The Pathophysiological Management of the Deceased Organ Donor: From Brain Death to the Operating Room
Dr Neeraj Manikath , claude.ai
Abstract
The management of the deceased organ donor represents one of the most complex and time-sensitive challenges in critical care medicine. Following brain death, a cascade of pathophysiological derangements transforms a hemodynamically stable patient into a critically unstable donor, requiring sophisticated ICU interventions. This review examines the evidence-based strategies for donor management, from the catecholamine storm through to organ procurement, with emphasis on the physiological rationale underlying each intervention. Understanding these mechanisms is crucial for maximizing the number and quality of transplantable organs, potentially saving multiple lives from a single donor.
Keywords: Brain death, organ donation, donor management, catecholamine storm, endocrine resuscitation, hemodynamic optimization
Introduction
Despite advances in transplant medicine, the gap between organ supply and demand continues to widen, with over 100,000 patients awaiting transplantation in the United States alone. Each potential organ donor represents the possibility of saving up to eight lives through solid organ transplantation. However, the physiological devastation following brain death creates a hostile environment for organ preservation, with up to 25% of potential donors lost due to cardiovascular collapse before organ recovery can occur.
Brain death triggers a predictable yet devastating sequence of events: the catecholamine storm, subsequent cardiovascular collapse, hypothalamic-pituitary axis failure, and progressive multi-organ dysfunction. The intensivist's role shifts from treating the patient to becoming a "guardian of the organs," requiring a fundamental paradigm shift in management priorities. This review provides a comprehensive, evidence-based approach to donor management, integrating pathophysiology with practical clinical strategies.
The "Catecholamine Storm" and its Aftermath: Managing the Initial Hypertensive Crisis Followed by Profound Vasodilatory Shock
Pathophysiology of the Autonomic Storm
The progression to brain death involves a critical period of intracranial hypertension that triggers the Cushing reflex—a desperate attempt by the medullary vasomotor center to maintain cerebral perfusion. As intracranial pressure approaches mean arterial pressure, medullary ischemia provokes a massive, unregulated sympathetic discharge known as the "autonomic storm" or "catecholamine storm."
During this phase, plasma catecholamine levels may increase 1,000-fold above normal, with norepinephrine levels reaching 10,000-20,000 pg/mL. This surge produces severe hypertension (often >200 mmHg systolic), tachycardia, and myocardial stress. The consequences extend far beyond hemodynamic instability: subendocardial ischemia, myocardial stunning, neurogenic pulmonary edema, and direct catecholamine-mediated myocyte toxicity can render organs unsuitable for transplantation.
Histologically, catecholamine excess causes myofibrillar degeneration, contraction band necrosis, and inflammatory infiltration—findings that mimic acute myocardial infarction. Cardiac troponin elevation is nearly universal, but does not necessarily preclude cardiac donation if ventricular function recovers with appropriate management.
The Biphasic Hemodynamic Response
Phase 1: Hypertensive Crisis (Minutes to Hours)
The immediate post-brain death period is characterized by:
- Severe hypertension (SBP >180-200 mmHg)
- Tachycardia or reflex bradycardia
- Increased systemic vascular resistance
- Myocardial oxygen demand-supply mismatch
- Acute neurogenic pulmonary edema
Phase 2: Vasodilatory Shock (Hours to Days)
Following sympathetic denervation with complete brain death, a profound vasodilatory state emerges:
- Loss of sympathetic vascular tone
- Distributive shock with SVR <800 dynes·sec·cm⁻⁵
- Relative or absolute hypovolemia
- Impaired baroreceptor reflexes
- Progressive hypothermia
Clinical Management Strategies
Hypertensive Phase Management
The primary goal during the catecholamine storm is organ protection, not blood pressure normalization per se. Aggressive treatment of extreme hypertension (>180 mmHg systolic) is warranted to prevent:
- Cardiac dysfunction from afterload excess
- Disruption of vascular anastomoses
- Exacerbation of pulmonary edema
Pearl: Use short-acting agents that can be rapidly titrated as the patient transitions to vasodilatory shock. Esmolol (β-blocker with 9-minute half-life) is ideal for managing both tachycardia and hypertension, reducing myocardial oxygen consumption without prolonged effect.
Nicardipine or clevidipine (ultra-short-acting dihydropyridine calcium channel blockers) provide smooth blood pressure control without the negative inotropic effects of diltiazem or verapamil. Target mean arterial pressure of 60-70 mmHg during this phase.
Oyster: Avoid long-acting antihypertensives (labetalol, hydralazine) that may compromise management during the subsequent hypotensive phase. The transition from hypertensive crisis to vasodilatory shock can occur within hours, and overly aggressive treatment may precipitate cardiovascular collapse.
Vasodilatory Shock Management
The foundation of shock management in the brain-dead donor differs fundamentally from standard critical care:
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Volume Resuscitation: Initial approach with crystalloids to restore intravascular volume, but with careful attention to avoid pulmonary edema. Target CVP 6-10 mmHg, recognizing that traditional filling pressure targets may be misleading.
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Vasopressor Selection: The choice of vasopressor has significant implications for organ viability:
- Norepinephrine remains first-line, but doses >0.1 mcg/kg/min suggest inadequate hormonal resuscitation
- Vasopressin (discussed below) should be introduced early as first-line or adjunctive therapy
- Phenylephrine may be considered for pure vasodilatory shock without cardiac dysfunction
- Dopamine should be avoided due to excessive β-adrenergic effects and arrhythmogenicity
Hack: The "Rule of 0.1" – If norepinephrine requirements exceed 0.1 mcg/kg/min, initiate endocrine replacement therapy immediately rather than escalating to high-dose vasopressors. This approach recognizes that refractory shock in brain death often reflects hormonal deficiency rather than true catecholamine resistance.
- Monitoring and Targets:
- Mean arterial pressure: 60-70 mmHg (higher targets do not improve outcomes and may worsen organ function)
- Urine output: ≥1 mL/kg/hr (but may be misleading in diabetes insipidus)
- Lactate clearance: >10% per hour
- Mixed venous oxygen saturation: >70%
Pearl: Dynamic indices (pulse pressure variation, stroke volume variation) may be more reliable than static filling pressures for guiding fluid therapy in the brain-dead donor, particularly when using advanced hemodynamic monitoring.
Endocrine Resuscitation: The Evidence for Using Vasopressin, Levothyroxine (T3/T4), and Corticosteroids
The Neuroendocrine Collapse
Brain death destroys the hypothalamic-pituitary axis, resulting in:
- Posterior pituitary failure → diabetes insipidus (78% of donors)
- Anterior pituitary failure → thyroid hormone deficiency (60-80%)
- Adrenal insufficiency (50-80%)
- Growth hormone and gonadotropin deficiency (variable clinical significance)
This triad of endocrine deficiencies contributes directly to cardiovascular instability, explaining why some donors require escalating vasopressor support despite adequate volume resuscitation.
