raised_icp
Table of Contents
raised intracranial pressure (ICP)
see also:
introduction
- raised ICP may cause fatal further cerebral injury, and thus in those patients at risk, it should be considered as a possible complication and actively managed.
- raised ICP may result in decreased blood perfusion of the brain
- cerebral blood perfusion pressure = mean arterial pressure - ICP
physiology
- normal ICP is ≤ 15mmHg in adults and lower in children
- significant raised ICP is said to occur when ICP > 20mmHg, although transient rises do also occur with Valsalva, cough, sneeze, etc.
- the adult skull has a fixed volume of ~1.5L and contains 80% brain tissue, 10% blood and 10% CSF
- ICP is generally maintained at a relatively constant pressure
- CSF is produced at a rate of ~500mL/day and mostly is absorbed via arachnoid granulations to ensure CSF volume remains constant
- cerebral blood flow (CBF) is determined by:
- (carotid arterial pressure - jugular venous pressure) / cerebrovascular resistance
- cerebrovascular resistance is reduced and thus CBF is increased if there is hypoxia or hypercapnia
- CBF is autoregulated to maintain a relatively constant CBF, however, this autoregulation may fail in stroke or intracranial trauma
- any increase in intracranial mass will first displace CSF into the spinal subarachnoid space
- further increase of ICP to 40-50mmHg results in compression of brain capillaries and resultant global cerebral ischaemia
- raised ICP may also result in herniation of brain tissue through the various anatomic compartments
aetiology of raised ICP
increased tissue volume
- cerebral oedema
- hypoxic brain injury
- acute stroke (CVA)
- acute brain trauma
- intracranial infections
- cerebral abscess
- cerebral abscess
increased extravascular blood
- intracranial haemorrhage:
- subdural haematoma
- extradural haematoma
raised CSF volume
-
- increased CSF production:
- choroid plexus papilloma
- impaired CSF absorption:
- arachnoid adhesions
- post-meningitis
- obstructive:
- pressure from neoplasia / cancer / tumours
increased cerebral blood volume
- hypercapnia
- hypoxia
- head down position
- stroke
- brain trauma
- venous outflow obstruction
- venous sinus thrombosis
- jugular vein compression
other causes
- benign raised intracranial hypertension / pseudotumor cerebri
- often young, obese females with amenorrhoea or irregular cycles
clinical features of raised ICP
- vomiting
- confusion
- spontaneous periorbital bruising
- may cause brain tissue herniations with their respective features:
- subfalcine herniation
- displacement of the cingulate gyrus from one hemisphere to the other, under the falx cerebri.
- can compress the pericallosal arteries, causing an infarct in their distribution (corpus callosum and medial surfaces of cerebral hemispheres) such as callosal disconnection syndromes, and contralateral hemiparesis with a lower limb predominance (more pronounced distally)
- central transtentorial herniation
- diencephalon stage: small reactive pupils, may have Cheyne Stokes respiration, may develop decorticate posturing
- midbrain/upper pons stage: fixed, mid-position pupils, hyperventilation or Cheyne Stokes respiration, impaired or absent vestibulo-ocular reflexes, decerebrate posturing or no movement
- lower pons/medulla stage: fixed, mid-position pupils, absent vestibulo-ocular reflexes, no movement, ataxic respiration
- medulla stage: fixed, mid-position pupils, absent vestibulo-ocular reflexes, no movement, irregular or no respiration
- uncal transtentorial herniation
- herniation of the medial temporal lobe from the middle into the posterior fossa, across the tentorial opening
- compresses the ipsilateral oculomotor nerve, causing a fixed and dilated pupil
- collapses the ipsilateral posterior cerebral artery, causing an infarct in its distribution resulting in cortical blindness
- displaces the midbrain laterally, compressing the contralateral cerebral peduncle against the edge of the tentorium, causing paralysis on the same side as the primary lesion
- may displace the brainstem caudally causing brainstem haemorrhages affecting the RAS and also causing focal neurology and coma
- upward cerebellar herniation
- cerebellar tonsillar/foramen magnum herniation
- pressure from above compresses the pons against the clivus and displaces the cerebellar tonsils into the foramen magnum
- may cause neck stiffness, head tilt
- pressure on pons and medullary cardioresp. centres may result in cardiorespiratory arrest
- transcalvarial herniation
- terminal phase presumable due to brainstem compression results in Cushing's triad:
- bradycardia
- hypertension
- respiratory depression
Dx
- CT scan brain:
- suggestive signs include:
- mass lesions
- midline shift
- effacement of basilar cisterns
- effacement of sulci
- does not exclude raised ICP nor its subsequent development
- role of the lumbar puncture (LP):
- in general, LP is C/I in patients with suspected raised ICP as there is risk of herniation
- it is useful in assisting Dx for those patients with suspected benign raised intracranial hypertension with a normal CT brain
- ICP monitoring:
- invasive procedure reserved for cases where:
- at risk of developing raised ICP, and,
- GCS < 8, and
- aggressive care warranted
Mx of the patient with raised ICP NOT due to benign raised incranial hypertension
- resuscitate as per usual guidelines to ensure hypercapnia, hypoxia, hypotension, rapid rise in blood pressure, and further rise in ICP is avoided
- head up position at 30deg is usually advocated
- avoid restrictive neck taping which may impair venous return
- adequate sedation and paralytic agents if rapid sequence induction (RSI) for emergency intubation indicated
- iv fluids as needed (usually no need to restrict fluids other than free water, as aim to maintain serum osmolality in the 295 to 305 mOsm/L range, and watch for hyponatraemia)
- avoid fever
- ongoing sedation such as propofol
- urgent CT brain mainly to search for aetiology
- consider hyperventilation to maintain PCO2 26-30mmHg (maybe C/I in brain trauma or stroke except in terminal phases)
- consider osmotic agents such as iv mannitol 1-1.5g/kg
- AVOID corticosteroids in patients with brain trauma, intracranial haemorrhage or stroke BUT consider use in those with brain tumours or CNS infections
- discuss with neurosurgical service ASAP to Rx the cause and consider other invasive measures
raised_icp.txt · Last modified: 2014/05/06 02:04 by 127.0.0.1