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Disturbances in Perception and Coordination

Spinal Cord Injury


Description:

Injuries affecting the spinal cord commonly results from trauma,


gunshot wounds and motor vehicle accidents. Many cases of SCI are caused
by falls, sports-related injury and minor trauma. The principal risk factors for
SCI include age, gender, and alcohol and drug use. Males are affected four
times more often than females. Over half of the victims are 16 to 30 years of
age.

The most common vertebrae involved in SCI are the 5th, 6th and 7th
cervical, the 12th thoracic, and the 1st lumbar. These vertebrae are the most
vulnerable because there is a greater range of mobility in the vertebral
column in these areas. Damage to the spinal cord ranges from transient
concussion, to contusion, laceration and compression of the cord substance,
to complete transection of the cord.

Injury can be categorized as primary which is usually permanent or


secondary wherein nerve fibers swell and disintegrate as a result of
ischemia, hypoxia, edema, and hemorrhagic lesions. The type of injury on
the other hand, refers to the extent of injury to the spinal cord itself.
Incomplete spinal cord lesions are classified according to the area of spinal
cord damage: central, lateral, anterior, or peripheral. A complete spinal cord
injury can result in paraplegia, which is paralysis of the lower body or
quadriplegia which is the paralysis of all four extremities.

Risk Factors:

• Trauma such as automobile crashes, falls, gunshots, diving accidents,


war injuries, etc.
• Tumor such as meningiomas, ependymomas, astrocytomas, and
metastatic cancer.
• Ischemia resulting from occlusion of spinal blood vessels, including
dissecting aortic aneurysms, emboli, arteriosclerosis.
• Developmental disorders, such as spina bifida, meningomyolcoele,
and others
• Neurodegenerative diseases, such as Friedreich's ataxia,
spinocerebellar ataxia, etc.
• Demyelinative diseases, such as Multiple Sclerosis.
• Transverse myelitis, resulting from stroke, inflammation, or other
causes.
• Vascular malformations, such as arteriovenous malformation (AVM),
dural arteriovenous fistula (AVF), spinal hemangioma, cavernous
angioma and aneurysm.

Pathophysiology:

This condition is generated by spinal cord and splanchnic reflex


mechanisms that remain operative despite the spinal cord injury. The
triggering events produce afferent impulses that are transmitted to the
dorsal column and spinothalamic tracts. As these tracts ascend, they
synapse with sympathetic neurons in the intermediolateral columns and
generate a generalizes sympathetic reflex response. Normally, descending
supraspinal inhibitory signals modulate these autonomic reflexes, but
because of the spinal lesion above the sympathetic outflow, inhibitory
impulses cannot effectively descend in the sympathetic chain to block the
autonomic response. The result if peripheral and splanchnic vasoconstriction
and the development of acute hypertension. Sweating and piloerection also
occur as a result of the mass sympathetic discharge. With increase in blood
pressure, the aortic arch and carotid sinus receptors are stimulated, which
can result in reflex bradycardia and vasodilation above the level of lesion.

Clinical Manifestations:

