FRCA Notes

Major Haemorrhage

This topic was an SAQ back in 2016, with a pass rate of 85%.

Over 50% of the marks were for knowing the principles of management in major haemorrhage.

The remaining marks were for a definition of major haemorrhage and the complications of massive transfusion.

Resources


Definitions of major haemorrhage
Loss of one circulating volume in 24hrs
Loss of >50% circulating volume within 3hrs
Blood loss >150ml/minute
Haemorrhage enough to cause physiological signs of shock i.e. hypotension <90mmHg and tachycardia >110bpm
  • When significant haemorrhage is recognised, urgent attempts to identify and control the source of bleeding should be undertaken

  • Damage control resuscitation is a trifecta of interventions in major traumatic haemorrhage

1 - Permissive hypotension

  • Allow SBP approximately 70-90mmHg (or MAP 50mmHg) for up to an hour to balance benefits of organ perfusion and risks of disturbing clotting process
  • In the case of head injury, judicious 250ml fluid challenges to a SBP 100mHg may balance bleeding vs. CPP

2 - Haemostatic resuscitation

  • Early use of blood products rather than excessive crystalloid
  • Resuscitate using a 1:1:1:1 ratio of FBC : FFP : cryoprecipitate: platelet
    • The optimal ratio of RBC : FFP in transfusion is not known, but 1:1 or 1:2 provide improved mortality in military patients
    • The PROPPR trial (2015) demonstrated no difference in outcome between a 1:1:1 and 1:1:2 ratio

3 - Damage control surgery

  • Damage control surgery aims to control bleeding and prevent contamination, but leave definitive treatment until a later, planned time
  • It is followed by post-operative resuscitation in a critical care environment and subsequent definitive surgery
Indications for damage control surgery (after initial resuscitation)
Transfusion >10 units i.e. massive transfusion
pH <7.30
Hypothermia <35'C
Coagulopathy (clinical or biochemical)
Lactate >5
  • If performed effectively this initial, abbreviated intervention may prevent or mitigate the lethal trial of major trauma

  • The lethal triad of major trauma includes:
    1. Hyothermia
    2. Acidosis
    3. Coagulopathy

Hypothermia

  • Hypothermia exacerbates coagulopathy, acidosis and organ failure in major haemorrhage
Respiratory Cardiovascular Neurological Metabolic Renal Haematological
Left-shift of oxyHb dissociation curve leads to tissue hypoxia Myocardial depression: ↓ CO and MAP ↓CMRO2 7% for each 1°C Slowed enzymatic reactions Diuresis ↑ blood viscosity
Pulmonary oedema if severe Bradycardia, VF, asystole Reduced CPP and ICP Altered drug metabolism Reduced renal function leads to acidosis ↓ platelet activation
Apnoea once <24°C J-waves (<30°C) Confusion <35°C Prolonged NMBA activity ↑ platelet sequestration
Shivering artefact Loss of consciousness <30°C Hyperglycaemia Inhibits fibrinolysis
Earlier return of GI motility ↓ factor 11 and 12 function

Acidosis

  • Tissue hypoperfusion and hypoxaemia results in anaerobic metabolism and metabolic acidosis
  • This exacerbates coagulopathy by impairing the activity of clotting factors 5,7a, 10 and thrombin
  • Lactate levels and clearance are closely related to outcome
  • Restoration of adequate tissue perfusion and oxygenation will treat acidosis

Coagulopathy - see next section


  • There are two distinct mechanisms of coagulopathy in trauma
    1. Acute coagulopathy of trauma shock
    2. Haemodilution

  • The net effect is:
    • Consumption of clotting factors
    • Systemic anticoagulation
    • Hyperfibrinolysis
  • I.e. a DIC-like syndrome

Acute coagulopathy of trauma shock

  • Acute coagulopathy is seen in 1/4 trauma patients
  • It is associated with a 4x increase in mortality, though active treatment improves outcomes

  • It is present prior to any fluid administration and before the advent of hypothermia
  • It is thought to be due to:
    • Endothelial exposure
    • Activation of the protein C pathway

Haemodilution

  • Administration of IV fluids dilutes clotting factors leading to coagulopathy
  • Some colloids may have a direct, negative impact on clot formation
  • Transfusion with RBC's alone will also dilute clotting factors; concomitant administration of FFP is required
  • The effect of this haemodilution is exacerbated by hypothermia
    • Sequestration of platelets occurs
    • Standard laboratory tests are calibrated to 37°C and may overestimate in vivo clotting


Factor Target Intervention
Hb >70g/L RBC transfusion
Haematocrit >0.3 (30%) RBC transfusion
Platelets >50-75 x 109/L Platelet transfusion
Fibrinogen >1.5g/L Cryoprecipitate | PCC | FFP
Prothrombin time (INR) <15s (<1.5) FFP
Ionised calcium >1mmol/L IV calcium 10ml 10%
Temperature >36°C Active warming
pH Avoid acidosis Resuscitation | I&V


Non-pharmacological

  • Viscoelastic haemostatic assays to provide real-time testing of coagulopathy, although mayn't improve outcome (ITACTIC trial, 2021)

  • Direct pressure
  • Splinting fractured limbs
  • Pelvic binders
  • Limb tourniquets

Pharmacological

  • Haemostatic agents e.g. Celox, Quicklot

  • Reversal of existing anticoagulants e.g. PCC for warfarin

  • TXA within 3hrs, 1-2g

  • Recombinant factor 7a
    • Aims to produce supra-physiological levels of factor 7a to initiate thrombin bursts at the site of injury
    • Is only likely to be effective if adequate platelets, FFP, temperature and acid-base balance have been established
    • Was associated with reduced blood transfusion but not mortality in one RCT

Surgical

  • IR-guided embolisation
  • Pelvic packing
  • External fixation