washington manual survival guide otolaryngology.docx

WASHINGTON MANUAL SURVIVAL GUIDE OTOLARYNGOLOGYABBREVIATIONS

BPPN benign paroxysmal positional nystagmus BPPV benign paroxysmal positional vertigo Cr creatinine CXR chest x-ray DVT deep venous thrombosis EAC external auditory canal ETT endotracheal tube FESS functional endoscopic sinus surgery N/V nausea and vomiting OM otitis media ORIF open reduction and internal fixation PCA patient-controlled analgesia PE pulmonary embolism PTA pure-tone average RSV respiratory syncytial virus SCC semicircular canal SOB shortness of breath SRT speech reception threshold TEF tracheoesophageal fistula UMN upper motor neuron VOR vestibuloocular reflex KEY TO SURVIVALHow to Make It through ResidencyResidency, particularly a surgical residency, can be a difficult and challenging time. In addition to working long hours and having a heavy workload, you are also expected to read regularly and learn a great deal about your field. You will be making decisions every day that significantly impact the lives of your patients. This can be a stressful time. Here are a few suggestions that may help: You and the other residents in your program should be a cohesive team. This means that everyone should do whatever it takes to help each other out. If one of your co-residents just had a baby, take a call or two so that he can spend some time with his new child. If your junior resident has dinner reservations for her 1-yr anniversary, offer to cover her floor work so that she can make it to the restaurant on time. If everyone makes an effort to help out, everyone will be much happier. Eat something before you come to work in the morning. You never know when you will be called to the OR unexpectedly, and you don't want to have an empty stomach. Do something for yourself on a regular basis. This can be whatever you find relaxing: go for a run, make a nice dinner for friends, and so forth. Start reading early in your residency. You may think that you will have more time as a senior resident than you do now. However, it will not be the case. Get into the habit of reading at least a few days a week right away. Treat everyone in the hospital with respect. Most employees at a hospital are there because they want to do their jobs and make an impact. However, we have all also met people who do not fall into that group. Getting into an argument with hospital support staff never benefits anyone. It just increases your stress level and gives you the reputation of being the "jerk ENT resident." Remember that your goal is to benefit the patient. Ask for help. You are not expected to know it all. Don't panic. Respect the airway. Patients will often look pretty good right before they completely lose their airways. Otolaryngology is one of the most competitive fields to get into because it is an absolutely wonderful job full of challenges, variety, and the opportunity to directly benefit your patients. ENT job satisfaction is high. You have worked hard to get to this point in your career. Now it is time to demand as much from yourself and your teachers to make you the best physician and surgeon possible. INTRODUCTION TO OTOLARYNGOLOGYOverview of the Specialty Otolaryngology is a broad and interesting surgical subspecialty. It includes the fields of otology/neurootology, rhinology/sinus disease, laryngology/voice disorders, head and neck oncology, microvascular surgery, skull base surgery, facial plastic and reconstructive surgery, and allergy. Due to the breadth of the field, otolaryngologists are skilled in a wide variety of surgical techniques, including soft tissue surgery, endoscopic procedures, and delicate microsurgery of the ear and skull base. They are also called on to perform the medical management of a wide variety of local and systemic diseases that affect the head and neck in infants, children, and adults. This variety provides a constant stream of new and interesting challenges to the individual who chooses to pursue training in otolaryngology.Overview of the Residency Training in most programs within the United States is 5 yrs (1 yr of general surgery internship followed by 4 yrs of otolaryngology). Responsibility and operative experience are usually progressive. Senior residents spend their days performing the more complex surgeries and seeing patients in the clinic. Junior residents see to the day-to-day routine care of inpatients and perform the more straightforward procedures. There are many similarities between otolaryngology and the other surgical fields in that time is divided between the OR, following patients on the floor, and seeing outpatients in clinic. Therefore, work hours can be long. However, otolaryngology residents remain among the happiest and most satisfied physicians in the hospital.The Otolaryngology Team A wide variety of health care professionals are involved in the care of otolaryngology patients due to the variety of their pathology and needs.Otolaryngologist The otolaryngologist is the captain of the team. He or she should be familiar with all aspects of the patient's management, including any surgical procedures, pre- and postop care, and outpatient medical management. Because it is impossible for the M.D. to personally perform all the duties of the team, it is important to know what is going on so that you can coordinate care. Remember that your ultimate responsibility is to assure the best care possible for each patient.Nurses Nurses are the well-trained eyes and ears of the medical profession. They probably spend more time with your patient than you are able to devote. Therefore, it is important that you communicate with the nursing staff. Tell them about your plan of care or if there is anything in particular to watch for with your patient. You can't be on the floor watching your patients all the time because you have to be in clinic and the OR. Therefore, you trust nurses to call you if there is something wrong; if you don't tell the staff what to look for, they may not notice the problem.Audiologists Most training programs have a staff of audiologists. They perform audiograms and other tests, such as auditory brainstem response and vestibular testing. Audiologists also fit and dispense hearing aids. Many academic institutions also perform cochlear implantation in partnership with audiology.Speech Therapists Many of your patients will have problems with their voice or with swallowing. Much of the testing and therapy for these disorders falls on the shoulders of speech therapists. They perform video stroboscopy/laryngoscopy, modified swallow studies, and speech and swallow rehabilitation.Physical Therapists Physical therapists are especially helpful for patients after cancer surgery. They teach stretching and strengthening exercises to help patients avoid frozen shoulder after a neck dissection. Also, they are responsible for conditioning postop.Nutritionists Many otolaryngology patients have poor nutrition due to dysphagia/odynophagia. Also, cancer resections of the head and neck alter a patient's ability to swallow, and many postop patients require a special diet or tube feeding for a period of time. For these reasons, it is important to have a nutritionist involved in the care of any patient with feeding issues.Daily Routine Your daily routine as a junior otolaryngology resident will vary according to the program you are attending and whether you have an intern. A significant portion of the "scut" and floor work can be covered by the intern, leaving you free to go to clinic or the OR. However, remember that it is the junior resident's responsibility to ensure that all floor work is completed correctly and on time. Also, many ENT patients have tenuous airways, tracheostomies, and various other special needs that are not appropriate to leave for the intern. In addition, many otolaryngology services do not have an intern, leaving only you to perform the work on the floor. Because every otolaryngology junior resident has completed a general surgery internship, a detailed description of daily tasks is not necessary in this text, but a brief overview follows. More detailed discussion of the daily routine can be found in The Washington Manual Surgery Survival Guide.Prerounding Prerounding includes getting everything together so that rounds can proceed efficiently. Make an updated list of the patients. Have the vitals, ins, outs, and drain outputs for patients. Speak to the nurses who took care of your patient overnight to see if there were any issues. Contact the physician on call the night before for the same reason. Ideally, see the patients and take down any dressings so that the team can see wounds on rounds. Rounds Every patient needs to be seen and evaluated efficiently. Dressings will need to be changed, so have supplies with you on rounds. The senior resident will examine and speak to the patient. He or she will generate a series of things that need to be done for the patient that day. It is your job to generate a coherent to-do list and make sure the tasks are completed. It is also your job to make sure all the notes are completed; it may be done on rounds or shortly thereafter. Lab analyses must be checked and corrected. Any consults or radiographic studies needed should be called in early in the day. Also, discharges should be processed early so that the patient can go home in a timely manner.Operating Room The amount of time you spend in the OR and clinics varies by program. Whenever you have the chance, go to both. Soon you will be performing these surgeries and managing your own patients in clinic. It is in your best interest to "get your hands dirty" right away and at least observe how the various procedures are done.Evening Rounds Before evening rounds, you should preround again. See the patients and make sure there are no new issues. Check on the status of all consults and studies. Read over the charts to make sure that consultant's recommendations have been followed. Evening rounds will proceed similar to morning rounds. Again, make sure you make a list of items that need to be done. After rounds, finish the work that has been assigned, sign out to the resident on call that night, and get out of the hospital.HEAD AND NECK EXAMINATIONInstrument, Illumination, and Additional Equipment Hand-held otoscope (pneumatic)Tuning forks (256, 512 (if you only carry one tuning fork, use the 512), 1024 Hz)Head mirror or headlightNasal speculumNasal and ear suctionsTongue bladesGlovesCentimeter rulerLaryngeal mirrorNasal anesthetic/vasoconstrictor sprayFiberoptic nasopharyngoscopeOtomicroscopeHand-held ear speculaCerumen curettesAlligator forceps4 4 gauze spongesNOSE AND PARANASAL SINUSESNote skin: lesions, trauma, scarring.

Note basic configuration of bony-cartilaginous skeleton: cosmetic relation to face, presence of dorsal hump, deviation of nasal bones or cartilages.

Examine base of nose with head back before inserting speculum: note width of columella; evaluate for deviated caudal septum; inspect external and internal nasal valves, mucus/crusts, foreign body.

Assess airflow: alternate occlusion; should be silent at rest; and should not distort ala with quiet inspiration.

On nasal speculum exam: inspect cartilaginous septum, bony septum, turbinates, mucosa.

Percuss maxillary teeth and face over maxillary, frontal, and ethmoid sinuses.

Anatomy of the external nose

A: Anterior view. B: Anterolateral viewCoronal cross-section of the sinuses

EARAuricle: Inspect skin, shape of cartilaginous ridges, postauricular area.

External auditory canal (lateral two-thirds cartilage, medial one-third bone): Assess patency, cerumen, skin integrity, canal skin or bony lesions, foreign body.

Tympanic membrane: Identify annulus, notch of Rivinus, pars tensa, pars flaccida; evaluate translucency, integrity, color, mobility, shape, vascularity, light reflexes, retractions, debris.

Middle ear space: Inspect through translucent drum or perforation; inspect ossicles and mucosa; assess presence of fluid or mass.

Anatomy of the external ear

Tuning fork testing: May be performed with the 512-Hz fork. May be repeated with the 256- and 1024-Hz forks if there are any abnormalities.

Weber Place tuning fork in center of patient's forehead. Ask patient if sound is louder on one side or is heard midline.For Weber "negative," patient response is "Sound is midline." Interpretation: Bone-conducted sound equal in both ears.

