Background
Major haemorrhage is a life-threatening event. Haemorrhagic shock accounts for 50% of deaths in the first 24 hours following trauma, and 80% of deaths in the operating theatre are due to haemorrhage. Knowledge of major haemorrhage and its management is important for the anaesthetist, as the patient is critically ill, requires advanced resuscitation, and often usually requires therapeutic intervention involving general anaesthesia. This case study will highlight the issues of major haemorrhage and outline the steps required to reduce morbidity and mortality and thus optimize patient outcome.
Learning outcomes
1 Understand the pathophysiology of major haemorrhage
2 Understand the rationale of management by simultaneous resuscitation and haemorrhage control
3 Make appropriate choice of fluids, blood products, and drugs in managing major haemorrhage
4 Understand the rationale for a local major haemorrhage protocol
5 Recognize the sequelae of major haemorrhage and massive transfusion.
CPD matrix matches
2A02; 2A05
Case history
A 20-year-old man was the driver of a car that was struck side-on by a lorry travelling at approximately 60 miles/hour. Whilst entrapped in the vehicle, he remained conscious, complaining of pain in his lower abdomen. He was placed in a hard collar, had an IV cannula sited, and observations monitored before extrication, showing a respiratory rate (RR) of 18/min, an oxygen saturation (SpO2) of 95%, a heart rate (HR) of 110, and a blood pressure (BP) of 90/60 mmHg. He was transferred to the emergency department (ED) within a major trauma centre. In the ambulance, his systolic BP decreased to 70 mmHg on three occasions but responded to a bolus of 250 mL 0.9% NaCl on each occasions, resulting in a systolic BP of 90–95 mmHg.
You are a member of the trauma team in the ED. Primary survey reveals a conscious, pale young man who is:
◆ A: talking coherently
◆ B: RR of 22 breaths/min, saturation of 95%, clear chest, and normal chest X-ray (CXR)
◆ C: pulse of 120/min, BP 75/40, capillary refill time (CRT) 4 s, heart sounds I + II, tender lower abdomen, and deformed pelvis
◆ D: GCS 15, pupils equal and reactive, BM 6.0
◆ E: temperature 35.9°C.
What features of this case suggest haemorrhage, and how can its severity be graded?
Trauma is a mechanism of injury that is associated with vascular disruption, organ rupture, and long bone fracture, leading to loss of blood from the vasculature. Haemorrhage should be suspected and actively excluded in all trauma patients. Sites for blood loss are ‘the floor plus four,’ i.e. external, thorax, abdomen, pelvis, and femur.
The clinical signs of acute blood loss preceding the loss of pressure in the vasculature are the compensatory changes that occur to maintain oxygen delivery to body tissues, including increased ventilation, increased HR, and a reduction of perfusion initially to non-essential organs, including skin and kidneys. Then the perfusion of vital organs is reduced, e.g. reduced cerebral perfusion which is revealed by an altered conscious level. These signs occur progressively as blood loss increases and have been grouped into the four stages of hypovolaemia (see Table 2.1).
Table 2.1 The stages of hypovolaemic shock in adults
From Table 2.1, it should be appreciated that the first signs of blood loss may be subtle but denote significant loss. BP does not drop until 1.5 L have been lost and is a late sign denoting failure of compensatory mechanisms to maintain pressure in the vasculature.
Major haemorrhage has been defined by various criteria, including:
◆ Adult patients:
• Any life-threatening bleed
• The loss of one circulating volume in a 24-hour period
◆ Obstetric patients:
• The loss of 1500 mL, the requirement of >4 U of red cells, or a drop in Hb concentration of 40 g/L
◆ Paediatric patients:
• The actual or anticipated loss of 40 mL/kg of blood.
Measurement of Hb concentration is a poor indicator of blood loss in early haemorrhage, as blood remaining within the vasculature will likely have near-normal Hb concentration.
As organ perfusion and oxygen delivery worsen, cells will begin anaerobic metabolism, resulting in lactic acid production. Serum lactate and base deficit measurements are sensitive in estimating the degree of bleeding and shock.
