Eye

Eye Socket Inflammation: Orbital Cellulitis – Symptoms, Causes, and Treatment

What are the symptoms of orbital cellulitis? What causes orbital cellulitis? How is orbital cellulitis treated?

Содержание

Understanding Orbital Cellulitis

Orbital cellulitis is a serious infection that affects the soft tissues within the eye socket. It is a condition that, if left untreated, can lead to permanent vision loss and even life-threatening complications. This type of infection develops behind the orbital septum, a thin membrane that covers the front of the eyeball. Orbital cellulitis is distinct from periorbital or preseptal cellulitis, which refers to infections occurring in front of the orbital septum and is generally less serious.

Symptoms of Orbital Cellulitis

The primary symptoms of orbital cellulitis include pain, swelling, and proptosis (protrusion or forward displacement of the eye). Other common symptoms are:

  • Limited eye movement or pain when trying to move the eye
  • Impaired vision or sudden vision loss
  • Red, swollen eyelid
  • Difficulty or inability to open the eye
  • Discharge from the infected eye
  • Fever
  • Fatigue
  • Loss of appetite
  • Headache

Causes of Orbital Cellulitis

What is the primary cause of orbital cellulitis? Research suggests that up to 86-98% of people with orbital cellulitis also have sinusitis, or an infection of the sinuses. Without prompt treatment, sinus infections can spread to the fat and muscle surrounding the eye socket, leading to orbital cellulitis.

The most common bacterial causes of orbital cellulitis are Staphylococcus aureus and Streptococcus species. Less commonly, orbital cellulitis can also result from:

  • An injury to the eye that penetrates the orbital septum
  • Complications from eye surgery
  • Abscesses in the mouth
  • A foreign object becoming trapped in the eye
  • Asthma

Diagnosing Orbital Cellulitis

How is orbital cellulitis diagnosed? The diagnostic process typically begins with a physical examination by an ophthalmologist, who will look for signs of infection in the eye socket, such as redness, swelling, pain, and fever. The ophthalmologist may then order additional tests, such as:

  • Blood sample analysis to identify the causative bacteria
  • Discharge sample analysis from the eye
  • Imaging tests, like MRI or CT scans, to evaluate the extent of the infection and check for complications

Early diagnosis is crucial for preventing severe complications from orbital cellulitis.

Treating Orbital Cellulitis

The standard treatment for orbital cellulitis involves a combination of antibiotics and, in some cases, surgery.

Antibiotics

Healthcare professionals typically administer broad-spectrum antibiotics intravenously to treat orbital cellulitis. These antibiotics are effective against a wide range of bacteria, including Staphylococcus and Streptococcus species. The person with orbital cellulitis will usually need to remain in the healthcare facility while receiving antibiotic treatment, as the infection can spread quickly and require close monitoring.

Surgery

Surgical treatment may be necessary if the infection does not respond to antibiotics or if it spreads to other parts of the head. People with orbital cellulitis may require surgery if they experience worsening symptoms or vision impairment while taking antibiotics, or if they have developed an abscess in the eye.

Complications of Orbital Cellulitis

Orbital cellulitis is a serious condition that, if left untreated, can lead to severe complications, including:

  • Permanent vision loss
  • Life-threatening complications, such as spread of the infection to the brain or central nervous system

Therefore, it is crucial for anyone with symptoms of orbital cellulitis to seek immediate medical attention to prevent these potentially devastating outcomes.

Preventing Orbital Cellulitis

The best way to prevent orbital cellulitis is to promptly treat any underlying sinus infections or other conditions that could lead to the spread of infection to the eye socket. Maintaining good hygiene, avoiding eye injuries, and seeking prompt medical attention for any eye-related issues can also help reduce the risk of developing orbital cellulitis.

Orbital cellulitis: Symptoms, causes, and treatment

Orbital cellulitis is an infection of the soft tissues within the eye socket. It is a serious condition that, without treatment, can lead to permanent vision loss and life-threatening complications.

Orbital cellulitis, which is sometimes called postseptal cellulitis, can occur at any age, but it most commonly affects young children. The infection develops behind the orbital septum, a thin membrane that covers the front of the eyeball.

Periorbital, or preseptal, cellulitis refers to infections that occur in front of the orbital septum. Periorbital cellulitis can spread to the skin around the eye and the eyelid. This condition is less serious than orbital cellulitis but still requires immediate treatment.

In this article, we discuss the symptoms and causes of orbital cellulitis. We also cover the diagnosis, treatment, and complications of this condition.

Orbital cellulitis is a serious infection that affects the fat and muscle tissues within the eye socket, or orbit.

The infection causes inflammation that can push the eye out of the socket. Pain, swelling, and proptosis, which is the protrusion or forward displacement of the eye, are common symptoms of orbital cellulitis.

Other symptoms of orbital cellulitis can include:

  • limited eye movement or pain when trying to move the eye
  • impaired vision or sudden vision loss
  • a red, swollen eyelid
  • finding it difficult or impossible to open the eye
  • discharge from the infected eye
  • fever
  • fatigue
  • loss of appetite
  • a headache

The main cause of orbital cellulitis is sinusitis, which is an infection of the sinuses. Research suggests that up to 86–98 percent of people with orbital cellulitis also have sinusitis.

Without treatment, sinus infections can spread to the fat and muscle surrounding the eye socket. Bacteria such as the Staphylococcus aureus and Streptococci species are the most common cause of orbital cellulitis.

Minor infections of the eyelid can also spread to the back of the eye, causing orbital cellulitis. Less commonly, bacterial infections in other parts of the body can travel through the bloodstream into the eye socket.

Other, less common causes of orbital cellulitis include:

  • an injury to the eye that penetrates the orbital septum
  • complications of eye surgery
  • abscesses in the mouth
  • a foreign object becoming trapped in the eye
  • asthma

Share on PinterestA doctor will perform a physical examination to diagnose orbital cellulitis.

It is vital that anyone with symptoms of orbital cellulitis sees a healthcare professional immediately. Early diagnosis of orbital cellulitis is crucial for preventing severe complications.

The diagnosis of orbital cellulitis begins with a physical examination of the person’s eye. An ophthalmologist, a doctor who specializes in the eyes, will usually carry out the exam.

The ophthalmologist will check for physical signs of an infection of the eye socket, such as redness, swelling, pain, and fever. They may then order other tests to help determine the extent of the infection and the appropriate course of treatment.

An ophthalmologist or another healthcare professional may take a sample of the person’s blood or the discharge from their eye. They will then analyze these samples to determine what kind of germ is causing the infection.

The ophthalmologist may also recommend imaging tests, such as an MRI or CT scan, which create images of the inside of a person’s head. These tests allow a healthcare professional to evaluate how far the infection has spread and to check for complications involving the brain or central nervous system.

Orbital cellulitis infections can spread quickly and cause serious complications, so immediate treatment is essential.

The standard treatment options for orbital cellulitis are antibiotics and surgery.

Antibiotics

After diagnosing orbital cellulitis, a healthcare professional is likely to recommend immediate treatment with antibiotics. They usually administer these antibiotics continuously through an intravenous line.

Healthcare professionals typically use broad-spectrum antibiotics to treat people with orbital cellulitis. These drugs are effective against a wide range of bacteria, including both Staphylococcus and Streptococcus bacteria.

People with orbital cellulitis usually need to remain in the healthcare facility while they receive antibiotic treatment. Orbital cellulitis can spread quickly, so a healthcare professional will need to monitor the person closely for any signs that the infection is worsening or not responding to the antibiotics.

Surgery

Surgical treatment may be necessary if the infection does not respond to antibiotics or spreads to other parts of the head.

People with orbital cellulitis may also require surgery if they:

  • experience worsening symptoms or vision impairment while taking antibiotics
  • have developed an abscess in the eye socket or the brain
  • have a foreign object trapped in the eye
  • have a fungal or mycobacterial infection

Surgical procedures for treating orbital cellulitis include:

  • draining fluid from an infected area or abscess
  • removing a foreign object
  • obtaining a culture sample for further analysis

Early diagnosis and treatment of orbital cellulitis are vital to prevent serious complications.

Possible complications of orbital cellulitis include:

  • vision loss
  • hearing loss
  • blood infection, or sepsis
  • meningitis, which is an inflammation of the membranes lining the brain and spinal cord
  • cavernous sinus thrombosis, which is the formation of a blood clot at the base of the brain
  • intracranial abscess, which is an accumulation of pus inside the skull

Young children may experience more severe symptoms, and they have a higher risk of complications because their immune system is still developing.

Orbital cellulitis is a serious infection that causes inflammation of the soft tissue behind the eye. It can cause pain, swelling, and protrusion of the eyeball.

Orbital cellulitis most commonly occurs when bacteria from a sinus infection spread to the eye. People of all ages can develop this condition, but it primarily affects young children.

Without treatment, orbital cellulitis can lead to severe and potentially life-threatening health complications, such as sepsis and meningitis, as well as vision loss. It is crucial that people with symptoms of orbital cellulitis seek immediate medical attention.

Doctors usually treat orbital cellulitis with intravenous antibiotics, but some people may also require surgery.

Eyelid Eye Socket Infections and Inflammation Houston Treatment Options

The Berkeley Eye Center of Houston oculoplastics clinic focuses on problems that affect the appearance and function of the eyes, eyelids and areas surrounding the eyes. Ophthalmologist Dr. Aida Bounama is an oculoplastics surgeon with extensive experience performing a wide range of cosmetic and reconstructive oculoplastic procedures as well as treating the diseases, infections and other conditions that can affect health of the structures surrounding the eye, such as the eye socket, eyelids and tear ducts.

Infections of the eyelids and orbital structures can develop into a serious problem if left untreated. These types of infections are usually caused by bacteria but may also occur after exposure to a virus or fungus. One or both eyes may become infected.

Symptoms That You Might Have an Eyelid or Orbital Infection

Inflammation of the eye and surrounding tissue can be a major indication of an eye infection. Other symptoms of an eye infection include:

  • Red eyes
  • Itchy eyes
  • Pain in and around the eye
  • Discharge
  • Fever
  • Swelling and redness of the eyelids and soft tissue around the eye
  • Vision difficulties – decreased or double vision
  • Problems with eye mobility
  • Increased pressure in the eye

You may also experience concurrent sinus problems, such as a runny nose and congestion.

Common Types Of Eye Socket And Eyelid Infections

Orbital Cellulitis

Orbital cellulitis is an infectious condition that affects the tissue within the orbit (eye socket) around the eye. It usually begins as a bacterial sinus infection that spreads to the eye socket. Orbital cellulitis is an emergency condition. Left untreated it can result in blindness and can also spread to other parts of the body such as the brain and spinal cord.

Conjunctivitis

Also known as “pink eye,” conjunctivitis is a contagious infection of the conjunctiva, the membrane that lines the eyelid and covers the white part of the eyeball. Inflammation affects the blood vessels, giving the eye a pink or red appearance.

Styes

Styes are small red bumps that form along the edges of the eyelid. They can be caused by a bacterial infection of the eyelash follicle. Styes may result in pain, swelling and tearing of the eye.

Blepharitis

Inflammation of the eyelids that can also affect the eyelashes and oil glands of the eyelids. Infection is one cause of blepharitis.

Treatment options

A thorough examination will be needed to exactly diagnose the cause of the inflammation or infection. The good news: eyelids and orbits often respond well to treatments that can include antibiotics, antihistamines and steroids. Over the counter medications may be recommended to relieve the pain. Serious cases of cellulitis may require surgery to drain fluids from the eye socket and sinuses.

Schedule an Exam with Dr. Bounama at Berkeley Eye Center

If you have been experiencing pain or irritation due to inflammation around or behind the eye, it may be due to an eyelid or orbital infection. Dr. Bounama has the knowledge and skills to diagnose the cause of your problem and prescribe the most effective treatment available. Delaying treatment only makes it the condition worse. Call Berkeley Eye Center today to schedule your examination.

Inflammation of the eye: symptoms, causes and treatment

Symptoms of eye inflammation

When an eye is inflamed, it entails an inflammatory process around the eye. It can affect different parts of the eye. The term “inflammation of the eye” serves as an umbrella term for the various inflammatory diseases. Different symptoms and complaints are prevalent depending on the clinical picture. In rare cases, there can be a serious disease present which is a threat to the eyesight.
Most commonly, inflammation affects the conjunctiva, followed by the cornea and the eyelid.
 

