AnswersDBCA E
I mention here that PE is an elusive diagnosis.
More than 25 years often Eugene Robin wrote a landmark article
on the diagnosis and management of PE, even today, we still are
puzzled over the best approach to this clinical entity.
So, lets take a few minutes and go over the goals of this topic.
So let us beginPulmonary embolism is the most serious complication
of venous thrombosis
It is the third most common cause of death in the US
As many as 60% of deaths in hospitalized patients are found to
have pulmonary emboli
So, generally speaking it is a hard diagnosis to make.
As clinicians we must consider the diagnosis in patients to put
us on the right pathPE It has a wide spectrum of patient
presentation, which leads us to do suboptimal testing. This can
stand in the way of a timely diagnosis
Its important, because prompt diagnosis and treatment can
dramatically reduce the mortality rate and morbidity of this
disease.
Unfortunately, the diagnosis is missed far more than it is made.
I want to offer you a historical perspective of the disorderUntil
the 1930s, PTE was viewed almost universally fatal, with surgery
the only treatment despite an operative mortality of 100%
Enter heparin, circa 1930s, heparin was discovered and its wide
spread use were so immediate and dramatically apparent that this
become the mainstay of treatment for the next 70 years!
In 1977, a physician be the name of Eugene Robin published a
landmark article which stimulated immense change in medicines
approach to diagnosing PE.
It was robin contention the while lung scintigraphy was
sensitive to the presence of clots, but also non-specific. He
questioned the value of ventilation scans when the perfusion
defects were small. He felt angiography was being underused, and
that PE.was being OVER diagnosed.
Jump ahead to 1990. The PIOPED investigators, stimulated by
Robins article published their data on the sensitivities and
specificities of V/Q scans for PE.
In summary, a random sample of 933 of 1493 patients were studied
prospectively. 931 had scintography and 755 underwent
angiography.
Their conclusion: clinical assessment combined with the V/Q scan
can establish the diagnosis or exclusion of pulmonary embolism only
for a minority of patients
Enter the electronic era, Craig Feied, MD, who has read every
published article about PE written in the last 100 years and who
has written the chapter in Rosens in the last two editions
published this statement:
Massive PE is one of the most common causes of unexpected death,
being second only to coronary artery disease as a cause of sudden
unexpected natural death at any age. Most clinicians do no
appreciate the extent of the problem, because the diagnosis is
unsuspected until autopsy in approximately 80% of cases. Do we
under diagnose or over diagnose?
If we over diagnose, is it such a big deal? Its just a few month
of inconvenience of heparin and warfarin.
Aside from the potential morbidity of the anticoagulants,there
are other problems.
The diagnoses carries a stigma which will contaminate all future
medical encounters. Women may be barred from oral contraceptives,
future pregnancies will be considered high risk. Elective surgery
may be denied.
So, really after all these years, we are still left in the dark.
We still dont have a collective conscience on a standard approach
to this problem.
Before we can answer any questions we have to understand the
condition and this take us to virchow.
Everyone Im sure is familiar with Virchows triad. It was first
described by this German pathologist.
If we think of risk factors, we should think of them as the
embodiment of the triad: hypercoagulability, stasis, and vessel
injury.
So, essentially, under normal conditions, microthrombi are
continually formed and lysed with the venous circulatory
system.
When any one of the risk states exists, potential microthrombi
may escape the normal fibrinolytic system and grow and propagate.
Pulmonary Emboli occurs when fragments of thrombus break loose and
are carried through the right side of the heart into the pulmonary
arterial tree. Cancers of primarily adenocarcinoma and CNS tumors
most often cause thrombosis.
We need to make special mention about patients with a prior
history of DVT or PE.
Studies have revealed these patients have between a 5 to 30
times increased risk of a new DVT in response to a triggering event
compared to those who have not had prior episodes. All the above
symptoms are a manifestation of cardiopulmonary stress caused by
the cloth in the lung.
These produce symptoms perceived by the patient and the signs
observed by you!
There are three common clinical presentations that you should be
aware of:
1. Patients with pulmonary infarction may have pleuritic chest
pain and can be hard to distinguish between that patient with
infection pneumonitis
2. Submassive embolism are the hardest of all. By definition,
they have an angiographically defined blockage of flow to an area
served by less than two lobar arteries. These patients have acute
or unexplained dyspnea with exertion or at rest. So, they can be
easily confused with infection, asthma, CHF and the like.
3. Finally, Massive PE, or a clot which obstructs two lobar
arteries, so-called Saddle Embolus. These patients have acute cor
pulmonaly often with syncope. You might think there having an MI or
look septic!
While its true the most common symptom is shortness of breath,
even patients with circulatory collapse may have no dyspnea,
tachypnea, or pleuritic pain!
In fact, A normal paO2 > 80 is more prevalent in patients
with pulmonary infarction syndrome.
As a simple rule, if you have a patient in your department and
you dont have a good reason to explain there dyspnea, its a good
idea to consider PE!
These are the common symptoms that are associated with PE
As we mentioned in the previous slide, dyspnea and chest pain
are not always preset.
The explanation is that with a small V/Q mismatch, the adaptive
physiology of the pulmonary vasculature and bronchi produce
intermittent shortness of breath. Because of this, we are easily
distracted and looking for a cardiogenic cause of the dyspnea.
What about pleuritic chest pain, still not a home run!
In fact, up to 25% of patients ultimately diagnosed with a PE,
never had any chest pain!
This is what makes the diagnosis so difficult! Lets look a t a
couple of these:
Tachycardia!
Myth #2 We are all taught this is a key component of the
diagnosis. Right?
In fact, actually not having tachycardia is more commonly seen
in patients who are found to have a PE!
