Raised Intracranial Pressure Flashcards
(24 cards)
State 3 symptoms of raised ICP in an adult patient
Headache Bursting / Throbbing (exacerbated by sneezing, exertion, recumbency, [lying down] and the raised PaCO2 associated with sleep)
Vomitting (often accompanies the headache and so tends to be worse in the morning after waking)
Visual Disturbance
State the signs of raised ICP in an adult
Progressive reduction in consciousness (due to caudal displacement of the midbrain)
“Eye signs”
i.e. papiloedema, fundal hemorrhages, pupillary dilatation,ptosis, impaired upward gaze (due to midbrain compression) and CN 6 adbucens nerve palsy (lateral rectus muscle)
“Motor features”
i.e. ataxia, abnormal posturing, focal neurological deficit, seizure activity
Respiratory Irregularity i.e. Cheyne Stokes Breathing, or hyperventilation due to tonsillar herniation.
Cushings Triad (which are indicative of brainstem ischemia associated with herniation):
Hypertension (with high pulse pressure)
Bradycardia
Irregular Respiration
What is the upper limit of normal ICP in an adult in mmHg?
15mmHg
Name 2 invasive monitoring methods to measure ICP in a patient with a traumatic brain injury
Extra ventricular Drain (aka Intraventricular Catheter) which can be calibrated and used to therapeutically drain CSF
Transducer pressure monitoring in subdural, intraparenchymal, subarachnoid or epidural space. (The transducer may be a balloon, strain gauge, or fibreoptic tip. Once it is sited, there is no ability to recalibrate it. It is important to note that it may not reflect variations in ICP in different parts of the brain).
What management goals may be undertaken in the Emergency Department of a non neurosurgical centre to initiate optimal treatment of a patient with a traumatic brain injury
Tracheal Intubation If: GCS <8, not maintaining adequate gas exchange, lost protective laryngeal reflexes, spontaneously hyperventilating or has irregular respirations
Avoid Hypoxia (PaO2 >13kPa)
Normocarbia (PaCO2 between 4.5 and 5.0kPa)
Maintain MAP >80mmHg
Adequate sedation +/- analgesia to reduce the cerebral metabolic demand for O2
Muscle paralysis if needed to facilitate ventilation to desired PaO2 and PaCO2 or if patient not synchronising with the ventilator
Aid Venous Drainage by: Head up by 30-45 degree tilt , Avoid tube ties, avoid PEEP >12cmH2O or high peak airway pressures
Treatment of Seizures
Maintainence of normoglycaemia <10mmol/l
Maintainence of Normothermia
Discuss with a regional neurosurgical centre to arrange transfer
Give 2 pharmacological options with doses that may be used to treat acute rises in ICP whilst preparing for definitive neurosurgical intervention
Mannitol 0.25-1g/kg
Hypertonic Saline 3% 2ml/kg
Thiopentone must also be an option
Name one non-pharmacological temporising measure for the management of acute rises in ICP
Hyperventilation to a PaCO2 of 4-4.5kPa
What is secondary brain injury and when is it likely to occur?
Primary Brain injury causes a series of metabolic, inflammatory and vascular processes that may lead to secondary tissue damage beyond the initial site of injury in the hours and days that follow the original insult.
It may occur as a result of cerebral oedema, localised tissue hypoxia, excitotoxicity or metabolic dysfunction.
Additionally systemic complications of traumatic brain injury may result in cardiovascular dysfunction causing further damage due to cerebral hypoperfusion and hypoxia
What physiological and Cellular changes are associated with secondary brain injury?
Raised ICP in association with systemic hypotension:
Can cause reduced cerebral perfusion pressure which can result in cerebral hypoperfusion with tissue ischaemia and inadequate substrate delivery.
Local Tissue Damage:
Causes excessive release of excitatory neurotransmitters, resulting in calcium influx into cells, cell oedema and death
Injured cells release inflammatory mediators, (platelet activating factors, leukotrienes, reactive oxygen species) that affect the blood brain barrier and increase blood vessel permeability resulting in vasogenic oedema raising ICP further
Impaired cell membrane function:
Leads to the accumulation of intracellular water and cytotoxic oedema, this increases ICP and worsens tissue perfusion causing a worsening injury.
Impaired cerebral autoregulation:
May cause increased cerebral blood flow and vasogenic oedema
with subsequent raised ICP
Hypoxia, Hypotension, Hyper or Hypocapnia Hyper or Hypo glycaemia:
All will exacerbate secondary brain injury, reduce the ability to auto regulate and cause direct changes to brain tissue size and therefore impact on ICP and perfusion, thus perpetuating a doward vicious cycle
Seizures:
These will cause a significant increase in cerebral metabolism leading to ischaemia, cellular dysfunction and increased ICP. Generalised tonic clonic seizures will also raise the metabolic rate and if ventilation is not increased lead to a raised PaCO2 causing further increases in ICP
What indications are there for intubating a patient with a traumatic brain injury
Coma / GCS <8
Loss or impairment of laryngeal reflexes
Ventilatory insufficiency Pa O2 <13kPa or PaCO2 >6kPa
Spontaneous Hyperventilation causing PaCO2 <4kPa
Irregular respiration
What respiratory goals would you aim for to minimise the risk of secondary brain injury in a patient with traumatic brain injury?
