MANAGEMENT OF TRAUMATIC HEAD INJURY MODES OF HEAD INJURY Contusion injury: Results from a direct force over the brain. It is histopathologically defined by areas of micro-haemorrhages often aligned at right angles to the cortical surface or as a confluent haemorrhage. Typically affecting gyral crests and progressing to areas of necrosis involving subjacent white matter. Axonal injury: Results from acceleration-deceleration mechanism of injury. It is histopathologically defined by an initial axonal deformation with interruption of axoplasmic transport and subsequent accumulation of cytoskeletal components, leading to axonal swelling. After 12h, there is distal axonal Wallerian degeneration. Deep punctate haemorrhages occur in areas of cleavage planes, where the variation of the angular momentum is more pronounced.

Fig 1: Mechanism of axonal injury

Initial Management

Resuscitation

This should be according to ATLS guidelines. Specific points: AVOID prophylactic hyperventilation (aim ETCO2 35-40mmHg) AVOID arterial oxygen desaturation (aim Sat O2>96%) ENSURE stabilisation of the cervical spine AVOID hypotension (BPs > 90mmHg) - Level II BTF

ICU admission Standard monitoring and line insertion.

Basic Management Principles

The basic principles in the ICU management of patients with severe brain injury are to identify any treatable surgical pathologies, and to prevent secondary brain injury by monitoring and control of intracranial pressure and cerebral perfusion pressure. Consideration must also be given to identification and management of any other non cerebral injuries sustained a. Decrease Risk of “SECONDARY INJURY” (“the golden hour”)

Maintenance of normothermia – specifically avoid hyperthermia Maintenance of normocapnia - aim ETCO2 35-40mmHg Avoid arterial oxygen desaturation (goal: O2Sat > 96% or PaO2 >60mmHg) Avoid hypotension (aim BPs > 90mmHg, lesser data regarding Mean Arterial

Pressure) Avoid sustained hyperglycemia as well as ANY episode of hypoglycemia

(shown to increase lactate production and brain injury Phenytoin load (15mg/kg) with maintenance (5mg/kg/day) to decrease risk of

early seizures (<7 days). Does not prevent delayed seizures.

The rationale for these measures is based in experimental models showing: More than 40% of all head injuries develop swelling and raised ICP. CBF is reduced in more than 50% of baseline during the first 24h after head

injury, with studies showing mismatch perfusion and histological evidence of ischemia.

Cerebral autoregulation and cerebral vasoreactivity are impaired within the 72h after a brain injury, being cerebral blood flow directly dependant on cerebral perfusion pressure and therefore to mean systemic blood pressure.

Prophylactic hyperventilation has been correlated with worse neurological outcome.

There is a trend towards cerebral hypoperfusion in early phases after brain injury, so an adjusted balance of oxygen delivery and consumption is necessary.

b. Treat Underlying Process

Neurosurgical intervention for evacuation of hematoma, repair of depressed skull fractures etc, if indicated.

ICP monitoring indications - BTF:

1).GCS <9 on scene post-resuscitation AND Abnormal CT head

2) GCS <9 on scene post-resuscitation AND Normal CT head with age>40yo and either:

Abnormal motor posturing or hypotension (MAP<50mmhg).

ICP monitoring has not been shown to improve outcome but allows titration of therapy. Raised ICP’s (>20) are associated with worse outcome.

Type of ICP monitoring: determined by local protocols:

Type of Catheter

EVD Camino Richmond-Bold

Position Intraventricular Intraparenchymal Subdural Advantages Monitoring and therapeutic

purpose, as drains CSF. Allows administration of intraventricular drugs.

Recognised Gold StandardNo drift

Recalibration in vivo

Inserted through a sheath that

allows monitoring of PTi02, tissue

temperature and microdialysis.

Can be calibrated under sterile conditions

Minimally invasive, it is

extraparenchymalMinimal risk of bleeding during

insertion.

Disadvantages Leads to ventriculitis if prolonged insertion (>10% risk infection beyond day

6 insertion) Insertion can lead to bleed

Can block or show poor transduction

Shows a phase shift related to

the days of insertion

Insertion can lead to bleed

Low reliability

Graphic representation of types of ICP Monitors:

c. Ensure Cerebral Perfusion Pressure (CPP) Aim for CPP > 60mmHg - 70 mmHg < -BTF (3,4)

Optimal fluid resuscitation (crystalloids, colloids. 4% Albumin not recommended in this population for trend towards increased mortality [SAFE study]).

Use of vasopressors Noradrenaline is the agent of choice in the unit,

The rationale for these measures is: CPP target therapy has shown to lead to better neurological outcomes than

an ICP target therapy. A CPP >60mmHg ensures brain perfusion without the systemic complications

related to pursuing higher levels of pressure – Ref Claudia Robertson 1999

Whilst the classical “vasodilator cascade of Rosner” approach advocated maintaining CPP>70 mmHg, the Lund approach advocated a CPP>50 mmHg – Ref Nordstrom 2003. The bottom-line is that the state of the cerebral autoregulation will determine whereas there is higher risk of vasogenic edema or tissue ischemia respectively.

