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Baue, Arthur E.

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doi: 10.1097/01.shk.0000228172.32587.7a
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Though old the thought and oft expressed, tis his at last who says it best. James Russell Lowell, For an Autograph, 1868


Early in World War II, the major problem after injury was hemorrhagic shock (wound shock). As blood transfusions were made available and fluids, along with surgical intervention, were used, this became less of a problem (1). Late in World War II, renal failure or post-traumatic renal insufficiency was found to be a problem in the severely wounded, which continued through the Korean conflict (2). With more rapid fluid resuscitation, renal failure was prevented more frequently. The problem then became the lungs-post-traumatic pulmonary insufficiency (shock lung), which was most evident during the Vietnam conflict (3). Burke et al. reported on high-output respiratory failure as an important cause of death with peritonitis in 1963 (4). Acute respiratory distress syndrome (ARDS) was described by Ashbaugh et al. in 1967 (5). Early aggressive use of positive pressure ventilation decreased the incidence of pulmonary failure. Thus, single organ failure as a cause of death decreased. There was identification of multiple organ problems. Skillman et al. (6) described respiratory failure, hypotension, sepsis, and jaundice as a complication leading to death in stress ulceration of the stomach.

The descriptions of multiple organ problems began with sequential systems failure (SSF) after ruptured abdominal aneurysms by Tilney et al. (7) in 1973. Then I described multiple progressive or SSF, a syndrome of the 1970s, in 1975 (8). Eiseman et al. (9) first used the term multiple organ failure (MOF) in 1977.

Border et al. (10) wrote about multiple system organ failure in 1976. In 1977, Polk and Shields (11) described remote organ failure as a valid sign of occult intra-abdominal infection. In 1980, Fry and colleagues (12) stressed the role of uncontrolled infection in multiple system organ failure. Chaudry and I (13) wrote about the prevention of multiple system failure at the same time. There was then an explosion of contributions to our knowledge and more acronyms about organ failure (Table 1). Goris et al. (14) described MOF as a problem of generalized acute destructive inflammation, and later, a model for MOF without sepsis and bacteria. Faist et al. (15) described MOF in polytrauma patients. McMenamy et al. (16) described the basal state in MOF. Meakins (17) emphasized the 1-hit/2-hit multiple hits in the development of MOF. He, along with Marshall (18), called the gastrointestinal tract the "motor of MOF." Carrico et al. (20) used the expression "multiple organ failure syndrome."

Knaus and colleagues (21) developed a scoring system for acute organ system failure and emphasized the high mortality. This became the Acute Physiology and Chronic Health Evaluation scoring system. Wilmore and Orlick (22) described the systemic responses to injury and wounds. Cerra (23) wrote about the hypermetabolism organ failure complex in 1987. Bell et al. (24) wrote about multiple organ system failure in 1983. Darling et al. (25) described multiorgan failure in critically ill patients in 1988. Crump et al. (26) described MOF after trauma.

Maier (27), in a review of critical care and metabolism, describes MOF as a "malignant systemic inflammatory response caused by the host's own immune system." Carrico et al. (28) described the incidence and problems of the multiple organ failure syndrome.

Members of the Canadian Multiple Organ Failure Study Group (29) proposed discriminating between the phenomenon of the effects of micro-organism (infection) and the response of the host (sepsis). Pruitt (30) reviewed the proposal of Nuytinek et al. of increased organ weight and intraorgan accumulation of neutrophils as the preclinical stage of MOF.

Ueno et al. (31) noted a correlation between thrombocytopenia and MOF in critically ill patients. A number of studies of the mediators and causes of MOF after trauma have been reported such as those by Waydhas et al. (32) and Nuytinck et al. (33), who described whole-body inflammation leading to MOF. Roumen et al. (34) studied inflammatory mediators leading to MOF after trauma. DeCamp and Demling (35) explored post-traumatic organ failure. A cellular injury score was developed by Oda et al. (36).