• Bladder control. Your bladder will continue to store urine from your
kidneys. However, your brain may no longer be able to control bladder
emptying, as the message carrier (the spinal cord) has been injured.
The loss of bladder control increases your risk of urinary tract
infections. It may also cause kidney infection and kidney or bladder
stones. Drinking plenty of clear fluids may help. And during
rehabilitation, you'll learn new techniques to empty your bladder.
• Bowel control. Although your stomach and intestines work much like
they did before your injury, your brain may no longer be able to control
the muscles that open and close your anus. This may cause fecal
incontinence. A high-fiber diet may help regulate your bowels, and
you'll learn techniques to better control your bowels during
rehabilitation.
• Impaired skin sensation. Below the neurological level of your injury,
you may have lost part or all skin sensations. Therefore, your skin can't
send a message to your brain when it's injured by things such as
prolonged pressure, heat or cold. This can make you more susceptible
to pressure sores, but changing positions frequently — with help, if
needed — can help prevent these sores. And, you'll learn proper skin
care during rehabilitation, which can help you avoid these problems.
• Circulatory control. A spinal cord injury may cause circulatory
problems ranging from spinal shock immediately following your spinal
cord injury to low blood pressure when you rise (orthostatic
hypotension) to swelling of your extremities throughout your lifetime.
These circulation changes may increase your risk of developing blood
clots, such as deep vein thrombosis or a pulmonary embolus. Another
problem with circulatory control is a potentially life-threatening rise in
blood pressure (autonomic hyperreflexia). Your rehabilitation team will
teach you how to prevent autonomic hyperreflexia.
• Respiratory system. Your injury may make it more difficult to
breathe and cough if your abdominal and chest muscles are affected.
These include the diaphragm and the muscles in your chest wall and
abdomen. Your neurological level of injury will determine what kind of
breathing problems you may have. If you have cervical and thoracic
spinal cord injury you may have an increased risk of pneumonia or
other lung problems. Medications and therapy can treat these
problems.
• Muscle tone. Some people with spinal cord injuries may experience
one of two types of muscle tone problems: spastic muscles or flaccid
muscles. Spasticity can cause uncontrolled tightening or motion in the
muscles. Flaccid muscles are soft and limp, lacking muscle tone.
• Fitness and wellness. Weight loss and muscle atrophy are common
soon after a spinal cord injury. However, limited mobility after spinal
cord injury may lead to a more sedentary lifestyle, placing you at risk
of obesity, cardiovascular disease and diabetes. A dietitian can assist
you in attaining a nutritious diet to sustain an adequate weight.
Physical and occupational therapists can help you develop a fitness
and exercise program.
• Sexual health. Sexuality, fertility and sexual function may be affected
by spinal cord injury. Men may notice changes in erection and
ejaculation; women may notice changes in lubrication. A spinal cord
injury may cause decreased or absent sensation and movement below
the level of injury, but a person may notice a heightened sensitivity in
areas above the level of injury. Doctors, urologists and fertility
specialists who specialize in spinal cord injury can offer options for
sexual functioning and fertility.

There's usually no physical change in women with a spinal cord injury


that inhibits sexual intercourse or pregnancy. Most women with a
spinal cord injury can experience labor, have a normal delivery and
breast-feed.

• Pain. Some people may experience pain, such as muscle or joint pain
from overuse of particular muscle groups. Nerve pain, also known as
neuropathic or central pain, can occur after a spinal cord injury,
especially in someone with an incomplete injury.

Medical Management:

Unfortunately, there's no way to reverse damage to the spinal cord.


But, researchers are continually working on new treatments, including
innovative treatments, prostheses and medications that may promote nerve
cell regeneration or improve the function of the nerves that remain after a
spinal cord injury.

In the meantime, spinal cord injury treatment focuses on preventing


further injury and empowering people with a spinal cord injury to return to an
active and productive life.

You may be sedated so that you don't move and sustain more damage
while undergoing diagnostic tests for spinal cord injury.

If you do have a spinal cord injury, you'll usually be admitted to the


intensive care unit for treatment. You may even be transferred to a regional
spine injury center that has a team of neurosurgeons, orthopedic surgeons,
spinal cord medicine specialists, psychologists, nurses, therapists and social
workers with expertise in spinal cord injury.

• Medications. Methylprednisolone (Medrol) is a treatment option for an


acute spinal cord injury. If methylprednisolone is given within eight
hours of injury, some people experience mild improvement from their
spinal cord injury. It appears to work by reducing damage to nerve
cells and decreasing inflammation near the site of injury. However, this
is not a cure for a spinal cord injury.
• Immobilization. You may need traction to stabilize your spine, to bring
the spine into proper alignment or both. Sometimes, traction is
accomplished by securing metal braces, attached to weights or a body
harness, to your skull to keep your head from moving. In some cases, a
rigid neck collar also may work. A special bed also may help immobilize
your body.
• Surgery. Often, surgery is necessary to remove fragments of bones,
foreign objects, herniated disks or fractured vertebrae that appear to
be compressing the spine. Surgery may also be needed to stabilize the
spine to prevent future pain or deformity.

Medications.

Medications may be used to manage some of the effects of spinal cord


injury. These include medications to control pain and muscle spasticity, as
well as medications that can improve bladder control, bowel control and
sexual functioning.

New technologies.

