CASE PRESENTATION

Otosclerosis












SUBMITTED TO : Mrs. Sukhpal kaur
Lecturer, N.I.N.E
P.G.I.M.E.R, Chandigarh

Submitted by:


MS. Davinder kaur, M.Sc 1st year
11/2/2010

Otosclerosis

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CASE PRESENTATION

BIODATA OF PATIENT

Name Jaswinder singh
Age 22 yrs
Sex Male
C.R No 524341
Marital Status Unmarried
Ward/Bed No ENT /35
Address VPO Mahilpur
Religion Sikh
Education Graduation
Occupation Not working
Monthly Family income 2501-5000
Date of Admission 12/07/09
Consultant Prof. S.Prbhakr
Diagnosis Otosclerosis

Chief Complaints
H/O decresed hearing x 25 days
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History of Present Illness
Jaswinder singh 22 yrs old male patient was admitted to PGI Chandigarh with
complaints of decresed hearings. Relieved with medication taken from some local
RMP. 2 Days before admission he was taken to some local hospital from where she
was refered to PGI for treatment.
History of Past illness
No H/O Diabetes, Hypertension,Tuberculosis, Bronchial Asthma or any other chronic
illness.
Family History
Patiemt lives in joint Family. There are total 8 members in her family. There is no history
of DM/TB/HT or any other illness in family members.
Health facility near home.
Patient lives in a villege near Patiala. There is a local dispensary near patients home.
Housing
Patient lives in her own pucca house. There are total 2 rooms. Indian toilet facility is
there. Source of drinking water is from tap and hand pump.
Patients sensitivity/allergy/precaution
Patient was not allergic to any drug, food material.
Personal History
Patient is vegetarian, usually had 3 meals per day. Bt due to fever and vomiting she had
anorexia for 4 to 5 days. She used to have 8 to 10 hrs of sleep at home.

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Elimination:
Patient used to have normal bowel movement. He had retention of urine one day before
admission.
Mobility and exercise
He dont have walking habits. He is a privte student of graduation. She used to help her
mother in household activities.


GENERAL PHYSICAL EXAMINATION

HEAD TO TOE ASSESSMENT
General Appeaarance: Thin built
Sensorium : Conscious
Posture : Normal
Vital Signs
Temp 38
o
c Pulse 90/min resp-18/min B.P- 126/90 mm of Hg
Skin The condition of skin is dry, pale. She And iv cannula.
Hair
Hair are clean, black and long. No pediculli or dandruff.
Eyes
Eyes are black in colour with no discharge, redness, swelling. Patient has normal 6/6
vision without spectacles.
ENT
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No discharge from ear or nose. No DNS. Patient has nasogastric tube and tracheostomy
tube.
Oral mucosa
Dental caries present in last molar tooth, gums are healthy without swelling and bleeding.
Glands
Lymph nodes are not enlarged
Chest
Shape is normal with symmetrica l chest movements. No dyspnea, orthopnea present.
Abdomen
Abdomen is flat , hard,& tender , due to constipation. Patient feels pain in umbilical
region.
Limbs
Upper limbs
Full range of motion is present in both the upper limbs.
Lower limbs
Weakness of lower limbs present. There is decreased muscle strength and tone. Power of
right lower limb is 1/5 and of left lower limb is 2/5.
Back
Patient feels pain and discomfort in back due to prolonged bed rest. There is no
tenderness. Shape and curvature of spine is normal. No lordosis, kyphosis, scoliosis.

Systemic examination
Nervous system
Cranial nerves: All the cranial nerves are intact.
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Motor system
Muscle tone and strength is decresed in lower limbs ( 1/5)
DTRs are diminished
Respiratory system:
Bilateal breath sounds are equal. No adventitious sounds: wheezing, crepts are absent.
RR: 20/min
Circulatory system
S1 & S2 normal. Hear rate : 92/min


Gastrointestinal system
Bowel sounds are present. Patient feels tenderness at umbilical region.
No bruits present
Musculoskeletal system:
Full range of motion present in upper limbs .
Urinary system
No urinary retention.






Otosclerosis

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Description of Disease
Definition
Otosclerosis involves the stapes and is thought to result from the formation of new,
abnormal spongy bone, especially around the oval window, with resulting fixation of the
stapes. The efficient transmission of sound is prevented because the stapes cannot vibrate
and carry the sound as conducted from the malleus and incus to the inner ear.

