Significant History

• Recent and rapid onset of symptoms
  
• Occasional fever and leukocytosis

Laboratory Tests

• Complete blood count (CBC) with differential: Leukemia, lymphoma
  
• Culture any discharge on blood (most bacteria), chocolate (Haemophilus sp., Neisseria gonnorrhoeae), and thioglycollate agar (aerobic and anaerobic bacteria)
  
• Computed tomography (CT), magnetic resonance imaging (MRI), or orbital ultrasound: Delineates extent of tissue involvement, especially indicated with proptosis, downward displacement of the globe, limited EOM motility, or decreased vision
  
• Blood titers for appropriate suspected viral etiologies: Mumps, Epstein-Barr, HIV
  
• Lacrimal gland biopsy: Atypical presentations or lack of appropriate treatment response

The Treatment

Broad-spectrum antibiotics should be initiated until cultures, titers, and laboratories can better direct therapy. Appropriate choices would include

• Amoxicillin/clavulanate 500/125 mg twice daily
  
• Cephalexin 250 to 500 mg four times daily
  
• Penicillin/cephalosporin sensitive: Azithromycin: 500 mg daily for 3 days or 250 mg twice a day for 1 day, then once daily for 4 days
  
• Severe presentations or pediatric cases: Referral for possible hospitalization with intravenous (IV) drug therapy

Viral Etiologies

• Cool compresses
  
• Topical lubricants
  
• Appropriate analgesic as needed
  
• Suspected herpetic: Acyclovir 400 mg five times a day (simplex) or 800 mg five times a day (zoster), Valacyclovir 1,000 mg three times a day, Famciclovir 500 mg three times a day

Chronic/Granulomatous Dacryoadenitis

Andrew Mick

ICD-9: 375.02

     THE DISEASE

The Patient

Clinical Symptoms

• Chronic or recurrent swelling and redness of the upper lid
  
• Bilateral cases more common than with acute dacryoadenitis
  
• Occasional pain and double vision

Clinical Signs

• Localized mass in the lateral upper eyelid area
  
• Lacrimal gland enlarged and inflamed
  
• Proptosis, downward displacement of the globe, or EOM disruption in severe cases

Chronic/granulomatous dacryoadenitits has a variety of etiologies: Inflammatory (sarcoidosis, Wegener’s granulomatosis, Crohn’s disease), infectious (tuberculosis, mumps, HIV, syphilis), and neoplastic (leukemia, lymphoma)

Significant History

• Symptoms/signs of systemic infectious, inflammatory, or neoplastic disease

Laboratory Tests

• Suspected leukemia/lymphoma: CBC with differential
  
• Suspected sarcoidosis: Chest x-ray, serum angiotensin-converting enzyme (ACE)
  
• Suspected Wegener’s granulomatosis: Sinus/chest x-ray, antineutrophil cytoplasmic antibody (ANCA) test, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP)
  
• Suspected Crohn’s disease: History of characteristic symptoms (weight loss, chronic diarrhea, abdominal pain), hematocrit/hemoglobin (gastrointestinal bleeding), ESR, x-ray with barium, abdominal CT
  
• Suspected tuberculosis: Purified protein derivative with anergy panel
  
• Suspected syphilis: Rapid plasma reagin or Venereal Disease Research Laboratory and fluorescent treponemal antibody absorption
  
• Suspected HIV: Serology
  
• CT, MRI, or orbital ultrasound: Delineates extent of tissue involvement, especially indicated with proptosis, downward displacement of the globe, limited EOM motility, or decreased vision.
  
• Lacrimal gland biopsy

The Treatment

• Treatment will depend on the underlying cause of the chronic dacryoadenitis and will involve referral to appropriate subspecialist for evaluation.

Dacryocystitis

Andrew Mick

ICD-9: 375.30

     THE DISEASE

Pathophysiology

The disorder is characterized by acute or chronic infection or inflammation of the lacrimal sac. Complete or partial obstruction of the nasolacrimal duct is often the precipitating event prior to infection. Obstruction can result from developmental anomalies, nasal/sinus disease, trauma, neoplasm, dacryolith formation (lacrimal calculi), or systemic inflammatory disease.

Etiology

Acute (ICD-9: 375.32)

• Lacrimal stenosis that results in secondary acute and severe infection
  
• Commonly cultured bacteria are Gram positive (Staphylococcus aureus, Staphylococcus epidermidis, Streptococcus pneumoniae) and Gram negative (Pseudomonas aeruginosa, Escherichia coli)
  
• Rarely anaerobic bacteria (Actinomyces israelii, Propionibacterium acnes)
  
• Rarely fungi (Aspergillus sp., Candida sp.)

Chronic (ICD-9: 375.42)

• Partial or complete blockage of the nasolacrimal system that results in secondary chronic infection
  
• Commonly cultured pathogens include Gram-positive bacteria (Staphylococcus sp., Streptococcus sp.), coagulase-negative staphylococci, Gram-negative bacteria (P. aeruginosa, E. coli), and fungi (Aspergillus sp., Candida sp.)

