MSN Sensory Disturbances

ASSESSING CLIENTS WITH EYE DISORDERS
REVIEW OF ANATOMY AND PHYSIOLOGY
The Eye and Vision
The eyes are complex structures, containing 70% of the sensory receptors of the body.
Each eye is a sphere measuring about 1 in (2.5cm) in diameter, surrounding and
protected by a bony orbit and cushions of fat. The primary functions of the eye are to
encode the patterns of light from the environment through photoreceptors and to carry
the coded information from the eyes to the brain. The brain gives meaning to the coded
information, allowing us to make sense of what we see. Both extraocular and intraocular
structures are considered a part of the eye.
Extraocular Structures
Extraocular or accessory structures of the eye are those portions of the eye outside the
eyeball yet vital to its protection. These structures are the eyebrows, the eyelids, the
eyelashes, the conjuctiva, the lacrimal apparatus, and the extrinsic eye muscles.
The eyebrows are short, coarse hairs located above the eyes over the superior orbital
ridges of the skull. The eye brows shade the eyes and keep perspiration away from
them.
The eyelids are thin, loose folds of skin covering the anterior eye. They protect the eye
from foreign bodies, regulate the entry of light into the eye, and distribute tears by
blinking.
The eyelashes are short hairs that project from the top and bottom borders of the
eyelids. When anything touches the eyelashes, the blinking reflex is initiated to protect
the eyes from foreign objects.
The conjunctiva is a thin, transparent membrane that lines the inner surfaces of the
eyelids and also folds over the anterior surface of the eyeball. The palpebral conjuctiva
lines the upper and lower eyelids, whereas the bulbar conjuctiva loosely covers the
anterior sclera (the white part of the eye). The conjuctiva is a mucous membrane that
lubricates the eyes.
The lacrimal apparatus is composed of the lacrimal gland, the puncta, the lacrimal sac,
and the nasolacrimal duct. Together, these structures secrete, distribute, and drain tears
to cleanse and moisten the eyes surface.
The six extrinsic eye muscles control the movement of the eye, allowing it to follow a
moving object. The muscles also help maintain the shape of the eyeball.
INTRAOCULAR STRUCTURES
The intraocular structures transmit visual images and maintain homeostasis of the inner
eye. Those lying in the anterior portion of each eyeball are the sclera and the cornea
(forming the outermost coat of the eye, call the fibrous tunic), the iris, the pupil, and the
anterior cavity.
The white sclera lines the outside of the eyeball. The functions of the sclera are to
protect and give shape to the eyeball.
The sclera gives way to the cornea over the iris and pupil. The cornea is transparent,
avascular and very sensitive to touch. The cornea forms a window that allows light to
enter the eye and is a part of its light-bending apparatus. When the cornea is touched,
the eyelids blink and tears are secreted.
The iris is a disc of muscles tissue surrounding the pupil and lying between the cornea
and the lens. The iris gives the eye its color and regulates light entry by controlling the
size of the pupil.
The pupil is the dark center of the eye through which light enters. The pupil constricts
when bring light enters the eye and when it is used for near vision; it dilates when light
conditions are dim and when eye is used for far vision. In response to intense light, the
pupil constricts rapidly in the papillary light reflex.
The anterior cavity is made up of the anterior chamber (the space between the cornea
and the iris) and the posterior chamber (the space between the iris and the lens). The
anterior cavity is filled with a clear fluid called the aqueous humor. Aqueous humor is
constantly formed and drained to maintain a relatively constant pressure of from 15-20
mm Hg in the eye. The Canal of Schlemm, a network of channels that circle the eye in
the angle at the junction of the sclera and the cornea, is the drainage system for fluid
moving between the anterior and posterior chambers. Aqueous humor provides nutrients
and oxygen to the cornea and lens.
The intraocular structures that lie in the internal chamber of the eye are the posterior
cavity and vitreous humor, the lens, the ciliary body, the uvea, and the retina.
The posterior cavity lies behind the lens. It is filled with a clear gelatinous substance
called the vitreous humor. Vitreous humor supports the posterior surface of the lens,
maintains the position of the retina, and transmits light.
The lens is a biconvex, avascular, transparent structure located directly behind the pupil.
It can change shape to focus and refract light onto the retina.
The uvea, also called the vascular tunic, is the middle coat of the eyeball. This
pigmented layer has three components: the iris, ciliary body, and choroid. The ciliary
body encircles the lens, and along with the iris, regulates the amount of light reaching
the retina by controlling the shape of the lens. Most of the uvea is made up of the
choroids, which is pigmented and vascular. Blood vessels of the choroids nourish the
other layers of the eyeball. Its pigmented areas absorb light, preventing it from scattering
within the eyeball.
The retina is the innermost lining of the eyeball. It has an outer pigmented layer and an
inner neural layer. The outer layer, next to the choroids, serves as the link between
visual stimuli and the brain. The transparent inner layer is made up of millions of light
receptors in structures called rods and cones. Rods allow for vision in dim light as well
as for peripheral vision. Cones allow for vision in bright light and for the perception of
color. The optic disk, a cream-colored round or oval area within the retina is the point at
which the optic nerve enters the eye. The slight depression in the center of the optic disc
is often called the physiologic cup. Located laterally to the optic disc is the macula, which
is a darker area with no visible blood vessels. The macula contains primarily cones. The
fovea centralis is a slight depression in the center of the macula that contains only cones
and is a main receptor of detailed color vision
THE VISUAL PATHWAY
The optic nerves are cranial nerves formed of the axons of ganglion cells. The two optic
nerves meet at the optic chiasma, which is just anterior to the pituitary gland in the brain.
At the optic chiasma, axons from the medial half of each retina cross to the opposite side
to form pairs of axons from each eye. These pairs continue as the left and right optic
tracts. The crossing of the axons results in each optic tract carrying information from the
lateral half of the retina of the left eye and the medial half of the retina of the right eye,
whereas the right optic tract carries visual information from the lateral half of the retina of
the right eye and the medial half of the retina of the left eye.
The ganglion cell axons in the optic tracts travel to the thalamus and create synapses
with neurons, forming pathways called optic radiation terminate in the visual cortex of the
occipital lobe. Here the nerve impulses that originated in the retina are interpreted.
The visual fields of each eye overlap considerably, and each eye sees a slightly different
view. Because of this overlap and crossing of the axons, information from both eyes
reaches each side of the visual cortex, which then fuses the information into one image.
This fusion of images accounts for the ability to perceive depth; however, depth
perception depends on visual input from two eyes that both focus well.
Refraction
Refraction is the bending of light rays as they pass from one medium to another medium
of different optical density. As light rays pass through the eye, they are refracted at
several points: as they enter the cornea, as they leave the cornea and enter the aqueous
humor, as they enter the lens, and as they leave the lens and enter the vitreous humor.
At the lens, the light is bent so that it converges at a single point on the retina. This
focusing of the image is called accommodation. Because the lens is convex, the image
projected onto the retina (the real image) is upside down and reversed from left to right.
The real image coded as electric signals that are sent to the brain the brain decodes the
image so that the person perceives it as it occurs in space.
The eyes are best adapted to see distant objects. Both eyes fix on the same distant
image and do not require any change in accommodation. For people with emmetropic
(normal) vision, the distance from the viewed object at which the eyes require no
accommodate the lens, constrict the pupils, and converge the eyeballs. Accommodation
is accomplished by contraction of the ciliary muscles. This contraction reduces the
tension on the lens capsule so that it bulges outward to increase the curvature. This
change in shape also achieves a shorter focal length, another requirement for the
focusing of close images on the retina. The closest point on which a person can focus is
called the near point of vision; in young adults with normal vision this is usually 8-10 in.
pupillary constriction helps eliminate most of the divergent light rays and sharpens focus.
Convergence (the medial rotation of the eyeballs so that each is directed toward the
viewed object) allows the focusing of the image on the retinal fovea of each eye.
Assessment of the Eyes
I. Health History
A. Current Health Status

1. Problems
2. Corrective lenses
B. Past Health Status

1. Lens change
2. Blurred vision
3. Spots, floaters, halos
4. Infections or inflammations of the eyes
5. Eye surgery or injury
6. Styes (hordeolums)
7. High blood pressure
8. Diabetes
9. Eye medications
C. Family health status
Equipment Needed
A Snellen Eye Chart or Pocket Vision Card
An Ophthalmoscope
Visual Acuity
In cases of eye pain, injury, or visual loss, always check visual acuity before before
proceeding with the rest of the exem or putting medications in your patients eyes.
1. Allow the patient to use their glasses or contact lens if available. You are
interested in the patient's best corrected vision.
2. Position the patient 20 feet in front of the Snellen eye chart (or hold a
Rosenbaum pocket card at a 14 inch "reading" distance).
3. Have the patient cover one eye at a time with a card.
4. Ask the patient to read progressively smaller letters until they can go no further.
5. Record the smallest line the patient read successfully
6. Repeat with the other eye.
7. Unexpected/unexplained loss of acuity is a sign of serious ocular pathology.
Inspection
1. Observe the patient for ptosis, exophthalmos, lesions, deformities, or asymmetry.

2. Ask the patient to look up and pull down both lower eyelids to inspect the
conjuntiva and sclera.
3. Next spread each eye open with your thumb and index finger. Ask the patient to
look to each side and downward to expose the entire bulbar surface.
4. Note any discoloration, redness, discharge, or lesions. Note any deformity of the
iris or lesion cornea.
5. If you suspect the patient has conjuntivitis, be sure to wash your hands
immediately. Viral conjuntivitis is highly contagious - protect yourself!
Visual Fields
Screen Visual Fields by Confrontation
1. Stand two feet in front of the patient and have them look into your eyes.
2. Hold your hands to the side half way between you and the patient.
3. Wiggle the fingers on one hand.
4. Ask the patient to indicate which side they see your fingers move.
5. Repeat two or three times to test both temporal fields.
6. If an abnormality is suspected, test the four quadrants of each eye while asking
the patient to cover the opposite eye with a card.
Extraocular Muscles
Corneal Reflections
1. Shine a light from directly in front of the patient.

2. The corneal reflections should be centered over the pupils.
3. Asymmetry suggests extraocular muscle pathology.
Extraocular Movement
1. Stand or sit 3 to 6 feet in front of the patient.

2. Ask the patient to follow your finger with their eyes without moving their head.
3. Check gaze in the six cardinal directions using a cross or "H" pattern.
4. Check convergence by moving your finger toward the bridge of the patient's
nose.
Pupillary Reactions
Light
1. Dim the room lights as necessary.

2. Ask the patient to look into the distance.
3. Shine a bright light obliquely into each pupil in turn.
4. Look for both the direct (same eye) and consensual (other eye) reactions.
5. Record pupil size in mm and any asymmetry or irregularity.
Accommodation
If the pupillary reactions to light are diminished or absent, check the reaction to
accommodation (near reaction): [5] ++
1. Hold your finger about 10cm from the patient's nose.

2. Ask them to alternate looking into the distance and at your finger.
3. Observe the pupillary response in each eye.
Ophthalmoscopic Exam
1. Darken the room as much as possible. ++

2. Adjust the ophthalmoscope so that the light is no brighter than necessary.
Adjust the aperture to a plain white circle. Set the diopter dial to zero unless you
have determined a better setting for your eyes.
3. Use your left hand and left eye to examine the patient's left eye. Use your right
hand and right eye to examine the patient's right eye. Place your free hand on
the patient's shoulder for better control.
4. Ask the patient to stare at a point on the wall or corner of the room.
5. Look through the ophthalmoscope and shine the light into the patient's eye from
about two feet away. You should see the retina as a "red reflex." Follow the red
color to move within a few inches of the patient's eye.
6. Adjust the diopter dial to bring the retina into focus. Find a blood vessel and
follow it to the optic disk. Use this as a point of reference.
7. Inspect outward from the optic disk in at least four quadrants and note any
abnormalities.
8. Move nasally from the disk to observe the macula.
9. Repeat for the other eye.
Special Tests
Upper Eyelid Eversion
This procedure is performed when a foreign body is suspected. ++
1. Ask the patient to look down.

2. Gently grasp the patient's upper eyelashes and pull them out and down.
3. Place the shaft of an applicator or tongue blade about 1 cm from the lid margin.
4. Pull the lid upward using the applicator as a fulcrum to turn the lid "inside out."
Do not press down on the eye itself.
5. Pin the eyelid in this position by pressing the lashes against the eyebrow while
you examine the palpebral conjuntiva.
Ask the patient to blink several times to return the lid to normal.
Notes
1. Visual acuity is reported as a pair of numbers (20/20) where the first number is
how far the patient is from the chart and the second number is the distance from
which the "normal" eye can read a line of letters. For example, 20/40 means that
at 20 feet the patient can only read letters a "normal" person can read from twice
that distance.
2. You may, instead of wiggling a finger, raise one or two fingers (unialterally or
bilaterally) and have the patient state how many fingers (total, both sides) they
see. To test for neglect, on some trials wiggle your right and left fingers
simultaneously. The patient should see movement in both hands.
3. Additional Testing - Tests marked with (++) may be skipped unless an
abnormality is suspected.
4. PERRLA is a common abbreviation that stands for "Pupils Equal Round Reactive
to Light and Accommodation." The use of this term is so routine that it is often
used incorrectly. If you did not specifically check the accommodation reaction use
the term PERRLA. Pupils with a diminished response to light but a normal
response to accommodation (Argyll-Robertson Pupils) are a sign of
neurosyphilis.
5. Diopters are used to measure the power of a lens. The ophthalmoscope actually
has a series of small lens of different strengths on a wheel (positive diopters are
labeled in green, negative in red). When you focus on the retina you "dial-in" the
correct number of diopters to compensate for both the patient's and your own
vision. For example, if both you and your patient wear glasses with -2 diopter
correction you should expect to set the dial to -2 with your glasses on or -4 with
your glasses off.
DIAGNOSTIC TESTS FOR THE EYE

A. FLUORESCEIN ANGIOGRAPHY
It is a detailed imaging and recording of ocular circulation by a series of

photographs after administration of a dye.
Preprocedure Interventions
a. Assess client to allergies and previous reactions to dyes.
b. Obtain informed consent
c. A mydriatic medication, which causes pupil dilation, is instilled in the

eye, 1 hour before the test.
d. The dye is injected into a vein of the clients arm.
e. Inform the client that the dye may cause the skin to appear yellow for
several hours after the test and is eliminated gradually through the
urine.
f. The client may experience nausea, vomiting, sneezing, paresthesia of

the tounge or pain at the injection site.
g. If hives appear, orally or intramuscularly administered antihistamines
such as diphenhydramine (Benadryl) are given as prescribed.
Postoperative Interventions
a. Encourage rest.
b. Encourage fluid intake to assist in eliminating the dye from the clients
system.
c. Remind the client that the tallow skin appearance will disappear.
d. Instruct the client that the urine will appear bright green until the dye is
excreted.
e. Instruct the client to avoid direct sunlight for a few hours after the test.
f. Instruct the client that the photophobia will continue until pupil size
returns to normal.
B. COMPUTED TOMOGRAPHY
It is a diagnostic test for the eye wherein there is a beam of x-rays scans the
skull and orbits of the eye. A cross-sectional image is formed by the use of a
computer and a contrast material is not usually administered.
Nursing Interventions
No special client preparation or follow- up care is required.
Instruct the client that he or she will be positioned in a confined

space and will need to keep their heads still during the procedure.
C. SLIT LAMP
A slit lamp allows the examination of the anterior ocular structures under
microscopic magnification. The client leans on a chin rest to stabilize the head
while a narrowed beam of light is aimed so that it illuminates only a narrow
segment of the eye.
Explain the procedure to the client.
Advise the client about the brightness of the light and the need to look
forward at a point over the examiners ear.
D. CORNEAL STAINING
A topical dye is instilled into the conjunctival sac to outline irregularities of the
corneal surface that are not easily visible. The eye is viewed to a blue filter, and a
bright green color indicatesareas of a non intact corneal epithelium.
If the client wears contact lenses, the lenses must be removed.
The client is instructed to blink after the dye has been applied to
distribute the dye evenly across the cornea.
E. TONOMETRY
This test is used primarily to assess for an increase of intraocular pressure

and potential glaucoma. Normal ocular pressure is 10- 21 mmHg.
Each dye is anesthetized.
The client is instructed to stare forward at a point above the

examiners ear.
A flattened cone is brought contact with the cornea.
The amount of pressure needed to flatten the cornea is measured.
The client must instructed to avoid rubbing the eye following the
examination if the eye has been anesthetized because the
potential for scrubbing the cornea exists.
F. FUNDUS PHOTOGRAPHY
Special retinal cameras are use to document fine details of the fundus for
the study and future comparison. One of the most common applications is the
evaluation of insidious optic nerve changes in the clients with glaucoma.
Photographs are compared over time to identify subtle changes in the clients with
glaucoma. Photographs are compared over time to identify subtle changes in
disc shape and color.
G. SPECULAR MIMOGRAPHY
Specular mimography is a photographic technique used to count cells of

the corneal endothelium. A camera is focused on the endothelial layer, and the
area is magnified 200 times; then the cell is counted. This layer of the cornea is
one cell thick . cells in this layer do not reproduce but rather they expand to fill
gaps in the endothelium. The number or lack of number, of cells may indicate
healing potential.
H. EXOPTHALMOMETRY
The exopthalmometer is an instrument designed to measure the forward

protrusion of the eye. This instrument provides a method of evaluating and
recording the progression and regression of the prominence of the eye in
disorders such as thyroid disease and tumors of the orbit.
I. OPTHALMIC RADIOLOGY
X-ray study, tomography, and CT scan are useful n the evaluation of

orbital and intracranial conditions. Common abnormalities evaluated by these
methods include neoplasms, inflammatory masses, fractures and extraocular
muscle enlargement associated with Graves eye disease. Radiology is also
useful in the detection of foreign bodies.
J. MAGNETIC RESONANCE IMAGING
MRI has the advantage of not exposing the patient to ionizing radiation.
Also, multidimensional views are possible without repositioning the patient. This
is used to image edema, areas of demyelination, and vascular lesions. However,
the availability of MRI equipment is often lmited and the examination takes
longer. MRI may also cause movement of a metallic foreign body.
K. ULTRASONOGRAPHY
Ultrasonography uses the principle of sonar to study structures not

directly visible high frequency sound waves are transmitted to a probe placed
directly on the eyeball. As the sound waves bounce back off the various tissue
components, they are collected by a receiver that amplifies them on an
oscilloscope screen. Sound waves derived from the most distal structures arrive
last, having travel the farthest. Ultrasonography may be used to evaluate tissue
characteristics of a lesion as well as size and growth over time. It may also be
used to measure axial length (distance from the cornea to the retina) in order to
calculate the power for an intraocular lens implant in cataract surgery.
L. OPTHALMODYNAMOMETRY
Opthalmodyanamometry is a test that consists of exerting pressure on the

sclera with a string plunger while observing the central retinal vessels emerging
from the disc through an opthalmoscope. This instrument gives an approximate
measurement of the relative pressures in the central retinal arteries and is an
indirect method of assessing the carotid arterial flow on either sound.
M. ELECTRORETINOGRAPHY
An electrical potential exist between the cornea and retina of the eye.
Because the retina is neurologic tissue, the normal retina is exhibit certain
electrical responses when stimulated by light. Electroretinography (ERG)
measures the normal change in electrical potential of the eye caused by a diffuse
flash of light. For this test, electrodes incorporated into a contact lens are placed
directly on the eye. Eye movements disrupt the values of the test, so the client
must be able to fixate on a target while keeping the eyes still. A normal ERG
signifies functional integrity of the retina. Examples of retinal diseases that may
be th evaluated with ERG include retinitis pigmentosa (progressive degeneration
of photoreceptor cells), massive ischemia, disseminated infection, or toxic effects
from drugs or chemicals.
N. VISUAL EVOKED RESPONSE
Visual evoked response (VER) is similar to ERG in that it also measures

the electrical potential resulting from a visual stimulus. The entire visual pathway
from the retina to the cortex maybe evaluated in the examination through the
placement of electrodes on the scalp. Reduces speed of neuronal conduction,
such as with demyelination, results in an abnormal VER. Retina or optic nerve
disease may be diagnosed by stimulating each eye separately.
EYE DISORDERS
Degenerative Disorders
A. GLAUCOMA
Glaucoma includes a group of ocular disorders characterized by increase intraocular

pressure, optic nerve atrophy and visual field loss. The individual response to intraocular
pressure varies. Therefore, some people sustain damage from relatively low pressures
and others sustain no damage from high pressure. The degree of increase pressure that
cause ocular damage is not the same in every eye, and some individuals may tolerate a
pressure for long periods of time that would rapidly blind another.
Incidence
It is estimated that over 50,000 persons in the US are blind as a result of glaucoma.
The incidence of glaucoma is about 1.5%, and in blacks, between the ages of 45 and 65,
prevalence is at least five times that of the whites in the same age group. In most cases,
blindeness can be prevented if treatment is began early.
Glaucoma is called the sneak thief of sight because it strikes without obvious
symptoms. People with glaucoma are usually unaware of it until they have a serious loss
of vision. In fact, about half of those who have glaucoma do not know it. Currently, that
damage cannot be reversed.
While there are usually no warning signs, some symptoms may occur in the later
stages of the disease, such as a loss of peripheral vision, difficulty focusing on close
work, seeing halos around lights, and frequent changes of prescription glasses.
Unfortunately, though, once the vision is lost, it is gone forever.
African Americans are at a higher risk of developing glaucoma than other racial groups.
Others at risk include:
Anyone with a close relative who has glaucoma;