Inventive medical devices can help people with a spinal cord injury
become more independent and more mobile. Some devices may also restore
function. These include:

• Modern wheelchairs. Improved, lighter weight wheelchairs are making


people with a spinal cord injury more mobile and more comfortable.
For some, an electric wheelchair may be needed. Some wheelchairs
can even climb stairs, travel over rough terrain and elevate a seated
passenger to eye level to reach high places without help.
• Computer adaptations. For someone that has limited hand function,
computers can be very powerful tools, but they're difficult to operate.
Some examples of computer adaptations range from simple to
complex, such as key guards or voice recognition.
• Electronic aids to daily living. Essentially any device that uses
electricity can be controlled with an electronic aid to daily living
(EADL). Devices can be turned on or off by switch or voice-controlled
and computer-based remotes.
• Electrical stimulation devices. These sophisticated devices use
electrical stimulation to produce actions. They're often called
functional electrical stimulation (FES) systems, and they use electrical
stimulators to control arm and leg muscles to allow people with a
spinal cord injury to stand, walk, reach and grip.

Nursing Care Plans:

1. Risk for ineffective breathing pattern related to impairment of


innervation of diaphragm secondary to spinal cord injury
2. Risk for trauma related to temporary weakness or instability of spinal
column secondary to spinal cord injury
3. Impaired physical mobility related to neuromuscular impairment
secondary to spinal cord injury
4. Distrubed sensory perception related to destruction of sensory tracts
with altered sensory reception, transmission, and integration
secondary to spinal cord injury
5. Acute pain related to physical injury secondary to spinal cord injury

Retinal Detachment
Description:
A retinal detachment is a separation of the retina from its attachments
to its underlying tissue within the eye. Most retinal detachments are a result
of a retinal break, hole, or tear. These retinal breaks may occur when the
vitreous gel pulls loose or separates from its attachment to the retina,
usually in the peripheral parts of the retina. The vitreous is a clear gel that
fills 2/3 of the inside of the eye and occupies the space in front of the retina.
As the vitreous gel pulls loose, it will sometimes exert traction on the retina,
and if the retina is weak, the retina will tear. Most retinal breaks are not a
result of injury. Retinal tears are sometimes accompanied by bleeding if a
retinal blood vessel is included in the tear.

Once the retina has torn, liquid from the vitreous gel can then pass through
the tear and accumulate behind the retina. The build-up of fluid behind the
retina is what separates (detaches) the retina from the back of the eye. As
more of the liquid vitreous collects behind the retina, the extent of the retinal
detachment can progress and involve the entire retina, leading to a total
retinal detachment. A retinal detachment almost always affects only one
eye. The second eye, however, must be checked thoroughly for any signs of
predisposing factors that may lead to detachment in the future.

Risk Factors:

Studies have shown that the incidence of retinal detachments caused


by tears in the retina is fairly low, affecting approximately one in 10,000
people each year. Many retinal tears do not progress to retinal detachment.
Nevertheless, many risk factors for developing retinal detachments are
recognized, including certain diseases of the eyes, cataract surgery, and
trauma to the eye. Retinal detachments can occur at any age. They occur
most commonly in younger adults (25 to 50 years of age) who are highly
nearsighted (myopic) and in older people following cataract surgery.

Pathophysiology:

Retinal detachment refers to separation of the inner layers of the


retina from the underlying retinal pigment epithelium (RPE, choroid). The
choroid is a vascular membrane containing large branched pigment cells
sandwiched between the retina and sclera. Separation of the sensory retina
from the underlying RPE occurs by the following 3 basic mechanisms:

• A hole, tear, or break in the neuronal layer allowing fluid from the
vitreous cavity to seep in between and separate sensory and RPE
layers (ie, rhegmatogenous RD)
• Traction from inflammatory or vascular fibrous membranes on the
surface of the retina, which tether to the vitreous
• Exudation of material into the subretinal space from retinal vessels
such as in hypertension, central retinal venous occlusion, vasculitis, or
papilledema

Retinal detachments may be associated with congenital malformations,


metabolic disorders, trauma (including previous ocular surgery), vascular
disease, choroidal tumors, high myopia or vitreous disease, or degeneration.

Of the 3 types of retinal detachment, rhegmatogenous RD is the most


common, deriving its name from rhegma, meaning rent or break. Vitreous
fluid enters the break and separates the sensory retina from the underlying
RPE, resulting in detachment.

