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Acute Pulmonary Embolism: Introduction, Clinical presentation, Classification, Diagnosis, Treatment.

Acute pulmonary embolism. Clinical presentation of Acute pulmonary embolism. Classification of Acute pulmonary embolism. Diagnosis strategies of acute pulmonary embolism. Treatment of acute pulmonary embolism.

Acute Pulmonary Embolism: Introduction, Clinical presentation, Classification, Diagnosis, Treatment.

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Acute Pulmonary
Embolism
INTRODUCTION
ACUTE PULMONARY EMBOLISM (PE) IS A FORM OF VENOUS
THROMBOEMBOLISM (VTE) THAT IS COMMON AND SOMETIMES
FATAL. THE CLINICAL PRESENTATION OF PE IS VARIABLE AND
OFTEN NONSPECIFIC MAKING THE DIAGNOSIS CHALLENGING. THE
EVALUATION OF PATIENTS WITH SUSPECTED PE SHOULD BE
EFFICIENT SO THAT PATIENTS CAN BE DIAGNOSED AND THERAPY
ADMINISTERED QUICKLY TO REDUCE THE ASSOCIATED MORBIDITY
AND MORTALITY.
INTRODUCTION
• Definition — Pulmonary embolus (PE) refers to
obstruction of the pulmonary artery or one of its
branches by material (eg, thrombus, tumor, air, or
fat) that originated elsewhere in the body. This
topic review focuses upon PE due to thrombus.
• 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, a process termed venous thromboembolism
(VTE).
Why is it important?
 PE is the most common preventable cause of death in
hospitalized patients
 Untreated mortality - 30%
 80% of pulmonary emboli occur without prior
warning signs or symptoms
 Diagnosis can be difficult
 Early treatment is highly effective
PATHOGENESIS: THE PATHOGENESIS OF PULMONARY EMBOLISM
(PE) IS SIMILAR TO THAT WHICH UNDERLIES THE GENERATION OF
THROMBUS (IE, VIRCHOW'S TRIAD). VIRCHOW'S TRIAD CONSISTS OF
VENOUS STASIS, ENDOTHELIAL INJURY, AND A HYPERCOAGULABLE
STATE
Stasis
 Immobility/cast/travel
 Advanced age
 Acute medical illness
 Major surgery
 Spinal cord injury
 Obesity
Endothelial
• Damage
• Major surgery
• Trauma
• Central venous
• Catheterization
Hypercoagulability
Hereditary Deficiencies:
• Antithrombin deficiency
• Protein C deficiency
• Protein S deficiency
• Factor V Leiden
• Prothrombin gene mutation
Dysfibrinogenemia
Acquired:
• Cancer
• Pregnancy & postpartum
period
• Oral contraceptives
• Hormone replacement
therapy
• Polycythemia rubravera
• Smoking
• Anti phospholipid syndrome
• Chemotherapy
Ad

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Acute Pulmonary Embolism: Introduction, Clinical presentation, Classification, Diagnosis, Treatment.

  • 2. INTRODUCTION ACUTE PULMONARY EMBOLISM (PE) IS A FORM OF VENOUS THROMBOEMBOLISM (VTE) THAT IS COMMON AND SOMETIMES FATAL. THE CLINICAL PRESENTATION OF PE IS VARIABLE AND OFTEN NONSPECIFIC MAKING THE DIAGNOSIS CHALLENGING. THE EVALUATION OF PATIENTS WITH SUSPECTED PE SHOULD BE EFFICIENT SO THAT PATIENTS CAN BE DIAGNOSED AND THERAPY ADMINISTERED QUICKLY TO REDUCE THE ASSOCIATED MORBIDITY AND MORTALITY.
  • 3. INTRODUCTION • Definition — Pulmonary embolus (PE) refers to obstruction of the pulmonary artery or one of its branches by material (eg, thrombus, tumor, air, or fat) that originated elsewhere in the body. This topic review focuses upon PE due to thrombus. • 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, a process termed venous thromboembolism (VTE).
