Regional citrate anticoagulation "non-shock" protocol with pre-calculated flow settings for patients with at least 6 L/hour liver citrate clearance.


Journal

BMC nephrology
ISSN: 1471-2369
Titre abrégé: BMC Nephrol
Pays: England
ID NLM: 100967793

Informations de publication

Date de publication:
02 07 2021
Historique:
received: 10 02 2021
accepted: 28 05 2021
entrez: 3 7 2021
pubmed: 4 7 2021
medline: 8 2 2022
Statut: epublish

Résumé

Regional citrate anticoagulation (RCA) for the prevention of clotting of the extracorporeal blood circuit during continuous kidney replacement therapy (CKRT) has been employed in limited fashion because of the complexity and complications associated with certain protocols. Hypertonic citrate infusion to achieve circuit anticoagulation results in variable systemic citrate- and sodium load and increases the risk of citrate accumulation and hypernatremia. The practice of "single starting calcium infusion rate for all patients" puts patients at risk for clinically significant hypocalcemia if filter effluent calcium losses exceed replacement. A fixed citrate to blood flow ratio, personalized effluent and pre-calculated calcium infusion dosing based on tables derived through kinetic analysis enable providers to use continuous veno-venous hemo-diafiltration (CVVHDF)-RCA in patients with liver citrate clearance of at least 6 L/h. This was a single-center prospective observational study conducted in intensive care unit patients triaged to be treated with the novel pre-calculated CVVHDF-RCA "Non-shock" protocol. RCA efficacy outcomes were time to first hemofilter loss and circuit ionized calcium (iCa) levels. Safety outcomes were surrogate of citrate accumulation (TCa/iCa ratio) and the incidence of acid-base and electrolyte complications. Of 53 patients included in the study, 31 (59%) had acute kidney injury and 12 (22.6%) had the diagnosis of cirrhosis at the start of CVVHDF-RCA. The median first hemofilter life censored for causes other than clotting exceeded 70 h. The cumulative incidence of hypernatremia (Na > 148 mM), metabolic alkalosis (HCO3- > 30 mM), hypocalcemia (iCa < 0.9 mM) and hypercalcemia (iCa > 1.5 mM) were 1/47 (1%), 0/50 (0%), 1/53 (2%), 1/53 (2%) respectively and were not clinically significant. The median (25th-75th percentile) of the highest TCa/iCa ratio for every 24-h interval on CKRT was 1.99 (1.91-2.13). The fixed citrate to blood flow ratio, as opposed to a titration approach, achieves adequate circuit iCa (< 0.4 mm/L) for any hematocrit level and plasma flow. The personalized dosing approach for calcium supplementation based on pre-calculated effluent calcium losses as opposed to the practice of "one starting dose for all" reduces the risk of clinically significant hypocalcemia. The fixed flow settings achieve clinically desirable steady state systemic electrolyte levels.