Exudative or serous detachments occur when subretinal fluid accumulates


and causes detachment without any corresponding break in the retina. The
etiologic factors are often tumor growth or inflammation.

Tractional retinal detachment occurs as a result of adhesions between the


vitreous gel and the retina. Centripetal mechanical forces cause the
separation of the retina from the RPE without a retinal break. Advanced
adhesion may result in the development of a tear or break. The most
common causes of tractional retinal detachment are proliferative diabetic
retinopathy, sickle cell disease, advanced retinopathy of prematurity, and
penetrating trauma. Vitreoretinal traction increases with age, as the vitreous
gel shrinks and collapses over time, frequently causing posterior vitreous
detachments in approximately two thirds of persons older than 70 years.

Clinical Manifestations:

• Bright flashes of light, especially in peripheralperipheral vision


• Blurred visionBlurred vision
• Floaters in the eye
• Shadow or blindnessblindness in a part of the visual fieldvisual field of
one eye

Medical Management:

Retinal holes or tears can be treated with laser therapy or cryotherapy


(freezing) to prevent their progression to a full-scale detachment. Many
factors determine which holes or tears need to be treated. These factors
include the type and location of the defects, whether pulling on the retina
(traction) or bleeding is involved, and the presence of any of the other risk
factors discussed above. Three types of eye surgery are done for actual
retinal detachment: scleral buckling, pneumatic retinopexy, and vitrectomy.

Scleral buckling

For many years, scleral buckling has been the standard treatment for
detached retinas. The surgery is done in a hospital operating room with
general or local anesthesia. Some patients stay in the hospital overnight
(inpatient), while others go home the same day (outpatient). The surgeon
identifies the holes or tears either through the operating microscope or a
focusing headlight (indirect ophthalmoscope). The hole or tear is then
sealed, either with diathermy (an electric current which heats tissue), a
cryoprobe (freezing), or a laser. This results in scar tissue later forming
around the retinal tear to keep it permanently sealed, so that fluid no longer
can pass through and behind the retina. A scleral buckle, which is made of
silicone, plastic, or sponge, is then sewn to the outer wall of the eye (the
sclera). The buckle is like a tight cinch or belt around the eye. This
application compresses the eye so that the hole or tear in the retina is
pushed against the outer scleral wall of the eye, which has been indented by
the buckle. The buckle may be left in place permanently. It usually is not
visible because the buckle is located half way around the back of the eye
(posteriorly) and is covered by the conjunctiva (the clear outer covering of
the eye), which is carefully sewn (sutured) over it. Compressing the eye with
the buckle also reduces any possible later pulling (traction) by the vitreous
on the retina.

A small slit in the sclera allows the surgeon to drain some of the fluid
that has passed through and behind the retina. Removal of this fluid allows
the retina to flatten in place against the back wall of the eye. A gas or air
bubble may be placed into the vitreous cavity to help keep the hole or tear in
proper position against the scleral buckle until the scarring has taken place.
This procedure may require special positioning of the patient's head (such as
looking down) so that the bubble can rise and better seal the break in the
retina. The patient may have to walk, eat, and sleep with the head facing
down for two to four weeks to achieve the desired result.

Pneumatic retinopexy

Pneumatic retinopexy is a newer method for repairing retinal


detachments. It usually is performed on an outpatient basis under local
anesthesia. Again, laser or cryotherapy is used to seal the hole or tear. The
surgeon then injects a gas bubble directly inside the vitreous cavity of the
eye to push the detached retina against the back outer wall of the eye
(sclera). The gas bubble initially expands and then disappears over two to six
weeks. Proper positioning of the head in the postoperative time period is
crucial for success. Although this treatment is inappropriate for the repair of
many retinal detachments, it is simpler and much less costly than scleral
buckling. Furthermore, if pneumatic retinopexy is unsuccessful, scleral
buckling still can be performed.

