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Christopher J. Patton, BSN Barnes-Jewish College

Anesthesia Considerations for Simultaneous Pancreas-Kidney Transplantation and Post-Reperfusion Syndrome: A Case Report and Review of the Literature. Christopher J. Patton, BSN Barnes-Jewish College. CASE STUDY. REPEAT SPKT. 43-year-old, ASA 3, 158 cm, 47 kg female

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Christopher J. Patton, BSN Barnes-Jewish College

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  1. Anesthesia Considerations for Simultaneous Pancreas-Kidney Transplantation and Post-Reperfusion Syndrome: A Case Report and Review of the Literature Christopher J. Patton, BSN Barnes-Jewish College

  2. CASE STUDY

  3. REPEAT SPKT • 43-year-old, ASA 3, 158 cm, 47 kg female • Underwent primary SPKT two years earlier • Pancreatic graft failure due to severe pancreatitis • Renal graft failure secondary to rejection • Medical History: IDDM, ESRD, anemia, GERD, HTN, HLD, IBS • Anesthesia History: Unremarkable • Allergy: Cephalexin (rash)

  4. PREOPERATIVE ASSESSMENT • Airway: Mallampati III, TM Distance = 5 cm, Normal Cervical Extension • Hypertensive: MAPs as high as 125 mm Hg noted • ECG: NSR with poor R-wave progression • Recent nuclear stress test: Negative • TTE: Normal LVEF, mild LVH/LAE, trace MR/TR • CXR: Remarkable for an in situ left subclavian HD catheter with its tip at the atriocaval junction

  5. PREOPERATIVE ASSESSMENT • Lungs CTA Bilaterally • Heart Tones Normal • No Carotid Bruits • Labs: • Elevated Cr and PO4 (4.43/6.0 mg/dL, respectively) • Decreased H & H (9.9/28.8 g/dL) • Severe N/V: three episodes of emesis in the holding area • Treated with transdermal scopolamine, two doses of odansetron, famotidine, and metoclopramide • Midazolam 2 mg administered prior to leaving holding

  6. INDUCTION

  7. MAINTENANCE OF ANESTHESIA • Desflurane titrated between 4.2-6.5% inspired concentration in equal mixture of oxygen and air • NMB maintained with atracurium totaling 160 mg • Piperacillin/Tazobactam 2.25 g per surgeon request • Serum glucose assessed Q30 minutes and regular insulin administered IV in small doses throughout the case per the surgeon’s request (9 units total)

  8. INITIATION OF IMMUNOSUPPRESSIVE THERAPY AND INITIAL HYPOTENSION Immunosuppressive therapy induced with methylprednisolone 350 mg IV (Over 15 min) Followed by a continuous infusion of anti-thymocyte globulin (ATG) 4.1 mg/hr Infusion decreased to 2 mg/hr after hypotension noted Small boluses of phenylephrine, calcium chloride and ephedrine to maintain MAP ~ 80 mm Hg BP stabilizes with 1.5 L of 0.9% NS, 250 mL of 5% albumin, and dopamine infusion at 5 g/kg/min

  9. WE’RE CRUISING… • Prepare for pancreas graft insertion • Heparin 3,000 units • Mannitol 12.5 g • Graft inserted • Vascular anastamoses completed • Surgeon announces venous clamp will be released • Student experiences SEVERE pudendal neuropathy as this happens……..

