A small pilot study on a convenience sample of children presenting to the emergency department with acute limb injury pain evaluated the use of intranasal ketamine(1).
Initial dose averaged 0.84 mg/kg and a third of the patients required a top up dose at 15 minutes, resulting in a total dose of about 1.0 mg/kg to provide adequate analgesia by 30 min for most patients. The authors suggest that this could guide investigators on an appropriate dose of IN ketamine for use in clinical trials.
Adverse events were all transient and mild.
Prior to administration, the ketamine was diluted with saline to a total volume of 0.5 mL and was administered as 0.25 mL per nare using a Mucosal Atomiser Device (MAD, Wolfe Tory Medical, Salt Lake City, UT, USA). According to the protocols in my Service, this device requires 0.1 ml to prime its dead space(2). It is unclear whether this factor may have affected the total dose delivered to the patient in this study.
OBJECTIVE: The present study aims to conduct a pilot study examining the effectiveness of intranasal (IN) ketamine as an analgesic for children in the ED.
METHODS: The present study used an observational study on a convenience sample of paediatric ED patients aged 3-13 years, with moderate to severe (≥6/10) pain from isolated limb injury. IN ketamine was administered at enrolment, with a supplementary dose after 15 min, if required. Primary outcome was change in median pain rating at 30 min. Secondary outcomes included change in median pain rating at 60 min, patient/parent satisfaction, need for additional analgesia and adverse events being reported.
RESULTS: For the 28 children included in the primary analysis, median age was 9 years (interquartile range [IQR] 6-10). Twenty-three (82.1%) were male. Eighteen (64%) received only one dose of IN ketamine (mean dose 0.84 mg/kg), whereas 10 (36%) required a second dose at 15 min (mean for second dose 0.54 mg/kg). The total mean dose for all patients was 1.0 mg/kg (95% CI: 0.92-1.14). The median pain rating decreased from 74.5 mm (IQR 60-85) to 30 mm (IQR 12-51.5) at 30 min (P < 0.001, Mann-Whitney). For the 24 children who contributed data at 60 min, the median pain rating was 25 mm (IQR 4-44). Twenty (83%) subjects were satisfied with their analgesia. Eight (33%) were given additional opioid analgesia and the 28 reported adverse events were all transient and mild.
CONCLUSIONS: In this population, an average dose of 1.0 mg/kg IN ketamine provided adequate analgesia by 30 min for most patients
In this study, the administration of an intravenous ketamine formulation to the nasal mucosa of a paediatric burn victim is described in the prehospital environment. Effective analgesia was achieved without the need for vascular or osseous access. Intranasal ketamine has been previously described for chronic pain and anaesthetic premedication. This case highlights its potential as an option for prehospital analgesia.
I ‘jumped ship’ from etomidate to ketamine for rapid sequence intubation (RSI) in sick patients about seven years ago. Good thing too, since I later moved to Australia where we don’t have etomidate. I’ve been one of the aggressive influences behind my prehospital service’s switch to ketamine as the standard induction agent for prehospital RSI. It’s no secret that I think propofol has no place in RSI in the critically ill.
I love ketamine for its haemodynamic stability compared with other induction agents. In fact, I very rarely see a drop in blood pressure when I use it for RSI even in significantly shocked patients. One should however try to remain open to evidence that disconfirms ones biases, lest we allow science to be replaced by religion. I therefore was interested to read a report of two cases of cardiac arrest following the administration of ketamine for rapid sequence intubation (RSI)(1).
The first case was a 25 year old with septic shock due to an intestinal perforation, with a respiratory rate of 30 ‘labored’ breaths per minute and hypoxaemia prior to intubation with 2mg/kg ketamine who became bradycardic and then had a 10-15 minute PEA arrest after ketamine administration (but prior to intubation). Pre-arrest oxygen saturation and pre-induction blood gases are not reported.
The second case was an 11 year old with septic shock and pneumonia, hypoxaemia, and a severe metabolic acidosis. She arrested with bradycardia then a brief period of asystole one minute after receiving 2.4 mg/kg ketamine with rocuronium for intubation.
