a) K-Phos MF contains potassium phosphate, monobasic 155 mg - sodium phosphate, monobasic 350 mg
b) K-Phos original contains potassium phosphate, monobasic 500 mg
c) K-Phos Neutral or Phospha 250 Neutral contains potassium phosphate, monobasic 155 mg - sodium phosphate, dibasic 852 mg - sodium phosphate, monobasic 130 mg
d) K-Phos No 2 contains potassium phosphate, monobasic 305 mg - sodium phosphate, monobasic 700 mg

a) ORAL SOLUTION: Sodium phosphate, dibasic 0.9 g/5 mL and sodium phosphate, monobasic 2.4 g/5 mL
b) RECTAL ENEMA: Fleet(R) Enema Extra(R) (sodium phosphate heptahydrate, dibasic 7 g/197 mL and sodium phosphate monohydrate, monobasic 19 g/197 mL)
c) RECTAL ENEMA: Fleet(R) Enema (sodium phosphate heptahydrate, dibasic 7 g/118 mL and sodium phosphate monohydrate, monobasic 19 g/118 mL)
d) RECTAL ENEMA: Fleet(R) Enema, Fleet(R) Pedia-LAX(R) Enema and Fleet(R) Enema for children (sodium phosphate heptahydrate, dibasic 3.5 g/59 mL and sodium phosphate monohydrate, monobasic 9.5 g/59 mL)
e) ORAL TABLET: Oral tablet contains sodium phosphate, dibasic 0.398 g and sodium phosphate, monobasic 1.102 g
f) IV SOLUTION: (sodium phosphate 3 mmol/mL (each mL contains monobasic sodium phosphate, monohydrate 276 mg; dibasic sodium phosphate, anhydrous 142 mg (equivalent to dibasic sodium phosphate, heptahydrate 268 mg)

a) POTASSIUM PHOSPHATE/SODIUM PHOSPHATE, MONOBASIC AND DIBASIC: Indicated in adults and children over 4 years of age to increase urinary phosphate and pyrophosphate (Prod Info PHOSPHA 250(TM) NEUTRAL oral tablets, 2011).
b) SODIUM PHOSPHATE DIBASIC/SODIUM PHOSPHATE MONOBASIC: Indicated to prevent or correct hypophosphatemia. It is also used for bowel cleansing prior to colonoscopy and the relief of occasional constipation (Prod Info sodium phosphates IV injection, 2006; Prod Info OSMOPREP(TM) oral tablets, 2006; Prod Info PHOSPHATE LAXATIVE oral liquid, 2005).

a) POTASSIUM PHOSPHATE DIBASIC is a buffering agent, a nutrient in culturing of antibiotics, a constituent in fertilizers, and a sequestrant in the manufacture of nondairy powdered coffee creams (Budavari, 1996).
b) SODIUM PHOSPHATE DIBASIC is used in foods as a buffering agent, an emulsifier, and a sequestrant. In industry, it is used in the manufacture of boiler compounds, ceramics, detergents, and enamels. In brazing and soldering it is used in place of borax. It is used as a buffering agent and reagent. It is also used in the dyeing, silk, and tanning industries (Budavari, 1996).
c) SODIUM PHOSPHATE MONOBASIC is used in foods as a dry acidulant and sequestrant and in baking powders. It is also used in boiler water treatments and as a urinary acidifier (Budavari, 1996).
d) SODIUM PHOSPHATE TRIBASIC is not discussed in this management. This phosphate compound is strongly alkaline.

1) Nausea, vomiting, and diarrhea are common after oral administration.

1) MILD TO MODERATE TOXICITY: Gastrointestinal irritation, nausea, vomiting, and diarrhea. Asymptomatic hyperphosphatemia may also occur.
2) SEVERE TOXICITY: Nausea, vomiting, abdominal pain, diarrhea, altered mental status, weakness, dehydration, hypernatremia, and hypotension may develop. Profound hypocalcemia and hypomagnesemia can cause tetany, seizures, bradycardia, prolonged QT interval, ventricular dysrhythmias, and cardiac arrest. Metabolic acidosis is a frequent occurrence following administration of hypertonic phosphate enema solutions.

1) Isolated gastrointestinal symptoms do not require treatment; occasionally patients may require antiemetics. Manage mild hypotension with IV fluids.

