Transcript Pulmonary Embolism Hidden Killer

Pulmonary Embolism
Hidden Killer
Dr. Hatem Said
Assistant Professor Anesthesia/ICU
Ain Shams University
Objectives
1.
2.
3.
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Definition
Epidemiology
Pathophysiology
Clinical Picture
Diagnostic Tools
Prophylaxis
Treatment
Conclusion
1-Definition
Pulmonary embolism (PE): is an obstruction
of the pulmonary artery or one of its branches
by a thrombus (or thrombi) that originates
somewhere in the venous system.
Infarction : The pathological changes which
develop in the lung as a result of pulmonary
embolism
The types of emboli :could be a blood clot
(most common), air, fat, amniotic, fluid, and
septic (from bacterial invasion of the
thrombus).
2-Epidemiology
PE : The cause of, or a major contributory
factor to, death in 7-9% of necropsy cases
650,000 cases in the US each year
150,000 – 200,000 US deaths each year
Most common preventable cause of hospital
death
3rd most common acute cardiovascular
emergency (MI and stroke)
3-Pathophysiology
Source of Thrombosis (Thrombo-embolic)
that originates in the venous system and
embolizes to the pulmonary arterial
circulation
1. DVT in veins of leg above the knee (>90%)
2. DVT elsewhere (pelvic, arm, calf veins,
etc.)
3. Cardiac thrombi
3-Pathophysiology
Risk factors for deep venous thromboembolism
Triad of Virchow
1. Endothelial injury: mainly caused by either direct
trauma (severed vein) or local irritation (by
chemotherapy, past DVT, phlebitis).
2. Stasis: mainly caused by heart failure, prolonged
immobility.
3. Hypercoagulation status: inherited :(AT III def.,
protein C, S deficiency) or acquired: (malignancy,
pregnancy, nephritic syndrome, DIC and liver
failure.
3-Pathophysiology
Risk Factors:
Strong Predisposing
factors
(Odds Ratio>10)
Moderate Predisposing factors
(Odds Ratio 2-9)
Weak Predisposing factors
(Odds Ratio <2)
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•Bed Rest<3 days
•Immobility due to
sitting(e.g prolonged car
or air travel)
•Increasing Age
•Laparoscopic surgery
(Cholecystectomy)
•Obesity
•Varicose veins
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Fracture (Hip or
Leg)
Hip or Knee
Replacement
Major General
Surgery
Major trauma
Spinal Cord Injury
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Arthroscopic Knee Surgery
Central venous line
Chemotherapy
Chronic heart or
respiratory failure
Hormonal replacement
therapy
Oral Contraceptive Pills
Paralytic Stroke
Pregnancy/Postpartum
Previous VTE
Thrombophelia
4-Clinical Picture
• Revised Geneva Score (Clinical Prediction)
Variable
Predisposing Factors:
•Age>65 years
•Previous DVT or PE
•Surgery or fracture within 1 month
•Active malignancy
Symptoms:
•Unilateral lower limb pain
•Haemoptysis
Clinical Signs
•Heart Rate
•75-94 bpm
•>95bpm
•Pain on LL deep vein and unilateral edema
Clinical probability:
•Low
•Intermidiate
•High
Points
+1
+3
+2
+2
+3
+2
+3
+5
+4
Total
0-3
4-10
4-Clinical Picture
• Wells Score (Clinical Prediction)
Variable
Points
Predisposing Factors:
•Previous DVT or PE
•Recent Surgery or immobilization
•Cancer
+1.5
+1.5
+1
Symptoms:
•Haemoptysis
+1
Clinical Signs
•Heart Rate
•>100 bpm
•Clinical signs of DVT
•Clinical Judgement
•Alternative diagnosis less likely than PE
Clinical probability:
•Low
•Intermidiate
•High
+1.5
+3
Total
0-1
2-6
>7
4-Clinical Picture
Most PE are small embolism will reach the
periphery of the lung, sometimes producing wedge
shaped shadow (pulmonary infarction) on CxR .
A large embolism suddenly obstructing a major
pulmonary vessel has marked effects on cardiac
function , often associated with anterior chest pain
and collapse.
Chronic recurrent pulmonary embolism may
develop pulmonary hypertension and right
ventricular failure
4-Clinical Picture
 SYMPTOMS :
• Dyspnea (84%).
• Pleuritic pain (74%).
• Anterior chest pain (68%).
• Cough (53%).
• Hemoptysis (30%).
