Amitriptyline/Ketamine as Therapy for Neuropathic Pruritus and Pain Secondary to Herpes Zoster

February 2015 | Volume 14 | Issue 2 | Original Article | 115 | Copyright © 2015

John R. Griffin MD and Mark D.P. Davis MD

Department of Dermatology, Mayo Clinic, Rochester, MN

Abstract

Frequent causes of morbidity secondary to herpes zoster include acute pain, secondary infection, and postherpetic neuralgia. A less documented complication is pruritus, which can be either acute or postinfectious when it persists more than 3 months after the rash has healed. We discuss a case of severe, acute neuropathic pruritus and pain secondary to active herpes zoster that was unresponsive to standard medical therapy, including oral antihistamines, topical lidocaine, oral gabapentin, and local wound care. Modest control of the pruritus and pain was achieved with continued multimodal therapy and the addition of topical 2% amitriptyline/0.5% ketamine gel.

J Drugs Dermatol. 2015;14(2):115-118.

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INTRODUCTION

Acute herpetic pain has been noted to markedly impact health-related quality of life.1,2 No studies have attempted to quantify the impact of herpetic pruritus, acute or postinfectious, on quality of life, though epidemiologic data give voice to its relative frequency (up to 17% of acute cases) and individual reports bring to light its negative impact in selected cases.3-5 A proposed mechanism of herpetic pruritus and neuralgia cites neuronal necrosis and subsequent imbalance of pruritogenic and nociceptive inputs as the culprit.5 Unfortunately, many drugs that alleviate neuropathic pain do not have the same efficacy for relief of neuropathic itch in the individual patient.6

Case Report

A 64-year-old man with Crohn disease was admitted for enterocutaneous fistula takedown. He did not have a prior history of herpes zoster. During his postoperative stay, he had hyperalgesia, erythema, and vesicles in a left V1 distribution with ipsilateral conjunctivitis and keratitis (Figures 1 and 2). Treatment with intravenous acyclovir was begun, and varicella zoster virus was confirmed with polymerase chain reaction of blister fluid.

Three days after the skin eruption, the patient began to report itch in the area. Over the next 2 weeks, this symptom progressed to severe pruritus and burning pain, each rated by the patient as 10/10 on the visual analog scale, initially localized to the area of infection, and unrelenting. Over 3 days, the pruritus extended to include the bilateral scalp, though the pain remained localized to the area of infection. Initial treatment recommendations included wound care with dilute acetic acid wet dressings and twice daily 2.5% hydrocortisone cream. The patient reported that he had a decrease in his symptoms— to 8/10 and lasting for several hours—with this regimen. This treatment was continued for the remainder of his hospital stay. Oral gabapentin therapy was begun at a dosage of 300 mg 3 times daily and was titrated to up to 400 mg 3 times daily before his dismissal from the hospital, which occurred when his renal function had normalized.

Low-dose oral opioid therapy was discontinued in favor of nonopioid analgesics, given that opioids may cause considerable pruritus in some patients. Topical lidocaine patches were applied to intact surrounding skin every 12 hours. Therapy with oral hydroxyzine (25 mg daily) was started; however, it was used only intermittently because of the patient’s concern about associated somnolence. After the combination of these interventions, his itch was 7/10 or 8/10 for most of the day and 10/10 for the remainder.

At this point, the patient’s primary medical and surgical conditions had stabilized; however, his recalcitrant pruritus and pain prohibited his dismissal. Treatment of conjunctivitis and keratitis consisted of erythromycin ophthalmic ointment initially. Unfortunately, he also had an immune stromal keratitis, which required the addition of ophthalmic corticosteroids.

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