DrRajiniENT

VERTIGO (GIDDINESS MANAGEMENT)
THE ABILITY OF NORMAL PEOPLE TO ORIENT THEMSELVES IN SPACE DEPENDS ON INFORMATION FROM THREE SETS OF SENSORS.
FIRSTLY-EYES (OPTO KINETIC)
SECONDLY- FROM THE BODY MUSCLES (PROPRIOCEPTORS)
THIRDLY- SEMI CIRCULAR CANALS IN THE INNER EAR CALLED “VESTIBULAR SYSTEM”

VERTIGO IS ONLY A SYMPTOM AND NOT A DISEASE.THERE ARE MAINLY THREE TYPES OF VERTIGO(DIZZINESS0
1.OBJECTIVE: PERSON FEELS THAT THE OBJECT AROUND HIM KEEPS ON MOVING.
2.SUBJECTIVE: PERSON FEELS THAT HIS HEAD IS ROTATING.
3.POSITIONAL:WHEN HIS BODY OR HEAD POSITION CHANGES(TURNING-BENDING)

SOMETIMES THIS SENSATION APPEAR ASSOCIATED WITH NAUSEA,VOMITTING,RINGING SOUND IN THE EAR(TINNITUS) WITH FULLNESS IN HEAD OR LOSS OF HEARING(MENIERS DISEASE)
SOME OTHERS NARRATE AS IF THEY TEND TO FALL WHILE WALKING(IMBALANCE).
THIS SYMPTOM MAY APPEAR INCASE OF VARIATIONS IN BLOOD PRESSURE .DIABETES MELLITUS OR EVEN WITH CASES OF CERVICAL SPONDY-LOSIS AND EVEN WITH VARYING ATMOSPHERIC PRESSURE(FLYING).HAEMODYNAMIC CHANGES,FUNCTIONS OF CAROTID & VERTEBRAL BLOOD SUPPLY TO THE BRAIN.
THEREFORE A PERSON SUFFERING FROM GIDDINESS NEEDS TO BE EVALUATED BY A PHYSICIAN,NEUROLOGIST.AN ENT SURGEON TO FIND OUT THE UNDERLINED PATHOLOGY AND FACE TREATMENT.THERE ARE MANY PEOPLE WHO ARE ON CONTINUOUS MEDICATION WITH AFEWAVAILABLE DRUGS.BUT WITH NO SIGNIFICANT IMPROVEMENT IN THE SENSITIVITY OF GIDDINESS.
BEFORE STARTING THE TREATMENT FOR GIDDINESS THE FOLLOWING INVESTIGATIONS ARE ESSENTIAL,
1. DETAILED HISTORY OF CASES
2. ENT OPINION AND OPTHALMOLOGY REPORT.
3. PURETONE AND SPEECH AUDIOMETRY.
4. IMPEDENCE AUDIOMETRY.
5. BERA(EVOKED POTENTIALS) IF REQUIRED.
6. CALORIC TEST
7. ELECTRONSTAGMOGRAPHY
8. VESTIBULAR FUNCTION ASSESSMENT.
9. CAROTID AND VERTEBRAL DOPPLER STUDIES
10. BLOOD INVESTIGATION
MANY TIMES THESE INVESTIGATIONS MAY NOT REVEAL ANY ABNORMILITY AT ALL THEY ARE A MUST TO RULE OUT ANY UNDERLINED ORGANIC PATHOLOGY.
MOST OF THE PATIENTS NARRATED THAT
1 THEY USED COLLARS OR
2.THEY USED MEDICINES LIKE VERTIN,STUGERON OR STEMITIL
3.THEY DID SOME POSTURAL NECK EXCERCISES.
ULTIMATELY ,THEY MIGHT NOT HAVE BEEN BENEFITTED.THESE PATIENTS KEEP ON CONSULTING ONE DOCTOR OR THE OTHER SPEACIALIST ALL THE TIME.FINALLY THEY BECOME DESPERATE AND A FEW MAY EVEN RESORT TO AYURVEDIC AND HOMEOPATHIC TREATMENT.IN MANY OF THE HOSPITAL ,NURSING HOMES AND CLINICS FACILITIES TO CARRYOUT ALL TESTS MAY NOT BE AVAILABLE.,BUT THIS DEPENDS ON MANY OTHER PARAMETERS AND CONDITION OF THE PATIENT.NOW ONE SHOULD THINK OF AN ADEQUATE APPROACH TO THIS PROBLEM OF TREATING GIDDINESS.IT IS KNOWN THAT THE ORGAN PROBABLY EFFECTED IS “VESTIBULAR HABITUATION: IS KNOWN IN THE LITERATURE.SO WE HAVE TO “STIMULATE”THESE ORGANS,i.e (SEMICIRCULAR CANALS,OTOLITHS,UTRICLE AND SACCULE)FOR MORE EFFECTIVE MANAGEMENT OF GIDDINESS.SO BEFORE TREATING VERTIGO PATIENTS THE EXACT CAUSE IS ESSENTIAL.
PSYCHOLOGICAL ASPECTS
LIKE ALL SENSORY SYSTEMS VESTIBULAR SYSTEM EXHIBITS A DECREASED RESPONSE TO STIMULI THAT ARE PERSISTENT(ADAPTATION)OR REPETITIVE(HABITUATION)
INCREASE IN PERCEPTUAL AND MOTOR RESPONSIVENESS TO VESTIBULAR STIMULATION IS TERMED A VESTIBULAR ENHANCEMENT THIS OCCURS WHEN STIMULATION IS NOVEL,THREATENING OR WHENEVER SOATIAL ORIENTATION IS RECEIVED TO BE IMPORATANT.IT IS BELIEVED TO BE DUE TO EFFERENT VESTIBULAR NERVOUS CONTROLLING THE GAIN OF THE VESTIBULAR SYSTEM SO AS TO EFFECT SUPPRESSION OR ENHANCEMENT ,ALSO HABITUATION DEPENDS ON “AROUSAL’ACTIVITY IN DRAIN SYSTEM NUCLEI.
ANYTHING WHICH KEEPS THE SUBJECT IN AN ALERT STATE(SUCH AS MENTAL ARITHMATIC)DELAYS OR PREVENTS HABITUATION WHILE DAY DREAMING OR LACK OF ATTENTION HELP HABITUATION.
SOME PEOPLE FEEL HABITUATION TO ANGULAR ACCELERATION
TRANSFER OF HABITUATION CANNOT BE OBTAINED FOR DIFFERENT CONDITIONS.
EACH CONDITION MUST BE PRACTICED SEPARATELY DESPITE THEIR SIMILARITY IN SENSATION AND NYSTAGMIC RESPONSES.
THERFORE IT IS ESSENTIAL TO INSTALL PARALLEL SWING FOR STIMULATING OTOLITH ORGAN AND TORISON CHAIR AND ROTATING CHAIR TO STIMULATE ALL CANALS AT THE SOMETIME.
OTHER BALANCE TESTS CAN ALSO WILL BE ADDED FOR THE BENEFIT OF THE PATIENTS.MORE THAN ANYTHING ELSE IT REQUIRES EXTREME CO-OPERATION FROM PATIENTS AND THEY HAVE TO ATTEND REGULARLY THERAPY SESSIONS ATLEAST FOR A PERIOD OF 10 TO 15 DAYS.AND THEY POSITIVELY DERIVE BENEFIT BY THESE NON MEDICAL ASPECTS OF TRAETMENT.THESE EQUIPMENTS WERE DESIGNED AND EXTENSIVELY USED ON SCIENTIFIC BASIS AND FOUND VERY MUCH BENEFICIAL .

VESTIBULAR REHABILITATION EXERCISES.(EPLEY’S AND SEMENTS)
EXERCISES TO BE CARRIED OUT FOR 15 MINUTES TWICE A DAY INCREASING TO 30 MINUTES.
EYE EXERCISES TO BE CARRIED OUT SITTING IN BED.
LOOK UP FORST AND THEN DOWN.SLOWLY AT FIRST ,QUICKLY LATER 20 TIMES.
HEAD AND NECK EXERCISES TO BE CARRIED SITTING ON BED.
BEND HEAD FORWARDS ,THEN BACKWARD WITH EYES OPEN.SLOWLY FIRST,THEN QUICKLY 20 TIMES .TURN HEAD LEFT TO RIGHT THEN VICE VERSA.SLOWLY FIRST,THEN VICE VERSA.SLOWLY FIRST ,THEN QUICKLY 20 TIMES.AS DIZZINESS IMPROVES ,THESE EXERCISES SHOULD BE CARRIED OUT WITH EYES CLOSED.
SHOULDER AND TRUNK EXERCISES TO BE CARRIED OUT SITTING IN BED.
SHRUG YOUR SHOULDERS UP AND THEN DOWN SLOWLY 20 TIMES
TUM SHOULDERS TO THE RIGHT AND THEN TO THE LEFT,SLOWLY FIRST THEN QUICKLY 20 TIMES.
BEND FORWARDS AND PICK UP OBJECTS FROM THE GROUND AND SIT UP 20 TIMES.
STANDING UP EXERCISES
CHANGE FROM SITTING TO STANDING UP AND BACK AGAIN WITH EYES OPEN 20 TIMES REPEAT WITH EYES CLOSED.
THROW SMALL RUBBER BALL FROM HAND TO HAND ABOVE EYE LEVEL.
THROW BALL FROM HAND TO HAND UNDER ONE KNEE.BALL BOUNCING AND CATCHING.
MOVING ABOUT EXERCISE
WALKS ACROSS ROOM WITH EYES OPEN AND THEN CLOSED-10 TIMES
WALK UP AND DOWN A SLOPE WITH EYES OPEN AND THEN CLOSED-10 TIMES.
WALK UP AND DOWN STEPS WITH EYES OPEN AND THEN CLOSED-10 TIMES.
ANY GAME INVOLVING STOPPING OR TURNING IS GOOD .
THE ABOVE MENTIONED EXERCISES HAVE BEEN NARRATED BY EPLEY AND SEMONT

Labels: GIDDINESS

Introduction:
Otitis externa is inflammation and infection of the external auditory canal (EAC) and is a common occurrence both in the emergency room and within the pediatric community. As such, it is important to recognize the common historical information, presenting symptoms, and physical findings associated with this condition in order to treat appropriately.
The auricle, or pinna, is the visible part of the ear located outside of the head. Its purpose is to collect sound. It does so by acting as a funnel, amplifying the sound and directing it to the ear canal. While reflecting from the pinna, sound also goes through a filtering process that adds directional information to the sound. The filtering effect of the human pinna preferentially selects sounds in the frequency range of human speech.
Embryology:
To better understand some of the congenital malformations that may predispose a patient to acquiring otitis externa, or to broaden your differential diagnosis in a pediatric setting, embryology is key. The auricle begins development during the 6th week of gestation. It is derived from mesoderm of the 1st and 2nd branchial arches, forming 6 His hillocks. Adult shape is attained by the 20th week of gestation, but the adult size is not reached until the age of 9 years.
The EAC begins to form during the 8th week of gestation, when the surface ectoderm of the 1st pharyngeal groove thickens and grows toward the middle ear. This core of tissue begins to resorb by 21 weeks gestation to form a channel that is complete by 28 weeks gestation. The canal ossifies completely by age 3 years and reaches adult size by age 9 years.
Knowledge of embryology will help especially in the case of preauricular cyst and fistula, where abnormal development of the first and second branchial arch may manifest as persistent discharge or recurrent infection around the EAC. A draining sinus may be present anterior to the tragus; when infected, the cyst distends with pus and the overlying skin is erythematous. These lesions are managed by complete surgical excision if they become repeatedly infected. The facial nerve is at risk of injury during the excision of these lesions because of the close relationship of the preauricular cyst or fistula to the superior branches of the facial nerve within the parotid gland. First branchial cleft anomalies have a more complex embryologic origin than preauricular cysts and fistulas. These lesions may not have an obvious sinus tract on the skin and may manifest as an abscess extending deeply into the EAC, parotid, and/or neck.
Incidence and Symptoms:
Fortunately, malformations usually do not accompany the classic presentation of otitis externa and are generally easy to visualize upon examination. It should be noted that most ear canal infections are due to excessive moisture providing suitable conditions for bacterial overgrowth.
Statistically, acute otitis externa occurs in 4 of every 1000 people per year. Otitis externa is defined as chronic when the duration of the infection exceeds 4 weeks or when more than 4 episodes occur in 1 year.
Important clues for otitis externa reside in the patient history:
• 1 to 2 days of progressive ear pain
• Exposure to water
• Itching
• Purulent discharge
• Conductive hearing loss
• Feeling of fullness or pressure

Phyical exam:
• sine qua non of otitis externa = pain on gentle traction of the external ear
• Periauricular adenitis
• Speculum examination reveals erythema, edema of the epithelium, and accumulation of moist debris in the canal
• The tympanic membrane may be difficult to visualize, may be mildly inflamed, but it should be normally mobile on insufflation
• Spores and hyphae may be seen in the external canal, if etiology is fungal
• Eczema of the pinna may be present and represent the 1st visible sign of external otitis to the examiner
• (CN) involvement is not associated with simple otitis externa.

