Sketchy IM - Electrolytes
Sketchy IM - Electrolytes
Hypernatremia
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Hypernatremia = serum sodium > 145 mEq/L (ultimately represents a net LOSS of free
water compared to serum sodium)
Hypernatremia = serum sodium > 145 mEq/L (ultimately represents a net LOSS of free
water compared to serum sodium)
Elderly patients and very young patients are most at risk of hypernatremia due to lack of
access to water (very young, very old, immobilized, long term care facilities) or loss of thirst
response (dementia); patients with intact thirst response and access to fresh water should
not develop hypernatremia, as high sodium stimulates thirst response ( → increased free
water intake), and ADH release ( → kidneys preserve free water)
Chronic hypernatremia (lasting >48 hours) may be asymptomatic or present with very mild,
nonspecific symptoms
Hypernatremia causes osmotic fluid to shift out of brain → decreased brain volume
(shrinkage)
Osmotic fluid loss of brain volume → intracranial hemorrhages (subdural and intracerebral)
due to venous rupture
Osmotic fluid shifting out of brain → osmotic demyelination due to osmotic destruction of
myelin sheath cells (oligodendrocytes)
Dehydration (net loss of free water instead of loss of volume) causes confusion, lethargy,
hypotension, tachycardia, poor skin turgor, dry mucous membranes, and delayed capillary
refill
Unreplaced hypotonic fluid loss (e.g. GI losses (vomiting, diarrhea, NG tube suction), skin
losses (excessive sweating, burns) = extrarenal cause of hypernatremia
Lack of access to water (very elderly or very young, AMS, dementia, immobilization, thirst
impairment) = extrarenal cause of hypernatremia
Sodium overload (e.g. sodium poisoning, hypertonic saline use) = extrarenal cause of
hypernatremia
Peeing and drinking with nightcap:
Lesson
Sodium Abnormalities
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Candy trapeze:
Raspberry sorbet:
Causes of isotonic hyponatremia = irrigation with isotonic glycine and/or sorbitol (during
urologic or gynecologic surgery)
For hypovolemic hyponatremia, order a urine Na+ to differentiate between extrarenal and
renal losses
#1 adrenal beanie:
Lesson
Sodium Abnormalities
2/8
Fishbone
Fishbone:
Honey:
Tall man:
Chicken wings:
Acute hyponatremia requires faster correction rate (4 to 6 mEq/L over a few hours) to
improve neurologic symptoms and prevent brain herniation
Max correction rate for chronic hyponatremia patients with mild to moderate symptoms = 0.5
mEq/L/hr
Potassium Abnormalities
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“5imian 5afari”
Normal potassium level is approx 3.5 - 5 mEq/L; Hyperkalemia is a serum potassium ≥ 5.5
mEq/L and symptomatic hyperkalemia usually occurs ≥ 6.5
“5imian 5afari”:
Normal potassium level is approx 3.5 - 5 mEq/L; Hyperkalemia is a serum potassium ≥ 5.5
mEq/L and symptomatic hyperkalemia usually occurs ≥ 6.5
Metabolic acidosis can result from hyperkalemia secondary to reduced urinary ammonium
excretion
Hyperkalemia can cause cardiac arrhythmias including bradycardia, AFib/VFib and asystole,
as well as muscle weakness that can progress to ascending flaccid paralysis
EKG changes seen in hyperkalemia include peaked T waves, shortening of QT, QRS
widening and progression to a sine wave
Metabolic acidosis will cause hydrogen to move into the cell, and potassium to move out into
the serum which can lead to hyperkalemia
Torn pant:
Muted beta-bugle:
Beta blockers, digoxin toxicity, calcineurin inhibitors and succinylcholine can all lead to
hyperkalemia
DJ Foxglove mixtape:
Beta blockers, digoxin toxicity and succinylcholine can all lead to hyperkalemia
Candy key:
Dominoes:
Potassium Abnormalities
Hyperkalemia: Management
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Pseudohyperkalemia can result from technique used during lab draw (drawing from line near
potassium infusion, hemolysis, prolonged tourniquet, delayed processing, sample cooling) or
elevated platelets or WBC
Pseudohyperkalemia can result from technique used during lab draw (drawing from line near
