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10 Frailty andMobility Degeneration inDiabetes andDiabetic Foot Ulceration

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40. de Oliveira AL, Moore Z.Treatment of the diabetic foot by ofoading: a systematic review. J Wound Care. 2015;24(12):560. https://doi.org/10.12968/

jowc.2015.24.12.560, 2–70. PubMed PMID:

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41. Schwenk M, Mohler J, Wendel C, D’Huyvetter K, Fain M, Taylor-Piliae R, et al. Wearable sensorbased in-home assessment of gait, balance, and physical activity for discrimination of frailty status: baseline results of the Arizona frailty cohort study. Gerontology. 2015;61(3):258–67. https://doi.

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43. Fried LP, Tangen CM, Walston J, Newman AB, Hirsch C, Gottdiener J, etal. Frailty in older adults: evidence for a phenotype. J Gerontol A Biol Sci Med Sci. 2001;56(3):M146–56. https://doi.org/10.1093/

gerona/56.3.m146. PubMed PMID: 11253156.

44. Naja B, Armstrong DG.Gait inefciency induced by ofoading – critically unintended consequences for the diabetic foot in remission. 8th International Symposium on the Diabetic Foot 2019, The Hague, The Netherlands; 2019.

45. Zhou H, Park C, Shahbazi M, York MK, Kunik ME, Naik AD, etal. Digital biomarkers of cognitive frailty: the value of detailed gait assessment beyond gait speed. Gerontology. 2021;68:1–10.

46. Alalo J, Karunananthan S, Eisenberg MJ, Alexander KP, Bergman H. Role of frailty in patients with cardiovascular disease. Am J Cardiol. 2009;103(11):1616–21.

47. Kulmala J, Nykänen I, Hartikainen S.Frailty as a predictor of all-cause mortality in older men and women. Geriatr Gerontol Int. 2014;14(4):899–905.

48. Lee H, Joseph B, Enriquez A, Naja B.Toward using a smartwatch to monitor frailty in a hospital setting:

using a single wrist-wearable sensor to assess frailty in bedbound inpatients. Gerontology. 2017;64:389.

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49. Theou O, Cann L, Blodgett J, Wallace LM, Brothers TD, Rockwood K. Modications to the frailty phenotype criteria: Systematic review of the current literature and investigation of 262 frailty phenotypes in the Survey of Health, Ageing, and Retirement in Europe. Ageing Res Rev. 2015;21:78–94. https://

doi.org/10.1016/j.arr.2015.04.001. PubMed PMID:

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50. Theou O, Brothers TD, Mitnitski A, Rockwood K. Operationalization of frailty using eight commonly used scales and comparison of their ability to predict all-cause mortality. J Am Geriatr Soc. 2013;61(9):1537–51. https://doi.org/10.1111/

jgs.12420. PubMed PMID: 24028357.

51. Rockwood K, Jones D, Wang Y, Carver D, Mitnitski A.Failure to complete performance-based measures is associated with poor health status and an increased risk of death. Age Ageing. 2007;36(2):225–8. https://

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52. Rockwood K, Song X, MacKnight C, Bergman H, Hogan DB, McDowell I, etal. A global clinical measure of tness and frailty in elderly people. CMAJ. 2005;173(5):489–95.

53. Kojima G, Iliffe S, Walters K.Frailty index as a predictor of mortality: a systematic review and metaanalysis. Age Ageing. 2018;47(2):193–200.

54. Cesari M, Gambassi G, van Kan GA, Vellas B.The frailty phenotype and the frailty index: different instruments for different purposes. Age Ageing. 2014;43(1):10–2. https://doi.org/10.1093/ageing/

aft160. PubMed PMID: 24132852.

55. Naja B, Armstrong DG.Smart technology for the diabetic foot in remission. In: Boulton AJM, etal., editors. The foot in diabetes. NewYork, NY: Wiley;

2020. p.201–24.

56. Toosizadeh N, Yen TC, Howe C, Dohm M, Mohler J, Naja B. Gait behaviors as an objective surgical outcome in low back disorders: A systematic review. Clin Biomech. 2015;30(6):528–36. https://

doi.org/10.1016/j.clinbiomech.2015.04.005. PubMed

PMID: 25921552; PubMed Central PMCID: PMC4714541.

