MEDICAL REVIEW
Governance Shingles
Fatimah Fitriani, Harijono Kariosentono, Budi Eko Prasetyorini, Putri Oktriana, Nathania Amelinda
Department of Skin and Venereology
Dr. Moewardi/ Faculty of Medicine, Sebelas Maret University, Surakarta
ABSTRACT
Shingles(HZ) is a neurocutaneous disease caused by reactivation and multiplication of varicella zoster virus (VZV) in infected ganglions.
The clinical characteristics of HZ include a painful, unilateral dermatomal rash. The rash is in the form of grouped, maculopapular vesicles with a reddish base localized in the ganglion innervation area. Herpes zoster is a common disease and has the potential to cause serious complications that affect quality of life.
Keywords :shingles, varicella zoster virus
ABSTRACT
Herpes zoster is a neurocutaneous disease caused by reactivation and multiplication of varicella zoster virus in infected ganglions.
Herpes zoster is characterized by unilateral and dermatomal painful rash. The rash appears as erythematous maculopapular and vesicular lesions that are clustered within a single dermatome. Shingles is a common disease and it has potential serious complications that could affect quality of life.
Keywords:herpes zoster, varicella zoster virus
I. Introduction
Shingles(HZ) is a neurocutaneous disease caused by reactivation and multiplication of varicella zoster virus (VZV) in latently infected ganglions in the dorsal roots of sensory fibers and cranial nerve ganglions. The characteristics of HZ are grouped vesicles with a reddish base that feels painful in the ganglion innervation area which is unilateral and dermatomal.1Herpes zoster is a common disease and has the potential to cause serious complications that affect quality of life.2
The global incidence of HZ averages 3.4-4.82 per 1,000 people every year, and the incidence is higher, up to 11 per 1,000 people every year in people aged 80 years.3The incidence of HZ in the United States and Europe is 2.5 per 1,000 people aged 20-50 years, 5 per 1,000 people aged 51-79 years, and 10 per 1,000 people aged over 80 years.4.5Women have a higher predisposition to experience this case than men, with the average age affected being 70-80 years.2A study of the incidence of HZ in the 2011-2013 period reported from 13 teaching hospitals in Indonesia showed that the group that most frequently experienced HZ was the 45-64 year age group, namely 851 (37.95% of the total HZ cases).6
Symptoms of HZ include pain such as burning, prickling, or itching accompanied by vesicles clustered in certain parts of the body. The clinical manifestations of HZ begin with erythematous macules within 12-24 hours which then develop into grouped, unilateral vesicles that do not cross the midline of the body and are limited to the skin area innervated by one sensory ganglion.7.8The most common complication symptom is postherpetic neuralgia (PHN), including dysesthetic pain (eg burning or prickling sensation, allodynia) that persists after the skin lesion has healed. HZ complications occur in 10-20% of HZ cases and can increase in incidence and severity with increasing age.5.9
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Therapy for HZ aims to speed up the healing process of lesions, reduce complaints of acute pain, reduce the risk of PHN complications, and improve the patient's quality of life.5HZ management is based on the 6A strategy, namely assessing the patient from the start with a complete history and physical examination, assessing the patient completely based on special conditions, antiviral management, pain relievers, antidepressant drugs, and anxiety counseling.6The purpose of writing this paper is to understand HZ management as a guide in diagnosing HZ early in order to provide appropriate management and prevent further complications in patients.
