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Head Injury Management Guidelines

The document outlines guidelines for managing head injuries, including performing an emergency evaluation to assess injuries and monitor vital signs, taking steps to prevent secondary brain injuries like hypoxia and hypotension, and monitoring for signs of increased intracranial pressure like headache, vomiting, and changes in mental status which require interventions to reduce pressure. The presentation provides objectives, classifications of head injuries, and guidelines for general management, specific treatments, and predicting outcomes.

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0% found this document useful (0 votes)
427 views87 pages

Head Injury Management Guidelines

The document outlines guidelines for managing head injuries, including performing an emergency evaluation to assess injuries and monitor vital signs, taking steps to prevent secondary brain injuries like hypoxia and hypotension, and monitoring for signs of increased intracranial pressure like headache, vomiting, and changes in mental status which require interventions to reduce pressure. The presentation provides objectives, classifications of head injuries, and guidelines for general management, specific treatments, and predicting outcomes.

Uploaded by

dhabe
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPTX, PDF, TXT or read online on Scribd
  • Management of Head Injury: Introduction to the session covering the management of head injuries including presentation details.
  • Outline: Provides an overview of key topics discussed such as emergency evaluation and specific management techniques concerning head injuries.
  • Objectives: Details the aims of the presentation including evaluation methods and management of critical brain injury indicators.
  • Introduction to Head Injuries: Describes traumatic brain injury, causes, and potential consequences for young adults.
  • Data and Statistics: Highlights various statistics regarding head injuries, including common causes and patient demographics.
  • Classification of Head Injuries: Outlines classification of head injuries based on mechanism, severity, and morphology.
  • Primary vs Secondary Brain Injuries: Explains the differences between primary and secondary brain injuries, including examples of each type.
  • Secondary Injuries: Discusses secondary injuries occurring alongside primary brain injuries, including examples such as hypoxia.
  • Emergency Evaluation and Examination: Reviews procedures and principles of conducting emergency evaluations and neurological examinations for head injuries.
  • General Management: Comprehensive overview of head injury management, focusing on the primary aspects of life support and observation regimes.
  • Intracranial Hypertension: Examines the causes, symptoms, and clinical significance of intracranial hypertension in patients.
  • Clinical Manifestations of ICP: Identifies the symptoms and clinical signs associated with elevated intracranial pressure.
  • ICP Monitoring: Details the methods and indications for monitoring intracranial pressure in head injury patients.
  • Treatment for Elevated ICP: Provides guidelines for the management of elevated intracranial pressure, including accepted thresholds for treatment.
  • Fluid and Electrolyte Management: Focuses on fluid and electrolyte management strategies for head injury patients.
  • Seizure Management: Reviews seizure management protocols, including details about early and late post-traumatic seizures.
  • Surgical Interventions: Explores surgical procedures and criteria for interventions such as burr holes and managing cranial injuries.
  • Skull Fractures and Treatment: Discuss differential diagnosis of skull fractures and provides guidelines for treatment interventions.
  • Parenchymal Injuries: Discusses injuries to the brain tissue such as concussions and diffuse axonal injuries.
  • Subdural and Epidural Hemorrhages: Explains the characteristics and management strategies for different types of hemorrhages often seen in head trauma.
  • Pediatric Traumatic Brain Injuries: Focuses on the specific features and treatment considerations for head injuries in children.
  • Outcome of Head Injury: Focuses on outcome measures following head injury, including the Glasgow Outcome Scale and factors affecting recovery.
  • Summary and Conclusions: Final thoughts on head injuries, emphasizing the importance of early diagnosis and intervention.
  • References: Lists references and further reading sources for advanced study on head injuries.

