1. Identify patients at high risk of developing MODS.
2. Identify causes and pathophysiology of MODS.
3. Identify the priorities needed for prevention and treatment measures of MODS .

CW, a 53 year old caucasian male with COPD (chronic obstructive pulmonary disease) arrives at the Emergency Department after suffering trauma to the chest from a motor vehicle accident.  He complains of dyspnea with an increased respiratory rate and pulse. 
Cultures revealed pneumococci in the sputum and Chest X-ray showed bilateral lower lobe pneumonia and multiple lung contusions.  CW was admitted to the medical unit and treated with bronchodilators, fluid, morphine, and antibiotics.

On day two, the patient was found to be confused, hypotensive, and having severe respiratory distress.  The patient had labored respirations at 36/min, blood pressure 80/52 mmHg, a pulse of 148 beats/min, and temperature of 102 degrees.  He had 4+ pitting edema and noted periorbital edema.  Auscultation of the lungs revealed bilateral crackles, increased resonance, and fremitus.  The patient's schlera showed jaundice. 
CW's once adequate urine output was now only 70cc in 8 hours per foley, despite IV fluids running at 250 cc/hr.  CW was transferred to a Medical Intensive Care Unit (MICU).  Orders were a 12 lead ECG, Chemistry and Metabolic labs, and PA (Posterior/Anterior) chest radiograph to determine differential diagnosis of pulmonary hypertension, ARDS (Acute Respiratory Distress Syndrom), Shock, Sepsis, or MODS.

Multiple organ dysfunction syndrome is a progressive failure of two or more organs.  This can be the result of acute illness, sepsis, trauma, systemic inflammatory responses, ARDS, burns (severe full thickness), a single organ failure, and other bodily insults. These causes of MODS are aggravated by the body's natural cascades and feedback loops ( Slutsky, Tremblay , 1998).  The pathophysiology is not completely known, but is understood on the basis of each system failure.  Altered tissue perfusion and oxygen delivery affect all organ systems.  This explains why it usually begins in the pulmonary, or hemodynamic systems, altering tissue perfusion to the renal, cardiac, hepatic, and gastrointestinal systems.  Diagnostic criteria include the following organ systems:

1.  Cardiovascular failure
2.  Respiratory failure
3.  Renal failure
4.  Neurologic failure
5.  Hepatic Failure
6.  Hematologic failure
(Black, Matassarin-Jacobs, 1997)

Predicting factors for MODS 12 hours after insult or injury include;  severity of tissue injury, the number of blood tranfusions given, use of inotropes, platlet count, and age.  The severity of tissue injury increases the occurance of MODS, by the immune and inflamatory processes that follow.  More than 6 units of blood has statistically shown a correlation to the development of MODS. Signs of shock, such as lower platelets and longer prothrombim time (PT), are signifigant indicators of MODS.  Age greater than 45 years increases the chances of developing MODS by two times compaired to younger ages.  The development of an infection is a preceeding factor in MODS (Sauaia et al., 1998).

At first MODS may show signs of low-grade fever, tachycardia, dyspnea, hypermetabolism, and altered mental status (Huether et al., 1996).

CW had been a smoker for 30 years, used to work in asbestos removal, and had an antero-septal MI (Myocardial infarction) six years ago.  He was diagnosed NIDDM (Non-Insulin Dependent Diabetes Mellitus) and is diet controlled.

Risk factors for developing MODS:

• Impaired immune response
• Prolonged inflammatory response
• Malnutrition
• Age/Elderly
• Cancer
• Malnutrition
• Chronic illness (Sauaia et al., 1998)
• Persisitent infectious agent (Black, Matassarin-Jacobs, 1997)
• Full-thickness Burns (Cryer et al., 1999)
• Certain drug over doses (Miller et al., 2001)
• Alcohol abuse (Moss et al., 1999)

CW is married with adequate income and medical insurance.  Father had chronic renal failure and died of a stroke at the age of 62.

While there has yet to be evidence of familial risk factors, research continues. 
Socioeconomic status may be an area of concern for healthcare providers due to the extensive ICU costs of care and length of stay needed with a grim prognosis.  With this prognosis comes the fact that MODS is a relatively new described disease process, first discussed around 1975.  Mortality of MODS ranges from 60 to 100% (Huether et al., 1996).
 

