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Severe
blunt head injury
Immediate management
Indications for immediate neurosurgical
consultation
Indications for CT brain with 2-4 h (in addition to
above)
Pathophysiology of secondary brain injury
Treatment
ICP monitoring
Treatment of raised intracranial pressure
Prognosis
The management of severe blunt head injury revolves around minimizing further
neurological injury due to secondary injury
Immediate management
3 main priorities:
- resuscitation. Avoid hypotension and hypoxia - both significantly increase
mortality and morbidity
- rapid diagnosis of a brain lesion from head injury
- measures to inhibit secondary brain insults and to prevent rise in ICP
Resuscitation
- Airway
- Breathing
- Apnoea or cyanosis in the field or PaO2 < 60 mm Hg
associated with poor outcome
- Intubation and ventilation to prevent aspiration and ensure adequate
oxygenation. PEEP of up to 12 cmH2O well tolerated in terms of rise
in ICP
- consider pre-treatment with lignocaine (1-2 mg/kg 4 mins prior to
intubation) to blunt rise in ICP in response to laryngoscopy
- consider defasciculating dose of non-depolarizing muscle relaxant
to prevent suxamethonium induced rise in ICP
- Sedation and neuromuscular block may be necessary to prevent coughing,
which may result in prolonged rises in ICP. Use short acting agents.
- Circulation
- NB shock is rarely due to isolated head injury except in young
children and in patients with medullary injuries or large scalp lacerations
- Hypotension is an independent predictor of poor outcome and the only one of the
five major predictors which can be altered
- Aim for
MAP > 90 mm Hg in an attempt to maintain adequate cerebral perfusion pressure
- Fluid resuscitation to re-establish normal cerebral blood flow as soon as
possible -the
most likely cause of hypotension in a trauma patient is hypovolaemia
- Although
it is not currently standard practice there are data supporting use
of small volume resuscitation with hypertonic or hyperoncotic
solutions. Small volume resuscitation with hypertonic/hyperoncotic
solutions is associated with a faster restoration of normal cardiac
output in severe haemorrhagic shock than any other form of fluid
resuscitation. Use of hypertonic saline instead of isotonic fluid
has been demonstrated to reduce ICP in patients with traumatic brain
injury and intracranial hypertension. Retrospective subgroup
analysis of a RCT of patients with severe traumatic brain injury
demonstrated a higher systolic blood pressure and improved survival
in patients resuscitated with hypertonic saline and a meta-analysis
has shown that patients who receive hypertonic saline/dextran are
about twice as likely to survive as patients who receive standard
therapy. However an, as yet unpublished, large RCT shows no benefit
from use of hypertonic saline.
- patients resuscitated with albumin have a worse outcome thoan
those resuscitated with saline. (Click
here
to view paper)
- Note that blood-brain barrier does not
function like other membranes: tonicity and not osmolality is important in
determining fluid shifts.
- Aim for mild dehydration
- Specific treatment aimed at intracranial hypertension only if signs
of transtentorial herniation or progressive neurological deterioration not
attributable to extracranial causes are present.
- Hyperventilation
- Mannitol after adequate volume resuscitation
- Secondary survey including:
- GCS: initial score of 3-8 indicative of severe head injury
- Pupil size
- Motor function
Rapid diagnosis of brain injury
Indications for immediate consultation with
neurosurgeon (usually prior to urgent CT)
- Coma persisting after resuscitation
- Deteriorating consciousness or progressive neurological signs
- Skull fracture with any of:
- Confusion
- Fits
- Neurological symptoms or signs
- Open injury: depressed compound fracture of skull vault, fracture of base
of skull, penetrating injury
Indications for CT within 2-4 h of admission (in
addition to above)
- age>60 yrs
- failure to reach GCS of 15 within 2 h
- skull fracture
- fit
- headache
- vomiting
- focal neurological signs
- unstable systemic state precluding transfer to neurosurgery
- uncertain diagnosis
- tense fontanelle or suture diastasis in a child
Refer all patients with an abnormal CT scan or unsatisfactory clinical
progress despite normal scan to neurosurgeon.