1) Administer intravenous fluids to restore electrolyte balance. Replace calcium and magnesium intravenously, but over-aggressive repletion can theoretically cause precipitation of calcium phosphate in tissue. Treat severe hypotension with IV fluids, dopamine, or norepinephrine. Patients with respiratory failure should be intubated and ventilated. Institute continuous cardiac monitoring and monitor ECG for evidence of QT prolongation or dysrhythmias. Symptomatic patients with severe electrolyte abnormalities should be treated with hemodialysis. Treat seizures with IV benzodiazepines; barbiturates or propofol may be needed if seizures persist or recur.

1) PREHOSPITAL: Administration of an aluminum based antacid may bind phosphate and decrease absorption. Activated charcoal is not recommended.
2) HOSPITAL: Phosphates are not bound by activated charcoal. Aluminium salts will bind phosphate and form insoluble aluminum phosphate, so administration of an aluminum based antacid may decreased phosphate absorption, but there are no reports describing this treatment.

1) Is unlikely to be required following overdose. Consider early intubation in patients who develop weakness. Patients with respiratory failure should be intubated and ventilated.

1) None.

1) Phosphates are rapidly cleared by dialysis. Dialysis can also be used to treat other electrolyte abnormalities such as hypernatremia, hypocalcemia, and hypomagnesemia.

1) HOME CRITERIA: Sip ingestions can be managed at home. However, ingestion of only 30 to 60 mL by a child can produce severe electrolyte abnormalities, so if the history is not clear, the patient should be evaluated in a healthcare facility.
2) ADMISSION CRITERIA: Patients who require dialysis or who have persistent severe electrolyte abnormalities should be admitted to a monitored setting.
3) CONSULT CRITERIA: Consult a poison center or medical toxicologist for assistance in decision making whether or not admission is advisable, managing patients with severe toxicity or in whom the diagnosis is not clear. Consult a nephrologist for dialysis in patients with severe toxicity.

1) Phosphates are rapidly absorbed following ingestion and can be absorbed after retention enema. Phosphate is minimally protein bound, and highly concentrated in cells (intracellular concentrations are 100-fold higher than serum concentrations). Elimination is primarily renal (90%).

1) In healthy children with phosphate overdose, half-life was 4.8 to 10.6 hours, and was prolonged to 17 hours in a child with renal insufficiency.

1) Hyperphosphatemia may occur with renal failure. Hypocalcemia may occur with hydrofluoric acid poisoning. Hypernatremia may occur following ingestion of other sodium containing products (eg, sodium bicarbonate).

1) Patients with renal insufficiency are at greater risk of toxicity.

1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

1) An elevation of body temperature has been reported in association with toxicity resulting from phosphosoda enemas given to children with Hirschsprung's disease (Moseley & Segar, 1968).
2) CASE REPORT: An elevated temperature (101 degrees F) was reported in an 8-week-old infant after mistakenly receiving a hypertonic phosphate enema solution instead of bottled water when both were placed in a refrigerator (Hung et al, 1998).

1) CASE REPORT: Tachycardia was seen in a 2.5-year-old who received 2 pediatric dihydrogen phosphate enemas and became hyperphosphatemic, hypocalcemic, and hypernatremic (Sotos et al, 1977).
2) CASE REPORT: A pulse rate of 170 beats per minute was reported in an 8-week-old infant who inadvertently received a hypertonic phosphate enema solution instead of bottled water. The infant also experienced lethargy, bradycardia, seizures, and electrolyte imbalances (Hung et al, 1998).

1) CASE REPORT: A 60-year-old man developed bradycardia (40 beats/minute) after receiving 11 sodium phosphate-based enemas (approximately 1100 mL) in a 2-hour period (Pitcher et al, 1997).
2) CASE REPORT: An 8-week-old infant became lethargic and unresponsive, necessitating intubation, after inadvertent oral administration of a hypertonic phosphate enema solution. The infant developed bradycardia (50 beats/minute) shortly after intubation, but was responsive to administration of multiple doses of atropine and epinephrine (Hung et al, 1998).
3) CASE REPORT: A 6-week-old premature infant developed hypocalcemia (serum calcium level 2.4 mg/dL; normal range 8.4 to 10.2 mg/dL) and hyperphosphatemia (serum phosphorus level of 28.5 mg/dL; normal range, 2.4 to 4.5 mg/dL) after receiving a full pediatric Fleets enema. He presented with generalized seizures, apnea, and bradycardia, necessitating intubation and cardiopulmonary resuscitation. Following supportive therapy for 12 days, he recovered completely (Walton et al, 2000)