Sections du résumé

BACKGROUND
Regional citrate anticoagulation (RCA) for the prevention of clotting of the extracorporeal blood circuit during continuous kidney replacement therapy (CKRT) has been employed in limited fashion because of the complexity and complications associated with certain protocols. Hypertonic citrate infusion to achieve circuit anticoagulation results in variable systemic citrate- and sodium load and increases the risk of citrate accumulation and hypernatremia. The practice of "single starting calcium infusion rate for all patients" puts patients at risk for clinically significant hypocalcemia if filter effluent calcium losses exceed replacement. A fixed citrate to blood flow ratio, personalized effluent and pre-calculated calcium infusion dosing based on tables derived through kinetic analysis enable providers to use continuous veno-venous hemo-diafiltration (CVVHDF)-RCA in patients with liver citrate clearance of at least 6 L/h.
METHODS
This was a single-center prospective observational study conducted in intensive care unit patients triaged to be treated with the novel pre-calculated CVVHDF-RCA "Non-shock" protocol. RCA efficacy outcomes were time to first hemofilter loss and circuit ionized calcium (iCa) levels. Safety outcomes were surrogate of citrate accumulation (TCa/iCa ratio) and the incidence of acid-base and electrolyte complications.
RESULTS
Of 53 patients included in the study, 31 (59%) had acute kidney injury and 12 (22.6%) had the diagnosis of cirrhosis at the start of CVVHDF-RCA. The median first hemofilter life censored for causes other than clotting exceeded 70 h. The cumulative incidence of hypernatremia (Na > 148 mM), metabolic alkalosis (HCO3- > 30 mM), hypocalcemia (iCa < 0.9 mM) and hypercalcemia (iCa > 1.5 mM) were 1/47 (1%), 0/50 (0%), 1/53 (2%), 1/53 (2%) respectively and were not clinically significant. The median (25th-75th percentile) of the highest TCa/iCa ratio for every 24-h interval on CKRT was 1.99 (1.91-2.13).
CONCLUSIONS
The fixed citrate to blood flow ratio, as opposed to a titration approach, achieves adequate circuit iCa (< 0.4 mm/L) for any hematocrit level and plasma flow. The personalized dosing approach for calcium supplementation based on pre-calculated effluent calcium losses as opposed to the practice of "one starting dose for all" reduces the risk of clinically significant hypocalcemia. The fixed flow settings achieve clinically desirable steady state systemic electrolyte levels.

Identifiants

pubmed: 34215201
doi: 10.1186/s12882-021-02443-6
pii: 10.1186/s12882-021-02443-6
pmc: PMC8249839
doi:

Substances chimiques

Anticoagulants 0
Solutions 0
Citric Acid 2968PHW8QP

Types de publication

Journal Article Observational Study Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

244

Subventions

Organisme : NIDDK NIH HHS
ID : T32 DK007378
Pays : United States

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Auteurs

Lenar Yessayan (L)

Division of Nephrology, Department of Medicine, University of Michigan, 3914 Taubman Center, 1500 E. Medical Center Dr. 5364, Ann Arbor, MI, 48109-5364, USA. lenar@med.umich.edu.

Ryann Sohaney (R)

Division of Nephrology, Department of Medicine, University of Michigan, 3914 Taubman Center, 1500 E. Medical Center Dr. 5364, Ann Arbor, MI, 48109-5364, USA.

Vidhit Puri (V)

Division of Nephrology, Department of Medicine, University of Michigan, 3914 Taubman Center, 1500 E. Medical Center Dr. 5364, Ann Arbor, MI, 48109-5364, USA.

Benjamin Wagner (B)

Division of Nephrology, Department of Medicine, University of Michigan, 3914 Taubman Center, 1500 E. Medical Center Dr. 5364, Ann Arbor, MI, 48109-5364, USA.

Amy Riddle (A)

Division of Nephrology, Department of Medicine, University of Michigan, 3914 Taubman Center, 1500 E. Medical Center Dr. 5364, Ann Arbor, MI, 48109-5364, USA.

Sharon Dickinson (S)

Division of Acute Care Surgery, Department of Surgery, University of Michigan, Ann Arbor, MI, USA.

Lena Napolitano (L)

Division of Acute Care Surgery, Department of Surgery, University of Michigan, Ann Arbor, MI, USA.

Michael Heung (M)

Division of Nephrology, Department of Medicine, University of Michigan, 3914 Taubman Center, 1500 E. Medical Center Dr. 5364, Ann Arbor, MI, 48109-5364, USA.

David Humes (D)

Division of Nephrology, Department of Medicine, University of Michigan, 3914 Taubman Center, 1500 E. Medical Center Dr. 5364, Ann Arbor, MI, 48109-5364, USA.

Balazs Szamosfalvi (B)

Division of Nephrology, Department of Medicine, University of Michigan, 3914 Taubman Center, 1500 E. Medical Center Dr. 5364, Ann Arbor, MI, 48109-5364, USA. bszamos@med.umich.edu.

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