ABBREVIATIONS

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 SURVIVAL

How to Make It through Residency Residency, 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 OTOLARYNGOLOGY
Overview 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-today 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. 3

 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 EXAMINATION

Instrument, 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 headlight Nasal speculum Nasal and ear suctions Tongue blades Gloves Centimeter ruler Laryngeal mirror Nasal anesthetic/vasoconstrictor spray 4

 Fiberoptic nasopharyngoscope Otomicroscope Hand-held ear specula Cerumen curettes Alligator forceps 4 4 gauze sponges

NOSE AND PARANASAL SINUSES

Note 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 view

Coronal cross-section of the sinuses

EAR
Auricle: 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 PATIENT

Spontaneous Nystagmus Action: Target fixation in neutral gaze, Frenzel lenses Normal: No nystagmus or excessive saccades Abnormal: 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 plane Normal: Physiologic end gaze or no nystagmus Abnormal
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 Jerk 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 vertical Normal: Smooth pursuit movements Abnormal Saccadic pursuit = CENTRAL (cerebellum, brainstem, parietal lobe) Irregular tracking = acuity, age, medications, attention Saccades Action: Alternate gaze between finger Normal: Rapid, accurate, conjugate eye movements Abnormal Overshoots, 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 nystagmus Normal: No nystagmus Abnormal Unidirectional 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 target Normal: No loss of fixation

Abnormal: Refixation saccade = PERIPHERAL (loss of vestibuloocular reflex) Dynamic visual acuity Action: Have patient read eye chart with head still, then with 2-Hz head shake Normal: Less than three-line drop in acuity with head shaking Abnormal: More than three-line drop = PERIPHERAL (bilateral vestibuloocular reflex loss) Fixation suppression test Action: Subject fixates on own thumb while rotating body in chair Normal: No nystagmus Abnormal: Nystagmus in direction of rotation = CENTRAL (flocculus) Position tests Action: Place the head in left/right Hall pike, left/right lateral, supine Normal: No nystagmus Abnormal Torsional (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 motion Normal: Accurate movements Abnormal: Dysmetria, dysdiadochokinesia = CENTRAL (cerebellum) Posture tests Action: Romberg test, sharpened Romberg test, eyes closed foam Normal: Minimal sway, no falls

Abnormal Excessive sway, falls on Romberg = VARIABLE/APHYSIOLOGIC Falls on foam eyes closed = PERIPHERAL/MIXED/APHYSIOLOGIC Gait tests Action: Observation of gait; Fukuda step test Normal: Normal gait, <30-degree rotation on Fukuda test Abnormal: >30-degree rotation in the direction of the lesion

ORAL CAVITY AND OROPHARYNX

Lips: 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.

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Teeth and occlusion

NECK
Skin 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 HYPOPHARYNX

Assess 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.
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 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 larynx Laryngeal muscles

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CRANIAL NERVE EXAMINATION

I: 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: Vision Test: Visual fields by confrontation and acuity. III: Oculomotor nerve

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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 membrane Test: 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 glands Test: Note flow of tears, saliva.

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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)

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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 SCALE

Each 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
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 Eye: incomplete closure Mouth: asymmetric with maximum effort V. Severe dysfunction Forehead: none Eye: incomplete closure Mouth: slight movement VI. Total paralysis No movement

OTOLOGY
ANATOMY
External 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

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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

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Contents of the Middle Ear Bones of Hearing Malleus Incus Stapes Muscles The 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 25 33 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
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ASSESMENT OF AUDITORY FUNCTION

Many 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.

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 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%.

Audiograms

A. Normal:
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B. Conductive hearing loss:

C. Sensorineural hearing loss:

D. Mixed hearing loss:

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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

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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

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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

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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
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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 mixedsloping 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 EXTERNA
Otitis externa is an infection of the cartilaginous external auditory canal. Symptoms Otalgia Otorrhea Pruritus
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 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 CANAL

External 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
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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.

OSTEOMA
Osteomas 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 PERFORATIONS

Classification 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.

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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 (<1015%) central perforations that do not heal spontaneously can be repaired by paper patch or fat graft placement. In performing a paper patch graft, first the margins of the perforation are abraded with a Fraser tip suction or a Rosen needle to induce inflammation and tissue ingrowth. A round disc of rice paper or similar material is then placed onto the perforation, providing a scaffold for reepithelialization. Although the procedure has only an approximately 50% success rate, it is simple to perform and minimally invasive. Fat patch The theory behind a fat patch graft is similar to that for a paper patch. The fat acts as a scaffold for new cell growth along the tympanic membrane. Again, the edges of the perforation are gently freshened with suction. A piece of fat the size of the perforation is then harvested from the retroauricular tissue or the lobule. The fat is then placed snugly within the perforation so that an equal amount of the graft lies on each side of the tympanic membrane. This procedure is also uncomplicated but has a success rate just slightly greater than paper patch repair. It is also appropriate for central perforations <20%. Tympanoplasty Larger perforations require more extensive repair. Two graft techniques are commonly used: the lateral graft and medial graft (referring to the placement of the graft relative to the tympanic membrane and fibrous annulus). In both cases, temporalis fascia is harvested by a retroauricular incision. Fascia is then placed either medial, after reflection of the ear and tympanic membrane, or lateral to the fibrous annulus atop the tympanic membrane. The middle ear and external auditory canal are packed with absorbable Gelfoam to provide stability to the graft immediately postoperatively. The patient must be advised to sneeze with an open mouth and refrain from nose blowing and heavy lifting. These maneuvers increase middle ear pressure and can result in graft blowout.

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OTITIS MEDIA
Definition Otitis media is defined as inflammation of the middle ear mucosa. Classification Otitis media is divided into three groups based on the duration of symptoms: Acute: infection lasts <3 wks. Subacute: infection lasts 3 wks to 3 mos. Chronic: infection presents >3 mos. Acute Otitis Media Acute otitis media is common in the pediatric population, affecting 80% of children <2 yrs. Predisposing factors in children include Narrow lumen Horizontal position of the eustachian tube in children Poor control of muscles involved in opening the eustachian tube Attendance at daycare and other areas where they are exposed to bacteria that cause upper respiratory infections and otitis media Bottle feeding Passive smoke inhalation Signs and Symptoms Pain. Fever. Child tugging at the ears. Irritability. On otoscopy, the tympanic membrane appears dull and occasionally bulging from fluid accumulation behind the eardrum. Pneumatic otoscopy confirms this diagnosis with decreased mobility of the tympanic membrane. Type B tympanogram (Fig. 4-5). Ear drainage does not occur unless an accompanying perforation also exists. Microbiology The three most common organisms: Streptococcus pneumoniae Nontypeable Haemophilus influenza Moraxella catarrhalis
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Treatment Medical management consists of oral antibiotics, initially amoxicillin at 50 70 mg/kg/day for 10 days. Initial treatment failure is usually the result of subtherapeutic drug concentrations or antibiotic resistance and should be treated with second-line antibiotics, such as amoxicillin and clavulanic acid (Augmentin), cefprozil (Cefzil), and cefuroxime axetil (Ceftin). Keep in mind that the typical patient who presents to an otolaryngology practice for otitis media has already had multiple courses of antibiotics. Surgical management of otitis media consists of myringotomy with tube placement. This is a surgical procedure and has risks, including perforation and damage to hearing (rare). The general guidelines for tube placement for acute otitis media are Acute infection that does not respond to numerous courses of antibiotics Complication of acute otitis media (see below) At least six episodes of acute otitis media in 1 yr At least four episodes of acute otitis media/year for 2 consecutive yrs Recurrent otitis media in a child with a craniofacial disorder (e.g., cleft palate) Persistent fluid in the middle ear can lead to a conductive hearing loss with a theoretic risk of speech delay Chronic Otitis Media Chronic otitis media is characterized by irreversible inflammatory changes of the middle ear and mastoid, resulting in fluid present in the middle ear space for 3 mos. The factors allowing acute otitis media to progress into chronic otitis media are unclear. It is proposed that aeration of the middle ear, antrum, and mastoid are impaired. Inflammation results in obstruction of the normal draining mechanism of the middle ear, specifically the communication between the middle ear, antrum, attic, and mastoid cavity. Treatment A course of antibiotics is appropriate to try to clear the middle ear fluid. If this is unsuccessful, myringotomy and tubes should be inserted, particularly if the child is experiencing a conductive hearing loss due to the fluid. Complications of Otitis Media Complications of otitis media are defined as spread of infection beyond the spaces lined by middle ear mucosa. Although vigilant use of antibiotic by pediatricians, primary care physicians, and otolaryngologists has decreased the incidence of these complications dramatically, close monitoring must occur due to the rapid development of permanent sequelae if left untreated. All of these complications are serious and require immediate attention.

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Intratemporal Mastoiditis Petrositis Labyrinthitis Facial paralysis Intracranial Extradural abscess Sigmoid sinus thrombophlebitis Brain abscess Otic hydrocephalus Subdural abscess Meningitis

OTOSCLEROSIS
Otosclerosis is a disease of the otic capsule resulting in conductive and sensorineural hearing loss. Fixation of the stapes footplate occurs from resorption and deposition of new bone. Epidemiology Otosclerosis is transmitted as an autosomal dominant trait with variable penetrance. A child of a parent with otosclerosis has a 20% risk of developing otosclerosis. In 50% of patients with otosclerosis, a positive family history is obtained. Women are affected twice as often as men, with acceleration of the process during pregnancy. Otosclerosis usually presents during the second and third decades of life. The disease occurs more frequently in whites, and clinical disease is rare in Asians, Africans, and Native Americans. The disease is bilateral in 70% of cases. Pathogenesis There are two phases of otosclerosis. In the early phase, bone resorption predominates. Osteocytes are active along the periphery of blood vessels. Schwartze sign, a reddish hue behind the tympanic membrane secondary to increased vascularity of the promontory, is present. Although Schwartze sign is a classic finding dating back to 1873, it is visualized in only 10% of patients. New spongy bone formation, otospongiosis, occurs during the early phase of disease. Histologically, this new spongy bone contains blue finger-like projections on hematoxylin and eosin stain, producing the characteristic "blue mantles of Manasse" on microscopy. The late phase is characterized by formation of dense sclerotic bone in the areas of previous bone
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resorption. Signs and Symptoms There is no pathognomonic sign for otosclerosis. In fact, the only way to definitively diagnose the disease is either histologically or by manipulating the ossicles in the OR. Therefore, a good history and interpretation of the audiogram are crucial. Clinically, most patients experiencing otosclerosis present with a gradual hearing loss over several years. Tinnitus is present in 75% of patients. The audiogram is the diagnostic tool most useful in otosclerosis. The hallmark of the disease is a low-frequency conductive hearing loss in the early stages. A characteristic depression of the bone line at 2000 Hz is referred to as Carhart's notch. As the disease progresses, a mixed or sensorineural hearing loss may develop. Cochlear reserve refers to the falsely decreased bone level on an audiogram of a patient with otosclerosis. After surgical repair, the bone line is improved by 5 dB at 500 Hz, 10 dB at 1000 and 4000 Hz, and 15 dB at 2000 Hz. Treatment The primary symptom of otosclerosis is hearing loss, and management involves improving the patient's hearing. Hearing aids for amplification can be used for all patients with otosclerosis. In fact, hearing aids work extremely well because the majority of the hearing loss is conductive. Therefore, speech recognition is usually not affected. All patients should be offered amplification as a reasonable option. Surgical candidates are those patients with a conductive hearing loss with good discrimination and a negative Rinne test (bone conduction greater than air conduction). Stapedectomy is 90% successful in treating otosclerosis and can be performed as an outpatient under local anesthesia. The risks of surgery include 2% chance of cochlear deafness 23% chance of tympanic membrane perforation Postop vertigo Dysgeusia (abnormal sense of taste or metallic taste) secondary to trauma or transection of the chorda tympani Facial paralysis

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Cholesteatoma
Cholesteatomas are epithelial inclusion cysts of the middle ear. These cysts contain keratin and desquamated debris. Although the suffix -oma is used in the nomenclature, these are not tumors but aggressive growths of tissue that can destroy bony structures. Classification There are three types of cholesteatomas relating to the etiology of the disease. Congenital cholesteatomas are embryonic rests of epithelial cells in the pneumatized portion of the temporal bone. They occur behind an intact tympanic membrane in a patient without a history of otorrhea or otologic surgery. Two-thirds occur in the anterior-superior quadrant of the tympanic membrane and are visualized as a white mass. The average age at presentation is 4.5 yrs, and 75% occur in male patients. Primary acquired cholesteatomas are believed to be the result of retraction pockets. They usually form in the epitympanum in the area of Prussak's space. Prussak's space is the area medial and superior to the pars flaccida. The boundaries include the tympanic membrane laterally, the head of the malleus medially, and the posterior and lateral malleolar folds (Fig. 4-6). The mechanism of formation involves negative pressure in the middle ear, causing retraction of the pars flaccida, the weakest portion of the tympanic membrane. Epithelial debris then accumulates in the pocket and is pulled into the middle ear. As the retraction pocket deepens, the normal cleaning mechanisms of the external auditory canal and tympanic membrane are overcome, and debris collects in this pocket. Management includes frequent inspection and removal of the epithelial debris under microscopic visualization. Persistently retracted eardrums can be treated with a myringotomy tube to allow equalization of middle ear pressure and aeration of the middle ear. If the entire extent of the cholesteatoma is not visualized, further exploration is necessary. Secondary acquired cholesteatomas are the result of ingrowth of tissue from a tympanic membrane perforation. Three mechanisms are proposed to explain this form of cholesteatoma: The implantation theory poses that epithelial tissue is implanted into the middle ear space as a result of iatrogenic manipulation from surgery or a foreign body. This can result from tympanostomy tube placement or myringotomy. The invasion theory involves invasion of skin from the meatal wall through a perforation into the middle ear. This is supported by experimental evidence demonstrating epithelial migration that progresses until the epithelium contacts another epithelialized surface. This explanation is the most widely accepted theory of secondary acquired cholesteatoma. The metaplasia theory states that desquamated epithelium in the middle ear is transformed into keratinized squamous epithelium, a result of exposure to chronic middle ear infection. Signs and Symptoms The patient with a cholesteatoma is usually asymptomatic in the early stages of disease. History of unilateral hearing loss. History of unilateral aural drainage is usually elicited. On microscopic exam, a pearly white plaque of skin or granulation tissue is visualized. Granulation tissue can be removed in the office, but care must be taken to avoid aggressive removal, as
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granulation tissue may be adherent to the ossicles allowing ossicular disruption with forceful removal. Treatment Surgery is the treatment for advanced cholesteatomas. CT scanning is a useful adjunct to surgery to define the extent of disease. The goal of surgery is removal of disease, with restoration of hearing a secondary benefit. A mastoidectomy is performed to remove all visualized cholesteatoma, with procedure modifications for each individual case. Complications of Untreated Cholesteatoma Hearing loss from ossicular chain erosion Labyrinthine fistula Facial paralysis Periosteal or brain abscess Brain herniation Ossicles of the middle ear

Mnire's disease
Mnire's disease is a disorder of the peripheral vestibular system. Epidemiology The incidence is variable, with reports stating 7.5157.0 cases/100,000 people. Peak onset is in those patients 4060 yrs of age.
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 Bilateral disease is found in 4070% of patients. Pathogenesis The disease is believed to be caused by endolymphatic hydrops due to mechanical obstruction, viral infection, autoimmune infection, or ischemia of the inner ear. Signs and Symptoms The classic symptom complex is Episodic attacks of vertigo lasting minutes to hours (96%) Fluctuating low-frequency sensorineural hearing loss (88%) Tinnitus (91%) Aural fullness (94%) Acute attacks can awaken a patient from sleep and typically last 23 hrs. Treatment There is no cure for Mnire's disease, but many treatments can decrease the incidence of symptoms. A low-salt diet and diuretic are initial treatment for all patients with Mnire's disease. The salt restriction is believed to decrease the endolymphatic volume by fluid removal or decreased production. 5070% of patients have symptom control with this treatment. Antivertiginous medications, along with antiemetics, sedatives, and antidepressants, are additional recommended treatments. In severe disease refractory to medical treatment (10% of patients), surgery is available. The endolymphatic shunt, selective vestibular neurectomy, and labyrinthectomy are possible surgical options. Intratympanic gentamicin injection is a minimally invasive procedure aimed at abolishing vertiginous attacks. Aminoglycosides are ototoxic, with gentamicin preferentially affecting the vestibular apparatus. The drug is injected into the middle ear by needle injection through the tympanic membrane. The procedure has a 60% success rate.

BENIGN PAROXYSMAL POSITIONAL VERTIGO

Benign paroxysmal positional vertigo (BPPV) is a disease of the posterior semicircular canal causing vertigo that lasts seconds. Epidemiology BPPV is the most common type of vertigo seen by an otolaryngologist. The incidence is 10 60/100,000. There is a slight female predominance.
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Pathogenesis Pathogenesis is deposition of otoconia in the posterior semicircular canal. Signs and Symptoms Most patients present with severe rotary vertigo associated with particular head movements. Common head movements that cause vertigo include Looking up to remove an object from the shelf Rising from a bending position Flipping the head over to wash hair in the sink Turning over in bed Diagnosis Diagnosis of BPPV is made by the Dix-Hallpike maneuver. This maneuver consists of turning the head 45 degrees toward the affected ear while the patient is sitting upright. The patient is then brought to a supine position with the head overhanging the table by 45 degrees. Frenzel lenses, which inhibit fixation suppression, can be used to more easily identify nystagmus. In a patient with BPPV, the Dix-Hallpike maneuver can provide characteristic findings leading to diagnosis. First, an onset latency of 210 secs is observed. The nystagmus typically lasts <1 min and is upbeat and torsional, directed toward the affected down-hanging ear. The nystagmus fatigues, obtaining less of an effect with repeated maneuvers. Treatment The Eppley maneuver is a procedure that repositions the otolith from the semicircular canal into the vestibule where it can no longer cause vertigo. Begin by placing the patient in the Dix-Hallpike position with affected ear down. After the initial nystagmus subsides, the head is rotated 90 degrees, with a pause to allow the nystagmus to subside once again. The head is rotated another 90 degrees and to a position with the affected ear up and the nose pointing toward the ground. The patient is then brought to an upright seated position. This maneuver is 90% effective in eliminating symptoms of BPPV. Posterior semicircular canal plugging is a surgical option for severe, refractory cases.

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RHINOSINUSITIS
Definition Sinusitis may be defined as an inflammatory condition involving the mucous membranes of the paranasal sinuses, as well as the fluids within the sinuses. Most patients develop the symptoms of nasal congestion with obstruction, purulent discharge, postnasal drip, facial pressure, and pain. Because the mucous membrane of the nasal cavity is in continuity with that of the sinuses, sinusitis may be more accurately referred to as rhinosinusitis. Controversy exists as to the appropriate definition of sinusitis and its temporal course. A recent Task Force on Rhinosinusitis has agreed that symptoms lasting 4 wks could be accurately described as acute sinusitis. Symptoms lasting from 412 wks could be characterized as subacute rhinosinusitis, and those lasting >12 wks are characterized as chronic rhinosinusitis [1]. Classification of adult rhinosinusitis From Lanza DC, Kennedy DW. Adult rhinosinusitis defined. Otolaryngol Head Neck Surg Suppl 1997;117:S5, with permission. Acute Duration: 4 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: Fever or facial pain does not constitute a suggestive history in the absence of other nasal signs or symptoms. Consider acute bacterial rhinosinusitis if symptoms worsen after 5 days, if symptoms persist for >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

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 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

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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
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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
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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 rhinosinusitis Major 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.

