A synopsis on Head injury and management

1. Traumatic Brain Injury
Dr. Abimanyu Sakthivelu MD
Assistant Professor
Department of Accident, Emergency & Critical care.
Vinayaka Mission University
Salem, Tamil nadu, India

2. Cerebral Hemodynamics
Brain
Blood
Artery Arteriole Capillary
The blood-brain
barrier (BBB)
maintains the
microenvironment
of the brain tissue
Introduction

3. Movement across BBB regulates
extracellular ion and
neurotransmitter concentrations
Prolonged disruption of the BBB
contributes to the development of
post-traumatic vasogenic cerebral
edema

4. The brain has an extremely high
metabolic rate
Uses up to 20% of oxygen volume
consumed by the body
The brain requires approximately
15% of the total cardiac output
Optimal regional CBF is maintained
by altering cerebral vessel diameter
in response to changing physiologic
conditions

5. Cerebral
Blood
vessel
Cerebral
vasoconstricti
on
Cerebral
vasodilatio
n
Hypertension
Alkalosis
Hypocarbia
Hypotension
Acidosis
Hypercarbia
Hypoxia
Ischemia
Increased
ICP

6. Cerebral Perfusion Pressure
 The cerebral perfusion pressure (CPP) is the pressure gradient
required to perfuse the cerebral tissue
 CPP is calculated as the difference between the mean arterial
pressure (MAP) and the intracranial pressure (ICP):
MAP – ICP = CPP
MAP = DBP + [(SBP – DBP)/3]
 The local adjustment of cerebral blood flow within the brain
microcirculation is termed autoregulation.

7. Cerebral autoregulation
 Cerebral autoregulation is a homeostatic mechanism that
minimizes deviations in cerebral blood flow (CBF) when
cerebral perfusion pressure (CPP) changes.
 CBF is 50 to 55 ml per 100g of brain tissue per minute
CBF is maintained at constant levels
MAP of 60 to 150 mm Hg
CPP of 50 to 160 mm Hg

9. Biomechanics of Head Trauma

10. Direct impactCompression
Energy
applied
Cranium absorbs
Shock waves
Travel distant to the site of impact or
compression
Distort and disrupt intracranial
contents
Alter regional
ICP

11. Prolonged application
Ability of the skull to absorb the force is
overwhelmed
Multiple linear skull fractures
High-energy rapid
compression force to a small
area of the skull.
Depressed fractures
Compressio
n

12. Cranial contents are set into vigorous
motion
Bridging subdural vessels are
strained
Indirect brain
injury
DAI/Concussio
n
SDH
Differential acceleration –
one brain region slides past
another
Shear and strain injuries results in diffuse
injuries
Abrupt arrest of intracranial
contents
Contrecoup
contusions

13. Primary brain injury
 It is mechanical irreversible damage that occurs at the time of
head trauma and includes brain lacerations, hemorrhages,
contusions, and tissue avulsions
Secondary brain injury
 It results from intracellular and extracellular derangements
that are probably initiated at the time of trauma by a massive
depolarization of brain cells and subsequent ionic shifts

14.  Hyperpyrexia (core body temperature >38.5 °C) – The
mechanism involves stimulation of metabolism in injured
areas of the brain, thus recruiting blood flow with a resultant
increase in ICP
 Anemia (hematocrit <30%) – reduces the oxygen-carrying
capacity of the blood, thus reducing the amount of necessary
substrate delivered to the injured brain tissue.
Secondary Systemic Insults

15. Secondary Systemic Insults
 Hypoxia (Po2 less than 60 mm Hg) – cerebral vessels dilate to
ensure adequate oxygen delivery to brain tissue
Brainstem compression or injury – transient or prolonged
apnea
Partial airway obstruction
Chest wall injury interfering with expansion
Pulmonary injury reducing effective oxygenation
Ineffective airway management,
The overall mortality from
severe head injury may
double or quadruple