For Weber right, patient response is "Sound louder on right." Interpretation: Unilateral right conductive hearing loss or unilateral left sensorineural hearing loss.

For Weber left, patient response is "Sound louder on left." Interpretation: Unilateral left conductive hearing loss or unilateral right sensorineural hearing loss.

Rinne Place tuning fork lateral to ear canal, then place it firmly on mastoid process. Ask patient if sound is louder by canal or on mastoid bone.For Rinne "positive," patient response is "Sound louder when fork by canal." Interpretation: Air conduction louder than bone conduction; normal.

For Rinne "negative," patient response is "Sound louder when fork on mastoid process." Interpretation: Bone conduction louder than air conduction; conductive hearing loss.

For Rinne "equal," patient response is "Sound equal." Interpretation: Air and bone conduction equal.

10-MINUTE EXAM OF THE DIZZY PATIENTSpontaneous Nystagmus Action: Target fixation in neutral gaze, Frenzel lensesNormal: No nystagmus or excessive saccadesAbnormal:Jerk nystagmus Direction fixed, increases with Frenzel lenses = PERIPHERAL

Direction changing, increases with fixation = CENTRAL (periodic alternating nystagmus, congenital)

Pendular = CENTRAL (congenital nystagmus)

Gaze nystagmus Action: Hold eccentric gaze 2030 degrees for 10 secs in horizontal and vertical planeNormal: Physiologic end gaze or no nystagmusAbnormalJerk nystagmus (exponentially decreasing slow phase) in direction of gaze = CENTRAL (flocculus, drug effect, alcohol)

Downbeat nystagmus in lateral gaze = CENTRAL (Arnold-Chiari, midline cerebellum)

Smooth pursuit Action: Track finger moving, 60 degrees/sec through 60-degree arc horizontal and verticalNormal: Smooth pursuit movementsAbnormalSaccadic pursuit = CENTRAL (cerebellum, brainstem, parietal lobe)

Irregular tracking = acuity, age, medications, attention

Saccades Action: Alternate gaze between fingerNormal: Rapid, accurate, conjugate eye movementsAbnormalOvershoots, undershoots = CENTRAL (dorsal vermis, fastigial nuclei)

Slow saccades = CENTRAL (brainstem)

Late saccades = CENTRAL (frontal lobe, brainstem, Parkinson's disease)

Disconjugate = CENTRAL (medial longitudinal fasciculus syndrome)

Head-shake test Action: Shake head for 20 secs at 2 Hz (horizontal and vertical) eyes closed, then open eyes (Frenzel lenses) and observe for nystagmusNormal: No nystagmusAbnormalUnidirectional nystagmus in plane of head shake = PERIPHERAL (toward intact side except hydrops)

Vertical nystagmus after horizontal head shake = CENTRAL

Head-thrust test Action: Thrust head 2030 degrees while fixating on targetNormal: No loss of fixationAbnormal: Refixation saccade = PERIPHERAL (loss of vestibuloocular reflex)Dynamic visual acuity Action: Have patient read eye chart with head still, then with 2-Hz head shakeNormal: Less than three-line drop in acuity with head shakingAbnormal: More than three-line drop = PERIPHERAL (bilateral vestibuloocular reflex loss)Fixation suppression test Action: Subject fixates on own thumb while rotating body in chairNormal: No nystagmusAbnormal: Nystagmus in direction of rotation = CENTRAL (flocculus)Position tests Action: Place the head in left/right Hall pike, left/right lateral, supineNormal: No nystagmusAbnormalTorsional (geotropic) nystagmus with upbeat and ageotropic horizontal components = benign paroxysmal positional nystagmus (downmost posterior semicircular canal)

Horizontal (geotropic or ageotropic) paroxysmal nystagmus = benign paroxysmal positional nystagmus (downmost lateral canal)

Horizontal sustained nystagmus = PERIPHERAL/CENTRAL

Cerebellar tests Action: Finger to nose, heel-shin, rapid alternating motionNormal: Accurate movementsAbnormal: Dysmetria, dysdiadochokinesia = CENTRAL (cerebellum)Posture tests Action: Romberg test, sharpened Romberg test, eyes closed foamNormal: Minimal sway, no fallsAbnormalExcessive sway, falls on Romberg = VARIABLE/APHYSIOLOGIC

Falls on foam eyes closed = PERIPHERAL/MIXED/APHYSIOLOGIC

Gait tests Action: Observation of gait; Fukuda step testNormal: Normal gait, 30-degree rotation in the direction of the lesion

ORAL CAVITY AND OROPHARYNXLips: Note color, skin and mucosal surfaces, presence of any lesions.

Gingiva and teeth: Note the color and condition of the gingiva and general appearance of the teeth; remove dentures if present.

Buccal mucosa: Note hyperkeratosis, discoloration, evidence of trauma, saliva, parotid duct opening opposite second molar tooth.

Tongue: Inspect mucosa; assess mobility in protrusion and side-to-side motion; evaluate for masses, tremors, atrophy; palpation is crucial for evaluation of submucosal tumors and tongue base tumors.

Floor of mouth: Examine mucosa and orifice of submandibular ducts just lateral to the lingual frenulum; palpate carefully for masses/duct stones.

Submandibular glands: Palpate with one hand in floor of mouth and one hand beneath angle of mandible; assess for tenderness or masses.

Hard and soft palate: Inspect, palpate, note soft palate elevation.

Palatine tonsils/anterior and posterior tonsillar pillars, posterior pharyngeal wall: Inspect using a tongue blade to depress tongue in midline; evaluate for lesions/masses/asymmetry.

Teeth and occlusion

NECKSkin lesions: induration, abnormal pigmentation, vascular pulsations.

Thoroughly palpate soft tissue triangles of neck.

Masses: Note location, texture, color, size, tenderness, fixation, pulsation.

Larynx: Identify hyoid bone and thyroid and cricoid cartilages

Thyroid gland: Have patient swallow with head flexed while you palpate for masses and any asymmetry.

Auscultation: carotid bruits, vascular tumors, arteriovenous malformations.

LARYNX AND HYPOPHARYNXAssess voice quality (if hoarse, characterize voice quality as breathy/harsh/strained).

Assess breathing pattern: Is there airway noise (e.g., stridor, stertor)?

For mirror exam: Remove dentures.

Sit patient in "sniffing" position.

Explain to patient exactly what you are going to do.

Grasp tongue with 4 4 gauze and retract anteriorly.

Test temperature of warmed mirror on back of your hand before inserting into oral cavity.

Advance mirror to level of oropharynx and use back of mirror to elevate soft palate without touching posterior tongue.

Inspect the epiglottis, arytenoids, aryepiglottic folds, vallecula, tongue base, pyriform sinuses, false vocal folds, and true vocal folds.

Assess true vocal cord mobility while having patient say "eee"; pyriform sinuses are better visualized by turning head to the left or right to open contralateral pyriform.

Endoscopic view of the larynxLaryngeal muscles

CRANIAL NERVE EXAMINATIONI: Olfactory nerve Function: Olfaction (smell)Test: Use substances that do not illicit trigeminal nerve stimulation (e.g., coffee, not ammonia salts). If olfactory dysfunction is present, consider site of lesion: olfactory mucosa, bulb, tract, nucleus, or frontal or temporal lobe.II: Optic nerve Function: VisionTest: Visual fields by confrontation and acuity.III: Oculomotor nerve Function: Levator palpebrae superioris, superior rectus, medial rectus, inferior rectus, and inferior oblique muscles (somatic motor)Test: Extraocular movements and levator function.Function: Constrictor pupillae and ciliary muscles of the eye (visceral motor)Test: Pupillary light reflex; separate afferent from efferent deficits.IV: Trochlear nerve Function: Superior oblique muscle (somatic motor)Test: Palsy gives ipsilateral extortion (upper pole rotated laterally) at rest, head tilt preference.V: Trigeminal nerve Function: Sensation of face, conjunctiva, mucous membranes of paranasal sinuses, nasal and oral cavities, part of tympanic membraneTest: Light touch with wisp of cotton applicator.Function: Muscles of mastication, tensor tympani, tensor veli palatini, mylohyoid, and anterior belly of digastric (branchial motor)Test: Temporalis bulge with jaw clenched or with chewing.VI: Abducens nerve Function: Lateral rectus muscle (somatic motor)Test: Palsy gives restriction of ipsilateral lateral gaze.VII: Facial nerve Function: Muscles of facial expression; stapedius, stylohyoid, and posterior digastric muscles (branchial motor)Test: Full range of facial expressions (upper motor neuron lesions preserve function of the contralateral forehead) stapedius reflex.Function: Lacrimal, submandibular, and sublingual glandsTest: Note flow of tears, saliva.Function: Taste to the anterior two-thirds of tongue and the hard and soft palates (special sensory)Test: Sweet, salty, bitter, sour.VIII: Vestibulocochlear nerve Function: Cochlea and vestibule (special sensory)Test: Hearing (best with full audiogram) and vestibular function.IX: Glossopharyngeal nerve Function: Stylopharyngeus (branchial motor)Test: Function: Otic ganglion/parotid gland (visceral motor)Test: Function: Carotid body and sinus (visceral sensor)Test: Function: Posterior one-third of tongue, oropharynx, part of external auditory canal and tympanic membrane (general sensory)Test: Gag reflex.Function: Taste of posterior one-third tongue (special sensory)Test: X: Vagus nerve Function: Pharyngeal muscles, palatoglossus, and larynx (branchial motor)Test: Vocal cord movement, palate elevation.Function: Mucosal glands of pharynx and larynx (visceral motor)Test: Function: Larynx, trachea (visceral sensory)Test: Cough reflex with endoscopy.Function: Skin at back of ear and part of external auditory canal, tympanic membrane, and pharynx (general sensory)Test: XI: Spinal accessory nerve Function: Sternomastoid and trapezius (branchial motor)Test: Shoulder beyond 90 degrees, muscle atrophy including downward and lateral rotation of scapula.XII: Hypoglossal nerve Function: All intrinsic and extrinsic muscles of the tongue, except palatoglossus (somatic motor)Test: Tongue deviates toward side of lesion in lower motor neuron lesion, away in upper motor neuron lesion.

