ENT

De La Salle Health Sciences InstituteDe La Salle University Medical CenterCollege of MedicineDepartment of Otorhinolaryngology-Head and Neck Surgery

OPD CLINICAL CASE DISCUSSIONAugust 16-22, 2011

Bryan Paul G. RamirezJunior Intern

Dr. Brendan R. FerrolinoPreceptor

De La Salle University Medical CenterCollege of Medicine

Department of Otorhinolaryngology – Head and Neck Surgery

SUBMITTED BY: JI BRYAN PAUL RAMIREZPRECEPTOR: DR. BRENDAN R. FERROLINO

OPD CLINICAL CASE DISCUSSION (AUGUST 16-22, 2011)

1. Miranda, Jian Khurt 6 mo./M

This is the case of J.M, 6 months old male who came in for follow up and was last seen Aug. 12, 2011, with a chief complaint of Right Lateral Neck Mass, beneath the post-auricular area.

4 months prior to consult, the mother noticed bluish-purple patch beneath the patient’s right posterior auricular area around the size of 1 peso coin. There were no ear discharge, fever, bleeding, cough and colds. The patient was seen and examined by ENT OPD last 7/14/2011 and was diagnosed with reactive lymphadenitis r/o hemangioma. He was prescribed with Clindamycin 75/5ml 1.25 ml q6 x 7 d. However there was no decrease in size noted. On physical examination, there was a 3x3 cm tender, non-movable, hard, bluish purple lateral neck mass below the preauricular area. On otoscopy, there were cerumen on both Eustachian tubes. Otherwise, the other ENT findings were normal.

The patient was diagnosed to have Hemangioma and was referred to a tumor clinic. Hemangiomas are proliferative lesions as compared to AV malformations which are vessel malformations. Visible lesion on the face or neck may signify presence of another internal hemangioma such as in the oral cavity, larynx or pharynx. Hemangiomas are sometimes associated with certain syndromes such as Sturge-Weber or posterior fossa lesion in the brain, arterial lesions in the neck or in the face, cardiac or coarctation problems and eye abnormalities. Superficially located lesions appear flat and reddish in color. Deep lesions are bluish. Compound lesions such as in this case is both deep and superficial and may appear purple. Cavernous hemangiomas are compressible, globular, bright red or deep purple involving deep structures. This is the most likely clinical type of hemangioma in this patient. Capillary hemangiomas on the other hand are plaque-like lesions, slightly elevated and more superficial. Port-wine stains are capillary type, flat and mostly in the dermis. Strawberry marks are capillary type with cavernous component.

Hemangiomas are usually just observed since they may involute in time. Indications for treatment may include involvement of vital organs, recurrent bleeding, ulceration, crusting or infection and rapid growth and deformity. CT scan is usually warranted but MRI may be needed for deep and large lesions. For small areas not involving the face, intralesional injection with steroids may be done with or without liquid nitrogen cryosurgery also with pulsed dye laser. Larger hemangiomas require oral steroids. For lesions that are life-threatening or non-responsive to steroids Alpha-interferon may be warranted. Careful surgical excision may be the last resort which can be very bloody since hemangioma is a vascular lesion.

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2. Fernandez, Nancy Contreras 43/F

This is the case of N.F. 43, female who sought consult for tinnitus of the left ear. 3 months prior to consult patient noticed sudden onset of ringing sensation on the left ear associated with dizziness, hearing difficulty and occasional headaches. Otherwise there is no associated ear discharge, cough or colds. 2 months prior to consult patient consulted in a private clinic and was prescribed with Polynerve Vitamins. However, patient noticed persistence of symptoms. On otoscopy both ET are patent with scanty cerumen and intact TM. Tuning fork test was done with the following results:

Weber’s: Lateralization on R ear

Rinne’s: AC>BC R ear; BC>AC L ear

Schwabach’s: (+)

The patient was diagnosed with Sensorineural Hearing Loss, T/C Meniere’s and was advised for PTA, ST and tympanometry. In Sensory Hearing Loss, the pathology may involve the inner and outer hair cells of the Cochlea, hence the transmitted sound waves does not stimulate those structures. HL is usually severe to profound and more so in high frequency sounds (4,000-8,000 kHz). The clarity of speech sound is usually distorted. The hearing is worse in the presence of background noise hence understanding speech is impaired. Etiology may include congenital aplasias of the cochlea, presbyacusis, perilymph fistula, noise-induced, infection or ototoxic drugs such as quinine, aminoglycosides or aspirin or Meniere’s disease. In Neural Hearing loss, the pathology is in the spiral ganglion and CN VIII. There is impaired nerve impulse transmission even if the cochlea is stimulated. There is poorer speech discrimination as compared with sensory hearing loss. It is associated with very severe hearing loss and tinnitus. The etiology may be an acoustic neuroma or vestibular schwannoma. In this case, the etiology of the SNHL is considered to be Meniere’s disease.

Meniere’s disease involves a triad of vertigo, fluctuating hearing loss and tinnitus all of which are present in this patient. It usually occurs in the 3rd or 4th decade of life (the patient is 43 years old) It is secondary to distention or increased volume of endolymphatic system. There is remission and relapses and with bilateral involvement in 30% of cases. In treating Meniere’s, the goal is to increase the circulation in the inner ear to decrease the pressure of the lymphatic system. Betahistine HCL may be given as prophylaxis. Diuretics such as Hydrochlorthiazides and Azetazolamide may be given to reduce the distention. Intratympanic gentamycin may be injected. Methotrexate may be given as immunologic treatment.

3. Nario, Dennis Asis 25/M

This is the case of D.N. 25 year old male who consulted for a 10 year history of enlarged tonsils. There is no pain, dysphagia, odynophagia, difficulty sleeping or apnea. He has tonsillitis 3x/year in 2 years. On inspection of the oral cavity and pharynx, there are enlarged tonsils, Grade 3. There is no hyperaemia or exudates noted. He was diagnosed with Chronic Hypertrophic Tonsillitis.

Human tonsil tissue includes the pair of tonsils at the back of the mouth, the adenoids behind the nose and a final area of soft tissue behind the tongue. Cases of chronic tonsillitis or infection may become difficult to treat using only antibiotics. Surgery to remove the tonsils is sometimes required, especially if a condition known as hypertrophic tonsils develops. The term hypertrophic tonsils, also referred to as tonsillar hypertrophy, describes tonsils that are so enlarged that they may obstruct breathing. It can be most bothersome at night when trying to sleep. The condition can also cause difficulty swallowing. All of which are not present in this patient. Most cases of hypertrophic tonsils also involve enlarged adenoids. The combination of swollen tissue can lead to more than breathing problems. In fact, ear infections, sinus infections, oral and mental maldevelopment, and eustachian (auditory) tube blockages can also occur.

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Biopsies of hypertrophic tonsils that have been surgically removed often show signs of bacterial pathogens. Hypertrophic tonsils contain significantly higher amounts of microbes than that of healthy tonsils. This pathogenic bacterium has been found to collect in the crypts of hypertrophic tonsils, causing infection and excessive inflammation. A diagnosis of hypertrophic tonsils is often visually based. They are very pronounced and tend to bulge out towards the front of the mouth. The tonsils are often so large that they touch one another---often termed "kissing tonsils." Chronic infections, breathing problems and maldevelopments are also taken into consideration along with other symptoms that may develop. Chronic halitosis, weight loss, decreased appetite and fatigue are also considered in a diagnosis of hypertrophic tonsils.

Hypertrophic tonsils generally warrant surgical intervention. When enlarged tonsils or adenoids interfere with sleeping by causing snoring or severe sleep apnea, surgery is often recommended. Surgery is also recommended when swallowing difficulties occur or dental problems are involved.

4. Cabahug, Nissa Yvonne 10/F

This is the case of N.C. 10 year old female who sought consult for ear pain. 2 days PTC, patient noted pain on both ears with decreased hearing. There were no noted discharge, cough or colds. Otoscopic findings revealed impacted cerumen on right ear and some on the left ear. The visualized portion of the left TM is intact. The patient is diagnosed with Retained Cerumen, AS; Impacted Cerumen, AD and was prescribed with Paracetamol Tablet 250mg 1 Tab every 4 hours as necessary for pain. Aural flushing was done. The patient was advised to come back after one week if pain persists.

Ear wax, also known as cerumen, is the result of mixing skins cells of the outer ear canal with glandular secretions that protect the ear against infections by cleaning and trapping dirt in the ear canal. The amount of ear wax produced varies by individual. Some individuals produce very little wax; others overproduce ear wax to the point that blockage may occur. Cerumen normally works itself out of the ear; however, there are situations when ear was begins to plug up the outer ear canal. When ear wax blocks the ear canal so that it begins to cause problems, it results in impacted ear wax, or cerumen impaction. Impacted ear wax is a common phenomenon. It is most likely caused when an individual cleans the outer ear with a cotton-tipped applicator, which ends up pushing the wax down so much that it plugs the outer ear canal. This condition is also prevalent among the population who wear hearing aids. Individuals who have impacted ear wax often complain about hearing loss, pain in the ear, tinnitus, cough, vertigo, or itching of the ear. Cerumen accumulation can occur if there is an overproduction of ear wax in response to infections or loud noises. An individual with an abnormally shaped ear canal may also encounter ear wax build-up. It may be removed by flushing after softening the ear wax with oil-based agents such as mineral oil. Docusate sodium may also be used to soften the impacted cerumen prior to flushing.

5. Felonia, Renato Esrellado 31/M

This is the case of RF 31 year-old male who presented with ear pain, AS. 4 days PTC, patient had rhinorrhea. 3 days PTC, he experienced ear fullness, AS and decreased hearing. No itchiness was noted. On otoscopy, the left ET is hyperaemic with scanty cerumen. The left TM is intact and also hyperaemic and bulging. Weber’s test does not lateralize and Rinne’s test revealed AC>BC. The patient was diagnosed with Acute Otitis Media, AS and was prescribed with Amoxicillin 500mg/cap, 1 cap q8 x 7 days and Mefenamic acid 500mg/cap, 1 cap q6.

The middle ear cleft connects middle ear with nasopharynx and is lined by columnar ciliated secretory epithelium. It is normally closed and opens on contraction of Tensor Veli Palatini muscle. The Eustachian tube is the key to normal middle ear function. In infants the ET is shorter and horizontally oriented, prone to reflux from nasopharynx and has poor TVP function. In adults, the ET is longer and angulated at 45o and drains better than an

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infant’s. The ET functions to drain middle ear secretions via mucociliary clearance of respiratory epithelium. It also protects the middle ear from nasopharyngeal secretions and sound pressure changes thru the action of the TVP. Its most important function is that it ventilates the middle ear for optimum hearing.

Otitis media is the inflammation of the middle ear. Based on duration it is classified as acute (<3 weeks), subacute ( 3 weeks-3months) and chronic (>3 months). In this case the inflammation occurred in 3 days hence it is classified as acute otitis media. Factors that contribute to the pathogenesis of Otitis Media include infection (URTI which is most likely the etiology in this case), ET dysfunction, immunologic status, allergy, environment and social factors. In this case, the URTI caused mucosal congestion. The ET may be dysfunctional too causing persistent negative middle ear pressure. The ET suddenly opened causing insufflations of nasopharynx secretions. The secretions may have caused bacterial inoculation in the middle ear hence there is inflammation leading to otitis media. The microbiology of OM includes S. Pneumonia, H. Influenza, Moraxella catarrhalis and others. Diagnosis of otitis media is usually made with clinical history and otoscopic findings. Pnuematic otoscopy, audiometry and tympanometry may also be done. Management of AOM includes antimicrobial agents for 7-14 days. If symptomatic failure occurs, change of antimicrobial agents, examination for other foci or tympanocentesis or myringotomy may be performed. After 7-14 days, re-examination may be done, if no effusion is appreciated, periodic follow up may be done. If there is effusion change of antimicrobial agent/s is warranted. If effusion occurs >3 months, myringotomy with tympanostomy tube is done.

6. Ante, Teresita Flores 52/F

This is the case of TA 52 year-old female who came in for follow-up and was previously diagnosed with nasal polyposis. 13 years PTC patient had anosmia and consulted at PGH and was diagnosed with nasal polyps. Patient had recurrent rhinorrhea and nasal congestion. At present the patient is asymptomatic and is awaiting schedule of FESS. On anterior rhinoscopy there is a grade I whitish mass near the right middle turbinate, and a grade II pale, whitish boggy mass at the left middle turbinate.

Nasal polyps are polypoidal masses arising mainly from the mucous membranes of the nose and paranasal sinuses. They are overgrowths of the mucosa that frequently accompany allergic rhinitis. They are freely movable and nontender. Nasal polyps are usually classified into antrochoanal polyps and ethmoidal polyps. Antrochoanal polyps arise from the maxillary sinuses and are the much less common, ethmoidal polyps arise from the ethmoidal sinuses. Antrochoanal polyps are usually single and unilateral whereas ethmoidal polyps are multiple and bilateral. Symptoms of polyps include nasal block, sinusitis, anosmia (loss of smell), and secondary infection leading to headache. Despite removal by surgery, nasal polyps are found to reoccur in about 70% of cases. Sinus surgery requires great amount of precision as this involves risk of damage to orbit matter. The tendency to manifest multiple polyps is referred to as “polyposis”.

The pathogenesis of nasal polyps is unknown. Nasal polyps are most commonly thought to be caused by allergy and rarely by cystic fibrosis although a significant number are associated with non-allergic adult asthma or no respiratory or allergic trigger that can be demonstrated. These polyps have no relationship with colonic or uterine polyps. Irregular unilateral polyps particularly associated with pain or bleeding will require urgent investigation as they may represent an intranasal tumour. There are various diseases associated with polyp formation: Chronic rhinosinusitis, Asthma, Aspirin intolerance, Cystic fibrosis, Kartagener's syndrome, Young's syndrome, Churg-strauss syndrome and Nasal mastocytosis. Exposure to some forms of chromium can cause nasal polyps and associated diseases. They are also linked to salicylate sensitivity.

Nasal polyps are most often treated with steroids or topical, but can also be treated with surgical methods. Pre-post surgery, sinus rinses with a warm water (240 ml / 8 oz) mixed with a small amount (teaspoon) of salts (sodium chloride & sodium bicarbonate) can be very helpful to clear thesinuses. This method can be also used as a preventative measure to discourage the polyps from growing back and should be used in combination with a nasal steroid. The removal of nasal polyps via surgery lasts approximately 45 minutes to 1 hour. The surgery

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http://en.wikipedia.org/wiki/Paranasal_sinus

http://en.wikipedia.org/wiki/Sodium_bicarbonate

http://en.wikipedia.org/wiki/Sodium_chloride

http://en.wikipedia.org/wiki/Salts

http://en.wikipedia.org/wiki/Sinus_rinses

http://en.wikipedia.org/wiki/Steroid

http://en.wikipedia.org/wiki/Salicylate_sensitivity

http://en.wikipedia.org/wiki/Chromium

http://en.wikipedia.org/wiki/Mastocytosis

http://en.wikipedia.org/wiki/Churg-strauss_syndrome

http://en.wikipedia.org/wiki/Young's_syndrome


http://en.wikipedia.org/wiki/Kartagener's_syndrome

http://en.wikipedia.org/wiki/Cystic_fibrosis

http://en.wikipedia.org/wiki/Aspirin_intolerance

http://en.wikipedia.org/wiki/Asthma

http://en.wikipedia.org/wiki/Rhinosinusitis



http://en.wikipedia.org/wiki/Pathogenesis

http://en.wikipedia.org/wiki/Headache

http://en.wikipedia.org/wiki/Infection

http://en.wikipedia.org/wiki/Anosmia

http://en.wikipedia.org/wiki/Sinusitis

http://en.wiktionary.org/wiki/bilateral

http://en.wikipedia.org/wiki/Ethmoidal_sinus


http://en.wikipedia.org/wiki/Maxillary_sinus

can be done under general or local anaesthesia, and the polyps are removed usingendoscopic surgery. Recovery from this type of surgery is anywhere from 1 to 3 weeks.

7. Violanda, Brenda Gucilatar 40/F

This is the case of BV a 40 year-old female who came in for follow-up with UTZ results showing enlarged nodular thyoid. 2 years PTC, patient had dysphagia and odynophagia. On PE, there is a palpable thyroid with no cervical lymphadenopathy. TSH, FT3, FT4 were requested but showed normal values. She was diagnosed with Nodular Nontoxic goiter. She was started with levothyroxine 5 mcg. 1 tab. BID x 14 days.

Thyroid Gland has two pear-shaped lobes, isthmus (which connects the left and right lobes), and a pyramidal lobe (may present as a superior extension of the embryological thyroid duct). A nontoxic goiter is a diffuse or nodular enlargement of the thyroid gland that does not result from an inflammatory or neoplastic process and is not associated with abnormal thyroid function. The histopathology varies with etiology and age of the goiter. Initially, uniform follicular epithelial hyperplasia (diffuse goiter) is present, with an increase in thyroid mass. As the disorder persists, the thyroid architecture loses uniformity, with the development of areas of involution and fibrosis interspersed with areas of focal hyperplasia. This process results in multiple nodules (multinodular goiter). On nuclear scintigraphy, some nodules are hot, with high isotope uptake (autonomous) or cold, with low isotope uptake, compared with the normal thyroid tissue (as demonstrated in the images below). The development of nodules correlates with the development of functional autonomy and reduction in thyroid-stimulating hormone (TSH) levels. Clinically, the natural history of a nontoxic goiter is growth, nodule production, and functional autonomy (resulting in thyrotoxicosis in a minority of patients). The overall risk of malignancy is the same in a patient with a nodular goiter as with a solitary nodule.

