Helu Neuro

Management
Of
Head Injury
By Hani E.
Hana L.
Haileysus A. & Helen B.
Feb 21/2014
Moderator Dr. Abat
Objectives
• Introduction & Epidemiology of HI
• Mechanisms of Injury
• Pathophysiology
• Scales & Clinical Features
• Evaluation of the Patient with HI
• Management of HI
• Sequelae of Head Injury
Ghana Emergency
Ghana Emergency Medicine
MedicineCollaborative
Collaborative
Advanced Emergency Trauma
Advanced Emergency Trauma Course
Course
Introduction
• Traumatic Brain Injury has long been
recognized as a important medical entity
– Traumatic Brain Injury [TBI] first came into use in

1996.
– It is a non degenerative, non congenital insult to the

brain from an external mechanical force possibly
leading to temporary/permanent impairment.
– Hippocrates first commented on mechanisms

of head injury and first described trephination http://commons.wikimedia.org/wiki/
File:Trepan1b.gif
as modality to treat head injury
Ghana
Emergency Medicine Collaborative
Collaborative
Advanced Emergency
Trauma Course
Course
Epidemiology
• WHO global burden of injury estimates :
- Among the top ten leading causes of death, with an
estimated 5 million deaths annually related mortality rates
in the world
- Among African nations the rate of injury mortality was the
highest in Nigeria, South Africa and Ethiopia were 2 nd& 3rd .
- Injury is more common among men 15–44 years of age &
road traffic crashes was the highest in Egypt (41%) followed
by Ethiopia (30%)
JUSH- Significantly more males had cut, (AOR=2.0; 95% CI=1.2, 3.3)
and stab, (AOR=3.0; 95% CI=1.6, 5.7), injuries compared to females.
Cont…..
• 194 neurosurgical cases were
performed at BLH from 2006-7 ^
Procedures for head trauma
comprised 50 %of the total
number of operations :
- 46% had depressed skull # the

predominant mechanism of injury
was stick fighting > 80%
- The remainder of the patients

presented after auto-pedestrian
accidents or other motor vehicular
accidents, and kicks by farm
animals
Spectrum of Injury
– Results from:
• Direct Forces = Object Striking or penetrating cranium
• Indirect Forces = Acceleration/Deceleration or

Rotational Mechanism [Blunt]
• Parts involved during injuries= Scalp injuries

Skull injuries
Brain injuries
Normal Cerebral Autoregulation
• The brain is a semi-solid organ that occupies ≈ 80% of the cranial

vault
• Monroe-Kelli Doctrine
– Defines the relationship between the volumes of the three
compartments to maintain a stable ICP
CPP = CBF = MAP – ICP
• Cerebral autoregulation is a protective mechanism designed to

maintain a tightly controlled intracranial environment where
fluctuations in systemic arterial pressure or ICP do not have a large
impact on cerebral blood flow
SCALP Lacerations
• It extends from external occipital protuberance & superior nuchal lines to
the supra orbital margins
• Skin
• Connective tissue
• Galea Aponeurotica – deep fascia – percied by numerous emissary veins
connect with intracranial venous circulation
• Loose connective tissue – dangerous area of scalp – allow accumulation of
blood/pus
• Periosteum
Cont…
• Types – Stellate
- Linear
- Y shaped
- Penetrating
- Crescent
 Often incised looking lacerations- Use hand lens to
differentiate
 Bleed profusely
 Usually heals rapidly
 Sometimes infection may spread to brain through unnoticed
fissured #s- make take weeks to cause death
SKULL FRACUTERS
Classification- based on
 pattern: Linear…Diastatic…Comminuted…Depressed
 location: Convexity…Skull base
 Type: Open …Closed
• Linear Skull Fracture

¯ Single fracture line:
– Passing through the entire thickness of the skull
• Diastatic fracture line:

– Separation of a cranial suture
– Common in infants < 3y/r
– In older pts only as part of a more extensive fracture pattern
Cont…..
Treatment:
• Closed: observe
• Open:
– Non-penetrating:
• Clean & debride scalp and close primarily
– Penetrating
• Only need to explore dura if known penetrating injury, e.g.,
knife
• Do craniotomy around fracture site
• Do not cross the fracture line with the saw
• Do limited debridement of brain and close dura mater-tight
Cont…
• Comminuted Skull Fracture
- When more than one linear skull fracture is present
- Usually a central impact point with multiple fractures radiating away from it.
Rx:-----treat as per linear fractures
• Depressed Skull Fracture