potassium infusion, hemolysis, prolonged tourniquet, delayed processing, sample cooling) or
elevated platelets or WBC
Continuous cardiac monitoring and frequent EKGs are essential to monitor cardiac rhythm
and morphology changes
Labs (assess renal function, WBC, PLTs, glucose, calcium level). Also consider specific
situations (digoxin level, CPK/myoglobin if rhabdomyolysis suspected, uric acid if tumor lysis
suspected, and aldosterone if mineralocorticoid deficiency suspected
Monkeys with 6.5-shaped tails:
First step is to stabilize cellular membrane with IV calcium; generally calcium gluconate is
preferred as it can be given peripherally
Insulin shifts potassium into cells and glucose decreases likelihood of hypoglycemia
Beta bugle:
Beta-2 agonists (albuterol, for example) shifts K into cells by increasing Na-K ATPase activity
In patients with metabolic acidosis, sodium bicarbonate ↑pH & activates Na+-K+-pump
Thiazide & loop diuretics; potassium wasting diuretics remove potassium from body
Zirconium earring:
Sodium zirconium cyclosilicate (GI cation exchanger) is preferred over older polystyrene
sulfonate which is less effective, and can cause colonic necrosis
If hyperkalemia is mild or chronic, less urgent correction needed, may consider diet and
medication adjustment (trials of diuretics or chronic GI cation exchangers)
Lesson
Potassium Abnormalities
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Hypokalemia <3.5 mEq/L (normal reference range for potassium is 3.5 - 5 mEq/L) and
severe hypokalemia is less than 2.5 mEq/L
Hypokalemia <3.5 mEq/L (normal reference range for potassium is 3.5 - 5 mEq/L) and
severe hypokalemia is less than 2.5 mEq/L
Ileus can occur with hypokalemia and can result in abdominal distention, abdominal pain,
constipation, nausea and vomiting
More profound hypokalemia can lead to more severe muscular symptoms including flaccid
paralysis, hyporeflexia and respiratory depression secondary to weakness
Heart beating out of chest:
Hypertension and various arrhythmias can occur with hypokalemia including PACs/PVCs,
bradycardia, junctional tachycardias, Vtach/Vfib and Torsades de pointe
Transcellular shift is a way potassium leaves the serum and moves into the cell via the Na-
K-ATPase pump
Insulin causes potassium to be moved inside the cell by directly stimulating the Na-K-
ATPase pump
Beta-bugle:
Increased beta adrenergic activity causes potassium to shift intracellularly. Examples include
medications like albuterol, ephedrine, pseudoephedrine
Hypokalemic periodic paralysis is an inherited or acquired disorder that can cause sudden
recurrent attacks of generalized muscle weakness secondary to rapid intracellular shift of
potassium; severe cases can be fatal
Domino:
Vine bowtie:
Potassium Abnormalities
Hypokalemia: Management
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EKG vine
EKG vine:
Candy:
Fishbone:
Magazine:
Obtaining a 24-hr urine K collection will help distinguish between renal causes vs other
causes (transcellular shift, GI losses)
Higher pool of yellow water:
In the setting of metabolic acidosis & ↑urinary potassium, hypokalemia may be due to renal
tubular acidosis, DKA or a carbonic anhydrase inhibitor
In the setting of metabolic acidosis & ↓ urinary potassium, hypokalemia may be due to
diarrhea; consider infectious diarrhea, laxative abuse, villous adenoma, VIPoma
Metabolic alkalosis & ↑ urinary potassium can indicate hypokalemia is due to inherited
tubulopathies (specifically Bartter and Gitelman) or due to loop and thiazide diuretics
Metabolic alkalosis & ↑ urinary potassium with ↑ BP may indicate the cause of hypokalemia
is due to excess mineralocorticoids (hyperaldosteronism, Cushings) or renovascular disease
Metabolic alkalosis & ↓urinary potassium may indicate the cause of hypokalemia is vomiting;
could be due to NG tube losses, bulimia, infectious vomiting
Potassium repletion can be PO or IV, will raise serum potassium 0.1 mEq/L for every 10
mEq given and should be accompanied by magnesium repletion, if indicated
In DKA, K level must be >3.3 before insulin is given; additional potassium supplementation
should occur concurrently
Calcium Abnormalities