HOUSE RACKMAN FACIAL PARALYSIS SCALEEach grade is followed by the associated facial movements.I. Normal Normal facial function at all times

II. Mild dysfunction Forehead: moderate to good function

Eye: complete closure

Mouth: slight asymmetry

III. Moderate dysfunction Forehead: slight to moderate movement

Eye: complete closure with effort

Mouth: slightly weak with maximum effort

IV. Moderately severe dysfunction Forehead: none

Eye: incomplete closure

Mouth: asymmetric with maximum effort

V. Severe dysfunction Forehead: none

Eye: incomplete closure

Mouth: slight movement

VI. Total paralysis No movement

OTOLOGYANATOMYExternal Ear The external ear (Fig. 4-1) extends from the pinna to the lateral border of the tympanic membrane.

The pinna is composed of fibroelastic cartilage covered by perichondrium and skin. The skin on the lateral surface of the pinna adheres firmly to the perichondrium, whereas that of the medial surface is loosely attached and contains areolar tissue below the epidermis.

External ear

The external auditory canal (EAC) is approximately 2.5 cm in length and slightly S-shaped, pointing anteroinferiorly. Due to the EAC's sloping course, posterior superior retraction on the antihelix straightens the canal and provides optimal visualization of the tympanic membrane.The lateral third of the EAC is cartilaginous, containing cerumen-producing glands and hair follicles, whereas the medial two-thirds is osseous, containing periosteum without subcutaneous tissue.Function Localization of sound is a primary objective of the external ear.

At frequencies >2 kHz, a head-shadow effect occurs, and interaural differences of 1015 dB are used to localize sound.

Middle Ear The middle ear (Fig. 4-2) consists of the tympanic cavity and the osseous eustachian tube.Ligaments of the incus; muscles of the middle ear; and middle ear spaces, wall, and recesses

Boundaries of Tympanic Cavity Lateral: tympanic membrane

Medial: osseous labyrinth

Roof: tegmen

Floor: jugular bulb

Anterior: carotid wall, eustachian tube, tensor tympani

Posterior: mastoid air cells, pyramidal eminence, stapedius muscle

Contents of the Middle Ear Bones of HearingMalleus

Incus

Stapes

MusclesThe tensor tympani connects the medial surface of the malleus with the cochleaform process and is innervated by the trigeminal nerve. It is proposed that the tensor tympani contracts in response to loud noises, stiffening the tympanic membrane and ossicular chain and therefore protecting the cochlea from loud noises.

The stapedius muscle serves a similar function. This muscle originates from the pyramidal process and attaches to the posterior surface of the neck of the stapes. The stapedial branch of the facial nerve innervates this muscle, and involuntary contraction occurs in response to loud noises.

Function The function of the middle ear is transmission of acoustic energy from the air-filled external canal to the fluid-filled cochlea.

Fluid has higher impedance than air, and this interface would result in an approximately 30-dB loss if other factors were not involved.

Three aspects of the middle ear contribute to an overall gain of 2533 dB sound pressure generated by the middle ear.First and most significant is the size difference between the tympanic membrane and the oval window. The vibrating surface of the tympanic membrane is 1720 times larger than the surface area of the stapes footplate at the oval window.

The second factor relates to the lever action of the ossicles. The length of the malleus is 1.3 times greater than the long process of the incus, creating a lever to generate additional force.

Finally, the shape of the tympanic membrane contributes minimally to the sound intensification. The curvature of the tympanic membrane allows portions of the membrane to vibrate at greater amplitude, providing additional leverage to the system.

Inner Ear The inner ear (Fig. 4-3) consists of the cochlea and semicircular canals. The cochlea is a bony, coiled tube containing the organ of Corti, which is responsible for sound transmission in the inner ear. The semicircular canals are three paired canals responsible for balance and equilibrium.

Membranous labyrinth of the inner ear. SCC, semicircular canal

ASSESMENT OF AUDITORY FUNCTIONMany audiometric tests are available to evaluate auditory function. The most basic assessment is a tuning fork exam. It is quick, can be performed in any quiet room, and can provide a great deal of information. Two fork tests are commonly performed (see Head and Neck Exam). Weber test: A 512-Hz tuning fork is struck and placed on the patient's skull in the midline either on the maxilla or the vertex of the head. Lateralization, hearing the sound louder in one ear, indicates a conductive loss in the louder ear or a sensorineural loss in the opposite ear. Patients with normal hearing or symmetric hearing loss hear the sound equally loud in both ears. Rinne test: a tuning fork test that differentiates a conductive hearing loss from a sensorineural hearing loss. A tuning fork is struck and placed on the mastoid process. Once the patient hears the noise, place the tuning fork just outside the external auditory canal on the same side. In normal hearing, air conduction is greater than bone conduction, and the patient should be able to hear the sound louder when presented to the external auditory canal. If air conduction is greater than bone conduction, the normal state, the test is considered positive. If the Rinne test is negative (bone conduction is greater than air conduction), then a 25-dB conductive hearing loss is present. Pure-tone audiometry is another basic measure of hearing sensitivity. The audiogram is a relative measure of hearing compared to established hearing of normal subjects. A range of frequencies of pure tones is presented to each ear individually. 250, 500, 1000, 2000, 4000, and 8000 Hz are the standard frequencies tested (Fig. 4-4). Suprathreshold sounds are presented to the ear and decreased in 5-dB increments until the sound is inaudible. The sound level that is just audible is then recorded for air and bone conduction. During a standard audiogram, the audiologist presents pure tones to each ear individually via headphones or an ear insert to test air conduction. Air conduction assesses the external, middle, and inner ear. The audiologist also presents pure tones via a probe attached to the mastoid process to test bone conduction. This bypasses the middle ear structures and directly stimulates the cochlea. The pure-tone average (PTA) is an estimate of hearing within the speech frequencies. Although the human ear can perceive frequencies of 2020,000 Hz, the speech frequencies fall between 300 and 3000 Hz. Air conduction hearing thresholds at 500, 1000, and 2000 are averaged and given as one number in dB. Speech audiology is used to confirm the pure-tone findings on audiogram and reflects the patient's speech reception abilities. The speech reception threshold (SRT) test is performed by presenting a set of spondees to the patient. Spondees are two-syllable words with equal emphasis on each syllable, such as hotdog, popcorn, and eardrum. The SRT is the minimum level at which the patient is able to repeat 50% of the presented words. Because the PTA assesses the speech frequencies, the PTA and SRT should be within 68 dB. If a >8-dB difference exists, one or both of the tests is invalid, and a nonorganic cause, such as malingering, should be suspected. The speech discrimination test evaluates the patient's ability to recognize speech. 2550 standardized single-syllable words are presented for the patient to repeat. The score is reported as a percentage of words correctly repeated. Normal values are >90%. AudiogramsA. Normal:B. Conductive hearing loss:

C. Sensorineural hearing loss:

D. Mixed hearing loss:

Tympanogram Picture Tympanometry is an objective form of pneumatic otoscopy (Fig. 4-5). It is a sensitive measure of the mobility or compliance of the tympanic membrane and middle ear structures. As an electrophysiologic test, it does not require behavioral cooperation of the patient, making this test extremely useful in children. The following is a description of tympanogram types (From Roseser RJ, Valente M, Hosford-Dunn H. Audiology diagnosis. New York: Thieme Medical Publishers, 2000:10, with permission.):Tympanogram type A

A: Represents normal middle ear function. The peak (point of maximum compliance) occurs within normal statis compliance limits and at pressures between +50 and 100 mm/H2O.Tympanogram type As

As: Represents abnormal stiffness in the middle ear system, resulting from a fixation of the ossicular chain as in otosclerosis. Compliance measures are abnormally low.Tympanogram type Ad

Ad: Represents a flaccid tympanic membrane resulting from scar tissue or a possible disarticulation of the middle ear ossicles. Compliance measures are abnormally high.B: Represents restricted tympanic membrane mobility and would indicate that some pathologic condition exists in the middle ear. Static compliance measures are abnormally low.Tympanogram type B

C: Represents significant negative pressure in the middle ear cavity (considered significant for treatment when more negative than 200 mm/H2O). This may indicate a precursory state of otitis media or the resolution of an ear infection. Compliance measures are usually within normal limits.Tympanogram type C

A probe is inserted into the external auditory canal, creating a seal between the probe and canal. Air pressure is then increased and decreased within the closed space. The compliance, movement of the tympanic membrane, is recorded relative to the air pressure on a graph. Maximal compliance occurs when air pressure is equal on both sides of the tympanic membrane.Normal compliance is between 50 and 150 mm water pressure. Five tympanograms are commonly seen, termed types A, As, Ad, B, and C (see descriptions above).Interpretation and Diagnosis These audiometric tests are used together to differentiate the two general types of hearing loss, conductive and sensorineural.An airbone mismatch or gap on the audiogram of >20 dB indicates a conductive hearing loss. Common causes of conductive hearing loss include Foreign bodies in the ear.

Cerumen impaction. Cerumen impaction is the most common cause of conductive hearing loss in adults and contributes, at most, 3040 dB of hearing loss.

Otitis media. In children, otitis media with effusion is the most common etiology of conductive hearing loss.

Hemotympanum (blood in the middle ear space).

Cholesteatoma.

Ossicular chain discontinuity.

Otosclerosis. Excluding cerumen impaction, otosclerosis is the most common cause of conductive hearing loss in adults.

5060 dB is the largest conductive hearing loss that can occur purely from a conductive cause. This generally results from ossicular discontinuity with an intact tympanic membrane.

The best treatment for conductive hearing loss is to treat the underlying disorder. This includes cerumen disimpaction, antibiotics, ossiculoplasty, and stapedectomy to treat cerumen impaction, otitis media, ossicular discontinuity, and otosclerosis, respectively.

Sensorineural hearing loss is caused by abnormalities of either the cochlea or neural transmission to the central nervous system. In this type of hearing loss, both the air and bone lines are depressed on the audiogram.