CT of
subdural haematoma
Subdural
haematoma: gross pathology
CT of extradural haematoma
EDH:
gross pathology
Pathophysiology of secondary brain damage
Extracranial causes
- Failure of adequate cerebral perfusion from
circulatory shock
- Failure of cerebral oxygenation from disturbance of pulmonary
ventilation from:
- aspiration
- instability of chest wall (eg flail chest)
-
neurogenic disturbances of ventilatory drive
Intracranial mechanisms
- rise in ICP due to mass lesions and cerebral oedema
leading to fall in cerebral perfusion pressure and to herniation of brain is a
major factor in poor outcome
- cerebral blood flow of great significance in pathophysiology of secondary
brain damage. Almost all patients dying from severe head injury have
pathomorphological evidence of cerebral ischaemia. CBF heterogenous with areas
of hyperperfusion and hypoperfusion. Hyperperfusion of damaged brain may
increase cerebral oedema and thus ICP
- cerebral autoregulation impaired
Prevention of secondary injury
ICP monitoring and management
Intracranial
hypertension is important for two reasons:
-
in patients in
whom ICP exceeds central venous pressure, cerebral perfusion pressure is
determined by the difference between mean arterial pressure and intracranial
pressure
-
intracranial
hypertension may lead to coning
Indications for ICP monitoring:
- severe head injury with abnormal admission CT (ie haematoma, contusion,
oedema, or compressed basal cisterns)
- severe head injury and normal CT but ≥2 of: age
> 40 yrs, unilateral or bilateral motor posturing, systolic BP < 90 mm
Hg
- not routinely indicated in patients with mild/moderate head injury however
may be appropriate in certain conscious patients with traumatic mass lesions
Method:
- ventricular catheter attached to external strain gauge is most accurate, low
cost method and allows drainage of CSF. ICP transduction via fibreoptic or
strain gauge devices placed in ventricular catheters provide similar benefits
but at higher cost
- parenchymal ICP monitoring with fibreoptic or strain gauge catheter tip
transduction is similar to ventricular ICP monitoring but has the potential
for measurement drift
- subarachnoid, subdural and epidural
Complications:
- include infection, haemorrhage(1.5%),
malfunction (~10%), obstruction or malposition
- rarely produce long term morbidity in patients
- most studies define infection as positive CSF culture in ventricular and
subarachnoid bolt devices however this would better be defined as colonization
as there have been no reports in large prospective series of clinically
significant intracranial infections associated with ICP monitoring devices
Treatment of raised ICP: (hierachical)
- evacuate extradural/subdural haematomas +/- intracerebral haematomas, drain
hydrocephalus
- analgesia and sedation, nurse head up (30o), position head and neck to
ensure venous drainage is not obstructed, control temperature (and treat cause
of pyrexia) and fits to minimize rise in CMRO2
- ventricular drainage
- mannitol (0.3-1 g/kg initially followed by 0.25-0.5 g/kg 6 hourly).
Alternative: hypertonic saline (2ml/kg of 7.5% saline)
- hyperventilation to PaCO2 30-35 mm Hg
- second line therapy eg high dose barbiturate therapy, hyperventilation to
PaCO2 <30 mm Hg (monitoring of SjO2, AVdO2
and/or CBF recommended
- ICP treatment should be initiated at an upper threshold of 20-25 mm Hg.
Impact of ICP on outcome appears to lie in its role in determining CPP and as
an indicator of mass effect. As CPP can be managed by manipulation of MAP to a
great extent risk of herniation is a more important consideration in
determining the treatment threshold
Cerebral perfusion pressure
- aim for a CPP (ie MAP-ICP) of >60 mmHg by maintaining an adequate MAP
(use norepinephrine if necessary) and control of ICP (NB the choice of this
threshold is based on class III evidence)
Hyperventilation
- prophylactic hyperventilation to PaCO2 £ 35 mm
Hg during first 24h associated with a worse prognosis probably because it
reduces already low CBF
- hyperventilation may be necessary for brief periods when there is acute
neurological deterioration or for longer periods if there is intracranial
hypertension refractory to sedation, paralysis, CSF drainage and osmotic
diuretics
- SjO2, AVdO2 and CBF monitoring may help to identify
cerebral ischaemia if hyperventilation (with PaCO2<30 mm Hg)
necessary
- Probably has 2 distinct effects in the brain:
- Immediate plasma expanding effect. Reduces hct and blood viscosity.
