RAISED
INTRACRANIAL PRESSURE
Pathophysiology
·
Normal intracranial pressure 5 to 15
mmHg in the adult at rest.
·
ICP varies with venous pressure and gravitational
drainage and manoeuvres that raise intrathoracic pressure (coughing, Valsalva,
positive pressure ventilation) or lower it (normal inspiration).
Aetiology
of raised intracranial pressure
The
principle causes of raised ICP are
·
Mass lesions,
·
Hydrocephalus and
·
Cerebral oedema.
The
Monro–Kellie doctrine - the skull as a rigid container that
encloses the brain, CSF and arterial/venous blood.
·
The addition of a new mass lesion
initially be compensated for by the egress of CSF and venous blood from the
skull.
·
During this compensation phase, there is
only a small ↑ in ICP.
·
When compensation is maximal, there is
then a rapid ↑ in ICP for relatively small ↑ in volume > compression and
herniation of the brain
Cerebral
oedema
·
Cytotoxic
oedema - cerebral swelling as a result of cellular
engorgement and can occur in both neurones and glia in response to insults such
as ischaemia.
·
Vasogenic
oedema - results from an accumulation of extracellular
cerebral fluid, usually as a result of breakdown of the BBB and leakage of
fluid through ‘leaky’ capillaries (commonly seen with tumours such as
metastases, malignant gliomas and meningiomas)
Raised
intracranial pressure and cerebrovascular physiology
·
Brain does not store much energy -
unable to utilize anaerobic metabolism.
·
Dependent on a constant flow of O2 and
glucose
·
In the absence of arterial blood flow,
brain tissue will be viable for only a few minutes.
·
Cerebral autoregulation - In normal
circumstances, is maintained CBF at a constant rate despite fluctuations in
mean arterial pressure (MAP) of between 50 and 150 mmHg.
·
These mechanisms include neural regulation (via aortic and carotid
baroreceptors) and local factors ( arteriolar
responsiveness to O2 and CO2).
·
MAP ↑ > ICP ↑, MAP ↓ > ICP ↑
·
Cerebral perfusion pressure (CPP)=MAP – ICP.
·
An poor prognostic factors = ICP
of >20–25 mmHg or a CPP of < 60 mmHg.
Cerebral
herniation
·
Sub-falcine
herniation
- shift of the cingulate gyrus of one hemisphere under the falx cerebri and
across to the contralateral side.
·
Uncal
herniation
- shift of the medial temporal lobe (uncus) medially towards the tentorial
hiatus > 3rd nerve is
stretched > dilatation and fixation of the ipsilateral pupil ± a rapidly
progressive contralateral hemiparesis as pressure is exerted on the ipsilateral
cerebral peduncle.
·
Tentorial
herniation
- downwards shift of midbrain structures through the tentorial hiatus.
·
Tonsillar
herniation
- downwards shift of the cerebellar tonsils and medulla through the foramen
magnum - death due to compression and/or ischaemia of the cardiorespiratory
centres.
Clinical
features
·
Headaches (to be worse in
the early morning or on lying down)
·
may
be exacerbated by coughing, straining or bending
·
Associated
symptoms
- nausea, vomiting or visual disturbance (double vision or blurred vision).
·
Symptoms
relevant to the location of the
pathology- eg: cognitive and personality change, unsteadiness of gait and
incontinence of urine in frontal lobe pathology
·
As
ICP ↑ further > lethargy or drowsiness f/b unconsciousness and coma
·
Raised
ICP may be associated with papilloedema
on fundoscopy
·
Diplopia due to a 6th
nerve palsy
·
There
may be abnormalities of conjugate gaze.
In particular, impaired upgaze or sun-setting may be seen as part of Parinaud’s syndrome, caused by pressure
on the dorsal midbrain.
Treatment
Medical
·
Mannitol is an osmotic diuretic
that can be used in emergency settings to reduce ICP: the dose is 0.5–1.0 g kg-1.
·
Vasogenic oedema - high-dose
steroids in the form of dexamethasone ( example 8 mg Bd)
·
Steroids ↓ the permeability of
the BBB and are useful in reducing cerebral swelling prior to definitive
treatment
·
A carbonic anhydrase inhibitor (
acetazolamide )↓ ICP by ↓ CSF production.