  10. PANCREATIC GRAFT REPEFUSION • Within 5 min, MAP acutely decreased from a pre-reperfusion value of 79 mm Hg to 28 mm Hg, and heart rate increased to approximately 140 beats per minute • The ATG infusion paused and sodium bicarbonate 1 ampule, calcium chloride 500 mg, phenylephrine 400 g, ephedrine 10 mg, norepinephrine 64 g, and epinephrine 200 g, were all administered IV over the next 5 minutes before the MAP recovered to 60 mm Hg • One unit of packed red blood cells infused and continuous infusion of norepinephrine 0.05 g/kg/min was initiated and quickly titrated to 0.2 g/kg/min

  11. Over the next 80 minutes… • Norepinephrine infusion titrated to 0.25 g/kg/min • An additional six 64 g boluses of norepinephrine were administered • 2L 0.9% NS bolused to maintain a MAP > 60 mm Hg • Remember, goal MAP ~80 mm Hg • Diphenhydramine (25 mg) and esmolol (10 mg) also administered with no observed response • Heart rate remained 120 – 140 bpm • About four hours into the case, MAP stabilized at 70 mm Hg • Per the surgeon’s request, 2,000 units of heparin administered prior to clamping for vascular anastamoses of renal graft • 12.5 g mannitol administered prior to reperfusion of renal graft • Anesthesia grimaces….

  12. RENAL GRAFT REPEFUSION Upon reperfusion of renal graft, MAP again acutely fell from 72 mm Hg to 51 mm Hg A norepinephrine 128 g bolus administered and second unit of PRBCs transfused Furosemide 10 mg also administered, per the surgeon’s request CardioQ SV monitor (Deltex Medical, Greenville, SC) utilized to assess fluid status 4.5 L of crystalloid infused over remainder of case, per fluid optimization protocol In total, patient received 8 L crystalloid and approximately 1.5 L colloid Estimated blood loss was 500 mL A total of three ampules of sodium bicarbonate were administered to correct acidosis

  13. EMERGENCE • By the end of the case, hemodynamics stabilized • Norepinephrine infusion decreased to 0.08 g/kg/min • Dopamine infusion discontinued • ATG infusion reinitiated at full dose • Neuromuscular blockade was antagonized with glycopyrrolate 0.5 mg and neostigmine 3.5 mg after surgical incision closed (fascia left open) • Patient awoke and followed commands, but was determined to be too weak to safely extubate • Propofol infusion initiated and patient transported to ICU in stable condition

  14. POSTOPERATIVE COURSE • Patient was extubated the following morning and transferred out of the ICU two days later • Eight days after SPKT, patient returned to OR for closure of fascia • Wound infection and edematous pancreas with multiple necrotic areas discovered • Four days later, returned OR for I&D of the abdomen, debridement of several small necrotic areas on the pancreas, and closure of the fascia and skin • Patient remained hospitalized for a month prior to being discharged to a rehabilitation facility

  15. DISCUSSION

  16. WHO BENEFITS FROM SPKT? • Approximately 50-60% of insulin-dependent diabetics develop diabetic nephropathy, the leading cause of renal failure requiring hemodialysis (HD) in young and middle-aged adults in the United States (US).1,2 • While pancreatic transplantation may be indicated for the treatment of disease states such as pancreatitis or cancer, an overwhelming 96% of the total pancreatic transplants in the US are performed in patients with underlying IDDM.3,10

  17. WHY SPKT? • SPKT is curative treatment for both IDDM and ESRD • SPKT has become far more prevalent over the past 40 years2,3,10

  18. WHAT HAPPENS WHEN SPKT FAILS? • Uncommon • Serious • Few institutions with much experience

  19. PANCREATIC ANASTAMOSES Bifurcation of donor Iliac Artery anastamosed to Superior Messenteric and Splenic Arteries during bench preparation of pancreatic graft to improve ease of anastamosis to recipient’s Right Common Iliac Artery during transplantation

  20. RENAL ANASTAMOSES

  21. ANESTHESIA CONSIDERATIONS • Preoperative Assessment, Planning & Collaboration • Minimizing Consequences of IDDM and ESRD • Glycemic Control • Autonomic Neuropathy • Avoidance of Drugs with Renal-Dependent Metabolism • Fluid Management • Management of Immunosuppressive Therapy • Optimization of Graft Function • Commonly Utilized Intraoperative Drugs • Ensure Adequate Graft Perfusion • Appropriate Fluid/Pressor Management • Management of Post-Reperfusion Syndrome (PRS)

