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CLINICAL UPDATE
Year : 2019  |  Volume : 6  |  Issue : 6  |  Page : 61-63

Phosphate


Senior Professor and Incharge PICU and Respiratory Clinic, Pt B D Sharma, PGIMS Rohtak, Haryana, India

Date of Submission25-Oct-2019
Date of Acceptance23-Nov-2019
Date of Web Publication20-Dec-2019

Correspondence Address:
Kundan Mittal
Senior Professor Pediatrics, Pt B D Sharma, PGIMS, Rohtak Haryana
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.21304/2019.0606.00552

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  Abstract 


Phosphate plays an important role in cell structure and metabolism. Less than 1% of phosphate is in circulating serum and maintained within narrow range by hormones PTH, calcitonin, FGF23, vitamin D. Children require higher amount of phosphate compared to adults. Kidneys play a crucial role in extracellular phosphate homeostasis.

Keywords: Phosphate, hypophosphatemia, hyperphosphatemia


How to cite this article:
Mittal K. Phosphate. J Pediatr Crit Care 2019;6:61-3

How to cite this URL:
Mittal K. Phosphate. J Pediatr Crit Care [serial online] 2019 [cited 2022 Dec 6];6:61-3. Available from: http://www.jpcc.org.in/text.asp?2019/6/6/61/279483



Phosphate constitute approximately 1% of total body weight (85% in bones and teeth, 14% in soft tissues, and 1% in ECF). The concentration of intracellular phosphate is higher than plasma concentration. 70% of phosphate is in organic form and 30% in physiologically active inorganic form, of which 10% is bound to albumin. Phosphate circulates in the form of HPO42- and H2PO4-, in a ratio of 4:1 at normal pH. The ratio between intra to extra cellular phosphate is 99:1 which is influenced by multiple factors including glucose metabolism, acid-base status, insulin and catecholamines. Phosphate concentration is not influenced by change in albumin concentration but diurnal variation is present, with a peak at midnight. Phosphate homeostasis is mainly regulated by intestines, kidneys and bones. Phosphate has significant role in mitochondrial respiration, oxidative phosphorylation, oxygen transport, cell signalling and skeletal muscle metabolism. Daily requirement of phosphate is 20mg/kg/day. Atomic weigh of phosphorus is 31g/mol and valence is 1.8.Normal serum levels are 0.9–1.5 mmol/L (2.7–4.7 mg/dl) in adolescents, 1.3–2.3 mmol/L (4–7 mg/dl) in children and 1.6–2.6 mmol/L (5–8 mg/dl) in the first week of life and cell phosphorus level is 100mEq/L. Only 0.1% of phosphorus is present in ECF. Most of phosphorus is absorbed from jejunum and excreted by kidneys (90%) and rest by GIT. Low phosphorus diet causes kidney to reabsorbs more phosphate to maintain serum levels. Phosphorus is also regulated by PTH, which is indirectly controlled by calcium level and there is an inverse relationship between calcium and phosphate.


  Hypophosphatemia Top


Hypophosphatemia can result either due to decrease in total phosphate or altered transcellular distribution of phosphorus. It is defined as serum phosphate level <2.5mg/dL (mild 2.0-2.5mg/dL, moderate 1.0-1.9mg/ dL and severe <1.0mg/dL). Pseudo hypophosphatemia can occur in patients receiving mannitol therapy.


  Etiology Top


  • Shift from extracellular to intracellular compartment: Insulin, catecholamines, refeeding syndrome, rapid cellular proliferation, respiratory alkalosis, salicylate toxicity.
  • Decreased intake and intestinal absorption: Vitamin D deficiency, aluminium containing antacids, malabsorption, starvation, laxative abuse
  • Renal loss: RTA,dopamine infusion, theophylline overdose, hyperparathyroidism, bicarbonate therapy.
  • Drugs: Osmotic diuretics, loop diuretics, acyclovir, corticosteroids, aminoglycosides, valproic acid, catecholamines, salbutamol, acetaminophen.
  • Miscellaneous: DKA, toxic shock syndrome, Gram negative sepsis, burns, massive fluid resuscitation.



  Clinical manifestations Top


  • Neurological and neuromuscular: Confusion, irritability, seizure, ataxia, central pontine myelinolysis, peripheral neuropathy, coma, muscle weakness, rhabdomyolysis, proximal myopathies.
  • Cardiac: Cardiomyopathy and decreased cardiac output.
  • Respiratory: Muscle weakness, diaphragm dysfunction, hypoxia, respiratory failure, left shift of oxy-haemoglobin dissociation curve.
  • Bone and skeletal muscle: Pain, rickets, osteomalacia, osteopenia, muscle weakness, rhabdomyolysis (CK >1.5 of upper limit), bone demineralization.
  • Hematologic: Decreased RBC life span, haemolysis, increased oxygen affinity, thrombocytopenia, decreased 2-3DPG, decreased bactericidal activity due to low level of ATP in WBC, abnormal platelet function.
  • Biochemical: Decreased glucose metabolism, insulin resistance, hypomagnesemia, decreased GFR, hypercalciuria, hypophosphaturia, decrease PTH.
  • Renal: Decrease GFR, hypercalciuria, hypermagnesuria, stone formation.



