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ELECTROLYTE
EMERGENCIES Katie Rose Flannery, MD
Henry Ford Hospital – Emergency
Medicine
Grand Rounds, December 4, 2014
OBJECTIVES
Define significant electrolyte disturbances
Identify clinical signs/symptoms of electrolyte abnormalities
Understand etiologies of electrolyte abnormalities
Evaluate diagnostic and ancillary testing
Discuss treatment options
Identify immediate life threatening electrolyte emergencies
WHAT IS AN ELECTROLYTE?
Electrolyte “any substance that has free ions and therefore can conduct
an electrical charge when in solution” –Rosen’s, 7th Ed. 1615
“It’s like the stuff in gatorade that helps your body work right”
CASE 1
51 yo female ESRD on MWF presents on a Thursday morning stating
she has not gone to dialysis since last week
Chief complaint: SOB
EKG on the chart:
What are you thinking? What would you give?
HYPERKALEMIA
Serum K+ > 5.0 mEq/L
Etiologies
Increased Intake
Impaired Renal Excretion
Transcellular shift – Acidosis, insulin deficiency
Cellular deficiency – tumor lysis syndrome, crush/burn injuries
Pseudohyperkalemia – hemolysis, thrombocytosis, leukocytosis
CLINICAL FEATURES
Cardiovascular – dysrhythmias
Second degree heart block
Third degree heart block
Wide-complex tachycardia
Ventricular fibrillation
Asystole
Neurologic
Muscle cramps, weakness, paralysis, paresthesia, tetany, focal
neurologic deficits
EKG FINDINGS HYPERKALEMIA
Tall peak T waves – best seen in precordial leads
Tall peak T waves, Prolonged PR interval, widening QRS complex
Absent p wavers, bundle branch/fascicular blocks, SINE wave
MANAGEMENT
A. Calcium Gluconate (peripheral)/Calcium Chloride
(central) – stabilizes cardiac membrane
B. Sodium Bicarbonate – shifts K into cells, duration 2 hours,
less efficacious than insulin/albuterol
C. Glucose/Insulin – shifts K into cells, duration 4-6 hours
D. Beta2-agonists – shifts K into cells, duration 2 hours
E. Exchange Resins (eg kayexalate) – PO dose takes effect in 1-
2 hours; rectal works in 30 mins
F. Dialysis
G. DON’T FORGET TO TREAT UNDERLINING CAUSE!
WHEN DO YOU USE CALCIUM?
Why not just give it? Calcium will decrease QTc
Increase risk Ventricular Dysrhythmias
Use Calcium when QRS widens
Serum K 6.0-7.0
Calcium stabilizes cardiac membrane
Duration approximately 20 minutes
WHEN DO YOU USE BICARB?
Use Bicarb when patient is acidotic
Why?
Bicarb alkalinizes serum, H+ out of cell, K+ into cell
HCO3 H+
K+
HYPOKALEMIA
Serum K < 3.5 mEq/L
Etiologies
Decreased Intake - rare
Increased Excretion – eg. Renal/GI losses, Diuretics
Transcellular Shifts
Alkalosis
Insulin
Beta2-agonists
CLINICAL FEATURES Symptomatic: serum K < 2.5 mEq/L
Neurologic
CNS: lethargy, depression, irritability, confusion
PNS: paresthesias, depressed DTRs, fasciculations, myalgias, muscle weakness
**Muscular paralysis occurs K < 2.0 mEq/L
Cardiovascular
Palpitations, ectopy, dysrhythmias (PVCs, afib, Vfib)
GI
Nausea, vomiting, abdominal distension, ileus
Renal
Polyuria, polydipsia, inability to concentrate urine
MANAGEMENT
**Check Serum Magnesium**
PO replacement preferred over IV replacement
Lower risk of hyperkalemia
PO replacement: 20-40 mEq packets
KDUR: large pill, hard for some patient’s to swallow
KLOR: Liquid, Tastes bad
IV replacement: 10-20 mEq per hour
Common side effect: burning at infusion site
Monitor for dysrhythmias
ANTERIOR SHOULDER DISLOCATION
Most common shoulder dislocation
Young men 20-30s -> athletic events
Older women 50-60s -> fall
For all shoulder dislocation – examine neurovascular status
(distal pulses, axillary nerve)
CASE 2
51 yo female pmh HTN, HLD, chronic alcohol abuse presents with
complaints of generalized fatigue and weakness. She states she might
have had “one beer” today. Denies any falls
VS: 98.7*F, HR: 77, BP: 132/78, RR: 18, SatO2: 97% RA
Blood ethanol: 0.24, patient ambulating without difficulty
BMP: Na 118, K 3.4, BUN/Cr: 13/1.13, Cl 96
What do you do next?