  22. PREOPERATIVE ASSESSMENT • Begins with a review of the health history, with special attention to co-existing diseases that often accompany ESRD and IDDM: • Hypertension, anemia, uremia, and cardiac disease11 • CXR, ECG, echocardiography and stress testing warranted in most patients due to risk for silent ischemia secondary to autonomic neuropathy9,10

  23. PREOPERATIVE LABORATORY STUDIES • Laboratory tests should include: CBC, CMP, hemoglobin A1C, coagulation studies, and a T&C for at least two units of washed PRBCs8,11 • The transplant workup will also include screening test for a multitude of infectious diseases, as well as ABO and human leukocyte antigen (HLA) compatibility11

  24. PREOPERATIVE EXAM • Primary concerns: cardiopulmonary system and airway • VS, orthostatics, and dialysis details facilitate estimation of blood volume status9 • Difficult airway? • Few studies propose intubation difficult in diabetics • Subsequent studies did not substantiate these fears2 • Nonetheless, prudent to assess joint mobility in neck and jaw and to prepare for difficult visualization of laryngeal structures12 • Identify HD shunts/fistulas and verify adequate padding, as pressure may cause thrombosis2,8

  25. GLYCEMIC CONTROL • Many proposed management strategies • Most authors agree BG should be assessed at least Q30-60 minutes and treated with IV regular insulin • Avoid complications such as ketoacidosis, depressed immune function, decreased wound healing, and risk for significant neurologic insult in the setting of cerebral ischemia.2,6,8,12 • Keep BG > 150 mg/dL prior to pancreatic graft insertion • Glucose concentrations decrease ~ 50 mg/dL/hr after reperfusion • Hypoglycemia difficult to detect due to decreased autonomic from anesthesia and diabetic and renal disease-related neuropathy2,8 • Another complicating factor is routine administration of high-dose corticosteroid for immunosuppressive therapy

  26. ANESTHETIC TECHNIQUE • Regional anesthesia has been successfully used for SPKT in a small number of reported cases • Most authors encourage general endotracheal anesthesia2,6,8,12 for the following reasons: • The long, tedious nature of these surgeries • The benefit of muscle relaxation • The potential for hemodynamic instability • Furthermore, splanchnic perfusion to the transplanted organs is a major concern and the sympatholytic effect of regional anesthesia may pose a danger to adequate graft perfusion2,8

  27. IMMUNOSUPPRESSIVE THERAPY • Transplant function dependent on immunosuppression • Induction Agents: Started at time of transplantation • May continue for a few doses while maintenance agents initiated • Maintenance Agents: Will be continued indefinitely • Commonly encountered induction regimens include either monoclonal or polyclonal antibodies which may be supplemented with a large dose of corticosteroid6,10 • Regimens vary between patients and institutions • Imperative that anesthetist clarifies schedule and dosing with transplant team6

  28. SIDE EFFECTS Clinical Anesthesia, 6th ed., 2009 Miller’s Anesthesia, 7th ed., 2010

  29. AUTONOMIC NEUROPATHY • Diabetics, especially those with ESRD, prone to autonomic neuropathy that may cause:2 • Gastroparesis increases risk for aspiration1,7,8,12,13 • Cardiovascular lability: possible intraoperative hypotension requiring pressors, dysrhythmias, and bradycardia resistant to atropine1,12,13 • Regardless of volume status, patients with ESRD often experience exaggerated hypotension with induction of anesthesia1,9

  30. INDUCTION OF ANESTHESIA • No standard induction drugs specifically contraindicated • All patients presenting for SPKT should be considered at risk for aspiration • RSI with cricoid pressure and slight reverse trendelenberg positioning indicated2,6,8

