Hypophosphatemia
Hypophosphatemia
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 carbohydrate ingestion or insulin administration. Large doses of aluminum or magnesium-containing antacids, severe burns, inadequate phosphorus supplementation duringhyperalimentation, diabetic ketoacidosis, alcohol withdrawal, and prolonged respiratory alkalosis can all produce a negative phosphorus balance and lead to severe hypophosphatemia (<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 associated with widespread organ dysfunction. Cardiomyopathy, impaired oxygen delivery (decreased 2,3-diphosphoglycerate levels), hemolysis, impaired leukocyte function, platelet dysfunction, encephalopathy, skeletal myopathy, respiratory failure, rhabdomyolysis, skeletal demineralization, metabolic acidosis, and hepatic dysfunction have all been associated with severe hypophosphatemia.
Oral phosphorus replacement is generally preferable to parenteral replacement because of the increased risk of phosphate precipitation with calcium, resulting in hypocalcemia, and also because of the increased risks of hyperphosphatemia, hypomagnesemia, and hypotension. Accordingly, intravenous replacement therapy is usually reserved for instances of symptomatic hypophosphatemia and extremely low phosphate levels (<0.32 mmol/L). In situations where oral phosphate replacement is utilized, vitamin D is required for intestinal phosphate absorption.
Anesthetic management of patients with hypophosphatemia requires familiarity with its complications (see above). Hyperglycemia and respiratory alkalosis should be avoided to prevent further decreases in plasma phosphorus concentration. Neuromuscular function must be monitored carefully when NMBs are given. 
Some patients with severe hypophosphatemia may require mechanical ventilation postoperatively because of muscle weakness.
Hypophosphatemia
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 carbohydrate ingestion or insulin administration. Large doses of aluminum or magnesium-containing antacids, severe burns, inadequate phosphorus supplementation duringhyperalimentation, diabetic ketoacidosis, alcohol withdrawal, and prolonged respiratory alkalosis can all produce a negative phosphorus balance and lead to severe hypophosphatemia (<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 associated with widespread organ dysfunction. Cardiomyopathy, impaired oxygen delivery (decreased 2,3-diphosphoglycerate levels), hemolysis, impaired leukocyte function, platelet dysfunction, encephalopathy, skeletal myopathy, respiratory failure, rhabdomyolysis, skeletal demineralization, metabolic acidosis, and hepatic dysfunction have all been associated with severe hypophosphatemia.
Oral phosphorus replacement is generally preferable to parenteral replacement because of the increased risk of phosphate precipitation with calcium, resulting in hypocalcemia, and also because of the increased risks of hyperphosphatemia, hypomagnesemia, and hypotension. Accordingly, intravenous replacement therapy is usually reserved for instances of symptomatic hypophosphatemia and extremely low phosphate levels (<0.32 mmol/L). In situations where oral phosphate replacement is utilized, vitamin D is required for intestinal phosphate absorption.
Anesthetic management of patients with hypophosphatemia requires familiarity with its complications (see above). Hyperglycemia and respiratory alkalosis should be avoided to prevent further decreases in plasma phosphorus concentration. Neuromuscular function must be monitored carefully when NMBs are given. Some patients with severe hypophosphatemia may require mechanical ventilation postoperatively because of muscle weakness.
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 carbohydrate ingestion or insulin administration. Large doses of aluminum or magnesium-containing antacids, severe burns, inadequate phosphorus supplementation duringhyperalimentation, diabetic ketoacidosis, alcohol withdrawal, and prolonged respiratory alkalosis can all produce a negative phosphorus balance and lead to severe hypophosphatemia (<0.3 mmol/dL or <1.0 mg/dL).
In contrast to respiratory alkalosis, metabolic alkalosis rarely leads to severe hypophosphatemia.
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Nerve, bone, red and white blood cells, membrane, and muscle functional problems.