Kidney Transplant Flashcards
So, tell me about which hypertensive states will cause you to delay surgery:
What pressure are you trying to get it to?
I would prefer to delay elective surgery for at least 6-8 weeks to optimize
the blood pressure of any patient who: I) has stage 3 baseline hypertension, 2) has
stage 1 or stage 2 hypertension with concomitant end-organ damage, and/or 3) is
undergoing cardiac surgery, carotid surgery, or pheochromocytoma resection.
However, as I mentioned, the decision to delay any case (and the length of that delay)
must weigh the risks of blood pressure optimization against the risk of surgical delay.
Jn the case of emergency surgery, I would carefully reduce the patient’s blood
pressure to less than 160/110 mmHg and ensure adequate B-blockade (if not
contraindicated) to reduce the risk of perioperative hemodynamic !ability and
myocardial ischemia, while avoiding end-organ hypoperfusion.
How long do the kidneys last prior to transplant?
Fortunately,
current preservation techniques allow for up to 48 hours of cold-ischemia time prior
to transplant, providing sufficient time for pre-operative dialysis.
If his potassium level were > 5.5 mEq/L, I would
delay surgery for dialysis and correction of this el~6~olyte disturbance.
What would be your choice of anesthesia for this case?(Kidney transplant)
Kidney transplant has been successfully performed under regional
anesthesia. However, the subsequent sympathectomy may complicate systemic blood
pressure management, and uremic platelet dysfunction and/or residual heparin from
preoperative dialysis may increase the risk of neuraxial hematoma. Therefore,
assuming he did not have a difficult airway, I would choose to provide a balanced
general anesthetic, using a volatile agent (avoid sevoflurane -7 the production of
fluoride and compound A have been implicated in renal toxicity), a short acting
opioid (consider using opioids without active metabolites that depend on renal
excretion), and a muscle relaxant (mivacurium, atracurium, cisatracurium do not
depend on renal excretion) in order to provide optimal operating conditions, while at
the same time, maintaining hemodynamic stability and adequate end-organ perfusion.
Qualms about regional anesthesia for kidney transplant?
In the case of a difficult airway or strong patient preference, and
assuming there were no contraindications, I would consider utilizing regional
anesthesia. In preparing for regional anesthesia, I would inform the patient of
potential complications; ensure adequate hydration; prepare to address any acute
hypotension; obtain coagulation studies (specifically a PTT); and look for signs of
coagulopathy such as marked or easy bruising, bleeding at the IV sight, and/or
mucosal bleeding (CRF patients may have platelet dysfunction that results in
abnormal coagulation despite normal coagulation studies). In performing the
procedure, I would take precautions to avoid vascular trauma (i.e. single pass,
injection oflocal or saline through epidural needle prior to placing the catheter) and
slowly raise the block to avoid rapid sympathectomy. Finally, I would develop a plan
to convert to general anesthesia should regional anesthesia prove insufficient.
Sevo and kidney transplants:
Given the potential risk of nephrotoxicity with the use of sevo:flurane,
I don’t believe it would be a good choice for kidney transplant surgery. The concern
of nephrotoxicity stems from the fact that sevo:flurane metabolism leads to the
formation ofpotentiallynepbroto:xic levels of inorganic fluoride (>50 μmoVL), and
that degradatiOn by sodium or barium hydroxide (barium hydroxide > soda lime) can
lead to the production of compound A, which has been associated with renal toxicity
in animals. However, despite these theoretical or potential risks, sevo:flurane has
been successfully used for kidney transplant surgery. If using sevo:flurane became
necessary for some reason, I would minimize the length of patient exposure to the
agent, ensure gas flow rates of at least 2 L per minute (> 1 L per minute is ok for cases
lasting less than 1 hour), and make sure my carbon dioxide absorbent is not
desiccated
Fluids in Renal transplant:
I would replace blood loss with an isotonic
solution, such as normal saline or Plasma-Lyte, at a ratio of 3:1 (??? Is this because the pt’s about to have a new kidney)
, avoiding potassium
containing solutions, such as Ringer lactate, that could exacerbate intraoperative
hyperkalemia. If the administration of blood became necessary, I would transfuse
cytomegalovirus-negative packed red blood cells.
Are there any drugs you would give prior to clamping of the vessels? What’s given prior to revascularization and why? What is given following repercussion?
Usually heparin is administered prior to clamping the iliac vessels to
prevent clotting. Just prior to revascularization, a calcium channel blocker
(verapamil) or papaverine is often injected into the arterial circulation of the graft io
prevent arterial vasospasm and/or reperfusion injury. Finally, mannitol and/or
furosemide are given following reperfusion to induce diuresis. Mannitol has the
added advantage of acting as a free radical scavenger.
After unclamping, his blood pressure falls to 61/40 mmHg. What do you think is
going on?
Hypotension immediately following unclamping is most likely
secondary to the washout of vasoactive substances from previously ischemic tissues
and the acute increase of up to 300 ml to the intravascular space. However, I would
also consider 1) congestive heart failure, secondary to fluid overload or cardiac
ischemia; 2) dysrhythmia, secondary to cardiac ischemia or acute hyperkalemia; 3)
anaphylaxis, secondary to antibiotics, thymoglobulin, etc.; 4) blood loss; 5) tension
pneumothorax (possibly secondary to central line placement); 6) anesthetic overdose;
7) hypoxia; and 8) monitor error. In response, I would ensure adequate oxygenation
and ventilation; auscultate the lungs; check the EKG for dysrhythmia; check the CVP
and PAC pressures (if available); consider transesophageal echocardiography, if the
etiology of the hypotension remains unclear; inspect the surgical field for bleeding;
check serum electrolytes (i.e. hyperkalemia, hyponatremia); and prepare to treat with
fluids, inotropes, and vasopressors, as indicated.
