Sudden onset hearing loss bilateral knee,jhumka earrings buy online,child hearing protection ear muffs - Test Out

Send Home Our method Usage examples Index Contact StatisticsWe do not evaluate or guarantee the accuracy of any content in this site. The aim of this study was to determine the effects of various treatment modalities employed for patients with sudden sensorineural hearing loss (SHL).
Sudden sensorineural hearing loss (SHL) is defined as hearing loss equal to or greater than 30 dB at three or more consecutive frequencies, the onset of which takes place over a period of 3 days or fewer [1]. Treatment is controversial and can involve anti-inflammatory drugs (steroids), vasodilators, antiviral agents, plasma expanders, diuretics, calcium channel antagonists, hyperbaric chamber use, carbogen, anticoagulants and, more recently, intratympanic corticosteroids [6-11].
The aim of this study was to observe the progression of SHL in patients who underwent different treatments at the SHL outpatient facility of our institution and to describe clinical and epidemiological aspects.
This retrospective study analyzed the records of patients treated in the sudden hearing loss section of the Otolaryngology Department, Clinic Hospital School of Medicine, University of Sao Paulo, Brazil, between 1996 and 2006. All patients underwent imaging tests (temporal bone magnetic resonance imaging or computed tomography) and complete blood cell counts.
The patients underwent serial audiometric testing at baseline and after 30, 90, 120, and 180 days of treatment. Considering all the cases, we observed significant posttreatment reductions in low- and high-frequency PTA (Table 3).
Estimates have shown that among patients with SHL, the mean age ranges from 43 to 53 years, the gender distribution is equivalent, and the hearing loss is unilateral in more than 95% of cases [2,4,11,13,14], similar to what we observed in our study.
Approximately 25-40% of patients with SHL present with concomitant upper-airway infection [11]. According to Rauch [11], vestibular symptoms were identified in 28-57% of cases, as compared with 32-40% reported by Nakashima et al.
The most common etiological factors identified for SHL were those that are not the most frequent but can be directly identified through clinical history, blood samples, or imaging studies, including autoimmune diseases, acoustic trauma, ototoxic drugs, Lyme disease, and ear malformations.
Theoretically, this anatomical presentation predisposes to hypoxia, spasms, thrombi, and hemorrhage, especially at the cochlear apex, primarily affecting the response to low frequencies [23].
When we analyzed the cases in which PTA normalized, we observed that in most cases baseline PTA was moderate and the etiology was unknown. Among the five treatment groups, the differences in ΔPTA were not statistically significant at any frequency.
For low-frequency and high-frequency PTA, we observed an inverse linear correlation between time from onset to treatment and audiometric response presented by the patients. On the basis of our analysis, we can infer that plasma expanders do not improve the efficacy of the corticosteroidacyclovir combination used in managing SHL in patients. Zones of the Neck This actually applies to penetrating trauma but is useful to review when discussing neck anatomy. Morbidity: Esophageal Injury Odynophagia, dysphagia, hematemesis Airway injury ? 25% have esophageal injury Transcervical trajectory Saliva in wound, subcutaneous emphysema Prevertebral air on lateral neck X ray Kietdumrongwong P & Hemachudha T 2005 Kietdumrongwong P & Hemachudha T.
Morbidity: Airway Injury More common in blunt trauma 5-15% PNI will have laryngotracheal trauma Hoarseness, stridor, hemoptysis, difficulty breathing, pain Air leak in wound, difficult airway ? surgery!!!
Auricular Hematoma accumulation of blood in the subperichondrial space, secondary to blunt trauma.
Nasal trauma Timing of repair : Within 1 - 3 hours of the time of injury before significant edema has developed. We retrospectively evaluated the records of patients treated in the sudden hearing loss section of the Otolaryngology Department at Clinic Hospital, School of Medicine, University of Sao Paulo, Brazil, between 1996 and 2006.
Approximately one-third of affected patients improve spontaneously, most within the first 2 weeks of disease progression [1,3]. The inclusion criterion was SHL of sudden onset over a 72-hour period, equal to or greater than 30 dB at three or more consecutive frequencies. Group II included patients who had a 0- to 15-day history of SHL and in whom the use of plasma expanders was contraindicated owing to systemic hypertension, cardiopathy, coagulation disorder, or renal failure. The laboratory exams included erythrocyte sedimentation rate, fasting glucose, cholesterol, triglycerides, free thyroxine and thyroid-stimulating hormone, circulating immunocomplex, complement, rheumatoid factor, and antinuclear factor. The only epidemiological study of SHL published to date was performed in Japan in three different years and different decades [13].