Many symptoms of eye inflammation overlap with those of dry eyes. These include:

 

On top of that other, more specific symptoms can occur:

  • pain
  • eyelids sticking together
  • clouding of vision
  • sensitivity to light
  • secretion of pus
     

A purulent discharge is a sign of bacterial infection. Some people affected suffer from severe pain and a significant reduction in vision.
 

Causes of eye inflammation

Eye inflammation can be traced back to numerous different causes. Infections due to bacteria, viruses or fungi are the main causes. The eyes are one of the ports of entry for pathogens in the human body. They put up a fight against the “invaders” on a daily basis, but when there is inflammation, the germs have outsmarted the immune defence system.
 

Dry eyes are particularly susceptible to eye inflammation. The eye’s immune system has only a limited effect when the tear film is impaired. In such conditions, pathogens can gain access more easily and cause inflammation. Dry eyes can be cared for with lubricating eye drops which can also help to reinforce the protective barrier against germs.

Further reasons for eye inflammation are allergic reactions such as hay fever, autoimmune diseases and environmental irritants such as draughts, dust particles or sunshine. Mechanical irritants, like when an eyelash grows into the eye, can also result in inflammation of the eye.
 

Diagnosis and treatment of eye inflammation

You should visit an eye doctor if symptoms of eye inflammation are present and they will conduct a slit lamp examination. Suitable treatment will be prescribed as soon as the doctor has ascertained which part of the eye is inflamed.

If eye inflammation is recognized and treated in time, the healing process is usually uncomplicated. Antibiotic eye drops are used for treatment if bacteria are the cause of the infection.

In the case of an allergic reaction, contact with the allergen should be avoided where possible. Allergic inflammation of the eye can be alleviated with special eye drops such asHYLODUAL®.

Antiviral eye drops are frequently used against viral infections. Eye ointments containing cortisone are also often prescribed.
 

Household remedies for eye inflammation?

In general, inflammation of the eye should always be examined by an eye doctor. At worst, inflammation can take a severe course and lead to permanent decreases in, or even loss of, vision.

Lubricating eye drops or ointments help to regenerate the eyes. Warm, damp compresses laid upon the affected eye can help with the healing of inflammation of the eyelid or with styes. Attention must be paid to strict hygiene when using compresses as otherwise there is a risk of spreading the germs.

It is not advisable to use washes or compresses containing camomile, as there is a risk of an allergic reaction. In addition, the eye can be greatly irritated by the fine hairs in the camomile blossoms.

Swollen Eyelid Causes & Symptoms

Why is My Eyelid Swollen?

Swollen eyelids are a fairly common eye condition caused by inflammation or excess fluid in the connective tissues surrounding the eye. Depending on the cause, swollen eyelids can sometimes be somewhat painful, affecting the upper eyelid, lower eyelid, or both. Swollen eyes can also be caused by many other factors, including allergies, styes, a blocked gland, traumatic eye injury, and conjunctivitis (“pink eye”).

Other Swollen Eyelid Causes & Symptoms

In some cases, swollen eyelids may be symptomatic of a bigger health problem, such as orbital cellulitis (a sudden infection of the tissue surrounding the eye), Graves’ disease (an autoimmune eye disorder associated with abnormalities of the thyroid gland), and ocular herpes (a recurrent viral infection that can cause inflammation and scaring of the cornea). In general, swollen eyelids are accompanied by symptoms such as itching or scratching sensations, excessive tear production resulting in watery eyes, obstructed vision, redness of the eyelid, eye discharge, and eyelid dryness or flaking. Pain generally accompanies swollen eyelids that are caused by an infection.

Many people also use the term “puffy eyes” interchangeably with swollen eyelids. However, for medical professionals, swollen eyes are generally used to describe an immune system response to an allergy, infection, or injury. Puffy eyes typically refer to eyes that are swollen from external reasons, such as water retention, a lack of sleep, or even genetic traits like hereditary dark circles under the eyes.

Eye allergies are the most common cause for swollen eyes. In this case, the swollen eyes are symptomatic of the body’s overreaction to a foreign substance, known as an allergen. Common allergens that can trigger swollen eyes include pollen, dust and pet dander, and can sometimes be due to the changing of the seasons. Some types of contact solution and eye drops may also trigger an allergic reaction in certain individuals with sensitive eyes.

Diagnosis and Treatment

The treatment of swollen eyes depends on the cause. Generally, if eyes are swollen due to allergies, antihistamine drops or oral allergy medication will be an effective treatment. For severe allergic reactions, an eye care professional may also recommend mild steroid drops. Ocular herpes and conjunctivitis are treated with anti-viral medications or anti-inflammatory eye drops, ointments, or antibiotics.

For at home care, remove contact lenses (if you wear them) until the swelling stops. Applying a cool compress can relieve swelling and pain. Most importantly, do not rub the eyes as this will only aggravate the condition. Speak with an eye care professional should conditions worsen or pain intensify, in order to rule out the possibility of a more serious cause for this pain.

Our ophthalmologists at Carolina Vision Center proudly serve patients throughout Fayetteville, Clinton, Raeford, Hope Mills, and Ellizabethtown, NC. Please contact our office today to schedule an appointment.

Like this:

Like Loading…

Eye Swelling – Symptoms, Causes, Treatments

Swelling around the eyes is a common symptom of allergy, infection, inflammation, or even physical irritation. The medical term for swelling involving the skin around the eyes is periorbital edema. Chemosis is the term used to describe swelling of the outer coats of the eyeball (common with eye allergies). Eye swelling results from excess fluid (edema) escaping from inflamed blood vessels into the soft tissues surrounding the eyes. It may occur in conditions affecting the eye area itself or in association with more generalized conditions, such as colds or hay fever.

Inflammation of the surface of the eye (conjunctivitis) and inflammation of the eyelids (blepharitis) are common causes of swollen eyes. Other common causes include crying, lack of sleep, or excessive rubbing of the eyes. Wearing contact lenses can also result in eye swelling. Depending on the cause, swelling may occur in one or both eyes, and it may be accompanied by redness, pain, itching, excessive tear production, or other types of discharge from the affected eyes.

Allergic reactions can lead to swelling of both eyes and, sometimes, of the entire face, especially in severe cases such as anaphylactic reactions. In rare cases, eye swelling is a symptom of serious infections of the soft tissues around or behind the eye, such as orbital cellulitis. The thyroid condition known as Graves’ disease may be accompanied by swelling of the conjunctiva (chemosis) in addition to bulging eyes (proptosis). Injuries or trauma to the eyes, including corneal abrasions, orbital bone fracture, and foreign bodies in the eye, can all lead to swelling.

Eye swelling can be a sign of a serious condition.
Seek prompt medical care if eye swelling is persistent or causes you concern.
Seek immediate medical care (call 911) if you experience eye swelling along with facial swelling, difficulty breathing, or fever, or if you experience eye swelling as a result of head injury or trauma. Other symptomsthat require immediate medical care include swelling around the eye with fever, chills, pus, or redness around the eye. These are symptoms of orbital cellulitis, which, left untreated, can rapidly lead to serious complications, such as meningitis or a blood infection.

Orbital inflammatory disease: a diagnostic and therapeutic challenge

  • 1

    Gordon LK . Diagnostic dilemmas in orbital inflammatory disease. Ocul Immunol Inflamm 2003; 11: 3–15.

    PubMed 

    Google Scholar 

  • 2

    Shields JA, Shields CL, Scartozzi R . Survey of 1264 patients with orbital tumors and simulating lesions: The 2002 Montgomery Lecture, part 1. Ophthalmology 2004; 111: 997–1008.

    PubMed 

    Google Scholar 

  • 3

    Stevens JL, Rychwalski PJ, Baker RS, Kielar RS . Pseudotumor of the orbit in early childhood. J AAPOS 1998; 2: 120–123.

    CAS 
    PubMed 

    Google Scholar 

  • 4

    Gordon LK, Goldberg RA, Krauss HA . Orbital inflammatory disease. In: Pepose JS, Holland GN, Wilhelmus KR (eds). Ocular Infection and Immunity. Mosby:St Louis, 1996, pp 609–625.

    Google Scholar 

  • 5

    McCluskey P, Powell RJ . The eye in systemic inflammatory diseases. Lancet 2004; 364: 2125–2133.

    PubMed 

    Google Scholar 

  • 6

    Rootman J . Inflammatory diseases of the orbit. Highlights. J Fr Ophtalmol 2001; 24: 155–161.

    CAS 
    PubMed 

    Google Scholar 

  • 7

    Rootman J . Why ‘orbital pseudotumour’ is no longer a useful concept. Br J Ophthalmol 1998; 82: 339–340.

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • 8

    Rubin PA, Foster CS . Etiology and management of idiopathic orbital inflammation. Am J Ophthalmol 2004; 138: 1041–1043.

    PubMed 

    Google Scholar 

  • 9

    Snebold NG . Orbital pseudotumor syndromes. Curr Opin Ophthalmol 1997; 8: 41–44.

    CAS 
    PubMed 

    Google Scholar 

  • 10

    Weber AL, Romo LV, Sabates NR . Pseudotumor of the orbit. Clinical, pathologic, and radiologic evaluation. Radiol Clin North Am 1999; 37: 151–168, xi.

    CAS 
    PubMed 

    Google Scholar 

  • 11

    Weber AL, Jakobiec FA, Sabates NR . Pseudotumor of the orbit. Neuroimaging Clin North Am 1996; 6: 73–92.

    CAS 

    Google Scholar 

  • 12

    Yuen SJ, Rubin PA . Idiopathic orbital inflammation: distribution, clinical features, and treatment outcome. Arch Ophthalmol 2003; 121: 491–499.

    PubMed 

    Google Scholar 

  • 13

    Yuen SJ, Rubin PA . Idiopathic orbital inflammation: ocular mechanisms and clinicopathology. Ophthalmol Clin North Am 2002; 15: 121–126.

    PubMed 

    Google Scholar 

  • 14

    Kennerdell JS, Dresner SC . The nonspecific orbital inflammatory syndromes. Surv Ophthalmol 1984; 29: 93–103.

    CAS 
    PubMed 

    Google Scholar 

  • 15

    Ajitsaria R, Dale R, Ferguson V, Mayou S, Cavanagh N . Psoriasis, psoriatic arthropathy and relapsing orbital myositis. Clin Exp Dermatol 2001; 26: 274–275.

    CAS 
    PubMed 

    Google Scholar 

  • 16

    Bahn RS . Clinical review 157: pathophysiology of Graves’ ophthalmopathy: the cycle of disease. J Clin Endocrinol Metab 2003; 88: 1939–1946.

    CAS 
    PubMed 

    Google Scholar 

  • 17

    Bradley D, Baughman RP, Raymond L, Kaufman AH . Ocular manifestations of sarcoidosis. Semin Respir Crit Care Med 2002; 23: 543–548.

    PubMed 

    Google Scholar 

  • 18

    Carvounis PE, Mehta AP, Geist CE . Orbital myositis associated with Borrelia burgdorferi (Lyme disease) infection. Ophthalmology 2004; 111: 1023–1028.

    PubMed 

    Google Scholar 

  • 19

    Dhaliwal U, Arora VK, Singh N, Bhatia A . Clinical and cytopathologic correlation in chronic inflammations of the orbit and ocular adnexa: a review of 55 cases. Orbit 2004; 23: 219–225.

    PubMed 

    Google Scholar 

  • 20

    Fadini GP . A case of orbital myositis associated with rheumatoid arthritis. Ann Rheum Dis 2003; 62: 383–384.

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • 21

    Foley MR, Moshfeghi DM, Wilson MW, Haik BG, Pappo AS, Hill DA . Orbital inflammatory syndromes with systemic involvement may mimic metastatic disease. Ophthalmol Plast Reconstr Surg 2003; 19: 324–327.

    Google Scholar 

  • 22

    Heuser K, Kerty E . Neuro-ophthalmological findings in sarcoidosis. Acta Ophthalmol Scand 2004; 82: 723–729.

    PubMed 

    Google Scholar 

  • 23

    Hwang IP, Jordan DR, Acharya V . Lacrimal gland inflammation as the presenting sign of Crohn’s disease. Can J Ophthalmol 2001; 36: 212–213.

    CAS 
    PubMed 

    Google Scholar 

  • 24

    Kawasaki A, Borruat FX . An unusual presentation of herpes zoster ophthalmicus: orbital myositis preceding vesicular eruption. Am J Ophthalmol 2003; 136: 574–575.

