Download Free Medical Multiple Organ Dysfunction Syndrome PowerPoint Presentation

Multiple Organ Dysfunction Syndrome PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical PowerPoint presentation titled "Multiple Organ Dysfunction Syndrome".

This medical PowerPoint presentation talks about Multiple Organ Dysfunction Syndrome (MODS), a serious and potentially life-threatening condition that occurs when two or more organ systems in the body fail to function properly as a result of a variety of underlying diseases or injuries. MODS typically affects critically ill patients in intensive care units (ICUs) and is considered a major cause of morbidity and mortality in these patients.

MODS can occur as a result of a wide range of underlying conditions, including severe infections, trauma, burns, pancreatitis, liver disease, and acute respiratory distress syndrome (ARDS). The underlying causes of MODS can trigger an inflammatory response in the body that can lead to widespread damage to multiple organs and systems.

The symptoms of MODS can vary depending on which organ systems are affected, but commonly include low blood pressure, altered mental status, rapid breathing, rapid heart rate, and low urine output. Treatment of MODS typically involves supportive care, such as mechanical ventilation, dialysis, and medication to support blood pressure and organ function.

Prevention of MODS is an important aspect of critical care management and may involve early recognition and treatment of the underlying causes of the condition, aggressive resuscitation, and careful monitoring of vital signs and laboratory values to detect signs of organ dysfunction early on.

Tags : Multiple Organ Dysfunction Syndrome, MODS, intensive care units, ICUs, critical care medicine, critical care medicine PowerPoint presentation

Published on : Mar 28, 2023 | Views : 2027 | Downloads : 1

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Multiple Organ Dysfunction SyndromeDefinition Diagnosis Management
Slide 2-

Definitions Multiple Organ Dysfunction Syndrome “MODS” 1991 Consensus conference of the American College of Chest Physicians (ACCP) and the Society of Critical Care Medicine (SCCM) Dysfunction replaced failure to accentuate the reversible nature of the condition Underlying concept Sepsis, systemic inflammatory response syndrome (SIRS), acute respiratory distress syndrome (ARDS), and MODS are closely related phenomena
Slide 3-

Definition of systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndrome (MODS) Systemic inflammatory response syndrome The systemic inflammatory response to a variety of severe clinical insults is manifest by two or more of the following conditions: Temperature > 38°C or < 36°C Heart rate > 90 beats/min Respiratory rate > 20 breaths/min or Paco2 < 32 mmHg (or ventilator dependence) White blood cell count > 12 000 cells/mm3, < 4000 cells/mm3 or > 10% band forms Multiple organ dysfunction syndrome The presence of altered function involving at least two or more organ systems in an acutely ill patient such that homeostasis cannot be maintained without intervention
Slide 4-

MODS is the most common cause of late trauma deaths Approximately 50% of ICU patients will develop MODS (estimates 25-80+%) Estimates of 20% to up to 75% mortality in patients having at least two-organ failure As each organ fails the average risk of death increased 11 to 23 percent Ulvik A, Kvale R, Wentzel-Larsen T, et al. Multiple organ failure after trauma affects even long-term survival and functional status. Crit Care 2007;11:R95.
Slide 5-

Mortality in intensive care unit black Mortality to hospital discharge black + dark grey Mortality to 1 year black + dark grey + light grey. Mayr VD et al Causes of death and determinants of outcome in critically ill patients Crit Care 10:R154, 2006.
Slide 6-

Most organ failure assessment systems assign values to six organ systems Respiratory Cardiovascular Renal Hematology, Hepatic Central nervous system. Definitions
Slide 7-

Most commonly Respiratory Failure followed by the cardiovascular, renal, and hematologic systems. Respiratory failure Hypoxemia, reduced P/F, require mechanical ventilation Cardiovascular failure Hypotension that is unresponsive to adequate fluid resuscitation and requires vasopressors. Renal dysfunction Diminished urine output, increased serum creatinine, Hematologic failure Anemia, thrombocytopenia, and disseminated intravascular coagulation. General Definitions
Slide 8-

