Managing the Trauma Patient Presenting with the Lethal Trial

PRACTICE DEVELOPMENT IN ORTHOPAEDICS AND TRAUMA

Managing the trauma patient presenting with the lethal trial

Nicola Credland University of Hull

Practice development in orthopaedics and trauma

It is essential that orthopaedic and trauma practitioners develop and maintain their own skills and knowledge in order to help improve and deliver quality care for patients. The utilisation of research in practice development is an important part of the process for nurses endeavouring to deliver evidence based practice to improve care and service user experience.

This new series entitled 'Practice development in orthopaedics and trauma' aims to showcase initiatives and innovations in practice development that have transformed delivery of quality care around the world and to provide readers with brief summaries of current thinking in relation to clinical issues that are common features of orthopaedic and trauma nursing practice. The feature will provide readers with a summary of an evidence base with the aim of empowering them to initiate discussion with colleagues and question their own practice. There will be associated CPD activities incorporating self-directed learning that will enhance the series and provide nurses with an opportunity to extend their learning.

The International Journal of Orthopaedic and Trauma Nursing invites contributions from clinical staff, educators and students normally of between 1000 and 2500 words. Items may focus on, but are not restricted to, best practice and practice development initiatives relating to clinical care issues, implementation of research findings and education and development of the workforce in the clinical environment.

INTRODUCTION

Musculoskeletal injury brings with it a pattern of physical trauma that can result in death in

the hours, days and months that follow. It is important that orthopaedic trauma

© 2016, Elsevier. Licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International http://creativecommons.org/licenses/by-nc-nd/4.0/ practitioners have the knowledge and skills to provide care for the injured patient that takes

into account the physiological impact of trauma so that they can deliver best evidence

based care for their patients. An understanding of the actual and potential physiological

response to trauma can help practitioners care for those whose condition deteriorates or

who have recently been transferred from a critical care setting to an orthopaedic ward.

Studies have demonstrated a significant reduction in mortality among patients with

polytrauma within the last 10 years (MacKenzie et al 2007; 2010, Cameron et al 2008).

Advances in medical and surgical care, the emergence of major trauma centres and the

development of trauma systems have been associated with improved mortality (Durham et

al 2006, Brown et al 2010, Sampalis et al 1997, Harris et al 2010). Research suggests that

poly trauma patients managed at a major trauma centre have a significant reduction in

mortality than those patient managed at general hospitals (Cameron et al 2008, McDermott

et al 2007). Advances in trauma care generally and care in major trauma centres have

focused on early management and “damage control” to reduced immediate life threatening

complications.

The “lethal triad” of trauma is a term that describes the relationship between hypothermia,

acidosis, and coagulopathy (Mitre et al 2012, Rotondo et al 1997) that can lead to patient

death following major trauma. The incidence of patients presenting with the trauma triad is

low, but in trauma patients with significant bleeding this combination forms a vicious circle

that can be impossible to recover from (Mitre et al 2012). This has not improved in line with

the improvement in general trauma care and the management and resuscitation of patients

with severe trauma remains controversial.

© 2016, Elsevier. Licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International http://creativecommons.org/licenses/by-nc-nd/4.0/ Orthopaedic and trauma practitioners provide care to individuals following trauma in a

variety of clinical settings and at various stages in the recovery trajectory. The aim of this

paper is to provide practitioners working outside of the intensive care / critical care setting

with an overview of the physiological cascade that can lead to the trauma triad along with

an outline of management. Through an enhanced understanding of these, the practitioner

will be better equipped to provide care to the deteriorating trauma patient receiving care in

the general orthopaedic setting. A list of useful terms is provided in box 1.

