Lecture 12- Pulmonary embolism Flashcards
Embolism
Obstruction of blood vessel by a foreign substance or blood clot that travels through the bloodstream, lodging in a blood vessel, plugging the vessel
- Material may or may not derived from the
- circulation itself
- Clots from artery (heart arrack) or venous (PE)
- thrombus
- Air
- Tumour
- Fat- e.g. motor vehicle accident when bone marrow can go into circulation if bone crushed
- Amniotic fluid
- Clots from artery (heart arrack) or venous (PE)
- Pulmonary embolism means that the material passes through the
-
right side of the heart and lodges in the pulmonary arteries
- Can be smaller branches
- Could be main pulmonary trunk deadly
Angiogram showing the right pulmonary artery
- Loss of vasculature due to embolism stopping significant blood flow to the lung
- 90% of PE arise from
DVTs in legs, particularly popliteal vein and more proximal veins including pelvic veins
- only …..% of patients with PE have symptoms or signs of DVT
25%
upper extremity clots are formed by
‘lines’ e.g. used to give chemotherapy, forming clots which pass through the venous system
PE stats
- 3rd cause of vascular death after MI and stroke
- Commonest cause of preventable death in hospital
- One of the commonest cause of unexpected death in hospital pts
- Risk factors same for DVT
risk factors for PE
virchows triad
- Virchow’s triad
- Endothelial injury
- Statis of blood flow
- Hypercoagulability
- Endothelial injury
e.g. Hip fracture damages blood vessels
- Statis or turbulence of blood flow
- E.g long haul flight
- E.g. immobility – fractured hip
- Blood hypercoagulability
e.g.
- Cancer
- COCP
- pregnancy
Pathology of deep venous thrombosis
- Changes in blood composition, reduced blood flow and changes to vessels can result in the formation of fibrous clots
- Clots form through activation of the coagulation cascade
- if clots form in legs= DVT
- If part of the clot goes to the lungs = PE
- Anticoagulants guideline treatment
coagulation cascade
fibrinogen –> fibrin –> fibrin mesh –> insoluble
full coagulation cascade
risk factors for thromboembolism
- pregnancy X6
- prolonged immobolisation x3
- previous VTE x3
- contraceptive pill x3
- long haeul travel x3
- cancer
- heart failure
- obesity
- surgery >30 mins
- HRT
- thrombophilia
ALLL MAKES YOU HYPERCOAGULABLE
Presence of risk factors in patients with PE
- 50% have an identifiable temporary risk factor
- Surgery
- Oestrogen treatment
- 25% have cancer (permanent risk factor)
- 25% have no identifiable risk factor
- Need to consider undetected malignancy- evaluate risk factors e.g. smoking and cancer
Pancreatic cancer=
highest risk of DVT/PE
Hypercoagulable conditions
*
- Hypercoagulation workup performed if no obvious cause for embolic disease- screen for:
- Antithrombin III deficiency- natural blood thinner
- Factor C or protein S deficiency or resistance
- Factor V Leiden mutation- causing resistance to activated protein C is the most common risk factor for DVT/PE in younger people
- Lupus anticoagulant
- Homocystinuria
- Occult neoplasm
- Connective tissue disorders such as RA
sudden death in
20% - many asymptomatic
Pathophysiology of clinical outcomes in PE:
- Acute right ventricular overload (death)
- Pulmonary artery pressure increases if more than 30% of the total cross section of pulmonary arterial bed occluded
- This leads to acute right ventricular dilatation and strain
- Also inotropes are released by the body in attempt to maintain systemic BOL these cause pulmonary artery vasoconstriction that further exacerbates situation- right heart collapse
- Main cause of death in PE is acute right sided heart failure leading to:
- Cardiogenic shock with circulatory failure
- Increased afterload for RV Right heart collapse
- Because the right ventricle is working so hard it pushes into the left ventricle through the interventricular septum
- Decreases amount of space in LV
- EDV decreased- preload decreases
- Cardiogenic shock and death
- Cardiac arrest secondary to arrhythmias
- Cardiogenic shock with circulatory failure
Pathophysiology of clinical outcomes in PE:
- respiratory failure
- Due to areas of ventilation perfusion mismatch
- Low right ventricle output
- Shunt with patent foramen ovale
Pathophysiology of clinical outcomes:
- Pulmonary infarction
- Small distal emboli may create areas of alveolar haemorrhage
- Resulting in haemoptysis, pleuritis and small pleural effusion
- Pulmonary infarction
- Relatively uncommon- approx. 10-20% cases- may be visible on CXR as wedge shape
- Symptoms of PE
some people have zero symptoms- need to consider PE in context of risk factors
- dyspnea
- pleuritic chest pain
- cough
- substernal chest pain
- haemoptysis
- syncope
- unilateral leg pain
- fever of less than 39oC
- chest wall tenderness upon palpation without hisotry of trauma, may be sole physical finding in rare cases
- Haemoptysis-
coughing up blood
signs of PE
- tachypnea>16/min
- rales or decreased breath sounds
- accentuated second heart sounds
- tachycardia
- fever >37.8
- diaphoresis
- thrombophlebitis
- lower extremity oedema
- cardiac murmus
- cyanosis
diaphoresis
sweating
Thrombophlebitis
(throm-boe-fluh-BY-tis) is an inflammatory process that causes a blood clot to form and block one or more veins, usually in your legs.
