Closed Head Injuries: Mechanisms and Diagnosis

Closed Head Trauma Epidemiology

• Trauma is the leading cause of death in young individuals.
• Head injuries account for nearly half of all trauma-related deaths.
• Head trauma leads to over 1.5 million emergency department visits annually, most of which are for mild traumatic brain injuries.
• Falls are a common cause of head trauma in the youngest and oldest age groups.
• Assaults, falls, and motor vehicle collisions are common causes of head trauma in the 15-55 age group.
• Significant morbidity and mortality are associated with head trauma, particularly among the elderly.

Brain Anatomy and Intracranial Pressure (ICP)

• The rigid and inflexible nature of the skull makes the brain susceptible to increases in Intracranial Pressure.
• Dura-mater partitions divide the brain:
  • Falx Cerebri separates the hemispheres,
  • Tentorium Cerebelli separates the occipital lobe from the cerebellum,
  • Falx Cerebelli separates the cerebellar hemispheres.
• The brain occupies approximately 80% of the intracranial cavity.

Central Nervous System Regions

• The three major regions of the central nervous system are:
  • Cerebrum,
  • Cerebellum,
  • Brain stem.

Cerebrospinal Fluid (CSF)

• Cerebrospinal Fluid cushions the brain and spinal cord, protecting against trauma.
• The choroid plexus produces CSF within the ventricles.
• It flows through the ventricular system and down around the spinal cord.
• The adult brain contains ~150cc of CSF.

Cerebral Blood Flow (CBF)

• CBF is significantly impacted by CO2 and oxygen levels.
  • Hypercapnia increases CBF.
  • Hypocapnia decreases CBF.
  • Hypoxia increases CBF.

Intracranial Pressure (ICP)

• Intracranial Pressure is determined by three components: brain, blood, and CSF.
• Normal ICP is less than 15 mmHg.
• Intracranial mass, hematoma, or cerebral edema raises ICP.
• CSF is displaced from ventricles when ICP rises.
• Blood is displaced from the brain when ICP rises.

Monro-Kellie Doctrine

• The Monro-Kellie doctrine describes the compensatory mechanisms within the skull to maintain a stable ICP.

Herniation

• Transtentorial (uncal) herniation occurs when a developing hematoma causes a rise in ICP, forcing the medial aspect of the temporal lobe (uncus) through the tentorium opening.
• Herniation leads to deteriorating LOC.
• Herniation compresses the corticospinal tract, causing weakness on the arm/leg.
• It compresses the 3rd cranial nerve, resulting in a "down and out" pupil on the side of herniation.
• Herniation is an ominous sign and requires immediate intervention to prevent death.

Head Trauma History

• Key questions to ask include:
  • Was there LOC? How long did it last?
  • If a fall, how far did the patient fall?
  • Was there any drug or alcohol use?
  • What medications is the patient taking?
  • Are there any distracting injuries?

Head Trauma Assessment

• Assess vital signs, noting that hypoxia and hypercarbia increase ICP, and hypotension is unlikely from head trauma alone.
• Perform a neurologic exam including:
  • Level of consciousness using the Glasgow Coma Scale (GCS),
  • Pupil size and reactivity,
  • Motor exam,
  • Brainstem function (corneal/gag reflexes),
  • Repeated exams.
• Conduct a full physical exam to assess for other injuries.

Head Trauma Evaluation

• Standard evaluation involves a CT head scan with or without contrast.
• CT c-spine indicated for:
  • Neck pain,
  • Decreased LOC,
  • Neurological deficits,
  • Significant or distracting injury,
  • Age or underlying disease.
• Skull X-rays can be useful for penetrating injuries but are uncommonly used otherwise.
• Trauma labs are part of the evaluation.

Management of Major Head Injury

• 5 Distinct Major Head Injuries described by Frequency:
  • Epidural hematoma
  • Subdural hematoma (SDH)
  • Traumatic SAH
  • Diffuse axonal injury
  • Intraparenchymal hemorrhage
• Key management includes:
  • ABCs and C-spine immobilization,
  • Reversing anticoagulation,
  • Considering seizure prophylaxis.
• Reduce Intracranial Pressure by:
  • Intubating,
  • Hyperventilating,
  • Elevating the head of the bed to 30 degrees,
  • Administering IV mannitol, osmotic diuretic.
  • Neurosurgery is needed in Rapid evacuation.

