Cochlear Implantation after Bromate Intoxication-Induced Bilateral Deafness: A Case Report.

Hearing loss is a common consequence of the strong acidosis induced by bromate poisoning. Partial hearing recovery has been achieved through medical or rehabilitative therapy but reports of surgical otology treatment for this condition are rare. We report the case of a 48-year-old female patient who underwent cochlear implantation after bromate intoxication had induced bilateral deafness. In cases with life-threatening renal damage, the diagnosis of hearing loss is sometimes delayed, but in our case, hearing impairment was unavoidable despite early detection of symptoms and early disruption of the use of diuretics that could cause hearing damage. Hearing loss 12 hours after bromate ingestion was successfully reversed through cochlear implantation (CI) six months after completing acute phase treatment, including dialysis for acute kidney injury. The benefit of CI for deafness by bromate intoxication is highlighted by this case.

Toxicity and carcinogenicity of potassium bromate--a new renal carcinogen.

Potassium bromate (KBrO3) is an oxidizing agent that has been used as a food additive, mainly in the bread-making process. Although adverse effects are not evident in animals fed bread-based diets made from flour treated with KBrO3, the agent is carcinogenic in rats and nephrotoxic in both man and experimental animals when given orally. It has been demonstrated that KBrO3 induces renal cell tumors, mesotheliomas of the peritoneum, and follicular cell tumors of the thyroid. In addition, experiments aimed at elucidating the mode of carcinogenic action have revealed that KBrO3 is a complete carcinogen, possessing both initiating and promoting activities for rat renal tumorigenesis. However, the potential seems to be weak in mice and hamsters. In contrast to its weak mutagenic activity in microbial assays, KBrO3 showed relatively strong potential inducing chromosome aberrations both in vitro and in vivo. Glutathione and cysteine degrade KBrO3 in vitro; in turn, the KBrO3 has inhibitory effects on inducing lipid peroxidation in the rat kidney. Active oxygen radicals generated from KBrO3 were implicated in its toxic and carcinogenic effects, especially because KBrO3 produced 8-hydroxydeoxyguanosine in the rat kidney. A wide range of data from applications of various analytical methods are now available for risk assessment purposes.

Acute renal failure and hearing loss due to sodium bromate poisoning: a case report and review of the literature.

Acute renal failure with hearing loss due to sodium bromate intoxication is described. A 48-year-old woman who ingested permanent wave neutralizer in a suicide attempt and developed anuria was admitted to our hospital for hemodialysis. Bromate intoxication was suspected and hemodialysis was carried out; she required maintenance dialysis 3 times a week. Irreversible severe sensorineural hearing loss continued and peripheral polyneuropathy developed in the lower limbs. We measured the concentration of bromine in the serum before and after the first hemodialysis and found its removal rate to be 61.3%. This is the first report that proved the utility of hemodialysis for bromate intoxication in a clinical setting.

[Acute renal failure, neuropathy and deafness due to sodium bromate intoxication: report of one case].

The clinical manifestations of sodium bromate intoxication include among others acute renal failure and deafness. Most of the toxic manifestations are reversible with the exception of renal failure and deafness. This patient ingested about 7.5 g of sodium bromate powder, which produced gastrointestinal irritation, hypotension, fatigue, deafness, acute renal failure, anemia and peripheral neuropathy. Hemodialysis was performed three times due to acute renal failure, although the renal function improved, it did not recover completely. The patient was discharged with BUN: 42 mg/dL and creatinine: 3.4 mg/dL; she was still deaf.

[A case of sodium bromate intoxication with cerebral lesion].

We confirmed a cerebral lesion due to sodium bromate intoxication on MRI, SPECT, auditory brainstem response (ABR) and sensory evoked potential (SEP). The patient was 34 years old, and ingested sodium bromate (14 g) to commit suicide. Vomiting, epigastralgia, watery diarrhea and anuria appeared after 30 minutes and he became deaf within 12 hours. Renal function recovered after hemodialysis. Renal biopsy revealed acute renal tubular necrosis. After one month, burning pain appeared in bilateral lower extremities. Sporadic, clear and small high intensity spots were observed in the deep white matter of the right occipitotemporal border zone and bilateral centrum semiovale on T2 and proton weighted images of brain MRI. IMP-SPECT disclosed partial low perfusion in the left parietal gray matter. Central conduction time was delayed on ABR and SEP. The clinical symptoms and course together with laboratory studies suggest that the cerebral lesion was due to direct sodium bromate intoxication.