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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 <2% of acute rhinosinusitis patients, it is almost never seen in patients with allergic rhinitis. The diagnosis may be confounded by the fact that patients with rhinitis may be prone to develop a concurrent rhinosinusitis because of the resulting mucosal edema and obstruction of the sinus ostia. Patients with upper respiratory infections may display a tendency for fevers and malaise. The mucosa of the nose tends to be more dry but can develop into nasal congestion and drainage from the inflammation. Cough tends to be a nonspecific symptom and can be seen in patients with asthmatic conditions as well as rhinosinusitis. This symptom tends to present mainly at night in the latter condition. Although most patients who present with rhinosinusitis develop similar symptoms, localization of the complaints can help identify the source of the infection. For example, maxillary sinusitis may cause upper teeth, cheek, or infraorbital pain mainly in the distribution of V2. Ethmoidal disease may cause pain over the nasal dorsum or radiate towards the temporal region. Frontal sinusitis tends to cause supraorbital pain and Pain radiation involved in rhinosinusitis

tenderness especially in the distribution of V1. Sphenoidal disease tends to spread towards the occiput or vertex areas of the cranium but can also refer to the upper canine teeth or even the shoulder region. The complex nature of referred sinus pain can be seen in Fig. 5-2. Additionally, the symptomatology may differ slightly for acute vs chronic rhinosinusitis. There is usually a moderate to severe degree of symptoms involved in the acute phase of the disease. With chronic inflammation, many symptoms are diminished in nature and may only
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present with mild aching of the associated sinus. Many times, the characteristics may imitate those of migraine or cluster headache as well. Because these aspects may be more subtle, the physician may find that nasal congestion and persistent thick nasal secretions are more common. Physical Exam The physical exam is essential in supporting the diagnosis of rhinosinusitis. Patients with an acute infection may display maxillary region swelling, edema, or erythema of the overlying skin. The symptoms are worse in the early morning and tend to improve throughout the day as the patient becomes more upright. These regions should be palpated for increased tenderness, confirming the diagnosis. Transillumination is usually not reliable for diagnosis of sinus disease but can be helpful. Poor lighting can cause the observer to falsely assume an obstructed sinus when this may not be the case at all. Anterior rhinoscopy is much more reliable and, with adequate illumination, is invaluable in the physical exam. This should be accompanied by nasal endoscopy (rigid or flexible) as well. Any initial exam should assess nasal septal deviation leading to symptoms of obstruction. Other causes of obstruction may include concha bullosa and a lateralized middle turbinate. The mucosa of the nose should be carefully inspected. Erythema and edema are more consistent with an active infection. Allergic rhinitis tends to display more edematous mucosa with pale mucosa. Often, crusting of the nasal mucosa may be seen, caused by nasal drying or purulence. A careful inspection of the middle meatus, sphenoethmoidal recess, and superior meatus can help to differentiate between allergic rhinitis, upper respiratory infection, and rhinosinusitis. For example, purulent discharge seen from the middle meatus can confirm a diagnosis of acute rhinosinusitis of the maxillary, ethmoidal (anterior), and frontal sinuses. More posterior discharge is typically seen in posterior ethmoidal and sphenoidal disease. The nasopharyngeal region should be carefully inspected for adenoid hypertrophy, masses, tumors, and postnasal purulence. Associated nasal polyposis may be seen, especially in patients with chronic rhinosinusitis. These tend to have a glistening mucosal surface with a pedunculated stalk. They can contribute to the patient's symptoms due to their obstructive nature. Radiographic Studies Although most cases of rhinosinusitis can be diagnosed with a complete history and physical exam, there still are situations in which radiographic tests can be helpful. They may include (a) evaluation of chronic rhinosinusitis, (b) evaluation of recurrent rhinosinusitis and an anatomic basis for the infections, (c) evaluation of an impending or evolved complication, and (d) evaluation of the anatomy of the paranasal sinuses before surgical treatment.

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Early in the course of a sinus infection, signs and symptoms may be vague and ill defined. Radiologic confirmation may be needed. A sinus series is usually not beneficial in the early stages of the disease due to lack of sensitivity and specificity. U/S can be helpful; however, it is limited to maxillary sinus imaging and can be inconsistent with plain radiographic tests. CT scanning has improved the level of sinus imaging and is now an essential tool in evaluation of sinonasal pathology. The unreliability of plain radiographs compared to CT scanning was shown in a prospective study by McAlister et al. [10]. A lack of correlation between CT and plain films was seen in 74% of patients. Plain x-rays tended to both underestimate and overestimate the degree of sinus disease compared to CT scans. MRI provides an additional modality to evaluate the sinonasal system. It is useful in the investigation of soft tissue masses, extension beyond the confines of the sinonasal passages, and in related complications. MRI allows clear delineation of soft tissue and fluid states and may help to differentiate inflammatory disease from neoplastic processes. MRI typically has not been found to be as useful for routine sinus evaluation and assessment of the ostiomeatal unit. Treatment The goal of medical treatment for rhinosinusitis is to reestablish the normal sinonasal anatomy and function. Nasal irrigation with saline solutions accomplishes this by moisturizing, removing debris and crusting from the airway, and clearing inspissated mucus. Mucolytics are another useful adjunct to treatment. Guaifenesin, found in many decongestants, helps to thin mucous secretions and promote clearance. This may be particularly helpful in specific conditions of chronic nasal mucous stasis, such as cystic fibrosis and immotile cilia syndrome. Medications that minimize mucosal edema and swelling promote patency of the ostiomeatal complex and improve ventilation. Decongestants do this by stimulating alpha-adrenergic receptors found within the mucosa of the upper airway. Topical [oxymetazoline hydrochloride (Afrin); pseudoephedrine hydrochloride (Afrinol)] and systemic [pseudoephedrine hydrochloride (Cenafed)] medications have been used to alleviate symptoms and promote rapid recovery. Of note, because of the risk of rebound edema (and rhinitis medicamentosa), these agents should be used sparingly and generally in situations of acute rhinosinusitis or exacerbation of chronic conditions. Antihistamines have been used frequently to manage symptoms as well. These medications have been shown to work by competitively binding to H1-receptors on various muscle or nerve endings to reduce the effects of histamine release. Although most first-generation compounds cause side effects such as drowsiness, the newer second-generation antihistamines do not exhibit anticholinergic effects and are safer. Caution should still be applied, however, because many times the drying action may actually impair clearance by thickening secretions. For the most part, antihistamines have been used in cases in which patients display an allergic component exacerbating their rhinosinusitis. They are not used for chronic sinusitis alone.
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Steroids, both topical and systemic, have been shown to benefit a variety of inflammatory conditions. Many physicians have seen favorable results in both allergic and nonallergic rhinitis and rhinosinusitis. Systemic steroids have also been used with success in cases of nasal polyposis and allergic fungal disease. The main problem with systemic application is the suppression of the hypothalamic-pituitary-adrenal axis and the risk of adrenal insufficiency on sudden discontinuation. Other effects include gastric ulcers, mucosal itching, sleep disturbances, HTN, weight gain, osteoporosis, and altered insulin requirements in diabetic patients. The benefits of topical application include minimal systemic absorption and systemic effects as well as the efficacy of local application. Generally, systemic steroids are reserved for chronic rhinosinusitis because of the risk of numerous side effects from long-term use. Antibiotics generally are directed toward the main offenders involved in acute or chronic rhinosinusitis. These may include S. pneumoniae, H. influenza, M. catarrhalis, Staphylococcus, and anaerobic species. For cases of acute disease, a 10- to 14-day course is generally enough to cover the infection. Longer duration of therapy (4 6 wks) is recommended for chronic infections. Some antibiotics considered effective in treatment of acute rhinosinusitis include amoxicillin (Amoxil), amoxicillin-clavulanate (Augmentin), azithromycin (Zithromax), cefpodoxime (Vantin), proxetil (Vantin), cefprozil (Cefzil), loracarbef (Lorabid), and TMP-SMX (Bactrim, Septra, Co-trimoxazole) [7]. Clindamycin (Cleocin) or metronidazole (Flagyl) may be incorporated as well for coverage of chronic infections. Physicians should include various factors (e.g., previous antibiotic usage and response, resistance patterns, side effects, medical interactions, drug allergy information, and dosing schedule) when choosing an antibiotic. Immunotherapy is intuitively viewed as essential in controlling refractory allergies, which can lead to chronic rhinosinusitis after surgery. No studies to date, however, have conclusively demonstrated the beneficial effects of immunotherapy for patients with allergic rhinitis and chronic rhinosinusitis. Most people would agree that allergic rhinitis predisposes a patient to chronic rhinosinusitis, and by controlling the resulting mucosal edema and hypersecretory state, symptoms can be alleviated. Because of the cause effect relationship, immunotherapy can still be considered an appropriate adjunct in controlling chronic rhinosinusitis if allergic rhinitis is deemed to be a major factor in the patient's pathophysiology. Surgical treatment for rhinosinusitis has become more accepted with the advent of newer technology such as surgical instrumentation, more accurate imaging techniques, and realtime image-guided systems. The Task Force on Rhinosinusitis has agreed on various absolute and relative indications for surgery (Table 5-3). Although the absolute indications for surgery have created a more uniform and rigid protocol, the majority of patients who undergo sinus surgery are those with chronic but uncomplicated adult rhinosinusitis, which is considered a relative indication for surgery. These patients have undergone numerous medical treatments with unsatisfactory responses. At this point, irreversible mucosal disease is assumed, and surgical treatment is needed to remove the diseased tissue. Although there has been no definitive study on the success of FESS, most studies have seen adequate improvement of symptoms after surgery. Gliklich and Metson [11] found that 82% of patients who underwent
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FESS for chronic sinusitis demonstrated statistically significant improvement in their sinusitis-specific health status. Absolute indications for surgery in rhinosinusitis Bilateral extensive and massive obstructive nasal polyposis with complications Complications of adult rhinosinusitis Subperiosteal or orbital abscess Pott's puffy tumor Brain abscess Meningitis Chronic adult rhinosinusitis with mucocele or mucopyocele formation Invasive or allergic fungal adult rhinosinusitis Diagnosis of tumor of nasal cavity and paranasal sinuses CSF rhinorrhea Complications Complications associated with sinusitis may occur in the acute, subacute, or chronic phase. The orbit is commonly involved due to its proximity. Usually from acute ethmoidal disease (mainly in children) or frontal disease in adults, bacterial extension can cause symptoms involving the periorbita and orbit. Although infection may spread via arteries, veins, or lymphatics, direct extension through the lamina papyracea is the most common route. Chandler has proposed a classification for orbital complications (Fig. 5-3), which can help to direct treatment modality and prognosis [12]. Careful exam for visual changes, changes in ocular pressure and mobility, and worsening proptosis should be done. Early ophthalmologic consultation should be performed as well. Immediate surgical treatment may be needed for any worsening changes of the orbit to decompress the eye and prevent permanent blindness. Additionally, visual changes may occur not only from direct involvement of the orbit but also from inflammation of the sphenoid sinus with its location near the cavernous sinus and cranial nerves III, IV, and VI. Eradication of the infection by surgery may be needed to prevent permanent neurologic injury of the eye. Extension into the intracranial space may cause epidural and subdural abscess, meningitis, brain abscess, and cavernous sinus thrombosis. These patients should be treated aggressively, and the physician should have a low threshold for surgical treatment. Neurosurgical consultation should be obtained early on to assist in treatment options. Osteomyelitis of the frontal bone and maxilla rarely occurs due to rhinosinusitis. Surgical treatment is warranted to remove infected or necrotic areas and to reconstruct defects in the sinus wall.

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A-E: Chandler classification for orbital complications due to acute rhinosinusitis

SURGICAL TREATMENT OF THYROID DISEASE

Surgery on the thyroid gland comprises a substantial component of head and neck surgery. Previously, thyroid surgery was performed for treatment of goiter or hyperthyroidism; however, this is now a relatively infrequent indication for such operations. The primary goal of current thyroid surgery is to remove malignant or potentially malignant lesions. Accordingly, the principal concerns of the otolaryngologist with regard to thyroid disease are to identify patients with surgically treatable disease and those who would benefit from medical management and to correct any medical abnormalities that may be present before surgery. Anatomy The human thyroid gland is a bilobed structure with a midline isthmus that may also be accompanied
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by a pyramidal process that can extend as superior as the hyoid bone. Each thyroid lobe is attached to the trachea by a band of dense connective tissue called Berry's ligament. Laterally, it extends into the tracheoesophageal groove, where it lies in close proximity to the recurrent laryngeal nerve. The arterial supply to the thyroid gland is from paired superior and inferior thyroid arteries. The superior thyroid artery is the first branch of the external carotid system, whereas the inferior thyroid artery derives from the thyrocervical trunk. The venous drainage of the gland consists of superior thyroid veins that drain to the internal jugular system as well as middle and inferior thyroid veins that generally drain to the brachiocephalic veins. Lymph drainage goes to the prelaryngeal and pretracheal nodes for the central region of the gland and to the paratracheal and lower deep cervical nodes for the lateral aspects of the thyroid gland. Patient Evaluation As with any disease, evaluation of thyroid disease begins with the patient history and physical exam. Symptoms relating to hypothyroidism, commonly attributed to autoimmune disease or thyroiditis, should be sought during the patient interview. A variety of symptoms may be found in the hypothyroid patient, including lethargy, constipation, thickening of skin, weight gain, and cold intolerance. In addition, hearing loss, vertigo, and hoarseness may constitute otolaryngologic manifestations of hypothyroidism. Conversely, hyperthyroidism presents with nearly opposite symptoms: anxiety, weight loss, heat intolerance, flushed appearance, tachycardia, and tremor. Grave's disease, toxic adenoma, multinodular goiter, and thyroid cancer are all considerations in patients with hyperthyroidism. Physical exam should be directed toward identification of signs related to the above symptoms. In addition, careful palpation of the thyroid gland should be performed. Characteristics such as thyroid gland size, consistency, heterogeneity, and nodularity should all be noted at the time of exam. Complete evaluation of patients with possible thyroid disease includes functional evaluation of the thyroid gland. A biochemical assessment to measure TSH is the most sensitive means of assessing thyroid function. Such a test detects a suppressed TSH level in cases of hyperthyroidism in contrast to the elevated TSH level seen in hypothyroidism. In cases of hyperthyroidism in which a low TSH level is noted, further evaluation of free thyroxine or triiodothyronine should be performed to establish the diagnosis. These levels can then be followed after initiation of either medical or surgical treatment to monitor the patient's response to therapy. Thyroid Lesions Primary concerns of the head and neck surgeon with regard to the thyroid gland involve evaluation of the thyroid nodule to identify and treat malignancy. A thyroid nodule is a discrete mass in the thyroid gland. Nodules can be found in 5% of women and 12% of men. Roughly half of thyroid nodules are caused by goiter with a dominant nodule. Goiter is a physiologic response to inadequate levels of thyroid hormone. The subsequent enlargement of the gland and resulting dominant nodule are benign. Other benign enlargements of the gland include thyroid cysts, teratoma, and lymphadenopathy. The most common benign lesion of the gland, however, is the follicular adenoma. Follicular adenomas are comprised of tissue similar in histologic appearance and function to normal thyroid tissue and may
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contribute to a hyperthyroid state. Malignancy of the Thyroid There are principally four primary malignancies of the thyroid gland: papillary, follicular, medullary, and anaplastic carcinoma. Papillary carcinoma is the most common, comprising 6070% of thyroid cancer. Papillary carcinomas are often multicentric lesions that spread via regional lymphatics to the paratracheal and cervical nodes. The cricothyroid node, also known as the Delphian node, is a common location of regional metastasis for papillary carcinoma. Up to 30% of patients with papillary carcinoma have evidence of regional spread at the time of diagnosis; however, this does not exert a significant impact on survival. Follicular carcinoma is the next most frequent malignancy, comprising 20% of thyroid cancer. These lesions generally occur only in patients >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. Longterm 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 <5%, whereas it may be up to 25% in "cold" nodules. In this fashion, imaging modalities can offer additional information; however, the decision regarding treatment should be made on a case-by-case basis, with thorough discussion with the patient.
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Surgical Therapy The appropriate surgical treatment for thyroid disease depends on numerous factors, including patient characteristics, tumor pathology, regional metastasis, and others. The basic list of operations includes hemithyroidectomy, subtotal thyroidectomy, and total thyroidectomy. These can be combined with neck dissection or paratracheal node dissection if required. A detailed description of these procedures is beyond the scope of this text. General concepts include identification of the recurrent laryngeal nerve, preservation of the parathyroid glands, and control of superior and inferior thyroid vessels during dissection. It should be noted that ablation of residual thyroid tissue with radioactive iodine is a common practice for eradication of cancer after total thyroidectomy, depending on the underlying pathology. Complications of Thyroid Surgery Thyroid surgery performed by an experienced thyroid surgeon generally produces few complications. In the majority of cases, patients are ambulatory, are able to speak, can tolerate oral intake, and have normal breathing in the postop period. There are certain potential complications that do merit consideration. Given the proximity of dissection to the recurrent laryngeal nerve, injury of this structure is a potential complication. It may result in hoarseness or voice change postop. It may also cause little voice change and would only be noted on postop laryngeal exam. Risk of weakness of the nerve can be reduced through use of intraop steroids. In the case of total thyroidectomy, bilateral injury is possible and may have potentially life-threatening consequences. Bilateral vocal cord paralysis can result in stridor with airway compromise that may require urgent intubation versus tracheotomy for airway management. Hemorrhage with hematoma formation is also a risk of this procedure. Because of the location, such an occurrence may present with respiratory difficulty, which can be managed acutely by opening of the incision and immediate drainage by blunt dissection if warranted by patient distress. Further bleeding can then be controlled in a more appropriate setting if needed. Hypocalcemia is a potential complication of thyroid surgery. Dissection in the region of the thyroid gland may result in injury to the parathyroid glands or their vascular supply, resulting in decreased parathyroid hormone and serum calcium. This complication is generally not seen in hemithyroidectomy, as only half of the gland may be disturbed by the procedure.