II. ETIOLOGY
Varicella zoster virus(VZV) is another name for human herpesvirus 3 (HHV-3), which is a type of herpes virus which causes two types of disease, namely chickenpox (varicella) and herpes zoster/HZ (shingles).10Varicella zoster virus is a member of the herpesviridae family, such as herpes simplex virus (HSV) types 1 and 2, cytomegalovirus (CMV), Epstein-barr virus (EBV), human herpesvirus 6 (HHV-6), human herpesvirus 7 (HHV-7 ), and human herpesvirus 8 (HHV-8).6,11
Varicella zoster virusis a type of virusdeoxyribonucleic acid (DNA), alphaherpesvirus which has a genome size of 125,000 bp, enveloped, with a diameter of 80-120 nm. This virus codes for approximately 70-80 proteins, one of which is the thymidine kinase enzyme which is susceptible to antiviral drugs because it phosphorylates aciclovir, thereby inhibiting viral DNA replication.10.6The viral protein coat is thought to play a role in interactions with cell surface molecules such as the mannose-6-phosphate receptor or myelin glycoprotein. VZV glycoproteins B (gB), gH and L function as the core complex and other envelope glycoproteins function as accessory proteins. Tegument proteins including immediate-early protein 62 (IE62) as the main protein function as transcription factors or are called viral transactivators, come out and are moved to the nucleus before protein synthesis occurs.10
III. PATHOGENESIS
The course of HZ disease includes a viremia phase and a latent phase. During the viremia phase, VZV can attack epidermal cells, causing varicella which manifests as scattered vesicles (generalized), then enters sensory nerve fibers at mucocutaneous locations and moves retrogradely by axons to the dorsal root of the sensory ganglion in the spinal cord, where the virus can persists in a latent phase in the cranial nerves, dorsal roots, and autonomic ganglion, especially in the cell bodies of neurons, because these locations are associated with the most common sites affected by varicella.11,12VZV reactivation in the latent phase can occur spontaneously or be induced by stress, fever, radiation therapy, local trauma, or immunosuppressant agents.5
Figure 1.Different phases of varicella zoster virus (VZV) infection. Primary VZV infection in someone who is susceptible will cause chickenpox (varicella). Varicella zoster virus can remain in the latent period in nerve ganglions and experience reactivation and replication
of the virus which then spreads to the skin which is innervated by neurons and causes herpes zoster disease. Increasing age and being immunocompromised are risk factors for complications from VZV infection. Postherpetic neuralgia can also occur without any
predisposing factors.5
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MEDICAL REVIEW
In the latent phase, VZV DNA is circular and does not replicate, but when reactivation occurs, the virus continues to replicate at the base of the dorsal ganglion, causing the ganglion to become necrotic and hemorrhagic and inducing ganglionitis which is characterized by pain (Figure 1).5When ganglionitis occurs there is regulation of MHC class I and protein II, infiltration of CD4 T cells+and CD8+. Ganglionitis and CD8 T cell infiltration+can persist after HZ occurs.11Neuronal inflammation and necrosis can cause neuralgia that gets worse as the virus spreads along the sensory nerves. Fluid from HZ vesicles can spread VZV to seronegative individuals resulting in primary infection, namely chicken pox (varicella).13Varicella zoster virus can survive in the intracellular environment in the human body with its main targets being T lymphocytes, epithelial cells and ganglions, and is different from herpes simplex virus (HSV).11
IV. DIAGNOSIS
a. Clinical manifestations
The clinical manifestations of HZ can vary between individuals. In children and young adults generally no severe clinical manifestations occur.12Herpes zoster begins with prodromal symptoms which can resemble the symptoms of other diseases involving visceral organs such as myocardial infarction, cholecystitis, or renal colic so that it can make diagnosis difficult and delay appropriate treatment.5Prodromal symptoms can include headache, photophobia, malaise, and fever. An uncomfortable sensation on the skin is the most common symptom.12
Prodromal symptoms are not common in immunocompromised patients under 30 years of age, but the majority occur in patients >60 years of age. Pain and paresthesia may precede the HZ rash from the first to the third day, a week, or longer.9Pain and paresthesia are one of the clinical manifestations of zoster without skin abnormalities (zoster sine herpete) or acute segmental neuralgia without skin eruption. Discomfort such as a burning sensation, prickling, skin becoming more sensitive, unbearable itching, with varying intensity can feel superficial to deep.12Pain can be continuous or intermittent, and can be accompanied by stiffness or hyperesthesia of the affected skin dermatome.9Patients may experience enlarged lymph nodes in the affected area.4The characteristic of HZ is that it has a predilection for affecting any part of the body, especially in the thoracic, cervical and ophthalmic areas.4The distribution of the rash in HZ is unilateral and limited to the skin innervated by a single sensory ganglion and does not cross the midline of the body.
