CASE PRESENTATION

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

Submitted by:MS. Davinder kaur, M.Sc 1st year11/2/2010

CASE PRESENTATION

BIODATA OF PATIENT

NameJaswinder singhAge22 yrsSexMaleC.R No524341Marital StatusUnmarriedWard/Bed NoENT /35AddressVPO MahilpurReligionSikhEducationGraduationOccupationNot workingMonthly Family income2501-5000Date of Admission12/07/09ConsultantProf. S.PrbhakrDiagnosisOtosclerosis

Chief ComplaintsH/O decresed hearing x 25 days

History of Present IllnessJaswinder 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 illnessNo H/O Diabetes, Hypertension,Tuberculosis, Bronchial Asthma or any other chronic illness.Family HistoryPatiemt 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.HousingPatient 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/precautionPatient was not allergic to any drug, food material.Personal HistoryPatient 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.

Elimination:Patient used to have normal bowel movement. He had retention of urine one day before admission.Mobility and exerciseHe 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 ASSESSMENTGeneral Appeaarance:Thin builtSensorium : ConsciousPosture :NormalVital SignsTemp 38oc Pulse 90/min resp-18/min B.P- 126/90 mm of HgSkin The condition of skin is dry, pale. She And iv cannula.HairHair 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.ENTNo discharge from ear or nose. No DNS. Patient has nasogastric tube and tracheostomy tube.Oral mucosaDental caries present in last molar tooth, gums are healthy without swelling and bleeding.GlandsLymph nodes are not enlargedChestShape is normal with symmetrica l chest movements. No dyspnea, orthopnea present.AbdomenAbdomen is flat , hard,& tender , due to constipation. Patient feels pain in umbilical region.LimbsUpper limbsFull range of motion is present in both the upper limbs. Lower limbsWeakness 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.BackPatient 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 examinationNervous systemCranial nerves: All the cranial nerves are intact.Motor systemMuscle tone and strength is decresed in lower limbs ( 1/5)DTRs are diminishedRespiratory system:Bilateal breath sounds are equal. No adventitious sounds: wheezing, crepts are absent. RR: 20/minCirculatory systemS1 & S2 normal. Hear rate : 92/min

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

Description of DiseaseDefinitionOtosclerosis 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 incidenceOtosclerosis is the most frequent cause of middle ear hearing loss in young adultsotosclerosis 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. 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 % ofcases. This is known as Van der Hoeve syndrome or Adair - Dighton syndromeTypes of otosclerosis:Accoridng to effect on area1. 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.

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

PathophysiologyFormation of spongy bony starts from bony labyrinthFixation of footoplatePoor conduction of soundHearing loss

Clinical Manifestations

According to BookAccording to Patient

DeafnessMany 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 earsPresent

Rarely mild vertigoAbsent

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 peopleAbsent

Diagnostic tests

According to BookAccording to Patient

Otoscopic examinationOtosclerosis 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.

AudiogramDone

Tympanometry Not Done

ManagementMedical management : Hearing loss associated with otosclerosis may stabilized by the use of sodium fluride with vitamin D caco3 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.StapedotomyA 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 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(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 INDICATIONS 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 ACTION Essential for nervous, muscular, and skeletal systems Maintain cell membrane and capillary permeability 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: Replacement of calcium in deficiency states. PHARMACOKINETICSAbsorption: 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. CONTRAINDICATIONS AND PRECAUTIONSOtosclerosis

20

Contraindicated in: Hypercalcemia Renal calculi Ventricular fibrillation. Use Cautiously in: Patients receiving digitalis glycosides Severe respiratory insufficiency Renal disease Cardiac disease.

ADVERSE REACTIONS AND SIDE EFFECTS*CNS: syncope (IV only), tingling. CV: CARDIAC ARREST (IV only) , arrhythmias , bradycardia. GI: constipation , nausea, vomiting. GU: calculi, hypercalciuria. Local: phlebitis (IV only) . INTERACTIONSDrugDrug: 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 DOSAGEDoses are expressed in mg, g, or mEq of calcium. 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