Organ donation


Organ harvest

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Related conditions

Brain death

Non-beating-heart donor

1. Description of the problem

Management of the organ donor can often be challenging as it requires in-depth knowledge of the pathophysiologic effects of brain death and knowledge about attenuating these responses to maximize donor physiology for preservation of potential organ viability.

Clinical features

Cardiovascular collapse

Hypothalamic-hypophyseal axis dysfunction

Cardiac, pulmonary, renal, and hepatic dysfunction and preservation

Key management points

Preserve organ (heart, liver, kidney) perfusion and oxygenation

Preservation of pulmonary mechanics and alveoli for potential transplantation

Diabetes insipidus

Treatment of infections

Screening for viral infection, viability of organs, blood matching, etc.

Hyperglycemia due to insulin resistance

Adrenal insufficiency secondary to stress cortisol response from primary brain injury

2. Emergency Management

Ensure declaration of brain death and potential donor status.

Standard monitoring of clinical signs and symptoms of adequate organ perfusion.

Continued optimal intensive care therapy and management.

Maintain mean arterial pressure >70 mmHg.

Maintain urine output >0.5 and <3 ml/kg/hr.

Maintain normovolemia with central venous pressure between 8 and 12 mmHg.

Maintain central venous oxygen saturation (ScvO2) >70%.

Monitor for and aggressively treat diabetes insipidus and hyperglycemia.

Consider antibiotics for possible or documented infections.

Correct extremely aberrant electrolyte abnormalities.

Transfuse packed red blood cells for a hemoglobin <7 to 8 gm/dl.

Maintain heart rate between 60 and 120 beats/min.

Consider pulmonary artery catheter for fluid management, especially with depressed ejection fraction, to maintain pulmonary capillary wedge pressure between 8 and 12 mm Hg, cardiac index >2 l/min*m2, and systemic vascular resistance between 800 and 1200 dynes/s/cm.

When able, institute lung protective strategies for possible procurement with arterial partial pressure of oxygen >80 mmHg, lowest tolerated inhaled fraction of oxygen and positive end expiratory pressure, tidal volumes between 5 and 7 ml/kg and adequate minute ventilation to maintain normocapnea, and peak airway pressures <30 mm Hg.

Management points not to be missed

Continue full intensive care therapy and management (nutrition, nursing, hygiene, etc.).

Has brain death been declared?

Is the patient a potential organ donor?

Is the mean arterial pressure >70 mmHg?

Has normovolemia been achieved?

Are there any signs of diabetes insipidus?

Are any infections being treated?

Can any electrolyte abnormalities be corrected?

Are the ventilator settings maximized for lung protection?

3. Diagnosis

A. Cardiovascular compromise

Brain death leads to loss of vasomotor CNS centers with subsequent loss of sympathetic tone and results in multifactorial cardiac dysfunction.

Diagnostic criteria include:

Mean arterial pressure <60 mmHg

Systemic vascular resistance <600 dynes/s/cm

Cardiac index <2 l/min*m2

Central venous oxygen saturation (ScvO2) <60%

Hypovolemia with central venous pressure <6 mmHg and urine output <0.5 ml/kg/hr

Electrocardiogram abnormalities

Depressed ejection fraction or wall motion abnormalities by transthoracic and/or transesophageal echocardiogram

B. Endocrine dysfunction

Brain death results in the destruction of the hypothalamus and causes disruption of pituitary hormones, which nearly always results in diabetes insipidus and may cause anterior pituitary dysfunction (thyroid hormone, adrenocorticotropin hormone, and human growth hormone).

Diagnostic criteria include:

Diabetes insipidus: >4 ml/kg/hr of urine with specific gravity <1, urine osmolality <200 mosm/L and serum osmolality >310 mosm/l, and serum sodium >145 mEq/ml

Anterior pituitary dysfunction – tachycardia >120 beats/min, hypotension with mean arterial pressure < 60 mm Hg, decreased to non-existent concentrations of thyroxine, adrenocorticotropin hormone, and human growth hormone.

C. Pulmonary dysfunction

Brain death often results in neurogenic pulmonary edema. In addition, often the primary injury that resulted in brain is accompanied by traumatic lung damage, pneumonia, etc.

Diagnostic criteria include:

Ratio of arterial partial pressure of oxygen to fraction of inhaled oxygen (P:F ratio) <200

Consolidation on chest radiography

Increasing mechanical ventilatory requirements to maintain arterial partial pressure of oxygen >80 mmHg, including increasing positive end expiratory pressure, mean airway pressure, and fraction of inhaled oxygen

Pathophysiological alterations are often multifactorial. Management is aimed at maintaining adequate organ perfusion, recognizing endocrine abnormalities, prophylactically treating likely infections, and reversing acid-base and electrolyte disturbances.

