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High Acuity Final Study Material > SIRS, MODS, DIC, SEPSIS > Flashcards

SIRS, MODS, DIC, SEPSIS Flashcards

1
Q

What are some ABNORMAL responses to an injury

A
  • 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
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2
Q

What are some Infectious Causes of SIRS?

A
  • Candidiasis
  • Pneumonia
    • Community-acquired
    • Nosocomial
  • Influenza
  • Urinary tract infections
  • Intra-abdominal – diverticulitis, appendiciti
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3
Q

What are some nonInfectious Causes of SIRS?

A
  • Pancreatitis
  • Multiple trauma/tissue injury
  • Burns, blood transfusion reaction
  • Hemorrhagic shock – UGI Bleed
  • Ischemia/reperfusion
  • Medication side effect (theophylline)
  • Immune-mediated organ damage
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4
Q

What is SIRS?

A
  • ™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.
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5
Q

What are the effects of Nitric Oxide ?

A
  • –Protect tissue toxicity
  • –Vasodilation
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6
Q

What are the effects of Prostaglandins in SIRS?

A

They are ™released from endothelial damage and cause:

  • ™Vasodilation
  • ™Platelet Aggregation
  • ™Increase vascular permeability
  • ™Chemotaxis
  • ™Pain
  • ™Fever
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7
Q

What are the risk factors for developing SIRS?

A

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

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8
Q

What is the criteria for SIRS?

A

™2 or more of the following:

  • –Temperature > 100 F or < 96.8 F (> 38C or < 36C)
  • –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
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9
Q

What are the clinical manifestations of SIRS?

A

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.
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10
Q

Describe the difference between a normal response to an injury and an abnormal response

A

™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
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11
Q

What is MODS?

A

A progressive failure of two (2) or more organ systems resulting from malignant intravascular inflammation and resultant tissue hypoxia

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12
Q

What are the primary and secondary causes of MODS?

A
  • *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)
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13
Q

Describe how SIRS can develop into MODS

A
  1. Initiating event (Tissue Injury, Inadequate perfusion, Infection)
  2. SIRS
  3. Early MODS (1st 72 hrs, Conseq of 1st insult) **OR **Late MODS (After 72 hrs, Conseq of SIRS) OR Recovery

4.

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14
Q

What are some risk factors for developing MODS?

A
  • ™Age > 45 years (2 - 3x > risk)
  • ™Presence of pre-existing conditions:
    • –Cirrhosis
    • –COPD
    • –Ischemic heart disease
    • –Diabetes Type 1 or 2–
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15
Q

Describe the 7 major Pathophysiologic Changes in MODS

A

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
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16
Q

What are some signs, symptoms, and lab values associated with pulmonary dysfunction?

A

Signs

  • –Tachypnea
  • –ARDS patterns
  • –Pulmonary HTN

™Symptoms

  • –Restlessness
  • –Dyspnea
  • –Anxiety
  • –Mental status change

–Lab Values:

  • Respiratory rate < 5 bpm or > 49bpm
  • –PaCO2 > 50 mm Hg
  • –Alveolar-arterial oxygen difference > 350 mm HG
  • –Vent or CPAP dependent on 2nd day
  • –Need for mechanical ventilation for > 5 days at FiO2 40%
17
Q

What are some signs and lab values associated with cardiovascular dysfunction

A

Signs:

  • –Restlessness
  • –Dyspnea
  • –Palpitations
  • –Tachycardia
  • –Hypotension
  • –Poor capillary refill
  • –Skin mottling
  • –Increased CVP, PAOP
  • –Arrythymias
  • –Decreased SVR, LVSWI

Lab values:

  • –Pulse < 54
  • –SBP < 60
  • –MAP < 49 for at least 1 hour despite adequate fluid resuscitation, adequate volume status, and/or vasopressors
  • –Increased pulse adjusted heart rate
    • ™(HR X CVP-MAP) or (HR X RA-MAP)
  • –Occurrence of V tach or V Fib
  • –CI < 2L/min/m2
18
Q

What are some signs of Central Nervous System Dysfunction?

A
  • –Confusion
  • –Coma
  • –Psychosis
  • –Restlessness
  • –Disorientation
  • –Glasgow Coma Scale < 8 if no other injuries (e.g., head trauma)
  • ICP > 15; decreased CPP
19
Q

What are some signs of renal dysfunction?

