MANAGEMENT OF TRAUMATIC HEAD INJURY AND ICP

1. Management of Adult
Head Trauma &
Intracranial Hypertension

2. Head Trauma Statistics
 50-60% of patients with Glasgow Coma Scale≤8
have 1 or more other organ system injured
 25% of these patients have “surgical” lesions
 ~15% of patients with head trauma who do not
initially exhibit signs of significant brain injury
may deteriorate in a delayed fashion (75% of
these will be intracranial hematomas)

3. Classification of Head Injury
 Mechanism: blunt (high or low velocity) or penetrating
 Morphology
 Skull fractures
 Intracranial lesions
 Focal lesions: hematoma
 Diffuse: Concussion, DAI
 Severity
 Mild
 Moderate
 Severe

4. Glasgow Coma Scale
Points Best Motor Best Verbal* Best Eye
6 Obeys
5 Localizes Oriented
4 Withdraws Confused Spontaneous
3 Flexor Inappropriate To Speech
2 Extensor Incomprehensible To Pain
1 None None None
*there is also a T modifier for intubated patients

5. Initial Assessment

6. Initial Assessment
 ABCs!
 Physical Exam
 Immobilization of spine, hard cervical collar
 Stat labs, including urine/blood tox screens
 Determine home medications
 Head CT. Consider imaging C-spine as well
 4-5% incidence of associated spine fractures with
significant head injury (mostly C1-C3)

7.  GCS, best motor exam in all 4 extremities
 Brain stem reflexes: pupils, corneals, cough, gag
 No oculocephalic reflex (Doll’s eyes) in hard
collar
 Scalp lacs, look for evidence of basilar skull
fracture (raccoon’s eyes, Battle’s sign-
postauricular ecchymosis, CSF
rhinorrhea/otorrhea, hemotympanum)
Initial Assessment

9. Initial Assessment
 ATLS trauma evaluation (ABC’s, fluid
resuscitation, labs eval)
 Rapid neurologic exam (pupils, corneals, cough
gag, motor,reflexes,rectal tone), adjusting your
exam based on level of consciousness.
 Look for signs of basilar skull fxs (raccoon eyes,
battles sign, CSF otorrhea, rhinorrhea)
 Spine precautions at all times
 Signs of herniation or worsening level of
consciousness indicate increasing ICP
 Stat CT of brain and secondary survey for
concomitant injuries

10. Initial Assessment
 Auscultate over carotids (carotid
dissection), over globe (traumatic carotid-
cavernous fistula)
 Palpate spine for step-offs, tenderness
 Check rectal tone, lower extremity
reflexes, bulbocavernosus reflex (tug foley
or squeeze glans to check for sphincter
contraction)

11. Initial Measures
 Load Dilantin 20mg/kg, then 100mg IV Q8
 Antibiotics for open fractures, CSF leak:
Vancomycin 1gm, Rocephin 2gm
 For rapid deterioration or signs of
herniation: hyperventilation, Mannitol
1gm/kg IV if euvolemic
 Rapid CT brain without contrast

12. Intracranial Injury Risk Stratification
 Low Risk:
 Asymptomatic
 Headache
 Dizziness
 Scalp hematoma
 Laceration
 Contusion
 Abrasion
 No higher risk criteria
 No LOC

13. Low Risk Injuries
 CT or skull plain films NOT indicated
 Discharge to home, observe

14. Intracranial Injury Risk Stratification
 Moderate Risk:
 Change/loss of consciousness
 Progressive headache
 EtOH/drug intoxication
 Posttraumatic seizure
 Unreliable history
 Age <2yr (unless trivial)
 Vomiting
 Posttraumatic amnesia
 Signs of basilar skull fracture
 Multiple trauma
 Serious facial trauma
 Possible skull penetration or depressed fracture
 Suspected child abuse
 Significant subgaleal swelling

