When examining the litany of documented adverse events associated with tourniquet use, there are three easily-identified, broad categories of tourniquet-related complications: muscle injury; nerve injury; and coagulopathy. All of these complications fundamentally relate to ischemia and compression resulting from tourniquet use. While one can instinctively think of nerve and muscle damage as related to direct pressure (or compression), all three categories are more likely secondary to a combination of both ischemic and compressive factors.
What Is The Relationship Between Muscle Injury And Tourniquet Use?
Muscle Injury. This can manifest as decreased contractile strength; reperfusion injury; pain or post-tourniquet syndrome. Skeletal muscle injury in relation to tourniquet use is reasonably well-documented and is influenced both by the compression and ischemia created from a tourniquet. The skeletal muscles distal to the tourniquet experience these effects at a molecular level, primarily through prolonged inadequate blood flow (i.e. ischemia) and subsequent restoration of circulation (i.e. reperfusion injury).
When creating an ischemic environment in skeletal muscle via application of a tourniquet, the response at the cellular level includes decreased protein synthesis, increased degradation of protein and an up-regulation of cell stress pathways (including increased glycerol), creating an environment for reperfusion injury.1-3 The rate of skeletal muscle metabolic recovery with reperfusion depends on the duration of ischemia;1-2 this recovery rate lengthens significantly after three hours of ischemia secondary to adenosine triphosphate (ATP) depletion in an anaerobic metabolic environment.4-8
Aside from reperfusion injury at a cellular level, one can also observe muscular injury changes at the histologic level. Following one to three hours at a 350mmHg (400mmHg for human reference) tourniquet setting, early signs of muscle damage in human, canine and rabbit studies included inflammatory reactions, intra-fiber and extracellular edema, mild focal and regional necrosis, and granular degeneration.6,7,9-11 The combined effect of muscle ischemia with micro-traumatic changes from tourniquet use results in the coined phenomena “post-tourniquet syndrome,” characterized by stiffness, pallor, weakness and subjective numbness of the affected extremity (without objective anesthesia).12
Along with ischemic injury to skeletal tissues, compression injuries via tourniquet application can result in muscular deficits post-operatively.4,13-16
In a rabbit model, quadriceps musculature compressed at 350 mmHg for two hours demonstrated markedly decreased function at two days postop (21 percent of normal) with restoration to only 83 percent of normal at three weeks.6,17 Longer periods of post-operative monitoring in total knee arthroplasty (TKA) trials (up to three months), which demonstrate quadriceps muscular deficits with tourniquet use at the three-month mark in comparison to the control group (no tourniquet utilized).18
When considering the use of a tourniquet during surgery, the complications on a physiologic level may seem remote, however, these changes could potentially result in functional abnormalities that interfere with patient rehabilitation and overall outcomes. Currently, increased interest in tourniquet-induced muscle injury and its implication on post-operative outcomes may shed additional light on proposed tourniquet standards.18,19
What You Should Know About Nerve Injury And Surgical Tourniquets
Nerve Injury. Though seemingly rare, the reported risk of neurological complications (sensory neuropathy, pain, paralysis) stemming from tourniquet use is documented to range between 0.1 and 7.7 percent, primarily been documented in studies utilizing thigh tourniquets.20-25 Along with incidence, the severity of nerve injuries related to tourniquet usage also varies. Reports range anywhere from a mild transient functional loss to permanent irreversible damage.24 One might question the exact relationship between tourniquet use and nerve function based on this variance.
Generally well-studied via multimodal examination techniques, including histologic evaluation, nerve conduction velocity (NCV) studies and electromyography (EMG), the two primary postulated etiologies that we observed for tourniquet-induced nerve injury are ischemia and direct mechanical effects (i.e. pressure, shearing forces, etc.).