Common causes of sensorineural hearing loss include Presbycusis

Ototoxicity

Noise-induced hearing loss

Hereditary

Mnire's disease

Acoustic neuroma

Trauma

Definition of hearing loss Normal hearing, 020 dB

Mild hearing loss, 2040 dB

Moderate hearing loss, 4060 dB

Severe hearing loss, 6080 dB

Profound hearing loss, 80100 dB

Total hearing loss, >100 dB

The audiogram is described in terms of symmetry and the morphology of the curve. Many disease processes produce classic audiograms. Presbycusis, or hearing loss of advanced age, produces an audiogram that is symmetric and downward sloping in the high frequencies.

Noise-induced hearing loss presents with a downward slope, with a nadir at 46 kHz and rising at 8 kHz.

Otosclerosis initially presents as a conductive hearing loss. As the disease progresses, a mixed-sloping curve is demonstrated, with a maximal 15-dB bone loss at 2 kHz.

Mnire's disease presents as a fluctuating low-frequency sensorineural hearing loss rising toward normal levels.

Any asymmetric high-frequency sensorineural hearing loss in an adult should prompt an evaluation for acoustic neuroma.

Presbycusis is the most common cause of sensorineural hearing loss followed by noise-induced hearing loss. Gunfire is the most common cause of nonoccupational hearing loss.

Sensorineural hearing loss is most commonly treated with hearing aids.

OTITIS EXTERNAOtitis externa is an infection of the cartilaginous external auditory canal.Symptoms Otalgia

Otorrhea

Pruritus

Aural fullness

Pathogenesis A warm and humid environment predisposes the ear canal to otitis externa, as demonstrated by the higher incidence in swimmers during the summer months.

Moisture disrupts the lipid layer covering the canal skin, allowing the stratum corneum to absorb fluid, creating edema and obstruction of the auditory canal.

Aposebaceous glands (which produce cerumen) in the external auditory canal are blocked, resulting in a warm, moist canal lacking bacteriostatic cerumen.

This provides an ideal environment for bacterial growth.

Microbiology Pseudomonas is the most common organism cultured from ears with otitis externa.

Staphylococcus aureus is also commonly identified.

Treatment Aural toilet: clean the external auditory canal with irrigation and a Frazier tip suction under microscopic visualization. This may need to be repeated multiple times during the first 2 wks of therapy.

A steroid and antibiotic combination otic drop is then used three times a day for 1 wk.

If the canal is extremely edematous, a small wick may be placed in the external auditory canal to allow the otic drops to penetrate the medial aspect of the canal.

FOREIGN BODIES IN THE EXTERNAL AUDITORY CANALExternal auditory canal foreign bodies are commonly seen in children, although they can be found in adults. Common foreign bodies include beads, rocks, and insects.Treatment Removal should be performed with an operative microscope to avoid trauma to the canal or tympanic membrane.

A Buck curette or right-angle pick is placed just past the foreign body and used to pull the object out of the external auditory canal.

If the object has been present for a long time and the canal is inflamed, conscious sedation or general anesthesia may be necessary for removal.

Irrigation must be avoided with vegetable material because this causes swelling of the object and makes removal more difficult.

Insects Mineral oil is used to drown live bugs in the external auditory canal.

Alligator or Hartman ear forceps are then used to remove the insect.

A small watch battery presents an emergency and must be removed immediately because alkali material can leak into the external auditory canal.

If inflammation or irritation of the external canal or tympanic membrane is present, a steroid otic drop should be used for 35 days.

It is imperative that both ears and nostrils are examined to verify that the child did not insert foreign bodies in multiple sites.

OSTEOMAOsteomas are benign, solitary, pedunculated tumors occurring in middle-aged adults. The tympanosquamous suture line is the most common site for these tumors. Removal is performed if the growth produces canal obstruction resulting in pain or hearing loss.TYMPANIC MEMBRANE PERFORATIONSClassification Perforations of the tympanic membrane are classified into two types:Central perforations are usually inferior to the umbo of the malleus and do not involve the annulus.

Marginal perforations involve the fibrous annulus and are more difficult to repair.

Signs and Symptoms Recurrent infections

Otorrhea

Hearing loss

Occasional pain

Assessment Microscopic exam is the best diagnostic tool for assessing a perforation. The degree of perforation is described as a percentage of the total tympanic membrane surface area.Pathogenesis In children, tympanic membrane perforations are often the result of retained myringotomy tubes.The chance of tympanic membrane perforation after placement of myringotomy tubes is directly proportional to the length of time the tube is in place. For this reason, myringotomy tube removal is recommended if still in place after 3 yrs in a child without craniofacial abnormalities.

Children with cleft palate and other craniofacial syndromes are prone to chronic eustachian tube dysfunction, and the risk of persistent perforation is offset by the risk of recurrent retractions and serous otitis media after removal.

Treatment Most small perforations heal spontaneously. After a perforation, only the inner and outer layers of the tympanic membrane regrow, resulting in a weakened hypermobile area termed a monomer.

Keep in mind that presence of a perforation does not necessitate repair. The indications for surgery are persistent drainage, recurrent infection, and hearing loss. The ear should be free of infection before proceeding with surgery.

Paper patch Small (10 days, or in the presence of symptoms out of proportion to those typically associated with viral infection.

Subacute Duration: 412 wks

Strong history: Same as chronic

Include in differential: Same as chronic

Special notes: Complete resolution after effective medical therapy.

Recurrent acute Duration:4 episodes/yr, with each episode lasting 710 days and absence of intervening signs and symptoms of chronic rhinosinusitis

Strong history: Same as acute

Chronic Duration:12 wks

Strong history:2 major factors, 1 major factor and 2 minor factors, or nasal purulence on exam

Include in differential: One major factor or 2 minor factors

Special notes: Facial pain does not constitute a suggestive history in the absence of other nasal signs or symptoms.

Acute exacerbations of chronic Duration: Sudden worsening of chronic rhinosinusitis, with return to baseline after treatment

Anatomy Anatomically, there are four pairs of sinuses within the facial skeleton: the frontal, ethmoid (anterior and posterior), maxillary, and sphenoid (Fig. 5-1). The function of these sinuses has been theorized to involve humidification of inspired air, voice resonance, and diminished Anatomy of paranasal sinuses and ostiomeatal complex

weight of the skull. At birth, the ethmoid and maxillary sinuses are present, whereas the sphenoid and frontal sinuses appear by the third year of life. Drainage of the frontal, anterior ethmoid, and maxillary sinuses is into the middle meatus. The posterior ethmoid sinus empties into the superior meatus, whereas the sphenoid sinus drains into the sphenoethmoid recess. The anterior ethmoidmiddle meatus region is classically believed to play a major role in the etiology of sinusitis. This area has been labeled as the ostiomeatal complex and is believed to be where sinusitis initially develops. Involvement of this region may then spread to any of the sinuses.Pathophysiology There are three major factors involved in the pathophysiology of sinus disease: patency of the ostia, function of the cilia, and quality of the nasal secretions [2]. First, a diminished ostia size can lead to a lower oxygen content within the sinus, which can lead to a favorable situation for infection. Anaerobic and facultative bacteria may flourish in such an environment. Hypoxia can also contribute to a diminished immune system from impaired polymorphonuclear function, immunoglobulin production, and mucociliary clearance. Studies have also shown that because ciliary clearance of mucus occurs toward the natural ostium, fluid still accumulates even if a new ostium is surgically created in a more gravity-dependent position [3]. Factors that may play a role in ostia patency include nasal polyposis, septal deviation, mucosal edema, allergies, and concha bullosa.The sinus cavities depend on the mucociliary transport system to create a bacteria-free environment. Sinuses are lined with a ciliated, pseudostratified columnar epithelium, which clears mucus, bacteria, and particulate matter from the area. Impaired ciliary function can occur in hypoxic conditions (from an obstructed ostium), which can alter the effectiveness of sinus clearance. Ciliated cells may also be lost or damaged from airway pollutants, surgical trauma, and chronic sinus disease.Changes in the mucus composition can also occur in patients with dehydration or cystic fibrosis. Likewise, airway irritants and pollutants, allergens, and cold air can increase the amount of mucus produced by goblet cells, resulting in an increased viscosity index. This can diminish the effectiveness of ciliary clearance and serve as a medium for bacteria growth.Microbiology Cultures taken directly from the nasal sinuses are much more accurate than those from the oro- or nasopharynx. It has been well established that little correlation exists between cultures taken from the anterior nares and nasal pharynx compared with sinus aspiration [4]. Although it can be done through sinus puncture or at the time of functional endoscopic sinus surgery (FESS), cultures can also be taken accurately with endoscopic assistance.The most commonly found pathogens in acute rhinosinusitis generally include Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis. One study by Gwaltney et al. [5] demonstrated a predominance of S. pneumoniae (31%), H. influenzae (21%), anaerobes (6%), Staphylococcus aureus (4%), and M. catarrhalis (2%). Subacute rhinosinusitis demonstrates similar microorganisms; however, the causative pathogens tend to differ once the chronic phase develops. Most studies on chronic sinusitis demonstrate a predominance of coagulase-negative Staphylococcus species (51%), S. aureus (20%), and anaerobes (3%) [6]. This increase in anaerobic activity can be seen in chronic infections of both adults and children.Additionally, the microorganisms found in chronic maxillary sinus disease tend to differ from those seen in chronic ethmoid disease. One review from Benninger et al. [7] shows that maxillary sinus pathogens tend to include S. pneumoniae, H. influenzae, anaerobes, and Streptococcus viridans; ethmoid cultures grow S. aureus, coagulase-negative Staphylococcus, and Enterobacteriaceae. The fact that most organisms within the maxillary sinus were anaerobic is consistent with the trapped environment of the sinus compared to the more open anatomic nature of the ethmoids.A search for atypical pathogens may be prudent in patients with immunodeficient conditions. These pathogens may include Pseudomonas, Listeria monocytogenes, atypical mycobacteria, and various fungi (Aspergillus, Candida, and Mucor).Allergic Fungal Sinusitis Allergic fungal sinusitis should always be entertained as an etiology of chronic sinusitis, especially if both medical and surgical treatments seem to promote minimal improvement. This process begins as an allergic reaction (types I and III Gell-Coombs hypersensitivity) to the colonized fungus of the sinus cavity. The resulting inflammatory process damages ciliary function and impairs clearance of debris and secretions from the sinus. Although this disease characteristically has noninvasive fungus elements, bony erosion may occur. It has been believed to be from buildup of mucus within the sinus (pressure effect) or osteoclastic factors secreted by the fungus itself or cytokine-mediated activation [2]. Although infrequent, orbital and intracranial extension has been reported. On inspection of the sinus, one usually sees thick, brown-green mucus similar to a peanut butter consistency. Eosinophils, Charcot-Leyden crystals, and fungal hyphae can be found within this mucus material. Tissue biopsy usually does not produce any organisms due to the lack of invasiveness from this disease process.Diagnostic criteria may include (a) testing or history positive for fungal atopy, (b) nasal polyposis, (c) CT scan demonstrating hyperdense material in the sinus cavity, (d) allergic mucus with high eosinophilic content, and (e) no histologic evidence of fungal invasion on tissue biopsy [8].Treatment consists of surgical removal of the offending mucus material and frequent sinus irrigations. Some have advocated postop nasal steroid sprays or systemic steroids, although no conclusive studies are present. Immunotherapy had previously been believed to be ineffective and possibly detrimental, although new studies have demonstrated a clinical benefit from its use [9]. Systemic antifungal agents do not typically play a role in treatment because of the disease process' noninvasive nature.Diagnosis A complete patient history and physical exam had previously been thought to be inadequate for making the diagnosis of rhinosinusitis. Supportive evidence by radiologic tests tended to be favored. Recently, a task force agreed that these two aspects would be sufficient for the proper diagnosis of rhinosinusitis. Currently, the task force has defined five different classifications of adult rhinosinusitis (Table 5-1). These classifications emphasize the temporal nature of the infection and the various symptomatology involved [1]. For example, acute rhinosinusitis tends to be very acute in onset, lasting 4 wks. Nasal congestion, purulent nasal discharge, and facial pain (worsened by head motion or bending over) have all been commonly seen. A "strong" history of acute rhinosinusitis includes two or more major factors or one major and two minor factors (Table 5-2). Additionally, the symptoms of fever and facial pain themselves do not support a diagnosis unless other nasal signs or symptoms are present. Many times, these symptoms may be seen in viral upper respiratory infections. A worsening of symptoms after 5 days or continuation of symptoms for >10 days suggests acute bacterial rhinosinusitis.Factors associated with rhinosinusitisMajor factors Facial pain/pressure (Facial pain/pressure alone does not constitute a suggestive history for rhinosinusitis in the absence of another major nasal symptom or sign.)

