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raised intracranial pressure (ICP)


  • 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


  • 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

increased extravascular blood

raised CSF volume

increased cerebral blood volume

  • hypercapnia
  • hypoxia
  • head down position
  • stroke
  • brain trauma
  • venous outflow obstruction
    • venous sinus thrombosis
    • jugular vein compression

other causes

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


  • 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
    • 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

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