IMPORTANT
- Symptoms of PE may be mild and generally recognised symptoms may be absent in pts with the largest PE
- High or intermediate probability objective clinical assessment may suggest need for diagnostic studies, but low probability objective clinical assessment may be present even in pts with PE
- Maintenance of high level of suspicion is critical for the identification of pts in whom diagnostic tests may be necessary
- History
- Risk factors key
Main differential diagnoses
- Pneumothorax
- Pneumonia
- MI
- Pericarditis
- Pleurisy
- Musculo-skeleta; chest pain
Investigations
- blood gases
- CXR
- ECG
- Blood gases
- May show hypoxaemia and hypocapnia (resp alkalosis) due to hyperventilation
- Undertake if evidence of hypoxaemia requiring oxygen
- In a small proportion of pts arterial PaO2 may be normal
CXR
- By far most common finding in PE is a normal CXR
- May be used to exclude other diagnosis
- Not useful as primary diagnostic tool
- Classic finding- peripheral wedge shape
classic ECG finding in pulmoanry embolism
SIQIIITIII
SI
deep S wave in lead I
QIII
Q wave in III
TIII
inverted T wave in III
ECG will show
- Signs of right ventricular strain
- T wave inversion in V1-V4 and inferior leads II, III and aVF
- Classic finding is SIQIIITIII
- Deep s wave in lead I, Q wave in III, intervted T In III- 20% of pts with PE
*
- Deep s wave in lead I, Q wave in III, intervted T In III- 20% of pts with PE
- People who have PE are prone to
Supraventiruclar Tachyarrhythmias
further investigations
D -dimer
what is D-dimer
- Fibrin degradation product, a small protein fragment released into blood when a thrombus is degraded by fibrinolysis
- Normal D-dimer
rules out PE in those at LOW risk of PE
in those at HIGH risk of PE, negative D-dimer
- does not have a high enough negative predictive value need further imaging tests
what is used to decide likelihood of PE
modified wells score
-
Modified Wells score
*
- Stratify people into different risk categories, so that most appropriate diagnostic pathway or treatment pathways can be followed
-
Two risk categories
- Likely
- Unlikely
Imaging for PE
CT pulmonary angiography (CTPA)
e.g. saddle embolus
Treatment of PE
- Do not forget oxygen
- Decrease hypoxic vasoconstriction
- Immediate heparinisation
- Reduces mortality
- Subcutaneous low molecular weight heparin used
How does heparinisation reduce mortality
- Stops thrombus propagation in pulmonary arteries and allows body’s fibrinolytic system to lyse thrombus
- Stops thrombus propagation at the embolic source and reduces frequency of further pulmonary embolism
- Does NOT DISSOLVE THE CLOT- body does that
what do we have to be careful with heparinisation
for heparin induced thrombocytopenia (0.1-0.2% )
heparin induced thrombocytopenia (0.1-0.2% )
- Heparin induced thrombocytopenia (HIT) most important and frequent drug induced, immune mediated type of thrombocytopenia
- Much lower incidence with LMW heparin- but may still occur
- Body produces antibodies to a portion of heparin that also recognise heparin-platelet complexes- binding of antibody to platelets activates them, platelet clumps are formed leading to thrombi
- LOW PLATELET COUNT- but paradoxically increased risk thrombosis
- Thromboembolic complications can be venous, arterial or both
- Include DVT, PE, myocardial infarction, thrombotic stroke and occlusion of limb arteries
treatment of heparin induced thrombocytopenia
-
immediate cessation of all formulations of heparin
- But may not stop continuing thrombin generation nor avoid thrombotic events (40% pts)- need to use non-heparin based anti-coagulants
Treatment of high risk PE patients
- Haemodynamic support
- Resp support
- Exogenous fibrinolytics (streptokinase/tPA)
- Peripheral intravenous
- Delivered directly via a percutaneous catheter into the pulmonary arteries
- Percutaneous catheter directed thrombectomy
- Surgical pulmonary embolectomy
- Surgical pulmonary embolectomy
What happens after initial heparinisation? Long term treatment
*
- Oral anticoagulant e.g. warfarin or direct oral anticoagulant DOAC e.g. rivaroxaban now increasingly prescribed- lowerk risk bleeding
- For 3 months if there is an identifiable temporary risk factor (50%)
- Indefinitely if cancer or no identifiable risk factor (50%)
- Which pts cannot be safely anticoagulated?
- Oesophageal varices
- Previous haemorrhagic stroke
- Retroperitoneal bleed
- Severe thrombocytopenia
What if cant use any form of anti-coagulation
Inferior vena cava filter
Prevention DVT/PE (outpatient)
*
- Should an obese women who smokes me on COCPs or HRT
- Advice for people with thrombophilia who travel >4 hours
- Prevention DVT/PE (Inpatient)
- DVT prophylaxis after surgery
- DVT prophylaxis for patients with malignancy
- Reduce immobility
Need to balance risk of DVT vs risks of
bleeding re active prophylaxis