1) WITH POISONING/EXPOSURE

1) WITH POISONING/EXPOSURE

1) WITH POISONING/EXPOSURE

1) WITH THERAPEUTIC USE

1) CASE REPORT: A middle-aged man developed weakness, seizures, and asystolic cardiac arrest associated with two separate enemas of sodium phosphate in preparation for a barium enema examination. Electrical activity occurred after administration of calcium. A pulse was established after administration of a second bolus of calcium. Normal sinus rhythm and blood pressure were established within minutes (Martinez, 1987).
2) CASE REPORT: Cardiac arrest occurred during induction of anesthesia in a 17-month-old child with a history of chronic constipation. He as given 2 Fleet(R) pediatric enemas at 0600 and 0830 in preparation for a rectal biopsy in a day surgery facility He responded to resuscitation efforts after calcium gluconate 200 mg was administered intravenously (Reedy & Zwiren, 1983).
3) CASE REPORT: A 64-year-old man with theophylline intoxication and significant comorbidity developed a colonic ileus after receiving decontamination with activated charcoal with sorbitol. The patient died following a cardiac arrest as a result of hyperphosphatemia secondary to oral and rectal administration of a hypertonic phosphate enema solution used to facilitate clearance of the activated charcoal (Feig et al, 1982).

1) CASE REPORT: A 60-year-old man developed bradycardia (40 beats/minute) after receiving 11 sodium phosphate-based enemas (approximately 1100 mL) in a 2-hour period (Pitcher et al, 1997).
2) CASE REPORT: An 8-week-old infant became lethargic and unresponsive, necessitating intubation, after inadvertent oral administration of a hypertonic phosphate enema solution. The infant developed bradycardia (50 beats/minute) shortly after intubation, but was responsive to administration of multiple doses of atropine and epinephrine (Hung et al, 1998).
3) CASE REPORT: A 6-week-old premature infant developed hypocalcemia (serum calcium level 2.4 mg/dL; normal range 8.4 to 10.2 mg/dL) and hyperphosphatemia (serum phosphorus level of 28.5 mg/dL; normal range, 2.4 to 4.5 mg/dL) after receiving a full pediatric Fleets enema. He presented with generalized seizures, apnea, and bradycardia, necessitating intubation and cardiopulmonary resuscitation. Following supportive therapy for 12 days, he recovered completely (Walton et al, 2000)

1) WITH THERAPEUTIC USE
2) WITH POISONING/EXPOSURE

1) Hyperventilation may be noted secondary to hypocalcemia (Levitt et al, 1973).

1) Coma was seen due to hypocalcemia caused by hyperphosphatemia (Sotos et al, 1977; Rohack et al, 1985; Hung et al, 1998). Lethargy is a common presenting symptom.

1) WITH THERAPEUTIC USE
2) Seizures may occur in association with electrolyte imbalances secondary to administration of hypertonic phosphate enema solutions (Walton et al, 2000; Hung et al, 1998; O'Callaghan et al, 1995).

1) Tetany was associated with hypocalcemia caused by hyperphosphatemia in patients following administration of hypertonic phosphate enemas (Honig & Holtzapple, 1975; Levitt et al, 1973; Oxnard et al, 1974; Sotos et al, 1977; Edmondson & Almquist, 1990; Escalante et al, 1997; Hung et al, 1998).
2) CASE REPORT (CHILD): A 23-month-old child with renal insufficiency developed hypocalcemic tetany, as well as hyperphosphatemia and hypokalemia, approximately 6 hours after receiving 2 phosphate enemas for treatment of fecal retention. With supportive care, the duration of the patient's tetany was 10 hours and her electrolytes normalized within 2 days (Craig et al, 1994).

1) CASE REPORT: A 9-month-old child who received two phosphate-containing enemas developed a cardiac arrest secondary to hypocalcemia, and had residual spasticity and retardation (Loughnan & Mullins, 1977).