Prevalance and incidence
Otosclerosis is the most frequent cause of middle ear hearing loss in young adults
otosclerosis affects about 1 or 2 of 100 people in India. It usually first develops between
the ages of 15 and 35, but sometimes develops in younger children. Women are affected
twice as often as men. Pregnancy is not a cause but may make the condition worse, so
symptoms are commonly first noticed during pregnancy.. Deafness due to otosclerosis
may be initiated or made worse by pregnancy.
Etiology
Many theories have been proposed to explain the etiological factors of
otosclerosis. They are:

1. Metabolic

2. Immune disorders

3. Vascular disease

4. Infection (Measles) currently accepted

5. Trauma : The petrous bone doesnot have regenerative capacity. This is because of the
fact that the enzymes released during reparative phase are very toxic to the inner ear hair
cells.
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Pockets of tissue capable of regeneration may be sequestered in various portions of
labyrinthine bone. These tissue could be activated by the presence of regenerative
enzymes in the blood following bone fracture elsewhere in the body.
6. Temporal bone abnormalities (congenital)

Genetic factors predisposing to otosclerosis: The tendency for otosclerosis to run in
families has been documented. Authors have postulated an autosomal dominant mode of
inheritance with varying degrees of penetration.
Otosclerosis is associated with osteogenesis imperfecta in 0.15 % of cases. This is
known as Van der Hoeve syndrome or Adair - Dighton syndrome
Types of otosclerosis:
Accoridng to effect on area
1. Histological otosclerosis: Otosclerotic foci does not cause any symptoms and
hence known as histological otosclerosis.
2. Stapedial otosclerosis: is the classical otosclerosis with fixation of stapedial foot
plate causing conductive deafness.
3. Cochlear otosclerosis: The foci involves the cochlea causing sensorineural
deafness.
4. Combined otosclerosis: Here in addition to fixation of foot plate of stapes there is
also associated sensorineural hearing loss due to involvement of cochlea.
Classification of various clinical types of otosclerosis is based on microscopic
appearances of the diseased foot plate.

Rim fixation: Here the otosclerotic foci starts from the anterior portion of the oval
window niche. It gradually expands to involve the anterior portion of the foot plate
causing fixation of the anterior portion of the foot plate only leaving the centre of the
plate free.
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Biscuit foot plate: This type occur less frequently. The focus originates in the foot plate
itself and as it expands it gives rise to the biscuit or rice grain foot plate with delineated
margins.

Obliterative otosclerosis: Rarely a large mass of otosclerotic new bone fills up the oval
window niche obscuring the entire foot plate. This condition is known as obliterative
otosclerosis. It is a difficult condition to manage surgically


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Pathophysiology
Formation of spongy bony starts from bony labyrinth
Fixation of footoplate
Poor conduction of sound
Hearing loss


Clinical Manifestations

According to Book According to Patient
Deafness
Many people with otosclerosis first notice that
they cannot hear low-pitched sounds or that they
can no longer hear a whisper.

Present

get tinnitus (a ringing sound in your ears Present
Rarely mild vertigo Absent
Paracusis is common. This means you tend to
hear better when there is a lot of background
noise. For example, when talking to someone in
a pub or cafe that is full of other people
Absent



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Diagnostic tests

According to Book According to Patient
Otoscopic examination Otosclerosis may reveal a reddish blush
of the tympanum (schwatrzs
sign)caused by the vascular and bony
changes within middle ear .
Tuning fork tests

In rinnes test heraing longer when the
tuning fork is touched on mastiod
process than placed on next to ear.
Webers test :sound is better through the
skull bone in the ear with the greater
conductive hearing loss than through the
skull bone in the ear with greater
conductive hearing loss than through
air.

Audiogram
Done
Tympanometry
Not Done









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Management
Medical management :
Hearing loss associated with otosclerosis may stabilized by the use of sodium fluride with
vitamin D caco
3
to retard bone growth resorption and encourage ccalcification of bone
lesions can be effective for because ethe inner ear is intact.

