eMedicine Specialties > Emergency Medicine > Endocrine & Metabolic
Hyperphosphatemia
Updated: Jan 31, 2008
Introduction
Background
Phosphorus is the sixth most abundant element in the human body. It is critical for bone mineralization, cellular structure, genetic coding, and energy metabolism. Many organic and inorganic forms exist. The adult body contains approximately 1000 g of phosphorus, of which 80-90% is in bone. An additional 10-14% is intracellular and the remaining 1% is extracellular.
The phosphorus in plasma is 12-17% protein bound. Free serum compounds represent much less than 1% of the total body phosphorus content. This fraction also varies with shifts between the intracellular and extracellular compartments. Thus, serum phosphorus levels may not reflect accurately the total body phosphorus content.
Levels are expressed in terms of serum phosphorus mass (mg/dL). One mg/dL of phosphorus is equal to 0.32 mmol of phosphate. The normal adult range is 2.5-4.5 mg/dL (0.81-1.45 mmol/L). Levels are 50% higher in infants and 30% higher in children because of growth hormone effects.
Hyperphosphatemia is considered significant when levels are greater than 5 mg/dL in adults or 7 mg/dL in children or adolescents.
Pathophysiology
Phosphorus homeostasis normally is maintained through several mechanisms. Gastrointestinal (GI) absorption must be matched by renal excretion, and cellular release is balanced by uptake in other tissues. Hormonal control is provided mainly by parathyroid hormone.
Hyperphosphatemia occurs when the phosphorus load (from GI absorption, exogenous administration, or cellular release) exceeds renal excretion and tissue uptake.
GI absorption
Phosphorus is present in nearly all foods, and GI absorption of dietary forms is very efficient. With low dietary intake, 80-90% is absorbed. When intake is greater than 10 mg/kg daily, 70% is absorbed. Normal daily dietary intake varies from 800-1500 mg.
Absorption occurs mainly in the jejunum, although some absorption occurs throughout the intestinal tract. A small amount of phosphorus is secreted into the GI tract.
Serum phosphorus levels
Serum phosphorus levels rise after a large meal. Antacids decrease absorption because calcium, aluminum, and magnesium bind phosphorus into insoluble complexes. Aluminum is the most efficient binder found in antacids.
Renal excretion and reabsorption
To maintain homeostasis, renal phosphorus excretion normally matches the amount of daily GI absorption. Excretion occurs in the proximal tubule and is largely dependent on the filtered phosphorus load. As the filtered load increases, a higher fraction of excreted phosphorus is reabsorbed.
Reabsorption is also dependent on concurrent sodium transport. However, while sodium that is not reabsorbed at the proximal tubule may be reabsorbed distally, this is not true for phosphorus. Proximal diuretics, which decrease sodium reabsorption, also increase phosphorus excretion. The usual load excreted is 5-15% of the filtered load or 600-800 mg/d in the normal net steady state. This amount may increase markedly in hyperphosphatemia. Marked hyperphosphatemia is unusual in chronic renal insufficiency unless the glomerular filtration rate (GFR) is less than 25 mL/min. Secretion plays an insignificant role in renal phosphorus excretion.
Hyperphosphatemia occurs most often in patients with renal insufficiency. Most patients with acute or chronic renal failure have hyperphosphatemia in some degree. To avoid hyperphosphatemia, patients with end-stage renal disease and a GFR <30 must restrict their intake of dietary phosphorus. If dietary restriction alone does not reduce serum phosphate levels into the normal range, oral phosphate binders should be added to reduce absorption.
Sequelae of hyperphosphatemia
Hyperphosphatemia causes hypocalcemia by precipitating calcium, decreasing vitamin D production, and interfering with parathyroid hormone-mediated bone resorption. Severe life-threatening hypocalcemia may result. Signs and symptoms of acute hyperphosphatemia are due to the effects of hypocalcemia.
Prolonged hyperphosphatemia promotes metastatic calcification, an abnormal deposition of calcium phosphate in previously healthy connective tissues such as cardiac valves and in solid organs such as muscles. The calcium-phosphate product predicts the risk of metastatic calcification.
