The document provides an overview of head injuries, including definitions, risk factors, and anatomy related to traumatic brain injury (TBI). It describes the classification, evaluation methods, and management strategies for TBI, emphasizing the importance of monitoring cerebral perfusion pressure and intracranial pressure. Critical treatment protocols are outlined, focusing on preventing secondary brain injury and the necessity of timely interventions.

1. HEAD INJURY
Presented by Dr NDAYISABA CORNEILLE
CEO of CHG
MBChB, DCM,BCSIT,CCNA

2. Introduction
■ Definition: Head injury is Alteration in mental or physical
functioning related to trauma
■ Central nervous system injuries remain the leading cause of
morbidity and mortality for young people throughout the
world.
■ The risk of incurring a traumatic brain injury (TBI) is
especially high among adolescents, young adults, and elderly
people.
– For example, the management of depressed skull fractures in
children at Muhimbili Medical Centre, Dar es Salaam, Tanzania is
described by Mlay and Sayi.
– The fractures were located in the frontal or parietal bone in 27
(76.3%) patients.
– Casualty officers should note the indications for surgery were
cosmetics in 15 patients, compound fracture in 3 patients, focal
neurological deficit in 2 patients, and torn dura presenting with
Pseudo-meningocele in 2 patients.
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3. Anatomy:
Axial T1-weighted MRI
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Parietal
Occipital
Temporal
Frontal

4. Anatomy: Brain
■ Brain: Cerebrum
■ Frontal Lobe
– Emotions
– Motor Function
– Expression of
speech
■ Temporal Lobe
– Comprehension of
speech
– Memory
■ Parietal Lobe
– Sensory function
– Spacial orientation
■ Occipital Lobe
– Vision
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5. Anatomy: Brain
■ Brain:
– Cerebellum:
■ Coordination and balance
– Brainstem (Midbrain,
Pons, Medulla)
■ Alertness (RAS)
■ Cardiorespiratory centers
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6. Anatomy: Meninges
■ The meninges of the brain and potential sites for
hemorrhage
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Brain
Calvarium
Dura Mater
Arachnoid
Pia Mater
Potential Space
CSF
Potential Space
Epidural Hematoma (meningeal arteries)
Subdural Hematoma (bridging veins)
Subarachnoid Hemorrhage into CSF

7. Physiology
■ Cerebral Blood Flow (CBF):
– Normal CBF = 50 ml/100 gm of tissue
– Loss of cell function occurs at < 20-25
– Cell death of irreversible damage occurs at < 5
■ Autoregulation:
– the brain can maintain a constant CBF with a CCP
(Cerebral Perfusion Pressure) of 50-150 mm Hg
through vasoconstriction and vasodilatation
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8. Physiology
■ Cerebral Perfusion Pressure (CPP): CPP = MAP – ICP
■ Intracranial Pressure (ICP):
■ Normal 5-15 mm Hg
■ Abnormal > 20
■ Severe > 40
■ CCP must be maintained > 70 mm Hg
■ The autoregulatory function is often lost in TBI patients
■ MAP and ICP must be carefully monitored in TBI patients
■ Low CPP must be treated aggressively to maintain CBF
– Increase MAP
– Decrease ICP
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9. Classification of TBI - Mechanism
■ Mechanism:
– Blunt
■ High velocity (MVC)
■ Low velocity (fall, assault)
– Penetrating
■ Gunshot wounds
■ Other penetrating injuries
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10. Classification of TBI - Morphology
■ Scalp Lacerations
– Can result in major blood loss
– Treatment
■ Direct pressure
■ Ligation of the bleeding vessels
■ Injection of lidocaine with epinephrine into the bleeding
areas
■ Multi-layer closure of the wound (always close torn
galea)
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11. Skull Fractures
■ Cranial vault fractures
■ Linear or stellate
■ Open or closed
■ Depressed or non-depressed
– Fragments depressed greater than skull
thickness require elevation
■ Basilar skull fractures (BSF)
■ Periorbital ecchymosis (raccoon eyes)
■ Retroauricular ecchymosis (Battle’s sign)
■ CSF leaks (rhinorrhea, otorrhea)
■ Hemotympanum (blood behind the eardrum)
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12. Basilar Skull Fractures (BSF)
■ DO NOT place NGT’s in
patients with suspected or
known BSF!!!
■ This patient clearly has
physical signs of a BSF, yet
inappropriately had an NGT
placed!!!!!
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13. Basilar Skull Fractures (BSF)
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What is the PROBLEM in this picture?

