To the Editor,

We are writing in response to your recent article “Acute Skeletal Muscle Wasting Is Associated With Prolonged Hospital Stay in Critical Illness With Brain Injury” by Kangalgil et al. [1]. This study must be complimented for drawing attention to muscle wasting in relation to prolonged hospital stay. This article provides details about acute muscle loss in hospitalized patients with brain injury.

It is remarkable that the study has stressed dietary assessment, including daily energy and protein adequacy. Consequently, we consider that the study should have included the protein turnover in hospitalized patients in critical illness with brain injury. Proteolysis surpasses protein synthesis, leading to a net catabolic effect [2]. There are four crucial systems that play significant roles in protein degradation in skeletal muscle atrophy. These are the ubiquitin protease system, the cysteine aspartate protease system, the autophagy-lysosome system, and the calcium-dependent calpain system [3, 4].

In addition, a physiological principle is applied to skeletal muscles: “use it or lose it”. Reduced muscle activity in patients with brain injury leads to muscle wasting and metabolic disturbance [5]. The study did not emphasize the impact of disuse atrophy in hospitalized patients. Classic models of muscle atrophy due to disuse include bed rest, joint immobilization, mechanical ventilation, spaceflight, and denervation [6]. Muscle atrophy is primarily due to protein imbalance; thus, the loss of muscle strength results in a reduction two times its size [7]. For treating disuse atrophy, exercise and amino acid supplements stand out as the best modality of management [5].

Furthermore, the study has not mentioned the correlation of the urea to creatinine ratio (UCR) in evaluation of muscle mass wasting. This ratio can provide a biochemical marker for assessment of muscle breakdown in patients with prolonged hospital stay due to brain injury [8]. Physiologically, the UCR holds a strong base. In a catabolic state, urea synthesis increases, and because of muscle wasting, creatinine levels fall. Hence, both move in opposite directions, leading to an overall increase [9]. Raised levels of the UCR run parallel with muscle atrophy; hence, it can serve crucially beneficial in determination of muscle catabolism [8].

Moreover, this study has emphasized the use ultrasonography for measurement of the cross-sectional area of the rectus femoris, whereas other techniques, such as computerized tomography (CT) and magnetic resonance imaging (MRI), can also be used. Even though ultrasonography is a noninvasive, easy, and quick technique, it only manages to measure muscle area and thickness and not muscle mass. Muscle thickness underestimates muscle loss as compared with a cross-sectional area. CT scans and MRI both measure fat-free skeletal muscle, but CT scans also provide evaluation of deep muscles. The results of both techniques are highly accurate and reliable, thus conclusively serving as a much appreciable diagnostic measure [10].

Thus, having the aspects addressed in the prior discussion, one can indeed find enhancements to the overall efficacy of the article concerned in this letter.