Journal of Anesthetics and Anesthesiology

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Case Report - Journal of Anesthetics and Anesthesiology (2022) Volume 4, Issue 3

Multimodal anesthesia for kidney retransplantation in patients with advanced renal osteodystrophy.

Lucia Caroline Schons1, Carlos Darcy Alves Bersot2, Rafael Linhares3, Jose Eduardo Guimaraes Pereira4,5*

1Department of Anesthesiology, Pedro Ernesto University Hospital, University of the State of Rio de Janeiro, Rio de Janeiro, RJ, Brazil

2Department of Anaesthesiology, Hospital Federal Lagoa, Rio de Janeiro, RJ, Brazil

3Department of Anaesthesiology, Hospital Municipal Miguel Couto, RIode Janeiro, RJ, Brazil

4Department of Anaesthesiology, Valença Medical School, Valença, Rio de Janeiro, RJ, Brazil

5Department of Anaesthesiology, Hospital Unimed Volta Redonda, Volta Redonda, RJ, Brazil

*Corresponding Author:
Jose Eduardo Guimaraes Pereira
Department of Anaesthesiology
Valença Medical School
Valença, Hospital Unimed Volta Redonda
Volta Redonda RJ, Brazil
E-mail: dudunest@gmail.com

Received: 30-Apr-2022, Manuscript No. AAAA -22-62274; Editor assigned: 02-May-2022, PreQC No. AAAA -22-62274(PQ); Reviewed: 16-May-2022, QC No. AAAA -22-62274; Revised: 13-Jun-2022, Manuscript No. AAAA -22-62274(R); Published: 20-Jun-2022, DOI:10.35841/aaaa-4.3.111

Citation: Schons LC, Bersot CDA, Linhares R, et al. Multimodal anesthesia for kidney retransplantation in patients with advanced renal osteodystrophy. J Anesthetic Anesthesiol. 2022;4(3):111

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Abstract

End-stage renal failure is a chronic, progressive, debilitating disease that causes disability and high mortality, and the incidence and prevalence have increased in the world population. Among the chronic diseases, dialysis chronic kidney disease is among those that generate the greatest impact on the patient's quality of life, such as living with an incurable disease, dependence on a dialysis machine to survive, rigorous therapeutic regimen, changes in body image and dietary and water restrictions. Dialysis therapy does not completely replaces renal functions and, for this reason, prolonged stay on hemodialysis causes bone complications (ostedystrophy due to secondary hyperparathyroidism), cardiovascular (left ventricular hypertrophy, vascular calcification), brain (advanced arteriosclerosis). The chance of death among hemodialysis patients is 20 times greater than that of the general population. Kidney transplantation is the best treatment for patients with end-stage renal disease. Anesthesia requires an understanding of these metabolic and systemic abnormalities. In addition, associated comorbidities increase perioperative morbidity and mortality, so for a better outcome, multidisciplinary collaboration with well-planned anesthetic strategies is necessary, with individualization of cases.

Keywords

Renal osteodystrophy, Anesthesia, Outcome, Kidney retransplantation.

Introduction

Chronic Kidney Disease (CKD) is a worldwide health problem, with an increasing prevalence and adverse outcomes [1,2]. Mineral and bone disorders are important complications of this disease, which can result in numerous consequences, such as bone pain, skeletal deformities, bone fractures, vascular calcification, cardiovascular disease and even death [3,4]. Levels of calcium, phosphorus and intact PTH (PTHi) should be determined in all patients with CKD in which the Glomerular Filtration Rate (GFR) is below 60 mL/min/1.73 m2. [5]. These measures should be even more frequent in renal transplant patients or in any patient with CKD who is being treated for disorders of calcium and phosphorus metabolism. In CKD, hyperphosphatemia and hypocalcemia occur due to loss of renal function, deficit of active vitamin D, and imbalance in the maintenance of the calcium-phosphorus product. As a consequence of hypocalcemia, there is an increase in the secretion of parathormone, responsible for the reabsorption of bone salts, increasing the levels of Ca++ in the extracellular fluid. The resulting trend is the establishment of a picture of HPTS, which can cause pathological fractures, bone deformities and decrease in patients' survival [6].

