This document provides an overview of head injury management. It discusses evaluating head injuries in the emergency setting, classifying injuries as primary or secondary, monitoring intracranial pressure, and treating increased intracranial pressure and secondary injuries. Specific management strategies are outlined to prevent secondary brain injury and optimize outcomes for patients with head trauma.

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• Management Of Head Injury
Presenter : Dr.Dawit Mekonnen (gsr3)

2. • Out line
– Introduction
– Emergency evaluation
– General management of head injury
– Specific head injury management
– Summary
– References
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3. • 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
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4. • 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.
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5. • 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.
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• CLASSIFICATION
• Practical categorizations
– Mechanism
– Severity
– Morphology

7. • 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)
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8. • 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.
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9. • 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.
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10. • 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
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13. • 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.
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14. • 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
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• Hypoxia and Hypotension- 'Deadly Combo' in TBI
– "The EPIC project”,2014
– 9194 moderate to severe TBI

17. • 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
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18. • 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) more than
doubles mortality.
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20. • 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.
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Monro-Kellie doctrine

22. • 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 autoregulation).
• May be more significant than edema in raising
ICP
– traumatically induced masses
• A. epidural hematoma
• B. subdural hematoma
• C. intraparenchymal hemorrhage
(hemorrhagic contusion)
• D. foreign body (e.g. bullet)
• E. depressed skull fracture
– Hypoventilation (causing hypercarbia →
vasodilatation)
– Increased muscle tone and valsalva
maneuver as a result of agitation or
posturing
– Sustained posttraumatic seizures (status
epilepticus)
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23. • 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
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25. • CLINICAL MANIFESTATIONS
• Global symptoms of elevated ICP
– Headache
– depressed global consciousness
– vomiting.
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26. • 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.
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27. • 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
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28. • 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.
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29. • 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)
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30. • Types of monitors
• There are four main anatomical sites used in the clinical
measurement of ICP:
– Intraventricular,
– Intraparenchymal,
– Subarachnoid, and
– Epidural
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31. • 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.
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32. • 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
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33. • 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)
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34. • 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).
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35. • MANAGEMENT
– General management
– Specific management
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36. • 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
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37. • “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.
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39. • 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
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40. • 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
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41. 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
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42. • 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
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43. • 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
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44. • 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
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45. • 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.
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46. • 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.
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47. • 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.
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48. • 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
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49. • 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)
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50. • 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)
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51. • 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

52. Technique to convert burr-hole(s) into trauma flap

53. • 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

54. Specific injuries management
• Scalp
• Superficial or deep
• Transverse or sagittal
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55. Skull Fractures
• Linear #
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56. • 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
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57. • 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
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58. • 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
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59. • 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.
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60. • 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)
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• 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

62. • 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
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63. • 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.
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64. • 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
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65. Compression or absence of the BCs carries a threefold risk of increased ICP, and the status of
the BCs correlates with outcome

66. • Contusion(TICH)
– High density areas on CT
– Produce much less mass effect.
– Areas where sudden deceleration
of the head causes the brain to
impact on bony prominences
– Often enlarge and/or coalesce with
time as seen on serial CTs.
– CT scans months later often show
surprisingly normal.
• Indications for surgery:
– progressive neurological
deterioration referable to the TICH
– Volume > 50 cm3
– GCS = 6-8 with
– Frontal/ temporal volume > 20cm3
– midline shift ≥ 5 mm and/or
– compressed basal cisterns on CT
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67. • 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
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68. • 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.
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70. 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.
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71. • 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.
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72. • Treatment Of EDH
– Surgical indications
• Volume >30 cm3
• Thickness > 15 mm
• Midline shift (MLS) >5 mm
• GCS < 8
• focal neurologic deficit
• Low threshold in pediatrics
• Surgical objectives
– To remove the clot
• Wide exposure
– Absolute haemostasis
• Coagulate bleeding soft tissue
• Apply bone wax to diploic bleeders
– Prevent reaccumulation
• Hitch /tack-up suture
• Central tack-up /Poppen’s suture
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73. • 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.
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74. • 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
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75. • Treatement
• Indications for surgery
– ASDH with thickness > 10 mm or
– midline shift (MLS) > 5 mm (on CT)
– ASDH with thickness < 10 mm and MLS < 5
mm should undergo surgical evacuation if:
• GCS drops by ≥ 2 points
• Pupils are asymmetric or fixed and dilated
• ICP is > 20 mm Hg
• The aim of surgery
– To evacuate the haematoma and any
associated underlying lesions.
– A wide decompressive craniotomy.
– With/without duraplasty
– Burr-hole usually unsuccessful
– “Four hour rule”
• Mortality
– 50-90% (mostl from the underlying brain
injury).
– Traditionally thought to be higher in aged
patients (60%).
– 90-100% in patients on anticoagulants.
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• Venous Sinus Injury
– Results in raised ICP.
– Anterior, middle , posterior 1/3
– Transverse sinus dominance.
• Preoperative angiography or
MR angiography

77. • 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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78. • 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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79. • 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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80. • 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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81. • 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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82. – Penetrating missile Injury
• Primary Injury by bullet
– Cavitation
– shock waves
– Coup & Contrecoup Injury
• Secondary Injury
– Cerebral edema
– ICP may rise rapidly within
minutes
• Management
• Initial stabilization
• Goals of surgery
– Debridement of devitalized tissue
– Evacuation of hematomas
– Removal of accessible bone fragments
– Retrieval of bullet fragment for
forensic purposes
• Only accessible fragments shouldbe
sought and removed
• Large intact fragments should be sought
as they tend to migrate
– Obtaining hemostasis
– Watertight dural closure
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83. • 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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84. • 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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85. • 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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86. • 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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87. 12/2/2017 87
Thank you