Surgical treatment:
Stapdectomy : Stapedectomy is a microsurgical procedure. The operation can be done
through the ear canal. Anaesthesia can be either general (completely asleep), or local (the
ear being anaesthesized with an injection). An incision is made in the ear canal near the
ear drum. The ear drum is then carefully raised and the ear surgeon uses the operating
microscope to see the structures in detail. The middle ear is now opened. The bones of
hearing are evaluated, confirming the surgeon's diagnosis of otosclerosis.
The calcium deposit is usually visible, and the stapes bone is tested. It does not move
when pressed. The stapes bone is now separated from the incus (anvil.)
Freed from the stapes, the incus and malleus (hammer) bones can now move when
pressed. A laser or other micro instrument vaporizes the tendon and the arch of the stapes
bone, and the stapes bone remnant is removed from the middle ear.
The window that joins the middle ear to the inner ear and which serves as a platform for
the stapes bone, is now opened. With a very low power setting, the laser is directed at the
window and a miniscule opening (.6 mm or 1/40") is made. Once the opening is made in
the window, the artificial bone (prosthesis) is placed onto the incus bone and gently
inserted. The prosthesis is then clipped gently onto the incus and the new assembly is
gently pressed to confirm that its movement is correct. A piece of fat or other tissue is
taken from a small incision behind the ear lobe and used to help seal the hole in the
window and the space around the prosthesis. The ear drum is then folded back into its
normal position and held down with a small gelatin sponge.
Stapedotomy
A modified stapes operation, called a stapedotomy, is thought by many otologic
surgeons to be safer and reduce the chances of postoperative complications. In
stapedotomy, instead of removing the whole stapes footplace, a tiny hole is made in the
footplate - either with a microdrill or with a laser,and a prosthesis is placed to touch this
area with movement of the tympanic membrane. This procedure greatly reduces the
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chance of a perilymph fistula (leakage of cochlear fluid) and can be further improved by
the use of a tissue graft seal of the fenestra.
Laser stapedotomy is a well-established surgical technique for treating conductive
hearing loss due to otosclerosis. The procedure creates a tiny opening in the stapes (the
smallest bone in the human body) in which to secure a prosthetic. The CO2 laser allows
the surgeon to create very small, precisely placed holes without increasing the
temperature of the inner ear fluid by more than one degree, making this an extremely safe
surgical solution. The hole diameter can be predetermined according to the prosthesis
diameter. Treatment can be completed in a single office visit using anesthesia.
[5]

Surgery is performed under local anasthesia with sedation.the ear with poor hearing is
treated first and other ear may be operated on 6 months to one year later.an endural
incision is made using the operating microscope for visualisation.gelfoam is used on the
incision flap to liomit bleeding . a cooton ball is placed in the ear canal and a small
covering is used to cover the ear.
During the surgery the patient will reoprt an immediate improvement in hearing in the
operative ear. Because of the accumulation of blood and fluid in the middle ear, the
hearing level decreases postoperatively, but will improve with healing.after stapdectomy
90% of the patients experience improvement in hearing ,in many instances to near
normal.

Complications of stapedectomy:
Facial palsy
Vertigo in the immediate post op period
Vomiting
Perilymph gush
Floating foot plate
Tympanic membrane tear
Dead labyrinth
Perilymph fistula
Labyrinthitis
Granuloma (Reparative)
Granuloma (Reparative
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(Prognosis)
Otosclerosis gets worse without treatment, but surgery may restore at least partial
hearing. Most complications of surgery get better by themselves within a few weeks.
To reduce the risk of complications after surgery:
Do NOT blow your nose for 1 week after surgery.
Avoid people with respiratory or other infections.
Avoid bending, lifting, or straining, which may cause dizziness.
Avoid loud noises or sudden pressure changes such as scuba diving, flying, or
driving in the mountains until healed.
If surgery is unsuccessful, total hearing loss may occur. Treatment then involves
developing skills to cope with deafness, including use of hearing aids and visual cues.



