Pulmonary Embolism and Fat Embolism
Syndrome
Presentor
Nur Safwanah
Ng Ser Hui
Supervisor: Dr. Dhanraj
Pulmonary Embolism
Venous thromboembolism
• Comprises of deep vein thrombosis (DVT)
and pulmonary embolism (PE)
• 70% are hospital acquired
• PE accounts for 6% hospital deaths
Natural history
• risk of VTE highest following major
orthopedic surgery - vessel damage and
immobility
• risk of fatal PE highest 3-7 days after
surgery
• 50% resolution occurs 2-4 weeks of
treatment
• complete resolution in 2/3rd of patients
• active cancer and APLS are risk factors for
recurrence
Pathogenesis
•Accidental injury
•Surgical insult
•Smoking
Hereditary
•Thrombophillia
Virchow's
Acquired Triad
•Cancer
•Chemotherapy •Immobility
•OCP/HRT •Varicose veins
•Pregnancy •Venous obsctruction
•Obesity
Risk factors
• obesity (BMI>30) • family h/o VTE
• smoking • recent leg trauma / plaster
• malignancy • recent abdominal / pelvic
• APLS surgery
• estrogen containing • bedridden >3 days
OCP • nephrotic syndrome
• HRT • sickle cell disease
• pregnancy • thalassemia
• post partum (12w) • inflammatory bowel
• previous VTE disease
Identify patients at risk of VTE
• Surgical or trauma patients:
– surgical procedure with a total anaesthetic and surgical time
of >90 mins or >60 mins if the surgery involving pelvis or
lower limbs
– acute surgical admission with inflammatory or intra-abdominal
condition
– expected significant reduction in mobility
– one or more risk factors for VTE
Symptoms & Signs
• sudden onset pleuritic • tachypnea (RR>20)
chest pain • tachycardia (PR>100)
• fever (T>37.8)
• shortness of breath
• diaphoresis
• cough • mental confusion
• hemoptysis • hypotension
• calf or thigh pain • elevated JVP
• asymptomatic
PE - Wells' score
Clinical feature Points
Clinical signs & symptoms of DVT (minimum leg swelling & pain with 3
palpitation of deep vein)
An alternative diagnosis is less likely than PE 3
Heart rate > 100 bpm 1.5
Immobilization or surgery in previous 4 weeks 1.5
Previous DVT / PE 1.5
Haemoptysis 1
Malignancy (on treatment, treated in the last 6 months / palliative) 1
PE likely > 4 points
PE unlikely <= 4 points
Investigations
1. ABG: low PaO2 and low O2 saturation
2. ECG: non-specific; S1Q3T3 / RBBB / RV hypertrophy
3. CXR: exclude differential diagnoses
Westermark sign – area of oligaemia Hampton hump – well-defined pleural based
distal to large vessel occluded by opacity representing haemorrhage and necrotic
pulmonary embolus lung tissue in a region of pulmonary infarction
4. ECHO: Right side strain / thrombus visualisation
5. CTPA - gold standard
6. Duplex ultrasonography
Resuscitation
• ABC
• Oxygen / mechanical ventilation
• IV access
• Fluid resuscitation
• Analgesia – IV morphine 5-10mg with
antiemetics
• Inotropes – dopamine, dobutamine,
noradrenaline
• Blood investigations, CXR, ECG
VTE prophylaxis
Mechanical
Intermittent
Anti-embolic Foot impulse pneumatic
stockings device compression
device
• calf pressure 14-15mmHg
•do not offer if:
- PAD
- neuropathy
- local conditions
- allergy
- cardiac failure
- severe edema
- major deformity
Pharmacological
Low molecular Enoxaparin 40mg daily
weight heparin Tinzaparin 3500-4500 units daily
Fondaparinux Fondaparinux 2.5mg daily (6H after surgery)
sodium CI: severe renal impairment
Rivaroxaban Rivaroxaban 10mg daily (6-10H after surgery)
Dabigatran etexilate Dabigatran 110mg (1-4H after surgery), then 220mg
daily
for severe renal impairment (eGFR<15)
Unfractionated
heparin UFH 5000 units BD
platelet monitoring every 2-3 days
Treatment
1. LMW heparin (5 days or INR >2 for 24H) + warfarin
- enoxaparin 1mg/kg BD or tinzaparin 175units/kg OD
2. Thrombolytic therapy
- for patients with PE and hemodynamic instability (SBP<90)
- t-PA 100mg over 2H --> therapeutic heparin infusion
- streptokinase 250,000IU bolus --> 100,000IU/hr for 24H
- Thoracotomy (unsuitable for thrombolysis) – embolectomy
3. Graduated elastic compression stockings - 2 years
