Pulmonary Embolism
Pathophysiology |
• A thrombus in another area of the body embolizes to the pulmonary vasculature via the RV and PA.
• Blood flow distal to the embolus is obstructed, causing increased PVR, PA pressure, and RV pressure. If severe, acute cor pulmonale can occur.
• Blood flow decreases in some areas, dead space is created where there is ventilation but no perfusion.
• Hypoxemia and hypercarbia occur and drive tachypnea.
If dead space is large, signs are more overt (SOB). PE and DVT are on a continuum. |
Source |
• Most PE arise from thromboses of deep veins of lower extremities above the knee (iliofemoral DVT).
• Can also arise from deep veins of pelvis.
• Calf vein thrombi have a low incidence of embolizing to the lungs, but they can progress into the proximal veins and increase the risk of PE.
• Upper extremity DVT is rare (seen in IVDU).
• Fat emboli from long bone fractures, amniotic fluid emboli during or after delivery, air emboli (trauma, lines), septic emboli (IVDU), schistosomiasis. |
Sympotms |
• Not a reliable indicator of the presence of PE.
• Dyspnea (73%), cough (37%), pleuritic chest pain (65%), hemoptysis (13%).
• Only 1/3 of patients will have signs and symptoms of a DVT.
• Syncope seen in large PE. |
Signs |
• Tachypnea (70%), rales (51%), tachycardia (30%), S4 (24%), increased P2 (23%).
• Shock with rapid circulatory collapse in massive PE.
• Others include low-grade fever, decreased breath sounds, and dullness on percussion. |
Risk Factors for DVT and PE. |
• Age>60, malignancy, prior history, hereditary, hyper coagulable states, prolonged immobilization, cardiac disease (esp. CHF). obesity, nephrotic syndrome, major surgery (esp. pelvic or orthopedic), major trauma, pregnancy, and estrogen use. |
Prognosis |
• PE is usually clinically silent.
• Recurrences are common, which can lead to chronic pulmonary HTN and chronic cor pulmonale.
• When undiagnosed, mortality approaches 30%.
• When PE is diagnosed, mortality is 10% in first 60 minutes. Of those who survive initial event, 30% will die of recurrent PE if untreated.
• Most are recurrent in the first few hours.
• Treatment with anticoagulation decreases mortality to 2-8%. |
Diagnosis |
• If suspected PE, stabilize with IVF and O2. {{nl}• }If PE is likely, start anticoagulation before diagnostic tests.
• If PE is unlikely, get testing first.
• If the patient has contraindications to anticoagulation, get testing first and then consider IVC filter. |
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Testing
D-Dimer |
• Specific fibrin degradation product whose levels can be elevated in PE or DVT.
• Sensitive (90-98%).
• If results are normal and clinical suspicion is low, PE is very unlikely.
• Specificity is low, as it can be elevated in MI, CHF, pneumonia, and postop.
• Any cause of clot or increased bleeding can elevate D-Dimer. |
Venous Duplex Ultrasound |
• If positive, treat with IV heparin.
• False positives will lead to anticoagulation in patients without PE.
• If negative, the test is of very little value and the patient may still have a PE (up to 50% of patients with PE). |
Echocardiogram |
• Acute massive PE is accompanied by RV dilation and failure due to RV outflow obstruction and increased PVR.
• The dilated RV pushes the septum towards the LV, causing further decrease in LV preload and CO.
• This shows up as dilated RV cavity and hypokinesis of the RV free wall with sparing of the apex (McConnell's sign). |
Helical CT |
• >90% sensitivity and good specificity.
• Can visualize very small clots (>2mm). Can miss clots in small sub segmental vessels.
• Test of choice.
• If negative and high clinical probability of PE, there is a 5% incidence of PE.
• Contraindicated in patients with renal insufficiency because of IV contrast. |
CXR |
• Usually normal. Atelectasis or pleural effusion may be present.
• Mainly useful to exclude competing diagnoses.
• Hampton's hump or Westermark's sign are rarely present |
V/Q Scan |
• Important when there is a contraindication to helical CT.
• Results can either be normal, low-probability, intermediate-probability, or high-probability.
• A normal V/Q scan rules out PE and no further testing is needed.
• A high probability scan is very sensitive for PE and indicates treatment with heparin.
• If low or intermediate probability, clinical suspicion determines next step.
• If high, pulmonary angiography is indicated. |
Arterial Blood Gas |
• Not diagnostic.
• PaO2 and PaCO2 are low (latter due to hyperventilation) and pH is high.
• Typically respiratory alkalosis.
• The A-a gradient is usually elevated. A normal A-a gradient makes PE less likely but does not exclude it. |
Pulmonary Angiography |
• Gold standard. Definitively diagnoses or excludes PE.
• But the test is invasive. Contrast is injected into the PE branch after percutaneous catherization of the femoral vein.
• Consider when noninvasive testing is equivocal and risk of anticoagulation is high, or if the patient is unstable and embolectomy may be required. Rarely performed due to 0.5% mortality. |
Rules Out PE |
Normal or low-probability V/Q scan or helical scan and low clinical suspicion, negative pulmonary angiogram (definite), and negative D-Dimer with low suspicion |
Wells Criteria |
Symptoms and signs of DVT (3 points), alternative diagnosis less likely than PE (3 points), HR>100 (1.5 points), immobilization >3 days or surgery in last 4wks (1.5 points), previous DVT or PE (1.5 points), hemoptysis (1 point) and malignancy (1 point). If >4, PE is likely. |
Indications for Treatment |
intraluminal defects in central, segmental or lobular PAs on helical CT (or high probability with a scan) and clinical suspicion, DVT diagnosed with clinical suspicion, and positive pulmonary angiogram (definitively proves PE). |
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Treatment
Oxygen Therapy |
• To correct hypoxemia.
• Severe hypoxemia or respiratory failure requires intubation and mechanical ventilation. |
Heparin |
• Either unfractionated or LMWH (enoxaparin) to prevent recurrence.
• Prevents further clot formation but does not lyse existing emboli or diminish thrombus size.
• Start immediately based clinical suspicion. Do not wait for studies if high.
• Give one bolus, followed by infusion for 5-10days.
• Goal aPTT of 1.5-2.5x normal.
• Acts by promoting antithrombin III.
• Contraindications include active bleeding, uncontrolled HTN, recent stroke, and HIT.
• LMWH has less complications but NOT used in ESRD. |
Warfarin |
• For long-term treatment. Can start with heparin on day 1.
• Goal INR is 2-3. Continue for 3-6 months depending on risk factors.
• Some patients with significant risk for recurrence (malignancy, hyper coagulable state) should receive lifelong therapy. |
Thrombolytic Therapy |
• Streptokinase, TPA.
• Speed up lysis of clots.
• Does not improve mortality rates.
• Should be considered for use in patients with massive PE who are unstable, and patients with evidence of RHF. |
IVC Filter |
• Have not been proven to reduce mortality.
• Patients are at a higher risk of recurrent DVT but lower risk of recurrent PE.
• Complications include filter migration or misplacement, filter erosion and perforation of IVC, and IVC obstruction due to filter thrombosis.
• Indicated for patients with contraindications to anticoagulation, complication of current anticoagulation, failure of adequate anticoagulation evidence by recurrence, and low pulmonary reserve (high risk of death due to PE). |
NOACs |
Fondaparinox is an injectable factor Xa inhibitor. Rivaroxaban is an oral factor Xa inhibitor. Neither can be used in severe CKD (GFR<30). Epixaban is approved for use in CKD. |
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