The spinal accessory nerve innervates trapezius. The entire muscle will retract the scapula. However, its upper and lower fibres act together to upwardly rotate it.

l Charcot Foot Pathogenesis: Requires peripheral neuropathy and repetitive microtrauma (often minor or completely forgotten by the patient). l Charcot Foot Neuropathy: Involves both sensory-motor neuropathy (insensate walking) and autonomic neuropathy (increased blood flow). l Charcot Foot Early Phase Presentation: Mimics cellulitis with localized erythema, warmth, swelling, and bounding foot pulses. l Charcot Foot Deformity: Continued weight-bearing on an insensate, hyperemic foot leads to progressive joint destruction and the classic "rocker-bottom" foot. l Charcot Foot Bounding Pulses: Autonomic neuropathy leads to arteriovenous shunting, creating bounding distal pulses despite active local destruction.

l Compartment Syndrome Splinting: Immediate initial management involves removing all constrictive dressings or casts down to the skin and elevating the limb to the level of the heart (not above, as this reduces perfusion pressure). l Myoglobinuria Risk: Muscle necrosis in compartment syndrome releases myoglobin, leading to dark tea-colored urine and a high risk of acute kidney injury (AKI).

l Compartment Syndrome Diagnosis: Suspected in any patient with a crush injury, severe limb swelling, and an inability to actively or passively move digits. l Compartment Syndrome Treatment: Urgent surgical decompression via emergency fasciotomy is the definitive treatment. l The Late Signs Trap: Paralysis and loss of distal pulses are very late signs of compartment syndrome; waiting for them to appear before acting leads to irreversible necrosis.

A post-operative patient becomes drowsy, bradypnoeic, and has pinpoint pupils after receiving morphine. What is the most appropriate immediate treatment?