Once a declaration of brain death has been confirmed, cardiovascular, endocrine and pulmonary pathophysiologic changes are not subtle, if they occur. Due to the primary injury mechanism that resulted in brain death, the loss of sympathetic tone and hypothalamic-pituitary axis that occurs with brain death, and the patient’s own comorbidities prior to injury, diagnosis of pathophysiologic mechanisms is less relevant than maintaining organ perfusion and oxygenation.

Frequent, serial laboratory studies are essential, including arterial blood gas, serum electrolytes, and serum glucose. Echocardiography is useful to determine focal wall abnormalities and assess volume status.

Lab values

Pulmonary artery catheter:

Mean arterial pressure <60 mmHg

Systemic vascular resistance <600 dynes/s/cm

Cardiac index <2 l/min*m

Central venous oxygen saturation (ScvO2) <60%

Central venous pressure <6 mmHg

Pulmonary capillary wedge pressure between 10 and 12 mmHg

Electrocardiogram: ST segment changes, heart block

Echocardiography: wall motion abnormalities, depressed ejection fraction, under- or overfilling of the left ventricles (hypovolemia or pulmonary edema)

Diabetes Insipidus: >4 ml/kg/hr of urine with specific gravity <1, urine osmolality <200 mosm/L and serum osmolality >310 mosm/l, and serum sodium >145 mEq/ml

Chest radiograph: discrete infiltrate (pneumonia, pulmonary contusion), diffuse edema (adult respiratory distress syndrome, heart failure, etc.), effusion (volume overload, infection)

Partial pressure of oxygen <70 mmHg

Abnormal electrolytes including serum sodium, potassium, calcium, blood urea nitrogen, bicarbonate, magnesium

Altered acid-base status by arterial blood gas (pH <7.38)

Hyperglycemia (serum glucose >140 gm/dl)

4. Specific Treatment


Guided by rational strategy based on pulmonary artery catheter monitors

Usually initial therapy should include vasopressin infusion

Of note, beta-agonism should be used with caution as it may result in a poor hemodynamic profile and vasoconstriction in potential donated organs.

In addition, noradrenergic augmentation may result in worsening acidemia and pulmonary edema.

Endocrine dysfunction

Diabetes insipidus is treated with volume replacement and vasopressin infusion (at 0.5 to 4 U/hr) to maintain urine output <4 ml/kg/hr and euvolemia.

Triiodothyronine infusion for refractory hypotension (mean arterial pressure <60 mmHg) at 3 ug/hr

Methylprednisolone infusion for adrenocorticotropin insufficiency at 5 mg/kg q6hr


Maintain lowest possible inhaled fraction of oxygen.

Maintain lowest possible mean airway pressure.

Tidal volume should be aimed at 5 to 8 ml/kg.

Transfuse to optimize hemoglobin oxygen carrying capacity (<7 gm/dl).

Insulin infusion to maintain serum glucose <140 gm/dl

Bicarbonate infusion to maintain arterial pH >7.2

Vasopressin infusion (at 0.5 to 4 U/hr) to maintain urine output <4 ml/kg/hr and euvolemia

Triiodothyronine infusion for refractory hypotension (mean arterial pressure <60 mmHg) at 3 ug/hr

Methylprednisolone infusion for adrenocorticotropin insufficiency at 5 mg/kg q6hr

Add secondary and tertiary vasopressor agents, such as norepinephrine, epinephrine, or phenylephrine.

Transfuse to a higher hemoglobin (8 to 10 gm/dl).

Increase bicarbonate infusion.

Broad-spectrum antibiotics

Increase inhaled oxygen fraction and mean airway pressures with profound hypoxemia and/or worsening hypercapnea

Proceed with urgent/emergent organ donation.

5. Disease monitoring, follow-up and disposition

All attempts should be made at maintaining homeostasis with a variety of fluid resuscitation, lung protection strategies, vasopressor agents infusion, hormone replacement, correction of metabolic disturbances, and transfusion of blood products. If end organs maintain function, then the likelihood of their being appropriate for transplant is high.

Choice of vasopressor agent and/or hormone replacement should be based on goal-directed therapy. If adequate perfusion of end organs is not being preserved, then changes should be made to the regimen.

Alterations in therapy should occur on a minute-to-minute basis as response to treatment is determined.


Brain death results from cerebral herniation as a result of raised intracranial pressure due to a variety of insults (infarction, mass effect, edema, etc.). As intracranial pressure increases, mean arterial pressure increases in an attempt to maintain cerebral perfusion. Left unchecked, raised intracranial pressures results in lack of adequate perfusion, which leads to ischemia and, ultimately, infarction of cerebral tissue. As this occurs, herniation is completed with midbrain destruction resulting in parasympathetic activation and sinus bradycardia, pontine infarction causing superimposed hypertension, and compromise of the medulla oblongata ending with loss of the baroreceptor reflexes. This Cushing’s reflex, or autonomic storm, compromises blood flow to potential donor organs.

