Ketamine Boluses Are Associated with a Reduction in Intracranial Pressure and an Increase in Cerebral Perfusion Pressure: A Retrospective Observational Study of Patients with Severe Traumatic Brain Injury

Abstract

Background. Increased intracranial pressure (ICP) and hypotension have long been shown to lead to worse outcomes in the severe traumatic brain injury (TBI) population. Adequate sedation is a fundamental principle in TBI care, and ketamine is an attractive option for sedation since it does not commonly cause systemic hypotension, whereas most other sedative medications do. We evaluated the effects of ketamine boluses on both ICP and cerebral perfusion pressure (CPP) in patients with severe TBI and refractory ICP. Methods. We conducted a retrospective review of all patients admitted to the neurointensive care unit at a single tertiary referral center who had a severe traumatic brain injury with indwelling intracranial pressure monitors. We identified those patients with refractory intracranial pressure who received boluses of ketamine. We defined refractory as any sustained ICP greater than 20 mmHg after the patient was adequately sedated, serum Na was at goal, and CO2 was maintained between 35 and 40 mmHg. The primary outcome was a reduction in ICP with a subsequent increase in CPP. Results. The patient cohort consisted of 44 patients with a median age of 30 years and a median presenting Glasgow Coma Scale (GCS) of 5. The median reduction in ICP after administration of a ketamine bolus was −3.5 mmHg (IQR −9 to +1), and the postketamine ICP was significantly different from baseline ( p < 0.001 ). Ketamine boluses led to an increase in CPP by 2 mmHg (IQR −5 to +12), which was also significantly different from baseline ( p < 0.001 ). Conclusion. In this single-institution study of patients with severe traumatic brain injury, ketamine boluses were associated with a reduction in ICP and an increase in CPP. This was a retrospective review of 43 patients and is therefore limited in nature, but further randomized controlled trials should be performed to confirm the findings.

Acute Effects of Ketamine on Intracranial Pressure in Children With Severe Traumatic Brain Injury*

“…These represent Oxford level 2b, Grading of Recommendations Assessment, Development and Evaluation C evidence supporting the assertion that ketamine does not raise ICP in sedated, ventilated patients with sTBI and that, in some instances, ketamine may lower ICP (16). More recently, a retrospective study of 44 adults with sTBI corroborated these observed favorable effects, with lower ICP and higher CPP after ketamine doses (25).…”

The management of severe traumatic brain injury in the initial postinjury hours – current evidence and controversies

“…Induction agents such as propofol should be cautiously used, possibly only in conjunction with induction inotropes, in view of the risk of systemic hypotension resulting in an impaired cerebral blood flow (CBF) [19]. Ketamine is a commonly used option, although early studies using ketamine in sTBI patients implied that it could increase ICP and decrease cerebral perfusion pressure (CPP) [25 ▪ ]. To date, an ICP-reducing effect of ketamine is suggested and in hypotensive sTBI patients ketamine may be preferred due to less risk of hypotension compared with other induction agents [26].…”

Recent advancements in the practice of neuroanaesthesia and neurocritical care: An update

“…The use of ketamine is on an increasing trend due to better understanding of its effect in improving cerebral perfusion pressure and reducing intracranial pressure (ICP). [ 1 , 2 ] The role of ketamine during thrombolytic therapy in acute ischaemic stroke is under evaluation for its utility in amelioration of cerebral infarction at a dose of 0.15 mg/kg intravenous (IV) bolus (maximum 15 mg) followed by an IV infusion of 0.15 mg/kg over 60 minutes (maximum 15 mg). [ 3 ]…”