CRACKCast E125 – Electrolyte Disorders

In CRACKCast, Featured, Podcast by Adam ThomasLeave a Comment

This episode of CRACKCast covers Rosen’s Chapter 117, Electrolyte Disorders. This episode will help you manage those electrolyte disturbances like the slick medical professional you are! Check out the shownotes for a deeper dive into the material.

Shownotes – PDF Here

Core questions

[1] What are the five most common causes of hyperkalemia?

Box 117.1: “SPARK+”

  1. Spurious elevation
  2. Acidosis
  3. Renal failure (Including nsaids, ACE/ARB)
  4. Kell (Cell) death
  5. Drugs
  • Spurious elevation: Hemolysis due to drawing or storing of the laboratory sample or post–blood sampling leak from markedly elevated white blood cells, red blood cells, or platelets
  • Renal failure: Acute or chronic
  • Acidosis: Diabetic ketoacidosis (DKA), Addison’s disease, adrenal insufficiency, type 4 renal tubular acidosis
  • Cell death: Rhabdomyolysis, tumor lysis syndrome, massive hemolysis or transfusion, crush injury, burn
  • Drugs: Beta-blockers, acute digitalis overdose, succinylcholine, angiotensin-converting enzyme inhibitors, angiotension receptor blockers, nonsteroidal anti-inflammatory drugs (NSAIDs), spironolactone, amiloride, potassium supplementation

[2] Describe the ECG features seen with hyperkalemia. List at least 5.

  1. the peaked T wave,
  2. flattened p wave with prolonged PR interval or
  3. a totally absent P wave,
  4. wide QRS,
  5. and sine wave pattern, portending imminent cardiac arrest

[3] How is hyperkalemia managed? How does each intervention work, and how long do the effects typically last? (Table 117.1)  

Table 117.1. Treatment of Hyperkalemia 

TREATMENT MEDICATION FEATURES
Stabilize cardiac membrane Calcium chloride (10 mL, maximum 20 mL) or calcium gluconate (10 to 30 mL), IV push 1.     For wide QRS, restores the electrical gradient; does not decrease serum potassium

2.     Onset within minutes; lasts 30 to 60 minutes

Shift potassium into cells 1.     Insulin, 10 units, IV push, combined with 100 mL of 50% dextrose, IV push

2.     High-dose nebulized albuterol by face mask (15 to 25 mg by continuous inhalation)

3.     Bicarbonate 50 to 100 mL

4.     Normal saline 100 to 250 mL

1.     Insulin: Onset <15 minutes; maximum effect 30 to 60 minutes (~0.6 mEq/L decrease)

2.     Nebulized albuterol: Onset <15 minutes (0.5 to 1 mEq/L decrease)

3.     If severely acidotic

4.     In conjunction with nephrologist if dialysis dependent

Remove potassium from the body 1.     Hemodialysis

2.     Normal saline and furosemide

3.     Ion exchange resin

1.     Emergently in cardiac arrest, urgently in renal failure; may delay if renal function is normal

2.     In patients with rhabdomyolysis or tumor lysis syndrome with intact urine output, not effective acutely

[4] What are the five most common causes of hypokalemia?

Most common cause in the outpatient world = thiazide diuretics.

The five most common causes of hypokalemia are:

  1. renal losses,
  2. increased nonrenal losses (sweating, diarrhea, vomiting, laxatives)
  3. decreased potassium intake,
  4. intracellular shift,
  5. endocrine etiologies.

[5] Describe the ECG features seen with hypokalemia. List at least 4.

No clear stepwise progression with these findings.

  • Flat T wave
  • U wave
  • Non-specific S-T changes
  • Prolonged QT

[6] How is hypokalemia managed?

It’s not just a benign disorder: in patients with cardiac ischemia or heart failure, even mild to moderate hypokalemia increases the likelihood of cardiac arrhythmias secondary to potassium’s effect on the action potential. So our goal K+ in these groups is between 4-5 mmol/L.

