guidelines for the management of traumatic brain injurytbi traumatic brain injury 4. references and...

DEPARTMENT OF CRITICAL CARE CLINICAL GUIDELINE

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Date: Mar 2017 Review Mar 2019 �1 Authors: IHL/GC/GR/JS/JW

Guidelines for the Management of Traumatic Brain Injury

AIM: To provide guidance on the management of patients with traumatic brain injury. SCOPE: All adult ICUs within Brighton and Sussex University Hospitals

Initial ABCDE

• Evacuate significant SOL• 30 degrees head up/tilt if no contraindications• Avoid venous obstruction• CPP 60-70 unless otherwise instructed by a

Consultant Neurosurgeon• ICP<20 mmHg• Optimise haemodynamic and volume status• PaO2>13kPa• PaCO@ 4.5-5 kPa• Core temperature 36-37 degrees• Propofol and Fentanyl +/- neuromuscular

blockade• Phenytoin/Keppra if indicated• Blood glucose 4.5-10 mmols• If LICOX brain oxygen 20-40mmHg and

temperature <37 degrees

Is ICP<20

mmHg and CPP>60-

70

Recent CTRisk of SOL low? CT scan

Does patient have significant

SOL?

YES

Evacuate SOL• Bolus sedation and increase• Consider neuromuscular blockers if not already used• Mannitol 20% 0.25-1 g/kg• Consider hypertonic saline• Volume, vasoactive drugs +/- PICCO• If >24 hours post-injury reduce PaCO2 4-4.5 kPa• Consider EVD• EEG- if this shows seizure activity commence/increase anti epileptics• Consider: • LICOX• Thiopentone coma• Decompressive craniectomy

YES

NONO

YESNO


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P4 Admission and C spine

P5 Initial neurosurgical management

P6 Specific management TBI

P7 Ventilation

P9 Sedation and analgesia

P12 NMJ blockers

P13 Barbiturate coma

P14 Mannitol and hypertonic saline

P17 Fluids

P18 Specific treatments to reduce ICP

P20 Temperature control

P22 Seizures and phenytoin

P27 General ICU Care

P28 Glossary

Appx 1 C spine clearance

Appx 2 Nerve stimulator use

Appx 3 Steroid deficiency screening

1. INTRODUCTION

Outcome and potential; for successful rehabilitation after brain injury depend on the primary brain damage and on the quality of early management, prompt diagnosis and treatment of mass lesions as well as preventing, limiting and treating processes leading to secondary brain damage.Complete standardisation of treatment is impractical, but a common “core approach” is desirable. The mainstay of head injury management is based on the concept that little can be done about the primary brain injury, but that a lot can be done to minimise secondary brain injury because the duration and severity of secondary insults influence outcome1.The trend in reduced mortality and improved outcomes from traumatic brain injury (TBI) has been the result of the use of evidence-based protocols that emphasise monitoring and maintaining adequate cerebral perfusion.

Much of the supporting evidence for the guidelines comes from:

EBIC: European Brain Injury Consortium 1997 guidelines based on consensus and expert opinion1

BTF: Brain Foundation Guidelines 2016 evidence based guidelines2



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�Pathophysiology

Damage to the brain following trauma includes the immediate (primary) injury caused by the impact itself and secondary brain injury developing in the hours or days after the initial impact.

PRIMARY BRAIN INJURY

• Disruption of brain vessels• Haemorrhagic contusion• Diffuse axonal injury• Haematoma

Duration and severity of secondary insults influence outcome. Head injury management in ICU is focused on preventing, detecting and correcting these secondary insults1.

SECONDARY BRAIN INJURY

Systemic secondary insults Intracranial secondary insults

Events Main causes Events Main causes

Hypoxaemia • Hypoventilation• Thoracic injury• Aspiration

pneumonia• Anaemia Hb less

than 80 g/l

Raised intracranial pressure and/or brain shift

• mass lesion• vascular

engorgement:• vasodilation• impaired cerebral

venous drainage (position, ET tube ties, coughing etc.)

• oedema• hydrocephalus

Hypotension • hypovolaemia• cardiac failure• sepsis• spinal cord injury

VasospasmStroke/infarction

• Traumatic subarachnoid haemorrhage?

Hypercarbia • respiratory depression

Seizures • cortical brain injury

Hypocarbia • hyperventilation, spontaneous or induced

Infection • skull base fracture• compound

depressed skull fracture

Hyperthermia • hyper metabolism• stress response• infection

Hyperglycaemia • hypothermia• i.v. infusion dextrose• stress response

Hypoglycaemia • inadequate nutrition

Hyponatraemia • dilution (SIADH)• hypovolemic (CSW)



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Admission and initial assessment

Initial Management of C spine

Recommendation (Action) Justification (Rationale)

Essential monitoring and access

Standard ICU monitoring plus:• wide bore oro-gastric tube or naso-gastric tube if no base of

skull fracture or suspected base of skull fracture. • Temperature monitoring• ICP monitoring if appropriate• BIS monitoring to ensure adequate sedation

Certain patients may need additional monitoring

1.Cardiac output monitoring:• To be inserted if no response to crystalloid and no response

to 0.1µg/kg/min of Noradrenaline• If acute or pre-existing cardiac disease• Systemic sepsis• Cardiac contusion• Pulmonary oedema2. Peripheral nerve stimulator if administering muscle relaxants3. Consider EEG if suspecting seizures or during barbiturate coma

Specific investigations above baseline

• Troponin if chest trauma or >50 yrs or if history indicates• Triglyceride level as baseline (specifically triglyceride not

lipid levels)• CK • Consider urine and serum osmolality and urine electrolytes

if polyuric• 9am Cortisol level in case of pituitary injury (must be off

steroids)


Clear the Cervical Spine if possible

The cervical spine should be cleared according Intensive Care Society (ICS) Guidelines (4) Appendix 1 or BSUH guidelines

If a hard collar is required change to an Aspen

This is less likely to cause ulceration

If injury detected Management of a detected injury must involve a consultant neurosurgeon

Recommendation (Action)


http://rxhws001/ICU/Home/ClinicalGuidelines/tabid/68/Default.aspx


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Initial General Neurosurgical Management

Clearing the Cx Spine If CT scans/X-rays are interpreted as normal by senior radiologist, the cervical spine may be assumed stable (this must be documented in the medical notes) and the hard collar can be removed.

It is strongly recommended that the thoracolumbar spine of a trauma victim who remains unconscious be cleared within 48-72 hours.

Beyond this time the morbidity and mortality of spinal precautions (secondary to skin ulceration, pneumonia, thromboembolism, and venous access and airway complications) probably exceed the risk of missed spinal injury4

Justification (Rationale)Recommendation (Action)


Sedation Fully sedated and analgesia, ± paralysis if required.

Ventilation SIMV as per ARDS ventilation guidelines • Target PaO2 > 13kPa• Target PaCO2 4.5-5.0kPa5

• Aggressive hyperventilation should be avoided unless PbtO2 is measured.

• Avoid PaCO2 <4.0kPa except in critical situations when a PaCO2 <4.0 kPa may be needed to “buy time” (e.g. prior to theatre or CT scan) but in these instances the patient must be on 100% O2.

