Tint7 Ch 21 Electrolytes Potassium Calcium Magnesium Chloride

Front 1

• Hypermagnesemia is rarely encountered in emergency medicine practice.
• A small elevation in serum concentration has little clinical significance.

• The most common causes for hypermagnesemia:

Back 1

• The most common cause for hypermagnesemia can be found in patients with renal insufficiency or renal failure who ingest [Mg2+]-containing drugs.

• Hypermagnesemia is more commonly seen in the perinatal setting in patients secondary to the treatment of Preeclampsia or Eclampsia.
• Other causes of hypermagnesemia include
o lithium ingestion,
o volume depletion, or
o familial hypocalciuric hypercalcemia (Table 21-21).

Table 21-21 Causes of Hypermagnesemia

• Renal failure
o Acute or chronic

• Increased magnesium load
o Magnesium-containing laxatives, antacids, or enemas*
o Treatment of preeclampsia/eclampsia (mothers and neonates)
o Diabetic ketoacidosis (untreated)*
o Tumor lysis
o Rhabdomyolysis*

• Increased renal magnesium absorption
o Hyperparathyroidism
o Familial hypocalciuric hypercalcemia
o Hypothyroidism
o Mineralocorticoid deficiency, adrenal insufficiency


*Most likely presentation relevant to the ED.

Front 2

• Hypermagnesemia rarely produces symptoms.
• [Mg2+] decreases the transmission of neuromuscular messages and thus acts how?

Back 2

• Hypermagnesemia rarely produces symptoms.
• [Mg2+] decreases the transmission of neuromuscular messages and thus acts as a CNS depressant and decreases neuromuscular activity.

Front 3

• Approximate [Mg2+] causing signs and symptoms can be found in Table 21-22.
o [Mg2+] 2.0–3.0:
o [Mg2+] 3.0–4.0:
o [Mg2+] 4.0–8.0
o [Mg2+] 8.0–12.0:
o [Mg2+] 12.0–15.0:

Back 3

• Approximate [Mg2+] causing signs and symptoms can be found in Table 21-22.
o [Mg2+] 2.0–3.0: Nausea
o [Mg2+] 3.0–4.0: Somnolence
o [Mg2+] 4.0–8.0: Loss of deep tendon reflexes
o [Mg2+] 8.0–12.0: Respiratory depression
o [Mg2+] 12.0–15.0: Hypotension, Heart block, Cardiac arrest

Front 4

Treatment of Hypermagnesemia:

Back 4

EVALUATION AND TREATMENT
• Serum [Mg2+] is usually diagnostic.

• The possibility of Hypermagnesemia should be considered in patients with Hyperkalemia or Hypercalcemia.
• Hypermagnesemia also should be suspected in patients with renal failure, particularly in those who are taking magnesium-containing antacids (Table 21-21).

• The primary treatment available is the immediate cessation of [Mg2+] administration.

• If renal failure is not evident, dilution by IV fluids followed by Furosemide (40 to 80 milligrams IV) may be helpful.

• Calcium directly antagonizes the effects of magnesium;
o severe symptomatic hypermagnesemia can be treated with 5 mL 10% CaCl2 IV over 5 minutes.
• Patients with renal failure may benefit from dialysis using a decreased [Mg2+] bath that lowers serum [Mg2+].

Front 5

• Hypercalcemia is relatively common. It is defined as a
o total [Ca2+] >10.5 milligrams/dL or an
o ionized calcium level >2.7 mEq/L.

Back 5

• Hypercalcemia is relatively common. It is defined as a
o total [Ca2+] ___ milligrams/dL or an
o ionized calcium level ___

Front 6

• More than 90% of Hypercalcemia occurrences are associated with:

Back 6

• More than 90% of occurrences are associated with
o Hyperparathyroidism or
o Malignancy (malignancy being the most likely underlying presentation in the ED).

