FES & PE

1. FAT EMBOLISM SYNDROME
&
PULMONARY EMBOLISM FARAH AZUREEN ABD ZAIM

2. FAT EMBOLISM SYNDROME
BACKGROUND
EPIDEMIOLOGY
CAUSES
PATHOPHYSIOLOGY
CLINICAL FEATURES
DIAGNOSTIC CRITERIA
INVESTIGATIONS
TREATMENT
REFERENCES

3. BACKGROUND
First diagnosed in 1873 by Ernt Von Bergmann
A systemic inflammatory cascade affecting multiple
organ systems, particularly involving the triad of
lungs, brain, and skin.
___Key points
Fat embolism syndrome is a clinical diagnosis with non-specific/insensitive diagnostic tests;
A high index of suspicion is important to ensure diagnosis;
The classic triad of respiratory changes, neurological abnormalities, and petechial rash is not always present;
Treatment is supportive;
Prophylactic steroid therapy may be considered for patients at a high risk

4. DEFINITION
Fat Emboli : Fat particles or droplets that
travel through the circulation.
Fat Embolism : A process by which fat
emboli passes into the bloodstream and
lodges within a blood vessel.
Fat Embolism Syndrome (FES) : A
physiological response to fat within the
systemic circulation. It occasionally causes
multisystem dysfunction, the lungs are
always involved and next is brain.

5. EPIDEMIOLOGY
 Most commonly associated with long bones fractures and the
pelvis and more frequent in closed rather than open fractures.
 Incidence increases with number of fractures involved.
 3-4% with isolated long bone trauma
 10-15% with polytrauma
Some cases are associated with trauma in the absence of
fractures and rare cases.
Mortality is estimated to be 5–15% overall, but most patients will
recover fully.
Orthobullet

6. CAUSES
TRAUMA RELATED NON TRAUMA RELATED
Long bone fractures (e.g. femur, tibia) Acute pancreatitis
Pelvic fractures Diabetes mellitus
Fractures of other marrow-containing
bones
Osteomyelitis
Orthopaedic procedures (e.g.
intramedullary nailing, pelvic and knee
arthroplasty)
Bone tumor lyses
Soft tissue injuries (e.g. chest
compression with or without rib
fractures)
Steroid therapy
Liposuction Sickle cell hemoglobinopathies
Bone marrow harvesting and transplant Alcoholic (fatty) liver disease
Burns Lipid fusion

7. PATHOPHYSIOLOGY
Exact pathophysiology of FES remains unclear.
Two theories have been proposed regarding causes of FES :
1. Mechanical theory
 embolism is caused by droplets of bone marrow fat released into venous system
2. Biochemical theory
 stress from trauma causes changes in chylomicrons which result in formation of fat
emboli

9. 1. Mechanical Theory
Fat droplets, released by marrow of adipose tissue following injury,
embolise throughout circulation causing microvascular occlusion.
As they travel through the venous system, they trigger rapid
aggregation of platelets and accelerated fibrin generation, eventually
lodging in the pulmonary arterial circulation.
Pulmonary capillary obstruction leads to interstitial hemorrhage and
edema, alveolar collapse, and reactive hypoxemic vasoconstriction.
Massive fat emboli may also lead to macrovascular obstruction and
shock.
 Fat cells may also enter the arterial circulation via a patent foramen
ovale or directly through the pulmonary capillary bed, causing the
characteristic neurological and dermatologic findings FES.

11. 2. BIOCHEMICAL THEORY
Toxicity of Free Fatty Acid (FFA)
Circulating FFA directly affect pneumocytes, producing abnormalities
in gas exchange.
Co-existing shock, hypovolemia and sepsis impair liver function and
augment effect of FFA
Hormonal changes caused by trauma or sepsis induce systemic
release of FFA as chylomicrons.
Acute-phase reactants (CRP) cause chylomicrons to coalesce.
It explains non traumatic form of FES and why symptoms take 12
hours to develop.