Speculum findings:
• The canal may be so swollen that a view into the ear is impossible
• In swimmers, divers and surfers, chronic water exposure can lead to the growth of bony swellings in the canal known as exostoses. These can interfere with the drainage of wax and predispose to infection

Differential Diagnosis
Conditions that warrant exclusion prior to the diagnosis of simple otitis externa include:
Otitis media:
Otitis media is usually diagnosed by the combination of symptoms (ear pain and reduced hearing), and direct observation of an inflamed tympanic membrane with fluid behind it. Fever may be present and a recent history of an upper respiratory infection is likely. Hearing in otitis media and otitis externa is generally reduced in a "conductive" pattern, to a modest amount (20-50 dB). Auditory testing is often done to be sure that the condition is improving. The fluid behind the eardrum is associated with immobility and a "flat" tympanometer trace. Differentiation can be difficult, especially in the case of current otitis externa, where occlusion of the EAC prevents visualization of the tympanic membrane. In the absence of systemic symptoms and fever, treat the otitis externa first with topical antibiotics and wait to give oral antibiotics when symptoms persist.
Ramsay Hunt syndrome
This condition, more accurately known as herpes zoster oticus, is caused by varicella-zoster viral infection. Ramsay Hunt syndrome is characterized by facial nerve paralysis and sensorineural hearing loss, with bullous myringitis and a vesicular eruption of the concha of the pinna and the EAC. A painful otitis externa may be present as well. Treatment includes use of an antiviral agent (eg, valacyclovir) and systemic steroids. The role of facial nerve decompression remains controversial.
Furuncle:
Staphylococcal infection of a hair follicle is the usual cause of a furuncle. This infection occurs in the lateral cartilaginous hair-bearing portion of the EAC. On otoscopic examination, a furuncle is a localized infection, which may develop into an abscess, rather than the diffuse inflammatory process characteristic of otitis externa.
Skull base osteomyelitis:
This serious infection, also known as malignant otitis externa, occurs most often in patients who are diabetic or immunocompromised. The pathogenic bacteria are usually Pseudomonas aeruginosa. Other predisposing conditions include arteriosclerosis, immunosuppression, chemotherapy, steroid use, and other immunodeficient states. The diagnosis is strongly suggested by a history of diabetes mellitus, severe otalgia, cranial neuropathies, and characteristic EAC findings. The EAC may be filled with friable granulation tissue, which is primarily found inferiorly. Because this presentation may be identical to that of a soft tissue malignancy, prudence dictates a tissue biopsy, even if a history of diabetes mellitus is present. Bare bone of the EAC floor may be exposed; small bony sequestra may be observed as well. CT scanning demonstrates bone erosion, and gallium scanning can be performed at points throughout treatment to monitor resolution. Treatment consists of administration of an antipseudomonal IV antibiotic such as ceftazidime (in some cases) or oral ciprofloxacin (in less dramatic cases). Extended treatment for at least 6 weeks is most appropriate. Hyperbaric oxygen therapy may also be effective. Surgical debridement is reserved for granulation tissue, necrosis and bony sequestra.
Preauricular cyst and fistula: previously discussed.
Lacerations:
Full-thickness auricular lacerations may be observed after blunt or sharp trauma. These injuries are managed surgically by closing both the perichondrium and the skin. In contrast, external canal lacerations may occur after attempts at cleaning the ear canal using cotton-tipped applicators. Microscopically replacing any skin flaps in their normal position, packing the ear canal, and administering topical antibiotic drops usually manage EAC lacerations.
Atopic dermatitis:
Drug sensitivity to topical antibiotic solutions is well known. Neomycin allergy occurs in up to 5% of patients treated with the medication. Suspect drug sensitivity if worsening of symptoms associated with skin excoriation and weeping occurs in the distribution of the topical medication exposure after application of drops. Metal sensitivity also manifests as excoriation, erythema, and edema around the exposure site (eg, a piercing hole). A common allergen is nickel, an impurity that may be present in precious metals. Atopic dermatitis is managed by removal of the allergen, such as an earring, and beginning topical steroid and antibiotics if the wound is secondarily infected. The diagnosis of metal sensitivity is confirmed by performing a skin patch test.
Cerumen impaction:
Cerumen impaction is the most common abnormality found on otoscopic examination, yet only a small proportion of the general population requires regular disimpaction because the EAC has the innate ability to produce and clear itself of cerumen. Cerumen may vary in color and consistency and may exist with other pathologies. Of note, debris in the EAC from cholesteatoma or tumors may be confused with cerumen, indicating that considerable care is required when attempting debridement of the EAC. Debridement may be accomplished with microinstruments or by aspirating the ear canal contents with a No 5 or No 7 Barton suction, while under direct vision through the otoscope or microscope. Irrigation of the ear canal is another option, but use of a pressurized irrigation system entails the risk of trauma.
Exostosis and osteoma:
The two most common bony lesions of the EAC, exostoses and osteomas, differ histologically and clinically. Exostoses tend to arise from the anterior and/or posterior floor of the medial EAC. Exostoses have a sessile base and are covered with normal-appearing skin. Both anterior and posterior exostoses may be found simultaneously. Osteomas may arise from any region of the bony EAC and often are pedunculated. Osteomas may also be either single or multiple and are covered by normal skin. Exostosis and osteomas require surgical treatment only if they are so large that they lead to a conductive hearing loss or intractable otitis externa.
Foreign body:
Foreign bodies are not infrequently encountered in the EAC. In children, parts of toys or even food may be found in the EAC, and thus, appearance varies. In adults, fragments of cotton swabs are the most common finding. Erythema and edema surrounding the foreign body are commonly present. Using microinstruments, the foreign body may be removed under a microscope, depending on the patient's ability to cooperate.
Acute (bullous) and chronic (granular) myringitis:
Acute myringitis is usually caused by a mycoplasma or viral infection and is observed in adults and children. It is characterized by hemorrhagic bullae involving the tympanic membrane and a flulike syndrome. It is self-limiting and requires pain and fever management.Chronic myringitis is defined as deepithelization of the tympanic membrane, granulation tissue formation, and discharge. Treatment includes topical application of eardrops, a caustic solution in unresponsive cases, and mechanical removal of polypoidal granulations.
Organisms
The most common organisms causing otitis externa are:
1. Pseudomonas species
2. Staphylococci
3. Streptococci/Gram negative rods
4. Fungi (Aspergillus & Candida species)

On exam, it is important to note the observation of black dots (spores) within the EAC as this is highly suggestive of a fungal infection with aspergillus niger. In other fungal species the spores may be white or yellow.
In chronic otitis externa, although the canal wall is not swollen to the same extent as it is in the acute presentation, the skin is excoriated and red. The examiner should note that the drum is essentially normal in appearance without evidence of fluid behind the tympanic membrane.
Labs/workup
Usually after failed empiric therapy with topical antibiotics or antifungals:
• Bacterial and fungal culture
• Gram stain
• KOH prep smear (if available)
• Adults with otitis externa: screening blood glucose and/or a urine dipstick test to rule out occult diabetes.

Imaging
Imaging studies are not required for simple otitis externa. However, in patients with suspected malignant otitis media (diabetic or immunocompromised):
• CT scanning or MRI of the temporal bone
• triple-phase bone scanning
• gallium scanning

Treatment for simple Otitis Externa
First line treatment is topical application of various drying agents, antibiotics, or antifungals. Most preparations require an intact tympanic membrane in order to prevent damaging vital middle ear structures. Acetic acid acts as a drying agent and should not be used if a perforation is present. Neomycin, nystatin, and boric acid also should only be used with an intact tympanic membrane. It should be noted that ciprofloxacin and ofloxacin are safe to use with a perforated eardrum.
• Acetic acid with and without hydrocortisone (EarSol HC, VoSoL HC, Acetasol HC)
5-10 gtts in affected ear TID
• Neomycin, polymyxin B, and hydrocortisone (Cortisporin Otic)
5 gtt in affected ear TID
• Ciprofloxacin (Ciloxan)
5-10 gtt in affected ear BID
• Ofloxacin (Floxin)
-10 gtt in affected ear BID
or
10 drops in affected ear QD
• Nystatin powder (Mycostatin, Nilstat) or boric acid powder
1-2 puffs from handheld nebulizer for 1wk

Case Presentation: ER consult
Mr. A.T is a 53 y/o Hispanic male with PMHx sig. for well controlled DM (HbA1C 6.5) and severe fungal otitis externa 7 yrs ago requiring gross debridement and hospitalization.
CC: clear, non-purulent, non-odorous d/c from his left ear for the past 10 days following an URI. Pt. denies dizziness, increasing pain, or fever.
Physical exam:
Right Ear: right TM intact, non-erythematous, no fluid present
Left Ear: EAC appears white and wet with friable cheesy material present. Non-bloody. Large central perforation present.

Next step in management
This patient has risk factors that include a PMHx of diabetes, past surgery on the ear that is symptomatic, past severe fungal infection, and a large perforation that limits the treatment available. It is now important to consider what labs should be ordered, remembering that the patient is not currently in severe pain or having other evidence of a systemic infection. In addition to laboratory studies, imaging studies could be considered if deemed necessary for proper treatment. Does this patient simply need empiric therapy and follow up? If this is the plan, what medication(s) are indicated?
Treatment plan
Based on history and clinical presentation, the plan for this patient was to:
• Obtain fungal and bacterial cultures
• No imaging necessary
• Tolnaftate 1% topical in L ear BID x 7 days
• Ofloxacin 0.3% otic, 4 gtts in L ear BID x 7 days
• F/U in 2 wks

What if’s discussion
Instead of the patient just discussed, what if on arriving in the ER for a simple external otitis consult you find that the patient has:
• Severe, unrelenting, deep-seated otalgia
• Temporal headaches
• Purulent otorrhea
• Dysphagia, hoarseness, and/or facial nerve dysfunction

Suspecting Malignant External Otitis (MEO)
The previous history and physical exam findings point to a more serious clinical picture that warrants immediate intervention. If malignant otitis externa is high on your differential, it is important to look for the following:
Physical exam:
• Inflammatory changes are observed in the external auditory canal and the periauricular soft tissue
• The pain is out of proportion to the physical examination findings
• Marked tenderness is present in the soft tissue between the mandible ramus and mastoid tip
• Granulation tissue is present at the floor of the osseocartilaginous junction. This finding is virtually pathognomonic of malignant external otitis (MEO).
• Fever is uncommon, but if present, it is usually > 39C

Orders
When suspecting MEO, it is imperative that the following labs are obtained:
• Cultures (bacteria & fungi)
• Glucose monitoring

Next step
The following should be performed in all cases:
• Admit patient
• Place on empiric IV antibiotics until organism is isolated through culture
• Pain relief (morphine or other appropriate analgesic)
• Once organism isolated, treat appropriately
• Consult Infectious Disease
• Use decreased severe pain as marker of improvement
• Surgery is necessary only if necrosis is present

Imaging
Appropriate imaging when high suspicion of MEO is present:
• CT scanning or MRI of the temporal bone
• triple-phase bone scanning
• gallium scanning

It should be noted that CT scan is the most readily available and best choice for evaluation of bone. All of these choices are present in the literature and are acceptable choices. Gallium scanning will be discussed in greater detail in regard to therapy continuation and assessing response to treatment.
Treatment
The following are highly recommended general guidelines for the care of MEO:
• meticulous glucose control
• aural toilet
• systemic and ototopic antimicrobial therapy (fluoroquinolone)
• hyperbaric oxygen therapy
• debridement (generally reserved for exposed bone or necrosis)

