Repeating the DUS testing in 5-7 days and 12-14 days
is a safe strategy in suspected PE with nondiagnostic
lung imaging.

TREATMENT of PULMONARY
EMBOLISM

TREATMENT of PULMONARY
EMBOLISM

Both Pulmonary embolism and

DVT are treated the same
An adequate level of
anticoagulation is essential
Patients will have variable effect of
anticoagulants
Treatment requires monitoring

Bolus of 5-10,000 units of (unfractionated)

HEPARIN + maintenance dose with
heparin nomogram

Heparin Nomogram

APTT Bolus Stop

Rate
Repeat
(sec) Dose infusion change
PTT
<64 5,000u 0 min.
150u/hr 6 hours
65 74
0
0 min.
100u/hr 6 hours
75100
0
0 min. 0 change Next am
101-110
0
0 min.
50u/hr. Next am
111-125
0
30 min. 100u/hr 6 hours
>125
0
60 min. 200u/hr 6 hours

Low Molecular Weight Heparin if patient

is hemodynamically stable

TREATMENT of PULMONARY
EMBOLISM

Start oral anticoagulants in 24 -72 hrs.

with 5 day crossover with heparin
Duration: - 3 - 6 months if correctable
cause e.g. surgery
- indefinitely if no known cause or
recurrent or ongoing risk e.g cancer

19

TREATMENT of PULMONARY
EMBOLISM

TREATMENT of PULMONARY EMBOLISM

Side effects of heparin

Low Molecular Weight Heparin

abnormal bleeding especially if

predisposed e.g. peptic ulcer disease

increased half life

Increased bioavailability
low frequency of bleeding
administered once a day
less monitoring
More Expensive*

Heparin induced trombocytopenia which is

associated with increased clotting

TREATMENT of PULMONARY EMBOLISM

Take Home Points

TREATMENT of PULMONARY EMBOLISM

Take Home Points

DVT and PE are the same disease

Assigning pretest probability for VTE is an
essential step in diagnosis
A noninvasive testing strategy can result in safe
management for most patients suspected of
having VTE
Always consider VTE prophylaxis in inpatients

20