Defn- the outer table lies below the anatomical level of the inner table of
the surrounding intact skull
- results from impact of energy over a small area
- many pts. suffer an initial LOC, then lucid
- 85% have assoc. scalp laceration, but this may be 1-2 cm away from actual
skull fracture
- Can have significant underlying brain injury
NB: skull fragments usually rebound somewhat to lie more superficial than at
the moment of impact
Cont….
Treatment:
Indication for Elevation
I) Cosmoses- usu. forehead with a # depth of >3mm
- usu. can be done within days, unless- dural laceration/brain
penetration,- frontal sinus #, - mass effect & hematoma presents
II) OPEN - should do <12 hours
- clean scalp, bone, brain
- debride devitalized tissue
- watertight dural closure
- should delay cosmetic bone repair if: multiple severe injuries
Technique
 Incorporate scalp laceration into an “S” incision
 Lift off bone fragments only if they come easily
 If they are impacted, then do a craniotomy around the
fracture site and lift off as one piece
 Debride devitalized dura/brain/bone fragments
 Watertight dural closure  use pericranium or temporalis fascia
 Clean bone fragments in saline
 Irrigate thoroughly
 Dural tack-up stitches
- 3-10% get infection
Cont…
Depressed Fracture over Dural Venous Sinus
- Do only a superficial debridement! unless…
 Indications for elevating fracture:
- # is grossly contaminated with foreign body
- Major cosmetic defect
- Intracranial hypertension
Basal skull #
Classified into: Anterior, Middle & Posterior
Signs according to the site of # respectively:
 Bilateral perioribital edema “raccoon eyes”
 CSF rhinorrhea or otorrhea
 Hemotympanium/ bleeding from ear
 Battle’s sign- bruising over mastoid
TRAUMATIC BRAIN INJURY
– Primary Brain Injury [TBI]
• Types of Primary Brain injury
• Cellular Injury Mechanisms
– Secondary Brain Injury
• Systemic Insults
• Intracranial Insults
– Mechanisms of TBI
• Skull Fractures
• Extra-axial Fluid Collections
• Intraparenchymal Hemorrhage
• Subarachnoid Hemorrhage
Ghana
Collaborative
Advanced Emergency
Trauma Course
Course
Types of primary brain injury
 Direct or indirect force to brain tissue,
resulting in cellular injury
– Cortical Brain Contusion
– Brain Concussion
– Diffuse Axonal Injury[ DAI]

• Rotational Mechanism
– Widespread shearing strain at deep
cerebral white matter that disrupts normal
axonal organization resulting in disruption
of axonal fibers and myelin sheaths
• Non-lateralizing neurological deficits
• Generalized edema occurs after injury, typically

within 6 hours without any focal lesion on
imaging
Primary Brain Injury - Cellular Level
Primary Cellular Injury
Oxygen Free Radical Lipid Peroxidation
Massive Depolarization of
Pathway Activation Cell Membrane Dysfunction
Brain Cells
Cell Lysis
“Neurotransmitter
Storm”
Glutamate
High Nitric Oxide Cell Death
Levels
Calcium Nitric Oxide

Synthase
NMDA Disruption of normal cellular processes:

Protein Phosphorylation Membrane and
Microtubule Construction Cytoskeleton Breakdown
Enzyme Production
Intracellular Signaling
Ghana Emergency Medicine Collaborative
Processes Advanced Emergency Trauma Course
Secondary Brain Injury
– Systemic or Intracranial processes that contributes

to the primary brain injury cycle and results in
greater tissue injury
– Categorized into:
Ghana
Collaborative
Advanced Emergency
Trauma Course
Course
Cont….
– Hypoxia (PaO2 < 60 mmHg)
• Mortality of TBI pts with hypoxia = doubled
– Hypotension (SBP < 90 mmHg)

• Present in 33-35% of TBI patients
• Hypotension → ↓Cerebral Perfusion→↑Cerebral Ischemia
→↑Doubles Mortality
– Anemia (↓Oxygen Carrying Capacity)
– Hypo/ Hypercapnia
• Hyperventilation → ↓pCO2 Levels → ↑Serum pH → Cerebral
Vasoconstriction → ↓Cerebral Blood Flow
• Previously was a mainstay of treatment and will help to buffer an
expanding hematoma in short-term
Ghana Emergency
Collaborative
Course
Cont….
• Other Systemic Insults
– Seizures - Coagulopathy
– Electrolyte Abnormalities - Infections
– Coagulopathy - Hyperthermia
– Iatrogenic (Under resuscitation)
– Extra-axial Lesions
– Cerebral Edema (Peaks at 24-48 hrs post injury)
– Intracranial Hypertension
Ghana Emergency
Collaborative
Course
Concussion Vs contusion
• Concussion
– Concussion represents a subset of mild traumatic brain injury. “To shake
violently”
– It is a transient brief interruption of neurologic function with or w/o brief