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The majority of hypercalcemia is found incidentally, and patients are either asymptomatic or
minimally symptomatic
The majority of hypercalcemia is found incidentally, and patients are either asymptomatic or
minimally symptomatic
Kidney-shaped stone:
Brain bandana:
Lesson
Calcium Abnormalities
2/8
Inventory checklist:
Employee album:
Order albumin to calculate total corrected calcium; for every 1 g drop in albumin below 4
g/dL → add 0.8 mg/dL to the measured total calcium
Standing PthD:
#1 ribbon:
Urine calcium < 100 mg/day on 24 hour urinary calcium excretion test → FHH
PTHrP kid:
Blood-red crab:
Causes of PTH-independent hypercalcemia = humoral hypercalcemia of malignancy (↑
PTHrP); e.g. squamous cell carcinomas of lung, head, or neck, breast, ovarian, renal, and
bladder carcinomas
Bone-breaking crab:
1, 25 - Calcitron robot:
Soccer ball:
Lesson
Calcium Abnormalities
Hypercalcemia: Management
2/8
Most common cause of hypercalcemia = high PTH from primary hyperparathyroidism 2/2
parathyroid adenoma
Most common cause of hypercalcemia = high PTH from primary hyperparathyroidism 2/2
parathyroid adenoma
Most common cause of hypercalcemia = high PTH from primary hyperparathyroidism 2/2
parathyroid adenoma
Scalpel scissors:
14 L milk bottle:
“C-tones”:
“To Donate”:
“Dialyzer”:
Patients with severe hypercalcemia and underlying renal insufficiency or heart failure should
receive hemodialysis
Shriveled kidney-shaped plate:
Patients with severe hypercalcemia and underlying renal insufficiency or heart failure should
receive hemodialysis
Patients with severe hypercalcemia and underlying renal insufficiency or heart failure should
receive hemodialysis
Lesson
Calcium Abnormalities
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Free ionized calcium is active; Bound calcium is inactive and is mostly bound to albumin
(small amount bound to phosphate, citrate)
Boxed up milk:
Free ionized calcium is active; Bound calcium is inactive and is mostly bound to albumin
(small amount bound to phosphate, citrate)
Alkalosis promotes calcium binding; the higher the amount of bound calcium, the lower the
ionized “free” active calcium
For every 1 gram below normal albumin value (4 gm/dL), add 0.8 to the calcium level to
calculate corrected calcium or use the following equation: Corrected Calcium mg/dL =
Serum calcium + (0.8 x (4 - albumin level))
Stunned kid:
Hypocalcemia can cause Chvostek’s sign which is contraction of facial muscles when the
facial nerve is tapped just in front of the ear
Hand of clown:
Trousseau’s sign is the resulting carpopedal spasm that occurs when the upper arm is
compressed in patients with hypocalcemia
Q u a l i T y sign:
The most common cause of hypocalcemia with LOW parathyroid hormone is surgical
damage, radiation, or removal the parathyroid gland; autoimmune destruction is the second
most common cause; genetic abnormalities and infiltrative diseases are less common
causes
Door broken in antibody Y shape:
The most common cause of hypocalcemia with LOW parathyroid hormone is surgical
damage, radiation or removal the parathyroid gland; autoimmune destruction is the second
most common cause; genetic abnormalities and infiltrative diseases are less common
causes
Lesson
Calcium Abnormalities
Hypocalcemia: Management
2/8
Calculate corrected calcium: obtain albumin level, then for each 1 g/dL decrease in albumin
below 4 g/dL, add 0.8 mg/dl to calcium level
Calculate corrected calcium: obtain albumin level, then for each 1 g/dL decrease in albumin
below 4 g/dL, add 0.8 mg/dl to calcium level
Q u a l i T y sign:
Obtain EKG to rule out QT prolongation
Selfie picture:
IV calcium gluconate is less likely to cause tissue necrosis, and can be given via peripheral
IV so is preferred, but contains less elemental calcium (Ca gluconate 1 gram = 90mg
elemental calcium)
IV calcium chloride carries risk of tissue necrosis if extravasation occurs but has higher
concentration of elemental Ca (Ca chloride 1 gm = 270 mg elemental calcium)
“FortifieD” carton:
Non-emergent oral calcium and Vit D is adequate for asymptomatic or mild hypocalcemia
Lesson