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”

4 ELECTROLYTES

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

#1 CAUSE HYPERKALEMIA

Error in collection

Redraw

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+

Hyperkalemia Or STEMI?

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

EKG FINDINGS HYPOKALEMIA

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

TAKE HOME MESSAGE

Hypokalemia = Hypomagnesemia

SHOULDER REDUCTIONS

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)

REDUCTION TECHNIQUES

Hennepin Technique Stimson Technique

Scapular Manipulation Traction-Countertraction

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

DIAGNOSTIC STUDIES

Serum Sodium

Urine sodium

Serum osmolarity

Urine osmolarity

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

Google images, keyword: calcium homeostasis

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

CHVOSTEK’S SIGN

Twitching of ipsilateral facial muscles when tapping facial nerve

Google images

TROUSSEAU’S SIGN

Carpal spasm with BP inflated 20 mmHg above SBP for 3 minutes

Google images

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

EKG CHANGES CALCIUM

HYPERCALCEMIA EKG

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

DR. COREY SLOVIS

QUESTIONS

REFERENCES

Rosen’s Emergency Medicine, 8th Edition, 2013

Tintinalli’s Emergency Medicine, 7th Edition, 2010

Access Emergency Medicine via SLADEN library

Reichman et al. Emergency Medicine Procedures

Google images

Dr. Corey Slovis, electrolyte emergencies lectures

EMRAP