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Iournal of Analytical Toxicology, Vol. 28, September 2004
ICase Report
A Non-Fatal Caseof SodiumToxicity
Thomas C. Kupiec
Analytical ResearchLaboratories,840 ResearchParkway, Suite 546, OklahomaCity, Oklahoma 73104
John M. Goldenring
Riverside PhysiciansNetwork, 1650Iowa Street,#200, Riverside, California 92507
Vishnu Raj
Departmentof ForensicScience, Universityof Central Oklahoma (UCO), 100 N. University Drive, Edmond,Oklahoma 73034
I Abstract I
A non-fatal case of sodium toxicity in a six-year-old boy is
presented. Hypernatremia is the clinical term for an excessive
concentration of sodium relative to water in the body. The
diagnosis of hypernatremia was made at serum sodium (Na +)
concentrations exceeding 150 mEq/L, and few people have been
reported to survive concentrations greater than 160 mEq/L. This
case involves a six-year-old boy who was taken to the hospital
following a seizure attack, and lab analyses revealed serum sodium
(Na § levels of 234 mEq/L and serum chloride (CI-) levels of 205
mEq/L. Clinical tests ruled out diabetes insipidus, dehydration,
renal pathology, and other primary causes of hypernatremia. The
child's purported history of pica, and the lab results indicating
corresponding increases in levels of serum sodium (Na +) and serum
(CI-), led to a diagnosis of acute sodium toxicity by ingestion of
sodium chloride. A search of the boy's house led to the discovery of
rock salt in the cabinet and a container of table salt. Extrapolating
from the serum sodium (Na +) level, it was estimated that the child
had ingested approximately four tablespoons of rock salt, leading to
the acute toxicity. A literature search revealed that the serum
sodium (Na +) concentration in the present report was the highest
documented level of sodium in a living person.
Introduction
Sodium (Na) is a frequently encountered element, and it is
also a key component of the body's electrolyte system. The daily
intake of sodium is chiefly in the form of common salt, or
sodium chloride (NaCl). Hypernatremia, or very high sodium
concentration, may be due to a variety of causes like dehydration, diabetes insipidus (DI), sodium ingestion, and kidney disease. The cutoff for a diagnosis of hypernatremia is a serum
sodium (Na+) level of 150 mEq/L. However, reports describe a
few non-fatal cases with serum sodium (Na+) levels ranging
from 193 to 209 mEq/L (1-3). Prior to this report, Dominguez
et al. (4) have documented a case of hypernatremia with sodium
526
ion levels of 216 mgq/L, which was the highest known level of
serum sodium (Na§ in a non-fatal case. The following is a
case of sodium toxicity secondary to the suspected ingestion of
rock salt in a six-year-old boy.
Case History
A six-year-old boy was taken to the hospital following respiratory failure after a seizure attack. The patient was thrashing
in his sleep, thus awakening the foster parents, who attempted
to give him CPR after he turned unresponsive. The foster parents called emergency services, and an ambulance transported
him to the hospita]. At the hospital, the lab findings indicated
serum sodium levels in excess of 200 mEq/L; the result was beyond the linearity of the instrument. The child was then transferred to a children's hospital, where the presenting symptoms
included respiratory failure and altered mental status.
ACT scan revealed the presence of bilateral chronic subdural
hematomas. Lab results at the children's hospital indicated
severe hypernatremia with a serum sodium (Na+) value of 234
mEq/L. Additionally, hyperchloremia was observed, with a
serum chloride (Cl-) value of 205 mEq/L. Other metabolic abnormalities included hypokalemia and metabolic acidosis. In the
ER, the patient was administered fluids, lorazepam (Ativan|
and vecuronium. Subsequently, the patient was placed on
saline, sodium bicarbonate, potassium chloride, potassium
phosphorus, and Ringer's lactate.
The patient had a general history of pica, a disorder involving
the ingestion of non-food items, and a specific history of glass
ingestion. He displayed signs of a burn wound on his left hand,
and the wound looked approximately two-weeks old. Records
also revealed that he had a past history of physical and sexual
abuse and was diagnosed with Post Traumatic Stress Disorder
(PTSD) and Attention Deficit Hyperactivity Disorder (ADHD).
The foster parents of the child reported that he complained of
thirst, urinated frequently, and had vomited twice in two days.
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Journal of Analytical Toxicology, Vol. 28, September 2004
However, they denied any knowledge of salt ingestion.
