Beruflich Dokumente
Kultur Dokumente
2008-Apr.-11
Outline
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1. Introduction
2. Epidemiology & Pathophysiology
3. Risk Factors
4. Diagnostic Approaches
5. Treatment
6. Pregnancy & APE
7. Conclusions
Introduction-1
most commonly originating from deep
venous
thrombosis ( DVT ) of the legs
Asymptomatic
incidentally
discovered emboli
massive embolism causing immediate
death
Introduction-2
Chronic sequelae of venous
thromboembolism(VTE) (DVT & PE)
post-thrombotic syndrome
chronic thromboembolic pulmonary H/T
Introduction-3
Acute pulmonary
embolism ( APE )
may occur rapidly & unpredictably
may be difficult
to diagnose
Introduction-4
Treatment can reduce the risk of death
appropriate
primary prophylaxis : effective
rate of death in the next year: 1.5% vs.
0.4%
Patients treated for
APE appear to die of
recurrent thromboembolism (1.5% )
patients
treated for DVT (0.4% )
Epidemiology &
Pathophysiology
Epidemiology & Pathophysiology-1
Thrombi commonly form in deep veins
in
the calf
propagate into the proximal veins,
including
& above the popliteal veins
from which they are more likely
to
embolize
Epidemiology & Pathophysiology-2
About 79% of patients with PE have
evidence of DVT in their legs
PE occurs in up to 50% of patients with
proximal DVT
Dual pulmonary circulation ( pulmonary
&
bronchial arteries ), pulmonary infarction :
not usually
present
Epidemiology & Pathophysiology-3
APE, anatomical obstruction
is the most
important cause of compromised
physiology
release of vasoactive & bronchoactive
agents (serotonin from platelets )----
deleterious ventilationperfusion
matching
Epidemiology & Pathophysiology-4
As RV afterload increases, tension
in RV
wall rises
dilatation,
dysfunction, & ischemia of RV
Death results
from RV failure.
Epidemiology & Pathophysiology-5
VTE is a worldwide problem, esp. in
people
with known risk factors
Less common in certain regions, eg. Asia
Average annual incidence in US : 1
episode
per 1000 registered patients
US :300,000
people/year die from APE
Dx is often not made until autopsy
Hospitalized
pts are at particularly high
risk
Risk Factors
Acquired Risk Factors
Certain risk factors increase the likelihood
Overall, acute medical illness may be the
most common
setting
Prolonged air or ground travel increases
the risk
eThrombosis:extended
periods of sitting
at a computer terminal
Advancing age is
another clear risk factor,
with the risk increasing after
age 40
Genetic Disorders & Thromboembolic Risk
Risk Factors for VTE
Virchow's classic triad of risk
Hypercoagulability
Stasis
Venous
injury
Diagnostic Approaches
Clinical Manifestations -1
Recognition of the symptoms & signs of
VTE may reduce diagnostic delays
Symptoms of cough,
palpitations, &
dizziness & signs of fever,
wheezing, &
crackles : PE or
concomitant illnesses
Tachypnea & tachycardia : common
but
nonspecific findings
Clinical Manifestations -2
Signs of pulm. HTN : elevated neck veins,
loud
P
2
, right-sided gallop, & RV lift
Signs
& symps. of VTE : highly suggestive
but neither sensitive nor specific
extent of symptoms depends on the
thromboembolic
burden
massive PE:sudden onset of
near syncope
or syncope,hypotension,severe hypoxemia,
EM
dissociation, or cardiac arrest.
Clinical Manifestations -3
Leg pain, warmth, or swelling:DVT
dyspnea or
chest pain, either sudden
onset or evolving over a period
of days to
weeks:APE
Pleuritic chest pain , a pleural rub (more
peripheral emboli ) & hemoptysis:
pulmonary infarction
Preliminary Lab. Testing & Pretest Probability -1
Hx., PE, & known risk factors
EKG,
CXR, & ABG analysis
Preliminary Lab. Testing & Pretest Probability -2
EKG:unexplained tachycardia:common in
APE but nonspecific
acute
cor pulmonale: S1, Q3, T3 pattern,
RBBB , P-wave pulmonale, or RAD : more
common
with massive embolism ---
nonspecific
CXR: generally nondiagnostic
arterial
oxygen tension may be normal
Aa
oxygen difference may be normal
Preliminary Lab. Testing & Pretest Probability -3
D-dimer
test (+): VTE are possible
diagnoses
this test is nonspecific
infection,other inflammatory states, cancer,
& trauma
D-dimer testing is best considered
together with clinical
probability
Clinical Prediction Scores for Suspected APE-
1
Clinical Prediction Scores for Suspected APE-
2
Clinical Prediction Scores for Suspected APE-
3
Preliminary Lab. Testing & Pretest Probability -4
D-dimer test (-):with a low
or moderate
pretest probability, likelihood of VTE is low
precludes the need
for specific imaging
studies
high pretest
probability: imaging should be
performed instead of
D-dimer testing
Other biomarkers: cardiac
troponin levels,
plasma levels of brain natriuretic
peptide
Imaging Studies -1
Contrast-enhanced CT arteriography
the
greatest sensitivity & specificity for
detecting emboli in
the main, lobar, or
segmental pulmonary arteries
false (+) CT arteriography
: unusual
sensitivity of spiral CT arteriography
alone
= 83%, combination of this &
CT
venography ,up to 90%
Imaging Studies -2
Ventilationperfusion scan : diagnostic
in
the absence of cardiopulmonary disease
A normal perfusion
lung scan effectively
rules out APE
high probability scan:APE should be
considered diagnostic , unless clinical
suspicion is
low or Hx. of PE with an
identical
previous scan
Imaging Studies -3
if the clinical story strongly
suggests
PE,with a nondiagnostic VP
scan, Dx.
should be rigorously pursued
nondiagnostic VP
scan :
with low
probability or with moderate probability
but negative
D-dimer test , no additional
testing or therapy
is indicated
Imaging Studies -4
a recent study of 221 patients
with susp.
