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Raised Intracranial Pressure Section of the Algorithm for the Management of Meningococcal Disease in Children and Young People, Edition 7a, 2013. Reproduced with the kind permission of the Meningitis Research Foundation
Airway opening manoeuvres (avoid head-tilt and chin-lift in trauma, use jaw thrust) as required with high flow oxygen (10-15 litre/minute via face-mask with reservoir bag) and suction airway as needed. Immobilise cervical spine in trauma patient. Consider oropharyngeal airway if difficultly maintaining airway and GCS depressed while preparations for intubation are made (avoid nasopharyngeal airway in trauma due to risk of basal skull fracture).
Indications for intubation include inability to maintain/protect airway (GCS < 8), apnoea/hypoventilation, hyperventilation, to allow CO2 control for the treatment of raised ICP or to facilitate neuroimaging.
If intubation is required a rapid sequence induction should be performed with manual in-line stabilisation of the cervical spine (remove collar). For the potentially haemodynamically unstable patient e.g. sepsis, multi-trauma, ketamine is the preferred induction agent. The traditional teaching that ketamine causes elevation in intracranial pressure is based on weak evidence and other agents such as propofol and thiopentone (despite their beneficial effects on reducing ICP) are more likely to cause a greater overall reduction in cerebral perfusion pressure due to the frequent hypotension experienced when using these agents. Consider adding fentanyl (1 – 2 mcg/kg) to blunt the sympathetic pressor response to laryngoscopy. Thiopentone may be the preferred induction agent in the patient who is markedly hypertensive or actively seizing, however hypotension must be avoided and the dose should be adjusted according to the patients haemodynamic status.
As for any intubation in the critically ill child, have volume e.g. 10 – 20 ml/kg of 0.9% saline and vasoactive drugs e.g. push dose adrenaline 1 in 100,000, prepared in case of haemodynamic instability on induction – hypotension must be promptly and aggressively treated (ensure blood pressure cycling every minute during induction).
Gentle hand ventilation during the apnoea period is common practise in small infants and younger children – hypoxia and hypercapnia must be avoided.
Due to limited movement of cervical spine expect a suboptimal view at laryngoscopy and have an appropriately sized bougie to hand (ETT < 4.0mm use 5CH bougie; ETT 4.0 – 5.5mm use 10CH bougie; ETT > 5.5mm use 15CH bougie).
Use a cuffed oral endotracheal tube.
Routine settings on ventilator i.e I:E ratio 1:2, PEEP 5 cm H2O (excessive PEEP will impair cerebral venous drainage), Ti < 1 year = 0.6 – 0.8 seconds, 1-5 years = 0.8 – 1 seconds, 5-12 years = 1-1.2 seconds, >12years = 1.2-1.5 seconds and adjust depending on blood gases.
A volume mode of ventilation should be used where possible, as it maintains a stable minute ventilation despite changes in lung compliance and should therefore provide better control of CO2 than a pressure mode where the tidal volume delivered will change with changes in lung compliance. Start with a tidal volume of 6-8 ml/kg (or peak pressure around 20 cmH2O if using pressure mode) and adjust depending of chest movement and blood gases.
Target a PaCO2 of 4.5 – 5 kPa and PaO2 > 12 kPa (continuously monitor end tidal CO2 and correlate this with PaCO2).
Hypoxia and hypercapnia must be avoided – pre-oxygenate prior to suctioning and monitor ETCO2 during handbagging.
Chest radiograph following intubation for endotracheal tube position.
Ensure patient has two working peripheral or intraosseous access (in non-fractured limb). Transfer to CT or to a neurosurgical centre must not be delayed for central and arterial line insertion in a patient needing a time critical imaging/transfer e.g. suspicion of intracranial haematoma or blocked VP shunt. However in patients that are not time critical e.g. generalised cerebral oedema secondary to a medical cause, insertion of peripheral arterial and femoral central venous lines (avoid internal jugular lines as they impair cerebral venous drainage) prior to transfer can be considered, as it will allow more accurate monitoring and control of cerebral perfusion pressure (providing local skills and expertise allow).