1) WITH POISONING/EXPOSURE

1) WITH POISONING/EXPOSURE

1) WITH POISONING/EXPOSURE

1) CASE REPORT: Colonic perforation, identified by laparotomy, occurred in a 55-year-old woman who received a phosphate enema through a rectal tube, which had been passed blindly into the recto-sigmoid region. Sixteen hours after administration of the enema, the patient developed peritonitis and renal insufficiency, with an increased serum creatinine, hepatic enzyme, and potassium levels. The patient was also hyperphosphatemic and hypomagnesemic.

1) Absorbed saline compounds may act as a mild diuretic (Sollmann, 1957).

1) WITH THERAPEUTIC USE

1) WITH THERAPEUTIC USE

1) WITH THERAPEUTIC USE
2) WITH POISONING/EXPOSURE

1) Carpopedal spasm is a common presenting sign in inorganic phosphate poisoning, and is associated with low serum calcium levels (Larson et al, 1986; Swerdlow et al, 1974; Craig et al, 1994).

1) Hypotonia is a common finding.

1) DIBASIC SODIUM PHOSPHATE ANHYDROUS/MONOBASIC POTASSIUM PHOSPHATE/MONOBASIC SODIUM PHOSPHATE MONOHYDRATE: At the time of this review, no data were available to assess the teratogenic potential of this combination product (Prod Info PHOSPHA 250(TM) NEUTRAL oral tablets, 2011).
2) POTASSIUM PHOSPHATE: At the time of this review, no data were available to assess the teratogenic potential of this agent (Prod Info Potassium Phosphates intravenous injection, 2011).

1) DIBASIC SODIUM PHOSPHATE ANHYDROUS/MONOBASIC POTASSIUM PHOSPHATE/MONOBASIC SODIUM PHOSPHATE MONOHYDRATE: There are no adequate and well-controlled studies of dibasic sodium phosphate anhydrous/monobasic potassium phosphate/monobasic sodium phosphate monohydrate combination treatment use in pregnant women. The effects, if any, on the developing fetus are unknown (Prod Info PHOSPHA 250(TM) NEUTRAL oral tablets, 2011).
2) POTASSIUM PHOSPHATE: There are no adequate and well-controlled studies of potassium phosphate use in pregnant women. The effects, if any, on the developing fetus are unknown (Prod Info Potassium Phosphates intravenous injection, 2011).

1) The manufacturers have classified the dibasic sodium phosphate anhydrous/monobasic potassium phosphate/monobasic sodium phosphate monohydrate combination product and potassium phosphate as FDA pregnancy category C (Prod Info Potassium Phosphates intravenous injection, 2011; Prod Info PHOSPHA 250(TM) NEUTRAL oral tablets, 2011). Due to the lack of human safety information, the manufacturer recommends that potassium phosphate should be used in pregnant women only if clearly needed (Prod Info Potassium Phosphates intravenous injection, 2011).

1) DIBASIC SODIUM PHOSPHATE ANHYDROUS/MONOBASIC POTASSIUM PHOSPHATE/MONOBASIC SODIUM PHOSPHATE MONOHYDRATE: Lactation studies with dibasic sodium phosphate anhydrous/monobasic potassium phosphate/monobasic sodium phosphate monohydrate combination treatment have not been conducted in humans. It is not known whether this combination treatment is excreted in human breast milk. Due to the lack of human safety information, the manufacturer recommends exercising caution when administering dibasic sodium phosphate anhydrous/monobasic potassium phosphate/monobasic sodium phosphate monohydrate combination treatment to lactating women (Prod Info PHOSPHA 250(TM) NEUTRAL oral tablets, 2011).
2) POTASSIUM PHOSPHATE: At the time of this review, no data were available to assess the potential effects of exposure to this agent during lactation in humans (Prod Info Potassium Phosphates intravenous injection, 2011).

1) DIBASIC SODIUM PHOSPHATE ANHYDROUS/MONOBASIC POTASSIUM PHOSPHATE/MONOBASIC SODIUM PHOSPHATE MONOHYDRATE: At the time of this review, no data were available to assess the potential effects on fertility from exposure to this agent (Prod Info PHOSPHA 250(TM) NEUTRAL oral tablets, 2011).
2) POTASSIUM PHOSPHATE: At the time of this review, no data were available to assess the potential effects on fertility from exposure to this agent (Prod Info Potassium Phosphates intravenous injection, 2011).

1) At the time of this review, no data were available to assess the carcinogenic or mutagenic potential of this agent.

