NDT Advance Access originally published online on December 15, 2005
Nephrology Dialysis Transplantation 2006 21(4):1096-1099; doi:10.1093/ndt/gfi339
© The Author [2005]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Case Report
Hyperlactataemia induced by CVVHDF with low lactate bicarbonate-buffered solutions in patients with liver dysfunction
K. M. Ho
Intensive Care Unit, Royal Perth Hospital, Perth, WA 6000, Australia
Correspondence and offprint requests to: K. M. Ho, Consultant Intensivist, Intensive Care Unit, Royal Perth Hospital, Perth, WA 6000, Australia. Email: kwok.ho{at}health.wa.gov.au
Keywords: acute renal failure; dialysis lactate acidosis
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Introduction
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Critical illness is often complicated by hyperlactataemia, acute
renal failure, and multi-organ failure [
1]. Sodium lactate is
the most commonly used nonbicarbonate buffer in both dialysate
and replacement solutions and as a result, significant quantities
of lactate could be transferred to the patient resulting in
hyperlactataemia during continuous veno-venous haemodiafiltration
(CVVHDF) [
2]. Hyperlactataemia is well described during CVVHDF
when the lactate load exceeds the capacity of lactate metabolism
in critically ill patients [
1]. The liver accounts for approximately
50% of the total lactate clearance of the body and therefore
patients with liver dysfunction have a reduced capacity to metabolize
lactate [
1]. As such, bicarbonate-buffered solutions instead
of lactate-buffered solutions are recommended in these patients
[
2–4]. Significant hyperlactataemia induced by the use
of low lactate bicarbonate-buffered replacement and dialysate
solutions during CVVHDF in critically ill patients has not been
described [
5]. We report on two critically ill patients, both
with circulatory failure and acute liver dysfunction, who developed
significant hyperlactataemia during CVVHDF with the use of low
lactate bicarbonate-buffered solutions.
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Case 1
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A 63-year-old woman with a history of mitral stenosis, atrial
fibrillation and chronic renal failure was admitted to the Royal
Perth Hospital, Perth, Australia, with severe right-sided pneumonia.
Her renal failure was normally treated with peritoneal dialysis
and she was anticoagulated with warfarin for the valvular heart
disease. The patient deteriorated rapidly in the ward and developed
severe hypoxaemic respiratory failure and septic shock requiring
mechanical ventilation and noradrenaline infusion (0.1 µg/kg/min)
in the intensive care unit (ICU). The liver function of the
patient was deranged on admission to the ICU (bilirubin 33 µmol/l,
ALT 144 U/l, ALP 303 U/l, INR 3.4). The INR remained elevated
after treatment with 4 units of fresh frozen plasma, 2 vials
of prothrombin complex concentrate (Prothrombinex-HT, CSL limited,
Australia) [
6] and 10 mg of intravenous vitamin K
1. Ultrasound
of the abdomen showed good hepatic blood flow to the liver and
the blood ammonia concentration was mildly elevated (62 µmol/l,
normal range: 10–50). Urgent transoesophageal echocardiography
showed severe mitral stenosis with a large clot adherent to
the wall of the left atrium but no echocardiographic evidence
of infective endocarditis.
Because the patient was normally anuric, CVVHDF was commenced immediately, through a femoral venous double lumen catheter by a blood pump at a flow rate of 180 ml/min, to facilitate fluid and electrolyte management. Bicarbonate dialysate solutions (Hemosol B0® by Hospal, Sondalo, Italy) were infused through the haemofilter, countercurrent to the blood flow, at a constant rate of 1 l/h. The replacement solutions were the same as the dialysate solutions in composition, infused continuously into the blood circuit in a prefilter fashion at a rate of 1 l/h, aiming at a neutral balance in the fluid status of the patient. Sixteen hours after the commencement of CVVHDF, the serum lactate concentration started to increase and it peaked at 8.5 mmol/l after 25 h of CVVHDF (Patient A in Figure 1). The haemodynamic status of the patients remained steady and there was no significant increase in requirement of noradrenaline infusion (0.1 µg/kg/min). Because the patient had a high risk of embolic complications due to the presence of atrial fibrillation and a large left atrial clot, the clinical diagnosis of ischaemic bowel disease was made despite her stable haemodynamic status. However, the bowel perfusion was normal and no abnormal pathology was found at the laparotomy. The serum lactate concentration slowly returned to the normal range over a period of 8 h while the patient was not on CVVHDF after the operation. The hyperlactataemia reappeared again after 16 h of treatment with the same regimen of CVVHDF. Hyperlactataemia induced by CVVHDF was suspected and CVVHDF was withheld for another 24 h and the hyperlactataemia slowly resolved. The liver function and the cardiovascular status of the patient improved 2 days after the laparotomy and hyperlactataemia did not reappear when the same regimen of CVVHDF was recommenced again.
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Fig. 1. The changes in serum lactate concentrations, base excess, pH and bicarbonate concentrations after commencement of CVVHDF.
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Case 2
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A 64-year-old man with a history of hypertension was admitted
to the Emergency Department of Royal Perth Hospital with a ruptured
abdominal infra-renal aortic aneurysm. He was in profound hypovolaemic
shock and had a short period of cardiac arrest at the Emergency
Department before the emergency surgery. The patient had severe
lactic acidosis during the surgery and was treated with 300
mmol of intravenous sodium bicarbonate. The patient was transferred
to the ICU after emergency grafting of the ruptured abdominal
aorta in the operating theatre. The patient developed signs
of intra-abdominal bleeding soon after the operation and urgent
re-laparotomy was required to achieve haemostasis. The patient
was in circulatory failure requiring noradrenaline infusion
(0.2 µg/kg/min) when he was transferred to ICU after the
second operation.
