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200

In other patients with mild

and moderate hypophosphatemia, who have evidence of phosphorus deficit, oral

supplementation is the safest and preferred mode of replacement. Skim or low-fat

milk is a convenient source of phosphorus and calcium. Whole milk, because of its

high fat content, can cause diarrhea if a large amount is consumed. Several oral

phosphorus preparations can be used in patients who cannot tolerate milk products.

When hypophosphatemia is severe, as in M.R., or when the patient is vomiting or

unable to take oral medication, parenteral phosphorus replacement is needed.

Several empiric regimens have been evaluated. IV administration of 0.08 to 0.5

mmol/kg body weight of phosphorus over the course of 4 to 12 hours is safe and

effective in restoring the serum phosphorus concentration.

228,229 More aggressive

regimens, such as infusion over the course of 30 minutes to 2 hours, have also been

suggested for critically ill and surgical patients.

230,231 Parenteral phosphorus

replacement should be stopped once the serum phosphorus concentration reaches 2.0

mg/dL and also when oral supplementation is started. In general, no more than 32

mmol (1 g) of phosphorus should be administered IV in a 24-hour period. Regardless

of the regimen used, serum phosphorus, calcium, and magnesium concentrations

should be monitored closely because IV phosphorus administration can induce

hyperphosphatemia quite rapidly, as well as hypocalcemia and hypomagnesemia.

Monitoring of urine phosphorus concentration also helps determine the adequacy of

therapy. Metastatic soft tissue calcification, hypotension, and, depending on the

preparation used, potassium, sodium, or volume overload may occur. This could be

significant in patients such as M.R. who have a history of HF and hypertension.

Therefore, renal function and volume status should be monitored during therapy.

Diarrhea, a common dose-related side effect of oral phosphorus replacement, can be

minimized by diluting the supplement and slowly titrating the dose. Large doses can

also result in metabolic acidosis.

228

Phosphorus can be administered orally in doses of 30 to 60 mmol/day, usually

given in two to four divided doses to minimize GI adverse events, using any

commercially available oral supplement (e.g., Fleet or Neutra-Phos). Fleet PhosphoSoda (5 mL twice daily) delivers 40 mmol/day of phosphorus. Skim milk, the

preferred agent for diluting the supplement, contains approximately 7 mmol of

phosphorus/cup and provides calcium and potassium as well.

In M.R., oral supplementation was not feasible because she had intermittent

diarrhea and vomiting. Potassium phosphate 15 mmol (providing 22 mEq of

potassium) was therefore infused IV in 250 mLof 0.45% saline over the course of 12

hours. The regimen was repeated once until the serum phosphorus concentration

reached 2 mg/dL. Oral supplementation with Fleet Phospho-Soda then was begun by

adding one teaspoonful twice daily to her enteral tube feeding.

Hyperphosphatemia

Refer to the Mineral and Bone Disorders section in Chapter 28, Chronic Kidney

Disease.

MAGNESIUM

Homeostasis

Magnesium is an intracellular cation found primarily in bone (65%) and muscle

(20%). Only 2% of the total body store of 21 to 28 g (1,750–2,400 mEq) is located

in the extracellular compartment. Serum magnesium concentrations, therefore, do not

reflect the total magnesium body store accurately. In healthy adults, the serum

magnesium concentration is 1.5 to 2.4 mEq/L, with approximately 20% of the serum

magnesium bound to proteins.

Magnesium plays an important role in different metabolic processes, particularly

in energy transfer, storage, and utilization. Cation deficiency can impair many ATPmediated energy-dependent cellular processes as well as the action of

phosphatases.

232 Magnesium is necessary for many enzymes involved in the

metabolism of carbohydrate, fat, and protein, as well as RNA aggregation, DNA

transcription, and degradation. The normal operation of many sodium, proton, and

calcium pumps and the regulation of potassium and calcium channels are all

dependent on the availability of intracellular magnesium.

233,234

In addition, adequate

magnesium stores are needed to maintain normal neuronal control, neuromuscular

transmission, and cardiovascular tone.

The average diet in North America contains about 20 to 30 mEq of magnesium.

