Otology Physicians & Surgeons - Long Beach,California



	John Wix Thomas III M.D. (562) 498-6653

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Medical Topics

: Otorhinolaryngology
(oto- + Gr. rhis nose + larynx larynx + -logy)that branch of medicine concerned with medical and surgical treatment of the head and neck, including the ears, nose and throat.
Tonsillitis
Septal Deviation And Perforation
Earache
Tinnitus
Migraine

Tonsillitis
Acute inflammation of the palatine tonsils, usually due to streptococcal or, less commonly, to viral infection.

Epidemics of viral tonsillitis occur among military recruits. Tonsillitis is characterized by sore throat and pain, most marked when swallowing and often referred to the ears. Very young children may not complain of sore throat, but they refuse to eat. High fever, malaise, headache, and vomiting are common.

Diagnosis
The tonsils are edematous and hyperemic. There may be a purulent exudate from the crypts and a membrane--white, thin, nonconfluent, and confined to the tonsil--that peels away without bleeding. Differential diagnosis includes diphtheria, Vincent's angina (trench mouth), and infectious mononucleosis. In diphtheria, the membrane is dirty gray, thick, and tough; it bleeds if peeled away, and smear and culture show Corynebacterium diphtheriae. Vincent's angina, characterized by superficial, painful ulcers with erythematous borders, is caused by a fusiform bacillus and a spirochete that are demonstrable on smear. Inflamed tonsils in infectious mononucleosis are characteristically associated with micropetechiae of the soft palate; atypical lymphocytes on smear and a positive monospot test confirm the diagnosis of Mononucleosis.

Treatment
For viral tonsillitis, symptomatic therapy is the same as that for pharyngitis (see above). Penicillin V 250 mg po q 6 h or, for children < 6 yr, penicillin V 125 mg po q 8 h is the treatment of choice for streptococcal tonsillitis and should be continued for 10 days. If possible, another throat culture should be performed 5 to 6 days later. Throat cultures of family members should be performed initially so that carriers may be treated at the same time. Tonsillectomy should be considered if acute tonsillitis returns repeatedly after adequate treatment or if chronic tonsillitis and sore throat are relieved only temporarily by antibiotic therapy.
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Sinusitis
Inflammation of the paranasal sinuses due to viral, bacterial, or fungal infections or allergic reactions.

Acute sinusitis is caused by streptococci, pneumococci, Haemophilus influenzae, or staphylococci and is usually precipitated by an acute viral respiratory tract infection. Chronic sinusitis may be exacerbated by a gram-negative rod or anaerobic microorganisms. In a minority of cases, chronic maxillary sinusitis is secondary to dental infection.

In a URI, the swollen nasal mucous membrane obstructs the ostium of a paranasal sinus, and the O2 in the sinus is absorbed into the blood vessels of the mucous membrane. The resulting relative negative pressure in the sinus (vacuum sinusitis) is painful. If the vacuum is maintained, a transudate from the mucous membrane develops and fills the sinus; the transudate serves as a medium for bacteria that enter the sinus through the ostium or via a spreading cellulitis or thrombophlebitis in the lamina propria of the mucous membrane. An outpouring of serum and leukocytes to combat the infection results, and painful positive pressure develops in the obstructed sinus. The mucous membrane becomes hyperemic and edematous.

Symptoms, Signs, and Diagnosis
Acute sinusitis and chronic sinusitis produce similar symptoms and signs. The area over the affected sinus may be tender and swollen. Maxillary sinusitis causes pain in the maxillary area, toothache, and frontal headache. Frontal sinusitis produces pain in the frontal area and frontal headache. Ethmoid sinusitis causes pain behind and between the eyes and a frontal headache often described as splitting. Pain from sphenoid sinusitis is less well localized and is referred to the frontal or occipital area. Malaise may be present. Fever and chills suggest an extension of the infection beyond the sinuses.

The nasal mucous membrane is red and turgescent; yellow or green purulent rhinorrhea may be present. Seropurulent or mucopurulent exudate may be seen in the middle meatus with maxillary, anterior ethmoid, or frontal sinusitis and in the area medial to the middle turbinate with posterior ethmoid or sphenoid sinusitis.

