fat embolism

FAT EMBOLISM SYNDROMEFAT EMBOLISM SYNDROME

FAT EMBOLISM

Indicates the presence of fat globules in lung parenchyma & peripheral circulation after # of a long bone or major trauma.

Usually occurs within 72 hrs of skeletal trauma.

Often asso with multiple #res, major bone #res, pelvic #res, multi system injuries like chest& abdomen, head injuries etc.

Causes a devastating clinical deterioration within hrs.

The overall prevalence of fat embolism syndrome is 1% to 3.5% of patients with a fracture of tibia or femur.

Patients with bilateral femoral fractures are at particular risk & have a higher risk of ARDS & death.

CAUSES Traumatic & non traumatic factors.

1. Traumatic causes are;

Fractures – long bones, pelvis Burns Surgery – IM nailing, arthroplasty Sub cutaneous adipose tissue injuries.

2. Non traumatic causes;• Diseases – DM, collagen diseases, severe

infections, c/c pancreatitis, c/c alcoholism, osteo myelitis, sickle cell anemia.

Procedures – cardio pulmonary bypass, blood transfusion, renal transplantation, liposuction.

PATHO PHYSIOLOGY Mechanical theory& Bio chemical theory

-Toxic theory

-Obstructive theory• Mechanical theory;

Suggests that fat globules are forcibly intravasated from marrow thru disrupted vessels & then they are transported to the pulmonary vascular bed & are trapped as emboli in the lung capillaries.

Some reaches systemic circulation causing embolization in areas such as brain,kidney,retina or skin.

2. Bio chemical theory;

Toxic theory – Lung lipase hydrolyzes neutral fat to chemically toxic free fatty acids. This causes severe inflammatory changes by producing endothelial damage, inactivation of lung surfactant & increase in capillary permeability leading to ARDS.

Obstructive theory –

A chemical event at the site of # releases mediators that affect the solubility of lipids, causing coalescence & subsequent embolization. Normal chylomicrons may coalesce & form fat globules which are capable of occluding the lung capillaries.

Gurd’s criteria for diagnosis

Major criteria:

- Axillary & sub conjunctival petechiae.

- Pa O2 < 60 mm Hg

- CNS depression Minor criteria:

- pulse>110/mt

- pyrexia>38.5

-retinal embolism

-fat in urine

- reduced platelet count- increased ESR- Fat globules in sputum

…..At least 1 from major criteria & 4 from minor criteria.

The classic syndrome involves pulmonary, cerebral & cutaneous manifestations.

- Pulmonary: tachypnoea,dyspnoea,cyanosis,tachy cardia,& rhonchi

Cerebral: headache,irritability,delirium, stupor,convulsions & coma.

Cutaneous and retinal: retinal exudates, edematous patches,cotton wool spots & petechial haemorrhages.

Three presentations:

1.Sub clinical fat embolism syndrome:

Lab abnormalities present..but non specific clinical symptoms.

Tachy cardia>100beats/mt, tachypnoea >25breaths/mt, temp>37.8.

Moderate hypoxemia(Pa O2< 80mm Hg)& moderate decrease in platelets is a common finding.

2.Non fulminant sub acute fat embolism syndrome

Characterised by respiratory failure, fever, tachycardia, petechiae & cerebral signs etc.

Petechial rashes are pathognomonic of fat embolism syndrome.This rashes appears between 12 to 96 hrs following injury.

Retinal lesions are described as cotton wool spots & flame like haemorrhages on fundoscopy.

PaO2 <60 mm Hg,anemia,thrombocytopenia & lung opacities on CXR.

3.Fulminant fat embolism syndrome Severe variant. Patients may present with sudden hypotension,

cerebral signs, severe hypoxemia, frank pulmonary edema or acidosis.

Petechiae arise from occlusion & distention of dermal capillaries by fat globules & increased CP.•They are present across the chest,axilla,root of neck &conjunctiva and they fades rapidly.

Laboratory investigations

Shows hypoxemia(<60mm Hg),thrombocytopenia(<1.5 lakhs), anemia & hypo calcemia.

The most useful diagnostic test is arterial blood gas analysis.

PT & ESR increases. Demonstration of fat globules in urine, sputum or

blood. Raised serum lipase level& Raised blood lipid levels.

X ray chest:

Pathognomonic snow storm appearance.

ECG:

S waves prominent.

DIAGNOSTIC TRIAD:

1. Thromboctopenia

2. PaO2 < 60 mm Hg

3. Rashes

Management Non specific: 3 vital steps.1. Keep airway patent & #

immobilized.2. Restore blood volume, fluid &

electrolyte balance.3. Avoid careless handling of the

injured.

Specific: 3 vital steps.1. Respiratory support: Can

range from O2 administration to full respiratory support with mechanical ventillation.

2.Drug therapy

Treatment of shock: Aggressive fluid resuscitation under appropriate monitoring.

Albumin is preferred because it not only restores blood volume but also binds free fatty acids.

Steroids: Helps gas exchange by decreasing inflammation

in the lungs.Methyl prednisolone appears to modify the pulmonary response to injury by relative preservaton of arterial oxgenation.

Heparin: Increases serum lipase activity &

decreases no of circulating fat globules.

Low molecular wt dextran: Useful in prophylaxis. Acts by increasing plasma

volume,decreases blood viscosity & reduces platelet adherence.

Hypertonic glucose: Decreases free fatty acid production. Improves arterial oxygenation.

Intra venous alcohol: Reduces serum lipase activity. Thus limits free fatty acid production.

3. Definitive fracture treatment: Early fixation of fractures is advocated to

prevent worsening of the situation.