Was the ketamine responsible for the arrests? Ketamine usually exhibits a stimulatory effect on the cardiovascular system, through effects which are incompletely understood but include a centrally mediated sympathetic response and probable inhibition of norepinephrine (noradrenaline) reuptake. However ketamine can have a direct depressant effect on cardiac output which is usually overridden by the sympathetic stimulation. In critically ill severely stressed patients the depressant effect may predominate. In a study on 12 critically ill surgical patients, haemodynamic indices were measured using pulmonary artery catheters within 5 minutes of ketamine administration (at a mean of 70 mg)(2). Six patients demonstrated decreases in ventricular contractility, and four had decreases in cardiac output. Mean arterial blood pressure decreased in four patients. The authors commented:
The patients..were septic, hypovolemic, or cirrhotic, and had severe stress preoperatively. It is possible that in these ill patients adrenocortical and catechol stores had been depleted prior to ketamine administration. Alternatively, in the setting of prolonged preoperative stress, there may be resistance to further sympathetic and/or adrenocotical stimulation by ketamine. In either case, preoperative stress may blunt the usual physiologic responses to ketamine, setting the stage for possible adverse effects.
The negative cardiovascular effects of ketamine may also be precipitated by larger doses or repeated doses of ketamine(3).
While this small case series of cardiac arrest following ketamine administration is interesting, we should bear in mind the other possible precipitants of arrest in these patients, which are not all discussed by the authors:
i) Both patients were hypoxaemic prior to induction and their peri-intubation oxygen saturations are not reported. Arrests following bradycardia at the time of induction in the critically ill are frequently related to hypoxaemia.
ii) The second patient had a severe metabolic acidosis and the first – an abdominal sepsis patient with a labored respiratory rate of 30 – very probably did too. A failure to match a patient’s compensatory respiratory alkalosis with hyperventilation after anaesthesia is known to precipitate arrest in acidaemic patients.
iii) Finally, if the ketamine was responsible for the arrests, one should consider that the doses given to these shocked and highly unstable patients were well in excess of what many of us would recommend, and doses in the range of 0.5-1 mg/kg might not have been associated with adverse effects.
The takehome points for me are that this report is a helpful reminder that the cardiovascular stimulation-inhibition balance of ketamine may be altered by severe critical illness, and that doses of any induction agent should be significantly reduced in the critically ill patient. In no way does this convince me that I should discard ketamine as my preferred choice for RSI in such patients.
Given their relative hemodynamic stability, ketamine and etomidate are commonly chosen anesthetic agents for sedation during the endotracheal intubation of critically ill patients. As the use of etomidate has come into question particularly in patients with sepsis, due to its effect of adrenal suppression, there has been a shift in practice with more reliance on ketamine. However, as ketamine relies on a secondary sympathomimetic effect for its cardiovascular stability, cardiovascular and hemodynamic compromise may occur in patients who are catecholamine depleted. We present 2 critically ill patients who experienced cardiac arrest following the administration of ketamine for rapid sequence intubation (RSI). The literature regarding the use of etomidate and ketamine for RSI in critically ill patients is reviewed and options for sedation during endotracheal intubation in this population are discussed.
Anesthetic induction with ketamine has been reported to maintain or improve cardiovascular performance in severely ill patients. Using invasive cardiovascular monitoring, we studied physiologic responses to a single dose of ketamine in 12 critically ill patients. Six patient demonstrated decreases in ventricular contractility, and four had decreases in cardiac output. Mean arterial blood pressure decreased in four patients. Pulmonary venous admixture increased in four of six patients, while oxygen consumption decreased in eight of 11 patients. Thus, a single dose of ketamine produced decreases in cardiac and pulmonary performance and in peripheral oxygen transport in this group of patients. It is proposed that in severely ill patients, preoperative stress may alter the usual physiologic responses to ketamine administration, and adverse effects may predominate. Ketamine, therefore, should be used with caution for induction of anesthesia in critically ill and in acutely traumatized patients until additional studies and further information on cardiovascular responses to ketamine are available.
Cardiorespiratory effects of ketamine and Althesin were measured in two groups of premedicated patients with cardiac disease. The drugs were given in clinically equivalent doses with a second dose administered about 10 min after induction. The first dose of ketamine caused a marked increase in systemic and pulmonary arterial pressure, heart rate, and central venous and wedge pressures and cardiac index. The first dose of Althesin caused a decrease in systemic arterial pressure, central venous pressure, cardiac index and heart work, but little change in heart rate. The second dose of induction agent was administered before the cardiorespiratory effects of the initial dose had resolved. The second dose of Althesin caused changes similar to those following the first dose, but less marked. The changes following the second dose of ketamine were opposite to those following the first dose.