57. Lee H, Joseph B, Enriquez A, Naja B. Toward using a smartwatch to monitor frailty in a hospital setting: using a single wrist-wearable sensor to assess frailty in bedbound inpatients. Gerontology. 2018;64(4):389–400.

58. Kang GE, Naik AD, Ghanta RK, Rosengart TK, Naja B. A wrist-worn sensor-derived frailty index based on an upper-extremity functional test in predicting functional mobility in older adults. Gerontology. 2021;67:1–9.

59. Kang GE, Zhou H, Varghese V, Naja B.Characteristics of the gait initiation phase in older adults with diabetic peripheral neuropathy compared

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to control older adults. Clin Biomech. 2020;72: 155–60.

60. Kang GE, Yang J, Naja B. Does the presence of cognitive impairment exacerbate the risk of falls in people with peripheral neuropathy? An application of body-worn inertial sensors to measure gait variability. Sensors. 2020;20(5):1328.

61. Zahiri M, Wang C, Gardea M, Nguyen H, Shahbazi M, Sharafkhaneh A, et al. Remote physical frailty monitoring–the application of deep learning-based image processing in tele-health. IEEE Access. 2020;8:219391–9.

62. Cacciatore F, Testa G, Galizia G, Della-Morte D, Mazzella F, Langellotto A, etal. Clinical frailty and long-term mortality in elderly subjects with diabetes. Acta Diabetol. 2013;50(2):251–60.

63. Chode S, Malmstrom T, Miller D, Morley JE.Frailty, diabetes, and mortality in middle-aged African Americans. J Nutr Health Aging. 2016;20(8):854–9.

64. Takeji Y, Yamaji K, Tomoi Y, Okazaki J, Tanaka K, Nagae A, etal. Impact of frailty on clinical outcomes in patients with critical limb ischemia. Circ Cardiovasc Interven. 2018;11(7):e006778.

65. O’Donovan M, Sezgin D, O’Caoimh R, Liew A.The impact of and interaction between diabetes and frailty on psychosocial wellbeing and mortality in Ireland. Int J Environ Res Public Health. 2020;17(24):9535.

66. Bąk E, Młynarska A, Marcisz C, Bobiński R, Sternal D, Młynarski R.The inuence of frailty syndrome on quality of life in elderly patients with type 2 diabetes. Qual Life Res. 2021;30:1–9.

67. Kang GE, Naja B. Sensor-based daily physical activity: towards prediction of the level of concern about falling in peripheral neuropathy. Sensors. 2020;20(2):505.

68. Van Epps P, Oswald D, Higgins P, Hornick T, Aung H, Banks R, etal. Frailty has a stronger association with inammation than age in older veterans. Immun Ageing. 2016;13(1):1–9.

69. Morley JE, Vellas B, Van Kan GA, Anker SD, Bauer JM, Bernabei R, et al. Frailty consensus: a call to action. J Am Med Dir Assoc. 2013;14(6):392–7.

70. Kang GE, Sharafkhaneh A, Bryant MS, Nguyen C, Ruiz I, Sharafkhaneh S, etal. Efcacy of telerehabilitation on exercise capacity and frailty in veterans with chronic pulmonary obstructive disease: 1397. Med Sci Sports Exerc. 2021;53(8S):458.

71. McAdams-DeMarco MA, Isaacs K, Darko L, Salter ML, Gupta N, King EA, et al. Changes in frailty after kidney transplantation. J Am Geriatr Soc. 2015;63(10):2152–7.

72. Armstrong DG, Lavery LA, Fleischli JG, Gilham KA. Is electrical stimulation effective in reducing neuropathic pain in patients with diabetes? J Foot Ankle Surg. 1997;36(4):260–3.

73. Naja B, Talal TK, Grewal GS, Menzies R, Armstrong DG, Lavery LA.Using plantar electrical stimulation to improve postural balance and plantar sensation among patients with diabetic peripheral neuropathy: a randomized double blinded study. J Diabetes Sci Technol. 2017;11(4):693–701.