  • 4. Why is it important?  PE is the most common preventable cause of death in hospitalized patients  Untreated mortality - 30%  80% of pulmonary emboli occur without prior warning signs or symptoms  Diagnosis can be difficult  Early treatment is highly effective
  • 5. PATHOGENESIS: THE PATHOGENESIS OF PULMONARY EMBOLISM (PE) IS SIMILAR TO THAT WHICH UNDERLIES THE GENERATION OF THROMBUS (IE, VIRCHOW'S TRIAD). VIRCHOW'S TRIAD CONSISTS OF VENOUS STASIS, ENDOTHELIAL INJURY, AND A HYPERCOAGULABLE STATE
  • 6. Stasis  Immobility/cast/travel  Advanced age  Acute medical illness  Major surgery  Spinal cord injury  Obesity Endothelial • Damage • Major surgery • Trauma • Central venous • Catheterization Hypercoagulability Hereditary Deficiencies: • Antithrombin deficiency • Protein C deficiency • Protein S deficiency • Factor V Leiden • Prothrombin gene mutation Dysfibrinogenemia Acquired: • Cancer • Pregnancy & postpartum period • Oral contraceptives • Hormone replacement therapy • Polycythemia rubravera • Smoking • Anti phospholipid syndrome • Chemotherapy
  • 7. PREDISPOSING FACTORS Threre is an extensive collection of predisposing environmental and genetic factors for VTE Strong risk factors Moderate risk factors Weak risk factors •Fracture of lower limb •Hospitalization for heart failure or atrial fibrillation/flutter (within previous 3 months) •Hip or knee replacement •Major trauma •Myocardial infarction (within previous 3 months) •Previous VTE •Spinal cord injury •Arthroscopic knee surgery •Autoimmune diseases •Blood transfusion •Central venous lines •Intravenous catheters and leads •Chemotherapy •Congestive heart failure or respiratory failure •Erythropoiesis-stimulating agents •Hormone replacement therapy (depends on formulation) •In vitro fertilization •Oral contraceptive therapy •Bed rest >3 days •Diabetes mellitus •Arterial hypertension •Immobility due to sitting (e.g. prolonged car or air travel) •Increasing age •Laparoscopic surgery (e.g. cholecystectomy) •Obesity •Pregnancy •Varicose veins Predisposing factors for venous thromboembolism
  • 8. Pathophysiology The pathophysiology of pulmonary embolism: Although pulmonary embolism can arise from anywhere in the body, most commonly it arises from the calf veins. The venous thrombi predominately originate in venous valve pockets (inset) and at other sites of presumed venous stasis. To reach the lungs, thromboemboli travel through the right side of the heart.
  • 10. THE TEMPORAL PATTERN OF PRESENTATION (ACUTE, SUBACUTE, OR CHRONIC) – PATIENTS WITH PE CAN PRESENT ACUTELY, SUBACUTELY, OR CHRONICALLY: • ACUTE – PATIENTS WITH ACUTE PE TYPICALLY DEVELOP SYMPTOMS AND SIGNS IMMEDIATELY AFTER OBSTRUCTION OF PULMONARY VESSELS. • SUBACUTE – SOME PATIENTS WITH PE MAY ALSO PRESENT SUBACUTELY WITHIN DAYS OR WEEKS FOLLOWING THE INITIAL EVENT. • CHRONIC – PATIENTS WITH CHRONIC PE SLOWLY DEVELOP SYMPTOMS OF PULMONARY HYPERTENSION OVER MANY YEARS (IE, CHRONIC THROMBOEMBOLIC PULMONARY HYPERTENSION; CTEPH). CLASSIFICATION OF PULMONARY EMBOLISM
  • 11. THE PRESENCE OR ABSENCE OF HEMODYNAMIC STABILITY (HEMODYNAMICALLY UNSTABLE OR STABLE) • HEMODYNAMICALLY UNSTABLE PE IS ALSO CALLED "MASSIVE" OR "HIGH-RISK" PE. • HEMODYNAMICALLY STABLE PE IS CALLED "SUBMASSIVE" OR "INTERMEDIATE-RISK" PE IF THERE IS ASSOCIATED RIGHT VENTRICULAR STRAIN • "LOW-RISK" PE IF THERE IS NO EVIDENCE OF RIGHT VENTRICULAR STRAIN. CLASSIFICATION OF PULMONARY EMBOLISM
  • 12. Hemodynamically stable and unstable PE are defined as the following:  Hemodynamically unstable PE is that which results in hypotension. Hypotension is defined as a systolic blood pressure <90 mmHg or a drop in systolic blood pressure of ≥40 mmHg from baseline for a period >15 minutes or hypotension that requires vasopressors or inotropic support and is not explained by other causes such as sepsis, arrhythmia, left ventricular dysfunction from acute myocardial ischemia or infarction, or hypovolemia.  Although hemodynamically unstable PE is often caused by large (ie, massive) PE, it can sometimes be due to small PE in patients with underlying cardiopulmonary disease. Thus, the term "massive" PE does not necessarily describe the size of the PE as much as its hemodynamic effect. CLASSIFICATION OF PULMONARY EMBOLISM
