EICP Management

CPP 60-70 mmHg

ICP < 22 mmHg

Normocapnoea

Normothermia

Avoid Hypoxia

OPTIMAL VENOUS DRAINAGE

> Head of bed 30-45 degrees

> Head in neutral position

> Brown tape tube ties or EDAT

> Remove cervical collar and replace with sandbags

SEDATION AND ANALGESIA

> Propofol (2-4 mg/kg/hr) and/or fentanyl (1-4 mcg/kg/hr)

MAINTENANCE OF CPP

> Fluid boluses or noradrenaline infusion

VENTILATION

> Ensure ventilator synchrony

> Avoid unnecessary PEEP

> Aim SpO2 >94% and PaCO2 35-40 mmHg

SODIUM MANAGEMENT

> Aim sodium >135 mmol/L

TEMPERATURE MANAGEMENT

> Paracetamol and/or ‘Active Cooling Protocol’

ACCURATE ICP MEASUREMENT

> CSF draining and oscillating

> Non-dampened ICP waveform

> No kinks, debris or bubbles, antibacterial filter not soiled

> EVD appropriately zeroed and leveled

> No sign of EVD catheter migration

> Is ICP real & sustained?

> Communicated to right people?

> What’s the cause? 

> Repeat CT indicated?

> Surgery indicated?

CSF DRAINAGE

> Increase drainage via EVD

OSMOTHERAPY

> 3% Hypertonic saline bolus (3 ml/kg) to max 155 mmol/L e.g 250 ml bolus OR

> Mannitol (0.25-1 g/kg) to max 320 mEq/L, e.g. ≈ 350 ml of 20% solution bolus

VENTILATION

> PaCO2 35-38 mmHg

SEDATION

> Propofol boluses (0.2 mg/kg)

> Midazolam boluses (0.1 mg/kg)

ANALGESIA

> Fentanyl boluses (0.2 mcg/kg)

TREAT SEIZURES

> EEG and empirical seizure management

> Is ICP real & sustained?

> Communicated to right people?

> What’s the cause? 

> Repeat CT indicated?

> Surgery indicated?

NEUROMUSCULAR BLOCKADE

> Bolus rocuronium (50 mg) or cisatracurium (10 mg)

> Assess for effect: if effective commence cisatracurium infusion

> Ensure adequate sedation prior to paralysis

DEEPEN SEDATION

> Repeat propofol and fentanyl boluses and increase infusion rates

> Bolus midazolam (0.1 mg/kg) and commence midazolam infusion (0.1-0.4 mg/kg/h)

LOW DOSE THIOPENTONE BOLUSES

• Prepare 500 mg thiopentone in 20 mL sterile water then give 100 mg boluses up to 7 mg/kg.
• Inject first dose over 15 seconds and allow at least 20 to 40 seconds between doses to assess response.
• An ongoing infusion, with its associated risks, may not be required.

MILD HYPOCAPNOEA

> Aiming PaCO2 32-35 mmHg

MAP CHALLENGE

> Increase MAP by 10 mmHg, assess effect on ICP

> Is ICP real & sustained?

> Communicated to right people?

> What’s the cause? 

> Repeat CT indicated?

> Surgery indicated?

THIOPENTONE COMA

> 5 -10 mg/kg bolus then 3-8 mg/kg/h, titrated to ICP

> Do account for boluses already given

> Requires EEG monitoring

> Don’t exceed a dose that achieves burst suppression

MILD HYPOTHERMIA

> Aiming temperature 35-36 degrees C using active cooling

DECOMPRESSIVE CRANIECTOMY

> Is this survivable?

> Should focus switch to palliative measures?

Options for increasing cerebral venous outflow include:

> Head of bed 30-45’. In patients with spinal precautions, position the bed in a reverse Trendelenburg position.

> Avoid constrictive ETT ties. Instead opt for brown ‘neuro’ tube tapes or EDATs

> Keep the head in a neutral position

> Avoid straining as this may raise intrathoracic pressure e.g. coughing, pain, constipation, ventilator asynchrony

> Replace cervical collars with sandbags

Pain can increase ICP so analgesia should be given to prevent this contributing to EICP.

There is no evidence that very high doses of analgesics are beneficial.

Sedation decreases ICP and reduces cerebral metabolic rate, therefore reduces demand. All sedatives used in ICU also reduce seizures.

Propofol has the benefit of being short acting, permitting cessation and neurological assessment. However, it causes hypotension and at high doses can cause PRIS.