    PubMed 

    Google Scholar 

  • 25

    Knox RJ, Gigantelli JW, Arthurs BP . Recurrent orbital inflammation from metastatic orbital carcinoid tumor. Ophthalmol Plast Reconstr Surg 2001; 17: 137–139.

    CAS 

    Google Scholar 

  • 26

    Kubota T, Hirose H . Ocular changes in a limited form of Wegener’s granulomatosis: patient with cutaneous ulcer of upper eyelid. Jpn J Ophthalmol 2003; 47: 398–400.

    PubMed 

    Google Scholar 

  • 27

    Kyhn M, Herning M, Prause JU, Heegaard S . Orbital involvement in multifocal fibrosclerosis. Acta Ophthalmol Scand 2004; 82: 323–324.

    PubMed 

    Google Scholar 

  • 28

    Levy J, Monos T, Levy J, Shelef I, Nash M, Lifshitz T . Intrasinus wood foreign body causing orbital cellulitis in congenital insensitivity to pain with anhidrosis syndrome. Ophthal Plast Reconstr Surg 2004; 20: 81–83.

    PubMed 

    Google Scholar 

  • 29

    Lynch III JP . Neurosarcoidosis: how good are the diagnostic tests? J Neuroophthalmol 2003; 23: 187–189.

    PubMed 

    Google Scholar 

  • 30

    Maiorano E, Favia G, Capodiferro S, Montagna MT, Lo ML . Combined mucormycosis and aspergillosis of the oro-sinonasal region in a patient affected by Castleman disease. Virchows Arch 2005; 446: 28–33.

    PubMed 

    Google Scholar 

  • 31

    Maurer I, Zierz S . Recurrent orbital myositis: report of a familial incidence. Arch Neurol 1999; 56: 1407–1409.

    CAS 
    PubMed 

    Google Scholar 

  • 32

    McCarty ML, Wilson MW, Fleming JC, Thompson JW, Sandlund JT, Flynn PM et al. Manifestations of fungal cellulitis of the orbit in children with neutropenia and fever. Ophthal Plast Reconstr Surg 2004; 20: 217–223.

    PubMed 

    Google Scholar 

  • 33

    Mombaerts I, Schlingemann RO, Goldschmeding R, Koornneef L . Idiopathic granulomatous orbital inflammation. Ophthalmology 1996; 103: 2135–2141.

    CAS 
    PubMed 

    Google Scholar 

  • 34

    Nabili S, McCarey DW, Browne B, Capell HA . A case of orbital myositis associated with rheumatoid arthritis. Ann Rheum Dis 2002; 61: 938–939.

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • 35

    Peterson EA, Hymas DC, Pratt DV, Mortenson SW, Anderson RL, Mamalis N . Sarcoidosis with orbital tumor outside the lacrimal gland: initial manifestation in 2 elderly white women. Arch Ophthalmol 1998; 116: 804–806.

    CAS 
    PubMed 

    Google Scholar 

  • 36

    Rao VB, Sahare P, Varada V . Acquired brown syndrome secondary to superior oblique muscle cysticercosis. J AAPOS 2003; 7: 23–27.

    PubMed 

    Google Scholar 

  • 37

    Reittner P, Riepl T, Goritschnig T, Preidler KW, Koele W, Szolar DH . Bilateral orbital pseudotumour due to Ormond’s disease: MR imaging and CT findings. Neuroradiology 2002; 44: 272–274.

    CAS 
    PubMed 

    Google Scholar 

  • 38

    Schaffler GJ, Simbrunner J, Lechner H, Langmann G, Stammberger H, Beham A et al. Idiopathic sclerotic inflammation of the orbit with left optic nerve compression in a patient with multifocal fibrosclerosis. AJNR Am J Neuroradiol 2000; 21: 194–197.

    CAS 
    PubMed 

    Google Scholar 

  • 39

    Selva D, Dolman PJ, Rootman J . Orbital granulomatous giant cell myositis: a case report and review. Clin Exp Ophthalmol 2000; 28: 65–68.

    CAS 
    PubMed 

    Google Scholar 

  • 40

    Shovlin JP . Orbital infections and inflammations. Curr Opin Ophthalmol 1998; 9: 41–48.

    CAS 
    PubMed 

    Google Scholar 

  • 41

    Stavrou P, Murray PI, Batta K, Gordon C . Acute ocular ischaemia and orbital inflammation associated with systemic lupus erythematosus. Br J Ophthalmol 2002; 86: 474–475.

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • 42

    Thorne JE, Volpe NJ, Wulc AE, Galetta SL . Caught by a masquerade: sclerosing orbital inflammation. Surv Ophthalmol 2002; 47: 50–54.

    PubMed 

    Google Scholar 

  • 43

    Thorne JE, Jabs DA . Ocular manifestations of vasculitis. Rheum Dis Clin North Am 2001; 27: 761–779, vi.

    CAS 
    PubMed 

    Google Scholar 

  • 44

    Wall JR . Graves’ disease is a multi-system autoimmune disorder in which extra ocular muscle damage and connective tissue inflammation are variable features. Thyroid 2002; 12: 35–36.

    PubMed 

    Google Scholar 

  • 45

    Wardyn KA, Ycinska K, Matuszkiewicz-Rowinska J, Chipczynska M . Pseudotumour orbitae as the initial manifestation in Wegener’s granulomatosis in a 7-year-old girl. Clin Rheumatol 2003; 22: 472–474.

    PubMed 

    Google Scholar 

  • 46

    Wells TS, Harris GJ . Orbital dermoid cyst and sinus tract presenting with acute infection. Ophthalmol Plast Reconstr Surg 2004; 20: 465–467.

    Google Scholar 

  • 47

    White ES, Lynch III JP . Sarcoidosis involving multiple systems: diagnostic and therapeutic challenges. Chest 2001; 119: 1593–1597.

    CAS 
    PubMed 

    Google Scholar 

  • 48

    Lee AG, Tang RA, Feldon SE, Pless M, Schiffman JS, Rubin RM et al. Orbital presentations of giant cell arteritis. Graefes Arch Clin Exp Ophthalmol 2001; 239: 509–513.

    CAS 
    PubMed 

    Google Scholar 

  • 49

    Colombo F, Holbach LM, Naumann GO . Chronic inflammation in dermoid cysts: a clinicopathologic study of 115 patients. Orbit 2000; 19: 97–107.

    PubMed 

    Google Scholar 

  • 50

    Goh AS, Francis IC, Kappagoda MB, Filipic M . Orbital inflammation in a patient with extrascleral spread of choroidal malignant melanoma. Clin Exp Ophthalmol 2001; 29: 97–99.

    CAS 
    PubMed 

    Google Scholar 

  • 51

    Fairley C, Sullivan TJ, Bartley P, Allworth T, Lewandowski R . Survival after rhino-orbital-cerebral mucormycosis in an immunocompetent patient. Ophthalmology 2000; 107: 555–558.

    CAS 
    PubMed 

    Google Scholar 

  • 52

    Tovilla-Canales JL, Nava A, Pomar JL . Orbital and periorbital infections. Curr Opin Ophthalmol 2001; 12: 335–341.

    CAS 
    PubMed 

    Google Scholar 

  • 53

    Brooks SE, Pillai JJ, Bains H . Orbital cellulitis due to occult orbital lymphangioma. South Med J 2001; 94: 532–535.

    CAS 
    PubMed 

    Google Scholar 

  • 54

    Schick U, Hassler W . Neurosurgical management of orbital inflammations and infections. Acta Neurochir (Wien) 2004; 146: 571–580.

    CAS 

    Google Scholar 

  • 55

    Clement CI, Hassall ME . Necrotizing fasciitis of the face and orbit following complications with a tooth abscess. ANZ J Surg 2004; 74: 85–87.

    PubMed 

    Google Scholar 

  • 56

    Maccheron LJ, Groeneveld ER, Ohlrich SJ, Hilford DJ, Beckingsale PS . Orbital cellulitis, panophthalmitis, and ecthyma gangrenosum in an immunocompromised host with pseudomonas septicemia. Am J Ophthalmol 2004; 137: 176–178.

    PubMed 

    Google Scholar 

  • 57

    Uddin JM, Rennie CA, Moore AT . Bilateral non-specific orbital inflammation (orbital ‘pseudotumour’), posterior scleritis, and anterior uveitis associated with hypothyroidism in a child. Br J Ophthalmol 2002; 86: 936.

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • 58

    Boonman ZF, De Keizer RJ, Graniewski-Wijnands HS, Watson PG . Orbital myositis in scleritis. Br J Ophthalmol 2003; 87: 38–42.

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • 59

    Uehara F, Ohba N . Diagnostic imaging in patients with orbital cellulitis and inflammatory pseudotumor. Int Ophthalmol Clin 2002; 42: 133–142.

    PubMed 

    Google Scholar 

  • 60

    Dhariwal DK, Kittur MA, Farrier JN, Sugar AW, Aird DW, Laws DE . Post-traumatic orbital cellulitis. Br J Oral Maxillofac Surg 2003; 41: 21–28.

    CAS 
    PubMed 

    Google Scholar 

  • 61

    O’Sullivan RM, Nugent RA, Satorre J, Rootman J . Granulomatous orbital lesions: computed tomographic features. Can Assoc Radiol J 1992; 43: 349–358.

    CAS 
    PubMed 

    Google Scholar 

  • 62

    Kalina PH, Lie JT, Campbell RJ, Garrity JA . Diagnostic value and limitations of orbital biopsy in Wegener’s granulomatosis. Ophthalmology 1992; 99: 120–124.

    CAS 
    PubMed 

    Google Scholar 

  • 63

    Woo TL, Francis IC, Wilcsek GA, Coroneo MT, McNab AA, Sullivan TJ . Australasian orbital and adnexal Wegener’s granulomatosis. Ophthalmology 2001; 108: 1535–1543.

    CAS 
    PubMed 

    Google Scholar 

  • 64

    Talar-Williams C, Sneller MC, Langford CA, Smith JA, Cox TA, Robinson MR . Orbital socket contracture: a complication of inflammatory orbital disease in patients with Wegener’s granulomatosis. Br J Ophthalmol 2005; 89: 493–497.

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • 65

    Hoffmann EM, Muller-Forell W, Pitz S, Radner H . Erdheim–Chester disease: a case report. Graefes Arch Clin Exp Ophthalmol 2004; 242: 803–807.

    PubMed 

    Google Scholar 

  • 66

    Sheidow TG, Nicolle DA, Heathcote JG . Erdheim–Chester disease: two cases of orbital involvement. Eye 2000; 14: 606–612.

    PubMed 

    Google Scholar 

  • 67

    Takanashi T, Uchida S, Arita M, Okada M, Kashii S . Orbital inflammatory pseudotumor and ischemic vasculitis in Churg-Strauss syndrome: report of two cases and review of the literature. Ophthalmology 2001; 108: 1129–1133.

    CAS 
    PubMed 

    Google Scholar 

  • 68

    Metzler C, Hellmich B, Gause A, Gross WL, de Groot K . Churg Strauss syndrome—successful induction of remission with methotrexate and unexpected high cardiac and pulmonary relapse ratio during maintenance treatment. Clin Exp Rheumatol 2004; 22: S52–S61.

    CAS 
    PubMed 

    Google Scholar 

  • 69

    Kline LB, Hoyt WF . The Tolosa–Hunt syndrome. J Neurol Neurosurg Psychiatry 2001; 71: 577–582.

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • 70

    Gunalp I, Gunduz K, Yazar Z . Idiopathic orbital inflammatory disease. Acta Ophthalmol Scand 1996; 74: 191–193.

    CAS 
    PubMed 

    Google Scholar 

  • 71

    Hannerz J . Recurrent Tolosa-Hunt syndrome: a report of ten new cases. Cephalalgia 1999; 19 (1Suppl 25): 33–35.

    PubMed 

    Google Scholar 

  • 72

    Wasmeier C, Pfadenhauer K, Rosler A . Idiopathic inflammatory pseudotumor of the orbit and Tolosa–Hunt syndrome—are they the same disease? J Neurol 2002; 249: 1237–1241.

    CAS 
    PubMed 

    Google Scholar 

  • 73

    Yousem DM, Atlas SW, Grossman RI, Sergott RC, Savino PJ, Bosley TM . MR imaging of Tolosa–Hunt syndrome. AJNR Am J Neuroradiol 1989; 10: 1181–1184.

