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Multiple Organ Dysfunction Syndrome Timothy G. Buchman, Ph.D., MD

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Multiple Organ Dysfunction Syndrome Timothy G. Buchman, Ph.D., MD Physiologic Failure: Multiple Organ Dysfunction Syndrome Timothy G. Buchman, Ph.D., M.D. Edison Professor of Surgery Professor of Anesthesiology and of Medicine Washington University School of Medicine St. Louis, Missouri 63110 [email protected] Acknowledgement: This work was supported, in part, by award GM48095 from the National Institutes of Health 2 Buchman Humans, like other life forms, can be viewed as thermodynamically open systems that continuously consume energy to maintain stability in the internal milieu in the face of ongoing environmental stress. In contrast to simple unicellular life forms such as bacteria, higher life forms must maintain stability not only in individual cells but also for the organism as a whole. To this end, a collection of physiologic systems evolved to process foodstuffs; to acquire oxygen and dispose of gaseous waste; to eliminate excess fluid and soluble toxins; and to perform other tasks. These systems—labeled respiratory, circulatory, digestive, neurological, and so on—share several features. • Physiological systems are spatially distributed. Food has to get from mouth to anus. Urine is made in the kidneys but has to exit the urethra. Blood may be pumped by the heart but has to reach the great toe. • Physiologic systems are generally spacefilling and structurally fractal. Each cell has demand for nutrients; each cell excretes waste. Information has to travel from the brain throughout the body. While not every physiologic system is self-similar at all levels of granularity, there is typically a nested architecture that facilitates function: microvillus to villus to intestinal mucosa; alveolus to alveolar unit to bronchial segment; capillary to arteriole to artery. • Physiologic systems are functionally integrated. After eating, blood is redistributed to the gut and splanchnic circulation. When alveoli become atelectatic, blood is shunted away from these hypoxic regions. Ingestion 3 Buchman and delivery of excess fluid to the circulation is quickly followed by augmented production of urine. • Physiologic systems have characteristically variable time signatures that lose their variability in aging and disease. (1) Instantaneous cardiac and respiratory rates vary from one event (heart beat or breath) to the next. Many hormones exhibit not only diurnal variation, but also a superimposed pattern or irregular pulses. The product of physiologic systems—such as gait which combines neural, musculoskeletal, cardiac and respiratory systems into a semivoluntary activity (one usually doesn’t think about putting one foot in front of the next) –display characteristically variable time signatures. The first three features of physiologic systems have medical consequences. Both aging and illness can compromise one or more physiologic systems. Management of such compromise was, until about fifty years ago, directed exclusively towards minimizing the performance demand placed on the system. For example, in advancing pulmonary insufficiency, patients were progressively confined to home, to chair and finally to bed. Each organ system had a critical level of compromise, and once the compromise exceeded the critical level, the patient simply died. Two major advances in the last half-century have changed the clinical trajectory. The first major advance was the development of mechanical 4 Buchman supports for failing mechanical systems. Ventilators (respirators), ventricular assist devices and renal replacement therapies (dialysis machines) have come into widespread clinical use. These supports have evolved to the point that individual system failures can be managed by outpatient use of these devices: many patients thus gain years of useful life. The second advance was the development of organ transplantation. Beginning with blood components (transfusion is a type of transplantation) and progressing to kidney, heart, lung, pancreas and intestine, component replacement is increasingly frequent and relatively safe. Both advances—mechanical support and tissue transplantation—compromise immune system function, but this compromise is usually a good trade for survival. It is hardly surprising that organ dysfunction and failures accumulate. Like the aging automobile with worn bearings, cracked hoses and leaking engine valves, many humans eventually acquire an illness to which they cannot successfully respond even with medical care—a bleed into the brain, a metastatic cancer or a high speed motor vehicle crash. They die with multiple organs failing to perform their appropriate function. The subject of this chapter, however, is a syndrome of widespread, progressive and disproportionate multiple organ dysfunction (MODS) that rapidly accumulates following a minor or modest insult. (2) Despite timely and appropriate reversal of the inciting insult—whether a pneumonia, intraabdominal abscess, pancreatitis or simply the stress of an anesthetic and elective surgery—many 5 Buchman patients develop the syndrome. Mortality is proportional to the number and depth of system dysfunctions (4), and the mortality of MODS after (for example) repair of ruptured abdominal aortic aneurysm is little changed despite three decades of medical progress. (2,5) Unfortunately, MODS remains the leading cause of death in most intensive care units. MODS: The Phenotype Autopsy findings in patients who succumbed to MODS are surprisingly bland. Tissue architecture is preserved, cells do not appear abnormal, there is no widespread thrombosis. At least anatomically, the body appears to be largely intact. (The exception is lymphatic tissues, which are often exhausted through accelerated programmed cell death [apoptosis] (6) ) Nor does organ function appear to be irretrievably lost: among MODS survivors, many—especially younger survivors—experience return of multiple organ performance to levels approaching that which they enjoyed prior to the syndrome. (7) These two observations –anatomic integrity and the potential for near-complete recovery—led to replacement of the old descriptor (“multiple organ failure”) with the current and more apt label of multiple organ dysfunction syndrome. Using the jargon of information technology, the focus shifted from the hardware to the software.(8) Bearing in mind that MODS is only three decades old (multiple organ supports had to be developed and used in enough patients before it could be 6 Buchman observed that the patients were dying despite the treatments), its phenotype has changed somewhat as physicians have tried to preempt its occurrence and progression. In its original –and perhaps purest-- form, organ dysfunctions would accumulate in a more or less predictable sequence.(2,3) The lungs would fail first, and the patient would require intubation and mechanical ventilation. A few days later, evidence of gut and liver failure would appear—patients would fail to absorb nutrients and fail to manufacture critical proteins such as clotting factors. Artificial nutrition and transfusion medicine were therefore administered. A few days after that. kidney failure would become apparent and the patient would require dialysis. Not only was the dysfunction sequential, but this particular sequence precisely mirrored the sequence in which organs matured in fetal life—kidneys first, then the liver/gut and lastly, the lungs. For this reason, multiple organ failure began to be recast as organ systems “falling off line”, each functionally separating from the whole. For this reason, physicians initiate organ-specific support earlier and earlier—at the first sign of dysfunction. This strategy of early intervention has muddied the failure sequence, unfortunately with little effect on outcome: four-organ failure is still quite lethal. Physiologic Stability How do organisms maintain function in the face of external stress? There appear to be two general ways. (9) One way relies on purpose-specific mechanisms that have arisen and been refined in the course of evolution. At 7 Buchman the resolution of the individual cell, the “stress response”—originally called the “heat shock response” because it was observed in polytene chromosomes of Drosophila cells exposed to high temperatures—activates specific transcription factors, modulates RNA splicing and applies selection filters to translation. The phenotype of this stress response is marked alteration in protein synthesis while the cell becomes (temporarily) refractory to additional external stimuli. At the resolution of the intact organism, circulating blood sugar levels are tightly maintained by the secretion of insulin and of glucagon, which sequester and mobilize (respectively) carbohydrates. Such engineered mechanisms have been identified at all levels of granularity, and their product was termed “homeostasis” by Walter B. Cannon early in the 20th century. A central dogma of medical care as articulated by Cannon instructs the physician to render “external aid” when homeostatic mechanisms are overwhelmed by disease. This has been translated by the medical community into the “fix-the-number” imperative: if the bicarbonate level is low, give bicarbonate; if the urine output is low, administer a diuretic; if the bleeding patient has a sinking blood pressure, make the blood pressure normal. Unfortunately, such interventions are commonly ineffective and even harmful. (10, 11) For example, sepsis—which is a common predecessor of MODS—is often accompanied by hypocalcemia. In controlled experimental conditions, administering calcium to normalize the laboratory value increases mortality.
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