Traumatic Cat Haem part 2

Acute Traumatic Coagulopathy and the Lethal Trauma Triad:

Acute Traumatic Coagulopathy (ATC) is an internal process that is initiated by major trauma due to a cascade of negatively impacting pathophysiological effects stemming from major trauma and hypoperfusion (due to hypovolaemic shock). These negative processes include activation of protein C, platelet dysfunction, and endothelial glycocalyx disruption. ATC has a significant effect on the body’s normal response to major haemorrhage as it disrupts its’ ability to arrest significant bleeding.

ATC is made worse through the 3 elements of the lethal trauma triad, Hypothermia, Acidosis, and further Coagulopathy:


Within trauma, hypothermia is determined by many as a temperature below 36⁰C. Hypothermia can be caused by several reasons in the traumatic setting:

  • Environmental factors
  • Length of time exposed/entrapped
  • Administration of cold Intra Venous (IV) fluids
  • Haemorrhage

Hypothermia has multiple negative pathophysiological effect on the patients’ ability to stem haemorrhage and maintain homeostasis.

  • Trauma induced hypothermia switches cellular energy production from aerobic to anaerobic. This increases blood acidity levels
  • The production of Thrombin is reduced which overall increases coagulation time
  • Platelet function is decreased with their activation, aggregation, and adhesion properties impaired
  • At further hypothermic levels <33⁰C, the blood’s clotting factors are further impaired, having a direct affect on the synthesis of fibrinogen

Any hypothermia in a major trauma patient with ATC will have drastic negative effects on their overall outcome. As part of patient management it is imperative that active warming is done through use of heat pads, blankets/foil blankets, use of warm fluids, and removal from the cold environment.


ATC present in a major trauma patient will already cause disruption to the coagulation process. This coagulopathy can be made worse by the clinician through aggressive use of fluid therapy. Large boluses of fluids in the major trauma patient can cause disruption of clots through increased hydrostatic pressure, a dilution of coagulation factors, and a subsequent reduction in the patient’s body temperature.

When looking to administer fluid boluses, a targeted systolic of 60 mmHg or central carotid pulse should be aimed for in penetrating torso trauma, and systolic of 90 mmHg or peripheral radial pulse in blunt trauma or penetrating limb trauma. This is to try and stop hydrostatic pressure from dislodging any formed clots.

It is vital that clinicians look at reducing the effects of the ATC and the lethal trauma triad in order to best try and maintain the patients’ homeostatic balance.


Blood pH normal ranges between 7.35-7.45. Below that figure is classed as acidotic. As major haemorrhage occurs, this reduces the body’s oxygen carrying capability. As oxygen levels reduce, less is available for cellular respiration. Cellular activity switches from aerobic to anaerobic resulting in production of by-products such as carbon dioxide and lactic acid. Carbon dioxide and lactic acid in the blood result in a build-up of hydrogen ions (H+) and a subsequent decrease in the blood’s pH. To compound this process further, cell membranes become leaky, resulting in cellular oedema, which further impairs oxygen delivery to tissues.

Coagulation is less effective in acidic blood, with the activity of clotting factors reduced when the pH of blood falls below 7.3. Further drops in pH further impact the bloods’ clotting process.

Combating acidosis, administration of high flow Oxygen can help with cellular metabolism, providing greater oxygen supply to the cells and reducing the anaerobic acidosis effect.