Vasopressin Therapy
Physiological Rationale
The posterior pituitary's destruction eliminates antidiuretic hormone (ADH/vasopressin) production, causing:
- Diabetes insipidus with massive diuresis (>4 mL/kg/hr)
- Severe hypernatremia (Na⁺ >155 mEq/L in 80% of donors)
- Intravascular volume depletion
- Loss of vasopressin's vascular V₁ receptor-mediated vasoconstriction
Evidence Base
Multiple observational studies and randomized trials demonstrate vasopressin's benefits:
- Reduces catecholamine requirements by 30-50%
- Corrects diabetes insipidus within 1-2 hours
- Improves hemodynamic stability in 75-85% of donors
- Associated with increased organ yield per donor
The landmark study by Pennefather et al. (1995) demonstrated that low-dose vasopressin (1-2 units/hour) restored hemodynamic stability in 93% of previously unstable donors, allowing organ recovery in all cases.
Clinical Application
Standard Protocol:
- Initiate vasopressin 0.5-2.4 units/hour (do not use boluses)
- For diabetes insipidus: DDAVP 1-4 mcg IV bolus, repeat every 4-6 hours as needed
- Target urine output <3 mL/kg/hr
- Monitor serum sodium every 2-4 hours, target 135-150 mEq/L
Hack: The "Vasopressin First" strategy—start vasopressin as a first-line vasopressor in brain-dead donors rather than as adjunctive therapy. This approach acknowledges the physiological vasopressin deficiency and often prevents the need for escalating norepinephrine doses. Combine 1 unit/hour vasopressin with low-dose norepinephrine (0.03-0.05 mcg/kg/min) as initial therapy.
Oyster: Avoid excessive sodium correction. Rapid reduction of hypernatremia (>10 mEq/L per 24 hours) risks cerebral edema in solid organs with intact blood-brain barriers, particularly in kidney allografts. Chronic hypernatremia (>160 mEq/L for >6 hours) may render kidneys unsuitable for transplantation due to tubular injury.
Thyroid Hormone Replacement
Pathophysiology of Thyroid Hormone Deficiency
Thyroid hormone exerts profound cardiovascular effects:
- Enhances myocardial contractility via genomic and non-genomic mechanisms
- Increases β-adrenergic receptor expression and sensitivity
- Reduces systemic vascular resistance
- Improves diastolic function
- Regulates cellular metabolism and ATP production
Following brain death, free T₃ levels decline by 30-40% within hours, contributing to:
- Myocardial dysfunction (reduced ejection fraction)
- Vasopressor dependency
- Metabolic derangements (reduced oxygen consumption)
- "Euthyroid sick syndrome" pattern
Evidence and Controversy
The use of thyroid hormone in donor management remains somewhat controversial, with mixed evidence:
Supporting Evidence:
- Meta-analysis by Novitzky et al. showed improved cardiac function and increased hearts transplanted (RR 1.54, 95% CI 1.20-1.98)
- Observational studies demonstrate reduced vasopressor requirements
- Improved donor stability during organ procurement
Neutral Evidence:
- Several randomized trials (including Venkateswaran et al., 2009) showed no significant benefit in cardiac function or transplantation rates
- The HOTT trial (2011) found no difference in hearts transplanted with T₃ therapy
Current Understanding:
Despite mixed evidence, most transplant programs include thyroid hormone in their hormonal resuscitation protocols, particularly for cardiac donors. The rationale: potential benefit with minimal risk, and biological plausibility given the known cardiovascular effects.
Clinical Protocol
Two approaches exist:
1. Triiodothyronine (T₃) – Preferred
- Loading dose: 4 mcg IV bolus
- Maintenance: 3 mcg/hour continuous infusion
- Onset of action: 4-6 hours
- Advantages: Active form, rapid onset
2. Levothyroxine (T₄)
- Loading dose: 20 mcg IV bolus
- Maintenance: 10 mcg/hour infusion
- Requires peripheral conversion to T₃
- Slower onset (12-24 hours)
Pearl: Start thyroid hormone replacement early (immediately upon brain death declaration) to allow adequate time for cardiovascular effects before organ procurement. Waiting until hemodynamic instability develops may be too late for optimal benefit.
Hack: For donors with severe cardiac dysfunction (EF <40%), consider higher T₃ doses: 0.8 mcg bolus followed by 0.113 mcg/kg/hour. This "aggressive thyroid protocol" was associated with improved cardiac allograft function in the study by Rosendale et al. (2003).
Corticosteroid Therapy
Physiological Basis
Adrenal insufficiency in brain death occurs through:
- Loss of hypothalamic CRH and pituitary ACTH
- Reduced cortisol production (levels <20 mcg/dL in 60% of donors)
- Inflammatory cytokine release
- Capillary leak and vascular instability
Evidence
High-quality evidence supports corticosteroid use:
- Improves hemodynamic stability (reduced vasopressor requirements)
- Reduces inflammatory cytokine levels
- Improves oxygenation (important for lung donation)
- Associated with increased organs transplanted per donor
- May improve post-transplant graft function, particularly for lungs
The CORTICOME trial (2006) demonstrated that methylprednisolone significantly reduced vasopressor requirements and improved organ yield.
Clinical Application
Standard Protocol:
- Methylprednisolone 15 mg/kg IV (maximum 1 gram) as single bolus, OR
- Hydrocortisone 300 mg bolus followed by 100 mg every 8 hours
Pearl: Administer corticosteroids to all potential donors, regardless of baseline hemodynamic status. Benefits extend beyond shock reversal to include anti-inflammatory effects that may improve organ quality, particularly for lungs and kidneys.
Combined Hormonal Therapy: The "Rule of 100s"
An easy-to-remember protocol for hormonal resuscitation:
- Vasopressin: 1 unit/hour
- T₃: 4 mcg bolus, then 3 mcg/hour (or T₄: 20 mcg bolus, then 10 mcg/hour)
- Methylprednisolone: 15 mg/kg bolus (often rounds to ~1000 mg)
Oyster: Do not delay hormonal therapy waiting for laboratory confirmation of deficiency. Hormone assays take hours to result and are often unreliable in the critical care setting. The risk-benefit ratio strongly favors empiric replacement.
