|The Merck Manual of Medical Information--Home Edition
|Section 12. Disorders of Nutrition and Metabolism
Salts are simple chemical compounds made up of atoms that carry either a positive or a negative electrical charge. For example, table salt (sodium chloride) is made up of positively charged sodium and negatively charged chloride atoms. Sodium chloride forms crystals when it's dry but, like many other salts found in the body, readily dissolves in water.
When a salt dissolves in water, its components exist separately as charged particles called ions. These dissolved, charged particles are collectively known as electrolytes. The level (concentration) of each electrolyte in a solution of dissolved salts can be measured and is generally expressed as the amount in milliequivalents (mEq) per volume of solution (usually per liter).
Major Electrolytes in the Body
|Positively Charged||Negatively Charged|
Phosphates (HPO4= and H2PO4-)
Electrolytes are dissolved in the three major compartments of body water (see page 664 in Chapter 136, Water Balance): the fluid within the cells, the fluid in the space surrounding cells, and the blood (electrolytes are actually dissolved in the serum, or fluid part of blood). The normal concentrations of electrolytes in these fluids vary. Some electrolytes are found in high concentrations inside cells and in low concentrations outside them. Other electrolytes are found in low concentrations inside cells and in high concentrations outside them.
To function properly, the body must maintain the concentration of electrolytes in each of these compartments within very narrow limits. It does so by moving electrolytes into or out of cells. The kidneys filter the electrolytes in the blood and excrete enough of them in the urine to maintain a balance between daily intake and output.
Electrolyte concentrations can be measured in a sample of blood or urine by a laboratory. Doctors measure blood electrolyte concentrations to determine if an abnormality exists and, if so, to use the results to follow the response to treatment. Sodium, potassium, calcium, phosphate, and magnesium are the electrolytes most often involved in disorders of salt balance. Chloride and bicarbonate are also commonly measured; however, the blood chloride concentration usually parallels the blood sodium concentration, and bicarbonate is involved in disorders of acid-base balance. (see page 676 in Chapter 138, Acid-Base Balance)
Regulation of Sodium
Most of the body's sodium is in the blood and the fluid that surrounds cells. Sodium is taken in through food and drink and lost through sweat and urine. Normal kidneys can adjust the amount of sodium excreted in the urine so that the total amount of sodium in the body varies little from day to day.
A disturbance in the balance between sodium intake and output affects the total amount of sodium in the body. Changes in the total amount of sodium are closely linked to changes in the volume of water in the blood. An overall loss of sodium from the body doesn't necessarily cause the blood sodium concentration to fall but rather may cause the blood volume to drop. When the blood volume drops, the blood pressure falls, the heart rate rises, and light-headedness and sometimes shock occur.
What Causes the Syndrome of Inappropriate Antidiuretic Hormone?
Meningitis and encephalitis
Lung diseases (including pneumonia and acute respiratory failure)
Cancer (especially of the lung or pancreas)
- Chlorpropamide (a drug that lowers blood sugar levels)
- Carbamazepine (an antiseizure drug)
- Vincristine (an anticancer drug)
- Clofibrate (a drug that lowers cholesterol levels)
- Antipsychotic drugs
- Aspirin, ibuprofen, and many nonprescription analgesics
- Vasopressin and oxytocin (synthetic antidiuretic hormones)
Conversely, the blood volume may rise when there's too much sodium in the body. The extra fluid accumulates in the space surrounding the cells and results in a condition called edema. One sign of edema is swelling of the feet, ankles, and lower legs. When both excess water and sodium are lost or gained by the body, both the blood volume and the blood sodium concentration can be affected.
The body continually monitors the blood sodium concentration and the blood volume. When the sodium concentration becomes too high, the brain senses thirst, prompting the person to drink water. (see box, page 665) Sensors in the blood vessels and kidneys detect when blood volume is becoming low and trigger a chain reaction that attempts to increase the volume of fluid in the blood. The adrenal gland secretes the hormone aldosterone, which causes the kidneys to retain sodium. (see page 712 in Chapter 146, Adrenal Gland Disorders) The pituitary gland secretes antidiuretic hormone, which causes the kidneys to conserve water. The retained sodium and water lead to decreased urine production, which eventually leads to an increase in blood volume, and the blood pressure returns to normal. When sensors in the blood vessels and kidneys detect increased blood pressure and sensors in the heart detect increased blood volume, the kidneys are stimulated to excrete more sodium and urine, thus reducing blood volume.
