Surgical Critical Care

Organ Donation

Our regional organ donation team is "Donor Network West" (DNW).  The type of donation related to Brain Death is considered a 'deceased donation'. When a patient is thought to be moving towards brain death, we notify DNW of a potential donor. AT NO TIME should any member of the health care team discuss the idea of donation with a family member. Even if family bring up the topic with you, the appropriate response is: "We have specially trained support staff who can answer all your questions regarding this donation".​

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In transplant, there are two major types of donation, 'deceased' and 'living'. Since we do not have a transplant program on-site, we do not deal with 'living' donors. The subcategories of deceased donations are: 

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• Donation after brain death declaration

• Donation after cardiac death

• Tissue donation

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Since this page deals particularly with 'brain death' we will focus on that aspect of management here. 

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Criteria for Donation​

Eligibility

• The donor must be declared brain dead or have suffered a cardiac arrest that is not reversible. 

• The donor's organs must be in good health and suitable for transplantation. 

• The donor must not have any active infections, uncontrolled diseases, or certain types of cancer. 

Consent: 

• The donor must have registered as an organ donor or their family must consent to donation. 

• In the United States, most states have organ donor registries where individuals can register their intent to donate. 

• If the donor is not registered, their family will be asked for their consent. 

Age: 

• There is no upper age limit for organ donation. 

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Physiologic Support in the setting of Brain Death

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When a patient progresses to brain death, multiple aspects of their physiology can be affected. As the physiology becomes more and more dysregulated, homeostasis is lost and there is risk of arrhythmias, volume loss, and maldistribution of blood flow. All these issues can lead to cardiovascular collapse and cardiac death. In the 'waiting period' prior to brain death declaration, it is important to support patient's physiology so that family may say goodbye, and the potential for donation is preserved, should the family choose to pursue it. 

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Physiology of Brain Death

1. Cardiovascular: there is an intense sympathetic outflow that accompanies

brain stem death. This leads to a substantial rise in circulating

catecholamine levels. Norepinephrine, epinephrine and dopamine levels have been measured in animal models after brainstem death, and were found to be from 100 - 800% increased from normal baseline levels. The physiologic affect of this sympathetic surge can be:

• Intense systemic vasoconstriction

• Hypertension

• Tachycardia

• Increase in myocardial oxygen demand

• Coronary vasoconstriction and sub-endocardial ischemia

Catecholamines can also directly injure the myocardium. Ventricular dysfunction is seen in even previously healthy hearts. Baroldi and colleagues showed the presence of contraction band necrosis in 89% of hearts from patients with brain death. ​

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After the initial catecholamine surge, there is a loss of sympathetic tone and a significant reduction in systemic vascular resistance (SVR). This subsequent hemodynamic dysfunction is primarily distributive in nature instead of cardiogenic. 

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Since the myocardium is already under stress in this clincal setting, isolated use of vasoconstrictors and ionotropic agents is discouraged. To counteract the decreases in SVR in the setting of brain death, a comprehensive strategy is needed. 

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Other contributing factors for decreased SVR in brain dead patients include: 

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• Loss of endogenous catecholamines

• Thyroid dysfunction

• Loss of volume from central diabetes insipidus

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To manage these patients, invasive cardiovascular monitoring (e.g. arterial line) and targeted resuscitation are imperative. 

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Pulmonary sequellae of brain death​

​There are many respiratory complications related to severe TBI such as:

• pneumonia

• aspiration

• neurogenic pulmonary edema

• pulmonary trauma

• Adult Respiratory Distress Syndrome (ARDS)

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These conditions can be worsened by the catecholamine surge associated with brain stem death. The increase in SVR during catecholamine surge can contribute to elevated left atrial pressures and increased pressure across pulmonary vascular beds. Sympathetic surge and the inflammatory response can trigger pulmonary microvascular leak and subsequent pulmonary edema. As lung dysfunction progresses, ventilator support is increased in an effort to maintain oxygenation goals. These efforts can have negative repercussions since prolonged high FiO2 levels cause oxygen toxicity, high levels of PEEP cause barotrauma and can reduce cardiac output. It has also been shown that sustained high levels of PEEP can trigger the release of vasopressin and activate the renin / angiotensin system, resulting in vasoconstriction leading to impaired perfusion to vital organs. 

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Endocrine abnormalities after Brain Death

Pituitary Influence:

Once the brainstem dies, anterior and posterior pituitary glands cease to function. Antidiuretic hormone (ADH)  levels drop and Primary Diabetes Insipidus (DI) can occur. Almost eighty percent of brain death organ donors will show some degree of DI. 

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Symptoms of DI

• ​Inappropriate diuresis

• Severe hypovolemia

• Hyperosmolality

• Hypernatremia

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The fluid shifts related to these symptoms can result in cardiovascular collapse if DI goes untreated. 

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​Thyroid stimulating hormone (TSH)  is another hormone affected by the loss of the pituitary axis. Impaired TSH results in a decline in serum free triiodothyronine (T3) and peripheral conversion to tetraiodothyronine (T4).  Low T3 is thought to cause progressive loss of cardiac contractility. T3 infusions to support cardiac function have been recommended by some researchers. 

 Insulin levels decrease after brain death. This causes a decrease in intracellular glucose leading to an energy deficit. When cells have less energy they shift to anaerobic metabolism and become acidotic. Serum levels of glucose rise resulting in increased osmolarity of the serum. If untreated, the hyperglycemia induced hyperosmolar state causes an osmotic diuresis... causing further hypovolemia with resultant decreased organ perfusion. 

Cortisol levels drop after the brain stem dies. This is likeley due to the loss of Adrenocorticotropic hormone (ACTH), produced by the anterior pituitary gland. The milieu created by low cortisol and T3 can contribute to cardiovascular instability. Stabilization of organ function has been seen in donors when exogenous corticosteroids were given. 

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Other systemic repercussions of brain death:

• Hepatic dysfunction

  • depletion of hepatic glycogen​

  • reduction in sinusoidal perfusion b/c of leukocyte activation

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• Disseminated Intravascular Coagulation (DIC)

  • Ischemic / necrotic brain releases tissue thromboplastin ​

  • TTP activates coagulation pathway

  • Endothelial lining is compromised

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• Hypothermia

  • loss of hypothalamic temperature regulation ​

  • Endogenous heat production is lost due to fall in metabolic rate and loss of muscle activity

  • Increase heat loss due to dilation of peripheral vasculature  

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• Inflammatory response

  • Increases in cytokines, chemokines, adhesion molecules increase​

  • Likely due to interrelated events

    • Central injury​

    • Hypotension

    • Circulating factors

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Strategies for physiologic support during brain death 

• Cardiovascular

  • Invasive cardiac monitoring ​

  • Mean Arterial Pressure > 60

  • Maintain normo-volemia, avoid hypervolemia!

  • Ionotropic support 

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• Pulmonary

  • Protective lung strategies (i.e. ARDSnet protocols)​

  • Keep FiO2 as low as possible to avoid oxygen toxicity

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• Sytem level support

  • Thermal regulation w/ heating, cooling as needed to maintain normothermia​

  • In setting of DIC - give products as needed to maintain normal coagulation profile

    • Fresh Frozen Plasma​

    • Cryoprecipitate

    • Platelets

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• Hormonal - Adjuncts which 'may' be helpful

  • Methyprednisolone​

  • T3 / T4 infusions

  • Arginine Vasopressin

  • Insulin for normoglycemic target​​​​​

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Please note* there is a "gift of life" order set! (It is poorly named).

You may use this order set for any brain dead patient who is fully resuscitated yet still showing signs of physiologic compromise.