• The decision to reduce PaCO2 to <4.0kPa must be made by a Consultant Neurosurgeon and Consultant Intensivist and ideally only with a LICOX in situ.

Consider surgery Early evacuation of SOL

Optimise CPP ICP < 20 mmHgCPP > 60 - 70mmHg2 Unless otherwise specified by the Consultant Neurosurgeon or LICOX suggests a lower CPP. 50-60mmHg can be considered in certain situations in consultation with the Consultant Neurosurgeon. Target CPP should never be <50mmHg

Target brain O2 PbtO2 20-40mmHg

Consider EVD Consider CSF drainage to manage intracranial hypertension

Manage temperature

Core temperature 36-37oC. Treat pyrexias vigorouslyBrain temperature < 37 oC

Optimise CVS Optimal haemodynamic and volume status




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Specific Management of Severe TBI

Prevent fits Tight seizure control

Feed Establish early enteral feeding within 24 hours if possible

Control glucose Blood sugar control 4.5-10.0 mmols (minimum of daily blood sugars, 2-6hrly if high)

Treat infection Treat established or clinically significant infection vigorously



ICP monitoring ICP should be monitored in all salvageable patients with a severe TBI (GCS3-8 after resuscitation) and an abnormal CT scan. An abnormal CT scan of the head is one that reveals haematomas, contusions, swelling, herniation or compressed cisterns.2

ICP monitoring is indicated in severe TBI with a normal CT scan if two or more of the following features are noted at admission :age over 40 years, unilateral or bilateral motor posturing, or systolic blood pressure (BP) <90 mmHg.

Maintain SBP at >100mmHg for patients 50-69 years old or at >110mmHg or above for patients 15-49 or over 70 years ol, may decrease mortality and improve outcomes.2

The Councils of NACCS and SBNS would recommend that when calculating CPP in TBI the MAP used in the equation CPP=MAP−ICP should be the mean cerebral arterial pressure estimated to exist at the level of the middle cranial fossa, which can be approximated by positioning (levelling) the arterial transducer at the tragus of the ear. They also recommend that the arterial transducer is repositioned to remain levelled with the tragus following changes in body elevation or position.

Targets Initial management is directed at maintaining ICP < 22mm Hg and CPP > 60 - 70mm Hg

LICOX If brain tissue oxygen monitoring (LICOX) in use then increase CPP in stages and record PbtO2. Then set optimal CPP parameter to achieve PbtO2




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Ventilation

Autoregulation Patients with intact pressure autoregulation tolerate higher CPP values2.Aggressive attempts to maintain CPP above 70mmHg is associated with an increased risk of developing adult respiratory distress syndrome2

Evacuate Ensure early evacuation of intracranial space occupying lesions.

Drain If ICP > 25mmHg persists consider external ventricular drain (EVD) and cerebrospinal fluid (CSF) drainage

Hyperaemic phase After 24 - 72 hours a hyperaemic phase can occur in 25 - 30% of patients, where autoregulation starts to recover with improved cerebral blood flow and this can continue for 7-10 days. During this phase, the combination of hyperaemia, intracranial inflammation and altered blood –brain permeability may result in vasogenic cerebral oedema. In this context, medical therapies directed at maintaining adequate cerebral perfusion pressure may result in increased intracranial pressure. During this phase the lower cerebral perfusion pressure may be acceptable In some circumstances a CPP of 50-60mmHg may be acceptable2. This decision must be discussed with the consultant neurosurgeon. Target CPP should never be <50mmHg



Justification (Rationale)

Initial ventilation Ventilate on SIMV for minimum of first 48 hours then consider BIPAP. Use ARDS net ventilation guidelines PBW Vt 6ml/kg.(http://rxhws001/ICU/Home/GuidelinesProtocols/ClinicalGuidelines/tabid/68/Default.aspx)

Ensure that VT and minute volume are constant

• Variations in ventilation will result in PaCO2 fluctuations and episodic rises in ICP. The fluctuations can have a significant detrimental effect on cerebral blood flow. Set alarm limits for minimum volume close to desired target (± 0.5 L) to detect varying minute volume due to changes in respiratory compliance.

• Remember when adjusting ventilation that only small changes should be made, one at a time, and time allowed for these to take effect. Monitor blood gases 15-20mins after all changes in ventilator settings and record response to change.



http://(http://rxhws001/ICU/Home/GuidelinesProtocols/ClinicalGuidelines/tabid/68/Default.aspx)


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Monitor blood gases Target PaO2 = 13 kPa (A lower PaO2 = 11kPa may be acceptable in patients who have a previous history of lung disease).

Target PaCO2 4.5 – 5.0 kPa

If more than 24 hours post injury and ICP> 25mmHg persists consider PaCO2 4.0-4.5 kPa in conjunction with brain oxygen monitoring (CBF is considerably reduced in the first 24 hours so hyperventilating the patient at this stage to a PaCO2 < 4.5 kPa may significantly increase the risk of ischaemia5)

Aggressive hyperventilation should be avoided unless PbtO2 is measured.

Avoid PaCO2 < 4.0 kPa if PbtO2 is not measured except in critical situations when a PaCO2 <4.0 kPa may be needed to “buy time” (e.g. prior to theatre or CT scan), but in these instances the patient must be on 100% O2. The decision to reduce PaCO2 to <4.0kPa must be made by a Consultant Neurosurgeon and Consultant Intensivist

On transfer to CT scan use ETCO2 and ICP blocks from patient’s bedside monitor in transport monitor. Stabilise PaCO2 and check correlation of PaCO2 with ETCO2 prior to moving patient.

Acute Lung Injury Acute lung injury (ALI) is common after traumatic brain injury and occurs secondary to direct pulmonary injury, aspiration injury, neurogenic pulmonary oedema and may occur as a complication of the induced arterial hypertension used to maintain CPP constant in the presence of raised intracranial pressure.Diagnosis requires acute onset of bilateral pulmonary infiltrates on chest X-ray, a PaO2/FiO2 ratio < 300 mmHg or 40 kPa and no clinical evidence of left atrial hypertensionFor guidance on managing sepsis induced ALI/ARDS see Surviving Sepsis Guidelines20 and ARDSnet guidelines on intranet.




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Sedation and Analgesia

Neurogenic Pulmonary Oedema

Neurogenic pulmonary oedema occurs in the absence of underlying heart and lung dysfunction and may occur within minutes to hours of the injury or it may have a delayed onset. The pathogenesis is not clear. It is believed it is caused by a massive sympathetic discharge with resultant systemic and pulmonary hypertension leading to increased pulmonary capillary pressure leading to oedema or by a neurally induced increase in capillary permeability or an element of both.Symptoms usually resolve in 24 – 72 hours.Treatment is supportive and should focus on maintaining pulmonary function while preventing increases in ICP. Therefore activities associated with patients with diagnosed pulmonary oedema such as frequent suctioning and turning should be done with caution. Treatment Urgent discussion with ConsultantVentilation managementIncreased inspired O2 concentrationControl of CO2 Increased PEEP with caution to avoid unacceptable rises in ICPConsider alteration in mode of ventilation (Consultant intensivist decision)



Justification (Rationale)

Initially Propofol and Fentanyl

• Propofol 2% 2-4mg/kg/hour - maximum 400 mg/hr (20mL/hr of Propofol 2%)

• Monitor for signs of Propofol Infusion Syndrome – see table 1.

