Head Injuries and Trauma

Head Injuries (Traumatic Brain Injuries)

• Head injuries are a broad term encompassing injuries to the scalp, skull, or brain.
• Traumatic Brain Injury (TBI) is a traumatic insult to the brain resulting in physical, intellectual, emotional, social, and vocational changes, according to the National Head Injury Foundation.
• Head injuries can range from mild to severe, with very severe injuries potentially fatal due to profound brain damage.

Head Trauma Epidemiology

• Head injuries account for 25-50% of all trauma deaths in the U.S.
• Head injuries account for 60% of all vehicle crash deaths.
• Approximately 2 million injuries and 400,000 hospitalizations occur per year due to head injuries.
• The death rate from head injuries ranges from 24 to 36 per 100,000 per year.
• Cumulative mortality from head injuries admitted to trauma centers is 15-40%.
• Delayed or prolonged effects of head trauma, even minor, include headaches, memory loss, behavioral/learning/psychologic dysfunction.

Head Injury Types

• Common types of head injuries include scalp lacerations, skull fractures, and brain injuries.
• Brain injuries can be diffuse (concussion, diffuse axonal injury, cerebral edema) or focal (intracranial hemorrhages, brain lacerations).

Traumatic Brain Injury (TBI) Causes

• Falls account for 28% of TBIs, making them the leading cause.
• Traffic accidents are responsible for 20% of TBIs.
• Being struck by/against objects causes 19% of TBIs.
• Assaults contribute to 11% of TBIs.
• Unknown causes account for 9% of TBIs.
• Other causes (excluding bicycle accidents) account for 7%
• Bicycle accidents contribute to 3% of TBIs.
• Suicide attempts and other transport incidents each account for 1%.

Classification of TBI

• Approximately one million patients attend A&E each year in the UK with head injuries.
• 80% of TBIs are classified as minor, with a Glasgow Coma Scale (GCS) score of 13-15.
• 10% of TBIs are moderate, with a GCS score of 9-12.
• 10% of TBIs are severe, with a GCS score of less than 8.
• Severe head injuries account for 50% of trauma-related deaths.

TBI Classification: Mild, Moderate, Severe

• Mild TBI:
  • Predominantly blast, non-penetrating mechanism.
  • Alteration or loss of consciousness lasts less than 30 minutes.
  • Amnesia lasts less than 24 hours.
  • Outcome typically involves transient neuropsychiatric deficits, mostly full recovery, but repeated injuries can lead to frequent long-term neuropsychiatric issues.
• Moderate TBI:
  • Frequently mixed mechanism involving blast + acceleration/deceleration, typically non-penetrating.
  • Alteration or loss of consciousness lasts more than 30 minutes but less than 24 hours.
  • Amnesia lasts more than 24 hours but less than 7 days.
  • Outcome is mild-to-moderate, typically involving chronic, neurological, and neuropsychiatric abnormalities.
• Severe TBI:
  • Complex mechanism involving blast + acceleration/deceleration + penetration.
  • Alteration or loss of consciousness lasts more than 24 hours.
  • Amnesia lasts more than 7 days.
  • Outcomes include death, significant neurological and neuropsychiatric deficits, and severe, chronic physical and neuropsychiatric disabilities.

Pathophysiology of Brain Injury

• Initial injury leads to primary injury, causing fracture and hematoma.
• Secondary injury may result in hypercarbia, cerebral edema, increased intracranial pressure (ICP), hypotension, and hypoxemia.
• Compensation mechanisms include initial damage, decreased autoregulation, and compensatory mechanisms.
• Brain injury is categorized into primary and secondary types.
  • Primary brain injury is a direct consequence of the trauma and isn't preventable or easily treated.
  • Secondary brain injury ensues after energy transfer and is preventable and amenable to treatment.

Mechanisms of Brain Injury

• Brain injury results from energy transfer (low or high) due to blunt or penetrating injuries, often occurring in road traffic accidents (RTA), falls, industry-related incidents, sports, and assaults.
  • Closed head injuries: Acceleration or deceleration of the brain is the primary mode of injury.
    • Low energy transfer causes temporary disruption of function (e.g., brief loss of consciousness or amnesia).
    • High energy transfer may cause neuron disruption, contusions, or lacerations.
  • Open (penetrating) head injuries: Involve an injuring agent penetrating the skull and meninges.
    • Low-velocity missile wounds result in direct disruption.
    • High-velocity missile wounds cause shock waves that destroy the entire brain.