Lung-Protective Ventilation for the Donor: Strategies to Prevent Ventilator-Associated Lung Injury
The Challenge of Donor Lung Management
Lungs are the most frequently injured organs following brain death, with only 15-25% of donated lungs ultimately suitable for transplantation. The etiology is multifactorial:
Injury Mechanisms:
- Neurogenic pulmonary edema from catecholamine storm
- Aspiration at time of neurological injury
- Ventilator-induced lung injury (VILI) from prolonged mechanical ventilation
- Inflammatory cascade triggered by brain death
- Fluid overload during resuscitation
- Infection (ventilator-associated pneumonia)
Pathophysiology of Ventilator-Induced Lung Injury
Traditional ICU ventilation strategies—designed for gas exchange optimization—may be harmful to donor lungs:
Mechanisms of VILI:
- Barotrauma: Excessive airway pressures causing alveolar rupture
- Volutrauma: Overdistension from excessive tidal volumes
- Atelectrauma: Repetitive opening/closing of alveoli causing shear stress
- Biotrauma: Release of inflammatory mediators (IL-6, IL-8, TNF-α)
The "baby lung" concept is relevant: only non-injured lung regions participate in ventilation. Excessive tidal volumes distributed to these compliant areas cause regional overdistension even when plateau pressures seem acceptable.
Evidence-Based Lung-Protective Strategies
1. Low Tidal Volume Ventilation
Strategy:
- Tidal volume: 6-8 mL/kg ideal body weight (IBW)
- Calculate IBW: Males = 50 + 2.3(height in inches - 60); Females = 45.5 + 2.3(height in inches - 60)
- Accept permissive hypercapnia (PaCO₂ 40-60 mmHg)
Evidence: The landmark ARDS Network trial principles apply to donor management. Mascia et al. (2010) demonstrated that lung-protective ventilation in brain-dead donors increased lungs suitable for transplantation from 27% to 54% (p<0.001).
Pearl: Don't be distracted by traditional ICU targets. Brain-dead patients don't require "normal" blood gases—organs need adequate oxygen delivery, not PaO₂ >100 mmHg or PaCO₂ 35-45 mmHg. Accept PaO₂ 80-100 mmHg and pH >7.25.
2. Optimal PEEP Strategy
Target: PEEP 8-10 cm H₂O (higher if ARDS present)
Rationale:
- Prevents atelectasis
- Maintains functional residual capacity
- Reduces cyclic alveolar collapse/reopening
- Improves V/Q matching
- Reduces inflammatory mediator release
Evidence: Higher PEEP (10 cm H₂O vs 5 cm H₂O) in donors improved post-transplant outcomes, with better oxygenation and reduced primary graft dysfunction in recipients (Mascia et al., 2013).
Hack: The "PEEP trial" in unstable donors—if hemodynamically tolerant, incrementally increase PEEP from 5 to 10 cm H₂O while monitoring blood pressure and oxygenation. Many donors tolerate this well with improved lung compliance. If hypotension develops, the problem is likely inadequate preload, not excessive PEEP.
Oyster: Be cautious with very high PEEP (>12 cm H₂O) in non-ARDS donors, as this may impair venous return and cardiac output in the absence of intact autonomic reflexes. The risk-benefit ratio shifts toward lower PEEP if hemodynamics deteriorate.
3. Plateau Pressure Limitation
Target: Plateau pressure (Pplat) <30 cm H₂O, ideally <28 cm H₂O
Measurement: Perform inspiratory hold maneuver every 4 hours to assess Pplat
Management: If Pplat >30 cm H₂O:
- Reduce tidal volume to 5-6 mL/kg IBW
- Accept higher PaCO₂ (permissive hypercapnia)
- Consider prone positioning for severe ARDS
- Avoid aggressive fluid resuscitation
4. Recruitment Maneuvers
Controversial but potentially beneficial:
- Sustained inflation (30-40 cm H₂O for 30-40 seconds)
- Stepwise PEEP increments
- Prone positioning for refractory hypoxemia
Evidence: Limited data specific to donors, but recruitment maneuvers improved oxygenation in observational studies without clear harm. Use judiciously in hemodynamically stable donors with recruitable atelectasis.
5. Fraction of Inspired Oxygen (FiO₂) Management
Target: Lowest FiO₂ to maintain SpO₂ 92-95%, PaO₂ 80-100 mmHg
Rationale:
- Oxygen toxicity contributes to lung injury
- High FiO₂ promotes absorption atelectasis
- Hyperoxia may worsen reperfusion injury post-transplant
Pearl: The "P/F ratio rule of 300"—lungs are typically suitable for transplantation if PaO₂/FiO₂ ratio >300 mmHg on FiO₂ 1.0 and PEEP 5 cm H₂O. However, this must be assessed after optimization of ventilation strategy, fluid balance, and hemodynamics.
Practical Ventilator Settings Protocol
Initial Settings:
- Mode: Volume control or pressure-regulated volume control
- Tidal volume: 6-8 mL/kg IBW
- Respiratory rate: 10-16 breaths/min (adjust for pH >7.25, PaCO₂ <60 mmHg)
- PEEP: 8-10 cm H₂O
- FiO₂: Titrate to SpO₂ 92-95%
- Inspiratory flow: 60 L/min (adjust for I:E ratio ~1:2)
Monitoring:
- Arterial blood gas every 4 hours
- Plateau pressure with every ABG
- Dynamic compliance trending
- Chest X-ray daily (or more frequently if concerns)
Adjustments:
- If Pplat >30: Reduce VT, increase RR if needed for pH
- If severe hypoxemia (P/F <200): Consider recruitment, prone positioning, higher PEEP
- If hypercapnia with acidosis (pH <7.20): Increase RR (but maintain low VT priority)
Adjunctive Strategies for Lung Protection
1. Conservative Fluid Management
Goal: Zero or negative fluid balance after initial resuscitation
- Extravascular lung water increases by 30-50% post-brain death
- Aggressive diuresis (furosemide) after hemodynamic stabilization
- Target CVP 4-6 mmHg (lower than typical ICU targets)
2. Airway Management
- Maintain ETT cuff pressure 20-25 cm H₂O (prevents aspiration, minimizes tracheal injury)
- Frequent suctioning with sterile technique
- Elevate head of bed 30-45°
- Oral care every 4 hours
3. Bronchoscopy
Consider for:
- Significant secretions or atelectasis
- Aspiration suspected
- Assessment before lung procurement
4. Antimicrobial Therapy
- Early broad-spectrum antibiotics if aspiration or pneumonia suspected
- Directed therapy based on cultures
- Balance infection control with antibiotic stewardship
Hack: The "60-minute recruitment protocol" for marginal lungs: aggressive bronchoscopy, recruitment maneuvers, diuresis, and prone positioning performed sequentially over 60 minutes before declaring lungs unsuitable. This salvages 15-20% of lungs initially thought non-viable.
