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    Fat Embolism

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    Suhanthi Mani
    Fat embolism syndrome occurs when fat particles migrate from bone marrow into the bloodstream following trauma or surgery, typically to long bones or the pelvis. This can cause lung damage and hypoxemia as the fat emboli become lodged in the pulmonary capillaries. Clinical diagnosis is difficult as there is no confirmatory test, but symptoms include respiratory issues, neurological changes, and a characteristic rash. The most effective prevention is early surgical fixation of long bone fractures to limit further fat release. Management is otherwise supportive care to address respiratory compromise, hemodynamics, and other issues. Prognosis is generally good if the patient survives the initial critical period, though neurological deficits can occasionally linger.

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    Fat Embolism

    Uploaded by

    Suhanthi Mani
    642 views26 pages
    Fat embolism syndrome occurs when fat particles migrate from bone marrow into the bloodstream following trauma or surgery, typically to long bones or the pelvis. This can cause lung damage and hypoxemia as the fat emboli become lodged in the pulmonary capillaries. Clinical diagnosis is difficult as there is no confirmatory test, but symptoms include respiratory issues, neurological changes, and a characteristic rash. The most effective prevention is early surgical fixation of long bone fractures to limit further fat release. Management is otherwise supportive care to address respiratory compromise, hemodynamics, and other issues. Prognosis is generally good if the patient survives the initial critical period, though neurological deficits can occasionally linger.

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    Fat embolism syndrome occurs when fat particles migrate from bone marrow into the bloodstream following trauma or surgery, typically to long bones or the pelvis. This can cause lung damage and hypoxemia as the fat emboli become lodged in the pulmonary capillaries. Clinical diagnosis is difficult as there is no confirmatory test, but symptoms include respiratory issues, neurological changes, and a characteristic rash. The most effective prevention is early surgical fixation of long bone fractures to limit further fat release. Management is otherwise supportive care to address respiratory compromise, hemodynamics, and other issues. Prognosis is generally good if the patient survives the initial critical period, though neurological deficits can occasionally linger.

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    © All Rights Reserved
    Download as PPT, PDF, TXT or read online from Scribd
    Download as ppt, pdf, or txt
    642 views26 pages

    Fat Embolism

    Uploaded by

    Suhanthi Mani
    Fat embolism syndrome occurs when fat particles migrate from bone marrow into the bloodstream following trauma or surgery, typically to long bones or the pelvis. This can cause lung damage and hypoxemia as the fat emboli become lodged in the pulmonary capillaries. Clinical diagnosis is difficult as there is no confirmatory test, but symptoms include respiratory issues, neurological changes, and a characteristic rash. The most effective prevention is early surgical fixation of long bone fractures to limit further fat release. Management is otherwise supportive care to address respiratory compromise, hemodynamics, and other issues. Prognosis is generally good if the patient survives the initial critical period, though neurological deficits can occasionally linger.

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    © All Rights Reserved
    Download as PPT, PDF, TXT or read online from Scribd
    Download as ppt, pdf, or txt
    of 26

    By

    Dr Nethiya Vengataraman
    Fat Embolism Syndrome
    Fat embolism can occur due to the
    migration of fat particles from the bone
    marrow at the time of trauma or during
    reaming of the intramedullary canal. This
    causes the release of inflammatory
    mediators ,with endothelial lung damage
    and hypoxemia.



    First diagnosed in 1873 by Dr Von Bergmann

    Published in 1879 Fenger and Salisbury.
    Fat Embolism:
    Traumatic fat embolism occurs in up to 90% of
    individuals with severe skeletal injuries, but < 10% of
    such patients have any clinical symptoms / signs

    Fat Embolism Syndrome:
    FE with clinical manifestation .
    Incidence: 1-3% femur #, 5-10% if bilateral or multiple.

    Mortality: 5-15%

    Clinical diagnosis :No specific laboratory test is
    diagnostic

    Mostly associated with long bone/pelvic #s, and more
    frequent in closed fractures.

    Onset is 24-72 hours from initial insult

    A high index of suspicion is needed for diagnosis is to
    be made.

    An asymptomatic latent period - 12-48 hours.

    The fulminant form presents as acute cor pulmonale,
    respiratory failure, - death within a few hours of injury.

    Mechanical and biochemical Theory
    1. Two theories about fat embolism exist. First, the mechanical theory states
    that large fat droplets are released into the venous system. These droplets are
    deposited in the pulmonary capillary beds and travel through arteriovenous
    shunts
    to the brain. Micro vascular lodging of droplets produces local ischemia and
    inflammation, with concomitant release of inflammatory mediators, platelet
    aggregation, and vasoactive amines.

