Managing Major Haemorrhage in the Emergency Department

Author: Isabella Vielba / Reviewer: Henry Greenslade / Codes: HP3, RP4, RP7, SLO3, SLO4, SuP5, TP4 / Published: 04/02/2015 / Reviewed: 19/03/2024

Major Haemorrhage in the Emergency Department (ED) is common, with around 4700 cases of traumatic major haemorrhage reported in England and Wales annually. (1) If you are outside of the trauma centre, it is estimated that in the U.K. every 6 minutes a patient presents to hospital with a GI bleed. This blog aims to look at current concepts in haemorrhage management, as well as some general mechanics of the major haemorrhage protocol (MHP).

1) Recognise the fact that your patient is bleeding

No prizes for recognising major haemorrhage (simply defined as life-threatening bleeding likely to require massive transfusion) in your trauma patient who is pale, clammy and hypotensive; but the diagnosis is not always immediately obvious.

Think early about the potential for life-threatening blood loss when your differential includes a ruptured AAA, GI haemorrhage, obstetric emergencies or in patients that have undergone recent surgical procedures.

When looking for the source of the blood loss think, ‘Blood on the floor and four more’ – or another great acronym from Life in the Fast Lane is SCALPeR.

If we want a more specific definition of sorts – major haemorrhage is often recognised as:

• Loss of more than one blood volume in 24 hours (70ml/kg)
• 50% of total blood volume in 3 hours
• 150ml/minute of blood loss

These are perhaps less helpful to calculate when you have a sick patient in front of you – and so often major haemorrhage protocols (MHP) will include bleeding + vital signs (e.g., HR >110, systolic BP < 90mmHg) in their activation criteria.

However – Vital signs can be misleading

We are well versed in the fact that hypotension is a late sign (ATLS shock classification), but the absence of tachycardia does not exclude potentially life-threatening haemorrhage

Patients with major haemorrhage can be bradycardic.

Traditional teaching suggests that a decrease in heart rate is an indicator of irreversible and terminal shock. But recent research has suggested that in some patients. (2)

• The heart rate demonstrates a biphasic response to volume loss – initial vasoconstriction and tachycardia followed by what is thought to be a vagally mediated bradycardia which is potentially reversible.
• There is relative bradycardia (i.e., they never mount a tachycardia)

Elderly patients may be bleeding significantly with “normal vital signs” – with evidence suggesting elderly trauma patients have worse outcomes with systolic <110mmHg and HR >90.

Anticoagulation can obviously contribute to risk of haemorrhage, with an ever-widening variety of novel oral anti-coagulants and reversal agents now available.

For more reading – there are some useful RCEM Learning blogs on silver trauma and anticoagulation reversal.

Pregnancy brings a vast number of changes that can both raise a woman’s risk of traumatic haemorrhage, and also potentially mask a significant amount of blood loss. In particular – increased vascularity and cardiac output mean that a significant percentage (>35%) of blood volume can be lost before classic signs show. (3)

In addition to having a suspicious mind and a thorough systematic approach to your clinical examination consider:

• FAST for suspected occult intra-abdominal bleeding, taking in to account that this has good specificity but cannot be used as a rule out test.
• Pan-CT scan in trauma patients – to identify otherwise missed injuries and potential sources of bleeding.
• Lactate measurement. Levels > 4mmol/L are associated with increased mortality. (4) The response of lactate to resuscitation is also a useful marker of shock severity.
• Haemoglobin – obviously a low Hb points you in the direction of a large bleed, but important to note that a significant number (5) of patients with significant haemorrhage can have a normal haemoglobin. A good blog discussing this can be found here.
• Early group and save/cross-match – ideally taken before the first donor blood has gone in!

2) Control and stop the bleeding

Your first thought once major haemorrhage is suspected/identified should be, ‘Who do I need to turn off the tap?’ Call for Help immediately!

Depending on the source this will include a senior/consultant member of the  surgical/orthopaedic/obstetric/endoscopy team or an interventional radiologist.

You will undoubtedly need the assistance of ITU+/ anaesthetics as well. IV access is critical, and for the code-red haemorrhage may require placement of a central line.

Immediate actions you can do in the ED whilst facilitating definitive management include:

• Direct pressure/ haemostatic dressings to wounds
• Application of tourniquets
• Splint/bind fractures
• Suture or tie off bleeding vessels

3) Start Damage Control Resuscitation (DCR)

Avoidance of the lethal triad is the rationale behind the concept of DCR. It incorporates:

• Permissive hypotension
• Early damage control surgery
• Haemostatic resuscitation

Permissive Hypotension – a compromise between ensuring adequate tissue perfusion whilst reducing the risk of dilutional coagulopathy and clot disruption. (Based on animal studies, evidence is limited, and BP target will vary from patient to patient. LITFL summary suggests a target MAP of 65mmHg.) *note – in children the idea of permissive hypotension is not practiced – as hypotension is so often a peri-arrest indicator in this group.

