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Emergency And Acute Medicine – Herpes Zoster
Definition And Overview
Herpes zoster, commonly known as shingles, is characterized by a unilateral eruption of painful vesicles distributed along a single dermatome. It results from reactivation of latent varicella zoster virus (VZV) in dorsal root ganglia. Dissemination is rare in immunocompetent hosts but occurs more frequently in immunocompromised patients. The disease is most common in individuals with impaired cell-mediated immunity, particularly adults older than 50 years, patients with malignancy, and those receiving immunosuppressive therapy.
Etiology And Risk Factors
Herpes zoster is caused by reactivation of VZV, a DNA virus in the Herpesviridae family. Most cases occur in individuals with a history of primary varicella (chickenpox), and only rarely in vaccinated individuals. Declining cell-mediated immunity with aging or immunosuppression is the primary risk factor.
Pregnancy is not associated with an increased risk of congenital varicella syndrome. In children, herpes zoster may occur following in utero exposure or primary varicella infection during the first six months of life.
Clinical Features
Dermatomal zoster typically begins with a prodrome of pain, paresthesias, or pruritus in the affected dermatome, occurring in approximately 75% of patients. Pain may be sharp, burning, tingling, or severe. The classic rash consists of grouped vesicles on an erythematous base, which progress to crusting over 7–10 days, with complete resolution in 2–3 weeks. Thoracic and lumbar dermatomes are most commonly involved, followed by trigeminal and cervical distributions.
Zoster sine herpete presents with dermatomal pain without rash and can be diagnostically challenging.
Herpes zoster ophthalmicus results from involvement of the ophthalmic division of the trigeminal nerve. Hutchinson sign, defined as vesicles on the tip of the nose, suggests nasociliary nerve involvement and increased risk of ocular complications. Ocular findings may include punctate keratitis or corneal pseudodendrites, which are less ulcerative and show less fluorescein uptake than HSV dendrites.
Ramsay Hunt syndrome is caused by involvement of cranial nerves VII and VIII and presents with vesicles in the external auditory canal, peripheral facial palsy, vertigo, and altered sensation of the anterior two-thirds of the tongue.
Disseminated disease may occur, particularly in immunocompromised patients, and can involve the central nervous system, liver, or lungs, leading to complications such as meningoencephalitis, myelitis, hepatitis, pneumonitis, and peripheral neuropathy.
Postherpetic neuralgia is defined as pain persisting at the site of zoster lesions for more than three months after cutaneous healing. It occurs in 10–70% of patients, with risk increasing in those older than 50 years and in patients with severe initial rash or pain.
Diagnostic Evaluation
Diagnosis is primarily clinical in typical presentations. Laboratory testing is reserved for atypical cases, disseminated disease, or immunocompromised patients. Tzanck smear may show multinucleated giant cells but cannot distinguish VZV from HSV and has low sensitivity. PCR testing from vesicle fluid, blood, cerebrospinal fluid, or bronchoalveolar lavage is the preferred diagnostic method due to high sensitivity and specificity. Serologic testing is less reliable in the acute setting, and viral culture is slow and insensitive.
Differential Diagnosis
Conditions to consider include primary varicella, herpes simplex infection, cellulitis, allergic contact dermatitis, bullous impetigo, molluscum contagiosum, insect bites, trigeminal neuralgia, radiculopathy, biliary or renal colic, Bell palsy, peripheral vertigo, conjunctivitis, and HSV keratitis.
Emergency Management
Herpes zoster is usually self-limited. Management focuses on reducing pain, shortening disease duration, and preventing postherpetic neuralgia. Lesions should be covered, and universal precautions maintained, as zoster can transmit varicella to nonimmune individuals.
In immunocompetent patients, oral antiviral therapy should be initiated within 72 hours of rash onset, though treatment may still be beneficial if new lesions are forming. Valacyclovir is preferred for ease of dosing, though acyclovir or famciclovir are acceptable alternatives. Analgesia should be tailored to pain severity, ranging from nonsteroidal anti-inflammatory drugs to opioids. Corticosteroids remain controversial and may modestly improve acute pain and rash healing but do not prevent postherpetic neuralgia.
Immunocompromised patients require intravenous acyclovir and close monitoring.
Herpes zoster ophthalmicus requires urgent ophthalmology consultation. Oral antivirals are indicated, with intravenous therapy for immunocompromised patients or those with cranial nerve involvement.
Postherpetic neuralgia is managed with analgesics, tricyclic antidepressants, gabapentin or pregabalin, and topical lidocaine; antivirals are not effective once PHN is established.
Postexposure Prophylaxis And Prevention
Varicella zoster immune globulin (VariZIG) is recommended within 72 hours of exposure for immunocompromised patients, pregnant individuals, and certain neonates. The live-attenuated zoster vaccine is recommended for adults over 60 years of age but is contraindicated in pregnancy and immunocompromised patients. Vaccination does not treat active disease or prevent postherpetic neuralgia in those with established zoster.
Disposition And Follow-Up
Most patients can be managed as outpatients. Admission is indicated for immunocompromised patients, disseminated disease, severe or intractable pain, neonatal infection, or herpes zoster ophthalmicus with cranial nerve involvement. Patients should be advised to avoid contact with pregnant or immunocompromised individuals until all lesions have crusted. Long-term follow-up may be required for management of postherpetic neuralgia.
Clinical Pearls And Pitfalls
Always assess for ocular involvement when lesions appear on the tip of the nose. Consider herpes zoster in patients with unexplained dermatomal pain, even in the absence of rash. Fully expose the skin in patients presenting with chest or abdominal pain. Counsel patients early about the risk and chronic nature of postherpetic neuralgia.
