The EM blogosphere has been abuzz with talk of ketamine the past week or so. We stated in the 4th LITFL Review that “an irrational fear of ketamine’s “bite” makes it one of the most under-rated drugs in the ED doc’s arsenal.” Emergency Medicine Updates provided some great tips on Taming the Ketamine Tiger and featured a number of recent publications from the Annals of Emergency Medicine including a link to ACEP’s Clinical Practice Guideline for Emergency Department Ketamine Dissociative Sedation: 2011 Update. Also, just released, is Scott Weingart’s brilliant podcast on the use of ketamine for a controversial technique he calls Delayed Sequence Intubation — something that makes a huge amount of sense to me.
Now, this post is a Q-and-A review of last month’s article from @EBMedicine (which I finally got round to reading…) which is all about using ketamine for procedural sedation in children:
Madati PJ (2010). Ketamine: Procedural Pediatric Sedation In The Emergency Department. Pediatric Emergency Medicine Practice, 8(1). [Abstract and subscription link]
So, without further ado, here are 10 questions highlighting some of the key learning points:
Q1. Compare the IV and IM routes of ketamine administration for procedural sedation.
Ketamine for procedural sedation can be given intravenously or intramuscularly. The dose of ketamine to produce profound dissociation is:
- 1 to 1.5 mg/kg IV
This is given over 1-2 minutes, is effective within 1-2 minutes, results in effective sedation lasting 10-20 minutes, and if inadequate a further 0.5 mg/kg dose may be given
- 4 to 5 mg/kg IM
This is effective within 2 to 5 minutes, results in effective sedation lasting 15-30 minutes and a repeat IM dose (2-4 mg/kg) can be given after 10 to 15 minutes if the initial effect is inadequate
The IM route is useful when IV access is problematic, but the downsides include:
- a longer recovery time (mean of 120 minutes for IM vs. 80 minutes for IV)
- vomiting is more likely (usually occurs during emergence)
- sedation doses are less easily titrated
Higher doses, or even a continuous infusion, may be required in small children due to their relatively higher volume of distribution.
Q2. Should an anticholinergic agent be used with ketamine?
Atropine (0.02 mcg/kg, up to maximum of 0.6mg) or glycopyrrolate are often administered as a co-medication to reduce the hypersalivation caused by ketamine.
The weight of evidence at this time, based on meta-analyses of controlled trials, suggests that anticholinergics should not be routinely used:
- glycopyrrolate appears to increase airway complications.
- atropine confers no benefit.
However, atropine may be beneficial for certain procedures where having dry oral mucosae may be beneficial to the proceduralist rather than the sedationist, e.g. repair of tongue lacerations.
Q3. What are emergence reactions and how can the likelihood of them occurring be decreased?
Emergence phenomena include recovery agitation, dreams, hallucinations and depersonalisation.
They are less common in children than adults:
- adults: 10-20% (as high as 30% in some studies), with 1-2% clinically significant.
- children: 7.6%, with 1.4% clinically significant.
Benzodiazepines are useful for treating emergency reactions, but they do not decreased the likelihood of an emergence reaction occurring. Furthermore, co-administration of midazolam increases the risk of respiratory complications, although emesis is reduced.
In one study, involving adult patients in a non-emergency department setting, no emergence phenomena occurred if ketamine was adminstered in the following circumstances:
- patients were interviewed in the preoperative area:
- they were assured that the medication was safe and would provide complete analgesia during the procedure.
- they were told that the anesthetic medication would allow them to dream about a topic of their choice
- they were instructed to concentrate on that pleasant thought/dream during induction of anesthesia.
- they were encouraged to share their thoughts and feelings before undergoing ketamine sedation.
- ambient operating room and recovery room stimuli were minimized (e.g. noise and lighting).
Q4. What benefit does low dose ketamine with propofol offer over ketamine alone?
Studies performed in non-emergency department settings suggest that ketamine (0.5 to 1 mg/kg IV) followed by propofol (1mg/kg IV) results in more rapid recovery times (time from administration to discharge is halved in some studies) with no increase in clinically significant adverse effects.
Although ‘ketafol’ (sometimes mixed in the same syringe) is being used in emergency departments, there are currently no RCTs in an emergency department setting to support this practice.
Q5. Why might ketamine be a poor choice for the sedation of children requiring imaging (e.g. CT or MRI)?
Ketamine can cause hypertonia and semi-purposeful movements that may interfere with imaging if the patietn is required to lie still.
Q6. Is ketamine contra-indicated in head an/or ocular trauma?
Ketamine is traditionally contra-indicated in situations where raised intra-cranial or intra-ocular pressure may be harmful or poorly tolerated.
These contra-indications are largely based on data from the 1970s. More recent studies in animals and ICU patients have undermined the belief that ketamine causes clinically significant increases in either intra-cranial or intra-ocular pressures. Indeed, some believe ketamine may be neuroprotective as a result of maintaining a stable ICP but with increased cerebral blood flow.
At present, it is probably best to choose an agent other than ketamine in these settings, unless other agents are less suitable for other reasons.
Q7. How are the dissociative effects of ketamine related to the dose administered?
The dissociative state is a lack of response to external stimuli due to ‘disconnection’ of the thalamoneocortical system from the limbic system, as a result of non-competitive antagonism at NMDA receptors.
Above a dose of about 1mg/kg IV the dissociative effects of ketamine do not exhibit dose-responsive effects. Once a patient is fully dissociated, higher doses do not result in a deeper level of sedation.
‘Sub-dissociative’ doses (<1mg/kg IV or <2 mg/kg IM) of ketamine provide potent analgesia, due to agonism of mu, delta, and kappa opioid receptors.
Q8. What are the effects of ketamine on the airway and respiration?
- maintenance of airway reflexes
- risk of laryngospasm — rare (~0.4%)
- excessive salivation
- no suppression of respiratory drive
Q9. How long should a patient be fasted before they are sedated with ketamine?
Most guidelines state that patients should be fasted for 4-6 hours prior to procedural sedation. However, no relationship between adverse respiratory events and fasting times has been found in any studies thus far.
Fasting time should be tailored to the risks of aspiration versus the benefit of an early procedure. Fasting times should not be an issue in true emergencies (e.g. neurovascular compromise due to a displaced fracture).
Q10. Why is ketamine contra-indicated in children less than 3 months of age?
For two main reasons:
- increased rates of respiratory complications
- animal studies implicate NMDA antagonists as a cause of apoptosis and neurodegeneration in developing brains.
Ketamine is also absolutely contra-indicated in patients with a history of overt psychosis.
Want to test your knowledge some more?
Other stuff the proceduralist/ sedationist needs to know is explored in a case-based Q&A called Nasal foreign body, ketamine and laryngospasm.