Pathogenesis of multiple organ dysfunction Crit Care Clin 2000;16:337-352
Slide 9-

Multiple System Organ Failure Score Afessa et. Al, Severity of Illness and Organ Failure Assessment in Adult Intensive Care Units Crit Care Clin 23 (2007) 639–658
Slide 10-

Sequential Organ Failure Assessment (SOFA) score Afessa et. Al, Severity of Illness and Organ Failure Assessment in Adult Intensive Care Units Crit Care Clin 23 (2007) 639–658
Slide 11-

Definitions and grading of organ dysfunction (MODS score) Mayr VD et al Causes of death and determinants of outcome in critically ill patients Crit Care 10:R154, 2006.
Slide 12-

Denver Postinjury MOF Score Ciesla et al, The role of the lung in postinjury multiple organ failure Surgery 01-OCT-2005; 138(4): 749-57
Slide 13-

Diagnosis by Definition Syndrome wide spectrum of pathophysiology under one term believed to be related by common cascade of events culminating in organ dysfunction Heterogeneous collection Approximately 50%–70% of patients with MODS do not have an identifiable focus of infection Approximately 1/3 do not have lung involvement Trauma patients may form a distinct subset
Slide 14-

The role of the lung in postinjury multiple organ failure 1,344 Trauma patients (age greater than 16 years, trauma intensive care unit admission, Injury Severity Score greater than 15, and survival longer than 48 hours) 75% developed Organ dysfunction 25% MODS MODS Morality 26% (80% of total mortality of 112) The onset of MOF occurred an average of 3.4 ± 0.2 days postinjury Lung dysfunction established within 72 hours in 89% patients followed by cardiac dysfunction at 0.6 +/- 0.2 days hepatic dysfunction at 4.8 +/- 0.2 days kidney dysfunction at 5.5 +/- 0.5 days Lung dysfunction was noted in : 94% with with1 or more organ dysfunctional 99% with 2 or more organ dysfunctional Ciesla DJ - Surgery - 01-OCT-2005; 138(4): 749-57
Slide 15-

Potential Pathophysiologic Mechanisms Producing MODS Circulating immune/inflammatory mediators Primary cellular injury Mitochondrial Injury/ down-regulation Inadequate tissue/organ perfusion Hypoperfusion Ischemia/reperfusion Microaggregation and/or DIC Diffuse endothelial cell injury Circulating humoral factors Protein calorie malnutrition Bacterial-toxin translocation Adverse effect of directed treatment or medication
Slide 16-

Models Meakins “two-hit” model of postinjury MOF. The first hit (trauma / shock ) primes neutrophils and macrophages The second hit (nosocomial infection/complication) results in detrimental inflammatory response
Slide 17-

Inflammatory Model MODS is caused by an overwhelming imbalance between systemic inflammatory response and counter regulation (anti-inflammatory) response. May be activated by a number of external and internal factors, including pro-inflammatory (e.g., infection, sepsis, shock, and trauma) and immunosuppression (e.g., Blood transfusion, infection, and steroids) . The imbalance in favor of inflammatory response causes loss of the host's ability to localize the inflammation to ijnitial inciting factor, leading to systemic inflammation and tissue damage.
Slide 18-

Karima et. al, The molecular pathogenesis of endotoxic shock and organ failure Mol Med Today 1 March 1999, 123-132
Slide 19-

Karima et. al, The molecular pathogenesis of endotoxic shock and organ failure Mol Med Today 1 March 1999, 123-132
Slide 20-

Multiple organ dysfunction is the results of the dysregulation of mitochondria Mitochondrial activity is down-regulated as a protective reflex to inciting factors Failure to recover mitochondrial function results in self perpetuating cycle of cell damage furthering shutdown of mitochondria Bioenergetics Model Mervyn Singer, Mitochondrial function in sepsis: Acute phase versus multiple organ failure (Crit Care Med 2007; 35[Suppl.]:S441–S448)
Slide 21-

