17. MECHANISMMECHANISM
Mobility of brain in relation to skull & membranes
because of firm attachment to skull by dura mater,
falx cerebri & tentorium, if the brain moves against
them , there is damage to brain.
Configuration of interior of the skull
rough surface in ant: fossa, sphenoidal ridge , and also
at falx & tentorium with sharp edges
Preexisting state of the brain
aging brain has less reserve than the younger brain
Deceleration & acceleration
Coup & counter coup
41. Brain metabolism
Brain oxygen consumption is about 3.5 ml/ 100 g/min.
Cerebral blood flow and autoregulation
approximately 55 ml/ 100 g/min
maintained at a constant level via cerebral autoregulation,
in MAP of between 50 and 150 mmHg.
In TBI,autoregulation become disordered.
Cerebral blood flow then fluctuates with MAP and the
brain is mor e vulnerable to hypotension.
PATHOPHYSIOLOGYPATHOPHYSIOLOGY
42.
43. * Rigid box
* Content about 1400 - 1600 ml
brain cellular space 65 - 70 %
interstitial space 10 - 15 %
blood 5 %
CSF 5 %
* Intracranial volume is relatively constant.
* Any increase in vol: in one space leads to decrease in
others.
44. Monro-Kellie doctrine
Kellie, George
Monro, secundus, Alexander
A doctrine stating that any increase in the volume of the cranial will elevate intracranial
pressure and that an increase in one element must occur at the expense of the others.
Description
In 1783 Alexander Monro deduced that the cranium was a "rigid box" filled with a
"nearly incompressible brain" and that its total volume tends to remain constant. The
doctrine states that any increase in the volume of the cranial contents (e.g. brain, blood
or cerebrospinal fluid), will elevate intracranial pressure. Further, if one of these three
elements increase in volume, it must occur at the expense of volume of the other two
elements. In 1824 George Kellie confirmed many of Monro's early observations.
Bibliography
A. Monro:
Observations on the structure and function of the nervous system.
Edinburgh, Creech & Johnson 1823, page 5.
G. Kellie:
An account of the appearances observed in the dissection of two of the three individuals
presumed to have perished in the storm of the 3rd, and whose bodie were discovered in the
vicinity of Leith on the morning of the 4th November 1821 with some reflections on the
pathology of the brain.
The Transactions of the Medico-Chirurgical Society of Edinburgh, 1824, 1: 84-169
45.
46.
47.
48. CPP = MAP - ICP
( 70 – 80 ) = ( 80 – 90 ) - ( 5 – 15 ) mmHg
CPP < 50 mmHg cerebral ischaemia
CPP < 30 mmHg death
ICP CPP
Brain herniation
As EDH enlarges , it pushes the temporal lobe
medially causing herniation of uncus & hipocampal gyrus into
tentorial opening . ( Tentorial or uncal herniation )
If Pr: increases further, medulla & cerebellum
are forced downwards into the foramen magnum.( coning )
49.
50.
51. Uncal herniation syndrome
- decreasing level of consciousness
- early dilatation of ipsilateral pupil
- contralateral hemiparesis due to decussation of
decending pyramidal tract with deep tendon
hyperreflexia & Babinski’s sign.
With severe intracranial hypertension, Cushing’s response
may occur –
- systolic hypertension
- sinus bradycardia
- respiratory depression
52. situation deteriorates further if ventilation is impaired, as
hypoxia produces additional cerebral swelling.
Hypercarbia results in vasodilatation of the blood vessels
in the uninjured parts of the brain, thereby increasing
intracranial pressure.
Hypotension & hypovolemia
53. Eliminate hypoxia and hypovolaemia; each can
alone induce coma. If they are coupled with head
trauma, mortality increases.
54.
55. Features of increased ICP
symptoms - headache
- nausea, projectile vomiting
- drowsiness
- blurring of vision
- fit
signs - Cushing’ triad
- papilloedema
- fall in GCS
- uncal herniation syndrome
Focal neurological deficit
56. MANAGEMENTMANAGEMENT
Primary survey with resuscitation
A - clear & protect AIRWAY , control cervical spine
B - assess & maintain adequate BREATHING
C - assess & maintain adequate CIRCULATION
D - briefly assess neurological function, DISABILITY
E - EXPOSE the whole body, check the ENVIROMENT
Multidisplinary team approach
57.
58. Q. At the scene of an accident tracheal intubation
may have been carried out. What evidence is there
that this benefits head injury patients?
A. Clear evidence is elusive. A widely accepted view is that
intubation should be carried out ‘as soon as safely
possible’ in selected patients. When transport times are
long and trained personnel are available such
management seems logical. In this context the adverse
effects of transporting a severely head-injured patient with
a compromised airway outweigh the possible
complications of intubation in the field.
