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Surgical Management of Diabetic Peripheral Neuropathy in Type 2 Diabetes Mellitus

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Surgical Management of Diabetic Peripheral Neuropathy in Type 2 Diabetes Mellitus

Samarth B. Patel1, Frederick Tiesenga2, Tina M. Stanco1, Denelle Mohammed1 and Lincey Alexida1*

1Saint James School of Medicine, 1480 Renaissance Drive, Suite 300, Park Ridge, IL 60068, USA

2West Suburban Medical Center, 3 Erie St, Oak Park, IL 60302, USA

*Corresponding author: Lincey Alexida, Saint James School of Medicine, 1480 Renaissance Drive, Suite 300, Park Ridge, IL 60068, USA, E-mail: [email protected] 

Citation: Patel SB, Tiesenga F, Stanco TM, Mohammed D, Alexida L (2018) Surgical Management of Diabetic Peripheral Neuropathy in Type 2 Diabetes Mellitus. Arc Cas Rep Med 4(1):115.

 

Abstract

 

Type 2 diabetes mellitus (T2DM) is a metabolic disorder that often presents with a multitude of complications when poorly regulated. One of the most common and worrisome complication is diabetic peripheral neuropathy (DPN). DPN increases the risk of foot ulcers which are prone to infections and subsequent therapeutic amputation. This complication is often aggravated with the presence of other comorbid conditions such as peripheral artery disease (PAD). Here we present a case of a T2DM patient with a past medical history of PAD who presented with a necrotic toe as a complication of this DPN. The patient was surgically treated with a toe amputation and intravenous Pipercillin-Tazobactam. This article provides a literature review of the implications of DPN on the quality of life of T2DM patients. 

Keywords: Diabetes mellitus the 1 last update 02 Jun 2020 type 2; MSSA; Diabetic peripheral neuropathy; HyperglycemiaKeywords: Diabetes mellitus type 2; MSSA; Diabetic peripheral neuropathy; Hyperglycemia

 

Introduction

 

reverses diabetes type 2 explanation (⭐️ guidelines 2020) | reverses diabetes type 2 veteranhow to reverses diabetes type 2 for Diabetes mellitus is a type of metabolic pathophysiology that affects the generation of insulin within the body, either by an absence of production of insulin or a resistance to conventional insulin production, resulting in subsequent hyperglycemia [1]. The main classifications of diabetes are: Type 1 Diabetes Mellitus, Type 2 Diabetes Mellitus and Gestational Diabetes Mellitus [1]. Furthermore, there are two subsets of Type 1: Type 1A which is secondary to autoimmune destruction of beta cells in the pancreas and Type 1B which refers to non-autoimmune obliteration of the beta cells in the pancreas [2]. The mechanism behind Type 2 is due to the cellular resistance to insulin production by beta cells; this leads to eventual destruction of these cells and an insulin deficiency, since hyperglycemia can impede beta cell activity [3]. Gestational diabetes mellitus can be attributed to a multiplicity of factors; it is usually due to the production of human placental lactogen that controverts the purpose of insulin in addition to synergistic factors such as subprime lifestyle practices of obesity, amongst others, as well as a genetic inclination to the development of diabetes [4]. In the United States of America, the latest statistical analysis conducted by the CDC gauges the prevalence of diabetes, solidified with an actual diagnosis in addition to non-diagnosed cases at 9.4%, as of 2015 [5]. The prevalence of diabetic patients with a concrete diagnosis was 7.2% [5]. As of 2015, the incidence of diabetes in the American population was 1.5 million cases [5].

In addition, the complications of diabetes mellitus are numerous and affect most organ systems in the body, over a period of time [6]. The nervous system is affected by cerebral strokes as well as neuropathies that encompass both the peripheral and autonomic systems [6]. The renal system can be afflicted by proteinuria, nephropathy and eventual renal demise [7]. From a cardiovascular standpoint, atherosclerotic cardiovascular disease and hypertension are main complications [8]. The gastrointestinal system is impacted by postponed gastric emptying and dyspepsia [9]. A myriad of other complications includes cataracts, defective wound healing, erectile dysfunction, osteopenia, ulceration of the extremities, polyhydramnios, preeclampsia and neonatal cardiomyopathy [10]. We present a case of a patient with Type 2 Diabetes Mellitus affected by gas gangrene of the lower extremity and subsequent clinical approaches to this pathophysiology.

 

Case Presentation

 

A 62-year-old Hispanic male, with a history of diabetes, presented to the emergency department with complaints of left foot pain and blackening of his toe (Figure 1).  The patient’s symptoms began a few days before he sought treatment with pain and swelling of the left foot, and subjective fevers which progressed to his present condition. The patient had a normal BMI of 26 kg/m2 and a past medical history significant of peripheral vascular disease and T2DM which was poorly controlled based on previous hyperglycemic events requiring hospitalization. Physical examination showed a normal appearing patient in no acute distress, with normal vital signs. However, the patient had intermittent fever after admission with a T-max of 101.3 degrees Fahrenheit.

