Oral Sucrose and Pain Relief for Preterm Infants

Anita Mitchell, RN, PhD, Patricia A. Waltman, RNC, EdD, NNP

Disclosures

Pain Manag Nurs. 2003;4(2) 

In This Article

Physiologic Mechanisms and Background of Oral Sucrose

Studies support the theory that sucrose and pain relief are interrelated through the body's endogenous opioid system that provides natural analgesia (Barr et al., 1995; Nikfar, Abdollahi, Etemad, & Sharifzadeh, 1997). Sucrose as an analgesic was first studied using laboratory rats. In 1987, researchers demonstrated that rats receiving an oral infusion of 7.5% sucrose experienced a significant elevation in pain thresholds compared with groups of rats that received an oral infusion of water or no infusion (Blass, Fitzgerald, & Kehoe, 1987). The analgesic effect of sucrose is reversed with administration of naloxone, an opioid antagonist, suggesting that sucrose activates the central endogenous opioid system with an action similar to that of opioid analgesics (Barr et al., 1995; Blass et al., 1987). The analgesic action of sucrose may involve descending pain-modulating mechanisms, with inhibition of pain transmission at the spinal level. The presence of sucrose in the mouth also may stimulate the release of endorphins from the hypothalamus (Ren, Blass, Zhou, & Dubner, 1997).

Studies with infants indicate that the pain-reducing qualities of sucrose appear to be in its sweet taste, and do not rely on systemic absorption. In a double-blind crossover study of 30 preterm infants of 32 to 36 weeks' gestational age, sucrose effectively reduced pain when given by mouth but not when administered through a nasogastric tube (Ramenghi, Evans, & Levene, 1999). In another study that examined the action of sweet-tasting solutions, 60 full-term newborns were assigned randomly to four treatment groups. Each infant received one of the following: sterile water, 25% sucrose, 50% sucrose, or Calpol (a sweet-tasting solution). The artificially sweetened solution was as effective as both sucrose solutions in relieving pain, which suggests that the analgesic effect was due to sweet taste and not systemic absorption of sucrose products (Ramenghi, Griffith, Wood, & Levene, 1996). Similar results were found in a study that compared the effectiveness of the artificial sweetener aspartame with 24% sucrose (Barr, Pantel, Young, Wright, Hendricks, & Gravel, 1999). These authors described the analgesic action as a "sweetness effect" (p. 415).

Questions arose regarding the use of glucose, or breast milk as a substitute for sucrose. However, no studies have examined the use of alternate sweet liquids with preterm infants. A study with term newborn infants found that 30% glucose significantly reduced crying time (p < .01) and reduced increases in heart rate during heelsticks. The researchers concluded that 30% glucose was effective in relieving pain during procedures (Skogsdal, Eriksson, & Schollin, 1997). In a study that compared the effectiveness of breast milk with 25% sucrose as an analgesic during heelsticks in term newborns, sucrose was found to be effective in reducing crying time and heart rate, but breast milk did not make a significant difference in crying time or heart rate (Ors et al., 1999).

The peak response time for sucrose is compatible with the time needed to activate the endogenous opioid system. In a study that focused on response time, infants received oral sucrose followed by heelsticks at 30, 60, 90, 120, and 240 seconds. The maximum reduction in crying was noted in the 120-second heelstick group. This time delay is consistent with the time needed for the release of endogenous opioids by taste stimulation and the time needed to occupy opioid receptor sites (Blass & Shah, 1995).

At this time, there are no reports of side effects associated with the administration of single, small (< 2 ml) doses of 24% sucrose to term or preterm infants. Sucrose solution used in small doses for analgesia has not been shown to cause hyperglycemia in preterm infants (Bucher et al., 1995).

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