Head Injury

Outline

• Epidemiology
• Anatomy and Physiology Review
• Classification of Head Injuries
• Management: Medical and surgical
• Specific types of head traumas

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Epidemiology

• Head injury accounts for 3-4% of emergency department attendances.

• Nearly 90% of prehospital trauma-related deaths involve brain injury.
• The leading cause of death and disability from childhood to early middle age.
• RTAs are the leading cause of head injury, being responsible for up to 50% of
cases.
• Other common mechanisms of injury include falls and assault
• 75% have mild injuries, 15% moderate, and 10% severe.

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Anatomy

• Scalp: Highly vascular

S= Skin
C= Connective tissue
A= Aponeurosis
L= Loose areolar tissue
P= Periosteum
• Skull: Calvaria and base
• Brain tissue
• CSF and ventricles
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Physiology: ICP and CBF

• Normal CBF: 55 ml/min. for every 100 grams of brain tissue.

• Ischemia: when CBF is below 20 ml/min. and lower levels result in
infarction.
• Flow depends on CPP:
• CPP (75–105 mmHg) = MAP (90–110 mmHg) – ICP (5–15 mmHg)
• Raised ICP can compromise cerebral perfusion, resulting in a cycle of
secondary brain injury and swelling

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Physiology Cont’d

• Pressure autoregulation: A MAP of 50 to 150 mm Hg is

“autoregulated” to maintain a constant CBF.
• Chemical regulation: Cerebral blood vessels constrict or dilate in
response to changes in the PaO2 and the PaCO2 in the blood.
• In severe TBI this regulatory mechanism is lost.
• Therefore, secondary injury can occur from hypotension, hypoxia,
hypercapnia, and iatrogenic hypocapnia.

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The Monro-Kellie doctrine and herniation syndromes

• The cranial vault is a rigid structure and therefore the total volume of
its contents determine ICP.
• ICP is determined by three compartments:
• Brain Parenchyma (1300ml)
• Intravascular blood (150 ml)
• CSF (150 ml)
• Normal ICP for adults is 10-15 mmHg.

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 The Monro-Kellie doctrine

Volume–Pressure Curve.

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 Raised ICP and Herniation syndromes
Herniation syndromes
• Clinical signs of raised ICP:
• Severe headache, visual
changes, focal weakness,
nausea and vomiting,
seizure, change in mental
status
• Hypertension,
bradycardia, irregular
respiration (Cushing
reflex)
• Coma 1. Subfalcine herniation
2. Uncal Herniation
3. Central transtentorial herniation
4. Tonsillar herniation
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 Classification of head injuries
• Based on GCS Score
Mild TBI Moderate TBI Severe TBI
13-15 9-12 3-8
• Based on morphology
• Skull fractures:
• Open/closed
• Depressed/Non-depressed
• Vault/Basilar skull fractures
• Intracranial lesions
• Focal: Epidural hematoma, subdural hematoma, contusion
• Diffuse: Concussion, multiple contusions, Hypoxic ischemic injury, DAI
• Based on mechanism:
• Blunt: RTAs, Falls, assault
• Penetrating: Gun shot wounds, Stabs

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Approach

• ABCDEs: Resuscitation and evaluation

• History:
• Mechanism of injury: fall from a height or a high-speed RTA
• Loss of consciousness and its duration
• Amnesia: retrograde, antegrade
• Seizure, headache (Mild, moderate, severe), nausea and vomiting.
• Medication: anticoagulants and antiplatelets
• P/E: Serial neurologic examination- GCS and Pupillary responses and focal
neurologic deficits.
• CT in all cases of moderate and severe TBI

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The GCS Score

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Primary Survey

• ABCDEs
• Ensure adequate oxygenation and circulation
• Stop bleeding from scalp lacerations
• C-spine protection
• Check Pupillary reflex, GCS and gross focal neurological deficits.
• Measure Blood glucose level

N.B: Assess GCS Score after resuscitation but before giving sedatives/intubation

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Secondary survey

• Pay particular attention to head, neck and spine.

• Head
• Inspection and palpation of the scalp for evidence of subgaleal hematoma and
scalp lacerations, which may bleed profusely, and potentially overlie fractures.
• Examine the face for evidence of fractures, especially to the orbital rim, zygoma
and maxilla.

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 Cont’d

• Clinical evidence of a skull base fracture may include:

• Battle’s sign
• ‘Racoon’ eyes
• Hemotympanum or overt bleeding from the ear
• CSF rhinnorrhea or otorrhea
• CN examination: CN VII or CN VIII damage associated with skull base fracture.
• Re-evaluate the GCS and pupil status

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Neck and spine

• Cervical fracture in association with moderate and severe TBI is upto 10% .
• Motor and sensory examinations to identify spinal pathology.
• Log-roll and palpate for thoracic or lumbar deformity and c-spine tenderness and
do per rectal examination assessing for anal tone, sensation in the awake patient
and anal wink.
• Priapism is a strong predictor of severe cord injury.

