Neurology - Raised ICP and herniation syndromes Flashcards
Definition of intracranial pressure (ICP)
= Pressure within intracranial compartment, it is distributed evenly throughout the intracranial cavity and corresponds to pressure in the brain tissue and CSF
Lumbar CSF pressure in a supine patient equates to the ICP
How is ICP measured?
Measured relative to the foramen of Monroe (usually approximated to the external auditory meatus)
5-15mmHg in normal supine adults (can be much higher in coughing, straining or valsalva)
Infants
CBF
CBF = Cerebral blood flow
Raised ICP is only a problem if CBF is compromised
Flow = Pressure/ Resistance
So, CBF = Cerebral perfusion pressure (CPP)/ Cerebral vascular resistance (CVR)
CBF is reduced if CPP decreases or if CVR increases
What controls CVR?
i) Autoregulation (changes in vessel calibre in response to changes in cerebral perfusion pressure; myogenic response)
- Increased pressure = CONSTRICTION
- Decreased pressure = DILATION
ii) Metabolic changes:
- Hypoxia, hypercapnia, acidosis, increased metabolic products = DILATION
- Hypocapnia, alkalosis, and decreased metabolic by products = CONSTRICTION
CPP
CPP = Cerebral perfusion pressure
= MABP - ICP
Normally > 50mmHg
Therefore, if ICP increases CPP decreases (due to loss of pressure gradient) leading to reduced cerebral blood flow causing ischaemic damage
How far does CBF need to fall before brain damage occurs?
Brain damage occurs when CBF falls to
When does auto regulation of cerebral blood flow begin to fail?
Autoregulation maintains cerebral blood flow over certain limits despite changes in cerebral perfusion pressure (MABP - ICP)
Autoregulation only works between a CPP of 60-160mmHg after which blood flow is determined directly by perfusion pressure
How is auto regulation affected during brain injury?
In the damaged brain autoregulation is impaired
Decreased CPP is more likely to cause reduced CBF and ischaemia
High CPP may raise CBF, break down the BBB and produce cerebral oedema
Causes of raised ICP
1) Intracranial mass lesion
- Tumor
- Infection: Abscess/ subdural empyema/ tuberculoma
- Haematoma: Traumatic or spontaneous
2) Increased CSF volume
- Obstructive or communicating hydrocephalus
3) Increase in cerebral blood volume
- Venous outflow obstruction (e.g. venous sinus thrombosis)
- Vasodilation (e.g. reactive hyperaemia due to loss of auto regulation following head injury)
4) Cerebral oedema
5) Prevention of normal skull growth (children)
- Multisutural synostosis (premature fusion of skull sutures) - e.g. Crouton’s syndrome
How does oedema appear on CT?
Affected brain is hypotenuse (darker) on CT
2 types of oedema - vasogenic and cytotoxic (both are often present in variable portions in trauma and schema)
Vasogenic oedema
- Secondary to breakdown of BBB, leakage of intravascular proteins and fluid into interstitial space
- Primarily affects white matter
- Seen around tumours or abscesses
When causes vasogenic oedema?
- Can occur in late stages of cerebral ischaemia due to ischaemic damage to cerebral blood vessels
- PRES = posterior reversible encephalopathy syndrome; type of vasogenic oedema that arises secondary to malignant hypertension
- Altitude sickness (HACE = high altitude cerebral oedema)
Appearance of vasogenic oedema on MRI
Elevated apparent diffusion co-efficient (ADC) - i.e. increased water diffusion
Cytotoxic oedema
Increased intracellular fluid in glia (particularly astrocytes) and neurones due to failure of cellular metabolism (ATP dependent ion channels)
Predominantly affects grey matter
What are the common causes of cytotoxic oedema?
1) Early cerebral ischaemia (failure of oxygen delivery to the brain) - e.g. stroke, near drowning, cardiac arrest, carbon monoxide poisoning
2) Drugs and toxins - e.g. hepatic encephalopathy (secondary to elevated ammonia), isoniazid
Appearance of cytotoxic oedema on MRI
Reduced ADC (decreased water diffusion)
Which type of oedema is most responsive to therapy?
Vasogenic oedema, not cytotoxic, is helped with dexamethasone therapy
3 stages in pathogenesis of ICP
1) Stage of compensation
2) Stage of decompensation
3) Vasomotor paralysis
What happens during the stage of compensation in raised ICP?
An expanding lesion (e.g. tumour, oedema, haematoma etc) leads to a potential increase in ICP
Initially there is:
- Vasoconstriction - reduces intracranial blood volume (predominantly venous)
- Increased CSF absorption and decreased formation - decreases CSF volume
This allows the brain to expand without serious effects but is only temporary
What happens during decompensated raised ICP?
At this stage there are herniations (with associated complications) and raised ABP with bradycardia (Cushing reflex)
Vasomotor paralysis
Raised ICP leads to reduced CPP this leads to reduced CBF and hypoxia and hypercapnia. This damages neurones and causes vasodilation with further increases ICP - vicious cycle
Monro-Kellie doctrine
Cranial compartment is of fixed volume. Any increase in one of the intracranial contents (blood, CSF or brain tissue) must be compensated by a decrease in another
What happens in infants with raised ICP?
Infants are the exception because their skull sutures have not fused
When volume increases their sutures separate (diastasis) and the cranial vault enlarges to accommodate increased volume
History of raised ICP
- Headache: global headache; usually persistent; may be relieved on standing or by vomiting; may wake from sleep in early morning due to headache; worse on coughing or straining
- Vomiting
- Drowsiness
- Confusion