The thyroid gland usually grows outward because of its location anterior to the trachea. Occasionally, the thyroid wraps around and compresses the trachea and/or esophagus or extends inferiorly into the anterior mediastinum. Determining whether the goiter has been present for many years and whether a change has occurred in the recent past is important. Recent or accelerated growth of a discrete nodule or thyroid lobe should raise the suspicion of malignancy.Goiters associated with unilateral adenopathy should raise the suspicion of malignancy. Goiters rarely are painful or grow quickly unless recent hemorrhage into a nodule has occurred.

Tracheal compression is generally asymptomatic until critical narrowing has occurred. Patients develop a dry cough, dyspnea, and stridor, especially with exertion. In patients with intrathoracic goiter, the dyspnea and stridor may be nocturnal or positional (ie, occurring when the patient's arms are raised) when the thoracic outlet is narrowed. Hemorrhage into a nodule or cyst or development of bronchitis may acutely worsen the respiratory symptoms in a patient with tracheal narrowing. The esophagus is more posterior in the neck, and a goiter occasionally extends posteriorly and causes solid food and pill dysphagia. Compression of the recurrent laryngeal nerve by a goiter or invasion by a thyroid malignancy results in vocal cord dysfunction and may cause hoarseness. The superior laryngeal nerve controls the pitch of the voice. An expanding goiter may cause a change in the character of the voice, especially in individuals who use their voice extensively (eg, in certain occupations). Compression of the venous outflow through the thoracic inlet by a mediastinal goiter results in facial plethora and dilated neck and upper thoracic veins.

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http://emedicine.medscape.com/article/383062-overview





http://en.wikipedia.org/wiki/Endoscopic_surgery

http://en.wikipedia.org/wiki/Anaesthesia

9. Raposon, Virgilio Requejo 65/M

This is the case of VR 65 year old male who came in for follow-up with a chief complaint of hoarseness for 2 weeks. There is throat itchiness and non-productive cough, with no dysphagia or odynophagia. On indirect laryngoscopy, the TVCs are mobile. The FVC is mobile and swollen. There is no subglottic masses, the arythenoids are nonedematous; the epiglottis is nonhyperemic and nonedematous. There is no pooling in the pyriform. She was diagnosed with Chronic Laryngitis.

More common in males than females, chronic laryngitis is aggravated by: habitual shouting; faulty voice production coupled with excessive vocal use seen in teachers, actors, singers; smoking; spirit drinking; and chronic upper airway infection, such as sinusitis. The voice is hoarse and fatigues easily. There may be discomfort and a tendency to clear the throat constantly. Examination shows the cords to be thickened and pink and the surrounding mucosa is often red and dry. Treatment is often ineffective. The voice should be rested as far as possible, any upper airway sepsis dealt with and steam inhalations given to humidify the larynx. Voice therapy may be helpful in cases of faulty voice production and referral to a singing teacher is of value to professional or amateur singers.

10. Garcia, Rowelyn 14/F

This is the case of RG 14 year old female diagnosed with Conductive Hearing Loss, and was advised for PTA, ST and tympanometry. In CHL, the pathology lies in the external ear canal, ear drum (tympanic membrane), ossicles or middle ear. Because of the pathology, impaired conduction of sound occur; hence, there is decreased intensity of sound reaching the cochlea. Unlike SNHL, there is no distortion of sound hence understanding speech is no problem with adequate intensity. Persons with CHL tends to speak softly because they hear the speech louder (bone>air conduction), hence they lower their voices since they perceive that they are speaking loudly. Hearing loss is mild to moderate around 30-40 dB. The most common etiology is Impacted cerumen and other foreign bodies. Other possible etiology include: ear canal atresia, otitis externa/media, otosclerosis, ear canal tumors, and myringitis. Diagnosis of CHL includes otoscopic findings of the ear canal and ear drum; Weber’s test that lateralizes to the affected ear; a negative Rinne test (bone>air conduction); a higher air conduction threshold on PTA. Treatment is directed at the specific etiology. For instance, in cases of impacted cerumen, the cerumen is flushed out; or in AOM, the infection is relieved by antimicrobial agents.

12. Panelo, Arnold 42/M

This is the case of AP, 42 year old male who consulted for nasal obstruction and was diagnosed with New growth, Right nasal concha. The causes of Nasal Obstruction may be structural, such as congenital deformities, deformities from trauma or infection, neoplastic masses or polyps, or foreign bodies. It may also be systemic: physiologically it can be because of the nasal cycle or the position or temperature; pathologically, it can be rhinosinusitis, atrophic rhinitis, metabolic or endocrine or specific chronic rhinitis.

In this patient a new growth was appreciated at the right nasal concha, which can either be a polyp or malignant neoplasm. Nasal polyps are polypoidal masses arising mainly from the mucous membranes of the nose and paranasal sinuses. They are overgrowths of the mucosa that frequently accompany allergic rhinitis. They are freely movable and nontender. Nasal polyps are usually classified into antrochoanal polyps and ethmoidal polyps. Antrochoanal polyps arise from the maxillary sinuses and are the much less common, ethmoidal polyps arise from the ethmoidal sinuses. Antrochoanal polyps are usually single and unilateral whereas ethmoidal polyps are multiple and bilateral. Symptoms of polyps include nasal block, sinusitis, anosmia (loss of smell), and secondary infection leading to headache. Despite removal by surgery, nasal polyps are found to reoccur

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http://en.wikipedia.org/wiki/Headache

http://en.wikipedia.org/wiki/Infection

http://en.wikipedia.org/wiki/Anosmia

http://en.wikipedia.org/wiki/Sinusitis

http://en.wiktionary.org/wiki/bilateral


http://en.wikipedia.org/wiki/Maxillary_sinus

in about 70% of cases. Sinus surgery requires great amount of precision as this involves risk of damage to orbit matter. The tendency to manifest multiple polyps is referred to as “polyposis”.

The pathogenesis of nasal polyps is unknown. Nasal polyps are most commonly thought to be caused by allergy and rarely by cystic fibrosis although a significant number are associated with non-allergic adult asthma or no respiratory or allergic trigger that can be demonstrated. These polyps have no relationship with colonic or uterine polyps. Irregular unilateral polyps particularly associated with pain or bleeding will require urgent investigation as they may represent an intranasal tumour. There are various diseases associated with polyp formation: Chronic rhinosinusitis, Asthma, Aspirin intolerance, Cystic fibrosis, Kartagener's syndrome, Young's syndrome, Churg-strauss syndrome and Nasal mastocytosis. Exposure to some forms of chromium can cause nasal polyps and associated diseases. They are also linked to salicylate sensitivity.

Nasal polyps are most often treated with steroids or topical, but can also be treated with surgical methods. Pre-post surgery, sinus rinses with a warm water (240 ml / 8 oz) mixed with a small amount (teaspoon) of salts (sodium chloride & sodium bicarbonate) can be very helpful to clear thesinuses. This method can be also used as a preventative measure to discourage the polyps from growing back and should be used in combination with a nasal steroid. The removal of nasal polyps via surgery lasts approximately 45 minutes to 1 hour. The surgery can be done under general or local anaesthesia, and the polyps are removed usingendoscopic surgery. Recovery from this type of surgery is anywhere from 1 to 3 weeks.

On the other hand, virtually all malignant tumours of the nasopharynx are squamous cell carcinoma, but rarely lymphoma or adenoid cystic carcinoma may occur. Cancer of the nasopharynx spreads locally to invade the skull base and Eustachian tube and metastasizes early to the upper deep cervical lymph nodes. The Epstein–Barr virus may play a role in the aetiology of nasopharyngeal malignancy. Other tumors f the nasal region includes the following.

Osteomata occur in the frontal and ethmoidal sinuses. They are slow growing and cause few symptoms but may eventually call for surgical removal.

Nasopharyngeal angiofibroma is a rare tumour of adolescent boys. It presents as epistaxis and nasal obstruction and is usually easily visible by posterior rhinoscopy. Being highly vascular, the tumour is locally destructive and extends into the surrounding structures. Diagnosis is confirmed by angiography and treatment is by surgical removal.

Though not truly neoplastic, malignant granuloma is a sinister condition characterized by progressive ulceration of the nose and neighbouring structures. There are two main varieties: the Stewart type, in which the lesion is limited to the skull and is characterized by a pleomorphic histiocytic infiltration and which is a form of lymphoma; and the Wegener type, in which the kidneys, lungs and other tissues may show periarteritis, the local nasal lesion containing multinucleated giant cells. It is probable that Wegener’s granuloma is an auto-immune disease. Radiotherapy, steroids and cytotoxic agents are used in its treatment and occasionally are successful.

Malignant melanoma is fortunately rare in the nose and sinuses. Treatment is by radical surgery but the prognosis is extremely poor.

13. Domingo, Lita 56/F

This is the case of LD 56 year old female with a chief complaint of tinnitus and was diagnosed with Impacted Cerumen AU, removed. Flushing was done and was advised to keep ears dry.

Cerumen is the result of mixing skins cells of the outer ear canal with glandular secretions that protect the ear against infections by cleaning and trapping dirt in the ear canal. The amount of ear wax produced varies by individual. Some individuals produce very little wax; others overproduce ear wax to the point that blockage may occur. Cerumen normally works itself out of the ear; however, there are situations when ear was begins to plug up

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http://en.wikipedia.org/wiki/Endoscopic_surgery

http://en.wikipedia.org/wiki/Anaesthesia

http://en.wikipedia.org/wiki/Paranasal_sinus

http://en.wikipedia.org/wiki/Sodium_bicarbonate

http://en.wikipedia.org/wiki/Sodium_chloride

http://en.wikipedia.org/wiki/Salts

http://en.wikipedia.org/wiki/Sinus_rinses

http://en.wikipedia.org/wiki/Steroid

http://en.wikipedia.org/wiki/Salicylate_sensitivity

http://en.wikipedia.org/wiki/Chromium

http://en.wikipedia.org/wiki/Mastocytosis

http://en.wikipedia.org/wiki/Churg-strauss_syndrome



http://en.wikipedia.org/wiki/Kartagener's_syndrome


http://en.wikipedia.org/wiki/Aspirin_intolerance


http://en.wikipedia.org/wiki/Rhinosinusitis



http://en.wikipedia.org/wiki/Pathogenesis

the outer ear canal. When ear wax blocks the ear canal so that it begins to cause problems, it results in impacted ear wax, or cerumen impaction. Impacted ear wax is a common phenomenon. It is most likely caused when an individual cleans the outer ear with a cotton-tipped applicator, which ends up pushing the wax down so much that it plugs the outer ear canal. This condition is also prevalent among the population who wear hearing aids. Individuals who have impacted ear wax often complain about hearing loss, pain in the ear, tinnitus, cough, vertigo, or itching of the ear. Cerumen accumulation can occur if there is an overproduction of ear wax in response to infections or loud noises. An individual with an abnormally shaped ear canal may also encounter ear wax build-up. It may be removed by flushing after softening the ear wax with oil-based agents such as mineral oil. Docusate sodium may also be used to soften the impacted cerumen prior to flushing.

14. Dela Cruz, Luz 69/F

This is the case of LD 69 year old female who presented with a chief complaint of neck mass. He was diagnosed with anterior neck mass S/P lobectomy, L (1984). She was advised for ultrasound, TSH and FT3 and FT4. In this patient, the diagnosis of nontoxic nodular goiter is considered. A nontoxic goiter is a diffuse or nodular enlargement of the thyroid gland that does not result from an inflammatory or neoplastic process and is not associated with abnormal thyroid function. The histopathology varies with etiology and age of the goiter. Initially, uniform follicular epithelial hyperplasia (diffuse goiter) is present, with an increase in thyroid mass. As the disorder persists, the thyroid architecture loses uniformity, with the development of areas of involution and fibrosis interspersed with areas of focal hyperplasia. This process results in multiple nodules (multinodular goiter). On nuclear scintigraphy, some nodules are hot, with high isotope uptake (autonomous) or cold, with low isotope uptake, compared with the normal thyroid tissue (as demonstrated in the images below). The development of nodules correlates with the development of functional autonomy and reduction in thyroid-stimulating hormone (TSH) levels. Clinically, the natural history of a nontoxic goiter is growth, nodule production, and functional autonomy (resulting in thyrotoxicosis in a minority of patients). The overall risk of malignancy is the same in a patient with a nodular goiter as with a solitary nodule.


Tracheal compression is generally asymptomatic until critical narrowing has occurred. Patients develop a dry cough, dyspnea, and stridor, especially with exertion. In patients with intrathoracic goiter, the dyspnea and stridor may be nocturnal or positional (ie, occurring when the patient's arms are raised) when the thoracic outlet is narrowed. Hemorrhage into a nodule or cyst or development of bronchitis may acutely worsen the respiratory symptoms in a patient with tracheal narrowing. The esophagus is more posterior in the neck, and a goiter occasionally extends posteriorly and causes solid food and pill dysphagia. Compression of the recurrent laryngeal nerve by a goiter or invasion by a thyroid malignancy results in vocal cord dysfunction and may cause hoarseness. The superior laryngeal nerve controls the pitch of the voice. An expanding goiter may cause a change in the character of the voice, especially in individuals who use their voice extensively (eg, in certain occupations). Compression of the venous outflow through the thoracic inlet by a mediastinal goiter results in facial plethora and dilated neck and upper thoracic veins.

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15. Impis, Dindo B. 41/M

This is the case of DI, 41 year old male who presented with a chief complaint of discharge, AD. He is diagnosed with Chronic Otitis Externa. He was advised application of PND with ear wick, PND 2-3 drops TID.

Otitis externa is a diffuse inflammation of the skin lining the external auditory meatus. It may be bacterial or fungal (otomycosis), and is characterized by irritation, desquamation, scanty discharge and tendency to relapse. The treatment is simple, but success is absolutely dependent upon patience, care and meticulous attention to detail. Some people are particularly prone to otitis externa, often because of a narrow or tortuous external canal. Most people can allow water into their ears with impunity but in others otitis externa is the inevitable result. Swimming baths are a common source of otitis externa. Poking the ear with a finger or towel further traumatizes the skin and introduces new organisms. Further irritation occurs, leading to further interference with the ear, so causing more trauma. A vicious circle is set up.Otitis externa may occur after staying in hotter climates than usual where increased sweating and bathing are predisposing factors. Underlying skin disease, such as eczema or psoriasis, may occur in the ear canal and produce very refractory otitis externa. Ear syringing, especially if it causes trauma, may result in otitis externa.

A mixed infection of varying organisms is not infrequent, the most commonly found types being: Staphylococcus pyogenes, Pseudomonas pyocyanea, diphtheroids, Proteus vulgaris; Escherichia coli; Streptococcus faecalis; Aspergillus niger and Candida albicans. Symptoms include irritation, discharge (scanty), pain (usually moderate, sometimes severe, increased by jaw movement) and deafness. Signs that may be present are Meatal tenderness, especially on movement of the pinna or compression of the tragus; moist debris, often smelly and keratotic, the removal of which reveals red desquamated skin and edema of the meatal walls and often the tympanic membrane. Scrupulous aural toilet is the key to successful treatment of otitis externa. No medication will be effective if the ear is full of debris and pus. Investigation of the offending microorganism is essential.

16. Celaje, Julieta M. 45/F

This is the case of JC 45 year old female who consulted because of frequent sneezing. She is diagnosed with Allergic rhinitis. She was prescribed with Fluticasone nasal spray and NaCl nasal spray (0.65%) 2 prays on both nostril TID.

Following exposure to a particular allergen, the susceptible individual produces reaginic antibody (IgE), which becomes bound to the surface of a mast cell. Such cells abound in nasal mucosa and when fixed to IgE molecules are said to be sensitized. Further exposure to the specific allergen causes its binding to the IgE of the sensitized mast cell, degranulation of the cell and release of histamine, slow-reacting substance and vasoactive peptides. These substances cause vasodilation, increased capillary permeability and smooth-muscle contraction—the features of allergic airways disease.

The allergens responsible for nasal allergy are inhaled and may be seasonal, e.g. mould spores in autumn, tree and grass pollen in spring; or perennial,e.g. animal dander (especially cats), house dust mite.

Symptoms include watery rhinorrhea, sneezing attacks—often violent and prolonged, nasal obstruction. conjunctival irritation and lacrimation. In taking a history, it is important to relate the onset of the symptoms toexposure to the suspected allergen.

The nasal mucosa is edematous and usually pale or violet in colour. There is excessive clear mucus within the nose, and this usually contains an increased number of eosinophils. Children may develop a transverse nasal skin crease from rubbing the nose—the allergic salute.

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Avoidance of contact with the allergen may be possible, especially in the case of domestic pets. Antihistamines are useful in acute episodes but tolerance develops. The latest generation of antihistamines (H1 receptor antagonists) do not produce drowsiness. Vasoconstrictor nasal drops provide temporary relief but are not advisable, as prolonged use leads to chronic rhinitis medicamentosa. Sodium cromoglycate (Rynacrom) applied to the nose 4–6 times daily as prophylaxis is particularly suitable for children. Topically applied steroid preparations (beclomethasone, flunisolide) are probably the most effective treatment of nasal allergy. Systemic effects of steroid therapy are absent but such treatment is not advisable in young children. Desensitization by administration of increasing dosages of allergen is no longer widely practised, as it is of little benefit in most cases and carries therisk of anaphylaxis. If gross hypertrophy of the nasal mucosa has occurred, surgical reduction by diathermy or laser may be beneficial.

