Radical meatoplasty in the treatment of severe chronic external otitis.

In the beginning, external otitis is an inflammation of the skin of the external ear canal. Partial or total obliteration of the meatus causes cleaning problems, which worsen the obliteration, and hence, the infection. Immunosuppressive medication or illness, certain dermatological problems or frequent infections may lead to irreversible changes and to the malignant form of external otitis with life-threatening sequelae. Conservative treatments in the beginning are aimed at regaining the normal skin functions by helping the cleaning process and curing the acute infection with repeated irrigation, proper antibacterial medication and corticosteroids and anti-inflammatory analgesics. In rare prolonged cases, surgical procedures are needed to help the cleaning process by removing the irreversibly thickened skin and bone affections, and using grafts. On the basis of our experience, even the removal of the diseased skin and enlarging of the external ear canal are insufficient procedures in the most difficult cases. In the present paper, we describe a new surgical method that we have performed to treat chronic bilateral obliterative external otitis in 2 patients, with favorable results.

Treatment of severe tinnitus.

In 1995-96 we selected a group of 26 patients who were suffering from severe invalidating idiopathic tinnitus (IT) in order to evaluate the efficacy of rehabilitation and some alternative therapies. All patients were assessed thoroughly by means of audiology and radiology regarding any objective cause for the symptom. In order to help patients control their symptom by increasing knowledge and adding supportive elements, they were given basic education (presentations of the anatomy and physiology of the ear and hearing system, psychological and social aspects of IT, guided and non-guided group discussions, relaxation therapy, physiotherapy, music therapy) for 4 months, comprising one 2-h session bi-weekly. This type of group therapy was found to be extremely helpful, although no objective evaluation revealed effects on IT sensation (VAS) or psychometric measures (SLC-90). In a second limb of the study, the same patients attended a 6-day intensive course in a spa. The purpose was to evaluate the possible usefulness of the widely recommended alternative therapies for IT. All patients had an opportunity to sample the treatments. Six months later only a few had tried any of these treatments, but all reported that the lessons were the most helpful in association with supportive group discussions. The results indicated that none of these therapies can be recommended, based on rational medical practise.

Betahistine increases vestibular blood flow.

Betahistine is used for treatment of several vestibular disorders. Despite the accepted use of this histamine-like substance, its mechanism of action is not well understood. The purpose of this study was to assess the possibility that one of the activities of betahistine is increasing blood flow in the peripheral vestibular end organs. Using a novel surgical approach, we identified the posterior semicircular canal ampulla of guinea pigs and placed a laser Doppler probe in position to obtain blood flow measurements from the posterior semicircular canal ampulla. Blood pressure, heart rate, and vestibular blood flow were continuously recorded. Concentration-response curves were obtained for betahistine (2.5, 5, 7.5, and 10 mg/kg) and control-vehicle (0.15 mol/L NaCl) infusions. A separate group of subjects was pretreated with the competitive selective H3 agonist, thioperimide maleate, before betahistine treatment. Increases in vestibular blood flow and decreases in blood pressure were observed in response to betahistine infusions. Pretreatment with thioperamide maleate abolished these changes at low doses of betahistine and attenuated the responses at higher doses of betahistine. These results show that betahistine administration induces increases in vestibular blood flow. These findings support the potential use of betahistine for treatment of vestibular disorders, which may be caused by compromised circulation.

Effects of intratympanically delivered lidocaine on the auditory system in humans.

Since lidocaine is used to relieve the symptoms of Meniere's disease and tinnitus, its effects on the human cochlea is of specific interest. In experimental animals, topically administered lidocaine affects cochlear electrophysiology in a specific, dose-dependent manner. In the current study, lidocaine (40 mg in 1 ml of saline) was delivered intratympanically in six patients with essentially normal hearing in an attempt to alleviate tinnitus. Auditory function was assessed by pure tone audiometry, auditory evoked brain stem responses (ABR), and transiently evoked otoacoustic emissions (TEOAE) to observe possible drug effect in the auditory system. In five patients, saline was injected prior to lidocaine for control purposes. Saline injection did not create significant changes in any of the measures. After a 2 hr follow-up period, intratympanic injection of lidocaine caused a 2 to 10 dB reduction in TEOAE level at 1 to 3 kHz frequencies. This reduction was at its maximum at the 30 min post-injection sampling point, and was followed by a slow recovery. At 2 hr post-injection, TEOAE amplitude was still 2 to 4 dB below baseline level. Pure tone thresholds were slightly affected 30 min after intratympanic lidocaine injection, but were fully recovered 1 hr after the injection. Lidocaine injection did not cause any changes in ABR latencies or amplitudes in any of the patients. These results suggest that the dose of intratympanically administered lidocaine used here has a specific effect on the organ of Corti structures in human subjects, without significantly affecting the auditory nerve or central auditory pathways. The relationship of the drug effect in conjunction with a possible effect on inner ear disorder might help to localize the site of disorder.

Plasma concentrations of lidocaine (lignocaine) after cranial subcutaneous injection during neurosurgical operations.

After cranial subcutaneous injection of lidocaine 0.8-3.7 mg/kg+adrenaline (epinephrine) 1:200,000 in neurosurgical patients, fast drug absorption was found with peak plasma concentrations of 0.6-1 microgram/ml in 5-10 min. However, the concentrations remained above the lowest effective antiarrhythmic level of 0.6 microgram/ml for only about 10 min. In one patient, simultaneously administered intravenous lidocaine had an additive effect on those levels. Induced hypotension (sodium nitroprusside) during aneurysm operations decreased the arterial plasma level of lidocaine and was followed by a new peak after discontinuation. Thus the absorption of a drug during induced hypotension from subcutaneous tissue is often erratic.

Plasma lidocaine concentrations after different methods of releasing the tourniquet during intravenous regional anaesthesia.

Different methods of tourniquet release have been proposed to decrease the concentrations of local anaesthetic released into the systemic circulation at the end of intravenous regional anaesthesia. The effect of releasing the tourniquet intermittently with 5 seconds (group I) and 30 seconds (group II) deflation periods or at once (group III) was studied in 25 adult patients after intravenous regional anaesthesia with 40 ml of 0.5% lidocaine. The venous plasma lidocaine concentrations from the contralateral arm were measured by gas chromatography. There was no leakage of lidocaine from the occluded arm into the systemic circulation. The mean maximum plasma lidocaine concentration in group I 1.99 +/- 1.45 (SD) microgram/ml, in group II 1.33 +/- 0.54 microgram/ml and in group III 1.56 +/- 0.88 microgram/ml (P greater than 0.05) was below the toxic concentrations reported in the literature. There were subjective complaints such as dizziness and ringing in the ears in 4 out of the 7 patients in group I, in 2 out of the 9 patients in group II and in one of the 9 patients in group III (P greater than 0.05). There was no correlation between the duration of tourniquet time (range 12-87 minutes) and the maximum plasma lidocaine concentration. The intermittent release of the tourniquet did not decrease the venous plasma lidocaine concentrations in the contralateral arm; neither did comparing the lidocaine pharmacokinetics in 5 patients of group II after tourniquet release and in the 5 healthy volunteers after a single 100 mg intravenous lidocaine injection reveal any differences.