Post-Traumatic Seizures

• There is an increased risk of seizure following brain trauma.
• Keppra or phenytoin is commonly prescribed as post-traumatic prophylaxis for about 1 week.
• Patients can develop post-traumatic epilepsy, which anti-epileptic drugs may not prevent.

Glasgow Coma Scale (GCS)

• The GCS assesses eye opening, verbal response, and motor response.
• Minor brain injury is 13-15 points, moderate is 9-12, and severe is 3-8.

Mild, Moderate, Severe TBI

• Mild: GCS 13-15
• Moderate: GCS 9-12, some clinicians consider GCS 13 as moderate due to high morbidity at GCS 13 vs 14.
• Severe: GCS < 8.

General Management of TBI

• CT head w/o contrast ASAP is needed for moderate to severe brain injuries, reverse anticoagulation, and consult neurosurgery.
• For mild brain injuries:
  • Use validated decision rules to obtain imaging judiciously,
  • Often can be discharged after initial workup with PCP or concussion specialist follow-up,
  • Maintain a low threshold for imaging in elderly/anticoagulated patients.

Diffuse Lesions

• Diffuse lesions are concussion and diffuse axonal injury.

Concussion Overview

• This is an alteration in mental status caused by trauma, with or without loss of consciousness.
• It is also Minor head injury and also a minor head trauma or mild traumatic brain injury.
• The pathology is unknown, but is a mild diffuse axonal injury and excitotoxic neuronal injury.
• It is seen as a functional disturbance.

Concussion Symptoms

• Early acute symptoms:
  • headache,
  • dizziness, Imbalance, N/V, Confusion/Disorientation.
• Following hours-days: Photo-/phonophobia, Mood/cognitive changes, Difficulty concentrating, Sleep disturbances

Concussion Examination

• Patients are usually normal on exam.
• Orientation and attention, short-term memory, reaction time may be affected.
• Make sure to note: Signs of scalp laceration, Facial or skull fracture, Neck injury.
• Persistent or progressive decline in LOC → imaging is needed

Concussion Imaging

• CT is needed in following CMDT situations: GCS <15, Focal neuro deficit, Seizure, Coagulopathy, Age > 65yo old, Skull Fx, Retrograde amnesia > 30, Intoxication, Soft tissue injury head or neck, Persistent headache or vomiting.

Concussion Disposition and Management

• Treatments aim to promoting resolution of current symptoms.
• avoid Second Impact Syndrome: recurrent concussion while still still symptomatic from first concussion can be detrimental for healing.
• Most can be discharged with observation and follow up with pcp or concussion.
• Uncomplicated concussions can return to work after 24h of physical and cognitive rest.
• Athletes remove from play; graduated supervised return is implemented for safety concerns.

Concussion Prognosis

• Post-concussion syndrome
  • Symptoms and disability from the concussion,
  • Greatest in first 7-10 days,
  • Symptoms resolve in most patients by 1 month; vast majority by 3 months. 10-15% of people have symptoms at a year.
• Persistent headaches: migraine, can be treated with prophylaxis.
• There may be chronic traumatic encephelopathy, where there are mood and cognitive changes. These are correlated with lifetime exposure to repetitive head injury

Post Concussion Syndrome

• The Post Concussion Syndrome is seen as common sequelae of TBI (30-80%).
• Sx: HA, dizziness, neuropsychiatric sx, cognitive impairment for days- weeks after injury
• There may be complication definition and diagnosis that involves: Symptoms vague and subjective Can be caused by varying degrees of head injury, Underlying pathophysiology not clearly defined, Tests can be normal or abnormal and not consistent.

