SIRS AND MODS

Inflammation
Inflammation is immediate response to cellular
injury
Triggered response to variety of causes
Ischemia, infection, trauma, foreign substances,
malignancies
Limited to specific area localized inflammation
Large number or persistent inflammatory
mediators released generalized & systemic
inflammatory response SIRS

SIRS
Systemic inflammatory response syndrome
(SIRS)- systemic inflammatory response to a
variety of insults
Generalized inflammation in organs remote from
initial insult
Triggers
Mechanical tissue trauma: burns, crush injuries, surgical
procedures
Abscess formation: intra-abdominal, extremities
Ischemic or necrotic tissue: pancreatitis, vascular disease, MI
Microbial invasion: Bacteria, viruses, fungi
Endotoxin release: Gram-negative bacteria
Global perfusion deficits: Postcardiac resuscitation, shock states
Regional perfusion deficits: Distal perfusion deficits




Characterized by presence of any 2 of the following
clinical findings in response to tissue injury
Temp > 38C or < 36C
HR > 90
RR > 20 or respiratory alkalosis
WBC > 12,000 or < 4,000 cells/mm
3
or > 10%
immature WBCs (bands)

Can lead to altered circulation & coagulation; edothelial
dysfunction; impaired tissue perfusion
MODS
Multiple organ dysfunction syndrome
(MODS)- failure of two or more organ
systems
Homeostasis cannot be maintained without
intervention-Results from SIRS
SIRS and MODS represent ends of a
continuum
Transition from SIRS to MODS DOES NOT
occur in a clear-cut manner

SIRS and MODS
Consequences of
inflammatory response

Release of mediators
Direct damage to endothelium
Hypermetabolism
Vasodilation leading to dec SVR
Inc in vascular permeability
Activation of coagulation cascade
Relationship Shock, Sirs &
Mods
SIRS and MODS
Pathophysiology
Organ and metabolic dysfunction
Hypotension
Decreased perfusion
Formation of microemboli
Redistribution or shunting of blood
SIRS and MODS
Pathophysiology
Respiratory system
Alveolar edema
Decrease in surfactant
Increase in shunt
V/Q mismatch
End result: ARDS
Cardiovascular system
Myocardial depression
and massive vasodilation


SIRS and MODS
Pathophysiology
Renal system
Acute renal failure
Hypoperfusion
Release of mediators
Activation of reninangiotensin aldosterone system
Nephrotoxic drugs, especially antibiotics

SIRS and MODS
Pathophysiology
GI system
Motility decreased: Abdominal distention and paralytic ileus
Decreased perfusion: Risk for ulceration and GI bleeding
Potential for bacterial translocation
Hypermetabolic state
Hyperglycemiahypoglycemia
Insulin resistance
Catabolic state
Liver dysfunction
Lactic acidosis

SIRS and MODS
Pathophysiology
Hematologic
system
DIC
Electrolyte
imbalances
Metabolic acidosis
SIRS and MODS
Collaborative Care
Prognosis for MODS poor
Goal: Prevent progression of SIRS to MODS
Vigilant assessment-ongoing monitoring to
detect early signs of deterioration or organ
dysfunction-critical
Prevention and treatment of infection
Aggressive infection control strategies to dec risk
for nosocomial infections
Once an infection suspected, institute interventions
to control source !~
SIRS and MODS- Collaborative Care
Maintain tissue oxygenation
Dec O
2
demand
Sedation
Mechanical ventilation
Paralysis
Analgesia
Optimize O
2
delivery
Maintain normal hemoglobin level
Maintain normal PaO
2

Individualize tidal volumes with PEEP

SIRS and MODS- Collaborative Care
Maintenance of tissue oxygenation
Enhance CO
Inc preload or myocardial contractility
Reduce afterload
SIRS and MODS- Collaborative Care
Nutritional and metabolic needs
Goal of nutritional support: Preserve
organ function-total energy expenditure-
often inc 1.5 to 2.0 times
Nutritional and metabolic needs
Use of enteral route preferred to parenteral
nutrition
Monitor plasma transferrin & prealbumin levels
to
assess hepatic protein synthesis
SIRS and MODS- Collaborative Care
Support of failing organs
ARDS: Aggressive O
2
therapy and mechanical
ventilation
DIC: Appropriate blood products
Renal failure: Continuous renal replacement
therapy or dialysis
Is the systemic response to infection