*each 0.3 mEq potassium drop below normal correlates with an approximately 100 mEq total body deficit.*

Replacement:

  • Potassium chloride is the most commonly used supplementation, and 40 to 60 mEq orally every 2 to 4 hours is typically well tolerated.
  • If IV infusion is necessary, potassium chloride can be safely given at a rate of 10 to 20 mEq/hr. In the rare instance when IV repletion is planned at more than 20 mEq/hr, the patient should have continuous cardiac monitoring and central line access established.
  • Hypokalemia is associated with hypomagnesemia, and the severity of the hypokalemia correlates with a similar degree of hypomagnesemia. Magnesium replacement should usually accompany potassium repletion.
    • Unless the patient receives at least 0.5 g/hr of magnesium sulfate along with potassium replacement, potassium will not move intracellularly and the patient will lose potassium through excretion.

Correction of large potassium deficits may require several days, with simultaneous oral and IV replacement.

[7] What are the three main types of hypernatremia? Give 3 examples of each.

By far, the most common cause is a patient with an altered thirst mechanism (elderly, disabled patient) without access to free water.

Hypernatremia can be divided into three physiologic pairings:

  1. hypernatremia with dehydration and low total body sodium,
  2. hypernatremia with low total body water and normal total body sodium,
  3. hypernatremia with increased total body sodium

[1] Double loss:

  • Heatstroke
  • Increased insensible losses: Burns, sweating
  • Gastrointestinal loss: Diarrhea, protracted vomiting, continuous gastrointestinal suction
  • Osmotic diuresis: Glucose, mannitol, enteral feeding

[2] Loss of body water: 

  • Diabetes insipidus
  • Neurogenic
  • Elderly with “reset” osmostat
  • Hypothalamic dysfunction
  • Suprasellar or infrasellar tumors
  • Renal disease
  • Drugs (amphotericin, phenytoin, lithium, aminoglycosides,methoxyflurane)
  • Sickle cell disease

[3] Increased sodium: 

  • Salt tablet ingestion
  • Salt water ingestion
  • Saline infusions
  • Saline enemas
  • IV sodium bicarbonate
  • Poorly diluted interval feedings
  • Primary hyperaldosteronism
  • Hemodialysis
  • Cushing’s syndrome
  • Conn’s syndrome

[8] List four central and four nephrogenic causes of diabetes insipidus.

Box 117.4

Central

  1. Idiopathic
  2. Familial disease
  3. Cancer
  4. Hypoxic encephalopathy
  5. Infiltrative disorders
  6. Post supraventricular tachycardia
  7. Anorexia nervosa

Nephrogenic

  1. Chronic renal insufficiency
  2. Polycystic kidney disease
  3. Lithium toxicity 
  4. Hypercalcemia
  5. Hypokalemia
  6. Tubulointerstitial disease
  7. Hereditary
  8. Sickle cell disease

[9] What are the four broad categories of hyponatremia?

These are the five most common causes.

in adults are therapy with thiazides, the postoperative state the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), psychogenic polydipsia, exercise-associated hyponatremia, and unintentional water intoxication.

Here are the broad categories:

  • pseudohyponatremia,
    • large molecular particles that do not contribute to plasma osmolality relative to sodium.
      • Severe hypertriglyceridemia and
      • hyperproteinemia are two common causes of this condition.
  • hyponatremia with dehydration and decreased extracellular volume,
  • hyponatremia with increased extracellular volume,
  • euvolemic hyponatremia with increased TBW

 

  • Sometimes a fifth category of “dilutional hyponatremia” is added. This occurs with HYPERglycemia – where the extra glucose draws fluid into the intravascular space.

See Box 117.5

[10] Give an example of two clinical conditions for each: hypovolemic, euvolemic and hypervolemic hyponatremia.