Vitrectomy

Certain complicated or severe retinal detachments may require a more


complicated operation called a vitrectomy. These detachments include those
that are caused by the growth of abnormal blood vessels on the retina or in
the vitreous, as occurs in advanced diabetes. Vitrectomy also is used with
giant retinal tears, vitreous hemorrhage (blood in the vitreous cavity that
obscures the surgeon's view of the retina), extensive tractional retinal
detachments (pulling from scar tissue), membranes (extra tissue) on the
retina, or severe infections in the eye (endophthalmitis). Vitrectomy surgery
is performed in the hospital under general or local anesthesia. Small
openings are made through the sclera to allow positioning of a fiberoptic
light, a cutting source (specialized scissors), and a delicate forceps. The
vitreous gel of the eye is removed and replaced with a gas to refill the eye
and reposition the retina. The gas eventually is absorbed and is replaced by
the eye's own natural fluid. A scleral buckle is usually also performed with
the vitrectomy.

Nursing Care Plans:

1. Fear related to sensory impairment, loss of eyesight, scheduled


surgery, or inability to regain eyesight secondary to retinal
detachment
2. Risk for injury related to decreased vision secondary to retinal
detachment
3. Social Isolation related to decreased visual acuity, fear of injury,
or fear of embarassment secondary to retinal detachment
4. Self-Care Deficit (dressing/grooming) related to perceptual
impairment secondary to retinal detachment
5. Impaired Home Maintenance related to age, limited vision, or
activity restrictions imposed by surgery secondary to retinal
detachment

Glaucoma
Description:

Glaucoma is a disease in which the optic nerve is damaged, leading to


progressive, irreversible loss of vision. It is often, but not always, associated
with increased pressure of the fluid in the eye.

The nerve damage involves loss of retinal ganglion cells in a


characteristic pattern. There are many different sub-types of glaucoma but
they can all be considered a type of optic neuropathy. Raised intraocular
pressure is a significant risk factor for developing glaucoma (above 21
mmHg or 2.8 kPa). One person may develop nerve damage at a relatively
low pressure, while another person may have high eye pressure for years
and yet never develop damage. Untreated glaucoma leads to permanent
damage of the optic nerve and resultant visual field loss, which can progress
to blindness.

Glaucoma can be divided roughly into two main categories, "open


angle" and "closed angle" glaucoma. Closed angle glaucoma can appear
suddenly and is often painful; visual loss can progress quickly but the
discomfort often leads patients to seek medical attention before permanent
damage occurs. Open angle, chronic glaucoma tends to progress at a slower
rate and the patient may not notice that they have lost vision until the
disease has progressed significantly.

Glaucoma has been nicknamed the "silent thief of sight" because the
loss of vision normally occurs gradually over a long period of time and is
often only recognized when the disease is quite advanced. Once lost, this
damaged visual field cannot be recovered. Worldwide, it is the second
leading cause of blindness. It is also the first leading cause of blindness
among African Americans. Glaucoma affects 1 in 200 people aged fifty and
younger, and 1 in 10 over the age of eighty. If the condition is detected early
enough it is possible to arrest the development or slow the progression with
medical and surgical means.

Risk Factors:

• Age over 45 years


• Family history of glaucoma
• Black racial ancestry
• Diabetes
• History of elevated intraocular pressure
• Nearsightedness (high degree of myopia), which is the inability to see
distant objects clearly
• History of injury to the eye
• Use of cortisone (steroids), either in the eye or systemically (orally or
injected)
• Farsightedness (hyperopia), which is seeing distant objects better than
close ones (Farsighted people may have narrow filtering angles, which
predispose them to acute (sudden) attacks of closed-angle glaucoma.)

Pathophysiology:

The major risk factor for most glaucomas and focus of treatment is
increased intraocular pressure. Intraocular pressure is a function of
production of liquid aqueous humor by the ciliary processes of the eye and
its drainage through the trabecular meshwork. Aqueous humor flows from
the ciliary processes into the posterior chamber, bounded posteriorly by the
lens and the zonules of Zinn and anteriorly by the iris. It then flows through
the pupil of the iris into the anterior chamber, bounded posteriorly by the iris
and anteriorly by the cornea. From here the trabecular meshwork drains
aqueous humor via Schlemm's canal into scleral plexuses and general blood
circulation. In open angle glaucoma there is reduced flow through the
trabecular meshwork; in angle closure glaucoma, the iris is pushed forward
against the trabecular meshwork, blocking fluid from escaping.