Case report

A 35 year-old, female patient, weighing 50 kg and measuring 1.50 meter tall, with a history of nephrotic syndrome onset at age 15, was diagnosed with post-biopsy glomerulonephritis [7]. At the age of 20, she presented anasarca, systemic arterial hypertension, dialysis was initiated and she was submitted to her first kidney transplant, which evolved with immediate loss due to thrombosis [8]. New transplant was performed at age 23, with new graft loss, but now without a clear cause.

Medicines in use: Losartan, Atenolol, Renagel, AC F, Hemax, Complex B, CACO3. Previous Surgeries: Kidney Transplantation, Parathyroidectomy. Main etiology of Chronic Kidney Disease: Glomerulopathy. Comorbidities: Systemic Arterial Hypertension. Echocardiography: Concentric left ventricular hypertrophy, 66% ejection fraction, Grade 2 diastolic dysfunction, mild mitral insufficiency [9]. ECG: Sinus Bradycardia. Chest: Bell. Chest X-ray: dextroconvex thoracic scoliosis and morph structural alteration of the costal arches, dorsal spondyloarthrosis; Elongated and atheromatous aorta; Free Costophrenic sinuses. Computed Tomography: Infra-renal Vein Hypoplasia. Two previous renal implants in right and left iliac arteries [10]. Anesthesia: Monitoring performed with cardioscopy, pulse oximeter, invasive blood pressure with catheterization of the right radial artery, Bispectral Index (BIS), capnography and gas analyzer. Pre- induction sedation: dexmedetomidine 40 mcg, magnesium sulfate 2 grams, midazolam 5 mg. Epidural Puncture was performed at T8, with the passage of an Epi Dural Catheter (EDC). Anesthetic induction in rapid sequence: lidocaine 100 mg, fentanyl 100 mcg, propofol 100 mg, and rocuronium 60 mg [11]. Orotracheal intubation was performed with the aid of a video laryngoscope. During the surgery, 5 ml of 0.5% ropivacaine + 1% lidocaine were administered through the epidural catheter to maintain analgesia. Heparinization was performed with 2500 IU intravenous heparin and guided by Activated Clotting Time (ACT) and was not reversed at the end of the procedure.

At the end of the surgery, 2 mg of morphine was administered by EDC [12]. Dipyrone 2 grams and ondansetron 8mg were given intravenously.

Surgery was performed by a xipho-pubic incision with transperitoneal access and organ implantation in vena cava at the level of the renal veins, arterial implantation in the right common iliac artery and ureter implantation of intraperitoneal vesical graft [13,14].

The patient maintained hemodynamic stability throughout the procedure, maintaining mean arterial pressure above 90 mmHg, heart rate around 60 bpm and BIS between 40-60 [15,16]. At the end of the surgery, she was extubated in the room and taken to the ICU, stable and ventilated on room air, without pain complaints.

Discussion

In surgery for kidney transplantation, modified Gibson incisions are made. However, in this specific case, the patient was undergoing her third kidney transplant due to the loss of the previous two grafts [17]. Therefore it was necessary to enlarge the surgical incision to a midline xipho-pubic access to gain intraperitoneal access for implantation in both vena cava and common iliac artery [18-20]. Thus resulting in greater pain stimulation and surgical complexity. Multimodal anesthesia aims to maximize analgesic efficacy and minimize side effects of a single medication. The choice of neuraxial block combined with general multimodal anesthesia in this case, despite the great technical difficulty of the chest with bone deformity helped to maintain analgesia and with greater hemodynamic stability in this case, in addition to analgesic maintenance in the postoperative period [21-23].

Vasodilation can be induced by lidocaine doses higher than 40 μg/ml. And it has been demonstrated that a better diuresis in time zero and within three days after transplantation (early polyuria) is associated with a better graft function [24,25].

Dexmedetomidine is a short acting selective alpha 2 agonist and has a stabilizing effect on hemodynamics mediated by reducing sympathetic tone, decreasing inflammatory response, alleviating I/R injury, inhibiting renin release, increasing glomerular filtration rate, increasing secretion of sodium and water by the kidneys, and decreasing insulin secretion [26,27]. Additionally, in renal cells, Dexmedetomidine can also decrease apoptosis and downregulate monocyte chemo- attractant protein-1 through suppressing injury-induced activation of the Janus kinase/signal transducer and activator of transcription signaling pathways during renal I/R injury [28-30]. These immune modulatory effects may underlie an organ protective effect of Dexmedetomidine from I/R injury. Considering the importance of inflammation and apoptosis, as well as potential anti-inflammation and apoptosis effects.