DRUG PRESENTATION
Calcium carbonate
I NDI CATI ONS
PO, IV: Treatment and prevention of hypocalcemia
PO: Adjunct in the prevention of postmenopausal osteoporosis
IV: Emergency treatment of hyperkalemia and hypermagnesemia and adjunct in
cardiac arrest (calcium chloride, calcium gluconate)
Calcium carbonate: May be used as an antacid
ACTI ON
Essential for nervous, muscular, and skeletal systems
Maintain cell membrane and capillary permeability
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Act as an activator in the transmission of nerve impulses and contraction of
cardiac, skeletal, and smooth muscle
Essential for bone formation and blood coagulation.
Therapeutic Effects:
o Replacement of calcium in deficiency states.
PHARMACOKI NETI CS
Absorption: Absorption from the GI tract requires vitamin D. IV administration results
in complete bioavailability.
Distribution: Readily enters extracellular fluid. Crosses the placenta and enters breast
milk.
Metabolism and Excretion: Excreted mostly in the feces; 20% eliminated by the
kidneys.
Half-life: Unknown.
CONTRAI NDI CATI ONS AND PRECAUTI ONS
Contraindicated in:
Hypercalcemia
Renal calculi
Ventricular fibrillation.
Use Cautiously in:
Patients receiving digitalis
glycosides
Severe respiratory insufficiency
Renal disease
Cardiac disease.
ADVERSE REACTI ONS AND SI DE EFFECTS*
CNS: syncope (IV only), tingling.
CV: CARDIAC ARREST (IV only) , arrhythmias , bradycardia.
GI: constipation , nausea, vomiting.
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GU: calculi, hypercalciuria.
Local: phlebitis (IV only) .
I NTERACTI ONS
DrugDrug:
Hypercalcemia increases the risk of digoxin toxicity
Chronic use with antacids in renal insufficiency may lead to milk-alkali syndrome
Ingestion by mouth decreases the absorption of orally administered tetracyclines ,
fluoroquinolones , phenytoin , and iron salts
Excessive amounts may decrease the effects of calcium channel blockers
Decreases absorption of etidronate and risedronate (do not take within 2 hr of
calcium supplements)
May decrease the effectiveness of atenolol
Concurrent use with diuretics (thiazide) may result in hypercalcemia
May decrease the ability of sodium polystyrene sulfonate to decrease serum
potassium.
DrugFood:
Cereals , spinach , or rhubarb may decrease the absorption of calcium
supplements
Calcium acetate should not be given concurrently with other calcium supplements.
ROUTE AND DOSAGE
Doses are expressed in mg, g, or mEq of calcium.
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PO (Adults): Prevention of hypocalcemia, treatment of depletion, osteoporosis
12 g/day. Antacid 0.51.5 g as needed (calcium carbonate only).
PO (Children): Supplementation 4565 mg/kg/day.
PO (Infants): Neonatal hypocalcemia 50150 mg/kg (not to exceed 1 g).
IV (Adults): Emergency treatment of hypocalcemia, cardiac standstill 714
mEq. Hypocalcemic tetany 4.516 mEq; repeat until symptoms are controlled.
Hyperkalemia with cardiac toxicity 2.2514 mEq; may repeat in 12 min.
Hypermagnesemia 7 mEq.
IV (Children): Emergency treatment of hypocalcemia 17 mEq. Hypocalcemic
tetany 0.50.7 mEq/kg 34 times daily.
IV (Infants): Emergency treatment of hypocalcemia <1 mEq. Hypocalcemic
tetany 2.4 mEq/kg/day in divided doses..
.
TIME/ACTION PROFILE (effects on serum calcium)