The visible skin lesions can be grouped vesicles with an erythematous base (Figure 2).5
Figure 2.Manifestations of herpes zoster rash. Clustered vesicles with an erythematous base5
b. Diagnosis
In the early stages of development of HZ lesions, erythematous macules appear which develop into papules, then within 1-2 days they develop into vesicles and will become clearer in 3-4 days. Pustular lesions occur starting one week after the onset of redness and within 3-5 days become ulcers and crusts. Crusts are completed within 3-4 weeks. Scars, hypopigmented and hyperpigmented lesions can persist after shingles heals.14In the elderly group, local eruptions sometimes become necrotic, heal within a few weeks, and are followed by heavy scarring.
Mucous membranes included in the dermatomal area may also be affected.4
In children and young adults with good immunity, HZ generally recovers without residual symptoms. The intensity of pain, skin lesions, and severity of HZ complications can worsen with age and if there are immune disorders.5Recurrence of herpes zoster is generally rare and limited to immunocompromised patients.15
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VOL. 34 ISSUE 3, DECEMBER 2021The clinical diagnosis of HZ can be made based on the history and clinical picture. On physical examination, grouped vesicles were found with a reddish base, unilateral and dermatomal distribution. Characterized by an atypical rash, disseminated HZ, or with minimal lesions or no skin abnormalities; zosteriform herpes simplex, redness due to enterovirus, poxvirus, zoster without skin disorders (zoster sine herpete) but sometimes marked by facial paralysis, meningitis, stroke, myelitis and gastrointestinal infections.11
c. Supporting investigation
Supporting examinations are carried out to help confirm the diagnosis of HZ. A simple examination using a Tzank smear with Giemsa staining can help establish a diagnosis quickly to identify the presence of cytological changes in epithelial cells that show a picture of multinucleated giant cells..5
Examination of vesicles with immunofluorescence or immunoperoxidase staining to observe cell material that detects VZV is more significant and faster than culture.9Serum antibody testing provides accurate results but takes time for antibodies to form in the patient. Serum anti-VZV IgM antibodies are generally unhelpful and nonspecific.11
Another laboratory examination that can be used is examinationpolymerase chain reaction(PCR) which is used to identify VZV antigen/nucleic acid.6.16The material taken comes from vesicles (swabs, fluids), saliva from patients who do not have skin manifestations, and cerebrospinal fluid if there are neurological signs.5DNA examination via PCR has the highest sensitivity and specificity and is the gold standard for diagnosis by knowing the genome of VZV.16,17Viral culture is a very specific but not sensitive examination, besides that the results can only be obtained in more than 1 week.17
Serological examination can help confirm the diagnosis of VZV if in serum convalescence there is a 4-fold increase in VZV titer relative to acute serum. PCR is a very sensitive, relatively fast examination, and is starting to be widely used as a VZV detection method. PCR can also be used to determine the presence of aciclovir resistance.11
d. Differential diagnosis
The differential diagnosis of HZ can be differentiated based on the pre-eruption stage and the eruption stage.6.9History and physical examination are important to distinguish HZ lesions from other differential diagnoses (Table 1).
Table 1. Differential diagnosis of HZ9
Stage before eruption
Segmental acute pain is localized and as pain that occurs due to hyperalgesia or
Acute segmental pain damage to sensory receptors and is usually chronic. The locations usually affected are the lateral elbow, Achilles tendon, shoulder.
Eruption stage Zosteriform herpes simplex
Irritant contact dermatitis
Venenous dermatitis
It looks similar to HZ which is dermatomal in nature, the skin disorder manifests in the form of grouped vesicles located in the mouth and genital area.
