Hypophosphatemia is usually the result of either a negative phosphorus balance or cellular uptake of extracellular phosphorus (an intercompartmental shift). Intercompartmental shifts of phosphorus can occur during alkalosis and following carbo-hydrate ingestion or insulin administration. Large doses of aluminum or magnesium-containing ant-acids, severe burns, inadequate phosphorus sup-plementation during hyperalimentation, diabetic ketoacidosis, alcohol withdrawal, and prolonged respiratory alkalosis can all produce a negative phos-phorus balance and lead to severe hypophosphate-mia (<0.3 mmol/dL or <1.0 mg/dL). In contrast to respiratory alkalosis, metabolic alkalosis rarely leads to severe hypophosphatemia.
Mild to moderate hypophosphatemia (1.5–2.5 mg/ dL) is generally asymptomatic. In contrast, severe hypophosphatemia (<1.0 mg/dL) is often associ-ated with widespread organ dysfunction. Cardio-myopathy, impaired oxygen delivery (decreased2,3-diphosphoglycerate levels), hemolysis, impaired leukocyte function, platelet dysfunction, encepha-lopathy, skeletal myopathy, respiratory failure, rhab-domyolysis, skeletal demineralization, metabolic acidosis, and hepatic dysfunction have all been asso-ciated with severe hypophosphatemia.
Oral phosphorus replacement is generally preferable to parenteral replacement because of the increased risk of phosphate precipitation with calcium, result-ing in hypocalcemia, and also because of the increased risks of hyperphosphatemia, hypomagnesemia, and hypotension. Accordingly, intravenous replacement therapy is usually reserved for instances of symptom-atic hypophosphatemia and extremely low phosphate levels (<0.32 mmol/L). In situations where oral phos-phate replacement is utilized, vitamin D is required for intestinal phosphate absorption.
Anesthetic management of patients with hypophos-phatemia requires familiarity with its complications (see above). Hyperglycemia and respiratory alkalo-sis should be avoided to prevent further decreases in plasma phosphorus concentration. Neuromus-cular function must be monitored carefully when NMBs are given. Some patients with severe hypophosphatemia may require mechanicalventilation postoperatively because of muscle weakness.
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