Multisystem Problems
antigen reaction
A. Shock
An acute. Widespread process of
impaired tissue perfusion.
- Life threatening
- Organs don’t receive enough
oxygen nutrients
Ineffective tissue perfusion:
 Imbalance in cellular oxygen
supply and demand
 Cellular dysfunction – death
Shock Syndrome
 Complex pathologic process
o Multi-Organ Dysfunction
Syndrome and death
 All types of shock
o Ineffective tissue perfusion
and acute circulatory
failure.
 Shock Syndrome:
o Pathway involving a variety
of pathologic processes.
o 4 stages
 Initial- tissue perfusion
threatened.
 Compensatory –
mechanism to counter the
decrease in tissue perfusion
 Progressive- compensatory
begin to fail. The shock
become steadily worse until
death
 Refractory- poor tissue
perfusion, hypotension, and
organ failure.
Types of Shock
Distributive Shock
 Mal distribution of circulating blood
volume
o Septic – microorganisms entering
body
o Anaphylactic- Severe antibody –
o Neurogenic – Loss of sympathetic
tone.
Hypovolemic Shock
 Loss of intravascular volume
Cardiogenic Shock
 Cardiac pump failure
Obstructive Shock
 Anatomical Obstruction of the
great vessels of the heart.
Consequences of Shock
 Cardiovascular – Ventricular failure,
microvascular thrombosis
 Neurologic – SNSD, Cardiac and respi
depression, Thermoregulatory failure,
coma.
 Pulmonary - Acute lung failure , ARDS
 Renal –AKI
 Hematologic – Disseminated
intravascular coagulation.
 GI – GIT, Liver and Pancreatic failure
Assessment and Diagnosis
Shock State
 MAP <60 mmHg
 Hypotension
 Compensatory Mechanisms:
Produce normal hemodynamic
values even when tissue perfusion
is compromised
Medical Management
 Improvement and Preservation of
tissue perfusion
 Adequate tissue perfusion
o Oxygen transport – gas
exchange, CO, hemoglobin level
 o Oxygen use: internal metabolic Nursing Management
environment and mitochon
 Psychosocial needs of the patient
function.
and family
 Focuses on supporting O2 delivery
o Situational, familial and patient-
 Adequate airway, ventilation and
centered variables.
oxygenation
Nursing Interventions
 Administration of supplemental
and mechanical ventilator  Providing info and explaining
support. procedures and routines
 Adequate CO and hgb level  Encouraging the expression of
 Fluids : indicate for decrease feelings
preload related to IV volume  Facilitating problem solving and
depletion shared decision making
o Crystalloids- balanced  Visitation schedules
electrolyte solutions (PNS, PLRS)  Involving the family in patient
o Colloids – protein containing care and establishing contracts
solutions. with necessary resources.
 Blood – Augment oxygen HYPOVOLEMIC SHOCK
transport MOST COMMONLY OCCURING FORM
o Stored RBC – does not OF SHOCK
substantially increase oxygen
consumption ↓↓ IV volume
o Transfusion-related acute lung ↓↓ Venous Return
injury: from immune and
↓↓ Cardiac Output
nonimmune activation (leading
cause of transfusion-related  Occurs from inadequate fluid
death) volume
Medications:  Lack of adequate circulating vol.
↓ tissue perfusion and initiation of
 Vasoconstrictor – improving BP ,
the general shock response
↑SVR
 Absolute hypovolemia – ↓Volume
 Vasodilator – ↓ preload and after
 Absolute factors
load or both by ↓ venous return
o Loss of whole blood
and SVR
o Loss of plasma
 Positive inotropic agents -↑
o Loss of other body fluids
contractility
 Relative hypovolemia - ↑ in
 Antidysrhythmic agents –
vascular capacitance
Influence heart rate
 Relative Factors
 Enteral Nutrition support therapy
o Vasodilation
started within (24-48hrs)
o ↑ capillary membrane
 Nutrition supplementation varies
permeability
according to the cause of shock
o Decreased colloidal osmotic
 PN when enteral feeding is
pressure.
contraindicated
 Glucose control - 140-180 mg/dL
o ↓ incidence of infection, renal
failure, sepsis and death
ASSESSMENT AND DIAGNOSIS  Limiting blood sampling
 Observing for accidental
Simpler Approach
disconnection
