Download Head injury mgmc

Dr. S. Parthasarathy
MD., DA., DNB, MD (Acu),
Dip. Diab. DCA, Dip. Software statistics, Phd (physio)
Mahatma Gandhi Medical college and research
institute puducherry , India
What is this ??
 Head injury can be defined as any trauma to
the head, other than superficial facial injuries.
 This term is often used interchangeably with
both
brain
injury.(TBI)
injury
and
traumatic
brain
Incidence and classification
 1 million / year in UK
 1 % of all adult deaths
 In India one person dies every 10 minutes due
to TBI, and this will treble by 2020.
 80% -- Mild - == GCS 13 -15
 10-15 % –Moderate 9-12
 5-10% -
Severe < 8
( mortality of 25 % )
One more classification
 Primary
 Instantaneous neuronal injury at the impact time
 Can we do something ??
 Secondary
 We can do something !! Why does it happen ??
We want to decrease it !!
TBI itself causes these !!
 1.DECREASE CBF[ ESP < 18
CC/100G/MIN]
 2.IMPAIR AUTOREGULATION
 3.INCREASE ICP
 4. HYPERTENSION
 5. IRREGULAR RESPIRATION
 6. HYPERTHERMIA
Response to
head injury
Types of injuries
 Haemorhagic contusion
 Intracerebral hematomas
 Subdural hematomas
 Extradural hematomas
 Vascular injuries
 Diffuse axonal injuries
 Skull fractures
Look for
 Chest injuries
 Bleeding profuse external injuries
 Abdominal injuries
 Spine injuries
 Ophthalmic injuries
 Vitals
 Breathing and airway injuries
Then come to brain
Initial assessment
 Conscious status – GCS – pupils
 Cervical spine injuries _ 5 %
 Extra cranial injuries upto 50 % !!
 GCS – 8 or below – intubate
 Don’t sedate any patient with head injury for
CT scan if uncooperative
 Better intubate and control
 Good dose of thio will obliterate scoline
induced ICP problem !!
When to intubate ??
Airway
Breathing
– High or
slow
Fits or low
GCS
B/L mand.
#
When to take CT scan
 GCS < 13 on initial assessment
 GCS < 15 on assessment 2 hours post-injury
 Definite or suspected open or depressed skull fracture
 Signs of basal skull fracture
 Post-traumatic seizure
 Focal neurological deficit
 >1 episode of vomiting
 Any history of amnesia or loss of consciousness post-
injury in a patient
 who is coagulopathic (clotting disorder, warfarin
treatment)
During transfer for CT
 Good dose of IV agents and narcotics
 20 degree head up tilt decrease their ICP.
 Avoid ties obstructing neck veins,
 prevention of coughing (all patients should be fully
paralysed after intubation and until they are delivered
to the ICU),
 avoidance of PEEP
Neck veins compressed !!
Sub,
extra,
ICH, diffuse axonal
Monitoring is a must - waste time ??
 Lines like cavafix
 Arterial lines
 Foleys catheter
 Use the head shaving time to do these !!
 ICP monitoring is mainly used in head injured
patients undergoing non neurological surgeries
ICP monitoring
GCS
Back again to the same picture !!
compliance curve
Preoperative preparation
 Routine investigations
 Blood grouping and reservation
 Coagulation profile
 Possible neuroprotective role
 Potassium
 Magnesium
 Female gender hormones
Aims of anaesthesia
 Avoid secondary brain damage
 Optimize cerebral perfusion and
oxygenation
 Provide adequate surgical conditions for the
neurosurgeons.
Induction
 Usually intubated
 If not start propofol/thio / suxa / intubation
 Difficult airway – awake fibreoptic
 Glidescope
 Never allow hypoxemia. Hypercarbia etc..
 Be aggressive
Manual inline stabilization
Maintanance
 Ketamine Can be avoided
 Studies say – can coadminister with propofol
 Continue propofol infusion with hemodynamic
stability
 Nitrous oxide can increase CMRO2 and cause
cerebral vasodialation and increased ICP and
should be avoided
 Inhalational agents with titration( < 1 MAC ) – OK
 tight brain – stop and switch over to IV agents
Keep it at 0.5 MAC approx
Gastric drain tubes
 Orogastric and aspirate
 Nasogastric ??
 Coil back into the brain ?
Appropriate blood pressure ?
 Edingurgh concept
 emphasizes
low
postinjury
CBF,
impaired
autoregulation, and the necessity to support CPP
[MAP] — [ICP]) ---- MAP to 70mm Hg.
 The "Lund concept“
 CPP of 60 -70 mm Hg
 The"Birmingham”concept,entails
pharmacological induced hypertension.????
