PULMONARY EMBOLISM

Dr. M. A. Sofi MD; FRCP; FRCPEdin; FRCSEdin

Pulmonary Embolism PE is the most common

preventable cause of death in hospitalized patients

600,000 deaths/year 80% of pulmonary emboli

occur without prior warning signs or symptoms

2/3 of deaths due to pulmonary emboli occur within 30 minutes of embolization

Death due to massive PE is often immediate

Diagnosis can be difficult Early treatment is highly

effective

40-50% of pts with DVT develop PE, often “silent”

PE presents 3-7 days after DVT Fatal within 1 hour after onset of respiratory

symptoms in 10% Shock/persistent hypotension in 5-10% (up to

50% of patients with RV dysfunction) Most fatalities occur in untreated pts Perfusion defects completely resolve in

75% of all patients (who survive)

Natural History of VTE

Inherited Risk Factors

Family History (+)

Acquired risk factor (+)

Prior deep venous thrombosis

Inherited Risk Factors (2)

Antithrombin III deficiency

Protein C deficiency

Protein S deficiency

Protein C resistance (Factor V Leiden)

Hyperhomocystinemia

Abnormal fibrinogen

Abnormal fibrinolytic system

RISK FACTORS

Acquired Risk factors (III) Prior DVT Nephrotic Syndrome Antiphospholipid Syndrome PNH Waldenström

Macroglobinemia

Major risk factors: relative risk of 5-20

Surgery: Major abdominal/pelvic

surgeryor hip/knee replacement(risk lower if prophylaxis used).

Postoperative intensive care.Obstetrics: Late pregnancy. Puerperium. Caesarean sectionLower limb problems: Fracture. Varicose veins - previous

varicose vein surgery;superficial thrombophlebitis; varicose veins per se are not a risk factor

Minor risk factors: relative risk of 2-4

Cardiovascular: Congenital heart disease. Congestive cardiac failure. Hypertension. Paralytic stroke.Oestrogens: Pregnancy (but see major risk

factors for late pregnancy and puerperium).

Combined oral contraceptive. Hormone replacement

therapy.Renal: Nephrotic syndrome. Chronic dialysis. Paroxysmal nocturnal

haemoglobinuria

Risk Factors:

Major risk factors: relative risk of

Malignancy: Abdominal/pelvic. Advanced/metastatic.Reduced mobility: Hospitalization. Institutional care.Previous proven VTE: Intravenous (IV) drug use

(could be major orminor risk factor:no data on relative risk).

Other: Major trauma. Spinal cord injury. Central venous lines.

Minor risk factors: relative risk of

Hematological: Thrombotic disorders

Consider this in cases of PE aged <40 years, recurrent VTE or a positive family history.

Myeloproliferative disordersMiscellaneous: Chronic obstructive pulmonary

disease (COPD). Neurological disability. Occult malignancy. Long-distance sedentary travel. Obesity. Other chronic diseases:

inflammatory bowel disease, Behçet's disease.

Risk Factors:

The classic presentation of PE is the abrupt onset of pleuritic chest pain.

Shortness of breath. Hypoxia. Most patients with PE have

no obvious symptoms at presentation.

Symptoms may vary from sudden catastrophic hemodynamic collapse to gradually progressive dyspnea.

The diagnosis of pulmonary embolism should be suspected in patients with respiratory symptoms unexplained by an alternative diagnosis

Patients with PE may present with atypical symptoms, such as the following:

Seizures Syncope Abdominal pain Fever Productive cough Wheezing Decreasing level of

consciousness New onset of atrial fibrillation Hemoptysis Flank pain Delirium (in elderly patients)

Presentation:

Evidence-based literature supports the practice of using clinical scoring systems to determine the clinical probability of pulmonary embolism before proceeding with testing.

