Elevated ICP

Etiology

• intracranial space-occupying lesion:

  • tumour

  • Pus

  • blood [trauma → hematoma (most common), subarachnoid hemorrhage]

  • depressed skull fracture

  • foreign body

• increased intracranial blood volume

  • vasodilatation (increased pCO2/decreased pO2/decreased extracellular pH, e.g. hypoventilation)

  • venous outflow obstruction (venous sinus thrombosis, superior vena cava syndrome, space occupying lesion)

  • cranial dependency

• cerebral edema

  • vasogenic (vessel damage, e.g. hypertensive encephalopathy, tumour) - Infarction/neoplasm → destroy BBB tight junctions → vasgoenic edema

  • cytotoxic (tissue/cell death, e.g. hypoxia, brain injury)

  • osmotic (acute hyponatremia, hepatic encephalopathy)

• impaired autoregulation (hypotension, hypertension, brain injury)

• hydrocephalus (obstructive, non-obstructive)

• tension pneumocephalus (gas within the cranial cavity)

• pseudotumour cerebri (idiopathic intracranial hypertension)

• status epilepticus (chronic seizure resulting in brain edema)

Clinical Features

Investigations

• Pts /w suspected elevated ICP require an urgent CT/MRI

• ICP monitoring where appropriate

Tx

• CT or MRI to identify etiology, assess for midline shift/herniation

• treat primary cause (i.e. remove mass lesions, ensure adequate ventilation)

• if elevated ICP persists following treatment of primary cause, consider therapy when

• ICP >20 mmHg

• goals: keep ICP <20 mmHg, CPP >65 mmHg, MAP >90 mmHg

Conservative Measures

• elevate head of bed at 30°, maintain neck in neutral position → increases intracranial venous outflow with minimal effect on arterial pressure

• prevent hypotension with fluid and vasopressors, dopamine, norepinephrine prn

• ventilate to normocarbia (pCO2 35-40 mmHg) → prevents vasodilatation

• oxygen to maintain pO2 >60 mmHg → prevents hypoxic brain injury

• osmolar diuresis (mannitol 20% IV solution 1-1.5 g/kg, then 0.25 g/kg q6h to serum osmolarity

• of 315-320)

  • can give rapidly, acts in 15-30 min, must maintain sBP >90 mmHg

• corticosteroids → decrease edema over subsequent days around brain tumour, abscess, blood

  • no proven value in head injury or stroke

Aggressive Measures

• sedation ("light" e.g. barbiturates/codeine → "heavy" e.g. fentanyl/MgSO4)

• paralysis with vecuronium → reduces sympathetic tone, reduces HTN induced by muscle

• contraction

• hyperventilate to pCO2 30-35 mmHg

  • use for brief periods only - also results in decreased cerebral blood flow

• drain 3-5 mL CSF via ventricles, assess each situation independently

• insert EVD (if acute) or shunt

• barbiturate-induced coma induced with pentobarbital to reduce cerebral blood flow and

• metabolism (10 mg/kg over 30 min, then 1 mg/kg q1h continuous infusion)

  • decreases mortality, but no improvement in neurological outcome

• decompressive craniectomy is a last resort

• no role for the use of hypothermia in head injury