Transcript Slides - Philippe Le Fevre

Head Injury in the ICU
Tim Cowan
ED Registrar
November 16 2011
Overview
Epidemiology
Physiology, primary and secondary injury
Initial care and resuscitation
ICP control

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Surgical
Medical
Retrieval considerations
Research focus
Epidemiology
Roughly 110/100 000 of hospital visits are
for traumatic brain injury
Males twice the rate of females
Peaks at age 15-24 and greater than 75
years
Estimated cost $4.8 billion every year in
Australia
MVA, falls and assaults account for the
majority of severe brain injuries
"Ute surfing": a novel cause of severe head
injury
Rodney S Allan, Peter J Spittaler and John G
Christie
MJA 1999; 171: 681-682
Impact at the cellular level
• Excitotoxicity
• Inflammatory changes
• Cytotoxic oedema
• Vasogenic oedema
Monro-Kellie Doctrine
CSF ~8%
Blood ~ 12%
Brain ~80%
• Cranium is a rigid structure
containing three components:
brain, CSF and blood
• Normal ICP is <15 mmHg
• An increase in the volume of one
of the components increases ICP
unless there is a compensatory
decrease in the volume of another
component
• These mechanisms are
exhausted by about 25 mmHg
Cerebral perfusion pressure
=
Mean arterial pressure
Intracranial pressure
The vicious circle of ICP and CBF
Raised intra-cranial
pressure
Increased cellular injury,
local hypoxia and
hypercapnoea
Increased cerebral
blood flow
Primary vs secondary brain injury
Primary occurs at the time of
impact and is usually
refractory to medical
treatment
Secondary occurs
subsequently and for the
most part is preventable or
treatable
Secondary brain injury
Major extracranial causes

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Hypoxia
Hypo or hypercapnia
Hypotension
Why is hypoxia bad?
Brain uses ~20% of total oxygen consumption
Hypoxia leads to cell changes in seconds and quickly
becomes irreversible
Low arterial oxygen tension has profound effects on
cerebral blood flow. When it falls below 50 mmHg, there
is a rapid increase in CBF and arterial blood volume
0
50
100
150
What does CO2 do?
Carbon dioxide causes cerebral vasodilation. As the
arterial tension of CO2 rises, CBF increases.
When PaCO2 is reduced vasoconstriction is induced.
100
Cerebral blood flow
(ml/100g/min)
50
0
0
25
50
Arterial pCO2
(mmHg)
75
100
What’s wrong with hypotension?
Brains like blood – receiving up to 15% of cardiac output
Normally autoregulation maintains a constant blood flow
between MAP of about 50 mmHg and 150 mmHg.
Autoregulation is a poorly understood local vascular
mechanism.
In traumatised or ischaemic brain, CBF may become
blood pressure dependent.
Retrospective analysis of a large group of matched
patients has suggested a single prehospital episode of
hypotension


doubled risk of mortality and
was independent of age, GCS, pupillary status, GCS motor
score and intracranial pathology
Secondary brain injury
Other extracranial causes

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Hyperthermia
Hyponatraemia
Hypo/perglycaemia
Acidosis
Secondary brain injury
Intracranial causes

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Hemorrhage
Oedema
Infection
Initial care
ABCDE
Usual ATLS guidelines
Particular attention to
avoiding secondary injury
Don’t forget the C spine
Airway and breathing
Usually ETT required in severe TBI
Useful to perform a limited neurological exam first if
possible
RSI

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Ketamine no longer contraindicated
Opiates can blunt stress
response to intubation
Cervical spine injuries
common
Aim