Irritant contact dermatitis is characterized by reddish patches, fissures and oozing, pain and a history of exposure to irritants at the affected location.9
In venenata dermatitis as an irritation reaction due to insect bites that appears 24 hours after contact, there is a history of insect exposure, generally the lesions are linear, last several days, kissing lesions appear
Burns
Local bacterial infection of HZ:
herpes zoster
There is a history of exposure to heat, fire, electricity, chemicals. Burns can cause redness, blisters and deeper skin tissue damage at grade III
Local bacterial infections that can occur include cellulitis and bullous impetigo
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MEDICAL REVIEW
V. COMPLICATIONS OF HERPES ZOSTER Postherpetic neuralgia
A common complication of herpes zoster (HZ) is postherpetic neuralgia (PHN), which is a type of neuropathic pain that persists for 90 days or more after the red rash has healed. Pain can persist for several months or years, and impact the sufferer's quality of life because it disrupts sleep and daily activities, causes anorexia, weight loss, weakness, interferes with social function, productivity, and causes dependency.18There are two characteristic forms of pain in PHN, namely continuous pain with decreased touch sensation, or intermittent pain with itching accompanied by paresthesia. This pain is the most disturbing complaint and occurs in 90% of people with PHN.5Risk factors for PHN include age over 40 years, severity of pain in acute conditions, severity of reddish skin lesions, and severity of prodromal symptoms with the location most at risk being the trigeminal area.14
Muscle weakness
Apart from pain, HZ can also cause permanent disabilities, such as eye complications, neurological complications (peripheral and cranial nerve paralysis, motor deficits, paresis) followed by pain in the lesion area.6Herpes zoster affecting the sacral region can manifest as urinary retention and defecation disorders.4.11In the condition of herpes sine herpete, Bell's palsy, Ramsay Hunt syndrome (manifested by the presence of vesicles in the external auditory canal, loss of taste sensation in the anterior 2/3 of the tongue, facial weakness), transverse myelitis, meningoencephalitis, a syndrome involving the cerebral arteries or called varicella zoster can occur. Viral vasculopathy can cause stroke syndrome.5,19,18
Shinglesdissemination
The incidence of HZ severity increases in conditions of immune failure such as malignant conditions (lymphoma) or when a person is undergoing therapy with immunosuppressant agents.19The skin lesions that occur can be scattered, numbering more than 20 lesions or extending from the primary dermatome, and there is involvement of internal organs in the form of pneumonia, hepatitis, and brain inflammation.4.14
VI. MANAGEMENT OF HERPES ZOSTER
Basically, shingles is self-limiting or can heal by itself.4Therapy for HZ aims to speed up the healing process of lesions, reduce complaints of acute pain, reduce the risk of PHN complications, and improve the patient's quality of life.5.14HZ management is based on the 6A strategy, namely:
1.Attract patients early(early patient assessment with history and physical examination) 2.Assess patient fully(assess the patient completely based on specific conditions) 3.Antiviral therapy(treatment with antivirals)
4.Analgesics(pain management)
5.Antidepressantand anticonvulsant (treatment with antidepressants and anticonvulsants in cases that require it) 6.Allay anxiety-counsellingor anxiety counseling.6
1. Early patient assessment (attract patient early)
A complete history and physical examination is needed to obtain a correct diagnosis so that the patient can receive appropriate therapy. Treatment is carried out within 72 hours after the skin eruption appears to obtain optimal results.6
2. Complete patient assessment (asses patient fully)
A complete patient assessment is by paying attention to the patient's special conditions such as advanced age, risk of PHN, risk of eye complications, Ramsay Hunt syndrome, immunocompromised conditions, motor deficits, and possible internal organ complications in the form of pneumonia, hepatitis and brain inflammation.6
3. Antiviral treatment (antiviral therapy)
The main goal of administering antiviral drugs is to reduce the severity, shorten the duration of the lesion, and prevent the spread of the lesion from being limited to the primary dermatome.9Various studies regarding the management of HZ recommend administering antivirals within 72 hours of the development of skin lesions.5.20Antiviral administration can be given earlier since lesions appear in several conditions such as age over 50 years, risk of PHN, Ramsay Hunt syndrome, immunocompromised conditions with generalized spread, HZ with complications, as well as in children and pregnant women with the drug dosage stated in Table 2.6Antivirus in HZ infection has a working target to inhibit viral DNA activity in the transcription process so that it can suppress viral replication. Antivirals that have this mechanism, namely the nucleoside analog group such as aciclovir, famciclovir, valaciclovir, brivudine, and foscarnet, have shown efficacy in managing VZV infections.9.21Systemic therapy via both oral and parenteral routes
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VOL. 34 ISSUE 3, DECEMBER 2021is preferred over topical therapy because it has a better pharmacokinetic profile and is able to overcome limitations in the presence of a barrier for the entry of antiviral drugs into tissues at the sites of VZV replication.9
Aciclovir, famciclovir, and valaciclovir are drugs approved byFood and Drug Administration (FDA) for HZ therapy in immunocompetent patients and results in reduced disease severity, duration of skin lesions, and pain.5Aciclovir is a guanosine analog that is selectively phosphorylated by VZV thymidine kinase (a weak substrate for cellular thymidine kinase) and becomes concentrated in infected cells.