Primary Brain Injury

• Damage occurs at the time of impact and can be focal or diffuse.
• Diffuse axonal injury is due to deceleration and shearing forces.
• Severity depends on the extent of initial injury and is often difficult to treat

Types of Primary Brain Injury

• Cerebral Concussion
• Cerebral Contusion
• Cerebral Laceration
• Diffuse Axonal Injury
• Skull Fractures
• Intra-Cranial Hematoma
• Coup & Counter Coup

Types of Primary Brain Injury: Details

• Cerebral Concussion:
  • Brief, temporary physiological paralysis without organic structural damage which results in transient Loss Of Consciousness followed by complete recovery
• Cerebral Contusion:
  • Occurs beneath the skull at the site of impact or when the brain strikes bony or Dural structures.
  • Indicates more severe damage, leading to pathological changes.
• Cerebral Laceration:
  • Brain surface is torn, coupled with changes similar to cerebral contusion.
• Diffuse Axonal Injury:
  • Involves widespread disruption of axonal fibers and myelin sheaths, causing severe neurological deficits.
  • Example: Baby Shaking Syndrome.
  • GCS is usually low, and ICP is often normal.
  • CT scans may appear normal or show small punctate brain edema.
• Skull Fracture:
  • Can be closed or open.
  • Vault fractures are linear, satellite, diastasis of the sutures line, or depressed fractures.
  • Basal skull fractures can result in CSF rhinorrhea or otorhea, subconjunctival hemorrhage, raccoon eyes, Battle's sign, and hemotympanium.
    • GCS of 15 without skull fracture has an I.C. hematoma risk of 1:6000.
    • Adding skull fractures bring a GCS 15 risk to 1:30
    • Skull fractures with a GCS of 14 raise the risk to 1:4

Skull Fractures: Location Types

• Frontal fracture
• Temporal fracture
• Parietal fracture
• Posterior fossa fracture
• Orbital fracture
• Basilar skull fracture

Skull Fractures

• Open fractures allow communication with the external environment and have an increased risk of infection.
  • Linear Fracture:
    • Most are asymptomatic and have no LOC
    • Rare complications include subgaleal and epidural hematomas.
  • Vault Fracture:
    • Scalp hematomas may be asymptomatic with LOC.
  • Basilar Fracture:
    • Clinical signs include Battle's sign, periorbital ecchymosis, hemotympanum, CSF otorrhea/rhinorrhea, and cranial nerve deficits.
    • Potential complications include conductive hearing loss, CN V, VI, VII, VIII, as well as Jugular foramen issues affecting CN IX, X, and XI.
  • Depressed Fracture:
    • Typically caused by blunt trauma to a small surface area, leading to bony defects and a "step-off" appearance.
    • LOC is common
    • Can cause epidural hematoma, dural/brain laceration, and seizures.

Signs of Basal Skull Fracture

• Blood or CSF from the nose or ear.
• Peri-orbital hematoma.
• Mastoid hematoma (Battle's sign).
• Hemotympanium.
• Radiological evidence of intracranial air.
• Radiological evidence of fluid levels in the sinuses.

Depressed Skull Fracture: Management

• Inspect the scalp injury and order a tangential skull X-ray.
• If there is no depression, perform debridement and suture.
• In the presence of depression, if there is bone overlap less than 50% and neurological deficit is present, debride and suture.
• If bone overlap is more than 50%, debride/elevate and repair.

Intra-Cranial Hematoma

• Types of intra-cranial hematomas:
  • Extra-Dural Hematoma
  • Sub-Dural Hematoma
  • Intra-Cerebral Hematoma
  • Sub-Arachnoid Hemmorage (SAH)

Extradural (Epidural) Hematoma

• It's the most common intracranial hematoma. Epidural Hematoma is the result of Fractured Temporal bones causing Middle Meningeal artery injury resulting in Arterial hemorrhage.
• Clinical features include an initial loss of consciousness followed by a lucid interval, but continued hematoma accumulation may cause brain herniation and LOC.
• Treatment involves a burr hole or craniotomy + hematoma evacuation.
• Has a good prognosis following early treatment.
• Signs and symptoms include, loss of consciousness, lucid intervals, headache, dilated pupils on side of injury, weakness, paralysis, and seizures.
  • Skull fracture middla meningeal artery rupture resulting in collection of blood between dura mater and skull. Biconvex or lenticular shaped on CT
  • Blow to the head results in skull fracture.
  • Bleeding occurs rapidly d/t arterial tear.
  • Craniotomy or burr hole for larger hematomas, conservatives with smaller hematomas.