Seniors;
People with diabetes;
People taking steroid medications for extended periods of time.
Pathophysiology
Intraocular pressure is determined by the rate of aqueous production in the

cilliary body and the resistance to outflow aqueous from the eye. Increase intraocular
pressure (usually greater that 23mm Hg) indicates the need for further evaluation.
Intraocular pressure varies with diurnal cycles. (the highest pressure is usually on
awakening) and position of the body (increase when lying down). Normal variation do
not usually exceed 2-3 mm Hg. Intraocular pressure and blood pressure are
independent of each pther but variations in the systemic blood pressure may be
associate with corresponding variations in the intraocular pressures. Increase intraocular
pressure may result from hyper production of aqueous or obstruction of the outflow. As
aqueous fluid builds up in the eye, the increase pressure inhibits blood supply to the
optic nerve and the retina. These delicate tissues become ischemic and gradually loss
function.
Etiology/ Risk Factors
Many terms are used to describe the various types of glaucoma. The terms primary
and secondary refer to whether the etiology is the disease alone or due to another
condition. Acute and chronic refer to the onset and/ duration of the disorder. The terms
open (wide) and closed (narrow) describe the width of the ngle between the cornea and
the iris. Anatomically narrow anterior chamber angles predispose clients to an acute
onset of angle-closure glaucoma.
TYPES OF GLAUCOMA
Primary Open-Angle Glaucoma
Approximately 90% of primary glaucoma cases occur in clients with open angles.
It is a multifunctional disorder that is often genetically determined, bilateral, ininsidious in
onset, and slow to progress. Symptoms appear late when vision is impaired by damage
to the optic nerve. Because there are no early warning symptoms, it is imperative that
regular ophthalmic examinations include tonometry and assessment the optic nerve
head (disc). This type of glaucoma is often referred t as the THIEF IN THE NIGHT
because there are no early symptoms alerting the client that vision is being lost. The
most common cause of chronic open angle glaucoma is degenerative change in the
trabecular meshwork, resulting in the decrease outflow of aqueous humor.
Angle- Closure Glaucoma
An acute attack of angle-closure glaucoma can develop only in an eye in which

the anterior chamber angle is anatomically narrow. The attack occurs due to a sudden
blockage of an anterior angle by the base of the iris. When the aqueous flow is
obstructed, intraocular pressure becomes markedly elevated, causing severe pain and
blurred vision or vision loss. Some client will see rainbow halos around lights, and some
will experience nausea and vomiting.
Low Tension Glaucoma
Low-tension glaucoma resembles primary open-angle glaucoma. The angle is

normal, the optic nerves are cupped and the visual fields show characteristic
glaucomatous effects. (peripheral vision deficits). These changes, however, develop in
the presence statistically normal intraocular pressures. The etiology of low tensions
glaucoma is not known. Although the pressure readings are in the normal range,
treatment is indicated to lower the pressure even further to avoid progressive optic nerve
damage and visual field loss.
Secondary Glaucoma
Increase intraocular pressure may occur as a post operative complication.

Edematous tissue may inhibit the outflow of aqueous through the trabecular meshwork.
Delayed healing of corneal would edges may result in epithelial cell growth into the
anterior chamber.
Glaucoma may occur as a result of trauma. Lens displacement, hemorrhage into
the anterior chamber, laceration, and contusions can dirupt the flow pattern of aqueous
humor.
Clinical Manifestations
Clinical manifestations of glaucoma include:

1. Increase intraocular pressure,
2. Cupping or indentation of the optic nerve head (disc) and
3. Visual field defects
Diagnostic Assessment
An opthalmoscopic examination shows atrophy (pale color) and cupping

(indentation) of the optic nerve head. The visual field examination is used to determine
the extent of peripheral vision loss (see the section on visual fields). In chronic open
angle glaucoma, a small crescent- shape scotoma (blind spot) appears early in the
disease. In acute angle-closure glaucoma, the fields demonstrate larger areas significant
vision loss.
In clients with angle-closure glaucoma, a slit lamp examination may demonstrate an
erythematous conjunctiva and corneal cloudiness. The anterior chamber aqueous may
also appear turbid and the pupil may be non reactive. Slit lamp examination is used in
open angle glaucoma to look for any secondary causes and associate findings.
Intraocular pressure is measured at the slit lamp with the applanation tonometer.
Gonioscopy is performed to determine the depth of the anterior chamber and to examine
the entire circumference of the angle for any abnormal change in the filtering meshwork.
Medical Management
The goal of medical management is to facilitate the outflow of aqueous through

remaining channels. This is achieved through the use of
Topical miotics, which constricts the pupil and increase outflow;
Topical epinephrine, which also increase the outflow;
Topical beta blockers or alpha adrenergics, which suppress the secretion of
aqueous humor; and
Oral carbonic anhydrase inhibitors, which also reduce the production of aqueous
humor.
When mediacal management is no longer effective, surgical intervention may be

indicated.
Surgical Management
When maximum medical therapy has failed to halt the progression of visual field loss
and optic nerve damage, surgical intervention is recommended. There are many
procedures that are use to correct the aqueous outflow; however, there is no operation
that is uniformly successful.
Laser Trabeculocospy
The use of laser to create an opening in the trabecular meshwork is often indicated
before filtration surgery is considered. The laser produces scars in the trabecular
meshwork fibers. The tightened fibers allow increased outflow of aqueous. Intraocular
pressure is reduced through improved outflow in about 80% of cases.
Filtering Procedures
Operative procedures such as trephination, thermal sclerostomy, or scleroctomy

create an outflow channel from the anterior chamber to the subconjunctival space.
These are called filtering procedures. Aqueous is absorbed through the conjunctival
vessels. In about 25% of cases, the opening closes due to scar tissue formation, and
reoperation is necessary.
Ciliodestructive Procedures
When other surgical procedures have failed, cyclocryotherapy (application of

freezing tip) or cyclophotocoagulation may be used to damage the ciliary body and
decrease the production of aqueous.
ASSESSMENT
Progressive loss of peripheral vision followed by loss of central vision

Elevated intraocular pressure (normal pressure is 10- 21 mmHg)
Vision worsening in the evening with difficulty adjusting to dark rooms
Blurred vision
Halos around white lights
Frontal headaches
Eye pain
Photophobia
Lacrimation
Progressive loss of central vision
NURSING INTERVENTIONS
Acute Glaucoma
Administer medications s prescribe to lower intraocular pressure. And prepare
the client for peripheral indectomy, which allows aqueous humor to flow from the
posterior to anterior chamber.
Chronic Glaucoma
Instruct the client on the importance of medications (miotics) to constrict the
pupils, (carbonic anhydrase inhibitors) to decrease production of aqueous humor,
and beta blockers to decrease the production of aqueous humor and intraocular
pressure.
Instruct the client on the need for lifelong medication use and to avoid
anticholinergic medications.
Instruct the client to report eye pain, halos around the eyes, and changes in
vision to the physician.
Teach the client that when maximal medical therapy has failed to halt the
progression of visual field loss and optic nerve damage, surgery will be
recommended.
Prepare the client for trabeculoplasty as prescribed to facilitate aqueous humor
drainage and to allow drainage of aqueous humor into the conjunctival spaces b
the creation of an opening.
B. CATARACT
Definition
A cataract is a cloudy or opaque area (an area you cannot see through) in the
lens of the eye. It is an opacity of the lens that distorts the image projected onto the
retina and that can progress to blindness.
Alternative Names
Lens opacity
Causes, incidence, and risk factors
The lens of the eye is normally clear. If the lens becomes cloudy, the condition is
known as a cataract. Rarely, cataracts may be present at or shortly after birth. These are
called congenital cataracts.
Adult cataracts usually develop with advancing age and may run in families.
Cataracts develop more quickly in the presence of some environmental factors, such as
smoking or exposure to other toxic substances. They may develop at any time after an
eye injury. Metabolic diseases such as diabetes also greatly increase the risk for
cataracts. Certain medications, such as cortisone, can also accelerate cataract
formation.
Congenital cataracts may be inherited. The gene for such cataracts is dominant
(autosomal dominant inheritance), which means that the defective gene will cause the
condition even if only one parent passes it along. I families where one parent carries the
gene, there is a 50% chance in every pregnancy that the child will be affected.
Congenital cataracts can also be caused by infections affecting the mother during
pregnancy, such as rubella. They are also associated with metabolic disorders such as
galactosemia. Risk factors include inherited metabolic diseases, a family history of
cataracts, and maternal viral infection during pregnancy.
Adult cataracts are generally associated with aging. They develop slowly and
painlessly, and vision in the affected eye or eyes slowly gets worse.
Visual problems may include the following changes:
Difficulty seeing at night

Seeing halos around lights
Being sensitive to glare
Vision problems associated with cataracts generally move towards decreased vision,
even in daylight.
Adult cataracts are classified as immature, mature, and hypermature. A lens that
has some remaining clear areas is referred to as an immature cataract. A mature
cataract is completely opaque. A hypermature cataract has a liquefied surface that leaks
through the capsule, and may cause swelling and irritation of other structures in the eye.
Most people develop some clouding of the lens after the age of 60. About 50% of
people aged 65-74, and about 70% of those 75 and older, have cataracts that affect their
vision.
Most people with cataracts have similar changes in both eyes, although one eye
may be worse than the other. Many people with this condition have only slight visual
changes, and are not aware of their cataracts.
Factors that may contribute to cataract development are low serum calcium
levels, diabetes, long-term use of corticosteroids, and various inflammatory and
metabolic disorders. Environmental causes include trauma, radiation exposure, and too
much exposure to ultraviolet light (sunlight).
Symptoms
Cloudy, fuzzy, foggy, or filmy vision
Loss of color intensity
Frequent changes in eyeglass prescription
The glare from bright lights causes vision problems at night, especially
while driving
Sensitivity to glare from lamps or the sun
Halos around lights
Double vision in one eye
Decreased contrast sensitivity (the ability to see shades, or shapes
against a background)
Signs and tests
Standard ophthalmic exam, including slit lamp examination
Ultrasonography of the eye in preparation for cataract surgery
Other tests that may be done (rarely) include:
Glare test
Contrast sensitivity test
Potential vision test
Specular microscopy of the cornea in preparation for cataract surgery
Treatment
The only treatment for cataract is surgery to remove it. This is done when a person
cannot perform normal activities, even with glasses. For some people, changing glasses,
getting stronger bifocals, or using a magnifying lens is helpful enough. Others choose to
have cataract surgery.
If a cataract is not bothersome, then surgery is usually not necessary. Sometimes

there is an additional eye problem that cannot be treated without first having cataract
surgery.
Cataract surgery consists of removing the lens of the eye and replacing it with an
artificial lens. A cataract surgeon will discuss the options with the patient, and together
they will decide which type of removal and lens replacement is best.
LENS REMOVAL:
There are 2 types of surgery that can be used to remove lenses that have a cataract.
Extracapsular surgery consists of surgically removing the lens, but leaving the
back half of the capsule (the outer covering of the lens) whole. High-frequency sound
waves (phacoemulsification) may be used to soften the lens to help removing it through
a smaller cut. With extracapsular extraction, the lens is lifted out without removing the
lens capsule; the procedure may be performed by phacoemulsification in which the lens
is broken up by ultrasonic vibrations and is extracted.
Intracapsular surgery involves surgically removing the entire lens, including the
capsule. Today this procedure is done very rarely. In this procedure, lens is removed
within capsule through a small incision.
LENS REPLACEMENT:
People who have cataract surgery are usually fitted with an artificial lens at the same
time. The artificial lens is a synthetic (manufactured) disc called an intraocular lens. It is
usually placed in the lens capsule inside the eye.
Other options include contact lenses and cataract glasses.
Surgery can be done in an outpatient center or hospital. Most people do not need to stay
overnight in a hospital. The patient will need a friend or family member to assist with
travel and home care after outpatient surgery. Follow-up care by the surgeon is
important.
NURSING INTERVENTIONS
Preoperative Interventions
Instruct the client regarding the postoperative measures to prevent or decrease

intraocular pressure.
Administer eye medications preoperatively, including mydriatics and cycloplegics
as prescribed.
Elevate the head of the bed 30- 45 degrees.

Turn the client to the back or unoperative side
Maintain an eye patch; orient the client to the environment
Position the clients personal belongings to the unoperative side
Use side rails for safety
Assist with ambulation
AGE RELATED MACULAR DEGENERATION
Previously known as the senile macular degeneration, age related macular

degeneration is an atrophic degenerative process that affects the macula and
surrounding tissues, resulting in central visual deficits.
Age related macular degeneration can be found in some degree to some adults
over the age of 65. It is one of the most common causes of visual loss in the elderly. The
exact etiology is unknown, but the incidence increases with each decade over 50. It may
also be hereditary.
Age- related macular degeneration falls into two categories:
1. Nonexudative
2. Exudative
Both are usually bilateral and progressive.

Also referred to as dry macular degeneration, nonexudative age related
macular degeneration is characterized by atrophy and degeneration of the outer retina
and underlying structures. Yellowish round spots called drusen may be seen in the retina
and macula with an opthalmoscope. Drusen are deposits of amorphous material from
the pigment epithelial cells of the retina. Overtime, these spots increase, enlarge and
may calcify.
At this, wet, exudative stage of age-related macular degeneration, Bruchs
membrane, which lies just beneath the pigment epithelial cell layer of the retina,
becomes compromised and this results in serous fluid leaks from the colloid with
accompanying proliferation of choroidal blood vessels.
A dome-shaped retinal pigment epithelium may be seen when examining the
fundus. These leak produce a visual effect called tamorphopsia, which is the blurred,
wavy distortion vision. The client may also notice blurred scotomo or decrease central
visual acuity. Fundus photograpghy and angiography may be performed on a regular
basis of documents and evaluate changes.
Management
There is no known means of medical treatment or prevention for age elated macular
degeneration. Further damage from exudative macular degeneration sometimes may be
arrested by the use of argon photocoagulation, even though laser bamage to the retina
in this area results in a blind spot. When the fovea is involved, central vision is lost and
he only helpful measures are low-vision aids.
The client with age-related macular degeneration is threatened with the loss of
central vision. In order to evaluate change in vision, the client is taught to use an Amsler
grid at home. The nurse may be able to assist the client to maximize remaining vision
with low vision aids and community referral to a low vision specialist and low vision
support groups.
C. RETINAL DETACHMENT
Retinal detachment occurs when the layers of the retina separate because of the
accumulation of fluid between them, or when both retinal layers elevate away from the
choroid as a result of a tumor. Partial separation becomes complete if untreated. When
detachment becomes complete, blindness occurs.
Assessment
Flashes of lights
Floaters
Increase in blurred vision
Sense of curtain being drawn
Loss of a portion of the visual field
Immediate Interventions
Provide bed rest
Cover both eyes with patches to prevent further detachment
Speak to the client before approaching
Position the client head as prescribed
Protect the client from injury
Avoid jerky head movements
Minimize eye stress
Prepare the client for the surgical procedure as prescribed.
Surgical Procedures
Draining fluid from the subretinal space so that the retina can return to the normal
position.
Sealing retinal breaks by cryosurgery, a cold probe applied to the sclera, to
stimulate an inflammatory response leading to adhesions.
Diathermy, the use of an electrode needle and heat through the sclera, to
stimulate an inflammatory response.
Laser therapy to stimulate an inflammatory response, to seal small retinal tears
before the detachment occurs.
Sclera buckling, to hold the choroid and retina together with a splint until scar
tissue forms closing the tear.
Insertion of gas or silicon oil to encourage attachment because these agents
have a specific gravity less than vitreous or air and can float against the retina.
Maintain eye patches bilaterally as prescribed.

