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Eye (Current Medical Diagnosis & Treatment, 45th Edition)

edwien — Sun, 27 Nov 2011 17:15:20 +0000

Tierney, Lawrence M., McPhee, Stephen J., Papadakis, Maxine A.

Current Medical Diagnosis & Treatment, 45th Edition

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Eye

Paul Riordan-Eva FRCS, FRCOphth

See http://www.cmdtlinks.com

SYMPTOMS OF OCULAR DISEASE

Redness

Redness is the most frequently encountered symptom of
ocular disorders. It is due to hyperemia of the conjunctival,
episcleral, or ciliary vessels; erythema of the eyelids; or
subconjunctival hemorrhage. The major differential diagnoses are
conjunctivitis, corneal disorders, acute glaucoma, and acute uveitis (Table 7-1).

Vafidis G: When is red eye not just conjunctivitis? Practitioner 2002;246:469.

Ocular Discomfort

Ocular pain may be caused by trauma, infection, inflammation, or sudden increase in intraocular pressure.

Foreign body sensation may
be due to corneal or conjunctival foreign bodies, disturbance of the
corneal epithelium, or rubbing of eyelashes against the cornea
(trichiasis).

Photophobia is usually due
to corneal inflammation (keratitis) or iritis. Other causes are
albinism, aniridia, cone dystrophy, aphakia, or fever associated with
various systemic infections.

Itching is characteristically associated with allergic eye disease.

Scratching and burning due
to dryness of the eyes may be due to dry environment, ocular surface
disease, systemic disorders (eg, Sjögren’s disease), or drugs (eg,
atropine-like agents).

Watering is usually due to
inadequate tear drainage through obstruction of the lacrimal drainage
system or malposition of the lower lid. Reflex tearing occurs with any
disturbance of the corneal epithelium.

“Eyestrain” & Headache

Eyestrain is discomfort associated with prolonged
reading or close work. Refractive error including presbyopia,
inadequate illumination, and latent ocular deviation are the usual
causes. Headache is rarely due to ocular disorders but is a major
symptom of giant cell arteritis, an important cause of visual loss in
older individuals.

Conjunctival Discharge

Purulent discharge usually indicates bacterial infection
of the conjunctiva, cornea, or lacrimal sac. Viral conjunctivitis or
keratitis produces watery discharge; allergic conjunctivitis results in
tearing, ropy discharge, and itching.

Visual Loss

Causes of blurred vision include refractive error,
cataract, macular degeneration, diabetic retinopathy, vitreous
hemorrhage, retinal detachment involving the macula, central retinal
vein occlusion, central retinal artery occlusion, intraocular
inflammation (uveitis), corneal opacities, and optic nerve disorders.

Monocular field loss usually indicates disease of the
retina or optic nerve. Important causes are chronic glaucoma, retinal
detachment, branch retinal artery or vein occlusion, optic neuritis,
and anterior ischemic optic neuropathy, all of which, especially
chronic glaucoma, may be bilateral. Lesions of the optic chiasm due to
pituitary tumors usually result in bitemporal field loss. Retrochiasmal
lesions cause contralateral homonymous field defects. The more
posterior the lesion in the visual pathway, the more similar are the
defects in the two eyes. Cerebrovascular disease and tumors are
responsible for most lesions of the retrochiasmal visual pathways.

Visual Impairment & Blindness

An individual is visually impaired if best corrected
distant visual acuity in the better eye is 20/80 or less or if visual
fields are significantly restricted. Legal blindness is defined as
visual acuity for distant vision of 20/200 or less in the better eye
with best correction or widest diameter of the visual field subtending
an angle of less than 20. Most states require best corrected visual
acuity with both eyes of 20/40 for an unrestricted driving license.

The World Health Organization (WHO) estimates that of
the world’s population over 160 million people are visually impaired
and about 37 million are blind. The most frequent causes of blindness
worldwide are cataract, glaucoma, age-related macular degeneration, and
diabetic retinopathy, all of which are increasing in prevalence,
especially in older individuals, as well as

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trachoma. In the United States, over 3 million adults aged 40 years or over are blind or visually impaired.

Table 7-1. The inflamed eye: Differential diagnosis of common causes.

	Acute Conjunctivitis	Acute Uveitis	Acute Glaucoma¹	Corneal Trauma or Infection
Incidence	Extremely common	Common	Uncommon	Common
Discharge	Moderate to copious	None	None	Watery or purulent
Vision	No effect on vision	Often blurred	Markedly blurred	Usually blurred
Pain	Mild	Moderate	Severe	Moderate to severe
Conjunctival injection	Diffuse; more toward fornices	Mainly circumcorneal	Mainly circumcorneal	Mainly circumcorneal
Cornea	Clear	Usually clear	Steamy	Clarity change related to cause
Pupil size	Normal	Small	Moderately dilated and fixed	Normal
Pupillary light response	Normal	Poor	None	Normal
Intraocular pressure	Normal	Commonly low but may be elevated	Elevated	Normal
Smear	Causative organisms	No organisms	No organisms	Organisms found only in corneal ulcers due to infection
¹Angle-closure glaucoma.

Evans
JR et al: Causes of visual impairment in people aged 75 years and older
in Britain: an add-on study to the MRC Trial of Assessment and
Management of Older People in the Community. Br J Ophthalmol
2004;88:365.

Friedman
DS et al: Racial variations in causes of vision loss in nursing homes:
The Salisbury Eye Evaluation in Nursing Home Groups (SEEING) Study.
Arch Ophthalmol 2004;122:1019.

Resnikoff S et al: Global data on visual impairment in the year 2002. Bull World Health Organ 2004;82:844.

Diplopia

Double vision typically results from acquired ocular
misalignment. This may be caused by central disorders of eye movements
or cranial nerve palsies due to head injury, vascular, neoplastic, or
inflammatory intracranial disease, or Wernicke’s syndrome; myasthenia
gravis; or intraorbital lesions including Graves’ ophthalmopathy and
muscle entrapment as a result of orbital blowout fracture. Monocular
diplopia, which persists when the fellow eye is covered, is usually due
to refractive error or lens opacities.

“Spots Before the Eyes” & “Flashing Lights”

Spots before the eyes (floaters) are often caused by
benign vitreous opacities. However, they may also be caused by
posterior vitreous detachment, vitreous hemorrhage, or posterior
uveitis. Sudden onset of floaters, particularly when associated with
flashing lights (photopsia), necessitates dilated fundal examination to
exclude a retinal tear or detachment.

Polkinghorne
PJ et al: Analysis of symptoms associated with rhegmatogenous retinal
detachments. Clin Exp Ophthalmol 2004;32:603.

OCULAR EXAMINATION

Abbreviations and symbols commonly used in ophthalmology are listed in the accompanying box.

Visual Acuity (VA)

Corrected distant visual acuity should be tested for
each eye in turn, using a Snellen or logMAR (EDTRS) chart, annotated
according to the distance at which each line can be read by a normal
individual. It is traditionally measured at 20 feet (6 meters in
Europe) or nearer if vision is poor, but other test distances may be
used. Visual acuity is expressed as a fraction—the test distance over
the figure assigned to the lowest line the patient can read. If the
patient is unable to read the top line of the chart, acuity is recorded
as counting fingers (CF), hand movements (HM), perception of light
(LP), or no light perception (NLP). A corrected acuity of less than
20/30 (6/9) is abnormal.

Near acuity is tested with a reduced Snellen chart or
standardized reading test types. The patient must be wearing
appropriate reading correction.

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Visual Fields

Confrontation testing, preferably using a 5-mm red
target, is valuable for rapid assessment of field defects. Amsler
charts are the easiest method of detecting central field abnormalities
due to macular disease.

Corbett JJ: The bedside and office neuro-ophthalmology examination. Semin Neurol 2003;23:63.

Pupils

The pupils are examined for absolute and relative size
and reactions to both light and accommodation. A large, poorly reacting
pupil may be due to third nerve palsy, iris damage caused by acute
glaucoma, or pharmacologic mydriasis. A small, poorly reacting pupil is
observed in Horner’s syndrome, inflammatory adhesions between iris and
lens (posterior synechiae), or neurosyphilis (Argyll Robertson pupils).
Physiologic anisocoria is a common cause of unequal pupils that react
normally.

A relative afferent pupillary defect, in which the
pupillary light reaction is reduced when light is shined into the
affected eye compared with the normal eye, generally indicates optic
nerve disease. It is detected with the “swinging light test,” in which
the pupillary light reactions are compared as a bright light is moved
from one eye to the other.

Extraocular Movements

Examination of extraocular movements begins with an
assessment of whether the two eyes are correctly aligned. A
misalignment of the visual axes under binocular viewing conditions is
known as a manifest deviation, or tropia. A deviation when binocular function is disrupted is known as a latent deviation, or phoria.
A manifest deviation may be apparent by comparing the relative
positions of the corneal light reflexes. A more reliable test is the cover test,
in which the deviated eye moves to take up fixation when the other eye
is occluded. The correctional movement is in the direction opposite to
that of the original manifest deviation. If no manifest deviation is
present, occlusion of one eye will elicit any latent deviation because
binocular function will have been disrupted. As the occluder is removed
(uncover test), latent deviation is then
detected by any correctional movement that occurs to reestablish the
normal alignment of the eyes. Latent deviation is common among normal
individuals.

Horizontal diplopia indicates dysfunction of the medial
and lateral rectus muscles; vertical diplopia results from dysfunction
of the superior or inferior recti or the obliques. The false outer
image arises from the affected eye. If muscle contraction is impaired,
the image separation will be greatest in its normal direction of
action; if a muscle cannot relax, image separation will be greatest in
the direction opposite to its normal action. For example, a paretic
lateral rectus or a tethered medial rectus of the right eye will cause
maximal image separation on looking to the right.

ABBREVIATIONS & SYMBOLS USED IN OPHTHALMOLOGY

A or Acc

Accommodation

Ax or x

Axis of cylindric lens

BI or BO

Base-in or base-out (prism)

Counting fingers

Cyl

Cylindric lens or cylinder

Diopter (lens strength)

Esophoria

EOG

Electro-oculography

EOM

Extraocular muscles or movements

ERG

Electroretinography

Hyperphoria

Hand movements

Hypertrophia

IOP

Intraocular pressure

IPD

Interpupillary distance

J1—J20

Test types (Jaeger) for testing reading vision

Keratic precipitates

Light perceptions

L Proj

Light projection

NLP

No light perception

NPC

Near point of convergence

Hand movements

OD (R, or RE)

Oculus dexter (right eye)

OS (L, or LE)

Oculus sinister (left eye)

Oculi unitas (both eyes)

Prism diopter

Pinhole

PRRE

Pupils round, regular, and equal

S or Sph

Spherical lens

Esotropia (with L or R)

Visual acuity

VER

Visual evoked response

Exophoria

Exotropia

Plus or convex lens

Minus or concave lens

[combined with]

Combined with

∞

Infinity (6 meters [20 feet] or more distance)

Degree (measurement of strabismus angle)

Prism diopter

Nystagmus in the primary position is always abnormal.
Minor degrees of nystagmus at the extremes of gaze are normal. Other
forms of physiologic nystagmus include optokinetic nystagmus and
nystagmus induced by rotation or caloric stimulation. Exaggerated
gaze-evoked nystagmus may be due to drugs or posterior fossa disease.

Proptosis (Exophthalmos)

Proptosis is suspected when there is widening of the palpebral aperture, with exposure of sclera both superiorly

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and inferiorly. (Eyelid retraction causes more exposure superiorly than
inferiorly.) By viewing from above while the patient is asked to look
down and the upper lids are lifted by the examiner, a further estimate
of the degree of proptosis can be made. Exophthalmometry provides
objective assessment. In nonaxial proptosis, there is also horizontal
or vertical displacement of the globe, indicating the presence of a
mass lesion outside the extraocular muscle cone.

The most frequent cause of proptosis in adults is
dysthyroid eye disease. Other causes include cellulitis, tumors, and
orbital pseudotumor.

Ptosis

Ptosis is usually due to eyelid disease. Neurologic
causes of ptosis include Horner’s syndrome, in which the pupil is
constricted, and third nerve palsy, in which there are abnormalities of
eye movements and the pupil may be dilated and react poorly to light.
In myasthenia gravis, the pupils are normal and characteristically the
ptosis is fatiguable.

Anterior Segment Examination

Although slit-lamp examination is more sensitive,
examination with a flashlight and loupe usually provides sufficient
information for initial assessment. Patterns of redness indicate the
site of the problem. In conjunctivitis, it extends diffusely across the
globe and the inner surface of the lids. Keratitis, intraocular
inflammation, and acute glaucoma lead to predominantly circumcorneal
injection. Episcleritis and scleritis cause localized or diffuse deep
injection, which in the case of scleritis is associated with blue
discoloration.

Focal lesions of the cornea due to infection or trauma
can be differentiated from the diffuse corneal haze of acute glaucoma
and from the cloudiness of the anterior chamber and perhaps hypopyon
(white cells within the anterior chamber) of iritis. Instillation of
fluorescein and examination with a blue light aid in detection of
corneal epithelial defects.

Direct Ophthalmoscopy

Direct ophthalmoscopy, ideally following pupil dilation
with tropicamide 0.5–1%, which rarely induces angle-closure glaucoma,
is used for examining the retina. Assessment of the red reflex and
clarity of fundal details indicate the degree of media opacity.
Abnormalities may then be localized to the cornea, lens, or vitreous by
variations of focus of the ophthalmoscope and use of parallax.

The optic disk is examined for swelling, pallor, and
glaucomatous cupping. Macular lesions causing poor central vision are
usually apparent. The retinal vessels are scrutinized for caliber and
wall changes. Retinal hemorrhages, exudates, and cotton-wool spots are
noted. In hospital patients, dilation should be noted in the record to
avoid confusion on neurologic examination.

OPHTHALMOLOGIC REFERRALS

Sudden loss of vision requires emergency ophthalmologic
consultation. Important causes in an uninflamed eye are vitreous
hemorrhage, retinal detachment, exudative age-related macular
degeneration, retinal artery or vein occlusions, anterior ischemic
optic neuropathy, giant cell arteritis, and optic neuritis. In an
inflamed eye, acute anterior uveitis, acute glaucoma, and corneal ulcer
are possibilities. Other emergencies include orbital cellulitis,
gonococcal keratoconjunctivitis, and ocular trauma.

Patients developing gradual loss of vision should also
be referred. The principal causes are cataract, atrophic age-related
macular degeneration, chronic glaucoma, chronic uveitis, and
intraorbital and intracranial tumors.

Patients with diabetes must undergo annual examination
through dilated pupils. Any patient with myopia should be warned of the
increased risk of retinal detachment and made aware of the importance
of reporting relevant symptoms. First-degree adult relatives of
patients with glaucoma should undergo screening annually.

Goldzweig CL et al: Preventing and managing visual disability in primary care: clinical applications. JAMA 2004;291:1497.

REFRACTIVE ERRORS

Refractive errors are the most common cause of blurred
vision, and may be a treatable component of poor vision in patients
with other diagnoses. In emmetropia (the
normal state), objects at infinity are seen clearly with the
unaccommodated eye. Objects nearer than infinity are seen with the aid
of accommodation, which increases the refractive power of the lens. In hyperopia,
objects at infinity are not seen clearly unless accommodation is used,
and near objects may not be seen because accommodative capacity is
finite. Hyperopia is corrected with plus (convex) lenses. In myopia,
the unaccommodated eye brings to a focus images of objects closer than
infinity, the distance of such objects from the patient becoming
progressively shorter with increasing myopia. Thus, the high myope is
able to focus on very near objects without glasses. Objects beyond this
distance cannot be seen without the aid of corrective (minus, concave)
lenses. In astigmatism, the refractive errors in the horizontal and vertical axes differ.

Various surgical techniques are available for the
correction of refractive errors, particularly myopia, including
photorefractive keratectomy (PRK), in which the excimer laser is used
to reshape the anterior cornea; laser in situ keratomileusis (LASIK)
and laser subepithelial keratomileusis (LASEK), in which laser
remodeling of the corneal stroma is performed after lifting away a flap
of epithelium and stroma (LASIK) or just epithelium (LASEK), which is
then replaced; intrastromal corneal ring segments (INTCS); and
extraction of the clear crystalline lens. Overall visual outcomes from
such procedures are impressive and many individuals seek treatment.
However, outcomes for individual cases are not completely predictable,
regression of effect from laser surgery may necessitate repeated

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treatment,
and there is risk of complications with the possibility of severe
permanent visual loss. Topical pirenzepine, a selective muscarinic
antagonist, and rigid contact lens wear during sleep (orthokeratology)
are also being investigated for myopia.

Presbyopia is the natural
loss of accommodative capacity with age. Emmetropes usually notice
inability to focus on objects at a normal reading distance at about age
45. Hyperopes experience symptoms at an earlier age. Presbyopia is
corrected with plus lenses for near work. Various surgical techniques,
particularly insertion of multifocal or accommodative intraocular
lenses, are being evaluated.

Use of a pinhole will overcome most refractive errors
and thus allows their exclusion as a cause of visual loss. Transient
refractive errors occur in patients with diabetes—typically when
diabetic control is erratic— and may be the presenting feature.
Autoinoculation of scopolamine from seasickness patches or atropine
from vials for parenteral use leads to inadvertent pupillary dilation
and loss of accommodation.

Claoue
C: Functional vision after cataract removal with multifocal and
accommodating intraocular lens implantation: prospective comparative
evaluation of Array multifocal and 1CU accommodating lenses. J Cataract
Refract Surg 2004;30:2088.

Rad AS et al: Progressive keratectasia after laser in situ keratomileusis. J Refract Surg 2004;20:S718.

Rau
M et al: Intrastromal corneal ring implantation for the correction of
myopia: 12-month follow-up. J Cataract Refract Surg 2003;29:322.

Tan
DT et al: One-year multicenter, double-masked, placebocontrolled,
parallel safety and efficacy study of 2% pirenzepine ophthalmic gel in
children with myopia. Ophthalmology 2005;112:84.

Taneri
S et al: Evolution, techniques, clinical outcomes, and pathophysiology
of LASEK: review of the literature. Surv Ophthalmol 2004;49:576.

Contact Lenses

Contact lenses are used mostly for correction of
refractive errors, for which they often provide a better optical
correction than glasses, as well as for management of diseases of the
cornea, conjunctiva, or lids. The various types are hard lenses, rigid
gas-permeable lenses, and soft lenses. Hard lenses are much more
durable and easier to care for than soft lenses but are more difficult
to tolerate. Rigid gas-permeable lenses are an effective compromise.

Contact lens care includes cleaning and sterilization
whenever the lenses are removed and removal of protein deposits as
required. Sterilization is accomplished by thermal or chemical methods.
For individuals developing reactions to preservatives in contact lens
solutions, preservative-free systems are available. All contact lenses
can be inserted in the morning and removed at night. Soft lenses are
also available for extended wear. Disposable soft lenses to avoid the
necessity for lens cleaning and sterilization are available for daily
or extended wear.

The major risk from contact lens wear is corneal
ulceration, potentially a blinding condition. Soft lenses present the
major hazard, particularly with extended wear, for which there is an
approximately eightfold increase in risk of corneal ulceration compared
with daily wear. The increased risk from extended wear begins with the
first night of overnight wear and increases progressively thereafter.
Disposable lenses are also associated with corneal ulceration.

Contact lens wearers should be made aware of the risks
they face and ways to minimize them, such as avoiding extended-wear
soft lenses and maintaining meticulous lens hygiene, including not
using tap water for lens cleaning. Whenever there is ocular discomfort
or redness, contact lenses should be removed. Ophthalmologic care
should be sought if symptoms persist.

Mah-Sadorra JH et al: Trends in contact lens-related corneal ulcers. Cornea 2005;24:51.

Najjar DM et al: Contact lens-related corneal ulcers in compliant patients. Am J Ophthalmol 2004;137:170.

DISORDERS OF THE LIDS & LACRIMAL APPARATUS

Hordeolum

Hordeolum is a common staphylococcal abscess that is
characterized by a localized red, swollen, acutely tender area on the
upper or lower lid. Internal hordeolum is a meibomian gland abscess
that points onto the conjunctival surface of the lid; external
hordeolum or sty is smaller and on the margin.

Warm compresses are helpful. Incision may be indicated
if resolution does not begin within 48 hours. An antibiotic ointment
(bacitracin or erythromycin) applied to the eyelid every 3 hours may be
beneficial during the acute stage. Internal hordeolum may lead to
generalized cellulitis of the lid.

Chalazion

Chalazion is a common granulomatous inflammation of a
meibomian gland that may follow an internal hordeolum. It is
characterized by a hard, nontender swelling on the upper or lower lid
with redness and swelling of the adjacent conjunctiva. If the chalazion
is large enough to impress the cornea, vision will be distorted.
Treatment is by incision and curettage.

Tumors

Verrucae and papillomas of the skin of the lids can
often be excised by the general physician if they do not involve the
lid margin; otherwise, surgery should be performed by an
ophthalmologist so as to avoid permanent notching of the lid. Basal
cell epithelioma, squamous cell carcinoma, meibomian gland carcinoma,
and malignant melanoma should be excluded by microscopic examination of
the excised material since 2% of lesions thought to be benign
clinically are found to be malignant. Basal cell epithelioma

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is
the most common of these lesions. Mohs’ technique of intraoperative
examination of excised tissue is particularly valuable in ensuring
complete excision of eyelid tumors.

Blepharitis

Blepharitis is a common chronic bilateral inflammatory
condition of the lid margins. Anterior blepharitis involves the eyelid
skin, eyelashes, and associated glands. It may be ulcerative, because
of infection by staphylococci, or seborrheic dermatitis, and associated
with seborrhea of the scalp, brows, and ears. Both types may be
present. Posterior blepharitis results from inflammation of the
meibomian glands. There may be bacterial infection, particularly with
staphylococci, or primary glandular dysfunction, in which there is a
strong association with acne rosacea.

Symptoms of blepharitis are irritation, burning, and
itching. In anterior blepharitis, the eyes are “redrimmed,” and scales
or granulations can be seen clinging to the lashes. In posterior
blepharitis, the lid margins are hyperemic with telangiectasias; the
meibomian glands and their orifices are inflamed, with dilation of the
glands, plugging of the orifices, and abnormal secretions. The lid
margin is frequently rolled inward to produce a mild entropion, and the
tears may be frothy or abnormally greasy.

Blepharitis is a common cause of recurrent
conjunctivitis. Both anterior and, more particularly, posterior
blepharitis may be complicated by hordeola or chalazions; abnormal lid
or lash positions, producing trichiasis; epithelial keratitis of the
lower third of the cornea; marginal corneal infiltrates; and inferior
corneal vascularization and thinning.

In anterior blepharitis, cleanliness of the scalp,
eyebrows, and lid margins is effective local therapy. Scales must be
removed from the lids daily with a damp cotton applicator and baby
shampoo. An antistaphylococcal antibiotic eye ointment such as
bacitracin or erythromycin is applied daily to the lid margins with a
cotton-tipped applicator. Antibiotic sensitivity studies may be
required in severe staphylococcal blepharitis.

In mild posterior blepharitis, regular meibomian gland
expression may be sufficient to control symptoms. Inflammation of the
conjunctiva and cornea indicates a need for more active treatment,
including long-term low-dose systemic antibiotic therapy, usually with
tetracycline (250 mg twice daily), doxycycline (100 mg daily),
minocycline (50–100 mg daily) or erythromycin (250 mg three times
daily), and short-term topical steroids, eg, prednisolone, 0.125% twice
daily. Topical therapy with antibiotics such as ciprofloxacin 0.3%
ophthalmic solution twice daily may be helpful but should be restricted
to short courses.

Ta
CN et al: Effects of minocycline on the ocular flora of patients with
acne rosacea or seborrheic blepharitis. Cornea 2003;22:545.

Entropion & Ectropion

Entropion (inward turning of usually the lower lid)
occurs occasionally in older people as a result of degeneration of the
lid fascia, or may follow extensive scarring of the conjunctiva and
tarsus. Surgery is indicated if the lashes rub on the cornea. Botulinum
toxin injections may also be used for temporary correction of the
involutional lower eyelid entropion of older people.

Ectropion (outward turning of the lower lid) is common
with advanced age. Surgery is indicated if there is excessive tearing,
exposure keratitis, or a cosmetic problem.

Dacryocystitis

Dacryocystitis is infection of the lacrimal sac due to
obstruction of the nasolacrimal system. It may be acute or chronic and
occurs most often in infants and in persons over 40 years. It is
usually unilateral.

The usual infectious organisms are Staphylococcus aureus and β-hemolytic streptococci in acute dacryocystitis and S epidermidis, anaerobic streptococci, or Candida albicans in chronic dacryocystitis.

Acute dacryocystitis is characterized by pain, swelling,
tenderness, and redness in the tear sac area; purulent material may be
expressed. In chronic dacryocystitis, tearing and discharge are the
principal signs, and mucus or pus may also be expressed.

Acute dacryocystitis responds well to systemic
antibiotic therapy. Surgical relief of the underlying obstruction is
usually undertaken electively but may be performed acutely. The chronic
form may be kept latent with antibiotics, but relief of the obstruction
is the only cure. In adults, the standard procedure for obstruction of
the lacrimal drainage system is dacryocystorhinostomy, which involves
surgical exploration of the lacrimal sac and formation of a fistula
into the nasal cavity. Laser-assisted endoscopic dacryocystorhinostomy
and balloon dilation or probing of the nasolacrimal system are
alternatives. Congenital nasolacrimal duct obstruction often resolves
spontaneously but if necessary can be treated by probing of the
nasolacrimal system.

Singh
Bhinder G et al: Repeated probing results in the treatment of
congenital nasolacrimal duct obstruction. Eur J Ophthalmol 2004;14:185.

CONJUNCTIVITIS

Conjunctivitis is the most common eye disease. It may be
acute or chronic. Most cases are due to bacterial (including gonococcal
and chlamydial) or viral infection. Other causes include
keratoconjunctivitis sicca, allergy, chemical irritants, and deliberate
self-harm. The mode of transmission of infectious conjunctivitis is
usually direct contact via fingers, towels, handkerchiefs, etc, to the
fellow eye or to other persons. It may be through contaminated eye
drops.

Conjunctivitis must be differentiated from acute uveitis, acute glaucoma, and corneal disorders (Table 7-1).

