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Educational Objectives - After evaluating this article, participants will be able to:

1. Incorporate a rational approach to the NPO status of patients receiving procedural sedation

2. Effectively utilize ondansetron as a pre-treatment agent in procedural sedation

3. Develop evidence-based strategies for consideration of atropine use with ketamine

Q. Do children who have been fasting do better than those who have not fasted prior to using ketamine?

A.“No!” The citation below shows that children who fasted more than 3 hours prior to ketamine use had a higher incidence of vomiting than children who were NPO for less than one hour

Citation:

Treston G.Prolonged pre-procedure fasting time is unnecessary when using titrated intravenous ketamine for paediatric procedural sedation. Emerg Med Australas. 2004 Apr;16(2):145-50.

Objectives: To prospectively address the relationship between preprocedure fasting time and intraprocedure or postprocedure vomiting in children aged 1-12 years undergoing procedural sedation with intravenous ketamine in the ED.

Methodology: From January 1999 to May 2000 all children presenting to the Royal Darwin Hospital Emergency Department with a condition requiring ketamine PPS were enrolled for data collection after parental consent was obtained. Titrated intravenous ketamine was administered via protocol. Prospective ED procedural sedation data collection forms of 272 consecutive cases of titrated intravenous ketamine sedation were reviewed.

Findings: Fasting time was accurately recorded on 257 (95%) data collection forms. There was no intraprocedure vomiting. Overall rate of postprocedure vomiting was 13.9%. No statistically significant association between decreased fasting time and increased incidence of vomiting was found. In fact, there was a trend towards increased incidence of vomiting with increased fasting time (P = 0.08). The rate of vomiting of those children fasted 3 h or greater preprocedure (20/127 or 15.8%) was over twice the rate of those fasted less than 1 hour (2/30 or 6.6%). Incidence of vomiting was significantly associated with increasing age (P = 0.0007). No clinically evident aspiration pneumonitis occurred.

Conclusion: Prolonged preprocedure fasting time did not reduce the incidence of postprocedure vomiting in this case series; to the contrary there was a increased incidence of vomiting with longer fasting times (P = 0.08). There was an increase in postprocedure vomiting with increasing age of the patients.

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Q. Does the pre-sedation use of ondansetron decrease the incidence of post-ketamine vomiting?

A.The use of ondansetron significantly decreased the incidence of vomiting after ketamine sedation- 4.7% in the ondansetron group versus 12.6% in patients who did not receive ondansetron.

Citation:

Langston WT, Wathen JE, Roback MG, Bajaj L. Effect of ondansetron on the incidence of vomiting associated with ketamine sedation in children: a double-blind, randomized, placebo-controlled trial. Ann Emerg Med2008 Jul;52(1):30-4. Epub 2008 Mar 19.  

Objective: We investigate the effect of ondansetron on the incidence of vomiting in children who receive intravenous (IV) ketamine for procedural sedation and analgesia in the emergency department (ED).

Methodology: In this double-blind, randomized, placebo-controlled trial in a children’s hospital ED, patients receiving IV ketamine (1 mg/kg) for ED procedures were randomized to receive either IV ondansetron (0.15 mg/kg; maximum 4 mg) or placebo. We recorded whether vomiting occurred in the ED postsedation or up to 12 hours after discharge with telephone follow-up and compared ED length of stay and parental satisfaction.

Findings: One hundred twenty-seven children were randomized to placebo and 128 to ondansetron. The groups were similar in age, sex, and fasting duration. ED vomiting was less common with ondansetron: 6 of 128 (4.7%) versus 16 of 127 (12.6%), P=.02, difference 7.9% (95% confidence interval 1.1% to 14.7%), number needed to treat 13. Follow-up was successful in 82.7%, with vomiting in the ED or after discharge less frequent with ondansetron: 10 of 128 (7.8%) versus 24 of 127 (18.9%), P=.01, difference 11.1% (95% confidence interval 2.7% to 19.5%), number needed to treat 9. ED length of stay and parental satisfaction were similar between groups.

Conclusion: IV ondansetron significantly reduces the incidence of vomiting associated with IV ketamine procedural sedation in children.

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Q. Is atropine use necessary when using ketamine?

A.This one is a bit tougher as there are two recent articles on this issue. The first one states that atropine is not necessary, the other states that atropine is useful in decreasing salivation (analysis of study #2, Heinz 2006, is available online at epmonthly.com). My take on this topic is that I would use atropine if I am suturing a tongue as any assistance is helpful. However, since ketamine and atropine as individual agents can make patients tachycardic, it is probably not necessary for routine sedations.