Hypotension must be promptly and aggressively treated. Ensure non-invasive blood pressure is cycling at least every 5 minutes. Target the age related minimum value for cerebral perfusion pressure (see table below).
After restoring circulating volume (use blood products in trauma patients) use noradrenaline to maintain minimum target blood pressure. In patients needing time critical transfer by the local team a dilute noradrenaline infusion (see drugs section for reconstitution instructions) can be administered via a good peripheral or intraosseous with non-invasive blood pressure cycling every few minutes. In multi-trauma patients who have had active bleeding increasing the blood pressure to the above levels will increase the risk of bleeding, so slightly lower target may need to be considered on a case by case basis depending on individual risks – discuss and agree targets with the retrieval team. Even if patient is meeting the blood pressure targets without support, it is good practise to prepare and attach a noradrenaline infusion to the patient and set the rate on the infusion pump (but leave infusion on hold). This approach will limit the duration of suboptimal CPP, should hypotension occur during the transfer.
Perform a neurological assessment (GCS and pupillary reflexes at a minimum) prior to induction of anaesthesia where possible (predicts severity of head injury and likelihood of finding a time critical lesion allowing early discussion with a neurosurgeon).
Ensure the following neuroprotective measures are initiated in all patients with suspicion of elevated intracranial pressure:
- Encourage cerebral venous drainage – head up 30° and in the midline (tilt whole bed to 30° in trauma), ensure neck collar/endotracheal tube ties are not too tight, avoid internal jugular lines and use minimal PEEP.
- Control blood supply to brain – maintain PaCO2 4.5 – 5.0 kPa, PaO2 > 12 kPa and reduce cerebral metabolic demand (keep well sedated/paralysed, prevent/treat seizures and maintain normothermia). Maintain target CPP (see circulation).
- Treat cerebral oedema – treat generalised cerebral oedema with 3 ml/kg of 3% hypertonic saline over 5 minutes or 0.5 g/kg of mannitol over 30 minutes. For local swelling round a space-occupying lesion only, administer 0.5 mg/kg of dexamethasone (maximum dose = 20 mg). Consider tapping VP shunt if shunt blockage is suspected (discuss with neurosurgery).
Sedate with morphine (10 – 60 mcg/kg/hr) and midazolam (1 – 4 mcg/kg/min). Administer fentanyl 1-2 mcg/kg prior to suctioning/painful procedures. Keep paralysed.
Observe for seizures (this will be more difficult in the paralysed patient) and treat as per seizure protocol (see status epilepticus). Administer prophylactic phenytoin loading dose of 20 mg/kg over 20 minutes in non-time critical patients with traumatic brain injury (providing it is not contraindicated).
In head trauma patients aim to perform CT scan of brain within 30 minutes of presentational the emergency department. This should be reported immediately and if this shows a time critical lesion, local team transfer to a neurosurgical centre should be organised aiming to depart within one hour of completing the scan at the latest.
Don’t tape the eyes closed as pupils will need to be assess regularly as part of ongoing regular CNS observations (every 15 minutes minimum including on transfer).
Monitor blood glucose (hypoglycaemia and hyperglycaemia are both associated with worse outcome). Insulin sliding scale not normally initiated outside PICU environment.
If raised ICP is related to meningitis/encephalitis ensure adequate antimicrobial cover is administered (see sepsis section). Routine administration of antibiotics in traumatic brain injury is not normally indicated, even if suspected CSF leak (unless requested by the neurosurgeon).
Pyrexia will increase intracranial pressure by increasing cerebral metabolic demand and thus cerebral blood flow. Aim for normothermia and treat any pyrexia aggressively.
Restrict intravenous fluids to 80% maintenance.
Use isotonic fluids (risk of SIADH):
< 2 years – 0.9% saline and 5% dextrose +/- KCL
≥ 2 years – 0.9% saline +/- KCL
Catheterise bladder in non-time critical transfers (pain associated with full bladder will increase ICP).