Box 1 - Useful terminology relating to the trauma triad

Acidosis – an increased acidity in the blood and other body tissue that causes an acid base

disturbance

Anaerobic respiration – cellular respiration in the absence of oxygen

Coagulation cascade – Two separate pathways, the intrinsic and extrinsic, that join together

to form the common pathway which leads to the clotting of blood through the production

of fibrin in order to achieve haemostasis

Coagulopathy – impairment of the blood’s ability to clot

DIC (Disseminated Intravascular Coagulation) – the widespread activation of the clotting

cascade that causes blood clots to form in the small blood vessels, reducing blood flow and

leading to organ damage

Endogenous – produced within an organism, tissue or cell

Fibrinolysis – the normal breakdown of blood clots that prevents blood clots becoming

problematic

© 2016, Elsevier. Licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International http://creativecommons.org/licenses/by-nc-nd/4.0/ Lactic acid – produced in muscles when they are working anaerobically (without oxygen)

Lactic acidosis – increased amount of lactic acid in the blood caused a drop in the blood pH

Metabolic acidosis – a drop in the blood pH caused by build-up of acid or impaired kidney

function

Permissive hypotension – the use of restricted fluid resuscitation that increases systolic

blood pressure without reaching normal blood pressure

THE LETHAL TRIAD OF TRAUMA

The term “lethal triad” describes the combination of hypothermia, acidosis and

coagulopathy (figure 1). Haemorrhage from injured organs, viscera, bones and soft tissue

reduces the circulating volume leading to a drop in core temperature and a reduction of

oxygen rich blood supply to the tissues. This causes anaerobic metabolism which creates

lactic acid production and metabolic acidosis. Anaerobic metabolism limits endogenous heat

production which exacerbates any existing hypothermia caused by exposure at the scene

and during pre-hospital care and subsequent emergency care and resuscitation (Jansen et al

2009). The combination of acidosis and hypothermia slow the coagulation cascade causing a

loss in clotting ability known as coagulopathy (Moffatt 2012). Coagulopathy prevents

haemostasis and haemorrhaging continues causing further heat loss and hypoxia. The

hypothermia and acidosis continue to deteriorate which further inhibits coagulation and

encourages further haemorrhage.

© 2016, Elsevier. Licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International http://creativecommons.org/licenses/by-nc-nd/4.0/ Studies have reported that a core temperature of less than 35oC on admission is an

independent predictor of mortality in trauma patients. Several studies also suggest a

fourfold increase in mortality when an established early coagulopathy is present (Brochi et

al 2003; 2007, McLeod et al 2003, Maegele et al 2007). When acidosis is present alongside

hypothermia, the impairment of coagulation is exacerbated (Dirkmann et al 2008, Martini et

al 2005, Maani et al 2009).

Insert figure 1 near here

HYPOTHERMIA

Trauma patients may have lost heat through exposure during entrapment, haemorrhage,

administration of cold resuscitation fluids, removal of clothing, exhaustion and a cold

environment (Lundgren et al 2011). Hypothermia is defined as a core body temperature of

less than 35oC (Tortora and Derrickson 2014). Body temperature is regulated by the

hypothalamus via a negative feedback loop. The hypothalamus receives feedback from the

peripheral nervous system and from its own receptors that body temperature has dropped.

This activates heat generating mechanisms to bring the body temperature back within the

normal range. The hypothalamus stimulates skeletal muscles to shiver which ultimately

leads to increased heat production but which uses up the body’s fuel; adenosine

triphosphate (ATP). Blood absorbs this heat and distributes it to other tissues during

circulation. As the body temperature continues to fall and the blood vessels that supply the

skin constrict blood flow is restricted to the vital organs (Tortora and Derrickson 2014). Heat

© 2016, Elsevier. Licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International http://creativecommons.org/licenses/by-nc-nd/4.0/ can also be lost because of decreased blood flow through organs (hypoperfusion) due to

hypovolaemic shock (loss of circulating volume) (Spahn et al 2005). Decreased heat

production alongside impaired circulation means that blood loss can have a rapid and

significant effect on core body temperature. Hypothermia can cause haemoglobin to release

oxygen less readily, reduces cardiac output and can instigate cardiac arrhythmias (Moffatt

2013) which can lead to cardiac arrest.