  • Hypovolemic hyponatremia = decreased extracellular volume combined with an even greater loss of sodium.
    • GI, skin, urine losses (diuretics)
    • Third spacing – burns, pancreatitis
  • Euvolemic hyponatremia =
    • Water intoxication / psychogenic polydipsia
    • SIADH
  • Hypervolemic hyponatremia water retention exceeds sodium retention. THEY HAVE EDEMA!*
    • “The failures”
      • Heart failure
      • Renal failure
      • Liver failure / cirrhosis

*The fluid retention in these states is secondary to renal hypoperfusion, resulting in increased aldosterone secretion and a decrease in free water excretion.

[11] What are the three most common causes of SIADH?

 

The three most common causes of SIADH are (1) pulmonary lung masses and infections (PNA or TB), (2) CNS disorders, and (3) drugs*

*thiazide diuretics, narcotics, lithium, oral hypoglycemics, barbiturates, and antineoplastics.

Box 117.6: Three most common causes of Inappropriate secretion of antidiuretic hormone

Lung Masses

  1. Cancer (especially small cell)
  2. Pneumonia
  3. Tuberculosis
  4. Abscess

Central Nervous System Disorders

  1. Infection (meningitis, brain abscess)
  2. Mass (subdural, postoperative, cerebrovascular accident)
  3. Psychosis (with psychogenic polydipsia)

Drugs

  1. Thiazide diuretics
  2. Narcotics
  3. Oral hypoglycemic agents
  4. Barbiturates
  5. Antineoplastics

Treatment: free water restriction!

[12] Describe the management of hyponatremia in the following patients:

  • Actively seizing
    • In more severe cases when the sodium value is 120 mEq/L or less and the patient has alterations in mental status, has focal findings, or is seizing, 3% hypertonic saline (513 mEq/L of sodium) is indicated.
      • 100 mL of 3% Saline over 10 mins
  • Euvolemic with acute hyponatremia
    • If altered mental status and Na <120 = hypertonic saline
    • If focal findings = hypertonic saline
    • If asymptomatic:
      • Search for the underlying cause of
        • SIADH*, drugs causing SIADH, adrenal insufficiency, hypothyroidism, etc.
        • Water restriction  
        • *In patients with SIADH, normal saline may cause the serum sodium concentration to fall even more as free water is retained and hypertonic urine is excreted. If a patient is symptomatic because of a rapid decrease in serum sodium concentration, treatment with hypertonic saline is recommended.
  • Hypovolemic with chronic hyponatremia
    • Correct any hypotension / instability with normal saline
    • Slowly correct with IV saline once stable (go slow, 6-8 mmol/L in 24 hrs is safe)
    • Then search for the underlying cause (GI, skin, renal losses; third spacing)
  • Hypovolemic with acute hyponatremia
    • If altered mental status and Na <120 = hypertonic saline
    • If focal findings = hypertonic saline
    • If asymptomatic, but hypotensive
      • IV normal saline resuscitation till no longer hypotensive
      • Search for the underlying cause of the hyponatremia
        • GI, skin, renal losses
        • Third spacing (burns, pancreatitis, rhabdo)
        • Diuretics
      • Probably can continue IV saline with a goal of correcting no more than 10-12 mmol/L in 24 hrs.

[13] What are the five most common causes of hypercalcemia?

80% of cases are due to – malignancy (inpatients) or hyperparathyroidism (outpatients).

Box 117.7: Five Most Common Causes of Hypercalcemia

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

[14] What are the five Most Common Symptomatic Causes of Hypocalcemia Seen in the Emergency Department? 

Box 117.9: Five most common symptomatic causes of hypocalcemia seen in the Emergency department

  • Hyperventilation: Anxiety, sympathomimetics
  • Ethanol abuse, chronic malnutrition: Hypoalbuminemia
  • Massive blood transfusion: More than 10 units
  • Toxins: Hydrofluoric acid, ethylene glycol
  • Severe pancreatitis 

HE Bleeds Pure Acid

[15] What ECG features are seen in hypercalcemia vs. hypocalcemia? How is each managed?