A prospective open-label randomised controlled trial in prehospital patients receiving morphine for traumatic pain compared intravenous ketamine with additional morphine.
Analgesia was superior in the ketamine group, with some minor (expected) adverse effects.
This small study adds to the prehospital ketamine literature and provides some support to ambulance services considering introducing ketamine analgesia.
Study objective: We assess the efﬁcacy of intravenous ketamine compared with intravenous morphine in reducing pain in adults with signiﬁcant out-of-hospital traumatic pain.
Methods: This study was an out-of-hospital, prospective, randomized, controlled, open-label study. Patients with trauma and a verbal pain score of greater than 5 after 5 mg intravenous morphine were eligible for enrollment.
Patients allocated to the ketamine group received a bolus of 10 or 20 mg, followed by 10 mg every 3 minutes thereafter. Patients allocated to the morphine alone group received 5 mg intravenously every 5 minutes until pain free. Pain scores were measured at baseline and at hospital arrival.
Results: A total of 135 patients were enrolled between December 2007 and July 2010. There were no differences between the groups at baseline. After the initial 5-mg dose of intravenous morphine, patients allocated to ketamine received a mean of 40.6 mg (SD 25 mg) of ketamine. Patients allocated to morphine alone received a mean of 14.4 mg (SD 9.4 mg) of morphine. The mean pain score change was 5.6 (95% conﬁdence interval [CI] 6.2 to 5.0) in the ketamine group compared with 3.2 (95% CI 3.7 to 2.7) in the morphine group. The difference in mean pain score change was 2.4 (95% CI 3.2 to 1.6) points. The intravenous morphine group had 9 of 65 (14%; 95% CI 6% to 25%) adverse effects reported (most commonly nausea [6/65; 9%]) compared with 27 of 70 (39%; 95% CI 27% to 51%) in the ketamine group (most commonly disorientation [8/70; 11%]).
Conclusion: Intravenous morphine plus ketamine for out-of-hospital adult trauma patients provides analgesia superior to that of intravenous morphine alone but was associated with an increase in the rate of minor adverse effects.
A case is reported in Prehospital Emergency Care1 in which an agitated patient (due to mania and alcohol intoxication) received 5 mg/kg (500 mg) of ketamine intramuscularly by an EMS crew which dissociated him within a few minutes. He subsequently developed episodes of laryngospasm in the emergency department which were unrelieved by head tilt, chin lift and simple airway adjuncts but responded to bag-mask ventilation (BMV). The patient was intubated because the laryngospasm recurred, although it had again responded to BMV.
The authors make the point that because of the response of laryngospasm to simple manoeuvres, and because in the prehospital environment a patient will not be left without an EMS provider present, ‘restricting ketamine to EMS units capable of rapid-sequence intubation therefore seems unnecessary.‘
This is one for EMS directors to consider seriously. Personally, I think practicing prehospital care without access to ketamine is like having a hand tied behind my back. Ketamine opens up a world of possibilities in controlling combative patients, optimising scene safety, providing sedation for painful procedures including extrication, and enabling severe pain to be controlled definitively.
I’ve been using ketamine regularly for prehospital analgesia and emergency department procedural sedation in both adults and kids for more than a decade. I’ve seen significant laryngospasm 5 times (twice in kids). On one of those occasions, a 3 year old child desaturated to around 50% twice during two episodes of laryngospasm. We weren’t slow to pick it up – that was just her showing us how quickly kids can desaturate which continued while we went through a stepwise approach until BMV resolved it. It was however an eye opener for the registrar (senior resident) assisting me, who became extremely respectful of ketamine after that. Our ED sedation policy (that I wrote) required that suxamethonium was ready and available and that an appropriate dose had been calculated before anyone got ketamine. Paralysis may extremely rarely be required, but when it’s needed you need to be ready.