The reactions of the clotting cascade are all temperature dependant. Both prothrombin

time (PT) and partial thromboplastin time (PTT) increase in hypothermic patients (Dirkmann

et al 2008). The optimum temperature for the activity of clotting factors is 37oC.

Hypothermia prolongs coagulation, leading to increased clotting times and as the

temperature drops, bleeding increases dramatically (Moffatt 2013). Hypothermia therefore

has significant consequences for the trauma patient with one study finding a core body

temperature of less than 32oC associated with a zero survival rate (Jurokovich et al 1987).

Strategies for limiting hypothermia include using warmed blood products and resuscitation

fluids, limiting patients’ exposure time, air warming blankets and warmed oxygen.

ACIDOSIS

The cause of acidosis following trauma is usually inadequate tissue perfusion (the amount of

blood that a tissue is getting from the circulation). In homeostasis, aerobic respiration

provides the energy required for cellular function in the form of ATP. This is reliant on a

supply of oxygen to the tissues that meets their demand. A reduction in oxygen carrying

capacity causes hypoxaemia. Anaerobic respiration then occurs which leads to a metabolic

© 2016, Elsevier. Licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International http://creativecommons.org/licenses/by-nc-nd/4.0/ acidosis usually described as a ‘lactic acidosis’ due to the accumulation of lactic acid (Marieb

2009).

Arguably, the most dangerous effect of acidosis in the trauma patient is coagulopathy.

Normally blood is slightly alkaline with a pH of between 7.35 and 7.45 (Tortora and

Derrickson 2014). The coagulation system does not function in an acidic environment. The

natural qualities of clotting enzymes (activated clotting factors) are altered and when pH

levels drop below 7.3, thrombin generation is impaired and clotting factors break down.

(Sorenson et al 2012). Studies suggest that PT and PTT are increased in acidosis suggesting

that acidosis has a negative effect on both the intrinsic and extrinsic clotting pathways

(Dunn et al 1979). Potant procoagulant drugs cannot work when the pH is low (Mong et al

2003).

Acidosis also decreases cardiac contractility, causes arrhythmias, reduces cardiac output,

causes vasodilation and hypotension and decreases renal and hepatic blood flow

(Withdenthal et al 1968). As the acidosis worsens, cardiac output decreases and

catecholamines (neurotransmitters such as adrenaline and dopamine) become less effective.

Fluid resuscitation with unbalanced crystalloids such as 0.9% normal saline can cause a

metabolic acidosis due to its high concentration of chloride. Administration of sodium

bicarbonate has historically been used to treat acidosis but there is no evidence to support

its effectiveness (Boyd et al 2008). Sodium bicarbonate produces carbon dioxide which can

require large increases in respiratory minute volume (volume of gas inhaled or exhaled per

minute) to clear. It also decreases ionised calcium concentrations which has a negative

effect on cardiac and vascular contractility (Boyd et al 2008).

Coagulopathy refers to an INR (International Normalised Ratio – measure of clotting

efficiency) of greater than 1.5 times normal (Hodgetts et al 2007). Severe tissue damage

such as traumatic amputation and head injuries can result in disseminated intravascular

coagulopathy (DIC). Traumatised tissues activate the clotting cascade in an abnormal way

that causes fibrinolysis (clot breakdown) out of proportion to the injury and in areas distant

to the site of bleeding. DIC is a result of the severe inflammatory response that can occur

following trauma which causes clotting factors to become abnormally active resulting in

small clots being formed in the blood vessels (Johansson et al 2011). The clots obstruct the

blood supply to vital organs causing organ damage and, ultimately, organ failure. DIC uses

up the clotting factors leading to a deficiency of these at a time when they are in greatest

need. This leads to further haemorrhage and compounds the coagulopathy. This lack of

clotting factors can cause failure of haemostasis, haemorrhage from relatively minor injuries,

stroke, limb ischaemia and organ failure (Johansson et al 2011).