Excess free serum phosphorus is taken up into vascular smooth muscle via a sodium-phosphate cotransporter. The increased cellular phosphate activates a gene, cbfa-1, that promotes calcium deposition in the vascular cell, making smooth muscle cells engage in osteogenesis. Vascular walls become calcified and arteriosclerotic, leading to increased systolic blood pressure, widened pulse pressure, and subsequent left ventricular hypertrophy.
Hyperphosphatemia is an independent risk factor contributing to the increased incidence of aortic and mitral stenosis and other cardiovascular disease among dialysis-dependent patients. A peripheral form known as calcific uremic arteriolopathy (calciphylaxis) can induce necrotic ulceration and gangrene in affected extremities.
Hyperphosphatemia-induced resistance to parathyroid hormone contributes to secondary hyperparathyroidism and renal osteodystrophy.
Frequency
United States
Patients with end-stage renal disease make up the bulk of patients with hyperphosphatemia. Approximately 250,000 persons are affected.
Mortality/Morbidity
Prolonged hyperphosphatemia is an independent risk factor for cardiovascular disease in patients with renal failure. Patients with chronic phosphate levels above 6.5 have an 18-39% higher mortality compared with patients with renal failure with near-normal serum phosphate levels.
Sex
Although women have physiologic elevation of serum phosphate levels after menopause, this has no known clinical significance.
Age
- Phosphorus levels are naturally higher in infants, children, and postmenopausal women.
- A phosphate-driven rise of erythrocyte 2,3-diphosphoglycerate and ATP in children may account for the physiologic anemia of childhood.
Clinical
History
- Patients with hyperphosphatemia most commonly complain of muscle cramping secondary to low calcium levels. This may progress to tetany, delirium, and seizures. A search for the following historical clues may help identify those patients at risk for increased phosphorus levels.
- Renal disease
- Past or present hemodialysis
- Adherence to renal (low phosphorus) diet
- Use of oral phosphate binders
- Cancer
- Leukemia
- Lymphoma
- Bone tumors
- Other cancers
- Chemotherapy treatment
- Endocrinopathies
- Trauma
- Burns or heat-related illnesses
- Prolonged immobilization
- Metabolic or hematologic disorders including genetic predisposition
- Medications
- Oral phosphate binders
- Potassium phosphate
- Antacid use
- Bisphosphonate therapy
- Use of laxatives (oral/rectal) and enemas
- Use of nutritional supplements or hyperalimentation
- Ischemic bowel (possible phosphorus elevations)
Physical
The nervous and cardiovascular systems are most commonly affected.
- Central nervous system (CNS)
- Altered mental status
- Delirium
- Obtundation
- Coma
- Convulsions and seizures
- Muscle cramping or tetany
- Neuromuscular hyperexcitability (ie, Chvostek and Trousseau signs)
- Paresthesias (particularly perioral and distal extremities)
- Cardiovascular system
- Hypotension and heart failure
- Prolongation of the QT interval
- Ocular - Cataracts
Causes
Phosphorus balance between intracellular and extracellular compartments and between bone and other tissues may be influenced by many factors. The most common cause of hyperphosphatemia is decreased renal excretion due to renal insufficiency from any cause. All marked elevations of phosphorus involve significant addition of phosphorus to the extracellular compartment, usually with some impairment of renal function.
