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• To provide a consistent approach to TBI within PICU
• To minimise the incidence of secondary brain injury within PICU
This guideline is intended for all healthcare professionals caring for traumatic brain injury patients within the Paediatric Intensive Care Unit at the Royal Hospital for Sick Children, Glasgow.
All medical, nursing and allied professionals caring for patients who have traumatic brain injury should be familiar with the protocol.
Traumatic Brain injury (TBI) is a major source of mortality amongst older children. Public health measures have had the biggest impact on reduction in mortality and morbidity in recent years (safety helmets, seatbelts, speed reduction).
The intensive care management of these injuries focus on preventing secondary injury and being alert to a surgically remedial event. This includes trying to prevent or reduce any further factors that may increase brain injury. Avoidance of hypoxia, hypotension, pyrexia and hypoglycaemia are probably the only factors that clinicians agree should be avoided. There is general acceptance that trying to minimise further swelling of the brain and control the intracranial pressure (ICP) may be useful. Therefore in some brain injuries particularly if the GCS<8 and with an abnormal CT a direct monitor for ICP may be placed.
Maintaining the cerebral perfusion pressure (CPP) of the brain is felt to be even more important.
CPP= MAP -ICP
This formula is most useful when both the ICP and MAP are directly measured. See below for age-related values.
A basic strategy for preventing secondary brain injury is good basic intensive care. Sedate and minimise oxygen demand, employ minimal handling to prevent surges in ICP, oxygenate well, maintain blood pressure (therefore keeping CPP adequate), treat pyrexia and avoid hypoglycaemia.
Until fairly recently it was standard management to hyperventilate patients and aim for a low pCO2 – this definately reduced the ICP but as it works via cerebral vasoconstriction it also reduced oxygen delivery to the brain. A more conservative approach is now taken aiming for a low normal pCO2 (4.5-5 kPa) and only resorting to hyperventilation if there are concerns of impending cerebral herniation. Judicious use of inotropes to maintain and support CPP is important. There is some evidence that noradrenaline is superior to dopamine. However it is more important to maintain CPP than differentiate between agents.
If the above basic management fails other steps may be taken to control ICP. Mannitol and hypertonic saline (osmotic diuretics) are both highly effective at reducing ICP quickly. The debate as to whether one is superior to the other continues.
If the ICP is difficult to control sometimes an external ventricular drain (EVD) will be placed by the neurosurgeon. An EVD can be technically difficult to insert in a swollen brain and may require the aid of a volume CT scan which is only performed during the day. If an EVD is present then one response to raised ICP is to let some CSF drain out and allow the ICP to normalise. (See EVD guideline).
The evidence for all secondary therapeutic measures to reduce ICP and prevent secondary brain injury is patchy at best. There was and remains great hope on the basis of animal, neonatal and adult data that therapeutic hypothermia may minimise secondary brain injury. Cooling appears to improve survival and function in both neonatal encephalopathy and post-cardiac arrest in adults. However most head injury trials have failed to correlate cooling with improved survival. The only randomised controlled trial (RCT) in paediatrics to date cooled for 24hours and found no benefit. It may be that we just don’t know how long, how quickly or how cold to cool patients as yet to be effective. Alternatively in the future it may be that cooling is discounted as a treatment strategy. Meanwhile it is common practice to undertake cooling as a secondary intervention if ICP remains problematic. If actively cooling paralysis should be commenced to prevent shivering which increases ICP and oxygen demand.
Thiopentone coma remains a standard treatment when ICP is difficult to control but needs to be undertaken carefully. Thiopentone infusion will lead to a fall in blood pressure and measures must be in place to avoid this (eg. noradrenaline). CFAM monitoring or EEG should be used in conjunction with thiopentone coma aiming for a reduction in ICP primarily or burst suppression. Thiopentone is a particularly toxic substance which has a long half-life. An irritating side-effect of thiopentone is that it may induce fixed dilated pupils. This removes one of the key areas of brain function assessment when paralysed and sedated. Brain stem testing cannot be performed until thiopentone levels have fallen. A Cochrane Review concluded that barbiturate therapy did not improve outcome in head injury
Decompressive craniectomy is an age old surgical treatment which literally allows the rigid box of the skull to be opened. This allows room for the brain to swell and therefore reduces ICP. There is concern that decompressive craniectomy may increase survival but at a very poor functioning level (eg. persisitent vegetative state). A recent randomised study DECRA did not include children and failed to reveal a positive outcome. Decompressive craniectomy may have a place in a few well selected cases, current consensus is that outcomes may be improved if decompressive craniectomy is performed early.
