Fatal Barium Chloride Poisoning Four Cases Report and Literature Review

Introduction

Barium is an alkaline metal. Its salts are used in a variety of industries including mining, ceramics, plastics, adhesives, and every bit a dark-green coloring in fireworks. It is too used every bit a rodenticide. In the 18th and 19th centuries it was used medicinally as a tonic and in the handling of a wide variety of conditions including asthma, tuberculosis, and heart failure. With its ascent in popularity as a therapeutic agent, came its first report of toxicity in overdose in 1794 [1].

Barium poisoning is uncommon, merely potentially life-threatening. It blocks passive efflux potassium channels without affecting the Na/M-ATPase pump resulting in an increase in intracellular potassium and extracellular hypokalemia [two]. When severe, the hypokalemia leads to weakness which may progress to respiratory paralysis and cardiac arrhythmia.

Instance

A 44-year-old homo self-presented to hospital vi hours following deliberately ingesting 10 g of barium carbonate with suicidal intention. He had purchased the pulverization from the cyberspace for this purpose afterward researching methods of suicide. To improve palatability, he mixed information technology into his coffee. Two hours following ingestion he began vomiting and before long after adult diarrhea. His vomiting and diarrhea worsened, prompting him to telephone call an ambulance. On their arrival vi hours mail ingestion, he was complaining of generalized weakness and tingling to his face. His heart rate was 92 bpm and blood pressure was 182/119 mmHg.

On arrival to hospital one-half an 60 minutes later, it was noted he had global weakness with 4/5 ability in upper and lower limbs with macerated reflexes. His ECG (Figure 1) was in sinus rhythm with outset degree AV block, diffuse T-wave flattening, and U-moving ridge formation consistent with hypokalemia. His potassium was found to exist critically low at 2.4 mmol/50 (reference range three.5–5.2 mmol/L). The balance of his blood investigations were unremarkable autonomously from a mildly elevated lactate at 3.5 mmol/L (reference range 0.5–2.2 mmol/L).

Effigy 1. ECG on arrival to hospital.

He received intravenous ondansetron, potassium, and magnesium supplementation and was observed overnight. Over the subsequent sixteen h he received a full of fourscore mmol potassium chloride (Effigy 2). By the next twenty-four hour period, he was asymptomatic, and his potassium had stabilized at 3.seven mmol/L. He was reviewed past the mental health squad and discharged abode.

Figure 2. Potassium concentration during admission (reference range 3.5–five.2 mmol/Fifty). Arrow indicates the assistants of 20 mmol potassium chloride intravenously.

Give-and-take

Barium toxicity has been reported with ingestions as modest as 200 mg [iii]. The toxicity of private barium salts depends on their solubility. The more than soluble salts such as chloride, hydroxide and nitrate are more toxic while insoluble salts such as arsenate, fluoride, and sulfate are rarely associated with toxicity. Some, like barium carbonate, while poorly soluble, are converted to the more soluble chloride by tum acids when ingested.

The clinical features of barium toxicity are well described. In 1945, Dr William Morton reported three stages of toxicity following ii outbreaks caused by barium carbonate contaminated flour in 85 British troops [4]. Stage 1 occurred within ninety minutes and consisted of tingling around the rima oris and neck forth with vomiting followed past diarrhea. The pupils were initially dilated and there was a slow pulse. Stage ii occurred within two to three hours. The face and neck tingling was replaced past tingling of the limbs. Gastrointestinal effects continued for up to 20-four hours. Varying degrees of motor weakness and hyporeflexia occurred. Improvement occurred within hours post ingestion and resolution expected by 36 h. A minority went on to develop phase 3, defined every bit the progression to more than significant paralysis including respiratory compromise. In this group, recovery occurred by day 4. There were no deaths. Further epidemics have been described with contaminated flour in Bangladesh, potato flour in State of israel [v], and salt in People's republic of china [6]. Individual exposures take been reported with industrial exposure to barium salts [seven], ingestion of barium containing shaving powder [8], and fireworks [9]. Additional clinical features that accept been described with barium poisoning include hypertension, metabolic acidosis, elevated lactate, hypophosphatemia, and rhabdomyolysis.

The management of barium toxicity is largely supportive with a focus on potassium replacement. Activated charcoal is ineffective. The utilize of oral sulfate salts such as sodium or magnesium sulfate may be considered early to decrease absorption by converting the barium into the nontoxic barium sulfate in the gastrointestinal tract [10]. Intravenous sulfates should be avoided to prevent the theoretical take chances of intravascular precipitation and subsequent acute kidney injury. Hemodialysis has been shown to rapidly increase barium clearance while stabilizing potassium levels and may be considered in cases of astringent toxicity not responding to potassium supplementation [11].

Barium poisoning is an uncommon only potentially life-threatening poisoning that results in gastrointestinal toxicity and severe hypokalemia. Management is supportive with intravenous potassium supplementation. There may be a office for oral sulfate salts to decontaminate early on, and in severe poisoning hemodialysis to aid elimination.

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Source: https://www.tandfonline.com/doi/full/10.1080/24734306.2019.1691340

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