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Bacterial Conjunctivitis

The organisms isolated most commonly in bacterial conjunctivitis are staphylococci, streptococci (particularly S pneumoniae), Haemophilus species, Pseudomonas, and Moraxella.
All may produce a copious purulent discharge. There is no blurring of
vision and only mild discomfort. In severe cases, examination of
stained conjunctival scrapings and cultures is recommended.

The disease is usually self-limited, lasting about 10–14
days if untreated. A sulfonamide (eg, sulfacetamide, 10% ophthalmic
solution or ointment) instilled locally three times daily will usually
clear the infection in 2–3 days. Povidone-iodine may also be effective.
The use of topical fluoroquinolones is rarely justified for treatment
of a generally self-limiting, benign infection.

A. GONOCOCCAL CONJUNCTIVITIS

Gonococcal conjunctivitis, usually acquired through
contact with infected genital secretions, is manifested by a copious
purulent discharge. It is an ophthalmologic emergency because corneal
involvement may rapidly lead to perforation. The diagnosis should be
confirmed by stained smear and culture of the discharge. In this
disorder, a 5-day course of parenteral ceftriaxone, 1–2 g daily, is
required. Topical antibiotics such as erythromycin and bacitracin may
be added. In such patients, other sexually transmitted diseases,
including chlamydiosis, syphilis, and HIV infection, should be tested
for.

B. CHLAMYDIAL KERATOCONJUNCTIVITIS

1. Trachoma

(Chlamydia trachomatis
serotypes A–C.) Trachoma is a major cause of blindness worldwide.
Recurrent episodes of infection in childhood are manifest as bilateral
follicular conjunctivitis, epithelial keratitis, and corneal
vascularization (pannus). Cicatrization of the tarsal conjunctiva leads
to entropion and trichiasis in adulthood, with secondary central
corneal scarring.

Immunologic tests or polymerase chain reaction on
conjunctival samples will confirm the diagnosis but treatment should be
started on the basis of clinical findings. Single-dose therapy with
oral azithromycin, 20 mg/ kg, is effective. Alternatively, oral
tetracycline or erythromycin, 250 mg four times a day, or doxycycline,
100 mg twice a day, is given for 3–4 weeks. Local treatment is not
necessary. Surgical treatment includes correction of eyelid deformities
and corneal transplantation.

2. Inclusion conjunctivitis

(C trachomatis serotypes
D–K.) The agent of inclusion conjunctivitis is a common cause of
genital tract disease in adults. The eye is usually involved following
accidental contact with genital secretions. Adult inclusion
conjunctivitis thus occurs most frequently in sexually active young
adults. The disease starts with acute redness, discharge, and
irritation. The eye findings consist of follicular conjunctivitis with
mild keratitis. A nontender preauricular lymph node can often be
palpated. Healing usually leaves no sequelae. Diagnosis can be rapidly
confirmed by immunologic tests or polymerase chain reaction on
conjunctival samples. Treatment is with oral tetracycline or
erythromycin, 500 mg four times a day, or doxycycline, 100 mg twice a
day, for 3 weeks. Single-dose therapy with azithromycin, 1 g, may also
be effective. Before treatment, all cases should be assessed for
genital tract infection so that management can be adjusted accordingly,
and other venereal diseases sought.

Melese
M et al: Feasibility of eliminating ocular Chlamydia trachomatis with
repeat mass antibiotic treatments. JAMA 2004;292:721.

Solomon AW et al: Mass treatment with single-dose azithromycin for trachoma. N Engl J Med 2004;351:1962.

Viral Conjunctivitis

One of the most common causes of viral conjunctivitis is
adenovirus type 3. Conjunctivitis due to this agent is usually
associated with pharyngitis, fever, malaise, and preauricular
adenopathy (pharyngoconjunctival fever). Locally, the palpebral
conjunctiva is red, and there is a copious watery discharge and scanty
exudate. Children are more often affected than adults, and contaminated
swimming pools are sometimes the source of infection. The disease
usually lasts 10 days.

Epidemic keratoconjunctivitis is caused by adenovirus
types 8, 19, 29, and 37. It is more likely to be complicated by visual
loss due to corneal subepithelial infiltrates. The disease lasts at
least 2 weeks. Local sulfonamide therapy prevents secondary bacterial
infection and cold compresses reduce the discomfort of the associated
lid edema.

Keratoconjunctivitis Sicca (Dry Eyes)

This is a common disorder, particularly in elderly
women. A wide range of conditions predispose to or are characterized by
dry eyes. Hypofunction of the lacrimal glands, causing loss of the
aqueous component of tears, may be due to aging, hereditary disorders,
systemic disease (eg, Sjögren’s syndrome), or systemic and topical
drugs. Excessive evaporation of tears may be due to environmental
factors (eg, a hot, dry, or windy climate) or abnormalities of the
lipid component of the tear film, as in blepharitis. Mucin deficiency
may be due to malnutrition, infection, burns, or drugs. Hormone
replacement therapy may increase the risk of dry eyes.

The patient complains of dryness, redness, or a scratchy
feeling of the eyes. In severe cases there is persistent marked
discomfort, with photophobia, difficulty in moving the eyelids, and
often excessive mucus secretion. In many cases, inspection reveals no
abnormality, but on slitlamp examination there are subtle abnormalities
of tear film stability and reduced volume of the tear film meniscus
along the lower lid. In more severe cases, damaged corneal and
conjunctival cells stain with 1% rose bengal, which is to be avoided in
severe cases because of the intense pain. In the most severe cases
there is marked conjunctival injection, loss of the normal conjunctival

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and
corneal luster, epithelial keratitis that may progress to frank
ulceration, and mucous strands. Schirmer’s test, which measures the
rate of production of the aqueous component of tears, may be helpful,
but false-positive and false-negative results are frequent.

Treatment depends upon cause. In most early cases, the
corneal and conjunctival epithelial changes are reversible. Aqueous
deficiency can be treated by replacement of the aqueous component of
tears with various types of artificial tears. The simplest preparations
are physiologic (0.9%) or hypo-osmotic (0.45%) solutions of sodium
chloride. Balanced salt solution is more physiologic but also more
expensive. All of these drop preparations can be used as frequently as
every half-hour, but in most cases are needed only three or four times
a day. More prolonged duration of action can be achieved with drop
preparations containing methylcellulose (eg, Isopto Plain) or polyvinyl
alcohol (eg, Liquifilm Tears or HypoTears), or by using petrolatum
ointment (Lacri-Lube). Such mucomimetics are particularly indicated
when there is mucin deficiency. If there is tenacious mucus, mucolytic
agents (eg, acetylcysteine, 20% six times daily) may be helpful. The
presence of ocular surface and lacrimal gland inflammation in dry eyes
has prompted trials of topical antiinflammatory agents such as
cyclosporin A.

Lacrimal punctal occlusion by canalicular plugs or
surgery is useful in severe cases. Blepharitis is treated as described
above. Associated blepharospasm responds to botulinum toxin injections.

Artificial tear preparations are generally very safe and
without side effects. However, the preservatives necessary to maintain
their sterility are potentially toxic and allergenic and may cause
keratitis and cicatrizing conjunctivitis in frequent users.
Furthermore, the development of such reactions may be misinterpreted by
both the patient and the doctor as a worsening of the dry eye state
requiring more frequent use of the artificial tears and leading in turn
to further deterioration, rather than being recognized as a need to
change to a preservative-free preparation.

Moss SE et al: Incidence of dry eye in an older population. Arch Ophthalmol 2004;122:369.

Pflugfelder SC: Antiinflammatory therapy for dry eye. Am J Ophthalmol 2004;137:337.

Allergic Eye Disease

Allergic eye disease takes a number of different forms
but all are expressions of atopy, which may also manifest as atopic
asthma, atopic dermatitis, or allergic rhinitis. Symptoms include
itching, tearing, redness, stringy discharge, and, occasionally,
photophobia and visual loss.

Allergic conjunctivitis is a benign disease, occurring
usually in late childhood and early adulthood. It may be seasonal,
developing usually during the spring or summer, or perennial. Clinical
signs are limited to conjunctival hyperemia and edema (chemosis), the
latter at times being marked and sudden in onset. Vernal
keratoconjunctivitis also tends to occur in late childhood and early
adulthood. It is usually seasonal, with a predilection for the spring.
Large “cobblestone” papillae are noted on the upper tarsal conjunctiva.
There may be lymphoid follicles at the limbus. Atopic
keratoconjunctivitis is a more chronic disorder of adulthood. Both the
upper and the lower tarsal conjunctivas exhibit a fine papillary
conjunctivitis with fibrosis, resulting in forniceal shortening and
entropion with trichiasis. Staphylococcal blepharitis is a complicating
factor. Corneal involvement, including refractory ulceration, is
frequent during exacerbations of both vernal and atopic
keratoconjunctivitis. They may also be complicated by herpes simplex
keratitis.

For mild and moderately severe allergic eye disease, a topical histamine H₁-receptor
antagonist, such as levocabastine hydrochloride 0.05% or emedastine
difumarate 0.05%, or ketorolac tromethamine, a nonsteroidal
anti-inflammatory agent, is applied topically four times daily.
Ketotifen 0.025%, which has histamine H₁-receptor
antagonist, mast cell stabilizer, and eosinophil inhibitor activity, is
applied two to four times daily; olopatadine 0.1%, applied twice daily,
reduces symptoms by a similar mechanism. Topical mast cell stabilizers,
such as cromolyn sodium 4% or lodoxamide tromethamine 0.1%, applied
four times daily, or nedocromil sodium 2%, applied twice daily, produce
longer-term prophylaxis but the therapeutic response may be delayed.
Topical vasoconstrictors and antihistamines are advocated in hay fever
conjunctivitis but are of limited efficacy and may produce rebound
hyperemia and follicular conjunctivitis. Systemic antihistamines may be
useful in prolonged atopic keratoconjunctivitis. Topical
corticosteroids are essential to the control of acute exacerbations of
both vernal and atopic keratoconjunctivitis. Steroid-induced side
effects, including cataracts, glaucoma, and exacerbation of herpes
simplex keratitis, are major problems. Topical cyclosporin may be
effective. Systemic steroid therapy and even plasmapheresis may be
required in severe atopic keratoconjunctivitis. In allergic
conjunctivitis, specific allergens may be identifiable and thus
avoidable. In vernal keratoconjunctivitis, a cooler climate often
provides significant benefit.

Ono
SJ et al: Allergic conjunctivitis: update on pathophysiology and
prospects for future treatment. J Allergy Clin Immunol 2005;115:118.

Owen
CG et al: Topical treatments for seasonal allergic conjunctivitis:
systematic review and meta-analysis of efficacy and effectiveness. Br J
Gen Pract 2004;54:451.

PINGUECULA & PTERYGIUM

Pinguecula is a yellow elevated nodule on either side of
the cornea, more commonly the nasal side, in the area of the palpebral
fissure. It is common in persons over age 35 years. Pterygium is a
fleshy, triangular encroachment of the conjunctiva onto the nasal side
of the cornea and is usually associated with constant exposure to wind,
sun, sand, and dust. Pterygium may be either unilateral or bilateral.

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Pingueculae rarely grow, but inflammation
(pingueculitis) may occur. No treatment is usually required for
pingueculitis or for inflammation of pterygium, but artificial tears
are often beneficial, and short courses of topical nonsteroidal
anti-inflammatory agents or weak steroids (prednisolone, 0.125% three
times a day) may be necessary.

The indications for excision of pterygium are growth
threatening vision by approaching the visual axis, marked induced
astigmatism, or severe ocular irritation. Recurrence is common and
often more aggressive than the primary lesion.

Hirst LW: The treatment of pterygium. Surv Ophthalmol 2003; 48:145.

CORNEAL ULCER

Corneal ulcers are most commonly due to infection by
bacteria, viruses, fungi, or amebas. Noninfectious causes—all of which
may be complicated by infection— include neurotrophic keratitis
(resulting from loss of corneal sensation), exposure keratitis (due to
inadequate eyelid closure), severe dry eyes, severe allergic eye
disease, and various inflammatory disorders that may be purely ocular
or part of a systemic vasculitis. Delayed or ineffective treatment of
corneal infection may lead to devastating consequences with intraocular
infection or corneal scarring. Prompt referral is essential.

Patients present with pain, photophobia, tearing, and
reduced vision. The eye is red, with predominantly circumcorneal
injection, and there may be purulent or watery discharge. The corneal
appearance varies according to the organisms involved.

Bacterial Keratitis

Bacterial keratitis pursues an aggressive course.
Precipitating factors include contact lens wear—especially soft contact
lenses worn overnight—and corneal trauma, including laser surgery. The
pathogens most commonly isolated are Pseudomonas aeruginosa, Pneumococcus, Moraxella
species, and staphylococci. The cornea is hazy, with a central ulcer
and adjacent stromal abscess. Hypopyon is often present. The ulcer is
scraped to recover material for Gram stain and culture prior to
starting treatment with high-concentration topical antibiotics applied
hourly day and night for at least the first 24 hours. Fluoroquinolones
such as ciprofloxacin 0.3%, ofloxacin 0.3%, and norfloxacin 0.3% are
commonly used as first-line agents. Experience with levofloxacin 0.5%,
which is more effective against pneumococci than ciprofloxacin, and the
fourth-generation fluoroquinolones (moxifloxacin 0.5% and gatifloxacin
0.3%), which are active against mycobacteria, is limited. Gram-positive
cocci can also be treated with a cephalosporin such as cefazolin, 100
mg/mL; and gram-negative bacilli with an aminoglycoside such as
tobramycin, 15 mg/mL. If no organisms are seen, these two agents can be
used together.

Hwang
DG: Fluoroquinolone resistance in ophthalmology and the potential role
for newer ophthalmic fluoroquinolones. Surv Ophthalmol 2004;49(Suppl
2):S79.

Hyon
JY et al: Comparative efficacy of topical gatifloxacin with
ciprofloxacin, amikacin, and clarithromycin in the treatment of
experimental Mycobacterium chelonae keratitis. Arch Ophthalmol 2004;122:1166.

Mah
FS: Fourth-generation fluoroquinolones: new topical agents in the war
on ocular bacterial infections. Curr Opin Ophthalmol 2004;15:316.

Herpes Simplex Keratitis

Herpes simplex keratitis is an important cause of ocular
morbidity in adults. The ability of the virus to colonize the
trigeminal ganglion leads to recurrences precipitated by fever,
excessive exposure to sunlight, or immunodeficiency.

The dendritic (branching) ulcer is the most
characteristic manifestation of this epithelial keratitis. More
extensive (“geographic”) ulcers also occur, particularly if topical
corticosteroids have been used. These ulcers are most easily seen after
instillation of fluorescein and examination with a blue light.
Epithelial disease in itself does not lead to corneal scarring. It
responds well to simple debridement and patching. More rapid healing
can be achieved by the addition of topical antivirals such as
trifluridine drops, vidarabine ointment, acyclovir ointment, or
ganciclovir gel. Long-term oral acyclovir reduces the rate of recurrent
epithelial disease, for which topical corticosteroids must not be used.

Stromal herpes simplex keratitis produces increasingly
severe corneal opacity with each recurrence. Topical antivirals alone
are insufficient to control stromal disease. Thus, topical
corticosteroids are used in combination, but steroid dependence is a
common consequence. Corticosteroids may also enhance viral replication,
exacerbating epithelial disease. Oral acyclovir, 200–400 mg five times
a day, may be helpful in the treatment of severe herpetic keratitis and
for prophylaxis against recurrences, particularly in atopic or
HIV-infected individuals. Corneal grafting is necessitated by severe
stromal scarring, but the overall outcome is relatively poor. Caution:
For patients with known or possible herpetic disease, topical
corticosteroids should be prescribed only with ophthalmologic
supervision.

Uchoa
UB et al: Long-term acyclovir use to prevent recurrent ocular herpes
simplex virus infection. Arch Ophthalmol 2003;121:1702.

Wilhelmus KR: Interventions for herpes simplex virus epithelial keratitis. Cochrane Database Syst Rev 2003;3:CD002898.

Fungal Keratitis

Fungal keratitis tends to occur after corneal injury
involving plant material or in an agricultural setting, in eyes with
chronic ocular surface disease, and in contact lens wearers. It is an
indolent process, with the cornea characteristically having multiple
stromal abscesses and relatively little epithelial loss. Intraocular
infection

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is
common. Corneal scrapings are cultured on media suitable for fungi
whenever the history or corneal appearance is suggestive of fungal
disease.

Srinivasan M: Fungal keratitis. Curr Opin Ophthalmol 2004;15:321.

Acanthamoeba Keratitis

Acanthamoeba is an important cause of suppurative
keratitis in contact lens wearers. Although severe pain with perineural
and ring infiltrates in the corneal stroma is characteristic, earlier
forms with changes confined to the corneal epithelium are identifiable.
Culture requires specialized media. Treatment is hampered by the
organism’s ability to encyst within the corneal stroma. Various agents
have been used, including neomycin-polymyxin-gramicidin, chlorhexidine,
the investigational agents propamidine isethionate and polyhexamethyl
biguanide, and oral and topical imidazoles such as ketoconazole,
miconazole, and itraconazole. Epithelial debridement may be useful in
early infections. Corneal grafting may be required in the acute stage
to arrest the progression of infection or after resolution to restore
vision. Systemic immunosuppression may be needed if there is scleral
involvement.

Kilvington
S et al: Acanthamoeba keratitis: the role of domestic tap water
contamination in the United Kingdom. Invest Ophthalmol Vis Sci
2004;45:165.

Herpes Zoster Ophthalmicus

Herpes zoster frequently involves the ophthalmic
division of the trigeminal nerve. It presents with malaise, fever,
headache, and periorbital burning and itching. These symptoms may
precede the eruption by a day or more. The rash is initially vesicular,
quickly becoming pustular and then crusting. Involvement of the tip of
the nose or the lid margins predicts involvement of the eye. Ocular
signs include conjunctivitis, keratitis, episcleritis, and anterior
uveitis, often with elevated intraocular pressure. Recurrent anterior
segment inflammation, neurotrophic keratitis, and posterior subcapsular
cataract are long-term complications. Optic neuropathy, cranial nerve
palsies, acute retinal necrosis, and cerebral angiitis are infrequent
problems in the acute stage. HIV infection is an important risk factor
for herpes zoster ophthalmicus and increases the likelihood of
complications.

High-dose oral acyclovir (800 mg five times a day),
valacyclovir (1 g three times a day), or famciclovir (250–500 mg three
times a day) started within 72 hours after the appearance of the rash
reduces the incidence of ocular complications but not of postherpetic
neuralgia. Anterior uveitis requires treatment with topical
corticosteroids and cycloplegics. Neurotrophic keratitis is an
important cause of long-term morbidity.

Liesegang TJ: Herpes zoster virus infection. Curr Opin Ophthalmol 2004;15:531.

Zaal
MJ et al: Prognostic value of Hutchinson’s sign in acute herpes zoster
ophthalmicus. Graefes Arch Clin Exp Ophthalmol 2003;241:187.

ACUTE ANGLE-CLOSURE GLAUCOMA

General Considerations

Primary acute angle-closure glaucoma occurs only with
closure of a preexisting narrow anterior chamber angle, found in
elderly persons (owing to enlargement of the lens), hyperopes, and
Asians. In the United States, about 1% of people over age 35 years have
narrow anterior chamber angles, but many never develop acute glaucoma.
Angle closure may be precipitated by pupillary dilation and thus can
occur from sitting in a darkened theater, at times of stress, or,
rarely, from pharmacologic mydriasis. Anticholinergic or
sympathomimetic agents (eg, nebulized bronchodilators, atropine for
preoperative medication, antidepressants, or nasal decongestants) are
also causes. Secondary acute angle-closure glaucoma may be observed
with anterior uveitis, dislocation of the lens, or topiramate therapy.
Symptoms are the same as in primary acute angle-closure glaucoma, but
differentiation is important because of differences in management.
Chronic angleclosure glaucoma is particularly common in eastern Asia.
It presents in the same way as open-angle glaucoma (see below).

Clinical Findings

Patients with acute glaucoma usually seek treatment
immediately because of extreme pain and blurred vision, though there
are subacute cases. The blurred vision is associated with halos around
lights. Nausea and abdominal pain may occur, and acute glaucoma must be
remembered in the differential diagnosis of the acute abdomen. The eye
is red, the cornea steamy, and the pupil moderately dilated and
nonreactive to light. Intraocular pressure is usually over 40 mm Hg.

Differential Diagnosis

Acute glaucoma must be differentiated from conjunctivitis, acute uveitis, and corneal disorders (Table 7-1).

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Treatment

A. PRIMARY

Initial treatment in primary angle-closure glaucoma is
control of intraocular pressure. A single 500-mg intravenous dose of
acetazolamide, followed by 250 mg orally four times a day, is usually
sufficient. Osmotic diuretics such as oral glycerol and intravenous
urea or mannitol—the dosage of all three being 1–2 g/kg—may be
necessary if there is no response to acetazolamide. Laser therapy to
the peripheral iris (iridoplasty) or anterior chamber paracentesis is
also effective. Once the intraocular pressure has started to fall,
topical 4% pilocarpine, 1 drop every 15 minutes for 1 hour and then
four times a day, is used to reverse the underlying angle closure. The
definitive treatment is laser peripheral iridotomy or surgical
peripheral iridectomy, which should also be performed prophylactically
on the fellow eye. Cataract extraction is a possible alternative. If it
is not possible to control the intraocular pressure medically, glaucoma
drainage surgery as for uncontrolled open-angle glaucoma (see below)
may be required.

B. SECONDARY

In secondary acute angle-closure glaucoma, systemic
acetazolamide is also used, with or without osmotic agents. Further
treatment is determined by the cause.

Prognosis

Untreated acute angle-closure glaucoma results in severe
and permanent visual loss within 2–5 days after onset of symptoms.
Affected patients need to be kept under review for development of
chronic glaucoma.

Aung T et al: Long-term outcomes in Asians after acute primary angle closure. Ophthalmology 2004;111:1464.

Fraunfelder FW et al: Topiramate-associated acute, bilateral, secondary angle-closure glaucoma. Ophthalmology 2004;111:109.

Saw
SM et al: Awareness of glaucoma, and health beliefs of patients
suffering primary acute angle closure. Br J Ophthalmol 2003;87:446.

CHRONIC GLAUCOMA

General Considerations

Chronic glaucoma is characterized by gradually
progressive—over a period of months or years—excavation (“cupping”) and
pallor of the optic disk with loss of vision varying from slight
constriction of the peripheral fields to complete blindness. In chronic
openangle glaucoma, the intraocular pressure is elevated due to reduced
drainage of aqueous through the trabecular meshwork. In chronic
angle-closure glaucoma, flow of aqueous into the anterior chamber angle
is obstructed. In normal-tension glaucoma, intraocular pressure is not
elevated above the normal range but the same pattern of optic nerve
damage occurs, probably due to vascular insufficiency.

The cause of the reduced drainage of aqueous in primary
open-angle glaucoma has not been clearly established. A number of
mutations, such as in the myocilin gene on
chromosome 1, have been identified in a small proportion of cases. The
disease is bilateral, and there is an increased prevalence in
first-degree relatives of affected individuals and in diabetics. In
blacks, primary open-angle glaucoma is more frequent, occurs at an
earlier age, and results in more severe optic nerve damage. Secondary
open-angle glaucoma may result from uveitis or the effects of trauma.
Elevation of intraocular pressure is also a complication of steroid
therapy, whether it be topical, systemic, inhaled, or administered by
nasal spray.

In the United States, it is estimated that 2% of people
over 40 years of age have glaucoma, affecting more than 2 million
individuals and being three times more prevalent in blacks. At least
25% of cases are undetected. Over 90% of cases are of the open-angle
type, either primary open-angle or normal-tension glaucoma. Worldwide,
about 50% of all cases of glaucoma are due to acute (see above) or
chronic angle closure due to the very high prevalence of angle closure
in Asians.

Clinical Findings

Because patients with chronic glaucoma have no symptoms
initially, diagnosis is often made incidentally at routine eye tests.
On examination, there may be slight cupping of the optic disk observed
as an absolute increase—or an asymmetry between the two eyes—of the
ratio of the diameter of the optic cup to the diameter of the whole
optic disk (cup-disk ratio). (Cup-disk ratio of greater than 0.5 or
asymmetry of cup-disk ratio of 0.2 or more is suggestive.) Changes in
the retinal nerve fiber layer may be observed as an earlier finding in
some patients. The visual fields gradually constrict, but central
vision remains good until late in the disease.

Diagnosis requires consistent and reproducible
abnormalities in at least two out of three parameters— intraocular
pressure, optic disc cupping, and central visual field. The normal
range of intraocular pressure is 10–21 mm Hg. In many individuals,
elevated intraocular pressure is not associated with optic disk or

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visual
field abnormalities. These ocular hypertensives are at increased risk
of developing glaucomatous damage. Treatment to reduce intraocular
pressure is justified if there is a moderate to high risk of the
development of glaucoma. Risk is determined by several factors,
including age, optic disk appearance, level of intraocular pressure,
and corneal thickness. Conversely, a significant proportion of patients
with glaucoma have normal intraocular pressure when it is first
measured, and only repeated measurements identify the abnormally high
pressure. Furthermore, in patients with normal-tension glaucoma, the
intraocular pressure is always within the normal range despite repeated
measurement. There are many other causes of optic disk abnormalities or
visual field changes that mimic glaucomatous damage, and visual field
testing may prove unreliable in some patients, particularly the
elderly. Taken together, these factors mean that the diagnosis of
glaucoma is not always straightforward, hampering the effectiveness of
screening programs.

Prevention

All persons over age 40 years should have intraocular
pressure measurement and optic disc examination every 2–5 years. In
diabetics and in individuals with a family history of glaucoma, annual
examination is indicated.

Treatment

The prostaglandin analogs (latanoprost 0.005%,
bimatoprost 0.03%, and travoprost 0.004% once daily at night; or
unoprostone isopropyl 0.15% twice daily) are commonly used as
first-line therapy because of their efficacy, the convenience of
once-daily administration, and their lack of systemic side effects. All
may produce conjunctival hyperemia, permanent darkening of the iris and
eyebrow color, and eyelash growth. Latanoprost has been associated with
reactivation of uveitis and macular edema. Topical β-adrenergic
blocking agents such as timolol 0.25% or 0.5%, carteolol 1%,
levobunolol 0.5%, and metipranolol 0.3% solutions twice daily or
timolol 0.5% gel once daily may be used alone or in combination with a
prostaglandin analog. They are contraindicated in patients with
reactive airway disease or heart failure. Betaxolol, 0.25% or 0.5%, a
β-receptor selective blocking agent, is theoretically safer in reactive
airway disease but less effective at reducing intraocular pressure.
Brimonidine 0.2%, a selective α₂-agonist, and dorzolamide 2%
or brinzolamide 1%, topical carbonic anhydrase inhibitors, also can be
used in addition to a prostaglandin analog or a β-blocker (twice daily)
or as initial therapy when prostaglandin analogs and β-blockers are
contraindicated (brimonidine twice daily, dorzolamide and brinzolamide
three times daily). Both are associated with allergic reactions. The
combination drops Xalacom (latanoprost 0.005% and timolol 0.5%) used
once daily in the morning and Cosopt (dorzolamide 2% and timolol 0.5%)
used twice daily improve compliance when multiple medications are
required.

