The Lab Who Ate the Sun

Erika Loftin, DVM, DACVECC, presents a case of a dog that ingested toxic levels of salt via homemade “play-dough”.

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A 9-year-old male neutered retriever presented to DoveLewis with a primary complaint of tremors. His owners reported that he had ingested the sun from a homemade play dough (50% salt and 50% flour) solar system earlier in the day. He began having diarrhea and vomiting shortly thereafter, followed by marked generalized tremors. The dog was otherwise healthy, and not on any medications.

On presentation, he was hyperthermic with a rectal temperature of 107.2 F, tachycardic with a heart rate of 220 bpm, and estimated to be 10 percent dehydrated. He was non-ambulatory with severe generalized tremors. His pupils were equal and responsive to light, but full neurologic evaluation was not possible initially. Watery hemorrhagic diarrhea was noted on rectal examination. His blood pressure was normal at 145 mmHg systolic. His body weight was 85 pounds (38kg).

Therapy was initiated with diazepam 15 mg intravenously (which resulted in mild improvement in the tremors), as well as active cooling (wet towels, fans, and alcohol applied to his feet). Due to persistent tremors, he was administered two sequential 1500 mg doses of methocarbamol with some reduction in the tremors. His rectal temperature improved to 105.1 F.

At this time, STAT bloodwork results (see Table 1) became available, which revealed severe hypernatremia (sodium 193.1 mEq/L, normal range 144-160 mEq/L), mild hyperkalemia (potassium 6.23 mEq/L, normal range 3.5-5.8 mEq/L), severe hyperchloridemia (chloride 159.3 mEq/L, normal range 109-112 mEq/L), moderate hypermagnesemia (magnesium 0.79 mmol/L, normal range 0.44-0.58 mmol/L), moderate hyperlactatemia (5.7 mmol/L, normal range 0.5-2.0 mmol/), and elevated packed cell volume and total solids (58 percent/9.5 g/dL), consistent with hemoconcentration.

Table 1 – Initial Emergency Data Base
  Normal Value
Na (mEq/L) 144-160 193.1
K (mEq/L) 3.5-5.8 6.23
Cl (mEq/L) 109-112 159.3
iCa++ (mmol/L) 1.12-1.42 1.33
iMg++ (mmol/L) 0.44-0.58 0.79
Gluc (g/dL) 77-125 122
Lac (mmol/L 0.5-2.0 5.7
BUN (mg/dL) 7.0-27 15
Creat (mg/dL) 0.5-1.8 1.7
PCV/TS   58/9.5

Following diagnostic results, the dog was started on Normosol-M intravenously (IV) at 1 liter/hour to begin rapidly replacing his free water deficit and ameliorating the consequences of acute severe hypernatremia. Active cooling was discontinued when his temperature reached 103.8 F. Due to continued tremors and a need to control excessive muscle activity pending correction of his hypernatremia, he was administered a 16 mg/kg phenobarbital loading dose IV over 30 minutes. He was also started on metronidazole 380 mg IV twice daily due to hemorrhagic diarrhea and concern for bacterial translocation, as well as dolasetron 23 mg IV once daily as an anti-emetic.

Recheck labwork (see Table 2) was performed after 3 liters of Normosol-M had been administered, which revealed significant improvement in his hypernatremia (sodium 166.9 mEq/L). Packed cell volume and total solids measurements were consistent with improved hydration (55 percent/7.1 g/dL). The Normosol-M was continued at a reduced rate (150 mL/hr). Hyperglycemia was noted (521 mg/dL) likely due to the volume of dextrose-containing fluid that had been recently administered. Hyperlactatemia was mildly improved, likely due to successful tremor control as well as improved perfusion.

Table 2 – Recheck Emergency Data Base (EDB) three hours after commencing therapy
  Normal Value
Na (mEq/L) 144-160 166.9
K (mEq/L) 3.5-5.8 3.74
Cl (mEq/L) 109-112 139.1
iCa++ (mmol/L) 1.12-1.42 0.95
iMg++ (mmol/L) 0.44-0.58 0.57
Gluc (g/dL) 77-125 521
Lac (mmol/L) 0.5-2.0 4.5
BUN (mg/dL) 7.0-27 11
Creat (mg/dL) 0.5-1.8 1.2
PCV/TS   55/7.1

The dog’s clinical signs improved and he was able to drink some water by mid-afternoon, but then subsequently vomited hemorrhagic liquid. He was started on pantoprazole 38 mg IV once daily and carafate 1 gram orally every eight hours for gastroprotection, as well as maropitant 38 mg subcutaneously once daily for additional anti-emetic effect.

Recheck electrolytes later that evening revealed mild worsening of hypernatremia (sodium 170.6 mEq/L). The Normosol-M rate was increased back to 200 mL/hr, and the patient was offered oral water in small amounts as well. Electrolyte monitoring and therapeutic adjustment in the fluid plan were continued overnight (see Table 3) until serum sodium normalized and monitoring was discontinued.

The patient's neurologic status normalized, but he remained inappetant. He was discharged home the day after presentation. His discharge medications included metronidazole 500 mg orally twice daily for seven days, omeprazole 20 mg orally once daily for seven days, carafate 1 gram orally every eight hours for five days, and maropitant orally as needed for nausea or vomiting. His owners were instructed to offer small amounts of water orally as tolerated for the first 24 hours after discharge, and then to make water available free choice. A subsequent phone call to his owners indicated that he made a full recovery.

