Pulmonary Embolism

Dr.V.Maruthi Rama Krishna Rao Assistant prof EMD

• Pulmonary embolism (PE) refers to the lodging of a embolic material from a distant site in the pulmonary circulation

• The term embolus describe objects that lodge in blood vessels and obstruct the flow of blood. • Thrombotic • NonThrombotic

EMBOLIC MATERIAL • Thrombotic :Venous thromboembolism (VTE)

• PE & VTE together constitute one of the “big three” cardiovascular diseases, the other two being myocardial infarction (MI) and stroke.

• Nonthrombotic

• include fat, • tumor, • air, • amniotic fluid.

• FAT EMBOLISM most often occurs after blunt trauma complicated by long bone fractures.

• mechanical obstruction and biochemical injury • Fat embolism syndrome. characterized pulmonary

insufficiency, neurologic symptoms, anemia, and thrombocytopenia

• Thrombocytopenia platelet adhesion to fat globules and subsequent aggregation;red cell aggregation and/or hemolysis

• Release of free fatty acids from the causing local toxic injury to endothelium, and platelet activation and granulocyte recruitment (complete the vascular assault).

• AIR EMBOLUS can occur during placement or removal of a central venous catheter, operations on head & neck, trauma,

Intravenous infusions, Angiography, Cardiothoracic surgeries.

• Gas bubbles in the vasculature cause edema, hemorrhage, and focal atelectasis or emphysema, leading to a form of respiratory distress called the chokes.

• Air more than 5ml/kg, complications have been reported at 20ml

• AMNIOTIC FLUID embolism may be catastrophic anaphylactoid syndrome of pregnancy

• The onset is characterized by sudden severe dyspnea, cyanosis, and shock, followed by neurologic impairment ranging from headache to seizures and coma.

• If the patient survives the initial crisis, pulmonary edema typically develops, along with (in half the patients) DIC, as a result of release of thrombogenic substances from the amniotic fluid.

• Intravenous drug abusers sometimes self inject hair, talc, and cotton as contaminants of the drug of abuse.

• Septic PE, which can cause endocarditis of the tricuspid or pulmonic valve.

• Sudden death, right heart failure (cor pulmonale), or cardiovascular collapse occurs when emboli obstruct 60% or more of the pulmonary circulation

• Most pulmonary emboli (60% to 80%) are clinically silent because they are small. With time they become organized and are incorporated into the vascular wall

• Paradoxical Embolism that embolizes to the arterial system, usually through a patent foramen ovale

MOLECULAR PATHOPHYSIOLOGY

• Endothelial injury/insult, Inflammation, hypercoagulability activate the pathophysiologic cascade leading to VTE. Venous thrombi contain fibrin, red blood cells, platelets, and neutrophils

• Activated platelets release polyphosphates, procoagulant microparticles, and proinflammatorymediators.

• These activated platelets bind neutrophils and stimulate them to release their nuclear ,DNA, histones, and neutrophil granule constituents. These networks are called neutrophil extracellular traps (NETs).

• They are prothrombotic and procoagulant. • Almost all emboli represent some part of a

dislodged thrombus, hence the term thromboembolism.

CARDIOPULMONARY DYNAMICS • INCREASED PULMONARY VASCULAR RESISTANCE

through not only mechanical obstruction but also pulmonary artery vasoconstriction from hypoxia,neural reflexes, and humoral factors.

• IMPAIRED GAS EXCHANGE caused by increased alveolar dead space from vascular obstruction and hypoxemia from alveolar hypoventilation.

• ALVEOLAR HYPERVENTILATION caused by reflex stimulation of irritant receptors; increased airway resistance due to bronchoconstriction; and decreased pulmonary compliance due to lung edema, lung hemorrhage, and loss of surfactant.

CARDIOPULMONARY DYNAMICS • As obstruction increases, pulmonary

artery pressure rises. Pulmonary vascular resistance result from secretion of vasoconstricting.

• The sudden rise in pulmonary artery pressure abruptly increases right ventricular afterload, with consequent elevation of right ventricular wall tension followed by right ventricular dilation and dysfunction.

Perpetuation of this cycle can lead to right ventricular infarction, circulatory collapse, and death.

pro-BNP, BNP, troponin.

CARDIOPULMONARY DYNAMICS

• Pulmonary Infarction Pulmonary infarction is characterized by pleuritic chest pain that may be unremitting , occasionally is accompanied by hemoptysis.

