Association between cerebrospinal fluid biomarkers of neuronal injury or amyloidosis and cognitive decline after major surgery.


Journal

British journal of anaesthesia
ISSN: 1471-6771
Titre abrégé: Br J Anaesth
Pays: England
ID NLM: 0372541

Informations de publication

Date de publication:
02 2021
Historique:
received: 26 06 2020
revised: 16 09 2020
accepted: 19 09 2020
pubmed: 14 11 2020
medline: 2 2 2021
entrez: 13 11 2020
Statut: ppublish

Résumé

Postoperative neurocognitive decline is a frequent complication in adult patients undergoing major surgery with increased risk for morbidity and mortality. The mechanisms behind cognitive decline after anaesthesia and surgery are not known. We studied the association between CSF and blood biomarkers of neuronal injury or brain amyloidosis and long-term changes in neurocognitive function. In patients undergoing major orthopaedic surgery (knee or hip replacement), blood and CSF samples were obtained before surgery and then at 4, 8, 24, 32, and 48 h after skin incision through an indwelling spinal catheter. CSF and blood concentrations of total tau (T-tau), neurofilament light, neurone-specific enolase and amyloid β (Aβ1-42) were measured. Neurocognitive function was assessed using the International Study of Postoperative Cognitive Dysfunction (ISPOCD) test battery 1-2 weeks before surgery, at discharge from the hospital (2-5 days after surgery), and at 3 months after surgery. CSF and blood concentrations of T-tau, neurone-specific enolase, and Aβ1-42 increased after surgery. A similar increase in serum neurofilament light was seen with no overall changes in CSF concentrations. There were no differences between patients having a poor or good late postoperative neurocognitive outcome with respect to these biomarkers of neuronal injury and Aβ1-42. The findings of the present explorative study showed that major orthopaedic surgery causes a release of CSF markers of neural injury and brain amyloidosis, suggesting neuronal damage or stress. We were unable to detect an association between the magnitude of biomarker changes and long-term postoperative neurocognitive dysfunction.

Sections du résumé

BACKGROUND
Postoperative neurocognitive decline is a frequent complication in adult patients undergoing major surgery with increased risk for morbidity and mortality. The mechanisms behind cognitive decline after anaesthesia and surgery are not known. We studied the association between CSF and blood biomarkers of neuronal injury or brain amyloidosis and long-term changes in neurocognitive function.
METHODS
In patients undergoing major orthopaedic surgery (knee or hip replacement), blood and CSF samples were obtained before surgery and then at 4, 8, 24, 32, and 48 h after skin incision through an indwelling spinal catheter. CSF and blood concentrations of total tau (T-tau), neurofilament light, neurone-specific enolase and amyloid β (Aβ1-42) were measured. Neurocognitive function was assessed using the International Study of Postoperative Cognitive Dysfunction (ISPOCD) test battery 1-2 weeks before surgery, at discharge from the hospital (2-5 days after surgery), and at 3 months after surgery.
RESULTS
CSF and blood concentrations of T-tau, neurone-specific enolase, and Aβ1-42 increased after surgery. A similar increase in serum neurofilament light was seen with no overall changes in CSF concentrations. There were no differences between patients having a poor or good late postoperative neurocognitive outcome with respect to these biomarkers of neuronal injury and Aβ1-42.
CONCLUSIONS
The findings of the present explorative study showed that major orthopaedic surgery causes a release of CSF markers of neural injury and brain amyloidosis, suggesting neuronal damage or stress. We were unable to detect an association between the magnitude of biomarker changes and long-term postoperative neurocognitive dysfunction.

Identifiants

pubmed: 33183737
pii: S0007-0912(20)30844-8
doi: 10.1016/j.bja.2020.09.043
pii:
doi:

Substances chimiques

Amyloid beta-Peptides 0
Biomarkers 0
MAPT protein, human 0
Neurofilament Proteins 0
Peptide Fragments 0
amyloid beta-protein (1-42) 0
neurofilament protein L 0
tau Proteins 0
Phosphopyruvate Hydratase EC 4.2.1.11

Types de publication

Journal Article Observational Study Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

467-476

Informations de copyright

Copyright © 2020 The Authors. Published by Elsevier Ltd.. All rights reserved.

Auteurs

Mattias Danielson (M)

Department of Anesthesiology and Intensive Care Medicine, Institute of Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, Sahlgrenska University Hospital, Gothenburg, Sweden.

Andreas Wiklund (A)

Department of Physiology and Pharmacology, Section of Anesthesiology and Intensive Care Medicine, Karolinska Institutet, Stockholm, Sweden.

Fredrik Granath (F)

Clinical Epidemiology, Department of Medicine, Karolinska Institutet, Stockholm, Sweden.

Kaj Blennow (K)

Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden; Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.

Souren Mkrtchian (S)

Department of Physiology and Pharmacology, Section of Anesthesiology and Intensive Care Medicine, Karolinska Institutet, Stockholm, Sweden.

Bengt Nellgård (B)

Department of Anesthesiology and Intensive Care Medicine, Institute of Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, Sahlgrenska University Hospital, Gothenburg, Sweden.

Jonatan Oras (J)

Department of Anesthesiology and Intensive Care Medicine, Institute of Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, Sahlgrenska University Hospital, Gothenburg, Sweden.

Malin J Fagerlund (MJ)

Department of Physiology and Pharmacology, Section of Anesthesiology and Intensive Care Medicine, Karolinska Institutet, Stockholm, Sweden.

Anna Granström (A)

Function Perioperative Medicine and Intensive Care, Karolinska University Hospital, Stockholm, Sweden.

Anna Schening (A)

Function Perioperative Medicine and Intensive Care, Karolinska University Hospital, Stockholm, Sweden.

Lars S Rasmussen (LS)

Department of Anaesthesia, Centre of Head and Orthopaedics, Rigshospitalet, and Institute of Clinical Medicine University of Copenhagen, Copenhagen, Denmark.

Helena E Harris (HE)

Rheumatology Unit, Center for Molecular Medicine, Department for Medicine Solna, Karolinska Institutet, Stockholm, Sweden.

Henrik Zetterberg (H)

Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden; Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden; Department of Neurodegenerative Disease, UCL Institute of Neurology, And UK Dementia Research Institute at UCL, London, UK.

Sven-Erik Ricksten (SE)

Department of Anesthesiology and Intensive Care Medicine, Institute of Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, Sahlgrenska University Hospital, Gothenburg, Sweden.

Lars I Eriksson (LI)

Department of Physiology and Pharmacology, Section of Anesthesiology and Intensive Care Medicine, Karolinska Institutet, Stockholm, Sweden. Electronic address: Lars.I.Eriksson@ki.se.

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Classifications MeSH