Q. Please review management of sepsis in dogs.
A. Dr. Amy DeClue at the 2007 American College of Veterinary Internal Medicine in Seattle gave an excellent lecture on management
of canine sepsis. Here are some relevant points from it:
Sepsis in dogs most commonly originates from the GI tract (e.g., canine parvoviral enteritis), followed by the respiratory
tract (e.g., bacterial pneumonia), severe dental disease, chronic urinary-tract disease and contaminated wounds.
Products for management of bacterial infection or canine parvoviral enteritis
Gram-negative bacterial infections predominate, with E. coli being the most common isolate. However, any bacterial, fungal, parasitic or viral organism may cause sepsis.
Sepsis is diagnosed based on the presence of an underlying infection and identification of systemic inflammatory response
syndrome (SIRS). Bacteremia often is not identified and therefore a negative blood culture does not rule out the presence
of existing sepsis.
Systemic Inflammatory Response Syndrome (SIRS): a clinical syndrome caused by systemic inflammation of infectious (i.e., sepsis) or non-infectious origin. In dogs, the diagnosis
of SIRS is based on fulfillment of at least two of these criteria: tachycardia, tachypnea, hypothermia or hyperthermia and
leukocytosis, leukopenia or greater than 3 percent band neutrophils.
Sepsis: the systemic inflammatory response to infection
Severe sepsis: the systemic inflammatory response to infection associated with organ dysfunction and manifestations of hypoperfusion or
Septic shock: the systemic inflammatory response to infection with hypotension refractory to volume expansion
Bacteremia: the presence of bacteria in the blood stream
The sequence of events leading to sepsis is complex and not completely understood. In the initial phases of infection, microbial
products (e.g., endo-toxin from gram-negative bacteria; exotoxins, peptidoglycans and super antigens from gram-positive bacteria;
and fungal cell-wall material) induce systemic inflammation through activation of immune cells, resulting in an imbalance
between pro-inflammatory mediators (e.g., TNF) and anti-inflammatory mediators (e.g., IL-10).
Tumor necrosis factor (TNF), IL-1 beta, IL-6, IL-8 and leukotrienes are examples of important pro-inflammatory mediators contributing
to the pathologic effects of sepsis in dogs. Ultimately, induction of pro-inflammatory mediators leads to inflammatory cell
infiltration, altered thermoregulation, vasodilation, vascular leakage and coagulation.
Dogs can have either a hyper-dynamic or hypodynamic response during sepsis. The hyperdynamic response is characterized by
fever, brick-red mucous membranes, tachycardia and bounding pulses. With disease-process progression, a hypodynamic response
characterized by hypotension, pale mucous membranes and hypothermia can be observed.
Often dogs will have GI or respiratory signs associated with the sepsis. Possible serum chemistry profile abnormalities may
include hyperglycemia or hypoglycemia, hypoalbuminemia, azotemia, hyperbilirubinemia and elevated serum ALT and/or ALP.
Coagulation abnormalities are common. Anticoagulant proteins (protein C and antithrombin) are significantly decreased and
PT, PTT and D-dimer concentrations are significantly increased in naturally occurring sepsis in dogs.
Altered microcirculation and tissue hypoxia may lead to metabolic acidosis in septic dogs. Little is known about the prevalence
of organ dysfunction or failure during canine sepsis, although hemodynamic derangement, renal failure and respiratory failure