• Paradoxically, severe pleuritic pain often signifies that the embolism is small, not life-threatening, and located in the distal pulmonary arterial system, near the pleural lining.

• Tissue infarction usually occurs 3 to 7 days after embolism.

• Signs and symptoms often include fever, leukocytosis, elevated erythrocyte sedimentation rate, and radiologic evidence of infarction.

DIAGNOSIS • clinical assessment of likelihood, based on

presenting symptoms and signs, in conjunction with diagnostic testing

• Symptoms and signs of PE are nonspecific • Dyspnea is the most frequent symptom,

and tachypnea is the most frequent sign of PE

• Most common symptom: • dyspnea (82% to 85%) • Tachypnea (30% to 60%) • Chest pain: may be nonpleuritic or

pleuritic (infarction) (40% to 49%) • Syncope (massive PE) (10% to 14%) • Fever, diaphoresis, apprehension • Hemoptysis (2%)

• PE should be suspected in hypotensive patients when there is evidence of (1) venous thrombosis or predisposing VTE risk factors; (2) acute cor pulmonale (acute right ventricular failure), with features such as distended neck veins, right-sided S3 gallop, right ventricular heave, tachycardia, or tachypnea; (3) there are echocardiographic findings of right ventricular dilation and hypokinesis.

• Classic Wells Criteria to Assess Clinical Likelihood of Pulmonary Embolism CRITERION SCORING*

DVT symptoms or signs 3 An alternative diagnosis is less likely than PE 3 Heart rate > 100 beats/min 1.5

Immobilization or surgery within 4 weeks 1.5

Previous DVT or PE 1.5

Hemoptysis 1

Cancer treated within 6 months or metastatic 1

>4 score points = high probability

CATEGORY PRESENTATION

Massive PE (5%-10%)

Systolic blood pressure < 90 mm Hg or poor tissue perfusion or multisystem organ failure plus extensive thrombosis, such as “saddle” PE or right or left main pulmonary artery thrombus

Submassive PE (20%-25%)

Hemodynamically stable but moderate or severe right ventricular dysfunction or enlargement, coupled with elevation biomarker of right ventricular microinfarction and/or right ventricular pressure overload

Small to moderate PE (70%)

Normal hemodynamics and normal right ventricular size and function

Differential Diagnosis of Pulmonary Embolism Anxiety, pleurisy, costochondritis Pneumonia, bronchitis Acute coronary syndromes Pericarditis Congestive heart failure Aortic dissection Idiopathic pulmonary hypertension

Diagnostic Methods

• Plasma D-dimer level is useful to exclude PE in patients with a low pretest probability of PE.

• However, it cannot be used to “rule in” the diagnosis because it increases with many other disorders (e.g., metastatic cancer, trauma, sepsis, postoperative state).

LABORATORY TESTS • ABGs may reveal hypoxemia and respiratory

alkalosis (decreased Pao2 and Paco2 and increased pH).

• Elevated cardiac troponin levels also occur in patients with PE because of right ventricular dilation and myocardial injury.

• Elevated serum BNP levels in patients with acute PE may reflect RV overload.

Electrocardiogram •Abnormal in 85% of patients with acute PE. •Frequent abnormalities are sinus tachycardia,nonspecific ST-segment or T-wave changes •S-1, Q-3, T-3 pattern (10% of patients); •S-1, S-2, S-3 pattern; T-wave inversion in V1 to V6; acute RBBB; ST segment depression in lead II; right ventricular strain. •A right ventricular strain pattern on ECG with normal blood pressure is associated with adverse short-term outcome.

IMAGING STUDIES • CHEST X-RAY suggestive findings include elevated diaphragm, pleural effusion, dilation of pulmonary artery, infiltrate or consolidation, abrupt vessel cut-off, oligemia distal to the PE (Westermark sign). A wedge-shaped consolidation in the middle and lower lobes is suggestive of a pulmonary infarction and is known as “Hampton’s hump.”

Hamptons hump Westermark sign

CHEST COMPUTED TOMOGRAPHY • Chest CT initial imaging test in patients with

suspected PE, allowing ready visualization of massive PE

• detect other pulmonary diseases that manifest in conjunction with PE ,that mimics PE include pneumonia, atelectasis, pneumothorax, and pleural effusion, which may not be well visualized on the chest radiograph.