Treatment options
The role of systemic antibiotics is essential in the treatment of MEO to prevent further spread of infection to bone or meninges.
• Ciprofloxacin 1500-2250 mg/d PO/IV divided bid/tid
o Resistance seen in up to 33% of pts with MOE who fail initial outpatient treatment
• Ceftazidime 1-2 g IV q8h
• Ticarcillin/clavulanate (Timentin) 3.1 g IV q6h

Ciprofloxacin remains the current preferred treatment in mild to moderate cases. Severe cases warrant IV ceftazidime and, in conjunction with an Infectious Disease consult, combined drug therapy.
Duration of Treatment
This is a subject of debate and disagreement. Osteomyelitis of the skull base is the most severe form of malignant otitis externa and the following discussion represents a minority of cases encountered in general practice. However, if encountering a virulent case of MEO, current literature strongly suggests treating at least as long as osteomyelitis in any other location (minimum of 6 weeks of IV antibiotics).
Benecke et al developed a method of staging and monitoring this malady using gallium and technetium scanning techniques. Ga-67 accumulates in areas of active inflammation by binding to leukocytes and forming a complex with lactoferrin. Hence, nuclear scanning with gallium-67 will be positive for soft tissue and bone infections. Enhanced uptake will be present in areas of skull base osteomyelitis, but unlike the technetium-99 scan, it returns to normal sooner once the infection has resolved. They devised a staging system where Stage I is localized to soft tissues, Stage II is limited osteomyelitis, and stage III represents extensive skull base osteomyelitis. All stages were treated with appropriate anti-pseudomonal antibiotics. They recommended ending treatment 1 week after the gallium citrate scan findings return to normal and confirming this with a repeat scan 1 month after the treatment is stopped. Using this protocol, average duration of treatment was 8.8 weeks with a range of 4-17 weeks. It should be noted that this study followed 13 pts gathered over 4 yrs in the Los Angeles area, highlighting the extreme nature of these infections and their relative rarity.

Introduction
Rhinosinusitis is manifested clinically by an inflammatory response involving the upper respiratory airway tract including the following: the mucous membranes (possibly including the neuroepithelium) of the nasal cavity and paranasal sinuses, fluids within these cavities, and/or underlying bone. Broadly speaking, rhinosinusitis is defined as an inflammation and/or infection involving the nasal mucosa and at least one of the adjacent sinus cavities. Traditionally this condition was called sinusitis but the Task Force on Rhinosinusitis believes that for issues of clarity the entity should be referred to as rhinosinusitis to reflect that the condition affects the nasal passages and the sinus mucosa simultaneously. Rhinosinusitis syndromes are discussed in temporal terms and the disease state is categorized by how long symptoms have been present. The incidence of rhinosinusitis in the United States has been estimated at 14% of the adult population as determined by surveys conducted.
Acute rhinosinusitis (AS) is defined as the persistence and worsening of upper respiratory symptoms for greater than a 7-day period but less than 4 weeks. Subacute rhinosinusitis (SAS) is defined as nasal symptoms lasting 4 weeks to 12 weeks. The infectious pathogens involved in SAS are similar to those found in AS. 11 Acute Bacterial Rhinosinusitis (ABS) is the fifth most common diagnosis, in the primary care setting, prompting antibiotic administration and accounts for 0.4% of ambulatory diagnoses. The economic burden of this disease is greater than $1.77 billion per year. Acute rhinosinusitis may lead to chronic rhinosinusitis (CRS).
CRS diagnosis is symptom based and requires persistence of patient complaints of mucosal inflammation for more than 3 consecutive months despite optimal medical therapy or episodes have occurred more than four times a year with persistent radiographic changes. Chronic Recurrent Rhinosinusitis (CRRS) consists of multiple episodes of sudden worsening of CRS with return to baseline between episodes. Typically the acute symptoms are alleviated but the chronic symptoms persist. Rhinosinusitis is rarely life threatening, but the close proximity of the paranasal sinuses to the central nervous system, the multiple fascial planes of the neck, and the associated venous and lymphatic channels can lead to serious complications.
Incidence and Epidemiology
CRS ranks fifth compared to all diseases in frequency of antibiotic use associated with treatment. CRS affects approximately 32 million persons each year and accounts for 11.6 million visits to physicians' offices. Internationally, CRS is a common disease, particularly in places where atmospheric pollution levels are high. Damp, temperate climates along with higher concentrations of pollens are associated with a higher prevalence of this disease in the northern hemisphere. Epidemiological data for CRRS is scarce due to physician to physician variability in diagnosis and uncertainty in differentiation between CRS and CRRS.
Anatomy
Embryology
Classic anatomic treatises attribute initial paranasal sinus development to lateral nasal wall ridges called ethmoturbinals. A series of five to six ridges first appear during the eighth week of development; through regression and fusion, however, three to four ridges ultimately persist the first ethmoturbinal regresses during development; its ascending portion forms the agger nasi, while its descending portion forms the uncinate process. The second ethmoturbinal ultimately forms the middle turbinate, the third ethmoturbinal forms the superior turbinate, and the fourth and fifth ethmoturbinals fuse to form the supreme turbinate. These structures are all considered to be ethmoid in their origin. An additional ridge, the maxilloturbinal, arises inferior to these structures. This ridge ultimately forms the inferior turbinate but is not considered ethmoid in its embryologic origin.
In addition to the ridge and furrow development, a cartilaginous capsule surrounds the developing nasal cavity and has an important role in sinonasal development. Bighman et al. highlighted the role of the cartilage capsule through cross-sectional histologic analysis of fetal specimens. At 8 weeks, three soft-tissue elevations or preturbinates are seen that correlate to the future inferior, middle, and superior turbinates. At 9 to 10 weeks, two cartilaginous projections invade into the soft tissue preturbinates. An additional soft tissue elevation with an underlying cartilaginous bud emerges at this time, corresponding to the future uncinate process. This structure enlarges, and by 13 to 14 weeks, a space develops lateral to the structure that corresponds to the ethmoidal infundibulum. By 16 weeks, the future maxillary sinus begins to develop from the inferior aspect of the infundibulum. The cartilaginous structures resorb or ossify as development progresses. The cartilaginous capsule, therefore, plays an important role in sinonasal development
The ethmoid sinus is commonly referred to as “the labyrinth” due to its complexity and inter-subject variability. Fortunately, several rhinologists and surgeons have reduced the complex ethmoidal labyrinth of the adult into a series of lamellae on the basis of embryologic precursors. These lamellae are obliquely oriented and lie parallel. With experience, these structures are relatively easy to recognize during surgery and are invaluable in maintaining orientation in ethmoid procedures. The first lamella is the uncinate process; the second lamella corresponds to the ethmoidal bulla; the third is the basal or ground lamella of the middle turbinate; and the fourth is the lamella of the superior turbinate. The basal lamella of the middle turbinate is especially important, as it divides the anterior and posterior ethmoids. The frontal, maxillary, and anterior ethmoids arise from, and therefore drain into, the middle meatus. The posterior ethmoid cells arise from, and therefore drain into, the superior and supreme meati, while the sphenoid sinus drains into the sphenoethmoid recess. The lamellae are relatively constant features between human subjects, making intra-operative recognition important.
Agger Nasi
On anterior rhinoscopy, a prominence can be easily appreciated at and just anterior to the middle turbinate’s insertion into the lateral nasal wall. This region was designated the agger nasi, taken from the Latin agger, meaning mound or eminence, and nasi, meaning nose. This mound or eminence is a very consistent feature on nasal examination. In many but not all cases, the agger nasi region is pneumatized by an anterior ethmoid cell, referred to as the agger nasi cell. This cell usually takes its origin from the superior aspect of the infundibulum or the frontal recess region. The agger nasi cell is bordered anteriorly by the frontal process of the maxilla, superiorly by the frontal recess/sinus, anterolaterally by the nasal bones, inferomedially by the uncinate process of the ethmoid bone, and inferolaterally by the lacrimal bone. The intimate relationship of the cell to the lacrimal bone readily explains the finding of epiphora in select patients with sinus disease. The agger nasi can also be important in frontal sinusitis and its treatment. The superior aspect of the cell serves as the anteromedial floor of the frontal sinus and a significant portion of the anterior border of the frontal recess. This is relevant for understanding the pathophysiology of frontal sinusitis and the surgical treatment of the frontal sinus. The agger nasi can pneumatize inferomedially to pneumatize the uncinate process. In a small percentage of patients, the pneumatization can be significant, and bulla formation of the uncinate may occur.
Uncinate Process
The uncinate process is most easily appreciated by viewing a sagittal gross anatomic specimen after deflecting the middle turbinate superiorly. This ethmoid structure is nearly sagittally oriented, nearly paralleling the ethmoidal bulla. It is approximately 3 to 4 mm wide and 1.5 to 2 cm in length. Through most of its course, its posterior margin is free as it has no bony attachments. The hiatus semilunaris lies directly behind the posterior margin of the uncinate (Figure 1–3). Anteriorly and superiorly, it attaches to the ethmoidal crest of the maxillae, just inferior to the lateral attachment of the anterior aspect of the middle turbinate and agger nasi. Directly inferior to this, it fuses with the posterior aspect of the lacrimal bone. Its anterior inferior aspect does not have a bony attachment.
Posteriorly and inferiorly, the uncinate attaches to the ethmoidal process of the inferior turbinate bone. The attachment here is thick, and the uncinate often splits or widens in this region to fuse with the stouter inferior turbinate bone. At its posterior and superior limit, the uncinate also gives off a small bony projection to attach to the lamina perpendicularis of the palatine bone. The uncinate has no bony attachment anterior and posterior to its attachment to the inferior turbinate bone. Here, the lateral nasal wall is made not of bone but rather middle meatal mucosa, a small layer of intervening connective tissue, and sinus mucosa. These areas are referred to as the anterior and posterior fontanelles. The posterior fontanelle is much larger and more distinct than its anterior counterpart. An opening into the maxillary sinus, the accessory ostium, can often be seen here and can be mistaken for the natural maxillary sinus ostia. Accessory ostia are frequently encountered in the posterior fontanelle region, occurring in approximately 20 to 25% of patients. Returning to its superior aspect, the uncinate projects posterior and superior to the middle turbinate attachment and most commonly bends laterally to insert on the lamina papyracea of the orbit. Inferior and lateral to this portion of the uncinate lies the superior aspect of the infundibular air space, the recessus terminalis. Superior and medial to this portion of the uncinate (most commonly) lies the floor of the frontal recess. Alternatively, the uncinate can attach centrally to the skull base or medially to the superior aspect of the vertical lamella of the middle turbinate near the turbinate’s insertion to the cribriform plate. It can also fuse with an anterior ethmoid cell, such as the agger nasi. Stammberger highlights that the superior portion of the uncinate can divide to attach to the lamina papyracea, skull base, and middle turbinate. Each leaflet can develop variably to produce partial or complete septations with accompanying inlets. The inlets vary as well, from shallow, blind pouches to small cells and, of course, include the native frontal recess. These observations underscore the complexity and variability of this region.
The uncinate process forms the anteromedial boundary of the ethmoidal infundibulum. For most of its course, the uncinate is a three-layer structure, comprising nasal or middle meatal mucosa on its anteromedial aspect, ethmoid bone, and infundibular mucosa on its more posterolateral aspect. The most common orientation of the uncinate to the lateral wall and lamina papyracea is approximately 140°; however, there is a significant amount of variability. The uncinate can be displaced laterally against the orbit, as commonly occurs in maxillary sinus hypoplasia, or it can be displaced medially, as commonly occurs in cases with extensive polypoid disease within the infundibulum. In select cases, the uncinate is displaced medially to such an extent that it recurves on itself and has been misinterpreted is a duplication of the middle turbinate. Additionally, in a small percentage of cases, the uncinate process can be pneumatized. An appreciation of uncinate variability is important. If lateral displacement of the uncinate with accompanying atelectasis of the infundibulum is not appreciated during infundibulotomy incision, inadvertent orbital injury can occur.
Ethmoid Bulla
The ethmoid bulla is one of the most constant and largest of the anterior ethmoid air cells. It is located within the middle meatus directly posterior to the uncinate process and anterior to the basal lamella of the middle turbinate. The cell is based on the lamina papyracea and projects medially into the middle meatus. The cell has the appearance of a bulla, that is, a hollow, thin-walled, rounded, bony prominence. Superiorly, the anterior wall of the ethmoid bulla can extend to the skull base and form the posterior limit of the frontal recess. Posteriorly, the bulla can blend with the ground lamella. Anatomic variations can occur in the ethmoid bulla. When highly pneumatized, the ethmoid bulla can be one of the largest ethmoid air cells and can lie in the lower aspect of the middle meatus. In select cases, a low-lying bulla can potentially narrow the ethmoidal infundibulum and impair mucociliary transport and ventilation. The ethmoid bulla is formed by pneumatization of, and behind, the second basal lamella or bulla lamella. When unpneumatized, a bony projection from the lamina papyracea results and is referred to as the torus lateralis.3 It is estimated that this occurs in approximately 8% of subjects.
Hiatus Semilunaris
The hiatus semilunaris can be more easily understood by translating the Latin roots directly into English: hiatus, a gap, cleft or passageway, and semilunaris, crescent-shaped. Indeed, the hiatus semilunaris is a crescent-shaped gap between the posterior-free margin of the uncinate process.
Ostiomeatal Unit
The ostiomeatal unit is not a discrete anatomic structure but refers collectively to several middle meatal structures: the uncinate process, the ethmoid infundibulum, anterior ethmoid cells, and ostia of the anterior ethmoid, maxillary, and frontal sinuses. The ostiomeatal unit is a functional rather than an anatomic designation, coined by Naumann in discussing the pathophysiology of sinusitis. He emphasized that a small amount of obstruction in this critical region could lead to significant disease in the larger frontal and maxillary sinuses.
Frontal Recess and Sinus
The frontal sinus drains into the middle meatus and nasal cavity through a complex passage. Review of the anatomic nomenclature of this region has produced much discussion. Several authors describe a “nasofrontal duct” that forms the nasofrontal connection. Anatomic dissection reveals that a true duct, that is, “a tubular structure conducting any fluid,” does not exist. In an attempt to refine the nomenclature and more accurately characterize the anatomy, the term frontal recess has been recommended. The frontal recess is the most anterosuperior aspect of the anterior ethmoid sinus that forms the connection with the frontal sinus. The boundaries of the frontal recess are the lamina papyracea laterally, the middle turbinate medially, the posterosuperior wall of the agger nasi cell (when present) anteriorly, and the anterior wall of the ethmoid bulla posteriorly. If the anterior wall of the ethmoid bulla does not reach the skull base and form a complete posterior wall, the frontal recess may communicate with the suprabullar recess. The frontal recess tapers as it approaches the superiorly located internal os of the frontal sinus; above the os, it again widens, as the anterior and posterior tables diverge to their respective positions. An hourglass-like appearance is evident, with the narrowest portion being the frontal ostium. There is tremendous variation with respect to the pattern of the nasofrontal connection. The anatomic complexity of this region is better understood when the effect of the surrounding ethmoid cells, such as the agger nasi cell, frontal cells, and supraorbital ethmoid cells, are considered. An intimate relationship therefore exists between the agger nasi cell and the frontal recess. Secretions from the frontal sinus destined for the nasal cavity usually follow a path through the frontal recess and over the posterior and medial surface of the agger nasi cell. If the agger nasi cell is extensively pneumatized, the frontal recess can be relatively narrowed, and hence the patient may be predisposed to frontal sinusitis. In surgery, an extensively pneumatized agger nasi can be mistaken for the frontal recess or sinus. If a large agger nasi cell is opened and mistaken for a frontal sinus, the residual superoposterior wall of the agger nasi cell can scar posteriorly to the ethmoid roof, and iatrogenic stenosis or obstruction of the nasofrontal connection can occur. In addition to the agger nasi cell, there are other ethmoid cells that have an intimate relationship with the frontal recess. Van Alyea reported that approximately 50% of anatomic specimens had anterior ethmoid cells that encroached into the frontal sinus, and that one-third of these encroached into the area of the frontal ostium. He termed these cells “frontal cells.” Schaeffer pointed out that anterior ethmoid cells could pneumatize sufficiently into the frontal sinus to give the appearance of duplication of the sinus. Stammberger points out that “from the frontal recess, anterior ethmoid cells can develop into the frontal bone along side the frontal sinus.” These were called “the bulla frontalis” by Zuckerkandl.
Ethmoid Roof
An area that deserves special attention is the ethmoid roof. From its orbital plate, the frontal bone sends an extension across the ethmoids, which are open superiorly, to join with the lateral lamella of the cribriform plate. The extension of frontal bone forms the ethmoid roof, which is indented by various ethmoid air cells and clefts to form indentations or foveolae: specifically, the foveolae ethmoidales ossis frontalis. The ethmoid roof may vary in its orientation from being nearly horizontal to nearly vertical; however, in most patients, the ethmoid roof lies above the level of the cribriform plate, and therefore, the roof has a superomedial aspect. The medial aspect of the ethmoid roof is formed by the lateral lamellae of the cribriform plate, also known as the lamina lateralis of the lamina cribrosa because it projects superiorly or superomedially from the cribriform plate. Keros has described three types of skull-base conformations that have clinical relevance in sinus surgery. In type one, the olfactory sulcus is 1 to 3 mm deep, the corresponding lateral lamella is short, and there is a significant portion of frontal bone that backs the ethmoid roof, making the roof thick and the sinus less hazardous to operate in. In type two, the olfactory sulcus is 3 to 7 mm deep, and the corresponding lateral lamella forms a considerable portion of the medial ethmoid roof. In type three, the olfactory sulcus is 7 to 16 mm deep, and the ethmoid roof lies at a significant level above the cribriform plate. The thin lateral lamella is a much larger component of the roof, and a significant portion of the ethmoid roof is not backed by thick frontal bone, making this the most hazardous sinus to operate in. Extreme caution must be exercised when operating along the skull base, especially medially in the region of the thin lateral lamellae of the cribriform plate. In an anatomic study using microscopic techniques, the extension of frontal bone that backs the ethmoid roof measured 0.5 mm, while the lateral lamella was noted to be only 0.2 mm thick. At the ethmoidal sulcus, a groove in the lateral lamella for the anterior ethmoidal artery, the bone measured only 0.05 mm, a 10-fold reduction in the thickness of the roof.
Patient Evaluation
When evaluating a patient for complaints related to sinus symptoms it is important to pay close attention to the following aspects (in addition to a complete history and physical), a detailed chief complaint, history of allergies, asthma, aspirin sensitivity and polyps. In patients with a history of with CRS, it is important to note facial pain, congestion, nasal obstruction, drainage and hyposmia. Of note a review of the medical care a patient has received prior to evaluation is also important.
A complete head and neck exam should be completed with particular attention to basic ocular examination such as visual fields, extraocular eye movement and a basic visual acuity. Anterior rhinoscopy should be performed to evaluate septal deviations, character of mucosa, and the presence of polyps. Nasal endoscopy (typically 30° or 45°) should be used to evaluate the nasal floor, nasopharynx, middle meatus, and sphenoethmoidal recess.
Pre-operative evaluation includes a review of CT imaging. A technique used at UTMB is the CLOSE Technique.
• C – Cribriform – Asses for Keros type, asses asymmetry
• L – Lamina Papyracea - Check for dehiscence or pathologic fractures to avoid injuring vital structures.
• O – Orbits, Onodi cell, Optic Nerve – Check for dehiscence of the optic nerve in the sphenoid sinus, asses the presence of Onodi cells (superior-lateral to sphenoid) and determine the angle of the orbital slope
• S – Sphenoid, Skull Base - Assess for Carotid dehiscence and aeration patterns such as Conchal, Pre-sellar, & Sellar (thickness of clivus).
• E – Ethmoid Arteries – evaluate the location of the artery and the presence of a mesentery around the artery.