The inconsistent relationship of glaucomatous optic neuropathy with ocular


hypertension has provoked hypotheses and studies on anatomic structure,
eye development, nerve compression trauma, optic nerve blood flow,
excitatory neurotransmitter, trophic factor, retinal ganglion cell/axon
degeneration, glial support cell, immune, and aging mechanisms of neuron
loss.
Clinical Manifestations:

HEENT:

• Diminished field of vision (+)


• Decreased accomodation (+)
• Pale optic disc
• Reports halos around lights (+)
• Moderately dilated, nonreactive pupil (+)
• Reports aching pain (+)

Medical Management:

Intraocular pressure can be lowered with medication, usually eye


drops. There are several different classes of medications to treat glaucoma
with several different medications in each class.

Each of these medicines may have local and systemic side effects.
Adherence to medication protocol can be confusing and expensive; if side
effects occur, the patient must be willing either to tolerate these, or to
communicate with the treating physician to improve the drug regimen.
Initially, glaucoma drops may reasonably be started in either one or in both
eyes.

Poor compliance with medications and follow-up visits is a major


reason for vision loss in glaucoma patients. A 2003 study of patients in an
HMO found that half failed to fill their prescription the first time and one in
four failed to refill their prescriptions a second time. Patient education and
communication must be ongoing to sustain successful treatment plans for
this lifelong disease with no early symptoms.

The possible neuroprotective effects of various topical and systemic


medications are also being investigate. Prostaglandin analogs like
latanoprost (Xalatan), bimatoprost (Lumigan) and travoprost (Travatan)
increase uveoscleral outflow of aqueous humor. Bimatoprost also increases
trabecular outflow

• Topical beta-adrenergic receptor antagonists such as timolol,


levobunolol (Betagan), and betaxolol decrease aqueous humor
production by the ciliary body.
• Alpha2-adrenergic agonists such as brimonidine (Alphagan) work by a
dual mechanism, decreasing aqueous production and increasing
trabecular outflow.
• Less-selective sympathomimetics such as epinephrine decrease
aqueous humor production through vasoconstriction of ciliary body
blood vessels.
• Miotic agents (parasympathomimetics) like pilocarpine work by
contraction of the ciliary muscle, tightening the trabecular meshwork
and allowing increased outflow of the aqueous humour. Ecothiopate is
used in chronic glaucoma.
• Carbonic anhydrase inhibitors like dorzolamide (Trusopt), brinzolamide
(Azopt), acetazolamide (Diamox) lower secretion of aqueous humor by
inhibiting carbonic anhydrase in the ciliary body.
• Physostigmine is also used to treat glaucoma and delayed gastric
emptying.

Surgery:

Generally, these operations are a temporary solution, as there is not yet a


cure for glaucoma.

Canaloplasty

Canaloplasty is a nonpenetrating procedure utilizing microcatheter


technology. To perform a canaloplasty, an incision is made into the eye to
gain access to Schlemm's canal in a similar fashion to a viscocanalostomy. A
microcatheter will circumnavigate the canal around the iris, enlarging the
main drainage channel and its smaller collector channels through the
injection of a sterile, gel-like material called viscoelastic. The catheter is then
removed and a suture is placed within the canal and tightened. By opening
the canal, the pressure inside the eye may be relieved, although the reason
is unclear since the canal (of Schlemm) does not have any significant fluid
resistance in glaucoma or healthy eyes. Long-term results are not available.

Laser surgery

Laser trabeculoplasty may be used to treat open angle glaucoma. It


is a temporary solution, not a cure. A 50 μm argon laser spot is aimed at the
trabecular meshwork to stimulate opening of the mesh to allow more outflow
of aqueous fluid. Usually, half of the angle is treated at a time. Traditional
laser trabeculoplasty utilizes a thermal argon laser. The procedure is called
Argon Laser Trabeculoplasty or ALT. A newer type of laser trabeculoplasty
exists that uses a "cold" (non-thermal) laser to stimulate drainage in the
trabecular meshwork. This newer procedure which uses a 532 nm frequency-
doubled, Q-switched Nd:YAG laser which selectively targets melanin pigment
in the trabecular meshwork cells, called Selective Laser Trabeculoplasty or
SLT. Studies show that SLT is as effective as ALT at lowering eye pressure. In
addition, SLT may be repeated three to four times, whereas ALT can usually
be repeated only once.

