PULMONARY THROMBOEMBOLISM

Perspective
 A Common disorder and potentially deadly

 650,000 cases occurring annually

 Highest incidence in hospitalized patients

 Autopsy reports suggest it is commonly “missed”

diagnosed

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 Perspective
 Presentation is often “atypical”

 Signs and symptoms are frequently vague and

nonspecific and rarely “classic”

 Untreated mortality rate of 20% - 30%, plummets to

5% with timely intervention

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Pulmonary thromboembolism
 Embolism : Impaction of a thrombus or foreign matter in the
pulmonary vascular bed.

 Blood clot , usually from the deep veins of the leg, also
air, fat, tumor, that occludes pulmonary vasculature
Epidemiology:

 Epidemiology Most deaths from PE are due to failure

to diagnose rather than failure to treat adequately.
 Two thirds of patients die within 1 hour of symptom
onset; this is the golden hour .
 Third most common acute cardiovascular disease
Mortality rate remains unacceptably high: With
treatment: 5% to 8% Without treatment: 25% to
30%

 Pathophysiology
Rudolph Virchow, 1858

Triad:
 Hypercoagulability
 Stasis to flow
 Vessel injury

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Risk Factors Virchow’s triad (SHE)

 S tasis
 H ypercoagulability
 E ndothelial damage
Risk Factors
Hypercoagulability
Malignancy
Nonmalignant thrombophilia
Pregnancy
Postpartum status (<4wk)
Estrogen/ OCP’s
Genetic mutations (Factor V Leiden, Protein C & S deficiency, Factor
VIII, Prothrombin mutations, anti-thrombin III
deficiency)
Venous Statis
Bedrest > 24 hr
Recent cast or external fixator
Long-distance travel or prolong automobile travel

Venous Injury
Recent surgery requiring endotracheal intubation
Recent trauma (especially the lower extremities and pelvis)
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Risk Factors (for DVT)
 Virchow’s Triad
 Alterations in blood flow (stasis): best rest, inactivity/immobilization, CHF,
paralysis
 Injury to endothelium: trauma, surgery
 Thrombophilia: Factor V Leiden, Protein C or S deficiency, etc.
 Age >50
 History of varicose veins
 History of MI
 History of malignancy
 History of atrial fibrillation
 History of ischemic stroke
 History of diabetes mellitus
 obesity, pregnancy
 Clinical Presentation
 The Classic Triad: (Hemoptysis, Dyspnea, Pleuritic Pain)
 Not very common!
 Occurs in less than 20% of patients with documented PE

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 Clinical Features
Symptoms in Patients with Angio Proven PTE

Symptom Percent

Dyspnea 84
Chest Pain, pleuritic 74
Anxiety 59
Cough 53
Hemoptysis 30
Sweating 27
Chest Pain, nonpleuritic 14
Syncope 13

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 Clinical Features
Signs with Angiographically Proven PE
Sign Percent

Tachypnea > 20/min 92

Rales 58
Accentuated S2 53
Tachycardia >100/min 44
Fever > 37.8 43
Diaphoresis 36
S3 or S4 gallop 34
Thrombophebitis 32
Lower extremity edema 24

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Clinical Presentation
 Asymptomatic
 Sudden onset of unexplained dyspnea
 Pleuritic chest pain
 Tachypnea
 Tachycardia
 Anxiety/agitation, cough, hemoptysis, syncope, fever,
cyanosis, isolated crackles, pleural friction rub, loud P2,
right-sided S3, pulmonary insufficiency murmur, right
ventricular heave, acute worsening of heart failure or
lung disease
Symptoms:
 Dyspnea
 Chest pain (pleuritic)
 Apprehension
 Cough
 Hemoptysis
 Syncope
 Palpitations
 Wheezing
 Leg pain
 Leg swelling
Signs
 Tachycardia
 Tachypnea
 Hypoxemia
 Accentuated S2
 Fever
 Diaphoresis
 Signs of DVT
 Cardiac murmur
 Jugular venous distention
 Cyanosis
 Hypotension
Nonspecific Workup
 Chest X-ray: abnormal in 88% of acute PE
 Atelectasis (60-70%): most common finding in
PE without infarction
 “Classic” findings:
 Westermark sign (increased lucency in area of
embolus)/ Decreased pulmonary vascularity
 Hampton Hump (wedge-shaped pleural-based
infiltrate)
 Abrupt cutoff of vessel
 Pleural effusion
 EKG
 Most common: sinus tachycardia +/-
nonspecific ST-segment and T-wave changes
 “Classic S1-Q3-T3 pattern”
 Other signs of right heart strain (ie, new RBBB
and ST changes in V1,2
 ABG
 Normal does NOT rule out PE
 “Classic” findings:
 Hypoxia, hypocapnia, respiratory alkalosis,
increased A-a gradient
Diagnostic modalities:

 D-dimer Lung Scanning

 Helical/Spiral Computed Tomography
 Leg Ultrasonography
 Pulmonary Angiography

 Chest X-ray Eponyms of PE
 Westermark's sign

 A dilation of the pulmonary vessels proximal to the embolism

along with collapse of distal vessels, sometimes with a sharp
cutoff.

 Hampton’s Hump

 A triangular or rounded pleural-based infiltrate with the apex

toward the hilum, usually located adjacent to the hilum.

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Westermark Sign
Hampton Hump

Occurs 12 to 36 hours after symptoms begin;

usually indicates pulmonary infarction
EKG Findings
VQ Scan :

 VQ Scan :Perfusion Ventilation Mismatch

 V/Q scans Old standard Currently reserved for Renal

impairment; IV contrast allergies ;Pregnancy ;Chronic PE
(controversial)

CT scan:
 CT scan New Standard Data suggests CT is as accurate as
invasive angiography (gold standard)
Pulmonary Angiography
 “Gold Standard”
 Invasive study
 5% morbidity
 < 0.5% mortality
 Indicated if the diagnosis remains uncertain after noninvasive
testing
Broad Differential
 Pneumothorax
 Myocardial ischemia
 Pericarditis
 Asthma
 Pneumonia
 MI with cardiogenic shock
 Cardiac tamponade
 Aortic dissection
Differential diagnosis:

 Pneumothorax
 Thoracic herpes zoster
 Rib fracture
 Musculoskeletal pain primary or metastatic intrathoracic
cancer
 hyperventilation syndrome
 infradiaphragmatic processes (e.g. acute cholecytitis)
 Dr. Batizy explaining the CT
results

Treatment: Patient
replies:
“Uh-huh,
when do I
get to eat!”

Goals:
 Prevent death from a current embolic event

 Reduce the likelihood of recurrent embolic events

 Minimize the long-term morbidity of the event

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 Treatment
 Anticoagulants
 Heparin
 Provides immediate thrombin inhibition, which prevents thrombus
extension

 Does not dissolve existing clot

 Will not work in patients with antithrombin III def.

 In this case use hirudins

 Few absolute contraindications

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 Treatment
 Anticoagulants
 Heparin
 Available as Unfractionated or LMW Heparin

 FDA approved dosing:

o Unfractionated: 80 units/kg bolus, 18 units/kg/hr

o LMWH: 1 mg/kg Q 12 or 1.5mg/kg Q D

 LMWH (Lovenox) prefered in pregnant patients

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 Treatment
 Anticoagulants
 Warfarin (Coumadin)
 Interferes with the action of Vit-K dependent factors: II, VII, IX, and X, as
well as protein C & S

 Causes temporary hypercoagulable state in first 5 days of treatment

 Important a patient is anticoagulated with heparin before initiating warfarin

therapy

 Target INR is 2.5 – 3.0

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 Treatment
 Fibrinolytic Therapy (Alteplase)
 Indications:
 Documented PE with:
 Persistent hypotension
 Syncope with persistent hemodynamic compromise
 Significant hypoxemia
 +/- patient with acute right heart strain

 Approved Altivase regimen is 100mg as a continuous IV infusion.

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 Treatment
 Embolectomy
 Prefininolytic therapy this was only therapy for massive PE

 Carries a 40% operative mortality

 Alternative is Transvenous Catheter Embolectomy

 Thrombolytic therapy: Streptokinase

 Urokinase
 Altepase (t-PA) In haemodynamically unstable patients even with heparin

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Adverse events and clinical outcome:

 Recurrent PE
 Death
 Bleeding
 Complications: Intracranial bleed Pulmonary hypertension
Prevention:

 heparin low-molecular-weight heparin graded compression

stockings have been shown to reduce the incidence of
pulmonary embolism in hospitalized patients.