Get documents about "5aa1Acute Pulmonary embolism
Shared by: amrik7300
-
Stats
- views:
- 4
- posted:
- 8/21/2012
- language:
- English
- pages:
- 91
Document Sample
Pulmonary Embolism
EPIDEMIOLOGY
• 65 000 cases per year in Canada1
• Estimated incidence of acute PE in
community/teaching general hospitals is 0.27% -
0.40% (95/34567)3
• Mortality of treated PE is 5% (stable) to 20%
(hypotensive)4
• Mortality from unrecognized PE is up to 30% 1
• PE was not suspected in 70% of those
diagnosed with PE at autopsy! 2
PATHOPHYSIOLOGY
Pulmonary embolus exists in the spectrum of venous
thromboembolism (VTE) which includes deep
venous thrombosis (DVT).
DVT is found in 70% of those with PE.4
In the remaining 30%, embolization is assumed to
have already occurred.
Other sources of emboli include iliac, renal and
upper extremity veins, right heart. Emboli do not
come from the calf, nor do they occur in situ.
Up to 50% of those with popliteal or proximal DVT will
have PE, usually asymptomatic.4
PATHOPHYSIOLOGY: Risk
Factors
PREEXISTING DISEASE AND RISK FACTORS IN 500 PATIENTS WITH CLINICALLY SUSPECTED PULMONARY
EMBOLISM (PE) 5
PE Present (n = 202) PE Absent (n = 298) p Value
n (%) n (%)
Preexisting disease
Cardiovascular 53 (26) 96 (32) 0.18
Pulmonary 14 (7) 72 (24) < 0.00001
Neoplastic* 36 (18) 43 (14) 0.37
Endocrine 21 (10) 32 (11) 0.98
Risk factors
Immobilization > 3 d 119 (59) 138 (46) 0.007
Surgery* 81 (40) 116 (39) 0.72
Thrombophlebitis (ever) 69 (34) 57 (19) 0.0002
Bone fractures (lower limb) 46 (23) 36 (12) 0.002
Estrogen use 1 (0.5) 1 (0.3) 1.0
Pregnancy/postpartum 1 (0.5) 4 (1) 0.34
* Clinically active malignancy with pathologic diagnosis within 3 mo of study entry.
* Within 4 wk of study entry.
VIRCHOW’S
IMMOBILITY
TRAUMA CANCER
ORTHO ATIII, PROTEIN C,S DEF.
SURGERY POLYCYTHEMIA
CV PERIPARTUM
CATHETERS
PATHOPHYSIOLOGY
• Most PE are multiple.
• Humoral mediators -- thromboxane and
serotonin from activated platelets may
increase the pulmonary hypertension and
severity of disease
• The burden of clot obstructing the
pulmonary arterial bed and the duration of
obstruction dictate symptoms:
Presentation DYSPNEA ALTERED RIGHT
HEMO- HEART
DYNAMICS FAILURE
Clot Burden < 50%, >50%, acute >50%,
acute (massive) subacute
Reason V/Q mismatch +/- RV overload with Over several
shunting decr. CO weeks the RV can
partially
compensate
Up to 1/3 of patients will have infarction with pleuritic pain +/- fever
CHALLENGES TO DIAGNOSIS
• PE can mimic many other conditions
• PE may coexist in those with diseases that
present similarily
• History and physical exam are of limited
utility
• We have multiple tests which have varying
availability and utility in combination
UTILITY OF HISTORY
SYMPTOMS IN 500 PATIENTS WITH
CLINICALLY SUSPECTED PULMONARY EMBOLISM (PE) 5
PE Present (n = 202) PE Absent (n = 298) p Value
n (%) n (%)
Symptoms
Dyspnea (sudden onset) 158 (78) 87 (29) < 0.00001
Dyspnea (gradual onset) 12 (6) 59 (20) 0.00002
