Pulmonary Embolisim .pdf

PULMONARY EMBOLISM ILOs At the end of this session, the student will be able to: State the definition of pulmonary embolism, its causes, and risk factors. Define the different clinical presentations and types of pulmonary embolism. Recognize the complications of pulmonary...

PULMONARY EMBOLISM ILOs At the end of this session, the student will be able to: State the definition of pulmonary embolism, its causes, and risk factors. Define the different clinical presentations and types of pulmonary embolism. Recognize the complications of pulmonary embolism. Explain the pathophysiology of pulmonary embolism. Classify pulmonary embolism according to severity. Outline pulmonary embolism work-up: laboratory and imagining techniques. Discuss the management plan of pulmonary embolism. Identify Pulmonary hypertension and corpolmonale definitions and classifications. ▪ Pulmonary embolism (PE) is an Obstruction of the pulmonary artery or one of its branches by a substance that has traveled from elsewhere in the body through the bloodstream (embolism). ▪ PE most commonly results from deep vein thrombosis (a blood clot in the deep veins of the legs or pelvis) that breaks off and migrates to the lung, lodges in the pulmonary vascular bed, and restricts circulation to the corresponding part of lung vasculature a process termed venous thromboembolism (VTE). ▪ Less commonly PE is due to the embolization of: ▪ Fat: which can escape from the bone marrow with fracture of a long bone, lipolysis, or burns ▪ Cancerous tumor fragments, which may break free into the bloodstream ▪ Air bubbles: may be introduced during intravenous delivery of drugs or fluids, vein is operated on, or when a person is being resuscitated because of the force of having pressure put on their chest. 1 ▪ Amniotic fluid: which may be forced into the pelvic veins during childbirth. ▪ Talc in drugs of intravenous drug abusers Source of Emboli: ▪ Most cases (80–95 percent) of VTE occur as a result of a thrombus originating in the lower extremity. ▪ Most thrombi originate in the deep veins of the calf and propagate proximally to the popliteal and femoral veins. ▪ Calf-limited thrombi pose a minimal embolic risk while those that extend into and above the popliteal vein represent the most common source of acute symptomatic pulmonary embolism. Emboli may originate from other sites, ▪ Most often from the pelvic veins (pregnancy, or pelvic infection, or recent pelvic surgery). ▪ Upper-extremity thrombosis associated with central venous catheters or intravascular cardiac device. ▪ Right side of the heart: Mural thrombi or vegetations on tricuspid valve (subacute bacterial endocarditis). Course: After traveling to the lung, large thrombi can lodge at the bifurcation of the main pulmonary artery or the lobar branches and cause hemodynamic compromise. Smaller thrombi typically travel more distally, occluding smaller vessels in the lung periphery. These are more likely to produce pleuritic chest pain by initiating an inflammatory response adjacent to the parietal pleura. Risk factors for DVT& pulmonary embolism Virchow described a triad for thrombosis to occur on the wall of a deep vein: 1. Stasis: leads to accumulation of clotting factors and fibrin, resulting in thrombus formation in veins, occurs in: old age, immobility, 2  obesity, pregnancy, Labour, malignancy, major surgery. 2. Hypercoagulability states: Altered balance between coagulation and anticoagulation by many diseases (e.g., malignancy), trauma After surgery. Use of oral contraceptive pills Deficiency of natural anticoagulants: Protein C,S deficiency, Anticardiolipin antibodies. 3. Vessel wall injury.g. inflammation or trauma Clinical presentation Different possible presentations according to the size of the embolus and obstruction can occur: 1. Acute massive pulmonary embolism: It is due to obstruction of one of the main pulmonary arteries and causes hemodynamic compromise. It is associated with: - Sudden onset of severe retrosternal chest pain due to sudden distension of the pulmonary trunk. - Severe dyspnea - Manifestations of cardiogenic shock: Hypotension, tachycardia, disturbed conscious state, collapse, tachypnea, cyanosis, and cold extremities, low urine output. - Even sudden death. - Signs of acute corpulmonal. 