Case update
The patient is given 500 mL of crystalloid which returns his systolic BP to 85 mmHg.
A pelvic binder device is applied, following the IV administration of 5 mg of morphine. He is not catheterized, because of blood in the urethral meatus.
He has a bedside HemoCue® performed which shows Hb 100 g/L, and an ABG shows lactate 3.0 mmol/L, base deficit 3.0 mmol/L, and hydrogen ion (H+) of 48 nmol/L. Venous blood is drawn and sent for full blood count (FBC), urea and electrolytes (U&E), coagulation screen, and cross-match for 4 U of packed red cells (PRC). The ED consultant informs blood transfusion service (BTS) that a major haemorrhage is likely to be present.
What are the pathophysiological features of a major haemorrhage?
◆ Hypovolaemia: the loss of volume of blood from the vasculature results in reduced intravascular pressure and reduced organ perfusion, resulting in cellular hypoxia, acidosis, and organ dysfunction
◆ Anaemia: oxygen carriage is dependent upon Hb concentration. A low concentration of Hb results from the loss of red cell mass and physiological measures that increase water reabsorption, including the action of aldosterone and vasopressin. Volume resuscitation with clear fluids will further reduce the Hb concentration, thus reducing the oxygen-carrying capacity of the blood, contributing to cellular hypoxia and acidosis
◆ Acute coagulopathy of trauma (ACoT): this is associated with a higher risk of mortality and may be due to several mechanisms, including:
• Consumption
• Dilution
• Protein C activation
• Hyperfibrinolysis
• Hypocalcaemia
• Drugs, including anticoagulants and antiplatelet medications
• Hypothermia
◆ Acidosis: this is the end result of anaerobic metabolism. The change in pH within cells will lead to enzyme dysfunction and uncoupling of the processes which maintain ion gradients that, in turn, maintain cell activities
◆ Free radical formation: under stress conditions, there is failure of the electron transport chain to fully reduce oxygen to water. The resulting oxygen species are charged free radicals that cause irreversible damage to mitochondria.
The combination of coagulopathy, acidosis, and hypothermia is often referred to as the ‘triad of death’ in trauma, as they increase the risk of mortality.
What are the priorities in managing this patient with suspected pelvic fracture and major haemorrhage?
Optimal management of major haemorrhage should be aimed at the cessation of blood loss with concurrent resuscitation. This process is a continuum, beginning in the pre-hospital environment and continued in the ED, theatre, and intensive care unit (ICU). Unnecessary delays in achieving haemostasis should be avoided, as these will adversely affect outcome.
The trauma patient may have multiple life-threatening injuries, including thoracic, cervical spine, neurological, and intra-abdominal injuries, and long bone fracture. The primary survey is a means of rapidly assessing for life-threatening injuries, with an intrinsic order of prioritization that should allow recognition and management of the most pressing injury, before attention is directed to the next. It has been traditionally taught as ‘ABCDE’.
In the immediate pre-hospital environment, control of catastrophic external haemorrhage has become the first priority, before cervical spine control, airway, breathing, and circulation (C-A-B-C). The Combat Application Tourniquet (CAT) is a device that can be applied rapidly to prevent exsanguination from an injured limb.
Unstable skeletal cervical spine injury may lead to devastating injury to the spinal cord, and anyone with neck symptoms, or a mechanism consistent with a cervical spine injury, should have their cervical spine immobilized. This can be achieved rapidly with two-hand manual in-line stabilization, then replaced with a rigid collar, blocks, and tape (triple immobilization).
Airway management and breathing are aimed at optimizing the oxygenation of blood and include the administration of high-flow oxygen, intubation for respiratory failure, and management of life-threatening intrathoracic injuries.
The ‘circulation’ aspect of the primary survey is aimed at identifying and resuscitating shocked patients, i.e. those with failure of delivery of oxygen to their tissues. Circulatory failure has four mechanisms whereby the pressure in the arterial vasculature can be diminished (see Table 2.2).
