Hypernatremia, a high concentration of sodium in the blood, is not usually caused by an intentional salt overdose.
More commonly, hypernatremia is caused by free water losses due to either decreased water intake or excessive gastrointestinal or renal losses.
As little as 25 grams, or fewer than 4 tablespoons of salt, has been lethal in adults.1 Lethal salt ingestion has occurred when salt is used as an antiemetic, confused for sugar, or used in suicide attempts.2
A 22-year-old male was brought into the ED by emergency medical services (EMS) due to altered mental status and seizures. The patient’s landlord called EMS after finding him unresponsive in his bedroom surrounded by white powder and an empty bottle of salt (NaCl) tablets. The landlord informed EMS that the patient possibly was being treated for a “mineral disorder.” No further medical history or collateral information was available at the time. EMS treated his seizure successfully with midazolam and transported the patient.
In the ED, the patient’s eyes were open with minimally reactive, 5 mm pupils bilaterally. He was nonverbal and withdrew to painful stimuli. There was no evidence of continued seizure activity. His initial vital signs were blood pressure of 153/110 mm Hg, heart rate of 130 beats/min, respiratory rate of 21 breaths/min, oxygen saturation of 98% on a non-rebreather, and a temperature of 37.2°C. The remainder of his physical exam was notable only for dry mucous membranes.
Due to his altered mental status, concern for airway protection, and need for extensive medical work-up, the decision was made to intubate the patient. The venous blood gas sample shortly returned with a mild acidosis of 7.23, pCO2 of 53 mm Hg, pO2 of 39 mmHg, and bicarbonate of 21.7 mmol/L. Our venous blood gasses included electrolytes which showed critical sodium of 198 mmol/L, chloride above detectable ranges, glucose of 167 mg/dL, and lactate of 3.3 mmol/L.
Subsequently, the patient’s basic metabolic panel confirmed the diagnosis of severe hypernatremia with sodium >180 mmol/L. Additional blood tests were notable for a serum osmolality of 415 mOsm/kg, an AKI, and mild leukocytosis. His head CT without contrast was concerning for peripheral subarachnoid hemorrhages.
In the ED, hypernatremia is generally due to free water losses and volume depletion. Less frequently, it is a consequence of excessive sodium intake. Historically, salt has been used as an antiemetic, which has led to several deaths. Other fatal cases have included mistaking salt for sugar and the ritual use of salt in exorcisms.1 In animal models, the LD50 (lethal dose in 50% of animals) of salt is 3g/kg, but significantly lower doses have been fatal in humans.3 In large ingestions, sodium chloride is rapidly absorbed through the GI system, overwhelming its renal excretion. If there is no additional free water intake, the patient will become increasingly hypernatremic.4
Patients with acute hypernatremia can present with encephalopathy, seizures, and focal neurological deficits. Central nervous system (CNS) effects predominate as the brain is especially sensitive to the tonicity changes associated with acute hypernatremia. The increased tonicity can result in osmotic demyelination syndrome (ODS) due to damage to oligodendrocytes.5 More commonly, ODS occurs in the setting of rapid correction of hyponatremia; however, it has also been reported in acute salt ingestion.6,7 The pons is more susceptible to these osmotic changes and is frequently involved in ODS.
Unfortunately, diagnosis is often delayed after the initial insult due to the lag of symptom onset. It is usually diagnosed after an MRI shows demyelinating disease consistent with ODS and carries a poor prognosis with no clear treatments.5This highlights the importance of well-controlled sodium correction, which requires frequent monitoring every 2-4 hours in the acute phase.
Acute hypernatremia is also associated with intracranial hemorrhage, which can be another contributor to altered mental status and seizures.8 In the setting of high tonicity, neurons shrink in size to achieve osmotic equilibrium with the extracellular space. This leads to the retraction of cerebral tissue, causing shear stress on blood vessels and hemorrhage.