Monitor for hemorrhage.
Prevent nausea and vomiting and monitor for restlessness, which can cause
hemorrhage.
Monitor for sudden sharp eye pain and monitor the physician.
Encourage deep breathing exercise but avoid coughing.
Provide bed rest for 1-2 days and position the client as prescribed.
If gas has been inserted, position the client as prescribed on the abdomen
and turn the head so unaffected eye is down.
Administer eye medications as prescribed.
Assist the client with activities of daily living.
Avoid sudden head movements or anything that increases intraocular
pressure.
Instruct the client to limit reading for 3-5 weeks.
Instruct the client to avoid squinting, straining and constipation, lifting heavy
objects and bending from the waist.
Instruct the client to wear dark glasses during the day and an eye patch at
night.
Encourage follow-up care because of the danger of recurrence in the other
eye.
REFRACTIVE DISORDERS
Light is bent (refracted) as it passes through the cornea and lens of the eye.
Refractive errors exist when light rays are not focused appropriately on the retina
of the eye. Three basic abnormalities of refraction occur in the eye: 1) myopia 2)
hyperopia, and 3) astigmatism. Optical correction is important to distinguish
between visual loss caused by disease and visual loss caused by refractive error.
Refractometry is the measurement of refractive error and should not be confused
with refraction, the method used to determine which lens or lenses (if any) will
most benefit the client.
a. Myopia
Myopia, or nearsightedness, is a condition in which the light rays come
into focus in front of the retina. In this case the refractive power of the eye
is too strong and a concave, or minus, lens is used to focus light rays on
the ey. In most cases myopia is caused by an eyeball that is longer than
normal, which may be a familial triat. Transient myopia may occur with the
administration of a variety of medications (sulfonamides, acetozolamide,
salicylates, and steroids) and has been associated with other disorders,
such as influenza, typhoid fever, severe dehydration, and large intakes of
antacids. Correction is accomplished with eyeglasses or contact lenses.
b. Hyperopia
The hyperopic, or farsighted, eye focuses light rays behind the eye, and
consequently the image that falls on the retina is blurred. Vision may be
brought into focus by placing a convex, or plus, lens in front of the eye.
The lens supplies the magnifying power that the eye is lacking. Hyperopia
may be caused by an eyeball that is shorter than normal or a cornea that
has less curvature than normal. Because children have a greater ability to
accommodate, they are less often affected than adults. Demands for
close work and reading usually bring on manifestations of headache or
eye strain. Correction is based on a persons age and individual needs
and complaints.
c. Astigmatism
Astigmatism is a refractive condition in which rays of light are not bent
equally by the cornea in all direction so that a point of focus is not
attained. In most instances, astigmatism is caused because the curvature
of the cornea is not perfectly spherical. This is the cause of poor vision for
both distant and near objects. Astigmatism is corrected with cylindrical
lenses.
Surgical management
The following are the three main types of refractive surgery and new procedure.
Laser in situ keratomileusis (LASIK) is currently the most commonly used corrective
surgery for nearsightedness in the United States. An extremely thin layer of the cornea is
peeled back for the laser reshaping on the middle layer of the cornea and then put back
in place. There is little postoperative discomfort, rapid recovery of clear vision, and quick
stabilization of refractive change. LASIK is performed in a surgeons office or samed-
day surgery center and does not require a hospital stay. It takes about 10-15 minutes per
eye. It has a high success rate and low complication rate for low to moderate
nearsightedness and may also be used to correct more severe nearsightedness.
Excimer laser photorefractive keratectomy (PRK) uses short-wavelenght, high-energy

ultraviolet radiation laser to reshape the corneal surface. In PRK for myopia, the central
cornea is flattened with the excimer laser. The same laser may be used to reshape the
cornea by making the central curvature steeper to correct hyperopia. It may be used to
correct nearsightedness and astigmatism at the same time. PRK is performed on an
outpatient basis in a surgeons office or same-day surgery center. The PRK procedure
takes about 30 minutes, most of which is spent teaching the client to hold the eye still.
The actual treatment takes less than a minute. Recovery from PRK is longer and more
painful than recovery from ether radial keratotomy (RK) or LASIK. Vision will be reduced
for several days after surgery.
Radial keratotomy (RK) involves making tiny cuts in the cornea, which flatten it and
reduce nearsightedness. In people who have both astigmatism and nearsightedness, the
surgeon may make additional cutrs to flatten the misshapen part of the cornea that is
causing the astigmatism. RK is an outpatient procedure. It is done under local or topical
anesthesia in a surgeons office or same day surgery center.
Corneal ring implants are clear pieces of acrytic that can be surgically implanted into
the cornea. The implants are shaped like crescents or half circles. Two implants are
used for each eye, and the implants are inserted along the sides of the cornea.
Nursing management of the surgical client

Clients are assessed preoperatively for degree of myopia or astigmatism. Clients with a
severe case usually cannot achieve full correction. Surgery is performed on an out
patient basis with local anesthesia. Eye protection is used, such as goggles to prevent
dry eyes. Vigorous activities, activities that cold get water in the eye, and eye makeup
are to be avoided. The eye is treated with steroid eyed drops, and most clients report
watering of the eyes and minimal pain. Refraction slowly stabilizes after surgery. There is
a period of adjustment during which visual acuity waxes and wanes. Reduced contrast
sensitivity in night vision and daytime glare is common. Some clients require re
treatment for scarring that is unresponsive to topical steroids.
Infectious and Inflammatory Conditions
Inflammation and infection of eye structures are common. Eye infection is a leading
cause of blindness worldwide.
Dry eye syndrome

Dry eye syndrome, or keratoconjuctivitis sicca, is a deficiency in the production of any of
the aquaeous, mucin, or lipid tear film components; lid surface abnormalities; or
epithelial abnormalities related to systemic diseases (eg, thyroid disorders, Parkinsons
disease), infection, injury, or complications of medications (eg. Antihistamines, oral
contraceptives, phenothiazines)
Clinical manifestations
The most common complaint in dry eye syndrome is a scratchy or foreign body
sensation. Other symptoms include itching, excessive mucus secretions, inability to
produce tears, a burning sensation, redness, pain, and difficulty moving the lids.
Assessment and diagnostic findings

Slit-lamp examination shows an absent or interrupted tear meniscus at the lower lid
margin, and the conjuctiva is thickened, edematous, and hyperemic and has lost its
luster. A tear meniscus is the crescent-shaped edge of the tear film in the lower lid
margin. Chronic dry eyes may result in chronic conjuctival and corneal irritation that can
lead to corneal erosion, scarring, ulceration, thinning, or perforation that can seriously
threaten vision. Secondary bacterial infection can occur.
Management
Management of dry eye syndrome requires the complete cooperation of the patient with
a regimen that needs to be followed at home for a long period; otherwise, complete relief
of symptoms is unlikely. Instillation of artificial tears during the day and an ointment at
night is the usual regimen to hydrate and lubricate the eye and preserve a moist ocular
surface. Anti-inflammatory medications are also used, and moisture chambers (eg,
moisture chamber spectacles, swim goggles) may provide additional relief.
Patients may become hypersensitive to chemical preservatives such as benzalkonium

chloride and themerosal. For these patients, preservative-free ophthalmic solutions are
used. Management of the dry eye syndrome also includes the concurrent treatment of
infections such as chronic blepharitis and acne rasacea, and treating the underlying
systemic disease.
Conjunctivitis
Conjunctivitis (inflammation of the conjuctiva) is the most common ocular disease
worldwide. It is characterized by a pink appearance (hence the common term pink eye)
because of subconjuctival blood vessel congestion.
Clinical manifestations
General symptoms include foreign body sensation, scratching or burning sensation,
itching, and photophobia. Conjunctivitis may be unilateral or bilateral, but the infection
usually starts in one eye and then spreads to the other eye by hand contact.
Assessment and Diagnostic Findings

The four main clinical features important to evaluate are the type of discharge (watery,
mucoid, purulent, or mucopurulent), type of conjuctival reaction (follicular or papillary),
presence of pseudomembranes or true membranes, and presence or absence of
lymphadenopathy (enlargement of the preauricular and submandibular lymph nodes
where the eyelids drain). Pseudomembranes consist of coagulated exudates that
adheres to the surface to the superficial layer of the ocnjuctiva, and moval results in
bleeding. Follicles are multiple, slightly elevated lesions encircled by tiny blood vessels;
they look like grains of rice. Papillae are hyperplastic conjuctival epithelium in numerous
projections that are usually seen as a fine mosaic pattern under slit-lamp examination.
Diagnosis is based on the distinctive characteristics of ocular signs, acute or chronic
presentation, and identification of any precipitating events. Positive results of swab
smear preparations and cutures confirm the diagnosis
Types of conjunctivitis:
1. Microbial conjunctivitis
Bacterial conjunctivitis can be acute or chronic. The acute type can develop into a
chronic condition. Signs and symptoms can vary from mild to severe. Chronic bacterial
conjunctivitis is usually seen in patients with lacrimal duct obstruction, chronic
dacryocystitis, and chronic blepharitis. The most common causative microorganisms are
streptococcus pneumoniae, haemophilus influenzae, and staphylococcus aureaus. It is
manifested with an acute onset of redness, burning, and discharge.
2. Viral conjunctivitis
Viral conjunctivitis can be acute and chronic. The discharge is watery, and follicles are
prominent. Severe cases include psudomemebranes. The common causative organisms
are adenovirus and herpes simplex virus. Conjunctivitis caused by adenovirus is highly
contagious. The condition isusually preceded by symptoms of upper respiratory
infection. Corneal involvement causes extreme photophobia. Symptoms include extreme
tearing, redness, and foreign body sensation that can involve one or both eyes. There is
lid edema, ptosis, and conjuctiva hyperemia (dilation of the conjuctival blood vessels).
These signs and symptoms vary from mild to sever and may last for 2 weeks.
3. Allergic conjunctivitis
Immunologic or allergic conjunctivitis is a hypersensitivity reaction that occurs as part of
allergic rhinitis (hay fever), or it can be an independent allergic reaction. The patient
usually has a history of an allergy to pollens and other environmental allergens. There is
extreme pruritus, epiphora (excessive secretion of tears), injection, and usually severe
photophobia.
4. Toxic conjunctivitis
Chemical conjunctivitis can be the result of medications; chlorine from swimming pools;
exposure to toxic fumes among industrial workers; or exposure to other irritants such as
smoke, hair sprays, acids, and alkalis.
Management
The management of conjunctivitis depends on the type. Most types of mild and viral
conjuctivits are self-limiting, benign conditions that may not require treatment and
laboratory procedures. For more severe cases, topical antibiotic therapy, eye drops, or
ointments are prescribed. Patients with gonococcal conjunctivitis require urgent antibiotic
therapy. If left untreated, this ocular disease can lead to corneal perforation and
blindness. The systemic complications can include meningitis and generalized
septicemia.
UVIEITIS
Inflammation of the uveal tract (uveitis) can affect the iris, the ciliary body, or the
choroids. There are two types of uveitis: nongranulomatous and granulomatous.
The more common type of uveitis is the nongranulomatous type, which manifests as an
acute condition with pain, photophobia, and a pattern of conjuctival injection, especially
around the cornea. The pupil is small or irregular, and vision is blurred. There may be
small, fine precipitates on the posterior corneal surface and cells in the aqueous humor.
If the uveitis is severe, a hypopyon (accutmulation of pus in the anterior chamber) may
occur. The condition may be unilateral or bilateral and may be recurrent.
Management
Because photophobia is a common symptom, patients should wear dark glasses
outdoors. Ciliary spasm and synechia are best avoided through mydriasis;
cyclopentolate and atropine are commonly used. Local corticosteroid drops such as
Pred Forte 1% and Flarex 0.1%, instilled four to six times a day are also used to
decrease inflammation. In very severe cases, systemic corticosteroids as well as
intravitreal corticosteroids, may be used.
DISORDER OF THE AUDITORY SYSTEM
Ear disease causes significant discomfort and hearing loss. It also creates work
loss and decreased productivity-- this increases as the persons communicative skills
decrease when associated hearing loss increases. In children, developmental delays
and academic failure my result due to manifestation of auditory problem if not properly
treated. Ear Complications such as deafness, meningitis, brain abscesses, and facial
nerve paralysis may also occur. Proper management of ear disease is critical and
immediate attention is necessary.
COMMON DISEASES AND DISORDER OF THE MIDDLE EAR
Otitis Media (Middle Ear Infections)
The basic underlying problem causing most forms of otitis is eustachian tube
dysfunction. Most otitis occurs in patients whose eustachian tube, the tube between the
nose and the middle ear the area behind the eardrum, does not work properly. When air
cannot adequately get through this tube to the middle ear, the negative pressure created
can "suck" fluid out of the lining of the middle ear/mastoid, filling the middle ear and
mastoid air cells with fluid. A mild hearing loss usually accompanies the fluid. The
hearing loss disappears when the fluid is gone as long as there are no other causes for
the hearing loss. Three kinds of otitis can result from eustachian tube dysfunction. They
are serous and secretory otitis, where fluid fills the middle ear and mastoid, acute otitis,
where pus fills the middle ear and mastoid but its presence is of short duration, and
chronic otitis, where pus fills the middle ear and mastoid and it has been present for
months or years. Chronic otitis is associated with infection of the bone itself and
thickening and polyp formation of the mucosal lining of the middle ear and mastoid. The
highest incidence of otitis media occurs in preschool children and decreases gradually
after age 6. The highest incidence occurs poor children, children in day care, and Native
Americans. Additional factors that cause or aggravate otitis include the presence of
enlarged adenoid tissue, lack of proper muscle in the back of the throat (as in those with
a cleft palate), allergy, immune deficiencies, sudden change in atmospheric pressure
(like poor pressurization in an airplane dropping from a high altitude), scarring or tumors
in the nasopharynx, and abnormal cell function of the mucosa of the ear and nose.
Diabetes does not increase the incidence of otitis, but can make it much more difficult to
treat.
Types of Otitis Media
Serous otitis- where fairly clear fluid fills the middle ear and mastoid occurs with
fairly sudden obstruction of the eustachian tube. A sudden descent of an airplane
with poor pressurization or a bad cold are two of the most common causes of
acute serous otitis media. Usually decongestants will clear the fluid or even
bloods that can be sucked from the mucosa into the middle ear with wither of
these processes. If the fluid does not clear within a few weeks, it is considered
chronic serous otitis. Older people with poorly functioning eustachian tubes
commonly have recurrent serous otitis and may require intermittent tube
placement over many years. Hearing loss is present depending on the amount of
fluid in the ear. The hearing loss usually resolves when the fluid is cleared out of
the ear, either medically or surgically.
Secretory otitis- where somewhat thicker fluid fills the middle ear and mastoid is
common in small children and is often "outgrown" by the time they reach their
teens. It is the most common disease process requiring the placement of PE
tubes. This thicker fluid has components that are actually "secreted" by the
mucous glands of the middle ear. There are actually tissue breakdown enzymes
in this fluid; that, if left untreated, can gradually eat away bone and cause chronic
hearing loss/damage. Luckily, it generally takes quite a while for these enzymes
to cause damage to the ear, so treating secretory otitis in children with
medication for a few weeks or months is safe. Leaving this kind of fluid in an ear
for more than several months, however, places the ear tissues (including the tiny
ear bones) at risk of damage or destruction by these enzymes. Not treating
infections with antibiotics at all places the ear structure at even higher risk of
permanent damage/destruction by the fluid.
Acute otitis- occurs when pus fills the middle ear. It is usually sudden in onset
and is often associated with sudden obstruction of the eustachian tube at the
same time infections bacteria are present to cause the acute otitis. Without
antibiotic treatment, a true bacterial acute otitis is often associated with sudden
perforation of the eardrum, with profuse drainage from the ear. Often the eardrum
will spontaneously heal over after the infection has resolved, but a perforation
can be left and damage to the middle ear and/or the inner ear can accompany
the infection. The eardrum may be bright red or the creamy color of the fluid can
sometimes be seen through the eardrum. It sometimes looks "soggy." Pain and
fever may accompany an ear infection, but usually disappear rapidly if the
eardrum perforates. Pain and fever are rarely present if there is a whole
(perforation) in the eardrum before the infection starts. The standard treatment of
acute otitis media is oral antibiotics. Ear drops are added if the eardrum
perforates. IV antibiotics are indicated for severe infections, if the mastoid bone is
also infected, or if the facial nerve becomes paralyzed as a "complication" of the
acute infections. Hearing loss is present but usually goes away when the
infection clears.
Chronic otitis-occurs when chronic infection fills the middle ear space and
mastoid cavity. True chronic otitis media is almost always a form of chronic
mastoiditis, where the bone of the mastoid cavity (the honeycombed bone behind
the ear) is chronically infected along with the tissues of the middle ear space. It is
important to realize that antibiotics alone usually cannot remove infection from
the bone; surgical removal of the infected bone is usually necessary to
accomplish this. Even IV antibiotics do not often eradicate a true bone infection,
especially in the mastoid, which has its connection to the bacteria-filled nose
through the eustachian tube. A cholesteatoma is a common additional finding
along with chronic otitis and mastoiditis. A cholesteatoma is a skin sac that grows
back into the middle ear or mastoid from the eardrum, creating a mass of skin
and debris that keeps getting larger and larger over time, destroying anything in
its path. The ear bones, the inner ear, the facial nerve (the nerve that makes all
the muscles of one side of your face work), and the brain next to the ear can all
be damaged or destroyed by either spreading infection or cholesteatoma. These
diseases must be removed fore the safety of the ear, the head, and the brain.
Infection or cholesteatoma involving the inner ear, facial nerve, or the brain
requires immediate attention by an ear surgeon and often required immediate
surgery.
Symptoms of Middle Ear Infection
Earache
Headache
Fever
Discharge from the ear
Mild deafness
Difficulties in sleeping
Loss of appetite.
The causes of middle ear infection:
A progressive head cold

A viral sinus infection that spreads
An otitis externa infection left too long that spreads to the inner ear
Blowing the nose too hard, forcing sinal or eustachian material into the middle
ear.
An opportunistic infection entering through a perforated eardrum
Treatments for Otitis Media
Mild bacterial infections often clear up by themselves in a matter of days. Over-

the-counter painkillers can help alleviate the pain. Warm olive oil dripped in the ear can
also soothe the pain as long as there is no ruptured eardrum. Repeat every few hours.
In more severe cases, antibiotics might be needed which usually includes an

initial antibiotic shot, antibiotic pills and ear drops.
In many cases of middle ear infection, the Eustachian tube is blocked and can
cause or at least contributes to a middle ear infection. A Eustachian tube can become
blocked from any combination of the following:
The body's inflammation reaction to an infection, swelling the Eustachian

tube to where it closes completely.
A contributing factor can be the discharge of the dead bacteria and dead
lymphocytes from the middle ear. The lymphatic system contains the white
blood cells or lymphocytes which are the body's defense against foreign
objects such as bacteria. When the white blood cells kill bacteria, the
lymphatic fluid becomes pus-like due to a build up of dead white blood cells
and dead bacteria. This discharge from the middle ear can irritate the
Eustachian tube causing it to close.
A blocked Eustachian tube is often what causes the pain of a middle ear
infection. Pus builds up in the inner ear cavity with no where to go, putting pressure on
the inner ear and the ear drum. If left without treatment, the pressure can be so great
that it bursts the ear drum. The initial excruciating pain of a burst eardrum is immediately
compensated for by pain reduction from the release of pressure. Whereas, prior to the
burst eardrum, sleep was impossible, the pain relief from the pressure reduction allows
the sufferer to finally sleep. If the middle ear infection is cured on its own, the ruptured
ear drum will also usually heal on its own, although sometimes surgery (tympanoplasty)
is indicated if the rupture is extremely large.
Chronic Suppurative Otitis Media (CSOM)
CSOM is the name given to a condition when there is an infection of the middle ear
which fails to heal and is draining all the time.
Glue Ear
There is a natural flow of fluids from the middle ear (the fluids keep the middle
ear cavity moist) that migrate through the Eustachian tube to the back of the throat. A
blocked Eustachian tube prevents air from reaching the middle ear. When this happens
the middle ear can fill up with the fluid that can becomes thick, like glue over time. This
problem is called glue ear or otitis media with effusion. The buildup of fluid in the middle
ear reduces the movement of the eardrum and ossicles, and hearing is reduced. This
condition is quite prevalent in children. Glue Ear is not a disorder in itself, it is just a
visible symptom of a discharge of bacterial waste from the middle ear.
Note: Glue ear is sometimes confused by anxious parents with the normal
discharge of wax from a child's ear canal. During an infant or child's growth, there may
be periods when ear wax is produced more copiously than normal, causing wax to leak
from the ear.
How to tell the difference:
If the child has not had a fever then it is a normal wax discharge
If the child has not complained of earache then it is a normal wax discharge
If the discharge does not have a really smelly odor then it is a normal wax discharge
(there is a slight odor to normal wax, but nothing like that from waste bacteria from the
middle ear)
Predisposition factors for Otitis Media and Glue Ear
There are factors that can increase the risk of a child being susceptible to otitis media
and glue ear:
being a male
short length of breastfeeding
attendance at day care centers
parental smoking
wet climate
winter season
upper respiratory infection
housing with mold
allergies
Symptoms of Glue Ear
A thick liquid discharge from the ear that looks like liquid wax and is orange in
color.
Ear aches
Headaches
Fever
Listlessness
They may be clumsy. With very small infants (1-3 years old), it might also take
them longer to start to walk, speak or understand language.
Older children may be able to tell you if they cannot hear very well. Or you may
notice that they say 'pardon' or 'what' a lot or that they turn the television up loud.
Glue ear also makes older children clumsy and dizzy.
Treatment for Glue Ear
1. Many children recover naturally from glue ear once the Eustachian tube opens.
Doctors usually adopt a wait-and-see approach to begin with. Your child will normally
be observed for about three months to see if they need further treatment. If the
eardrum has burst, it should heal over time approximately 3-6 weeks.
2. Self medication can be performed by means of an OTC pediatric oral

decongestant to thin the fluid in the ear and help it drain away. The main purpose of
a decongestant is to dry the nasal passages so the Eustachian tube opens and the
fluid drains into the throat. If that does not work you might want to try a small dose of
an antihistamine such as Benadryl. Have your pharmacist recommend a child's
dosage. If that treatment still doesn't work, see your family doctor or physician. They
might prescribe stronger antihistamines or nasal steroids in the form of drops or
sprays - both of which will help reduce the swelling of the Eustachian tube.
3. The second treatment is if there is a suspected infection. If the eardrum has burst,
this is usually the case. Antibiotics are sometimes prescribed, often initially by
injection, then a regimen orally three times a day for at least 7 days. In the past,
antibiotics such as penicillin, erythrosine, or erythromycin were prescribed. However,
in the last few decades, many in the general population have become immune to the
effects of these antibiotics, and stronger ones are often prescribed. (The cause of
immunity is often blamed on antibiotics fed to the food supply (chickens and beef)
before they are brought to market).
Surgical Treatments for Glue Ear
Grommets-myringotomy
If your child has had glue ear over a few months and the eardrum has not
burst and antibiotics have not worked, the other option is to have a small
ventilation drain known as a grommet inserted into the ear drum. The
grommet is made of either stainless steel or plastic. This procedure
involves making a small hole in the eardrum and inserting the grommet
through the hole to keep it open. Initially fluid is sucked out of the middle
ear through this hole, then over a few months, the grommet lets air into
the middle ear space and lets fluid in the middle ear drain away. There
are only simple precautions to stop water getting into ear like swimming
on the surface of the water only and not dive and you need to use
earplugs or cotton wool with Vaseline to stop soap water getting into the
ears when showering or washing hair.
Plastic grommet to drain middle ear fluids