  • 13. • HEMODYNAMICALLY STABLE PE IS DEFINED AS PE THAT DOES NOT MEET THE DEFINITION OF HEMODYNAMICALLY UNSTABLE PE. THERE IS A SPECTRUM OF SEVERITY WITHIN THIS POPULATION RANGING FROM PATIENTS WHO PRESENT WITH SMALL, MILDLY SYMPTOMATIC OR ASYMPTOMATIC PE (ALSO KNOWN AS "LOW-RISK PE") TO THOSE WHO PRESENT WITH MILD OR BORDERLINE HYPOTENSION THAT STABILIZES IN RESPONSE TO FLUID THERAPY, OR THOSE WHO PRESENT WITH RIGHT VENTRICLE DYSFUNCTION (ALSO KNOWN AS "SUBMASSIVE" OR "INTERMEDIATE-RISK" PE). CLASSIFICATION OF PULMONARY EMBOLISM
  • 15. • PULMONARY EMBOLISM (PE) HAS A WIDE VARIETY OF PRESENTING FEATURES, RANGING FROM NO SYMPTOMS TO SHOCK OR SUDDEN DEATH. THE MOST COMMON PRESENTING SYMPTOM IS DYSPNEA FOLLOWED BY CHEST PAIN (CLASSICALLY PLEURITIC IN NATURE), COUGH, AND SYMPTOMS OF DEEP VENOUS THROMBOSIS. • HEMOPTYSIS IS AN UNUSUAL PRESENTING SYMPTOM. • RARELY DO PATIENTS PRESENT WITH SHOCK, ARRHYTHMIA, OR SYNCOPE. • MANY PATIENTS, INCLUDING SOME WITH LARGE PE, ARE ASYMPTOMATIC OR HAVE MILD OR NONSPECIFIC SYMPTOMS. THUS, IT IS CRITICAL THAT A HIGH LEVEL OF SUSPICION BE MAINTAINED SUCH THAT CLINICALLY RELEVANT CASES ARE NOT MISSED. THE SIGNS AND SYMPTOMS OF PE ARE DISCUSSED IN DETAIL SEPARATELY. Clinical presentation
  • 16. Symptom Frequency Dyspnea 73 percent Pleuritic chest pain 66 percent Cough 37 percent Hemoptysis 13 percent Sign Tachypnea 70 percent Rales 51 percent Tachycardia 30 percent Fourth heart sound 24 percent Accentuated pulmonic component second heart sound 23 percent Circulatory collapse 8 percent Clinical presentation
  • 17. Assessment of clinical (pre-test) probability Of these, the most frequently used prediction rules are the revised Geneva rule (Table 5) and the Wells rule. Both prediction rules have been simplified in an attempt to increase their adoption into clinical practice; the simplified versions have been externally validated.
  • 18. The revised Geneva clinical prediction rule for pulmonary embolism
  • 19. The Wells clinical prediction rule for pulmonary embolism
  • 20. Laboratory tests and biomarkers  D-dimer testing  White blood cell count  Arterial blood gases  Markers of myocardial injury - serum troponin  Markers of right ventricular dysfunction - brain natriuretic peptide
  • 21. D-Dimer  Fibrin degradation product.  Non specific (~40%): cancer, sepsis, severe infection or inflammation disease increase D-dimer levels. Negative D dimer with Low clinical Probability is sufficient to exclude PE : 92% sensitive. Raised D- dimer does not imply VTE ( negative predictive value ) D dimer should not be done if clinical probability is high Laboratory tests and biomarkers
  • 22.  Markers of right ventricular dysfunction In normotensive patients with PE, the positive predictive value of elevated BNP or NT-proBNP concentrations for early mortality is low. Haemodynamically stable patients with low NT-proBNP levels may be candidates for early discharge and outpatient treatment  Markers of myocardial injury Elevated plasma troponin concentrations on admission have been reported in connection with PE and were associated with worse prognosis (troponin T concentrations >14pg/mL). Elevated serum creatinine levels and a decreased (calculated) glomerular filtration rate are related to 30-day-all- cause mortality in acute PE. Laboratory tests and biomarkers
  • 23. Imaging studies that aid in the diagnosis of pulmonary embolism
  • 24. Chest radiograph  Nonspecific abnormalities on chest radiography are common (eg, atelectasis, effusion) in PE, but a normal chest radiograph can be seen in 12 to 22 percent of patients.  A Hampton's hump and Westermark's sign are rare but, when present, should raise the suspicion for PE
  • 25. Hampton's hump  Hampton's hump is a shallow, hump-shaped opacity in the periphery of the lung, with its base against the pleural surface and hump towards the hilum
  • 26. Westermark's sign The sign results from a combination of:  The dilation of the pulmonary arteries proximal to the embolus and  The collapse of the distal vasculature creating the appearance of a sharp cut off on chest radiography. Has a low sensitivity (11%) and high specificity (92%) for the diagnosis of pulmonary embolism.
