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What is sepsis?
systemic inflammatory response due to an infection that may be d/t bacteremia, viremia, fungemia, or other causes.
What are the steps of acute inflammation?
- 1. vascular changes
- 2. leukocyte recruitment
- 3. leukocyte activation
- 4. termination
Describe step 1 of acute inflammation, vascular changes.
- Interstitial edema
What causes vasodilation during the first step of acute inflammation? (3)
d/t histamine from mast cells, serotonin from platelets, and nitric oxide from endothelial cells
What causes interstitial edema during step 1 of acute inflammation? (3)
- modifications of starlings forces
- endothelial cell contraction
- endothelial cell death
Interstitial edema depends on 3 factors, including....
oncotic pressure, hydrostatic pressure, vascular permeability.
Describe step 2 of acute inflammation, leukocyte recruitment.
- from the blood stream to the site of injury by:
- 1. margination (d/t blood stasis)
- 2. rolling and adhesion (adhesion molecules)
- 3. diapedesis
- 4. migration by chemotaxis (neutrophils then macrophages)
Describe step 3 of acute inflammation, leukocyte activation.
- Goal of inflammation- to remove source of breakdown and removal of damaged tissue and/or infectious agents by:
- arachidonic acid pathway--> prostaglandins/ leukotrienes
- oxidative burst and reactive oxygen species
- cytokine release
The arachidonic acid pathway leads to production of __(3)__, resulting in... (3)
- prostaglandins, leukotrienes, platelet-activating factor
- vasodilation/ vasoconstriction (prostaglandins)
- chemotaxis (leukotrienes)
- thrombosis (PAF)
- **inflammation and coagulation are linked**
Oxidative burst leads to production of ___________, which results in... (4)
- reactive oxygen species
- lipid peroxidation and plasma membrane damage, DNA damage, amino acid damage, and induction of apoptosis
How does phagocytosis play a role in leukocyte activation? (3)
opsonization, engulfment of microbe, fuse with lysosome and digestion of microbial products
Describe step 4 of acute inflammation, termination. (3)
- removal of primary insult stops stimulation
- release anti-inflammatory cytokines
- switch to anti-inflammatory pathway
What are the functions of inflammation? (3)
- eliminate the cause of the injury
- increase immune defenses
- balanced, controlled response
What is SIRS?
- systemic inflammatory response syndrome
- uncontrolled or excessive inflammatory response, causing normal tissue to be damaged due to excessive host response (rather than from the primary disease)
How does inflammation progress to SIRS?
- local overflow of pro-inflammatory mediators into systemic circulation
- prolonged or severe inflammation eventually overwhelms the natural anti-inflammatory mechanisms
Contrast the local signs of inflammatory response to the systemic signs (SIRS)?
- Local: redness, pain, heat, swelling
- Systemic: tachypnea, tachycardia, temperature, WBC changes
What are the criteria for diagnosing SIRS in dogs?
- HR >150
- RR > 40
- Temp >103 or <99
- WBC >19 or <5
- **Must have 2 of these criteria + a disease process susceptible to induce SIRS**
What are the criteria for diagnosing SIRS in cats?
- HR >200 or <140
- RR >40
- Temp >103 or <99
- WBC >20 or <5
- **Must have 3 of these criteria + a disease process susceptible to induce SIRS**
What are causes of SIRS? (11)
- non-infectious inflammatory diseases (meningitis, pancreatitis)
- Immune-mediated diseases (IMHA, IMPA)
- Infectious (sepsis)
- Snake venom
- Heat stroke
- ischemia/ reperfusion
What is MODS?
Multiple Organ Dysfunction Syndrome: presence of altered organ dysfunction in an acutely ill patient such that homeostasis cannot be maintained without intervention
Describe the relationship between inflammation/ infection, SIRS/ sepsis, and MODS.
- not all inflamed/ infected patients have SIRS/ sepsis
- not all SIRS/ sepsis patients go into MODS and die
- all patients with MODS had SIRS/sepsis that was allowed to progress unnoticed
- the more organs dysfunctioning, the higher the mortality rate
What are the 5 stages of SIRS/ Sepsis?
- Stage 1: establishment of infection- sets up initial inflammation and cytokine release, body begins regulating
- Stage 2: preliminary systemic response- spill-over of mediators into systemic circulation; fever
- Stage 3: an overwhelming systemic response- excessive release of pro-inflammatory mediators; clinical syndrome of SIRS
- Stage 4: compensatory anti-inflammatory reaction- body attempts to down-reg pro-inflammatory mediators; if anti-inflamm reaction goes to far--> compensatory anti-inflammatory response syndrome (CARS)
- Stage 5: immunomodulatory failure-immune failure--> infection progresses, organ failure, death
What is compensatory anti-inflammatory response syndrome (CARS)?
the anti-inflammatory reaction goes too far, causing the immune system to become paralyzed and potentially allows the initial infection to spiral out of control
For MODS to occur, the starting point is thought to be __________, which progresses through the following steps... (7)
- pro-inflammatory cytokines
- 1. endothelial activation--> clotting cascade, microthrombosis--> ischemia, tissue hypoxia
- 2. direct injury by ROS and complement--> further loss of functional tissue
- 3. direct tissue damage from initial injury
- 4. edema formation d/t altered starling forces
- 5. microvascular dysfunction--> loss of tissue perfusion
- 6. apoptosis
- 7. impaired oxygen delivery from hypoperfusion, anemia, +/- hypoxemia
Everything that is pro-inflammatory is ___________.
Why is it important that the criteria for sepsis is very sensitive, but not specific?
- not a lot of false negative, but lots of false positive
- important because we need to recognize SIRS in the early stages and not let it progress without treatment
What are the general concepts of treatment of SIRS/ sepsis?
- Shock treatment w/ early, aggressive fluid therapy
- Antibiotics early and aggressive (if infectious- sepsis)
- Support of
- Organ function
- Nutrition early
What are the findings with septic shock? (5)
- [hyperdynamic findings]
- red MMs
- fast CRT
- bounding pulses
- decreased mental state
- warm extremities
What are the targets for early, goal-directed therapy for sepsis? (4)
- CVP 8-12mmHg
- MAP >65mmHg
- Urine output > 0.5mL/kg/hr
- ScvO2> 70%
What organ systems are usually involved with MODS? (8)
- renal- AKI
- lungs- ALI/ARDS
- coagulation- DIC
- immune system- CARS
- adrenal- CIRCA/ RAI
What cardiovascular parameters should you monitor with sepsis? (4)
What treatments are directed toward this? (4)
- hypovolemia, vasodilation, decreased inotropy, dysrrhythmia
- fluid therapy, vasopressors, positive inotropes, anti-arrhythmics
What coagulation parameters should you monitor with sepsis? (6)
What treatments are directed toward this? (3)
- clotting times
- platelet numbers
- FDPs/ D-Dimrs
- serial measurements
- Treatments: treat primary cause of sepsis, +/- heparin for patients in prothrombotic phase, plasma for patients in bleeding phase
What renal parameters should you monitor with sepsis? (3)
What treatments are directed toward this? (5)
- urine cytology, oliguria/anuria (urine output <1mL/kg/hr), azotemia
- fluid therapy, mannitol, furosemide, hemodialysis, peritoneal dialysis
What pulmonary parameters should you monitor with sepsis? (2)
What treatments are directed towards this? (4)
- SpO2, radiographs
- oxygen, fluid therapy, diuretics, mechanical ventilation