Blood loss is further exacerbated by the dilution of clotting factors (dilutional coagulopathy)

when fluid resuscitation is undertaken with fluids that do not contain clotting factors.

DAMAGE CONTROL RESUSCITATION

Damage control resuscitation combines permissive hypotension and haemostatic

resuscitation with damage control surgery (Holcomb et al 2007) (Figure 2). Permissive

hypotension involves fluid resuscitation that is limited to a volume sufficient to maintain a

© 2016, Elsevier. Licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International http://creativecommons.org/licenses/by-nc-nd/4.0/ radial pulse (Martin et al 2005). Blood and blood products are used early as primary

resuscitation fluids to treat acute traumatic coagulopathy and to prevent the development

of dilutional coagulopathy (Duchesne et al 2010). Resuscitation and surgery are undertaken

simultaneously allowing an integrated approach to the management of the severe trauma

patient.

Permissive hypotension

Permissive hypotension is a strategy for restricting fluid resuscitation until haemorrhage is

controlled in order to avoid a rise in blood pressure that is likely to lead to worsening

haemorrhage while accepting a period of suboptimal organ perfusion (Jansen et al 2009).

No published evidence currently exists to support permissive hypotension but the concept

has not been disregarded. Whilst replacing lost volume in patients with self-limiting or

controlled haemorrhage is appropriate, for patients with uncontrolled haemorrhage,

permissive hypotensive combined with expert resuscitation and rapid control of

haemorrhage may be more appropriate. In recognition of the challenges seen in trauma

following combat situations, permissive hypotension has been incorporated into military

trauma management protocols (Hodgetts et al 2007). The National Institute for Health and

Clinical Excellence (NICE) and the Advanced Trauma Life Support Guidelines (2012) support

the need for a balance between end organ perfusion, the risk of exacerbating bleeding and

maintaining an adequate blood pressure. Guidance from NICE regarding the assessment and

management of airway, breathing and ventilation, circulation, haemorrhage and

temperature control in major trauma is due for publication in February 2016.

Haemostatic resuscitation

© 2016, Elsevier. Licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International http://creativecommons.org/licenses/by-nc-nd/4.0/ Proactive management of coagulopathy is crucial to improving the outcome for trauma

patients (Hodgetts et al 2007, Kirkman et al 2008). Common tests such as PT and PTT lack

sensitivity when guiding treatment in such situations and the decision to replace clotting

factors is often a clinical one (Miller 2013,Kirkman et al 2008). In trauma patients expected

to require massive transfusion, administration of fresh frozen plasma (FFP), packed red

blood cells (PRC) and Platelets in a 1:1:1 ratio is associated with improved survival (Miller

2013, Holcomb 2010, Jansen et al 2009).

FFP

Current military practice is to give FFP and PRC in a 1:1 ratio (Miller 2013, Kirkman et al 2008,

Holcomb et al 2007, 2010). A retrospective study of military casualties showed a statistically

significant reduction in mortality for patients (46%) who has been resuscitated with 1:1 ratio

compared to a more conventional 1:8 ratio (Borgman et al 2007).

Platelets

The administration of platelets to RBC in a 1:1 ratio is recommended by military guidelines

(Miller 2013, Borgman et al 2007, Kirkman et al 2008). There is limited evidence to support

this with few studies investigating the high platelet to packed cell ratio (Gunter et al 2008,

Holcomb et al 2008). These studies show improved survival with a 1:1 ratio compared to the

lower rates but further research is needed.