• Asymptomatic (10%).
 SIGNS:
• Tachypnea (70%).
• Rales (51%).
• Tachycardia (30%).
• S4 (24%).
• Accentuated P2.
Massive PE:
-Shock.
-Dyspnea, Cyanosis.
-Apprehension, Sweating.
-Chest pain, Tachycardia, AF
4-Clinical Picture
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Differential Diagnosis:
Myocardial Infarction.
Pluerisy/Pericarditis.
Tachyarrhythmia.
Musculoskeletal/rib fracture.
Lobar Collapse secondary to tumor.
Asthma.
Pneumonia.
Pneumothorax.
Perforating Peptic Ulcer.
Acute Pancreatitis.
Differential Diagnosis of Massive Pulmonary Embolism:
Acute pulmonary edema
Cardiac tamponade.
Dissecting Aortic Aneurysm.
Shock/sepsis.
5-Diagnostic Tools
Duplex US with compression of the
lower extremities
• Non-invasive test that accurately detects
proximal DVT in LE (70-80% of pts with PE
have concomitant proximal DVT)
• Often used in workup of PE before going to
more invasive procedures
Invasive test: Venography (definitive
diagnosis)
5-Diagnostic Tools
Laboratory Investigations (Non Specific):
leukocytosis , ESR elevation, LDH, SGOT elevation
with normal bilirubin.
• CK, CK MB or Troponin I should be checked to rule
out AMI
• ABG
– Normal does NOT rule out PE
• Hypoxia, hypocapnia, respiratory alkalosis.
• D-Dimer: High sensitivity but poor specificity
• Negative prediction<500 ng /ml is a powerful
excluding tool for PE
5-Diagnostic Tools
Chest X-ray: Abnormal in 88% of acute PE
• Atelectasis (60-70%): most common finding
in PE without infarction.
• Westermark sign (increased lucency in area
of embolus)
• Hampton Hump (wedge-shaped pleuralbased infiltrate)
• Abrupt cutoff of vessel
• Pleural effusion
Westermark Sign: represents a focus of oligemia (vasoconstriction )seen
distal to a pulmonary embolism
Hampton Hump: Radiologic sign which consists of a shallow wedge-shaped opacity in the
periphery of the lung with its base against the pleural surface. Occurs 12 to 36 hours after
symptoms begin;
usually indicates pulmonary infarction
5-Diagnostic Tools
 ECG:
– Most common: sinus tachycardia +/- nonspecific STsegment and T-wave changes
– “Classic S1-Q3-T3 pattern”
– Other signs of right heart strain (ie, new RBBB and ST
changes ,T wave inversion in V1,2
 Echocardiography:
• It may be helpful after a large PE in a compromised patient,
as it can show right heart dilatation , occasionally thrombus
and increased pulmonary arterial pressure readings if
tricuspid regurgitation developed.
• Convenient and rapidly available
ECG findings
Echocardiography Findings
Echocardiography Findings
Transesophageal echocardiographic findings
showing the floating thrombus (arrow) into
central pulmonary artery
(PA, pulmonary artery; RA, right atrium; Ao,
aorta)
Transesophageal echocardiographic shows
the reduction in size of the clot (arrow)
(PA, pulmonary artery; RA, right atrium; Ao,
aorta)
Helical(Spiral) CT
• Sensitivity 85% (more sensitive for proximal emboli
but is less good at detecting peripheral emboli,
which may account for up to 30% of PE vessels)
• Specificity 95%
• It may be used as a first line investigation when
V/Q Scan is delayed and when a large PE is
suspected and early diagnosis is needed first-
V/Q Scan
 Identifies mismatches between areas that are ventilated
but not perfused
 Best initial test in patients with clear CXR
1. Normal: rules out PE
2. High-probability scan: is diagnostic of PE if the clinical
suspicion is also high
3. Low-probability scan: rules out PE only in a pt with low
pretest clinical probability (because PE is found in
roughly 15% of pts with low-probability scans)
4. Intermediate-probability scan: requires further
evaluation (16-66% chance of PE depending on pretest
probability)
Pulmonary Angiography
“Gold Standard” but is invasive, time
consuming, needs experienced radiologists
5% morbidity
< 0.5% mortality
Indicated if the diagnosis remains uncertain
after noninvasive testing
6- Prophylaxis
 Encourage all patients to ambulate as soon as possible
 determine patient at risk:
• Low risk :(<40 years old, ambulating, minor surgery)
don't need prophylaxis.