Cellular enzymes are then converted from aciclovir monophosphate to aciclovir triphosphate which affects viral DNA synthesis by inhibiting viral DNA.9AciclovirAvailable in oral, topical and intravenous dosage forms. Oral aciclovir has low bioavailability with an absorption rate of only around 15-30%. The dose of aciclovir in HZ is as listed in Table 2. Aciclovir cannot prevent the occurrence of PHN.22Intravenous aciclovir can be given in HZ conditions with internal organ involvement, retinitis, and immunocompromised patients experiencing HZ (after 4 months post allogeneic stem cell transplantation, patients with graft versus host disease (GVHD), blood cell transplantation, patients taking transplant rejection drugs) .5.22Intravenous aciclovir is dissolved in 100 ml of 0.9% NaCl and given intravenously over one hour.6
Table 2.Dosage of antiviral drugs for the management of shingles Normal
Children
Age <50 years
Age ≥50 years and patients with cranial nerve involvement
(e.g. ophthalmic herpes zoster)
Immunocompromise
Moderate immunocompromise, including HIV infection
Severe immunocompromise
Resistance to aciclovir (advanced AIDS)
HZ: shingles; HIV: human immunodeficiency virus; AIDS: acquired immune deficiency syndrome.
Valaciclovirand famciclovir works as an antiviral drug with better absorption than aciclovir, so it requires a smaller dose. Valaciclovir is converted enzymatically to aciclovir after absorption. Famciclovir as a prodrug of penciclovir has a mechanism of action similar to aciclovir and other antiviral activities against VZV and HSV.5.9Famcicloviror valaciclovir is preferred over aciclovir for oral therapy of VZV infection.
Brivudineis a uracil analogue with high antiviral activity against VZV. Although effective in the therapy of herpes zoster and registered for use outside the United States, it is not registered in the United States due to a potentially lethal interaction with 5-fluorouracil. Foscarnet is an inorganic pyrophosphate analog that inhibits VZV replication in vitro. The antiviral activity of this drug occurs through selective inhibition of the pyrophosphate binding side of virus-specific DNA polymerase and reverse transcriptase at concentrations that have no effect on DNA
polymerase. Foscarnet does not require thymidine kinase phosphorylation for activation, and when active foscarnet is also effective against aciclovir-resistant VZV, thereby reducing activity.
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thymidine kinase.9 Aciclovir resistance in HZ has been reported in AIDS patients due to mutations in the VZV thymidine kinase gene, resulting in cross-resistance to ganciclovir, valaciclovir, famciclovir, and penciclovir. These resistant cases generally respond to intravenous foscarnet therapy 40 mg every 8 hours, although these infections can generally recur after therapy ends.9
4. Analgesic treatment
The degree of pain in HZ can be assessed using a standardized pain scale.9Several types of pain medication and the doses that can be used can be seen in Table 3. Moderate intensity pain can be treated with paracetamol and non-steroidal anti-inflammatory drugs.