17. Campos, Proceso Q. 52/M

This is the case of PC, 52 year old male who consulted at the OPD because of decreased hearing, AU. He was diagnosed with Otomycosis, AU. Aural cleaning was done and he was advised to keep ear dry.

The cerumen usually have saprophytic fungi that have no pathologic significance. Aspergillus, Candida, Mucor, may infect the medial EAC when it is treated with steroids or antibiotics especially during warm summer months. It is usually manifested by severe itching and ear fullness rather than pain. On otoscopy, the fungi may appear as white, black or yellow lining in the EAC. It has a refractory course and has a tendency to recur. Once the ears are cleaned and dried, local antimycotics may be given. But in most cases aural cleaning is adequate.

18. Cosatnilla, Gaudioso 60/M

This is the case of GC 60 year old male who presented with a chief complaint of ear pain, AD. He is diagnosed with Acute suppurative otitis media, AD. Aural cleaning was done. He was advised to continue Amoxicillin 500mg TID x 5 more days, and to keep ears dry. Mefenamic acid 500mg cap, 1 cap q6 is also prescribed for the pain.

Acute suppurative otitis media results from bacterial infection of the middle ear cleft, often as a bacterial complication of the common cold. This is more frequent in children than in adults.

The common infective organisms are beta hemolytic streptococcus, pneumo-coccus, Hemophilus influenzae, and staphylococcus. In the Eustachian tubes it could be caused by viral upper respiratory infection, enlarged adenoids, sinus infections, allergy-causing edema in the eustachian tube region, and cleft palate. Other cause: traumatic rupture , perforation of the tympanic membrane , from infection following ear surgery. ASOM is a self-limiting disease, and when treated adequately it rarely leaves any residual change.

Fever, malaise, otalgia, decrease in hearing, discharge from the ear canal: muco-purulent or purulent (perforation of the tympanic membrane. In the early stage, the tympanic membrane will show retraction and lack of mobility. Next with the onset of edema and exudation the drum will lose its landmarks, appear thick and dull, and may have a fluid level. The fluid is thick and not clear, as in the case of serous otitis media. Tympanic membrane outward and cause bulging of the drum. If untreated the tympanic membrane will rupture, giving rise to a serosanguinous and then mucopurulent or purulent discharge from the ear. Perforation occurs in tympanic membrane central.

After perforation, pain and fever may not be as marked as in the earlier stages, but there is persistence of purulent discharge and recurrence of pain. Pressure on the mastoid tip will produce pain mastoid tenderness. Infection may spread to mastoid cause mastoiditis.

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19. Torno, Sean Mae Daniaye M. 1/M

This is the case of ST 1 year old male who was diagnosed with Impacted cerumen. Aural flushing was done after instillation of mineral oil.

Cerumen is the result of mixing skins cells of the outer ear canal with glandular secretions that protect the ear against infections by cleaning and trapping dirt in the ear canal. The amount of ear wax produced varies by individual. Some individuals produce very little wax; others overproduce ear wax to the point that blockage may occur. Cerumen normally works itself out of the ear; however, there are situations when ear was begins to plug up the outer ear canal. When ear wax blocks the ear canal so that it begins to cause problems, it results in impacted ear wax, or cerumen impaction. Impacted ear wax is a common phenomenon. It is most likely caused when an individual cleans the outer ear with a cotton-tipped applicator, which ends up pushing the wax down so much that it plugs the outer ear canal. This condition is also prevalent among the population who wear hearing aids. Individuals who have impacted ear wax often complain about hearing loss, pain in the ear, tinnitus, cough, vertigo, or itching of the ear. Cerumen accumulation can occur if there is an overproduction of ear wax in response to infections or loud noises. An individual with an abnormally shaped ear canal may also encounter ear wax build-up. It may be removed by flushing after softening the ear wax with oil-based agents such as mineral oil. Docusate sodium may also be used to soften the impacted cerumen prior to flushing.

20. Polido, Gladys 25/F

This is the case of GP 25 year old female who came in for follow-up with a history of anterior neck mass, palpitations once or twice a week and dryness of throat. There is a non-tender anterior neck mass around 4x 2cm which moves with deglutination. Patient had an UTZ guided biopsy of the mass which showed colloid goiter with cystic degeneration. She was diagnosed with Nontoxic nodular goiter.

A nontoxic goiter is a diffuse or nodular enlargement of the thyroid gland that does not result from an inflammatory or neoplastic process and is not associated with abnormal thyroid function. The histopathology varies with etiology and age of the goiter. Initially, uniform follicular epithelial hyperplasia (diffuse goiter) is present, with an increase in thyroid mass. As the disorder persists, the thyroid architecture loses uniformity, with the development of areas of involution and fibrosis interspersed with areas of focal hyperplasia. This process results in multiple nodules (multinodular goiter). On nuclear scintigraphy, some nodules are hot, with high isotope uptake (autonomous) or cold, with low isotope uptake, compared with the normal thyroid tissue (as demonstrated in the images below). The development of nodules correlates with the development of functional autonomy and reduction in thyroid-stimulating hormone (TSH) levels. Clinically, the natural history of a nontoxic goiter is growth, nodule production, and functional autonomy (resulting in thyrotoxicosis in a minority of patients). The overall risk of malignancy is the same in a patient with a nodular goiter as with a solitary nodule.


Tracheal compression is generally asymptomatic until critical narrowing has occurred. Patients develop a dry cough, dyspnea, and stridor, especially with exertion. In patients with intrathoracic goiter, the dyspnea and stridor may be nocturnal or positional (ie, occurring when the patient's arms are raised) when the thoracic outlet is narrowed. Hemorrhage into a nodule or cyst or development of bronchitis may acutely worsen the respiratory

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symptoms in a patient with tracheal narrowing. The esophagus is more posterior in the neck, and a goiter occasionally extends posteriorly and causes solid food and pill dysphagia. Compression of the recurrent laryngeal nerve by a goiter or invasion by a thyroid malignancy results in vocal cord dysfunction and may cause hoarseness. The superior laryngeal nerve controls the pitch of the voice. An expanding goiter may cause a change in the character of the voice, especially in individuals who use their voice extensively (eg, in certain occupations). Compression of the venous outflow through the thoracic inlet by a mediastinal goiter results in facial plethora and dilated neck and upper thoracic veins.

21. Sagun, Marty G. 31/M

This is the case of MS 31 year old male who presented with discharge, AD. He was diagnosed with Otitis externa. He was prescribed with PND otic drops 2-3 gtts TID and Mefenamic acid 500mg q6 for pain.

Otitis externa is a diffuse inflammation of the skin lining the external auditory meatus. It may be bacterial or fungal, and is characterized by irritation, desquamation, scanty discharge and tendency to relapse. The treatment is simple, but success is absolutely dependent upon patience, care and meticulous attention to detail. Some people are particularly prone to otitis externa, often because of a narrow or tortuous external canal. Most people can allow water into their ears with impunity but in others otitis externa is the inevitable result. Swimming baths are a common source of otitis externa. Poking the ear with a finger or towel further traumatizes the skin and introduces new organisms. Further irritation occurs, leading to further interference with the ear, so causing more trauma. A vicious circle is set up.Otitis externa may occur after staying in hotter climates than usual where increased sweating and bathing are predisposing factors. Underlying skin disease, such as eczema or psoriasis, may occur in the ear canal and produce very refractory otitis externa. Ear syringing, especially if it causes trauma, may result in otitis externa.


22. Padilla, Catherine G. 37/F

This is the case of CP, 37 year old female with a chief complaint of Right ear fullness. She was diagnosed with Otitis externa. Aural cleaning was done. She was advised to avoid ear manipulation. PND 2-3 gtts TID was also prescribed.

Otitis externa is a diffuse inflammation of the skin lining the external auditory meatus. It may be bacterial or fungal, and is characterized by irritation, desquamation, scanty discharge and tendency to relapse. The treatment is simple, but success is absolutely dependent upon patience, care and meticulous attention to detail. Some people are particularly prone to otitis externa, often because of a narrow or tortuous external canal. Most people can allow water into their ears with impunity but in others otitis externa is the inevitable result. Swimming baths are a common source of otitis externa. Poking the ear with a finger or towel further traumatizes the skin and introduces new organisms. Further irritation occurs, leading to further interference with the ear, so causing more trauma. A vicious circle is set up. Otitis externa may occur after staying in hotter climates than usual where increased sweating and bathing are predisposing factors. Underlying skin disease, such as eczema or psoriasis, may

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occur in the ear canal and produce very refractory otitis externa. Ear syringing, especially if it causes trauma, may result in otitis externa.


23. Lacasa, Danica Fe L. 6/F

This is the case of DL 6 year old female, with a chief complaint of ear pain. She is diagnosed with diffuse otitis externa, AD. She was prescribed with Amoxicillin 250/5mg, 5ml q6 and Aplosyn otic drops 2-3 gtts TID on AD. Otitis externa is a diffuse inflammation of the skin lining the external auditory meatus. It may be bacterial or fungal, and is characterized by irritation, desquamation, scanty discharge and tendency to relapse. The treatment is simple, but success is absolutely dependent upon patience, care and meticulous attention to detail. Some people are particularly prone to otitis externa, often because of a narrow or tortuous external canal. Most people can allow water into their ears with impunity but in others otitis externa is the inevitable result. Swimming baths are a common source of otitis externa. Poking the ear with a finger or towel further traumatizes the skin and introduces new organisms. Further irritation occurs, leading to further interference with the ear, so causing more trauma. A vicious circle is set up.Otitis externa may occur after staying in hotter climates than usual where increased sweating and bathing are predisposing factors. Underlying skin disease, such as eczema or psoriasis, may occur in the ear canal and produce very refractory otitis externa. Ear syringing, especially if it causes trauma, may result in otitis externa.


25. Manalo, Rose Ann 18/F

This is the case of RM, 18 year old female who presented with Ear discharge, AS. She was diagnosed with Chronic suppurative otitis media AS, resolved. She was advised to keep her ear dry.

Chronic suppurative otitis media (CSOM) is the result of an initial episode of acute otitis media and is characterized by a persistent discharge from the middle ear through a tympanic perforation. It is an important cause of preventable hearing loss, particularly in the developing world. A history of at least 2 weeks of persistent ear discharge should alert primary health workers to the problem; if the ear could be dry mopped well enough to see the eardrum, then the diagnosis of CSOM can be confirmed by visualization of the perforation in the tympanic membrane. Chronic suppurative otitis media involves a perforation (hole) in the tympanic membrane and active bacterial infection within the middle ear space for several weeks or more. There may be enough pus that it drains

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to the outside of the ear (otorrhea), or the purulence may be minimal enough to only be seen on examination using a binocular microscope. This disease is much more common in persons with poor Eustachian tube function. Hearing impairment often accompanies this disease.

26. Ramirez, Consolacion C. 58/F

This is the case of CR, a 50 year old female who consulted because of ear pain. She is diagnosed with Otitis externa, AU resolving and was prescribed with Aplosyn otic drops 2-3 drops TID x 5 days and Mefenamic Acid 500mg TID PRN.



27. Wael, Rose Ann M. 2/F

This is the case of RW, a 2 year-old female with a chief complaint of ear pain and discharge, AU. She is diagnosed with Otitis Media, AU. She was prescribed with Amoxicillin 250mg/5ml, 5ml q8 x 10 days; Disudrin syrup ½ tsp TID x 5 days. She was also advised to keep her ear dry.

The middle ear cleft connects middle ear with nasopharynx and is lined by columnar ciliated secretory epithelium. It is normally closed and opens on contraction of Tensor Veli Palatini muscle. The Eustachian tube is the key to normal middle ear function. In infants the ET is shorter and horizontally oriented, prone to reflux from nasopharynx and has poor TVP function. In adults, the ET is longer and angulated at 45o and drains better than an infant’s. The ET functions to drain middle ear secretions via mucociliary clearance of respiratory epithelium. It also protects the middle ear from nasopharyngeal secretions and sound pressure changes thru the action of the TVP. Its most important function is that it ventilates the middle ear for optimum hearing.

Otitis media is the inflammation of the middle ear. Based on duration it is classified as acute (<3 weeks), subacute ( 3 weeks-3months) and chronic (>3 months). In this case it is classified as acute otitis media. Factors that contribute to the pathogenesis of Otitis Media include infection (URTI which is most likely the etiology in this case), ET dysfunction, immunologic status, allergy, environment and social factors. In this case, the URTI caused mucosal congestion. The ET may be dysfunctional too causing persistent negative middle ear pressure. The ET 15 | P a g e

http://en.wikipedia.org/wiki/Purulence

suddenly opened causing insufflations of nasopharynx secretions. The secretions may have caused bacterial inoculation in the middle ear hence there is inflammation leading to otitis media. The microbiology of OM includes S. Pneumonia, H. Influenza, Moraxella catarrhalis and others. Diagnosis of otitis media is usually made with clinical history and otoscopic findings. Pnuematic otoscopy, audiometry and tympanometry may also be done. Management of AOM includes antimicrobial agents for 7-14 days. If symptomatic failure occurs, change of antimicrobial agents, examination for other foci or tympanocentesis or myringotomy may be performed. After 7-14 days, re-examination may be done, if no effusion is appreciated, periodic follow up may be done. If there is effusion change of antimicrobial agent/s is warranted. If effusion occurs >3 months, myringotomy with tympanostomy tube is done.

28. Casimsiman, Randy Sr. D. 34/M

This is the case of RC, a 34 year old male who was diagnosed with Conductive Hearling Loss and was advised for PTA, ST and tympanometry.

In CHL, the pathology lies in the external ear canal, ear drum (tympanic membrane), ossicles or middle ear. Because of the pathology, impaired conduction of sound occur; hence, there is decreased intensity of sound reaching the cochlea. Unlike SNHL, there is no distortion of sound hence understanding speech is no problem with adequate intensity. Persons with CHL tends to speak softly because they hear the speech louder (bone>air conduction), hence they lower their voices since they perceive that they are speaking loudly. Hearing loss is mild to moderate around 30-40 dB. The most common etiology is Impacted cerumen and other foreign bodies. Other possible etiology include: ear canal atresia, otitis externa/media, otosclerosis, ear canal tumors, and myringitis. Diagnosis of CHL includes otoscopic findings of the ear canal and ear drum; Weber’s test that lateralizes to the affected ear; a negative Rinne test (bone>air conduction); a higher air conduction threshold on PTA. Treatment is directed at the specific etiology. For instance, in cases of impacted cerumen, the cerumen is flushed out; or in AOM, the infection is relieved by antimicrobial agents.

29. Cabonce, Mary Ann P. 32/F

This is the case of MC, a 32 year old female with a chief complaint of decreased hearing. She was diagnosed with Chronic Suppurative Otitis Media and was prescribed with Co-amoxiclav 625mg BID x 7 days as well as Mefenamic Acid 500 mg q6 PRN.

Chronic suppurative otitis media is the result of an initial episode of acute otitis media and is characterized by a persistent discharge from the middle ear through a tympanic perforation. It is an important cause of preventable hearing loss, particularly in the developing world. A history of at least 2 weeks of persistent ear discharge should alert primary health workers to the problem; if the ear could be dry mopped well enough to see the eardrum, then the diagnosis of CSOM can be confirmed by visualization of the perforation in the tympanic membrane. Chronic suppurative otitis media involves a perforation (hole) in the tympanic membrane and active bacterial infection within the middle ear space for several weeks or more. There may be enough pus that it drains to the outside of the ear (otorrhea), or the purulence may be minimal enough to only be seen on examination using a binocular microscope. This disease is much more common in persons with poor Eustachian tube function. Hearing impairment often accompanies this disease.

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30. Dormitorio, Roselle S. 25/f

This is the case of RD, a 25 year old female who presented at the OPD with ear discharge, AD. She was diagnosed with Acute Otitis Media and was prescribed with Amoxicillin 500 mg q8 x 7 days. For the pain, she was prescribed with Mefenamic Acid 500mg q6 PRN.


Otitis media is the inflammation of the middle ear. Based on duration it is classified as acute (<3 weeks), subacute (3 weeks-3months) and chronic (>3 months). In this case it is acute otitis media. Factors that contribute to the pathogenesis of Otitis Media include infection (URTI which is most likely the etiology in this case), ET dysfunction, immunologic status, allergy, environment and social factors. In this case, the URTI caused mucosal congestion. The ET may be dysfunctional too causing persistent negative middle ear pressure. The ET suddenly opened causing insufflations of nasopharynx secretions. The secretions may have caused bacterial inoculation in the middle ear hence there is inflammation leading to otitis media. The microbiology of OM includes S. Pneumonia, H. Influenza, Moraxella catarrhalis and others. Diagnosis of otitis media is usually made with clinical history and otoscopic findings. Pnuematic otoscopy, audiometry and tympanometry may also be done. Management of AOM includes antimicrobial agents for 7-14 days. If symptomatic failure occurs, change of antimicrobial agents, examination for other foci or tympanocentesis or myringotomy may be performed. After 7-14 days, re-examination may be done, if no effusion is appreciated, periodic follow up may be done. If there is effusion change of antimicrobial agent/s is warranted. If effusion occurs >3 months, myringotomy with tympanostomy tube is done.

31. Embuscado, Audrey Nicole V. 1/F

This is the case of AE, 1 year old female who presented with ear discharge. She is diagnosed with Otitis Externa, AS. She was prescribed with PND otic drops 2-3 drops TID and Paracetamol 200mg/5ml, 4ml q4 PRN.