Hypercalcemia Hypocalcemia
ECG features Short QT – (may or may not be present)

**ST elevation – the most common finding (according to Rosen’s)

Bradydyrhythmias

AV block

Atrial fibrillation

VTach

LONG QT

Dysrhythmia

Management Bolus normal saline until perfusion / hemodynamically stable

Continue IV NS at 200-300 ml/hr

Goal 2 L urine output per day

Consider advanced therapies with specialist supervision:

IV bisphosphonates

Calcitonin

Glucocorticoids

Asymptomatic/mild symptoms = use PO calcium carbonate

Symptomatic:

IV calcium chloride through CVC

IV calcium gluconate through good peripheral line

 

 

[16] What are the five most common causes of hypermagnesemia?

Box 117.10: Five Most Common Causes of Hypermagnesemia

  • Iatrogenic: IV administration, dialysate
  • Oral administration: Laxatives, antacids, vitamins, cathartics, dialysate, parental
  • Impaired elimination—hypomotility: Bowel obstruction, chronic constipation
  • Impaired elimination—medications: Anticholinergics, narcotics, lithium therapy
  • Miscellaneous: Hypothyroidism, tumor lysis syndrome, adrenal insufficiency, milk-alkali syndrome

[17]List five clinical manifestations of hypermagnesemia.

Table 117.5: Clinical Effects of Hypermagnesemia

 

EFFECT LEVEL (mg/dL)
Decreased deep tendon reflexes 4 to 5
Hypotension 5 to 7
Respiratory insufficiency 10
Heart block 10 to 15
Cardiac arrest 10 to 24

 

[18] List five common causes of hypomagnesemia?

Five most common ED populations with low Mg.

  • Patients on diuretics
    • Due to loop or thiazide diuretics
  • Malnourished and alcoholic patients
    • Lack of green vegetables, legumes, fruits, shellfish, fresh meat, and cocoa on a regular basis to maintain normal total body magnesium stores.
    • Patients with chronic diarrhea or bowel disease/short gut
  • Patients with hypoKalemia:
    • Both potassium and magnesium are critical to help stabilize the membrane potential, to decrease cell excitability, and for function of the Na+ K+-ATPase pump.
  • Patients With Acute Coronary Artery Disease and Ventricular Arrhythmias
    • Make sure you check and correct any low serum K / Mg levels, otherwise these patients are at high risk for dysrhythmias
  • Patients on certain medications:
    • Long term PPI use, patients with bowel preps for colonoscopy
    • aminoglycosides, amphotericin B, cisplatin, and pentamidine

[19] What are the five most common causes of hyperphosphatemia?

Hyperphosphatemia can occur because of five major pathways:

(1) decreased phosphate excretion

  • Acute and Chronic Renal Failure

(2) excessive phosphate intake

(3) increased renal tubular reabsorption

  • Hypoparathyroidism,
  • vitamin D intoxication,
  • thyrotoxicosis increase renal phosphate reabsorption and may cause elevated phosphate levels.

(4) shift of phosphate from intracellular to extracellular space.

  • rhabdomyolysis, tumor lysis syndrome, and DKA.
  • Make sure you look for the concomitant hypocalcemia!

(5) spurious elevation:

  • hyperproteinemia, such as multiple myeloma, hyperlipidemia,hemolysis, or hyperbilirubinemia.

[20] What the five most common causes of hypophosphatemia in the ED? How do they manifest clinically?

Acute hypophosphatemia is most commonly due to a rapid intracellular shift.

Here are the most common causes seen in ER patients:

  • malnourished with alcohol withdrawal,
  • acute hyperventilation or sepsis
  • patients with DKA or alcohol ketoacidosis in whom reintroduction of insulin and glucose causes phosphate uptake into cells.