  • 27. Computed tomographic pulmonary angiography  Sensitivity of 83% and a specificity of 96% for CTPA in PE diagnosis.  In patients with a low or intermediate clinical probability of PE, a negative CTPA had a high negative predictive value for PE (96 and 89%, respectively). But its negative predictive value was only 60% if the pre-test probability was high.  Conversely, the positive predictive value of a positive CTPA was high (92- 96%) in patients with an intermediate or high clinical probability, but much lower (58%) in patients with a low pre- test likelihood of PE.
  • 28. Lung scintigraphy With multiple tracers such as xenon-133 gas, Tc- 99m-labelled aerosols, or Tc-99m-labelled carbon microparticles The high-probability criteria are as follows:  Two large (>75% of a segment) segmental perfusion defects without corresponding ventilation or chest radiographic abnormalities  One large segmental perfusion defect and 2 moderate (25-75% of a segment) segmental perfusion defects without corresponding ventilation or radiographic abnormalities  Four moderate segmental perfusion defects without corresponding ventilation or chest radiographic abnormalities
  • 29. Pulmonary angiography  For several decades, pulmonary angiography was the ‘gold standard’ for the diagnosis or exclusion of acute PE, but it is now rarely performed as less-invasive CTPA offers similar diagnostic accuracy.  The diagnosis of acute PE is based on direct evidence of a thrombus in two projections, either as a filling defect or as amputation of a pulmonary arterial branch.
  • 30. Magnetic resonance angiography  А large pulmonary embolus in the left main branch of the pulmonary artery
  • 36. Treatment TREATMENT IN THE ACUTE PHASE 1. HAEMODYNAMIC AND RESPIRATORY SUPPORT: • OXYGEN THERAPY AND VENTILATION. • PHARMACOLOGICAL TREATMENT OF ACUTE RIGHT VENTRICULAR FAILURE • MECHANICAL CIRCULATORY SUPPORT AND OXYGENATION 2. INITIAL ANTICOAGULATION • PARENTERAL ANTICOAGULATION • NON-VITAMIN K ANTAGONIST ORAL ANTICOAGULANTS • VITAMIN K ANTAGONISTS 3. REPERFUSION TREATMENT • SYSTEMIC THROMBOLYSIS • PERCUTANEOUS CATHETER-DIRECTED TREATMENT • SURGICAL EMBOLECTOMY
  • 37. Treatment in the acute phase Haemodynamic and respiratory support:  Hypoxaemia is one of the features of severe PE, and is mostly due to the mismatch between ventilation and perfusion. Administration of supplemental oxygen is indicated in patients with PE and SaO2 <90%.  Further oxygenation techniques should also be considered, including high-flow oxygen (i.e. a high-flow nasal cannula) and mechanical ventilation (non-invasive or invasive) in cases of extreme instability (i.e. cardiac arrest)
  • 38. Pharmacological treatment of acute right ventricular failure
  • 39. Mechanical circulatory support and oxygenation  The temporary use of mechanical cardiopulmonary support, mostly with veno–arterial extracorporeal membrane oxygenation (ECMO), may be helpful in patients with high-risk PE, and circulatory collapse or cardiac arrest
  • 40. Parenteral anticoagulation  In patients with high or intermediate clinical probability of PE, anticoagulation should be initiated while awaiting the results of diagnostic tests.
  • 41. Vitamin K antagonists  When VKAs are used, anticoagulation with UFH, LMWH, or fondaparinux should be continued in parallel with the oral anticoagulant for ≥5 days and until the international normalized ratio (INR) value has been 2.0–3.0 for 2 consecutive days.
  • 42. Systemic thrombolysis  Accelerated i.v. administration of recombinant tissue-type plasminogen activator (rtPA; 100 mg over 2 h) is preferable to prolonged infusions of first-generation thrombolytic agents (streptokinase and urokinase).
  • 44. Percutaneous catheter-directed treatment  For patients contraindications with to absolute thrombolysis Surgical embolectomy • Aortic cross-clamping and cardioplegic cardiac arrest should be avoided. • With bilateral PA incisions, clots can be removed from both pulmonary arteries down to the segmental level under direct vision.