13. CLINICAL FEATURES
May develop 24-72h after trauma or surgery
Characterized by classic triad of FES:
i. Respiratory failure
ii. Neurological abnormalities
iii. Dermatological changes

14. i. RESPIRATORY CHANGES
1st clinical feature to present (earliest)
Dyspnea, tachypnea, hypoxemia
May progress to respiratory failure and acute respiratory distress
syndrome (ARDS)

16. ii. NEUROLOGICAL
ABNORMALITIES
Typically manifest after the respiratory changes.
Resulted from cerebral embolism which produce neurological signs
in up to 86% of cases.
Leads to wide spectrum of changes: mild confusion and drowsiness
to severe seizures.
More common presentation : acute confusional state.
Focal neurological signs may also present including hemiplegia,
aphasia, apraxia, visual field disturbances, anisocoria and decorticate
posturing.
Almost all neurological deficits are transient and fully reversible.

17. iii. DERMATOLOGICAL CHANGES
Petechial rash (non palpable). It occurs in up to 60% of cases.
Last component of the triad to develop. Appears within first 36h and
is self-limiting and disappear within 7 days.
Due to embolization of small dermal capillaries leading to
extravasation of erythrocytes.
Location : conjunctiva, oral mucous membrane, skin fold of the
upper body especially neck and axilla.

19. OTHER CHANGES..
Pyrexia
Cardiovascular changes include tachycardia, myocardial depression,
ECG changes indicative of right heart strain
Retina shows soft fluffy retinal exudates with macular oedema
scotomata (Purtscher's retinopathy)
Renal changes such as oliguria, lipiduria, proteinuria, or haematuria.
Hepatic damage may manifest as jaundice.

20. DIAGNOSIS CRITERIA
Diagnosis of FES is usually made from clinical findings.
The most commonly used criteria is Gurd’s and Wilson’s Criteria.
Other indexes:
Lineques’s criteria
Schonfeld’s criteria

21. GURDS’S DIAGNOSTICCRITERIA
MAJOR
Hypoxemia (Pao2 < 60mmHg)
CNS depression (changes in mental
status)
Petechial rash
Pulmonary edema
MINOR
Tachycardia
Pyrexia
Retinal emboli
Fat in urine or sputum
Jaundice
Renal changes
Laboratory features:
• Thrombocytopenia
• Elevated ESR
• Anemia
• Microglobulinemia
AT LEAST 1
MAJOR +
4 MINOR

22. LINDEQUE’S CRITERIA

23. SCHONFELD’S CRITERIA
-a quantitative measure to diagnose FES
-it ranks signs and symptomsof fes in relation to their incidence of
presentation

24. LABORATORY STUDIES
ARTERIAL BLOOD GAS
Hypoxemia (PaO2<60mmHg)
HEMATOLOGICAL TESTS
Thrombocytopenia
Anemia
High ESR

25. BIOCHEMICAL TESTS
Liver function test
Renal profile
Serum electrolytes, e.g hypocalcemia
URINE & SPUTUM EXAMINATION
May detect fat globules
Non specific
Blood lipid concentration is not helpful for diagnosis because
circulating fat concentrations do not correlate with the severity of the
syndrome.

26. IMAGING
CHEST X-RAY
May be normal initially
Shows multiple flocculent shadows (snow storm appearance)
Serial radiographs reveal increasing diffuse bilateral pulmonary
infiltrates
ECG
Evidence of right heart strain / ischemic patterns and tacycardia.

28. TREATMENT & PREVENTION
There are no specific therapy for FES.
Prevention, early diagnosis, and adequate symptomatic treatment
are important.
Mainstay of treatment : supportive

29. SUPPORTIVE MEDICAL CARE
Maintenance of adequate oxygenation and ventilation
Maintenance of hemodynamic stability
Administration of blood products as clinically indicated
Adequate hydration
Prophylaxis of deep venous thrombosis
Nutrition
Adequate analgesia

30. Maintenance of adequate oxygenation and ventilation
High flow rate oxygen is given to maintain the arterial oxygen
tension in the normal range.
Mechanical ventilation and PEEP may be required to maintain arterial
oxygenation.
Hemodynamic stability
Maintenance of intravascular volume is important, because shock
can exacerbate the lung injury causes by FES.
Albumin has been recommended for volume resuscitation in addition
to balanced electrolyte solution.
It restores blood volume and also binds with fatty acid and thus
decrease of lung injury.