• CT scan serves as a prognostic and diagnostic test.

• CT scan can detect signs of right ventricular dysfunction by analyzing • (1) right ventricular–to–left ventricular diameter

ratio • (2) right ventricular–to–left ventricular volume

ratio, • (3) interventricular septal bowing, and • (4) reflux of contrast medium into the inferior vena

cava. • A right to- left ventricular dimensional ratio of 0.9

indicates right ventricular enlargement. • a right-to-left volumetric ratio of 1.2 or greater is

predictive of adverse clinical outcomes.

30.58mm

47.36 mm

RV diameter of 47 mm and an LV diameter of 31 mm. The RV/LV diameter ratio of 1.5 is abnormally high.

Pulmonary radionuclide perfusion scintigraphy (lung scanning) • V/Q scan is reserved for patients with clinically significant

contrast allergies or renal insufficiency.

A, A normal pattern on the ventilation scan. B, The complete disappearance of the entire left lung from the perfusion scan indicates proximal occlusion of the left pulmonary artery.

• Angiography: pulmonary angiography is the historic gold standard;

• however, it is invasive, expensive, and not readily available in some clinical settings.

• Gadolinium-enhanced magnetic resonance angiography (MRA) of the pulmonary arteries has a moderate sensitivity and high specificity for the diagnosis of PE. Performed only if other imaging tests are contraindicated.

ECHOCARDIOGRAPHY • Right ventricular dilation hypokinesis or akinesis • Right ventricular free-wall hypokinesis with apical

sparing (the McConnell sign) • Paradoxical movement of the interventricular septum

persistent pulmonary hypertension, patent foramen ovale, and free-floating right heart thrombus are markers for increased risk of death or recurrent thrombosis.

VENOUS ULTRASONOGRAPHY • The primary diagnostic criterion for DVT on

ultrasound imaging is loss of vein compressibility.

• Normally, the vein collapses completely when gentle pressure is applied to the skin overlying it.

CFV

RT CFV

GSV CFA

Overall Strategy: An Integrated Diagnostic Approach

MANAGEMENT • Providing adequate oxygen promptly reduces

PAP and improves cardiac output in patients with pulmonary hypertension.

• Intravenous (IV) fluid to be used with caution RV dilation and failure can further compromise cardiac output

• Vasopressor therapy should be considered early in massive PE in order to maintain RVCPP and minimize RV ischemia and infarction.

• both norepinephrine and phenylephrine showed restoration of hemodynamics, but norepinephrine group showed improved RV function, presumably through its beta-1

• DOBUTAMINE should be used cautiously, as it can worsen hypotension through systemic vasodilation

• MECHANICAL VENTILATION • Intubation, positive-pressure ventilation

can lead to decrease in venous return and an increase in PVR, resulting in further RV decompensation and subsequent hypotension

• A low tidal volume (6 mL/kg ideal body weight) with plateau pressure goal below 30 cm H2O should be used in massive PE

Parenteral Anticoagulation Drug Dose Remarks

Unfractionated heparin (intravenous infusion)†

80 IU/kg of body weight as an intravenous bolus, followed by continuous infusion at the rate of 18 IU/kg/hr

maintain aPTT between 1.5 and 2.5 times control, monitor platelet count at baseline and every other day from day 4 to day 14 or until heparin is stopped; heparin-induced thrombocytopenia if platelet count falls by ≥50%

Low-molecular-weight heparins (subcutaneous injection)§

monitoring of anti–factor Xa levels may be helpful in patients at increased risk for bleeding, particularly in renal impairment;

Enoxaparin 1.0 mg/kg every 12 hr or 1.5 mg/kg once daily

If creatinine clearance is <30 ml/min, reduce enoxaparin dose to 1 mg/kg once daily; consider unfractionated heparin infusion as an alternative.

Fondaparinux 5 mg (body weight, <50 kg); 7.5 mg (body weight, 50-100 kg); or 10 mg (body weight, >100 kg), administered once daily

This drug is contraindicated in patients with severe renal impairment (creatinine clearance, <30 ml/min); no routine platelet monitoring is necessary.

•Warfarin Anticoagulation • Warfarin is a vitamin K antagonist, It prevents

gamma-carboxylation activation of coagulation factors II, VII, IX, and X.