Keep nil by mouth.
Insert and aspirate nasogastric tube (to remove any swallowed air splinting the diaphragm), then leave on free drainage.
Labs & Electrolytes
Check FBP, Clotting, Crossmatch, U&E, LFTs, amylase, Ca, Mg, Phosphate, CRP, glucose, blood gas and lactate. Send blood culture if sepsis concerns. Consider toxicology screen and ammonia/metabolic screen if cause of cerebral oedema unknown.
Hyponatraemia should be treated by administering 3 ml/kg of 3% hypertonic saline over 15 minutes (don’t wait for formal lab results – treat the sodium on the blood gas).
Don’t forget to administer tranexamic acid/correct coagulopathy in the bleeding trauma patient.
Drugs & Infusions
Hypertonic Saline 3%
Indicated for the treatment of cerebral oedema (avoid if Na > 160 mmol/l) or hyponatraemia in the setting of raised ICP.
Administer 3 ml/kg over 5 – 15 minutes for cerebral oedema and over 30 minutes for asymptomatic hyponatraemia.
A bag of 3% hypertonic saline can be constituted by removing 36 ml from a 500 ml bag of 0.9% saline and replacing it with 36 ml of 30% saline.
Dose range for the treatment of cerebral oedema is 0.25 – 1.5 g/kg by infusion over 30 – 60 minutes, repeating after 4-8 hours if required (providing serum osmolarity < 310 mOsm/L).
Therefore give aliquots of 0.5 g/kg (2.5 ml/kg of 20% mannitol) over 30 minutes, repeating up to two times if needed.
Dexamethasone is only indicated for the treatment of oedema surrounding a space occupying lesion (not for generalised cerebral oedema).
An initial dose of 0.5 g/kg (maximum dose = 20 mg) should be given by slow intravenous injection over 3 – 5 minutes. A smaller dose if often continued 2-3 hourly under specialist advice.
For the maintenance of CPP targets in the setting of raised ICP.
Peripheral Strength – dilute 1 mg of noradrenaline to 50 ml with 0.9 % saline and start at 0.3 x weight in kg ml/hr (0.1 mcg/kg/min) via a good peripheral or intraosseous line and titrate to effect
Central Strength – dilute 0.3 x weight in kg mg of noradrenaline to 50 ml with 0.9% saline and start at 1 ml/hr (0.1 mcg/kg/min) via a central line and titrate to effect (use peripheral strength noradrenaline while CVL is being sited).
It is vital to quickly identify the patient who has raised intracranial pressure and to prevent secondary injury by avoiding hypoxia, hypercapnia, hypotension and initiating the neuroprotective measures outlined above.
Identifying the patient where a specialist intervention such as neurosurgery will relieve the elevated intracranial pressure by performing an urgent CT scan and then organising a time critical transfer by the local team should be the next priority. To ensure this happens in a timely manner this requires good planning and communication with the different professionals involved e.g. having CT on standby with radiologist/ neurosurgeon ready to report scan, ambulance crew called early and transferring directly to theatre in receiving centre. Avoid unnecessary interventions in time critical transfers e.g. arterial/central lines or urinary catheter and remember to handover what still needs to be done e.g. completion of secondary survey, safeguarding concerns.
- Observe the patient closely for any signs of increasing intracranial pressure throughout the transfer e.g. bradycardia, hypertension and pupillary changes. Should this occur:
- Keep moving urgently towards neurosurgical intervention (don’t stop ambulance).
- Ensure patient well sedated and paralysed. Consider a thiopentone bolus (avoid hypotension) – this will sedate patient, treat any seizure activity and reduce intracranial pressure.
- Consider administration of further osmotic agents e.g. hypertonic saline or mannitol.
Hyperventilation to reduce intracranial pressure can be used in an emergency e.g. suspected coning but should only be used for as brief a period as possible.
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