Bioenergetics and Sepsis Mervyn Singer, Cellular Dysfunction in Sepsis Clin Chest Med 29 (2008) 655–660
Slide 22-

Progression of Bioenergetics Dysfunction Mervyn Singer, Mitochondrial function in sepsis: Acute phase versus multiple organ failure (Crit Care Med 2007; 35[Suppl.]:S441–S448)
Slide 23-

Pathophysiology of multiple organ dysfunction syndrome (MODS). Shock Model Hypoperfusion causes dysfunction due to hypoxia and secondary injury
Slide 24-

Multifactor Models Gut-liver-lung axis Initiation of the inflammatory state can occur in any of these organs following trauma or shock. The gut can leak inflammatory mediators into the portal circulation, causing a response in the liver. Inflammatory mediators then travel in the hepatic vein to the inferior vena cava and to the lungs. The lungs may become injured and release inflammatory substances themselves, which travel systemically to distant organs (including the gut). Martinez-Mier G, Toledo-Pereyra LH, Ward PA: J Trauma 51:408, 2001
Slide 25-

LPS, Lipopolysaccharide. Gut-liver-lung axis in response to shock and hemorrhage Martinez-Mier G, Toledo-Pereyra LH, Ward PA: J Trauma 51:408, 2001.
Slide 26-

Abraham 2007, Crit Care Med All In Models
Slide 27-

Composite model Current Therapy of Trauma and Surgical Critical Care Asensio and Trunkey 2008
Slide 28-

Therapy
Slide 29-

Targeted therapy Activated Protein C Modulating the systemic inflammatory, procoagulant, and fibrinolytic host responses Vasopressin Therapy Replacing falling plasma levels of vasopressin seen in shock Steriods Replacement reversible failure of the hypothalamic-pituitary-Adrenal (HPA) axis
Slide 30-

Activated Protein C for Severe Sepsis The properties of activated protein C include (1) Antithrombotic activity inhibition of thrombin formation inhibition of factors V and VIII (2) Profibrinolytic activity inhibition of PAI-1 (plasminogen-activator inhibitor 1) (3) Anti-inflammatory activity Direct effect inhibitory effect monocytes, neutrophils, and endothelial cells indirectly through reduced thrombin resulting in less tumor necrosis factor and interleukin-1 production, Bernard et al, N Engl J Med, Vol. 344, No. 10 March 8, 2001
Slide 31-

James A Russell MD. Management of Sepsis. N Engl J Med 2006; 355:1699-1713 Yong Lee, Pharm.D. Jackson Memorial Hospital Trauma Critical Care Pharmacist
Slide 32-

Bernard et al, N Engl J Med, Vol. 344, No. 10 March 8, 2001
Slide 33-

EFFICACY AND SAFETY OF RECOMBINANT HUMAN ACTIVATED PROTEIN CFOR SEVERE SEPSIS 1690 randomized patients with a known or suspected infection on the basis of clinical data who meet the following criteria within a 24-hour period: 1) three or more signs of the Systemic Inflammatory Syndrome 2) the sepsis-induced dysfunction of at least one organ or system that has lasted no longer than 24 hours Study group received drotrecogin alfa (activated) 24 μg per kilogram of body weight per hour for a total duration of 96 hours Bernard et al, N Engl J Med, Vol. 344, No. 10 March 8, 2001 RCT: PROWESS
Slide 34-

Findings Absolute reduction in the risk of death of 6.1 percent Mortality rate 30.8 percent in the placebo 24.7 percent in the drotrecogin alfa activated group Bernard et al, N Engl J Med, Vol. 344, No. 10 March 8, 2001 RCT: PROWESS
Slide 35-

Drotrecogin Alfa (Activated) for Adults with Severe Sepsis and a Low Risk of Death 2640 adults patients with severe sepsis and a low risk of death (defined by an Acute Physiology and Chronic Health Evaluation [APACHE II] score <25 or single organ failure) Randomized intravenous infusion DrotAA (24 Μg per kilogram of body weight per hour) for 96 hours or placebo Trial was terminated early No benefit from treatment Increased incidence of serious bleeding complications, Conclusion DrotAA should not be used in patients with severe sepsis who are at low risk for death Abraham, et al N Engl J Med 353;13 Sept 29,2005 RCT: ADDRESS
Slide 36-

