fat_embolism.pdf

7/25/2019 fat_embolism.pdf

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Fat Embolism Syndrome

Dr. Alex Rabinovich


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Introduction

Zenker (Pathologist) first identified fat

embolism syndrome (FES) at autopsy in1862.

von Bergmann was the first physician toidentify FES clinically in 1873.

Initial clinical description was respiratory

and neurological manifestations with

petechial hemorrhages.


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Introduction

Most commonly associated with LONG BONE

(Femur, Tibia, Humerus, ), PELVIC andSPINAL #s

More frequent in CLOSED > OPEN #s

Younger pts (more bone marrow) > Older Pts

A single long bone # has 1-5% chance of

developing FES, this directly correlates with thenumber of long bone #s

FES has been reported as high as 33% in

bilateral femoral fractures.


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Introduction


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Pathophysiology

2 Theories

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 sepsisinduce systemic release of free fatty acids (FFA) as

chylomicrons which cause the systemic FES.


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Pathophysiology

Mechanical

This theory is supported by research onOrthopaedic long bone (IM reaming) andspinal surgeries which cause fat globules to

enter the blood circulation when vigorousreaming/fixation is done.

Increased Pressure + Volume

Extravasation Measuring fat globules pre and post reaming

shows significant difference in concentration.


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Pathophysiology

Mechanical

But what makes this clinically significant? Fat droplets are deposited in the pulmonary capillary

beds and travel through arteriovenous shunts to the

brain. Systems affected include LUNG, BRAIN andCIRCULATION.

Microvascular lodging of droplets produces local

ischemia and inflammation, with concomitant releaseof inflammatory mediators, platelet aggregation, and

vasoactive amines.


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Pathophysiology

Biochemical

FES is dependent upon degradation of the embolizedfat into free fatty acids.

Neutral fat does not cause an acute lung injury, it is

hydrolyzed over the course of hours to severalproducts, including FFA, which cause ARDS in animal

models.

CRP (acute phase reactant), which is elevated intrauma patients, appears to be responsible in lipid

agglutination (FES) for both traumatic and non-

traumatic FES.


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Pathophysiology

Biochemical

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 andcircumstantial at best.


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Clinical

Diagnosis is made clinically NOT

chemically. It does not matter how muchfat globules are in your circulation, it justmatters if you have their side effects.

FES typically manifests 24 to 72 hoursafter the initial insult. Rarely 72 hrs.

Classic triad: Hypoxemia; Neurologicabnormalities; and a Petechial Rash


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Clinical

SOB, Inc RR, Hypoxemia are early findings.50% of pts with symptoms will need ventilationsupport. Respiratory dysfunction is major causeof mortality, which is about 10-20%.

Neurologic symptoms usually develop after lunginjury, and include: Confusion, altered LOC,Headaches, +/- Seizures, +/- Strokes with FocalDeficits.

Petechial rash is usually a late finding(frequency of 20-50% of pts). Head, neck,

anterior thorax, subconjunctiva, and axillae aremost common regions.


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Clinical Petechiae result from the occlusion of dermal

capillaries by fat globules, leading toextravasation of erythrocytes.

No abnormalities of platelet function have beendocumented.

The rash resolves in five to seven days. Other Findings

Scotomata (Purtscher's retinopathy)

Lipiduria Fevel

Coagulation Abnormalities (DIC like)

Myocardial Depression


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Diagnosis FES is clinical diagnosis

CXR (n) mostly. Some have patchy

consolidations at periphery or bases due toalveolar hemorrhages, but not sensitive norspecific (snow storm pattern).

Ventilation/perfusion scans may demonstrate a

mottled pattern of subsegmental perfusiondefects with a normal ventilatory pattern.

Focal areas of ground glass opacification with

interloblar septal thickening are generally seenon chest CT

MRI of the brain may reveal high intensity T2

signal, which correlates with the degree ofclinical neurologic impairment


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Diagnosis Common misconception that the presence of fat

globules, either in sputum, urine, or a wedgedPA catheter, is necessary to confirm the

diagnosis of FES In 50% of fracture patients, fat globules was

demonstrated in the serum, without symptoms of

FES.

HOWEVER

Growing literature on the use of bronchoscopywith bronchoalveolar lavage to detect fatdroplets in alveolar macrophages as a means to

diagnose fat embolism. Sensitivity and specificityare unknown, being studied in Trauma patients.


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Diagnosis Classic Gurds criteria 1 major criteria and at least 4 minor criteria

Major Criteria

PaO2 < 60mmHg &

FiO2 >40%

Altered mentation Petechial rash

Minor Criteria

Temp > 38.5 0C

HR > 120/min

PLTs < 150 X 109/L Retinal fat emboli

Oliguria/anuria

Fat globules in urine

HCT not attributed to

blood loss or IVF dilution

Fat macroglobulemia


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Treatment ATLS protocol

High clinical suspicion during 3rd survey

1. Early immobilization of fracture and early

definitive reduction (open or closed).