Stage Volume  Direct pressure to bleeding sites
Loss Compensatory  Volume replacement
mechanism o Insertion of large-bole
Class I 15%-20% Slight anxiety, peripheral iv catheters
MILD -750 ml volume loss o Rapid administration of
worsens, cool prescribed fluids
extremities, ↑ CARDIOGENIC SHOCK
capillary refill
LEADING cause of death of patients
time
with MI
Class II 15%-30% Overwhelmed
Moderate -750- and  Lack of adequate pumping
1500 ml ineffective function leads to ↓ tissue perfusion
tissue and circulatory failure
perfusion; BP ↓  5% -8% of patient with ST segment
but often MI
hypoperfusion.  Acute hypo perfusion and
Class III 30%-40% Same as class hypoxia
Moderate -1500- 2
2000ml Etiologic Factors
Class IV >40% Refractory in
Severe -2000ml nature  MUSCULAR
o Ischemic injury
o Acute decompensated heart
MEDICAL MANAGEMENT failure
To correct the cause of the o Cardiomyopathy
hypovolemia, restore tissue perfusion o Acute myocarditis
and prevent complications o Myocardial contusion
o Prolonged cardiopulmo bypass
 Identifying and stopping the o Septic shock
source of fluid loss o Hemorrhagic shocl
 Administer fluid o Medications
 Vasopressor therapy to maintain  Beta-adrenergic blockers
tissue perfusion until volume is  Calcium channel
restored antagonists
NURSING MANAGEMENT  Cytotoxic agents
 Prevention  MECHANICAL
o Identification of pt at risk &  RHYTHMIC
frequent assessment of the pt’s o Bradydysrhythmias
fluid volume. (decreased o Tachydysrhythmias
mortality)
 Accurate I/O and wts monitoring ASSESMENT AND DIAGNOSIS
 Continuous evaluation S/SX
 Minimizing fluid loss
 Assessment  Systolic bp <90mmHg
 Providing comfort and emotional  Acute drop in BP >30 mmHg
support  >100 bpm
 Preventing and maintaining  Weak, thread pulse
surveillance for complication  Diminished heart sounds
  Change in sensorium
 Cool, pale, moist skin
 Urine output <30 ml/hr
 Chest pain
 Dysrhythmias
 Tachypnea
 Crackles
 Decreased CO
 Cardiac Index <2.2 Lm/m2
 ↑ Pulmonary artery occlusion
pressure
 ↑ right atrial pressure
 Variable systemic vascular
resistance
MEDICAL MANAGEMENT
AGGRESSIVE APPROACH
 Enhance the effectiveness of the
pump and improve tissue
perfusion
 Inotropic agents : ↑ contractility
and maintain BP and tissue
perfusion (DOBUTAMINE)
 Vasopressor: norepinephrine to
maintain BP when hypotension is
severe
o ↑myocardial demand, lowest
possible doses should be used
 Diuretics : preload reduction
 Vasodilating agents
 Antidysrhythmic agents : suppress
and control dysrhythmias than
can affect CO
 Intubation and mechanical
Ventilation: support oxygenation
NURSING MANAGEMENT
 Prevention of cardiogenic shock
 Identification of patient at risk
 Facilitation of early reperfusion
therapy for acute MI
 Frequent assessment
 Limiting myocardial oxygen
demand
o Analgesics, sedatives and
antidysrhythmic agents
o Position the patient for comfort
o Limit activities
o Calm and quiet environment
o Offering support
o Health teaching
 Enhancing myocardial oxygen
supply
o Supplemental oxygen
o Monitoring RR
o Prescribed medications
o Managing device therapy
 Maintaining adequate tissue
perfusion
 Providing comfort and emotional
support and preventing and
maintaining surveillance
complications
o Infection, bleeding,
thrombocytopenia, hemolysis,
embolus, stroke, device
malfunction, circulatory
compromise of a cannulated
extremity and sepsis
ANAPHYLACTIC SHOCK
 Type of Distributive shock
 Life-threatening requires prompt
intervention
 ↓ decreased tissue perfusion and
initiation of the general shock
response.
 Anaphylaxis
-Caused by an immunologic antibody
response or non-immunologic
activation of mast cells and basophils
 Triggers
-Introduce by injection or ingestion
through the skin or respi tract and
venoms.
-Can be physical factors and idiopathic
-Latex (extreme problematic agent
Etiologic Factors in Anaphylactic Shock
 Environmental Agents
o Pollens, molds and spores
o Sunlight
o Cold or heat
 o Animal dander
o latex
 Venoms
o Bees, hornets, yellow
