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Water Intoxication, Acute 1047.e1

Water Intoxication, Acute
VetBooks.ir Etiology and Pathophysiology Diseases and Disorders

BASIC INFORMATION
• Urinalysis: low specific gravity
• Excessive water intake results in low solute • Chemistry panel: panhypoproteinemia
Definition concentrations in the extracellular fluid • Thoracic radiographs (rule out pulmonary
Acute water intoxication (AWI) is a rare but compartment compared with intracellular edema)
potentially fatal condition in dogs resulting fluid. • Oxygen saturation (if pulmonary edema)
from rapid overconsumption of water without • The greatest concern is hyponatremia (p.
sufficient electrolyte replenishment. Initial 518); low serum concentrations of other Advanced or Confirmatory Testing
clinical signs of AWI can include polydipsia, electrolytes (notably chloride and potassium) Serum osmolality < 280 mOsm/kg
polyuria, hypersalivation, and vomiting quickly are also expected.
followed by disorientation, ataxia, seizures, • Hyponatremia can result in reduced plasma TREATMENT
and death. Excessive water intake can lead osmolality, causing a fluid shift (water move-
to significant decrease in serum osmolality ment into cells) through osmosis and leading Treatment Overview
mainly due to hyponatremia; this in turn to neuronal swelling, cerebral edema, and • Distinguish between acute hyponatremia
could cause cerebral edema, ataxia, seizures, and increased intracranial pressure. (clinical signs within hours after consuming
death. • Cerebral edema/increased intracranial pres- excessive water) and chronic hyponatremia
sure can cause central nervous system (CNS) (signs > 24 hours after exposure).
Synonyms signs (ataxia, disorientation, blindness, ○ Treat acute hyponatremia quickly to
Overhydration, hyponatremic encephalopathy seizures, and/or coma), respiratory depres- avoid cerebral edema, brain herniation,
sion/failure, neurogenic pulmonary edema, and demyelination syndrome.
Epidemiology and bradycardia (due to pressure on vagal ○ Treat chronic hyponatremia (>24 hours’
SPECIES, AGE, SEX control mechanisms in medulla [Cushing’s duration) slowly.
Dogs of all ages and both sexes; rare in reflex]).
cats • Death may occur due to demyelination Acute General Treatment
syndrome, brain herniation, and mechani- • Patient presents with polydipsia/polyuria but
RISK FACTORS cal compression of vital midbrain functions no CNS signs.
Pre-existing renal disease can increase the (respiration, heart rate), pulmonary edema, ○ Limit water intake.
likelihood of developing AWI. or a combination of these factors. ○ Check serum electrolytes, and monitor
• Impaired renal water excretion secondary in-clinic for 8 hours for development of
to a concurrent nonosmotic release of DIAGNOSIS CNS signs.
antidiuretic hormone (ADH) with excessive ○ Remove excessive water from stomach (if
intake of hypotonic fluid or due solely to Diagnostic Overview present) with a gastric tube.
an ingestion of excessive volumes of fresh AWI is suspected mainly from the history • Treat acute hyponatremia promptly (p. 518).
water can overwhelm normal renal excretory of swimming/playing in the water and rapid ○ Correct serum sodium with hypertonic
mechanisms and lead to AWI. development of polydipsia, polyuria, neurologic or isotonic saline.
• Solute loss (mainly sodium) or water reten- signs, physical exam findings, hyponatremia, and ○ Furosemide 2.2-4.4 mg/kg IV (preferred),
tion can cause hyponatremia. In general, low concentrations of other electrolytes (and low IM, PO q 6-8h to enhance excretion of
hyponatremia occurs only when there is a serum osmolality). Typically, severe neurologic free water through the kidney to normalize
defect in renal water excretion. dysfunction in dogs occurs when serum sodium osmolality
is < 120 mEq/L. ○ Monitor electrolytes every few hours until
GEOGRAPHY AND SEASONALITY normalization.
In dogs, more likely in summer months (e.g., Differential Diagnosis • Treat seizures with diazepam 0.5-2 mg/kg
exposure to sources of fresh water) Toxicologic: IV.
• Ethylene glycol (polyuria, polydipsia, • Correct hypothermia with warming methods
ASSOCIATED DISORDERS lethargy, acute GI signs) as needed.
Hyponatremia • Marijuana (urinary incontinence, ataxia) • Do not use atropine to treat bradycardia
• Ivermectin toxicosis (CNS signs, blindness) because bradycardia is thought to be second-
Clinical Presentation • Pesticide toxicosis (pyrethrins/pyrethroids, ary to the Cushing’s reflex.
HISTORY, CHIEF COMPLAINT organophosphate, carbamate) • Frequently monitor body weight to help
A history of swimming, intense exercise, or play Nontoxicologic: assess hydration.
for several hours in or near water (e.g., lake, • Head trauma
boat, garden hose) with excessive consumption • Fluid overload Chronic Treatment
of fresh water is typical. This is followed by the • Congestive heart failure • Patients with chronic hyponatremia (>24
acute onset of polydipsia, polyuria, ptyalism, • Psychogenic polydipsia (rare) hours’ duration) may have mild signs or
vomiting, ataxia, disorientation, seizures, and/ • Syndrome of inappropriate antidiuretic no clinical signs at admission due to brain’s
or coma. hormone secretion (SIADH): thought to ability to adapt to hypotonicity over time.
be uncommon in dogs; urine osmolality ○ For asymptomatic patients, restrict water
PHYSICAL EXAM FINDINGS > 100 mOsm/kg with hyponatremia and intake, and monitor serum sodium level
• See History, Chief Complaint serum hypoosmolality supports SIADH in and other electrolytes as needed.
• Bradycardia possible (heart rate < 60 beats/ dogs • Treat patients with signs due to chronic
min) (>24 h) hyponatremia slowly (p. 518).
• Dyspnea, tachypnea possible due to pulmo- Initial Database ○ Overly rapid correction of chronic hypo-
nary edema • Serum electrolytes: hyponatremia, hypoka- natremia can lead to neurologic syndrome
• Hypothermia if patient is comatose lemia, hypochloremia (myelinolysis).

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