16. Secondary Systemic Insults
 Hypercarbia
 Hyperthermia
 Coagulopathy
 Seizures

17. Pathophysiology

18. Increased Intracranial Pressure
 It is defined as CSF pressure greater than 15 mm Hg (or
195 mm H2O) and is a frequent consequence of severe head
injury.
 ICP represents a balance of the pressures exerted by the
contents of the cranial cavity.
 This relationship is explained by the Monro-Kellie doctrine

19. Monro-Kellie doctrine
Total intra cranial volume remains constant as the cranial
vault is a rigid non expansile container

20. Hayreh SS, Br J Ophthalmol, 1964;48:522–43.
FUNDOSCOPY
** CT BRAIN
Clinical signs
*ONSD or invasive monitoring

21. Traumatic mass lesion or edema
increases ICP
CSF displaced from cranial vault to
spinal canal
Compromise of compensatory mechanism
Accommodat
es volume of
50 to 100 ml
Vasodilation, CSF obstruction, or small areas of focal
edema
Compromise of CPP, vasoparalysis & Loss of
autoregulation
Offsets increased blood or brain
volume
Brain tissue compression compensates the
increase in ICP

22. The CBF directly depends on systemic
MAP
Loss of autoregulation cause massive cerebral
vasodilation
Systemic pressure is transmitted to the
capillaries
Outpouring of fluids into the extravascular
space
Vasogenic edema further increase
ICP
ICP rises to the level of the systemic
arterial pressure, CBF ceases and
brain death occurs

23. Cerebral edema
 Cerebral edema is an increase in brain volume caused by an
absolute increase in cerebral tissue water content.
On computed tomography scans
Bilateral compression of the
ventricles
Loss of definition of the cortical
sulci
Effacement of the basal cisterns
Vasogenic edema arises from
transvascular leakage caused by
mechanical failure of the tight
endothelial junctions of the BBB
Cytotoxic edema is an intracellular
process resulting from membrane
pump failure when CBF ≤ 40% of
baseline

24. Cushing's Reflex

25. Cerebral Herniation

26. New Orleans and Canadian CT Clinical Decision Rules
New Orleans Criteria—GCS 15* Canadian CT Head Rule—GCS 13–15*
Headache GCS <15 at 2 h
Vomiting Suspected open or depressed skull
fracture
Age >60 y Any sign of basal skull fracture
Intoxication More than one episode of vomiting
Persistent antegrade amnesia Retrograde amnesia >30 min
Evidence of trauma above the clavicles Dangerous mechanism (fall >3 ft or struck
as pedestrian)
Seizure Age 65 y
Identification of patients who have an intracranial lesion on CT
100% sensitive, 5% specific 83% sensitive, 38% specific
Identification of patients who will need neurosurgical intervention
100% sensitive, 5% specific 100% sensitive, 37% specific
*Presence of any one finding indicates need for CT scan.
Limitations: Not applicable for children and patients on anticoagulation

27. Classification Of Head injury
Morphology
Severity
Mechanism

28. Mechanism
Blunt Penetrating
High Velocity Low velocity Gun shot
Automobile
collision
Falls & assault
Stab wounds
Severity
Moderate - GCS 9-13Mild - GCS 14-15 Severe - GCS 3-8
Morphology
Skull fractures
Vault Basilar
Linear/stellate
Depressed/non
depressed
Open/closed
±CSF leak
±7th -nerve palsy
Intracranial lesions
Epi Dural Hematoma
Sub Dural
Hematoma
Intra Cerebral
Hematoma
Focal Diffuse
Concussion
Multiple contusion
Hypoxic/ischemic
injury

29. Pre-Hospital Care

30. Airway
Airway interventions to prevent
hypoxia
Unsuccessful attempts at field
intubations delays IN – HOSPITAL CARE
and increase the risk for aspiration or
hypoxia
Unintentional hyperventilation of
intubated patients

31. Outcome of Out – Of – Hospital
Endotracheal intubations in TBI

32. Prehospital hyperventilation

33. Circulation
Compression of the brainstem and
medulla have profound effects on
the cardiovascular system - cardiac
dysrhythmia
Establishing intravenous (IV)
access
Cardiac monitor during transport
Scalp lacerations should be secured
with less bulky dressing and firm
constant manual pressure should be
applied to avoid excessive blood
loss