Goal-Directed Fluid and Hemodynamic Management: Using Advanced Monitoring
The Hemodynamic Dilemma
Donor management requires balancing competing priorities:
- Adequate perfusion of all organs to prevent ischemic injury
- Minimal fluid administration to prevent pulmonary edema and cardiac distension
- Optimization of each organ system which may have conflicting requirements
This challenge is compounded by:
- Loss of normal compensatory mechanisms
- Unreliable clinical examination (absent brainstem reflexes)
- Rapidly changing physiology
- Need to optimize multiple organs simultaneously
Advanced Hemodynamic Monitoring
Traditional Monitoring Limitations:
- Central venous pressure (CVP): Poor predictor of fluid responsiveness, influenced by PEEP, cardiac function
- Pulmonary artery catheter: Infrequently used, interpretation complicated by changing vascular compliance
- Urine output: Misleading in diabetes insipidus (may be high despite hypovolemia)
Advanced Monitoring Modalities:
1. Transthoracic/Transesophageal Echocardiography
Indications:
- All potential cardiac donors (mandatory)
- Hemodynamically unstable donors
- Suspected cardiac dysfunction
- Guiding fluid management
Assessment Parameters:
- Left ventricular ejection fraction and wall motion
- Right ventricular function
- Valvular function
- Volume status (IVC collapsibility, LV end-diastolic area)
- Cardiac output estimation
Pearl: Serial echocardiography (every 6-8 hours) in cardiac donors documents recovery from catecholamine-induced stunning. An initially reduced EF (35-45%) may improve to >50% within 24 hours with hormonal resuscitation, making the heart suitable for transplantation.
2. Pulse Contour Cardiac Output Monitoring
Systems: FloTrac/Vigileo, LiDCO, PiCCO
Advantages:
- Continuous cardiac output monitoring
- Stroke volume variation (SVV) and pulse pressure variation (PPV) for fluid responsiveness
- Less invasive than PA catheter
Targets:
- Cardiac index: 2.4-4.0 L/min/m²
- SVV or PPV: <13% suggests fluid responsiveness
- Systemic vascular resistance: 800-1200 dynes·sec·cm⁻⁵
Hack: The "SVV-guided fluid challenge" protocol: If SVV >13% and donor hypotensive, give 250 mL crystalloid bolus. Reassess SVV after 10 minutes. If SVV decreases and hemodynamics improve, repeat. If SVV unchanged or hemodynamics don't improve, stop fluids and consider vasopressors. This prevents both under-resuscitation and fluid overload.
3. End-Tidal CO₂ Monitoring
Often underutilized but valuable:
- Sudden decrease: Suggests reduced cardiac output, PE, circuit disconnection
- Gradual increase: May indicate hypercapnia, increased dead space
- Trending more useful than absolute values
Goal-Directed Therapy Protocol
Phase 1: Initial Resuscitation (First 4-6 hours)
Goals:
- MAP 60-70 mmHg
- Cardiac index >2.5 L/min/m²
- ScvO₂ or SvO₂ >70%
- Lactate clearance >10%/hour
- Urine output >1 mL/kg/hr (if not in DI)
Approach:
- Volume resuscitation with crystalloids (target CVP 6-8 mmHg initially)
- Early vasopressin (1 unit/hour)
- Norepinephrine if needed (target <0.1 mcg/kg/min)
- Initiate hormonal therapy immediately
Phase 2: Optimization (6-24 hours)
Goals:
- Achieve euvolemia (zero or negative fluid balance)
- Minimize vasopressor support
- Optimize organ-specific parameters
- Maintain normothermia
Approach:
- Transition from volume loading to maintenance fluids
- Aggressive diuresis if lungs being considered (target CVP 4-6 mmHg)
- Fine-tune hormonal support
- Implement lung-protective ventilation
- Correct metabolic derangements
Oyster: The "one-size-fits-all" approach fails in donor management. A cardiac donor may require higher filling pressures and cardiac output, while a lung donor benefits from aggressive diuresis and lower CVP. Prioritize organs based on recipient need and organ quality assessment.
Fluid Selection
Crystalloids vs Colloids:
Crystalloids (Preferred):
- Balanced crystalloids (Lactated Ringer's, Plasma-Lyte) preferred over normal saline
- Avoid hyperchloremic acidosis from excessive NS
- Lower cost, readily available
Colloids:
- 5% albumin may be considered for refractory hypotension with low oncotic pressure
- Synthetic colloids (HES, dextrans) generally avoided due to concerns about kidney injury
Blood Products:
- Target hemoglobin 7-9 g/dL (transfusion threshold lower than typical ICU)
- Higher thresholds for cardiac donors or active ischemia
- FFP/platelets only if coagulopathy with active bleeding
Pearl: The "restrictive transfusion strategy" in donors improves outcomes. Higher hemoglobin doesn't improve oxygen delivery in the absence of metabolic demand, and transfusions increase inflammation and allosensitization risk for recipients.
Organ-Specific Hemodynamic Targets
For Cardiac Donors:
- Higher cardiac output acceptable (CI 2.8-4.0 L/min/m²)
- Maintain adequate coronary perfusion (MAP 65-70 mmHg)
- Avoid excessive preload (maintain CVP <10 mmHg)
For Lung Donors:
- Restrictive fluid strategy (target CVP 4-6 mmHg)
- Negative fluid balance preferred
- MAP 60-65 mmHg acceptable if organs well-perfused
For Abdominal Organ Donors:
- Balance perfusion with avoiding congestion
- MAP 65-70 mmHg
- CVP 6-8 mmHg
- Maintain renal perfusion (UOP >0.5 mL/kg/hr)
Hack: Use point-of-care lactate measurements every 2 hours during optimization. Falling lactate indicates adequate perfusion regardless of other parameters. Rising lactate (or failure to clear) should prompt reassessment of volume status, cardiac output, and vasopressor requirement—not simply increasing vasopressors.
Diagnostic and Monitoring Challenges: Interpreting Labs and Vitals in a Body Without Cerebral Function
The Paradigm Shift in Monitoring
The brain-dead donor presents unique interpretative challenges:
- Absent cerebral autoregulation and metabolic demand
- Disrupted neuroendocrine feedback loops
- Loss of compensatory mechanisms
- Traditional clinical signs unreliable
- Laboratory values may not reflect true organ function
Laboratory Monitoring and Interpretation
1. Arterial Blood Gas Analysis
Unique Considerations:
- pH and PaCO₂: Permissive hypercapnia acceptable (pH >7.25)
- PaO₂: Target 80-100 mmHg, not supranormal values
- Base deficit: May reflect inadequate perfusion, guide resuscitation
- Lactate: Most reliable marker of global perfusion
Oyster: Respiratory alkalosis or hypocapnia is not beneficial and may be harmful (reduces cerebral blood flow in transplanted organs with intact autoregulation post-transplant, shifts oxygen-hemoglobin dissociation curve).
2. Electrolyte Management
Sodium:
- Hypernatremia universal (diabetes insipidus)
- Target 135-150 mEq/L
- Rapid correction risks organ injury
- Free water deficit calculation: 0.6 × body weight (kg) × [(Na⁺/140) - 1]
- Replace deficit over 12-24 hours with D5W or hypotonic saline
Pearl: The "145 rule"—maintain serum sodium <145 mEq/L during donor management. Higher levels associated with reduced kidney graft survival, likely reflecting prolonged tubular injury.
