The presence of altered organ function in a client who is acutely ill such that hemeostasis cannot be maintained without intervention. MODS is present when two or more organs fail .MODS results from SIRS

1. BY- PINKY RATHEE
M.Sc. Nursing
Multiple Organ
Dysfunction Syndrome
(MODS).

2. SIRS is an inflammatory
clinical response of the whole
body without a proven source
of infection. SIRS is non-
specific and can be caused by
ischemia, inflammation,
trauma, infection, or a
combination of several insults.
SYSTEMIC INFLAMMATORY
RESPONSE SYNDROME (SIRS)

3. SIRS with a confirmed source of infection,
through blood or tissue cultures, is called sepsis.

4. SIRS is defined as two or more of the following variables:
*Temperature of more than 38 degree Celsius or less
than 36 degree Celsius.
*Heart rate of more than 90 beats per minute.
*Respiratory rate of more than 20
breaths per minute or a PaCO2
level of less than 32 mm of Hg.
*Abnormal white blood cell count (>12,000/ L or
<4000 L)

5. *
MULTIPLE ORGAN DYSFUNCTION
SYNDROME (MODS)

6. MULTIPLE ORGAN DYSFUNCTION
SYNDROME (MODS)
The presence of altered organ
function in a client who is
acutely ill such that
hemeostasis cannot be
maintained without
intervention. MODS is present
when two or more organs fail
.MODS results from SIRS

7. MULTIPLE ORGAN DYSFUNCTION SYNDROME (MODS)

8. *
MULTIPLE ORGAN DYSFUNCTION
SYNDROME (MODS)

9. PRIMARY MODS
SECONDARY MODS
CLASSIFICATION OF MODS
There are two types of MODS.

10. PRIMARY MODS
*The direct insult initially
causes a localized
inflammatory response that
may or may not progress to
SIRS. e.g. primary
pulmonary injury, such as
aspiration. Only a small
percentage of clients
develop primary MODS.

11. SECONDARY MODS
It is the consequence of widespread systemic
inflammation, which develops after a variety of
insults, and results in dysfunction of organs not
involved in initial insult. The client enters a
hypermetabolic state that lasts for 14-21 days.
During this time the body catabolizes muscle and
fat for energy, which causes profound changes in
the body metabolic processes. Unless the process
can be stopped, the outcome for client is death.
Secondary MODS occurs with conditions such as
ARDS and septic shock.

12. *
MULTIPLE ORGAN DYSFUNCTION
SYNDROME (MODS)

13. Elderly
patients
Shock episode associated
with a rupture aneurysm,
acute pancreatitis, sepsis,
burns or surgical
complications.

14. Chronic illness
and Malnutrition
Severe trauma, multiple
injury, massive blood
loss, hypovolemic shock
and infection.

15. Prolonged
inflammatory
responses are at risk,
like clients with sepsis.
Surgery, massive
blood
transfusion.

16. *
MULTIPLE ORGAN DYSFUNCTION
SYNDROME (MODS)

17. Infection, injury
(accident,
surgery), hypoperfusion
and hypermetabolism.
SIRS and sepsis could
ultimately progress to
multiple organ
dysfunction syndrome.

18. MULTIPLE ORGAN DYSFUNCTION
SYNDROME (MODS)

19. Local injury from trauma, infection, or lack of
perfusion.
Disturbed Inflammatory Immune Response.
Bacteria enter into the wound and releases toxins.
Activation of systemic mediators of inflammation.
Chemical mediators or endotoxins target
endothelium & damage of endothelial.

20. When this inflammatory response is
unchecked it produces damage to organs
(respiratory system, cardiovascular
system, nervous system, renal system) and
tissues by altering perfusion, disturbing
oxygen supply or demand or metabolic
dysfunction and coagulopathy
SIRS + infection
Sepsis→ Severe Sepsis
Multiple Organ Dysfunction Syndrome
(MODS).

22. *
Inflammatory mediators have a direct effect on the pulmonary vasculature.
Endothelial damage from the release of inflammatory mediators.
Increase in capillary permeability
Movement of proteinaceous fluid from the pulmonary vasculature into the
pulmonary interstitial spaces.
The alveoli collapse, creating an increase in shunt
Worsening of the ventilation-perfusion mismatch.
ARDS.