Adenoidectomy
It is a surgical treatment for glue ear which aimed to remove the adenoids. The
adenoids are located above the tonsils, at the back of the throat and are thought
to assist the body in its defense against incoming bacteria and viruses by helping
the body to form antibodies. With ear infections, the adenoids often swell, usually
due to an infection in the immediate area, in this case, the middle ear.
Tubo-Tympanic Otitis Media
The tubo-tympanic form usually involves a perforation of the central part of

the eardrum. This can be caused by infection, injury or surgery.
Symptoms of tympanic otitis media (triad)
Hearing loss
Discharge (which may come and go, and will become noticeable
particularly if you get a cold or the ear gets wet)
Tinnitus.
Treatment of tympanic otitis media
If the opening is not too large, it may close and heal on its own. Failing
that, an ENT specialist may close it with surgery or by covering it with a special
material to keep the opening closed while it heals.
You can usually help the symptoms by taking simple steps like wearing an
ear plug or keeping the ear dry when you are having a bath or swimming.
However, you may need an operation to repair the hole in the eardrum
(tympanoplasty or myringoplasty).
Attico-antral
The attico-antral form of CSOM might also involve a hole in the

eardrum usually in the upper part. This form of CSOM can be more of a
problem than the tubo-tympanic form because the eardrum sheds dead skin
which can build up and enter the middle ear. There are two major
complications of the attico-antral variant of CSOM - Cholesteatomas and
Mastoid infections (Mastoiditis).
Burst Eardrum
(Perforation of eardrum, Rupture of the tympanic membrane)
In the final stages of a middle ear infection, if the pressure becomes

too much, the eardrum may burst. This is actually a positive event if
controlled properly. The burst eardrum will immediately relieve the pressure in
the middle ear and the accompanying earache will diminish. A smelly
discharge (bacteria detritius from the middle ear) will spill out of the ear and
can be sopped up with a wet rag or a tissue.
Causes of a burst eardrum
External Causes of a Burst Eardrum - An external cause for a burst

eardrum is a head trauma such as a blow to the ear or an object
penetrating the ear canal and penetrating the eardrum. Usually, the larger
the perforation, the greater the loss of hearing. The location of the
perforation in the eardrum also affects the degree of hearing loss. If
severe trauma (skull fracture) disrupts the bones in the middle ear which
transmit sound or causes injury to the inner ear structures, the loss of
hearing maybe quite severe. With a traumatic or explosive event, the loss
of hearing can be great and tinnitus may be severe. Side effects of a
perforated eardrum will definitely be excruciating pain. You will probably
also suffer from vertigo and tinnitus
Internal Causes of a Burst Eardrum- Perforated eardrums from internal
causes are usually from middle ear infections or otitis Media. Detritus
from the infection in the inner ear causes pressure to build in the middle
ear cavity and if not relieved, the eardrum will burst outward.
Symptoms of a burst eardrum from internal causes
Sharp pain as the eardrum bursts, then initial pain relief.

Pus discharge from the ear, and usually very smelly
Bleeding from the ear
Hearing loss
Tinnitus
Vertigo
Throbbing pain as the middle and inner ear is subject to direct contact with the air
Treatments for a Burst Eardrum
If you have had a middle ear infection that pushed out the eardrum, then
the throbbing pain has been greatly diminished. Wipe off the smelly pus
with a damp cloth, and sit quietly with a warm compress on that side of
the head.
Antibiotics are usually prescribed, sometimes initially by injection, then a
regimen orally three times a day for at least 7 days.
If the perforation is very small and it does not heal after 2-3 weeks, an
ENT may decide not to operate and allow nature to take its course and let
the eardrum heal naturally.
For a larger tear, an outpatient visit to the ENT will allow a small patch
(taken from under the skin behind the ear perhaps) to be attached (not
completely covering the hole) over the hole to help it shrink and
encourage new skin growth.
Another technique an ENT may use to encourage healing is to add a

chemical to the edges of the hole to stimulate growth and then place a
thin paper patch on the eardrum to act as a base for skin growth over the
hole.
There are a variety of surgical techniques, but all basically place tissue
across the perforation allowing healing. The name of this procedure is
called tympanoplasty or myringoplasty . Surgery is typically quite
successful in closing the perforation permanently, and improving hearing.
Allowable sound exposure times

Sound Level Intensity Maximum Hours of Exposure
In dBa Per 8-Hours Workday
Mastoid
80 dBa 24 hrs.
Infection
82 dBa 16 hrs.
83 dBa 12 hrs., 40 mins.
85 dBa 8 hrs.
88 dBa 4 hrs.
91 dBa 2 hrs.
92 dBa 1 hr., 34 mins.
93 dBa 1 hr., 16 mins.
94 dBa 1 hr.
95 dBa 48 mins.
96 dBa 38 mins.
97 dBa 30 mins.
98 dBa 24 mins.
99 dBa 19 mins.
100 dBa 15 mins.
101 dBa 12 mins.
102 dBa 9 mins., 6 secs.
103 dBa 7 mins., 30 secs
106 dBa 3 mins., 45 secs
108 dBa 1 min., 52 secs
112 dBa 56 secs
115 dBa 28.07 secs
118 dBa 14.03 secs
121 dBa 7.01 secs
124 dBa 3.31 secs
127 dBa 1.45 secs
130 dBa .52 secs
133 dBa .26 secs
136 dBa .13 secs
139 dBa .06 secs
(Mastoiditis)
The mastoid is part of the skull and is made up of spongy bone just behind
the ear. Mastoiditis is an infection of the bony air cells in the mastoid bone. In fact
the middle ear and the inner ear are embedded in the mastoid bone.
Indications of a mastoid infection are reddening and swelling behind the ear. The
cause is usually from an untreated middle ear infection, so otitis media symptoms are
often present. An untreated middle ear infection can slowly spread into the mastoid cells.
When infection becomes trapped in the mastoid it is known as mastoiditis.
Another example showing a
Note the mastoid bone
child's right ear being pushed
swelling behind the ear
forward by the mastoid infection
Symptoms of mild mastoiditis
Reddening behind the ear

Swelling
Sensitive to touch.
Symptoms of acute mastoiditis
Pronounce bulbous swelling that can push the ear forward (acute)
Large swelling behind the ear
High fever
Ear pain
Sensitive to touch
Hearing loss
Paralyzed facial nerves (serious cases)
Treatment for Mastoiditis
Antibiotics are the normal treatment for the mild form of mastoiditis. There are a
number of antibiotics available to treat. Because there are few blood vessels permeating
the mastoid area, a normal 10 day protocol of antibiotics may be extended to 14 days to
make sure the medicine penetrates the bony mass. While in acute form mastoidectemy
is inevitably needed.
Diagnostic Procedures for Mastoiditis
A number of procedures will usually be performed in a hospital setting to

ascertain the extent of the disease's progress and to rule out any complications. A CT-
scan and X-rays will be used to assess the extent of the infection. To assist with
diagnostic procedures an antibiotic therapy through IV is needed, and if the eardrum has
not burst, a small incision will be made in the eardrum (myringotomy) to allow drainage
of the infection.
Mastoid Surgery -Mastoidectomy
A mastoidectomy is done under general surgery. It involves drilling away the

infected bone. This aims to remove all the infected bone. An incision is made behind the
ear and the flap is lifted forward.
A circle is cut out of the bone covering the mastoid and showing the infected
area. The spongy mass that is infected is then cut away and removed. The remaining
cavity is cleaned, coated with antibiotics and if possible the bone cover is place back to
the rest of the skull, and the flap of skin stitched back together. An outer pressure
dressing is then worn for 1-2 days after surgery. If too much mastoid material has been
removed, and it is not possible to reattach the bone covering, it is left off and the skin
flap is stitched back to the surrounding tissue. After healing, there will be depression
behind the ear.
The stay in the hospital is usually 1-3 days. After discharged from the hospital, a
full regimen of antibiotics will be given (10-14 day regimen). The stitches will be removed
after about 2 weeks. Full recovery will take 3-4 weeks with possibly bouts of dizziness
and headaches during this time. Over time the headaches and dizziness should
diminish.
Cholesteatoma
A cholesteatoma occurs if skin from the inner side of the tympanic

membrane sloughs off and mixes with ear wax that penetrates the open
hole in the eardrum to the middle ear chamber and fails to drain through
the Eustachian tube. Over time the accumulation of dead skin and wax
causes a cyst-like mass to grow -cholesteatoma. If left untreated and the
mass becomes larger, the mass can put pressure to nearby parts of the
ear causing serious damage such as the eardrum and ossicles. In serious
cases, cholesteatomas have been known to penetrate into the mastoid
area causing infection or into the cranial chamber causing meningitis-
infection of the covering of the brain or the meninges.
Symptoms
The attico-antral form of the condition initially causes a smelly discharge to leak
from the ear. You may also have a hearing loss and sometimes tinnitus. You can
get vertigo - dizziness - if the semicircular canals, which form part of the balance
system, are also affected.
Signs of cholesteatoma
Extreme pain, especially in the side of the head where the problem is
Continual vertigo and nausea
Loss of hearing
A gradual weakening of the facial muscles causing a droopy look on one side as
if recovering from a stroke
Headaches similar to migraines
Treatment for Cholesteatoma
It is important to remove the cholesteatoma and all traces of infection. For this,
it is usually necessary to have a surgical procedure known as mastoidectomy.
Once the middle ear chamber is opened, the mass is removed and the surgeon
will check to make sure the ossicles are not damaged and that the
cholesteatoma has not penetrated to other areas of the cranium.
Damaged Ossicles (Ossicular Chain Disruption)

Causes of Damaged Ossicles
Trauma to the ear drum from external sources.

Continuous infections can slowly dissolve one or all three of the bones that make
up the ossicles.
Genetics: Babies are sometimes born with malformed ossicles. They can be
repaired or replaced by having an operation called an ossiculoplasty.
Surgical Procedures (Ossiculoplasty)
As with mastoid surgery, an incision is made behind the ear and a flap of skin
pulled back to access the inner ear chamber. The damaged ossicles is removed
and matched against various sized artificial bones to get a close match.
Titanium is often used to replace one or more of the bones and is custom
fitted for each patients unique bone lengths. Titanium is used as the body will
not reject the metal and after time will actually grow a slime covering over the
metal. The ossicles are very small and this makes the surgery very delicate.
Patients are put under local or general anesthesia in a hospital and the implant
procedure usually lasts about two hours. Because of the small size of the bones
and the small workspace of the middle ear (about a 1" chamber), surgery is
performed using a special microscope. For more serious middle and inner ear
operations that are performed under general surgery, robotic machines are used.
Otosclerosis
Otosclerosis is a spongy bone-like tissue that grows at the place where

the stapes meets the oval window of the cochlea. As this growth grows, it slowly
prevents the ossicles from moving well. Otosclerosis is the most frequent cause
of middle ear hearing loss and affects about 10% of the United States
population. It is most commonly seen in more women than men often during
pregnancy, implying a hormonal cause. Caucasians are more likely to have this
disorder than any other race. Only 1% of African Americans have otosclerosis. It
is also rare among Orientals and Native Americans.
Image of otosclerosis occurring between the stapes and the oval window of the cochlea
Causes of Otosclerosis
The causes of otosclerosis are not exactly known. However, the most
generally accepted theory is that it has a genetic basis, combined with hormonal
production abnormalities. The gene that cause the otosclerosis appears to be a
dominant, rather than a recessive gene, but it has a characteristic called
reduced penetrance meaning it does not always dominate over a normal gene.
At first, hearing loss occurs in the low frequencies. High frequencies are affected
next, followed by the loss of hearing in the middle frequencies. Otosclerosis
usually begins in one ear, but the other ear often develops it as well. If left
untreated, otosclerosis will cause the hearing to steadily get worse and can lead
to profound deafness. It is rare for otosclerosis to occur after the age of fifty.
Categories of Otosclerosis
Subclinical Otosclerosis- occurs when the tissue does not interfere

with the ossicles. A person may have this form for many years and not
know it.
Clinical Otosclerosis- This type can be present in the teen years,
but not detected until the young adult years.
Histologic Otosclerosis- occurs when the tissue is present, but it

does not grow larger. This rare condition may or may not cause a hearing
loss. Very occasionally, otosclerosis can also affect the inner ear. The
condition can affect either one, or more commonly, both ears.
Symptoms of Otosclerosis
Tinnitus
Hearing loss, often at lower frequencies
You may also find that your hearing is better in noisy surroundings.
People with otosclerosis tend to speak quietly.
Treatments for Otosclerosis
In the early stages of otosclerosis, or when the condition is mild, you might not
need any treatment. Hearing aids are very useful initially. However, as the tissue builds
up on the stapes you will gradually lose your hearing. Sodium fluoride tablets have been
shown to help prevent the progression of otosclerosis, but only if the condition has also
affected the inner ear.
Surgical procedures for Otosclerosis
Stapedectomy- this operation aims to improve hearing by replacing the stapes -

one of the ossicles, with a piston. The piston helps to restore the movement of
the ossicles, so transmitting sound into the inner ear.
Most of the stapes bone is removed, leaving just the portion called the footplate,
which sits in contact with the oval window. The oval window is the link between the
middle and inner ear. A small hole is then drilled in the footplate and the piston is
inserted so that it sits in contact with the oval window. At its other end, the piston is
attached to the incus, the middle of the three ossicles.
About 85% of people find the operation a success and report a good
improvement in hearing. However, there is a very small risk of fluid loss in the years
following surgery -for example, if you have a sudden blow to the head or sudden
pressure change that causes the piston to penetrate the membrane of the oval window.
Fenestration- the idea of the operation is that since the

oval window is obliterated by bony growth, a new window (fenestra) needs to be
made, and usually this window is to be drilled into the lateral semicircular canal
level of the promontory.
Stapedolysis (stapes mobilization) - The principle of this surgery is so simple, if

the stapes is stuck, free it. The procedure involves raising the tympanic
membrane, exposing the contents of the middle ear, attaching the hook like
instrument to crus of the stapes, and by jerking it, freeing the footplate from the
otosclerosis growth.
COMMON DISEASE AND DISORDER OF THE INNER EAR
It is estimated that up to 25% of any population in the industrialized world will

experience dizziness, with or without vertigo, at some point in their lives. Older people
experience it more than the younger population. It is important to understand that all
vertigo comes with dizziness, but not all dizziness comes with vertigo.
Dizziness
The main symptoms of dizziness include a feeling of light headedness.

There are numerous reasons why a person may be experiencing dizziness. It
may be related to anxiety or panic disorders, or mood disorders. Dizziness in the
form of light-headedness may result from a cardiovascular problem such as an
irregular heart beat (arrhythmia) or if your blood pressure drops when you
change positions (postural hypotension).
There are some medications that may cause light-headedness or

imbalance such as some blood pressure medications (antihypertensives),
medications to control convulsions or spasms (anticonvulsants), calming
medications (sedatives) or medications that help with sleep (hypnotics).
Problems with chemical changes within your body (metabolic problems) may also
cause dizziness, such as if your blood sugar drops too low (hypoglycemia) or
hormonal imbalances.
Symptoms of Dizziness
Light headedness
Motion sickness or nausea
Faintness or weakness
Tinnitus
Another symptom that is sometimes associated with true vertigo is

tinnitus. Tinnitus is noise in the ear that may be heard on and off, continuously
or in a pulsation form. This noise may be buzzing, ringing, roaring, whistling or
hissing. It often goes with many ear disorders, including Menieres disease,
infections such as an inflammation of the middle ear -otitis media, or
inflammation of the internal ear labrynthitis, eustachian tube obstruction or
noise-induced hearing loss.
Two general classes of Tinnitus
Vibratory- appears when the underlying etiology originates from outside

the patients like loud noise and head trauma.
Nonvibratory appears when the cause is due to disease, drugs or some
other internal process
The Semi-Circular Canals as Balancers
The body senses its different positions and controls its balance through
organs of equilibrium (balance) that make you feel stable, or normal. These
organs of balance are located in the inner ear and are called the semicircular
canals. These canals look like loops of tubes. Their connections on one side are
to the cochlea where they receive sounds, and to the aural nerves going to the
brain.
The semicircular ducts are arranged roughly at right angles with each
other so that they represent all three planes in three-dimensional space. The
horizontal duct lies in a plane pitched up approximately 30 degrees from the
horizontal plane of the earth-erect head. The front canals are located in vertical
planes that project forward and outward by approximately 45 degrees. The rear
canals are located in vertical planes that project backward and outward by
approximately 45 degrees.
If you could take the upper portion of each inner ear on each side of the
head, they would be symmetrical the front canal on one side of the head is
parallel to the rear canal on the other.
Messages to the brain as to the head's changes in position are generated

by calcium carbonate crystals that shift on their bed of sensory hairs in the
utriculus and the sacculus. The changes as to which hairs are being stimulated
by the presence of crystals are reported to the cerebellum which in turn,
translates the information into knowledge of the position of the head relative to
gravity.
Vertigo
A major symptom of a balance disorder, it is the sensation of spinning or

swaying while the body is stationary with respect to the earth or surroundings.
The word vertigo comes from the Latin vertere to turn and igo, a condition,
meaning a condition of turning about.
Two classes of vertigo:
Subjective vertigo- is when a person feels a false sensation of

movement.
Objective vertigo- is when the surroundings will appear to move past a
person's field of vision
Symptoms of True Vertigo
Sense of movement
An illusion of spinning and circling
Worsened with head movements
Nausea/vomiting
Episodes come and go
Rhythmic Eye Movement (Nystagmus)
Causes of Vertigo
The cause of all vertigo is when the semi-circular canals are not
functioning properly, ether due to infection, inflammation, trauma, hormonal
imbalances, blood disorders, or scarring. However, for vertigo that lasts off and
on or continuously for a few days, the following are some probable causes.
Low tolerance for vehicular motion such as cars, boats, cruise ships, and
airplanes that cause motion sickness.
A head cold or some infection of the ear or nasal passages that blocks or
swells the eustachian tube.
The subsequent inability of the middle ear to equalize air pressure in the
middle ear chamber causes undue pressure on the inner ear, and
subsequently the semicircular canals where balance is registered.
High blood pressure
High cholesterol
Diabetes
Anemia
Calcium disorders
Alcohol or drug abuse
Brain tumors and Syphilis (rare cause)
Most Common Types of Vertigo
Menieres Disease
Vertigo with hearing loss on one-side, noise in the ear and aural fullness.
Menieres Disease is an inner ear disorder that brings spontaneous episodes of
vertigo that can last minutes to hours. Along with the vertigo, there may be
some hearing loss in the affected ear that comes and goes, as well as an
increase in tinnitus and a sense of fullness in the Menieres affected ear. Between
episodes, you may have a persistent hearing loss and tinnitus in the affected
ear. The vertigo associated with Menieres Disease may happen suddenly, or
may build in intensity over several hours and you may begin to experience
nausea or vomiting.
Causes of Meniere's Disease
The underlying cause of Meniere's Disease is unknown. Meniere's Disease

is felt to be due to an abnormality in the fluid balance of the inner ear.
Symptoms of Meniere's Disease
Lasts minutes to hours

Usually an accompanying hearing loss or a change in hearing
Tinnitus
Feeling of pressure in ears
Possible Treatments for Menieres Disease
The first is to treat the symptoms of vertigo with anti-vertigo medication.