Sepsis
Sepsis
- SIRS
+ Infection


Severe Sepsis
- Sepsis
+ Organ dysfunction

Septic shock
Sepsis
+ Hypotension despite fluid resuscitation


Complications
Organ System Involvement
Circulation
Hypotension,
increases in microvascular permeability
Shock

Lung
Pulmonary Edema,
hypoxemia,
ARDS

Hematologic
DIC, coagulopathy
(DVT)
Organ System Involvement

GI tract
stress ulcer
Translocation of bacteria,
Liver Failure,
Gastroparesis and ileus,
Cholestasis


Kidney
Acute tubular necrosis,
Renal Failure

Organ System Involvement

Nervous System
Encephalopathy

Skeletal Muscle
Rhabdomyolysis

Endocrine
Adrenal insufficiency

MODS
Biliary tract
infection
Shock
Pancreatitis
Burn
Intra-abdominal
infection
Infective diseases Non-infective diseases
Multiple trauma
MODS
Biliary tract
infection
Shock
Pancreatitis
Burn
Intra-abdominal
infection
Infective diseases Non-infective diseases
Multiple trauma
Bacterial translocation
The viable bacili locomote from the
gastrointestinal tract to the other organs.
Intestinal flora imbalance
Intestinal mucosal ischemia
Immune dysfunction
Causes for the translocation
Infective diseases Non-infective diseases
MODS
Ischemia/reperfusion injury
Mechanism
Uncontrolled inflammatory response
Microcirculatory hypo-perfusion
Inflammation
Inflammatory cells
Inflammatory cytokines
MODS is the failure of the balance
Uncontrolled inflammatory response
Systemic Inflammatory Response Syndrome (SIRS)
An uncontrolled inflammation process
Pro-inflammatory signals exceed its normal
domain or degree


Result in end-organ damage and multi-
system
failure.
Definition
Anti-inflammatory reaction
IL-10, IL-4, TGF-
IL-1ra ,Lipoxin
Cell eliminate
Pro-inflammatory reaction
TNF-a, IL-1, IL-6, IFN
TXA
2
, PAF
Cell activation
Infection/ injury
Local inflammatory
cell activated
(M,PMN,VEC,)
Pro-inflammatory
mediators released
Inflammatory stimulator
Tissue injury
Infection/Injury
Host
response
SIRS CARS
MODS
Uncontrolled
inflammatory
response
Excessive
Adequate
Death
Inadequate
Infection/injury
controlled
Summary
Shock
Syndrome characterized by decreased tissue
perfusion and impaired cellular metabolism
Imbalance in supply/demand for O2 and nutrients
Shock
Classification of shock
Cardiogenic
Hypovolemic
Distributive
Obstructive
Low Blood Flow- Cardiogenic Shock
Definition
Systolic or diastolic dysfunction
Compromised cardiac output (CO)
Precipitating causes
Myocardial infarction
Cardiomyopathy
Blunt cardiac injury
Severe systemic or pulmonary hypertension
Cardiac tamponade
Myocardial depression from metabolic problems


Pathophysiology of Cardiogenic Shock
39
Fig. 67-1. Relationship of shock, systemic inflammatory response syndrome, and multiple
organ dysfunction syndrome. CNS, Central nervous system.
Low Blood Flow-Cardiogenic Shock
Early manifestations
Tachycardia; Hypotension
Narrowed pulse pressure
myocardial O2 consumption
Physical examination
Tachypnea, pulmonary congestion
Pallor; cool, clammy skin
Dec capillary refill time
Anxiety, confusion, agitation
in pulmonary artery wedge pressure
Dec renal perfusion and UO

