Transcript Anesthesia Considerations for Simultaneous Pancreas

ANESTHESIA CONSIDERATIONS
FOR SIMULTANEOUS PANCREASKIDNEY 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, 47 kg female
• Underwent primary SPKT two years earlier
– Pancreatic graft failure due to severe pancreatitis
– Renal graft failure secondary to rejection
• History: IDDM, ESRD, Anemia, GERD, HTN, HLD
• Anesthesia History: Unremarkable
• Allergy: Cephalexin (rash)
PREOPERATIVE ASSESSMENT
• Airway: Mallampati III, TM distance = 5 cm,
normal cervical extension
• Hypertensive: MAP 100 - 125 mm Hg
• ECG: NSR with poor R-wave progression
• Negative nuclear stress test
• TTE: Normal EF, mild LVH/LAE, trace MR/TR
• CXR: Remarkable only for an in situ left subclavian
HD catheter with its tip at the atriocaval junction
PREOPERATIVE ASSESSMENT
•
•
•
•
Lungs CTA bilaterally
Normal heart tones
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
INDUCTION
MAINTENANCE OF
ANESTHESIA
• Desflurane titrated between 4.2-6.5 %
• NMB maintained with atracurium
• Serum glucose assessed Q30 minutes
• Regular insulin administered IV in small doses
throughout the case as directed by surgeon
IMMUNOSUPPRESSIVE THERAPY
• Induced with methylprednisolone 350 mg IV (15 min)
• Followed by infusion of anti-thymocyte globulin
• Infusion rate halved 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
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……
PANCREATIC REPEFUSION
OVER THE NEXT 80 MINUTES…
• Norepinephrine infusion titrated to 0.25 g/kg/min
• Six 64 g boluses of norepinephrine were administered
• 2L NS bolused to maintain a MAP > 60 mm Hg
– Recall, goal MAP ~80 mm Hg
• Diphenhydramine (25 mg) and esmolol (10 mg)
administered
• No observed response
• Heart rate remained 120 – 140 bpm
• Four hours into the case, MAP stabilized at 70 mm Hg
• Heparin and mannitol administered prior to vascular
clamping and reperfusion of renal graft
• Anesthesia grimaces….
RENAL GRAFT REPEFUSION
•
•
•
•
•
•
•
•
•
MAP acutely fell from 72 to 51 mm Hg after reperfusion
128 g norepinephrine bolus administered
Second unit of PRBCs transfused
10 mg furosemide administered, per the surgeon’s request
CardioQ SV monitor utilized to assess volume status
4.5 L of crystalloid infused over remainder of case,
Fluid total: 8 L crystalloid and ~ 1.5 L colloid
Estimated blood loss was 500 mL
A total of three ampules of sodium bicarbonate were
administered to correct acidosis
POST-REPERFUSION SYNDROME
EMERGENCE
• By the end of the case, hemodynamics stabilized
– Norepinephrine infusion decreased to 0.08 g/kg/min
– Dopamine infusion discontinued
– Anti-thymocyte globulin infusion reinitiated at full dose
• NMB antagonized with 0.5 mg glycopyrrolate and 3.5 mg
neostigmine 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
POSTOPERATIVE COURSE
• Patient was extubated the following morning and
transferred out of the ICU two days later
• Patient back to OR for closure of fascia POD 8
– Wound infection and edematous pancreas with multiple
necrotic areas discovered
• Returned to OR on POD 12 for I&D and closure of
the fascia and skin
• Patient remained hospitalized for one month prior to
being discharged to a rehabilitation facility
DISCUSSION
WHO BENEFITS FROM SPKT?
• Patients with brittle diabetes and ESRD
• ~ 50-60% of insulin-dependent diabetics develop
diabetic nephropathy
• Leading cause of renal failure requiring hemodialysis in
young and middle-aged adults in the United States
• 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
(Lin, 2007; Yost & Niemann, 2010; Gruessner, 2011)
SPKT VS. PTA & PAK
(Gruessner, 2011)
WHAT HAPPENS WHEN SPKT FAILS?