Apraclonidine, 0.5–1%, another α₂-agonist,
can be used three times a day to postpone the need for surgery in
patients receiving maximal medical therapy, but long-term use is
limited by drug reactions. It is more commonly used to control acute
rises in intraocular pressure such as after laser therapy. Epinephrine,
0.5–1%, and the prodrug dipivefrin, 0.1%, are being used much less
frequently because of adverse effects on the outcome of subsequent
glaucoma surgery. Pilocarpine 1–4% (and sometimes higher concentrations
in patients with dark irides) four times a day is little used because
of the induced myopia in younger patients and the pupillary
constriction that compromises vision in patients with cataract. Oral
carbonic anhydrase inhibitors (eg, acetazolamide) may still be used on
a long-term basis if topical therapy is inadequate and surgical or
laser therapy is inappropriate.

Laser trabeculoplasty is used as an adjunct to topical
therapy to defer surgery and is also advocated as primary treatment.
Surgery is generally undertaken when intraocular pressure is
inadequately controlled by medical and laser therapy, but it may also
be used as primary treatment. Trabeculectomy remains the standard
procedure. Adjunctive treatment with subconjunctival fluorouracil or
mitomycin is used perior postoperatively in difficult cases.
Viscocanalostomy and deep sclerectomy with collagen implant—two
alternative procedures that avoid a full-thickness incision into the
eye—may be as effective as trabeculectomy but are more difficult to
perform.

In chronic angle-closure glaucoma, laser peripheral
iridotomy or surgical peripheral iridectomy may be helpful in the early
stages.

Prognosis

Untreated chronic glaucoma that begins at age 40–45
years will probably cause complete blindness by age 60–65. Early
diagnosis and treatment can preserve useful vision throughout life. In
primary open-angle glaucoma—and if treatment is required in ocular
hypertension—the aim is to reduce intraocular pressure to a level that
will adequately reduce progression of visual field loss. In eyes with
marked visual field or optic disk changes, intraocular pressure must be
reduced to less than 16 mm Hg. In normal-tension glaucoma with
progressive visual field loss, it is necessary to achieve even lower
intraocular pressure such that surgery is often required.

Bonovas S et al: Diabetes mellitus as a risk factor for primary openangle glaucoma: a meta-analysis. Diabet Med 2004;21:609.

Cohen CS et al: The dawn of genetic testing for glaucoma. Curr Opin Ophthalmol 2004;15:75.

Friedman
DS et al: Eye Diseases Prevalence Research Group. Prevalence of
open-angle glaucoma among adults in the United States. Arch Ophthalmol
2004;122:532.

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Higginbotham
EJ et al: The Ocular Hypertension Treatment Study: topical medication
delays or prevents primary openangle glaucoma in African American
individuals. Arch Ophthalmol 2004;122:813.

Weinreb RN et al: Primary open-angle glaucoma. Lancet 2004;363:1711.

Wong EY et al: Detection of undiagnosed glaucoma by eye health professionals. Ophthalmology 2004;111:1508.

UVEITIS

Uveitis means inflammation of the uveal tract, which is
formed by the iris (iritis), ciliary body (cyclitis), and choroid
(choroiditis). Inflammatory eye disease may also originate primarily in
the retina (retinitis) or retinal blood vessels (retinal vasculitis).

Intraocular inflammation is classified as anterior
uveitis, posterior uveitis, or panuveitis. Uveitis may also be termed
acute or chronic and granulomatous or nongranulomatous. In most cases
the pathogenesis of uveitis is primarily immunologic, but in
immunodeficiency states infection may be the cause.

Clinical Findings

Anterior uveitis is characterized by inflammatory cells
and flare within the aqueous. In severe cases, there may be hypopyon
(layered collection of white cells) and fibrin within the anterior
chamber. Cells may also be seen on the corneal endothelium as keratic
precipitates (KPs). In granulomatous uveitis, these are large
“mutton-fat” KPs, and iris nodules may be seen. In nongranulomatous
uveitis, the KPs are smaller and iris nodules are not seen. The pupil
is usually small, and with the development of posterior synechiae
(adhesions between the iris and anterior lens capsule), it also becomes
irregular.

Nongranulomatous anterior uveitis tends to present
acutely with unilateral pain, redness, photophobia, and visual loss.
Granulomatous anterior uveitis is more indolent, causing blurred vision
in a mildly inflamed eye.

In posterior uveitis, there are cells in the vitreous.
Inflammatory lesions may be present in the retina or choroid. Fresh
lesions are yellow, with indistinct margins, whereas older lesions have
more definite margins and are commonly pigmented. Retinal vessel
sheathing may occur adjacent to such lesions or more diffusely. In
severe cases, vitreous opacity precludes visualization of retinal
details.

Posterior uveitis tends to present with gradual visual
loss in a relatively quiet eye. Bilateral involvement is common. Visual
loss may be due to vitreous haze and opacities, inflammatory lesions
involving the macula, macular edema, retinal vein occlusion, or,
rarely, associated optic neuropathy.

Etiology

The systemic disorders associated with acute
nongranulomatous anterior uveitis are the HLA-B27related conditions
ankylosing spondylitis, reactive arthritis, psoriasis, ulcerative
colitis, and Crohn’s disease. Behçet’s syndrome produces both anterior
uveitis with recurrent hypopyon in 5% of patients and posterior uveitis
with retinal vein occlusions on occasion. Both herpes simplex and
herpes zoster infections may cause nongranulomatous anterior uveitis.

Diseases producing granulomatous anterior uveitis also
tend to be causes of posterior uveitis. These include sarcoidosis,
tuberculosis, syphilis, toxoplasmosis, Vogt-Koyanagi-Harada syndrome
(bilateral uveitis associated with alopecia, poliosis [depigmented
eyelashes, eyebrows, or hair], vitiligo, and hearing loss), and
sympathetic ophthalmia following penetrating ocular trauma. Syphilis
produces a characteristic “salt and pepper” fundus, often with
surprisingly little visual loss unless there is also primary syphilitic
optic atrophy. In congenital toxoplasmosis, there is usually evidence
of previous episodes of retinochoroiditis. The principal agents
responsible for ocular inflammation in AIDS are cytomegalovirus, herpes
simplex and herpes zoster viruses, mycobacteria, cryptococcus,
toxoplasma, and candida.

Autoimmune retinal vasculitis and pars planitis (intermediate uveitis) are idiopathic conditions that produce posterior uveitis.

Retinal detachment, intraocular tumors, and central nervous system lymphoma may all masquerade as uveitis.

Treatment

Anterior uveitis will usually respond to topical
corticosteroids. Occasionally, periocular steroid injections or even
systemic steroids may be required. Dilation of the pupil is important
to relieve discomfort and prevent posterior synechiae.

Posterior uveitis more commonly requires systemic
corticosteroid therapy and occasionally systemic immunosuppression with
agents such as azathioprine or cyclosporine. Pupillary dilation is not
usually necessary.

If an infectious cause is identified, specific
antimicrobial therapy may be indicated. In general, the prognosis for
anterior uveitis, particularly the nongranulomatous type, is better
than that for posterior uveitis.

Fernandez-Melon
J et al: Uveitis as the initial clinical manifestation in patients with
spondyloarthropathies. J Rheumatol 2004;31:524.

Monnet
D et al: Ophthalmic findings and frequency of extraocular
manifestations in patients with HLA-B27 uveitis: a study of 175 cases.
Ophthalmology 2004;111:802.

Smith JR: Management of uveitis. Clin Exp Med 2004;4:21.

Tugal-Tutkun I et al: Uveitis in Behcet disease: an analysis of 880 patients. Am J Ophthalmol 2004;138:373.

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CATARACT

General Considerations

Cataract is a lens opacity. Cataracts are usually
bilateral. They may be congenital (owing to intrauterine infections
such as rubella and cytomegalovirus, or inborn errors of metabolism
such as galactosemia); traumatic; or secondary to systemic disease
(diabetes, myotonic dystrophy, atopic dermatitis), systemic or inhaled
corticosteroid treatment, or uveitis. Senile cataract is by far the
most common type; most persons over age 60 have some degree of lens
opacity. Cigarette smoking increases the risk of cataract formation.

Clinical Findings

Even in its early stages, a cataract can be seen through
a dilated pupil with an ophthalmoscope or slitlamp. As the cataract
matures, the retina will become increasingly more difficult to
visualize, until finally the fundus reflection is absent and the pupil
is white.

Treatment

Functional visual impairment is the prime criterion for
surgery. The cataract is usually removed by one of the techniques in
which the delicate posterior lens capsule remains (extracapsular).
Laser treatment may be required subsequently if the posterior capsule
opacifies. Ultrasonic fragmentation (phacoemulsification) of the lens
nucleus allows cataract surgery to be performed through a small
incision without the need for sutures, thus reducing the postoperative
complication rate and accelerating visual rehabilitation.

It is routine practice to insert an intraocular lens at
the time of surgery. This dispenses with the need for heavy cataract
glasses or contact lenses. Multifocal and accommodative intraocular
lenses have been used with some success to reduce the need for both
distance and reading glasses.

Prognosis

If surgery is indicated, lens extraction improves visual
acuity in 95% of cases and can have a profound impact on quality of
life, although expectations must be realistic. The remainder either
have preexisting retinal damage or develop perioperative or
postoperative complications.

Dick HB: Accommodative intraocular lenses: current status. Curr Opin Ophthalmol 2005;16:8.

Harwood
RH et al: Falls and health status in elderly women following first eye
cataract surgery: a randomized controlled trial. Br J Ophthalmol
2005;89:53.

Pager
CK: Expectations and outcomes in cataract surgery: a prospective test
of 2 models of satisfaction. Arch Ophthalmol 2004;122:1788.

Shichi H: Cataract formation and prevention. Expert Opin Investig Drugs 2004;13:691.

RETINAL DETACHMENT

General Considerations

The primary event in rhegmatogenous retinal detachment
is the development of a retinal tear. This is usually spontaneous,
related to changes in the vitreous, but may be secondary to trauma.
Spontaneous detachment occurs most frequently in persons over 50 years
of age. Myopia and cataract extraction are the two most common
predisposing causes. Once there is a tear in the retina, fluid vitreous
is able to pass through the tear and lodge behind the sensory retina.
This, combined with vitreous traction and the pull of gravity, results
in progressive detachment. The superior temporal area is the most
common site of detachment. The area involved rapidly increases, causing
corresponding progressive visual loss. Central vision remains intact
until the macula becomes detached.

The basis of traction retinal detachment is the
development of preretinal fibrosis, such as in association with
proliferative retinopathy secondary to diabetic retinopathy or retinal
vein occlusion. Serous retinal detachment results from accumulation of
subretinal fluid, such as in exudative age-related macular degeneration
or secondary to choroidal tumors.

Clinical Findings

On ophthalmoscopic examination in rhegmatogenous retinal
detachment, the retina is seen hanging in the vitreous like a gray
cloud. One or more retinal tears will usually be found on further
examination. In traction retinal detachment, there is irregular retinal
elevation with fibrosis. With serous retinal detachment, the retina is
dome-shaped and the subretinal fluid may shift position with changes in
posture.

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Treatment

All cases of retinal detachment must be referred
immediately to an ophthalmologist. During transportation, the patient’s
head is positioned so that the detached portion of the retina will fall
back with the aid of gravity. Treatment of rhegmatogenous retinal
detachment is directed at closing the tears. A permanent adhesion
between the neurosensory retina, the retinal pigment epithelium, and
the choroid is produced in the region of the tears by applying
cryotherapy to the sclera or laser photocoagulation to the retina. To
achieve apposition of the neurosensory retina to the retinal pigment
epithelium while this adhesion is developing, indentation of the sclera
with a silicone sponge or buckle; subretinal fluid drainage via an
incision in the sclera; and injection of an expansile gas into the
vitreous cavity may be required. Certain types of uncomplicated retinal
detachment may be treated by pneumatic retinopexy, in which an
expansile gas is initially injected into the vitreous cavity followed
by positioning of the patient’s head to facilitate reattachment of the
retina. Once the retina is repositioned, the tear is sealed by laser
photocoagulation or cryotherapy. All the stages of pneumatic retinopexy
can be performed under local anesthesia as an office procedure. The
last stage is the same as is used to seal retinal tears without
associated detachment as prophylaxis against recurrence.

In complicated retinal detachments—particularly those in
which fibroproliferative tissue has developed on the surface of the
retina or within the vitreous cavity, ie, traction retinal
detachments—retinal reattachment can be accomplished only by removal of
the vitreous, direct manipulation of the retina, and internal tamponade
of the retina with air, expansile gases, or even silicone oil. (The
presence of an expansile gas within the eye is a contraindication to
air travel, mountaineering at high altitude, and nitrous oxide
anesthesia. Such gases persist in the globe for weeks after surgery.)
(See Chapter 38.) Treatment of serous retinal detachments is determined by the underlying cause.

Prognosis

About 80% of uncomplicated rhegmatogenous retinal
detachments can be cured with one operation; an additional 15% will
need repeated operations; and the remainder never reattach. The
prognosis is worse if the macula is detached or if the detachment is of
long duration. Without treatment, retinal detachment often becomes
total within 6 months. Spontaneous detachments are ultimately bilateral
in up to 25% of cases.

Gariano RF et al: Evaluation and management of suspected retinal detachment. Am Fam Physician 2004;69:1691.

Lee EJ: Use of nitrous oxide causing severe visual loss 37 days after retinal surgery. Br J Anaesth 2004;93:464.

VITREOUS HEMORRHAGE

Patients with vitreous hemorrhage complain of sudden
visual loss, abrupt onset of floaters that may progressively increase
in severity, or, occasionally, “bleeding within the eye.” Visual acuity
ranges from 20/20 to light perception only. The eye is not inflamed,
and the clue to diagnosis is the inability to see fundal details
clearly despite the presence of a clear lens. Causes of vitreous
hemorrhage include diabetic retinopathy, retinal tears (with or without
detachment), retinal vein occlusions, exudative age-related macular
degeneration, blood dyscrasias, trauma, and subarachnoid hemorrhage. In
all cases, examination by an ophthalmologist is essential. Retinal
tears and detachments necessitate urgent treatment (see above).

AGE-RELATED MACULAR DEGENERATION

Age-related macular degeneration is the leading cause of
permanent visual loss in the elderly. The exact cause is unknown, but
the incidence increases with each decade over age 50 years (to almost
30% by age 75). Other associations in addition to age include race
(usually white), sex (slight female predominance), family history, and
a history of cigarette smoking.

Age-related macular degeneration includes a broad
spectrum of clinical and pathologic findings that can be classified
into two groups: atrophic (“dry”) and exudative (“wet”). Although both
are progressive and usually bilateral, they differ in manifestations,
prognosis, and management. The precursor to age-related macular
degeneration is age-related maculopathy, the hallmark of which is the
development of retinal drusen. Hard drusen appear ophthalmoscopically
as discrete yellow deposits, usually in the macular region. Soft drusen
are larger, paler, and less distinct. Large, confluent soft drusen are
particularly associated with exudative age-related macular degeneration.

Atrophic degeneration is characterized by gradually
progressive bilateral visual loss of moderate severity due to atrophy
and degeneration of the outer retina, retinal pigment epithelium,
Bruch’s membrane, and choriocapillaris. In exudative degeneration,
visual loss is of more rapid onset and greater severity, and the two
eyes are frequently affected sequentially over a period of a few years.
The exudative form accounts for about 90% of all cases of legal
blindness due to this disorder. Impairment of the barrier function of
Bruch’s membrane (between the retinal pigment epithelium and the
choriocapillaris) allows serous fluid or blood to leak into the retina
to produce elevation of the retinal pigment epithelium from Bruch’s
membrane (retinal pigment epithelial detachment) or separation of the
neurosensory retina from the retinal pigment epithelium (serous retinal
detachment). These changes may resolve spontaneously, with variable
visual outcome, but are often associated with neovascularization
arising from the

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choroidal
vessels and extending between the retinal pigment epithelium and
Bruch’s membrane (subretinal neovascular membrane). This membrane
produces permanent visual loss.

Sudden visual loss in patients with exudative agerelated
macular degeneration occurs at the time of pigment epithelial or
sensory retinal detachment or hemorrhage from a subretinal neovascular
membrane. All these changes may occur in previously undiagnosed
patients, in patients known to have atrophic changes, and in the other
eye of patients with exudative disease. Laser photocoagulation of
subretinal neovascular membranes may delay the onset of permanent
visual loss but only when the membrane is far enough away from the
fovea to permit such treatment, which is relatively infrequent.
Conventional laser photocoagulation of subfoveal neovascular membranes
is associated with an inevitable immediate reduction in vision because
of associated retinal damage. Photodynamic laser therapy (PDT),
involving intravenous injection of verteporfin activated by subsequent
laser irradiation to produce cytotoxic derivatives that induce
selective vascular damage, is particularly indicated when the
neovascular membrane is well defined (“classic”) and may be helpful
when it is not (“occult”). Treatment often needs to be repeated, but
the relatively high cost can limit ongoing therapy. Various surgical
techniques to excise subfoveal neovascular membranes—or to reposition
the macula away from them—continue to be investigated. Older patients
developing sudden visual loss due to macular disease—particularly
paracentral distortion or scotoma with preservation of central
acuity—should be referred urgently to an ophthalmologist for assessment.

There is no specific treatment for atrophic age-related
macular degeneration, but—as with the exudative form—patients often
benefit from low vision aids. The disorder results in loss of central
vision only. Peripheral fields and hence navigational vision are always
maintained, though these may become impaired by cataract formation for
which surgery may be helpful. The value of oral antioxidants and other
dietary supplements in preventing visual loss in age-related macular
degeneration continues to be assessed.

Klein R et al: The epidemiology of age-related macular degeneration. Am J Ophthalmol 2004;137:486.

Liu
M et al: A review of treatments for macular degeneration: a synopsis of
currently approved treatments and ongoing clinical trials. Curr Opin
Ophthalmol 2004;15:221.

Meads
C et al: Photodynamic therapy with verteporfin is effective, but how
big is its effect? Results of a systematic review. Br J Ophthalmol
2004;88:212.

Moshfeghi DM et al: Age-related macular degeneration: evaluation and treatment. Cleve Clin J Med 2003;70:1017.

Zarbin MA: Current concepts in the pathogenesis of age-related macular degeneration. Arch Ophthalmol 2004;122:598.

CENTRAL & BRANCH RETINAL VEIN OCCLUSIONS

The severity of visual loss in central retinal vein
occlusion is variable. The visual impairment is commonly first noticed
upon waking. Ophthalmoscopic signs include disk swelling, venous
dilation and tortuosity, retinal hemorrhages, and cotton-wool spots.

In those with initially good acuity (20/60 or better),
the visual prognosis is good. With poor initial acuity (20/200 or
worse), extensive hemorrhages and multiple cotton-wool spots indicate
widespread retinal ischemia, which can be confirmed by demonstrating
extensive areas of capillary closure on fluorescein angiography. These
eyes are at high risk of developing neovascular (rubeotic) glaucoma,
typically within 3 months after venous occlusion, and should be
monitored by an ophthalmologist so that laser panretinal
photocoagulation can be undertaken if it occurs. Visual prognosis in
such cases is poor. Improvement in vision has been reported in central
retinal vein occlusion after direct injection of tissue plasminogen
activator into the retinal venous system, incision of the sclera at the
edge of the optic disk (radial optic neurotomy), and intravitreal
corticosteroid injection when macular edema is present.

Branch retinal vein occlusions may present in a variety
of ways. Sudden loss of vision may occur at the time of occlusion if
the fovea is involved or some time afterward from vitreous hemorrhage
due to retinal new vessels. More gradual visual loss may occur with
development of macular edema.

In acute branch retinal vein occlusion there are signs
similar to those of central retinal vein occlusion but affecting only
the retina drained by the obstructed vein. If retinal
neovascularization develops, the areas of ischemic retina should be
laser photocoagulated. Macular edema may respond to laser treatment or
possibly vitrectomy with surgical incision of the retinal vascular
adventitia (arteriovenous sheathotomy) and injection of tissue
plasminogen activator.

All patients with retinal vein occlusion should be
referred urgently to an ophthalmologist. They should be screened for
diabetes, systemic hypertension, hyperlipidemia, and glaucoma. In
younger patients, antiphospholipid antibodies, inherited thrombophilia,
and hyperhomocysteinemia should be excluded. Hyperviscosity syndromes
are rarely associated with retinal vein occlusions but may worsen their
prognosis.

Bashshur
ZF et al: Intravitreal triamcinolone for the management of macular
edema due to nonischemic central retinal vein occlusion. Arch
Ophthalmol 2004;122:1137.

Charbonnel
J et al: Management of branch retinal vein occlusion with vitrectomy
and arteriovenous adventitial sheathotomy, the possible role of
surgical posterior vitreous detachment. Graefes Arch Clin Exp
Ophthalmol 2004;242:223.

Garcia-Arumi
J: Management of macular edema in branch retinal vein occlusion with
sheathotomy and recombinant tissue plasminogen activator. Retina
2004;24:530.

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Mason J
3rd et al: Sheathotomy to decompress branch retinal vein occlusion: a
matched control study. Ophthalmology 2004;111:540.

CENTRAL & BRANCH RETINAL ARTERY OCCLUSIONS

Central retinal artery occlusion presents as sudden
profound monocular visual loss. Visual acuity is reduced to counting
fingers or worse, and visual field is restricted to an island of vision
in the temporal field. Ophthalmoscopy reveals pallid swelling of the
retina, most obvious in the posterior segment, with a cherryred spot at
the fovea. The retinal arteries are attenuated, and “box-car”
segmentation of blood in the veins may be seen. Occasionally, emboli
are seen in the central retinal artery or its branches. The retinal
swelling subsides over a period of 4–6 weeks, leaving a relatively
normal retinal appearance but a pale optic disk and attenuated
arterioles.

The patient is referred emergently to an
ophthalmologist. If seen within a few hours after onset, emergency
treatment—including laying the patient flat, ocular massage, high
concentrations of inhaled oxygen, intravenous acetazolamide, and
anterior chamber paracentesis—may influence the visual outcome. Studies
of thrombolysis, particularly by local intra-arterial injection but
also intravenously, have shown variable results.

Branch retinal artery occlusion may also present with
sudden loss of vision if the fovea is involved, but more commonly
sudden loss of visual field is the presenting complaint. Fundal signs
of retinal swelling and adjacent cotton-wool spots are limited to the
area of retina supplied by the occluded vessel. Patients with branch
retinal artery occlusions should be referred urgently to an
ophthalmologist.

Giant cell arteritis must be excluded in patients 55
years of age or older, especially because of the risk— highest in the
first few days—of involvement of the other eye. If giant cell arteritis
is suspected, either by clinical features, particularly jaw
claudication, or markedly elevated serum inflammatory markers, usually
erythrocyte sedimentation rate and C-reactive protein, immediately
institute high-dose corticosteroids (oral prednisolone 1–1.5 mg/kg/d,
if necessary preceded by intravenous hydrocortisone 250–500 mg stat)
and proceed promptly to temporal artery biopsy. In patients with
bilateral visual loss, initial treatment with methylprednisolone 1 g/d
for 1–3 days should be considered.

In central and particularly in branch retinal artery
occlusion, carotid and cardiac sources of emboli must be identified so
that appropriate treatment is given to reduce the risk of stroke (see Chapter 12).
Migraine, oral contraceptives, systemic vasculitis, congenital or
acquired thrombophilia, and hyperhomocysteinemia should be considered
in young patients, internal carotid artery dissection when there is
neck pain or a recent history of neck trauma, and diabetes,
hyperlipidemia, and systemic hypertension in all patients.

Lichtstein DM et al: Heeding clues to giant cell arteritis. Prompt response can prevent vision loss. Postgrad Med 2004;115: 91.

Yuzurihara D et al: Visual outcome in central retinal and branch retinal artery occlusion. Jpn J Ophthalmol 2004;48:490.

AMAUROSIS FUGAX

Amaurosis fugax (“fleeting blindness”) is usually caused
by retinal emboli from ipsilateral carotid disease. The visual loss is
usually described as a curtain passing vertically across the visual
field with complete monocular visual loss lasting a few minutes and a
similar curtain effect as the episode passes. To reduce the risk of
stroke, patients with high-grade stenosis (70–99%) of the ipsilateral
internal carotid artery should be considered for carotid endarterectomy
or angioplasty with stenting. Patients with medium-grade (30–69%)
stenosis, unless there are other risk factors for stroke, or low-grade
(up to 29%) stenosis are generally better treated medically with
aspirin or other antiplatelet drugs. The most reliable method of
evaluating carotid stenosis is intra-arterial angiography, but this is
associated with a number of complications including stroke. The
noninvasive techniques of duplex ultrasonography and magnetic resonance
angiography are suitable screening methods. Emboli from cardiac sources
may also be responsible for amaurosis fugax. Electrocardiography should
be performed in all cases, particularly to identify atrial
fibrillation. Echocardiography should be undertaken in young patients
and in any patient with clinical evidence of a potential cardiac source
of emboli. In younger patients without carotid or cardiac disease,
amaurosis fugax may be due to choroidal or retinal vascular spasm, in
which case calcium channel blockers such as slow-release nifedipine, 60
mg/d, appear to be effective. Antiphospholipid syndrome should be
excluded.

Similar obscurations of vision, characteristically on
exposure to bright light, may occur with poor ocular perfusion due to
severe occlusive carotid disease or to aortic dissection. More
transient episodes (lasting only a few seconds to 1 minute) affecting
both eyes occur in patients with raised intracranial pressure. In all
cases of episodic visual loss, early ophthalmologic consultation is
advisable.

Alamowitch
S et al: The risk and benefit of endarterectomy in women with
symptomatic internal carotid artery disease. Stroke 2005;36:27.

