Painful Rash on Right Flank


  • Eruption of vesicles on the right side.

A 65-year-old woman presents to the clinic with a painful rash on her right side. On examination, there is a group of vesicles on an erythematous base on her right flank. The patient reports the rash appeared the day before, but the region around the vesicles “felt like it was on fire” the past week. The patient has never experienced these symptoms before. Medical history confirms the patient had chicken pox when she was 7 years old.

Herpes zoster (HZ), or shingles, is a painful dermatomal rash caused by reactivation of latent varicella-zoster virus (VZV) that persists in neurons after varicella (chicken pox) infection.1 HZ has been recognized since ancient Greece: its name derives from the Greek...

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Herpes zoster (HZ), or shingles, is a painful dermatomal rash caused by reactivation of latent varicella-zoster virus (VZV) that persists in neurons after varicella (chicken pox) infection.1 HZ has been recognized since ancient Greece: its name derives from the Greek herpein zoster, meaning “to creep” and “girdle or zone.”2 It was first associated with peripheral nerves in 1818 by Mehlis, and in 1861, von Bärensprung linked it to sensory neuron cell bodies.3,4 In 1900, Head and Campbell described a viral inflammation in the cell bodies,5 but it was not until the 1950s that it was confirmed that the same VZV caused varicella and herpes zoster.6

HZ has no seasonal prevalence, and the incidence increases with age. Half the yearly cases occur in individuals older than 60 years.1 In the community, HZ has an incidence of 2 to 5 cases per 1000 person-years, which increases to 8 to 12 per 1000 years in adults ≥70 years of age.1,7 The primary risk factor in developing HZ is a prior varicella infection.1

HZ occurs when latent VZV becomes reactivated, which leads to the appearance of painful vesicles in the regions where the sensory neurons project, referred to as a dermatome pattern.1,8 A depressed immune system is a major risk factor in the reactivation of VZV, accounting for 10% of HZ cases. At-risk, immunocompromised individuals include organ transplant patients or patients with tumors or immunological/rheumatological diseases.1 HZ is also a prominent sign of HIV immune deficiency, and therefore HIV should be considered especially in young patients presenting with HZ.1 Other risk factors include being female, trauma to a sensory dermatome, family history of HZ, Caucasian race, and certain genetic predispositions including interleukin 10 gene polymorphisms.1,9

Histologically, HZ resembles an intraepidermal blister.1 Key features include acantholysis with solitary keratinocytes in the blister cavity.1 Because of the viral infection, keratinocytes will have nuclear changes, including multinucleation and nuclear inclusions, as well as viral inclusions in the nucleus that resemble small pink deposits with a clear halo.1 Tzanck smears can be used to identify multinucleated giant cells.1

Patients with HZ will often have a prodrome of pain and paresthesia in the affected areas.1 The pain can be as severe as pain associated with diseases from visceral organs, such as myocardial infarction or cholecystitis.10 Altered sensations in the areas include itching, tingling, or burning.10 Select patients can develop the skin eruption without prodromal pain, known as zoster sine herpete.11

The distinctive skin eruption is a unilateral rash limited to a body region innervated by a single sensory ganglion.1 The most common areas affected are the ophthalmic division of the trigeminal nerve and the truncal region between sensory levels of T3-L2.12

On examination, the HZ rash will appear as tightly grouped vesicles on an erythematous base.1 The vesicles begin as macules and papules, with vesicles forming within 24 hours, transitioning to pustules in about 3 days, and then a dry crust in 7 to 10 days, which can persist up to 3 weeks. Other key clinical features of HZ include pain, which is often severe and can lead to decreased physical and social functioning, and pruritus, which can remain until all crusts are gone.

In the prodromal phase of HZ, diagnosis can be difficult, as the pain can be confused with other causes of localized pain such as cholecystitis, myocardial infarction, gastritis, and so on. The diagnosis is usually clinical, with a dermatomal eruption along with pain and sensory abnormalities. HZ is most often confused with zosteriform herpes simplex, as both present with a cluster of vesicles, although with zosteriform herpes simplex, the cluster often appears near the mouth or genitals.1 A history of multiple recurrences in the same region often differentiates the 2 diagnoses.

In addition to zosteriform herpes simplex, the differential diagnoses includes contact dermatitis, insect bites, and burns, and less likely, drug eruptions, scabies, popular urticaria, erythema multiforme, and molluscum contagiosum.1 For most of these, the unilateral dermatomal patterned painful rash is often sufficient to diagnose HZ; however, a biopsy can be used to confirm HZ. Polymerase chain reaction is the optimal diagnostic test to detect VZV, can distinguish between VZV and herpes simplex virus, and can be performed from vesicular fluid, lesion or crust scrapings, or tissue biopsy.13