• Uncommon
• Serious
• Few institutions with much experience
(Gruessner, 2011)
PANCREATIC
ANASTAMOSES
During bench preparation
of pancreatic graft, the
bifurcation of donor’s Iliac
A. is anastamosed with the
Superior Messenteric A. &
Splenic A. from graft for
ease of anastamosis to
recipient’s R Common Iliac
A. during transplantation
RENAL ANASTAMOSES
ACS Surgery Principles and Practice
ANESTHESIA CONSIDERATIONS
• Preoperative Assessment, Planning & Collaboration
• Minimizing Consequences of IDDM and ESRD
• Glycemic Control
• Autonomic Neuropathy
• Renal pharmacological considerations
• Management of Immunosuppressive Therapy
• Optimization of Graft Function
• Fluid Management
• Commonly Utilized Intraoperative Drugs
• Adequate Graft Perfusion
• Management of Post-Reperfusion Syndrome (PRS)
PREOPERATIVE ASSESSMENT
• Begins with a review of the health history
• Special attention to co-existing diseases that often
accompany ESRD and IDDM:
• Hypertension, anemia, uremia, and cardiac disease
• Cardiac workup warranted due to risk for silent
ischemia secondary to autonomic neuropathy
• Coronary angiography vs. non-invasive testing such as
EKG, TTE, Nuclear Stress Testing, etc
(Garwood, 2008; Evenson & Fryer, 2009; Ouellette, 2010; De Lima, et al., 2003)
PREOPERATIVE LABS
• Laboratory tests should include: CBC, CMP,
hemoglobin A1C, coagulation studies, and T&C
for at least two units of washed PRBCs
• The transplant workup will also include
screening tests for a multitude of infectious
diseases, as well as ABO and human leukocyte
antigen (HLA) compatibility
(Busque, 2009; Ouellette, 2010)
PREOPERATIVE EXAM
• Primary concerns: cardiopulmonary system and airway
• Orthostatics and dialysis details facilitate estimation of
blood volume status
• Difficult airway?
– Few studies propose intubation difficult in diabetics
– Subsequent studies did not substantiate these fears
– Nonetheless, prudent to assess joint mobility in neck and
jaw and to prepare for difficult visualization of laryngeal
structures
• Identify HD shunts/fistulas and verify adequate
padding, as pressure may cause thrombosis
(Yost & Niemann, 2010; Garwood, 2008; Busque, 2009; Palmer, 2010)
GLYCEMIC CONTROL
• Many proposed management strategies
• Most authors agree BG should be assessed at least Q30-60 min
• Treat with regular insulin IVP or via continuous infusion
• Mitigates risk for ketoacidosis, depressed immune function,
decreased wound healing, and worsened neurologic insult in the
setting of cerebral ischemia
• Keep BG > 150 mg/dL prior to pancreatic graft insertion
• Serum glucose decreases ~ 50 mg/dL/hr after reperfusion
• Hypoglycemia difficult to detect due to anesthesia and diabetic
and renal disease-related neuropathy
• Another complicating factor is routine administration of
high-dose corticosteroid for immunosuppressive therapy
(Yost & Niemann, 2010; Csete & Glas, 2009; Busque, 2009; Palmer, 2010)
ANESTHETIC TECHNIQUE
• Regional anesthesia has been successfully used for isolated
pancreas and kidney transplants
• Most authors encourage general endotracheal anesthesia
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
perfusion
(Hadimioglu, Ertug, Bigat, Yilmaz, & Yegin, 2005; Pichel & Macnab, 2005; Busque et al., 2009; Csete & Glas, 2009; Palmer, 2010; Yost & Niemann, 2010).