[Peripheral nerve disease associated with acute renal failure due to bromate poisoning].

A case of 21 year old male with neuropathy caused by renal insufficiency was present. He had taken bromate (mixed powder of potassium bromate and sodium bromate) for the purpose of suicide and suffered from acute renal insufficiency and hard of hearing. Renal dysfunction improved gradually by peritoneal dialysis and hemodialysis. However, on the 32th day after the onset, burning pain appeared in the bilateral feets. Following this, he began to complain of the disturbances of superficial and deep sensory below the ankle jerks and the weakness of his toes. Considering the clinical features, we supposed that the disturbance of the peripheral nerve was caused by uremia due to taking bromate. N. suralis was biopsied on the 80th day after the onset and examined electron microscopically. Electroscopical findings was as follows. Degeneration of the Schwann cells and irregularity or destruction of the myelin sheaths were observed. The axoplasm of the myelinated nerve fiber were relatively preserved as compared with the changes of the myelin sheaths. In the unmyelinated nerve fibers, cavity formations were observed. The findings of regeneration were not observed. From the electron microscopical findings, we speculate that the changes of the Schwann cells and the myelin sheaths are primary resulting from the disturbance of the metabolism of the Schwann cells. We speculate that anemia and hypoproteinemia caused by bromate disturbed regeneration.

[A case of acute potassium bromate intoxication].

We experienced a case of a 44 year old man who had ingested potassium bromate solution for suicide attempt. Soon after the ingestion, nausea, vomiting, abdominal pain and diarrhea developed in him. Several hours later, he began to complain of auditory disturbance and, in addition, anuric acute renal failure occurred. Direct hemoperfusion and hemodialysis was performed on the patient for the treatment purpose. Five weeks later, he was released from hemodialysis procedure. Gradually, on the other hand, progressing anemia was observed until 90th hospital day, which slowly improved thereafter. Further, pruritus, lower leg pain, headache, tinnitus and loss of sense of taste, etc. were observed in the clinical course. Renal biopsy was performed on the 119th hospital day and the specimen showed the regenerative stage of acute tubular necrosis. In our case, acute renal failure was reversible and, many other clinical manifestations were observed. However slight anemia and irreversible severe auditory disturbance remained unimproved.

An elderly patient with severe acute renal failure due to sodium bromate intoxication.

Accidental or deliberate ingestion of bromate solution has been reported in pediatric as well as adult cases; however there have been no reports of such intoxication in the elderly. We report a 78-year-old woman who suffered severe acute renal failure due to the accidental ingestion of sodium bromate solution. The patient was successfully treated with hemodialysis therapy and renal function recovered without hearing loss. This case suggests that emergency therapeutic measures, including hemodialysis, should be taken as soon as possible, and the rapid removal of bromate is essential to prevent severe intoxication and its sequelae. To the best of our knowledge this is the first report of an elderly patient that demonstrates the clinical benefit of hemodialysis therapy for bromate intoxication.

Acute bromate poisoning associated with renal failure and deafness presenting as hemolytic uremic syndrome.

A case of bromate-induced acute renal failure (ARF) in an infant associated with hemolysis, thrombocytopenia and deafness is presented. The initial clinical and laboratory features suggested the diagnosis of hemolytic uremic syndrome (HUS). The serum bromide level was in the nontoxic range (1.2 mg/dl). However, further investigation of the ingested material revealed the toxic agent to be bromate rather than bromide. The spectrum of bromate (BrO3-) toxicity is different from bromide (Br-) and includes the induction of ARF and deafness. This combined with clinical evidence of behavioral regression and speech loss led to detection of deafness in this patient and confirmed the diagnosis of bromate toxicity.

Toxic mechanism of bromate poisoning in a dog: a case study.

Efforts to link the observed signs in a canine poisoning event with 1 or more possible permanent wave solution chemicals ingested are described. A scenario is presented describing the mechanisms by which the most likely of those compounds, ammonium thioglycolate and sodium or potassium bromate, could have acted to cause both the immediate and delayed signs of acute vestibular dysfunction.