Pulmonary embolism

PULMONARY EMBOLISM

Dr. HOSAM ATEF

LECTURER OF ANESTHESIOLOGY&ICU

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 Thrombo-embolism

• 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

• 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


• 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


• Locally: No Physical Findings, Consolidation, Diminished Intensity of Breath Sounds, Crepitus, Wheezing Chest

• Pleural Rub• Signs of Pleural Effusion


• 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

Without Infarction Breathlessness, Tachycardia, Anxiety, Restlessness

Usually Transient

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 PTEWith Hemodynamic Impairment

Angina, Tachycardia, 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, Wedge-shaped opacity, Atelectasis, Pleural Effusion

It may be Normal after acute PE

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

Chest X-Ray and ECG should be Routine


Isoenzyme Pattern

Normal Only helpful in distinguishing PE from MI

Leucocytic Count

Under 15 000 If over 15 000, consider Bacterial Sepsis


Arterial Blood Gases ( ABG )

Hypoxemia, Hypocapnia

Non-specific

Alveolar-Arterial Oxygen Tension Difference

Increased Difference

More Sensitive but Non-specific .


Radioactive Scanning

Abnormal Lung 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 .


Pulmonary Angiogram

Intravacular Filling Defect or Vessel Cut-off

The Most Reliable but Invasive

D-Dimers A Good Negative Predictive Test

Elevated in DIC, Pregnancy, Severe Infection, Trauma, Malignancy, Surgery, Liver Disease


Spiral Computed Tomography

•Comparable to Angiography.•Cases with Ventilation-Perfusion scan of Intermediate Probability

Poor Quality may be obtained as a result of motion artifacts.

Clinical Assessment

Clinical Scoring Plus ECG, Radiographic Findings, Perfusion Scan.

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.


• 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.


• Low Probability (10%): Absence of the above three symptoms, or identification 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 Ventilation-Perfusion 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.


• 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.


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

Pulmonary embolism

Health & Medicine

Transcript of Pulmonary embolism