Peaked T waves on EKG during renal transplant, what do you want to do?
Remember to have that defibrillator ready for reperfusion!
Peaked T waves on the EKG are consistent with significant
hyperkalemia, which may occur with perfusion of the newly transplanted kidney and
subsequent washout of potassium-containing preservative solution into the systemic
circulation. Therefore, I would order a plasma potassium level, notify the surgeon,
and initiate treatment, with the goals of: 1) eliminating any factors that may
exacerbate hyperkalemic cardiotoxicity, such as acidosis, hyponatremia, and
hypocalcemia (all of which occur in the presence of impaired renal :function); 2)
depressing cardiac membrane hyperexcitability; and 3) reducing extracellular fluid
potassium, by either shifting it into cells or removing it from the body. I would also
ensure immediate access to a cardiac defibrillator and prepare to treat cardiovascular
dysrhythmias and instability as necessary.
Tell me about EKG changes in hyperkalemia: At what level is V fib happening?
EKG signs associated with hyperkalemia, (usually when plasma
potassium levels exceed 6 mEq/L) characteristically progress from peaked T waves,
to prolongation of the PR interval, to decreasing amplitude, to loss of the P wave, to
widening of the QRS complex (representing the loss of atrial activity), to a sine wave
pattern, and fmally, to ventricular fibrillation and asystole (usually occurring at levels
around 8-9 mEq/L).
How would you treat this hyperkalemic patient with associated
electrocardiographic changes?
Given the presence of EKG changes, I would: 1) give calcium chloride
or calcium gluconate to depress cardiac membrane excitability (immediate affect); 2)
ensure immediate access to a cardiac defibrillator and prepare to treat cardiovascular
dysrhythmias and instability as necessary; 3) attempt to correct any factors that may
exacerbate hyperkalemic cardiotoxicity, such as acidosis, hyponatremia, and
hypocalcemia; 4) attempt to shift extracellular potassium into cells by administering
insulin and glucose (effective in 10-20 minutes), Bradrenergic drugs (albuterol,
salbutamol), ; 5) hyperventilate the patient to promote alkalosis and subsequent
intracellular movement of potassium; and 6) consider hemodialysis, if temporizing
measures are insufficient.
After extubation in the operating room, the patient develops rapid and labored
breathing. Auscultation of the lungs reveals diffuse rales. Will you reintubate?
Assuming the patient were st~ble enough to allo~ further investigation, I would
provide supplemental oxygen and assess oxygenation and ventilation by carefully
auscultating all lung fields, evaluating the patient’s oxygen saturation and inspiratory
effort, and obtaining an ABG. Next, I would evaluate his cardiovascular function by
checking the CVP, PAC (if present), EKG, and arterial blood pressure; and by
ordering a chest x-ray and, possibly, an echocardiogram. Additionally, I would check
the patient’s electrolytes and review all medications, giving careful consideration to
whether renal excretion played a significant role in the elimination of the parent
compounds and/or their active metabolites. Finally, depending on my findings, I
would consider diuretics, hemodialysis, bronchodilators, inotropes, afterload reducing
agents, and re-intubation.
Renal transplant:The chest x-ray suggests bilateral pulmonary edema and his oxygen saturation is
84%. How might mechanical ventilation prove beneficial?
Mechanical ventilation, and more specifically PEEP, may prove
beneficial for patients with pulmonary edema, secondary to a positive-pressure-
induced redistribution of alveolar fluid into areas that are less involved in gas
exchange, which leads to improved oxygenation. However, in the presence ofleft
ventricular dysfunction, positive ventilation and PEEP must be applied with caution
to prevent worsening cardiac function secondary to decreased preload
If you didn’t place a pulmonary artery catheter for the case, (renal transplant and now pt in PACU with rales) would you place
one now?
UBP Answer: Given the presence of significant pulmonary edema, potentially
compromised cardiac function (normal cardiac function is required for CVP to
accurately reflect left heart filling pressures), and the importance of maintaining
adequate renal blood flow in this post-transplant patient, I would certainly consider
placing a pulmonary artery catheter to aid in fluid management, assess cardiac
function, and help differentiate cardiac and noncardiac causes of his pulmonary
edema.
Patient is bleeding from his surgical site in PACU (renal transplant case)
The most common cause of post-operative coagulopathy is platelet
dysfunction, which may result secondary to uremia (interferes with vWF formation
and release), hypothermia (affects the morphology and function of platelets), drug
· effect, or severe anemia (with decreased viscosity, the platelets tend to travel in the
center of the blood column, instead of near the endothelial surface). However, I
would also consider other causes of coagulopathy such as residual heparin effect,
inadequate surgical hemostasis, metabolic acidosis (interferes with the generation of
thrombin), thrombocytopenia, and DIC. Therefore, I would check a platelet count,
PT, PTT, INR, CBC, fibrinogen level, and fibrin degradation products. TEG analysis
may also prove helpful, if available.
