Today we will talk about venous thromboebolism, lets take this case:
A 55 years old female patient (actual patient), presented with sudden dyspnea,
some chest pain in the emergency room, she denied cough, wheezes and
hemoptysis, so the main complaint is dyspnea and chest pain, now on further
history taking she had renal cell carcinoma on her left side and she do left
nephrectomy two weeks prior to her admission to the ER, she is obese and the
BMI is high, and she is hypotensive, has tachycardia, tachypnea and she has a low
grade fever, chest examination was normal, abdominal examination and heart
examination are within normal except for nephrectomy scar, and no swelling or
redness on her legs.
So this is by history, this is how she presented, the physician will think of a lot of
things when he face a patient like this, if you notice this patient that she dont
have a label or a diagnosis to the ER doctor or the internal doctor, so you as a
doctor must read between these lines and understand what the history and
physical examination do.
A basic investigation were done to her and we find that she has hypoxia,
tachypnea, hypocapnea and on ECG she has sinus tachycardia and she was normal
on chest x-ray
So what are the differential diagnoses that may be present in this case?
1) Metastasis is a possibility but for a patient who did nephrectomy before two
weeks it is difficult that her doctor was so ignorant that he didnt work up for
metastasis that will appear in a couple of weeks of time.
2) Acute pulmonary embolism (PE) which is the diagnosis of the emergency
doctor.
3) She has fever and shortness of breath so it could be an infection, so pneumonia
could be a possibility of her case.
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What comes in our mind that this patient has either pulmonary embolism or an
infection.
-The first question that must come to your mind is what is the likely diagnosis?
It is not a must that our diagnosis is true, but this is our likely diagnosis, but to
support this diagnosis I must know what are the risk factors that lead to this
diagnosis?, that she had risk factors for pulmonary embolism.
What is the pathophysiology? which is very important in understanding how to
handle the disease, initial and long term management, like when you know that
this disease causes airway obstruction from the pathophysiology like asthma so we
must do a test to confirm a pulmonary obstruction and so on.
How to confirm the diagnosis?:
Now we know what is her diagnosis, what is the likely diagnosis and what is the
pathophysiology, so I need a way to confirm the diagnosis.
And what is the appropriate treatment for this patient and then is this problem
preventable or not?
We have other things rather than pulmonary embolism like:
Pneumonia, pneumothorax, pleural effusion, pericarditis, dissecting aortic
aneurism, all of them are possibilities.
-Pericarditis will appear clearly on the ECG but we said that the patient ECG shows
sinus tachycardia without anything else.
-But if there is pneumothorax, pulmonary effusion or pulmonary edema it will
appear on the examination and on chest x-ray, but the examination was normal
and the chest x-ray was normal also.
So by just examine the patient we will rule out most of these diseases.
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-Dissecting aneurism is a possibility even if normal x-ray, but this patient did a
recent surgery and there is nothing suggesting this possibility.
-Whats remain is acute MI and pneumonia, but her ECG didnt show any signs of
acute MI, and pneumonia as we said that she dont have cough or sputum
production and chest x-ray is normal.
The classic presentations of PE are non specific, because a lot of things can do
dyspnea, chest pain, cough, hemoptysis, dizziness, fever, all the diseases that we
said previously can do these things, so by history taking from the patient herself
(these symptoms) I cant be sure 100% or 90% or even 80% to say that this case is
PE.
What makes PE more complicated that it can deceive you because it can be
presented as death, like for example this patient suddenly her family came to
wake her up and they discover that she is dead, so they insist to do autopsy to find
finally that she has a large pulmonary embolism, so she diagnosed after her death,
actually they start discover PE by post mortem analysis.
Pulmonary embolism could be silent, the patient has nothing but when you do a
CT-scan or any investigations looking for something else you will find that there is
a PE, I remember the first time that someone has an experience in CT-angio
pulmonary thromboembolism and we shown him a CT-scan for something else
which is lung cancer and he discovered a lung embolism, so she had a lung
embolism while she is a symptomatic.
Now when we examine patients with pulmonary embolism, there physical signs
are also non specific like: tachycardia, tachypnea, low grade fever (38.9c), forth
heart sound, accentuated p2, signs of pleural effusion, hypotension, all of them
are non specific signs, so far the history is not helping me 100% to rule in the
diagnosis, but all of these findings suggestive of the disease.
Whats make me think of pulmonary embolism is thinking about risk factors for
this disease, if someone of your colleagues has sudden shortness of breath in the
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middle of the hall, PE is unlikely because if yyou

ou look at the risk factors not knowing
everything about the student but because those patients are more than 40 years
old, and they have history of similar disease
diseases,, prolonged immobility for acute
illness, recent surgery, they have heart failure, trauma, estrogen therapy (OCP),
look at this table:

Now we have renal catheters of the central line will make deep vein thrombosis,
obesity, caesarean section, recent delivery, pregnancy itself, venous compression,
cancer.
So what are the risk factors in this patient that we said?
She had renal cell carcinoma so malignancy, she had recent surgery and it is a
major surgery, she is obese, and she has varicose veins (not mentioned earlier),
after these risk factors this patient is at risk of acute pulmonary
ry embolism, just
from looking at her risk factors.
The pathophysiology : what makes this patient to have PE?
The answer for this question is deep vein thrombosis (DVT)
(DVT),, whenever you hear PE
means that there is a thrombus embolized because the lung is not the primary
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organ, the lung is a receiving organ for a disease process that occur somewhere
else and usually it is a deep vein thrombosis, so most of the cases originate from
deep veins of the lower limbs, they can originate from renal veins, or from the
upper extremities, they can originate from the inferior vena cava, but most of
them come from femoroiliac veins( from the femoral and iliac veins).
The calf veins which are distal, they can be a source of embolism if they propagate;
and extended cross the knee then they can propagate to become DVT.
Now distal DVT not all of them will become proximal and the proximal DVT they
become pulmonary embolism, they dislodge, the minority will be large clots and
they will remain going up and close the artery, but the majority of them are small
and multiple clots.
There is an important relationship between DVT and PE and they are named as
venous thromboembolic disease, why? Because the relation between them is very
close, there are about 30% of the patients with PE have symptoms of DVT that
means if you come to 100 patients you will find 30 patients of them have pain and
swelling in their legs, but 70% of them they dont have anything in their legs, but I
know that the PE came from there, so they do have DVT but it is not visible to the
eye, it is not showing itself clinically.
Also patients with DVT about 50% of them have a symptomatic PE, means it will go
to the lungs even a small part of it but it doesnt show any symptoms.
Now what to do with that patient, how to diagnose her, how to approach, now we
reached 3 different diagnosis, which are pneumonia, PE, metastasis, the approach
normally will not be PE targeted, it will be patient targeted or complain targeted or
complex of signs and symptoms targeted and not targeted to that diagnosis, this
means that not every patient come with chest pain I will do cardiac enzymes and
ECG, and if they are normal then said to the patient go to somewhere else, so
rather than targeted the diagnosis we targeted the complex of signs and
symptoms.
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Knowing these differential diagnoses, I will do cardiac enzymes to rule out acute
MI, I will do ECG also to rule out acute MI (ST elevation MI, non ST elevation MI)
and also pericarditis, I will do chest x-ray to rule out a lot of these diagnoses like
pneumonia, pneumothorax, and pleural effusion, also we do arterial blood gases
(ABGs) to confirm if there is a physiology problem, means this is a real complaint
like when somebody cant breathe well but if we look at his ABGs and it is within
normal that makes it unlikely that he has a real physiological problem, so this is to
confirm and differentiate between PE and historical attack which is a psychogenic
hyperventilation.
Start talking about the D-dimer test which is a blood test (we take a blood sample
from the patient), it is a degradation of an active thrombus, if the patient has an
active thrombosis the D-dimer will be positive, but there are other disease
processes like pregnancy, liver disease, trauma, cancer which can make the Ddimer test positive, so it is non specific test when it is positive, because there may
be other things rather than PE or DVT can make it positive, but my concern when
it is negative because negative D-dimer unlikely to be PE or DVT so its importance
when it is negative not positive.
Chest x-ray: the majority of patients will have normal chest x-ray, like this patient,
so we do the chest x-ray for a couple of reasons; to rule out other diagnosis like
pneumothorax, pleural effusion, etc.
There is saying in medicine which said:
If the chest x-ray was normal, and the examination was normal, and the patient
has severe hypoxia and distress, then PE is a possibility.
You rule out pneumothorax, pulmonary effusion, pulmonary edema and a lot of
things, and then you will be limited to pulmonary vascular disease, so the
importance of the x-ray if it is normal incase of PE.
ABGs as we said it is not diagnostic but it help you to confirm if there is
physiological problem.
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The finding of the ECG is non specific, but is it possible that this patient coming
with chest pain and sudden shortness of breath and we dont do an ECG for her, it
is more common that she has acute MI, but acute MI is something that should be
ruled out.
This is the S1QT3 which is:
*Deep S wave on lead 1
*And we have Q wave and T
inversion on lead 3.
-This is more specific for
pulmonary embolism than
anything else.