Lab Work

Initial laboratory testing showed leukocytosis of 17.6 x 103/μL, however, before discharge this resolved with a final white blood cell count of 9.6 x 103/μL. Gram staining performed from specimens obtained during the amputation showed, rare white blood cells, gram-positive cocci in pairs and gram-positive cocci in clusters. The culture was positive for the following three isolates: Escherichia coli, Proteus mirabilis and Methicillin susceptible Staphylococcus aureus (MSSA) with their respective sensitivities shown in table I, II, and III. An x-ray performed showed swelling of the soft tissue which was centered about the fifth metatarsophalangeal joint thought the 1 last update 02 Jun 2020 to be indicative of soft tissue gas. There was, however, no evidence of acute osteomyelitis on x-ray. A venous Doppler was also performed which showed no evidence of a deep vein thrombosis. A left leg angiogram showed occlusions in the anterior and posterior tibial artery a highly stenotic lesion of 90% stenosis in the peroneal artery.Initial laboratory testing showed leukocytosis of 17.6 x 103/μL, however, before discharge this resolved with a final white blood cell count of 9.6 x 103/μL. Gram staining performed from specimens obtained during the amputation showed, rare white blood cells, gram-positive cocci in pairs and gram-positive cocci in clusters. The culture was positive for the following three isolates: Escherichia coli, Proteus mirabilis and Methicillin susceptible Staphylococcus aureus (MSSA) with their respective sensitivities shown in table I, II, and III. An x-ray performed showed swelling of the soft tissue which was centered about the fifth metatarsophalangeal joint thought to be indicative of soft tissue gas. There was, however, no evidence of acute osteomyelitis on x-ray. A venous Doppler was also performed which showed no evidence of a deep vein thrombosis. A left leg angiogram showed occlusions in the anterior and posterior tibial artery a highly stenotic lesion of 90% stenosis in the peroneal artery.

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The patient was managed with a left foot 5th metatarsal head amputation with foot debridement including the skin, subcutaneous muscle, bone and the fascia (Figure 2). Surgical pathology of the specimen showed a gangrenous fifth left toe with atherosclerotic peripheral vascular disease and active necrosis of the bone. The patient was also treated with atherectomy of left peroneal artery to address lower vessel ischemia and promote post-operative healing. The patient necessitated three subsequent left foot debridement to address complex necrosis post toe amputation operation. The patient was discharged to his home on intravenous Pipercillin-Tazobactam and a diabetic pharmacologic regimen of pre-meal insulin and insulin Glargine nightly. A final six-month post-operative follow-up showed that the infection had cleared and the patient had completely healed from the amputation (Figure 3). 

the 1 last update 02 Jun 2020   

Discussion

 

Type 2 diabetes mellitus (T2DM) is particularly ubiquitous in the world, with substantial complications leading to mortality in the uncontrolled state of the disease. Although appropriate management diminishes the risk of T2DM related complications, many patients with various reasons fail to adhere to the meticulous management of this disease. T2DM continues to increase mainly due to decreases in physical activity and increases in obesity [11]. This indicates a tremendously escalating encumbrance in un-industrialized countries [11]. Furthermore, diabetes mellitus is a prevalent phenomenon in today’s society, with approximately 400 million adults being affected worldwide, as of 2015 [12]. Furthermore, the occurrence in the combined regions of the Caribbean and North America is currently at 11.5% [12]. Type 1 Diabetes accounts for 5% of total diabetic cases while Type 2 Diabetes constitutes approximately 90% of cases [12].

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It is imperative that clinicians acknowledge the connotation concerning T2DM and vascular disease due to its mounting prevalence in the United States [15]. Since the hyperglycemia in T2DM is the cause of its countless complications, current healthcare interventions are intended towards management and prophylaxis to ensure the tissues of the body are not harmed by the hyperglycemia [15]. The outcomes of hyperglycemia on the vasculature for 1 last update 02 Jun 2020 are detrimental and literature has upheld how this is a foremost source of morbidity and mortality [15]. The injurious consequences of hyperglycemia can be parted into two types of complications; microvascular and macrovascular [15]. Microvascular complications incorporate diabetic nephropathy, neuropathy and retinopathy; macrovascular complications comprise stroke, coronary artery disease (CAD) and peripheral arterial disease (PAD) [15]. Trends of complications in Type 2 diabetics are variable by gender [16]. Lower extremity amputations and morbid obesity were more prevalent in men while females had a higher incidence of coronary disease, stroke, vascular complications and dialysis secondary to diabetic nephropathy [16]. Nephropathy was equally distributed between both genders [16].It is imperative that clinicians acknowledge the connotation concerning T2DM and vascular disease due to its mounting prevalence in the United States [15]. Since the hyperglycemia in T2DM is the cause of its countless complications, current healthcare interventions are intended towards management and prophylaxis to ensure the tissues of the body are not harmed by the hyperglycemia [15]. The outcomes of hyperglycemia on the vasculature are detrimental and literature has upheld how this is a foremost source of morbidity and mortality [15]. The injurious consequences of hyperglycemia can be parted into two types of complications; microvascular and macrovascular [15]. Microvascular complications incorporate diabetic nephropathy, neuropathy and retinopathy; macrovascular complications comprise stroke, coronary artery disease (CAD) and peripheral arterial disease (PAD) [15]. Trends of complications in Type 2 diabetics are variable by gender [16]. Lower extremity amputations and morbid obesity were more prevalent in men while females had a higher incidence of coronary disease, stroke, vascular complications and dialysis secondary to diabetic nephropathy [16]. Nephropathy was equally distributed between both genders [16].

