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Oral Sedation Postdischarge Adverse Events in Pediatric Dental Patients
Annie HuangDMD and
Thomas TanbonliongDDS
Article Category: Research Article
Volume/Issue: Volume 62: Issue 3
Online Publication Date: Jan 01, 2015
DOI: 10.2344/0003-3006-62.3.91
Page Range: 91 – 99

combinations of a narcotic (eg, morphine or meperidine), a sedative-hypnotic (eg, chloral hydrate), a benzodiazepine (eg, midazolam or diazepam), and/or an antihistamine (eg, hydroxyzine HCl) ( Figure 1 ) at the following dosages: 0.66 mg/kg for morphine, 2 mg /kg for meperidine, 0.5–0.7 mg/kg for midazolam, 0.5–.7 mg/kg for diazepam, and 2 mg/kg for hydroxyzine HCl. Figure 1. Distribution of oral sedation regimens. Figure 1. Distribution of oral sedation regimens. Following the

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Figure 3; Molecular structures of morphine, codeine, and derivatives. Codeine and its derivatives differ from their morphine-derived counterparts only in a methyl substitution (circled). This methyl group prevents adequate binding to the mu opioid receptor that mediates most opioid effects. However, these prodrugs are capable of producing nausea and constipation, which are problematic when high doses are administered to generate enough active metabolite for analgesia. (Asterisks indicate molecular alterations from morphine and codeine.)
Daniel E. Becker and
James C. Phero
Figure 3
Figure 3

Molecular structures of morphine, codeine, and derivatives. Codeine and its derivatives differ from their morphine-derived counterparts only in a methyl substitution (circled). This methyl group prevents adequate binding to the mu opioid receptor that mediates most opioid effects. However, these prodrugs are capable of producing nausea and constipation, which are problematic when high doses are administered to generate enough active metabolite for analgesia. (Asterisks indicate molecular alterations from morphine and codeine.)

Figure 3; Molecular structures of morphine, codeine, and derivatives. The top row illustrates molecular structures for morphine and its two derivatives, hydromorphone and oxymorphone. The subtle changes indicated by the asterisks enhance affinity for the opioid receptors, which accounts for greater potency. The bottom row illustrates codeine and its derivatives, which differ from their morphine-derived counterparts only in a methyl substitution (circled). Approximately 60% of an oral dose of codeine-related products is absorbed and may be subjected to varying degrees of demethylation by CYP2D6 to its active metabolite. Framed molecules are those credited with the analgesic effect provided by various codeine-related products. Codeine has little affinity for opioid receptors. Roughly 10% of an absorbed dose is demethylated to morphine, which is credited with its analgesic effect. Hydrocodone and oxycodone have good receptor affinity and provide an analgesic effect. The analgesic effect of hydrocodone is credited to both the parent drug and its active metabolite, hydromorphone, but analgesia provided by oxycodone is almost entirely the result of the parent drug. Very little is demethylated to oxymorphone.
Daniel E. Becker
Figure 3
Figure 3

Molecular structures of morphine, codeine, and derivatives. The top row illustrates molecular structures for morphine and its two derivatives, hydromorphone and oxymorphone. The subtle changes indicated by the asterisks enhance affinity for the opioid receptors, which accounts for greater potency. The bottom row illustrates codeine and its derivatives, which differ from their morphine-derived counterparts only in a methyl substitution (circled). Approximately 60% of an oral dose of codeine-related products is absorbed and may be subjected to varying degrees of demethylation by CYP2D6 to its active metabolite. Framed molecules are those credited with the analgesic effect provided by various codeine-related products. Codeine has little affinity for opioid receptors. Roughly 10% of an absorbed dose is demethylated to morphine, which is credited with its analgesic effect. Hydrocodone and oxycodone have good receptor affinity and provide an analgesic effect. The analgesic effect of hydrocodone is credited to both the parent drug and its active metabolite, hydromorphone, but analgesia provided by oxycodone is almost entirely the result of the parent drug. Very little is demethylated to oxymorphone.

Figure 1 ; Analgesic prodrugs, codeine and tramadol, require metabolism by CYP 2D6 to their active metabolites, morphine and o-desmethyltramadol, respectively. CYP2D6 inhibition by SSRIs (fluoxetine, paroxetine) may result in inadequate analgesia. From Hersh EV, Moore PA. JADA. 2004;135:298–311.
Mana Saraghi,
Leonard Golden, and
Elliot V. Hersh
<bold>Figure 1</bold>
Figure 1

Analgesic prodrugs, codeine and tramadol, require metabolism by CYP 2D6 to their active metabolites, morphine and o-desmethyltramadol, respectively. CYP2D6 inhibition by SSRIs (fluoxetine, paroxetine) may result in inadequate analgesia. From Hersh EV, Moore PA. JADA. 2004;135:298–311.

Figure 2; Analgesic efficacy. This graph illustrates a typical dose-response curve for orally administered (PO) analgesics. The dose-response curve for opioids such as morphine demonstrates unlimited efficacy in which greater doses provide greater analgesia. At equipotent doses, all opioids demonstrate a similar dose response. In contrast, nonopioids demonstrate a “ceiling” effect that generally is adequate for relief of mild to moderate pain (pain relief rating of 4–5 in this scale). For ibuprofen, doses greater than 400 mg do not provide further analgesia. For aspirin (ASA) and acetaminophen (APAP), this ceiling effect is achieved at 1000 mg and is somewhat lower than that provided by nonsteroidal anti-inflammatory drugs (NSAIDs).
Daniel E. Becker
Figure 2
Figure 2

Analgesic efficacy. This graph illustrates a typical dose-response curve for orally administered (PO) analgesics. The dose-response curve for opioids such as morphine demonstrates unlimited efficacy in which greater doses provide greater analgesia. At equipotent doses, all opioids demonstrate a similar dose response. In contrast, nonopioids demonstrate a “ceiling” effect that generally is adequate for relief of mild to moderate pain (pain relief rating of 4–5 in this scale). For ibuprofen, doses greater than 400 mg do not provide further analgesia. For aspirin (ASA) and acetaminophen (APAP), this ceiling effect is achieved at 1000 mg and is somewhat lower than that provided by nonsteroidal anti-inflammatory drugs (NSAIDs).

Figure 1.; Distribution of oral sedation regimens.
Annie Huang and
Thomas Tanbonliong
Figure 1.
Figure 1.

Distribution of oral sedation regimens.

Figure 2.; Frequency of time to return to normal behavior and routine.
Annie Huang and
Thomas Tanbonliong
Figure 2.
Figure 2.

Frequency of time to return to normal behavior and routine.

Figure 3.; Comparison of sedation levels versus various presedation factors and behaviors.
Annie Huang and
Thomas Tanbonliong
Figure 3.
Figure 3.

Comparison of sedation levels versus various presedation factors and behaviors.

Figure 4.; Comparison of responsiveness to treatment versus presedation factors and behaviors.
Annie Huang and
Thomas Tanbonliong
Figure 4.
Figure 4.

Comparison of responsiveness to treatment versus presedation factors and behaviors.

Figure 5.; Comparison of sedation efficacy versus presedation factors and behaviors.
Annie Huang and
Thomas Tanbonliong
Figure 5.
Figure 5.

Comparison of sedation efficacy versus presedation factors and behaviors.