Hyponatremia and Other Critical Electrolyte Abnormalities Phillip D. Levy, MD, MPH, FACEP Associate Professor and Associate Director of Clinical Research Department of Emergency Medicine Assistant Director of Clinical Research Cardiovascular Research Institute Wayne State University School of Medicine
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Hyponatremia and Other Critical
Electrolyte Abnormalities
Phillip D. Levy, MD, MPH, FACEPAssociate Professor and Associate Director of Clinical Research
Department of Emergency MedicineAssistant Director of Clinical Research
Cardiovascular Research InstituteWayne State University School of Medicine
Disclosures• None relevant to this presentation
Objectives• To provide a brief review of
common electrolyte abnormalities encountered in the ED and discuss basic treatment
• To take a closer look at hyponatremia and evolving approaches to management
Potassium• Hyperkalemia
- Most common life-threatening electrolyte abnormality
- Three stage approach to treatment• Membrane stabilization• Shift potassium into cells• Remove potassium from the body
Common Causes
Pfenning et al. Critical Decisions in Emergency Medicine 2011;10;2-11.
Potassium• Hyperkalemia
- Most common life-threatening electrolyte abnormality
- Three stage approach to treatment• Membrane stabilization• Shift potassium into cells• Remove potassium from the body
Typical ECG Changes
Pfenning et al. Critical Decisions in Emergency Medicine 2011;10;2-11.
Potassium• Hyperkalemia
- Most common life-threatening electrolyte abnormality
- Three stage approach to treatment• Membrane stabilization• Shift potassium into cells• Remove potassium from the body
Potassium• Hyperkalemia
- Most common life-threatening electrolyte abnormality
- Three stage approach to treatment• Membrane stabilization• Shift potassium into cells• Remove potassium from the body
Potassium• Hypokalemia
- Often coupled with hypomagnesemia- Frequently asymptomatic
• Cramps, weakness- Classic ECG findings
Common Causes
Pfenning et al. Critical Decisions in Emergency Medicine 2011;10;2-11.
Potassium• Hypokalemia
- Often coupled with hypomagnesemia- Frequently asymptomatic
• Cramps, weakness- Classic ECG findings
Potassium• Hypokalemia
- Often coupled with hypomagnesemia- Frequently asymptomatic
• Cramps, weakness- Classic ECG findings
Potassium• Hypokalemia
- Replete orally for mild to moderate decreases
• Each 0.3 mEq < normal = 100 mEq deficit- Prolonged therapy may be needed for
severe cases- Requires concurrent magnesium to
move intracellularly
Potassium• Hypokalemia
- Replete orally for mild to moderate decreases
• Each 0.3 mEq < normal = 100 mEq deficit- Prolonged therapy may be needed for
severe cases- Requires concurrent magnesium to
move intracellularly
Potassium• Hypokalemia
- Replete orally for mild to moderate decreases
• Each 0.3 mEq < normal = 100 mEq deficit- Prolonged therapy may be needed for
severe cases- Requires concurrent magnesium to
move intracellularly
Calcium• Hypercalcemia
– Most often caused by parathyroid disease and malignancy
– “Bones, moans, groans and stones”• Arrhythmias with concomitant electrolyte
abnormalities– Primary treatment is normal saline
• Furosemide can help with associated diuresis but no longer routinely recommended
• Bisphosphonates = definitive therapy
Common Causes
Pfenning et al. Critical Decisions in Emergency Medicine 2011;10;2-11.