A mixed infection of varying organisms is not infrequent, the most commonly found types being: Staphylococcus pyogenes, Pseudomonas pyocyanea, diphtheroids, Proteus vulgaris; Escherichia coli; Streptococcus faecalis; Aspergillus niger and Candida albicans. Symptoms include irritation, discharge (scanty), pain (usually moderate, sometimes severe, increased by jaw movement) and deafness. Signs that may be present are Meatal tenderness, especially on movement of the pinna or compression of the tragus; moist debris, often smelly and 17 | P a g e

keratotic, the removal of which reveals red desquamated skin and edema of the meatal walls and often the tympanic membrane. Scrupulous aural toilet is the key to successful treatment of otitis externa. No medication will be effective if the ear is full of debris and pus. Investigation of the offending microorganism is essential.

32. Gerillo, Derek Albert T. 6/M

This is the case of DG, a 6 year old male who presented with ear fullness. He is diagnosed with Impacted Cerumen, AU. Aural flushing was done, and the Tympanic membrane visualized. He was advised to avoid ear manipulation and to continue Paracetamol for pain.


33. Barcelon, Arnold E. 36/M

This is the case of AB 36 year old male who presented with epistaxis. He is diagnosed with Nasopharyngeal Carcinoma (Squamous Cell Carcinoma), Stage 1. He is advised to undergo radiation therapy.

Nasopharyngeal CA is considered rare in the west. It is endemic in the far east. The highest incidence is in China, HK and Singapore. Its peak incidence occurs at age 45-55. It has a genetic predisposition. The implicated environmental factors include nitrosamines from salted fish, polycyclic hydrocardbons, chronic sinusitis, poor hygiene and nickel exposure. It is associated with Epstein Barr Virus, since high levels of antibodies against EBV has been identified.

Signs and symptoms include: neck mass, aural fullness, hearing loss, epistaxis, nasal obstruction, head pain, otalgia, neck pain, weight loss and diplopia. Hearing loss occurs when the Eustachian tube is affected. When the tumor is large, there is nasal obstruction. Diplopia may be a sign of distant metastasis.

Diagnosis is based on high index of suspicion. Endoscopy, biopsy and serology may be done. MRI is the imaging of choice since it is a soft tissue mass. For bone involvement and lymph nodes CT scan can complement the MRI.

Initial treatment for all forms is radiation to the primary tumor and both sides of the neck. Chemotherapy and radiation is done for distant metastasis. Neck dissection is necessary for persistent neck disease with control of the primary.

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34. Salminao, Ester 7/F

This is the case of E.S. a 7 year old female who sought consult for ear discharge. Patient was diagnosed with Chronic Suppurative Otitis Media, AU and was advised to continue Ciprofloxacin otic drops. Patient was also advised for culture of ear discharge and patient is for possible mastoidectomy.

If an attack of acute otitis media fails to heal, the perforation and discharge may in some cases persist. This leads to mixed infection and further damage to the middle-ear structures, with worsening conductive deafness. The predisposing factors in the development of chronic suppurative otitis media (CSOM) are: late treatment of acute otitis media: inadequate or inappropriate antibiotic therapy; upper airway sepsis; lowered resistance, e.g. malnutrition, anaemia,immunological impairment; and particularly virulent infection, e.g. measles.

There are two major types of CSOM. Mucosal disease with tympanic membrane perforation (tubo-tympanic disease, relatively safe) and Bony: osteitis cholesteatoma—dangerous (attico-antral disease). Chronic suppurative otitis media (CSOM) is the result of an initial episode of acute otitis media and is characterized by a persistent discharge from the middle ear through a tympanic perforation. It is an important cause of preventable hearing loss, particularly in the developing world. A history of at least 2 weeks of persistent ear discharge should alert primary health workers to the problem; if the ear could be dry mopped well enough to see the eardrum, then the diagnosis of CSOM can be confirmed by visualization of the perforation in the tympanic membrane. Chronic suppurative otitis media involves a perforation (hole) in the tympanic membrane and active bacterial infection within the middle ear space for several weeks or more. There may be enough pus that it drains to the outside of the ear (otorrhea), or the purulence may be minimal enough to only be seen on examination using a binocular microscope. This disease is much more common in persons with poor Eustachian tube function. Hearing impairment often accompanies this disease.

35. Lazaro, Fernando 62/M

This is the case of F.L. a 62 year old male who sought consult for dizziness. After examination and tests were done, patient was diagnosed with Mixed Hearing Loss. Patient was prescribed with Polynerve 1 tablet OD x 2 weeks and was advised to follow-up. In mixed hearing loss, there is a combination of Conductive Hearing Loss and Sensorineural Hearing Loss. There is greater air conduction loss compared with bone conduction indicating impaired sound conduction. There is an increased threshold of bone conduction.

In Sensory Hearing Loss, the pathology may involve the inner and outer hair cells of the Cochlea, hence the transmitted sound waves does not stimulate those structures. HL is usually severe to profound and more so in high frequency sounds (4,000-8,000 kHz). The clarity of speech sound is usually distorted. The hearing is worse in the presence of background noise hence understanding speech is impaired. Etiology may include congenital aplasias of the cochlea, presbyacusis, perilymph fistula, noise-induced, infection or ototoxic drugs such as quinine, aminoglycosides or aspirin or Meniere’s disease. In Neural Hearing loss, the pathology is in the spiral ganglion and CN VIII. There is impaired nerve impulse transmission even if the cochlea is stimulated. There is poorer speech discrimination as compared with sensory hearing loss. It is associated with very severe hearing loss and tinnitus. The etiology may be an acoustic neuroma or vestibular schwannoma.

In CHL, the pathology lies in the external ear canal, ear drum (tympanic membrane), ossicles or middle ear. Because of the pathology, impaired conduction of sound occur; hence, there is decreased intensity of sound reaching the cochlea. Unlike SNHL, there is no distortion of sound hence understanding speech is no problem with adequate intensity. Persons with CHL tends to speak softly because they hear the speech louder (bone>air conduction), hence they lower their voices since they perceive that they are speaking loudly. Hearing loss is mild to moderate around 30-40 dB. The most common etiology is Impacted cerumen and other foreign bodies. Other possible etiology include: ear canal atresia, otitis externa/media, otosclerosis, ear canal tumors, and myringitis. Diagnosis of CHL includes otoscopic findings of the ear canal and ear drum; Weber’s test that lateralizes to the

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affected ear; a negative Rinne test (bone>air conduction); a higher air conduction threshold on PTA. Treatment is directed at the specific etiology. For instance, in cases of impacted cerumen, the cerumen is flushed out; or in AOM, the infection is relieved by antimicrobial agents.

36. Abulon, Leonard

This is the case of L.A., a 2 year old male who sought for ear pain and itchiness. After examination and tests were done, patient was diagnosed with retained cerumen on left ear. Aural flushing was done and patient was advised to follow-up anytime if with problems.

Cerumen is produced in the ear canal by sebaceous and cerumen glands. A protective film is formed consisting of lysozymes, fatty acids, acid milleu which protects the skin from various infections. The ear canal is also cleansed via epithelial migration from the tympanic membrane towards the external meatus which effectively removes the cerumen. Disturbance of this normal self-cleansing mechanism or excessive cerumen secretion may cause impacted cerumen. It is usually precipitated by excessive cleaning of the ears with cotton-tipped swabs. A cerumen plug may be formed which further hinders normal expulsion of the cerumen. Impaction may occur especially when there is contact with water. Drying of the meatal skin and decrease in secretions may cause hardening of the cerumen which causes retention especially in narrow ear canals.

Although impacted cerumen may cause vertigo and tinnitus, ear pressure symptoms such as ear fullness and hearing difficulty in the affected ear are the usual encountered symptoms. It is mainly diagnosed by visualization through an otoscope wherein a yellowish, brownish to blackish material is observed to obstruct the ear canal. Impacted cerumen also sometimes lead to otitis externa. It may be removed via a small instrument such as a hook or curette or be flushed away by aural cleaning with irrigation jet or a syringe.

37. Alano, Alpha Grace 23/F

This is the case of A.A., a 23 year old female who sought for decrease hearing on left ear. After examination and tests were done, patient was diagnosed with chronic tympanomastoiditis left ear. Patient was status post radical mastoidectomy, of right ear (2001) and grafted right tympanic membrane. Patient was prescribed with Ciprofloxacin + Dexamethasone otic drops 2-3 drops on both ears three times a day for 7 days. Also, patient was advised to come back on Monday for CP clearance. Mastoiditis is the inflammation of the air cells in the mastoid process involving the mucus membrane. It usually originates from an infection of the middle ear and is actually the most common complication of otitis media. Pathogenetic factors include degree of mastoid pneumatisation, infecting organism’s virulence, host’s immune system and treatment for otitis media especially if antibiotic treatment is inadequate. Wegener’s disease can also cause mastoiditis as well as infections and abscess formation. Local pain and fever are the most frequent complaints. A prominent auricle with retroauricular swelling, mastoid tenderness and otorrhea compose the classic clinical triad of mastoiditis. The triad may not always be present hence mastoiditis should be investigated in opatients treated for otitis media who fails to improve or worsens in 2-3 weeks. Complications include epidural abscess, brain abscess, meningitis, subdural abscess, thrombophlebitis, bezoid abscess in the SCM, and subperiosteal abscess. Definitive treatment includes mastoidectomy, with IV antibiotics. In early stages of mastoidectomy, IV antibiotics and inpatient assessment may suffice.

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38. Lacasa, Danica Fe 6/F

This is the case of D.L. a 6 year old female who came in for ear pain. Patient was diagnosed with diffuse otitis externa right ear. Aural cleaning was done. Patient was advised to continue Cloxacillin 200 mg/5ml and for daily cleaning of ear.

Diffuse Otitis Externa is an acute bacterial infection of the ear canal skin with a mixed flora of gram negative organisms and anaerobes. It is usually precipitated by an inflammatory condition of the EAC such as eczema, allergies, dermatitis etc. The Tympanic membrane is also usually involved and its development is promoted by a warm, moist environment. Itching is the primary symptom. Pain is also observed as well as crusting, purulent discharge and obstruction which may lead to conductive hearing loss. Complications include perichondritis, cellulitis, abscess formation or necrotizing otitis externa in predisposed patients. Treatment includes meticulous aural cleaning and hygiene while keeping the ear dry. Antibiotics with steroids as otic drops may be given for not more than 2 weeks.

39. Fabros, Elmar M. 3/M

This is the case of E.F a 3 year old male who came for mass on the R post auricular area. Patient was diagnosed with impacted cerumen. Aural flushing was done on the right ear, mineral oil of 2-3 drops QID was prescribed for the left ear and patient was advised to follow up on Saturday.


40. Ynot, Andrew Emerson

This is the case of A.Y. who came in due to ear pain on both ears. Patient was diagnosed with Acute Otitis Media on both ears. Patient was prescribed with Amoxicillin 250/5ml to 6.5 ml every 8 hours if with pain and was advised for follow-up after 1 week.

Acute Otitis Media is an acute infection (<3 weeks) causing inflammation of the middle ear space It is the second most common disease in children (upper respiratory infection is the most common). Its pathophysiology includes eustachian tube dysfunction which results in negative middle ear pressures leading to transudative fluid collection in the middle ear space and subsequent infection. Common pathogens include S. pneumoniae (most common), H. influenza, Moraxella (Branhamella) catarrhalis; gram negative bacilli and Group B Streptococcus may be found in infants; viral pathogens are often present alone (sterile otitis media) or concurrently with bacterial pathogens.

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Risk factors that may contribute to eustachian tube dysfunction include craniofacial or skull base abnormalities, recurrent upper respiratory infections, nasal allergy, attendance at a child care facility, bottle feeding or supine baby feeds (reflux into ear), smoking or presence of second-hand smoke, history of immunological disorders (especially IgA and IgG subclass 2 and 3 deficiencies) or ciliary dysfunction (Kartagener syndrome), gastroesophageal reflux, prolonged nasotracheal intubation or nasogastric tubes, and adenoid hypertrophy. Signs and symptoms include otalgia (irritability and tugging of ears in children), aural fullness, hearing loss, tinnitus, fever, hyperemic or thickened TM, fluid in middle ear space (nonmobile or bulging TM, air-fluid levels, bubbles, yellow hue). Diagnosis is usually made by clinical and physical exam, audiogram (CHL <30 dB) and tympanometry.

Treatment includes antimicrobial therapy. First-line antimicrobials should include gram positive and gram negative coverage, may consider beta lactamase resistant agents due to increasing beta-lactamase activity in certain regions. Treatment duration is at least 7–10 days (typically resolves infection within 72 hours). If no resolution, broader spectrum coverage or beta-lactamase resistant agents may be used. Adjunctive Therapy includes antipyretics, analgesics, oral or nasal decongestants (to relieve associated nasal congestion, no provenbenefit in the treatment of acute otitis media). Myringotomy may be considered for severe otalgia or toxic patients

41. Berras, Eldrigo 3/M

This is the case of E.B. a 3 year old male, who came in for mass on right pre-auricular area. Patient was diagnosed with lymphadenitis to consider primary complex infection. Patient was advised for chest xray, to put warm compress on affected area. Patient was prescribed with Co-Amoxiclav 250mg/5ml, 5 mlevery 8 hours and was advised to come back once with result.

Reactive adenitis is typically secondary to a nasopharyngeal infection, may occur from any infection of the head and neck. The primary infection may have resolved with persistent, enlarged cervical lymph nodes. Signs and symptoms include painful swelling of the cervical lymph nodes, induration, fluctuating size or tenderness.

Diagnosis is made by clinical history and exam. The patient must undergo a careful exam for the primary infection. Open biopsy is done if malignancy is suspected. Treatment is targeted to address the primary infection. If no primary infection site is identified, a trial of broad-spectrum antibiotics versus close observation may be done.

42. Aglipay, Errol 63/M

This is the case of E.A. a 63 year old male who came in because of dysphagia. We are considering presbyesophagus. Paitent was advised to increase oral fluid intake and was referred to IM due to hypertension.

Presbyesophagus is a term used to describe an abnormal shape of the swallowing tube (esophagus) that occurs in some individuals. In this situation, the esophagus appears wavier than a typically straight esophagus. This change may impact esophageal movement (motility). The term presbyesophagus (presby is Latin for old) was originally used to describe a change in esophagus movement related to aging even though there has been limited evidence that aging by itself causes trouble swallowing.

Some people with presbyesophagus have trouble swallowing liquids or solids or have heartburn. A sensation of food being stuck or slow to pass through the esophagus is often described. Many people, however, experience no symptoms at all.

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Tests used to diagnose presbyesophagus could include a barium swallow x-ray, an upper endoscopy (EGD), or an esophageal motility test (manometry). Treatment includes diet modification. The patient is advised to eat slowly and to take smaller bites. Talk while eating is prohibited. Patient is also advised to sit in an upright position after meals, use a blender to puree solid foods if needed, thicken liquids with milk, juice, broth, gravy or starch to make swallowing easier.

43. Villedo, MEliza 10/F

This is the case of M.V. a 10 year old female who came in for wound on the right ear. Patient was diagnosed with acute otitis media on right ear. Patient was prescribed with Amoxicillin 250mg/5ml, 5 ml every 8 hours for 7 days. Also, patient was prescribed with Paracetamol 250 mg/5ml, 5 ml every 4 hours for pain. Patient was advised for follow-up after 1 week.



44. Siat, Bernardino 34/M

This is the case of B.S. a 34 year old male who came in for itchiness on both ears. Patient was diagnosed with Otitis Externa, OU. Patient was prescribed with Aplosyn otic drops 2-3 drops three times a day for 5 days.

Otitis externa is a diffuse inflammation of the skin lining the external auditory meatus. It may be bacterial or fungal, and is characterized by irritation, desquamation, scanty discharge and tendency to relapse. The treatment is simple, but success is absolutely dependent upon patience, care and meticulous attention to detail. Some people are particularly prone to otitis externa, often because of a narrow or tortuous external canal. Most people can allow water into their ears with impunity but in others otitis externa is the inevitable result. Swimming baths are a common source of otitis externa. Poking the ear with a finger or towel further traumatizes the skin and introduces new organisms. Further irritation occurs, leading to further interference with the ear, so causing more trauma. A vicious circle is set up.Otitis externa may occur after staying in hotter climates than usual where

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increased sweating and bathing are predisposing factors. Underlying skin disease, such as eczema or psoriasis, may occur in the ear canal and produce very refractory otitis externa. Ear syringing, especially if it causes trauma, may result in otitis externa.


45. Salazar, Gorgonio Jr. 55/M

This is the case of G. S. a 55 year old male who came in for ff-up regarding submandibular mass. Patient was diagnosed with Pleomorphic adenoma, submandibular area, R. Patient was advised excision under general anesthesia and to come back once decided.

Pleomorphic adenoma or mixed benign tumor is a benign heterogeneous tumor composed of variable epithelial and myoepithelial components. It is the most common tumor of the salivary glands and may also be found in the respiratory tract and nasal cavity. It is slightly more common in women. It may present as a slow growing (over years), unilateral, painless, firm mass (usually toward the tail of the parotid). It rarely progresses todysphagia (if there is pharyngeal extension), dyspnea, or hoarseness (laryngeal involvement), or facial nerve palsies. Deep lobe (10%) involvement may present with intra-oral swelling. Recurrent signs and symptoms include multilobular nodules, not discrete; may arise in scar, subcutaneous tissue, deep lobe, or facial nerve sheath. Complications may include rare malignant transformation (Carcinoma Ex-Pleomorphic Adenoma and Sarcoma) or “benign” metastasizing.