  31. NEUROMUSCULAR BLOCKADE • Succinylcholine usually safe in patients with ESRD • Serum potassium should be < 5.5 mEq/L • 0.6 mEq/L increase in serum potassium after intubating dose of succinylcholine2,8,14 • CAUTION: risk for hyperkalemia after succinlycholine administration may be increased in patients with motor and sensory neuropathy secondary to diabetes and uremia12 • Alternative to succinylcholine for RSI is rocuronium • Subsequent doses should be carefully titrated based upon train-of-four monitoring with a peripheral nerve stimulator2,6,8 • Cisatracurium and atracurium ideal due to extrarenal metabolism via Hoffman degredation and plasma cholinesterase2,6,8,11,14 • Primary metabolite, laudanosine, may cause seizures via stimulation of CNS at high plasma concentrations9

  32. MAINTENANCE OF ANESTHESIA • Balanced anesthetic technique likely best method to sustain hemodynamic stability2 • Drugs selected based upon known side effects9 • N2O often omitted • Morphine and meperidine should also be avoided due to the action of their metabolites2 • Desflurane and isoflurane are commonly used inhaled anesthetics2 • While the metabolism of sevoflurane has been implicated in nephrotoxicity, there is a lack of evidence clearly substantiating these concerns

  33. FLUID CHOICES • Multiple considerations • Electrolyte Balance • Edema/Third-Spacing • Acid-Base Balance • Which Crystalloid? • NS vs. LR vs. Plasmalyte? • NS widely used, but LR and Plasmalyte may be better • Which Colloid? • Albumin vs. HES Solutions? • Albumin demonstrated to be best colloid

  34. MONITORING • Standard ASA monitors placed upon entering OR • HD catheters may be used if CVC access warranted • CVP 10 – 15 mm Hg optimizes CO/Renal Blood Flow2,6,8 • Pulmonary Artery Catheter based upon H&P • Higher filling pressures (>20/15 mm Hg) indicative of better graft function than lower pressures in one study2 • A-Line based upon H&P • Non-invasive cardiac stroke volume monitors • These have been found to facilitate goal directed fluid therapy • Demonstrated to PONV, morbidity, and hospital stay15

  35. INTRAOPERATIVE HEMODYNAMICS • Moreover, despite the anesthetist’s best efforts, major hemodynamic shifts are common during organ transplantation • One illustration of these hemodynamic shifts was provided by a large series that found substantial changes in intraoperative hemodynamics, with hypotension more likely than hypertension (49.6% vs. 26.8%)6

  36. SPKT HEMODYNAMICS CONTINUED • Another study followed 17 patients presenting for SPKT reported similar hemodynamic shifts4

  37. POST-REPERFUSION SYNDROME • PRS was first described by Aggarwal (1987), in the context of orthotopic liver transplantation (OLT) • A systemic phenomenon generally defined as a 30% decrease in MAP, sustained > 1 minute, occurring < 5 minutes after organ reperfusion5,20-22 • PRS has been reported in surgeries other than OLT • Cardiopulmonary bypass, aneurysm repair, ischemic limb reperfusion, and intestinal and renal transplants • Literature describing incidence of PRS is inconsistent, with rates between 20-55% of all OLT patients and 4% of renal transplants reported5,20

  38. PRS PHYSIOLOGY • While the exact mechanism of PRS remains controversial, some of the initially proposed causes included: • Cold preservation solution into systemic circulation20 • Acid-base and electrolyte derangements20,21 • Release of pro-inflammatory mediators, including nitric oxide (NO), due to massive induction of oxidative stress21 • However, one prospective study found no statistical correlation between serum pH, core temperature, potassium and calcium levels, or arterial blood-gas tensions and PRS5 • In the same study, a decreased SVR was the only variable that correlated significantly with PRS.