jackets, and wasps
o Snakes, jellyfish
o Deer flies
o Fire ants
 Medications
o Antibiotics
o Aspirin
o Nonsteroidal anti-
inflammatory drugs
o Opioids
o Dextran
o Vitamins
o Muscle relaxants
o Neuromuscular blocking
agents
o Barbiturates
o Nonbarbiturates hypnotics
o Protamine
o Infliximab (Remicade)
o Ethanol
 Immunologic anaphylactic
reactions: either IgE or non IgE
mediated responses.
 IgE: antibody
o The first time an antigen
enters the body, an
antibody IgE, specific for the
antigen, is formed.
o The antigen-specific IgE
antibody is then stored by
attachment to mast cells
and basophils.
o This initial contact with the
antigen is known as a
primary immune response.
 Some immunologic anaphylactic
reactions are non IgE-mediated.
ASSESSMENT AND DIAGNOSIS
Anaphylactic Shock : severe systemic
reaction that can affect multiple organ
systems
 Usually starts to appear within
minutes of exposure to the
antigen
 Symptoms may appear after 1-72
hrs window of resolution termed a
biphasic reaction.
 Late phase reactions may be
similar to initial response, milder or
more severe
 In protracted anaphylaxis
symptoms may last 32 hrs
S/SX
MEDICAL MANAGEMENT
 Requires an immediate and direct
approach to prevent death
 Goals
o Remove offending antigen
o Reverse the effects of the
biochemical mediators
o Promote adequate tissue
perfusion
 When hypersensitivity reaction
occurs infusion should be
immediately discontinued.
 Often impossible to remove the
antigen]
 Reversal of the effects of
biochemical mediators involves
preservation and support of the
patient’s airway, ventilation and
circulation.
o Oxygen therapy
o Intubation
o Mechanical ventilation
o Administration of
medication and fluids
  Epinephrine
o First line
o Promotes bronchodilation,
vasoconstriction and ↑
myocardial contractility and
inhibits further release of
biochemical mediators
o Mild cases:
 0.2 to 0.5 mg ( 0.3 to 0.5 ml ) of a
1:1000 dilution IM into the
anterolateral thigh
 Repeated every 5-10 mins until
anaphylaxis is resolved.
o Anaphylactic shock with
hypotension:
 IV dose is 0.05 to 0.1 mg (1Ml) of
a 1:10,000 dilution over 5 mins.
 If hypotension persist a
continuous of epi is
recommended, administered at
1-4 mcg/min with titration up to
10 mcg/min as needed
o IV glucagon - 20- to 30- mcg/kg
bolus over 5 mins followed by
continuous infusion at 5-15
mcg/min is recommended to
treat bronchospasm and
hypotension in this patients.
o Rapid volume replacement
 1L in 5-10 minutes is suggested if
needed to restore perfusion
 Vasopressors may be necessary
to reverse the vasodilation and
increase blood pressure.
o Beta-adrenergic agents- for
bronchospasm unresponsive to
epi
o Diphenhydramine- 1 -2 mg/kg
given by slow IV push
o Corticosteroids- to prevent a
prolonged or delayed reaction.
NURSING MANAGEMENT
 PREVENTIVE MEASURES:
o Identification of patient at risks
o Complete and accurate hx of
patient’s allergies
o Detailed description of the type
of response for each allergy
should be obtained.
 Administering epi
 Ventilation
o Positioning the patient to assist
with breathing]
o Instructing the patient to breathe
slowly and deeply
 Administering volume
replacement
o Inserting large-bole
peripheral IV catheters and
rapidly administering
prescribed fluids
 Providing comfort and emotional
support
o Administering medications
to relieve itching
o Applying warm soaks to skin
 Maintaining surveillance for
recurrent reactions and
preventing and maintaining
surveillance for complications
 Patient education- to avoid
allergens
 Education on how to recognize
and respond to a future episode
including self-administration of epi
to prevent future life-threatening
event.
Neurogenic Shock
• Another type of distributive shock, is
the result of the loss or suppression of
sympathetic tone.
• The lack of sympathetic tone leads to
decreased tissue perfusion and
initiation of the general shock response.
• Most uncommon form of shock.
 Assessment and Diagnosis

