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Primer of Postoperative Pruritus for Anesthesiologists Beverly Waxler, M.D.,* Zerin P

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Primer of Postoperative Pruritus for Anesthesiologists Beverly Waxler, M.D.,* Zerin P Ⅵ REVIEW ARTICLE David C. Warltier, M.D., Ph.D., Editor Anesthesiology 2005; 103:168–78 © 2005 American Society of Anesthesiologists, Inc. Lippincott Williams & Wilkins, Inc. Primer of Postoperative Pruritus for Anesthesiologists Beverly Waxler, M.D.,* Zerin P. Dadabhoy, M.D.,* Ljuba Stojiljkovic, M.D., Ph.D.,† Sara F. Rabito, M.D., F.A.H.A.‡ pruritus. There is still much unknown about postopera- Downloaded from http://pubs.asahq.org/anesthesiology/article-pdf/103/1/168/358674/0000542-200507000-00025.pdf by guest on 23 September 2021 This article has been selected for the Anesthesiology CME Program. After reading the article, go to http://www. tive itching in patients with diseases associated with asahq.org/journal-cme to take the test and apply for Cate- pruritus, e.g., (1) the incidence of pruritus after receiving gory 1 credit. Complete instructions may be found in the opioids via the neuraxial route, (2) whether the use of CME section at the back of this issue. opioids in patients with these disorders would potenti- ate their pruritus, (3) whether the development of pru- Postoperative itching is an important problem in the post- ritus in these patients when treated with neuraxial opi- operative care unit. Pruritus after surgery may be drug induced oids is a side effect of the opioid or the natural (including intrathecal opioids) or secondary to a preexisting manifestation of the disease. systemic disease. Mechanisms of itching are complex and not The purpose of this review is to facilitate an under- completely understood. The purpose of this review is to high- standing of the pathways and mediators involved in the light new discoveries in pathways and mechanisms of pruritus and to summarize up-to-date knowledge about treatment of development and central transmission of the itch sensa- itching after surgery. More basic and clinical studies are needed tion, to describe the methods available to evaluate itch, to address the effects of drugs on specific receptors and im- and to provide a basis for its rational therapy. We also prove the treatment of postoperative pruritus. wanted to summarize the up-to-date knowledge about systemic diseases that have pruritus as a symptom and UNDERSTANDING different mechanisms of pruritus is may be associated with an increase in the incidence of necessary to diagnose and treat postoperative pruritus. pruritus in the perioperative period. Pruritus is an unpleasant, localized or generalized sen- sation on the skin, mucous membranes, or conjunctivae, which the patient instinctively attempts to relieve by Pathways scratching or rubbing. Itching is a disturbing feeling (or sensation), and scratching is the response (or action). The mechanisms of pruritus have been poorly under- Itch can be induced by nonpathologic conditions such as stood in the past because it was considered solely from the movement of a hair, whereas pruritus represents a the neurophysiologic point of view as a submodality of condition in which itch is present without a normal pain. However, more recent studies have shown that cause. pain and pruritus are sensations transmitted through The origin of pruritus can be cutaneous (prurito- different populations of primary sensory neurons. A sub- ceptive), neuropathic, neurogenic, mixed, or psycho- class of C-nociceptors, which is mechano-insensitive and genic.1–6 The use of opioids intrathecally or epidurally histamine-sensitive, transmits itch.7 These fibers, which frequently results in itching. This uncomfortable adverse originate in the skin at the junction of the dermis and event requires the use of therapeutic agents in most epidermis, have thin axons but extensive terminal circumstances, which can be ineffective or even reverse branching. These unmyelinated C-fibers transmit itch the analgesic effect of the opioid. impulses to the ipsilateral dorsal horn of the spinal Several systemic and skin diseases are associated with cord,3 where they synapse with itch-specific secondary neurons. These secondary neurons immediately cross over to the opposite anterolateral spinothalamic tract3 to * Assistant Professor, † Anesthesiology Resident, ‡ Associate Professor. the thalamus and then to the somatosensory cortex of Received from the Department of Anesthesiology and Pain Management, John 6 H. Stroger Jr. Hospital of Cook County, Chicago, Illinois, and Rush Medical the postcentral gyrus (fig. 1). C-fibers that mediate itch College of Rush University, Chicago, Illinois. Submitted for publication April 14, have extremely low conduction velocities (mean, 2004. Accepted for publication December 3, 2004. Support was provided solely from institutional and/or departmental sources. Presented at the Midwestern 0.5 m/s), approximately half those of mechano-heat no- Residents’ Conference, Rochester, Minnesota, March 19–21, 2004 (Stojiljkovic L, ciceptors, and receptor fields that are approximately Waxler B, Dadabhoy Z, Rabito S: Post-operative itching: Possible mechanisms and 7–9 associated systemic conditions). three times larger (up to 85 mm in diameter). This Address reprint requests to Dr. Waxler: Division Chair, Division of Postanes- pathway is the only one identified so far, but others not thesia Care, Department of Anesthesiology and Pain Management, John H. Stroger Jr. Hospital of Cook County, 1901 West Harrison Street, Chicago, Illinois yet discovered may exist. 