HYPONATREMIA
Serum sodium < 135 mEq/L
5 broad categories:
Hypovolemic hyponatremia
Euvolemic hyponatremia
Hypervolemic hyponatremia
Pseudohyponatremia
Redistributed hyponatremia
HOW TO ASSESS VOLUME STATUS
Mucous membranes
Skin turgor
Vital signs – HR, BP
Orthostatic blood pressure
Capillary refill
Extremity Edema
JVD
Ultrasound: IVC (<1cm, >2cm)
CLINICAL FEATURES
CNS symptoms
Lethargy, apathy, confusion, disorientation, agitation, depression,
psychosis
“Hey staff doctor, remember that patient I had in MHT…”
Focal neurologic deficits, ataxia, seizures
Muscle cramps
Anorexia
Nausea
Weakness
MANAGEMENT
Based on severity of symptoms - chronic hyponatremia
are more at risk from rapid correction
Hypovolemic hyponatremia: 0.9% NS
Euvolemic hyponatremia: free water restriction
***Patients with SIADH (or on Lithium) can have worsening
hyponatremia after normal saline***
Hypervolemic hyponatremia: fluid restriction
SYMPTOMATIC HYPONATREMIA
Severely symptomatic (eg Seizures) – consider 3% NS
Goal is increase in 10 mEq/L in 24 hours
Acute hyponatremia: 1-2 mEq/L/hr
Chronic hyponatremia: 0.5 mEq/L/hr
Why do we not correct too rapidly?
CENTRAL PONTINE MYELINOLYSIS
aka CEREBRAL DEMYELINATION
More common in chronic hyponatremia
CN palsies, quadriplegia, coma
Siddiqi TA, Sim Y, Nguyen T, Sam A. Medical image of the week: central pontine myelinolysis. Southwest J
Pulm Crit Care. 2013;8(1):18-9. 38 yo alcoholic with initial sodium 116, developed motor weakness, clonus,
ataxia, hyporeflexia
HYPERNATREMIA
Serum sodium >145 mEq/L
#1 Cause: decrease free water
A) decreased water intake
B) increased water loss (GI, renal, skin)
CAUSES Hypernatremia with dehydration and low
total body sodium
•Heatstroke
•Increased insensible losses: burns, sweating
•Gastrointestinal loss: diarrhea, protracted vomiting,
continuous gastrointestinal suction
•Osmotic diuresis: glucose, mannitol, enteral feeding
Hypernatremia with low total body water
and normal total body sodium
•Diabetes insipidus
•Neurogenic
•Elderly with “reset” osmostat
•Hypothalamic dysfunction
•Suprasellar or infrasellar tumors
•Renal disease
•Drugs (amphotericin, phenytoin, lithium,
aminoglycosides, methoxyflurane)
•Sickle cell disease
Hypernatremia with increased total body
sodium
•Salt tablet ingestion
•Salt water ingestion
•Saline infusions
•Saline enemas
•Intravenous sodium bicarbonate
•Poorly diluted interval feedings
•Primary hyperaldosteronism
•Hemodialysis
•Cushing's syndrome
•Conn's syndrome
CLINICAL FEATURES
Symptoms:
Anorexia
Nausea/vomiting
Fatigue
Irritability
Signs:
Dehydration
Lethargy/Confusion/Stupor/Coma
Muscle twitching, tremor, spasticity, ataxia
DIAGNOSTIC STUDIES
UA
Urine Osmolality
Serum Osmolality
Low specific gravity + low urine osmolality: Diabetes
Insipidus
MANAGEMENT
Hypovolemic Hypernatremia: GIVE FLUIDS!
