Coagulopathy
Coagulation depends upon a cascade of enzymatic reactions that are adversely affected by hypothermia. Hypothermia prolongs coagulation times.6 A team led by Andrea Ferrara, MD, found that patients who were hypothermic and acidotic developed clinically significant bleeding despite adequate blood, plasma and platelet replacement in the hospital.7 If hypothermia can be avoided with simple prehospital measures, it may avert coagulation problems.

Acidosis
Metabolic acidosis is implicated in coagulopathy, but the mechanism is poorly defined. Physician Brian Murray reported a case of a 49-year-old woman with severe hypothermia (87.0ºF) and metabolic acidosis (pH 6.67) in 1961, and speculated that her acidosis was secondary to hypothermia.8 Surgeon Walter Ballinger and colleagues found in an experiment with dogs that lactate produced by hypoxic metabolism increased during cooling, indicating a metabolic acidosis.9 Acidosis, in turn, impairs coagulation.10,11 Although one study found acidosis alone produced no significant coagulopathy, when coupled with hypothermia it had a profound effect.12

Disseminated Intravascular Coagulation
DIC is a complex condition involving the coagulation process. It has many causes, among them trauma, infections, obstetrical complications and cancer. It begins with release of clotting factors, followed by formation of microclots in the circulation and eventual consumption of all reserve clotting factors, resulting in uncontrolled bleeding from multiple sites such as gums, wound sites and even IV sites.13

In the case of trauma, the clotting process is activated with traumatic damage to the tissues. Hypothermia and acidosis, however, interfere with normal clotting, leading to tissue hypoxia, production of lactic acid and toxic byproducts of cellular necrosis that promote agglutination of blood cells, eventual sludging of the blood, further interference with tissue perfusion, production of more toxins, more interference with clotting, more microclot formation, and eventual depletion of clotting factors.14,15 Hypothermia and acidosis contribute to further coagulation problems and more bleeding. DIC can be an explosive and life-threatening disorder, although it may also be mild, depending upon underlying causes.15

Acute Respiratory Distress Syndrome
As early as 1821, French physician Rene Laennec described a condition known as pulmonary edema without heart failure, and to this day ARDS is also described as non-cardiac pulmonary edema.16
ARDS is characterized by increased permeability of the pulmonary capillaries, resulting in fluid leaking into the interstitial and alveolar space—a different mechanism entirely from cardiogenic pulmonary edema, which involves increased hydrostatic pressures in the pulmonary circulation.
This leaking in turn leads to decreased blood volume, decreased ventilation, increased tissue perfusion and worsening shock.14 At one time, patients with ARDS were almost certain to die, but with today’s ventilatory techniques and improved ICU care, mortality has dropped to between 30%–60%. Patients with underlying medical conditions such as chronic liver disease, cirrhosis, chronic alcohol abuse, chronic immunosuppression, sepsis, chronic renal disease and non-pulmonary organ failure are at greater risk.17