Subdural Hematoma

• Venous hemorrhage bleeds slower than arteries (contrasting epidural hematoma) and is less common.
• Rupture of veins crossing the Subdural space (from the brain to the Dural venous sinuses).
• Can be Acute, Sub-Acute, or Chronic.
  • Acute subdural hematoma: Young adult-massive acceleration head injury-tears in the cortical surface & hemorrhage in the Subdural space through tears in the Subarachnoid.
  • Sub-acute subdural hematoma is less than 2 weeks.
• Elderly patients are more prone, minor trauma may result in tearing of the Subdural veins & formation of small subdural hematoma.
• Infants can have vein rupture due to mobile skull bones crossing the subdural space.
• Clinical features: Past history of minor trauma, confusion, decreased level of consciousness, headache, vomiting, hemi-paresis.
  • A craniotomy + evacuation of Hematoma is the recommended treatment

Etiologies of acute subdural hematomas

• Trauma: Motor vehicle collisions, falls, assaults, accidents.
• Coagulopathy or medical anticoagulation: Warfarin, heparin, hemophilia, liver disease, thrombocytopenia.
• Nontraumatic hemorrhage: Cerebral aneurysm, arteriovenous malformation, tumor (especially meningioma or dural metastasis).
• Postsurgical Craniotomy, CSF shunting.
• Intracranial hypotension: Lumbar puncture, lumbar CSF leak, lumboperitoneal shunt, spinal epidural anesthesia.
• Inflicted injury: Usually pediatric age group; also can be seen in the elderly. Rare spontaneous or unknown.

Clinical features of SDH

• Recent head A history of recent head SDH
• Loss of consciousness/fluctuating consciousness levels
• Irritability & Seizures
• Numbness
• Dizziness & Disorientation
• Amnesia & Weakness/lethargy
• Nausea or vomiting& Personality changes
• Inability to speak or slurred speech & Ataxia, or difficulty walking
• Altered breathing patterns & Blurred Vision
• Conservative SDH treatment options includes Bed rest, Osmotic diuresis, Corticosteroids and Surgery

Intracerebral Hematoma

• Results in a worse prognosis.
• Minor injury: Petechial hemorrhage.
• Major Injuries Rupture of the larger blood vessels & formation of a large Intra-cerebral hematoma.

Coup & Counter Coup

• Coup: Positive generated force beneath the collision site.
  • Injuries include Scalp laceration, Skull fracture, Extradural hematoma, Subdural hematoma, Intra-cerebral hematoma, Cerebral contusion & laceration & brain oedema
• Counter Coup: Involves negative pressure on the opposite diagonal of the collisions site. Injuries include Subdural hematoma, Cerebral contusion and laceration, brain oedema & Intra-cerebral hematoma

Secondary Brain Injury

• Secondary insult occurs after the initial injury may be due to
  • Hypoxemia & Hypercapnea
  • Systemic Hypotension.
  • Intracranial hematoma & Intracranial Hypertension
• Early treatment aims to prevent it because auto regulation of cerebral blood flow is lost after head injury.
• Mechanism of common causes include:
  • Brain Swelling: Congestion & dilatation of the blood vessels + increase in the brain blood volume causes an increase in ICP. -Brain Oedema: Accumulation of intracellular or extracellular fluid in the focal or diffuse regions may also result in increased ICP.
• Can result from:
  • Hypercapnea (INCREASE PCO2): Occurs in Chest injuries & over sedation causing Cerebral vasodilation which result in Cerebral Swelling & eventually increase of the ICP (ICP approach MAP).
  • Hypocapnea (DECREASE PCO2): Due to hyperventilation results in Cerebral vasoconstriction which give rise to decrease of CBF & Cerebral ischemia and eventually increase ICP.
  • Hypoxia (DECREASE PO2): The injured brain is less able to tolerate hypoxia & hypotension, so avoid hypoxia and preserve normo tension.
    • Respiratory Insufficiency may aggravate cerebral ischemia and venous congestions.
    • Its essential that the PCO2 & PO2 are maintained at normal levels

Coning

• Herniation of the Medulla oblongata through the foramen magnum which results in Cerebellar compression, high B.P., & bradycardia.
• Herniation of the contents of the supratentorial compartment through Tentorial hiatus may result in a medial temporal lobe herniation & interfere with the descending contralateral motor pathway. This results in consciousness deteriorations, ipsilateral pupil dilation & contralateral hemi-paresis.
• This can lead to expansion of mass lesions and herniation syndromes
• Signs and Symptoms include Pupilary dilation, Systemic hypertension, Bradycardia and Extensor posturing
• Emergent treatment needed: Hyperventilation with FiO2 1.0, Mannitol or hypertonic saline and Thiopental or etomidate before CT scan prior to surgery

