Pulmonary Embolism Symptoms, Causes and Treatment

Pulmonary embolism (PE) is the obstruction of the pulmonary artery or one of its branches by a substance that has moved from elsewhere in the body through the bloodstream (embolism).

Pulmonary embolism

Pulmonary embolism can be:

1. Thrombotic: Venous thromboembolism (VTE) (Most common)

PE most commonly results from deep vein thrombosis (DVT); 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).

Pulmonary Embolism

Pulmonary Embolism

Sources of emboli:

a) Most common (90% of VTE):

Lower limb DVT (deep veins of the calves, popliteal, and femoral veins) 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.

b) Other less common sources

  • Pelvic veins (in pregnancy, pelvic thrombophlebitis or infection, recent pelvic surgery, prostatic diseases)
  • Upper limb DVT (associated with central venous catheters or intravascular cardiac devices).
  • The right side of the heart: Mural thrombi or tricuspid vegetations (subacute bacterial endocarditis).

2. Non-thrombotic (Less common)

Fat embolism (which can escape from the bone marrow with fracture of a long bone, lipolysis, or bums)

  • Tumor embolism (detached tumor fragments).
  • Air embolism (IV drug administration, chest compressions during CPR, vascular surgery).
  • Amniotic fluid embolism: which may be forced into the pelvic veins during childbirth.
  • Parasitic: Bilharzial Ova.
  • Talc embolism (IV drug abusers).

After traveling to the lung, large thrombi can lodge at the bifurcation of the main pulmonary artery of 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.

Pathophysiology: (Virchow’s Triad)

  1. Stasis: sluggish circulation resulting in accumulation of clotting factors and fibrin, resulting in thrombus formation in veins, occurs in: old age, immobility, obesity, pregnancy, peripartum period, malignancy, post-operative, multiple comorbidities.
  2. Hypercoagulable state: Imbalance between coagulation and anticoagulation factors. e.g., obesity, post-operative, malignancy, oral contraceptive pills, protein C and S deficiency, anticardiolipin antibodies.
  3.  Vessel wall (endothelial) injury: c.g., inflammation or trauma.

Risk factors

A. Medical risk factors

  • Prior history of DVT or PE.
  • Age > 65.
  • Malignancy (especially pancreatic, stomach, colon, lung, and breast cancer).
  • Obesity.
  • Prolonged immobility: IHD, CHF, stroke.
  • Pregnancy and postpartum period.
  • Contraceptive pills (Estrogen-containing birth control pills).
  • Estrogen hormonal therapy.
  • Antiphospholipid antibody syndrome.
  • Varicose vein.
  • Polycythemia.
  • Hyperlipidemia.

B. Surgical risk factors:

  • Major surgery (e.g. hip joint, vascular, prostate, extensive abdominal, and pelvic surgeries).
  • Fractures (e.g., femur and tibia, pelvic, spinal).
  • Surgical and accidental traumas predispose patients to VTE by activating clotting factors as well as by causing immobility.

Clinical Presentation

Different possible presentations according to the size of the embolus and obstruction can occur.

1. Acute massive pulmonary embolism

• Due to obstruction of one of the main pulmonary arteries resulting in hemodynamic instability

• C/P:

  • Sudden onset of severe retrosternal chest pain due to sudden distension of the pulmonary trunk and interference with coronary circulation
  • Severe dyspnea
  • Manifestations of cardiogenic shock: hypotension, tachypnea, tachycardia, cyanosis, disturbed level of consciousness, cold extremities, low urine output.
  • Signs of acute corpulmonale
  • Sudden death may occur.

2. Pulmonary infarction

• Due to obstruction of lobar pulmonary arteries.

• C/P:

  • 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.
  • Pleural effusion may be present.

3. Small pulmonary emboli

  • No pathological effect apart from obstruction of small arteries in the lung leading to reflex hyperventilation.
  • C/P: Tachypnea.

