Clinical Anatomy: Head Injuries & TBI

• The information covers the clinical anatomy of head injuries, focusing on traumatic brain injuries (TBI) and intracranial hemorrhages and concussion.

Traumatic Brain Injuries (TBI)

• Primary TBIs can be focal or diffuse
• Mechanisms include coup and contrecoup injuries, and diffuse axonal injury (DAI)
• Diffuse Axonal Injury (DAI): Shearing forces from rotational forces cause damage to different tissue layers.
• Coup Injury: Direct impact causes fracture and positive pressure with forward brain movement.
• Contrecoup Injury: Indirect damage from negative pressure and backward brain movement, specifically impacting rough bones.

Concussion

• Brain injury that involves acute and transient alteration of mental functioning after trauma
• Direct blow to the head is not always required, can occur during whiplash
• Pathophysiology involves axonal stretching and shearing leading to neuronal dysfunction
• Ionic and chemical flux happens when potassium exits and calcium enters the cell, with neurotransmitters released
• Deranged ionic balance and neuronal depolarization
• Excitotoxicity is possible
• Brain uses Increased energy to depolarize
• Impaired blood flow to the brain
• Energy crisis happens when the process persists
• Cytokines are released and an inflammatory response which can lead to permanent injury
• Common signs and symptoms include confusion, headache, transient amnesia and loss of consciousness, imbalance, and photophobia
• Long-term sequelae include second impact syndrome, post-concussion syndrome, psychosocial effects, and brain degeneration
• Recovery is more difficult with severe DAI or repeated stresses

Traumatic Intracranial Hemorrhages

• Head injury that includes 4 types: epidural/extradural (EDH), subdural (SDH), subarachnoid (SAH), and intracerebral
• Each type can occur in isolation or in combination

Anatomy of Intracranial Hematomas

• Pia mater is tightly attached to the brain
• Arachnoid mater does not follow sulci
• Dura has 2 layers:       - The endosteal layer attaches to the skull. Attachment strengthens with age.       - The meningeal layer is present.
• Dural venous sinuses are between the two layers
• Subarachnoid space is a continuous space containing cerebral vessels
• Subdural space is considered a continuous space
• Epidural space is only a potential space with cross connections between the dura and pericranium through suture lines
• Middle meningeal vessels are located in the epidural space
• Bridging veins cross the subdural space
• Dural venous sinuses are formed by separation of 2 layers of dura, lined by endothelium and drain into the internal jugular vein
• Superficial cortical veins drain cerebral and cerebellar cortex into adjacent venous sinuses via bridging veins.

Extradural Hemorrhage (EDH)

• Bleeding between the skull and endosteal dura, usually with skull fractures (inner table tears meningeal vessels)
• Common in the pterion region
• Middle meningeal artery most commonly implicated
• Arterial bleeding causes progression and elastic deformation can separate the dura
• Can be associated with venous bleeding, like tear of dural venous sinuses in the posterior cranial fossa
• Blood accumulates lifting dura off cranial bones
• More common in young people (20-30 yrs) as elderly have stronger attachment of dura
• Usually is a biconvex shape because of tight dura attachment to skull and sutures causing a limited space that prevents the sutures from extending
• Clinically associated with raised ICP
• Lucid interval can be present
• Compresses cortical areas
• Radiological features includes appears hyperdense (bright white) in non-contrast CT, biconvex in shape and does not cross suture lines, suture line damage may cause it to cross suture lines.
• Management involves surgical evacuation if volume is >30ml, thickness >15mm, midline shift >5mm or GCS score <8, presence of focal neurological signs/herniation or the case is managed conservatively
• Emergency burr hole and evacuation may be needed

Subdural Hemorrhage (SDH)

