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Multiorgan Dysfunction Syndrome Justin Chandler Oct 27, 2010 Epidemiology Exact incidence is not known In one study of 938 consecutive SICU pt, about 50% had MODS Mortality was 30% Infection related severe sepsis is estimated at ~750,000 cases/yr nationally If non-infectious causes is included (trauma, pancreatitis), the rate doubles Mortality is about 28% or 215,000 deaths/yr Mechanism Clinical picture is of generalized systemic inflammatory response (SIRS) Typically in response to infection or uncontrolled inflammation (severe trauma, pancreatitis) “Can be viewed as a systemic process involving the excessive stimulation of certain inflammatory responses mediated by circulating factors whose effects contribute to injury or dysfunction in organs not involved in the initial insult”1 SIRS Criteria Requires two of the following: Current Concepts Earliest reports of postinjury MODS identified occult intraabdominal infection as the etiology in half of the cases However, we know now 50%–70% of MOF do not have an identifiable infectious focus Therefore uncontrolled infection is not the universal cause of MODS It was then realized the host’s own response to tissue injury or shock could result in a noninfectious sepsis The immunoinflammatory response to infection, injury, necrotic tissue, or shock was similar led to the hypotheses that immune cell products contributed to MODS Current Concepts Concept of an excessive immunoinflammatory response from activated macrophages and other immune cells led to cytokinemediated tissue injury (and thereby SIRS and MODS) Supported by several experimental and clinical observations Cytokine levels were increased in trauma patients Administration of (TNF-α) to humans elicited a clinical response similar to SIRS Preclinical animal studies documented that TNF- α neutralization improved survival after receiving a lethal dose of endotoxin However, there have been multiple clinical trials of anti-inflammatory agents that have failed along with more complex preclinical animal studies It is now recognized that cytokines have many beneficial functions, such as the control of infection Elevated cytokine levels appear to be more markers or predictors of the host response than inducers Diagnosis Term “MODS” was introduced in 1991 by a consensus of the American College of Chest Physicians (ACCP) and the Society of Critical Care Medicine (SCCM) Concept that there exists a continuous spectrum from mild to full-blown dysfunction Several MODS scoring systems have been established grade the severity of MODS Most correlate, on a patient population level, with mortality and morbidity Scoring Systems for MOF SOFA Scoring Beneficial in critically ill patients. Use in the daily clinical evaluation of a patient’s response Epidemiologic studies Assessment of new therapies in clinical Although systems use slightly different parameters the clinical utility of these scoring systems is comparable Management No cure… Treatment is largely symptomatic and dedicated to supporting organs and systems that have failed Resuscitation Central goal: restoration of an effective blood volume, optimization of microcirculatory blood flow (and hence tissue perfusion), and the prevention/limitation of ischemia-reperfusion injury Increasing emphasis on the adequacy of volume resuscitation Primary endpoint of resuscitation, however, remains controversial Blood pressure and urine output may not reflect the adequacy of volume resuscitation Base deficit, lactate, oxygen delivery, gastric intramucosal pH (pHi), and pulmonary artery catheters have all been used patients who cleared their base deficient or lactate levels within 48 hours had a reduced incidence of ARDS and MODS plus a higher survival rate resuscitative goal should be to reduce base deficit below –2 mmol/l and/or lactate less than 1.5 mEq/l. Resuscitation - Fluids Choice of resuscitative fluid has become more controversial Ringers lactate is proinflammatory Large-volume resuscitation with crystalloids contributes to abdominal compartment syndrome Attention has refocused on the early resuscitation of trauma patients with hypertonic (7.5%) saline Has demonstrated similar survival, but decreased complications (renal failure and ARDS) with hypertonic saline Not enough data to determine if hypertonic saline resuscitation is superior to standard crystalloid resuscitation Splanchnic-directed antioxidant therapy helps prevents MODS in trauma patients investigations into novel resuscitation fluids with pharmacologic actions (i.e., gut-protective, immune modulatory) continues Resuscitation - Fluids Blood is immune-suppressive and that blood transfusions are an independent predictor of MODS TRICC trial showed a significant reduction in severity of organ dysfunction when transfusion withheld until Hb <7 g/dl Two general conclusions Prophylactic transfusions to raise the hemoglobin above 7 g/dl does not improve tissue oxygen consumption consistently Prophylactic transfusion is not associated with improvements in outcome, and may result in worse outcomes in several subgroups Resuscitation - Fluids Attempts to identify optimal hemodynamic values Tissue-specific resuscitation endpoints Gastric pH (tonometry) Early studies suggested supranormal CO and DO2 for increased oxygen demands improved survival Cardiac index, oxygen delivery, and oxygen consumption Refuted by numerous prospective randomized trials Use of prophylactic blood transfusions, inotropes, and large volumes of crystalloids may be deleterious Some data suggesting