    CAS 
    PubMed 

    Google Scholar 

  • 74

    Zakir R, Manners RM, Ellison D, Barker S, Crick M . Idiopathic sclerosing inflammation of the orbit: a new finding of calcification. Br J Ophthalmol 2000; 84: 1322–1324.

    CAS 
    PubMed 

    Google Scholar 

  • 75

    Billing KJ, Hsuan J, Selva D . Idiopathic sclerosing inflammation of the orbit: a case of steroid-responsive disease in a patient with auto-immune hemolytic anemia. Eur J Ophthalmol 2005; 15: 263–266.

    CAS 
    PubMed 

    Google Scholar 

  • 76

    Valvassori GE, Sabnis SS, Mafee RF, Brown MS, Putterman A . Imaging of orbital lymphoproliferative disorders. Radiol Clin North Am 1999; 37: 135 xi.

    CAS 
    PubMed 

    Google Scholar 

  • 77

    Stidham DB, Sondhi N, Plager D, Helveston E . Presumed isolated inflammation of the superior oblique muscle in idiopathic orbital myositis. Ophthalmology 1998; 105: 2216–2219.

    CAS 
    PubMed 

    Google Scholar 

  • 78

    Menon GJ, Hollman AS, Dutton GN . Granulomatous orbital myositis. Eye 2000; 14: 676–678.

    PubMed 
    PubMed Central 

    Google Scholar 

  • 79

    Magrini L, Rotiroti G, Conti F, Viganego F, Alessandri C, Picardo V et al. Orbital myositis in a patient with primary biliary cirrhosis: successful treatment with methotrexate and corticosteroids. Isr Med Assoc J 2003; 5: 825–826.

    PubMed 

    Google Scholar 

  • 80

    Caramaschi P, Biasi D, Carletto A, Bambara LM . Orbital myositis in a rheumatoid arthritis patient during etanercept treatment. Clin Exp Rheumatol 2003; 21: 136–137.

    CAS 
    PubMed 

    Google Scholar 

  • 81

    Hatton MP, Rubin PA . The pathophysiology of thyroid-associated ophthalmopathy. Ophthalmol Clin North Am 2002; 15: 113–119.

    PubMed 

    Google Scholar 

  • 82

    Kazim M, Goldberg RA, Smith TJ . Insights into the pathogenesis of thyroid-associated orbitopathy: evolving rationale for therapy. Arch Ophthalmol 2002; 120: 380–386.

    CAS 
    PubMed 

    Google Scholar 

  • 83

    Yan J, Wu Z, Li Y . The differentiation of idiopathic inflammatory pseudotumor from lymphoid tumors of orbit: analysis of 319 cases. Orbit 2004; 23: 245–254.

    PubMed 

    Google Scholar 

  • 84

    Siatkowski RM, Capo H, Byrne SF, Gendron EK, Flynn JT, Munoz M et al. Clinical and echographic findings in idiopathic orbital myositis. Am J Ophthalmol 1994; 118: 343–350.

    CAS 
    PubMed 

    Google Scholar 

  • 85

    Scott IU, Siatkowski MR . Thyroid eye disease. Semin Ophthalmol 1999; 14: 52–61.

    CAS 
    PubMed 

    Google Scholar 

  • 86

    de Heide LJ, Talsma MA . Giant-cell arteritis presenting as an orbital pseudotumor. Neth J Med 1999; 55: 196–198.

    CAS 
    PubMed 

    Google Scholar 

  • 87

    Tychsen L, Tse DT, Ossoinig K, Anderson RL . Trochleitis with superior oblique myositis. Ophthalmology 1984; 91: 1075–1079.

    CAS 
    PubMed 

    Google Scholar 

  • 88

    Yanguela J, Pareja JA, Lopez N, Sanchez DR . Trochleitis and migraine headache. Neurology 2002; 58: 802–805.

    PubMed 

    Google Scholar 

  • 89

    Hykin PG, Spalton DJ . Bilateral perineuritis of the optic nerves. J Neurol Neurosurg Psychiatry 1991; 54: 375–376.

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • 90

    Fay AM, Kane SA, Kazim M, Millar WS, Odel JG . Magnetic resonance imaging of optic perineuritis. J Neuroophthalmol 1997; 17: 247–249.

    CAS 
    PubMed 

    Google Scholar 

  • 91

    Frohman L, Wolansky L . Magnetic resonance imaging of syphilitic optic neuritis/perineuritis. J Neuroophthalmol 1997; 17: 57–59.

    CAS 
    PubMed 

    Google Scholar 

  • 92

    Purvin V, Kawasaki A, Jacobson DM . Optic perineuritis: clinical and radiographic features. Arch Ophthalmol 2001; 119: 1299–1306.

    CAS 
    PubMed 

    Google Scholar 

  • 93

    Ersahin Y . Orbital pseudotumor. Pediatr Neurosurg 1999; 31: 53.

    CAS 
    PubMed 

    Google Scholar 

  • 94

    Srivastava SK, Newman NJ . Pseudo-pseudotumor. Surv Ophthalmol 2000; 45: 135–138.

    CAS 
    PubMed 

    Google Scholar 

  • 95

    Jacobs D, Galetta S . Diagnosis and management of orbital pseudotumor. Curr Opin Ophthalmol 2002; 13: 347–351.

    PubMed 

    Google Scholar 

  • 96

    Goldberg RA, McCann JD, Shorr N . Idiopathic orbital inflammatory disease. Arch Ophthalmol 2004; 122: 1092–1093.

    PubMed 

    Google Scholar 

  • 97

    Caruso K, Marrion R, Silver G . What is your diagnosis? Retrobulbar mass indenting the inferior aspect of the right globe. J Am Vet Med Assoc 2002; 221: 1553–1554.

    PubMed 

    Google Scholar 

  • 98

    Notter M, Kern T, Forrer A, Meister F, Schwegler N . Radiotherapy of pseudotumor orbitae. Front Radiat Ther Oncol 1997; 30: 180–191.

    CAS 
    PubMed 

    Google Scholar 

  • 99

    Mahr MA, Salomao DR, Garrity JA . Inflammatory orbital pseudotumor with extension beyond the orbit. Am J Ophthalmol 2004; 138: 396–400.

    PubMed 

    Google Scholar 

  • 100

    Zborowska B, Ghabrial R, Selva D, McCluskey P . Idiopathic orbital inflammation with extraorbital extension: case series and review. Eye 2006; 20: 107–113.

    CAS 
    PubMed 

    Google Scholar 

  • 101

    Nassar DL, Raab SS, Silverman JF, Kennerdell JS, Sturgis CD . Fine-needle aspiration for the diagnosis of orbital hematolymphoid lesions. Diagn Cytopathol 2000; 23: 314–317.

    CAS 
    PubMed 

    Google Scholar 

  • 102

    Mooy CM . Comments on ‘Clinical and cytopathologic correlation in chronic inflammations of the orbit and ocular adnexa: a review of 55 cases’ by Upreet Dhaliwal et al. Orbit 2004; 23: 211–212.

    CAS 
    PubMed 

    Google Scholar 

  • 103

    Wirostko BM, Wirostko E, Wirostko RF . Orbital pseudotumors treated with systemic corticosteroids. Ophthalmology 1996; 103: 1519–1520.

    CAS 
    PubMed 

    Google Scholar 

  • 104

    Jordan DR . Orbital pseudotumors treated with systemic corticosteroids. Ophthalmology 1996; 103: 1519.

    CAS 
    PubMed 

    Google Scholar 

  • 105

    Mombaerts I, Schlingemann RO, Goldschmeding R, Koornneef L . Are systemic corticosteroids useful in the management of orbital pseudotumors? Ophthalmology 1996; 103: 521–528.

    CAS 
    PubMed 

    Google Scholar 

  • 106

    Isobe K, Uno T, Kawakami H, Ueno N, Kawata T, Abe H et al. Radiation therapy for idiopathic orbital myositis: two case reports and literature review. Radiat Med 2004; 22: 429–431.

    PubMed 

    Google Scholar 

  • 107

    Smitt MC, Donaldson SS . Radiation therapy for benign disease of the orbit. Semin Radiat Oncol 1999; 9: 179–189.

    CAS 
    PubMed 

    Google Scholar 

  • 108

    Ferris JD, Dawson EL, Plowman N, Adams GG, Fells P, Lee JP . Radiotherapy in thyroid eye disease: the effect on the field of binocular single vision. J AAPOS 2002; 6: 71–76.

    PubMed 

    Google Scholar 

  • 109

    Smith JR, Rosenbaum JT . A role for methotrexate in the management of non-infectious orbital inflammatory disease. Br J Ophthalmol 2001; 85: 1220–1224.

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • 110

    Sen HN, Suhler EB, Al Khatib SQ, Djalilian AR, Nussenblatt RB, Buggage RR . Mycophenolate mofetil for the treatment of scleritis. Ophthalmology 2003; 110: 1750–1755.

    PubMed 

    Google Scholar 

  • 111

    Baltatzis S, Tufail F, Yu EN, Vredeveld CM, Foster CS . Mycophenolate mofetil as an immunomodulatory agent in the treatment of chronic ocular inflammatory disorders. Ophthalmology 2003; 110: 1061–1065.

    PubMed 

    Google Scholar 

  • 112

    Garrity JA, Coleman AW, Matteson EL, Eggenberger ER, Waitzman DM . Treatment of recalcitrant idiopathic orbital inflammation (chronic orbital myositis) with infliximab. Am J Ophthalmol 2004; 138: 925–930.

    CAS 
    PubMed 

    Google Scholar 

  • 113

    Smith JR, Spurrier NJ, Martin JT, Rosenbaum JT . Prevalent use of complementary and alternative medicine by patients with inflammatory eye disease. Ocul Immunol Inflamm 2004; 12: 203–214.

    PubMed 

    Google Scholar 

  • 114

    Wilson MW, Shergy WJ, Haik BG . Infliximab in the treatment of recalcitrant idiopathic orbital inflammation. Ophthalmol Plast Reconstr Surg 2004; 20: 381–383.

    Google Scholar 

  • 115

    Chiu CS, Rubin PA . Pharmacotherapies and nonpharmacotherapies for orbital inflammatory diseases. Int Ophthalmol Clin 2004; 44: 165–185.

    PubMed 

    Google Scholar 

  • 116

    Baughman RP, Lower EE, Bradley DA, Raymond LA, Kaufman A . Etanercept for refractory ocular sarcoidosis: results of a double-blind randomized trial. Chest 2005; 128: 1047–1062.

    Google Scholar 

  • 117

    Thorne JE, Jabs DA, Qazi FA, Nguyen QD, Kempen JH, Dunn JP . Mycophenolate mofetil therapy for inflammatory eye disease. Ophthalmology 2005; 112: 1472–1477.

    PubMed 

    Google Scholar 

  • 118

    Zierhut M, Stubiger N, Siepmann K, Deuter CM . MMF and eye disease. Lupus 2005; 14 (Suppl 1): s50–s54.

    CAS 
    PubMed 

    Google Scholar 

  • 119

    Zwerina J, Redlich K, Schett G, Smolen JS . Pathogenesis of rheumatoid arthritis: targeting cytokines. Ann N Y Acad Sci 2005; 1051: 716–729.

    CAS 
    PubMed 

    Google Scholar 

  • 120

    Braiteh F, Boxrud C, Esmaeli B, Kurzrock R . Successful treatment of Erdheim-Chester disease, a non-Langerhans cell histiocytosis, with interferon-alpha. Blood 2005; 106: 2992–2994.

    CAS 
    PubMed 

    Google Scholar 

  • 121

    Atzeni F, Turiel M, Capsoni F, Doria A, Meroni P, Sarzi-Puttini P . Autoimmunity and Anti-TNF-{alpha} Agents. Ann N Y Acad Sci 2005; 1051: 559–569.

    CAS 
    PubMed 

    Google Scholar 

  • 122

    Van Assche G, Vermeire S, Rutgeerts P . Medical treatment of inflammatory bowel diseases. Curr Opin Gastroenterol 2005; 21: 443–447.

    CAS 
    PubMed 

    Google Scholar 

  • 123

    Smolen JS, Redlich K, Zwerina J, Aletaha D, Steiner G, Schett G . Pro-inflammatory cytokines in rheumatoid arthritis: pathogenetic and therapeutic aspects. Clin Rev Allergy Immunol 2005; 28: 239–248.

    CAS 
    PubMed 

    Google Scholar 

  • Thyroid Eye Disease (TED or Graves Eye Disease) | Kellogg Eye Center

    What Is Graves’ Eye Disease or Thyroid Eye Disease?