The Patient

Clinical Symptoms

Acute

• Pain, redness, and swelling around the lacrimal sac
  
• Tearing and discharge
  
• Occasional fever

• Tearing may be the only symptom in many cases
  
• Occasional swelling around the lacrimal sac
  
• Discomfort with local digital pressure

Clinical Signs

Acute

Canaliculitis

Andrew Mick

ICD-9: 375.31—ACUTE CANALICULITIS, LACRIMAL

ICD-9: 375.41—CHRONIC CANALICULITIS

     THE DISEASE

Pathophysiology

The disorder is characterized by infection or inflammation of the canaliculi.

Etiology

Infectious agents include bacteria (A. israelii, Propionibacterium propionicum), fungi (Candida sp., Aspergillus sp.), and viruses (Herpes simplex). Canaliculitis is rarely associated with intracanalicular punctal plug occlusion.

The Patient

Clinical Symptoms

• Irritation, redness, and swelling over medial portion of eyelids
  
• Tearing and discharge

Clinical Signs

• Mucopurulent discharge or concretions expressed from punctum
  
• Concretions felt while probing canaliculus
  
• Conjunctivitis more severe nasally
  
• Erythematous area around punctal openings
  
• Periocular skin vesicles (herpes simplex)

Demographics

Canaliculitis can affect people of all ages but is more common in elderly populations.

Significant History

• Chronic/recurrent conjunctivitis
  
• Epiphora
  
• History of herpetic eye disease

Laboratory Tests

• Culture any discharge from punctum on blood (all bacteria), chocolate (children: Haemophilus sp.), thioglycollate (aerobic and anaerobic bacteria), and Sabouraud’s (fungi) agar

The Treatment

• Cultures positive for bacteria: Polymyxin B/trimethoprim solution four times a day or as directed by cultures
  
• Cultures positive for fungus: Natamycin 5% suspension four times a day
  
• Suspected herpetic infection: Trifluridine 1% solution four times a day
  
• Removal of debris in canaliculus with irrigation
  
• Canaliculotomy or snip punctoplasty may be indicated in nonresponsive canaliculitis

Epiphora

Andrew Mick

ICD-9: 375.20

     THE DISEASE

Pathophysiology

• Dry eye or other secondary causes of reflex hypersecretion of tears
  
• Blockage within the lacrimal drainage apparatus or punctal malposition
  
• Secondary hypersecretion of the lacrimal gland due to mechanical effects
  
• Primary hypersecretion of the lacrimal gland

Etiology

Clinical Signs

• Negative Jones I or II tests
  
• Asymmetric dye disappearance test
  
• Increased lacrimal tear lake
  
• Lid, punctum, caruncle abnormalities
  
• Tender swollen lacrimal gland or sac area
  
• Expression of purulent material from the punctum

Demographics

Epiphora can present in all age groups.

Significant History

• Persistent tearing
  
• Recurrent sinusitis or dacryocystitis
  
• Swelling or pain over lacrimal sac
  
• History of facial trauma or lid surgery

Laboratory Tests

• Culture any discharge if infectious etiology is suspected on blood (all bacteria), chocolate (children: Haemophilus sp.), thioglycollate (aerobic and anaerobic bacteria), and Sabouraud’s (fungi) agar
  
• Suspected thyroid disease: Serology for T3, T4, TSH
  
• Suspected sarcoidosis: Chest x-ray, serum ACE
  
• Suspected Wegener’s granulomatosis: Sinus and chest x-ray, ANCA test, ESR, CRP
  
• Suspected Sjögren’s syndrome: Consistent history (dry mucus membranes, enlarged salivary, or parotid glands), ESR, CBC, rheumatoid factor, antinuclear antibodies
  
• Dacryocystography (DCG)
  

  1. Conventional DCG: Contrast medium is passed through canaliculus and nasolacrimal system and imaged with CT, sequential radiographic images, or fluoroscopy

  
  

  2. Magnetic Resonance DCG: Dilute contrast medium is used and ionizing radiation is avoided

  
  
• CT: Axial and coronal views allow visualization of bony lacrimal canal, nasal cavity, and sinuses. Indicated with history of trauma and sinus surgery or concern about the presence of a tumor

Other Diagnostic Tests

Punctal Malposition

ICD-9: 375.51

• Blepharoplasty: When ectropion or entropion is leading to malposition of the punctum and subsequent epiphora
  
• Carunculectomy: When underlying cause of punctal malposition is megalocaruncle

Congenital Obstruction

ICD-9: 375.55 or 743.65

• Treat any suspected infection
  
• Massage lacrimal sac from the common canalicular junction down to the ampulla: Technique is best accomplished while feeding the infant, ten strokes four times a day, most obstructions spontaneously resolve within the first year
  
• Lacrimal probing between 6 and 12 months of age: Probing after 12 months decreases success rate, probing before 6 months carries inherent risks of anesthesia
  
• Balloon dacryocystoplasty (DCP), silicone tube intubation, or DCR:
  