• Propofol is contraindicated for the sedation of ventilated children receiving intensive care aged 16 years and below. Propofol should only be given in the very short term and for no longer than 24 hours in this age group. Particular caution should be used when administering Propofol to patients who are 17-18 years of age.

• Fentanyl 1-6 micrograms/kg/hr -maximum 600 micrograms/hour (12mL/hour of fentanyl 50mcg/mL)

• Prior to increasing dose consider using a test bolus of 25mcg (with caution) to see the impact on ICP. If test bolus has no impacts then consider appropriateness of increasing dose. Need to consider this bolus!!!!

• If rapid sedation reversal is anticipated within 24 hours or difficult to manage patient’s intracranial pressure consider Propofol and Remifentanyl as per BSUH ITU Remifentanyl guideline. This decision must be made in consultation with the consultant.




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Consider changing at 48 hours

• After 48 hours if long term sedation seems likely e.g. weaning is not imminent, neurological assessment is not planned, or there is not a possibility of brain death critieria then consider a change sedation to:

• Morphine 1-15mg/hour (1-15ml/hour of 1mg/ml concentration)

• Midazolam 1-15mg/hour (1-15ml/hour of 1mg/ml concentration)The rationale for administering dosages greater than this should be documented in the medical notes and reviewed at least once daily.

Bolus A Propofol bolus of 10-20mg (1-2mL of propofol 1%, or 0.5 – 1mL of Propofol 2%)can be considered to allow nursing, medical or physiotherapy intervention if required, but be aware of the potential hypotensive effect.

Beware withdrawal

Avoid excessive doses of Morphine. Ensure adequate analgesia and then if necessary, increase Midazolam (within prescribed dosage range) rather than Morphine to manage intracranial pressure. Tachyphylaxis is extremely common with morphine infusion leading to a possible need for dose escalation and a prolonged period of “withdrawal” when therapy is discontinued2. Tachyphylaxis and withdrawal symptoms may also occur after prolonged use of fentanyl2.

Use scoring systems

Use sedation scoring and in the acute phase - aim for no eye opening, no limb movements, no coughing spontaneously or on suctioning and no respiratory effort.

Maintain BIS score between 20-30 initially, depending on ICP.

In the acute phase sedate to level to-4 on Ramsey Agitation and Sedation Score and maintain BIS score between 35-50 based on clinical judgement. Aim for a score that maintains the ICP below 20mmHg

Consider NMBs

If ICP >25mmHg persists ensure patient is on maximum sedation and analgesia and consider neuromuscular blockade




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Table 1 Propofol Infusion Syndrome

PROPOFOL INFUSION SYNDROME 11-15 Caution should be exercised when using doses of Propofol in excess of 4mg/kg/hour and for longer than 48 hours1Symptoms typically become evident 24-48hrs into the infusion at infusion rates >4mg/kg/hr Consider stopping Propofol if arrhythmias or metabolic acidosis.

EARLY MARKERS COMMON CLINICAL FEATURES

PREDISPOSING FACTORS

Unexplained metabolic acidosis

Metabolic acidosis Young age

Elevated serum lactate, creatinine kinase and myoglobin or hyperlipidaemia/triglycerides

Cardiac arrhythmias particularly bradycardia

Severe head injury

Early sign is Rt BBB with convex-curved ST elevation in the right precordial leads.Brugada like changes. Cases of Lt BBB have also been seen

Severe critical illness of central nervous system or respiratory origin

Hyperkalaemia High dose exogenous catecholamine or steroidadministration

Rhabdomyolisis Inadequate carbohydrate intake

Hyperlipideamia Subclinical mitochondrial disease

Hepatomegaly Sepsis

Renal Failure

Rapidly progressive cardiac failure which may be unresponsive to inotropes

Send serum on a daily basis for triglyceride levels and CK if patient on doses of Propofol 4mg/kg/hr or on Propofol for longer than 48 hours. Lactate should also be monitored on a regular basis. (CK avoid over interpreting minor increases. CK values associated with rhabdomyolisis are very high.)



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Neuromuscular blockade


Should be considered if ICP remains high or is LABILE despite full sedation.

• A BIS monitor must be in place to ensure patients have adequate analgesia and sedation prior to administration of neuromuscular blockade.

• Neuromuscular blockade masks neurological changes and potential seizure activity. It is also associated with a longer intensive care unit stay due to an increased incidence of pneumonia. Therefore the appropriateness of its use should be reviewed on a daily basis.

• Using Cisatracurium 150mg/30mL (5mg/mL or 5000 micrograms/mL) as per National Injectable Medicines Guide Monograph administer an initial bolus dose of Cisatracurium 150 micrograms/kg (calculate using patient’s ideal body weight if they are obese) followed by a continuous infusion of 180 micrograms/kg/hr titrated to achieve 1-2 twitches using the train of four test.

• Usual dose range 30 – 600 micrograms/kg/hourA peripheral nerve stimulator must be used when administering neuromuscular blockade.

•

PNS • Instructions for setting up and using the peripheral nerve stimulator are in Appendix 1.

• Prior to commencing the neuromuscular blockade the supramaximal stimulation -SMS which is a baseline response for the particular patient should be identified using the peripheral nerve stimulator, (Appendix 1).

• The SMS should be recorded on the patients observation chart. If you are not able to identify the SMS e.g the patient is already receiving a neuromuscular blockade then an SMS of 50mA for a normal adult or 60mA for an obese adult can be used.The peripheral nerve stimulator (PNS) delivers 4 pulses over 2 seconds (train of four).

• The use of a PNS minimises the complications of prolonged paralysis by monitoring the degree of neuromuscular blockade.

• After starting the continuous infusion allow time for drug to reach a steady state, at least 0.5 – 1 hour then the train of four test should be performed hourly until the goal of 1-2 twitches is achieved17



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Table 2 Management of Cisatracurium infusion using PNS

Specific Drugs

0 twitches Reduce infusion by 20% increments until 1-2 twitches

achieved.

1 – 2

twitches

Maintain present infusion rate

3 twitches Reload with 75micrograms/kg Increase infusion rate by 50%

4 twitches Reload with 150micrograms/kg Increase infusion rate by

100%


Barbiturates • High dose barbiturate administration is recommended to control elevated ICP refractory to maximum standard medical and surgical treatment (level IIb evidence)2. should only be given on the instructions of a Consultant Neurosurgeon in consultation with the Consultant Intensivist.

• Haemodynamic stability is essential before and during barbiturate therapy2. Follow Thiopental guidelines on intranet. http://rxhws001/ICU/Home/GuidelinesProtocols/ClinicalGuidelines/tabid/68/Default.aspx

• Monitor the BIS during barbiturate coma therapy. The bispectral index value and the suppression ratio values have shown to correlate well with the standard EEG based method to titrate barbiturate therapy.

