Fat Emboli

DR. dr. Pamudji Utomo, SpOT (K)

Program Studi Ortopedi Traumatologi FK UNS / RS Ortopedi Prof. Dr. R. Soeharso Surakarta
History

 Zenker, a pathologist, 1st identified fat embolism syndrome at autopsy, 1862.

 First diagnosed in 1873 by Dr Von Bergmann

 In 1879, Fenger and Salisbury published description of FES

Definitions

 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): Serious manifestations of fat

embolism occasionally causes multisystem dysfunction. The
lungs are always involved and next is brain.
Fat Embolism Syndrome

 Clinical diagnosis. No specific laboratory test is diagnostic.

 Mostly associated with long bone and pelvic fractures, and more frequent in closed
fractures than open fractures.
 Single long bone fractures have 1-5% chance of developing FES, increases with number of
fractures.
 Onset is 24 – 72 hours from initial insult.
 Mortality: 5 – 15%.
Causes

Trauma-related Non trauma-related

Long bone fractures Pancreatitis
Pelvic fractures Diabetes mellitus
Fractures of other marrow-containing Osteomyelitis and panniculitis
bones
Orthopedic procedures Bone tumor lysis
Soft tissue injuries (ex. chest compressions Steroid therapy
with or without rib fractures)
Burns Sickle cell hemoglobinopathies
Liposuction Alcoholic (fatty) liver disease
Bone marrow harvesting and transplant Lipid infusion
Cyclosporin A solvent
 Blunt trauma (90%)
 Non trauma
Agglutination of chylomicrons and VLDL by high levels of plasma CRP.

a. Disease-related : Diabetes, acute pancreatitis, burns, SLE, sickle cell crisis

b. Drug-related : Parenteral lipid infusion
c. Procedure-related : Orthopedic surgery, liposuction
Pathophysiology

Exact mechanism is unknown, but two main hypothesis

Mechanical vs Biochemical
Mechanical : Fat globules from disrupted bone marrow or adipose tissue are forced into torn
venules in areas of trauma
Biochemical : Hormonal changes caused by trauma and/or sepsis induce systemic release of free
fatty acids (FFA) as chylomicrons which cause the systemic FES.
Mechanical Hypothesis

 Fractures of marrow-containing bone (Femur and Pelvis) have the highest incidence of FES
and cause the largest volume of fat emboli, because the disrupted venules in the marrow
remain tethered open by their osseous attachments.
 The marrow contents enter the venous circulation with little difficulty. This theory is
supported by research on Orthopedic long bone (IM reaming) and spinal surgeries which
cause fat globules to enter the blood circulation when vigorous reaming/fixation is done.
 Increase pressure + volume extravasation
 Measuring fat globules pre and post reaming shows significant difference in concentration.
 Fat droplets are deposited in the pulmonary capillary beds and travel through arteriovenous
shunts to the brain. Systems affected include LUNG, BRAIN and CIRCULATION.
 Microvascular lodging of droplets produces local ischemia and inflammation, with
concomitant release of inflammatory mediators, platelet aggregation and vasoactive amines.
Biochemical

 FES is dependent upon degradation of the embolized fat into free fatty acids.
 Neutral fat does not cause an acute lung injury, it is hydrolyzed over the course of hours to
several products, including FFA, which cause ARDS in animal models.
 CRP (acute phase reactant), which is elevated in trauma patients, appears to be responsible
in lipid agglutination (FES) for both traumatic and non-traumatic FES.
 The process of Neutral fat cells  FFA  Agglutination with CRP may explain the time
sequence of clinical findings in FES.
 Onset of symptoms may coincide with agglutination.
 This theory is animal model based and circumstantial at best.
Clinical Presentation

 Diagnosis is made CLINICALLY, NOT CHEMICALLY. It doesn’t matter how much fat
globules are in your circulation, it just matters if you have their side effects.

 FES typically manifests 24 to 72 hours after the initial insult. Rarely <12 hours or
>72 hours.
 TRIAD OF FES Early Signs of FES
 Hypoxemia  Dyspnea

 Neurological abnormalities  Tachypnea

 Petechial rash  Hypoxemia

Pulmonary

 Hypoxia, rales, pleural friction rub

 Breath sounds: Loud harsh, crepts & wheeze
 ARDS may develop (fat emboli obstructs lung vessel (20
microns) platelets and fibrin adhere)
 ½ of patients with FES require mechanical ventilation
 CXR usually normal early on, later may show
‘snowstorm’ pattern- diffuse bilateral infiltrates
 CT Chest: ground glass opacification with interlobular
septal thickening
Neurological Findings

 Usually occur after respiratory symptoms

 Incidence 80% patients with FES
 Minor global dysfunction most common, but ranges from mild delirium to coma
 Seizures/focal deficits not common but can occur
 Transient and reversible in most cases
 CT Head: General edema, usually non specific
 MRI brain: Low density on T1, and high intensity T2 signal, correlates to degree of impairment
Rash

 Petechial
 Usually on conjunctiva, neck, axillae
 Results from occlusion of dermal capillaries by fat globules
and then extravasations of RBC
 Fleeting & last short. Resolves in 5-7 days
 PATHOGNOMONIC, but only present in 20-50% of patients
Other findings

 Retinopathy (exudates, cotton wool spots, hemorrhage)

 Lipiduria
 Fever (39-40 C)
 DIC
 Myocardial depression (prominent S, T depression, RBBB, arrhythmia)
 Thrombocytopenia / anemia
 Hypocalcemia
Diagnosis