  1. Children who do not respond to lacrimal massage and probing

Acquired Obstruction

ICD-9: 375.56

While commonly referred to as simply dry eye, any abnormality to the composition or quantity of tears, disruption of the normal eyelid anatomy, or dysfunction of the blink mechanism can result in tissue damage and inflammation. The surface epithelium and tear film of patients with ocular surface disease show unique characteristics. There is an increase of the tear osmolarity as the deficiency of the aqueous component concentrates the tear film. The increased osmolarity and overall dryness results in damage to the cornea and conjunctiva and elicits an inflammatory response. The role of inflammation is evidenced by an increased number of lymphocytes and inflammatory cytokines in the tears of patients with ocular surface disease and is the basis behind the usage of topical steroidal and immunosuppressive therapies in dry eye patients.

Etiology

Ocular surface disease can be classified into two main groups that have different etiologies but often have overlap in the final injury and inflammation pathways. These two categories are evaporative tear loss and aqueous deficiency.

Evaporative Tear Loss

The main cause of evaporative tear loss is blockage or a deficiency in the production of the normal lipid layer by the meibomian glands. With the loss of the stabilizing lipid layer, the aqueous component of the tear film is lost at a higher rate. Meibomian gland dysfunction can occur in isolation but often accompanies dermatologic disorders such as acne rosacea (see “Ocular Rosacea”) and seborrheic dermatitis. Staphylococcal and seborrheic blepharitis (see “Bacterial Blepharitis”/“Meibomianitis”) also can influence the stability of the tear film by producing toxins and lipases that irritate the corneal epithelium and induce an inflammatory response. The lipid layer can also be influenced by the placement of a contact lens into the tear film, abnormalities in the blink mechanism, or prolonged exposure secondary to disrupted lid anatomy.

Aqueous Deficiency

This form of ocular surface disease is primarily caused by a decrease in the secretion from the primary and accessory lacrimal glands and subsequent deficiency in the aqueous component of the tear film. Classically, this condition is caused by Sjögren’s syndrome, but other etiologies exist.

Sjögren’s Syndrome Sjögren’s syndrome is a generalized systemic autoimmune disease characterized by lymphocytic infiltration of the exocrine glands. In the primary form, the glands throughout the body are affected, resulting in keratoconjunctivitis sicca, xerostomia (dry mouth), and dryness to other mucus membranes including the nose and vagina. Secondary Sjögren’s syndrome has the same signs in addition to a systemic autoimmune disorder (see Sjögren’s syndrome).

Non-Sjögren’s Syndrome Other less common causes of decreased aqueous layer production by the lacrimal glands exist. Disruption of the neuronal secretion control can occur after surgical procedures such as laser-assisted in situ keratomileusis. Damage of the accessory conjunctival glands and ducts of the primary gland can result from scarring processes in disorders such as trachoma, ocular cicatricial pemphigoid, Stevens-Johnson’s syndrome, and chemical burns. Infiltrative diseases, such as sarcoidosis and lymphoma, can result in destruction of the glands. Systemic medications such as oral contraceptives, β-blockers, antihistamines, tricyclic antidepressants, and benzodiazepines can depress aqueous tear production as well.

Clinical Symptoms

• Foreign body sensation
  
• Gritty, burning, or soreness of the eyes
  
• Red eyes
  
• Photophobia
  
• Discharge on the lashes
  
• Symptoms exacerbated by wind, arid environments, and air conditioning

Clinical Signs

• Conjunctival injection
  
• Punctate epithelial defects (concentrated inferiorly and in the interpalpebral zone)
  
• Decreased height of inferior tear meniscus
  
• Mucus debris in the tear film
  
• Increased blink rate
  
• Decreased TBUT
  
• Fluorescein and vital dye staining
  
• Positive Schirmer’s test

Demographics

The incidence of dry eye increases with age and is extremely common in the elderly. The condition is more prevalent in women, especially in the postmenopausal period. Dry eye is a common sequela of a variety of autoimmune diseases. Those people who live in dry environments or whose work requires prolonged near or computer tasks are often afflicted. Contact lens wearers also have a higher rate of dry eye symptoms.

Significant History

• Bilateral (may be asymmetrical)
  
• Long-standing
  
• Symptoms often worse in the morning
  
• Symptoms exacerbated by smoke, wind, heat, low humidity, prolonged near or computer work
  
• Taking systemic β-blockers, antihistamines, tricyclic antidepressants, benzodiazepines, or oral contraceptives
  
• Additional systemic symptoms that might signal the presence of Sjögren’s syndrome or other autoimmune disease

Aqueous Deficiency

In this disorder, the main problem is a deficiency in the aqueous component of the tear film. Consequently, the treatment focuses on replacing lost tears, conserving present tears, and controlling the secondary inflammation.

Mild

• Artificial tears four times a day (nonpreserved formulations are always preferred and should be used if more than four times a day dosing is required to relieve symptoms)
  
• Lubricating ophthalmic ointment at bedtime

Moderate