- Renal insufficiency (acute or chronic)
- Medications - Liposomal amphotericin B
- Increased catabolism or cellular injury
- Rhabdomyolysis
- Trauma, burns, crush injuries, shock
- Exhaustive exercise
- Prolonged immobilization
- Heat-related illnesses
- Malignant hyperthermia
- Hypothermia
- Massive hemolysis
- Severe infections
- Ischemic bowel
- Endocrinopathies
- Hypoparathyroidism
- Pseudohypoparathyroidism
- Abnormal parathyroid hormone
- Acromegaly and other causes of growth hormone excess
- Thyrotoxicosis
- Glucocorticoid withdrawal or deficiency
- Poisoning, excessive intake or administration
- Bisphosphonate therapy
- Vitamin D intoxication or other causes of increased vitamin D (sarcoidosis)
- Ingestion or administration of phosphate salts (eg, oral/rectal laxatives, enemas, intravenous phosphate)
- Hyperalimentation (including lipid administration)
- White phosphorous burns
- Milk-alkali syndrome
- Transfusion of outdated blood
- Neoplasms
- Leukemia
- Lymphoma
- Bone tumors
- Tumor lysis after chemotherapy
- Acidosis
- Acute respiratory acidosis
- Lactic acidosis
- Diabetic ketoacidosis
- Alcoholic ketoacidosis
- Alkalosis
- Miscellaneous
- Tumoral calcinosis
- Cortical hyperostosis
- Syndrome of familial intermittent hyperphosphatemia
- Hyperbilirubinemia (controversial as cause)
Differential Diagnoses
Hypercalcemia
Hypermagnesemia
Hypocalcemia
Other Problems to Be Considered
Pseudohyperphosphatemia is most commonly due to paraproteinemia from the following:
Waldenström macroglobulinemia
Multiple myeloma
Monoclonal gammopathy of unknown significance
Workup
Laboratory Studies
- Serum phosphate level
- Reference range in adults - 2.5-4.5 mg/dL
- Reference range in children - 3-6 mg/dL
- Serum calcium level
- Electrolytes
- BUN and creatinine levels
- Serum magnesium level (may be low)
- Hemolysis or hyperlipidemia of the serum sample may lead to falsely elevated phosphorus levels.
Imaging Studies
- Radiographs are not necessary for the workup but may show evidence of metastatic calcifications (eg, bilateral, symmetric calcifications of the basal ganglia; periarticular calcifications around large joints; soft-tissue calcifications at pressure point areas).
Other Tests
- The ECG may show QT interval prolongation.
Treatment
Prehospital Care
- The diagnosis of hyperphosphatemia rarely is evident in the prehospital setting. No specific disease-directed prehospital management is indicated.
- In patients without a history of renal failure or evidence of cardiac compromise, volume repletion may be initiated.
Emergency Department Care
Most symptoms and sequelae are due to secondary hypocalcemia. Initial care is aimed at management and correction of the hypocalcemia and its sequelae. Endpoints of therapy include resolution of symptoms and a serum calcium level within the low reference range.
- A secondary goal is to decrease the incidence of sequelae, which requires reducing serum phosphate to nearly normal levels, less than 5.5 mg/dL, and maintaining the calcium phosphate product less than 60.
- The ultimate goal is resolution of the underlying disease state(s) responsible for the hyperphosphatemia.
- Saline diuresis and treatment of the primary cause usually lead to improvement.
- Hypocalcemia is treated directly when symptoms arise.
- Patients with symptomatic hypocalcemia and those with a corrected serum level of 1.875 mmol/L or less should be treated with parenteral calcium. The rate and extent of calcium replacement is determined clinically, based on the severity of the symptoms.
- Calcium replacement carries a theoretical risk of acceleration of metastatic calcification, but the clinical significance of this risk is not known.
- Oral binders are given to decrease GI absorption of phosphorus. Binders containing calcium may cause hypercalcemia and promote vascular calcium deposition by increasing the calcium-phosphate product. Resin binders like sevelamer (Renagel) promote phosphorus excretion without affecting calcium. Sevelamer has been shown to decrease incidence of vascular calcium deposition in patients with renal failure. Phosphate binders containing aluminum should be avoided in patients with renal failure due to a heightened potential for aluminum toxicity. Diuretics that act on the proximal renal tubules, such as acetazolamide, may be considered to increase urinary excretion.
- Hemodialysis or peritoneal dialysis is indicated for severe refractory cases and for patients with renal failure. As with hyperkalemia, glucose and insulin may force translocation of intracellular phosphorus, and this can be a useful temporizing measure.
- For toxic ingestions, gastric lavage and oral phosphate binders are given to prevent further absorption.
Consultations
- Nephrology consultation is necessary for patients with renal failure.
- Poison control consultation is helpful for poisonings involving phosphorus.
Medication
Oral phosphate binders are used to decrease the highly efficient GI absorption of phosphorus. Calcium salts are widely used but may produce hypercalcemia. Aluminum salts are effective binders but may induce aluminum toxicity. Newer compounds containing iron or bile acid sequestrants are replacing calcium and aluminum binders.
Proximal diuretics are phosphuretic to the same extent they are natriuretic. Acetazolamide is particularly efficient in promoting renal phosphate excretion.
Oral phosphate binders
These agents decrease GI phosphate absorption.
