When organs fail one by one

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 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

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 ventilatorassociated 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 oxygencarrying 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 Cdrotrecogin 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.

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:

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.