Fat embolism syndrome occurs when fat droplets from bone marrow or adipose tissue embolize into the pulmonary circulation or systemic circulation following trauma or surgery. It is characterized by a clinical triad of respiratory issues, neurological abnormalities, and petechial rash. Diagnosis is based on clinical criteria and supportive investigations include imaging, blood tests, and identification of fat globules. Management is supportive with oxygen supplementation, ventilation if needed, intravenous fluids, diuretics, steroids, and anticoagulants to prevent further emboli and reduce inflammation. Outcomes depend on severity but most patients recover fully with treatment.

1. FAT EMBOLISM
SYNDROME
- DR PRATIK DHABALIA
RESIDENT IN ORTHOPEDICS
Dr DY Patil Hospital, Navi Mumbai

2. INTRODUCTION
• In 1862, Zenker first described this syndrome at autopsy, presence of fat droplets
in the lung capillaries in a railroad worker who sustained a fatal thoracoabdominal
crush injury.1
• In 1865, Wagner described the pathologic features of fat embolism.
• In 1873, Von Bergmann, for the first time clinically diagnosed and used the term
fat embolism syndrome (FES).
1. Scuderi CS. The present status of fat embolism. Bibliographic review. Int Surg Digest. 1934;18:195–215.

3. • Fat embolism syndrome (FES) occurs when fat droplets become
impacted in pulmonary microcirculation and other microvascular
beds, and is characterized by respiratory failure, cerebral dysfunction
and petechiae.
• While almost all patients will have fat globules detected in the blood
or develop transient hypoxia, the incidence of FES is much lower.

4. EPIDEMIOLOGY
• The incidence of FES ranges from < 1 to 29% in different studies. It varies
considerably according to the cause.
• This is most commonly seen following orthopedic trauma; however,
patients with many other clinical condition may have FES.
• More common in males
• More common in young patients
• More common in closed fractures
• More common in polytrauma than single bone fractures

5. ETIOLOGY
Traumatic causes:
• Fractures of long bones
(Shaft of femur, tibia, NOF – 90% Closed
fractures and multiple fractures produce more
emboli than open fractures.
• Pelvic and acetabulum fractures
• Extensive soft tissue injury.
• Higher degree burns injury.
• Sternotomy
• BM Transplant
Non-traumatic causes:
• Hemoglobinopathy like sickle cell anaemic
crisis
• Decompression sickness and Deep sea divers
• Diabetes mellitus
• Severe infection and sepsis
• Emboli from Neoplasm
• Blood transfusion
• Hepatic steatosis (fatty liver)
• Long duration corticosteroid therapy
• Acute pancreatitis
• Osteomyelitis

6. Iatrogenic causes:
• Major orthopedic surgeries like,
intramedullary nailing of tibia
and femur shaft fractures,
especially when both sides
operated in same sitting
• Arthroplasty procedures of hip
• Arthroplasty procedure of knee,
especially when done both sides
in same sitting
• Cardiopulmonary bypass
• Removal of large volume of
adipose tissue in liposuction
• Bone marrow biopsy

7. PATHOPHYSIOLOGY
The exact mechanism producing fat embolism is not known; different
theories have been proposed. They may act singly or in combination
with each other.

8. 1. Mechanical theory (Gassling et. al)
Traumatic injury forces liquefied fat droplets from disrupted bone
marrow into torn venules.
These droplets then enter into the pulmonary capillary beds
travel through arteriovenous shunts to the brain.
Microvascular deposition of droplets produces local ischemia by
occlusion of the vessels
platelet aggregation in the capillaries setting up a vicious loop of
ischemia.

9. 2. Biochemical theory
Toxic theory:
Baker suggested that local hydrolysis of fat emboli by lung lipase generates
chemically toxic free fatty acids, which causes severe inflammatory changes
by producing endothelial damage, inactivation of lung surfactant and
increasing lung permeability. They can also enter into systemic circulation
causing multiorgan dysfunction.
Obstructive theory:
This theory states that changes caused by trauma and/or sepsis in the patient
leads to systemic release of free fatty acids as chylomicrons. Subsequently
chylomicrons coalesce because of elevated acute-phase reactant in these
patients, such as C-reactive proteins, which leads to embolization and causes
the physiologic reactions

11. During reaming, in IMIL Nailing
procedure,
Rise in intramedullary pressure
pushes fat into broken vessels and
sinusoids which then reach lung
and can cause FES

13. CLINICAL FEATURES
Fat embolism syndrome typically presents 24–72 hours after the initial
injury. Rarely, cases occur as early as 12 hours or as much as 2 weeks
later.
Patients present with a classic triad:
• Respiratory changes
• Neurological abnormalities
• Petechial rash

14. Cardiopulmonary features
• Early persistent tachycardia.
• Respiratory signs like tachypnea, dyspnea, and hypoxemia are the
earliest to manifest and seen in 75% of patients.
• hey are liable to progress to respiratory failure in 10% of the cases.
• Moderate fever with inproportionate tachycardia

15. Dermatologic features:
• The characteristic petechial rash develops in about 20–60% of cases.
• The petechial rash develops due to embolization of small dermal
capillaries which causes extravasation of erythrocytes.
• Petechial rashes are seen in mucous membrane (oral), the
conjunctiva, and skin folds of the neck and axilla.
• Usually, they appear within first 36 hours and are transient
disappearing nearly completely within 7 days.