However, other authors [2] observed that, unlike our finding, only 11% of their SHL patients presented with concomitant upper-airway infection. The autoimmune diseases that can lead to SHL are autoimmune inner-ear disease and immunemediated systemic disease leading to a secondary innerear injury. One piece of evidence supporting this hypothesis is the fact that various authors have reported among patients with SHL seropositivity for a number of viruses, including herpes simplex, varicella zoster, cytomegalovirus, influenza, parainfluenza, rubella, and mumps [9, 18-20].
Studies involving patients with SHL have shown evidence of sudden-onset cochlear ischemia and an association between SHL and systemic vascular diseases [23].
In fact, vascular etiology is a very promising theory, but confirming and explaining it is difficult. Despite the lack of a control group, the findings of our study can be compared with those presented in the literature.


Among the remaining cases, the most common etiology was diabetes mellitus, followed by viral causes. The improvement in PTA was less pronounced in patients in groups IV and V (who started treatment at least 15 days after the onset of SHL) than in the other patients, although the difference was not statistically significant. This finding is in agreement with those of other studies showing that earlier initiation of treatment improves prognosis [1,4,25].
Retropharyngeal carotid artery important for presurgical planning Esophageal injury can track air into RP, prevertebral space Missed esophageal injuries can present as retropharyngeal abscess, mediastinitis, sepsis Bleeding that displaces prevertebral muscles anteriorly is associated with vertebral body fractures. Majority airways managed by rapid sequence intubation (RSI) at scene or ED Mandavia DP 2000RetrospectiveN = 74811% emergent intubation -67% RSI with ? 100% success -33% fiberoptic ? 91% success -3 fiberoptic failures ? RSI Eggen JT 1993 N = 11460% intubated, 22% ED No intubation complications Shearer VE 1993 N = 10783% RSI with DL ? 100% success 6% surgical airway ? 100% 7% awake fiberoptic ? 98% 4% blind nasotracheal ? 75% Eggen JT et al.
This creates a barrier for diffusion between the cartilage and the perichondrial vascularity, leading to necrosis of the cartilage. However, patients rarely present this early and often require reevaluation within 3 -7 days to allow for extensive facial edema to subside. Our study included patients with SHL of sudden onset (occurring over a 72-hour period) at equal to or greater than 30 dB at three consecutive frequencies. Approximately one-third of cases are accompanied by complaints of tinnitus, dizziness, and ear fullness [2,3].
Risk factors associated with poor prognosis include time of disease progression prior to the initiation of treatment, extreme age (being very young or very old), severe initial hearing loss, concomitant vestibular symptoms, and a descending pure-tone audiometry curve [1,4,12].
The treatment regimen was the same as that used in group I patients, minus dextran or minus dextran and acyclovir if the SHL onset was greater than 5 days. Serological tests were also conducted for herpes simplex virus type I, cytomegalovirus, syphilis, rubella, measles, Lyme disease, and the human immunodeficiency virus.
Nevertheless, none of those authors compared their results with the prevalence observed in epidemiological studies of upper-airway infection in the corresponding populations. However, those authors found that prevalence of these disorders among patients with SHL was lower than that reported for patients with dizziness [15], which is in agreement with the findings by Cadoni et al. In our study, the etiology was vascular in 4.3% of the cases of SHL, one of which was very severe. We cannot state with confidence that the likelihood of complete recovery is greater in such cases of SHL, as other factors such as gender and age at SHL onset might exert some influence.
In groups I, II, and III, treatment was initiated within the first 15 days after the onset of SHL. We observed a genderbased difference in ΔPTA, with a tendency toward statistical significance, suggesting that the SHL prognosis is poorer for men. Oral steroid treatment of sudden sensorineural hearing loss: A ten year retrospective analysis. Sudden complete or partial loss of function of the octavus system in apparently normal persons.
Antiviral treatment of idiopathic sudden sensorineural hearing loss: A prospective, randomized, double-blind clinical trial. Treatment of idiopathic sudden sensorineural hearing loss with antiviral therapy: A prospective, randomized, double-blind clinical trial. Prognosis for sudden sensorineural hearing loss: A retrospective study using logistical regression analysis. Clinicoepidemiologic features of sudden deafness diagnosed and treated at university hospitals in Japan.
The implication of viruses in idiopathic sudden hearing loss: Primary infection or reactivation of latent viruses? The relationship of the herpesvirus family to sudden hearing loss: A prospective clinical study and literature review. The anterior part ( little area ) of the nasal septum is the most frequent site for bleeding, because of rich blood supply. We divided patients into five groups by profile and treated them with dextran, dexamethasone, acyclovir, nicotinic acid, and papaverine hydrochloride (with or without vitamin A). Group III included patients who had a 6- to 15-day history of SHL and who were hospitalized and treated with the same treatment used in group I minus acyclovir.
If no improvement occurred in the auditory threshold after 3 days, treatment was discontinued and the patient was discharged.