2. Pulmonary infarction 3  It is due to obstruction of lobar pulmonary arteries. Patient presented by: ▪ Sudden onset of localized pleuritic chest pain, ▪ Hemoptysis, ▪ Dyspnea ▪ Fever in the first 48 hours. ▪ Pleural friction rub may be audible over the affected area of the lung. ▪ A pleural effusion is sometimes present. 3. Small pulmonary emboli They cause no pathological effect apart from obstruction of small arteries in the lung leading to reflex hyperventilation. 4. Chronic pulmonary embolism Recurrent PE (multiple showers of minute emboli over a long period of time) may gradually obstruct the pulmonary vasculature, increase resistance to blood flow in the pulmonary vessels and ultimately lead to chronic obstructive pulmonary hypertension, increased RV stain and corpulmonale (when the degree of pulmonary vascular bed obstruction exceeds 60%). Patient presented with progressive exertional dyspnea, signs of pulmonary hypertension, corpulmonale. Complications: 1. Pulmonary hypertension, cor pulmonale. 2. Respiratory failure. 3. Arrhythmia. 4. Sudden Death. Physiology ▪ During the ideal gas exchange, blood flow and ventilation would perfectly match each other, resulting in no alveolar-arterial oxygen tension (PO2) gradient. ▪ However, even in normal lungs, not all alveoli are ventilated and perfused perfectly. For a given perfusion, some alveoli are underventilated, while others are overventilated. Similarly, for known alveolar ventilation, some units are underperfused, while others are overperfused. 4  ▪ The optimally ventilated alveoli that are not perfused well have a large ventilation-to-perfusion ratio (V/Q) and are called high-V/Q units (which act like dead space). ▪ Alveoli that are optimally perfused but not adequately ventilated are called low-V/Q units (which act like a shunt) Pathophysiology: PE contributes to gas exchange abnormalities and hypoxemia, but it is predominantly the hemodynamic consequences of PE that are responsible for increased morbidity and mortality. 1. Hypoxemia and Gas Exchange: ▪ Though a normal partial arterial pressure of oxygen (PaO 2) does not exclude PE, hypoxemia is the most common physiologic consequence of acute PE. ▪ The most common mechanisms of hypoxemia are ventilation–perfusion inequalities and shunt. ▪ There is a redistribution of blood flow from obstructed regions of the vascular bed to uninvolved areas of the pulmonary vascular bed. This results in areas of low ratios of ventilation to perfusion in some lung gas exchange units and areas of high ratios of ventilation to perfusion in other units. ▪ Shunting can be due to intrapulmonary or intracardiac. 5  ▪ Areas that retain blood flow but no ventilation such as atelectasis due to loss of surfactant or areas of pulmonary hemorrhage or infarct can contribute to shunt. ▪ Elevated right atrial pressures in the setting of acute PE can open a patent foramen ovale and cause right-to-left intracardiac shunting. ▪ Vascular obstruction leads to increased dead space because lung units continue to be ventilated despite reduced or absent perfusion. ▪ Though increased dead space is expected to impair the elimination of carbon dioxide, hypercapnia in acute PE is rare because medullary receptors sense the increase in partial pressure of carbon dioxide and increase minute ventilation. Most patients with PE therefore have respiratory alkalosis. 2. Hemodynamics Decreased RV cardiac output leads directly to decreased return to the LV and therefore decreased LV cardiac output. Furthermore, RV overload and dilatation compresses the interventricular septum which impinges on the LV and further decreases the LV cardiac output Classification of PE according to severity: ❖ Non-massive PE patients are those who are normotensive with normal RV function. ❖ Massive PE implies hemodynamic instability from RV failure. ❖ Sub-massive PE patients may clinically be normotensive but have evidence of RV dysfunction by echocardiography or CT imaging. Diagnosis: Diagnosis is based on: ▪ The clinical findings in combination with laboratory tests (such as the D- dimer test) and imaging studies, usually CT pulmonary angiography. ▪ Prompt and accurate diagnosis of PE is facilitated by a clinical evaluation that assesses the probability of PE (pretest probability) and makes appropriate use of the plasma d-dimer ELISA and chest CT scanning. ▪ Wells et al developed a simple clinical model to predict the likelihood of PE. 6  Simplified interpretation ▪ Score 4 — PE likely. Consider diagnostic imaging. ▪ Score 4 or less — PE unlikely. Consider D-dimer to rule out PE. Simplified PE severity score: 7 Investigations: A) Laboratory Tests: Although none of these laboratory studies confirm the diagnosis of VTE, but can provide support for therapeutic intervention or confirm alternative diagnosis. 