446 - Tourniquet-induced nerve compression injuries caused by high pressure levels and gradients

this progression in safety was evident from the introduction of a non-pneumatic elastic tourniquet ring which produced high pressure gradients and uncontrolled applied pressure levels, resulting in reports of nerve injuries and pulmonary embolism [6 – 8]. While automatically controlled pneumatic tourniquets have improved the safety, accuracy and reliability of restricting and occluding blood flow into limbs, it remains important to review the evidence of how and why tourniquet-related nerve injuries occur to identify and ameliorate key risk factors associated with tourniquet use. It is estimated that tourniquet systems are used in more than 15,000 surgical procedures around the world daily [8], but their widespread adoption is not without clinical risk of injuries. Skin, muscle, nerve, blood vessels and connective tissue (in isolation or combination) are subject to potential tourniquet damage manifested by numbness, paresis or paralysis with muscle atrophy [2, 8]. Present evidence has demonstrated that lower tourniquet pressure levels and pressure gradients applied for short durations of time de- creases both frequency and severity of tourniquet-induced injuries [1, 9]. Nevertheless, clinical protocols for tourniquet usage have not significantly evolved since safer automated technology was introduced [1, 5, 8]. Further motivation to review the existing evidence of the causes of tourniquet-related injuries has arisen from the recent use of tourniquets more broadly in periopera- tive and non-operative applications, including pre- hospital trauma settings and newly established blood flow restriction (BFR) therapies [1, 3, 10, 11]. The les- sons learned through advancements in surgical tourni- quet technology should be applied to these broader settings. A better understanding of how tourniquets are being used outside of the surgical setting may enable surgeons to improve the treatment of their patients. Due to key differences in both the design and application of pre-hospital tourniquets compared with classical surgical tourniquets, there is a need for guidelines to establish best practices for admitting patients to the hospital with a pre-applied tourniquet. In another application, the use of surgical-grade tourniquets in blood flow restriction therapy can be incorporated into the surgical treatment plan during both the prehabiliation and rehabilitation phases. BFR therapy has been shown to increase muscle strength and mass at low loads to protect the healing limb, reducing overall recovery times [10]. Surgeons can play a key role in the prescription of safe and effective use of BFR therapy based on their knowledge of risks as- sociated with surgical tourniquet use. Main text Nerve compression injury It is almost 50 years since Ochoa et al. [12] demonstrated that the damage to nerve fibers resulting from a compression tourniquet was the direct result of the ap- plied pressure, and not a consequence of secondary ische- mia, and that the pressure gradient was higher near the edges rather than in the middle of a tourniquet. Subse- quent studies have shown that ischemia is also of rele- vance, particularly at the distal cuff edge and below [13]. In patients with tourniquet-induced paralysis there is focal conduction delay at the level of the tourniquet border zone which likely reflects the functional equivalent of the structural abnormalities observed by Ochoa et al. (Fig. 1) [12]. Tourniquet compression nerve injuries are typically transient, and resulting symptomatology is mild to moder- ate [14]. However, when the applied pressure gradient is high, there is a risk of axonal injury with subsequent axonal degeneration and accompanying target muscle fibre atrophy [14]. If this happens recovery may be pro- longed (lasting weeks or even months). Further, because of potential mal-innervation, recovery may be incomplete with functionally impaired fractionation of movement and/or permanent sensory deficit. This is especially true when the upper limb is involved. Because upper extremity nerves are closer to the skin surface, or adjacent to bone they are more susceptible to direct compression injury [1, 4]. Upper extremity nerve injuries are more commonly re- ported than in the lower limb, with the radial nerve being the most vulnerable [1, 15, 16]. Thus location of tourni- quet placement is also significant for reducing the risk of direct nerve compression [1, 8, 15]. Although there has been considerable investigation into the pathological sequelae of chronic nerve compres- sion, both in humans and a variety of animal models, much less is known about acute effects of compression as they may occur initially with tourniquet use. In the acute phase of nerve compression conventional nerve conduction studies are of limited value and usually nor- mal. Nerve excitability studies have emerged as a recent novel, non-invasive technique, that allows for the assess- ment of peripheral axonal biophysical properties that in- clude ion channels, energy-dependent pumps and membrane potential in both health and disease [17, 18]. These biophysical properties likely become deranged during compression. Temporary compression-related symptoms are common and predominantly sensory. After 30 – 60 min, inflation of a tourniquet is frequently followed by the development of a dull aching pain, despite adequate re- gional anaesthesia. Tourniquet pain reflects selective pain transmission of unmyelinated, slowly conducting C fibres, which are continuously stimulated by skin compression. Muscle injury After tourniquet application there is progressive cellular hypoxia, acidosis, and cooling in the occluded limb [19]. | The Surgical Technologist | FEBRUARY 2021 68