Complications of HZ include bacterial superinfection of the lesions, scarring (from excessive scratching), or cutaneous dissemination through nearby neurons or spinal cord.1,7 Visceral adverse effects can also occur, such as pneumonitis, hepatitis, esophagitis, gastritis, and so on.7 Neurological complications include nerve palsies, sensory loss, ocular complications (especially with ophthalmic HZ), and most important, postherpetic neuralgia (PHN).2,7 PHN is defined as pain that continues after the rash is healed, and can last up to 6 months from onset. PHN occurs in 5% to 30% of patients.2,7

Effective treatment of HZ includes antiviral agents such as acyclovir, famciclovir, and valacyclovir.8 These treatments are most effective at reducing acute pain and preventing PHN if started within 72 hours of rash onset.8 Importantly, for HZ affecting the ophthalmic region of the trigeminal nerve, antiviral treatment is necessary and must be started even if more than 72 hours have elapsed since rash onset.8 For ophthalmic HZ, topical antiviral cream should also be used along with oral corticosteroids.8

Oral prednisolone with acyclovir reduces pain, increases the healing speed of lesions, and allows for a faster resolution, especially for nonophthalmic HZ.14 Therefore, the addition of oral steroids to antiviral treatment should be considered when there are no contraindications. Other treatment agents include tricyclic antidepressants, which have been shown to reduce the prevalence of PHN at 6 months; however, these agents should be used with caution in older patients because of anticholinergic adverse effects precipitating delirium or tachycardia.8 Opioids and nonsteroidal anti-inflammatory drugs can also be used for pain management: oxycodone has been shown to reduce acute pain, and tramadol has used to treat PHN.8

The advent of the varicella vaccine and eradication of primary varicella should lead to the eventual eradication of HZ. Although there were concerns that the loss of childhood chicken pox could lead to an increase in HZ, analyses of the prevalence of HZ after varicella vaccination has not supported this claim.15 In addition, in patients who may have had a primary varicella infection as children, administration of the varicella zoster virus vaccine in patients older than 60 years was effective at reducing the number of HZ cases and the incidence of PHN.16

The patient in the case was treated with oral valacyclovir. Her lesions crusted over and disappeared over the course of 2 weeks.

Jay Patel, BS, and Yelena Dokic, BSA, are medical students at Baylor College of Medicine, and Christopher Rizk, MD, is a dermatologist at Elite Dermatology in Houston, Texas.


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3. von Bärensprung FGH. Die Gürtelkrankheit. Ann d char krankenh zu Berl. 1861;9:40-128.

4. Meyer R, Brown HP, Harrison JH. Herpes zoster involving the urinary bladder. N Engl J Med. 1959;260(21):1062-1065.

5. Head H, Campbell AW, Kennedy PGE. The pathology of herpes zoster and its bearing on sensory localisationRev Medical Virol. 1997;7(3):131-143.

6. Weller TH, Witton HM. The etiologic agents of varicella and herpes zoster; serologic studies with the viruses as propagated in vitro. J Exp Med. 1958;108(6):869-890.

7. Kawai K, Gebremeskel BG, Acosta CJ. Systematic review of incidence and complications of herpes zoster: towards a global perspective. BMJ Open. 2014;4(6):e004833.

8. Wareham DW, Breuer J. Herpes zoster. BMJ. 2007;334(7605):1211-1215.

9. Haanpää M, Nurmikko T, Hurme M. Polymorphism of the IL-10 gene is associated with susceptibility to herpes zoster. Scand J Infect Dis. 2002;34(2):112-114.

10. Chen TM, George S, Woodruff CA, Hsu S. Clinical manifestations of varicella-zoster virus infection. Dermatologic Clinics. 2002;20(2):267-282.

11. Lewis GW. Zoster sine herpete. Br Med J. 1958;2(5093):418-421.

12. Ragozzino MW, Melton LJ, Kurland LT, Chu CP, Perry HO. Population-based study of herpes zoster and its sequelae. Medicine (Baltimore). 1982;61(5):310-316.

13. Harbecke R, Oxman MN, Arnold BA, et al. A real-time PCR assay to identify and discriminate among wild-type and vaccine strains of varicella-zoster virus and herpes simplex virus in clinical specimens, and comparison with the clinical diagnoses. J Med Virol. 2009;81(7):1310-1322.

14. Whitley RJ, Weiss H, Gnann JW, et al. Acyclovir with and without prednisone for the treatment of herpes zoster. A randomized, placebo-controlled trial. The National Institute of Allergy and Infectious Diseases Collaborative Antiviral Study Group. Ann Intern Med. 1996;125(5):376-383.

15. Jumaan AO, Yu O, Jackson LA, Bohlke K, Galil K, Seward JF. Incidence of herpes zoster, before and after varicella-vaccination-associated decreases in the incidence of varicella, 1992-2002. J Infect Dis. 2005;191(12):2002-2007.

16. Oxman MN, Levin MJ, Johnson GR, et al. A vaccine to prevent herpes zoster and postherpetic neuralgia in older adults. N Engl J Med. 2005;352(22):2271-2284.

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