No statistically significant difference was noted among the treatment groups in terms of audiometric progression determined by calculating the difference between the low- and high-frequency PTAs seen at baseline and after 180 days (Table 7). Owing to differences in design and population, we cannot directly compare our sample with theirs. However, despite advances, serological diagnosis remains difficult, as most tests are nonspecific and have a low accuracy rate [17]. Blood circulation in the inner ear is of the terminal type, the cochlear artery running from the base to the apex of the cochlea. In that case, SHL was detected after an episode of aplastic anemia (severe erythrocytopenia and thrombocytopenia) resulting from prolonged use of a nonsteroidal antiinflammatory drug (potassium diclofenac used daily for more than 1 year to treat acne).


To our knowledge, no previous studies have attempted to identify the etiologies that are most often associated with audiometric normalization in patients with SHL.
However, the greatest improvement in PTA was observed in group II patients, who were the only ones not treated by dextran. A recent study demonstrated a statistically significant association between less recovery of hearing loss and male gender [16]. 2009 Volume 9 Number 1 CT shows right thyroid cartilage fracture & air escape suggesting tracheal tear.
Open :usually reserved for cases in which either a prior closed reduction has failed or malunion has occurred. Worldwide, SHL accounts for approximately 1% of all cases of deafness, and 15,000 new cases occur annually [1,4]. Patients were divided into five treatment groups on the basis of SHL duration and clinical profiles that indicated the use or absence of the current drugs prescribed. Group IV included patients with a 16- to 30-day history of SHL and who were treated with the group I regimen minus dextran and acyclovir.
However, the fact that the time to first medical visit was longer in our study might be attributed to patients' lack of knowledge concerning the symptoms or difficulty in patients' gaining access to treatment. In our sample, tinnitus was much more prevalent (95% of cases) and was often the main reason for the disturbance, leading us to recommend that future clinical trials investigate therapeutic possibilities in preventing and managing this symptom in SHL patients.
In our sample, diagnoses were made by determining erythrocyte sedimentation rates and levels of antinuclear factor and rheumatoid factor. Intracochlear hemorrhage can be revealed through the use of magnetic resonance imaging, showing the importance of this procedure in making the diagnosis [24].
The authors estimated that audiometric recovery resulting from treatment translated to an increase in mean PTA of approximately 25 dB, similar to what we observed for low-frequency PTA. However, we agree with Mattox and Simmons [25], who reported a fundamental difference between hearing losses at low frequencies and those affecting high frequencies, stating that low-frequency losses are more easily reversed. Although some underlying diseases can impair innerear microcirculation and hinder clinical improvement of SHL, the comorbidities presented by patients in group II were not indicators of poor prognosis. The better prognosis in women merits further analyses, given a possible bias that might be related to indicators of good prognosis.
We determined outcome as the difference between day-0 and day-180 pure-tone averages (PTAs). Since SHL was first described 62 years ago [5], various etiologies have been proposed, including the infectious, traumatic, neoplastic, immune, ototoxic, vascular, ischemic, neurological, and metabolic. Group V included patients with more than a 30-day history of SHL who were treated with nicotinic acid, papaverine hydrochloride, and vitamin A. If audiometric improvement occurred, the treatment regimen was maintained for up to 10 days. Possibly these discrepancies in the prevalence of upper-airway infection accompanying SHL are the result of geographical differences. In two patients, the diagnoses were made based on a clinical history of vasculitis (Churg-Strauss syndrome) and thrombophilia, respectively. This was also observed in our study in which low-frequency PTA normalized in 28 cases as compared with 15 cases of high-frequency PTA normalization. In our study, dextran was not found to act as an adjuvant to dexamethasone or acyclovir in the treatment of SHL, as the patients presenting the best response to treatment were those in the group not treated by dextran. We observed significant improvements in PTAs after 180 days of treatment and noted a significant linear correlation between time from SHL onset to initial visit and recovery.
The low-frequency PTA was determined by averaging the pure tones of the 250-, 500-, and 1,000-Hz frequencies, and the high-frequency PTA was based on those of the 2,000-, 4,000-, and 8,000-Hz frequencies. We determined audiometric evolution of the responses in the different treatment groups by subtracting baseline PTA from final PTA (after 180 days of treatment). Pitkaranta and Julkunen [21] investigated the protein MxA (a specific marker of systemic viral infection) in patients with SHL and found evidence of viral etiology in 6.5% of the cases. In the treatment of SHL, dextran provided no more benefit than did dexamethasone or acyclovir. We found mumps (paramyxovirus) to be the most common etiology, although we did not test for influenza or parainfluenza. These discrepancies can be attributed to the difficulty of making the viral diagnosis, given that the time to the first medical visit (interval between the onset of SHL and blood collection) varied from study to study, which can influence seropositivity. Of note in our study and in a previous study [22] is that some of the patients presented seropositivity for the bacterium that causes Lyme disease.



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