LOC followed usually blunt injuries
– Symptoms of a concussion range from mild to severe and can last for hours
to weeks
– Four main categories of symptoms predominate by

* Headache, confusion & amnesia
– Most people recover early from concussion

Cont…
• According to AAN & ICC, 2004
- A complex pathophysiological process affecting the brain,
induced by traumatic biomechanical forces that typically
includes:
- Maybe caused by either a direct blow to the head, face, neck or elsewhere on the
body with an “impulsive” force transmitted to the head
- Rapid onset of short lived impairment of neurologic function

that resolves spontaneously
- The acute clinical symptoms largely represent a functional

disturbance rather than structural injury
- Concussion results in a graded set of clinical syndromes that may or may

not involve LOC [ not brief] and grossly associated with normal
Extra-axial Fluid Collections
 EPIDURAL HEMATOMA [EDHs}
-Clots outside the dura beneath c.vault
Epidemiology
< 2% of HI
R are in adults > 60 years and infants < 2 y/o
Pathogenesis
Impact causes inbending of skull and stripping of the Dura
Skull is usually fractured: in 90% of adults, but less common in
children
Bleeding source:
– MMA 50%
– MMV 30%
– Diploic vein/ Dural sinus 20%
Predominantly results from direct mechanical forces that will lead

to skull # [ usu. mild parenchymal injury]
Cont….
Clinically Radiologic finding
• classically, LOC, followed by lucid • Biconvex, lenticular hyper dense lesion
interval, then LOC again [30%] • appear more flattened if:
– posterior fossa
– d/t dural venous sinus laceration or
• delayed EDH can occur in approx. 10% of diploic vein
series
NB: Note in children esp. two special types of
• Temporo-parietal region is the commonest EDH:
site for EDH – posterior fossa
– bilateral convexity, esp. bifrontal –
usually venous origin
• Most often EDHs are unilateral
Management
• A rapid deterioration of a patient from • Urgent craniotomy
arterial bleeding • Do one burr hole first to provide immediate
decompression then complete craniotomy
* In general, S/s depends entirely on how

Cont…
 SUBDURAL HEMATOMAS
[SDHs]
- Blood accumulation b/n the dura matter
& the brain. Defn-< 3 days  acute [ASDH]
- 3 days – 3 weeks  subacute
- > 3 weeks  chronic [CSDH]
Epidemiology
- More common than EDHs
- Incidence 2 per 100,000
- 12 to 29% in severe TBI
- Common in elders >50 and infants <2yrs
- 30-50% of pts have no hx of HI

Cont….
Risk Factors: • Pathogenesis
-Brain atrophy most important factor Initial bleeding within the DBC
- Old age * layer - (subdural space is only a
- Alcoholism * potential space
- Epilepsy • Potential causes of bleeding:
- Pre-existing acute SDH > 1cm
– 34% cerebral contusions
- Malnutrition
- Hemodialysis
– 26% dural tears
- VP shunt – 19% bridging veins
- Coagulopathies – Parenchymal vessels from
cortical contusion
– Arachnoidal arteries/veins
Sequential steps in SDH formation
 Initial hemorrhage incites reaction  attempts to organize hematoma 
this mostly occurs on the outer dural surface
 Within 1st day – outer surface covered by fibrin & fibroblasts
 Proliferating fibroblasts & capillaries penetrate the clot to a depth of
several mm
 By 4-7 days this outer membrane begins to develop
 Hematoma starts to liquefy  more hypo dense on CT
 Inner membrane:
– Develops later (about 2-3 weeks)
– More delicate lamina developed by fibroblasts (or DBC)
– lacks the capillaries of the outer membrane
– never as thick as the outer membrane
Cont….
Mechanisms of hematoma enlargement:
• Diffusion of albumin into cavity – little supportive evidence ? ??
• osmotic electrolyte diffusion of CSF into cavity – DISPROVED
• Recurrent hemorrhage – most likely