15. Moderate Risk Head Injury
 Non-contrasted head CT
 Can observe at home if:
Normal CT, initial GCS≥14, no moderate
criteria except LOC, now neuro intact, has
supervision,remains close to ED
 Otherwise, admit for observation

16. Intracranial Injury Risk Stratification
 High Risk:
Decreased level of consciousness not clearly
due to EtOH, drugs, metabolic abnormalities,
postictal, etc.
Focal neurological findings
Decreasing level of consciousness
Penetrating skull injury or depressed fracture

17. High Risk Head Injury
 CT scan
 Admit
 Consider OR, possible emergency burr
holes, possible ICP monitoring

18. Head Injury with GCS 9-13
 10% of head injured patients
 Somnolent, confused, focal deficit, does
follow commands
 10-20% deteriorate, 8% need surgery

19. Severe Head Injury, GCS 3-8
 Hypotension single SBP<90 and hypoxia PaO2 < 60 increase
morbidity and mortality several fold
 Initially focus on cardiopulmonary stabilization
 Early intubation
 Fluid resuscitation with 2L NS
 SBP>100 and no signs of increased ICP on exam, use sedation
for transport and get head CT with trauma CTs
 SBP>100 and dilated pupil or hemiparesis, ventilate to PaCO2
30-35mmHg, mannitol 1gm/kg IVP, and stat head CT
 SBP does not respond to fluids, DPL or abd U/S and ex lap if
necessary.
 ICP monitor

20. Intracranial Pressure
 60% of patients with closed head injury
and abnormal CT will have intracranial
hypertension
 13% of head injury patients with a normal
CT scan will have intracranial
hypertension

21. ICP Management
 Prevention of secondary injury to brain
becomes the primary goal of therapy
following the treatment of any surgical
lesions
 Cerebral Blood Flow 50cc/100g/min
 CPP = MAP – ICP
 Monro-Kellie doctrine

22. Changes in ICP with Space
Occupying Lesions
A space occupying lesion causes the ICP to increase more rapidly with any
further increase in size of the space occupying lesion, shifting the curve
upwards and making it steeper.

23. Alteration of Autoregulation in
Head Injury
Cerebral Blood Flow = Cerebral Perfusion Pressure / Cerebrovascular Resistance
B: When ICP increases, a higher CPP is needed to overcome the ICP and keep the
same CBF. This shifts the curve to the right
C: Impaired autoregulation with head injury causes passive increases in CBF with
increases in CPP

24. ICP Waves
 Normal: large peak from arterial systolic
pressure followed by small dicrotic notch, then
smaller and less distinct peaks, then peak
corresponding to central venous A wave from
right atrium.
 ICP changes with respiration. Expiration
increases pressure in SVC, reduces venous
outflow so elevates ICP
 Opposite when mechanically ventilated

25. ICP Waves
 Lundberg A (plateau waves)
 ICP >50 mm Hg for 5-20 minutes, accompanied by
simultaneous increase in MAP

26. ICP Waves
 Lundberg B
 Lower amplitude, 10-
20mm Hg, variation
with types of
breathing, last 30 sec -
2 minutes
 Lundberg C
 4-8 /minute, transmission of Hering-Traube-Wave,
related to variations in vasomotor tone

27. The Anatomy of
Tentorial Herniation

28. Herniation Syndromes
 Increasing ICP does not distribute evenly across normal and damaged brain.
Therefore a pressure gradient forms which lead to herniation.
 In an infant, check the fontanelle to directly feel intracranial pressure
 Subfalcine herniation: A unilateral expanding mass forces midline structures across
the falx. The ACA can become occluded, leading to bilateral leg weakness.
 Uncal herniation: A mass in the middle cranial fossa causes the medial portion of
the hippocampal gyrus between the free edge of the tentorium and midbrain. This
causes CNIII palsy, hemiparesis from the Cerebral peduncle getting compressed,
and hemianopsia from occlusion of the PCA.
 Tectal herniation: the presence of bihemispheric lesions causes bilateral posterior
herniation of temporal lobes. This causes bilateral ptosis and loss of upward gaze.
 Central herniation: Depression of consciousness, decerebrate rigidity, irregular
respiration, hypertension, apnea
 Tonsillar herniation: Sudden apnea

