Transcript Acute Pulmonary Embolism

Acute Pulmonary Embolism
黃華桓 醫師
2008-Apr.-11
Outline
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Introduction
Epidemiology & Pathophysiology
Risk Factors
Diagnostic Approaches
Treatment
Pregnancy & APE
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 ventilation–perfusion 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 P2, 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
• A–a 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 APE1
Clinical Prediction Scores for Suspected APE2
Clinical Prediction Scores for Suspected APE3
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
• Ventilation–perfusion 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 V–P scan, Dx.
should be rigorously pursued
• nondiagnostic V–P 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 anti–factor 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 veryhigh-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