– fibrinolytic activity and coagulation abnormalities
within CSDH
– repeat bleeding d/t fragile neocapillaries with
encapsulation creates multiple membranes
Fate of CSDH:
Cont….
- Can slowly grow and become symptomatic - Some Calcify
- Acute bleed with rapid neurological deterioration - Some shown resoln
Clinically
• The “great imitator”…can present as almost anything…is in the differential for
any LOC/personality/deficit in elderly
-Altered mental state 50-70%
-Headache 50-60%
-Motor deficit 50%
- Lucid interval at some point 12-38%
-Transient neuro deficit 10%
- Seizure 6%
* Most pts presents with a GCS score of <8

- During its expansion, its slow & constant presurre increment often cause
extensive parenchymal tissue damage surrounding the clot..
Cont…
Imaging
• CT – Hyperdense crescent
shaped lesion
CT can miss
– bilateral isodense SDH
– vertex, skull base, post fossa
CSDH
• MRI - follows the usual
progression of hematoma,
except hemosiderin is rarely
seen
Cont…
Cont….
Cont….
Cont…
Cont…
Cont…
Management
Observation
- For small asymptomatic SDH or patients considered too ill for surgery
- In non-selected geriatric series (i.e., non-neurosurgical cases) only 40% of patients
receive surgery
Surgery need for re-operation:

• Twist drill drainage 60%
• Burr hole drainage 11%
• Burr hole with SD drain 7%
• Craniotomy 9%
• Subdural-peritoneal shunt: value in pediatric population
Complications
• 20-30% symptomatic recurrence - New acute SDH or ICH
• 11% post-op seizure - Infections
• 8% tension pneumocephalus
Prognosis
- Overall mortality of pts who have SDH is b/n 40-60%
at 6 months
- In operative series- ≈ 6% mortality & 16% morbidity.
 SUBDURAL HYGROMA Etiology
-Subdural collection of clear (i.e. CSF) -Trauma  arachnoid tear - CSF
fluid following HI efflux
Epidemiology -Post-meningitic  “meningitis
• 10% of traumatic intracranial mass serosa traumatica”
lesions -Iatrogenic  post crani
• bilateral > 50% “compensated hydrocephalus”
• skull fracture ~40%
Pathogenesis:
Clinically – Tear in arachnoid membrane
- Many asymptomatic  CSF leak into subdural
-  LOC compartment
-Focal neuro deficit – Most are low-pressure
Cont…..
Imaging Rx
• Most asymptomaticno Rx
CT -Low-density (i.e. CSF • For large, symptomatic
density) fluid collection in
lesion:
subdural space – burrhole  drain
-Often minimal/absent shift – subdural-peritoneal shunt
- Lack of enhancing membrane • Outcome chiefly related to
underlying brain injury
Intracerebral Hemorrhage
 Subarachnoid Hemorrhage
Bleeding beneath the arachnoid
membrane over the surface
of the brain
– Disruption of subarachnoid
vessels
– Common in moderate to
severe brain injury
– Worse prognosis
* 2X as likely as other head
injured patients to suffer from
death, PVS or severe
disability
Cont…
Cont…
 Intracranial
hematoma
-Focal areas of
hemorrhage within the
parenchyma
Clinical Features and Measurements of
TBIs
Spectrum of clinical presentations
– Hallmark Symptoms
• Confusion and amnesia w/ or w/o LOC
– Severe brain injury often characterized by
decreased mental status and presence of
neurological deficits
– Patients may also deteriorate from mild to severe
head injury during course of evaluation
C/Fs
• Confusion
– Characterized by three cardinal features
• Disturbance of vigilance and heightened distractibility
• Inability to maintain a coherent train of thought
• Inability to carry out a sequence of goal directed
movements
• Amnesia
– Anterograde or retrograde
– Often characterized by repetitive questioning, inability to
follow commands, inability to retain information during
medical evaluation
– Amnesia will decrease slowly over time and small amount
of memory deficit remains
Ghana
Collaborative
Advanced Emergency
Trauma Course
Course
Cont….
– No loss of biographical data
• i.e. Name, etc. – typically the result of hysterical rxn or
malingering
– Duration does correlate with severity and outcome of head
injury
• LOC
– Results from rotational forces at the junction of the upper
midbrain and thalamus that results in disruption of reticular
neuron function and inability to maintain alertness
– Presence of LOC is not a predictor of long term
neuropsychiatric sequelae of head injury
Measurements
 Glasgow Coma Scale [GCS}
– Developed by Teasdale and Jennett in 1974
– Originally designed for measure 6 hours after injury to
provide long term prognostic information about
mortality and disability
– Now, standardized to measure 30 min after injury and
repetitive measurements throughout patient’s stay
– Should be performed after adequate resuscitation b/c
scale is sensitive to hypotension, hypoxia, intoxication
and pharmacologic interventions
* Best prognostic indicator of outcome = CT Scan
Cont….
• GCS
Glasgow Coma Scale (GCS)
Eye Opening Opens spontaneously 4
Responds to verbal command 3
Responds to pain 2
No eye opening 1
Verbal Oriented 5
Disoriented 4
Inappropriate words 3
Incomprehensible speech 2
No verbal response 1
Motor Obeys commands 6
Localizes to pain 5
Withdraws to pain 4
Flexion to pain (Decorticate posturing) 3
Extension to pain (Decerebrate posturing) 2
No motor response 1
Ghana Emergency
Collaborative
Course
Mild HI [14-15]
• Mild Head Injury
– Signs and symptoms (early/late)
Signs and Symptoms of Head Injury
Cognitive Somatic Affective
Confusion Headache Emotional Lability
Anterograde amnesia Fatigue Irritability
Retrograde amnesia Disequilibrium Sadness
Loss of consciousness Dizziness
Disorientation Nausea/vomiting
Feeling “zoned out” Visual disturbances
Feeling “foggy” Photophobia
Vacant stare Phonophobia
Inability to focus Difficulty sleeping
Delayed verbal/motor response Ringing of the ears
Slurred or incoherent speech
Excessive Drowsiness
Ghana Emergency
Collaborative
Course
Cont…
• Grading scale for mild head injury with GCS
b/n 14-15 and Concussion syndrome
– Developed by Colorado Medical Society and
American Academy of Neurology
– Composite Grading System
• Grade 1 – Any head injury with transient confusion, no
LOC and symptoms that last less than 15 minutes
• Grade 2 – Transient confusion, no LOC, symptoms that
last longer than 15 minutes
• Grade 3 – All head injury with LOC
Ghana Emergency
Collaborative
Course
Moderate HI [9-13]
– Clinical presentation varies widely
– 10% of patients
– Specialized Subset = “Talk and Die Syndrome”
• Initially, talkative and without significant signs of external
injury
• Within 48 hours of injury, rapidly deteriorate
• EDH is cause in 78-80% of cases
• Patients with “talk and die syndrome” who present with a
GCS > 9 but who deteriorate have been shown to have a
worse outcome than patients who present with severe TBI at
outset
– ? Delayed Diagnosis
Ghana
Collaborative
Advanced Emergency
Trauma Course
Course
Severe Head Injury [GCS<9]
- 10% of patients with TBI
- Early aggressive treatment is required with airway control, resuscitation, admission

