Search

Several studies have demonstrated that noise exposure may result in local vasoconstriction of cochlear vessels. The subsequent decrease in cochlear blood flow may lead to hypoxia and predispose to the formation of free oxygen radicals (FORs). If hypoxia occurs in response to noise exposure, then drugs that scavenge or block the formation of FORs should protect the cochlea from damage resulting from hypoxic or ischemic events as well as noise trauma. Rats were exposed to 60 hours of continuous broad-band noise (90 dB SPL) and treated with superoxide dismutase — Polyethylene glycol (SOD-PEG), allopurinol, or a control vehicle. Exposure to noise resulted in significant threshold shifts at each frequency tested (3, 8, 12, and 18 kHz) as measured by tone burst-evoked compound action potentials and cochlear microphonics recorded from the round window. Both of these thresholds In drug-treated animals were attenuated compared with animals exposed to noise alone. These findings show that SOD-PEG and allopurinol may preserve cochlear sensitivity associated with noise exposure. This suggests that noise-induced damage to the cochlea may be related to the activity of FORs.

Angioedema is a disorder characterized by well-demarcated nonpitting edema involving the tongue, floor of the mouth, larynx, lips, and face. This condition can progress to upper airway obstruction and death. Angiotensin-converting enzyme inhibitors (ACEIs), relatively new antihypertensive agents, act by blocking the formation of angiotensin II, a potent vasoconstrictor and stimulator of aldosterone formation. ACEIs also retard the breakdown of bradykinin, a potent vasodilator, which may lead to the edema seen in nonhereditary angioedema. These ACEIs include enalapril, Captopril, ilsinopril saralasin acetate, and a combination of ACEl with diuretics (for example, Capozide) From August 1987 to January 1989, we treated six patients with a nonhereditary form of angioedema related to ingestion of angiotensin-converting enzyme inhibitors Symptoms developed in all patients within 12 hours after their initial dose of an ACEl They presented with shortness of breath and dysphagia associated with tongue and floor of the mouth edema. Two Of the six required intubation and monitoring in the surgical intensive care unit for 36 to 48 hours. Three required supportive treatment and observation in an intermediate care unit, and one received supportive care in the clinic and was discharged the same day. Specifically, treatment consisted of cessation of inciting agent, steroids, antihistamines, and epinephrine. If not otherwise contraindicated. Assays of C, esterase inhibitor levels and C4were normal in all six patients; this was important in order to rule out hereditary forms of angioedema. These cases will be discussed, including a review of the literature, methods of diagnosis, pathophysiology and treatment of angioedema.

The purpose of this study was to assess the protective effects of allopurinol, a blocker of free oxygen radical (FOR) formation, and superoxide dismutase-polyethylene glycol (SOD-PEG), a scavenger of FORs, on Ischemic and reperfusion-induced cochlear damage. Fifteen Wistar Kyoto rats (WKY) were randomly assigned to three groups: (1) a control group (5 animals) that was exposed to 15 minutes of cochlear ischemia by clamping the anterior inferior cerebellar artery (AICA), followed by 15 minutes of reperfusion as documented by laser Doppler flowmetry; (2) a drug-treated group (5 animals) that received allopurinol before ischemia/reperfusion; and (3) a drug-treated group (5 animals) that received SOD-PEG before ischemia/reperfusion. In the control group, the tone burst-evoked compound action potential (CAP) recorded from the round window (RW) of the cochlea was abolished, and the cochlear microphonic (CM) was reduced after ischemia. In contrast, both allopurinol and SOD-PEG–treated animals showed post-reperfusion sensitivity in CAP and CM measures. We interpret these results to indicate that damage to the cochlea from ischemia and subsequent reperfusion can be attenuated by pretreatment with allopurinol or SOD-PEG. This provides indirect evidence that FORs may be partially responsible for cochlear damage resulting from ischemic conditions.

In the early period after chronic ear surgery, the reasons for conductive hearing loss may be difficult to determine. Patients who cannot autoinflate the middle ear after 3 weeks, or who have a negative Rinne test result with the 512 Hz tuning fork, are treated with a transtympanic injection of 0.5 cc of air with a 27-gauge needle and tuberculin syringe. This represents 20% of patients who had chronic ear surgery. Results show that hearing may be immediately improved, the sensation of pressure in the ear may be reduced, and fluid may be cleared from the middle ear. Other benefits may include the release of adhesions. The surgeon is better able to assess the thickness of the graft, and the status of the ossicular chain reconstruction can be determined. There have been no complications of middle ear infection or failure of the micropuncture site to heal. In our practice, middle ear air injection is a routine procedure in patients with inadequate eustachian tube function after chronic ear surgery. This report describes the results of 100 patients over 14 years who received middle ear air injections after chronic ear surgery compared with a control group of 100 patients who did not meet the criteria for requiring air injection. Hearing was immediately improved in 74% of patients as determined by Rinne testing. Audiograms were performed in 25 of these patients, documenting a mean improvement in pure-tone average of 16 dB. The long-term hearing results in patients undergoing air injection, who by definition had evidence of poor eustachian tube function, are similar to the results in the control group. This may indicate a lasting benefit of air injection. (OTOLARYNGOL HEAD NECK SURG 1993;109:488-92.)

An algorithm has evolved for the management of patients with acoustic neuroma. Decisions as to surgery vs. observation, surgical approach, and whether hearing preservation should be attempted depend on age, patient symptoms, size of the tumor, residual hearing, and degree of facial nerve involvement at the time of surgery. Conservative management is used for patients over 65 years of age. This consists of observation or subtotal resection through a translabyrinthine approach, depending on the absence or presence of brainstem signs or symptoms. In patients under 65 years of age, hearing preservation is attempted through the retrosigmoid approach in tumors 1.5 cm or less if pure-tone average is less than 30 dB and the discrimination score is greater than 70%. The translabyrinthine approach is our preferred approach for tumors of any size when hearing is not serviceable. A near-total excision is performed when the facial nerve cannot be separated from the tumor. The rationale for this algorithm in the management of 130 cases of acoustic neuroma over the past 17 years is presented.

We have recently demonstrated that allopurinol, a blocker of free oxygen radical (FOR) production, and superoxide dismutase (SOD), a scavenger of FOR, protect the cochlea from damage associated with ischemia/reperfusion. The purpose of this present study was to determine if tirilated mesylate (U74006F), a potent inhibitor of lipid peroxidation, can also protect the cochlea from ischemia/reperfusion. Eleven Wistar-Kyoto rats were randomly assigned to two groups: (1) a control group (6 animals) that was exposed to 15 minutes of cochlear ischemia by clamping the anterior-inferior cerebellar artery (AICA), followed by 15 minutes of reperfusion, and (2) a drug-treated group (5 animals) that received U74006F before ischemia/reperfusion. In the control group, the tone burstevoked compound action potential (CAP) recorded from the round window (RW) was abolished and cochlear microphonic (CM) was reduced. In contrast, the U74006F-treated animals showed post-reperfusion sensitivity in CAP, and less of a CM threshold shift. We interpret these results to indicate that U74006F lessens cochlear damage occurring as a result of ischemia/reperfusion and supports the hypothesis that FOR-induced lipid peroxidation may be partly responsible for the cochlear damage that occurs from ischemia.

Educational objectives: To understand the involvement of FOR in otolaryngology, including noise-induced hearing loss, cis-platin ototoxicity, presbycusis, myocutaneous free flaps, neural injury, and aging, and to begin to develop a potential intervention for the damaging effects of FOR.