Low Sodium Levels
Hyponatremia (low sodium blood level) is a blood sodium concentration below 136 milliequivalents (mEq) per liter of blood.
The sodium blood concentration falls too low when sodium has been overdiluted by too much water in the body. Sodium can be overdiluted in people who drink enormous amounts of water, as occasionally occurs in certain psychiatric disorders, and in hospitalized patients who receive large amounts of water intravenously. In either case, the amount of fluid taken in exceeds the kidneys' capacity to eliminate the excess. Smaller amounts of water intake--sometimes as little as 1 quart a day--can lead to hyponatremia in people whose kidneys aren't functioning properly, such as those with kidney failure. Hyponatremia also often occurs in people with heart failure and cirrhosis of the liver, in whom the blood volume is increased. In these conditions, the increased blood volume results in the sodium being overdiluted, although the total amount of sodium in the body is generally increased as well.
Hyponatremia occurs in people who have underactive adrenal glands (Addison's disease), (see page 712 in Chapter 146, Adrenal Gland Disorders) who excrete too much sodium. The wasting of sodium in the urine is caused by a deficiency of the adrenal hormone aldosterone.
People who have the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) have low sodium concentrations for a different reason. In this disorder, the pituitary gland at the base of the brain secretes too much antidiuretic hormone. (see page 698 in Chapter 144, Pituitary Gland Disorders) The antidiuretic hormone causes the body to retain water and dilute the amount of sodium in the blood.
The speed at which the blood sodium concentration falls partly determines the severity of symptoms. When the concentration falls slowly, symptoms tend to be less severe and don't begin until the concentration becomes extremely low. When the concentration falls quickly, symptoms are more severe and tend to occur with even minor decreases. The brain is particularly sensitive to changes in the blood sodium concentration. Therefore, lethargy and confusion are among the first symptoms of hyponatremia. As hyponatremia becomes more severe, muscles may twitch and seizures may occur. In the most severe cases, stupor, coma, and death may follow.
Severe hyponatremia is an emergency that requires immediate and intensive treatment. After performing any necessary emergency measures, doctors slowly increase the blood sodium concentration with intravenous fluids; increasing the concentration too rapidly can result in permanent brain damage.
Fluid intake is restricted, and doctors attempt to identify and correct the underlying cause of the hyponatremia. In those with the syndrome of inappropriate secretion of antidiuretic hormone, potential causes are identified and treated if possible. Demeclocycline or thiazide diuretics, drugs that can decrease the effect of antidiuretic hormone on the kidneys, may be given if hyponatremia worsens or doesn't improve despite the restriction of fluid.
High Sodium Levels
Hypernatremia (high sodium blood level) is a blood sodium concentration above 145 milliequivalents (mEq) per liter of blood.
Major Causes of High Sodium Levels
- Head trauma or neurosurgery involving the pituitary
- Disorders of other electrolytes (high calcium levels and low potassium levels)
- Use of drugs such as lithium, demeclocycline, or diuretics
- Excess water losses (diarrhea, vomiting, fever, excessive sweating)
- Sickle cell disease
- Diabetes insipidus
- Limited access to water (especially in combination with any of the other causes)
In hypernatremia, the body contains too little water relative to the amount of sodium. The blood sodium concentration generally rises abnormally high when water loss exceeds sodium loss, usually when a person drinks too little water. A high blood sodium concentration implies that a person either doesn't feel thirsty when he should, or he is thirsty but can't obtain enough water to drink. Hypernatremia may also be seen in people with abnormal kidney function, diarrhea, vomiting, fever, or excessive sweating.
Hypernatremia is most common among the elderly. Usually, the sense of thirst is slower to develop in the elderly and is less intense than in younger people. Elderly people who are bedridden or demented may be unable to obtain water to drink even if their sense of thirst is functioning. In addition, the kidneys are less able to concentrate the urine in advanced age, so the elderly can't conserve water as well. Older people who take diuretics, which force the kidneys to excrete more water, are particularly at risk for hypernatremia, especially when the weather is hot or they become ill and do not drink enough water. Hypernatremia is always serious but is especially so in the elderly. Nearly half of the older people hospitalized for this condition die. However, the death rate may be high because many of the victims have a severe underlying illness that allowed the hypernatremia to develop.