Validated clinical prediction rules should be used to estimate pretest probability of pulmonary embolism and to interpret test results

Physical signs of pulmonary embolism include the following:

Tachypnea (respiratory rate >16/min): 96%

Rales: 58%

Accentuated second heart sound: 53%

Tachycardia (heart rate >100/min): 44%

Fever (temperature >37.8°C): 43%

Diaphoresis: 36% S3 or S4 gallop: 34% Clinical signs and symptoms

suggesting thrombophlebitis: 32%

Lower extremity edema: 24%

Cardiac murmur: 23% Cyanosis: 19%

Presentation:

Perform diagnostic testing on symptomatic patients with suspected Pet o confirm or exclude the diagnosis or until an alternative diagnosis is found.

Routine laboratory findings are nonspecific and are not helpful in pulmonary embolism.

A hypercoagulation workup should be performed if no obvious cause for embolic disease is apparent, including screening for conditions such as the following:

Antithrombin III deficiency Protein C or Protein S deficiency

Lupus anticoagulant Homocystinuria Occult neoplasm Connective tissue disordersPotentially useful laboratory

tests in patients with suspected pulmonary embolism include the following:

D-dimer testing Ischemia-modified albumin

level White blood cell count Arterial blood gases: Serum troponin levels Brain natriuretic peptide

Testing:

Imaging studies that aid in the diagnosis of pulmonary embolism include the following:

Computed tomography angiography (CTA): Multidetector-row CTA (MDCTA) is the criterion standard for diagnosing pulmonary embolism

Pulmonary angiography: Criterion standard for diagnosing pulmonary embolism when MDCTA is not available

Chest radiography: Abnormal in most cases of pulmonary embolism, but nonspecific

V/Q scanning: When CT scanning is not available or is contraindicated

ECG: Most common abnormalities are tachycardia and nonspecific ST-T wave abnormalities

MRI: Using standard or gated spin-echo techniques, pulmonary emboli demonstrate increased signal intensity within the pulmonary artery

Echocardiography: Transesophageal echocardiography may identify central pulmonary embolism

Venography: Criterion standard for diagnosing DVT

Duplex ultrasonography: Noninvasive diagnosis of pulmonary embolism by demonstrating the presence of a DVT at any site

Imaging:

Chest Radiography Usually nonspesific

Not sensitive or specific

Proximal, large segmental artery

Multiple small segmental artery

Chest Radiography (II) Atelectasis

Elevation of the hemidiaphragm

Pleural efusion

Dilatation of the main branches of PA

Paranchymal densities (in the lower lung fields, pleural based)

Zones of oligemia

Laboratory Tests

S1 Q3 T3 and T WAVE CHANGES

If PE is suspected, use the two-level PE Wells' score to estimate the clinical probability of PE

Offer patients in whom PE is suspected and with a likely two-level PE Wells' score either

An immediate computed tomography pulmonary angiogram (CTPA) or

Immediate interim parenteral anticoagulant therapy followed by a CTPA,

If a CTPA cannot be carried out immediately.

Consider a proximal leg vein ultrasound scan if the CTPA is negative and DVT is suspected.

AssessmentNB: treatment may precede investigations if the patient is very ill

D-dimer test if the result is positive:

Immediate CTPA or immediate interim parenteral anticoagulant therapy followed by a CTPA, if a CTPA cannot be carried out immediately.

For patients who have an allergy to contrast media, or who have renal impairment, or whose risk from irradiation is high:

Assess the suitability of a ventilation/perfusion single-photon emission computed tomography (V/Q SPECT)

If offering a V/Q SPECT or planar scan that will not be available immediately, offer immediate interim parenteral anticoagulant therapy.

AssessmentNB: treatment may precede investigations if the patient is very ill

Wells' Two-level PE Score Clinical feature Point Clinically suspected DVT (minimum leg swelling and pain on palpation of deep veins).

3.0

Alternative diagnosis less likely than PE. 3.0

Tachycardia (heart rate above 100 beats per minute).

1.5

Immobilization for more than three days or surgery in the previous four weeks

1.5

History of DVT or PE. 1.5

Haemoptysis. 1.0

Malignancy (on treatment in the preceding six months or palliative stage).

1.0Clinical probability4 points or less = PE unlikely.More than 4 points = PE likely.

