Sensory Disorders
CATARACT
Acataract is a gradually developing opacity of the lens or lens capsule. Light shining through the cornea is blocked by this opacity, and a blurred image is cast onto the retina. As a result, the brain interprets a hazy image. Cataracts commonly occur bilaterally, and each progresses independently. Exceptions are traumatic cataracts, which are usually unilateral, and congenital cataracts, which may remain stationary.
AGE ALERT
Cataracts are most prevalent in people older than age 70. The prognosis is generally good; surgery improves vision in 95% of affected people.Causes
Aging
Trauma, foreign body injury
Exposure to ionizing radiation or infrared rays
Exposure to ultraviolet radiation
Drugs that are toxic to the lens, such as prednisone, ergot alkaloids, dinitrophenol, naphthalene, phenothiazines, or pilocarpine
Genetic abnormalities
Infection such as maternal rubella during the first trimester of pregnancy
Maternal malnutrition
Metabolic disease, such as diabetes mellitus or hypothyroidism
Myotonic dystrophy
Uveitis, glaucoma, retinitis pigmentosa, or retinal detachment
Atopic dermatitis
Pathophysiology
Pathophysiology varies with each form of cataract. Congenital cataracts are particularly challenging. They may result from chromosomal abnormalities, metabolic disease, intrauterine nutritional deficiencies, or infections during pregnancy (such as rubella). Senile cataracts show evidence of protein aggregation, oxidative injury, and increased pigmentation in the center of the lens. In traumatic cataracts, phagocytosis of the lens or inflammation may occur when a lens ruptures. The mechanism of a complicated cataract varies with the disease process — for example, in diabetes, increased glucose in the lens causes it to absorb water.
Typically, cataract development goes through these four stages:
immature — partially opaque lens
mature — completely opaque lens; significant vision loss
tumescent — water-filled lens; may lead to glaucoma
hypermature — lens proteins deteriorate; peptides leak through the lens capsule; glaucoma may develop if intraocular fluid outflow is obstructed.
COMPLICATIONS
Vision loss
Signs and Symptoms
Gradual painless blurring and loss of vision
Milky white pupil
Blinding glare from headlights at night
Poor reading vision caused by reduced clarity of images
In central opacity — vision improves in dim light; as pupils dilate, patients able to see around the opacity
AGE ALERT
Elderly patients with reduced vision may become depressed and withdraw from social activities rather than complain about reduced vision.Diagnostic Test Results
Indirect ophthalmoscopy and slit-lamp examination show a dark area in the normally homogeneous red reflex.
Visual acuity test confirms vision loss.
Treatment
Phacoemulsification cataract extraction to remove lens but leave capsule in place:
phacoemulsification to fragment the lens with ultrasonic vibrations
aspiration of pieces
implantation of intraocular lens.
Extracapsular cataract extraction:
lens removed in one piece, capsule left intact
implantation of intraocular lens.
Intracapsular cataract extraction of entire lens and capsule:
rarely performed; may be necessary in trauma cases
intraocular lens placed in front of iris.
Laser surgery to restore visual acuity if a secondary membrane forms in the intact posterior lens capsule after an extracapsular cataract extraction
Discission (an incision) and aspiration possibly still used in children with soft cataracts
Contact lenses or lens implantation after surgery to improve visual acuity, binocular vision, and depth perception
 CATARACT |
CLEFT LIP AND CLEFT PALATE
Cleft lip and cleft palate — an opening in the lip or palate — may occur separately or in combination. Cleft lip and cleft palate are twice as common in males as in females; isolated cleft palate is more common in females.
Causes
Isolated birth defect: normal development of orofacial structures disrupted by a combination of genetic and environmental factors
Part of a chromosomal or Mendelian syndrome (cleft defects are associated with over 300 syndromes)
Exposures to specific teratogens during fetal development
CLINICAL TIP
A family history of cleft defects increases the risk that a couple may have a child with a cleft defect. Likewise, an individual with a cleft defect is at an increased risk to have a child with a cleft defect. Children with cleft defects and their parents or adult individuals should be referred for genetic counseling for accurate diagnosis of cleft type and recurrence risk counseling. Recurrence risk is based on family history, the presence or absence of other physical or cognitive traits within a family, and prenatal exposure information.Pathophysiology
Cleft deformities originate in the 2nd month of pregnancy, when the front and sides of the face and the palatine shelves fuse imperfectly. Cleft deformities usually occur unilaterally or bilaterally, rarely midline.
COMPLICATIONS
Speech difficulties
Failure to thrive related to feeding difficulties
Dentition problems
Otitis media
Hearing defects
Physical deformity and self-image issues
Signs and Symptoms
Cleft lip may range from a simple notch in the upper lip to a complete cleft from the lip edge through the floor of the nostril.