Post Concussion Syndrome - Symptoms

• Headaches,
• Sleep Disturbances
• Psychological and cognitive symptoms - 15-20% meet criteria for psychiatric disease such as:
• Personality changes
• Irritability
• Anxiety and/or depression
• Intolerance to noise
• Sensitivity to alcohol -Impaired memory and concentration

Post Concussion Syndrome - Diagnosis & Management

• Diagnosis Neuropsychological testing, Neuroimaging as in CT scan and/or MRI brain, EEG that is usually not needed.
• Management
  • Unique to patient and symptoms - most need reassurance/education, Cognitive and physical rest, Headache management, Sleep/wake management, Psychological interventions.

Diffuse Axonal Injury Overview

• Persistent loss of consciousness, coma, or persistent vegetative state resulting from severe rotational shearing forces or deceleration,
• The Pathology: Tearing/shearing of nerve fibers at time of impact,
• CT scan can be normal despite profound neurological deficit : could also show scattered white matter hemorrhages → torn axons, the is best seen on MRI, Has high Mortality 33% due to cerebral edema.

Focal Lesions

• these involve: Skull Injury, Cerebral Contusion, Intracerebral Hemorrhage, SubarachnoidHemorrhage, Subdural Hematoma, Epidural Hematoma.

Skull Fractures

• Linear non-depressed fracture:
  • No tx needed if scalp is intact. Depressed skull fracture:
  • Requires surgical intervention
• Open fractures:
  • Associated with large scalp lacerations and depressed skull fractures,
  • IV antibiotics and possible neurosurgical intervention.

Basilar Skull Fractures overview

• Fracture through base of skull:
• Most common fracture is the - Temporal bone,
• There are racoon eyes due to - tarsal plate sparing,
• Also Hemotympanum due to - blood behind TM,
• Visible Battle's sign
• Ring/Halo is present due to sign due to CSF leakage
• Tx: Most often monitoring, but monitor closely especially for bleeding.
• In pediatrics, think non-accidental trauma - "Egg shell" like breaks in skull

Cerebral Contusion overview

• Focal area of hemorrhage in brain, causes surrounding edema. Pathology of Contusion
  • Same side as impact (Coup),
• Opposite side of impact, (Contrecoup). Clinical Features: Often LOC longer than with concussion; focal deficits common. Imaging: CT scan Treatment: Control ICP

Intracerebral Hemmorhage overview

• Parenchymal hemorrhage from the Disruption of small intraparenchymal vessels,
• It leads to expanding mass lesion
• Varies widely depending on size and location
• Causes: Headache, Nausea, vomiting, Hemiparesis, LOC
• Treatment: Decrease ICP, Evacuation of hematoma.

Subarachnoid Hemmorrhage overview

• Traumatic SAH: results from Accumulation of blood between the surface of brain, and the arachnoid membrane.
• Direct extravasation from adjacent cerebral contusion, Arterial dissection, Direct damage to smaller veins or arteries,
• The symptoms are similar to Intracerebral Hemorrhage but include photophobia as well.
• Patients are managed with supportive care and close observation with frequent neurological assessments

Subdural Overview

• Location is within the location Subdural space.
• Shearing of bridging veins causes: acute motor vehicle collision blunt force falls and older patients and acute and chronic.
• Signs and symptoms is a spectrum of manifestations with additional bleeds like
  • epidural SAH and cerebral contusions. Can have additional bleeds, Focal neurologic signs like; frontal lobe, parietal lobe, etc. seizures stupor with herniation
• There is an asymetrical bleed with "Sickle shaped" and "Crescent shaped" edges, and Bleed can cross the suture line - needs Reverse anticoagulation, Neurosurgical consult, Surgical burr hole or craniotomy.

Epidural Hematoma overview

• This is a neurosurgical emergency
• The Location is on the Epidural space,
• Results due to middle meningeal artery.
• It has rapid progression to Herniation
• It will present with brief lucidity followed by deteriorating metal status: headache, Nausea, tentorial herniation etc
• Treatment is emergent craniotomy with management of inter cranial preasure (ICP)
• The appearance is Lens shaped and may not cross suture line with good resolution.

Explore the mechanisms and diagnosis of closed head injuries. Understand intracranial pressure, Glasgow Coma Scale, and the pathophysiology of diffuse axonal injury. This lesson synthesizes the role of advanced neuroimaging techniques in managing such injuries.