PULMONARY EMBOLISM

Dr. Mohammad ABD-EL-SABOUR Professor of Pulmonary Medicine Ain Shams University

Pulmonary Embolism, Infarction

Embolism : Impaction of a thrombus or foreign matter in the pulmonary vascular bed. Infarction : The pathological changes which develop in the lung as a result of pulmonary embolism.

Pulmonary Thromboembolism
Thrombosis of peripheral veins , embolization of pulmonary arteries , and pulmonary infarction. Primary thrombosis in pulmonary arteries and veins

Pulmonary Embolism, Prevalence

PE : The cause of, or a major contributory factor to, death in 7-9% of necropsy cases PM Pul. Angiographic technique : 14-18% Considering smaller thrombi : 60% PE is a major contributory factor to death in 50 000-200 000 patients per year in USA

EMBOLUS
Thrombotic Non-thrombotic : Fat, Air, Tumour , Amniotic fluid, IV Drug abusers.

Pathogenesis of Vascular Thrombosis

Decrease in blood flow below a certain critical level. Increase in coagulability of blood. Damage of the vessel wall.

RISK FACTORS
Bed rest Post-operative After severe blood loss and trauma CCP CHF Varicose veins Advancing age Obesity Post-partum Malignancy DM Pneumonia Debilitating diseases 1ry polycythemia Race, Diet

PE, Clinical Features

Size of the embolus and blood vessel occluded. State of the lung. Associated disease(s).

PE , Clinical Features
Massive Pulmonary Embolism ( MPE ) Pulmonary Infarction ( PI ) Obliterative Pulmonary Hypertension

Massive Pulmonary Embolism MPE

CLINICAL SETTING ELDERLY,POSSIBLY OBESE AROUND THE 10th DAY POST-OP. CALLING FOR BED-PAN EXPIRING SUDDENLY OR WHILE IN THE ACT OF DEFECATION IMMEDIATELY FATAL,2/3 DIE IN THE FIRST TWO HOURS

Massive Pulmonary Embolism MPE

SHOCK DYSPNEA APPREHENSION TACHYCARDIA SWEATING CHEST PAIN FAINTNESS CYANOSIS AF COLLAPSE

MPE, Differential Diagnosis

Myocardial Infarction. Dissecting Aortic Aneurysm. Peumothorax. Major Pulmonary Collapse. Shock. Perforating Peptic Ulcer. Acute Pancreatitis.

CARDIOGENIC PULMONARY EDEMA

SUDDEN ONSET OF DYSPNEA SOMETIMES SEVERE CHEST PAIN PINK FROTHY SPUTUM EXTREME ANXIETY AND ORTHOPNEA DIAPHORESIS AND CYANOSIS TACHYPNEA AND AIR HUNGER WHEEZING DIFFUSE MOIST RALES,GALLOP

ACUTE PULMONARY EDEMA IN COPD

HISTORY OF PREVIOUS HEART DIS. SUDDEN,NOT ACUTE OR INSIDIOUS, ONSET OF DYSPNEA PINK FROTHY SPUTUM DIFFUSE MOIST RALES,PULSUS ALTERNANS,GALLOP,MURMURS CXR,ECG,ABG

PNEUMOTHORAX
SHARP UNILATERAL CHEST PAIN DYSPNEA;EXTREME IN TENSION PNX PRIMARY, SECONDARY, TRAUMATIC, BAROTRAUMA TACHYPNOEIC RAPID LOW VOLUME PULSE HYPOTENSION SURGICAL EMPHYSEMA

PNEUMOTHORAX
UNILATERAL BULGE TRACHEAL SHIFT HYPER-RESONANCE DIMINISHED INTENSITY OR ABSENT BREATH SOUNDS CXR

INTERCOSTAL TUBE DRAINAGE

MASSIVE PULMONARY COLLAPSE

CLINICAL SETTING TRACHEAL SHIFT UNILATERAL DULLNESS DIMINISHED OR ABSENT BREATH SOUNDS CXR BRONCHOSCOPY

COMPREHENSIVE ASSESSMENT

HISTORY : PT., PT.S RELATIVES, WITNESS PHYSICAL EXAMINATION: GENERAL RESPIRATORY CARDIOVASCULAR

COMPREHENSIVE ASSESSMENT
INVESTIGATIVE STUDIES ECG ABG CXR ELECTROLYTES ENZYMES

Pulmonary Infarction, Pathology

Blood Vessels: Engorgement, Hemorrhage from distended necrotic capillaries, Granulation tissue repair , Fibrous scar Bronchioles: usually survive, may turn bronchiactatic

Pulmonary Infarction, Pathology

Bacterial Infection : Abscess Source : embolus, blood-borne, bronchi . Pleural Complications : Pleurisy, Pleural effusion, Empyema.

