Death from salt and baking soda ingestion

Abstract

Table salt (sodium chloride) and baking soda (sodium bicarbonate) are rarely included on the list of potentially dangerous household toxins and many clinicians are unfamiliar with the management of ingestion or overdose. Table salt overdose has been reported after attempted induction of emesis and improper preparation of infant formula. The latter have resulted in severe toxicity and death. Sodium bicarbonate use for the treatment of dyspepsia and in religious exorcism rituals has also been reported to cause severe toxicity and death. Specifically, large quantities of sodium chloride have been reported to cause hemodynamic instability, electrolyte abnormalities, seizures, altered mental status, cerebral edema, and thrombi secondary to red blood cell crenation. Acute ingestions of sodium bicarbonate have been reported to cause metabolic alkalosis, electrolyte abnormalities, altered mental status, dysrhythmias, tachypnea, and rhabdomyolysis. We report a case of ingestion of sodium chloride and sodium bicarbonate in an attempt to induce emesis, which resulted in death.

Keywords:

• Salt
• sodium chloride
• baking soda
• sodium bicarbonate
• hypernatremia

Introduction

Table salt (sodium chloride) and baking soda (sodium bicarbonate) are rarely included on the list of potentially dangerous household toxins, and many clinicians are unfamiliar with the management of ingestion or overdose. Table salt overdose has occurred after attempted induction of emesis and improper preparation of infant formula, resulting in severe toxicity and death [1–3,9,10]. Sodium bicarbonate use for the treatment of dyspepsia and in religious exorcism rituals has also caused severe toxicity and death [4,5]. Specifically, large quantities of sodium chloride have caused hemodynamic instability, electrolyte abnormalities, seizures, altered mental status, cerebral edema, and thrombi secondary to red blood cell crenation [1,2,6]. Acute ingestions of sodium bicarbonate have caused metabolic alkalosis, electrolyte abnormalities, altered mental status, dysrhythmias, tachypnea, and rhabdomyolysis [4,5,7]. We report a case of ingestion of sodium chloride and sodium bicarbonate in an attempt to induce emesis, which resulted in death.

Case

A 57-year-old female reported taking an intentional overdose of an unknown amount of tramadol, which was her only known medication. Her boyfriend contacted the regional Poison Center (PC) to enquire about inducing emesis. The PC advised that he seek medical attention immediately and that he should not attempt to induce emesis. Despite the recommendation, he administered “a few glasses” of table salt and baking soda mixed with water to the patient prior to leaving for the hospital. En route to the hospital the patient had an episode of emesis. On arrival to the Emergency Department (ED) she was awake and oriented. She had a heart rate of 66 beats per minute, blood pressure of 119/68 mmHg, temperature of 36.3⁰C, and an oxygen saturation of 97% on room air. Her physical exam was documented to be entirely normal. About five hours post-ingestion her mental status deteriorated, and the poison center was consulted by the treating emergency physician. The physician reported the patient had experienced a self-limited, tonic-clonic generalized seizure. At that time laboratory workup (Table 1) revealed a serum sodium of 168 mmol/L. Serum acetaminophen, salicylate, and ethanol concentrations were undetectable. She was admitted to the intensive care unit and seizure activity began again. Attempts to treat the seizure with three doses of intravenous (IV) lorazepam 2 mg were unsuccessful. A loading dose of phenobarbital (975 mg) was administered IV and the patient was intubated. Status epilepticus persisted for three hours despite propofol and lorazepam infusions. Repeat lab work revealed a serum sodium of >175 mmol/L (Table 1) and a metabolic alkalosis with respiratory compensation (Table 2). She underwent 3 h of hemodialysis, which transiently improved the serum sodium from >175 mmol/L to 161 mmol/L. Due to concerns from the primary management team regarding the rate of correction of the serum sodium, no further hemodialysis was performed.

Table 1. Basic Metabolic Panel results including timing of dialysis and DDAVP administration.

	HD 1: 1222	1745	2113	HD 2: 0142	0638	1416	HD 3: 0344	1008
Sodium mmol/L	168	>175	>175	161	170	167	153	148
			Dialysis		DDAVP
Potassium mmol/L	2.6	2.3	2.0	2.4	1.8	1.9	2.3	2.8
Chloride mmol/L	119	130	130	107	113	110	112	111
Bicarbonate mmol/L	43	>48	48	46	>48	>48	37	30
Anion gap	9	–	–	10	7	4	6	10
Calcium mg/dL	9.3	8.8	8.7	8.4	7.7	7.4	7.1	7.4
Blood Urea Nitrogen mg/dL	10	14	16	8	11	11	10	12
Creatinine mg/dL	<0.5	0.9	1.2	0.8	1.1	1.0	0.7	0.7
Glucose mg/dL	156	219	172	177	192	164	157	113

Table 2.  Blood Gas results for the first three days of the patient's admission.

