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ALOK SINHA
Department of Medicine
Manipal College of Medical Sciences
Pokhara, Nepal
Clinically significant obstruction of part
or all of the pulmonary vascular tree,
usually caused by thrombus from a
distant site
Massive P E
Medium size P E
Small P E
Incidence

Account for up to 15% of all post-operative
deaths

Commonest cause of death following
elective surgery

Commonest cause of

Improved diagnostic methods mean that it is
probably reported more frequently
maternal death
75% thrombi generated in deep venous
system of the lower limbs and pelvis
•Heart failure
•Increased viscosity
•Small blood clots
•Prolonged immobilization
•Anti coagulant factor deficiencies
•Auto immune disorders
•Certain cancers
•Platelet disorders
•Smoking
•Contraceptive pills
Wells scoring system (to asses the clinical probability of DVT)
Score
Active cancer (patient receiving treatment for cancer within the previous 6 months or
currently receiving palliative treatment)
1
Paralysis, paresis or recent plaster immobilisation of the lower extremities
1
Recently bedridden for 3 days or more, or major surgery within the previous 12 weeks
requiring general or regional anaesthesia
1
Localised tenderness along the distribution of the deep venous system
1
Entire leg swollen
1
Calf swelling at least 3 cm larger than that on the asymptomatic side (measured 10 cm
below tibial tuberosity)
1
Pitting oedema confined to the symptomatic leg
1
Collateral superficial veins (non-varicose)
1
Previously documented DVT
1
Alternative diagnosis at least as likely as DVT
-2
Clinical probability
Total score
DVT unlikely
<2
DVT likely

.
RISK FACTORS FOR VENOUS
THROMBOEMBOLISM
Surgery
•Major abdominal/pelvic surgery
•Hip/knee surgery
•Post-operative intensive care
Obstetrics
•Pregnancy/puerperium
Cardiorespiratory disease
•COPD
•Congestive cardiac failure
•Other disabling disease
Lower limb problems
• Fracture
• Varicose veins
• Stroke/ spinal cord injury

.
Malignant disease
• Abdominal pelvic
• Advanced/metastatic
• Concurrent chemotherapy
Miscellaneous
•
•
•
•
•
Increasing age
Previous proven VTE
Immobility
Thrombotic disorders
Trauma
Cancer and venous
thromboembolism (VTE)

Previously undiagnosed cancer is frequent in
patients with unprovoked VTE

prevalence of previously undiagnosed cancer in patients with unprovoked (idiopathic) VTE (venous
thromboembolism) was 6.1% (95% CI, 5.0% to 7.1%) at baseline and 10.0% (CI, 8.6% to 11.3%) from
baseline to 12 months
risk of cancer was 4-fold greater in patients with unprovoked VTE (10%) than in those with a clear
precipitating factor (2.6%)
an extensive screening strategy using computed tomography of the abdomen and pelvis statistically
significantly increased the proportion of previously undiagnosed cancer detected from 49.4% (CI, 40.2% to
58.5%) (with limited screening alone - history and examination, routine blood tests, CXR) to 69.7% (CI, 61.1%
to 77.8%) in patients with unprovoked VTE


Inherited Thrombophilia
(propensity to develop thrombosis due to an abnormality in the coagulation system )
• 25 - 50% of patients with VTE have an identifiable
inherited thrombophilia

Antiphospholipid syndrome


Among the identified acquired thrombophilic states, it is the most common

lupus anticoagulant (LA)

anticardiolipin antibodies (ACA)
Deficiency of Protein C & S & antithrombin III
small protein molecule that inactivates several enzymes of coagulation system

Factor V leiden
Factor V
+
COAGULATION
-
Protein C & S
Anti thrombin III
• These usually need to interact with an
additional acquired risk factor to cause VTE
Inherited
thrombophilia
+
Dehydration
=
Pulmonary
embolism
(DVT)
Symptoms of DVT

Warmth, swelling, redness,
and /or pain in a leg
DVT of the calf – symptoms in the calf
 In thigh – symptoms in both thigh &/or calf

Vast majority of DVTs occurs in only one leg at
a time
 Other medical conditions can cause pain and/
or swelling in the legs

Thrombi can develop in

The heart following
• Atrial fibrillation
• Myocardial infarction
• Prosthetic valve
• Endocarditis
• In association with intraventricular septal defects
(paradoxical emboli)

AV shunts

With central venous access
Clinical features are:
Very varied
 Non specific
 Strong degree of suspicion required for diagnosis
 All information has to be examined carefully
before giving a verdict

Wow ! What a
geeeenius yar !!
I
Like a detective
am “Saarlak Homes”

The clinical features of PE depend upon
Size of embolism
 Pre existing state of myocardium & lung parenchyma
 Co-morbidity


Encompass a spectrum from
Small emboli with few or no
haemodynamic consequences
Cardiovascular collapse
Thrombi/embolus can be
Massive
Medium
Small
Acute massive PE
Large clot lodge at the bifurcation of the main
pulmonary arteries causing haemodynamic
compromise
Pathophysiology:

Major haemodynamic effects:
↓ Cardiac output
 Acute right heart failure
Symptoms:
 Severe dyspnoea
on sitting up ?
 Faintness or collapse
 Central chest pain
 Apprehension

Platypnoea
(some times)
 Isolated
dyspnoea: Acute breathlessness
in the absence of circulatory collapse
 Suspect
PE: sudden onset of unexplained
breathlessness, in the presence of risk factors
for VTE
Chest X-ray:
 Usually normal. May be subtle oligaemia

Wester mark sign
Westermark’s Sign
ECG:
 S1 Q3 T3 anterior T-wave inversion
 Right bundle branch block (RBBB)
S1-Q3-T3
•Right heart strain or
acute cor pulmonale
•Tall peaked p-waves
in II,III,AVF
•Right axis deviaton
(S>R in lead I)
•Right bundle branch
block
Arterial blood gases:
 Markedly abnormal with ↓ PaO2 and ↓ PaCO2
 Metabolic acidosis
.
Acute small/medium PE
Smaller clot travel more distally
• May infarct lung
• Pulmonary infarction is an uncommon consequence because of the
bronchial arterial collateral circulation
• Causes pleural involvement ± effusion
Symptoms:
 Pleuritic chest pain
 Restricted breathing
 Haemoptysis
• Found most often in the lower lobes, where blood
flow is greater
Some times
 Collapse (clinical deterioration)
 In
(10%)
an elderly patient with limited cardio
respiratory reserve
 Can rapidly decompensate with even a
relatively small PE
 Clinical findings non-specific and reflect the
underlying disease process, rather than the
PE itself
Signs:
 Tachycardia
 Pleural rub
 Crackles or crepitations
 Effusion (often blood-stained)
 Low-grade fever
ECG:
– Sinus tachycardia
Arterial blood gases:
– May be normal or ↓ PaCO2
Chest X-ray:
 Pleuropulmonary
 Pleural
opacities
effusion
 Linear shadows
 Raised hemidiaphragm
X Ray findings
.
Pulmonary infarction – triangular
opacity with base towards
periphery – Hamptons sign
Fleischner lines
Chronic PE
Pathophysiology:
– Chronic occlusion of pulmonary microvasculature
– right heart failure
Symptoms:
– Exertional dyspnoea
– Late symptoms of pulmonary hypertension or right
heart failure
Signs:
– May be minimal early in disease
– Later-RV heave
– loud, split P2
– Terminal-right heart failure
Chest X-ray: features of pulmonary hypertension
– Enlarged pulmonary artery trunk
– enlarged heart
– prominent RV
ECG:
– RV hypertrophy and strain
Arterial blood gases:
– Exertional ↓ PaO2 or desaturation on formal
exercise testing

DIFFICULT




Varied clinical features
Physical - signs non-specific
Lack of sensitive and specific diagnostic tests
Ask three questions:
1.
2.
3.
Is the clinical presentation consistent with PE?
Does the patient have risk factors for PE?
Is there any alternative diagnosis that can explain
the patient's presentation?
BTS PRE-TEST CLINICAL PROBABILITY SCORING

A. Patient has clinical features compatible with PE:
– raised respiratory rate
– ± haemoptysis
– ± pleuritic chest pain

Plus 2 other factors:
– 1. Absence of another reasonable clinical explanation
– 2. Presence of a major risk factor
A. + 1 and 2
 A. + 1 or 2:
 A. alone:

HIGH
INTERMEDIATE
LOW pre-test clinical probability


In > 80% cases the X ray & ECG are normal
All patients with suspected PE should have
– chest X-ray
– ECG
– arterial blood gas analysis

Help to exclude important differential diagnoses


Variety of radiographic appearances -usually
non-specific
Suspect P E in
– Normal X ray in an acutely breathless and
hypoxaemic patient
– bilateral changes in a patient presenting with
unilateral pleuritic chest pain

Most important role of the chest X-ray is to
exclude important D D
– heart failure
– pneumonia
– pneumothorax
– tumour
Arterial blood gases


Ventilation-perfusion mismatch and reduced
cardiac output with a low mixed venous
oxygen saturation and hyperventilation
Arterial blood gases show a
– Reduced Pa O 2 and a normal or low Pa C O2
– Normal in a significant minority
– Metabolic acidosis may be seen in acute massive PE with
cardiovascular collapse
Bedside echocardiography extremely helpful in:
– differential diagnosis
– assessment of acute circulatory collapse



Acute dilatation of the right heart usually
present in massive PE
Thrombus may be visible
Alternative diagnoses
– left ventricular failure
– aortic dissection
– pericardial tamponade
Can be established with confidence
Patient with acute pulmonary hypertension
due to pulmonary embolism
After clot lysis
1.
2.
3.
4.
D-dimer & other circulating markers
Ventilation-perfusion scanning
Pulmonary angiography
CTPA & MRPA
D-dimer
D-dimer: degradation product of fibrin
undergoing endogenous fibrinolysis
 Low D-dimer has a high negative predictive
value useful screening test
 Non-specific elevation of the D-dimer

myocardial infarction
 pneumonia
 sepsis


Suggestive clinical picture in a high-risk patient
must be investigated further even when Ddimer level is normal
Ventilation-perfusion scanning

