By Francisco Gomez (left), MD, Mohammad El-Ghanem (center), MD and Fawaz Al-Mufti, MD (right)
The authors have no actual or potential conflict of interest in relation to the topics discussed in this column. This article may discuss non-FDA approved devices and “off-label” uses. The NCS and Currents do not endorse any particular device.
A significant portion of critically ill patients admitted to the ICU will eventually exhibit severe loss of strength and muscle mass, a phenomenon which has been termed ICU Acquired Weakness (ICUAW). ICUAW is clinically detectable acquired muscle strength deficit manifesting in all limbs. At the seven-day mark, an estimated 24-77 percent of critically ill patients will be affected. Muscle mass loss has been tallied at 5-13 percent on the first week of ICU stay alone, and resulting weakness carries with it far-ranging complications and consequences.
ICUAW is associated with aspiration events, delayed ventilator weaning, as well as increased length of stay and costs and higher mortality rate. Additionally, strength impairment may persist for up to eight years after discharge, resulting in decreased independence and quality of life. It has been posited that each day of bed rest in this population confers a 3-11 percent relative decrease in muscle strength over two-year follow-up.
Several risk factors have been identified for ICUAW such as sepsis, systemic inflammatory response syndrome, multiple organ failure and hyperglycemia. Other risk factors include medications such as corticosteroids, cathecolamines, aminoglycosides and colistin. Several of these factors are also associated with entities such as critical illness myopathy (CIM) and critical illness polyneuropathy (CIP), which can be causative of ICUAW. The pathophysiology behind CIP/CIM has been linked to pro-inflammatory cytokines, namely IL-1, IL-6 and TNF-alpha. Said inflammatory factors mediate axonal degeneration in CIP and myosin loss in CIM. TNF-a promotes muscle atrophy and has a direct catabolic action on differentiated muscle cells. In CIP, endothelial damage and local tissue edema impairing nerve microcirculation has been posited as the pathogenic mechanism.
Special attention has been given to immobility as a modifiable factor leading to ICUAW. Early mobilization and physical therapy can improve patient outcomes, lengths of stay and, potentially, long-term recovery. However, a subgroup of critically ill patients may be precluded from participating in rehabilitation given clinical instability, severity of illness and altered sensorium or consciousness.
Thus, neuromuscular electrical stimulation (NEMS) has emerged as an adjuvant therapy modality, with the advantage of not necessitating patient participation, or even consciousness. This intervention comprises the application of an electrical current to muscles via surface electrodes with activation of intramuscular nerve branches, leading to non-voluntary contraction. NEMS has exhibited the potential to preserve myocyte protein synthesis and prevent muscle catabolism or atrophy during prolonged immobilization. Other benefits of NEMS have been proposed, as NEMS was shown to increase circulating endothelial progenitor cells (EPCs) in critically ill septic patients. This cell lineage is associated with endothelial repair, which the authors theorized may aid recovery of systemic microcirculation in this patient group.
Initially showing benefit in patients with chronic diseases such as COPD and CHF, NEMS has been increasingly studied in the ICU setting, showing promise.
Systematic reviews have shown NMES when combined with standard therapy proves more effective than usual care alone for preventing strength loss in the critically ill. Most data has shown NEMS groups retain more strength than their counterparts. While muscle mass preservation analyses have yielded mixed data, most suggest NEMS does provide benefit.
One RTC in Brazil involving 24 patients focused on the rectus abdominus and pectoral muscles demonstrated a significant (p<0.001) difference in muscle cross section between the intervention and control groups. While the NEMS group had no loss of mass at the tested muscles at seven days, the control group demonstrated significant atrophy. In secondary outcome analysis, the NEMS group also demonstrated significantly decreased lengths of stay.
The CATASTIM2 study in Vienna demonstrated no significant changes in muscle mass between the treatment and control groups; however, observed strength recovery was increased by 450 percent in the treated group. In conclusion, there is moderate to strong evidence suggesting NEMS is beneficial and results in improved muscle strength outcomes. Notably, NMES in combination with usual therapy may result in accelerated ventilator weaning, and improvements in six-minute walking distance and bed to chair transfer as well as reducing incidence of critical illness CIM, CIP and ICUAW.
Implementation of NEMS as adjuvant therapy would pose an advantageous cost-benefit ratio. This therapy is low-risk, non-invasive and does not require patient cooperation. The apparatuses themselves are relatively inexpensive and are not overly complicated in their operation. Given potential benefits, NEMS seems to poses a beneficial proposition for our patients.
There are some limitations to the routine use of NEMS in critical care medicine. Firstly, as this technology is nascent there is a significant amount of heterogeneity among the described protocols. Existing studies varied in muscle groups treated or applied electrical current parameters leaves us without a clear guideline or operational consensus. Additionally, evaluation and reporting of muscle mass and cross-sections has been confounded by observed edema. Ultimately pathophysiological mechanisms of ICUAW and their interplay with NMES remain to be fully elucidated, and as with all incompletely understood variables, should be approached with caution.
Dall’Acqua, A et. al, Use of neuromuscular electrical stimulation to preserve the thickness of abdominal and chest muscles of critically ill patients: a randomized clinical trial . J Rehabil Med 2017; 49: 40–48Stefanou et al. Neuromuscular electrical stimulation acutely mobilizes endothelial progenitor cells in critically ill patients with sepsis Ann. Intensive Care (2016) 6:21 Fischer A, et al. Muscle mass, strength and functional outcomes in critically ill patients after cardiothoracic surgery: does neuromuscular stimulation help? The Catastim 2 randomized control trial.
Maffiuletti et al. Neuromuscular electrical stimulation for preventing skeletal-muscle weakness and wasting in critically ill patients: a systematic review
BMC Medicine 2013, 11:137 #LeadingInsights #TechCorner #FranciscoGomez #MohammedEl-Ghanem #FawazAl-Mufti #June2018