Fatal Poisoning From Sodium Phosphate Enema

Martin, Robert R.; Lisehora, George R.; Braxton, Maceo; Barcia, Peter J.

doi:10.1001/jama.1987.03390160076030

Cited by 77 publications

(15 citation statements)

References 12 publications

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“…tionship between the phosphate enema dose (and duration of exposure) and the plasma concentrations of Na and P0 4 , and a concomitant fall in the plasma Ca concentration and pH. 22 There are similar data in humans.v In the pig model, the lethal dose of a phosphate enema was 20-30 mLlkg (35-50 mmol/kg P0 4 and 45-65 mmol/kg Na), which is equivalent to two Travad enemas for a two-year-old child. 22 The parenteral administration of calcium for hypocalcaemic tetany secondary to hyperphosphataemia is problematic owing to the risk of metastatic calcium deposition.…”

Section: Triquilar Ed Lowest Dose Optimal Performancementioning

confidence: 98%

Phosphate enema poisoning in children

Craig

Hodson

Martin

1994

Medical Journal of Australia

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ObjectiveTo report a case of hypocalcaemic tetany occurring in a child secondary to two phosphate enemas administered for faecal retention, and review the literature of phosphate enema toxicity in children. Clinical FeaturesA 23‐month‐old child with a repaired anorectal malformation and associated unilateral renal hypodysplasia presented with hypocalcaemic tetany (minimum serum calcium level, 1.11 mmol/L), hyperphosphataemia (maximum serum phosphate level, 6.06 mmol/L), hypokalemia (minimum serum potassium level, 1.9 mmol/L) and dehydration 10 hours after the administration of two phosphate enemas for acute on chronic faecal retention. Management and outcomeManagement consisted of parenteral rehydration, potassium supplementation, calcium gluconate, an enterally administered phosphate binder and saline bowel washouts to evacuate the remaining enema. She was discharged on day eight, with normal biochemical parameters and no neurological sequelae. ConclusionThe use of phosphate enemas in children under five years of age is associated with significant morbidity due to hyperphosphataemia, hypocalcaemia, hypokalaemia and dehydration. They should not be used in children under two years of age, and should be used only with extreme caution in children aged two to five years, especially in those with underlying bowel or renal dysfunction.

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Section: Triquilar Ed Lowest Dose Optimal Performancementioning

confidence: 98%

Phosphate enema poisoning in children

Craig

Hodson

Martin

1994

Medical Journal of Australia

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“…These in vivo genetic and dietary manipulation studies clearly demonstrated that the mammalian aging process could be adversely influenced by phosphate toxicity to compromise survival. In a separate animal study, when acute phosphate toxicity (7- to 20-fold increase over control by 4 h) was induced by using a commercially available phosphate-containing enema (30–50 ml/kg), 100% mortality was noted in the experimental animals [79]. Moreover, genetically inducing phosphate toxicity could significantly impair survival of leptin -deficient obese mice [80].…”

Section: Experimental Phosphate Toxicitymentioning

confidence: 99%

Can features of phosphate toxicity appear in normophosphatemia?

Osuka

Razzaque

2012

J Bone Miner Metab

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Phosphate is an indispensable nutrient for the formation of nucleic acids and the cell membrane. Adequate phosphate balance is a prerequisite for basic cellular functions ranging from energy metabolism to cell signaling. More than 85% of body phosphate is present in the bones and teeth. The remaining phosphate is distributed in various soft tissues, including skeletal muscle. A tiny amount, around 1% of total body phosphate, is distributed both in the extracellular fluids and within the cells. Impaired phosphate balance can affect the functionality of almost all human systems, including muscular, skeletal, and vascular systems, leading to an increase in morbidity and mortality of the involved patients. Currently, measuring serum phosphate level is the gold standard to estimate the overall phosphate status of the body. Despite the biological and clinical significance of maintaining delicate phosphate balance, serum levels do not always reflect the amount of phosphate uptake and its distribution. This article briefly discusses the potential that some of the early consequences of phosphate toxicity might not be evident from serum phosphate levels.

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“…In contrast, osteo-renal miscommunication through dysregulation of FGF23-klotho system provokes phosphate imbalance and induces pathological changes in a wide range of organs/tissues including blood vessels, bone and kidney. Of clinical importance, phosphate toxicity induced by excessive exogenous phosphate administration in humans can be fatal (90–93). Acute phosphate toxicity can provoke hypocalcemia and associated complications, whereas chronic phosphate toxicity can induce ectopic calcification.…”

Section: Resultsmentioning

confidence: 99%

Osteo‐renal regulation of systemic phosphate metabolism

Razzaque

2011

IUBMB Life

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Summary Impaired kidney function and subsequent skeletal responses play a critical role in disrupting phosphate balance in chronic kidney disease (CKD) patients with mineral and bone disorder (CKD-MBD). In patients with CKD-MBD, the inability of the kidney to maintain normal mineral ion balance affects bone remodeling to induce skeletal fracture and extraskeletal vascular calcification. In physiological conditions, bone-derived fibroblast growth factor 23 (FGF23) acts on the kidney to reduce serum phosphate and 1,25-dihydroxyvitamin D levels. In humans, increased bioactivity of FGF23 leads to increased urinary phosphate excretion, which induces hypophosphatemic diseases (e.g., rickets/osteomalacia). However, reduced FGF23 activity is associated with hyperphosphatemic diseases (e.g., tumoral calcinosis). In patients with CKD, high serum levels of FGF23 fail to reduce serum phosphate levels and lead to numerous complications, including vascular calcification, one of the important determinants of mortality of CKD-MBD patients. Of particular significance, molecular, biochemical and morphological changes in patients with CKD-MBD are mostly due to osteo-renal dysregulation of mineral ion metabolism. Furthermore, hyperphosphatemia can partly contribute to the development of secondary hyperparathyroidism in patients with CKD-MBD. Relatively new pharmacological agents including sevelamer hydrochloride, calcitriol analogs and cinacalcet hydrochloride are used either alone, or in combination, to minimize hyperphosphatemia and hyperparathyroidism associated complications to improve morbidity and mortality of CKD-MBD patients. This article will briefly summarize how osteo-renal miscommunication can induce phosphate toxicity, resulting in extensive tissue injuries.

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Fatal Poisoning From Sodium Phosphate Enema

Cited by 77 publications

References 12 publications

Phosphate enema poisoning in children

Phosphate enema poisoning in children

Can features of phosphate toxicity appear in normophosphatemia?

Osteo‐renal regulation of systemic phosphate metabolism

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