34. Neurologic assessment
Should focus on
GCS
Pupillary responsiveness and
size
Level of consciousness
Motor strength and symmetry
Determine the subsequent effectiveness
of treatment

35. Need for sedation
Agitated patients
Exacerbate physical injury
Cause an increase in ICP
Interfere with appropriate
stabilization and management
Lorazepam
Diazepam
Midazolam
Haloperidol
Droperidol
Tripardol

36. Emergency Department
management

37. Management Of Mild Head Injury
(GCS14 -15)
History
General Examination to exclude systemic injuries
Limited Neurologic Examination
C-spine and other X-rays as indicated
Blood alcohol level and urine toxicology screening
CT scan is indicated if criteria for high or moderate risk of
neurosurgical intervention are present
Observe or admit to hospital Discharge from hospital

38. Observe or admit to hospital
No CT scanner available
Abnormal CT scan
All penetrating head injuries
H/O prolonged loss of consciousness
Deteriorating level of consciousness
Moderate to severe headache
Significant alcohol / drug intoxication
Skull fracture
CSF leak – rhinorrhea or otorrhea
Significant associated injuries
No reliable companion at home
Abnormal GCS score (<15)
Focal neurological deficits

39. Discharge from hospital
Patient does not meet any of the criteria for admission
Discuss need to return if any problems develop and issue a
“warning sheet”
Schedule a follow – up visit

40. Management of moderate head injury
(GCS 9-13)
Initial Examination
Same as for mild head injury plus baseline blood work
CT scan brain – obtained in all cases
Admit to a facility capable of definitive neurosurgical care
After Admission
Frequent Neurologic Checks
Follow up CT if condition deteriorates or preferably before discharge
Improves (90%) Deteriorates (10%)
Discharge when appropriate
Follow up in clinic
If the patient stops following simple
commands repeat CT scan
Manage as per severe head injury protocol

41. Management of severe head injury(3 - 8 )
ABCDEs
Primary Survey and Resuscitation
Secondary Survey and ‘AMPLE’
history
Admit to facility – neurosurgical care
Neurologic Re-evaluation
Eye opening
Motor response
Verbal response
Pupillary reaction
Therapeutic agents (administered after Neurosurgical consult)
Mannitol
Moderate hyperventilation (Pco2 ~ 35 mmHg)
Anti convulsants
CT Brain

42. Airway
Attention must be given to the
increased ICP that can potentially
occur with any physical
stimulation of the respiratory tract
Lidocaine (1.5–2 mg/kg IV push)
Suppresses
Cough reflex
Hypertensive response
Increased ICP associated with
intubation
Etomidate (0.3 mg/kg IV)
Short-acting sedative-hypnotic
agent
Beneficial effects on ICP by
reducing CBF and
metabolism.
Has minimal adverse effects
on blood pressure and cardiac
output
Fewer respiratory depressant
effects than other agents.

43. Hypotension
A cause other than the head injury should be sought
Scalp lacerations can cause
hypovolemic hypotension
Hemorrhage into an epidural or
subgaleal hematoma (children)
Neurogenic hypotension in
concomitant high spinal cord
injury
Fluids should never be withheld in the head trauma patient with hypovolemic
hypotension for fear of increasing cerebral edema and ICP

44. Hyperventilation
Acute hyperventilation prevents or
delays herniation in the patient with
severe TBI
Goal is to reduce the pco2 to the
range of 30 to 35 mm hg
The onset of effect is within 30
seconds and peaks within 8 minutes
Hyperventilation lowers the ICP by
25%

46. Osmotic Agents
Mannitol is the mainstay for control
of elevated ICP acute severe TBI.
Mannitol (0.25–1 g/kg)
Hypertonic saline (HTS)
Preclinical studies have
demonstrated that HTS can
significantly reduce ICP
Adverse events - Renal Failure,
Central Pontine Myelinoysis,
Rebound ICP elevation