Cryoprecipitate

Fibrinogen deficiency develops before any other clotting derangement. Fibrinolysis carries a

mortality rate of over 50% in severely injured trauma patients (Kashuk et al 2010, Schochl et

al 2009, Theusinger et al 2011). The CRASH -2 trial (Shakur et al 2010, 2011) is the only class

© 2016, Elsevier. Licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International http://creativecommons.org/licenses/by-nc-nd/4.0/ 1 evidence showing a 30-day benefit from using cryoprecipitate or fibrinogen concentrate as

part of resuscitation management. Cryoprecipitate contains fibrinogen, factor VIII, factor XIII

and von Willebrand factor. Current British and European guidelines recommend giving

cryoprecipitate or fibrinogen concentrate if plasma fibrinogen levels drop below 1.0g/l

(Jansen et al 2009).

Damage control surgery

Following major trauma patients lack the physiological reserve to survive complex,

prolonged or reconstructive surgery. The aim of damage control surgery is to restore normal

physiology, not anatomical integrity. Haemorrhage is stopped by temporary clamping,

packing, shunting or ligation and hollow injuries are closed or resected without anastomosis

(Jansen et al 2009). Unstable musculoskeletal injuries are stabilised using minimally invasive

techniques such as external fixation (Roberts et al 2005).Planned re-operation to definitively

restore anatomy and achieve definitive repair is undertaken when normal physiology

returns. Damage control surgery is associated with potential morbidity and should not be

carried out in isolation. There is currently no evidence to support its use despite being an

accepted part of the trauma patient’s management (Ball 2014).

Insert figure 2 near here

COMPLICATIONS ASSOCIATED WITH THE RESUSCITATION OF THE TRAUMA PATIENT

Following the initial resuscitation there are numerous complications which can affect the

major trauma patient. The management of early post resuscitation complications can affect

mortality and morbidity.

Transfusion related acute lung injury (TRALI) is the leading cause of blood transfusion

related mortality (Vamvacas 2010). Typically TRALI occurs within six hours of a blood

transfusion with no evidence of circulatory overload or alternative risk factors. Patients

present with acute onset hypoxaemia and bilateral infiltrates on chest xray. ICU admission is

required for invasive ventilation and monitoring. Transfusions should be limited to avoid

worsening outcomes. In patients where it is not appropriate to restrict transfusion

avoidance of plasma with pathogenic antibodies, administration of washed blood products

and use of products with the shortest length of storage are recommended (Vamvakas 2010).

Transfusion- associated circulatory overload (TACO) is the second most common cause of

transfusion related mortality (Narick 2012, Popovsky 2009). TACO does not rely on large

volume transfusion and is seen particularly in children and the elderly. Treatment involves

supportive care, diuretic therapy for hypervolaemia and reduced infusion rate for future

transfusions.

Complications of fluid resuscitation

Reperfusion injury occurs when perfusion is re-established to an area that has been

ischaemic. In tissues which have been without oxygen, cellular mechanisms are disrupted.

When the circulation is restored these conditions result in oxidative damage which initiates

the inflammatory response and involves the mechanisms of apoptotic cell death (Tortora

and Derrickson (2014). These factors can lead to acute respiratory distress syndrome (ARDS)

and multi organ failure.

RENAL AND ELECTROLYTE COMPLICATIONS

© 2016, Elsevier. Licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International http://creativecommons.org/licenses/by-nc-nd/4.0/ Rhabdomyolysis is the elevation of serum creatinine kinase (CK) due to the destruction or

disintegration of striated muscle (Huerta-Alardin et al 2005). Muscular trauma is the most

common cause with 10-50% of patients developing acute renal failure (Ward 1998, Better et

al 1997). Muscular trauma may be as a result of compartment syndrome. CK and myoglobin

levels are used to diagnose and monitor patients with rhabdomyolysis. Treatment involves

early and aggressive fluid resuscitation to achieve a target of 100-200mls urine per hour

(Shere-Wolfe et al 2012). Renal replacement therapy may be required for those patients

concurrently suffering acidosis and hyperkalaemia. With appropriate treatment CK levels

rise within the first 12 hours of injury, peak by 3 days and fall 3-5 days following that

(Huerta-Alardin et al 2005).