Here’s the table of causes from Rosen’s: (Box 117.13)

Decreased Intake or Increased Absorptive States

  1. Chronic alcoholism
  2. Home parenteral nutrition
  3. AIDS
  4. Chemotherapy
  5. Vomiting
  6. Malabsorption syndromes
  7. Secretory diarrhea
  8. Vitamin D deficiency

Hyperventilatory States

  1. Sepsis
  2. Alcohol withdrawal
  3. Salicylate poisoning
  4. Neuroleptic malignant syndrome
  5. Panic attacks
  6. DKA
  7. Hepatic coma

Hormonal and Endocrine Effects

  1. Insulin loading
  2. Glucose loading
  3. Exogenous epinephrine
  4. Hyperparathyroidism

Medicationsa

  1. Diuretics
  2. Chronic antacid ingestion
  3. Steroids
  4. Phosphate binders
  5. Xanthine derivatives
  6. Beta2-agonists

Disease States

  1. Trauma
  2. Severe thermal burns
  3. Acute renal failure
  4. Gout

The symptoms:

Most symptoms don’t appear until it is in the severe range:

Nonspecific complaints including joint pain, myalgias, irritability, and depression.

severe hypophosphatemia can be manifested as seizures, arrhythmias, cardiomyopathy, insulin resistance, acute tubular necrosis, rhabdomyolysis, and acute respiratory failure.

Box 117.14: Clinical Manifestations of Hypophosphatemia

Central Nervous System

  1. Irritability
  2. Confusion
  3. Paresthesias
  4. Depression
  5. Dysarthria
  6. Seizure
  7. Coma

Cardiovascular

  1. Cardiomyopathy
  2. Depressed myocardial contractility
  3. Arrhythmias

Respiratory

  1. Acute respiratory failure
  2. Depressed myocardial contractility

Gastrointestinal

  1. Ileus, dysphagia

Hematologic

  1. Depressed levels of 2,3-diphosphoglycerate and adenosine triphosphate
  2. Leukocyte dysfunction
  3. Hemolysis
  4. Platelet dysfunction

Renal

  1. Acute tubular necrosis
  2. Metabolic acidosis
  3. Hypercalcemia

Endocrine

  1. Insulin resistance
  2. Hyperparathyroidism

WiseCRACKS

[1] What other electrolyte abnormalities are often seen with hypomagnesemia?

  • Hyponatremia
  • Hypokalemia
  • Hypocalcemia

Look at the ECG and correct any long QT!!

[2] How do you estimate the total body water?

Table 117.2 Calculation of Body Water

POPULATION TOTAL BODY WATER
Children and adult men Body weight (kg) × 0.6
Adult women Body weight (kg) × 0.5
Elderly men Body weight (kg) × 0.5
Elderly women Body weight (kg) × 0.45

Sodium deficit = Total body water * (desired Na – pt’s Na) (TBW = 0.6 if male and 0.5 if female)

 

Water deficit in Hypernatremia

FORMULA

FW Deficit (Adult Male) = 0.6 x weight (kg) x (current NA / 140-1)

FW Deficit (Adult Female) = 0.5 x weight (kg) x (current NA / 140-1)

FW Deficit (Elderly Male) = 0.5 x weight (kg) x (current NA / 140-1)

FW Deficit (Elderly Female) = 0.45 x weight (kg) x (current NA / 140-1)

FW Deficit (Child) = 0.6 x weight (kg) x (current NA / 140-1)

 

This post was uploaded and copyedited by Owen Scheirer (@OwenGregg1)

Adam Thomas

Adam Thomas

Adam Thomas is a MedEd re-purpose-r. He cofounded the CrackCast project to fill the obvious gap in current FOAMed. He is a true podcasting supporter, and finds it to be the best way he learns. Currently a resident in the FRCP program at the University of British Columbia.
Adam Thomas
- 6 days ago
Adam Thomas

Latest posts by Adam Thomas (see all)

Chris Lipp
Chris Lipp is one of the founding Fathers for CrackCast and an EM Resident in Victoria, BC. His interests are in sports, exercise, and wilderness medicine. When he isn’t out on one of his accidental 20km trail runs, you can find him jamming with friends, or outdoors, and reading Rosen’s…..