What about fever? If a patient has a fever, it must not be a PE,
right?
Not true.
Although not common, Among patients with PE and no other source
of fever, fever was present in one study in 43 of 311 patients
(14%).
For example
This could represent the likelihood that a specific patient ,
say a middle-aged man, with a specific past history, say
hypertension and tobacco smoking who presents with a specific
symptom complex: Chest pain, Dsypnea, or Diaphoresis has a specific
diagnosis.
Final Statement:Because PE can present with or with any of the
classic signs and symptoms and even the risk factors which
contribute to PE are varied in frequency, we are left with a
intuition at best!
As you can see there are a variety of test that we use to arrive
at a diagnosis.
Some better than others!
So, lets talk about these individually. Granted that most are
abnormal, but certainly not diagnostic.
It is true that in the original PIOPED study it was recommended
but the main value is to exclude diagnoses the mimic PE and to aid
in the interpretation of the V/Q scanCardiomegaly was the most
frequent finding in those with PE of In-patients
Out-patients, it seemed to be atelectasis in the above
study.
Here we see the dilated vessels and oligemia of westermarks
sign
And below Hamptons HumpA brief mention about the classic
S1-Q3-T3, its appearance on the EKG may suggest PE, but study after
study has shown it has no predictive value what so ever!
But you got to know it because question writers for the boards
love it!Actually, it is opposite of what you might think!As with
most dogma, we are taken back by what we thought was truth.
About 15% of patients with proven pulmonary embolism have a pO2
of 85mmHg or higher!
In one study, researches drew from there data various
combinations of the PaO2 of 80mm Hg or more, the PaCO2 of 35mmHg or
higher, and the A-a gradient of 20 mmHg or less.
They found that PE could not be excluded in more than 30% of
patients with no prior cardiopulmonary disease.
Moreover, PE could not be excluded in more than 14% of patients
with prior cardiopulmonary disease.
Conclusion, Blood gas levels are poor discriminate value to
permit the exclusion of PE.
Diagnosing of early right ventricular strain is important
because it is a strong predictor of subsequent death
Important to recommend echocardiogram with your admitting
internist if a pattern of right heart strain is suggested by
EKG.
Studies have documented that lives are saved with early
fibrinolysis is considered in these patients.
Well, what is it?
Basically, the assay is enzyme-linked monoclonal antibody test
used to identify the protein, D-Dimer.
D-Dimer itself is a unique degradation product that is produced
by a plasmin mediated breakdown of cross-linked fibrin
Good test with respect to its negative predictive value.
The drawbacks are some of the false positives that we commonly
see in the ER.
Two types,
Qualitative RBC agglutination assay, low sensitivity and
specificity and not good enough to comfortably rule out PE.
Quantitative, which measure the accurately the amount using a
spectrophotometer.
Our lab uses the 2nd generation VIDAS d-dimer with a negative
predictive value of 99.3%!
Essentially, a patient is injected with a radioisotope that
travels through the pulmonary microcirculation and are detected by
a gamma camera over the patient
A normal Perfusion study will have evenly distributed blood
flow.
Then a patient inhales a radioactive gas and it is viewed as it
washes over the bronchopulmonary tree.
A mismatch, areas of blocked perfusion and normal ventilation is
interpreted by the radiologist and given reading as normal (never),
high probability, or non-diagnostic/low-probability
The reason the low probability or non diagnostic scan category
is so suspect is because in the PIOPED study this group had
terrible inter-reader reliability. So, just beware.
The entire lung can be scanned while the patient holds there
breath.
Advantages:CT most useful benefit is in providing evidence for
an alternative diagnosis or excluding it entirely.
Disadvantages:The clinical significance for subsegmental PE are
not well known, but may be a marker for a larger PE
Given that the majority of V/Q studies are non-diagnostic, I
prefer the CT as the initial test of choice in place of V/Q
scan.
Right now there is no better test on the horizon of the
immediate present to virtually rule out or in PE.
I thought this cartoon kind of summarizes how patients sometimes
feel about the medical jargon we throw about and the puzzled look
are there face when we try to explain this condition and how to
treat it.
So what are our goals???Heparin is the most frequently used drug
in the treatment of PE.
Because heparin works by activating antithrombin III, this
genetic mutation makes heparin ineffective.
FDA approved dose for Unfractionated heparin is 80units/kg IV
bolus, then 18 units/kg/hr infusion to maintain the INR at
2.5-3
Lovenox is dosed at 1mg/kg every 12 hours or 1.5 mg/kg per
day.
LMWH in pregnancy only preferred for convenience sake.
This is because the anticoagulants protein C and S have short
half-lives compared with the procoagulant vitamin K-dependent
proteins.
So, this gives rise to the clinical importance that heparin must
be continued for at least five days after beginning Coumadin
The incidence of progressive thrombosis and embolization is 40%
when starting warfarin directly, compared to only 8% when beginning
after a patient has been anticoagulated with heparin.
Treatment is usually for 6 months, but may continue lifelongFor
critically ill patients, a very rapid infusion of 100mg over 10
minutes is preferred.
Alternative is Retavase, you can give it as two IV doses of 10
units, each over two minutes. This is a procedure where a suction
tip catheter is placed in contact with the thrombus under
fluoroscopy and sucked out while catheter is withdrawnThe simplest
algorithm says you can safely rule out PE in a low pre-test patient
with a negative D-dimer
I believe our institution and my personal practice is similar to
the Mayo Clinic Group who uses a combination of pre-test
probability, D-dimers, and CT angio, and limited V/Q to arrive at a
disposition.
These patients are difficult if not impossible to image. D-dimer
may be useful if < 500 and you can support an alternative
diagnosis.
Pregnant patients
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