一个头部创伤,三个耳鼻喉科症状

Santos Pedro, Rego Ângela, Carvalho Isabel, Meireles LuÍs
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引用次数: 0

摘要

导读:众所周知,头部创伤(HT)可引起听觉减退;良性体位性阵发性眩晕(BPPV)和嗅觉缺失,这些通常被称为HY的后遗症。然而,BPPV、听觉减退和嗅觉缺失在同一患者中出现的情况极为罕见,文献中仅报道了2例。在此病例报告中,我们希望描述一个临床病例,该病例导致听觉减退,BPPV和嗅觉缺失作为后遗症,并回顾耳鼻喉科评估在某些HT病例中的重要性,即使在没有颅骨骨折的情况下。结果:我们描述了一个病例71岁的病人转到耳鼻喉科咨询,投诉嗅觉变化,眩晕和左侧听力损失恶化,耳鸣后HT。体格检查发现嗅觉缺失(UPSIT®:7个正确答案),左侧后半圆管BPPV和左耳传导性听力损失(左侧为Rinne阴性,左侧为Weber偏侧)。听力学上,患者为中度I级左耳混合性耳聋,辨别良好,与以前的检查相比恶化。创伤后数小时内的CE-CT显示左侧额基底部和颞部挫伤,并伴有分散的蛛网膜下腔出血和硬膜下血肿。一个周期的全身皮质类固醇治疗尝试没有有利的发展嗅觉。结论:即使没有颅骨骨折的痕迹,htent后受累也可能是复杂的。HT后,膜性迷路可能受到Corti器官震荡/拉伸的影响。另一方面,颅内出血后可能出现内耳压下降。高温还可以将耳聋转移到不同的半规管,这是创伤后BPPV的机制。最后,额部和/或颞部脑震荡,以及嗅觉片的破坏,是ht后嗅觉变化的最常见原因,这些变化通常是不可逆的。总之,耳鼻喉科医师应注意耳鼻喉科创伤后的各种表现,早期发现和治疗创伤后后遗症可改善预后。
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One Head Trauma, Three ENT Manifestations
Introduction: It is well known that head trauma (HT) can cause hypoacusis; as well as benign positional paroxysmal vertigo (BPPV) and anosmia, which are frequently referred as sequelae of HY. However, the post-HT triad of BPPV, hypoacusis and anosmia is extremely rare to occur in the same patient, with only two cases reported in the literature. With this case report we wish to describe a clinical case of HT that caused hypoacusis, BPPV and anosmia as sequelae, and to review the importance of ENT evaluation in some cases of HT, even in the absence of cranial fractures. Results: We describe the case of a 71-year-old patient referred to ENT consultation with complaints olfactory changes, vertigo and worsening of left hearing loss with tinnitus after HT. Physical examination revealed the presence of anosmia (UPSIT®: 7 correct answers), left posterior semi-circular canal BPPV and left ear conduction hearing loss (Rinne negative on the left and Weber lateralized to the left). Audiometrically, the patient had moderate grade I mixed deafness of the left ear, with good discrimination and worsening compared to previous exams. CE-CT performed within hours after trauma showed left frontobasal and temporal contusion with scattered subarachnoid hemorrhage and subdural hematoma. A cycle of systemic corticosteroid therapy was attempted without favourable evolution of the anosmia. Conclusion: Even without traces of cranial fracture, post-HT ENT involvement can be complex. After HT the membranous labyrinth may be affected by concussion/ stretching of the Corti organ. On the other hand, after intracranial hemorrhage there may be decreased inner ear pressure. HT can also shift otoconia to different semicircular canals, which is the proposed mechanism for post-traumatic BPPV. Finally, frontal and/or temporal concussions, as well as disruption of olfactory fillets, are the most common causes of post-HT olfactory changes, which are often irreversible. In conclusion, otolaryngologists should be aware of the various post-traumatic ENT manifestations, as early identification and treatment of post-HT sequelae can improve the prognosis.
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