Cleft palate may be partial or complete, involving only the soft palate or extending from the soft palate completely through the hard palate into the upper jaw or nasal cavity.
CLINICAL TIP
The constellation of U-shaped cleft palate, mandibular hypoplasia, and glossoptosis (downward displacement and retraction of the tongue) is known as Pierre Robin sequence, or Robin sequence. It can occur as an isolated defect or one feature of many different syndromes; therefore, a comprehensive genetic evaluation is suggested for infants with Robin sequence. Because of the mandibular hypoplasia and glossoptosis, careful evaluation and management of the airway are mandatory for infants with Robin sequence.Diagnostic Test Results
Prenatal ultrasonography reveals the defect.
Treatment
Surgical Correction (Timing Varies)
Cleft lip:
within the first few days of life to make feeding easier
delay lip repairs for 2 to 8 months to minimize surgical and anesthesia risks, rule out associated congenital anomalies, and allow time for parental bonding.
Cleft palate:
performed only after the infant is gaining weight and is infection-free
usually completed by age 12 to 18 months
two steps: soft palate between ages 6 and 18 months; hard palate as late as age 5 years.
Speech Therapy
Palate is essential to speech formation (structural changes, even in a repaired cleft, can permanently affect speech patterns).
Hearing difficulties are common in children with cleft palate because of middle ear damage or infections.
CONJUNCTIVITIS
Conjunctivitis (also known as pinkeye) is characterized by hyperemia of the conjunctiva. The three main types of conjunctivitis are infectious, allergic, and chemical. This disorder usually occurs as a benign, self-limiting condition; it may also be chronic, possibly indicating degenerative changes or damage from repeated acute attacks. Epidemic keratoconjunctivitis is an acute, highly contagious viral conjunctivitis. Careful handwashing is essential to prevent the spread of conjunctivitis.
Causes
Infectious Conjunctivitis
Most commonly by:
bacterial — Staphylococcus aureus, Streptococcus pneumoniae, Neisseria gonorrhoeae, Neisseria meningitidis
chlamydial — Chlamydia trachomatis (inclusion conjunctivitis)
viral — adenovirus types 3, 7, and 8; herpes simplex 1; coxsackie; varicella zoster.
Allergic Conjunctivitis
Hypersensitivity to:
pollen, grass, unknown seasonal allergens (vernal conjunctivitis), or animals
topical medications, cosmetics, or fabrics
air pollutants or smoke
contact lenses or solutions
Chemical Conjunctivitis
Chemical reaction to:
environmental irritants (wind, dust, smoke, swimming pool chlorine)
occupational irritants (acids, alkalies)
Pathophysiology
Conjunctivitis is an inflammation of the conjunctiva, the transparent layer covering the surfaces in the inner eyelid (palpebral conjunctiva) and the front of the eyeball (bulbar conjunctiva). It usually begins in one eye and rapidly spreads to the other by contamination of towels, washcloths, or the patient’s own unwashed hands.
Vernal conjunctivitis (so called because symptoms tend to be worse in the spring) is a severe form of immunoglobulin E-mediated mast cell hypersensitivity reaction. This form of conjunctivitis is bilateral. It usually begins between ages 3 and 5 years and persists until about 10 years or age. It’s sometimes associated with other signs of allergy commonly related to pollens, asthma, or allergic rhinitis.
COMPLICATIONS
Corneal infiltrates
Corneal ulcers
Signs and Symptoms
Hyperemia of the conjunctiva
Discharge or tearing
Pain or photophobia (red flags, may indicate more serious conditions such as iritis, keratitis)
Acute Bacterial Conjunctivitis (Pinkeye)
Usually lasts only 2 weeks
Itching, burning, and the sensation of a foreign body in the eye
Crust of sticky, mucopurulent discharge (greenish) on the eyelids
N. gonorrhoeae Conjunctivitis
Itching, burning, or foreign body sensation
Profuse and purulent discharge
Viral Conjunctivitis
Copious tearing (epiphora), minimal exudate
Enlargement of the preauricular lymph node
In children, sore throat or fever if the cause is an adenovirus
Variable time course, depending on the virus:
some self-limiting, lasting 2 to 3 weeks
others chronic, producing a severe disabling disease
Diagnostic Test Results
In stained smears of conjunctival scrapings, the predominance of lymphocytes indicates viral infection; of neutrophils, bacterial infection; and of eosinophils, allergy-related infection.
Culture and sensitivity tests identify the causative organism (not routinely done).
