Hyperphosphatemia: Difference between revisions
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==Background== | ==Background== | ||
===Major Causes=== | ===Major Causes=== | ||
*Increased phosphate intake (Vitamin D, laxative abuse | *Increased phosphate intake (Vitamin D, laxative abuse) | ||
*Increased renal reabsorption ([[Hypoparathyroidism]]) | |||
*Decreased excretion ([[Renal failure]] | *Decreased excretion ([[Renal failure]] | ||
*Transcellular shifts ([[Tumor lysis syndrome]], [[Rhabdomyolysis]]) | *Transcellular shifts ([[Tumor lysis syndrome]], [[Rhabdomyolysis]]) | ||
Revision as of 00:04, 27 January 2019
Background
Major Causes
- Increased phosphate intake (Vitamin D, laxative abuse)
- Increased renal reabsorption (Hypoparathyroidism)
- Decreased excretion (Renal failure
- Transcellular shifts (Tumor lysis syndrome, Rhabdomyolysis)
Clinical Features
- Fatigue
- Shortness of breath
- Anorexia
- Nausea
- Vomiting
- Insomnia
Differential Diagnosis
- Calciphylaxis
- Vitamin D intoxication
- Tumor lysis syndrome
- Laxative (Phospho-soda) abuse
- Rhabdomyolysis
- Hypoparathyroidism
- Pseudohypoparathyroidism
- Multiple myeloma
Evaluation
- >4.5mg/dL[1]
Labs
Symptoms usually related to associated renal failure, hypocalcemia or hypomagnesemia
- Metabolic Panel (with calcium, Magnesium, and Phosphorus)
Management
Hyperphosphatemia treatment
- Treat the underlying cause
- Restrict calcium phosphate intake
- IV Normal Saline (if normal renal fx)
- Acetazolamide (500mg IV q6hr) - if normal renal function
- Phosphate Binder - Aluminum hydroxide (50-150mg/kg PO q4-6h) - limited effect
- Dialysis if refractory
Disposition
See Also
References
- ↑ Hawley C. Serum phosphate. Nephrology. Apr 2006. 11(S1):S201-5.