In acute and chronic sinusitis, the swollen mucous membrane and retained exudate cause the affected sinus to appear opaque on x-rays. CT provides better definition of the extent and degree of sinusitis. X-rays of the apices of the teeth may be required in chronic maxillary sinusitis to exclude a periapical abscess.

Treatment
In acute sinusitis, improved drainage and control of infection are the aims of therapy. Steam inhalation effectively produces nasal vasoconstriction and promotes drainage. Saline nasal washes may promote drainage. Topical vasoconstrictors, such as phenylephrine 0.25% spray q 3 h, are effective but should be used for a maximum of 7 days; systemic vasoconstrictors, such as pseudoephedrine 30 mg po (for adults) q 4 to 6 h, are less effective.

In acute and chronic sinusitis, antibiotics should be given for at least 10 to 12 days. In acute sinusitis, penicillin V 250 mg po q 6 h is the initial antibiotic of choice, and erythromycin 250 mg po q 6 h is the second choice. In exacerbations of chronic sinusitis, a broad-spectrum antibiotic, such as ampicillin 250 or 500 mg or tetracycline 250 mg po q 6 h, is better. In chronic sinusitis, prolonged antibiotic therapy for 4 to 6 wk often results in complete resolution. The sensitivities of pathogens isolated from the sinus exudate and the patient's response guide subsequent therapy. Sinusitis not responsive to antibiotic therapy may require an operation (maxillary sinusotomy, ethmoidectomy, or sphenoid sinusotomy) to improve ventilation and drainage and to remove inspissated mucopurulent material, epithelial debris, and hypertrophic mucous membrane. These operations are usually performed intranasally with the aid of an endoscope (functional endoscopic sinus surgery). Chronic frontal sinusitis is managed with osteoplastic obliteration of the frontal sinuses but may be treated endoscopically in selected patients.

SINUSITIS IN METABOLICALLY OR IMMUNOLOGICALLY COMPROMISED PATIENTS

In patients with poorly controlled diabetes or with immunodeficiency, aggressive and even fatal fungal or bacterial sinusitis can occur.

Mucormycosis (phycomycosis)--a mycosis due to fungi of the order Mucorales, including species of Mucor, Absidia, and Rhizopus--may develop in patients with poorly controlled diabetes. It is characterized by black, devitalized tissue in the nasal cavity and neurologic signs secondary to retrograde thromboarteritis in the carotid arterial system. Diagnosis is made by the histopathologic demonstration of mycelia in the avascularized tissue, and treatment requires control of the diabetes and IV administration of amphotericin B.

Aspergillosis and candidiasis of the paranasal sinuses may occur in a patient who is immunologically compromised as a result of therapy with cytotoxic drugs or the underlying disease process in leukemia, lymphoma, multiple myeloma, AIDS, or other immunosuppressive diseases. Aspergillosis is characterized by polypoid tissue in the nose and paranasal sinuses. Biopsy and culture of this tissue are required for diagnosis; aggressive paranasal sinus surgery and IV amphotericin B therapy are advocated as attempts to control these often fatal infections.
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Septal Deviation And Perforation
Deviations of the nasal septum due to developmental abnormalities or trauma are common but often are asymptomatic and require no treatment. Septal deviation may cause nasal obstruction and predispose the patient to sinusitis (particularly if the deviation obstructs the ostium of a paranasal sinus) and to epistaxis as a result of drying air currents. Treatment of symptomatic septal deviation consists of septoplasty (septal reconstruction).

Septal ulcers and perforations may result from nasal surgery; repeated trauma, such as that from picking the nose; cocaine use; or conditions such as TB, syphilis, leprosy, and Wegener's granulomatosis. Crusting around the margins and repeated epistaxis may result. Small perforations may whistle. Topically applied bacitracin 500 U/g in a petrolatum base reduces crusting. Symptomatic perforations of the nasal septum are occasionally repaired using buccal or septal mucous membrane flaps; closing the perforation with a Silastic septal button is a reliable option.