Facial congestion/fullness

Nasal obstruction/blockage

Nasal discharge/purulence/discolored postnasal drainage

Hyposmia/anosmia

Purulence in nasal cavity on exam

Fever (acute rhinosinusitis only) (Fever in acute sinusitis alone does not constitute a strongly suggestive history for acute in the absence of another major nasal symptom or sign.)

Minor factors Headache

Fever (all nonacute)

Halitosis

Fatigue

Dental pain

Cough

Ear pain/pressure/fullness

Clinical Evaluation The initial clinical evaluation is an important part of the diagnosis and management of rhinosinusitis. On history, predisposing factors should be investigated. These include general debilitating conditions such as malnutrition, uncontrolled diabetes mellitus, and patients undergoing chemotherapy or radiation. Immune deficiencies should be investigated, including HIV infections. It has been published that as many as 80% of HIV patients may have some symptoms consistent with rhinosinusitis [4]. Problems with mucociliary transport may predispose to infections of the sinuses. Immotile cilia syndrome and cystic fibrosis should be considered in children with recurrent ear, sinus, or pulmonary infections. Patients in the ICU tend to have risk factors for sinus disease. Placement of a nasogastric or tracheal tube for long periods may cause rhinosinusitis. Many ICU patients also have multiple organ dysfunction and a hypermetabolic state, leading to colonization of the respiratory tract with enteric gram-negative bacilli that may predispose to an active sinus infection.Patients presenting with asthma, gastroesophageal reflux, or allergic rhinitis must be differentiated from those with rhinosinusitis because of the different treatments. Those with allergic rhinitis, for example, tend to have more clear, watery nasal discharge, paroxysmal sneezing, and itchy eyes and nose. The symptoms may be seasonal, and there may be a strong family history of these symptoms. Although fever occurs in 40 yrs. These lesions demonstrate follicles of malignant cells with evidence of capsular invasion and invasion of surrounding vasculature. Regional metastasis is seen less frequently than with papillary carcinoma; however, distant hematogenous metastasis is more typical.

Anaplastic carcinoma constitutes 1020% of thyroid cancer. It generally occurs in patients >60 yrs. Anaplastic carcinomas demonstrate giant and spindle cells with little evidence of normal thyroid architecture. Prognosis is uniformly poor, and roughly 20% live 1 yr from the time of diagnosis. Long-term survival is essentially unheard of in patients with this disease. The vast majority of these patients are treated with chemotherapy or radiation, as surgery is rarely of benefit.

Medullary carcinoma accounts for the remaining 510% of thyroid cancer. These tumors originate from the parafollicular cells that produce calcitonin (C cells). They are characterized by nests of small cells with irregular regions of calcification. The majority of cases are sporadic; however, 2030% are familial and may be associated with the multiple endocrine neoplasia syndromes. Regional metastasis may be present at the time of diagnosis and has a substantial negative effect on prognosis.

Evaluation of the Thyroid Lesion A variety of tests and imaging modalities are available to the head and neck surgeon in the evaluation of the thyroid mass.Most physicians agree that the most critical diagnostic modality is the fine-needle aspirate. A needle aspirate of the lesion can be performed and sent for cytologic exam by the pathologist. This procedure often categorizes lesions as benign, malignant, or intermediate. Benign lesions can be followed conservatively, whereas malignant lesions can be treated by surgical resection as warranted by type of pathology. Patients with intermediate lesions can be further evaluated by other means.

U/S can be used to distinguish nodules from cysts. Purely cystic lesions are rarely malignant and may be followed conservatively.

Radioisotope scanning can be performed to evaluate uptake of nodules. These can be categorized as "hot" or "cold" according to the scan. The incidence of malignancy in "hot" nodules is 2 cm but not >4 cm in greatest dimension

T3: >4 cm in greatest dimension

T4: Lip: invades through cortical bone, into deep (extrinsic) muscle of tongue, maxillary sinus, or skin of face

T4a: Oral cavity: invades through cortical bone, into deep (extrinsic) muscle of tongue, maxillary sinus, or skin of face

T4b: Oral cavity: involves masticator space, pterygoid plates, or skull base and/or encases external carotid artery

T Staging Criteria: Pharynx Nasopharynx T1: Confined to the nasopharynx

T2: Extends to soft tissues

T2a: Extends to the oropharynx and/or nasal cavity without parapharyngeal extension

T2b: Any tumor with parapharyngeal extension

T3: Invades bony structures and/or paranasal sinuses

T4: Intracranial extension and/or involvement of cranial nerves, infratemporal fossa, hypopharynx, orbit, or masticator space

Oropharynx T1: 2 cm in greatest dimension

T2: >2 cm but not >4 cm in greatest dimension


T4: Invades lateral pterygoid plates, lateral nasopharynx, or skull base and/or pterygoid muscle, encases carotid artery

Hypopharynx T1: Limited to one subsite of the hypopharynx (e.g., pyriform sinus, posterior wall, postcricoid) and 2 cm in greatest dimension

T2: Invades more than one subsite of the hypopharynx or an adjacent site, without fixation of the hemilarynx, and tumor 4 cm or with fixation of hemilarynx

T4a: Invades thyroid/cricoid cartilage, hyoid bone, thyroid gland, esophagus, or central compartment soft tissue

T4b: Invades prevertebral fascia, encases carotid artery, or involves mediastinal structures

T Staging Criteria: Larynx Supraglottis T1: Limited to one subsite of supraglottis with normal vocal cord mobility

T2: Invades more than one subsite of supraglottis or glottis, with normal vocal cord mobility

T3: Limited to larynx with vocal cord fixation or invades postcricoid area, preepiglottic tissues, paraglottic space, or minor thyroid cartilage erosion

T4a: Invades through thyroid cartilage and/or extends to other tissues beyond the larynx (e.g., oropharynx, soft tissues of the neck)

T4b: Invades prevertebral space, encases carotid artery, or involves mediastinal structures

Glottis T1: Limited to vocal cords with normal mobility

T1a: Limited to one vocal cord

T1b: Involves both vocal cords

T2: Extends to supraglottis or subglottis, or with impaired vocal cord mobility

T3: Limited to the larynx with vocal cord fixation and/or invades paraglottic space and/or minor thyroid cartilage erosion

T4a: Invades through the thyroid cartilage or extends to other tissues beyond the larynx (e.g., oropharynx, soft tissues of the neck)


Subglottis T1: Limited to the subglottis

T2: Extends to the vocal cord(s) with normal or impaired mobility

T3: Limited to larynx with vocal cord fixation

T4a: Invades through cricoid or thyroid cartilage or extends to other tissues beyond the larynx (e.g., oropharynx, soft tissues of neck)


T Staging Criteria: Maxillary Sinus T1: Limited to the antral mucosa, with no erosion or destruction of bone

T2: Erosion or destruction of the infrastructure, including hard palate and/or middle nasal meatus

T3: Invades skin of cheek, posterior wall of maxillary sinus, floor or medial wall of orbit, ethmoid sinus, pterygoid fossa, or SC structures

T4a: Invades orbital contents and/or cribriform plate, posterior ethmoid or sphenoid sinuses, nasopharynx, soft palate, pterygomaxillary or temporal fossa or base of skull

T4b: Invades any of the following: orbital apex, dura, brain, middle cranial fossa, cranial nerves other than V2, nasopharynx, or clivus