• Management Of Head Injury

Presenter : Dhabessa M.
(MD)
Moderator : Dr.Sintayehu
(Consultant Surgeon)

04/10/2020 1
• Out line
– Introduction
– Emergency evaluation
– General management of head injury
– Specific head injury management
– Summary
– References

04/10/2020 2
• Objectives
– How to do emergency evaluation of head injury
– How to manage deadly ICP In Head Injury
– How to prevent secondary brain injury
– Predict outcome in head injury

04/10/2020 3
• Introduction
– Traumatic brain injury (TBI) is a disruption or alteration of brain function
– due to external forces.
• Acceleration or deceleration,
• direct compression,
• penetrating objects,
• combined effects
– Leading cause of death and long term disability, particularly in young adults
– Subtle effects , focal injuries such a fractures, contusion, SDH, EDH, or IPH , or
more widespread damage such as DAI.
– All injuries and symptoms should be taken seriously.
04/10/2020 4
• US data
– 1.4 million per year suffer TBI.
• 1.1 million are treated and released
• 240,000 are hospitalized, and 50,000
die.
– Common causes for TBI are
• falls (28%),
• motor vehicle accidents (20%),
• pedestrian impact (19%), and
• assault (11%).
– TBI has a bimodal age distribution
• greatest risk in 0–4 & 15- to 19yrs.

04/10/2020 5
• CLASSIFICATION
• Practical categorizations
– Mechanism
– Severity
– Morphology

04/10/2020 6
• Primary VS Secondary Brain injuries
– Primary injury occurs at the time of impact
• Direct injury to the brain parenchyma
– Contusion, lacaration
• Injury to the long white-matter tracts through acceleration-deceleration
forces
– Concussion, DAI
• Shearing or laceration of vascular structures
– Intracranial hemorrhage(EDH, SDH)

04/10/2020 7
• Secondary injuries
– Systemic and intracranial events that occur in response to the primary
injury
– Further contribute to neuronal damage and cell death.
– The systemic events
• hypotension, hypoxia, and hypercapnia
– direct result of primary injury to the central nervous system (CNS) or
– as a consequence of associated injuries in a person with multiple traumas.
– Intracranial events
• cerebral edema, increased ICP, hyperemia, and ischemia.

04/10/2020 8
• Emergency evaluation
– The basic principles of trauma resuscitation.
• Rapid assessment and maintenance of an airway (and cervical spine) , breathing,
circulation & disability
• Primary and secondary surveys should evaluate for systemic
injuries
– Neurological Examination
• An accurate neurological examination is essential to determine diagnosis,
treatment strategies, and prognosis in TBI patients.

04/10/2020 9
• Evaluation of the head
– Palpation of the head
• scalp lacerations
– Evaluated for depth, and depressed or open skull fractures.
• The eye examination
– Pupillary size and reactivity
– visual acuity and for hemorrhage within the globe
– perform the eye examination early, because significant orbital swelling
– raccoon eyes
– The tympanic membrane is examined
• hemotympanum, otorrhea, or rupture

04/10/2020 10
04/10/2020 11
04/10/2020 12
• Radiographic Evaluation
– Plain X-Rays
• skull #, c-spine
– Brain CT
• Presence of any moderate or high risk criteria which include:
– GCS ≤ 14
– Focal deficit,
– Amnesia for injury,
– Altered mental status,
– Deteriorating neuro status,
– Seizures
– Signs of basal or calvarial skull fracture
– All elderly patients(>65)
– All patients on antiplatelet agents or anticoagulation
– MRI SCANS IN TRAUMA
• Usually not appropriate for acute head injures.

04/10/2020 13
• General management of head injury
– ABC of life should be followed.
– Concomitant injury should be evaluated
• Admission and observation
– NICE guidelines
• Continuing worrying signs ( persistent vomiting, severe headaches).
• Clinically significant abnormalities on imaging
• GCS <15
• Drug or alcohol intoxication
• Suspected non-accidental injury
• Cerebrospinalfluid leak

04/10/2020 14
04/10/2020 15
• Hypoxia and Hypotension- 'Deadly Combo' in TBI
– "The EPIC project”,2014
– 9194 moderate to severe TBI

04/10/2020 16
• Hypoxia ( PaO2 < 60 mm Hg on ABG)
• Indications for intubation
1. depressed level of consciousness ; GCS≤ 7
2. need for hyperventilation (HPV)
3. severe maxillofacial trauma : patency of airway tenuous or concern for inability to
maintain patency with further tissue swelling and/or bleeding
4. need for pharmacologic paralysis for evaluation or management

04/10/2020 17
• Hypotension (shock) is rarely attributable to head injury except:
– In terminal stages (i.e. with dysfunction of medulla and cardiovascular
collapse)
– In infancy, where enough blood can be lost intracranially or into the subgaleal
space to cause shock
– Where enough blood has been lost from scalp (exsanguination)
• Hypotension (defined as a single SBP < 90 mm Hg) doubles mortality.
• Hypoxia ( PaO2 < 60 mm Hg on ABG) also increases mortality).
• The combination of both triples mortality.

