Page 208 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice
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198 ELECTROLYTE DISORDERS
concurrent phosphate depletion. 99 Hypophosphatemia BOX 7-1 Causes of
decreases erythrocyte concentrations of ATP, which
increases erythrocyte fragility, leading to hemolysis. Hypophosphatemia
Hemolysis usually is not observed until serum phospho-
rus concentration decreases to 1.0 mg/dL or less. Maldistribution (Translocation)
Hypophosphatemia also reduces erythrocyte 2,3-DPG • Treatment of diabetic ketoacidosis
concentrations, which impairs oxygen delivery to tissues. • Carbohydrate load or insulin administration
Leukocytes in hypophosphatemic patients have impaired • Respiratory alkalosis or hyperventilation
chemotaxis, phagocytosis, and bacterial killing. 38 This • Total parenteral nutrition or nutritional recovery
altered function may promote sepsis in hypophos- • Hypothermia
phatemic patients receiving total parenteral nutrition. Increased Loss (Reduced Renal
Platelet-associated abnormalities include shortened sur- Reabsorption)
vival time, impaired clot retraction, megakaryocytosis in • Primary hyperparathyroidism
the bone marrow, and thrombocytopenia. Hemolytic • Renal tubular disorders (e.g., Fanconi syndrome)
anemia, thrombocytopenia, and impaired clot retraction • Renal transplantation
occurred in starved dogs that were made hypophos- • Major hepatic resection (?)
phatemic by infusion of amino acids, ostensibly because • Proximally acting diuretics (e.g., carbonic anhydrase
of depletion of cellular ATP stores. 178 Clinically, hemoly- inhibitors) (?)*
sis has been reported in hypophosphatemic dogs and cats • Eclampsia
• Hyperadrenocorticism (?)
with diabetic ketoacidosis, hepatic lipidosis, and other
2,80,173
disorders. Hemolysis was reported in four other Decreased Intake (Reduced Intestinal
hypophosphatemic diabetic cats, but cause and effect Absorption)
were obscured by the possibility of Heinz body anemia. 23 • Dietary deficiency (?)
Neuromuscular effects of hypophosphatemia include • Vomiting (?)
weakness and pain associated with rhabdomyolysis, as • Malabsorption (?)
well as anorexia, vomiting, and nausea secondary to intes- • Phosphate binders
tinal ileus. 88,89 Decreased phosphate may impair central • Vitamin D deficiency
nervous system glucose use and ATP production, leading Laboratory Error
to metabolic encephalopathy, which has a wide range of
manifestations in people (e.g., coma, seizure, confusion,
irritability). 99,177 Reversible impairment of cardiac con- *(?) Importance in veterinary medicine uncertain.
tractility occurs in dogs with experimentally induced
hypophosphatemia and in people with naturally occur-
ring hypophosphatemia. 65,66,180 Hypophosphatemia also of hypophosphatemia in hospitalized people. 15,79 Insulin
causes proximal tubular bicarbonate wasting, reduction facilitates entry of glucose and phosphate into cells, where
in titratable acidity, and impaired renal ammoniagenesis. glucose is phosphorylated to glycolytic intermediates.
However, serious acid-base disturbances do not arise in Interestingly, infusion of a higher concentration (e.g.,
phosphate-deprived dogs. 151 Phosphate deficiency 10%dextrose)forashortertimeseemstobelessdetrimental
produces bone demineralization via effects of PTH and than infusing 4% glucose continuously. 99 Malnourished
calcitriol, and release of carbonate from bone may prevent patients receiving total parenteral nutrition are particularly
serious metabolic acidosis. Hypomagnesemia frequently susceptibletohypophosphatemiabecauseoftheaccelerated
is found in hypophosphatemic people, but the reasons rate of tissue repair as phosphate is incorporated into new
32 88,136
for this association are not clear. cells and phosphate use during glycolysis.
Hypophosphatemia as part of the “refeeding syndrome”
CAUSES OF HYPOPHOSPHATEMIA (i.e., severe electrolyte changes in malnourished patients
Hypophosphatemia may be caused by translocation of that are being fed parenterally or enterally) was more likely
phosphate from extracellular to intracellular fluid (maldis- inpatientsthatweremoreseverelyemaciated,hadlowerini-
tribution), increased loss (decreased renal reabsorption of tialserumphosphateconcentrations,andexperiencedmore
phosphate), or decreased intake (decreased intestinal aggressive initial infusion of parenteral nutrition. 107 Respi-
absorption of phosphate). 99,136 Clinical conditions ratory alkalosis likewise causes translocation because it
associated with hypophosphatemia are presented in stimulates glycolysis by activating phosphofructokinase. 88
Box 7-1. In confusing cases, one can measure fractional This effect has been demonstrated in experimental dogs
urinary phosphorus excretion to help determine if renal but was marked only when hyperventilation was combined
losses are responsible. with glucose administration. 19 Increased intracellular pH
Translocation related to administration of a carbohy- may be more important than increased extracellular pH
drate load (e.g., 5% dextrose infusion) is a common cause for causing hypophosphatemia in respiratory alkalosis,