What are the risks of shingles affecting the eye. How can shingles cause vision impairment or blindness. What treatments are available for shingles in the eye. How effective is the shingles vaccine at preventing ocular complications.

Understanding Shingles and Its Ocular Manifestations

Shingles, medically known as herpes zoster, is a viral infection that can have serious consequences, particularly when it affects the eye. This condition arises from the reactivation of the varicella-zoster virus, the same virus responsible for chickenpox. After an initial chickenpox infection, the virus remains dormant in the body’s nerves, held in check by the immune system. However, factors such as aging, illness, or immunosuppressive medications can weaken the immune system, increasing the risk of shingles.

Approximately one million cases of shingles occur annually in the United States. Of these cases, up to 20% involve the nerves of the head, potentially affecting various parts of the eye. This ocular involvement can lead to significant complications, including vision impairment and, in severe cases, blindness.

How does shingles affect the eye?

Shingles can impact different parts of the eye, including:

• The eyelid
• The eye surface
• Deeper portions of the eye

When shingles affects the eye, it can cause a range of symptoms, including:

• Pain
• Drainage
• Redness
• Sensitivity to light

Herpes Zoster Ophthalmicus: Shingles in the Front of the Eye

One of the most common ocular manifestations of shingles is herpes zoster ophthalmicus (HZO). This condition typically involves one side of the upper face, forehead, and scalp. HZO can lead to keratitis, an inflammation of the cornea, which is the transparent dome of tissue at the front of the eye.

How common is keratitis in HZO patients?

More than half of patients with HZO may develop keratitis. This complication usually occurs within one month of the shingles rash appearing.

What are the potential consequences of keratitis?

Keratitis can result in several serious complications:

• Numbness of the cornea
• Scarring
• Additional infections
• Further corneal damage
• Potential blindness

Given these risks, it is crucial for individuals experiencing shingles in the upper face, forehead, or scalp area to seek immediate evaluation by an ophthalmologist, regardless of whether they notice any eye symptoms.

Treatment Approaches for Ocular Shingles

The primary treatment for HZO, like other forms of shingles, involves oral antiviral medications. These medications target the underlying viral infection and can significantly reduce the risk of eye complications.

How effective are antiviral medications in preventing eye complications?

When administered promptly, antiviral treatments can decrease the risk of later eye complications by approximately 40% to 60%. For optimal efficacy, treatment should be initiated within 72 hours of symptom onset.

What are the additional benefits of early antiviral treatment?

Beyond reducing the risk of eye complications, early antiviral treatment offers several advantages:

• Reduces the overall severity of the infection
• Decreases the risk of post-herpetic neuralgia, a form of long-term pain that can persist after a shingles episode

Shingles Affecting the Back of the Eye: Viral Retinitis

While less common than HZO, shingles can also affect the structures at the back of the eye, including the retina and optic nerve. This condition, known as viral retinitis, can cause significant damage to the retina through a combination of infection and inflammation.

What are the main forms of viral retinitis associated with shingles?

Viral retinitis can manifest in two primary forms:

1. Acute retinal necrosis (ARN)
2. Progressive outer retinal necrosis (PORN)

Unlike HZO, viral retinitis typically does not present with a skin rash or symptoms at the eye surface, making diagnosis more challenging.

Acute Retinal Necrosis: A Serious Complication

Acute retinal necrosis (ARN) is a severe form of viral retinitis that can occur in otherwise healthy, middle-aged individuals. This condition requires careful examination by an ophthalmologist for proper diagnosis.

How is ARN diagnosed and treated?

Diagnosis of ARN involves:

• A thorough eye examination
• Possible collection of a sample from the inside of the eye to confirm the presence of the varicella-zoster virus

Treatment approaches for ARN vary based on severity:

• Mild cases: Oral antiviral medications, with or without intraocular antiviral injections
• Severe cases or those unresponsive to initial treatment: Intravenous (IV) antiviral medications until improvement is observed

Progressive Outer Retinal Necrosis: A Rare but Severe Condition

Progressive outer retinal necrosis (PORN) is a rare and aggressive form of viral retinitis. This condition typically affects individuals with severely compromised immune function and progresses rapidly.

What is the recommended treatment approach for PORN?

Due to its aggressive nature, PORN requires immediate and intensive treatment:

• Intraocular antiviral injections
• Intravenous (IV) antiviral medications

The treatment regimen for PORN is generally more aggressive than that for ARN due to the rapid progression and severe nature of the condition.

Managing Immune Function in Ocular Shingles

For patients with ocular shingles, including those with HZO or ARN, managing immune function is a crucial aspect of treatment. This may involve various strategies depending on the patient’s underlying health status and current medications.

How is immune function managed in patients with ocular shingles?

Several approaches may be employed:

• For patients on immunosuppressive medications: Reducing the dose or temporarily discontinuing the medication
• Allowing time for the infection to respond to antiviral treatment before administering another dose of immunosuppressive medication
• In cases of severe inflammation: Using steroids to control inflammation and prevent eye damage

It’s important to note that the use of steroids in ocular shingles is carefully balanced against the need to control the viral infection. Steroids are typically introduced only after the infection has been adequately addressed with antiviral medications.