On histopathology, cellular components include: myoepithelial component: spindle shaped with hyperchromatic nuclei, may be more than one cell layer thick; epithelial components: varied growth patterns (trabecular, solid, cystic, papillary); and stromal components: product of myoepithelial cells: myxoid, chondroid, fibroid, or osteoid components. Fibrous pseudocapsule (except minor glands) and micro-pseudopod extensions can also be seen.

Diagnosis is made by biopsy specimen (parotidectomy), or Fine Needle Aspiration. Surgical resection (superficial or total parotidectomy) may be performed with wide margin for pseudopod extensions to prevent recurrence (>90% 10-year cure, approximately 30% recurrence rate for enucleation alone). It is radioresistant.

46. Garnatas, Reynaldo 44/M

This is the case of R.G. a 44 year old male who came in for ff-up regarding his right ear discharge. Patient was diagnosed with acute otitis media on the right ear. Patient was asked to consume Ciprofloxacin 500 mg BID for 3 more days and to follow-up if with problem.

Acute Otitis Media is an acute infection (<3 weeks) causing inflammation of the middle ear space It is the second most common disease in children (upper respiratory infection is the most common). Its pathophysiology includes eustachian tube dysfunction which results in negative middle ear pressures leading to transudative fluid collection in the middle ear space and subsequent infection. Common pathogens include S. pneumoniae (most

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common), H. influenza, Moraxella (Branhamella) catarrhalis; gram negative bacilli and Group B Streptococcus may be found in infants; viral pathogens are often present alone (sterile otitis media) or concurrently with bacterial pathogens.

Risk factors that may contribute to eustachian tube dysfunction include craniofacial or skull base abnormalities, recurrent upper respiratory infections, nasal allergy, attendance at a child care facility, bottle feeding or supine baby feeds (reflux into ear), smoking or presence of second-hand smoke, history of immunological disorders (especially IgA and IgG subclass 2 and 3 deficiencies) or ciliary dysfunction (Kartagener syndrome), gastroesophageal reflux, prolonged nasotracheal intubation or nasogastric tubes, and adenoid hypertrophy. Signs and symptoms include otalgia (irritability and tugging of ears in children), aural fullness, hearing loss, tinnitus, fever, hyperemic or thickened TM, fluid in middle ear space (nonmobile or bulging TM, air-fluid levels, bubbles, yellow hue). Diagnosis is usually made by clinical and physical exam, audiogram (CHL <30 dB) and tympanometry.

Treatment includes antimicrobial therapy. First-line antimicrobials should include gram positive and gram negative coverage, may consider beta lactamase resistant agents due to increasing beta-lactamase activity in certain regions. Treatment duration is at least 7–10 days (typically resolves infection within 72 hours). If no resolution, broader spectrum coverage or beta-lactamase resistant agents may be used. Adjunctive Therapy includes antipyretics, analgesics, oral or nasal decongestants (to relieve associated nasal congestion, no provenbenefit in the treatment of acute otitis media). Myringotomy may be considered for severe otalgia or toxic patients

47. Valdez, Loraine C. 14/F

This is the case of L.V. a 14 year old female who came in for ff-up regarding her right cheek mass. We are considering an epidermal inclusion cyst on the right cheek. Patient was advised for FNAB of right cheek mass.

Epidermoid cysts represent the most common cutaneous cysts. While they may occur anywhere on the body, they occur most frequently on the face, scalp, neck, and trunk. Historically, epidermoid cysts have been referred to by various terms, including follicular infundibular cysts, epidermal cysts, and epidermal inclusion cysts. The term epidermal inclusion cyst refers specifically to an epidermoid cyst that is the result of the implantation of epidermal elements in the dermis. Because most lesions originate from the follicular infundibulum, the more general term epidermoid cyst is favored. The term sebaceous cyst should be avoided because it implies that the cyst is of sebaceous origin. Finally, the term milia refers to very small, superficial epidermoid cysts.

Epidermoid cysts are benign lesions; however, very rare cases of various associated malignancies have been reported. Epidermoid cysts result from the proliferation of epidermal cells within a circumscribed space of the dermis. Analysis of their lipid pattern demonstrates similarities to the epidermis. In addition, epidermoid cysts express cytokeratins 1 and 10, which are constituents of the suprabasilar layers of the epidermis. The source of this epidermis is nearly always the infundibulum of the hair follicle, as evidenced by the observation that the lining of the 2 structures is identical.

Inflammation is mediated in part by the horny material contained in epidermoid cysts. Extracts of this material have been shown to be chemotactic for polymorphonucleocytes. Studies have suggested that human papillomavirus (HPV) and exposure to ultraviolet light (UV) may play a role in the formation of epidermoid cysts. The manner in which carcinomas may arise within epidermoid cysts is unclear. In a series of epidermoid cysts with carcinoma, immunohistochemical results for HPV were negative, suggesting that HPV is not likely to play a role in the development in squamous cell carcinoma (SCC) in epidermoid cysts. Chronic irritation or repetitive trauma to the epithelial lining of the cyst has been suggested to play a role in malignant transformation; however, this relationship has not been established.

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Epidermoid cysts are usually asymptomatic. Discharge of a foul-smelling “cheeselike” material may be described. Less frequently, the cysts can become inflamed or infected, resulting in pain and tenderness. In the uncommon event of malignancy, rapid growth, friability, and bleeding may be reported. Epidermoid cysts appear as flesh–colored-to-yellowish, firm, round nodules of variable size. A central pore or punctum may be present. Reportedly, epidermoid cysts are most common (in descending order of frequency) on the face, trunk, neck, extremities, and scalp. Rare cases of epidermoid cysts occurring in bone, breast, and various intracranial locations have been reported. Epidermoid cysts in the breast and genital area are not uncommon in the general population. The ocular and oral mucosae can also be affected and, cysts have been reported on the palpebral conjunctivae, lips, buccal mucosa, tongue, and uvula.

Asymptomatic epidermoid cysts do not need to be treated. Intralesional injection with triamcinolone may hasten the resolution of inflammation. Oral antibiotics may occasionally be used. Epidermoid cysts may be removed via simple excision or incision with removal of the cyst and cyst wall though the surgical defect. If the entire cyst wall is not removed, the lesion may recur. Excision with punch biopsy technique may be used if the size of the lesion permits. Minimal-incision surgery, with reduced scarring, has been reported. Incision and drainage may be performed if a cyst is infected. This may facilitate the clearing of infection; however, it will not eradicate the cyst.

48. Dagium, Anna Luna 19/F

This is the case of A.D. a 19 year old female who came in for ff-up regaring nasal polyp. Patient was diagnosed with Chronic Rhinosinusitis with nasal Polyposis on the right. Patient was advised to continue Clarithromycin for 1 more week, NaCL Nasal spray. Also, patient was advised Nasonexx nasal spray 2 sprays once a day for 2 weeks. Patient was advised to come back for biopsy of nasal mass.

Sinus inflammation or sinusitis often occurs in the setting of rhinitis hence the term rhinosinusitis is often used. The pathophysiology includes anatomical (compromised patency of ostia causes hypooxygenation and impairment of sinus drainage), dysfunction of cilia motility, change in quality of secretions and immune dysfunction. Pathogens involved include anaerobes, S. aureus, H. influenzae, and in 1–2% of cases, fungal pathogens.

Patients with chronic rhinosinusitis present with more subtle symptoms of nasal obstruction, less fever and pain complaints as compared with patients with acute form of the disease. Associated Symptoms include anosmia/hyposmia, loss of taste, allergic components (sneezing, watery eyes), fever, malaise, lethargy, cough, eustachian tube dysfunction. Physical exam is done via rhinoscopy/nasopharyngoscopy to look for osteomeatal unit obstruction, nasal masses and obstruction, purulence, hypertrophied adenoid tissue. There may also be decreased sinus transillumination (not reliable) polyps and edema.

The following should be evaluated: anatomically, there may be deviated septum, mucosal edema (rhinitis, allergic), hypertrophic adenoids, nasal masses, nasal foreign bodies, nasogastric tubes, nasal packing, facial fractures, concha bullosa, lateral deviated uncinate process, paradoxical middle turbinate, uncinate hypoplasia, nasal polyposis. Ciliary dysfunction may also be present. It is also common in immunocompromised (HIV, diabetes, malnutrition), cystic fibrosis, smoker, and elderly. Local causes include apical dental infection, trauma, and barotraumas.

Chronic Sinusitis is treated with Antibiotics: 3–6 weeks regimen with broad spectrum agents (eg, amoxicillin-clavulanate, cefuroxime, ciprofloxacin, clarithromycin, cefpodoxime, cefprozil). Nasal corticosteroid sprays, nasal hypertonic saline irrigations, oral decongestants, and mucolytic agents are useful for chronic sinusitis.

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Medical management often fails with chronic sinus disease, hence surgical management is frequently required. A functional endoscopic sinus surgery may be done. Allergy management is also advised.

In Nasal Polyposis, the pathophysiology is unclear. It may be secondary to abnormal cellular homeostasis from chronic inflammation resulting in polypoidal degeneration, typically arises from lateral nasal wall. It is associated with chronic sinusitis (approximately 50%), ASA intolerance, and asthma (Samter’s Triad), allergy, fungal sinusinfection, cystic fibrosis, trauma, and metabolic diseases. It usually presents as a smooth, pale, intranasal clustered grape-like masses (usually bilateral), nasal obstruction, anosmia, postnasal drip, rhinorrhea, and hyposomia. Diagnosis is done via anterior rhinoscopy, nasal endoscopy, CT of paranasal sinus (nonenhancing nasal mass with partial or complete sinus opacification may reveal expansion of superior nasal fossa and ethmoid air cells in advanced cases, also required to evaluate for potential encephalocele, gliomas, or inverting papillomas) Histopathology Types include edematous (few inflammatory cells with edematous stroma), inflammatory (predominantly inflammatory cells), and fibrous (collagen stoma). Complications may include proptosis, diplopia, bone erosion, osteitis, and even meningitis.

Medical Management includes allergy desensitization, avoidance of aspirin or other allergens, nasal corticosteroid sprays or oral corticosteroids, and hypertonic saline irrigations. Polypectomy is effective in short term (high rate of recurrence), and provides a biopsy specimen. Endoscopic Sinus Surgery is the treatment of choice, includes polypectomy, complete sphenoethmoidectomy, antrostomy for ventilation and drainage. The polypoid specimen should be sent as specimen to evaluate for potential underlying tumor. Lipoxygenase pathway inhibitors should also be considered.

49. Cleofe, Cecilia P. 55/F

This is the case of C.C. a 55 year old female who came in for ff-up regarding hoarseness. Patient is having laryngopharyngeal reflux and was advised to continue Omeprazole 20mg/cap, 1 cap BID for 7 weeks.

Reflux-induced laryngitis is an inflammatory response of laryngeal mucosa from Laryngopharyngeal Acid Reflux (LPR). Symptoms include hoarseness (worse in the morning), choking spells at night, regurgitation, bitter taste in mouth, globus sensation, cough, chronic throat clearing, and postprandial heartburn (seen <50% of the time in LPR). Laryngeal Findings includes erythema and edema of the posterior commissure, arytenoids, superior surface of the vocal folds, and laryngeal surface of the epiglottis; diffuse supraglottic edema; laryngeal pachydermia (interarytenoid); and granulomas of the vocal process.

Because of reservations regarding specificity of the laryngoscopic examination, many physicians have opted to begin a trial of empiric therapy. Four categories of drugs are used in treating laryngopharyngeal reflux (LPR): proton pump inhibitors (PPIs), H2-receptor agonists, prokinetic agents, and mucosal cryoprotectants. PPIs are the mainstay of treatment. PPIs are the most effective drugs in treating GERD that involves the esophagus. Acid reflux events are decreased by greater than 80%, and healing of esophagitis is reported in 80-90% of patients. The response to medical therapy in patients with suspected supraesophageal complications of GERD is not as efficacious as that noted in esophageal complications of GERD. Although PPIs appear to be effective, higher doses for a longer duration are necessary as compared with esophageal GERD disease.

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50. Bonola, Kycel Jane 10/F

This is the case of K.B. a 10 year old female who came in for ear discharge. Patient is diagnosed with chronic suppurative otitis media in remission for both ears which is now resolving. Patient was advised to continue Ofloxacin for 1 more week and was advised.



51. Callada, Cedric 4/M

This is the case of C.C.a 4 year old male who came in for right ear pain, Patient had foreign body (pellet) on his right ear. Removal of foreign body was done. Patient was advised to keep ear dry.

In small children, most cases occur when small objects such as beads or pellet in this case is inserted inside the EAC. In adults, it consists of noise reducing ear plugs or cleaning materials stuck inside the canal. Insects may also be stuck inside the canal. History is often adequate to make a diagnosis and is confirmed via otoscopy. Injuries, swelling, inflammation or bleeding may make the visualization difficult. Differential diagnosis includes dry blood, impacted cerumen, cholesteatoma, ear canal tumors, or otitis externa especially fungal infections. If the FB is deeply penetrating, a secondary middle ear and inner ear damage may occur. Prolonged retention may also cause secondary otitis externa usually associated with foul-smelling discharge. Treatment is directed at removing the foreign body by a small instrument such as an extraction hook. It should not be irrigated with water for possibility of pushing the FB further inside the canal. In children, extraction is sometimes necessarily done under GA. Insects may be killed with a 10% lidocaine solution. Rarely indicated, surgical incision may be done to extract the retained FB.52. Tortosa, Maria S. 50/F

This is the case of M.T a 50 year old female who came in pain on both ears. Patient is diagnosed with otitis externa both ears. Polymyxin+Neomycin+Dexamethasone 2-3 drops QID for 7 days was prescribed. Also, Mefenamic acid Q6, PRN for pain was given.

Diffuse Otitis Externa is an acute bacterial infection of the ear canal skin with a mixed flora of gram negative organisms and anaerobes. It is usually precipitated by an inflammatory condition of the EAC such as eczema, allergies, dermatitis etc. The Tympanic membrane is also usually involved and its development is

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promoted by a warm, moist environment. Itching is the primary symptom. Pain is also observed as well as crusting, purulent discharge and obstruction which may lead to conductive hearing loss. Complications include perichondritis, cellulitis, abscess formation or necrotizing otitis externa in predisposed patients. Treatment includes meticulous aural cleaning and hygiene while keeping the ear dry. Antibiotics with steroids as otic drops may be given for not more than 2 weeks.

53. Morales, Teresa G. 32/F

This is the case of T.M. a 32 year old female who came in because of decrease hearing. Patient is diagnosed with traumatic tympanic membrane perforation left ear and was advised to keep ear dry.

Pathophysiology of TM perforation includes acute/chronic suppurative otitis media (most common cause), persistent perforation after extrusion of a pressure equalization tube, trauma (hand blow to the ear, barotrauma, diving, water skiing, explosion, forceful irrigation, slag burns), iatrogenic, cholesteatoma (associated with peripheral perforations). Spontaneous closure of a perforated TM results in a monomeric membrane (misnomer: actually has two layers, outer epidermal and inner mucous) Types of TM perforation includes:

1. Central: perforation does not involve the annulus, typically infectious etiology.2. Marginal: involves the annulus, less likely to resolve spontaneously, and has a higher association with

cholesteatomas.3. Subtotal: large defect completely surrounded with an intact annulus

Symptoms of TM perforation includes CHL and tinnitus. It is diagnosed via an otoscopic exam and audiogram. Treatment includes keeping the ear dry. Tympanoplasty may be considered for a persistent perforation.

54. Rivera, Dwight Aaron 7/M

This is the case of D.R a 7 year old male who came in came in because of wound on left ear. Patient is diagnosed with Otitis externa left ear and impacted cerumen on right ear. Patient was prescribed with Cloxacillin 250 mg/5ml, 5ml every 6 hours and Ibuprofen 200mg/5ml, 4ml every 6 hours for pain. Also, patient was advised to avoid manipulation of ears.

Acute Otitis Externa is a bacterial infection involving the skin of the external auditory canal. Pathophysiology includes an aggressive washing of cerumen or retention of water (“Swimmer’s Ear”) results in a more alkalotic EAC; decreased production of antibacterial agents (eg, lysozyme) which are permissive for bacterial overgrowth and penetration into the apopilosebaceous unit; and microtrauma (eg, cotton swabs, fingernails, or hairpins) directly injure EAC soft tissue. Pathogens include Pseudomonas aeruginosa (most common, opportunistic infection), Staphylococcus, and gram-negative bacilli. Imunocompromised patients (diabetics, HIV), and swimmers are more at risk to develop Otitis Externa.

Signs and symptoms include pain with posterosuperior manipulation of auricle, tragal tenderness, otalgia, and pruritus; edematous and erythematous EAC (may have exudative or purulent discharge). Patients may have a conductive hearing loss. Clinical history and physical exam is adequate to make a diagnosis. Perforation of the TM may suggest an underlying chronic otitis media.

Management includes thorough and frequent ear canal debridement with fine suction to allow opening of apilosebaceous unit. For diabetics, aggressive management of diabetes is necessary. Signs and symptoms of malignant external otitis (granulation tissue in the canal, cranial nerve involvement) must also be evaluated. Otic Drops may be prescribed for acidification, drying, antibiotic, or antibiotic/corticosteroid combination drops for 7–10 days (consider placing an otowick to aid drops to reach medial EAC if canal is too edematous to visualize TM).

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Oral Pain Medication may also be given and some may require narcotics. Oral Antibiotics is typically not required unless signs of cellulitis, concurrent otitis media, persistent or severe symptoms, or systemic illness. Culturing the EAC for recalcitrant infection may be considered.