04/10/2020 18
04/10/2020 19
• Autoregulation Impairment in TBI
– The majority of the severe TBI patients experienced impaired AR
within the first 48 hours after the injury
• Myogenic, Neurogenic And Metabolic
– AR response after TBI is highly associated with the severity of primary
and secondary brain damage.
– Brain is highly sensitive during this period to trauma.

04/10/2020 20
• Intracranial Hypertension

Monro-Kellie doctrine

04/10/2020 21
• Traumatic IC-HTN (alone or in various
combinations):
– cerebral edema
– hyperemia: the normal response to head
injury.
• Possibly due to vasomotor paralysis (loss of cerebral – Hypoventilation (causing
autoregulation). hypercarbia → vasodilatation)
• May be more significant than edema in raising ICP
– traumatically induced masses – Increased muscle tone and valsalva
• A. epidural hematoma maneuver as a result of agitation or
• B. subdural hematoma posturing
• C. intraparenchymal hemorrhage (hemorrhagic
contusion) – Sustained posttraumatic seizures
• D. foreign body (e.g. bullet) (status epilepticus)
• E. depressed skull fracture

04/10/2020 22
• Compensation mechanisms
– The craniospinal axis(CSF) can buffer small increases in volume.
• CSF can be displaced from the ventricles and subarachnoid spaces and exit
the intracrania compartment via the FM
– Intravenous blood can displaced via the IJVs as pressure continues to
rise
– Arterial blood is displaced and CPP decreases, eventually producing
diffuse cerebral ischemia.
• Cerebral herniation

04/10/2020 23
04/10/2020 24
• CLINICAL MANIFESTATIONS  
• Global symptoms of elevated ICP
– Headache
– depressed global consciousness
– vomiting.

04/10/2020 25
• Signs include
– CN VI palsies,
– papilledema secondary to impaired axonal transport and congestion,
– triad of bradycardia, respiratory depression, and hypertension
(Cushing's triad).
• Mechanism of Cushing's triad remains controversial,
• many believe that it relates to brainstem compression.
• The presence of this response is an ominous finding that requires urgent
intervention.

04/10/2020 26
• Focal symptoms
– mass lesions or
– herniation syndromes.
• Herniation results when pressure gradients develop between two regions of the cranial
vault.
• The most common anatomical locations affected by herniation syndromes include
– subfalcine,
– central transtentorial,
– uncal transtentorial,
– upward cerebellar,
– cerebellar tonsillar/foramen magnum, and
– transcalvarial

04/10/2020 27
• Diagnostic accuracy of signs and symptoms is limited
• Use of radiologic studies may support the diagnosis
• The most reliable method of diagnosing elevated ICP is to
measure it directly.

04/10/2020 28
• ICP MONITORING  
– Empiric therapy for presumed elevated ICP is unsatisfactory
• because CPP cannot be monitored reliably without measurement of ICP.
• Indications For ICP Monitoring
• For Salvageable Patients With Severe Traumatic Brain Injury
– With An Abnormal Admitting Brain CT
– With A Normal Admitting Brain CT, But With ≥ 2 Of The Risk Factors For IC-HTN.
• Age > 40 Yrs
• SBP < 90 Mm Hg
• Decerebrate Or Decorticate Posturing On Motor Exam (Unilateral Or Bilateral)

04/10/2020 29
• Types of monitors  
• There are four main anatomical sites used in the clinical
measurement of ICP:
– Intraventricular,
– Intraparenchymal,
– Subarachnoid, and
– Epidural

04/10/2020 30
• Duration Of Monitoring
• D/C monitor when ICP normal x 48-72 hrs after withdrawal of ICP
therapy.
• Caution:
• IC-HTN may have delayed onset
• often starts on day 2-3, and
• day 9-11 is a common second peak especially in peds.
• Avoid a false sense of security imparted by abnormal early ICP.