RETINAL DISORDERS ASSOCIATED WITH SYSTEMIC DISEASES

Many systemic diseases are associated with retinal
manifestations. These include diabetes mellitus, essential
hypertension, preeclampsia-eclampsia of pregnancy, blood dyscrasias,
and AIDS. The retinal changes caused by these disorders can be easily
observed with an ophthalmoscope.

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Diabetic Retinopathy

Diabetic retinopathy is the leading cause of new
blindness among adults in the United States aged 20–65 years. It is
broadly classified as nonproliferative or proliferative.

Nonproliferative retinopathy
shows dilation of veins, microaneurysms, retinal hemorrhages, retinal
edema, and hard exudates. A major subgroup includes those patients in
whom visual loss develops owing to edema, exudates, or ischemia at the
macula (diabetic maculopathy). This is the most common cause of legal
blindness in maturity-onset diabetes.

Proliferative retinopathy is
characterized by neovascularization, arising from either the optic disk
or the major vascular arcades. Vitreous hemorrhage is a common sequela.
Proliferation into the vitreous of blood vessels, with their associated
fibrous component, leads to tractional retinal detachment. Without
treatment, the visual prognosis with proliferative retinopathy is
generally much worse than that with nonproliferative retinopathy.
Severe proliferative retinopathy is often complicated by maculopathy.

Nonproliferative retinopathy is occasionally present at
the time of diagnosis in type 2 diabetes. Treatment includes optimizing
control of blood glucose, blood pressure, and serum lipids. Institution
of intensive insulin therapy can be associated with temporary
exacerbation of retinopathy, with multiple cotton-wool spots. Laser
photocoagulation is helpful in the treatment of focal macular edema but
may also be used when there is diffuse macular edema, which may also
respond to intravitreal injection of corticosteroid. The presence of
macular edema can be detected only by stereoscopic examination of the
retina or by fluorescein angiography. The level of visual acuity is a
poor guide to the presence of treatable maculopathy—hence the need for
regular ophthalmologic follow-up.

Proliferative retinopathy must be recognized early and
treated by panretinal laser photocoagulation to prevent blindness.
Neovascularization is all too often diagnosed only at the time of
vitreous hemorrhage. In some patients, a “preproliferative” retinopathy
may be identified. Whether panretinal laser photocoagulation should be
undertaken at this time can be determined by the degree of retinal
ischemia as assessed by fluorescein angiography.

Surgical treatment (vitrectomy) is used either to remove
vitreous hemorrhage and thus allow perioperative panretinal laser
photocoagulation for the underlying retinal neovascularization, to deal
with retinal detachments involving the macula, to manage rapidly
progressive proliferative disease, or to treat persistent macular edema.

Patients with diabetes should have yearly
ophthalmoscopic examination through dilated pupils. Examination by an
ophthalmologist is advisable in type 1 diabetes of more than 5 years’
duration; at the time of diagnosis in type 2 diabetes; in early
pregnancy, prior to conception in women contemplating pregnancy, and
every 4–8 weeks throughout pregnancy; if ocular symptoms develop; or if
there are suspicious findings of retinopathy, especially
neovascularization or macular exudates. Failure to diagnose diabetic
retinopathy by ophthalmoscopic examination is common, particularly if
the pupils are not dilated. The severity of diabetic retinopathy can be
decreased by control of blood glucose levels, but good diabetic control
is more important in preventing the development of retinopathy than in
influencing its subsequent course. Proliferative diabetic retinopathy,
especially after successful laser treatment, is not a contraindication
to treatment with thrombolytic agents, aspirin, or warfarin unless
there has been recent vitreous or preretinal hemorrhage.

Centers
for Disease Control and Prevention (CDC): Prevalence of visual
impairment and selected eye diseases among persons aged 50 years with
and without diabetes—United States, 2002. MMWR Morb Mortal Wkly Rep
2004;53:1069.

Colucciello M: Diabetic retinopathy. Control of systemic factors preserves vision. Postgrad Med 2004;116:57.

Massin
P et al: Intravitreal triamcinolone acetonide for diabetic diffuse
macular edema: preliminary results of a prospective controlled trial.
Ophthalmology 2004;111:218.

Matthews
DR et al: Risks of progression of retinopathy and vision loss related
to tight blood pressure control in type 2 diabetes mellitus: UKPDS 69.
Arch Ophthalmol 2004;122:1631.

Sinclair
SH et al: The internist’s role in managing diabetic retinopathy:
screening for early detection. Cleve Clin J Med 2004;71:151.

Sjolie AK et al: Medical management of diabetic retinopathy. Diabet Med 2004;21:666.

Hypertensive Retinochoroidopathy

Systemic hypertension affects both the retinal and
choroidal circulations. The clinical manifestations vary according to
the degree and rapidity of rise in blood pressure and the underlying
state of the ocular circulation. The most florid disease occurs in
young patients with abrupt elevations of blood pressure, such as may
occur in pheochromocytoma, malignant hypertension, or
preeclampsia-eclampsia.

Chronic hypertension accelerates the development of
atherosclerosis. The retinal arterioles become more tortuous and narrow
and develop abnormal light reflexes (“silver-wiring” and
“copper-wiring”). There is increased venous compression at the retinal
arteriovenous crossings (“arteriovenous nicking”), an important factor
predisposing to branch retinal vein occlusions. Flame-shaped
hemorrhages occur in the nerve fiber layer of the retina.

Acute elevations of blood pressure result in loss of
autoregulation in the retinal circulation, leading to the breakdown of
endothelial integrity and occlusion of precapillary arterioles and
capillaries. These pathologic changes are manifested as cotton-wool
spots, retinal hemorrhages, retinal edema, and retinal exudates, often
in a stellate appearance at the macula. In the choroid,
vasoconstriction and ischemia result in serous retinal detachments

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and
retinal pigment epithelial infarcts. These infarcts later develop into
pigmented lesions that may be focal, linear, or wedge-shaped. The
abnormalities in the choroidal circulation may also affect the optic
nerve head, producing ischemic optic neuropathy with optic disk
swelling. Malignant hypertensive retinopathy was the term previously
used to describe the constellation of clinical signs resulting from the
combination of abnormalities in the retinal, choroidal, and optic disk
circulation. When there is such severe disease, there is likely to be
permanent retinal, choroidal, or optic nerve damage. Precipitous
reduction of blood pressure may exacerbate such damage.

Luo BP et al: Update on the ocular manifestations of systemic arterial hypertension. Curr Opin Ophthalmol 2004;15:203.

Wong TY et al: Hypertensive retinopathy. N Engl J Med 2004;351:2310.

Blood Dyscrasias

In conditions characterized by thrombocytopenia or
severe anemia, various types of hemorrhages occur in both the retina
and choroid and may lead to visual loss. If macular hemorrhages have
not occurred, it is possible to regain normal vision with treatment.

Proliferative retinopathy (sickle cell retinopathy) is
particularly common in hemoglobin SC disease but may also occur with
other hemoglobin S variants. Severe visual loss is rare. Retinal
photocoagulation reduces the frequency of vitreous hemorrhage. Surgery
is occasionally needed for unresolving vitreous hemorrhage or
tractional retinal detachment.

AIDS

Cotton-wool spots, retinal hemorrhages, and microaneurysms are the most common ophthalmic abnormalities in AIDS patients.

Cytomegalovirus (CMV) retinitis
occurs when CD4 counts are below 50/mcL. It is characterized by
progressively enlarging yellowish-white patches of retinal
opacification, which are accompanied by retinal hemorrhages; they
usually begin adjacent to the major retinal vascular arcades. Patients
are often asymptomatic until there is involvement of the fovea or optic
nerve or until retinal detachment develops.

The commonly used agents are intravenous or intravitreal
ganciclovir, foscarnet, and cidofovir, which has the significant
advantage of a prolonged intracellular half-life such that no more than
weekly administration is required. Major side effects are neutropenia
with systemic ganciclovir and nephrotoxicity with foscarnet and
cidofovir. Dosage of both ganciclovir and foscarnet is adjusted in
renal failure. Oral probenecid and intravenous hydration are used to
minimize nephrotoxicity from cidofovir. Oral valganciclovir and
intravitreal fomivirsen are also effective. All the available agents
are virostatic.

Initial therapy is as follows: (1)
intravenous—ganciclovir 5 mg/kg twice a day, foscarnet 60 mg/kg three
times a day, or cidofovir 5 mg/kg once weekly, usually for 2 weeks; (2)
oral—valganciclovir 900 mg twice daily; or (3) by local administration,
using either intravitreal injection of ganciclovir, foscarnet, or
fomivirsen or the sustained-release ganciclovir intravitreal implant.
Intravitreal cidofovir is effective, but there is a high incidence of
uveitis, low intraocular pressure, and ciliary body necrosis.
Maintenance therapy can be conducted with lower-dose intravenous
therapy (ganciclovir 3.75 mg/kg/d or foscarnet 60 mg/kg/d for 5 days
each week, or cidofovir 5 mg/ kg once every 2 weeks), with oral
ganciclovir (3 g/d) or oral valganciclovir 900 mg once daily, or with
intravitreal therapy. Local therapy tends to be more effective than
systemic therapy and avoids systemic side effects, but there is a risk
of intraocular complications, and the incidence of retinitis in the
fellow eye and of extraocular CMV infection is higher. Unresponsive
disease or reactivation during maintenance therapy can be managed by
changing to a different agent or by use of combination therapy. Retinal
detachment, either due to retinitis or as a complication of
intravitreal therapy, requires vitrectomy and intravitreal silicone
oil. Oral ganciclovir as prophylaxis against cytomegalovirus retinitis
in patients with low CD4 counts or high CMV burdens has not been found
to be worthwhile.

Antiretroviral therapy may result in reduction of HIV
virus load and increase in CD4 counts, and even regression of CMV
retinitis without the use of anticytomegalovirus therapy. If the CD4
count is maintained above 100/mcL, it may be possible to discontinue
maintenance anticytomegalovirus therapy. Highly active antiretroviral
therapy (HAART) occasionally leads to “immune recovery” uveitis, which
may lead to visual loss.

Other opportunistic ophthalmic infections occurring in
AIDS patients include herpes simplex retinitis, toxoplasmic and
candidal chorioretinitis, and herpes zoster ophthalmicus. Kaposi’s
sarcoma of the conjunctiva and orbital lymphoma may also be seen on
rare occasions.

Dunn
JP et al: Complications of ganciclovir implant surgery in patients with
cytomegalovirus retinitis: the Ganciclovir Cidofovir Cytomegalovirus
Retinitis Trial. Retina 2004;24: 41.

Hodge WG et al: Clinical risk factors for cytomegalovirus retinitis in patients with AIDS. Ophthalmology 2004;111: 1326.

Jabs
DA et al: Course of cytomegalovirus retinitis in the era of highly
active antiretroviral therapy: 1. Retinitis progression. Ophthalmology
2004;111:2224.

Jabs
DA et al: Course of cytomegalovirus retinitis in the era of highly
active antiretroviral therapy: 2. Second eye involvement and retinal
detachment. Ophthalmology 2004;111:2232.

Vrabec TR: Posterior segment manifestations of HIV/AIDS. Surv Ophthalmol 2004;49:131.

P.169

ANTERIOR ISCHEMIC OPTIC NEUROPATHY

Anterior ischemic optic neuropathy—due to inadequate
perfusion of the posterior ciliary arteries that supply the anterior
portion of the optic nerve—produces sudden visual loss, usually with an
altitudinal field defect, and optic disk swelling. In older patients,
it is often caused by giant cell arteritis, which necessitates
high-dose systemic steroid treatment to prevent visual loss in the
fellow eye. (See Central and Branch Retinal Artery Occlusions,
above.) The predominant factor predisposing to nonarteritic anterior
ischemic optic neuropathy is congenitally small optic disks. Other
causative factors include systemic hypertension, diabetes,
hyperlipidemia, systemic vasculitis, inherited or acquired
thrombophilia, and ingestion of sildenafil.

Rucker JC et al:. Ischemic optic neuropathies. Curr Opin Neurol 2004;17:27.

OPTIC NEURITIS

Optic neuritis is characterized by unilateral loss of
vision, which usually develops over a few days. Vision ranges from
20/30 to no perception of light. Commonly there is pain in the region
of the eye, particularly on eye movements. Field loss is usually a
central scotoma, but a wide range of monocular field defects is
possible. There is marked loss of color vision and a relative afferent
pupillary defect. In about two-thirds of cases, the optic nerve is
normal during the acute stage (retrobulbar optic neuritis). In the
remainder, the optic disk is swollen (papillitis) with occasional
flame-shaped peripapillary hemorrhages. Visual acuity usually improves
within 2–3 weeks and returns to 6/ 12 or better in 95% of previously
unaffected eyes. Optic atrophy subsequently develops if there has been
destruction of sufficient optic nerve fibers.

Optic neuritis is strongly associated with demyelinating
disease, particularly multiple sclerosis. Among patients with
clinically isolated optic neuritis, about 40% will develop multiple
sclerosis within 10 years but the visual and neurologic prognosis is
good. The major risk factors are female gender, multiple white matter
lesions on brain magnetic resonance imaging (MRI), and cerebrospinal
fluid oligoclonal bands.

In acute demyelinating optic neuritis, intravenous
methylprednisolone therapy accelerates visual recovery. Use in an
individual patient is determined by the degree of visual loss, the
state of the fellow eye, and the patient’s visual requirements. In
patients with a first episode of optic neuritis and multiple cerebral
white matter lesions, long-term interferon therapy reduces the risk of
subsequent development of multiple sclerosis by 25% at 2–3 years.

Optic neuritis also occurs with viral infections
(including measles, mumps, influenza, and those caused by the
varicella-zoster virus), with various autoimmune disorders,
particularly systemic lupus erythematosus, and by spread of
inflammation from meninges, orbital tissues, or paranasal sinuses.
Optic neuritis due to herpes zoster or systemic lupus erythematosus
generally has a poorer prognosis and requires high-dose intravenous
corticosteroid therapy.

All patients with optic neuritis should be referred
urgently for neuro-ophthalmologic assessment. Any patient with isolated
optic neuritis in which visual recovery does not occur requires
exclusion of a compressive lesion or an intrinsic optic nerve tumor.

Beck RW et al: Neurologic impairment 10 years after optic neuritis. Arch Neurol 2004;61:1386.

Beck
RW et al: Visual function more than 10 years after optic neuritis:
experience of the optic neuritis treatment trial. Am J Ophthalmol
2004;137:77.

Pirko I et al: The natural history of recurrent optic neuritis. Arch Neurol 2004;61:1401.

OPTIC DISK SWELLING

Optic disk swelling may result from intraocular disease,
orbital and optic nerve lesions, severe hypertensive
retinochoroidopathy, or raised intracranial pressure. Intraocular
causes include central retinal vein occlusion, posterior uveitis, and
posterior scleritis. Optic nerve lesions causing disk swelling include
optic neuritis; anterior ischemic optic neuropathy; optic disk drusen
(pseudopapilledema); optic nerve sheath meningioma; and nerve
infiltration by sarcoidosis, leukemia, or lymphoma. Any orbital lesion
causing nerve compression may produce disk swelling.

Papilledema (optic disk
swelling due to raised intracranial pressure) is usually bilateral and
most commonly produces enlargement of the blind spot without loss of
acuity. Chronic papilledema, as in idiopathic intracranial hypertension
and dural venous sinus occlusion, may be associated with progressive
visual field loss and occasionally with profound loss of acuity. All
patients with chronic papilledema must be monitored
carefully—especially their visual fields—and optic nerve sheath
fenestration or lumboperitoneal shunt is considered in those with
progressive visual failure not controlled by medical therapy (weight
loss where appropriate and acetazolamide).

Optic disk drusen are a
possibility when disk swelling is not associated with any visual
disturbance or symptoms of raised intracranial pressure. Exposed optic
disk drusen may be obvious clinically or can be demonstrated by their
autofluorescence. Buried drusen are best detected by orbital ultrasound
or computed tomographic (CT) scanning. Other family members may be
similarly affected.

Friedman DI et al: Idiopathic intracranial hypertension. J Neuroophthalmol 2004;24:138.

Wilkins JM et al: Visual manifestations of visible and buried optic disc drusen. J Neuroophthalmol 2004;24:125.

P.170

OCULAR MOTOR PALSIES

In complete third nerve paralysis,
there is ptosis with a divergent and slightly depressed eye.
Extraocular movements are restricted in all directions except laterally
(preserved lateral rectus function). Intact fourth nerve (superior
oblique) function is detected by the presence of inward rotation on
attempted depression of the eye.

Pupillary involvement (dilated pupil that does not react
to accommodation or to light shone in either eye) is an important sign
differentiating “surgical” from “medical” causes of isolated third
nerve palsy. Compressive lesions of the third nerve—eg, aneurysm of the
posterior communicating artery and uncal herniation due to a
supratentorial mass lesion—characteristically have pupillary
involvement. Patients with painful isolated third nerve palsy and
pupillary involvement are assumed to have a posterior communicating
artery aneurysm until this has been excluded. Medical causes of
isolated third nerve palsy include diabetes, hypertension, and giant
cell arteritis.

Fourth nerve paralysis
causes upward deviation of the eye with failure of depression on
adduction. There is vertical diplopia that becomes most apparent on
attempted reading and descending stairs. Many cases of isolated fourth
nerve palsy are due to a congenital lesion. Trauma is a major cause of
acquired—particularly bilateral—fourth nerve palsy, but cerebral
neoplasms and medical causes such as in third nerve palsies should also
be considered.

Sixth nerve paralysis causes
convergent squint in the primary position with failure of abduction of
the affected eye, producing horizontal diplopia that increases on gaze
to the affected side and on looking into the distance. It is an
important sign of raised intracranial pressure. Sixth nerve palsy may
also be due to trauma, neoplasms, brain stem lesions, or medical causes.

An intracranial or intraorbital mass lesion should be
considered in any patient with an isolated ocular motor palsy. In
patients with isolated ocular motor nerve palsies presumed to be due to
medical causes, brain MRI is generally only necessary if recovery has
not begun within 3 months, although a recent study suggests that it
should be undertaken in all cases.

Ocular motor nerve palsies occurring in association with
other neurologic signs may be due to lesions in the brain stem, the
cavernous sinus, or in the orbit. Lesions around the cavernous sinus
involve the upper divisions of the trigeminal nerve, the ocular motor
nerves, and occasionally the optic chiasm. Orbital apex lesions involve
the optic nerve and the ocular motor nerves.

Myasthenia and dysthyroid eye disease must always be
considered in the differential diagnosis of disordered extraocular
movements.

Chou
KL et al: Acute ocular motor mononeuropathies: prospective study of the
roles of neuroimaging and clinical assessment. J Neurol Sci
2004;219:35.

Patel
SV et al: Incidence, associations, and evaluation of sixth nerve palsy
using a population-based method. Ophthalmology 2004;111:369.

DYSTHYROID EYE DISEASE

Dysthyroid eye disease is a clinical syndrome caused by
deposition of mucopolysaccharides and infiltration with chronic
inflammatory cells of the orbital tissues, particularly the extraocular
muscles. Patients may have clinical or laboratory evidence of thyroid
dysfunction, elevated thyroid autoantibodies, or no detectable
abnormality outside the orbit. Radioiodine therapy and cigarette
smoking increase its severity.

The primary clinical features are proptosis, lid
retraction and lid lag, conjunctival chemosis and episcleral
inflammation, and extraocular muscle abnormalities due to restriction
of their actions. Resulting symptoms are cosmetic abnormalities,
surface irritation, which usually responds to artificial tears, and
diplopia, which should be treated conservatively (eg, with prisms) in
the active stages of the disease and only by surgery when the disease
has been static for at least 6 months.

The important complications are corneal exposure and
optic nerve compression, both of which may lead to marked visual loss.
Treatment is by urgent orbital decompression, either medically, with
high-dose systemic steroids (prednisolone 80–100 mg/d)—although this is
often of only short-term benefit—by radiotherapy, or by surgery,
usually consisting of extensive removal of bone from the medial,
inferior, and lateral walls of the orbit.

The optimal management of moderately severe dysthyroid
eye disease without visual loss is controversial. Systemic steroids and
radiotherapy do not provide definite long-term benefit. Peribulbar
steroid injections have been advocated. Surgical decompression may be
justified in patients with marked proptosis. Lateral tarsorrhaphy may
be used for moderately severe corneal exposure. Other procedures are
particularly useful for correcting lid retraction but should not be
undertaken until the orbital disease is quiescent and orbital
decompression or extraocular muscle surgery has been undertaken.
Establishing and maintaining euthyroidism are important in all cases.

Ebner
R et al: Treatment of thyroid associated ophthalmopathy with periocular
injections of triamcinolone. Br J Ophthalmol 2004;88:1380.

Kim JM et al: The relation of Graves’ ophthalmopathy to circulating thyroid hormone status. Br J Ophthalmol 2004;88:72.

ORBITAL CELLULITIS

Orbital cellulitis is manifested by an abrupt onset of
fever, proptosis, restriction of extraocular movements, and swelling
with redness of the lids. Infection of the paranasal sinuses is the
usual underlying cause. Immediate treatment with intravenous
antibiotics is necessary to prevent optic nerve damage and spread of
infection to the cavernous sinuses, meninges, and brain. The response
to antibiotics is usually excellent, but abscess formation may
necessitate surgical drainage. In immunocompromised patients,
zygomycosis must be considered.

P.171

Greenberg
RN et al: Zygomycosis (mucormycosis): emerging clinical importance and
new treatments. Curr Opin Infect Dis 2004;17:517.

Howe L et al: Guidelines for the management of periorbital cellulitis/ abscess. Clin Otolaryngol 2004;29:725.

OCULAR TRAUMA

Conjunctival & Corneal Foreign Bodies

If a patient complains of “something in my eye” and
gives a consistent history, a foreign body is usually present on the
cornea or under the upper lid even though it may not be visible. Visual
acuity should be tested before treatment is instituted, as a basis for
comparison in the event of complications.

After a local anesthetic (eg, proparacaine, 0.5%) is
instilled, the eye is examined with a hand flashlight, using oblique
illumination, and loupe. Corneal foreign bodies may be made more
apparent by the instillation of sterile fluorescein. They are then
removed with a sterile wet cotton-tipped applicator.
Polymyxin-bacitracin ophthalmic ointment should be instilled. It is not
necessary to patch the eye, but the patient must be examined 24 hours
later for secondary infection of the crater. If a corneal foreign body
cannot be removed in this manner, the patient should be referred to an
ophthalmologist.

Steel foreign bodies usually leave a diffuse rust ring.
This requires excision of the affected tissue and is best done under
local anesthesia using a slitlamp. Caution: Anesthetic drops should not be given to the patient for self-administration.

If there is no infection, a layer of corneal epithelial
cells will line the crater within 24 hours. The intact corneal
epithelium forms an effective barrier to infection, but once it is
disturbed the cornea becomes extremely susceptible to infection. Early
infection is manifested by a white necrotic area around the crater and
a small amount of gray exudate. These patients are referred immediately
to an ophthalmologist; untreated corneal infection may lead to loss of
the eye.

In the case of a foreign body under the upper lid, a
local anesthetic is instilled and the lid is everted by grasping the
lashes gently and exerting pressure on the mid portion of the outer
surface of the upper lid with an applicator. If a foreign body is
present, it can easily be removed by passing a wet sterile
cotton-tipped applicator across the conjunctival surface.

Intraocular Foreign Body

Intraocular foreign body requires emergency treatment by
an ophthalmologist. Patients giving a history of “something hitting the
eye”—particularly while hammering on metal or using grinding
equipment—must be assessed for this possibility, especially when no
corneal foreign body is seen, a corneal or scleral wound is apparent,
or there is marked visual loss or media opacity. Such patients must be
treated as for corneal laceration (see below) and referred without
delay. Intraocular foreign bodies significantly increase the risk of
intraocular infection.

Corneal Abrasions

A patient with a corneal abrasion complains of severe
pain and photophobia. There is often a history of trauma to the eye,
commonly involving a fingernail, piece of paper, or contact lens.
Visual acuity is recorded, and the cornea and conjunctiva are examined
with a light and loupe to rule out a foreign body. If an abrasion is
suspected but cannot be seen, sterile fluorescein is instilled into the
conjunctival sac: the area of corneal abrasion will stain a deeper
green than the surrounding cornea.

Treatment includes polymyxin-bacitracin ophthalmic
ointment, mydriatic (cyclopentolate 1%), and analgesics either topical
or oral nonsteroidal anti-inflammatory agents. Padding the eye is
probably not helpful. The patient should be reviewed within 48 hours to
be certain the cornea has healed. Recurrent corneal erosion may follow
corneal abrasions.

Wilson SA et al: Management of corneal abrasions. Am Fam Physician 2004;70:123.

Contusions

Contusion injuries of the eye and surrounding structures
may cause ecchymosis (“black eye”), subconjunctival hemorrhage, edema
or rupture of the cornea, hemorrhage into the anterior chamber
(hyphema), rupture of the root of the iris (iridodialysis), paralysis
of the pupillary sphincter, paralysis of the muscles of accommodation,
cataract, dislocation of the lens, vitreous hemorrhage, retinal
hemorrhage and edema (most common in the macular area), detachment of
the retina, rupture of the choroid, fracture of the orbital floor
(“blowout fracture”), or optic nerve injury. Many of these injuries are
immediately obvious; others may not become apparent for days or weeks.
Patients with moderate to severe contusions should be seen by an
ophthalmologist.

Any injury causing hyphema involves the danger of
secondary hemorrhage, which may cause intractable glaucoma with
permanent visual loss. The patient should be advised to rest until
complete resolution has occurred. Daily ophthalmologic assessment is
essential. Aspirin and any drugs inhibiting coagulation increase the
risk of secondary hemorrhage and are to be avoided. Sickle cell anemia
or trait adversely affects outcome.

Lacerations

A. LIDS

If the lid margin is lacerated, the patient should be
referred for specialized care, since permanent notching may result.
Lacerations of the lower eyelid near the inner canthus often sever the
lower canaliculus. Lid lacerations not involving the margin may be
sutured like any skin laceration.

P.172

B. CONJUNCTIVA

In lacerations of the conjunctiva, sutures are not
necessary. To prevent infection, sulfonamides or other antibiotics are
instilled into the eye until the laceration is healed.