Table 2.2 Types of shock
| Mechanism of shock | Examples |
|---|---|
|
Hypovolaemia |
Major haemorrhage |
|
Cardiogenic |
Myocardial contusion, arrhythmia |
|
Obstructive |
Cardiac tamponade, tension pneuomnthorax |
|
Distributory (vasodilatory) |
Septic shock, neurogenic shock |
In trauma, hypovolaemia is the most common cause of shock and should be actively sought and managed as the most likely cause. The priorities in managing the hypovolaemic patient are:
1 Haemostasis: the process of stopping further blood loss, including:
(a) Immediate measures: various methods are available to rapidly reduce blood loss. These include direct pressure over a bleeding wound, limb tourniquets, pelvic binders, and femoral traction devices (see Figure 2.1a–c). If a suitably qualified surgeon is present, abdominal packing or aortic cross-clamping may be employed, if deemed necessary
(b) Investigation to confirm haemorrhage: the practice of ultrasonography in ED to confirm haemorrhage is growing, but CT scanning has better sensitivity and specificity, and, in the multiply injured patient, full body CT scanning is the most rapid means to achieve a definitive diagnosis of their injuries. Unstable patients with suspected haemorrhage may need immediate transfer to theatre without imaging
(c) Definitive control: this has traditionally been performed surgically, but interventional radiology is being increasingly employed
2 Resuscitation: to occur simultaneously with the process of confirming haemorrhage and achieving haemostasis. The overall aim is the improvement in oxygen delivery to tissues to reduce acidosis. Resuscitation consists of:
(a) Improving intravascular volume
(b) Optimizing Hb concentration with red cell transfusion
(c) Prevention and managing coagulopathy
3 Minimizing delays at all stages of the care pathway.
Fig. 2.1 Devices for immediate haemorrhage control, rapidly applied to reduce haemorrhage. (a) Combat Application Tourniquet. (b) Pelvic-binding device. (c) Femoral traction device.
The patient’s pelvic fracture is suspected from the mechanism of injury and clinical signs. Pelvic fracture is associated with major haemorrhage due to the associated vascular disruption of bones and pelvic vessels.
The immediate measure to reduced blood loss was achieved by the pelvic binder to reduce the volume of the pelvic cavity and encourage tamponade of the bleeding vessels. Simultaneously, resuscitation by means IV volume restoration was instituted.
Investigation of the polytrauma patient is ideally carried out by whole body imaging with CT scanning. The advantage is this allows a rapid identification of all injuries in one investigation. However, it requires the patient to have a degree of cardiovascular stability, as it requires transfer to the radiology suite and limits access to the patient during the scan. Severely unstable patients are unable to undergo CT scanning for these reasons. In such cases, the site of haemorrhage can be identified from clinical findings and bedside radiology tests, including CXR, pelvic X-ray, and focussed assessment sonography in trauma (FAST) scan. Transfer to theatre on confirming the site of haemorrhage should be prompt to minimize delays in definitive haemostatic control.
How should this patient be resuscitated in terms of fluids, blood products, and drugs?
Initial fluid and patient response
The aim of fluid resuscitation is the improvement in organ perfusion via an increase arterial pressure.
NICE guidelines recommend the administration of IV fluids in the pre-hospital setting only when the radial pulse has diminished. The loss of a radial pulse is traditionally said to occur when the systolic pressure falls below 80 mmHg. Crystalloid 250 mL boluses are advised until the return of the radial pulse. This strategy is known as hypotensive resuscitation, aimed at reducing the stress on fragile fibrin clots to prevent secondary haemorrhage.
