Sepsis is defined as the systemic inflammatory response to an infection. We commonly see patients that have a clinical presentation
that appears similar to sepsis, but no source of infection can be identified. This syndrome has been termed the systemic
inflammatory response syndrome or SIRS. SIRS can result from activation of the immune and inflammatory system in response
to trauma, tissue injury, heat stroke, pancreatitis, burns or hypoxia. In humans, there are established criteria for the
diagnosis of SIRS. Table 1 includes proposed criteria for definition of SIRS in dogs and cats and humans. It is important
to realize that only 2 of the 4 potential criteria need to be met for a patient to qualify for SIRS. Sepsis includes these
SIRS criteria plus evidence of a source of infection. Because the primary source of infection may not be identified initially
and SIRS can lead to secondary sepsis, for the purpose of this discussion, the term sepsis will be used to describe both conditions.
SIRS criteria are not particularly useful in the clinical management of patients because they lack specificity and sensitivity.
A more recent classification scheme called PIRO, has been proposed to attempt to identify which patients are at risk of poor
outcome in sepsis.
Overview of patients at risk
Several risk factors for sepsis have been identified in human patients. It appears that many of these risk factors are equally
relevant in our veterinary patients. The most obvious risk factor is a known infectious focus, such as pneumonia, prostatitis
or peritonitis. These patients should be monitored carefully for systemic signs of systemic infection and activation of the
inflammatory cascade. Patients with hypotension, ischemia/reperfusion injury (e.g. gastric dilatation and volvulus), or intestinal
compromise (e.g. parvovirus, infiltrative intestinal disease or cancer) are at risk for bacterial translocation and sepsis.
Major trauma or surgery can predispose patients to hypotension, ischemia/reperfusion or SIRS as a result of tissue injury.
Burn patients have both tissue injury and are at risk for infection. Immunosuppression from drugs or disease can also predispose
patients to overwhelming infections and sepsis.
Early aggressive treatment to control infection is the first line of therapy. This includes early administration of appropriate
antibiotics and removal of the infectious/inflammatory focus. For abscesses or injured tissue, this may require surgical
debridement and drainage. For patients with pneumonia, this may require nebulization and coupage as well as maintaining adequate
hydration. Nebulization is generally performed using humidified oxygen, this delivers moisture to the airways, which in conjunction
with coupage (physical therapy involving clapping on the chest to loosen pulmonary exudates) facilitates elimination of the
infection. It is recommended that animals with pneumonia are nebulized 3-4 times daily for 10-15 minutes followed by coupage.
The second line of therapy is aimed at supporting the normal organ function, preserving tissue perfusion, and preventing secondary
organ failure. There have been multiple attempts to identify a third line of therapy to control or inhibit the actions of
the inflammatory cascade, however to date the only therapy that has been beneficial in human clinical trials, activated protein
C is not feasible for use in veterinary patients.
Clinically, sepsis is associated with the development of distributive shock. This form of shock results from massive vasodilation.
The consequence of this vasodilation is that the amount of blood in circulation is inadequate to fill the vascular space,
creating an effective hypovolemia. As a result, there is insufficient delivery of oxygen and nutrients to vital tissues. In
response to tissue hypoxia, there is an increase in heart rate (in dogs and variably in cats) and cardiac contractility (early)
which provide a compensatory increase in cardiac output and tissue perfusion. In contrast to hypovolemic shock, where peripheral
vasoconstriction is part of the compensatory response, sepsis leads to vasodilation and maldistribution of blood flow, resulting
in regions of excess blood flow and other regions that remain underperfused. Vasodilation in septic shock is a consequence
of the production and release of inflammatory mediators by the activated immune system. The vasodilation is responsible for
the bright red appearance of the mucous membranes. The vasodilation leads to a decrease in peripheral vascular resistance,
lower diastolic blood pressure and the sensation of hyperdynamic or bounding pulses. Bounding pulses can be thought of as
a normal volume of blood (pulse duration) that is propelled forward into the vessels but the pulse wave drops off rapidly
(increased intensity). The stress response triggered by sepsis will result in an initial hyperglycemia, however the inflammatory
mediators subsequently promote hypoglycemia from decreased production and increased consumption of glucose.
Fever is generated centrally by inflammatory mediators and external cooling will not eliminate the increase temperature. The
use of antipyretics can lead to serious complications as well as loss of monitoring of response to therapy and is generally
reserved for patients with dangerously high temperatures. As sepsis progresses and the animal is no longer able to compensate,
perfusion is further impaired and the rectal temperature will decrease. Septic cats in particular have a high frequency of
hypothermia. Hypothermia, as measured by rectal temperature, is often a reflection of poor perfusion to the rectum. Treatment
should focus first on volume resuscitation with warm fluids while preventing heat loss (e.g. wrap the patient in blankets
to minimize heat loss and prevent contact with cold metal tables). Forced air warming blankets are very effective in rewarming
and maintaining temperature in critically ill animals and are safer than electric heating pads.