This document discusses pulmonary embolism (PE), including its causes, symptoms, diagnosis, and treatment. Some key points: - PE is a common cause of preventable death, often occurring without warning signs. Prompt diagnosis and treatment are important. - PE usually originates from blood clots that form in the deep leg veins. Symptoms can include chest pain, difficulty breathing, and syncope. - Diagnosis is difficult as symptoms are non-specific. Imaging tests like CT scans are often needed along with blood tests like d-dimers. - Treatment involves blood thinners to prevent further clots. Thrombolysis may be used in high-risk cases but risks need to be weighed

1. Pulmonary Embolism
Dr. Prabhu Dayal Sinwar
Assistant Professor

2.  PE is the most common preventable
cause of death in hospitalized patients
 ~600,000 deaths/year
 80% of pulmonary emboli occur
without prior warning signs or
symptoms
 2/3 of deaths due to pulmonary emboli
occur within 30 minutes of embolization
 Death due to massive PE is often
immediate
 Diagnosis can be difficult
 Early treatment is highly effective
 YOU WILL TAKE CARE OF PATIENTS
WITH PE!

3. Pathology
At least 90% of pulmonary
emboli originate from major leg
veins.

6.  40-50% of pts with DVT develop PE, often
“silent”
 PE presents 3-7 days after DVT
 Fatal within 1 hour after onset of respiratory
symptoms in 10%
 Shock/persistent hypotension in 5-10% (up to 50% of
patients with RV dysfunction)
 Most fatalities occur in untreated pts
 Perfusion defects completely resolve in 75% of
all patients (who survive)

7.  Dyspnea, tachypnea, or pleuritic chest pain
most common
 Pleuritic pain = distal emboli pulmonary infarction
and pleural irritation
 Isolated dyspnea of rapid onset= central PE with
hemodynamic sequlea
 Retrosternal angina like sxs= RV ischemia
 Syncope=rare presentation, but indicates
severely reduced hemodynamic reserve
 Sxs can develop over weeks
 In pts with pre-existing CHF or COPD,
worsening dyspnea may indicate PE

8. Non-Specific!!

9.  Usually abnormal, but non-specific
 Study of 2,322 patients with PE:
 Cardiac enlargement (27%)
 Normal (24%)
 Pleural effusion (23%)
 Elevated hemidiaphragm (20%)
 Pulmonary artery enlargement (19%)
 Atelectasis (18%)
 Parenchymal pulmonary infiltrates (17%)
Chest Radiographs in Acute Pulmonary Embolism: Results From the International
Cooperative Pulmonary Embolism Registry. Chest July 2000 118:3338;
10.1378/chest.118.1.33

10.  Usually non-specific ST/T waves changes and
tachycardia
 RV strain patterns suggest severe PE
 Inverted T waves V1-V4
 QR in V1
 Incomplete RBBB
 S1Q3T3

12.  Implicit clinical judgement is fairly accurate:
“Do you think this patient has a PE?”
 Validated prediction rules standardize clinical
judgement
 Wells
 Geneva

13. Proportion with PE
65%
30
10%

15.  D-Dimer
 Fibrin degradation product
 ELISA tests are highly sensitive (>95%)
 Non specific (~40%): cancer, sepsis, inflammation
increase d-dimer levels

16. • Direct visualization of emboli.
• Both parenchymal and mediastinal structures
can be evaluated.
•Optimally used when incorporated into a
validated diagnostic decision tree

18. 3 month
VTE rate 0.5% (all non fatal) 1.3%
This algorithm allowed for a management decision in 98% of
patients presenting with symptoms suggestive of PE

19. RISK STRATIFICATION

20.  Hypotension (not caused by arrhythmia,
sepsis, or hypovolemia)
 SBP <90 mm Hg = 53% 90-day all cause mortality
 SBP drop of 40 mm Hg for at least 15 minutes = 15%
in–hospital mortality
 Syncope= bad
 Shock= really bad