Orthopnea 2 (1) 27 (9) 0.00004
Chest pain (pleuritic) 89 (44) 89 (30) 0.002
Chest pain (substernal) 33 (16) 29 (10) 0.04
Fainting 53 (26) 38 (13) 0.0002
Hemoptysis 19 (9) 16 (5) 0.12
Cough 22 (11) 45 (15) 0.22
Palpitations 36 (18) 46 (15) 0.56
UTILITY OF PHYSICAL EXAM
SIGNS IN 500 PATIENTS WITH
CLINICALLY SUSPECTED PULMONARY EMBOLISM (PE)5
PE Present (n = 202) PE Absent (n = 298) p Value
n (%) n (%)
Signs
Tachycardia > 100/min 48 (24) 69 (23) 0.96
Cyanosis 33 (16) 44 (15) 0.73
Hypotension < 90 mm Hg 6 (3) 5 (2) 0.15
Neck vein distention 25 (12) 28 (9) 0.36
Leg swelling (unilateral) 35 (17) 27 (9) 0.009
Fever > 38° C 14 (7) 63 (21) 0.00003
Crackles 37 (18) 76 (26) 0.08
Wheezes 8 (4) 39 (13) 0.001
Pleural friction rub 8 (4) 11 (4) 0.93
PE: Differential Diagnosis
• Myocardial infarction
• Pneumonia
• Congestive heart
failure ("left-sided")
• Cardiomyopathy
(global)
• Primary pulmonary
hypertension
• Asthma
• Pericarditis
• Intrathoracic cancer
• Rib fracture
• Pneumothorax
• Costochondritis
• "Musculoskeletal pain"
• Anxiety
‘PRETEST’ TESTS
• What diagnostic tests do we use prior to
our V/Q, spiral CT, or pulmonary
angiogram?
– ABG
– CXR
– D-dimer
– EKG
– Leg imaging (duplex ultrasound, impedence
plethysmography (IPG), contrast venography)
ECG FINDINGS
• Sinus Tachycardia 43%
• “T” wave inversion 40%
• ST segment depression 33%
• Low voltage 16%
• L axis 12%
• S1 Q3 T3 11%
• ST elevation 11%
• R Bundle Branch Block 11%
ABG
• A-aDO2 is usually elevated in PE… and in many other
conditions so it is NOT SPECIFIC ENOUGH
• 30% of those <40 years with PE have a PaO2 >80mmHg
so it is NOT SENSITIVE ENOUGH
(This falls to 3% of those over 40… but many are still in the
70-79mmHg range)
A-aDO2 gradient has a sensitivity of 84%, specificity of
27%, PPV of 27% and NPV of 84%8
D-Dimer
1. Latex Agglutination: not reliable!
2. SimpliRED (“whole blood”) 9,10
Anti-D-dimer antibodies, faster than ELIZA
Good sensitivity with 95% NPV
3. ELIZA Sensitivity: >95% negative predictive
value for a low reading (<500ng/mL)… but only
25% of normal subjects have a value that low
ie. Specificity is poor!
• Different manufacturers have different assays
with different S&S. Few outcome studies yet.
D-Dimer
• May be useful in the settings of low clinical
suspicion and non-diagnostic lung scan to
rule out PE9,11
PIOPED
(Prospective Investigation of Pulmonary Embolism Diagnosis, 1990)6
PERCENT OF PATIENTS WITH PROVEN
PULMONARY EMBOLISM
V/Q Scan Probability Clinical Suspicion for PE
High Intermediate Low
High 96 88 56
Intermediate 66 28 16
Low 40 16 4
Normal 0 6 2
.
CXR
• With PE we may see
– atalectasis
– pleural effusion
– pulmonary infiltrates
– pulmonary consolidation (Hampton’s Hump is
a peripheral consolidation on infarcted lung)
– elevated hemidiaphragm
– oligemia (Westermark’s sign)
CXR
• A normal Xray in the setting of marked
dyspnea (with no evidence of
bronchospasm or cardiac shunt) is
strongly suggestive of PE.11
Hampton’s
Pulmonary infarct
Oligemia?