low gastric mucosal pHs have a worse outcome Measuring gastric mucosal pH has not been shown to be as effective as base deficit or lactate as markers resuscitation Operative Intervention Judicious use of damage-control laparotomy to limit both acute and delayed MODS Prolonged attempts at definitive control can result in hemodynamic instability, acidosis, and coagulopathy Morbidity and mortality of damage-control laparotomies is significant Incidence of MODS appears to be reduced and survival increased A planned reoperation is safer and easier Occurs after pts have been warmed, resuscitated, and had their acidosis and coagulopathy corrected Operative Intervention A second example reduce the incidence of ARDS and MODS with early fixation of long-bone fractures Compared with delayed fracture fixation is associated with lower rates of renal, respiratory, and liver failure and death Early fracture fixation in the presence of major thoracic or head injury is controversial Early fixation have shown no added morbidity with either chest or head injury Others cite increases in secondary brain injury and ARDS Overall, most evidence supports early fracture fixation as an effective method ICU MOF can be prevented through: Continued resuscitation Management of infectious complications Early empiric abx in suspected pneumonia has been shown to reduce pneumonia mortality Selective decontamination of the digestive tract (SDD) reduces infectious complications as well as mortality in trauma and surgical pts Early nutritional and specific organ support Prevention SDD Gut is a major reservoir for organisms causing pneumonias and bacteremias By controlling intestinal bacterial flora, including upper GI, incidence of infections and hence mortality will be reduced The failure to employ SDD appears to relate to the labor intensiveness Has only recently been shown by metaanalyses to improve survival Activated Protein C With the exception of activated protein C, immunomodulatory agents have been disappointing APC is both anticoagulant and anti-inflammatory activity, thereby protecting the microcirculation as well as limiting the inflammatory response More rapid resolution of cardiovascular, respiratory, and hematologic dysfunction in severe sepsis Improved 28-day survival Steroids Low-dose steroids Effective therapy in patients with pressor-refractory septic shock and impaired response to ACTH stimulation Trials have documented in this pt group the administration of 50 mg of hydrocortisone every 6 hours and 50 mcg of fludrocortisone improves survival Surviving sepsis recommends 300 mg/day divided doses, with mineralocorticoid being superfluous Other Therapies Other beneficial interventions include Early enteral alimentation Based on limiting atrophy to limit gut-origin sepsis by loss of barrier funct Effectively reduces infectious complications, ICU, and total hospital length of stay, but does not improve survival Glucose control Elevated serum glucose is associated with an increased incidence of infectious complications and poorer outcomes Excessively tight glucose control has been shown to increase complications and mortality for most subsets Ventilator Therapies Ventilator-induced lung injury (VILI) Reduced vent volumes and pressures outcomes with ALI or ARDS are similar whether lower or higher PEEP levels are used end-inspiratory plateau pressure under 30 cm of water While oxygenation is maintained with low tidal volumes, permissive hypercapnia and increased CO2 levels may develop High volumes and increased pressures cause, rather than prevent, lung injury by inducing lung inflammation does not appear to be harmful Other ventilatory strategies have either failed to show consistent benefit (such as inhaled nitric oxide) or remain to be proven beneficial (such as prone ventilation or high-frequency ventilation). Other Therapies Other beneficial interventions include Elevation of the head of the bed In ventilated patients reduces the incidence of pneumonia and helps to preserve pulmonary function Daily cessation of sedative infusions Reduces ICU length of stay and morbidity Renal Support Renal support Prophylactic use of low-dose dopamine, have not been found to be effective Best way to limit renal failure Once renal failure occurs, continuous venovenous hemodialysis (CVVHD) appears to be superior to hemodialysis Avoid underresuscitation Promptly diagnose and treat infectious complications Avoids the need for systemic anticoagulation Less likely to cause hypotension Renal replacement therapy Allows regulation of fluid and electrolytes Has the potential to remove toxins and circulating mediators of inflammation Abdominal Compartment Syndrome Recently recognized and treatable cause of MODS As the intra-abdominal pressure rises Pts at highest risk include: Abdominal visceral perfusion decreases Ventilation is impaired Cardiac output declines Polytrauma Massive hemorrhage Prolonged operations with massive volume resuscitation Massive hemorrhage requiring intra-abdominal packing Diagnosis Clinical signs: decreasing urine output, inadequate ventilation associated w/ elevated peak airway pressures, and hypotension Made or confirmed by measuring the abdominal pressure through a Foley catheter placed in the bladder (> 25 mm Hg), progressive organ dysfunction (UO < 0.5 ml/kg/hr, PaO2/FIO2 < 150, PIP 45 cm H2O or cardiac index <3 L/min/m2 despite resuscitation) Improved organ function after surgical abdominal decompression Prevention Strategies References Current Therapy of Trauma and Surgical Critical Care http://www.medicalcriteria.com