A
  • Creatinine > 2 mg/dl or double that of admission
  • –Creatinine clearance < 30 ml/min
  • –Urine output < 0.5 ml/kg/hr for 1 hour despite adequate fluid resuscitation
  • –Signs of prerenal azotemia
  • –Oliguria, anuria or polyuria consistent with ATN
  • –Increased BUN
20
Q

What are some nursing interventions for patients with MODS?

A

Prevent and early identification/treatment of inflammation

  • ™Hand washing
  • ™Assessment –signs

–Prevent infections –

  • ™HOB 30
  • ™Oral care
  • ™Prevent pressure wounds
  • ™Aseptic dressing changes

–Restore oxygen supply/demand balance –

  • ™Assessment – Decreased CO and increased HR
  • ™Mixed venous oxygen saturation -SvO2
  • ™Hgb oxygen delivery
  • ™Preload/afterload, vasoactives
  • ™Activities to decrease oxygen demand
  • ™Ventilators, NMB. Lung protection strategies

Correct perfusion defects

  • Pulmonary Toilet

​​Provide nutritional/metabolic support

  • Control glucose levels, insulin drip
  • Glucose lvls < 150, you want them lower
21
Q

What are the advantages to early feeding in MODS?

A

Stress

  • –Hypermetabolic
  • ™Mediators – ACTH, growth hormone, catecholamines, cortisol, glucagon, epinephrine, norepinephrine
  • ™Insulin resistance due to cortisol – increased problem with the rising glucose levels

™Decreased Albumin (from the vasodilation)

  • –Impaired immune function
  • –Decreased wound healing
  • ¡Decreased catabolic response to injury
    ¡Maintenance of bowel mucosal integrity
    ¡Decreased bacterial translocation
    ¡Improved wound healing
    Decreased sepsis-associated mortality
22
Q

What is sepsis?

A
  • –Infection (documented or suspected)

AND

  • –Some ™Categories of Possible Manifestations:
    • ™General variables of sepsis
    • ™Inflammatory variables
    • ™Hemodynamic variables
    • ™Organ dysfunction variables
    • ™Tissue perfusion variables
23
Q

What are the criteria for sepsis?

A
  • ™Heart rate >90 beats/min (SIRS)
  • ™Temperature >101° F (38.3° C) or <96.8° F (36° C) (SIRS)
  • ™Altered mental status (SEPSIS)
  • ™Significant edema or positive fluid balance (>20 mL/kg over 24 hours) (SEPSIS)
  • ™Hyperglycemia (SEPSIS)

™SBP <90 mm Hg or
™MAP <70 mm Hg or
™SBP decrease > 40 mm Hg in adults or < 2 standard deviations below normal for age

24
Q

Severe Sepsis Definition

A

™Sepsis + Sepsis-induced tissue hypoperfusion or Organ dysfunction

  • ™Phase 1 : Hyperdynamic, warm, early
    • they are trying to compensate
  • ™Phase 2 : Hypodymanic, cold, late.
    • they are not able to compensate any longer, late stage
25
Q

What are the manifestations of phase 1 of Septic Shock?

A

(Hyperdynamic, Warm, Early phase of septic shock)

Manifestations of Hyperdynamic Septic Shock

1. Warm

  • Endotoxin increases temperature
  • Vasodilation (capillaries near skin have more blood)

2. Afterload [SVR, BP] Low to Normal

  • Low= vasodilation
  • Normal= compensatory mechanism

3. Preload [CVP] Low to Normal

  • Vasodilation
  • Compensatory mechanism

4. Contractility [LVSWI] increased

  • SNS stimulation
  • Compensatory mechanisms

5. HIGH Cardiac Output

  • SNS stimulation
  • Less resistance since pathological vasodilation started
26
Q

What are the manifestations of Phase 2 of Septic Shock?

A

(Hypodynamic, Cold, Late phase of shock)

Manifestations of Hypodynamic Septic Shock

–1. Cold: Poor perfusion
–2. Afterload [SVR, BP] Low

  • ™Severe vasodilation
  • ™Relative vasoconstriction 20 to vasopressor use, uncompensated state of shock

–3. Relative Increased Preload

  • ™Myocardial depressant factor (MDF)àDecreased Contractility causes fluid to backflow

–4. Decreased contractility [LVSWI]

  • ™MDF
  • ™Myocardial ischemia

–5. LOW Cardiac Output

  • ™Tachycardic
  • ™Less preload, contractility and afterload
27
Q

What are some interventions to help septic shock patients once their CVP is <8 mmHg?

A

Goal is to get their CVP back up to 8-12, give them either crystalloid fluids or colloid fluids.