    Graves’ eye disease, also known as thyroid eye disease, is an autoimmune condition in which immune cells attack the thyroid gland which responds by secreting an excess amount of thyroid hormone. As a result, the thyroid gland enlarges and excess hormones increase metabolism. The hypermetabolic state is characterized by fast pulse/heartbeat, palpitations, profuse sweating, high blood pressure, irritability, fatigue, weight loss, heat intolerance, and loss of hair and alterations in hair quality. When the immune system attacks the tissues around the eyes, it causes the eye muscles or fat to expand.

    The eyes are particularly vulnerable to Graves’ eye disease, because the autoimmune attack often targets the eye muscles and connective tissue within the eye socket. This likely occurs because these tissues contain proteins that appear similar to the immune system as those of the thyroid gland. Ocular symptoms can range from mild to severe; but only 10-20% of patients have sight threatening disease. Another tissue that can also be involved in the immune attack of Graves’ eye disease is the skin of the shins.

    Thyroid Glands Relation to the Eye

    Although Graves’ disease and Graves’ eye disease both stem from the immune system’s attack on healthy tissue, one disease does not directly cause the other. That’s why treatment of the thyroid gland, while important, does not improve the eye disease. The two diseases run their separate courses and do not necessarily occur at the same time. 

    Signs and Symptoms of Graves’ Eye Disease

    In Graves’ eye disease the tissue around the eye is attacked, and the result is inflammation and swelling, causing:

    • Redness and pain
    • Puffiness around the eyes
    • Bulging of the eyes
    • Dry eye and irritation, occurring when the eyelids cannot close completely over bulging eyes

    Progressive swelling may cause: 

    • Increased pressure inside the eye socket
    • Pressure-pain or deep headache, which worsens with eye movements
    • Decreased vision, when swollen tissues push on the optic nerve

    The muscles around the eye are particularly susceptible to the attack of lymphocytes. As they tighten and lose their ability to stretch, these symptoms can occur:

    • The eye is pushed forward in its socket causing a “staring” appearance
    • Restriction of the eye’s normal movements, resulting in double vision

    As symptoms build, many patients fear they will lose their vision. Fortunately, patients almost never go blind from Graves’ eye disease.

    Causes

    When the immune system attacks the muscles and other ocular tissues in the eye socket, the swelling and scarring resulting from the inflammation causes symptoms and signs noted above. In severe cases, the clear covering of the eye (cornea) may ulcerate, or the optic nerve may be damaged, either of which may result in a permanent loss of vision if not treated appropriately. The former is often due to a combination of the eyes bulging forward and scarring resulting in the eyelids retracting backward. The latter is due to thickened, inflamed and/or scarred muscles impinging on the optic nerve at the back of the socket.

    In most patients who develop Graves’ ophthalmopathy, the eyes bulge forward or the eyelid retracts to some degree. Many patients with mild to moderate Graves’ ophthalmopathy will experience spontaneous improvement over the course of two to three years or will adapt to the abnormality. Severe ophthalmopathy will affect 10% of patients. It is caused by inflammation of the muscles, which causes them to swell. They can also become stiff (scarred), which interferes with movement of the eyes and causes double vision or impinges upon the optic nerve, causing loss of vision. In some patients, eye protrusion makes it difficult for the lids to close properly and the cornea becomes exposed and vulnerable. When the optic nerve is compromised, progressive and irreversible vision loss occurs. Rarely, orbital swelling may precipitate glaucoma that also affects the optic nerve.

    Risk Factors

    Approximately one million Americans are diagnosed with Graves’ eye disease each year. Women are five to six times more likely than men to get the disease. Cigarette smokers are at significantly increased risk to develop the disease, and when they do, often have more severe and prolonged activity that threatens vision.

    Although Graves’ disease and Graves’ eye disease both stem from the immune system’s attack on healthy tissue, one disease does not directly cause the other. That’s why treatment of the thyroid gland, while important, does not improve the eye disease. The two diseases run their separate courses and do not necessarily occur at the same time. 

    Tests and Diagnosis

    If your doctor suspects you have an overactive thyroid gland, your thyroid function must first be evaluated and treated appropriately by an internist trained in doing so. Treatments include medications to suppress the production of hormone by the thyroid gland, radioactive iodine to eliminate hormone-producing cells, and surgery to remove the thyroid tissue. In most cases, replacement thyroid hormone is required following the natural course of the Graves’ autoimmune attack on the thyroid gland or following effective treatment.  Once your thyroid function is treated and returned to normal, the eye disease must be monitored as it often continues to progress. Eye involvement must be evaluated on a continuing basis by an ophthalmologist during the active phase of the disease and, if necessary, treated. Although symptoms often resolve on their own, activity, scarring, and visual loss not readily apparent to the patient may otherwise go unnoticed and cause permanent changes.

    Treatment and Drugs 

    Treatment for thyroid eye disease generally occurs in two phases. The first phase involves treating the active eye disease. This active period usually lasts two to three years and requires careful monitoring until stable. Treatment during the active phase of the disease focuses on preserving sight and the integrity of the cornea as well as providing treatment for double vision when it interferes with daily functioning and becomes bothersome. 

    Most patients experience relief from dry eyes by using artificial tears throughout the day and gels or ointments at night. Some patients also use eye covers at night or tape their eyes shut to keep them from becoming dry if the eyelids do not close properly. Dryness occurs because the lids are retracted and cannot blink properly, because the tear-producing glands have been affected by the autoimmune process and aren’t functioning well, and/or because the forward bulging of the eyes prevents them from being completely covered by the lids. In some cases, acute swelling causing double vision or loss of vision may be treated for a limited time with prednisone. However, prednisone given for more than a few weeks at the dosages required to suppress the autoimmune inflammation always causes bothersome side-effects that may become severe. In patients who respond to prednisone, radiation therapy may be offered to reduce swelling, double vision, and, in severe cases, loss of vision. Most people get relief from their symptoms within two months of the radiation. However, radiation treatment is only marginally effective at reducing these abnormalities and may cause ocular dryness. It can only be used at most twice in a person’s lifetime and bears a slight risk for inducing tumors. Surgical decompression can also be used during the active phase, most often to relieve optic neuropathy. It is also helpful in reducing congestion, redness, pain, and ocular exposure.

    Treatment during the remission phase that lasts indefinitely in most cases, involves correcting unacceptable permanent changes that persist after the ocular conditions of the active phase have stabilized. In the second phase, treatment of permanent changes may require surgery to correct double vision and reduce eyelid retraction. Surgery may be helpful in returning the eye to a normal position within the socket (orbital decompression).

    It is important to stop smoking in order to reduce the severity, duration of activity, degree of scarring, and risk of optic nerve involvement, greatly improving the success of treating Graves’ eye disease.

    New Study: ‘Breakthrough’ Drug Reduces Graves’ Eye Disease Symptoms

    A clinical trial led by the University of Michigan Kellogg Eye Center offers hope for those with moderate to severe active TED. Patients had a significant reduction in the severity of symptoms after treatment with teprotumumab, a study drug the Food and Drug Administration designated a “breakthrough therapy.” Learn more about the results of this clinical trial.

    Find a Doctor or Location 

     

    Reviewed by Raymond S. Douglas, M.D., Ph.D.

    90,000 Inflammatory eye diseases, barley, demodicosis, blepharitis, dacryoadenitis, canaliculitis, conjunctivitis, thrombophlebitis, exophthalmos, iritis, endophthalmitis

    Inflammatory processes , developing in various parts of the eye – is a fairly common pathology . Inflammation can affect one or more parts of the eyeball, as well as surrounding tissues, and it can be both infectious and non-infectious in nature. Any of the inflammatory diseases of the organs of vision is characterized by similar clinical signs and leads to dysfunction of the eyes.

    An ophthalmologist (ophthalmologist) is engaged in the diagnosis and treatment of inflammatory eye diseases.

    Types and localization of eye inflammations

    The eye is one of the most complex organs of our body, consisting of a variety of parts that have a special purpose and perform important functions in the work of the visual system. The term “inflammatory eye disease” usually refers to a variety of processes that affect any part of the eye. Depending on the location of the inflammatory process, pathologies can be classified as follows:

    • inflammation of the eyelids (barley, demodicosis, blepharitis, etc.)
    • inflammation of the lacrimal organs (dacryoadenitis, canaliculitis, etc.)
    • inflammation of the conjunctiva (bacterial, viral conjunctivitis)
    • inflammation of the orbit (thrombophlebitis, exophthalmos, etc.)
    • inflammation of the eye vessels (iritis, endophthalmitis, etc.)
    • corneal inflammation (viral, fungal keratitis, etc.).

    The type of inflammation can also differ. So, in medicine, the following types of inflammatory processes that can affect the eyes are distinguished:

    • catarrhal
    • rheumatic
    • granulosa
    • syphilitic
    • gonorrheal
    • scrofulous
    • inflammation resulting from mechanical trauma
    • inflammation caused by overexertion
    • , arising after rash infectious diseases, etc.e.

    The inflammatory process of various types can occur in both acute and chronic forms.

    Reasons for the development of inflammatory eye diseases

    • infectious diseases (streptococcal and staphylococcal infections, herpes, tuberculosis, etc.)
    • eye injury
    • eye irritation by aggressive substances
    • inflammatory diseases of the nasopharynx
    • vitamin deficiency in the body
    • lack of personal hygiene.

    You should also be careful if you often have to experience irritating effects of corrosive smoke and other substances, if you are hit in the eye or have any other mechanical impact. Also, you can enter a risk group if you are used to malnutrition, because with a lack of necessary substances in the body, metabolic processes can be disrupted, which often leads to the development of inflammatory diseases, including the organs of vision.

    General signs and symptoms

    Any inflammation affecting the organs of vision is characterized by some general clinical symptoms:

    • redness of the skin and mucous membranes
    • the appearance of edema
    • pain
    • with some diseases itching and burning are possible
    • lacrimation
    • narrowing of the eye gap
    • sensitivity to light
    • painful mobility
    • eyelash loss and deformation of their growth
    • with barley and some other inflammatory diseases, a nodular formation is formed on the eyelid, which is painful and can secrete pus.

    In severe, advanced cases, you may also feel that your vision has become worse. Such a sign cannot be ignored, because poor vision not only significantly reduces the quality of life, but signals a serious eye pathology and possible complications of inflammation.

    Do not ignore existing symptoms! When they appear, it is recommended not to postpone an appointment with an ophthalmologist.

    Diagnostics in our clinic

    Our experienced ophthalmologist will be able to prescribe highly effective treatment only after a comprehensive examination and a reliable diagnosis.For this, an examination of the eye by the method of ophthalmoscopy and with the help of a slit lamp, the function of vision is checked, and the intraocular pressure is measured. To check for infection, it is also necessary to conduct a number of laboratory tests that will determine the causative agent of the disease.

    Particular attention is paid to differential diagnosis, because many inflammatory eye diseases follow a similar scenario. Our doctor can apply the following examination methods in the clinic:

    • PCR analysis of scrapings from the conjunctiva and cornea, as well as PCR analysis of blood for accurate qualitative and quantitative analysis of the infectious agent;
    • bacterial inoculation of the detachable eye, which allows you to accurately identify the infectious pathogen and determine its sensitivity to various groups of antibiotics;
    • Conducting allergy tests, with the help of which the doctor can find out if your body is sensitive to certain substances;
    • examination of eyelashes under a microscope for fungal infections or demodicosis;
    • some instrumental research methods.

    Treatment of inflammatory eye diseases

    Competent therapy for eye inflammation is impossible without eliminating the main factor causing the disease. If inflammation of the organs of vision develops in you against the background of systemic pathology, it must be identified and cured. In our clinic, you always have the opportunity to undergo not only complex ophthalmological diagnostics, but also, if necessary, get advice from various narrow specialists.

    In the course of the complex therapy of inflammatory diseases affecting the organs of vision, the doctor may prescribe you:

    • antiviral, antibacterial and other medicines, the action of which is aimed at combating the infectious agent
    • medical massage of the eyelids
    • specific immunotherapy
    • allergy therapy
    • conjunctival cavity ozone therapy
    • laser treatment
    • magnetostimulation
    • color therapy, etc.e.

    If your disease was diagnosed late and serious complications began to appear, our specialists will be able to perform sparing microsurgical treatment. However, we strongly recommend to see a doctor at the first signs of inflammation , especially since modern diagnostic methods allow you to recognize any eye disease at the earliest stages of development.