Often an anti-nausea agent is necessary to combat the sick feeling that
comes with vertigo. During and following a vertigo attack, the affected
patient should avoid movements as they may increase the severity of the
symptoms.
The second form of treatment is prevention of further vertigo attacks.

Certain medications are effective in reducing the frequency and severity of
vertigo attacks.
Surgery may be necessary to treat Meniere's Disease. One option is
having surgery to place an antibiotic directly into the inner ear. This may
reduce the attacks of vertigo.
Lifestyle and Diet Changes
There are some changes to diet and lifestyle that may help you manage
Menire's Disease. These include a low-salt diet to help reduce fluid retention as
well as taking a medication that encourages urination. You should also avoid
sudden movements as they may aggravate these symptoms.
Recurrent Vestibulopathy
Severe vertigo, with or without hearing loss
Patients who suffer multiple episodes of severe vertigo without hearing

loss likely have what is known as recurrent vestibulopathy. These attacks of
vertigo come and go, and last from minutes to hours. This disorder is therefore
similar to the later, but without any hearing loss or noise in the ear. There is no
evidence of brain dysfunction with recurrent vestibulopathy, and it usually goes
away over time. Some recurrent vestibulopathy may turn into Meniere's Disease
or benign paroxysmal positional vertigo (BPPV).
Causes of Recurrent Vestibulopathy
The cause or causes of recurrent vestibulopathy are unknown.
Symptoms of Recurrent Vestibulopathy
Lasts minutes to hours

No hearing loss or tinnitus
Treatments for Recurrent Vestibulopathy
Treatment for recurrent vestibulopathy is similar to Mnire's Disease.

These may include an anti-vertigo medication and anti-nausea agent to combat
the sick feeling that comes with vertigo.
There are some changes to diet and lifestyle that may help you manage
this type of vertigo. These include a low-salt diet to help reduce fluid retention as
well as taking a diuretic.
Benign Paroxysmal Positional Vertigo or BPPV
Vertigo caused by free floating particles in the inner ear organ of balance
or vestibule
Debris in the posterior semicircular canal of the inner ear (BPPV)
The vestibular system located in and around the ear controls our body's sense of
balance. When your head moves, the vestibular system sends information to the organs
inside the ear, and these organs then pass the information on to the brain.
Symptoms of BPVV
Benign paroxysmal positional vertigo (BPPV) results from debris particles

that move freely within fluid in the canals of the inner ear. The debris is not
related to getting anything in the ear canal, it just forms on its own.
A change in your head position, lying down, getting up, turning over in
bed, or tipping your head backwards to look up may cause the debris to shift.
This shifted debris affects the balance receptor in the ear and causes vertigo.
The vertigo associated with BPPV comes on suddenly and usually only lasts for
seconds to minutes. There are usually no hearing symptoms.
Possible Treatments for BPPV
A skilled doctor can perform some maneuvers that can move the debris
out of the sensitive part of the ear (posterior canal). Your doctor can also teach
you how to do certain exercises at home, placing your head in various positions
at different angles. This may help move the debris in your ear as well.
The need for surgery is very rare, but in such cases a procedure known as
posterior canal plugging can be done. This blocks most of the canals function,
which can reduce the symptoms.
Vestibular Neuronitis
Disruption of vestibular input to the brain
The brain and the inner ear communicate information via nerves. The
cochlear nerve carries information about noise and hearing, the vestibular
nerve carries information about balance and body position. Viruses can affect
either or both nerves and the symptoms will vary according to which nerve
has been affected.
Vestibular neuronitis is an inflammation of the vestibular nerve that

causes a disruption of the message sent by the vestibular nerve to the brain.
The first attack of vertigo is usually severe, and is associated with nausea
and vomiting, lasting days to weeks. People with vestibular neuronitis do not
have hearing loss or tinnitus.
Symptoms of Vestibular Neuronitis
Vertigo Lasts days to weeks

No hearing changes
Viral Labyrinthitis
Viral infection of the inner ear
It is a sudden disruption of the messages to the brain from within the

inner ear as a result of a sudden viral infection. As a result of this virus, you may
experience severe vertigo that usually comes on suddenly and can last from days
to weeks, depending on the length of time the body builds up anti-bodies to the
virus. There are no other symptoms related to the ear.
Symptoms of Viral Labyrinthitis
Vertigo Lasts days to weeks

May have hearing changes
Possible Treatments for Either Cause
It is important for people suffering from such symptoms to be examined

and diagnosed by an ENT specialist since other conditions, such as stroke can
present with similar symptoms. There are several medications that your
physician may recommend if they feel that the vertigo associated with the
vestibular neuronitis or viral labyrinthitis requires treatment. These include anti-
vertigo agents, antihistamines, sedatives and or anti-nausea agents.
There are some other things that you can do to help alleviate the
symptoms. Bed rest is recommended for the first 2 to 3 days from the initial
onset of your symptoms. If your vertigo symptoms last more than a few days,
staying active may be more helpful. There are also some exercises that your
doctor may suggest once the vertigo has subsided.
Viral diseases that cause hearing loss:

Cytomegalovirus
Mumps
Acquired Immunodeficiency Syndrome
Herpes
Bacterial diseases that cause hearing loss:

Meningitis
Syphilis
Hearing loss associated with systemic disease

Thyroid Disease
Diabetes Mellitus
Kidney Disease
Multiple Sclerosis
Connective Tissue Disease
Menieres Disease
PEDIATRIC DEAFNESS
Normal hearing requires that all parts of the auditory pathway are working
correctly. This pathway includes the external ear, middle ear, inner ear, auditory
nerve, and the connection between the auditory nerve and the brain. The exact
location and nature of the problem in the auditory pathway determines the type
and severity of a person's hearing loss.
Some causes of hearing loss occur before a baby is born. These include genetic
disorders such as Warrensburg syndrome or Crouzon syndrome and infections
such as congenital rubella or congenital syphilis.
Genetic Factors
About half of all cases of hearing loss among children are thought to result from
genetic factors. Sometimes these children have a syndrome of which hearing
loss is only one feature. However, in most children with hearing loss that is due
to a genetic cause, the hearing loss is not part of a syndrome. A variant of the
connexin 26 gene is responsible for much of the hearing loss in this latter group
of children.
Postpartum Factors
Problems during or soon after birth can also be risk factors for developing
hearing loss. These include hypoxia, bleeding in the brain, and
hyperbilirubinemia. Children who are born early or at low birth weight are more
likely to have problems that may lead to hearing loss. However, children who are
normal birth weight can have hearing loss.
Other Factors
Hearing loss can also occur later in a child's or adult's life. Causes during this
time include infection such as meningitis, chronic middle ear infections, or
measles, injuries such as head injury, or certain drugs such as the antibiotic
gentamycin. High noise levels such as from firecrackers or loud rock concerts can
also damage a person's hearing. About 30 million workers are exposed to
dangerous noise levels on their jobs. Another nine million are at risk of hearing
loss as a result of working with certain metals or solvents. Some causes of
hearing loss can be prevented. For example, vaccines can prevent certain
infections, such as H-flu meningitis or measles, which can cause hearing loss.
The Technology of Hearing Aids

Body worn aids
This was the first type of hearing aid invented by Harvey Fletcher while
working at Bell Laboratories. These aids consist of a case containing the
components of amplification and an ear mold connected to the case by a cord.
The case is about the size of a pack of playing cards and is worn in the pocket or
on a belt. Because of their large size, body worn aids are capable of large
amounts of amplification and were once used for profound hearing losses.
Behind the ear aids (BTE)
BTE aids have a small plastic case that fits behind the ear and provides
sound to the ear via air conduction of sound through a small length of tubing, or
electrically with a wire and miniature speaker placed in the ear canal. The
delivery of sound to the ear is usually through an earmold that is custom made,
or other pliable fixture that contours to the individuals ear. BTEs can be used for
mild to profound hearing losses and are especially useful for children because of
their durability and ability to connect to assistive listening devices such as
classroom FM systems.
In the ear aids (ITE)
These devices fit in the outer ear bowl or pinna they are sometimes visible
when standing face to face with someone. ITE hearing aids are custom made to
fit each individual's ear. They can be used in mild to some severe hearing losses.
Feedback, a squealing/whistling caused by sound leaking out of the aid and
being amplified again, may be a problem for severe hearing losses. Some
modern circuits are able to provide feedback regulation or cancellation to assist
with this. Traditionally, ITEs have not been recommended for young children
because their fit could not be as easily modified as the earmold for a BTE, and
thus the aid had to be replaced frequently as the child grew.
Receiver In the ear aids (RITE)
At a first glance, these devices are similar to the BTE aid. There is
however one crucial difference, the receiver of the hearing aid is placed inside
the ear canal of the user and thin electrical wires replaces the acoustic tube of
the BTE aid. There are some advantages with this approach. First, the sound of
the hearing aid is arguably smoother than that of a traditional BTE hearing aid.
With a traditional BTE hearing aid, the amplified signal is emitted by the receiver
which is located within the body of the hearing aid behind the ear. The amplified
signal is then directed to the ear canal through an acoustic tube, which creates a
peaky frequency response. With a RITE hearing aid, the receiver is right in the
ear canal and the amplified output of the hearing aid does not need to be pushed
through an acoustic tube to get there, and is therefore free of this distortion.
Secondly, RITE hearing aids can typically be made with a very small part behind-
the-ear and the wire connecting the hearing aid and the receiver is extremely
inconspicuous. For the majority of people this is one of the most cosmetically
acceptable hearing device types.
In the canal (ITC) and completely in the canal aids (CIC)
ITC aids are smaller, filling only the bottom half of the external ear. You
usually cannot see very much of this hearing aid when you are face to face with
someone. MIC and CIC aids are often not visible unless you look directly into the
patients ear. These aids are intended for mild to moderately-severe losses. CICs
are usually not recommended for people with good low frequency hearing, as the
occlusion effect is much more perceivable.
Open-fit devices
"Open-fit" or "Over-the-Ear" OTE hearing aids are small behind-the-ear type

devices. This type is characterized by a small plastic case behind the ear, and a
very fine clear tube running into the ear canal. Inside the ear canal, a small soft
silicone dome or a molded, highly vented acrylic tip holds the tube in place. This
design is intended to reduce the occlusion effect. Conversely, because of the
increased possibility of feedback, they are limited to moderate high frequency
losses.
Bone Anchored Hearing Aids (BAHA)
The BAHA is an auditory prosthetic which can be surgically implanted. The

BAHA uses the skull as a pathway for sound to travel to the inner ear. For people
with conductive losses, the BAHA, bypasses the external auditory canal and
middle ear, stimulating the functioning cochlea. For people with unilateral
hearing loss, the BAHA uses the skull to conduct the sound from the deaf side to
the side with the functioning cochlea. The implant vibrates the skull and inner
ear, which stimulate the nerve fibers of the inner ear, allowing hearing.
Eyeglass aids
Recently, a new type of eyeglass aid was introduced. These hearing

glasses feature directional sensitivity: four microphones on each side of the
frame effectively work as two directional microphones, which are able to discern
between sound coming from the front and sound coming from the sides or back
of the user. This allows for amplification of the sound coming from the front, the
direction in which the user is looking, and active noise control for sounds coming
from the sides or back. Only very recently has the technology required become
small enough, in size, to be put in the frame of the glasses.
Hearing aids are built from analog or digital circuits. Each technology processes
sound differently. Until recently, all hearing aids were analog. Digital hearing
aids are the newest kind of hearing aid and are superior to analog. All hearing
aids, whether analog or digital, are designed to increase the loudness of sounds
reaching the ear drum so that the hearing-impaired person can better
understand speech.
Components of Hearing Aids
1. A microphone to gather acoustic energy (sound waves in the air) and

convert it to electrical energy.
2. An amplifier to increase the strength of the electrical energy.
3. A receiver, which is like a miniature speaker that converts the electrical
energy back into acoustic energy (sound waves).
Difference between digital hearing aids and analog hearing aids

in terms of functioning
Analog Hearing Aids
Analog hearing aids use a continuously varying electrical signal to produce

sound, just like a microphone and loudspeaker. Analog hearing aids have a microphone
that picks up sound and converts the sound into small electrical signals. These signals
vary according to the pattern of the sound. The signals are then amplified (made louder)
by transistors and fed to the ear phone on the hearing aid which is next to your ear drum
so you can hear them. Most of the better analog hearing aids compress the sound using
automatic gain control (AGC). This amplifies quiet sounds until they are loud enough to
be heard, but gives less amplification to sounds that are already loud, so you're
protected against uncomfortably loud sound levels. Analog hearing aids dont have all
the features that come with advanced digital aids, but they are less expensive.
Digital Hearing Aids
Digital aids take the signal from the microphone and convert it into "bits" of data
- numbers that can be manipulated by a tiny computer chip in the hearing aid.
This makes it possible to tailor and process sounds very precisely in ways that
are impossible with analog aids. The digital chip takes the bits representing the
sound and analyzes and manipulates them using what is called DSP or Digital
Signal Processing. Software algorithms (a set of instructions), are used to
perform the precise complex DSP actions, and are then converted back into
electricity, which is finally changed back into sound that goes into the ear. This
process happens very rapidly with several million calculations occurring in the
hearing aid each second.
The digital sound representations can be manipulated in almost any way

imaginable, and this is what gives the digital hearing aid its big advantage.
When someone talks, you usually want to hear what they are saying, rather than
whatever noise is going on in the background. People who use traditional analog
hearing aids often complain that they find it difficult or impossible to follow
conversations in noisy places. Many digital aids are designed to reduce steady
kinds of background noise, such as crowds in a restaurant or the rumble of traffic
or the whirr of a fan. This makes listening more comfortable. But it does not
necessarily help you to pick out a single voice from everything else that's going
on, especially when several people are talking. Some digital hearing aids also
have circuitry to protect whatever hearing is left. If a loud sound is detected
above the 90-100 Db range which can cause damage, dampening circuitry cut
out the sound.
To effectively use any sensory aid, clients must know and understand
the following:
1. Component parts and their specific function.

2. Benefits and limitation of available sensory aids.
3. How to clean and maintain the aid for daily use.
4. How to troubleshoot the operation and performance of selected aids.
5. How to adjust the aid for everyday use.
6. How to mange minor problem.
7. Who to contact in the event of a problem with the aid.
8. Cost of replacement aids and batteries on how to acquire them.
9. How to use aids in combination to enhance the performance over a single aid.
10. Insurance and manufacturer warranty conditions.
COCHLEAR IMPLANTS
Advances in computer technology as well as in ear surgery itself have

given us the opportunity to offer the world of sound, music, and speech to those
who would otherwise have spent their lives in a soundless cocoon.
Those who are born deaf prelingual deafness, as well as children and
adults who lost their hearing from either disease or trauma post lingual
deafness, can experience the gift of hearing thanks to cochlear implants.
Development of the devices came about through the surgical experiments

of a group of French medical scientists as well as the pioneering work of William
House of Los Angeles, Dr. Robert Schindler of San Francisco and a cochlear
implant team from Melbourne Australia. Miniaturization and advances in
computer technology over the last 30 years set the stage for the further
development of more sophisticated and effective cochlear implant devices.
Today, over 30,000 individuals have been implanted worldwide, over 3,000
cochlear implants were performed in 1999 alone.
Sound is picked up through a tiny microphone housed in a headpiece that
is worn at the ear. The sound is sent along a cable to a processor, a mini-
computer that converts the sound into digital signals. The processor is worn on
the belt or, in some models at ear level.
Once processed, the digital signals go back up to a transmitter (in some

models, the transmitter and the microphone are in the same piece in other
models, the microphone is in a behind-the-ear piece that looks like a
conventional hearing aid). The transmitter, which is held by a magnet on the
side of the head behind the ear, sends the coded signals via radio waves across
the skin to the implant. The implant delivers the signals to electrodes that have
been inserted into the cochlea. The electrodes stimulate the auditory nerve,
sending impulses to the brain where they are interpreted as sound.
Initial experiments with deaf participants indicated that if an electrode

was placed on the bony wall of the inner ear and an electric current was passed
through the electrode, the deaf individual could perceive the sensation of sound.
From this very basic observation the concept of placing an active electrode into
the inner ear by way of the round window -the only non-bony entry into the
cochlea of the inner ear was born.
Initial implants were thus placed against the outer wall of the inner ear.
Soon, they were introduced into the cochlear chamber itself through the round
window. Not only was this introduction more effective in stimulating the residual
nerve endings of the inner ear, but it also allowed the surgeon to better anchor
the implant into the inner ear without risk of loosing contact with the nerve
endings.
Individuals with deafness usually have lost most of their hair cell nerve
endings which normally conduct sound from the ear to the brain. Significant
residual nerve endings are needed to be present in the deaf to allow for their
direct stimulation by the neighboring electrodes. The cochlear implant is thought
to function by directly stimulating the surviving nerve population in the cochlea
and spiral ganglion.
The earliest cochlear implants consisted of a single active electrode,
introduced into the inner ear, through the cochlear wall next to the round
window. Today, most investigators in the cochlear implant field agree that
stimulating the residual nerve cell population with multiple electrodes at different
sites within the cochlea, combined with sophisticated computer assisted
processing strategies allows for better recognition and understanding of speech.
Both the Nucleus 24 Contour and the Clarion High Focus devices have
further refined this concept with the closer placement of the electrode array to
the residual spiral ganglion cells of the auditory nerve.
The active electrodes in these newest devices allow them to hug the bony inner
wall of the cochlea instead of loosely fitting into the cochlear chamber. This
concept may allow for lower electrical stimulation levels of individual electrodes
which would prevent cross chatter between electrodes (jumping of electrical
fields from one electrode to another) and conserve battery life as well.
Long lasting batteries requiring little electric current will allow for a
completely implantable cochlear device in the future. For the present, the
implantable portion includes the electrode array and wire from the electrodes to
an implanted portion of the device which is behind the ear. The remaining
hardware of the device includes the microphone, receiver, speech processor and
magnetic link between the outer scalp and the implanted portion of the device.
The external portion of the unit receives and processes sounds which are
then fed into a specific electrode pair. These, in turn, stimulate the auditory
nerve and finally the auditory center of the brain.
O L FA C T I O N
Anatomy and Physiology
NOSE
The nose is the organ involved in smell and breathing. It is located in the
middle of the face. The internal part of the nose lies above the roof of the
mouth. It processes the air that you breathe before it enters your lungs. Most of
this activity takes place in and on the turbinates, located on the sides of the
nasal passages. In an adult, 18,000 to 20,000 liters of air pass through the nose
each day.
The nose is consists of:
External Nose- triangular-shaped projection in the center of the face.