Prevention: The Role of Shingles Vaccination

The most effective way to prevent shingles and its ocular complications is through vaccination. The current recommended vaccine in the United States is Shingrix, which has replaced the older Zostavax vaccine.

How effective is the Shingrix vaccine in preventing shingles?

Shingrix is a highly effective vaccine:

• It is more than 90% effective at preventing shingles
• It is a non-live vaccine, making it safer for a broader range of individuals
• It is recommended for adults over age 50
• The vaccine is administered in two doses

By preventing shingles, the Shingrix vaccine also reduces the risk of ocular complications associated with the disease. This makes vaccination a crucial preventive measure, particularly for older adults and those at higher risk of developing shingles.

Are there any contraindications for the Shingrix vaccine?

While Shingrix is generally safe and recommended for most adults over 50, there are some considerations:

• Individuals with a history of severe allergic reactions to any component of the vaccine should not receive it
• People who are currently experiencing an active shingles outbreak should wait until the symptoms resolve before getting vaccinated
• Those who are pregnant or breastfeeding should consult with their healthcare provider before receiving the vaccine

It’s important to discuss individual circumstances with a healthcare provider to determine the appropriateness of the Shingrix vaccine.

Long-Term Management and Follow-Up for Ocular Shingles

For individuals who have experienced ocular shingles, long-term management and follow-up are crucial to monitor for potential complications and ensure optimal eye health.

What does long-term management of ocular shingles involve?

Long-term management may include:

• Regular follow-up appointments with an ophthalmologist
• Monitoring for recurrence of viral activity
• Managing any residual inflammation or scarring
• Addressing potential complications such as glaucoma or cataracts
• Visual rehabilitation if significant vision loss has occurred

The frequency and nature of follow-up care will depend on the severity of the initial infection and the presence of any ongoing complications.

Can ocular shingles recur?

While recurrence of ocular shingles is relatively rare, it can happen. Factors that may increase the risk of recurrence include:

• Weakened immune system
• Advanced age
• Severe initial infection

Patients who have experienced ocular shingles should be vigilant for any signs of recurrence and seek prompt medical attention if symptoms develop.

Research and Future Directions in Ocular Shingles Management

The field of ocular shingles management is continually evolving, with ongoing research aimed at improving prevention, diagnosis, and treatment strategies.

What are some areas of current research in ocular shingles?

Current research focuses on several key areas:

• Development of more effective antiviral medications
• Improvement of diagnostic techniques for early detection of ocular involvement
• Investigation of novel therapies to reduce inflammation and prevent long-term complications
• Exploration of strategies to boost the immune response against the varicella-zoster virus
• Refinement of vaccination strategies to provide more comprehensive protection against shingles and its complications

As research progresses, it is hoped that new innovations will further reduce the incidence and severity of ocular shingles, ultimately improving outcomes for affected individuals.

How might future developments impact the management of ocular shingles?

Potential future developments could include:

• More targeted antiviral therapies with fewer side effects
• Advanced imaging techniques for earlier detection of retinal involvement
• Personalized treatment approaches based on genetic or immunological factors
• Improved vaccines that provide longer-lasting protection against shingles
• Novel interventions to prevent or minimize post-herpetic neuralgia

These advancements could significantly improve the prognosis for patients with ocular shingles and reduce the risk of vision-threatening complications.

Patient Education and Awareness: Key to Early Intervention

Raising awareness about the potential ocular complications of shingles is crucial for ensuring early intervention and optimal outcomes. Patient education plays a vital role in this process.

What key information should patients be aware of regarding ocular shingles?

Important points for patient education include:

• Recognition of early signs and symptoms of shingles, particularly those involving the face or head
• Understanding the importance of seeking prompt medical attention if shingles is suspected
• Awareness of the potential for ocular involvement, even in the absence of obvious eye symptoms
• Knowledge of the benefits of early treatment in reducing the risk of complications
• Understanding the importance of follow-up care and long-term monitoring
• Awareness of vaccination options and their role in preventing shingles and its complications

By empowering patients with this knowledge, healthcare providers can help ensure that cases of ocular shingles are identified and treated as early as possible, potentially preventing vision-threatening complications.

How can healthcare providers effectively educate patients about ocular shingles?

Effective patient education strategies may include:

• Providing clear, concise written materials about shingles and its potential ocular complications
• Using visual aids to illustrate the parts of the eye that can be affected by shingles
• Discussing the importance of shingles vaccination during routine health check-ups
• Encouraging patients to ask questions and voice any concerns about shingles and eye health
• Utilizing telemedicine platforms to provide education and follow-up care when appropriate

By implementing comprehensive patient education programs, healthcare providers can play a crucial role in reducing the impact of ocular shingles and promoting overall eye health.

