Post-traumatic cerebral fat embolism

Introduction to brain fat embolism after trauma Cerebral fat embolism is more common in craniocerebral injury with long bone fractures, or fat wounded with large area crush injury. Fat drops enter the ruptured sinus and reach blood circulation, causing fat embolism of multiple organs in the body, where the embolus passes through the lungs. A anterior bronchial capillary branch or a foramen ovale through the right atrial occlusion enters the systemic circulation. Although there is lung filtration, some blood vessels enter the cerebral blood vessels and form brain fat embolism. basic knowledge The proportion of illness: 0.001% Susceptible people: no special people Mode of infection: non-infectious Complications: interstitial pneumonia, acute pulmonary edema, cerebral edema, cerebral palsy

Causes of brain fat embolism after trauma

(1) Causes of the disease

When patients with craniocerebral injury have multiple systemic injuries or long bone fractures, fat particles can free human blood to become fat emboli, causing fat embolism in multiple organs in the body, most of which stay in the lungs, causing pulmonary fat plugs However, the granules enter the systemic circulation through the pulmonary-bronchial anterior capillary traffic branch or through the foramen ovale of the right atrial occlusion, and fat embolism occurs in important organs such as brain, kidney, heart and liver.

(two) pathogenesis

Generally, fat embolism firstly causes mechanical obstruction of blood vessels in the lungs, and then decomposes into free fatty acids by the action of lipase. The latter causes damage to vascular endothelial cells and abnormally increases the permeability of blood vessel walls, thereby promoting hemorrhagic Pneumonia and acute pulmonary edema, fat emboli into the cerebral blood vessels often embolize most small blood vessels in the brain, causing extensive punctate erythema and hemorrhagic infarction in the white matter and cerebellar hemisphere of the brain. The cerebral edema reaction is also more serious. Therefore, patients often have aggravation or new neurological damage. At present, the main pathological changes of post-traumatic fat embolism syndrome are in the brain or in the lungs. Sevitt believes that the main lesion is in the brain, emphasizing the occurrence of tissue lesions. The size and number of fat emboli, the time of hypoxia, the presence or absence of collaterals in small blood vessels, and the sensitivity of organs to hypoxia are all related. The brain tissue is sensitive to ischemia, hypoxia and poor tolerance. It is easy to cause damage. Clinically, cases with neurological damage and preceded with pulmonary symptoms have been found. Cerebral embolism is the leading cause of death. Eltier believes that the main lesion is in the lungs, stressing the primary lesion of fat embolism in the lungs, respiratory insufficiency caused by pulmonary fat embolism and hypoxemia are the main causes of secondary hypoxia in brain tissue. Hypoxia is hypoxic hypoxia rather than ischemic hypoxia. From this point of view, it is necessary to see which pathological changes are more serious, so each patient is different.

Prevention of brain fat embolism after trauma

Avoid trauma and pay more attention to rest.

Complications of brain fat embolism after trauma Complications interstitial pneumonia acute pulmonary edema cerebral edema cerebral palsy

Fatal embolism may occur in the system, such as interstitial pneumonia, acute pulmonary edema and cerebral edema. Patients with increased intracranial pressure may have cerebral palsy. If there is no timely and reasonable treatment, the patient often dies within a short period of time.

Symptoms of brain fat embolism after trauma Common symptoms Difficulty breathing High fever twitching cyanosis Increased intracranial pressure Increased heart rate Increased coma Blood pressure decreased hemoptysis consciousness

In the wounded person with craniocerebral trauma and long bone fracture, there is unconsciousness or coma 1 to 2 days after the injury. After a few days, the disturbance of consciousness is aggravated, accompanied by hemiplegia, convulsions, aphasia, high fever, rapid heart rate, blood pressure drop, cough , breathing difficulties, cyanosis and other cardiopulmonary symptoms, there may be subcutaneous congestion at the neck, shoulder, chest, abdominal wall, etc., retinal hemorrhage and intravascular fat embolus can be seen in the fundus, due to the occurrence and development of cerebral edema, patients often have epilepsy And increased intracranial pressure, but the signs of localized neurological deficits are rare. Depending on the location and extent of vascular involvement, light cases can only be temporarily suppressed for a few days, headaches, lethargy, and more complete recovery after sputum. The change of transient consciousness is often attributed to the reaction of brain injury without paying attention. In severe cases, the brain fat embolism is serious, and the onset is rapid. The patient can change from awake to coma, respiratory distress, weak pulse and blood pressure drop within a few hours after the injury. The venous pressure is elevated and the hemoptysis is paralyzed. If there is no timely and reasonable treatment, the patient often dies in a short period of time .

Examination of brain fat embolism after trauma

Laboratory inspection

Urine, sputum, cerebrospinal fluid can be seen in erythrocytosis, with fat globules, patients with arterial blood oxygen tension decreased (60mmHg or below 8.0kPa), hemoglobin decreased (less than 100g / L), thrombocytopenia, increased erythrocyte sedimentation rate, serum lipase Increase (3 to 4 days after injury, and peak at 7 to 8 days).

Film degree exam

1. X-ray film: a wide range of "blizzard"-like flocculent shadows visible in the lungs.

2. CT and MRI scan: CT scan and evolution are the same as cerebral infarction, but have the following two characteristics:

(1) often hemorrhagic infarction.

(2) Different arterial blood supply areas showed multiple cortical infarctions. MRI showed more high-signal lesions in white matter on both T1 and T2-weighted images.

Diagnosis and differentiation of brain fat embolism after trauma

Early diagnosis of post-traumatic brain fat embolism is often difficult, especially in patients with severe brain trauma, often confused, easy to miss diagnosis, many patients until the death of the autopsy began to be a clear diagnosis, therefore, the head of the head after trauma The disturbance of consciousness caused by sexual injury has improved, the condition has deteriorated again, accompanied by obvious respiratory symptoms, the bleeding point of the skin and the heart rate that is difficult to explain increase. When the blood pressure drops, the disease should be thought of. Generally, the fundus examination can be more. Hemorrhagic spots were found. Occasionally, fat emboli in the blood vessels could be seen. At the same time, fat globules were also found in the patient's sputum, urine and cerebrospinal fluid. X-ray pictures of the lungs showed a unique "storm"-like change, brain CT scan. In addition to cerebral edema, there were many abnormal findings, and MRI showed high-signal lesions on T1 and T2-weighted images.

In patients with complex injury, new brain symptoms appear after the condition is stable or improved. Considering the intracranial hematoma, the possibility of brain fat embolism should be considered. CT scan can help diagnosis.

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