later in life to cause herpes zoster, or shingles. Patients who were vaccinated against chickenpox as a child can also develop shingles later in life, though it considered less common than developing shingles after chicken pox disease. Estimates show that approximately one out of every three people in the United States will develop shingles in their lifetime; over 1.2 million cases occur per year in the United States. Risk factors for reactivation include (Albrecht & Levin, 2021): ● Age . A significant, age-related increase in incidence of herpes zoster starts at approximately 50 years of age, with 20% of cases affecting people between 50 and 59 years of age. Ap- proximately 50% of 85-year- old patients have had an episode of herpes zoster. ● Immunocompromised status . The reduced T-cell immunity of patients who are immunocompromised increases the risk of herpes zoster in this group. This group includes patients with autoimmune disease, those who have had an organ trans- plant, and patients with human immunodeficiency virus (HIV). ● Race . White Americans experience significantly higher inci - dence of herpes zoster compared with African Americans. ● Physical trauma . Patients over 65 who experience trauma are significantly more likely to develop a case of herpes zoster. ● Gender . Women are more likely to develop herpes zoster than men. ● Other comorbidities . Other conditions that increase the risk of herpes zoster infection include malignancy, chemotherapy, and chronic lung or kidney disease. Upon reactivation, the virus can spread along the sensory neurons until it reaches the skin, where it establishes infection. This infec- tion results in inflammation and the characteristic shingles rash. Pain is typically related to nerve inflammation and hemorrhagic necrosis of nerve cells (Albrecht & Levin, 2021). Symptoms Before the characteristic rash appears, some patients with shin- gles experience fatigue or a general “run-down” feeling. Before developing a rash, around 75% of patients experience pain in the area of infection, known as prodromal pain . This prodromal pain is often misinterpreted as other diseases, such as appendicitis or cholecystitis, depending on the location (Albrecht & Levin, 2021). Two to three days later, the shingles rash begins. It starts as red patches of skin with small bumps that develop into blisters over the course of several days. The blisters are associated with itchi- ness, and the pain is often described as a deep burning or stab- bing sensation. The blisters typically dry up within 7 to 10 days, leaving behind scabs that are commonly yellow in color. Skin symptoms of shingles typically clear up within 2 to 4 weeks; pain lasts at least 30 days in 18% of patients. Shingles patients are con- sidered contagious, after the lesions crust over. Fluid from blisters can cause chickenpox in patients without prior infection history (Albrecht & Levin, 2021). The rash is commonly located in one area on a single side of the body, although it is possible to occur in multiple areas at once. Shingles most commonly affects the torso or chest, though it is possible to develop just about anywhere on the body, including arms, face, head, and even ears or eyes. A small percentage of patients present with only pain and skin sensations with no rash. Less than 20% of patients report flu-like symptoms during acute herpes zoster infections, and helplessness and depression have also been reported (Albrecht & Levin, 2021). Complications Patients with compromised immune systems are more likely to experience complications as well as a more severe, longer-lasting shingles rash. Pain and skin sensations associated with the shin- gles rash can persist for weeks, months, or even years, causing the most common complication of herpes zoster infection, referred to as post-herpetic neuralgia. Post-herpetic neuralgia is defined as significant pain that persists for at least 90 days after the onset of the shingles rash. It can affect between 10% and 15% of shingles patients. Risk of developing post-herpetic neuralgia increases
with age, with 50% of cases occurring in patients over 60 years of age (Albrecht & Levin, 2021). Scratching shingles blisters can cause a bacterial skin infection or lead to scarring. In rare cases, blisters can spread to neighboring skin areas and, even more rarely, spread over the whole body. This spread is often related to a significantly weakened immune sys - tem, similar to that occurring in cancer or transplant patients. Un- der these rare situations, shingles can be life-threatening. Chang- es in skin pigmentation can occur in the involved skin area after resolution of the infection, causing lighter or darker pigmentation than surrounding skin (Albrecht & Levin, 2021). Other complications are related to the site of zoster infection. In- volvement near the eye can lead to herpes zoster ophthalmicus, causing conjunctivitis, ulcers on the cornea, and even blindness. Ramsey-Hunt syndrome, also known as herpes zoster oticus, oc- curs when the varicella zoster virus affects the nerves that serve the ear. This syndrome can lead to ear pain, facial nerve palsies, shingles rash in the ear canal, balance issues, and hearing loss. Nerve palsies can affect other areas of the body, depending on the affected nerve (Albrecht & Levin, 2021). Herpes zoster can also affect the nerves of the central nervous system, leading to meningitis, encephalitis, peripheral motor neu- ropathy, myelitis, Guillain-Barré syndrome, and stroke syndromes. These rare but serious complications appear to be more likely in patients with a significantly weakened immune system (Albrecht & Levin, 2021). Diagnosis Some people who develop shingles initially think they have a non-contagious skin infection, such as eczema. This initial misdi- agnosis can delay a correct diagnosis and treatment. Diagnosis during the early stages of shingles development can be difficult because the characteristic rash often develops after pain starts. Depending on the affected area, other causes may be initially suspected, such as appendicitis, hernia, or myocardial infarction (Albrecht & Levin, 2021). Diagnosis is often based on the characteristic rash that develops on one side of the body, as well as the accompanying pain and sensations related to nerve inflammation. If the diagnosis is un - clear, fluid from blisters can be tested to determine whether it contains varicella zoster virus. Blood tests to detect antibodies to varicella zoster virus can also be helpful in the diagnostic phase (Albrecht & Levin, 2021). Treatment Antiviral medications, such as acyclovir, famciclovir, and valacy- clovir, which are effective at inhibiting viral replication, are cor- nerstones in the management of herpes zoster. Goals of antiviral therapy include reducing the duration and severity of pain, pro- moting the healing of skin lesions, preventing new lesion forma- tion, reducing viral shedding to decrease the contagious aspect of shingles, and preventing post-herpetic neuralgia. Antiviral ther- apy should be initiated as soon as possible after the rash appears to maximize effectiveness – ideally within 72 hours. Antivirals are most beneficial if initiated while new lesions are actively forming since this formation of lesions indicates ongoing vital replication. The benefit of using antivirals after new lesions have stopped forming is unknown (Albrecht & Levin, 2021). Acyclovir is the prototype antiviral medication, available for both oral and intravenous administration. It is less bioavailable than other antiviral options, and its frequent administration require- ments make it less favorable for treating shingles. It is commonly administered at a dose of 800 mg five times daily for 7 days. Intra - venous use is typically reserved only for patients with severe com- plications. Dose adjustments may be necessary in patients with severe renal insufficiency because of its renal clearance. Acyclovir is a generic medication, associated with the brand name Zovirax (Albrecht & Levin, 2021). Valacyclovir is a prodrug of acyclovir, meaning it is converted into acyclovir in the body after ingestion. Valacyclovir is more bioavailable than acyclovir, with oral dosing producing antiviral
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