• Aim for BIS values of 10-20 and SR values of 60-80%. This has been shown to correspond to 3-5 bursts per minute on EEG.

• Hypokalaemia has been reported commonly in patients receiving Thiopental infusions15. The fall in serum K+ is not due to an increase in urinary excretion of potassium, it is thought to be due to metabolic changes within the brain. Therefore any potassium supplementation may lead to hyperkalaemia if the Thiopental infusion is ceased. Supplement low plasma K+ cautiously, if ECG changes indicate need.


http://rxhws001/ICU/Home/GuidelinesProtocols/ClinicalGuidelines/tabid/68/Default.aspx


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Mannitol • Hyperosmolar therapy works not only by reducing ICP through simple brain dehydration but also by reducing brain viscosity, leading to improved microcirculatory flow of blood constituents and consequent constriction of the pial arteries, resulting in decreased cerebral blood volume and intracranial pressure.

• Mannitol is effective for the control of ICP and may be required if intracranial hypertension persists, if unilateral pupillary dilatation or unilateral progressing to bilateral dilatation. (Primary bilateral dilatation may represent fitting, drug intoxication or overdose, or overwhelming brain injury).

• If a patient is requiring repeated doses of Mannitol to control ICP they should have a LICOX considered.

• Mannitol 20% (20g in 100mls): 1.25 – 5mL/kg (0.25-1g/kg) over 15-30 minutes. This can be repeated 6hrly if serum osmolarity remains < 320mOsm/L. (Mannitol elevates plasma osmolarity thus enhancing diffusion of water from the cerebrospinal fluid). Arterial hypotension (systolic blood pressure<90mmHg) should be avoided.

• A serum osmolarity of 300 – 320 mOsm/L is recommended for patients with poor intracranial compliance/elastanceMannitol administered when the patient’s serum osmolarity has risen above 320 mOsm/L is likely to lead to renal failure, metabolic acidosis and death23.

• Crystallisation of mannitol 20% can occur during storage particularly if the solution is very cold. Solutions may be warmed to dissolve crystals but it must always be administered via a buretrol administration set with a 15micron in-line filter added. The filter should allow an adequate flow rate to administer Mannitol over 15-20mins (e.g. Alaris Ref No: MFX1822 which flows at 7.4mls/min) Solutions should not be administered if crystals are visible.




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Hypertonic Saline • Studies suggest that hypertonic saline may be an effective adjuvant or alternative to mannitol in the treatment of intracranial hypertension2. If Intracranial hypertension persists following two doses of mannitol consider hypertonic saline in conjunction with LICOX.

• Sodium Chloride 5% intravenous 500ml Polyfusor (Management of intracranial hypertension is an unlicensed indication)

• Dose 1-2ml/kg infused slowly over 15-20 minutes • Can be given up to every 4-6 hours if needed • Maximum daily dose 8ml/kg over 24 hours.• Must be administered via a central line Monitoring

including criteria for stopping:Hyponatraemia should be excluded prior to administration (Hypertonic saline infusion bears the risk of central pontine myelinolysis when given to a patient with a pre-existing chronic hyponatraemia).

• Twice daily serum sodium levels and daily measurement of serum osmolality, serum potassium and chloride. Check chloride prior to use if metabolic acidosisAvoid use if hyperchloraemia

• Not to be administered to patients with a serum osmolality > 320mOsm/L or serum sodium level > 155 mmol/L without consultant approval.

Contraindications serum osmolality > 320 mosmserum sodium level > 155 mmol/L(In some patients a serum osmolality of 325 mosm/L and a serum sodium of 160 mmol/L will be tolerated but this must be a consultant decision)

Unwanted effects sodium overloadrapid infusion can cause cardiac arrest or circulatory overloading. Use with caution in patients with impaired renal function, cardiac failure, pulmonary oedema and the elderly.

Interactions No clinically significant interactions.

Incompatibilities Amiodarone, amphotericin, and sodium nitroprusside are always incompatible with saline..

Tranexamic acid There are currently three randomised trials of tranexamic acid versus placebo in patients with isolated TBI the most well know being CRASH 3, due to the uncertainty of whether tranexamic acid improves outcome no patient with an isolated head injury should receive it unless in the context of a random controlled trial.




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�Recommendation (Action) Justification (Rationale)

Steroids • The use of steroids is not recommended for improving outcome or reducing ICP. In patients with severe TBI, high dose methylprednisolone was associated with increased mortality and is contraindicated( CRASH trial)

• Approximately 15%–20% of TBI patients may develop chronic hypopituitarism, which clearly suggests that TBI-induced hypopituitarism is a frequent problem, in contrast with previous assumptions. However, there are no epidemiological studies showing the burden of the disease in the population. Post-traumatic hypopituitarism is generally characterized by isolated anterior pituitary hormone deficiency rather than multiple hormone deficiencies, and growth hormone deficiency seems to be the most common disorder.

• Current evidence implies that insufficiency in the hypothalamic-pituitary-adrenal axis during the acute phase after head trauma is associated with a worse neurological outcome, increased need for vasoactive drug therapy due to hemodynamic instability, relative or absolute hypoglycaemia, hyponatraemia, and rapidly progressive hypotension, all of which may increase the risk of morbidity and mortality.

• Therefore, the emphasis during the acute phase of brain injury should be on detecting adrenal insufficiency although this is reported as anything from rare 4% to frequent 78%. (See Appendix 3)

Chronic problems In the chronic phase most of the pituitary hormone deficiencies improved over time, but there have been reports of significant rates of pituitary hormone deficiency 5 years after TBI (28% growth hormone, 4% ACTH, and 4% gonadotropin)



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�Fluid management


Intravenous fluids • Fluid input: 2.5-3.0 litres / 24 hours unless otherwise indicated

• Maintain hydration with early enteral feeding• Supplement with IV 0.9% Sodium Chloride or

Hartmanns if enteral feeding not established/ appropriate.

• 0.45% Sodium Chloride if hypernatraemic (>150 mmol/L) and IV fluid needed.

• Treat low volumes with Hartmans / RBCs as appropriate to maintain haemodynamics with:

• Hct 30-35% (Hb 8-10g/dl)• Normal or near normal clotting, especially

postoperatively.• Platelet count > 100,000• PT 11-14 seconds• APPT 22.5-34.5 seconds • Avoid dextrose/saline as routine maintenance fluid

Renal • Urine output~ 0.5-1 ml/Kg/Hr• Urine specific gravity should be measured daily, more

frequently if urine output is in excess of 250mls/hr• Diabetes insipidus should be suspected if urine output >

250mls/hr for more than 3 hrs and specific gravity <1005. Confirm by measuring plasma and urinary osmolalities and electrolytes.

• In DI plasma osmolality rises with a marked rise in Na+ > 150 mmols/l and urine osmolality is very low with low electrolyte concentrations. In later stages diuresis may be appropriate (do they have a low plasma and urine osmolality, do they have a previous high cumulative balance)

• If confirmed on laboratory results, urine output continuing to rise and plasma Na+ >155 mmols/l give DDAVP 0.5micrograms – 1 micrograms subcutaneously. Replace fluid with 5% Dextrose or enteral water.