N Staging Criteria: Regional Lymph Nodes N0: No regional lymph node metastases

N1: Single ipsilateral lymph node, 3 cm in greatest dimension

N2a: Single ipsilateral lymph node, >3 cm but not >6 cm in greatest dimension

N2b: Multiple ipsilateral lymph nodes, none >6 cm

N2c: Bilateral or contralateral lymph nodes, all 6 cm

M Staging Criteria: Distant Metastases Mx: Distant metastases cannot be assessed

M0: No distant metastases

M1: Distant metastases

Stage Grouping of Oral Cavity, Lip, Pharynx, and Larynx 0: Tis, N0, M0

I: T1, N0, M0

II: T2, N0, M0

III: T3, N0, M0

T1, N1, M0

T2, N1, M0

T3, N1, M0

IVA: T4a, N0, M0

T4a, N1, M0

T1, N2, M0

T2, N2, M0

T3, N2, M0

T4a, N2, M0

IVB: Any T, N3, M0

T4b, Any N, M0

IVC: Any T, Any N, M1

ESOPHAGEAL CARCINOMATNM Staging Criteria: Esophagus T Staging Criteria: Primary Tumor T1: Invades lamina propria or submucosa

T2: Invades muscularis propria

T3: Invades adventitia

T4: Invades adjacent structures

N Staging Criteria: Regional Lymph Nodes N0: No regional lymph node metastases

N1: Regional lymph node metastases

M Staging Criteria: Distant Metastases M0: No distant metastases


Stage Grouping of Esophageal Carcinoma 0: Tis, N0, M0

I: T1, N0, M0

IIA: T2, N0, M0

T3, N0, M0

IIB: T1, N1, M0

T2, N1, M0

III: T3, N1, M0

T4, Any N, M0

IV: Any T, Any N, M1

IVA: Any T, Any N, M1a

IVB: Any T, Any N, M1b

SALIVARY GLAND TUMOURSTNM Staging Criteria: Salivary Gland T1: 2 cm in greatest dimension

T2: >2 cm but not >4 cm in greatest dimension without extraparenchymal extension

T3: >4 cm and/or having extraparenchymal extension

T4a: Invades skin, mandible, ear canal, or facial nerve

T4b: Invades skull base and/or pterygoid plates or encases carotid artery

Note: N and M staging criteria are the same as those for lip, oral cavity, pharynx, and larynx staging.

Stage Grouping of Salivary Gland Tumors I: T1, N0, M0

II: T2, N0, M0

III: T3, N0, M0

T1, N1, M0

T2, N1, M0

T3, N1, M0

IVA: T4a, N0, M0

T4a, N1, M0

T1, N2, M0

T2, N2, M0

T3, N2, M0

T4a, N2, M0

IVB: T4b, Any N, M0

Any T, N3, M0


THYROID CANCERT Staging Criteria: Thyroid T1: 2 cm in greatest dimension, limited to thyroid

T2: 2 cm but not 4 cm in greatest dimension, limited to thyroid

T3: >4 cm, limited to thyroid or any tumor with minimal extrathyroid extension

T4: Tumor of any size extending beyond the thyroid capsule to invade SC soft tissues, larynx, trachea, esophagus, or recurrent laryngeal nerve

N Staging Criteria: Thyroid N0: No regional lymph nodes

N1a: Level V1 lymph nodes

N1b: Ipsilateral, midline, or contralateral cervical or mediastinal lymph nodes

M Staging Criteria: Thyroid M0: No distant metastases


Stage Grouping of Thyroid Cancer Papillary or follicular (45 yrs)I: T1, N0, M0

II: T2, N0, M0

III: T3, N0, M0

T1, N1a, M0

T2, N1a, M0

T3, N1a, M0

IVA: T4a, N0, M0

T4a, N1a, M0

T1, N1b, M0

T2, N1b, M0

T3, N1b, M0

T4a, N1b, M0

IVB: T4b, Any N, M0


Medullary carcinomaI: T1, N0, M0

II: T2, N0, M0

T3, N0, M0

III: T1, N1a, M0

T2, N1a, M0

T3, N1a, M0

IVA: T4a, N0, M0

T4a, N1a, M0

T1, N1b, M0

T2, N1b, M0

T3, N1b, M0

T4a, N1b, M0

IVB: T4b, Any N, M0


Anaplastic carcinoma (All anaplastic carcinomas are considered stage IV.)IVA: T4a, Any N, M0

IVB: T4b, Any N, M0


Note: Separate stage groupings are recommended for papillary or follicular, medullary, and anaplastic (undifferentiated) carcinoma.

SKIN CARCINOMAT Staging Criteria: Skin T1: 2 cm in greatest dimension

T2: >2 cm but not >5 cm in greatest dimension


T4: Invades deep extradermal structures (cartilage, skeletal muscle, or bone)

N Staging Criteria: Skin N0: No regional lymph node metastases

N1: Regional lymph nodes

M Staging Criteria: Skin M0: No distant metastases


Stage Grouping of Skin Carcinoma 0: Tis, N0, M0

I: T1, N0, M0

II: T2, N0, M0

T3, N0, M0

III: T4, N0, M0

Any T, N1, M0


MELANOMA OF THE SKIN (EXCLUDING EYELID)T Staging Criteria: Melanoma of the Skin (Excluding Eyelid) Tis: Melanoma in situ

T1: 1.0 mm in thickness

T2: 1.012.0 mm in thickness

T3: 2.014 mm in thickness

T4: >4 mm

Note: All T stages are divided into a (no ulceration) and b (with ulceration).N Staging Criteria: Melanoma of the Skin (Excluding Eyelid) N0: No regional lymph nodes

N1: Metastases in one regional lymph node

N2: Metastases in two to three regional lymph nodes

N3: Metastases in four or more regional lymph nodes; matted nodes; or in-transit metastases/satellite lesion with regional nodes

M Staging Criteria: Melanoma of the Skin (Excluding Eyelid) M0: No distant metastases

M1a: Metastases to skin, SC tissue, or distant lymph nodes

M1b: Metastases to lung

M1c: Metastases to all other visceral sites or metastases with elevated serum lactic dehydrogenase

Stage Grouping of Melanoma Pathologic stage grouping0: Tis, N0, M0

IA: T1a, N0, M0

IB: T1b, N0, M0

T2a, N0, M0

IIA: T2b, N0, M0

T3a, N0, M0

IIB: T3b, N0, M0

T4a, N0, M0

IIC: T4b, N0, M0

IIIA: T14a, N1a, M0

T14a, N2a, M0

IIIB: T14b, N1a, M0

T14b, N2a, M0

T14a, N1b, M0

T14a, N2b, M0

T14a/b, N2c, M0

IIIC: T14b, N1b, M0

T14b, N2b, M0

Any T, N3, M0


Clinical stage grouping0: Tis, N0, M0

IA: T1a, N0, M0

IB: T1b, N0, M0

T2a, N0, M0

IIA: T2b, N0, M0

T3a, N0, M0

IIB: T3b, N0, M0

T4a, N0, M0

IIC: T4b, N0, M0

III: Any T, N1, M0

Any T, N2, M0

Any T, N3, M0


Antimicrobial therapy in otolarygologyhead and neck surgeryPROPHYLAXIS AGAINST MICROBIALS: GENERAL PRINCIPLES.Therapeutic concentration should be present before incision. Oral antibiotics should be given 1 hr before surgery. IV antibiotics should be administered shortly before induction of anesthesia.

During a long case, it may be necessary to administer a second dose to maintain therapeutic levels.

Antibiotic therapy >24 hrs postop has not been shown to reduce wound infections. However, some clinicians choose to continue antibiotics until all drains and packing are removed from the wound.

See Table 9-1 for a list of antibiotics commonly used.

Clean SkinOnly Incisions in Healthy Patients Risk of infection is low. Adequate skin preparation and sterile technique is sufficient.

Antibiotics are unnecessary.

If you choose to use an antibiotic, it should cover skin organisms (Staphylococcus aureus). Primary choices are cefazolin (Ancef), 1 g IV before induction, or cephalexin (Keflex), 500 mg PO 1 hr before induction.

In PCN-allergic patients, clindamycin can be given as 600 mg IV or 300 mg PO.

Oral/Pharyngeal Surgery Higher risk for infection by mixed aerobe/anaerobe infections from the oral flora.

Organisms to cover include Streptococcus

Peptostreptococcus

Bacteroides

Fusobacterium

Prevotella

Spirochetes

First-line antibiotics Ampicillin/sulbactam (Unasyn), 3 g IV at induction or

Amoxicillin/clavulanate (Augmentin), 1 hr preop

Second-line antibiotics Clindamycin (Cleocin Oral, Cleocin T), 600 mg IV or

Combination of cefazolin (Ancef), 1 g IV, and metronidazole (Flagyl, Flagyl 375, Flagyl ER, Protostat), 500 mg IV

Every patient should receive a topical antibiotic rinse with chlorhexidine or amoxicillin/clavulanate (Augmentin) preop to reduce intraoral bacterial counts.

Major Head and Neck Surgery Involves both skin and oral/pharyngeal incisions

High risk for mixed infections Staphylococcus

Streptococcus

Anaerobes

Aerobes

Possibly Pseudomonas

First-line antibiotic Clindamycin, 600 mg IV

Second-line antibiotics Cefazolin, 1 g IV, and metronidazole, 500 mg IV

Ampicillin/sulbactam, 3 g IV

If Pseudomonas is a concern, one of the following should also be administered preop: Gentamycin (Garamycin)

Tobramycin (Tobrex)

Ceftazidime (Fortaz)

Aztreonam (Azactam)

Every patient should receive a topical antibiotic rinse with chlorhexidine (Peridex, PerioGard) or amoxicillin/clavulanate preop to reduce intraoral bacterial counts.

Nasal Surgery: Clean and Contaminated Clean For example: septorhinoplasty

Considered a clean case

Antibiotics unnecessary

Contaminated For example: functional endoscopic sinus surgery for sinusitis or maxillofacial procedures

Must cover oropharyngeal contaminants Aerobes

Anaerobes

S. aureus

First-line antibiotics Ampicillin/sulbactam, 3 g IV, or clindamycin, 600 mg IV

Otologic Surgery: Clean (Dry Ear) and Contaminated Clean (Dry Ear) Considered a clean case.