• characteristically presents with

hypotension, bradycardia, and warm,
dry skin.

• decreased BP from massive

peripheral vasodilation.

• decreased HR due to inhibition of the

baroreceptor response and unopposed
parasympathetic control of the heart.

• Hypothermia from uncontrolled

peripheral heat loss.

• Can be caused by anything that • warm, dry skin occurs as a

disrupts the SNS. consequence of pooling of blood in the
extremities and loss of vasomotor
• occur as the result of interrupted
control in surface vessels of the skin that
impulse transmission or blockage of
control heat loss.
sympathetic outflow from the
vasomotor center in the brain.

• most common cause: spinal cord Medical Management

injury (SCI).
Goals of therapy:
• Neurogenic shock may mistakenly be • treat or remove the cause
referred to as spinal shock. • prevent cardiovascular instability,
and promote optimal tissue perfusion.
• The latter condition refers to loss of
• Cardiovascular instability can result
neurologic activity below the level of
from hypovolemia, bradycardia, and
SCI, but it does not necessarily involve
hypothermia.
ineffective tissue perfusion.
• Hypovolemia treated with careful
fluid resuscitation.

• The minimal amount of fluid is

administered to ensure adequate
tissue perfusion.
 • Volume replacement is initiated for
systolic blood pressure less than 90
mm Hg or evidence of inadequate
tissue perfusion.
• The patient is carefully observed
for evidence of fluid overload.
• Vasopressors: used as necessary to
maintain BP and organ perfusion.
• All patients at risk for DVT should be
started on prophylaxis therapy.
• monitoring of passive range-of-
motion exercises,
• application of sequential pneumatic
stockings, and
• administration of prescribed
anticoagulation therapy.

• Bradycardia: rarely requires specific

treatment, but atropine, intravenous
infusion of a beta-adrenergic agent, or
electrical pacing can be used when
necessary.
• Hypothermia: treated with warming
measures and environmental
temperature regulation.
Nursing Management
• Prevention of neurogenic shock is one
of the primary responsibilities of the
nurse in the critical care unit.
• identification of patients at risk
• constant assessment of the
neurologic status.
• Vigilant immobilization of SCIs and
slight elevation of the head of the
patient’s bed after spinal anesthesia
are essential components of preventive
nursing care.
Sepsis and Septic Shock
• Sepsis: a life-threatening clinical
syndrome caused by an infection and
dysregulated physiologic systemic
response.
• The host response results in perfusion
abnormalities with organ dysfunction
(sepsis) and eventually circulatory,
cellular, and metabolic abnormalities
(septic shock).
• Septic shock differs from sepsis in that
the complications are more severe,
and the risk of patient mortality is
greater.
• Primary mechanisms: maldistribution
of blood flow to the tissues,
hypovolemia, and myocardial
dysfunction.