Day 2 for CW in MICU.  Vital signs have progressively deteriorated, but have instead worsened with a pulse of 162, BP (Blood Pressure) 80/44, temp 101 (Tylenol 650 mg given 1 hour prior), respiratory rate 40/min, labored breaths, using accessory muscles, jaundice present in schlera and on skin tone.
Lungs dull to percussion.  Crackles and rales present upon auscultated.  Edema is present 4+ in extremities and periorbital edema.  Heart sounds muffled S1 and S2.  No bowel sounds are present, urinary output remains under 10cc per hour per Foley catheter.  CW lost consciousness after transfer to MICU.  CW was intubated, and placed on mechanical ventilation and sputum cultures were taken.

After initial injury the body releases stress hormones.
Inflamatory mediators released make the vasculature permeable, allowing fluid leak, hypotension, and microvascular coagulation.  Extreme inflammation and coagulation causes cardiovascular problems, clotting, and edema.  The massive cascades cause the immune system to respond.  Maldistribution of blood flow, hypotension, and decreased oxygen transportation follows creating tissue hypoxia (Huether et al., 1996).

The lungs are usually the first organ to fail, commonly by ARDS.  Common associated conditions with MODS are pulmonary, cardiac, renal, neurologic, and hepatic conditions in conjuncture with sepsis and DIC (disseminated intravascular coagulation).
For more about DIC click here
It is important to monitor for any system failure to prevent MODS in susceptible patients.  Patients usually show signs of organ failure 24-72 hours after insult (Cryer et al., 1999).  Clinical manifestations of MODS usually include, fever, leukocytosis, tachycardia, tachypynea, hemodynamic finding of sepsis and DIC.
One third of septic deaths are due to MODS (White, 1997).
For more information about sepsis click here.
 

CW's lab tests returned:
 

Lab	Patient Value	Normal Range
hemoglobin	9.5 g/dL	14-18 g/dL
platelets	22 X 109	150-450 X 109
hematocrit	27%	40-54%
WBC	13.5 X 109	4.5-11.0 X 10 9
BUN	98 mg/dl	5-20 mg/dL
creatinine	5.2 mg/dl	0.6-1.3 mg/dL
AST	539 IU/L	8-26 IU/L
ALT	382 IU/L	54 IU/L
bilirubin	5.1 mg/dl	0.1-0.4 mg/dL
ABG's		on vent at 40% O2
pH	7.31	7.35 - 7.45
PCO2	30	35-45
PO2	52	90 and above
HCO3	15 mmol/L	22-26 mmol/L

Chest X-ray revealed fluid accumulation within alveolar spaces.  CW was diagnosed with ARDS.
For more information on ARDS click here
CW was given a pulmonary artery catherization. CW's PAWP (Pulmonary Artery Wedge Pressure) - 10 mmgHg, cardiac index was 2.5 L/min, and systemic vascular resistance (SVR) 1620 dyne sec/cm.

With inury to lungs and alveolar capillary edema, inflammatory mediators are released into the blood stream.  These mediators play a role in the pathophysiology of multisystem organ failure.  Experimental data suggests that mechanical ventilation can cause or increase lung injury and increase surfactant and alveolar collapse, and this can cause ventilator induced MODS.  During this condition, the body is in a hypermetabolic state and needs more oxygen.  In CW's case, there is a lack of oxygen.  ARDS and septic shock are initialting events in MODS (Black, Matassarin-Jacobs, 1997).

Modified Apache II Diagnostic Criteria for Multiple System Organ Failure
Cardiovascular Failure (presence of one or more of the following)

• Heart Rate < 54 beats/min
• Mean artierial pressure < 49 mm Hg (systolic pressure < 60 mm Hg)
• Occurrence of ventricular tachycardia or ventricular fibrilation
• Serum pH < 7.24 with a PaCO2 of < 40 mm Hg

• Respiratory rate < 5 breaths/min or > 49 breaths/min PaCO2 > 50 mm Hg
• Alveolar-arterial oxygen difference > 350 mm Hg (calculate as follows, at sea level): (713 X % oxygen in inspired gas) - PaCO2 - PaO2
• Dependent on ventilator or CPAP on the second day

• Urine output < 479 ml/24 hr or < 159 ml/8 hr
• Serum BUN > 100 mg/dl (35.7 mmol/L)
• Serum creatinine > 3.5 mg/dl (309 µmol/L)

• WBC count < 1000/µl ( 1 X 10⁹ /L)
• Platelets < 20,000/µl (20 X 10⁹/L)
• Hematocrit < 20%

• Glasgow Coma Score < 6 (in absence of sedation)

• Serum bilirubin > 6 mg%
• Prothrombin time > 4 sec over control in the absence of systemic anticoagulation (Black, Matassarin-Jacobs, 1997)

There has been evidence that Multisystem Organ Failure is an auto-destructive inflammatory process involving specific mediators.  These mediators increase the pulmonary edema, hypermetabolism, need for oxygen, systemically the lack of oxygen and sepsis or shock.