    2. Second, the biochemical theory states that hormonal changes caused by
    trauma and/or sepsis induce systemic release of free fatty acids as chylomicrons.
    Acute-phase reactants, such as C-reactive proteins, cause chylomicrons to coalesce
    and create the physiologic reactions described above. The biochemical theory
    helps explain nontraumatic forms of fat embolism syndrome.
    [1]




    The biochemical theory


    Circulating FFAs -directly toxic to Pneumocytes / capillary
    Endothelium in the lung - interstitial hemorrhage, edema
    & chemical pneumonitis.

    Coexisting shock, hypovolemia and sepsis - reduce liver
    flow exacerbate the toxic effects of FFAs.

    H/E stain lung

    - blood vessel with
    fibrinoid material and

    -optical empty space -lipid
    dissolved during the
    staining process.
    TRAUMA
    Hypoxemia
    Neurological
    abnormalities
    Petechial
    rash


    Dyspnea,

    Tachypnea

    Hypoxemia PaO2 < 60 mm Hg
    Clinically Tachpnea, Dyspnea, Hypoxia, rales, pleural
    friction rub & ARDS.
    High spiking temperatures.
    Hypoxemia - ventilation-perfusion mismatch &
    intrapulmonary shunting. Acute cor pulmonale -
    respiratory distress, hypoxemia, hypotension and
    elevated CVP.
    of pts require mechanical ventilation
    CXR normal early on - later may show snowstorm
    pattern- diffuse bilateral infiltrates
    CT chest: ground glass opacification with interlobular
    septal thickening
    CNS signs usually occur after respiratory symptoms -
    nonspecific - features of diffuse encephalopathy

    Acute confusion, stupor, coma, rigidity, or convulsions
    - Transient and reversible in most cases

    CT Head: general edema nonspecific

    MRI brain: Low density on T1 & High intensity T2
    signal - correlates to degree of impairment

    Reddish-brown non-palpable Petechial rash - upper
    anterior body, chest, neck, upper arm, axilla, shoulder,
    oral mucous membranes and conjunctivae in 20 - 50%
    patients.

    Pathognomonic, however, it appears late and
    disappears within hours.

    Results from occlusion of dermal capillaries by fat
    globules - extravasations of RBC

    Retinopathy (exudates, cotton wool spots,
    hemorrhage)
    Lipiduria(fat globulin in the urine)
    Fever
    DIC
    Myocardial depression (R heart strain)
    Thrombocytopenia
    Anemia, Decreased Hematocrit
    Hypocalcemia
    Gurds criteria

    Most commonly used

    1 major, plus 4 minor
    The most effective prophylactic measure - operative
    reduction/rigid fixation of long bone fractures as soon
    as possible. Higher incidence (5 fold) when fixation
    delayed greater than 24 hours.

    Supportive care includes maintenance of adequate
    oxygenation and ventilation, stable hemodynamics,
    blood products as clinically indicated, hydration,
    prophylaxis of DVT and stress-related GI bleeding.
    Continuous pulse oximetry monitoring - at-risk
    patients ( those patients with long bone fractures) -
    detecting desaturations early.

    Consultations recommended include orthopedists,
    neurologists/ neurosurgeons, trauma care specialists,
    critical care specialists, pulmonologists,
    hematologists, and nutritionists.
    Albumin has been recommended - not only restores
    blood volume / binds fatty acids - may decrease the
    extent of lung injury.

    High dose corticosteroids have been effective in
    preventing development of FES in several trials, but
    controversy on this issue still persists.

    Heparin has also been proposed as it activates lipase,
    but no evidence exists for its use in FES.


    DURATION OF FES
    Difficult to predict FES is frequently subclinical or
    overshadowed by other illnesses or injuries.

    Increased alveolar-to-arterial oxygen gradient and
    neurologic deficits, including coma, may last days or
    weeks.

    SEQUELAE
    As in ARDS, pulmonary sequelae usually resolve
    almost completely within 1 year.

    Residual subclinical diffusion capacity deficits may
    exist.

    Residual neurologic deficits may range from
    nonexistent to subtle personality changes to memory
    and cognitive dysfunction to long-term focal deficits.

    SUMMARY FES
    Clinical diagnosis so high index of suspicion.

    Most effective management is prevention with rigid
    fixation of fractures within 24 hours

    When developed management is supportive.

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