MULTIPLE ORGAN
irreversible organ failure. The
DYSFUNCTION SYNDROME
HISTORY
○ World War II - seen in soldiers
with severe non-thoracic
injuries developed respiratory
failure and subsequent renal
failure. May be related to the
severity and duration of pre-
hospital hypotension and the
‘shock lung’ (subsequent
respiratory failure)
○ 1970’s - patterns of ‘distant’
organ failure was reported in
critically ill patients following
trauma, surgical hemorrhage,
abdominal sepsis, pneumonia
and pancreatitis
○ 1975 - it was described by Baue
in his editorial that it is
“multiple, progressive or
sequential systems failure” that
became the basis of a new
clinical syndrome
DESCRIPTION
o Multiple organ dysfunction
syndrome (MODS) is defined as
the progressive physiological
dysfunction of two or more
organ systems where
homeostasis cannot be
maintained without
intervention (Osterbur et al.
2014; Nickson 2019).
○ Multiple organ dysfunction
syndrome (MODS) is a RISK FACTORS
continuum, with incremental
degrees of physiologic
derangements in individual
organs; it is a process rather
than a single event. Alteration
in organ function can vary
widely from a mild degree of
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organ dysfunction to completely
degree of organ dysfunction has
a major clinical impact.
○ Eventually, the term MODS was
proposed as a more appropriate
description. MODS is defined as
a clinical syndrome
characterized by the
development of progressive and
potentially reversible
physiologic dysfunction in 2 or
more organs or organ systems
that is induced by a variety of
acute insults, including sepsis
CAUSES
Multiple organ dysfunction
syndrome is induced by illness,
injury or infection that triggers
an unregulated systemic
inflammatory response (known
as systemic inflammatory
response syndrome), resulting in
tissue injury
o SEPSIS
○ Major trauma
○ Burns
○ Pancreatitis
○ Acute heart failure
○ Exposure or ingestion of
Poisons/toxins
○ Reperfusion injury
○ Ischemia
○ Multisystem injury
○ Autoimmune disease
○ Genetics
○ Patient with comorbidities - are
more likely to have further
deterioration of organ
functions
○ Medications, Therapies, and
ICU support
 ■ ventilator-induced lung
injury contributing to
pulmonary cytokine
release and ARDS
○ Elderly patients (>65 years old)
- because of decreased organ
reserve and presence of
comorbidities
○ Shock episodes - associated
with a rupture aneurysm,
acute pancreatitis, sepsis,
burns, or surgical
complications
○ Patient with severe trauma,
multiple injury, massive blood
loss, Infection is at risk of
developing MODS
○ Malnutrition
○ Prolonged inflammatory
response associated with
SEPSIS
CLASSIFICATIONS
○ Immediate Type (Primary) -
the direct result of a well-
defined insult in which organ
dysfunction occurs early and
can be directly attributable to
the insult itself
○ Delayed Type (Secondary) -
organ dysfunction caused by
the systemic inflammatory
response syndrome or sepsis
SIGNS AND SYMPTOMS
Organ Dysfunction may present
as:
○ Acute Kidney Injury (AKI) and
uremic acidosis
○ Acute Respiratory Distress
Syndrome (ARDS)
○ Cardiomyopathy
○ Encephalopathy
○ Gastrointestinal dysfunction
○ Hepatic dysfunction
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○ Coagulopathy and bone
marrow suppression
● The patient may display some of
the following symptoms
depending on which organs are
affected:
○ Altered mental state
○ Decrease in urine output
○ Respiratory deterioration
○ Decrease in cardiac function
○ Decrease in cardiac output
○ Deranged metabolic status
○ Compromised fluid balance
○ Pale, clammy, peripherally cool
skin, and faint pedal pulses
Systemic inflammatory response:
○ Increased body temperature
○ Increased resting heart rate
○ Increased respiratory rate
○ Increased amount of WBC
PROGNOSIS
○ MODS involves 2 organ
systems fail, (3+ organ systems
fail = 80-90% mortality)
○ Usually, the lungs fail first
because of the cytokine
released at the massive
inflammation leading to ARDS
follows by kidneys, liver, GI
system fail and if it spreads so
far that it affects the
cardiovascular system and
neurologic system are affected,
it leads to 100% mortality
■ Circulatory failure is
the most important
predictor of poor
outcome
■ About 50% of people
with MODS will not
return to work or
normal function at 1
year follow-up
 ■ Hemodynamic
DIAGNOSTICS monitoring
How to assess for multiple organ ■ Fluid infusion - to
dysfunction syndrome expand and maintain
- Undertake a system approach the intravascular
assessment (head-to-toe compartment
assessment).
○ Look for signs and symptoms
- Document and analyze data from
the patient’s vital signs, taking of acute renal failure
into account any trends. ■ Hourly monitoring of
- A Sequential Organ Failure urine output
Assessment (SOFA) score can be ○ Medications
used in line with other ■ Antibiotics (Infection) -
assessment tools. third-generation
• (SOFA) score is a simple and cephalosporin or 2
objective score that allows for broad spectrum
calculation of both the number antibiotics
and the severity of organ (azithromycin,
dysfunction in six organ systems amoxicillin,
(respiratory, coagulatory, liver, tetracycline, and
cardiovascular, renal, and quinolones)
neurologic) ■ Vasopressors (Low
• Mortality 15-20%: SOFA Score 7 blood pressure) -
to 9. Mortality 40-50%: SOFA dopamine and
Score 10 to 12. Mortality 50- norepinephrine
60%: SOFA Score 13 to 14. ○ Isotonic crystalline for
Mortality >80%: SOFA Score 15. expansion of intravascular
Mortality >90%: SOFA Score 15 fluid spaces (Normal Saline
to 24. and Lactated Ringer’s Solution)
○ Colloids for plasma volume
MANAGEMENT expansion without risking for
○ Early prevention is the best fluid overload (Albumin)
management. Detecting and
documenting the initial signs HEALTH TEACHING
of infection are essential in ○ Educate the patient/family
managing MODS especially in about:
elders. Warning signs: subtle ■ the disease, diagnosis,
change in mentation and and treatment
gradual rise in temperature ■ the medications
required and adverse
TREATMENT drug reaction
○ Respiratory and circulatory ■ Purpose and intent of
function support. therapies
■ Mechanical ventilation
■ Supplemental oxygen