Westermark Sign
PE appears like a mass
pulmonary PE with hemorrhage or
pul edema
PE with effusion
and elevated diaphragm
CXR
CHEST RADIOGRAPHIC FINDINGS IN 500 PATIENTS WITH
CLINICALLY SUSPECTED PULMONARY EMBOLISM (PE)5
PE Present (n = 202) PE Absent (n = 298) p Value
n (%) n (%)
• Finding
• Right heart enlargement 77 (38) 43 (14) < 0.00001
• Left heart enlargement 10 (5) 30 (10) 0.06
• Cardiomegaly 36 (18) 65 (22) 0.33
• Amputation of hilar artery 72 (36) 3 (1) < 0.00001
• Oligemia 91 (45) 3 (1) < 0.00001
• Consolidation (infarction) 31 (15) 2 (1) < 0.00001
• Consolidation (no infarction) 12 (6) 54 (18) 0.0001
• Platelike atelectasis 65 (32) 70 (23) 0.04
• Interstitial edema 1 (0.5) 27 (9) < 0.00001
• Elevated diaphragm (unilateral) 86 (43) 89 (30) 0.005
• Elevated diaphragm (bilateral) 39 (19) 57 (19) 0.95
• Pleural effusion 91 (45) 104 (35) 0.02
Echo
Diagnosis of Pulmonary Embolism
Suspected PE
V/Q Scan
(CT, MRI)
NORMAL (14%) HIGH PROB. (13%)
No Rx Treat
NONDIAGNOSTIC (73%)
Diagnosis of PE ~ Ventilation –
perfusion scintigraphy 1
• Most commonly used non-invasive
technique with clinical suspicion
• Perfusion lung scan : not specific enough
for diagnosis of PE
• Ventilation imaging : differentiate vascular
occlusion from disorder of ventilation
Diagnosis of PE ~ Ventilation –
perfusion scintigraphy
Segmental defect
• Occlusion of a branch of a branch of the
pulmonary artery
• Wedge shape and pleural based
• Conforms to segmental anatomy of the lung
• Large (>75%), moderate(25~75%), small(<25%)
Nonsegmental defect
Diagnosis of PE ~ Ventilation –
perfusion scintigraphy 3
V / Q match
• Both scintigrams are abnormal in the
same area, defects of equal size
V / Q mismatch
• Abnormal perfusion in the area of normal
ventilation or much larger perfusion
abnormality than ventilation defect
Diagnosis of PE ~ Ventilation –
perfusion scintigraphy 4
High probability
• Segmental or lobar perfusion defect with
normal ventilation
Low probability of PE
• Perfusion defect with matched ventilation
abnormality
Diagnosis of PE ~ Ventilation –
perfusion scintigraphy 5
Modified PIOPED Criteria
High probability (>80%)
• 2 large mismatched segmental defects without
radiographic abnormality
• Any combination of mismatched defects
equivalent to the above
• (2 moderate = 1 large)
Intermediate probability (20~80%)
Low probability (<20%)
• Nonsegmental perfusion defect
• Any perfusion defect with a substantially larger
radiographic abnormality
• Matched ventilation and perfusion defects with
normal chest radiograph
• Small subsegmental perfusion defects
Normal
( No perfusion defect )
Condition associated with V/Q mismatch
• Acute or chronic PE
• Other cause of embolism : drug abuse,
iatrogenic
• Bronchogenic carcinoma
• Hypoplasia or aplasia of pulmonary artery
• Vasculitis
• Post radiation therapy
• Mediastinal or hilar adenopathy with obstruction
of pulmonary artery or veins
Determinining Clinical Likelihood of PE
• Assessment of risk factor for venous
thromboembolism (leg paralysis, bed rest,
malignancy, CHF, presence of central
venous catheter …)
• Evaluation of symptoms and signs
• Interpretation of preliminary investigation
(eg. chest radiograph and
electrocardiogram)
VQ Scan
V/Q Scan Clinical Suspicion for PE
High Intermediate Low
High 96 88 56
Intermediate 66 28 16
Low 40 16 4
Normal 0 6 2
Positive V/Q Scan
Spiral tomographic scan 1
• capable of imaging nearly the entire thorax
during a single breath-hold intravenous
contrast can be timed to arrive pulmonary
vasculature
• Sensitivity : 64 ~ 93 %
Specificity : 89~100 %
Especially when PE is involved the main,
lobar, or segmental pulmonary arteries
Advantage
• High sensitivity and specificity
• Visualize the clot
• Indentify other disease states that can
mimic PE (lung tumor, pleyral disease,
pericardial disease) provide alternative
diagnosis
• Cost : 1/6 ~ 1/8 angiography
Limitation
• Inability of spiral scanning to detect PE in
subsegmental pulmonary arteries
(sensitivity : 29%)
Clinical guidelines
• It should be used as a ”rule-in” modality,
rather than a ”rule-out” procedure
• if an alternative diagnosis is being
considered in addition to pulmonary
embolism, spiral CT scanning can provide
new information that a ventilation-
perfusion scan cannot.
