Traumatic Brain Injury

1. CASE - 2
DR.SHRADDHA TOSHNIWAL

2. CASE SCENARIO – 2A
24 year old male was brought by EMS with H/O
closed head injury while driving a car and had
high velocity impact on a tree besides the road.
EMS personnel gave history of a co passenger
thrown out of vehicle and didn’t survived.
• O/E- neurologic status GCS-7/15
• Pupils equal reacting to light
• HR-110/min, BP.-86/60 mmHg.
• fracture shaft femur.
• No instability, crepitations at chest and pelvis.
• How will you proceed in this case?

3. STEP 1- INITIAL ASSESMENT
ABC takes precedence in spite of the obvious
head injury.
1. Airway and Breathing :
• Apply the cervical collar and check airway
• Hypoxia (PaO2 < 60 mmhg or O2 sat <90 %)
should be avoided.Intubate and ventilate the
patient with 100 % oxygen in case of threatened
airway with manual in-line cervical
immobilisation.
• Mild Hyperventilation ( PaCO2 >_32 mmhg and
<_ 36 mmhg) is recommended as a temporiszing
measure for reduction of raised ICP.

4. • Prophylactic Hyperventilation is not
recommended.(PaCO2 <25 mmhg)
2. Circulation :
• Maintain systolic BP > 100 mmhg.
• Avoid antihypertensives in head injury
patients, because hypertension is a part of
Cushing’s reflex to maintain cerebral
perfusion.
• If at all we need to treat hypertension,
Labetalol is a drug of choice.

5. STEP 2- SECONDARY ASSESSMENT
• Assess Glassgow coma score and pupillary
reaction, and check localising signs (weakness
in limbs).
• All patients with GCS of 8 or less should be
intubated and electively ventilated(if not done
at step 1).

6. STEP-3 ASSESS SEVERITY OF HEAD
INJURY
GCS Grading :
GCS of 14-15:Mild head injury
GCS of 9-13:Moderate head injury
GCS of 8 or less:Severe head injury

7. Level Of Consciousness
• Glasgow Coma Scale
Eye Opening Best Verbal Best Motor
Spontaneous 4 Oriented 5 Obeys Command
6
To Voice 3 Confused 4 Localizes 5
To Pain 2 Inappropriate 3 Withdraws 4
None 1 Incomprehensible 2 Flexion 3
None 1 Extension 2
None 1

9. • Mild Head Injury :
STEPS MANAGEMENT
STEP A Shift to observational area
STEP B Maintain Airway, Breathing and
Circulation
STEP C Send for a NCCT of head and cervical
spine(if any neck pain or tenderness) in
the following conditions: Loss of
conciousness for >5 mins, Amnesia,
Severe headcahe,,GCS <15,FND
STEP D Inform the Neurosurgeon

10. • Moderate Head Injury :
STEPS MANAGEMENT
STEP A Shift to observational area
STEP B Maintain Airway, Breathing and
Circulation
STEP C Inform the Neurosurgeon
STEP D Send for the plain CT scan of the head
cervical spine ( including C 7 Vertebra)

11. • Severe Head Injury :
STEPS MANAGEMENT
STEP A Shift to resuscitation room
Simultaneously inform the
neurosurgeon
STEP B Maintain Airway, Breathing and
Circulation
Maintain temperature
STEP C -Send baseline investigations
-Caogulation profile and platelet count
TEG if available (plt function)
-Arrange PCV and FFP
-ABG (repeat after 1 hr)

12. • Severe Head Injury :
STEPS MANAGEMENT
STEP C Contineud……….
-Foley’s catheterization
-IV Fluid Maintainance-avoid dextrose
-Proton Pump Inhibitors
-Antiepileptics
-Mannitol (after BP correction)
-Diuretics (after BP correction)
STEP D FAST ( any other site of free blood loss)
STEP E NCCT Brain and Cervical spine after
stabilisation.