Functional Endoscopic Sinus Surgery – Concepts of Surgery
Significant controversy reigned throughout the 20th century with regard to the extent of surgery that should be performed in chronic sinusitis. Debate is sure to continue until the pathogenesis of chronic sinusitis is better understood. The concept of “irreversibly diseased” mucosa that needs to be surgically removed has now largely been eliminated. Indeed, the problems associated with exposure of bone from mucosal stripping during surgery have been increasingly appreciated. Moriyama and colleagues have shown that denuded bone results in extremely delayed healing. The bone may remain exposed for 6 months or more, and ciliary density may never return to normal at these sites. Greater emphasis thus should be placed on mucosal preservation within the ethmoid sinus during surgery. The initial understanding of functional endoscopic sinus surgery (FESS), namely, that drainage of the involved sinuses is sufficient to induce disease resolution, currently has been modified somewhat, based on continued improvement of the understanding of the disease process.
Controversy in Sinus Surgery
ANTROSTOMY
Several theoretic considerations need to be kept in mind when considering the most appropriate size of antrostomy opening. Experimental evidence clearly demonstrates that, in rabbits, exposure of the maxillary sinus to airflow results in dramatic slowing or cessation of mucosal clearance. Theoretically, therefore, the maxillary sinus ostium and the maxillary sinus mucosa should ideally remain protected from airflow. Additionally, it has been demonstrated that nitric oxide is actively liberated from the sinus mucosa at levels that may reach bacteriostatic concentrations.8 Theoretic advantages would appear to exist for keeping the surgically created ostium small. On the other hand, a significant part of the medial wall of the maxillary sinus is composed of the uncinate process, and this bone frequently displays osteitic changes. When the uncinate process is diseased and not completely resected, persistence of disease and scarring are typically seen at this site. Therefore, when disease is very mild, a minimal opening of the ostium, if necessary at all, is preferable. However, in the presence of long-standing diffuse chronic sinusitis, when there is evidence of osteitis on CT or at the time of surgery, or when there is a strong likelihood that significant local care may be required to the maxillary sinus following surgery, a wide middle meatal antrostomy, with careful and complete removal of the uncinate process anteriorly and inferiorly, is preferable. In addition, if the maxillary sinus extends medially so that the medial wall posterior to the antrostomy is displaced into the nasal air- flow, this medially displaced wall should be removed posteriorly to the pterygoid plate, to avoid air being directed into the sinus cavity during inspiration.
FRONTAL SINUSOTOMY
The frontal sinus continues to present the surgeon with the most challenge, both in terms of the surgical procedure and in terms of the potential for persistent and recurrent disease. At minimum, exploration of the frontal recess commits both the patient and the surgeon to a prolonged period of postoperative care and endoscopic observation. At worst, unnecessary exploration of the frontal sinus or inadvertent stripping of mucosa in this area can result in prolonged morbidity and multiple surgical procedures. Therefore, the most difficult decision in FESS is whether the frontal recess should be explored. In some cases of frontal sinus involvement, it is clearly better to perform just an ethmoid dissection and then monitor the patient to see if the frontal recess disease resolves. The decision should, in part, depend on the surgeon’s experience, the regional anatomy as seen on CT, and the availability of through-cutting mucosal-sparing instrumentation, as well as on the pathology present. Preoperative evaluation of the frontal sinus and frontal recess anatomy requires careful evaluation of the coronal and axial CT. A reconstructed sagittal view, as provided in computer assisted stereotactic navigation, is also of benefit, particularly in cases of complicated frontal recess pneumatization. In evaluating the frontal recess for potential surgical intervention, attention is paid to its size in the anteroposterior and lateral diameters, the presence of neo-osteogenesis, and an evaluation of the underlying disease process. Additionally, attention should be paid to the extent of the pneumatization of the frontal sinus itself, as a hypoplastic frontal sinus appears to be significantly more likely to result in frontal recess stenosis than one that is well pneumatized, irrespective of the anatomy of the frontal recess. One possible explanation for this phenomenon is that mucociliary clearance from a well pneumatized sinus is greater than from a hypoplastic sinus, and mucociliary flow may aid in maintaining patency.
Balloon Sinuplasty
Balloon sinuplasty was developed in 2006 and this new iteration of it is considered different from prior french biliary catether in that the new technique can fracture bones. Kennedy concluded in a recent study that this technique may lead to bacterial introduction and subsequent osteitis, mucositis, and mucoceles.
Bolger et. al. published results in 2007 in which he demonstrated the usefulness of balloon sinuplasty. The trial involved a 24 week follow up and they enrolled 115 patients. Exclusion criteria for the study was patients with extensive sinonasal polyps, prior surgery, or cystic fibrosis. At 24 weeks the patency of the frontal sinus was noted to be 80%, 17.9 % of the sinuses could not be assess secondary to normal anatomy of the area and only 1.6% of patients were non-patent. Revision surgery was required in three sinuses (1%) and three patients (2.75%), in addition SNOT-20 scores were shown to improve with balloon sinuplasty alone. Of note, they only reported 9 cases of bacterial sinusitis, which were all managed with oral antibiotics. No other adverse events reported.
Extended Maxillary Antrostomy
The extended maxillary antrostomy has been advocated by some R. Casiano in cases where maxillary sinus disease is refractory to medical and prior surgical treatment. His group has published a small series with impressive results. In their description of the procedure they state the middle meatal sinusotomy is opened widely anteriorly (up to NLD), posteriorly to post wall of max sinus, superiorly to roof of max sinus and inferiorly to inferior turbinate. The inferior maxillary antrostomy performed inferiorly into the inferior meatus, post to Hasner’s valve (lacrimal punctum). They noted 60% of patients had a complete symptomatic response and 50% of the patients had no evidence of disease upon nasal endoscopy.
Conclusions
Functional endoscopic surgery is a complex and constantly evolving field with new techniques, instruments and approaches continually described. The most important aspect to remember when performing sinus surgery is that one must be safe and the best way to assure one is safe is to have an excellent understanding of the anatomy of the paranasal sinuses. Even in the advent of image guidance, it is paramount to have a good understanding of the proximity of structures to avoid damage to them. The second most important aspect of sinus surgery, as in all other surgery, is understanding the indications and knowing what type of surgery is best fitted for each individual patient.