The general aims of PICU management of children with severe head injuries are to meticulously maintain adequate oxygenation of the arterial blood, achieve a blood pressure that will perfuse the brain and an intracranial pressure of less than 20mmHg. It is also necessary to bear in mind continually the possibility of the development of an intracranial lesion that may require surgery.
Treat all TBI as having a C-spine injury
Oral ETT placed. (avoid nasal route as may have basal skull fracture). The aim of ventilation is to maintain adequate oxygenation with low normocapnia.
PaO2 >10 -13kPa PaCO2 4.5- 5 kPa
This should be achieved at the lowest possible PIP and PEEP (<5mmHg).
Some literature suggest there may be a place for Pressure Regulated Volume Controlled Mode of ventilation (ie SIMV Autoflow, rather than BIPAP). More important than mode is to measure end-tidal pCO2 continuously and react to changes.
Arterial gases should be performed at least 4-6 hourly in the first few days of admission. A change in end-tidal pCO2 or rise in ICP should result in a repeat gas.
Endotracheal suctioning (ETS) may produce significant (usually transient) rises in ICP. It remains necessary, but should be minimised and some means of prophylaxis –sedation boluses ( Fentanyl 2micrograms/kg IV) or endotracheal instillation of lignocaine 1% (max 2mls)- should be considered.
C-spine – ensure correct collar placement and careful moving and handling as per APLS guidelines. Log-roll –no straight lifting. See separate moving and handling guideline.
Hypotension should be considered an emergency
If adequate filling alone fails to produce an adequate blood pressure then judicious use of inotropic support will be necessary. Consider noradrenaline/ dopamine/adrenaline to titrate to BP. Arterial and central venous catheters will generally be placed to allow continual monitoring of arterial and CVP. Transducers will be levelled to the right atrium. Femoral lines are preferred in view of less disruption to cerebral venous return. Aim for a CVP 6-10mmHg.
Fluids: 0.9% saline (75-100% calculated maintenance) Glucose should be withheld from the IV solution if the serum glucose is above 10 mmol/l. When serum glucose reaches the normal range the IV solution should be changed to 5% dextrose/0.9% saline.
Avoid hypoglycaemia -if found treat quickly and ensure followed up carefully. Give 2ml/kg of 10% dextrose and repeat sugar at 30 mins and 1 hour minimum.
Electrolytes Hyponatraemia may produce further brain swelling in this context (particularly if inappropriate ADH syndrome occurs) therefore target:
[Na] at >140mmol/l and a serum osmolality of >280mOsm
Aim for normokalaemia.
Maintaining an optimal Cerebral Perfusion Pressure (CPP) is critical, as well as controlling the ICP.
CPP = MAP – ICP
Threshold for ICP
(or infants with
1.5 – 5 mmHg
3 –7 mmHg
but assess whether
3 – 7 mmHg
<10 – 15 mmHg
Agree target ICP and CPP for intervention for each individual patient with intensivist and neurosurgeon.
Neuro-observations must be performed regularly – every 30 minutes if an ICP monitor is not in-situ. 2 hourly if ICP monitor in place. Any changes should be alerted to a doctor.
ICP monitoring – If present be alert to changes. For set up and background to ICP -See separate ICP monitoring guideline.
If elevation of ICP is >20mmHg for >5min then move on to CONTROL ICP ALGORITHM
Analgesia and Sedation
Patients should receive an infusion of narcotic (morphine or fentanyl) and midazolam. Inadequate sedation should be a first consideration for raised ICP Once adequately sedated, a muscle relaxant may be added prn as a bolus to prevent coughing on suction. If cooled, paralysis should be delivered as a continous infusion to prevent shivering and its associated metabolic demands.
Patients have a high risk of seizures which can be difficult to recognise in a sedated +/- paralysed child. Seizures increase ICP substantially, therefore a prophylactic approach has been adopted. Load with phenytoin IV (18mg/kg over 30 mins) and then continue maintenance dose for at least 7 days.