Shingles of the eye can cause lasting vision impairment

Shingles, or herpes zoster, is a viral infection known for its characteristic painful, burning, or itchy rash. This rash appears along a particular affected nerve, for example in a band on one side of the chest or abdomen that extends around to the back. In fact, the name shingles comes from cingulum, the Latin word for girdle, belt, or sash.

Shingles is caused by reactivation of the varicella zoster virus, the virus that causes chickenpox. After the initial chickenpox infection resolves the virus lives on in nerves all over the body, but is kept in check by the immune system. The risk of shingles therefore increases with any process that can weaken the immune system, including age, illness, and immune-suppressing medications. About one million cases of shingles occur in the US each year.

Up to 20% of shingles episodes involve nerves of the head, where the infection can affect various parts of the eye, including the eyelid, the eye surface, and the deeper portions of the eye. Viral infection of the eye can cause pain, drainage, redness, and sensitivity to light. In some cases it can lead to vision impairment, including blindness.

Shingles in the front of the eye

Shingles can affect the cornea, the curved, transparent dome of tissue at the front of the eye. This is called keratitis, and it can occur as a complication of herpes zoster ophthalmicus (HZO), which refers to shingles with a rash that typically involves one side of the upper face, forehead, and scalp. More than half of patients with HZO may have keratitis.

If you have shingles involving the upper face, forehead, or scalp area, it is important to see an ophthalmologist for a formal eye examination, whether or not you notice any eye symptoms. Keratitis usually develops within one month of the shingles rash and can lead to numbness of the cornea, scarring, additional infections, and more corneal damage, which can ultimately cause blindness.

HZO, like episodes of shingles on other areas of the body, is typically treated with oral antiviral medications to address the underlying viral infection. Treatment decreases the risk of later eye complications by about 40% to 60%. When started within 72 hours of the onset of symptoms, antiviral treatment also reduces the overall severity of the infection and the risk of post-herpetic neuralgia, a form of long-term pain that can occur after an episode of shingles.

Shingles in the back of the eye

Shingles involving the retina or optic nerve — structures found at the back of the eye — typically is not associated with a skin rash or other symptoms at the eye surface. This type of shingles infection is called viral retinitis and occurs much less commonly than HZO. But it can significantly damage the retina through a combination of infection and inflammation. Viral retinitis can take the form of acute retinal necrosis (ARN) or progressive outer retinal necrosis (PORN).

In contrast to patients with HZO or other forms of shingles that are associated with a skin rash, patients with ARN are often middle-aged and generally healthy. Diagnosis of ARN requires a careful eye exam by an ophthalmologist, and a sample may be collected from the inside of the eye for testing to confirm that the infection is caused by the varicella zoster virus. In mild cases, ARN can be treated with oral antiviral medications, with or without injections of antiviral medications into the eye. In more severe cases, or if there is no improvement with oral medications and intraocular injections, these infections are treated with intravenous (IV) antiviral medications until the infection starts to improve.

Fortunately, PORN is rare. It typically occurs in people who have severely compromised immune function, and progresses rapidly. PORN is treated aggressively, with intraocular injections and IV antiviral medications.

Often for patients with shingles, including those with HZO or ARN, efforts are made to strengthen the immune system until the infection is under control. For people taking immune-suppressing medications, this may mean decreasing the dose, or allowing time for the infection to respond to antiviral treatment before administering another dose of immune-suppressing medication. Sometimes the inflammation associated with shingles of the eye is so severe that steroids are needed to control the inflammation before it damages the eye.

Shingles vaccine is the best prevention

The best way to prevent shingles, including shingles of the eye, is with a shingles vaccine. The Zostavax live shingles vaccine is no longer used in the US. Shingrix is a newer, more effective, and non-live shingles vaccine. Shingrix is a two-dose vaccine recommended for adults over age 50. It is more than 90% effective at preventing shingles. Unfortunately, the shingles vaccine does not treat shingles or post-herpetic neuralgia; the vaccine is effective only as a prevention strategy.

Can Shingles Cause Blindness?

October 4, 2017

Latest News cornea, dry eye, eye infections, glaucoma, herpes zoster, optic nerve, permanent vision loss, shingles, shingles vaccine

At Georgia Eye, we know that caring for the eyes can often be more complicated than most people think.   Even though many of the conditions that can affect vision, like common refractive errors or chronic dry eye, are relatively straightforward and easy to diagnose, it is also important to remember that the eyes are complicated and delicate organs and that they may be seriously affected by conditions that seem to have nothing to do with them.  Take, for example, shingles.  Many people are familiar with shingles as a kind of skin condition that can cause an extremely painful rash, but most are unaware that it actually affects the nerves and, if it occurs on the face, can potentially cause serious damage to the eyes or even long-term vision loss.  Here are the important things that you need to know about how the shingles virus can impact your vision and what you can do to help prevent it.