Arterial Blood Gases Acute PaCO2 decreases

Massive PaO2 decreases

Submassive Normal / Near

normal

Echocardiography

Shows emboli in main pulmonary arteries, but not in lober and segmentaL arteries

Dilated hypokinetic RV

Distorsion of the interventricular septum in diastole

Tricuspid regurgitation associated with increase in systolic pressure in pulmonary artery

Laboratory Tests

Perfusion (-) and Ventilation (+) PE

Perfusion (N) and Clinical sym and signs (N) PE excluded

Low probability PVLS and low probability of

clinical sym and signs PE excluded

High probability PVLS and high probability of

clinical symp and signs Anticoagulation

Ventilation-Perfusion Lung ScanIt remains the first line investigation of possible PE. It should be performed in all clinically stable patients. A Ventilation Perfusion scan is most useful when the result category is one of normal , low or high probability.

Deep Vein Thrombosis

PERFUSION/VENTILATION LUNG SCAN

PERFUSION/VENTILATION LUNG SCAN

This algorithm allowed for a management decision in 98% of patients presenting with symptoms suggestive of PE

Anticoagulation medications include the following:

Unfractionated heparin Low-molecular-weight

heparin Factor Xa Inhibitors Fondaparinux Warfarin

Thrombolytic agents used in managing pulmonary embolism include the following:

Alteplase Reteplase Urokinase StreptokinaseSurgical options Surgical management

options include the following:

Catheter embolectomy and fragmentation or surgical embolectomy

Placement of vena cava filters

Management:

Anticoagulation and thrombolysis

Immediate full anticoagulation is mandatory for all patients suspected of having DVT or pulmonary embolism.

Diagnostic investigations should not delay empirical anticoagulant therapy.

Thrombolytic therapy should be used in patients with acute pulmonary embolism who have hypotension (systolic blood pressure< 90 mm Hg)

who do not have a high bleeding risk.

In selected patients with acute pulmonary embolism not associated with hypotension who have a low bleeding risk and whose initial clinical presentation or clinical course suggests a high risk of developing hypotension.

Management:

Direct visualization of emboli. Both parenchymal and mediastinal

structures can be evaluated. Offers differential diagnosis in 2/3 of cases

with a negative scan. BUT… Dye load and large radiation dose Optimally used when incorporated into a validated diagnostic decision tree

Spiral CT

Clinical Probability of acute PE

High Probability (80-100%)

Risk factors (+) Dyspnea

Tachypnea Chest pain

Radiology (+) PaO2 decreases

P (A-a)O2 increases

Intermediate Probability (20-79%)

Low Probability (1-19%)

Risk Factors (-)

Clinical and laboratory findings can be explained

Treatment To prevent death

To reduce morbidity

To prevent pulmonary hypertension

Progresing due to thromboemboli

Anticoagulation

1. Unfractioned heparin

2. LMWH

3. Thrombolysis

4. Embolectomy

Prognosis Mortality rate – 30%

Depends on associated pathology

Resolution – 5 days 36%

2 weeks 52%

3 months 73%

Pulmonary hypertension

recurrent microemboli (rare)

TREATMENT

Unfractioned Heparin

IV 5000 U bolus + 30-35 000 U/kg

aPTT- twice the control value

Thrombocytopenia

Early: thrombocyte aggregation slight, reveresible, no need to stop

Late: antibodies against thrombocytes arterial and venous thromboemboli

Osteopenia

LMWH

long acting

less binding to plasma

protein

greater bioavailibity

no need monitoring

TREATMENT

Thrombolysis

Massive pulmonery emboli with hemodynamic instability

Streptokinase

Urokinase

t-PA

**serious bleeding

Secondary prevention UFH + oral anticoagulan

(6 months) LMWH SC + oral

anticoagulan (6 months )

LMWH (pregnancy)

Recurrance / unknown origin / permanantly increased risk (throughout life)

TREATMENT

Catheter Embolectomy & FragmentationAn alternative in high-risk PE patients when thrombolysis is absolutely contraindicated or has failed