It seems like over the past three years, we’ve been hearing more and more about ketamine and how it seems to be the answer to everything in the acute care setting and beyond. The flowchart above is not just an attempt at some topical comedy. I borrowed this from Steve Carroll’s (EMbasic Podcast) Twitter post because it is really an accurate depiction of ketamine’s utility.
Ketamine seems to have fallen out of favor in the late 1980s and early 1990s for several different reasons, a lot of which centered on the hallucinations and emergence effects that it can cause. After all, ketamine is synthetically derived from the stimulant/hallucinogen phencyclidine, also known as PCP. As so often happens, ketamine has fallen back into favor over the last decade or so, and new research is appearing almost weekly on new and improved uses for it. We see it being used for everything from analgesia and sedation to respiratory and psychiatric emergencies. For our purposes though, I’m going to go over the drug itself and its current uses from the perspective of EMS and prehospital medicine.
As I mentioned before, ketamine is derived from the street drug PCP and has similar stimulant and hallucinogenic effects. The former gives ketamine a very important place in our toolbox and the latter is rather easily treated. Most sedatives that we use today (benzodiazepines, opioids, propofol, etc.) have an annoying property of dropping our patients’ blood pressures, some more than others. This can make effective sedation of the hypotensive trauma or septic patient tricky. Ketamine on the other hand, triggers a release of endogenous catecholamines, creating a sympathetic response that increases blood pressure and heart rate and dilates the airways. This makes it safer and easier to use in hypotensive patients and a great choice for respiratory patients. Closed head injury remains a contraindication for ketamine use in many systems because of fears that the sympathetic response will increase intracranial pressure. However, several studies and meta-analyses have come out recently that disprove this (Wang et al., 2014 and Zeiler et al., 2014), so we will hopefully see ICP-related concerns surrounding ketamine use finally disappear soon.
Ketamine’s effects are dose-dependent, with analgesic effects starting at lower doses than sedation/induction doses. For me, in the average size adult I give 20-30 mg doses every 20 minutes to achieve an analgesic effect. This is similar to how U.S. military pararescue medics have been giving it for most of Operation Enduring Freedom (Rush et al., 2015). For rapid sequence induction for intubation, I go for 1-2 mg/kg for initial sedation, then 3 mcg/kg/min for continued sedation. Lastly, I think ketamine has a lot of potential for sedation of the agitated delirium patient in the prehospital setting. Aside from some small pockets of ongoing research (see Keseg et al., 2014 and Scheppke et al., 2014), we aren’t using it much for this in the U.S. yet, but it’s gained popularity in other countries, especially in Australia and New Zealand. For a great introduction to this, I strongly suggest listening to Rob Orman’s ERCast podcast episode “Art of the Chemical Takedown”. You’ll hear from physicians all over the globe and their preferences for chemical takedown pharmacology. It’s a great episode, and you’ll hear from Australian emergency medicine and retrieval physicians Cliff Reid and Minh Le Cong on ketamine for this purpose.
Before I wrap it up, two important cautionary notes. First, the emergence effects can be intense and truly terrifying to patient and provider alike. Thankfully, these are easily mitigated with a dose of your benzo of choice (I like 4-5 mg midazolam) timed to coincide with the ketamine wearing off. See the 2015 paper by Perumal et al. for more on this. Secondly, ketamine is a dissociative drug and NOT a hypnotic per se. This means that it will not put your patient “to sleep”, even after a big induction dose. Your patient will likely appear awake and be staring back at you, but they will be endlessly cooperative and for all intents and purposes will feel no pain. This can be extremely unnerving if you aren’t used to working with the drug so be prepared. It will feel odd intubating this patient that appears awake and responsive from a distance. However, ketamine essentially severs the mind-body connection so even though they look awake, they have no sense of anything happening from the brainstem down.
Anyway, that’s my brief two cents on prehospital ketamine. I hope to do a more in-depth post in the near future and expand on a lot of these points. Please leave me feedback in the comments section and thanks for reading!
- Keseg D, Cortez E, Rund D, Caterino J. The Use of Prehospital Ketamine for Control of Agitation in a Metropolitan Firefighter-based EMS System. Prehosp Emerg Care. 2014;19(1):110-115. doi:10.3109/10903127.2014.942478.
- Perumal DK, Adhimoolam M, Selvaraj N, Lazarus SP, Mohammed MAR. Midazolam premedication for Ketamine-induced emergence phenomenon: A prospective observational study. J Res Pharm Pract. 2015;4(2):89-93. doi:10.4103/2279-042X.155758.
- Rush S, Boccio E, Kharod CU, D’Amore J. Evolution of Pararescue medicine during operation Enduring Freedom. Mil Med. 2015;180(3 Suppl):68-73. doi:10.7205/MILMED-D-14-00403.
- Scheppke KA, Braghiroli J, Shalaby M, Chait R. Prehospital use of i.m. ketamine for sedation of violent and agitated patients. West J Emerg Med. 2014;15(7):736-741. doi:10.5811/westjem.2014.9.23229.
- Wang X, Ding X, Tong Y, et al. Ketamine does not increase intracranial pressure compared with opioids: meta-analysis of randomized controlled trials. J Anesth. 2014;28(6):821-827. doi:10.1007/s00540-014-1845-3.
- Zeiler FA, Teitelbaum J, West M, Gillman LM. The ketamine effect on ICP in traumatic brain injury. Neurocrit Care. 2014;21(1):163-173. doi:10.1007/s12028-013-9950-y.