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Diagnostic procedures

• CBC, blood group and cross match

• Coagulation Profile
• CT: Non contrast CT is the gold standard
• Repeat head CT with in 24 hours:
• Subfrontal/ temporal intraparenchymal contusions
• Receiving anticoagulation therapy
• > 65 years
• Intracranial hemorrhage volume >10 mL
• C-spine x-ray
• Lateral view important

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Mild Head Injury
• If patients are asymptomatic, fully awake and alert, and have no neurological abnormalities, they may
be observed for several hours, reexamined, and, if still normal, safely discharged
• Avoid discharge during the ‘lucid interval’ that may precede delayed deterioration due to an
expanding intracranial hematoma.
• National Institute for Health and Care Excellence discharge criteria in mild head injury:
• GCS 15/15 with no focal deficits
• Normal CT brain if indicated
• Patient not under the influence of alcohol or drugs
• Patient accompanied by a responsible adult
• Verbal and written head injury advice: seek medical attention if:
• Persistent/worsening headache despite analgesia
• Persistent vomiting
• Drowsiness
• Visual disturbance
• Limb weakness or numbness
• Admit: All penetrating head injuries, CT abnormal or not available, skull fracture, CSF leak, history
of prolonged loss of consciousness, Focal neurological deficit or GCS does not return to 15 within 2
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hours
 National Institute for Health and Care Excellence guidelines for
computed tomography (CT) in head injury.
Indications for CT imaging within 1 hour
GCS <13 at any point
GCS <15 at 2 hours
Focal neurological deficit
Suspected open, depressed or basal skull fracture
More than one episode of vomiting
Post-traumatic seizure
Indications for CT imaging within 8 hours
Age >65 years
Coagulopathy (e.g. aspirin, warfarin use)
Dangerous mechanism of injury (e.g. fall from a height, road
traffic accident)
Retrograde amnesia >30 minutes

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Concussion, second impact syndrome and postconcussive
syndrome
• Concussion: temporary neuronal dysfunction following non-penetrating head
trauma.
• Generally used to describe mild head injury without imaging abnormalities
• Key features of concussion include: headache, brief loss of consciousness and
retrograde amnesia.
• Second Impact Syndrome: a second minor injury triggering a form of malignant
cerebral edema refractory to treatment.
• should be considered in advice to individuals engaged in sports or activities carrying a risk of
further injury.
• Post-concussive syndrome: headache, dizziness and disorders of hearing and
vision, difficulty with concentration and recall, insomnia, emotional lability,
fatigue, depression and personality change.
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Moderate Brain Injury

• Initial examination is same as mild TBI

• CT in all cases
• Frequent neurologic checks
• If patient improves follow up CT and management and if patient deteriorates
treated as severe TBI

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Severe brain injury

• ABCDE is a priority
• If the patient’s systolic BP cannot be raised to > 100 mmHg, establish the cause of
the hypotension- FAST, DPL, Laparotomy
• If the patient’s systolic BP is > 100 mmHg after resuscitation and there is clinical
evidence of a possible intracranial mass (e.g., unequal pupils or asymmetric
results on motor exam), obtain a CT head scan.

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Management principles

1. ATLS primary survey: ABCs and C-spine protection

2. Prevent secondary insults:
• Hypoxia
• Hypotension
• Hypo/Hyperglycemia
• Hyperthermia
3. Identify treatable mass lesions
4. Identify other life threatening injuries

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Medical therapies for brain injury

• aim to minimize secondary brain injury, through avoidance of hypoxia and

hypotension and control of ICP.

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Medical therapies for brain injury

• Include intravenous fluids, correction of anticoagulation, temporary

hyperventilation, mannitol, hypertonic saline, barbiturates, and anticonvulsants.
• Fluids: use isotonic fluids (N/S or R/L)
• Anticoagulation reversal:
Anticoagulant Treatment
Antiplatelets (e.g., aspirin, Clopidogrel) Platelets
Warfarin FFP, Vitamin K, prothrombin
complex concentrate, Factor VIIa
Heparin Protamine sulfate
LMWH e.g. Enoxaparin Protamine sulfate

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 Medical management cont’d
• Raising the head of the bed to 300
• Hyperventilation: not in the first 24 hours post-
trauma; brief. • Indications for anticonvulsant:
• Mannitol: • Depressed skull #
• Seizure at time of injury
• Indicated in patients with acute neurologic • Seizure in the ED
deterioration.
• Penetrating brain injury
• Bolus of mannitol (1 g/ kg) rapidly and transport • GCS < 8
to the OR or CT room • Acute SDH, EDH, ICH
• Do not give if patient is hypotensive (Systolic BP • History of seizures
<90 mm Hg) • Load phenytoin IV 1gm over 1 hour then 300mg
• Hypertonic Saline: od X 7 days
• Preferred for patients with hypotension • Prophylactic antibiotics:
• Anticonvulsants • Penetrating brain injury
• Open skull fracture
• Risk factors to a high incidence of late epilepsy
are: • Involvement of sinuses
• Seizures occurring within the first week • Nutrition: enteral nutrition should be
• Intracranial hematoma commenced within 72 hours of injury
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• Depressed skull # 26
 Goals of treatment of brain injury: clinical, laboratory and monitoring parameters

