CRUSH SYNDROME AND FAT EMBOLISM SYNDROME FOR UNDERGRADUATES

1. FAT EMBOLISM SYNDROME
AND
CRUSH SYNDROME
DR KISHORE.V
ASSISTANT PROFESSOR OF ORTHOPAEDICS
KIMS-RF, AMALAPURAM.

2. • a 24year male sustained RTA came to casuality .on examination
found closed fractures of both femur shafts. No head or chest injury.
Patient stabilized hemodynamically and admitted in orthopaedic
ward. There was a delay in orthopaedic procedure for 2 days. After
2nd day patient become restless and agitated , with decreasing
saturations, and fall in blood pressure. Oxygen and hemodynamic
support unable to stabilize the patient and patient is ventilated. Chest
xray shows diffuse lung infiltrates and snowstorm appearance. What
is your clinical diagnosis….

3. FAT EMBOLISM VS FAT EMBOLISM SYNDROME
Fat embolism (FE) and fat embolism syndrome(FES) are a clinical
phenomenon that are characterized by systemic dissemination of fat
emboli within the system circulation. The dissipation of fat emboli will
disrupt the capillary bed and affect microcirculation, causing a systemic
inflammatory response syndrome and End-organ damage.
• Fat embolism syndrome is a continuum of fat embolism.
• Fat embolism syndrome is most common in patients with orthopedic
trauma.
• In most instances, diagnosis is usually established during the autopsy

4. EPIDEMOLOGY
• Zenker first described the clinical presentation of fat embolism
syndrome in 1863 in a patient suffering from crush injury.
• In 1873, Von Bergmann clinically diagnosed the condition for the first
time
about 67% of orthopedic trauma patients have fat globules in their blood. if
the blood sample was taken from a site close to the area of the fracture, the
incidence is closer to 95%.
• Most recent studies show an incidence of about 1% to 11%.

5. ETIOLOGY
TRAUMATIC (most common)
•# femur, tibia, pelvis
• Massive soft tissue damage
• Crush injury
• Prolonged cardiopulmonary resuscitation
• Severe burn involving more than 50% of body
surface area
Risk factors
• Young
• Multiple fractures
• Closed fractures
• Prolonged conservative treatment
• Intraoperative abnormal reeming for insertion of
nails
NON TRAUMATIC (very rare)
• Bone marrow transplantation
• Liposuction
• Median sternotomy
• Fatty Liver
• Acute or chronic pancreatitis
• Therapy with corticosteroid
• Infusion of fat emulsion
• Lymphography
• Hemoglobinopathies
• Sickle cell disease
• Thalassemia

6. Clinical presentation
• A fat embolism can travel to most of the organs in the body. Fat embolism and fat
embolism syndrome are multiorgan diseases that can damage the kidneys, heart, skin,
brain, and lungs.
• Fat embolism typically manifests at around 24 to 72 hours after the initial insult.
• The symptoms in fat embolism and fat embolism syndrome are nonspecific. Patients
might complain of the following:
• Pain related to bone fracture
• Nausea
• General weakness
• Malaise
• Difficulty breathing
• Headache

7. Clinical presentation continued….
Most patients with fat embolism syndrome will be anxious, agitated and
ill-looking
Respiratory
• Tachypnea
• Tachycardia
• Respiratory distress and failure
Skin
• Petechial rash over neck, anterior
chest wall, anterior axillary
folds,conjunctiva, palate
Eye
• Retinal hemorrhages
Central nervous system
(due to cerebral edema not
ischemia)
• Agitation from hypoxia
• Restlessness
• Change in mental status
• Seizure
• Coma
• A GCS<8 indication for ventilator

8. Gurd`s criteria for FES…
(2 major or 1 major + 4 minor criteria)
• Major Criteria
• Petechial rash
• Respiratory insufficiency
• Cerebral involvement in non-head
injury patients
• Minor Criteria
• Fever greater than 38.5 C
• Tachycardia heart rate greater than 110
beats per minutes
• Retinal involvement
• Jaundice
• Renal signs
• Anemia
• Thrombocytopenia
• High erythrocyte sedimentation rate
• Fat macroglobulinemia

10. Work up……
• Anaemia and thrombocytopenia are common
• Elevated urea and sr creatinine, metabolic acidosis
• ABG:
Ventilation-perfusion mismatch is a hallmark of fat embolism
syndrome.
The arterial blood gas analysis usually has a low partial pressure of
oxygen, causing hypoxemia.
An increased alveolar-arterial (A-a) gradient is common in fat embolism
syndrome.

