• Clinical science

Elevated intracranial pressure and brain herniation

Abstract

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.

Etiology

References:[1][2][3][4][5][6][7]

Pathophysiology

Physiology

  • The skull is nearly inflexible , which has two major implications
    • The intracranial volume is fixed → if one of the constituents (e.g., blood, CSF, tissue) increases in volume, the volume of one (or more) of the other components must decrease.
    • If sufficient reduction of volume can no longer occur, the intracranial pressure rises.
  • 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).

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

References:[8][3][9]

Clinical features

References:[8][3][10][11]

Subtypes and variants

Cerebral herniation syndromes

References:[8][12][13][14][15][16][17]

Diagnostics

Imaging

  • 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.
  • Contraindications: no absolute contraindications exist.
  • 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
      • Disadvantages: risk of infection
    • Intraparenchymal
      • Technique: insertion of monitoring device into the brain parenchyma via a small hole in the skull
      • Advantages: easier placement, lower risk of infection
      • Disadvantages: lower accuracy, no drainage system, higher risk of technical problems
    • Subarachnoid
      • Technique: device is placed on the inside of the skull adjacent to the dura (which is then punctured to allow CSF to reach the epidural space)
      • Advantages: relatively low risk of infection and bleeding
      • Disadvantages: relatively low accuracy and reliability
    • Epidural
      • Technique: device is placed between on the outside of the dura
      • Advantage: low risk of hemorrhage
      • Disadvantages: low accuracy and reliability
  • Analysis: 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)

References:[8][3]

Treatment

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

Special considerations in children and infants

  • General principles are similar to the treatment of adults.
  • Initial stabilization and emergency treatment must be performed according to Pediatric Advanced Life Support (PALS) protocols
  • pCO2 should generally be kept at 35–38 mm Hg

References:[18][8]

Complications

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: normally allows for keeping the visual representations of objects fixed on the eye's fovea, despite movement
        • 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)
      • 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)
      • Cerebral angiography
      • Transcranial Doppler ultrasonography
      • Cerebral scintigraphy
  • Factors that falsely suggest cerebral function
    • Spontaneous or reflexive complex motor activity (e.g., repetitive leg movements)
    • False triggering of ventilator detection system for spontaneous breathing drive
  • 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 and hemodynamics
    • Cytotoxic: intracellular accumulation of fluids as a result of impaired Na+/K+-ATPase function
    • Interstitial: interstitial (therefore extracellular) accumulation of fluids as a result of increased CSF influx into the brain parenchyma (which is itself due to blocked CSF drainage)
  • 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

References:[18][19][20][21][22][23][24][25]

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