1) Phosphate is a normal constituent of intracellular fluid; normal concentration in plasma range from 0.8 to 1.6 mmol/Liter (JEF Reynolds , 1990).
2) Obtain arterial blood gases if serum electrolytes indicate metabolic acidosis.

1) ECG

A) Patients who require dialysis or who have persistent severe electrolyte abnormalities should be admitted to a monitored setting.

A) Sip ingestions can be managed at home. However, ingestion of only 30 to 60 mL by a child can produce severe electrolyte abnormalities, so if the history is not clear, the patient should be evaluated in a healthcare facility.

A) Consult a poison center or medical toxicologist for assistance in decision making whether or not admission is advisable, managing patients with severe toxicity or in whom the diagnosis is not clear. Consult a nephrologist for dialysis in patients with severe toxicity.

1) Monitor vital signs and mental status.
2) Monitor serum electrolytes (including magnesium, calcium, and phosphate) if there is more than a trivial exposure.
3) Obtain an ECG and institute continuous cardiac monitoring.

1) Rapid correction of fluid and electrolyte deficits with oral or IV fluid therapy and careful monitoring of intake and output are essential. Restrict solid food and maintain high fluid intake until diarrhea resolves. Oral fluid should consist of polyionic hypotonic solution containing appropriate electrolytes.

1) Coma, lethargy, or CNS depression may be a result of dehydration and will respond to fluid replacement. Correct hypocalcemia, hypernatremia, hyperphosphatemia, hypomagnesemia, and hyperkalemia or hypokalemia as needed.

1) Correct hypocalcemia with intravenous CALCIUM CHLORIDE (10% SOLUTION): ADULT 2 to 4 mg/kg (0.02 to 0.04 mL/kg) with repeat doses as necessary. PEDIATRIC: 10 to 30 mg/kg (0.1 to 0.3 mL/kg) infused slowly with repeat doses as necessary. Ideally, repeat doses should be based on measured deficits of ionized calcium. CALCIUM GLUCONATE (10% solution) may also be used, but the dose is 3 times the amount of the dose for calcium chloride.

1) Correct hypomagnesemia with intravenous MAGNESIUM SULFATE: ADULT: 2 grams is diluted in 50 to 100 mL of D5W and administered over 5 minutes. PEDIATRIC: 100 to 200 mg/kg diluted to less than 10 mg/mL administered slowly over 5 minutes. Repeat doses may be necessary.
2) Serial evaluation of the patient's knee jerk reflex is the most important and reliable guide to magnesium treatment. Serum magnesium levels are not a reliable indicator for what is a "therapeutic level". Patient should be monitored with ECG continuously.

1) Aluminum hydroxide gel may bind phosphate in the intestine and aid in phosphate excretion. Dose will vary by patient and amount of phosphate elevation. Monitor electrolytes closely (Sotos et al, 1977).

1) Correct with 0.9% or 0.45% saline intravenously.

1) Patients developing congestive heart failure from sodium intoxication may be treated with fluid restriction and/or diuretic therapy, furosemide 1 milligram/kilogram intravenously to a maximum of 40 milligrams.

1) SUMMARY
2) DIAZEPAM
3) NO INTRAVENOUS ACCESS
4) LORAZEPAM
5) PHENOBARBITAL
6) OTHER AGENTS

1) SUMMARY
2) DOPAMINE
3) NOREPINEPHRINE

1) ATROPINE/DOSE
2) ISOPROTERENOL INDICATIONS

1) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

1) Dose and rate of IV infusion is patient specific. Potassium phosphates injection contains 3 mmol/mL of phosphorus and 4.4 mEq/mL of potassium. Calculate the volume needed to provide the required number of mmol of phosphorus and mEq of potassium. The potassium component must be calculated into the total electrolyte content of prepared solutions (Prod Info Potassium Phosphates intravenous injection, 2011).

1) 1 or 2 tablets (852 mg dibasic sodium phosphate anhydrous/155 mg monobasic potassium phosphate/130 mg monobasic sodium phosphate monohydrate) orally 4 times a day (Prod Info PHOSPHA 250(TM) NEUTRAL oral tablets, 2011).