Treatment
Bacterial conjunctivitis: topical appropriate broad-spectrum antibiotic
Viral conjunctivitis:
resist treatment; most important aspect of treatment is preventing transmission
herpes simplex infection generally responsive to treatment with trifluridine drops, vidarabine ointment, or oral acyclovir
secondary infection possibly prevented by sulfonamide or broad-spectrum antibiotic eyedrops
Vernal (allergic) conjunctivitis:
corticosteroid drops followed by cromolyn sodium
cold compresses to relieve itching
occasionally, oral or ophthalmic antihistamines
 CLINICAL MANIFESTATIONS OF CONJUNCTIVITIS |
CORNEAL ULCER
Corneal ulcers produce corneal scarring or perforation and are a major cause of blindness worldwide. They occur in the central or marginal areas of the cornea, vary in shape and size, and may be singular or multiple. Marginal ulcers are the most common form. Prompt treatment (within hours of onset) and referral to an ophthalmologist are imperative to prevent visual impairment.
Causes
Protozoan Infection
Acanthamoeba
Bacterial Infections
Staphylococcus aureus
Pseudomonas aeruginosa
Streptococcus viridans
Streptococcus (Diplococcus) pneumoniae
Moraxella liquefaciens
Viral Infections
Herpes simplex 1
Variola
Vaccinia
Varicella zoster
Fungal Infections
Candida
Fusarium
Acremonium
Other
Trauma
Exposure reactions to bacterial infections, toxins, trichiasis, entropion, allergens, or contact lenses
Vitamin A deficiency (xerophthalmia)
Fifth cranial nerve lesions (neurotropic ulcers)
Pathophysiology
The introduction of a causative factor, such as bacterial or herpes virus infection, trauma, or misuse of contact lenses, starts the process. This leads to epithelial destruction of the stoma with inflammation and tearing. Superficial ulceration results in photophobia, epiphora, foreign body sensation, discomfort (eye pain), and decreased visual acuity.
Deep ulcerations penetrate the epithelial layers of the eye, leading to perforation and allowing infection of deeper eye structures and extrusion of eye contents. Fibrous tissue can form during healing of deep ulcerations, leading to scarring and eventual opacity of the cornea. These processes can lead to partial or total vision loss.
COMPLICATIONS
Corneal scarring
Loss of the eye
Vision loss (permanent)
Signs and Symptoms
Pain aggravated by blinking
Foreign body sensation
Increased tearing
Photophobia
Pronounced visual blurring
Purulent discharge (with bacterial ulcer)
Diagnostic Test Results
Flashlight examination reveals an irregular corneal surface.
Fluorescein dye instilled in the conjunctival sac stains the outline of the ulcer and confirms the diagnosis.
Culture and sensitivity testing of corneal scrapings may identify the causative bacteria or fungus.
Treatment
All Corneal Ulcers
Prompt treatment and referral to ophthalmologist to prevent complications and permanent visual impairment
Systemic and topical broad-spectrum antibiotics until culture results identify the causative organism
Measures to eliminate the underlying cause of the ulcer and relieve pain
Fungal Infection
Topical instillation of natamycin for Fusarium, Acremonium, and Candida infections
Infection with Herpes Simplex 1
Topical application of trifluridine drops or vidarabine ointment
Trifluridine for recurrence
Vitamin A Deficiency
Correction of dietary deficiency or GI malabsorption of vitamin A
Infection with P. aeruginosa
Polymyxin B and gentamicin administered topically and by subconjunctival injection
Hospitalization and isolation and I.V. carbenicillin and tobramycin to stop the rapid spread of infection and prevent corneal perforation, which can occur within 48 hours
CLINICAL TIP
Treatment for a corneal ulcer caused by bacterial infection should never include an eye patch. Use of an eye patch creates the dark, warm, moist environment ideal for bacterial growth. Steroid drops should be utilized cautiously and only under the supervision of an ophthalmologist.Neurotropic Ulcers or Exposure Keratitis
Frequent instillation of artificial tears or lubricating ointments and use of a plastic bubble eye shield
Infection with Varicella Zoster
Topical sulfonamide ointment applied three to four times daily to prevent secondary infection
Analgesics for pain
Cycloplegic eyedrops for associated anterior uveitis
 LOOKING AT CORNEAL ULCERS |
ECTROPION AND ENTROPION
Ectropion, the outward turning or eversion of the eyelid, may be congenital or acquired. Acquired ectropion may be involutional, paralytic, cicatricial, or mechanical. Involutional ectropion is the most common form and usually stems from age-related weakness in the lid. Paralytic ectropion may occur with seventh cranial nerve palsy from diverse causes, such as Bell’s palsy, tumors, herpes zoster oticus, and infiltrations or tumors of the parotid gland. Cicatricial ectropion results from scarring of the anterior lamella from facial burns, trauma, chronic dermatitis, or excessive skin excision with blepharoplasty. Mechanical ectropion can occur with lid tumors that cause the lower eyelid to evert.
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