Potassium:
- Aggressive repletion needed (K⁺ losses from diuresis)
- Target 4.0-5.0 mEq/L
- Hypokalemia increases arrhythmia risk
Calcium:
- Ionized calcium: 1.0-1.2 mmol/L
- Critical for cardiac contractility
- Supplement aggressively if low
Magnesium:
- Target 2.0-2.5 mg/dL
- Prevents arrhythmias
- Potentiates calcium effects on cardiac function
3. Glucose Management
Target: 120-180 mg/dL (moderate control)
Rationale:
- Hyperglycemia (>180 mg/dL) associated with impaired graft function
- Hypoglycemia (not detected clinically) causes cellular injury
- Insulin has anti-inflammatory effects
Protocol:
- Continuous insulin infusion for glucose >180 mg/dL
- Check glucose every 1-2 hours until stable
4. Hemoglobin and Hematocrit
Target: Hemoglobin 7-9 g/dL (restrictive strategy)
Rationale:
- No cerebral oxygen demand requiring higher levels
- Lower viscosity may improve microcirculatory flow
- Reduces transfusion-related complications
- Exception: Cardiac donors may benefit from 9-10 g/dL
5. Coagulation Parameters
Monitoring:
- PT/INR, aPTT every 6-12 hours
- Fibrinogen, D-dimer if concerned about DIC
- Platelet count
Management:
- Correct coagulopathy only if bleeding or before procurement
- Vitamin K 10 mg IV for elevated INR
- Cryoprecipitate if fibrinogen <150 mg/dL
- Platelet transfusion if <50,000 and bleeding
Pearl: Mild coagulopathy (INR 1.5-2.0) without bleeding does not require correction. Over-aggressive correction increases thrombotic risk in organs and recipient.
6. Liver Function Tests
Interpretation Challenges:
- Transaminase elevation common (hepatic ischemia, shock liver
, congestion)
- ALT/AST: May rise 2-5× above normal during resuscitation
- Bilirubin: Less affected acutely, more important for liver donor assessment
- Alkaline phosphatase: Rises slowly, less useful for acute assessment
Clinical Approach:
- Trending more important than absolute values
- Declining transaminases suggest improving perfusion
- Rising transaminases (>1000 IU/L) may indicate ongoing ischemia
- Lactate clearance better reflects hepatic function than isolated enzyme levels
Hack: The "transaminase trajectory rule"—if ALT/AST are rising at 6-hour intervals despite optimization, increase MAP target by 5 mmHg and reassess. Hepatic perfusion pressure (MAP - CVP) should be >60 mmHg for optimal liver perfusion.
7. Renal Function Assessment
Challenges:
- Diabetes insipidus produces misleading urine output
- Creatinine reflects baseline function, not acute changes
- Acute kidney injury common (50% of donors)
Monitoring Strategy:
- Hourly urine output (but interpret cautiously)
- Serum creatinine every 12 hours
- Calculate eGFR for baseline assessment
- Urine electrolytes (FENa) if oliguria develops
- Consider bladder pressure monitoring if abdominal compartment syndrome suspected
Management of Oliguria (UOP <0.5 mL/kg/hr):
- Assess volume status (echo, CVP, dynamic indices)
- Optimize MAP (target 65-70 mmHg)
- Trial of furosemide if volume replete (1 mg/kg)
- Consider dopamine 2-3 mcg/kg/min (controversial, limited evidence)
- Avoid nephrotoxins (contrast, aminoglycosides unless essential)
Oyster: High urine output (>200 mL/hour) does not guarantee adequate renal perfusion—it may simply reflect untreated diabetes insipidus. Always correlate with sodium levels, serum osmolality, and urine-specific gravity.
8. Cardiac Biomarkers
Troponin:
- Elevated in 80-90% of donors (catecholamine storm)
- Level does not predict cardiac graft function
- Serial measurements more useful (trending downward = recovery)
- Troponin >10 ng/mL may warrant echocardiographic assessment
BNP/NT-proBNP:
- Limited utility in acute donor management
- May reflect volume overload or cardiac dysfunction
- Not routinely measured in most protocols
Pearl: Elevated troponin with normal or improving echocardiographic function does not preclude cardiac donation. Many "stunned" hearts recover excellent function within 24-48 hours. The key is demonstrating functional recovery, not biomarker normalization.
Hemodynamic Monitoring Interpretation
1. Blood Pressure Measurement
Challenges:
- Loss of cerebral autoregulation means traditional BP targets may not apply
- Peripheral vasoplegia may cause wide pulse pressure
- Invasive arterial monitoring essential (radial or femoral)
Targets (Revisited):
- MAP 60-70 mmHg (organ-specific adjustment as noted)
- Systolic BP 90-120 mmHg
- Avoid extreme hypotension (MAP <55 mmHg for >10 min associated with worse outcomes)
- Avoid excessive hypertension (increases cardiac work, may worsen pulmonary edema)
Hack: The "differential MAP strategy"—use slightly higher MAP targets (65-70 mmHg) during initial resuscitation and organ assessment, then liberalize to 60-65 mmHg once stability achieved and lung-protective strategy prioritized. This maximizes organ assessment quality while minimizing lung injury.
2. Heart Rate Interpretation
Denervation Effects:
- Loss of vagal tone → relative tachycardia common (90-110 bpm)
- Loss of baroreceptor reflexes → absent compensatory tachycardia with hypotension
- Atropine ineffective (no vagal tone to block)
- Beta-blockers still effective (direct myocardial action)
Management:
- Persistent tachycardia >110 bpm: rule out hypovolemia, pain (yes, spinal reflexes remain), hypoxia, metabolic derangement
- Esmolol for HR >120 bpm if hemodynamically stable
- Amiodarone for atrial fibrillation (common post-catecholamine storm)
Oyster: Bradycardia (<60 bpm) in brain-dead donors is concerning and unusual. Consider:
- Hypothermia (most common cause)
- High-dose vasopressin (can cause bradycardia via V1a receptors)
- Electrolyte abnormalities (hyperkalemia, hypocalcemia)
- Beta-blocker effect (if given during hypertensive phase)
- Cardiac ischemia
3. Temperature Management
The Universal Problem:
- Hypothermia universal (loss of hypothalamic thermoregulation)
- Temperature drifts to ambient (core temp may fall to 32-35°C)
- Each 1°C drop reduces metabolic rate by ~7%
- Coagulopathy worsens below 35°C
- Cardiac irritability increases below 32°C
Target: Core temperature 36-37°C
Strategies:
- Forced-air warming blankets (Bair Hugger)
- Warmed IV fluids (all fluids through warmer)
- Increase ambient room temperature (24-26°C)
- Heated humidified ventilator circuits
- Warming mattresses
- Warmed bladder/gastric irrigation if severe
Pearl: Active rewarming takes time—start early and aggressively. It may take 4-6 hours to rewarm a donor from 34°C to 36°C despite maximal efforts. Cold organs are dysfunctional organs; prioritize normothermia from the moment of brain death declaration.