• Bleeding into the space between dura and arachnoid, more common than EDH
• Sudden acceleration/deceleration tears bridging veins, bleeding into space
• Is often caused by contrecoup injuries
• Violent/high speed injury mechanism causes other primary damage to brain
• 1/3 of patients with severe TBI have SAH
• Signs of neurologic damage are associated with raised ICPs
• May be lucid but brain is damaged or you may not be able to tell cause there are seizures
• Slow venous bleed with delayed presentation
• There is larger SD space with cerebral atrophy, especially in elderly
• In children, suspect child abuse if not birth trauma
• Can deteriorate due to smaller intracranial space
• Evacuate SDH by craniotomy if size ≥ 10 mm, there is midline shift ≥ 5 mm or present with signs of cerebral herniation
• Other types include acute which arise within 3 days, subacute which arise between 4-20 days, or chronic SDH, which arise Symptoms onset after ≥ 21 days
• Chronic presentations are Confusion, headache, ataxia, seizures, memory deficit
• There is association with minor or non-traumatic causes, common among elderly, with alcohol or alzheimers
• They stem from stretched, unsupported Bridging Veins leading to cerebral atrophy
• Radiological features include appearing hyperdense on CT and being crescent shaped while chronic SDH appear isodense

Traumatic Subarachnoid Hemorrhage (SAH)

• SAH happens when cerebral vessels running the in the SA space are damaged
• bleeding from damaged brain tissue or associated SDH
• Associated with brain contusions, SDH, etc
• Trauma is most common cause of SAH, Mild TBI
• Unlike non-traumatic SAH, the blood is seen in superficial sulci
• Non-traumatic SAH is from ruptured aneurysms which happens mostly in the basal aspect and the outcome is generallY good

Secondary Brain Injuries

• Results from the biochemical, metabolic, and cellular processes that occur after the initial injury, significantly worsening brain damage
• Molecular and cellular responses involve influx and efflux of potassium, calcium, and neurotransmitters causing cell death
• Metabolic changes cause neuronal deprivation, impaired cerebral blood flow, and energy crisis
• Blood brain barrier damage which causes increased permeability
• Neuroinflammation causes inflammatory mediators
• These processes cause cerebral ischemia and oedema
• Extracranial factors such as hypotension and hypoxia also play a role
• Increased intracranial mass effect leads to compensatory mechanisms until exhaustion and high ICP
• The goal of secondary preventative care is to prevent brain herniation

Expanding Masses and Compensatory, Exhaustion

• The skull is non expandable so masses must be controlled
• Intracranial pressure is limited by the ability of the brain to compensate, which involves managing the Brain + blood + CSF equilibrium
• If the intracranial pressure is disrupted and increases, brain herniation is possible

Increasing ICP - Cushing’s Triad

• Increasing cerebral pressure can manifest through: Increased ICP, Ischemia, reduced MAP etc.
• The cerebral body’s response is for example, elevate Peripheral Resistance to increase MAP and heart contraction
• Cushing's Triad, caused by cerebral ischemia, is when the body manifests hypertension, bradycardia, and irregular respiration

Management Principles for TBI

• Maintain CPP/oxygenation. 
• Control bleeding, fluid resuscitation, and reduce cerebral metabolic demands (sedation, seizure control, hypothermia) so the patient isn't restless.
• Control ICP by raising the head, administering osmotheraputics and draining fluid
• Avoid hyperventilation because it's harmful
• Aim to achieve CPP of 60-70 mmHg; control by use of CPP=MAP-ICP, or if ICP is unknown consider it 30mmHg

Osmotherapy Mechanism

• Mannitol is osmotic diuretic for edema management because it uses fluid to draw water out, however this may require replacement
• hypertonic management requires more water management because it’s a water barrier management
• Hyperventilation can be also managed, be careful since it limits flow and oxygen

Radiological Findings

• Effacement of ventricles and midline shift
• May have specific herniation

Brain Herniation

• Brain can herniate from one compartment to the other, different type of herniation include: cingulate, transtenorial, uncal, tonsillar
• Central herniation pushes midbrain, pons, and medulla downwards, and can cause Duret hemorrhages
• Subfalcine herniation occurs when the cingulate gyrus is shifted under the falx cerebri, the clinical effects on the anterior cerebral artery compression are non-fatal
• The uncal compression of the cerebral peduncle or CNIII causes hemiparesis
• Tonsillar herniation compresses the respiratory and cardiac control center in the medulla

Final Steps

• Raised ICP has symptoms that can be seen in the optic disc
• Early Signs to look for to identify increasing ICP include deterioration of consciousness, confusion, agitation, and declining GCS scores
• Need to do Head/Brain CT in mild TBI with risk factors and moderate or severe head injuries
• Glasgow Coma Scale (GCS) assesses neurological consciousness.