235

The daily requirement is approximately 18 to 33 mEq for young persons and 15 to 28

mEq for women.

236 Normally, 30% to 40% of the elemental magnesium is absorbed,

primarily in the jejunum and ileum. However, absorption may be increased to 80% in

deficiency states and reduced to 25% during high magnesium intake. In patients with

uremia, GI absorption of magnesium is decreased; however, absorption in the

jejunum can be normalized by physiologic doses of 1α,25-dihydroxyvitamin D3

.

237

In

addition, PTH also modulates magnesium absorption.

238

Magnesium is eliminated primarily by the kidneys; only 1% to 2% of the

endogenous magnesium is eliminated by the fecal route.

182 The magnitude of renal

removal is determined by GFR and tubular reabsorption. Approximately 20% to 30%

of the tubular reabsorption takes place in the proximal tubule, whereas Henle’s loop,

primarily the thick ascending limb, is responsible for up to 65% of the total

reabsorption.

238 Only about 5% to 6% of the filtered magnesium is generally

eliminated in the urine. The extent of magnesium reabsorption changes in parallel

with sodium reabsorption, which is affected by the ECF volume. The renal threshold

for urinary magnesium excretion is 1.3 to 1.7 mEq/L, which is similar to the normal

plasma magnesium concentration. Slight changes in plasma magnesium concentration,

therefore, may substantially alter the amount of magnesium excreted in the urine.

239

Urinary magnesium reabsorption is affected by many factors, including sodium

balance; ECF volume; serum concentrations of magnesium, calcium, and phosphate;

and metabolic acidosis and alkalosis.

240 Concurrent use of loop and osmotic diuretics

will also modulate the reabsorption.

241 Hormones, such as PTH, and possibly

calcitonin, glucagon, and mineralocorticoids may affect the routine maintenance of

magnesium balance as well.

242,243

p. 593

p. 594

Hypomagnesemia

ETIOLOGY

CASE 27-13

QUESTION 1: R.J., a 61-year-old man, is admitted to the hospital because of trauma to his forehead after

falling at home. He has a long history of conditions related to his alcohol abuse: liver disease, ascites, seizures,

pancreatitis, and malabsorption. R.J. complained of abdominal pain, nausea, vomiting, and diarrhea for the past

several days. At admission, R.J. was confused, apprehensive, and combative, and he had marked tremors. He

also had delirium, as evidenced by hallucinations, screaming, and delusions, and he was having multiple tonic–

clonic seizures. The medical record revealed that R.J. had been taking furosemide for the last 2 months.

Pertinent laboratory test results obtained at admission were as follows:

K, 2.5 mEq/L

Magnesium, 0.8 mEq/L

Creatinine, 0.8 mg/dL

Phenytoin was administered for seizure control and R.J. was placed on nasogastric suction. Fluid restriction

was instituted and furosemide therapy was continued to control his ascites. What are the circumstances that

have contributed to R.J.’s hypomagnesemia?

Magnesium body stores are difficult to assess because magnesium is primarily an

intracellular ion, and serum magnesium concentrations do not provide an accurate

indication of the total body load. In fact, cellular magnesium depletion may be

present with low, normal, or even high serum magnesium concentrations.

243,244

Conversely, hypomagnesemia may be seen without a net loss of body magnesium.

Refeeding after starvation will result in increased trapping of magnesium by newly

formed tissue, resulting in hypomagnesemia. Similarly, acute pancreatitis and

parathyroidectomy can cause hypomagnesemia without a net loss of the cation.

245,246

The prevalence of hypomagnesemia in ambulatory and hospitalized patients is

approximately 6% to 12%.

247 The incidence increases to 42% in patients who are

hypokalemic

248 and to 60% to 65% in those under intensive care.

249 Multiple risk

factors and clinical conditions can contribute to the high rate of hypomagnesemia in

critically ill patients.

Magnesium depletion and hypomagnesemia can develop owing to GI, renal, and

endocrinologic causes. Depletion can occur in patients whose dietary magnesium

intake is severely restricted

250 and in those who have protein calorie malnutrition.