Front 7

• Table 21-17 Causes of Hypercalcemia:

Back 7

• Table 21-17 Causes of Hypercalcemia

• Malignancy*
o Breast
o Lung (squamous cell cancer)
o Kidney
o Myeloma
o Leukemia

• Endocrinopathies
o Primary Hyperparathyroidism
o Hyperthyroidism
o Pheochromocytoma
o Adrenal Insufficiency
o Acromegaly

• Drugs
o Hypervitaminosis D and A
o Thiazides
o Lithium*
o Hormonal therapy for breast cancer

• Granulomatous disease*
o Sarcoidoses
o Tuberculosis
o Histoplasmosis
o Coccidioidomycosis

• Immobilization

• Miscellaneous
o Paget disease of bone
o Postrenal transplantation
o Recovery from acute renal failure
o Phosphate depletion syndrome


*More likely to be encountered in the ED.

Front 8

• The effects of hypercalcemia can be:

Back 8

• The effects of hypercalcemia can be
o neuromuscular,
o cardiovascular,
o GI,
o renal, and
o skeletal.

Front 9

Hypercalcemia neuromuscular changes

Back 9

• Hypercalcemia Neuromuscular changes include
o decreased sensitivity, responsiveness, and strength of muscular contraction and
o decreased nerve conduction.


• Neurologic
o Confusion
o Apathy, Depression, Stupor
o Decreased memory
o Irritability
o Hallucinations
o Headache
o Ataxia
o Hyporeflexia, Hypotonia
o Mental retardation (infants)


• Neurologic
o Confusion
o Apathy, Depression, Stupor
o Decreased memory
o Irritability
o Hallucinations
o Headache
o Ataxia
o Hyporeflexia, Hypotonia
o Mental retardation (infants)

Front 10

• In mild hypercalcemic states, cardiovascular effects:

Back 10

• In mild hypercalcemic states, the
o conduction of the heart is slowed and
o automaticity is decreased with a
o shortening of the refractory period.
o Increased sensitivity to cardiac glycosides may be seen.

• Cardiovascular
o Hypertension
o Dysrhythmias
o Vascular calcifications
o ECG abnormalities
• QT shortening
• Coving of ST-T wave
• Widening of T wave
• Digitalis sensitivity

Front 11

Hypercalcemia renal effects:

Back 11

• Loss of concentrating ability is the most frequent renal effect of hypercalcemia.
o This is a reversible tubular defect, which results in polyuria and volume depletion even in the presence of thirst.
• Potassium wasting results in hypokalemia in up to one third of patients.
• Nephrocalcinosis and Nephrolithiasis may result from hypercalcemia and be exacerbated by volume depletion.
• As the hypercalcemia persists, increasing microscopic [Ca2+] deposits in the kidney can lead to progressive renal insufficiency.

• Urologic
o Polyuria, Nocturia
o Renal insufficiency
o Nephrolithiasis

Front 12

Table 21-18 Symptoms and Signs of Hypercalcemia:
• General
• Neurologic
• Metastatic Calcification
• Skeletal
• Cardiovascular
• GI
• Urologic

Back 12

Table 21-18 Symptoms and Signs of Hypercalcemia:
• General
o Malaise, weakness
o Polydipsia, dehydration

• Neurologic
o Confusion
o Apathy, Depression, Stupor
o Decreased memory
o Irritability
o Hallucinations
o Headache
o Ataxia
o Hyporeflexia, Hypotonia
o Mental retardation (infants)

• Metastatic Calcification
o Band keratopathy
o Conjunctivitis
o Pruritus

• Skeletal
o Fractures
o Bone pain
o Deformities

• Cardiovascular
o Hypertension
o Dysrhythmias
o Vascular calcifications
o ECG abnormalities
• QT shortening
• Coving of ST-T wave
• Widening of T wave
• Digitalis sensitivity

• GI
o Anorexia, weight loss
o Nausea, vomiting
o Constipation
o Abdominal pain
o Peptic ulcer disease
o Pancreatitis

• Urologic
o Polyuria, Nocturia
o Renal insufficiency
o Nephrolithiasis

Front 13

Hypercalcemia ECG changes:

Back 13

o ECG abnormalities
• QT shortening
• Coving of ST-T wave
• Widening of T wave
• Digitalis sensitivity

Front 14

• Hypercalcemic patients with plasma total [Ca2+] ___ are usually asymptomatic, but
• total [Ca2+] of ___ higher levels can cause a wide variety of symptoms and signs.

Back 14

• Hypercalcemic patients with plasma total [Ca2+] below 12.0 milligrams/dL are usually asymptomatic, but
• total [Ca2+] above 12.0 milligrams/dL higher levels can cause a wide variety of symptoms and signs (Table 21-18).

