Hi Peter,

Having 20 years of experience of attending ICU ward rounds every other day, I can offer two explanation, one complex and one simple:

1. Starting with the complex:: Normally the kidneys work as an effective lactate clearing organ even during septic shock, whilst the liver may suffer inhibition of glycolysis and reduction of lactate consumption via gluconeogenesis during sepsis leading to hyperlactataemia. If lactate buffered fluids are used during haemodialysis of septic patients then blood lactate levels could significantly rise exacerbating metabolic acidosis. On the other hand, if bicarbonate buffered fluids are used then lactate rise won’t happen to a significant degree and amelioration of acidosis takes place. High citrate level could somehow inhibit gluconeogenesis thus reducing hepatic clearance of lactate via Cori cycle leading to its accumulation.

2. The simple explanation: many iv drugs used in ICU, like diazepam, lorazepam and midazolam, contain propylene glycol as excipient (diluent) which is metabolised via alcohol dehydrogenase to lactate. Cases of severe lactic acidosis has been described with prolonged use of such IV drugs in ICU.

3. I could be wrong on both counts and somebody else could offer a third explanation.

Best regards

Mohammad

Dr. M. A. Al-Jubouri

MBChB, FRCP Edin, FRCPath

Consultant Chemical Pathologist

Clinical Director of Pathology

St. Helens & Knowsley Teaching Hospitals

Description: Description: Description: Description: HSJ logo (2)

From: Clinical biochemistry discussion list [mailto:[log in to unmask]] On Behalf Of Peter Beresford
Sent: 29 March 2017 15:10
To: [log in to unmask]
Subject: Use of citrate in haemodialysis

Dear Mailbase,

Can anyone help with this query?

One of our Consultants in ICU has contacted me with an observation about patients on haemodialysis using citrate as an anticoagulant in the dialysis machine.

There seems to be a small proportion of patients (generally the very sick ones) who respond with a significant increase in lactate. The cause of this is not clear, and it does not happen in most patients. There don’t appear to be an reports of this in the literature, but I’m told it happens often enough to be a recognised pattern. An anecdotal example is a patient with a lactate of 3 mmol/L that increased to around 8 mmol/L following haemodialysis, then slowly settled after dialysis was stopped. Because of concern about the rising lactate, these patients may be taken off the citrate filter early, which is not ideal.

The clinical question that arises from this is whether that lactate rise is of clinical concern, indicating a genuine problem with tissue oxygen delivery for some reason, or whether it could just be a by-product from metabolism of the citrate. Conventional wisdom is that any citrate returning to the patient’s circulation from the dialysis circuit is quickly metabolised via the TCA cycle in the liver and skeletal muscle to carbon dioxide and water. Is there a plausible mechanism for this citrate load to be converted to lactate under hypoxic conditions in sick patients?

I would be interested to know if anyone has come across this before or has any insights

Regards

Pete

Peter Beresford│Consultant Clinical Biochemist

Severn Pathology

North Bristol NHS Trust, Pathology Building, Southmead Hospital,

Southmead Road, Westbury-On-Trym, Bristol BS10 5NB

Tel: 0117 4148415 │ Fax: 0117 4148438

Website: www.severnpathology.com

Please note new telephone numbers from May 2016

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