04/10/2020 31
• Complications Of Icp Monitors
– 1. infection
– 2. hemorrhage: overall incidence is 1.4% for all devices
• Risk of significant hematoma requiring surgical evacuation is ≈ 0.5–2.5%
– 3. malfunction or obstruction: with fluid coupled devices, higher rates of
obstruction occur at ICPs > 50 mm Hg
– 4. malposition: 3% of IVCs require operative repositioning

04/10/2020 32
• Adjuncts to ICP monitoring
• Jugular Venous Oxygen Monitoring
• jugular venous oxygen saturation (SjVO2)
• jugular vein oxygen content (CVO2)
• Arterial-jugular venous oxygen content difference
• Brain Tissue Oxygen Tension Monitoring (Pbto2)

04/10/2020 33
• Treatment measures for elevated ICP
• Intracranial pressure treatment thresholds
• The optimal ICP at which to begin treatment is not known.
Generally accepted level: ICP ≥ 20-25 mm Hg
– treatment for IC-HTN should be initiated for ICP > 20 mm Hg
– the need for treatment should be based on ICP in combination with
clinical examination & brain CT findings
• Caution: patients can herniate even at ICP < 20 (depends on
location of intracranial mass).
04/10/2020 34
• MANAGEMENT
– General management
– Specific management

04/10/2020 35
• Indications for mannitol in Emergency:
– 1. evidence of intracranial hypertension
– 2. evidence of mass effect (focal deficit, e.g. hemiparesis)
– 3. sudden deterioration prior to CT (including pupillary dilatation)
– 4. after CT, if a lesion that is associated with increased ICP is identified
– 5. after CT, if going to O.R.
– 6. to assess “salvageability”: in patient with no evidence of brainstem function,
look for return of brainstem reflexes
• If IC-HTN persists , give strong consideration to cranial CT to rule out a
surgical condition
04/10/2020 36
• “Second tier” therapy for persistent IC-HTN
– High dose barbiturate therapy
– Hyperventilate to PaCO2 = 25-30 mm Hg.
– Hypothermia
– Decompressive craniectomy
• Controversial (may enhance cerebral edema formation).
• Removal of large areas of contused hemorrhagic brain
– No more than 4-5 cm on dominant side, 6-7 cm on non-dominant or frontal lobectomy.
• Early decompressive craniectomy in emergent surgery (fracture, EDH, SDH)
• Flap must be at least 12 cm in diameter, and duraplasty is mandatory.

04/10/2020 37
04/10/2020 38
• Fluid and electrolytes
– The aim of fluid therapy should be to maintain euvolaemia.
– Full maintenance
– Isotonic fluid usually 0.9% normal saline
– Given at 35 mL/kg per day.
– Avoid hypotension

04/10/2020 39
• Consider fluid and electrolytes disturbances
– SIADH, CSWS,DI
• SIADH-excess ADH from posterior pituitary
-hyponatremia with volume retention
-treat with volume restriction
• CSWS- excess brain natriuretic factor
-failure to retain sodium and water with dehydration
-treated with sodium and water replacement
resolves spontaneously (2-4wks)
• Central DI-hypernatremia

04/10/2020 40
Nutrition in the head-injured patient
• Full caloric replacement should be attained by post-trauma day 7
• Enterally or parenterally:
• non-paralyzed patients: 140% BEE
• paralyzed patients: 100% of predicted BEE
• provide ≥ 15% of calories as protein
• Nutritional replacement should begin within 72 hrs of head injury

04/10/2020 41
• The enteral route is preferred.
– Isotonic solutions should be used at full strength starting at 30 ml/hr.
– Check gastric residuals q 4 hrs and hold feedings if residuals exceed ≈
125 ml in an adult.
– Increase the rate by ≈ 15-25 ml/hr every 12-24 hrs as tolerated until
the desired rate is achieved

04/10/2020 42
• Hyperglycemia
– Hyperglycemia has been associated with poor neurological outcome.
– Exacerbates secondary injury processes.
• Tight glucose control
– blood glucose levels of less than 110-120 mg/dl
– by using continuous insulin infusions
v/s
• Conventional glucose control group
– insulin was not given unless serum glucose levels exceeded 200 mg/dl