Front 15

Hypercalcemia treatment:

Back 15

• Treatment for hypercalcemia should be initiated in any symptomatic patient, or if [Ca2+] is above 14 milligrams/dL. Treatment consists of
o volume repletion (with NS),
o decreasing [Ca2+] mobilization from bone, and
o correction of the underlying disorder.
o Up to one third of patients with hypercalcemia have associated Hypokalemia. Hypomagnesemia also is common.

• The use of loop diuretics for malignancy-related hypercalcemia is no longer recommended because
o No direct evidence supports the common practice of using furosemide or other loop diuretic to enhance [Ca2+] elimination.
o Furthermore, diuresis can worsen volume depletion, hypokalemia, and hypomagnesemia.

• Decreased mobilization of [Ca2+] from bone through reduction of osteoclast activity can be accomplished with several medications. Recommendations for initiating the following medications in the ED are generally lacking, but consideration should be given to using them if the patient is symptomatic or the [Ca2+] is >14 milligrams/dL.
o Bisphosphonates, such as Pamidronate, 90 milligrams IV over 24 hours,
o or etidronate, 7.5 milligrams/kg/day IV for 3 consecutive days,
o or zoledronic acid, 4 milligrams IV over 15 minutes, represent the principal support of treatment and work by potent inhibition of osteoclast-mediated bone resorption.

• Calcitonin inhibits bone reabsorption and increases excretion of calcium. Calcitonin 4 units/kg SC, may also be given to patients with severe symptoms.

Front 16

Hyperkalemia is defined as measured serum [K+] of

Back 16

• Hyperkalemia is defined as measured serum [K+] of >5.5 mEq/L.

Front 17

• Hyperkalemia is defined as measured serum [K+] of >5.5 mEq/L.

• The most common cause is:

Back 17

• Hyperkalemia is defined as measured serum [K+] of >5.5 mEq/L.

• The most common cause is Factitious Hyperkalemia due to release of intracellular potassium caused by hemolysis during phlebotomy.

Front 18

Causes of Hyperkalemia

Back 18

Causes of Hyperkalemia

o Pseudohyperkalemia
 Tourniquet use
 Hemolysis (in vitro)*
 Leukocytosis
 Thrombocytosis

o Intra- to extracellular potassium shift
 Acidosis*
 Heavy exercise
 -Blockade
 Insulin deficiency
 Digitalis intoxication
 Hyperkalemic periodic paralysis

o Potassium load
 Potassium supplements
 Potassium-rich foods
 IV potassium
 Potassium-containing drugs
 Transfusion of aged blood
 Hemolysis (in vivo)
 GI bleeding
 Cell destruction after chemotherapy
 Rhabdomyolysis/crush injury*
 Extensive tissue necrosis

o Decreased potassium excretion
 Renal failure*
 Drugs—potassium-sparing diuretics,* -blockade, NSAIDs, angiotensin-converting enzyme inhibitors
 Aldosterone deficiency*
o Selective defect in renal potassium excretion
 Pseudohypoaldosteronism,
 Systemic lupus erythematosus,
 Sickle cell disease,
 Obstructive uropathy,
 renal transplantation,
 type IV renal tubular acidosis

*Frequent or important ED diagnostic considerations.

Front 19

Clinical manifestations of hyperkalemia usually result from ___

Back 19

Clinical manifestations of hyperkalemia usually result from disordered membrane polarization.

Front 20

• Table 21-12 ECG Changes Associated with Hyperkalemia:
o [K+] 6.5–7.5 mEq/L:
o Prolonged PR interval,
o tall peaked T waves,
o short QT interval
o [K+] 7.5–8.0 mEq/L
o Flattening of the P wave,
o QRS widening
o [K+] 10–12 mEq/L
o QRS complex degradation into a sinusoidal pattern

Back 20

ECG Changes Associated with Hyperkalemia:
o [K+] 6.5–7.5 mEq/L:
o Prolonged PR interval,
o tall peaked T waves,
o short QT interval
o [K+] 7.5–8.0 mEq/L
o Flattening of the P wave,
o QRS widening
o [K+] 10–12 mEq/L
o QRS complex degradation into a sinusoidal pattern