Adequate skin prep and sterile technique are sufficient.

Antibiotics are unnecessary.

Contaminated For example: tympanomastoiditis or cholesteatoma

Cover for Staphylococcus

Proteus

Haemophilus influenzae

Pseudomonas

Bacteroides

First-line antibiotic regimen Ampicillin/sulbactam, 3 g IV, plus aztreonam, 2 g IV

Second-line regimens Ceftriaxone (Rocephin), 2 g IV

Rifampin (Rifadin, Rimactane) plus metronidazole plus aztreonam for PCN-allergic patients

ANTIBIOTICS COMMONLY USED IN OTOLARYNGOLOGYPCNs PCN V Trade, route, dose: Pen Vee K, PO, 500 mg qid

Cost for 10-day course (U.S. $): 12

Antibacterial spectrum: Streptococcus, Pneumococcus (emerging resistance)

Side effect: 5% of individuals allergic to all the PCN family

Dicloxacillin Trade, route, dose: Dycill, PO, 500 mg qid


Antibacterial spectrum: PCN-resistant Staphylococcus

Amoxicillin Trade, route, dose: Amoxil, PO, 500 mg tid


Antibacterial spectrum: Streptococcus, Pneumococcus, Haemophilus influenzae, proteus

Side effect: Causes rash when given to patient with infectious mononucleosis

Amoxicillin with clavulanate Trade, route, dose: Augmentin, PO, 875 mg bid


Antibacterial spectrum: Gram-positive and -negative aerobes and anaerobes

Side effect: GI irritation (nausea, vomiting, diarrhea), which can be minimized by taking drug at mealtime and following the meal with a lactobacillus preparation

Ampicillin with sulbactam Trade, route, dose: Unasyn, IV, 3 g q6h


Antibacterial spectrum: Gram-positive and -negative aerobes and anaerobes

Piperacillin with tazobactam Trade, route, dose: Zosyn, IV, 3 g q6h


Antibacterial spectrum: Gram-positive and -negative aerobes and anaerobes, plus Pseudomonas coverage

Cephalosporins Antibacterial spectrum: Gram-positive cocci

Side effect: 20% of PCN-allergic patients cross-react with cephalosporins

Cefazolin Trade, route, dose: Ancef, IV, 1 g q8h


Cephalexin Trade, route, dose: Keflex, PO, 500 mg qid


Cefaclor Trade, route, dose: Ceclor, PO, 500 mg tid


Cefuroxime Trade, route, dose: Ceftin, PO, 500 mg bid


Loracarbef Trade, route, dose: Lorabid, PO, 200 mg bid


Macrolides Erythromycin Trade, route, dose: Erythrocin, PO, 500 mg qid


Clarithromycin Trade, route, dose: Biaxin, PO, 500 mg bid


Azithromycin Trade, route, dose: Zithromax, PO, Z-pack


Quinolones Side effect: Do not give quinolones to children.

Ciprofloxacin Trade, route, dose: Cipro, PO, 500 mg bid


Levofloxacin Trade, route, dose: Levaquin, PO, 500 mg qd


Gatifloxacin Trade, route, dose: Tequin, PO, 400 mg qd


Other classes Tetracycline Trade, route, dose: Achromycin V, PO, 500 mg qid


Clindamycin Trade, route, dose: Cleocin, PO, 300 mg qid


Side Effect: Pseudomembranous colitis.

Metronidazole Trade, route, dose: Flagyl, PO, 500 mg qid


Side effect: Metallic taste.

Otic drops Ciprofloxacin Trade, form: Cipro HC, 10-mL bottle


Ofloxacin Trade, form: Floxin Otic, 5-mL bottle


Neomycin and polymyxin B sulfate Trade, form: Cortisporin Otic, 10-mL bottle


Side Effect: May cause hearing loss if placed in middle ear.

Aluminum acetate Trade, form: Domeboro, 60-mL bottle


Hydrocortisone and acetic acid Trade, form: VoSoL HC, 10-mL bottle


Tobramycin and dexamethasone Trade, form: TobraDex, 5-mL bottle


INFECTIOUS DISEASES IN OTOLARYNGOLOGYACUTE OTITIS MEDIAMicrobiology Streptococcus pneumoniae and H. influenzae together account for half of all cases.

Moraxella catarrhalis accounts for an additional 1520% of cases.

Viruses and other bacteria make up the remainder.

Treatment Over half of all cases of acute otitis media resolve spontaneously.

Antibiotic therapy is indicated to Prevent mastoiditis and other complications

Prevent hearing loss

Relieve pain

Antibiotic choice First-line therapy for first time uncomplicated, untreated acute otitis media is amoxicillin for 10 days. However, in young children, seriously ill children, those with frequent otitis media episodes, and those with recent antibiotic use, the first-line treatment is amoxicillin/clavulanate for 10 days.

Second-line therapy should be employed for treatment failures. Choice of Amoxicillin/clavulanate for 10 days.

Cefuroxime (Ceftin) or equivalent for 10 days.

Quinolones for 710 days.

Ceftriaxone IM, one injection every other day for three injections.

If second-line therapy fails, consider culture-directed therapy from a myringotomy.

CHRONIC SUPPURATIVE OTITIS MEDIAMicrobiology Chronic ear drainage in chronic suppurative otitis media (with tympanic membrane perforation) is typically from mixed aerobic/anaerobic infections.

Pseudomonas aeruginosa.

S. aureus.

Klebsiella.

Escherichia coli.

Anaerobes. Bacteroides fragilis is often present when there is cholesteatoma.

Treatment Most chronic draining ears can be dried with ofloxacin (Floxin) or ciprofloxacin (otologic drops) topical therapy alone.

The patient should be instructed to keep the ear dry.

Pearl If a course of antibiotic drops does not dry up a chronically draining ear, there should be a high index of suspicion forFungal infection

Chronic mastoiditis

Cholesteatoma

ACUTE OTITIS EXTERNA (SWIMMERS EAR)Microbiology Most common organism is P. aeruginosa.

Number two is S. aureus.

Treatment Primary therapy is ototopical drops and aural toilet.Alcohol/boric acid (Domeboro) for 510 days

Cortisporin drops for 510 days

Alternative therapy includes ofloxacin drops or ciprofloxacin drops

Pearl In patients with diabetes or who are otherwise immunocompromised, it is necessary to have a high index of suspicion for necrotizing otitis externa.

NECRITIZING OR MALIGNANT OTITIS EXTERNAMicrobiology Caused by P. aeruginosa in diabetic patients.Treatment Must be treated by topical and systemic therapy.Biopsy of external auditory canal wall is often indicated to rule out squamous cell carcinoma.

Topical drops can be either ofloxacin or ciprofloxacin.

Systemic therapy choices include Imipenem (Primaxin)

Meropenem (Merrem IV)

Ciprofloxacin (Cipro)

Cefepime (Maxipime)

Ceftazidime

Admission Indicated until patient symptoms are improving.Complications Malignant otitis externa can rapidly advance to death or serious intracranial complications.

SINUSITIS ACUTE AND CHRONICAcute Sinusitis Microbiology Similar to acute otitis media. The more common offending organisms, in decreasing prevalence, areH. influenzae

S. pneumoniae

M. catarrhalis

Viruses

Treatment 50% resolve without treatment.

First-line antibiotic is still amoxicillin (Amoxil) or erythromycin (E-Mycin) plus TMP-SMX (Bactrim, Septra) for PCN-allergic patients for 710 days.

Second-line therapy is indicated in nonresponders, for children (in whom resistance is prevalent), and for moderately to severely ill patients. Second-line therapy is a 14-day course of any of the following: Amoxicillin/clavulanate

Cefuroxime

Cefpodoxime (Vantin)

Levofloxacin (Levaquin)

Gatifloxacin (Tequin)

Chronic Sinusitis Microbiology Usually polymicrobial and includes aerobic and anaerobic organisms.

P. aeruginosa is common in patients with polyps, particularly those patients with cystic fibrosis.

Treatment Primary therapy is with an extended course (23 wks) of amoxicillin/clavulanate (Augmentin).

In those with polyps and pseudomonas, the primary therapy is ciprofloxacin plus metronidazole.

Second-line antibiotics include Clindamycin

Cefuroxime plus metronidazole

Gatifloxacin

TONSILLITIS AND ADENOIDITISMicrobiology Streptococcus pyogenes is the most important pathogen. However, tonsil infections, particularly chronic tonsillitis, are caused by mixed aerobic/anaerobic infections. Most organisms are beta-lactamase producing.Treatment Rule out mononucleosis in patients with exuberant exudate.

Length of antibiotic treatment should be 510 days.

First-line drugs are the first-generation cephalosporins, such as cephalexin (Keflex).

Alternative therapies are Cefuroxime

Cefpodoxime

Clindamycin

Amoxicillin/clavulanate

Levofloxacin

Gatifloxacin

THRUSH (MUCOCANDIDIASIS)Microbiology: Candida albicans

Treatment: nystatin (Mycostatin) swish and swallow

EPIGLOTTITISMicrobiology Classically, epiglottitis is caused by H. influenzae type b. It is also caused by Pneumococcus, Staphylococcus, and S. pyogenes.Treatment The first step is to secure the airway (see Common Consults and Emergency Room Calls: Airway Problems).

After this is accomplished, the primary antibiotic is IV cefuroxime. Second-line antibiotics are Ceftriaxone

Ampicillin/sulbactam

Trovafloxacin (Trovan) in those allergic to PCN

DEEP NECK SPACE ABSCESSESMicrobiology Neck abscesses usually contain mixed aerobic/anaerobic organisms:Staphylococcus

Streptococcus

Fusobacterium

Bacteroides

Eikenella

Enterobacter

E. coli

Treatment With few exceptions, neck abscesses need to be drained surgically in addition to antibiotic therapy.

IV clindamycin or ampicillin/sulbactam is given until overlying cellulitis and fevers resolve.