USE CRYSTALLOID FLUIDS 1ST

28
Q

What is the goal range for MAP in septic shock patients and what are interventions to get it in that range?

A

MAP in septic shock patients should be <65 mmHg and >90mmHG. Give vasoactive medications to increase the resistance if it is too low.

29
Q

What is the goal range for ScvO2 in septic shock patients and what are interventions to get it in that range?

A
  1. We want ScvO2 >70%, but if ScvO2 is less than 70% transfuse rbc’s until hematocrit >30%.
  2. If this doesn’t work then give inotropic agents also

This value is an early warning indicator of tissue hypoxia

30
Q

What should be completed within 3 hours of suspecting sepsis in a patient?

A
  1. Measure lactate level
  2. Obtain blood cultures prior to the adminstration to abx
  3. Administer broad spectrum abx
  4. Administer 30mL / kg crystalloid for hypotension or lactate greater than or equal to 4mmol/L
31
Q

What should be completed within 6 hours of suspecting sepsis in a patient?

A
  1. Apply vasopressors (for hypotension that does not respond to inital fluid resuscitation) to maintain a MAP greater than or equal to 65 mmHg
    1. Norepinephrine (1st choice) or vasopressor
    2. Epinephrine (2nd choice)
  2. In the event of persistant arterial hypotension despite volume resuscitation (septic shock) or initial lactate greater than or equal to 4mmol/L (36 mg/dL):
    1. Measure CVP
    2. Measure ScvO2 (central venous oxygen saturation)
  3. Remeasure lactate if initial lactate was elevated
32
Q

What intervention can be provided to a patient in vasopressor refractory spetic shock?

A

For patients in vasopressor refractory septic shock (when vasopressors aren’t helping the shock state) it is recommended that IV hydrocortisone be infused. 200mg/24 hours

33
Q

How would a nurse manage sepsis & severe sepsis with antibiotics?

A
  1. Start ABX within the 1st hour
  2. Culture prior to abx if possible
  3. Combination of abx; recommended combination therapy for patient with suspected pseudomonas or neutropenic patients
34
Q

Describe the pathophysiology of DIC

A
  • Sepsis, trauma, organ destruction, cancer, obstetric complications, vascular malformations, severe liver failure, or severe toxic or immunologic reactions –>
  • Trigger excessive activation of the blood coagulation, with or without concomitant inflammation –>
  • Widespread fibrin formation in the microvasculature, rather than the normal concentration of a clot to an injured locus –>
  • Can lead to MODS—
35
Q

What are the 2 major mechanisms that trigger DIC?

A

—1. Release of Tissue Factor or thromboplastic substances into the circulation

  • Placenta
  • Leukemic cells
  • Adenocarcinomas
  • Bacterial endotoxins
  1. —Widespread injury to endothelial cells
  • Release of Tissue Factor
  • Promotes platelet aggregation
  • Activates intrinsic pathway
36
Q

What are some intrinsic causes of DIC?

A

All occur because of endothilial injury

  • Trauma
  • Burns
  • Gram-negative sepsis
  • Hypoxia
  • Acidosis
  • Shock
  • Vasculitis
    *
37
Q

What are some extrinsic causes of DIC?

A

Tissue injury:

  • Trauma
  • Obstetrical complications
  • Complications of cancer
38
Q

What are the clinical manifestations of DIC?

A

Bleeding related:

  • Superficial
    • Petechia, ecchymoses
    • Bleeding/continuous oozing from arterial lines, catheters, and injured tissue
  • Internal
    • bleeding in the GI tract, lungs, and CNS (potentially life threatening)

Thrombosis related:

  • Superficial
    • Cyanosis/ischemia, or gangrene of fingers, nose, and ears
  • Internal
    • Renal: oliguria/anuria, azotemia, hematuria
    • Pulmonary: transient hypoxemia, pulmonary hemorrhage, ARDS
    • CNS: delirium, coma, cerebral hemorrhage, meningeal irritation
    • Hepatic: jaundice
    • Skin: necrosis, gangrene
39
Q

What are some nursing interventions for DIC?

A
  • Complete assessment (**Neuro, Resp [PE, DVT])
  • Check 6 P’s of perfusion: pain, pallor, pulse, paralysis, paresthesia, poikilothermia (coolness)
  • Sites for bleeding
  • Hemetest all excretions (NG, feces, urine, wound drainage, nasal, ear/eyes, vagina, urethra)
  • Mucosal surfaces (petechiae, purpura, ecchymosis)

High Acuity Final Study Material (4 decks)

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