Target a PaO2 of >13kPa
Target a PaCO2 of 4.5 to 5kPa
Avoid Excessive PEEP (aim <12cmH2O) and high mean airway pressures (while also ensuring adequate ventilation and ensuring a lung protective strategy)
What cardiovascular goals would you aim for to minimise the risk of secondary brain injury in a patient with traumatic brain injury?
Maintain MAP >80mmHg:
Replacing any lost volume with a non-hypotonic fluid and blood if indicated
Use Vasopressors is if needed
Facilitate Venous Drainage:
30-45 degree head up tilt
avoidance of tight tube ties
Avoidance of Excessive PEREP or mean high airway pressures
Use Neuromuscular Blocking Drugs if coughing or straining on tube
What non respiratory or cardiovascular goals could be undertaken to minimise the risk of secondary brain injury in a patient with traumatic brain injury?
Adequate sedation and analgesia (to reduce cerebral O2 demand)
Treatment of Seizures
Maintenance of Normoglycemia (<10mmol/L)
Maintenance of Normothermia
Muscle Paralysis to facilitate ventilation to desired PaO2 and PaCO2 or if patient not synchronising with the ventilator
What is the normal range for Intracranial Pressure in adults and children?
Adults 10-15mmHg
Older Children 5-15mmHg
Infants 3-4mmHg
Describe the normal appearance of ICP waveforms
The normal ICP waveform is triphasic, and analysis of the waveform appearance alongside the ICP value can help to assess if cerebral compliance is changing.
The triphasic waveform comprises:
P1: The percussion wave - this waveform is transmitted by arterial pulsation
P2: The tidal wave - this is a reflection of P1 and so represents intracranial compliance. If brain compliance decreases P2 will rise and may become higher than or merge with P1
P3: The dicrotic wave - this is due to aortic valve closure, and is the lowest wave of the 3
State the equation of cerebral perfusion pressure
Cerebral Perfusion Pressure = Mean Arterial Pressure - Intracranial Pressure
What indications are there for ICP monitoring following a traumatic brain injury?
All patients with a traumatic brain injury, GCS < or equal to 8 and abnormal CT brain
OR
Patients with a severe traumatic brain injury and normal CT brain scan if they have 2 or more of the following:
Age > 40 years
Motor Posturing
SBP <90mmHg
What methods of invasive monitoring of ICP are there for a patient who has received a traumatic brain injury
Intraventricular catheter aka extraventricular drain - these can be calibrated and used to therapeutically drain CSF
Transducer pressure monitoring in subdural, intraparenchymal, subarachnoid or epidural space. (The transducer may be a balloon, strain gauge, or fibreoptic tip. Once it is sited, there is no ability to recalibrate it. It is important to note that it may not reflect variations in ICP in different parts of the brain).
At what level is an intracranial pressure monitor zeroed
The foramen of Monro, which correlates with the external acoustic meatus in the supine patient with the head in a neutral position.
Above what pressure should management be instigated to lower intracranial pressure?
22mmHg
Which physiological parameters can be used as a surrogate for the measurement of jugular venous oxygen saturations (SjvO2)?
Cerebral Oxygenation
Cerebral Blood Flow
Describe the correct positioning of a catheter for jugular venous oxygen saturation monitoring and state why malposition will cause error.
A catheter is inserted in a retrograde direction in the internal jugular vein to the jugular bulb, usually on the dominant side.
Which is determined by comprising each internal jugular vein and seeing which causes the greatest rise in ICP.
The catheter is inserted until the tip reaches the C1/2 intervertebral level on a lateral C-spine x-ray.
Poor positioning will result in admixture from extracranial blood and hence lead to error.
What factors might cause a low jugular venous oxygen saturation (SjvO2)?
Reduction in oxygen delivery due to: raised ICP, cerebral ischaemia, hypoxia, profound hypocarbia
Increased cerebral oxygen demand due to: seizures, pyrexia
NB normal SjvO2 is between 55 and 75,% and as with measuring mixed venous O2 sats when assessing systemic O2 delivery, it is a question of supply and demand.
What factors might cause a high jugular venous oxygen saturation (SjvO2)?
Reduction in cerebral O2 consumption due to: Coma, hypothermia, cerebral infarction.
Increased O2 delivery due to hypercaponia or vasodilation
NB normal SjvO2 is between 55 and 75,% and as with measuring mixed venous O2 sats when assessing systemic O2 delivery, it is a question of supply and demand.
