186
U N I T 2
Integrative Body Functions
also needed for normal function of white blood cells
and platelets.
Hypophosphatemia
Hypophosphatemia is commonly defined by a serum
phosphorus level of less than 2.5 mg/dL (0.81 mmol/L) in
adults; and is considered severe at a concentration of less
than 1.0 mg/dL (0.32 mmol/L).
3,44
Hypophosphatemia
may occur despite normal body phosphorus stores as a
result of movement from the ECF into the ICF compart-
ment. Serious depletion of phosphorus may exist with
low, normal, or high plasma concentrations.
The most common causes of hypophosphatemia
are depletion of phosphorus because of insufficient
intestinal absorption, transcompartmental shifts, and
increased renal losses.
3,44
Often, more than one of these
mechanisms is active. Unless food intake is severely
restricted, dietary intake and intestinal absorption of
phosphorus are usually adequate. Intestinal absorption
may be inhibited by administration of glucocorticoids,
high dietary levels of magnesium, and hypothyroidism.
Prolonged ingestion of antacids may also interfere with
intestinal absorption. Antacids that contain aluminum
hydroxide, aluminum carbonate, and calcium carbonate
bind with phosphate, causing increased phosphate losses
in the stool. Because of their ability to bind phosphate,
calcium-based antacids are sometimes used therapeu-
tically to decrease plasma phosphate levels in persons
with chronic kidney disease.
Malnutrition increases phosphate excretion and
phosphorus loss from the body. Refeeding of malnour-
ished persons increases the incorporation of phosphorus
into nucleic acids and phosphorylated compounds in
the cell. The catabolic events that occur with diabetic
ketoacidosis also deplete phosphorus stores. Usually the
hypophosphatemia does not become apparent, how-
ever, until insulin and fluid replacement have reversed
the dehydration and glucose has started to move back
into the cell. Chronic alcohol use is a common cause
of hypophosphatemia. Contributing factors include
poor food intake and the effect that chronic alcohol use
has on the renal threshold for phosphate reabsorption,
causing more phosphate to be eliminated in the urine.
Administration of hyperalimentation solutions with-
out adequate phosphorus can cause a rapid influx of
phosphorus into the body’s muscle mass, particularly if
treatment is initiated after a period of tissue catabolism.
Respiratory alkalosis due to prolonged hyperventilation
can produce hypophosphatemia through increased PTH
levels and increased phosphate excretion. Clinical con-
ditions associated with hyperventilation include sepsis,
withdrawal from chronic alcoholism, fever, and primary
hyperventilation.
Manifestations.
Many of the manifestations of phos-
phorus deficiency result from a decrease in cellular
energy stores associated with a deficiency in ATP and
impaired oxygen transport due to a decrease in red
blood cell 2,3-diphosphoglycerate (2,3-DPG).
3,44
The
decrease in cellular energy can cause altered neural func-
tion, disturbed musculoskeletal function, and hemato-
logic disorders (Table 8-7).
Red blood cell metabolism is impaired by phos-
phorus deficiency; causing the cells to become rigid,
undergo increased hemolysis, and have diminished ATP
and 2,3-DPG levels (see Chapter 14). The chemotactic
and phagocytic functions of white blood cells and the
hemostatic functions of the platelets are also impaired.
Anorexia and dysphagia can occur. Neural manifesta-
tions (intention tremors, paresthesias, hyporeflexia,
stupor, coma, and seizures) are uncommon but serious
manifestations.
Chronic phosphorus depletion interferes with min-
eralization of newly formed bone matrix. In growing
children, this process causes abnormal endochondral
growth and clinical manifestations of rickets. In adults,
TABLE 8-7
Manifestations of Hypophosphatemia and Hyperphosphatemia
Hypophosphatemia
Hyperphosphatemia
LaboratoryValues
LaboratoryValues
Serum phosphorus < 2.5 mg/dL (0.8 mmol/L)
Serum phosphorus >4.5 mg/dL (1.45 mmol/L)
Neural Manifestations
Neuromuscular Manifestations
Intentional tremor
Paresthesias
Ataxia
Tetany
Paresthesias
Confusion, stupor, coma
Seizures
Musculoskeletal Manifestions
Cardiovascular Effects
Joint stiffness
Hypotension
Bone pain
Cardiac arrhythmias
Osteomalacia
Blood Disorders
Hemolytic anemia
Platelet dysfunction with bleeding tendency
Impaired white blood cell function