Advanced trauma life support (ATLS) teaching on fluid administration advocates 1–2 L of warmed crystalloid to the hypovolaemic trauma patient. European guidelines agree with the initial use of crystalloids. A rise in BP and a reduction in HR are used to assess for improvement in response to fluid, as they reflect a reduction in the need of the cardiovascular system to compensate for low blood volume; such patients are labelled as ‘fluid responders.’ This response may be: (1) sustained or (2) transient, with the latter more likely to have an ongoing haemorrhage. The third group is labelled as ‘non-responder,’ indicating that the haemorrhage is so profound and ongoing that fluid therapy does not expand blood volume to improve BP or allow a reduction in HR. Fluid non-responders may have another reason for their profound shock, and causes such as tension pneumothorax or cardiac tamponade should be excluded. Based on fluid responsiveness, the urgency blood products and surgical intervention can be predicted (see Table 2.3).
Table 2.3 Stratifying patients according to fluid response
Blood pressure target
Whilst aiming to restore an arterial pressure consistent with organ perfusion, it should be noted that overly aggressive fluid resuscitation and elevation of arterial pressure can increase bleeding by clot disruption, coagulation dilution, and hypothermia. The concepts of ‘low volume’ and ‘hypotensive’ resuscitation aim to minimize fluid administration before definitive haemostasis. Minimal volume resuscitation is preferable to aggressive volume resuscitation, before active bleeding has been controlled. There is insufficient evidence to determine an optimal BP level during active haemorrhagic shock, but European guidelines recommend a target systolic BP of 80–100 mmHg in those without traumatic brain injury. If brain injury is suspected, then maintenance of cerebral perfusion pressure (CPP) by achieving a normal mean arterial pressure (MAP) is recommended.
Blood product use
The continual administration of crystalloid or colloid fluids will expand the intravascular volume and improve BP but has no oxygen-carrying capacity and will dilute Hb, clotting factors, and platelets. Thus, with ongoing haemorrhage, the need for administration of red cells, clotting factors, and platelets becomes increasingly likely to sustain oxygen delivery and haemostasis.
Red cell replacement
Hb concentration is central in determining arterial oxygen concentration in non-hyperbaric conditions, according to the formula:
(where 0.003 represents the solubility constant for dissolved oxygen in plasma, i.e. 0.003 mL oxygen/PO2 in mmHg/dL)
The corresponding figure in kPa is 0.023, i.e.
It is not possible to determine the optimal Hb levels in patients with traumatic haemorrhagic shock, because no studies have assessed the relationship between Hb levels and the adverse outcomes in patients with traumatic haemorrhage. The European guidelines produced by the Task Force for Advanced Bleeding Care in Trauma in 2010 recommend a target Hb of 70–90 g/L. Near-patient testing can rapidly quantify Hb concentrations and reduce delays in the decision to transfuse. Fully cross-matched blood is preferable, but clinical urgency may necessitate the use of group-specific or O-negative units to optimize Hb.
Clotting factors and platelets
Monitoring and measures to control coagulopathy should be undertaken as early as possible. Traditional means of assessing coagulation have consisted of measuring PT (or international normalized ratio, INR), APTT, fibrinogen concentration, and platelet concentration. These parameters, although widely used, reflect only the early stage of clot formation, provide no information on clot strength, and provide no information on fibrinolysis. TEG is a technique that provides near-patient assessment of the kinetics, strength, and dissolution of blood clotting. It is used routinely in cardiothoracic anaesthesia to rapidly identify the likely cause of coagulopathy and guide decision making in product administration and is increasingly used in other settings, including obstetric haemorrhage, major vascular surgery, and trauma.
FFP administration should begin as soon as possible, following red cell transfusion, initially 10–15 mL/kg. Further FFP can be administered if PT ratio or APTT ratio are >1.5.
Platelet transfusion is recommended when their concentration is <50 × 109/L, or <100 × 109/L in traumatic brain injury.
Fibrinogen deficiency is treated with fibrinogen concentrate or cryoprecipitate. The target range for treatment during active bleeding is 1.5–2.0 g/L.