74. Zulbaran-Rojas A, Park C, El-Refaei N, Lepow B, Naja B.Home-based electrical stimulation to accelerate wound healing—a double-blinded randomized control trial. J Diabetes Sci Technol. 2021;17:15.

75. Kang GE, Zahiri M, Lepow B, Saleem N, Naja B.The effect of daily use of plantar mechanical stimulation through micro-mobile foot compression device installed in shoe insoles on vibration perception, gait, and balance in people with diabetic peripheral neuropathy. J Diabetes Sci Technol. 2019;13(5):847–56.

76. Geirsdottir O, Arnarson A, Briem K, Ramel A, Jonsson P, Thorsdottir I. Effect of 12-week resistance exercise program on body composition, muscle strength, physical function, and glucose metabolism in healthy, insulin-resistant, and diabetic elderly Icelanders. J Gerontol A Biomed Sci Med Sci. 2012;67(11):1259–65.

77. Zhou H, Al-Ali F, Kang GE, Hamad AI, Ibrahim RA, Talal TK, etal. Application of wearables to facilitate virtually supervised intradialytic exercise for reducing depression symptoms. Sensors. 2020;20(6):1571.

78. Rahemi H, Chung J, Hinko V, Hoeglinger S, Martinek WA, Montero-Baker M, et al. Pilot study evaluating the efcacy of exergaming for the prevention of deep venous thrombosis. J Vasc Surg Venous Lymph Disord. 2018;6(2):146–53.

79. Grewal GS, Schwenk M, Lee-Eng J, Parvaneh S, Bharara M, Menzies RA, etal. Sensor-based interactive balance training with visual joint movement feedback for improving postural stability in diabetics with peripheral neuropathy: a randomized controlled trial. Gerontology. 2015;61(6):567–74.

Anesthesia fortheDLS Patient: Minimizing Risk andMaximizing Safety

KasraRazmjou andAndyLiao

Preoperative Optimization

In an effort to accommodate an aging population with chronic diseases, the American Society of Anesthesiologists (ASA) developed the perioperative surgical home [1]. The PSH aims to optimize patient care through the process of surgery and recovery, beginning in the preoperative stage. During this period, the anesthesiology service will collaborate with the surgeon and primary care physician to evaluate the patient’s history, comorbidities, and goals of surgery. They will also make recommendations on additional testing and medical management in preparation for surgery. At this point, the patient’s team is focused on optimizing the patient for successful surgery and postoperative recovery. The DLS patient will likely require multiple surgeries and hospitalizations; thus the PSH model is ideal in maintaining anesthesiology’s continual presence in the patient’s care.

DLS patients tend to have several medical comorbidities including hypertension, coronary artery disease (CAD), arrhythmia, cerebrovascu-

K. Razmjou (*) Regional Anesthesia and Acute Pain Medicine, MedStar Medical Group Anesthesiology, Baltimore, MD, USA e-mail: kasra.a.razmjou@medstar.net

A. Liao North American Partners in Anesthesia, Melville, NY, USA

lar disease (CVD), obesity, hyperlipidemia, renal disease, elderly age (60+ years of age), chronic lung disease, and history of smoking [2, 3]. These disease processes all negatively impact the cardiovascular system and should be medically optimized in preparation for anesthesia.

In 2014, the American College of Cardiology (ACC) and American Heart Association (AHA) developed guidelines for perioperative cardiovascular evaluation for the management of patients undergoing noncardiac surgery [4]. These guidelines provide a stepwise algorithm stratifying the risk of patients with potential cardiovascular conditions. The rst step assesses the urgency of surgery for patients with risk factors or a history of CAD [5]. Risk factors for CAD were rst introduced by the Framingham Heart Study [6], but now can be taken from the ACC/AHA Atherosclerotic Cardiovascular Disease (ASCVD) risk calculator [7]. This tool considers age, low-density lipoprotein (LDL), total cholesterol, blood pressure, diabetes, and smoker status. These risk factors and the urgency of surgery should be evaluated in a discussion between the surgeon and anesthesiologist. If surgery can be delayed, the ideal plan of action involves treating the underlying cardiovascular issues prior to surgery. Unfortunately, in the DLS population critical limb ischemia and sepsis are common causes of urgent and emergent surgical interventions [8]. The second step evaluates the patient for acute coronary syndrome (ACS), which requires