Sevelamer hydrochloride (Renagel)
The polymer forms ionic and hydrogen bonds with phosphates and bile acids to promote fecal excretion. Lowers serum phosphate to near normal levels in hemodialysis patients as effectively as calcium acetate without inducing hypercalcemia or increased aluminum levels. Maintains stable iPTH levels and increases alkaline phosphatase levels compared to calcium acetate.
Dosing
Adult
2.4-4.8 g PO divided tid with meals
Pediatric
Not established
Interactions
May decrease absorption of oral medications causing a decrease in levels of antiarrhythmics and antiepileptics
Contraindications
Documented hypersensitivity; bowel obstruction, hypophosphatemia
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in patients with dysphagia, altered GI motility or GI tract surgery; measure serum phosphate and calcium frequently to adjust dose to keep serum phosphate <6 mg/dL
Calcium acetate (PhosLo)
Combines with dietary phosphate to form calcium acetate, which is then excreted in feces.
Dosing
Adult
4-8 g PO divided tid with meals
Pediatric
Not established
Interactions
May increase effect of quinidine; may decrease effects of tetracyclines, atenolol, salicylates, iron salts, and fluoroquinolones; IV administration antagonizes effects of verapamil; large intakes of dietary fiber may decrease calcium absorption and levels
Contraindications
Documented hypersensitivity; hypercalcemia or hypercalcuria may occur when therapeutic amounts are given
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Monitor serum calcium and phosphate frequently; adjust dose to keep serum phosphate less than 6 mg/dL; avoid use of over-the-counter antacids
Lanthanum carbonate (Fosrenal)
Noncalcium, nonaluminum phosphate binder indicated for reduction of high phosphorus levels in patients with end-stage renal disease. Directly binds dietary phosphorus in upper GI tract, thereby inhibiting phosphorus absorption.
Dosing
Adult
Initial: 250-500 mg PO tid pc (chewable tabs); adjust dose q2-3wk to target serum phosphorus level
Maintenance: 500-1000 mg PO tid pc
Pediatric
Not established
Interactions
Drugs known to interact with antacids (eg, alendronate, amprenavir, ciprofloxacin, itraconazole, tetracycline, thyroid hormones) should not be administered within 2 h
Contraindications
Documented hypersensitivity; bowel obstruction; hypophosphatemia
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Deposited into developing bone, including growth plate (long-term effects unknown); common adverse effects typically diminish over time but include headache, abdominal pain, nausea, diarrhea, constipation, and vomiting; in clinical trials, dialysis graft occlusion occurred more frequently than with placebo; caution with GI motility diseases (eg, Crohn disease, ulcerative colitis) or recent GI surgery
Calcium salts
These agents are used to treat symptomatic hypocalcemia resulting from hyperphosphatemia by replacing calcium.
Calcium gluconate (Kalcinate)
IV preparation used in treatment of symptomatic hypocalcemia, particularly for treatment of tetany. In absence of symptoms, hypocalcemia may be treated with oral supplements rather than IV infusions. Calcium gluconate 10% solution contains 100 mg/mL = 0.45 mEq elemental calcium/mL.
Dosing
Adult
2 g (20 mL) IV over 10-30 min initially, followed by maintenance dose of 0.5-2 mg/kg/h
Pediatric
Neonates: 200-800 mg/kg/d IV continuous infusion or divided qid
Infants and children: 100-200 mg/kg IV over 10 min initially, followed by maintenance dose of 200-500 mg/kg/d IV continuous infusion or divided qid
Interactions
May decrease effects of tetracyclines, atenolol, salicylates, iron salts, and fluoroquinolones; antagonizes effects of verapamil; large intakes of dietary fiber may decrease calcium absorption and levels
Contraindications
Renal calculi; hypercalcemia; hypophosphatemia; renal or cardiac disease; digitalis toxicity
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in digitalized patients, respiratory failure, acidosis, or severe hyperphosphatemia
Calcium chloride
IV preparation used in treatment of severe symptomatic hypocalcemia. Do not confuse calcium chloride with calcium gluconate; calcium chloride contains approximately 3 times as much elemental calcium per unit weight as does calcium gluconate. In absence of symptoms, hypocalcemia may be treated with oral supplements rather than IV infusions. Calcium chloride 10% solution contains 100 mg/mL = 1.4 mEq/mL.