 FES is CLINICAL diagnosis, not biochemical

 A high degree of suspicion is needed to make diagnosis
 Common misconception is that the presence of fat globules, either in sputum, urine
or a wedged PA catheter, is necessary to confirm the diagnosis of FES. In 50%
fracture patients, fat globules was demonstrated in the serum, without the
symptoms of FES.
 However, growing literature on the use of bronchoscopy with bronchoalveolar
lavage to detect fat droplets in alveolar macrophages as a means to diagnose fat
embolism. Sensitivity and specificity are unknown, being studied in trauma patients.
Gurd’s Criteria
 FES = 1 MAJOR + 4 MINOR + fat microglobulinemia
 Still widely used today Major features
Petechial rash
Respiratory symptoms plus bilateral
signs with positive radiographic
changes
Cerebral signs unrelated to head
injury
Minor features
Tachycardia > 120x/min
Pyrexia > 39,4 C
Retinal fat or petechiae
Urinary fat globules or oligoanuria
Sudden drop in Hb level > 20%
Sudden thrombocytopenia > 50%
High ESR > 71 mm/h
Lindeque’s Criteria

 FES = femur fracture ± tibia fracture + 1 feature

 Based on respiratory parameters

A sustained PaO2 < 8 kPa (60 mmHg)

A sustained PaCO2 > 7,3 kPa(55 mmHg) or pH < 7,3
A sustained respiratory rate > 35x/min even after adequate sedation
Increased work of breathing judged by dyspnea, use of accessory muscles,
tachycardia and anxiety
 Sevitt’s Classification

Subclinical FES

●
± 3 days post trauma
●
Probably occurs in almost all long bone fractures of the lower extremity and fractures of the pelvis
●
Characterized by decreased PaO2, decreased Hb% and platelets. No clinical signs and symptoms of respiratory insufficiency

Nonfulminant FES

●
Any time, up to 6 days post trauma
●
Clinical signs and symptoms are clearly evident, but no definitive test. The diagnosis remains a clinical ones.
●
Petechiae, tachycardia, respiratory failure and signs of CNS embolism
●
Thrombocytopenia, anemia and coagulation abnormalities can be found, as well as pulmonary alveolar and interstitial opacities on CXR
 Fulminant FES

●
Occurs suddenly and rapidly after injury, and progresses quickly, often resulting in death within a few hours of the
initial trauma
●
Clinical features are: acute respiratory failure, acute cor pulmonale and embolic neurological changes
●
These occur shortly after injury and often result in the death of the patient
●
Multiple fractures are particularly susceptible to this form of the syndrome, which, although it is relatively rare, is of
immense clinical significance because of its high mortality
Management

Treatment is largely supportive

 Constant Positive Airway Pressure (CPAP)
 Mechanical ventilation
 Antibiotics
 Nutritional support
 Corticosteroids
 Heparins
Initial Treatment
 Adequate airway
 Start IV line – correct fluid deficit
 Basic investigation – including baseline chest
x-ray and ABG assay (v. imp)
 Nasogastric tube – should be inserted in
patient with severe trauma and gastric
contents suctioned to prevent aspiration and
ARDS
Monitoring
 TPR, BP
 I/O chart – maintain output 50-100cc/hr
 CVP – to correct fluid deficit
 If overload  pulmonary edema (4-8 cm
H20)
 Pulmonary haemodynamics – PCWP to
accurate mean of deficit correction (5 – 12
mm of Hg)
 Arterial blood gas monitoring
Specific drug therapy

 Many drugs have been tried, mostly without demonstrable benefit in established ARDS, except
corticosteroids but with some prophylactic benefit

 Drugs which may be tried in fat embolism associated ARDS are:

 Ethanol: Lipase inhibitor, low incidence when level > 20 mg
 Heparin: ↓ PL aggregation useful in DIC associated ARDS also controversial in trials. 10000 –
15000 iu stat & 10000 iu 4-6hly with PTT at 1.5-2.5 INR
 Hypertonic glucose: block post traumatic mobilization of FFA – may improve oxygenation
 Corticosteroids: stabilize cell member, ↓ PMN adhesion, prevent surfactant reduction, protect
capillary endothelium, ↓ compliment activation and minimize transudation
Corticosteroids

 Value in ARDS of fat embolism, aspiration, sepsis, shock and cerebral edema
 Helpful in late stage in recovering patients in reducing fibrotic change
 Improve and preserve arterial oxygenation and stimulate proliferation and maturation of Type II
pneumocyte

Prophylactic dose: 10 mg/kg /8h

or
80 mg/kg bolus
or
1-2gm IV over 24hr and maintain for 48-96hr by gradual reduction
ATLS Protocol

 Early immobilization of fracture and early definitive reduction (open or closed)

 Maintain intravascular volume to maintain cardiovascular stability (hypovolemic
shock resuscitation), may use colloids (albumin) as it can expand fluid and bind FFA
 Mechanical ventilation with PEEP
 IV Ethanol has been used in Russia, Europe and some American centers to decrease
rate of FES
 Studies showed that a raised level of alcohol in blood was associated with lower
incidence of fat embolism
Role of fracture stabilization

 Highly debated issue

 Accumulated evidence over past decade support early fixation within 24hr of injury

 Early IF – decompress fractures hematoma as ongoing source of fat emboli and retained necrotic
debris, eliminate pain and physiologic stress with continued fracture motion, optimize pulmonary
function, contributes to reduced ventilator dependence and improve survival

 But transient increasing pulmonary pressure and worsening pulmonary gas exchange observed during
reaming of medullary canal. So, undreamed nailing is suggested for femoral fixation in multiple
fracture patients
Prognosis

 Mild : undetected
 Moderate : Low mortality
 Severe : Fatal, unless if treatment instituted early. Survivors have pulmonary sequele