Successful Rescue of Deep Coma, Shock, and Arrhythmia Caused by Bittern Poisoning

Abstract

Bittern has been used as the main ingredient of tofu coagulant, and poisoning events usually occurred in the rural of North China. Bittern intoxication may induce electrolyte imbalances, the most important of which is hypermagnesemia, and may be fatal if ingested. The patient without any medical history presented with sinoatrial block, atrioventricular block, paroxysmal atrial tachycardia, and atrial fibrillation on electrocardiography over a short period. The initial diagnosis was unclear and the treatment was difficult. Arterial blood gas analysis indicated severe metabolic acidosis. Her serum concentration of magnesium and chlorine attained 15.14 mEq/L and 130 mEq/L, respectively. After supportive therapy and continuous veno-venous hemofiltration sessions, we observed full recovery without any sequelae. After regaining consciousness, the patient reported ingesting “brine,” confirming the diagnosis of “brine poisoning.” To the best of our knowledge, such sever hyperchloremia after bittern intoxication has not been previously reported in the literature. However,successful rescue of severe hypermagnesemia in Chinese patients by treatment has only rarely been reported in the current literature.

INTRODUCTION

Bittern is bitter in flavor and low toxicity, the major components of which include magnesium chloride, calcium sulfate, calcium chloride, and sodium chloride. In this report, we present a case of sever electrolyte disturbance in a 67-year-old woman admitted for drinking an unknown amount of bittern and without renal dysfunction. Examination revealed coma, shock, hypotension, and arrhythmia. Laboratory investigations confirmed a severe hypermagnesemia[1] ([Mg2+] 15.14 mEq/L) and hyperchloremia ([CL−] 130 mEq/L). The patient immediately received continuous renal replacement therapy as well as the supportive treatment including fluids, diuresis, and maintaining the body homeostasis. She received treating over 48 h until reaching normal electrolyte levels. Supportive care and treatment were continued to promote excretion after discontinuing continuous veno-venous hemofiltration (CVVH), and her electrolyte levels did not rise again. Five days later, she was discharged from the hospital without any sequelae. Brine poisoning can cause severe electrolyte imbalances, particularly hypermagnesemia, which has inhibitory effects on the cardiovascular and nervous systems, and carries a high mortality rate. CVVH could not only reduce blood magnesium but also lower blood calcium and chloride, correct hyperchloremic acidosis, and prevent the rebound of hypermagnesemia and hyperchloremia. To the best of our knowledge, cases of hyperchloremia following bittern poisoning are rare.

CASE REPORT

A 69-year-old female patient without any medical history was found unconscious 2 h prior and brought to the emergency department with no fever and convulsions. On physical examination, her heart rate was 39 beats/rain, temperature 36.5°C, blood pressure 65/32 mmHg, and respiratory rate 6 breaths/rain. Neurological examination revealed a comatose state with a GCS score of 3 (E1V1M1). She was immediately given dopamine (4-8μg/kilogram/minute) to raise blood pressure and atropine (0.25 mg) to increase heart rate based on personal experience of emergency doctors. The patient was then transferred to the intensive care unit (ICU) after emergency endotracheal intubation.

On admittance to ICU, initial laboratory values were significant for the following: a serum magnesium concentration of 5.7 mEq/L and a serum chlorine concentration of 112 mEq/L. Arterial blood gas analysis demonstrated acid–base disturbance (pH 7.16; pCO₂, 45 mmHg; bicarbonate, 15.4 mEq/L; lactate, 2.1 mmol/L). A complete blood count and the values for creatinine (0.34 mg/dl), calcium (5.7 mEq/L), and blood urea nitrogen (5.7 mg/dl) were normal. After admission, an electrocardiography (ECG) revealed atrioventricular (AV) block, QT interval prolongation, and scarce supraventricular premature beats [Figure 1].

Figure 1.

Changes in the electrocardiogram of a patient following bittern intoxication at admission

Initial supportive treatments included isoproterenol to increase heart rate, fluid resuscitation, correction of acidosis, vasopressor (for perfusion), and mechanical ventilation. The craniocerebral computed tomography was negative for acute cerebrovascular accident. There was no fever, and infection markers were not elevated, ruling out cerebrovascular events, common infections, and cardiogenic shock. Upon admission, the patient’s blood magnesium levels were significantly elevated, confirming the diagnosis of hypermagnesemia. A 10% calcium gluconate injection was administered to prevent arrhythmia. Her serum concentration of magnesium rose to a peak of 11.4 mEq/L after 6 h; meanwhile, her serum concentration of calcium and chlorine levels gradually increased (5.42 and 130 mEq/L, respectively). She was emergently hemofiltrated using specially configured magnesium-free and chlorine-low bicarbonate replacement solutions, because of its high efficiency in removing magnesium and chlorine. Elimination of magnesium and glucose were monitored by the measurements of electrolyte concentrations every 6 h.

After 48 h of hemofiltration, her serum magnesium and chloride levels decreased to 1.96 mEq/L and 111 mEq/L, and the acidosis gradually improved. After discontinuing CVVH, fluid replacement was continued to promote excretion, and electrolyte levels did not rise again [Figure 2].

Figure 2.

Graphical representation of magnesium and chlorine serum levels measured in the study patient

The patient’s hemodynamics stabilized, spontaneous breathing increased, and she regained consciousness, nodding indicates self-ingestion of brine. Thirty-six hours later, she was successfully weaned off mechanical ventilation and had her endotracheal tube removed. After correcting the electrolyte imbalances, the ECG returned to normal. During the hospitalization period, the patient did not indicate abnormal kidney function, and 5 days later, she was discharged from the hospital without any sequelae.