Laryngospasm is rare but most regular prescribers of ketamine will have seen it; the literature says it occurs in about 1-2% of sedations, although anecdotally I think it’s a bit less frequent. Importantly for those weighing the risks of allowing non-RSI competent prescribers, the requirement for intubation is exceptionally rare (2 of 11,589 reported cases in one review). Anyone interested should read this excellent review of ketamine-related adverse effects provided by Chris Nickson at Life in The Fast Lane. Chris reminds us of the Larson manouevre, which is digital pressure in the notch behind and below the ear, described by Larson2 as follows:
The technique involves placing the middle finger of each hand in what I term the laryngospasm notch. This notch is behind the lobule of the pinna of each ear. It is bounded anteriorly by the ascending ramus of the mandible adjacent to the condyle, posteriorly by the mastoid process of the temporal bone, and cephalad by the base of the skull. The therapist presses very firmly inward toward the base of the skull with both fingers, while at the same time lifting the mandible at a right angle to the plane of the body (i.e., forward displacement of the mandible or “jaw thrust”). Properly performed, it will convert laryngospasm within one or two breaths to laryngeal stridor and in another few breaths to unobstructed respirations.
I use this point most often to provide painful stimuli when assessing GCS in a patient, particular those I think may be feigning unconsciousness (I’ve done this for a number of years since learning how painful it can be when I was shown it by a jujitsu instructor). Dr Larson says he was taught the technique by Dr Guadagni, so perhaps we should be calling it the ‘Guadagni manouevre’. The lack of published evidence has led to some appropriate skepticism3, but as it can be combined with a jaw thrust it needn’t delay more aggressive interventions should they become necessary, it may work, and it’s likely to be harmless.
I presented the following suggested algorithm for management of laryngospasm during ketamine procedural sedation at a regional emergency medicine ‘Fellows Forum’ meeting in November 2007 in the UK. Since many paediatric procedural sedations were done using intramuscular (im) ketamine, it gives guidance based on whether or not vascular access has been obtained:
Some things I considered were:
Neuromuscular blockade (NMB) isn’t always necessary – laryngospasm may be managed with other sedatives such as propofol. However, titrating further sedatives in a desaturating child in my view is inferior to definitive airway management and laryngeal relaxation with suxamethonium and a tube.
Laryngospasm may be managed with much smaller doses of suxamethonium than are required for intubation – as little as 0.1 mg/kg may be effective. However, I think once we go down the NMB route we’re committed to intubation and therefore we should use a dose guaranteed to be effective in achieving intubating conditions.
In the child without vascular access, I considered intraosseous and intralingual sux. However, intramuscular suxamethonium is likely to have a relaxant effect on the laryngeal muscles within 30-45 seconds, which has to be compared with time taken to insert and confirm intraosseous needle placement. I do not think the traditionally recommended intralingual injection has any role to play in modern airway management.
At the time I wrote this most paediatric resuscitation bays in my area in the United Kingdom had breathing circuits capable of delivering PEEP – usually the Ayr’s T-Piece (specifically the Mapleson F system), which is why PEEP was included early in in the algorithm prior to BMV.
I have since modified it for two reasons: firstly, we might as well do the Larson manoeuvre during the jaw thrust; secondly, many Australasian and US EDs will only be able to deliver PEEP with a PEEP valve attached to a BVM, so PEEP has been moved to the BVM stage.
I would love to hear what people are doing in their prehospital and inhospital practice. Should ketamine only be administered by providers who can offer RSI? Do you have a laryngospasm protocol? If so, I’d love to see it. If not, feel free to use or adapt my unvalidated one at your own risk.
ABSTRACT An advanced life support emergency medical services (EMS) unit was dispatched with law enforcement to a report of a male patient with a possible overdose and psychiatric emergency. Police restrained the patient and cleared EMS into the scene. The patient was identified as having excited delirium, and ketamine was administered intramuscularly. Sedation was achieved and the patient was transported to the closest hospital. While in the emergency department, the patient developed laryngospasm and hypoxia. The airway obstruction was overcome with bag–valve–mask ventilation. Several minutes later, a second episode of laryngospasm occurred, which again responded to positive-pressure ventilation. At this point the airway was secured with an endotracheal tube. The patient was uneventfully extubated several hours later. This is the first report of laryngospam and hypoxia associated with prehospital administration of intramuscular ketamine to a patient with excited delirium.
What are the best sedatives for patients with traumatic brain injury? A systematic review found no evidence that one sedative agent is better than another for improvement of neurologic outcome or mortality in critically ill adults with severe TBI. Thirteen randomised trials including around 380 patients were reviewed.
reduce metabolic requirements of the injured brain to avoid ischemic progression of the traumatic lesion in presence of increased ICP
facilitate mechanical ventilation to control PaCo2
avoid ICP rises due to airway instrumentation such as those induced by coughing
Sedation generally improved intracranial pressure (ICP) and cerebral perfusion pressure (CPP) vs. baseline in most trials.
