Pulmonary Embolism - NCI

Pulmonary Embolism - NCI

Pulmonary Embolism - NCI


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Pulmonary Embolism

Pulmonary Embolus is a fragment of the

thrombus that breaks off and travels in

the blood until it lodges at the

pulmonary vasculature.

-The majority of clinically significant

pulmonary emboli begin in the pelvic or

lower extremity veins.

-The morbidity and mortality associated

with this disease remains unacceptably


-It is estimated that 500,000 suffer from

pulmonary emboli each year and that

50,000 of those will die

Diagnosis of Pulmonary Embolism (PE)

1-Clinical picture.

2-Look for risk or predisposing factors for DVT

3-Look for ventilation-perfusion mismatch

4-Testing for PE.

-A chest radiograph


-Ventilation-perfusion scanning (V/Q scanning).


-Spiral CT


1-Signs and Symptoms of PE

• Dyspnea 73%

• Pleuritc Pain 66%

• Cough 43%

• Leg Swelling 33%

• Leg Pain 30%

• Hemoptysis 15%

• Palpitations 12%

• Wheezing 10%

• Angina-Like pain 5%

The signs and symptoms serve only to raise the suspicion of

pulmonary embolus

2-Predisposing Factors

Primary risk factors


Major Trauma


Congestive Heart Failure

Myocardial infarction


Minor risk factors


Bed Rest

Estrogen therapy

3-Look for ventilation-perfusion mismatch

By calculating A-a O2 gradient = PaO2 (alveolar) - PaO2


Normal A-a O2 gradient is 5-20 and increases with age.

-Elevated in 80% to 90% in PE

-Normal in 10% to 20% in PE

PAO2 (alveolar) = 150 - 1.2(PaCO2), assuming patient

breathing room air

150 - 1.2 (40) = 102 150 – 1.2 (35) = 108

102-100 = 2 108 -100 = 8

4-Testing for PE

-A chest radiograph


-Ventilation-perfusion scanning (V/Q scanning).


-Spiral CT


Abnormalities on Chest Radiography

14% Normal

68% Atelectasis or parenchymal density

48% Pleural Effusion

35% Pleural based opacity

24% Elevated diaphragm

15% Prominent central pulmonary artery

7% Cardiomegally

5% Pulmonary edema

Figure 1

Atelectasis 68%


Atelectasis and parenchymal densities are quite common. Most

of these densities are caused by pulmonary hemorrhage and


Pleural Effusion 48%

Figure 2

Pleural effusions are common and most often unilateral

occupying less than 15% of a hemithorax

Figure 4

Elevated diaphragm 24%

A diaphragm may be elevated, reflecting

volume loss in the affected lung.

ECG of Acute pulmonary embolus

-An S1Q3T3 pattern:

prominent S wave in lead I, Q wave and

inverted T wave in lead III

-Sinus tachycardia

-T wave inversion in leads V1 - V3

-Right Bundle Branch Block

-low amplitude deflections

ECG of Acute pulmonary embolus

Ventilation-perfusion scanning

It visualizes the gas exchange in the lungs using

Xenon-133 and the perfusion of the lung using

technetium99m-labeled albumin aggregates.

In practical terms, the test can be:

* High probability.

• Intermediate probability.

• Low probability.

*Normal .

High probability V/P scan


This V/P scan demonstrates a high probability

scan with multiple segmental defects and normal

ventilation in those areas

Intermediate probability V/P scan

scans with sub segmental defects or defects of any

size that match abnormalities on the chest x-ray

or the ventilation scan.

Interpretation of V/Q Scan




Probability of



High probability

High or


96% +

Treat for PE

Medium probability

Medium probability





Need further


Need further


Low probability

Low probability




4% <

Need further







Pulmonary angiogram

It is the "gold standard" test

If you absolutely must know whether the patient had pulmonary

embolism there is no substitute for a well done angiogram.

With the angiogram you look for cut-offs in

the vascular tree or for intraluminal filling


Pulmonary angiogram showing

intraluminal filling defects.



The typical appearance of a pulmonary

infarct on CT includes a pleural based

density with convex borders and a

linear strand at the apex of the triangle.

The differential diagnosis for this

abnormality includes infarct,

hemorrhage, pneumonia, fibrosis,

neoplasia and edema.


-A marker for thrombosis and fibrinolysis, can

be useful in the exclusion of PE.

- Specific conditions that will give positive D-

dimer tests include trauma, postoperative state,

and malignancies.

-30% with PE will have normal D-dimer

Treatment of Pulmonary Embolism

1- Treat as for any respiratory distress including O2,

monitoring, fluid resuscitation for secondary

right-sided heart failure, Inotropic.