This drug cannot reduce pain in PHN, but can be used as a first-line drug to control pain in HZ.17Severe acute pain is a risk factor for PHN, which contributes to central sensitization and causes chronic pain, so it is necessary to consider giving opioid analgesics such as tramadol and codeine.6More severe acute pain may require short-acting opioids.17Randomized studies with placebo report that opioids are more effective than gabapentin for HZ-related pain.18
5. Antidepressant/anticonvulsant treatment (antidepressant/anticonvulsant)
Tricyclic antidepressants play a role in controlling pain in HZ and PHN.17Low-dose tricyclic antidepressants show fairly good efficacy and work through an indirect mechanism of their antidepressant effect. The frequently used tricyclic antidepressant, namely amitriptyline, can significantly reduce pain in PHN compared to nortriptyline and desiramine because their use is associated with cholinergic side effects.17In a randomized controlled study it was found that combination therapy of nortriptyline and gabapentin could reduce pain more than the use of these agents alone. In one open study, the use of gabapentin together with valaciclovir during the acute period of herpes zoster was more effective in preventing the occurrence of PHN than the use of valaciclovir alone. Although treatment with prednisone along with aciclovir can reduce acute pain in patients with herpes zoster, several controlled studies have failed to show any difference in the incidence or severity of PHN with the combination of these drugs versus the use of aciclovir monotherapy.5
Table 3.Use of steroids and analgesics in the management of herpes zoster
Drug Initial dose Titration Maximum dose Side effects
Opioid analgesics
Tramadol
There is no maximum dose with careful titration, consider pain evaluation at doses >120 mg/day, 400 mg/day (100 mg, 4 times/day) for patients >75 years, 300 mg per day in divided doses
Nausea, vomiting, constipation, sedation and dizziness
Nausea, vomiting, constipation, sedation, dizziness, convulsions, postural hypotension
Gabapentin
Pregabalin
300 mg at night or 100-300 mg, 3 times a day
75 mg at night or 75 mg, 2 times a day
The dose can be increased from 100-300 mg, 3 times a day every 2 days
The dose may be increased from 75 mg, 2 times daily every 3 days if tolerated
3,600 mg daily (1,200 mg, 3 times a day) the dose can be reduced if failure occurs
600 mg per day (300 mg, 2 times a day) can be reduced if kidney abnormalities occur
Drowsiness, dizziness, extremity edema
Drowsiness, dizziness, extremity edema
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VOL. 34 ISSUE 3, DECEMBER 2021Antidepressant
Steroids oral (dose prednisone)
Dose increased from 25
mg daily, on 2-3 days 150 mg per day if tolerable
After a dose of 60 mg per day 60 mg per day for 7 days, dose can be
reduced to 30 mg per day for 7 days then reduced to 15 mg per day for 7 days then stopped
Weight gain, drowsiness, blurred vision, dry mouth Stomach pain, nausea, mood changes and oedema
6. Counseling to overcome anxiety (allay anxiety-counselling)
Education regarding HZ disease to patients aims to reduce anxiety and provide information about the disease, risk of transmission, complications and therapy plans to patients.14Education to maintain optimal mental condition and physical activity, provide attention in order to help patients overcome HZ disease, and improve the patient's quality of life.6.14Patients are given education to keep reddish skin lesions clean and dry to reduce the risk of bacterial superinfection.14
VII. PREVENTION OF HERPES ZOSTER
The varicella vaccine was first developed in Japan by Takahashi and his colleagues in 1974. Varicella was isolated from a boy with varicella infection, then cultivated 33 times through human and guinea pig fibroblasts at 34oC. VZV reactivation is associated with a decrease in cell-mediated immunity, so the varicella vaccine is being studied as a prophylactic method for HZ.11The Advisory Committee on Immunization Practices (ACIP) recommends administering a single dose of vaccine to all immunocompetent individuals aged ≥60 years, regardless of previous history of varicella or HZ. The dosage for HZ vaccine can be seen in Table 4.22
The recombinant HZ vaccine should be given to all psoriasis and psoriatic arthritis patients aged >50 years and <50 years who are classified as high risk groups.23This vaccine is not indicated in active HZ or PHN conditions. Contraindications for the HZ vaccine are primary immunodeficiency diseases (humoral immunity failure including hypogammaglobulinemia), hematological malignancies, blood cell transplantation within 24 months,acquired immune deficiency syndrome (AIDS) with CD value4+ ≤200 mm3or ≤15% of total lymphocytes), use of immunosuppressant drugs, including use of high doses of steroids (equivalent to prednisone ≥20 mg/day or patients receiving biological agent therapy (infliximab, adalimumab and etanercept). Vaccination can be done after stopping these drugs for at least 1 months. Pregnancy should be avoided for 1 month after HZ vaccination.22.24
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Table 4.Recommended shingles vaccine dosage table1
Vaccine Vaccine type Recommended dosage Category dosage
Zostavax®
Shingrix® Recombinant
Single dose contains virus (0.65 ml, contains VZV ≥19,400 plaque forming units (PFU). Given subcutaneous injection
2 doses, each dose contains (50 μg of VZV glycoprotein E with an initial dose at month 0 followed by a second dose after 2-6 months. The second dose is important to ensure maximum vaccine efficacy and duration of HZ protection.