19. Neurologic features :
• They result from cerebral embolism and seen in up to 86% of cases.
• The common presentation is an acute confusional state.
• Focal neurological signs, such as aphasia, apraxia, hemiplegia, visual
field disturbances, seizures and decorticate posturing, are also
sometimes seen.
• Fundoscopic examination reveals retinal hemorrhages with intra-
arterial fat globules.

21. Miscellaneous:
• Right heart failure pattern is common
• Myocardial ischemia causing reduced efficacy of myocardium
• Macular edema causing scotomata associated with soft fluffy retinal
exudates (Purtscher’s retinopathy).
• Coagulation abnormalities similar to disseminated intravascular
coagulation.
• Renal symptom presenting as oliguria, lipiduria, proteinuria or
hematuria.

22. DIAGNOSIS
• Fat embolism syndrome is mainly a clinical diagnosis whereby other
causes are systematically excluded.
• Gurd’s and Wilson’s criteria
• Schonfeld’s criteria
• Lindeque’s criteria

23. Gurd’s and Wilson’s criteria

24. Schonfeld’s criteria

25. Lindeque’s criteria
• FES can be diagnosed on the basis of respiratory system involvement
alone.

26. INVESTIGATIONS
• Fall in hematocrit occurs within 24–48 hours and is due to intra-alveolar
hemorrhage. Coagulation abnormalities and thrombocytopenia and.
• Raised ESR and CRP
• Arterial blood gas: Unexplained increase in pulmonary shunt fraction
(PaO2-PaO2) difference is strongly suggestive of the syndrome especially if
it occurs immediately after (24–48 hours). Arterial blood gas analysis will
reveal hypoxia, with a PaO2 of less than 60 mm Hg along with
hypocapnia— paCO2 less than 30 mm Hg.
• Demonstration of fat globules—staining of urine, blood and sputum with
Sudan or Oil Red O may show fat globules. Fat globules in the urine are as
such common after bone injuries or polytrauma.

28. LFT – Derranged enzymes
RFT – Creat and Creat clearance
PT INR and BT/CT
ECG – “S1Q3T3” pattern (McGinn-White Sign)

29. Imaging studies
Plain chest radiograps: within 24–
48 hours of onset
• Diffusely distributed bilateral
pulmonary infiltrates
• “Snow storm” appearance of
fleck-like pulmonary shadows
• Prominent pulmonary
bronchiolar markings
• Enlargement of the right side of
the heart

30. • Noncontrast head CT and MRI:
Usually it is normal, only in some
cases do they show diffuse white
matter petechial hemorrhages
related to microvascular injury.
• It is also used to rule out other
causes of decreased
consciousness.

31. • V/P Lung studies
• MRI Brain
• HRCT Chest
• TEE

32. MANAGEMENT
• No specific treatment is available for FES.
• Most modalities of management are directed to prevention, early
diagnosis and adequate symptomatic relief.
• ATLS procedure for trauma, followed by stabilizing the patient.
• Shift patient to Intensive care.
• Regular monitoring of oxygen saturations, input output and
hematocrit levels.
• GCS charting

33. Supportive management
• Maintain hemodynamic stability – IVF and BTs
• Maintatin adequate oxygenation – ET + ventilatory support
• Maintain fluid balance – restrict fluid intake, diuretics (tab furosemide
40mg BD or Intravenously)
• Maintain nutrition – specially protein levels

34. • Pharmacological
Steroids:
• Decrease inflammatory reaction in lungs caused by free fatty acids.
• Decrease capillary leakage by stabilizing lysosomal and capillary
membrane.
Prophylactic dose of methyl prednisolone: 1.5 mg/kg IV can be
administered every 8 hours for six doses

35. Anticoagulants
Prophylaxis for DVT - LMWH, Aspirin, Rivaroxaban
Ionotropic support with dobutamine may be necessary
Ethanol
Hypertonic glucose
IVC Filters
IV Albumin

36. Orthopedic management and prevention
• Immobilization of all long bone fractures as early as possible.
• Early Internal fixation procedures within 24-48 hours have shown to
reduce chances of post operative FES
• Unreamed nailing
• Narrower reamers and reamer irrigator aspirator devices
• Gradually increase reamer sizes, 0.5
• Decrease RPM while reaming
• Flexible reamer > rigid reamer

37. • Don’t fix all the long bone fractures in same sitting.
• Slowly deflate tourniquet after the procedure.
• Computer assisted Navigation in arthroplasty > conventional
• Distal venting of bone
• Physiotherapy – chest, ankle pumps and joint mobilization
• Compression bandages for lower limbs
• Post op anticoagulants and monitoring