Hypoacusis was found as a factor present in the family, which substantiates the risk of hearing loss in children due to genetic factors, as well as delayed language that can be associated to hearing losses and unspecified neurological pathology.
5% of children whose etiology is based on prematurity and all the risk factors underlying to this condition can generate false hypoacusis cases that corresponded to early stages of hearing maturity, as stated in the study by Talero et al.
Delayed auditory pathway maturation in the differential diagnosis of hypoacusis in young children.
Table 1 Classification of the degree of hypoacusis * Degree dB HL Normal hearing 0--10 Minimum hypoacusis 11--25 Slight hypoacusis 25--40 Moderate hypoacusis 40--55 Moderate to severe hypoacusis 55--70 Severe hypoacusis 70--90 Profound hypoacusis >90 * Ross and Downs, 2004--ANSI 1996 Table 2 Family antecedents Positive antecedents in 55.
Once all eligible charts had been selected, we reviewed them for each patient's age, sex, degree of hypoacusis
, and type of prosthesis.
Sudden hypoacusis is defined as a sensorineural hearing loss of rapid progression and unknown etiology that can progress to severe deafness.
The difficulty in pinpointing the etiology of sudden hypoacusis has hindered efforts to treat it.
In addition to all these therapies, another effective treatment for sudden hypoacusis is hyperbaric oxygen therapy (HOT).
In this article, we describe our comparison of outcomes in a group of 50 patients with sudden hypoacusis who were treated with either HOT or intravenous vasodilation within 48 hours of the onset of their symptoms.
We studied 50 patients with sudden hypoacusis of unknown etiology who had been referred to the ENT Clinic at Pisa University within 48 hours of the onset of acute symptoms.
In the treatment of sudden hypoacusis
, hyperbaric oxygen therapy (HOT) works, in part, by:
The neurologic examination detected anacusis on the left, severe hypoacusis
on the right, a complete vestibular loss bilaterally, a very slight paresis of the right facial nerve, and no signs of compression of the cerebral structures.