• If Na+ < 135mmols/l consider hypovolaemic hyponatraemia (Cerebral Salt Wasting) or Syndrome of Inappropriate Antidiuretic Hormone (SIADH)

• To assist in defining the abnormality a sodium clearance calculation can be provided from the laboratory by sending a timed sample of urine (e.g. 6 hours) in a plain bottle along with a plasma sample. This must be sent to the pathology department with a request for a Lolinogram profile.



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�Specific treatments to reduce ICP


Decompressive craniectomy • Decompressive craniectomy, the surgical removal of a portion of the skull (unilateral or bifrontal) may be performed to relive elevated intracranial pressure. place of this therapy remains controversial.

• In the first large randomised in 2011 the DECRA trial showed there was no benefit from bifrontal surgical decompressive craniectomy to reduce intracranial pressure although the definition of refractory intracranial –pressure elevation of >20 mmHg for 15 minutes within a one hour period was called into question.

• Since then the RESCUEicp trial has addressed these concerns by defining the refractory intracranial –pressure elevation(>25mmHg for 1-12 hours) this trail showed better intracranial pressure control in the surgical group , lower mortality but higher rates of vegetative states, lower severe disability and upper severe disability in the surgical groups. The rates of moderate and good recovery were similar in the two groups. The rates of upper severe disability (patients who may be independent in the home but rely on others for assistance outside the home) did not show a favourable outcome in the surgical group compared with the medical group at 6 months(42.8% and 34.6% respectively=0.12) but there was a significant difference at 12 months(45.4% vs 32.4%;P=0.01).

• In view of these results the decision to perform this procedure most be a consultant decision, which has involved the patients surrogates in discussions focusing on patient’s previously stated wishes and personal values and emphasizing that lifesaving procedures may not lead to a return to normal functioning, with particular regard to the larger proportion of survivors in the vegetative state in the surgical group.

Cerebrospinal Fluid Drainage • An EVD system zeroed at the midbrain with continuous drainage of CSF may be considered to lower ICP burden more effectively than intermittent use ( Level III) 2.

• Use of CSF drainage to lower ICP in patients with an initial Glasgow Coma Scale (GCS)<6 during the first 12 hours after injury may be considered( Level III) 2



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�Additional Brain monitoring


LICOX There is NO level III evidence that supports the use of jugular venous saturation and brain tissue oxygen monitoring, in addition to standard intracranial pressure monitoring2. The LICOX brain tissue oxygen monitoring system provides direct, real-time measurement of partial pressure of brain tissue oxygenation (PbtO2)Consider insertion in patients with unstable/labile ICP and/or potential for secondary brain oedema. For management of LICOX please see full guidelines

Oxygen Challenge Test

After insertion of the PbtO2 catheter it takes 1-2 minutes before the local brain oxygen tension is correctly displayed. However the readings are influenced by the local microtrauma of probe implantation into the brain tissue so may not initially represent the oxygen tension of the surrounding tissue. This stabilisation time may be as long as two hours. The PbtO2 values displayed during this initial phase after implantation therefore do not provide relevant information about tissue oxygenation.After brain tissue has had time to settle from the initial insertion, perform an oxygen challenge particularly if the PbtO2 reading is unexpectedly low or there is a question of probe accuracy, reliability or validity. To do this, place the ventilator FiO2 on 100% for 2 to 5 minutes. An accurate probe will demonstrate an increase in PbtO2. If the PbtO2 does not rise check all connections and cables etc. then repeat the challenge if there is still no rise in PbtO2 consider CT scan to check correct positioning of catheter. Aim to maintain PbtO2 20-40mmHg and ICP < 20mmHg – follow LICOX algorithms (see LICOX guidelines)Complete LICOX data chart when you make changes as a result of brain tissue oxygen reading to monitor effect of intervention. IMPORTANT: When removing the LICOX loosen the compression cap on the introducer and remove sensors before removing bolt



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Physiological Consequences of TBI

Hyperthermia


Hyperthermia should be avoided

• Hyperthermia following TBI may be due to post-traumatic cerebral inflammation (often seen in the first 24 hours), direct hypothalamic damage (known as neurogenic fever or central fever, is not usually seen in the hyperacute phase) or secondary infection.

• If the patient has an unexplained fever and they have sustained a DAI or frontal injury there should be an increased suspicion of neurogenic fever.Increased temperature in the post injury period is associated with poorer outcomes.

• For every 1oC rise in body temperature there is a 13% increase in the metabolic rate25. It is important to establish the cause of the hyperthermia as they need to be treated differently. The diagnosis of neurogenic fever is currently a diagnosis of exclusion24.

• There is currently no consensus regarding the most efficacious therapeutic strategy to treat hyperthermia following TBI.Hypothermia is well known for its ability to reduce intracranial pressure however it bears risks, including coagulopathy, immunosuppression and arrhythmia and currently it is not recommended as a recent trial demonstrated that hypothermia to 32-35oC worsened clinical outcome and increased mortality compared to standard care alone.

• Maintain core temperature at 36-37 oC (Core temperature may underestimate brain temperature at a time when the brain is vulnerable to secondary insult25).If no PiCCO in situ consider monitoring core temperature with an oropharyngeal or nasopharyngeal probe (a nasopharyngeal probe should not be used in patients with of base of skull fracture or suspected base of skull fracture).

• If LICOX system in situ maintain brain temperature at < 37oC Identify the cause of the pyrexia (It may be due to a combination of central damage and secondary infection). Pyrexia should be treated aggressively

Infection Screen for infection and treat if indicated.




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Sympathetic Storm

Active cooling • Discuss appropriate method of cooling with medical team.

• To maintain normothermia use antipyretic e.g. Paracetamol and consider using Medicool System.• Each pack contains 2 sets (one blue and one white) 1

x blanket, 1 x cap, 1 x groin pads and 2 x axilla pads made of water absorbing polymer.

• Immerse the blue set in water and then place in plastic bag in freezer. Once frozen apply the blue set to the patient and place the white set in the freezer. Change the blue set for the white set after two hours and repeat the cycle.

• When changing sets monitor skin for signs of thermal burns. It may only be appropriate to apply the cap in cases where hypothermia (33-35oC) is being induced. The seam at the top of the cap will need to be undone prior to freezing to allow for ICP/LICOX monitoring. Record changing of sets on ventilator chart.

• Cautions when using Medicool system: • Shivering should be avoided as it increases oxygen

consumption through aerobic muscle activity25. If actively cooling patient must be on a paralysing agent.

• Monitor skin for thermal burns when changing sets. If you are concerned about the skin the ice packs can be placed over a gown or similar.

• If inducing hypothermia insulin resistance may develop. Monitor Blood glucose 1-2hourly and commence sliding scale insulin if indicated.



Sympathetic Storm • Dysautonomia, sometimes referred to as sympathetic storming, is an exaggerated stress response that occurs in 15-33% of patients with severe traumatic brain injury. It can occur within the first 24 hours or up to 2 weeks after injury.