SaO2 >97%,
pCO2 35-40 mmHg
Circulation
Hypotension clearly linked to poor
outcome
BTF guidelines suggest aim for SBP>90
JHH TBI protocol suggests MAP of 90
rather than SBP
Consider permissive hypotension in
multitrauma
Correct coagulopathy
Disability
Limited exam
GCS and pupils
Monitor trends as well as initial
Expedite CT brain
Blown pupil
Medial temporal lobe
herniates
Pressure on CN III
interrupting
parasympathetic input
to the eye
Transtentorial
herniation also
compresses the
brainstem.
Consider other causes
(briefly!)
ICP monitoring
Clinically

track GCS, pupillary responses
Invasive


operative insertion of an ICP monitor
can be intraventricular or intraparenchymal
Management of raised ICP in the
resuscitative setting
Simple things (if you don’t have a
Black and Decker)
Nurse 30 degrees head up if able

Can tilt whole bed if spine not cleared
Avoid impeding cranial venous drainage

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Tapes not too tight on ETT
Subclavian or femoral CVC rather than IJ
Sandbag and tape vs collar
Mannitol
Osmotic agent (sugar alcohol)
0.5gm/kg/dose
Initially volume expander
(decreases Hct, reduces viscosity,
improves oxygen delivery)
Osmotic effects take about 15-30
minutes, last from 90 minutes to
several hours
Filtered and not reabsorbed, thus
net volume loss.
Useful to ‘buy time’
Use with caution in hypotension
Surgical intervention
There is a clot. I must fix it.
Different operations

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External ventricular drain
(EVD)
Burrholes
Craniotomy (bone window
replaced)
Craniectomy (bone removed
and sent to bone bank,
stored in subcutaneous
pouch, or discarded)
Can leave a drain in situ
EVD
Medical intervention
Mannitol
Driving MAP
Sedation
Paralysis
Hypertonic saline
Barbiturates
CPP = MAP-ICP
CPP needs to be greater than 60mmHg
Ideally preferable to reduce ICP rather
than increase MAP
If ICP optimised as possible, and CPP not
satisfactory, use noradrenaline to drive
MAP
Sedation +/- paralysis
Routinely sedated until ICP controlled >24h
First line treatment of ICP ‘spike’

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Bolus of M and M
If that works, increase background rate
Propofol reduces cerebral metabolism and blood flow
Paralysis decreases straining, eg from
coughing/ventilator dyssynchrony

But can mask seizure, and causes complications if
used long term
Hypertonic saline
“Current evidence is not strong enough to make
recommendations on the use, concentration and
method of administration of hypertonic saline for
the treatment of traumatic intracranial
hypertension.” Brain Trauma Foundation
guidelines
JHH ICU guideline – if serum Na+ <155, and
CVP <12 give a dose
(30ml 23.4% saline over 10 min)
Barbiturates
About 55% of the glucose and oxygen utilisation
by the brain is meant for its electrical activity and
metabolism
Barbiturates depress cerebral metabolism and
as a result, CBF needs are reduced
Also inhibit free radical-mediated lipid
peroxidation and excitotoxicity, cause alterations
in vascular tone and resistance
Improve ICP but not outcome - Cochrane
Hypotension, myocardial depression,
accumulation can all be associated problems.
Other ICU care
Nutrition and glycaemic control
Analgesia
DVT prophylaxis