Pulmonary Infarction, Clinical Picture

Pleuritic chest pain, Pleural rub, Pleural effusion Hemoptysis: in only 50% of cases Finding the source of embolization: in only 60% of cases Tachcardia( more than 100/ min ) Tachypnoea Jaundice, Cyanosis

Pulmonary Infarction, Clinical Picture

Locally: No Physical Findings, Consolidation, Diminished Intensity of Breath Sounds, Crepitus, Wheezing Chest Pleural Rub Signs of Pleural Effusion

Pulmonary Infarction, Clinical Picture

With Infection: Worsening of the Clinical Status: Abscess or Empyema Persistent Fever, Malaise, Sweating Increasing Pulse Rate Leucocytosis more than 20 000 Chest X-Ray

Clinical Features of PTE

Silent Asymptomatic Probably more frequent than we realize Usually Transient

Without Infarction

Breathlessness, Tachycardia, Anxiety, Restlessness

Clinical Features of PTE

With Infarction Dyspnea, Hemoptysis, Pleutitic Pain, Friction Rub, Fever, Brochospasm. If you wait for these features, you will miss perhaps 60% of patients with embolism

Clinical Features of PTE

With Angina, Hemodynamic Tachycardia, Impairment P++, Gallop, JVP++, Hypotension, Cyanosis, Syncope This means obstruction of 30-50% of pulmonary vascular bed

Value of Diagnostic Tests in PTE

Chest X-Ray Elevated Diaphragm, It may be Normal Wedge-shaped after acute PE opacity, Atelectasis, Pleural Effusion

ECG

Sinus Tachycardia, S1, Q3, T3, Rt. Axis P-Pulmonale, Incomplete RBBB , Arrhythmias

Chest X-Ray and ECG should be Routine

Value of Diagnostic Tests in PTE

Isoenzyme Pattern Normal Only helpful in distinguishing PE from MI

Leucocytic Count

Under 15 000

If over 15 000, consider Bacterial Sepsis

Value of Diagnostic Tests in PTE

Arterial Blood Hypoxemia, Gases ( ABG ) Hypocapnia Non-specific

AlveolarArterial Oxygen Tension Difference

Increased Difference

More Sensitive but Non-specific .

Value of Diagnostic Tests in PTE

Radioactive Abnormal Lung Scanning Perfusion with Normal Ventilation . High, Intermediate and Low Probability . Non-specific, Too many False-positive . A Normal Perfusion Scan with a Normal CXR rules out PE .

Value of Diagnostic Tests in PTE

Pulmonary Angiogram Intravacular Filling Defect or Vessel Cut-off The Most Reliable but Invasive

D-Dimers

A Good Negative Elevated in DIC, Predictive Test Pregnancy, Severe Infection, Trauma, Malignancy, Surgery, Liver Disease

Value of Diagnostic Tests in PTE

Spiral Computed Comparable to Tomography Angiography. Cases with VentilationPerfusion scan of Intermediate Probability Clinical Assessment Clinical Scoring Plus ECG, Radiographic Findings, Perfusion Scan. Poor Quality may be obtained as a result of motion artifacts.

This may restrict the need for Angiography to a minority.

Clinical Probability of PE
High Probability ( 90% ): Presence of at least one of three symptoms ( Sudden onset Dyspnea, Chest Pain, or Fainting ) not explained otherwise and associated with : (1) Any two of the following abnormalities: ECG signs of RV overload, Radiographic signs of Oligemia, Amputation of hilar artety, or Pulmonary consolidations compatible with infarction; (2) Any one of the above three radiographic abnormalities.

Clinical Probability of PE
Intermediate Probability (50%): Presence of one of the above symptoms, not explained otherwise, but not associated with the above ECG and Radiographic abnormalities, or associated with ECG signs of RV overload only.

Clinical Probability of PE
Low Probability (10%): Absence of the above three symptoms, or idetification of an alternative diagnosis that may account for their presence (e.g.,exacerbation of COPD, Pneumonia, Lung Edema, Pneumothorax, Myocardial Infarction, and others).

A Normal VentilationPerfusion Scan Excludes Pulmonary Embolism

The Combination of A High-Probability Ventilation-Perfusion Scan Plus A High Clinical Suspicion is Diagnostic for Pulmonary Embolism.

A Low-Probability or Normal Lung Scan with a Low Clinical Suspicion makes the diagnosis of Pulmonary Embolism Unlikely

Spiral CT is A Primary Diagnostic Modality in Suspected Pulmonary Embolism.

.It is the Diagnostic Test of Choice when

Ventilation-Perfusion Scans are judged to be Intermediate.

Massive Pulmonary Embolism MPE

2/3 die in the first 2 hours. A Medical Emergency. Resuscitate : Succeed : Pulmonary Angiography. Less than 75% decrease in peripheral perfusion : Streptokinase. 75% or more decrease in peripheral perfusion : Embolectomy.

Massive Pulmonary Embolism MPE

Recombinent-tissue type plasminogen activator ; t-PA Altepase : 100mg over 2 hours.

Pulmonary Embolism, Prevention

Patients at risk: Early Ambulation. Risk Factors. During Operations. Prophylactic Heparin. Vein Ligation. Filters.

Pulmonary Embolism, Active Treatment

Embolectomy. Recombinant tissue-plasminogen activator, t-PA. Streptokinase and Urokinase.

Pulmonary Embolism, Active Treatment

Heparin, Low-Molecular-Weight Heparin. Oral Anticoagulants. Filters, Vein Ligation. Adjuvants: Oxygen, Antibiotics, Rest in bed.

Streptokinase
600 000 U in 1/2 h, Then 100 000 U/h for 72h. Thrombin clotting time. EACA: Local and Systemic, Fresh Blood, and Fresh Frozen Plasma.

Heparin
15 000 - 25 000 U iv Bolus, Then 40 000 - 60 000 U/ 24 h, or 20 U/Kg/h Partial Thromboplastin Time ( PTT ). Infusion Pump. Absolute and Relative Cotraindications. Protamine Sulphate.

Low-Molecular-Weight-Heparin
Greater Bioavailability. Can be given Subcutaneously. Longer duration of Anticoagulant effect. A fixed dose can be used, PTT monitoring is not necessary. Enoxaparin: 1 mg/kg every 12h.

Oral Anticoagulants
For How Long ? Prothrombin Time. Drug-Drug Interaction. Vitamin K.

THANK YOU