1) CONSTIPATION (ORAL SOLUTION): 20 to 45 mL oral liquid orally (Prod Info PHOSPHATE LAXATIVE oral liquid, 2005). Do not exceed one dose in a 24 hour period (U.S. Food and Drug Administration (FDA), 2014).
2) HYPOPHOSPHATEMIA (IV): Dose and rate of IV infusion is patient specific; usual concentration in total parenteral nutrition, 10 to 15 mmol/L (310 to 465 mg elemental phosphorus); larger amounts may be required in hypermetabolic states (Prod Info sodium phosphates IV injection, 2006).
3) COLONOSCOPY BOWEL PREPARATION (ORAL TABLETS): sodium phosphate, dibasic - sodium phosphate, monobasic 0.398 g-1.102 g each tablet:Total of 32 tablets (48 g of sodium phosphate) taken orally over 2 days. 4 tablets orally every 15 minutes for a total of 20 tablets the day before procedure; 4 tablets orally every 15 minutes for a total of 12 tablets, starting 3 to 5 hours before the procedure (Prod Info OSMOPREP(TM) oral tablets, 2006).

1) Dose and rate of IV infusion is patient specific. Potassium phosphates injection contains 3 mmol/mL of phosphorus and 4.4 mEq/mL of potassium. Calculate the volume needed to provide the required number of mmol of phosphorus and mEq of potassium. The potassium component must be calculated into the total electrolyte content of prepared solutions (Prod Info Potassium Phosphates intravenous injection, 2011).

1) It is not indicated in pediatric patients 4 years of age or under (Prod Info PHOSPHA 250(TM) NEUTRAL oral tablets, 2011).
2) CHILDREN OVER 4 YEARS OF AGE: 1 tablet (852 mg dibasic sodium phosphate anhydrous/155 mg monobasic potassium phosphate/130 mg monobasic sodium phosphate monohydrate) orally 4 times a day (Prod Info PHOSPHA 250(TM) NEUTRAL oral tablets, 2011).

1) INTRAVENOUS
2) ORAL SOLUTION
3) ORAL TABLETS
4) RECTAL SOLUTION

a) A 69-year-old woman received two 90-mL doses of Fleet(R) Phospho(R)-Soda buffered oral saline laxative 5 hours apart. This represented double the recommended dose with half the dosing interval. The patient developed hypocalcemic tetany and hyperphosphatemia (Vukasin et al, 1997).
b) In a retrospective case series, 11 elderly patients developed severe metabolic disorders after receiving sodium phosphate enemas; 3 patients received a 500 to 798 mL dose and 8 received a 250 to 266 mL dose. Although most patients presented within 24 hours of receiving the enemas, 4 patients presented late (2 after 72 hours, 1 after 13 days, 1 after 38 days). The following adverse effects were reported: hypotension (n=9), severe hyperphosphatemia (n=8), severe hypocalcemia (n= 8); hypernatremia (n=9); hypokalemia (n=7); hyperkalemia (n=4); metabolic acidosis (n=8); prolonged QT intervals (n=7); grand mal seizures (n=1); and acute renal failure (n=11). Two patients underwent hemodialysis. Five patients died (Ori et al, 2012).

a) A 15-month-old, 10 kg boy developed hyperphosphatemia (24.6 mg/dL), hypocalcemia, and hyperosmolarity. This occurred 3 hours following an ingestion of 60 mL of a buffered sodium biphosphate and sodium phosphate solution (24 grams of phosphate), given for an iron ingestion. He recovered uneventfully after calcium and fluid administration (Geffner & Opas, 1980).
b) Reported administration of 10 to 30 mL of phosphosoda resulted in severe toxicity in a 4-month-old child (Larson et al, 1986); it is likely that up to 53 mL was actually ingested.
c) Administration of 30 mL of phosphosoda produced severe toxicity (coma, serum phosphorus 13.3 millimoles/liter, 41.5 mg/dL) in a 6-week-old infant (Smith et al, 1973).