Shingles, which is medically known as herpes zoster, is a relatively common condition that is believed to affect as many as one in three people over the course of their lifetimes.  If you have ever had chicken-pox, the varicella-zoster virus that causes it never goes away, but instead remains inactive deep inside the roots of the nerves.   Generally, your immune system is sufficient to keep the virus dormant, but as we grow older our natural defenses tend to become less effective.  In some people, this can allow the virus to reactivate and spread up the nerves and to the skin, where it ultimately manifests as a red, blistering rash, usually accompanied by deep, penetrating pain from the nerve endings.  Most often, the rash occurs as a band or strip on one side of the abdomen and back.  However, because there are nerve endings across the entire skin surface, herpes zoster can potentially flare up anywhere on the body.  If the forehead, temple, or nose becomes infected, the eye may become infected as well, and this can have serious ramifications.

The blisters and sores caused by the herpes zoster rash easily become infected, so if that rash is close to the eye it can easily lead to eye infections that cause pain, redness, light sensitivity, and eyelid swelling.  Unfortunately, this may only be the tip of the iceberg.   The infection can also cause the cornea (the clear layer in front of the iris and pupil) to become swollen, severely damaged, and scarred.  When the structures behind the cornea become inflamed the pressure of the fluids inside the eye can increase to the point that it begins to damage the optic nerve.  Ultimately this can result in glaucoma, a serious condition which can result in permanent vision loss.

Fortunately, if shingles is caught early and treated with antiviral drugs within the first three days, the duration of the rash and the risk of eye complications can be significantly reduced.  Corticosteroids, usually in the form of eye drops, can be used to control dangerous inflammation as well.  The eye care specialists at Georgia Eye can diagnose this and help you treat it, so call us immediately if you think you may be starting to exhibit symptoms.  Finally, a shingles vaccine is also recommended for healthy people aged 60 or over, regardless of whether they have had chickenpox or shingles. This vaccine not only decreases the chance of getting shingles but also makes any outbreaks that do occur less severe than they would be in people who have not been vaccinated.  If you are concerned with your eyesight, or would like to schedule a comprehensive medical eye examination, please contact Georgia Eye Physicians and Surgeons today to make an appointment. Be sure to follow us on Facebook, Twitter, and Google+ for more to keep your vision healthy.

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Shingles | Korsunskaya I.M.

Key words: Herpes – virus – nervous system – ganglia – sensitivity – antiviral drugs – metisazon – acyclic nucleotides – analgesics.

Herpes zoster is a viral disease that often occurs, especially against the background of immunosuppression. Diagnosis is based on clinical manifestations. Treatment should be comprehensive and include antiviral drugs, ganglion blockers, analgesics.

Key words: Herpes – virus – nervous system – ganglia – antiviral agents – methisazone – acyclic nucleosides – analgetics.

Herpes zoster is a viral disease that is most common especially in immunodeficiency. The diagnosis is based on its clinical manifestations. Treatment should be combined and include antiviral, ganglion-blocking, and analgetic agents.

I.M. Korsunskaya – Ph.D. honey. Sci., Assistant, Department of Dermatovenereology, Russian Medical Academy of Postgraduate Education

I.M. Korsunskaya, Candidate of Medical Sciences, Assistant, Department of Dermatovenereology, Russian Medical Academy of Postgraduate Training

O Shingles (Herpes zoster) is a common viral disease that attracts the attention of not only dermatologists, neuropathologists and virologists, but also doctors of other specialties.

Etiology

The history of this disease is very old, but only at the end of the last century neuropathologists Erb (1893) and Landori (1885) first suggested the infectious genesis of Herpes zoster, which was confirmed by the following clinical data: fever, cyclic course , the disease of two members of the same family or more. The virus (Varicella zoster – VZ) belongs to the group of DNA-containing viruses. The size of the virus is from 120 to 250 microns. The virion core consists of DNA covered with protein. The composition of the virion includes more than 30 proteins with a molecular weight of up to 2.9• 10 daltons. Viruses of this group begin to reproduce in the nucleus. In cross-neutralization experiments performed by Taylor-Robinson (1959), the varicella-zoster virus and the Herpes zoster virus were equally neutralized by the sera of convalescents. At the same time, sera taken from patients with Herpes zoster in the acute period had a greater neutralizing activity than sera taken at the same time from patients with chickenpox. A. K. Shubladze and T. M. Maevskaya believe that this is apparently due to the fact that Herpes zoster is a secondary manifestation of an infection caused by the varicella-zoster virus. Most modern researchers consider the VZ virus to be the cause of this disease.