  39. PRS PHYSIOLOGY CONTINUED • Another study exploring PRS hemodynamics found preload in PRS patients was significantly lower than non-PRS patients • Despite equal LV function, as observed by TEE • Thus, acute vasodilation could explain both the decrease in SVR and preload • This phenomenon may be mediated by the release of vasoactive inflammatory mediators, secondary to an immunogenic response, resulting in a massive extracellular fluid shift • Supported by another study that identified increased levels of neutrophil and macrophage activation, with simultaneous anaphylatoxin formation, in patients experiencing PRS5 • Another proposed mechanism is the release of ROS2,6

  40. WHY IS PRS IMPORTANT? • PRS implicated in a number of undesirable outcomes: • Longer mechanical ventilation times and ICU stays, poor graft function, acute organ dysfunction unrelated to the surgical site, and increased mortality5 • One study examining PRS in renal transplant patients found the rate of graft failure at six months was increased by 10% in patients experiencing PRS • Additionally, the number of post-transplant hospitalization days was almost twice that of non-PRS patients who had the same surgery • Another study, following OLT patients who developed PRS, reported the relative risk of severe kidney dysfunction to be over three times greater that the non-PRS group • More frightening, the relative risk of death was determined to be almost three times greater than non-PRS cohorts

  41. WHO IS AT RISK FOR PRS? In the previously referenced study examining PRS in renal transplant patients, a significant correlation was identified between PRS and patients who were either diabetic, Asian, older than 60, or transplanted with an organ from an extended criteria donor (ECD)5

  42. PRS & AUTONOMIC DYSFUNCTION • A separate study reported an increased prevalence of PRS in patients with autonomic dysfunction • As previously discussed, both IDDM and ESRD are associated with autonomic dysfunction23 • Thus, these pathologies may be good markers for predicting PRS in surgical patients.

  43. PRS TREATMENTS? • Unfortunately, there does not yet appear to be a consensus in the literature regarding effective treatment regimens for PRS • Proposed strategies include2,5-8,11,12,20,21 : • Methylene Blue to inhibit inducible NO synthase and scavenge NO • On retrospective study of 700 patients found methylene blue to have no effect on changes in MAP, vasopressor or blood transfusion requirements, or end-organ effects • Prophylactic administration of epinephrine and atropine to attenuate hypotension and bradycardia • Mannitol to scavenge ROS • Sodium bicarbonate to buffer the increased acid load • Nonetheless, despite 25 years of research, there remains much to learn about PRS • However, as more definitive explanations of the mechanism and treatment of PRS emerge, it is reasonable to expect outcomes for a number of surgical procedures to improve

  44. HINDSIGHT IS 20/20

  45. AREAS FOR IMPROVEMENT • More proactive/aggressive treatment of N/V • Haldol/droperidol, diphenhydramine, etc • Tighter glycemic control • Continuous insulin infusion • Earlier utilization of SV Monitor • Aggressive treatment of early PRS with Epi? • Fluid Selection • LR only or more balanced ratio of LR/NS

