Management of Peritonsillar Abscess Within a Local Emergency Department: A Quality Analysis Study.

OBJECTIVE: Peritonsillar abscess (PTA) is the most common deep space infection of the head and neck, affecting thousands of people annually with high treatment costs. The purpose of this project was to determine how in-network emergency departments (EDs) adhere to generally accepted guidelines regarding diagnosis and management of potential PTAs. METHODS: The authors performed a retrospective chart review to identify patients with PTA in five EDs in one year. Information pertaining to diagnostic tests, treatment, and airway status was also collected. Descriptive analysis was used to assess if EDs were consistent with generally accepted guidelines. RESULTS: Six hundred twenty-one patient records were identified and 140 were included in final analysis. Out of 140 patients, 71 were admitted for inpatient management and 23 were admitted for observation. Of the 46 patients diagnosed and discharged from the ED, 61% received a computerized tomography (CT) scan and only 39% had PTA drainage performed. Four (3%) patients received a point of care ultrasound and a CT scan and no patient received only an ultrasound. Out of all patients, 116/140 received a CT scan and 22 received drainage in the ED. The remainder of these patients either had drainage performed by an otolaryngologist or had no drainage performed. Of the 94 patients admitted for inpatient or observation, 84 received a CT scan and six received drainage by an ED physician. Only 62% of patients were given a penicillin derivative and 29% were given clindamycin, which has no Gram-negative coverage. CONCLUSION: One-third of PTA patients were managed within the ED, far less than similar studies. Of these, over 50% received a CT scan and less than 50% had PTA drainage. PTA drainage can improve patients\u27 symptoms and antibiotic effectiveness. The majority of patients were prescribed a penicillin derivative with or without another antibiotic

The Growth of Hearing Loss in Neonatal Chicks Exposed to Intense Pure Tones.

One-day-old chicks were exposed to an intense pure tone (0.9 kHz, 120 dB SPL) and assigned to one of eight groups based on continuous exposure durations from 1 to 200 h. As each animal was removed from the exposure, it was anesthetized and an electrode was placed in the nucleus magnocellularis. Sound-evoked potentials were used to measure absolute thresholds and frequency selectivity. Thresholds were measured at 10 frequencies between 0.1 and 4.5 kHz while frequency selectivity was assessed by a simultaneous masking tuning-curve procedure at five probe-tone frequencies between 0.3 and 2.5 kHz. Threshold shift was greatest at 1.3 kHz and reached a maximum loss of approximately 57 dB between 48 and 200 h of exposure. The shape of the threshold-shift curve as a function of exposure duration (for frequencies between 0.9 and 2.5 KHz) suggested the presence of an early and late effect. The loss in tuning sharpness was evaluated by comparing the values of Q10 dB for control and exposed tuning curves and expressing the difference between them as a percent change. Probe-tone tuning curves above 0.9 kHz became less selective as exposure duration increased. A maximum decrease in tuning of about 54 percent was reached by 48 h and this remained constant to 200 h. The low-frequency tuning curves (below 0.9 kHz) did not show any systematic loss in selectivity. The changes in sensitivity and selectivity are discussed in relation to the patterns of cochlear injury that occurred on the basilar papilla as exposure duration lengthened

The Chiari-I malformation.

We have described the important clinical features and aspects of the Chiari-I malformations, with particular emphasis on Chiari-I malformation. Previously thought to be a rare finding with only minor significance, Chiari-I malformation is an important cause of a variety of symptoms, and will be diagnosed even more frequently as the use of MRI increases. The clinician must consider Chiari-I malformation in any patient with unexplained sensorineural hearing loss, headache, vertigo, ataxia, dysequilibrium, dysphagia or other cranial nerve symptom, especially if accompanied by more classic symptoms of this disorder, such as cervical pain or weakness

The use of diagnostic testing in asymmetric sensorineural hearing loss.

The etiology of an asymmetric sensorineural hearing loss can often be difficult to determine. Because a wide variety of pathologic processes may be responsible for the hearing loss, numerous diagnostic tests are usually used in the initial evaluation, including pure-tone audiometry, acoustic reflex testing, imaging, serologic testing, and auditory brainstem response testing. The diagnostic evaluations of 225 consecutive cases of asymmetric sensorineural hearing loss are reviewed. A cochlear site-of-lesion was demonstrated in the majority (194) of patients. Because all retrocochlear lesions (31) were associated with an abnormal auditory brainstem response, imaging should be performed in that group of patients. Magnetic resonance imaging offers greater specificity than computed tomography. Reflex decay, acoustic reflex testing, and rollover were all associated with a high false-negative rate. Whereas serologic testing for syphilis yielded several cases of otosyphilis, thyroid function testing was of little value. A diagnostic protocol for asymmetric sensorineural hearing loss is presented

Angiotensin-converting enzyme inhibitor induced angioedema of the head and neck.

Angiotensin-converting enzyme (ACE) inhibitors are now in widespread use for the treatment of essential and renovascular hypertension. Consequently, angioedema, an uncommon complication of ACE inhibitor therapy is being encountered with increasing frequency. Since ACE inhibitor angioedema predominantly involves the face, lips, oral cavity, and occasionally the larynx the otolaryngologist is often consulted to evaluate affected patients. Treatment ranges from simple cessation of the drug to emergent airway intervention. The pertinent pharmacologic properties of ACE inhibitors and the pathophysiology of angioedema are discussed. The authors\u27 experience with the evaluation and treatment of ACE inhibitor induced angioedema is presented