The neuropathy linked with T2DM leads to decreased pain sensation in the extremities which leads to an enormous risk of the breakdown of skin along with infection and joint destruction [17]. The most common complications of diabetic neuropathy are foot ulcerations which therefore lead to amputation [17]. A literature review showed how peripheral neuropathy can ominously surge the risk for amputation, in-fact over 80% of amputations shadow a foot ulcer or injury [18,19]. Male patients who have had T2DM for over 10 years with meager glucose control are at utmost peril for ulcers or amputations [15,17]. The American Diabetes Association (ADA) classifies several foot-related risk factors associated with an increased risk for amputation; peripheral neuropathy with loss of protective sensation, altered biomechanics in the presence of neuropathy, erythema or hemorrhage under a callus, body deformity, PAD, history of ulcers or amputations and severe nail pathology [17]. For this reason, the ADA recommends all diabetic patients should receive foot exams annually along with education regarding their risk factors and proper management [17]. Therefore, patients who have increased risk expressively benefit from early recognition, education regarding pathophysiology and appropriate foot care; this can lessen the frequency of ulcer formation and ensuing amputation [19].

The scope of neuropathy in diabetes is quite vast, however most complications are attributed to distal symmetric polyneuropathy (DPN) which is usually of a chronic nature [19]. Since microvascular injury encompasses the small blood vessels that fund the vasa nervorum, up to 50% of DPN may be asymptomatic leading to a large risk of unconscious damage to the feet [19]. The diagnosis of asymptomatic DPN is made when a patient presents with a painless foot ulcer [19]. The other 50% of patients can present with symptoms of the lower limbs such as burning pain, electrical or stabbing sensations, paresthesia, hyperesthesia and deep aching pain that is worse at night [19]. During examination of the lower limb, sensory loss of vibration is seen along with loss of pressure, pain and temperature and absent ankle reflexes [19]. Warm or cold feet, distended dorsal foot veins, dry skin and calluses mark peripheral sympathetic dysfunction that are also frequently observed [19].

According to literature, the injury to peripheral nerves from hyperglycemia is likely related to injury from advanced glycation end products (AGEs) and oxidative stress [17]. Small vessel narrowing is the first pathological change and occurs because blood vessels undergo capillary basement membrane thickening and endothelial hyperplasia that lead to decreased oxygen tension and ultimately hypoxia [17,20]. Since blood vessels are reliant on normal nerve function and normal nerve function is reliant on proper blood flow, neuronal ischemia is a major characteristic of diabetic neuropathy [20]. Therefore, we can associate the correspondence of early small vessel dysfunction to the succession of neuronal dysfunction [17,20]. Hyperglycemia triggers a non-enzymatic covalent bonding amid proteins when exposed to sugars, ultimately leading to alterations in their structure and subsequently inhibiting their function; these are called AGEs [21]. AGEs contribute to macrovascular complications through establishing cross-links amongst molecules of the extracellular matrix (ECM) and through engagement of the receptor for advanced glycation end products (RAGE) [21]. In the ECM, AGEs produce lipids, collagen, laminin, elastin and vitronectic; this increases the stiffness of the ECM and eventually leads to small vessel and neural dysfunction [21]. When RAGE is activated by AGEs, an upregulation occurs of the transcription factor nuclear factor-kB leading to increased ECM formation [21]. This AGE bound to RAGE substantially increases the permeability of the endothelium to macromolecules such as endothelin-1, ICAM-1, E-selectin and tissue factor; all leading to vessel and neuronal dysfunction [21]. The effects of nitric oxide are blocked by AGEs in the endothelium which subsequently leads to production of reactive oxygen species [21]. Activated monocytes through AGEs increase the expression of macrophage scavenger receptors which lead to an increased uptake of oxidized LDL and foam cell formation, causing oxidative stress [21].

In conclusion, the compromise of blood supply from microvascular disease predisposes patients to foot infections. The loss of sensation due to neuropathy along with local trauma or pressure greatly increases the risk of foot infections and ultimately amputation. One of the strongest etiologies of diabetic ulceration includes neuropathy, and it is crucial to do annual foot examinations along with providing proper education to the patient regarding pathophysiology and proper foot care.

 

Conflict of interest

 

All the authors receive no financial supports and have no conflicts of interest.

 

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Copyright: © 2018 Patel SB, et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.