• Signs and symptoms include posturing, dystonia, hypertension, tachycardia (> 130), pupillary dilatation, diaphoresis, hyperthermia (> 38.5oC), and tachypneoa (>20b.p.m.).

• The precise mechanism for the increase in activity of the sympathetic nervous system is unknown but is believed to be a stage of recovery. It is more common in patients with diffuse axonal injury.

• In sympathetic storming the feedback mechanism, when the parasympathetic nervous system dampens down the effect of increased activity, does not occur.




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Control of Seizures

• Episodes can be unprovoked with the signs and symptoms occurring within seconds and can vary from episode to episode. Triggers that may precede an episode include suctioning, repositioning, environmental sensory stimulation (alarms etc.) or fever.

• It is important to identify the triggers so measures can be taken to reduce the length of the episode, lessen its intensity or even abort the episode.

• Diagnosis is usually based on clinical examination, but can be confirmed by elevated serum levels of adrenaline or catecholamines (samples are needed before and during episodes).

• Careful assessment is needed as the differential diagnoses include, an expanding lesion or oedema, seizures, deep vein thrombosis, pulmonary embolus, malignant hyperthermia, central fever, and drug or alcohol withdrawal.

• Medical management focuses on treating the signs and symptoms in order to reduce the potential adverse effects of prolonged activity of the sympathetic nervous system.

Medications In Intensive Care I.V. medications e.g. fentanyl, morphine, midazolam or clonidine are first line drugs used to control the episodes. Consequently episodes of sympathetic storming frequently coincide with weaning from the ventilator. It is important to explain these episodes to the family/carers.



Avoid seizures Seizure activity in the early post traumatic period following head injury may cause secondary brain damage as a result of increased metabolic demands, raised intracranial pressure and excess neurotransmitter release.

Drugs There is evidence that prophylactic anti-epileptic drugs reduce early seizures, but this is not supported by a reduction in late seizures Anticonvulsants are indicated to decrease the incidence of early post traumatic seizures (within 7 days of injury) 2.There is no evidence that prophylactic anti-epileptics used at any time after head injury reduce death and disability 2. The rationale for using prophylactic anti-epileptic drugs should be clearly stated in the medical notes. The most commonly used anticonvulsants in this institution are phenytoin or levetiracetam (Keppra) although at present comparative studies are insufficient to support a recommendation for or against levetiracetam (Keppra).




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Table 3 Intravenous Phenytoin administration

Refer to National Injectable Medicines Guide Monograph for administration guidance. Administration of undiluted phenytoin carries a much lower risk profile than diluted phenytoin.

Phenytoin If phenytoin is used prophylactically then consider stopping after one week (reduces risk of acute idiosyncratic reactions) 34. Prophylactic use of phenytoin is not recommended for preventing late post traumatic seizures2.If used prophylactically and no evidence of seizures phenytoin must be stopped after six – eight weeks. Consider prophylaxis in patients who are at increased risk of early seizure activity i.e:

• Previous epileptic on treatment• Compound skull fracture• Depressed skull fracture• Linear skull fracture• Immediate seizures• Chronic alcoholism• Sub/epi/intracerebral haematoma• Cerebral abscess• Penetrating injury• Temporal/cortical contusions• GCS score of ≤10• Age ≤65 years• Post traumatic amnesia >30 mins

Dose Loading dose:20mg/kg (max 2g)Rate of infusion: Maximum rate 50mg/min (50mg/mL neat solution run at 60mL/h)Maintenance dose: Start maintenance dose 24 hours after the loading dose at 3 – 4mg/kg each day (see table below)Administer in 3 divided doses when using IV route, or one dose at night for the enteral route.

Contra Indications to Phenytoin

Sinus bradycardiaSA block 2nd and 3rd degree A-V blockAdams –Stokes syndromeAllergy to phenytoin Acute porphyria

Alternatives Levetiracetam 250mg IV bdCarbamazepine (oral or rectal only) or Sodium valproate IV 400-800mg - max 10mg/kg (with careful consideration as it may not provide protection against posttraumatic seizures and has been associated with higher death rates)




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Weight IV loading Dose 20mg/kgRun at undiluted

60mL/hour

IV Maintenance DoseBolus at 50mg/min

Enteral Maintenance

DoseUp to 56kg 1000mg in 20mL 50mg om, 50mg pm, 100mg nocte 200mg od

57 – 68kg 1250mg in 25mL 50mg om, 100mg pm, 100mg nocte 250mg od

69 – 81kg 1500mg in 30mL 100mg om, 100mg pm, 100mg nocte 300mg od

82 – 93kg 1750mg in35mL 100mg om 100mg pm, 150mg nocte 350mg od

≥94kg 2000mg in 40mL 100mg om, 150mg pm, 150mg nocte 400mg od


Interactions • Phenytoin has complex interactions with many classes of drugs. It is an enzyme inducer and induces the metabolism of many drugs.Ideally ask the pharmacist to review the prescription for interactions, or refer to the BNF if necessary.

• Some common interactions to be aware of (not an exhaustive list):Other Anticonvulsants, Amiodarone, Aminophylline, Antibiotics, Anticoagulants, Antidepressants, Antifungals, Antiretrovirals.

• There is also a physical interaction between enteral phenytoin liquid and enteral feed. Enteral feed must be stopped 2 hours before the phenytoin dose and restarted 2 hours after the dose has been given.




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Phenytoin levels and Monitoring

• The therapeutic range for Total Phenytoin is 10 – 20mg/L.

• The sample sent should be a trough – one hour before the dose is due.

• Phenytoin is highly protein bound. An albumin level should be requested at the same time as the phenytoin level. Pathology will then report a phenytoin level corrected for the albumin level.

• Steady state phenytoin levels may not be reached for up to 2 weeks. Levels can be measured on day 3 after loading and then on day 7 and weekly thereafter. Total phenytoin is measured routinely.

• In an acute setting this can be misleading and will require interpretation if:• Hypoalbuminaemia • Renal or hepatic impairment• Protein binding displacement by other drugs• Increased/variable metabolism

• Care should be taken when adjusting the maintenance dose as a small increase in dose can produce a large increase in plasma levels.

• Inadequate blood concentrations of anticonvulsants can be related to the hypermetabolic state of injured patients, it is therefore advisable to keep the concentrations at the higher end of the therapeutic range




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Topping up a low level

• If the adjusted level is below 10mg/L following initial loading and maintenance dosing, give a “top-up dose” calculated as follows:

• Top-up phenytoin dose [mg] = (0.7 [L/kg] x weight [kg]) x (required level [mg/L] – measured level [mg/L])

Usual required level = 15mg/L • For Example: • An 85kg patient has a corrected phenytoin level of

4.8mg/L.• Aiming for a level in the range 10-20mg/L – target level

15mg/L(0.7L/kg x 85kg) x (15mg/L - 4.8mg/L) = 59.5L x 10.2mg/L = 606.9mg

• Round the calculated dose up to the nearest 25mg for ease of administration.

