ICP and Hydrocephalus

ICP: the pressure exerted by the cranium onto brain tissue, CSF and intracranial circulating blood volume

Aetiology

Causes of increased ICP

  • Mass effect e.g. tumour - distort surrounding brain
  • Brain swelling due to e.g. ischaemia, acute liver failure
  • Increase in central venous pressure e.g. venous sinus thrombosis
  • Problems with CSF flow
    • Obstruction ('obstructive hydrocephalus') - masses, Chiari syndrome
    • Increased production - choroid plexus papilloma
    • Decreased absorption ('communicating hydrocephalus') - SAH, meningitis, malignant meningeal disease

Pathophysiology

  • ICP is constantly fluctuating but at rest 7-15 mmHg
    • Can be negative in vertical position
  • The Monroe-Kellie Doctrine is a compensatory mechanism for expanding masses
    • Immediate: decrease in CSF volume by moving it out of FM, decrease in blood volume by squeezing sinuses
    • Delayed: decrease in ECF
  • CSF is secreted by the choroid plexus → ventricular system → subarachnoid space (Magendie and Luschka) → venous system (arachnoid granulations)
    • Any obstruction in this flow will lead to hydrocephalus and increased ICP
  • Cerebral perfusion pressure (CPP) = MAP - ICP
  • Cerebral blood flow = CPP/cerebral vascular resistance
  • Autoregulation of CBF over wide range of BP, CBF remains constant, exact mechanism is unknown
    • Pressure autoregulation - arterioles dilate or constrict in response to changes in BP or ICP
    • Metabolic autoregulation - arterioles dilate in response to chemicals e.g. CO2
    • Other theories include myogenic theory (direct reaction of smooth muscle to stretch)

Clinical presentation of raised ICP

Early signs

  • Decreased level of consciousness
  • Headache
  • Pupillary dysfunction +/- papilloedema
  • Changes in vision
  • Nausea and vomiting

Later signs

  • Coma
  • Fixed, dilated pupils
  • Hemiplegia
  • Bradycardia → Cushing's triad
  • Hyperthermia
  • Increased urinary output

Normal pressure hydrocephalus

  • Idiopathic disease of the elderly, possibly due to decreased brain elastance

Clinical presentation

  • Hakim's triad: abnormal gait, urinary incontinence, dementia

Investigations

  • LP, lumbar drain test, lumbar infusion studies

Management

  • VP shunt, medium-low or low-pressure valve

Idiopathic intracranial hypertension

  • Condition characterized by increased intracranial pressure (pressure around the brain) without a detectable cause

Aetiology

  • Typically develops in younger, overweight female patients, many of whom have polycystic ovaries
  • Probably results from reduced CSF resorption

Clinical presentation

  • Headache
  • Double vision, visual blurring
  • Tinnitus
  • Radicular pain
  • Morning N+V
  • Papilloedema → 25% severe/permanent visual loss

Investigations

  • No ventricular dilation → normal CT
  • LP, CT/MR head, CTV, fundoscopy +/- opthalmology review

Management

  • Weight loss
  • Carboanhydrase inhibitors - acetazolamide, topiramate
  • Ventricular atrial/lumbar peritoneal shunt
  • Monitor visual fields and CSF pressure

Management of other causes of rasied ICP

  • Goals of therapy are to maintain CPP and prevent ischaemia and brain compression

Initial management

  • Maintain head in midline to facilitate blood flow
  • Loosen tube ties, collars etc.
  • HoB 30-45 degrees elevation
  • Avoid gagging, coughing etc.
  • Decrease environmental stimuli
  • Treat hyperthermia
  • Maintain fluid balance and electrolytes
  • Maintain normocarbia

Medical management

  • Diuretics - hypertonic saline
  • Barbiturate coma
  • Antiepileptics

Surgical management

  • Surgical decompression
  • Other surgical treatment - remove mass lesions, CSF diversion