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    When organs fail one by one

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    CE Center

    RN/Thomson AHC Home Study Program

    CE credit is no longer available for this article. (Expired May 2008)


    Originally posted May 2006

    By Jennifer L. Duhon, RN, MSN

    JENNIFER DUHON is assistant professor of nursing at Illinois Central College in East Peoria, IL. The author has no financial relationships to disclose.

    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.

    Defenses take a destructive turn

    MODS can develop quickly following major surgery, trauma, or severe burns, or slowly as in the case of an infection that turns into sepsis. While it's not clear why some patients develop MODS while others don't, there are predisposing factors that increase the likelihood. Risk factors include:

    • Age (very young or very old),
    • Chronic disease, such as diabetes, cancer, or renal insufficiency,
    • Immunosuppressant therapy, and
    • Multiple blood transfusions.1

    Regardless of whether the insult to the body is infectious or not, it is the body's own defenses— the immune system and stress response—that 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 system—the 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 system.) As dysfunction progresses to failure, organs become so significantly altered that homeostasis can't be maintained without intensive medical support.1,3,7

    When organs malfunction

    Treating the cause, providing support

    Eliminating or minimizing potential triggers for SIRS by treating the underlying cause takes top priority. Thus, the physician may drain an abscess or remove an infected invasive line, vascular graft, or orthopedic device, for example.1,2

    Nursing care is mainly supportive, and geared toward preventing or limiting further destruction of each system. Controlling infection is paramount. Meticulous line care, thorough handwashing, and scrupulous attention to sterile technique is a must. Since more than half of all cases of MODS are triggered by a pathogen, patients should get broad-spectrum antibiotics, as ordered and without delay.3 Culture and sensitivity tests of sputum, blood, catheter tips, and urine must be done for all patients who are febrile.1 The physician will adjust the antibiotic regimen if a pathogen is discovered.

    Supporting oxygenation is critical: This involves increasing oxygen delivery with supplemental oxygen and fluid resuscitation.9 While noninvasive positive pressure ventilation can be used, most SIRS patients require mechanical ventilation. The goal of ventilator therapy is to maintain an SpO2 >90% and a PaO2 >60 mm Hg.9 But achieving this in a patient whose lungs are failing without causing further injury can be tricky.

    To protect the lungs, the patient should be given the lowest tidal volumes (6 ml/kg and end inspiratory plateau pressure <30 cm H2O), FiO2 levels, and amount of positive end-expiratory pressure (PEEP) possible to achieve the goals of therapy.2,9 Since PEEP changes the intrathoracic pressure and causes a drop in venous blood return to the heart, you'll need to closely monitor the cardiovascular status of patients in whom this system may already be compromised.

    At the same time, you'll want to prevent complications of ventilator therapy.10 Sedation and neuromuscular blockade may keep the patient from fighting the vent, which worsens hypoxemia. Other strategies include elevating the head of the bed 30 degrees; using a special endotracheal tube to suction away oral secretions that accumulate above the cuff, preventing ventilator-associated pneumonia; and positioning patients on a bed that provides continuous lateral rotation.10

    You'll also want to prevent other complications linked to ventilator therapy, such as deep vein thrombosis and peptic ulcers.10 The treatment of choice for DVT is low-dose heparin or one of the low molecular weight heparins, such as enoxaparin (Lovenox) or dalteparin (Fragmin). Peptic ulcers are prevented by administering H2 receptor inhibitors such as cimetidine (Tagamet) and ranitidine (Zantac).