Be liberal in
vasopressors
Fluids
 Warm, non-glucose containing isotonic crystalloid






solution is preferable for TBI patients.
Hypertonic saline may be beneficial resuscitation fluid
for TBI patients because it increases intravascular fluid
and decreases ICP.
Keep the osmolarity – 280 mosmoles
Albumin – no demonstrable usefulness.
Hetastarch – proved usefulness – not better than NS
No dextrose containing fluids
Blood - blood - blood -- anemia is the worst offender
What can anemia do ??
Potential mechanisms of cerebral injury due to
anemia include tissue hypoxia, injury caused by
reactive oxygen species, inflammation, disruption
of blood-brain barrier (BBB) function, vascular
thrombosis and anemic cerebral hyperemia
POINT TO NOTE
Hypertonic saline
Improved
hemodynamics
vasoregulation
Increased
Cerebral
perfusion
Decreased
Cerebral edema
Decreased
ICP
Avoiding secondary
injury
Cellular
modulation
BUT THE PROBLEMS REMAIN
 Hypernatremia
 osmotic demyelination syndrome (ODS),
 Pulmonary edema, CCF, acute renal insufficiency
 Rebound brain edema
 hematologic
abnormalities
including
increased
hemorrhage, coagulopathy, and red cell lysis.
Hyperventilation
 MAY BE USEFUL
 acute increases in ICP
 need to improve surgical exposure
 Paco2 can decrease ICP
but cerebral ischemia ?? –
 short lived action of hypocarbia
 Studies – beneficial Paco2 is around 30 -35
Miscellaneous
 Routine stress ulcer prophylaxis is required.
 Seizure prophylaxis is currently recommended for
7 days following the injury in patients with severe
TBI.
 The agent most commonly recommended is
phenytoin,
 loading dose of 18 mg/kg
 maintenance dose of 5 mg/kg/d
 serum drug levels 10 to 20 mg/L.
Hyponatremia, hypomagnesemia !!
Miscellaneous
 Both hypoglycaemia and hyperglycaemia can worsen
brain injury.
 A blood glucose of 4 – 8 mmol/l is targeted
 majority of studies indicate that 15-30°head elevation
reduces ICP without compromising CPP or cerebral
oxygenation.
 Marked degrees of head elevation (>30°) may actually
increase ICP in some patients by causing
autoregulatory vasodilatation
 Keep it at 20
Miscellaneous
 Mild hypothermia (32-34°C) is beneficial in head
injuries.
 It reduces CMR, CBF, ICP and improves outcome
 Steroids have no role in head injury !!
 Diuretics have definite role – detailed earlier
 Mannitol – 1gm/kg followed by frusemide –
ICP, ? Brain herniation, slackness
Coagulopathy
 Coagulation disorder could result from TBI and cause
secondary brain injury.
 A recent review reported that the overall prevalence of
coagulopathy was 32.7% after TBI and more than 60%
in severe TBI
 presence of coagulopathy was associated with an
increased mortality and poor outcome.
 Novoseven . Tranexamic acid
End op decisions
NONNEURO NEXT SURGERY
PLAN ??
 If the patient had normal preop consciousness
 End op - patient is able to follow commands and
move extremities. Then -- early extubation would be preferable
 No bucking and coughing
 Intravenous lidocaine for smooth emergence.
 Short acting opiates, particularly remifentanil, can
provide a patient that is hemodynamically stable,
tolerating the endotracheal tube, and following
commands.
DURING TRANSFER
 VENTILATION,OXYGENATION,CPP
MUST
BE
CAREFULLY MAINTAINED.
 MONITOR BP,CAPNOGRAPHY,SaO2,ICP
 EMERGENCE CAN RESULT IN INCREASE IN BP,ICP,
ADDITIONAL SEDATIVE,NARCOTIC,LABETALOL MAY
BE REQUIRED
 ALVEOLAR VENTILATION MUST BE CAREFULLY
SUPPORTED AND MONITORED UNTIL TO ICU
Summary
 Definition
 Intubate ?
OTHER
INJURIES
 CT scan ?
 Aggressive
 Other injuries
 Aims of anaesthesia
 Induction and intubation
 Recovery
PREVENT
SECONDARY
BRAIN
INJURY
Summary of targets
 PaO2 > 13kPa (98mmHg)
 PaCO2 of 4.5 – 5.0kPa (34- 38mmHg)
 MAP ≥ 80 mmHg (in the absence of ICP
monitoring)
 Glucose 4 – 8 mmol/l
 Temperature < 37°C
 Hematocrit
 If ICP monitoring in situ
 ---- CPP 60 – 70mmHg -----ICP < 20mmHg
Carry home message