Increases cerebral blood flow and oxygen delivery causing autoregulatory
vasoconstriction. Probable explanation for
reduction in ICP within a few mins and why reduction is most marked in those
with low CPP
- Osmotic dehydration of brain. Delayed for 15-30 mins and persists for 90
mins to ≥6h
- significant risk of renal failure if mannitol given in large doses,
particularly if serum osmolality >320 mOsm. May be increased risk in
patient receiving other potentially nephrotoxic drugs, in septic patients or
patients with pre-existing renal disease. At levels >350 serious cellular
damage may occur.
- should be discontinued if does not cause a diuresis
- euvolaemia should be maintained by adequate fluid replacement
- may cause cardiovascular collapse in hypovolaemic patient.
Contra-indicated in the unresuscitated patient
- in common with other osmotics "opens" BBB with the result that
mannitol and other small molecules in circulation may pass into brain. This
effect becomes harmful after many doses because mannitol may accumulate in
brain causing a reverse osmotic shift. Accumulation most marked when
mannitol is in circulation for long periods (eg with continuous infusion)
and therefore should be given as repeated boluses (0.25-1 g/kg)
- frusemide may produce less changes in electrolytes and osmolality than
mannitol. Reduction in cerebral oedema may be due to factors other than just
diuresis. ? acts synergistically with mannitol. Little data to support use
of frusemide in addition to mannitol
Barbiturates
- decrease ICP
- high dose barbiturate therapy may be considered in haemodynamically stable
salvageable patients with intracranial hypertension refractory to maximal
medical and surgical ICP lowering therapy.
- titrate dose to achieve EEG burst suppression
- >85% of patients with intractable intracranial hypertension requiring
barbiturates die
Other treatment
Prognosis
- Main determinants:
- age
- patients >60 yrs have a worse prognosis.~75% mortality in
severely brain injured.
- GCS on admission, especially motor function
- 20% of patients with an initial GCS=3 survive and 8-10% will be
moderately disabled or better
- pupillary response
- bilaterally unresponsive pupils associated with poor outcome (90%
mortality in one study, ~75% dead, vegetative or severely disabled
in two smaller studies)
- interaction between pupillary response and pathology. Unresponsive
pupils (prior to surgery) due to extradural haematoma: 56%; subdural
haematoma: 88%
- hypotension (systolic BP <90)
- hypotension consistently one of the strongest predictors of poor
outcome and the only one of the five major predictors that is
amenable to treatment
- evidence that correcting hypotension improves outcome
- iatrogenic hypotension also associated with worse outcome. As a
result great care should be taken to avoid intra-operative
hypotension or procedures should be delayed until patient is more
stable
- CT appearance (initial CT). Features associated with worse outcome
- abnormal CT associated with better prognosis
- acute subdural haematoma worse than diffuse injury which is worse
than extradural
- higher abbreviated injury score CT component
- absent or compressed basal cisterns
- traumatic subarachnoid haemorrhage
- midline shift (probably less important than other parameters)
- presence of hypoxia or ischaemia
- ICP > 20 mmHg
- Coma persisting > 6 hrs following head injury associated with a 40% 6
month mortality
- Overall mortality in severe head injury: approx. 30-50%
- Recovery may continue for up to 18-24 months after head injury although the
most significant gains are made in the first 6 months
Further reading
Brain Trauma
Foundation & American Association of Neurosurgeons. Management and prognosis
of severe traumatic brain injury. Published 2000
Update to BTF guidelines (2003)
Guidelines for children
Vincent JL, Berré J. Primer on
medical management of severe brain injury. Critical Care Medicine, 2005;
33:1392-99 |