APE, MRI of the lung followed by MR
venography ---successfully search for
both DVT & PE
Echocardiography may reveal findings that
strongly support hemodynamically
significant PE, offering the potential to
guide treatment
Treatment
Anticoagulation-1
Bed rest is not recommended for DVT
unless
substantial pain & swelling
PE diagnosed, inpatient therapy
with initial
bed rest for 24 to 48 hrs : often
recommended
Anticoagulation-2
APE (+):IV anticoagulation
with LMW
heparin ,
or standard, UF heparin should
be initiated unless
contraindicated
Not thrombolytic, but decreasing the
thromboembolic burden
If the suspicion of PE is high, parenteral
anticoagulation
should be considered even
before imaging
Anticoagulation-3
Warfarin can
be initiated on day 1 of
therapy
SC LMWH or weight-based UFH IV should
be administered for at least 5 days until
INR=2.0 to 3.0 for 2 consecutive days
With standard heparin,aPTT checked Q6h
until it is =1.5 to 2.5 X control
Achieving
a therapeutic aPTT within 24
hours ,reduce the risk of recurrence
Anticoagulation-4
LMWHs have advantages over UFH :
greater bioavailability, more predictable
dosing, SC delivery, & a lower risk of
heparin-induced thrombocytopenia ( HIT )
Monitoring LMWH by antifactor Xa
:
morbidly obese (weighing
>150 kg) or
very small (<40 kg), pregnant,
& very
severe renal insufficiency
or rapidly
changing renal function
Anticoagulation-5
VTE require long-term
anticoagulation to
prevent extension & recurrence
Documented VTE with transient
risk
factors should treat 3 to 6 months, but
more extended
treatment is appropriate
when significant risk factors persist,
idiopathic or previous episodes
of VTE
D-dimer levels may help guide decisions
about
the duration of therapy
Anticoagulation-6
Tx. with a direct thrombin inhibitor (e.g.,
argatroban
or lepirudin) for HIT with
thrombosis
Tx. with warfarin should not be initiated
until disease process has been controlled
& platelet
count has returned to the
normal range---potential
for worsening
thrombotic complications :venous limb
gangrene & warfarin-induced skin necrosis
Placement of a Vena Caval Filter
contraindications to anticoagulation
major bleeding
during anticoagulation
recurrent embolism
under adequate
therapy
filters are effective in reducing the
incidence of PE, they increase the
subsequent incidence of DVT,but do not
increase overall survival
Treatment of Massive PE
PE causing hemodynamic instability
resulting RV failure---compromised LV
preload
If saline is infused for hypotension,
it
should be done with caution
Vasopressor therapy (e.g., dopamine)
should be considered if BP is not rapidly
restored
Complications of Thrombolytic Therapy-1
most widely accepted indication for
thrombolytic therapy :proven PE with
cardiogenic shock
frequently considered : systemic
hypotension without shock
may be considered : severely
compromised oxygenation or a massive
embolic burden identified by image
Complications of Thrombolytic Therapy-2
The most devastating complication :ICH
retroperitoneal & GI bleeding & bleeding from
surgical wounds or sites of recent invasive
procedures
Contraindications : intracranial, spinal, or ocular
surgery or disease, recent major surgery or
other invasive procedures, active or recent
major bleeding, pregnancy, & clinically obvious
risks of bleeding
Prognosis
The 3-month overall mortality :15 - 18%
Shock at presentation : increase in
mortality by a factor of 3 to 7
post-thrombotic syndrome (chronic leg
pain & swelling) & chronic
thromboembolic pulmonary
hypertension :possible long-term sequelae
of APE
Prevention-1
Without prophylaxis, risk of VTE among
acutely ill, hospitalized medical patients :
as high as 15%
Unfortunately, prophylaxis is grossly
underused ( U.S. & international studies )
Anticoagulant prophylaxis is more
effective than lower-limb mechanical
prophylaxis
Prevention-2
After total hip or knee replacement, the
risk of venous thrombosis : 50% or higher
without prophylaxis
Trauma & spinal cord injury :also very-
high-risk scenarios
Every hospitalized patient should be
assessed for the need for prophylaxis
Pregnancy & Acute
Pulmonary Embolism
Pregnancy & APE-1
increased risk for VTE : pregnancy ,
postpartum period ,& hormone therapy
Risk of a first episode of VTE= 5-fold as
high in the postpartum period as during
pregnancy
Risk of PE = 15-fold as high during the
postpartum period as during pregnancy
Pregnancy & APE-2
Low-dose oral contraceptives increase the
risk of VTE : a factor of 2 to 5
HRT increases the risk of VTE : a factor of
2 to 4
Pregnant patients with acute VTE require
the same initial approach as other patients
with regard to the need for parenteral
anticoagulation, placement of an IVC filter,
or embolectomy
Conclusions
Conclusions
Untreated PE is associated with high
mortality
Suspected PE demands prompt diagnostic
testing & assessment of risk factors &
clinical probability, with empirical clinical
assessment & a validated clinical
prediction score when possible