Hypernatremia can also result when the kidneys excrete excessive water, as in diabetes insipidus. In people with diabetes insipidus, either the pituitary gland secretes too little antidiuretic hormone (antidiuretic hormone causes the kidneys to retain water) or the kidneys don't respond appropriately to the hormone. (see page 703 in Chapter 144, Pituitary Gland Disorders) Despite the excess water loss from the kidneys, people with diabetes insipidus rarely develop hypernatremia if they have a normal thirst and access to water.
As with hyponatremia, the major symptoms of hypernatremia result from brain dysfunction. Severe hypernatremia can lead to confusion, muscle twitching, seizures, coma, and death.
Hypernatremia is treated by replacing water. In all but the most mild cases, fluid is given intravenously. Blood tests are performed every few hours to help determine when enough fluid has been given. The blood sodium concentration is reduced very slowly, because correcting the condition too rapidly can cause permanent brain damage.
Doctors may perform additional blood or urine tests to determine why the sodium concentration is high. Once the underlying cause is identified, treatment can become more specific. For example, if a person has diabetes insipidus, doctors can give antidiuretic hormone (vasopressin).
Regulation of Potassium
Potassium has major roles in cell metabolism and in nerve and muscle cell function. Unlike sodium, most of the body's potassium is located inside cells, not in the surrounding fluid or in the blood.
Sources of Potassium
- Potassium supplements
- Salt substitutes (potassium chloride)
- Potatoes and sweet potatoes
- Spinach, turnip greens, collard greens, kale, and other green leafy vegetables
- Most peas and beans
The concentration of potassium in the blood must be maintained within a narrow range. A potassium concentration that is too high or too low can have serious consequences, such as an abnormal heart rhythm or cardiac arrest. The potassium stored within the cells helps keep the potassium concentration in the blood constant.
As with other electrolytes, potassium balance is achieved by matching the amount of potassium taken in through food with the amount excreted. Although some potassium is lost through the gastrointestinal tract, most of the potassium leaves the body in the urine. Normally, the kidneys adjust the excretion of potassium to match changes in dietary intake. Some drugs and certain conditions cause potassium to move into or out of cells, also greatly affecting the potassium concentration in the blood.
Low Potassium Levels
Hypokalemia (low potassium blood level) is a blood potassium concentration below 3.8 milliequivalents (mEq) per liter of blood.
Normal kidneys are extremely good at conserving potassium. If the blood potassium concentration drops too low, usually it's because the kidneys aren't functioning normally or too much potassium has been lost through the gastrointestinal tract (because of vomiting, diarrhea, chronic laxative use, or colon polyps). Since many foods contain potassium, hypokalemia rarely is caused by too little intake.
Potassium may be lost in the urine for several reasons. By far the most common is the use of certain types of diuretics that cause the kidneys to excrete excess sodium, water, and potassium. Other causes of hypokalemia are rare. In Cushing's syndrome, the adrenal glands produce excess amounts of corticosteroid hormones including aldosterone, a hormone that causes the kidneys to excrete large amounts of potassium. (see page 714 in Chapter 146, Adrenal Gland Disorders) The kidneys also excrete excessive potassium in people who eat large amounts of licorice or chew certain types of tobacco. People with Liddle's syndrome, Bartter's syndrome, and Fanconi's syndrome are born with rare defects in the kidneys' mechanism for conserving potassium.
Certain drugs, such as insulin and the asthma drugs albuterol, terbutaline, and theophylline, increase the movement of potassium into cells and can result in hypokalemia. However, use of these drugs is rarely the sole cause of hypokalemia.
Mild decreases in the blood potassium concentration usually cause no symptoms at all. A more severe deficiency (levels below 3.0 mEq per liter of blood) can cause muscle weakness, twitches, and even paralysis. The heart may develop abnormal rhythms, especially in people with heart disease. For this reason, hypokalemia is particularly dangerous in those taking the drug digoxin.
Potassium usually can be replaced relatively easily by eating foods rich in potassium or by taking potassium salts (potassium chloride) orally. Because potassium can irritate the gastrointestinal tract, potassium supplements are given in small doses several times a day with food rather than in a single large dose.
Most people who take diuretics don't need to take potassium supplements. Nevertheless, doctors periodically check the blood potassium concentration so that the drug regimen can be altered if necessary.
When potassium deficiency is severe, potassium can be given intravenously. This is done cautiously, and generally only in the hospital, to avoid raising the blood potassium concentration too much.
