Skull fractures
Blunt head trauma often leads to disruption of the bone framework integrity. Injuries are divided into skull base and skull vault fractures. Vault fractures are classified into linear and depressed. Depressed defects vary in shape: they can be perforated, comminuted, or terraced.
Open skull vault fractures present a particular clinical hazard. In this mechanism of injury, not only bone structures are involved in the pathological process, but also the skin, underlying soft tissues, as well as the anatomical formations of the middle ear and paranasal sinuses.
Maxillofacial injuries
Facial injuries are distinguished by a high risk of combined complications. The main bone injuries include fractures of the nasal bones, zygomatic bone, maxilla, and mandible, as well as temporomandibular joint dislocation and dental trauma.
A critical aspect is the threat of upper airway obstruction. This life-threatening condition can develop against the background of:
- massive hemorrhages and pronounced edema in the oral cavity;
- maxillary or mandibular fractures;
- aspiration of knocked-out teeth.
In addition, maxillofacial trauma is frequently accompanied by soft tissue facial injuries and cervical spine trauma, requiring a comprehensive approach during examination.
Diffuse brain injuries
This group includes conditions where the brain substance suffers globally, without a clearly demarcated local focus.
- Concussion. Occurs due to direct mechanical impact. Pathological anatomy is limited to soft tissue head injuries, while skull vault and base fractures are absent.
- Diffuse axonal injury. Develops due to rapid, sudden angular head rotation. Initially, macroscopic changes and structural defects on computed tomography (CT) are absent. Primary traumatic axonal injury and diffuse white matter degeneration occur. In young patients, signs of atrophy and a sharp decrease in brain weight may be detected. Macroscopic signs, such as brainstem hemorrhages or corpus callosum tears, are only discovered in prolonged coma progressing to a vegetative state or death.
Focal injuries and brain compression
Focal injuries include contusions and various types of intracranial hemorrhages resulting from direct impact or contrecoup.
Brain contusion is accompanied by focal changes on CT. Primary hemorrhages form at the site of impact, contrecoup impact, along the wound tract, or in the area of bone fragment penetration. Severity ranges from punctate cortical hemorrhages (mild) to cortical and white matter foci (moderate) and complete destruction of brain tissue with pial tears (severe).
Brain compression is most commonly caused by hematomas:
- Epidural hematoma: accumulation of blood between the periosteum and the dura mater. The source is arterial bleeding (often in temporal bone fractures when the fracture line crosses the middle meningeal artery sulcus). Appears on CT as a high-density, biconvex lens-shaped zone.
- Subdural hematoma: localized between the dura and arachnoid mater. Occurs upon rupture of pial veins or sinuses. Passes through acute (up to 2 days, liquid blood, neuronal ischemia), subacute (2–14 days, fibrin and erythrocyte clot), and chronic (more than 14 days, brain atrophy) stages.
- Subarachnoid hemorrhage: blood collects between the arachnoid mater and the brain surface, filling sulci, cisterns, and ventricles. Fresh erythrocytes are found in the cerebrospinal fluid.
For quick memorization of hematoma locations: Epidural — between the bone and dura mater (arterial, lens shape on CT); Subdural — between the dura and arachnoid mater (venous); Subarachnoid — between the arachnoid mater and brain surface (blood in sulci and CSF).
Class and exam questions
How to distinguish an epidural hematoma on CT?
It has a characteristic biconvex lens shape and high density. This shape is due to the fact that the dura mater is tightly adhered to the inner table of the bone, preventing diffuse spreading of blood.
What is the main feature of diffuse axonal injury?
It occurs upon rapid angular head rotation. The main feature is the absence of visible structural CT damage and macroscopic brain changes in the early stages, despite the patient's severe condition.
How do the stages of subdural hematoma differ?
In the acute stage (up to 2 days), the hematoma consists of liquid blood, accompanied by edema and ischemia. In the subacute stage (2–14 days), a clot of fibrin strands and erythrocytes forms. In the chronic stage (more than 14 days), atrophy of adjacent brain areas develops.
What else to study on this topic
- Mechanisms of contrecoup focus formation in brain contusions.
- Topography of the middle meningeal artery and its relationship with temporal bone fractures.
- Pathogenesis of ischemic neuronal injury in acute subdural hematoma.
- Spontaneous subdural hematomas upon rupture of vascular malformations.
- Brain laceration foci and compression in depressed skull fractures.
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