Association of North Western Intensive Care
Units
The General ICU Management of Patients with Severe Traumatic
Brain Injury
Adapted for ANWICU by Dr Charlie Granger, Lancaster Hospital and
Dr Duncan Hancox, Royal Preston Hospital from the Toronto guidelines
and proposed AMICU Guidelines
Last Revised Oct. 2000
ICU NEUROLOGICAL SUPPORT SUMMARY
This is a guideline NOT a protocol. Staff should only undertake treatments and procedures
that they are familiar with or trained to perform.
SUMMARY:
Discuss the patient with the neurosurgeons.
1. Insert arterial and CVP monitoring lines and ICP bold / jugular bulb catheter if trained
Indications for ICP placement include:
a) initial GCS <9,
2.
3.
4.
5.
6.
b) b) changes present on head CT,
c) c) clinical deterioration
Avoid hypotension at any time (Systolic Blood Pressure below 95 mmHg). Maintain
CPP >70 mmHg or MAP>90mmHg if no ICP bolt
Avoid hypoxia at any time (Pa02 below 60 mmHg) - PEEP is permitted
Treat pyrexia prophylactically - Paracetamol 4hrly and /or active cooling to reduce
hyperthermia
Avoid hypercarbia (PaCO2 >40mmHg / 5.3KPa)
Avoid excessive hypocarbia (PaCO2 <35 mmHg / 4.6kPa)
7. Treat abnormalities in glucose, electrolytes or coagulation
8. Ensure patient is adequately sedated with adequate analgesia
9. Paralyse patient if necessary, but only if necessary
10. Nurse patient at 15-30 degrees head-up tilt with head in neutral position
11. Avoid constriction of neck, to permit adequate jugular venous drainage
12. Avoid hypovolaemia. Use isotonic fluids or colloids.
13. Treat or avoid rises in the ICP above 20 mmHg
14. Start NG feeding early
15. Treat fitting rapidly
16. see guidelines for more details
NEUROLOGICAL SUPPORT
Secondary brain damage can occur at any time after the initial cerebral injury and is, to a large
extent, avoidable. The aim of providing neurological support is to minimise the risk of secondary
damage, by avoiding the factors that cause it, and to provide the optimum environment for
recovery from the primary brain injury.
Causes of secondary injury include:
Systemic:
Hypoxaemia
Arterial hypotension
Anaemia
Pyrexia
Hypercarbia
Excessive hypocarbia
Hyponatraemia
Hypo/hyperglycaemia
Severe arterial hypertension
Intracranial:
Haematoma
Cerebral oedema
Seizures
Vasospasm
Infection
Hydrocephalous
If secondary brain damage is to be avoided, meticulous attention to the following points is
necessary:
General Points
Secure the airway – by definition the severely head injured will have a GCS < 9
Insert monitoring to enable patient management – arterial line, central line and ICP monitoring
bolt (trained personnel only)
Hypotension.
In adults, hypotension is not a normal consequence of an isolated head injury, so other causes
should be actively sought. A systolic blood pressure below 95mmHg doubles the risk of death
after head injury. The duration of hypotension, and its severity, strongly influence the severity of
secondary brain injury (1). Because of the crucial influence of arterial pressure on secondary
head injury, an arterial line should be inserted in all patients with severe brain injury (GCS < 9),
and a CVP line can also be very useful, especially in patients with additional injuries - i.e. major
trauma. The traditional emphasis is on the Cerebral Perfusion Pressure (CPP), which is defined
as the Mean Arterial Pressure less the Intracranial Pressure (ICP), but in reality the most
important consideration is the cerebral blood flow (CBF). In the absence of any measure of CBF,
in a head-injured patient, in whom cerebral autoregulation may be imperfect, the CPP should be
maintained above 70mmHg (2).
In the absence of ICP monitoring then mean arterial pressure should be >90mmHg.
After euvolaemic fluid resuscitation, adequate arterial pressure should be maintained with
inotropes. Noradrenaline may be the preferred choice.
Hypoxia.
A PaO2 below 60 mmHg is the second most powerful predictor of a poor outcome after head
injury (3). PEEP of 5 to 15 cm H20 will not usually raise the ICP, but may help to reduce the
risk of hypoxia (4). In a head injured patient, a GCS below 9 mandates intubation - which must
be performed with the possibility of an unstable injury to the cervical spine permanently in mind
(4).
Pyrexia.
