Duchenne muscular dystrophy (DMD) is the most common and severe muscular dystrophy with an incidence of 1 in 3000 male newborns; it is caused by a mutation in the dystrophin gene located on chromosome Xp21. As de-novo mutations are frequent, a positive familial history is lacking in 30% of cases: in those cases, the mean age of diagnosis is between 3 and 5 years. Some females carrying the gene on one X can present with a muscular or cardiac pathology. This mutation results in a deficit of dystrophin, an important sarcolemmnal structural protein in muscle cells. The clinical course of DMD is severe and there is no causative therapy available but some patients are on chronic corticoid therapy because this slows the progression of the disease. The disorder is characterized by progressive skeletal muscle weakness with an early onset in childhood. Muscle remodelling with fibrous and fatty tissue leads to loss of ambulation at a mean age of 10 years. Most of these patients require corrective orthopaedic surgery in the early stage of the disease for foot deformities and later for severe scoliosis to improve quality of life. The main anaesthetic concern in the treatment of patients with DMD is the use of depolarizing relaxants and volatile (halogenated) anaesthetics because of the potential for severe hyperkalimia and rhabdomyolysis.