• Omit maintenance doses on the day of the top-up and recommence the following day. If this is the second time or more that a top-up dose is being given, increase the daily maintenance dose by 25mg.

For example: Increase enteral dose from 300mg OD to 325mg OD Increase IV dose from 100mg TDS to 125mg mane, 100mg lunchtime, 100mg nocte • If persistent fits or problems with levels consider using

Levetiracetam, sodium valproate, carbamazepine (only available orally or rectally) or clonazepam. If still uncontrolled consider thiopental.




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�General ICU Care


Positioning • Avoid venous congestion• Nurse 30o head up unless contraindicated (caution:

ensure this does not compromise CPP). If spine not cleared tilt bed 30o head up.

• Head and neck in neutral alignment with no neck flexion.• Avoid excessive hip flexion > 90o.• Turn and reposition patient with caution. Use a minimum

of 3 nurses to maintain head and neck in neutral alignment when turning or repositioning.

• Jugular vein compression can be seen as an increase in mean ICP and an increase in ICP waveform amplitude, mainly P2 and P3

• If patient unconscious and cervical spine needs clearance follow unit protocol

• If cervical spine fracture confirmed, management is dictated by the precise nature of the injury and its stability – position according to instructions from neurosurgical team or orthopaedic surgeons.

DVT Prophylaxis • Graduated compression stockings or intermittent pneumatic compression stockings are recommended unless lower extremity injuries prevent their use2.

• Tinzaparin or low dose unfractionated heparin as per BSUH VTE prophylaxis guideline should be considered after the acute stage of injury is resolved and following discussion with Consultant Neurosurgeon as an increased risk for expansion intracranial hernia.

Transfer Minimum monitoring when transferring patient (e.g. to CT scan) • ECG• Oxygen saturation• ETCO2

• Arterial BP• ICPThe blocks that are in the patient’s bedside monitor should be used for the transfer.As soon as the patient is on the portable ventilator and attached to transport monitor you must stabilise ETCO2 prior to transfer. Check ABG

Consider Ophthalmology review

If a patient has facial injuries and there is a suspicion that there may be eye damage or there is obvious eye damage refer to the Consultant Ophthalmologist.




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3. GLOSSARYCPP Cerebral perfusion pressureCSF Cerebrospinal fluidICP Intracranial pressureMAP Mean arterial blood pressureNMB Neuromuscular junction blocking muscle relaxantsPNS Peripheral nerve stimulatorSAH Sub-Arachnoid HaemorrhageTBI Traumatic Brain Injury

4. REFERENCES AND ONLINE RESOURCES

1. European Brain Injury Consortium. EBIC-Guidelines for Management of Severe Head Injury in Adults. Acta Neurochir 1997; 139: 286-294

2. Guidelines for the Management of Severe Traumatic Brain Injury 4th edition. September 2016. Braintrauma.org

Nutrition Severe head injury patients are in a hypermetabolic and hypercatabolic state. High dose IV vitamins (Pabrinex ®) on admission if any suspicion of chronic alcohol abuse or chronic malnutrition followed by regular enteral vitamins. Dose as per BSUH alcohol withdrawal prescribing or refeeding syndrome guidelines.Early enteral feeding - aim to start within 24 hours of admission. Patients should be fed to attain full caloric replacement by day 7 post injury2. Follow guidelines for confirming correct positioning of naso gastric tubes see trust intranet Follow unit protocol for establishing enteral nutrition. Monitor for refeeding syndrome in at risk patients as per BSUH refeeding syndrome guidelines for adults

Control blood glucose Monitor blood glucose with 2-4 hourly measurements on admission. If blood glucose stable within 4.5-10mmol/L then reduce frequency. Monitor blood glucose at least once a day.Commence sliding scale if indicated. It is recommended that patients receiving intravenous insulin receive a glucose calorie source and that blood glucose values are monitored every 1-2 hours until glucose values and insulin infusion rates are stable and then every 4 hours thereafter.Low glucose levels obtained with point of care testing of capillary blood should be interpreted with caution; as such measurements may overestimate arterial blood or plasma glucose values20.




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3. Hogarth DK, Hall J. Management of sedation in mechanically ventilated patients. Curr Opin Crit Care. 2004;10:40–46

4. Intensive Care Society. Evaluation of spinal injuries in unconscious victims of blunt polytrauma; guidance for critical care 2005 Available online at http://www.ics.ac.uk/icmprof/standards.asp?menuid=7

5. Morris CGT & E McCoy. Clearing the Cervical spine in Polytrauma victims, balancing risks and effective screening Anaesthesia 2004; 59(5): 464-482.

6. Calculation of cerebral perfusion pressure in the management of traumatic brain injury: joint position statement by the councils of the Neuroanaesthesia and Critical Care Society of Great Britain and Ireland (NACCS) and the Society of British Neurological Surgeons (SBNS)Br. J. Anaesth. (2015) 115 (4): 487-488. doi: 10.1093/bja/aev233

7. Martin NA, Patwardhan RV, Alexander MJ et al. Characterization of cerebral haemodynamic phases following severe head trauma: hypoperfusion, hyperaemia and vasospasm. J Neurosurg 1997; 87: 9-19.

8. Bouma GJ, Muizelaar JP,Choi SC et al. Cerebral Circulation and metabolism after severe traumatic brain injury: the elusive role of ischaemia. J Neurosurg 1991; 75: 685-93

9. Dunn-Meynell AA, Hassanian M, Levin BE. Norepinephrine and traumatic brain injury: a possible role in post traumatic oedema. Brain Res 1998; 800: 245-52

10. Playfor S, et al. Consensus guidelines on sedation and analgesia in critically ill children. Intensive Care medicine. 2006; 32: 1125-1136

11. Kang T. Propofol Infusion Syndrome in Critically Ill Patients The Annals of Pharmacotherapy. 2002; 36: 1453-1456

12. Propofol Infusion available on www.surgicalcriticalcare.net

13. Burow BK, Johnson ME, Packer DL.. Metabolic Acidosis Associated with Propofol in the Absence of Other Causative Factors. Anesthesiology. 2004; 101: 239-41

14. Kam, P.C.A. & D. Cardone. Propofol infusion syndrome. Anaesthesia. 2007; 62: 690-701

15. LohP.Nair N, Propofol infusion syndrome Contin Educ Anaesth Crit Care Pain (2013) 13 (6): 200-202.

16. Kerr ME, Sereika SM, Orndoff P, et al. Effect of Neuromuscular blockers and opiates on the cerebrovascualr response to endotracheal suctioning in adults with severe head injuries. Am J Crit Care 1998; 7: 205-217



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17. Riker R.R., G. Fraser & M. Wilkins. Comparing the Bispectral Index and Suppression Ratio with Burst Suppression and the Electroencephalogram During Pentobarbitol Infusions in Adult Intensive Care Patients. Pharmacotherapy. 2003; 23(9): 1087-1093

18. Schalen W., K. Messeter & C.H. Nordstrom. Complications and side effects of during Thiopentone therapy in patients with severe head injuries. Acta Anaesthesiol Scand. 1992; 36:369-377