04/10/2020 43
• Fever
– Fever increases the body’s metabolic rate by approximately 10%
to 13% per °C.
– Fever is common during recovery from a head injury.
• Potent cerebral vasodilator and can raise ICP.
• Raise cerebral metabolic requirements.
– Infectious causes of fever should be investigated with appropriate
cultures and treated with antibiotics

04/10/2020 44
• Seizure
– Immediate, i.e. w ithin minutes to an hour.
– Early :≤ 7 days after head trauma.
– Late :>7days
• Early PTS
– 30% incidence in severe head injury
– ≈ 1% in mild to moderate injuries.
– Occurs in 2.6% of children < 15 yrs age.
– Precipitate adverse events as a result of
– elevation of ICP,
– alterations in BP,
– changes in oxygenation, and
– excess neurotransmitter release.

04/10/2020 45
• Late onset PTS (> 7 days after head trauma)
– Estimated incidence 10–13% within 2 yrs after significant head
trauma.
• 3.6 times control population.
– Incidence in severe head injury > > moderate > mild.
– Late seizures less frequent in children.

04/10/2020 46
• Option of treatement:
– Begin AEDs within 24 hrs of injury in the presence of any of the high risk
criteria.
• Levetiracetam , phenytoin or carbamazepine or phenobarbital
– Phenytoin: load with 18 mg/kg; Maintenance: 5mg/kg
– Switch to phenobarbital if PHT not tolerated.
• 10-20 mg/kg loading dose
• then 3-5 mg/kg/d divided bid/tid
– Levetiracetam
• 500 mg bid IV or PO
• advance to 1000 mg bid.

04/10/2020 47
• Discontinuation of AEDs
– Taper AEDs after 1 week of therapy except in the following:
• penetrating brain injury
• development of late PTS (i.e. a seizure > 7 days following head trauma).
• prior seizure history
– For patients not meeting the criteria to discontinue AEDs after 1
week:
• maintain ≈ 6–12 month of therapeutic AED level

04/10/2020 48
• Exploratory burr holes
• INDICATIONS
• Clinical criteria
– Neurologically stable patient undergoes witnessed deterioration
– Indicators of transtentorial herniation/brainstem compression:
• Sudden drop in Glasgow Coma Scale (GCS) score
• One pupil fixes and dilates
• Paralysis or decerebration (usually contralateral to blown pupil)

04/10/2020 49
• Choice of side for initial burr hole
• Start with a temporal burr hole on the side:
– ipsilateral to a blown pupil.
• This will be on the correct side in > 85% of epidurals and other extra-axial mass
lesions
– if both pupils are dilated, use the side of the first dilating pupil (if known)
– if pupils are equal, or it is not known which side dilated first, place on side
of obvious external trauma
– if no localizing clues, place hole on left side (to evaluate and decompress
the dominant hemisphere)

04/10/2020 50
• Approach
• Burr holes are placed along a path that can be connected to form a “trauma
flap”.
• First outline the trauma flap with a skin marker:
– 1. start at the zygomatic arch < 1 cm anterior to the tragus
• spares the branch of the facial nerve to the frontalis muscle and the anterior branch of the
superficial temporal artery
– 2. proceed superiorly and then curve posteriorly at the level of top of the pinna
– 3. 4-6 cm behind the pinna it is taken superiorly
– 4. 1-2 cm ipsilateral to the midline (sagittal suture) curve anteriorly to end behind the
hairline
Technique to convert burr-hole(s) into trauma flap
• Burr hole locations
• First (temporal) burr-hole: over middle cranial fossa just superior
to the zygomatic arch.
• If no epidural hematoma, the dura is opened if it has bluish
discoloration (suggests subdural hematoma) or if there is a
strong suspicion of a mass lesion on that side
• If completely negative, usually perform temporal burr hole on
contralateral side
• Proceed to ipsilateral frontal burr hole
• Subsequent burr holes may be placed at parietal region and
lastly in posterior fossa
Specific injuries management