23. *
Increasing tissue demands.
Myocardial depression and massive vasodilation.
Decreased Systemic Vascular Resistance and blood
pressure.
To compensate for hypotension, cardiac output increases
by increase in heart rate and stroke volume.
Increases in capillary permeability causes a shift of
albumin and fluid out of vascular space.
Diminishing venous return and thus preload.

24. NERVOUS SYSTEM-
Acute alteration in mental status can
be an early sign of MODS. The
patient may become confused and
agitated, disoriented, lethargic or
comatose. These changes may be
due to hypoxemia, the direct effect
of inflammatory mediators, or
impaired perfusion.

25. Acute renal failure can be caused by hypoperfusion
and also by effects of mediators. When there is
decreased perfusion to the kidneys, the
sympathetic nervous system and rennin
angiotensin system are activated. The stimulation
of rennin angiotensin system results in systemic
vasoconstriction and aldosterone mediated sodium
and water reabsorption. Another risk of developing
ARF is the use of nephrotoxic drugs. Antibiotics
commonly used to treat gram negative bacteria,
such as aminoglycosides, can also be nephrotoxic.
RENAL SYSTEM

26. MODS trigger a hypermetabolic response. Glycogen stores
are rapidly converted to glucose (glycogenolysis). Once a
glycogen is depleted, amino acids are converted to glucose
(gluconeogenesis), reducing protein stores. Fatty acids are
mobilized for fuel. Catecholamines and glucocortecoids are
released and result in hyperglycemia and insulin resistance.
The net result is a catabolic state and muscle is lost.
METABOLIC DISTURBANCE

27. Failure of coagulation system manifests as
Disseminated Intravascular Coagulopathy
(DIC). DIC results in simultaneous micro-
vascular clotting and bleeding because of the
depletion of clotting factors and platelets in
addition to excessive fibrinolysis.
COAGULOPATHY-

28. MULTIPLE ORGAN DYSFUNCTION
SYNDROME (MODS)

29. Respiratory-
Dyspnea
Bilateral fluffy infiltrates on chest X ray
Ventilation perfusion mismatch
Pulmonary hypertension
Increased respiratory rate
Decreased compliance
Decrease in surfactant
Alveolar edema
Hypoxemia

30. Myocardial depression
Hypotension
Vasodilation
Increased cardiac output, SVR, Heart rate
Decrease stroke volume, mean arterial
pressure
CARDIOVASCULAR-

31. Acute change in
neurologic changes
Seizures
Confusion
Hepatic encephalopathy
NEUROLOGIC SYSTEM-

32. Mucosal ischemia
GI bleeding
Mucosal ulceration
Hypoperfusion due to
decrease peristalsis, paralytic
ileus
GASTROINTESTINAL-

33. Increase in bleeding time,
increase PT, increase APTT
Decrease platelet count
Leucocytosis
Anemia
Leukopenia
HEMATOLOGIC-

34. Hyperglycemia
Increased ADH
production and ACTH.
ENDOCRINE SYSTEM-

35. RENAL SYSTEM
Oliguria
Fluid electrolyte
imbalances
Increase creatinine

36. MULTIPLE ORGAN DYSFUNCTION
SYNDROME (MODS)

37. History
 Underlying diseases
 Hypotension
 Oliguria or anuria
 Tachypnea or hyperpnea
 Immunocompromised patient
 Community or nosocomial infection
 Hypothermia without obvious cause

38. Physical Examination
 In all neutropenic patients and pelvic
infection the physical examination
should include rectal, pelvic, and genital
examinations
 Perirectal, and/or perineal abscesses
 Pelvic inflammatory disease and/or
abscesses, or prostatitis

39. Blood studies-
 CBC
 Procalcitonin (PCT)
 CRP
 Blood cultures
 Cardiac enzymes
 Urinalysis and culture
 Basic metabolic profile
 Amylase, lipase
 Spinal fluid and
 Liver profile

