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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.

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., (© 2018 John Wiley & Sons Ltd.)

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.

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.

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.

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.

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.

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.

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.

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.

Bromism, the chronic intoxication with bromide is rare and has been almost forgotten. In the recent past bromide is rediscovered as an anticonvulsive drug. The increasing frequency of bromism in children coming to admission induced this report. We describe the cause, the symptoms and the pseudohyperchloremia associated with bromism. If unclarified neurological or psychiatric symptoms are associated with the determination of an elevated serum chloride concentration and a diminished anion gap chronic intoxication with bromide has to be excluded.

A 49-year-old woman who had noted increasing fatigue and found it difficult to concentrate became confused and uncoordinated with rapid speech. Anxious and suffering from insomnia she had for 6 weeks taken a prescription-free bromide-containing drug mixture (daily 0.09 g potassium bromide and 1.8 g sodium bromide), to a total bromide intake of 60 g. The admission diagnosis of chronic bromism was confirmed by a markedly increased serum bromide concentration (325 mg/l). Once she had stopped taking the drug and had increased her salt intake she became symptom-free within 8 days. The case demonstrates that, while chronic bromism has become rare, it should still be included in the differential diagnosis, even after intake of supposedly harmless medication.

Although cold syrup containing dextromethorpan bromide is widely administered, the bromism due to cold syrup has not been reported. We report a patient who had negative anion gap with hyperchloremia and conscious loss because of daily intake of cold complex syrup (containing dextromethorphan bromide 0.4 mg/ml, acetaminophen 8.33 mg/ml) for headache for 4-5 years. The bromide content in cold complex syrup resulted in serum levels of bromide that interfered with the automated analyzers for chloride content. When conscious change is due to bromism, hemodialysis instead of forced hydration and diuresis should be performed immediately. Therefore, patients with a markedly negative anion gap with hyperchloremia should be considered as having halide intoxication.

Increased serum bromide may result from the ingestion of various drugs and from environmental exposures. Chloride methods that are less susceptible to bromide interference have a clinical disadvantage in that they are less likely to arouse suspicion in cases of bromide toxicity. When there is a clinical suspicion of bromide toxicity, differences among various analyzers in the amount of interference caused by bromide may be exploited to confirm this suspicion and to estimate the concentration of bromide in serum.

The diagnosis of bromide intoxication is often aided by the detection of a low or negative anion gap due to the laboratory detection of bromide as chloride. A 59-year-old woman with myasthenia gravis who received a large dose of pyridostigmine bromide developed postoperative psychosis and was diagnosed as having bromide intoxication. The diagnosis was suspected in the setting of a negative anion gap and only later confirmed by direct measurement of the serum bromide level. To our knowledge , this is the first reported case of bromide intoxication due to pyridostigmine bromide administration.

Hyperchloremia in a patient with intoxication by a bromide containing mixture is described. Loss of the normal anion gap in combination with hyperchloremia is only seen in bromide intoxication. An explanation for this observation is suggested.

The method developed by Chang for using in collodion and albumin encapsuled charcoal as artificial cells for hemoperfusion has been studied in vitro. The capacity for the absorption of more or less dialysable exogenous substances (barbiturate, Diazepam, Parathion) and an endogenous toxic metabolite (p-hydroxyphenyl acetic acid) has been examined. With the absorption unit one can eliminate 80 to 90 per cent of the initial concentration of barbiturate, Diazepam and p-hydroxyphenyl acetic acid in about 90 min, of Parathion about 50 per cent in the same time, whereas bromide and ammonia are not absorbed. Attempts to avoid regional heparinisation by the incorporation of heparin into the capsule of charcoal granules were not successful. Assuming correct preparation of the hemoperfusion system, observance of steril precoutions and regional heparinisation, the use of the "detoxication shunt" is a promising means in the treatment of severe exogenous and endogenous intoxications which are not accessible by conventional therapeutic means.

Current methods for determining serum chloride concentration vary in specificity. Laboratory detection of bromide in serum is usually dependent on spuriously high chloride values. In the absence of historical information, the chemical identification of bromide in serum may be the only diagnostic sign of bromism. Bromide may be found in as many as 1% of sera obtained from inpatients of a general hospital. Ion-selective electrodes and some thiocyanate methods for chloride analysis can be highly sensitive to bromide (interference). Chloride electrodes are also sensitive to iodide.