PULMONARY THROMBOEMBOLISM

1
PULMONARY THROMBOEMBOLISM

• Dr Elizabeth Veitch
• Respiratory Unit
• Concord Repatriation General Hospital

2
Terminology

• Thrombosis is the process of formation of a solid
  mass in living blood vessels or the heart, from
  the constituents of blood.
• Thrombus is the mass resulting from thrombosis.
• Embolus is an intravascular mass (solid, liquid
  or gaseous) carried in the blood stream to a site
  removed from its origin.
• Thrombi emboli - ARTERIAL or VENOUS

3
When I cut myself why dont I bleed to death ?
4
Normal Haemostasis

• 3 main components-
• 1. Blood vessel
• 2. Platelets
• 3. Coagulation Clotting Factors

5

• The normal blood vessels has-
• 1. Continuous lining endothelium which provides a
  non-reactive interface.
• 2. Endothelial surface contains sulfated
  mucoploysaccharides (anticoagulant effect).
• 3. Endothelial cells elaborate substances which
  are anti-thrombotic
• Some prostaglandins...inhibit platelet
  aggregation
• Plasminogen activatorfibrinolysis

6
Thrombus Formation

• 1. Loss of integrity of the blood vessel wall
  leads to exposure of subendothelial tissues.
• 2. Adherence of passing platelets.
• 3. Platelets change morphologically and release
  their granules.
• 4. Granule products cause
• - Vasoconstriction of blood vessel (serotonin)
• - Trigger coagulation cascade, leading to the
  formation of a stable fibrin polymer

7
Once I start clotting how do I stop?
8
Normal Anticoagulation

• 4 main components-
• Haemodynamic forces
• Depletion of coagulation factors
• - especially local depletion of thrombin
• Fibrinolytic system
• Clot retraction

9
What is a PE?
10

• An embolus, carried via the venous circulation,
  which lodges in the pulmonary arteries and
  arterioles.
• solid masses are by far the most common
• most originate from thrombus in the lower limb
  and pelvic veins
• common annual incidence 1 in 1000
• 3rd most common acute cardiovascular event
• one of the few causes of sudden death (10-15)

11
(No Transcript)
12
Who gets PE?
13

• Anyone!!!!
• but there are factors which greatly enhance the
  risk of VTE (DVT and PE)
• These risk factors act via 3 mechanisms to
  predispose to thrombosis-
• Injury to the vascular endothelium
• Alterations in normal blood flow
• Alterations in the blood (hypercoagulability)

14
Acquired Risk Factors

• Old age
• - Age lt 15 AI 1/1,000,000 vs gt85 AI 1/100
• Immobility
• - Surgery, Medical illness, Paraplegia, Long
  distance travel
• Malignancy
• Lower limb problems
• Pregnancy and puerperium
• Intravascular foreign bodies
• Drugs
• - OCP, HRT, Tamoxifen, Estrogen receptor
  modulators

15
Inherited Risk Factors

• Inherited thrombophilias
• Factor V Leiden mutation
• Deficiencies of endogenous anticoagulants (AT
  III, Protein C and S)
• Prothrombin gene mutation
• Not uncommon, may be present in up to 50 of
  patients with VTE
• Generally also need acquired risk factors to
  trigger VTE
• Look for only if unprovoked recurrent VTE,
  especially in younger patients

16
Risk Factors

• May be
• Acquired or Inherited
• Major (RR 5-20) or Minor (RR 2-4)
• Are often multiple
• An elderly patient with cancer, who is post-op
  and dehydrated (thus hyperviscous blood) with a
  central venous line.
• Usually act via more than 1 mechanism.

17
How can I tell if someone has a PE?
18
Clinical Suspicion

• PE causes symptoms-
• Dyspnoea 70-80
• Chest pain/pleurisy 50-60
• Cough 20-30
• Haemoptysis 10-15
• Syncope 10-15
• Infrequently have symptoms/signs of DVT (PIOPED
  30)
• Only a minority (5-10) are asymptomatic

19
Clinical Suspicion

• PE causes signs-
• Tachopnea (RR gt 20/min) 60-70
• Tachycardia (PR gt 100/min) 30-40
• Hypotension 4-8
• Fever (T gt 38C) 10-15
• Lung crackles 50
• Loud P2 20

20
Clinical Suspicion

• Unfortunately the signs and symptoms of PE are
  neither sensitive nor specific
• The same spectrum of symptoms/signs was seen in
  the 850 patients in PIOPED who did NOT have PE
• The diagnosis must be considered in patients
  presenting with the above symptoms and signs
• Autopsy series PE only considered antemortem in
  30 of patients who are found to have PE at
  post-mortem
• The main alternate diagnosis is pneumonia

21
Can I prove that my patient has a PE?
22

• Sometimes only!!!
• BECAUSE the symptoms and signs are neither
  sensitive nor specific
• BECAUSE the investigations findings are
  non-specific or indeterminant
• An INTEGRAL PART of diagnosing PE is the
  exclusion of an alternate diagnosis that would
  explain the patients presentation
• AND assignment of a clinical pretest probablilty.

23
Basic Test Findings

• Arterial Blood Gases (ABGs)
• - Usually low O2, low CO2
• - O2 normal in 10-15
• - High CO2 if massive PE or underlying
  respiratory disease
• Other blood tests
• Not uncommon to see mild increases in WCC, ESR
• Elevated cardiac enzymes (troponins) have been
  found to correlate with right heart infarction
  and a poorer outcome.