55. Monteverde, Elieza Cyrene 11/M

This is the case of E.M.. a 11 year old female who came in came in with enlarged parotid. We were considering suppurative lymphadenitis. Patient was advised to have soft diet, for CBC and to put warm compress on area. Patient was also prescribed with Clindamycin 75mg/5ml, 65 ml every 6 hours and Ibuprofen syrup 200 mg/5ml every 6 hours for pain. Patient was advised to follow-up on the ER the following day

Suppurative lymphadenopathy is most frequently caused by Staphylococcus aureus and group A B-Streptococcus. These neck masses usually develop in the submandibular or jugulodigastric region and are often accompanied by sore throat, skin lesions, and symptoms of upper respiratory tract infection. Empirical antibiotic therapy against anaerobic and gram-positive organisms is recommended as the first line of management. If this fails, either FNA or incision and drainage may be indicated.

56. Raquel, Lanz Patrick 6/M

This is the case of L.R.. a 6 year old male who came in came in for pain on right ear. Patient is having impacted cerumen on both ears and was advised to put in mineral oil and to come back on Aug. 20.



57. Balondo, Carmencita 37/F

This is the case of C.B. a 37 year old female who came in came in because of decrease hearing on right ear. Patient is diagnosed with traumatic perforation of eardrum on right ear and was prescribed with Mefenamic acid every 6 hours as necessary for pain. Patient was advised to come back on Saturday.

Acute tympanic membrane (TM) perforations are caused by direct penetrating trauma, barotrauma, otitis media, corrosives, thermal injuries, and iatrogenic causes (foreign-body removal, tympanostomy tubes). TM perforations are occasionally accompanied by injuries to the ossicular chain and temporal bone.

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Patients complain of a sudden onset of ear pain, vertigo, tinnitus, and altered hearing after a specific event. Physical examination of the TM reveals a slit-shaped tear or a larger perforation with an irregular border. An acute perforation can have blood on the perforation margin and blood or clot in the canal. Subacute or chronic perforations have smooth margins and a round or ovoid shape.

Treatment of acute TM perforations is tailored to the mechanism of injury. All easily removable foreign bodies should be extracted. Corrosive exposures require face, eye, and ear decontamination. Antibiotics and irrigation do not improve the rate or completeness of healing unless the injury is associated with OM. Systemic antibiotics should be reserved for perforations associated with OM, penetrating injury, and possibly water-sport injuries. Topical steroids impede perforation healing.

Patients are instructed to avoid allowing water to get into the ear while the perforation is healing and to return if symptoms of infection appear. Even though nearly 80% of all TM perforations heal spontaneously, all TM perforations should be referred to an otolaryngologist for follow-up for possible myringoplasty.

58. Villamor, Remedios

This is the case of R.V. a 70 year old female who came in for decrease hearing in left ear. Patient has chronic perforation of left ear and chronic suppurative otitis media on right ear. Patient was prescribed with Ofloxacin otic drops 2-3 drops on right ear for 1 week. Patient was also advised to keep ear dry and to ff-up after 1 week.

Chronic suppurative otitis media is defined as a persistent or intermittent infected discharge through a nonintact tympanic membrane (ie, perforation or tympanostomy tube). There are a number of mechanisms by which a persistent tympanic membrane perforation may develop. In most cases, CSOM occurs as a consequence of an episode of AOM with perforation, with subsequent failure of the perforation to heal. There is also an association between OME and chronic perforation. The continued presence of a middle ear effusion leads, in some cases, to degeneration of the fibrous layer of the tympanic membrane. This weakness of the tympanic membrane both predisposes to perforation and reduces the likelihood of spontaneous healing. Although most tympanic membranes heal spontaneously after the extrusion of ventilation tubes, a small percentage do not. Traumatic perforations, particularly if large, may fail to heal.

There are two main mechanisms by which a chronic perforation can lead to continuous or repeated middle ear infections: (1) Bacteria can contaminate the middle ear cleft directly from the external ear because the protective physical barrier of the tympanic membrane is lost. (2) The intact tympanic membrane normally results in a middle ear "gas cushion," which helps to prevent the reflux of nasopharyngeal secretions into the middle ear via the eustachian tube. The loss of this protective mechanism results in the increased exposure of the middle ear to pathogenic bacteria from the nasopharynx. The most commonly isolated bacteria responsible for CSOM are P aeruginosa, S aureus, and the Proteus species.

Typically, a patient with CSOM presents with a history of otorrhea, which may be either intermittent or continuous, and hearing loss. The discharge is usually mucopurulent, although chronic infection of the middle ear may lead to polyp or granulation tissue formation, which can result in bloodstained otorrhea. Pain is not a usual feature of CSOM and its presence should alert the physician to the possibility of a more invasive pathology.

Inspection may reveal scars from previous surgery for chronic ear disease. To properly visualize the tympanic membrane, it is necessary to suction the discharge from the external auditory canal with an operating microscope. The middle ear mucosa, seen through the perforation, is edematous, sometimes to the point of polyp formation. If the perforation is of sufficient size, it may be possible to identify the presence of ossicular discontinuity due to necrosis of the long process of the incus.

The treatment goals of uncomplicated CSOM are to eliminate infection, prevent further infection, and restore normal functioning to the middle ear. Both medical and surgical interventions play a role in achieving these

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aims. Aural toilet is important for the successful treatment of CSOM, particularly when topical medication is used. Clearing the discharge from the external auditory canal allows the topical agent to reach the middle ear in an adequate concentration. Although topical antibiotics are more effective than systemic antibiotics in the treatment of CSOM, many contain aminoglycosides, which are potentially ototoxic. Despite the risk of ototoxicity, topical aminoglycosides are widely prescribed by otolaryngologists for the treatment of CSOM because the benefits of effective treatment outweigh the risks. The recent availability of topical ofloxacin preparations may prove to be as effective as topical aminoglycosides without the ototoxic potential.

Systemic antibiotics tend to have a poor penetration of the middle ear and are therefore less effective than topical antibiotics. Because P aeruginosa is the primary pathogen responsible for CSOM, the choice of oral systemic antibiotics is limited. Both ciprofloxacin and ofloxacin have good antipseudomonal activity. Some cases of CSOM resolve with medical treatment, and if the patient is asymptomatic, then no further intervention is required. However, if otorrhea recurs or persists despite medical treatment or if the patient feels handicapped by a residual conductive hearing loss, surgical therapy should be considered.

Ideally, surgery should be carried out when the infection has been adequately treated and the middle ear mucosa is healthy, since the chance of a successful outcome is increased. In this situation, a tympanoplasty, with repair of the tympanic membrane and ossicular chain (if required), is recommended.

In cases that are refractory to medical treatment, it is necessary to perform tympanomastoid surgery (tympanoplasty combined with a cortical mastoidectomy). The aims of this procedure are to aerate the middle ear and mastoid, remove chronically inflamed tissue, repair the tympanic defect, and reconstruct the ossicular chain. The achievement of all of these goals often requires more than one procedure.

59. Leynes, Lorenza 76/F

This is the case of L.L a 76 year old female who came in due to neck mass. Upon history and thorough examination, patient has been found out to have essentially normal ENT findings.

Evaluation of neck masses starts with history. The character of Neck Mass should be elicited including onset, duration, and progression of growth, and pain. Contributing factors include recent upper respiratory infection, sinus infection, otitis media, or other head and neck infection; exposure to pets and other animals; recent travel; exposure to tuberculosis; risk of malignancy (previous excision of skin or scalp lesions, family history of cancer, smoking and alcohol abuse, radiation therapy, other malignancies); recent trauma; immunodeficiency (risk of HIV, corticosteroids, uncontrolled diabetes); age (often infectious in children, higher risk of malignancy in adults). Associated Symptoms may include fever, postnasal drip, rhinorrhea, sore throat, otalgia, night sweats, weight loss, malaise, dysphagia, and hoarseness.

On Physical Exam, the character of Neck Mass is evaluated on size (normal hyperplastic nodes rarely exceed 2 cm), distribution, mobility, tenderness and fluctuance (infectious), consistency (firm, elastic, soft, compressible), solitary mass versus general cervical adenopathy, lesions and character of the overlying skin (eg, erythematous, blanching, vascular signs, fistulas, induration, radiodermatitis, necrotic). The following should also be done: thorough head and neck exam for primary malignancies (attention to nasopharynx, oral cavity, base of tongue, tonsilar fossa, nasal cavity, external ear canal, scalp, thyroid, and salivary glands); palpate other lymphatic sites (eg, inguinal, axillary, supraclavicular); palpate thyroid gland, liver, and spleen (lymphoma, mononucleosis); auscultation for vascular abnormalities.

CT/MRI of Neck provides greater differentiation of abscess, neoplasms, vascular lesions, hematomas, or congenital abnormalities. Laboratory Evaluation includes complete blood count with differential, monospot, Purified Protein Derivative (PPD), HIV testing, cat-scratch antigen titers, toxoplasmosis titers, and Epstein-Barr virus serology tests. Ultrasound identifies cystic masses, and when combined with Doppler further defines vascular lesions. Fine-needle Aspirate (FNA) provides fluid for culture and sensitivity, indicated for nonresolving masses

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suspicious for malignancy (firm, large [>2 cm], nontender, asymmetric neck masses) without a known primary. Open Biopsy is indicated for persistent idiopathic adenopathy or high suspicion of malignancy (if FNA is negative or nondeterminate and complete work-up does not reveal a primary site), prepare for possible completion of neck dissection if frozen section is positive. Angiography demonstrates primary vascular diseases. Panendoscopy which includes direct laryngoscopy, esophagoscopy, and bronchoscopy may be considered to evaluate for a primary site for malignancy.

60. Nuada, Jhameran 9mo./M

This is the case of N.J., a 9 month old male who came in due to ear discharge on both ears. Patient is diagnosed with Acute otitis media and was prescribed with Amoxicillin suspension 125/5ml, 2.5 ml every 6 hours. Mother was advised to for follow-up on Aug 25, 2011.



61. Balondo, Carmencita 37/F

This is the case of C.B., a 37 year old female who came in came in because of decrease hearing on right ear. Patient is diagnosed with traumatic perforation of eardrum on right ear and was prescribed with Mefenamic acid every 6 hours as necessary for pain. Patient was advised to come back on Saturday.

Pathophysiology of TM perforation includes acute/chronic suppurative otitis media (most common cause), persistent perforation after extrusion of a pressure equalization tube, trauma (hand blow to the ear, barotrauma, diving, water skiing, explosion, forceful irrigation, slag burns), iatrogenic, cholesteatoma (associated with peripheral perforations). Spontaneous closure of a perforated TM results in a monomeric membrane (misnomer: actually has two layers, outer epidermal and inner mucous).

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Types of TM perforation includes: Central wherein perforation does not involve the annulus, typically infectious etiology. Marginal TM perforation involves the annulus, less likely to resolve spontaneously, and has a higher association with cholesteatomas. Subtotal TM perforation has a large defect completely surrounded with an intact annulus. Symptoms of TM perforation includes CHL and tinnitus. It is diagnosed via an otoscopic exam and audiogram. Treatment includes keeping the ear dry. Tympanoplasty may be considered for a persistent perforation.

62. Grimaldo Ma Rhea 26/F

This is the case of M.G. a 26 year old female, who came in came in for ff-up regarding Bell’s Palsy. Patient is diagnosed with Bell’s Palsy HB class III and was advised to continue Prednisone. Patient was also advised to start physical therapy sessions and to come back after two weeks.

Character of Facial Paralysis must be elicited inluding onset, duration, and progression of Paralysis. Contributing Factors include recent infection or illness, trauma (birth trauma in neonates), surgery (otologic, parotid, or neurologic surgery); recent tick bites or outdoor activity; history of syphilis, HIV, tuberculosis, or herpes infections; toxin exposure (lead); history of otologic, neurologic, diabetic, or vascular disorders; and previous history of facial nerve paralysis. Associated symptoms include fever, facial pain, hearing loss, aural fullness, otalgia, vertigo, other neurologic deficits, change in taste sensation, vision changes, drooling, cheek biting, epiphora, dysacusis, and pain (auricular, postauricular, or facial).

Observation of facial symmetry at rest and with movement is necessary, as well as differentiation of paresis vs paralysis, hemifacial spasms, and facial tics at rest. Evaluation must include unilateral versus bilateral weakness, eye closure, quality of Bell’s phenomenon (globe turns up and out during attempts to close eyes), tear production, corneal reflex, and visual acuity.

House-Brackmann Grading is used to evaluate recovery of paralysis (eg, recovery from Bell’s palsy, preoperative versus postoperative results). It includes:House-Brackmann System of Grading Facial Nerve Paralysis*

Grading FunctionI normal function

II mild dysfunction: weakness on close inspection, normal symmetry and tone at rest, moderate to good facial function (slight mouth asymmetry, complete eye closure with minimal effort)

III moderate dysfunction: obvious weakness, and/or asymmetry (not disfiguring), contracture, and/or hemifacial spasms, normal symmetry and tone at rest; moderate facial function (weak mouth and forehead function, complete eye closure with effort)

IV moderately severe dysfunction: disfiguring asymmetry and/or obvious weakness, normal asymmetry and tone at rest, incomplete eye closure, no forehead motion, asymmetric mouth motion with maximal effort

V severe dysfunction: barely perceptible motion, asymmetry at rest, incomplete eye closure, no forehead motion, slight mouth motion

VI total paralysis

Other Head and Neck assessment should be done to evaluate for mass or fluid in the middle ear, presence of vesicles in the EAC and concha, Hitselberger sign (hypesthesia of the sensory division of the facial nerve at the

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superior posterior concha), other cranial nerve involvement, other lateralizing signs (hemiparesthesias, hemiparalysis, aphasia), and parotid masses.

Ancilliary studies include Electromyography (EMG) wherein electrodes are inserted into muscle, and measures muscle response to voluntary contraction. It is useful to demonstrate the existence of functional motor units. Fibrillations from deinnervated nerve appear after 1–2 weeks whereas polysynaptic signals indicate reinnervation. Presence of voluntary action potentials indicates at least partial continuity of nerve. In Electroneuronography (ENoG), it is essentially an evoked EMG (muscle response is recorded by electromyogram). It records muscle response via electrodes after stimulation of the facial nerve with a transcutaneous impulse at the stylomandibular foramen. It objectively compares muscle compound action potential amplitudes (related to intact motor axons) and latencies from the paralyzed and normal sides. In an acute setting ENoG is typically not useful until after 24–72 hours when wallerian degeneration occurs. It can distinguish neuropraxia versus more severe injuries, and is valuable in determining prognosis for idiopathic paralysis. Other Ancillary Studies which may be considered in select cases includes an Audiogram, usually indicated for all intratemporal injuries and for preoperative baseline hearing. CT of Temporal Bones may detect temporal bone lesions and fractures. MRI of Temporal Bones is most sensitive imaging for examining the intratemporal segment of the facial nerve, and gadolinium enhancement may reveal acoustic or facial neuromas and other tumors. Complete Blood Count may suggest inflammatory process whereas ACE level may suggest active sarcoidosis.T

Idiopathic Facial Paralysis (Bell’s Palsy) is the most common cause of facial paralysis. Facial paralysis or paresis may be due to impaired axoplasmic flow from edema of the facial nerve within the fallopian canal secondary to a herpes simplex virus type 1 (HSV-1) infection (may be reactivated from dormancy in geniculate ganglion). Possible etiologies include immunological or vascular (ischemia) pathology. Risks include diabetes mellitus, pregnancy, and past history (7–12% recur). It presents as an acute, unilateral paresis (approximately 1/3) or paralysis (approximately 2/3) of the face, rapid onset (<48 hours); may have a viral-like prodrome 3–4 days prior to paralysis, postauricular pain, and dysgeusia. Approximately 70–85% will have full recovery by 6 months. Favorable prognosis is associated with the presence of any facial movement. Poorer prognosis is associated with complete facial paralysis (ENoG reveals >90% weakness) within 2 weeks of onset.

Diagnosis is based on exclusion of other causes of facial nerve paralysis as well as clinical history and exam. Medical Management includes oral antivirals (acyclovir) and corticosteroids with taper for 10 days for acute phases. Eye Protection is indicated and includes artificial tears, ocular ointment at night, eye patch at night. Progression may be followed with serial exams (may consider ENoG testing). Surgical Decompression is controversial and is considered if ENoG reveals >90% weakness within two weeks after onset and no voluntary movement on EMG. It is most effective if performed within 2 weeks of onset. It typically requires a transmastoid and middle cranial fossa approach with decompression of the tympanic segment, geniculate ganglion, labyrinthine segment, and meatal foramen.

64. Juanillo, Jimboy 18/M

This is the case of J.J. a 18 year old male who came in for ff-up regarding hemangioma excision. Patient had hemangioma, L pinna and status post excision. Ascorbic acid 1 tab once a day and ff-up after 1 week was advised to the patient.

Hemangiomas are proliferative lesions as compared to AV malformations which are vessel malformations. Visible lesion on the face or neck may signify presence of another internal hemangioma such as in the oral cavity, larynx or pharynx. Hemangiomas are sometimes associated with certain syndromes such as Sturge-Weber or posterior fossa lesion in the brain, arterial lesions in the neck or in the face, cardiac or coarctation problems and eye abnormalities. Superficially located lesions appear flat and reddish in color. Deep lesions are bluish. Compound lesions such as in this case is both deep and superficial and may appear purple. Cavernous hemangiomas are

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compressible, globular, bright red or deep purple involving deep structures. This is the most likely clinical type of hemangioma in this patient. Capillary hemangiomas on the other hand are plaque-like lesions, slightly elevated and more superficial. Port-wine stains are capillary type, flat and mostly in the dermis. Strawberry marks are capillary type with cavernous component.

