Management of Increased Intracranial Pressure





Brain tissue, cerebrospinal fluid (CSF), and blood are contained within the confined space of the skull. An increase in volume of one of these components necessarily results in a compensatory reduction in another. Normal physiologic compensatory mechanisms include egress of CSF or venous blood into the lumbar cistern or extracranial blood compartment. However, with a sufficiently large intracranial mass lesion, such as intracranial hemorrhage, or diffuse brain swelling, such as with traumatic brain injury, these compensatory mechanisms are overwhelmed, leading to decreased intracranial blood flow and/or direct compression of brain tissue, both of which may cause brain injury and potentially brain death. As a general rule, the patient with increased intracranial pressure (ICP) should be intubated and mechanically ventilated to facilitate management. Measures to lower ICP aim to prevent this injury and can be broadly divided into therapies that (1) reduce brain tissue volume, typically osmotic agents (e.g., mannitol, hypertonic saline) or surgical procedures to remove mass lesions; (2) reduce intracranial blood volume, typically through hyperventilation, which causes vasoconstriction; and (3) reduce the volume of CSF, typically through an external ventricular drain. An ICP greater than 20–25 mmHg that is sustained for a period of greater than 5 minutes generally warrants treatment.



  • A.

    Simply raising the head of the bed may reduce ICP. Likewise, the head should be maintained in the midline position to avoid compression of the jugular veins. Hypoosmotic fluids should be avoided. Seizure activity may increase cerebral metabolic demand and result in ICP elevation, so if present, it should be aggressively treated.


  • B.

    Mild hyperventilation (PaCO 2 30–35 mm Hg) will rapidly reduce ICP by causing vasoconstriction, but the effect is not durable. It should therefore generally be used only in the setting of impending herniation as a bridge to more definitive ICP-lowering therapy.


  • C.

    If ICP is elevated due to a focal mass lesion, such as hemorrhage or tumor, surgical evacuation of the mass or decompressive craniectomy should be pursued if appropriate. CSF diversion with an external ventricular drain (EVD) may also be considered. If there is hydrocephalus, placement of an EVD is essential, and allows both direct monitoring of ICP and treatment by draining CSF. Steroids may be used when a tumor is present. For other conditions, such as intracerebral hemorrhage, traumatic brain injury, and ischemic stroke, steroids are ineffective and should be avoided.


  • D.

    Administration of an intravenous (IV) bolus of 20% mannitol (1 g/kg) rapidly reduces ICP. It may be repeatedly administered every 6 hours. The osmolar gap (measured serum osmolarity minus calculated serum osmolarity) should be calculated prior to each dose to assess for accumulation; if > 20 mOsm/L, additional mannitol should not be given. Given the osmotic diuresis induced by mannitol, urinary losses should be carefully repleted to avoid hypovolemia. If hypovolemia is present initially, a bolus of hypertonic saline (150 mL of 5%; or 30 mL of 23.4% solution every 6 hours) may be used instead of mannitol. If serum sodium is > 160, hypertonic saline (HTS) should be stopped; it should also be avoided in the setting of severe acidosis. In the setting of renal failure, mannitol should be avoided and HTS used instead.


  • E.

    HTS is available in various concentrations and for bolus or continuous administration. It is preferable to administer higher-concentration formulations via a central venous catheter to minimize infusion site reactions. Serial assessment of serum sodium is recommended for patients receiving repeated doses or continuous infusion of HTS. HTS induces a hyperchloremic metabolic acidosis and may cause volume overload or pulmonary edema.


  • F.

    Neuromuscular paralysis may reduce ICP in patients with refractory persistently elevated ICP. A test bolus should be given first, and a continuous infusion may be instituted if the patient responds.


  • G.

    Barbiturate (e.g., pentobarbital) coma can be considered for those who fail to respond to all other aggressive interventions to control ICP. Hypotension is a side effect, so patients should be carefully volume resuscitated, and vasopressors may be used as needed. Pentobarbital has potent immunosuppressive effects, and prolonged use should therefore be with caution. Continuous electroencephalogram should be used to target the infusion to burst suppression or ICP within target range (whichever occurs sooner). Therapeutic hypothermia may also be considered. If there is felt to be increased intraabdominal pressure, for instance in cases of major abdominal or thoracic injuries, laparotomy to reduce intraabdominal pressure may in some cases lower ICP by increasing venous drainage.


Algorithm 59.1


Flowchart for the treatment of a patient with increased intracranial pressure. EEG, Electroencephalogram; EVD, external ventricular drain; HOB, head of bed; IV, intravenous; HTS, hypertonic saline; ICP, intracranial pressure.

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May 3, 2021 | Posted by in NEUROLOGY | Comments Off on Management of Increased Intracranial Pressure
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