DISSCUSSANT- Remarks by Patricia Maeso, MD 2009-05-29:
A sphenoethmoid cell (Onodi cell) is formed by lateral and posterior pneumatization of the most posterior ethmoid cells over the sphenoid sinus. The presence of Onodi cells increases the chance that the optic nerve and/or carotid artery would be exposed (or nearly exposed) in the pneumatized cell.
It’s important to define what the agger nasi cell is. The agger nasi is a bony prominence that is often pneumatized in the ascending process of the maxilla. Its location below the frontal sinus also defines the anterior limit of the frontal recess. Approximately 75-80% of patients have agger nasi cells.
You mentioned hyposmia in your discussion. To prevent this when we do sphenoid surgery we remove the inferior 1/3 of the superior turbinate, but leave the rest of it to preserve the olfactory neuroepithelium.
Further, we avoid producing any senechiae or any trauma to the area between the middle turbinate and the septum (olfactory cleft) so that it doesn’t scar down and cause anosmia.
The other important thing about the sphenoid and the skull base is the sphenoid intersinus septum. In 25% of patients it may insert directly on the carotid, so don’t crack it so that you don’t open directly into the carotid.
You mentioned a Haller cell. This is really an infraorbital ethnoidal cell. The Haller cell (infraorbital cell) is usually situated below the orbit in the roof of the maxillary sinus. It is a pneumatized ethmoid cell that projects along the medial roof of the maxillary sinus. Enlarged Haller cells may contribute to narrowing of the ethmoidal infundibulum and recurrent sinus disease, despite previous (perhaps incomplete) surgery.
There are patients who can’t properly get rid of their secretions- for example – CF patients or patients with immotile cilia. We help them to get rid of their secretions by extending the antrostomy to the floor of the maxillary sinus. Otherwise I like to stay with my normal middle meatus antrostomy. This gives the mucosa a chance to regenerate and the mucosa will regenerate usually if you get rid of the disease.
There are several theories in sinus surgery and one is the Kennedy theory of operating.
He’s done multiple studies and the Kennedy theory of operating says that the bone itself may be osteitic and houses osteomyelitis so that apart from removing the mucosa, the “billiard ball” sinus, you have to remove the infected/inflamed bone as well.

Injuries resulting from trauma to the middle and inner ear can cause minor temporary symptoms or permanent debilitation. Knowledge of the anatomy of the many fragile sensory structures within the middle and inner ear is vital to proper diagnosis and appropriate management of such injuries. Appropriate evaluation takes into account the spectrum of severity and the sometimes-unappreciated subtle symptoms of otologic trauma.

Anatomy

The tympanic membrane is an elliptically shaped structure creating the lateral border of the middle ear. It consists of three germinal layers: 1) outer keratinizing squamous epithelium from ectoderm, 2) middle fibrous layer from mesoderm, and 3) inner cuboidal mucosa from endoderm. It is composed of the large inferiorly located sound conducting pars tensa, and the smaller superiorly located pars flaccida. These two areas differ in structure and in function. The pars flaccida has a thicker epithelial layer and contains collagen within the middle layer, which allows for more flexibility, making it less susceptible to barotrauma. The pars tensa is taut compared to the pars flaccida. The thickened periphery sits firmly within the tympanic sulcus of the temporal bone to create the tympanic annulus. The average surface area of the tympanic membrane is 90mm2, the effective vibratory portion consisting of the pars tensa averages 55mm2.

The three ossicles of the middle ear (the malleus, incus, and stapes) bridge the gap between the tympanic membrane and the oval window while conducting sound as a lever system. The average area of the oval window being 3.2mm2 gives a 17:1 (55/3.2) magnification. Likewise the handle of the malleus being 1.3 times the length of the incus contributes additional amplification of sound energy to a final amplification of 22:1. The ossicles are supported as a chain by the walls of the tympanic cavity. The malleus is firmly embedded with the tympanic membrane as well as being suspended by three suspensory ligaments, and a tendinous attachment. The stapes sits firmly within the oval window by the annular ligament and is further secured by the stapedial tendon. The incus, supported by two ligaments, is the weakest part and is the most likely to be sheared by external forces. The chorda tympani branch of the facial nerve traverses the middle ear between the malleus and incus.

The delicate sensory organs of the inner ear consist of the cochlea, vestibule, and semicircular canals housed within the petrous portion of the temporal bone. The semicircular canals are well hidden with the bony labyrinth , and their injury requires extreme disruption of the temporal bone. On the other hand, the vestibule and cochlea lie immediately medial to the middle ear, behind the TM. Penetrating trauma to the TM jeopardizes the auditory labyrinth by possible violation of the oval and round windows or the cochlear promontory.

Epidemiology

The TM is much more frequently traumatized than the middle or inner ear, but usually to a less serious degree. Annual incidence rates of traumatic perforations vary between 1.4 and 8.6 per 100,000. It occurs in all age groups with a predisposition for children likely due to their inquisitive nature and habit of placing foreign bodies into the external ear canal. Young men are more commonly found to have perforation injuries. Due to the rise in domestic violence, women have increasingly become victims of open-handed slap injuries with subsequent TM perforations.

Reliance on motorized transportation has greatly increased the risk of head injury. It has been estimated that 30-75% of blunt head trauma had associated temporal bone lesions. Gunshot wounds are an increasing source of temporal bone trauma. Increased mortality is more frequently seen in this group due to the high association with intracranial trauma. New laws governing the use of safety restraints and child seats for MVAs and head protection for motorcyclists have been very beneficial as forms of secondary prevention.

Etiology

TM perforations occur by various mechanisms and sources of energy, and therefore can be of many shapes and sizes. They are described in relation to the four quadrants of the TM as determined by the handle of the malleus. Size is normally described as a percentage perforation (ex. 40% perforation) or directly for smaller perforations (ex 2, 3, or 4mm perforation). Further classification of central versus marginal perforations is important for management.

1. Compression injuries:
Sudden changes in air pressure (blast or slap injuries) as well as gradual changes (barotrauma) can lead to significant TM damage. Blast injuries are more severe when there is less reflection or obstruction of the blast energy wave en route to the TM. Water skiing accidents are frequently seen during summer months. Changes in water pressure during the descent of SCUBA divers can led to compression type injuries as well.

2. Penetrating injuries:
The second most common cause of TM perforations include Q-tips, bobby pins, keys, and paper clips often used in an attempt to clean the external ear canal.

3. Thermal injuries:
In industrial communities such as ours, hot welding slag is occasionally encountered as the culprit for TM injuries. Because of the tissue damage and associated risk of infection, these are felt to be less amenable to observational treatment.

4. Lightning injuries:
The instantaneous electrical conduction of lightning strikes is thought to cause damage to the TM by either compression or rarefaction pressure changes. These injuries are also less likely to heal spontaneously.

Temporal bone trauma can be classified into blunt, penetrating, blast, and barotrauma. Blunt trauma to the skull occurs when there is a rapid collision between the head and a solid or semisolid object. The most common temporal bone fracture occurring from blunt trauma is the longitudinal fracture (80%). Directly applied lateral forces travel through the path of least resistance along the petrosquamous suture line and continues anterior to the otic capsule. This path usually involves major foramina in the skull base. The most common being the carotid artery and jugular bulb. The anterior extension may also include the temporomandibular joint. The most frequent structures involved are the tympanic membrane, the roof of the middle ear, and the anterior portion of the petrous apex. 15-20% will have involvement of the facial nerve, and injury occurs near the geniculate ganglion or in the horizontal portion. The facial paralysis is often delayed in onset, attributed to edema rather than direct interruption of the nerve. Vestibular involvement and sensorineural deficits are relatively uncommon and are attributed to concussive effects rather than direct trauma on the vestibular labyrinth and cochlea.

Twenty percent of temporal bone fractures are transverse in nature generated by forces in the anterior-posterior axis. These fractures often require much greater energy and are more commonly associated with more serious or even fatal head injuries. The facial nerve is involved in 50% of cases. The otic capsule and internal auditory canal are frequently involved as well.

Penetrating trauma usually resulting from firearms and violence is becoming more prominent. Unfortunately, their outcomes are more dismal. Victims may present with destructive lesions to the facial nerve, conductive hearing loss, TM perforation, ossicular disruption, labyrinthine fractures, and cochlear nerve transection. Intracranial injuries include laceration of the internal carotid artery, dura, or brain.

Barotrauma principally results from air travel or scuba diving. Rapid transient pressure fluctuations may jar the ossicular chain, and cause displacement of the stapes footplate, resulting in sensorineural hearing loss and vertigo. These same pressure events occurring on the oval or round window can lead to fluctuating auditory and vestibular symptoms known as inner ear barotraumas. Scuba divers descending beyond 30 feet must undergo decompression stages during ascent. Too rapid an ascent can cause percolation of nitrogen bubbles known as “the bends”, causing severe CNS or musculoskeletal dysfunction. Blast injuries occur by similar rapid pressure fluctuations yet cause more mechanical injuries.

Evaluation and Management

Along with an adequate history of the patient and the events of the injury, a thorough head and neck examination is necessary. The patient with multiple systems trauma must proceed according to the ATLS protocol of emergency resuscitation. Immobilization or clearance of cervical spine injuries are immediately performed. The signs of middle and inner trauma can be very prominent. Evidence of a basilar skull fracture includes hemotympanum, Battle’s sign, and periorbital ecchymosis. Blood in the external ear canal may be more representative of longitudinal versus transverse fractures of the temporal bone. Foreign bodies are more accountable for injuries to the TM, ossicles, facial nerve, or labyrinth without temporal bone fractures. The external ear canal may be lacerated in longitudinal fractures, whereas the transverse fracture will reveal hemotympanum. Pneumatic otoscopy may initiate the nystagmus and vertiginous symptoms of a perilymphatic fistula, or reveal a subtle fracture of the malleus.

Hearing Loss
Hearing loss is a common complaint after middle and inner ear trauma. Evaluation of hearing should be done with formal audiometry, however in the emergency room setting a tuning fork test should be enough preliminary data. Autophony may indicate a conductive hearing loss. 71% of patients with temporal bone trauma relate hearing loss. The type and degree of deficit is related to the force of injury and location of the fracture.