4. Chronic pulmonary embolism

Recurrent PE (multiple showers of minute emboli over a long period) gradually increases pulmonary vascular resistance leading to pulmonary hypertension, right ventricular strain, and eventually corpulmonale. “Chronic thromboembolic pulmonary hypertension” “CTEPΗ”.

•C/P:

  • Progressive exertional dyspnea
  • Signs of pulmonary hypertension and corpulmonale

Complications of VTE

  1. Pulmonary hypertension, corpulmonale.
  2. Respiratory failure.
  3. Pulmonary edema.
  4. Arrhythmia.

Diagnosis

1. Clinical Evaluation

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.

2. Laboratory tests:

Although none of these laboratory studies confirm the diagnosis of VTE but can provide support for therapeutic intervention or confirm alternative diagnosis.

  • D-Dimer: D-dimer is elevated in almost all patients with acute thrombotic disorders because of endogenous ineffective fibrinolysis, which causes plasmin to digest some of the fibrin clots and release d-dimers into the systemic circulation. The strength of the test lies in its very high sensitivity and, thus, high negative predictive value. D-dimer is considered a good negative test where it allows the exclusion of VTE diagnosis in patients with a lower pretest probability of VTE.
  • Other tests indicating activation of coagulation cascade: Thrombin- antithrombin Ill complex
  • Tests indicating increased RBC hemolysis: increased LDH, increased serum bilirubin.
  • Tests to detect the cause or the precipitating factor in cases with unprovoked VTE: Anticardiolipin antibodies, protein C. S deficiency, ANA. anti-ds-DNA, anti-thrombin III deficiency, factor V Leiden deficiency or mutation.
  • Normal AST: help to rule out myocardial infarction from DD.

3. Imaging:

Chest X-ray:

  • Usually normal (most common)
  • May show abnormal signs such as: enlargement of the descending pulmonary artery, the elevation of the copula of the diaphragm, localized area of hyper translucency (Westermark sign), lamellar atelectasis, minimal pleural effusion, wedge-shaped area of pulmonary infarction with the base directed to the periphery and the apex towards the hilum.

B. Computed tomography with pulmonary angiography (CTPА)

  • It is the most diagnostic imaging modality for the detection of pulmonary embolism.
  • It allows the detection of emboli up to segmental and subsegmental branches, as well as the detection of any underlying parenchymal lesions.
  • 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. Spiral CT is more helpful.
  • Multi-detector CT with pulmonary angiography: 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.

C. MRI: Current MRI technology demonstrates high specificity and high sensitivity for proximal PE, but still limited sensitivity for distal PE and 30% of inconclusive results. Although a positive result can aid in clinical decision-making, MRI cannot be used as a stand-alone test to exclude PE.

D. Pulmonary angiography: It used to be the gold standard for diagnosing PE, but it is no longer used given its invasiveness and the feasibility of CTPA.

E. Ventilation/perfusion lung scan (V/Q):

  • It is used when there is a contraindication for IV contrast administration in CTPA (e.g., renal failure, pregnancy). It is also used for the detection of CTEPH.
  • A perfusion scan is done by IV injection of radioactive technetium or radioactive iodine while a 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. It is particularly useful in people who have an allergy to iodinated contrast or impaired renal function.

F. Contrast venography, Doppler ultrasound (duplex study): It is used to detect DVT in the lower extremity.

4. ECG

ECG most commonly shows sinus tachycardia but may produce S1Q3T3 with a large PE, and 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.

5. Echocardiography

It can detect right ventricular enlargement, dilated pulmonary artery, pulmonary hypertension, and large thrombi in the pulmonary artery.

6. Arterial blood gases

Arterial blood gases are helpful, although not definitive:

  • PE often does not cause hypoxemia. Hypoxemia may be present, the more severe the hypoxemia, the more massive obstruction.
  • Hypoxia: V/Q mismatch (low V/Q): PE causes a redistribution of blood flow so that some lung gas exchange units are over-perfused and have low ratios of V/Q. Atelectasis: caused by loss of surfactant.
  • • Hypocapnia occurs due to hyperventilation and is associated with respiratory alkalosis.