Hemangiomas are usually just observed since they may involute in time. Indications for treatment may include involvement of vital organs, recurrent bleeding, ulceration, crusting or infection and rapid growth and deformity. CT scan is usually warranted but MRI may be needed for deep and large lesions. For small areas not involving the face, intralesional injection with steroids may be done with or without liquid nitrogen cryosurgery also with pulsed dye laser. Larger hemangiomas require oral steroids. For lesions that are life-threatening or non-responsive to steroids Alpha-interferon may be warranted. Careful surgical excision may be the last resort which can be very bloody since hemangioma is a vascular lesion.

65. Corvera, John Bersh T. 4/M

This is the case of J. C. a 4 year old male who came in came in for ff-up regarding his otitis media. Patient is diagnosed with resolved CSOM and was advised to continue Ofoxacin for 1 more week.



66. Sarsagal, Jazlyn S. 3/M

This is the case of J. S. a 3 year old female who came in came in regarding impacted cerumen. Patient is diagnosed impacted cerumen on right ear. Aural flushing on right ear was done. Patient was advised to discontinue mineral oil.

Cerumen is a protective secretion produced by the outer portion of the ear canal. In most persons, the ear canal is self-cleansing. Recommended hygiene consists of cleaning the external opening with a washcloth over the index finger without entering the canal itself. In most cases, cerumen impaction is self-induced through ill-advised attempts at cleaning the ear. It may be relieved with detergent ear drops (eg, 3% hydrogen peroxide;

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6.5% carbamide peroxide), mechanical removal, suction, or irrigation. Irrigation is performed with water at body temperature to avoid a vestibular caloric response. The stream should be directed at the posterior ear canal wall adjacent to the cerumen plug. Irrigation should be performed only when the tympanic membrane is known to be intact.

Use of jet irrigators designed for cleaning teeth (eg, WaterPik) for wax removal should be avoided since they may result in tympanic membrane perforations. Following professional irrigation, the ear canal should be thoroughly dried (eg, by instilling isopropyl alcohol or using a hair blow-dryer on low-power setting) to reduce the likelihood of inducing external otitis. Specialty referral for cleaning under microscopic guidance is indicated when the impaction is frequently recurrent, has not responded to routine measures, or if the patient has a history of chronic otitis media or tympanic membrane perforation.

67. Mandac, Christian Paul 3/M

This is the case of C.M., a 3 year old male who sought consult for left ear pain Patient was diagnosed with acute otitis media left ear and otitis externa on right. Patient was prescribed with Amoxicillin to complete for 10 days and Paracetamol 6.5ml every 4 hours. He was prescribed with Aplosyn otic drops 3 drops three times a day. Patient was instructed to keep her ear dry and to have warm compress 15 minutes every 6 hours.

Acute otitis media is a bacterial infection of the mucosally lined air-containing spaces of the temporal bone. Purulent material forms not only within the middle ear cleft but also within the pneumatized mastoid air cells and petrous apex. Acute otitis media is usually precipitated by a viral upper respiratory tract infection that causes eustachian tube obstruction. This results in accumulation of fluid and mucus, which becomes secondarily infected by bacteria. The most common pathogens both in adults and in children are Streptococcus pneumoniae, Haemophilus influenzae, andStreptococcus pyogenes. Acute otitis media is most common in infants and children, although it may occur at any age. Presenting symptoms and signs include otalgia, aural pressure, decreased hearing, and often fever. The typical physical findings are erythema and decreased mobility of the tympanic membrane. Occasionally, bullae will be seen on the tympanic membrane.

The treatment of acute otitis media is specific antibiotic therapy, often combined with nasal decongestants. The first-choice oral antibiotic treatment is amoxicillin (20–40 mg/kg/d) orerythromycin (50 mg/kg/d) plus sulfonamide (150 mg/kg/d) for 10 days. Alternatives useful in resistant cases are cefaclor (20–40 mg/kg/d) or amoxicillin-clavulanate (20–40 mg/kg/d) combinations.

Surgical drainage of the middle ear (myringotomy) is reserved for patients with severe otalgia or when complications of otitis (eg, mastoiditis, meningitis) have occurred. Recurrent acute otitis media may be managed with long-term antibiotic prophylaxis. Single daily oral doses of sulfamethoxazole (500 mg) or amoxicillin (250 or 500 mg) are given over a period of 1–3 months. Failure of this regimen to control infection is an indication for insertion of ventilating tubes.

Otitis externa is an inflammatory and infectious process of the EAC. Pseudomonas aeruginosa and Staphylococcus aureus are the most commonly isolated organisms. Less commonly isolated organisms include Proteus species, Staphylococcus epidermidis, diphtheroids, and Escherichia coli.

In the preinflammatory stage, the ear is exposed to predisposing factors, including heat, humidity, maceration, the absence of cerumen, and an alkaline PH. This can cause edema of the stratum corneum and occlusion of the apopilosebaceous units. In the inflammatory stage, bacterial overgrowth ensues, with progressive edema and intensified pain. Incomplete resolution or persistent inflammation for more than 3 months refers to the chronic inflammatory stage.

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Symptoms of otitis externa may vary, depending on the stage and extent of disease. The clinical diagnosis is suggested by the presence of otalgia, otorrhea, aural fullness, pruritus, tenderness to palpation, and varying degrees of occlusion of the EAC. The patient may also present with hearing loss that results from occlusion of the EAC by edema and debris. Signs of otitis externa include pain on distraction of the pinna, EAC erythema, edema, otorrhea, crusting, and, in more advanced disease, lymphadenopathy of the periauricular and anterior cervical lymph nodes. Skin changes of cellulitis may be present as well. In the chronic stage, the skin of the EAC may be thickened.

Treatment for otitis externa involves meticulous atraumatic debridement of the EAC with the aid of a microscope. Analgesia can be achieved with nonsteroidal anti-inflammatory drugs (NSAIDs), opioids, or topical steroid preparations. After cleansing is complete, otic drop preparations that are antiseptic, acidifying, or antibiotic (or any combination of these) should be used. If the degree of stenosis of the canal is severe, a wick may be carefully placed in an effort to deliver the drops to the medial portion of the canal.

Available antibiotic preparations include ofloxacin, ciprofloxacin, colistin, polymyxin B, neomycin, chloramphenicol, gentamicin, and tobramycin. Polymyxin B and neomycin preparations are often used in combination for the treatment of S aureus and P aeruginosa infections. Ofloxacin and ciprofloxacin are single-agent antibiotics with an excellent spectrum of coverage for pathogens encountered in otitis externa. Preparations with steroids help to reduce edema and otalgia. Systemic antibiotics are indicated for infections that spread beyond the EAC. For chronic otitis externa, a canalplasty may be indicated for thickened skin that has caused canal obstruction. Patients must be instructed to avoid EAC manipulation and water exposure if they have a history of recurrent otitis externa.

68. Bejo, Bobby 38/M

This is the case of B.B., a 38 year old who came in for follow up and was last seen Aug. 12, 2011. Patient had foreign body (dentures) and was status post emergency esophagoscopy. Extraction of foreign body via lateral pharyngotomy (8/5/11) was done. During the follow-up, removal of suture was done. Patient was advised wound care two times a day. Removal of NGT was also done. Patient was allowed to have general liquids for 3 hours ; soft diet for overnight then cereal diet.

Most common objects that may cause foreign body ingestion in adults are fish bones, dentures, and meat (most common objects in pediatrics are coins). 95% of esophageal foreign bodies are located at the cricopharyngeus (other common sites are the gastroesophageal junction and the indentation from the aortic arch and left mainstem bronchus). Signs and symptoms include dysphagia, drooling, weight loss, chest pain and fever. Chest x-ray is used to identify the object, whereas barium swallow should be avoided since it may obscure the field with endoscopy. Complications include esophageal perforation, mediastinitis, pneumomediastinum, pneumothorax, and aspiration.

Rigid Esophagoscopy is indicated for foreign bodies that remain in the esophagus for >24 hours, large object in the esophagus, any batteries; if possible may obtain similar object in order to determine a strategy for instrumental removal. A second foreign body is always checked. Fogarty catheters may be used for distal objects. If no endoscopy indicated, consider following with abdominal films and straining stool. Long-term Management icludes oral corticosteroids for presence of edema and prophylactic antibiotics, as well as close follow-up.

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69. Mazo, Christian Joy 6/M

This is the case of C.M. a 6 year old male who came in came in for in regarding impacted cerumen. Patient is diagnosed with resolved impacted cerumen. Patient was advised to come back once with problems.



70. Sinco, Zosimo Sr. 70/M

This is the case of Z.S. a 70 year old male who came in came in regarding ear pain on both ears. Patient is diagnosed with conductive hearing loss on the right and with aural polyp. Ear wick was placed. PND otic drops 2-3 drops three times a day fro 7 days, Cloxacillin 500 mg/cap 1 cap every 6 hours for 7days and Mefenamic Acid 500 mg/ cap, 1 cap every 6 hours for pain were prescrive

In CHL, the pathology lies in the external ear canal, ear drum (tympanic membrane), ossicles or middle ear. Because of the pathology, impaired conduction of sound occur; hence, there is decreased intensity of sound reaching the cochlea. Unlike SNHL, there is no distortion of sound hence understanding speech is no problem with adequate intensity. Persons with CHL tends to speak softly because they hear the speech louder (bone>air conduction), hence they lower their voices since they perceive that they are speaking loudly. Hearing loss is mild to moderate around 30-40 dB. The most common etiology is Impacted cerumen and other foreign bodies. Other possible etiology include: ear canal atresia, otitis externa/media, otosclerosis, ear canal tumors, and myringitis. Diagnosis of CHL includes otoscopic findings of the ear canal and ear drum; Weber’s test that lateralizes to the affected ear; a negative Rinne test (bone>air conduction); a higher air conduction threshold on PTA. Treatment is directed at the specific etiology. For instance, in cases of impacted cerumen, the cerumen is flushed out; or in AOM, the infection is relieved by antimicrobial agents.

An aural polyp is a growth in the outside (external) ear canal. It may be attached to the eardrum (tympanic membrane), or it may grow from the middle ear space. Aural polyps may be caused by: cholesteatoma, foreign object, inflammation and tumor. Bloody drainage from the ear is the most common symptom. Hearing loss can also occur. An aural polyp is diagnosed through an examination of the ear canal and middle ear using an otoscope or microscope. Treatment depends on the underlying cause. Avoiding water in the ear, steroid medications, and antibiotic ear drops are part of the management. If a cholesteatoma is the underlying problem or the condition fails to clear, then surgery may be needed.

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71. Clomera, Christian 6/M

This is the case of CC, a 6 year old male diagnosed with Chronic Suppurative Otitis Media and came in for follow-up. Resolution of the CSOM was seen hence medications and ofloxacin was discontinued.

Chronic suppurative otitis media is typically a persistent disease, insidious in its onset. This disease often causes severe destruction and irreversible sequelae. It manifests clinically as discharge and deafness. Chronic otitis media develops after long-standing inflammation in the middle ear and mastoid. It is commonly associated with perforation of the tympanic membrane and, often, cholesteatoma. The actual cause of chronic otitis media maybe difficult to ascertain; however, it seems to be associated with a history of eustachian tube dysfunction, regardless of the cause. Poor socioeconomic status, overcrowding, poor nutrition, poor hygiene, and infectious diseases (eg, measles) have been found to contribute to the development of chronic suppurative otitis media. The disorder is more prevalent in some specific populations, such as Eskimos and American Indians, as well as in people with cleft palates. Adenoid hypertrophy and chronic sinusitis also contribute to the development of chronic suppurative otitis media.

Chronic otitis media develops after longstanding inflammation of the middle ear cleft. There are likely a number of a reasons for the inflammation, including acute otitis media, perforation of the tympanic membrane and eustachian tube dysfunction. The exposure to chronic inflammatory mediators leads to weakening of the tympanic membrane while causing mucosal edema. Eventually eustachian tube dysfunction leads to negative middle ear pressure that causes tympanic membrane retraction and perforation. Longstanding negative pressure can damage surrounding bone and ossicles, leading to cholesteatoma or loss of ossicular continuity.

Chronic negative pressure can lead to an atticoantral type of chronic suppurative otitis media is characterized by the formation of cholesteatoma. Cholesteatoma is simply skin that has migrated medially to the tympanic membrane. The cholesteatoma sac tends to slowly expand along the path of least resistance, collecting keratin debris within that tends to become infected. Clinical symptoms of discharge and hearing loss develop because of chronic inflammation and interruption of the ossicular chain. If left untreated, cholesteatoma can cause life-threatening complications such as permanent hearing loss, facial nerve dysfunction, and brain abscess.

Ear discharge and hearing loss are the typical symptoms of a patient with chronic suppurative otitis media. The examination of the ear may reveal a central perforation in the eardrum, which is typically painless, with some mucopurulent ear discharge.

72. Duran, Estelita 28/F

This is the case of ED, a 28 year old female with conductive hearing loss and chronic suppurative otitis media of the left ear. She is status post mastoidectomy and came in for suture removal.

The external ear, the external auditory canal, and the middle ear apparatus is designed to collect and amplify sound and efficiently transfer the mechanical energy of the sound wave to the fluid-filled cochlea. Factors that obstruct the transmission of sound or serve to dampen the acoustical energy result in conductive hearing loss. Conductive hearing loss can occur from obstruction of the external auditory canal by cerumen, debris, and foreign bodies; swelling of the lining of the canal; atresia or neoplasms of the canal; perforations of the tympanic membrane; disruption of the ossicular chain, as occurs with necrosis of the long process of the incus in trauma or infection; otosclerosis; or fluid, scarring, or neoplasms in the middle ear. Rarely, inner ear malformations or pathologies may also be associated with conductive hearing loss.

Eustachian tube dysfunction is extremely common in adults and may predispose to acute otitis media (AOM) or serous otitis media (SOM). Trauma, AOM, or chronic otitis media are the usual factors responsible for tympanic membrane perforation. While small perforations often heal spontaneously, larger defects usually require surgical intervention. Tympanoplasty is highly effective (>90%) in the repair of tympanic membrane perforations. Otoscopy is usually sufficient to diagnose AOM, SOM, chronic otitis media, cerumen impaction, tympanic

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membrane perforation, and eustachian tube dysfunction; tympanometry can be useful to confirm the clinical suspicion of these conditions.

Cholesteatoma, a benign tumor composed of stratified squamous epithelium in the middle ear or mastoid, occurs frequently in adults. This is a slowly growing lesion that destroys bone and normal ear tissue. Theories of pathogenesis include traumatic immigration and invasion of squamous epithelium through a retraction pocket, implantation of squamous epithelia in the middle ear through a perforation or surgery, and metaplasia following chronic infection and irritation. On examination, there is often a perforation of the tympanic membrane filled with cheesy white squamous debris. A chronically draining ear that fails to respond to appropriate antibiotic therapy should raise suspicion of a cholesteatoma. Conductive hearing loss secondary to ossicular erosion is common. Surgery is required to remove this destructive process.

Conductive hearing loss with a normal ear canal and intact tympanic membrane suggests either ossicular pathology or the presence of "third window" in the inner ear (see below). Fixation of the stapes from otosclerosis is a common cause of low-frequency conductive hearing loss. It occurs equally in men and women and is inherited as an autosomal dominant trait with incomplete penetrance; in some cases, it may be a manifestation of osteogenesis imperfecta. Hearing impairment usually presents between the late teens and the forties. In women, the otosclerotic process is accelerated during pregnancy, and the hearing loss is often first noticeable at this time. A hearing aid or a simple outpatient surgical procedure (stapedectomy) can provide adequate auditory rehabilitation. Extension of otosclerosis beyond the stapes footplate to involve the cochlea (cochlear otosclerosis) can lead to mixed or sensorineural hearing loss. Fluoride therapy to prevent hearing loss from cochlear otosclerosis is of uncertain value.

Disorders that lead to the formation of a pathologic "third window" in the inner ear can be associated with conductive hearing loss. There are normally two major openings, or windows, that connect the inner ear with the middle ear and serve as conduits for transmission of sound; these are, respectively, the oval and round windows. A third window is formed where the normally hard otic bone surrounding the inner ear is eroded; dissipation of the acoustic energy at the third window is responsible for the "inner ear conductive hearing loss." The superior semicircular canal dehiscence syndrome resulting from erosion of the otic bone over the superior circular canal can present with conductive hearing loss that mimics otosclerosis. A common symptom is vertigo evoked by loud sounds (Tullio phenomenon), by Valsalva maneuvers that change middle ear pressure, or by applying positive pressure on the tragus (the cartilage anterior to the external opening of the ear canal),. Patients with this syndrome also complain of being able to hear the movement of their eyes and neck. A large jugular bulb or jugular bulb diverticulum can create a "third window" by eroding into the vestibular aqueduct or posterior semicircular canal; the symptoms are similar to those of the superior semicircular canal dehiscence syndrome.



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73. Delloro, Robi 3/M

This is the case of RD, a 3 year old male who presented with a chief complaint of Epistaxis. He is diagnosed with epistaxis, anterior, inactive 2O to mucositis. He is prescribed with NaCl Nasal Spray (0.65%), 2 sprays on both nostrils TID; Cetirizine syrup ½ teaspoon once daily for 1 week and multivitamins 1 tablespoon once daily.