24
Basic Test Findings

• 3. Electrocardiogram (ECG)
• - Often abnormal (70-85), even in those without
  cardiovascular disease
• - Tachycardia 40-50
• - Non-specific T wave and ST changes 50
• More specific changes are less common 20-30
• right axis deviation
• RBBB
• S1Q3T3

25
(No Transcript)
26
Basic Test Findings

• 4. Chest X-Ray (CXR)
• Is rarely normal (10), but the changes are
  non-specific and often subtle
• Common findings are atelectasis, parenchymal
  shadowing and pleural effusions (usually small
  and bilateral)
• Specific findings (Hamptons hump and
  Westermarks sign) are rare.

27
Basic Test Findings

• 5. Echocardiogram
• May show
• RH dilatation
• bowing of the interventricular septum
• reduced contractility of the RV
• elevated RH pressures
• Regurgitation of the pulmonary and tricuspid
  valves
• - A marker of more severe PE and poorer outcome.

28
(No Transcript)
29
(No Transcript)
30
Specific Investigations

• D-dimer
• A degradation product released into the
  circulation when cross-linked fibrin undergoes
  endogenous fibrinolysis
• Elevated when thrombosis is present
• Marked recent interest coupled with evolution of
  the assays for D-dimer
• Sensitivity for DVT/PE is improving (87-98), but
  poor specificity (increased in cancer, post-op)
• Main role excellent negative predictive value in
  low risk patients

31
Specific Investigations

• Demonstration of DVT
• - Leg Ultrasound
• - Venography
• Demonstration of PE
• - Ventilation/Perfusion Lung Scanning (VQ)
• - Computerized Tomography Pulmonary
• Angiography (CTPA)
• - Pulmonary Angiography (PA)

32
Pulmonary Angiography

• Dye is injected into the pulmonary artery and
  x-rays are taken of the lungs
• Generally regarded as the gold standard
  investigation for PE
• Very low rate of subsequent PE (1 over a year)
  in those with a negative PA
• But, it carries a small but relevant morbidity
  (2-3) and mortality (0.5)
• Many now question its status and role (difficult
  to perform, falling expertise, inter-observer
  disagreement).

33
(No Transcript)
34
(No Transcript)
35
VQ Scanning

• Patient inhales technetium labeled gas and
  receives injection of labeled blood. The lungs
  are scanned and V and Q images compared.
• The number and pattern of defects yields a
  probability of PE
• High probability 88 PE
• Intermediate probability 33 PE
• Low probability 12 PE
• Normal test 4 PE
• Accuracy is increased by combining a consistent
  pretest probability.

36
(No Transcript)
37
CT Pulmonary Angiography

• CT scan of the lungs is done following iv
  administration of a contrast agent. Look for
  filling defects in pulmonary arteries.
• Attractive to clinicians because
• It yields a Yes/No answer
• Can demonstrate an alternate diagnosis
• Is not affected by pulmonary disease
• Evolving technology has led to improvements in
  sensitivity some now regard it as 1st line.

38
(No Transcript)
39
(No Transcript)
40
(No Transcript)
41

• Thus, PE can be a difficult diagnosis to make
• Big emboli are easy to find on all tests, small
  PE arent.
• MUST exclude alternate diagnoses
• MUST have in your mind a clinical pretest
  probability (after consideration of risk factors,
  symptoms, signs and basic investigations)
• OFTEN need more than 1 specific investigation
• SOMETIMES need to treat for PE without conclusive
  proof.

42
How do I fix a PE?
43
Treatment modalities

• Prevent thrombus from propagating
• - While awaiting endogenous fibrinolysis
• Dissolve embolus
• Thrombolytic agents, Catheter fragmentation/suctio
  n
• Physically remove embolus (surgical embolectomy)
• Physically prevent thrombus from reaching the
  lungs (venacaval filter)
• Supportive measures

44
Treatment

• Treatment does work!!!
• Untreated PE mortality 30 (mainly due to further
  PE)
• Treated PE mortality 2-8
• Prompt recognition and treatment are essential
• Supportive measures
• Oxygen
• Support BP (volume expanders, inotropes)

45
Treatment

• Mainstay of treatment is anticoagulation to
  prevent thrombus propagation/embolism
• Heparin initially, then warfarin tablets
• Generally treat provoked PE for 3 months and
  unprovoked PE for 6 months
• Lifelong anticoagulation is sometimes needed
• Recurrent unprovoked PE, continuing major risk
  factor
• Recurrence rate for PE-
• 3 per year for PE provoked by transient risk
  factor
• 10 per year if unprovoked PE, or persistent risk
  factor

46
Treatment

• Thrombolysis (with iv Steptokinase, Urokinase,
  TPA) leads to
• Quicker resolution of clot (on VQ, CTPA, PA)
• Improved haemodynamics
• Probably improved long term outcomes
• But NOT
• Reduced mortality
• Reduced PE recurrence
• Risky, thus only used in those with massive PE
• (ICOPER 22 major bleeding, 12 transfusion, 3
  ICH)

47
Treatment

• Other modalities are infrequently used
• Surgical embolectomy
• For massive, central clot
• Patients often succumb prior to surgery
• Little experience with this procedure
• Catheter fragmentation/suction
• - Research tool
• Venacaval filters
• - If anticoagulation CI or further PE would be
  fatal

48
(No Transcript)
49
Prevention better then cure!

• Well documented that the DVT rate can be
  substantially reduced in certain high risk
  situations, by the use of low dose prophylactic
  heparin or LMWH
• Orthopedic and general surgery, Medical illness
• This is now the standard of care!
• Physical therapies are also important
• Calf stimulators during surgery, TED stockings
  post-op and early mobilization.