When re-warming after hypothermia:
Infection and Sepsis
In the case of a patient who has no known radiological injury to the cervical spine and who is well sedated and immobile (paralysed), the purpose of the cervical collar is to serve as a warning of a potential neck lesion. The initial hard collar should be exchanged for a suitably sized long –term collar (eg.Miami –J). The collar should be left in situ but should be left open except when the patient is being moved to scan etc. or log rolled. The head should still be protected with sandbags either side. A sign should be placed above the bed declaring “ C-spine not cleared” .The collar must not be allowed to obstruct venous return or become a source of pressure necrosis. The collar MUST be fastened up again when the child is moved, log rolled, woken up or when the paralysis is discontinued.
• Good oxygenation at all times
• Avoid / Treat aggressively any drops in Cerebral Perfusion Pressure
• If these measures fail to control ICP: elevation of ICP is >20mmHg for >5min then move on to CONTROL ICP ALGORITHM
Treatment threshold is a sustained ICP rise above target limit for > 5 minutes.
Ensure all general management outlined is being achieved if not correct this first.
→ Consider mass lesion – CT SCAN & Neurosurgical Opinion
First Tier Therapy
If ICP still raised:
ICP STILL RAISED
Second Tier Therapies (all lack conclusive proof of benefit)
ICP STILL RAISED or impending cerebral herniation?
*Thiopentone is a potent and toxic drug. It acts on GABA A and offers cerebral protection. It should be used with caution, using the smallest dose possible and titrated to effect, aiming to lower ICP. CFAM monitoring should always be used. It accumulates over time as it undergoes zero-order kinetics. Levels need to be checked prior to being able to perform brain stem testing. Alternatively propofol infusion can be considered in older children but consider carefully propofol syndrome.
The above is intended as a guide. It may be more appropriate in individual cases to tolerate a mildly elevated ICP (eg. 25mmHg) rather than proceed to second tier therapies.
1. Intracranial Pressure Monitoring Guidelines – Neurosurgical Institute Glasgow
2. Medical Management of Traumatic Brain Injuries – PICU Guidelines – Alder Hey hospital, Liverpool.
3. Guidelines for the Management of Severe Traumatic Brain Injury – Birmingham
4. The Guidelines for the Acute Medical Management of Severe Traumatic Brain Injury in Infants, Children, and Adolescents. Paed Crit Care Med Supplement-2003
5. Dean NP, Boslaugh S, Adelson PD, Pineda JA, Leonard JR et al Physicians Agreement with Evidence-Based Recommendations for the Treatment of Severe Traumatic Brain Injury Journal of Neurosurgery 2007; 107(5 Suppl): 387-91
6. The Epidemiology of Urban Paediatric Neurotrauma: Evaluation of, and Implications for,Injury Prevention Programs. Neurosurgery:Vol 42(2);300-31
7. Pediatric Brain Injuries: The Nature, Clinical Course and Early Outcomes in a Defined United States’ Population. Kraus JF,Fife D, Conroy C. Pediatrics 1987; 79: 501-507
8. Epidemiology of Traumatic Brain Injury in Children Receiving Intensive Care in the UK. Parslow RC, Morris K, Tasker R, Forsyth R, Hawley C. Archives of Diseases in Childhood 2005;90:1182-1187
9. Report of Working Party on Management of Head Injuries – RCS (Lancet 1997;349:821-4
10. Quayle KS, Jaffe DM, Kuppermann N, et al. Diagnostic testing for acute head injury in children: when are head computed tomography and skull radiographs indicated? Pediatrics 1997;99:11–17.
11. Chambers I.R, Stobbart L, Jones P.A, Kirkham F.J, Marsh M, Mendelow A.D, Minns R.A, Struthers S, Tasker R.C et al Child's Nervous System 2005; 21 (3): 195-199 Age-related differences in intracranial pressure and cerebral perfusion pressure in the first 6 hours of monitoring after children’s head injury:association with outcome
12. Philip S, Chaiwat O, Udomphorn Y, Moore A, Zimmerman J.J, Armstead W Variation in cerebral blood flow velocity with cerebral perfusion pressure >40 mm Hg in 42 children with severe traumatic brain Crit Care Med 2009(37);11:2973
13. Tume L, Baines P, Lisboa P The Effect of Nursing interventions on the Intracranial Pressure in Pediatric Traumatic Brain Injury Nursing in Critical care 2011;16:77-84
14. White H , Venkatesh B Cerebral perfusion pressure in neurotrauma: a review Anesth Analg 2008;107:979-988
15. Wakai A, Roberts I, Schierhout G Mannitol for acute traumatic brain injury. Cochrane Database Syst Rev. 2005 19;(4):CD001049.
