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Shock: septic

ISSN 2398-2950


  • Bacteremia: presence of liver organisms in the blood stream.
  • Sepsis: life-threatening organ dysfunction caused by a dysregulated host response to infection.
  • Septic shock: subset of sepsis in which underlying circulatory and cellular/metabolic abnormalities are profound enough to substantially increase mortality. Patients suffer persistent, volume-unresponsive hypotension requiring vasopressors to maintain a mean arterial pressure over 65 mmHg.
  • Cause: dysregulated inflammatory response to an infection (bacterial, viral, protozoal or fungal). The release of circulating inflammatory mediators causes signs of systemic inflammatory response syndrome (SIRS) that can range from mild to moderate and severe, ultimately developing septic shock.
  • Clinical signs and diagnostic: depend on location of the infection, virulence of the organism, co-morbities of the host as well as age and immunocompetence. SIRS criteria typically consists of tachycardia (or bradycardia), tachypnea, hyper/hypothermia. Usually, patients tend to have hyperemic ('congested/injected') mucous membranes with a shortened capillary refill time due to severe peripheral vasodilation. Additional laboratory findings in sepsis include leukopenia or normal white blood cell count with a band neutrophil count of over 10%, increased levels of C-reactive protein and other acute phase proteins and inflammatory makers and/or hyperlactatemia. Further abnormalities can be encountered if the patient suffers from multiple organ dysfunction syndrome (MODS).
  • Treatment: treatment of the infection source, treatment of secondary organ failure/coagulopathy, appropriate and timely antimicrobial administration, intravenous fluid therapy and vasopressors when required.
  • Prognosis: guarded, worsening as the patient progresses from mild SIRS to progressive systemic inflammation to organ dysfunction and vascular collapse. Associated with high mortality rates.
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Presenting signs

  • Most dependent on location of infection and secondary organ failure.
  • Most patients present with depressed mental status and recumbent. They will usually have congested mucous membranes and shortened capillary refill times. Tachycardia and hypotension (hypotension may or may not be responsive to fluid therapy) are often seen as well as pyrexia.
  • Septic peritonitis patients Peritonitis usually suffer from abdominal pain and the abdomen can be distended and will be positive for free fluid.
  • Patients that suffer sepsis originating in the thorax (bronchopneumonia, pyothorax, etc) will likely suffer dyspnea, but can become hypoxemic/cyanotic.
  • If they suffer secondary organ failure they may present coagulopathic (disseminated intravascular coagulation DIC Disseminated intravascular coagulation is often encountered secondary to septic shock), or present with signs secondary to liver or kidney failure.

Acute presentation

  • Collapse.
  • Sudden death.



  • Common pathogen will depend on the location of the septic foci.
  • Most common etiological agents include E. coli Escherichia coli, Enterococcus spp, Staphylococcus spp, B-hemolytic Streptococcus spp, Enterobacter spp, Klebsiella spp, Pasteurella spp Pasteurella multocida, Pseudomonas spp, Acinetobacter spp, Corynebacterium spp, Bartonella spp.
  • Some etiological agents will be more common than others depending on the location of the septic focus, eg urosepsis is usually caused by organisms of gastrointestinal origin.
  • Key to the etiology of sepsis/septic shock is the dysregulation of the host inflammatory response: this may be the result of an over-exuberant pro-inflammatory state, and inapproptiate anti-inflammatory state, or differing combinations of these extremes at different time points during the disease.
  • Whilst the majority of clinically-recognized sepsis results from bacterial infections, sepsis can occur secondary to viral, fungal, parastic or other pathogenic infections.

Predisposing factors


  • Septic peritonitis is the most common cause in sepsis (in dogs) often occurring following leakage of contents from the GI tract. This can happen secondary to neoplasia, perforation due to foreign body ingestion, dehiscence of previous surgical sites, use of non-steroidal anti-inflammatory therapy associated with perforating ulcers or severe colitis. Septic peritonitis is also described secondary to contamination from urine (the animal must have suffered from a urinary tract infection prior to this), bile or after uterine rupture.
  • Other less common causes of sepsis include pyelonephritis, pneumonia, septic arthritis, deep pyoderma, bacterial endocarditis, tick borne diseases, septic meningitis, pyothorax, trauma, bite wounds, septic prostatitis, pyometra, osteomyelitis, etc.
  • Widespread use of catheters/other invasive equipment can be a source for sepsis.
  • Use of corticosteroids/other immunosuppressive agents can predispose an animal to sepsis. Animals receiving chemotherapy are also at a higher risk.
  • Antibiotic use prior to onset of sepsis may lead to presence of resistant bacteria.


  • Septic shock is a form of shock Shock which is caused by the presence of micro-organisms (usually bacteria) or their products (endotoxins) in the systemic circulation. This leads to a dysregulated host immune.
  • The gram-negative bacterial cell wall contains lipopolysaccharides (LPS) that are recongized as one of the most potent stimuli for an inflammatory host response. Activation of the inflammatory cascade due to gram positive bacterial occurs in response to cell wall components or bacterial DNA. Stimulation of the innate immune system from a variety of pathogen antigens results in the production of inflammatory cytokines.
  • The most important cytokines related to sepsis are tumor necrosis factor alpha and interleukins 1,6 and 8. These cytokines attract and activate neutrophils and stimulate other cells in the immune response.
  • Cytokines can cause extensive host tissue damage secondary to the release of reactive oxygen species (ROS) and proteases among others.
  • Overproduction of nitric oxide (NO) during sepsis is a major contributing factor to dysregulation of the vasomotor tone (vasoplegia). This vasodilatory state will cause severe hypotension, typically unresponsive to fluid therapy.


  • Usually acute over hours.


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Further Reading


Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Prescott J F, Miller C W, Mathews K A et al (1999) Update on canine streptococcal toxic shock syndrome and necrotizing fasciitis. Can Vet J 38 (4), 241-242 PubMed.
  • Dernell W S & Kreegan J (1992) Peracute, necrotizing mastitis as a cause of fatal septicemia and endotoxemia in a dog. Canine Pract 17 (6), 25-29 VetMedResource.
  • Nostrandt A C (1990) Bacteremia and septicemia in small animal patients. Probl Vet Med (2), 348-361 PubMed.

Other sources of information

  • Boller E M & Otto C M (2015) Sepsis and septic shock. In: Small Animal Critical Care Medicine. 2nd edn. Silverstein and Hopper. Elsevier, Philadephia. pp 472-479.
  • Kirby R (1995) Septic shock. In: Kirk's Current Veterinary Therapy XII. Ed J D Bonagura. Philadelphia: W B Saunders. pp 139-146.