14. Concussion
■ Diffuse injury
■ GCS 14 to 15
■ Headache
■ Dizziness
■ Normal Neurologic Exam
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15. Cerebral Contusion
■ Common injury
■ Often seen in association with
SDH and SAH
■ Most common in frontal and
temporal lobes, occasionally in
occipital lobes
■ “Coup” or “contrecoup” injuries
■ Tissue disruption leads to
increased vascular
permeability and edema
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16. Epidural Hematoma
■ Relatively uncommon
■ More common in young & active
■ Between the dura and skull
■ Biconvex in shape
■ Result of tearing of meningeal
arteries
■ Often associated with skull
fracture
■ Usually minimal damage to brain
parenchyma
■ Prognosis good if evacuated
quickly
■ Classic History: Lucid interval
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17. Subdural Hematoma
■ More common injury (30%)
■ More common in older & alcoholics
■ Under the dura
■ Crescent shaped
■ Covers surface of hemisphere
■ Result of tearing bridging veins
■ Associated with blunt trauma to
underlying parenchyma
■ Prognosis worse due to more diffuse
injury
■ Requires prompt evacuation
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SDH with MLS

18. Subarachnoid Hemorrhage
■ Most common finding in moderate to
severe TBI (40%)
■ Blood noted in cisterns and sulci
■ Results from tear in subarachnoid
vessels
■ May precipitate vasospasm
■ Often associated with meningeal
signs:
– Photophobia
– Neck stiffness
– Headache
■ Requires neurosurgical consultation
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19. Diffuse Axonal Injury
■ Occur with rapid acceleration and
deceleration injuries
■ Causes disruption of axonal fibers
by shear forces in white matter and
BS
■ Effects are rapid and irreversible
■ Associated with edema and
increased ICP
■ Non-specific pattern on CT with loss
of G-W interface and diffuse swelling
■ “Shaken-baby syndrome”
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20. Glasgow Coma Scale (GCS)
■ Main Components
– Eyes
– Verbal
– Motor
■ Scoring
– Mild Injury 14-15
– Moderate Injury 9-13
– Severe Injury 3-8
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21. Glasgow Coma Scale (GCS)
■ Eyes
– 1 – Closed
– 2 - Opens to pain
– 3 - Opens to voice
– 4 - Open
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22. Glasgow Coma Scale (GCS)
■ Verbal
– 1 – Silent
– 2 – Moans
– 3 - Inappropriate words
– 4 - Disoriented or confused
– 5 - Oriented and appropriate
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23. Glasgow Coma Scale (GCS)
■ Motor
– 1 - No response
– 2 - Extension to pain
– 3 - Flexion to pain
– 4 - Withdraws from pain
– 5 - Localizing pain
– 6 - Follows commands
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24. Evaluation
■ Critical Components of History:
■ Age
■ Sex
■ Mechanism of injury
■ Time of injury
■ Loss of consciousness
■ Level of alertness
■ Amnesia
■ Headache
■ Seizures
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25. Evaluation
■ Critical components of physical exam:
■ GCS (Eye, Verbal, Motor)
■ Pupillary light reaction (brainstem)
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26. Pupil Evaluation
Pupil Size Light Response Interpretation
Unilateral dilation Sluggish or fixed 3rd nerve compression due
to tentorial herniation
Bilateral dilation Sluggish of fixed Inadequate brain perfusion
Bilateral 3rd nerve palsy
Unilateral dilation or
equal
Swinging flashlight +
(Marcus-Gunn)
Optic nerve injury
Bilateral constriction None or minimal Drugs (opiates)
Metabolic encephalopathy
Pontine hemorrhage
Unilateral
constriction
Intact Injured sympathetic path
(ie: carotid sheath injury)
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27. Evaluation of TBI
■ CT scan is the imaging modality of choice
– Indications for CT scan in trauma patient:
■ Loss of consciousness
■ Amnesia
■ Neurological signs or symptoms
■ Decreased level of consciousness (GCS < 14)
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28. Evaluation of TBI