SURGICAL TREATMENT OF PARATHYROID DISEASE

Author: Urjeet A. Patel Surgical excision of the parathyroid glands is principally focused on treatment of hyperparathyroidism. Hyperparathyroidism is characterized by an abnormally high production of PTH and has a variety of causes. These are divided into primary, secondary, and tertiary categories. Primary hyperparathyroidism reflects dysfunction of the glands themselves in the form of adenoma
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or diffuse hyperplasia. Secondary hyperparathyroidism describes a scenario in which the parathyroid glands are hypersecreting PTH in response to dysfunction of another organ system, principally the kidneys. In this situation, renal failure may result in low serum calcium, which in turn causes hypertrophy of the parathyroid glands as they secrete abnormally high levels of PTH that then cause bone wasting. Tertiary hyperparathyroidism occurs in long-standing cases of secondary hyperparathyroidism in which the PTH production becomes autonomous and the glands continue to secrete high levels of PTH despite normal serum calcium levels. Anatomy The parathyroid glands consist of two pairs of discrete glands that derive from the third and fourth branchial pouches. Third arch parathyroid gland tissue descends through the neck and eventually comes to rest along the inferior border of the thyroid gland to constitute the inferior parathyroid glands. Parathyroid tissue from the fourth arch does not migrate in this fashion and remains closer to the superior pole of each thyroid lobe. This tissue then constitutes the superior parathyroid glands. Both the superior and inferior parathyroid glands are supplied by the inferior thyroid artery. Although this generally describes the normal anatomy, numerous variations have been found. As many as six glands may be found in a single patient, and they can be found in many locations, including the carotid bifurcation, the prevertebral region, and the superior mediastinum. Therefore, parathyroid surgery should be performed only by the experienced head and neck surgeon who is familiar with this varied anatomy. Patient Evaluation The most common cause of hypercalcemia in the general population is primary hyperparathyroidism, followed by patients with malignancy and bone metastasis. Patients with hyperparathyroidism demonstrate elevated levels of PTH as well as serum calcium. In contrast, patients with malignant bone metastasis may have high calcium levels but should have low or normal levels of PTH. The most common cause of hyperparathyroidism is parathyroid adenoma, which constitutes approximately 85% of cases. These patients generally have a single hyperfunctioning gland caused by adenoma. The remaining glands in such patients are often smaller than normal, reflecting an appropriate negative response to the high PTH levels from the adenomatous gland. Diffuse hyperplasia of all four glands comprises 15% of primary hyperparathyroidism cases. In these patients, all glands have undergone some degree of hyperplasia and are contributing to the high PTH level. Carcinoma of the parathyroid glands can cause hyperparathyroidism; however, this is rare and comprises <1% of such cases. Manifestations of hyperparathyroidism are primarily related to the resulting hypercalcemia. These include fatigue, bone and joint pain, abdominal pain and cramping, headache, and renal stones. Lab evaluation should demonstrate elevated levels of PTH and serum calcium. Serum protein levels should also be assessed, as this is required for an accurate calculation of calcium levels. Imaging studies are routinely performed to identify the exact cause of hyperparathyroidism and to localize the responsible glands.
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 U/S may be useful; however, it has several limitations. It cannot accurately locate retrotracheal or mediastinal glands, and it depends on an experienced ultrasonographer. CT scan does not provide sufficient resolution to clearly identify parathyroid glands and is generally quite expensive. The most useful imaging technique available to date is the technetium-99m sestamibi scan, which uses a radioisotope that is taken up by the parathyroid glands and can then be imaged. This technique is 90% sensitive and 98% specific for the diagnosis of parathyroid adenoma in patients with hyperparathyroidism. Subsequently, it can be a very useful tool to identify whether a single adenoma is present as well as the specific location of such a lesion. Surgical Therapy The primary goal of the parathyroid surgeon is to localize the hyperfunctioning parathyroid gland(s) and remove it. The traditional surgical approach to parathyroidectomy involves a bilateral exploration with identification of all four parathyroid glands. Normal parathyroid glands are left in place, whereas enlarged glands are sent for intraop pathologic evaluation. If hyperplasia is noted in a gland, it is removed, and the search for remaining glands is continued. If normal glands are then identified, the exploration can be concluded with reasonable confidence that the offending gland has been identified and removed. If second or third glands identified also show evidence of hyperplasia, then the patient likely suffers diffuse hyperplasia with all parathyroid glands involved. Accordingly, the general practice is that three complete glands and half of the fourth are to be removed. Alternatively, all four can be resected, with reimplantation of roughly 20 g of tissue from one gland into an easily identifiable muscle bed such as the sternocleidomastoid muscle or a forearm muscle. In this situation, the remaining parathyroid tissue is often able to regulate normal calcium homeostasis. Using such a surgical plan, >95% of patients return to normal PTH and calcium levels postop. With use of good preop localization studies such as the sestamibi scan, some surgeons advocate a more directed approach. If the scan suggests the location of a single adenoma, a unilateral exploration can be undertaken with resection of a single gland. The belief is that with reliable imaging studies, a bilateral exploration can be avoided, thereby reducing both operative time and cost. Regardless of surgical plan, a small percentage of patients have persistently elevated levels of PTH after surgery. These are patients who likely have parathyroid tissue in aberrant locations, such as the mediastinum or a retroesophageal location. Secondary procedures are occasionally required in this setting, and further imaging studies are mandatory. The variability in location of parathyroid glands further underscores the need for an experienced head and neck surgeon for such procedures. Complications of Parathyroid Surgery Complications for parathyroidectomy are essentially the same as for thyroidectomy, described in Surgical Treatment of Thyroid Disease. Recurrent laryngeal nerve injury, hematoma, and hypocalcemia are the leading concerns during the postop period.

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 Approximately 25% of patients experience transient hypocalcemia that does not require supplementation. Serum calcium levels reach a nadir on approximately the second or third postop day. Such low levels then stimulate the remaining normal parathyroid tissue to release PTH and correct this hypocalcemia. If the patient begins to show symptoms during this time or demonstrates positive signs of hypocalcemia, such as Chvostek's or Trousseau's sign, then supplemental calcium and vitamin D are indicated.

HEAD AND NECK CANCER STAGING

Staging of head and neck cancers can be quite confusing. However, it is important to know this information in order to best advise your patient on chances for survival and treatment options. (Staging information in this chapter is based on Greene FL, Page DL, Fleming ID, et al., eds. AJCC cancer staging manual, 6th ed. New York: Springer-Verlag, 2002. Head and neck cancers are characterized using the TNM system. T stands for the primary tumor site. The T criteria are different for each region within the head and neck. N stands for the regional lymph nodes; the classification is the same for all tumors. Similarly, M stands for distant metastases and is characterized as M0 (no distant metastases) or M1 (distant metastases). This section contains a list of the tumor staging for head and neck carcinomas. It provides a good reference for when you see tumors in the clinic and the operating room. Pearls Accurate staging of head and neck cancers is crucial for determining appropriate therapy and prognosis. Criteria vary based on the site of the tumor. Therefore, it can be confusing to just memorize the staging criteria. Instead, review the criteria for a particular tumor before you stage it. Be warned that many attendings love to pimp on staging. Also, it is crucial to consider the different treatment options for the tumor and to rule out any contraindications for a particular therapy that may exist in a given patient. For instance, interarytenoid involvement by tumor does not necessarily change the stage of a laryngeal primary. However, it eliminates partial laryngectomy as a treatment option.
ORAL CAVITY, LIP, PHARYNX AND LARYNX CARCINOMA

T Staging Criteria: Oral Cavity and Lip T1: 2 cm in greatest dimension T2: >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
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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 T3: >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 T3: >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
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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) T4b: Invades prevertebral space, encases carotid artery, or involves mediastinal structures 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) T4b: Invades prevertebral space, encases carotid artery, or involves mediastinal structures 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 N3: Any lymph node >6 cm M Staging Criteria: Distant Metastases Mx: Distant metastases cannot be assessed M0: No distant metastases M1: Distant metastases
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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 CARCINOMA
TNM 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 M1: Distant metastases Stage Grouping of Esophageal Carcinoma

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 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 TUMOURS

TNM 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
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 IVC: Any T, Any N, M1

THYROID CANCER
T 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 M1: Distant metastases Stage Grouping of Thyroid Cancer Papillary or follicular (<45 yrs) I: Any T, Any N, M0 II: Any T, Any N, M1 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
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 T4a, N1b, M0 IVB: T4b, Any N, M0 IVC: Any T, Any N, M1 Medullary carcinoma I: 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 IVC: Any T, Any N, M1 Anaplastic carcinoma (All anaplastic carcinomas are considered stage IV.) IVA: T4a, Any N, M0 IVB: T4b, Any N, M0 IVC: Any T, Any N, M1 Note: Separate stage groupings are recommended for papillary or follicular, medullary, and anaplastic (undifferentiated) carcinoma.

SKIN CARCINOMA

T Staging Criteria: Skin T1: 2 cm in greatest dimension T2: >2 cm but not >5 cm in greatest dimension T3: >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
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 N1: Regional lymph nodes M Staging Criteria: Skin M0: No distant metastases M1: 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 IV: Any T, Any N, M1

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
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Stage Grouping of Melanoma Pathologic stage grouping 0: 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 IV: Any T, Any N, M1 Clinical stage grouping 0: 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:
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 Any T, N1, M0 Any T, N2, M0 Any T, N3, M0 IV: Any T, Any N, M1

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Antimicrobial therapy in otolarygologyhead and neck surgery

PROPHYLAXIS 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
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 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
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 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 OTOLARYNGOLOGY

PCNs 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 Cost for 10-day course (U.S. $): 29 Antibacterial spectrum: PCN-resistant Staphylococcus Amoxicillin Trade, route, dose: Amoxil, PO, 500 mg tid Cost for 10-day course (U.S. $): 12 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 Cost for 10-day course (U.S. $): 122 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 Cost for 10-day course (U.S. $): 2290 Antibacterial spectrum: Gram-positive and -negative aerobes and anaerobes Piperacillin with tazobactam Trade, route, dose: Zosyn, IV, 3 g q6h Cost for 10-day course (U.S. $): 2290 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
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 Cefazolin Trade, route, dose: Ancef, IV, 1 g q8h Cost for 10-day course (U.S. $): 2220 Cephalexin Trade, route, dose: Keflex, PO, 500 mg qid Cost for 10-day course (U.S. $): 28 Cefaclor Trade, route, dose: Ceclor, PO, 500 mg tid Cost for 10-day course (U.S. $): 140 Cefuroxime Trade, route, dose: Ceftin, PO, 500 mg bid Cost for 10-day course (U.S. $): 170 Loracarbef Trade, route, dose: Lorabid, PO, 200 mg bid Cost for 10-day course (U.S. $): 85 Macrolides Erythromycin Trade, route, dose: Erythrocin, PO, 500 mg qid Cost for 10-day course (U.S. $): 28 Clarithromycin Trade, route, dose: Biaxin, PO, 500 mg bid Cost for 10-day course (U.S. $): 87 Azithromycin Trade, route, dose: Zithromax, PO, Z-pack Cost for 10-day course (U.S. $): 54 Quinolones Side effect: Do not give quinolones to children. Ciprofloxacin Trade, route, dose: Cipro, PO, 500 mg bid Cost for 10-day course (U.S. $): 107 Levofloxacin Trade, route, dose: Levaquin, PO, 500 mg qd Cost for 10-day course (U.S. $): 106 Gatifloxacin Trade, route, dose: Tequin, PO, 400 mg qd Cost for 10-day course (U.S. $): 86 Other classes Tetracycline Trade, route, dose: Achromycin V, PO, 500 mg qid Cost for 10-day course (U.S. $): 11 Clindamycin Trade, route, dose: Cleocin, PO, 300 mg qid Cost for 10-day course (U.S. $): 90 Side Effect: Pseudomembranous colitis. Metronidazole Trade, route, dose: Flagyl, PO, 500 mg qid
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 Cost for 10-day course (U.S. $): 25 Side effect: Metallic taste. Otic drops Ciprofloxacin Trade, form: Cipro HC, 10-mL bottle Cost for 10-day course (U.S. $): 60 Ofloxacin Trade, form: Floxin Otic, 5-mL bottle Cost for 10-day course (U.S. $): 37 Neomycin and polymyxin B sulfate Trade, form: Cortisporin Otic, 10-mL bottle Cost for 10-day course (U.S. $): 16 Side Effect: May cause hearing loss if placed in middle ear. Aluminum acetate Trade, form: Domeboro, 60-mL bottle Cost for 10-day course (U.S. $): 16 Hydrocortisone and acetic acid Trade, form: VoSoL HC, 10-mL bottle Cost for 10-day course (U.S. $): 15 Tobramycin and dexamethasone Trade, form: TobraDex, 5-mL bottle Cost for 10-day course (U.S. $): 38

INFECTIOUS DISEASES IN OTOLARYNGOLOGY

ACUTE OTITIS MEDIA

Microbiology 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.
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 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 MEDIA

Microbiology 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 for Fungal 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
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 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 EXTERNA

Microbiology 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 CHRONIC

Acute Sinusitis Microbiology Similar to acute otitis media. The more common offending organisms, in decreasing prevalence, are
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 H. 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 ADENOIDITIS

Microbiology 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.
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 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

EPIGLOTTITIS

Microbiology 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 ABSCESSES

Microbiology Neck abscesses usually contain mixed aerobic/anaerobic organisms: Staphylococcus Streptococcus Fusobacterium Bacteroides Eikenella Enterobacter E. coli

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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 Trauma

Head and Neck Trauma: General Principles Soft 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 FRACTURES
Diagnosis 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.

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NASAL SEPTAL HEAMATOMA

Diagnosis 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 HEAMATOMA
Diagnosis
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.

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 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.

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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

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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 FRACTURE

Diagnosis 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.

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

MANDIBLE FRACTURE
Diagnosis 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.

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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 FRACTURE

The 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.
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 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. Make sure the patient is on prophylactic antibiotics. Displaced Significantly displaced and comminuted fractures of the posterior table require either obliteration or cranialization of the sinus cavity. If there is no significant bone loss associated with the posterior table fracture, obliteration with plugging of the nasal frontal ducts is a viable option. Otherwise, cranialization should be performed.

FACIAL LACERATION
Diagnosis Facial (soft tissue) wounds are frequent in the multiply injured trauma patient. As such, all other trauma imperatives must be satisfied (ABCD) before initiating evaluation and repair of facial soft tissue injuries. All wounds are invariably contaminated and frequently more extensive than superficial exam reveals. Facial nerve function must be documented before any administration of local anesthesia or attempted repair. In addition, parotid duct injury must be ruled out for all injuries below a line from the tragus to the vermilion border at Cupid's bow. The duct may be cannulated intraorally with a long, fine angiocatheter before wound exploration to assist with this determination. Management Facial (soft tissue) wounds are categorized as contusions, abrasions, lacerations, or avulsions. A systematic approach allows effective management of even the most extensive injuries.

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 Contusions are generally self-limited but may mask underlying fractures. Abrasions are frequently contaminated with embedded foreign matter and require thorough dbridement; a surgical scrub sponge works well. Lacerations are frequently irregular and deep. All wounds should be copiously irrigated with 1 L of sterile saline and probed with forceps and cotton-tipped applicators after local anesthesia has been given. Special attention is given to precise anatomic landmarks, the specific layers violated, and the presence of underlying fractures. Lacrimal system injuries are generally referred to ophthalmology. Facial lacerations should be closed as soon as the patient's overall condition allows. Extensive injuries frequently require repair in the OR, especially when associated injuries require repair in the OR as well. Precise alignment of the vermilion border and margins of the brow and alar rim are critical to achieve an aesthetic repair. Layered closure technique is critical. Principal layers include skin, facial musculature, and mucosa. Forehead and scalp lacerations may also require galeal repair. Pinna lacerations are closed in perichondrial and skin layers. (Small pinna avulsions are reattached in the same way.) Through-and-through lip lacerations require repair of skin, SC tissue, and muscle. Mucosal lacerations are only loosely closed, if at all, as this allows a dirty wound to heal from the inside out. All diabetics need PO clindamycin prophylaxis. Tissue deficits secondary to avulsions should be dealt with conservatively; achieve good tensionless primary closure while minimizing areas of tissue loss. Definitive local flap closure is deferred to a secondary procedure. Facial nerve and parotid duct injuries require repair in the OR; this may be performed immediately in conjunction with the wound repair or the next day through your suture line or other incision. Disposition If discharged, patients should follow up in 12 days for a wound evaluation. Clean wound with half-strength peroxide twice daily to decrease crusting. After cleansing, triple-antibiotic ointment should be applied. Anti-Staphylococcus antibiotics (cephalexin, 250500 mg qid) may be given for rather contaminated wounds. PCN V (Pen Vee K), 500 mg qid, or clindamycin, 300 mg tid, should be given for deep or extensive oral cavity wounds. Patients should sleep in a recliner or with the head of the bed elevated 30 degrees for 3 days to minimize edema.

LARYNGEAL TRAUMA MANAGEMENT

Management protocol for the acutely injured larynx is shown in Fig. 10-5.

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Management protocol for the acutely injured larynx. Note: CT, computed tomography; ORIF, open reduction and internal fixation. (See the section General Notes on Management for an explanation of the superscript numbers in this figure.) Acutely injured larynx History of neck trauma Elicit symptoms or signs of injury Grossly assess airway Signs Tenderness, crepitance, hematoma, subcutaneous emphysema, stridor Symptoms Hoarseness, dysphonia, dysphagia, odynophagia hemoptysis, dyspnea, pain General Notes on Management
1. SC emphysema indicates a perforation of the upper aerodigestive tract: pharynx, larynx, trachea, or esophagus. Marked emphysema is usually a result of subglottic airway injury and can in itself create airway obstruction from extraluminal compression. 2. ER tracheotomy should be performed for any patient in immediate distress or in whom deterioration may occur before the OR can be made completely ready. 3. Endolaryngeal hematomas, lacerations, or edema; mild to moderate airway compromise; vocal fold immobility; no cartilage exposed. 4. Evaluate thyroid cartilage, cricoarytenoid joints, and endolaryngeal soft tissue. 5. Evaluation is generally performed in the OR with full instrumentation to prevent further injury. Be prepared to perform ER tracheotomy if stable airway deteriorates. 6. Conservative management for laryngeal trauma includes at a minimum monitoring in an ICU, bedrest, head of bed elevation, voice rest, humidified air, and avoidance of sedatives. Additional management may include antibiotic prophylaxis, adjunctive nutrition, antacid and antireflux measures, or diverting tracheostomy.

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COMMON CONSULTS AND EMERGENCY ROOM CALLS: AIRWAY PROBLEMS

Role of the ENT Surgeon As subspecialists, otolaryngologists are often called by the ER or to see patients on the floor. This chapter highlights the most common topics. Although it is not an exhaustive list, it encompasses approximately 90% of the consults that you will receive. The ENT surgeon is the airway expert in the hospital. Therefore, he or she is often called to urgently manage a difficult airway. An airway that is incorrectly managed often results in asphyxiation of the patient. Therefore, it is imperative to act quickly and aggressively when consulted on an airway problem. Many airways can be managed conservatively with medical therapy and close observation. However, always maintain a low threshold to treat it more aggressively (e.g., intubation, tracheostomy) if you are concerned that the airway is not secure. Managing the Airway of the Crashing Patient The first time that you are called to manage a patient who is not breathing, you will probably forget to breathe yourself. Do not panic. After you arrive at the bedside and find that the airway is obstructed, call for help. Do whatever it takes to get experienced medical staff to assist you. Some suggestions are to call a fellow ENT resident, have someone page in-house anesthesia, get the in-house senior surgery or medicine resident in the room, or call a code. Most people in the room are probably going to panic. The ENT physician is the airway expert and is in charge of the room. Therefore, it is your job to stay calm, delegate responsibilities appropriately, and obtain an airway. Call for the supplies that you will need. This includes O2, a mask and bag to ventilate the patient, the code cart, supplies to intubate the patient, and a tracheostomy tray (or at least a scalpel). If the patient is moving some air on his or her own, provide a calm environment and O2 and position the patient however is easiest for him or her to breathe. If the patient has no respiratory effort or is not moving air, the first step is to try to bag ventilate the patient. Using a jaw thrust may help to open the airway. If masking the patient does not work, intubation should be attempted. An emergency tracheostomy or cricothyroidotomy should be performed only if the above are unsuccessful. Workup for Airway Obstruction There are many causes of airway obstruction. However, the initial workup and management for all causes are similar.

