Prehospital administration of calcium in trauma

Hypothermia, coagulopathy and acidosis are known collectively as the lethal triad (Ditzel et al, 2020). Together with haemostatic measures and replacement of blood, managing the lethal triad is a significant focus of ‘damage control resuscitation’ for haemorrhagic shock (Joint Trauma System, 2019). Calcium ion (Ca²⁺) depletion is also suspected of influencing mortality in traumatic haemorrhage, leading to the addition of hypocalcaemia to the lethal triad and the theorisation of the lethal diamond (Figure 1).

Calcium ions initiate actin-myosin filament binding, resulting in myofibril (muscle-fibre) shortening and muscle contraction. Depletion of calcium ions because of loss during haemorrhage and consumption from clot formation can therefore reduce myocardial contractility and vascular smooth-muscle tone, thereby reducing cardiac output and blood pressure, exacerbating shock (Spahn et al, 2019).

Calcium is also essential for platelet adhesion and factors II, VII, IX and X in the clotting cascade. Hypocalcaemia therefore has the potential to exacerbate coagulopathy, leading to further haemorrhage. Patients who receive transfusions to replace blood loss are at risk of experiencing further depletion of calcium ions from citrate, a chelating (ion-binding) agent that is added to transfusion products to prevent calcium from causing donor blood to coagulate (Spahn et al, 2019). This is a pertinent consideration for prehospital administration of blood products, as well as for paramedics who may not carry or transfuse blood products but expect a patient with shock from traumatic haemorrhage to receive blood transfusions on arrival at hospital.