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 CONCEPT MAP tachycardia and
anxiety, can be fatal.
MECHANISM OF MODS: ■ Resuscitation: The
○ Multiple organ dysfunction restoration of
syndrome can affect any or all consciousness to a
of six organ systems: person who appears
respiratory, cardiovascular, dead.
renal, hepatic, neurologic and ■ Reperfusion of ischemic
hematologic. gut leads to cascade of
○ In general, the cause of the post events: gut
injury MODS involves a mixed translocation of
layering of patient, injury, and microorganisms
treatment factors. The precipitating and/ or
dysregulated immunological perpetuating this
response is the crucial factor in inflammatory response-
the pathophysiology of post compensatory anti-
injury MODS inflammatory response
○ Following the initial injury, the (CARS) results in
following changes are proposed immunosuppression
to occur: and anergy
■ Shock: Medical ■ Coagulation cascade:
emergency in which the triggered by tissue
organs and tissues of factor, endotoxins,
the body are not cytokines, and bacterial
receiving an adequate antigens
flow of blood. This ■ Cytokines: pro-and
deprives the organs and anti-inflammatory
tissues of oxygen cytokines are released
(carried in the blood) excessively during the
and allows buildup of initial phase of trauma.
waste products. Shock The role of anti-
can result in serious inflammatory cytokines
damage or even death. is to down regulate the
■ Whole body production of
hyperfusion: a proinflammatory
condition of acute cytokines. Normally,
peripheral circulatory the balance of pro and
failure due to anti-inflammatory
derangement of cytokines is in
circulatory control or equilibrium. However,
loss of circulating fluid. when this natural
It is marked by balance is unbalanced
hypotension and with the release of
coldness of the skin, predominantly
and often by proinflammatory

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 cytokines, this leads to ● Ventilator-
Systemic inflammatory induced lung
response syndrome, injury
while predominance of contributing to
anti-inflammatory pulmonary
cytokines causes cytokine release
immunosuppression and acute
■ Neuro-endocrine respiratory
factors: neurally distress
mediated immune- syndrome
suppression: stress (ARDS)
responses involving ● Fluid therapy,
adrenal hormones: hypothermia,
Hypothyroid state due extracorporeal
to production of inert membrane
reverse T3 (Reverse T3 oxygenation
is sort of a hibernation (ECMO),
hormone, in times of immobility,
stress and chronic inotropes, blood
illness, it lowers your products, etc.
metabolism)
■ Mitochondrial
dysfunction: may be
mediated by humoral
factors and may
contribute to cellular
dysoxia and organ
dysfunction
○ Other factors include:
■ Genetics: differences in
gene expression and
the proteome may
account for individual
differences in the
likelihood and severity
of MODS following a
given stimulus.
■ Comorbidities: patients
with premorbid organ
dysfunction are more
likely to have further
deterioration of organ
dysfunction.
■ Medications, therapies,
and ICU supports:

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