Treatment of canine sepsis: First identify, eradicate the cause

Treatment of canine sepsis: First identify, eradicate the cause

Feb 01, 2008

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:

Products for management of bacterial infection or canine parvoviral enteritis
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.

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 hypotension
  • 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.

Clinical effects

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 are recognized.