Citation:

Brown L, Christian-Kopp S, Sherwin TS,etal  Adjunctive atropine is unnecessary during ketamine sedation in children. Acad Emerg Med. 2008 Apr;15(4):314-8.  

Background: The prophylactic coadministration of atropine or other anticholinergics during dissociative sedation has historically been considered mandatory to mitigate ketamine-associated hypersalivation. Emergency physicians (EPs) are known to omit this adjunct, so a prospective study to describe the safety profile of this practice was initiated.

Objectives: To quantify the magnitude of excessive salivation, describe interventions for hypersalivation, and describe any associated airway complications.

Methodology: In this prospective observational study of emergency department (ED) pediatric patients receiving dissociative sedation, treating physicians rated excessive salivation on a 100-mm visual analog scale and recorded the frequency and nature of airway complications and interventions for hypersalivation.

Findings: Of 1,090 ketamine sedations during the 3-year study period, 947 (86.9%) were performed without adjunctive atropine. Treating physicians assigned the majority (92%) of these subjects salivation visual analog scale ratings of 0 mm, i.e., “none,” and only 1.3% of ratings were >or= 50 mm. Transient airway complications occurred in 3.2%, with just one (brief desaturation) felt related to hypersalivation (incidence 0.11%, 95% confidence interval = 0.003% to 0.59%). Interventions for hypersalivation (most commonly suctioning) occurred in 4.2%, with no occurrences of assisted ventilation or intubation.

Conclusion: When adjunctive atropine is omitted during ketamine sedation in children, excessive salivation is uncommon, and associated airway complications are rare. Anticholinergic prophylaxis is not routinely necessary in this setting.

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Q. Isn’t ketamine contraindicated in head injury?

A. Great news is emerging from the pediatric literature supporting the use of ketamine in patients with head injury as it can help maintain cerebral perfusion pressure and does not decrease blood pressure. The studies to date have been on intubated patients and while there are no ED studies to date, the critical care literature is very promising and we will hopefully be seeing increased use of ketamine for patients with acute head injury in our departments. Stay tuned for more articles on this topic!

Citation:

Bar-Joseph G, Guilburd Y, Tamir A, Guilburd JN.Effectiveness of ketamine in decreasing intracranial pressure in children with intracranial hypertension. Neurosurg Pediatr. 2009 Jul;4(1):40-6.  

Summary: Deepening sedation is often needed in patients with intracranial hypertension. All widely used sedative and anesthetic agents (opioids, benzodiazepines, propofol, and barbiturates) decrease blood pressure and may therefore decrease cerebral perfusion pressure (CPP). Ketamine is a potent, safe, rapid-onset anesthetic agent that does not decrease blood pressure. However, ketamine’s use in patients with traumatic brain injury and intracranial hypertension is precluded because it is widely stated that it increases intracranial pressure (ICP). Based on anecdotal clinical experience, the authors hypothesized that ketamine does not increase-but may rather decrease-ICP.

Methodology: The authors conducted a prospective, controlled, clinical trial of data obtained in a pediatric intensive care unit of a regional trauma center. All patients were sedated and mechanically ventilated prior to inclusion in the study. Children with sustained, elevated ICP (> 18 mm Hg) resistant to first-tier therapies received a single ketamine dose (1-1.5 mg/kg) either to prevent further ICP increase during a potentially distressing intervention (Group 1) or as an additional measure to lower ICP (Group 2). Hemodynamic, ICP, and CPP values were recorded before ketamine administration, and repeated-measures analysis of variance was used to compare these values with those recorded every minute for 10 minutes following ketamine administration.

Findings: The results of 82 ketamine administrations in 30 patients were analyzed. Overall, following ketamine administration, ICP decreased by 30% (from 25.8 +/- 8.4 to 18.0 +/- 8.5 mm Hg) (p < 0.001) and CPP increased from 54.4 +/- 11.7 to 58.3 +/- 13.4 mm Hg (p 2 mm Hg during the distressing intervention in only 1 of 17 events. In Group 2, when ketamine was administered to lower persistent intracranial hypertension, ICP decreased by 33% (from 26.0 +/- 9.1 to 17.5 +/- 9.1 mm Hg) (p < 0.0001) following ketamine administration.

Conclusion: In ventilation-treated patients with intracranial hypertension, ketamine effectively decreased ICP and prevented untoward ICP elevations during potentially distressing interventions, without lowering blood pressure and CPP. These results refute the notion that ketamine increases ICP. Ketamine is a safe and effective drug for patients with traumatic brain injury and intracranial hypertension, and it can possibly be used safely in trauma emergency situations


 

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