Earache
Earache (otalgia) occurs with infections and neoplasms in the external or middle ear or is referred to the ear from remote disease processes. Even mild inflammation in the ear canal produces severe pain; perichondritis of the pinna produces severe pain and tenderness. Eustachian tube obstruction causes abrupt changes in middle ear pressure relative to atmospheric pressure, which may result in painful retraction of the tympanic membrane. Infection in the middle ear produces painful inflammation of its mucous membrane and pain from increased pressure in the middle ear, with bulging of the tympanic membrane. The most common cause of earache in children, acute otitis media, requires prompt examination by a physician and antibiotic therapy to prevent serious sequelae.

If there is no disease in the ear, the source of referred pain should be sought in areas receiving sensory supply from the cranial nerves that subserve sensation in the external and middle ear--ie, the 5th (trigeminal), 9th (glossopharyngeal), and 10th (vagus) nerves. Specifically, the cause of obscure otalgia should be sought in the nose, paranasal sinuses, nasopharynx, teeth, gingiva, temporomandibular joint, mandible, parotid glands, tongue, palatine tonsils, pharynx, larynx, trachea, and esophagus. Occult neoplasms (most often, carcinoma of the nasopharynx) in these locations are sometimes first manifested by pain referred to the ear. Otalgia commonly occurs after a tonsillectomy.
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Tinnitus
Perception of sound in the absence of an acoustic stimulus.

Tinnitus, a subjective experience of the patient, is distinguished from bruit, noise that may be heard by the examiner and often also by the patient.

Tinnitus may be a buzzing, ringing, roaring, whistling, or hissing, or it may involve more complex sounds that vary over time. It may be intermittent, continuous, or pulsatile (synchronous with the heartbeat). An associated hearing loss is usually present.

The mechanism causing tinnitus is obscure. Tinnitus may occur as a symptom of nearly all ear disorders, including obstruction of the ear canal by cerumen or a foreign body, infections (external otitis, myringitis, otitis media, labyrinthitis, petrositis, syphilis, meningitis), eustachian tube obstruction, otosclerosis, middle ear neoplasms (eg, glomus tympanicum and glomus jugulare tumors), Meniere's disease, arachnoiditis, cerebellopontine angle tumors, ototoxicity (eg, due to salicylates, quinine and its synthetic analogs, aminoglycoside antibiotics, certain diuretics, carbon monoxide, heavy metals, alcohol), cardiovascular diseases (eg, hypertension, arteriosclerosis, aneurysms), anemia, hypothyroidism, hereditary sensorineural or noise-induced hearing loss, acoustic trauma (blast injury), and head trauma.

Evaluation of a patient with tinnitus requires the minimum comprehensive audiologic assessment (see above) as well as CT of the temporal bone and MRI of the head. If a sensorineural hearing loss is found, tests to differentiate sensory and neural hearing losses (see above) are indicated. Pulsatile tinnitus requires investigation of the vascular system with carotid and vertebral arteriograms to exclude arterial obstruction, aneurysms, and vascular neoplasms.

Treatment
The ability to tolerate tinnitus varies among patients. Treatment should be directed toward the underlying disease, because its amelioration may lessen the tinnitus. Correcting the associated hearing loss usually relieves the tinnitus; a hearing aid often suppresses the tinnitus. Although there is no specific medical or surgical therapy for tinnitus, many patients find relief by playing background music to mask the tinnitus and may go to sleep with the radio playing. Some patients benefit from using a tinnitus masker, a device worn like a hearing aid that presents a sound more pleasant than the tinnitus. Electrical stimulation of the inner ear, as with a cochlear implant, occasionally reduces the tinnitus but is appropriate only for the profoundly deaf.
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Migraine
Headache that lasts 4 to 72 h, is throbbing, is moderate to severe in intensity, is unilateral, becomes worse with exertion, and is associated with nausea, vomiting, or sensitivity to light, sound, or smell.

Only three or four of the above criteria must be present for accurate diagnosis.