• Moderate risk: (>40 years old, abdominal, pelvic or
thoracic surgery) pneumatic compression, or low dose
heparin prophylaxis.
• High risk: (>60years old, prior DVT or PE malignancy,
orthopedic surgery hypercoagulability state)
combination of pneumatic compression and low dose
heparin prophylaxis or Dextran.
Coumadine or IVC filter are considered.
IVC Filter: if anticoagulation is contraindicated (e.g., active GI bleed,
intracranial neoplasm, Ophthalmology patient , known bleeding diathesis), if
thrombus formed despite adequate anticoagulation, or with a large burden of
thrombosis in the LE that could be fatal if embolized.
6- Prophylaxis
Rivaroxaban (Oral factor X a inhibitor)
• New Drug that provide a simple, fixed-dose
regimen for treating acute DVT and for continued
treatment, without the need for lab. Monitoring.
• Approved (FDA) for prophylaxis in post-operative
period after knee & hip replacement and chronic
AF.
• Nearly it will approved for treatment of acute PE.
• Antidote: Thrombin Complex Concentrate.
7-Treatment
 Primary Treatment:
• Supplemental oxygen for hypoxemia.
• If the PE is large, supportive treatments for hypotension or
reduced CO should be given IVF , Levophed , or
Dopamine/Mechanical Ventilatory Support
• Specific treatment is with intravenous unfractionated heparin
infusion following an initial bolus dose 80 U/kg bolus, then 18
U/kg/hr
• a PTT should be monitored 6 hours after initiation, 6 10 hours
after any dosage change, then daily with a target of 46-70
seconds.
• Heparin does not reduce acute mortality but significantly
reduces further events
7-Treatment
 LMWH: Current guidelines for patients with acute
nonmassive pulmonary embolism recommend LMWH
over UFH.
 LMWHs have many advantages over UFH:
• These agents have a greater bioavailability,
• can be administered by subcutaneous injections,
• and have a longer duration of anticoagulant effect.
• - A fixed dose of LMWH can be used ( 30mg, sc, bid),
and laboratory monitoring of a PTT is not necessary
• Chest. Jun 2008;133(6 Suppl):454S-545S
7-Treatment
 Oral Anticoagulation:
• Oral Warfarin can be given with the initiation of
Heparin keep INR between 2- 3 with initial dose of
5mg/day for 2 days (The peak effect does not occur
until 36-72 hours after drug administration) .
• An overlap of 4- 5 days with a therapeutic INR and a
PTT is recommended .
• Persistent oral Warfarin should be prescribed for 3
months till the absence of risk factors
• LMWH can be used when Warfarin is contraindicated
(e.g. pregnancy) .
7-Treatment
Long-term anticoagulation
• 1st event with reversible risk factors: 3-6 months
Warfarin.
• Idiopathic PE/DVT: 6 months Warfarin.
• 2nd event, cancer, preexisting irreversible risk
factors, such as deficiency of antithrombin III,
protein S and C Deficiency: 12 month to life long
Warfarin.
• BMJ. Mar 31 2007;334(7595):674
7-Treatment
 Potential indications for THROMBOLYTIC THERAPY in venous
thromboembolism (acceptable risk of bleeding
complications) :
• significant cardiac compromise , RV strain (Dysfunction) .
• presence of hypotension related to PE not responding to IVF
and vasopressor resuscitation.
• Presence of severe hypoxemia.
• Substantial perfusion defect.
• Extensive DVT.
• Thrombolytic therapy achieves faster resolution of the
thrombus and more rapid recovery of normal vascular flow
than simple anticoagulation.
7-Treatment
Regimens for thrombolysis in Pulmonary
Embolism:
Drug
Regimen
• Streptokinase
250.000 IU in 20-30 min
followed by 100.00 IU/Hour up to 24 Hours
• t-PA
10 MG IV over 1-2 min
followed by an infusion of 90 MG over 2 Hours
Cerebral hemorrhage can occur in up to 1% of cases
It has been used successfully and safely in a
pregnant woman and this is not a contraindication
unless immediately postpartum
7-Treatment
Pulmonary Embolectomy:
• This is reserved for severe cardiac compromise
where thrombolysis has either failed or is
contraindicated.
• It requires an experienced team to be successful
and, although used infrequently, small studies
(Doerge et al, 1999) have shown favorable
outcomes.
8-Conclusion
• 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.