Drugs
Tranexamic acid is a drug with several mechanisms of action, including inhibition of fibrinolysis. In a large randomized controlled trial (RCT) of trauma patients (CRASH-2) it was shown to reduce mortality without increasing thromboembolic complications. It should be administered to all haemorrhagic trauma patients as a 10–15 mg/kg loading dose, followed by 1–5 mg/kg over 8 hours (1 g loading dose, followed by 1 g over 8 hours for an average-sized adult). The greatest reduction in haemorrhagic deaths is seen when the drug is administered within 1 hour of injury and is now often administered by pre-hospital trauma teams when transfer to hospital is delayed.
Recombinant factor VIIa has failed to show an improvement in the mortality rate in haemorrhagic shock but is associated with an increased risk of thromboembolic events. It has no place in the routine management of haemorrhagic shock.
Calcium chloride should be administered if ionized calcium levels are deficient.
A new approach
A novel approach to major haemorrhage has been advocated, based on the management of recent battlefield casualties. This approach has advocated the minimization of clear fluids and the early use of red cells, plasma, and platelet units in a ratio of 1:1:1 to improve outcome in trauma, although controversy exists. This evidence has been questioned by the optimum ratio effect of red cells:plasma due to ‘survivor bias’, i.e. that those patients who died early were much more likely to have received a higher ratio of red cells:plasma due to the time factor in thawing and administering plasma. Furthermore, the survival benefit may have been as a result of a highly organized major haemorrhage protocol where delays were minimized.
The optimum ratio of red cells:plasma remains controversial, and further research is warranted on this question. In contrast, early administration of red cells and plasma is not controversial, and the simultaneous early administration of plasma with red cells, as part of a regimented major haemorrhage protocol, likely improves outcomes in major haemorrhage.
Case update
The patient remains haemodynamically stable, with HR 110 and BP 88/50. You decide to transfer him to the radiology suite for whole body CT scanning.
The investigation shows a pelvic fracture with significant blood in the pelvic cavity. The pelvis is fractured, as shown in Figure 2.2:
Fig. 2.2 A three-dimensional reconstruction of a complex pelvic fracture with involvement of the right ilium, right acetabulum, right ramus, pubic symphysis, and left side of the sacrum.
The addition of IV contrast to the study reveals bleeding from a branch of the internal iliac artery.
There is no evidence of primary brain, C-spine, thoracic, intra-abdominal, or other skeletal injuries.
What are the options for definitive haemorrhage control in trauma?
The options for management in haemorrhagic trauma patients are:
1 Non-operative management:
(a) Observation: employed for haemodynamically stable patients when organ preservation is desirable, e.g. splenic laceration
(b) Interventional radiology (IR): a minimally invasive approach to achieve haemostasis in blunt abdominal trauma and pelvic fracture. IR procedures may involve:
(i) Embolization of smaller vessels
(ii) Stent graft placement in larger vessels
2 Operative management: surgical exploration and repair.
Traditionally, surgical exploration and repair have been the means of definitive haemorrhage control. However, the surgical process is a further trauma (‘second hit’) that will evoke a stress response, contributing to cellular dysfunction and increasing the risk of morbidity and mortality.
Benefits of minimally invasive IR include:
◆ Avoiding the stress response associated with laparotomy or pelvic exploration
◆ Better access to the retroperitoneal space and pelvic cavity.
Although originally employed only in the haemodynamically stable patients, IR has been demonstrated to be of benefit in haemodynamically unstable patients with pelvic fracture. This approach now forms part of the trauma protocol for a growing range of haemodynamically unstable injuries associated with blunt abdominal trauma in many centres. Although prospective studies have shown that the number of laparotomies performed in blunt abdominal trauma can be halved with the use of IR, the overall quality of the evidence for interventional radiological and surgical interventions in trauma is poor. The decision on intervention should be made by the consultant in surgical and radiological teams.
Case update
The consultant interventional radiologist, consultant orthopaedic surgeon, and general surgeon discuss the findings of the CT scan whilst you are transferring the patient off the CT scanner. They agree the best management strategy is to use IR to achieve definitive haemostatic control. You transfer the patient to the IR suite along the corridor where you anaesthetize him for the procedure.