Pathogenesis

To understand the pathogenesis of Herpes zoster, the data of post-mortem studies are important, indicating the connection of rash areas with lesions of the corresponding ganglia. Later, Head and Campbell (1900), on the basis of histopathological studies, came to the conclusion that both neurological phenomena in Herpes zoster and the zones of skin rashes that characterize them arise as a result of the development of a pathological process in the intervertebral nodes and their homologues (Gasser’s node, etc.) . But already Volville (1924), having studied the nervous system of patients who died from the generalized form of Herpes zoster, came to the conclusion that the defeat of the intervertebral ganglia in Herpes zoster is not mandatory. The spinal cord is often involved in the inflammatory process, and not only the posterior horns are affected, but also the anterior ones. Volville and Shubak (1924) described cases when herpetic eruptions were the first manifestations of a polyneurotic process proceeding according to the type of Landry’s paralysis. Volville believes that the inflammatory process first affected the sensitive neurons, and then spread to the spinal segments and peripheral nerves. In the case described by Schubak, a pathoanatomical examination revealed nests of inflammatory infiltration in the sciatic nerves, cervical sympathetic nodes and the corresponding spinal ganglia, dorsal horns of the spinal cord.
Stamler and Stark (1958) described the histological picture of fulminant ascending radiculomyelitis zoster, in which death occurred as a result of bulbar and spinal respiratory paralysis. Demyelination of the spinal cord conductors with glial and lymphocytic reaction, perivascular infiltration and proliferation, changes in neurons of the spinal ganglia, dorsal horns, and dorsal roots were found.
In 1961, Kro, Dunivits and Dalias reported seven cases of Herpes zoster affecting the central nervous system. The disease proceeded in the form of aseptic meningitis, meningoencephalitis involving the cranial nerves, encephalomyelitis, polyradiculoneritis. Histopathological examination revealed a picture of “posterior poliomyelitis”. The authors consider it sufficient for the histological diagnosis of Herpes zoster, when the disease occurs without clear herpetic eruptions.

Pathomorphological and virological studies indicate that the Herpes zoster virus is widely disseminated throughout the body: during illness, it can be isolated from the contents of vesicles, saliva, lacrimal fluid, etc. This gives reason to believe that herpetic eruptions may be due not only to the deposition of the virus in the sensitive ganglia and the defeat of the parasympathetic effector cells located in them, but also to its direct penetration into the skin. Penetrating into the nervous system, it is not only localized within the peripheral sensory neuron (spinal ganglia, etc. ), but also spreads to other parts of the central nervous system. When it is introduced into the motor cells and roots, a picture of amyotrophic radiculoplexitis occurs, in the gray matter of the spinal cord – myelitis syndrome, in the cerebrospinal fluid system – meningoradiculoneuritis or serous meningitis, etc.

Clinic

The clinical picture of Herpes zoster consists of skin manifestations and neurological disorders. Along with this, most patients have general infectious symptoms: fever, enlargement of hormonal lymph nodes, changes (in the form of lymphocytosis and monocytosis) of the cerebrospinal fluid. Usually, erythematous spots of round or irregular shape, raised, edematous, are found on the skin, when you run a finger over them, some pebbly skin (tiny papules) is felt. Then, in these areas, groups of bubbles appear sequentially, often of different sizes. Bubbles can merge, but most often they are located in isolation, although close to one another – the vesicular form of Herpes zoster. Sometimes they look like a small bubble surrounded by a red rim around the periphery. Since the rash occurs simultaneously, the elements of the rash are at the same stage of their development. However, the rash may appear within 1 to 2 weeks in the form of separate groups. In the latter case, when examining a patient, rashes of various stages can be detected. In typical cases, the bubbles have a transparent content for the first time, quickly turning into a cloudy one, and then dry into crusts. A deviation from the type described is the milder abortive form of Herpes zoster. With this form, papules also develop in the foci of hyperemia, which, however, do not transform into vesicles, this form differs from vesicular. Another variety is the hemorrhagic form of Herpes zoster, in which the vesicles have bloody contents, the process extends deep into the dermis, the crusts become dark brown. In severe cases, the bottom of the vesicles becomes necrotic – the gangrenous form of herpes zoster, after which cicatricial changes remain. The intensity of the rashes in this disease is very variable: from confluent forms, leaving almost no healthy skin on the side of the lesion, to individual vesicles, although in the latter case the pain can be pronounced. Such cases have given rise to the assumption that Herpes zoster can exist without skin eruption.