Now all these things make me suspicious of pulmonary embolism, now to confirm
we have two tests; one of them is old whi
which is ventilation perfusion scan which is a
radio labeled material injected in the vein so we see the perfusion of the lung, and
another one inhaled to check for the ventilation, so what you suspect in PE case?
There is ventilation but there is no perfusio
perfusion
n and this is what we call match-defect.
match
in this picture If you look at the patient from the posterior aspect, looking at his
right lung you will see that it is lighted because it is perfused but the left lung is
disappeared, so this is a large perfusion
defect, and the same thing from the
anterior if you look at the right
right, It is well
perfused and the left is largely absent.
So this is a positive V-Q
Q scan for PE.

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There is this slide which is related to the clinical probability that there is a group
gro
of
patients even if there V-Q
Q test is low probability still there is a number of patients
have PE.

The problem of this test that it doesnt give

You the answer 100% to the problem.
What is the meaning of highly likely,
Uncertain, unlikely this is the cclinical
Suspension, I am as a doctor when I send
the patient to the radiology I will say I really
dont know what she has, I dont know if she has PE or not, this patient has SOB
and we dont know what she has so see her !
The intermediate when the doctor doesnt know and the radiology doesnt know
still one third off the patients have PE, when the doctor is certained and the
radiologist is certained it is 96%, but if the doctor is certained and the radiologist
isnt still 40% of the patients could have PE, so this is the difficulty in the
interpretation of the V-Q
Q scan
scan,, this principle is important which is called pre-up
pre
or
pre-test
test probability in medicine.
Now we do something called C
C-T angio which is contrast that is injected in the vein
and we wait until it reaches the pulmonary artery
artery, it needs around 20 sec then we
take a photo of the pulmonary artery by the C
C-T scan,, searching for filling defect, it
has a lot of qualities, like either seeing the clot or not, but the problem that it may
cause contrast nephropathy
phropathy in patients with diabetes, renal impairment, and those
whom have allergy to the die, it could be fatal, but it is now becoming the
procedure of choice.
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This is the newer CT-scan,

CT
this is the
major pulmonary artery, this is the
trunk, if you notice in the left
pulmonary artery it is filled and
there is no contrast so this is the
clot.

And here the right pulmonary artery

all of it is closed because of the clot

So in this technique you see the clot by your eyes and there is no probability or
anything else.

Someone may ask why we are so concerned about PE?

The mortality rate of PE is nearly the same as MI but MI is more common, the
mortality reach 12% which is not small, even the DVT cause nearly 5% mortality
rate, But manyy patients with pulmonary embolism may recover completely and go
home with or without treatment.
Chronic thromboembolic disease is also another complication of PE, means that
the immediate death because of the pulmonary artery closure, will lead to
pulmonary hypertension, cor pulmonale and then accumulation of fluids
fluid (ascites)
and lower limb edema, etc
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Now shift to the DVT(deep vein thrombosis): lets take this case which is a real one
also:
This patient came complaining of right leg swelling of two days duration, it was
painful and getting worse (getting bigger and more painful over a couple of days),
he is 24 years old, he works in JUST university, he is an employee (office
employee), previously healthy, view of systems within normal, he doesnt have GI,
pulmonary, cardiac, urogenital or any other complains, He denies trauma, recent
illness, this is how you take history, when you suspect DVT you start asking about
risk factors like trauma, or recent surgery, but he was In CHICAGO for 3 weeks
visiting his brother, and he came one week ago, he smoked 1 pack\day for the last
5 years, he doesnt take any medication, his brother died suddenly at age of 28
and the causes are not known, his legs are warm, swollen, and red from the calf to
the mid thigh, and he has pitting edema, chest was normal on examination, his
basic lab investigations doesnt show hypoalbuminemia, finally the platelets and
WBCs are normal.
So what is the likely diagnosis?
The possibilities are DVT, rupture baker cyst which is the differential diagnosis for
unilateral leg swelling but this is usually affects older women with rheumatoid
arthritis, and it may be cellulitis which is an infection and this patient may have an
infection, it could be trauma, hematoma but he denied any recent trauma or
hematoma, it couldnt be a lymphatic obstruction because it causes non pitting
edema, so DVT our main top differential diagnosis, but it could be cellulitis or MSS
injury, venous stasis but the most common is cellulitis vs. DVT.
The classic presentation for DVT is unilateral leg swelling; it is usually painful and
associated with skin changes, whether it is redness or dusky colour of the limbs,
the pain usually worse with activity or moving around.
One student asks if the patient could have an autoimmune disease like
antiphospholipid antibody?
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The answer was: that what the patient had, this is the real diagnosis but he came
with DVT, this is a thrombogenic disorder and sometimes the anti phospholipid
associated with SLE and sometimes not.
To cause clot formation in one of his legs the patient must have one of many
problems, to have a thrombosis you must have a stasis in an immobilized patients.
The doctor asked about a disease that causes vessel wall damage?
The answer was: vasculitis and the most common cause of it in our area is BEHGET
disease which causes endothelial problems.
What are the causes of a hypercoaguable state?
It can be caused by anti thrombin deficiency, DIC (disseminated intravascular
coagulation), cancer because malignancy can cause a hypercoaguable state,
pregnancy.
So we look to our patient, does he have any of these risk factors?
Traveling that will lead to immobilization, and he has history of sudden death to
his brother that could be related to this disorder, but otherwise he dont have
other risk factors so this is make us suspicious of thrombophilia, which you think
about it in young patients, in patients that have un provoked events, this means
the patient is healthy and do normal activities but suddenly he will have PE, so in
any age the patient is, we should think of thrombophilia.
If the patient has DVT in the left leg and then in the right leg then PE between
them periods of months, so we think of thrombophilia, if there is family history of
this disorder (even if it is not strong) because usually it is an autosomal dominant,
so they run in families and the most common one of them is factor 5 Leiden
(activated protein c resistance) question site as the doctor said.
What is the importance of activated protein c?

