Transplant Anesthesia Flashcards
Before initiating brain death testing, we must make sure that these factors have been ruled out ass possible causes of cerebral dysfunction
Hypothermia
Hypotension
Metabolic/endocrine instability
Drug overdose (recreational, is pt paralyzed?)
What is the definition of comatose?
Unresponsive to verbal stimuli
How can you tell if cerebral cortical function is absent?
No spontaneous movement, and no response to painful stimulus
What are two supporting studies that can be used in the brain death exam?
EEG and TCDs
What is the oculocephalic reflex?
Doll’s eyes response
Oculo–eyes
Cephalic – head
Seeing how their eyes move in relation to their head
What is the oculovestibular reflex?
Cold caloric testing
Stimulating the inner ear with cold water
What are the components of the brain death exam?
Absence of pupillary response to light Absent corneal reflex Absent oculocephalic reflex Absent oculovestibular reflex Absent cough and gag reflex Absent respiratory reflex (apnea test)
How do you perform an apnea test?
Give 100% FiO2 for 10 minutes. Ensure that PaCO2 is normal with an ABG. Take the patient off the vent and connect to a t piece for 7-10 minutes. Get another ABG. Absence of respiratory effort and PaCO2 > 60 is a positive test.
Hemodynamic goals for preserving organ function in the brain death donor patient for organ harvest
SBP > 100 UO 1-1.5cc/kg/hr Hgb > 10 CVP 5-10 FiO2 7.5 (again to avoid lung damage) SaO2 > 95% PaO2 75-150 Core temp > 34-35C
Why do we avoid phenylephrine in the organ harvest patient?
It can reduce splanchnic blood flow to the organs we are trying to procure
What do we give for pressers instead of neo in the organ harvest patient?
Dopamine, dobutamine, epi, and norepi
What do we give for bradycardia in the organ harvest patient?
They will be resistant to atropine, so give either epic or isoproterenol
When someone donates a kidney, which one do they usually take?
The left
In healthy liver segment donors, why do they experience more hypotension with clamping of the hepatic pedicle?
Because unlike those with liver disease, they are healthy and haven’t developed collaterals. To prevent this, we pretreat with albumin boluses.
How are the organs preserved once removed?
Kept cold to reduce metabolism.
Kept in a preservative solution (helps to maintain cellular integrity, prevent cellular swelling, prevent vasospasm, prevent the buildup of toxic metabolites, and to provide a source of energy for the organ
This solution is used to intraabdominal organs
UW solution
This solution is used or hearts
Celsior
Once out of the body, organs are cooled to this temperature
4C
This is an ABSOLUTE contraindication to organ transplant
Active infection (pt will be immunosuppressed, and needs to be able to fight off the infection)
These are RELATIVE CIs to organ transplant
Malignancy, systemic disease, physical/social factors, and advanced age (although, by itself is not a CI)
What are some of the potential SEs of the immunosuppressive agents used?
Life-threatening infection
Increased risk of tumors and malignancy (body isn’t fighting off abnormal cells)
Progressive vascular disease
Renal compromise
This is the sensitization stage
The interaction between the graft cells and the host’s T cells. They’re meeting each other for the very first time, and the T cells are pretty suspicious of these new cells they’re seeing.
This is the effector stage
Those T cells be activated. They realized this shit ain’t what dey used to, and shit’s about to get real. The T cells become activated and secrete cytokines, and amplify T cell activation via DNA synthesis and T cell proliferation.
Why are glucocorticoids given? What glucocorticoid is commonly given?
They decrease macrophage production of interleukins. This decreases T cell development and proliferation of T helper cells.
Methylprednisolone is commonly given, and can cause adrenal suppression, infection, and DM.
These are two Calcineurin Inhibitors used in transplant. What are their names and how do they work? What are their SEs?
Cyclosporine and Tacrolimus
These inhibit T cell differentiation and cytokine synthesis.
SE: Nephrotoxic, hepatotoxic, neurotoxic, HTN, HLD, and hyperglycemia.
Cyclosporine can prolong NM blockade
Tacrolimus is also called FK5
FK506
This is a monoclonal antibody used as an immunosuppressant
Daclizumab. Has no major SEs.
These immunosuppressants work by inhibiting adhesion molecules
Rabbit/Horse Antithymocyte Globulin
- Can cause anaphylaxis, increased CMV or epstein-barr viral infection, and pulmonary edema
Antilymphotcyte globulin (ALG) - Decreased the availability of activated T cells and their proliferation. Specific for T3 complex located on the surface of mature T cells and blocks their function.
This immunosuppressant works by inhibiting DNA synthesis
Azathroprine.
SE include pancytopenia, severe upper airway edema (rare), and antagonist of NM blockade
These are some common causes of ESRD
DM HTN Glomerulonephritis PKD Chronic pyelonephritis Obstructive uropathy SLE Alport's syndrome
Matching tests needed for renal transplant
ABO
HLA
Patient specific crossmatch
Hemodynamic goals for kidney transplant
SBP > 90
MAP > 60
CVP 10-15
Why are lasix and mannitol administered before reperfusion of the kidney?
To stimulate diuresis. Mannitol, along with adequate volume decreases the risk for ATN. Adequate volume increases renal blood flow, and improve immediate graft function.
This is the first choice vasoactive infusion in kidney transplants if pressure does not come up with fluids
Dopamine
Emergence in kidney transplant
May have hyper dynamic responses, especially in those with uncontrolled HTN
Avoid excessive coughing, which could disrupt the graft
ESRD patients may have delayed emergence from anesthesia
Extubatne awake d/t aspiration risk (we want to know they’re awake and capable of protecting their own airway before we remove the tube)
Key during organ reperfusion
Watch for hypotension. This is expected d/t release of ROS, but should be avoid to maintain graft perfusion
What is the most common indication for liver transplant?
Hep C
When the pressure gradient between hepatic and portal veins is severe (__-__mmHg), complications such as ascites, esophageal varices, encephalopathy, and hepatorenal syndrome can develop
10-12
Why do ESLD patients have hyper dynamic circulation?
Hyperdynamic circulation is high CO, low BP, and low SVR.
It is caused by portal HTN-induced production of vasodilators, most importantly, NO. The overproduction of vasodilators is responsible for reduced circulatory responsiveness to sympathetic stimulation. Clinically, this frequently results in a need for increased doses of vasopressors.
What is hepatopulmonary syndrome?
A syndrome that is defined as having portal HTN, PaO2
What is portopulmonary HTN?
Defined as pulmonary hypertension in the presence of portal hypertension in a patient without other predisposing factors. Diagnosis: Mean PAP > 25 PVR > 240 PCWP
What are some examples of natural anticoagulants?
Protein C, Protein S, and AT-III