2. Maintain intravascular volume tomaintain cardiovascular stability

(hypovolemic shock resuscitation), mayuse colloids (albumin) as it can expand

fluid and bind FFA.

3. Mechanical ventilation with PEEP


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Treatment

4. IV Ethanol has been used in Russia,

Europe and some American centres todecrease rate of FES.J Bone Joint Surg Am. 1977 Oct;59(7):878-80

A raised level of alcohol in the bloodwas associated with a lower incidence offat embolism all other variables

controlled.

Other studiesCan J Surg. 1970 Jan;13(1):41-9Br Med J. 1978 May 13;1(6122):1232-4


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Treatment5. Corticosteroids (controversial) Surg Gynecol Obstet. 1978 Sep;147(3):358-62

Ann Intern Med. 1983 Oct;99(4):438-43

J Trauma. 1987 Oct;27(10):1173-6

J Bone Joint Surg [Br] 1987 Jan;69(1):128-31

Methylprednisolone is the study drug

Randomized double blind studies Specific to fractures and all other variables

controlled. RCTs with control drugs.

Differences was dosing and timing of drugadmin.

Major S/E looked at: GI Bleeds, Infections,Delayed healing, Cortisol issues, and CVSstability (cardiac mostly), Mortality


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Treatment

5. Corticosteroids

Other doses: 1.5 mg/kg q8h X 48 hrs

Statistical Significance in reduction of clinical diagnosed FES

No major complications were noted

Potential for complications is the major concern (bleeds, infection,

cardiac compromise)

Key is to initiate treatment early and for a short period of time Be cautious of the S/E

12 doses


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Treatment

The overall outcomes of FES with respect toisolated long bone, pelvis and spine fractures isgood with standard immobilization and reductionof fracture, fluid resuscitation and ventilatorsupport as needed.

Steroids and Ethanol treatments can be adjunctsto treatment, but most be started early.Recommended to start with low dose and for aperiod of 24-48 hours.

No evidence on Steroids or Ethanol Tx onceFES is diagnosed. This is only for Prophylaxis


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Almost Over

Now that you have learned the basics of

FES. Its time for your final exam


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Questions

What percentage of people with skeletal

trauma would normally develop fat emboli, andwhat percentage of these would then develop

the Fat Embolism Syndrome?

1. 30% and 12%

2. 50% and 10%3. 70% and 1%

4. 90% and 5%


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Questions

What percentage of people with skeletal

trauma would normally develop fat emboli, andwhat percentage of these would then develop

the Fat Embolism Syndrome?

1. 30% and 12%

2. 50% and 10%

3. 70% and 1%

4. 90% and 5%


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Questions

How does fat emboli enter the systemic

circulation (arterial vs. venous)?


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Questions

How does fat emboli enter the systemic

circulation (arterial vs. venous)?

Patent Foramen Ovale


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What percentage of the generalpopulation are considered to have apatent foramen ovale?

5%

15%

25%

40%

Questions


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What percentage of the generalpopulation are considered to have apatent foramen ovale?

5%

15%

25%

40%

Questions


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Questions

A biochemical theory suggests that a chemical eventduring trauma, or during the activation of the stress

response, affects the solubility of circulating lipidscausing them to coalesce and form systemic emboli.These emboli travel to lungs, brain and skin to give theFES triad of signs.

There are some very unusual causes of FES in the non-trauma patients, including the strikingly unusual:liposuction, chemotherapy, renal transplant.

1. True

2. False


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Questions

A biochemical theory suggests that a chemical eventduring trauma, or during the activation of the stress

response, affects the solubility of circulating lipidscausing them to coalesce and form systemic emboli.These emboli travel to lungs, brain and skin to give theFES triad of signs.

There are some very unusual causes of FES in the non-trauma patients, including the strikingly unusual:liposuction, chemotherapy, renal transplant.

1. True

2. False


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Questions The pulmonary signs are usually noted first and include

tachypnoeia, dyspnoea and cyanosis. These signsresult from the embolic fat being hydrolised by lung

lipase with the release of lung-toxic FFA. These FFAsinduce an acute lung injury and subsequent ARDS.

This process accounts for the time period betweeninjury and onset of clinical signs of FES. Time period isusually:

1. 6 to 12 hours

2. 12 to 24 hours

3. 24 to 72 hours

4. 72 to 84 hours


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Questions The pulmonary signs are usually noted first and include

tachypnoeia, dyspnoea and cyanosis. These signsresult from the embolic fat being hydrolised by lung

lipase with the release of lung-toxic FFA. These FFAsinduce an acute lung injury and subsequent ARDS.

This process accounts for the time period betweeninjury and onset of clinical signs of FES. Time period isusually:

1. 6 to 12 hours

2. 12 to 24 hours

3. 24 to 72 hours

4. 72 to 84 hours


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Questions

The cutaneous signs are usually seen within 72hours. On a critically ill patient they may go

unnoticed, thereby losing the chance forconfirmation of diagnosis.

