Osteoporosis

Confirm which bone disease you're dealing with - A DXA T-score at or below -2.5, or a low-trauma fracture, makes the diagnosis; FRAX gives the 10-year risk of hip and of major osteoporotic fracture. If calcium or phosphate is low with a raised alkaline phosphatase, you're looking at osteomalacia instead — different mechanism, different fix.

Handling is the intraoperative hazard - Pathologic fractures occur with little or no trauma. Lift rather than pull, log-roll, support the arms and hips through every transfer, pad the bony prominences, and never use a limb as a lever.

Kyphosis costs lung reserve - Vertebral compression fractures produce thoracic kyphosis, height loss, chronic pain, respiratory compromise, and a high risk of developing pneumonia. Expect reduced reserve, and plan for pulmonary toilet and early mobilization afterward.

Fixed kyphosis fights your positioning - Thoracic kyphosis and lost height change how the patient can sit for a neuraxial block and how flat they can lie. Plan the block around the spine the patient actually has rather than the one the textbook drawing shows.

Cement is the moment to watch - Hip fracture repair and femoral head replacement are the classic osteoporotic cases. Systolic pressure falls after cement insertion, with intravascular embolization and, rarely, cardiac arrest; the proposed mechanism is right ventricular failure from a rise in pulmonary artery pressure. Risk climbs with hypertension, obesity, and a previously uninstrumented femoral canal.

Vertebroplasty and kyphoplasty - Polymethyl methacrylate is injected percutaneously to restore vertebral body height, reduce pain, and stabilize the fracture. You are positioning, usually prone, a spine that already fractures easily.

Bisphosphonates leave marks - Use beyond 5 years is associated with osteonecrosis of the jaw and with atypical low-trauma femur fractures; the class also causes gastritis and esophagitis and is contraindicated below a GFR of roughly 30-35 mL/min. Look in the mouth before instrumenting the airway and document what you find.

A hip fracture is a life event, not just a case - Most patients lose the ability to live independently after an osteoporotic hip fracture, and recovery is prolonged. That belongs in the risk conversation, and it's the argument for pushing hard on early mobilization.

Find the secondary cause - Glucocorticoid use, hyperthyroidism, hypogonadism, diabetes (a 3-fold risk of any fracture and 7-fold risk of hip fracture in type 1), chronic kidney disease, COPD (about one-third of patients affected), and spinal cord injury each drive bone loss and each carry their own anesthetic weight.

Osteoporosis is low bone mineral density caused by deteriorated bone microarchitecture — the bone that remains is normally mineralized, there is simply not enough of it — which predisposes to low-impact fragility fractures. Osteoblast activity slows while osteoclast resorption continues, and the two fall out of balance with aging and hormonal change.

Primary disease follows aging and estrogen loss; secondary disease follows glucocorticoids, hyperthyroidism, hypogonadism, diabetes, chronic kidney disease, transplantation, COPD, cystic fibrosis, and spinal cord injury. It is silent until something breaks, and is usually picked up either on DXA or by the fragility fracture itself. Perioperatively it means two things: a skeleton that can fracture during ordinary handling and transfer, and a thoracic spine collapsing into kyphosis with the chest restriction that follows.