16. Knapp JM Hyperosmolar therapy in the treatment of severe head injury in children: mannitol and hypertonic saline. AACN Clin Issues. 2005;16(2):199-211.
18. Forsyth RJ, Parslow RC, Tasker RC, Hawley CA, Morris KP Prediction of raised intracranial pressure complicating severe traumatic brain injury in children: implications for trial design. Pediatr Crit Care Med. 2008 Jan;9(1):8-14.
19.Gluckman P ,Wyatt J,Azzopardi D, Ballard D et al Selective Head Cooling with Mild Systemic Hypothermia After Neonatal Encephalopathy Lancet 2005;365:663-670
20.Denis V. Azzopardi, Brenda Strohm, A. David Edwards, Leigh Dyet, Henry L. Halliday, Moderate Hypothermia to Treat Perinatal Asphyxial Encephalopathy N Engl J Med 2009; 361:1349-1358
21. The Hypothermia after Cardiac Arrest Study Group Mild Therapeutic Hypothermia to Improve the Neurologic Outcome after Cardiac Arrest N Engl J Med 2002; 346:549-556
22. McIntyre et al Prolonged Therapeutic Hypothermia After Traumatic Brain Injury in Adults Systematic Review JAMA 2003; 289(22):2992-9
23. Henderson, Dhingra V, Chittock D, Fenwick j, Ronco J et al Hypothermia in the Management of Traumatic Brain Injury Int Care Med 2003;29 (10):1637-44
24. Sydenham E, Roberts I, Alderson P Hypothermia for traumatic head injury Cochrane 2009
25. Clifton et al Lack of effect of induction of hypothermia after acute brain injury NEJM 2001;344:556-563
26. Biswas et al Treatment of acute traumatic brain injury in children with moderate hypothermia improves intracranial hypertensionCrit Care Med 2002;30:2742-51
27. Adelson P.D, Ragheb J, Muizelaar J, Kanev P, Brockmeyer D, Beers S et al Phase II Clinical Trial of Moderate Hypothermia after Severe Traumatic Brain Injury in Children Neurosurgery 2005;56(4):740-75
28. Hutchison JS, Ward RE, Lacroix J, Hébert PC, Barnes MA, Bohn DJ et al Hypothermia therapy after traumatic brain injury in children. NEJM 2008;358:2447-2456
29.Schierhout G, Roberts I. Anti-epileptic drugs for preventing seizures following acute traumatic brain injury. Cochrane Database Syst Rev. 2001;(4):CD000173
30. Roberts I Barbiturates for acute traumatic brain injury Cochrane Database Syst Rev. 2000;(2):CD000033.
31. Gough S, Tume L, Sinha A Efficacy of CSF Drainage on ICP Reduction After Severe Paediatric Traumatic Brain Injury. World Congress of Paediatric Critical Care, Geneva 2007
32. Sahuquillo J Decompressive craniectomy for the treatment of refractory high intracranial pressure in traumatic brain injury Cochrane Database 2009
33. Kan P, Amini A, Hansen K, White GL Jr, Brockmeyer DL, Walker ML et al Outcomes after decompressive craniectomy for severe traumatic brain injury in children. J Neurosurg. 2006;105(5 Suppl):337-42.
34. Jagannathan J, Okonkwo DO, Dumont AS, Ahmed H, Bahari A, Prevedello DM et al Outcome following decompressive craniectomy in children with severe traumatic brain injury: a 10-year single-center experience with long-term follow up.
J Neurosurg. 2007;106(4 Suppl):268-75.
35. Cooper DJ, Rosenfeld JV, Murray L, Arabi YM, Davies AR, D'Urso P et al Decompressive craniectomy in diffuse traumatic brain injury N Engl J Med. 2011 Apr 21;364(16):1493-502
Last reviewed: 01 March 2014
Next review: 30 November 2020
Author(s): J. Richardson
Co-Author(s): Anne McGettrick
Approved By: Paediatric Clinical Effectiveness & Risk Committee
Document Id: 12