During the procedure, you are phoned by the haematology laboratory, with results of FBC and coagulation screen taken just before leaving the ED. They are as follows:
◆ Hb 65 g/L
◆ WCC 7.5 × 109/L
◆ Plt 100 × 109/L
◆ PT ratio 1.7
◆ APTT ratio 1.6
◆ Fibrinogen 2.0 g/L
◆ ABG showing base excess (BE) –4.0 mmol/L, H+ 50 nmol/L, lactate 3.8 mmol/L.
You speak with BTS and request an emergency transfusion pack consisting of 4 U of PRC, 4 U of FFP, and 1 U of platelets.
They inform you that the red cells are ready and will be delivered immediately and they had begun thawing the plasma as soon as the patient’s coagulation results were available, as the major haemorrhage protocol had been activated by the ED consultant.
How has the introduction of a major haemorrhage protocol influenced management and outcome?
The timely and comprehensive delivery of care in major haemorrhage must coordinate the efforts of front-line medical and nursing staff, laboratory biomedical scientists, BTS, and support staff, including switchboard operators and porters. The introduction of major haemorrhage protocols have been shown to improve several markers of quality of care, including reduced exposure to crystalloid, improved temperature control, and better blood product use. Systematic reviews of major haemorrhage protocols have associated full compliance of protocols with improved survival. However, full compliance with protocols has been shown to be poor. Each institution must have a locally agreed major haemorrhage protocol, given their demonstrable benefit. The anaesthetist must be familiar with the content of the local protocol to achieve full compliance and improve survival. A sample generic protocol is shown in Figure 2.3.
Major haemorrhage protocol
To trigger the major haemorrhage protocol (MHP)
1 Phone 2222 and state that there is a major haemorrhage and the location of the patient. Remain on the line whist the switchboard operator transfers your call to Blood Bank. Tell Blood Bank:
• The diagnosis, e.g. ruptured aortic aneurysm, obstetric emergency
• The patient’s details: name, DOB, CHI number (A&E/ARU number for unidentified patients)
• What blood components are required, e.g. red cells, FFP, platelets, and how many units
• How urgently the blood components are required
• The patient’s current location and planned moves
• Your name and contact details
• What samples are being sent to Blood Bank/Haematology and whether they are ready for collection (Blood Bank will inform you whether a sample for blood grouping is required).
Switchboard will inform:
• Porters: a dedicated emergency porter will report to Blood Bank
• Haematology lab and on-call haematology doctor
2 Send the following blood samples with the major haemorrhage porter:
• A sample for blood grouping to Blood Bank (unless Blood Bank have informed you this is not required because they already have a suitable sample)
• FBC and coagulation screen samples to Haematology.
If further blood components are required, contact Blood Bank directly. Send FBC and coagulation screen samples, as indicated. Haematology advice is available from the on-call haematology doctor—via switchboard. When the major haemorrhage is over: inform Blood Bank directly. Red cells can be obtained rapidly from Blood Bank without triggering the MHP.
Contact numbers for Blood Bank in an emergency: MHP trigger 2222; Blood Bank phone 3333; Switchboard 0.
O-negative blood location: inform Blood Bank immediately if used; Blood Bank at each hospital A&E—6 U, labour ward 2 U.
Fig. 2.3 Major haemorrhage protocol example.
Case update
Over the next 40 min, the patient is transfused with the requested blood products, using a rapid infusion device with heating ability. You then send further blood samples to haematology and also an ABG sample.
Meanwhile, the interventional radiologist performs catheterization of the left internal iliac artery, as shown in Figure 2.4a. Good haemostasis is then achieved by the selective embolization of the bleeding vessel (see Figure 2.4b), and the patient remains cardiovascularly stable.
Fig. 2.4 (a) Interventional radiology: contrast-enhanced demonstration of the internal iliac artery. Black arrow indicates bleeding point from a branch of the anterior division, with characteristic ‘blushing’ of contrast.
Fig. 2.4 (b) Interventional radiology: embolization of the bleeding vessel by microcatheterization.