■ CT scan is the imaging modality of choice
– Indications for CT scan in trauma patient:
■ Seizure activity
■ Mental status difficult to evaluate: drugs, alcohol, anesthesia
■ Prior to surgery if surgery is required for other injuries
■ (Headache without these other signs is no longer included)
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29. Management - General Principles
■ Address ABC’s first
■ If ABC’s are intact and patient has a
depressed level of consciousness, ASSUME
head injury
■ If patient has a head injury, ASSUME C-spine
injury
■ In patient with significantly depressed level of
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30. Treatment
■ East African practitioners will often:
– Perform hourly neurological observations which
should be recorded clearly and include:
■ Glasgow coma score
■ Blood pressure, pulse and respiratory rate
■ Pupil size and reaction
■ Limb movements (normal, mild weakness, severe
weakness, spastic flexion, extension, no response)
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31. Treatment to Control ICP
■ Intravenous fluids
■ Mannitol
■ Anesthesia and sedation
■ Anticonvulsants
■ ICP monitoring
■ Raise the head of the bed 30 degrees for increased ICP
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32. Ventilation
■ Prevent Hypoxia
– Maintain PO2 > 60 mm Hg
■ Maintain Low Normal PCO2
– PCO2 = 30-35 mm Hg
– Hyperventilation with
hypocapnea causes
constriction of cerebral
vessels, possibly leading to a
reduction in CBF
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33. Intravenous Fluids
■ Volume Status:
– Maintain the patient NORMOVOLEMIC
■ Use venous or Swan-Gantz catheter to monitor volume
status
■ Fluid Types:
– Isotonic only
■ NS or LR
– No glucose containing solutions
■ Glucose is broken down into lactic acid in the damaged
tissue and further increases brain injury
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34. Mannitol
■ Mechanisms
■ Immediate:
– Expands circulating volume and decreases viscosity
– Increases CBF and O2 delivery
■ Delayed (15-30 min):
– Osmotic diuretic
– Assists in drawing free water from CNS across BBB
■ Dose:
■ 0.5-1 gm/kg
■ Given as one time bolus
■ Do NOT use for long term
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35. Sedation and Anesthesia
■ Keep patient sedated and anesthetized
■ Reduces muscles tone and contractions to minimize ICP
elevation
■ Barbituate Coma
■ Indications:
– Increase ICP with no surgical lesion
– Other methods have failed to control ICP
– Low GCS
■ Benefits:
– Decreases cerebral metabolic rate
– Decreases cerebral blood volume and ICP
– Promotes hypothermia
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36. Anticonvulsants
■ Seizure can increase tissue damage by:
■ Increasing hypoxia
■ Increasing ischemia
■ Increasing ICP
■ Risk factors:
■ Intracranial hemorrhage
■ Depressed skull fracture
■ Recommendations for severe TBI:
■ Anticonvulsant prophylaxis for 1 week post event
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37. ICP Monitoring
■ Intraventricular Catheter (IVC):
■ Invasive measure of ICP
■ Most accurate and reliable method to
monitor ICP
■ Can be used for continuous monitoring
■ Catheter placed through burr hole in
calvarium and through parenchyma into
lateral ventricle
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38. Burr Hole
■ Criteria for
explorative burr hole
– No CT scan
– No neurosurgical
services
– Rapid deterioration
– Herniation
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39. Burr holes
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41. Summary
■ Address the ABC’s First
■ Primary Goals:
■ Identify life-threatening injuries and treat immediately
■ Prevent secondary brain injury by avoiding hypoxia
and hypotension
■ Identify decompressible mass lesions early by CT
■ Intubate early
■ Treat hypotension aggressively
■ Frequently reassess the patient’s neuro status and
vitals
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42. THANKS FOR BEING
ATTENTION
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