• Management Of Head Injury

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

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 • Out line
– Introduction
– Emergency evaluation
– General management of head injury
– Specific head injury management
– Summary
– References

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• 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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• 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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• 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

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• 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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• 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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• 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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• 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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• 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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• 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

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• 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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• 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.

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• 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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• Intracranial Hypertension

Monro-Kellie doctrine

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• 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

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• 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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 • CLINICAL MANIFESTATIONS  
• Global symptoms of elevated ICP
– Headache
– depressed global consciousness
– vomiting.

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• 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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• 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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• 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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• 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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• 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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• 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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• 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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• 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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• 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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• MANAGEMENT
– General management
– Specific management

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• 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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• “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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• 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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• 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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 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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• 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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• 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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• 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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• 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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• 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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• 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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• 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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• 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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• 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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• 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

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 Skull Fractures
• Linear #

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• 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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• 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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• 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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• 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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• 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

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• 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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• 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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• 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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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.

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• 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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• 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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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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• 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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• 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
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• 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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• 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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• 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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 • 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
• Primary Injury by bullet
– Cavitation
– shock waves
– Coup & Contrecoup Injury
• Secondary Injury
– Cerebral edema
– ICP may rise rapidly within
minutes
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• 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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• 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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