9.6 + 9.7 · Acute problems: Primary brain trauma and Secondary brain trauma

Primary brain injury

Damage caused directly by impact

Closed head injury

Dura mater stays intact, due to blunt trauma

Open or penetrating head injury

Break in the dura mater exposing cranial contents to the environment

Focal brain injury

Observable brain lesions occurring in a precise location, such as contusion, hematoma, or open penetrating lacerations

Contusion

Local leakage of blood from damaged blood vessels; a bruise

Coup injury

Contusion under the location of impact as momentum forces the brain against the skull

Contrecoup injury

Contusion at the region opposite the impact site as the brain bounces against bony ridges

Contusion manifestations

Momentary loss of consciousness and loss of reflexes so the individual falls to the ground, lasting a few minutes

Contusion pathogenesis

Leaked blood forms hematomas with local compression, local ischemia, and inflammatory response causing edema, necrosis, and neutrophil invasion

Peak of acute contusion effects

18-36 hours after injury

Hematoma

Localized collection of blood outside blood vessels

Extradural (epidural) hematoma

Bleeding between the dura mater and the skull, usually from a fracture, predominantly arterial

Epidural hematoma classic scenario

Brief loss of consciousness, then a lucid period of 2-3 hours, then rapid deterioration as ICP rises

Focal signs of epidural hematoma

Ipsilateral pupil dilation and contralateral hemiparesis, from uncal herniation

Epidural hematoma prognosis

Recovery is good if the hematoma is removed before the person lapses again into unconsciousness

Subdural hematoma

Typically venous, low pressure, slow bleeding

Acute subdural hematoma

Post-traumatic and can still develop within hours, clinically resembling epidural hematoma

Chronic subdural hematoma

Develops over weeks or months, related to conditions such as cerebral atrophy or alcoholism

Intracerebral hematoma

Bleeding within the brain from penetrating injury or shearing forces; may be delayed, appearing 3-10 days after injury

Diffuse axonal injury (DAI)

Diffuse and widespread damage to neural axons from shaking, rotational, and twisting movements with rapid acceleration and deceleration

How DAI is observed

Only with a microscope, at the axon fibers

Functional effect of DAI

Reduces the speed of information processing

Least severe form of DAI

Concussion

Mild concussion

No loss of consciousness, but CSF pressure increases, confusion lasts several minutes, and there is amnesia

Classic cerebral concussion

Loss of consciousness up to 6 hours, confused state for several hours, headache, nausea, and more serious retrograde amnesia

Mild DAI

6-24 hour coma; may display decerebrate or decorticate posturing with extended periods of stupor and restlessness

Moderate DAI

Coma over 24 hours; on awakening often a permanent deficit in memory, reasoning, and language

Severe DAI

Usually emerge from coma within the first 3 months; results in compromised coordinated movements, verbal and written communication, and inability to learn and reason

Secondary brain injury

Damage caused by subsequent swelling, infection, or hypoxia; an indirect result of primary trauma

Mechanisms of secondary brain injury

Cerebral edema, increased intracranial pressure, decreased cerebral perfusion pressure, ischemia, and brain herniation

Timing of secondary brain damage

Occurs hours to days after the primary trauma