Author: Isabella Vielba / Codes: CMP5, HMP3, HMP4, RP4, RP7, SLO1, SLO4, SLO6 / Published: 04/02/2015
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
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:
- 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)
In addition to having a suspicious mind and a thorough systematic approach to your clinical examination consider:
- FAST for suspected occult intra-abdominal bleeding.
- 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 mortality2. The response of lactate to resuscitation is also a useful marker of shock severity.
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.
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) Do your best to avoid the lethal triad
Once established the lethal triad of hypothermia, acidosis and coagulopathy are irreversible and will lead to the death of your patient. 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 – rectal probe useful.
- Use warming blankets – forced air if available.
- Facilitate rapid transfusion of warmed blood products.
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).
- Liase 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 a number of 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 thromboelastography can provide more real time information on the speed of clot initiation, clot strength and lysis which can help guide management.
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.
4) Start Damage Control Resuscitation (DCR)
Avoidance of the lethal triad is the rationale behind the concept of DCR. It incorporates:
- Permissive hypotension
- Haemostatic resuscitation
- Early damage control surgery
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.)
Haemostatic Resuscitation – major haemorrhage protocols and transfusion ratios vary from hospital to hospital. Your role is to initiate and coordinate safe and rapid transfusion. The ideal ratio of blood products is debatable. An aggressive approach such as 2:1:1 Packed Red Blood Cells: Fresh Frozen Plasma: Platelets has been suggested to improve survival. (JPAC transfusion guidelines)
Monitor the following every 30-60 minutes to guide your management:
- Acid base
- Ionised Calcium – on your ABG/VBG
- PT/APTT/Clauss Fibrinogen and platelets
Consider the following adjuncts:
- Tranexamic acid (1g bolus followed by 1g over 8 hours) in all cases (CRASH2)
- Calcium Chloride – 10mls 10% over 10 minutes if ionised Ca <1.1
- Vitamin K and prothrombin complex in patients who are warfarinised
Early damage control surgery – Liaise 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.
1. Thomas I, Dixon J. Bradycardia in acute haemorrhage. BMJ 2004;328:451-3
2. Nguyen H, Rivers E, Knoblich et al. Early lactate clearance is associated with improved outcome in severe sepsis and septic shock. Crit Care Med 2004;32(8):1785-6