High Potassium Levels
Hyperkalemia (high potassium blood level) is a blood potassium concentration higher than 5.0 milliequivalents (mEq) per liter of blood.
In general, a high blood potassium concentration is more dangerous than a low one. A potassium concentration above 5.5 mEq per liter of blood begins to affect the heart's electrical conducting system. If the blood concentration continues to rise, the heart rhythm becomes abnormal and the heart may stop beating.
Hyperkalemia usually results when the kidneys don't excrete enough potassium. Probably the most common cause of mild hyperkalemia is the use of drugs that block the kidneys' excretion of potassium, such as triamterene, spironolactone, and angiotensin converting enzyme inhibitors. Hyperkalemia can also be caused by Addison's disease, in which the adrenal glands don't produce sufficient amounts of the hormones that stimulate the kidneys to excrete potassium. (see page 712 in Chapter 146, Adrenal Gland Disorders) Addison's disease is becoming an increasingly common cause of hyperkalemia, as more people with AIDS develop problems with their adrenal glands.
Partial or complete kidney failure can result in severe hyperkalemia. Thus, people with poor kidney function generally must avoid foods high in potassium.
Hyperkalemia can also result when a large amount of potassium is suddenly released from the reservoir in cells. This might happen if a large amount of muscle tissue is destroyed (as in a crush injury), if a person has a severe burn, or if a person overdoses on crack cocaine. The rapid influx of potassium into the bloodstream can overwhelm the kidneys' ability to excrete it and result in life-threatening hyperkalemia.
Mild hyperkalemia causes few if any symptoms. Usually, hyperkalemia is first diagnosed in routine blood tests or when a doctor notices changes on an electrocardiogram. Occasionally, symptoms such as an irregular heartbeat occur; an irregular heartbeat may be experienced as palpitations.
Immediate treatment is essential when the blood potassium concentration rises above 5 mEq per liter in someone with poor kidney function or above 6 mEq per liter in someone with normal kidney function. Potassium can be removed from the body through the gastrointestinal tract or the kidneys or by dialysis. Potassium can be removed by inducing diarrhea and by swallowing a preparation that contains a potassium-absorbing resin. This resin isn't absorbed from the gastrointestinal tract, so the potassium leaves the body in the stool. If the person's kidneys are functioning, a diuretic can be given to increase potassium excretion.
When treatment is needed even more rapidly, the person may be given an intravenous solution containing calcium, glucose, or insulin. Calcium helps protect the heart from the effects of high potassium, but this effect lasts only a few minutes. Glucose and insulin drive potassium from the blood into cells, thus lowering the blood potassium concentration. If these measures fail or if a person has kidney failure, dialysis may be necessary.
Regulation of Calcium
Calcium is essential for various body functions, including muscle contraction, nerve conduction, and the proper functioning of many enzymes. Most of the body's calcium is stored in the bones, but calcium is also found in cells and in the blood. The body controls precisely the amount of calcium in both cells and the blood.
Maintaining a normal calcium concentration in the blood depends on ingesting at least 500 to 1,000 milligrams of calcium a day, absorbing an adequate amount of this calcium from the gastrointestinal tract, and excreting excess calcium into the urine. Calcium moves out of the bones into the bloodstream as needed to maintain the blood calcium concentration. However, mobilizing too much calcium from the bones eventually weakens them and can lead to osteoporosis.
The calcium concentration in the blood is regulated by two hormones: parathyroid hormone and calcitonin. Parathyroid hormone is produced by the four parathyroid glands located around the thyroid gland in the neck. When the calcium concentration in the blood falls, the parathyroid glands produce more parathyroid hormone; when it rises, the parathyroid glands produce less hormone. Parathyroid hormone stimulates the gastrointestinal tract to absorb more calcium and causes the kidneys to activate vitamin D. Vitamin D further enhances the ability of the gastrointestinal tract to absorb calcium. Parathyroid hormone also stimulates the bones to release calcium into the blood and causes the kidneys to excrete less calcium into the urine. Calcitonin, a hormone produced by cells of the parathyroid, thyroid, and thymus glands, lowers the blood calcium concentration by stimulating the movement of calcium into the bones.
Low Calcium Levels
Hypocalcemia (low calcium blood level) is a blood calcium concentration below 8.8 milligrams (mg) per deciliter of blood.