29. ICP Normal Values
 Infant <7.5 mm Hg
 Child <10 mm Hg
 Adult <15 mm Hg

30. Indications for ICP Monitoring
 Any pt with GCS < 8 and abnormal CT
 GCS < 8 with normal CT scan if age >45,
motor posturing, or SBP < 90
 Treat ICP > 20-25 mmHg to maintain CPP
> 70 mmHg

31. Treatment of ICP
 Preemptive Measures
HOB at 30 degrees
PaCO2 35-40 mmHg
Euvolemia
Seizure prophylaxis
Sedation, paralytics
CPP > 70
Prevent clot expansion with FFP, Novo VII,
Vitamin K, Platelets as appropriate

32. Treatment of ICP
 CSF drainage from ventric. + hyperventilate to PaCO2
30-35 mmHg
 Mannitol 0.5-1 gm/kg to Ser Osm <320, Hypertonic
saline
 Consider cooling the patient
 If present, remove surgical lesion, or consider
hemicraniectomy
 Barbiturate coma with pentobarb
 10mg/kg/30 mins
 3 mg/kg q 1h x 3
 1 mg/kg/hr

33. Intracranial Injury Types
 Epidural Hematoma
 Subdural Hematoma
 Acute
 Chronic
 Intraparenchymal Hematoma
 Subarachnoid Hemorrhage
 Skull Fractures
 Penetrating Injuries
 Diffuse Injury

34. Epidural Hematoma
 Result from blunt trauma
 Biconvex, respects suture lines, arterial (often middle
meningeal), classically lucid interval
 30-90% have an associated linear fx
 70-90% occur in temporal area
 Less common in the elderly
 50% of pts become unconscious from initial concussion
 Compression of underlying brain, swelling, increased
ICP cause rapid deterioration  herniation symptoms

35. EDH Management
 Surgical drainage
 Coagulate the source. Most commonly middle meningeal artery.
May have to expose f. spinosum.
 Look for SDH if dura appears tense or blue.
 Obliterate epidural space to minimize recurrence.
 May observe with serial neuro exam if
 Minimal neuro deficits GCS >8 without focal deficits and
improving exam
 Minimal midline shift <5mm and patent basal cisterns
 EDH < 15mm (smaller cutoff for peds)
 <30 cubic centimeters

36. EDH
 Delayed EDH
 May occur from lowering ICP, rapid correction of
shock, coagulopathies, or underlying known fractures
 Many pts show delayed neurologic deterioration
 Posterior fossa EDH
 Most common in <20 yrs old.
 May be due to dural sinus tears
 Mortality 26%

37. Epidural Hematoma Outcomes
 Rapid treatment is key to survival
GCS>8 90-100% survival
GCS<8 30-70% survival
 Pupillary Exam
ERRL 80-100%
Asymmetric 55-100%
Both fixed 100% mortality

38. Acute SDH
 Highest morbidity and mortality of head injuries
30-90%. Only 20-30% have functional recovery.
 Caused by loading stresses from high rates of
acceleration and deceleration.
 High M&M secondary to associated brain injury.
Profound and sustained drop in CBF under
injury, with evidence of ischemic brain injury in
animal models.
 Anticoagulation therapy increases risk 7 - 26 fold

39. Acute SDH
 CT shows crescentic high attenuation
mass next to inner table
 Usually a high degree of edema in
underlying brain
 Usually venous
 Respects falx