• Scalp
• Superficial or deep
• Transverse or sagittal

04/10/2020 54
Skull Fractures
• Linear #

04/10/2020 55
• Depressed skull fractures
– Closed (simple fracture) or open (compound fracture).
• Indications for surgery
– Open fractures
• Fractures depressed > thickness of calvaria
• Evidence (clinical or CT) of dural penetration.
• Significant intracranial hematoma
• Depression is > 1 cm
• Frontal sinus involvement
• wound infection or gross contamination
• gross cosmetic deformity
– Closed (simple) depressed fractures
• may be managed surgically or non-surgically
– More conservative treatment is recommended for fractures overlying a major dural venous sinus

04/10/2020 56
• Timing of surgery
– Early surgery to reduce risk of infection
– Antibiotics should be used for all compound depressed fractures
• Surgical goals
– Debridement of skin edges
– Elevation of bone fragments
– Repair of dural laceration
– Debridement of devitalized brain
– Reconstruction of the skull
– Skin closure
04/10/2020 57
• Basal skull fractures
– Most are extensions of fractures through the
cranial vault.
– Most commonly through the temporal bone and
at high risk for EDH.
• DIAGNOSIS
– Clinical diagnosis
• CSF otorrhea or rhinorrhea
• hemotympanum or laceration of external auditory canal
• postauricular ecchymoses (Battle’s sign)
• periorbital ecchymoses (raccoon’s eyes)
• cranial nerve injury:
– VII and/or VIII: temporal bone fracture
– Cr. N. I injury: anterior fossa BSF
– VI injury: fractures through the clivus

04/10/2020 58
• Radiographic diagnosis
– CT scan is often poor for directly
demonstrating BSF.
• Sensitivity of CT diagnosis can be
increased by the use of bone windows
together with thin cuts (≤ 5 mm) and
coronal images.
– Plain skull x-rays and clinical
criteria are usually more sensitive.

04/10/2020 59
• TREATMENT
– The majority of CSF leaks resolve spontaneously within one week of injury and
without CNS complications.
– NG tubes: Caution
– Prophylactic antibiotics: The routine use of prophylactic antibiotics is
controversial.
• The risk of meningitis has been estimated at 3 percent in the first week.
• The incidence of meningitis rises substantially if the leak persists past 7 days
• Most ENT physicians recommend
• Antibiotic selection is identical to that for penetrating head trauma.
– Surgery – CSF fistula, cerebral abscess, facial N palsy (immediate/ delayed)
04/10/2020 60
• FRONTAL SINUS FRACTURES
– 5-15% of facial fractures.
• The risks of posterior wall fractures:
– brain abscess
– CSF leak with risk of meningitis
– Cyst or mucocele formation

04/10/2020 61
• Indications for surgery
– Anterior and posterior wall #.
– Linear fractures of the anterior wall
• Treated expectantly.
– Technique
• Incorporation of the laceration
• Bicoronal skin incision or a butterfly
incision.
• Options
– Obliteration(fat, muscle, bone or
hydroxyapatite).
– Cranization & exentration

04/10/2020 62
• PARENCHYMAL INJURIES
– Diffuse Cerebral Injuries
– Concussion
• Alteration of consciousness resulting from
nonpenetrating injury to the brain.
• Classic symptoms include headache, confusion,
amnesia, and sometimes
LOC.
• Other symptoms
– motor function (incoordination, stumbling),
– speech (slowed, slurred, incoherent),
– memory or processing (amnesia, difficulty
concentrating)
– orientation (vacant stare, unable to orient )
– presence of irritability.

04/10/2020 63
• Diffuse Axonal Injury
– Axonal stretch injury
– Cerebral cortex and deep brain structures moving at different relative
speeds.
– Mild and transient to permanent neuronal damage.
– 50% of all primary intra-axial TBI lesions
– 80–100% of autopsy patients in fatal injuries.
50-80% are microscopic and nonhemorrhagic
– 20-50% Hemorrhagic DAI, the most severe form, is visible on CT/MRI.
– Number of lesions & depth from the cortex to corpus callosum to brainstem

04/10/2020 64
Compression or absence of the BCs carries a threefold risk of increased ICP, and the status of
the BCs correlates with outcome
• Contusion(TICH)
• Indications for surgery:
– High density areas on CT
– progressive neurological
– Produce much less mass effect.
deterioration referable to the TICH
– Areas where sudden deceleration
– Volume > 50 cm3
of the head causes the brain to
– GCS = 6-8 with
impact on bony prominences
– Often enlarge and/or coalesce with – Frontal/ temporal volume > 20cm3
time as seen on serial CTs. – midline shift ≥ 5 mm and/or
– CT scans months later often show – compressed basal cisterns on CT
surprisingly normal.