• Early identification allows for early

treatment and decreased mortality.

• Nursing interventions:
• treating hypovolemia and
maintaining tissue perfusion,
• maintaining normothermia
• monitoring for and treating
dysrhythmias,
• providing comfort and emotional
support, and
• preventing and maintaining
surveillance for complications.

• Venous pooling in the lower

extremities promotes the formation of
deep vein thrombosis (DVT), which can
result in a pulmonary embolism.
• Sepsis: caused by a wide variety of
microorganisms, including gram-
negative and gram-positive aerobes,
anaerobes, fungi, and viruses.
• Common sources of infection:
respiratory, GU, and GI systems; the skin;
and the soft tissues.
• Sepsis and septic shock are associated
with intrinsic and extrinsic precipitating
factors.
• All factors interfere directly or indirectly
with the body’s anatomic and
physiologic defense mechanisms.
• Several of the intrinsic factors are not
modifiable or are very difficult to
control.
• Several of the extrinsic factors may be
required for diagnosis and
management.
• Therefore all critically ill patients are at
risk for septic shock.
Assessment and Diagnosis
• Effective treatment of sepsis and septic
shock depends on timely recognition.
• Sepsis-3 advocates the use of the
Sequential (Sepsis-related) Organ
Failure Assessment (SOFA) score to
facilitate early identification of patients.
• The SOFA score is a mortality prediction
tool that is based on the degree of
dysfunction of six different organ
systems (respiratory, cardiovascular,
hepatic, coagulation, renal, and
neurologic).
• score: calculated on admission and q24
hrs until discharge.
• 2 most common organs to demonstrate
dysfunction in sepsis:
CARDIOVASCULAR SYSTEM and LUNGS.
• Cardiovascular dysfunction: persistent
hypotension requiring vasopressor
therapy despite adequate volume
resuscitation
• Pulmonary dysfunction: PaO2/fraction of
inspired oxygen (FIO2) ratio of less than
300, indicating ARDS.
• Signs indicating septic shock are
hypotension despite adequate fluid
resuscitation and the presence of
perfusion abnormalities such as lactic
acidosis, oliguria, or acute change in
mentation.
Medical Management
• Treatment of a patient in sepsis or septic
shock requires a multifaceted
approach.
• The goals of treatment:
• control the infection,
• reverse the pathophysiologic
responses, and
• promote metabolic support.
• Approach:
• identifying and treating the infection,
• supporting the cardiovascular system
and enhancing tissue perfusion,
• limiting the systemic inflammatory
response,
• restoring metabolic balance
• initiating nutrition therapy.
• Guidelines for the management of
sepsis and septic shock have been
developed and updated under the
auspices of the Surviving Sepsis
Campaign (SSC), an international effort
of more than 11 organizations to
improve patient outcomes.
• Early recognition and treatment of • preventing and maintaining
sepsis and septic shock is critical for surveillance for complications
optimal patient outcomes.

• The Hour-1 Bundle lists interventions that Systematic Inflammatory Responses

should be implemented within the first Syndrome (SIRS)
hour after recognition.
•exaggerated defense response of the
body to a noxious stressor (infection,
trauma, surgery, acute inflammation,
ischemia or reperfusion, or malignancy,
to name a few) to localize and then
eliminate the endogenous or
exogenous source of the insult.