Low Blood Flow-Hypovolemic Shock
Absolute hypovolemia: loss of intravascular
fluid volume
Hemorrhage; GI loss (e.g., vomiting, diarrhea)
Fistula drainage; Diabetes insipidus
Hyperglycemia; Diuresis
Relative hypovolemia
Results when fluid volume moves out of vascular
space into extravascular space (e.g., interstitial or
intracavitary space)
Termed third spacing

Pathophysiology of Hypovolemic Shock
42
Fig. 67-3. The pathophysiology of hypovolemic shock.
Response to acute volume loss depends
on:
Extent of injury or insult
Age
General state of health
Low Blood Flow
Hypovolemic Shock
Clinical manifestations
Anxiety
Tachypnea
Inc in CO, heart rate
Dec in stroke volume, PAWP, urinary output
If loss is >30%, blood volume is replaced.
Distributive Shock
Neurogenic Shock
Hemodynamic phenomenon
that can occur within 30
minutes of a spinal cord
injury at the fifth thoracic
(T5) vertebra or above and
last up to 6 weeks
Can occur in response to
spinal anesthesia
Results in massive
vasodilation > lead to
pooling of blood in vessels

Distributive Shock-Neurogenic Shock
Clinical manifestations
*Hypotension
*Bradycardia
Temperature dysregulation (resulting in heat loss)
Dry skin
Poikilothermia (taking on the temperature of the
environment)
Distributive Shock-Anaphylactic Shock
Copyright 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
Acute, life-threatening hypersensitivity reaction
Massive vasodilation; Release of mediators
capillary permeability
Clinical manifestations
Anxiety, confusion, dizziness
Sense of impending doom; Chest pain
Incontinence
Swelling of the lips and tongue, angioedema
Wheezing, stridor; Flushing, pruritus, urticaria
Respiratory distress and circulatory failure


Distributive Shock-Septic Shock
Sepsis: systemic
inflammatory response to
documented or suspected
infection
Severe sepsis = Sepsis +
Organ dysfunction
Presence of sepsis with
hypotension despite fluid
resuscitation
Presence of tissue perfusion
abnormalities

Distributive Shock-Septic Shock
Clinical manifestations
coagulation and inflammation
fibrinolysis
Formation of microthrombi
Obstruction of microvasculature
Hyperdynamic state: inc CO and dec SVR
Tachypnea/hyperventilation
Temperature dysregulation
urine output
Altered neurologic status
GI dysfunction
Respiratory failure common.

Obstructive Shock
Develops when physical obstruction to blood
flow occurs with dec CO
From restriction to diastolic filling of right ventricle
due to compression
Abdominal compartment syndrome
Patient experience
Dec CO
Inc afterload
Variable left ventricular filling pressures
Rapid assessment and immediate treatment
important
Stages of Shock
Initial Stage
Usually not clinically apparent
Metabolism changes from aerobic to
anaerobic.
Lactic acid accumulates -must be removed by
blood and broken down by liver.
Process requires unavailable O2.
Clinically apparent Neural, Hormonal
&Biochemical compensatory mechanisms
Attempts aimed to overcome consequences of
anaerobic metabolism and maintaining
homeostasis.

Compensatory Stage of Shock
52
Fig. 67-7. Compensatory stage: reversible stage during which compensatory mechanisms are
effective and homeostasis is maintained.
Baroreceptors in carotid and aortic bodies
activate SNS in response to BP.
Vasoconstriction while blood to vital
organs maintained-
blood to kidneys > activates renin
angiotensin system venous return
to heart, CO, BP
Impaired GI motility- Risk for paralytic
ileus
Cool, clammy skin from blood
Except septic patient who is warm
and flushed

Stages of Shock-Compensatory Stage
Shunting blood from lungs increases
physiologic dead space.
arterial O2 levels
Increase in rate/depth of respirations
V/Q mismatch
SNS stimulation increases myocardial O2
demands.
If perfusion deficit corrected, patient recovers
with no residual sequelae
If deficit not corrected, patient enters
progressive stage