Generally, acute salt ingestion should be rapidly corrected to reduce serum osmolality. This can be done with an infusion of hypotonic solutions, such as 5% dextrose in water (D5W), with a goal reduction of 1 mmol/L/hr.9 Isotonic solutions should not be used unless the patient is hemodynamically unstable and requires volume expansion. Other methods such as hemodialysis have also been used to rapidly correct sodium levels, with good neurological outcomes.10
In this case, there was concern for a more subacute ingestion, given the patient’s history of an unknown mineral disorder treated with salt tablets. Therefore, rapid correction could result in significant brain edema. Over time, the brain parenchyma equilibrates to the higher extracellular osmolality by increasing intracellular osmoles, restoring normal cellular volumes.11 In cases of chronic hypernatremia, sodium should be reduced no more than 10 mmol/L/day with enteric free water or hypotonic solutions.9 If this is not done, the osmotic gradient will drive free water into the hyperosmotic cells, leading to increased cellular volume and brain edema.
After discussions with toxicology and nephrology, the patient’s sodium was slowly corrected with a D5W infusion after an initial D5W bolus. While in the ED, the patient was identified and was found to have a history of attention-deficit/hyperactivity disorder and anxiety. Notably, he was evaluated in the ED three months prior for persistent nausea and self-reported concerns that he had a “mineral imbalance.” The patient had purchased supplements to fix his imbalance despite having normal labs, including sodium, at that time.
Given the concern of chronic salt ingestion leading to longstanding hypernatremia, the decision was made to slowly correct the patient’s hypernatremia. He was admitted to the medical intensive care unit on a D5W infusion. His sodium was slowly corrected with a D5W infusion and enteric free water flushes. An MRI, with and without contrast, of his brain was done, which unfortunately showed pontine and extrapontine osmotic demyelination consistent with ODS. It also demonstrated cerebral edema and subarachnoid hemorrhage. His sodium normalized on hospital day nine, and he was extubated. After a prolonged hospital course, he was discharged to a short-term rehab facility. At the point of discharge, the patient was noted to have mild lower extremity weakness and an unsteady gait due to mild truncal ataxia. The patient was also noted to have a flat affect but was cognitively intact.
- Campbell N, Train E. A Systematic Review of Fatalities Related to Acute Ingestion of Salt. A Need for Warning Labels? Nutrients. 2017;9(7):648.
- Metheny NA, Krieger MM. Salt Toxicity: A Systematic Review and Case Reports. Journal of Emergency Nursing. 2020;46(4):428-439.
- Acros Organics. Safety Data Sheet: Sodium Chloride. Published 2015. Accessed June 7, 2022.
- Sterns RH. Disorders of Plasma Sodium — Causes, Consequences, and Correction. New England Journal of Medicine. 2015;372(1):55-65.
- Martin RJ. Central pontine and extrapontine myelinolysis: The osmotic demyelination syndromes. Neurology in Practice. 2004;75(3):22-28.
- Han MJ, Kim DH, Kim YH, Yang IM, Park JH, Hong MK. A case of osmotic demyelination presenting with severe hypernatremia. Electrolyte and Blood Pressure. 2015;13(1):30-34.
- Ismail FY, Szóllics A, Szólics M, Nagelkerke N, Ljubisavljevic M. Clinical semiology and neuroradiologic correlates of acute hypernatremic osmotic challenge in adults: A literature review. American Journal of Neuroradiology. 2013;34(12):2225-2232.
- Hughes A, Brown A, Valento M. Hemorrhagic encephalopathy from acute baking soda ingestion. Western Journal of Emergency Medicine. 2016;17(5):619-622.
- Adrogué HJ, Madias NE. Hypernatremia. New England Journal of Medicine. 2000;342(20):1493-1499.
- Sakai Y, Kato M, Okada T, et al. Treatment of salt poisoning due to soy sauce ingestion with hemodialysis. Chudoku Kenkyu. 2004;17(1):61. Accessed July 15, 2020.
- Gullans SR, Verbalis JG. Control of Brain Volume During Hyperosmolar and Hypoosmolar Conditions. Annual Review of Medicine. 1993;44(1):289-301.