    The goal of fluid resuscitation is to maintain a central venous pressure of 8 – 12 mm Hg (12 – 15 mm Hg for patients on a ventilator to account for increased thoracic pressure) and a urine output of at least 0.5 mg/kg/hr.2,9 Either crystalloids or colloids can be used. There's no evidence supporting the use of crystalloids over colloids.9 In fact, crystalloids require more volume to achieve the same ends, so they may exacerbate edema more than other fluid choices.9

    If fluids alone fail to support circulation, the physician will add an IV infusion of a vasopressor such as dopamine (Intropin) or norepinephrine (Levophed).2,9 You will need to titrate these drips to maintain a mean arterial pressure of at least 65 mm Hg.2,9 However, if the patient's oxygenation is still poor (mixed venous saturation <70%), you'll be ordered to administer dobutamine (Dobutrex) for inotropic support or packed red blood cells to improve the oxygen-carrying capacity of the blood. The goal here is a hemoglobin level of 7 – 9 gm/dL.2,9

    To reduce oxygen demand, you'll need to control fever by using cooling devices or antipyretics such as acetaminophen. Manage pain with analgesia and anxiety with sedation, as needed.2

    Attention in recent years has focused on limiting direct tissue destruction caused by MODS. Recombinant activated protein C—drotrecogin alfa (Xigris)—is one of the most promising drug therapies and works by dampening both inflammation and coagulation.9 It blocks the release of inflammatory mediators, limits endothelial damage, inactivates the coagulation cascade, and breaks down clots. It's indicated for patients with three or more signs of SIRS and evidence of early organ dysfunction. Because activated protein C has both antithrombotic and profibrinolytic properties, it's contraindicated in those at risk for bleeding.2,9

    To support the patient's increased need for energy, providing adequate nutrition is a must. Enteral feeding is preferred over parenteral.2,9 Enteral feeding helps restore the gut mucosa and prevents gut atrophy.7 Another plus is that a patient who can tolerate enteral feedings may be able to forgo peptic ulcer prophylaxis.

    Keeping blood sugar below 150 mg/dL is a measure that has been proven to reduce mortality from MODS.2,9 Patients should be started on an infusion of IV insulin. You'll need to assess serum glucose every hour and adjust the rate, as ordered. Keep in mind that as organs fail, hypoglycemia may become a problem, and patients may require an infusion of dextrose, 5% or 10%, prophylactically.9

    Other interventions include renal replacement strategies, such as intermittent hemodialysis or continuous venovenous filtration, to treat renal failure, and steroid therapy to treat adrenal insufficiency.2,9 Regardless of the specialty bed, good nursing care includes assessing the skin, particularly the occiput in patients on rotating beds, and repositioning as needed to prevent skin breakdown.

    Remember to support the family, too.2 Encourage them to ask questions and let them know that their presence at the bedside is an important part of the patient's healing. Keeping the communication lines open is fundamental to a smooth discussion should end-of-life care decisions need to be made.

    A positive outcome to a downward spiral

    Mr. Sherman, the patient whose case was described earlier, demonstrated the classic physiologic response to trauma and the development of MODS. He had many of the major risk factors, including tissue hypoxia, multiple transfusions, sepsis, and respiratory failure. When his condition continued to deteriorate despite treatment with antibiotics, he was started on continuous activated protein C. He remained on the drug for 96 hours, at an infusion rate of 24 mg/kg/hr.1

    During that time, his condition started to stabilize. His temperature dropped from 103° F (39.4° C) to 100° F (37.8° C) and his WBC count fell from 27,600/mm3 to 12,100/mm3. Mr. Sherman's chest X-rays also revealed great improvement and his hemodynamic parameters normalized.

    Less than three weeks after the accident, he was transferred to a rehabilitation facility. And six months after his injury, he could walk without the use of an assistive device. Only minimal pain in his left sacroiliac joint remained.

    Mr. Sherman was among the lucky ones. Many, if not most, patients who develop MODS do not have such a positive outcome. In some cases, having a nurse who watches carefully for subtle changes that could signal organ dysfunction in a severely ill or injured patient can make the difference.


    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).


    Suspect SIRS if a patient has two or more of the following:

    • Temperature >100.4° F (38° C) or <96.8° F (36° C)
    • Heart rate >90 beats per minute
    • Respiratory rate >20 breaths per minute
    • White blood cell count >12,000/mm3 or <4,000/mm3
    • >10% immature neutrophils (bands)

    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.

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    Jennifer L. Duhon, RN, MSN
    JENNIFER DUHON is assistant professor of nursing at Illinois Central College in East Peoria, IL.