Stages of Shock-Progressive Stage
Begins when compensatory
mechanisms fail
Aggressive interventions to
prevent multiple organ
dysfunction syndrome
(MODS)
Hallmarks - cellular
perfusion & altered capillary
permeability
Leakage of protein into
interstitial space
systemic interstitial edema

Stages of Shock-Progressive Stage
Anasarca
Fluid leakage affects solid organs and peripheral tissues.
blood flow to pulmonary capillaries
Movement of fluid from pulmonary vasculature to
interstitium
Pulmonary edema
Bronchoconstriction
residual capacity
Fluid moves into alveoli
Edema-Dec surfactant
Worsening V/Q mismatch
Tachypnea, Crackles
Inc work of breathing


Stages of Shock-Progressive Stage
CO begins to fall
Dec peripheral perfusion
Hypotension
Weak peripheral pulses
Ischemia of distal extremities
Myocardial dysfunction results in
Dysrhythmias
Ischemia; Myocardial infarction
End result: complete deterioration of cardiovascular
system


Stages of Shock-Progressive Stage

Liver fails to metabolize drugs and waste.
Jaundice; Elevated enzymes
Loss of immune function
Risk for DIC and significant bleeding
Mucosal barrier of GI system becomes ischemic
Ulcers
Bleeding
Risk of translocation of bacteria
Dec ability to absorb nutrients
Stages of Shock--Irreversible Stage
Copyright 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
Exacerbation of anaerobic
metabolism
Accumulation of lactic acid
capillary permeability
Profound hypotension and
hypoxemia
Tachycardia worsens.
Failure of one organ system
affects others.
Recovery unlikely


Diagnostic Studies
Thorough history and physical examination
No single study to determine shock
Blood studies
Elevation of lactate
Base deficit
12-lead ECG
Chest x-ray
Hemodynamic monitoring
Collaborative Care
Successful management includes
Identification of patients at risk for shock
Integration of patients history, physical
examination, and clinical findings to establish
diagnosis
Interventions to control or eliminate cause of dec
perfusion
Protection of target and distal organs from
dysfunction
Provision of multisystem supportive care

Collaborative Care
General management strategies
Ensure patent airway.
Maximize oxygen delivery.
Cornerstone of therapy for septic, hypovolemic, and
anaphylactic shock = Volume expansion
Isotonic crystalloids (e.g., normal saline) for initial
resuscitation of shock
Volume expansion
If patient does not respond to 2 to 3 L of
crystalloids, blood administration & central venous
monitoring may be instituted.
Complications of fluid resuscitation
*Hypothermia & Coagulopathy



Collaborative Care
Primary goal of drug therapy = Correction of
decreased tissue perfusion
Vasopressor drugs (e.g., norepinephrine)
Achieve/maintain MAP >60 to 65 mm Hg.
Reserved for patients unresponsive to fluid
resuscitation
Vasodilator therapy (e.g., nitroglycerin,
nitroprusside)
Achieve/maintain MAP >65 mm Hg.


Collaborative Care
Nutrition is vital to decreasing morbidity from
shock.
Initiate enteral nutrition within the first 24 hours.
Initiate parenteral nutrition if enteral feedings
contraindicated or fail to meet at least 80% of
caloric requirements
Monitor protein, nitrogen balance, BUN, glucose,
electrolytes
Collaborative Care-Cardiogenic Shock
Restore blood flow to myocardium by restoring
balance between O2 supply and demand.
Thrombolytic therapy
Angioplasty with stenting
Emergency revascularization
Valve replacement
Hemodynamic monitoring
Drug therapy (e.g., diuretics to reduce preload)
Circulatory assist devices (e.g., intraaortic balloon
pump, ventricular assist device)

Collaborative Care-Hypovolemic Shock
Management focuses on stopping loss of fluid
and restoring circulating volume.
Fluid replacement is calculated using a 3:1 rule
(3 mL of isotonic crystalloid for every 1 mL of
estimated blood loss).
Collaborative Care-Septic Shock
Fluid replacement to restore perfusion
Hemodynamic monitoring
Vasopressor drug therapy
Vasopressin for patients refractory to vasopressor
therapy
IV corticosteroids for patients who require
vasopressor therapy, despite fluid resuscitation, to
maintain adequate BP
Antibiotics after cultures obtained (e.g., blood,
wound exudate, urine, stool, sputum)
Drotrecogin alfa (Xigris)-Major side effect: bleeding