About 24 million Americans have migraines. Migraines may occur at any age but usually begin between ages 10 and 40, more often in women than in men. Headaches often partially or completely remit after age 50. More than 50% of patients have a family history of migraine.

Etiology and Pathophysiology
The cause is unknown, and the pathophysiology is not fully understood. Changes in brain and scalp arterial blood flow occur, but whether vasodilation and vasoconstriction are a cause or an effect of the migraine is unclear. Cortical spreading depression (fundamental changes in the brain cortex in which a crest of hyperpolarization is followed by depolarization) may induce neurogenic inflammation, with vasodilation, activated WBCs and permeable capillaries. The inflammation leads to irritation of perivascular trigeminal sensory fibers. A cascade of events follows, causing changes in blood flow and the severe headache. Intracranial vascular malformations are a rare cause of migraine-like headaches.

The mechanism for migraines is not well defined, but several triggers are recognized. Cycling estrogen, a significant trigger, may explain why there are three times as many women with migraines as men. Evidence of estrogen's role as a trigger includes the following: During puberty, migraine becomes much more prevalent in females than in males; migraines are particularly difficult to control in the premenopausal period; and oral contraceptives and estrogen replacement therapy often make migraine worse. Other triggers include insomnia, barometric pressure change, and hunger. The association of diet and migraine is usually overstated. No prospective study has proved an association.

Symptoms, Signs, and Diagnosis
Migraine may be preceded by a short prodromal period of depression, irritability, restlessness, or anorexia and may be associated with an aura (in 10 to 20% of occurrences). An aura usually precedes the headache by no more than 1 h but is often concurrent. An aura is a transient, reversible neurologic visual, somatosensory, motor, or language deficit. Most persons report visual auras, including flashing lights, scintillating scotoma, and fortification spectrums.

Symptoms usually follow a pattern in each patient, except unilateral headaches may not always occur on the same side. The patient may have attacks daily or only once every several months. Diagnosis is based on the symptom patterns when there is no evidence of intracranial pathologic changes. Migraine is more probable when the patient has a family history of migraine or of visual prodromata. No diagnostic tests are useful, except to exclude other causes.

Treatment
Treatment depends on the frequency of attacks and the presence of comorbid illness. In general, treatment can be classified as prophylactic, abortive, or analgesic.

If a person has more than one migraine a week, long-term prophylaxis should be considered. -blockers, calcium channel blockers, tricyclic antidepressants, or anticonvulsants may be used. The choice is empiric but is guided by the presence of comorbid illness. For example, if hypertension coexists, -blockers or calcium channel blockers would be most efficient. If depression or sleep dysfunction coexists, tricyclic antidepressants should be tried first.

Abortive drugs are used for acute treatment. A new class of drugs that activate serotonin receptors (5-hydroxytryptamine [5-HT] 1B/1D agonists) block neurogenic inflammation and can abort migraine pain in about 70% of patients. Sumatriptan, the prototype, is available in oral and subcutaneous injection forms. Subcutaneous dosing is more effective but has more adverse effects, which include flushing, nausea, esophageal constriction, and, rarely, coronary artery constriction. Caution is advised in prescribing sumatriptan to men > 55 yr, postmenopausal women, or persons with a history of heart disease. The next generation of 5-HT 1B/1D agonists (eg, eletriptan, naratriptan, rizatriptan, zolmitriptan) promises to increase the benefits and reduce the adverse effects. Ergot alkaloid derivatives, such as ergotamine tartrate and dihydroergotamine, in oral and parenteral preparations can be used effectively. Dopamine antagonist antiemetics, such as metoclopramide and prochlorperazine, are effective, even if nausea is not prominent.

Analgesics should be used sparingly. They are effective in some patients but cause rebound headache with dose escalation in others. NSAIDs are probably best for mild to moderate headaches. Opioids should be avoided except under special circumstances and strict guidelines.
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John Wix Thomas III M.D. � 1703 Termino Ave #210, Long Beach,CA 90804 � (562) 498-6653
Ears, Nose, Throat Specialist

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