One of the leading symptoms of the disease is neurological disorders , usually in the form of pain. Most often it occurs 1 – 2 days before the appearance of rashes. The pains, as a rule, are of an intense burning character, the zone of their distribution corresponds to the roots of the affected ganglion. It should be noted that the pain syndrome intensifies at night and under the influence of a variety of stimuli (cold, tactile, kinesthetic, barometric) and is often accompanied by vegetative-vascular dystonia of the hypertonic type. In addition, patients have objective sensitivity disorders: hyperesthesia (the patient can hardly tolerate the touch of linen), hypoesthesia and anesthesia, and hyperalgesia may exist simultaneously with tactile anesthesia.
Objective sensory disturbances are variable in form and intensity, usually limited to temporary sensory disturbances in the area of ​​the rash or scarring. Anesthesias concern all kinds of sensitivity, but in some cases a dissociated type of disorder is observed; sometimes within the same kind of sensitivity, such as hot and cold. Occasionally, hyperesthesia takes on the character of irritation in the form of causalgia.
Not in all cases, the intensity of the pain syndrome corresponds to the severity of skin manifestations. In some patients, despite the severe gangrenous form of the disease, the pain is minor and short-lived. In contrast, a number of patients have a prolonged intense pain syndrome with minimal skin manifestations.
Some patients in the acute phase have diffuse cephalgia, aggravated by a change in head position, which may be associated with a shell reaction to Herpes zoster infection. In the literature there are indications of damage to the brain and its membranes.
According to a number of authors (A.A. Kalamkaryan and V.D. Kochetkov 1973; M.K. Zucker 1976, etc.), herpetic ganglionitis of the gasser node are more common than ganglionitis of the intervertebral nodes. In most patients with this localization of the process, there is an increase in temperature and swelling of the face on the affected side, as well as pain at the exit points of the trigeminal nerve.
The cornea is often affected in the form of keratitis of a different nature. In addition, other parts of the eyeball are affected (episcleritis, iridocyclitis, iris zoster). The retina is involved very rarely (hemorrhages, embolisms), more often the changes concern the optic nerve – optic neuritis with an outcome in atrophy, possibly due to the transition of the meningeal process to the optic nerve. With ophthalmic herpes (iritis), glaucoma may develop; usually, with zoster, gynotension of the eyeball is observed, which is apparently caused by damage to the ciliary nerves. Complications of zoster from the motor nerves are quite common, they are arranged in the following order: III, IV, VI nerves. Of the branches of the oculomotor nerve, both external and internal branches are affected. Ptosis is often observed. Skin rashes in ophthalmic zoster tend to be more severe than in other parts of the body, possibly depending on the structure of the skin around the eye. Quite often, necrosis of the vesicles, severe neuralgia, accompanied by lacrimation, are observed. Bubbles pour out not only on the skin, but also on the mucous membranes of the eye.
As a result of the process in the cornea with ophthalmic zoster, atrophy of the optic nerve and complete blindness may develop. In addition, some patients note the loss of eyebrows and eyelashes on the side of the lesion.
The maxillary branches of the trigeminal nerve are affected both in the area of ​​the skin and in the area of ​​the mucous membranes (half of the hard and soft palate, the palatine curtain, the upper gum, the inner surface of the buccal mucosa, while the nasal mucosa may remain unaffected). Branches supplying mucous membranes may be more affected than cutaneous branches, and vice versa. Damage to the nerves of the upper and lower jaws does not always remain strictly localized, since pain sometimes radiates to the region of the ophthalmic and other branches.
Herpes zoster usually affects the autonomic nervous system. However, clinical observations have shown that the animal nervous system can also be involved in the pathological process. Evidence of this is that in some patients, simultaneously with the defeat of the Gasser node, there was a peripheral paresis of the facial nerve on the side of herpetic eruptions. With ophthalmic zoster, both the external and internal muscles of the eye are paralyzed. IV pair paralysis is rare. Oculomotor paralysis is usually partial rather than complete; more often than other muscles, m. levator palpebrae. There are cases of ophthalmic zoster with an isolated change in the shape and size of the pupil; unilateral Argil-Robertson symptom (Guillen). These paralysis sometimes partially or completely disappear spontaneously, without special treatment.

