Written by: Kevin Dyer, MD (NUEM PGY-3) Edited by: Simiao Li-Sauerwine, MD (NUEM Alum ‘18) Expert commentary by: David Zull, MD
A 76-year-old man with a history of metastatic colon cancer (on Bevacizumab), HTN, and DM2 presents with a skin rash on his back wrapping around to his groin. He went on to say that 4 days ago he began having a dull, aching pain in this region and about 18 hours ago this rash appeared. He denied having a rash in any other location, and also denied oral sores, vision changes, confusion, neck pain, fevers, cough, or shortness of breath. His last infusion of bevacizumab was 9 days prior to ED presentation and he did not receive the shingles vaccine.
Upon examination he had a unilateral erythematous vesicular rash in the distribution of his T12 and L1 dermatomes that was classic for Herpes Zoster (HZ) along with erythema at the base that was concerning for an underlying cellulitis. His labs were remarkable for a white count of 2,200 and an absolute neutrophil count of 1,200.
Given his immunocompromised status, he was given Acyclovir 750mg (10mg/kg) IV and Ancef 2g IV in the ED and admitted for continued IV anti-viral therapy.
To me, this case was much more interesting than the average case of HZ given the patient’s immunocompromised status and it served as an important reminder that there are several pitfalls and complications surrounding HZ that the ED physician must be aware of and constantly on the lookout for.
Post-Herpetic Neuralgia (PHN)
PHN is defined as pain that persists more than 30 days after the onset of rash. Both the incidence (8-70%) and duration are directly correlated with the patient’s age.[1-3] Symptoms of PHN include pain, numbness, dysesthesias, and allodynia. While PHN is not applicable to the patient with an acute attack of HZ, it is included here because it is the most common complication of HZ and should be included in the counseling given to patients who are discharged from the ED.
Herpes Zoster Ophthalmicus
Herpes Zoster Ophthalmicus (HZO) is an ocular and peri-ocular disease that is the result of virus reactivation in the trigeminal ganglion.
Patients with HZO may present with a vesicular eruption along the trigeminal dermatome, conjunctivitis, episcleritis, and lid droop. Clinicians should also pay particular attention the nose and be on the lookout for vesicular lesions at the base, side, or tip of the nose. Commonly known as Hutchison’s sign, lesions on the nose indicate involvement of the nasociliary branch and are strong predictors of ocular involvement, which occurs in 50-72% of HZO cases.[4,5]
Corneal involvement can lead to significant vision loss and should be evaluated for via fluoroscein staining in all patients with suspected HZO. Keratitis may present as punctate or dendriform lesions that are easily mistaken for Herpes Simplex Keratitis.
Herpes Zoster Oticus
Often referred to as Ramsay Hunt Syndrome (RHS), Herpes Zoster Oticus manifests as a triad of ipsilateral facial paralysis, ear pain, and vesicles in both the auditory canal and auricle. RHS is considered a polyneuropathy affecting cranial nerves V, VII, VIII, IX, and X.7 Involvement of these nerves leads to tinnitus, hearing loss, hyperacusis, dysgeusia, and vertigo. It is worth noting that when compared to those with Bell’s Palsy, patient’s with RHS were found to have more severe palsy and a less favorable recovery.
Disseminated cutaneous HZ is a complication that is often accompanied by visceral organ involvement. Though it is more common in immunocompromised hosts, it can also be seen in immunocompetent patients, as well. As the name implies, patients with disseminated zoster will have midline-crossing vesicular skin lesions in multiple dermatomes. Visceral involvement can be life threatening and may present as fulminant pneumonia, hepatitis, or encephalitis.11
Patients with HZ lesions are at an increased risk for skin superinfection regardless of immune status. The most likely causative agents are Staphylococcus and Streptococcus species. When encountering a patient with HZ, the clinician should be sure to look for signs of bacterial infection and treat with antibiotics in addition to antivirals.
In immunocompetent patients, antiviral therapy should be started within 72 hours of rash occurrence or if new lesions continue to occur as this is a sign of ongoing virus replication. For immunocompromised patients, antiviral therapy should be started regardless of when the lesions appeared.
The three antivirals currently recommended for use are acyclovir, valacyclovir, and famciclovir, with dosing regimens as follows:
Acyclovir – 800mg, 5 times per day for 7 days
Valacyclovir – 1000mg, 3 times per day for 7 days
Famciclovir – 500mg 3 times per day for 7 days
A meta-analysis of placebo-controlled trials have shown that patients who received acyclovir within 72 hours of rash onset are more likely to have resolution of neuritis and PHN. A commonly used alternative option is valacyclovir which, when compared to acyclovir, has equal efficacy in the resolution of cutaneous lesions, and the added benefit of accelerated resolution of neuritis. The TID dosing is also thought by many clinicians to lead to better patient compliance. The caveat to this, however, is valacyclovir is much more expensive than acyclovir and can be cost prohibitive depending on the patient’s insurance status.