47. Brain cell VesselMannitol
Expands
vessel
volume in
hypovolemic
shock
Decrease
ICP (6 to 8
hrs) provides
space for
expansion of
hematoma
Reduces
blood viscosity
&
microcirculator
y resistance &
promotes CBF
Free radical
scavenger
In large doses
Renal failure &
Hypotension
Induce a paradoxical
effect

49. Crystalloids Vs Colloids

50. Role of Albumin in TBI

51. Mannitol Vs 7.45% Hypertonic
Saline Solution (HSS)

52. Barbiturates
Reduce cerebral metabolic
demands of the injured brain tissue
Affect vascular tone and inhibit
free radical-mediated cell
membrane lipid peroxidation

53. Role of Barbiturates

54. Furosemide
 To reduce ICT in conjunction with mannitol
 Dose 0.3 to 0.5 mg/kg
 Never use in Hypovolemia

55. Biomarkers for TBI

56. Admission serum albumin levels –
Effective indicator of outcome of TBI

57. Role of Hypothermia TBI

59. Role of hyperglycemia in TBI

60. Seizure Prophylaxis
INDICATIONS FOR ACUTE SEIZURE
PROPHYLAXIS IN SEVERE HEAD TRAUMA
Depressed skull fracture
Paralyzed and intubated patient
Seizure at the time of injury
Seizure at emergency department
presentation
Penetrating brain injury
Severe head injury (GCS score ≤8)
Acute subdural hematoma
Acute epidural hematoma
Acute intracranial hemorrhage
Prior history of seizures
Early seizures can cause hypoxia, hypercarbia, release of
excitatory neurotransmitters, and increased ICP, which can
worsen secondary brain injury
Lorazepam (0.05–
0.15 mg/kg IV over 2–5
minutes up to a total of
4 mg)
Diazepam (0.1 mg/kg, up to
5 mg IV, every 10 minutes
up to a total of 20 mg)
Phenytoin (18–20 mg/kg IV)
Fosphenytoin (15–18
phenytoin equivalents/kg) IV
or IM can be given

61. Recombinant factor VIIa (rFVIIa)

62. Role of steroids in TBI

63. Cranial Decompression
Emergency trephination
Signs of herniation
Refractory rise of ICP
Rapid detoriation
Blind invasive procedure
Chances of localizing the expanding lesions are
uncertain
May temporarily reverse or arrest the herniation
syndrome
Provides time formal craniotomy

64. Specific indications for craniotomy
 Clinical deterioration
 Size > 1cm thick extracerebral clot. Volume > 25 – 30 ml in
intracerebral hematomas.
 Midline shift > 5 mm.
 Enlargement of contralateral ventricle (temporal horn).
 Obliteration of basal cisterns or third ventricle.
 Raised or increasing ICP

65. EDH
Need surgical evacuation
 Timing – Any patient with
EDH in coma
or
Any EDH with >30cm3
irrespective of the GCS
Can wait
 EDH<30cm3
 <15mm thickness
 <5mm midline shift
 GCS> 8
Ref:-neurosurg-58,2006

66. When to operate in Acute SDH
Acute SDH >10mm or midline shift >5mm on CT
regardless of GCS
If GCS is decreased in hospital from time of injury to
Admission by >2, Anisocoria or ICP>20mmhg
Ref:-neurosurg-58,2006

67.  Operations definitely indicated only if it is a compound
(open) fracture (not over sagittal sinus) or if the fracture
is so extensive that it causes mass effect.
 Closed depressed skull fractures are usually treated
conservatively, but operation may be appropriate in
selected cases to reduce mass effect or correct
defigurement.

68. Role of probiotics and early entral
nutrition in TBI

69. Researches and ongoing trials

72. ACHIEVE
To explore the efficacy of albumin as a neuroprotective
agent for TBI in humans, a randomized controlled trial,
Albumin for Intracerebral Hemorrhage Intervention
(ACHIEVE), is currently underway

73. THANK YOU