The patient can then be switched to PO clindamycin or amoxicillin/clavulanate for an additional 710 days.

Head and Neck TraumaHead and Neck Trauma: General PrinciplesSoft tissue injuries to the face account for a fair proportion of ER visits.

Complicated injuries require the surgical skill of someone conversant with both facial anatomy and the special techniques of reconstruction of facial injuries.

Fractures of the facial skeleton are also reasonably common. Because of the force required to create a facial fracture, you must exclude associated injuries to the cervical spine, skull, and eye. Appropriate consultation is required for these injuries.

Always ensure the stability of the airway in all patients undergoing facial trauma evaluation.

NASAL FRACTURESDiagnosis Nasal fractures are primarily diagnosed on physical exam by asymmetry, angulation, and edema of the nose.

Radiographs are not particularly useful.

It is important to exclude septal hematoma and associated injuries to the facial skeleton and surrounding soft tissue.

Management Associated epistaxis should be controlled first (frequently, it is self-limiting).

On occasion, nasal fractures may be reduced immediately with local anesthesia. Usually, they are reduced under general anesthesia in the OR.

It is often difficult to assess the deviation from normal shape until the soft tissue swelling has subsided, which may take 57 days.

The bones are typically firmly set approximately 3 wks after the injury. Therefore, the patient should be reassessed 57 days after the initial trauma.

If closed reduction in the OR is indicated, it should be scheduled for within 2 wks from the trauma.

NASAL SEPTAL HEAMATOMADiagnosis A septal hematoma is a surgical emergency. Failure to diagnose and treat in a timely manner results in necrosis of the cartilaginous septum and subsequent nasal deformity due to the development of a septal abscess.

A septal hematoma can occur after any injury to the nose. It causes complete nasal obstruction and is easily recognized as gross swelling of one or both sides of the nasal septum visualized on anterior nasal exam.

Management The hematoma must be evacuated immediately. The area over the hematoma should be anesthetized with topical and/or injected lidocaine. A No. 11 blade is used to incise the mucosa and drain the blood collection.

The patient should be discharged on antibiotics that cover Staphylococcus, such as cephalexin (Keflex), 250500 mg qid.

AURICULAR HEAMATOMADiagnosis An auricular hematoma is generally the result of blunt trauma or shearing trauma to the ear.

Classically, it is seen in wrestlers because they have their ears pressed into the mat and twisted.

Hematomas are confined to the anterior aspect of the pinna and result from blood collecting between the cartilage and perichondrium.

The blood supply to the cartilage comes from the perichondrium. Therefore, failure to drain these hematomas results in ischemia and necrosis of the auricular cartilage, leading to the classic "cauliflower ear."

Management An auricular hematoma requires operative drainage.The ear is prepped and draped in a sterile fashion.Local anesthesia is obtained with lidocaine 1% with epinephrine.Multiple stab incisions adjacent to the conchal margin may be necessary.The hematoma is then evacuated through this incision.Cotton roll bolsters (dental rolls) are then secured anteriorly and posteriorly with through-and-through nylon sutures. This is done to obliterate the dead space of the evacuated hematoma so that the perichondrium will seat on the cartilage.The patient is discharged on antistaphylococcal antibiotics [cephalexin, 250500 mg qid, or cefprozil (Cefzil), 250 mg PO bid] and follows up in 1 wk for bolster removal.The patient should be warned that these frequently reaccumulate. If this occurs, the patient should return immediately for a repeat of the same procedure.Otohematoma

A: Hematoma of the auricle. B: Hematoma incised and evacuated. C: Anterior dental rolls tied to the posterior dental roll on the surface of the ear. D: Side view showing how the bolsters are secured.

ORBITAL FLOOR/WALL BLOWOUT FRACTURE.Diagnosis Fractures of the orbital walls or orbital floor may occur in association with, or in isolation from, other bony facial trauma.

Direct blunt trauma to the globe increases intraorbital pressure, causing the thin bones of the orbit to "blow out."

Typically, the inferior orbital wall is most commonly involved due to its thin bone and dehiscence caused by the infraorbital canal.

Findings may include injury to the orbital contents (often note hyphema: blood in the anterior chamber that layers out), SC emphysema, restriction of extraocular movements, or visual complaints.

Management Plain radiographs may show disruption of the floor of the orbit or fluid in the maxillary sinus. A coronal CT scan is required for accurate diagnosis and assessment of the fracture.

Ophthalmologic evaluation in the ER is mandatory for blowout fractures, as the globe is intimately involved in the energy transfer that produces the fracture. Vision should be tested as well as extraocular eye movements to test for muscle entrapment.

Discharge instructions should include head elevation, cold compresses, and no nose blowing. Give antibiotics (cephalexin, 250500 mg qid, or cefprozil, 250 mg bid) as prophylaxis against sinusitis.

Definitive surgery may be necessary later if there is cosmetic deformity or entrapment.

ZYGOMATICO-MAXILLARY COMPLEX FRACTURES.Diagnosis Zygomatico-maxillary complex fractures result from significant blunt trauma to the midface.

Findings may include malocclusion, trismus, facial flattening, orbital contents injury, diplopia secondary to extraocular muscle entrapment, or pain with chewing.

Bony stepoffs may be felt at the following fracture sites: frontozygomatic suture, inferior orbital rim, zygomatico-maxillary buttress, or the zygomatic arch.

Sensation in all divisions of the trigeminal nerve should be tested and documented along with facial nerve function, reactivity of pupils, and extraocular muscle function.

Radiologic evaluation consists primarily of a coronal facial CT to demonstrate fracture sites at the orbital floor. Axial cuts demonstrate well zygomatic arch and inferior orbital rim fractures. Maxillary sinus fractures always occur concomitantly with fluid seen on CT.

Fig. 10-2

The external arcs of contour of the zygoma have been disrupted (dotted lines), with comminution of the inferior orbital rim and lateral antral wall. Totally accurate three-point reduction of the lower end of the vertical arc and the anterior end of the horizontal arc may not be possible, necessitating open reduction of the zygomatic arch.Management Ophthalmologic evaluation is mandatory for injuries to the orbital floor or medial wall or in which obvious injury to orbital contents has occurred.

Stable patients can be discharged from the ER if they can take medication PO and associated injuries have been excluded or adequately treated.

Discharge instructions should include elevation of the head of the bed to 30 degrees when lying down, no nose blowing, only open-mouth sneezing, and cold compresses. Give antibiotics (cephalexin, 250500 mg qid, or cefprozil, 250 mg bid) as prophylaxis against sinusitis.

Patients should follow up in 12 days to arrange for definitive treatment.

NASO ORBITAL ETHMOID FRACTUREDiagnosis A blow of considerable magnitude to the nasal dorsum may fracture the nasal bone(s) and adjacent bones of the orbit and ethmoid labyrinth. The fragment, which often carries the medial canthal tendon, is pushed back into the ethmoid air cells in an accordion-like fashion.

Patients frequently report pain, epistaxis, and nasal airway obstruction.

Findings may include traumatic telecanthus (wherein the medial canthus and the involved globe are displaced laterally), loss of "bowstring sign," flattening of the nasal dorsum, extraocular movement impairment, CSF rhinorrhea, epistaxis, or epiphora.

Blindness may result if the optic nerve is compressed.

Management Axial and coronal CT scanning with 2-mm cuts is required for accurate diagnosis and treatment planning.

Ophthalmologic evaluation is mandatory for nasoorbital ethmoid fractures.

Neurosurgical consultation should be obtained for associated head or cervical spine injuries.

All patients require admission for immediate repair.

The nasoethmoidal orbital region. Inf., inferior; Sup., superior

MANDIBLE FRACTUREDiagnosis Mandibular fractures usually result from blunt trauma sustained during motor vehicle collisions, assaults, and falls.

Occasionally, penetrating trauma to the mandible resulting in fracture is encountered.

Findings include malocclusion, trismus, open bite deformity, mandibular mobility, dental injury, and occasionally airway compromise. Document sensation of both inferior alveolar/mental nerves and facial nerve function.

Radiologic evaluation consists of a Panorex and a mandible series.

Usually two fractures occur, but more or less are possible.

Be sure to document the exact fracture location, displacement, comminution, and associated dental injuries.

Management Stable patients can be discharged from the ER if they can take medication PO, have no airway difficulty (and are not likely to develop difficulty), have relatively nondisplaced fractures, and have no other injuries.

Discharge medicines should include oral rinse [chlorhexidine (Peridex)], antibiotics [PCN V (Pen Vee K), 500 mg qid, or clindamycin (Cleocin Oral, Cleocin T), 300 mg tid], and mild narcotic analgesics.

Patients should follow up in 12 days to arrange for definitive treatment.

Patients with airway difficulty, greatly displaced fractures, inability to take medication PO, or other injuries should be admitted and definitive treatment arranged.

Mandibular fracture angulations and their relationship to muscle pulls

A: Horizontally unfavorable. B: Horizontally favorable. C: Vertically unfavorable. D: Vertically favorable. (From Stanley RB. Pathogenesis and evaluation of mandibular fractures. In: Mathog RH, ed. Maxillofacial trauma. Baltimore: Williams and Wilkins, 1984:136, with permission.)FRONTAL SINUS FRACTUREThe main goals in the treatment of frontal sinus fractures are to prevent intracranial complications (i.e., meningitis), prevent frontal sinus disease (i.e., sinusitis and mucocele), and provide cosmesis.Anterior Table Nondisplaced Fractures that are nondisplaced or minimally displaced and cause no cosmetic deformity can be treated conservatively.

Usually, fractures of the anterior table do not involve the nasal frontal duct unless there is an associated fracture of the supraorbital rim or the nasoethmoid complex.

Displaced Surgical intervention is strictly for cosmetic reasons as long as the nasal frontal duct is not injured (see above).

Repair is done via any number of approaches to the frontal sinus (e.g., direct brow, bicoronal), and the comminuted and displaced fragments are reduced and plated.

Again, obliteration of the frontal sinus is not required as long as the nasofrontal duct is intact.

Posterior Table Nondisplaced As long as there is no CSF leak, nondisplaced fractures of the posterior table can be observed.

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