The vasoconstrictive effect of the autonomic surge associated with brain death impairs end-organ perfusion. This is followed by a loss of sympathetic tone that results in hypotension. End-organ ischemia begins a cascade of effects similar to multi-organ failure from other etiologies (e.g. sepsis, severe trauma, etc.).




There are few data that verify that organ protection strategies translate into increased harvest rates. Evidence for practice guidelines is largely observational or based on preclinical models. However, there is evidence to support the use of ‘triple hormone’ therapy, consisting of vasopression, glucocorticoids, and triiodothyronine, to increase the potential for harvestable organs. Also, aggressive lung protective strategies have been demonstrated to increase the incidence of potential lung donation.

High troponin levels correlate with cardiac allograft rejection by the recipient.

Increased serum sodium levels >155 mmol*L correlate with hepatic allograft rejection by the recipient.

Special considerations for nursing and allied health professionals.

The prevailing theme for the health care team is to continue intensive care nursing, including turning, pulmonary toilet, hygiene, nutrition, ulcer and deep venous thrombosis prophylaxis.

What's the evidence?

Description of the Problem

Mackersie, RC, Bronsther, OL, Shackford, SR. “Organ procurement in patients with fatal head injuries. The fate of the potential donor”. Ann Surg. vol. 213. 1991. pp. 143-50.

Nygaard, CE, Townsend, RN, Diamond, DL. “Organ donor management and organ outcome: a 6-year review from a level 1 trauma center”. J Trauma. vol. 30. 1990. pp. 728-32.

Cho, YW, Cecka, JM. “Organ Procurement Organization and transplant center effects on cadaver renal transplant outcomes”. Clinical Transpl. 1996. pp. 427-41.

Emergency Management

Donor management: critical pathway.


Wood, KE, Becker, BN, McCartney, JG, D’Alessandro, AM, Coursin, DB. “Care of the potential organ donor”. N Engl J Med. vol. 351. 2004. pp. 2730-9.

Tuttle-Newhall, JE, Collins, BH, Kuo, PC, Schoeder, R. “Organ donation and treatment of the multi-organ donor”. Curr Probl Surg. vol. 40. 2003. pp. 266-310.

Zaroff, JG, Rosengard, BR, Armstrong, WF, Babcock, WD, D’Alessandro, AD. “Consensus conference report on maximizing use of organs recovered from cadaver donor: cardiac recommendations”. Circulation. vol. 106. 2002. pp. 836-41..

Specific Treatment

Yoshioka, T, Sugimoto, H, Uenishi, M. “Prolonged hemodynamic maintenance by the combined administration of vasopressin and epinephrine in brain death: clinical study”. Neurosurgery. vol. 18. 1986. pp. 565-7.

Hunt, SA, Baldwin, J, Baumgartner, W. “Cardiovascular management of a potential heart donor: a statement from the Transplantation Committee of the American College of Cardiology”. Crit Care Med. vol. 24. 1996. pp. 1599-601.

Edgar, P, Bullock, R, Bonner, S. “Management of the potential heart-beating organ donor”. Contin Educ Anaesth Crit Care Pain. vol. 4. 2004. pp. 86-90.

Disease Monitoring


Salim, A, Martin, M, Brown, C, Belzberg, H, Rhee, P, Demetriades, D. “Complications of brain death: frequency and impact on organ retrieval”. Am Surg. vol. 72. 2006. pp. 377-81.

Lagiewska, B, Pacholczyk, M, Szostek, M, Walaszewski, J, Rowinski, W. “Hemodynamic and metabolic disturbances observed in brain-dead organ donors”. Transplant Proc. vol. 28. 1996. pp. 165-6.


Figueras, J, Busquets, J, Grande, L. “The deleterious effect of donor high plasma sodium and extended preservation in liver transplantation: a multivariate analysis”. Transplantation. vol. 61. 1996. pp. 410-3.

Wheeldon, DR, Potter, CD, Oduro, A, Wallwork, J, Large, SR. “Transforming the “unacceptable” donor: outcomes from the adoption of a standardized donor management technique”. J Heart Lung Transplant. vol. 14. 1995. pp. 734-42.

Potapov, E, Ivanitskaia, E, Loebe, M. “Value of cardiac troponin I and T for selection of heart donors and as predictors of early graft failure”. Transplantation. vol. 71. 2001. pp. 1394-400.

Rosendale, JD, Kauffman, HM, McBride, MA. “Hormonal resuscitation yields more transplanted hearts, with improved early function”. Transplantation. vol. 75. 2003. pp. 1336-41.