The group in Denver with Ofner and Moore, Moore et al., and Sauaia et al. (37-41) made many contributions to our knowledge of MOF. They emphasized the risk factors for MOF in trauma patients, including massive blood transfusions, major abdominal trauma, and multiple fractures. They found that early deaths were associated with interleukin 6 going up (inflammation out of control), and late deaths were due to infection (42). In 1983, Ozawa et al. (43) developed a redox theory for the metabolic abnormalities associated with postoperative organ failure.

Hyers et al. (44) reviewed cellular interactions in the multiple organ injury syndrome. Bumaschny et al. (45) describe MOF occurring after postoperative acute gastrointestinal tract hemorrhage. Godin and Buchman (46) offered a complementary hypothesis, the uncoupling of biological oscillators in the pathogenesis of multiple organ dysfunction syndrome (MODS). Vincent and DeBacker (47) emphasized the importance of treatment of circulatory shock to prevent MSOF.

A number of books have been written about MOF. The first was my book on MOF in 1990, (48) which I wrote myself, with a chapter written by my wife Rosemary on the "Patient as a Person: Ethical Considerations of Patients with MOF." et al. (49) edited a multiauthored book on MOF. Matuschak (50), and also Deitch (51), edited multiauthored books on MOF. Fry (52) also wrote a book. There are other books resulting from symposia and Congresses. MOF has been reported in patients with burns, after liver transplantation and cardiac surgery, in children, in patients with perforated viscera, splanchnic ischemia, and many other problems.

A change in focus occurred with the development of the concept of MODS and its score and the systemic inflammatory response syndrome (SIRS). Systemic inflammatory response syndrome was defined by a consensus conference of the American College of Chest Physicians and the Society of Critical Care Medicine (53) as a clinical syndrome that is thought to be the result of an overly active inflammatory response. Vincent (54), Bone (55), Opal (56), and others believe that the concept of SIRS does not help, and I agree. Systemic inflammatory response syndrome is defined as two or more of the following conditions:

  1. Temperature greater than 38°C or less than 36°C;
  2. Heart rate greater than 90 beats/min;
  3. Respiratory rate greater than 20 breaths/ min or PaCO2 less than 32 torr;
  4. White blood cell (WBC) greater than 12,000 cells mm−3 or less than 4000 cells mm−3 or greater than 10% immature (band) forms.

I have no problem with the use of SIRS as a nonspecific description of being sick. I do have a problem with going beyond that such as using SIRS criteria for randomized trials of therapy. No one has reported on the appearance of patients with SIRS. Don't they look sick? Can't clinical observation also tell you that they are sick? Anyone with SIRS is sick. Systemic inflammatory response syndrome has been highly touted as a way to define and measure sickness. Has it helped? Is it worthwhile? Let us go beyond the hype of those who have a vested interested in SIRS because they invented the concept. The trained clinician observes his patients beyond just vital signs. I recommend to my students and residents that during rounds, they should go into the patient's room or cubicle in the intensive care unit or elsewhere and observe and talk to the patient before they check the chart and the vital signs. This allows them to determine the patient's state as the patient feels it or experiences it.

On the other hand, MODS emphasized an early phase of organ dysfunction before overt failure occurred. It is defined as "the presence of altered organ function in an acutely ill patient such that homeostasis cannot be maintained without intervention." The concept of MODS was developed by Marshall et al. (57) Identification of this abnormality might occur in a period when organ support can yield better function and prevention of organ failure. Systemic inflammatory response syndrome was an attempt to describe a state of illness resulting from trauma or infection-the early response of the individual by inflammation and the clinical characteristics of that state.

