Background/Objectives: Kienböck disease (idiopathic avascular necrosis of the lunate) is treated almost exclusively surgically; its pharmacological evidence base comprises fewer than five primary publications and ~20 patient-level observations. Femoral-head, jaw, and knee osteonecrosis have decades of evidence, including randomised trials. We ask whether extra-carpal evidence can be translated to Kienböck disease and the wider Carpal Avascular Necrosis Family (lunate, scaphoid/Preiser, capitate, hamate, triquetrum). Methods: We conducted a narrative review reported per SANRA, searching PubMed, CrossRef, Google Scholar and three specialty registries from inception to 2026 across eleven drug classes and eleven skeletal sites. All references were independently verified against primary sources (PubMed/CrossRef). No Kienböck-specific randomised or controlled data exist; all conclusions therefore rest on indirect, extra-carpal evidence. Results: Three pathways (subchondral insufficiency fracture, microvascular ischaemia, hypercoagulability) predict drug-class plausibility differently by site. Iloprost is the candidate most consistently aligned across the translation axes, though no direct lunate data exist; teriparatide provides the only randomised evidence suggesting reversal of established osteonecrosis at any site (medication-related osteonecrosis of the jaw). The lunate sits within a coherent carpal AVN family sharing end-arterial supply, Lichtman-grade trajectories, and a near-identical evidence vacuum. Conclusions: A Four-Axis Translation Framework (mechanistic alignment, anatomic concordance, Lichtman-stage applicability, lunate-specific risk-benefit geometry) is proposed to evaluate which extra-carpal evidence is admissible at the lunate; with the carpal AVN family construct, these are the review's two novel contributions.

Atrioventricular block (AVB) resulting from injury or ischaemia of the atrioventricular node (AVN) artery remains a key concern in inferior MI and procedures near the AVN. Given that ECG findings alone may be insufficient to reliably predict AVB occurrence or reversibility, anatomy-based risk assessment is essential. However, in vivo identification of the AVN artery is limited by its small size and marked anatomical variability and by the lack of specific markers for the AVN itself to confirm the artery's terminal distribution. A main AVN artery typically arises near the cardiac crux and courses through the inferior pyramidal space, although its origin and trajectory vary. In addition, supplementary arterial supply may reach the node via anatomically distinct pathways, most commonly through the antero-inferior buttress of the atrial septum. These separate pathways variably contribute to nodal perfusion. Combined with positional variability of the AVN, this complexity limits precise anatomical risk stratification and may explain the heterogeneity of AVB occurrence and reversibility.

Left ventricular non-compaction cardiomyopathy (LVNC) is a rare myocardial disorder associated with heart failure and arrhythmias. Cardiac resynchronisation therapy (CRT) is an established treatment in patients with electrical dyssynchrony; however, achieving optimal response remains challenging in complex clinical scenarios. We report a 51-year-old male with LVNC, severe left ventricular dysfunction, morbid obesity, and recurrent atrial and ventricular arrhythmias. Despite initial improvement following CRT-D implan-tation, the patient developed progressive heart failure and recurrent ventricular tachycardia with high atrial arrhythmia burden, resulting in ineffective biventricular pacing. Following unsuccessful device optimisation strategies, a multidisciplinary decision was made to proceed with atrioventricular node ablation. This resulted in marked clinical and echocardiographic improvement, including recovery of left ventricular ejection fraction and symptomatic status. This case highlights the importance of ensuring adequate CRT delivery and demonstrates the pivot-al role of atrioventricular node ablation in patients with refractory atrial arrhythmias and suboptimal CRT response.

Assessment of fracture healing in carpal bones is commonly performed using computed tomography (CT). However, CT may not accurately reflect bone viability. Magnetic resonance imaging (MRI) is more sensitive in detecting early changes in bone marrow and vascularity. A diagnostic challenge arises when CT suggests fracture union while MRI demonstrates features of avascular necrosis (AVN). We conducted a retrospective case series of three patients with prior carpal bone fractures (one scaphoid and two lunate) who presented with persistent or new-onset wrist pain following apparent fracture healing. All patients underwent MRI evaluation, and a CT was performed in one case for correlation. Magnetic resonance imaging (MRI) demonstrated features suggestive of AVN in all three cases despite prior imaging indicating fracture union. Two cases showed T1 hypointensity with corresponding hyperintensity on fluid-sensitive sequences, consistent with early AVN, while one case demonstrated persistent low signal on both sequences, suggestive of chronic AVN. In the case of CT correlation, there was apparent fracture union with mild sclerosis and no evidence of collapse, highlighting discordance between structural and biological assessment. Hence, persistent wrist pain following a healed fracture should prompt MRI evaluation to assess bone viability and guide appropriate management.

Talar neck fractures are relatively uncommon but potentially devastating injuries with often life-altering sequelae. The talus is located in the hindfoot and permits pain-free motion of the ankle, subtalar, and transverse tarsal joints. Talar neck fractures are associated with high-energy mechanisms, with severe soft tissue injury, bony comminution, and fracture displacement commonly co-occurring. Injury to the talar neck with resulting displacement can lead to permanent stiffness, deformity, and pain, with hindfoot arthrosis estimated to occur in greater than 90% of displaced talar neck fractures. The uncommon nature of these injuries partially explains the lack of high-quality literature to drive evidence-based treatment strategies. Open reduction internal fixation is the predominant treatment for displaced talar neck fractures, with nonoperative approaches reserved for the uncommon nondisplaced injury pattern or cases involving patients ineligible for surgery. Classic complications following open fixation of talar neck fractures include osteonecrosis or avascular necrosis, posttraumatic arthritis, and malunion. The high-energy traumatic mechanism is often a feature in these injuries, and fracture fragment displacement can disrupt the tenuous supply to the talus, resulting in necrosis. Unrecognized comminution of the medial talar neck predisposes these injuries to malreduction, leading to varus malunion deformity. Many of these injuries ultimately require hindfoot arthrodesis procedures for pain relief, regardless of the fixation timing and reduction quality. The high-energy mechanism of talar neck fractures also leads to significant soft tissue injury, making surgical wound healing a considerable concern.