Trabeculectomy

The most common conventional surgery performed for glaucoma is the


trabeculectomy. Here, a partial thickness flap is made in the scleral wall of
the eye, and a window opening made under the flap to remove a portion of
the trabecular meshwork. The scleral flap is then sutured loosely back in
place. This allows fluid to flow out of the eye through this opening, resulting
in lowered intraocular pressure and the formation of a bleb or fluid bubble on
the surface of the eye. Scarring can occur around or over the flap opening,
causing it to become less effective or lose effectiveness altogether. One
person can have multiple surgical procedures of the same or different types.

Nursing Care Plans:


1. Disturbed visual Sensory Perception related to altered status of sense
organs secondary to glaucoma
2. Anxiety related to change in health status secondary to glaucoma
3. Deficient Knowledge regarding condition related to lack of
exposure/unfamiliarity with resources secondary to glaucoma
4. Low Self-Esteem related to perception of helplessnes secondary to
glaucoma
5. Impaired physical mobility related to perceptual or cognitive
impairment secondary to glaucoma

Otitis Media
Description:

Otitis media is inflammation of the middle ear. "Otitis" means


inflammation of the ear, and "media" means middle. This inflammation often
begins with infections that cause sore throats, colds or other respiratory
problems, and spreads to the middle ear. These can be caused by viruses or
bacteria, and can be acute or chronic.

Acute otitis media is usually of rapid onset and short duration. Acute
otitis media is typically associated with fluid accumulation in the middle ear
together with signs or symptoms of ear infection; a bulging eardrum usually
accompanied by pain, or a perforated eardrum, often with drainage of
purulent material (pus). Fever can be present.

Chronic otitis media is a persistent inflammation of the middle ear,


typically for a minimum of a month. This is in distinction to an acute ear
infection (acute otitis media) that usually lasts only several weeks. Following
an acute infection, fluid (an effusion) may remain behind the ear drum
(tympanic membrane) for up to three months before resolving. Chronic otitis
media may develop after a prolonged period of time with fluid (effusion) or
negative pressure behind the eardrum (tympanic membrane). Chronic otitis
media can cause ongoing damage to the middle ear and eardrum and there
may be continuing drainage through a hole in the eardrum. Chronic otitis
media often starts painlessly without fever. Ear pressure or popping can be
persistent for months. Sometimes a subtle loss of hearing can be due to
chronic otitis media.

Risk Factors:

Upper respiratory infections predispose to acute otitis media. Exposure


to groups of children (as in child care centers) results in more frequent colds,
and therefore more earaches. Exposure to air with irritants, such as tobacco
smoke, also increases the chance of otitis media. Children with cleft palate or
Down syndrome are prone to ear infections. Children who have episodes of
acute otitis media before six months of age tend to have more ear infections
later in childhood.

Pathophysiology:

The three most common forms of otitis media are acute otitis media,
chronic otitis media, and serous otitis media. Each type affects the middle
ear but has slightly different causes, incidences, and pathologic changes. If
otitis progresses or remains untreated, permanents conductive hearing loss
may occur. Otitis media is less common in adults than in children.

Acute otitis media and chronic otitis media, also known as supprant or
purulent otitis media, are similar. An infecting agent introduced into the
middle ear causes inflammation of the mucosa, leading to swelling and
irritaion of the ossicles within the middle ear. A purulent inflammatory
exudate follows. Acute disease has a sudden onset and a duration of 3 weeks
or less. Chronic otitis media often follows repeated acute episodes, has a
longer duration, and causes greated middle-ear injury.

The eustachian tube and mastoid, connected to the middle ear by a


sheet of cells, are also affected by the infection. If the eardrum membrane
perforates and infective materials spill into the external ear, external otitis
also develops, which thickens and scars the middle ear if left untreated.
Necrosis of the ossicles destroys middle-ear structures.

Clinical Manifestations:

• Unusual irritability
• Difficulty sleeping
• Tugging or pulling at one or both ears
• Fever
• Fluid draining from the ear
• Loss of balance

Medical Management:

To treat the pain caused by otitis media oral as well as topical analgesics are
effective. Oral agents may include ibuprofen, acetaminophen, or narcotics.
Topical agents shown to be effective include antipyrine and benzocaine ear
drops.

