Spinal motion restriction is used to prevent iatrogenic spinal cord injury until spinal stability is established

How this is achieved is variable, with hard collars used in some regions and not in others e.g. Denmark
During intubation, manual in-line stabilisation (MILS) to prevent excessive movement of the C-Spine is recommended

Maintain oxygen saturation > 90%.

Hypoxia, defined as O2 saturation < 90% or a PaO2 < 60 mmHg, even for a brief period, is associated with increased mortality following a TBI.

Prehospital hypotension WITH hypoxia are doubles the risk of death compared to hypotension or hypoxia alone.

Intubation tips

Oxygenation and ventilation are both important.
Assess this first and consider intubation if:

• Insufficient airway protection, often if GCS < 8
• Hypoventilation – a high or rising PaCO2
• Any degree of hypoxemia
• Unable to safely manage without e.g for CT scan
• Borderline situation and about to have an anaesthetic for procedure e.g. EVD insertion, craniotomy

Intubation / anaesthesia for TBI is slightly different to ICH or aSAH
The priority is to intubate quickly, mainly trying to avoid hypotension.
Take these factors into account:

• In trauma patients, hypotension from haemorrhagic shock is a big threat to cerebral perfusion pressure
• Avoid hypotension (SBP < 100 mmHg) to maintain cerebral perfusion to damaged brain
• There is a higher risk of blood in the airway, increasing risk of aspiration and affecting video laryngoscopy
• Avoid induction drugs that will exacerbate hypotension
• Ketamine is a safe induction agent in TBI
• If hypotensive from blood loss, resuscitate with blood products

An Approach

Decide whether intubation is required quickly
Use local algorithm and checklist
Most experienced available intubator should do it, this is not the one to learn on
Haemodynamically stable induction agents e.g.

• Ketamine 1-2mg/kg
• Rocuronium 1.5 mg/kg
• Consider fentanyl if normotensive to prevent hypertension

Anticipate blood & secretions

• Have suction ready
• Use a laryngoscope that permits a view if the video screen gets covered in blood

Aim to maintain oxygenation and normocapnoea throughout
More resources on the Neurocritical Care Intubation
MORE ON NEUROCRIT CARE INTUBATION

Aim ET CO2 35-40 mmHg

Use a standard pressure and volume limited mode, targeting a constant end-tidal CO2 (ETCO2) 35-40 mmHg

> If ETCO2 is not available start with 6ml/kg x 12 breaths and get an ABG as soon.

> If no lung injury, use PEEP 5 (PEEP can affect cerebral perfusion pressure)

> If there are signs of herniation (e.g. dilated pupil) slightly hyperventilate aiming ETCO2 30-35 or (RR= 20 if no ETCO2)

Prophylactic hyperventilation should be avoided unless there are signs of brain herniation.

Hypoventilation causes a high PaCO2 which may cause cerebral vasodilatation, increased cerebral blood flow and increased intracranial pressure. This may compromise cerebral blood flow.

Hyperventilation decreases PaCO2, which causes cerebral vasoconstriction and a reduction in cerebral blood flow, which may cause cerebral ischaemia.

SBP ≥ 110 mmHg for patients 15-49 or > 70 years

SBP ≥ 100 mmHg for patients 50 – 69 years old.

> Evidence suggests different ages benefit from different targets

> Hypotension results in brain hypoperfusion, secondary brain injury and increased mortality.

> Prehospital hypotension AND hypoxia double the risk of death compared to hypotension or hypoxia alone.

As part of the trauma resuscitation you need to:

• Obtain IV / IO access
• FAST assessment for internal bleeding
• Achieve haemorrhage control ASAP

In the context of active bleeding in penetrating trauma, it may be acceptable to aim for NISBP > 90 mmHg until haemorrhage is controlled, as long as that is quickly!

