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Transfusion for Massive Blood Loss

Managing massive transfusion events

, November 24, 2006

Massive transfusion is a relatively uncommon event even for large volume trauma centres. Trauma centres should have defined protocols for massive transfusion so that blood and blood products are rapidly…

Massive Transfusion & Traumatic Coagulopathy: State of the Art Symposium

London Trauma Conference 2008

Karim Brohi, London, UK, October 17, 2009

Online video presentations from the Massive Transfusion & Traumatic Coagulopathy State of the Art Symposium held at the London Trauma Conference in 2008.

Trauma Massive Transfusion: Epidemiology & Outcomes - LTC2008

Prof Mark Midwinter

Karim Brohi, London, UK, October 18, 2009

Mark Midwinter, Defence Professor of Surgery at the Royal Centre of Defence Medicine, discusses the epidemiology and outcomes of massive transfusion in both civilian and military trauma.

Massive Transfusion: National Patterns & Practice - LTC2008

Dr Fiona Lecky

Karim Brohi, London, UK, October 18, 2009

Dr. Fiona Lecky, Research Director of the Trauma Audit & Research Network discusses the work of TARN and the practice patterns and outcomes for massive transfusion across the UK.

Prediction of Massive Transfusion - LTC2008

Tom König

Karim Brohi, London, UK, October 18, 2009

Tom König, Trauma Surgery Fellow at the Royal London Hospital, discusses whether the need for massive transfusion can be predicted on arrival in the trauma centre.

Trauma Induced Coagulopathy - LTC2008

Karim Brohi

Karim Brohi, London, UK, October 18, 2009

Karim Brohi, Professor of Trauma Sciences at Barts and the London School of Medicine, discusses the incidence, mechanisms and outcomes of Trauma Induced Coagulopathy (TIC).

Diagnosis of Acute Traumatic Coagulopathy - LTC2008

Ross Davenport

Karim Brohi, London, UK, October 18, 2009

Ross Davenport, Trauma Surgery Research Fellow at the Royal London Hospital, discusses the potential modalities available for the diagnosis of Acute Traumatic…

Management of Massive Haemorrhage in Trauma - Hospital experience - LTC2008

Joanthan Wallis

Karim Brohi, London, UK, October 18, 2009

Jonathan Wallis, Consultant in Haematology & Transfusion Medicine at the Freeman Hospital Newcastle, discusses the management of massive transfusion in trauma from a real-world hospital's perspective.

Can we deliver pre-thawed and high-dose fresh frozen plasma? - LTC2008

Heidi Doughty

Karim Brohi, London, UK, October 18, 2009

Heidi Doughty, Consultant in Haematology & Transfusion Medicine with the National Blood & Transplant Service, discusses the logistics and practicalities of providing pre-thawed and high-dose fresh frozen plasma for trauma…

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Research Blog Entries

PubMed ID: 19628092
Surgery. 2009 Aug;146(2):325-33.
Authors: Alam HB, Shuja F, Butt MU, Duggan M, Li Y, Zacharias N, Fukudome EY, Liu B, Demoya M, Velmahos GC.


BACKGROUND: We have demonstrated previously that valproic acid (VPA), a histone deacetylase inhibitor, can improve survival in lethal models of hemorrhagic shock. This study investigated whether VPA treatment would improve survival in a clinically relevant large animal model of poly-trauma/hemorrhagic shock, and whether the protective effects are executed through the Akt survival pathway. METHODS: Yorkshire swine were subjected to a poly-trauma protocol including: (1) Pre-hospital phase- Femur fracture, 60% hemorrhage, 30 min of shock (mean arterial pressure [MAP]: 25-30 mmHg), and infusion of 154mM NaCl (3 x shed blood); (2) Early hospital phase A Grade V liver injury (simulating rupture of a previously contained hematoma) followed by liver packing; (3) Treatment/monitoring phase randomization to 3 treatment groups (n = 6-8/group): no treatment (control), fresh whole blood (FWB), and intravenous VPA (400 mg/kg, given during the pre-hospital phase). Animals were monitored for 4 h, with survival being the primary endpoint. Liver tissue was subjected to Western blot analysis. RESULTS: FWB (n = 6) and VPA treatments (n = 7) significantly increased survival (100% and 86%, respectively) compared to control group (n = 8) (25%). The protocol produced significant anemia (Hb<6 g/dL) and lactic acidosis (lactate 3-5 mmol/L). Acidosis improved after blood transfusion and worsened in the other two groups. VPA treatment increased phospho-Akt (activated), phospho-GSK-3beta (Glycogen synthase kinase 3beta), beta-catenin and Bcl-2 (B-cell leukemia/lymphoma 2) protein levels compared to control group (P = .01, .01, .03, and .02, respectively). There was no significant difference in the level of these proteins between the control and FWB groups. CONCLUSION: Treatment with VPA without blood transfusion improves early survival in a highly lethal poly-trauma and hemorrhagic shock model. The survival advantage is due not to improvement in resuscitation but to better tolerance of shock by the cells, in part due to the preservation of the Akt survival pathway.