40. Acute SDH

41. Acute SDH
 Surgical drainage
 SDH > 1cm or MLS > 5mm
 GCS <8, SDH 5mm – 1cm, if:
 declining loc (decreased GCS by 2 or more points from time of injury to arrival at
hospital), or
 Pupil asymmetry or fixed and dilated pupils, or
 ICP >20mm Hg, or
 if located in middle fossa with mass effect
 Large frontotemporoparietal craniotomy
 Consider resection of pulped cortex
 May observe with serial neuro exam if
 Minimal neuro deficits GCS 14-15 or GCS 9-13 without focal deficits and
improving exam
 Minimal midline shift <5mm and patent basal cisterns
 SDH < 10mm

42. Acute SDH Outcomes
 Time to surgery
4 hour rule: 30% mortality if operated within 4
hours of injury, 90% if >4 hours, but not quite
this clear
 Controversial, studies flawed, some have shown a
statistically insignificant trend
Outcome definitely worse if > 12 hrs delay

43. Acute SDH Outcomes
 GCS GCS Mortality Functional
Survival
3 90 5
4 76 10
5 62 18
6&7 51 44

44. Chronic SDH
 Hematomas at least 2 weeks old. SDH occurs,
a vascularized membrane forms around clot
which can rehemorrhage with trivial trauma.
 Mostly in elderly >65 yo. Present with
symptoms of increasing ICP, TIA like symptoms,
dementia, or increasing seizures.
 <50% h/o trauma. Increased in alcoholism,
VPS, seizure disorders.

45. Chronic SDH CT Appearance
 Appears hypodense to the brain
 Loculations often present

46. SDHs

47. Chronic SDH treatment
 Surgery if > 1cm or if symptomatic.
 Twist drill
 Easy, can be done under local at bedside.
 Incision over maximal thickness, 45% angle of drill, pass catheter
and tunnel.
 Slow drainage x 1 hr, then drain at – 15cm.
 5-14% failure rate. No other complications reported.
 New option of bedside bolt drain available
 Burr holes
 5% failure rate.
 Tension pneumocephalus <16%, hemorrhage 1-5%, SD empyema
1%, increased seizure frequency
 Craniotomy

48. Chronic SDH Post op care
 Flat bedrest x 24-48hrs
 Elevate HOB slowly after drain out
 Maintain euvolemia
 Maximize nutrition
 Maintain therapeutic anticonvulsant levels for at
least one week
 Have high index of suspicion for ICH, acute
SDH, or tension pneumocephalus

49. Intracerebral Hematoma
 Occurs in 15% of fatal head injuries
 Indicates severe parenchymal injury
 Due to biomechanics of brain these mainly occur in
temporal or frontal lobe white matter
 Commonly associated with DAI, contusions and SDH
 Delayed hematomas occur from 6h to 30 days following
injury and can effect up to 7.4% of all HI patients. May
be due to posttraumatic fragility of blood vessels
 Mortality up to 40%

50. Intracerebral Hematoma
 Debate about resection
 Size, location, associated lesions, and response
to medical management of ICP
 IH >2cm can be removed
 IH < 2cm with effacement basal cisterns, >5mm MLS
in frontal pole or temporal tip can be removed
 Expectant treatment of IH in eloquent cortex, or if <
5mm MLS and stable exam.
 Do not operate on basal ganglia or internal capsule
hematomas

51. Intracerebral Hematoma
 Good functional outcome in up to 25% of
patients who survive, regardless of
management

52. Bifrontal
hemorrhagic contusion

53. Evolution of Hemorrhagic
Contusion Over 8Hr

54. Subarachnoid Hemorrhage
 Trauma most common cause
Consider angiogram or CT angiography if
trauma history unclear

55. Skull Fractures
 3/4 in frontal and parietal regions, 10% temporal, 5%
occipital
 Compound fractures have overlying scalp laceration or
involve the posterior wall of paranasal sinuses. These
have higher incidence of dural tears.
 Focal neurologic deficits are due to the initial brain injury
and will not improve with elevation
 Closed linear fractures usually heal themselves
 Caused by deformation distant from impact

