SIRS, MODS, DIC Flashcards
What are some ABNORMAL responses to an injury
- Homeostasis not restored
- Inflammation is no longer localized, becomes a systemic reaction
- Cytokines now causing destruction instead of protection
- Endothelial system activated
- Protective cascades activated (antibodies from plasma cells, opsonization, phagocytosis, coagulation, complement)
- Loss of circulatory integrity
- Leads to:
- SIRS
- MODS
What are some Infectious Causes of SIRS?
- Candidiasis
- Pneumonia
- Community-acquired
- Nosocomial
- Influenza
- Urinary tract infections
- Intra-abdominal – diverticulitis, appendiciti
What are some nonInfectious Causes of SIRS?
- Pancreatitis
- Multiple trauma/tissue injury
- Burns, blood transfusion reaction
- Hemorrhagic shock – UGI Bleed
- Ischemia/reperfusion
- Medication side effect (theophylline)
- Immune-mediated organ damage
What is SIRS?
- Prolonged exaggerated intravascular inflammation due to mediators
- Self defense mechanism– at the beginning
- Limits injury
- Promotes healing
- Cytokines tissue necrosis factor–alpha (TNF-α) and interleukin-1 (IL-1) are released first and initiate several cascades.
What are the effects of Nitric Oxide ?
- Protect tissue toxicity
- Vasodilation
What are the effects of Prostaglandins in SIRS?
They are released from endothelial damage and cause:
- Vasodilation
- Platelet Aggregation
- Increase vascular permeability
- Chemotaxis
- Pain
- Fever
What are the risk factors for developing SIRS?
Patient related:
•Age > 45
•Chronic disease states: Diabetes, CA, Renal Insufficiency
•Alcohol abuse
Treatment related:
•Immunosuppression
•Mechanical Ventilation
•Malnutrition
•Inadequate fluid resuscitation
•Tip the balance SIRS vs. CARS
•Severity of initial insult
What is the criteria for SIRS?
2 or more of the following:
- Temperature > 100 F or 38C or
- HR > 90 beats/min
- Respirations > or equal to 20/min or PaCO2 , 32 mm Hg
- WBC count:
- Greater than or equal to 12,000/mL or
- Less than or equal to 4,000/mL or
- >10% immature neutrophils/bands
What are the clinical manifestations of SIRS?
The systemic inflammatory response syndrome (SIRS) is a clinical response arising from a nonspecific insult manifested by two or more of the following:
- Fever or hypothermia
- Tachycardia
- Tachypnea
- Leukocytosis, leukopenia, or a left-shift (increase in immature neutrophilic leukocytes in the blood)
- Respiratory Rate – most sensitive indicator
- Hypotension – important indicator, may not be evident
in SIRS unless dehydrated
- Recent evidence indicates that hemostatic changes play a significant role in many SIRS-linked disorders.
Describe the difference between a normal response to an injury and an abnormal response
Normal
- Inflammation = local, effective response to injury
- Physiologic mechanism = orchestrated response of vasodilatation, microvascular permeability, cellular activation & coagulation
Abnormal (as in SIRS)
- Inflammation = systemic response to nonspecific injury
- Physiologic mechanisms = quaternary chaotic overreaction, AEB altered body temp, fever, heart rate & WBC count
What is MODS?
A progressive failure of two (2) or more organ systems resulting from malignant intravascular inflammation and resultant tissue hypoxia
What are the primary and secondary causes of MODS?
- *Primary causes:**
- *High severity of injury: Hypoxemia, Hemorrhage, Shock states (poor VO2 & microcirculation failure)**
- Sepsis = Infection + SIRS
- Persistent inflammatory focus
- Injury
- Necrotic tissues
- Shock
- SIRS
Secondary causes:
- Age
- Pre-existing conditions
- Deregulated apoptosis
- Transfusion
- Multiple surgical operations (second insult reactivates initial problem at intense level)
Describe how SIRS can develop into MODS
- Initiating event (Tissue Injury, Inadequate perfusion, Infection)
- SIRS
- Early MODS (1st 72 hrs, Conseq of 1st insult) OR Late MODS (After 72 hrs, Conseq of SIRS) OR Recovery
4.
What are some risk factors for developing MODS?
- Age > 45 years (2 - 3x > risk)
- Presence of pre-existing conditions:
- Cirrhosis
- COPD
- Ischemic heart disease
- Diabetes Type 1 or 2
Describe the 7 major Pathophysiologic Changes in MODS
1. Misdistribution of Circulating Volume
- Excessive persistent inflammatory response
- Actual/relative volume loss
- Decreased cardiac output
- Hemorrhage
- Opportunistic infections
- CMV
- HHV-6 (increased cytokines)Desachy et al. (2001)
2. Microvascular Coagulopathy
- Release of endotoxins/cellular mediators
- Protein C
3. Imbalance of Oxygen Supply/Demand
- Decreased supply
- Decreased utilization (deranged microcirculation)
- Increased demand
4. Metabolic Derangements
- Failure of microcirculation to remove end products
- Increase lymphocytes in GI, Liver, Kidney, Heart
- Decreased neutrophils
5. Uncontrolled Systemic Inflammation
- Pro-inflammatory mediators:
- Immune cells activated, then down regulated (creating immune deficiency state )
- Increase cap permeability (organ edema- ARDS, Brain)
- Vasodilation (NOx)
- Oxygen Free Radicals (tissue damage)
6. Unregulated Apoptosis
- Apoptosis= regulated normal cell death
- Lymphocytes and Gut cells have increased apoptosis
- Other organ cells have excessive apoptosis:
- Liver
- Kidney
- Heart
7. Gut-Origin Sepsis to MODS Theory
- During low flow and hypoxic states, the gut looses barrier function (increased endothelial permeability)
- Endotoxin from intestinal gram negative bacteria move into portal and lymphatic circulation
