SN4 SHORT NOTE 5M ★ High-yield

Describe fat embolism syndrome with its pathogenesis and clinical features.

Pathology · 2nd Professional — Para-Clinical

Definition

Fat embolism is the presence of globules of fat in the circulation, and fat embolism syndrome is the clinical illness that follows when they cause respiratory, neurological and cutaneous disturbance.

Fat globules are found in about 90% of patients with severe skeletal injury, but fewer than 10% develop the syndrome — the distinction matters

Causes

Fracture OF A long bone — especially the femur and tibia; the commonest cause by far
Orthopaedic procedures — reaming, intramedullary nailing, joint replacement
Extensive soft tissue trauma and severe burns
Non-traumatic causes — acute pancreatitis, sickle cell crisis (marrow infarction), liposuction, fatty liver, corticosteroid therapy

Pathogenesis

Mechanical theory → Marrow fat enters torn venous sinusoids, which are held open by bone → Globules travel to the pulmonary capillaries and obstruct them → Smaller globules pass through to the systemic circulation → brain and skin → biochemical theory — acting alongside → lipase hydrolyses the neutral fat to free fatty acids → These are directly toxic to endothelium and to pneumocytes → Increased permeability, oedema and platelet aggregation

The biochemical component explains the latent period of 24–72 hours — purely mechanical obstruction would be immediate

Clinical Features

System	Features	Frequency
Respiratory	Dyspnoea, tachypnoea, hypoxaemia; may progress to acute respiratory distress syndrome	Earliest and commonest — about 75%
Neurological	Restlessness, confusion, drowsiness, seizures, coma; usually reversible	About 60%
Cutaneous	Petechial rash over the upper chest, axillae, neck and conjunctivae; appears late and fades within a day	About 30–50%, but nearly pathognomonic
Other	Fever, tachycardia, retinal fat globules, thrombocytopenia, anaemia	—

CLINICAL PEARL

The latent period is the diagnostic clue. A patient who is stable after a femoral fracture and then becomes breathless and confused 24 to 72 hours later, with petechiae above the nipple line, has fat embolism syndrome until proved otherwise. Immediate collapse points to haemorrhage or pulmonary thromboembolism instead.

Diagnosis, Treatment and Applied Aspects

The diagnosis is clinical; no test confirms it. Gurd criteria combine the major features above with minor ones
Fat globules in urine, sputum and retinal vessels support it but are neither sensitive nor specific
Chest radiograph shows a "snowstorm" of bilateral patchy shadows; MRI brain shows a "starfield" pattern
Treatment is supportive — oxygen, ventilation if needed, fluids and analgesia; steroids and heparin are not established
Prevention is what matters — early immobilisation and operative fixation of long bone fractures within 24 hours substantially reduces the incidence
Mortality is 5–15%, and most survivors recover fully — so aggressive supportive care is well justified
Distinguish it from pulmonary thromboembolism — that occurs later, has no rash, and is associated with a deep vein thrombosis rather than a fresh fracture
Hypoxaemia is often the earliest sign, so pulse oximetry in every patient with a long bone fracture is a simple and effective precaution

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