Acute Bromide Intoxication in a Patient with Preserved Renal Function.

BACKGROUND Electrolyte imbalance is frequent in many situations, but severe hyperchloremia is markedly rare in the absence of renal impairment. We report a patient with preserved renal function who exhibited severe hyperchloremia and negative anion gap. CASE REPORT A 70-year-old female with preserved renal function presented with fatigue and impaired consciousness. Venous blood gas analysis was notable for a chloride level of 137 mEq/L and anion gap of -18.2 mEq/L. Careful history taking revealed that she had taken bromide-containing over-the-counter painkillers. Her symptoms and laboratory tests gradually improved after intravenous hydration and painkiller withdrawal. The serum level of bromide ions on admission was later found to be 4-times higher than that considered toxic. CONCLUSIONS It is important to recognize that hyperchloremia with a negative anion gap strongly suggests bromide intoxication, and that bromide intoxication can develop even in patients with preserved renal function. Careful history taking is essential to the diagnosis because some over-the-counter drugs that are widely available and a few prescription drugs contain bromides.

Effects of three infusion fluids with different sodium chloride contents on steady-state serum concentrations of bromide in dogs.

Potassium bromide overdose (bromism) in the management of canine epilepsy has been known. However, a protocol to reduce bromide concentrations rapidly has not been previously established. The effects of three infusion fluids with different chloride contents on the steady-state serum concentrations of bromide in beagles were determined. After stabilization of the serum bromide concentrations, seven dogs were infused with saline (Na+ 154 mmol/L; Cl- 154 mmol/L), lactated Ringer's (Na+ 131 mmol/L; Cl- 110 mmol/L), or maintenance solutions (Na+ 35 mmol/L; Cl- 35 mmol/L) at a rate of 2 or 10 ml kg-1  hr-1 for 5 hr. Serum and urine were collected hourly, and the bromide concentrations were measured. When saline and lactated Ringer's solutions were infused at a rate of 10 ml kg-1  hr-1 for 5 hr, serum bromide concentrations were decreased by 14.24% and urine bromide concentrations by 17.63%, respectively. Of all compositions of infusion fluids, only sodium and chloride contents were associated with the decreased serum concentrations and the increased renal clearance of bromide. In summary, saline and lactated Ringer's solutions reduced serum bromide concentrations in a sodium chloride-dependent manner in dogs were found when infused at 10 ml kg-1  hr-1 for 5 hr.

Bromism from daily over intake of bromide salt.

Bromide intoxication today is an infrequent disease, but preparations containing bromide are still available in nonprescription compounds, on the French market. We report a casewith bromide intoxication due to daily over intake (approximately 20 tablets per day; i.e. total elemental bromide intake approximately 6 g/day) of calcium bromo-galactogluconate (Calcibronat) for 1.5 months. A 30-year-old woman with a long history of psychotropic drug abuse was hospitalized in a psychiatric department for neuropsychological manifestations. She presented a seriously disturbed mental status with confusion, disorientation, auditory and visual hallucinations, and loss of short-time memory. A markedly increased serum bromide level of 1717 mg/L (21.5 mEq/L) measured on the first day after her admission confirmed the diagnosis of chronic bromism suspected based on her symptomatology. During her hospitalization, bromide plasma concentrations were measured and monitored using inductively coupled plasma mass spectrometry, a sensitive and very specific method. After withdrawal of the drug, the symptoms improved within 8 days. Serial bromide concentrations gradually declined throughout nearly 2 months of monitoring, until she was discharged from the hospital. We found an elimination half-life of bromide in blood of approximately of 10 days. This case demonstrates that, while today bromism occurs infrequently, it should still be included in the differential diagnosis of neuropsychiatric symptoms.

[False hyperchloremia in a bromide intoxication]. / Fausse hyperchlorémie révélant une intoxication aux bromures.

A false hyperchloremia in a patient with a history of depression suspected bromide intoxication. The diagnosis was confirmed by an increased bromide concentration > 20 mmoL.L-1. Rehydration was effective and allowed to decrease bromide concentration. In conclusion, hyperchloremia associated with a negative anion gap is a clue to the diagnosis.

Poisoning from a dietary supplement administered during hospitalization.

Increasing numbers of persons use dietary supplements (DS). Patients who believe in the effectiveness of DS may continue to take them on admission to a health care facility. We present the case of a child who received a DS on a daily basis as an outpatient, continued its use after admission to the hospital, and became poisoned by it during his hospitalization.

[Bromide poisoning and false hyperchloremia]. / Intoxication par les bromures et fausse hyperchlorémie.