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High risk patients
TEDS and SCUDS
Level III evidence supports the use of prophylaxis with low-dose
heparin or LMWH for prevention of DVT in patients with severe
TBI, but uncertainty remains around when to commence and
what dose to use
Ulcer prophylaxis
Pressure care, chest physio
Bowel care
Retrieval considerations.
Preventing secondary injury
Mannitol
Deep sedation +/- paralysis
Consider intracranial air
Expedite transfer to CT or surgery
Complications
Seizures
Prophylactic anticonvulsants reduce the
occurrence of post-traumatic seizures within the
first week of injury, but they do not improve longterm outcome.
Treat seizures immediately. Seizures raise ICP
and can increase the volume of
intraparenchymal and subarachnoid
hemorrhage.
Phenytoin load
Salt and the injured brain
Hyponatremia may lead to reduced
levels of consciousness and even
epileptic seizures.
Hyponatremia after head injury is often
due to SIADH, and less commonly to
cerebral salt wasting syndrome.
Hypernatraemia can also occur,
especially if there is HP axis injury
(causing diabetes insipidus)
Monitor sodium, urine output and
volume status, check osmolality if
abnormal and don’t correct too quickly
10mmol/L/day is generally a safe rate
to increase or reduce serum sodium
Dysautonomia (“Storming”)
Complex interactions between multiple
areas of brain (cortex, hypothalamus,
brainstem)
Hypertension, fever, tachycardia,
tachypnea, pupillary dilation, and
extensor posturing.
Diagnosis of exclusion
NMS, serotonin syndrome, malignant
hyperthermia, sepsis, withdrawal
syndromes and thyroid storm can
cause similar picture
Propanolol and clonidine can reduce
symptoms
Hydrocephalus
Acute or chronic post TBI
Communicating or noncommunicating