Collaborative Care-Septic Shock
Glucose levels <150 mg/dL
Stress ulcer prophylaxis with histamine (H2)-
receptor blockers
Deep vein thrombosis prophylaxis with low-
dose unfractionated heparin or low-molecular-
weight heparin
Collaborative Care
Neurogenic Shock
In spinal cord injury: spinal stability
Treatment of hypotension and bradycardia with
vasopressors and atropine
Fluids used cautiously as hypotension generally
is not related to fluid loss
Monitor for hypothermia.
Collaborative Care-Anaphylactic Shock
Epinephrine, diphenhydramine
Maintaining patent airway
Nebulized bronchodilators
Endotracheal intubation or cricothyroidotomy may be
necessary.
Aggressive fluid replacement
Intravenous corticosteroids if significant
hypotension persists after 1 to 2 hours of
aggressive therapy

Collaborative Care
Obstructive Shock
Early recognition and treatment is primary
strategy.
Mechanical decompression
Radiation or removal of mass
Decompressive laparotomy
Nursing Assessment
ABCs: airway, breathing, and circulation
Focused assessment of tissue perfusion
Vital signs
Peripheral pulses
Level of consciousness
Capillary refill
Skin (e.g., temperature, color, moisture)
Urine output


Nursing Assessment
Brief history
Events leading to shock
Onset and duration of symptoms
Details of care received before hospitalization
Allergies
Vaccinations
Nursing Diagnoses
Ineffective tissue perfusion: renal, cerebral,
cardiopulmonary, GI, hepatic, and peripheral
Fear
Potential complication: organ
ischemia/dysfunction

Goals for patient
Assurance of adequate tissue perfusion
Restoration of normal or baseline BP
Return/recovery of organ function
Avoidance of complications from prolonged states
of hypoperfusion
Planning
Nursing Implementation
Health promotion
Identify patients at risk.
Elderly patients
Those with debilitating illness
Those who are immunocompromised
Surgical or accidental trauma patients
Nursing Implementation
Health promotion (contd)
Planning to prevent shock
Monitoring fluid balance to prevent hypovolemic shock
Maintenance of hand washing to prevent spread of
infection
Nursing Implementation
Acute interventions
Monitor the patients ongoing physical and
emotional status to detect subtle changes in the
patients condition.
Plan and implement nursing interventions and
therapy.
Nursing Implementation
Acute interventions
Evaluate the patients response to therapy.
Provide emotional support to patient and family.
Collaborate with other members of health team
when warranted.
Nursing Implementation
Neurologic status: orientation and level of consciousness
Cardiac status
Continuous ECG
VS, capillary refill
Hemodynamic parameters: central venous pressure, PA pressures,
CO, PAWP
Heart sounds: murmurs, S3, S4
Respiratory status
Respiratory rate and rhythm
Breath sounds
Continuous pulse oximetry
Arterial blood gases
Most patients will be intubated and mechanically ventilated.

Nursing Implementation
Urine output
Tympanic or pulmonary arterial temperature
Skin: temperature, pallor, flushing, cyanosis,
diaphoresis, piloerection
Bowel sounds
Nasogastric drainage/stools for occult blood
I&O, fluid and electrolyte balance
Oral care/hygiene based on O2 requirements
Passive/active range of motion

Nursing Implementation
Assess level of anxiety and fear.
Medication PRN
Talk to patient
Visit from clergy
Family involvement
Comfort measures
Privacy
Call light within reach

Evaluation
Normal or baseline, ECG, BP, CVP, and PAWP
Normal temperature
Warm, dry skin
Urinary output >0.5 mL/kg/hr
Normal RR and SaO2 90%
Verbalization of fears, anxiety
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