60612. Address electronic mail to: [email protected]. When histamine induces itch, it activates both the Anesthesiology, V 103, No 1, Jul 2005 168 PRIMER OF PRURITUS 169 Fig. 1. Afferent itching pathways. Pri- mary neurons consist of unmyelinated subclass of C-nociceptors (mechano-in- sensitive and histamine-sensitive) that synapse with itch-specific second-order neurons in dorsal horn of the spinal cord. The secondary neurons immedi- ately cross over to join opposite antero- lateral spinothalamic tract and travel to the thalamus, where they synapse with third-order neurons. These third-order neurons travel to the somatosensory cor- Downloaded from http://pubs.asahq.org/anesthesiology/article-pdf/103/1/168/358674/0000542-200507000-00025.pdf by guest on 23 September 2021 -dor ؍ tex of the postcentral gyrus. DRG -aminobu-␥ ؍ sal root ganglion; GABA tyric acid. anterior cingulate cortex, thus both the sensorial and 85% of histamine receptors in the skin are of the H1 emotional aspects of itch, and the supplemental motor subtype, and the remaining 15% are H2 receptors.19 area. The latter is thought to participate in the prepara- Wheal-and-flare reactions may be associated with itch- tion of the scratching response.10–12 Although the itch ing. The addition of an H2 receptor antagonist to an H1 sensation seems to be transmitted by a subset of C-fibers, receptor blocker augments the inhibition of a histamine- which, as described above, are different from those induced wheal-and-flare reaction. Therefore, H2 recep- involved in the transmission of pain, increasing evidence tor antagonists have been combined with H1 receptor supports an interrelation between these two distinct antagonists in the treatment of chronic urticaria20 and sensations. Painful stimuli, such as thermal, mechanical, burn-wound itch.21 or chemical, can inhibit itching,13 and inhibition of pain processing may enhance itch.14 In addition, it has been Prostaglandins and Leukotrienes shown that the mechano-insensitive, histamine-sensitive Prostaglandins elicit very little or no pruritus when 22,23 nerve fibers are “selective” but not “specific” for pruri- applied to the skin, but they serve an important 24,25 togenic substances. The pruritic potency of a mediator synergistic function in itching. When administered increases with its ability to activate mechano-insensitive, in combination with histamine, prostaglandins potenti- histamine-sensitive nerve fibers (itch receptors) but de- ate the histamine-elicited itch. On the other hand, it creases with activation of mechano-responsive, hista- seems that prostaglandins are potent itch-producing sub- 26,27 mine-insensitive fibers.15 One interesting hypothesis is stances in the conjunctiva, and the antiitch efficacy that there are two types of histamine-sensitive primary of ketorolac in allergic conjunctivitis seems to involve afferent neurons:16 One type enhances pruritus, inhibition of conjunctival prostaglandin synthesis from 28 whereas the other attenuates it. arachidonic acid. Leukotriene B4 induces itch-associ- ated responses when injected intradermally, suggesting that leukotriene B4 may be an endogenous mediator of Mediators itch in the skin.29,30 Several substances have been identified as mediators of Acetylcholine itch that can stimulate the mechano-insensitive, hista- Acetylcholine is released from cholinergic nerves in mine-sensitive nerve fibers involved in itch transmission. the skin. The intradermal injection of acetylcholine elic- its burning pain in humans31 and evokes responses in Histamine nociceptive fibers in the superfused skin–saphenous Histamine can stimulate various nerve endings. When nerve preparation of the rat.32 In patients with atopic applied into the epidermis, it causes itch; when applied eczema, the intradermal injection of acetylcholine pro- more deeply into the dermis, it evokes pain, sometimes duces predominantly pruritus,31,33 rather than the usual 17 accompanied by itching. To induce itch, histamine burning pain. This pruritogenic action of acetylcholine directly stimulates type 1 histamine (H1) receptors on seems to be mediated by the activation of M3 muscarinic 7,18 the itch-specific C-fibers. However, only
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