04/10/2020 66
• Epidural hematoma
– 1-2% of head trauma admissions,15 % of fatal cases.
– Usually occurs in young adults,
– rare before age 2 yrs or after age 60
– 85% arterial bleeding.
– 15% bleeding from vein or dural sinus.
– Temporoparietal regions (73%)
– Anterior cranial fossa(11%)
– parasagittal regions(9%)
– posterior fossa(7%)
– Bruising of the overlying scalp is usually a reliable guide

04/10/2020 67
• One third have other signifcant brain injuries
• “Textbook” presentation (20%):
• brief posttraumatic loss of consciousness
• followed by a “lucid interval” for several hours
• then, obtundation, contralateral hemiparesis, ipsilateral pupillary dilatation
– 60% have a dilated pupil, 85% of which are ipsilateral.
– No initial loss of consciousness occurs in 60%.
– No lucid interval in 20%.
– Kernohan’s phenomenon is a false localizing sign.

04/10/2020 68
04/10/2020 69
Evaluation
– Plain skull x-rays
• Fracture is seen in 60%.
– CT scan
• High density biconvex (lenticular) shape.
• May cross the falx but not skull sutures.
• Swirl sign
• Mortality
– Overall: 20-55%.
– Optimal diagnosis and treatment :5-10%
mortality
– Death is mostly due to respiratory arrest
from uncal herniation.

04/10/2020 70
• Hematoma volume estimation  
– formula ABC/2, which approximates the volume of an ellipsoid.
– using the centimeter scale on the CT
– A is the greatest hemorrhage diameter on the CT slice with the largest area of
hemorrhage
– B is the largest diameter 90 degrees to A on the same CT slice
– C is the approximate number of CT slices with hemorrhage multiplied by the slice
thickness in centimeters
• full slice : area is >75 percent of the area on the slice with the largest hemorrhage.
• One-half : 25 to 75 percent of the area on the largest hemorrhage slice.
• The slice is not counted if <25 percent of the largest hemorrhage slice.

04/10/2020 71
• Treatment Of EDH • Surgical objectives
– Surgical indications – To remove the clot
• Volume >30 cm3 • Wide exposure
• Thickness > 15 mm – Absolute haemostasis
• Midline shift (MLS) >5 mm • Coagulate bleeding soft tissue
• GCS < 8 • Apply bone wax to diploic bleeders
• focal neurologic deficit – Prevent reaccumulation
• Low threshold in pediatrics • Hitch /tack-up suture
• Central tack-up /Poppen’s suture

04/10/2020 72
• Acute subdural hematoma
– The magnitude of impact damage is higher than EDH & more lethal.
– Associated underlying brain injury.
– Two common causes
• Accumulation around parenchymal laceration
• Surface or bridging vessel
– Clinical presentation is non-specific
– Mass effect
– Parenchymatous injury
• 40-50% of patients are unconscious at the time of their primary
injury
• Remain comatose for prolonged periods.

04/10/2020 73
• Imaging Features
• On CT scans(ASDH)
– Crescentric, hyperdense collection
– Cross sutural lines, but not cross
falx or the tentorium.
‒ Edema is often present.
‒ Usually over convexity

04/10/2020 74
• The aim of surgery
• Treatement – To evacuate the haematoma and any associated
underlying lesions.
• Indications for surgery – A wide decompressive craniotomy.
– ASDH with thickness > 10 mm or – With/without duraplasty
– midline shift (MLS) > 5 mm (on CT) – Burr-hole usually unsuccessful
– “Four hour rule”
– ASDH with thickness < 10 mm and
• Mortality
MLS < 5 mm should undergo – 50-90% (mostl from the underlying brain injury).
surgical evacuation if: – Traditionally thought to be higher in aged patients
• GCS drops by ≥ 2 points (60%).
• Pupils are asymmetric or fixed and – 90-100% in patients on anticoagulants.
dilated
• ICP is > 20 mm Hg