Nostrils - The two openings into the nasal passages.
Nasal passages - passages that are lined with mucous membranes and tiny
hairs (cilia) that help to filter the air and move nasal and sinus mucous to the
back of the throat. Nasal passages are separated by the nasal septum.
Septum - made up of cartilage and bone and covered by mucous membranes.
The cartilage also gives support to the lower part of the nose and divides the
nasal passages into right and left sides.
Sinuses - four-paired, air-filled cavities.
Sinuses
The sinuses are cavities, or air-filled pockets inside the face, near the nasal
passages. As in the nasal passages, the sinuses are lined with mucous membranes.
There are four sinuses:
Ethmoid sinus - located around the area of the bridge of the nose. This sinus is
present at birth, and continues to grow until puberty.
Maxillary sinus - located around the area of the cheeks. This sinus is also
present at birth, and continues to grow until puberty.
Frontal sinus - located in the area of the forehead. This sinus does not develop
until around 7 years of age.
Sphenoid sinus - located deep in the face, behind the nose. This sinus does not
fully develop until adolescence.
ASSESSMENT of the NOSE and SINUSES
The nurse uses inspection and palpation to examine the nose and sinuses.
The structures assessed include the external nose, vestibule, nasal mucosa,
septum, turbinates, nasal canals, and sinuses. Function of the first cranial nerve
(olfactory) is usually not tested unless a deficit in the sense of smell is reported
or suspected.
NOSE
External Nose
The external nose is inspected and palpated for deviations from normal
alignment, symmetry, color, discharge, nasal flaring, lesions, and tenderness.
Normal findings are listed. The skin color over the nose is the same as that of
the facial skin. Alignment is straight and symmetric without deviation from
midline. Discharge from the nares should be absent and the nares should not
flare (spread) with respirations. The client is able to breath quietly through the
nose rather than mouthbreathe. Masses, lesions, and tenderness are absent. The
nurse checks the nasal canals for patency by asking the client to occlude one
nares with a finger and to breathe through the open nares while closing the
mouth. This is repeated for the opposite nares. The client should be able to
breathe without difficulty through both nares. The nurse asks the client to tip the
head back and inspects the outer nares for crusting, bleeding, or dryness, which
should be absent.
Internal Nose
The nurse next inspects the vestibules with use of a penlight while the
clients head is tipped back. Normal findings include the presence of coarse hairs,
a clear passage without discharge, and a midline septum. Further examination of
the internal nose requires use of a nasal speculum; this is not done unless it is
indicated.
If detailed examination of the internal nose is done, the nurse either
attaches a nasal speculum tip to the otoscope head or uses a metal nasal
speculum and penlight for illumination. The client tips the head back, and the
nurse gently inserts the speculum into one nares with care being taken not to
scrape the mucosa. One nares is inspected at a time.
Hold the speculum correctly and inserts the blade gently about inch
into the nostril. Gain additional control of the speculum by resting the index
finger of the dominant hand on the side of the clients nose. Steady the clients
head with the nondominant hand. Open the blades gently and vertically, avoiding
pressure on the septum and turbinates. Slowly move the head to inspect all
areas of the nasal chamber. Observe the condition of the mucous membrane
(e.g., pallor, redness, swelling). Normally, the mucosa is moist and dark pink
without sign of inflammation, pallor, or blue color. Presence of discharge is
abnormal. The septum is midline without deviation, masses, perforation, or
exudates. The turbinates (only the inferior and part of the middle turbinates are
visible, the superior is not) have the same color as the mucosa and should be
free of exudates, swelling, or inflammation. Look for polyps and other masses.
Observe plugs of mucus for color, consistency, amount, and odor.
Inspection may be hampered by nasal congestion. It may be necessary to

shrink the nasal mucosa with a topical vasoconstrictor (e.g., ephedrine, cocaine,
phenylephrine hydrochloride) for adequate inspection. When these agents are
instilled into the nose, the client should be instructed to say e and hold the
sound. This technique raises the posterior tongue, occludes the upper airway,
and prevents the fluid from running into the pharynx.
Nasopharynx
The nasopharynx is best examined with a mirror with the tongue

depressed with a tongue blade or gauze. Prevent the mirrors fogging by
warming it before putting it into a mouth. Hold the mirror to one side of the
uvula and focus light on it. A small part of the nasopharynx can be observed with
a nasal speculum. Specialists may use a nasopharyngoscope to examine the
nasopharynx.
Paranasal Sinuses
Assess the paranasal sinuses by (1) inspecting and palpating the soft
overlying tissues, (2) observing any nasal secretions (it is possible to determine
which sinus is infected according to where purulent discharge appears), and (3)
transillumination of the maxillary and frontal sinuses.
The nurse palpates and percusses the frontal and maxillary sinuses to
assess for swelling and tenderness, which should be absent. The frontal sinuses
are palpated simultaneously by placing the thumbs above the eyes, just under
the bony ridge of the orbits, and applying gentle pressure. The maxillary sinuses
are palpated by use of either the index and third fingers or thumbs to gently
press on each side of the nose just under the zygomatic bones. Direct percussion
is used over the eyebrows for the frontal sinuses and on either side of the nose
below the eyes in line with the pupils for the maxillary sinuses.
TRANSILLUMINATION
Transillumination is a technique to further assess the sinuses if tenderness

is present. Either a penlight or the otoscope handle fitted with a transilluminator
head is used. The room is darkened. The light is placed against the orbital bones
immediately below the eyebrows and directed upward. The nurse shields the
light source with one hand. Normally, a reddish glow appears above the frontal
sinus area. Lack of illumination may indicate sinus congestion and pus
accumulation. The maxillary sinuses are assessed by placing the light beneath
the center of the eyes and the zygomatic bones and directing it down and in
toward the roof of the mouth. The nurse asks the client to open the mouth. A
glow should appear on the hard palate on the side being illuminated.
For more completely assessing sinus conditions, sinus radiographs may be
used. Air, normally present in the sinuses, appears as dark areas on a developed
film.
Smell
The senses of taste and smell are closely related. Many conditions affect
taste and smell, such as viral infections, normal aging, head injuries, and local
obstruction. Some medications can affect smell and taste, such as metronidazole
(Flagyl), local anesthetics, clofibrate (Atromid-S), some antibiotics, some
antineoplastics, allopurinol, phenylbutazone, levodopa, codeine, morphine,
lithium, and carbamazepine (Tegretol).
Smell impairment may be (1) hyposmia (decrease in smell sensitivity) or

(2) anosmia (bilateral and complete absence of smell sensitivity). Smell
assessment is done by having the client identify various odors. Various
substances are placed in individual test tubes (covered to eliminate visual cues).
Testing each nostril separately, have the client sniff the tubes (first with eyes
closed and then with eyes open). Document whether the client (1) can perceive
each odor and (2) can identify each odor accurately. Smell is perceived mainly
via the olfactory nerves, although some are perceived via the trigeminal nerves.
Trigeminal irritants are perceived even by clients experiencing anosmia.
(Therefore, a client who claims not to smell trigeminal irritants has a hysterical
loss of smell rather than hyposmia or anosmia.)
DIAGNOSTIC PROCEDURES for the NOSE and SINUSES
A. Flexible Rhinolaryngoscopy
Flexible rhinolaryngoscopy is currently one of the most commonly used

techniques for visualizing the nasal cavity, the sinuses, the pharynx, and the
larynx. The technique utilizes a small-caliber flexible endoscope and can be
performed in an office setting. Before the procedure, the patient's nasal cavity is
decongested and anesthetized for maximum visualization and minimal
discomfort. In the procedure, the examiner threads the end of the scope into the
nasal aperture along the floor of the nasal cavity. As the scope is advanced, the
examiner can visualize the nasal cavity proper for any evidence of lesions or
masses. Once the scope approaches the nasopharynx, it is directed inferiorly and
advanced slowly, allowing direct visualization of the entire pharynx and larynx.
B. Functional Endoscopic Sinus Surgery (FESS)
Before undergoing FESS, patients have lab tests, CT scans and other
screenings to confirm the exact nature of the problem. During FESS, our
otolargyngolgists (ear, nose and throat doctors) introduce an endoscope into the
interior of the patients nose and sinuses. The slender, fiberoptic device has a
tiny light at its end, enabling the physician to view the problem area. Once the
instrument is positioned, tiny scalpels and other surgical tools are passed
through the nostrils alongside the endoscope to remove polyps and other
obstructions. Since there are no external incisions, the patient rarely experiences
any bruising or swelling.
C. Image-guided Endoscopic Techniques
In select cases, UC Irvine Medical Center otolarngologists use image-

guided endoscopic techniques. By combining the power of computerized
tomography with endoscopy, theyre able to determine the anatomic location of
their instruments within the sinuses and perform three-dimensional
reconstructions of the surgical site.
D. Sinus X-ray
A sinus x-ray is a type of x-ray used to obtain images of the sinuses. The
sinuses are air-filled cavities lined with mucous membranes located within the
bones of the skull.
During a sinus x-ray, x-rays pass through the sinuses and form an image
on a special type of film. The sinuses are usually filled with air, which appears
black on x-ray film. An opaque (whitened) area on an otherwise normal film may
indicate the presence of sinusitis (inflammation of the mucous membranes of the
sinuses), hemorrhage, tumor, or other problems.
As computerized tomography (CT scan) and magnetic resonance imaging

(MRI) technologies are often able to provide improved imaging of the sinuses,
the use of these scans may replace sinus x-rays in certain circumstances.
Other related procedures that may be used to evaluate problems of the

sinuses include x-rays of the skull, CT scan of the brain, and MRI of the brain
and spine. Please see these procedures for more information.
E. Computed Tomography (Also called CT or CAT scan.)
A diagnostic imaging procedure that uses a combination of x-rays and

computer technology to produce cross-sectional images (often called slices),
both horizontally and vertically, of the body. A CT scan shows detailed images of
any part of the body, including the bones, muscles, fat, and organs. CT scans are
more detailed than general x-rays.
F. Cultures from the Sinuses
Laboratory tests that involve the growing of bacteria or other

microorganisms to aid in diagnosis.
SINUSITIS
Sinusitis is an infection of the sinuses near the nose. These infections usually
occur after a cold or after an allergic inflammation. There are four types of
sinusitis:
Acute - symptoms of this type of infection last less than four weeks and
get better with the appropriate treatment.
Subacute - this type of infection does not get better with treatment
initially, and symptoms last four to eight weeks.
Chronic - this type of infection happens with repeated acute infections or
with previous infections that were inadequately treated. These symptoms
last eight weeks or longer.
Recurrent - three or more episodes of acute sinusitis a year.
Causes of Sinusitis
Sometimes, a sinus infection happens after an upper respiratory infection

(URI) or common cold. The URI causes inflammation of the nasal passages that
can block the opening of the paranasal sinuses, and result in a sinus infection.
Allergies can also lead to sinusitis because of the swelling of the nasal tissue and
increased production of mucus. There are other possible conditions that can
block the normal flow of secretions out of the sinuses and can lead to sinusitis
including the following:
abnormalities in the structure of the nose
enlarged adenoids
diving and swimming
infections from a tooth
trauma to the nose
foreign objects stuck in the nose
cleft palate
gastroesophageal reflux disease (GERD)
secondhand smoke
When the flow of secretions from the sinuses is blocked, bacteria may begin
to grow. This leads to a sinus infection, or sinusitis. The most common bacteria
that cause sinusitis include the following:
Streptococcus pneumonia
Haemophilus influenzae
Moraxella catarrhalis
Symptoms of Sinusitis
The symptoms of sinusitis depend greatly on the age of the child. The
following are the most common symptoms of sinusitis. However, each child may
experience symptoms differently. Symptoms may include:
Younger Children:
runny nose
o lasts longer than seven to 10 days
o discharge is usually thick green or yellow, but can be clear
nighttime cough
occasional daytime cough
swelling around the eyes
usually no headaches younger than 5 years of age
Older children and adults:

runny nose or cold symptoms lasting longer than seven to 10 days
drip in the throat from the nose
headaches
facial discomfort
bad breath
cough
fever
sore throat
swelling around the eye, often worse in the morning
The symptoms of sinusitis may resemble other conditions or medical

problems. Always consult your child's physician for a diagnosis.
Treatment
Specific treatment for sinusitis will be determined by your child's physician

based on:
your child's age, overall health, and medical history
extent of the infection
your child's tolerance for specific medications, procedures, or therapies
expectations for the course of the infection
your opinion or preference
Treatment of sinusitis may include the following:

antibiotics, as determined by your child's physician (antibiotics are usually
given for at least 14 days)
acetaminophen (for pain or discomfort)
a decongestant (i.e., pseudoephedrine [Sudafed]) and/or mucus thinner
(i.e., guaifenesin [Robitussin])
cool humidifier in your child's room
nasal spray (to reduce inflammation)
medications to treat GERD
surgery to remove the adenoids
endoscopic sinus surgery
Antibiotics may be withheld for 10 to 14 days, unless severe symptoms

develop, such as: fever, facial pain or tenderness, or swelling around the eye.
Surgery should be considered only if other treatments have failed.
Referral to an allergist/immunologist is often needed, particularly for people

with chronic or recurrent sinusitis and for patients who have had sinus surgery,
but still experience sinusitis.
Antihistamines do not help the symptoms of sinusitis unless an allergy is

involved.
RHINITIS
Rhinitis is a reaction that occurs in the eyes, nose and throat when
airborne irritants (allergens) trigger the release of histamine. Histamine causes
inflammation and fluid production in the fragile linings of nasal passages,
sinuses, and eyelids.
The two categories of rhinitis are:
Allergic Rhinitis
There are two types of allergic rhinitis:
o Seasonal - occurs particularly during pollen seasons

o Perennial - occurs throughout the year
The most-common causes of allergic rhinitis are:
o pollen
o dust mites
o mold
o animal dander
Reactions from allergic rhinitis include:

o sneezing
o congestion
o runny nose
o itchy nose, throat, eyes, and ears
Preventive measures for avoiding allergic rhinitis include:

o environmental controls, such as air conditioning, during
pollen season
o avoiding areas where there is heavy dust, mites, molds
o avoiding pets
Treatments for allergic rhinitis, as determined by your physician

and based on your condition, may include:
o oral medications
o inhaled medications
o immunotherapy
o allergy injections
Nonallergic Rhinitis
Types of nonallergic rhinitis are:
o vasomotor rhinitis (irritant rhinitis)
o eosinophilic
o rhinitis medicamentosa
o neutrophilic rhinosinusitis
o structural rhinitis
o nasal polyps
o primary vasomotor instability
Causes of nonallergic rhinitis include:
o fumes
o odors
o temperature
o atmospheric changes
o smoke
o other irritants
Reactions from nonallergic rhinitis include:

o sneezing
o congestion
o runny nose
o itchy nose, throat, eyes, and ears
The preventive measure for avoiding nonallergic rhinitis is avoiding
the primary cause.
Treatments for nonallergic rhinitis, as determined by your physician

and based on your condition, may include:
o oral medications
o inhaled medications
o immunotherapy
o allergy injections
o surgery for some conditions
TONSILO-PHARYNEAL
Anatomy and Physiology
Tonsils
Tonsils are clusters of lymphatic tissue just under the mucous membranes
that line the nose, mouth, and throat (pharynx). There are three groups of
tonsils. The pharyngeal tonsils are located near the opening of the nasal cavity
into the pharynx. When these tonsils become enlarged they may interfere with
breathing and are called adenoids. The palatine tonsils are the ones that are
located near the opening of the oral cavity into the pharynx. Lingual tonsils are
located on the posterior surface of the tongue, which also places them near the
opening of the oral cavity into the pharynx. Lymphocytes and macrophages in
the tonsils provide protection against harmful substances and pathogens that
may enter the body through the nose or mouth.
Tonsils are lymphoepithelial organs at the opening of the upper

aerodigestive tract. From above downwards, they can be divided into:
1. pharyngeal tonsil, adenoid, which lies on the roof and posterior wall of the
nasopharynx
2. tubal tonsil which lies around the eustachain tube
3. palatine tonsil which lies between the anterior and posterior faucial pillars
4. lingual tonsil which lies at the base of the tongue
These lymphoid organs developed from the epithelium of the primitive

oronasal cavity, the mesenchymal stroma and lymphoid cells then infiltrate these
areas. Although the tonsils are present at embryonal stage, they only acquire
their typical structure in the postnatal period. They begin increasing rapidly in
size between the first and third year of life, with peaks in the third and seventh
year. They involute slowly at early puberty. In contrast to other lymphoid
aggregates, tonsils do not filter lymph.
The palatine tonsil is supplied by the facial artery, ascending pharyngeal
artery, lingual artery and the maxillary artery. Venous drainage is by the lingual
and pharyngeal veins.
Immunology
Tonsils are composed primarily of B-lymphocytes. T-cell lymphocytes

constitute 40% of total volume in contrast to 70% in circulating plasma.
According to present knowledge, tonsils are involved in production of antibodies,
interferon-gamma and lymphokines and in inducing secretory immunity.
Pharynx
The pharynx is a tubular structure extending from the base of the skull to
the esophageal inlet. Superiorly, it opens into the nasal and oral cavities;
inferiorly, it opens into the larynx and the esophagus. It is lined with mucous
membrane. The adenoids are located in the nasopharynx, the palatine tonsils in
the pharynx, and the lingual tonsils in the hypopharynx; all are lymphoid tissue.
The pharynx is subdivided into the nasopharynx, the oropharynx, and the
hypopharynx.
Nasopharynx. The nasopharynx extends from the posterior choanae to the