to ICU setting
- Outcome is poor with mortality as high as 60%
• Cushing’s Triad = Acute entity seen in severely head injured patients with
significant increased intracranial pressure and impending herniation
– Results from ischemia to hypothalamus with poor perfusion to the brain,
resulting in sympathetic stimulation of the heart to correct poor perfusion. The
sympathetic stimulation results in hypertension, but carotid baroreceptors
respond with parasympathetic stimulation resulting in bradycardia
– Characterized by:
• Progressive Hypertension
• Bradycardia
• Irregular or impaired respiratory pattern
Ghana Emergency
Collaborative
Course
Evaluation of H. Injured patients
Includes:- Neurological exam & imaging
 Glasgow Coma Score
 Pupil size & response
 Lateralising sign
 Signs of basal skull #
 Full neurological examinations
Neurological Exams
– Pupillary Size + Reactivity
• Fixed Dilated Pupil = Ipsilateral Intracranial Hematoma resulting in uncal herniation
• Bilateral Fixed + Dilated = Poor Brain Perfusion, bilateral uncal herniation or severe
hypoxia
– Indicative of very poor neurological outcome
– Neurological Posturing
• Decorticate Posturing = Upper extremity flexion with lower extremity extension
– Cortical Injury above the midbrain
• Decerebrate Posturing = Arm extension and internal rotation with wrist flexion
– Indicative of brainstem injury
– Very Poor predictor of outcome
– Full, Complete Neurological Exam

