EM@3AM: Herpes Zoster

Authors: Elizabeth Adams, MD (EM Resident Physician, UTSW, Dallas, TX); Samuel Parnell, MD (Assistant Professor of EM / APD, UTSW, Dallas, TX) // Reviewed by: Alex Koyfman, MD (@EMHighAK) and Brit Long, MD (@long_brit)

Welcome to EM@3AM, an emDOCs series designed to foster your working knowledge by providing an expedited review of clinical basics. We’ll keep it short, while you keep that EM brain sharp.

A 27-year-old pregnant female presents to your ED with a painful rash to the right side of her face that started 4 days ago. She is G1P0 and currently 26 weeks pregnant with reported routine prenatal care. She had been doing well until 4 days prior when she began to experience tingling and pain to her right cheek, followed by the development of small, painful, erythematous bumps to the area. She denies fevers, chills, shortness of breath, vision changes, or other symptoms at this time.

Vital signs on arrival to the ED include BP 110/76, HR 86, RR 18, SpO2 98% on room air, and temperature 98 F.  She is non-toxic appearing but uncomfortable due to pain. On exam, she has a vesicular rash across her right cheek in the V2 cranial nerve distribution. The rest of the exam is unremarkable.

What is the most likely cause of this woman’s rash?

Diagnosis: Shingles (Herpes Zoster)



  • Shingles, also known as herpes zoster, is the result of reactivation of the varicella-zoster virus (VZV) and is estimated to occur in more than 1.2 million Americans annually1.
  • The CDC estimates that approximately 30 percent of people living in the US will experience shingles in their lifetime2.
  • Varicella-zoster virus can cause two clinically distinct diseases. Primary infection leads to varicella (aka chickenpox), and reactivation of latent VZV causes herpes zoster (aka shingles).
  • Following the initial infection, VZV can lie dormant in the sensory ganglia for decades before reactivation.



  • Varicella-zoster virus is a member of the herpesvirus family.
  • Primary infection with VZV (known as acute varicella or chickenpox) occurs through direct contact with skin vesicles, or through exposure to airborne or respiratory droplets.
  • Virus particles in the skin vesicles during primary infection can move retrograde along sensory axons toward the nerve ganglia where the virus can lie dormant for years.
  • Stress, immunocompromised state, pregnancy, or illness can lead to reactivation of the virus, at which point the virus can spread from the ganglia down the sensory nerve to create the characteristic dermatomal rash of herpes zoster.
  • The most important risk factor for developing shingles is age; individuals greater than 50 years old are at an increased risk of developing shingles, with 40% of cases occurring in patients over the age of 601,3.
  • Shingles can also occur in vaccinated individuals who received the live-attenuated varicella vaccine.


History and Exam:

  • The most common presenting signs of shingles are a rash and acute neuritis.
  • The characteristic rash of herpes zoster is a painful, vesicular rash on an erythematous base that is unilateral and involves 2 or fewer adjacent dermatomes (usually 1 dermatome)1,4.
  • Initially, the rash may appear as erythematous macules or papules and edematous plaques before evolving into the characteristic grouped vesicles or bullae4.
  • Immunocompromised individuals with herpes zoster may present with lesions involving more than 2 dermatomes, or even disseminated skin lesions similar to acute varicella5.
  • Along with the characteristic rash, patients typically experience associated neuritis with the pain frequently described as burning, stabbing, or throbbing6.
  • Approximately 75% of patients will experience prodromal pain, tingling, or itching in a dermatomal distribution that can occur days before the rash develops6.
  • In addition to the rash, some patients with herpes zoster will have associated headache, fatigue, abdominal discomfort, or fever.