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It is an anti coagulant, because if there is nothing that counter coagulation then if

somebody has coagulation in the big toe will end in the brain, but this mechanism
is closely monitored, whenever coagulation occurs anti coagulation happens, but
here there will be resistance to protein c, also we have other risk factors of
thrombophilia like prothrombin gene mutation, hyperhomocystinemia,
anticardiolipin antibodies or lupus anticoagulant, protein c and protein s
deficiency, anti thrombin deficiency and behget disease, so these are the
thrombogenic disorders that you will see it around, in our country behget disease
is a forgotten disease, it is not a true thrombophilia because the problem is not in
the blood but it is in the blood vessels.
Here the doctor talked about a case which is about:
:            
!"#$  % '

The first thing that I must think of it when the patient comes to the ER is the Ddimer test, and as we said its importance when it is negative.
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The best test to confirm the diagnosis of the patient is the ultra sound, you will put
the probe on the vein and the vein is a low pressure system, if you press on it and
it is empty it will be compressible, but if there is a clot then it is not compressible,
and if the ultra sound has Doppler you will see the blood flow, it is operator
dependent and cant be used to rule out PE, because they dont relate to each
other, by this test either the patient has DVT or not.
There are complications of the DVT which are PE and it is the most serious one,
and there is something called post thrombotic syndrome, and this causes a
problem because it has pain, edema, hyper pigmentation, skin ulceration, so it is a
disfiguring problem, and it is common, all these diseases are called
thromboembolic disease.
The treatment:
Someone may ask if we didnt treat what will happen?
It will lead to a high mortality rate, and it is the most common preventable cause
of death in hospitalized patients, if it is remained untreated it is associated with
high mortality rate, but if treated the mortality drops, so there should be a good
doctor that diagnose the case and start treatment as soon as possible.
Treatment depends if it is DVT or PE, there is supportive treatment, like someone
with DVT, he may need pain control, rise his leg, prevent the movement in the first
day, in PE the patient will be afraid, tachypnic, dyspnea, he needs some analgesics,
oxygen, if there is chest pain then they need pain relief.
But the primary treatment is anticoagulation, which may be either IV heparin
although we dont do that anymore, we use low molecular weight heparin because
this is easy to use subcutaneously, and doesnt need monitoring, predictable per
Kg, enoxaparin 60 mgs twice daily or 90 mgs once daily, it is very easy to use.
The problem of heparin that it must be given by infusion.

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When we start treatment on day one we should start the patient on warfarin
which is the only available safe oral anticoagulant so far.
Now how long we treat?
Look at this slide which summarizes things for you:

In the past they used to treat DVT from 3 to 6 months and the PE from 6 to 12
months, but it depends on if it is the first episode or not,, caused by transient event
like surgery,, idiopathic pulmonary embolism, means we dont know what is the
cause, so in this case we treat for longer time to prevent recurrence, patients with
genetic factors like anti phospholipid are given for 12 months and others say in
different treatment so it is dependable, but the patients which are un provoked at
least one month, and the provoked patients from 6-9
9 months, there are some
studies because we are afraid from recurrence, the studies shown that the longer
you treat the lower the recurrence.
Prevention:
If I have a patient 60 years old, obese and she take estrogen therapy, and she has a
history of inflammatory bowel disorder and she have malignancy (colon cancer
14 | P a g e

because of the ulcerative colitis) and they did to her colectomy, so she has
multiple risk factors, so these patients we target them for prevention, the most
important thing in prevention iin
n surgery cases is mobilization, adequate hydration,
mechanical devices and heparin.

This elastic stocking in combination with these boots they pump the blood from
the lower to the upper and they are very effective.
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