Blood Pressure & Blood Volume

• CPP=MAP - ICP is important to maintain
• CBF is directly related to MAP after head injury because autoregulation is damaged
• Minimum target of CPP > 60mmhg to maintain sustain adequate Cerebral perfusion
• Hypotension may decreases CPP
• Its essential to maintain normal C.O.P. & to replace blood loss from other injuries.
• Decreased COP cause irreversible ischemic changes & conversely increased ICP can impair the protective Cerebral blood flow.

Fluids & Temperature Considerations

• Patients should avoid hypotonic solution (5% Dextrose) which decreases Plasma Osmolarity, so the fluid may be drawn into the brain tissues; use Isotonic Crystalloid Solution instead dedicated to blood replacement. IADH Syndrome with Hyponatremia may result from brain injury.
• Body temperature increase body metabolic demands & catabolites so keep it down. Severe head injuries may experience deteriorating Neurological states as a result.

Increased Intracranial Pressure (ICP)

• Factors which Increase Brain Swelling, Brain oedema, Contusion, I.C.Haematoma, infection or Hydrocephalus.
• Increasing ICP can disturb CBF leading to Ischemia & further brain damage.
• auto-regulatory mechanism may fail with resulting ishemic changes when ICP rises severely
• Sustained ICP > 25 mmhg is associated with poor prognosis
• Severely brain injured patients require sedation & ventilation with ICP monitoring

Infections & Post-Traumatic

• Infections- increase risk of infection of the brain or meninges, Skull fracture, Fracture at base of Skull / Penetrating missile trauma are examples
• Hydrocephalus- Occurs generally between 7 to 10 days after injury, Hemmoraging can cause fluid to accumulate and dilate the Cerebral Ventricles
• Cerebral arterial Spasm- Can be so severe at times that severe Ischemia & Infarction occur.
• Post-Traumatic epilepsy- can be Generalized or Focal and occurs in 5% of all cases, with 30 to 40% after missile injury.

Increased Risk of Epilepsy Factors

• Penetrating missile injury, Depressed Skull fracture, Fracture base of the Skull, I.C. hematoma, I.C. Infection, early epilepsy (1 - 7 days)& presence of focal Neurological Signs.

Management of Head Injuries

• Patients should be managed due to secondary brain injury and the spine should be checked: 5-10% patients with severe head injury have cervical spine injury and its important to follow ATLS protocols
• Full assessment requires:
  • Glasgow Coma Scale -Pulse/blood pressure readings
  • Pupil assesments and limbic functions 4 those with a GCS lower then 8 need Eartly Intubation and Mechanical Ventilation.

Signs and Symptoms of Head Injuries

• Wary depending on the injury
• Common symptoms- coma, headache, lucid intervals and nausea/vomiting
• Look for leaking cerebrospinal fluid and deviated or unmovable eyes which may be signs of basilar skull fracture as well as those that occur at the base of the skull
• Associated with Battle's sign, a subcutaneous bleed over the mastoid hemotympanum, and cerebrospinal fluid rhinorrhea and otorrhea.

Indications of C.T. Scans

• LOC or amnesia may recommend scanning
• GCS score less then 15 may recommend scanning
• 65 year old +

Admission & Consultation Criteria

• LOC & Confusion due to Symptoms are signs that indicate skull fractures in combination with neurological damage that must be considered in addition to other factors

Head Injury Management

• A Mild head injured patient (80%) can be discharged home

###Management of Severe Head Injury

• Primary Survey: Airway Cervical Control, Breathing, Circulation, Disability
• Secondary Survey: Injuries & AMPLE history and then definitive treatment Nurse the patient with head elevated for drainage and avoid blowing nose if there are factures
• Keep osmolity even

###Medical & Invasive Treatments in head injuries

• Medical Therapy:
  • Diuretics to alleviate swelling while anti-convulsants can mitigate potential seizures
  • Antacids can prevent the onset of cushings
  • Reduce fever where possible
  • Antidotes for possible OD
• Invasive Therapu:
  • Increased ICP can mitigated with increased blood volume & All acute hematomas need craniotomy.
• Burr hole exploration & evacuation
• Inpatient indications may be made through GCS and symptoms with additional neurosurgical consults
• ICP indication is suggested it the patient may need mechanical ventilation or if the brain is edema is present