Electrolyte disorders

Question 1

Hypernatremia

Answer 1

Serum sodium above 145. Usually due to free water loss rather than sodium gain

Question 2

History and PE for HyperNa

Answer 2

1) Presents with thirst (due to hypertonicity) as well as with oliguria or polyuria (depending on etiology)
2) Neurologic symptoms include AMS, weakness, focal neuro deficits, and seizures
3) Exam reveals doughy skin and signs of volume depletion

Certain patients (infants, intubated patients, those with AMS) may not drink enough water to replace insensible losses. This can cause or worsen hypernatremia

Question 3

Causes of hyperNa

Answer 3

the 6 Ds

1) Diuresis
2) Dehydration
3) Diabetes Insipidus
4) Docs (iatrogenic)
5) Diarrhea
6) Disease (kidney, sickle cell)

Question 4

dx of hyperNa

Answer 4

Assess volume status by conducting clinical exam and measuring urine volume and osmolality

1) Hypertonic Na gain: Due to hypertonic saline/tube feeds or increased aldosterone (suppresses ADH)
2) Pure water loss: Due to central or nephrogenic DI. Characterized by large volumes of dilute urine. Do not neglect dermal and respiratory insensible losses
3) Hypotonic fluid loss: Due to low intake, diuretics, intrinsic renal disease, GI loss (diarrhea), burns, and osmotic diuresis (mannitol, glucose in DKA, urea with high protein feeds)

Question 5

Tx of hyperNa

Answer 5

1) Treat underlying causes and replace the free water deficit depending on volume status.
a) hypovolemic: use D5W. If vital signs are unstable use isotonic saline (0.9) before correcting free water deficits
b) Euvolemia: use hypotonic fluids - D5W or 0.45 Saline
c) Hypervolemia: use combo of diuretics and D5W to remove excess sodium
2) Correction of chronic hypernatremia (more than 36-48h) should be accomplished gradually over 48-72h to prevent neurologic damage secondary to cerebral edema (high to low your brain will blow)

Question 6

Hyponatremia

Answer 6

Serum sodium less than 135. Almost always due to high ADH

Question 7

History and physical for hypoNa

Answer 7

1) May be asymptomatic or may present with confusion, lethargy, muscle cramps, hyporeflexia, and nausea
2) Can progress to seizures, coma, or brainstem herniation

Question 8

Dx of hypoNa

Answer 8

Hyponatremia can be categorized according to serum and urine osmolality as well as by volume status (clinical exam).

High osmolality (above 295) = hyperglycemia, hypertonic infusion (mannitol)

Normal (280-295) = hypertriglyeridemia, paraproteinemia (pseudohyponatremia)

Low (below 280) = Applies to majority of cases. Hypotonic etiologies.

Question 9

Hyponatremia diagnostic algorithm

Answer 9

1) First you look at serum osmalality. If high it’s hypertonic. You then check glucose. Causes could be glucose, mannitol or contrast agents. If isotonic measure glucose, lipids, protein. Causes are hyperlipidemia, hyperproteinemia, glucose and mannitol.
2) If low serum osmolality we have hypotonic case. Next thing we do is clinically assess extracellular fluid volume.
3) If ECF volume is low, we have hypovolemic hypotonic hypoNa. Check Urine Na. If it is below 10, causes include GI loss (diarrhea, vomit, NG suction), third spacing, and skin losses (burns). If urine Na is above 10 causes include diuretics, urinary obstruction, adrenal insufficiency, bicarbonaturia (RTA, metabolic alkalosis)
4) If ECF volume is normal causes include psychogenic polydipsia, SIADH, drugs, hypothyroid, glucocorticoid deficiency
5) If ECF is high we measure urine Na. If it is below 10, causes are cirrhosis, CHF and nephrotic syndrome. If urine sodium is above 10, causes are acute kidney injury or chronic renal failure

Question 10

Tx of hypoNa

Answer 10

Treat according to volume status

1) Hypervolemia - water restriction. Consider diuretics. Cortisol replacement with adrenal insufficiency. Thyroid replacement with hypothyroid
2) Euvolemia - water restriction
3) Hypovolemia - replete volume with NS

Chronic (more than 72h) should be corrected slowly (no more than 0.5 mEq per L per hr) in order to prevent central pontine myelinolysis (paraparesis/quadriparesis, dysarthria, and coma)

Question 11

When do you consider hypertonic saline in treatment of hypoNa?