2-Anticoagulant : Heparin, oral anticoagulant

and LMWH.

3- Thrombolysis.

4- Caval Interruption.



- A loading dose of 5,000 U followed by approximately 1,000


OR: a bolus dose of 10,000-15,000 u for PE.

weight-based dosing.

A bolus with 80 U/kg and start a drip at 18 U/kg/h.

-Check PTT in 6 hours. Keep the PTT at 1.5 to 2 times

control. Adjust dose as per protocol in. Use clinical judgment!

Adjustment of weight-based dosing

APTT (sec)

Dose Change

Additional Action

Next PTT



( hr)

-Heparin, 25,000 IU in 250 ml D5W. Infuse at rate

dictated by body weight through an infusion

apparatus calibrated for low flow rates.

-During the first 24 hr, repeat APTT every 6 hr.

Thereafter, monitor APTT once every morning

unless it is outside the therapeutic range.

- Hypercoagulable state will exist when heparin is

stopped (if the duration of heparin has been at least

72 hours.)


It depletes vitamin K-dependent clotting factors (II, VII, IX, and X).

-It is taken orally. Begin with 5 mg QHS.

-Warfarin therapy can begin on day one of heparin therapy.

- A ratio of treated to control PT (INR-International

normalization ratio) of 2 to 3 is considered therapeutic.

- Monitor daily using the PT (Prothrombin time), until

a stable INR for 2 days. Then 2 to 3 times weekly for 1 to 2

weeks, and then monthly.

-Heparin should be continued for at least 4 days total and for at

least 2 days after a therapeutic INR is obtained.

-Continue using anticoagulation (warfarin) for at least

6 months.


(Patients still require heparin)

If PE is confirmed with angiogram or high-probability V/Q and

there is:

- Evidence of right heart failure, unresponsive to standard


- Respiratory failure from PE, but the benefits are less well


* Regimens approved by FDA:

- Streptokinase 250,000 IU over 30 minutes followed by 100,000

IU/hr for 24 to 72 hours.

-TPA 100 mg as continuous infusion over 2 hours.-

* Catheter-directed thrombolysis. is rarely used.


Caval Interruption:

-If anticoagulation is contraindicated or

ineffective, consider vena cava

interruption with a filter such as the

Greenfield filter.

-Vena cava filters are less effective than

anticoagulation and may lead to

increased rates of DVT and may not

protect against PE (same PE and death

rates as controls).

Postoperative DVT Prophylaxis

- If not given prophylaxis, 15% to 30% of

those with abdominal surgery will

develop a DVT.

-DVT prophylaxis after surgery is cost

effective and reduces the incidence of

DVT and PE.

-Heparin (unfractionated): 5000 units SQ Q12h.

-Graded compression stockings: Effective and

have few side effects.

-low-molecular-weight heparin .

-Warfarin: Less effective than LMWH

-Aspirin: Not very effective.

Only low-molecular-weight heparin and

graded compression stockings have

been shown to reduce the incidence of

pulmonary embolism.

low-molecular-weight heparin LMWH

(anti-factor Xa )

- Enoxaparin: (Clexane)

- Dalteparin.

-Nadroparin calcium. (Fraxiparine)

-Tinzaparin sodium . (Innohep)




(100IU=mg=0.01ml) (2000IU=20 mg =0.2ml & 4000IU= 40

mg= 0.4ml)

No need to follow PT/INR/PTT.

The best studied LMW heparin.

DVT prophylaxis after abdominal surgery 40mg SQ once -

daily starts 2 hours before surgery.

-In high risk 12 h before surgery. -

-In spinal or epidural anesthesia, it should be 10-12 h before

and subsequent dose 2h after removal of catheter.

Continue until patient is ambulatory (7-10) or up to 14 days.

The dose must be adjusted for renal function. Use with caution

in renal and hepatic disease.

low-molecular-weight heparin in PE

-Enoxaparin sodium100IU/kg twice

daily injection

-Oral anticoagulant should be initiated and

Enoxaparin sodium should be continued

until therapeutic effect (INR 2-3)

Preoperative Management of Patient with


-When to Stop Oral Anticoagulation? 3-5 days

-Heparin Coverage Needed Preoperatively? Yes, if

history of thromboembolism 1 month

-Restart Anticoagulation Postoperatively with IV

heparin or SQ LMWH (Note: Simultaneously Resume

Prior Oral Anticoagulation)

-Restart heparin 12 hours after surgery, unless there is

bleeding, in this case it should be delayed.

Thank You •

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