4. Urine Output Pitfalls
The Diabetes Insipidus Conundrum:
- Massive polyuria (5-10 L/day) common
- High UOP does not indicate adequate resuscitation
- Oliguria may indicate undertreated DI (paradoxically hypovolemic despite low UOP)
Diagnostic Approach:
- Measure urine specific gravity (<1.005 suggests DI)
- Check urine osmolality (<200 mOsm/kg confirms DI)
- Serum sodium trend (rising Na confirms DI)
- Assess volume status independently of UOP
Management Algorithm:
- Polyuria + rising Na = DI → DDAVP 1-4 mcg IV
- Polyuria + normal Na = Adequate replacement → continue monitoring
- Oliguria + high Na + low UOP specific gravity = Severe DI with hypovolemia → aggressive fluid resuscitation + DDAVP
- Oliguria + normal Na + high UOP specific gravity = Inadequate perfusion → optimize hemodynamics
Neuromonitoring and Brainstem Function
Key Point: After brain death declaration, neuromonitoring is discontinued. However, be aware:
Spinal Reflexes Persist:
- Deep tendon reflexes may be present
- Spontaneous movements can occur (Lazarus sign)
- Triple flexion response to painful stimuli
- These do NOT indicate retained brain function
- Staff and family education essential
Implications for Management:
- Continue sedation/analgesia for OR (prevents spinal reflexes during procurement)
- No paralysis needed for declaration, but often continued for ventilator synchrony
- Monitor for seizure-like movements (rare, but spinal myoclonus possible)
Oyster: Family members may witness reflexive movements and question brain death. Proactive education by the OPO (Organ Procurement Organization) coordinator is essential. These movements do not change the diagnosis or prognosis.
Advanced Monitoring Pitfalls
1. Central Venous Pressure
Problems:
- Poor predictor of volume responsiveness (only 50% accurate)
- Affected by PEEP, chest wall compliance, venous tone
- Target varies by organ type (lungs vs cardiac vs abdominal)
Better Approach:
- Use as trending parameter, not absolute target
- Combine with dynamic indices (SVV, PPV)
- Integrate with echocardiographic assessment
2. Mixed Venous Oxygen Saturation
Interpretation in Brain Death:
- Absence of cerebral oxygen consumption increases SvO₂
- Normal SvO₂ >70% may not indicate adequate DO₂
- Low SvO₂ (<65%) definitely indicates inadequate DO₂
- High SvO₂ (>80%) may indicate:
- Adequate oxygen delivery (good)
- Distributive shock with impaired oxygen extraction (concerning)
- Left-to-right shunting (rare)
Clinical Use: More useful for detecting inadequate DO₂ than confirming adequate resuscitation.
3. Lactate and Base Deficit
Gold Standards for Global Perfusion:
- Lactate: Most reliable single marker
- Target: <2.0 mmol/L, but <3.0 acceptable if clearing
- Clearance rate >10%/hour indicates adequate resuscitation
- Persistent elevation (>4.0 mmol/L) poor prognostic sign
Base Deficit:
- Target: > -4 mEq/L
- Correlates with mortality risk in trauma, likely applicable to donors
- Reflects global tissue perfusion and oxygen debt
Pearl: Lactate clearance is more important than absolute value. A lactate of 3.5 mmol/L that was 6.0 mmol/L two hours ago indicates improving perfusion. A stable lactate of 2.5 mmol/L suggests marginal perfusion adequacy.
Special Situations and Troubleshooting
The Refractory Hypotensive Donor
Definition: MAP <60 mmHg despite:
- Adequate volume resuscitation (CVP 6-10 mmHg)
- Vasopressin 1-2 units/hour
- Norepinephrine >0.2 mcg/kg/min
- Complete hormonal resuscitation protocol
Stepwise Approach:
1. Reassess Volume Status:
- Perform bedside echo (IVC diameter, LV end-diastolic area)
- Check SVV/PPV if available
- Trial fluid bolus (250-500 mL) with reassessment
2. Review Hormonal Therapy:
- Is T₃/T₄ infusing correctly? (Check IV access patency)
- Has adequate time elapsed for effect? (4-6 hours for T₃)
- Consider increasing T₃ dose to 4 mcg/hour
- Redose methylprednisolone (may repeat 15 mg/kg once)
3. Increase Vasopressin:
- Titrate to 2.4 units/hour (maximum recommended)
- Monitor for excessive vasoconstriction (mesenteric, digital ischemia)
4. Add Second Vasopressor:
- Norepinephrine + vasopressin synergistic
- Consider phenylephrine if predominantly distributive (rare to need)
- Avoid epinephrine (increases myocardial oxygen demand, arrhythmogenic)
5. Assess for Reversible Causes:
- Cardiac dysfunction: Echo to assess EF, valvular function
- If reduced EF (<40%): Dobutamine 2.5-5 mcg/kg/min
- If severe: Consider epinephrine 0.01-0.05 mcg/kg/min
- Tamponade: Rare but assess for pericardial effusion on echo
- Tension pneumothorax: Particularly after central line placement
- Massive pulmonary embolism: Sudden cardiovascular collapse, consider thrombolysis
- Adrenal crisis: Although steroids given, consider hydrocortisone supplementation
- Thyroid storm (paradoxical): Rare, but catecholamine storm can present similarly
6. Consider Cardiac Support:
- Inotropic agents: Dobutamine, milrinone (if phosphodiesterase inhibitor not contraindicated)
- Mechanical support: Rarely, ECMO considered for cardiac donors with reversible dysfunction
Hack: The "quad therapy protocol" for refractory shock:
- Vasopressin 2 units/hour
- Norepinephrine 0.1-0.15 mcg/kg/min
- T₃ 4 mcg/hour
- Hydrocortisone 100 mg IV q8h (in addition to initial methylprednisolone)
This aggressive approach salvages 60-70% of "refractory" donors when implemented early.
The Severely Hypothermic Donor
Problem: Core temperature <34°C with refractory hemodynamic instability
Physiology:
- Cardiac irritability (arrhythmias common)
- Coagulopathy (platelet dysfunction, clotting cascade impairment)
- Left-shifted oxygen-hemoglobin dissociation curve
- Reduced drug metabolism
- Insulin resistance
Management:
- Aggressive active rewarming (all modalities simultaneously)
- Correct coagulopathy (warm FFP, platelet transfusion if needed)
- Anticipate arrhythmias (have defibrillator ready, magnesium supplementation)
- Adjust drug dosing (may need higher vasopressor doses that can be weaned during rewarming)
- Delay procurement if possible until core temp >35°C
Pearl: Don't declare a donor "unsuitable" due to hemodynamic instability until normothermia achieved. Profound hypothermia causes reversible cardiac dysfunction that resolves with warming.
