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It's important to know who's at risk for organ failure after infection or injury. Your early
intervention can prevent the development of the often-fatal syndrome known as MODS.
When his safety belt broke, a 27-year-old construction worker I'll call Matt Sherman fell from
scaffolding and fractured his left tibia-fibula and femur. A set of X-rays done during his initial
trauma workup in the ED revealed multiple left rib fractures, a large hemopneumothorax, and a
left vertical shear fracture of the pelvis.1
After surgeons repaired a splenic laceration and stabilized his pelvis, femur, and tibia, Mr.
Sherman was transferred to the ICU in critical condition. For the next three days, he had
numerous problems with his hemodynamic parameters, urine output, and temperature.
His oxygenation saturation level dropped, his respiratory rate increased, and chest X-rays
showed diffuse, fluffy white infiltrates. His blood pressure was below 90 mm Hg systolic and he
looked like he was going into shock. After studying Mr. Sherman's clinical, hemodynamic, and
laboratory data, physicians diagnosed early sepsis with multiple organ dysfunction syndrome
(MODS).
A progressive impairment of two or more organ systems, MODS is caused by the immune
system's uncontrolled inflammatory response to a severe illness or injury.2,3
It's a common cause of death for patients in the ICU. Mortality rates for MODS range from an
estimated 50% to just under 100%, with the outcome dependent upon the underlying cause, the
number of organ systems involved, and the degree of organ damage.2,4
Identifying those at risk for MODS and acting quickly to stop its progression can keep your
patient from becoming a statistic. Knowing what to look for and how to respond is crucial,
whether you work in the ED, on a med/surg unit, or in the ICU.
Regardless of whether the insult to the body is infectious or not, it is the body's own defenses
the immune system and stress responsethat together damage organs one by one.4 The immune
system triggers inflammation that's supposed to contain the intruder, injured area, or irritant, get
rid of dead tissue, and restore balance. But as inflammation progresses from a local to a systemic
response, it gathers intensity and can end up doing the body more harm than good.3,4
This systemic reaction to injury or infection has its own name: systemic inflammatory response
syndrome. SIRS can lead to organ damage independent of the trigger that sets it off. That's
because the powerful inflammatory mediators (cytokines and chemokines) that drive the process
cause both direct and indirect tissue damage, which in turn triggers the release of more
inflammatory mediators in a self-perpetuating downward spiral.5,6
And what happens when these mediators run amok? The mediators that promote peripheral
vasodilation end up causing severe hypotension. Those that increase capillary permeability cause
the body's fluids to shift out of the vascular bed and into the interstitial spaces, causing
pulmonary and generalized edema. Those that activate the clotting cascade create microemboli
that lodge in capillary beds all over the body. The result: global tissue hypoxia.5
Without oxygen, organs rapidly fail. The body tries to defend itself by activating the sympathetic
nervous systemthe stress response. But like the immune system, it too ends up doing more
harm than good. Catecholamines (adrenaline and norepinephrine) boost the falling cardiac output
by increasing the heart rate and shunting the blood supply back toward the heart.2,5
Unfortunately, they do so at the expense of the gut and kidneys.
Taking blood from the gut leads to necrosis and allows gut bacteria to translocate into the
bloodstream, exacerbating or causing sepsis.7 Taking blood from the kidneys impairs their ability
to eliminate toxins and maintain acid-base balance. Stress hormones (glucagon, cortisol,
glucocorticoids, others) block inflammation and bolster the body's energy needs by pulling
glucose out of storage.2,5 But their side effects cause numerous problems, including insulin
resistance, hyperglycemia, sodium and water retention, and stress-induced ulcers.2
Starved for oxygen, the body's tissues turn to anaerobic metabolism for energy; lactate is a
byproduct. Without intervention, lactic acidosis leads to death.
Since the lungs are highly sensitive to mediator-induced inflammation, they are often the first
system to show signs of failure in the progression of SIRS to MODS.5,8 Damage to lung tissue
can occur within 90 minutes of the onset of SIRS. That's why there's no time to waste in
detecting SIRS and providing targeted intervention.5,8(For the signs and symptoms of SIRS, see
the box at the end of this article.)
Once the lungs start failing, the liver, kidneys, and gut follow.3 The sequence of organ failure is
not set in stone, however. (The table below lists the signs of dysfunction and failure for each
REFERENCES
1. Walsh, C. R. (2005). Multiple organ dysfunction syndrome after multiple trauma. Orthop Nurs, 24(5), 324.
2. Kleinpell, R. M. (2006). Multisystem problems. In Chulay, M., & Burns, S. M., AACN essentials of critical care nursing. (pp. 267 278). New York:
McGraw-Hill.
3. Sharma, S., & Eschun, G. "Multisystem organ failure of sepsis." 2004. www.emedicine.com/med/topic3372.htm (15 Feb. 2006).
4. Marshall, J. C. "The multiple organ dysfunction syndrome." 2001. www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=surg.chapter.5364 (15 Feb. 2006).
5. Kaplan, L. "Systemic inflammatory response syndrome." 2004. www.emedicine.com/MED/topic2227.htm (1 Mar. 2006).
6. Vincent, J., & De Backer, D. (2005). Does disseminated intravascular coagulation lead to multiple organ failure? Crit Care Clin, 21(3), 469.
7. Deitch, E. A. "Role of the gut in multiple organ dysfunction syndrome." 2004. www.umdnj.edu/research/publications/fall 04/03_multiple_organ.htm (15
Feb. 2006).
8. Bhatia, M., & Moochhala, S. (2004). Role of inflammatory mediators in the pathophysiology of acute respiratory distress syndrome. J Pathol, 202(2),
145.
9. Delinger, R. P, Carlet, J. M., et al. (2004). Surviving Sepsis Campaign guidelines for management of severe sepsis and septic shock. Crit Care Med,
32(3), 858.
10. Institute for Healthcare Improvement. "Implement the ventilator bundle." www.ihi.org/IHI/Topics/CriticalCare/Intensive
Care/Changes/ImplementtheVentilatorBundle.htm (24 Mar. 2006).
SIGNS OF SIRS
Suspect SIRS if a patient has two or more of the following:
Source: Kleinpell, R. M. (2006). Multisystem problems.In Chulay, M., & Burns, S. M., AACN
essentials of critical care nursing. (pp. 267 278). New York: McGraw-Hill.