Answer 11

Only when patient has seizures due to hypoNa, and when serum Na is less than 120

In most cases, NS is best

Question 12

Hyperkalemia

Answer 12

Serum potassium over 5. Etiologies:

1) Spurious: Hemolysis of blood samples, fist clenching during blood draws, delays in sample analysis, extreme leukocytosis or thrombocytosis
2) Lower excretion: Renal insufficency, drugs (spironolactone, triamterene, ACEIs, trimethoprim, NSAIDs), hypoaldosteronism, type 4 RTA, calcineurin inhibitors
3) Cellular shifts: Cell lysis, tissue injury (rhabdo), insulin deficiency, acidosis, drugs (succinylcholine, digitalis, arginine, B-blockers), exercise, resorption of blood (GI bleeding, hematomas)
4) Iatrogenic

Question 13

History and physical of hyperK

Answer 13

May be asymptomatic or may present with nausea, vomiting, intestinal colic, areflexia, weakness, flaccid paralysis, arrhythmias, and parasthesias

Question 14

Dx of hyperK

Answer 14

1) Confirm hyperK with a repeat blood draw. In setting of extreme leukocytosis or thrombocytosis, check plasma potassium
2) ECG findings include tall, peaked T waves; wide QRS; PR prolonged; and loss of P waves. Can progress to sine waves, VFib and cardiac arrest

Question 15

Treating hyperK

Answer 15

C BIG K

Calcium
Bicarb
Insulin
Glucose
Kayexalate

1) Values above 6.5 or ECG changes (esp PR prolongation or wide QRS) require emergent treatment
2) First step is always to give calcium gluconate for cardiac cell membrane stabilization (it also has quickest onset of a few minutes)
3) Then give bicarb and/or insulin and glucose to temporarily shift K into cells
4) B-agonists (albuterol) promote cellular reuptake of K
5) Eliminate K from diet with IV fluids
6) Kayexalate (sodium polystyrene sulfonate) to remove K from body. Contraindications include ileus, bowel obstruction, ischemic gut, or pancreatic transplants (can cause bowel necrosis)

Loop diuretics can be used for increasing urinary excretion of K

Dialysis is appropriate for patient with renal failure or for severe, refractory cases.

Question 16

What things bring K into ICF from ECF?

Answer 16

1) Insulin
2) B-agonists
3) Alkalosis

Question 17

What brings K out of ICF into ECF?

Answer 17

1) Hyperosmolarity
2) Exercise
3) Cell lysis
4) Acidosis

Question 18

HypoK

Answer 18

Serum K less than 3.6. Etiologies:

1) Transcellular shifts causing K to move into cells from ECF
2) GI losses - diarrhea, chronic laxative abuse, vomiting, NG suction
3) Renal losses - diuretics (loop or thiazide), primary mineralocorticoid excess or secondary hyperaldosteronism. Low circulating volume. Bartter’s and Gitelman’s syndromes, drugs (gentamicin, amphotericin), DKA, hypoMg, type 1 RTA (defective distal H secretion) and polyuria

Question 19

Drugs that cause HypoK

Answer 19

1) Diuretics (loop or thiazide)
2) Gentamicin
3) Amphotericin

Question 20

Drugs that cause HyperK

Answer 20

1) spironolactone
2) triamterene
3) ACEIs
4) trimethoprim
5) NSAIDs
6) Calcineurin inhibitors
7) succinylcholine
8) digitalis
9) arginine
10) B-blockers

Question 21

History and physical for hypoK

Answer 21

Presents with fatigue, muscle weakness or cramps, ileus, hypotension, hyporeflexia, paresthesias, rhabdo, and ascending paralysis

Question 22

Dx of hypoK

Answer 22

1) 24h or spot urine K may distinguish renal from GI losses
2) ECG may show T wave flattening, U waves (additional wave after T wave), and ST depresion, leading to AV block and later arrest
3) Consider RTA in setting of metabolic acidosis

Patients with metabolic alkalosis, hypoK and normal BP likely have one of the following conditions:

1) Surreptitious vomiting
2) Diuretic abuse
3) Bartter’s
4) Gitelman’s

Question 23

Tx of hypoK

Answer 23

1) Treat underlying disorder
2) Oral and/or IV K repletion. Do not exceed 20 mEq per L per hr
3) Replace Mg as this deficiency complicates K repletion
4) Monitor ECG and plasma K levels frequently during replacement

Question 24

Digitalis and K levels

Answer 24

Can cause hyperK on its own

On the flip side, hypoK sensitizes the heart to digitalis toxicity since K and digitalis compete for same sites on Na/K pump.