    See also : Cataract: causes, symptoms, treatment, Glaucoma: symptoms, diagnosis, treatment.

    Orbital abscess

    Orbital abscess is a limited inflammation of the tissues of the orbit with the formation of a cavity filled with pus.

    Etiology and pathogenesis . More often occurs in diseases of the paranasal sinuses, as a result of caries and necrosis of the bone walls, inflammation of the veins passing through them, osteoperiostitis. It can develop as a result of infection of the tissues of the orbit with pyogenic microbes when it is damaged, the introduction of foreign bodies, as well as hematogenous-metastatic by various infectious diseases and purulent processes in the body.

    Distinguish between subperiosteal and retrobulbar abscess of the orbit. The first is localized between the periosteum and the bony wall of the orbit, the second – in the retrobulbar space.

    Clinical picture. Onset is usually acute. Hyperemia of the skin of the eyelids, their edema, chemosis of the conjunctiva, soreness of the eyelids and the edges of the orbit appear. Often, body temperature rises, headache, general weakness occur. In a subperiosteal abscess associated with purulent inflammation of the paranasal sinuses, the location of the abscess usually corresponds to the topography of the sinuses.The process from the maxillary sinus rarely spreads.When the ethmoid sinus is affected, edema occurs mainly in the area of ​​the inner corner of the palpebral fissure, the frontal sinus – in the middle third of the eyelid at the upper edge of the orbit. Sometimes there is fluctuation here. The eyeball is shifted to the side, its mobility is impaired. As a result, diplopia occurs. Visual acuity may decrease slightly.

    The posterior subperiosteal and retrobulbar abscess is characterized by edema and congestive hyperemia of the eyelids, exophthalmos, limited mobility of the eyeball, optic neuritis and decreased visual acuity.When the abscess is located close to the edge of the orbit, fluctuation is determined. If the process is localized at the apex of the orbit, then a syndrome of the superior orbital fissure occurs: the eyelid is lowered, the eyeball is motionless, the pupil is dilated, does not respond to light, skin sensitivity in the area of ​​distribution of the first branch of the trigeminal nerve is absent, visual acuity is sharply reduced, there is a stagnant optic nerve head … The sub-periosteal purulent process of tuberculous or syphilitic etiology usually proceeds subacutely or are reactive in the form of a cold abscess.

    An abscess can dissolve, especially under the influence of treatment, or open through the soft tissues of the eyelids and periorbital region, and a fistular passage is formed. A breakthrough of pus into the cavity of the orbit can lead to a developed inflammation of its cellulose – phlegmon of the orbit.

    Diagnosis is based on acute onset and characteristic clinical presentation. To identify the source of the process, X-ray and clinical examination of the paranasal sinuses is necessary. It should be differentiated from the phlegmon of the orbit, which is distinguished by more pronounced local and general manifestations and a more severe course.

    Prevention. Timely treatment and elimination of diseases of the paranasal sinuses and other foci of infection that can cause purulent inflammation of the tissues of the orbit.

    Treatment. Elimination of the primary focus of infection, primarily the inflammatory process in the paranasal sinuses. Antibiotics and sulfonamides: benzylpenicillin sodium salt parenterally 300 000 ED 3-4 times a day, streptomycin sulfate intramuscularly 0.5 g in 1-2 doses a day, tetracycline inside 0.2 g.3 times a day, sulfadimezin inside 0.5 g 6-8 times a day. Fortifying treatment: to reduce perifocal inflammation and collateral edema, anemize the nasal mucosa by lubricating it with 5% cocaine hydrochloride solution with 0.1% adrenaline hydrochloride solution. When an abscess forms, surgical intervention is necessary. With clinical signs of a subperiosteal abscess, a subperiosteal orbitotomy is performed – a wide incision to the bone without opening the tarzoorbital fascia.If a retrobulbar abscess has formed, then the periosteum is also opened. The wound is drained.

    Forecast. With timely active treatment, as a rule, complete recovery occurs with the restoration of the normal position of the eye, its mobility and functions. With an unfavorable course of the process, the development of phlegmon of the orbit is possible.

    Orbital cellulite (phlegmon of the eye socket) “Lakhta Clinic

    Terminology

    The origin and meaning of the term “Cellulite” in different contexts, as well as more detailed information about phlegmonous inflammation, are presented in the relevant materials on our website (“Lipodystrophic Cellulite” and “Phlegmon” ).See also Periorbital Cellulite .

    Orbital cellulite – phlegmonous inflammation of the adipose tissue of the orbit, i.e. diffuse acute purulent-inflammatory process in deep soft tissues surrounding the eyeball. This variant of cellulite (panniculitis) is itself a dangerous serious condition, and, in addition, carries the risk of life-threatening intracranial complications.

    According to current epidemiological estimates, orbital cellulitis is up to 16 times more common in young children than in the adult population, and about twice as often in boys than in girls.A certain seasonality is noted: the disease is more often diagnosed in the cold season, which is associated by researchers, first of all, with an increased frequency of sinusitis in the autumn-winter period. In general, orbital cellulite is rare. On the other hand, among all inflammatory diseases of the orbit, purulent forms of inflammation account for about a fifth; the risk of blindness in this case reaches, according to various sources, 20-50%, and death – 25-29%. According to other sources, such a high level of unfavorable outcomes was characteristic of the historical period preceding the “era of antibiotics”, and now the prognosis should be considered much more favorable.One way or another, this condition is an urgent one, and a prerequisite for its successful relief is the immediate provision of adequate ophthalmosurgical assistance – however, even in this case, orbital cellulite leaves a high probability of the development of long-term complications (strabismus, amblyopia, blindness due to retinal detachment and atrophy of the optic disc). nerve).

    Reasons

    Orbital cellulitis is an acute purulent infectious and inflammatory process of bacterial etiology, the causative agents of which are usually streptococci, staphylococci, pneumococci, or, less often, Escherichia coli.

    A typical developmental mechanism is associated with hematogenous penetration of a pyogenic microorganism from the foci of infection located in the immediate vicinity. In the overwhelming majority of cases (up to 70%), such a focus is ethmoiditis and other inflammations of the paranasal sinuses (paranasal sinuses). It is also possible phlegmonous inflammation of the orbit due to trauma, with purulent-inflammatory diseases of the eyelid, lacrimal glands, facial skin, teeth and periodontal tissues, as well as a complication of sepsis.

    Symptoms

    Orbital cellulite develops sharply, within a few hours (maximum 1-2 days). There is a pronounced pain syndrome, the pain usually pulsates, aggravated by turning the eyeball and touching the affected area. The eyelids acquire a crimson-red hue and swell so much that independent opening of the palpebral fissure becomes impossible. Typical symptoms also include ophthalmoplegia (limited mobility of the eyeball) and exophthalmos (displacement, protrusion of the eyeball anteriorly).The general condition is severe, infectious and toxic symptoms are expressed and progressing in the form of hyperthermia, chills, general weakness, nausea, headache, sometimes with disorders of the central nervous system. In the absence of immediate help, retinal blood supply disturbances leading to blindness, ulcerative keratitis, as well as life-threatening and highly lethal complications such as brain abscess, meningoencephalitis, and sepsis, may develop. Spontaneous opening of suppuration with the release of the accumulated exudate outside can somewhat alleviate the patient’s condition, but does not reduce the risk of critical complications.

    Diagnostics

    Most often, the diagnosis is made by an ophthalmologist during an urgent appointment, however, urgent consultation of related specialists (ENT doctor, maxillofacial surgeon, etc.) is often required. In addition to standard procedures for collecting complaints and anamnesis, examination and palpation, ultrasound, X-ray and / or other imaging studies of the orbit and paranasal sinuses are prescribed, since it is important to exclude symptomatically similar conditions (e.g., foreign body, oncological process, retrobulbar hemorrhage, etc.).etc.). It is mandatory to select material for laboratory clinical blood analysis, identification of the pathogen and determination of its drug sensitivity.

    Treatment

    In all cases, the patient is urgently admitted to a specialized ophthalmic surgery department or center. Without waiting for the results of laboratory diagnostics, an antibacterial drug cover is prescribed in shock doses, often in a combination of systemic and injection (for the eyeball, under the conjunctiva).An urgent surgical intervention is performed, the volume and nature of which is determined by a specific clinical picture and data of express diagnostics. Measures are taken to remove accumulated purulent-necrotic masses and drain purulent exudate, prescribe detoxification measures, and perform antiseptic sanitation of the operating field. In the rehabilitation period, vitamin complexes, physiotherapy methods, antibiotic washings, drops, ointments, etc. are used.

    90,000 Inflammation of the eyes. Symptoms and Prevention.

    3.May 2017

    The most common ocular problem is inflammation of the eye, which is the totality of various inflammatory processes that can affect any part of the eye.

    As a rule, eye inflammation manifests itself in reddening of the connective tissue elements of the organ, and due to plethora, the vascular pattern of the eye is sharply expressed.The inflammatory process can also affect the areas around the eye (for example, the eyelids), resulting in uncomfortable phenomena. The causes of inflammatory processes in the eye are not so numerous and consist of several main groups.

    So, eye inflammation can be caused by:

    Any infectious inflammation (tuberculosis, syphilis, herpes, staphylococcal, streptococcal infections).

    Traumatic injury to the eye (blow, hit of a foreign object in the eye, and so on).

    Impact of aggressive substances (acids, alkalis, dust, etc.)

    Symptoms of eye inflammation.

    In inflammatory diseases of the eyes (both outside and inside) and eyelids, as a rule, there is pain in the eyes, which has a different intensity. In the event that the mucous membrane of the eyes is inflamed (conjunctivitis), then, as a rule, there is redness of the eye, as well as discharge from the eyes. With inflammation of the muscles of the eye – the eyes also hurt, and the pain can be observed in the depths of the orbit, and can increase with the movement of the eyeball.If the vascular tract of the eye becomes inflamed, pain in the eyes appears again, which increases with pressure on the eyeball. In addition to all this, with inflammation of the eyes, there can be a burning sensation in the eyes, they can watery and even fester.

    A few words about the prevention of inflammation:

    You should never rub your eyes with the inside of your fingers, unless you have just washed them, because this is the easiest way to get an infection.

    If inflamed eyes itch and hurt, then wipe them with a clean napkin or clean handkerchief.As a last resort, you can use the outside of the finger joints.

    Remember to remove makeup before bed.

    Try to blink more often.

    If you have to work a lot at the computer, take breaks. So you can easily restore the water balance of the eyes and relieve tension. Due to the concentration of attention, the person stops blinking, because of this, the mucous membrane of the eye dries up and there is a burning sensation, pain. You will get the impression that there is sand in the eyes.Take off every 30-40 minutes from the monitor and look at the foreign objects that surround you.

    Buy special drops that are almost identical in composition to a human tear. They will help moisturize the retina and relieve irritation. Drop such drops several times a day if you are constantly sitting at the computer.

    Treatment of eye inflammation.

    Treatment of eye inflammation, as a rule, begins with a visit to a doctor (ophthalmologist), who will determine the cause of the disease, as well as select the treatment appropriate for the disease.Thus, the correct treatment for eye inflammation is chosen depending on the cause that caused this inflammation. If a foreign body gets into the eye, the doctor will remove it and prescribe medications that prevent infection from entering. If eye inflammation is caused by contact lenses, then it is recommended to start treatment with a temporary refusal to wear them.

    In the event that the eyes become inflamed, as a result of infection, antimicrobial drugs are usually prescribed.Well, when eye inflammation is of a viral nature, special drugs are used that are aimed at fighting viruses. If there is an allergic inflammation of the eyes, then antiallergic drugs are recommended. It should be noted that during the treatment of eye inflammation, you should protect your eyes from ultraviolet rays (for this, you should choose glasses with a special coating that absorbs ultraviolet light).

    90,000 Diagnostics and treatment of ethmoiditis in Moscow, price

    Etmoiditis – inflammation of the mucous membrane of ethmoid cells.Allocate acute and chronic forms of the disease.

    Causes and pathogenesis of ethmoiditis

    The disease can be caused by viruses, bacteria – staphylococci, streptococci, etc.

    Causes of acute ethmoiditis – as a rule, rhinitis, ARVI, influenza, inflammation of other paranasal sinuses. Risk factors for the development of ethmoiditis are curvature of the nasal septum, vasomotor and allergic rhinitis, hypertrophy of the turbinates, nasal polyps, adenoids in children. The inflammatory process affects the anterior and posterior cells of the ethmoid bone.Possible damage to the maxillary, frontal, sphenoid sinuses. Inflammation of the mucous membrane leads to its swelling and swelling, which becomes the cause of impaired drainage.

