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With hyperkalemia, especially if the patient is asymptomatic and the EKG is normal, you should wonder whether the lab specimen is hemolyzed. Hemolysis causes a false'hyperkalemia. Repeat the test.

Signs and symptoms may include weakness or paralysis, but the most important (and most tested) effects are cardiac, EKG changes (in order of increasing potassium value) include tall, peaked T waves; widening of QRS; PR interval prolongation; loss of P waves; and a sine wave pattern. Arrhythmias include asystole and ventricular fibrillation.

Common causes of hyperkalemia include renal failure (acute or chronic), severe tissue destruction, hypoaldosteronism (watch for hyporeninemic hypoaldosteronism in diabetes), medications (potassium-sparing diuretics, beta blockers, nonsteroidal anti-inflammatory drugs, or ACE inhibitors), and adrenal insufficiency (associated with low sodium and low blood pressure).Try stopping all implicated medications.

The best method of therapy is oral (decreased intake, sodium polystyrene resin). If, however, potassium is very high (> 6.S) and/or cardiac toxicity is apparent (more than peakedT-waves), immediate IV therapy is needed. First give calcium gluconate, which is cardioprotective, even though it does not change potassium levels.Then give sodium bicarbonate (alkalosis causes potassium to shift inside cells) and glucose with insulin, which also forces potassium inside cells. If the patient has renal failure or initial treatment is ineffective, prepare to institute dialysis emergently.

Plypocalcemia produces neurologic findings, the most tested of which is tetany. Tetany is evidenced by tapping on the facial nerve to elicit contraction of the facial muscles (Chvostek's sign) or applying a tourniquet or blood pressure cuff and inflating it to elicit hand muscle (carpopedal) spasms (Trousseau's sign). Other symptoms are depression, encephalopathy, dementia, laryngospasm, and convulsions. EKG shows QT interval prolongation.

Common causes:

a DiGeorge's syndrome (tetany shortly after birth, absent thymic shadow)

* Renal failure (because of the kidney's role in vitamin D metabolism)

■ Hypoparathyroidism (watch for posttbyroideetomy patients; all four parathyroids may have been accidentally removed)

» Vitamin D deficiency a Pseudohypoparathyroidism (short fingers, short stature, mental retardation, and normal levels of parathyroid hormone |PTH| with end organ unresponsiveness to PTH) a Acute pancreatitis « Renal tubular acidosis

Important points:

1. Hypoprotei.nem.ia of any etiology may cause hypocalcemia because the protein-bound fraction of calcium will be decreased. In this instance, however, the patient is asymptomatic:, because the ionized (unbound) fraction of calcium is unchanged.

2. Hypomagnesemia of any cause makes it difficult to correct the hypocalcemia until die by poniagiieseuua is also corrected.

3. Rickets and osteomalacia are the skeletal effects of vitamin D deficiency in children and adults, respectively.

4. Alkalosis may cause symptoms similar to hypocalcemia because of effects on the ionized fraction of calcium. Treat by correcting the pH.

5. Phosphorus and calcium levels are usually in opposite directions, and derangements in one may cause problems with the other, In. renal failure, therefore, you should not only raise calcium but also restrict phosphorus and give P04-binding agents, such as alu milium hydroxide.

Hypercalcemia is usually asymptomatic and discovered by routine labs. When symptoms are present, remember "bones, stones, groans, and psychiatric overtones" (bone changes such as osteopenia or pathologic fractures; kidney stones and polyuria; abdominal pain, anorexia, constipation, ileus, nausea, vomiting; depression, psychosis, del.iriu.ro, and confusion). EKG shows QT interval shortening.

Causes. Hypercalcemia in outpatients is due most commonly to hyperparathyroidism. in inpatients, the most common cause is malignancy. Other causes include vitamin A or D intoxication, sarcoidosis, thiazide diuretics, familial hypocaiciuric hypercalcemia (look lor low urinary calcium, which is rare with hypercalcemia), and immobilization. Hyperprotemenua of any cause may cause hypercalcemia because of an increase in the protein bound fraction of calcium, but the patient is asymptomatic because the ionized (unbound) fraction is unchanged.

Treatment. First, give IV fluids. Once the patient is well hydrated, give furosenh.de to cause calcium diuresis (thiazides are contraindiait«!). Other treatments include phosphorus administration (oral; IV is rarely used because it is dangerous), calcitonin, dipiiosphonates (e.g., etidronate, often used in Paget's disease), plicamycin, prednisone (especially for malignancy-induced hypercalcemia), and gallium nitrate.

Note; Severe prolonged hypercalcemia may cause nephrocalcinosis and renal failure from calcium salt deposits in kidney.

Hypomagnesemia is seen most often in alcoholics. Signs and symptoms, which include EKG changes and tetany, are similar to those of hypocalcemia, Hypomagnesemia is notorious because it makes hypokalemia and hypocalcemia difficult to correct. Treat: with, oral replacement.

Hypermagnesemia almost al ways is iatrogenic in pregnant patients treated for preeclampsia (but may also be seen in patients with renal failure). In patients treated with magnesium sulfate, check for decreased deep- tendon reflexes, hypotension, and respiratory depression.

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