13. Clinical Features In Head Trauma
• Scalp Injuries
• Skull Fractures
• Depressed Skull Fractures
• Basilar Skull Fractures
• Vascular Injuries
• Penetrating Head Injury
• Intracranial Hemorrhage
– Epidural Hematoma
– Subdural Hematoma
– Subarachnoid Hemorrhage
– Intracerebral Hemorrhage

14. Scalp Injuries
• Most are laceration
– Simple Linear/ Stellate  ED Rx
– Extensive, Degloving/Avulsion  Repair GA
– Overlying Depressed Skull#, Infections 
Repair+ Elevation Of #
– Hematomas
Subgaleal Cephalohematomas
Galeal Apo & Periost Periost & Skull
Cross Suture Lines Limited By S.Lines
Hypotension & Anemia(bp,hct) Calcify And Disfiguring Sx

15. Skull Fractures
• Thin skull #’s common place.
• Risk of # associated intracranial injuries?
• CT to R/o
1. Open
2. Closed
3. Linear (3/4)
4. Comminuted ( multiple branches)
5. Diastatic ( edges split apart)<3yrleptomeningeal
cyst, cephalomalacia,
6. Depressed
7. Basilar

16. Epidural Hematomas (EDH)
• Peak incidence in 2nd decade
• Source  meningeal vessel, Dural venous
sinus, diploic vein from skull #
• H/o minor head injury Viz fall
• C/f  wrt size, location, rate of accumulation
– Lucid interval (33%), non specific
– Confusion, lethargy, agitation, focal neurological
deficits.

17. Diagnosis
• CT is diagnostic
• Initial Ct Hyperdense Lentiform collection
beneath skull
• Actively bleeding- Mixed densities
• Severe anemia- isodense/hypodense
• Untreated EDH imaging over days
Hyperdense Isodense Hypodense w.r.t.
brain

19. Treatment
Non surgical Surgical
Minimal / no symptoms
Should be located outside of Temporal or
Post fossae
Should be < 40 ml in volume
Should not be associated with intradural
lesions
Should be discovered 6 or more hours
after the injury

20. Subdural Hematoma
• Common in infants.
• Cause  high velocity impact/ assault/ child
abuse/ fall from significant height.
• Associated with cerebral contusions + DAI
• Source  cortical bridging veins/ Dural
venous sinuses.
Adults Child/infants
Cerebral convexities over frontal/
temporal regions
Occipital + Parietal cortex
Parafalcine ( post falx cerebri),
supratentorial
{ abuse}

21. 50% are unconscious
immediately.
Focal deficits common
Hemiparesis – 50%
Pupillary abnormality- 28-78%
Seizures – 6-22%
Rx- larger- urgent removal
Small -
Small with mass effect/
significant change in
conscious/ focal deficits
Removed
Small with significant brain
injuries + mass effect out of
proportion to size of clot
Non operative approach

22. SDH’s are High density
collections on CT
conforming to convex
surface of brain
Cant cross falx cerebri/
tentorium cerebelli {
compartmentalized}
Can cross beneath suture
lines
Distorstion of cortical
surface/ effacement of
ipsilateral ventricle/ shift
of midline often noted.

23. SAH
• Trauma is leading cause.
• Acute from disruption of
perforating vessels around
circle of Willis in basal
cistern
• Delayed from ruptured
pseudo aneurysm.
• Rx maintain intravascular
vol to prevent ischemia
from vasospasm.
• Mortality 39% { national
traumatic coma databank}

24. Intracerebral
Bleed
• CT- hyperdense/mixed
• MRI- small petechial bleed+
DAI
• Rx- small- non operative.
Resolve in 2-3 weeks
• Large- Sx drainage.
• Repeat CT in small bleeds
after 12-24 hr is warranted
to r/o coalescence to form
large hematoma.
Rare in Peds.
60% from small contusions
coalesce to form larger
hematoma.
Rarely , violent angular
acceleration bleed in deep
white matter, basal ganglia,
thalamus
Transtentorial Herniation 
midbrain bleed ( Duret
hemorrhages)
Common sites
Ant Temporal and Inf Frontal
lobes { impact against lateral
sphenoid bone/ floor of ant
fossa}