    In most cases, the infection enters the rhinogenic route, less often with the blood stream or as a result of trauma.

    Provided a general decrease in immunity, inflammation of other paranasal sinuses, and the absence of treatment, the disease can become chronic. Viruses and bacteria have a destructive effect not only on the mucous membrane, but also on the bone tissue of the ethmoid bone.

    Symptoms of ethmoiditis

    Symptoms of acute ethmoiditis – nasal congestion, difficulty in nasal breathing, decreased sense of smell, a feeling of distention in the nasal cavity, profuse mucous or purulent discharge from the nose, headache, discomfort and a feeling of distention in the region of the bridge of the nose, the inner edge of the orbit. Also, patients complain of fever, weakness, malaise.

    Chronic ethmoiditis is characterized by nasal congestion, pain in the bridge of the nose, the inner edge of the orbit, headaches, minor mucopurulent nasal discharge, impaired smell, the formation of polyps and, as a result, severe difficulty in nasal breathing.The patient’s general condition is deteriorating. With an exacerbation of the disease, the clinical picture is identical to acute ethmoiditis.

    Diagnosis of ethmoiditis at the Clinical Hospital on Yaza

    Specialists of the Clinical Hospital on Yaza use an integrated approach when making a diagnosis.

    We carry out the following studies:

    • bacteriological examination of discharge from the nasal cavity
    • rhinoscopy
    • computed tomography of the nasal cavity and paranasal sinuses
    • Radiography
    • endoscopic examination of the nasal cavity and nasopharynx

    These methods make it possible to determine the state of the mucous membrane of the nasal cavity and ethmoid labyrinth cells, the prevalence of the inflammatory process, the structural features of the paranasal sinuses and the nasal septum, identify swelling, determine the nature and volume of exudate in the ethmoid cells, as well as the degree of polyposis changes in the mucous membrane and the presence of polyps in nasal cavity.

    Treatment of ethmoiditis at the Clinical Hospital on Yaza

    When detecting ethmoiditis, our specialists carry out both conservative and surgical treatment.

    Conservative treatment is indicated in the acute form of the disease, as well as in exacerbation of chronic ethmoiditis. For the unhindered outflow of the discharge by removing the edema of the mucous membrane, the patient is prescribed topical vasoconstrictor drugs in the form of drops or spray, as well as broad-spectrum antibiotics, mucolytic drugs, pain relievers, at elevated temperatures – antipyretic drugs.

    In case of a severe course of the disease in the absence of the effect of drug therapy or a chronic form of sphenoiditis, surgical treatment is necessary – surgical opening of the cells of the ethmoid labyrinth and the patient is recommended an endoscopic operation.

    The most effective and less traumatic method is the endoscopic method. The surgeon has a good view of the operating field on the monitor and, using special endoscopic instruments, performs manipulations in the narrow anatomical space of the middle sections of the nasal cavity at the base of the skull.In case of chronic ethmoiditis and the presence of polyps in the nasal cavity, we use a modern apparatus for removing polyps – a shaver. It allows you to remove polyps with an accuracy of tenths of a millimeter without damaging healthy tissues and structures of the nasal cavity.

    The use of “breathing” tampons and silicone stents relieves our patients from unpleasant sensations in the postoperative period. The low invasiveness and bloodlessness of endoscopic surgery using a shaver allows patients to quickly return to their usual rhythm of life after spending only one day in the hospital.

    Prices for services You can look at the price list or specify by phone, indicated on the website.

    Orenburg Regional Clinical Hospital

    We are glad to welcome you on the pages of the official website of our hospital!

    The State Autonomous Healthcare Institution “Orenburg Regional Clinical Hospital” (GAUZ “OOKB”) has been a leader in health care in the region for over 140 years. Thanks to the activities of the staff of our institution and respect for the traditions laid down by our predecessors, we continue to improve the quality and efficiency of medical care.A powerful material and technical base, high human potential, the use of effective methods of diagnosis and treatment make it possible to provide specialized, including high-tech, medical care to the population of the Orenburg region and other regions.

    Hospital capacity is 933 beds. Since 2007, GAUZ “OOKB” has been included in the list of institutions providing high-tech medical care under federal quotas. Since January 10, 2013, a regional vascular center for 120 beds has been operating in our hospital, and on January 1, 2014, a regional nephrological center began operating on the basis of the nephrology department.

    The capacity of the consultative polyclinic is 600 visits per shift, admission is carried out in 28 specialties.

    Annually over 24 thousand patients are treated in inpatient departments of the hospital.

    In addition, the specialists of the Emergency Consultative Medical Aid Department provide emergency assistance in case of complicated diseases, injuries, and, if necessary, perform surgical interventions, every day, with road and air ambulance trips to the site.

    Of the 404 doctors working in the hospital, 4 have a doctorate in medical sciences, 33 are candidates of medical sciences, 159 doctors have the highest qualification category. Of the 719 paramedical workers, 249 have the highest qualification category, 26 nurses have higher nursing education. 7 doctors of our hospital bear the honorary title “Honored Doctor of the Russian Federation”, 6 – the honorary title “Honored Health Worker of the Russian Federation”. The badge “Excellence in Health Care” was awarded to 31 doctors and 6 paramedical workers.32 employees of the hospital have a certificate of honor from the Ministry of Health of the Russian Federation, and a certificate of honor from the Ministry of Health of the Orenburg region – 94.

    The joint work of the regional clinical hospital and the Orenburg State Medical University (institute, academy) for the training of high-level medical personnel has more than 70 years of history. At present, five departments of the Orenburg State Medical University are working on our base.

    For the training of middle-level personnel, an evening department and a department of postgraduate training of specialists with secondary medical and pharmaceutical education of the regional medical college operate on the basis of the institution.

    Our institution is licensed for all types of medical activities, including work and services in the provision of high-tech medical care in 14 specialties.

    We hope that our site will not only help you find the information you need, but also leave you with the most pleasant impressions.

    Chief Physician

    GAUZ “Orenburg Regional Clinical Hospital”

    A. V. Redyukov


    Solving together

    Waste garbage not removed, hole in the road, lantern off? Faced a problem – report it!

    Report an issue

    The frequency of ophthalmologic manifestations of granulomatosis with polyangiitis (Wegener’s) and their relationship to systemic diseases | Ismailova

    Aim.To estimate the frequency of lesions in the organ of vision in granulomatosis with polyangiitis (GPA) (Wegener’s) and to determine their relationship to systemic diseases. Subjects and methods. The retrospective study enrolled 218 patients followed up at the E.M. Tareyev Clinic of Nephrology, Internal and Occupational Diseases, with a diagnosis of GPA. The frequency and association of ophthalmic manifestations with systemic involvement were statistically analyzed using PASW Statistics 18. Results.The organ of vision was impaired in 48.1% of the patients with GPA. The most common manifestations were orbital space-occupying lesion (22.9%), conjunctivitis / episcleritis (14.7%), dacryocystitis (6.0%), and scleritis (4.6%). Orbital space-occupying lesions occurred more frequently in the local type of the disease (p = 0.0003), and, on the contrary, the involvement of the conjunctiva and eyeball was seen in patients with the systemic types of GPA (p = 0.02). Conclusion. The findings may suggest that the orbital lesion is an independent manifestation of GPA, which develops more commonly in its local type.Conjunctivitis / episcleritis is, on the contrary, more frequently seen in the active phase of the disease and generally in the involvement of other organs and systems.

