Pulmonary Embolism
Moderator : Dr. Hardika
Presenter : Dr. Mohit Jagga
Introduction
•Pulmonary embolism (PE) is a medical emergency where
pulmonary artery or its branches are blocked with
embolic substances like- Fat, tumour cells, air, amniotic
fluid and most commonly blood clots.
•Most cases are not life threatening.
•Incidence: 23-69 cases/100,000 population/year in India
•Mortality of acute PE is approx. 30%, which can be
reduce to 2-10% by appropriate management
Types of PE
•Massive PE: Acute PE with obstructive shock or SBP < 90
mmhg or a drop in SBP > 40 mmhg for > 15 minutes
•Sub-massive PE: Acute PE without systemic hypotension
(SBP ≥90 mm Hg) but with either RV dysfunction or
myocardial necrosis
•Non-massive or low risk PE: None of the above severe
features.
Risk factors for PE
•Alteration of blood flow:
–Prolonged immobilisation
–Obesity
–Pregnancy
–Cancer
•Factors in blood vessel wall:
–Surgery
–Catheterisation
–Trauma
•Hypercoagulable states:
–Estrogen containing OCP
–Genetic thrombophilia (Factor V Leiden deficiency,
Protein C and Protein S deficiency, antithrombin III
deficiency)
–Acquired thrombophilia (antiphospholipid
syndrome, nephrotic syndrome, paroxysmal
nocturnal haemoglobinuria)
Virchow’s Triad
Clinical features for PE
Symptoms
•Dyspnea
•Pleuritic chest pain
•Cough
•Calf or thigh pain or swelling or both
•Haemoptysis
•Syncope
Signs
•Tachypnea
•Tachycardia
•Arrhythmia
•Jugular venous distension
•ABG
•ECG
•Chest x-ray
•Blood investigation:
–D-dimer
–Prothrombin time (PT)
–Partial thromboplastin time (PTT)
–Platelet count
–Troponin and NT ProBNP
•Trans-oesophageal echocardiography
•Precordial doppler USG
•CT pulmonary angiography
•V/Q Scan (lung scan)
Investigations
ABG findings
•pH = ↑
•PaO2 = ↓
•PaCO2 = ↓
•HCO3 = Normal
•Aa gradient = Large (PAO2 - PaO2)
•Hypoxemia, widened A-a oxygen gradient, respiratory
alkalosis
•Massive pulmonary embolism - Combined respiratory
(hypercapnia) and metabolic acidosis due to hemodynamic
collapse
•Sinus tachycardia
•Tall peaked T waves in V1- V4
•S1Q3T3 pattern: Not specific. Can be seen in any Cor
pulmonale syndrome
•RBBB
•Supraventricular and ventricular tachyarrhythmias
ECG findings
S1Q3T3 pattern ECG
•Mostly normal findings
•Done to exclude other pathology
•Pleural effusion
•Specific signs:
–Hampton’s hump - Dome shape pleural based
opacification in lung.
–Westermark sign – Focus of oligemia seen
distal to PE
–Palla sign – enlarged right pulmonary artery
Chest x-ray findings
Hampton’s hump
Westermark sign
Palla sign
D-dimer test
•D-dimer is a type of Fibrin degradation product
•Can be raised due to a number of reasons
•Level less than 500 ng/ml exclude pulmonary
embolism
•Negative D-dimer rules out PE/DVT in 98% cases
•False positive D-dimer: infection, pregnancy, renal
failure, post-operative
Other investigations
•Prothrombin time (PT)
•Partial thromboplastin time (PTT)
•Platelet count
•Troponin and NT ProBNP to risk stratify
•Invasive
•Most sensitive
•Detect macro and micro emboli
•Direct visualisation of thrombus in pulmonary artery
•Right heart changes:
–increased RV size
–decreased RV function
–Tricuspid regurgitation
•Abnormal septal wall motion
•Small left ventricle
•McConnell's sign- regional RV dysfunction, with akinesia of the
mid free wall but normal motion at the apex.
Trans-esophageal echocardiography
Echocardiogram in PE
Precordial Doppler USG
•Most sensitive in non-invasive techniques
•Probe positioning – either the right or left sternal border
(2
nd
to 4
th
intercostals space)
•The probe is placed along right heart border to pick up the
signal from the right ventricular outflow tract
•Positioning is confirmed by injection or bubble test
(Injection of an air agitated 10 ml bolus mixture of 1 ml air
in 9 ml saline
•Bubble test is helpful in obese patients
–The 1
st
evidence of pulmonary air embolism is a change
in the character and intensity of the emitted sound
–Turbulent resonance of normal blood flow passing
through the right cardiac chambers is superimposed by
an erratic high pitch swishing roar.
CT Pulmonary angiography
Gold standard for diagnosis of PE
Indications:
- Suspected PE
Contra-indications:
- Renal failure
- Pregnancy
- Allergy to radio-contrast
Procedure:
- Radioactive iodine administered IV
- CT scan performed
Treatment options
•Non-massive PE: Anticoagulation
•Sub-massive PE: Strongly consider
thrombolysis/embolectomy but need to
balance risk of bleeding
•Massive PE: Thrombolysis/embolectomy
Treatment Of PE
•Symptomatic treatment:
–ABCD approach
–Oxygen
–Analgesia
•Anticoagulation
•IVC filter: If there is contra-indications for anti-coagulation
•Thrombolysis: tPA eg: Alteplase, Tenectaplase
•Surgical procedures: Pulmonary embolectomy
Anticoagulation
IV Unfractionated Heparin:
–80 units/kg or 5000 IU bolus followed by
–18 units/kg/hr infusion
•Monitor aPTT - keeping between 1.5 – 2.5 times the control
value (in sec.)