25. Penetrating
Head Injury
• CT- localizes bullet and
bone fragments
• MRI- non advised till
magnetic properties of
bullet known.
• Rx. Surgical
– Debridement of entry
and exit wounds
– Remove accessible bullet
and bone
– Control hemorrhage
– Repair Dural lacerations
+ closure of wounds.
– NO ATTEMPT TO
REMOVE BULLET OR
BONE BEYOND ENTRY
AND EXIT WOUNDS.
Infants and children fall on sharp objects with thin
skull and open foraminae could predispose for these
injuries.
R/o child abuse
Rx Surgical.
Entry wound debrided and FB removed with in driven
bone fragments.
Peri and post op ABX
Prophylactic anticonvulsants
Adolescents and children  Gun Shot Wounds. (
12%) and increasing annually.
Higher mortality when
1.Low GCS on presentation (3-4)
2.B/L hemispheric /brainstem injury/ intraventricular
tracking
3.Hemodynamic instability/ apnea/both
4.Uncontrolled ICP.

26. STEP 5 - ICP MONITORING
Indications for ICP Monitoring :
1.GCS <8 and abnormal CT scan
2.Abnormal CT scan of head that reveals
hematomas, contusions ,or herniation
3.Severe TBI with a normal CT scan if two or
more of the following : Age>40,u/l or b/l motor
posturing, SBP<90 mmhg.
4.All children (<12 yrs) irrespective of CT or GCS

27. Intracranial Hypertension
• Pathophysiology
– ICP monitoring and control are the cornerstones of TBI
management
– Normal ICP
• Adults  <10mmhg
• Children  3-7mmhg
• Infants 1.5- 6mmhg
– When to treat?
• Adults  > 20
• Children  >15
• Infants >10 { Arbitrary numbers most commonly used,
pending outcome studies}

29. Device / method Risk / benefit
1. Intraventricular catheter Adv- drainage of CSF to reduce ICP
DisAdv- infection/ ventricular compression
leads to inaccuracy
2. subdural/ subarachnoid bolts
( Philadelphia, Leeds, Richmond bolts)
Occlusion of port in device leads to
inaccuracy
3. Fiberoptic cath ( Camino labs) Improved fidelity & longevity
Can be placed Intraparenchymal/
intraventricular/ subdural
Used to drain CSF
Accuracy maintained even with fully
collapsed ventricles
Single cath can be used as long as needed

30. Non invasive ICP measurement
Ultrasonographic tech Pediatr Crit Care Med 2010 Vol. 11, No. 5
Audiological tech- displacement of TM
and perilymphatic pressure as a correlate
of ICP
Infrared light- thickness of CSF from
reflected light as a correlate of ICP
Arterial BP wave contours and blood flow
velocity – mathematical model
Changes In optical nerve head with
optical coherent tomography
IOP as correlate of ICP With ICP cutoff of 20mmhg it has
Specificity of 0.7 and sensitivity of 0.97

33. Mangement of ICP
• Goal  to maintain CPP by
– Reducing ICP, and/or
– Increasing MAP { hyper/normo volumia preffered
as opposed old school Hypovol}
Brief periods of hypotension can double the
mortality rates
CPP should be match with cerebral metabolic
demand to avoid hypoperfusion / hypeeperfusion.

34. Hyperdynamic therapy
• To maintain CPP of about >70, by increasing MAP
• { CPP= MAP-ICP}
• IVF- crystalloid/colloid
• PRBC if low HCT(<30%)
• Pressors as needed ( Dopa, Dobu,Phenylephri)
• if autoregulation is intact? incres CPP
vasoconstriction constant CBFless volume
reduction in ICP.
• Systemic Hypo ? Vice versa

36. Increasing CPP by reducing ICP
Sedation and pain control Fentanyl/ midazolam drip
Etomidate in initial phase
Quiet envir + min extern stimuli
Pharmacological paralysis if needed Increase in Pneumonia+ sepsis
IV/ ET lidocaine ( ET > IV) During intubation, before ET suctioning,ET
manipulation
Elevation of head end by 20-30deg Red venous press ICP
Can cause orthostatic changesfall
CPP rebound ICP rise
Excessive PEEP, tight cervical collar, neck
flexion/ rotation
Can rise ICP
Bladder distention  rise Contin drainage
Occult seizures unexplained rise Prophylactic Anticonvulsants
Fever  rise Rx + hypothermia.