11. • Bronchoalveolar Lavage (BAL) has been researching extensively
as a diagnostic tool for fat embolism syndrome. Lipid inclusion in the
macrophages might point to a diagnosis of fat embolism syndrome
but is not specific
• Transesophageal echocardiography may be utilized
intraoperatively to monitor the release of fat globules or bone
marrow materials into the bloodstream during the process of
intramedullary nailing and reaming

12. The chest X-ray will reveal the presence of the following:
• Diffuse interstitial marking
• Pulmonary edema
• Lung infiltrate
• Flake-like pulmonary marking (snowstorm appearance)31
CT scan of the chest
• Area of increased vascular congestion
• Pulmonary edema
Imaging of the brain
• CAT scan
• This is not a very sensitive imaging study of the brain in fat
embolism syndrome, but it can be used to exclude other
causes of altered mental status such as epidural, subdural or
subarachnoid bleed.
• MRI
• This is the most sensitive test that can be used to
demonstrated changes in the brain related to fat embolism
syndrome

13. MANAGEMENT OF FES….
There is no specific treatment for fat embolism or fat embolism
syndrome
• DEXTROSE INFUSION TO DECREASE FFA MOBILIZATION
• HEPARIN
• CORTICOSTEROIDS-( 77% REDUCTION OF RISK OF FES.)
None of them proved effective in clinical trails and not recommended

14. Supportive Care
This is the mainstay treatment once a patient develops fat embolism syndrome.
Supportive care is geared towards adequately oxygenating the end organs.
• Goals of Supportive Care
• Provision of adequate oxygenation and ventilation
• Maintenance of adequate hemodynamic stability
• Transfusion of packed red blood cells to improve
oxygen delivery if indicated
• Prophylaxis of deep venous thrombosis with a
sequential compression device
• Adequate nutrition and hydration
• Supplemental oxygen might be required, and if the
patient develops fulminant acute
respiratory distress syndrome, intubation and
mechanical ventilation might be required.
•
• Albumin
• Albumin is recommended as part of the
resuscitation tools for hypovolemia. It
restores intravascular volume and helps to
bind free fatty acid. This prevents the
systemic dissemination of fat globules.
• Indications for Intubation
• Altered mental status with Glasgow coma
score of less than 8
• Moderate to several respiratory distresses
with no improvement on noninvasive support
• fat embolism syndrome might also cause
pulmonary hypertension with right ventricular
failure. Inotropic support with dobutamine or
a phosphodiesterase inhibitor like milrinone
might be required.

15. To prevent FES intraoperatively….
• It is highly recommended to start early open reduction and internal
fixation of long bone fractures
• During operative fixation of the long bone fracture, care must be
taken to limit the intramedullary pressure, as a high pressure is
associated with an increased amount of fat emboli entering the
systemic circulation

16. Crush injury vs crush syndrome
Also termed rhabdomyolysis, involves a series of metabolic
changes produced due to an injury of the skeletal muscles of
such a severity as to cause a disruption of cellular integrity and
release of its contents into the circulation.

18. • Pathophysiology of crush syndrome…
• EFFLUX
• INFLUX
• Myoglobin
• Potassium
• Magnesium
• Phosphates
• Lactic acid
• Sodium
• Water
• Calcium
• Creatinine phosphokinase (CPK)
• Lactate dehydrogenase (LDH)
• Serum aldolase
•
EFFLUX
Muscle cell

19. Myoglobinemia
Myoglobinuria
Hypovalemic shock
hyponatremia
Hyperkalemia
Hypermagnesemia
Hyperphosphatemia
Metabolic acidosis
Hypocalcemia
CPK
LDH
ALDOLASE
tea or cola’ coloured urine, acute renal tubular
acidosis
oliguria and renal failure are the sequence of
events Petechiae, blisters,
Nausea, vomiting, agitation and delirium
muscle bruising, and superficial injuries are seen.
Myalgia, muscle paralysis and sensory deficit are
common.
Fever, cardiac arrhythmia, pneumonia,
‘
.aciduria

20. Myoglobinemia
Myoglobinuria
Hypovalemic shock
hyponatremia
Hyperkalemia
Hypermagnesemia
Hyperphosphatemia
Metabolic acidosis
Hypocalcemia
CPK
LDH
ALDOLASE
Complete hemogram, blood urea , sr creatinine
Serum and urine myoglobin
Urine output, CVP
Serum electrolytes ( sodium, potassium, mag, phosp)
Arterial blood gas analysis(ABG)
Sr lactic acid
Sr calcium
CK > 1000 – indicative of crush syndrome
It raises steeply in 1-3 days
It is a better prognostic indicator of recovery

21. Myoglobinemia
Myoglobinuria
Hypovalemic shock
hyponatremia
Hyperkalemia
Hypermagnesemia
Hyperphosphatemia
Metabolic acidosis
Hypocalcemia
CPK
LDH
ALDOLASE
Fluid resuscitation is main stay of treatment
NS preferred , need large amounts of fluids
Monitor urine output and CVP
Maintain urine output of 300ml per hr
Correct acidosis with sodium bicarbonate
Oral citrate along with flids
Hemodialysis – to restore kidney function
-Required in setting of anuria, elevated BUN,
creatinine,fluid overload
Sr potassium >8meq/l is important predictor of
hemodialysis.
Correct hyperkalemia:
Insulin infusion

22. Surgical management of crush injuries
• Massive debridement may require including removal of dead and
necrotic sluff and muscle
• Amputations
• Compartment release by fasciotomy
• Fix fractures temporarily

23. Thank you…..