C. CORNEA OR SCLERA

Patients with suspected corneal or scleral lacerations
must be seen promptly by an ophthalmologist. Manipulation is kept to a
minimum, since pressure may result in extrusion of the intraocular
contents. The eye is bandaged lightly and covered with a metal shield
that rests on the orbital bones above and below. The patient should be
instructed not to squeeze the eye shut and to remain still. The eye is
routinely studied by x-ray, and CT scanning if necessary, to identify
and localize any metallic intraocular foreign body. MRI is
contraindicated owing to the risk of movement of the foreign body in
the magnetic field. Endophthalmitis occurs in over 5% of open globe
injuries.

Essex RW et al: Post-traumatic endophthalmitis. Ophthalmology 2004;111:2015.

ULTRAVIOLET KERATITIS (ACTINIC KERATITIS)

Ultraviolet burns of the cornea are usually caused by
use of a sunlamp without eye protection, exposure to a welding arc, or
exposure to the sun when skiing (“snow blindness”). There are no
immediate symptoms, but about 6–12 hours later the patient complains of
agonizing pain and severe photophobia. Slitlamp examination after
instillation of sterile fluorescein shows diffuse punctate staining of
both corneas.

Treatment consists of binocular patching and
instillation of 1–2 drops of 1% cyclopentolate (to relieve the
discomfort of ciliary spasm). All patients recover within 24–48 hours
without complications. Local anesthetics should not be prescribed.

Chemical Conjunctivitis & Keratitis

Chemical burns are treated by irrigation of the eyes
with saline solution or plain water as soon as possible after exposure.
Neutralization of an acid with an alkali or vice versa generates heat
and may cause further damage. Alkali injuries are more serious and
require prolonged irrigation, since alkalies are not precipitated by
the proteins of the eye as are acids. It is important to remove any
retained particulate matter such as is typically present in injuries
involving cement and building plaster. This may require double eversion
of the upper lid. The pupil should be dilated with 1% cyclopentolate, 1
drop twice a day, to relieve discomfort and prophylactic topical
antibiotics should be started. In moderate to severe injuries,
intensive topical corticosteroids and topical and systemic vitamin C
are also necessary. Complications include mucus deficiency, scarring of
the cornea and conjunctiva, symblepharon (adhesions between the tarsal
and bulbar conjunctiva), tear duct obstruction, and secondary
infection. It can be difficult to assess severity of chemical burns
without slit-lamp examination.

PRINCIPLES OF TREATMENT OF OCULAR INFECTIONS

Before determining the drug of choice for treatment of
ocular infection, the causative organisms must be identified, but in
most cases empirical treatment is used in the first instance. In the
treatment of conjunctivitis and for prophylaxis against ocular
infection, it is preferable to use a drug that is not given
systemically. Although fluoroquinolones, including the
fourth-generation fluoroquinolones, are advocated for the treatment of
conjunctivitis, they should be reserved for treatment of bacterial
keratitis and other serious infections. Of the available local
antibacterial agents, the sulfonamides are effective and inexpensive;
sulfisoxazole and sodium sulfacetamide are examples. The sulfonamides
have the added advantages of low allergenicity and effectiveness
against the chlamydial group of organisms. They are available in
ointment or solution form. Combined bacitracin-polymyxin ointment is
often used prophylactically after corneal foreign body removal for the
protection it affords against both grampositive and gram-negative
organisms.

Among the most effective broad-spectrum antibiotics for
ophthalmic use are fluoroquinolones (ciprofloxacin, ofloxacin,
norfloxacin, levofloxacin, moxifloxacin, and gatifloxacin), gentamicin,
tobramycin, and neomycin. For pneumococcus, one of the newer
fluoroquinolones, penicillin G, or nafcillin (if β-lactamase resistance
is present) is required. Allergic reactions to neomycin are common.
Other antibiotics frequently used are erythromycin, the tetracyclines,
and the cephalosporins.

Method of Administration

Most ocular anti-infective drugs are administered
locally. Ointments have greater therapeutic effectiveness than
solutions, since contact can be maintained longer. However, they do
cause blurring of vision; if this must be avoided, solutions should be
used.

Systemic administration is required for all intraocular
infections, orbital cellulitis, dacryocystitis, gonococcal
keratoconjunctivitis, inclusion conjunctivitis, and severe external
infection that does not respond to local treatment.

Kowalski RP et al: Infectious disease: changing antibiotic susceptibility. Ophthalmol Clin North Am 2003;16:1.

TECHNIQUES USED IN THE TREATMENT OF OCULAR DISORDERS

Table 7-2 lists commonly used ophthalmic drugs and their indications and costs.

Table 7-2. Topical ophthalmic agents.

Agent	Representative Cost/Size¹	Sig	Indications
AGENTS FOR GLAUCOMA AND OCULAR HYPERTENSION
Sympathomimetics
Apraclonidine HCl 0.5% solution (Iopidine)	$66.48/5 mL	1 drop three times daily	Reduction of intraocular pressure. Expensive. Reserve for treatment of resistant cases.
Apraclonidine HCl 1% solution (Iopidine)	$11.03/unit dose 0.1 mL	1 drop 1 hour before and immediately after anterior segment laser surgery	To control or prevent elevations of intraocular pressure after laser trabeculoplasty or iridotomy.
Brimonidine tartrate 0.2% solution (Alphagan)	$32.65/5 mL	1 drop two or three times daily	Reduction of intraocular pressure.
Dipivefrin HCl 0.1% solution (Propine)²	$14.07/5 mL	1 drop every 12 hours	Open-angle glaucoma.
Epinephrine HCl 0.25%, 0.5% (Epifrin), 1%, and 2% solution (various)³	1%:$49.69/15 mL 2%:$54.36/15 mL	1 drop twice daily
β-Adrenergic blocking agents
Betaxolol HCl 0.5% solution and 0.25% suspension (Betoptic S)⁴	0.5%:$44.56/10 mL 0.25%:$78.24/10 mL	1 drop twice daily	Reduction of intraocular pressure.
Carteolol HCl 1% solution (Ocupress)⁵	$37.07/10 mL	1 drop twice daily
Levobunolol HCl 0.25% and 0.5% solution (Betagan)⁵	0.5%:$32.25/10 mL	1 drop once or twice daily
Metipranolol HCl 0.3% solution (OptiPranolol)⁵	$26.85/10 mL	1 drop twice daily
Timolol 0.25% and 0.5% solution (Betimol)⁵	0.5%:$42.84/10 mL	1 drop once or twice daily
Timolol maleate 0.25% and 0.5% solution (Timoptic) and 0.25% and 0.5% gel (Timoptic-XE)⁵	0.5% solution:$32.29/10 mL 0.5% gel:$32.30/5 mL	1 drop once or twice daily
Miotics
Pilocarpine HCl (various)⁶ 1–4%, 6%, 8%, and 10%	2%:$11.80/15 mL	1 drop three or four times daily	Reduction of intraocular pressure, treatment of acute or chronic angle-closure glaucoma, and pupillary constriction.
Pilocarpine HCl 4% gel (Pilopine HS)	$42.00/4 g	Apply 0.5-inch ribbon in lower conjunctival sac at bedtime
Carbonic anhydrase inhibitors
Dorzolamide HCl 2% solution (Trusopt)	$55.88/10 mL	1 drop three times daily	Reduction of intraocular pressure.
Brinzolamide 1% suspension (Azopt)	$67.80/10 mL	1 drop three times daily	Reduction of intraocular pressure.
Prostaglandin analogs
Bimatoprost 0.03% solution(Lumigan)	$66.45/2.5 mL	1 drop once daily at night
Latanoprost 0.005% solution (Xalatan)	$58.84/2.5 mL	1 drop once or twice daily at night
Travoprost 0.004% solution (Travatan)	$59.70/2.5 mL	1 drop once daily at night	Reduction of intraocular pressure.
Unoprostone 0.15% solution (Rescula)	$51.50/5 mL	1 drop twice daily	Reduction of intraocular pressure.
Combined preparations
Xalacom (latanoprost 0.005% and timolol 0.5%)	Not available in the United States	1 drop daily in the morning	Reduction of intraocular pressure.
Cosopt (dorzolamide 2% and timolol 0.5%)	$53.51/5 mL	1 drop twice daily	Reduction of intraocular pressure.
ANTI-INFLAMMATORY AGENTS
Nonsteroidal anti-inflammatory agents⁷
Diclofenac sodium 0.1% solution (Voltaren)	$67.61/5 mL	1 drop to operated eye four times daily beginning 24 hours after cataract surgery and continuing through first 2 postoperative weeks	Treatment of postoperative inflammation following cataract extraction and laser corneal surgery.
Flurbiprofen sodium 0.03% solution (various)	$8.73/2.5 mL	1 drop every half hour beginning 2 hours before surgery; 1 drop to operated eye four times daily beginning 24 hours after cataract surgery	Inhibition of intraoperative miosis. Treatment of cystoid macular edema and inflammation after cataract surgery.
Ketorolac tromethamine 0.5% solution (Acular)	$71.53/5 mL	1 drop four times daily	Relief of ocular itching due to seasonal allergic conjunctivitis.
Corticosteroids⁸
Dexamethasone sodium phosphate 0.1% solution (various)	$17.31/5 mL	1 or 2 drops as often as indicated by severity; use every hour during the day and every 2 hours during the night in severe inflammation; taper off as inflammation decreases	Treatment of steroid-responsive inflammatory conditions of anterior segment.
Dexamethasone sodium phosphate 0.05% ointment (various)	$6.34/3.5 g	Apply thin coating on lower conjunctival sac three or four times daily
Fluorometholone 0.1% suspension (various)⁹	$26.16/10 mL	1 or 2 drops as often as indicated by severity; use every hour during the day and very 2 hours during the night in severe inflammation; taper off as inflammation decreases
Fluorometholone 0.25% suspension (FML Forte)⁹	$37.60/10 mL
Fluorometholone 0.1% ointment (FML S.O.P.)	$34.00/3.5 g	Apply thin coating on lower conjunctival sac three or four times daily
Medrysone 1% suspension (HMS)	$33.24/10 mL	1 or 2 drops as often as indicated by severity of inflammation; use every hour during the day and every 2 hours during the night in severe inflammation; taper off as inflammation decreases
Prednisolone acetate 0.12% suspension (Pred Mild)	$36.14/10 mL
Prednisolone acetate 0.125% suspension (various)	$36.96/10 mL
Prednisolone sodium phosphate 0.125% solution (various)	$27.29/10 mL
Prednisolone acetate 1% suspension (various)	$23.10/10 mL	1 or 2 drops as often as indicated by severity of inflammation; use every hour during the day and every 2 hours during the night in severe inflammation; taper off as inflammation decreases	Treatment of steroid-responsive inflammatory conditions of anterior segment.
Prednisolone sodium phosphate 1% solution (various)	$24.06/10 mL
Rimexolone 1% suspension (Vexol)	$49.32/10 mL
Mast cell stabilizers
Cromolyn sodium 4% solution (Crolom)	$37.20/10 mL	1 drop four to six times daily	Allergic conjunctivitis.
Ketotifen fumarate 0.025% solution (Zaditor)	$66.80/5 mL	1 drop two to four times daily	Allergic conjunctivitis.
Lodoxamide tromethamine 0.1% solution (Alomide)	$69.12/10 mL	1 or 2 drops four times daily (up to 3 months)	Allergic conjunctivitis and vernal keratoconjunctivitis.
Nedocromil sodium 2% solution (Alocril)	$79.85/5 mL	1 drop twice daily	Allergic conjunctivitis.
Olopatadine hydrochloride 0.1% solution (Patanol)	$74.16/5 mL	1 drop twice daily	Allergic conjunctivitis.
ANTIBIOTIC OINTMENTS AND SOLUTIONS
Bacitracin 500 units/g ointment (various)¹⁰	$4.75/3.5 g	Refer to package insert (instructions vary)	Infections involving lid, conjunctiva, or cornea.
Chloramphenicol 1% (10 mg/g) ointment (Ocu-chlor)¹¹	$1.65/3.5 g		As above, with both gram-positive and gram-negative coverage.
Ciprofloxacin HCl (Ciloxan)	0.3% solution: $50.46/5 mL 0.3% ointment: $50.46/3.5 g
Erythromycin 0.5% ointment (various)¹²	$5.62/3.5 g
Gatifloxacin 0.3% solution (Zymar)	$56.42/5 mL
Gentamicin sulfate 0.3% solution (various)	$8.17/5 mL
Gentamicin sulfate 0.3% ointment (various)	$19.67/3.5 g
Moxifloxacin sulfate 0.5% solution (Vigamox)	$51.24/3 mL
Norfloxacin 0.3% solution (Chibroxin)	Not available in the United States
Ofloxacin 0.3% solution (Ocuflox)	$50.81/5 mL
Polymyxin B sulfate 500,000 units, powder for solution (Polymyxin B Sulfate Sterile)¹³	$12.60/500,000 units
Tobramycin 0.3% solution (various) Tobramycin 0.3% ointment (Tobrex)	$15.00/5 mL $53.88/3.5 g	Refer to package insert (instructions vary)	As above, with both gram-positive and gram-negative coverage.
Sulfacetamide sodium 10% solution (various)	$5.08/15 mL	1 or 2 drops every 1–3 hours	Conjunctivitis, corneal ulcer, and other superficial ocular infections due to susceptible microorganisms.
Sulfacetamide sodium 10% ointment (various)	$8.10/3.5 g	Apply small amount (0.5 inch) into lower conjunctivitis sac once to four times daily and at bedtime	Conjunctivitis, corneal ulcer, and other superficial ocular infections due to susceptible microorganisms.
Note: Many combination products containing antibiotics, antibiotics and steroids, or sulfonamides and steroids are available as solutions, suspensions, or ointments.
TOPICAL ANTIFUNGAL AGENTS
Natamycin 5% suspension (Natacyn)	$147.36/15 mL	1 drop every 1–2 hours	Fungal blepharitis, conjunctivitis, and keratitis caused by susceptible organisms. Drug of choice for Fusarium solani keratitis.
TOPICAL ANTIVIRAL AGENTS
Ganciclovir 4.5 mg surgical insert (Vitrasert)	$5000.00 each	1 implant every 5–8 months	Treatment of cytomegalovirus retinitis in patients with AIDS.
Trifluridine 1% solution (Viroptic)	$104.95/7.5 mL	1 drop onto cornea every 2 hours while awake for a maximum daily dose of 9 drops until resolution occurs; then an additional 7 days of 1 drop every 4 hours while awake (minimum five times daily)	Primary keratoconjunctivitis and recurrent epithelial keratitis due to herpes simplex virus types 1 or 2.¹⁴
TOPICAL ANTIHISTAMINICS¹⁵
Levocabastine HCl 0.05% ophthalmic solution (Livostin)	$81.29/10 mL	1 drop four times daily (up to 2 weeks)	Allergic conjunctivitis; temporary relief of seasonal allergic conjunctivitis.
Emedastine difumarate 0.05% solution (Emadine)	$54.60/5 mL	1 drop four times daily	Allergic conjunctivitis.
¹Average wholesale price (AWP, for AB-rated generic when available) for quantity listed. Source: Red Book, Update, Vol. 24, April 2005. AWP may not accurately represent the actual pharmacy cost because wide contractual variations exist among institutions. ²Macular edema occurs in 30% of patients. ³May (rarely) increase blood pressure. Caution: Avoid in patients with sulfite hypersensitivity (some brands contain sulfite). ⁴Cardioselective (β1) β-blocker. Nonselective (^β1 and ^β2) ^β-blocker. Monitor all patients for systemic side effects, particularly exacerbation of asthma. ⁶Decreased night vision, headaches possible. ⁷Cross-sensitivity to aspirin and other nonsteroidal anti-inflammatory drugs. ⁸Long-term use may increase intraocular pressure or cause cataracts. ⁹May be less likely to elevate intraocular pressure. ¹⁰Little efficacy against gram-negative organisms (except Neisseria). ¹¹Aplastic anemia has been reported with prolonged ophthalmic use. Use only in serious infections for which less toxic drugs are ineffective or contraindicated. ¹²Also indicated for prophylaxis of ophthalmia neonatorum due to N gonorrhoeae or C trachomatis. Increasing resistance of S pneumoniae and P aeruginosa has been noted. ¹³No gram-positive coverage. ¹⁴Recurrences are common and call for additional 7-day treatment. ¹⁵Antihistamines (topical) are potential sensitizers and may produce local reactions.

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P.174

P.175

P.176

P.177

Instilling Medications

The patient is placed in a chair with head tilted back,
both eyes open, and looking up. The lower lid is retracted slightly,
and 2 drops of liquid are instilled into the lower cul-de-sac. The
patient looks down while finger contact is maintained, so that the eyes
are not squeezed shut. Ointments are instilled in the same general
manner.

For self-medication, the same techniques are used except
that medications are usually better instilled with the patient lying
down.

Eye Bandage

Most eye bandages should be applied firmly enough to
hold the lid securely against the cornea. An ordinary patch consisting
of gauze-covered cotton is usually sufficient. Tape is applied from the
cheek to the forehead.

Eyelid Taping

Eyelid taping, such as for corneal protection in facial
palsy, is best achieved with 1-inch-width transparent plastic adhesive
tape (eg, Transpore or even Sellotape) placed horizontally over the
closed eyelids from the side of the nose to the temple.

PRECAUTIONS IN MANAGEMENT OF OCULAR DISORDERS

Use of Local Anesthetics

Unsupervised self-administration of local anesthetics is
dangerous because the patient may further injure an anesthetized eye
without knowing it. The drug may also interfere with the normal healing
process.

Pharmakakis NM et al: Corneal complications following abuse of topical anesthetics. Eur J Ophthalmol 2002;12:373.

Pupillary Dilation

Dilating the pupil can very occasionally precipitate
acute glaucoma if the patient has a narrow anterior chamber angle and
should be undertaken with caution if the anterior chamber is obviously
shallow (readily determined by oblique illumination of the anterior
segment of the eye). A short-acting mydriatic such as tropicamide
should be used and the patient warned to report immediately if ocular
discomfort or redness develops. Angle closure is more likely to occur
if pilocarpine is used to overcome pupillary dilation than if the pupil
is allowed to constrict naturally.

Corticosteroid Therapy

Repeated use of local corticosteroids presents several
hazards: herpes simplex (dendritic) keratitis, fungal infection,
open-angle glaucoma, and cataract formation. Furthermore, perforation
of the cornea may occur when the corticosteroids are used for herpes
simplex keratitis. Topical nonsteroidal anti-inflammatory agents are
being used increasingly. The potential for causing or exacerbating
systemic hypertension, diabetes mellitus, gastritis, or osteoporosis
must always be borne in mind when systemic corticosteroids are
prescribed, such as for uveitis or giant cell arteritis.

Garrott HM et al: Glaucoma from topical corticosteroids to the eyelids. Clin Exp Ophthalmol 2004;32:224.

Ross JJ et al: Facial eczema and sight-threatening glaucoma. J R Soc Med 2004;97:485.

Contaminated Eye Medications

Ophthalmic solutions are prepared with the same degree
of care as fluids intended for intravenous administration, but once
bottles are opened there is always a risk of contamination,
particularly with solutions of tetracaine, proparacaine, fluorescein,
and any preservative-free preparations. The most dangerous is
fluorescein, as this solution is frequently contaminated with P aeruginosa,
which can rapidly destroy the eye. Sterile fluorescein filter paper
strips are recommended for use in place of fluorescein solutions.

Whether in plastic or glass containers, eye solutions
should not remain in use for long periods after the bottle is opened.
Four weeks after opening is an absolute maximal time to use a solution
containing preservatives before discarding. Preservative-free
preparations should be kept refrigerated and discarded within 1 week
after opening.

If the eye has been injured accidentally or by surgical
trauma, it is of the greatest importance to use freshly opened bottles
of sterile medications or singleuse eyedropper units.

Uchio
E et al: Adenovirus detected by polymerase chain reaction in multidose
eyedrop bottles used by patients with adenoviral keratoconjunctivitis.
Am J Ophthalmol 2002;134:618.

Toxic & Hypersensitivity Reactions to Topical Therapy

Patients receiving long-term topical therapy may develop
local toxic or hypersensitivity reactions to the active agent or
preservatives, especially if there is inadequate tear secretion.
Preservatives in contact lens cleaning solutions may produce similar
problems. Burning and soreness are exacerbated by drop instillation or
contact lens insertion; occasionally, fibrosis and scarring of the
conjunctiva and cornea may occur.

An antibiotic instilled into the eye can sensitize the
patient to that drug and cause an allergic reaction upon subsequent
systemic administration.

Systemic Effects of Ocular Drugs

The systemic absorption of certain topical drugs (through the conjunctival vessels and lacrimal drainage

P.178

system) must be considered when there is a systemic medical
contraindication to the use of the drug. Ophthalmic solutions of the
nonselective β-blockers, eg, timolol, may worsen patients with
congestive heart failure or asthma. Atropine ointment should be
prescribed for children rather than the drops, since absorption of the
1% topical solution may be toxic. Phenylephrine eye drops may
precipitate hypertensive crises and angina. Also to be considered are
adverse interactions between systemically administered and ocular
drugs. Using only 1 or 2 drops at a time and a few minutes of
nasolacrimal occlusion or eyelid closure ensure maximum efficacy and
decrease systemic side effects of topical agents.

Table 7-3. Adverse ocular effects of systemic drugs.

Drug	Possible Side Effects
Respiratory drugs Oxygen Anticholinergic bronchodilators Cetirizine	Retinopathy of prematurity. Angle-closure glaucoma due to mydriasis, blurring of vision due to cycloplegia. Oculogyric crisis.
Cardiovascular system drugs Digitalis Quinidine Thiazides (Diuril, etc) Carbonic anhydrase inhibitors (acetazolamide) Amiodarone	Disturbances of color vision, scotomas, photopsia. Optic neuritis (rare). Xanthopsia (yellow vision), myopia. Ocular hypotony, transient myopia. Corneal deposits, optic neuropathy, thyroid ophthalmopathy.
Gastrointestinal drugs Anticholinergic agents	Risk of angle-closure glaucoma due to mydriasis, blurring of vision due to cycloplegia (occasional).
Central nervous system drugs Barbiturates Chloral hydrate Phenothiazines Amphetamines Monoamine oxidase inhibitors Tricyclic agents Phenytoin Neostigmine Morphine Haloperidol Lithium carbonate Diazepam Topiramate Paroxetine Vigabatrin	Extraocular muscle palsies with diplopia, nystagmus, ptosis, cortical blindness. Diplopia, ptosis, miosis. Deposits of pigment in conjunctiva, cornea, lens, and retina, oculogyric crises. Widening of palpebral fissure, blurring of vision due to mydriasis. Nystagmus, extraocular muscle palsies, optic atrophy. Angle-closure glaucoma due to mydriasis, blurring of vision due to cycloplegia. Nystagmus, diplopia, ptosis, slight blurring of vision (rare). Nystagmus, miosis. Miosis. Capsular cataract. Exophthalmos, oculogyric crisis, nystagmus. Nystagmus. Angle-closure glaucoma. Angle-closure glaucoma. Visual field constriction.
Hormonal agents Corticosteroids	Cataract (posterior subcapsular); local immunologic suppression, causing susceptibility to viral (herpes simplex), bacterial, and fungal infections; steroid-induced glaucoma.
Female sex hormones	Retinal artery occlusion, retinal vein occlusion, papilledema, ocular palsies with diplopia, nystagmus, optic neuropathy.
Tamoxifen	Crystalline retinal deposits.
Antibiotics Chloramphenicol Streptomycin Tetracycline Minocycline	Optic neuropathy. Optic neuropathy. Papilledema, transient myopia. Papilledema.
Antimalarial agents Chloroquine, etc	Retinal degeneration principally involving the macula, keratopathy, ocular palsies, ptosis.
Amebicides Iodochlorhydroxyquin	Optic atrophy.
Chemotherapeutic agents Sulfonamides Ethambutol Isoniazid	Stevens-Johnson syndrome. Optic neuropathy. Optic neuropathy.
Heavy metals Gold salts Lead compounds	Deposits in the cornea and conjunctiva. Optic atrophy, papilledema, ocular palsies.
Chelating agents Penicillamine	Ocular pemphigoid, optic neuritis, ocular myasthenia.
Oral hypoglycemic agents Chlorpropamide	Transient change in refractive error, diplopia, Stevens-Johnson syndrome.
Vitamins Vitamin A Vitamin D	Papilledema, retinal hemorrhages, loss of eyebrows and eyelashes, nystagmus, diplopia, blurring of vision. Band-shaped keratopathy.
Antirheumatic agents Salicylates Indomethacin Phenylbutazone	Nystagmus, retinal hemorrhages, cortical blindness (rare). Corneal deposits. Retinal hemorrhages.
Dermatologic agents Isotretinoin Retinoids (isotretinoin, tretinoin, acitretin, and etretinate)	Blepharoconjunctivitis, corneal opacities, decreased dark adaptation, decreased contact lens tolerance, teratogenic ocular abnormalities. Papilledema.
Bisphosphonates Pamidronate Alendronate	Scleritis, uveitis, conjunctival hyperemia. Scleritis.

Fraunfelder
FW et al: Adverse systemic effects from pledgets of topical ocular
phenylephrine 10%. Am J Ophthalmol 2002; 134:624.

ADVERSE OCULAR EFFECTS OF SYSTEMIC DRUGS

Systemically administered drugs produce a wide variety of adverse effects on the visual system. Table 7-3 lists the major examples.

Flach AJ, Fraunfelder FW: Ocular and systemic side effects of drugs. In: Vaughan & Asbury’s General Ophthalmology, 16th ed. Riordan-Eva P, Whitcher JP (editors). McGraw-Hill, 2004.

Filed under: Medical

Aplikasi Mematikan Komputer Otomatis

edwien — Sun, 19 Jun 2011 07:06:45 +0000

Wah lama gak posting blog ini aku cuma mau berbagi ajah aku ada aplikasi untuk mematikan komputer/laptop secara otomatis

Jadi waktu kita pake laptop dengerin musik sambil tiduran jalan aplikasi ini sebelumnya so komputer bisa mati sendiri gak perlu begadang semaleman komputernya.. ini Link nya heh

Download Aplikasi Mematikan Komputer otomatis

Filed under: Software

Patofisiologi Gagal jantung

edwien — Mon, 10 Jan 2011 04:48:48 +0000

Patofisiologi CHF terjadi karena interaksi kompleks antara faktor-faktor yang memengaruhi kontraktilitas, after load, preload, atau fungsi lusitropik (fungsi relaksasi) jantung, dan respons neurohormonal dan hemodinamik yang diperlukan untuk menciptakan kompensasi sirkulasi. Meskipun konsekuensi hemodinamik gagal jantung berespons terhadap intervensi farmakologis standar, terdapat interaksi neurohormonal kritis yang efek gabungannya memperberat dan memperlama sindrom yang ada.