•Side effects:
–HITS (Heparin induced thrombocytopenia syndrome):
paradoxical hypercoagulable state leads to clots
–Bleeding
Low molecular weight Heparin (LMWH)
Enoxaparin (Clexane):
•1.5mg/kg s/c once a day Or 1mg/kg s/c twice a day
•1 mg/kg s/c once a day in renal impairment
Duration: 6 to 9 months
Side effect: Low HITS (Heparin induced thrombocytopenia
syndrome)
Dalteparin:
•5000 units s/c twice daily or 200 units/kg daily
Tinzaparin:
•175 units/kg once daily
Fondaparinux:
•Wt < 50kg – 5mg s/c once a day
•Wt 50-100kg – 7.5mg s/c once a day
•Wt >100kg – 10mg s/c once a day
Thrombolysis
•Indications:
–Massive PE
–Sub-massive PE where risk of bleeding low
•Contraindications:
–Bleeding, recent stroke, current GI bleeding, bleeding
PUD, surgery within 7 day, prolonged CPR
•Drugs:
–Alteplase 100mg IV: 15mg IV stat followed by 85mg
over 2 hours
–Followed by Heparin infusion
IVC filter
Indications:
- DVT with massive pulmonary embolus
- Recurrent PE not treatable with anticoagulation
- Absolute contra-indications for anti-coagulation
- Trauma patients
PE in Pregnancy
•All three components of Virchow’s triad are affected during
pregnancy
•D-dimer has high negative predictive value. False positive result
is common
•V/Q scan is preferred technique
•CTPA can be done if VQ is inconclusive
•Preferred treatment option: LMWH
•Warfarin is contraindicated
•Neck procedures
- Radical neck dissection
- Thyroidectomy
•Ophthalmologic
- Eye surgeries
•Cardiac
- Coronary surgeries
2.Previous history of PE
3.Manipulation of tumour with intravascular extension
Diagnosis
Clinical signs
•Sudden cardiovascular collapse
•Hypoxemia
•Bronchospasm
•Desaturation or central cyanosis
•Air in surgical field and vascular line
Monitoring
•Raised CVP or distended neck veins
•Decrease end tidal co2 concentration
•Changes in ECG
•Decrease Spo2(%)
Management of Intraoperative PE
1.The surgeon should be notified so that he/she can flood the surgical
field with saline or pack it with wet gauge
2.Nitrous oxide if used should be discontinued
3.Institute high flow oxygen- 100%
4.If central venous catheter is present it should be aspirated in an
attempt to retrieve the entrant air in case of air embolism
5.Intravascular volume infusion
6.Vasopressors should be given to treat hypotension
7.If persistent circulatory arrest then do chest compressions
and CPR
8.Anticoagulants- Low molecular weight heparin
9.Thrombolytic agents
10.Pulmonary embolectomy
11.Post operative IVC filter
Prevention of PE
•Control of obesity
•Stop smoking
•Stockings
•For hospitalized patients (immobility/bedrest):
–Heparin: 5000 units/day IV
–Pneumatic compression
Complications of PE
•Acute bleeding during treatment
•Pulmonary infarction
•Cardiac arrest or death
•Chronic thromboembolic pulmonary
hypertension
•Heparin associated thrombocytopenia
•Recurrent venous thromboembolic event
Case Scenario
•A 67-year-old male patient was admitted to
hospital with severe community-acquired
pneumonia and acute respiratory failure. He was
treated with antibiotics and mechanical
ventilation. He improved with the treatment and
was extubated on day 4. On day 7, he suddenly
developed acute severe breathlessness and
chest pain.
1.Initiate Resuscitation
–Provide oxygen.
–If the patient is hypotensive, administer 500-1000 mL isotonic crystalloid
–Vasopressor therapy
–Mechanically ventilate if there is respiratory collapse
–Record a detailed medical history and perform physical examination.
2.Assess the Risk Factors
3.Assess Clinical Probability of PE: They may vary from asymptomatic, mild
symptoms to shock or sudden death. Clinical probability of PE is based on
clinical decision rules Revised Geneva score or Revised Wells score.
4.Initiate Treatment: While diagnostic confirmation is awaited, anticoagulant
treatment with subcutaneous low-molecular-weight heparin (LMWH),
fondaparinux, or intravenous unfractionated heparin (UFH) should be initiated
as soon as possible.
5.Order Investigations:
–Electrocardiogram, X-ray chest (PA view), and arterial blood gas analysis
should be ordered in all these patients. Although these tests are nonspecific,
they do increase the index of suspicion.
–Baseline prothrombin time (PT), partial thromboplastin time (PTT), and
platelet count. Renal functions test to assess safety of contrast for CTA.
Troponin and NT ProBNP to risk stratify.
–If the patients is hemodynamically stable- CT pulmonary angiography (CTP),
–If the patients is hemodynamically unstable- transesophageal
echocardiography (TEE) and lower extremity ultrasonography with Doppler
–V/Q scan is reserved for patients in whom the CTPA is contraindicated like in
severe contrast allergy, high risk of contrast nephropathy, hypotension,
advanced heart failure.
–When both CTPA and V/Q scan both are contraindicated, Magnetic
Resonance Pulmonary Angiography (MRPA)
6.Identify the Risk of Adverse Outcome
7.Consider Thrombolysis
8.Consider Invasive Treatment
9.Hemodynamically Stable Patients with PE without Myocardial Dysfunction
or Injury
And finally…
PE is often over-diagnosed;
PE is often under-diagnosed;
Both conditions result in increased cost,
morbidity, mortality and medico-legal issues.