• The full anticoagulant effect of warfarin becomes evident after 5 to 7 days,

• The usual target INR range is between 2.0 and 3.0. • monitoring of INRs • initial prescription of intravenous UFH, LMWH,

fondaparinux, as a bridge to warfarin anticoagulation

• ADVANCED THERAPY (IN ADDITION TO ANTICOAGULATION) FOR ACUTE PULMONARY EMBOLISM

• These advanced therapy options include • full-dose systemic thrombolysis, • pharmacomechanical catheter–directed

therapy (usually with lowdose thrombolysis), • surgical embolectomy, • inferior vena cava filter placement.

Systemic Thrombolysis Administered Through a Peripheral Vein

• Thrombolysis reverses right-sided heart failure by physical dissolution of anatomically obstructing pulmonary arterial thrombus.

• Streptokinase: 250,000 IU IV bolus over 30 minutes followed by 100,000 IU/hour for 12 to 24 hours (or 1.5 million IU IV over 2 hours)

• Urokinase: 4,400 IU/kg IV bolus over 10 minutes followed by 4,400 IU/kg/h for 12 to 24 hours (or 1 million IU IV bolus over 10 minutes followed by 2 million IU IV over 110 minutes73)

• Alteplase: 100-mg IV infusion over 2 hours (or 0.6 mg/kg IV over 15 minutes with maximum dose of 50 mg74,75)

• Patients who receive thrombolysis up to 14 days after onset of new symptoms or signs can derive benefit, probably because of the effects on the bronchial collateral circulation.

• Patients being considered for thrombolysis require screening for contraindications. Intracranial hemorrhage is the most feared and severe complication.

Advances in Pharmacomechanical Catheter–Directed Therapy, Including Thrombolysis • Pharmacomechanical catheter– directed reperfusion, however, holds the promise of good efficacy, with lower rates of major bleeding owing to lower doses of thrombolytic agent.

• The typical dose of tissue plasminogen activator in a pharmacomechanical catheter-based procedure, for example, is 25 mg or less—compared with 100 mg for systemic administration

• Inferior Vena Cava Filters (1) contraindications to anticoagulation; (2) recurrent PE despite therapeutic levels of

anticoagulation; and (3) very poor cardiopulmonary reserve, including

patients with massive PE. • For patients with a temporary contraindication to

anticoagulation, placement of a nonpermanent, retrievable filter is appropriate. Retrievable filters can be left in place for weeks to months or can remain permanently, if necessary, for a trapped large clot or a persistent contraindication to anticoagulation.

MANAGEMENT OF AIR EMBOLISM

• Hyperbaric oxygen therapy • Direct removal of air from the venous circulation

by aspiration from a central venous catheter in the right atrium may be attempted.

• Immediately place the patient in the left lateral decubitus (Durant maneuver) and Trendelenburg position.

• This helps to prevent air from traveling through the right side of the heart into the pulmonary arteries

Amniotic Fluid Embolism Management Treatment is supportive and includes the following: • Administer oxygen. Intubate if necessary. • Initiate cardiopulmonary resuscitation (CPR) if the

patient arrests. If she does not respond to resuscitation, perform a perimortem cesarean delivery.

• Treat hypotension with crystalloid and blood products. Use pressors as necessary.

• Avoid excessive fluid administration.

• Continuously monitor the fetus. Deliver immediately following cardiac arrest if gestational age is ≥ 23 weeks.

• Early evaluation of clotting status and early initiation transfusion is recommended.

• Treat coagulopathy and transfuse platelets for platelet counts less than 20,000/µL.

• Hemodialysis with plasmapheresis and extracorporeal membrane oxygenation (ECMO) with intra-aortic balloon counterpulsation [have been described in case reports with successful outcomes in treating AFE patients with cardiovascular collapse.

Fat Embolism Management • Maintenance of adequate oxygenation and ventilation with

open lung strategies such as the use of airway pressure release ventilation (APRV)

• Maintenance of hemodynamic stability • Administration of blood products as clinically indicated • Hydration Prophylaxis of deep venous thrombosis • Nutrition • Judicious use of crystalloids, colloids. • Continuous pulse oximetry monitoring in at-risk patients (eg,

patients with long-bone fractures and multiple trauma), may facilitate early detection of desaturation, allowing prophylactic administration of oxygen and possibly steroids, thereby decreasing the chances of hypoxic injury and systemic complications of FES.

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