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Cerebral tumours

Up ADEM Brain abscess Brain death Cerebral oedema Cerebral tumours CVT CVA Coma Cord compression Delirium Encephalitis Guillain Barre syndrome ICU acquired weakness ICH Meningitis Myasthenia gravis Periodic paralysis Nerve lesions SAH Status epilepticus Subdural empyema SjO2 Tick paralysis Transverse myelitis Weakness

Cerebral tumours

ICU problems

Raised ICP and cerebral oedema

  • rapidly growing tumours usually lead to earlier and more serious deterioration as a result of a decompensation of brain mechanisms that normally control pressure within cranium. These tumours displace brain structures along the paths of least resistance and from one intracranial compartment to another: "herniation syndromes". Often fatal unless rapidly treated
  • cerebral oedema of vasogenic type: responsive to steroids. Dexamethasone most commonly used steroid for the treatment of brain tumours. Minimal mineralocorticoid effect. Compared to other treatments for ­ ICP onset is slow. Dose 16-40 mg/day in divided doses. Oral and IV doses are the same
  • 21-aminosteroids may provide anti-oedema effect of steroids without associated glucocorticoid side effects
  • in brain tumour patients too rapid an infusion of mannitol may cause a deterioration in neurological function by expanding vascular volume and hence CBV. Pretreatment with 5-10 mg of frusemide may prevent this response

Tumour related hydrocephalus


  • results from obstruction of bulk flow of CSF along its normal route of circulation or an overproduction of CSF relative to absorption (very rare)
  • tumour may block flow of CSF in ventricles or connecting channels within the brain (foramina or aqueduct) causing non-communicating or obstructive hydrocephalus or in the subarachnoid pathways causing communicating hydrocephalus.


  • presentation is with signs and symptoms of raised ICP
  • CT shows dilatation of ventricular system proximal to obstruction with normal sized pathways distal to block (noncommunicating) or with dilatation of all four ventricles (communicating)


  • drainage (temporary/permanent)
  • treatment of tumour


  • important cause of morbidity
  • approximately 40% of patient with glioma present with fits and 55% have at least one episode by the time their tumour is diagnosed
  • classically cause focal fits but can cause almost any type
  • phenytoin first line treatment. Patients on dexamethasone frequently require higher doses for therapeutic levels and seizure control. As steroid dose is decreased phenytoin levels may become toxic. Cranial irradiation predisposes some patients on anticonvulsants (especially phenytoin) to Stevens-Johnson and erythema multiforme reactions
  • prophylactic anticonvulsants are not indicated for patients who have not had fits. However may be indicated in the perioperative period (stop 7 days post-op) or when ICP significantly elevated to prevent acute detioration

Complications of surgery

  • infection
  • haemorrhage
  • shunt obstruction

Complications of radiation

Stereotactic radiosurgery

  • seizures, nausea and vomiting at time of procedure occur occasionally. N & V probably due to transient rise in ICP. Prophylactic anticonvulsants and steroids commonly used
  • major late complication is focal radiation necrosis which can behave as an expanding mass and mimic tumour progression. Can be distinguished from tumour using PET scanning

Interstitial brachytherapy

  • haemorrhage, oedema and infection may result from catheter placement or following removal

External beam radiotherapy

  • may result in early, or delayed symptomatic deterioration
  • early reactions primarily related to steroid-responsive oedema

Radiological appearances


  • CT: solitary, irregular mass surrounded by oedema. Usually low density but may be high or mixed. Mass effect usual. ± calcification (especially low grade tumours). Most show partial enhancement; may involve only outer portion resulting in "ring enhancement"
  • MRI: mass, often with adjacent oedema. Variety of signal intensities but in general lower in signal intensity than normal brain on T1 weighted images and higher on T2 weighted images


  • CT: high or low density. Usually enhance. Often surrounded by substantial oedema. Typically multiple. A single met cannot be distinguished from a glioma by either CT or MRI
  • MRI: similar to CT


  • CT: arise from vault, falx or tentorium in characteristic sites the commonest being the parasaggital region, over cerebral convexities and sphenoid ridges. Slightly denser than brain due to calcium. Marked enhancement. May be sclerosis and thickening of adjacent bone
  • MRI

Acoustic neuroma

  • enhance on both CT and MRI

Pituitary tumours

  • CT: pituitary adenoma may enhance vividly. Similar appearances may be seen with large aneurysm, meningioma or craniopharyngioma
  • SXR: may be enlargement or destruction of sella


  • most frequently seen cerebral metastases are from lung and breast cancer. Melanoma and systemic lymphoma also tend to spread to brain

Further reading

Fiandaca MS, Recht LD. Neurooncologic problems in the Intensive Care Unit. In Rippe JM, Irwin RS, Fink MP, Cerra FB (eds), Intensive Care Medicine, 3rd ed. Little Brown & Co., Boston, 1996, pp 2020-30


© Charles Gomersall December 1999


©Charles Gomersall, February, 2015 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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