Early damage control surgery – From an ED point of view, this involves liaising with the surgical team to select the right patient for abbreviated lifesaving surgery to arrest bleeding. Secondary surgery can take place once the lethal triad is under control and further resuscitation has taken place.

4) Replace like for like

One of the roles of the ED team in these situations is to recognise and commence urgent blood transfusion – replacing blood with blood.

How do we do this? In the U.K. this is often structured in a local Major Haemorrhage Protocol (MHP), which signals to blood bank to release products early.

This will allow blood products to be available as needed – but there is some delay which will vary depending on where you work e.g., there may be a minimum time of thawing for products such as FFP (generally at least 20 minutes). In some centres there will obviously be O-negative blood in the ED fridge for the initial management.

So, getting an early call out is important – and it is probably best to allocate someone to co-ordinate this in a busy resus situation, thinking about typical human factors and closed loop communication.

Don’t forget the TXA!

In a field with lots of unclear evidence for interventions, Tranexamic acid (TXA) generally (!) has got some higher quality evidence indicating it’s benefit in major haemorrhage, at least in certain situations. (a few caveats then).

Certainly, in trauma – there is good evidence that early (<3 hour) administration of TXA (1g bolus in adults) is associated with reduction in mortality. (6) This reduces the closer to the 3-hour mark we get, which is why often this is given pre-hospital. Important to remember that this bolus should be followed up by a further 1g infusion, typically over 8 hours.

Recent studies in GI bleeds, e.g. HALT-IT (7) have shown no benefit for TXA in Gi bleeds, and possibly a small risk of harms – and at present the BSH do not recommend TXA for GI bleeds.

What’s in a major haemorrhage pack?

A MHP Consists of various blood products, and usually extra items e.g., calcium chloride if needed.

Balanced resuscitation

Evidence for the best balance of blood products is still not conclusive, but current British Society for Haematology (BSH) guidelines advocate for 1:1 ratio of red blood cells (RBC) to fresh frozen plasma (FFP) in trauma, and no more than 1:2 for most major haemorrhage situations. This means generally giving 1 unit of blood for every unit of FFP. Some centres will also include platelets in 1:1:1 ratio.

The reason behind this is to try and promote normal clotting parameters, which can be commonly deranged in the trauma patient. For this reason – although 1:1 is a good starting point – it is also recommended to check clotting parameters early to guide further management – see below.

Possible harms of massive transfusion

• The more widespread use of rapid infusers has meant we can deliver large volumes of blood very quickly – over a couple of minutes.
• This brings obvious benefits but perhaps can also raise risk of blood transfusion.
• One case study highlights the potential for rapid hypothermia for a patient who received unwarmed blood products through a rapid infuser that was accidentally unplugged from a mains supply (and so stopped warming incoming fluids).

Important things to consider with rapid blood administration

• Calcium – can often drop due to the patient’s calcium binding to citrate in donor samples. Important to frequently monitor on ABG/VBG – treatment is generally calcium chloride/gluconate (depending on local preference). Generally, hypocalcaemia is more dangerous in haemorrhage.
• Potassium ­– Hyperkalaemia sometimes seen in rapid delivery of old stored blood e.g., from the resus fridge.
• The potential for typical blood transfusion reactions – particularly with large volume resus in the older population e.g., transfusion related acute lung injury (TRALI), transfusion associated circulatory overload (TACO).

Keeping track

In a massive haemorrhage – blood packs are often being exchanged every 5-10 minutes or less and it can be hard to keep track. It can be helpful to allocate a member of the trauma team to ensure each unit has been prescribed and recorded. There is a legal duty to ensure complete traceability of each blood product in the U.K. – and so each product used requires a slip completing and sending back to blood bank – something which can be easily lost, particularly as patients transfer between resus and elsewhere e.g., theatre.

Sometimes a patient may not require the full MHP. In which case early stand-down of the blood bank team is helpful – it lets the haematology team return to routine work and means that unused blood products may be able to be used for another patient. Again, lots to remember when someone is peri-arrest in front of you! So having that early allocation of roles is helpful.

