• Clinical science

Elevated intracranial pressure and brain herniation


Intracranial pressure (ICP) is the pressure that exists within the skull and all of its compartments (e.g., the subarachnoid space and the ventricles). ICP varies with the relative position of the head towards the rest of the body and is periodically influenced by normal physiological factors (e.g., cardiac contractions). Adults in supine position have a physiological ICP of 15 mm Hg or less while a pressure of 20 mm Hg or more indicates pathological intracranial hypertension.

Elevation of ICP may occur in a variety of conditions (e.g., intracranial tumors) and can result in a decrease in cerebral perfusion pressure (CPP) and/or herniation of cerebral structures. Symptoms of raised ICP are generally nonspecific (e.g., impaired consciousness, headache, vomiting). However, more specific symptoms may be present depending on the affected structures (e.g., Cushing triad if the brainstem is compressed). Brain imaging (e.g., showing a midline shift) and physical examination (e.g., papilledema) can detect ICP elevation, but not necessarily rule it out. Therefore, ICP monitoring and quantification is vital in at-risk patients. Management usually involves osmotic diuretics such as mannitol or hypertonic saline. Further therapeutic options include controlled hyperventilation, removal of CSF, and decompressive craniectomy.





  • Physiological ICP is ≤ 15 mm Hg in adults (in supine position), children generally have a lower ICP
  • ICP varies with the relative position of the head towards the rest of the body and is influenced by certain physiological processes (e.g., cardiac contractions, sneezing, coughing, Valsalva maneuver).
  • Expansion of either blood, CSF, or tissue within the skull → limited capacity for the intracranial volume to increase within the rigid skull → increase in intracranial pressure

Consequences of elevated ICP

  • Decreased cerebral perfusion pressure (CPP)
    • CPP is the effective pressure that delivers blood to the cerebral tissue.
    • CPP = mean arterial pressure - ICP
    • Therefore, if the ICP rises, the CPP diminishes (as long as the arterial pressure remains constant).
  • Herniation
    • As a bony structure, the skull is rigid and can not expand to compensate elevated internal pressure.
    • Increased pressure gradient within the skull in the presence of inflexible brain structures (e.g., tentorium cerebelli) → flexible brain tissue shifts → possible brain tissue herniation
    • This may result in direct physical damage or in blocking of cerebral vessels and subsequent ischemia.
  • Cushing triad


Clinical features


Subtypes and variants

Cerebral herniation syndromes




  • CT/MRI: may indicate mass lesions, midline shift, or effacement of the basilar cisterns
  • Ultrasound (e.g., ocular sonography): measures the optic nerve sheath diameter

Clinical examination and imaging may indicate elevated ICP, but cannot rule it out! Additionally, these tests do not allow quantification of intracranial pressure, which is necessary to determine CPP!

Invasive ICP monitoring

  • Indications
    • Patients at risk of elevated ICP
    • Closed head trauma
    • Patients that have a non-surgical intracranial hemorrhage and undergo or have undergone major nonneurological surgery and can not be properly evaluated.
    • Patients suffering from moderate head injury.
  • Placement of monitors
    • Intraventricular (gold standard)
      • Technique: implantation of monitoring device directly into the ventricles
      • Advantages: highest accuracy, allows for treatment of elevated ICP and/or diagnostic collection of CSF samples via drainage system
  • Analysis: > 20 mmHg indicates elevated intracranial pressure that requires treatment
    • ICP is not static but influenced by cardiac action and other factors. → ICP changes in a complex cyclic manner. → represented as distinct waveforms (normal, A wave, B wave, C wave)



Acute stabilization and treatment

  • Resuscitation and emergency measures (head elevation, controlled hyperventilation and IV mannitol)
  • Cardiopulmonary support
  • Sedation, analgesia, antipyretic therapy, antiseizure medication