19. Cooper D et al. Decompressive Craniectomy in Diffuse Traumatic Brain Injury N Engl J Med 2011; 364:1493-1502April 21, 2011

20. PJ. Hutchinson et al. Trial of Decompressive Craniectomy for Traumatic Intracranial Hypertension. N Engl J Med 2016; 375:1119-1130September 22, 2016

21. Lori A. Shutter, M.D., and Shelly D. Timmons, M.D., Ph.D.Intracranial Pressure Rescued by Decompressive Surgery after Traumatic Brain Injury N Engl J Med 2016; 375:1183-1184September 22, 2016

22. Pyeron A.M. Respiratory Failure in the Neurological Patient: The Diagnosis of Neurogenic Pulmonary Oedema. Journal of Neuroscience Nursing. 2001; 33(4): 203-207

23. Dollery C. 1999. Therapeutic Drugs 2nd ed. Churchill Livingstone

24. Bhardwaj A. & J. Ulatowski. Hypertonic Saline Solutions in Critical Care. Current Opinions in Critical Care. 2004; 10(2): 126-131

25. Thompson, HJ, Pinto-Martin, J & MR Bullock. Neurogenic fever after traumatic brain injury: an epidemiological study. J Neurol Neurosurg Psychiatry. 2003; 74:614-619.

26. Thompson, HJ et al. Hyperthermia following traumatic brain injury: a critical evaluation. Neurobiology of Disease. 2003; 12:163-173.

27. Andrews PJ et al. Hypothermia for intracranial hypertension after traumatiuc brain injury. N.Engl J Med 2015;373(25):2403-12.

28. Edwards P et al. Final results of MRC CRASH, a randomised placebo-controlled trial of iontravenous corticosteroids in adults with head injury-outcomes at 6 montyhs. Lamcet Jun 2005;365(9475) 1957-1959.

29. Fatih Tanriverdi, Fahrettin Kelestimur. Pituitary dysfunction following traumatic brain injury: clinical perspectives

30. Neuropsychiatr Dis Treat. 2015; 11: 1835–1843. Published online 2015 Jul 27. doi: 10.2147/NDT.S65814

31. Tanriverdi F, De Bellis A, Ulutabanca H, et al. A five year prospective investigation of anterior pituitary function after traumatic brain injury: is hypopituitarism long-term after head trauma associated with autoimmunity? J Neurotrauma. 2013;30(16):1426–1433

32. Lemke D M. Sympathetic Storming After Severe Traumatic Brain Injury. Critical Care Nurse. 2007; 27(1): 30-37


http://www.nejm.org/toc/nejm/364/16/



https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4524578/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4524578/


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34. Schierhout G, Roberts I. Anti-epileptic drugs for preventing seizures following acute traumatic brain injury. Cochrane Database of Systematic Reviews 2001, Issue 4. Art. No.: CD000173. DOI: 10.1002/14651858.CD000173.

35. Chadwick D. Seizures and Epilepsy after traumatic brain injury. Lancet 2000; 355: 334-5

36. Martindale ‘The Complete Drug Reference’ accessed via MedicinesComplete on 16/02/2017

37. Dikeman S et al. Neuropsychlogical effects of valproate in traumatic brain injury: A randomised trial. Neurology 2000; 54(4): 895-906

38. Meixensberger et al. Influence of body position on tissue-pO2, cerebral perfusion pressure and intracranial pressure in patients with acute brain injury. Neurological Research 1997; 19: 249-253

39. Winkelman C. Effect of Backrest Position on Intracranial and Cerebral Perfusion Pressures in Traumatically Brain-Injured Adults. American Journal of Critical Care. 2000; 9(6): 373-380

40. Sullivan J. Positioning of Patients with Severe Traumatic Brain Injury: Research Based Practice. Journal of Neuroscience Nursing. 2000; 32(4): 204-209

41. Kirkness et al. Intracranial Pressure Waveform Analysis: Clinical and Research Implications. Journal of Neuroscience Nursing. 2000; 32(5): 271-277

42. Association of Anaesthetists of Great Britain and Ireland. 2006. Recommendations for the Safe Transfer of Patients with Brain Injury. Available online at www.aagbi.org

43. ACPIN (1998), Clinical Practice Guidelines on Splinting Adults with Neurological Dysfunction


http://www.survivingsepsis.org/.../SSC-Statements-Sepsis-Definitions-3-2016.pdf


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Appendix 1 BSUH Cervical Spine Immobilisation Guidelines



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Appendix 2 Setting Up the Peripheral Nerve Stimulator (Innervator 242)

Perform an equipment test prior to use. Clip the alligator clips together with the leads plugged in. Turn on PNS (Innervator 242), increase the current to 40mA and test the demand buttons. If no error is indicated, then the unit is delivering the current requested.

Prior to placing the electrodes the skin should be cleaned with alcohol. Two electrodes (or one dual electrode) are placed on the skin of the forearm, along the course of the ulnar nerve (see picture). The leads are connected to the nerve stimulator where the PROXIMAL output jack is positive (red) and the DISTAL output jack is negative (black). The ends of the lead are colour coded. Connect the other end of the lead to the patient electrodes – the PROXIMAL being positive and closer to the centre of the body and the DISTAL being negative and closer to the hand.

When a peripheral nerve is electrically stimulated by a short current pulse, the response is seen as a contraction of the muscle or a twitch. In the case of the ulnar nerves this results in a twitch of the adductor pollicis muscle in the hand. The adductor pollicis adducts the thumb and is considered the gold standard in research on relaxants.Note: The distance between the electrode and the nerve being stimulated determines the skin resistance. A higher skin resistance will require a greater output by the PNS to achieve supramaximal stimulation (SMS).Before administering neuromuscular blockade it is necessary to establish the baseline response. Clip on the distal and proximal leads, turn the unit on and select 10mA. Use the TW and observe or palpate the thumb and hand for response. Wait 10 seconds then increase to 20mA and observe. If the reaction is greater wait 10 seconds then increase to 30mA and so on until there is no change in the response between two settings. Use the lower of these two settings as the baseline (supramaximal stimulation -SMS). The SMS should be recorded on the patients observation chart. If you are not able to identify the SMS e.g the patient is already being administered a neuromuscular blockade then an SMS of 50mA for a normal adult or 60mA for an obese adult can be used. After drug administration do not change this mA setting on the particular patient.



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�Appendix 3 Steroid deficiency screening in TBI


The use of this guideline is subject to professional judgement and accountability. This guideline has been prepared carefully and in good faith for use within the Department of Critical Care at Brighton and Sussex University Hospitals.The decision to implement this guideline is at the discretion of the on-call critical care

consultant in conjunction with appropriate critical care medical/ nursing staff.

Patients with complicated mild, moderate and severe TB

abnormal formal endocrine review

On day 5-10 measure morning basal cortisol in cases of clinical suspicion

including hyponaturemia, hypotension or need for high dose

vasopressors, hypoglycaemia

Assess ACTH deficiency by measuring morning basal cortisol

levels in the acute phase (on day 1-4 post injury)

guidelines for the management of traumatic brain injurytbi traumatic brain injury 4. references and...

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