Interestingly boluses or short infusions of opioids resulted in (often transient) increases in ICP and decreases in MAP and CPP in three RCTs. An accompanying editorial suggests this may be due to large opioid doses (up to 3 μg/kg of fentanyl) and consequent hypotension; hypotension itself may trigger autoregulatory cerebral vasodilatation and increase ICP and decrease CPP. Although opioids have been linked with increased ICP through decreased cerebrovascular resistance, increased cerebral blood flow or Paco2, and disturbed cerebral autoregulation, they state that in studies in which hypotension after opioid administration was prevented, an ICP increasing effect was not seen. It is important to note the small sample sizes studied and the long time period of studies included, dating back some decades.
Importantly, ketamine did not result in the increase in ICP purported by older literature.
OBJECTIVES: To summarize randomized controlled trials on the effects of sedative agents on neurologic outcome, mortality, intracranial pressure, cerebral perfusion pressure, and adverse drug events in critically ill adults with severe traumatic brain injury.
DATA SOURCES: PubMed, MEDLINE, EMBASE, the Cochrane Database, Google Scholar, two clinical trials registries, personal files, and reference lists of included articles.
STUDY SELECTION: Randomized controlled trials of propofol, ketamine, etomidate, and agents from the opioid, benzodiazepine, α-2 agonist, and antipsychotic drug classes for management of adult intensive care unit patients with severe traumatic brain injury.
DATA EXTRACTION: In duplicate and independently, two investigators extracted data and evaluated methodologic quality and results.
DATA SYNTHESIS: Among 1,892 citations, 13 randomized controlled trials enrolling 380 patients met inclusion criteria. Long-term sedation (≥24 hrs) was addressed in six studies, whereas a bolus dose, short infusion, or doubling of plasma drug concentration was investigated in remaining trials. Most trials did not describe baseline traumatic brain injury prognostic factors or important cointerventions. Eight trials possibly or definitely concealed allocation and six were blinded. Insufficient data exist regarding the effects of sedative agents on neurologic outcome or mortality. Although their effects are likely transient, bolus doses of opioids may increase intracranial pressure and decrease cerebral perfusion pressure. In one study, a long-term infusion of propofol vs. morphine was associated with a reduced requirement for intracranial pressure-lowering cointerventions and a lower intracranial pressure on the third day. Trials of propofol vs. midazolam and ketamine vs. sufentanil found no difference between agents in intracranial pressure and cerebral perfusion pressure.
CONCLUSIONS: This systematic review found no convincing evidence that one sedative agent is more efficacious than another for improvement of patient-centered outcomes, intracranial pressure, or cerebral perfusion pressure in critically ill adults with severe traumatic brain injury. High bolus doses of opioids, however, have potentially deleterious effects on intracranial pressure and cerebral perfusion pressure. Adequately powered, high-quality, randomized controlled trials are urgently warranted.
As well as the benefits of cardiovascular stability, maintenance of cerebral perfusion pressure, possibly lowering ICP and providing other neuroprotective benefits, ketamine may have other advantages. These are reviewed in a British Journal of Anaesthesia article from which I’ve selected those benefits of interest to practitioners of emergency medicine and critical care.
Additional Beneficial Effects of Ketamine
the dysphoric, or ’emergence’ reactions associated with ketamine may be reduced by pre-administration or co-administration of sedatives, such as benzodiazepines, propofol, dexmedetomidine, or droperidol.
ketamine potentiates opioid analgesia in multiple settings, reducing opioid total dose and in some groups of patients reducing postoperative desaturation
ketamine has possible anti-inflammatory effects demonstrated in some types of surgical patients
ketamine may prevent awareness, recall, or both during general anaesthesia
I published a case report in the EMJ highlighting the use of intranasal ketamine in a pre-hospital paediatric burns case.
The lad had nasty scalds but did not need iv fluids and had no other indications for an iv line. The vigorous first aid had rendered him cold and veinless and an intraosseous would have been overkill. Ketamine was perfect for the job and Ambulance Service New South Wales paramedics carry a mucosal atomisation device (MAD) for the administration of i.n. fentanyl. I used the MAD to adminster 0.5 mg/kg ketamine, but there is a dead space in the device (0.1 ml) that probably resulted in actual delivery of 0.25mg/kg. This gave great analgesia and compliance enabling us to painlessly apply polyethylene film to the burns.
