Can ketamine cause intracranial pressure (ICP) elevation?

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Last updated: March 12, 2025View editorial policy

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From the Guidelines

Ketamine is no longer considered a significant risk for intracranial pressure (ICP) elevation in most patients, including those with head injury, and can be safely used in pre-hospital trauma care. The historical concerns about ketamine's potential to increase ICP are now deemed to be of little practical significance 1. This shift in perspective is based on the understanding that the benefits of ketamine, such as relative haemodynamic stability, outweigh the potential risks in many clinical scenarios.

When considering the use of ketamine, it's essential to weigh the potential benefits against the risks, particularly in patients with head injury or at risk for elevated ICP. The key to safe administration lies in careful patient selection, adequate sedation, controlled ventilation, and close monitoring of neurological status.

Some of the key points to consider when using ketamine in patients with potential ICP concerns include:

  • Ensuring adequate sedation beforehand to minimize the risk of increased ICP
  • Maintaining controlled ventilation to prevent hypercapnia, which can exacerbate ICP elevation
  • Monitoring neurological status closely for any signs of deterioration
  • Using ketamine in doses that are appropriate for the clinical scenario, typically ranging from 0.5-2 mg/kg IV for induction and 0.5-1 mg/kg/hr for continuous infusion

The mechanism behind ketamine's potential ICP effects involves NMDA receptor antagonism, leading to cerebral vasodilation and increased cerebral metabolic rate. However, in mechanically ventilated patients with controlled CO2 levels, these effects appear to be minimal 1. As a result, many clinicians now consider ketamine a viable option for patients with head injury or at risk for elevated ICP, particularly when hemodynamic stability is a priority.

From the FDA Drug Label

  1. 7 Increase in Cerebrospinal Fluid Pressure An increase in intracranial pressure has been reported following administration of ketamine hydrochloride. Patients with elevated intracranial pressure should be in a monitored setting with frequent neurologic assessments.

Ketamine can cause intracranial pressure (ICP) elevation. Patients with elevated ICP should be closely monitored. 2

From the Research

Ketamine's Effect on Intracranial Pressure (ICP)

  • Studies have investigated the impact of ketamine on ICP in various patient populations, including those with traumatic brain injury and intracranial hypertension.
  • The evidence suggests that ketamine does not increase ICP, and in some cases, it may even decrease ICP 3, 4, 5, 6, 7.
  • A study published in the Journal of Neurosurgery: Pediatrics found that ketamine administration resulted in a 30% decrease in ICP in pediatric patients with intracranial hypertension 3.
  • Another study published in Critical Care Research and Practice found that ketamine boluses were associated with a reduction in ICP and an increase in cerebral perfusion pressure in patients with severe traumatic brain injury 4.
  • A meta-analysis of randomized controlled trials published in the Journal of Anesthesia found that ketamine did not increase ICP compared to opioids 5.
  • Additional studies have reported similar findings, with ketamine decreasing ICP and cerebral blood flow velocity in patients undergoing craniotomy 6 and decreasing ICP and electroencephalographic activity in traumatic brain injury patients during propofol sedation 7.

Key Findings

  • Ketamine does not increase ICP in patients with traumatic brain injury and intracranial hypertension 3, 4, 5.
  • Ketamine may decrease ICP in certain patient populations, including pediatric patients with intracranial hypertension 3 and patients with severe traumatic brain injury 4.
  • Ketamine's effects on ICP are comparable to those of opioids, with no significant differences in mean arterial pressure values or cerebral perfusion pressure 5.
  • Ketamine can be used safely in patients with mildly increased ICP without adversely altering cerebral hemodynamics 6, 7.

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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