It is important to remember that SIRS, MODS, MOF, and all the other names and descriptions of multiple organ problems are not diseases or even syndromes. They are terms with arbitrary definitions that cannot be treated as such. The specific underlying diseases causing these conditions must be identified and treated while organ function is supported. Thus, trying to keep SIRS from progressing and trying to improve MODS and prevent MOF is all we can do. Success of the effort will depend primarily on whether we can find, diagnose, and treat the specific problem making the patient sick. Irrespective of whether it is an undrained abscess, a nosocomial infection, a severe injury, end-stage cardiac or pulmonary disease, or other problems, our success depends on being able to correct, treat, or stamp out the problem.

We all seem to have a great need to name things. The plethora of alphabet soups or acronyms, terms, and expressions for the pathophysiologic state of sick, injured patients is overwhelming. We try to reduce complex clinical problems in even more complex patients to simplistic concepts of sickness, inflammation, and sepsis. It is true that the human body can respond clinically to an insult in only so many ways. Similar changes in vital signs, respiration, mentation, organ function, and circulating blood elements or mediators occur with many clinical problems, but the question is, "Does this reductionism helps us to take better care of such patients?"

The information learned from molecular biology is extremely complex. The overlap and redundancy of mediators and receptors of cascades, of signaling, and mechanisms of remote organ damage in the endothelium and microcirculation are wondrous to behold but difficult to understand and put into a coherent whole. We are learning of so many pieces in the biological puzzle, but what is the picture? Can we inter-relate these complexities into an understandable pattern and, more specifically, can we use such information for therapy? So far, this has not been possible. The failure of so-called magic bullets attests to this dilemma. The terms, expressions, and acronyms used for organ difficulties after the description of MOF are shown in Table 1. Those used for infection and inflammation are shown in Table 2. The teleology of SIRS, MODS, and MOF is listed in Table 3. It is amazing how many articles on MOF do not refer to the original articles. It should be possible to summarize all of the definitions and scoring systems for organ failure into some coherent system. There are more than 20 definitions, descriptions, classifications, or scoring systems of organ failures-MOF. At least 6 of these went on to develop scoring systems to calculate the severity of MOF. These descriptions are all very similar and allow the development of a common definition, which can be acceptable to everyone, if they accept it and use it. Because these definitions have already been developed and can be collated and codified, it should not be necessary to develop a whole new system of multiple organ dysfunction definitions. Twenty-two examples of various scores are provided in Table 4. A scoring system has also been developed by DeCamp and Demling (35). Baker (70) collated the scoring systems into a very sensible one, with the list of organ systems put in the order in which they fail.

Table 1
Table 1:
Organ failure expressions
Table 2
Table 2:
Terms and xpressions for infection and inflammation
Table 3
Table 3:
The teleology of systemic inflammatory rsponse syndrome, multiple organ dysfunction syndrome, and multiple organ failure
Table 4
Table 4:
Scoring system
Table 4
Table 4:
Table 4
Table 4:
Table 4
Table 4:
Table 4
Table 4:
Table 4
Table 4:
Table 4
Table 4:

Siegel et al. (71) studied the early predictors of injury severity and death after blunt trauma. Deitch (72) reviewed the pathophysiology and therapy for MOF. Anderson and Harken (73) described the autologous tissue injury that can occur with inflammation. Goodwin and Session (74) provided an overview of MOF. I have also written about the horror autotoxicus and MOF (75); an update on MOF/MODS and SIRS (76); why there are no magic bullets for MOF, MODS, and SIRS (77); whether we are winning the battle against MOF Baue et al. (78); whether SIRS and MODS are important entities in the clinical evaluation of patients (79); and about MOF in this new millenium (80). Chaudry (81) has reviewed the cellular and molecular biologic approaches to MOF.

This article cites the most prominent contributions to MOF, MODS, and SIRS. I am sure there are others that I missed. The whole problem of organ failure continues to perplex clinicians and scientists, and it contributes to fatal outcomes for patients with illnesses, infections, and injuries after operations. We know a lot about these problems but frequently can do little. The best approach remains patient and organ support to prevent failure.


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