Causes of Low Calcium Levels
|Low levels of parathyroid hormone
||Usually occurs after damage to or accidental removal
of the parathyroid glands during surgery to remove the thyroid
|Congenital lack of parathyroid glands
||A rare hereditary condition or one that occurs as
part of DiGeorge syndrome
|An uncommon inherited disease; levels of parathyroid
hormone are normal, but bone and kidney have a decreased response to the hormone
|Vitamin D deficiency
||Usually caused by poor nutrition, insufficient exposure
to sunshine (vitamin D is activated when the skin is exposed to sunshine), liver
disease, gastrointestinal disease that prevents absorption of vitamin D, or the
use of barbiturates and phenytoin, which decrease the effectiveness of vitamin
||Interferes with vitamin D activation in the kidneys
|Low magnesium levels
||Results in decreased parathyroid hormone
|Poor nutrition or malabsorption
||Occurs with or without vitamin D deficiency
||Occurs when excess fatty acids in the blood from
the injured pancreas combine with calcium
|Low levels of albumin
||Reduces amount of calcium bound to albumin but doesn't
generally cause symptoms because the amount of free calcium remains normal
The blood calcium concentration can be low as a result of several different problems. Hypocalcemia is most common in disorders that result in chronic calcium loss from the urine or a failure to mobilize calcium from the bones. Since most of the calcium in the blood is carried by the protein albumin, too little albumin in the blood results in a low blood calcium concentration. However, hypocalcemia caused by too little albumin isn't usually important, because only the calcium that isn't bound to albumin can prevent the symptoms of hypocalcemia.
Symptoms and Diagnosis
The blood calcium concentration can be abnormally low without producing any symptoms. Over time, hypocalcemia can affect the brain and cause neurologic symptoms such as confusion, memory loss, delirium, depression, and hallucinations. These symptoms are reversible if the calcium is restored. An extremely low calcium concentration (below 7 mg per deciliter of blood) may cause muscle aches and tingling, often in the lips, tongue, fingers, and feet. Seizures and spasms of the muscles in the throat (leading to difficulty in breathing) as well as tetany (general stiffening and spasms of the muscles) can occur in severe cases. Changes in the heart's electrical conducting system occur and can be seen on an electrocardiogram.
An abnormal calcium concentration is usually first found during routine blood tests. Consequently, hypocalcemia is often diagnosed before symptoms become obvious. Once hypocalcemia is detected, a detailed history, complete physical examination, and other laboratory tests of blood and urine are required to establish the cause.
The treatment varies, depending on the underlying cause. Calcium can be replaced either intravenously or orally. People who have chronic hypocalcemia may be able to correct the problem by taking oral calcium supplements. Once symptoms appear, the intravenous route is generally warranted. Taking vitamin D supplements as well helps to increase the absorption of calcium from the gastrointestinal tract.
High Calcium Levels
Hypercalcemia (high calcium blood level) is a blood calcium concentration above 10.5 milligrams (mg) per deciliter of blood.
Hypercalcemia can be caused by either increased gastrointestinal absorption or increased intake of calcium. People who ingest large amounts of calcium, as is occasionally done by those with peptic ulcers who drink a lot of milk and also take calcium-containing antacids, can develop hypercalcemia. An overdose of vitamin D similarly can affect the blood calcium concentration by greatly increasing the absorption of calcium from the gastrointestinal tract.
However, the most common cause of hypercalcemia is hyperparathyroidism, the excessive secretion of parathyroid hormone by one or more of the four parathyroid glands. Some 90 percent of people with primary hyperparathyroidism have a noncancerous tumor (adenoma) in one of these small glands. In the remaining 10 percent, the glands simply enlarge and produce too much hormone. In rare cases, cancers of the parathyroid glands cause hyperparathyroidism.
Hyperparathyroidism is more common in women than in men. It is more likely to develop in older people and in those who have previously received radiation therapy to the neck. Sometimes hyperparathyroidism occurs as part of the syndrome of multiple endocrine neoplasia, a rare hereditary disease. (see page 726 in Chapter 149, Multiple Endocrine Neoplasia Syndromes)
People with cancer often have hypercalcemia. Cancers of the kidneys, lungs, or ovaries often secrete large amounts of a protein that has effects similar to those of parathyroid hormone--these effects are considered a paraneoplastic syndrome. (see page 797 in Chapter 165, Complications of Cancer) Cancer also may spread (metastasize) to bone, destroying bone cells and releasing calcium into the blood. This occurs most commonly with cancers of the prostate, breast, and lung. Multiple myeloma (a cancer involving bone marrow) also can lead to the destruction of bone and result in hypercalcemia. Other cancers raise the blood calcium concentration by means not yet fully understood.