Table 3 - Summary of serial electrolytes during hospitalization
Time Serum sodium Therapy adjustment


193.1 mEq/L Started 3 liters Normosol-M over 3 hours
1:30PM 166.9 mEq/L Decreased Normosol-M to 150mL/hr
5:45PM 170.6 mEq/L Increased Normosol-M to 200mL/hr, offered small amounts of water orally
9:30PM 162.8 mEq/L Decreased Normosol-M to 150mL/hr
1:35AM 151 mEq/L Changed to Normosol-R 150mL/hr
5:10AM 150.4 mEq/L Electrolyte monitoring was discontinued

Differential diagnoses for hypernatremia include pure water loss (caused by primary hypodipsia, central or nephrogenic diabetes insipidus, hyperthermia or fever, or inadequate access to water), hypotonic fluid loss (gastrointestinal losses, renal losses, third space losses such as can occur due to peritonitis, cutaneous losses such as with burns), or impermeant solute gain (salt poisoning, hypertonic fluid administration). Homemade play dough is a recently recognized cause of salt toxicity in domestic animals, but additional sources of excessive salt can include salt water (access to ocean water) as well as paintball toxicity.

In most cases of hypernatremia, the increase in serum sodium results from abnormalities in water handling due to either lack of access to water or to excessive free water losses as discussed above. However, in this case the hypernatremia was a direct consequence of salt ingestion. According to a study of cases at the ASPCA, ingestion of a dose of salt greater than 0.5-1 g/kg may cause signs of toxicity and greater than 4 g/kg can be lethal. In the case presented above, the rapid development of severe hypernatremia led to central nervous system signs (tremors) and consequently significant hyperthermia.

Clinical signs of acute severe hypernatremia occur due to osmotic movement of water out of the brain cells resulting in a rapid decrease in brain volume, rupture of cerebral vessels, and focal hemorrhage. The severity of clinical signs is related more closely to the rapidity of onset of hypernatremia rather than to the absolute magnitude of the change. Clinical signs can include vomiting, diarrhea, polydipsia, muscle weakness, tachycardia, muscle tremors/twitching (often starting with the facial muscles), seizures, disorientation, behavior changes, coma, and death. In patients that are hypernatremic due to sodium gain, signs of volume overload may also be present, particularly in patients with underlying cardiac disease.

In cases of chronic hypernatremia, the body compensates by manufacturing molecules known as idiogenic osmoles (including inositol) to increase intracellular osmolality, restore intracellular volume, and maintain an appropriate osmotic gradient between intracellular and extracellular contents. This response occurs over approximately 24 hours, and prevents dehydration of the brain, allowing patients with chronic hypernatremia to be relatively asymptomatic. It is because of this adaptation that treatment of chronic hypernatremia must be undertaken with caution, because excessively rapid correction can lead to cerebral edema as the administered fluid volume shifts to the intracellular space.

In cases of acute hypernatremia, the physiologic compensation has not had time to occur, and so correction of the hypernatremia can be (and should be) relatively rapid. Free water deficit (FWD) can be calculated by use of the following formula:

FWD = ([current Na+/normal Na+]-1) x (0.6 x body weight in kgs)

In chronic cases, this volume should be replaced at a rate that permits only a 0.5mEq/hr drop in the serum sodium, and frequent electrolyte monitoring is required to regulate the change. Intravenous fluid replacement can be performed with D5W (5 percent dextrose in water) or other crystalloid solutions (see Table 4 for electrolyte composition of commercially available crystalloids). Measured amounts of water can also be offered orally if the patient is able to drink, and this should be factored into the water replacement calculations.


Table 4 - Electrolyte composition of several commercially available IV fluids (adapted from DiBartola)
Fluid Na (mEq/L) Cl (mEq/L) K (mEq/L) Dextrose (g/L)
D5W 0 0 0 50
Normosol-M 40 40 13 50
Normosol-R 140 98 5 0
LRS 130 109 4 0
0.45% saline 77 77 0 0
0.9% saline 154 154 0 0


In the case described above, the free water deficit was calculated as approximately 6.1 liters (using a mid-range normal sodium value of 152 mEq/L in the equation). The dog was administered the first 3 liters of intravenous fluid over three hours to rapidly restore intravascular volume, lower his serum sodium, and resolve clinical signs. This rapid correction was appropriate due to the acute nature of his toxicity. Once these initial goals were achieved, his fluid plan was adjusted to continue to replacement of his free water deficit over the remainder of his time in the ICU.  Further measures that can be useful in some in cases of hypernatremia include enemas (to encourage colonic reabsorption of free water) and furosemide (to facilitate renal sodium excretion).

Additional therapeutic objectives included control of the generalized tremors via administration of diazepam, methocarbamol, and ultimately phenobarbital, as well as active cooling to prevent any further consequences of severe hyperthermia. Hyperthermia can lead to devastating complications including coagulopathy progressing to disseminated intravascular coagulation, and damage to the gastrointestinal, hepatic, and neurologic systems. In this case, rapid cooling and restoration of perfusion likely contributed to the minimization of hyperthermia-related complications. Gastrointestinal protectants were administered due to hemorrhagic gastroenteritis (suspected due to irritant effect of the salt as well as gastrointestinal injury subsequent to hyperthermia).

Patients that survive the acute effects of hypernatremia and therapeutic corrections can be expected to have a good long term prognosis, as seen in this case. Client education is important to ensure that recovery continues after discharge home as well as to prevent any further exposure to excessive amounts of salt.

Burkitt JM:  Sodium disorders.  In Silverstein DC and Hopper K:  Small animal critical care medicine.  St. Louis, MO: Elsevier; 2009, pp. 224-229.  
DiBartola SP: Disorders of sodium and water: Hypernatremia and hyponatremia. In  DiBartola SP, editor:  Fluid, electrolyte, and acid-base disorders in small animal practice, ed 3, St Louis, MO: Elsevier; 2006, pp. 47-79.
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