ICP management

  • General approach
    • Goal of ICP management is generally to keep ICP < 20 mm Hg.
    • Positioning : e.g., head elevation (about 30 degrees), avoiding neck flexion/rotation or circumstances that may provoke Valsalva responses
    • Fluid management: patients should be euvolemic, blood hypoosmolarity should be avoided
    • Hyperventilation: up to a pCO2 of 26–30 mm Hg
    • Hypothermia
    • Causal treatment (e.g., removal of brain tumor) if possible
  • Medical therapy
    • Osmotic diuretics
      • IV mannitol: can generally be administered every 6–8 hours, effects last for up to 24 hours
      • IV hypertonic saline: particularly for short-term treatment
  • Removal of CSF via an intraventricular monitor with drainage system (e.g., external ventricular drain or lumbar drain) or a cerebral shunt (e.g., in hydrocephalus patients)
  • Decompressive craniectomy



Irreversible loss of brain function (brain death)

  • Definition: irreversible, complete loss of function of the entire brain (including the brainstem), even if cardiopulmonary functions can be upheld by artificial life support.
  • Requirements for the diagnosis of brain death
    • Clinical setting
      • Loss of brain function must be attributable to a specific cause (e.g., clinical or radiologic evidence of acute, severe damage to the CNS that is consistent with brain death).
      • Irreversible loss of brain function
      • Factors that may impede proper clinical judgment must be absent.
        • Complicating or mimicking conditions (e.g., electrolyte imbalances, locked-in syndrome)
        • Abnormal core temperature
        • Abnormal systolic blood pressure
        • Intoxication or effects of CNS-depressing drugs/neuromuscular blockade
    • Neurological examination
      • Coma (with a known cause)
      • Absence of brainstem reflexes
        • Pupillary light reflex (shining of light into the eye normally causes pupils to constrict in adaptation to bright light)
        • Vestibuloocular reflex: stimulation of the vestibular system via e.g., rapid head movement or caloric stimulation in the ear, normally elicits eye movement in the opposite direction i.e., away from the stimulation
        • Oculocephalic reflex: rapid rotation of the head to one side normally elicits eye movement in the opposite direction; this allows the image on the eye's fovea to remain central and stabilized despite movement of the head
        • Corneal reflex (touching of the cornea, e.g., with a sterile cotton swab, normally triggers blinking)
        • Gag reflex (touching of either side of the pharynx, e.g., with a sterile tongue depressor, normally triggers gagging)
        • Cough reflex (stimulation of the larynx or the respiratory epithelium normally provokes coughing)
        • No reaction to irritation of trigeminal nerve branches (normally painful)
      • Deep tendon reflexes are occasionally seen in brain-dead patients who have intact spinal cords
      • Apnea (absence of breathing drive)
    • Ancillary tests: only to be performed if clinical examination and/or apnea testing are inconclusive, or if patient is < 1 year
      • Electroencephalography (EEG)
  • Practical steps for determination of brain death: The American Academy of Neurology has published a practical guide that consists of four steps. It cites specific measures and interpretations (e.g., limits of body temperature) that can be used to determine brain death, although not all of them are evidence-based (see “Tips & Links”)
  • Management: : If brain death is proven, no consent is required to remove life support or other forms of treatment (e.g., antibiotic therapy)

If spontaneous breathing is present, the medulla is intact! If the corneal reflex is present, the pons is intact! If the pupillary light reflex is present, the midbrain is intact!

Cerebral edema

  • Definition: excess accumulation of fluid within the brain parenchyma as a result of damage to the blood-brain barrier and/or the blood-CSF barrier
    • Vasogenic: extracellular accumulation of fluids as a result of impaired capillary permeability seondary to breakdown of epithelial tight junctions
    • Cytotoxic: intracellular accumulation of fluids as a result of impaired Na+/K+-ATPase function
  • Etiology
    • Cerebral infarction (stroke)
    • Iatrogenic (Rapid lowering of glucose or rapid correction of hypernatremia)
    • Trauma (particularly in closed head injury)
    • Toxic (e.g., lead intoxication)
    • Inflammatory (e.g., meningitis)
    • Space-occupying lesions (e.g., brain tumors, intracranial hemorrhage)
  • Management: treatment of raised ICP


We list the most important complications. The selection is not exhaustive.