• It involves the release of acute-phase

reactants, which are direct mediators
• Immediate resuscitation (crystalloids)
of widespread autonomic, endocrine,
• Intubation and mechanical ventilatory
hematological, and immunological
support
alteration in the subject.
• Antibiotic therapy
• IV insulin: < 180 mg/dL • The purpose is defensive, the
• Platelets and RBC transfusions :< dysregulated cytokine storm can cause
10,000/mm3, Hgb < 7 g/dL. a massive inflammatory cascade
• Nutrition therapy: enteral leading to reversible or irreversible end-
organ dysfunction and even death.
Nursing Management
• SIRS with a suspected source of
• Patient care management of the
infection is termed sepsis.
patient with sepsis focuses on infection
prevention and transmission, early • Sepsis with one or more end-organ
recognition and treatment, and failures is called severe sepsis, and
supportive nursing care. hemodynamic instability despite
intravascular volume repletion is called
• Prevention of sepsis and septic shock is
septic shock.
one of the primary responsibilities of the
nurse in the critical care unit. • Together they represent a physiologic
• identification of patients at risk and continuum with progressively worsening
• reduction of their risk factors, balance between pro and anti-
including exposure to invading inflammatory responses of the body.
microorganisms
• handwashing, aseptic technique,
and an understanding of evidence-
based practice to reduce
nosocomial infection
• Early identification allows for early
treatment and decreases mortality.

Nursing interventions:
• early identification of sepsis
syndrome;
• any 2 of the criterias:
• administering prescribed fluids,
• Body temp: > 38° or < 36° Celsius
medications, and nutrition;
• HR: > 90 bpm
• providing comfort and emotional
• RR: > 20 bpm
support; and
• Leukocyte count: > 12000 or < 4000
/ml
• Almost all septic patients have SIRS,
but not all SIRS patients are septic.

• Subgroups of hospitalized patients,

particularly at extremes of age, who do
not meet the criteria for SIRS on
presentation but progress to severe
infection and multiple organ
dysfunction and death.

• Establishing laboratory indices to

identify such subgroups of patients and
the clinical criteria that we currently rely
upon has been gaining prominence Assessment and Diagnosis
over recent years.
• A thorough history of location,
• Sequential Organ Failure Assessment character, radiation, and exacerbating
• Q SOFA – relieving factors of pain, duration, and
time correlation of symptom are
• SBP: < 100 mm Hg
important.
• Highest RR: > 21 cpm
• The etiology and primary source are not
• Lowest GCS: < 15 as obvious.

• History should focus on any alteration

from usual activities, including new
medications, food intake, exposure,
travel, or recreational agents of abuse.

• Identification of specific risk factors:

preexisting immunosuppression, diabetes
mellitus, solid tumors and leukemia,
dysproteinemias, cirrhosis of the liver, and
extremes of age.

• A complete physical examination

• The definition of systemic inflammatory

response syndrome has its basis in vital
signs other than evaluating leukocyte
count.

Management

• Ensuring hemodynamic stability is of

utmost importance.