CATEGORY PARAMETER NORMAL VALUES

Clinical Parameters Systolic BP ≥ 100 mm Hg
Temperature 36-38 0C
Laboratory Parameters Glucose 80-180 mg/dl
Hemoglobin ≥ 7 g/dl
INR ≤ 1.4
Na 135-145 meq/L
PaO2 ≥ 100 mm Hg
PaCO2 35-45 mm Hg
pH 7.35-7.45
Platelets ≥ 75 X 103/mm3
Monitoring Parameters CPP ≥ 60 mm Hg
ICP 5-15 mm Hg
PbtO2 ≥ 15 mm Hg
Pulse Oximetry ≥ 95 %
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 Surgical management

• Scalp Injury:
• apply direct pressure
• Don’t apply pressure when there is possible skull injury.
• If it is a simple laceration copious irrigation with primary closure.
• Long laceration with multiple arms: debridement and closure in the OR needed.

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• Fractures:
• Skull fractures:
• Skull vault fractures:
• Closed linear fractures of the skull vault- managed conservatively.
• Open or comminuted fractures - consider debridement and prophylactic antibiotic therapy
• Depressed skull fractures
• Skull base fractures:
• no treatment if asymptomatic
• CSF leak resolves spontaneously but
• Persistent leak: repair may be required.
• Blind NG tube placement is contraindicated
• Indications for craniotomy:
• Depression greater than the cranial thickness
• Intracranial hematoma
• Frontal sinus involvement.
• Do not remove any impaled object until patient is in the OR.

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Epidural hematoma

• A neurosurgical emergency
• Blood between inner table of the skull and the dura.
• Lens shaped/biconvex hyperdense lesions that do not cross suture lines on CT
• It results from rupture of an artery, vein or venous sinus, in association with a skull fracture.
• Classical presentation: only in 20-30% of patients.
• Signs of uncal herniation
• Management: Evacuation
• Conservative management in patients who meet all these criteria:
• Maximum thickness < 1.5 cm
• Clot volume < 30cm3 and
• GCS > 8.
• Prognosis

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Acute subdural Hematoma

• Occur in approximately 30% of patients with severe brain injuries

• Due to sudden acceleration-deceleration of the brain parenchyma inside the skull
• Blood beneath the dura, overlying the brain and arachnoid, resulting from tears to
bridging vessels
• Risk Factors: Elderly, alcoholics
• Bleeds of significant size (thickness >1cm), with significant associated midline
shift (>5mm) or with deteriorating neurology, require urgent evacuation.
• Smaller bleeds in neurologically stable patients may be managed conservatively,
at least initially: liquefaction of the clot over 7–10 days after the bleed may allow
for a much less invasive evacuation through burr holes.

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 Acute subdural Hematoma

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Traumatic subarachnoid hemorrhage

• Traumatic SAH is the most common CT abnormality seen in patients with

moderate to severe TBI
• Trauma is the commonest cause of subarachnoid hemorrhage
• Bleeding beneath the arachnoid membrane on the surface of the brain.
• Blood in CSF-containing cisterns of brain
• managed conservatively
• not usually associated with significant vasospasm, which characterizes
aneurysmal subarachnoid hemorrhage

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SAH

Blood in sulci, Sylvian fissure,

inter-hemispheric fissure

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 Cerebral contusion
• A “bruise” of the brain
• occur in 20% to 30% of patients with severe brain injuries.
• Frontal, temporal and occipital regions most commonly affected.
• Coup: Brain injury at the site of impact
• Counter-coup
• Contusions rarely require surgical intervention, but may warrant delayed evacuation
to reduce mass effect

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Diffuse Axonal Injury (DAI)

• Shear force to brain (acceleration/

deceleration/rotational)
• seen in high-energy accidents
• Traumatic disruption of axonal fibres
• Hallmarks of DAI: absence of lucid interval and clinical picture out of proportion
to CT findings.
• CT: Loss of gray-white matter distinction, punctate hemorrhages.
• High mortality rate (50%)

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References

• ATLS Student Course Manual, 10th edition

• Baily and Loves’ Short Practice of Surgery 27th edition
• Schwartz’s Principle of Surgery, 10th edition
• Sabiston textbook of Surgery, 20th edition
• Tintinallis Emergency Medicine 8th ed.

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 Thank You!!

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