Definition And Overview
Herpes zoster, commonly known as shingles, is characterized by a unilateral eruption of painful vesicles distributed along a single dermatome. It results from reactivation of latent varicella zoster virus (VZV) in dorsal root ganglia. Dissemination is rare in immunocompetent hosts but occurs more frequently in immunocompromised patients. The disease is most common in individuals with impaired cell-mediated immunity, particularly adults older than 50 years, patients with malignancy, and those receiving immunosuppressive therapy.
Etiology And Risk Factors
Herpes zoster is caused by reactivation of VZV, a DNA virus in the Herpesviridae family. Most cases occur in individuals with a history of primary varicella (chickenpox), and only rarely in vaccinated individuals. Declining cell-mediated immunity with aging or immunosuppression is the primary risk factor.
Pregnancy is not associated with an increased risk of congenital varicella syndrome. In children, herpes zoster may occur following in utero exposure or primary varicella infection during the first six months of life.
Clinical Features
Dermatomal zoster typically begins with a prodrome of pain, paresthesias, or pruritus in the affected dermatome, occurring in approximately 75% of patients. Pain may be sharp, burning, tingling, or severe. The classic rash consists of grouped vesicles on an erythematous base, which progress to crusting over 7–10 days, with complete resolution in 2–3 weeks. Thoracic and lumbar dermatomes are most commonly involved, followed by trigeminal and cervical distributions.
Zoster sine herpete presents with dermatomal pain without rash and can be diagnostically challenging.
Herpes zoster ophthalmicus results from involvement of the ophthalmic division of the trigeminal nerve. Hutchinson sign, defined as vesicles on the tip of the nose, suggests nasociliary nerve involvement and increased risk of ocular complications. Ocular findings may include punctate keratitis or corneal pseudodendrites, which are less ulcerative and show less fluorescein uptake than HSV dendrites.
Ramsay Hunt syndrome is caused by involvement of cranial nerves VII and VIII and presents with vesicles in the external auditory canal, peripheral facial palsy, vertigo, and altered sensation of the anterior two-thirds of the tongue.
Disseminated disease may occur, particularly in immunocompromised patients, and can involve the central nervous system, liver, or lungs, leading to complications such as meningoencephalitis, myelitis, hepatitis, pneumonitis, and peripheral neuropathy.
Postherpetic neuralgia is defined as pain persisting at the site of zoster lesions for more than three months after cutaneous healing. It occurs in 10–70% of patients, with risk increasing in those older than 50 years and in patients with severe initial rash or pain.
Diagnostic Evaluation
Diagnosis is primarily clinical in typical presentations. Laboratory testing is reserved for atypical cases, disseminated disease, or immunocompromised patients. Tzanck smear may show multinucleated giant cells but cannot distinguish VZV from HSV and has low sensitivity. PCR testing from vesicle fluid, blood, cerebrospinal fluid, or bronchoalveolar lavage is the preferred diagnostic method due to high sensitivity and specificity. Serologic testing is less reliable in the acute setting, and viral culture is slow and insensitive.
Differential Diagnosis
Conditions to consider include primary varicella, herpes simplex infection, cellulitis, allergic contact dermatitis, bullous impetigo, molluscum contagiosum, insect bites, trigeminal neuralgia, radiculopathy, biliary or renal colic, Bell palsy, peripheral vertigo, conjunctivitis, and HSV keratitis.
Emergency Management
Herpes zoster is usually self-limited. Management focuses on reducing pain, shortening disease duration, and preventing postherpetic neuralgia. Lesions should be covered, and universal precautions maintained, as zoster can transmit varicella to nonimmune individuals.
In immunocompetent patients, oral antiviral therapy should be initiated within 72 hours of rash onset, though treatment may still be beneficial if new lesions are forming. Valacyclovir is preferred for ease of dosing, though acyclovir or famciclovir are acceptable alternatives. Analgesia should be tailored to pain severity, ranging from nonsteroidal anti-inflammatory drugs to opioids. Corticosteroids remain controversial and may modestly improve acute pain and rash healing but do not prevent postherpetic neuralgia.
Immunocompromised patients require intravenous acyclovir and close monitoring.
Herpes zoster ophthalmicus requires urgent ophthalmology consultation. Oral antivirals are indicated, with intravenous therapy for immunocompromised patients or those with cranial nerve involvement.
Postherpetic neuralgia is managed with analgesics, tricyclic antidepressants, gabapentin or pregabalin, and topical lidocaine; antivirals are not effective once PHN is established.
Postexposure Prophylaxis And Prevention
Varicella zoster immune globulin (VariZIG) is recommended within 72 hours of exposure for immunocompromised patients, pregnant individuals, and certain neonates. The live-attenuated zoster vaccine is recommended for adults over 60 years of age but is contraindicated in pregnancy and immunocompromised patients. Vaccination does not treat active disease or prevent postherpetic neuralgia in those with established zoster.
Disposition And Follow-Up
Most patients can be managed as outpatients. Admission is indicated for immunocompromised patients, disseminated disease, severe or intractable pain, neonatal infection, or herpes zoster ophthalmicus with cranial nerve involvement. Patients should be advised to avoid contact with pregnant or immunocompromised individuals until all lesions have crusted. Long-term follow-up may be required for management of postherpetic neuralgia.
Clinical Pearls And Pitfalls
Always assess for ocular involvement when lesions appear on the tip of the nose. Consider herpes zoster in patients with unexplained dermatomal pain, even in the absence of rash. Fully expose the skin in patients presenting with chest or abdominal pain. Counsel patients early about the risk and chronic nature of postherpetic neuralgia.
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