    GPA – granulomatosis with polyangiitis URT – upper respiratory tract ANCA – antineutrophil cytoplasmic antibodies MPO – myeloperoxidase PR-3 – proteinase-3 Granulomatosis with polyangiitis (GPA), formerly known as Wegener’s granulomatosis, is a rare disease related to the group of systemic vasculitis antineutrophilic cytoplasmic antibodies (ANCA), with a predominant lesion of small-caliber vessels.The clinical manifestations of HPA are very diverse. They include damage to the upper respiratory tract and the organ of hearing in the local variant; in generalized disease, the lungs and kidneys are involved in the pathological process [1-4]. In addition, the disease may be accompanied by the involvement of the osteoarticular apparatus (arthritis, myalgia, etc.), the gastrointestinal tract, the cardiovascular system, as well as the central and peripheral nervous systems. Damage to the organ of vision in HPA occurs in 29–58% of patients and can significantly reduce their quality of life, leading to severe cosmetic defects, loss of vision, loss of an eye, and complications are potentially life-threatening [3–8].Among the ophthalmic manifestations, conjunctivitis, scleritis, granulomatous inflammation of the orbit, and dacryoadenitis are described. Less common are corneal lesions (stromal, or peripheral, ulcerative keratitis), ischemic optic neuropathy, and isolated cases of retinal lesions are described. Research is limited to determining the frequency and does not allow to properly characterize the relationship of certain manifestations with each other. The purpose of our study was not only to assess the frequency of various ophthalmic manifestations, but also to identify the relationship with the variant of the disease, as well as various systemic manifestations of HPA.Materials and Methods Statistical processing of the data of 218 patients with HPA who were treated at the Clinical Clinical Hospital No. 3 of the First Moscow State Medical University was carried out. THEM. Sechenov from 2010 to 2014. A prerequisite for inclusion in the study was the presence of an examination by an ophthalmologist, confirming or excluding damage to the organ of vision. Of the 218 patients included in the study, 143 (65.6%) were women and 75 (34.4%) were men; thus the male to female ratio was 1: 1.9. The age of the patients ranged from 16 to 86 years, with a median of 53 years.The main peak of the incidence occurred at the age of 50-55 years. There was also a slight increase in morbidity at the age of 20-30. The median time to diagnosis was 6.5 months (range 0 to 276 months). Thus, only 50% of patients were diagnosed within the first half of the year. This period is due to the complexity of diagnosing the disease, the lack of specific signs and alertness among doctors. The general clinical examination of patients was carried out on the basis of the Clinic of Nephrology, Internal and Occupational Diseases named after I.EAT. Tareeva. It included the collection of anamnesis, physical, laboratory and instrumental examination methods, consultations of related specialists – otorhinolaryngologists, neurologists, endocrinologists, pulmonologists, ophthalmologists and others, if necessary. The median follow-up period reached 65 months (from 3 months to 24.4 years). For statistical analysis, the criteria and parameters were calculated using the PASW Statistics 18 program. To characterize variables with a symmetric distribution, the arithmetic mean (expected mathematical) was calculated; to characterize variables with an asymmetric distribution, the median was calculated.When searching for the relationships of nominal variables, we used 2 × 2 contingency tables, the significance of differences was assessed using Fisher’s exact solution, the relationship was considered significant at p <0.05. To characterize the relationship with its reliability according to Fisher's criterion, the relative risks were calculated. Frequency of ophthalmic manifestations in patients with HPA Note. PUC - peripheral ulcerative keratitis; PION - anterior ischemic optic neuropathy; KOH - compression optic neuropathy.The prevalence of the pathological process was assessed by the median number of affected organs and organ systems in groups of patients, depending on the presence of one or another ophthalmological manifestation. Results Among 218 patients with various types of HPA included in the study, systemic variant, including early systemic and generalized, was diagnosed in 158 (72.5%), local - in 60 (27.5%). The diagnosis was confirmed morphologically in 146 (67%) patients. By localization, 61 (41.8%) underwent biopsy of the nasal cavity and upper respiratory tract (URT), 32 (21.9%) - orbits, 19 (11%) - lung, 10 (6.9%) - kidneys and 24 (16.4%) - other organs.Of 209 patients, analysis for ANCA to proteinase-3 (PR-3) was positive in 131 (62.6%), for ANCA to myeloperoxidase (MPO) - in 34 (16.2%). A negative result of the analysis for ANCA was in 51 (24.4%) patients, more often with a local variant of the disease. This is partly due to the examination performed against the background of immunosuppressive treatment when it is impossible to use bio-samples before starting therapy. In the group of patients with lesions of the organ of vision, ANCA analysis is available in 101 (96.2%) out of 105. Among them, ANCA to PR-3 was determined in 56.4%, ANCA to MPO - in 12.9%, i.e.That is, somewhat less frequently than in the general group. URT pathology occurred in 218 (94%) patients and included sinusitis, ulcerative necrotizing rhinitis, destructive rhinosinusitis with the formation of a saddle nose deformity, and subglottic laryngitis with the formation of laryngeal stenosis. The defeat of the organ of hearing was observed in 98 (45%) patients and was characterized by serous otitis media and purulent and / or destructive mastoiditis. Lung lesion was diagnosed in 136 (62.4%) cases, and in some patients it was asymptomatic, and changes were detected only by X-ray examination.The characteristic lesions of the lungs in GPA are infiltrates (granulomas), decay cavities, hemorrhagic alveolitis, pleurisy. Kidney damage was noted in 106 (48.6%) cases and was accompanied by the development of nephritic and / or nephrotic syndrome. Eight patients developed end-stage renal disease. In addition, joint damage was observed in 75 (34.4%) patients, muscles in 15 (6.9%), skin in 60 (27.5%), central and peripheral nervous system in 4 (1.8%) and 41 (18.8%) respectively.Among all patients, damage to the organ of vision was found in 105 (48.2%), in 12 (5.5%) it led to a pronounced decrease or loss of vision. The frequency of damage to the organ of vision did not differ significantly among men and women: in men in 49.3%, and in women in 47.6% of cases (p> 0.05). There was no reliable connection between the damage to the organ of vision and the involvement of other organs; when assessed by Fisher’s exact criterion, the frequency of damage to the organ of vision in the groups with or without the involvement of one or another organ or system of organs did not differ.The frequency of ophthalmic manifestations of the disease in the examined patients is presented in the table. When comparing groups depending on the variant of the disease (local / systemic), the local variant of lesion of the organ of vision was detected in 34 (56.7%) of 60, and among patients with systemic lesion – in 71 (44.9%) of 158 (p = 0.08) (Fig. 1). Fig. 1. The frequency of damage to the organ of vision, neoplasms of the orbit, damage to the eyeball, depending on the variant of the disease. The lesion of the orbit was one of the most frequent ophthalmic manifestations.There were both unilateral and bilateral masses of various localization, determined by the results of computed tomography and / or magnetic resonance imaging. In 16 (7.3%) patients, the lesion of the orbit began with the lacrimal gland with subsequent infiltration of tissue and extraocular muscles. Volumetric formations of the orbit were found significantly more often in the local variant of the disease (p = 0.0003) (see Fig. 1). The median number of organs and systems involved in the pathological process in patients with orbital neoplasm was 2, and in patients without orbital neoplasm – 4 (Fig.2). Fig. 2. Median number of affected organs and organ systems in patients, depending on the presence of damage to the organ of vision. Of the bony walls of the orbit, the most common destruction was medial (in 12, or 5.5%) in patients with destructive rhinosinusitis. In 2 (0.9%) cases, there were X-ray signs of destruction of the upper walls of the orbit. In 13 (6%) patients, chronic dacryocystitis was diagnosed as a result of necrotizing ulcerative or destructive rhinosinusitis. Dacryocystitis was observed equally often in patients with and without URT lesions, but in other groups – more often in the absence of lesions.The median number of interested organs and systems was 3 in both comparison groups (see Fig. 2). The defeat of the conjunctiva and the eyeball, on the contrary, was more common in patients with systemic variants of HPA (see Fig. 1) and included such nonspecific manifestations as conjunctivitis, episcleritis, scleritis, including necrotizing, inflammation of the choroid of the eye (iritis, iridocyclitis, uveitis), as well as thrombotic vascular lesions of the retina. Due to the ambiguity in the interpretation of retrospective data in our study, patients with conjunctivitis and episcleritis were combined into one group and accounted for 14.7% of all patients.At the same time, conjunctivitis / episcleritis was detected only in the active phase of the disease; the median number of involved organs and systems in groups of patients with or without conjunctivitis / episcleritis was 4 and 3, respectively (see Fig. 2). Scleritis in GPA has a necrotizing character and was noted in 10 (9.5%) patients, of whom 9 had a systemic variant of HPA, and 1 had a local variant. A small number of observations makes it impossible to talk about the presence of reliable connections of scleritis with damage to other organs and systems, but the trend is beyond doubt.The median number of involved organs and systems in patients with scleritis was 4, and in patients without scleritis – 3 (see Fig. 2). Retinal involvement is an atypical manifestation of HPA. We observed 5 (2.3%) patients with thrombotic lesions of the retinal vessels or the development of nonspecific chorioretinitis. Retinal damage occurred only in patients with generalized HPA, i.e., with damage to the upper respiratory tract, auditory organ, lungs and kidneys. There were no reliable connections with damage to other organs and systems due to the small number of observations, however, when assessing the median of the number of affected organs and systems, it was revealed that in patients with retinal damage, a much larger number of organs and systems are involved in the pathological process than in patients without damage. retina, – 6 and 3, respectively (see.fig. 2). Discussion The results of studies of the frequency of damage to the organ of vision in HPA are very different. The complexity of diagnosis, the nonspecificity of the clinical picture, the lack of generally accepted diagnostic criteria, the different prevalence of the disease depending on the climatic zone, as well as the different ratio of disease variants depending on the specialization of the clinics where the study is carried out, in combination with a small number of cases (the rarity of the disease) explain such pronounced statistical differences.In our study, we examined a large group of patients observed in the rheumatology department, which made it possible to most accurately characterize the frequency and likelihood of damage to the organ of vision in patients with HPA. This is the first study of this kind in Russia. The incidence of ocular damage in HPA was 48.2% (105 out of 218), which is comparable to the results of published worldwide studies (29–58%) [9–13]. The most common ophthalmic manifestations were orbital lesions (22.9%) and conjunctivitis / episcleritis (14.7%).In addition, cases of damage to other parts of the adnexa (lacrimal duct: stenosis, dacryocystitis), retina, choroid (uveitis), anterior ischemic optic neuropathy and others have been reported, but they were rare. In the literature, damage to the orbit is described in 6.7-12.9% of cases [10-16]. In our study, an orbital mass was diagnosed in 50 (22.9%) patients. Perhaps such a high percentage of eye socket lesions can be explained by the availability of special diagnostic methods (including computed tomography) and well-established continuity between doctors of different specialties (in particular, ophthalmologists and rheumatologists), as well as the recently increased share of local variants [6].The literature reports that episcleritis and conjunctivitis are the most common ophthalmic manifestations of HPA. So, according to different authors, conjunctivitis occurs in 15.9-17.8% [10, 15], and episcleritis – in 14.3-75% of patients with HPA [10, 14]. In our opinion, such a spread in frequency can be explained by the non-specificity of this manifestation, as well as by various criteria for making a diagnosis. As a rule, conjunctivitis / episcleritis are signs of active systemic inflammation and disappear without a trace by the time remission is achieved.Scleritis in HPA is of a necrotizing nature and is a potentially dangerous condition for the eye, namely, it can lead to perforation of the eyeball with prolapse of the inner membranes. In the literature, the incidence of scleritis is 0.9–74% [10, 11]. We observed 10 (9.5%) patients with necrotizing scleritis. It is important to note that careful observation of such patients should be carried out even during the period of remission of the disease due to the high risk of complications. Retinal damage is an atypical manifestation of HPA; in the literature, there are mainly descriptions of individual cases, and only in the largest studies the frequency of 0.7-1.7% is indicated [10, 11].Our study included 5 patients with retinal pathology associated with HPA. All had a generalized variant of the disease. One of the pressing issues is the relationship of ophthalmological manifestations with systemic ones. There is still no clear understanding of the existence of such a connection. The most significant study of the relationship between damage to the organ of vision and systemic manifestations of HPA was carried out by S. Harper et al. [5], however, scientists considered only patients with damage to the organ of vision and did not separate them depending on the type of lesion, while it is a comparison with the control group (without damage to the organ of vision) that would make it possible to conclude about the likelihood of damage to the organ of vision, depending on systemic manifestation.Conclusion Damage to the organ of vision in GPA occurs in 48.2% of patients, while the orbit (22.9%) and the surface of the eyeball (conjunctivitis / episcleritis – 14.7%) are most often involved in the pathological process. Based on the results of the study, it can be concluded that the volumetric formation of the orbit in most cases serves as an independent manifestation of HPA, which is observed more often with a local variant of the disease. Damage to the eyeball and conjunctiva, on the contrary, is more common in systemic variants and, as a rule, correlates with the activity of systemic inflammation.The authors declare that they have no conflicts of interest.

    1. V.A. Nasonova, E.L. Nasonov (ed.). Systemic vasculitis. In rn .: Rational pharmacotherapy of rheumatic diseases: A guide for practicing physicians. M .: Litterra Publishing House; 2003.
    2. Beketova T.V., Nasonov E.L., Semenkova E.N., Kozlovskaya L.V., Aleksandrova E.N., Tishchenko V.A., Samsonov M.Yu., Baranov A.A. Immunological methods for assessing the activity of necrotizing vasculitis (Wegener’s granulomatosis and microscopic polyarteritis) with kidney damage. Ter. archive. 1996; 68 (6): 50-52.
    3. Grusha Ya.O., Ismailova D.S., Novikov P.I., Abramova Yu.V. Ophthalmic manifestations of granulomatosis with polyangiitis (Wegener’s granulomatosis). Ter. archive. 2015; 12 (87): 111-116. doi: 10.17116 / terarkh30158712111-116
    4. Beketova T.V., Nasonov E.L. Current views on the classification and treatment of systemic vasculitis associated with antineutrophilic cytoplasmic antibodies: results of 2011.Ter. archive. 2012; 84 (5): 68-74.
    5. Harper SL, Letko E, Samson CM, Zafirakis P, Sangwan V, Nguyen Q, Uy H, Baltatzis S, Foster CS. Wegener’s granulomatosis: the relationship between ocular and systemic disease. J Rheumatol. 2001; 28 (5): 1025-1032. doi: 10.1016 / S0002-9394 (01) 01122-9
    6. P.I. Novikov, S.V. Moiseev, E.I. Kuznetsova, E.N. Semenkova, N.A. Mukhin Changes in the course of the disease and prognosis of granulomatosis with polyangiitis (Wegener): results of 40-year follow-up.Clinical pharmacology and therapy. 2014; 1: 32-37.
    7. Tan LT, Davagnanam I, Isa H, Taylor SR, Rose GE, Verity DH, Pusey CD, Lightman S. Clinical and Imaging Features Predictive of Orbital Granulomatosis with Polyangiitis and the Risk of Systemic Involvement. Ophthalmology. 2014; 121 (6): 1304-1309. doi: 10.1016 / j.ophtha.2013.12.003
    8. Julia U Holle, Christopher Voigt, Marcus Both, Konstanze Holl-Ulrich, Bernhard Nolle, Martin Laudien, Frank Moosig, Wolfgang L.Gross Orbital masses in granulomatosis with polyangiitis are associated with a refractory course and a high burden of local damage. Rheumatology (Oxford). 2013; 52 (5): 875-882. doi: 10.1093 / rheumatology / kes382
    9. Abdou NI, Kullman GJ, Hoffman GS, Sharp GC, Specks U, McDonald T, Garrity J, Goeken JA, Allen NB. Wegener’s granulomatosis: survey of 701 patients in North America. Changes in outcome in the 1990s. J Rheumatol. 2002; 29 (2): 309-316.
    10. Rothschild PR, Pagnoux C, Seror R, Brézin AP, Delair E, Guillevin L.Ophthalmologic manifestations of systemic necrotizing vasculitides at diagnosis: a retrospective study of 1286 patients and review of the literature. Semin Arthritis Rheum. 2013; 42 (5): 507-514. doi: 0.1016 / j.semarthrit.2012.08.003
    11. Bullen CL, Liesegang TJ, McDonald TJ, DeRemee RA. Ocular complications of Wegener’s granulomatosis. Ophthalmology. 1983; 90 (3): 279-290.
    12. Hoffman GS, Kerr GS, Leavitt RY, Hallahan CW, Lebovics RS, Travis WD, Rottem M, Fauci AS.Wegener granulomatosis: an analysis of 158 patients. Ann Intern Med. 1992; 116 (6): 488-498.
    13. Fauci AS, Haynes BF, Katz P, Wolff SM. Wegener’s granulomatosis: prospective clinical and therapeutic experience with 85 patients for 21 years. Ann Intern Med. 1983; 98 (1): 76-85.
    14. Watkins AS, Kempen JH, Choi D, Liesegang TL, Pujari SS, Newcomb C, Nussenblatt RB, Rosenbaum JT, Thorne JE, Foster CS, Jabs DA, Levy-Clarke GA, Suhler EB, Smith JR.