Osteomalacia

The labs that name it - Hypophosphatemia or hypocalcemia together with a raised bone alkaline phosphatase; some sources hold that combination is necessary even to suspect osteomalacia. Serum 25-hydroxyvitamin D is the best marker of vitamin D status and is usually below 10 ng/mL in nutritional cases.

Draw an ionized calcium, not just a total - Only about 40% of serum calcium is in the free ionized state, and alkalosis lowers that fraction by exchanging calcium for hydrogen ions. Hyperventilating an already hypocalcemic patient makes it worse — hold end-tidal CO2 at the patient's own baseline.

Treat symptomatic hypocalcemia immediately - Tetany or seizures get IV calcium: 10-20 mL of 10% calcium gluconate or 3-5 mL of 10% calcium chloride. Circumoral numbness, fingertip tingling, cramping, and a positive Chvostek or Trousseau sign are the warning signs. See the hypocalcemia entry for the full workup.

Phosphate and the ventilator - Hypophosphatemia weakens skeletal muscle, the diaphragm included, and can stall weaning from mechanical ventilation. Check a serum phosphate before committing to extubating a marginal patient; below 1 mg/dL it can also impair myocardial contractility and produce paresthesia and tremor.

Weakness is part of the disease, not just deconditioning - Diffuse bone pain, tenderness, muscle weakness, and fragility fractures are the typical presentation. Expect a patient who moves and coughs poorly, and plan the extubation criteria accordingly.

Bones break with almost no force - Looser zones (pseudofractures) sit bilaterally and symmetrically at the femoral necks and shafts and the pubic and ischial rami; fragility fractures also turn up in the pelvis, feet, tibiae, and ribs. Lift and log-roll rather than pull, and be gentle abducting the hips into lithotomy.

Long-standing disease bends the spine - Kyphoscoliosis has been reported in long-standing osteomalacia, which constrains both how the patient can be positioned and how a neuraxial approach lines up.

Hunt the underlying cause, because it brings its own anesthetic - Malabsorption (celiac, short bowel, gastric bypass, inflammatory bowel disease, pancreatic insufficiency, cystic fibrosis), chronic liver disease, and chronic kidney disease each change drug handling, volume status, and electrolytes on their own.

Correction takes months, not days - Serum calcium and phosphate may normalize within a few weeks of vitamin D and calcium repletion, but bone alkaline phosphatase lags and can stay elevated for months. Don't read a persistently high alkaline phosphatase as treatment failure.

Osteomalacia is softening of adult bone caused by defective mineralization of osteoid — the collagen scaffold gets laid down, but hydroxyapatite is not deposited into it. The usual cause is prolonged vitamin D deficiency: low vitamin D drops serum calcium, parathyroid hormone rises in response, and calcium is stripped out of bone to defend the serum level.

Anything that interrupts the vitamin D pathway will do it — poor sun exposure or intake, malabsorption from celiac disease, short bowel, gastric bypass, inflammatory bowel disease or cystic fibrosis, chronic liver disease blocking 25-hydroxylation, and chronic kidney disease blocking 1-alpha-hydroxylation. Hypophosphatemia and hypocalcemia can also cause it directly. Rickets is the same defect at the growth plates of children. This is a mineralization problem, not the bone-mass problem of osteoporosis, and the labs are what separate the two.