  • 45. Recommendations for acute-phase treatment of high-risk pulmonary embolism
  • 46. Recommendations for acute-phase treatment of intermediate- or low-risk pulmonary embolism
  • 47. Chronic treatment and prevention of recurrence • THE AIM OF ANTICOAGULATION AFTER ACUTE PE IS TO COMPLETE THE TREATMENT OF THE ACUTE EPISODE AND PREVENT RECURRENCE OF VTE OVER THE LONG-TERM. • ORAL ANTICOAGULANTS ARE HIGHLY EFFECTIVE IN PREVENTING RECURRENT VTE DURING TREATMENT, BUT THEY DO NOT ELIMINATE THE RISK OF SUBSEQUENT RECURRENCE AFTER THE DISCONTINUATION OF TREATMENT.
  • 49. References: 1. Harrison's Manual of Medicine 2. Bates' Guide to Physical Examination and History Taking: https://booksdoctor.blogspot.com/2019/12/bates-guide-to-physical- examination-and-history-taking-pdf-download.html 3. Davidson's Principles And Practics Of Medicine: https://www.elsevier.com/books/davidsons-principles-and-practice-of- medicine/ralston/978-0-7020-7028-0 4. Treatment, prognosis, and follow-up of acute pulmonary embolism in adults: https://www.uptodate.com/contents/treatment-prognosis-and- follow-up-of-acute-pulmonary-embolism-in-adults

Editor's Notes

  1. Figure 2 Key factors contributing to haemodynamic collapse and death in acute pulmonary embolism (modified from Konstantinides et al. with permission). A-V = arterio-venous; BP = blood pressure; CO = cardiac output; LV - left ventricular; O2 = oxygen; RV = right ventricular; TV = tricuspid valve. a The exact sequence of events following the increase in RV afterload is not fully understood.
  2. b.p.m. = beats per minute; DVT = deep vein thrombosis; PE = pulmonary embolism.
  3. venous thromboembolism
  4. Therefore, clinicians should consider further testing in case of discordance between clinical judgement and the CTPA result.
  5. Angiographic findings of acute PE. (A) Pulmonary arteriogram in a 34-year-old female with hemodynamically unstable PE demonstrates multiple filling defects throughout the pulmonary arteries including complete cutoff of the right interlobar artery (arrow), and occlusion of right upper lobar artery, left lower lobe pulmonary artery, and lingular branch; (B) large right upper lobe filling defect in a different patient consistent with acute PE (arrow). Also noted are areas of decreased perfusion within the peripheral upper and lower lobes consistent with sub segmental emboli. PE, pulmonary embolism.
  6. CTPA=computed tomography pulmonary angiography; CUS=compression ultrasonography; DVT=deep vein thrombosis; LV=left ventricle; PE=pulmonaryembolism;RV=rightventricle;TOE=transoesophagealechocardiography;TTE=transthoracicechocardiogram. aSeeTable4fordefinitionofhaemodynamicinstabilityandhigh-riskPE. bAncillary bedside imaging tests may include TOE, which may detect emboli in the pulmonary artery and its main branches; and bilateral venous CUS, whichmayconfirmDVTandthusVTE. cInthe emergencysituation ofsuspectedhigh-risk PE, this refers mainlyto a RV/LVdiameter ratio >1.0; the echocardiographic findings ofRVdysfunction, andthecorrespondingcut-offlevels,aregraphicallypresentedinFigure3,andtheirprognosticvaluesummarizedinSupplementaryDataTable3. dIncludes the casesin whichthe patient’sconditionissocritical thatit onlyallows bedside diagnostic tests.Insuchcases, echocardiographicfindings ofRV dysfunctionconfirmhigh-riskPEandemergencyreperfusiontherapyisrecommended
  7. CTPA=computedtomographypulmonaryangiography/angiogram;PE=pulmonaryembolism.
  8. This is the accelerated regimen for rtPA in pulmonary embolism; it is not officially approved, but it is sometimes used in extreme haemodynamic instability such as cardiac arrest.
  9. ECMO = extracorporeal membrane oxygenation; PE = pulmonary embolism; UFH = unfractionated heparin. aSee Table 4 for definition of high-risk PE. After haemodynamic stabilization of the patient, continue with anticoagulation treatment as in intermediate- or low-risk PE (section 6.7). bClass of recommendation. cLevel of evidence. dIf appropriate expertise and resources are available on-site