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900.e2 Salt Toxicosis
Salt Toxicosis
VetBooks.ir
as: glycerol, maltitol, and sorbitol can cause
BASIC INFORMATION
this fluid shift. Common sources of osmoti- Spontaneous, non-toxicologic:
• Water deficit
Definition cally active agents include activated charcoal, ○ Primary hypodipsia, diabetes insipidus
Salt (sodium chloride, table salt, NaCl) toxicosis paint balls, gummy candies, sugar-free candy, (central/nephrogenic), high ambient
(hypernatremia) results when an excessive and bulk artificial sweeteners. temperature, fever, restricted water access
amount of sodium has been ingested, intake Mechanism of toxicosis: • Hypotonic fluid loss
of potable freshwater is limited, and/or free • Signs of toxicosis typically appear when ○ GI loss, third-space loss (peritonitis,
water translocates from the vasculature into serum sodium is > 170 mEq/L (vomiting, pancreatitis), cutaneous (burns), osmotic
the gut following osmotically active agents. polydipsia), and central nervous system diuresis (diabetes mellitus, mannitol
(CNS) signs (tremors and seizures) begin infusion), chemical diuretics, acute and
Synonyms when serum sodium level is > 180 mEq/L chronic kidney disease (CKD)
Water deprivation, sodium ion toxicosis, (typical normal range in healthy dogs: ○ Other causes of hypernatremia (paint
osmotic hypernatremia, salt poisoning 145-157 mEq/L). NOTE: Changes in serum ball ingestion in dogs; administration of
sodium may lag behind clinical signs, and activated charcoal)
Epidemiology CNS signs may be seen at significantly • Solute gain (e.g., hyperaldosteronism)
SPECIES, AGE, SEX lower serum sodium levels if levels rise
Both sexes of dogs and cats at any age; dogs quickly. Serum sodium levels may take Initial Database
are more likely to be involved hours after the onset of clinical signs • CBC: stress leukocytosis
to peak. • Serum biochemistry profile
RISK FACTORS • Hypernatremia creates a hypertonic state in ○ Hyperalbuminemia
• Use of table salt as an emetic (now contra- the extracellular fluid (ECF). Initially, water ○ Prerenal azotemia
indicated for this reason) shifts from the interstitium to the vasculature • Acid-base
−
• Availability of homemade play dough and/ and then from intracellular fluid (ICF) to ○ Decreased serum HCO 3 possible (meta-
or paintballs in pet’s environment the ECF to maintain equilibrium. bolic acidosis)
• Swimming and drinking seawater when • The CNS is particularly vulnerable to • Electrolytes
availability of potable drinking water is initial tissue shrinkage as water leaves the ○ Hypernatremia
limited ICF, resulting in microvascular trauma and ○ Hyperchloremia
• Dehydration (increases risk) potential demyelination, with a rapid rise • Thoracic radiographs: pulmonary edema
• Vomiting (inability to maintain hydration to severe hypernatremia. possible (with concurrent sodium and water
despite polydipsia) • Sodium passively crosses the blood-brain load, especially if there is pre-existing heart
• Outdoor dogs in cold climates/frozen water barrier into the cerebrospinal fluid (CSF). disease)
Once in the CSF, excess sodium affects
Clinical Presentation neuronal function by inhibiting glycolysis Advanced or Confirmatory Testing
HISTORY, CHIEF COMPLAINT and decreased energy production. Sodium • NaCl can be analyzed in vomitus, food,
• Owner description of risk factor (see above) requires active transport to move from the water; may help determine the source
• Lack of drinking water or vomiting after CSF back to the serum; decreased energy and concentration of NaCl (rarely needed
ingesting excessive amounts of salt production limits this process. In the brain, a clinically)
• Polyuria and polydipsia (PU/PD) compensatory response to dehydration is the • Postmortem: brain sodium (>1800 ppm)
• Polydipsia, vomiting, ataxia, tremors, and formation of idiogenic osmoles or solutes 24
seizures within 1-4 hours after ingestion hours or more after onset of hypernatremia. TREATMENT
With rapid rehydration, these osmotically
PHYSICAL EXAM FINDINGS active solutes cause an influx of water into the Treatment Overview
• Vomiting, diarrhea, signs of abdominal brain, resulting in cerebral edema, seizures, The cornerstone of treatment is reduction
pain permanent neurologic dysfunction, and of serum sodium. Asymptomatic patients
• Signs of dehydration possibly death. presented within 2 hours of ingestion may
• Sinus tachycardia (secondary to dehydration) • Excess sodium is irritating to gastrointestinal be decontaminated (induce emesis, do NOT
• Depression, ataxia, tremors, seizures (GI) mucosa and can cause gastroenteritis give activated charcoal), and treatment aims
• Hyperthermia possible (secondary to tremors, and secondary dehydration. for rapid sodium excretion/dilution. Serum
seizures) sodium level can be returned to normal as
DIAGNOSIS quickly as possible in patients that have been
Etiology and Pathophysiology hypernatremic for less than 24 hours. Patients
Source: Diagnostic Overview that present after 24 hours require careful
• Sources of excess sodium chloride for animals A tentative diagnosis is made based on history lowering of serum sodium concentrations to
include homemade play dough and model- (excessive sodium intake, water deprivation, avoid iatrogenic CNS injury from cerebral
ing clay, table salt (used as an emetic or and/or ingestion of an osmotically active agent), edema.
simply ingested), improperly mixed feed, ice compatible clinical signs (polydipsia, vomiting,
melt, sea water, hypertonic saline solutions, ataxia, tremors, seizures), or both. Presence of Acute General Treatment
sodium bicarbonate, and sodium phosphate increased serum sodium levels confirm the • Decontamination of patient (p. 1087)
enemas. diagnosis. ○ Induction of vomiting if the animal is
• Ingestion of osmotically active agents leads to asymptomatic and vomiting is induced
hypernatremia from free water loss into the Differential Diagnosis within 2 hours of ingestion
gut, not excess sodium chloride. Polyethylene Toxicologic: see common sources for excessive ○ Activated charcoal is strictly contrain-
glycol (PEG) and some sugar alcohols such sodium chloride ingestion above. dicated. It does not adsorb NaCl and
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