  Diagnostic workup Top


  • Detailed history and clinical examination mainly musculoskeletal system, drug intake.
  • Serum phosphate, magnesium, calcium, alkaline.
  • phosphatase, PTH, and vitamin D3.
  • Urine phosphate, urinary fraction excretion of phosphate FEPO4 (<5 non-renal, >5 renal etiology), and creatinine.
  • Imaging studies: Plain radiographs, CT, PET.



  Treatment Top


Intravenous phosphate given in separate line 0.16- 0.32mmol/kg over 4-6hr (sodium phosphate and potassium phosphate contain 3mmol/mL phosphate and 1mmol contains 3.1mg/dL phosphate) dissolved in DW5 is recommended in symptomatic patients. Intravenous phosphate administration is associated with hypocalcaemia, hypomagnesemia, hyperkalaemia, hypotension, ECG abnormalities, kidney failure, soft tissue calcification, metabolic acidosis. Chronic hypophosphatemia needs oral treatment and treatment of underlying etiology. Monitor vital signs, neurological status, respiratory & cardiac assessment, muscle strength, electrolytes, WBC. Moderate hypophosphatemia may be treated using oral sodium-potassium-phosphate preparation (30-90mg/kg/day).


  Preparation Top


Intravenous: Sodium PO4 (pH 7.7, phosphate 3mmol/mL, sodium 4mEq/L), Neutral Na/K PO4 (pH 7.4, phosphate 1.1mmol/mL, sodium 0.02mEq/L, potassium 0.02mEq/L), Neutral NaPO4 (pH 7.35, phosphate 0.09mmol/mL, sodium 0.2mEq/L)

Oral: Skim milk (phosphate 1gm/L, sodium 28mEq/L, potassium 38mEq/L), Neutra-phos (pH 7.3, phosphate 250mg/packet, sodium 7.1mEq/packet, potassium 7.1mEq/packet), K-Phos Neutral (pH 7.4, phosphate 250mg/tab, sodium 13mEq/L, potassium 1.1mEq/L)


  Hyperphosphatemia Top


It is defined as serum level (Pi) >4.5mg/dL in adults and 6mg/dL in children. Causes of true hyperphosphatemia include addition of phosphate from ICF to ECF (haemolysis, tumour lysis syndrome, rhabdomyolysis, leukaemia, lactic acidosis, excessive intake, phosphorus containing enemas, respiratory acidosis, lactic acidosis, DKA), decrease renal excretion (acute and chronic kidney disease, hypoparathyroidism), acromegaly, and drugs (excessive vitamin D3, growth hormone, bisphosphonates, liposomal amphotericin-B, parenteral phosphates, laxatives containing phosphates), neoplastic diseases (leukaemia, lymphoma), enhanced catabolism (rhabdomyolysis, malignant hyperthermia). Elevated level of phosphate compound binds with calcium and forms insoluble. They may be deposited in heart, eyes, kidneys, lungs, and other soft tissues. Pseudo hyperphosphatemia is seen in association hyperbilirubinemia, hypertriglyceridemia, and hyperglobulinemia. Hyperphosphatemia is a risk factor for cardiac mortality and secondary hyperparathyroidism. Clinical features include pruritis, ectopic calcification, rhythm disturbances, muscle weakness, impaired mental status, seizures, paraesthesia, tetany, hypocalcaemia (phosphate and calcium have inverse relationship), calcific uremic arteriolopathy and osteoporosis. Diagnostic tests include serum level of phosphate, calcium, creatinine, ECG, and x-ray showing features of osteodystrophy. Treatment modalities include dietary restriction, use of phosphate binders (calcium carbonate, calcium acetate, aluminium hydroxide, sevelamer hydrochloride, ferric citrate), rehydration and rarely haemodialysis. Intravenous glucose and insulin infusion shift phosphate in to cells like potassium. Hypocalcaemia should be managed aggressively. Monitor serum level of phosphate, calcium blood urea nitrogen, creatinine and fluid intake. Avoid high phosphorus containing foods like dairy products, fish, meat, eggs and peanuts.

Source of Funding: Nil

Conflict of Interest: Nil



 
  References Top

1.
Schrier RW. Renal & Electrolyte Disorders. 8th ed. China: Wolter Kluwer:2018  Back to cited text no. 1
    
2.
Ichai C, Quintard H, Orban JC. Metabolic Disorders and Critically ill Patients: From Pathophysiology to Treatment. Paris: Springer; 2018  Back to cited text no. 2
    
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Reilly FR, Perazella MA. Nephrology in 30 Days. Texas: McGraw Hill;2015  Back to cited text no. 3
    
4.
Acid-Base Disorders. Reddi AS. Newark USA: Springer;2020  Back to cited text no. 4
    




 

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  In this article
Abstract
Hypophosphatemia
Etiology
Clinical manifes...
Diagnostic workup
Treatment
Preparation
Hyperphosphatemia
References

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