SPIRAL CT
Segmental Subsegmental
Sensitivity 94% 63%
Specificity 94% 89%
Only 6% of all PE are subsegmental
CT and Spiral CT
Diagnosis of Pulmonary Embolism
Suspected PE
V/Q Scan
(CT, MRI)
NORMAL (14%) HIGH PROB. (13%)
No Rx Treat
NONDIAGNOSTIC (73%)
Clinically Stable Hypotensive/Severely Hypoxemic
Bilateral lower extremity evaluation Angiogram
(US, IPG, CV, MRI)
Pulmonary Angiogram
• Most specific test available for diagnosis of
PE
• Can detect emboli as small as 1-2 mm
• Most useful when the clinical likelihood of
PE differs substantially from the lung scan
result or when the lung scan is
intermediate probability
Pulmonary Angiogram
Emboli on Angiogram
LEG STUDIES
• Contrast Venography
– Gold standard, nearly 100% sensitive and specific
– Invasive, expensive, requires a dye load
• Impedence plethysmography
– Detects increased venous outflow resistance using
electrical current
– Does not distinguish non-thrombotic obstruction
– Sensitivity and specificity up to 98%
LEG STUDIES
• Duplex Ultrasound
– Doppler blood flow +compression imaging
= 2-D cross sectional view of leg veins
– Sensitivity 89-100% Specificity 95-100%
– PPV 92-100% NPV 75%-100%
- operator dependent, not always available,
hard to see pelvic DVT
Diagnosis of Pulmonary Embolism
Suspected PE
V/Q Scan
(CT, MRI)
NORMAL (14%) HIGH PROB. (13%)
No Rx Treat
NONDIAGNOSTIC (73%)
Clinically Stable Hypotensive/Severely Hypoxemic
Bilateral lower extremity evaluation Angiogram
(US, IPG, CV, MRI)
DVT absent DVT present
or nondiagnostic Treat
Serial leg studies
or angiogram
SERIAL LEG IMAGING
Remember… >70% of pts with PE will have
DVT and half of pts with DVT will have PE.
Less than 2% of patients with a non-
diagnostic VQ had any thromboembolism
after negative serial US or IPG.
BEYOND THE AMERICAN THORACIC SOCIETY
GUIDELINES
• Better studies on available D-dimer testing
(ie. The SimpliRED test)
• Validated combinations of clinical
prediction rules and lab testing
EXCLUDING PE AT THE BEDSIDE WITHOUT
DIAGNOSTIC IMAGING
WELLS et al. 2001
• “Managing patients on the basis of pretest
probability and D-dimer result is safe and
decreases the need for diagnostic
imaging.”
Wells et al. 2001
• Clinical scoring system derived and
validated from 40 clinical variables on
1239 patients investigated for suspected
PE
• 930 consecutive ED patients evaluated by
ED physicians using the clinical score and
SimpliRED whole blood D-dimer testing.
The Wells PE Score
Clinical signs of DVT (swelling and pain) 3
HR > 100 1.5
Immobilization (>3d) or surgery (<4wks) 1.5
Prior DVT/PE 1.5
Hemoptysis 1
Malignancy 1
PE as likely or more likely as other Dx 3
Low Risk <2
Mod Risk 2-6
High Risk >6
Wells’ PE Algorithm
Pretest Probability
Low Moderate or High
D-dimer D-dimer
- +
PE EXCLUDED
VQ
Normal Indeterminate High
(Low or moderate)
PE EXCLUDED Treat for PE
Wells’ PE Algorithm
VQ
Normal Indeterminate High
(Low or moderate)
PE EXCLUDED Doppler US Treat for PE
No DVT DVT---> Treat
Low Pretest Risk Moderate High
PE EXCLUDED
- Dd + Dd -Dd +Dd
PE EXCLUDED SERIAL US ANGIOGRAPHY
Diagnosis of PE ~ MRI 1
• Helpful for the diagnosis of pelvic and thigh deep
venous thrombosis
• Acute, symptomatic, proximal deep vein
thromboses : sensitivity approaching 100%
• Less sensitive for detecting calf deep venous
thrombosis
• PE : can demonstrate an embolus directly as an
intrvascular filling defect
(sensitivity : < pulmonary angiography)
Diagnosis of PE ~ MRI 2
Treatment
Anticoagulation for PE #1
• Obtain baseline CBC with platelets, PT,
PTT
• Check for contraindications to heparin
• Start LMWH (preferred) or unfractionated
heparin (if severe renal failure)
• Enoxaparin 1mg/kg sc q 12h
• Unfractionated heparin weight-based nomogram
• Chest 2004;126:401S
Recheck aPTT every 6 hours until in therapeutic range, then daily.
