Page 1390 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

CHAPTER 99: Electrolyte Disorders in Critical Care 963

indicator of total body phosphorus. Isolated hypophosphatemia without Etiologies: There are three principal mechanisms by which hypophos-
intracellular depletion is of little consequence and is usually a transient phatemia can arise: transcellular redistribution, decreased intestinal
phenomenon. Severe symptoms from hypophosphatemia are due to absorption, and increased urinary excretion.
total body phosphorus depletion. The causes of hypophosphatemia are Transcellular redistribution is movement of phosphorus into cells.
listed in Table 99-13. This is usually transient, and in the face of normal total body phos-
phorus, harmless. However, in the face of preexisting phosphorus
depletion, this transcellular movement can provoke serious symp-
TABLE 99-13 Etiologies of Hypophosphatemia
toms including death. The most severe cases of hypophosphatemia
221
Intracellular Shift Decreased Phosphorus due to transcellular distribution are found with refeeding syndrome.
of Phosphorus Absorption Increased Renal Excretion Starvation decreases total body phosphorus due to decreased dietary
Carbohydrate infusion Dietary insufficiency Alcoholism intake. Despite the phosphorus depletion, serum phosphorus typi-
cally remains normal as phosphorus leaks out of cells. With refeeding,
Fructose Malabsorption Volume expansion/natriuretic insulin moves phosphorus into cells where it is consumed. Thirty-four
states percent of ICU patients experienced refeeding-associated hypophos-
222
Glucose Phosphate binders IV Bicarbonate phatemia after being NPO for as little as 48 hours. Alcoholics and
Glycerol Calcium Bicarbonaturia those with anorexia nervosa admitted to the hospital also commonly
suffer from refeeding syndrome. Both patient groups are often poorly
Lactate Magnesium Glucosuria
nourished and have a renal phosphorus leak, resulting in total body
Calcitonin Aluminum Diuretics phosphorus depletion.
Catecholamines Sevelamer Acetazolamide is the most One of the most common causes of intracellular phosphorus redis-
216
Epinephrine Lanthium phosphaturic tribution in hospitalized patients is respiratory alkalosis. The drop in
the partial pressure of carbon dioxide results in intracellular alkalemia,
Dopamine Steatorrhea Thiazides which stimulates glycolysis, consuming phosphorus. Metabolic alka-
223
Terbutaline a Vitamin D deficiency Loop diuretics c losis rarely causes hypophosphatemia because it typically fails to induce
the intracellular alkalemia essential for the phenomenon.
Albuterol Glucocorticoids Osmotic diuretics
Dietary insufficiency of phosphorus is rare, as phosphorus is ubiq-
Insulin b uitous in the diet and the body is efficient at reducing renal losses.
Respiratory alkalosis Miscellaneous High salt diet or saline infusion Decreased intestinal absorption can occur due to corticosteroids, either
Rapid cell proliferation Hungry bone syndrome endogenous or therapeutic. Antacids that contain magnesium, calcium,
or aluminum bind dietary phosphorus, preventing its absorption.
Treatment of anemia Burns Hyperaldosteronism Vitamin D deficiency decreases intestinal absorption of phosphorus and
CML in blast crisis Acetaminophen overdose SIADH the lack of calcitriol increases PTH release, further increasing urinary
AML Bisphosphonates Fanconi syndrome losses (Fig. 99-15).
Phosphorus is primarily resorbed in the proximal tubules (see
AMML Gallium nitrate Multiple myeloma Fig. 99-13). PTH enhances phosphorus excretion. Since phosphate is
Refeeding syndrome Aminoglycosides resorbed in conjunction with sodium, any process that decreases sodium
Rewarming hypothermia Heavy metal toxicity resorption (volume expansion, osmotic diuretics, or glucosuria) decreases
phosphorus resorption. Diuretics that act in the proximal tubules, such
Chinese herbs
as osmotic diuretics and carbonic anhydrase inhibitors, have particu-
Congenital larly potent phosphaturic effects because they block the primary site of
Ifosfamide phosphate resorption. Any process that damages the proximal tubule will
increase renal excretion of phosphorus. Fanconi syndrome is character-
Cisplatin
ized by proximal tubule dysfunction and has marked phosphaturia as one
Cystinosis of its components. Alcoholics develop a renal leak of phosphorus, which
Wilson disease is reversible following weeks of abstinence. 224
More recently phosphatonins such as fibroblast growth factor 23
Hereditary fructose intolerance
(FGF-23) have been found to play a role in increased urinary phosphate
Glucocorticoids excretion, particularly in the setting of hypophosphatemia post renal
Hyperparathyroidism transplantation. 225,226 β -Agonists, steroids, and IV fluids all increase
2
Hypercalcemia renal excretion of phosphorus. 227
Clinical Sequelae: Modest hypophosphatemia is devoid of clinical sym-
Metabolic acidosis ptoms. Symptomatic hypophosphatemia generally becomes apparent
Paraneoplastic syndrome as phosphorus falls below 1.0 mg/dL. Hypophosphatemia without
PTH-rP intracellular phosphate depletion (ie, transcellular redistribution)
228
Tumor-induced osteomalacia is typically benign. Severe hypophosphatemia in the presence of
intracellular phosphate depletion causes impaired energy metabolism
Renal transplantation resulting in significant cellular dysfunction, which can affect multiple
Acute malaria (falciparum) organ systems.
X-linked hypophosphatemic The oxygen affinity of hemoglobin is regulated by 2,3 diphosphoglyc-
rickets (vitamin D resistant rickets) erate (2,3 DPG). Severe hypophosphatemia decreases 2,3 DPG, which
Xanthines increases hemoglobin’s affinity for oxygen, decreasing oxygen delivery to
tissues. Since phosphate is a substrate for glycolysis, intracellular phos-
AML, acute myelogenous leukemia; AMML, acute myelomonocytic leukemia; CML, chronic myelogenous phate depletion can slow glycolysis, decreasing ATP levels.
leukemia; PTH-rP, parathyroid-hormone–related peptide; SIADH, syndrome of inappropriate secretion of CNS symptoms include weakness, tremors, and paresthesias.
antidiuretic hormone. Progressive hypophosphatemia can cause delirium, seizures, central
Data from these references: pontine myelinolysis, coma, and death. 229,230 CNS symptoms are particu-
243 c
227 b
a Brady et al ; Winter et al ; Fiaccadori et al 218 larly prominent with refeeding syndrome.

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