Sistem reniniangiotensinfaldosteron (RAA): Selain untuk meningkatkan tahanan perifer dan volume darah sirkulasi, angiotensin dan aldosteron berimplikasi pada perubahan struktural miokardium yang terlihat pada cedera iskemik dan kardiomiopati hipertropik hipertensif. Perubahan ini meliputi remodeling miokard dan kematian sarkomer, kehilangan matriks kolagen normal, dan fibrosis interstisial. Terjadinya miosit dan sarkomer yang tidak dapat mentransmisikan kekuatannya, dilatasi jantung, dan pembentukan jaringan parut dengan kehilangan komplians miokard normal turut memberikan gambaran hemodinamik dan simtomatik pada CHF.

Sistem saraf simpatis (SNS): Epinefrin dan norepinefrin menyebabkan peningkatan tahanan perifer dengan peningkatan kerja jantung, takikardia, peningkatan konsumsi oksigen oleh miokardium, dan peningkatan risiko aritmia. Katekolamin juga turut menyebabkan remodeling ventrikel melalui toksisitas langsung terhadap miosit, induksi apoptosis miosit, dan peningkatan respons autoimun.

Vasodilator endogen, seperti endotelin dan oksida nitrat, peptida jantung, dan peptida natriuretik: Perannya dalam CHF sedang diselidiki dan intervensinya sedang diuji.

- Sitokin imun dan inflamasi: Faktor nekrosis tumor alfa (TNFa) dan interleukin 6 (IL-6) menyebabkan remodeling ventrikel dengan apoptosis miosit, dilatasi ventrikel, dan penurunan kontraktilitas. Lebih lanjut, mereka juga berperan dalam efek sistemik seperti penurunan berat badan dan kelemahan yang terlihat pada CHF brat (kakheksia jantung).
• Kejadian etiologi awal memengaruhi respons awal miokardium, tetapi seiring dengan perkembangan sindrom, mekanisme umum mulai muncul sehingga pasien CHF lanjut memperlihatkan gejala dan respons yang sama terhadap intervensi farmakologis yang sama apapun penyebab awal CHF-nya.
• Meskipun banyak pasien mengalami disfungsi ventrikel kiri sistolik dan diastolik, kategori ini sebaiknya dianggap sebagai hal yang berbeda untuk dapat memahami efeknya terhadap homeostasis sirkulasi dan responsnya terhadap berbagai intervensi.

Disfungsi ventrikel kiri sistolik
1) Penurunan curah jantung akibat penurunan kontraktilitas, peningkatan afterload, atau peningkatan preload yang mengakibatkan penurunan fraksi ejeksi dan peningkatan volume akhir diastolik ventrikel kiri (LVEDV). Ini meningkatkan tekanan akhir diastolik pada ventrikel kiri (I-VEDP) dan menyebabkan kongesti vena pulmonal dan edema paru.

2) Penurunan kontraktilitas (inotropi) terjadi akibat fungsi miokard yang tidak adekuat atau tidak terkoordinasi schingga ventrikel kiri tidak dapat melakukan ejeksi lebih dari 60% dari volume akhir diastoliknya (LVEDV). lni menyebabkan peningkatan bertahap LVEDV (juga dinamakan preload) mengakibatkan peningkatan LVEDP dan kongesti vena pulmonalis. Penyebab penurunan kontraktilitas yang tersering adalah penyakit jantung iskemik, yang tidak hanya mengakibatkan nekrosis jaringan miokard sesungguhnya, tetapi juga menyebabkan remodeling ventrikel iskemik. Remodeling iskemik adalah sebuah proses yang sebagian dimediasi oleh angiotensin II (ANG II) yang menyebabkan jaringan parut dan disfungsi sarkomer di jantung sekitar daerah cedera iskemik. Aritmia jantung dan kardiomiopati primer seperti yang disebabkan olch alkohol, infeksi, hemakromatosis, hipertiroidisme, toksisitas obat dan amiloidosis juga menyebabkan penurunan kontraktilitas. Penurunan curah jantung mengakibatkan kekurangan perfusi pada sirkulasi sistemik dan aktivasi sistem saraf simpatis dan sistem RAA, menyebabkan peningkatan tahanan perifer dan peningkatan afterload.

3) Peningkatan afterload berarti terdapat peningkatan tahanan terhadap ejeksi LV. Biasanya disebabkan oleh peningkatan tahanan vaskular perifer yang umum terlihat pada hipertensi. Bisa juga diakibatkan oleh stenosis katup aorta. Ventrikel kiri berespon terhadap peningkatan beban kerja ini dengan hipertrofi miokard, suatu respons yang meningkatkan massa otot ventrikel kiri tetapi pada saat yang sama meningkatkan kebutuhan perfusi koroner pada ventrikel kiri. Suatu keadaan kelaparan energi tercipta sehingga berpadu dengan ANG II dan respons neuroendokrin lain, menyebabkan perubahan buruk dalam miosit seperti semakin sedikitnya mitokondria untuk produksi energi, perubahan ekspresi gen dengan produksi protein kontraktil yang abnormal (aktin, miosin, dan tropomiosin), fibrosis interstisial, dan penurunan daya tahan hidup miosit. Dengan berjalannya waktu, kontraktilitas mulai menurun dengan penurunan curah jantung dan fraksi ejeksi, peningkatan LVEDV, dan kongesti paru.

4) Peningkatan preload berarti peningkatan LVEDV, yang dapat disebabkan langsung oleh kelebihan volume intravaskular sama seperti yang terlihat pada infus cairan intra vena atau gagal ginjal. Selain itu, penurunan fraksi ejeksi yang disebabkan oleh perubahan kontraktilitas atau afterload menyebabkan peningkatan LVEDV sehingga meningkatkan preload. Pada saat LVEDV meningkat, ia akan meregangkan jantung, menjadikansarkomer berada pada posisi mekanis yang tidak menguntungkan sehingga terjadi penurunan kontraktilitas. Penurunan kontraktilitas ini, yang menyebabkan penurunan fraksi ejeksi, menyebabkan peningkatan LVEDV yang lebih lanjut, sehingga menciptakan lingkaran setan perburukan gagal jantung.

5) Jadi, pasien dapat memasuki lingkaran penurunan kontraktilitas, peningkatanafterload, dan peningkatan preload akibat berbagai macam alasan (mis., infark miokard [MI], hipertensi, kelebihan cairan) dan kemudian akhimya mengalami semua keadaan hemodinamik dan neuro-hormonal CHF sebagai sebuah mekanisme yang menuju mekanisme lainnya.

Disfungsi ventrikel kiri diastolik
1) Penyebab dari 90% kasus
2) Didefinisikan sebagai kondisi dengan temuan klasik gagal kongestif dengan fungsi diastolik abnormal tetapi fungsi sistolik normal; disfungsi diastolik mumi akan dicirikan dengan tahanan terhadap pengisian ventrikel dengan peningkatan LVEDP tanpa peningkatan LVEDV atau penurunan curah jantung.
3) Tahanan terhadap pengisian ventrikel kiri terjadi akibat relaksasi abnormal (lusitropik) ventrikel kiri dan dapat disebabkan oleh setiap kondisi yang membuat kaku miokard ventrikel seperti penyakit jantung iskemik yang menyebabkan jaringan parut, hipertensi yang mengakibatkan kardiomiopati hipertrofi, kardiomiopati restriktif, penyakit katup atau penyakit perikardium.
4) Peningkatan denyut jantung menyebabkan waktu pengisian diastolik menjadi berkurang dan memperberat gejala disfungsi diastolik. Oleh karena itu, intoleransi terhadap olahraga sudah menjadi umum.
5) Karena penanganan biasanya memerlukan perubahan komplians miokard yang sesungguhnya, efektivitas obat yang kini tersedia masih sangat terbatas. Penatalaksanaan terkini paling berhasil dengan penyekat beta yang meningkatkan fungsi lusitropik, menurunkan denyut jantung, dan mengatasi gejala. Inhibitor ACE dapat membantu memperbaiki hipertrofi dan membantu perubahan struktural di tingkat jaringan pada pasien dengan remodeling iskemik atau hipertensi.

Source: http://wihans.web.id/patofisiologi-gagal-jantung-kongestif-chf

Filed under: Kardio, Medical Tagged: jantung, Patofisiologi

Pendidikan Sex/Sex Education

edwien — Wed, 22 Dec 2010 23:37:17 +0000

Remaja selalu dipenuhi rasa penasaran termasuk mengenai istilah-istilah seks yang belum diketahuinya. Apa saja istilah seks yang membuat remaja penasaran?

Seperti dikutip dari buku Questions Kids Ask About Sex, karangan J. Thomas Fitch dan Melissa R. Cox, yang diterbitkan ANDI, Rabu (22/12/2010) ada beberapa istilah seks yang membuat remaja sangat ingin mengetahuinya yaitu:

1. Apa yang dimaksud dengan mimpi basah?
Mimpi basah adalah istilah untuk nocturnal emission (keluarnya air mani pada malam hari). Saat sedang tidur, remaja bisa mengalami ereksi pada penisnya yang disertai dengan keluarnya air mani. Ini adalah sesuatu yang normal dan terjadi pada semua laki-laki.

2. Apa yang dimaksud dengan ‘making out’?
Istilah ini sebenarnya tidak dapat didefinisikan. Tapi beberapa orang menganggap istilah tersebut berarti berciuman dan berpelukan, sementara beberapa orang lain mengganggapnya sebagai hubungan seks.

3. Apa itu seks kering (dry sex)?
Seks kering atau dry sex adalah tindakan merangsang orang lain secara seksual dengan masih menggunakan pakaian lengkap. Pada tahap awal, berciuman bisa menjadi hal yang membosankan, sehingga pasangan memilih untuk bercumbu dengan pakaian lengkap. Meskipun tampak aman, tapi hubungan ini mendekati hubungan seks sebenarnya.

4. Apa yang dimaksud dengan promiskuitas?
Promiskuitas adalah memiliki lebih dari satu pasangan seksual atau bergonta-ganti pasangan. Padahal semakin banyak pasangan seks makin besar pula kemungkinan terkena penyakit infeksi menular seksual dan risiko kehamilan.

5. Apa yang dimaksud dengan ‘date rape’?
Date rape adalah paksaan untuk berhubungan seks di luar keinginan seseorang, dalam hal ini misalnya dipaksa oleh pacar saat berkencan atau pergi.

6. Apa yang dimaksud dengan petting?
Petting sebenarnya memiliki arti menyentuh atau mencumbu. Dalam hal ini adalah memberikan rangsangan pada organ seksual atau payudara yang biasanya dilakukan dengan tangan atau mulut untuk memberikan kesenangan seksual.

7. Apa yang dimaksud dengan foreplay?
Foreplay adalah perangsangan yang didefinisikan sebagai kegiatan seksual sebelum melakukan hubungan seks yang sebenarnya. Kadang disebut juga pemanasan sebelum penetrasi. Kegiatan ini biasanya meliputi ciuman yang intim dan lama, belaian dan sentuhan mulut pada payudara atau kemaluan. Saat ini kegiatan tersebut dikenal juga sebagai outercourse.

8. Apa yang dimaksud dengan masturbasi?
Masturbasi adalah perangsangan alat kelamin dengan tangan. Kegiatan ini dapat dilakukan sendirian atau berpasangan.

9. Apa yang dimaksud dengan jerking off?
Istilah ini umumnya ditunjukkan pada masturbasi yang dilakukan oleh laki-laki.

10. Apa yang dimaksud dengan aphrodisiak?
Zat aphrodisiak adalah sesuatu yang dianggap mampu membangkitkan gairah seksual atau segala sesuatu baik obat atau makanan yang bisa merangsang gairah seksual.

11. Apa yang dimaksud dengan nimfomania?
Nimfomania adalah hasrat seksual yang tak terkendali pada laki-laki maupun perempuan.

12. Apa yang dimaksud dengan eksibisionisme?
Eksibisionisme adalah suatu penyimpangan seksual yang ditandai dengan keinginan berlebih untuk mempertontonkan alat kelamin di muka umum.

13. Apa yang dimaksud dengan pedofil?
Pedofil adalah orang dewasa yang tertarik secara seksual pada anak-anak (kadang menindaklanjuti keinginannya tersebut). Secara psikologis hal ini sangat merusak anak-anak yang dieksploitasi secara seksual oleh orang dewasa.

14. Apa yang dimaksud dengan voyeurisme?
Voyeurisme adalah minat yang berlebihan untuk melihat kegiatan seks atau organ seks orang lain, khususnya secara diam-diam.

15. Apa salahnya melakukan binge drinking?
Binge drinking sangat berbahaya dan bisa mematikan, karena ia mengonsumsi 4-5 gelas minuman alkohol secara cepat atau sekaligus. Kondisi ini menyebabkan kadar alkohol dalam darah meningkat dan meracuni otak. Studi menunjukkan otak remaja lebih mudah terpengaruh oleh efek racun alkohol.

Filed under: Remaja Tagged: Remaja, SEX

Sterilisasi Botol Susu

edwien — Wed, 22 Dec 2010 23:31:00 +0000

detikcom – Jakarta, Sterilisasi botol susu dan juga peralatan makan bayi lainnya penting dilakukan untuk mencegah kontaminasi bakteri atau kuman. Ini dia 9 hal yang harus diketahui tentang sterilisasi.

Proses sterilisasi perlu dilakukan secara teratur setiap kali botol atau alat makan tersebut digunakan. Hal ini sebaiknya dilakukan dengan benar sehingga bisa mengurangi masuknya bakteri atau kuman yang bisa mengkontaminasi notol. Jika terjadi kontaminasi bisa menyebabkan diare pada bayi. Sedangkan untuk mainan bayi umumnya cukup disiram dengan air panas.

Seperti dikutip dari Askamum.co.uk, Rabu (22/12/2010) ada 9 hal yang harus diketahui orangtua mengenai sterilisasi botol susu, yaitu:

1. Mengapa perlu sterilisasi?
Sterilisasi bisa membantu melindungi bayi dari kuman dan infeksi. Bakteri berbahaya bisa tumbuh cepat di dalam susu dan tubuh bayi yang berusia di bawah 1 tahun karena belum memiliki sistem kekebalan tubuh yang optimal. Selain itu sterilisasi juga membantu mencegah kematian bayi. Meskipun tidak bisa menciptakan lingkungan yang bebas kuman 100 persen, tapi dengan sterilisasi dapat mengurangi risiko bagi bayi.

2. Perlukah sterilisasi bagi ibu yang menyusui bayinya langsung?
Jika ibu memberikan ASI tanpa menggunakan bantuan pompa payudara, maka ibu tak perlu melakukan sterilisasi. Tapi jika menggunakan pompa, maka segala peralatannya perlu disterilisasi untuk menjaga kebersihannya. Peralatan dicuci secara menyeluruh sebelum di sterilisasi, termasuk empeng bayi.

3. Apakah semua sterilisasi sama?
Tidak semua alat sterilisasi itu sama. Ada tiga jenis utama alat sterilisasi, yaitu menggunakan air dingin (cold water), sterilisasi uap listrik dan microwave. Setiap alat ini memiliki kelebihan dna kekurangan masing-masing, untuk itu ketahui jenis mana yang lebih banyak membantu. Namun satu hal yang sama adalah semua botol harus dicuci bersih terlebih dahulu sebelum disterilisasi.

4. Sterilisasi air dingin (cold water steriliser)
Alat ini menggunakan larutan sterilisasi atau tablet untuk membunuh bakteri. Sisi positifnya alat ini tidak membutuhkan tenaga yang besar dan bisa praktis dibawa ketika sedang bepergian. Namun umumnya memakan waktu lama yaitu sekitar setengah jam dan harus mencuci kembali semua peralatan dengan air mendidih untuk menghilangkan bahan kimia dari larutan sterilisasi.

5. Sterilisasi uap listrik
Teknik ini lebih cepat dan mudah dilakukan dengan menggunakan uap panas untuk membunuh bakteri, yaitu hanya sekitar 6-8 menit per siklus. Kelebihannya tidak memerlukan pembilasan lagi setelahnya dan memiliki kapasitas besar. Namun alat ini tidak bisa dibawa-bawa karena memerlukan listrik, harus sering dibersihkan dan biasanya memiliki harga yang cukup mahal.

6. Microwave
Alat ini juga menggunakan uap untuk menghilangkakn bakteri, tapi harganya lebih murah. Mengenai waktu yang dibutuhkan tergantung dari seberapa besar kekuatan microwave yang dimiliki. Namun umumnya kapasitas yang dimiliki tidak terlalu besar dan alat ini tidak bisa mensterilkan alat makan seperti sendok atau mangkuk logam.

7. Sterilisasi untu perjalanan
Ukuran alat sterilisasi ini lebih kecil dan biasanya tidak lebih dari dua botol. Umumnya menggunakan teknik sterilisasi air dingin yang memungkinkannya melakukan sterilisasi tanpa bantuan listrik.

8. Berapa lama sterilisasi dengan air mendidih?
Jika tidak ada alat sterilisasi, bisa dengan cara merebus dalam air mendidih. Pastikan botol susu tidak rusak terkena air mendidih, lalu masukkan botol dalam panci berisi air mendidih selama 10-15 menit. Setelah itu segera angkat, tiriskan botol kemudian simpan botol yang sudah dibersihkan di tempat yang yang bersih dan kering. Jika dibiarkan hingga air menajdi dingin akan embuat mikroorganisme masuk dan menempel di botol.

9. Berapa lama ibu harus menggunakan alat sterilisasi?
Para ahli menyarankan alat tersebut digunakan sampai bayi berusia 1 tahun. Setelah 1 tahun umumnya bayi memiliki sistem kekebalan yang lebih kuat untuk melawan infeksi. Selain itu pada usia 1 tahun ke atas, bayi mulai diajarkan untuk minum menggunakan gelas dan melatih gerakan motoriknya.

Sumber;detik.com

Filed under: Makanan, Tips Tagged: makanan, Susu

Makanan Pemicu Kolesterol

edwien — Mon, 22 Nov 2010 11:14:43 +0000

Agar kadar kolesterol di darah tidak melonjak, penderita hipertensi pasti akan menghindari kambing guling. Langkah ini bisa jadi percuma jika masih mengonsumsi sumber kolesterol lainnya yang sama bahayanya meski sering tidak disadari.

Kadar kolesterol yang tinggi merupakan faktor risiko berbagai masalah jantung dan pembuluh darah. Risiko terburuknya, gumpalan-gumpalan lemak bisa menyumbat aliran darah sehingga bisa memicu kematian akibat serangan jantung atau stroke.

Kolesterol umumnya berasal dari lemak hewani seperti daging kambing, meski tidak sedikit yang berasal dari lemak nabati seperti santan dan minyak kelapa. Beberapa makanan yang selama ini diyakini sehat seperti telur, juga banyak mengandung kolesterol.

Dikutip dari Livestrong, Senin (22/11/2010), berikut ini adalah 4 jenis sumber kolesterol yang sering dikonsumsi sehari-hari:

Hati Sapi Goreng
Meski kaya akan protein, kandungan kolesterol dan lemak jenuh dalam makanan ini termasuk yang paling tinggi. Karena setiap 85 gram hati sapi mengandung 410 mg kolesterol, maka porsi normal yang rata-rata 255 gram memberikan tambahan kolesterol sebanyak 1.230 mg sekali makan.

Telur
Banyak yang mengira kolesterol tinggi hanya diperoleh dari telur yang didadar dengan mentega. Padahal kolesterol ada di telur itu sendiri, sebab telur rebus sekalipun masih mengandung 225 mg kolesterol. Menggorengnya dengan mentega akan menambahkan sekitar 200 mg kolesterol.

Untuk mengurangi ancaman kolesterol yang tinggi, orang yang dewasa yang ingin diet sebaiknya makan putih telurnya saja.

Daging Ayam
Jika dimasak tanpa kulit, dada ayam yang termasuk white meat bisa dikatakan sehat karena tidak banyak mengandung kolesterol. Namun bagian lain yang termasuk dark meat seperti paha, ceker dan sayap memiliki kandungan kolesterol yang sama tingginya dengan daging sapi dan kambing.

Kandungan kolesterol dalam daging ayam akan lebih tinggi lagi jika dimasak semur, salah satu jenis masakan yang sangat berminyak. Satu porsi semur ayam bisa mengandung 300-600 mg kolesterol.

Kue Bolu
Tanpa tambahan apapun, 100 gram kue bolu mengandung sekitar 260 mg kolesterol. Jika disajikan bersama dengan krim atau sirup cokelat dan es krim, kue bolu akan menjadi gudang kolesterol dengan tambahan 400 mg lemak jahat.

detik.com

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Filed under: Makanan Tagged: kolesterol, makanan

Kebiasaan Sehari-hari yang Bikin Postur Tubuh Buruk

edwien — Thu, 11 Nov 2010 13:42:24 +0000

Memiliki postur tubuh yang baik tentunya akan membuat Anda tampil lebih percaya diri. Sayangnya, tanpa disadari banyak orang sering melakukan hal-hal kecil yang ternyata bisa membuat postur tubuhnya buruk. Apa saja?

Dilansir Buzzle, Kamis (11/11/2010), berikut beberapa kebiasaan sehari-hari yang membuat postur tubuh Anda buruk:

1. Cara duduk
Membungkuk ke depan sambil duduk di depan komputer atau duduk dengan posisi ‘C’ di depan meja. Posisi ‘C’ berarti Anda terlalu condong ke depan sehingga menyebabkan banyak tekanan pada tulang belakang. Posisi ini dapat menyebabkan stres pada tubuh. Selain itu, menggeser kursi terlalu ke depan juga dapat membuat postur tubuh memburuk.

2. Membawa tas berat
Membawa tas yang berat pada 1 bahu untuk jangka waktu yang lama juga dapat menyebabkan kedua bahu menjadi tidak sama yang akhirnya memperburuk postur tubuh.

3. Tidur dengan bantal tinggi
Tidur dengan bantal terlalu tinggi atau dengan posisi membentuk lengkungan (membungkuk) dan memeluk lutut dapat membuat posisi tulang belakang membungkuk.

4. Sepatu hak terlalu tinggi
Menggunakan sepatu dengan hak terlalu lama juga dapat membuat postur tubuh Anda buruk.

5. Menjadi gemuk
Banyak makan makanan berlemak yang akhirnya membuat Anda gemuk juga dapat mempengaruhi postur tubuh.

Bagaimana mendapatkan postur tubuh yang baik?

Mendapatkan postur tubuh yang baik bukanlah sesuatu yang diperoleh dengan cara cepat dan mudah. Anda harus bisa mengubah kebiasaan buruk saat duduk, berdiri ataupun tidur.

Posisi duduk yang benar

1. Selalu menempatkan kedua kaki rata di lantai, ini bisa menyelaraskan tubuh ke tempat duduk Anda.
2. Ketika duduk, pastikan lutut berada pada tingkat yang sama seperti pinggul dan membentuk sudut 75 sampai 90 derajat dengan siku.
3. Jaga bahu lurus setiap saat. Hindari membungkuk dan bersandar ke depan ketika berada di depan komputer.
4. Selalu luangkan waktu untuk peregangan setelah duduk lama

Posisi berdiri yang benar
Selalu jaga kepala dalam keadaan lurus. Telinga harus sejalan dengan bahu dan bahu harus lurus dengan lutut agar membuat Anda tegak. Ingatlan untuk tidak bungkuk ketika berdiri.

Posisi tidur yang benar

1. Gunakan bantal dengan ketinggian sedang dan tidak terlalu tinggi
2. Tempatkan bantat di bawah kepala dan bukan di bawah bahu
3. Tidur dalam posisi yang membantu mempertahankan kurva punggung, hindari memeluk lutut ketika tidur.
4. Pastikan kualitas kasur yang nyaman untuk berbaring
5. Jika akan bangun dari posisi tidur, terlebih dahulu menggerakkan kaki yang kemudian didorong dengan bantuan tangan.

http://m.detik.com/read/2010/11/11/133032/1492186/766/kebiasaan-sehari-hari-yang-bikin-postur-tubuh-buruk

Filed under: Gaya Hidup, Tips Tagged: gaya hidup, Tips

Penyebab Aliran Balik Lambung

edwien — Thu, 11 Nov 2010 13:36:42 +0000

Beberapa faktor bisa meningkatkan risiko terjadinya refluks, yakni naiknya asam lambung dari perut menuju kerongkongan. Kondisi ini menyebabkan rasa nyeri seperti terbakar di sekitar dada, tenggorokan dan kerongkongan.

Refluks terjadi ketika katup yang menghubungkan lambung dengan kerongkongan tidak menutup sempurna. Tidak diketahui pasti apa penyebabnya, namun beberapa hal yakni kebiasaan merokok, kehamilan dan obesitas merupakan faktor risiko yang bisa memicunya.

Meski memiliki faktor-faktor risiko tersebut, seseorang tetap bisa mencegah terjadinya refluks atau setidaknya mengurangi risikonya. Dikutip dari Foxnews, Kamis (11/11/2010), beberapa hal yang bisa mempengaruhi refluks asam lambung adalah sebagai berikut.

1. Posisi dan postur tubuh mempengaruhi refluks
Berbaring bisa menyebabkan refluks makin parah dan berlangsung lebih lama, sehingga dianjurkan untuk tetap duduk atau berdiri. Untuk mencegah terjadinya refluks saat tidur atau berbaring, manfaatkan efek gravitasi dengan memposisikan kepala sedikit lebih tinggi.

Kadang-kadang refluks juga terjadi saat sedang membungkuk. Posisi ini memberi tekanan pada perut sehingga asam lambung lebih mudah mengalami refluks.

2. Pakaian longgar mengurangi risiko refluks
Tekanan di daerah perut merupakan salah satu pemicu terjadinya refluks. Oleh karena itu hindari penggunaan pakaian yang terlalu ketat jika sering mengalami refluks.

3. Olahraga meredakan gejala refluks
Segala jenis olahraga terutama latihan kardiovaskular bisa dilakukan untuk mengurangi gejala refluks asam lambung. Olahraga juga membantu mengurangi berat badan, yang juga termasuk salah satu faktor risiko refluks.

4. Hernia hiatus bisa memicu refluks
Ketika sebagian isi perut menonjol melewati diafragma atau pembatas dengan rongga dada, kondisi ini disebut hernia hiatus. Jika bagian yang menonjol ukurannya mencapai 3-4 cm, maka asam lambung bisa terjebak dan lebih berisiko untuk mengalami refluks.