56. Skull Fractures Treatment
 Surgical repair indicated for:
Open depressed fractures greater than
thickness of skull
Underlying area of brain compressed with
deteriorating function
CSF leakage
Cosmesis

57. Skull Fractures Treatment
 Consider nonoperative management if:
 Closed fracture
 No clinical or radiographic evidence of dural
penetration, no pneumocephalus
 No significant intracranial hematoma
 No depression >1cm
 No frontal sinus involvement
 No gross cosmetic deformity
 No concern for wound infection or gross
contamination

58. Skull Fractures
 Seizures
 ~20% of pts will develop epilepsy
 a dural tear, >24hrs amnesia, early seizure (<1wk) increases risk for
delayed epilepsy
 6 mos anticonvulsant use recommended by some authors
 Infection
 Post traumatic meningitis 2-13%
 Risk of infection minimal if closed within 4-8 hours
 If closure delayed 5-7 days of Abx recommended
 Gram positive and gram negative coverage with CSF penetration
required

59. Skull Fractures Surgical
Considerations
 Fractures anterior to hairline can be reached with bicoronal incision to
avoid forehead scar
 S shaped incision overlying fractures behind hairline will allow adequate
closure after elevation
 Devitalized scalp should be debrided and bone should be thoroughly
washed
 If bone appears infected, craniectomy with delayed closure or use of a
plate should be considered. If not, option available to reconstruct with
bone fragments
 Fractures overlying dural sinuses should be managed conservatively if
possible. Be prepared for massive blood loss, temporary sinus
occlusion, and sinus patch graft repair.

60. Skull Base Fractures
 Comprise 19-21% of all skull fractures
 Heralded by CSF rhinorrhea or otorrhea, hemotympanum, Battle’s sign,
Raccoon eyes
 Usually nonsurgical, but treatment indicated for repair of persistent CSF
leakage or CN palsy
 Facial nerve palsy with t-bone fractures
 Longitudinal fx are most common, parallel to EAC, and disrupt the
ossicles causing conductive deafness
 Transverse fx are perpendicular to EAC, associated with immediate CN
V, VI, VII, or VIII palsy in 50% of cases
 All CN VII palsy treated initially with steroids
 Surgical decompression indicated if VII palsy immediate and no
improvement with steroids, or if delayed CN VII palsy shows
deterioration on serial electoneuronography

61. Temporal Bone Fractures
Longitudinal Transverse

62. Gunshot Wounds to Head
 Three mechanisms of injury: penetration,
cavitation, shockwave
 Low velocity bullets (<250 m/s) injure by path of
bullet, injury path slightly wider than bullet itself
 High velocity bullets (750 m/s) path of injury
many fold greater than bullet, damage due to
shock waves and cavitation-cone of injury
causes low pressure region that can draw
surface debris into wound

63. Gunshot Wounds to the Head
 Poor prognosis: 73% die at scene, 12% die
during 1st 3 hrs in hospital, and 7% die after
protracted course = 92% mortality
 Surgery generally not helpful
 Goals would be to debride, evacuate hematoma,
remove only accessible bullet fragments, obtain
hemostasis, close dura
 Poor prognosis if bullet crosses midline, passes
through center of brain, traverses the ventricles,
and worse with the more lobes it enters

64. Diffuse Injuries
 As mechanical forces increase, brain
acceleration causes more shear, tensile, and
compression strains
 Mild physiological disruption of cortical activity
causes concussion. Temporary global
disruption of cortical activity occurs.
 Axonal injury and tissue tears take place,
causing prolonged coma.

65. Diffuse Injuries
 DAI
Severe shearing forces cause axonal
disruption
Axon bulbs form in lobar white matter at gray
white junction, CC, and upper brainstem
Initial CT usually normal, however, petechial
hemorrhage may be seen