7. Capnography

  • It is noninvasive monitoring of partial pressure of CO2 in exhaled breath and is expressed as CO2 concentration over time (capnogram).
  • End-tidal CO2 (EtCO2) is the CO2 concentration at the end of each tidal breath, and its normal level is 35-40 mm Hg.
  • EtCO2 is low in PE due to dead space ventilation.

Prophylaxis against VTE

  1. It is indicated in persons with moderate or high risk for VTE (e.g., immobile patients post-operatively, or due to fractures}.
  2. Early mobility is advised to reduce the risk of occurrence of VTE.
  3. In cases of surgery, heparin started 2 hours before the operation and continued every 12 hours after surgery for 7 days.
  4. Unfractionated heparin or low molecular weight heparin (LMWH) can be used for prophylaxis
  • Unfractionated heparin: 5000 U every 8- or 12-hours SC.
  • LMWH {e.g., enoxaparin): 40 mg (or 0.5 mg/kg) every 24 hours SC.

Treatment of VTE

1. Anticoagulation

  • Anticoagulant therapy is the mainstay of treatment of VTE (not associated with hemodynamic compromise) to prevent new clots from forming.
  • Parenteral and oral anticoagulation are started together. Parenteral anticoagulation (unfractionated heparin or LMWH) is continued till the oral anticoagulation (warfarin) reaches its full effect (which usually does not occur till after 36 to 72 hours after initiating oral anticoagulation). “Bridging”
  • For therapeutic parenteral anticoagulation, unfractionated heparin is given in a continuous IV infusion (monitored by PTT) and LMWH is given SC 1 mg/kg every 12 hours.
  • Warfarin is started at a minimal dose (10mg/day) and its dose is up-titrated every 2 to 3 days guided by PT and the international normalized ratio (INR) daily.
  • Once the target INR is reached (which is 2-3), parenteral anticoagulation is discontinued, and warfarin is continued at the dose that has achieved the target INR.
  • INR is monitored bi-weekly for further modification of the dose of warfarin.
  • New oral anticoagulant agents (e.g., rivaroxaban, apixaban) do not require bridging by parenteral anticoagulation.
  • Oral anticoagulants (especially warfarin) are teratogenic, therefore pregnant females with VTE are maintained on LMWH or unfractionated heparin.
  • LMWH are generally preferred over unfractionated heparin, since they do not require lab monitoring by PTT. However, unfractionated heparin is preferred over LMWH in patients with renal impairment.

2. Thrombolytic therapy

  • Thrombolysis is the enzymatic destruction of the thrombus by an agent {e.g., streptokinase, urokinase, TPA).
  • It is indicated in acute massive PE associated with hemodynamic instability (shock and/or hypotension, defined as a systolic blood pressure <90 mmHg or a pressure drop of 40 mmHg for >15 min if not caused by new-onset arrhythmia, hypovolemia or sepsis).
  • It is the best available medical treatment in this situation, supported by clinical guidelines and the absence of contraindication for this 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:
  1. Patients with acute VTE who have an absolute contraindication to anticoagulant therapy (e.g., recent surgery, hemorrhagic stroke, significant active or recent bleeding).
  2. Patients with massive pulmonary embolism who survived but in whom recurrent embolism invariably will be fatal.
  3. Patients who have objectively documented recurrent venous thromboembolism, despite adequate anticoagulant therapy.
  4. In patients with a time-limited indication for IVC filter placement (e.g., a short-term contraindication to anticoagulation.

4. Surgery

  • Embolectomy: A catheter or surgical embolectomy is recommended for patients with massive pulmonary embolism who have contraindications to thrombolysis or who remain unstable after receiving thrombolysis.
  • Pulmonary Thromboendarterectomy: It is indicated in cases with chronic thromboembolic pulmonary hypertension (CTEPH).

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