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 or may
not be supplemented with a large dose of corticosteroid
• Regimens vary between patients and institutions
• Imperative that anesthetist clarifies schedule and dosing
with transplant team
(Csete & Glas, 2009; Evenson & Fryer, 2009; Kaufmann et al., 2002)
SIDE EFFECTS
Clinical Anesthesia, 6th ed., 2009
Miller’s Anesthesia, 7th ed., 2010
AUTONOMIC NEUROPATHY
• Diabetics, especially those with ESRD, prone to
autonomic neuropathy that may cause:
– Gastroparesis increases risk for aspiration
– Cardiovascular lability: possible intraoperative
hypotension requiring pressors, dysrhythmias, and
bradycardia resistant to atropine
• Regardless of volume status, patients with
ESRD often experience exaggerated
hypotension with induction of anesthesia
INDUCTION OF ANESTHESIA
• No standard induction drugs specifically
contraindicated
• May require increased dose of propofol
• Titration better than large single bolus
• All patients presenting for SPKT should be
considered at risk for aspiration
– RSI with cricoid pressure and slight reverse
trendelenberg positioning indicated
NEUROMUSCULAR BLOCKADE
• Succinylcholine usually safe in patients with ESRD
• Serum potassium should be < 5.5 mEq/L
• 0.6 mEq/L increase in potassium after intubating dose
• Increased risk for patients with motor and sensory neuropathy
• Alternative to succinylcholine for RSI is rocuronium
• All short and intermediate acting NDNMBs safe with
careful titration based upon TOF monitoring
• Cisatracurium and atracurium ideal due to extrarenal
metabolism via Hoffman degredation and plasma
cholinesterase
• Primary metabolite, laudanosine, may cause seizures via
stimulation of CNS at high plasma concentrations
(Busque et al., 2009; Csete & Glas, 2009; Palmer, 2010; Yost & Niemann, 2010; Ouellette, 2010; Ma & Zhuang, 2002 )
MAINTENANCE OF ANESTHESIA
• Balanced anesthetic technique likely best method to
sustain hemodynamic stability
• Drugs selected based upon known side effects
• N2O often omitted
• Morphine and meperidine should also be avoided due to
the action of their metabolites
• Desflurane and isoflurane are commonly used
• While the metabolism of sevoflurane has been
implicated in nephrotoxicity, there is a lack of evidence
clearly substantiating these concerns
(Yost & Niemann, 2010; Garwood, 2008)
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
(O'Malley, Frumento, & Bennett-Guerrero, 2002; Csete & Glas, 2009; Garwood, 2008; Ouellette, 2010; O'Malley et al., 2005; Hadimioglu et al., 2008; Groeneveld, Navickis, & Wilkes, 2011)
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 Flow
• Pulmonary Artery Catheter based upon H&P
– Higher filling pressures (>20/15 mm Hg) indicative of better graft
function than lower pressures in one study
• 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 stay
(Yost & Niemann, 2010; Csete & Glas, 2009; Busque, 2009; Bundgaard-Nielsen, 2007; Benes et al., 2010)
INTRAOPERATIVE HEMODYNAMICS
• 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%)
(Csete & Glas, 2009)
SPKT HEMODYNAMICS
• Another study following 17 patients presenting for SPKT
reported similar hemodynamic shifts
(Mazza, et al., 1998)
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 reperfusion
• 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 reported
(Bruhl et al., 2012; Chung et al., 2012; Fukazawa & Pretto, 2011; Lomax, Klucniks, & Griffiths, 2010)
PRS PHYSIOLOGY
• While the exact mechanism of PRS remains controversial,
some of the initially proposed causes included:
• Cold preservation solution into systemic circulation
• Acid-base and electrolyte derangements
• Release of pro-inflammatory mediators, including nitric oxide
(NO), due to massive induction of oxidative stress
• However, one prospective study found no statistical
correlation between serum pH, core temperature,
potassium and calcium levels, or arterial blood-gas
tensions and PRS
• In the same study, a decreased SVR was the only variable
that correlated significantly with PRS
(Bruhl et al., 2012; Chung et al., 2012; Fukazawa & Pretto, 2011; Lomax, Klucniks, & Griffiths, 2010)
PRS PHYSIOLOGY CONTINUED
• Another study exploring PRS hemodynamics found preload
was significantly lower in PRS patients than non-PRS patients;
despite equal LV function, as observed by TEE
• Acute vasodilation could explain both the decrease in
SVR and preload
• Possibly mediated by 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 PRS
• Another proposed mechanism is the release of ROS
(Bruhl, 2012; Yost & Niemann, 2010; Csete & Glas, 2009)
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 mortality
• Bruhl reported a 10% increase in graft failure at six in renal
transplant patients experiencing PRS
• 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
(Bruhl, 2012)
WHO IS AT RISK FOR PRS?
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
(Bruhl, 2012)
PRS & AUTONOMIC DYSFUNCTION
• Increased prevalence of PRS in patients with
autonomic dysfunction
• Both IDDM and ESRD are associated with
autonomic dysfunction
• Thus, these pathologies may be good markers
for predicting PRS in surgical patients.
(Perez-Pena, et al., 2003)
PRS TREATMENTS?
• Unfortunately, there does not yet appear to be a consensus in the
literature regarding effective treatment regimens for PRS
• Proposed strategies include:
• 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
(Bruhl et al., 2012; Busque et al., 2009; Chung et al., 2012; Csete & Glas, 2009; Fukazawa & Pretto, 2011; Ouellette, 2010; Palmer, 2010; Yost & Niemann, 2010)
HINDSIGHT IS
20/20
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
THANK YOU!
QUESTIONS?
[email protected]
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