Dexmedetomidine has emerged as an effective organ protective agent. Gu and colleagues suggested that Dexmedetomidine activated Akt signaling via α2 adrenoceptor-dependent and independent-PI3K coupling to improve kidney cell survival [31-33]. Apart from its cytoprotection, Dexmedetomidine might inhibit HMGB1 release and suppress subsequently toll- like receptor 4-mediated inflammatory actions in the setting of renal ischemia. Studies in vivo have reported that the reno- protective property of Dexmedetomidine could be related to modulating vasoreactivity, presented as improved renal blood flow, preserved glomerular filtration, elevated secretion of water and sodium, as well as suppression of renin release [34,35]. Moreover, Dexmedetomidine could induce diuresis through the inhibition of arginine vasopressin in the collecting duct and aquaporin expression.

Epidural analgesia blocks the stress response, either by relieving pain or by blocking sympathetic activity. Epidural analgesia, with the association of local anesthetics and opioids, promotes better quality analgesia than the use of isolated opioids, either via epidural route or systemic administration [36-39]. Also, it is superior to the isolated epidural use of local anesthetics. This association allowed to reduce, not only the concentration of the local anesthetic in the epidural analgesic solution, but also the necessary doses of opioid for a better quality postoperative analgesia, with less adverse effects than that obtained when either one of the aforementioned agents are used alone [40-42].

The combination of these factors, along with other measures, such as active postoperative mobilization and early return to oral feeding [43-45] led to the proposal that epidural analgesia would improve the evolution of these patients and could reduce morbidity and mortality.

Hypomagnesemia is frequently observed after kidney transplantation, in part to immunosuppressive regimens including CalciNeurin Inhibitors (CNI) that induce Magnesium (Mg) urinary waste. Hypomagnesemia was observed in 6.6% of patients treated with tacrolimus and in 1.5% of patients on cyclosporine [46]. The mechanisms leading to hypomagnesemia are not fully understood, but it has been shown that CNI induce a down-regulation of renal expression of the epidermal growth factor and TRMP6 in the distal collecting tubule, leading to decreased Mg reabsorption. Sirolimus might induce hypomagnesemia through inhibition of Na-K-Cl co-transporter 2 expression in the thick ascending loop of Henle. Renal Mg wasting has been shown to be similar between rats treated with sirolimus and those treated with cyclosporine or tacrolimus [47]. Many other factors influence Mg levels after kidney transplantation, such as post- transplantation volume expansion, metabolic acidosis, insulin resistance, decreased gastro-intestinal absorption due to diarrhea, low Mg intake and medication such as diuretics or proton pump inhibitors. Post-transplant diabetes mellitus- associated mortality is mainly related to cardiovascular events, which are today the main cause of death in kidney transplant patients. Hypomagnesemia has been shown to play a role in the pathogenesis of arterial hypertension, endothelial dysfunction, dyslipidemia and inflammation, with all these factors contributing to Coronary Heart Disease (CHD) [48].

Conclusion

Kidney transplantation is the gold standard treatment for patients with end-stage kidney disease. These patients have several metabolic changes and associated comorbidities, in which the anesthetic-surgical procedure must be studied and individualized in order to be successful. Multimodal anesthesia with the combination of several drugs in lower doses helps to enhance analgesia quality and hemodynamic performance in the perioperative period. Dexmedetomidine was associated with a reduced incidence of DGF, infection, graft rejection, overall complications, and LOS in patients who undergo renal transplantation. Epidural anesthesia with opioid promotes longer postoperative analgesia, in addition to decreasing the morbidity and mortality of these patients. Lidocaine also demonstrates a positive effect during intraoperative period with vasodilation and improvement of diuresis during the postoperative period. Therefore multimodal anesthesia exerts a positive effect in kidney transplantation surgery when compared to opioid based anesthesia.

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