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referral to the cardiology service for evaluation and management. The third step proceeds if the surgery is deemed non-emergent; the patient does not have ACS, but the patient has risk factors for CAD. At this point, the anesthesiology service will assess the patient’s risk for major adverse cardiovascular events (MACE) dened as total death, myocardial infarction (MI), stroke, hospitalization due to heart failure (HF), and ACS requiring revascularization via percutaneous coronary intervention (PCI) or coronary artery bypass graft (CABG). This risk can be evaluated by the American College of Surgeons National Surgical Quality Improvement Program (NSQIP) or the Revised Cardiac Risk Index (RCRI). Although there has not been a clear consensus on which calculator is superior [9], the RCRI is easier to remember and simpler to use with only six risk factors. The RCRI risk factors include the type of surgery, ischemic heart disease, congestive heart failure (CHF), CVD, insulin dependence, and preoperative creatinine greater than 2mg/dL.These risk factors are each assigned one point, cumulatively translating into the risk of MACE.A score of two points indicates a 10% risk of MACE and suggests further evaluation and testing may be necessary.

The common comorbidities of the DLS population will likely fulll several risk factors for MACE and necessitate further cardiovascular evaluation. In patients with elevated risk for MACE, the next step evaluates functional capacity through the Duke Activity Status Index (DASI). This series of self-reported activities correlate with functional status or assesses metabolic equivalents (METs), which can be objectively tested through cardiopulmonary exercise testing. The ACC/AHA guidelines indicate that moderate functional capacity or about 4 METs (and a DASI score of 10) is the minimum requirement for proceeding to surgery. This can be estimated with the ability to walk up two ights of stairs without chest pain or shortness of breath. Most DLS patients will not be able to answer this question accurately and require further assessment due to unknown functional capacity. Exercise stress testing is typically the next step in objectively assessing functional status. This may

not be physically feasible for DLS patients, leaving pharmacologic stress testing as the best alternative. If the stress test results are abnormal, the ACC/AHA guidelines recommend considering coronary angiography and revascularization.

In the DLS population, glucose control is especially important in medically optimizing patients for surgery and recovery. Hospital systems may have their own guidelines for appropriate preoperative serum glucose, and the denition of glucose control may vary across groups. Based on the widely cited NICE-SUGAR study, serum glucose is ideally kept in the 140–180 mg/dL range [10]. Although this is based on patients in the intensive care unit, this can be translated to the realm of anesthesia where surgical stress, medically induced comas, and potentially signicant uid shifts can occur. Glucose control is important for proper wound healing and avoidance of hypoglycemic or hyperglycemic coma [11]. Preoperative glucose control will allow for more optimal control in the intraoperative and postoperative settings.

Intraoperative Risk Mitigation

Surgical interventions will inevitably require the specialty care of anesthesiologists, especially within the DLS patient population. This group typically has several comorbidities affecting the cardiovascular system and requires many anesthetic considerations to maximize patient safety.

Nil per os (NPO) guidelines were developed by the ASA in an effort to prevent aspiration risk associated with sedation and anesthesia [12]. The data was based on gastric pH and volumes relative to the time of fasting, resulting in the recommendation of at least 8h of fasting prior to surgery. However, these guidelines assume normal gastric motility. In the DLS population, diabetic gastroparesis is a possibility and delayed gastric emptying should be considered when assessing NPO status. Although the incidence of gastroparesis is 4.6% in type 1 diabetics and

1.3% in type 2 diabetics [13], abdominal fullness or bloating are associated with diabetic gastroparesis [14] and should be factored into determining

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whether a patient is appropriately NPO. The administration of increasing depths of anesthesia can lead to an inability to protect the airway and the aspiration of gastric contents. In the incidence of an increased risk of aspiration, the anesthetic may be modied to use minimal to no sedation with a regional anesthesia technique to preserve airway reexes, or general anesthesia with an endotracheal tube to ensure a secure airway.