Both hyperkalaemia and hypocalcaemia can become deranged due to resuscitation from

haemorrhage and hypovolaemic shock. Hyperkalaemia should be promptly treated with

insulin, glucose and calcium to protect the myocardium and increase the shift of potassium

into the cells. Renal replacement therapy is indicated for life threatening hyperkalaemia

with or without renal failure.

Hypocalcaemia occurs due to the binding of calcium to citrate preserves in blood products.

It can contribute to hypotension and haemostasis and should be treated promptly.

HYPERGLYCAEMIA

Elevated glucose levels are very common in critically injured trauma patients and are a

response to injury and stress. This is caused by acute metabolic and hormonal changes such

as increased cortisol, glucagon, catecholamines, growth hormone, gluconeogenesis (the

© 2016, Elsevier. Licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International http://creativecommons.org/licenses/by-nc-nd/4.0/ formation of glucose from non carbohydrate substances) and glycogenolysis (the

breakdown of glycogen to glucose). Strict glucose control has been associated with

improved mortality and morbidity (DuBose et al 2011). Maintaining blood glucose between

4.4-5.6mmol/L has been shown to decrease length of stay and mortality (Eriksson et al

2011).

INTRA-ABDOMINAL HYPERTENSION (IAH) AND ABDOMINAL COMPARTMENT SYNDROME

(ACS)

Damage control resuscitation and damage control surgery have improved our

understanding of IAH and ACS. IAH is an elevation of intra-abdominal pressure >12mmHg

and ACS the elevation of intra-abdominal pressure >20mmHg that are associated with end

organ dysfunction (Mohmand et al 2011). Hypothermia, acidosis, anaemia and blood

transfusion all increase the risk of ACS. Both IAH and ACS can cause cardiac failure due to

vena cava compression and reduced venous return. Oliguria can occur due to compression

of the intra-renal blood vessels (Mohmand et al 2011, Balogh et al 2011, Barnes et al 1985).

Management includes prompt diagnosis using transduced urinary bladder pressure

(Mohmand et al 2011). There are few non-surgical options available and in most cases

prompt opening of the abdomen is the only method for restoring end organ function

(Leppaniemi 2009).

SUMMARY

This article has explored the initial and continued management of the trauma patient

presenting with the triad of trauma and the major clinical challenges have been identified.

The last 10 years has seen major changes in the way this group of patients are resuscitated,

© 2016, Elsevier. Licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International http://creativecommons.org/licenses/by-nc-nd/4.0/ but there is still work to be done. Despite improvements in trauma care, mortality in

patients with the triad of trauma remains high. Nurses caring for trauma patients need to

understand the relationship between acidosis, hypothermia and coagulopathy in order to

identify and treat patient presenting with the lethal triad of trauma.

Table 1 Resources for further learning : the trauma triad

Resource Notes General Resources Ball C (2014) Damage Control Resuscitation: history, Ball reviews the current evidence base theory and technique Canadian Journal of Surgery 57(1) surrounding the use of damage control 55-60 resuscitation in the trauma population

Moffatt S (2012) Hypothermia in trauma Emergency Moffatt explores the pathophysiology of Medicine Journal 30:989-996 hypothermia as a contributor to the triad of trauma and the role that hypothermia has to play in the management of the trauma patient Mitra B, Tullio F, Cameron PA, Fitzgerald M (2012) Mitre et al undertake a retrospective, Trauma patients with the 'triad of death Emergency explicit chart review of patient presenting Medical Journal 29(8):622-5 with the triad of trauma

Shere-Wolfe R, Galvagno S, Grissom T (2012) Critical care Shere-Wolfe explores the management of considerations in the management of the trauma patient the critically ill trauma patient using a non- following initial resuscitation Scandinavian Journal of systematic literature review approach Trauma, resuscitation and emergency medicine 20:68

Continuing professional development It is essential that orthopaedic and trauma practitioners develop and maintain their own skills, knowledge and competence in order to improve and deliver safe, high quality care for patients and service users. This section is intended to provide a CPD learning opportunity, helping to support the requirements of your professional bodies in terms of lifelong learning. Continuing professional development serves as a catalyst in helping you to reflect upon and evaluate your practice. This learning activity may support you to make changes to the way you work so that you can improve the quality of care and services you provide. Alternatively, it may endorse existing practice meaning that you work as you did before, but you are more confident that your practice is safe, effective and responsive to the needs of your patients and service users (Health Care Professional Council, 2012).

