Controversy on CVP monitoring after renal transplantation: useful in all cases ? selective use ?? Gold standard or placebo??? Your views will be very much appreciated.
We do not routine use CVP measurements after kidney transplantation. Almost all our patients get a central line, because of thymoglobulin induction, but we don't use it for monitoring. Also, almost all our patients go to the floor, not the ICU. Urine is replaced cc for cc up to 1000cc/hr.
It is important to note, however, that almost all our renal allografts function right away, probably because we routinely pump all deceased donor kidneys; and for living donor kidneys, we wait until diuresis (as seen from the transected ureter) is present before removing the donor kidney. A well-functioning allograft makes CVP moot.
We do not routinely monitor the patient's CVP following transplantation unless clinically indicated, such as in hypotensive cases. As per Dr. Powelson, we routinely replace urine output cc for cc and support with pressor agents if necessary.
We also follow the same protocol. We monitor CVP only in cases of delayed graft function or not expected urine volumes post-Tx. All these apply during the fisrt 1-2 days post-op
Sometimes (DGF, polyuria..) and only first 1-3 days. Then we see on patient's weight
We do not use cvp monitor after transplantation in children routinely.Almost all our donors are living and rate of DGF is very low in our patients.We carefully monitor other parameters such as weight, BP ,urine output and clinlcal situation for better fluid balance. In critical cases cvp monitoring may be useful.
We do not measure CVP intra- or post- op. In fact we do not typically place a central line in our transplant recipients. They get two peripheral IV cannulas, and sometimes an arterial line intra-operatively. They are nursed on a normal ward post-operatievly. We give the thymo peripherally over 6 h - the nurses often give it into the fistula, or a peripheral IV.
Once or twice we have had our fingers burned with this approach - patients aggressively fluid loaded intra-operatively without CVP guidance needed re-intubated on the ward for respiratory failure precipitated by fluid overload.
I strongly recommend and rely on CVP monitoring in these groups: during the operation before and after declamping of the vessels, elderly patients, those patient with preoperative heart failure or low cardiac reserve, recipients with delayed graft function, , recipients with very high urine output (over 1litr/hour), those recipients which their urine output decreases abruptly in the first 24 hours after the operation. CVP monitoring should be continued till the stability of the patient at least for 24-48 hours or when the urine output decrease to the normal rate with normal serum creatinine level and acid-base balance.
Our patients routinely get a central venous line preoperatively. However, we monitor CVP post-operatively mainly in kidney transplant recipients with DGF and poor urine output in the first 48 hours. It is important to note that CVP post-operatively does not reflect fluid status very accurately and a lot of our patients with low CVP's get fluid overloaded. We carefully monitor other parameters such as blood pressure, urine output and patient weight.
We use CVP monitoring as one of the several other parameters of volume assessment. If graft functions immediately we remove it by day 3.
We monitor CVP for 24 hours and find it useful allowing for the medical complexity of some of our recipients. Also the CVL is useful for blood drawing-an issue for some of our recipients who have poor peripheral venous access.
We monitor the CVP for the first 24-36 hours.Our hospital does predominantly live related renal transplant and hence chance of deelayed graft function is very very less. Some times there is dicordance betweeen the CVP and volume status.
Dear Colleagues,
Wish you all a Merry Christmas and a lovely day today.
Many thanks for your time, personal views and reflection of your practice.
What I have learnt over the last two decaded is that monitoring of CVP, during both intra-operative and post-operative periods, as a guide to fluid therapy, is helpful and crucial in certain group of patients. Pre-emptive living (LD) / DBD donor transplants and LD transplants, and patients on CAPD sail through, whatever we do, due to their euvolaemic state. LD or deceased donor transplants on haemodialysis, particularly those on home haemodialysis (usually are very dry), DCD transplants, transplants with delayed graft functions, patients with compromised cardiac functions, and severe diabetics with advanced autonomic neuropathy (compromised GI motility) do benefit from CVP measurements.
Hypovolaemia or fluid overload, both, present with deleterious effects not only on the allograft function, but also systemically in general, that is, GI tract, cardiac and pulmonary functions due to hypervolaemia and the deleterious effects of compensatory mechanisms (hormonal effects). Prolonged ileus resulting from ischaemic injury (due to mesenteric vasoconstriction and ischaemia during hypovolaelmia) and metabolic acidosis (low bicarbonate in blood - due to skeletal muscle ischaemia from vasoconstriction) are two common manifestations of intra- and post-operative hypovolaemia, which sets up a vicious circle, if not appreciated early . Hypovolaemia is not only responsible for ATN, but also for vascular thrombosis and graft loss.
If CVP is monitored, this should be done continuously with hourly recordings, so that low or high CVP are picked up early and actions taken. Leaving abnormal CVP unattended is associated with poor outcomes, that is, ATN or fluid overload and their consequences. This is easily achievable and I observe its benefits in daily practice, although junior consultants, both surgeon and nephrologists, who are in their learning phase, barely appreciate its value.
Fluid therapy based on the monitoring of pulse, BP and urine output is unreliable as when changes in these parameters have occurred, it is TOO LATE !!. The changes in these parameters occur only when STAGE-3 hypovolaemia (loss of 30-40% blood volume) has occurred (ATLS-classification of hypovolaemia). When this stage is reached, that is, hypotension and tachycardia has occured, ATN / vascular thrombosis have already set in !!!!!!! In worst case scenario, cortical necrosis ensues resulting in primary non-function..... the hypovolaemia is never blamed as a cause of primary non-function, particularly after DCD transplants, where intrarenal pressure is very high and a higher perfusion pressure is required to keep the cortex well perfused !!!!!! It is interesting to find medullary necrosis that occurs first due to high oxygen consumption at the cortico-medullary junction ....!!!!!!!!!
Relying on the body weight and the attempts to restore the TARGET WEIGHT is a KILLER in the post-transplant period, which prolongs the recovery from ATN and perpetuates ATN due to repetitive ischaemia-reperfusion injury from repetitive hypovolaemia resulting from haemodialysis (!!! Target weight !!!)
Fluid overload, on the other had, has ledl not only to pulmonary oedema, hypoxia and ATN, but also, to cardiac failure, rupture of chodae tendinae in a young patient, rupture of annulus of mitral valve, requiring valve replacements in two occasions, which I am aware of.
Transoesophageal Doppler can be used intraoperatively as a guidance for infusion during surgery, but, in my personal experience, is unrelaiblein dialysis patients and the patients remain hypovolaemic. Also transoesophageal Doppler can not be used in awake patients postoperatively.
Major centres such as Mayo Clinic, Rochester and Addenbrooke's Hospital, Cambridge, monitor CVP routinely during and after transplants and have excellent outcomes (personal communication).
Many thanks for your views.
Best wishes
Badri Shrestha