A 36-year-old female patient was admitted at three different times for neuropsychiatric disorders. No diagnoses were made during the first two hospital stays. A pseudohyperchloraemia allowed the diagnosis of bromide poisoning during her third hospital stay. Chloraemia was measured over 16 days by potentiometric, colorimetric and coulometric methods, in order to assess the analytical interferences caused by bromides. Results are reported and discussed. Bromide poisoning was treated by saline diuresis.

[Factitious hyperchloremia disclosing bromide poisoning. 4 cases]. / Hyperchlorémie factice révélatrice d'intoxication par le brome. 4 observations.

BACKGROUND: When routine blood chemistry shows elevated chloride alone, another anion (bromide, iodine, fluoride) may be involved. CASE REPORTS: Hyperchloremia and decreased anion gap was observed in four patients. Chloremia ranged from 134 to 174 mmol/l at initial blood tests. Careful history taking led to the discovery of long-term use of calcium bromogalacto-glucomate. Specific assay with inductively coupled plasma mass spectrometry (ICPMS) confirmed the presence of bromide in the blood. Chloridemia returned to normal levels after discontinuing use of bromine. DISCUSSION: Bromism is not a common diagnosis. Risks include neurological and psychiatric disorders due to bromide diffusion through the blood-brain barrier. Clinical manifestations have been described including skin lesions, digestive intolerance, and fever. Bromide is contained in certain prescription drugs. Patients should be warned against the adverse effects of overuse.

Estudio de los efectos neurotóxicos del bromuro de metilo sobre trabajadores expuestos / Study of neurotoxic effects of methyl bromide over exposed workers

We studied prospectively 15 male middle age workers before and after a fumigation period with methyl bromide, that lasted 2 to 4 weeks. According to the initial assessment, 5 of these subjects had a chronic exposure to the chemical. As controls, 10 non exposed workers matched for age, sex and working conditions were studied in 2 occasions. The evaluation included the Who Neuro Behavior Core Test Battery, dynamometric and vibrator assessment of peripheral nerve function, the Nothingham test for psychological functioning and Titmus test for visual acuity. Methyl bromide levels were measured in blood and irine. Blood methyl bromide levels increased from 13.3 to 30 mg/dl after headache, paresthesiae, mood changes and loss of memory and concentration. In these subjects, the threshold for the Vibration test increased from 2.4 to 2.85 sec, dynamometry the score fro negative auto-perception in the Nothingham test from 11.2 to 13.6. No deterioration in these tests were observed in unexposed workers. Acute and chronic methyl bromide exposure causes important psychological and neurological derangement

Bromide toxicosis secondary to renal insufficiency in an epileptic dog.

Bromide toxicosis was diagnosed in an 8-year-old Labrador Retriever that had been treated for epilepsy with potassium bromide, at a dosage of 29 mg/kg of body weight/d. Clinical signs included hind limb weakness, ataxia, and disorientation. Renal insufficiency, diagnosed by determination of endogenous creatinine clearance, was believed to be responsible for the development of bromide toxicosis in this dog. Diuresis with physiologic saline solution and discontinuation of bromide and phenobarbital treatment resulted in rapid resolution of abnormal neurologic signs; however, serum bromide concentrations decreased dramatically during diuresis and seizures recurred. Although saline diuresis has been recommended for the treatment of bromide intoxication in human beings, more conservative measures, such as discontinuation of bromide and short-term fluid administration, may be more appropriate for epileptic dogs.

[Bromine poisoning]. / Bromintoxikationen.

Intoxication by medication containing bromid has become so rare in recent years, that the clinical syndrome is nearly forgotten. The revival of brom in neurology at present points to an increased rate of bromintoxications. With this background and a corresponding case-history the symptoms and therapy of bromintoxication is represented.

A negative anion gap as a clue to diagnose bromide intoxication.

We report on a patient with bromide intoxication, presenting with confusion, disorientation, and auditory and visual hallucinations after taking a sedative medication containing bromide (mixture menopause; 15 ml containing 1 g potassium bromide) for 1 month. Blood chemistry showed a high chloride level (176 mEq/l) and a negative anion gap (-60 mEq/l). The spurious hyperchloremia was due to interference of chloride ion determination by the ion-selective electrode method with a high level of bromide in serum: 352 mg/dl (44 mEq/l). In this case the only striking abnormality which alerted the physician to the possibility of halide intoxication was the negative anion gap. Hence, a negative anion gap is an important clue which leads to the diagnosis of halide intoxication.