Dosing
Adult
500-1000 mg slow IV q6h
Pediatric
10-20 mg/kg/dose slow IV q4-6h prn
Interactions
With digoxin may cause arrhythmias; with thiazides may induce hypercalcemia; may antagonize effects of calcium channel blockers, atenolol, and sodium polystyrene sulfonate
Contraindications
Ventricular fibrillation not associated with hyperkalemia; digitalis toxicity; hypercalcemia; renal insufficiency; cardiac disease
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Administer slowly (not to exceed 0.5-1 mL/min) to avoid extravasation; hypercalcemia may occur in renal failure
Diuretic carbonic anhydrase inhibitor
These agents increase renal excretion of phosphate.
Acetazolamide (Diamox)
Increases renal excretion of phosphorus.
Dosing
Adult
250-375 mg PO/IV qd in am
Pediatric
5 mg/kg PO/IV qd in am
Interactions
Can decrease therapeutic levels of lithium and alter excretion of drugs (amphetamines, quinidine, phenobarbital, salicylates) by alkalinizing urine
Contraindications
Documented hypersensitivity; hepatic disease; severe renal disease; adrenocortical insufficiency; severe pulmonary obstruction
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Patients with impaired hepatic function may go into coma; may cause substantial increase in blood glucose in some diabetic patients
Follow-up
Further Inpatient Care
- Patients with hyperphosphatemia due to administration of liposomal amphotericin B who continue to require antifungal therapy may be switched to the formulation amphotericin B lipid complex, which contains less inorganic phosphate.1
Inpatient & Outpatient Medications
- Phosphate binders
- Calcium supplements, if needed
Transfer
- Patients with severe hyperphosphatemia may require transfer to a facility with a dialysis center.
Complications
- Complications resulting from the underlying cause of the hyperphosphatemia vary with the specific etiology.
Prognosis
- Prognosis is determined primarily by the severity of the underlying disorder and of the hypocalcemia produced. With metastatic calcification, progressive organ damage occurs at areas of deposition.
Patient Education
- Dietary education is very important for patients at risk for recurrent hyperphosphatemia.
- Restrict dietary phosphorus to 0.6-0.9 g/d.
- Avoid milk and milk products, meat, fish, poultry, eggs, and peanuts.
- Avoid phosphorus-containing preparations such as laxatives, enemas, and supplements.
- Maintain adequate hydration status.
Miscellaneous
Medicolegal Pitfalls
- Use caution in ordering phosphate-containing enemas and laxatives for children and for patients with renal insufficiency.
References
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Keywords
phosphorus homeostasis, high phosphorus level, hyperphosphatemia, renal insufficiency, acute renal failure, chronic renal failure, end-stage renal disease, hypocalcemia, calcific uremic arteriolopathy, calciphylaxis, managing hyperphosphatemia and chronic kidney disease
Contributor Information and Disclosures
Author
Leigh A Patterson, MD, Assistant Professor, Interim Residency Director, Department of Emergency Medicine, Brody School of Medicine at East Carolina University
Leigh A Patterson, MD is a member of the following medical societies: American College of Emergency Physicians, American Institute of Ultrasound in Medicine, American Medical Association, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Coauthor(s)
Peter MC DeBlieux, MD, Professor of Clinical Medicine and Pediatrics, Section of Pulmonary and Critical Care Medicine, Program Director, Department of Emergency Medicine, Louisiana State University Health Sciences Center
Peter MC DeBlieux, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Radiological Society of North America, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.
Medical Editor
Robin R Hemphill, MD, MPH, Associate Professor, Director, Disaster Preparedness, Department of Emergency Medicine, Vanderbilt University Medical Center
Robin R Hemphill, MD, MPH is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Pharmacy Editor
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
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Managing Editor
Jeffrey L Arnold, MD, FACEP, Chairman, Department of Emergency Medicine, Santa Clara Valley Medical Center
Jeffrey L Arnold, MD, FACEP is a member of the following medical societies: American Academy of Emergency Medicine and American College of Physicians
Disclosure: Nothing to disclose.
CME Editor
John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Chief Editor
Rick Kulkarni, MD, Medical Director, Assistant Professor of Surgery, Section of Emergency Medicine, Yale-New Haven Hospital
Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
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