• Examine for subtle neurological deficits
• Look for specific injury patterns:
– Battle’s sign, CXF Otorrhea, CSF Rhinorrhea, Hemotympanum, peri-orbital
Ecchymosis is indicative of skull fracture and is concerning for underlying brain
injury
Ghana Emergency
Collaborative
Course
Neuro imaging
• Skull Radiography
• CT Scan (Gold Standard)
• Magnetic Resonance Imaging (MRI)
• Experimental Modalities for Neuroimaging
– Functional MRI (fMRI)
– PET Scanning
– SPECT Scanning
– Magnetic Source Imaging (MSI)
Ghana
Collaborative
Advanced Emergency
Trauma Course
Course
Cont….
 Skull Radiography
– Prior to CT, Skull radiography used as triage tool
– Can evaluate for
• Skull fractures
• Pneumocephalus
• Blood in sinus
• Penetrating foreign body
– Patients with abnormal findings are at increased risk of
intracranial findings
– However, still misses a large number of patients with
normal skull films but extensive injury
– Limited utility at very rural sites without access to CT
imaging
Ghana
Collaborative
Advanced Emergency
Trauma Course
Course
Cont…
 Computed Tomography (CT Scan)
– Imaging modality of choice
– Non contrast CT is the Gold standard
– Especially good in identifying skull fracture, extra-axial
fluid collection and hemorrhagic contusion
• New Orleans Criteria
• Canadian Head CT Rule
Ghana
Collaborative
Advanced Emergency
Trauma Course
Course
New Orleans Criteria
CT imaging is required for patients with minor head injury with any one of the following findings. The
Criteria only apply to patients who have a GCS of 15.
1.Headache
2.Vomiting
3.Age > 60 years
4.Drug or Alcohol Intoxication
5.Persistent anterograde amnesia
6.Visible trauma above the clavicle
7.Seizure
Canadian CT Head Rule

CT Imaging is only required for patients with minor head injury with any one of the following
findings. The criteria apply to patients with minor head injury who present with GCS of 13-15 after
witnessed LOC, amnesia or confusion.
High Risk for Neurosurgical Intervention
1.GCS < 15 at two hours after injury
2.Suspected open or depressed skull fracture
3.Any sign of basilar skull fracture (Hemotympanum, Peri-orbital Eccymosis, Otorrhea or
Rhinorrhea, Battle sign)
4.Two or more episodes of vomiting
5.Age > 65 years
Medium risk for Brain Injury Detection by CT Imaging
6.Amnesia before impact of 30 or more minutes
7.Dangerous mechanism (E.g. Pedestrican vs. Motor vehicle, Ejection from motor vehicle or fall
from an elevation of 3 or more feet or 5 stairs)
Basics of Management
• Mild Head Injury
– Admission Criteria
– Discharge Criteria
– Discharge Instructions
– Return to Play Guidelines
• Moderate and Severe Head Injury
– General Principles
– Airway Management
– Hemodynamic Assessment
– Seizure Prophylaxis
– Operative Management
– Intracranial Monitoring
Ghana Emergency
Collaborative
Course
Mild Head Injury Management
ABC’s + C-spine!
 Symptomatic treatment and prevention of secondary injury
– Appropriate management depends on assessment of risk of
neurological decompensation and risk factors for intracranial
hematoma
– Risk factors for intracranial hematoma
• Coagulopathy, Drug/Alcohol Intoxication, Previous neurosurgical
procedures, Pre-trauma epilepsy or older age (> 60 y/o)
– Low risk features
– All patients with mild traumatic brain injury should be
observed for 24 hours after that injury (either inpatient or
outpatient).
Ghana Emergency
Collaborative
Course
Cont….
 Admission Criteria
• GCS < 15
• Abnormal CT Scan
• Seizure Activity
• Abnormal Bleeding Parameters (Anticoagulation or bleeding diathesis)
• Unable to be observed at home
 Discharge Criteria
– Low risk patients can be discharged home wit h instructions [telling warning signs]
– Patients can be discharged if:
• GCS = 15
• Normal neurological exam
• Normal Head CT
• No predisposition for bleeding
Ghana Emergency
Collaborative
Course
Moderate/Severe HI Mgt
• ABC + C- spine !
 Prevention of hypoxia and hypoventilation are the keys to prevent
secondary insults
 Special attention should be paid to maintaining cervical spinal
immobilization
 Patients with GCS < 9, should have endotracheal airway placed after
removing secretions with suction
 Elevate the head 30-40ͦc
 Hyperventilate at least with nasal O2 and rush for intubation [if GCS <9]
 Iv fluid resuscitation [2/3rd of daily dose with NS/RL] & restrict oral
intake
 Diuretics
 Seizure prophylaxis [ To decrease metabolism & elevated ICP]
Cont…
• Seizure Prophylaxis
– Post-traumatic seizures = Seizures occurring in less than 7 days
post-injury
– Risk factors = GCS < 10, Cerebral Contusion, Depressed Skull
Fracture, EDH, SDH, Intracerebral bleeding, Penetrating head
injury or seizure activity within 24 hours of injury
– Brain Injury Foundation recommends anti-epileptic medications be
administered to high risk patients for first 7 days post-injury
– Acute management of seizure activity is managed with
benzodiazepines and other typical anti-epileptic agents
– No proven benefit to administration of anti-epileptic meds after 7
days to decreasing post-traumatic epilepsy
Ghana Emergency
Collaborative
Course
Surgical mgt of Head Injury
• Only 1/3rd of pts with severe TBI needs craniotomy.