Activated Protein C Here APACHE II score > 25 No benefit seen in patients w/ APACHE II score < 25 More than 1 organ system affected Drotrecogin had no benefit in patients with single organ dysfunction Must start Drotrecogin w/in 48 hrs of 1st sign of organ dysfunction To achieve benefit seen in PROWESS drotrecogin should be started w/in 24hrs Consider continuing prophylactic heparin when starting drotrecogin Yong Lee, Pharm.D. Jackson Memorial Hospital Trauma Critical Care Pharmacist
Slide 37-

Exclusion Criteria Anyone of the following: Active bleed Recent CVA (w/in 3 months) Recent head trauma or intracranial/spinal surgery (w/in 2 months) Intracranial mass lesion or aneurysm < 12 hrs post surgery req. general or spinal anesthesia Epidural catheter Trauma patient w/ increased risk of bleeding Patient is moribund Yong Lee, Pharm.D.Jackson Memorial Hospital Trauma Critical Care Pharmacist
Slide 38-

Inclusion Criteria Must be in an ICU or consulted by an ICU team Patient has known or suspected infection 1 of the following: Positive culture White cells in a sterile body fluid Perforated viscus CXR evident of PNA with purulent sputum production Patient has signs of SIRS ( >3 of the following): 360 < Temp > 380 HR > 90 RR > 20 or PaCO2 < 32 or mech vent 4000 < WBC > 12000 or > 10% immature neutraphils Yong Lee, Pharm.D.Jackson Memorial Hospital Trauma Critical Care Pharmacist
Slide 39-

Inclusion Criteria Patient has organ system dysfunction At least 2 of the following: Cardiovascular dysfunction: MAP < 70 or arterial SBP < 90 or vasopressor support Renal dysfunction: UOP < 0.5ml/kg/hr for > 1 hr Respiratory dysfunction: PaO2 /FiO2 < 250 or < 200 if the lung is the only dysfunction Hematologic dysfunction: plt < 80000 or 50% decline in 3 dys Unexplained metabolic acidosis: pH < 7.3 or BE > 5 w/ lactate > 1.5 X normal Yong Lee, Pharm.D. Jackson Memorial Hospital Trauma Critical Care Pharmacist
Slide 40-

Vasopressin Therapy for Septic Shock In early shock, appropriately high levels of vasopressin are produced to support organ perfusion. As the shock state progresses, plasma vasopressin levels fall from: depletion of pituitary stores of vasopressin exhaustive release in early septic shock central inhibition from elevated norepinephrine levels (endogenous or exogenous) central inhibition from increased nitric oxide release by vascular endothelium within the posterior pituitary during sepsis
Slide 41-

Vasopressinand Septic Shock Trial (VASST) Randomization trial of 778 patients with shock 396 patients received vasopressin, and 382 norepinephrine There was no significant difference : 28-day mortality rate (35.4% and 39.3%, respectively; P = 0.26) in 90-day mortality (43.9% and 49.6%, respectively; P = 0.11). Overall rates of serious adverse events (10.3% and 10.5%, respectively;P = 1.00). Russell et al, Vasopressin versus Norepinephrine Infusion in Patients with Septic Shock N Engl J Med 2008;358:877-87
Slide 42-

Hydrocortisone Therapy for Patients with Septic Shock 499 patients multicenter Randomized, double-blind, placebo-controlled trial Concluded Hydrocortisone did not improve survival or reversal of shock in patients with septic shock, either overall or in patients who did not have a response to corticotropin, although hydrocortisone hastened reversal of shock in patients in whom shock was reversed. Sprung et. Al N Engl J Med 358;2 January 10, 2008
Slide 43-