The reality is there is no magic number and there is a trade-off between reducing bleeding and perfusing the brain. REF

AMPLE history

A > Allergies
M > Medications already given, anticoagulants / anti-platelet agents
P > Past Medical History, comorbidities
L > Last ate or drank (relevant to induction of anaesthesia)
E > Events leading to trauma, mechanism of injury, helmet use,

Also:

• Any alcohol or drug use
• Any loss of consciousness and duration
• Post-traumatic amnesia
• Any seizures

The GCS

See our GCS page to see the definitive way to do this
Grades TBI:

Mild TBI: GCS 13-15

Moderate TBI: GCS 9-12

Severe TBI: GCS 3-8

Do a GCS early and repeat at least hourly – a change in GCS ≥ 2 may indicate secondary brain injury from:

• Haematoma expansion
• Increasing cerebral edema
• Brain herniation
• Seizures

Pupils

Size, shape, and reactivity to light

A difference in size of > 1 mm could be important

Ocular trauma may cause mydriasis (dilated pupils)

> Unilateral unreactive dilated pupil suggests tonsillar herniation of the temporal lobe compressing CN3.

This may be from an expanding haematoma on that side or generally raised ICP.

> Bilateral fixed dilated pupils suggests significant brainstem herniation and injury.

This means it’s an emergency but not a universally bad outcome – in one study of patients with traumatic EDH or SDH presenting with bilateral fixed dilated pupils, 30% died but 54% had a favourable neurological outcome. REF

If there are signs of EICP, treat empirically
Signs include:

> Asymmetric, dilated or non-reactive pupils

> Extensor posturing

> Cushing reflex (hypertension, bradycardia, irregular respirations)

> Drop in GCS of > 2 points

Initial EICP management

When you don’t have imaging or ICP monitoring yet

> Hyperventilate aiming for ETCO2 30-35 or respiratory rate of 20 breaths/minute

> Consider hyperosmolar therapy e.g. 3 ml/kg 3% hypertonic saline

> SBP > 110 mmHg

> Elevate the head of bed to 30 degrees

> Optimize analgesia and sedation see EICP Management Protocol

> Maintain normothermia

> Treat seizures

Seizures are common after moderate or severe TBI

Classification

Immediate seizure (within 24 hours of injury)

Early seizure (24 hours – 7 days after injury)

Late seizure (> 7 days after injury)

Choice of Drug

Prophylactic antiseizure medication is recommended for 7 days following TBI to decrease the incidence of early post-traumatic seizures.

Two commonly used antiseizure medications in the setting of moderate-severe TBI are:

> Levetiracetam e.g. 500 mg BD IV or NG for 7 days

> Phenytoin (more side effects, more interactions, less commonly prescribed now)

• FBC (anaemia may contribute to brain injury; thrombocytopenia exacerbates bleeding)
• EUC, LFT, CMP (electrolytes should be normalised; important to know baseline renal and liver function)
• Coags (must be normalised)
• Troponin (Look for evidence of Takotsubo’s cardiomyopathy)
• Blood alcohol level
• Tox screen if relevant

Non-contrast CT brain

Main purpose is to identify intracranial haemorrhage that needs urgent neurosurgical intervention
Look specifically for:

• Basal cisterns – normal, compressed or absent
• Midline shift in mm
• Presence of an EDH
• Presence of IVH
• Presence of tSAH

Obtain other relevant trauma imaging at the same time
CT C-Spine usually essential

Once aSAH diagnosed, early referral to Neurosurgery and Intensive Care is important.
If surgery is required, anaesthetics must be notified as well.

Cover:

• Age
• Sex
• Past medical history, medications (especially antiplatelet or anticoagulation)
• Mechanism and time of injury
• Loss of consciousness, seizure, post-traumatic amnesia,
• Post-resuscitation GCS and pupil size shape and reactivity
• Head CT findings
• C-spine: cleared, not cleared, ?injury
• Other injuries
• Vital signs
• Current ventilation settings, EtCO2, recent ABG
• Blood results
• All treatments given