inferior surface of the soft palate. Malignancies of the nasopharynx can present
as nasal obstruction, epistaxis, tinnitus, headache, diminished hearing, and facial
pain.
Oropharynx. The oropharynx extends from the junction of the hard and soft
palates and the circumvallate papillae to the valleculae. It includes the soft
palate and uvula, the base of the tongue, the pharyngoepiglottic and
glossoepiglottic folds, the palatine arch (which includes the tonsils and the
tonsillar fossae and pillars), the valleculae, and the lateral and posterior
oropharyngeal walls. Carcinomas of the oro pharynx can present as pain, sore
throat, dysphagia, and referred otalgia.
Hypopharynx. The hypopharynx extends from the superior border of the hyoid
bone to the inferior border of the cricoid cartilage. It includes the pyriform
sinuses, the hypopharyngeal walls, and the postcricoid region (i.e., the area of
the pharyngoesophageal junction). Malignancies of the hypopharynx can present
as odynophagia, dysphagia, hoarseness, referred otalgia, and excessive
salivation.
The pharynx is the region of the tonsils, back part of the nose and swallowing
area. It is probably the most examined of all body regions, and reflects many
diseases.
Assessment
To inspect the pharynx, the examiner asks the person to open the mouth
without protruding the tongue. A tongue blade is pressed firmly down on the
midpoint of the arched tongue; pressing farther back may cause gagging. The
person then says ah while breathing through the mouth to prevent gagging.
The oropharynx, that portion of the pharynx directly posterior to the oral
cavity bounded by the nasopharynx above and laryngopharynx below, is
examined with a tongue blade and a mirror. The anterior and posterior tonsillar
pillars, the uvula, tonsils and posterior pharynx are inspected for color,
symmetry, evidence of exudates, edema, ulceration, and tonsillar enlargement.
Redness and swelling of the tonsils, pillars and uvula with white or yellow
exudates on the tonsils may indicate streptococcal infection. Tonsils may be
enlarged without being infected.
Examination of oral cavity should be done properly. Very often, the size of
tonsils may be exaggerated during gagging and pressing hard with the use of a
tongue depressor. The proper way is to gently place the tongue depressor
anterior to the circumvallate papillae or if possible, just by inspection without the
use of tongue depressor. The size and percentage of the obstruction should be
recorded using the scale 0 to +4. 0 means the tonsil is in the fossa; +1 means
less than 25% obstruction; +2 is less than 50%; +3 is less than 75% and +4 is
more than 75% obstruction.
Examination of the Pharynx for Problems
The pharynx can be seen partially by forceful traction on the tongue, by

the fingers wrapped in a handkerchief. It begins in back of the one-half inch
uvula, which hangs down freely from the posterior rim of the palate.
1. Observe the sides of the pharynx where the tongue appears to originate, and
note the irregular flesh colored tonsils on each side. When removed, a small
cavity remains in their site. Adult tonsils may be atrophied to a pea size or if
irritated and infected, be as large as grapes and flecked with pus.
2. With a flashlight, examine the back of the pharynx while attempting to yawn.
An all-over redness, with noticeable soreness, usually means pharyngitis as in
colds, sore throats, etc.
3. Examine the wall of the pharynx on all sides and the back of the tongue, if
possible, for any one particular sore, ulcer or bleeding point, which may mean
cancer.
Diagnostic Procedures for the Tonsils and Pharynx
A. Indirect Laryngoscopy
Indirect laryngoscopy has been used since the 1800s for visualizing the
pharynx and larynx. In this technique, the head light source illuminates the
mirror, which in turn illuminates the laryngopharynx. The patient is seated in the
sniffing position and protrudes the tongue while a warmed laryngeal mirror is
introduced firmly against the soft palate in the midline to elevate the uvula out
of the field (gently, so as not to elicit the gag reflex). The image seen on the
mirror can be used to assess vocal cord mobility, as well as to inspect for a mass
or foreign body of the larynx or pharynx. This technique can be performed
rapidly and is inexpensive.
B. Flexible Rhinolaryngoscopy
Flexible rhinolaryngoscopy is currently one of the most commonly used

techniques for visualizing the nasal cavity, the sinuses, the pharynx, and the
larynx. The technique utilizes a small-caliber flexible endoscope and can be
performed in an office setting. Before the procedure, the patient's nasal cavity is
decongested and anesthetized for maximum visualization and minimal
discomfort. In the procedure, the examiner threads the end of the scope into the
nasal aperture along the floor of the nasal cavity. As the scope is advanced, the
examiner can visualize the nasal cavity proper for any evidence of lesions or
masses. Once the scope approaches the nasopharynx, it is directed inferiorly and
advanced slowly, allowing direct visualization of the entire pharynx and larynx.
C. Direct Laryngoscopy
Direct laryngoscopy has the advantage of permitting both diagnostic and

therapeutic intervention. It is performed with the patient under general
anesthesia and intubated. The procedure allows for direct visualization of the
pharynx and the larynx and permits the surgeon to perform biopsies and remove
small lesions. At the same time, the surgeon has the opportunity to palpate the
structures of the oral cavity, the oropharynx, and the hypo pharynx, which
cannot be properly palpated in an awake patient.
The laryngoscope can also be suspended from a table-mounted Mayo

stand (for hands-free use), and a microscope can be maneuvered into focal
distance to allow magnified visualization of the glottis and subglottis. During a
microscopic direct laryngoscopy, small lesions or topographic abnormalities can
be better characterized and removed if desired. Some examples of lesions that
can be diagnosed by direct laryngoscopy are vocal cord polyps, leukoplakia,
intubation granulomas, contact ulcers, webs, nodules, hematomas, and
papillomatosis. Additionally, small malignant lesions of the vocal cords can be
examined and ablated or extirpated by using a CO 2 laser under direct
microlaryngoscopic guidance.
D. Angiography
Angiography is a widely used examination in which radiopaque dye is

injected into the vessels by means of transcutaneous catheter insertion. It
visualizes the internal wall and caliber of the vessel lumen, as well as the
position of the vessel, which is usefl for the evaluation of certain parapharyngeal
masses.
Biopsy Procedures
A. Fine-needle Aspiration
FNA is often used to make an initial tissue diagnosis of a neck mass. The
advantages of this technique include high sensitivity and specificity; however,
5% to 17% of FNAs are nondiagnostic. Another advantage of FNA is speed: If a
cytologist or a pathologist is available, diagnosis can often be made within
minutes of the biopsy.
FNA is performed with a 10 ml syringe with an attached 21- to 25-gauge

needle. Larger needles are more likely to result in tumor seeding. The patient is
positioned to allow for optimal palpation of the mass. The skin overlying the
mass is prepared with a sterile alcohol prep sponge. Local anesthesia is not
necessary. The mass is grasped and held in a fixed and stable position. The
needle is introduced just under the skin surface. As the needle is advanced, the
plunger of the syringe is pulled back, to create suction. Once the mass is
entered, multiple passes are made without exiting the skin surface; this
maneuver is critical in maximizing specimen yield. After the final pass is
completed, the suction on the syringe is released and the needle withdrawn from
the skin. If a cyst is encountered, it should be completely evacuated and the
fluid sent for cytologic analysis.
A drop of aspirated fluid is placed on a glass slide. A smear is made by

laying another glass slide on top of the drop of fluid and pulling the slides apart
to spread the fluid. Fixative spray is then applied. Alternatively, wet smears are
placed in 95% ethyl alcohol and treated with the Papanicolaou technique and
stains.
FNA has several advantages over excisional biopsy. An FNA requires only
an office visit, with minimal loss of time from work for the patient. In contrast,
excisional biopsy is commonly performed in an operating room, so the patient
must undergo preoperative testing. Patients with a significant medical history
may require formal medical clearance. An excisional biopsy exposes the patient
to the risks of anesthesia, postoperative wound infection, and tumor seeding.
B. Ultrasound-Guided FNA
Ultrasonographic guidance of FNA enables the surgeon to obtain a

cytologic specimen of deeper or nonpalpable masses that are not amenable to
standard FNA. Real-time imaging of the needle's passage allows the surgeon to
plot a more accurate trajectory and avoid underlying vital structures.
Furthermore, it provides an image of the mass, allowing its characterization as
solid, cystic, or heterogeneous. With cystic or complex masses, it is imperative
to place the tip of the needle into the wall to increase specimen yield.
C. CT-Guided FNA
CT-guided FNA is most commonly employed to diagnose poorly accessible

or deep-seated lesions of the head and neck. Like ultrasound-guided FNA, CT-
guided FNA provides visualization of the needle as it is passed through the tissue
and into the underlying structures, thus allowing a more accurate needle
trajectory and avoidance of underlying vital structures. Additionally, visual
guidance of the needle greatly increases the likelihood of obtaining a specimen
from the mass rather than the surrounding tissues.
Imaging Procedures
Because many of the deep structures of the head and neck are
inaccessible to either direct evaluation by palpation or indirect evaluation via
endoscopy, further information must be obtained by radiography. Imaging
procedures such as CT, MRI, ultrasound, and positron emission tomography
(PET) scanning permit the diagnosis and analysis of pathologic conditions
affecting these deep structures, including the temporal bone, skull base,
paranasal sinuses, soft tissues of the neck, and larynx.
A. Ultrasonography
Ultrasonography is a safe and inexpensive method of gaining high-

resolution real-time images of the structures of the head and neck. Palpable
masses in the neck can be assessed for changes in size, for association with
other local structures, and for character (i.e., solid, cystic, or complex).
Applications of ultrasonography include assessment of masses such as
thyroglossal duct cysts, branchial cleft cysts, cystic hygromas, salivary gland
tumors, abscesses, carotid body tumors, vascular tumors, and thyroid masses.
Additionally, ultrasonography combined with FNA and cytologic evaluation can
provide both a detailed visual description and an accurate cytologic evaluation of
masses in the neck.
B. Computed Tomography
A CT scan with intravenous contrast is often the first-line imaging

technique used to evaluate a mass of the neck and to assess for pathologic
adenopathy. CT has proved to be an effective method for primary staging of
tumors and lymph nodes. Additionally, it has been shown to be effective in
studying capsular penetration and extranodal extension. It is clearly superior to
MRI in evaluating bone cortex erosion, given that MRI cannot assess bone cortex
status at all. CT scans are also widely used for posttreatment surveillance in
cancer patients.
C. Magneic Resonance Imaging
MRI avoids exposing the patient to radiation and provides the investigator
with superior definition of soft tissue. For example, MRI can differentiate mucous
membrane from tumor, as well as detect neoplastic invasion of bone marrow. In
patients with nasal cavity tumors, MRI can distinguish between neoplastic,
inflammatory, and obstructive processes. MRI is also valuable in assessing the
superior extent of metastatic cervical lymphadenopathy (i.e., intracranial
extension). A disadvantage of MRI is its limited ability to show bone detail; it
therefore cannot detect invasion of bone cortex by a neoplasm. Furthermore, an
MRI scan is significantly more expensive than a CT scan.
D. Positron Emission Tomography
PET scanning is a functional imaging technique that measures tissue

metabolic activity through the use of radioisotopically tagged cellular building
blocks, such as glucose precursors. A range of physiologic tracers has been
developed for PET imaging, with the glucose analogue 2-deoxy-2-[(18)F]fluoro-
D-glucose (FDG) the most commonly used. FDG has a half-life of 110 minutes.
Once given to the patient, FDG is taken up by glucose transporters and is
phosphorylated by hexokinase to become FDG-6-phosphate (FDG-6-P). Further
metabolism of FDG-6-P is blocked by the presence of an extra hydroxyl moiety,
which allows FDG-6-P to accumulate in the cell and serve as a marker for
glucose metabolism and utilization.
Because neoplastic cells have higher rates of glycolysis, localized areas of

increased cellular activity on PET scans may represent neoplastic tissue. In this
respect, PET is very different from CT and MRI, which depict tissue structure
rather than tissue metabolic activity.
Because FDG is nonspecifically accumulated in glycolytically active cells, it

demarcates areas of inflammation as well as neoplastic tissue, which can lead to
a false positive scan. Muscular activity during the scan can also lead to areas of
increased uptake in nonneoplastic tissue. Furthermore, healing bone, foreign
body granulomas, and paranasal sinus inflammation can produce false positive
results.
False negative scans occur when tumor deposits are very small (i.e., 3 to
4 mm or less in diameter). Thus, micrometastases are not reliably detected
using an FDG-PET image. Furthermore, a false negative scan can occur if the PET
scan is performed too soon after radiation therapy.
The role of PET imaging in head and neck oncology is rapidly expanding.
Currently, the majority of PET imaging used in head and neck oncology is FDG
based. FDG-PET is actively being used to look for unknown primary lesions and
second primaries, to stage disease before therapy, to detect residual or recurrent
disease after surgery or radiation therapy, to assess the response to organ
preservation therapy, and to detect distant metastases. Because false positive
and false negative PET scans do occur, accurate interpretation of PET scans
requires a thorough understanding of the potential confounding factors.
E. PET/CT
PET/CT is essentially an FDG-PET scan that has been coregistered with a

simultaneous CT scan to allow the radiologist to precisely correlate the area of
increased cellular activity with the anatomic structure. This technique removes
some of the guesswork involved with interpreting an area of increased activity on
a simple PET scan and provides the physician with a morphologic correlate for
the area of increased uptake.
After a histologic diagnosis has been made and correlated with the
imaging information, the patient and physician can have a comprehensive
discussion of the pathology, the stage of the disease, and the selection of
therapy.
NOSE DISORDERS
EPISTAXIS
Epistaxis is bleeding from the nose caused by irritation, trauma,

coagulation disorders, hypertension, chronic infection or tumor.
Epistaxis is thought to have occurred at least once in over 10 % of the
normal population. It is either a primary disorder or secondary to another
condition such as hemophilia or leukemia and many cases are idiopathic. In
children, who are twice as likely to have epistaxis as adults, the bleeding is
usually mild and tends to originate from the posterior septum so that the
bleeding point is more difficult to locate and the bleeding may be profuse.
Epistaxis is equally common in men and in women.
Although epistaxis is a frightening experience for the patient, it
generally looks and feels worse than it actually is. The blood is usually
briught red and the patient may swallow some of it, which is an unpleasant
sensation. Although adults can lose up to 1 L per hour during severe
bleeding, the mortality is extremely low. When the patient bleeds enough to
show signs of shock, the nosebleed usually stops because of low blood
pressure; some deaths are thought to have been causes by coronary
ischemia from blood loss.
PATHOPHYSIOLOGY
The most common cause of epistaxis is trauma to the nasal mucosa

from damage by a foreign object, picking crusts from the nasal septum, or
dryness of the nasal mucosa. Nosebleeds are fairly common in patients with
coagulation defects such as hemophilia, leukemia and purpura. Infection,
tumors and some drugs and toxins may cause nosebleeds; in many instances
however, the cause is simply not identified or is considered idiopathic.
There may be some relationship between the menstruation and
epistaxis. It may be that in some women with premenstrual syndrome the
nasal mucosa becomes congested at the time of menstruation, setting the
stage for epistaxis.
The incidence of epistaxis is no higher in hypertensive patients than in
normotensive patients. However, hypertensive patients may bleed more
profusely, partly because of the direct effect of the increased pressure and
also because the small nasal arteries and arterioles of hypertensive patients
tend to have much of their muscular walls replaced by fibrous tissue and are
incapable of contracting adequately to attain hemostasis.
Children experience frequent nosebleeds from the anteroinferior part
of the septum known as the Littles area or Kiesselbachs plexus. The etiology
is not clear, but the area is richly vascular and children have hyperemic and
congested upper respiratory tracts. Children also pick up and rub their noses
in the area where the mucosa is stretched over the cartilage and bone.
Intractable nose picking is another cause of anterior nosebleeds. Some
patients cannot stop picking their noses, either because of a nervous habit or
because crusts are present from an earlier ulceration or perforation. Constant
nose picking can cause septal ulceration or even a perforation which leads to
epistaxis.
A hereditary disease that is an unusual cause of epistaxis is Rendu-
Osler-Weber disease of hemorrhagic hereditary telangiectasia. This disease is
gene dominant and may be passed from either parent to a child of either sex.
Epistaxis is usually the initial symptom, but telangiectasis is commonly found
in other mucous membranes or anywhere on the external surface of the
body. Bleeding usually occurs from the nose and gastrointestinal tract
because mucosa in those areas is very fragile, whereas other areas have
protective layers of squamous epithelium.
Most nosebleeds in the anterior part of the nose originate from
Kiesselbachs plexus, the highly vascular network in the anterior septum. It is
also anatomically closer to the rapid inspiratory air flow, which may dry the
normal mucus flow especially in cold, dry weather. Because the vessels are
fairly small and easily accessible, these nosebleeds are the easiest to treat. If
the bleeding is from the posterior part of the nose, the exact source of
bleeding is more difficult to locate because it is sometimes impossible to see
and bleeding is more profuse. Usually just one source on one side of the nose
bleeds, although bleeding frequently originates from both sides in patients
with blood dyscrasias.
Diagnostic Studies and Findings

Hematocrit
Hemoglobin
Platelets
Prothrombin time
Partial thromboplastin time
Reticulocyte count and differential
- done to rule out coagulation defect, results usually normal;
bleeding from other parts of body likely in patients with hematologic
disorders.
Rhinoscopy
Nasopharyngoscopy
- to detect and localize site of planning
Medical and Surgical Management

1. Arterial ligation of ethmoid, maxillary or carotid artery if proper packing
fails to control nosebleed.
> an incision is made I the gumline above the incisor on the
affected side, and the maxillary sinus is entered. The artery
that supplies the area of bleeding is identified, and a metal
clip or suture is used to ligate the artery.
2. Endoscopic cautery chemical or electrical cauterization of bleeding
vessels using nasal endoscope to visualize bleeding.
3. Septal dermoplasty for Rendu-Osler-Weber disease - skin graft is

placed in nose to cover anterior parts of septum and floor and walls of
nose anteriorly to provide protective covering over fragile mucosa;
combined with laser therapy gains control of epistaxis for several years.
4. For anterior bleeding:

Anterior nasal packing may be all that is required. Antibacterial ointment
such as Bacitracin or Neosporin is applied to half inch gauze and gently,
but firmly inserted into the anterior nasal cavities to apply pressure to the
bleeding vessels
Nasal packing should be in place for a minimum of 48 to 72 hours.
For posterior plugs:
Figure 4. Posterior nasal packing. A. After adequate anesthesia has been

obtained, a catheter is passed through the affected nostril and through
the nasopharynx, and drawn out the mouth with the aid of ring forceps.
B. A gauze pack is secured to the end of the catheter using umbilical tape
or suture material, with long tails left to protrude from the mouth. C. The
gauze pack is guided through the mouth and around the soft palate using
a combination of careful traction on the catheter and pushing with a
gloved finger. This is the most uncomfortable (and most dangerous) part
of the procedure; it should be completed smoothly and with the aid of a
bite block (not shown) to protect the physician's finger. D. The gauze
pack should come to rest in the posterior nasal cavity. It is secured in
position by maintaining tension on the catheter with a padded clamp or
firm gauze roll placed anterior to the nostril. The ties protruding from the
mouth, which will be used to remove the pack, are taped to the patient's
cheek.
A small, red rubber catheter is passed through the nose into the
oropharynx and mouth. A small gauze pack is tied to the catheter, and it
is withdrawn; this moves the pack into proper placement in the
nasophrarynx and posterior nose to apply pressure.
The nasal cavity is packed with half-inch gauze and the strings from the
posterior pack are tied around a rolled gauze for maintaining its position.
The ties from the oral cavity are taped to the clients face in order to
prevent loosening or dislodgement of the plug.
General comfort measures such as humidification, the use of drip pad to
collect bloody drainage and mucus, and providing lubrication to the nares.
Nurse must monitor for bleeding, and the proper placement of the
posterior plug. If the plug is visible in the oral cavity, notify the physician
for readjustment of the packing.
Posterior nasal packs should be in place for 5 days.
Prophylactic antibiotics are administered to prevent toxic shock syndrome
and sinusitis.
5. Balloon pressure catheter tubes

stents look like very short ( about 6 inches) urinary catheters. These
tubes have an exterior balloon along the tube length in addition to an
anchoring balloon on the end. These tubes are inserted into both nares.
The physician first inflates the anchoring balloon to keep the tubes in
place. Then the pressure balloons are inflated carefully for both tubes at
the same time to compress bleeding vessels. Placement of posterior
packing or pressure tubes is uncomfortable and airway may be
obstructed.
Nurse should observe for respiratory distress and tolerance of the tubes.
Pain medication may be prescribed. Oral care and adequate hydration are
important because of mouth breathing.
The tubes are usually removed after 2-5 days; teach the client measures
for comfort and safety. Like the use of petroleum jelly for lubrication,
nasal saline sprays and humidification. Instruct the client to avoid
vigorous nose blowing, use of aspirin and other NSAIDS, and strenuous
activities.
Medications:
Fibrinolytics VITAMIN K (Aquamephyton) 10mg po or IM; useful in
some cases of epistaxis, but packing remains therapy of choice
Anti-infective agents PENICILLIN 1.5 million U, IV q6h recommended
for prophylaxis because packing obstructs drainage of paranasal
sinuses and may precipitate a sinus infection.
Nursing Assessment/ Interventions
1. Assess for:
Nasal Bleeding
Bright red blood comes from the nares; patient may also
swallow or expectorate blood; history of trauma, nose picking or
other unknown cause.
2. Examination of patients body for bruises or petechiae that may
indicate underlying hematologic disorder.
3. Nursing Diagnoses:
Risk for fluid volume deficit r/t nasal bleeding
Fear r/t loss of blood
Risk for aspiration r/t inability to clear secretions; gagging
Altered cerebral and cardiopulmonary tissue perfusion r/t
large-volume blood loss
4. Interventions for:
ANTERIOR BLEEDING
Assess the location of bleeding
Pinch the nose firmly and hold for at least 10 minutes. It is best
if you pinch the patients nose instead of asking the patient to
do so. This way, you can ensure steady and firm pinching.
If bleeding continues beyond the pinching 10 min. period,
prepare the client for additional treatment.
With the patient in a high Fowlers position, slightly hyper flex
the head and suction the clots in the nasal passage.
Observe the canal for continued bleeding. If present, apply
vasoconstriction agent such as 10% cocaine solution.
If bleeding continues, the nose may need to be cauterized with
silver nitrate or anterior nasal packing inserted.
POSTERIOR BLEEDING
The bleeding usually originates from the sphenopalatine artery,
anterior ethmoid artery or the nasopalatine artery.
Assess that the bleeding is posterior.
Place the patient in a high Fowler position.
As ordered, anesthetize the posterior nasal passage with 10%
cocaine solution
Pack the bleeding site with packing materials such epistaxis
catheter, Foley catheter tip and or tampon.
Monitor vital signs and estimate blood loss. If necessary,
provide fluid volume replacement
Instruct patient to (1) tilt head forward if bleeding occurs (2)
not to blow nose and (3) to apply steady pressure for at least 5
min. if bleeding recurs.
NASAL FRACTURES
A nasal fracture is a traumatic injury to the nasal bones. Most common

causes are accidents, sports injuries, and assaults. In children, falls are the
most common cause of nasal fractures. They occur more commonly in men,
however when nasal fractures are diagnosed, it is essential to rule out
fractures of the associated facial bones such zygomatic or mandibular
fractures because facial injuries or trauma may also damage \these bones.
Even a nasal fractures that appear simple usually have associated
damage to the mucosal lining of the nose. If the patient suffered a facial
trauma that causes epistaxis, damage to the bone-cartilage structures of the
nose is more likely.
PATHOPHYSIOLOGY
A nasal fracture occasionally occurs in the birth canal during delivery.

These are usually greenstick fractures, and the babys nose inclines slightly
to one side. The nose can be grasped at the tip and pulled toward the midline
to realign it.
Nasal fractures can be classified as unilateral, bilateral or complex.
Unilateral fracture may produce little no displacement and may appear
on an xray examination as a simple crack.
Bilateral fractures which are the most common, may be caused
by a swinging punch or blow that pushes both nasal bones to one side or by
a frontal blow that depresses the nasal bones and gives a flattened look to
the nose. The entire nose may be deviated and the nose may have a C or S
deformity.
Complex fractures are usually caused by a powerful frontal blow.
Such blows may shatter the nasal pyramid and frequently the frontal bones
as well, causing a marked depression of the nasal and frontal bones.
The usual findings are epistaxis, a noticeable facial deformity and a history of
trauma. Edema occurs quickly at the injury site and depending on the
severity may include a periorbital swelling. Ecchymosis is common, the nose
is exquisitely tender, and nasal obstruction occurs. Complex fractures of the
nose and face may result in diplopia and subscleral hemorrhage.
Diagnostic Studies and Findings:
X-ray examination of the face and nose shows fractures

and depressed areas of facial and nasal bones; done to
complement clinical, visual evaluation.
Ophthalmoscopy performed to rule out eye injury such
as corneal abrasion or laceration, also to check lacrimal
apparatus and orbit.

1. Reduction and Fixation of the fractures as quickly as

possible after injury (within first hour or two before swelling
beings, or after 3 or 4 days when swelling has decreased)
because fragments tend to stabilize quickly; bilateral nasal
packing or nasal splints usually inserted during surgery to
maintain stability and position of nasal structure.
2. Rhinoplasty is a surgical reconstruction of the nose for

cosmetic purposes and to improve airflow. The client returns
from surgery with packing on both nostrils; the gauze packing is
usually treated with antibiotic to reduce risk for infection. A
moustache dressing (or drip pad) often a folded 2x2 gauze
pad is usually placed under the nose. A splint or cast may cover
the nose for additional alignment and protection.
After surgery:
Observe for edema and bleeding.check v/s q4. the client
with uncomplicated rhinoplasty may be discharge the day
of surgery.
Place the patient in a semi-Fowlers postion and instruct
to move slowly
Apply cool compresses to nose, eyes or face to reduce
swelling and bruising.
To prevent bleeding, instruct patient to limit Valsava
maneuvers for the first few days after packing is
removed.
Laxatives or stool softeners may be prescribed to ease
bowel movement. Instruct client to avoid aspirin and
NSAIDS to prevent bleeding.
Explain that edema and discoloration may last for weeks
and the final surgical result will be evident in 6 to 12
months.
3. Medications: Narcotic analgesics or antipyretics

Acetaminophen (TYLENOL), 325-650 mg
with/without codeine po q4-q6 prn
3. General Management: Simple thumb pressure on convex side

of the nose occasionally enough to push bones back together.
Nursing Assessment/ Interventions

1. Assess for:
Facial swelling; deformity; ecchymosis; epistaxis; nose very
tender; history of trauma to face and nose; possible accompanying
lacerations; leak of CSF fluid, a clear fluid dripping from then nose
and/or ears.
Respiratory Status; difficulty in breathing through the nose;
mouth breathing
2. Nursing Diagnoses and Interventions:

PAIN r/t facial trauma
Assess need for pain medication and provide adequate analgesia for
pain relief; evaluate and document effectiveness.
INEFFECTIVE BREATHING PATTERN r/t nasal obstruction

and swelling
- Monitor vital signs and level of consciousness.
- Assess for shortness of breath, dyspnea from nasal obstruction or
difficulty in swallowing.
- Apply ice to face and nose to minimize swelling and bleeding
without pressure to nose.
- Monitor amount and color of epistaxis and record
- Keep head of bed elevated, even when sleeping to prevent
aspiration of blood or secretions and minimize edema.
- Prevent patient from swallowing blood or aspirating; encourage
patient to breathe through mouth.
- Have basin nearby for patient to expectorate blood.
Provide frequent oral hygiene and encourage intake of oral fluids.
SENSORY/PERCEPTUAL ALTERATIONS (visual) r/t periorbital
edema
- Assess for eye swelling; apply ice to minimize edema
- Observe for scleral hemorrhage and periobital edema
- If eyes are not completely closed, assess patients
ability to see.
NASAL POLYPS
Polyps are benign grapelike cluster of mucous membrane and

connective tissue growths that appear as soft, pale gray, non tender masses
and gradually form from recurrent, localized swelling of the sinuses or nasal
mucosa. Polyps are seen in about 90% of patients with chronic maxillary
sinusitis. Polyps may become quite large. They are usually bilateral, occur in
multiples and may cause actual distention and enlargement of bony
structures of the nose. Even after surgical removal, some nasal polyps recur.
Although rare in children, polyps are occasionally found in children with cystic
fibrosis and allergies and in those with Peutz-Jeghers syndrome. The
symptoms of this syndrome include pigmented spots on the skin, especially
around the mouth and polyposis of the gastrointestinal tract. Many patients
with polyps have anosmia or hyponosmia.
PATHOPHYSIOLOGY
The etiology of nasal polyps is not clear. They are often suspended in
the nasal cavity by stalks of varying lengths. The polyps and stalks usually
originate in the paranasal sinuses, particularly the ethmoid sinuses and pass
into the middle meatus of the nose through the ostia connecting them to the
nasal cavities. They are often called pseudotumors. Their pathogenesis is
thought to be the result of focal mucosal edema that causes a polypoid
swelling. Because of the polyps weight, the swelling tend to enlarge and
eventually becomes suspended on a stalk.
Polyps are usually found in the middle meatus near the openings of
the sinuses and in the roof of the nose. They are never found on the septum
or in the lower meatus; the reason for this is not known. Nasal polyps are
often found in patients with allergy, cystic fibrosis, asthma, disorders of
ciliary motility, chronic rhinitis and chronic sinusitis. The exact relationship is
unknown but may be related to an inflammatory response causing
hypertrophy of the mucosa, edema, and thinning of mucous membranes.
An interesting phenomenon that occurs in some patients with asthma
and nasal polyps is intolerance to aspirin, indomethacin and coal tar dyes.
The intolerance is severe, and can cause respiratory arrest if these
substances are ingested. This is thought to be related to the inhibitory action
of these substances on prostaglandin synthesis.
Diagnostic Studies and Findings:
X-ray examination of sinuses. Shadows over affected

areas ethmoid sinuses and sometimes maxillary sinuses
appear opaque.
Immunologic assessment. Performed if allergy is
considered a causative effect.
1. Polypectomy each polyp avulsed with wire snare.

2. Caldwell-Luc procedure may be performed if polyps
originate in maxillary sinus.
3. Functional endoscopic sinus surgery removal of polyps
using nasal endoscope.
Medications:
Corticosteroids. Prednisone high dose for 5 days.
Methyprednisolone decreasing doses may be used for severe nasal
obstruction to decrease size of polyps.
Steroids not recommended for long term use; steroid sprays may be
used for long term control of the size of polyps and to prevent
recurrence by reducing the inflammatory response.
Antihistamines
Decongestants
Anti infective agents
Nursing Assessment:
Nasal Obstruction; feeling of fullness in face or nose; nasal obstruction;

difficulty in breathing through nose; nasal discharge; anosmia; symptoms of
allergic rhinitis such as sneezing, watery eyes, eczema and asthma.
Nursing Dx and Interventions:
INEFFECTIVE AIRWAY CLEARANCE r/t swelling of the nasal mucosa

and nasal obstruction
Monitor patients vital signs.

Assess patients ability to clear secretions, and amount of swelling.
Increase humidification.
After polypectomy, elevate head of bed and apply ice compresses to
nose to minimize swelling and bleeding.
Change nasal drip pad as indicated and record amount and consistency
of drainage.
Encourage patient not to swallow blood or secretions and expectorate
into basin to prevent nausea.
Instruct patient not to blow nose to prevent tissue trauma and
promote healing.
Observe for bleeding, and if bleeding occurs, instruct patient to notify
physician, elevate head of bed, check vital signs, compress outside of
nose against septum and apply ice compress to nose.
If bleeding persists, packing may be necessary.
SENSORY/PERCEPTUAL ALTERATIONS (olfactory) r/t anosmia,

presence of nasal edema
Assess patients ability to smell.

Assure patient that sense of smell should return postoperatively after
swelling has decreased.
Instruct patient to make appropriate adaptations to environment.
SEPTAL DEVIATION AND PERFORATION
A deviated septum is a shift of the septum from the

midline, which is common in many adults. It is either S or C shaped.
Although the septum is usually straight at birth, it may shift from one side to
another as a result of trauma or injury.
A septal perforation is a hole in the nasal septum between
the nostrils, which is usually in the anterior or cartilaginous septum but may
occasionally occur in the bony septum. A small perforation, which can be
caused by infections, nasal crusting, or nose picking is often asymptomatic,
although a slight whistle may be heard as the patient breathes. Larger
perforations may produce rhinitis, nasal crusting or epistaxis.
PATHOPHYSIOLOGY
The nasal septum, the dividing structure of the nose, is

usually straight and divides the nose into two equal chambers. The septum is
occasionally bent during birth, and the infant may have a twisted appearing
nose. With aging, the septum has a tendency to become deviated or to form
a hump. There is frequently no history of injury to account for the deviation.
As a result, few adults have a totally straight septum. Trauma during
childhood may also contribute to septal deviations in the adult. There is also
a congenital disorder called choanal atresia, where the back of the nasal
passage is blocked, usually by abnormal bony or soft tissue. It can be
unilateral or bilateral. Sometimes, a unilateral choanal atresia is not detected
until much later in life because the baby manages to get along with only one
nostril available for breathing
Septal perforations may be small or large. They may be
asymptomatic or may cause annoying symptoms such as crusting, watery
discharge, or a whistling noise as the patient breathes. Small perforations are
usually caused by repeated irritation of the nose such as picking it: they may
also be caused by septal surgery. Less frequent causes are repeated
cauterization because of epistaxis, abuse of intranasal lidocaine, and chronic
nasal infections. Ninety percent of perforations are in the anterior
cartilaginous portions of the nose, less than 10% are in the posterior bony
portions.
Diagnostic Studies and Findings
Facial X-ray examination, examination with nasal speculum or endoscope.

- Show a shift of the septum or a septal
perforation.
For deviation:
Submucous resection (SMR) may be performed to reposition
septum and relieve nasal obstruction
Rhinoplasty may be done to correct nasal structure deformity
Septoplasty to replace septum in midline, may be done to relieve
nasal obstruction and to enhance external appearance of nose.
For perforation:
Surgical closure possible but not always successful; a Silastic
button prosthesis may be inserted to close perforation.
MEDICATIONS: Analgesics
Antihistamines
Decongestants
Antiinfective agents
General Management:
Local application of lanolin or petroleum twice a day to prevent

crusting
Irrigate nose with normal saline or a dilute solution of sodium
bicarbonate two or three times a day to keep the nasal mucosa
hydrated (for perforations)
Packing to control bleeding, if present. ( for deviation)
Nursing Assessment:
Irregularities or deformity of external nose; obstruction to nasal breathing;
feeling of facial fullness; headaches; epistaxis; crusting of nasal mucosa;
whistle sound when breathing (perforation); or sinusitis
Nursing Dx and Interventions:

INEFFECTIVE BREATHING PATTERN r/t septal deformity causing
obstruction
Assess and record respiratory status.
Postoperative care includes explanation in patient that facial and
periorbital edema may be present and that nasal packing or nasal
splints may be used.
Instruct patient to breathe though mouth during this time.
IMPAIRED SKIN INTEGRITY r/t surgery on septum

Keep head of bed slightly elevated to prevent edema and promote
drainage.
Use ice compresses on face to decrease edema, pain and bleeding.
Use cool mist vaporizer to assist in liquefying secretions.
Point out that patient may experience difficulty swallowing if nasal
packing is used.
Change drip pad as necessary, recording color, consistency and
amount of drainage.
Provide meticulous mouth care because patient is breathing through
mouth.
RISK FOR INJURY r/t bleeding or tissue trauma

Assess and report presence of excessive bleeding, swallowing or
purulent discharge
Caution patient against attempting to blow nose, may cause bruising,
edema and bleeding.
Caution patient not to smoke for at least 2 days; limit physical activity
for several days to prevent irritation or trauma to tissues, which may
cause bleeding.

MSN Sensory Disturbances

Transféré par

Informations du document

Titre original

Copyright

Formats disponibles

Partager ce document

Partager ou intégrer le document

Options de partage

Avez-vous trouvé ce document utile ?

Ce contenu est-il inapproprié ?

Droits d'auteur :

Formats disponibles

MSN Sensory Disturbances

Transféré par

Droits d'auteur :

Formats disponibles

ASSESSING CLIENTS WITH EYE DISORDERS

REVIEW OF ANATOMY AND PHYSIOLOGY

The Eye and Vision

THE VISUAL PATHWAY

Assessment of the Eyes

A. Current Health Status

B. Past Health Status

C. Family health status

1. Observe the patient for ptosis, exophthalmos, lesions, deformities, or asymmetry.

Screen Visual Fields by Confrontation

1. Shine a light from directly in front of the patient.

1. Stand or sit 3 to 6 feet in front of the patient.

1. Dim the room lights as necessary.

1. Hold your finger about 10cm from the patient's nose.

1. Darken the room as much as possible. ++

Upper Eyelid Eversion

This procedure is performed when a foreign body is suspected. ++

1. Ask the patient to look down.

DIAGNOSTIC TESTS FOR THE EYE

It is a detailed imaging and recording of ocular circulation by a series of

a. Assess client to allergies and previous reactions to dyes.

b. Obtain informed consent

c. A mydriatic medication, which causes pupil dilation, is instilled in the

d. The dye is injected into a vein of the clients arm.

f. The client may experience nausea, vomiting, sneezing, paresthesia of

No special client preparation or follow- up care is required.

Instruct the client that he or she will be positioned in a confined

Explain the procedure to the client.

If the client wears contact lenses, the lenses must be removed.

This test is used primarily to assess for an increase of intraocular pressure

Each dye is anesthetized.

The client is instructed to stare forward at a point above the

A flattened cone is brought contact with the cornea.

The amount of pressure needed to flatten the cornea is measured.

Specular mimography is a photographic technique used to count cells of

The exopthalmometer is an instrument designed to measure the forward

X-ray study, tomography, and CT scan are useful n the evaluation of

J. MAGNETIC RESONANCE IMAGING

Ultrasonography uses the principle of sonar to study structures not

Opthalmodyanamometry is a test that consists of exerting pressure on the

N. VISUAL EVOKED RESPONSE

Visual evoked response (VER) is similar to ERG in that it also measures

Glaucoma includes a group of ocular disorders characterized by increase intraocular

Anyone with a close relative who has glaucoma;

Intraocular pressure is determined by the rate of aqueous production in the

Angle- Closure Glaucoma

An acute attack of angle-closure glaucoma can develop only in an eye in which

Low-tension glaucoma resembles primary open-angle glaucoma. The angle is

Increase intraocular pressure may occur as a post operative complication.

Clinical manifestations of glaucoma include:

An opthalmoscopic examination shows atrophy (pale color) and cupping

The goal of medical management is to facilitate the outflow of aqueous through

When mediacal management is no longer effective, surgical intervention may be

Operative procedures such as trephination, thermal sclerostomy, or scleroctomy

When other surgical procedures have failed, cyclocryotherapy (application of

Progressive loss of peripheral vision followed by loss of central vision

Causes, incidence, and risk factors

Visual problems may include the following changes:

Difficulty seeing at night

Other tests that may be done (rarely) include:

If a cataract is not bothersome, then surgery is usually not necessary. Sometimes

Instruct the client regarding the postoperative measures to prevent or decrease

Elevate the head of the bed 30- 45 degrees.