And Nordal (1969) first pointed out the defeat of the geniculate node in this form of Herpes zoster. Usually on the auricle or around it, and sometimes in the ear canal and even on the eardrum, herpetic eruptions appear. There is a sharp pain in the circumference of the auricle, swelling of the lymph nodes, impaired sensitivity. Disorders of the functions of the facial, cochlear, vestibular nerves occur in the first days of rashes or precede them. Pain in such cases is localized in the depth of the auditory canal and auricle with irradiation to the mastoid, auricular and temporoparietal regions. Objective sensitivity disorders are found behind the ear, in the fold between the auricle and the mastoid process. This skin area is supplied by the ear branch of the X pair, which innervates the posterior walls of the ear canal. Finally, in cases of a very common ear zoster, the latter captures not only the external auditory canal, auricle, mastoid process, but also the tympanic membrane, which sometimes suffers extremely severely. In such cases, the area innervated by the V, VII and X pairs is affected, and the defeat of these nerves is accompanied by damage to the ganglia of the corresponding cranial nerves or anastomoses that connect the terminal branches of all the listed nerves.
Often, simultaneously with paralysis of the VII pair, paralysis of the soft palate, anesthesia and paresthesia in the tongue are observed, often a taste disorder in the anterior two-thirds of the tongue due to damage. The defeat of the Vlll pair usually begins with tinnitus, which sometimes persists for a long time after the disappearance of other phenomena. Hyperacusia in the defeat of the VIII pair is called paresis n. stapeblii, although this symptom may also occur in isolated and previous lesions of the auditory nerve and is in such cases a symptom of irritation. Hypoacusia can occur regardless of the damage to the auditory nerve due to local lesions of the middle ear, the rash of bubbles on the eardrum, the laying of the external auditory canal, due to swelling of the mucous membrane due to the rash of zoster.
Vestibular phenomena, in contrast to cochlear ones, usually develop extremely slowly and are expressed differently: from mild subjective symptoms of dizziness to significant static disorders.
Neuralgia in ear zoster, in contrast to ophthalmic zoster, is rare.
Long-term results are not always favorable, as persistent paresis of the facial nerve and deafness may occur.
Volville emphasizes that the combination of paralysis of the VlI and VIII pairs, although it occurs especially often in zoster, nevertheless happens with the defeat of the gasser node, ll, lll, cervical ganglia, and, finally, all these areas can be affected simultaneously.
Rashes of zoster are also described in the region of innervation of the IX pair: the back of the soft palate, arches, posterolateral parts of the tongue, part of the posterior pharyngeal wall; the same area is innervated, in addition to IX, also by the branches of the X pair: the root of the tongue, larynx, proglottis, basal and posterior part of the pharyngeal wall. Although zoster predominantly and even selectively affects the sensitive systems, however, movement disorders are sometimes observed with it, especially when rashes are localized in the head, neck, and extremities. Paralyzes in zoster are radicular in nature, and the defeat of the posterior roots in these cases is accompanied by phenomena from the corresponding anterior roots.
The defeat of the cervical sympathetic nodes is often accompanied by rashes on the skin of the neck and scalp. Pain in this case is observed not only in the places of rashes, but also in the area of ​​paravertebral points. Sometimes there may be seizures that mimic facial sympathy.
With ganglionitis of the lower cervical and upper thoracic localization, along with the usual symptoms of this disease, Steinbrocker’s syndrome can be observed. Dominant in the picture of this syndrome are pains of a sympathetic nature in the form of a burning sensation or pressure, which occur first in the hand, and then in the entire hand. Soon appears and quickly increases swelling of the hand, spreading to the entire arm. Trophic disorders are added in the form of cyanosis and thinning of the skin, hyperhidrosis, brittle nails. The movements of the fingers are limited, painful. Often, pain and other autonomic disorders persist even after the rash has disappeared. Ganglionitis of thoracic localization often simulate the clinical picture of myocardial infarction, which leads to errors in diagnosis.
With herpetic lesions of the ganglia of the lumbosacral region, rashes are most often localized on the skin of the lower back, buttocks and lower extremities; along with pain in the places of rashes, pain syndromes can occur that simulate pancreatitis, cholecystitis, renal colic, appendicitis. Herpetic lesions of the lumbosacral ganglia are sometimes accompanied by involvement in the process of the animal nervous system, which gives a picture of ganglioradiculitis (radicular syndrome of Nori, Matskevich, Wasserman).
Sometimes, along with rashes along the nerve trunk, vesicular rashes appear all over the skin – a hepatic form of herpes zoster. Usually the disease does not recur. However, it is known from the literature that there are recurrent forms of the disease against the background of somatic burden: HIV infection, cancer, diabetes mellitus, lymphogranulomatosis, etc.

Treatment

drugs. It is known that the composition of the virus includes proteins that form its shell and carry the enzymatic function, as well as nucleic acid – the carrier of its genetic properties. Penetrating into cells, viruses are released from the proteinaceous protective shell. It has been shown that at this moment their reproduction can be inhibited with the help of nucleases. These enzymes hydrolyze the nucleic acids of viruses, but do not damage the nucleic acids of the cell itself. It was found that pancreatic deoxyribonuclease sharply inhibits the synthesis of DNA-containing viruses, such as herpes viruses, vaccinia, adenoviruses. Taking into account the above, it is recommended for patients with Herpes zoster to prescribe deoxyribonuclease intramuscularly 1-2 times a day, 30-50 mg for 7 days. In addition, in patients with rashes on the oral mucosa, conjunctiva and cornea, the drug is used topically in the form of an aqueous solution. The appointment of deoxyribonuclease contributes to the rapid regression of skin rashes and a decrease in pain.
Good results are obtained by the use of metisazon. It is prescribed orally at the rate of 20 mg per 1 kg of the patient’s body weight per day in 3 divided doses after meals for 6 to 7 days. The drug is contraindicated in severe lesions of the liver and kidneys, gastrointestinal diseases in the acute stage. It is not recommended to take alcoholic beverages during treatment. No complications were observed during the use of the drug.
Metisazon does not affect the adsorption of the virus by the cell and its penetration into the cell. It does not affect the synthesis of viral DNA and does not interfere with the synthesis of many viral proteins. The drug apparently interferes with the synthesis of late proteins involved in the construction of a viral particle. It has also been suggested that metisazon induces the formation of a new ribonucleic acid in the cell, which provides the synthesis of a protein with antiviral properties. When administered orally, metisazon can be detected after 30-40 minutes in the blood serum, and after 2-3 hours – in the urine.
In recent years, antiviral chemotherapy drugs from the group of synthetic acyclic nucleosides have been used to treat Herpes zoster. The most well studied at present is acyclovir. The mechanism of action of acyclovir is based on the interaction of synthetic nucleosides with the replication enzymes of herpesviruses. Herpesvirus thymidine kinase binds to acyclovir thousands of times faster than cellular thymidine, so the drug accumulates almost exclusively in infected cells. This explains the complete absence of cytotoxic, teratogenic and mutagenic properties in acyclovir. The synthetic nucleoside is built into a chain of DNA being built for the “daughter” viral particles, and this process is interrupted, thus stopping the reproduction of the virus. The daily dose of acyclovir for herpes zoster is 4 g, which should be divided into 5 single doses of 800 mg. The course of treatment is 7 – 10 days. The best therapeutic effect is achieved with early administration of the drug; the terms of rashes are reduced, there is a rapid formation of crusts, intoxication and pain syndrome are reduced.
Acyclovir of the second generation – valacyclovir, retaining all the positive aspects of acyclovir, due to increased bioavailability, allows you to reduce the dose to 3 g per day, and the number of doses – up to 3 times. The course of treatment is 7 – 10 days.
Famciclovir has been used since 1994. The mechanism of action is the same as that of acyclovir. The high affinity of the thymidine kinase of the virus for famciclovir (100 times higher than the affinity for acyclovir) makes the drug more effective in the treatment of herpes zoster. The drug is prescribed 250 mg 3 times a day for 7 days.
Along with antiviral drugs, ganglionic blockers such as ganglerone are used to reduce pain. Gangleron is used intramuscularly in the form of a 1.5% solution of 1 ml 1 time per day for 10-15 days or 0.04 g in capsules 2 times a day for 10-15 days, depending on the severity of the pain syndrome. In addition, the use of carbamazepine gives good results, especially in Herpes zoster gasser node, the drug is prescribed from 0.1 g 2 times a day, increasing the dose by 0.1 g per day, if necessary, up to 0.6 g daily dose (in 3 – 4 doses). After the reduction or disappearance of pain, the dose is gradually reduced. Usually the effect occurs 3-5 days after the start of treatment.
With a pronounced pain syndrome, analgesics are prescribed per os and in the form of injections, reflexology. In reflexology, both points of general action and points corresponding to the affected ganglion are usually used, the course is 10-12 sessions. It is also recommended to prescribe multivitamins, in particular vitamins of group B. Local irrigation with interferon or ointments with interferon, aniline dyes, eridine aerosol, florenal ointments, helepin, alpizarin can be used locally. With gangrenous forms of herpes zoster, pastes and ointments containing an antibiotic, as well as solcoseryl, are used.
After resolution of skin rashes, treatment is carried out by neuropathologists until the disappearance of neurological symptoms.
Thus, the treatment of herpes zoster should be comprehensive and include both etiological and pathogenetic agents.

