Fat embolism syndrome

Fat Embolism Syndrome

Dr. Ankit Desai

Dr.B.L.Chandrakar

History

First diagnosed in 1873 by Dr Von Bergmann

Published in 1879 Fenger and Salisbury.

FE vs FES

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 .

Some 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 manifestation of fat embolism occasionally causes multi system dysfunction, the lungs are always involved and next is brain

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. commanly with lower limb injury

Onset is 24-72 hours from initial insult

Pathogenesis

Mechanical Theory Physical obstruction of the pulmonary & systemic

vasculature with embolized fat. Temporary rise in I/M pressure - forces marrow into

injured venous sinusoids. Cor pulmonale - inadequate compensatory pulmonary

vasodilatation. Microvascular lodging - local ischemia and inflammation. Release of inflammatory mediators, platelet aggregation,

& vasoactive amines,veno arterial shunting,hypoxemia leeds to alveolar hypoperfusion leading to PD

Size of fat globules 2 to 200 micron Blood vessele <75 micron

The biochemical theory

Free fatty acid is culprit Circulating FFAs -directly toxic to Pneumocytes /

capillary Endothelium in the lung – decrease surfactant ,nterstitial hemorrhage, edema & chemical pneumonitis.

Local hydrolysis of Triglycerides and fat emboli by pneumocyte lipase -- Increase fatty acid .

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.

Triad of FES

Pulmonary dysfunction

Neurological abnormalities

Petechial rash

Early Signs

Dyspnea,

Tachypnea

Hypoxemia PaO2 < 60 mm Hg confusion

Pulmonary Picture

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.

½ of pts require mechanical ventilation

Imagining

• Chest x-ray– shows multiple flocculent shadows (snow storm appearance). picture

may be complicated by infection or pulmonary edema.– CT chest: ground glass opacification with interlobular septal thickening

• CT Scan brain – may be normal or may reveal diffuse white-matter petechial

haemorrhages

• Helical CT Scan chest– may be normal as the fat droplets are lodged in capillary beds. Can

detect lung contusion, acute lung injury, or ARDS may be evident.

Chest X-ray

ER admitAP & expiratory film so we cannot comment on cardiac shadow. However, there is no evidence of lung contusion, pneumo, haemo or pneumohaemothorax.

SICU admit (12 hours later)upper lobe diversion and bilateral pulmonary infiltrates

Altaf Hussain: “A Fatal Fat Embolism.” The Internet Journal of Anesthesiology, 2004. Volume 8 Number 2.

Neurological findings 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

MRI showing foci of ischemia suggestive of fat embolism syndrome

post operative day 14 and shows evolving cortical infarctions

post operative day 2 showing multiple hyperintense areas consistent with multiple emboli

Source:http://www.ispub.com/journal/the_internet_journal_of_anesthesiology/volume_19_number_2/article/acute_fatal_fat_embolism_syndrome_in_bilateral_total_knee_arthroplasty_a_review_of_the_fat_embolism_syndrome.html

Rash Reddish-brown non-palpable Petechial rash - upper

anterior body, chest, neck, upper arm, axilla, shoulder, oral mucous membranes and conjunctivae in 20 - 50% patients.2 to 3re day

Resolvs in 7 day

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

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

Other findings

Retinopathy (exudates, cotton wool spots, hemorrhage)

Lipiduria Fever DIC Myocardial depression (R heart strain) Thrombocytopenia Anemia, Decreased Hematocrit Hypocalcemia

Diagnostic Criteria

Gurd’s criteria

Most commonly used

1 major, plus 4 minor

Gurd’s Criteria

Diagnosis Clinical examination preferred over diagnostic

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.

Treatment

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.

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.

Ethanol/alcohol in bolus dose iv :as lipase inhibitor

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.

Risk Factors

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