'Headaches’ Managing Traumatic brain injury TBIs and intracranial pressure ICP

describe the pathophysiology leading to increases intra cranial pressure

brain protected by skull

• good: stops impacts

• not good at flexibility → so incrs in pressure in brain → the skull cant be flexible for this → brain squash → cushing 2ndary to this

The total volume of the brain parenchyma, the cerebrospinal fluid and the blood must remain constant.

Any change in volume without compensation → Increased ICP

What can cause a rise in ICP ?

any change in blood, cerebrospinal fluid or brain parenchyma volume WITHOUT compensation

What maintains total intracranial pressure ?

autoregulation - alters blood volume, or CSF if needed

what happens when brain parenchyma swells due to insult ?

increase in ICP

to compensate the CSF and blood need to decrease

What occurs when ICP is increased?

Increased ICP -> a decreased cerebral perfusion -> cerebral ischemia and eventually neuronal death.

Severe increased ICP -> cerebral ischemic response (Cushing's reflex) in an attempt to maintain cerebral pressure.

These changes can cause a secondary injury to the brain

give some causes of increased ICP

- meningoencephalitis - immune mediated, or infectious

- neoplasia

- trauma: swelling, bruising, etc

- systemic hypertension -> cats

- hydrocephalus - too much spinal fluid

- infarcts - ischaemic stoke, haemorrhagic stroke

what is cushing's reflex?

physiological response to increase in intracranial pressure

what happens in cushings reflex

ICP increases -> cerebral perfusion decreases to maintain the total intracranial volume -> the body increases vascular resistance to try and still deliver enough blood to the brain (systemic hypertension) -> baroreceptors in the aorta sense the hypertension and decrease heart rate (bradycardia)

what clinical parameters should be monitored in patients with suspected intracranial disease?

- HR - bradycardia

- BP - hypertensive - often 1st

- decreased mentation

- SPO2

How do we reduce intracranial pressure?

- hyperosmotic agents

what options for hyperosmotic agents do we have?

- mannitol 0.5-1.5g/Kg, also free radical scavanger - may exarcebate kindey injury - take bloods - no azotaemia

- hypertonic saline - reduces more significantly - good for hypotensive and hypovolaemic, 7.5% NaCl 3-4ml/kg (vasculitis) or 3% NaCl 5.3ml/Kg - takes longer but lasts longer

use what you have access to

what is the prognosis of TBI?

very poor

high mortality

what are the most common causes of TBI in cats and dogs ?

- RTAs (dogs>cats)

- Falls

- Kicks - horse, cows

- Gunshot

- Crushing (cats>dogs)

- Bites (cats>dogs)

what is Primary brain injury ? + types

direct physical damage from traumatic event

- contusion

- laceration

- haemorrhage

- haematoma

- vasogenic oedema

what is secondary brain injury ?

- complex biochemical cascade following primary injury

minutes -> days after event

1. Primary injury

2. Excitatory neurotransmitters -> decrease ATP

3. Influx Na+ and Ca2+ -> more excitatory neurotransmitters

4. Increase Na+ -> cytotoxic oedema

5. Increase Ca2+ -> neuronal cell death

6. Acidosis/hypoperfusion -> O2 free radicals (damage membranes)

7. Inflammatory cytokines ->arachidonic acid + coagulation cascade

8. Damage to BBB

9.Release NO -> vasodilation -> loss autoregulation

10. Cerebral perfusion -> compromised

what needs to be considered with tbi management

Continuous cerebral blood flow is paramount

Brief episodes of systemic hypotension, hypoxia, hyperventilation are associated with worse outcomes

The Brain Trauma Foundation guidelines are aimed at reducing the secondary injury

What do you need to monitor to manage TBI?

- SpO2 sats >90%

- RR - capnography 35-45mmHg

- BP - sys and dis every 5-10 mins

- MM - cyanosis

- normothermia

- pupils - anisocoria, mydriasis, miosis, PLR

- neuro - modified glasgow coma scale every 30 mins

- cerebral blood flow

- episodes of systemic hypotension, hypoxia, hyperventilation are associated with poor prognosis - mitigate secondary injury

How to oxygenate TBI patients

- continous oxygen supplementation

- nasal cannula or flow-by

Airway should be achieved in all TBI GCSS <9 or if 9 and decompensating

if hypoxaemia persists despite inc flow rate???

- check airway position - occlusions

-> PPV - Hi-flow

-> intubate - manually IPPV

IV Fluids for TBI

IVFT administered to treat hypotension

Blood products in humans are utilized for hypotension for TBI although isotonic fluids can be used

Hypertonic fluid resuscitation is recommended for patients with GCSS <8

why should temperature be monitored in TBI?

hyperthermia - causes vasodilation and increased ICP

How to increase venous drainage from the cranium?

Raise the head at 15-30 degrees with neck extended

Reduced cerebral blood volume by increasing venous drainage

This decreases ICP and increases CPP

DO NOT compress the jugulars - don't blood sample these

What is your medication choice if your TBI patient begins seizuring?

Benzodiazepines first line

Levetiracetam is preferred due to less sedative effects

wean off after to see if seizures stop or are now a thing

what does the MGCS examine?

modified glasgow coma scale

18 checks

assess consciousness, brainstem function and posture

lower = worse

perform full neuro exam for TBI

how do you know when to intervene with a patient if sus they have intracranial pathology

→ borderline comatose → monitor MGCS → if going down need to intervene

You suspect TBI what are your first clincal steps ...

IVFT: Quickly correct hypovolemia and hypotension = maintain CPP. Aggressive IVFT is now recommended, quarter shock doses (90ml/kg dogs and 60ml/kg cats) of isotonic fluids

Hypertonic fluids or mannitol as discussed previously

Levetiracetam

Oxygenation: SPO2 >95 is the aim as it indicates a parital pressure of O2 of >80mmHg

Analgesia: Fentanyl CRI recommended as provides consistent analgesia dose 2-6 ug/kg/hr. Paracetamol 20mg/kg IV TID

Prognosis for TBI

A MGCS of <9 have a guarded to poor prognosis

>90% of cases w MCGS <9 die or have permanent severe neurological deficits

Complicating factors to TBIs include coagulopathies, pneumonia, sepsis, seizures

Ionized hypocalcemia is negative prognostic indicator