Trauma (including nose picking and vigorous nose blowing) and mucosal dehydration are the most common cause of epistaxis. Hypertension, aspirin (and other platelet inhibiting medications), and alcohol abuse account for the most common causes of refractory epistaxis. Colder temperatures and dryness (winter seasons) increase risk of vascular injury. Nasoseptal deformities may result in epistaxis secondary to the drying effects of turbulent airflow. The Kiesselbach’s Plexus (Little’s area) is a confluence of arterial vessels at the anterior nasal septum. It is susceptible to bleeding due to the fragile mucosa and tightly adherent to underlying mucosa affording little resistance to mechanical stress. Contributing Vessels include the anterior ethmoidal, superior labial, greater palatine, and sphenopalatine arteries.

After evaluating the ABCs (airway, breathing, intravenous access), a systematic evaluation of the patient ideally should be performed prior to controlling the bleeding (may not be possible for heavy bleeding, may consider neosynephrine soaked cotton pledgets as a temporizing procedure). The epistaxis should be characterized: estimate amount of blood loss, length of time of epistaxis, intermittent versus continuous bleeding, and side of bleeding; previous episodes, hospitalizations, packing, or other management for epistaxis. Medical history and blood dyscrasias should be elicited such as hypertension, arteriosclerosis, leukemia, idiopathic thrombocytopenic purpura, von Willebrand’s disease, renal and hepatic failure, anemia, and haemophilia (higher risk of arterial, pulsatile bleeding). Use of medications such as antiplatelet medications (ASA), anticoagulants (coumadin, heparin) should be elicited. Social history should also be investigated for cocaine abuse, alcoholism and smoking. Toxin exposure to ammonia, sulfuric acid, gasoline, phosphorus are associated with nasal dryness and crusting hence must be evaluated. Other contributing factors include previous septal or nasal surgery, recent trauma to nasal bone or septum, facial skeleton, dry environment, high altitude living (home CPAP ventilators or oxygen), symptoms of allergy, sinusitis, rhinitis, and URI (typically short-lived bleeding).

Patient should sit up with body tilted forward to allow blood to be spit out and not swallowed. Initial attempt to stop bleeding by applying pressure to nasal alae for several minutes. Decongestant/anesthetic agents (4% cocaine or 0.25% phenylephrine HCL) may be applied. Adequate lighting (head lamp), nasal speculum, bayonet forceps, frazier and Yankhauer suctions available to suction clot and attempt to localize active bleeding (examine for escoriations, foreign bodies, masses, nasoseptal deformities, etc.) should be acquired. For chronic or recurrent epistaxis without an obvious bleeding source patient should undergo an endoscopic exam. Lab Tests include PT/PTT, bleeding time, liver function tests, creatinine, CBC, type and cross.

Acute management includes the following. There may be a need to correct hypovolemia (3:1 Rule: for every 100 cc of blood loss, replace with 300 cc of crystalloid fluid), hypertension (antihypertensive agents), or coagulopathy (fresh frozen plasma, platelets, cryoprecipitate). Chronic management includes hypertonic nasal spray and humidification; long-term medical management of hypertension; antimicrobial ointment to excoriated lesions; avoid excess straining, nose blowing, and digital manipulation.

Cauterization may be done with the use of silver nitrate, chromic acid pearls, electrocautery (for deeperpenetration and posterior bleeding), and cryotherapy. Laser cauterization may be considered for vascular malformations. Endoscopic instrumentation may be used for posterior and difficult to visualize bleeding. It is indicated for minor bleeding, single bleeding points, and easily visualized regions (Kiesselbach’s plexus).

Anterior Nasal Packing with Gelfoam, Cellulose, or Microfibrillar Collagen Packing provides a procoagulant effect, gentler packing, and is useful for coagulopathies, dissolves (does not require removal), may be placed after initial coagulation. Nasal Tampons and Expandable Sponges expand with instillation of water to provide pressure against the nasal mucosa. Vaseline Strip-Gauze is a formal anterior packing placed to posterior choanae, and controls most posterior bleeding. The packing is kept in place for 3–5 days to allow vessel to develop amature thrombus. It may be supplemented with thrombin, oxycellulose, or fibrin. Indications include acute or recurrent epistaxis after failed medical management or cauterization.

Posterior Nasal Packing is done with gauze, sponge pack, Foley catheter, pneumatic nasal catheters, or

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tonsillar packing is placed to close off the choana to prevent escape of bleeding into the nasopharynx requires a formal anterior pack for stability. Nasal Balloons using a catheter with two balloons (one placed in the nasopharynx and the other in the nasal cavity), is designed for easier placement of a posterior pack, and provides less trauma and is simple to adjust pressure. Indications for posterior nasal packing includes failed anterior packing, skull base trauma, and hemorrhage from a major branch of the sphenopalatine artery.

Embolization may also be done and is indicated for intractable nasal hemorrhage, surgically inaccessiblesites, and inoperable candidates. Vascular Ligation on the other hand is Indicated for uncontrolled epistaxis (typically posterior bleeding) and identifiable bleeding site. Techniques include the following:

1. Anterior and Posterior Ethmoidal Artery Ligation: approach from a Lynch incision, anterior ethmoid artery is located 14–18 mm posterior to frontoethmoid suture line, posterior ethmoid artery is located 10 mm posterior to anterior ethmoid foramen, the optic nerve is located 4–5 mm posterior to the posterior ethmoid foramen

2. Maxillary Artery or Sphenopalatine Artery Ligation: may be approached transantrally, transorally, or endoscopically

3. External Carotid Artery Ligation: severe uncontrolled, life threatening bleeding, ligate above the origin of the lingual artery

Septoplasty/Submucous Resection is indicated septal defects (unable to pack), and Osler-Weber-Rendu Syndrome. It removes diseased mucosa and replaces with STSG (Saunder’s Dermoplasty), reduces drying effect by decreasing turbulent airflow. However, there is a risk of septal perforation.

74. Florece, Alberto 34/M

This is the case of AF, 34 year old male who presented with mass at the left parotid area. He was diagnosed with Acute Parotitis, bacterial. She was prescribed with Co-amoxiclav 625 mg/tab TID x 7days; Mefenamic acid 500mg/cap TID; Paracetamol 500mg/tab q4 for fever; and warm compress 15mins q6.

The parotid glands are small exocrine glands that rarely call attention to themselves. Perfect function throughout life is normal. Dry mouth, drooling, swelling, and pain are essentially the only symptoms caused by dysfunction of the salivary glands.

The major salivary glands and their ducts are strategically situated on either side of the dental occlusal planes to irrigate and saturate a food bolus with saliva during chewing. The parotid gland contacts the mandibular ramus and muscles of mastication, which massage the gland during chewing. The mechanical squeezing and the parasympathetic nervous system, which analyzes a number of sensory inputs, cause the glands to inject an appropriate quantity and quality of saliva into the oral cavity. Minor salivary glands are scattered throughout the oral cavity and pharynx to assist the major glands in moistening, lubricating, and protecting the teeth and mucosa. The normal flow of saliva though the duct prevents oral bacteria from ascending the duct to cause infection.

Inflammatory swelling of the glands may present a serious diagnostic challenge. Parotitis presents in many forms and the symptoms vary from modest to prostrating. Reading the numerous journal on parotitis articles reveals frequent contradictions in the classification, etiology, and treatment of the disorders. A pure viral or bacterial infection, an autoimmune inflammation, or a combination of these can be the etiology. In this article, evolution of the knowledge of parotitis, as well as the diagnosis and treatment, is discussed.

Acute bacterial parotitis is now infrequent, but its historical importance and occasional occurrence today necessitate in-depth knowledge of this entity by the otolaryngologist. Mumps and bacterial parotitis were differentiated by 1800, but neither was effectively treated. The mortality rate for bacterial parotitis was 80%. Before antibiotics and intravenous administration of fluids were available, bacterial parotitis occurred in postoperative patients or other severely ill patients who became dehydrated and contributed to their demise as an incurable sepsis.

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Early in the 20th century, surgeons were hesitant to incise and drain parotid abscesses and frequently used ineffective conservative measures until the process was irreversible. They feared the consequences of the unsightly scar and facial paralysis.

In 1917, Lilienthal described a surgical treatment that was very similar to what is used today. He called parotid abscesses celiac parotitis because they were believed to be metastatic from abdominal infections. Other authors used names such as acute surgical parotitis, acute necrotic parotitis, acute gangrenous parotitis, and other historical designations according to Hemenway and English in 1971.

Lilienthal designed a vertical incision just anterior to the auricle that coursed posteriorly and inferiorly below the ear to join and follow an upper cervical skin crease that paralleled the lower mandibular border. He elevated the outlined skin flap forward to expose the parotid gland and made multiple incisions into the gland parallel to the facial nerve branches. He then opened the fascia behind the angle of the mandible to drain deeper spaces. The wound was packed and healed by secondary intention, resulting in a surprisingly good cosmetic result. The number of patients treated by this drainage is not known, but this treatment was probably almost anecdotal to Lilienthal’s contemporaries.

In 1919, Zachary Cope, a British Army surgeon, described 7 patients with parotitis that he had treated in Baghdad during the exceptionally hot summer of 1917. He recorded that these soldiers had heatstroke or were severely affected by the extreme heat. The patients developed parotid swelling accompanied by fever and general malaise. Cope made wide T-shaped incisions in the gland to allow drainage. Four of the 7 survived after sloughing gangrenous parotid tissue. Cope stated that although the disease was a bacterial infection, the excessive heat and debilitating illness predisposed to its development.

In 1923, Blair and Padgett of St. Louis published an article stating that early surgical drainage of the infected gland was safe and frequently was life saving. They stated that acute suppurative parotitis was an ascending duct infection related to decreased salivary flow, fever, and general debilitation. They cultured the pus and found that Staphylococcus aureus was the most common organism. The treatment proposed by Blair and Padgett did not become the standard practice for several more years. However, the high mortality rate decreased early in the 20th century and was 30-50% by 1930, probably because of more prompt and effective drainage of the abscesses.

From the 1930s to the 1960s, irradiation treatment of numerous diseases became popular, and several authors advocated 4-6 Gy delivered over 4-5 days for bacterial parotitis. Most patients with severe infections required surgical drainage despite radiation treatment. By 1960, most published papers stressed large doses of antibiotics, improved oral hygiene, and increased fluid intake as treatment, with incision and drainage for failures. They found that the parotid capsule and septations required wide exposure and extensive deep incisions parallel to the facial nerve branches to exteriorize the diseased gland. Physicians recognized the importance of hydration and oral hygiene for debilitated patients, and the incidence of bacterial parotitis plummeted.

Acute bacterial parotitis is caused by bacteria that ascends from the mouth and most frequently occurs in chronically ill patients. The patient quickly becomes extremely ill. In the hospital setting, S aureus is apt to be methicillin resistant (MRSA). Gram stains and culture and sensitivity testing is ordered. Intravenous vancomycin at 500 mg every 6 hours is begun empirically. Therapy may be altered based upon cultures or infectious disease consultation.

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75. Pareja, Ginina 19/F

This is the case of GP, 19 year old female who presented with a pre-auricular mass and was diagnosed with preauricular sinus, AD. She was advised to undergo excision.

Preauricular sinuses are common congenital malformations first described by Heusinger in 1864. Preauricular sinuses are frequently noted on routine physical examination as small dells adjacent to the external ear, usually at the anterior margin of the ascending limb of the helix. However, preauricular sinuses have been reported to occur along the lateral surface of the helicine crus and the superior posterior margin of the helix, the tragus, or the lobule. Anatomically, preauricular sinuses are lateral and superior to the facial nerve and the parotid gland.

Preauricular sinuses are inherited in an incomplete autosomal dominant pattern, with reduced penetrance and variable power of expression. They can arise spontaneously. The sinus may be bilateral in 25-50% of cases, and bilateral sinuses are more likely to be hereditary. In unilateral cases, the left side is more commonly affected.

During embryogenesis, the auricle arises from the first and second branchial arches during the sixth week of gestation. Branchial arches are mesodermal structures covered by ectoderm and lined with endoderm. These arches are separated from each other by ectodermal branchial clefts externally and by endodermal pharyngeal pouches internally. The first and second branchial arches each give rise to 3 hillocks; these structures are called the hillocks of His. Three hillocks arise from the caudal border of the first branchial arch, and 3 arise from the cephalic border of the second branchial arch. These hillocks should unite during the next few weeks of embryogenesis. Preauricular sinuses are thought to occur as a result of incomplete fusion of these hillocks.

Preauricular sinuses are usually narrow, they vary in length (usually they are short), and their orifices are usually minute. They may arborize and follow a tortuous course in the immediate vicinity of the external ear. The preauricular sinuses are usually found lateral, superior, and posterior to the facial nerve and the parotid gland. In almost all cases, the duct connects to the perichondrium of the auricular cartilage. They can extend into the parotid gland.

Most people with preauricular sinuses are asymptomatic. Only one third of persons are aware of their malformations. Some patients with preauricular sinuses present with chronic intermittent drainage of purulent material from the opening. Draining sinuses are prone to infection. Once infected, these sinuses rarely remain asymptomatic, often developing recurrent acute exacerbations.

Patients with preauricular sinuses may present with facial cellulitis or ulcerations located anterior to the ear. These ulcerations are often treated without recognition of the primary source, and the preauricular sinus remains unnoticed. Subsequent to infection, a patient with preauricular sinuses may develop scarring and disfigurement. Infants of diabetic mothers are at increased risk for the oculo-auriculo-vertebral sequence, which includes sinuses.

The preauricular sinus usually presents as a small dell adjacent to the anterior margin of the ascending limb of the helix. Unless they are actively infected or have previously been infected with subsequent scarring, they are only small openings in the external ear. If associated conditions are present, one might see external ear anomalies, such as flop ears. Physical examination may reveal associated branchiogenic fistulas and/or hearing loss.

Conditions associated with preauricular sinuses include subcondylar impaction of a third molar, renal malformations, hearing loss, branchiogenic fistulas, commissural lip pits (3.8% of patients with these have preauricular sinuses), and external ear anomalies; however, these conditions rarely occur. Cleft palate, spina bifida, imperforate anus, renal hypoplasia or renal agenesis, reduplication of the duodenum, undescended testes, and umbilical hernias are reported associations.

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Preauricular sinuses are involved in the following syndromes: Treacher Collins syndrome; branchio-oto-renal (BOR) syndrome; hemifacial microsomia syndrome; a syndrome consisting of facial steatocystoma multiplex associated with pilar cysts and bilateral preauricular sinuses; and a syndrome that includes preauricular sinuses, conductive deafness, commissural lip pits, and external ear abnormalities. BOR syndrome consists of conductive, sensorineural, or mixed hearing loss; preauricular pits; structural defects of the outer, middle, or inner ear; renal anomalies; lateral cervical fistulas, cysts, or sinuses; and/or nasolacrimal duct stenosis or fistulas. Hemifacial microsomia syndrome can include preauricular sinuses, facial nerve palsy, sensorineural hearing loss, microtia or anotia, cervical appendages containing cartilage, and other defects.

Associated facial pathology is as follows: Preauricular sinuses can be associated with facial pathology. In one case, a preauricular sinus associated with a congential cholesteatoma resulted in a facial palsy by impinging on the facial nerves. Wound infections after rhytidectomy have also been associated. Calculi can develop in the preauricular sinuses, resulting in infection.

In one large study, 52% of patients had inflammation of their sinuses, 34% had their sinus abscesses drained, and 18% of sinuses were infected. Infectious agents identified included Staphylococcus epidermidis (31%), Staphylococcus aureus(31%), Streptococcus viridans (15%), Peptococcus species (15%), and Proteus species (8%). Once a patient acquires infection of the sinus, he or she must receive systemic antibiotics. If an abscess is present, it must be incised and drained, and the exudate should be sent for Gram staining and culturing to ensure proper antibiotic coverage.

Once infection occurs, the likelihood of recurrent acute exacerbations is high, and the sinus tract should be surgically removed. Surgery should take place once the infection has been treated with antibiotics and the inflammation has had time to subside. Controversy regarding indications for surgery exists. Some believe that the sinus tract should be surgically extirpated in patients who are asymptomatic because the onset of symptoms and subsequent infection cause scarring, which may lead to incomplete removal of the sinus tract and postoperative recurrences. The recurrence rate after surgery is 13-42% in smaller studies and 21% in one large study.

Most postoperative recurrences occur because of incomplete removal of the sinus tract. One way to prevent incomplete removal is to properly delineate the tract during surgery. Some surgeons cannulate the orifice and inject methylene blue dye into the tract 3 days prior to surgery under sterile conditions. The opening is then closed with a purse-string suture. This technique distends the tract and its extensions by its own secretion stained with methylene blue.

During surgery, some surgeons use either a probe or an injection of methylene blue dye for cannulation of the orifice. The most successful method is to use both modalities to delineate the entire tract.

Other surgical techniques have been studied. The standard technique for extirpation of the sinus tract involves an incision around the sinus and subsequent dissection of the tract to the cyst near the helix. A supposedly more successful technique is the supra-auricular approach, which unlike the former technique, does not allow for difficulties in properly identifying the entire tract. The supra-auricular approach extends the incision postauricularly. Once the temporalis fascia is identified, dissection of the tract begins. A portion of the auricular cartilage, which is attached to the tract, is also removed, decreasing the incidence of recurrence to 5%. Leopardi et al report that they prefer the supra-auricular approach for the surgical treatment of recurring preauricular sinus.

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