Trauma Anaesthesia Dr James Peerless December 2013

Approaching Trauma Airway + c-spine control Breathing Circulation Disability Exposure Multidisciplinary approach

Session Learning Points Shock Damage Control Resuscitation GSTT Major Haemorrhage Protocols

Shock

“Tissue and organ perfusion is not sufficient to meet metabolic demand” Haemorrhagic Non-haemorrhagic – Neurogenic – Anaphylactic – Cardiogenic – Septic

CLASS ICLASS IICLASS IIICLASS IV Blood Loss (mL) < >2000 Blood Loss (% blood vol.) < >40 Pulse< >140 BPNN  Pulse pressureN/   RR >35 Urine Output (mL.hr -1 ) > Negligible GCSSlight anxietyMild anxietyAnxious, confused Confused, lethargic

Recognition of Shock Recognition and initialisation of treatment important – Haemostasis and fluid replacement Beware occult haemorrhage – “on the floor and four more” Long bones Retroperitoneum Chest Pelvis

Fluid Resuscitation Fluid resuscitation delivery determined by Hagen-Poiseuille ΔP – level 1 infuser r/l – large bore, short cannula η – warm blood to reduce viscosity

Which Cannula? CannulaGaugeMax. flow rate (mL.min -1 ) Blue22G30 Pink20G60 Green18G90 Grey16G200 Orange14G300

Fluid Resuscitation Level One Infuser – Combined heat and pressured fluid delivery system – Max. flow 1400mL min -1 Cell Salvage

Damage Control Resuscitation

Concept of Damage Control Resuscitation Previously accepted concepts of trauma resuscitation challenged during Iraq and Afghanistan Wars Mortality amongst injured US servicemen: – First Gulf War (1990-1) – 24% – Afghanistan and Iraq – 10% Transferable concepts in civilian practice

The Lethal Triad

Acidosis – Hypoperfusion  reduced D a O 2  switch to anaerobic metabolism Lactate production Metabolic acidosis AVOID HYPOTHERMIA ACIDOSIS COAGULOPATHY

The Lethal Triad Hypothermia – Core temperature <35°C is independent predictor of mortality – Exposure – Administration of cold IV fluids – Heat production limited by anaerobic metabolism AVOID HYPOTHERMIA ACIDOSIS COAGULOPATHY

The Lethal Triad Acute Coagulopathy – Coagulopathy on arrival at hospital associated with a four-fold increase in mortality – Procoagulant losses secondary to bleeding and consumption – Dysfunction secondary to hypothermia and acidosis – More complex mechanisms triggered by hypoperfusion and tissue injury AVOID HYPOTHERMIA ACIDOSIS COAGULOPATHY

Management Strategies

Permissive Hypotension Strategy of restricting fluid administration until haemorrhage becomes controlled Accept a period of suboptimal end-organ hypoperfusion SBP < 90, palpable radial pulse Caveat to this: – Head injuries – maintenance of cerebral perfusion pressure highly important.

Haemostatic Resuscitation Treatment of coagulopathy perhaps the most important corner of the triad Treatment strategies: – Fresh frozen plasma – Platelets – Recombinant Factor VIIa – Cryoprecipitate – Tranexamic acid – Calcium

Blood Products Packed Red Cells – No. infective complications and MOF increases with age of stored blood – Shelf-life PRCs 6 weeks; risk significantly increased after 2 weeks if being transfused >6 units of blood FFP – Current military practice to give as 1:1 ratio (packs) – Attenuates the acute coagulopathy – One trial: mortality reduced by 46% when compared with 1:8 ratio (Borgman et al., 2007)

Blood Products Platelets – Also 1:1 ratio, as this approximates whole blood – In the civilian setting, this is perhaps impractical 1:5 is advocated in patients requiring massive transfusion Cryoprecipitate – Fibrinogen, Factor VIII, Factor XIII, vW Factor – Aim to maintain Fibrinogen > 1.5 g.L -1

Other Therapies Recombinant Factor VIIa – Factor VII a crucial initial component of the coagulation cascade – Also important as an enhancer of localised haemostasis Calcium – Important cofactor in most of the coagulation cascade – Citrate present as an anticoagulant in blood products Chelates Ca 2+ and exacerbates systemic hypocalcaemia – Maintain ionised Ca 2+ >0.9 mmol.L -1

CRASH-2 & Tranexamic Acid Tranexamic Acid – Synthetic antifibrinolytic: blocks binding sites on plasminogen – Hyperfibrinolysis a feature of acute trauma coagulopathy – Antifibrinolytics therefore have a role to play in trauma TXA known to reduce bleeding in patients in elective surgical patients – Reduction of blood transfusion by one-third This large multi-centre study (RCT) showed that risk of death was significantly reduced in bleeding trauma patients Most benefit found when given within 1h of injury (CRASH-2 trial collaborators, 2010)

Hypothermia Easier to prevent than to correct – Limit exposure – Warm all blood products – Use forced air blankets

Damage Control Surgery Surgical strategy aimed at: – Controlling haemorrhage – Limiting contamination – Restoring normal physiology as soon as possible Restoring anatomical integrity is not the primary aim, e.g.: – Bowel injuries are identified and brought out, not internally anastomosed – Temporary clamping, packing of bleeding areas Planned return to theatre after stabilisation

GSTT Haemorrhage Protocols

GSTT Transfusion Protocols Two pathways for obtaining urgent blood products – Code red – Crash blood

GSTT Transfusion Protocols

Summary Uncontrolled bleeding needs to be identified and acted upon – surgical control, not aggressive resuscitation Early treatment with blood products Prevent hypothermia with forced air blankets and fluid warmers

The End

Reference Jansen JO, Thomas R, Loudon MA et al. Damage control resuscitation for patients with major trauma. British Medical Journal 2009; Borgman MA, Spinella PC, Perkins JG et al. The ratio of blood products transfused affects mortality in patients receiving massive trasfusions at a combat support hospital. J Trauma 2007;63: American College of Surgeons Committee on Trauma. Advanced Trauma Life Support Student Course Manual, Eighth Edition, FAD/Applications/ClinicalGuidance/User/Details.aspx?id=2888 (accessed )