Intramuscular injections are given and the recommended area is the deltoid muscle
Low dose: 3,500 – 10,000 PFU x 1 dose.
Standard dose: 19,400 – 23,000 PFU x 1 dose
Standard dose: 40,000-200,000 PFU x1 dose
Low dose: 25 μg x 2 doses Standard dose: 50 μg x 2 doses High dose: 100 μg x 2 doses
VIII. PREVENTION AND MANAGEMENT OF POSTHERPETIC NEURALGIA
Postherpetic neuralgia(PHN) can occur due to inflammation of the sensory ganglion and adjacent nerve structures, so the use of glucocorticoids is necessary during the acute phase of HZ. The goal of PHN management is so that patients can immediately carry out daily activities without being disturbed. Glucocorticoids combined with antivirals are effective for acute pain due to facial nerve paralysis and cranial polyneuritis.9First-line pharmacological therapy can be seen in Table 5.6Combination therapy of gabapentin and nortriptyline, or opiates and gabapentin has been shown to be more effective for PHN than monotherapy, although it has a higher potential for side effects.18Other therapies used in treating PHN include analgesics such as paracetamol if mild pain occurs, and opioids can be used for PHN with moderate-severe pain.8
Topical therapy using topical lidocaine is one of the therapeutic options for controlling pain in cases of PHN. Its use is relatively easy and has a low potential for systemic side effects.4.17During the acute phase of shingles, topical therapy can be given in the form of cold compresses and calamine lotion to reduce symptoms and dry out vesicular lesions. Creams and lotions containing glucocorticoids and occlusive ointments should not be used.
Topical therapy with antiviral agents is ineffective. Salicylic acid should be avoided due to the possibility of Reye's syndrome.9Capsaicin patch 8%
was recently approved by the FDA as a therapy for PHN, data shows its use can reduce pain for up to 12 weeks after use for 1 hour.5A randomized controlled trial demonstrated the efficacy of improving PHN pain with treatment with gabapentin, tricyclic antidepressants, opioid analgesics, tramadol and
capsaicin.9
Table 5.Choice of drugs in the management of PHN Drug
Tricyclic antidepressants
Gabapentin
Pregabalin Lidocainetopical EMLA
Initial dose
10 hours every night (2 hours before bed) 100 mg 3 times per day
75 mg 2 times per day Lidocainegel 5%
Titration First line
Increased by 20 mg every 7 days to 50 mg, then to 100 mg and 150 mg every night
100 -300 mg increased every 5 days to a dose of 1,800- 3,600 mg per day
Increase to 150 mg 2 times per day for 1 week -
Second line
Tramadol
MEDICAL REVIEW
Another therapy in the management of PHN is low level laser therapy (LLLT) which is included in non-invasive therapy, namely using infrared light with low energy from a laser. LLLT in dermatology is usually used for PHN and wound healing. Currently, LLLT has been proven effective for reducing pain such as trigeminal neuralgia, neuropathic pain, and PHN.25
IX. PROGNOSIS
The prognosis of HZ in lesions involving internal organs, such as in patients undergoing chemotherapy with lymphocyte counts decreasing to <500/µl, indicates a mortality rate of up to 30%. Varicella pneumonia can appear 3-7 days after the attack of skin infection and lasts for 2-4 weeks. Symptoms of central nervous system abnormalities may appear 4-8 days after skin infection and carry a poor prognosis.6
X. CONCLUSION
Shingles(HZ) is a viral infection that is generally self-limiting, characterized by a very painful rash, carries a risk of secondary infection, and a 20% risk of complications in the form of postherpetic neuralgia (PHN). It is necessary to carry out preventive efforts and comprehensive management in cases of infection to minimize the impact of disease on quality of life during and after infection. The aim of HZ management is to speed up the lesion healing process, reduce complaints of acute pain, reduce the risk of PHN complications, and improve the patient's quality of life. The 6A approach can be a guide for comprehensive management of HZ cases, which includes early patient assessment with a complete history and physical examination to establish the diagnosis, complete patient assessment based on special conditions, antiviral treatment, as well as additional therapy in the form of analgesic treatment, antidepressant treatment , and anxiety counseling.
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