The patient remained oliguric despite aggressive fluid resuscitation. There was no evidence of intra-abdominal compartment syndrome, the intra-abdominal pressure was measured at 10 cm H2O. The liver function of the patient was deranged (bilirubin 13 µmol/l, ALT 505 U/l, ALP 51 U/l, INR 2.0) on admission to ICU. CVVHDF was commenced immediately, through a right subclavian vein double lumen catheter by a blood pump at a flow rate of 180 ml/min, to facilitate fluid and electrolyte management. Bicarbonate dialysate solutions (Hemosol B0® by Hospal, Sondalo, Italy) were infused through the haemofilter, countercurrent to the blood flow, at a constant rate of 1 l/h. The replacement solutions were the same as the dialysate solutions in composition, infused continuously into the blood circuit in a prefilter fashion at a rate of 1 l/h, aiming at a neutral balance in the fluid status of the patient. The serum lactate concentrations progressively increased over a period of 18 h during CVVHDF until it peaked at 8.6 mmol/l (Patient B in Figure 1). The dose of the noradrenaline infusion remained steady at 0.2 µg/kg/min during this period. Because there was no deterioration in the clinical status of the patient other than an elevated lactate concentration and, also with the experience of the first patient of this report, the CVVHDF regimen was CVVHD without the component of haemofiltration. The lactate concentrations slowly decreased and returned to the normal range after 22 h of CVVHD. CVVHDF was recommenced 2 days later after the liver function test had improved and the hyperlactataemia did not reappear again.
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Discussion
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Tissue hypoxia or ischaemia can induce hyperlactataemia and
serum lactate concentrations have been used as a marker of tissue
perfusion in critically ill patients [
7]. Daily fluid exchanges
in CVVHDF can reach more than 20–50 l, and as a result,
the composition of the replacement and dialysate solutions can
have a significant effect on the blood biochemistry of the patient.
Lactate has a low molecular weight, and is readily dialysed
or ultrafiltered [
2]. However, the amount of lactate removed
by CVVHDF using lactate free replacement and dialysate solutions
is very small when compared with the total plasma clearance
in patients with normal liver function (25 ml/min
vs 1400 ml/min)
[
8]. It has been suggested that using lactate free dialysate
and replacement solutions in CVVHDF will not mask any excessive
endogenous lactate production even when there is tissue hypoxia
and ischaemia [
1,
8]. Furthermore, in patients with liver dysfunction
or failure resulting in reduced lactate clearance, lactate accumulation
does not seem to be a problem if the replacement or dialysate
solutions used in CVVHDF is completely free of lactate [
2].
However, some commercially available bicarbonate-buffered solutions
are not completely free of lactate (
www.usa-gambro.com: bicarbonate
dialysate) (
Table 1) [
4,
9,
10]. The dialysate and replacement
solutions (Hemosol B0® by Hospal, Sondalo, Italy) that were
used in our two patients contain 3 mmol/l of lactate. There
was no report of hyperlactataemia induced by using such a low
concentration of lactate bicarbonate-buffered replacement or
dialysate solution during CVVHDF in critically ill patients.
We observed a significant increase in lactate concentrations
in both of our patients with the use of one of these low lactate
bicarbonate-buffered replacement and dialysate solutions (Hemosol
B0® by Hospal, Sondalo, Italy) during CVVHDF. Whether different
low lactate bicarbonate-buffered solutions manufactured by other
manufacturers will induce the same problem is uncertain. The
markedly elevated lactate concentrations led to the clinical
diagnosis of ischaemic bowel disease and a negative laparotomy
in our first patient. With the experience of our first patient
and also because the hyperlactataemia was not associated with
any significant haemodynamic deteriorations, hyperlactataemia
induced by the replacement and dialysate solutions was suspected
in our second patient. This led to a prompt cessation of infusion
of all exogenous lactate to the patient by removing the replacement
component of the CVVDHF and resulted in resolution of the hyperlactataemia
and avoided an unnecessary re-laparotomy.
The average daily lactate production in adults is approximately
1500 mmol [
8]. However, in critically ill patients with acute
liver failure and sepsis, there is an increased production as
well as reduced clearance of lactate [
11]. This explains why
such patients do not tolerate the use of lactate-buffered solutions
during CVVHDF because the excessive exogenous lactate load caused
by the lactate-buffered replacement solutions can easily exceed
the lactate metabolism or clearance by the patient. The lactate
infused into the patient's circulation through the replacement
solutions in the CVVHDF seems to be the main cause of the hyperlactataemia
in our patients. It is possible that even a small excessive
amount of exogenous lactate in the low lactate bicarbonate-buffered
replacement solutions can induce a slow accumulation of lactate
when the total lactate load, from both exogenous and endogenous
sources, has exceeded the capacity of lactate clearance of the
patient. This scenario is most likely to occur when the patient
has an increased production of lactate because of circulatory
failure, and at the same time, a reduced capacity to metabolize
lactate because of liver dysfunction.
In conclusion, the use of low lactate instead of no lactate bicarbonate-buffered replacement solutions in CVVHDF can potentially induce hyperlactataemia when the exogenous lactate load exceeds the lactate clearance in patients who have circulatory failure and liver dysfunction. When there is no other evidence of tissue hypoxia or deteriorations in haemodynamic status, physicians should interpret elevated serum lactate concentrations in this scenario with caution. Ceasing all exogenous source of lactate by removing the replacement component of CVVHDF or changing the replacement solutions to solutions that are completely free of lactate should be considered while investigating for other causes of hyperlactataemia.
Conflict of interest statement. None declared.
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References
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Received for publication: 13.10.05
Accepted in revised form: 23.11.05
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Introduction
Case 1