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Initial Goals of Therapy Assess the degree of airway distress. Determine the cause. Secure a stable airway. Physical Exam Hoarseness usually suggests a laryngeal cause. Muffled or "hot potato" voice may be caused by supraglottic involvement. Suprasternal retractions suggest the cause of airway obstruction is superior to the thoracic inlet. Fever and WBC count suggest an infectious cause. After trauma, palpable fractures of the tracheal or laryngeal cartilages can cause airway obstruction. Stridor (noisy respiration due to obstruction of airflow) arises from air moving through a narrow aperture and may spring from myriad causes, including glottic dysfunction (vocal cord paralysis), trauma, tumor, foreign body, or exacerbation of laryngeal disease. Stertor arises from air moving through floppy mucosa. The typical case is poor supraglottic airway tone. Both stridor and stertor are indicative of a marginal airway for which intervention is required. Stertorous patients can usually be intubated if in distress. Fiberoptic endoscopy may aid in the diagnosis of stridor and guide management. Differential Diagnosis of Pharyngeal Obstruction (Often Causing Stertor) Infectious (pharyngitis, peritonsillar or parapharyngeal abscess) Foreign bodies Pharyngeal tumor Ludwig's angina (described later in this section) Angioedema and allergic reactions Differential Diagnosis of Laryngeal/Tracheal Obstruction (Often Causing Stridor) Trauma Laryngeal tumor Infectious (croup, epiglottitis, tracheitis) Foreign body Vocal cord paralysis Tracheal compression Subglottic stenosis Congenital lesions Allergic Angioneurotic Edema Definition Painless, nonpitting, well-demarcated edema occurring in the face, oral cavity, oropharynx, or larynx.
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Common Etiologies Insect bites Aspirin ACE inhibitors (at any time during therapy) Not uncommonly, there is no certain precipitating exposure in most patients. Physical Exam A thorough exam, including nasopharyngoscopy to determine the extent of involvement, is essential. Management May progress from the initial involved site leading to airway obstruction. All patients must be treated as if they had potential rapidly progressive airway compromise. Initial therapy: Humidified O2 Diphenhydramine (Benadryl) IV (50 mg) IV steroids (125 mg solumedrol) IV cimetidine If the edema progresses, epinephrine (either inhaled racemic or SC) is helpful. Maintain a low threshold for intubating the patient if the larynx is edematous or any airway distress occurs. If there is significant oral edema, fiberoptic intubation may be required. Adult Supraglottitis Adult supraglottitis is similar to epiglottitis in the pediatric population. However, it involves bacterial infection of all portions of the supraglottic larynx and a much wider range of causative organisms. The clinical course is only slightly less precipitous, making early recognition and prompt intervention critical. The temporal relationship is important: Events that evolve over hours are likely to be very precipitous; those evolving over days, less so. Symptoms There is a classic triad for supraglottitis directly related to laryngeal infection: Fever and pharyngeal pain first Leading to inability to swallow saliva (dysphagia) and Airway compromise or obstruction (especially when recumbent) Diagnostic Workup In stable patients, begin with a history and physical. Proceed to lateral soft tissue radiographs. If these clearly show supraglottic edema, the diagnosis is made.
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 If airway films are negative, limited fiberoptic endoscopy may be performed in adults (not in children) by advancing the scope only into the nasopharynx. Be prepared for immediate intubation or surgical airway at all times. If the airway is at all unstable or there is any doubt about the ability of the patient to tolerate this exam, arrange to take the patient emergently to the OR for laryngoscopy with attempted intubation or tracheotomy. Treatment of the Stable Patient If airway obstruction is not imminent, patients may be admitted to the ICU. High-humidity O2. Voice rest. Head of the bed elevated 90 degrees. A tracheotomy tray, laryngoscope, and ETT should be kept at the bedside at all times. IV hydration. Ampicillin/sulbactam (Unasyn) (1.53.0 g q6h) or clindamycin (Cleocin T) (600 mg) IV given immediately. Acute Epiglottitis in Children Ages 26 are most frequently affected. Signs and Symptoms Sudden onset and rapidly progressive High fever Respiratory distress Odynophagia Drooling Important: Fiberoptic exam, or even tongue depressors, is contraindicated, as it may precipitate laryngospasm. Management CBC and blood cultures should be obtained. Begin antibiotics as soon as possible. Cefuroxime (Ceftin), ceftriaxone (Rocephin), ampicillin/sulbactam, aztreonam (Azactam), or chloramphenicol (Chloromycetin) provides good coverage. The surgeon should never leave the child's bedside once epiglottitis is diagnosed. A lateral neck radiograph may be performed only if the diagnosis is uncertain. The OR is immediately alerted to prepare for emergent laryngoscopy and intubation, possible bronchoscopy, and possible tracheotomy. A culture of the epiglottis should be obtained after the airway is secured.

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Epistaxis Etiology Most nosebleeds are due to ruptured blood vessels on the nasal septum. The fragile network of blood vessels covering the anterior septum (Kiesselbach's plexus) is frequently subjected to trauma from instrumentation (e.g., the patient's finger, nasogastric tubes, an O2 nasal cannula). In younger patients, a vein just posterior to the columella is typically the cause. In older patients, the bleeding is more likely to be arterial, from the caudal part of the nasal septum, where there is an area of multiple anastomosing vessels (Little's area). Causes of bleeding that must be ruled out include Blood dyscrasias/coagulopathies HTN Increased venous pressure Vascular lesions Tumors Treatment When you receive a consult about a nosebleed, there are a number of questions to ask right away over the phone. What is the estimated blood loss? How rapidly is the patient bleeding? If there has been a significant bleed, it is important to get a CBC, PT/PTT, and type and screen as soon as possible. Patients can go into hemorrhagic shock and die from epistaxis. Is the patient stable? What are the vital signs? If hypotensive and/or tachycardic, consider fluid resuscitation. If the patient is hypertensive, it needs to be addressed by the staff immediately because it will be difficult to stop the bleed. Consider using nifedipine (Procardia) or clonidine (Catapres) IV for pressure control. Do not use hydralazine due to its function as a vasodilator. What medications is the patient taking? Anticoagulants [heparin, coumadin, clopidogrel bisulfate (Plavix), aspirin, NSAIDs] will affect your ability to control the hemorrhage. Are there any other medical problems that can be addressed? Renal failure can cause platelet malfunction. Hepatic failure results in coagulopathies. Heart failure causes increased venous pressure. Instruct the staff to sit the patient upright with his or her chin slightly down. Constant pressure should be applied by squeezing the nostrils together firmly. Finally, you should see the patient right away. Epistaxis is a potentially life-threatening emergency.

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When you first arrive at the bedside: The first step is intranasal anesthesia and vasoconstriction. Soak cotton balls in a mix of 4% topical lidocaine and oxymetazoline (Afrin). A Frazier tip suction and headlight are used to remove all the clots from the nose, nasopharynx, and oropharynx. The cotton balls are then placed in each nostril, and the patient is again told to pinch the nostrils together. It will take several minutes for the medication to take effect. During this time, you can assemble all the necessary supplies. Following is a list of everything you could potentially need for a nosebleed: 4% lidocaine (topical), oxymetazoline (Afrin), or Neo-Synephrine Large Frazier tip and suction set up Cotton balls Headlight and light source Nasal speculum Tongue blade Merocel epistat sponges Vaseline gauze packing Silver nitrate sticks Surgicel Protective eyewear (the patient will cough blood in your face) Epistat nasal pack Stopping the bleed: With the headlight on, the nasal speculum in one hand, and the Frazier suction in the other, the cotton is removed from one side of the nose at a time. The nasal cavity is inspected for a site of bleeding. If there is no bleed, the cotton from the other nostril is removed. Cauterize a discrete lesion with silver nitrate. If this controls the bleeding, a small piece of Surgicel can be placed over the area to promote healing. Warning: Avoid cauterizing both sides of the same area of the septum, which can result in septal necrosis and perforation. If the bleeding is controlled, have the ER observe the patient for 3060 mins before discharge. The patient should be instructed to avoid trauma to the nose, use oxymetazoline (Afrin) tid for 3 days, and use nasal saline spray q2h while awake for 10 days. If the bleeding continues from the front of the nose or continues to drip from the nasopharynx, the Surgicel is not sufficient, and a larger pack is needed. Lubricate an 8-cm Merocel Epistat (nasal tampon), and insert it along the floor of the nose until none of the sponge is protruding from the nostril. Apply oxymetazoline to the sponge to expand it. This should stop 95% of nosebleeds. With the Merocel fully expanded, check the posterior pharynx again for bleeding. If there is continued bleeding, a Merocel can be placed in the other nostril, or you can remove the Merocel and continue to the next step. The next step is using Vaseline gauze 0.5 72 in. This is packed into the nose, accordion-style, from
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the posterior floor up. Anyone with either Merocel or Vaseline packing needs to be on toxic shock syndrome prophylaxis [cephalexin (Keflex), 250500 mg qid] as long as the packing is in. The patient can go home and be followed in clinic in 35 days for packing removal. If this doesn't work, the final step is an Epistat kit for posterior arterial bleeds. This looks like a short Foley catheter that has one posterior balloon and one balloon along the shaft of the Epistat. After inserting the Epistat, the posterior balloon is filled partially with sterile water. The anterior balloon around the shaft is then partially filled until the bleeding stops. Vaseline gauze is then placed around the nares to prevent alar necrosis. Any patient with an Epistat must be admitted to a monitored bed because it can cause a hypoxic reflex. Peritonsillar Abscess Inadequately treated episodes of bacterial tonsillitis may progress to abscess formation in the potential space between the tonsil and its fossa. Classic Presentation Patient develops a sore throat and tonsillitis that either is not treated with antibiotics or is treated with penicillin or erythromycin. 47 days after the initial sore throat, the patient develops Increased pain Trismus A "hot potato" voice Fever Inability to take PO fluids On physical exam, there is typically an obvious swelling of the tissue lateral to the tonsil and uvular deviation. Any patient suspected of having a peritonsillar abscess should have a diagnostic tap. Differential Diagnosis Acute tonsillitis Scarlet fever Diphtheria Vincent's angina Malignancy Management Before attempting drainage, the patient should have IV access. Morphine or other pain medicine to help relieve the trismus. IV steroids to decrease the swelling (some argue against steroids during an acute infection).
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 Hydrate with a normal saline or lactated Ringer's bolus. The patient is probably very dehydrated due to odynophagia. Assemble necessary equipment: Headlight Tongue blade Benzocaine/tetracaine (Cetacaine) spray 10-cc syringe with 1 cc of lidocaine 18-gauge needle 27- or 30-gauge needle Yankauer suction No. 11 blade Kelly clamp Draining the abscess Spray the throat with benzocaine/tetracaine (Cetacaine). Inject lidocaine into the mucosa overlying the suspicious area. The 18-gauge needle is then placed lateral to the superior pole of the tonsil and inserted up to 1.5 cm. Constant negative pressure is applied to the syringe. As the needle enters the abscess, purulent fluid fills the syringe. It may be necessary to make several passes with the needle to localize the abscess. This is done by marching inferiorly along the lateral aspect of the tonsil. The needle should not be passed inferior to the midtonsillar region to avoid entering the carotid artery. Controversy exists regarding whether needle decompression of a peritonsillar abscess is sufficient drainage. Some argue that formal incision and drainage decreases the chances of fluid reaccumulating within the cavity. Incision and drainage are performed by making a curvilinear 2-cm incision with a No. 11 scalpel blade along the anterior pillar of the tonsil, following the lateral border of the tonsil. The incision typically needs to be made lateral to where one might expect. After the abscess cavity is entered, all loculations are broken up with a blunt instrument, and the cavity is irrigated with normal saline. Purulent fluid should be sent for culture. Decompression of the abscess usually brings about immediate relief. If the patient is able to drink adequate fluids, he or she can be sent home on clindamycin (Cleocin), 300 mg PO qid, or amoxicillin/clavulanate (Augmentin), 875 mg bid for 710 days. Follow-up should be in 23 days to check that the abscess has not reaccumulated. If the patient cannot drink, he or she should be admitted for IV fluids and clindamycin. A negative aspiration may be consistent with phlegmon. The patient should be told to follow up in 23 days if the symptoms do not improve with clindamycin. Other Neck Space Abscesses Although peritonsillar abscesses are the most common, there are a number of other potential space infections in the head and neck. The spectrum of offending organisms is similar, and all can be treated with the same antibiotics as used for a peritonsillar abscess.

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Retropharyngeal Space Abscess Etiology Suppurative infection of the retropharyngeal lymph nodes presents typically in babies and young children. Diagnosis Clinically, the diagnosis is difficult to make unless you maintain a high index of suspicion. The patient will typically Appear toxic Be febrile Refuse to eat or drink Possibly have hyponasal speech Physical Exam Anterior displacement of the posterior pharyngeal wall; however, this is difficult to identify on physical exam because of the lack of depth perception in this region. Overlying pharyngeal mucosa may be boggy and inflamed. Radiology Lateral neck film demonstrates air in the retropharyngeal space or a widened soft tissue shadow overlying C2-6. Lateral films do give a number of false-positive results due to the angle of the child's neck when the film is taken. CT scan can give a definitive diagnosis if there is any question. Management Secure the airway first. This kind of abscess is usually drained in the OR under general anesthesia. The child is placed in Trendelenburg (head down) position so that the child does not aspirate the pus. The abscess is incised, and purulent material is suctioned out and cultured. The child is observed for airway issues and is placed on clindamycin for 710 days. Lateral Pharyngeal (or Parapharyngeal) Abscess Etiology Rare complication of tonsillitis. Suppuration in the region surrounding the great vessels of the neck. If untreated, can result in carotid artery rupture.
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Diagnosis Symptoms include Trismus Drooling Dysphagia Odynophagia Physical exam demonstrates medial displacement of the lateral pharyngeal wall with fullness of the retromandibular region. Management Operative drainage through an external incision parallel to the anterior border of the sternocleidomastoid muscle. Never drain intraorally due to risk of injury to the great vessels. IV antibiotics until afebrile for 2448 hrs, then PO antibiotics for 710 days. Ludwig's Angina Etiology Often results from a dental source, particularly in immunocompromised individuals. A rapidly advancing, life-threatening acute infection that involves the connective tissue, fascia, and mylohyoid muscle of the floor of the mouth, then rapidly spreads to the submandibular space. In general, there is no discreet abscess; rather, there is phlegmon throughout. If not treated appropriately, the phlegmon and swelling from the floor of mouth and tongue will cause the posterior two-thirds of the tongue to be deviated superiorly and posteriorly, causing airway obstruction. Diagnosis The patient often has a history of a toothache within the last month. The patient typically presents with high-spiking temperatures and shaking chills and is unable to handle his or her own secretions. Physical exam reveals firm swelling of the entire floor of the mouth. Management Airway obstruction can progress rapidly. Therefore, it is crucial to control the airway immediately. Typically, these patients require either fiberoptic intubation or tracheotomy. Operative incision and drainage of the floor of mouth. Drainage produces a serosanguineous, foul discharge but rarely produces frank pus. IV antibiotics (clindamycin or ampicillin/sulbactam). Steroids to reduce swelling. The patient can usually be extubated or decannulated within 48 hrs after drainage when oral airway is patent.
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Foreign Bodies in the Ear Although foreign bodies in the ear are not emergencies, patients often present to the ER with them. Objects such as beads, stones, and toys can often be removed in the ER with the operating microscope. If the canal is traumatized, place the patient on antibiotic drops for 35 days. Small insects, such as cockroaches, will crawl into the ear canal and become trapped. If the insect is already dead, it can be removed under direct visualization with the operating microscope. If the insect is still alive and there is no perforation of the tympanic membrane, the ear canal should be filled with mineral oil for 1015 mins to suffocate the insect. Then it can be removed with the microscope. If the tympanic membrane is perforated, do not flush out the ear because the fluid will migrate to the middle ear. Instead, use neomycin/polymyxin B sulfate (Cortisporin) otic drops. If the foreign body has been in the external auditory canal for an extended time, an inflammatory reaction occurs. Any manipulation to remove the object causes pain. Place the patient on antibiotic drops containing steroids [e.g., neomycin/polymyxin B sulfate (Cortisporin) or ciprofloxacin (Cipro HC)] for 57 days before removing the object. If an object cannot be removed in the ER easily due to the shape of the object or noncompliance, it is appropriate to schedule the patient for removal in the OR under anesthesia. Upper Aerodigestive Tract Foreign Body Not everything put in the mouth belongs there. Children swallow toys or coins. Adults usually experience a fishbone being caught in the throat. If the object swallowed is radiopaque (e.g., a coin), airway x-rays are helpful to localize the object. Evaluation Fishbones usually do not show on films; thus, fiberoptic exam is the best method of evaluating bones lodged in the upper airway. Bones tend to stick in soft places such as tonsils, the base of tongue, and the hypopharynx. Bones are small, white, and often mistaken for a string of saliva. Frequently, the foreign body sensation results from an already swallowed object. Exam will reveal no foreign body, and topical anesthesia usually relieves the sensation. In these cases, the patient can be sent home with instructions to watch for temperature spikes (suggesting perforation) and expect the foreign body sensation to resolve over 34 days. If the sensation persists, the patient should follow up for reevaluation. Management If a foreign body is identified, ER removal should be considered if airway compromise is extremely unlikely. Topical anesthesia by 4% lidocaine atomizer is performed. Wear a headlight and use a laryngeal mirror and long curved instrument to remove the object.
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 If removed without incident, the patient can be sent home on a regular diet. If symptoms worsen or if fever and neck tenderness develop, formal endoscopy and barium swallow to rule out perforation are indicated. Tracheal and Esophageal Foreign Bodies in Children Most children who aspirate foreign bodies are <3 yrs; almost all are <5 yrs. Vegetable matter accounts for the majority of airway foreign bodies, with plastic toy pieces second; neither is radiopaque. Coins, discs, and hardware are found most often in the esophagus. History A thorough history is critical; a high index of suspicion is usually warranted. Take every positive in the history seriously and be wary of negatives. Symptoms Symptoms often progress through three stages: The initial event involves choking, coughing, gagging, or transient airway obstruction. It can usually be elicited from the patient's history; however, he or she may minimize the event. A treacherous asymptomatic interval frequently follows as the immediate irritation subsides and often gives parents and sometimes physicians a false sense that a foreign body is unlikely. If the asymptomatic interval is allowed to progress, symptoms of complications (obstruction, erosion through lumen wall, or infection) constitute the third stage. Physical Exam Esophageal Foreign Bodies Drooling Refusal to take solids or liquids Overflowing secretions into the larynx Airway Foreign Bodies Asymmetric breath sounds Stridor Wheezing Cough Frank airway obstruction Inspiratory and expiratory chest x-rays are useful when positive in all foreign bodies. However, negative radiographs do not rule out foreign bodies. Otherwise, management is based on history and physical exam.

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Management The following four situations demand emergent removal of a foreign body in the OR: Acute or potential airway obstruction: usually from globular foreign bodies or balloons. Dried vegetables: can absorb moisture, swell, and obstruct the airway. Disc battery lodged in the esophagus: acid from the battery can be released and erode the esophagus. Esophageal perforation: usually from a sharp metal or glass object. The Heimlich maneuver and finger sweep are appropriate management for laryngeal obstructive foreign bodies. The remainder of foreign bodies require urgent, but not emergent, removal in the OR. Patients are admitted, kept NPO, and hydrated IV. Otalgia See Otology. Vertigo See Otology. Sinusitis See Rhinosinusitis. Dysphagia Dysphagia may be the sequela of an acute of subacute process or may represent the end result of a multifactorial disorder. It is important to identify life-threatening processes, including Supraglottitis Upper aerodigestive tract foreign body Deep neck infection Foreign body aspiration Any other process that may potentially compromise the airway Physical Exam Be mindful of the pearls and pitfalls of each of the airway problems in this section. Fiberoptic exam to rule out pharyngeal or laryngeal pathology is performed with caution (and not at all in children if epiglottitis is possible). Modified barium swallow to evaluate swallow mechanics, aspiration, and esophageal pathology may be scheduled when the sun rises the next day. Acute airway problems should be managed in a cause-specific manner. Nonlife-threatening causes, when identifiable, should be treated accordingly. For example: Tonsillitis: 10 days of PCN V or cephalexin (Keflex) or 57 days of clindamycin
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 Reflux laryngitis: trial of H2-antagonist or proton pump inhibitor Viral laryngitis/pharyngitis: voice rest, topical relief (lozenges) Caustic Ingestion A history of witnessed or just-missed ingestion of a product is the most common presentation. Determine the type of product ingested: Alkaline agents (e.g., hair relaxers, lye, batteries, ammonia, and Clinitest tablets) are most common and may cause rapid deep burns via liquefactive necrosis. Acids are next most common and slightly less likely to cause deep burns owing to coagulative necrosis. Bleach- and chloride-containing substances rarely cause significant mucosal injury unless ingested in high concentration. Presentation Children frequently present with burns of the hands, lips, and oral cavity. Drooling or refusal to take PO usually indicates mucosal injury. Management Management begins by ruling out airway compromise. Chest x-ray is routine. Fiberoptic endoscopy should be performed, if necessary, to assess the airway. Once the patient is stabilized, prevention and treatment of significant esophageal injury are the goals. Obtain the product name and determine the pH from poison control. Rinse the oral cavity and skin burns copiously with plain water. Do not give a neutralizing agent or charcoal. Nasogastric tube and lavage in the ER are not recommended. Social services should be notified to assess risks to siblings in the home. Ingested batteries require emergent removal if lodged in the esophagus to prevent ongoing injury. If obvious mucosal burns are noted or if a strong alkali or base are ingested, the child is admitted. IV antibiotics. Steroids. Antireflux therapy. Give water or milk to dilute the agent (if not proceeding to the OR). Definitive esophagoscopy is performed within 48 hrs. Children who ingest weak agents and in whom no mucosal injury is detected may be discharged with closer follow-up with the otolaryngologist.