Vasodilatory cascade of Rosner

d. Specific Treatment of High Intracranial Pressure 1. Step One

Ensure head up 30 degrees, if C--Spine stable Head in central position to avoid compression of jugular venous return and

minimize cerebral vascular congestion. CSF drainage through EVD monitor: height to be determined by neurosurgical

criteria. Daily quantity of CSF drainage as an marker of EVD dependency.

Maximise analgesia + sedation Ensure PaCO2 within acceptable limits are usually 35 + /– 2mm Hg Use of sedation scales BIS monitoring to avoid over sedation Follow up CT brain to exclude new neurosurgical indications and progress of

initial injuries. Exclude other pathological processes such as: traumatic dissection of carotids

or vertebral arteries; venous thrombosis; brainstem injury; posterior fossa compression.

2. Step Two

Osmotic therapy No level I evidence supporting the use of Mannitol versus hypertonic saline. Mannitol – Level II BTF.

- Dose of 0.25-1 gr /K as bolus - Avoid continuous infusions of Mannitol - Avoid hypovolemia secondary to induced osmotic polyuria. - Still controversial mechanism of action

Hypertonic saline - 3% saline versus 7.5% saline, versus 10% boluses. - Active provided blood brain barrier (BBB) is intact, by: Inducing

intracellular dehydration; Increasing cerebral vessel diameter and cerebral blood flow (CBF); improving blood rheology by increase cell deformability; decreasing neutrophil priming; decreasing glutamate reuptake.

- Avoid Na >160mmol and/or serum Osmolarity >320mOsm, to minimise risk of acute renal failure.

- No robust data supporting different types of hypertonic solutions.

Induced hypothermia - Achieved with: convective measures (cooling packs, cooling blankets) or

intravascular devices. - Muscle relaxants may be needed to avoid shivering, alternatively induced

hypermagnesemia has shown to reduce shivering (5). - Prophylactic hypothermia does not increase mortality and effectively

reduces ICP, if managed correctly. - Greater effect when sustained for > 48h and instituted early. - Associated with better Glasgow Outcome Scale (GOS) with targeted

temperatures 33-35 degrees C. - Unclear total length of treatment, degree of hypothermia and rate of

rewarming

3. Step Three Decompressive craniectomy Current studies have failed to demonstrate an improvement in neurological

outcome or in mortality but consensus inclusion criteria and a definition of the optimal timing are required (6).

2 international RCT: DECRA trial (7) and lately RESCUE trial (8) -currently in progress.

4. Step Four

Decrease metabolic rate and oxygen consumption with barbiturate or propofol induced burst-suppression (9)

Level II evidence for the use of barbiturates if refractory ICP –BTF Requires continuous EEG monitoring to ensure goal Propofol infusion < 4mg/k/h in adults (to avoid propofol syndrome) until

burst suppression. Thiopentone versus pentobarbital, only small randomised studies

suggesting benefit of Thiopentone at high doses (10). Risks involved with barbiturate coma: increased incidence of HAP/VAP,

drug interactions; critical illness polyneuro-myopathy enteral feed intolerance, rebound hyperkalaemia prolonged ICU stay.

Fig 2: Example of head injury management according to multi-monitoring:

Role of additional monitoring techniques

Neurological multi-monitoring: there is currently no data that shows a change in outcome by applying multi-monitoring strategies; however its usefulness relates to the specific therapy instituted (1,2). Multi-monitoring is applied depending on use of resources and local policies:

- Oximetry monitoring includes: NIRS spectroscopy: Near-Infrared wavelength of light penetrate the scalp and brain to few centimetres of death. These light waves are differently absorbed by oxygenated and de-oxygenated hemoglobin and cytocrome aa3. Based on the modified Beer-Lambert law, optical attenuation is quantified using reflectance spectroscopy.

PTi02: Through the insertion of intraparenchimal multi-channel pressure sensors, peri-contusional tissue oxygenation can be monitored to titrate perfusion pressure. (Values of <15mmHg during 30 minutes, increases mortality –Stiefel 2005).

SJ02: Retrograde jugular bulb oximetry catheters widely used in the past are currently more experimental due to the global rather than local information that provide. However, in difuse head injury has good correlation with tissue oxygenation and NIRS. It has been shown that values < 50% are associated with worse neurological outcomes Robertson 1993.

- Cerebral blood flow (CBF) monitoring: Transcranial Doppler for the assessment of cerebral autoregulation; diastolic perfusion pressures; differentiation between

hyperemia and post-traumatic vasospasm; intracranial hypertension or trend towards cerebral tamponade.

