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Cerebral Oedema

Learning objectives

  • Learning
  • Understand
  • Integrate
  • Reflect

Causes of Cerebral oedema
  • Tumours
  • ICH, Infarcts
  • Traumatic brain injury
  • Reye's syndrome
  • Diabetic Ketoacidosis
Cerebral oedema

Post Ischaemic stroke disorder of cell function leads to the development of cytotoxic oedema usually accompanies infarction and is seen in lesions after about 24 hrs and tends to peak at the 48-72 hr period. Oedema is usually cytotoxic and is due to a failure of cellular pumps due to ischaemia. Later oedema can be vasogenic due to break down in normal vascular blood brain barrier and it is this that causes raised ICP. It is cytotoxic oedema that we see on DWI causing restricted diffusion. Oedema is often a transient phenomenon but becomes more malign when a stroke involves a large volume of the brain causing a significant rise in intracranial pressure usually due to a large vessel occlusion - MCA or Internal carotid. There is no role for steroids. Vasogenic oedema is seen with tumours and does respond to steroids. As ICP rises patients may require decompressive surgery such as hemicraniectomy for large lobar strokes and to reduce pressure and prevent coning or with suboccipital decompression for malignant cerebellar infarcts. Patients with oedema are given isotonic fluids, e.g. N-Saline rather than Dextrose to try to reduce excess free water and oedema. Fluid restriction may even be considered in this period however there are concerns that this may be prothrombotic or reduce cerebral perfusion in those with stenotic lesions. Cerebral oedema can also be managed medically often as a bridge to surgery using either IV Mannitol or Hypertonic saline or Barbiturates or elevated head position at 30-45 degrees.

Cerebral Oedema with Ischaemic stroke

There are several types of cerebral oedema seen in stroke disease. Oedema can be a dramatic and life ending phenomena such as with a malignant MCA syndrome. Significant and progressive oedema usually happens day 2 to 4 of the stroke course. The oedema can cause swelling and increased ICP and compression of midline structures and uncal herniation. There are two major types of cerebral oedema which are cytotoxic (intracellular) and vasogenic (extracellular) oedema.

  • Cytotoxic oedema is felt to be due to a failure to produce ATP and failure of cell pumps. Sodium which is usually pumped out is not done so accumulates which pulls in water. The resultant tissue oedema in the bony skull of the box leads to increased pressure with physical effects such as hydrocephalus, malignant MCA syndrome.
  • Vasogenic oedema is felt to be due to increased vascular permeability. Proteins can leak across the vascular membrane into the interstitium. It may be partly sodium mediated too. There may be an inflammatory component too. Mediators such as NO synthase, aquaporins, free radicals and metalloproteinases may also play a role.
Cerebral Oedema with Haemorrhagic stroke

Perilesional haemorrhagic stroke oedema may be seen with ICH. It tends to develop and peak later than the above. Again, it can add to pressure effects and cause clinical worsening. The causes can involve and inflammatory reaction to blood products, complement, thrombin and other factors.

  • Mechanical Ventilation/hyperventilation Often felt to be helpful but no evidence base. There is however no RCT data to support it. It works by causing hypocapnia which leads to vasoconstriction and a reduction in Cerebral blood flow. There may be deleterious effects so generally without good evidence hyperventilation is not recommended.
  • Mannitol is often used to help using its osmotic effects to remove oedema from interstitial space back into the circulating intravascular blood volume. In doing so it may help BP and cerebral perfusion pressure. Doses range from a single bolus of 1g/kg to 2.5g/kg given every 4hrs. Despite its use for many years there is no quality evidence for its effectiveness in terms of clinical outcomes. There is no evidence to recommend it use in stroke patients.
  • Hypertonic saline again uses the process of osmosis to pull fluid back into the intravascular space. Concerns that it can cause CCF, pulmonary oedema, hyperchloremic acidosis and low K and low Mg and even Central pontine myelinolysis. It has been useful in other brain injury to reduce ICP.
  • Steroids: there is no evidence for effectiveness in stroke. They are more effective for Vasogenic oedema as may be seen with tumours.
  • Decompressive surgery Does not treat the oedema but helps prevent the rise in ICP that may be seen. Examples include decompressive hemicraniectomy for malignant MCA syndrome.