40. MULTIPLE ORGAN DYSFUNCTION
SYNDROME (MODS)

41. • Aggressive infection control strategies are essential to
decrease the risk for nosocomial infections.
• Appropriate cultures should be sent, and broad spectrum
antibiotics should be initiated.
• Early, aggressive surgery is recommended to remove
necrotic tissue (eg. Debridement of burn tissue) that may
provide culture medium for microorganisms.
• Once a specific organism is identified, therapy should be
modified if necessary.
• Aggressive pulmonary management, including early
ambulation, can reduce risk of infection.
• Strict asepsis can reduce infections related to intra- arterial
lines, endotracheal tubes, urinary catheters, IV lines and
other invasive lines or procedures.
Prevention and treatment of infection-

42. • Controlling the mediators of inflammation is both
directed at general levels of care and specific
treatments targeted at the problem cells.
• Maintenance of positive nitrogen balance via
nutrition, promotion of sleep and rest, and
management of pain are important general care
areas.
• Specific treatment includes monoclonal antibodies
to control mediators such as endotoxins,
interleukin-1, and tumor necrosis factors.
Controlling the mediators-

43. • Sedation, mechanical ventilation, analgesia,
paralysis, and rest may decrease oxygen demand
and should be considered.
• Oxygen delivery may be optimized by maintaining
normal levels of hemoglobin (eg. Transfusion of
packed RBCs) and PaO2(80-100 mm Hg), using
individualized tidal volumes with PEEP, increasing
preload or myocardial contractility to enhance
cardiac output, or reducing afterload to increase
cardiac output.
Maintenance of tissue perfusion-

44. • The goal of nutritional support is to preserve
organ function.
• Providing early and optimal nutrition
decreases morbidity and mortality rates in
patients with SIRS and MODS.
• The use of enteral route is preferable to
parenteral nutrition, as it may enhance
perfusion and decrease the bacterial load and
the effects of endotoxins.
Nutritional and metabolic needs-

45. • The client is intubated and mechanically ventilated
in order to maintain adequate oxygenation.
• Oxygen is given to the client until blood levels of
lactate decrease towards normal. Elevated serum
lactate levels indicate the use of anaerobic
metabolism.
• Problems such as fever, seizures, and shivering
increase oxygen demands. These problems should
be controlled by medications and environmental
changes (warming).
Protecting the organs affected-

46. • Used to support hemodynamic parameters.
The client often becomes more and more
unstable and needs more continuous
monitoring
• Nutritional support is also critical to reduce
catabolism that accompanies hyper-
metabolism.
• Dialysis is often used to reduce azotemia
from renal failure.
Fluids and ionotropic drugs-

47. PROGNOSIS
If the process of MODS is not reversed by day 21,
it is usually evident that the client will die. Death
usually occurs between days 21 and 28 after the
injury or precipitating event. Not all clients with
MODS die, however MODS remains the leading
cause of death in the intensive care unit, with
mortality rates from 50- 90% despite the
development of better antibiotics, better
resuscitation, and more sophisticated means of
organ support. For those clients who survive, the
average duration of intensive care unit stay is
about 21 days. The rehabilitation, which is
directed at recovery of muscle mass and
neuromuscular function, lasts about 10 months.

48. MULTIPLE ORGAN DYSFUNCTION
SYNDROME (MODS)

49. Ineffective tissue perfusion related to decreased myocardial
oxygen supply than demand.
Impaired gas exchange related to VQ mismatch, intrapulmonary
shunting, alveolar hypoventilation.
Imbalanced nutrition less than body requirement related to less
intake of exogenous nutrients and increased metabolic demand.
Impaired physical mobility related to monitoring devices,
mechanical ventilation & medications as characterized by
imposed restrictions of movement, decreased muscle strength
& limited range of motion.
Risk for impaired skin integrity related to prolonged bed rest,
prolonged intubation & immobility.
Knowledge deficit related to health condition, treatment
modalities & hospitalization as characterized by increased
frequency of questions posed by patient.

50. CONCLUSION
MODS is a syndrome of multiple organs
progressively falling due to prolonged
inflammatory responses. Early diagnosis
and interventions are necessary for best
possible outcomes. A critical component of
the nursing role is vigilant assessment and
ongoing monitoring to detect early signs of
deterioration or organ dysfunction.