The intraoperative management of DLS patients can include general or regional anesthesia. General anesthesia is dened as the lack of response to surgical stimulus, allowing the surgeon to safely focus on the procedure. General anesthesia involves administering a mixture of sedatives, hypnotics, and analgesics that invariably lead to hypotension and airway obstruction. This may potentially result in organ damage, brain injury, and death if not managed by an experienced anesthesiologist.

Anesthesiologists are prudent about which patients can safely be anesthetized as there are many considerations to be made prior to proceeding with general anesthesia. Other than cardiovascular catastrophes, the ACC/AHA guidelines do not address other concerns in the perioperative period. Patients with obstructive sleep apnea (OSA) are at risk for many anesthesia-related complications [15]. These same patients are commonly obese and may also have difcult airway placement, which can signicantly increase the danger of inducing a general anesthetic [16]. General anesthesia is notorious for having a high incidence of nausea, and prophylactic antiemetics are routinely administered [17]. Due to these risks and adverse effects, the use of regional anesthesia, which includes neuraxial anesthesia and peripheral nerve blockade, may be safer.

Neuraxial anesthesia involves the injection of local anesthetic into the epidural and/or intrathecal space to achieve surgical anesthesia at the spinal cord [18]. When neuraxial anesthesia is utilized, it obviates the need for general anesthesia. These patients generally tolerate surgery with minimal or no sedation, which allows the anesthesiologist to avoid the risks associated with general anesthesia.

Neuraxial anesthesia includes two techniques, spinal and epidural. Spinal anesthesia involves intrathecal injection of local anesthetic with or without an adjuvant, resulting in the abolition of motor and sensory transmission from the level of the injected site. Epidural anesthetics involve injection in the epidural space. Catheters may be used for both techniques, allowing for the continuous infusion of local anesthetic. In addition to providing surgical anesthesia, neuraxial catheters can be used postoperatively for pain control. However, the catheter may be a conduit for potential infection, increasing with the amount of time the catheter remains in place. For this reason, neuraxial catheters are usually used for short-term periods. Contraindications to neuraxial blockade include patient refusal, infection at the injection site, systemic infection, coagulopathy, hemodynamic instability or hypovolemia, preload-dependent states such as hypertrophic obstructive cardiomyopathy (HOCM), severe compressive radiculopathy at the level of insertion, and increased cranial pressure [19]. DLS patients are vasculopathic and are commonly on anticoagulation and/or antiplatelet regimen, especially if recently revascularized. This must be weighed in the decision to pursue neuraxial anesthesia due to the increased risk of epidural hematoma [20].

The use of neuraxial blockade intraoperatively raises concern as neural blockade of sympathetic bers may lead to hypotension; however, this is usually reversible and can be treated with intravenous hydration and vasopressors. Other intraoperative concerns of neuraxial anesthesia include paresthesia due to trauma to the spinal cord, cardiopulmonary compromise due to high spinal level, nausea and vomiting typically caused by hypotension, postdural puncture headache, urinary retention, and infection [21]. Additionally, neuraxial procedures require a cooperating patient to appropriately position, which may not be feasible for a bedbound, deconditioned DLS patient.

Peripheral nerve (or perineural) blockade extends the concept of neuraxial anesthesia, and entails depositing local anesthetics around nerves distal to the spinal cord. The local anesthetic acts to halt the transmission of pain to the spinal cord.

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Since injection around the spinal cord is avoided, peripheral nerve blockade circumvents many of the aforementioned adverse effects related to neuraxial anesthesia, especially autonomic blockade. For upper extremity procedures, common brachial plexus nerve blocks include interscalene, supraclavicular, infraclavicular, and axillary nerve blocks. For lower extremity procedures, common nerve blocks aim to block branches of the lumbar and sacral plexus, including the femoral, obturator, lateral femoral cutaneous, and sciatic nerves. Ankle blocks target the distal branches of the femoral and sciatic nerve and are commonly used for foot procedures. The type of block selected is based on the location of surgery and the associated dermatomes, myotomes, and osteotomes. Like neuraxial procedures, peripheral nerve blocks can be extended with the use of catheters for postoperative pain control.

