ISSN 2398-2977      

Septic shock



  • Cause: any condition leading to sepsis or SIRS from a septic origin that has developed such that the patient is hypotensive.
  • Signs: tachycardia, tachypnea, cool extremities, delayed capillary refill time, purple to red mucous membranes that may have toxic line, decreased jugular filling, decreased pulse pressure, altered mentation.
  • Diagnosis: clinical signs associated with SIRS with suspicion of septic focus and hypotension. Positive or suspected positive blood culture alongside hypotension.
  • Treatment: fluid expansion, management of source of sepsis including antibiotic therapy, anti-endotoxic therapy, anti-inflammatories, digital cryotherapy, positive inotropic and/or pressor support.
  • Prognosis: guarded.



Predisposing factors


  • Shipping.
  • Parturition.


  • Access to other horses with infectious agents (Salmonella, Clostridium, etc) known to cause gastrointestinal disease.
  • Chronic usage of non-steroidal anti-inflammatory drugs (NSAIDs).
  • Horses receiving antibiotics.
  • Retained placenta.
  • Grain overload.


  • Systemic circulation of lipopolysaccharide (LPS) either in its shed form (unbound) or membrane bound form (still attached to gram-negative bacterial cell wall) MAY start the process. It is now accepted that several proteins on the surface of gram-positive organisms can trigger an identical response and is now known that is not all about LPS and endotoxin. This is one of the reasons why the name of this condition was changed over three decades ago.
  • In the case of gram-negative organisms, LPS binds to either lipopolysaccharide binding protein (LBP), which in turn binds to CD14 (macrophage membrane bound endotoxin receptor) or directly to CD14 (skipping the step with LBP).
  • CD14 interacts with another membrane bound protein (MD2) to transfer a signal to Toll like receptor 4 (TLR-4).
  • TLR-4 is a transmembrane spanning receptor that transduces the signal to an intracellular signaling cascade which is comprised of a number of enzymatic steps of various kinases, culminating in the intra-nuclear activation of NF-KB.
  • Once the nucleus is activated transcription of proinflammation genes ensues. Representatives of these genes include TNF-α, IL-1, IL-6, IL-8, Platelet Activating Factor (PAF).
  • The genetic transcription of these proinflammatory cytokines/mediators leads to activation of:
    • The coagulation cascade leading to endotoxin-induced coagulopathies.
    • Systemic inflammation (SIRS) Systemic inflammatory response syndrome - prostaglandin and leukotriene mediated.
    • The complement pathway and macrophage lysis.
  • The cumulative effects of these pathways (most particularly systemic inflammation) are responsible for cardiovascular depression, pulmonary hypertension, and arterial hypoxemia.
  • These effects can then lead to endotoxin induced decreased tissue perfusion and peripheral hypoxia.
  • Eventually perfusion to major organ systems can be compromised and lead to multiple organ dysfunction syndrome (MODS) and death.
  • Gram-positive bacteria can also activate a similar cascade.
  • Bacterial components such as peptidoglycan and lipoteichoic acid activate the host defense by engaging pattern recognition receptors (such as NOD-1 and NOD-2) and toll-like receptors (particularly TLR-2) of the innate immune system.
  • TLR-2 is a transmembrane receptor similar to TLR-4 which initiates an intracellular enzymatic cascade that ends with NFkB translocation and subsequent gene expression of proinflammatory cytokines and mediators (TNF-α, IL-1, IL-6, IL-8).
  • Similar to the response seen with gram-negative bacteria, these mediators can lead to cardiovascular depression, pulmonary hypertension, arterial hypoxemia, decreased tissue perfusion, peripheral hypoxia, and ultimately, multiple organ dysfunction syndrome (MODS) and death.


  • 2-6 h.


  • Septic shock is typically secondary to a primary disease process within one patient. However, it can be associated with infectious disease, in which case epidemiologic considerations should be made per the specific infectious disease.


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Further Reading


Refereed Papers

  • Recent references from PubMed and VetMedResource.
  • Werners A H (2017) Treatment of endotoxaemia and septicaemia in the equine patient. J Vet Pharmacol Ther 40 (1), 1-15 PubMed.
  • Fogle J, Jacob M, Blikslager A et al (2017) Comparison of lipopolysaccharides and soluble CD14 measurement between clinically endotoxaemic and nonendotoxaemic horses. Equine Vet J 49 (2), 155-159 PubMed.
  • Moore J N & Vandenplas M L (2014) Is it the systemic inflammatory response syndrome or endotoxemia in horses with colic? Vet Clin North Am Equine Pract 30 (2), 337-351 VetMedResource.
  • Jacobs C C, Holcombe S J, Cook V L et al (2013) Ethyl pyruvate diminishes the inflammatory response to lipopolysaccharide infusion in horses. Equine Vet J 45 (3), 333-339 PubMed.
  • Tadros E M & Frank N (2012) Effects of continuous or intermittent lipopolysaccharide administration for 48 hours on the systemic inflammatory response in horses. Am J Vet Res 73 (9), 1394-1402 PubMed.
  • Forbes G, Church S, Savage C J & Bailey S R (2012) Effects of hyperimmune equine plasma on clinical and cellular responses in a low-dose endotoxaemia model in horses. Res Vet Sci 92 (1), 40-44 PubMed.
  • Senior J M, Proudman C J, Leuwer M & Carter S D (2011) Plasma endotoxin in horses presented to an equine referral hospital: correlation to selected clinical parameters and outcomes. Equine Vet J 43 (5), 585-591 PubMed.
  • Alcott C J, Sponseller B A, Wong D M et al (2011) Clinical and immunomodulating effects of ketamine in horses with experimental endotoxemia. J Vet Intern Med 25 (4), 934-943 PubMed.
  • Werners A H, Bull S & Fink-Gremmels J (2005) Endotoxaemia: a review with implications for the horse. Equine Vet J 37 (4), 371-383 PubMed.

Other sources of information

  • Rowe E (2008) Management of Horses with Gastrointestinal Disorders. In: The Equine Hospital Manual. Ed: Corley K & Stephen J. Wiley-Blackwell, UK. pp 499-519.
  • Marino P (2013) Marino’s the ICU Book. 4th edn. Ed: Marino P. Lippincott, Williams, & Wilkins, USA.

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