Transverse fractures involving the otic capsule and internal auditory canal frequently cause severe sensorineural hearing loss. Longitudinal fractures are more likely to cause conductive or mixed hearing loss. Even without temporal bone fractures, concussive injuries to the cochlea or labyrinth can cause hearing loss. In a review by Tos on the prognosis of hearing loss in temporal bone fractures, he found that 80% of conductive hearing losses from longitudinal fractures resolved spontaneously, while cases of sensorineural hearing loss due to transverse fractures showed no improvement.

TM perforations result in conductive hearing loss due to the loss of the effective vibratory portion of the TM and by the cancellation effects of sound waves reaching the remnant TM and oval window at nearly the same time. CHL greater than 40dB should alert the physician to the possibility of ossicular discontinuity.

Dizziness
The vestibular symptoms of vertigo or nausea and vomiting may be the result of a fracture through the otic capsule or a labyrinthine concussion. It is often times a late presentation due to the sedation, bed rest, and obtundation of this class of patients. In the majority of cases, the symptoms are temporary, and in injuries in which the lesion is permanent, recovery usually occurs as a result of compensation. Vestibular suppressants can be employed transiently for patients with extreme symptoms, however, they should reduced or discontinued as soon as possible to minimize the suppression of central compensation. Benign Paroxysmal Positional Vertigo can often follow an episode of head trauma and can occur at any time following the injury.

Perilymphatic fistulas may present as fluctuating episodes of dizziness/vertigo with or without hearing loss lasting a few seconds. Tullio’s phenomenon may be present. PLFs are initially treated conservatively as up to 40% should heal spontaneously. In certain cases in which there is progressive hearing loss or persistent vertigo beyond an observation period of 10-14 days, surgical options may be considered. There is controversy about whether the presence of a perilymph fistula represents an emergent situation requiring surgical exploration because of the risk of severe sensorineural hearing loss, labrynthitis, or meningitis.
The most common areas of fistulization are the oval and round windows, and therefore require elevation of a tympanomeatal flap and visualization. Suspected defects are repaired then plugged with fascia, muscle, or fat. Regardless of visualization of a specific leak site, the majority of patients achieve resolution of their symptoms.

CSF Otorrhea and Rhinorrhea
Temporal bone fractures account for the most common cause of CSF otorrhea. TM or external canal lacerations associated with longitudinal temporal bone fractures will allow CSF otorrhea, whereas in transverse fractures, the CSF may build behind an intact TM and eventually drain via the Eustachian tube. Because of the associated hemorrhage with traumatic lesions, the fluid is often not overtly characteristic of CSF. The test of choice for identification of CSF is confirmation of the beta-2-transferrin protein, and should be analyzed in any suspicious case. High resolution CT scan can help identify the site of CSF fistula. Severe fractures may also produce defects in the tegmen plate, predisposing the patient to meningocele or encephalocele development and delayed CSF leakage.

Sterile cotton should be placed within the external canal to prevent contamination. Measures to reduce intracranial pressure such as bed rest with head of bed elevation, stool softeners, no nose blowing, and lumbar drains are used. The use of prophylactic antibiotics is controversial. Otic antimicrobial solutions may only cause confusion in monitoring the CSF flow. The use of prophylactic antibiotics in CSF fistula is controversial, however, a meta-analysis by Brodie did reveal a significant reduction in meningitis when prophylactic antibiotics were applied compared to no antibiotics. The most common infecting organisms are Pneumococcus, Streptococcus, and Haemophilus influenza.

Conservative therapy is generally attempted for 7-10 days before surgical options are considered. The approach for surgical closure of CSF fistulas depend mainly on the status of hearing, presence of meningocele or encephalocele, and location of the fistula. Defects of the mastoid tegmen may require a transmastoid approach and plugging with fascial grafts. If brain herniation or significant defects are found, the middle cranial fossa approach may be justified. Tegmen tympani defects in a functional ear should be repaired through a middle fossa approach to preserve hearing.

Facial Nerve injuries
The facial nerve enters the temporal bone via the internal acoustic meatus. The nerve then travels 8-10mm within the anterosuperior quadrant of the internal auditory canal to the meatal foramen where the canal reaches its most narrow point (0.68mm). The labyrinthine segment then runs 2-4 mm to the geniculate ganglion where the greater superficial petrosal nerve exits to carry parasympathetic secretomotor fibers to the vidian nerve. The tympanic segment begins just distal to the geniculate ganglion where the nerve turns 40 to 80 degrees at the first genu and runs posteroinferiorly across the tympanic cavity to the second genu. Here the stapedial muscle branch exits. The nerve then turns 90 degrees inferiorly where the mastoid segment travels for 12-14mm in the anterior mastoid to exit the stylomastoid foramen.

Early evaluation and a careful and thorough history when evaluating the status of the facial nerve is crucial. Particular attention should be given to the time and characteristics of onset of facial weakness, whether sudden or delayed, and determination of complete versus incomplete paralysis. The previous status of the nerve should also be documented. It is also important to determine if the paralysis is central or peripheral. Supranuclear or central lesions produce contralateral voluntary lower facial paralysis. The frontalis is spared due to the bilateral innervation. An incomplete paralysis is termed a paresis, and if there is no movement in the facial musculature, the paralysis is described as complete. Care must be taken not to misdiagnose a facial nerve paralysis as a paresis by attributing movement of the levator palpebrae superioris muscle of CN III. The House- Brackman grading system was designed to classify the long term degree of facial nerve deficit but is also useful to describe acute facial weakness.


Grade Characteristics
I Normal Normal facial function
II Mild Slight synkinesis, no asymmetry, slight weakness
III Moderate Complete eye closure, noticeable synkinesis, no asymmetry at rest, obvious weakness, slight forehead movement
IV Moderately Severe Incomplete eye closure, no asymmetry at rest, no forehead movement
V Severe Asymmetry at rest, barely perceptible motion
VI Total No movement


Temporal bone fractures are the most common cause of traumatic injury to the facial nerve. Fortunately, the facial nerve is robust and has shown a remarkable regenerative response to mechanical injury. As previously mentioned, the facial nerve is involved in 15-20% of longitudinal fractures and 50% of transverse fractures. High resolution CT scanning with axial and coronal images is the diagnostic tool of choice for evaluating the facial nerve in temporal bone trauma. Chang and Cass’s review suggests that of longitudinal fractures; 43% had intraneural hematoma or contusion, 33% had bony impingement, 15% had transaction, and 12% had no identifiable pathology. In contrast, in transverse fractures, 92% had transection and 8% had bony impingement.

In a study by Haberkamp, Gadolinium enhanced MRI was found to be helpful in accurately predicting the site of facial nerve injury as a result of trauma. Likewise, MRI may play an important role in diagnosis and documentation of subclinical temporal lobe injuries, and other preexisting CNS injuries.

Electrophysiologic testing of the facial nerve includes the Nerve Excitability Test (NET), Maximal Stimulation Test (MST), Electroneuronography. These tests can only be used for unilateral paralysis because all three involve comparison to the contralateral side, which must be normal for valid results. Also, each will give normal results during the first 72 hours. The NET involves placement of a stimulating electrode over the stylomastoid foramen and measuring the lowest current necessary to produce a twitch on the affected side, which is then compared to the contralateral, normal side. A difference greater than 3.5mA indicates a poor prognosis for return of facial function. The MST is a modified NET. A maximal stimulus is used to depolarize all facial nerve branches and is compared to the contralateral side. ENoG is considered to be the most accurate prognostic test because it provides quantitative, objective measurement of neural degeneration. An electrode is placed near the stylomastoid foramen and a transcutaneous stimulis is applied. The muscular response is then measured using bipolar electrodes placed near the nasolabial groove. The peak-to-peak amplitude wave is then measured and compared to the contralateral side. A reduction of greater than 90% amplitude correlates with a poor prognosis for spontaneous recovery. A reduction of less than 90% gives an expected spontaneous rate of recovery of 80-100%. It should be noted that ENoG data is very well known for Bell’s Palsy, however there is limited definitive ENoG data for facial nerve injuries due to trauma. Development of muscular degeneration fibrillations does not develop for 10-14 days, therefore making EMG of limited value in the early detection. However, diphasic or triphasic potentials indicate normal voluntary contraction. Polyphasic potentials indicate reinervation, which develop 6-12 weeks before clinical return of function, which is useful in the evaluation of patients seen in the late post-traumatic period.

There is general consensus supporting the conservative treatment of patients with an incomplete paralysis. In an overview by Chang and Cass, it was concluded that surgical treatment was not required in patients who had 1) documented normal facial nerve function after injury regardless of its progression, 2) incomplete paralysis as long as there was no progression to complete paralysis, and 3) less than 95% degeneration by ENoG. Treatment of a complete paralysis is much more controversial, however. In 1974, Fisch recommended basing the decision for surgery on the time of onset of paresis, the degree of paresis, the degree and evolution of degeneration as measured by electroneurography, and the degree and evolution of regeneration. He noted a poor functional outcome in patients presenting with greater than 90% nerve degeneration by ENoG within 6 days of onset of palsy. Chang and Cass suggest that if decompression surgery is anticipated it should be done within a 14 day window from the time of injury based on animal studies by Yamamoto and Fisch. Despite the controversy, three general guidelines can be followed to select patients as surgical candidates:
1) Immediate paralysis with no evidence of clinical return after 1 week and absent electrical responses.
2) Immediate paralysis with significant disruption of the temporal bone on CT scan.
3) Immediate paralysis with progressive decline of electrical responses to less than 10% of responses on the normal side.

After deciding on facial nerve exploration, the suspect location of neural injury and hearing status are the two key factors in deermining an appropriate approach. Injuries of the facial nerve at or distal to the geniculate ganglion can be approached via the transmastoid procedure. Patients with transverse fractures are not candidates for this approach. Fractures can be identified laterally upon visualization of the mastoid cortex. Theses fractures can be chased medially to the point of injury. If there is no obvious fracture, a facial recess approach will help provide examination of the nerve from the geniculate ganglion to the second genu. Partial transections of less than 50% may be repaired with onlay nerve grafts. If transection exceeds 50%, an interposition nerve graft, such as the greater auricular nerve, should be used in approximation after the epineurium is trimmed and the nerve fascicles optimized. Of patients who undergo direct anastomosis or cable graft repair, the majority of patients (82%) will recover to a HB 3 or 4, and none have shown to recover to HB 1 or 2. It has not been shown whether early versus delayed repair leads to better functional outcome. If the nerve is found to be intact, decompression of the epineural sheath is performed in proximal and distal fashion until normal nerve is encountered. In Chang and Cass’s review, about 50% of patients undergoing facial nerve decompression obtain excellent functional outcomes. Histopathological analysis of patients with severe facial nerve injuries has shown that retrograde axonal degeneration takes place to the level of the labyrinthine segment and possibly the meatal segment. If this stands true, lesions that are distal to the geniculate ganglion may not adequately be addressed by a transmastoid approach alone.

Injuries medial to the geniculate ganglion may be approached in several ways, depending on the status of hearing. For patients in whom hearing is not useful, a transmastoid-translabyrinthine approach is reserved. The entire intratemporal course of the facial nerve can be seen after translabyrinthine skeletonization of the internal auditory canal.

For patients with intact hearing, a transmastoid-supralabrinythine approach or a middle cranial fossa approach is considered. Following complete mastoidectomy, the superior semicircular canal is skeletonized, thus allowing exposure of the labyrinthine portion of the facial nerve. If there are any concerns regarding adequate exposure or if grafting of the meatal portion is anticipated, the middle fossa approach is more suitable. The middle fossa approach is usually preceded by a mastoidectomy to aid in the identification of the internal auditory canal. The superior portion of the temporal bone is then exposed via an extradural craniotomy approach.

In summary, most lesions are of the perigeniculate and labyrinthine segments, and serious facial nerve injury may occur proximal to the fracture site. Therefore, during preoperative planning complete decompression of the nerve must be considered.