• initial administration of isotonic

crystalloids at a rate of 30 ml/kg bolus

• measurement of pulse pressure

variability or stroke volume variability with
passive leg raising
 • for a patient on mechanical ventilator
support, pulse pressure variability, stroke
volume variability, or IVC diameter
variability with respiration is an option.
• Vasopressors and inotropes
• Primary source control:
• surgical intervention – incision and
drainage of wound infection, tube
drainage of a contained abscess and
collection, or more exploratory surgery.
• Broad-spectrum antibiotics should still be
guided by:
• Suspicion of community vs. hospital-
acquired infection
• Prior microbiology patterns in the
individual
• Antibiogram for the facility
• Antiviral therapy: respiratory
exacerbation and systemic inflammatory
response syndrome in the influenza
season.
• Neutropenic patients and those on total
parenteral nutrition with central venous
access may need empiric antifungals if
they continue to show SIRS response after
empiric antibiotics.
Multiple Organ Dysfunction Syndrome
• Results from progressive physiologic
failure of two or more separate organ
systems in an acutely ill patient such that
homeostasis cannot be maintained
without intervention.
• Major cause of death in patients in
critical care units
• linked to the number of organ systems
involved.
• dysfunction or failure of two or more
organ systems is associated with an
estimated mortality rate of 54%, which
increases to 100% when five organ
systems fail
• Survivors
• may develop generalized
polyneuropathy and a chronic form of
pulmonary disease from ARDS,
complicating recovery.
• often require prolonged, expensive
rehabilitation
• Trauma patients are particularly
vulnerable to developing MODS,
because they often experience
ischemia-reperfusion events resulting
from hemorrhage, blunt trauma, or SNS-
induced vasoconstriction.
• Pt <65 y/o : increased risk due to
decreased organ reserve and
comorbidities.
• Other high-risk patients:
• patients who have experienced
infection,
• a shock episode,
• various ischemia reperfusion events,
• acute pancreatitis,
• sepsis,
• burns,
• aspiration,
• multiple blood transfusions, or
• surgical complications.
Primary MODS
-results from a well-defined insult in which
organ dysfunction occurs early and is
directly attributed to the insult itself.
• Direct insults initially cause localized
inflammatory responses.
• Primary MODS accounts for only a small
percentage of MODS cases.
• The inflammatory response in primary
MODS has a less apparent presentation
and may resolve without long-term
implications.
Examples of primary MODS:
• immediate consequences of
posttraumatic pulmonary failure,
• thermal injuries,
• AKI
• invasive infections.
• Primary MODS may “prime” physiologic
systems for a more sustained
exaggerated inflammatory response that
leads to secondary MODS.
Secondary MODS
- a consequence of widespread sustained
systemic inflammation that results in
dysfunction of organs not involved in the
initial insult.
• Secondary MODS develops latently after
an initial insult.
• The early impairment of organs normally
involved in immunoregulatory function,
such as the liver and the GI tract,
intensifies the host response to the insult.
• The initial insult may prime the
inflammatory system in such a way that
even a mild second insult (hit) may
perpetuate a sustained
hyperinflammatory response.
• This “two-hit hypothesis” is a contributor
to the morbidity and mortality in patients
with secondary MODS.
Assessment and Diagnosis
• Secondary MODS: a systemic disease
with organ-specific
manifestations.
• Organ dysfunction:
• organ host defense function,
• response time to the injury,
• metabolic requirements,
• organ vasculature response to
vasoactive medications,
• organ sensitivity to damage, and
• physiologic reserve.
A. Gastrointestinal Dysfunction
• The GI tract plays an important role in
MODS.
• GI organs normally have
immunoregulatory functions, and the
GI tract contains approximately 70% to
80% of the immunologic tissue of the
entire body.
• A normally functioning GI tract
prevents bacteria from entering the
systemic circulation.
• Normal gut flora and gut environment
are altered in patients with severe
inflammation.
• Healthy probiotics are decreased in
an inflammatory state, and
pathogenic organisms proliferate.
B. Hepatobiliary Dysfunction
• The liver plays a vital role in host
homeostasis related to the acute
inflammatory response.
• The liver responds to sustained
inflammation by selectively altering
carbohydrate, fat, and protein
metabolism.
• Consequently, hepatic dysfunction
threatens the patient’s survival.
• The liver normally controls the
inflammatory response by several
mechanisms.
• Kupffer cells, which are hepatic
macrophages, detoxify substances
that may normally induce systemic
inflammation and vasoactive
substances that cause hemodynamic
instability.
• Failure to detoxify gram-negative
bacteria causes endotoxemia,
perpetuates inflammation, and may
lead to MODS.
• The liver also produces proteins and
antiproteases to control the
inflammatory response; however,
