26 th international wintersymposium leuven 7-8 th january 2011 MANAGEMENT. A. Neyrinck, MD University Hospitals Leuven Department of Anesthesiology
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1 26 th international wintersymposium leuven 7-8 th january 2011 THORACIC C ORGAN DONOR O MANAGEMENT A. Neyrinck, MD University Hospitals Leuven Department of Anesthesiology Arne.neyrinck@uzleuven.be
2 outline: pathophysiology p of brain death the catecholamine roller coaster hormonal resuscitation biomarkers donor management protocols specific aspects of heart/lung donor p p g management
3 DONOR ORGAN INJURY INFLAMMATORY DONOR ORGAN INJURY OXIDATIVE STRESS INFLAMMATION HOMEOSTASIS PHYSICAL FORCES Donor NHBD Preservation Reperfusion? Warm Brain ischemia death
4 PATHOPHYSIOLOGY OF BRAIN DEATH
5 BRAIN DEATH Intracranial pressure Venous outflow obstruction Brain swelling At Arterial compression Pituitary + hypothalamic disregulation Cushing response: bradycardia and hypertension Autonomic storm: tachycardia and hypertension Vagal + sympathic (pontine) Vagal + sympathic (lower medulla) Vagal + sympathic Sympathic paralysis: bradycardia and hypotension BRAIN DEATH SOMATIC DEATH
6 BRAIN DEATH Intracranial pressure Venous outflow obstruction Brain swelling At Arterial compression Pituitary + hypothalamic disregulation Cushing response: bradycardia and hypertension Autonomic storm: tachycardia and hypertension Vagal + sympathic (pontine) Vagal + sympathic (lower medulla) Vagal + sympathic Sympathic paralysis: bradycardia and hypotension BRAIN DEATH SOMATIC DEATH
7 BRAIN DEATH: neural phase
8 BRAIN DEATH: humoral phase hypothalamic/ pituitary gland dysfunction adrenocortical dysfunction hypothyroidism diabetes insipidus glucose electrolyte l t disturbances fluid disturbances anaerobic metabolism
9 BRAIN DEATH: inflammatory phase BRAIN DEATH HORMONAL AND CATECHOLAMINE CIRCULATING RELEASE OF METABOLIC STORM MEDIATORS NEUROPEPTIDES DERANGEMENT VASOCONSTRICTION ISCHEMIC BRAIN PERIPHERAL ISCHEMIA ACTIVATION OF ENDOTHELIUM INFLAMMATION IN PERIPHERAL ORGANS
10 BRAIN DEATH: inflammatory phase DONOR Hyperdynamic storm Neurogenic hypotension Endothelial activation ICAM VCAM selectins Inflammatory cell infiltration Pro-inflammatory cytokines (IL-6, IL-8) Early graft dysfunction Late graft dysfunctin Kidney, Heart, Lung, (Liver)
11 DIRECT CARDIAC DYSFUNCTION CNS-injury Sympathetic discharge α-adrenergic Primary cardiac injury Indirect cardiovascular collapse Systemic vascular resistance interstitial norepinephrine Myocardial oxygen demand Coronary vasoconstriction Subendocardial ischemia Structural damage myocytolysis contraction band necrosis (calcium overload) edema formation cell infiltration ATP production Systemic vascular resistance
12 LOAD-DEPENDENT DEPENDENT CARDIAC DYSFUNCTION Loss of vasomotor tone afterload preload Coronary perfusion Frank Starling Affinity of contractile proteins to Ca2+ Intracellular Ca2+ release Stress activated Ca2+ channels reduced oxygen supply contractility
13 PULMONARY INJURY Brain death CNS-injury Sympathetic discharge α-adrenergic Inflammatory activation Systemic vascular resistance Lung blood volume Pulmonary arterial pressure Left ventricular output Left atrial pressure Pulmonary Capillary Pressure venoconstriction Donor lung injury Pulmonary Capillary Permeability
14 OPTIMAL TIME INTERVAL optimal time interval for heart donor management is limited to 72 h
15 DONOR CAUSE OF DEATH DONOR CAUSE OF DEATH n (%) Anoxia (12.3) Stroke (42.9) Head trauma (41,8) CNS Tumor 755 (0.9) other 1852 (2.2) Unos Registry Analysis Transpl Proc 2009; 41: 3539
16 DONOR CAUSE OF DEATH
17 THE CATECHOLAMINE ROLLER COASTER
18 norepinehrine i HISTORICAL FACTS decreased survival after heart transplantation dobutamine/dopamine < 10 μg/kg/min exogenous cathecholamines induce similar cardiac damage compared to the sympathetic storm after brain death B t t d l ti d Beta-receptor down regulation decreases response to inotropes after heart transplantation
19 RECENT CONTROVERSIES inotropes and alpha-agonists should be minimized impaired right ventricular function with NA Dobutamine/dopamine < 10 μg/kg/min noradrenaline < 0.6 μg/kg/min liberal use organ shortage restoration of loading conditions after loss of sympathetic tone adequate coronary perfusion pressures cathecholamines have immunomodulatory effects