Anticoagulation for PE #2
• Platelet count day 3 and 5 (HIT)
• Start warfarin 5mg on first treatment day
and use INR to adjust daily doses
• Stop LMWH/heparin after at least 5 days
and INR >2 for at least 2 days
• For massive PE or severe iliofemoral
thrombosis, continue heparin for 10 days
• Chest 2004;126:413S
Anticoagulation for PE #3:
Early discharge
• Minimal elements for early discharge
– Patient stable with normal vital signs
– Low bleeding risk
– Absence of severe renal failure
– Practical system for administration of LMWH
and warfarin and appropriate monitoring
– Availability of evaluation/treatment of
recurrent VTE and bleeding complications
• Chest 2001;119:176S
Anticoagulation for PE #4:
Duration of therapy
• 3-6 months:
• First event with reversible or time-limited risk factor
• 6 to 12 months:
• Antithrombin deficiency
• Protein C/S deficiency
• Factor V Leiden
• Prothrombin 20210 gene mutation
• High factor VIII levels
• Homocysteinemia
• Chest 2004;126:401S
Anticoagulation for PE #4:
Duration of therapy (cont.)
• Indefinitely or until cancer resolved:
• Patients with cancer
• Indefinite (high value placed on preventing
recurrent PE):
• First idiopathic episode
• Antiphospholipid Ab
• Two or more thrombophilic conditions
• Two or more episodes of documented PE
• Chest 2004;126:401S
Stabilizing the PE patient:
• Hypoxia
– Supplemental oxygen
– Intubate if necessary
• Hypotension
– 500-1000cc fluid resuscitation
– Norepinephrine or dopamine
• Persistent hypotension
– Unfractionated heparin rather than LMWH
– Consider thrombolysis or surgical embolectomy
Thrombolyic therapy
• Outcomes
• 24 hours: superior to heparin alone in resolution of
radiologic and hemodynamic abnormalities
• Seven days: no difference in echocardiograms
• No differences in mortality or resolution of
symptoms
• Use is “highly individualized”;
Thrombolytic therapy in venous thromboembolism;
UpToDate, 2005
Thrombolytic therapy in venous thromboembolism; UpToDate 2005
Thrombolytic therapy in venous thromboembolism;
UpToDate, 2005
Pulmonary Embolectomy
• Unnecessary for most patients
• Consider in selected highly compromised,
hemodynamically unstable patients
– Who are unable to receive thrombolytic
therapy
– Whose critical status does not allow sufficient
time to infuse thrombolytic therapy
• Chest 2004;126:401S
IVC Filters: Indications
• Contraindication to anticoagulation
• Complication of anticoagulation
• Recurrent PE despite adequate
anticoagulation
• Chronic recurrent PE with pulmonary
hypertension
• Concurrent with surgical pulmonary
embolectomy
“Optional” Filters
• “Option” to leave in permanently or to
remove, usually in two to four weeks
• Three types at UVA
• Tulip
• Opease
• Recovery
• Recovery rate at UVA about 95%
Conclusion
• PE is a common complication seen in hospitalized
pts.
• Clinical presentation of PE is nonspecific and
difficult to interpret.
• There are many diagnostic tools that complement
clinical assessments.
• To better improve early diagnosis of PE, preventive
measures should be in place that counter the risk
factors, and clinicians should have a greater
awareness for early signs/symptoms of PE.
Thank U