	HD 1: 1733	1826	HD 2: 0114	0608	HD 3: 0845
pH	7.23	7.35	7.47	7.49	7.38
PaCO2 mmHg	147	131	70.2	74	60.3
PaO2 mmHg	219	219	67	86	64
Bicarbonate mmol/L	59.4	70.3	50.3	55.2	34.9
Base Excess mmol/L	24.6	35.7	21.5	8.5	5.5

The patient received 2,814 mL of 5% Dextrose in water (D5W) and had 3,550 mL of urinary output reported on hospital day (HD) 1. On HD 2 the patient received 7,227 mL of D5W and had 6,650 mL of urinary output reported. No further seizure activity was noted, but she remained unresponsive with fixed and dilated pupils without sedation. A head CT revealed diffuse cerebral edema with subarachnoid hemorrhage. She was started on DDAVP when her urine was noted to be “dilute”, although the Poison Center did not obtain the urinalysis results. On HD 3 hypertonic saline was initiated for cerebral edema. A head computed tomography angiography (CTA) revealed progression of cerebral edema with tonsillar herniation and lack of significant blood flow in the intracranial vessels. She was declared brain dead on HD 5, care was withdrawn, and she expired.

Discussion

We present a sodium chloride and sodium bicarbonate overdose associated with metabolic derangements, neurologic toxicity, and death. The initial ingestant was tramadol, a mu-opioid agonist with serotonergic properties and the potential to cause seizure in overdose. In the context of a lack of opioid toxidrome on exam, the cerebral edema, and the patient’s severe hypernatremia it is extremely unlikely that the seizure and subsequent hospital course reflected tramadol toxicity.

The patient presented with hypernatremia, hyperchloremia, hypokalemia, and alkalemia. The initial arterial blood gas revealed a metabolic alkalosis with respiratory compensation. She developed altered mental status, seizures, subarachnoid hemorrhage, cerebral edema, and brain death after her ingestion. A similar clinical course has been reported after sodium chloride overdose [1–3,6,8,9]. Cases of sodium bicarbonate ingestion have also lead to significant electrolyte and acid/base abnormalities [4,5].

The primary manifestations of sodium bicarbonate toxicity include metabolic alkalosis, hypernatremia, hypertension, hypokalemia, hypochloremia, hyporeninemia, acute kidney injury, and urinary alkalinization [4,5,7]. Treatment with normal saline and electrolyte replacement are adequate treatment after minor ingestions, but critically ill patients may require dialysis.

Sodium chloride toxicity most commonly results in hypernatremia, hyperchloremia, and metabolic acidosis. Elevated serum and extracellular fluid tonicity causes neuron dehydration with subsequent metabolic dysfunction [2,3]. Carlberg et al. describe the lethal dose of sodium chloride be 0.75-3 g/kg based on fatalities reported in the literature [6]. One tablespoon of salt contains about 17 g of sodium chloride and can elevate the serum sodium by 15mEq/L in an average-sized adult. Based on this dose an ingestion of four tablespoons of salt could be lethal in a 70 kg individual.

Severe sodium chloride toxicity is infrequent and has no single widely accepted treatment. Most authors recommend rapid correction of acute changes in serum sodium concentration, and more gradual corrections in cases in which the change in serum sodium concentration occurred over a longer period of time [1,2,6,8,10].

Treatment options for correction of hypernatremia include electrolyte-free water administration (e.g. D5W) intravenously or enterally, and dialysis. A patient with a serum sodium concentration of 196 mmol/L after soy sauce ingestion underwent a rapid infusion of 6 L D5W over 30 min. The patient suffered no neurological sequelae [6]. Alternatively, IV infusion of normal saline was used in another case report and resulted in a decrease in sodium of 18 mmol/L over the first 3 h [10]. The authors suggest that rate of decrease may have been too rapid and may have caused the herniation ultimately found in their patient. The most appropriate rate of sodium correction for acute hypernatremia remains uncertain.

Hemodialysis may rapidly correct the sodium concentration while avoiding high volume fluid administration. This may be preferable depending on patient-specific factors and concerns for fluid overload, although time delays in initiation of hemodialysis may be problematic.

DDAVP has been used for apparent diabetes insipidus in other cases of acute hypernatremia [10]. In this setting, diabetes insipidus is likely related to the natural progression of severe cerebral edema.

Overdose of sodium chloride and sodium bicarbonate can result in significant acid/base and electrolyte abnormalities. We report a case of an acute overdose of both substances resulting in death from severe hypernatremia and cerebral edema. It is possible that more rapid correction of our patient’s sodium level may have improved the outcome. Fluid shifts from rapid changes in serum sodium later in her clinical course, after intracellular compensation had begun, may explain the cerebral edema. However, cerebral edema was present on admission in 3 fatalities from severe acute hypernatremia due to salt water ingestion [1], suggesting other unknown factors may also lead to cerebral edema. Based on the good result in the soy ingestion case discussed above, and the uniformly poor outcomes with other approaches, we would recommend that acute hypernatremia from exogenous overdose be managed by rapid correction with aggressive electrolyte-free water administration and serial electrolyte assessment.

Disclosure statement

No potential conflict of interest was reported by the author(s).