Midazolam is more haemodynamically stable but takes an unpredictable amount of time to wear off and disposes to delirium.

REF

HYPERTONIC SALINE

> Hypertonic Saline is available in a variety of preparations ranging between 3 and 23.5%.

> Hypertonic saline increases the serum sodium concentration, leading to an increased tonicity. This increased tonicity leads to diffusion of intracellular fluid into the intravascular compartment, reducing cerebral oedema.

> Care must be taken to not raise serum sodium concentration too rapidly, particularly in the presence of hyponatraemia.

> 3% Hypertonic Saline contains 513 mmol/L of sodium chloride.

> The amount of hypertonic saline that is required to reach target serum sodium concentration can be approximated from the following formula: 

Sodium requirement (mmol)= Lean Body Weight (Kg) x Proportion of weight that is water (0.5 for women, 0.6 for men) x (desired sodium – current sodium in mmol/L)

Typical doses for 80 kg:

3%: 3 ml/kg e.g. 240 ml

7%: 1.5 ml/kg e.g. 120 ml

23.5%: 0.4 ml/kg e.g. 30 ml

Infusions usually only used to treat hyponatremia e.g. in context of cerebral salt wasting, not REICP

The possible advantages of hypertonic saline for osmotherapy include:

• Cheap
• Stable
• Rapidly acting
• Endpoint can easily be measured (serum sodium on a blood gas)

The possible disadvantages of using hypertonic saline for osmotherapy include:

• Carries the risk of central pontine myelinolysis
• May induce a hyperchloraemic metabolic acidosis
• Thrombophlebitis if not administered through a central line

MANNITOL

Mannitol is an osmotic diuretic that acts by increasing the osmolality of blood and urine. In the nephron, this decreases the reabsorption of water in the loop of Henle.

The increased serum osmolality draws fluid across the blood brain barrier to decrease cerebral oedema.

It has an onset of roughly 15 minutes and a duration of up to three hours.

Monitor and keep osmolality < 320 mEq/L

The potential disadvantages of using mannitol for osmotic therapy include:

• Dehydration / hypovolaemia
• Electrolyte loss, especially hypokalaemia from diuresis
• Rebound raised ICP

Hypocapnoea causes cerebral vasoconstriction.

> This reduces the volume of blood in the brain and therefore reduces ICP.

However as there is no decrease in the cerebral metabolic rate, this carries the risk of cerebral ischaemia.

Routine hyperventilation is not recommended but hyperventilation to a PaCO2 of 32-35 mmHg may be used transiently, really as a bridging measure to allow another treatment to work or to facilitate an event such as lying flat for a CT scan

Hyperventilating below a PaCO2 of 30 mmHg is not recommended.

Interestingly, in PbtO2 guided management of severe brain injury, higher PaCO2 targets are sometimes targeted to cause cerebral vasodilatation and increase cerebral blood flow – up to 45-50 mmHg, illustrating how complex and nuanced brain injury management is.

Neuromuscular blockade may reduce ICP, especially if increased muscular tone is contributing to EICP.

First try a bolus dose. If this is effective in lowering the ICP, a continuous infusion may be started.

Prior to administering neuromuscular blockade, adequate sedation must be administered.

Cisatracurium

> A non-depolarising benzylisoquinolinium 3 to 4 times as potent as atracurium

> Cardiostable, induces less histamine release than atracurium and does not increase ICP

> Metabolized by Hoffman elimination to inactive metabolites

> Organ independent elimination allows continuous infusion without accumulation in organ failure.

> If continuous infusion is commenced, a “Train-of-Four” count of one to two is generally sufficient.

> Barbiturate that may be used in patients with refractory EICP

> Titrated to ICP but cease if burst suppression achieved.

> Thiopentone infusion is generally reserved until other strategies to control ICP have been tried.

Can be used as small bolus doses in Tier 2 or as high dose with infusion titrated to ICP as Tier 3 therapy

Mechanism of Action

Thiopentone acts on GABA-A receptors to depress post-synaptic sensitivity to neurotransmitters and presynaptic neurotransmitter release.

It is believe to increase the duration of opening of chloride channels leading to neuronal hyperpolarization.

This has the effect of decreasing cerebral metabolic rate (CMRO₂), decreasing cerebral blood flow and decreasing ICP. It also has anticonvulsant effects.

The potential complications of thiopentone infusion include:

1. Hypotension

• Hypovolaemia may precipitate dramatic hypotension.
• Barbituates have cardiac depressant effects and therefore should be used with caution in patients with cardiac disease.