37. Specific measures to reduce ICP
Hyperventilation Rapid & effective response.
Red Paco2/incr pH vasoconstricton
Red CBF
Disadvantages
1.paco2 < 30 torr red CBF to ischemic
level
2.Regional variation in autoreg 
hyperventilation induced reverse vascular
steal
Current recommendations
1. routine hypervent ( 35 ) not be used in
first 24 hrs
2.Chronic hypervent be avoided in
absence of documented ICP rise
3.Reserved for deterioration not
responding to other measures.
4.When needed with caution, PaCo2
never <30 torr.
5.svJo2 can be used as indicator of
extreme ischemia( CBF fall)
6.If used, withdrawn slowly to avoid
rebound rise

38. • CSF drainage- effective and safe.
• Provides gradient for bulk flow of edema fluid
from parenchyma of brain to ventricles.
• Continous – 5-10 torr gradient
• Intermittent for 1-5 min when needed.

39. CASE SCENARIO – 2 B
• He required intubation for airway
protection and invasive ventilation for 5
days. It was however difficult to wean
him and XRC showed a consolidation in
the right lower zone.
• He was on Cefotaxime, Gentamicin &
Flagyl and on RT feeds.
• What is your differential diagnosis?

40. Diuretics
Mannitol – works as osmotic diuretic 
extract extra and intra cellular edema
fluid from brain
Disadv- may preferentially affect normal
areas ( intact BBB) vs affected zones (
disrupted BBB)
Additional mech reduces blood
viscocity ( by hemodilution) and improves
Rheology Increas CBF vasocons
decreas volume red ICP.
3 dosing methods
• intermittant boluses when ICP 15-20
•Intermittant Q6 hrly
•Continous infusion
Risks
1. Repeated dose reduced osmotic
gradient
2. Hyperosmolar state ( serum osm>320
mOsm) renal failure,
rhabdomyolysis, hemolysis

41. • Steroids – No role currently in TBI
• Barbiturates- usually last resort med.
Pros Cons
Reduce ICP , CBF, CMRO2
Inhibit free lipid
peroxidation reduce cellular
damage
Close ICU monitoring
Hypotension
Hyponatremia
Myocardial depression

42.  In this patient with prolonged ventilation,
most likely differential diagnosis is VAP.
 Ventilator Associated Pneumonia – is defined
as development of new infiltrate in the chest X
ray along with fever and leukocytosis after 48
hrs of intubation, it is s/o ventilator associated
pneumonia.
 Occurs in 9-27%of intubated patients.
 Risk increases with duration of mechanical
ventilation.

43. • OTHER DD’S ARE:
1. Atelectasis- Common in post operative
period,due to hypoventilation.
2. Aspiration – Rt LL commonly involved. Bile
coloured ET secretion on suctioning,??
Chemical pneumonitis.
3. Pulmonary Embolism
4. Pulmonary Hemorrhage- Blood stained ET
secretions
5. ARDS
6. Fluid overload
7. Drug Reactions

44. CLINICAL PULMONARY INFECTION
SCORE

45. SEND CULTURES AND START EMPIRIC
ANTIBIOTICS
• Always send Blood and ET secretions for gram
stain and C/S before starting empiric antibiotic
therapy.
• But if there is any logistic delay of more than 1
hour before sending cultures,don’t delay for
starting antibiotics.
• Initial Choice of antibiotics is very important, an
inappropriate initial choice increases mortality.

46. Selection of Empiric Antibiotic is
Based On
• Patient Risk Factors
• Early and Late onset VAP
• Recent Antibiotic Exposure to specific classes
• Local epidemiology and Antibiogram
• Previous Antibiotic Therapy
• Cover common organisms responsible for
pneumonia, depending upon epidemiology and
sensitivity
• Cover ESBL in at risk patients
• Use parenteral antibiotics in adequate dose and
frequency.

49. Early Onset VAP

50. Late onset VAP

52. CASE SCENARIO -2C
• Treated with antibiotics.
• VAP cleared.
• Weaned of ventilator.
• GCS remained 7/15.
• Discuss long term management of
neurologically impaired .

53. • Patient is weaned off ventilator, But
neurological status is same.
• In this case, we have to evaluate for need for
tracheostomy depending upon the cough
reflex.
• As patient is neurologically compromised,
airway protection is needed or not, to prevent
aspiration.
• Need for Assisted feeding to considered-PEG
insertion.