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Common Floor Calls

Common Floor Calls: Introduction Calls from the nurse on a busy call night, especially about patients with whom you are not familiar, are a constant source of frustration. However, even the most trivial of calls can lead to important discoveries that may significantly change the management of a patient. The most important point to make about any call you will get is to go see the patient. If the problem is not acute, you may be able to delay until you finish whatever more pressing matter you are dealing with, but don't forget to see the patient as soon as possible. The usual scenario is that a nurse will call with an abnormal finding or complaint. Do not be fooled into thinking that the nurse knows the diagnosis; he or she is only giving you the data. Although you must address the symptom, your primary objective is to uncover the underlying problem. In other words, you must make the diagnosis. How you respond to each of these calls depends on a variety of factors and most certainly evolves over the course of your training. You initially need to let your senior resident know about any significant patient changes. Gradually, you will be allowed more responsibility and will be better equipped to handle common problems. In addition, how well you know the patient influences how you investigate the problem. In brief, the approach to dealing with patient problems is described below.

THE INITIAL CALL

When the nurse calls, you will need to get the necessary information to be able to prioritize the problem. The most important information to find out is what the patient's current vital signs are and if the patient is complaining of anything. In addition, the nurse's sense of urgency about the problem may help you sort out how soon you need to see the patient. If the call warrants an immediate trip to the bedside, go to the patient's room directly. Tell the nurse to get the chart and whatever other equipment you will need (e.g., ECG machine, IV fluids) and meet you at the bedside. Do not worry about getting any history or other information until the life-threatening problem is settled. Chart Review If the problem can wait, your time is best spent by going to the chart first and gathering basic information about the patient. This should include the following: Operation and postop day Indication for operation Postop course and any complications Significant medical history Current medications, diet orders, and lab results
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History When going into the room, introduce yourself and explain to the patient that you have been called because the nurse is concerned about whatever issue you are there to settle. Then give the patient time to tell you what is wrong. He or she can usually provide you with the most important information. Make sure to take a focused history relevant to the problem you are investigating. Physical Exam Always examine the patient. Do so in adequate light even if it is very late at night and the patient's roommate is sleeping. Make sure to look at the operative site. Take the dressing down if you need to. Always look at the drains and the fluid in them. This does not take long and often leads you to the diagnosis. Differential Diagnosis After you have the basic information, you should be able to generate a differential diagnosis. Think carefully; this is the critical step in evaluating all patient problems. If you don't consider a particular diagnosis, you are likely to miss it. Testing You should then decide what ancillary testing is needed. If the patient needs a chest x-ray (CXR), don't be afraid to tell the nurse that it needs to be done right away. Don't wait until morning because it may inconvenience the staff or the patient. Treatment Some benign problems require nothing more than reassurance. However, serious problems commonly occur on a surgical service, and your treatment plan may save a patient's life. Possible treatments include drugs, bedside procedures, and reoperation. In addition, the patient may require transfer to a more closely monitored setting, such as an ICU. These are the most common problems experienced on a surgical service. Ultimately, you will develop your own method of dealing with each. Here we present an efficient and effective management summary for these common issues.

LOW URINE OUTPUT

All patients requiring hospitalization for a surgical reason should have their urine output recorded. In other words, every time you write orders, you should include "strict ins and outs." Accordingly, the problem of low urine output can be detected quickly instead of waiting for renal function to deteriorate.
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The first question to answer is, "How low is the urine output?" In general, we expect a patient with euvolemia to make 0.5 cc of urine/kg/hr. This refers to the patient's lean body mass. So for a patient who weighs 50 kg, the expected urine output is 25 cc/hr. This means that in an 8-hr shift, the recorded value should be 200 cc. Before you start to worry about your patient with "low urine output," you should first ascertain that the value is accurate. Often it is not; patients without an indwelling Foley catheter are not in the habit of collecting their urine for measurement. The first questions to ask are 1. Does the patient have a Foley catheter? 2. Is the patient incontinent? 3. Did the patient void without having the amount measured? The easiest way to sort this out is, as always, to go to the bedside. Simply ask the patient if he or she recalls voiding without saving it. In addition, you should always ask the patient if he or she feels the urge to void currently. This may produce another 300 cc of urine, and the low urine output problem may disappear. Assuming you have verified that the patient does in fact have low urine output, you should proceed with the following workup. Chart Review Look carefully through the patient's ins and outs over the last 48 hrs. Note if the patient is receiving a diuretic of any kind or takes one at home. Look for the date of Foley catheter insertion or removal and whether it was a difficult Foley placement. Review the operative note to rule out a possible iatrogenic cause. Look up the patient's most recent lab tests, including BUN, creatinine (Cr), potassium, and bicarbonate levels. Look for any recent contrast studies. Review the medication list for nephrotoxins. History Review for vomiting, diarrhea, or fluid loss (e.g., drains, nasogastric tube). Elicit symptoms of bladder outlet obstruction (slow stream, nocturia, dribbling) and whether the patient normally takes medication for this. Always ask if the patient has the feeling of having a full bladder. Physical Exam Assess the patient's volume status carefully. Look for dry mucous membranes, low jugular venous pressure, decreased skin turgor, and lack of axillary sweat. These signs point toward volume depletion. Flush the Foley catheter with 3050 cc of sterile water. See whether it flows easily in and out of the
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bladder. Make sure the proper length of catheter is outside the patient. Check the balloon valve. Look at the urine (if any is available). Dark-colored urine usually means concentrated urine, but you can be fooled by pigments. A patient with elevated serum bilirubin or myoglobinuria will pass dark urine. Feel the suprapubic area to see if you can palpate or percuss the bladder. Differential Diagnosis Prerenal The major causes of a prerenal state are Volume depletion: This is the most common reason for surgical patients to have low urine output. To decide why a surgical patient is volume depleted, consider the following: Postop day: Patients who are postop day 03 are still in the period of third-spacing fluids into the interstitial space. This generality applies to patients who have undergone rather significant open abdominal procedures. Excessive losses: Determined by high nasogastric tube output, high drain output, or frequent diarrhea. Inadequate intake: Patients whose IV fluids have been stopped but who are without sufficient oral intake may become intravascularly depleted. Bleeding: Patients who have lost a large amount of blood intraop or those who are continuing to bleed postop will demonstrate decreased urine output. Perceived volume depletion: Occurs if the intravascular volume is adequate but the kidneys are not able to sense this. The major causes of this problem are Heart failure Cirrhosis Nephrosis Renal Patients with renal problems have normal intravascular volume but kidneys that have an intrinsic problem making urine. The major causes of this type of problem include the following. Acute Tubular Necrosis Acute tubular necrosis (ATN) is the state in which the kidney tubules have been damaged and are unable to continue the process of filtering urine properly. The causes of ATN include Prolonged hypotension (often intraop) IV contrast loads (cardiac catheters, CT scans, angiograms) Nephrotoxic drugs (aminoglycosides, amphotericin, chemotherapy) Endogenous tubular toxins (myoglobinuria from crush injuries) Acute Interstitial Nephritis
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Acute interstitial nephritis is most often due to medications such as NSAIDs or beta-lactam antibiotics. Embolic Disease Embolic disease is most common in the vascular patient who had an intervention that could cause embolization of plaque and thrombus to the renal arteries. Causes include Cardiac catheterization Angiography Left heart thrombi from large myocardial infarctions (MIs) or atrial fibrillation Graft Dysfunction Patients with newly transplanted kidneys fall into their own class when they have the problem of low urine output. One of the possible etiologies is intrinsic graft dysfunction. Other conditions that should be considered are acute vascular problems, such as renal artery thrombosis and anastomotic disruption of the ureter. Do not treat these patients like others with low urine output. Alert your senior resident immediately. Postrenal Patients with postrenal problems are making adequate urine at the level of the kidney but have some problem that is not allowing the urine to exit through the urethra. There are multiple possible etiologies: Ureter problems: Surgically transected ureters, extrinsically compressed ureters (blood clots, retroperitoneal fibrosis), and luminally blocked ureters (stones, clots) can all cause a decrease in urine output. Bladder problems: usually a bladder outlet obstruction issue and easily relieved by placing a Foley catheter. Prostate problems: Male patients usually give a history of prostate enlargement. Placement of a standard Foley catheter may be difficult, requiring a stiffer catheter (Coud) or even a urology consult. Urethral problem: The catheter is blocked with debris and not properly draining urine from the bladder, or it is malpositioned. Testing Chemistries BUN, Cr, potassium, bicarbonate. These can help you assess the severity of renal compromise (i.e., if the patient has developed acute renal failure) and the potential for complications (the development of hyperkalemia). Urine electrolytes can also be considered (sodium, Cr). Urine Sediment
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If you suspect a patient of having ATN, the best diagnostic test is urine sediment looking for "muddy brown casts." If you suspect acute interstitial nephritis, send off urine for eosinophil measurement. Complete Blood Cell Count Order a CBC when you suspect the patient may be volume depleted as a result of blood loss. Renal Ultrasound Renal U/S is almost never needed in the middle of the night but is a test to consider performing the following morning if things have not improved. It will tell you if there is hydronephrosis, which suggests a postrenal cause. Treatment Bolus of isotonic IV fluid: This will be the most frequent and successful treatment you will offer the surgical patient. However, do not simply "bolus the patient" without first considering comorbidities such as congestive heart failure. Don't bolus with half normal saline or any fluid with added potassium. Change the fluid balance: If your patient is volume depleted because of increased losses, just giving a bolus may only fix the problem transiently. The best way to deal with this is to replace whatever fluid is being lost. If the patient appears to be third-spacing fluid, consider either increasing the rate of maintenance fluid or changing to an isotonic solution. Insert a Foley catheter: Any patient with low urine output who does not respond to conservative measures should have a Foley catheter inserted for closer monitoring. In addition, a Foley catheter may definitively treat a patient with postrenal obstruction. Ensure proper Foley function: Always flush the Foley catheter to make sure it is patent and that the catheter will return the amount of fluid you have flushed. If this does not occur, you should manipulate or change it until you are assured that the catheter is adequately draining the bladder. Medications: If the patient not only has low urine output but also appears to be experiencing a change in renal function (increasing Cr), you should discontinue any medications that could be contributing to the problem. In addition, any medications that require renal dosing should be adjusted accordingly. Diuretics: It is often tempting to give a patient who does not respond to several boluses of fluid a dose of furosemide (Lasix) to see if the urine output improves. This is, at times, the correct management decision, but it is not one that you should do without very careful consideration. Giving IV fluids followed by diuretics does not improve renal function; it only increases the urine output. The argument for doing it is that it is easier to manage a patient who is nonoliguric than one who is oliguric. Diuretics in a hypovolemic patient worsen renal failure. Always consider central venous pressure monitoring before giving diuretics if the patient's volume status is unclear. Always check with a more senior resident before proceeding down this pathway. Monitor response to intervention: If the urine output does not respond quickly, you will need to reassess the problem and consider what further interventions are needed.

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FEVER

Although the request for an acetaminophen order may seem mundane, a postop patient with a fever presents an opportunity to make a real difference in that patient's care. Getting therapy started early for infectious problems is essential. Chart Review Preexisting pulmonary disease, immunocompromised state (diabetes, steroids, postsplenectomy), and allergies to antibiotics are essential. Briefly go through the daily notes to see if the patient has had other fevers and what workup has been done (UA, sputum cultures, CXR, blood cultures, CT scan). Check to see if the patient is currently on antimicrobial therapy. History Mental status: Confusion is one of the first signs of a serious infection; thus, you should ask basic questions of orientation. Pulmonary complaints: Ask about cough, sputum production, and shortness of breath. Ask the patient to use the incentive spirometer to see if he or she can take in decent tidal volumes. Urinary complaint: If the patient does not have a Foley catheter, ask if there is any burning with urination and any sense of urgency or frequency. If the patient is male, ask if he has symptoms of prostate enlargement. Lower extremity complaints: Ask about the sense of swelling or pain in either leg, particularly the calves. Neck pain: This may be very subjective. However, if you sense that the patient is having more discomfort than he or she was previously or that the patient is off the bell curve for his or her operation, you should be concerned about the possibility of an infection. GI complaints: Ask about nausea and vomiting. Always ask specifically about diarrhea and the color and consistency of the effluent. Physical Exam Indwelling Foreign Object Start by looking for the obvious things. If the patient has any of the things listed below, find out how long the object has been in place. Central lines, Port-a-caths, IVs: Look at the site carefully. Epidural catheters: Examine the site. Foley catheter: Determine character of the urine. Surgical neck drains: Determine character of the fluid in them.

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Pulmonary Exam Listen for localized findings that suggest a developing pneumonia or generalized crackles to suggest atelectasis. Make sure you know what the O2 saturation is. Wound Look closely at the patient's wound. Take down the dressing. Look for erythema or discharge. If the wound is packed, change the packing to make sure that you know the quality of the fluid in the wound. Always be thinking about the possibility of wound dehiscence and fistula. Abdominal Exam Watch for localized tenderness in the right upper quadrant to suggest cholecystitis or suprapubic tenderness to suggest a UTI. Lower Extremities Look for swelling, tenderness, or erythema to suggest a deep venous thrombosis (DVT). Differential Diagnosis Atelectasis Atelectasis describes the collapse of terminal airways that often occurs in surgical patients. The predisposing factors include lying supine, being unable to take deep breaths or sigh (usually secondary to incisional pain), and a prolonged period of time on the operating table. You will often hear the nurse report that the patient had a fever earlier, but it went away when the incentive spirometer was used and the patient got up to walk. As unbelievable as this sounds, it is actually true that these maneuvers aimed at decreasing postop atelectasis sometimes return a patient's temperature to normal. Atelectasis alone does not cause extreme temperature elevations, and it will never make the patient look sick or have other abnormal vital signs. You should never feel satisfied with the diagnosis of atelectasis; it is more a diagnosis of exclusion when the rest of your search uncovers nothing. Atelectasis is most commonly seen on postop day 1. Wound Infection Patients frequently develop erythema or discharge from a neck wound. There are many things that can cause it, but the most likely, particularly in a febrile patient, is a wound infection. There are very aggressive wound infections that occur early in the postop course (e.g., Clostridium and Streptococcus), so if you detect a significant amount of erythema, warmth, or particularly SC air on the first or second postop days, it is important to let your senior resident know as soon as possible. With any patient who received a pharyngotomy

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during a procedure, keep a high index of suspicion for orocutaneous fistula. For more information on surgical site infections, see the section below on wound drainage. Pneumonia You should suspect a pulmonary infection in patients with a history of smoking, in those with COPD, and in those with localized rales or rhonchi on physical exam. There is a spectrum of infection that ranges from mild bronchitis picture to lobar consolidated pneumonia. These types of infections can occur at any time depending on preop pulmonary status. Urinary Infection In patients with indwelling catheters, there is a high risk of bacterial seeding and subsequent urinary infection. In addition, stagnant urine in men with urinary retention from prostate enlargement may serve as a predisposing factor to infection. If the patient has any urinary complaints or has a Foley catheter, you need to consider a UTI. It can manifest on any postop day. Line Infection If the patient has an indwelling central venous line, you need to be very concerned about the possibility of a line infection. Even if the site appears clean, the catheter tip can still be harboring bacteria. Be particularly vigilant about line infections in patients whose lines have been in >3 days and whose lines were not placed under optimal conditions (e.g., in the ER, in the OR emergently). Deep Venous Thrombosis A DVT is a common surgical problem and can, at times, cause low-grade fevers. It will not make the patient sick and is not likely to cause a high fever. Additionally, a superficial thrombophlebitis can cause fever. Clostridium difficile Colitis C. difficile is a common infection in surgical patients due to the frequency of antibiotic therapy. Any patient with diarrhea should be considered a possible candidate for C. difficile colitis. It often is associated with abdominal pain and a leukocytosis. Bacteremia/Sepsis Any type of infection may progress to a bloodstream infection and begin to cause a systemic inflammatory response in your patient. These patients are generally sicker and have abnormal vital signs. It is essential that you recognize when a patient is beginning to become systemically ill, as these patients need to be more closely monitored and started immediately on broad-spectrum antibiotic therapy.

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Other Rarer causes, but etiologies to consider in special circumstances, include drug reactions, Addisonian crisis, thyroid storm, pheochromocytoma, and malignant hyperthermia. Testing CBC: The WBC count will be useful to you, particularly the trend. Blood cultures: You rarely need blood cultures, but draw blood if you suspect bacteremia or if the patient has an indwelling central line. UA and urine culture: Obtain from any patient with a Foley catheter or with urinary complaints. Sputum culture: Only obtain if the patient has a significant amount of sputum and is likely to have a pulmonary infection (e.g., has physical CXR findings). Keep in mind that almost all chronic tracheostomy wounds are colonized with bacteria. CXR: Obtain on any patient with physical findings, shortness of breath, or hypoxemia. C. difficile toxin assay: Obtain on any patient with diarrhea. Neck CT scan: The decision to get a CT will usually be made in consultation with a more senior resident, but consider this in patients in whom you suspect an abscess. Venous duplex: This is used to rule out a DVT. It can usually wait until the following morning. Treatment Always order incentive spirometry and walking regimens in patients you suspect of having atelectasis. If you suspect a wound infection, consider starting antibiotics and opening the wound. If there is a fistula, open the wound near the midline of the neck to prevent oral secretions from running over the great vessels of the neck. In patients with a suspected pulmonary infection, initiate antimicrobial therapy and a mobilization routine (out of bed, incentive spirometer). In patients with UTIs, start antibiotics and consider removing their Foley catheter or changing it if there are no contraindications to doing so. In patients with indwelling lines, always consider removing the line if the patient no longer needs it. If the patient needs central access, but you believe it is possibly the source of the infection, you will need to remove the first line and place a new one. Rewiring a line is a possibility if the risk of a central puncture is deemed to be too great. In addition, consider starting IV antibiotics until you get the results of blood cultures back. This is best done in consultation with your senior resident. In a patient with suspected C. difficile colitis, start treatment with oral metronidazole (Flagyl) after the stool sample has been sent. If you suspect a patient to be septic, start broad-spectrum antibiotics and consider moving him or her to a more closely monitored setting (step down or ICU).