  • Herpes simplex virus, hand-foot-mouth disease, primary varicella infection, contact dermatitis, drug eruption, scabies, dermatitis herpetiformis


ED Evaluation:

  • Shingles is typically a clinical diagnosis based on history and physical exam.
  • If the clinical presentation is uncertain, laboratory confirmation can be performed through PCR testing of fluid from the vesicles1.
  • Less commonly, direct fluorescent antibody (DFA) testing of skin scrapings and viral cultures can be sent to confirm the diagnosis if PCR is unavailable, but this is rarely done from the emergency department1.
  • Consider HIV serologic testing, especially in atypical presentations of herpes zoster involving multiple dermatomes or disseminated rash.
  • In cases of herpes zoster involving the cranial nerves of the face, perform a thorough HEENT exam to evaluate for complications including herpes zoster ophthalmicus and Ramsay Hunt syndrome (herpes zoster oticus) – see “Complications” section below for more information.



  • In acute, uncomplicated herpes zoster, the mainstays of treatment are pain control and antiviral therapy (which promotes faster resolution of rash and pain, as well as reducing risk of viral shedding and disease transmission)6.
  • Treat mild pain with NSAIDs and acetaminophen.
  • Consider a 10- to 14-day oral prednisone taper for more severe pain.
  • For pain that is not improved with prednisone taper and conservative management, consider the use of regional nerve blocks, gabapentin, TCA’s or narcotics for pain management7.
  • Antiviral therapy should ideally be started within 72 hours of onset of clinical symptoms, and the choice of antiviral agent depends on comorbidities.
  • Common oral antiviral regimens include7,8:
    • Acyclovir (800 mg five times daily x 7 days) – preferred agent in pregnant patients
    • Valacyclovir (1000 mg three times daily x 7 days) – dosage adjustment required for renal impairment
    • Famciclovir (500 mg three times daily x 7 days)
  • Immunocompromised patients, especially those with disseminated disease, should be admitted for intravenous antiviral therapy.



  • Herpes zoster ophthalmicus (HZO) is an ocular complication of herpes zoster, which occurs when the virus involves the ophthalmic branch of the trigeminal nerve (V1) and can lead to permanent vision loss and blindness8.
    • Suspect ophthalmic involvement if lesions are found on the tip or sides of the nose (termed “Hutchinson sign”).
    • A thorough eye exam with fluorescein/Wood’s lamp may reveal punctate and/or pseudodendritic keratitis8.
    • All patients with HZO should have IOP measured to assess for secondary glaucoma due to involvement of the trabecular meshwork9,10.
    • If the history or physical exam is concerning for ocular involvement, consider early ophthalmology consultation, even in the absence of fluorescein uptake on exam as deeper structures of the eye may be involved.
    • Treatment includes topical and/or oral corticosteroids and topical erythromycin ophthalmic ointment in addition to oral antivirals; however, IV antivirals are indicated in cases of immunocompromised patients or those with sight-threatening disease7,8,9,10.
  • Acute retinal necrosis is a sight threatening emergency that can occur in both immunocompetent and immunocompromised patients6. It is another serious ocular complication of herpes zoster.
    • Patients frequently present with blurry vision and ocular pain which can progress to permanent vision loss and retinal detachment6.
    • If you suspect acute retinal necrosis or any ocular involvement of herpes zoster, prompt ophthalmology consultation and a dilated fundoscopic examination are recommended.
    • Patients with acute retinal necrosis should be managed in conjunction with an ophthalmologist. Patients are usually treated with IV acyclovir and systemic glucocorticoids6. Treatment is based on expert opinion as there are no large clinical trials available to guide management.
  • Ramsay Hunt syndrome (herpes zoster oticus) is the otologic complication of herpes zoster, often involving the facial nerve (CN VII), characterized by unilateral facial paralysis, and vesicles involving the auricle and external auditory canal. It can be associated with tinnitus, hearing loss, or vertigo.
    • Perform thorough ear exam to evaluate for vesicles involving the external auditory canal.
    • Treatment includes oral antivirals and oral prednisone (1mg/kg once daily x 5 days) for most cases7.
    • For patients with severe vertigo, tinnitus or hearing loss, admission for intravenous antiviral therapy is appropriate.
  • Post-herpetic neuralgia (PHN) is the most common complication of shingles and is characterized by persistent pain more than one month following resolution of the rash10.
    • The CDC estimates that between 10% and 18% of people who experience shingles will go on to have PHN, which can be debilitating and difficult to treat11.
    • Current pain control options for PHN include gabapentin, TCAs, topical capsaicin, topical lidocaine, carbamazepine, SSRIs, botulinum toxin injections, glucocorticoid injections, and nerve stimulation12.
  • The best way to prevent complications of shingles, including PHN, is to prevent the disease all together by the use of the recombinant zoster vaccine – currently recommended for patients 50 years and older or those with immunocompromised states13.