An elevation in temperature is virtually universal after head injury, even in the absence of
infection. Any pyrexia will increase the oxygen consumption of the brain, and therefore worsen
the effect of hypoxia or local ischaemia, as well as increase the ICP (5). Every effort should be
made to anticipate and avoid pyrexia, including regular prophylactic medication with
paracetamol NG or PR. Active cooling may be appropriate if simpler measures fail to reduce the
temperature below 37.5oC. Cooling below 37C probably doesn’t improve outcome other than
helping to avoid hyperthermia more effectively.
Hypercarbia.
Carbon dioxide is a powerful cerebral vasodilator. Hypercarbia will therefore raise the ICP and
worsen the effect of the primary head injury. An elevated PaCO2 should be avoided unless there
are powerful reasons to the contrary.
Hypocarbia.
Reducing the CO2 can reduce the ICP by producing cerebral vasoconstriction. However, if the
vasoconstriction is excessive this can cause a significant reduction in cerebral perfusion, further
worsening the cerebral damage. Cerebral blood flow is usually reduced by up to 25% after head
injury. There is now good evidence that prophylactic hyperventilation is not indicated in the first
five days after head injury (6), and there is a growing consensus that during the management of
head injuries the PaCO2 should not be allowed to fall below 35mmHg unless neurological
deterioration while awaiting emergency CT scanning or neurosurgery, when other forms of
treatment have been exhausted, and in treatment of last resort during acute deterioration (7).
Electrolyte abnormalities.
These may interfere with cellular function and should be avoided. Hypoglycaemia may be
particularly harmful, through its effect on cellular metabolism. Blood glucose should be tightly
controlled within the range 6-10mmol/l using as much insulin as required. The usual cautions on
excessively rapid manipulations of the serum Na+ should be observed and Na+ should be kept
within the normal range.
a) Diabetes Insipidus is usually an indicator of a very grave prognosis, often only occurring after
evidence of coning has developed. The consequence of non-treatment is the risk of
hypovolaemia and cerebral sinus thrombosis, both of which are disastrous with a 'tight brain'.
However the consequence of too early/excessive treatment is water overload leading to worse
oedema and consequent organ dysfunction.
Diagnostic criteria:
Excessive urine output> 300ml/hr for >2hours Rising serum
sodium >150 and Osmolality> 300 Low urine SG <1005
and Osmolality <300 Maintain circulating volume with nonsodium containing fluids e.g. 5% dextrose (control sugar)
Treatment:
Administer 1 ug IV DDAVP repeating as necessary every
few hours. Smaller doses more frequently or an infusion
may avoid excessive swings in urine output.
b) Inappropriate ADH syndrome causes hyponatraemia due to excess water retention. – Low
serum Na+ and osmolality. Positive fluid balance. Normal 24hr urinary sodium. Raised urine
osmolality. Treat by fluid restriction 1.5-2 l/24 hours.
c) Cerebral Salt Wasting is due to excess natriuresis. Low serum Na+. Low-normal serum
osmolality Treat by sodium replacement.
Coughing, restlessness and fighting the ventilator.
These all raise the ICP and should be avoided by the use of adequate levels of sedation and, if
required, paralysis (8). Patients should not be routinely paralyed. Some coughing on suction
should be tolerated as long as any associated rise in ICP is not prolonged – this helps to reduce
chest infections.
Sedation should be titrated to a Ramsey score of 5-6 i.e. unresponsive to suction and pain.
Neuromuscular blockade should be monitored if used, and should ideally be stopped at least
once every 24 hours to observe for sedation level, fitting and to see if it is needed.
Posture.
The patient should be nursed at a 15 - 30 degree head-up tilt without anything, such as
excessively tight tube ties, to impede jugular venous drainage (5,9). The head should be in the
neutral position. Restoration of euvolaemia should precede a significant head-up posture, since
the damaging effect of orthostatic hypotension on the CPP may exceed the beneficial effect of
head elevation.
DVT Prophylaxis
A major dilemma, as patients are at high risk, but safety of pharmacological prophylaxis remains
controversial. It is important to use some form of DVT prophylaxis.
Suctioning and Physiotherapy
These should be used to clear secretions and avoid atelectasis. They have potential to raise ICP
so the patient should be well sedated.
Fluid management.
There is still some controversy about this. Not only is there is no strong evidence that fluid
restriction has a significant beneficial effect on brain oedema, but also marked fluid restriction
can result in episodes of hypotension which, as above, carry a high risk of a poor outcome. It is
probably better to have produced mild hypervolaemia than to have permitted mild hypovolaemia
(5). Solutions such as 5% Dextrose can increase brain water, and therefore ICP, and are probably
therefore a poor choice. Beyond this, colloids or isotonic crystalloids (Normal Saline or
Hartmanns solution) are equally useful. In the otherwise healthy head-injured patient, neither the
urine output (particularly if Mannitol has been used) nor the CVP (especially in the presence of
lung injury or mechanical ventilation) provide a reliable assessment of volume requirements.