• The role of surgery on the management of TBI depends on
subjective criteria or previous experience of surgeon
• Most pts with severe TBI have high ICP.
Posttraumatic mass volume measurement in TBI patients

• Modified ellipsoid method,
-Volume=ABC/2
• On axial CT images, identify the slice with largest area of
hemorrhage, slice 1
Indications for Operative mgt
 Penetrating injuries or blunt injuries with breech of the calvarium/skull
 Presence of expanding intracranial hematoma
– Epidural Hematoma
» If volume > 30 cm3 or if comatose (GCS < 9)
» Thickness >15 mm, midline shift >5 mm
» EDH in the middle fossa/inferortemporal lobe
– Subdural Hematoma
» If size > 10 mm on CT or if 5 mm shift regardless of GCS score
» Decompression if GCS decreases by 2 points from time of
injury to hospital arrival
» ICP > 20 mmHG or if pt with fixed, dilated pupils
 Malignant cerebral edema

Ghana Emergency
Medicine Collaborative
Advanced
AdvancedEmergency TraumaCourse
Emergency Trauma Course
Cont….
Depressed skull #
=Open and significant depression
=Clinical or radiologic evidence of dural laceration
=Involvement of frontal sinus & Gross cosmotic deformities
 Intraparenchymal hemorrhage & Contusion

= Progressive neurologic deterioration refer
= Lesion size greater than 50 cc
= Frontal/temporal contusion with size >20 cc & mass effect
 Posterior fossa Lesion