1. D-Dimer: The d-dimer is elevated in almost all patients with acute thrombotic disorders. The strength of the test lies in its very high sensitivity and, thus, high negative predictive value. Negative D-dimer allows the exclusion of VTE in patients with lower pretest probability (PTPs) of the disease. 2. Increased LDH 3. Increased serum bilirubin 4. Normal AST: helps to rule out myocardial infarction from DD 5. Protein C, S 6. Anticardiolipin antibodies B) Imaging: 1. Plain chest X-ray May be Normal, Enlargement of descending pulmonary artery, Cut-off sign, Elevation of the copula of the diaphragm, Localized area of hyper translucency (Westermark sign), Lamellar atelectasis, small pleural effusion or Wedge-shaped area of pulmonary infarction with the base directed to the periphery and the apex towards the hilum. 2. CT pulmonary angiography: It provides the ability to directly visualize emboli as well as detect parenchymal abnormalities (shows wedge-shaped area of pulmonary infarction) that may support the diagnosis of PE or provide an alternative diagnosis. It is recommended as a first-line diagnostic imaging test in most cases. It provides higher resolution and allows the detection of thrombi in segmental and subsegmental branches. 3. Pulmonary angiography: It is the gold standard for diagnosing pulmonary embolism (PE) but used less often due to wider acceptance of CT scans, which are non-invasive. Currently, the main clinical utility of conventional pulmonary angiography is for therapeutic intervention. 8  4. MRI: Current MRI technology demonstrates high specificity and high sensitivity for proximal PE, but still limited sensitivity for distal PE. Although a positive result can aid in clinical decision-making, MRI cannot be used as a stand-alone test to exclude PE. 5. Ventilation /perfusion lung scan (V/Q): Perfusion scan is done by IV injection of radioactive technetium or radioactive iodine while ventilation scan is done using inert gases e.g. Xenon or Krypton. It can detect areas of the lung that are being ventilated but not perfused with blood (due to obstruction by a clot). This type of examination is as accurate as multidetector CT but is often used less because of the more widespread availability of CT technology. What are the advantages of a VQ scan? It exposes you to less radiation than a CT scan. It’s safe for people whose kidneys don’t work properly (renal insufficiency). Contrast dye used in CT scans can cause kidney damage in people with renal insufficiency. It’s safe for people who are allergic to contrast dye used in CT scans. 7. Contrast venography, (duplex study): to detect DVT in lower extremity. 8. ECG Most commonly shows sinus tachycardia but may produce S1Q3T3 with a large PE, T wave inversion in V1-V2. It is not a specific test for PE but may help to rule out myocardial infarction from the differential diagnosis. 9. Echocardiography: Can detect right ventricular enlargement, dilated pulmonary artery, pulmonary hypertension, and large thrombi in PA. 10.Arterial blood gases: It is helpful, although not definitive. PE often does not cause hypoxemia. Hypoxemia may be present, the more severe the hypoxemia, the more massive the obstruction. Hypoxia Hypocapnia is usually present (due to hyperventilation) that is associated with respiratory alkalosis. 9 PE Prophylaxis: It is indicated in persons with moderate or high risk for DVT and PE. Low dose heparin 5000 units given subcutaneously every 8 or 12 hrs, is begun as soon as the risk of DVT is evident and continued until that risk has abated. Low molecular–weight heparin (LMWH) can also be used for prophylaxis. The patient should be encouraged to regain mobility quickly after surgery. Treatment of VTE 1. Anticoagulant: ▪ Anticoagulant therapy is the mainstay of treatment of VTE (not associated with hemodynamic compromise) to prevent new clots from forming. ▪ Unfractionated heparin or low molecular weight heparin (LMWH), is administered initially (Heparin works quickly ), while warfarin, therapy doesn't start working until a few days after the first dose ( i.e, the peak effect does not occur until 36-72 hours after drug administration). ▪ LMWH may reduce bleeding among patients with pulmonary embolism as