Instead, these estimations should be used in addition to physical examination and cardiovascular
stability, to arrive at an overall picture (10). In patients in whom mannitol is being used to reduce
the ICP it is particularly important to avoid a net fluid deficit. Hourly 1:1 replacement of urine
volume and electrolytes may be required (5). Diuretics have no routine place in the management
of head injury, except in the use of mannitol as an osmotic diuretic.
Intracranial pressure.
Ideally, all patients requiring admission to ICU because of blunt head injury and with a GCS
below 9 should have an ICP monitor of some sort in place, and active treatment to reduce the
ICP should be made once the ICP exceeds 20mmHg. There are a number of different monitors in
use, each with its own spectrum of complications and problems. The ventricular catheters have
the advantage that, in addition to measuring the ICP they allow removal of CSF to treat a raised
ICP. In many cases this may be the optimal treatment for a raised ICP. In the sedated and
ventilated patient, the decision to place an invasive monitor should be based on a combination of
the initial clinical findings and the CT scan results or further clinical developments. Any
deterioration is accompanied by a reconsideration of ICP monitor placement and re-imaging
(11). Changes in the ICP can then be used as a guide for therapeutic interventions such as
alterations in the blood pressure, C02 or the use of mannitol. Even better, inserting a jugular bulb
catheter (a fine bore single-lumen catheter in the jugular vein that is directed up, rather than
down, with X-Ray confirmation that its tip is within the skull), allows global cerebral blood flow
to be assessed through changes in the jugular venous saturation, and thereby permits even finer
therapeutic adjustments to the factors that control ICP and cerebral perfusion. In the absence of
these monitoring devices, management of the patient should be directed at avoiding known
secondary insults and maintaining a careful watch for signs of an increasing ICP - bradycardia,
hypertension, widening of the pulse pressure, deteriorating GCS, focal signs or pupil dilation. Of
these, an increase in pupil size is a late sign, which should not be awaited before repeat CT scans
are performed. In the presence of any of these signs, Mannitol 0.5g/kg is an appropriate initial
rescue therapy. Mannitol acts principally by creating an osmotic diuresis, and will not be
effective if the serum osmolality is >310 mOsm.
Cerebral Function Monitoring
This may be the only way of detecting seizure activity or arousal from inadequate sedation in the
paralysed patient. Its use is also important for the proper control of 'deep barbiturate coma' for
control of intractable ICP problems. However it does require experience and knowledge to
interpret the information, and therefore its appropriate use may not be practical in the DGH ITU,
because of the lack of availability of expert interpretation.
Feeding and Nutrition
Head-injured patients require feeding. Even if their injuries appear to be relatively limited, they
are in a hypercatabolic state - it is not good management to add starvation to trauma (12).
Paralysed patients should be fed at 100% basal metabolic requirements and unparalysed patients
at 140%. All patients should receive ulcer prophylaxis until feeding is established.
After intubation an orogastric tube should be passed to decompress the stomach – this can then
be used for feeding.
If enteral feeding is difficult to establish then consider cisapride / metoclopramide /
erythromycin or jejunal feeding tube.
Other management.
i. Antibiotics: The use of antibiotics will depend on any co-existent morbidity. There is no
indication for prophylactic antibiotics, even in a patient with an indwelling ICP monitor. The
choice of antibiotics will depend, as usual, on the presumed site of infection and the result of
bacterial cultures.
ii. Fitting: Patients already on anticonvulsants should be kept on them. Prophylactic use is not
indicated and they should only be given if seizures occur. Fitting increases the ICP and
cerebral oxygen consumption, and is therefore a potential cause of secondary head injury. It
should be controlled as soon as possible, using the normal means - Diazepam IV 0.2mg/kg,
followed by a loading dose of phenytoin (15mg/kg at a rate not exceeding 50mg/minute (in
adults)) or phenobarbitone (l5mg/kg at a rate not exceeding l00mg/min), and then
maintenance doses as appropriate (Phenytoin: l00mg 6/8 hrly, Phenobarb 50-200mg 6 hrly).