= Neurologic deterioration & Mass effect on CT
Increased Intracranial Pressure
• Most frequent cause of death and disability after severe head
injury
• Recommended ICP < 20 mmHg with CPP > 60 mmHg
• Initial First line treatment of increased ICP
– HOB – 30 degrees
• Subsequent first line treatment measures
– Short term hyperventilation
– Osmotic diuretic administration (i.e. Mannitol, Hypertonic
saline)
• Second Line Treatments
– High dose barbiturates
– Severe hyperventilation
– Mild/moderate hypothermia
– DecompressiveGhana GhanaEmergency
craniotomy Medicine
Emergency Medicine
Trauma Course
Advanced Emergency
Collaboratincy
Collaborative
Trauma Course
Preop. preparation
• Optimize pts neurophysiologic status while preparing
for surgery
• Preoperative assessment should rule out
coagulopathic state.
• Mannitol can be used while preparing patient for
operation
– Decompressive Craniotomy
• Salvage operation used to manage increasing ICP
• Removal of part of skull and underlying dura
• Decreases ICP, improves cerebral perfusion, prevents
ischemia
• Serves to limit secondary insults
Ghana
Collaborative
Advanced Emergency
Trauma Course
Course
Emergency Burr Hole Trephination
Indications
• Patient w/ TBI with evidence of rapid deterioration and signs of impending
transtentorial herniation with expected delay in neurosurgical management
• After medical management of increased ICP has failed
 Ideally, hematoma is localized by CT imaging but can be performed as
blind procedure
– 85% of the time will be on the same side as the dilated pupil
procedure
o Landmark = 6 cm anterior and superior to the tragus of the ear over the
tempopareital region
o Vertical incision is made through the scalp, subcutaneous tissue and temporalis
muscle until galea aponeurotica is reached
o A rotary or twist drill is then used to breach the inner table of the cranium and
the site is examined
o If no blood is identified, additional holes are made superior to the initial site and
if blood is still not identified, then the opposite side is attempted
 All sites should be covered with a sterile non-occlusive dressing
Ghana Emergency
Collaborative
Course
Sequelae of Head Injury
• Post Concussive Syndrome
– Constellation of symptoms that develops within 4 weeks of the
injury and may persist for months (90% at 1 month, 25% at 1
year)
– Treatment is with analgesia, anti-depressants and anti-emetics
• Post-traumatic Epilepsy
– Seizure activity > 7 days from traumatic injury
– Head trauma is cause of long term epilepsy in 3% of patients
with epilepsy
– Incidence is highest in patients with compound skull fracture,
intracranial hemorrhage or presence of early acute symptomatic
seizure (presence of all 3 factors increases risk by 50-80%)
– Cannot be prevented with prophylactic use of antiepileptics
Cont….
• Persistent Vegetative State
– Rare complication of severe head injury, first described in
1972 by Jennett and Plum
– Disruption of cerebral cognitive function with sparing of
brainstem function
– No awareness of themselves or environment and cannot
interact with others but will maintain normal sleep-wake
cycle
– Recovery is rare if symptoms persist for > 3 months, no
recovery documented after 12 months of symptoms
Summary
 TBIs can be caused by blunt or penetrating insults that will result in
disruption of the brain autoregulatory system
 Major Mechanisms of TBIs involves
- Skull #s
- Extra-axial collections
- Intraparenchymal hemorrhage
- Subarachnoid hemorrhage
 Quick & proper assessment of pts with HI is crucial for better mgt
outcome
 ABC+ C-spine protection with Medical & surgical interventions are the
main stay of mgt basics in TBIs.
 Well coherent, strong & continuous teaching to the society regarding
RTA
THANK YOU
…….
• Neurological Surgery, Youman’s 5th ed
• Emergency Medicine Clinics of North America
• www.neuroradiologyreference.

Helu Neuro

Uploaded by

Copyright:

Available Formats

You might also like

Helu Neuro

Uploaded by

Document Information

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Helu Neuro

Uploaded by

Copyright:

Available Formats

Management

– Traumatic Brain Injury [TBI] first came into use in

– It is a non degenerative, non congenital insult to the

– Hippocrates first commented on mechanisms

- 46% had depressed skull # the

- The remainder of the patients

• Direct Forces = Object Striking or penetrating cranium

• Indirect Forces = Acceleration/Deceleration or

• Parts involved during injuries= Scalp injuries

• The brain is a semi-solid organ that occupies ≈ 80% of the cranial

CPP = CBF = MAP – ICP

• Cerebral autoregulation is a protective mechanism designed to

• Linear Skull Fracture

• Diastatic fracture line:

• Depressed Skull Fracture

– Cortical Brain Contusion

– Diffuse Axonal Injury[ DAI]

• Non-lateralizing neurological deficits

• Generalized edema occurs after injury, typically

Calcium Nitric Oxide

NMDA Disruption of normal cellular processes:

– Systemic or Intracranial processes that contributes

– Hypotension (SBP < 90 mmHg)

– Anemia (↓Oxygen Carrying Capacity)

– Cerebral Edema (Peaks at 24-48 hrs post injury)

– It is a transient brief interruption of neurologic function with or w/o brief

– Four main categories of symptoms predominate by

– Most people recover early from concussion

- Rapid onset of short lived impairment of neurologic function

- The acute clinical symptoms largely represent a functional

- Concussion results in a graded set of clinical syndromes that may or may

Predominantly results from direct mechanical forces that will lead

* In general, S/s depends entirely on how

- Incidence 2 per 100,000

- 12 to 29% in severe TBI

- Common in elders >50 and infants <2yrs

- 30-50% of pts have no hx of HI

• osmotic electrolyte diffusion of CSF into cavity – DISPROVED

• Recurrent hemorrhage – most likely

* Most pts presents with a GCS score of <8

Surgery need for re-operation:

- Early aggressive treatment is required with airway control, resuscitation, admission

– Full, Complete Neurological Exam

Canadian CT Head Rule

• Only 1/3rd of pts with severe TBI needs craniotomy.

Posttraumatic mass volume measurement in TBI patients

 Presence of expanding intracranial hematoma

 Malignant cerebral edema

 Intraparenchymal hemorrhage & Contusion

 Posterior fossa Lesion

You might also like