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CHEST PAIN

The usual response to a call from a nurse concerning a patient with chest pain is to ask for vitals signs and a stat ECG. Go directly to the patient's room. Have someone bring you the chart. Chart Review History of coronary artery disease and previous interventions (e.g., catheters, coronary artery bypass grafting) Home cardiac medications Inpatient cardiac medications Recent cardiac stresses (e.g., tachycardia, prolonged OR time) History Nature of pain: Pressure, crushing, tearing, burning. Location of pain: Substernal, jaw, left arm. Duration of pain: Find out exactly how long the pain has been there. Similar pains in past: See if the patient has felt anything similar in the past. Difficulty breathing: Find out if the patient is short of breath and if there is a pleuritic component to the chest pain. Exacerbating factors: Anything that seems to make the pain worse, such as movement of the arm, sitting up, or walking to the bathroom. Physical Exam Overall appearance: The most telling feature of the physical exam in a patient with chest pain is the view from the end of the bed. If a patient looks distressed and pale, that appearance will alert you to a more serious problem that needs immediate intervention. Pulmonary: Listen for rales, wheezes, basilar crackles, or rubs. Cardiac: Listen for the heart rate, rhythm, and new murmurs. Extremity temperature: You will be able to get a sense of distal perfusion by feeling the lower extremities. Cool, clammy skin is a sign of poor perfusion. Recent procedures: Look for signs of recent line placement or placement attempts and procedures such as thoracentesis and chest tube insertion or removal. Differential Diagnosis Cardiac Ischemia Patients who have undergone a major operation have been placed under significant physiologic stress. It is not uncommon for patients with angina to have an exacerbation of their condition in the postop period. This will usually be fairly obvious in that this group of patients will describe the pain as similar to their angina, and it will usually be relieved by nitroglycerin.
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Myocardial Infarction There is a critical difference between the patient with angina and the patient who has had or is having an MI. Patients with MIs have pain that is more severe than their typical anginal pain, and the symptoms last longer. In addition, they usually do not respond completely to nitroglycerin. However, the key feature in distinguishing the patient with angina from the patient with an MI is the difference in the ECG. Angina frequently does not change the patient's ECG, whereas most MIs change the ST segments in the territory of the vessel that is occluded. Pneumothorax The patient may have a noncardiac cause of chest pain. Patients who have had recent procedures (tracheostomy, lines, thoracentesis, chest tube removals) or failed attempts at these procedures are at risk of having a pneumothorax. In addition, any patient with intrinsic lung disease who has been intubated and undergone positive pressure ventilation in the OR may also develop a pneumothorax. You will be able to recognize this by listening to the patient's chest closely and by examining the CXR. Pulmonary Embolism Surgical patients are at increased risk of DVT and, therefore, of pulmonary embolism (PE). These patients frequently describe chest pain as their most prominent symptom rather than shortness of breath. Always have a low threshold for investigating a patient with chest pain that is pleuritic in nature for PE. Aortic Dissection Aortic dissection is much less common, but you may encounter it in blunt trauma patients. Usually it is described as an intrascapular ripping or tearing pain. This is a true emergency, so any suspicion of aortic dissection should warrant an immediate call to a more senior resident. Rib Fractures In the multitrauma patient and patients who have undergone CPR, the presence of rib fractures is often overlooked in the search for the life-threatening injuries. However, rib fractures will cause the patient great discomfort and are diagnosed by CXR. Gastroesophageal Reflux Patients who have undergone intraabdominal surgery often have some symptoms of reflux during their postop course. It presents as a burning or warm feeling in the lower chest. Any patient who has had antireflux surgery (e.g., Nissen or Toupet fundoplication) who reports chest pain should be suspected of having a slipped wrap (intrathoracic migration) until proved otherwise, which requires an upper GI contrast study.
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Testing ECG: All patients need an immediate ECG that should be compared to any available old ECG. CXR: Patients suspected of having a pneumothorax or a PE should have a stat portable CXR. Do not send patients with chest pain off the floor. Rib films: Obtain in patients with suspected rib fractures. V/Q scan: Order in patients with a clear CXR suspected of having a PE. Cardiac enzymes (CK-MB, troponin-I), CBC, and electrolytes. Treatment O2 . Nitroglycerin: Sublingual nitroglycerin should be your first-line therapy for patients suspected of having cardiac-related chest pain. Be cautious in the patient with aortic stenosis. Morphine: IV morphine is essential in the treatment of cardiac-related chest pain. Remember to use it cautiously in the elderly patient with narcotics already on board (a patient with a patient-controlled analgesia) and in those with renal failure. Aspirin: A patient with chest pain that is cardiac in etiology should receive a chewable aspirin (81 mg) as soon as possible. Postop patients can tolerate this mild anticoagulation, but in patients with a high risk of bleeding, check with your senior resident first. Antacids: Patients suspected of having simple reflux-related chest pain can be treated acutely with liquid antacids and should be placed on H2-blockers. Chest tube placement: If a patient has a pneumothorax that is large and symptomatic, the treatment is chest tube placement. Anticoagulation: If a PE is highly suspected, you should consider immediate anticoagulation. This is always a difficult decision in the postop patient who is at risk for bleeding and should never be done without first consulting with a senior resident. Cardiology consultation: If a patient is showing signs of an MI or has coronary artery disease with angina at rest, you will need the help of a cardiologist. Remember that any patient suspected of having cardiac chest pain should be made chest pain free. If this cannot be accomplished rapidly (within 20 30 mins), you will likely need cardiac consultation.
SHORTNESS OF BREATH

Your first priority when seeing the patient is to decide if he or she is in critical condition. This means the patient appears to be nearing respiratory failure and needs to be intubated and mechanically ventilated. In such an instance, bypass the steps suggested below. Remember that the first two steps in the ABCs are airway and breathing. The expression shortness of breath (SOB) means quite different things to different patients. Sometimes you will discover that the true complaint is chest pain, heartburn, or even a sore throat. If the patient does not appear in critical condition, proceed with the steps below.

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Chart Review History of COPD, emphysema, smoking, or congestive heart failure with pulmonary edema History of DVT, PE, or inferior vena cava filter placement Trend of O2 saturations, particularly preoperatively Results of most recent CXR Ease of intubation in OR (from anesthesia sheet) History How long has the patient felt poorly? Is the dyspnea getting better or worse? Has the patient ever felt this way before? Is there associated chest pain? Is that pain pleuritic? Palpitations? Has the patient been receiving his or her home pulmonary medications, if any, while in the hospital? Have home diuretics been withheld? Have there been any recent procedures or attempts (thoracentesis, central lines)? Did the onset coincide with administration of blood or a new medication? Physical Exam Make sure you know what the patient's O2 saturation is and how much O2 he or she is on. Location of incision: The patient who has had neck surgery represents an important subgroup with SOB. In these patients, the first thing you need to do is to carefully inspect the operative site. Take the dressing down and assess if there appears to be an underlying hematoma or mass effect. The feeling of dyspnea can result from airway compression in these patients, and its presence is a true surgical emergency. If there is a hematoma, swab betadine over the area and immediately open the incision. Bluntly remove the clot from the wound. When the patient has stabilized, he or she should be taken back to the OR for wound irrigation, control of the bleeding site, and closure of the wound. Tracheostomy care: In every patient with a tracheostomy tube and SOB, you must rule out the tube as the cause. There are two common tracheostomy causes of SOB. The first is a tracheal plug. This can be ruled out by removing and cleaning the tracheostomy tube (if it was not recently placed) or by passing a large-bore suction catheter down the tube. The second cause is a tracheostomy tube that is not in position in the trachea. This can be ruled out by passing a suction catheter easily through the tracheostomy tube or by viewing the position with a fiberoptic endoscope. Pulmonary exam: Listen closely for any focal findings. You need to assess if the breath sounds are equal, if there is dullness or hyperresonance to percussion, if there is wheezing or stridor, and if there are basilar rales. Cardiac exam: Listen for gallops (an S4) that can represent volume overload and congestive heart failure. Lower extremities: Look for signs of DVT that can lead to PE.

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Differential Diagnosis Pneumothorax Listen to breath sounds closely and determine if there were any preceding events that could put the patient at risk (e.g., central lines, thoracentesis). Treat immediately if the patient is deteriorating. Congestive Heart Failure Surgical patients often have large volume shifts that can push any patient with decreased cardiac function into congestive heart failure. It often occurs on postop day 3 or 4 when the patient mobilizes fluid back into the intravascular compartment. It is also possible for a patient to be pushed into volume overload by boluses of IV fluid for low urine output or hypotension. Patients routinely on large doses of diuretics who have had them withheld postop are also at risk of volume overload. Exacerbation of Chronic Obstructive Pulmonary Disease/Emphysema/Asthma Patients with underlying lung disease often have persistent or worsened symptoms while they are in the hospital. The reasons for this are multifactorial but include inadequate inhaler use, the lack of routine doses of inhaled corticosteroids, and the atelectasis that most surgical patients experience. Developing Pneumonia Patients with underlying lung disease and those with prolonged illnesses may develop a hospital-acquired pneumonia. It is often associated with sputum production and focal findings on pulmonary exam. A CXR is essential to making this diagnosis. Pulmonary Embolism There are often no physical findings, so a high index of suspicion is critical. Patients to be very concerned about are those who have hypotension or tachycardia associated with dyspnea, those who report sudden-onset SOB with pleuritic chest pain, and those with lower extremity signs of DVT. Patients at high risk for DVT (lower extremity fractures, prolonged immobilization) should also be suspected. Getting a V/Q or CT scan is always worth considering. Remember that patients with inferior vena cava filters in place can still have a PE. Myocardial Infarction Although most patients have associated chest pain, some present solely with SOB, either as an anginal equivalent or as a result of flash pulmonary edema. Consider this diagnosis in every patient and proceed with further testing when appropriate.

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Arrhythmia Remember that a tachycardia, especially rapid atrial fibrillation, can cause SOB and palpitations. Neck Hematoma An enlarging neck hematoma can obstruct the trachea by mass effect. The treatment for this is to open the wound, drain the hematoma, control the source of the bleed, and close. It is preferably done in the OR under sterile conditions. However, in a crashing patient, it should be performed emergently at the bedside. Anaphylaxis or Allergic Reaction Patients can develop SOB as the initial expression of anaphylaxis. It is usually described as throat tightness. Testing ABG: Remember to record the amount of O2 the patient is on and what the saturation reads at the time that you draw the ABG. CXR: Mandatory in most patients with SOB. Without it, you cannot exclude a pneumothorax, congestive heart failure, or pneumonia. However, even a normal CXR will not let you off the hook. The patient with a PE often has a normal CXR. ECG: Can help in the diagnosis of an atypical MI and PE (right-sided strain characteristics). It will also rule out rapid tachyarrhythmias. Get an ECG in every patient with a history of cardiac disease. Consider cardiac enzymes if the ECG is suggestive. Sputum cultures: If you think a patient has a developing pneumonia, and he or she has copious sputum production, it is useful to get a sputum culture before antimicrobial treatment is initiated. V/Q scan, CT scan, or angiography: If you suspect PE, you should first get a routine CXR and then proceed with the above tests. Which tests you perform are specific to the situation and should be discussed with a more senior resident and a radiologist. Treatment O2: All patients get placed on O2 initially. Those whose O2 saturation is persistently low after therapy should remain on it continuously. Inhaled beta-agonists: Any patient with wheezing or home use of inhalers should get treatment with inhalers or nebulized medication early in the management of SOB. Chest physiotherapy: The patient with a collapsed lobe, significant atelectasis, or lobar pneumonia may benefit from chest physiotherapy. Morphine/nitroglycerin/diuretics: Any patient with signs of congestive heart failure should be treated with this combination. Remember to use caution when giving surgical patients diuretics. It may be necessary to give several doses of diuretics on postop days 3 and 4 to avoid volume overload or to treat it once it has occurred. Antibiotics: If the patient appears to have a developing pneumonia, early antimicrobial treatment is
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important. Start broad-spectrum coverage if you believe it to be a hospital-acquired pneumonia. IV heparin: If the suspicion for a PE is high enough, therapy is often begun at the onset of symptoms, before the diagnostic testing is performed. The postop patient is at risk for bleeding complications, so this must be decided carefully and with input from your senior resident. Subcutaneous epinephrine: If a patient appears to have signs of anaphylaxis, treat early with SC epinephrine, histamine blockers, and possibly steroids.
NAUSEA AND VOMITING

The sensation of nausea is triggered in the brain and can be due to a number of psychological and physiologic factors. The initial evaluation of the patient with nausea and vomiting (N/V) should center on differentiating the truly sick from the merely nauseated. Chart Review History of N/V or vertebrobasilar problems. History of antiemetic use. Allergy history: allergies attributed to narcotics usually mean N/V. History How long has the N/V been going on? Are the symptoms related to food or medication intake? Is there a history of narcotic sensitivity? Has there been any hematemesis? Physical Exam Assess the patient's volume status carefully. Look for dry mucous membranes, low jugular venous pressure, decreased skin turgor, and lack of axillary sweat. These signs point toward significant fluid loss from emesis. Abdominal exam: Assess for distention, gastric tympany, and pain. If it has been saved, evaluate the emesis for blood, color, and medication and food particles. Differential Diagnosis Postop pain: If severe enough, pain alone can induce N/V. Medications: The common culprits are narcotics, anesthetics, oral potassium, and antibiotics. A temporal relationship will be evident. Ileus: After any abdominal surgery, especially one in which significant dissection and manipulation has been done, the GI function will be slow to recover. Delayed gastric emptying and a bloated sensation are common. It may be exacerbated by abnormal electrolytes, narcotics, antiarrhythmic agents such as calcium channel blockers, or infection. Bowel obstruction: Usually accompanied by abdominal pain. Persistent emesis, history of obstruction, or absence of bowel movements should prompt investigation. The common causes of obstruction
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include adhesions, entrapment (internal or external hernias), volvulus, diverticulitis, tumors/inflammatory conditions, and abscesses. It is an unlikely cause in an otolaryngology patient. Testing Obstructive series: This will help you make the diagnosis of ileus, obstruction, or free air. CBC: This should be obtained if there is any suspicion of infection. Electrolytes: With significant vomiting comes electrolyte disturbances, and a chemistry panel should be obtained. Treatment Nasogastric tube: This relieves the symptoms and can often be curative in situations such as isolated gastroparesis. In addition, the nasogastric tube serves as a quantifiable drain, which is especially useful in preventing electrolyte abnormalities by appropriate fluid replacement. Antiemetics: A number of medications are in common use for the treatment of nausea: Serotonin inhibitors: Ondansetron (Zofran) and other members of its class. Very effective, very safe, but very expensive. Phenothiazine derivatives: These dopaminergic agents, such as prochlorperazine (Compazine) or promethazine (Phenergan), are related to a class of antipsychotics and neuroleptics. Absolute contraindications to their use include phenothiazine hypersensitivity and agranulocytosis. As their mechanism of action suggests, extrapyramidal symptoms (tardive dyskinesia and dystonia) are possible. Anticholinergic agents such as diphenhydramine (Benadryl) or benztropine (Cogentin) can treat the acute side effects. They may also lower seizure threshold. Metoclopramide (Reglan): Mixed cholinergic and dopaminergic activity that serves to increase GI motility. This agent should never be used in the setting of intestinal obstruction. It has a role in diabetic gastroparesis. Extrapyramidal symptoms are also a possibility.
HYPOTENSION

Chart Review Review the patient's pre- and postop vital sign and urine output trends. Many people live quite comfortably with a low BP. If the alarming value you were called about is consistent with the patient's preoperative BP, there may not be a problem. On the other hand, the chronically hypertensive patient may be symptomatic with a "normal" BP. Always consider the patient's preop baseline. Review preop medications. Most BP medications are given on the morning of surgery and may have long-acting properties. Be suspicious of once-daily and extended-release preparations. Once-daily ACE inhibitors and angiotensin-II receptor blockers may be responsible for postop hypotension even if the last dose was taken up to 48 hrs previously. Check for medication and food allergies. Finally, review the operative note for any mention of complications and the anesthesia flow sheet for evidence of intraop BP lability. Consider that a "stable" patient being transferred from the recovery room may be supported by a lingering dose of pressors that will invariably wear off on arrival to the ward.
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History Is the hypotension symptomatic (dizziness, lightheadedness, headache, sweating, or nausea)? Is there associated chest pain or SOB? Physical Exam Look for pallor, cool extremities, dry mucous membranes, and other signs of dehydration or poor perfusion. Assess mental status. Look for evidence of drainage or swelling compartments that may indicate bleeding. If the patient is stable enough to tolerate the positioning, orthostatic vital signs may help you assess the severity of the hypotension. Finally, ensure that the proper BP cuff size is used. An ill-fitting cuff will lead to false results. Differential Diagnosis Hypovolemic shock: This may be due to inadequate fluid intake or excessive losses. In the immediate postop period, bleeding should be your primary concern. Cardiogenic shock: Intrinsic pump failure from MI can lead to hypotension. Extrinsic pressure on the heart from tension pneumothorax or pericardial tamponade also affects BP. Anaphylactic shock: Allergic reactions can lead to life-threatening complications, including hypotension. Neurogenic shock: Primarily a concern in the spinal cordinjured patient who may have autonomic dysfunction. Septic shock: Serious and advanced infection, especially with associated bacteremia. Endocrine: Hypothyroidism or adrenal insufficiency can cause refractory hypotension. Iatrogenic: Many medications that we give patients, especially narcotics, may cause hypotension. Also, in treating the hypertensive patient, we may overshoot and cause hypotension. Preop medications: A diagnosis of exclusion, this is the result of previously taken long-acting antihypertensives. During the periop period, the patient's physiology changes and may demonstrate an exaggerated response to a previously stable medication regimen. Testing CBC: If there is any concern for ongoing blood loss. Cardiac evaluation: Consists of an ECG, CK-MB, and troponin-I to rule out cardiac causes. CXR: Check this for pneumothorax or free intraabdominal air. Treatment Fluid bolus: 5001000 cc of normal saline can temporize the patient with hypovolemic hypotension. Remember that you may also have to increase the rate of the continuous IV infusion to avoid a recurrent problem. Pressors/inotropes: The patient with hypotension related to cardiac failure should be managed in an ICU, although some hospitals will allow you to initiate IV pressors and inotropes on the regular ward
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while awaiting transfer. Dopamine or phenylephrine may be started at low doses and titrated up to maintain an acceptable BP during transfer. Anaphylaxis therapy: Severe anaphylactic reactions require transfer to a closely monitored setting. Initial treatment should consist of SC epinephrine, an H1-blocker such as diphenhydramine (Benadryl, Benylin), an H2-blocker such as cimetidine (Tagamet, Tagamet HB), and IV corticosteroids. These patients usually require significant volume resuscitation as well. Neurogenic shock: Patients with neurogenic hypotension may be asymptomatic and often adjust to the lower BP over time. Acutely, these patients can be treated with IV pressors. Sepsis: Septic shock should be treated in the ICU and requires antibiotics, fluid resuscitation, and often pressors. Hormone replacement: IV thyroid hormone and corticosteroids should be administered where appropriate. Iatrogenic and preop medication-induced hypotension are most often self-limited. The mainstay of treatment is cessation of the offending agent and careful observation. A small fluid bolus may help to mitigate the transient hypotension.
TACHYCARDIA

There's nothing like a patient with tachycardia to start your own heart racing. A mildly elevated heart rate may signify nothing more than inadequate pain control. At its extremes, however, tachycardia can be rapidly fatal. A heart rate >150 bpm is rarely benign. This section assumes a familiarity with basic arrhythmia interpretation. Subtleties of ECG interpretation are not necessarily crucial; determine the rhythm and fix the problem. Unstable tachycardia signifies a decrease in BP or critical signs of diminished end-organ perfusion, such as chest pain, shortness of breath, or altered mental status. These findings should lead to initiation of standard advanced cardiac life support protocols (see ACLS Protocols). Chart Review
History of arrhythmia or other cardiac conditions History of cardiac surgery or pacemaker implantation Prehospital use of antiarrhythmics or rate-controlling medications Recent BP and heart rate trends Recent urine output trend

History
Subjective sensation of palpitations or "pounding heart"

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 Chest pain, SOB, or dizziness Any other pain, especially in the postop setting

Physical Exam
Assess volume status by mucous membranes and skin turgor. Tachycardia is the first sign of volume depletion. Cardiac exam: Determine whether the rhythm is regular or irregular. Lower extremities: Look for signs of DVT, as subsequent PE frequently induces tachycardia.

