Hyponatraemia in Neck of Femur Fracture: A Narrative Review of Epidemiology, Pathophysiology, and Outcomes

Background: Hyponatraemia is the commonest electrolyte disturbance encountered in older adults admitted with neck of femur (NOF) fracture. It is now recognised both as associated with fragility fracture and as an independent prognostic indicator for adverse post-operative outcomes. Methods: Narrative review of the literature, with emphasis on cohort studies, meta-analyses and mechanistic investigations pertinent to hip fracture in adults. Results: Admission hyponatraemia affects approximately 13–20% of NOF patients, twice the prevalence observed in age-matched community-dwelling elders and broadly comparable to general geriatric inpatients. A further 20–30% develop in-hospital, predominantly post-operative, hyponatraemia. Mild hyponatraemia (130–135 mmol/L) accounts for 75–85% of cases. Pathophysiology is multifactorial: hypovolaemia from the fracture haematoma, fasting and pre-admission “long lie”; drug effects (thiazides, selective serotonin reuptake inhibitors (SSRIs), proton pump inhibitors, carbamazepine, opioids); and non-osmotic arginine vasopressin (AVP) release driven by pain, nausea and peri-operative stress. Chronic hyponatraemia is hypothesised to contribute to fracture risk through three convergent mechanisms, direct sodium-dependent stimulation of osteoclastogenesis with AVP-mediated bone resorption, subtle cerebral dysfunction producing gait and attention deficits, and sarcopenia, although much of this mechanistic evidence derives from animal and in vitro studies rather than from patients with hip fracture. Hyponatraemia is reproducibly associated with longer length of stay, delayed surgery, and an adjusted 30-day mortality hazard of approximately 1.15–1.40. A dose–response relationship with severity is demonstrable; pre-operative correction has not been shown to improve outcomes in any randomised trial. Conclusions: Hyponatraemia in NOF fracture is consistently a consequence of the acute event and, at minimum, a robust marker of frailty and adverse prognosis. Whether it also causally contributes to fracture risk remains unproven, since the supporting human evidence is entirely observational and mechanistic, each contributing study carries methodological weaknesses that warrant caution, and no interventional study has established causality. Where hyponatraemia is mild and isolated, current evidence does not support delaying surgery; moderate and severe hyponatraemia warrant individualised assessment, with cautious correction proceeding alongside surgical planning rather than postponing it. Given the absence of interventional evidence, no correction strategy can yet be recommended to improve fracture or surgical outcomes. Prospective trials of targeted correction strategies and rehabilitation outcomes are overdue.