Peripheral nerve blocks were historically performed based on anatomic landmarks and patient feedback via transient paresthesia. The advent of peripheral nerve stimulators allows the anesthesiologist to assess if the location of the needle is adequate based on the motor response elicited relative to a programmed current. The development of ultrasound technology has allowed providers to achieve successful nerve blockade at a higher rate with a lower amount of local anesthetic, thus reducing the risks of local anesthetic systemic toxicity among other adverse effects [22]. Similar to neuraxial anesthesia, peripheral nerve blockade can be used to obtain surgical anesthesia with minimal to no sedation. Peripheral nerve blocks also avoid many of the risks related to neuraxial anesthesia. Although rare, nerve injury, infection, and local anesthetic systemic toxicity may occur with any regional anesthesia technique. Due to the relative safety of this approach, peripheral nerve blockade is an attractive alternative [23].

Postoperative Recovery Optimization

Up to 40,000 amputations are performed in the United States (US) annually. In 2005, 1.6 million people in the US were living with a limb amputa-

tion [24]. Amputation may have sequelae of residual limb pain (RLP), sometimes referred to as stump pain, and phantom limb pain (PLP). Both phenomena can develop into chronic pain after amputation (CPAP) [25]. RLP occurs at the actual site of the amputated limb and is caused by nerve entrapment, neuroma formation, surgical trauma, ischemia, skin breakdown, or infection [26]. PLP is described as chronic, severe pain or unpleasant sensation in a part of the body that no longer exists after amputation. PLP develops as early as 24 h to 1 week after amputation. The prevalence of PLP varies from 40 to 80% depending on the site of amputation, causation leading to amputation, and time since amputation [27]. In differentiating RLP from PLP, a thorough physical exam of the amputation site can rule out RLP, and other pain ndings such as the quality and severity of pain, sensation, allodynia, and hyperalgesia should be noted as well. Patients with chronic back pain with radiculopathy can be mistaken for PLP and should be ruled out [28]. The exact cause for the development of PLP is unclear, but has been found to be multifactorial including peripheral, central, and psychological factors. Phantom limb sensation (PLS), RLP, preamputation pain, and diabetes are risk factors for developing PLP [29].

While treatment of RLP involves addressing the underlying cause, treatment for PLP) is more difcult and focuses on symptom management. Poor management of PLP may lead to increased incidence of obesity, cardiovascular disease, sleep disorders, chronic joint pain, and lower back pain [30]. A conservative, interdisciplinary approach to preventing PLP involving physical therapists, prosthetic professionals, mental health professionals, and pain specialists is benecial in addressing potential RLP and PLP.

Common pharmacotherapies for PLP such as NSAIDs and acetaminophen are starting points for any pain regimen. Opioids are commonly used, but should be used conservatively to avoid tolerance and dependence, and are best used with adjuvants. Adjuvant medications include tricyclic antidepressants (TCAs) such as amitriptyline, and anticonvulsants such as gabapentin and pregabalin. Although both TCAs and anticonvul-

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sants have been extensively studied, both show mixed results, and evidence has been inconclusive for recommendation. NMDA antagonists such as ketamine may be helpful, especially in patients with chronic pain syndromes. One review analysis recommends a regimen of intravenous ketamine and intravenous morphine for acute treatment of PLP and oral morphine for intermediate- to long-term treatment (8weeks to 1 year) [31]. Topical capsaicin can help reduce hypersensitivity, and botulinum toxin type B can improve hyperhidrosis to facilitate prosthetic use. However, a Cochrane review for the current pharmacologic interventions in treating PLP concluded the available studies are not large enough to demonstrate evidence that pharmacologic therapies should be recommended in the treatment of PLP [32]. Pharmacologic therapy will remain a mainstay in patient care due to familiarity with the usage of medications, and the convenience of having a treatment modality that physicians can prescribe in the outpatient setting for patients to self-administer at home.

There is much research without denitive evidence for non-pharmacologic options such as transcutaneous electrical nerve stimulation (TENS), spinal cord simulation (SCS), peripheral nerve stimulation (PNS), sympathetic nerve block, mirror therapy, augmented reality biofeedback, acupuncture, and stump revision. Surgical techniques include peri-neuromal lidocaine injection, targeted nerve implantation, and targeted muscle re-innervation. These techniques have shown some efcacy in preventing PLP.