21.  Troponin levels correlate with in-hospital
mortality and clinical course in PE
 Troponins do not necessarily mean “MI”
 Significantly increased mortality in patients
with troponin level >0.1 ng/ml (O.R.= 6)
 Normal troponin has very high NPV (99-100%)
Prognostic value of troponins in acute pulmonary embolism: a meta analysis. Circulation
2007;116:427-433

22.  Brain natriuretic peptide
 Elevated levels related to worse outcomes.
 Low levels can identify patients with a good
prognosis (NPV 94-100%)
Prognostic role of brain natriuretic peptide in acute pulmonary embolism.
Circulation 2003;107:2545-2547

23.  RV dilation
 RV/LV short axis >1= pulmonary
hypertension
 RV/LV short axis >1.5= severe PE
 Leftward septal bowing

26. Echocardiography-RV Dilation

27. Arch Intern Med. 2005;165:1777-1781

29.  Streptokinase 250 000 IU as a loading dose over
30 min, followed by 100 000 IU/h over 12–24 h
 Accelerated regimen: 1.5 million IU over 2 h
 Urokinase 4400 IU/kg as a loading dose over
10 min, followed by 4400 IU/kg/h over 12–24
h
 Accelerated regimen: 3 million IU over 2 h
 rtPA 100 mg over 2 h or 0.6 mg/kg over 15 min
(maximum dose 50 mg over 15 min)

31. An alternative in high-risk PE patients when thrombolysis
is absolutely contraindicated or has failed
Kucher N Chest 2007;132:657-663

32. Optimal rx?

33.  Controversial! Evidence is limited regarding
optimal therapy
 No clinical trial or meta-analysis has been large
enough to demonstrate a mortality benefit of
thrombolysis compared to anticoagulation
alone.

34.  A combination of alteplase (100 mg given over
a two-hour period) and heparin prevented the
need for escalation of treatment (with open-
label alteplase, catecholamine infusion, or
mechanical ventilation) due to clinical
deterioration more often than a combination of
placebo and heparin.
 Clinical deterioration usually meant worsening
symptoms, especially worsening respiratory
failure.

35. 1. Anticoagulation should be initiated without delay in
patients with high or intermediate clinical probability
of PE while diagnostic workup is still ongoing
2. Use of LMWH or fondaparinux is the recommended
form of initial treatment for most patients with non-
high-risk PE
3. In patients at high risk of bleeding and in those with
severe renal dysfunction, unfractionated heparin with
an aPTT target range of 1.5–2.5 times normal is a
recommended form of initial treatment
Guidelines on the diagnosis and management of acute pulmonary embolism
European Heart Journal (2008) 29, 2276–2315

36. 4. Initial treatment with unfractionated heparin, LMWH
or fondaparinux should be continued for at least 5
days and may be replaced by vitamin K antagonists
only after achieving target INR levels for at least 2
consecutive days
5. Routine use of thrombolysis in non–high-risk PE
patients is not (yet) recommended, but it may be
considered in selected patients with intermediate-
risk PE (RV dysfunction, elevated troponin, BNP) and
low bleeding risk
Guidelines on the diagnosis and management of acute pulmonary embolism
European Heart Journal (2008) 29, 2276–2315

37. Agnelli G, Becattini C. N Engl J Med 2010;363:266-274
Recurrent PE
or PE and uncured
cancer:
Consider long term
anticoagulation if
benefits>risk
First unprovoked PE:
rx for at least 3-6
months

38. •May provide lifelong protection against PE
•Unclear effect on overall survival
• Complications:
•DVT (20%)
•Post thrombotic syndrome (40%)
•IVC thrombosis (30%)
•Risk/benefit ratio difficult to determine since no RCT
•Use when there are absolute contraindications to
anticoagulation and a high risk of VTE recurrence
•Consider in pregnant women with extensive
thrombosis
•Optimal duration of retrievable filters is unclear