The sodium levels started to progressively decrease without
any additional treatment, and this was followed by a corresponding improvement in neurological status. The patient had
a past history of seizure activity and was taking the prescription
anti-convulsant drug divalproex sodium (Depakote| Other
medications administered to the patient during the hospital
stay included albuterol, epinephrine, norepinephrine,
dopamine, fosphenytoin, lorazepam, rocuronium, ranitidine
(Zantac| clindamycin, desmopressin acetate (DDAVP),vasopressin, and hydrochlorthiazide.
Discussion
Sodium is a critical electrolyte and changes in sodium concentration could manifest as hyponatremia or hypernatremia.
Increase in the sodium concentration may imply a relative decrease in the water concentration, or an absolute increase in
sodium concentration (1). Hypernatremia results in cellular
dehydration, because of the shift of water from the intracellular
to the extracel[ular compartment (5). Physiological compensatory mechanisms to combat the increase in Na concentrations
include polydipsia (thirst) and the release of the antidiuretic
hormone (ADH). As the sodium concentration in the body increases, it leads to the release of ADH/vasopressin,which decreases diuresis and the ensuing water loss, thereby maintaining homeostasis. Coulthard et al. (6) refer to the rare
disorder Essential Hypernatremia, in which escalating levels of
sodium do not produce a thirst response or release of antidiuretic hormone (hl)H). The etiology of hypernatremia includes
dehydration due to diarrhea and vomiting, use of diuretics,
renal disease, DI, and excessive intake of sodium. The clinical
features include thirst, lethargy, weakness, nausea and vomiting, hypertension, and irritability (5). Seizures, coma and pup
monary edema have also been reported in certain cases of hypernatremia (5,6). Serum Na levels above 160 mEq/L have been
associated with a high mortality rate (60%) and neurologic
damage (7). DI, which is a disorder of decreased secretion of
ADH, is a common cause of hypernatremia. There have also
been reports of lithium-induced DI leading to hypernatremia
(8).
This patient, however, did not have a history of medication
with lithium, which is often used to treat bipolar disorders.
Additionally, the lab findings were not consistent with a diagnosis of DI, with the urine appearing normal (specific gravity
1.01 and osmolality 457 mOsm/L) instead of dilute, as expected
in cases of DI and renal pathology (300 mmol/kg to 50
mmol/kg) (6). The administration of DDAVPand vasopressin,
drugs of choice for the treatment of DI, did not produce any results, thus ruling out DI as the cause of hyponatremia in this
case. No signs of dehydration were evident;the urine output was
elevated, heart rate was normal, and there was no increase in
hemoglobin/hematocritvalues. None of the medications taken
by the patient were known to cause this electrolyte imbalance.
The patient was also hyperchloremic (205 mEq/L), and this
finding was not consistent with any etiology other than the in-
gestion of sodium chloride (NaCl).
A search of the patient's house revealed a container of table
salt on a countertop and rock salt in a closet. The similarity between the serum concentrations of Na§ (234 mEq/L) and C1(205 mEq/L) and the patient's history of pica suggested that the
hypernatremia might have been a consequence of acute NaCl
ingestion. Salt poisoning is known to increase the serum
sodium (Na§ concentrations and also leads to an increased osmolality, often above 400 mOsm/kg, due to impaired renal excretion (9).
Pica refers to the ingestion of non-food substances, which
may include dirt, clay, chalk, cigarette ashes, sand, soil, and
paint. Mental retardation (10), stress resulting from maternal
deprivation (10), parental neglect, and a variety of behavior
disorders (11) have been suggested as possible etiologies of
pica. This patient was a victim of sexual abuse, neglect, and maternal deprivation and had a purported history of pica, particularly the ingestion of glass.
One of the statements by the child alleged that his foster
mother used to make him drink salt water. Adrogu~and Madias
(12) list sodium-chloride emetics as a possible cause of hypertonic sodium gain. Salt-water emetics have been known to
cause hypernatremia; however, cases of salt water emetic poisoning are not as frequently encountered as before (5,13,14).
Although there was no evidence to determine the manner of ingestion, we hypothesized that the child had ingested NaCl, as a
result of his pica condition, and thereby developedacute sodium
toxicity. Shapiro et al. (10) describe the case of a young woman
with salt pica, secondary to iron deficiency.In the present case,
however, there was no evidence of a deficiency of iron in the
diet.
