Patient hypothermia is one of the most serious “killers” because it is relatively easy to develop and difficult to correct. This is an axiom in so-called “trauma anaesthesia”[1].

 

In addition to the intraoperative heat loss we are used to—through radiation, convection, evaporation, and conduction—during wartime surgery on injured patients, all of these mechanisms of heat loss may already occur during the patient’s evacuation to the hospital.

 

Most enzymes in the human body function within specific temperature ranges. Hypothermia disrupts enzyme activity. Metabolic and physiological processes slow down. From the cardiovascular system perspective, this may lead to hypotension, bradycardia, and ventricular fibrillation in severe cases. The oxyhemoglobin dissociation curve shifts to the left—hemoglobin binds oxygen more readily but releases it less easily. There are at least three mechanisms by which hypothermia compromises the body’s defense against surgical wound contamination [2]. Examples of pathophysiological changes can be found in almost every body system.

 

However, one of the most undesirable intraoperative manifestations of hypothermia is coagulopathy. This occurs primarily due to a reversible impairment of platelet aggregation caused by reduced release of thromboxane A3, which worsens the formation of the initial platelet plug. Hypothermia also decreases the activity of enzymes in the coagulation cascade, which in turn reduces clot formation [3]. All of this leads to greater perioperative blood loss and an increased need for blood transfusion. In one meta-analysis, even mild (e.g., 1°C) hypothermia increased blood loss by approximately 20 percent [4].

 

Hypothermia-induced coagulopathy is often not detected by routine laboratory tests because these tests are performed at 37°C; therefore, the coagulation profile may appear normal, even though it would not be if adjusted for the patient’s actual temperature.

 

Another important effect of hypothermia is its impact on drug metabolism. For example, the duration of action of neuromuscular blocking agents (NMBAs) increases under hypothermic conditions. Studies show that the effect of atracurium is prolonged by 60% during hypothermia [5]. This affects the duration of anesthesia and recovery from anesthesia, as well as the risk of residual neuromuscular blockade when neuromuscular monitoring is unavailable. In combat conditions, this is certainly not an advantage.


 

Therefore, it is important to understand that at the evacuation stage the patient may already be hypothermic. Our simplest actions in the operating room for such patients include:

  • increasing the operating room air temperature as much as possible;

  • using patient warming devices whenever available;

  • warming intravenous fluids.

 

It is also important to understand that warming fluids alone does not warm the patient, since intravenous fluids can only be slightly warmer than the internal (core) body temperature. Thus, fluid warming does not compensate for the initial redistribution hypothermia (from peripheral tissues to the core) nor for subsequent heat loss from the skin surface and surgical incisions. Similarly, warming irrigation fluid for the abdominal cavity does not transfer a significant amount of heat to the patient. However, patients can be significantly cooled by the infusion of unwarmed intravenous fluids or exposure to unwarmed abdominal irrigation fluids. For example, each liter of fluid administered at room temperature decreases mean body temperature by 0.25°C in a 70 kg patient.

 

In combat conditions, the patient warming devices we are accustomed to may be unavailable, and operating rooms may be cold.

 

Therefore, the use of intravenous fluid warmers is a simple method and can be one of the key elements in preventing further hypothermia in patients and avoiding negative outcomes.