Differential Diagnosis Sinus Tachycardia

Inadequate pain control Volume depletion Fever/infection Anemia PE Pneumothorax

Atrial Flutter/Fibrillation Atrial flutter or fibrillation is commonly seen in elderly patients, especially those with a history of cardiac or pulmonary disease. Cardiac and thoracic surgeries increase the risk considerably. Atrial fibrillation may be considered either rate controlled or nonrate controlled. A ventricular rate of <100 bpm in an asymptomatic patient is considered stable and controlled. New-onset atrial fibrillation should be evaluated for an inciting event, such as PE, MI, hyperthyroidism, or electrolyte abnormalities. Paroxysmal Supraventricular Tachycardia Paroxysmal supraventricular tachycardia is frequently triggered by severe pain and has a ventricular rate of >150 bpm. Electrolyte abnormalities may contribute greatly. Ventricular Tachycardia Ventricular tachycardia is a true emergency, even when a pulse is present.
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Testing
ECG: Critical in evaluating the patient with tachycardia. If there will be some delay in finding a 12-lead machine, the patient can be hooked up to the cardiac monitor on the code cart. Cardiac evaluation: For anything more than pain-induced sinus tachycardia, a cardiac lab evaluation should be considered (CK-MB or troponin-I). Electrolytes: Derangements of sodium, potassium, magnesium, calcium, and phosphorus can contribute. ABG: An ABG helps to support the diagnosis of PE. Also, extremes of pH can trigger arrhythmias. V/Q scan, CT scan, or angiogram: To confirm PE.

Treatment The treatment of specific life-threatening arrhythmias is systematically presented in the American Heart Association Advanced Cardiac Life Support algorithms. However, some general principles apply:
Cardiac monitoring: Continuous cardiac monitoring should be established. The frequency of vital sign measurements must be increased, which may necessitate transfer to an ICU. O2: Begin low-flow O2 therapy until the tachycardia has resolved. Fluid bolus: If volume depletion is suspected, give a 500- or 1000-cc normal saline bolus IV. Remember that the maintenance IV infusion rate may also need to be increased. Analgesia: Adequately control pain, as this is a potent inducer of tachycardia. See the section on pain later in this chapter for more details.

Once atrial fibrillation is confirmed and the rate is controlled, consideration must be given to the long-term consequences of this arrhythmia. After approximately 72 hrs, thrombus can begin to form in the atria, predisposing to systemic embolization. If the rhythm does not spontaneously convert to sinus in that time period, the patient can be electively cardioverted. Alternatively, anticoagulation may be initiated.

HYPERTENSION

Unlike low BP, HTN is rarely an emergency. Of course, every rule has its exceptions, and patients with aortic dissections and vascular anastomoses, and those following carotid surgery should not be allowed to sustain a markedly elevated BP.

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You will be called frequently to address high BP, and you need to know which situations require intervention. Chart Review
Review recent vital sign trends. Check if the alarming BP is consistent with previous values. Home antihypertensive regimen. Inpatient antihypertensive regimen. Check if it coincides with the patient's home regimen. The timing of drug administration is important as well. The patient may be due for a scheduled antihypertensive shortly.

History
Ask about prehospital BP control. Does the patient normally run high? Are there neurologic symptoms such as headache, blurry vision, or dizziness? Is the patient experiencing chest pain or SOB? Is there an excessive amount of pain that may be contributing to the elevated BP?

Physical Exam
Assess BP in both upper extremities and compare. A systolic difference of >1020 mm Hg suggests a vascular disturbance such as dissection. Ensure that the proper-sized BP cuff is used.

Differential Diagnosis
Pain: This is likely the most common cause of postop HTN. Cardiac: Patients experiencing myocardial ischemia or infarction may have associated HTN. Essential HTN: Remember that patients may miss scheduled doses of medications due to procedures, and GI absorption may be impaired after surgery. HTN in the postop period may merely reflect inadequate control of a chronic condition. Endocrinologic disturbances: Rarely, profound hormone abnormalities may affect BP, as in hyperthyroidism or pheochromocytoma.

Testing
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 Cardiac: An ECG and cardiac enzymes should be ordered if there is concern for cardiac causes of HTN. Further ancillary testing for HTN is rarely indicated. Evaluation of essential HTN is usually not appropriate during a surgical admission.

Treatment
Analgesia: Pain should be treated rapidly and is often all that is needed for BP control. Cardiac: The management of cardiac abnormalities is covered in the section Chest Pain. Antihypertensives: Patients with essential HTN are best served by resuming their prehospital antihypertensive regimen. If the patient is shortly due for a scheduled antihypertensive, consider giving the dose early. Small doses of PO or IV antihypertensives are indicated for extremely high BP that has not yet responded to the patient's typical regimen. Clonidine (Catapres): A fast-acting, short-lived oral antihypertensive commonly used and acts as a central sympatholytic. The transdermal form is not useful acutely because of its relatively long time to onset. Hydralazine (Apresoline): IV direct vasodilator. Beta blockers: Also very effective but should only be given in a monitored setting due to their cardiac depressant and proarrhythmic potential.

Antihypertensive medications can be dangerous. Do not initiate them unless you are prepared to deal with the potential side effects. Most IV preparations should be used in a monitored setting. As a general rule, you should not start new, long-term antihypertensives. This can be done, however, in consultation with the patient's primary care provider. Most patients will tolerate several days of elevated BP during the postop period. If the patient is not symptomatic, it is often best to leave HTN untreated.

CONFUSION/MENTAL STATE CHANGE/AGITATION

General anesthesia, narcotics, and disruption of the normal sleep wake cycle contribute to the frightening loss of mental faculties. Nothing is scarier for a patient than to be in a strange place, in pain, and completely disoriented. Don't forget the family, who is seeing a loved one change before their eyes. No other problem will challenge both your medical and social skills as much as mental status change. Chart Review

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 History of neurologic disorders (e.g., senile dementia, Alzheimer's disease, seizures) History of prescription or illicit psychoactive drug use History of alcohol use Type and quantity of anesthetic drugs and postop narcotics and sedatives History Understand that the confused patient will always be frightened and sometimes verbally and physically abusive. Try to get a sense of whether the patient's disorientation includes paranoia, which will make the situation more difficult. It may be difficult to get direct answers from these patients, but try to gain an idea of the severity of their mental deficit. Ask the typical "alert and oriented 3" questions: name, place, and date. See if the patient understands the reason for being in the hospital. Physical Exam Again, the disoriented patient may not allow you to get close enough for a physical exam. Additionally, your own safety may be in doubt when dealing with an abusive patient. Do your best to perform a focused physical exam while disturbing the patient as little as possible. Look for signs of lateralizing neurologic findings. A facial droop, slurred speech, or weak extremity strongly suggests a stroke. Examine incisions and catheter sites for evidence of infection. Examine the head for evidence of a fall that has led to intracranial injury. Differential Diagnosis Hypoxemia: A low O2 saturation can lead to mental status changes, but remember to determine and fix the underlying cause of the hypoxemia. Hypoglycemia. Stroke or TIA: Suggested by lateralizing neurologic signs as mentioned above. Seizure: Classic seizure pattern includes a postictal stage of variable length characterized by lethargy and confusion. Infection: Mental status changes may be the only indication of occult infection. Medication: Especially narcotics and anesthetic agents. Alcohol or substance withdrawal: Chronic alcohol use is a significant risk factor for head and neck cancer. Therefore, it is not at all uncommon for postop cancer resection patients to withdraw from alcohol. "ICU psychosis": This is more often found in elderly patients who have been in intensive care or otherwise loud and disorienting settings. Testing Pulse oximetry and bedside glucosecheck: Should be performed immediately, as hypoxemia and hypoglycemia are easily correctable causes of confusion.
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 CBC: An elevated WBC count helps lead to the diagnosis of infection. Blood cultures can also be obtained. Electrolytes: An electrolyte panel should be ordered to check for hypo- or hypernatremia. Head CT: Have a low threshold for requesting a noncontrast head CT to rule out bleeding or elevated intracranial pressure. Drug levels: If the patient takes anticonvulsants, check serum levels of those drugs. Lumbar puncture: Although the incidence of meningitis is quite low on a surgical service, a lumbar puncture is at times indicated. Treatment First and foremost, ensure the patient's safety. Sometimes a soothing voice or the presence of a family member is all it takes to calm the agitated patient. If necessary, physical or chemical restraints can be used temporarily and only as a last resort. Restraining a patient is a serious matter and should be accompanied by frequent reevaluations. Supplemental O2 and dextrose should be given as indicated. Correction of electrolytes should also be undertaken. Once the patient recovers, do not forget to assess for the underlying cause of the metabolic disturbance. Acute stroke is an indication for an emergency neurology consult. A minority of patients may be candidates for thrombolytic therapy and anticoagulation. Once the diagnosis of stroke is confirmed, request physical, occupational, or speech therapy consults. Alcohol withdrawal can lead to life-threatening delirium tremens if not recognized and treated promptly. Benzodiazepines are used for agitation, and clonidine may be added to treat sympathetic hyperactivity. Treat infections as indicated. Indwelling central lines should be changed, and empiric antibiotics may be started if suspicion is high. Remember to obtain microbiology studies before the first dose of antibiotic is administered. If the patient remains a threat to himself or herself, or if the patient is a threat to others, consider asking a staff member to stay in the room. The staff member can verbally redirect the patient and prevent him or her from pulling out tubes and lines. Medications: Should be used cautiously and sparingly for agitation. Benzodiazepines: Very effective when administered IV. Avoid in the elderly. Haloperidol (Haldol): This antipsychotics can be given IV or IM if the patient has pulled out the IV. Avoid in the elderly. Atypical antipsychotics: Oral drugs, such as olanzapine (Zyprexa, Zyprexa Zydis), risperidone (Risperdal), and quetiapine (Seroquel), are generally safer in the elderly but require several days to take effect. Try to minimize disruptions and maintain a normal sleepwake cycle. If the patient is hemodynamically stable, you may be able to decrease the frequency of vital sign measurements. Try to move the patient closer to a window, and keep the lights off overnight.
INSOMNIA

The environment in the hospital is, in general, not conducive to sleep for your patients. They will frequently request a pill to help them get to sleep at night. They are under
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physiologic stress and need sleep to help them heal. Although it is tempting to give a sleeping pill to any patient who requests it, this is not always a prudent thing to do. Consider the following when deciding whether to administer a "sleeper": Patient age: Older patients can react poorly to most sleep-inducing medications, particularly benzodiazepines. They can become confused and disoriented. This is certainly worse than their not getting enough sleep. In general, we suggest avoiding giving older patients any sleeping pills. The only exception is in patients who take one routinely at home and know their medication type and dose. If you do give a new medication to an older patient, do so cautiously and warn them of potential side effects. Pulmonary function: Most sleeping pills depress respiratory drive to some extent. Any patient with underlying pulmonary disease (COPD, emphysema, obstructive sleep apnea) and those who have undergone thoracic surgery are at particularly high risk from this complication. Do not take risks in these fragile patients. Concomitant medications: Most surgical patients are receiving some form of parenteral narcotic for pain. Benzodiazepines act synergistically with narcotics. Thus, even a small dose of a benzodiazepine can have significant effects in a patient receiving IV narcotics. Reason for request: Although it seems obvious why the patient is requesting a medication, the real problem may be something other than insomnia. Often the patient can't sleep because of uncontrolled pain, need for frequent urination, a loud roommate, a hallway light, or a loud nurses' station. These problems should not be solved by administering a potentially dangerous medication. Do the right thing for your patient even if it is not as easy as writing a quick order. This may mean helping to arrange a room transfer, turning off lights, or placing a Foley catheter. If you do decide to give the appropriate patient a sleeping pill, you should consider carefully which pill to give. The available classes are basically benzodiazepines (and benzodiazepinelike medications) and histamine antagonists. Examples of frequently used medications include diphenhydramine (2550 mg), temazepam (Restoril) (1530 mg), triazolam (Halcion) (0.125 mg), and zolpidem tartrate (Ambien) (510 mg). If you decide not to give a patient a sleeping pill, it is important to explain to the patient why you are not able to honor his or her request. Patients are frequently understanding if you take a minute to explain your concerns about side effects.
WOUND DRAINAGE

Wound problems are common postop occurrences and range from mild drainage to overt dehiscence. Additionally, wounds may become infected, and careful inspection should be a part of the physical exam of every postop patient. Drainage from a wound is quite common immediately after surgery. Thin drainage is usually caused by irrigation fluid used intraop that leaks out over the first 12 days. Thicker or bloody drainage is more concerning. A small amount of postop bleeding is expected and is most often the result of SC bleeding that will stop spontaneously. Nurses often circle the stain on the bandage early on as a means of judging its spread over time.
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 Thin or serous drainage can be left alone. When a dressing becomes soaked and must be replaced, this should be done under sterile conditions. Bleeding from a wound should be closely monitored. It can reflect serious neck hemorrhage or merely minor superficial oozing. If the bleeding continues or the patient becomes hemodynamically unstable, a CBC should be sent to assess the magnitude of blood loss. A PT and PTT may be requested if there is concern for coagulopathy. In some instances, a patient may need reoperation to treat bleeding. Wound drainage that begins several days postop should be considered infection until proved otherwise. Other local signs of infection include erythema, pain, and fluctuance. If the drainage point can be localized, the wound is often opened at this site by removing staples or sutures. The wound can then be probed to assess the extent of infection. SC fluid collections should generally not be cultured, as contaminating skin flora make interpretation difficult. Wound infections are most often caused by gram-positive bacteria. Most patients should be started on appropriate antibiotics, and the wound should be packed with a dressing and allowed to heal by secondary intention. An orocutaneous fistula should be considered in any patient with would drainage who had a pharyngotomy during surgery. Fistulas should be suspected when there is fluid that is purulent or resembles saliva. These wound infections are caused by mixed aerobic/anaerobic oral flora. The drainage can be sent for amylase if you are unsure if there is a fistula.
LOST IV ACCESS

One of the most frequent calls you will get as an intern will concern the loss of IV access. The fundamental issue at stake is actually one of safety. If a patient does not have an indwelling IV line in place, the delivery of medications and fluid is impossible. Your job when called about a lost IV is first to clarify whether the patient in fact needs an IV. If this is indeed true (and it almost always is), then reestablish access, either peripherally or centrally. Does the Patient Need an IV? Almost all surgical patients will need an IV while in the hospital. There are, however, some exceptions. Patients who are eating and drinking, not receiving important IV medications, and who are clinically stable may be able to avoid having an IV replaced. The most common example is the patient who is to be discharged within the next 24 hrs. Patients who are within the first 48 hrs of their postop course (unless the operation was minor) should always have an IV. Make sure your patient does not have an SC Port-a-cath or indwelling central line before deciding to replace an IV. What Kind of Access Does the Patient Need? Once you have determined that your patient indeed needs IV access, you need to decide whether he or she needs peripheral or central access. Central access is needed in patients on total parenteral nutrition, patients who need measurement of central venous pressure, patients receiving certain medications (e.g., pressors, some chemotherapy), and patients who need frequent blood draws and have exhausted their peripheral access. Most patients need only peripheral access.
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How Do I Establish a Peripheral IV? Most interns believe that if the nurse (especially the IV nurse) cannot establish a peripheral IV, a peripheral IV cannot be established. This is absolutely not true. Any time you are faced with this problem, you must assess the peripheral veins yourself. At a minimum, you must look for any available vein. You will be surprised at the number of times you will succeed. Before placing an IV, make sure you know how large an IV is needed. If the patient is to receive a blood transfusion, you need a minimum of an 18-gauge IV. Establishing a Central Line Before deciding to establish central access, you will need to get the patient's consent and discuss it with a senior resident. If you have not had adequate training or do not feel comfortable with placing a central line, you will need to call for help.

PAIN

Pain is the one symptom that all surgical patients share. Simply ordering a dose of morphine in response to every call about a patient in pain is not adequate patient care. Evaluate the Patient Take a brief history from the patient. Examine the operative site. Look for co-contributors to the pain. Check the vital signs. Assess the amount of medication the patient has received so far. Determine the Cause Although it may seem obvious that pain is from the operative incision, it is not always the case. At times, pain can be secondary to a postop complication, such as intraabdominal bleeding. Other potential etiologies include Ineffective delivery of prior pain medication [infiltrated IV, patient-controlled analgesia (PCA) not available, misplaced epidural] Tolerance to narcotics (in drug users and alcoholics) Complications (bleeding, missed diagnosis) Local problems (tight-fitting dressing, patient malposition, Foley catheter)

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Determine the Severity Ask the patient to rate the pain on a scale from 110, with 10 being the most severe pain. Follow this over time so you will know how effective your interventions have been. Also assess the vital signs to see if the patient is markedly tachycardic. Treat the Pain There are many different ways to treat the pain, but the most important thing is to initiate treatment promptly. Consider the following when deciding what medication to deliver: Method of Delivery Intermittent IV dosing by nurse PCA Local delivery of anesthesia (epidural, local blocks) Oral medications Type of Medication Narcotics Local anesthetics NSAIDs Acetaminophen Patient Comorbidities Renal failure Hepatic insufficiency Patient age Bleeding potential In General There is no one specific way to treat pain, but here are some general principles to get you started: Start with an IV narcotic in a dose that is appropriate for the patient's age and pain severity. Usually this means morphine in 2- to 4-mg doses. In the elderly, start with 1 mg. In the patient with renal failure or hepatic insufficiency, narcotics need to be carefully selected. The best choices are fentanyl (Sublimaze) and hydromorphone (Dilaudid) due to problems with poor clearance. In renal failure, accumulated metabolites of meperidine (Demerol) lower the seizure threshold. NSAIDs should be given judiciously due to renal and platelet side effects. However, a dose of ketorolac tromethamine (Toradol) can be a miraculous thing to the postop patient in pain. Patients who have a PCA but have ongoing pain are difficult to deal with. You need to assess the
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degree of narcotization (pupil size, respiratory rate) and their understanding of how to use the PCA. If they have been getting the maximum dosage and are not overnarcotized, then the appropriate move is to give them several extra doses until they are comfortable and then to increase the dose of the PCA (not the interval). It is unwise to give a basal rate on a PCA in most situations. Patients who are refractory to narcotics and NSAIDs but who have substantial pain are good candidates to consider for an epidural placement. Call your pain team or anesthesia team to help in this decision. Patients with preop epidurals need to have their epidural tested to make sure it is positioned properly if the pain control is inadequate. Consider giving oral pain medications when the pain is not severe and when the patient is tolerating oral intake. Giving oral pain medications to patients who are NPO often leads to N/V. Assess the Response to Therapy After treating an acute episode of pain, you should later assess for overnarcotization and effective pain control. Finally, the most important aspect of reassessing the patient is to make sure the patient understands that you are an ally in terms of fighting the pain. Too often, the patient will feel left to suffer and that no one is concerned about his or her discomfort.

PATIENT DOES NOT LOOK RIGHT

"The patient doesn't look right." These are dreaded words to hear. Over the telephone, they provide little information. The bottom line: Go see the patient. The first questions you ask will determine the speed at which you go to the bedside. As vital signs are crucial, obtain them immediately. Go through the ABCs. Is the patient awake or obtunded; is the patient responsive; and is the patient breathing with normal vital signs? This basic triage information can be obtained over the telephone and guides the rapidity of your arrival at the bedside. When an experienced nurse calls, this implies the patient is sick, and a physician needs to be at the bedside. When an inexperienced nurse calls, this means he or she has no idea what is going on and needs a physician to evaluate the patient. Once at the bedside, use the standard approach of the ABCs, look at the chart, and follow the vital sign trends. Think about the comorbid conditions and the potential complications of the procedure performed. The patients we have are getting older and sicker. New problems constantly arise. For example, it would not be unusual for an 80-yr-old after a cholecystectomy to have a stroke; 80-yr-olds have strokes.