References:

1. Barinsky I.F., Shubladze A.K., Kasparov A.A., Grebenyuk V.N. – “Herpes”. – M. – 1986.
2. Shishov A.S., Leshinskaya E.V., Martynenko I.N. – Journal of Clinical Medicine. – 1991. – No. 6. – P. 60–72.
3. Batkaev E.A., Korsunskaya I.M. – Viral dermatoses. – M. – 1992.
4. Management of varicella zoster virus infection and the clinical implications of heresvirus latency. Building international congress. IHMF 1995;37.

Herpes can threaten blindness! – Polyclinic News

April 7, 2015

Spring does not come alone, but brings with it traditional seasonal diseases: gastritis, depression, colds and, of course, herpes. The worst enemy is not only your appearance, but also the health of the whole organism.

“The skin and mucous membranes are the entry gate for the virus,” says Oksana Semeshko, dermatovenereologist at the Polyclinic named after. EAT. Niginsky. – The causative agent concentrates on the surface of the skin, penetrates into it, so there is a local focus of inflammation. The virus can then enter the bloodstream and spread to various organs and tissues, primarily to the central nervous system and liver.”

Those who have already encountered this disease know that herpes simplex, which is transmitted mainly by airborne droplets, does not manifest itself for a long time, is latent with periodic exacerbations in the form of blisters on the skin and mucous membranes.
The doctor notes that such a “decoration” on the lips in the off-season is worn by 80% of the population. Unfortunately, getting rid of the virus is completely impossible, and reducing the frequency of relapses is a feasible task.

“First of all, you shouldn’t part with your hats too early – the cold wind will take advantage of the weakened immunity during the winter,” says Oksana Grigoryevna. – Combine your usual make-up with a hygienic lipstick with an antiviral effect. Those who are going on vacation to warm countries should not relax either: herpes can manifest itself with a sharp change in climate, swimming in the cool sea, and a long stay in the sun.

Most people associate herpes infections exclusively with sores on the lips or nose. But few people suspect that there are eight types of herpes infections. “Including the herpes virus, which is the causative agent of varicella (chickenpox), – doctor Oksana Semeshko comments on the problem. – After the chickenpox passes, the virus does not disappear, but “dozes” in the cells of the nervous system. While the body is healthy, the herpes virus does not manifest itself in any way, but when immunity decreases, it enters the blood again, causing symptoms of herpes zoster (severe pain, itching, burning).

In addition, herpes is dangerous with complications. In parallel with the skin, herpes stomatitis may appear, eye damage may occur, and the process may spread to the nervous system. And if stomatitis is not dangerous, then corneal damage can threaten blindness. And the nervous system can give the development of encephalitis.

Therefore, self-diagnosis and treatment of herpes is a big mistake for many people.