1. Pulmonary Embolism Hidden Killer
Dr. Hatem Said
Assistant Professor Anesthesia/ICU
Ain Shams University

2. Objectives Definition Epidemiology Pathophysiology Clinical Picture
Diagnostic Tools
Prophylaxis
Treatment
Conclusion

3. 1-Definition
Pulmonary embolism (PE): is an obstruction of the pulmonary artery or one of its branches by a thrombus (or thrombi) that originates somewhere in the venous system.
Infarction : The pathological changes which develop in the lung as a result of pulmonary embolism
The types of emboli :could be a blood clot (most common), air, fat, amniotic, fluid, and septic (from bacterial invasion of the thrombus).

4. 2-Epidemiology
PE : The cause of, or a major contributory factor to, death in 7-9% of necropsy cases
650,000 cases in the US each year
150,000 – 200,000 US deaths each year
Most common preventable cause of hospital death
3rd most common acute cardiovascular emergency (MI and stroke)

5. 3-Pathophysiology
Source of Thrombosis (Thrombo-embolic) that originates in the venous system and embolizes to the pulmonary arterial circulation
DVT in veins of leg above the knee (>90%)
DVT elsewhere (pelvic, arm, calf veins, etc.)
Cardiac thrombi

8. 3-Pathophysiology Risk factors for deep venous thromboembolism
Triad of Virchow
Endothelial injury: mainly caused by either direct trauma (severed vein) or local irritation (by chemotherapy, past DVT, phlebitis).
Stasis: mainly caused by heart failure, prolonged immobility.
Hypercoagulation status: inherited :(AT III def., protein C, S deficiency) or acquired: (malignancy, pregnancy, nephritic syndrome, DIC and liver failure.

9. 3-Pathophysiology Risk Factors: Strong Predisposing factors
(Odds Ratio>10)
Moderate Predisposing factors
(Odds Ratio 2-9)
Weak Predisposing factors
(Odds Ratio <2)
Fracture (Hip or Leg)
Hip or Knee Replacement
Major General Surgery
Major trauma
Spinal Cord Injury
Arthroscopic Knee Surgery
Central venous line
Chemotherapy
Chronic heart or respiratory failure
Hormonal replacement therapy
Oral Contraceptive Pills
Paralytic Stroke
Pregnancy/Postpartum
Previous VTE
Thrombophelia
Bed Rest<3 days
Immobility due to sitting(e.g prolonged car or air travel)
Increasing Age
Laparoscopic surgery (Cholecystectomy)
Obesity
Varicose veins

16. 4-Clinical Picture Revised Geneva Score (Clinical Prediction) Variable
Points
Predisposing Factors:
Age>65 years
Previous DVT or PE
Surgery or fracture within 1 month
Active malignancy +1 +3 +2
Symptoms:
Unilateral lower limb pain
Haemoptysis
Clinical Signs
Heart Rate
75-94 bpm
>95bpm
Pain on LL deep vein and unilateral edema +5 +4
Clinical probability:
Low
Intermidiate
High
Total
0-3
4-10
>11

17. 4-Clinical Picture Wells Score (Clinical Prediction) Variable Points
Predisposing Factors:
Previous DVT or PE
Recent Surgery or immobilization
Cancer
+1.5 +1
Symptoms:
Haemoptysis
Clinical Signs
Heart Rate
>100 bpm
Clinical signs of DVT
Clinical Judgement
Alternative diagnosis less likely than PE +3
Clinical probability:
Low
Intermidiate
High
Total
0-1
2-6
>7

18. 4-Clinical Picture
Most PE are small embolism will reach the periphery of the lung, sometimes producing wedge shaped shadow (pulmonary infarction) on CxR .
A large embolism suddenly obstructing a major pulmonary vessel has marked effects on cardiac function , often associated with anterior chest pain and collapse.
Chronic recurrent pulmonary embolism may develop pulmonary hypertension and right ventricular failure

19. 4-Clinical Picture SYMPTOMS : Massive PE: Dyspnea (84%). -Shock.
Pleuritic pain (74%) Dyspnea, Cyanosis.
Anterior chest pain (68%) Apprehension, Sweating.
Cough (53%) Chest pain, Tachycardia, AF
Hemoptysis (30%).
Asymptomatic (10%).
SIGNS:
Tachypnea (70%).
Rales (51%).
Tachycardia (30%).
S4 (24%).
Accentuated P2.