The blood results from samples taken post-transfusion of 4 U of red cells, 4 U of FFP, and 1 U of platelets show Hb 82 g/L, WCC 9.0 × 109/L, Plt 99 × 109/L, H+ 48 nmol/L, BE –4.5 mmol/L, bicarbonate (HCO3–) 15 mmol/L. Despite the use of warmed IV fluids and a warming blanket, his temperature is 35.8°C.
What is ‘damage control’ surgery?
This concept advocates doing minimum surgical intervention to achieve stability, thus minimizing the physiological insult to the patient, who is then given a period of physiological normalization in a level 3 setting. The systemic inflammatory response to trauma and haemorrhage, although increasing oxygen delivery, leads to cellular acidosis and dysfunction. Each iatrogenic intervention, although performed to improve survival, is a further stimulus to this pathophysiological process.
Indications for damage control surgery in the severely injured patient include deep haemorrhagic shock, signs of ongoing bleeding, coagulopathy, hypothermia, acidosis, inaccessible major anatomical injury, a need for time-consuming procedures, or concomitant major injury outside the abdomen.
Following the period of correction and stabilization, the patient may be returned to theatre for more definitive correction of their injuries whilst not in extremis. In this particular case, the patient was acidotic, coagulopathic, and cold, immediately following definitive haemostatic control of the haemorrhage. At this point, to proceed with open orthopaedic stabilization of the trauma would involve further blood loss and a worsening of the metabolic and haematological parameters. The resulting increase of cellular dysfunction would increase the risk of multiorgan dysfunction syndrome (MODS) and death. Hence, with the minimum necessary intervention to preserve life and allow stabilization, the patient should be given a period in which normal physiology is restored to allow further surgery to be carried out under more favourable metabolic conditions.
Case update
Given the patient’s metabolic acidosis, coagulopathy, and anaemia, you arrange intensive care admission with the consultant intensivist.
Over the next 18 hours, he is kept sedated and ventilated. He is warmed to normothermia, receives further blood products to achieve Hb of 8.0, PT ratio <1.5, and APTT ratio <1.5, and 10 mL of 10% calcium chloride to achieve normocalcaemia. His BE gradually returns to –2.0 mmol/L. He does not require inotropic or vasopressor support. His pelvic binder is kept on throughout this period.
The following morning, the orthopaedic trauma team plans to take him to theatre to internally fix his pelvis. This is performed with the loss of 500 mL of blood, but he remains otherwise stable. He is returned to ICU post-operatively for monitoring and correction of his haematological and acid–base disturbance. He is extubated later that day and stepped down to high dependency unit (HDU) care.
Summary
Haemorrhage in trauma is a common, time-critical injury and is responsible for half of all early deaths. The stress response following haemorrhage increases oxygen consumption, whilst reduced Hb and arterial pressure increase oxygen consumption, resulting in tissue acidosis and organ dysfunction. The priorities in the management of major haemorrhage should be directed at the identification and cessation of the bleeding site, with simultaneous resuscitation, whilst avoiding delays. Recent changes in the management of haemorrhagic shock have included the early administration of blood products in preference to clear fluids, early use of tranexamic acid, near-patient testing of Hb and coagulation function, and haemorrhage protocols. Minimizing acidosis, coagulopathy, and hypothermia by resuscitation and damage control surgery should reduce the risk of poor outcomes.
Bouige A, Harrois A, and Duranteau J (2013). Resuscitative strategies in traumatic haemorrhagic shock. Annals of Intensive Care, 3, 1.
Rossaint R, Bouillon, Cerny V, et al. (2010).Management of bleeding following major trauma: an updated European Guideline. Critical Care, 14, R52.
Westerman RW, Davey KL, and Porter K (2008). Assessing the potential for major trauma transfusion guidelines in the UK. Emergency Medicine Journal, 25, 134–5.
Zealley IA and Chakraverty S (2010). The role of interventional radiology in trauma. BMJ, 340, c497.