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Blockage of outflow (blood in 3rd/4th
ventricles)
Impaired reabsorption (blood/proteins
blocking arachnoid villi)
Neurology varies
May need LP, EVD or V-P shunt
Research focus
DECRA trial
2003-2010 Aust, NZ, Saudi Arabia
Prospective randomised controlled trial
155 enrolments
Randomized to craniectomy plus
maximum medical care, versus maximum
medical care only
DECRA - background
1000 ICU admissions/year with severe TBI
50% have a focal surgical lesion
10% have diffuse injury and swelling
refractory to drugs and drains
Decompressive craniectomy was
becoming more popular to manage these
patients
Inclusions and exclusions
15-59 years
Non penetrating head trauma
GCS 3-8 at admission
Exclusions
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Not suitable for full active treatment as per treating clinician
Fixed dilated pupils
Mass lesion requiring surgery
Spinal cord injury
CA at scene
ICP >20 mmHg for 15 minutes within one hour during
first 72 hours of care and despite optimised first tier
treatment
DECRA n=73, standard care n=82
Interventions
DECRA group underwent bifrontal
decompressive craniectomy with dural opening,
in addition to medical therapy as per control
group
Control group underwent medical therapy as per
BTF clinical practice guidelines
Both had scope for second tier interventions
Controls could have compassionate craniectomy
after 72 hours if ICPs remained high (15/82)
DECRA findings
No mortality difference – 19% in DECRA group vs 18%
in standard care
The craniectomy group had decreased intracranial
pressure, markedly decreased medical therapies
required for intracranial pressure, shortened mechanical
ventilation time, and shortened stay in the intensive care
unit by 5 days compared with the standard care group
But at 6 month follow-up, 19% more patients had poor
functional outcomes based on the extended Glasgow
Outcome Score in the decompressive craniectomy group
compared with patients who received standard care
alone. (70% vs 51%)
Why did the DECRA group do
worse?
?surgical complications (including
hydrocephalus), but surgical complications seem
an unlikely explanation given that the rates
overall were less than those reported in
published case series.
?”axonal stretch” that occurred during swelling of
the brain outside the skull through the
craniectomy defect
?release of pressure, in and of itself, may have
aggravated the development of brain edema that
would otherwise have been self-limiting
DECRA - criticisms
20mmHg low threshold for inclusion, and 15
minutes short duration of raised ICP
Only 155 of 3500 potential patients enrolled,
hard to generalise results
Despite being randomized, more patients in the
craniectomy arm had unreactive pupils (after
randomization but before surgery)
Some patients in the non-surgical arm went on
to have craniectomy after 72 hours, yet were
included in the medical group for analysis
Didn’t evaluate cerebral hypoxia and blood flow
What does it all mean?
It’s really hard to do good research!
Craniectomy will reduce ICP
Maybe that is not the key issue (as suggested in
barbiturate and hypothermia studies) and when
considering outcome intracranial pressure cannot be
used as a reliable short-term surrogate for the
effectiveness of therapies for severe TBI.
Need to consider ICP in the context of brain perfusion
and oxygenation – further studies looking at ICP as well
as transcranial dopplers, microdialysis catheters and
jugular venous bulb oxygen saturations
RESCUEicp trial
319/400 recruited so far
Craniectomy versus standard care
ICP >25mmHg for 1-12 hours
Previous haematoma evacuation does not
exclude entry
Either bifrontal or wide unilateral
decompression
Outcome at discharge and 6 months
Erythropoietin
EPO receptors upregulated after TBI
EPO crosses BBB, protects against further
injury by restoring mitochondrial function,
reducing glutamate exocytosis
Activates anti-inflammatory, anti-oxidant
and anti-apoptotic signalling.
Also stimulates neurogenesis
EPO-TBI trial
Commenced May 2010
Randomised, double blinded, placebo controlled
trial
EPO 40 000 IU s/c weekly x 3 weeks vs normal
saline placebo
Primary outcomes – severe disability or death at
6 months as per GOSE
Secondary outcomes – disability, quality of life at
6 months, cost, and rate of thrombotic events.
Inclusion criteria
Patients with non-penetrating moderate (GCS 9-12) or severe (GCS
3-8) TBI admitted to the ICU
Are ≥ 15 to ≤ 65 years of age
Are < 24 hours since primary traumatic injury
Are expected to stay ≥ 48 hours
Have a haemoglobin not exceeding the upper limit of the applicable
normal
Have written informed consent from legal surrogate
Exclusion criteria
GCS = 3 and fixed dilated pupils
History of DVT, PE or other thromboembolic event
A chronic hypercoagulable disorder, including known malignancy
Treatment with EPO in the last 30 days
First dose of study drug unable to be given within 24 hours of primary injury
Pregnancy or lactation or 3 months post partum
Uncontrolled hypertension (systolic blood pressure of >200 mm Hg or diastolic blood pressure of
>110 mm Hg)
Acute myocardial infarct within the past 12 months
Past history of epilepsy with seizures in past 3 months
Expected to die imminently (< 24 hours)
Inability to perform lower limb ultrasounds
Known sensitivity to mammalian cell derived products
Hypersensitivity to the active substance or to any of the additives
Pure red cell aplasia (PRCA)
End stage renal failure (receives chronic dialysis)
Severe pre-existing physical or mental disability or severe co-morbidity that may interfere with the
assessment of outcome
Spinal cord injury
Treatment with any investigational drug within 30 days before enrolment
The treating physician believes it is not in the best interest of the patient to be randomised to this
trial
Hypothermia isn’t cool. Yet.
Prophylactic hypothermia is not associated with
decreased mortality
Does appear to have some impact on GOS compared to
normothermia, BUT
Limited good research, clarity needed in particular re:
 Target cooling temperature (32-33°C or >33°C)
 Cooling duration (<48 h, 48 h, or >48 h)
 Rate of rewarming (1°C per hour, 1°C per day, or
slower)
Steroids
CRASH trial
10 008 patients GCS 14 or less
Randomised to 48h of methylpred or saline
Outcomes of


death within 2 weeks of injury
GOS at 6 months
Steroids
Placebo
%Mortality at 2 weeks
21.1
17.9
%Mortality at 6 months
25.7
22.3
%Death and severe
disability at 6 months
38.1
36.3
Steroids not recommended in management of head injury
Free radical scavengers
Oxidative stress and mitochondrial injury
leads to the formation of free radicals
These in turn can further damage neural
cells and promote inflammation
Scavengers ‘mop up’ free radicals
Mannitol is a free radical scavenger
Edaravone is being researched for stroke
That is all.
Make sure you wear a helmet.
Extradural haematoma
Subdural haematoma
Traumatic subarachnoid
haematoma
Intracerebral contusions
Trauma.org moulage