Compression to a nerve can result in axonal degeneration, as well as have a direct effect to the Nodes of Ranvier (via paranodal myelin invagination), thereby impacting the quality of nerve function.26,27
In their 1972 study, Ochoa and colleagues demonstrated and explained the functional impact of tourniquet use as it relates to nerve injury; with severe nerve injuries resulting in Wallerian degeneration, creating a loss of nerve excitability distal to the lesion origin (recovery may take many months), intermediate nerve injuries resulting in a local conduction block with preservation of distal excitability (recovery may take several weeks) and mild nerve injuries producing a physiological block (immediate recovery occurring with pressure release).26
Though utilizing much higher tourniquet pressures than currently acceptable, historical studies helped demonstrate that nerve injury and dysfunction is most prominent at the outer edges of the tourniquet cuff where shear stress is maximal, sparing the central cuff portion, and sparing the nerves distal to the cuff from direct injury.26 As with the natural history of nerve injuries, dependent on the severity, partial or incomplete nerve lesions are generally likely to undergo spontaneous resolution within six months.12
Though nerve injury correlated to tourniquet use variables (duration, pressure, population, etc.) in human subjects is not abundatnt in literature, some studies do exist. In 1979, one clinical study aimed to distinguish the relationship between EMG abnormalities, the duration of tourniquet inflation and patient clinical recovery time as it relates to thigh tourniquet use during orthopedic procedures.28
This study demonstrated that compression duration resulted in distinct differences in EMG abnormalities, with short tourniquet time (less than 15 minutes) revealing 22 percent of subjects with EMG abnormalities and longer tourniquet time (greater than 60 minutes) resulting in 85 percent of subjects with EMG abnormalities. In total, 62.5 percent of patients in the study had documented changes on EMG postop; with an average duration of 51 days (ranging from 27 days to five months) prior to resolution.28
The authors hypothesized this delayed recovery to result from a slowly-resolving axonal compression syndrome caused by prolonged inflation of the pneumatic tourniquet. This study supports the inverse relationship between duration of tourniquet use and nerve function; with greater duration of tourniquet use resulting EMG changes both in the proximal thigh muscles (quadriceps) and extending to posterior lower leg muscles (gastrocnemius). The authors also demonstrate a direct relationship between duration of use and time to clinical recovery (i.e. increased tourniquet inflation time is related to increased time to clinical recovery).28
Instead of looking at the specific changes in neurological function and characterizing the severity of nerve injury, some studies aim to quantify the overall probability of nerve injury with tourniquet use and identify any risk factors.20,26,29 As previously mentioned, the incidence of nerve injury ranges anywhere from 0.1 to 7.7 percent with the majority of literature derived from thigh tourniquet use.20-23,25
A 2018 retrospective review of close to 40,000 total knee arthroplasties, identified risk factors for nerve injury with tourniquet use and found a total incidence of 0.16 percent.25 One risk factor described in this review and others is the relationship demonstrated between increased peroneal nerve palsies (i.e. foot drop) and patients with lumbar pathologies (history of lumbar stenosis, lumbar spine surgery, etc.).25,30,31 This review also identified an increased incidence of nerve injury in the female gender, hypothesized to be secondary to reduced soft tissue (muscle/fat), thought to protect the nerve from direct injury via compression.25
From a 2006 retrospective review of neurologic complications during orthopedic procedures, authors noted that nerve palsies documented included peroneal and tibial nerves, 89 percent of the peroneal nerve palsies resolved, 100 percent of the tibial nerve palsies recovered, reperfusion intervals only modestly decreased the probability of nerve injury and, in general, the probability of neurologic dysfunction increased with tourniquet time (incidence of palsies increased when tourniquet time is greater than 150 minutes).20
Other studies echo the observance of mononeuropathy incidence being greater in sciatic (approximately 91 percent, tibial and peroneal) distributions, followed by femoral distribution (approximately nine percent of all tourniquet-related mononeuropathies) but fail to find a direct relationship between tourniquet time and nerve injury probability.20 Though tourniquet time and specific nerve-related injury could be ‘debatable,’ the use of a tourniquet for two or less hours is the standard of care until randomized control trials establish a more optimal tourniquet time.
What About CRPS?
When discussing nerve injuries and tourniquet usage, it is prudent to mention complex regional pain syndrome type I (CRPS-I; also referred to as reflex sympathetic dystrophy) and how, if at all, it relates to tourniquet usage. Some propose that CRPS-I may be secondary to an ischemia-reperfusion injury in which there is alteration on a microcirculatory level leading to persistent inflammation and symptoms resembling CRPS-I.32 Others researching this topic suggest a physiologic alteration of oxygen consumption that occurs with subsequent reperfusion after tourniquet deflation, leading to increased formation of toxic oxygen radicals and predisposing an individual to the development of CRPS.33
This theory has led to certain recommendations of perioperative prophylactic measures targeted to reduce the radicals and/or scavengers, thus hypothetically decreasing the chance of CRPS recurrence or progression of the condition.33 In 2009, Besse and colleagues attempted to elucidate the relationship between tourniquet use and CRPS development by evaluating for factors associated with CRPS occurrence after foot and ankle surgery. In this study, they demonstrated a 10-fold increased risk and statistically significant correlation for patients with prior history of CRPS and development of the condition after surgery.34
Though an association in literature between CRPS diagnosis and a history of CRPS exists34, the relationship between development of CRPS and tourniquet usage remains unclear. However, with the information at hand, surgeons planning to operate with use of a tourniquet on patients with a history of CRPS should consider implementation of preventative modalities and measures to decrease risk of CRPS recurrence until there is further clarification of the association between tourniquets and CRPS incidence.
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