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Cc 10 mods - MODS
Critical Care (408)
Loma Linda University
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Local Inflammatory Response
Endothelial cells* activated by alterations in local environment how endothelial cells respond to alterations in environment differ according to host genetics, age, gender, nature of pathogen & location of vascular bed “cross talk” to other cells including erythrocytes platelets leukocytes vascular muscle cells responsible for the release of mediators most important function is regulation of permeability
Mediators released from endothelial cells elicit (generate) the inflammatory response recruit white blood cells to the area promote localized clotting contain infection
body’s response to insult/injury/abnormal situation caused by physical, chemical, biological agent goal: move materials & inflammatory immune response cells to injury to prevent foreign invasion or extension of injury Causes of Cellular Injury tissue trauma hypoxia ischemia microbes genetic or immune defects malnutrition extreme temperature chemical agents & ionizing radiation
What Went Wrong containment of localized inflammatory response limits further damage to the host preserves the integrity of uninvolved endothelial cells when host response generalizes it escapes the well-developed checks & balances leads to unregulated inflammatory response (macrolides go everywhere)
Systemic Inflammatory Response Syndrome (SIRS)
SIRS –
Populations at Risk age – older than 65 y/o trauma patients substance abuse genetic factors that predispose them to infections burn patients
SIRS – Clinical Manifestations temperature >38C (100) <36C (96) heart rate >90bpm (tachycardia) respiration > PaCO2 (alkalosis) < WBC >12,000 or <4, or >10% immature cells
SIRS – Conditions Associated infection pancreatitis ischemia trauma shock immune mediated organ injury exogenous administration of cytokines aspiration massive transfusions host defense abnormalities
systemic inflammatory process – aka generalized host response that went wrong manifested even in absence of infection SIRS in presence of infection = sepsis complications of SIRS multiple organ dysfunction syndrome (MODS) acute lung injury (ALI) acute renal failure (ARF) diagnosed when at least 2 of 4 clinical manifestations occur in high risk patients Multiple Organ Dysfunction Syndrome (MODS)
Primary MODS results from a well-defined insult early organ dysfunction directly related to initial insult accounts for a small fraction of MODS result of inadequate oxygen delivery to cells & a failure of microcirculation to remove metabolic end products identifiable disease process such as trauma, pulmonary contusion, aspiration or inhalation injury, renal dysfunction, thermal injuries
Secondary MODS consequence of widespread systemic inflammation involvement of other organs not well-defined insult late organ dysfunction result of generalized SIRS or sepsis process
organ failure of two or more organs mortality rate: 45-55% patient outcome relative to number of failed organs failure of each organ: 15- 20% increase mortality three or more failed organs: 80-100% mortality sepsis and trauma patients highly susceptible patient outcome directly related to number of organs involved some patient’s w/ infection, trauma, or surgery will only have SIRS & minor organ dysfunction that resolves rapidly. others have massive
MODS – Pathologic Changes uncontrolled systemic inflammation tissue hypoxia unregulated cell death microvascular coagulopathy
inflammatory response & die from profound shock Inflammatory Cells & Chemical Mediators*
platelet activating factor phospholipid that releases serotonin serotonin = increase vascular permeability tumor necrotic factor polypeptide that stimulates clotting cascade and causes DIC permeability DIC: bleed & clot at the same time protease proteolytic enzyme damage endothelium contribute to vascular permeability & organ dysfunction
Factors Affecting ScvO2 and SvO (oxygen delivery) inflammatory cells (neutrophils, macrophages, mast cells, lymphocytes, ENDOTHELIAL cells) produce & release inflammation mediators leukotriene, bradykinin, prostaglandin, oxygen free radicals affect vasomotor tone & vascular permeability interleukins cytokine that causes: vascular congestion capillary leakage increased coagulation
CO (cardiac output) heart rate volume resistance pump Hgb (hemoglobin) bleeding hemodilution (dilute blood) anemia
SaO2 (arterial oxygen saturation) oxygenation FiO ventilation VO2 (oxygen consumption) shivering fever seizure muscle activity
Intraabdominal Pressure (IAP)
Interventions to Decrease intraabdominal pressure (IAP) sedation pain control avoid prone position (on chest) reposition bed - reverse Trendelenburg without flexion at the hips (head above feet) remove all constrictive bandages carefully assess fluid administration: do NOT over resuscitate goal directed volumes & reassess avoid unneeded fluid boluses concentrate all drips goal: neutral to negative fluid balance by day 3 nasogastric tube rectal tube enemas bowel prokinetic agents erythromycin metoclopramide
MODS - Treatment
normal: 0- increasing physio compromise: (12-15) inc SVR, IAP against diaphragm, ↓ gut perfusion, ↓ wound healing, lower extremity pooling, ↑ SIRS, ↓ UOP, vena cava compression, ↓preload, ↓ CO) IAP 16- ↑ ICP, ↓ CPP, ↑ lung dysf, ↑ bowel edema/ischemia, ↑ ACIDOSIS, ↓ perfusion of kidneys, oliguria, worsening venal caval compression, further ↓ CO, ↑ CVP, ↑ wedge pressure (falsely elevated) if IAP over 20 brain swelling/ischemia, ↑peak pressure/ARDS, ↑ gut ischemia/ necrosis, further acidosis, Anuria/ARF, venal caval FLATTENING, cardio instability organ failure often develops abdominal compartment syndrome (ACS)
fluid resuscitation hemodynamic support inotropes antidysrhythmic vasopressors prevention & treatment of infection maintenance of tissue oxygenation nutritional & metabolic support comfort & emotional support support for individual organ function CLINICAL manifestations Tachypnea, dyspnea, hypoxemia, pulm HTN, ARDS, thrombocytopenia, coagulopathy, ↓ protein C, ↑ D-dimer, metabolic acidosis, ELEVATED LACTATE (>4), jaundice, elevated liver enzymes, decreased albumin, coagulopathy, adrenal insufficiency, hyper/hypoglycemia, confusion, disorientation, psychosis, oliguria, anuria, elevated Cr, ARF, hypotension unresponsive to fluid therapy, dysrhythmias, edema, tachycardia
Cc 10 mods - MODS
Course: Critical Care (408)
University: Loma Linda University