20 ANOTHER POINT OF VIEW catecholamines are not deleterious no distinction between inotropes/vasopressors methodological pitfalls in limited studies catecholamine administration i ti after catecholamine storm not evaluated on myocardial injury
21 ANOTHER POINT OF VIEW catecholamines are needed loss of sympathetic tone fluids alone are not sufficient
22 ANOTHER POINT OF VIEW catecholamines are beneficial maintenance of coronary perfusion pressure catecholamines have immunomodulatory catecholamines have immunomodulatory effects
23 HORMONAL RESUSCITATION
24 HORMONE COCKTAIL T3-T4 vasopressin methylprednisone insulin increased organ procurement per donor increased suitable donors improved outcome in heart transplants benefit in hemodynamic unstable donors
25 T3 T4 rationale: reduced levels due to reduce TSH levels (hypothalamus/pituitary) and reduced conversion of T4 (euthyroid sick syndrome) reversal of anaerobic metabolism restoration of cardiac output reduction in inotropes and bicarbonate increased organ recovery preferable T3 (more T4 in clinical practice)
26 arginine vasopressin V1 receptor: blood vessel vasopressor V2 receptor: antidiuretic effect V3 receptor: anterior pituitary - adrenocorticotrope t hormone diabetes insipidus reduced inotropic requirements reduction of myocardial ATP depletion Doses: U/hr (half life of 15 min)
27 Desmopressin (DDAVP) V2 receptor activation Diabetes insipidus: Diuresis > 3-5 ml/kg/h Hypernatremia (> 150mM) R/ saline 0.45% and dextrose 5% Doses: 2 6 µg every 6 to 8 hours (duration of action 6 20 hours)
28 methylprednisone/hydrocortisone hydrocortisone 10mg/h catecholamine sparing effect methylprednisone adrenal insufficiency and anterior pituitary gland dysfunction catcholamine sparing effect immunomodulatory effect
29 Insulin Hyperglycemia followed by hypoglycemia Improves glycogene reserves in heart and liver No studies in donor populations Tight glycemic c control o benefits e at the ICU Doses: Baseline: 1 2 U hour
30 BIOMARKERS
31 BIOMARKERS IN DONOR HEART ctnt en ctni predictive for early graft failure predictive for rejection correlates with donor heart function TNF-α, IL-6, BNP/NT-proBNP, PCT, SMARCAL1
32 BIOMARKERS IN DONOR LUNG IL-8 levels in BAL donor lungs correlation primary graft dysfunction IL-6;IL-1B;IL-8;IL-10;IFN;TNF-A 6IL1B 8IL10 IFN donor lung biopsies IL6/IL10 ratio correlates with mortality micro-array studies
33 DONOR MANAGEMENT PROTOCOLS
34 IMPLEMENTATION OF DONOR MANAGEMENT PROTOCOLS aggressive donor management protocols improve organ recovery early identification of potential donors intensive care unit admission early and aggresive resuscitation specific targets specific donor interventional studies mainly focused on hemodynamic variables and donor heart management
35 Adjust volume status: target CVP = 6-10 mmhg Correct acidosis:target ph = Correct hypoxemia: target p02 > 80 mmhg, sat >95% Correct anemia: target HCT > 30%; Hb > 10 g/dl Adjust inotropics to keep MAP > 60 mmhg (dopamine/dobutamin < 10 µg/kg/min) Rule out structural abnormalities T3: 4 µg bolus + infusion 3 µg/hour Vasopressin: 1 unit bolus + infusion at units/hour methylprednisolone=: 15 mg/kg bolus Insulin: 1 unit/ hour minimum 1 st TOP-Course >ThoracicTransplantation Place PAC Adjust fluids, inotropes and pressors 15 min to minimize use of alpha agonists and meet targets: MAP > 60 mmhg PCWP 8-12 mmhg C.I. > 2.4 Dopamine or dobutamine < 10 µg/kg/min CVP 4-12 mmhg SVR dune/sec/cm-5 Crystal City Consensus circulation 2001
36 Du Bose J Intensive Care Med 2008
37 Dictus et al Clin transplant 2009
38 Rostron Transplant rev 2007
39 ASPECTS OF CARDIAC MANAGEMENT
40 DONOR RISK FACTORS FOR HEART TRANSPLANTATION Risk factors for primary graft failure donor age > 30 y Donor head trauma high donor inotropes ischemic time > 240 min
41 SELECTION CRITERIA FOR HEART DONORS characteristics of donors where caution is to be applied during selection older donors (> 55y) prolonged ischemic time (> 5h) hepatitis C chronic alcohol abuse cocaine abuse atraumatic intracranial bleed size (body weight) undersizing (<30%) in recipients with pulmonary hypertension oversizing (>30%) in recipients with LVADS
42 HEART DONOR ASSESSMENT ECG abnormalities ST depression/elevation and inverted T- waves atrial arrhythmias prolonged QT interval (hypokalemia) short QT interval (gunshot) conduction abnormalities Q-waves (without positive enzymes)
