Duchenne Muscular Dystrophy (DMD)

Nondepolarizing NMB sensitivity - Degenerating muscle is exquisitely sensitive to nondepolarizing blockers; give reduced doses, monitor with quantitative train-of-four (TOF), and reverse a rocuronium or vecuronium block with sugammadex. Expect prolonged recovery.

Difficult airway - Macroglossia, limited mouth opening, and jaw or cervical contractures in advanced disease can make laryngoscopy hard; plan for it and have video laryngoscopy available.

Aspiration risk - Smooth-muscle involvement slows gastric emptying and weakens airway-protective reflexes; treat advanced disease as a full stomach.

Positioning - Fixed contractures and fragile, osteoporotic bones; pad generously and position carefully.

Regional where feasible - Neuraxial or peripheral regional avoids both triggering agents and neuromuscular blockade entirely and is a strong choice when the surgery allows.

Emergence and disposition - Weak respiratory muscles plus any residual blockade or opioid make emergence slow and precarious; dose opioids conservatively and have a low threshold for postoperative monitoring or noninvasive ventilation.

Succinylcholine is contraindicated - It drives massive potassium efflux from the unstable muscle membrane, producing hyperkalemic cardiac arrest, and can trigger rhabdomyolysis. Never use it, including as a rescue for a difficult airway.

Volatile agents can trigger rhabdomyolysis - Halogenated volatiles can cause anesthesia-induced rhabdomyolysis with hyperkalemia and arrest. This is distinct from classic malignant hyperthermia (MH) but is managed with the same trigger-free approach: run a total intravenous anesthetic (TIVA) on a clean, flushed circuit.

Managing a hyperkalemic event - Unexplained arrest, peaked T waves, or a wide-complex rhythm should prompt immediate treatment of hyperkalemia with calcium, insulin and glucose, bicarbonate, and hyperventilation, plus dantrolene if a hypermetabolic MH-like picture coexists. Send a potassium and creatine kinase.

Dilated cardiomyopathy - Nearly universal by the late teens; obtain a recent echocardiogram and ECG. Expect reduced contractility and arrhythmias, and titrate anesthetics to avoid myocardial depression while maintaining preload.

Restrictive respiratory disease - Progressive respiratory-muscle weakness and scoliosis produce a restrictive pattern; review recent pulmonary function and any home noninvasive ventilation. Postoperative respiratory failure is a leading cause of morbidity.

Postoperative planning - Decide disposition up front for anything beyond minor surgery, resume home noninvasive ventilation early, and lean on multimodal or regional analgesia to spare respiratory depressants.

An X-linked recessive disorder caused by mutations in the dystrophin gene, so functional dystrophin is absent from the muscle-cell membrane. Without it the membrane is fragile and skeletal muscle progressively degenerates and is replaced by fat and fibrous tissue. It presents in early childhood in boys with proximal weakness, calf pseudohypertrophy, and a Gowers sign, with loss of ambulation by around age 12. Dystrophin is also expressed in cardiac and smooth muscle, so a dilated cardiomyopathy and gastrointestinal and respiratory involvement develop over time; death is usually from respiratory failure or cardiomyopathy. That same membrane fragility is why anesthetic triggers can provoke rhabdomyolysis and dangerous hyperkalemia.