monitored for progressive edema of the airway and anaphylaxis. Patients with stridor, wheezes, drooling, swollen uvula, and/ or difficulty breathing or swallowing should be evaluated in an acute care facility. Epinephrine 0.3 mg SubC/IM should be administered, and EMS transport to the emergency department should be initiated. The newer, second-generation H1 antihistamines are recommended as first-line therapy by published guidelines from both allergy and dermatology expert panels. These include cetirizine, levocetirizine, loratadine, desloratadine, and fexofenadine. The first-generation antihistamines include Herpes zoster (shingles) Varicella-zoster virus (VZV) infection causes two clinically distinct diseases. Primary infection with VZV results in varicella (chickenpox), which is characterized by vesicular lesions on an erythematous base in different stages of development; lesions are most concentrated on the face and trunk. Herpes zoster, also known as shingles, results from the reactivation of latent VZV that gained access to sensory ganglia during varicella. Herpes zoster is characterized by a painful, unilateral vesicular eruption, usually occurring in single or two contiguous dermatomes. Individuals who did not have chickenpox during childhood may develop it later. Those with chickenpox may develop herpes zoster, which is caused by latent varicella zoster virus reactivation. Incidence and severity increase with age and with increasing immunosuppression. In immunocompetent individuals, herpes zoster typically manifests as vesicular lesions distributed along a dermatome and ending at the midline (Albrecht & Levin, 2022). People with shingles can transmit varicella-zoster virus (VZV), causing varicella (chickenpox) in contacts who are varicella naïve (i.e., never had varicella or the varicella vaccine). VZV is spread by direct contact with the active herpes zoster lesions or via airborne transmission from individuals with localized herpes zoster. The lesions are considered noninfectious after crusting (Albrecht & Levin, 2022). Individuals immunized against VZV are not at risk of developing chickenpox. The presenting clinical manifestations of herpes zoster are usually rash and acute neuritis or nerve pain. Fewer than 20% of patients who develop a rash have significant systemic symptoms, such as headache, fever, malaise, or fatigue (Albrecht & Levin, 2022). The rash starts as erythematous papules, typically in a single dermatome or several contiguous dermatomes. Within several days, grouped vesicles or bullae are the predominant manifestations. Within 3 to 4 days, the rash becomes pustular. The rash can be hemorrhagic in immunosuppressed people and those of advanced age. In immunocompetent hosts, the lesions crust by 7 to 10 days and are no longer considered infectious. Self-Assessment Quiz Question #8 Which of the following statements about varicella-zoster virus (VZV) infection is true? a. Varicella (chickenpox) and herpes zoster (shingles) are caused by two different viruses. b. Herpes zoster is characterized by bilateral vesicular eruptions. c. Individuals who received the VZV vaccine are at risk of developing chickenpox. d. The lesions of herpes zoster become noninfectious after crusting.
diphenhydramine, chlorpheniramine, hydroxyzine, and others. Significant sedation and performance impairment (e.g., fine motor skills, driving skills, and reaction times) occur in more than 20% of patients taking first-generation antihistamines (Asero, 2022). This should be communicated to the patient, and anticipatory guidance on the conditions should be provided. Glucocorticoids do not appear to be necessary for isolated urticaria. However, a brief course (i.e., usually a week or less) of systemic glucocorticoids may be added to antihistamine therapy for patients with prominent angioedema or if symptoms persist beyond a few days (Asero, 2022).
Figure 15. Varicella-Zoster Viru
From Herrmann, K. L. (1966). 21507. https://phil.cdc.gov/Details. aspx?pid=21507. In public domain Although the rash can occur in any dermatome, the thoracic and lumbar dermatomes are most commonly involved. Herpes zoster occurs on the face in 10% or more of cases. Some patients may also have a few scattered vesicles located some distance from the involved dermatome, probably reflecting the presence of varicella-zoster virus (VZV) viremia early in herpes zoster. Herpes zoster keratitis or herpes zoster ophthalmicus can result from the involvement of the ophthalmic branch of the trigeminal cranial nerve (Albrecht & Levin, 2022). These complications can be sight-threatening and considered an emergency. The treatment goals for herpes zoster include: ● Lessen the severity and duration of pain associated with acute neuritis ● Promote more rapid healing of skin lesions ● Prevent new lesion formation ● Decrease viral shedding to reduce the risk of transmission ● Prevent postherpetic neuralgia Several lines of evidence suggest that antiviral therapy hastens the resolution of cutaneous lesions and the acute neuritis of herpes zoster. However, it is unclear if antiviral therapy prevents postherpetic neuralgia. This is because of conflicting study results, which are due in part to different methodologies of pain assessment, definitions of postherpetic neuralgia, and length of follow-up (Albrecht & Levin, 2022). The management of herpes zoster includes: ● Antiviral therapy to hasten the healing of cutaneous lesions and decrease the duration and severity of acute neuritis; whether antiviral therapy decreases the risk of post-herpetic neuralgia is less clear ● Analgesia for patients with moderate to severe acute neuritis ● The doses used to treat herpes zoster are as follows: ● Valacyclovir: 1,000 mg three times daily for 7 days ● Famciclovir: 500 mg three times daily for 7 days ● Acyclovir: 800 mg five times daily for 7 days
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