hepatic dysfunction limits this response.
C. Pulmonary Dysfunction
• The lungs are common and early
target organs for mediator-induced
injury and are usually the first organs
affected.
• ARDS is the pulmonary manifestation
of MODS.
• Patients who develop MODS usually
have pulmonary symptoms; however,
not all patients with ARDS develop
secondary MODS.
• Patients with ARDS who develop sepsis
concurrently with acute lung failure
are at the greatest risk for MODS.
D. Kidney Dysfunction
• AKI: common manifestation of MODS.
• The kidney is highly vulnerable to
hypoperfusion and reperfusion injury.
• Consequently, kidney ischemia-
reperfusion injury may be a major
cause of kidney dysfunction in MODS.
• A patient with AKI may demonstrate
oliguria or anuria resulting from
decreased renal perfusion and relative
hypovolemia.
• Early oliguria is likely caused by
decreases in renal perfusion related to
shock-like states; late oliguria is
typically a sign of evolving kidney injury
and ischemia.
E. Cardiovascular and Hematologic
System Dysfunction
• Initial cardiovascular response in
sepsis:
• myocardial depression;
• decreased RAP and SVR;
• and increased venous
capacitance, CO, and heart rate.
• Despite an increased CO, myocardial
depression occurs and is
accompanied by decreased SVR,
increased heart rate, and ventricular
dilation.
• These compensatory mechanisms help
maintain CO during the early phase of
sepsis.
• An inability to increase CO in response
to a low SVR may indicate myocardial
failure or inadequate fluid
resuscitation, and it is associated with
increased mortality.
Medical Management
• A patient with MODS requires
multidisciplinary collaboration in
clinical management.
Focus:
• fluid resuscitation and hemodynamic
support,
• prevention and treatment of
infection,
• maintenance of tissue oxygenation,
• nutrition and metabolic support,
• comfort and emotional support, and
• preservation of individual organs.
Identification and Treatment of
Infection
• Identification and treatment of the
underlying source on inflammation or
infection are important ways to reduce
mortality.
• Medical and surgical intervention to
remove sources of infection on
contamination may limit the
inflammatory response and improve
chances of recovery.
• Surgical procedures such as early
fracture stabilization, removal of
infected organs or tissue, and burn
excision are helpful.
• Appropriate antibiotics are needed if
the cause cannot be removed by
surgical debridement or incision and
draining.
Maintenance of Tissue Oxygenation
• Normally under steady-state
conditions, oxygen consumption (VO2)
is relatively constant and independent
of oxygen delivery (DO2) unless delivery
becomes severely impaired.
• The relationship is called supply-
independent oxygen consumption.
• Consequently, a percentage of
oxygen is not used (physiologic
reserve).
• Patients with MODS often develop
supply-dependent oxygen
consumption, in which VO2 becomes
dependent on DO2, rather than
demand, at a normal or high DO2.
• When VO2 does not equal demand,
a tissue oxygen debt develops,
subjecting organs to failure.
Nutrition and Metabolic Support
• Hypermetabolism in MODS results in
profound weight loss, cachexia, and
loss of organ function.
• Goal: preservation of organ structure
and function.
• Although nutrition support may not
definitely alter the course of organ
dysfunction, it prevents generalized
nutrition deficiencies and preserves gut
integrity.
• Enteral nutrition may exert a
physiologic effect that downregulates
the systemic immune response and
reduces oxidative stress.
• The enteral route is preferable to
parenteral support.
• Enteral feedings are given distal to
the pylorus to reduce the risk of
pulmonary aspiration.
• Enteral feedings may limit bacterial
translocation.
• In addition to early nutrition support,
the pharmacologic properties of
enteral feeding formulas may limit
inflammation for selected critical care
populations.
• providing a calm and quiet
environment, and
• educating the patient and family
about the condition.
• Measures to enhance tissue oxygen
supply
• administering supplemental
oxygen,
• monitoring the patient’s respiratory
status, and
• administering prescribed fluids and
medications.

Nursing Management

• Preventive measures include a

multitude of assessment strategies to
detect early organ manifestations of
this syndrome.
• Patients who continue to experience
sites of inflammation, septic foci, and
inadequate tissue perfusion may be at
higher risk.
• Handwashing, aseptic technique,
and an understanding of how
microorganisms can invade the body
are essential components of preventive
nursing care.

Nursing interventions:
• preventing development of
infection,
• facilitating oxygen delivery and
limiting tissue oxygen demand,
• facilitating nutrition support,
• providing comfort and emotional
support, and
• preventing and maintaining
surveillance for complications.
• Measures to limit tissue oxygen
consumption
• administering analgesics and
sedatives,
• positioning the patient for comfort,
• limiting activities,
• offering support to reduce anxiety,