Medical Excellence - Issue 2

right ear. There was no need to dissect the right ear as when the patient was discharged he was Hale and Harty. Slight improve- ment in hearing in the left ear after 8 days of therapy suggested control of hypertension and diabetes. Discussion Sudden sensorineural hearing loss (SSNHL) is defined as a dete- rioration of more than 35 dB. In at least three different frequen- cies occurring with in 3 days, with allowance for a longer period of onset if the loss is more severe [1]. There are many causes of SSNHL. These include trauma and labyrinthine membrane rupture, viral and bacterial infections, vascular lesions, immune complex diseases and acoustic neuroma. Diabetes and other metabolic disorders are also well known causes of sensorineural hearing loss. In our patient the hearing deteriorated at all frequencies after 8 days of therapy in the right ear. In the literature, there are several papers which investigated the relationship between diabetes and hearing loss and vertigo. There is no reported case of any patient presenting with bilateral sudden deafness with vertigo and tinnitus as the only symptoms of diabetes mellitus. Some authors found significant hearing loss in low and middle frequencies in diabetes compared to controls [2–3]. Others found the hearing loss to be significant in high frequencies [4–5]. Audiological tests in our patient showed the hearing loss to be cochlear. The site of lesion in diabetes is thought to be coch- lear [6–7], retrocochlear [8–9] or both. Most of the available experimental and clinical evidence suggests that the complications of diabetes mellitus are a con- sequence of the metabolic derangements, mainly hyperglycemia [10]. Hyperglycemia can cause complications by two important mechanisms: zz Non-enzymatic glycosylation in which glucose chemically attaches to the amino-groups of proteins without the aid of enzymes and after a series of chemical rearrangements, forms irreversible advanced glycosylation end products (AGE). In capillaries for example, plasma proteins such as albumin bind to the glycosylated basement membrane accounting for the increased basement membrane thickening of diabetic micro- angiopathy. AGEs can also bind to receptors on many cell types resulting in a variety of biological activities including increased procoagulant activity on endothelial cells and en- hanced proliferation of fibroblasts and smooth muscle cells. zz Intracellular hyperglycemia occurs in some tissues (e.g., nerve, lens, blood vessels and kidney) that do not require insulin for glucose transport. This mechanism may be re- sponsible for damage to Schwann cells and to pericytes of capillaries with resultant neuropathy and microaneurysms resulting in hemorrhage as is suggested in this patients right membranous labyrinthopathy. Platelets from diabetic patients show an exaggerated ten- dency to aggregate, perhaps mediated by altered prostaglandin metabolism. Plasma and whole blood viscosity are increased whereas red blood cell deformability is decreased. All these defects may cause stasis in the microvasculature, leading to in- creased intravascular pressure and to tissue hypoxia [11] again predisposing to hemorrhage as is suggested in this patients’ right membranous labyrinthopathy. In diabetes, fat may be released from tissues to enter the blood stream and cause fat embolism [12]. Mechanism of Simultaneous Bilateral Cochlear Hearing Loss in this Particular Patient Neuropathy [8], angiopathy [9] and a combination of both may be the underlying pathology of hearing loss in diabetes. Disturbances in the microcirculation of the cochlear end vessels may be prominent aetiological factor [4]. Ischemia of the VIIIth nerve secondary to involvement of small intraneural vessels may be the aetiology in some diabetic patients [9] Wackym and Linthicum [13] suggest that vascular thickening found around the endolymphatic sac may cause accumulation of toxic waste products in endolymph, which in turn could cause hair cell dysfunction. About 25–50% of patients with SSNHL recover their hearing partially or completely without any treatment. In the patient under report there was a probable hemorrhagic labyrinthopa- thy in the right ear, hearing deteriorated inspite of therapy. Since hyperglycemia is the main cause for reversible or irreversible complications, insulin therapy presumably played a major role in partial recovery of hearing in the patient’s left cochlea. This patient presented immediately after the onset of bilater- al sudden onset hearing loss with vertigo and tinnitus. It appears to be advisable to hospitalize all such patients of diabetes. The diagnosis is NIDDM/Type 2 diabetes with cochleopa- thy left ear and labyrinthopathy right ear. References 1. Ludman H (1988) Acquired sensorinerual deafness. Mawson’s diseases of the ear, 5th edition chapter 25, Edwan Arnold, London 605–609. 2. Jones NS, Davis A (1992) Hyperlipidemia and hearing loss a true association? Clin Otolaryngol 17:463. 3. Tay HL, Ray N, Ohri R, Frootko NJ (1995) Diabetic mellitus and hear- ing loss. Clin Otolaryngol 130–134. Issue-2  |  11 MEDICAL EXCELLENCE