Take-home Points:

  • Patients with shingles usually present with a painful, vesicular rash in a dermatomal distribution.
  • Utilize the immune status of your patient to help guide appropriate management and disposition from the ED.
  • Consider serologic testing for HIV for patients that have atypical presentations involving multiple dermatomes or diffuse lesions.
  • The mainstays of treatment for shingles are antiviral therapy and pain control.
  • In cases of shingles involving the face, always perform a thorough exam to evaluate for herpes zoster ophthalmicus and consider early ophthalmology consultation even in the absence of fluorescein uptake on the cornea if the history or other exam findings are concerning for ocular involvement.
  • The best way to prevent the complications of shingles is to encourage vaccination with the recombinant zoster vaccine for patients over the age of 50 and those that are immunocompromised.

Further Reading

Additional Reading:


  1. Albrecht, Mary A, and Myron J Levin. “Epidemiology, Clinical Manifestations and Diagnosis of Herpes Zoster.” UpToDate, 29 Jan. 2021.
  2. “Shingles Surveillance, Trends, Deaths.” Centers for Disease Control and Prevention, Centers for Disease Control and Prevention, 14 Aug. 2019, https://www.cdc.gov/shingles/surveillance.html.
  3. Schmader K. “Herpes zoster in older adults.” Clin Infect Dis 2001; 32:1481.
  4. Oakley, Amanda. “Herpes Zoster.” Herpes Zoster. Shingles | DermNet NZ, Oct. 2015, https://dermnetnz.org/topics/herpes-zoster.
  5. Ammar M Ahmed et al. “Managing herpes zoster in immunocompromised patients.” Herpes, Sep. 2007.
  6. Dworkin RH, Johnson RW, Breuer J, et al. Recommendations for the management of herpes zoster. Clin Infect Dis. 2007;44 Suppl 1:S1-S26. doi:10.1086/510206
  7. Albrecht, Mary A. “Treatment of Herpes Zoster in the Immunocompetent Host.” UpToDate, 11 Mar. 2020.
  8. Minor, Megan and Ethan Payne. “Herpes Zoster Ophthalmicus.” Stat Pearls, 11 Aug. 2021.
  9. Cason, John B, and Shannon S Joseph. “Herpes Zoster Ophthalmicus.” EyeWiki, 10 Jan. 2022, https://eyewiki.aao.org/Herpes_Zoster_Ophthalmicus#Physical_examination.
  10. Shaikh, Saad, and Christopher N Ta. “Evaluation and Management of Herpes Zoster Ophthalmicus.” Am Fam Physician. 1 Nov. 2002;66(9):1723-1730.
  11. “Complications of Shingles (Herpes Zoster).” Centers for Disease Control and Prevention, Centers for Disease Control and Prevention, 1 July 2019, https://www.cdc.gov/shingles/about/complications.html.
  12. Stankus, Seth John, et al. “Management of Herpes Zoster (Shingles) and Postherpetic Neuralgia.” American Family Physician 15 Apr. 2000;61(8):2437-2444.
  13. “Shingles Vaccination.” Centers for Disease Control and Prevention, Centers for Disease Control and Prevention, 24 Jan. 2022, https://www.cdc.gov/shingles/vaccination.html.

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