Antibiotics

Many guidelines suggest deferring the start of antibiotics in acute bacterial


otitis media for one to three days if pain is manageable with the above
measures. This is recommended for a number of reasons including: two out
of three children with acute otitis media resolve without antibiotic treatment,
no adverse effect on long term outcomes have been found when treatment
is withheld, antibiotics have significant rates of potential side effects, and a
recent trial has found increased rates of recurrence of otitis in children who
were treated with antibiotics.

The first line antibiotic treatment, if warranted, is amoxicillin. If the bacteria


is resistant, then amoxicillin-clavulanate or another penicillin derivative plus
beta lactamase inhibitor is second line. Five days of treatment has been
found to be as effective as ten days in otherwise healthy children.

Azithromycin has been shown to be as effective in treatment of AOM as


amoxicillin. Cases were resolved in 80% of children less than two years of
age. Treatment with azithromycin also showed greater patient compliance
compared with amoxicillin, as well as being associated with less occurrence
of diarrhea.

Nursing Care Plans:

1. Deficient Knowledge related to treatment and prevention secondary to


otitis media
2. Actiity Intolerance related to pain secondary to otitis media
3. Social Isolation related to pain and decreased hearing secondary to
otitis media
4. Risk for Injury related to altered auditory perception and infection
secondary to otitis media
5. Acute Pain related to an inflammatory process and fluid in the middle
ear secondary to otitis media

Meniere’s Disease
Description:

Ménière's disease is a disorder of the inner ear that can affect


hearing and balance to a varying degree. It is characterized by episodes of
vertigo and tinnitus and progressive hearing loss, usually in one ear. It is
named after the French physician Prosper Ménière, who first reported that
vertigo was caused by inner ear disorders in an article published in 1861.
The condition affects people differently; it can range in intensity from being a
mild annoyance to a chronic, lifelong disability.

Risk Factors:
• Age: 20 to 60
• Race: Caucasian
• Family history of Meniere's disease
• Stress
• Allergies
• Excess salt in the diet
• Excess noise

Pathophysiology:

Ménière's disease has three features: tinnitus, one-sided


sensorineural hearing loss, and vertigo, occuring in attacks that can last for
several days. Clients are almost totally incapacitated during an attack, and
several days are needed for full recovery. The pathology of Ménière's
disease is either overproduction or decreased reabsorption of endolymphatic
fluid, causing a distortion of the entire inner-canal system. This distortion
decreases hearing from dilation of the cochlear duct, vertigo because of
damage to the vestibular system, and tinitus from unknown cause. The inital
hearing loss is reversible, but repeated damage to the cochlea from
increased fluid pressure, leads to permanent hearing loss.

The cause of Ménière's disease is unknown but it often occurs with


infections, allergic reactions, and fluid imbalances. Long-term stress may
have role in Ménière's disease.

Clinical Manifestations:

• Episodes of vertigo (spinning sensation), often accompanied by:


o Nausea or vomiting
o Sweating
o Paleness of the skin
o Weakness or falling
o In some cases, headache or diarrhea
• Hearing loss may worsen during attacks of vertigo
• Tinnitus (ringing in the ears)
• Feeling of fullness or pressure in the ear
• Poor sense of balance
• A tendency for symptoms to worsen with movement

Medical Management:

Medications include:

• Drugs to treat vertigo, such as meclizine or scopolamine


• Antiemetics—medications to help control nausea
• Other medications that may improve hearing, control inner ear
swelling, or limit overall symptoms, including:
o Antihistamines
o Cortisone drugs for a short time
o Antidepressants or antianxiety medications
o Diuretics
• Aminoglycoside therapy (such as streptomycin or gentamicin) to
permanently destroy the part of the inner ear that deals with balance

Surgery:
• Endolymphatic sac decompression—removal of a portion of inner ear
bone and placing a tube in the inner ear to drain excess fluid
• Labyrinthectomy—destruction or removal of the entire inner ear, which
controls balance and hearing
• Vestibular nerve section

Nursing Care Plans:

1. Anxiety related to loss of control


2. Risk for Injury related to loss of balance
3. Powerlessness related to loss of control
4. Activity Intolerance related to perception of dizziness
5. Risk for Deficient Fluid Volume related to nausea and vomiting