Peripheral nerve blockade has been studied as a non-opioid, non-systemic, targeted pharmacological therapy for preventing and treating PLP). A pilot study in 1991 found that a catheter inserted in the transected nerve sheath infused with 0.25% bupivacaine at 10mL/h for 72h signicantly reduced postoperative opioid consumption. The patients did not develop PLP at the 12month follow-up despite the presence of preoperative limb pain. With the growing body of evidence, perineural analgesia is an essential component of the multimodal approach to postoperative limb amputation and in preventing the development of chronic pain.

Regional anesthesia is also benecial in managing early postoperative pain. A retrospective study in Turkey found that epidural anesthesia or peripheral nerve blockade can reduce RLP and PLP in the rst week after limb amputation compared to general anesthesia and spinal anesthesia, but has no difference across anesthetic techniques at 14–17 months postoperation [33]. Another cross-sectional survey found neuraxial anesthesia led to better pain control in the rst postoperative week, but was not different from general anesthesia in the development of RLP or PLP at the 14-month mark [34]. A large retrospective cohort study in South Korea determined that the incidence of PLP after limb amputation was highest when general anesthesia was used, then neuraxial anesthesia, and the least with perineural nerve blockade [35]. Although it appears that anesthetic technique does not impact long-term development of chronic pain, perhaps preoperative pain control helps in preventing postoperative pain. A prospective controlled study in England found that an epidural infusion of bupivacaine, clonidine, and diamorphine started 24–48h preoperatively and maintained for at least 3 days postoperatively led to a signicant reduction in the incidence of PLP) at the 1-year follow-up [36]. A randomized, prospective trial in Greece demonstrated perioperative pain control, whether via neuraxial or intravenous patient-controlled analgesia (PCA), will lead to better pain scores and reduced PLP at 6 months [37]. Despite the numerous studies on perioperative pain and the subsequent development of RLP, PLP, and CPAP, the sample subgroups remain relatively small and difcult to compare [38]. However, studies have shown that perioperative pain control can reduce acute perioperative pain [39] and perineural catheters are recommended as part of the analgesic regimen in all patients undergoing amputation [40]. Despite the promising results of these studies on the benets of perineural catheters in preventing the onset of RLP, PLP, and CPAP, the evidence remains small and the results are conicting [41].

Neuraxial and perineural catheters can lead to infection, especially in diabetic patients [42], and the recommendation is to remove and/or replace

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both neuraxial and perineural catheters after 4 days [43]; however, the practice varies by hospital. While any infection is a concern in this patient population, infections related to neuraxial catheters can be disastrous since the development of an epidural abscess may necessitate surgical intervention. Perineural catheter infections are generally less signicant and rarely require more than short-term antibiotic treatment. There is an ongoing investigation into colonization of catheters and eventual infection [44]. Coagulase-negative staphylococcus is the most commonly found microbe colonizing the catheter, and independent risk factors associated with increased colonization include catheter placement greater than 48h, diabetes, and use of antibiotics in the month prior to surgery [45]. In this same study, it was noted that the incidence of catheter colonization was mostly from interscalene and femoral catheters. It is imperative to consult the APS for managing these catheters.

The postoperative pain management of DLS patients relies on a robust acute pain service (APS). The APS can help place and manage epidural and perineural catheters, and includes replacing them if dislodged and/or are ineffective, or manipulating the dosage to effect. The APS can also help manage the complex analgesic medications that these patients may be administered.

The PSH model has been in practice for 20 years and is becoming more widespread nationwide. This multidisciplinary approach leads to more usage of Enhanced Recovery after Surgery (ERAS) protocols [46], improved outcomes, more meaningful perioperative measures, and improved costs and efciency [47]. The optimal care of DLS patients requires early involvement of anesthesia and acute pain services. The anesthesia service is essential to optimize patients prior to surgery and minimize risk intraoperatively. The utilization of an APS employing anesthesia providers with specialized skills for interventional procedures and managing pain syndromes is essential for a successful PSH, especially in the postoperative period [48]. Overall, the PSH model helps improve patient outcomes, improve patient satisfaction, and decrease medical expenditures.

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