Activity: Reflection Reflection on your own standard of practice is an integral part of your development. You should reflect on what you have learnt from this article in terms of the trauma triad and its assessment and consider the impact on your patients and the areas in which you work. (Nursing & Midwifery Council, 2011). A useful approach to this may be to write a reflective account of a patient’s care who has been at risk of or experienced the trauma triad. See Box 2 for further guidance.

Health care professionals have a key role in musculoskeletal assessment and management. This article together with the reflective exercise and further reading is designed to maximize the existing knowledge and skills of health care professionals and help them to undertake evidence-based accurate assessment of musculoskeletal injury.

Box 2 Reflection guide (adapted from Gibbs et al. 1998) Description Explain what you are reflecting on; describe your learning expectations and prior knowledge of musculoskeletal assessment in the trauma patient. Feelings Discuss your personal thoughts and feelings about your experiences of caring for the severely injured/polytrauma patient in your area of practice. Have your opinions about how the severely injured/poly trauma patient is managed changed after reading this article? Evaluation What did you learn? What was helpful, what was missing, how did it make you feel? Analysis What did you gain from reading this article; did it meet your expectations? How does the information in this article relate to your current practice? Is there further evidence you need to gather relating to caring for the trauma patient? What are the potential implications for practice? Conclusion Summarise your thoughts, what are your general and personal conclusions about management of the patient following severe trauma/polytrauma and why? Action Plan Use your reflection to initiate a discussion/debate on management of the trauma patient with your colleagues. Recommendations for good practice? What will you do differently? How will you disseminate any recommendations to the multi-disciplinary team?

Ball C (2014) Damage Control Resuscitation: history, theory and technique Canadian Journal

of Surgery 57(1) 55-60

Balogh ZJ, Malbrain M (2011) Resuscitation in intra-abdominal hypertension and abdominal

compartment syndrome American Surgery 77: S31-33

Barnes GE, Laine GA, Giam PY, Smith SS, Granger HJ (1985) Cardiovascular responses to

elevation of intra-abdominal hydorstatic pressure American Journal of Physiology 248: R208-

213

Better OS, Rubinstein I (1997) Management of shock and acute renal failure in casualties

suffering from the crush syndrome Renal Failure 19: 647-653

Boyd JH, Walley KR (2008) Is there a role for sodium bicarbonate in treating lactic acidosis

from shock? Current Opinion in Critical Care 14: 379-383

Brohi K, Cohen M, Davenport R (2007) Acute coagulopathy of trauma: mechanism,

identification and effect Current Opinion in Critical Care 13:680-685

Brohi K, Singh J, Hern M, et al (2003) Acute traumatic coagulopathy. Journal of Trauma.

54:1127–30.

Borgman MA, Spinella PC, Perkins JG, et al (2007) The ratio of blood products transfuse

affects mortality in patients receiving massive transfusions at a combat support hospital.

Journal of Trauma. 63:805–13.