5. Makan sesaat sebelum tidur menyebabkan refluks
Efek gravitasi saat berbaring membuat asam lambung lebih mudah untuk berbalik ke kerongkongan. Waktu yang tepat untuk tidur atau sekedar berbaring adalah sekurang-kurangnya 3 jam sesudah makan.

http://m.detik.com/read/2010/11/11/140927/1492251/766/yang-mempengaruhi-naiknya-asam-lambung

Filed under: Pencernaan Tagged: pencernaan, perut

Gerak Reflek

edwien — Tue, 09 Nov 2010 13:15:10 +0000

Secara umum, refleks dapat diartikan sebagai respon yang terjadi secara otomatis, tanpa kesadaran. Refleks saraf selalu dimulai dengan adanya stimulus yang mengaktifkan reseptor sensoris. Kunci dari jaras refleks adalah negative feedback. Jalur yang terlibat dalam terjadinya refleks dikenal sebagai lengkung refleks. Tidak seperti gerak biasa yang memiliki banyak variasi respon, respon untuk gerak refleks dapat diprediksikan karena jalurnya selalu sama.

Neural refleks bisa diklasifikasikan sebagai berikut :

1. Berdasarkan divisi efferent sistem saraf yang mengontrol respon

Refleks ini melibatkan somatic motor neuron dan otot skeletal yang dikenal sebagai refleks somatik. Refleks yang responnya dikontrol saraf otonom disebut refleks otonom.

2. Berdasarkan lokasi CNS di mana refleks diintegrasikan

Refleks spinal diintegrasikan di spinal kord. Refleks ini bisa dimodulasi oleh input yang lebih tinggi dari otak, namun bisa juga tanpa input tersebut. Refleks yang diintegrasikan di otak disebut refleks kranial.

3. Berdasarkan apakah refleks itu dipelajari atau didapat.

Refleks patella merupakan refleks yang didapat. Contoh refleks didapat adalah Pavlov’s dogs salivating saat mendengar sebuah bel. Refleks ini juga disebut conditioned reflex. Begitu juga saat seorang pianis memainkan jari-jarinya di atas piano yang merupakan refleks yang dipelajari.

4. Berdasarkan jumlah neuron di jaras refleks

Yang paling sederhana adalah monosynaptic reflex, yang merupakan refleks dengan sinapsis tunggal di antara dua neuron di jaras : satu afferen, satu efferen, yang bersinapsis di spinal kord. Sedangkan kebanyakan refleks terdiri dari tiga atau lebih neuron, disebut polysinaptic reflex. Jalur divergen memungkinkan stimulus tunggal mempengaruhi banyak target sedangkan konvergen mengintegrasikan input untuk memodulasi sebuah respon.

a. Refleks otonom

Refleks ini disebut juga refleks visceral karena sering melibatkan organ internal tubuh. Beberapa refleks visceral, seperti urinasi dan defekasi, merupakan refleks spinal yang bisa terjadi tanpa input dari otak. Meskipun begitu, refleks spinal juga sering dimodulasi oleh excitatory atau inhibitory signal dari otak yang dibawa oleh jaras descending dari pusat otak yang lebih tinggi. Misal, urinasi dapat diinisiasi secara sadar dengan kesadaran atau bisa juga dihambat oleh stress dan emosi, seperti dengan adanya orang lain (sindrom bashful bladder).

Refleks otonom lain diintegrasikan di otak , khususnya di hipotalamus, thalamus dan batang otak. Daerah ini berisi pusat koordinasi yang dibutuhkan untuk menjaga homeostatis seperti detak jantung, tekanan darah, nafas, makan, keseimbangan air dan menjaga temperatur. Di sini juga ada pusat refleks seperti salivating, muntah, bersin, batuk, menelan, dan tersendak.

Salah satu tipe reflex otonom yang menarik adalah konversi stimulus emosional ke respon visceral. Sistem Limbic, yang merupakan tempat operasi primitif seperti sex, takut, marah, agresif dan lapar, disebut sebagai “visceral brain” karena pengaruhnya dalam refleks emosional. Contoh lain adalah folikel rambut yang tertarik saat seseorang merasa takut.

Refleks otonom merupakan polysinaptic dengan sedikitnya satu sinapsis di CNS di antara neuron sensorik dan preganglion saraf otonom serta sinaps tambahan di ganglion, antara neuron preganglionic dan postganglionic.

b. Refleks Otot Skeletal

Eksitasi somatic motor neuron selalu menyebabkan kontraksi di otot rangka. Tidak ada inhibitory neuron yang bersinapsis di otot skeletal untuk membuatnya rileks. Relaksasi merupakan akibat dari tidak adanya eksitatory input.

Refleks otot skeletal memiliki komponen sebagai berikut :

1. Reseptor sensorik

Dikenal sebagai proprioceptor yang terletak di otot skeletal, kapsul sendi, dan ligament. Reseptor ini memonitor posisi tungkai, pergerakan dan upaya yang kita gunakan saat mengangkat benda.

2. Neuron sensorik yang membawa sinyal dari proprioceptor ke CNS

3. CNS, yang menintegrasikan sinyal masuk menggunakan jalur eksitatori dan inhibitori interneuron. Pada refleks, informasi sensorik diintegrasikan dan dilakukan secara bawah sadar. Meskipun begitu, informasi sensorik mungkin diintegrasikan di cerebral korteks dan menjadi persepsi serta beberapa refleks bisa dimodulasi sebagai sebagai input sadar.

4. Motor neuron somatik yang membawa sinyal output. Motor neuron somatik yang mempersarafi kontraktil otot disebut alpha motor neuron.

5. Efektor, yang merupakan serat kontraktil otot skeletal, juga dikenal sebagai muscle fiber ekstrafusal. Potensial aksi di alpha motor neuron akan menyebabkan serat ekstrafusal berkontraksi.

Ada tiga buah propioceptor ditemukan di tubuh: muscle spindel, organ golgi tendon, dan reseptor sendi.

1. Muscle spindel merespon peregangan otot

Muscle spindel merupakan reseptor peregangan yang mengirim informasi ke spinal kord dan otak mengenai panjang otot dan perubahan panjang otot. Kecuali pada rahang, semua otot skeletal tubuh memiliki banyak muscle spindel.

Masing-masing musle spindel terdiri dari kapsul jaringan ikat yang membentuk sekelompok serat saraf kecil yang dikenal sebagai serat intrafusal. Serat ini dimodifikasi sehingga ujungnya kontraktil, tetapi bagian tengahnya kekurangan miofibril. Ujung kontraktil ini mendapatkan persarafan sendiri dari gamma motor neuron. Bagian tengah yang nonkontraktil dibungkus oleh ujung saraf sensoris langsung dengan alpha motor neuron yang mempersarafi otot di mana spindel berada.

Saat sebuah otot beristirahat, daerah central dari masing-masing musle spindel akan cukup tertarik untuk mengaktifkan serat sensoris. Hasilnya, neuron dari spindel aktif secara tonik, mengirimkan arus stabil potensial aksi ke CNS. Karena itu, meski dalam posisi istirahat, otot tetap memiliki ketegangan tertentu yang dikenal sebagai musle tone.

Muscle spindel dilabuhkan secara paralel ke serat otot ekstrafusal. Pergerakan yang menyebabkan pemanjangan otot juga meregangkan muscle spindel dan menyebabkan serat sensorisnya “fire” dengan cepat. Hal ini menyebabkan refleks kontraksi otot yang akan mencegah otot melakukan over stretching. Jaras reflex yang mana regangan otot menyebabkan respon kontraksi dikenal sebagai “stretch reflex”.

2. Golgi tendon berespon pada ketegangan otot

Reseptor ini ditemukan di persimpangan tendon dan serat otot. Organ golgi tendon, berespon secara primer ke tension otot yang berkembang selama kontraksi isometrik dan menyebabkan reflek relaksasi. Respon ini berlawanan dengan reflek kontraksi yang disebabkan muscle spindel.

Organ golgi tendon disusun oleh tiga ujung saraf bebas yang membelit serat kolagen di dalam kapsul jaringan ikat. Saat sebuah otot berkontraksi, tendonnya akan menjadi sebuah komponen elastis fase isometrik kontraksi. Kontraksi akan menarik serat didalam tendon golgi dengan kuat, menjepit ujung sensoris saraf afferen dan menyebabkan mereka “fire”.

Input afferent dari aktivasi organ golgi tendon mengeksitasi inhibitory interneurons di spinal kord. Interneuron menghambat alpha motor neuron yang mempersarafi otot, dan kontraksi otot akan turun. Dalam kebanyakan keadaan, reflek ini memperpelan kontraksi otot saat kekuatan otot meningkat. Dengan kata lain, organ golgi tendon akan mencegah kontraksi berlebihan yang mungkin melukai otot.

3. Stretch refleks dan Inhibisi resiprok mengontol pergerakan di sekeliling sendi

Pergerakan di sekeliling sendi paling flexible dikontrol oleh sekelompok otot sinergis dan antagonis yang terkoordinasi. Kumpulan pathway yang mengontrol suatu sendi dikenal sebagai unit myotatic.

Refleks paling sederhana pada unit myotatic adalah monosynaptic stretch reflex, yang hanya melibatkan dua neuron, neuron sensorik dari muscle spindle dan neuron somatic motor neuron ke otot. Reflek hentakan lutut adalah contoh monosynaptic stretch reflex.

Saat tendon pattelar di bawah tempurung lutut di ketuk dengan palu kecil, ketukan akan meregangkan otot quadriceps. Ini akan mengaktifkan muscle spindles dan mengirim potensial aksi melalui serat sensoris ke spinal kord. Neuron sensoris bersinaps secara langsung ke motor neuron yang mengontrol kontraksi otot quadriceps. Eksitasi dari motor neuron menyebabkan unit motorik di quadriceps berkontraksi dan kaki bagian bawah akan maju ke depan.

4. Refleks fleksi menarik tungkai dari stimulus nyeri

Refleks fleksi merupakan polysinaptic reflex pathway yang menyebabkan tangan atau kaki tertarik saat ada rangsang nyeri, misalnya terkena peniti atau kompor panas. Refleks ini terjadi dengan jalur divergen.

Saat kaki kontak dengan titik paku, nocireseptor di kaki mengirim sensor informasi ke spinal kord. Disini sinyal akan berdivergen mengaktifkan multiple eksitatori interneurons. Beberapa neuron ini akan mengeksitasi alpha motor neuron menyebabkan kontraksi otot fleksi tungkai yang terstimulus. Beberapa interneuron secara simultan mengaktivasi inhibitory interneurons yang menyebabkan relaksasi sekelompok otot antagonis. Karena inhibisi resiprok inilah, tungkai akan fleksi, menarik dari stimulus nyeri. Tipe refleks ini membutuhkan waktu lebih banyak dari pada stretch reflex karena lebih polysinaptic.

Saat lengkung refleks untuk menghindari stimulus nyeri diinisiasi di sebuah kaki, kaki yang berlawanan juga akan mempersiapkan diri sehingga orang tersebut tidak kehilangan keseimbangan.

Tidak semua aktivitas refleks melibatkan lengkung refleks yang jelas, meskipun begitu prinsip dasar refleks tetap ada. Ada jenis refleks yang dimediasi baik oleh neuron atau hormon maupun keduanya, ada pula yang tidak melibatkan keduanya.

Daftar Pustaka

Disusun oleh Johny Bayu Fitantra

Silverthorn. Human Physiology : Homeostatis and Control. 5th Ed. San Fransisco: Pearson;2010. p. 449-57.

Sherwood L. Human Physiology : The Central Nervous System. 7th ed. Canada: Brooks/Cole Cengange Learning;2010. p. 176-79.

http://semuadokter.blogspot.com/2010/05/gerak-refleks.html

Filed under: Saraf

Makanan Sehat Saat Patah Hati

edwien — Tue, 09 Nov 2010 02:29:33 +0000

HAMPIR semua orang pernah mengalami patah hati. Saat merasakannya, yang kerap kita lakukan biasanya hanya termenung di kamar atau di depan televisi sambil menonton film-film romantis semisal Sleepless in Seattle sambil, semangkuk es krim, dan berpikir keras mengapa hal buruk ini bisa terjadi. Tapi apakah es krim dapat benar-benar membantu memulihkan kembali sakit hati kita?

Meski tak ada studi ilmiah yang membuktikan bahwa makanan dapat membantu mengatasi masalah kita, yang pasti hampir setiap perempuan yang patah hati biasanya memiliki naluri untuk mencari sesutu yang menyenangkan. “Setelah perpisahan, makanan yang mampu membuat Anda nyaman patut untuk dikonsumsi,” kata ahli gizi Stephanie Clarke, salah satu pendiri C&J Nutrition.

“Bermuram durja sambil menyendokkan makanan yang berkalori ke mulut dan akhirnya hanya menambah lemak tubuh seperti es krim, keripik, atau cokelat nantinya hanya akan membuat kita merasa lebih buruk. Lebih baik, saat merasa sedih, kita memilih makanan yang justru akan membuat kita merasa lebih berenergi, lebih langsing, dan siap menyambut hari yang baru,” ulasnya.

Berikut beberapa jenis makanan sehat kaya gizi, bukan kalori yang juga akan membuat tubuh merasa lebih nyaman saat patah hati:

1. Sup sayur: Semangkuk sup hangat dengan sayur-sayuran akan membuat tubuh lebih nyaman, relaks, sekaligus sehat.

2. Cokelat buatan sendiri: Buatlah cokelat hangat buatan Anda sendiri dan tuangkan ke mug yang berisi susu rendah lemak semisal susu kedelai. Pastikan pilih cokelat pekat atau dark chocolate supaya kebutuhan protein dan kalsium tubuh terpenuhi

3. Yoghurt : Ketimbang es krim, lebih baik Anda memakan yoghurt untuk membantu memulihkan perasaan sedih Anda. Terlebih, Anda tak akan merasa bersalah saat memakannya karena yoghurt justru akan membantu Anda melancarkan pencernaan tubuh.

4. Buah beri: Belilah buah beri sebanyak-banyaknya dan jadikan camilan sehat. Daripada mengambil keripik, mencamil buah beri seperti stroberi dan anggur tentunya akan menyehatkan dan membuat tubuh lebih berenergi

Filed under: Makanan, Remaja Tagged: cinta, pacaran, Remaja

Alasan Telur Pilihan Baik

edwien — Tue, 09 Nov 2010 02:22:04 +0000

MUNGKIN Anda tak sadar, telur yang biasa kita makan untuk sarapan ataupun sebagai bahan masakan pendamping seperti pada nasi goreng memiliki segudang manfaat lebih dari yang kita duga. Mari kita simak apa saja sih kelebihan telur, selain tentunya mudah didapat, harganya yang terbilang ekonomis, dan bisa dikombinasikan dalam berbagai masakan.

1. Sumber protein: kandungan dalam telur semuanya adalah bahan alami. Telur memiliki protein berkualitas tinggi yang menyediakan asam amino yang dibutuhkan tubuh.

2. Sumber energi: menurut hasil beberapa penelitian, dikemukakan bahwa memakan telur untuk sarapan mampu memberikan suplai energi yang cukup bagi seluruh anggota keluarga untuk melakukan aktivitas seharian.

3. Harganya ekonomis: dengan hanya Rp14.000, Anda sudah bisa mendapatkan satu kilogram telur yang bisa dimakan untuk satu minggu. Telur juga terbilang jauh lebih murah jika dibandingkan dengan bahan makanan berprotein lainnya yang dijual di pasar.

4. Baik untuk jantung: melalui sebuah penelitian yang telah digelar selama 30 tahun, diketahui, memakan telur tidak membahayakan orang dewasa ataupin lanjut usia karena tak memiliki dampak signifikan terhadap jantung.

5. Mudah dimasak: telur sangat mudah dan ringkas untuk dimasak, sama seperti halnya Anda membuat roti selai ataupun sereal.

6. Baik bagi pertumbuhan bayi: telur kaya akan kolin, nutrisi yang dibutuhkan bagi tumbuh kembang bayi dan janin. Untuk itu, dengan kandungan tersebut, perempuan hamil dapat meminimalisasi risiko cacat lahir dan membuat perkembangan otak bayi lebih baik.

7. Kaya nutrisi: satu butir telur mengandung 13 vitamin dan mineral. Kalorinya pun terbilang sedkit yakni 70 saja. Telur juga mempunyai kandungan karbohidrat, protein, dan delapan macam asam amino sehingga berguna bagi tubuh, terutama bagi anak-anak yang masih berada dalam masa pertumbuhan.

Sebenarnya, hampir semua jenis telur dapat dikonsumsi, tetapi hanya beberapa jenis yang lazim dimakan, baik sebagai lauk-pauk maupun sebagai obat. Telur yang biasa dikonsumsi antara lain telur yang berasal dari unggas seperti ayam, bebek, angsa, dan beberapa jenis burung seperti burung unta dan burung puyuh. (Pri/OL-06)

Filed under: Makanan Tagged: makanan, telur

Macam-Macam Ukuran Penis

edwien — Thu, 28 Oct 2010 07:39:45 +0000

Hasil survei ini yang pernah dilakukan Andrologi Andromedical menyurvei rata-rata panjang penis tebesar di seluruh negara dunia. Penelitian yang dipimpin Dr Eduardo Gomez de Diego mendapatkan rata-rata panjang penis pria di dunia sekitar 14 cm (5,5 inci)

Negara-negara yang disurvei diambil yang mewakili semua benua. Seperti dikutip dari Andromedical, Selasa (13/4/2010) beberapa negara memiliki panjang ereksi penis dan panjang penis normal yang berbeda-beda, yaitu:

Berdasarkan studi dari Master dan Johnson menunjukkan orang kulit putih memiliki jaringan yang lebih elastis dan retractile pada saat normal dibandingkan dengan orang kulit hitam. Karena itu orang kulit hitam selalu beranggapan memiliki penis yang lebih besar, tapi tidak berlaku saat ereksi.

Sementara itu American Plastic Surgery Academy, mengklasifikasikan ukuran penis saat ereksi menjadi 4 tipe, yaitu:

1. Mikropenis, kurang dari 7 cm (2,75 inci).
2. Penis kecil, kurang dari 10 cm (3,93 inci).
3. Penis menengah, antara 12 cm – 17 cm (4,72-6,69 inci).
4. Penis besar, lebih dari 18 cm (7,08 inci).

Sedangkan berdasarkan survei yang dilakukan oleh perusahaan kondom Durex yang diterbitkandalam koran Milenio, jika berdasarkan etnis maka ras Kaukasia memiliki penis paling panjang yang diikuti oleh ras Afrika, Hispanic dan terakhir adalah Asia.

1. Kaukasia: 16,2 cm (6,39 inci)
2. Afrika: 15,2 cm (6 inci)
3. Hispanic: 14,7 cm (5,8 inci)
4. Asia: 13,5 cm (5,31 inci)

Filed under: Aneh, Reproduksi Tagged: Penis, pria, seksual

Patofisiologi dan Pengobatan Asma

edwien — Thu, 21 Oct 2010 02:09:51 +0000

1. Definisi Asma

Asma adalah suatu penyakit dengan ciri meningkatnya respon trakea dan bronkhus terhadap berbagai rangsangan dengan manifestasi adanya penyempitan jalan nafas yang luas dan derajatnya dapat berubah-ubah secara spontan maupun sebagai hasil pengobatan (Soeparman, 1990).

Menurut Sylvia Anderson (1995 : 149) asma adalah keadaan klinis yang ditandai oleh masa penyempitan bronkus yang reversibel, dipisahkan oleh masa di mana ventilasi jalan nafas terhadap berbagai rangsang.

Asma adalah suatu inflamasi kronis saluran nafas yang melibatkan sel eosinofil, sel mast, sel netrofil, limfosit dan makrofag yang ditandai dengan wheezing, sesak nafas kumat-kumatan, batuk, dada terasa tertekan dapat pulih kembali dengan atau tanpa pengobatan (Cris Sinclair, 1994)

Samsuridjal dan Bharata Widjaja (1994) menjelaskan asma adalah suatu penyakit peradangan (inflamasi) saluran nafas terhadap rangsangan atau hiper reaksi bronkus. Sifat peradangan pada asma khas yaitu tanda-tanda peradangan saluran nafas disertai infliltrasi sel eosinofil.

Asma merupakan suatu keadaan gangguan / kerusakan bronkus yang ditandai dengan spasme bronkus yang reversibel (spasme dan kontriksi yang lama pada jalan nafas) (Joyce M. Black,1996).

Menurut Crocket (1997) asthma bronkiale didefinisikan sebagai penyakit dari sistem pernafasan yang meliputi peradangan dari jalan nafas dengan gejala bronkospasme yang reversibel.

2. Penyebab Asma

Faktor Pencetus Serangan Asthma Bronkiale

Faktor-faktor yang dapat menimbulkan serangan asthma bronkiale atau sering disebut sebagai faktor pencetus adalah :

(1) Alergen

Alergen adalah sat-zat tertentu bila dihisap atau di makan dapat menimbulkan serangan asthma, misalnya debu rumah, tungau debu rumah (Dermatophagoides pteronissynus) spora jamur, serpih kulit kucing, bulu binatang, beberapa makanan laut dan sebagainya.

(2) Infeksi saluran nafas

Infeksi saluran nafas terutama oleh virus seperti influenza merupakan salah satu faktor pencetus yang paling sering menimbulkan asthma bronkiale. Diperkirakan dua pertiga penderita asthma dewasa serangan asthmanya ditimbulkan oleh infeksi saluran nafas (Sundaru, 1991).

(3) Tekanan jiwa

Tekanan jiwa bukan sebagai penyebab asthma tetapi sebagai pencetus asthma, karena banyak orang yang mendapat tekanan jiwa tetapi tidak menjadi penderita asthma bronkiale. Faktor ini berperan mencetuskan serangan asthma terutama pada orang yang agak labil kepribadiannya. Hal ini lebih menonjol pada wanita dan anak-anak (Yunus, 1994).

(4) Olah raga / kegiatan jasmani yang berat

Sebagian penderita asthma bronkiale akan mendapatkan serangan asthma bila melakukan olah raga atau aktifitas fisik yang berlebihan. Lari cepat dan bersepeda paling mudah menimbulkan serangan asthma. Serangan asthma karena kegiatan jasmani (Exercise induced asthma /EIA) terjadi setelah olah raga atau aktifitas fisik yang cukup berat dan jarang serangan timbul beberapa jam setelah olah raga.

(5) Obat-obatan

Beberapa pasien asthma bronkiale sensitif atau alergi terhadap obat tertentu seperti penicillin, salisilat, beta blocker, kodein dan sebagainya.

(6) Polusi udara

Pasien asthma sangat peka terhadap udara berdebu, asap pabrik / kendaraan, asap rokok, asap yang mengandung hasil pembakaran dan oksida fotokemikal, serta bau yang tajam.

(7) Lingkungan kerja

Diperkirakan 2 – 15% pasien asthma bronkiale pencetusnya adalah lingkunagn kerja (Sundaru, 1991).

3. Patofisiologi

Suatu serangan asthma timbul karena seorang yang atopi terpapar dengan alergen yang ada dalam lingkungan sehari-hari dan membentuk imunoglobulin E ( IgE ). Faktor atopi itu diturunkan. Alergen yang masuk kedalam tubuh melalui saluran nafas, kulit, dan lain-lain akan ditangkap makrofag yang bekerja sebagai antigen presenting cell (APC). Setelah alergen diproses dalan sel APC, alergen tersebut dipresentasikan ke sel Th. Sel Th memberikan signal kepada sel B dengan dilepaskanya interleukin 2 ( IL-2 ) untuk berpoliferasi menjadi sel plasma dan membentuk imunoglobulin E (IgE).

IgE yang terbentuk akan diikat oleh mastosit yang ada dalam jaringan dan basofil yang ada dalan sirkulasi. Bila proses ini terjadai pada seseorang, maka orang itu sudah disensitisasi atau baru menjadi rentan. Bila orang yang sudah rentan itu terpapar kedua kali atau lebih dengan alergen yang sama, alergen tersebut akan diikat oleh Ig E yang sudah ada dalam permukaan mastoit dan basofil. Ikatan ini akan menimbulkan influk Ca⁺⁺ kedalam sel dan perubahan didalam sel yang menurunkan kadar cAMP.

Penurunan pada kadar cAMP menimbulkan degranulasi sel. Degranulasi sel ini akan menyebabkan dilepaskanya mediator-mediator kimia yang meliputi : histamin, slow releasing suptance of anaphylaksis ( SRS-A), eosinophilic chomotetik faktor of anaphylacsis (ECF-A) dan lain-lain. Hal ini akanmenyebabakan timbulnya tiga reaksi utama yaitu : kontraksi otot-otot polos baik saluran nafas yang besar ataupun yang kecil yang akan menimbulkan bronkospasme, peningkatan permeabilitas kapiler yang berperan dalam terjadinya edema mukosa yang menambah semakin menyempitnya saluran nafas , peningkatansekresi kelenjar mukosa dan peningkatan produksi mukus. Tiga reaksi tersebut menimbulkan gangguan ventilasi, distribusi ventilasi yang tidak merata dengan sirkulasi darah paru dan gangguan difusi gas ditingkat alveoli, akibatnya akan terjadi hipoksemia, hiperkapnea dan asidosis pada tahap yangsangat lanjut, (Barbara C.L,1996, Karnen B. 1994, William R.S. 1995 )

4. Klasifikasi Asma Berdasarkan Etiologi

a) Asma Bronkiale Tipe Atopik (Ekstrinsik)

Asma timbul karena seseorang yang atopi akibat pemaparan alergen. Alergen yang masuk tubuh melalui saluran pernafasan, kulit, saluran pencernaan dan lain-lain akan ditangkap oleh makrofag yang bekerja sebagai antigen presenting cells (APC). Setelah alergen diproses dalam sel APC, kemudian oleh sel tersebut, alergen dipresentasikan ke sel Th. Sel APC melalui penglepasan interleukin I (II-1) mengaktifkan sel Th. Melalui penglepasan Interleukin 2 (II-2) oleh sel Th yang diaktifkan, kepada sel B diberikan signal untuk berproliferasi menjadi sel plasthma dan membentuk IgE.