Calcium• Hypercalcemia
– Most often caused by parathyroid disease and malignancy
– “Bones, moans, groans and stones”• Arrhythmias with concomitant electrolyte
abnormalities– Primary treatment is normal saline
• Furosemide can help with associated diuresis but no longer routinely recommended
• Bisphosphonates = definitive therapy
Calcium• Hypercalcemia
– Most often caused by parathyroid disease and malignancy
– “Bones, moans, groans and stones”• Arrhythmias with concomitant electrolyte
abnormalities– Primary treatment is normal saline
• Furosemide can help with associated diuresis but no longer routinely recommended
• Bisphosphonates = definitive therapy
Calcium• Hypocalcemia
– Typically caused by hypoalbuminemia– Muscle cramping, paresthesias
• Chvostek sign• Trousseau sign
– Oral repletion for mild cases, IV for more significant deficits• Ionized calcium level more accurate than
total
Calcium• Hypocalcemia
– Typically caused by hypoalbuminemia– Muscle cramping, paresthesias
• Chvostek sign• Trousseau sign
– Oral repletion for mild cases, IV for more significant deficits• Ionized calcium level more accurate than
total
Calcium• Hypocalcemia
– Typically caused by hypoalbuminemia– Muscle cramping, paresthesias
• Chvostek sign• Trousseau sign
– Oral repletion for mild cases, IV for more significant deficits• Ionized calcium level more accurate than
total
Magenesium• Hypomagnesemia
– Typically caused by insufficient dietary intake, GI disorders, and medication effects
– Symptoms relatively non-specific– Treatment generally IV
• 0.5-2 gm/h• Watch for loss of deep tendon reflexes and
development of respiratory depression
Magenesium• Hypomagnesemia
– Typically caused by insufficient dietary intake, GI disorders, and medication effects
– Symptoms relatively non-specific– Treatment generally IV
• 0.5-2 gm/h• Watch for loss of deep tendon reflexes and
development of respiratory depression
Magenesium• Hypomagnesemia
– Typically caused by insufficient dietary intake, GI disorders, and medication effects
– Symptoms relatively non-specific– Treatment generally IV
• 0.5-2 gm/h• Watch for loss of deep tendon reflexes and
development of respiratory depression
Sodium• Hypernatremia
- Hypovolemia most common cause- Also consider diabetes insipidus
• Central (deficient production of AVP)• Nephrogenic (diminished response to AVP)
Sodium• Hypernatremia
- Hypovolemia most common cause- Also consider diabetes insipidus
• Central (deficient production of AVP)• Nephrogenic (diminished response to AVP)
Sodium• Hypernatremia
- Hypovolemic: replace free water deficit• TBW = 0.6 x current weight (kg)• Desired TBW = measured Na x current
TBW / normal Na• Body water deficit = desired TBW – current
TBW- Diabetes insipidus
• Central: DDAVP• Nephrogenic: thiazide diuretic
Sodium• Hypernatremia
- Hypovolemic: replace free water deficit• TBW = 0.6 x current weight (kg)• Desired TBW = measured Na x current
TBW / normal Na• Body water deficit = desired TBW – current
TBW- Diabetes insipidus
• Central: DDAVP• Nephrogenic: thiazide diuretic
Hyponatremia• Most common electrolyte
abonormality• Classified by volume status
– Hypovolemic hyponatremia• Decrease in total body water with greater
decrease in total body sodium– Euvolemic hyponatremia
• Normal body sodium with increase in total body water
– Hypervolemic hyponatremia• Increase in total body sodium with greater
increase in total body water
Hyponatremia• Most common electrolyte
abonormality• Classified by volume status
– Hypovolemic hyponatremia• Decrease in total body water with greater
decrease in total body sodium– Euvolemic hyponatremia
• Normal body sodium with increase in total body water
– Hypervolemic hyponatremia• Increase in total body sodium with greater
increase in total body water
Hyponatremia• Most common electrolyte
abonormality• Classified by volume status
– Hypovolemic hyponatremia• Decrease in total body water with greater
decrease in total body sodium– Euvolemic hyponatremia
• Normal body sodium with increase in total body water
– Hypervolemic hyponatremia• Increase in total body sodium with greater
increase in total body water
Hyponatremia• Most common electrolyte
abonormality• Classified by volume status
– Hypovolemic hyponatremia• Decrease in total body water with greater
decrease in total body sodium– Euvolemic hyponatremia
• Normal body sodium with increase in total body water
– Hypervolemic hyponatremia• Increase in total body sodium with greater
increase in total body water
Hyponatremia• Most common electrolyte
abonormality• Classified by volume status
– Hypovolemic hyponatremia• Decrease in total body water with greater
decrease in total body sodium– Euvolemic hyponatremia
• Normal body sodium with increase in total body water
– Hypervolemic hyponatremia• Increase in total body sodium with greater
Length of In-hospital Post-discharge Death or stay (days) mortality (%) mortality (%) rehospitalization
since discharge (%)
Vasopressin
Non-osmotic stimulation of AVP secretion
H20 retention Intravascular volume
Dilutional hyponatremia
Sympathetic activity
Vasoconstriction
Fibrosis Myocardial &
vascular hypertrophy
Aortic/ carotid sinus baroreceptors stimulation
Goldsmith and Gheorghiade JACC 2005;46:1785-91
Vasopressin Mediated
Maisel et al. Circ Heart Fail. 2011;4:613-20.
Hypotonic Hyponatremia• Treatment options
– Hypertonic saline (3% soln)• Reserved for acute, severe cases• Bolus 100 mL over 10 min q 1 hr x 2 doses• Infusion of 1-2 mL/kg/hr• Target correction: 0.5 mEq/L/hr
– Hypertonic saline (3% soln)• Reserved for acute, severe cases• Bolus 100 mL over 10 min q 1 hr x 2 doses• Infusion of 1-2 mL/kg/hr• Target correction: 0.5 mEq/L/hr