If a patient is on digitalis, monitor K levels closely

Digitalis can cause high K. Low K can cause toxicity.

Question 25

HyperCa

Answer 25

Serum calcium above 10.2. Most common causes are hyperparathyroidism and malignancy (breast, SCC, MM). Other causes are CHIMPANZEES

Calcium supplementation
Hyperparathyroidism/Hyperthyroidism
Iatrogrenic (thiazides, parenteral nutrition), Immobility (esp in ICU)
Milk - alkali syndrome
Paget's disease
Adrenal insufficiency/Acromegaly
Neoplasm
Zollinger-Ellison (MEN 1)
Excess vitamin A
Excess vitamin D
Sarcoidosis and other granulomatous disease

Question 26

History and PE for HyperCa

Answer 26

Usually asymptomatic, but may present with bones (osteopenia, fractures), stones (kidney stones), abdominal groans (anorexia, constipation), and psychiatric overtones (weakness, fatigue, AMS)

Question 27

Dx of hyperCa

Answer 27

Order a total/ionized calcium, albumin, phosphate, PTH, PTHrP, vitamin D, and ECG (may show a short QT interval)

Question 28

Tx of hyperCa

Answer 28

1) IV hydration followed by furosemide to increase calcium excretion
2) Calcitonin, bisphosphonates (pamidronate), glucocorticoids, calcimimetics, and dialysis are used for severe or refractory cases. Avoid thiazide diuretics, which increase tubular reabsorption of calcium

Question 29

Hypocalcemia

Answer 29

Serum calcium less than 8.5. Etiologies include

1) hypoparathyroidism (post surgical, idiopathic)
2) malnutrition
3) HypoMg
4) Acute pancreatitis
5) Vitamin D deficiency
6) Pseudohypoparathyroidism

In infants, consider DiGeorge (tetany shortly after birth; absence of thymic shadow)

Classic case is a patient who develops cramps and tetany following thyroidectomy

Question 30

History and physical for hypoCa

Answer 30

1) Presents with abdominal muscle cramps, dyspnea, tetany, perioral and acral parasthesias, and convulsions
2) Facial spasm elicited from tapping of the facial nerve (Chvostek’s sign) and carpal spasm after arterial occlusion by BP cuff (Trousseau’s sign) are classic findings that are most commonly seen in severe hypocalcemia

Question 31

Dx of hypoCa

Answer 31

1) Order an ionized Ca, Mg, PTH, albumin, 25-OH vit D, and 1,25-OH Vit D. If patient is postthyroidectomy, review the operative note to determine if there was any potential damage to parathyroid glands
2) ECG may show a prolonged QT interval

Serum calcium levels may be falsely low in hypoalbuminemia. Check ionized calcium

Question 32

Tx of hypoCa

Answer 32

1) Treat the underlying disorder
2) Mg repletion
3) Administer oral calcium supplements; give oral and IV calcium for severe symptoms

Question 33

HypoMg

Answer 33

Serum Mg less than 1.5. Etiologies:

1) Reduced intake: Malnutrition, malabsorption, short bowel syndrome, TPN
2) Increased loss: Diuretics, diarrhea, vomiting, hyperCa, alcoholism
3) Miscellaneous: DKA, pancreatitis, ECF volume expansion

Alcoholics are the most common patient population with low Mg

Question 34

History and exam for hypoMg

Answer 34

In severe cases, symptoms may include hyperactive reflexes, tetany, paresthesias, irritability, confusion, lethargy, seizures, and arrhythmias

Question 35

Dx of hypoMg

Answer 35

1) Labs may show concurrent hypoCa and hypoK

2) ECG may reveal prolonged PR and QT intervals

Question 36

Tx of hypoMg

Answer 36

1) IV and oral supplements

2) HypoK and hypoCa will not correct without Mg correction