  46. THANK YOU!

  47. References • Lin L. Endocrine and nutritional disease. In: Stoelting RK, Miller RD, eds. Basics of anesthesia. 5th ed. Philadelphia, PA: Churchill Livingstone; 2007:437-452. • Yost CS, Niemann CU. Anesthesia for abdominal organ transplantation. In: Miller RD, ed. Miller’s anesthesia. 7th ed. Philadelphia, PA: Churchill Livingstone; 2010:2155-2184. • Gruessner AC. 2011 Update on pancreas transplantation: comprehensive trend analysis of 25,000 cases followed up over the course of twenty-four years at the international pancreas transplant registry (IPTR). Rev Diabet Stud. 2011;8(1):6-16. • Mazza E, De Gasperi A, Corti O, et al. Hypotension after pancreatic reperfusion during combined kidney-pancreas transplantation. Transplant Proc. 1998;30(2):265-266. • Bruhl SR, Vetteth S, Rees M, Grubb BP, Khouri SJ. Post-reperfusion syndrome during renal transplantation: a retrospective study. Int J Med Sci. 2012;9(5)391-396. • Csete M, Glas K. Transplant anesthesia. In: Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC, eds. Clinical anesthesia. 6th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2009:1375-1392. • Niemann CU, Yost CS. Organ transplantation. In: Stoelting RK, Miller RD, eds. Basics of anesthesia. 5th ed. Philadelphia, PA: Churchill Livingstone; 2007:530-537. • Busque S, Melcher ML, Desai DM, Esquivel CO, Angelotti T, Lemmens HJM. Liver/kidney/pancreas transplantation. In: Jaffe RA, Samuels SI, eds. Anesthesiologist’s manual of surgical procedures. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2009:679-712. • Garwood S. Renal disease. In: Hines RL, Marschall KE, eds. Stoelting’s anesthesia and co-existing disease. 5th ed. Philadelphia, PA: Churchill Livingstone; 2008:323-348. • Evenson AR, Fryer JP. Transplantation for the general surgeon. In: Ashley S, Wilmore DW, eds. ACS Surgery: ACS Surgery: Principles and Practice. Hamilton, Ontario: BC Decker; 2009: 1-20. • Ouellette SM. Renal anatomy, physiology, pathophysiology, and anesthesia management. In: Nagelhaut JJ, Plaus KL, eds. Nurse anesthesia. 4th ed. St. Louis, MO: Saunders-Elsevier; 2010:694-726. • Palmer TJ. Hepatobiliary and gastrointestinal disturbances and anesthesia. In: Nagelhaut JJ, Plaus KL, eds. Nurse anesthesia. 4th ed. St. Louis, MO: Saunders-Elsevier; 2010:727-770. • Wall RT III. Endocrine disease. In: Hines RL, Marschall KE, eds. Stoelting’s anesthesia and co-existing disease. 5th ed. Philadelphia, PA: Churchill Livingstone; 2008:365-406. • Yost CS, Niemann CU. Renal, liver, and biliary tract disease. In: Stoelting RK, Miller RD, eds. Basics of anesthesia. 5th ed. Philadelphia, PA: Churchill Livingstone; 2007:425-436. • Bundgaard-Nielsen M, Ruhnau B, Secher NH, Kehlet H. Flow-related techniques for preoperative goal-directed fluid optimization. Br J Anaesth. 2007;98(1):38-44. • Pihusch R, Holler E, Muhlbayer D. The impact of antithymocyte globulin on short-term toxicity after allogeneic stem cell transplantation. Bone Marrow Transplant. 2002;30(6):347-354. • O’Malley CMN, Frumento RJ, Hardy MA, et al. A randomized, double-blind comparison of lactated ringer’s solution and 0.9% NaCl during renal transplantation. Anesth Analg. 2005;100(5):1518-1524. • Hokema F, Ziganshyna S, Bartels M, et al. Is perioperative low molecular weight hydroxyethyl starch infusion a risk factor for delayed graft function in renal transplant recipients?. Nephrol Dial Transplant. 2011;26(10):3373-3378. • Groeneveld ABJ, Navickis RJ, Wilkes MM. Update on the comparative safety of colloids: a systematic review of clinical studies. Ann Surg. 2011;253(3):470-483. • Chung IS, Kim HY, Shin YH, et al. Incidence an predictors of post-reperfusion syndrome in living donor liver transplantation [published online ahead of print December 14 2011]. Clin Transplant. 2011. http://onlinelibrary.wiley.com/doi/10.1111/j.1399-0012.2011.01568.x/full. Accessed July 23, 2007. • Fukazawa K, Pretto EA. The effect of methylene blue during orthotopic liver transplantation on post reperfusion syndrome and postoperative graft function. J Hepatobiliary Pancreat Sci. 2011;18(3):406-413. • Lomax S, Klucniks A, Griffiths J. Anaesthesia for intestinal transplantation. Contin Educ Anaesth Crit Care Pain. 2011;11(1):1-4. • Perez-Pena J, Rincon D, Banares R, et al. Autonomic neuropathy is associated with hemodynamic instability during human liver transplantation. Transplant Proc. 2003;35(5):1866-1868.

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