The rash is usually seen on:

1. Thighs / Calves / Ankles

2. Clustered around the fracture site3. Chest / Axilla / Conjunctiva

4. Back of the head and knees


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Questions

The cutaneous signs are usually seen within 72hours. On a critically ill patient they may go

unnoticed, thereby losing the chance forconfirmation of diagnosis.

The rash is usually seen on:

1. Thighs / Calves / Ankles

2. Clustered around the fracture site3. Chest / Axilla / Conjunctiva

4. Back of the head and knees

Q


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Questions

Cerebral signs are non-specific, very rarely focal:headache, irritability and delirium. Severe cases may

show coma and convulsions. These signs are producedby embolism of fat through a patent foramen ovale andsubsequent microvascular occlusion of the braincirculation by fat.

Embolic fat can produce the necessary right heartpressures to open a patent foramen ovale but what isanother causative factor?

1. Increased cardiac pressures from ventilation2. Pneumothorax or haemothorax

3. Poor positioning on the OR table

4. Pressure exerted on the chest by OR equipment

Q ti


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Questions

Cerebral signs are non-specific, very rarely focal:headache, irritability and delirium. Severe cases may

show coma and convulsions. These signs are producedby embolism of fat through a patent foramen ovale andsubsequent microvascular occlusion of the braincirculation by fat.

Embolic fat can produce the necessary right heartpressures to open a patent foramen ovale but what isanother causative factor?

1. Increased cardiac pressures from ventilation2. Pneumothorax or haemothorax

3. Poor positioning on the OR table

4. Pressure exerted on the chest by OR equipment

Q ti


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Questions Diagnosis is always made on clinical grounds, there is no specific"test" for FES. Various sets of criteria exist to make the diagnosis

more accurate, such as those of Gurd & Wilson or those ofVedrienne, Guillaume and Gagnieu.

Management is then supportive as there is no specific treatment ofthe FES. Guidelines for the management of FES would include:

1. Prompt immobilisation of the fracture / delayed internal fixation ofthe fracture / early use of steroids / early use of Heparin

2. Prompt immobilisation of the fracture / early internal fixation of thefracture / prompt treatment of hypoxia / maintenance of cardiacoutput

3. Prompt immobilisation of fracture / intraoperative surgicalembolectomy / early use of IV Ethanol / daily low dose Aspirin

4. Prompt immobilisation of the fracture / avoidance of intramedullarynails / early use of steroids / mandatory use of calf compressors

Q ti


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Questions Diagnosis is always made on clinical grounds, there is no specific"test" for FES. Various sets of criteria exist to make the diagnosis

more accurate, such as those of Gurd & Wilson or those ofVedrienne, Guillaume and Gagnieu.

Management is then supportive as there is no specific treatment ofthe FES. Guidelines for the management of FES would include:

1. Prompt immobilisation of the fracture / delayed internal fixation ofthe fracture / early use of steroids / early use of Heparin

2. Prompt immobilisation of the fracture / early internal fixation ofthe fracture / prompt treatment of hypoxia / maintenance ofcardiac output

3. Prompt immobilisation of fracture / intraoperative surgicalembolectomy / early use of IV Ethanol / daily low dose Aspirin

4. Prompt immobilisation of the fracture / avoidance of intramedullarynails / early use of steroids / mandatory use of calf compressors

Q ti


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Questions

A Pulmonary Artery Catheter is often inserted tofacilitate the use of inotropic agents and fluids in a

critically ill patient with FES. Bearing in mind that therewill be widespread microvascular occlusion with fat inthe pulmonary vasculature what would be the mosttypical finding?

1. A high Systemic Vascular Resistance (SVR)

2. A low Systemic Vascular Resistance (SVR)

3. A high Pulmonary Vascular Resistance (PVR)4. A low Pulmonary Vascular Resistance (PVR)

Q ti


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Questions

A Pulmonary Artery Catheter is often inserted tofacilitate the use of inotropic agents and fluids in a

critically ill patient with FES. Bearing in mind that therewill be widespread microvascular occlusion with fat inthe pulmonary vasculature what would be the mosttypical finding?

1. A high Systemic Vascular Resistance (SVR)

2. A low Systemic Vascular Resistance (SVR)

3. A high Pulmonary Vascular Resistance (PVR)4. A low Pulmonary Vascular Resistance (PVR)

Q ti


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Questions

A patient who does not develop a

petechial rash by day 2 or 3 on his or herchest, anterior axillary folds or

conjunctiva does not have either Fat

Embolism or Fat Embolism Syndrome.

1. True2. False

Questions


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Questions

A patient who does not develop a

petechial rash by day 2 or 3 on his or herchest, anterior axillary folds or

conjunctiva does not have either Fat

Embolism or Fat Embolism Syndrome.

1. True2. False

The END


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The END

Thank you

References

1. UpToDate website2. eMedicine website

Documents

fat_embolism.pdf