Management of Organ Donors after Brain Death (Part II)

Infectious Disease

Goals: Infected donors should receive antimicrobial therapy for 24-48 hrs and have clinical signs of improvement before organ procurement

Physiological Challenges: 

All organ donors should be screened for infections (ex: HIV, hepatitis, CMV, EBV, syphilis). 

Depending on which organ is being transplanted, additional tests may be needed.

Management:

Antimicrobials: As for all critically ill patients, these should be tailored and chosen based on diagnosis, length of stay, and MDR risk factors.

Heme

Goals: To prevent thrombosis and early allograft dysfunction

Physiological Challenges: 

Replacement of blood products should be based on usual care of the critically ill patient. 

Targeting a Hgb of 10 g/dL could improve tissue oxygenation.

One of the biggest factors affecting the success of a donated organ is blood circulation to the organ after reperfusion. Furthermore, thrombosis is a major issue after circulation is stopped during organ procurement.

Management:

Heparin: Heparin IV is commonly administered after brain death. Administering heparin before cross clamping the aorta has also been shown to help prevent thrombotic complications. Evidence for DVT prophylaxis with heparin is limited. However, a high pulmonary emboli burden is frequently found in patients during organ procurement so continuing DVT prophylaxis is reasonable. For patients with a history of HIT, direct thrombin inhibitors (ex: argatroban, bivalirudin) should be utilized.

Endocrine

Goals: When volume replacement and pressors are not enough to maintain hemodynamic instability, exogenous hormone replacement should be considered

Physiological Challenges: 

After brain death, HPA axis malfunction causes low hormone levels leading to hypotension and organ deterioration.

Several studies have shown an increase in the total number of transplantable organs if donors received pretreatment with hormone replacement.

Management:

The following can be given alone or in combination with one another. Data on optimal replacement is lacking.

Thyroid hormones (triiodothyronine, thyroxine, liothyronine, and levothyroxine): UNOS specifically recommends triiodothyronine for cardiothoracic donors. Triiodothyronine is more potent and has a shorter half-life than thyroxine, making it the preferred agent for donors. Liothyronine, a sodium salt of triiodothyronine, can also be used. Many facilities simply use levothyroxine as it is more obtainable. Levothyroxine is a sodium salt of thyroxine and is converted to active triiodothyronine in the body. The only caveat with using levothyroxine is that the conversion may take several hours meaning a delay in cardiac effects. 

ADH: HPA axis dysfunction can also lead to DI and decreased ADH levels. Pretreatment with vasopressin has been shown to improve the chances of being able to transplant the kidneys, heart, lungs, and pancreas. However, using vasopressin must be done cautiously since it does have potent vasoconstrictive effects and can decrease renal blood flow thereby endangering the kidneys. Desmopressin, an analog of vasopressin, is longer acting and less vasoconstrictive. It can be used as an alternative.

Steroids: Steroids help attenuate the inflammatory response which ensues after brain death by inhibiting cytokines and stabilizing cell membranes. Steroids have been shown to decrease early graft failure and rejection following transplantation. SCCM and UNOS recommend high dose methylprednisolone for cardiothoracic donors. Hydrocortisone can also be used; when compared to methylprednisolone in one study, donors who received hydrocortisone had decreased insulin requirements and better glycemic control.

Insulin: Hyperglycemia is common after brain death due to changes in peripheral insulin resistance and carb metabolism. This can cause damage to pancreatic beta cells leading to graft dysfunction in pancreas recipients. Insulin infusions should be used to maintain a BG goal of < 180 mg/dL as is consistent with general recommendations for glycemic control in ICU patients.