The Polytraumatic Donor
Challenges:
- Hemorrhagic shock complicating brain death physiology
- Abdominal compartment syndrome
- Fat embolism
- Coagulopathy (trauma-induced plus hypothermia)
Key Management Points:
- Damage control resuscitation principles apply during stabilization
- Balanced transfusion (1:1:1 ratio RBC:FFP:platelets if massive transfusion)
- Bladder pressure monitoring (decompress if >20 mmHg)
- Early definitive hemorrhage control (surgical or IR embolization)
- Reassess organ viability after stabilization (traumatized organs may not be suitable)
Acute Complications During Donor Management
1. Cardiac Arrest
Approach:
- Begin ACLS immediately (chest compressions, defibrillation as indicated)
- Most arrests are PEA/asystole (profound vasodilatory shock)
- Epinephrine may be needed (despite general avoidance)
- Notify OPO immediately (decision regarding continued resuscitation)
- Consider DCD (donation after circulatory death) if resuscitation unsuccessful
Pearl: Brief cardiac arrest (<5 minutes with ROSC) does not necessarily preclude organ donation. Lactate and organ function assessment after stabilization guide decision-making.
2. Arrhythmias
Common Arrhythmias:
- Atrial fibrillation (most common, from catecholamine storm)
- Ventricular tachycardia (catecholamine toxicity, electrolyte abnormalities)
- Bradycardia (hypothermia, excessive vasopressin)
Management:
- Atrial fibrillation:
- Amiodarone 150 mg IV over 10 min, then infusion
- Rate control with esmolol if RVR
- Anticoagulation NOT indicated
- Ventricular arrhythmias:
- Correct electrolytes (K⁺, Mg²⁺, Ca²⁺)
- Amiodarone
- Lidocaine second-line
- Defibrillation for unstable VT or VF
- Bradycardia:
- Rewarm if hypothermic
- Reduce vasopressin if >2 units/hour
- Pacing rarely needed (but available)
3. Ventilator Dyssynchrony
Causes:
- Pain response (spinal reflexes)
- Agitation (inadequate sedation)
- Auto-PEEP (dynamic hyperinflation)
- ETT malposition or obstruction
Management:
- Increase sedation (propofol or benzodiazepines)
- Consider neuromuscular blockade (vecuronium, rocuronium)
- Check ETT position, suction secretions
- Adjust ventilator settings (reduce RR, increase expiratory time if auto-PEEP)
Emerging Concepts and Future Directions
Normothermic Regional Perfusion (NRP)
Concept: Ex situ perfusion of abdominal organs after circulatory death with oxygenated blood, bridging gap between DCD and DBD (donation after brain death) quality.
Technique:
- ECMO circuit providing perfusion below diaphragm
- Clamp aorta above celiac to prevent brain reperfusion
- Allows assessment and optimization before organ recovery
Evidence: Improved kidney and liver graft function in DCD donors. Not applicable to standard DBD donors but represents evolution of donation paradigm.
Machine Perfusion
Ex Vivo Perfusion:
- Kidneys, livers, lungs, hearts can be perfused on machines
- Allows assessment, treatment, and optimization outside body
- May extend preservation time and improve marginal organs
Implication for ICU Management: Potentially allows for more marginal organs to be recovered, with optimization occurring ex vivo. May reduce pressure for perfect ICU optimization.
Biomarkers for Organ Quality
Emerging Markers:
- Cell-free DNA (organ injury marker)
- Micro-RNAs (organ-specific quality indicators)
- Metabolomics (assessment of cellular energetics)
Future Application: Real-time assessment of organ suitability during ICU management, guiding individualized optimization strategies.
Targeted Temperature Management
Concept: Mild therapeutic hypothermia (33-35°C) for neuroprotection translates to organ protection?
Rationale: Reduced metabolic demand, decreased inflammatory response
Current Status: Limited evidence, not standard practice. Most protocols still target normothermia.
Practical Pearls and Clinical Wisdom
Ten Commandments of Donor Management
- Start hormonal therapy early – Don't wait for instability; initiate at brain death declaration
- Protect the lungs religiously – They are most fragile; lung-protective ventilation is non-negotiable
- Think "low and slow" – Lower tidal volumes, lower blood pressures than traditional ICU targets
- Warm the donor aggressively – Hypothermia kills organs; normothermia should be first priority
- Follow the lactate – It's your most reliable guide to resuscitation adequacy
- Less fluid is more – After initial resuscitation, conservative strategy benefits all organs
- Vasopressin first – It replaces deficiency rather than adding catecholamines
- Echo frequently – Serial imaging guides therapy better than any single monitoring modality
- Individualize organ-specific strategies – Cardiac donors need different management than lung donors
- Communicate constantly – With OPO, surgeons, recipient teams; coordination is everything
Common Mistakes to Avoid
Oyster Collection:
- Over-aggressive fluid resuscitation – "More is better" doesn't apply; causes pulmonary edema
- Chasing normal PaCO₂ – Unnecessary ventilation strategy that injures lungs
- Delaying hormonal therapy – Waiting for labs or instability; should be prophylactic
- Using dopamine for pressure support – Causes more arrhythmias without benefit
- Ignoring hypothermia – Accepting temperatures <36°C; all organs function poorly when cold
- High-dose single vasopressor – Using norepinephrine >0.2 mcg/kg/min before optimizing other factors
- Interpreting UOP without context – Diabetes insipidus makes UOP unreliable
- Abandoning donors prematurely – Many "unstable" donors can be salvaged with proper management
- Forgetting sedation/analgesia – Spinal reflexes persist; comfort care continues
- Poor communication with OPO – They are partners in optimization, not adversaries
Quick Reference Protocol
Initial Orders at Brain Death Declaration:
1. HORMONAL RESUSCITATION:
- Vasopressin 1 unit/hour IV continuous
- Methylprednisolone 15 mg/kg IV × 1 (max 1000 mg)
- T₃: 4 mcg IV bolus, then 3 mcg/hour continuous
(or T₄: 20 mcg IV bolus, then 10 mcg/hour)
2. VENTILATOR SETTINGS:
- Tidal volume: 6-8 mL/kg IBW
- PEEP: 8-10 cm H₂O
- FiO₂: Titrate to SpO₂ 92-95%
- RR: Adjust for pH >7.25
- Plateau pressure: Check q4h, keep <30 cm H₂O
3. HEMODYNAMIC TARGETS:
- MAP 60-70 mmHg
- Norepinephrine if needed (goal <0.1 mcg/kg/min)
- CVP 6-8 mmHg initially, then 4-6 mmHg after stabilization
4. MONITORING:
- Arterial line (if not already present)
- Temperature monitoring (continuous)
- Glucose checks q1-2h
- ABG q4h
- Comprehensive metabolic panel q6h
- Lactate q2h until <2.0 mmol/L
5. SUPPORTIVE CARE:
- Active warming (forced air, warmed fluids, room temp 24-26°C)
- Sedation: Propofol or midazolam (comfort, prevent reflexes)
- DVT prophylaxis: SCD (continue anticoagulation only if already on)
- Stress ulcer prophylaxis: PPI or H2-blocker
- Glycemic control: Insulin for glucose >180 mg/dL
6. LABS:
- Troponin (if cardiac donor)
- Repeat sodium q2-4h (if DI suspected)
- Blood cultures (if febrile or infection suspected)
- Urine specific gravity/osmolality (if polyuria)
7. CONSULTATIONS:
- Notify OPO immediately
- Social work/chaplain for family support
- Ophthalmology (if corneal donation)
- Tissue bank (if tissue donation)
Conclusion
The management of the deceased organ donor represents a unique intersection of critical care medicine, transplant science, and end-of-life care. Success requires a sophisticated understanding of the pathophysiology of brain death, meticulous attention to physiological details, and the ability to simultaneously optimize multiple organ systems with sometimes competing requirements.
