When a patient with a craniocerebral injury also has multiple systemic injuries or long bone fractures, fat particles can enter the bloodstream and become fat emboli, leading to fat embolism in multiple organs. Most fat emboli lodge in the lungs, causing pulmonary fat embolism. However, some fat particles may bypass the pulmonary circulation through precapillary bronchial-pulmonary anastomoses or pass through a patent foramen ovale in the right atrium, entering the systemic circulation and resulting in fat embolism in critical organs such as the brain, kidneys, heart, and liver. The incidence of this condition is 0.5–2% in cases of long bone fractures and approximately 5–10% in cases of multiple fractures or pelvic fractures.

bubble_chart Pathological Changes

Fat emboli initially cause mechanical obstruction of pulmonary blood vessels. Subsequently, they are broken down into free fatty acids by the action of lipase, which damages vascular endothelial cells, leading to abnormally increased vascular permeability and contributing to hemorrhagic interstitial pneumonia and acute pulmonary edema. Fat emboli entering the cerebral vasculature often occlude numerous small blood vessels in the brain, causing widespread petechial hemorrhages and hemorrhagic infarcts in the cerebral white matter and cerebellar hemispheres. The cerebral edema reaction is also more severe than usual, so patients often experience worsening conditions or new neurological impairments. Currently, there is disagreement over whether the primary lesions of post-traumatic fat embolism syndrome are in the brain or the lungs. Sevitt believes the main lesions are in the brain, emphasizing that the development of tissue damage is closely related to the size and quantity of fat emboli, the duration of hypoxia, the presence of collateral circulation in small vessels, and the organ's sensitivity to hypoxia. Brain tissue is highly sensitive to ischemia and hypoxia and has very poor tolerance, making it prone to damage. Clinically, cases where neurological damage predominates and precedes pulmonary symptoms are frequently observed, with cerebral embolism being the primary cause of death. Peltier, however, argues that the primary lesions are in the lungs, stressing that the initial pathological changes of fat embolism occur in the lungs. The resulting respiratory insufficiency and hypoxemia due to pulmonary fat embolism are the main causes of secondary hypoxia in the brain. This cerebral hypoxia is hypoxic hypoxia rather than ischemic hypoxia. Thus, the severity depends on which pathological changes are more pronounced, and this varies from patient to patient.

Symptoms of cerebral fat embolism typically appear 1 to 2 days after trauma, characterized by fever, rapid pulse, restlessness, and progressively deepening disturbances of consciousness, accompanied by rapid breathing, cough, cyanosis, blood-streaked sputum, decreased blood pressure, and subcutaneous petechiae on the neck, shoulders, chest, and abdominal wall. Due to the occurrence and progression of cerebral edema, patients often exhibit seizures and signs of increased intracranial pressure, though focal neurological deficits are relatively uncommon and vary depending on the location and severity of vascular involvement. Mild cases may only present with transient suppression lasting a few days, along with headaches and drowsiness, with most patients recovering fully afterward. These transient changes in consciousness are often attributed to the brain's response to injury and thus overlooked. In severe cases, cerebral fat embolism is critical, with sudden onset. Patients may transition from alertness to unconsciousness within hours of injury, accompanied by respiratory distress, weak pulse, decreased blood pressure, elevated venous pressure, and expectoration of bloody sputum. Without prompt and appropriate treatment, patients often succumb within a short period.

bubble_chart Diagnosis

Early diagnosis of cerebral fat embolism after trauma is often difficult, especially in patients with severe concomitant brain injuries, where confusion is common and misdiagnosis as fistula disease occurs frequently. Many cases are only definitively diagnosed postmortem during autopsy. Therefore, when a patient with head trauma shows initial improvement in consciousness due to primary brain injury but subsequently deteriorates, accompanied by significant respiratory symptoms, petechial skin hemorrhages, and unexplained tachycardia or hypotension, this condition should be suspected. Fundoscopic examination often reveals hemorrhagic spots, and occasionally intravascular fat emboli may be observed. Additionally, fat globules can be detected in the patient's sputum, urine, and cerebrospinal fluid. The patient may exhibit a stirred pulse, progressive decrease in blood oxygen tension (below 60 mmHg or 8.0 kPa), decreased hemoglobin (below 100 g/L), thrombocytopenia, elevated erythrocyte sedimentation rate, and increased serum lipase (peaking 7–8 days after injury, with initial rise at 3–4 days). Chest X-rays typically show a distinctive "snowstorm" pattern. Brain CT scans usually reveal no abnormalities other than cerebral edema. On MRI, multiple high-signal lesions in the white matter can be observed in both T₁

bubble_chart Treatment Measures

The treatment of cerebral fat embolism after trauma must target the systemic fat embolism lesions, especially addressing interstitial pneumonia, acute pulmonary edema, and cerebral edema. Strong measures should be taken as early as possible to improve respiratory function and correct hypoxemia, thereby controlling the series of pathophysiological changes in vital organs such as the lungs, brain, and heart. First, administer sufficient oxygen inhalation at a concentration of 40–45% to rapidly increase the arterial oxygen tension and maintain it at normal levels. If the arterial oxygen tension falls below 60 mmHg (8.0 kPa), endotracheal intubation or tracheostomy should be performed, assisted by mechanical ventilation with positive end-expiratory pressure (PEEP). The expiratory port should maintain a positive pressure of 10 cmH₂O (0.98 kPa) to increase the alveolar-arterial oxygen gradient. Simultaneously, fractures should be properly immobilized to prevent further entry of fat emboli into the venous circulation, and a tourniquet may be used if necessary. If hemorrhagic shock is present, blood volume should be adequately replenished. Next, administer high-dose corticosteroid therapy to protect capillary wall integrity, reduce exudation, prevent vasospasm and platelet aggregation, and help control the progression of pulmonary and cerebral edema. The initial dose is typically methylprednisolone 125 mg intravenously, followed by 80 mg every 6 hours for 3 days. Alternatively, hydrocortisone 500–1000 mg/day may be used for 2 days, followed by 300–500 mg every 3 days. Additionally, necessary treatments such as dehydration, diuresis, antiepileptic therapy, hypothermia, and anti-infection measures should be implemented. Intravenous infusion of low-molecular-weight dextran (500–1000 ml/day) can reduce blood viscosity and improve peripheral circulation, but prolonged use should be avoided to prevent coagulation disorders. Platelet ratios should be monitored if necessary to guard against bleeding tendencies. Previously used treatments such as alcohol or heparin for fat embolism are now rarely employed due to limited efficacy and potential risks.