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FAT EMBOLISM

Fat embolism syndrome


Showering of fat emboli to pulmonary and systemic circulations in trauma and
orthopedic surgical patients usually results in subclinical symptoms
1-5% are associated with clinical symptoms termed FES
Cause:
2 theories
Mechanical theory:
injuries or surgeries of long bones or pelvis increase intramedullary pressure
force large fat droplets into systemic circulation
Enters Rt heart and lungs mechanical obstruction of pul microcirculation acute
pulmonary HTN & localized ischemia and inflammation fat induced ac lung injury
May enter systemic arterial circulation through intracardiac shunts or by traversing
pul capillary bed cerebral and cutaneous embolization
Biochemical theory: obstructive and toxic
Biochemical (sp hormonal) changes occur with trauma and sepsis systemic
release of FAs as chylomicrons coalesce (obstructive theory)
Free FAs directly toxic to pneumocytes and pul capillary endothelium interstitial
Hge and chemical pneumonitis (toxic theory)
Esp attractive when FES occurs in the absence of trauma
Clinical findings in FES
Fat embolism is primarily a clinical diagnosis
Missed b/c of
subclinical sym,
delay in onset of 24-72hrs,
presence of additional traumatic injuries
Predisposing conditions
Risk assessment
Orthopedic surgery of lower extremities, esp hip and knee arthroplasty and
intramedullary nailing of femoral shaft ( increases medullary pressure to 1000mm Hg
predisposes to FES)

More frequently in closed/undiaplced than open/displaced fractures vent for


medullary fat
Very less likely to occur in children compared to adults
Delayed stabilization (>24hrs) increases the risk
Intramedullary rod placement
Joint replacement surgery esp revisions or b/l
Femoral metastasis
Alcohol-induced fatty liver, blunt injury to liver
Acute FES
High index of suspicion: classic triad of
Petechial rash
Pulmonary dysfunction
Cerebral dysfunction
Early persistent tachycardia 1st sign of impending problems
Rash: reddish brown, nonpalpable petechial rash on head, neck,
ant thorax, axillae in 20-50% pts
Easily missed b/c it resolves quickly
Pul dysfunction: Within 24-72hrs of insult tachypnea, dysnpea,
hypoxemia (ventilation-perfusion abnormalities) may progress to ARDS
Cerebral dysfunction: confusion, sedation and coma
Other: Retinal Hges, with intra-arterial fat droplets on fundoscopy
Fulminant FES
Encountered in the operating room during joint replacement procedures
Large amounts of fat from medullary cavity into venous circulation
In pts with limited cardiac reserve, Ac pul HTN ppt Rt VF with hypotension,
bradycardia, hypoxemia and CV collapse
Subacute FES
Secondary to toxic effects of free FAs from hydrolysis of embolized fat droplets
Investigations
Support the clinical diagnosis but not pathognomonic
Hematologic:
Alveolar Hge & mild hemolysis Hb decrease
Platelets and fibrinogen decrease
Fat macroglobulinemia from pul capillary sample
Marked rise in ESR
Radiologic:
Diffuse bilateral infiltrates
snowstorm appearance
CT chest and CT head
Diagnosis
Management
Treatment as well as prevention centered on the support of failing organ systems
Oxygen administered immediately by mask and severity of pulmonary insufficiency
assessed with ABG
CPAP, intubation with mechanical ventilation may be necessary
Adequate intravascular volume
Resp failure directly related to degree and duration of hemodynamic instability
Albumin therapy
Binds to oleic acid decreasing FAs inflammatory effect on target organs
Meticulous pain control
Decrease catecholamine release and attenuate the rise of FFA
FES is best avoided by
Minimizing the extent of intramedullary HTN when
preparing the femoral canal,
During cementing of prosthetic devices
During intramedullary nailing
Prognosis
Mortality
5 and 15%
Due to resp failure and assoc injuries
Long-term morbidity
Neurologic defects
Persistent cognitive dysfunction
Commonest site of fracture leading to fat embolism is - (AI 99)
a) Tibia# b)Femur#
c) Humerus # d) Ulna#
Factors favoring fat embolism in trauma patient (PGI Dec 07)
a) Diabetes Mellitus
b) Mobility of joint
c) Resp. failure
d) Hypovolemic shock
True about Posttraumatic fat embolism syndrome - (PGI Nov. 10, June 09)
a) Fracture mobility is a risk factor
b) Associated diabetes pose a risk
c) Bradycardia occurs
d) Thrombocytopenia
e) On ABG Pa02 < 60 mm Hg on FI02 < 0.4
The management of fat embolism includes all of the following except (AI 04
a) Oxygen
b) Heparinization
c) Low Molecular weight dextran
d) Pulmonary Embolectomy
A person with multiple injuries develops fever, restlessness,
tachycardia, tachypnea and periumbilical rash. The likely diagnosis is -
(AIIMS Nov 08)
a) Air embolism
b) Fat embolism
c) Pulmonary embolism
d) Bacterial pneumonitis
Ramesh singh, a 40 yrs old man, was admitted with fracture shaft femur
following a road traffic accident. He was tachypnoeic, and had
conjunctival petechiae. Most likely diagnosis is - (A102)
a) Pulomary embolism b) Sepsis syndrome
c) Fat embolism d)Hemothorax
A 30 year old man had road traffic accident and sustained fracture of
femur. Two days later he developed sudden breathlessness. The most
probable cause can be - (AI05)
a) Pneumonia
b) Congestive heart failure
c) Bronchial asthma
d) Fat embolism
Clincial feature of fat embolism includes all excepts- (PGINov.10)
a) Tachypnoea
b) Systmic hypoxia may occur
c) Fat globules in urine are diagnostic
d) Manifests after several days of trauma
e) Petechiae in the anterior chest wall
A 64 year old hypertensive obsese female was undergoing surgery for
fracture femur under general anaesthesia. Intra-operatively her end-
tidal carbon dioxide decreased to 20 from 40 mm of Hg, followed by
hypotension and oxygen saturation of 85%. What could be the most
probable cause? (DPG 09, AI 03)
a) Fat embolism b) Hypovolemia
c) Bronchospasm d) Myocardial infarction
True about fat embolism - (PGI Dec 07)
a) Petechia in the anterior chest wall
b) Bradycardia
c) Fat globules in urine
d) Occurs after 1st week of polytrauma
e) Thrmbocytopenia