Iatrogenic Facial Nerve Injuries
Iatrogenic facial nerve injuries are rare but devastating complications of otologic surgery. The most common procedure resulting in facial nerve injury is Mastoidectomy (55%), followed by Tympanoplasty (14%), and removal of exostoses (14%). The region that is most commonly injuried is the lower tympanic segment. Green found that 79% of injuries were not identified at the time of surgery. In patients with less than 50% transection, decompression was performed and 75% of the patients had a HB 3 or better. For lesions greater than 50%, direct anastomosis or cable graft was performed and no patients had better than a HB 3. Along with facial nerve injuries in temporal bone trauma, there is still much controversy regarding the management of iatrogenic facial nerve injuries. However, it is generally agreed upon by otologic surgeons that an acute, complete, postoperative facial nerve paralysis should be surgically explored as soon as possible. It should be kept in mind that local anesthetic effects may mimic a mechanical surgical injury. For postoperative delayed onset weakness, serial electrophysiologic testing should be performed. If there is greater than 90% degeneration within one week, exploration is necessary.

Emergencies
Brain herniation and massive hemorrhage are two consequences of middle and inner ear trauma that are considered emergent and require rapid intervention. Brain herniation into the middle ear or the external canal requires patient stabilization and high resolution CT scan. Surgical repair of the defect as soon as possible is usually needed. If massive bleeding from the external auditory canal occurs, it should be immediately packed and carotid arteriography performed to determine the bleeding site. Embolization of the bleeding artery is usually the treatment of choice.

Introduction



Noise is a common occupational hazard that leads to one of the most common complaints in the adult population seen by the otolaryngologist—noise induced hearing loss (NIHL). The cause and effect relationship between noise exposure and hearing loss has been appreciated for many years. “Boilermaker’s deafness” was a term coined in the 1700s and 1800s to refer to a high frequency hearing loss seen in laborers that could be diagnosed with tuning forks. The increased mechanization seen during the Industrial Revolution was associated with a rise in the incidence of this disorder and today it is estimated that over 9 million American laborers are exposed to potentially hazardous levels of noise throughout their employment. An additional 1 million Americans are affected by non-industrial noise exposure. This means that nearly one third of the 30 million Americans with hearing loss have an impairment caused by noise, making it the most common preventable cause of permanent sensorineural hearing loss (14).



Characteristics of Noise



In everyday language, the term noise is used to refer to an unpleasant or unwanted sound. However, in the context of the medical literature, noise has come to refer to an excessively intense sound capable of producing damage to the inner ear. Noise can be further described by its temporal patterns. Intermittent noise is interrupted with periods of quiet while continuous noise remains constant and fluctuating noise rises and falls over time. Both impact and impulse noises are produced by a sudden intense sound wave but impact noise is caused by a collision while impulse noise is due to an explosion (5).



Noise is typically measured with a sound pressure meter in decibel (dB) units on the A-scale (dBA). This is a scale weighted to place more emphasis on those frequencies to which the human ear is most sensitive while minimizing the effects of the extreme low and high frequencies. Perhaps a more accurate measure of an individual’s exposure to noise is obtained with a dosimeter. This device, which is similar to that worn by staff in the radiology department, integrates constant and fluctuating noise over time so that total noise exposure may be calculated and risk estimated (13).



Acoustic Trauma



Acoustic trauma refers to a sudden permanent hearing loss caused by a single exposure to an intense sound. This is most often caused by an impulse noise, typically in association with an explosion. The sound pressure levels capable of causing acoustic trauma vary between individuals but average around 130-140dB. The degree of hearing impairment seen after acoustic trauma is also variable and may range from a mild to profound SNHL. The mechanism of injury in acoustic trauma is thought to be direct mechanical injury to the sensory cells of the cochlea.



Patients suffering from acoustic trauma tend to present within a short time period following the event. They report a sudden, sometimes painful hearing loss that is often followed by a new onset tinnitus. Otologic examination is often unremarkable but may reveal tympanic membrane disruption or evidence of ossicular damage. Audiogram may show the typical 3-6kHz sensorineural notch that is seen with chronic NIHL but down-sloping or flat audiograms that effect a broad range of frequencies are more common. Conductive losses will be seen in cases of tympanic membrane perforation or ossicular discontinuity. Management of acute acoustic trauma injuries most often involves observation with strict noise avoidance. Some improvement can generally be expected in the days immediately following the injury and serial audiograms are performed until hearing levels stabilize. Those patients that present with a complete hearing loss may benefit from middle ear exploration (5,14).



Chronic NIHL



Chronic NIHL, in contrast to acoustic trauma, is a disease process that occurs gradually over many years of exposure to less intense noise levels. This type of hearing loss is generally caused by chronic exposure to high intensity continuous noise with superimposed episodic impact or impulse noise. The amount of sound that is capable of producing cochlear damage and subsequent hearing loss is related by so-called “damage risk criteria” which is based upon the equal energy concept. That is to say that it is the total sound energy delivered to the cochlea that is relevant in predicting injury and hearing loss. Both an intense sound presented to the ear for a short period of time and a less intense sound that is presented for a longer time period will produce equal damage to the inner ear. An increase in sound intensity of 3dB is associated with a doubling of sound pressure. Therefore, for each 3dB increase in sound exposure, the time exposed must be cut in half in order to deliver equal sound energy to the ear. Because noise levels are likely to fluctuate throughout the time of exposure, the standard accepted by OSHA is known as the 5dB rule; for every 5dB increase in noise intensity, exposure time must be cut in half. A 90dBA exposure is allowed for 8 hours, a 95dBA exposure is allowed for 4 hours, and so on to a maximum allowable intensity of 115dBA for 15 minutes (1).



Like in acoustic trauma, the hearing loss associated with chronic NIHL is variable between individuals—a subject that will be discussed in more detail later. However, the principal characteristics of chronic, occupational NIHL as specified by the American College of Occupational Medicine Noise and Hearing Conservation Committee include the following:

1. It is always sensorineural.

2. It is nearly always bilateral and symmetric.

3. It will only rarely produce a profound loss.

4. It will not progress once noise exposure is stopped.

5. The rate of hearing loss decreases as the threshold increases.

6. The 4kHz frequency is the most severely effected and the higher frequencies (3-6kHz) are more affected than the lower frequencies (500Hz-2kHz).

7. Maximum losses typically occur after 10-15 years of chronic exposure.

8. Continuous noise is more damaging than intermittent noise (5,6).



The majority of chronic NIHL is due to occupational or industrial exposure. It is important to remember, however, that in today’s noisy society even people with quiet jobs may suffer from NIHL. Such non-occupational NIHL is also called socioacusis. Sources of non-occupational noise include gunfire, loud music—via concerts or headphones, open vehicles such as motorcycles, snowmobiles or tractors, and power tools to name just a few. This hearing loss also demonstrates the characteristics listed above. One caveat to these features would be the individual who had significant noise exposure secondary to rifle shooting. In this case, an asymmetrical loss, with the ear nearest the gun barrel (the left ear in a right handed shooter) demonstrating slightly worse hearing, would be expected (5)

.

The development of chronic NIHL progresses through two phases. The first stage is characterized by a temporary threshold shift (TTS). This is brief hearing loss that occurs after noise exposure and completely resolves after a period of rest. This can be thought of as auditory fatigue and most studies indicate that it is associated with no sensory cell damage or minimal, reversible cell changes. After repeated exposure to noises intense enough to produce TTS, eventually a permanent threshold shift (PTS) will occur. This is the second stage of chronic NIHL and is an irreversible increase in hearing thresholds. At this point, there has been irreversible hair cell damage (5,6).



Patients suffering from chronic NIHL commonly present at the urging of family members or friends who are frustrated by the patients hearing loss. Upon further questioning, patients report difficulty not so much with hearing speech as with understanding speech. This difficulty is primarily noticed in environments with significant background noise. High frequency hearing loss is characterized by a loss of consonant discrimination. Consonant sounds such as f, s, t, d, sh, and k are all high frequency sounds (3-6kHz) and although they are not responsible for the acoustic power of speech, they are very important to the intelligibility of speech. Otoscopic examination will most often be normal and the audiogram will likely demonstrate the characteristics as listed above (5,14).



Many studies have been done looking for an effective medicinal treatment for NIHL caused by either acute trauma or chronic exposure. Dextran-40, carbogen, nicotinic acid, vitamins A, B1, E, and ephedrine are just a few agents that have not proven themselves beneficial (11). A report published in 1998 treated patients with sudden SNHL, acoustic trauma or NIHL whose hearing loss had failed to improve after a short trial of medical therapy with hyperbaric oxygen therapy (HBO). This study found that if the onset of the hearing loss was 2-6 weeks prior to HBO therapy, 1/3 of patients showed a marked hearing improvement—more than 20dB in at least three frequencies. Another 1/3 of patients had a moderate hearing gain—10-20dB while 13% had no improvement. If the onset was between 6 weeks and 3 months prior to therapy, 13% had marked gain, 25% had moderate gain and 62% had no improvement. If the hearing loss had been present for more than 3 months, HBO offered no benefit in terms of hearing improvement. From this data, the conclusion was made that a new hearing loss diagnosed within 3 months may improve with HBO treatment (10). Obviously, further studies are required to support or refute these findings.



Although NIHL is not amendable to medical or surgical therapy, it is entirely preventable. To address the increasing concern over occupational NIHL, many industries have adopted hearing conservation programs (HCPs). An effective HCP has five components: 1.) assessment of noise levels, 2.) engineering controls, 3.) administrative controls, 4.) use of personal hearing protectors, and 5.) serial audiograms. Hazardous noise levels can be identified with sound pressure meters or individual dosimeters as mentioned previously. In order to obtain the most accurate measurement of noise, sound surveys are performed that measure noise levels over long periods of time. Once dangerous noise levels have been identified, various control measures are taken to minimize exposure. Engineering controls involve changes in the technology or equipment used in industry. Examples of this would include replacing riveting with welding, applying mufflers to pneumatic drills, or redesigning machinery to enclose noisy gear wheels. Administrative controls include limiting time of exposure to noise, providing a less noisy work environment, and educating workers about the prevention of NIHL (1). When engineering and administrative controls fail to reduce noise to an acceptable level, personal hearing protective devices (PHPD) are vital to prevent NIHL. Insert earplugs, earmuffs and canal caps are the three main types of PHPDs. Earplugs fit directly into the EAC and may be sized, custom-made or moldable. While earplugs are often felt to be less cumbersome than other devices, their effectiveness in attenuating sound depends on an adequate seal within the EAC and proper fit is essential. Earmuffs encompass both ears with rubber or plastic cups connected by a headband. Again, the effectiveness of these devices depends on an adequate seal and a snug fit. Canal caps seal the external meatus with a soft rubber or plastic cap that is held in place with a headband. They do not require sizing or custom fitting like earplugs and are less bulky than earmuffs, but still must be worn tightly to assure an adequate seal. PHPDs, in general, are more effective in attenuating sounds above 1kHz but the absolute reduction of sound reaching the inner ear is highly variable. Earmuffs with a tight seal are capable of reducing sound levels by about 45dB in the high frequencies while earplugs average about 30dB of attenuation. Worn together, they provide a maximum of approximately 50dB of sound reduction. Obviously no PHPD will be effective unless the worker consistently wears it. Therefore, the most important aspect of choosing a PHPD is worker comfort and confidence in using the device (1,7,13). Finally a HCP involves screening audiometry to allow early identification of individuals with worsening hearing and to assess the efficacy of the program. Changes of 10dB or greater at any frequency or an average change of 10dB or more at all frequencies may warrant a referral to an otolaryngologist for further evaluation and a reassessment of the HCP. This annual exam serves not only to identify hearing loss but also to provide a opportunity for counseling on the importance of hearing conservation and assuring proper fit and compliance with PHPDs (1).



Physiology, Pathophysiology and Histopathology



Although the histopathologic correlate to chronic NIHL is injury to the cells of the inner ear, the pathogenesis involves interactions between all three divisions of the auditory system—the external, middle and inner ears. The importance of the external ear centers on the resonant characteristics of the external auditory canal (EAC). Tubes that are open at one end have an inherent resonant frequency that is determined primarily by the length of the tube. The average human EAC is 25mm in length, using this value in the formula: resonant frequency = speed of sound/4 x EAC length, means the average resonant frequency of the human ear is 3200Hz. Additionally, the configuration of the EAC can serve to amplify mid-frequency sounds by as much as 20dB. The clinical importance of these characteristics is twofold. Studies have shown that the most severe hearing loss is demonstrated ½-1 octave higher than the offending noise. The broadband noise seen in industry is converted by the fundamental resonance of the EAC to a 3Hz noise. This leads to the characteristic 4Hz notch seen on the audiogram in noise-exposed individuals. Secondly, as mentioned previously, significant variability exists in different individuals response to similar noise exposure. One explanation for this variability could be differences in EAC configuration and inherent resonance (5,8).