20. 4-Clinical Picture Differential Diagnosis: Myocardial Infarction.
Pluerisy/Pericarditis.
Tachyarrhythmia.
Musculoskeletal/rib fracture.
Lobar Collapse secondary to tumor.
Asthma.
Pneumonia.
Pneumothorax.
Perforating Peptic Ulcer.
Acute Pancreatitis.
Differential Diagnosis of Massive Pulmonary Embolism:
Acute pulmonary edema
Cardiac tamponade.
Dissecting Aortic Aneurysm.
Shock/sepsis.

21. Duplex US with compression of the lower extremities
5-Diagnostic Tools
Duplex US with compression of the lower extremities
Non-invasive test that accurately detects proximal DVT in LE (70-80% of pts with PE have concomitant proximal DVT)
Often used in workup of PE before going to more invasive procedures
Invasive test: Venography (definitive diagnosis)

24. 5-Diagnostic Tools
Laboratory Investigations (Non Specific): leukocytosis , ESR elevation, LDH, SGOT elevation with normal bilirubin.
CK, CK MB or Troponin I should be checked to rule out AMI
ABG
Normal does NOT rule out PE
Hypoxia, hypocapnia, respiratory alkalosis.
D-Dimer: High sensitivity but poor specificity
Negative prediction<500 ng /ml is a powerful excluding tool for PE

25. 5-Diagnostic Tools Chest X-ray: Abnormal in 88% of acute PE
Atelectasis (60-70%): most common finding in PE without infarction.
Westermark sign (increased lucency in area of embolus)
Hampton Hump (wedge-shaped pleural-based infiltrate)
Abrupt cutoff of vessel
Pleural effusion

26. Westermark Sign: represents a focus of oligemia (vasoconstriction )seen distal to a pulmonary embolism

27. Hampton Hump: Radiologic sign which consists of a shallow wedge-shaped opacity in the periphery of the lung with its base against the pleural surface. Occurs 12 to 36 hours after symptoms begin;
usually indicates pulmonary infarction

29. 5-Diagnostic Tools ECG:
Most common: sinus tachycardia +/- nonspecific ST-segment and T-wave changes
“Classic S1-Q3-T3 pattern”
Other signs of right heart strain (ie, new RBBB and ST changes ,T wave inversion in V1,2
Echocardiography:
It may be helpful after a large PE in a compromised patient, as it can show right heart dilatation , occasionally thrombus and increased pulmonary arterial pressure readings if tricuspid regurgitation developed.
Convenient and rapidly available

30. ECG findings

31. Echocardiography Findings

32. Echocardiography Findings
Transesophageal echocardiographic shows the reduction in size of the clot (arrow) (PA, pulmonary artery; RA, right atrium; Ao, aorta)
Transesophageal echocardiographic findings showing the floating thrombus (arrow) into central pulmonary artery (PA, pulmonary artery; RA, right atrium; Ao, aorta)

33. Helical(Spiral) CT
Sensitivity 85% (more sensitive for proximal emboli but is less good at detecting peripheral emboli, which may account for up to 30% of PE vessels)
Specificity 95%
It may be used as a first line investigation when V/Q Scan is delayed and when a large PE is suspected and early diagnosis is needed first-

38. V/Q Scan
Identifies mismatches between areas that are ventilated but not perfused
Best initial test in patients with clear CXR
Normal: rules out PE
High-probability scan: is diagnostic of PE if the clinical suspicion is also high
Low-probability scan: rules out PE only in a pt with low pretest clinical probability (because PE is found in roughly 15% of pts with low-probability scans)
Intermediate-probability scan: requires further evaluation (16-66% chance of PE depending on pretest probability)

43. Pulmonary Angiography
“Gold Standard” but is invasive, time consuming, needs experienced radiologists
5% morbidity
< 0.5% mortality
Indicated if the diagnosis remains uncertain after noninvasive testing

47. 6- Prophylaxis Encourage all patients to ambulate as soon as possible
determine patient at risk:
Low risk :(<40 years old, ambulating, minor surgery) don't need prophylaxis.
Moderate risk: (>40 years old, abdominal, pelvic or thoracic surgery) pneumatic compression, or low dose heparin prophylaxis.
High risk: (>60years old, prior DVT or PE malignancy, orthopedic surgery hypercoagulability state) combination of pneumatic compression and low dose heparin prophylaxis or Dextran.
Coumadine or IVC filter are considered.

