Neuromuscular Electrical Stimulation During Immobilization Due to Ankle Fractures (ANKL-ES)

Maastricht University Medical Centre (MUMC)

Status

Terminated

Conditions

Muscle Disuse Atrophy

Immobilization

Treatments

Device: Neuromuscular Electrical Stimulation (NMES)

Study type

Interventional

Funder types

Other

Identifiers

NCT02469506

METC 14-3-050

Details and patient eligibility

About

Rationale: Situations such as fractures of the lower extremity can necessitate a prolonged period of immobilization in otherwise healthy individuals. Long-term immobilization of the lower extremity has shown to cause significant reductions in skeletal muscle mass, already occurring during the early stages of disuse. Accordingly, feasible strategies for attenuating this loss of muscle during disuse need to be pursued. Local neuromuscular electrical stimulation (NMES) offers such a potential strategy but, as yet, remains untested during prolonged muscle disuse in a clinical setting.

Objective: To investigate whether twice daily local (gastrocnemius/soleus) NMES attenuates muscle loss during 2 weeks of unilateral ankle immobilization.

Study design: Randomized, parallel (two groups) study design.

Study population: 30 adults (18-65 y) with any form of closed ankle fractures needing surgical treatment.

Intervention: Twice daily neuromuscular electrical stimulation (NMES) or no intervention.

Main study parameters/endpoints: Primary: Calf muscle (gastrocnemius) cross sectional area (CSA) as determined by CT scan. Secondary: type I and II muscle fiber CSA and SC content, intramuscular triglyceride content and mRNA and protein expression of anabolic signaling proteins.

Enrollment

1 patient

Sex

All

Ages

18 to 65 years old

Volunteers

No Healthy Volunteers

Inclusion criteria

Unilateral closed ankle fracture (Weber type A, B or C)
Aged from 18-65 years
18.5 < BMI < 30 kg/m2
Undergoing surgical treatment

Exclusion criteria

Additional fractures beside ankle fracture (e.g. multi-trauma following a car accident)
Use of oral anticoagulants such as vitamin K-antagonists (e.g. acenocoumarol and fenprocoumon) and direct-acting or new oral anticoagulants (e.g. apixaban, dabigatran and rivaroxaban).
Any family history of thrombosis
All co-morbidities interacting with mobility and muscle metabolism of the lower limbs (e.g. arthritis, spasticity/rigidity, all neurological disorders and paralysis).
Myocardial infarction within the last 3 years