The intensivist caring for organ donors must undergo a fundamental shift in therapeutic mindset—from patient-centered care to organ-centered care, from cure to preservation, from prolonging life to enabling life for others. This transition is both technically demanding and emotionally complex, requiring clinical excellence and compassionate communication with grieving families.
Evidence-based protocols incorporating early hormonal resuscitation, lung-protective ventilation strategies, goal-directed hemodynamic optimization, and careful attention to metabolic and endocrine derangements can dramatically improve both the quantity and quality of transplantable organs. Each intervention, from vasopressin infusion to tidal volume selection, should be understood not merely as a protocol step but as a physiologically-driven strategy to counteract the specific pathophysiology of brain death.
As the field evolves with machine perfusion technologies, advanced monitoring modalities, and emerging biomarkers, the principles outlined in this review will remain foundational. The intensivist's role as guardian of organs continues to be essential in addressing the critical shortage of transplantable organs and providing hope to thousands of patients awaiting life-saving transplantation.
In the end, optimal donor management represents one of critical care's highest callings: transforming tragedy into hope, death into life, and ensuring that one person's final act becomes another's second chance.
References
-
Wood KE, Becker BN, McCartney JG, et al. Care of the potential organ donor. N Engl J Med. 2004;351(26):2730-2739.
-
Mascia L, Pasero D, Slutsky AS, et al. Effect of a lung protective strategy for organ donors on eligibility and availability of lungs for transplantation: a randomized controlled trial. JAMA. 2010;304(23):2620-2627.
-
Pennefather SH, Bullock RE, Dark JH. The effect of fluid therapy on alveolar arterial oxygen gradient in brain-dead organ donors. Transplantation. 1993;56(6):1418-1422.
-
Rosendale JD, Kauffman HM, McBride MA, et al. Hormonal resuscitation yields more transplanted hearts, with improved early function. Transplantation. 2003;75(8):1336-1341.
-
Zaroff JG, Rosengard BR, Armstrong WF, et al. Consensus conference report: maximizing use of organs recovered from the cadaver donor: cardiac recommendations. Circulation. 2002;106(7):836-841.
-
Novitzky D, Cooper DK, Rosendale JD, Kauffman HM. Hormonal therapy of the brain-dead organ donor: experimental and clinical studies. Transplantation. 2006;82(11):1396-1401.
-
Venkateswaran RV, Steeds RP, Quinn DW, et al. The haemodynamic effects of adjunctive hormone therapy in potential heart donors: a prospective randomized double-blind factorially designed controlled trial. Eur Heart J. 2009;30(14):1771-1780.
-
Schnuelle P, Lorenz D, Mueller A, et al. Donor catecholamine use reduces acute allograft rejection and improves graft survival after cadaveric renal transplantation. Kidney Int. 1999;56(2):738-746.
-
Mascia L, Solidoro P, Boschi S, et al. Protective ventilation improves donor lung procurement: results of the RObust study of Protective Ventilation (PROPVE). J Heart Lung Transplant. 2013;32(4):S100-S101.
-
Kutsogiannis DJ, Pagliarello G, Doig C, et al. Medical management to optimize donor organ potential: review of the literature. Can J Anaesth. 2006;53(8):820-830.
-
McKeown DW, Bonser RS, Kellum JA. Management of the heartbeating brain-dead organ donor. Br J Anaesth. 2012;108(suppl 1):i96-i107.
-
Salim A, Velmahos GC, Brown C, et al. Aggressive organ donor management significantly increases the number of organs available for transplantation. J Trauma. 2005;58(5):991-994.
-
Dictus C, Vienenkoetter B, Esmaeilzadeh M, et al. Critical care management of potential organ donors: our current standard. Clin Transplant. 2009;23(Suppl 21):2-9.
-
Dupuis S, Amiel JA, Desgroseilliers M, et al. Corticosteroids in the management of brain-dead potential organ donors: a systematic review. Br J Anaesth. 2014;113(3):346-359.
-
Angel LF, Levine DJ, Restrepo MI, et al. Impact of a lung transplantation donor-management protocol on lung donation and recipient outcomes. Am J Respir Crit Care Med. 2006;174(6):710-716.
-
Pinsard M, Ragot S, Mertes PM, et al. Interest of low-dose hydrocortisone therapy during brain-dead organ donor resuscitation: the CORTICOME study. Crit Care. 2014;18(4):R158.
-
Kotloff RM, Blosser S, Fulda GJ, et al. Management of the potential organ donor in the ICU: Society of Critical Care Medicine/American College of Chest Physicians/Association of Organ Procurement Organizations Consensus Statement. Crit Care Med. 2015;43(6):1291-1325.
-
Tuttle-Newhall JE, Collins BH, Kuo PC, Schoeder R. Organ donation and treatment of the multi-organ donor. Curr Probl Surg. 2003;40(5):266-310.
-
Totsuka E, Dodson F, Urakami A, et al. Influence of high donor serum sodium levels on early postoperative graft function in human liver transplantation. Liver Transpl Surg. 1999;5(5):421-428.
-
Amatschek S, Wilflingseder J, Pones M, et al. The effect of steroid pretreatment of deceased organ donors on liver allograft function: a blinded randomized placebo-controlled trial. J Hepatol. 2012;56(6):1305-1309.
Disclosure Statement: The author has no conflicts of interest to declare.
Acknowledgments: The author acknowledges the organ procurement organizations, transplant coordinators, and critical care teams whose dedication to donor management makes transplantation possible, and honors the donors and their families whose generosity gives the gift of life.