© 2016, Elsevier. Licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International http://creativecommons.org/licenses/by-nc-nd/4.0/ Brown J, Stassen N, Bankey P et al (2010) Helicopters and the civilian trauma system:

national utilisation patterns demonstrate improved outcomes after traumatic injury Journal

of Trauma 69; 1030-1036

Cameron P, Gabbe B, Cooper D et al (2008) A statewide system of trauma care in Victoria:

effect on patient survival Medical Journal of Australia 189: 546-550

Dirkman D, Hanke A, Gorlinger K et al (2008) Hypothermia and acidosis synergistically impair

coagulation in human whole blood Anaesthetics Analogue 106: 1627-1632

Duchesne JC, McSwain NE Jr, Cotton BA, Hunt JP, Dellavolpe J, Lafaro K, Marr AB, Gonzalez

EA, Phelan HA, Bilski T, Greiffenstein P, Barbeau JM, Rennie KV, Baker CC, Brohi K, Jenkins

DH, Rotondo M (2010) Damage control resuscitation: the new face of damage control

Journal of Trauma 69: 976-990

Durham R, Pracht E, Orban B et al (2006) Evaluation of a mature trauma centre Annals of

Surgery 243: 783-785

Dunn E, Moore E, Breslich D et al (1979) Acidosis induced coagulopathy Surgical Forum 30:

471-473

DuBose JJ, Scalea TM (2011) Glucose elevations and outcome in critically injured trauma

patients Advances in Surgery 45:187-196

Eriksson EA, Christianson DA, Vanderkolk WE, Bonnell BW, Hoogeboom JE, Ott MM (2011)

Tight glucose control in trauma patients: who really benefits? Journal of Emergency Trauma

and Shock 4: 359-364

© 2016, Elsevier. Licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International http://creativecommons.org/licenses/by-nc-nd/4.0/ Gunter OL, Au BK, Isbell JM, Mowery NT, Young PP, Cotton BA (2008) Optimising outcomes

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Harris T, Davenport R, Hurst T et al (2010) Improving outcomes in severe trauma: trauma

systems and initial management – intubation, ventilation and resuscitation Postgraduate

Medical Journal doi:10.1136/pgmj.2008.074245

Hodgetts T, Mahoney P, Kirkman E (2007) Damage control resuscitation Journal of the Royal

Army Medical Corps 153: 299-300

Holcomb JB, Jenkins D, Rhee P, et al. (2007) Damage control resuscitation: directly

addressing the early coagulopathy of trauma. Journal of Trauma. 62:307–10.

Holcomb JB (2010) Optimal use of blood products in severely injured trauma

patients. Hematology Am Soc Hematol Educ Program 2010 465–469.

Johansson P, Sorenson A, Perner A et al (2011) Disseminated intravascular coagulopathy or

acute coagulopathy of trauma shock early after trauma? An observational study Critical Care

15: 272-282

Huerta-Alardin AL, Varon J, Marik PE (2005) Bench to bedside review: Rhabdomyolysis – an

overview for clinicians Critical Care 9: 158-169

Jurkovich GJ, Greiser WB, Luterman A et al (1987) Hypothermia in trauma victims: an

ominous predictor of survival Journal of Trauma 27: 1019-1024

© 2016, Elsevier. Licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International http://creativecommons.org/licenses/by-nc-nd/4.0/ Jansen J, Thomas R, Loudon M, Brooks A (2009) Damage control resuscitation for patients

with major trauma British Medical Journal 338: b1778

Kirkman E, Watts S, Hodgetts T, Mahoney P, Rawlinson S, Midwinter M (2008) A proactive

approach to the coagulopathy of trauma : the rationale and guidelines for treatment Journal

of the Army Medical Corps 153: 302-306

Kashuk JL, Moore EE, Sawyer M, Le T, Johnson J, Biffl WL, Cothren CC, Barnett C, Stahel P,

Sillman CC, Sauaia A, Banerjee A (2010) Post injury coagulopathy management: goal

directed resuscitation via POC thrombelastography Annals of Surgery 251: 604-614

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COAGULOPATHY

METABOLIC

HYPOTHERMIA Decreased myocardial performance ACIDOSIS

Figure 1 – The lethal triad of hypothermia, acidosis and coagulopathy

Damage Control Resuscitation

Permissive Hypotension Haemostatic Resuscitation Damage Control Surgery

Figure 2 – The Damage Control Resuscitation Paradigm