Scoop and run Versus Stay and play
59. Q. Will intubation and ventilation in these circumstances
require the patient to be anaesthetised? If so, what
techniques and drugs would you use and why?
A. The patient will require to be anaesthetised, even when
consciousness is already impaired, to minimise the risk of
secondary brain damage due to induced raised ICP
(intracranial pressure). Rapid sequence induction and
intubation is the recommended technique using a
combination of sedative with low cardiopressant effects
(e.g. midazolam, ketamine), analgesic (fentanyl) and
muscle relaxant (e.g.succinylcholine) agents.
60. Q. What pathophysiological process makes it unlikely
that isolated intracranial injury would cause
hypotension?
A. It takes only 100 to 150 mL of intracranial blood loss to
cause brain death by herniation. Thus hypotension
normally signifies extracranial injury.
Q. Do you know of the commonly quoted exception
to the above rule?
A . Only in newborn infants and babies can intracranial
haemorrhage result in significant hypotension.
62. Adjuncts to the primary survey
■ Blood – FBC, urea and electrolytes, clotting screen,
glucose, toxicology, cross-match
■ ECG, pulse oxymetry
■ Two wide-bore cannulae for intravenous fluids
■ Urinary and gastric catheters
■ Radiographs of the cervical spine and chest
63. Secondary survey
H/O - from pt or witness
- mechanism of injury
- Use of airbags, seat-belts, crash-helmets
- Neurological state and vital parameters at the
scene and during transport
- Estimated blood loss
- past medical history
- use of alcohol, drugs
P/E - scalp
- face … eye, ear, nose
- vital signs
- motor status
- GCS
AMPLE
64.
65. Paediatric GCS for children under five years of age
Feature Scale Score
Responses Notation
Eye opening Spontaneous 4
To voice 3
To pain 2
None 1
Verbal response Orientated/interacts/follows objects/ smiles/alert/coos/babbles
words to usual ability 5
Confused/consolable 4
Inappropriate words/moaning 3
Incomprehensible sounds/irritable/inconsolable 2
None 1
Best motor response Obey commands/normal movement 6
Localise pain/withdraw to touch 5
Withdraw to pain 4
Flexion to pain 3
Extension to pain 2
None 1
TOTAL COMA ‘SCORE’ 3/15 – 15/15
66. GCS 13 - 15 …….. Mild
9 - 12 …….. Moderate
3 - 8 …….. Severe ( < 8 - coma )
To consider
- treat the pt as OPD / In pt
- need investigation / stable for it / X ray or CT
- consult neurosurgeon / transfer
- urgent OT
It depends on
- severity
- local facilities
67. Criteria for admission
- GCS < 15
- GCS 15, additional risk factors
- N,V
- persisting post-traumatic amnesia
- fit after injury
- focal neurological signs in limbs & pupils
- irritability or abnormal behavior
- recent skull #
- abnormal CT
- significant medical co-morbidity or social problems
68. Investigations
1. Skull X ray
Indications – mechanism of injury is not trivial
- unconsciousness
- vomiting, amnesia
- full thickness laceration of scalp or boggy
haematoma
- medico legal evidence
69.
70. LinearLinear
FractureFracture
VesselVessel
groovegroove
Suture lineSuture line
DensityDensity Dark blackDark black GrayGray GrayGray
CourseCourse StraightStraight CurvingCurving AlongAlong
suture linessuture lines
BranchingBranching UsuallyUsually
nonenone
OftenOften
branchingbranching
Join withJoin with
otherother
suture linessuture lines
WidthWidth Very thinVery thin ThickerThicker
thanthan
fracturefracture
Jagged andJagged and
widewide
71.
72.
73.
74.
75. Risk of intracranial haematoma in head injury
GCS Skull fracture Risk
15 _ 1 in 31300
+ 1 in 81
9 - 14 _ 1 in 180
+ 1 in 5
3 - 8 _ 1 in 27
+ 1 in 4
78. NICE guidelines for CT in head injury
■ GCS < 13 at any point
■ GCS 13 or 14 at 2 hours
■ Focal neurological deficit
■ Suspected open, depressed or basal skull fracture
■ Seizure
■ Vomiting > one episode
Urgent CT head scan if none of the above but:
■ Age > 65
■ Coagulopathy (e.g. on warfarin)
■ Dangerous mechanism of injury (CT within 8 hours)
■ Antegrade amnesia > 30 min (CT within 8 hours)
79.
80.
81.
82.
