44. ICP

Question 1

What is normal intracranial pressure?

Answer 1

Around 10 mmHg or less

Sustained pressure of >15mmHg is termed ‘intracranial hypertension’

Areas of focal ischaemia if ICP > 20

Global ischaemia if ICP > 50

Treatment usually considered if ICP > 20

Question 2

Cerebral perfusion pressure:

Answer 2

CPP = MAP − ICP(or CVP if greater)

Normal CPP = 80–100mmHg.

Remember that adequate tissue perfusion is not just a function of CPP
but depends on blood flow and oxygen content.

Question 3

What are the causes of raised intracranial pressure?

Answer 3

According to the Munro–Kelly hypothesis (1852) the contents of the cranium
are not compressible. Any significant increase in the volume of brain tissue,
blood or CSF within the cranium will lead to a rapid rise in intracranial
pressure (ICP).

The causes of raised ICP may therefore be divided into three broad
categories:

1. Brain
   Tumours
   Infection/abscess
   Oedema – three types: vasogenic, cytotoxic, interstitial
2. Blood
   Extradural
   Subdural
   Intracerebral
   Subarachnoid
   Venous congestion (e.g. cavernous sinus thrombosis)
3. CSF
   Outflow obstruction, e.g. SAH, meningitis, tumours
   Increased production – choroid plexus papilloma (extremely rare !)
   Benign intracranial hypertension (usually young, obese women).

Question 4

What are the symptoms and signs of raised intracranial pressure?

Answer 4

Symptoms
Headache
Vomiting
Drowsiness
Confusion
Neck stiffness
Seizures.

Signs
Depressed GCS
Papilloedema (late sign)
Cushing reflex (hypertension and bradycardia)
Irregular respirations
Seizures
Hemiparesis
IV cranial nerve palsy (false localising sign due to long intracranial course)
III cranial nerve palsy due to tentorial coning

Question 5

Coning Two major types:

Answer 5

1. Tentorial – part of the temporal lobe compresses the
   brainstem on the contralateral side.
   This results in an ipsilateral IIIn palsy, decreased GCS, Cushing reflex and
   decerebrate rigidity.
2. Cerebellar- the medulla is compressed by the cerebellar
   tonsils passing through the foramen magnum resulting in
   Cheyne–Stokes breathing, sudden apnoea and neck stiffness.

Question 6

What are the indications for ICP monitoring following head injury?

Answer 6

GCS<8 with an abnormal CT scan

Normal CT scan but two or more of the following factors
Age >40
Hypotension
Unilateral posturing
Bilateral posturing

Question 7

How can you measure intracranial pressure clinically

Answer 7

There are four methods commonly used via the skull and a lumbar approach
via a CSF catheter.

1. Epidural catheter
   Strain gauge transducer at tip or
   fibre-optically supplied light reflecting off a
   pressure-sensitive membrane
2. Subdural bolt or catheter
   Prone to blocking and leak but less risk of
   infection than ventricular catheter
3. Ventricular catheter
   Gold standard, accurate, CSF can be drained
   but risk of infection
4. 4. Intraparenchymal catheter
      Light reflecting pressure-sensitive membrane

Question 8

The appropriate monitor will display the ICP and a waveform.

Answer 8

Lundberg waves:

A-waves
Sustained pressure waves (60–80mmHg) every 5–20 minutes
Life-threatening and represent cerebral vasodilatation in
response to ↓ CPP. Need urgent treatment.

B-waves
Small and short lasting waves (10–20mmHg) every 30–120
seconds. Caused by fluctuations in CBV.

C-waves Small oscillations (0–10 mmHg),
reflect changes in systemic
arterial pressure.

Question 9

The Management of Raised ICP

Answer 9

Moderate head-up position will reduce venous pressure without unduly affecting the
MAP (provided there is no physical constriction to drainage by artefacts such as
tracheal tube tapes). Moderate hypocapnia will reduce ICP, but the benefit is
short-lived, and there is a risk of rebound hyperaemia.

Mannitol 20% in a dose of 0.5 g kg1 has a marked but transient effect. It may shift the patient back down the
intracranial compliance curve and gain sufficient time for definitive treatment before
a catastrophic rise in ICP

High-dose dexamethasone
reduces oedema secondary to intracranial tumours but has no effect on raised ICP
following trauma. Hypertonic saline has a well-established role in the management of
raised ICP secondary to brain injury and neoplasm, although not in other conditions.
It also has a role in limiting secondary brain injury due to neurochemical changes.
Hyperthermia will increase the cerebral metabolic rate for oxygen (CMRO2) and
cerebral blood flow and must be avoided. Hypothermia has the opposite effect and
may confer some benefit. Intermittent cerebrospinal fluid drainage via an intraventricular
catheter can be very effective. (Continuous drainage risks emptying the
ventricles completely, which will then make ICP monitoring impossible.)