The body’s normal response to an infection is to raise its core temperature, creating a fever that helps fight off pathogens. In severe sepsis, however, this temperature control mechanism can fail dramatically, resulting in hypothermia, or an abnormally low body temperature, typically defined as a core temperature below 96.8°F (36°C). This shift to low body temperature is a serious sign of systemic collapse, indicating the body is overwhelmed. For a patient with sepsis, hypothermia is often associated with a significantly worse prognosis than if they presented with a fever.
Understanding Sepsis and Its Symptoms
Sepsis is a medical emergency where the body’s response to an infection becomes life-threatening, causing injury to its own tissues and organs. It is not the infection itself but the extreme, widespread inflammatory reaction that causes harm. This overwhelming immune response triggers a chain reaction throughout the body, leading to organ dysfunction, which can rapidly progress to tissue damage and death if not treated immediately.
The initial infection can start anywhere, most commonly in the lungs, urinary tract, or skin. Common signs of this systemic reaction include a rapid heart rate, confusion or disorientation, and breathing that is fast and shallow. Severe pain or discomfort, clammy skin, and shivering can also signal sepsis.
While many patients with sepsis will exhibit a high fever, a low body temperature is an equally important sign. In sepsis, inflammatory chemicals are released into the bloodstream, creating a whole-body reaction. This uncontrolled inflammation ultimately leads to widespread damage, including the failure of temperature regulation.
Why Severe Sepsis Causes Low Body Temperature
The development of hypothermia in severe sepsis involves both excessive heat loss and an inability to generate enough heat. Initially, the systemic inflammatory response releases chemical mediators, such as cytokines, which cause widespread vasodilation. This process widens the blood vessels, particularly those close to the skin’s surface, which allows a large amount of heat to escape quickly into the environment.
At the same time, the body’s central thermostat, regulated by the hypothalamus in the brain, is directly affected by the systemic inflammation, leading to a breakdown in temperature control. The body loses its ability to shiver or constrict blood vessels to conserve heat, which are normal protective mechanisms against cold. This failure of thermoregulatory mechanisms means the body cannot maintain its set temperature, resulting in a rapid drop in core heat.
The overwhelming metabolic demands of fighting a severe infection eventually exhaust the body’s energy reserves. The infection leads to cellular dysfunction, particularly in the mitochondria, which are responsible for generating energy and heat. When these cellular powerhouses fail, the body’s metabolic activity slows significantly, meaning it cannot produce the necessary heat to counteract the rapid loss. This metabolic crash is often seen in the most severe cases of septic shock, where low body temperature is a marker of profound physiological distress.
Emergency Medical Response to Hypothermia
Hypothermia in a septic patient requires immediate intervention, as it is associated with a higher mortality rate compared to febrile sepsis. The medical response focuses on stabilization, infection control, and careful rewarming to restore the core body temperature above 96.8°F (36°C). Rewarming techniques must be active and monitored closely to prevent complications from a too-rapid temperature change.
Medical teams use forced air warming systems, such as specialized blankets that blow warm air over the patient’s body, to promote surface warming. Intravenous fluids, which are often administered in large volumes during sepsis resuscitation, must be actively warmed before infusion to prevent further core cooling. Direct internal methods, like circulating warm fluids through catheters, may be used to address significant temperature deficits.
The immediate administration of broad-spectrum antibiotics is a time-sensitive requirement, often given before the specific pathogen is identified. Patients presenting with hypothermia often experience delays in receiving these antibiotics compared to those with fever, contributing to their worse outcomes. Stabilization protocols also include the use of vasopressors, medications designed to raise low blood pressure caused by the septic shock.