4. Temporary inferior vena cava filters (for patients contraindicated to
anticoagulants)
VTE prophylaxis for inpatients
• Orthopaedic surgery patients
• Offer combined mechanical and
pharmacological methods for lower limb
surgery
• Do not routinely offer to patients with
upper limb surgery
Fat Embolism Syndrome
Fat Embolism Syndrome
• FES: serious manifestation of fat embolism
occasionally causing multisystem dysfunction
• Highest incidence in closed, long bones
fracture of lower extremities, particularly femur
• Risk of FES highest in age 10 – 40 years old
• More frequently in men than women
Risk Factors
Causes
Trauma Non-Trauma
Blunt Trauma Pancreatitis
Long Bone (Femur, Tibia, Pelvis)
fractures, orthopedic procedures
Soft tissue injuries Osteomyelitis
Burn Bone Tumor Lysis
Liposuction Sickle Cell Crisis
- Bone Marrow necrosis due to
hypoxia
Bone Marrow Harvesting and
Transplant
Pathophysiology
• End Organ Pathology is thought to be
mediated by 2 processes
– Mechanic obstruction
– Biochemical injury
Mechanical Theory
• Fat cells in bone marrow gain access to
the venous sinusiods after trauma
– Fat cells have potent Proinflammatory and
prothrombotic potential
• Trigger rapid aggregation of platelet and
accelerate fibrin generation as they travel
through venous system and eventually
lodge into pulmonary arterial circulation
Mechanical Theory - cont
• Pulmonary capillary obstruction leading to
– Interstitial haemorrhage
– Edema
– alveolar collapse
– Reactive hypoxemic vasoconstriction
• Fat cells may also enter arterial circulation via patent
foramen ovale or directly through pulmonary capillary
bed
– Causing characteristic Neurological and Dermatological
findings
Biochemical Theory
• Bone marrow fat broken down by tissue lipase,
resulting in high concentration of glycerol and
toxic free fatty acids
• Intermediate product leads to end organ
dysfunction
– Lung: toxic injury to pneumocytes and pulmonar
endothelial cells causing vasogenic and cytotoxic
edema as well as hemorrhage
• Damaged pulmonary endothelium trigger
proinflammatory cascade, leading to
development of acute lung injury or ARDS
Clinical Presentation
• Multisystem dysfunction typically
presenting 12 – 72H after initial insult
• Classic Triad
– Hypoxemia
– Neurological abnormalities
– Petechiae
Clinical Presentation
• Pulmonary • Neurological Deficit
manifestation are – Focal deficits
among the most – Confusion
common initial signs – Lethargy
– Dyspnea – Restless
– Hypoxemia – Coma
– Tachypnea
– Respiratory Failure
Clinical Presentation
• Dermatological • Hematological
• Petechiae – Unexplained anemia
– Located in – Thrombocytopenia
nondependent regions • Other non specific
• Conjunctiva signs
• Head
– Fever
• Neck
• Anterior Thorax – Retinopathy
• Axilla
•Gurd’s criteria were used most
widely,
Laboratory and Imaging Findings of FES
Treatment and Prevention
• Principle of Management:
– Supportive treatment to maintain oxygenation
and ventilation
– Support hemodynamic
– Resuscitate with fluids and blood products
• because shock can exacerbate the lung injury
caused by FES
Treatment and Prevention
• Early Fracture stabilization in stable
patients (within 24 hours of trauma)
• Reducing risk of fat emboli
– External fixation or fixation with plates and
screws produces less lung injury than nailing
the medullary cavity
– Venting the medullary canal during nailing
reduces the number of emboli
– Use small diameter nails and unreamed nailing
Reference
• Rothberg, D. and Makarewich, C., 2019. Fat
Embolism and Fat Embolism Syndrome. Journal of
the American Academy of Orthopaedic Surgeons,
27(8), pp.e346-e355.
• Kosova, E., Bergmark, B. and Piazza, G., 2015. Fat
Embolism Syndrome. Circulation, 131(3), pp.317-
320.
• Uransilp, N., Muengtaweepongsa, S.,
Chanalithichai, N. and Tammachote, N., 2018. Fat
Embolism Syndrome: A Case Report and Review
Literature. Case Reports in Medicine, 2018, pp.1-6.