43 HEART DONOR ASSESSMENT echocardiography h after optimization of load-indices dobutamine stress echocardiography diffuse wall motion abnormalities limited role for repeat echocardiography Swan-ganz catheter Troponin-I -T
44 SODIUM LEVELS polyuria: diabetes insipidus (<>hyperglycemia) urine output > 4 ml/kg/h serum Na+ > 145 mmol/l serum Osm > 300 mosm/l urine Osm < 200 mosm/l desmopressin 2 4 μg/q 6h Na+ fluid > 145 dextrose 5% NaCl 0.3% + glucose 3,3% <130 NaCl 09% 0.9%
45 SODIUM LEVELS hypernatremia and intracellular sodium levels contribute to ischemia-reperfusion injury historical no clinical adverse effect on outcome in heart transplantation donor hypernatremia is an indicator of suboptimal donor management
46 SODIUM LEVELS donor hypo- and hypernatremia are predictors for increased 1-year mortality Hoefer et al Transplant International 2009; 23:589
47 ASPECTS OF PULMONARY MANAGEMENT
48 DONOR LUNG CRITERIA CURRENT DONOR LUNG CRITERIA GUIDELINES ABO compatible Age < 55y smoking history < 20 y clear chest radiograph Pa02 > 300 (FiO2 100%) and 5 cmh2o PEEP abscence of chest trauma no evidence of aspiration/sepsis no prior cardiothoracic surgery no organisms on donor gram stain no purulent secretions on bronchoscopy
49 DONOR LUNG CRITERIA NON COMPLIANCE WITH CURRENT STANDARD CRITERIA age > 55y 7.7% PO2 18% smoking history 21% abnormal chest radiograph 41% purulent secretions 12% confirmed blood infection 3.1% ABO compatibility 0.058% (accidents)
50 DONOR LUNG CRITERIA NEW DONOR CRITERIA WITH NEGATIVE IMPACT ON SURVIVAL african-american high recipient/donor BMI ratio diabetic blood type A CMV antibodies head trauma as cause of death race mismatch gender mismatch
51 PULMONARY MANAGEMENT no clear donor management protocols available recruitment prevention of atelectasis improvement of gas exchange increased organ recovery oxygenation as important target
52 PULMONARY MANAGEMENT SALT protocol (retrospective) recruitment (PEEP 15cmH20 and AwP 25 cmh20) when P/F ratio < 300 IPPV 10 ml/kg and PEEP 5 cmh20 head elevation and bronchoscopy
53 Angel LF et al Am J Respir Crit Care Med 2006
54 PULMONARY MANAGEMENT hemodynamic resuscitation of donor lungs donor catecholamines lead to impaired gas exchange CVP 4-10 mmhg PCWP mmhg alpha-adrenergic antagonism during hypertensive crisis correction of neurogenic hypotension
55 PULMONARY MANAGEMENT hormonal resuscitation of donor lungs methylprednisone (1g) +/- T3 (0.8μg bolus μg/kg/min) methylprednisone decreased EVLWI no effect on oxygenation
56
57 PULMONARY MANAGEMENT associated risk factors for lung quality aspiration pneumonia contusion ventilator-induced lung injury specific exams chest X-ray (CT-scan) bronchoscopy
58 VENTILATORY STRATEGY Overdistention (baby lung) volutrauma in functional reduced lung volume reduction in tidal volume interdependence Atelectrauma (open lung concept) Repetitive e opening and closure of atelectatic zones recruitment and PEEP
59 VENTILATORY STRATEGY: PROTECTIVE VENTILATION ARDS/ALI?
60 VENTILATORY STRATEGY: PROTECTIVE VENTILATION DONORS Ranieri i et al JAMA 2010 conventional (6h) n = 59 protective (6h) n = 59 TV cmh2o TV 6 8 cmh2o PEEP 3-5 cmh2o PEEP 8 10 cmh2o apnea test by disconnection apnea test by CPAP open circuit airway suction closed circuit airway suction Lung protectivee strategy increased organ recovery reduced d serum IL-6 no effect on 6-month survival
61 ALVEOLAR FLUID CLEARANCE Modulation of activity Modulation of expression Glucocorticoids EGF KGF β2-agonist β2-agonist Dopamine dobutamine Na ENaC ATII AIRSPACE Cl CFTR Na ENaC H2O camp K ATI camp aquaporin Na Matthay MA et Al. J Appl Physiol 2002; 93: K INTERSTITIUM
62 ALVEOLAR FLUID CLEARANCE Ware L B et al. J Appl Physiol 2002;93: EX VIVO ASSESSMENT OF REJECTED DONOR LUNGS
63 ALVEOLAR FLUID CLEARANCE Ware L B et al. J Appl Physiol 2002;93: EX VIVO ASSESSMENT OF REJECTED DONOR LUNGS
64 ALVEOLAR FLUID CLEARANCE Ware L B et al. J Appl Physiol 2002;93: EX VIVO ASSESSMENT OF REJECTED DONOR LUNGS
65 CONCLUSION hemodynamic and inflammatory changes following brain death are responsible for donor organ injury donor organ injury has impact on transpant outcome aggressive donor management protocols might improve organ recovery and outcome future donor organ intervention ti studies
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