Diseases in which bone is destroyed or resorbed may also cause hypercalcemia. One such disease is Paget's disease. People who are immobilized, such as paraplegics, quadriplegics, or those on prolonged bed rest, can also develop hypercalcemia because bone tissue is resorbed.
Symptoms and Diagnosis
Because hypercalcemia often causes no symptoms at all, the condition is usually first discovered during routine blood tests. The underlying cause is often apparent from the person's history and recent activities (for example, drinking large amounts of milk and taking calcium-containing antacid tablets for indigestion), but usually laboratory tests or x-rays are needed to find a cause.
The earliest symptoms of hypercalcemia are usually constipation, loss of appetite, nausea and vomiting, and abdominal pain. The kidneys may produce abnormally large amounts of urine. As excess urine is produced, the fluid in the body decreases and symptoms of dehydration can occur. (see page 665 in Chapter 136, Water Balance) Very severe hypercalcemia often causes symptoms of brain dysfunction such as confusion, emotional disturbances, delirium, hallucinations, weakness, and coma. Abnormal heart rhythms and death can follow.
Kidney stones containing calcium may form in people with chronic hypercalcemia. If hypercalcemia is severe and prolonged, calcium-containing crystals may form in the kidneys, causing permanent damage.
The treatment depends on how high and why the blood calcium concentration rose. If the calcium concentration is no higher than 11.5 mg per deciliter of blood, correcting the underlying cause is often sufficient. People who have normal kidney function and a tendency to develop hypercalcemia are usually advised to drink plenty of fluids, which stimulates the kidneys to excrete calcium and helps prevent dehydration.
If the calcium concentration is very high (higher than 15 mg per deciliter of blood) or if symptoms of brain dysfunction appear, fluids are given intravenously as long as the kidney function is normal. Diuretics such as furosemide increase the kidneys' excretion of calcium and are a mainstay of treatment. Dialysis is a highly effective, safe, reliable treatment but is usually reserved for those people with severe hypercalcemia not treatable by other methods.
Hyperparathyroidism is usually treated by surgically removing one or more of the parathyroid glands. For a successful result, the surgeon must remove all parathyroid tissue that's producing excessive amounts of hormone. Sometimes additional parathyroid tissue is located in places other than the parathyroid glands. In the hands of an experienced surgeon, surgery is successful in nearly 90 percent of cases.
Several other drugs can be used to treat hypercalcemia when other methods fail. They include plicamycin, gallium nitrate, calcitonin, bisphosphonates, and corticosteroids. The drugs work primarily by slowing the movement of calcium from bone.
Hypercalcemia caused by cancer is particularly difficult to treat. However, if the cancer can't be controlled, hypercalcemia usually returns despite the best treatment.
Regulation of Phosphate
Foods High in Phosphate
- Milk and dairy products
- Most peas and beans
- Spinach, turnip greens, collard greens, kale, and other green leafy vegetables
- Dark-colored soft drinks (except root beer)
The element phosphorus is present in the body almost exclusively in the form of phosphate (one phosphorus and four oxygen atoms). Most of the body's phosphate is contained in bone. The rest is primarily inside cells, where it's intimately involved in energy metabolism and is also used as a building block for such important molecules as DNA. Phosphate is excreted in the urine and stool.
Low Phosphate Levels
Hypophosphatemia (low phosphate blood level) is a blood phosphate concentration lower than 2.5 milligrams (mg) per deciliter of blood.
Chronic hypophosphatemia occurs in hyperparathyroidism, hypothyroidism (an underactive thyroid gland), poor kidney function, and long-term use of diuretics. Toxic amounts of the drug theophylline can reduce the amount of phosphate in the body. Taking large amounts of aluminum hydroxide antacids for a long time can also deplete the body's phosphate, especially in people undergoing kidney dialysis. Phosphate stores are depleted in people with severe malnutrition, diabetic ketoacidosis, severe alcohol intoxication, or severe burns. As people with these conditions recover, the blood phosphate concentration can quickly fall dangerously low because the body uses large amounts of phosphate.