54. Guidelines for the Management of
Severe Traumatic Brain Injury
4th Edition
September 2016

55. Decompressive Craniectomy
• Level I: There was insufficient evidence to support a
Level I recommendation for this topic.
• Level II A: Bifrontal DC is not recommended to improve
outcomes as measured by the Glasgow Outcome
Scale–Extended (GOS-E) score at 6 months post-injury
in severe TBI patients with diffuse injury (without mass
lesions), and with ICP elevation to values >20 mm Hg
for more than 15 minutes within a 1-hour period that
are refractory to first-tier therapies. However, this
procedure has been demonstrated to reduce ICP and to
minimize days in the intensive care unit (ICU).

56. • A large frontotemporoparietal DC (not less
than 12 x 15 cm or 15 cm diameter) is
recommended over a small
frontotemporoparietal DC for reduced
mortality and improved neurologic outcomes
in patients with severe TBI.

57. Prophylactic Hypothermia
• Level I and II A : There was insufficient
evidence to support a Level I or II A
recommendation for this topic.
• Level II B : Early (within 2.5 hours), short-term
(48 hours post-injury) prophylactic
hypothermia is not recommended to improve
outcomes in patients with diffuse injury

58. Hyperosmolar Therapy
• Level I, II, and III: Although hyperosmolar
therapy may lower intracranial pressure, there
was insufficient evidence about effects on
clinical outcomes to support a specific
recommendation, or to support use of any
specific hyperosmolar agent, for patients with
severe traumatic brain injury.

59. Cerebrospinal Fluid Drainage
• Level I and II: There was insufficient evidence
to support a Level I or II recommendation for
this topic.
• Level III: An EVD system zeroed at the
midbrain with continuous drainage of CSF may
be considered to lower ICP burden more
effectively than intermittent use. • Use of CSF
drainage to lower ICP in patients with an
initial Glasgow Coma Scale (GCS)

60. Ventilation Therapies
• Level I and II A : There was insufficient
evidence to support a Level I or II A
recommendation for this topic.
• Level II B: Prolonged prophylactic
hyperventilation with partial pressure of
carbon dioxide in arterial blood (PaCO2) of 25
mm Hg or less is not recommended.

61. Anesthetics, Analgesics, and Sedatives
• Level I and II A: There was insufficient
evidence to support a Level I or Level IIA
recommendation for this topic.

62. Level II B:
• Administration of barbiturates to induce burst suppression
measured by EEG as prophylaxis against the development
of intracranial hypertension is not recommended.
• High-dose barbiturate administration is recommended to
control elevated ICP refractory to maximum standard
medical and surgical treatment.
• Hemodynamic stability is essential before and during
barbiturate therapy.
• Although propofol is recommended for the control of ICP, it
is not recommended for improvement in mortality or 6-
month outcomes. Caution is required as high-dose propofol
can produce significant morbidity.

63. Steroids
• Level I: The use of steroids is not
recommended for improving outcome or
reducing ICP. In patients with severe TBI, high-
dose methylprednisolone was associated with
increased mortality and is contraindicated

64. Nutrition
• Level I: There was insufficient evidence to
support a Level I recommendation for this topic
• Level II A: Feeding patients to attain basal caloric
replacement at least by the fifth day and, at most,
by the seventh day post-injury is recommended
to decrease mortality.
• Level II B: Transgastric jejunal feeding is
recommended to reduce the incidence of
ventilatorassociated pneumonia.

65. Infection Prophylaxis
• Level I: There was insufficient evidence to support a
Level I recommendation for this topic.
• Level II A: Early tracheostomy is recommended to
reduce mechanical ventilation days when the overall
benefit is felt to outweigh the complications associated
with such a procedure. However, there is no evidence
that early tracheostomy reduces mortality or the rate
of nosocomial pneumonia.
• The use of povidone-iodine (PI) oral care is not
recommended to reduce ventilatorassociated
pneumonia and may cause an increased risk of acute
respiratory distress syndrome.

66. • Level III : Antimicrobial-impregnated catheters
may be considered to prevent catheter-related
infections during EVD.