Normal CBF (diastolic flow preserved and normal PI index) Cerebral tamponade: reversed diastolic flow

- Metabolic: Microdialysis monitoring after the consensus conference in 2004,

microdialysis in association with other brain monitoring techniches may assist in delivery of targeted therapy for prevention of secondary injury; therefore instituted in patients with subarachnoid hemorhage and head injury allows monitor the following markers:

* Energy-related metabolites: glucose, lactate, piruvate (Lactate/piruvate ratio is batter marker of tissue ischemia than lactate alone) –Persson 1996

* Neurotransmiters: glutamate, aspartate, gamma- Aminobutiric. * Exogenous substances: drugs levels.

- Physiological monitoring: EEG or Compressed Spectra Array (CSA) for burst

suppression and BIS for depth of sedation.

Fast Fourier Transformation of multiple frequencies over time Other trials in TBI: -Progesterone as neuroprotective agent. Primary endpoint is mortality at 30 days after trauma. Key points:

CPP target therapy aiming for CPP>60 minimises systemic complications related to fluid overload and cardiovascular complications when compared with higher targets (CPP>70) and minimises episodes of hypoperfusion pressure when compared with CPP>50

Hyperventilation should not be applied in the absence of acute signs of herniation and/or without Microdyalisis monitoring

If required, early decompresive craniectomy needs to be considered in cases of refractory ICP.

Thiopentone coma is an effective measure to control ICP, and its use is supported by the BTF guidelines

Avoiding hyperthermia is a fundamental measure in the treatment of head injury

Questions:

1. With regards to hyperventilation in the acute phase of TBI: a)- It is safe and necessary when ICP is raised b)- Should never be applied c)-Hyperventilation may be necessary when signs of herniation d)-Hyperventilation is recommended for refractory ICP when metabolic monitoring such as Microdyalisis or cerebral blood flow monitoring is applied. e)-c and d are correct

2. With regards to ICP monitoring a)- It is necessary in all head injuries to allow early treatment b)- The Intraparenchimal monitors are the gold standard c)- Intraventricular drains have lesser risk of infections than intraparenchimal monitors

d)- Intraparenchimal monitors are routinely calibrated and show minimal phase drift e) – none of above is correct 3. With regards to cerebral blood flow after head injury a)- Cerebral autoregulation is normally impaired in acute phase of head injury b)-Cerebral microcirculation can show heterogeneous distribution c)- CPP target therapy has shown to be more physiological than ICP targeted therapy. d)- The classical CPP > 70 target has shown to lead to vasogenic edema and more systemic complications. e)- all of above are true 4. With regards to hypothermia a)- A 2001 Randomised control trial (Clifton et al) suggested that hypothermia did not change outcome and was associated with adverse effects, however the methodology of this trial was later on criticized, leading to the need of further studies. b)- Hypothermia is effective in reducing ICP and it is supported by the BTF guidelines. c)- The rate of hypothermia and rewarming as well as the length of hypothermia are still controversial d)- Active rewarming is contraindicated when hypothermia is applied e)- all of above are true. 5. In the treatment of refractory ICP a)-The use of Mannitol is supported by the BTF guidelines b)- The use of hypertonic saline is effective but there is no strong data showing advantage among different types of solutions. c)- Early decompresive craniectomy is currently being assessed on the RESCUE trial d) the DECRA trial included patients having a delayed decompresive craniectomy e)-all of above are true Answers:

1- e 2- e 3- e 4- e 5- e

Reference List

(1) Andrews PJ, Citerio G. Intracranial pressure. Part one: historical overview and basic concepts 7. Intensive Care Med 2004; 30(9):1730-1733.

(2) Hlatky R, Robertson CS. Multimodality monitoring in severe head injury 3. Curr Opin Anaesthesiol 2002; 15(5):489-493.

(3) Hlatky R, Furuya Y, Valadka AB, Robertson CS. Management of cerebral perfusion pressure 11. Semin Respir Crit Care Med 2001;22(1):3-12.

(4) Robertson CS. Management of cerebral perfusion pressure after traumatic brain injury. Anesthesiology 2001 December;95(6):1513-7.

(5) Wadhwa A, Sengupta P, Durrani J et al. Magnesium sulphate only slightly reduces the

shivering threshold in humans. Br J Anaesth 2005; 94(6):756-762. (6) Munch E, Horn P, Schurer L, Piepgras A, Paul T, Schmiedek P. Management of severe

traumatic brain injury by decompressive craniectomy. Neurosurgery 2000; 47(2):315-322.

(7) The DECRA trial (8) The RESCUE Trial (9) Angelini G, Ketzler JT, Coursin DB. Use of propofol and other nonbenzodiazepine

sedatives in the intensive care unit 1. Crit Care Clin 2001; 17(4):863-880. (10) Perez-Barcena J, Llompart-Pou JA, Homar J et al. Pentobarbital versus thiopental in the

treatment of refractory intracranial hypertension in patients with traumatic brain injury: a randomized controlled trial