IgE yang terbentuk akan segera diikat oleh mastosit yang ada dalam jaringan dan basofil yang ada dalam sirkulasi. Hal ini dimungkinkan oleh karena kedua sel tersebut pada permukaannya memiliki reseptor untuk IgE. Sel eosinofil, makrofag dan trombosit juga memiliki reseptor untuk IgE tetapi dengan afinitas yang lemah. Orang yang sudah memiliki sel-sel mastosit dan basofil dengan IgE pada permukaan tersebut belumlah menunjukkan gejala. Orang tersebut sudah dianggap desentisisasi atau baru menjadi rentan

Bila orang yang sudah rentan itu terpapar kedua kali atau lebih dengan alergen yang sama, alergen yang masuk tubuh akan diikat oleh IgE yang sudah ada pada permukaan mastofit dan basofil. Ikatan tersebut akan menimbulkan influk Ca++ ke dalam sel dan terjadi perubahan dalam sel yang menurunkan kadar cAMP.

Kadar cAMP yang menurun itu akan menimbulkan degranulasi sel. Dalam proses degranulasi sel ini yang pertama kali dikeluarkan adalah mediator yang sudah terkandung dalam granul-granul (preformed) di dalam sitoplasma yang mempunyai sifat biologik, yaitu histamin, Eosinophil Chemotactic Factor-A (ECF-A), Neutrophil Chemotactic Factor (NCF), trypase dan kinin. Efek yang segera terlihat oleh mediator tersebut ialah obstruksi oleh histamin.

Hiperreaktifitas bronkus yaitu bronkus yang mudah sekali mengkerut (konstriksi) bila terpapar dengan bahan / faktor dengan kadar yang rendah yang pada kebanyakan orang tidak menimbulkan reaksi apa-apa, misalnya alergen (inhalan, kontaktan), polusi, asap rokok / dapur, bau-bauan yang tajam dan lainnya baik yang berupa iritan maupun yang bukan iritan. Dewasa ini telah diketahui bahwa hiper rektifitas bronkus disebabkan oleh inflamasi bronkus yang kronik. Sel-sel inflamasi terutama eosinofil ditemukan dalam jumlah besar dalam cairan bilas bronkus pasien asthma bronkiale sebagai bronkhitis kronik eosinofilik. Hiper reaktifitas berhubungan dengan derajad berat penyakit. Di klinik adanya hiperreaktifitas bronkhus dapat dibuktikan dengan uji provokasi yang menggunakan metakolin atau histamin.

Berdasarkan hal-hal tersebut di atas saat ini penyakit asthma dianggap secara klinik sebagai penyakit bronkhospasme yang reversibel, secara patofisiologik sebagai suatu hiper reaksi bronkus dan secara patologik sebagai suatu peradangan saluran nafas.

Bronkus pada pasien asma oedema di mukosa dan dindingnya, infiltrasi sel radang terutama eosinofil serta terlepasnya sel silia yang menyebabkan getaran silia dan mukus di atasnya sehingga salah satu daya pertahanan saluran nafas menjadi tidak berfungsi lagi. Ditemukan pula pada pasien asthma bronkiale adanya penyumbatan saluran nafas oleh mukus terutama pada cabang-cabang bronkhus

.Akibat dari bronkhospasme, oedema mukosa dan dinding bronkhus serta hipersekresi mukus maka terjadi penyempitan bronkhus dan percabangannya sehingga akan menimbulkan rasa sesak, nafas berbunyi (wheezing) dan batuk yang produktif.

Adanya stressor baik fisik maupun psikologis akan menyebabkan suatu keadaan stress yang akan merangsang HPA axis. HPA axis yang terangsang akan meningkatkan adeno corticotropic hormon (ACTH) dan kadar kortisol dalam darah. Peningkatan kortisol dalam darah akan mensupresi immunoglobin A (IgA). Penurunan IgA menyebabkan kemampuan untuk melisis sel radang menurun yang direspon oleh tubuh sebagai suatu bentuk inflamasi pada bronkhus sehingga menimbulkan asma bronkiale.

b) Asma Bronkiale Tipe Non Atopik (Intrinsik)

Asma non alergenik (asma intrinsik) terjadi bukan karena pemaparan alergen tetapi terjadi akibat beberapa faktor pencetus seperti infeksi saluran nafas atas, olah raga atau kegiatan jasmani yang berat, serta tekanan jiwa atau stress psikologik. Serangan asma terjadi akibat gangguan saraf otonom terutama gangguan saraf simpatis yaitu blokade adrenergik beta dan hiperreaktifitas adrenergik alfa. Dalam keadaan normal aktifitas adrenergik beta lebih dominan daripada adrenergik alfa. Pada sebagian penderita asma aktifitas adrenergik alfa diduga meningkat yang mengakibatkan bronkhokonstriksi sehingga menimbulkan sesak nafas.

Reseptor adrenergik beta diperkirakan terdapat pada enzim yang berada dalam membran sel yang dikenal dengan adenyl-cyclase dan disebut juga messengner kedua. Bila reseptor ini dirangsang, maka enzim adenyl-cyclase tersebut diaktifkan dan akan mengkatalisasi ATP dalam sel menjadi 3’5’ cyclic AMP. cAMP ini kemudian akan menimbulkan dilatasi otot-otot polos bronkus, menghambat pelepasan mediator dari mastosit / basofil dan menghambat sekresi kelenjar mukus. Akibat blokade reseptor adrenergik beta maka fungsi reseptor adrenergik alfa lebih dominan akibatnya terjadi bronkhus sehingga menimbulkan sesak nafas. Hal ini dikenal dengan teori blokade adrenergik beta. (baratawidjaja, 1990).

c) Asma Bronkiale Campuran (Mixed)

Pada tipe ini keluhan diperberat baik oleh faktor-faktor intrinsik maupun ekstrinsik.

Pernafasan (respirasi) adalah peristiwa menghirup udara dari luar yang mengandung oksigen kedalam tubuh. Serta menghembuskan udara yang banyak mengandung karbondioksida (CO2) sebagai sisa dari oksidasi keluar dari tubuh. Penghisapan ini disebut inspirasi dan menghembuskan disebut ekspirasi (Lorraine M.wilson,1995).

Secara garis besar saluran pernafasan dibagi menjadi dua zona, zona konduksi yang dimulai dari hidung, faring, laring,trakea, bronkus, bronkiolus segmentalis dan berakir pada bronkiolus terminalis. Sedangkan zona respiratoris dimulai dari bronkiolus respiratoris, duktus alveoli dan berakhir pada sakus alveulus terminalis (N.L.G.Yasmin, 1995 dan Syaifuddin,1997).

Saluran pernafasan mulai dari hidung sampai bronkiolus dilapisi oleh membran mukosa yang bersilia. Ketika udara masuk kerongga hidung, udara tersebut disaring, dihangatkan dan dilembabkan. Ketiga proses ini merupakan fungsi utama dari mukosa respirasi yang terdiri dari epiotel thorak yang bertingkat, bersilia dan bersel goblet.Permukaan epitel dilapisi oleh lapisan mukus yang sisekresi sel goblet dan kelenjar serosa. Partikel-partikel debu yang kasar dapat disaring oleh rambut-rambut yang terdapat dalam lubang hidung. Sedangkan partikel yang halus akan terjerat dalam lapisan mukus untuk kemudian dibatukkan atau ditelan. Air untuk kelembapan diberikan oleh lapisan mukus, sedangkan panas yang disuplai keudara inspirasi berasal dari jaringan dibawahnya yang kaya dengan pembulu darah, sehingga bila udara mencapai faring hampir bebas debu,bersuhu mendekati suhu tubuh dan kelembapanya mencapai 100%(Lorraine M. Wilson, 1995).

Asma ditandai dengan mengi (wheezing), batuk dan rasa sesak di dada berjalan atau kronis, sebagai akibat adanya bronkokonstriksi. Angka kesakitan dan kematian terus meningkat, dan meskipun telah dilakukan penelitian intensif, dasar penyebabnya masih belum diketahui. Namun terdapat 3 kelainan pada asma : sumbatan jalan napas yang sebagian reversible, inflamasi jalan napasserta hiperrespins jalan napas etrhadap berbagai rangsang. Adanya kaitan dengan alergi telah lama diketahui, dan kadar IgE plasma seringkali meningkat. Protein yang dilepaskan dari eosinofil pada reaksi inflamasi dapat merusak epitel saluran napas dan ikut berperan pada hiperrespons. Eosinofil dan sel mast melepaskan leukotrien yang menyebebakan bronkokonstriksi. Takikinin yang dilepas dari saraf sensorik pada saluran napas mungkin ikut berperan, dan didapatkan bukti adanya defisiensi VIP, suatu bronkodilator. Serangan asma lebih berat saat larut malam dan dini hari, karena seperti telah diuraikan sebelumnya, saat itu merupakan periode konstriksi maksimal irama sirkadian tonun bronkus. Udara dingin dan latihan fisik, yang keduanya biasanya menyebabkan brokokonstriksi, juga memicu serangan asma, dan pengaruh keduanya dicegah oleh penghambat sintesis atau kerja leukotrien. Rseptpr adrenergik-b memperantarai bronkodilatasi, dan pengobatan dengan inhalasi agonis adrenergik-b merupaka terapi standar ams. Reseptor muskarinik memperantarai bronkokonstriksi, dan obat penghambat muskarinik kolinergik juga digunakan untuk pengobatan asma. Obat tambahan lain yang lazim digunakan adalah kromolin, yang menghamat pelepasan produk sel mast, dan glukokortikoid, yang menghambat respons inflamasi.

Udara mengalir dari hidung kefaring yang merupakan tempat persimpangan antara jalan pernafasan dan jalan makanan. Faring dapat dibagi menjadi tiga bagian yaitu : nasofaring, orofaring dan laringofaring. Dibawah selaput lendir terdapat jaringan ikat, juga dibeberapa tempat terdapat follikel getah bening yang dinamakan adenoid. Disebelahnya terdapat dua buah tonsil kiri dan kanan dari tekak, (Syaifuddin,1997).

Laring merupakan saluran udara dan bertindak sebagai pembentukan suara terletak didepan bagian faring sampai ketinggian vertebra servikalis dan masuk ke trakea di bawahnya (Syaifuddin,1997). Laring merupakan rangkaian cincin tulang rawan yang dihubungkan oleh otot dan mengandung pita suara. Diantara pita suara terdapat glotis yang merupakan pemisah saluran pernafasan bagian atas dan bawah. Pada saat menelan, gerakan laring keatas, penutupan dan fungsi seperti pintu pada aditus laring dari epiglotis yang berbentuk daun berperan untuk mengarahkan makanan ke esofagus, tapi jika benda asing masih bisa melampaui glotis, maka laring mempunyai fungsi batuk yang akan membantu merngeluarkan benda dan sekret keluar dari saluran pernafasan bagian bawah, (Larroin M.W, 1995).

Trakea dibentuk 16 sampai dengan 20 cincin tulang rawan, yang berbentuk seperti kuku kuda dengan panjang kurang lebih 5 inci (9-11 cm), lebar 2,5 cm, dan diantara kartilago satu dengan yang lain dihubaungkan oleh jaringan fibrosa, sebelah dalam diliputi oleh selaput lendir yang berbulu getar(sel bersilia) yang hanya bergerak keluar. Sel-sel bersilia ini berguna untuk mengeluarkan benda-benda asing yang masuk bersama udara pernafasan, dan dibelakang terdiri dari jaringan ikat yang dilapisi oleh otot polos dan lapisan mukusa, (Syaifuddin,1997).

Bronkus merupakan lanjutan dari trakea ada dua buah yamg terdapat pada ketinggian vertebra torakalis ke IV dan V. Sedangkan tempat dimana trakea bercabang menjadi bronkus utama kanan dan kiri disebut karina. Karina memiliki banyak syaraf dan dapat menyebabkan bronkospasme dan batuk yang kuat jika batuk dirangsang . Bronkus utama kanan lebih pendek , lebih besar dan lebih vertikal dari yang kiri. Terdiri dari 6-8 cincin, mempunyai tiga cabang. Bronkus utama kiri lebih panjang,dan lebih kecil, terdiri dari 9-12 cicin serta mempunyai dua cabang,(Syaifuddin,1997).

Bronkiolus terminalis merupakan saluran udara kecil yang tidak mengandung alveoli (kantung udara) dan memiliki garis 1 mm. Bronkiolus tidak diperkuat oleh cincin tulang rawan, tapi dikelilingi oleh otot polos sehingga ukuranya dapat berubah. Seluruh saluran uadara ,mulai dari hidung sampai bronkiolus terminalis ini disebut saluran penghantar udara atau zona konduksi. Bronkiolus ini mengandung kolumnar epitellium yang mengandung lebih banyak sel goblet dan otot polos, diantaranya strecch reseptor yang dilanjutkan oleh nervus vagus,(Lorraine M. Wilson,1995).

Setelah bronkiolus terminalis terdapat asinus yang merupakan unit fungsional paru , yaitu tempat pertukaran gas. Asinus terdiri dari : Bronkiolus respiratoris, duktus alveolaris dan sakus alveolaris terminalis yang merupakan struktur akhir dari paru. (Lorraine M.Wilson,1995 ).

Secara garis besar fungsi pernafasan dapat dibagi menjadi dua yaitu pertukaran gas dan keseimbangan asam basa. Fungsi pertukaran gas ada tiga proses yang terjadi. Pertama ventilasi, merupakan proses pergerakan keluar masuknya udara melalui cabang-cabang trakeo bronkial sehingga oksigen sampai pada alveoli dan karbondioksida dibuang. Pergerakan ini terjadi karena adanya perbedaan tekanan. Udara akan mengalir dari tekanan yang tianggi ke tekanan yang rendah. Selama inspirasi volume thorak bertambah besar karena diafragma turun dan iga terangkat. Peningkatan volume ini menyebabkan menurunan tekanan intra pleura dari –4 mmHg (relatif terhadap tekanan atmosfir) menjadi sekita –8mmHg. Pada saat yang sama tekanan pada intra pulmunal menurun –2 mmHg (relatif terhadap tekanan atmosfir). Selisih tekanan antara saluran udara dan atmosfir menyebabkan udara mengalir kedalam paru sampai tekanan saluran udara sama dengan tekanan atmosfir. Pada ekspirasi tekanan intra pulmunal bisa meningkat 1-2 mmHg akibat volume torak yang mengecil sehingga udara mengalir keluar paru,(Lorraine M. Wilson,1995).

Proses kedua adalah difusi yaitu masuknya oksigen dari alveoli ke kapiler melalui membran alveoli-kapiler. Proses ini terjadi karena gas mengalir dari tempat yang tinggai tekanan parsialnya ketempat yang lebih rendah tekanan partialnya. Oksigen dalam alveoli mempunyai tekanan partial yang lebih tinggi dari oksigen yang berada didalam darah. Karbondioksida darah lebih tinggi tekanan partialnya dari pada karbondioksida dialveoli. Akibatnya karbondioksida mengalir dari darah ke alveoli,(John Gibson,1995).

Proses ketiga adalah perfusi yaitu proses penghantaran oksigen dari kapiler ke jaringan melalui transpor aliran darah. Oksigen dapat masik ke jaringan melalui dua jalan : pertama secara fisik larut dalam plasma dan secara kimiawi berikata dengan hemoglobin sebagai oksihemoglobin, sedangkan karbondioksida ditransportasi dalam darah sebagai bikarbonat, natrium bikarbonat dalam plasma dan kalium bikarbonat dalam sel-sel darah merah. Satu gram hemoglobin dapat mengika 1,34 ml oksigen. Karena konsentrasi hemoglobin rata-rata dalam darah orang dewasa sebesar 15 gram, maka 20,1 ml oksigen bila darah jenuh total ( Sa O2 = 100% ),bila darah teroksigenasi mencapai jaringan . Oksigen mengalir dari darah masuk ke cairan jaringan karena tekanan partial oksigen dalam darah lebih besar dari pada tekanan dalam cairan jaringan. Dari dalam cairan jaringan oksigen mengalir kedalan sel-sel sesuai kebutuhan masing-masing. Sedangkan karbondioksida yang dihasilkan dalam sel mengalir kedalam cairan jaringan. Tekanan partial karbondioksida dalam jaringan lebih besar dari pada tekanan dalam darah maka karbondioksida mengalir dari cairan jaringan kedalam darah (Lorraine M.Wilson, 1995).

Fungsi sebagain pengaturan keseimbangan asam basa : pH darah yang normal berkisar 7,35 – 7,45. Sedangkan manusia dapat hidup dalam rentang pH 7,0 – 7,45. Pada peninggian CO₂ baik karena kegagalan fungsi maupun tambahnya produksi CO₂ jaringan yang tidak dikompensasi oleh paru menyebabkan perubahan pH darah. Asidosis respiratoris adalah keadaan terjadinya retensi CO₂ atau CO₂yang diproduksi oleh jaringan lebih banyak dibandingkan yang dibebaskan oleh paru. Sedangkan alkalosis respiratorius adalah suatu keadaan Pa CO₂ turun akibat hiper ventilasi, (Hudak dan Gallo,1997 ).

Dampak yang Ditimbulkan Oleh Asthma Bronkiale

Dampak yang ditimbulkan oleh asma Bronkhiale adalah :

Sistem Pernafasan

Peningkatan frekuensi pernafasan, susah bernafas, perpendekan periode inspirasi, pemanjangan ekspirasi

2. Penggunaan otot-otot aksesori pernafasan (retraksi sternum, pengangkatan bahu waktu bernafas).

a. Pernafasan cuping hidung.

b. Adanya mengi yang terdengar tanpa stetoskop.

c. Batuk keras, kering dan akhirnya batuk produktif.

d. Faal paru terdapat penurunan FEV1.

Sistem Kardiovaskuler

1. Takikardia

2. Tensi meningkat

3. Pulsus paradoksus (penurunan tekanan darah) 10 mmHg pada waktu inspirasi).

4. Sianosis

5. Diaforesis

6. Dehidrasi

Psikologis

Peningkatan ansietas (kecemasan) : takut mati, takut menderita, panik, gelisah.
Ekspresi marah, sedih, tidak percaya dengan orang lain, tidak perhatian.
Ekspresi tidak punya harapan, helplessness.

Sosial

Ketakutan berinteraksi dengan orang lain.
Gangguan berkomunikasi
Inappropiate dress
Hostility toward others

Hematologi

Eosinofil meningkat > 250 / mm³
Penurunan limfosit dan komponen sel darah putih yang lain.
Penurunan Immunoglobulin A (IgA)

Pengobatan Asma

a) Agonis beta

Bentuk aerosol bekerja sangat cepat diberika 3-4 kali semprot dan jarak antara semprotan pertama dan kedua adalan 10 menit. Yang termasuk obat ini adalah metaproterenol ( Alupent, metrapel ).

b) Metil Xantin

Golongan metil xantin adalan aminophilin dan teopilin, obat ini diberikan bila golongan beta agonis tidak memberikan hasil yang memuaskan. Pada orang dewasa diberikan 125-200 mg empatkali sehari.

c) Kortikosteroid

Jika agonis beta dan metil xantin tidak memberikan respon yang baik, harus diberikan kortikosteroid. Steroid dalam bentuk aerosol ( beclometason dipropinate ) dengan disis 800 empat kali semprot tiap hari. Karena pemberian steroid yang lama mempunyai efek samping maka yang mendapat steroid jangka lama harus diawasi dengan ketat.

d) Kromolin

Kromolin merupakan obat pencegah asthma, khususnya anak-anak . Dosisnya berkisar 1-2 kapsul empat kali sehari.

e) Ketotifen

Efek kerja sama dengan kromolin dengan dosis 2 x 1 mg perhari. Keuntunganya dapat diberikan secara oral.

f) Iprutropioum bromide (Atroven)

Atroven adalah antikolenergik, diberikan dalam bentuk aerosol dan bersifat bronkodilator.

(Evelin dan joyce L. kee, 1994 ; Karnen baratawijaja, 1994 )

3. Pengobatan selama serangan status asthmatikus

a) Infus RL : D5 = 3 : 1 tiap 24 jam

b) Pemberian oksigen 4 liter/menit melalui nasal kanul

c) Aminophilin bolus 5 mg / kg bb diberikan pelan-pelan selama 20 menit dilanjutka drip Rlatau D5 mentenence (20 tetes/menit) dengan dosis 20 mg/kg bb/24 jam.

d) Terbutalin 0,25 mg/6 jam secara sub kutan.

e) Dexamatason 10-20 mg/6jam secara intra vena.

f) Antibiotik spektrum luas.

Filed under: Respirasi, Saluran Nafas Tagged: asma, penyakit, pernafasan

Meningkatkan Sistem Imun

edwien — Wed, 20 Oct 2010 00:04:56 +0000

CUACA ekstrem dan tak jelas yang melanda Tanah Air akhir-akhir ini menimbulkan permasalahan di berbagai sektor termasuk kesehatan. Berikut beberap tips yang akan membantu kita untuk melindungi tubuh dari penyakit yang bisa saja mengganggu aktivitas kita sehari-hari.
1. Kurangi makanan berlemak
Makanan berlemak dapat membuat fungsi sistem imun kita berkurang sehingga tubuh terasa lebih lemas dan lamban. Dengan mengurangi asupan lemak, sel T lymphocytes akan berfungsi lebih maksimal sehingga mampu menangkal segala infeksi yang mungkin menyerang tubuh. Usahakan tubuh mendapat asupan lemak sebesar 20-30 persen per harinya, lebih baik dari lemak tak jenuh. Lemak jenis ini dapat ditemukan pada minyak zaitun, alpukat, dan selai kacang. Juga hindari lemak tak jenuh pada susu, mentega, dan daging.

2. Perbanyak protein
Asam amino pada protein diibaratkan seperti dinding pelindung sistem imun kita dengan menghasilkan sel darah putih dan zat antibodi. Bagi kaum perempuan, disarankan mengonsumsi sekitar 50 gram protein per harinya dari beberapa makanan seperti ikan, daging unggas tanpa kulit, telur, kacang, daging sapi rendah lemak, atau produk kacang kedelai.

3. Banyak bergerak
Menurut beberapa penelitian, terbukti bahwa gerakan tubuh berupa jalan ringan, bersepeda, atau berenang selama 45 menit selama lima kali per minggu dapat meningkatkan sistem kekebalan tubuh dan memperkecil risiko terkena penyakit hingga 50 persen.

4. Bermusik
Hasil penelitian yang dilakukan di Universitas Johann Wolfgang Goethe di Frankfurt memperlihatkan bahwa menyanyi mampu meningkatkan suasana hati bahkan sistem kekebalan tubuh seseorang sehingga tak mudah terserang penyakit. Pada penelitian lain di Universitas Willamette, Salem, Oregon, ditemukan ketika seseorang tengah memainkan alat musik seperti perkusi, drum lalu bernyanyi mengiringinya, tingkat konsentrasinya bertambah lebih besar ketimbang yang hanya mendengarkan musik.

5. Sayangi hewan peliharaan
Mungkin ini tampak aneh, tapi nyata. Dari hasil penelitian yang diadakan di Universitas Wilkes, diketahui bahwa membelai anjing selama 18 menit membantu meningkatkan sekretori imunoglobulin (IgA) yang membantu melindungi tubuh dari kuman. Selain itu, membuat hewan peliharaan merasa senang, kita pun akan turut senang karena memicu pelepasan bahan kimia ke dalam otak yang meningkatkan fungsi kekebalan tubuh. Maka itu, sering-seringlah membelai dan memberi makan hewan peliharaan Anda

6. Makanan tiga warna
Sayuran dan buah berwarna merah, oranye, kuning, dan hijau kaya akan karotenoi yang membantu sel imun melindungi tubuh dan membunuh virus. Selain itu, makanan tersebut juga mengandung antioksidan dan vitamn A serta C yang memperkuat sel sehingga mereka mampu menangkal berbagai bakteri jahat.

7. Makan bakteri baik
Produk yang mengandung probiotik tertentu telah terbukti mampu mencegah atau mengurangi masalah gastrointestinal, urogenital, dan masalah pernapasan. Pilihlah makanan atau suplemen berprobiotik yang mengandung Lactobacillus rhamnosus GR-1 atau GG, L casei Immunitas, dan Bifidobacterium animalis DN 114 001. Jangan langsung percaya dengan produk bertuliskan ‘probiotik’ atau ‘acidophilus’.

8. Hindari tidur larut malam
Usahkan tidur tidak terlalu malam agar energi tubuh terisi kembali. Dsarankan, sebaiknya tidur selama 7-8 jam. Dalam sebuah penelitian diketahui bahwa perempuan yang beristirahat cukup memiliki sel darah putih pelindung tubuh yang lebih banyak ketimbang yang kurang istirahat.

9. Salurkan hobi
Lakukanlah kegiatan yang merupakan hobi atau seseuatu yang senang Anda lakukan seperti melukis atau bermain puzzle setiap hari. Dengan begitu, tingkat stres Anda akan berkurang karena sel imun bersirkulasi meningkatkan hormon kortisol sehingga tubuh Anda pun terhindar dari kuman.

reffrence: Media Hidup Sehat

Filed under: Tips Tagged: immune, sehat, Tips

Minuman Pereda Stress

edwien — Sat, 16 Oct 2010 09:56:22 +0000

ANDA tengah stres karena mengalami hari yang buruk? Jangan segera meraih permen, kue, atau makanan lainnya yang berada di dekat Anda. Cobalah minum salah satu jenis minuman di bawah ini. Niscaya stres akan mereda dan Anda pun akan merasa lebih tenang.

1. Minum segelas susu
Susu mengandung tryptophan yang melalui metabolisme tubuh diubah menjadi serotonin yang mampu meningkatkan mood. Plus, kalsium, magnesium, dan kalium yang menjaga tekanan darah.

2. Minum cokelat panas
Minuman hangat terutama cokelat akan menaikkan suhu tubuh sehingga kita akan merasa nyaman. Tak hanya untuk tubuh, efek serupa juga akan dirasakan otak kita.

3. Nikmati teh hitam
Ketimbang kopi, cobalah pesan teh hitam. Menurut studi yang dilakukan tim di Universitas College London, meminum teh hitam empat kali sehari ampuh menurunkan tingkat hormon kortisol yang menyebabkan stres.

4. Minum teh hijau
Bila sulit menemukan the hitam, minumlah saja the hijau. The hijau mengandung zat theanine yang akan meningkatkan hormon relaksasi pada otak dan memicu produksi gelombang alpha dan mengurangi ketegangan yang disebabkan gelombang beta.

5. Minum air dingin
Coba raih segelas air dingin dan berjalan-jalanlah ke luar ruangan. Dengan air, cairan dalam tubuh akan bergerak dan hormon endorfin pun terstimulasi sehingga stres mereda.

Filed under: Tips Tagged: Makananan, stress