I received the following email from TIm Wolfe, the inventor of the MAD nasal (reproduced with permission):
Nice contribution to the literature. There is a lot of interest in IN ketamine in these lower doses to treat pain but not cause sedation. You eluded to the military interest and the hospice interest. I think your insights for EMS are also cutting edge – hopefully this will lead others to design a larger trial.
Tim Wolfe, MD
More information on the use of intranasal medication is available at www.intranasal.net. I have no conflicts of interest to declare.
In adults undergoing procedural sedation with ketamine, 0.03 mg/kg IV midazolam reduced recovery agitation compared with placebo.
STUDY OBJECTIVE: We assess whether midazolam reduces recovery agitation after ketamine administration in adult emergency department (ED) patients and also compared the incidence of adverse events (recovery agitation, respiratory, and nausea/vomiting) by the intravenous (IV) versus intramuscular (IM) route.
METHODS: This prospective, double-blind, placebo-controlled, 2×2 factorial trial randomized consecutive ED patients aged 18 to 50 years to 4 groups: receiving either 0.03 mg/kg IV midazolam or placebo, and with ketamine administered either 1.5 mg/kg IV or 4 mg/kg IM. Adverse events and sedation characteristics were recorded.
RESULTS: Of the 182 subjects, recovery agitation was less common in the midazolam cohorts (8% versus 25%; difference 17%; 95% confidence interval [CI] 6% to 28%; number needed to treat 6). When IV versus IM routes were compared, the incidences of adverse events were similar (recovery agitation 13% versus 17%, difference 4%, 95% CI -8% to 16%; respiratory events 0% versus 0%, difference 0%, 95% CI -2% to 2%; nausea/vomiting 28% versus 34%, difference 6%, 95% CI -8% to 20%).
CONCLUSION: Coadministered midazolam significantly reduces the incidence of recovery agitation after ketamine procedural sedation and analgesia in ED adults (number needed to treat 6). Adverse events occur at similar frequency by the IV or IM routes.
What are the factors associated with laryngospasm in ketamine sedation? A large study was unable to identify specific predictors:
Objective: The objective of this study was to assess predictors of emergency department (ED) ketamine-associated laryngospasm using case-control techniques.
Methods: We performed a matched case-control analysis of a sample of 8282 ED ketamine sedations (including 22 occurrences of laryngospasm) assembled from 32 prior published series. We sequentially studied the association of each of 7 clinical variables with laryngospasm by assigning 4 controls to each case while matching for the remaining 6 variables. We then used univariate statistics and conditional logistic regression to analyze the matched sets.
Results: We found no statistical association of age, dose, oropharyngeal procedure, underlying physical illness, route, or coadministered anticholinergics with laryngospasm. Coadministered benzodiazepines showed a borderline association in the multivariate but not univariate analysis that was considered anomalous.
Conclusions: This case-control analysis of the largest available sample of ED ketamine-associated laryngospasm did not demonstrate evidence of association with age, dose, or other clinical factors. Such laryngospasm seems to be idiosyncratic, and accordingly, clinicians administering ketamine must be prepared for its rapid identification and management. Given no evidence that they decrease the risk of laryngospasm, coadministered anticholinergics seem unnecessary.
Despite the huge number of articles in the literature on paediatric sedation, one still encounters acrimonious debates about the appropriateness of non-anaesthetists doing it. How refreshing then, to see that the UK’s National Institute for Health & Clinical Excellence (“NICE”) has tackled this subject and come up with some reasonable recommendations. I’ve as yet only read the summary, but some of the good things are:
No unachievable ‘two doctors present’ rule: ‘Two trained healthcare professionals should be available during sedation‘
Differentiating painless imaging from painful procedures
Monitoring standards that are appropriate for the age of child and depth of sedation (no mandatory blood pressure or ECG monitoring unless deep sedation; end-tidal capnography in deep sedation).
Acknowledgement of the special features of ketamine: ‘Ketamine is a dissociative agent: the state of dissociative sedation cannot be readily categorised as either moderate or deep sedation; the drug is considered to have a wide margin of safety.’
Recognition that specialists other than anaesthetists may have specialist sedation and airway skills
There are some rather conservative recommendations on fasting, although the wording of the guideline in my interpretation allows some flexibility if ketamine is used for an emergency procedure.