2. Vasopressin resistant diabetes insipidus

• May require 4 mcg boluses of DDAVP to control urine output

3. Sepsis

• High dose barbiturate therapy is immunosuppressive and may be an indication to stop thiopentone infusion.

4. Hypokalaemia and rebound hyperkalaemia.

• Thiopentone coma causes an intracellular shift of potassium. When the infusion is cease, a rapid extracellular shift of potassium may lead to hyperkalaemia.
• Treatment of hypokalaemia is generally avoided unless serum potassium concentration decreases below 20mmol/L or cardiac arrhythmias occur.

Stopping thiopentone infusions:

• Continuous thiopentone infusion can be stopped if ICP remains less 22 mmHg for greater than 24 hours.
• After cessation, serum potassium should be monitored two to four hourly to monitor for rebound hyperkalaemia.

Description

Decompressive craniectomy is based on the principles of the Monro-Kellie doctrine and by removing a variable amount of bone, the skull is converted from a fixed volume closed space into an open space.

Surgical approaches differ in the bone removed and in the handling of the dura.

Decompressive craniectomy can be therapeutic or prophylactic.

Craniectomies can be classed as:

1. Hemicraniectomy: The ideal hemicraniectomy involves removal of bone along the entire supratentorial hemicranium
2. Bilateral craniectomy: This can be done by performing two separate hemicraniectomies, leaving a 2-3 cm wide bone strip along the midline covering the superior sagittal sinus. Alternatively a bifrontal craniectomy can be performed. This approach is most useful in patients whose primary problem is bifrontal contusion or diffuse brain swelling.

The dura may be left closed, opened, scarified or a duraplasty may be performed in order to allow more room for subdural contents.

The bone flap may be required for reconstructive cranioplasty once the patient is clinically improved.

There are three options for the handling of the craniectomy bone flap:

1. Discard the bone flap. This approach requires a future cranioplasty using titanium mesh, surgical cement or a pre-fashioned computer generated bone flap.
2. Create a separate abdominal subcutaneous incision in which to place the bone flap. This can be accessed when the cranioplasty is performed. Remodelling of the bone occurs, leaving the edges enlarged which may lead to difficulties in obtaining a tight bone edge at time of cranioplasty
3. Preserve the bone flap in a tissue bank.

Potential Indications

1. Malignant MCA infarction (in specific population)
2. Refractory intracranial hypertension
3. Severe cerebral oedema

Complications

Early and late‐surgical complications of DC can include:

• Expansion of pre‐existent hemorrhagic contusions
• Development of new ipsilateral or contralateral hematomas (subdural or intracerebral)
• Seizures
• CSF leaks
• Subdural hygroma
• Brain herniations through the craniectomy defect with infarction
• Post traumatic hydrocephalus
• Infection
• Syndrome of the trephined (‘sinking skin flap syndrome’) due to exposure to atmospheric pressure.

Evidence

Decompressive craniectomy is the most invasive therapy for EICP.

Although it effectively decreases ICP, its patient centered benefits are controversial. The DECRA trial (NEJM, 2011) showed a shorter duration of mechanical ventilation and shorter ICU stay but worse functional outcomes at 6 months. However, if adjusted for pupil reactivity, this difference disappeared.

The Rescue ICP trial (NEJM, 2016) again showed improved mortality with worse functional outcomes.

Decompressive craniectomy therefore needs to be discussed on a case by case basis.

Translation of Evidence Into Practice

DC remains a very controversial topic in the TBI field.

There was much hope that the 2 key RCTs, DECRA and RESCUEicp, would provide clarity on whether or not this is a procedure that neurosurgeons should perform amongst other therapeutic options available for severe TBI.

Unfortunately, neither DECRA nor RESCUEicp, together or separately, provides definitive evidence for or against the performance of DC, and they are both complex and challenging to interpret.

Perhaps the most important conclusion of these studies is that choosing to perform a DC is not a simple decision and that the potential benefits should be balanced against the complications and likely outcomes on a case-by-case basis.

Impact of Evidence on Practice

Anecdotal evidence suggests that these new RCTs have not markedly changed practice.

DC is often performed for EICP in TBI.

This likely reflects uncertainty in the prognosis of individual patients as well as the fact that it is hard to withhold a possibly life-saving therapy even when the odds of functional recovery are believed to be low. Indeed, despite important advances in our ability to predict prognosis on a population level for severe TBI patients early after injury, it remains hard to accurately predict outcomes for an individual patient.

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