For intractable seizures consider giving thiopentone boluses or infusion.
iii. Calcium-channel blockers: With the exception of the use of Nimodipine in patients with
sud-arachnoid haemorrhage, the potential therapeutic use of calcium channel blockers in head
injured patients remains unclear (13).
iv. Propofol and Barbiturates: Approx 10% of patient with severe raised ICP will not
respond to the above therapies. Propofol and high dose barbiturate therapy has been shown to
reduce the ICP in these patients, with a consequent small, but real, reduction in mortality.
There is no indication for the prophylactic use of high-dose barbiturates. Barbiturate therapy
is titrated against achieving burst suppression on the EEG, the main complications being
hypotension, hypothermia, infection and prolongation of ICU admission. Boluses of
thiopentone can be useful preceding or during stimulating procedures – e.g. doses of 125250mg may reduced the rises in ICP in response to physio / suctioning. Vasopressor therapy
is almost always required in patients receiving high dose barbiturates (15).
vi. Hypothermia: Moderate hypothermia may help to reduce the ICP -temperatures of 32 - 35
degrees centigrade. Below about 32 degrees centigrade coagulation pathways can become
unreliable. If testing coagulation in a hypothermic patient, ensure that the lab performs the test
at the patient's actual temperature.
Transfers.
Transferring head-injured patients within or between hospitals is a particularly high-risk period
for the development of factors leading to secondary head injury. Every effort should be made to
anticipate these factors prior to transfer, and the necessary equipment kept to hand to deal with
them rapidly should they occur.
Action for suspected secondary injury or raised intracranial pressure
Check for:
a) Jugular venous drainage is optimized
b) Airway is clear
c) Ventilation – minute volume, compliance, CO2
d) Oxygenation
e) MAP target is being met
f) Adequate sedation /paralysis if necessary (remember pain and full bladder)
g) Evidence of seizures
In the mean while, hyperventilate temporarily, if necessary give oxygen 100% and:
a) Administer mannitol 0.5-1g/kg over 15 minutes – check circulating volume is OK
b) Organize urgent CT
c) Contact neurosurgeons for further advice
d) Check for and correct other factors such as pyrexia, hyponatraemia etc
Indications for re-scanning
a)
b)
c)
d)
After 24 hours particularly if 1st scan very early (2-6hrs post injury)
Sudden or persistent rise in ICP
Abnormal pupil responses, lateralizing signs
Prior to stopping sedation if not previously rescanned to check that signs of brain swelling
have settled.
Following the above points can lead to an increase in high-quality survival without a
corresponding increase in vegetative patients who would otherwise have died.
Suggested Intervention for the Management of Cerebral Oxygenation and Raised Intracranial Pressure
Cerebral Oxygen
-------------------Extraction Ratio(O2ER)
= Cerebral Oxygen Consumption (CMRO2)
------------------------------------------------Cerebral Oxygen Delivery (CDO2)
O2ER = SaO2 – Jugular Bulb Sv02
------------------------------ X 100
SaO2
Cerebral O2 Extraction Ratio <40%
-
Maintain current PaCO2
-
Observe
Cerebral O2 Extraction Ratio >40%
-
ICP <20mm Hg
ICP >20mm Hg
-
Decrease stimulation
Sedation / analgesia / paralysis
Treat any fever
Hyperventilate to an O2ER no greater than 40%
If ventricular drain in place, drain CSF with bag levelled at
26cm H2O
Mannitol 20% 0.25-0.5g/kg bolus If repeated boluses keep
serum osmolality <310mosm
Repeat CT scan to exclude expanding mass lesion
Increase MAP; if CVP low add volume, if CVP is OK then
use Dopamine or Noradrenaline
Consider barbiturate therapy
(normal range 25-35%
and not >40%)
-
Maintain Hb >10g/dl
If Hyperventilated, allow PaCO2 rise until O2ER <40% or ICP
>20mmHg
Consider nursing patient supine
Decrease stimulation
Sedation / analgesia / paralysis
Treat any fever
Increase MAP; if CVP low add volume, if CVP is OK then use
Dopamine or Noradrenaline
Consider barbiturate therapy
Maintain current PaCO2
Maintain Hb >10g/dl
Decrease stimulation
Sedation / analgesia / paralysis
Treat any fever
If ventricular drain in place, drain CSF with bag levelled at 26cm H 2O
Mannitol 20% 0.25-0.5g/kg bolus If repeated boluses keep serum
osmolality <310mosm
Increase MAP; if CVP low add volume, if CVP is OK then use
Dopamine or Noradrenaline
Repeat CT scan to exclude expanding mass lesion
Consider barbiturate therapy
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