Patients should be treated with intravenous acyclovir 10 mg/kg if they are immunocompromised, have disseminated zoster, are found to have sight threatening disease on exam, or if they have symptomatic meningitis, encephalitis, or myelitis.
The overwhelming majority of patients with HZ can be treated as outpatients with an oral agent as discussed above. Admission is indicated for patients who meet the criteria for IV acyclovir as outlined in the previous section.
Take Home Points
When caring for a patient with herpes zoster, be on the lookout for herpes zoster ophthalmicus, herpes zoster oticus, signs of disseminated zoster, and underlying cellulitis.
Initiate antivirals if the onset of rash is within 72 hours of presentation or if the patient is immunocompromised.
Oral antivirals are acceptable for the majority of patients with herpes zoster, but those who are immunocompromised, have disseminated zoster, sight threatening involvement, or signs of CNS involvement should be treated with IV acyclovir.
It is estimated that up to one third of the population will develop Herpes Zoster virus infection (shingles) sometime during our lifetime, such that it is a very common ED presentation. Emergency physicians should be keenly aware of the complications of HZV and be able to recognize it early. Antiviral treatment within the first 72 hours of the skin eruption can limit progression of lesions, halt development of new lesions, minimize infectious risk to household contacts, decrease the risk of complications of HZV infection, and in particular ameliorate the severity of post herpetic neuralgia.
Ramsay Hunt syndrome is typically limited to a triad of Bell’s palsy (7th Nerve palsy), ear pain and vesicles in the auditory canal and external ear. The skin lesions are often subtle and frequently limited to just a few papules such that the syndrome is often missed. Other cranial nerves (5,8,9,10) can also be involved in Ramsay Hunt syndrome, most notably 8th nerve involvement with tinnitus, hearing loss or hyperacusis, and vertigo.
Herpes Zoster ophthalmicus is usually limited to punctate keratitis and is not vision threatening. Dendritic lesions can occur in HZV but they are referred to as pseudodendrites because they are composed of heaped up epithelial cells with no epithelial defects. These pseudodendrites do not take up fluorescein since the epithelium remains intact but fluorescein often collects at the edges thereby outlining the dendrites. In contrast, the dendrites of HSV are comprised of denuded epithelium which do take up fluorescein. The HSV dendrite can lead to corneal erosion, scarring, and even perforation. HZV can also affect the corneal stroma and not the corneal epithelium leading to white rounded opacities with no overlying fluorescein uptake. Pink eye can result from conjunctivitis or iritis but is often overlooked. The most feared ocular complication of V-1 Zoster is acute retinal necrosis which leads to rapidly progressive vision loss often complicated further by retinal detachment.
Disseminated herpes zoster is defined as the presence of more than 20 lesions outside the involved dermatome. This unusual presentation is more common in immunosuppressed patients. Lesions in an ipsilateral adjacent dermatome are usually not of concern. Disseminated zoster can resemble acute varicella or smallpox, as well as acute vesiculating drug eruptions like erythema multiforme and toxic epidermal necrolysis. Disseminated HZV is distinguished by the onset primarily in one dermatome before dissemination of lesions. Systemic organ involvement can occur with dissemination of HZV including pneumonia, hepatitis, aseptic meningitis, encephalitis, motor neuropathy, myelitis, GBS, and CNS vasculitis with stroke.
Post herpetic neuralgia, a common complication of HZV infection, is best prevented by prompt antiviral therapy in the acute phase. Although steroids may have some benefit in ameliorating the severity of pain in the acute setting, they have not been shown to decrease the development of PHN. Pain management of PHD frequently requires use of TCA’s, gabapentin or pregabalin.
A common complication of HZV dermatomal lesions is secondary bacterial infections with staph aureus, usually with an impetiginous superficial purulent discharge with or without local cellulitis. Staph septicemia and toxic shock syndrome is a rare complication in dermatomal zoster but is well described in primary varicella infections in neonates and immunocompromised children.
The emergency physician should have a low threshold for initiating antiviral therapy acute shingle, typically Valcyclovir 1gm TID or Acyclovir 800mg five times per day, for 7 days in immunocompetent hosts with uncomplicated disease, or 14 days in compromised hosts and those experiencing complications of HZV.
David N. Zull, MD, FACEP, FACP
Professor of Emergency Medicine & Internal Medicine
How to Cite This Post
[Peer-Reviewed, Web Publication] Dyer K, Li-Sauerwine S (2018, December 17). Herpes Zoster [NUEM Blog. Expert Commentary by Zull D]. Retrieved from http://www.nuemblog.com/blog/herpes-zoster
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