31. PROPHYLAXIS
1) Early fracture stabilization
Early fracture stabilization (within 24 hours) of long bone fracture
2) Reduce risk of fat emboli
Limit the elevation in intraosseous pressure during orthopaedic
procedures
It reduces the intravasation of intramedullary fat
E.g : use of external fixation for definitive fixation of long bone
fractures.
3) Adequate fluid resuscitation and maintenance of hydration
Maintenance + deficit

32. EXAMPLE OF CALCULATION:
A 70 kg man sustained closed fracture of
left tibia.
Eg:
Hip : 2L
Femur : 1.5L
Tibia : 1L
70kg
Maintenance
=1000mL+500mL+ 1000mL
=2500mL (5pints)
Deficit (tibia)
=1000 (2pints)
Total
=7 pints/24 hours

33. VENOUS THROMBOEMBOLISM
(VTE)
Encompasses two interrelated conditions
Pulmonary embolism (PE)
Deep vein thrombosis (DVT)
They share common risk factors,
pathophysiologies and management

34. RISK FACTORS
3 main factors contribute to the development of VTE:
Venous stasis
•Prolonged immobility
•Heart failure
Hypercoagulability
•Inherited condition
(Protein C or S def)
•Acquired (malignancy,
pregnancy)
Endothelial injury
•Direct trauma
•Local irritation
(chemotherapy, past DVT)

35. CONT’D
Inherited
• Factor V Leiden mutation
• Antithrombin III def.
• Protein C def.
• Protein S def.
• Activated protein C resistance
Acquired
• Malignancy
• Elevated hormone conditions (HRT, OCP)
• Elevated antiphospholipid antibody
conditions (lupus anticoagulant,
anticardiolipin antibody)
• Previous thromboembolism
• Obesity
• Aging
• Varicose vein
• Smoking
• Immobilization
• General anesthetic

36. PULMONARY EMBOLISM (PE)
PE is the obstruction of blood flow to one or more arteries of the lung by a
thrombus lodged in a pulmonary vessel.
Occur when deep venous thrombi detach and embolize to the pulmonary
circulation.
Pulmonary vascular occlusion occurs and impairs gas exchange and
circulation.
90% of PE results from DVT occurring in the deep veins of lower extremities.
Procedures associated with PE:
1. Hip fracture
2. Elective total hip arthroplasty (activation of the clotting cascade)
3. Elective total knee arthroplasty
4. Spine fracture with paralysis

38. EVALUATION
There are scoring systems to assist in the determination of likelihood
of PE and thromboembolic events.
1. Modified Wells Criteria

39. 2. Revised Geneva Score

40. INVESTIGATIONS
I. FBC : abnormalities in HB, WCC, Platelet
II. Coagulation Profile : prolongation of PT and APTT
III. Arterial blood gas : hypoxaemia, hypocapnea and respiratory
alkalosis
IV. Plasma D-Dimer : >500ng/mL. If less than 500ng/mL, PE is
excluded.
V. ECG : sinus tachycardia is often present. S1Q3T3 pattern

42. VI. Chest xray :
VI. nuclear medicine ventilation-perfusion scan (V/Q)
VII. pulmonary angiography ( gold standard)
VIII.helical chest CT (widely considered first line imaging modality)

43. PROPHYLAXIS
Prophylaxis treatment should be determined by weighing risk of
bleeding vs risk of pulmonary embolus
Prophylaxis in hip & knee replacement
mechanical prophylaxis
-compressive stockings recommended
-pneumatic compression devices (increase venous return and
decrease stasis)
medical treatment
-anticoagulation

44. TREATMENT
Continuous IV heparin infusion followed by warfarin
-as first line treatment
technique
 continuous IV heparin infusion typically given for 7-10 days
 monitor heparin therapy with PTT (partial thromboplastin time)
 warfarin therapy typically given for 3 months
 monitor warfarin therapy with INR (international normalized ratio)

45. THANK YOU..