48. IVC Filter: if anticoagulation is contraindicated (e. g
IVC Filter: if anticoagulation is contraindicated (e.g., active GI bleed, intracranial neoplasm, Ophthalmology patient , known bleeding diathesis), if thrombus formed despite adequate anticoagulation, or with a large burden of thrombosis in the LE that could be fatal if embolized.

51. 6- Prophylaxis Rivaroxaban (Oral factor X a inhibitor)
New Drug that provide a simple, fixed-dose regimen for treating acute DVT and for continued treatment, without the need for lab. Monitoring.
Approved (FDA) for prophylaxis in post-operative period after knee & hip replacement and chronic AF.
Nearly it will approved for treatment of acute PE.
Antidote: Thrombin Complex Concentrate.

52. 7-Treatment Primary Treatment: Supplemental oxygen for hypoxemia.
If the PE is large, supportive treatments for hypotension or reduced CO should be given IVF , Levophed , or Dopamine/Mechanical Ventilatory Support
Specific treatment is with intravenous unfractionated heparin infusion following an initial bolus dose 80 U/kg bolus, then 18 U/kg/hr
a PTT should be monitored 6 hours after initiation, 6 10 hours after any dosage change, then daily with a target of seconds.
Heparin does not reduce acute mortality but significantly reduces further events

53. 7-Treatment
LMWH: Current guidelines for patients with acute nonmassive pulmonary embolism recommend LMWH over UFH.
LMWHs have many advantages over UFH:
These agents have a greater bioavailability,
can be administered by subcutaneous injections,
and have a longer duration of anticoagulant effect.
- A fixed dose of LMWH can be used ( 30mg, sc, bid), and laboratory monitoring of a PTT is not necessary
Chest. Jun 2008;133(6 Suppl):454S-545S

54. 7-Treatment Oral Anticoagulation:
Oral Warfarin can be given with the initiation of Heparin keep INR between 2- 3 with initial dose of 5mg/day for 2 days (The peak effect does not occur until hours after drug administration) .
An overlap of 4- 5 days with a therapeutic INR and a PTT is recommended .
Persistent oral Warfarin should be prescribed for 3 months till the absence of risk factors
LMWH can be used when Warfarin is contraindicated (e.g. pregnancy) .

55. 7-Treatment Long-term anticoagulation
1st event with reversible risk factors: 3-6 months Warfarin.
Idiopathic PE/DVT: 6 months Warfarin.
2nd event, cancer, preexisting irreversible risk factors, such as deficiency of antithrombin III, protein S and C Deficiency: 12 month to life long Warfarin.
BMJ. Mar ;334(7595):674

56. 7-Treatment
Potential indications for THROMBOLYTIC THERAPY in venous thromboembolism (acceptable risk of bleeding complications) :
significant cardiac compromise , RV strain (Dysfunction) .
presence of hypotension related to PE not responding to IVF and vasopressor resuscitation.
Presence of severe hypoxemia.
Substantial perfusion defect.
Extensive DVT.
Thrombolytic therapy achieves faster resolution of the thrombus and more rapid recovery of normal vascular flow than simple anticoagulation.

57. 7-Treatment Regimens for thrombolysis in Pulmonary Embolism:
Drug Regimen
Streptokinase IU in min followed by IU/Hour up to 24 Hours
t-PA MG IV over 1-2 min followed by an infusion of 90 MG over 2 Hours
Cerebral hemorrhage can occur in up to 1% of cases
It has been used successfully and safely in a pregnant woman and this is not a contraindication unless immediately postpartum

58. 7-Treatment Pulmonary Embolectomy:
This is reserved for severe cardiac compromise where thrombolysis has either failed or is contraindicated.
It requires an experienced team to be successful and, although used infrequently, small studies (Doerge et al, 1999) have shown favorable outcomes.

59. 8-Conclusion
Untreated PE is associated with high mortality ,Suspected PE demands prompt diagnostic testing & assessment of risk factors & clinical probability, with empirical clinical assessment & a validated clinical prediction score when possible.