Rhabdomyolysis in the pathogenesis of local cold injury: 616-092.19

Abstract

Summary. Introduction. Cold alteration of muscle tissue is associated with the entry of cytotoxic degradation products of myocytes into the bloodstream. Myocytolysis derivatives are not specific markers of myoalteration, while free myoglobin is considered the only confirmation of muscle destruction. The role of myoglobin in the pathogenesis of any injury and in the effects of myoglobin-induced

cytodestruction have been demonstrated. However, there are no works focused on the involvement of free myoglobin in the pathogenesis of cryotrauma. Aim: to study the level of myoglobin and indicators of bioelectrical activity in the muscles of patients with local cold injury. Materials and Methods. The single-center prospective open-label non-randomized controlled trial included 88 patients (50 men and 38 women, aged 30–40 years) with III–IV degree frostbite of the lower extremities. Patients were divided into three groups based on the extent of cold-induced tissue damage: those with lesions at the level of the phalanges of the fingers (n = 20), those with lesions up to the level of the metatarsus (n=24), and those with lesions of the foot and lower third of the leg (n=44). Patients with the most severe injuries were identified and divided into 2 subgroups: subgroup IV — 22 individuals in the late reactive period (Day 5 after injury), subgroup V — 22 individuals in the granulation and epithelization period (Day 30). The control group consisted of 28 relatively healthy individuals aged from 27 to 40 years. In all examined perrsons we measured the level of peripheral myoglobin, evaluated the bioelectric activity of the muscles via non-invasive electroneuromyography, and assessed the state of the microcirculatory bed via non-invasive laser doppler flowmetry. Results. On day 5 following the cryoinjury, the myoglobin blood level of subgroup IV patients was 35.6 times higher than that of the control group. At the same time, these patients demonstrated a 5-fold decrease in the M-response amplitude, a 1.7-fold increase in the residual latency, and a 1.6-fold decrease in the microcirculation index compared with the control group. On Day 30 following cryoinjury, patients in subgroup V exhibited a myoglobin blood level 7.0 times greater than that of the control group, the M-response amplitude 1.8 times lower, a residual latency 1.5 times higher, and a microcirculation indicator value 1.3 times lower. On Day 30 following cryoinjury, patients in subgroup V exhibited a 3.9-fold decrease in myoglobin levels as well as a 1.7-fold decrease in residual latency when compared to group IV. The amplitude of the M-response and the microcirculation index exhibited an increase on Day 30 relative to Day 5 following cryoinjury (by 3.8-fold and 1.8-fold, respectively). Depending on the volume of tissues affected by cold, there was a decrease in the bioelectrical activity of muscles and an increase in the level of peripheral myoglobin in comparison to the control group. In group I patients, the amplitude of the M-response decreased by 3 times while the level of myoglobin increased by 3 times. In group II patients, the amplitude of the M-response decreased by 4 times. The amplitude of the M-response was decreased by 7 times, while myoglobin values increased by 6 times in all groups. In addition, group III exhibited an increase of 38 times in myoglobin levels. The residual latency was also increased in comparison to the control group, with patients in group I exhibiting an increase of 1.4 times, 1.7 times for patients in group II, and 2.4 times for patients in group III. Conclusion. In patients with deep frostbite, there is a rapid elevation in myoglobin levels during the early stages of cryoinjury, with myoglobinemia persisting in the long term after the injury. A high concentration of free myoglobin is linked with microcirculatory disorders and the development of localized neuropathy. Additionally, patients with frostbite experience a decrease in the amplitude of the M-response and an increase in residual latency.

For citation: Mikhailichenko M.I., Figursky S.A., Mudrov V.A., Dorzheev V.V., Mikhailichenko Yu.V., Shapovalov K.G. Rhabdomyolysis in the pathogenesis of local cold injury. Tromboz, gemostaz i reologiya. 2023;(4):68–74. (In Russ.).

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