83. TREATMENT PLANNING
Mild ( GCS 13 - 15 )
- GCS 15, no criteria for investigations D/C with
information
- criteria for X ray (+) skull x ray
no # observation
# CT & admit
- if criteria for CT (+), no need for X ray
normal CT observe for at
least one night abnormal CT discuss with
neurosurgical unit
84. Moderate ( GCS 9 – 12 )
- urgent CT
abnormal CT urgent transfer
normal CT exclude other causes of GCS
if (- ), discuss with neurosurgeon
transfer / observation at A&E
if GCS still decreases
transfer
85. Severe ( GCS 3 – 8 )
- immediate discussion with neuro: unit & transfer
- if motor response 5 or 6 no need ventilation
maintain SaO2>95%,Pco2<6kPa,Po2>12kPa at FiO2 40%
- if motor response 4 or less
ETT & ventilation, maintain Pco2 4 – 4.5kPa,
MAP at least 90 mmHg
- if transfer is inappropriate ( eg. d/t severe co-morbidity ),
keep pt at local ICU & continue neuro: consultation.
86. Medical management
Head up 300
if spinal clearance allows .
Ensure that the cervical collar doe not obstruct
venous return from the head.
Maintain normocapnia : PCO2 4.5–5.0 kPa.
Hyperventilation ??
Avoid hypotension
Sedation +/– muscle relaxant
Diuretics: furosemide, mannitol
Barbiturte, thiopentone
88. Sedation & analgesia
-decrease the reaction of the brain to stimulation
-reduce the incidence of seizures
-blunt autonomic responses to TBI
-propofol and remifentanil, or fentanyl
-midazolam or diazepam with fentanyl
89. Mannitol
-it stays in the vascular compartment and creates a
temporary osmotic gradient
-serum osmolarity exceeds 320 mOsmol
-0.3 g/kg intravenously, in 15 to 20 min
92. Q. What particular type of infection is associated with
the use of barbiturates in head-injured patients?
A. Respiratory infection.
Q. Give two reasons why this might occur with
barbiturates.
A. Reduced respiratory ciliary activity and immune
function.
Q. What other class of drug which has been used in
the management of severe head injury has been
reported to have a similar side effect?
A. Steroids.
93. Hypothermia
Moderate hypothermia reduces cerebral metabolism
three phases
- induction -temperature down to 34 °C quickly
- maintenance phase
- rewarming phase- slow and controlled warming
95. Q. A head-injured patient, several hours after evacuation of a large
extradural haematoma, has his sedation reduced to allow neurological
assessment prior to extubation. He is observed to start having a
generalised seizure. Presuming ABCs are addressed, outline your
pharmacological approach.
A. An intravenous bolus dose (10 mg or more) of diazepam will probably abort
the seizure. An intravenous infusion of phenytoin should then be
commenced.
Q. Outline your ongoing management of the phenytoin therapy?
A. Phenytoin should be given no faster than 25 mg/min (as it is cardiotoxic)
until the loading dose (usually 1000 mg in an adult) is given. Then start a
maintenance adult dose of 250–300 mg per day as guided by clinical response
and the plasma level of the drug.
Q. If the patient’s convulsions do not stop within 30 minutes, outline
further pharmacological steps.
A. Consider thiopentone (thiopental) (a 200 mg bolus followed by an infusion
of 5–15 mg/min). Clonazepam can be used if the seizures are mainly focal.
96. Other pharmacological agents
-agents are tested e.g. blockade of glutamate
receptors, scavenging of free radicals, and blockade
of calcium channels
-More recent research has moved toward the test of
drugs, hormones, and other endogenous substances
for multiple neuroprotective mechanisms.
97. Monitor
- level of consciousness by GCS
- pupils - size, symmetry & light response
- motor power – symmetry & pattern of limb movement
- vital signs - BP, PR, RR, T
-Pulse oximetry
-3-lead-ECG
-Capnography (ventilated patients)
98. Q. How frequently should such monitoring be
performed?
A. As frequently as indicated by the patient’s
condition. In a recently admitted or unstable patient,
recordings every 15 minutes (or more frequently) are
desirable.
99. ICP monitoring
should be placed in GCS less than 8T (after
resuscitation)
EVD, intraparenchymal fibreoptic catheter, epidural
may be discontinued when the ICP remains in the
normal range within 48-72 hours of withdrawal of ICP
therapy or if the pt is following commands.
100.
101.
102. Surgical treatment
- for scalp injury
- for # e.g.. depressed
- for intracranial h’age
exploratory Burr hole
craniectomy
- for increased ICP
CSF drainage via ventriculostmy
Delayed evacuation of swelling contusion
Decompressive craniectomy
103.
104.
105.
106.
107.
108.
109.
110.
111.
112.
113. Exploratory Burr hole
Without CT, exploratory Burr holes are made under
GA at following sites –
- first should be placed over skull # site
- if EDH (-), repeat in temporal, frontal & parietal
regions starting on site of first dilated pupil
- if (-), same procedure should be repeated in opposite
site
120. Q. What factors are most likely to affect outcome?
A.
-the nature and extent of intracranial and extracranial
damage
-the depth and duration of post-traumatic coma
-the patient’s age
-general medical health and previous state of function
-the quality of available clinical care.