compared to heparin. DOSE: ▪ The most widely used regimen includes an 80 units/kg IV bolus of unfractionated heparin followed by 18 units/kg /hr by IV infusion guided with PTT(to maintain partial thromboplastin time at 1.5–2.5 times the control value) until adequate replacement by oral warfarin. ▪ Alternatively, LMWH can be given subcutaneously twice daily in a dose of 1mg/kg/dose. ▪ LMWHs have advantages over UFH. o These agents are administered by subcutaneous injections, o Have a longer duration of anticoagulant effect. o A fixed dose of LMWH can be used, o Laboratory monitoring of a PTT is not necessary Warfarin Start warfarin on the first day of heparin therapy at 10 mg/day guided with PT and INR (international normalized ratio). Discontinue heparin after 5-7 days and continue warfarin for 3-6 months. 10  The recommended therapeutic range for venous thromboembolism is an INR of 2-3. This level of anticoagulation markedly reduces the risk of bleeding without the loss of effectiveness. Initially, INR measurements are performed on a daily basis; once the patient is stabilized on a specific dose of warfarin, the INR determinations may be performed every 1-2 weeks or at longer intervals. Most studies have reported that more advantages than disadvantages for NOACs when compared with VKAs, with the most important advantages of NOACs including safety issues (ie, a lower incidence of major bleeding), the convenience of use, minor drug and food interactions, a wide therapeutic window, and no need for laboratory monitoring). Pregnant women are often maintained on low molecular weight heparin to avoid the known teratogenic effects of warfarin, especially in the early stages of pregnancy. 2. Thrombolytic therapy ▪ Thrombolysis is the enzymatic destruction of the clot with medication (streptokinase, urokinase, TPA). ▪ It is indicated in massive PE causing hemodynamic instability (shock and/or hypotension in the absence of contraindication. ▪ Catheter Directed Thrombolytic Therapy 3. Inferior vena cava filter ▪ An ideal IVC filter should be mechanically stable, and able to trap emboli without causing occlusion of the vena cava. ▪ IVC interruption by the insertion of an IVC filter is only indicated in the following settings: ▪ Patients with acute VTE who have an absolute contraindication to anticoagulant therapy (eg, recent surgery, hemorrhagic stroke, significant active or recent bleeding) ▪ Patients with massive pulmonary embolism who survived but in whom recurrent embolism invariably will be fatal ▪ Patients who have objectively documented recurrent venous thromboembolism, in spite of adequate anticoagulant therapy. 4. Surgery Embolectomy Catheter embolectomy and fragmentation or surgical embolectomy is recommended for patients with massive pulmonary embolism who have 11  contraindications to thrombolysis or who remain unstable after receiving thrombolysis. Pulmonary Thromboendarterectomy Chronic pulmonary embolism leading to pulmonary hypertension (known as chronic thromboembolic hypertension) is treated with a surgical procedure known as a pulmonary thromboendarterectomy. Pulmonary hypertension & Corpulmonale I. Definition: PAH includes patients with mean pulmonary artery pressure >20 mm Hg measured by right heart catheterization. The term PAH describes a group of PH patients characterized by the presence of pre-capillary PH, defined by: A pulmonary artery wedge pressure (PAWP) ≤15 mmhg And a PVR >3 Wood units (WU) In the absence of other causes of pre-capillary PH such as PH due to lung diseases, CTEPH or other rare diseases. II. Classification of pulmonary hypertension ▪ Group 1: Pulmonary arterial hypertension ▪ Group 2: Pulmonary hypertension due to left heart disease ▪ Group 3: Pulmonary hypertension due to lung diseases and/or hypoxia ▪ Group 4: Chronic thromboembolic pulmonary hypertension (CTEPH) ▪ Group 5: Pulmonary hypertension with unclear and/or multifactorial mechanisms Corpulmonale ▪ Cor pulmonale is defined as an alteration in the structure and function of the right ventricle (RV) of the heart caused by a primary disorder of the respiratory system. Chronic respiratory diseases which may lead to corpulmonale: ▪ Those characterized by a limitation to airflow (COPD and other causes of chronic bronchial obstruction) ▪ Those characterized by a restriction of pulmonary volumes from extrinsic or parenchymatous origin (restrictive lung diseases) ▪ Pulmonary thromboembolic disease. 12 13 14