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• Venous Sinus Injury
– Results in raised ICP.
– Anterior, middle , posterior 1/3
– Transverse sinus dominance.
• Preoperative angiography or
MR angiography

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• Operative Technique
– potentially severe hemorrhage
• At least 2 to 4 units of packed cells
– head is elevated above the level of the
heart
• bleeding & air embolism are minimized
– Prevent venous obstruction in the neck
• Avoid extremes of flexion and rotation of
the head on the shoulders
– Sufficient bone is removed around the
margins of the sinus
• proximal and distal control of the sinus

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• Pediatric Traumatic Brain Injuries
• Children commonly sustain injury to the head’
– Susceptible to fall
– Less agile in escaping a dangerous situation
– Child’s head relative to the body is much larger(thrust forward or fall
headfirst )
– May be physically abused

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• The neuroplasticity : young children have significant advantages for
functional recovery.
• Increased water content in the child’s brain and continued process
of myelination
• The consumption rate of oxygen in children is twice that of adults.
• Greater compliance of the skull
– More kinetic energy can be transmitted directly to the brain
during trauma.
• Infants often show the worst developmental outcome after severe TBI
• Older children, have a higher incidence of post-traumatic epilepsy

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• Cerebral contusion and subdural hematomas are common injuries.
• EDHs are relatively more common in young children
• Children are less susceptible to mass lesions than adults
• More frequently develop diffuse cerebral hyperemia or diffuse edema
– Because of this propensity for diffuse hyperemia, mannitol is used with caution in
young children.
• Small infants may bleed sufficiently into the head to develop hemorrhagic
shock

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• Penetrating head injury
– Penetrating Nonmissile Injury
• lower-velocity objects (knives, arrows, lawn darts, ice pick)
• Embedded objects , and protruding, stabilize the object during transport.
• CT to localize the precise location of the foreign body or injury.
• Angiography :territory of any major vessels/sinuses.
• All radiographic evaluation performed with the foreign body still embedded.
• Removal should only proceed in the OR
• Open the dura before removing the object
• Removal of the object ideally should follow the entry trajectory if possible
• Broad-spectrum antibiotics should be administered

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– Penetrating missile Injury • Management
• Primary Injury by bullet • Initial stabilization
– Cavitation • Goals of surgery
– Debridement of devitalized tissue
– shock waves – Evacuation of hematomas
– Coup & Contrecoup Injury – Removal of accessible bone fragments
• Secondary Injury – Retrieval of bullet fragment for forensic
purposes
– Cerebral edema • Only accessible fragments shouldbe sought and
– ICP may rise rapidly within removed
• Large intact fragments should be sought as they tend
minutes to migrate
– Obtaining hemostasis
– Watertight dural closure

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• OUTCOME Of Head Injury
• The Glasgow Outcome Scale
– is a widely used outcome grading
• The patient’s ultimate
neurological outcome
– May not be fully evident until
weeks or months of treatment
• At hospitals, rehabilitation centers, and
at home.

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• Variables strongly influencing outcome:
– Mechanism of injury:
– the worst outcome was with motorcycle accidents
– unhelmeted patients
– age: > 65 yrs age, with 82% mortality and 5%
functional
– admission Glasgow Coma Scale
– Delayed Surgery >4-6hrs
– Persistent ICP 20 mm Hg
– Postoperative ICP
• Only the time to surgery and
postoperative ICP can be directly
influenced by the treating neurosurgeon.

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• Summary
– Head injury remain leading cause of mortality and morbidty
– Early diagnosis and management of brain pathology in trauma is of
paramount important

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• References
– Greenberg Handbook of Neurosurgery, 8th
– Kenneth L. Mattox TRAUMA 7th
– Youman’s Neurological Surgery’ 6th
– Ramamurthi and Tandon’s Textbook of Neurosurgery,3rd
– Principles of neurological surgery ,3rd
– Bailey & Love’s Short Practice Of Surgery, 26th
– Schwartz’s Principles of Surgery Tenth Edition

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Thank you
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