Following any of these processes comes shock and DIC.  When the patient goes into shock hemorrhage or a drop in organ perfusion causing secondary insult to all vital organs.  The heart is affected by decreased coronary blood flow and reduced myocardial oxygen supply.  Myocardial damage is usually an effect. Due to ARDS the gas exchange abnormalities decrease oxygen delivery to other organs.  Shock results in serious liver damage, which can aid in coagulation and excess toxins.  DIC could result during this coagulation process.  If preceeding symptoms of DIC or shock is noted early in this process, MODS can be prevented ( Slutsky, Tremblay, 1998). 

Initial cardiovascular pathophysiology effects are inflammatory mediator, hypovolemia, vasodilation, tissue hypoxia, and increased lactate (from anaerobic production) (Cryer et al., 1999).

Additional lab values include:

• Plasma cortisol levels increase, leading to sepsis and septic shock
• Leukocytes, Thrombocytopenia
• Activation of coagulation cascade
• Possible DIC
• Acute Tubular Necrosis from nephrotoxins (Swearingan et al., 2001).

CW's humidified O2 was increased using the mechanical ventilator and PEEP (Positive end expiratory pressure).  Sodium bicarbonate was given with an IV push 1mEq/kg and repeated .5mEq/kg every 10 minutes for 30 minutes to reverse the acidosis.  The patient was given fluid restriction, BUMEX, and Vasopressors (Dopamine 10mcg/kg/min) per IV drip, ABG's were taken every 15 minutes X 8.  IV colloids and crystalloids, total parental nutrition, and prophylactic antibiotics, were also given.  CW was stabilized later that night. This care was maintained throughout the evening.  Liver and renal functioning were improving, and urinary output was increasing close to 20 cc/hr.  CW was given methyl-prednisolone 40mg every 6 hours, PaO2 was 82, mechanical ventillator was back down to 40%oxygen.  BP was therapeutic at 125/65 with the Dopamine drip.  CW spent the next 28 days in ICU and maintained a slow progression.  He was weaned off of the vent and transferred to a step down unit and was discharged 22 days later to a rehabilitation hospital.

When treating a patient with MODS supportive measure are used, monitoring lab values, and hemodynamics. The priority is obviously ABC's (Airway, Breathing, Circulation); oxygen therapy must be monitored closely to prevent further trauma or oxygen toxicity.  It is essential to monitor for respiratory changes and maintain the patient's airway per sunctioning.  Nursing care such as repositioning can increase the oxygen consumption, nurses must monitor the paitent and avoid activity that may increase oxygen consumption.  It is also important to monitor the cardiac status for induced arrythmias, monitor the PEEP because it may lower CO (cardiac output), monitor blood pressure and titrate dopamine drip appropriately.  To prevent muscle wasting, a nitrogen equilibrium and adequate nutrition supply are necessary. Prevention is the key, monitor potential patients and be alert of common manifestations.  Oxygen and nutritional support are standard protocol for these patients.  Prevent or treat any infection, before the patient becomes septic. 

Prevention of MODS should be a priority of critical care providers.  Identifying patients at  risk, monitoring protocol and procedure, and early resucitation may prevent a devastating  disease process from occuring.

In a study to determine predicting factors to MODS, results showed being older than 45 years of age, having a high injury severity score, being given more than 6 units of RBC in 12 hours, and lactate levels may be early predictors of organ failure (Sauaia et al, 1998).

The mortalitiy rate of MODS is very high.  To understand why some people survive and others don't we must continue to try to understand MODS.  The research continues. One study showed mortality for patients with one organ failure was 40%, this increases with  two organ to 60% mortality(Zimmerman et al, 1996).  Therefore the more organs affected the higher mortality rate.  An additional study suggests the severity on the first day of organ failure is more associated with death than the number of organs affected (Anonymous, 1997). One research group found that MODS patient mortality is better predicted in the first 48 hours than thereafter (Ferreira et al., 2001).  Once MODS has been diagnosed supportive treatment to the organs effected is priority. There is no one preferred treatment for MODS, to reverse the occurrence or incidence of mortality (Vincent, 1996).A study found that patients with MODS who died had functional impairments and lower quality of life.  Limiting aggressive treatment might aid the family members of emotional suffering (Somogyi-Zalud et al., 2001).

