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Coagulopathy and haemorrhagic progression in traumatic brain injury: advances in mechanisms, diagnosis, and management.

Abstract Normal haemostasis depends on an intricate balance between mechanisms of bleeding and mechanisms of thrombosis, and this balance can be altered after traumatic brain injury (TBI). Impaired haemostasis could exacerbate the primary insult with risk of initiation or aggravation of bleeding; anticoagulant use at the time of injury can also contribute to bleeding risk after TBI. Many patients with TBI have abnormalities on conventional coagulation tests at admission to the emergency department, and the presence of coagulopathy is associated with increased morbidity and mortality. Further blood testing often reveals a range of changes affecting platelet numbers and function, procoagulant or anticoagulant factors, fibrinolysis, and interactions between the coagulation system and the vascular endothelium, brain tissue, inflammatory mechanisms, and blood flow dynamics. However, the degree to which these coagulation abnormalities affect TBI outcomes and whether they are modifiable risk factors are not known. Although the main challenge for management is to address the risk of hypocoagulopathy with prolonged bleeding and progression of haemorrhagic lesions, the risk of hypercoagulopathy with an increased prothrombotic tendency also warrants consideration.
PMID
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Authors

Mayor MeshTerms

Blood Coagulation Disorders

Brain Injuries, Traumatic

Cerebral Hemorrhage

Hemostasis

Keywords
Journal Title the lancet. neurology
Publication Year Start




PMID- 28721927
OWN - NLM
STAT- MEDLINE
DA  - 20170719
DCOM- 20170731
LR  - 20170731
IS  - 1474-4465 (Electronic)
IS  - 1474-4422 (Linking)
VI  - 16
IP  - 8
DP  - 2017 Aug
TI  - Coagulopathy and haemorrhagic progression in traumatic brain injury: advances in 
      mechanisms, diagnosis, and management.
PG  - 630-647
LID - S1474-4422(17)30197-7 [pii]
LID - 10.1016/S1474-4422(17)30197-7 [doi]
AB  - Normal haemostasis depends on an intricate balance between mechanisms of bleeding
      and mechanisms of thrombosis, and this balance can be altered after traumatic
      brain injury (TBI). Impaired haemostasis could exacerbate the primary insult with
      risk of initiation or aggravation of bleeding; anticoagulant use at the time of
      injury can also contribute to bleeding risk after TBI. Many patients with TBI
      have abnormalities on conventional coagulation tests at admission to the
      emergency department, and the presence of coagulopathy is associated with
      increased morbidity and mortality. Further blood testing often reveals a range of
      changes affecting platelet numbers and function, procoagulant or anticoagulant
      factors, fibrinolysis, and interactions between the coagulation system and the
      vascular endothelium, brain tissue, inflammatory mechanisms, and blood flow
      dynamics. However, the degree to which these coagulation abnormalities affect TBI
      outcomes and whether they are modifiable risk factors are not known. Although the
      main challenge for management is to address the risk of hypocoagulopathy with
      prolonged bleeding and progression of haemorrhagic lesions, the risk of
      hypercoagulopathy with an increased prothrombotic tendency also warrants
      consideration.
CI  - Copyright (c) 2017 Elsevier Ltd. All rights reserved.
FAU - Maegele, Marc
AU  - Maegele M
AD  - Department for Trauma and Orthopaedic Surgery, Cologne-Merheim Medical Center,
      University Witten/Herdecke, Cologne, Germany; Institute for Research in Operative
      Medicine, University Witten/Herdecke, Cologne, Germany. Electronic address:
      [email protected]
FAU - Schochl, Herbert
AU  - Schochl H
AD  - Department for Anaesthesiology and Intensive Care Medicine, AUVA Trauma Academic 
      Teaching Hospital, Paracelsus Medical University Salzburg, Salzburg, Austria.
FAU - Menovsky, Tomas
AU  - Menovsky T
AD  - Department for Neurosurgery, Antwerp University Hospital, University of Antwerp, 
      Edegem, Belgium.
FAU - Marechal, Hugues
AU  - Marechal H
AD  - Department of Anaesthesiology and Intensive Care Medicine, CRH La Citadelle,
      Liege, Belgium.
FAU - Marklund, Niklas
AU  - Marklund N
AD  - Department of Clinical Sciences, Division of Neurosurgery, University Hospital of
      Southern Sweden, Lund University, Lund, Sweden.
FAU - Buki, Andras
AU  - Buki A
AD  - Department of Neurosurgery, The MTA-PTE Clinical Neuroscience MR Research Group, 
      Janos Szentagothai Research Center, Hungarian Brain Research Program, University 
      of Pecs, Pecs, Hungary.
FAU - Stanworth, Simon
AU  - Stanworth S
AD  - NHS Blood and Transplant/Oxford University Hospitals NHS Foundation Trust,
      University of Oxford, John Radcliffe Hospital, Oxford, UK.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20170711
PL  - England
TA  - Lancet Neurol
JT  - The Lancet. Neurology
JID - 101139309
SB  - IM
MH  - *Blood Coagulation Disorders/diagnosis/drug therapy/etiology
MH  - *Brain Injuries, Traumatic/complications/drug therapy
MH  - *Cerebral Hemorrhage/etiology
MH  - *Hemostasis
MH  - Humans
EDAT- 2017/07/20 06:00
MHDA- 2017/08/02 06:00
CRDT- 2017/07/20 06:00
PHST- 2016/12/06 [received]
PHST- 2017/05/08 [revised]
PHST- 2017/05/30 [accepted]
AID - S1474-4422(17)30197-7 [pii]
AID - 10.1016/S1474-4422(17)30197-7 [doi]
PST - ppublish
SO  - Lancet Neurol. 2017 Aug;16(8):630-647. doi: 10.1016/S1474-4422(17)30197-7. Epub
      2017 Jul 11.