International task force by the American College of Critical Care Medicine Review published literature concluded most of the research supports treatment with moderate-dose corticosteroids in patients with septic shock who have responded poorly to volume resuscitation and vasopressor agents Tests of adrenal function are not routinely required in these patients. Recommendations for the diagnosis and management of corticosteroid insufficiency in critically ill adult patients: Consensus statements from an international task force by the American College of Critical Care Medicine Crit Care Med 2008 Vol. 36, No. 6
Slide 44-

Management Prevention Removal of inciting factors Support Recovery
Slide 45-

Current Therapy of Trauma and Surgical Critical Care eds Asensio and Trunkey 2008 Algorithm for preventing and managing MODS
Slide 46-

ALI, acute lung injury; DA, dopamine; DVT, deep vein thrombosis; NE, norepinephrine; PUD, peptic ulcer disease. Dellinger RP, Carlet JM, Masur H, et al: Surviving Sepsis Campaign guidelines for management of severe sepsis and septic shock. Crit Care Med 2004;32:858-873.) Surviving Sepsis Campaign Guidelines
Slide 47-

Hemodynamic Support Early Goal directed therapy 1. Preload Monitor/Support central venous pressure 8 - 12 mm Hg 12 - 15 mm Hg in mechanically ventilated patients 2. After-load Monitor/Support Mean arterial pressure >65 mm Hg Urine output >0.5 mL/Kg/h 4. Balance oxygen delivery and oxygen demand Monitor/Support Oxygen balance Central venous or mixed venous oxygen saturation >70%
Slide 48-

Hemodynamic Support Low-dose steroids administered for nonresponders to fluid and vasopressors Hydrocortisone dose should be < 300 mg/day Steroid therapy may be weaned once vasopressors are no longer required Activated Protein C administered in accordance policy here
Slide 49-

Infection Control Source Control Early Identification abscess, infection with imaging/studies ID treatable causes e.g., necrotizing fasciitis, diffuse peritonitis, cholangitis,intestinal infarction Early intervention Drainage of infected fluid collection Surgery to control /eliminate source if appropriate Debridement of infected solid tissue Removal of devices or foreign bodies Monitor/Address abdominal compartment syndrome Remove intravascular access devices if potentially infected Systemic Antibiotics Broad-spectrum antibiotic therapy started within the first hour Cultures (blood, urine, sputum,tissue) preferable prior, Therapy adapted to most appropriate single drug as soon as antibiogram available. Combination therapy for patients with known or suspected Pseudomonas infections and neutropenic patients with severe sepsis
Slide 50-

Sepsis Resuscitation Bundle 1. Serum lactate measured at clinical presentation 2. Blood cultures obtained before antibiotics administered 3. Broad-spectrum antibiotics within 3 hours 4. In the event of hypotension or lactate >4 mmol/L (36 mg/dL) a. deliver an initial minimum of 20 mL/kg of crystalloid (or colloid equivalent) b. apply vasopressors for ongoing hypotension 5. In the event of persistent hypotension despite fluid resuscitation or lactate >4 mmol/L (36 mg/dL) a. achieve central venous pressure of >8 mm Hg b. Achieve central venous oxygen saturation > 70% The Role of Bundles in Sepsis Care Crit Care Clin 22 (2006) 521–529
Slide 51-

On Going Intensive Care Support DVT/PE prevention Ulcer Prevention Nutritional Support Glucose Control/Insulin therapy as needed Specific organ Support Minimize Blood Transfusion Infection control Avoidance of Ventilator Associated Pneumonia Avoidance of Catheter (any type) Related Infection
Slide 52-

Long-term Outcome Follow up 322 patients Trauma related organ failure 47% had multiple organ failure (MOF), 28% had single organ failure. Long-term survival and functional status were the same for patients suffering single organ failure and no organ failure. MOF increased the overall risk of death 6.0 times. Complete recovery occurred in 52% of survivors 87% were able to look after themselves MOF had 3.9 times greater odds for requiring personal assistance in activities of daily living Ulvik A, Kvale R, Wentzel-Larsen T, et al. Multiple organ failure after trauma affects even long-term survival and functional status. Crit Care 2007;11:R95.
Slide 53-

ppt slide no 53 content not found