With knowledge and preparation we can improve a patient's care and outcomes before and after MODS.  It is necessary to understand the interventions and rationale to apply information to a personalized case of MODS. With so many causes, every intervention needs to be individualized to the patient's needs. Multisystem organ failure is not a simple disease process, many other processes are involved and with this in mind it may be better understood.
 

Anonymous. (1997). ICU studies focus on triage of low-risk patients and outcomes for patients with organ system failure. Research Activities(202),10.

Black, J.M., Matassarin-Jacobs, E., (1997). Medical-surgical nursing:  Clinical management for continuity of care. Philadelphia, PA: W.B. Saunders Company.

Cryer, H.G., Leong, K., McArthur, D.L., Demetriades, D., Bongard, F.S., Fleming, A. W., Hiatt, J.R., & Kraus, J.F., (1999).  Multiple organ failure: By the time you predict it, it's already there. Journal of Trauma-Inury Infection & Critical Care, 46 (4), 597-606.

Ferriera, F.L., Bota, D.P., Bross, A, Melot, C, & Vincent, J.L. (2001). Serial evaluation of the SOFA score to predict outcome in critically ill patients. Journal of the American Medical Association, 286(14),1754-1768.

Hurther, S.E., & McCance, K.L., (1996). Understanding pathophysiology . St Louis, MS: Mosby

Kirton, O.C., Windsor, J., Weddenburn, R., Hudson-Civetia, J. Shatz, D.V., Mataragas, N.R., Civetta, J.M. (1998). Failure of splanchnic resuscitation in acutely injured trauma patients correlates with multiple organ system failure and length of stay in the ICU. Chest, 113 (4),1064-1070.

Miller, H.M., Haller, C., Pialbo, M., Brown, C., & Aggarwal, A. (2001). Colchcine related death presenting as an unknown case of multiple organ failure. Journal of Toxicology: Clinical Toxicology, 29(5), 511.

Moss, M., Steinberg, K.P., Guiclot, D.M., Duhon, G.F., Treece, P., Wolken, R., Hudsen, L.D., & Parsons, P.E. (1999). The effect of chronic alcohol abuse on the incidence of ARDS and severity of multiple organ dysfunction syndrome in adults with septic shock. Chest, 116(1),97.

Sauaia, A, Moore, F.A. Moore, E.E., Norris, J.M., Lezotte, D.C., & Hannan, R.F. (1998). Multiple organ failure can be predicted as early as 12 hours after injury. Journal of Trauma-Injury Infection & Critical Care, 45(2), 291-303.

Slutsky, A.S., & Tremblay, L.N. (1998). Multiple system organ failure: Is mechanical ventilatoin a contributing factor? American Journal of Respiratory and Critical Care Management, 157 (6),1732-1725.

Somogyi-Zalud,E., Zhong,Z., Lynn, J., Dawson, N.A., Hamel, M.B., & Desbiens, N. A., (2000). Dying with acute respiratory failure or multiple organ system failure with sepsis. Journal of the American Geriatrics Society, 48 (5), 140-146.

Swearingan, P.L. & Keen, J.H., (2001). Manual of critical care nursing . St Louis, MS: Mosby.

Tan, K., Khoo, K.L., Hsu, A.A.L., Ong, Y.Y.,  &Eng, P. (1999). Organ dysfunction and outcomes of medical intensive care unit. Chest, 116(4),367.

Vincent, J.L.(1996). Prevention and therapy of multiple organ failure. World Journal of Surgery, 20, 465-470.

Weinbraoun, A.A., Hochhauser, E., Rudick, V., Kluger, Y., Karchevsky, E., Graf, E., Vidne, B.A. (1999). Multiple organ dysfunction after remote circulatory arrest: Common pathway of radical oxygen species.  Journal of Trauma-Inury Infection & Critical Care, 47(4), 691-699.

White, K.M. (1997). Understanding the hemodynamics of sepsis. Springnet Available online: [http://www.springnet.com/ce/s705a.htm]

Zimmerman, J.E., Knaus, W.A., Sun, X., & Wagner, D.P. (1996). Severity stratification and outcome prediction for multisystem organ failure and dysfunction. World Journal of Surgery, 20 , 401-405.
 
 

Matt Krebsbach RN BSN
SICU, Surgery

Contact Jo Voss for information or questions related to this case study.