A person may have hypophosphatemia without any illness. Symptoms occur only when the blood phosphate concentration drops very low. Initially the person may experience muscle weakness. Over time, bones can weaken, resulting in bone pain and fractures. An extremely low phosphate concentration (lower than 1.5 mg per deciliter of blood) can be very serious, leading to progressive muscle weakness, stupor, coma, and death.
The treatment is determined by the severity of symptoms and the underlying cause. A person with no symptoms can take phosphate in an oral solution, but this usually causes diarrhea. One quart of low-fat or skim milk provides a large amount of phosphate and is generally easier to take. Intravenous phosphate may be given if hypophosphatemia is very severe or if phosphate can't be taken orally.
High Phosphate Levels
Hyperphosphatemia (high phosphate blood level) is a blood phosphate concentration higher than 4.5 milligrams (mg) per deciliter of blood.
Normal kidneys are so efficient at excreting excess phosphate that hyperphosphatemia rarely occurs except in people with severe kidney dysfunction. In people with kidney failure, hyperphosphatemia is a problem because dialysis is not very effective at removing phosphate.
There are few outward signs of hyperphosphatemia. When the blood phosphate concentration is elevated in dialysis patients, the blood calcium concentration becomes low. This stimulates the parathyroid glands to produce parathyroid hormone, which in turn raises the blood calcium concentration by mobilizing calcium from the bone. If this condition continues, progressive bone weakness can occur, resulting in pain and fractures from minimal trauma. Calcium and phosphate can crystallize in the walls of the blood vessels and heart, causing severe arteriosclerosis (hardening of the arteries) and leading to strokes, heart attacks, and poor circulation. Crystals can also form in the skin where they cause severe itching.
Hyperphosphatemia in people with kidney damage is treated by decreasing phosphate intake and reducing the absorption of phosphate from the gastrointestinal tract. Foods high in phosphate should be avoided, and calcium-containing antacids should be taken with meals so that the calcium can bind to the phosphate in the intestines and not be absorbed.
Continuous stimulation of the parathyroid glands may cause hyperparathyroidism, requiring that the glands be surgically removed.
Regulation of Magnesium
A wide variety of enzymes in the body depend on magnesium to function properly. Most of the body's magnesium is found in bone; very little is in the blood. The amount of magnesium is maintained largely by eating a nutritious diet. Some magnesium is excreted in the urine; some is excreted in the stool.
Low Magnesium Levels
Hypomagnesemia (low magnesium blood level) is a blood magnesium concentration lower than 1.6 milliequivalents (mEq) per liter of blood.
The disorders in which hypomagnesemia occurs are complex and usually are the result of metabolic and nutritional disturbances. The most common causes of hypomagnesemia are decreased intake associated with starvation or intestinal malabsorption and increased excretion by the kidneys. Hypomagnesemia also occurs frequently in people who consume large amounts of alcohol or who have protracted diarrhea. High levels of aldosterone, antidiuretic hormone, or thyroid hormone can cause hypomagnesemia by increasing the excretion of magnesium by the kidney. Treatment with diuretics, the antifungal drug amphotericin B, or the anticancer drug cisplatin can also cause hypomagnesemia.
Hypomagnesemia can lead to loss of appetite, nausea and vomiting, sleepiness, weakness, personality changes, muscle spasms, and tremors. If hypomagnesemia occurs in conjunction with hypocalcemia, the magnesium must be replaced before the calcium disorder can be treated successfully.
Magnesium is replaced when the deficiency causes symptoms or when the magnesium concentration is very low (lower than 1 mEq per liter of blood). Magnesium can be taken orally or by injection into a muscle or vein.
High Magnesium Levels
Hypermagnesemia (high magnesium blood level) is a blood magnesium concentration higher than 2.1 milliequivalents (mEq) per liter of blood.
People almost never have hypermagnesemia unless they have kidney failure and are given magnesium salts or they take drugs that contain magnesium, such as some antacids or purgatives. Hypermagnesemia can lead to weakness, low blood pressure, and impaired breathing. The heart can stop beating if the magnesium concentration rises above 12 to 15 mEq per liter.
The treatment of severe hypermagnesemia requires the administration of intravenous calcium gluconate and support of the circulatory and respiratory systems. Powerful intravenous diuretics can increase the kidneys' excretion of magnesium. If the kidneys aren't functioning well, dialysis may be needed.