DISCUSSION

This patient presented with altered consciousness, and her family was unclear about the onset circumstances, leading to an early diagnostic challenge. Since brine is rarely used in rural tofu production nowadays, brine poisoning cases are uncommon. In addition, brine is colorless and odorless, and its clinical manifestations affect multiple systems without specific symptoms, making diagnosis difficult. Brine poisoning can cause severe electrolyte imbalances, particularly hypermagnesemia, which has inhibitory effects on the cardiovascular and nervous systems, and carries a high mortality rate.

Magnesium is the second most important intracellular cation in the human body and has numerous special physiological functions.[2,3] It can affect various organ systems, such as the central nervous system, cardiovascular system, and neuromuscular junctions.[4] Clinically, magnesium levels are not routinely monitored, and the initial symptoms of hypermagnesemia lack specificity, making it prone to misdiagnosis or missed diagnosis. Severe hypermagnesemia can cause lower blood pressure levels, arrhythmia[5] (due to calcium channel blocker), disturbance of consciousness,[6] and respiratory failure (due to inhibit the release of acetylcholine at the nerve synaptic terminal),[7] potentially leading to death.

The treatment of hypermagnesemia depends mainly upon the blood magnesium levels, renal function status, and the clinical symptoms. The two main principles in treating acute severe hypermagnesemia are inhibiting the effects of magnesium and reducing blood magnesium levels. The former is achieved by intravenous calcium (a magnesium antagonist) to counteract hypermagnesemia’s effects on neuromuscular and cardiac function.[5] The latter can be achieved by increasing urinary magnesium excretion and using blood purification to remove electrolytes.

The symptoms and signs of the patient can be explained by magnesium poisoning, but the cause of acidosis is unclear. We consider it to be possibly caused by high chloride acidosis. Chloride is the most abundant electrolyte in serum next to sodium, with an essential role in various body functions including the preservation of electrical neutrality, fluid-electrolyte balance, acid–base status, muscle activity, and osmotic pressure.[8] Hyperchloremia may result from disease processes or clinical interventions,[9] with common causes including severe diarrhea, excessive intake of chloride-rich fluids and chloride infusions (sodium 0.9%, albumin, total parenteral nutrition), etc.[8]

Studies have confirmed the relationship between chloride-containing solutions and hyperchloremic metabolic acidosis.[10] Many studies also report that hyperchloremia is associated with poor patient outcomes.[10,11,12,13]

Despite its significant physiological functions, chloride has rarely or never attracted attention compared to other routinely measured electrolytes (potassium and sodium) until recently, when the relationship between chloride-rich solutions and hyperchloremic metabolic acidosis was identified.[10,14]

Many studies also report that hyperchloremia is associated with poor patient outcomes. It has been found that hyperchloremia increases short-term mortality after non-cardiac surgery.[11] In a large retrospective study, Thongprayoon et al. found that changes in serum chloride at admission and increases in serum chloride after admission were predictive of poor outcomes.[12] In a retrospective study, the incidence of new-onset hyperchloremia within 72 h of neonatal intensive care unit admission was associated with increased odds of 30-day all-cause mortality and poor 6-month prognosis in critically ill stroke patients.[13]

Our patient’s serum magnesium level was 5.7 mEq/L prior to admission. Despite the discontinuation of bittern and administering intravenous calcium as Mg-antagonist, the plasma magnesium concentration was persistently increased, with concurrent increases in serum calcium and chloride concentrations (3.12 mmol/L and 130 mmol/L, respectively). The rebound hypermagnesemia and hyperchloremia were possibly caused by two reasons: the amount of Mg and Cl absorbed from the intestinal tract increases with the time Mg and Cl remains in the intestinal tract and reabsorption of Mg and Cl in the tissue organ. We used CVVH as a treatment method relatively early in the treatment process. This was based on some explanations and considerations: the unsuitability of calcium gluconate due to hypercalcemia, and for a treatment to decrease serum calcium concentration and chlorine concentration, meanwhile, to protect against rebound hypermagnesemia and hyperchloremia. Nevertheless, we used CVVH, a relatively novel treatment option, based on some literature reports and research.[15,16,17] Currently, the indication for specific treatment is still determined by the physician, mainly based on clinical presentation and severity.

In summary, brine poisoning usually affect multiple systems without specific symptoms, making diagnosis difficult. It causes hypermagnesemia, and there is also the possibility of hyperchloremic acidosis. It is necessary for emergency department doctors to pay attention to monitoring the concentration of serum magnesium and chlorine. Hypermagnesemia can lead to damage to multiple systems, including circulatory, respiratory, central systems, and even death. Brine poisoning should be suspected as a possible cause in any coma, shock and arrhythmia patient who presents to the hospital. For severe electrolyte and acid–base imbalances caused by this type of poisoning, blood purification may be considered, though further evidence is needed to confirm its efficacy.

Research quality and ethics statement

The authors followed applicable EQUATOR Network (https://www.equator-network.org/) guidelines, notably the CARE guideline, during the conduct of this report

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient has given her consent for her images and other clinical information to be reported in the journal. The patient understands that her name and initials will not be published and due efforts will be made to conceal her identity, but anonymity cannot be guaranteed.

Conflicts of interest

There are no conflicts of interest.

Funding Statement

Nil.