Surgical
·
Trauma - acute EDH,SDH,
intracerebral contusions and chronic subdural haematomas;
·
CVS - Haematomas associated with
ruptured aneurysms;
·
Neuro-oncology - a
variety of primary and secondary tumours.
·
Surgical control by a large bony
decompression (craniectomy), such as in traumatic brain injury or extensive middle
cerebral artery (MCA) infarction.
Hydrocephalus
Discuss about aetiology ,
investigation and management of hydrocephalus.
Definition An increase in the volume of
cerebrospinal fluid (CSF) occupying the cerebral ventricles secondary to either
impaired absorption or, less commonly, increased production of fluid.
Types of Hydrocephalus
Communicating This implies communication
between the ventricles and the subarachnoid space. Usually due to ↑CSF production, occasionally
due to ↓absorption or ↓drainage
Non-communicating CSF flow obstructed within the
ventricles or between the ventricles and the subarachnoid space.
Normal pressure hydrocephalus The
CSF pressure remains normal or is only intermittently raised. Failure to
reabsorb the CSF is compensated by ↓ production. The condition may be
congenital (+ myelomeningocoele or –myelomeningocoele [infantile
hydrocephalus]) or acquired.
Hydrocephalus ex vacuo This is seen in conditions
associated with cerebral atrophy and shrinkage, such as Alzheimer's Disease and
Pick's Disease. The ventricles expand and there is no increase in CSF pressure.
Aetiology
·
Congenital hydrocephalus
prevalence 82 per 100,000 live births
·
Acquired hydrocephalus
incidence is unknown.
Causes
Congenital causes in infants
and children
·
Stenosis of the aqueduct of
Sylvius
·
Dandy-Walker
malformation/Arnold-Chiari malformation type 1 and type 2
·
Agenesis of the foramen of
Monro
·
Congenital toxoplasmosis
·
Bickers-Adams syndrome
(stenosis of the aqueduct of Sylvius, severe mental retardation, and in 50% by
an adduction-flexion deformity of the thumb)
Acquired causes in infants and
children
·
Mass lesions (20% of all cases
in children, e.g. medulloblastoma, astrocytoma)
·
Intraventricular haemorrhage
(e.g.prematurity, head injury, or rupture of an AVM)
·
Infections - meningitis,
cysticercosis in some areas
·
↑Venous sinus pressure - related to achondroplasia, craniostenoses,
venous thrombosis
·
Iatrogenic - e.g.
hypervitaminosis A
·
Idiopathic
Causes of hydrocephalus in
adults
·
Subarachnoid haemorrhage
·
Idiopathic (one third of
cases)
·
Head injury
·
Tumours
·
Iatrogenic - posterior fossa
surgery
·
Congenital aqueductal stenosis
(may not be symptomatic until adulthood)
·
Meningitis, especially
bacterial
·
Normal pressure hydrocephalus
·
All causes of hydrocephalus
described in infants and children
Investigation
(1)
CT
scan - may be detected ventricular size,
generalized cerebral atrophy or localized neuronal cell loss
(2)
MRI
scan of brain can provide better anatomical detail of lesions and useful in
diagnosis of aqueduct stenosis
(3)
ICP
monitoring with parenchymal probe if shunt dysfunction is suspected
(4)
Lumbar
puncture may be both diagnosis and therapeutic in communication hydrocephalus
Management
(a) Medical
treatment
·
Drugs
- Temporizing measure: Frusemide and acetazolamide ↓secretion
of CSF. Isosorbide ↑absorption.
(b) Surgical
·
Treat the underlying cause The
cure rate is 80% if a tumour can be identified.
·
Repeated lumbar punctures is
only valid in communicating hydrocephalus.
·
Insertion of a ventriculoperitoneal shunt
– may be done by insertion of catheter
into lateral ventricle ( usually right frontal or occipital )and then connected
to a shunt valve under scalp,which is tunneled subcutaneously down to
peritoneal cavity.
Credit to – Dr Win Htet Ko
·
Other surgical procedures Choroid
plexectomy, choroid plexus coagulation, and endoscopic
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