Being a monobasic salt, NaC1contains similar proportions of
Na§ and CI-, and both serum sodium (Na+) and serum chloride
(Cl-) levels were elevated in this patient. In the current case, information about the methodology used by the ER to evaluate
electrolyte concentration was not available. However, these
electrolytes are typicallyassessed by ion selective electrodes. We
performed a series of back calculations to estimate the approximate quantity of ingested sodium that would produce a serum
concentration of 234 mEq/L. Cases of salt poisoning in the literature describe lethal doses ranging from 0.75 g/kg body
weight to 3 g/kg body weight (15). Extrapolating from the aforementioned data, the lethal dose for a child who weighs 25 kg
would range between approximately 19 g and 75 g. Assuming
the normal sodium concentration to be 140 mEq/L, and using
the following equation, the ingested quantity of NaC[ was calculated to be approximately 83 g.
Dose = (Cp)x (Vd)
where Vd= volume of distribution and Cp = plasma concentration.
The average tablespoon of rock salt contained about 21.6 g of
NaC1; therefore, the patient was suspected to have consumed
about four tablespoons of rock salt.
The CT scan of the patient exhibited the presence of bilateral
subdural hematomas. One of the prevailing theories in the
1950s was based on the dehydration induced by hypernatremia
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Journal of Analytical Toxicology,Vol. 28, September2004
leading to shrinkage of the brain (1), thereby decreasing its
size and stretching the bridging veins, resulting in a subdural
hematoma (9), subarachnoid hemorrhage, and cerebral
bleeding (12). Handy et al. (9), however, failed to identify any
causal link between hypernatremia and the subsequent occurrence of subdural hematomas.
References
1. Y.J. Park, Y.C. Kim, M.O. Kim, J.H. Ruy, S.W. Hart, and H.J. Kim.
Successful treatment in the patient with serum sodium level greater
than 200 mEo./L.J. Korean Med. ScL 15(6): 701-703 (2000).
2. M. Addleman, A. Pollard, and R.F.Grossman. Survival after severe
hypematremia due to salt ingestion by an adult. Am. J. Med. 78(1):
176-178 (1985).
3. K.G. Moder and D.L. Hurley. Fatal hypematremia from exogenous
salt intake: report of a case and review of the literature. Mayo Clin.
Proc. 65(12): 1587-1594 (1990).
4. R.R. Borrego Dominguez, A. Imaz Roncero, J. Lopez-Herce Cid,
and C. Serina Ramirez. Severe hypernatremia: survival without
neurologic sequelae (in Spanish). An. Pediatr. (Barc). 58(4):
376-380. (2003).
5. N. Bates. Poisoning: sodium chloride and sodium bicarbonate.
Emerg. Nurse 11(2): 33-37 (2003)
528
6. M.G. Coulthard and G.B. Haycock. Distinguishing between salt
poisoning and hypematremic dehydration in children. Br. Med. J.
326(7381): 157-160 (2003).
7. N.A. Snyder, D.W. Feigal, and A.I. Arieff. Hypernatremia in elderly
patients: a heterogeneous, morbid, and iatrogenic entity. Ann. Intern. Med. 107(3): 309-319 (1987).
8. D. Mukhopadhyay, L. Gokulkrishnan, and K. Mohanaruban.
Lithium-induced nephrogenic diabetes insipidus in older people.
Age Ageing 30(4): 347-350 (2001).
9. T.C. Handy, R. Hanzlick, L.B. Shields, R. Reichard, and S. Goudy.
Hypernatremia and subdural hematoma in the pediatric age group:
is there a causal relationship? J. Forensic Sci. 44(6): 1114-1118
(1999).
10. M.D. Shapiro and S.L. Linas. Sodium chloride pica secondary
to iron-deficiency anemia. Am. J. Kidney Dis. 5(1): 67-68
(1985).
11. M.S. Bhatia, S. Rai, P.K. Singhal, V.R. Nigam, N. Bohra, and
S.C. Malik. Pica: prevalence and etiology. Indian Pediatr. 25"
1165-1170(1988)
12. H.J. Adrogu~ and N.E. Madias. Hypernatremia. N. Engl. J. Med.
342:1493-1499 (2000).
13. G.A. Gresham and M.K. Mashru. Fatal poisoning with sodium
chloride. Forensic $ci. Int. 20(1): 87-88 (1982).
14. F.J.Smith and S. Palevsky. Salt poisoning in a two-year-old child.
Am. J. Emerg. Med. 8(6): 571-572 (1990).
15. M.J. Ellenhorn. Ellenhom's Medical Toxicology: Diagnosis and
Treatment of Human Poisoning, 2nd ed. Williams & Wilkins, New
York, NY, 1997, pp 971-1035.