0.9% NS
Euvolemic Hypernatremia
Diabetes Insipidus vs Insensible fluid loss
Oral fluids or 0.45% NS if DI; central DI: vasopressin
Hypervolemic Hypernatremia:
Loop diuretics followed by hypotonic saline administration
Symptomatic Hypernatremia: avoid rapid correction
Rapid hypotonic fluid administration shifts water into cells, leads to
cerebral edema
POSTERIOR SHOULDER DISLOCATION
4% shoulder dislocations
Frequently missed
Most common cause: seizures
Higher rate of neurovascular complications, consider
orthopedic consultation
REDUCTION METHODS
Traction/Countertraction
CALCIUM
Normal Serum Calcium 8.5-10.5 mg/dL
Need to correct for hypoalbuminemia
Ionized calcium measures ONLY metabolically active
Normal 1.00-1.15 mmol/L
99% total body calcium is mineral component
Remaining 1%
50% bound serum proteins (albumin)
10% serum anions (phosphate, lactate, bicarb)
40% free ionized calcium
HYPOCALCEMIA
Serum Ca < 8.5 mg/dL
Etiologies
PTH deficiency
Vitamin D deficiency
Pseudo-hypoparathyroidism
Calcium chelation
Hyperphosphatemia Alkalosis, Fluoride poisoning
CLINICAL FEATURES
Dependent on serum levels + rapidity of decline
CNS: seizures (focal or generalized)
PNS: paresthesias, muscle weakness, cramps, fasciculations,
tetany, hyperreflexia
Cardiac: decreased contractility, bradycardia, QT
prolongation, digitalis insensitivity
Respiratory: bronchospasm, laryngeal spasm (rare)
Psychiatric: anxiety, depression, confusion, irritability
MANAGEMENT
Check ionized calcium/Perform corrected calculation
IV replacement
Calcium chloride – central line; 10 mL 360 mg elemental Ca
Calcium gluconate – peripheral line; 10 mL 93 mg elemental Ca
Side effects: HTN, N/V, flushing; rare: Bradycardia
Asymptomatic patients: po calcium: 1-4 g per day
HYPERCALCEMIA
Serum Ca > 10.5 mg/dL
Mild symptoms ~ 12 mg/dL
Severe symptoms > 14 mg/dL
Etiologies
Hyperparathyroidism
Malignancy
Meds (thiazides, Lithium, Vit D tox, Vit A tox, Estrogens)
Granulomatous disease
ETIOLOGIES
Malignant disease •Ectopic secretions of parathyroid hormone, multiple myeloma,
cancer metastatic to bone
•Most common: breast, lung, hematologic, kidney, prostate
Endocrine Hyperparathyroidism, multiple endocrine neoplasias,
hyperthyroidism, pheochromocytoma, adrenal insufficiency
Granulomatous disease Sarcoidosis, tuberculosis, histoplasmosis, berylliosis,
coccidioidomycosis
Pharmacologic agents Vitamins A and D, thiazide diuretics, estrogens, milk-alkali
syndrome
Miscellaneous Dehydration, prolonged immobilization, iatrogenic,
rhabdomyolysis, familial, laboratory error
CLINICAL FEATURES
“Moans, Groans, Stones, Psychiatric Overtones”
Neuro: fatigue/weakness, Confusion, ataxia, Coma,
Hypotonia
Cardiovascular: HTN, sinus bradycardia, dysrhythmias EKG
abnormalities: short QT, BBB, Osborn waves
Renal: polyuria, polydipsia, dehydration, nephrolithiasis,
nephrocalcinosis
GI: Nausea, vomiting, anorexia, PUD, pancreatitis,
ileus/constipation
MANAGEMENT
Restore Intravascular Volume
Isotonic solution; 2-5 L per day NS for severe HyperCa
Loop diuretics (“Loops lose calcium”)
Osteoclastic inhibitors
Bisphosphonates, Calcitonin, Zoledronic acid, Hydrocortisone
Correct underlining etiology
INFERIOR SHOULDER DISLOCATION
AKA Luxatio erecta
Less than 1% all shoulder dislocation
Classic presentation:
MAGNESIUM
Normal Serum Mag 1.8 – 3.0 mg/dL
Total body Magnesium
~50% mineral componenet bone
40-50% Intracellular Compartment
1-2% Extracellular space
HYPOMAGNESEMIA
Most common electrolyte deficiency
Serum Magnesium <1.8 mg/dL
Etiologies
Diuretics
Alcoholism
Renal, GI, Endocrine
Pregnancy
Drugs
Congenital Disorders
CLINICAL FEATURES
*Non-specific, inconsistent*
CNS: apathy, irritability, dizziness, seizures, papilledema, coma
PNS: muscle weakness, tremors, hyper-reflexia, tetany,
+Chovstek’s/+Trousseau’s
Cardiovascular: dysrhythmia (SVT, PVC, VT, torsades), EKG
changes
EKG CHANGES HYPOMAGENESEMIA
Most common: Prolong QT, Torsades
Prolonged PR, QRS, QT
ST-T segment abnormalities
T wave flattening and widening
U waves
**Many associated with Hypokalemia**
Google images
MANAGEMENT
Severe symptoms: 4 g IV Magnesium over 30-60 mins
Do Not give bolus – cause bradycardia, heart block
Minor symptoms/asymptomatic: 2 g IV or PO supplement
HYPERMAGNESEMIA
Rare
Etiologies
#1: Impaired Renal Function
Rhabdomyolysis
Tumor Lysis Syndrome
Decreased GI motility – impaired excretion
Exogenous intake
Iatrogenic (Pre-Eclampsia patients)
CLINICAL FEATURES
Correlate with Serum Levels
Early:
Nausea, Vomiting, Weakness, Flushing
>4 mg/dL
Hyporeflexia Loss of reflexes
5-6 mg/dL
Hypotension
EKG changes: QRS wide, QT/PR prolongation
>9 mg/dL
Respiratory depression, coma, complete heart block
MANAGEMENT
Discontinue all exogenous magnesium
IV fluids
Loop diuretics
Severe hypermagnesemia should receive IV Calcium
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