ONSET PEAK DURATION

PO unknown unknown unknown
IV immediate immediate 0.52 hr

NURSI NG I MPLI CATI ONS
ASSESSMENT
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Calcium Supplement/Replacement: Observe patient closely for symptoms of
hypocalcemia (paresthesia, muscle twitching, laryngospasm, colic, cardiac
arrhythmias, Chvosteks or Trousseaus sign). Notify physician or other health care
professional if these occur. Protect symptomatic patients by elevating and padding
siderails and keeping bed in low position.
o Monitor blood pressure, pulse, and ECG frequently throughout parenteral
therapy. May cause vasodilation with resulting hypotension, bradycardia,
arrhythmias, and cardiac arrest. Transient increases in blood pressure may
occur during IV administration, especially in geriatric patients or in patients
with hypertension.
o Assess IV site for patency. Extravasation may cause cellulitis, necrosis, and
sloughing.
o Monitor patient on digitalis glycosides for signs of toxicity.
Antacid: When used as an antacid, assess for heartburn, indigestion, and
abdominal pain. Inspect abdomen; auscultate bowel sounds.
Lab Test Considerations: Monitor serum calcium or ionized calcium, chloride,
sodium, potassium, magnesium, albumin, and parathyroid hormone (PTH)
concentrations before and periodically throughout therapy for treatment of
hypocalcemia.
o May cause decreased serum phosphate concentrations with excessive and
prolonged use. When used to treat hyperphosphatemia in renal failure
patients, monitor phosphate levels.
Toxicity and Overdose: Assess patient for nausea, vomiting, anorexia, thirst,
severe constipation, paralytic ileus, and bradycardia. Contact physician or other
health care professional immediately if these signs of hypercalcemia occur.
POTENTIAL NURSING DIAGNOSES
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Nutrition, imbalanced: less than body requirements (Indications).
Injury, risk for , related to osteoporosis or electrolyte imbalance (Indications).
IMPLEMENTATION
High Alert : Errors with IV calcium gluceptate, gluconate, and chloride have
occurred secondary to confusion over which salt is ordered. Clarify incomplete
orders. Confusion has occurred with milligram doses of calcium chloride, calcium
gluconate, and calcium gluceptate, which are not equal. Chloride and gluconate
forms are routinely available on most hospital crash carts; physician should specify
form of calcium desired. Doses should be expressed in mEq.
General: Do not confuse Os-Cal (calcium carbonate) with Asacol (mesalamine).
o In arrest situations, the use of calcium chloride is now limited to patients
with hyperkalemia, hypocalcemia, and calcium channel blocker toxicity.
PO: Administer calcium carbonate or phosphate 11.5 hr after meals and at
bedtime. Chewable tablets should be well chewed before swallowing. Dissolve
effervescent tablets in glass of water. Follow oral doses with a full glass of water,
except when using calcium carbonate as a phosphate binder in renal dialysis.
Administer with meals for patients with hyperphosphatemia.
IM: IM administration of calcium gluconate and calcium gluceptate may be
tolerated in an emergency if IV administration is not feasible. For child, administer
only in thigh. For adult, administer only in gluteal region. Do not administer
calcium chloride IM.
IV: IV solution should be warmed to body temperature and given through a small-
bore needle in a large vein to minimize phlebitis. Do not administer through a scalp
vein. May cause cutaneous burning sensation, peripheral vasodilation, and drop in
blood pressure. Patient should remain recumbent for 3060 min after IV
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administration. High Alert : Administer slowly. High concentrations may cause
cardiac arrest.
o If infiltration occurs, discontinue IV. May be treated with application of
heat, elevation, and local infiltration of normal saline, 1% procaine HCl, or
hyaluronidase.
o Rapid administration may cause tingling, sensation of warmth, and a
metallic taste. Halt infusion if these symptoms occur, and resume infusion at
a slower rate when they subside.
o Do not administer solutions that are not clear or that contain a precipitate.
PATIENT/FAMILY TEACHING
General: Instruct patient not to take enteric-coated tablets within 1 hr of calcium
carbonate; this will result in premature dissolution of the tablets.
o Do not administer concurrently with foods containing large amounts of
oxalic acid (spinach, rhubarb), phytic acid (brans, cereals), or phosphorus
(milk or dairy products). Administration with milk products may lead to
milk-alkali syndrome (nausea, vomiting, confusion, headache). Do not take
within 12 hr of other medications if possible.
o Instruct patients on a regular schedule to take missed doses as soon as
possible, then go back to regular schedule.
o Advise patient that calcium carbonate may cause constipation. Review
methods of preventing constipation (increasing bulk in diet, increasing fluid
intake, increasing mobility) and using laxatives. Severe constipation may
indicate toxicity.
o Advise patient to avoid excessive use of tobacco or beverages containing
alcohol or caffeine.
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Calcium Supplement: Encourage patients to maintain a diet adequate in vitamin
D (see Appendix Q).
Osteoporosis: Advise patients that exercise has been found to arrest and reverse
bone loss. Patient should discuss any exercise limitations with health care
professional before beginning program



NURSING MANAGEMENT

NURSING DIAGNOSIS
Ineffective breathing pattern and impaired gas exchange related to respiratory
muscle weakness / paralysis

Impaired communication related to deafness

Self care deficit related to neuromuscular impairment

Imbalanced nutrition less than bodys requirement related to inability to ingest and
digest food

Impaired physical mobility related to paralysis

Fear and anxiety related to loss of control and paralysis

Risk for ineffective coping related to physiological changes/psychological
conflicts/multiple life changes/ inadequate coping methods

Ineffective family coping related to situational crisis
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Knowledge deficit regarding conditions, prognosis,complications, treatment,self
care related to lack of exposure/ unfamiliarity with the information resources
SUMMARY
Jaswinder kaur 22 yrs old female patient was admitted with complaints of hearing loss
.stapdectomy was planned for her

















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8. http://www.nhlbi.nih.gov/health/dci/Diseases/hvd/hvd_whatis.html