5) Do your best to avoid the lethal triad

Haemostatic resuscitation refers to attempting to maintain as normal a clotting profile as possible. Some of this occurs via balanced blood products (above) and trying to maintain optimal physiology.

Like most things in ED, it is trying to do the core things well, and avoiding potential factors that can worsen outcomes.

Once established the lethal triad of hypothermia, acidosis and coagulopathy are irreversible and have a grave prognosis. Therefore treat these three components before they manifest.

Hypothermia – impairs platelet function and enzymatic function within the clotting cascade.

• Limit exposure, remove wet clothing and ensure ambient temperature is appropriate.
• Continually monitor the temperature – consider catheter temperature probe (if no urethral trauma) or rectal probe.
• Use warming blankets – forced air if available.
• Facilitate rapid transfusion of warmed blood products – this can be done using rapid infusers e.g., a Belmont rapid infuser.

Acidosis – inadequate tissue perfusion leads to lactic acidosis which can impair clotting.

• Exacerbated by crystalloid administration which also has a dilutional anaemia effect. Restore tissue perfusion ASAP with haemostatic resuscitation and avoid the traditional teaching of giving 1-2 litres of crystalloid at the outset.
• Maximise oxygenation and minimise causes of hypoventilation to avoid any additional respiratory acidosis.

Coagulopathy – the aetiology of coagulopathy in major haemorrhage is multifactorial with hypothermia and acidosis synergistically aggravating it.

•  Avoid large volumes of crystalloid or unbalanced blood products which can cause dilutional coagulopathy. (up to date).
• Have a low threshold to discuss with haematology from the outset, irrespective of the initial coagulation screen. The screen is often normal in the acute situation (despite an evolving coagulopathy) for several reasons—it’s 45-60mins behind real time, provides no indication of platelet function or interaction between red cells and platelets and is not representative in hypothermic patients (as it’s carried out at 37 °).
• In patients without pre-existing coagulation defects a prolonged PT or APTT > 1.5 X normal defines coagulopathy. But manage the major haemorrhage patient as though they are already coagulopathic. I.e. Transfuse blood products as per major haemorrhage protocol. Don’t wait for lab results!
• If available haemostatic assays (TEG/ROTEM) can provide more real time information on the speed of clot initiation, clot strength and lysis which can help guide management and choice of further clotting products.

Acute coagulopathy of Trauma (ATC) – independent of the lethal triad and the other causes of coagulopathy. This phenomenon has been recognised in severely injured patients and is characterised by systemic anticoagulation mediated by protein C and hyperfibrinolysis. The endothelium is thought to be central to the response. Manage as above.

Summary and further reading

Hopefully this has been a recap of current concepts in major haemorrhage management in the ED. Below are some good resources, including the current 2022 guidelines from the BSH, as well as more of a deep dive into the physiology behind massive transfusion.

The BSH recommend that there are frequent “fire safety drills” for major haemorrhage protocols, and this may be a good quality improvement project if one does not exist in your current department.

Internet Book of Critical Care: Massive Transfusion Protocol

Haematological management of major haemorrhage: a British society for Haematology guideline

References

1. Griggs JE, Jeyanathan J, Joy M, Russel MQ, Durge N, Bootland D, et al. Mortality of civilian patients with suspected traumatic haemorrhage receiving pre-hospital transfusion of packed red blood cells compared to pre-hospital crystalloid. Scand J Trauma Resusc Emerg Med. 2018; 26(100).
2. Thomas I , Dixon J. Bradycardia in acute haemorrhage. BMJ. 2004; 328: 451-3.
3. Irving T, Menon R, Ciantar E. Trauma during pregnancy. BJA Educ. 2021 Jan;21(1):10-19.
4. Thomas I, Rivers E, Knoblich , Jacobsen G, Muzzin A, et al. Early lactate clearance is associated with improved outcome in severe sepsis and septic shock. Crit Care Med. 2004; 32(8): 1785-6.
5. Figueiredo S, Taconet C, Harrois A, Hamada S, et al. How useful are hemoglobin concentration and its variations to predict significant hemorrhage in the early phase of trauma? A multicentric cohort study. Ann. Intensive Care. 2018; 8(76).
6. Stanworth SJ, Dowling K, Curry N, et al. Haematological management of major haemorrhage: a British Society for Haematology Guideline. Br J Haematol. 2022; 198: 654-667.
7. Collaborators. HIT. Effects of a high-dose 24-h infusion of tranexamic acid on death and thromboembolic events in pa-tients with acute gastrointestinal bleeding (HALT-IT): an international randomised, double-blind, placebo-controlled trial. Lancet. 2020; 390(10241): 1927-36.