Most popular method to confirm PE

Available only in few centres
A normal V/Q scan virtually excludes PE
 Low probability scan in the presence of a low
clinical probability makes PE unlikely
 High probability scan in a patient with a high
clinical probability establishes diagnosis

CTPA & MRPA

Replaced conventional pulmonary angiography
Can exclude PE
 Highlight an alternative diagnosis
 Role limited in small peripheral emboli

Utility of contrast-enhanced magnetic
resonance scanning is also being explored
 Both CT and MRI may allow simultaneous
visualisation of the pelvic and leg veins

conventional pulmonary
angiography
CTPA
MRPA
What is 'gold standard' for diagnosis of PE ?
PULMONARY ANGIOGRAPHY
(has been largely superseded by CTPA)

.
Management of acute massive PE
(mortality20%)
Oxygen - 100%
 IV access
 Send baseline bloods,

profile

Perform ECG
including clotting
Different oxygen delivery systems
Nasal canula
Non re – breather masks

Analgesia
(if required)
– Opiates – morphine sulphate

Management of cardiogenic shock
– fluids
– inotropes
to maintain right ventricular filling
Unfractionated Heparin
L.M.W.H
molecular weight: 3000 Da
20000 Da
No need for monitoring of
PT -coagulation parameter
smaller risk of bleeding
need for monitoring of
PT -coagulation parameter
risk of bleeding is more
Smaller risk of
thrombocytopenia
risk of thrombocytopenia MORE
Anticoagulant effect: not
Reversible with protamine
sulphate
Acts by inhibiting Xa
Reversible with protamine
sulfate.
Inhibits both Xa & thrombin
(by augmenting antithrombin III)
Onset Of action:
Slower
faster
Heparin

Start IV heparin unless
–Active GI bleeding or
–Intracerebral haemorrhage:
– Bolus dose 5000 - 10,000 units or 80 IU/kg
– Maintenance infusion of 1300 IU/hr or 18 units/kg/hr


Adjust infusion rate until PT 1.5 - 2.5 of control
Check 4 - 6 hours after initial bolus and 6 - 10 hours
after any dose change
Low molecular weight heparin (LMWH)
– as effective as standard unfractionated
intravenous heparin
– Unfractionated heparin should be considered
in massive PE (faster onset of action) as a
first dose bolus prior to commencement of
LMWH
Oral anticoagulation


Should only be commenced once PE is
proven -along with Heparin
Target INR 2.0 - 3.0 - heparin stopped
Length of warfarin anticoagulation



Temporary risk factor: 4 - 6 weeks.
First episode of idiopathic PE: 3 months is
currently recommended
Recurrent idiopathic PE:
– no guidelines
– risk of bleeding balanced with risk of recurrent
event.
– often long-term anticoagulation

Persisting risk factors: lifelong anticoagulation
recommended

Thrombolysis
– Massive PE presenting with hypotension
– No active GI bleeding
– No intracerebral haemorrhage


Risk of major haemorrhage is 3 - 4 times that of heparin
Embolectomy
– if thrombolysis is contraindicated
Agents used

suspected massive PE, 50 mg IV alteplase immediately



Alteplase
Streptokinase
250 000 units in 20 minutes with 100 000 units/h for 24 hours (plus
hydrocortisone to prevent further circulatory instability)
 Urokinase
IVC filter placement
Acute VTE with an absolute
contraindication to anticoagulation
 Patients with massive PE who survive

(in whom a second PE may be fatal)

Recurrent VTE despite adequate
anticoagulation
summary




Analgesia
Oxygen
IV fluids & inotrops
Anticoagulation
– Heparin & LMWH initially
– Oral anticoagulats when proved



Thrombolysis
Embolectomy
IVC filter placement

Air embolism
–
–
–
–

Rare causes
Neck vein cannulation,
intrauterine manipulations -criminal abortion
bronchial trauma
barotrauma causing air to enter the pulmonary vein and left
heart
Amniotic fluid embolism
– 1 in 25,000 - 80,000 live births
– third commonest cause of maternal death,
– most common cause of death in the immediate post-partum
period.
– Amniotic fluid enters circulation because of torn fetal
membranes
– in Caesarean section,
– uterine or cervical trauma, or uterine rupture
Fat embolism
– during surgery
– trauma
– fracture of long bone (such as the femur or pelvis)


Fat emboli are small and multiple, and so have
widespread effects.
Symptoms 1-3 days after the insult, and are
predominantly:
•
•
•
•


Pulmonary - shortness of breath, hypoxemia
Neurological - agitation, delirium, or coma
Dermatological - petechial rash
Haematological - anaemia, low platelets
Steroid prophylaxis of high risk patients reduces the
incidence
Mortality rate approximately 5-15%
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