The contribution of the middle ear to the response to noise is the action of the acoustic reflex. The middle ear structures involved in this reflex are the tensor tympani muscle, which is attached to the head of the malleus and the stapedius muscle, which is attached to the head of the stapes. Two cranial nerves—the trigeminal (V) and facial (VII)—participate in the reflex. Stimulation of the reflex by a sudden intense sound causes muscle contraction. The action of the tensor tympani is to tense the tympanic membrane (TM) by pulling the malleus medially while the stapedius pulls the stapes perpendicular to its axis on the oval window. The combined action of these muscles is to stiffen the middle ear structures thereby reducing the sound energy reaching the inner ear. This system is most effective in attenuating low frequency sounds (<2kHz). Human and animal studies have shown that malfunction of the acoustic reflex is related to more temporary and permanent hearing threshold shifts. Specifically, patients with Bell’s palsy developed more TTS on the side of the facial paralysis when exposed to moderate noise. Additionally, differences in reflex latency, threshold, strength of muscle contraction and resistance to adaptation have been found and may help to explain inter-individual differences in NIHL (5,8,9).



The injurious action of noise is believed to affect not only the sensory cells of the inner ear, but also the supporting cells, nervous structures and blood vessels. The outer hair cells (OHC) are more vulnerable to noise injury than the inner hair cells (IHC). This is likely secondary to several characteristics including the location of the OHC, which is close to the point of maximal basilar membrane displacement, the direct shearing forces on the stereocilia of the OHC against the tectorial membrane, and the relative lack of supporting cells around the OHC. Early noise induced injury involves alterations in hair cell membranes which eventually lead to a failure in the regulation of intracellular ionic composition. A chain of events is set off that involves cell swelling or herniation, increased number of lysosomes and changes in essentially all cellular organelles. The hair cell cilia may become floppy, disordered, splayed, fractured or fused. Some of these changes seen in the cilia are reversible—this may be seen clinically as a TTS. However, at some point the cell is unable to recover from these injuries and degenerates—causing a PTS. With prolonged noise exposure, supporting cells and IHC undergo similar changes and eventual loss. After IHC loss, retrograde degeneration of cochlear nerve fibers may also be seen. Noise exposure has also been found to cause changes in the vascular system of the cochlea. Reductions in the number of capillaries, evidence of vessel occlusion, and alterations of RBC packing density have all been demonstrated in noise damaged ears. Although all of these pathologic changes have been well documented in both animal and human studies, a clear relationship between the degree of hearing loss and cochlear pathology has not been documented. Histologic study of ears that demonstrate identical audiograms may reveal markedly different pathology. Not only does this, once again, point to differences in susceptibility to NIHL, but it also has implications regarding differences in successful rehabilitation of hearing loss (5,8).



Susceptibility and Interactions



As has been mentioned several times, individual susceptibility to NIHL is highly variable. Several large studies have been done which have shown that, on average, 5% of individuals with long-term exposure to noise levels of 80dBA will have significant hearing loss. This risk increases to 5-15% with 85dBA noise and 15-25% with 90dBA noise (1). These averages are useful in terms of counseling patients on the risks of noise exposure, but we do not have a good understanding why, within a population exposed to the same noise intensity for the same time period, some individuals will have a significant reduction in hearing thresholds and others will not. Studies have evaluated the relationship between such things as gender, race, eye-color, other medical conditions or smoking history and susceptibility to noise but have not been able to demonstrate a connection (9). Attempts have also been made to predict the likelihood of a PTS based upon the degree of TTS after a noise exposure. Again, no such association has been proven (5).



One thing that we do know is that chronic noise exposure can interact with other factors to produce a hearing loss that may differ from that expected if each factor were delivered separately. Aging and noise exposure are the two most common causes of hearing loss. Since we know that chronic NIHL occurs over years of exposure, many patients will experience some degree of age induced hearing loss (AIHL) in addition to NIHL. The interaction between AIHL and NIHL follows the idea of decibel additivity up to a cumulative loss of approximately 40dB. This concept predicts that the normal progression of hearing loss associated with aging will occur in subjects with NIHL from an early age. Similarly, subjects with pre-existent AIHL will experience the same degree of NIHL with any given noise exposure as will those without AIHL. Once the total loss exceeds 40dB then one must factor in a “compression term” which takes into account that both AIHL and NIHL occur via the same mechanism—hair cell loss. Such that, when a number of hair cells have been previously damaged by one factor, there exists less chance for the other factor to cause further damage and the total loss will not simply be the sum of the two individual losses. In this case, total loss can be calculated with the following formula:



Total HL =


NIHL + AIHL –


(NIHL)(AIHL)

120



Simultaneous exposure to noise and ototoxic medications may have an amplifying affect on hearing loss, producing more threshold elevation than with either factor alone. This effect has been definitively demonstrated in noise- exposed animals given aminoglycoside antibiotics. The chemotherapy drug cisplatin was not found to cause hearing loss alone, but in animals given the drug and exposed to noise the hearing was worse than in animals exposed to noise alone. Although the diuretic furosemide is potentially ototoxic when given intravenously to patients with altered renal function, oral administration in people with normal kidneys has not been associated with hearing loss. It has also not been shown to worsen NIHL. The literature on the combined effect of salicylates and noise is contradictory. Some studies have demonstrated a potentiating effect, while others have not. Two separate studies done in the mid 1980’s found that in noise exposed individuals, if higher doses of aspirin (1.9 gr/day) were taken, their TTS was of greater magnitude and slower to recover. Therefore, it seems reasonable to counsel patients with significant noise exposure to avoid high dose aspirin therapy (5,9).



Simultaneous exposure to hazardous noise and certain chemical pollutants may have an additive effect on hearing loss. Toluene, carbon monoxide and carbon disulphide in combination with noise are known to cause a more severe high frequency hearing loss than noise alone. Other agents such as lead, mercury, xylene and trimethyltin are suspected to either worsen NIHL or alter susceptibility to NIHL (9,12).



It is not unusual for significant vibration to accompany noisy environments. Although vibration alone is known not to cause hearing loss, it is not known if vibration has any influence on NIHL. Animal studies have found more severe hearing loss and hair cell loss in animals exposed to both vibration and noise compared to those exposed to noise alone. In humans, vibration causes a larger TTS after a noise exposure, however, it is not clear if this can be translated to larger PTS also (5,12).



Impairment, Handicap and Disability



Hearing impairment, handicap and disability are terms that are frequently, though incorrectly, used synonymously. The correct definitions as set forth by the American Academy of Otolaryngology Committee on Hearing and Equilibrium in 1979 are as follows. Hearing impairment refers to “a change for the worse in either structure or function, outside the range of normal.” A hearing handicap is “the disadvantage imposed by an impairment sufficient to affect a person’s efficiency in the activities of daily living.” And, a hearing disability is “an actual or presumed inability to remain employed at full wages.” The otolaryngologist is often called to evaluate patients with hearing loss and should therefore be familiar with the appropriate use of these terms, particularly in those cases that may involve some compensation for the loss (2).



Although several methods exist to calculate hearing handicap, the most commonly accepted formula is the AAO-1979 rule. In this formula, pure tone audiometry is used to establish hearing thresholds at 500Hz, 1, 2, and 3kHz for each ear and the average monaural thresholds are calculated using these values. Then, using the assumptions that hearing handicap begins when PTA thresholds exceed 25dB and increases by 1.5% for each decibel loss above 25dB, the monaural percent impairment is calculated: MI = 1.5(PTA-25). Finally, the hearing handicap is calculated by applying a 5:1 weight favoring the better hearing ear: HH = [5(MIb) + (MIw)]/6. The following is an example of the calculation of hearing handicap:



PTA thresholds


500Hz


1kHz


2kHz


3kHz

Right ear


25


30


35


45

Left ear


35


40


55


70



1. Calculate monaural PTA.




Right ear:


25 + 30 + 35 + 45 =

4


135 =

4


33.8dB




Left ear:


35 + 40 + 55 + 70 =

4


200 =

4


50dB



2. Calculate monaural impairment.




Right ear:


33.8dB – 25dB = 8.8 x 1.5% =


13.2%




Left ear:


50dB – 25dB = 25 x 1.5% =


37.5%



3. Calculate hearing handicap.

HH = [5(13.2%) +(37.5%)]/6 = 66 + 37.5/6 = 103.5/6 = 17% (5,6).





The establishment of a hearing disability is an “administrative” decision. It is an estimate of the individual’s present and future ability to earn wages based, in part, on the hearing handicap. Any compensation that an individual will receive is dependent on the determination of a disability (2).



Legislation and Compensation



The introduction of legislation for noise regulation came in 1969 with the Walsh-Healey Public Contracts Act. This established a maximum noise exposure of 90dB over an eight-hour workday with increases of 5dB of exposure requiring a decrease in duration by half. The stipulation was made that when these levels were exceeded, employers must use control measures to limit exposure. In 1970, with the establishment of the Occupational Safety and Health Act, these requirements were applied to all employees involved in interstate commerce. Also in 1970, the Clean Air Act created the Office of Noise Abatement and Control within the EPA, which was designed to identify sources of noise and its effect on public health and welfare. Bulletin #334: Guidelines to the Department of Labor’s Occupational Noise Standards was published in 1971. In addition to restating the maximal allowable exposure levels (90dB for 8hr), this standard issued a requirement that employers provide personal protective equipment to those employees whose exposure exceeded these levels. Secondarily, industries in which noise exceeded the maximal levels were required to establish hearing conservation programs that included periodic screening audiograms and noise surveys. The Noise Control Act of 1972 served to establish noise emission standards for construction, transportation equipment, motors, engines and electrical equipment. Lastly, the Hearing Conservation Amendment, Final Rule was set forth by the Department of Labor in 1983. This lowered the noise exposure that necessitated implementation of a hearing conservation program to 85dB over eight hours instead of the previously stated 90dB. Employers were required to provide personal hearing protectors to those workers exposed to 90dB or greater noise levels (3,15).



During and immediately following the Industrial Revolution, the majority of responsibility for personal safety in the workplace rested upon individual employees. Employers limited their liability by establishing three common-law defenses. The fellow servant rule stated that the employer was not liable if an action of one worker caused injury to another. The assumption of risk policy stated that when a worker accepted wages they assumed the risks of the job. And, the limited responsibility policy stated that the employer could fire or transfer any worker who was negligent in their job. Thus, prior to 1948, compensation for occupational NIHL was essentially unheard of. However, between 1948 and 1959, several court decisions served to establish occupational hearing loss as a compensable injury. The original concept behind worker’s compensation was to provide payment to cover lost wages and medical expenses accrued by a worker as a result of an injury sustained on the job. Employers gave up their common-law defenses, employees gave up their right to sue, and limits were set on the amounts of liability. In the United States, the federal government oversees three worker’s compensation programs and each of the 50 states has such a program that covers occupational NIHL. The state programs are similar but may differ in terms of statute of limitations, waiting periods, exposure levels, use of hearing protectors or prior hearing loss. Hearing handicap is most often the criterion upon which compensation awards are based. Although other methods to calculate this are available, 32 of the 50 states use the AAO-1979 rule as outlined above (3). A study published in 1982 found that average compensation for hearing loss in private industry was $3,000 per claim, while federal employees received $8,000 per claim (15). In 1992, the average maximum payment for total bilateral hearing loss was $45,000 but in the majority of cases the claimant does not receive this maximum. Instead, the percentage handicap is multiplied by the state maximum to determine an individual award (4).



The otolarygologist’s role in cases of NIHL that may involve compensation centers on accurate diagnosis and succinct reporting of findings. Patients must undergo a complete otologic history and examination to rule out other potential sources of hearing loss. A complete audiogram is obtained and compared to previous studies if possible. Then, taking all of this data into account, the otolaryngologist must provide clear diagnostic conclusions in his or her report or testimony. In workers compensation cases the standard of “reasonable medical certainty” is utilized. This means that if a diagnosis is determined to be “more probable than not” the source of the disability, causation may be assigned and compensation awarded .