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788.e2 Phosphate Enema Toxicosis

Phosphate Enema Toxicosis Client Education
Sheet
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BASIC INFORMATION
of sodium and phosphate from the colon.
Prolonged retention, overdose, colonic TREATMENT
Definition disease (dilation or ulceration), or pre- Treatment Overview
Toxicosis due to administration of sodium existing electrolyte disturbances as seen with Treatment aims to correct hypernatremia and
phosphate enemas in cats and small-breed chronic kidney disease increase the risk of hypocalcemia and provide supportive care.
dogs results in severe hyperphosphatemia, toxicosis. Sepsis may occur in animals with compromised
hypernatremia, and hypocalcemia. • Hypocalcemia occurs if calcium-phosphorus colonic mucosa, requiring treatment.
solubility product is exceeded; phosphorus
Synonym binds and precipitates calcium, leading to Acute General Treatment
Fleet enema toxicosis hypocalcemia. • IV fluids to address hypernatremia (p. 498)
• Hyperosmolality ○ Initial choice (assuming < 24 hours since
Epidemiology ○ Hypernatremia enema administration): 5% dextrose in water
SPECIES, AGE, SEX ○ Hyperglycemia is a minor contributor or 0.45% saline with 2.5% dextrose (with
• Dogs and cats of any age and either sex to increased osmolality and is believed potassium supplementation if hypokalemia
• Younger animals, cats, and small-breed dogs to be due to stress release of catechol- is identified). Concurrent furosemide 2 mg/
may be at increased risk because small body amines and hypertonicity that alter kg IV can increase natriuresis.
size produces a disproportionate ratio of cellular glucose uptake and metabolism; ○ Initial rate: one to two times the
enema fluid to body weight. it can also result from pancreatic insulin maintenance rate (65-130 mL/kg/day
release. [30-60 mL/lb/day]) plus a dehydration
RISK FACTORS • Metabolic acidosis with increased anion deficit and ongoing losses compensation
Presence of constipation, obstipation, colonic gap if applicable; proceed with caution if the
disease, and kidney disease may increase patient has heart disease.
the risk of problems from administration of DIAGNOSIS ○ Adjustment/change in fluid type and rate
sodium phosphate enemas by decreasing sodium is based on response and results of ongoing
and phosphate excretion (renal disease) or Diagnostic Overview monitoring.
enhancing sodium and phosphate absorption History of administration of an enema to a • Plain-water enema
(others). patient weighing < 10 kg, with hyperphospha- ○ May help to reduce hypernatremia; the
temia, hypernatremia, and/or hypocalcemia colon has a large surface area and can
ASSOCIATED DISORDERS occurring within 12 hours of enema administra- absorb free water rapidly.
Hyperphosphatemia, hypernatremia, hypocal- tion, provide the clinical diagnosis. ○ Administer 10 mL/kg of plain water as a
cemia (potentially severe/critical) retention enema; repeat q 2-4h if needed.
Differential Diagnosis • Calcium gluconate for hypocalcemia-
Clinical Presentation • Hypernatremia: sometimes seen after associated tetany
HISTORY, CHIEF COMPLAINT activated charcoal administration (p. 1237) ○ IV route if tetany is severe and/or if
Possible signs within 30 minutes to 4 hours of • Hypocalcemia (p. 1239) hyperthermia is present concurrently
administration of enema: ○ 10% calcium gluconate = 100 mg/mL
• Depression Initial Database calcium gluconate, which corresponds
• Ataxia • CBC: generally unremarkable to 9.3 mg elemental calcium per milliliter.
• Vomiting • Serum chemistry panel; common ○ Give 50-200 mg/kg calcium gluconate
• Diarrhea with or without blood abnormalities: (≈0.5-2 mL/kg; typical cat dose = 3 mL)
○ Hyperphosphatemia slowly IV over a period of 15-30 minutes
PHYSICAL EXAM FINDINGS ○ Hypernatremia with electrocardiogram (ECG) monitoring,
Common: ○ Hypocalcemia administered to effect. Clinical normality
• Tachycardia ○ Hyperkalemia or hypokalemia usually does not occur immediately; mild
• Pallor ○ Metabolic acidosis (decreased serum to moderate improvement may be seen
−
• Prolonged capillary refill time [HCO 3 ]) with increased anion gap during the infusion, which warrants
−
+
+
• Weakness ■ Anion gap: ([Na ] + [K ]) − ([Cl ] + stopping administration.
−
Possible: [HCO 3 ]); normal = 12-24 mEq/L ○ If heart rate decreases significantly or if
• Hyperthermia or hypothermia ○ Hyperosmolality onset of ST-segment elevation/depression
• Tachypnea ■ Measured directly and calculated or QT-interval shortening is seen, the
+
+
• Tetany according to formula: 2[Na + K ] infusion must be stopped promptly.
• Seizure + blood urea nitrogen (BUN) (mg/ • Calcium gluconate in stable, hypocalcemic
dL)/2.8 + glucose (mg/dL)/18; result patient
Etiology and Pathophysiology is reported in milliosmoles per kilogram ○ 150-250 mg/kg calcium gluconate (1.5-
Source: (NOTE: if BUN and glucose units are 2.5 mL/kg), diluted with two to four
• Over-the-counter (without a prescription) reported in mmol/L, do not use cor- times more sterile water and given SQ
+
phosphate enemas are available at pharmacies rection factors: osmolarity = 2 Na + q 6-8h
+
and in the drug aisles of supermarkets and 2 K + glucose + urea) • Phosphate-binding agents (e.g., Amphojel
convenience stores. ■ Normally and in phosphate enema 64 mg Al(OH) 3/mL, AlternaGel 120 mg
Mechanism of toxicosis: toxicosis, the difference between Al(OH) 3/mL)
• Hypernatremia and hyperphosphatemia calculated and measured values (i.e., ○ 10-30 mg/kg (or higher) PO q 6-12h,
can occur after administration of sodium osmol gap) should be < 10 mOsm/kg. based on serum phosphorus levels; may
phosphate enemas by massive absorption • Urinalysis: generally unremarkable cause inappetence
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