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Monitoring and Intervention for the Critically Ill Small Animal The Rule of 20

  • Erscheinungsdatum: 10.10.2016
  • Verlag: Wiley-Blackwell
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Monitoring and Intervention for the Critically Ill Small Animal

Monitoring and Intervention for the Critically Ill Small Animal: The Rule of 20 offers guidance for assessing the patient, interpreting diagnostic test results, and selecting appropriate monitoring procedures. Based on Rebecca Kirby's time-tested Rule of 20, with a chapter devoted to each item on the checklist Provides comprehensive guidance for monitoring a critically ill small animal patient Emphasizes the interplay of each parameter with one another Designed for fast access on the clinic floor, with potentially life-saving ideas, tips, lists and procedures Presents tables, schematics, algorithms, and drawings for quick reference
Rebecca Kirby , DVM, DACVIM, DACVECC, was formerly an Associate Professor and Director of Emergency Services at the University of Pennsylvania, and served as owner of the Animal Emergency Center in Milwaukee, Wisconsin, USA for 21 years. Andrew Linklater , DVM, DACVECC, was trained at the Animal Emergency Center and is currently a Clinical Instructor at Lakeshore Veterinary Specialists in Milwaukee, Wisconsin, USA.


    Format: ePUB
    Kopierschutz: AdobeDRM
    Seitenzahl: 424
    Erscheinungsdatum: 10.10.2016
    Sprache: Englisch
    ISBN: 9781118900840
    Verlag: Wiley-Blackwell
    Größe: 40802 kBytes
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Monitoring and Intervention for the Critically Ill Small Animal

An introduction to SIRS and the Rule of 20

Rebecca Kirby

(Formerly) Animal Emergency Center, Gainesville, Florida
Introduction to the Rule of 20 and inflammatory response syndromes

Heat stroke, peritonitis, parvovirus diarrhea, systemic lymphosarcoma, leptospirosis, massive trauma, gastric dilation-torsion, aspiration pneumonia, pancreatitis, immune-mediated disease, and postoperative laparotomy are but a sampling of the multitude of potentially life-threatening disorders that can affect the small animal intensive care unit (ICU) patient. These and other disorders share a common pathophysiology: an inciting stimulus initiates the production and release of circulating mediators that cause systemic inflammatory changes.

Inflammation can be defined as a localized protective response elicited by injury or destruction of tissues that serves to destroy, dilute, or wall off both the injurious agent and the injured tissue [1]. Chemical mediators are released in response to an inciting antigen and initiate the innate immune response that causes inflammation. The classic signs of inflammation are heat, redness, swelling, pain, and loss of normal function. These are manifestations of the physiological changes that occur during the inflammatory process: (1) vasodilation (heat and redness), (2) increased capillary permeability (swelling), and (3) leukocytic exudation (pain). The initial inflammatory response to a localized insult is good, serving to localize the problem, destroy an offending pathogen, clean up damaged tissues, and initiate the healing process.

However, many ICU patients develop a negative trajectory when the inflammatory mediators and their response have systemic consequences. When this occurs due to an infection, it is called sepsis, and when it progresses, it often results in multiple organ dysfunction syndrome (MODS) or multiple organ failure (MOF).

It might appear logical that an overwhelming infectious agent could stimulate systemic inflammation. Yet, an almost identical clinical progression has been commonly observed in response to conditions that are not due to infection (such as trauma, surgery, and certain metabolic diseases). The term "sepsis syndrome" was first used to describe this in human patients when they appeared to be septic but had no obvious source of infection [2-4].

By the mid-1990s, sepsis syndrome had evolved into the nomenclature of systemic inflammatory response syndrome (SIRS). It was discovered that the body can respond to noninfectious insults and tissue injury in the same exaggerated manner that it does to microbial pathogens, with an almost identical pathophysiology [5]. In sepsis, pathogen-associated molecular patterns (PAMPs), expressed by the pathogen, stimulate pattern recognition receptors (PRRs) in the host. With noninfectious diseases, damaged tissues also release endogenous mediators, such as alarmins and damage-associated molecular pattern (DAMP) molecules (such as heat shock proteins, HMGB-1, ATP, and DNA). These will stimulate the toll-like receptor, PRRs or other receptor systems that typically respond to microbes and activate immune cell responses [6-8]. A list of proinflammatory cytokines associated with SIRS is provided in Table 1.1 . Figure 1.1 provides a schematic of many of the proinflammatory changes that occur in this syndrome.

Table 1.1 Inflammatory and hemostatic mediators of severe sepsis and their effects.

Adapted from: Balk RA, Ely EW, Goyette RE. Stages of infection in patients with severe sepsis. In: Sepsis Handbook, 2nd edn. Thomson Advanced Therapeutics Communication, 2004, pp 24-31.
Proinflammatory mediators Tumor necrosis factor IL-6 induction, TF expression, do

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