67. Deep Vein Thrombosis Prophylaxis
• Level I and II: There was insufficient evidence
to support a Level I or II recommendation for
treatment of deep vein thrombosis (DVT) in
severe TBI patients.
• Level III: Low molecular weight heparin
(LMWH) or low-dose unfractioned heparin
may be used in combination with mechanical
prophylaxis. However, there is an increased
risk for expansion of intracranial hemorrhage.

68. Seizure Prophylaxis
• Level I: There was insufficient evidence to support a Level I
recommendation for this topic.
• Level II A: Prophylactic use of phenytoin or valproate is not
recommended for preventing late PTS. • Phenytoin is
recommended to decrease the incidence of early PTS
(within 7 days of injury), when the overall benefit is felt to
outweigh the complications associated with such
treatment. However, early PTS have not been associated
with worse outcomes.
• At the present time there is insufficient evidence to
recommend levetiracetam over phenytoin regarding
efficacy in preventing early post-traumatic seizures and
toxicity.

69. Monitoring
three types of monitoring:
• intracranial pressure (ICP),
• cerebral perfusion pressure monitoring (CPP),
and
• advanced cerebral monitoring (ACM).

70. Intracranial Pressure Monitoring
• Level I and II A: There was insufficient
evidence to support a Level I or II A
recommendation for this topic.
• Level II B: Management of severe TBI patients
using information from ICP monitoring is
recommended to reduce in-hospital and 2-
week post-injury mortality.

71. Cerebral Perfusion Pressure
Monitoring
• Level I: There was insufficient evidence to
support a Level I recommendation for this
topic.
• Level II B: Management of severe TBI patients
using guidelines-based recommendations for
CPP monitoring is recommended to decrease
2-week mortality.

72. Advanced Cerebral Monitoring
Advanced cerebral monitoring techniques for blood
flow and oxygen include:
• transcranial Doppler (TCD)/duplex sonography,
• differences between arterial and arterio-jugular
venous oxygen (AVDO2), and
• measurements of local tissue oxygen.
Arterio-jugular AVDO2 globally measures cerebral
oxygen extraction.

73. • Level I and II: There was insufficient evidence
to support a Level I or II recommendation for
this topic.
(Although patients with desaturations identified
with advanced cerebral monitoring have
poorer outcomes, Level II evidence showed no
improvement in outcomes for monitored
patients.)

74. • Level III: Jugular bulb monitoring of
arteriovenous oxygen content difference
(AVDO2), as a source of information for
management decisions, may be considered to
reduce mortality and improve outcomes at 3
and 6 months post-injury

75. Thresholds
• blood pressure (BP),
• intracranial pressure (ICP),
• cerebral perfusion pressure monitoring (CPP),
and
• advanced cerebral monitoring (ACM)

76. Blood Pressure Thresholds
• Level I and II: There was insufficient evidence
to support a Level I or II recommendation for
this topic.
• Level III: Maintaining SBP at ≥100 mm Hg for
patients 50 to 69 years old or at ≥110 mm Hg
or above for patients 15 to 49 or over 70 years
old may be considered to decrease mortality
and improve outcomes

77. Intracranial Pressure Thresholds
• Level I and II A: There was insufficient
evidence to support a Level I or II A
recommendation for this topic.
• Level II B: Treating ICP above 22 mm Hg is
recommended because values above this level
are associated with increased mortality

78. • Level III: A combination of ICP values and
clinical and brain CT findings may be used to
make management decisions.

79. Cerebral Perfusion Pressure
Thresholds
• Level I and II A: There was insufficient evidence to
support a Level I or II A recommendation for this topic.
• Level II B: The recommended target cerebral perfusion
pressure (CPP) value for survival and favorable
outcomes is between 60 and 70 mm Hg. Whether 60 or
70 mm Hg is theminimum optimal CPP threshold is
unclear and may depend upon the patient’s
autoregulatory status.
• Level III: Avoiding aggressive attempts to maintain CPP
above 70 mm Hg with fluids and pressors may be
considered because of the risk of adult respiratory
failure

80. Advanced Cerebral Monitoring
Thresholds
• Level I and II: There was insufficient evidence
to support Level I or II recommendation for
this topic.
• Level III: Jugular venous saturation of less
than 50% may be a threshold to avoid in order
to reduce mortality and improve outcomes.

81. THANK YOU