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PEADIATRIC OTOLARYNGOLOGY
One of the enriching characteristics of otolaryngology is the opportunity to care for infants and children as well as adults. Children make up a substantial percentage of the average otolaryngologist's practice. In addition, children often cannot or will not give a good history. Therefore, it is important to have a solid understanding of the diseases that affect children. It is important to keep a number of things in mind when caring for children. First, they are often afraid of being in the hospital or office; it is important to gain their trust early in the encounter. Second, it is equally important to gain the trust of the parents. Third, remember that children are not little adults. They have a separate set of pathologies that require a different mindset to treat. Also, children (particularly infants) do not have the reserve that adults have. This is especially obvious when dealing with a child's airway. A small amount of edema can obstruct a child's airway; children desaturate extremely quickly when they stop ventilating. For these reasons, it is a good idea to keep your senior resident and attending closely involved if there is any change in the status of a pediatric patient.

PEADIATRIC NECK MASS

Introduction and Presentation There are numerous causes of neck masses in children. Thus, it is important to have an orderly means of classifying them. Neck masses can be broken into four main groups: congenital, infectious, autoimmune, and malignant. Congenital Masses and Cysts Branchial Cleft Cysts Branchial cleft cysts account for 33% of congenital masses. They typically present as lateral neck masses or a fistula that drains to the skin. First Branchial Cleft Cyst Type I: A duplication of membranous external auditory canal of ectodermal origin. It is typically medial to the concha and may extend to the postauricular region. This lesion is superior to the facial nerve. Type II: A mesodermal and ectodermal duplication of the external auditory canal. This tract occurs at the level of the mandible and may approximate the facial nerve, and excision may encompass superficial parotidectomy.

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Second Branchial Cleft Cyst A second branchial cyst, the most common, is in the high cervical (level II) region, deep to the anterior sternocleidomastoid, lateral to the carotid bifurcation. The tract goes between internal and external carotid, lateral to hypoglossal nerve, and empties into tonsil fossa. Third Branchial Cleft Cyst The third branchial cleft cyst presents in the lower neck. It is uncommon. Thyroglossal Duct Cysts Thyroglossal duct cysts account for 33% of congenital masses. They present as a midline neck mass that moves with swallowing and occur near the hyoid. Thyroid tissue may be found in 40% and may be the only thyroid tissue. Therefore, an U/S or radionucleotide scan is recommended before excision. A Sistrunk procedure includes resection of the hyoid midportion, and the tract may be followed to the tongue (foramen cecum). There is a recurrence rate of 10% after excision. Dermoid Cyst A dermoid cyst presents as a midline mass and is an epithelium-lined cyst with desquamated keratin debris inside. Thymic Cyst A thymic cyst is a remnant of the third pharyngeal pouch. They are usually unilateral and 90% cystic. Pathology shows Hassall's corpuscles. Lymphangiomas (Cystic Hygromas) Lymphangiomas present as a lateral neck mass above the clavicle. They are filled with clear or yellow lymph fluid and, therefore, transilluminate on exam. Often, they wrap around vital structures of the neck and can, therefore, be difficult to remove. Laryngoceles A laryngocele is a dilation of the saccule. Internal: within thyroid cartilage External: extrudes through the cricothyroid membrane as a midline neck mass

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Hemangiomas A hemangioma is a benign proliferation of blood vessels. It typically grows rapidly until 12 mos of age and begins to involute at 1824 mos. The size may expand with crying or straining. Teratomas Teratomas are neck masses that contain at least one germ layer (may contain hair, teeth, and so forth). Congenital Torticollis The child with congenital torticollis presents with a firm, painless mass of anterior sternocleidomastoid at 18 wks of age. The mass increases in size over 2 mos, involutes over 48 mos, and disappears completely in >80%. Infectious Mass/Lymphadenitis A pathologic node is a lymph node >1 cm. A single enlarged node should be treated as infectious, and the child should be given a trial of antibiotics that cover Staphylococcus and Streptococcus pathogens. If the node continues to enlarge or does not begin to resolve after 1 mo, then the options include serologies, imaging, aspirating, or excision. Differential Diagnosis Suppurative lymphadenopathy: Common in children, usually Staphylococcus aureus or Streptococcus. Cat scratch (Bartonella henselae) occurs usually at submandibular or high cervical neck. Serologies are diagnostic. No treatment necessary. Atypical Mycobacterium (M. avium complex, M. fortuitum, M. kansasii) presents as slowly enlarging upper cervical or submandibular triangle node. Patients may have violaceous skin changes, and 50% will have a moderate PPD induration (10 mm). With M. tuberculosis, the child presents with constitutional symptoms (50%) (fever, malaise, weight loss) and a history of immigration or known exposure (7090%). The incidence of tuberculosis increases with age. In infections caused by Mycobacterium in children >12 yrs, M. tuberculosis was the pathogen in 90%, whereas in children <12 yrs, in 90% the organism was atypical Mycobacterium. M. tuberculosis cervical lymphadenitis is bilateral in 30%, and 20% have an abscess or draining sinus tract (scrofula). 70100% have 15-mm induration on PPD. Treat medically. Tularemia is transmitted by rabbits, ticks, or contaminated water. The child presents with fever, tonsillitis, and fevers. Check serology titers. It is treated with IM streptomycin. Brucellosis is a gram-negative bacilli transmitted by unpasteurized milk. The child presents with generalized lymphadenopathy. Check serology. If the patient is <9 yrs, treat with TMP-SMX (Bactrim); if older, treat with tetracycline (discolors teeth in patients <8 yrs old). Viral: Usually presents as multiple enlarged nodes, not a single node. Viral adenitis: Caused by adenovirus, measles, mumps, rubella, and varicella. Mononucleosis (Epstein-Barr virus): Exudative tonsillitis with fever, malaise, hepatosplenomegaly,
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and atypical lymphocytosis. If these children are treated with penicillin, approximately 50% will develop a rash. CMV: Similar to mononucleosis. AIDS: Diffuse adenopathy of posterior triangle. Inflammatory and Autoimmune Causes of Masses Kawasaki's Mucocutaneous Lymphadenitis Usually occurs in children <5 yrs. It is a multisystem vasculitis. Child presents with a history of 5 days of fever and four of the following: Acute, nonsuppurative lymphadenopathy Erythema and desquamation of hands and feet Polymorphous exanthem Bilateral painless conjunctivitis Cheilitis erythema of lips Sequelae consist of thrombocytosis, pericardial effusion, and subacute coronary artery aneurysms in 15%. Therapy consists of aspirin and possibly gamma globulin. Sarcoid Multisystem Nonsuppurative Granulomatous Disease Diagnosed by lymph node biopsy and presents with a combination of the following: Bilateral nontender cervical lymphadenopathy Fever Weight loss Cough Uveitis Retinitis Parotid or neck masses Possible facial nerve palsy Malignancy Malignancy is rare in the pediatric population. The more common malignancies are lymphoma, rhabdomyosarcoma, and neuroblastoma. Check the CBC with differential, CXR, and MRI or CT scan. Consider surgical excision vs radiation vs chemotherapy.

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PEADIATRIC AIRWAY
Managing a pediatric airway can be quite tricky. In addition, children have poor pulmonary and cardiac reserve. Therefore, an inappropriately managed airway can quickly cause cardiopulmonary collapse. Anatomy The infant airway is predisposed to obstruction due to Relatively large head and oropharynx to small size of larynx and trachea. Pliability of airway (it can collapse on itself). Upper respiratory infections and airway edema (common in children). Increased chest wall compliance; respiratory muscles fatigue easily. >90% of preterm newborns and 20% of full-term newborns are obligate nasal breathers. Obligate nasal breathing usually resolves by 4 mos of age. Terminology of Airway Sounds Stertor: A term to describe snoring type of sound; implies nasopharyngeal obstruction such as in obstructive sleep apnea. Stridor: High-pitched noise caused by turbulent airflow through a narrow opening. Inspiratory: Near cords or above, seen in subglottic or laryngeal obstruction (subglottic stenosis, laryngomalacia). Biphasic: High or midtracheal obstruction (tracheomalacia). Prolonged expiratory phase: Tracheal and bronchial obstruction. Aspiration or cough: Possible sign of foreign body, reflux, tracheoesophageal fistula, laryngeal cleft, or vocal cord palsy. Causes of Stridor in Newborns 60% of stridor cases in the newborn occur at the level of the larynx. Laryngomalacia accounts for 60% of this subgroup. Laryngomalacia is an abnormal redundancy or prolapsing of larynx. On fiberoptic exam, one typically sees an omega-shaped epiglottis and infolding of arytenoids with inspiration. Child presents with stridor a few days to weeks after birth. Stridor is worse with supine position, feeding, and crying. Treatment is reassurance of parents that symptoms improve with age and resolve by 12 mos. However, in severe cases (cyanosis, cardiopulmonary HTN, failure to thrive), an endoscopic epiglottoplasty or division of aryepiglottic folds may be performed. Subglottic stenosis is the second most frequent laryngeal cause of stridor at 20% of cases. Vocal cord palsy accounts for 13%. Left cord paralysis is more common than right. Usually caused by birth trauma and recovers in 69 mos. Bilateral vocal cord paralysis is commonly associated with neurologic abnormalities such as Arnold133

Chiari malformation or hydrocephalus. The remaining 7% of cases are from laryngeal webs, cysts, or atresia. Recurrent laryngeal papillomatosis has been linked to the human papillomavirus. Management consists of repeated vaporization by laser or endoscopic dbridement when the child is symptomatic. Interferon-alpha may help slow the regrowth of the papillomas. This condition usually improves after puberty. 15% of stridor cases are tracheal in origin. Tracheomalacia accounts for 45% of this subgroup. Vascular compression accounts for 45% of this subgroup. Tracheal stenosis accounts for 10% of this subgroup. 5% of stridor cases are bronchial in origin, 5% are infectious in origin, and 15% have other causes. Miscellaneous Causes of Airway Obstruction Pierre-Robin Sequence Upper airway obstruction caused by mandibular hypoplasia, glossoptosis, and incomplete U-shaped cleft palate. Treat expectantly by prone position. Airway usually improves by 6 mos of age. Child may need nasopharyngeal airway, intubation, or tracheostomy. Gastroesophageal Reflux Extremely common in children. Gastroesophageal reflux disease may cause upper airway edema or exacerbate underlying problems, such as laryngomalacia and subglottic stenosis. The gold standard for diagnosis is a 24-hr pH dual-probe study and a mucosal biopsy. Treatment of gastroesophageal reflux disease ranges from changes of daily habits (elevating head of bed, thickening feed, shorter and more frequent feeds) to medical therapy to surgery (fundoplication).

ENDOTRACHEAL INTUBATION IN NEWBORNS

Newborns <6 mos of age tolerate prolonged endotracheal intubation. A tracheostomy should be considered depending on the infant's medical and neurologic condition, or if the infant is >6 mos of age and requires >1014 days of intubation. Formulas for estimating ETT size: Uncuffed tube if <8 yrs of age (cricoid narrower than vocal cords) Tube that correlates to the size of the child's finger ETT size = (age + 16)/4 (e.g., a 4-yr-old should have a size 5 ETT) Placement of the ETT = ETT size 3 (e.g., a size 4 tube should be 12 cm at the teeth/lips)

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STRIDOR AND RESPIRATORY DISTRESS

Differential Diagnosis of Stridor and Respiratory Distress Croup (viral laryngotracheitis) Cause: Parainfluenza, influenza, respiratory syncytial virus Age: 3 mos3 yrs Signs and symptoms: Barking cough, low-grade fever, coryza, hoarse voice, winter/spring peak Airway film: Unnecessary (steeple sign unreliable) Treatment: Cool mist tent, epinephrine, steroids, Ribavirin if respiratory syncytial virus positive Bacterial tracheitis Cause: Viral prodromepositive, Staphylococci, Streptococci, H. influenzae, Escherichia coli Age: 3 mos3 yrs Signs and symptoms: Improving croup then sudden increase: temperature, work of breathing, stridor, no drooling, fall/winter peak Airway film: Pseudomembrane may give soft tissue shadow Treatment: Intubation, antibiotics Retropharyngeal abscess Cause: Beta-hemolytic streptococci anaerobes Age: 6 mos3 yrs Signs and symptoms: Initial upper respiratory illness, drooling, toxic appearance, stridor, dysphagia, odynophagia Airway film: Radiograph shows retropharyngeal soft tissue mass Treatment: Surgical drainage, antibiotics

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Epiglottitis Cause: Haemophilus influenzae, Staphylococci, Streptococci Age: 27 yrs Signs and symptoms: Sudden onset of high fever, toxic appearance, dysphagia, stridor, drooling, "sniffing" position, no cough Airway film: Do not send to x-ray unless airway can be secured (thumbprint sign) Treatment: Never examine orally unless prepared to intubate. Intubation, antibiotics

OTITIS MEDIA IN CHILDREN

By age 3 yrs, 80% of children will have had at least one episode of otitis media (OM). Eustachian tube development plays a role in the etiology. The eustachian tube lies horizontally at birth and is 50% of its adult length; therefore, it is not as effective. The most common organisms in acute OM are Streptococcus pneumoniae Haemophilus influenzae Moraxella catarrhalis Indications for tympanostomy tube placement: Severe OM unresponsive to medical therapy or impending complication Recurrent acute OM (more than four episodes in 6 mos or six episodes in 12 mos) Chronic OM with effusion present >3 mos (with >30-dB hearing loss) Chronic retraction pocket Barotitis media Eustachian tube dysfunction causing autophony OM with effusion is the presence of nonpurulent fluid in the middle ear space. It resolves in 80% of children by 2 mos. Treatment is by expectant management. Some advocate a short-term course of antibiotics to hasten the clearance of the effusion. The use of steroids, decongestants, and antihistamines is controversial.

ADENOTONSILLAR DISEASE
Blood supply to tonsil is from five arteries: Facial artery (tonsillar branch) Dorsal lingual artery Ascending palatine artery Lesser palatine artery
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 Ascending pharyngeal artery Tonsillar Hypertrophy Grading 1+ tonsil obstructs 025% to midline 2+ = 2550% 3+ = 5075% 4+ = 75100% Tonsillectomy Indications from the American Academy of OtolaryngologyHead and Neck Surgery Recurrent infections Seven episodes of acute tonsillitis in a 12-mo period, or Five episodes of acute tonsillitis/yr for 2 consecutive yrs, or Three episodes of acute tonsillitis/yr for 3 consecutive yrs Tonsillar hypertrophy causing Upper airway obstruction with evidence of adenotonsillar hypertrophy. For obstructive sleep apnea, it is important to document the following: History of constant or near-constant snoring Mouth breathing Sleep disturbance Enuresis Respiratory distress Choking or gagging Poor sleep architecture and frequent awakenings Nightmares Dysphagia Cardiopulmonary complications Dental malocclusion documented by dentist Chronic tonsillitis with persistent foul taste or halitosis unresponsive to medical treatment. Chronic/recurrent tonsillitis in Streptococcus carrier unresponsive to beta-lactamase antibiotics. Peritonsillar abscess unresponsive to medical treatment. Lifetime recurrence risk is 10%. Suspected neoplasm: unilateral hypertrophy. Complications of Tonsillectomy Postop hemorrhage occurs in 25%. Airway obstruction. Pulmonary edema. Nasopharyngeal stenosis (linked to aggressive cauterization of the adenoid bed). Velopharyngeal incompetence in 1/1000 patients. Atlantoaxial subluxation (Grisel's syndrome), particularly in Down syndrome.

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VELOPHARYNGEAL INCOMPETENCE
Entity in which the velopharyngeal sphincter does not close appropriately, resulting in hypernasal voice and nasopharyngeal reflux Causes Neurologic, cerebrovascular accident Congenital Submucous cleft Iatrogenic (resulting usually from adenoidectomy) Down syndrome Velocardial facial syndrome Velopharyngeal Sphincter Formed by the following: Superior constrictor fibers (Passavant's ridge) Tensor veli palatini Levator veli palatini Muscular uvula Palatoglossus (anterior tonsil pillar) Palatopharyngeus (posterior tonsil pillar) Treatment Speech therapy is usually the first step. It is often sufficient to correct the defect. Obturator to lengthen palate. Surgical therapy Pharyngoplasty Pharyngeal flap Palatal lift Augmentation of posterior pharyngeal wall (Passavant's ridge)

CLEFT LIP AND PALATE

Terms Complete cleft lip: involves entire lip and alveolar arch Incomplete cleft lip: involves portion of lip Primary cleft palate: anterior to incisive foramen Secondary cleft palate: posterior to incisive foramen Submucous cleft palate: intact mucosa with deficiency in muscles; bifid uvula, notching of posterior hard palate, muscular diastasis, zona pellucida, blue midline streak
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Embryology Craniofacial development occurs at 48 wks' gestation. Primary palate is formed by fusion of the medial nasal prominences. Secondary palate is formed by fusion of the lateral palatine processes. Incidence 1/1000 births and increased in Native Americans and Asians. 80% are unilateral; 20% are bilateral. Etiology 3060% of clefts are syndromic. Other causative factors: Phenytoin Methotrexate Cigarette use Alcohol abuse There is documented decreased risk with maternal use of folic acid. Otitis media with effusion is common with cleft palate. Cleft Lip Repair Rule of 10s: surgery when infant is >10 wks old, weighs >10 lbs, and Hgb >10 Lip adhesiolysis Rotation advancement (Millard's technique) Triangular flaps (Tennison-Randall) Cleft Palate Repair Levator sling reconstruction is essential. Surgery is performed near 18 mos of age because repair at an earlier age allows for better speech but may hinder facial growth. Furrows palatoplasty (double reversing Z-plasty). V-Y pushback technique. von Langenbeck's palatoplasty: bipedicled mucoperiosteal flap. Schweckendieck procedure: primary veloplasty with closure of velum at 412 mos.

CONGENITAL INFORMATION: TRACHEOESOPHAGEAL FISTULAS

85% of cases are esophageal atresia with distal tracheoesophageal fistula (TEF). X-ray reveals stomach filled with air. 7% of cases are esophageal atresia without fistula (no air in stomach). 5% of cases are TEF without atresia (H-type). <5% of cases are esophageal atresia with proximal and distal TEF. 1% of cases are esophageal atresia with proximal TEF (no air in stomach).
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CONGENITAL INFORMATION: EXTERNAL EAR MALFORMATIONS

Prominent ear occurs when the antihelical fold is missing. Cup ear (lop ear) deformity occurs when the upper two-thirds of the auricle is bent forward >90 degrees from the mastoid. Microtia occurs when the auricle is not developed. It can occur with or without canal atresia (lack of external auditory canal). Microtia is graded from grade I (appears almost normal) and grade II ("question mark" appearance of pinna) to grade III (a small lobule or skin tag where the auricle should be).

CONGENITAL INFORMATION: CHOANAL ATRESIA

Occurs when the bucconasal membrane does not rupture Affects girls to boys 2:1 >80% bony atresia; <20% membranous atresia 80% unilateral; 20% bilateral Presents as respiratory distress at birth or with feeding because of obligate nasal breathing

HEAD AND NECK MALIGNANCIES IN CHILDREN

Head and neck malignancies account for <5% of childhood cancers. Lymphoma: 60% Rhabdomyosarcoma: 15% Thyroid cancer: 13% Neuroblastoma: 5% Nasopharyngeal carcinoma: <5% Soft tissue sarcomas: <5% Salivary gland cancers: 2% Malignant teratomas: 1%

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