a) A 4-year-old boy with a history of anorectoplasty for high imperforate anus and constipation, presented with shock, decreased mental status, seizures, and tetany after receiving 240-mL of sodium phosphate enemas (Fleet Phospho-Soda Enemas, 16-g monobasic sodium phosphate and 6-g dibasic sodium phosphate/100 mL) through a cecostomy every 2 to 3 days for 8 months. On presentation, he was unresponsive, tachypneic (respiratory rate of 80 breaths/min), and tachycardic (heart rate of 215 beats/min). Despite aggressive supportive care for hyperphosphatemia, hypocalcemia, and seizures, his condition deteriorated and he developed hemodynamic instability and continued to experience seizures. He underwent hemodialysis which decreased his serum phosphate concentrations, resulting in resolution of hypocalcemia, improvement of hemodynamic parameters, and normalization of the his neurological examination (Becknell et al, 2014).
b) A 5-month-old female was given a rectal adult sodium phosphate enema and developed lethargy, hypocalcemia, and hyperphosphatemia. The sodium, phosphate, and calcium levels were 159 mEq/L, 44.3 mg/dL, and 4.2 mg/dL, respectively. She recovered after intravenous fluid therapy (Wason et al, 1989).
c) Hypocalcemia, hyperphosphatemia, and dehydration were reported in a 4-month-old and a 3-year-old with normal renal function following administration of a single hypertonic phosphate enema. The authors suggested that these children had mild dehydration when the enema was administered and thus retarded renal clearance of phosphate (Davis et al, 1977).
d) A 3-year-old girl received 3 adult-sized hypertonic phosphate enemas and developed severe hyperphosphatemia and hypocalcemia with a serum phosphate level of 74.7 mg/dL and an ionized calcium level of 0.22 mEq/L. The patient recovered with supportive care (Helikson et al, 1997).
e) Three children (2.5 to 5 years of age) developed severe hyperphosphatemia (phosphate range: 46.04 to 58.36 mg/dL; normal values: 3.41 to 6.19 md/dL) and hypocalcemia (calcium range: 5.7 to 7.1 mg/dL; normal range: 8.5 to 10.5 mg/dL) after receiving 1 or 2 pediatric-sized sodium phosphate-containing enemas for severe constipation. All 3 patients recovered following supportive therapy. Two of the 3 patients required intensive care services (Ladenhauf et al, 2012).

1) NORMAL RANGE

1) TOXIC RANGE
2) FATAL RANGE

1) 250 mg/kg ((RTECS, 2000))

1) LD50- (ORAL)RAT:

1) LD50- (INTRAPERITONEAL)MOUSE:

1) LD50- (ORAL)RAT:

1) LD50- (ORAL)RAT:

a) ANHYDROUS: Hygroscopic powder (Budavari, 1996)
b) HEPTAHYDRATE: Granular powder or crystals (Budavari, 1996)
c) DODECAHYDRATE: Granules or translucent crystals (Budavari, 1996)

a) MONOHYDRATE: White, slightly deliquescent crystals or granules that are odorless (Budavari, 1996)
b) DIHYDRATE: Colorless, orthorhombic bisphenoidal crystals (Budavari, 1996)

a) ANHYDROUS (1% solution in water): 9.1 (at 25 degrees C) (Budavari, 1996)
b) HEPTAHYDRATE (solution in water): 9.5 (Budavari, 1996)
c) DODECAHYDRATE (solution in water): 9.5 (Budavari, 1996)

a) ANHYDROUS: 141.96 (Budavari, 1996)
b) DIHYDRATE: 177.99
c) HEPTAHYDRATE: 268.02
d) DODECAHYDRATE: 358.05

a) ANHYDROUS: 119.98 (Budavari, 1996)
b) MONOHYDRATE: 137.99
c) DIHYDRATE: 155.99

1) Toxicity noted included ataxia, bloody diarrhea, depression, mucous membrane pallor, stupor, and vomition.
2) Laboratory abnormalities included severe hyperphosphatemia, mild hypernatremia, hyperglycemia, hypocalcemia, lactic acidosis with an increased anion gap, and serum hyperosmolality.
3) One cat died 4 hours after administration of enema. No profound hypocalcemia nor tetany were noted in any cat (Atkins et al, 1985; Atkins, 1987).

1) Treatment is symptomatic and supportive.
2) Monitor fluid and electrolyte status carefully.

1) Recommended doses of sodium phosphate enemas of 60 or 120 mL were associated with signs of toxicity in 10 clinically healthy cats (Atkins et al, 1985).

1) An infusion of a 0.25 M phosphate solution with a final pH of 7.4 at 25 and 37 degrees C at 50 mL/hour for 1 hour produced no observable cardiac toxicity nor any significant reduction of ionized calcium in this rabbit model.

A) GENERAL TREATMENT