MULTIPLE ORGAN DYSFUNCTION SYNDROME (MODS) o Inadequate protein (children: Kwashiorkor

and Marasmus)
 #1 Organ affected is the LUNGS  Preexisting Chronic Disease
 Results from progressive physiological failure of two or o Hypertension
more separate organ system. o Diabetes
 Presence of altered organ function in an acutely ill o Arthritis
patient. o Anemia – Pernicious Anemia
o Pneumonia
SYSTEMIC INFLAMMATORY RESPONSE SYNDROME (SIRS/SEPSIS) o PTB
 Is a widespread inflammation that occurs in patients  Inadequate delayed resuscitation
suffering a variety of insults.  Burns (3rd Decree or more)
WIDESPREAD INFECTION  plenty of histamine o 3rd degree  fluid transferred from
intravascular to interstitial space  decrease
 It is called SEPSIS when the cause of SIRS is infection.
CO  affects brain
 SEVERE SEPSIS – is sepsis with HYPOPERFUSION.
 Sepsis
 SEPTIC SHOCK – is sepsis induced hypotension despite
 Tissue Hypoxemia
fluid resuscitation.
o Anemia  less oxygen in the blood
 Acute Pancreatitis
PRIMARY MODS
o It destroys the beta cells  Beta cells cannot
 Direct consequence of the insult
produce insulin  lots of glucose in the
o Thermal injuries
circulation  wound healing is compromised
o ATN (Pre Renal Failure) Shifting of fluid from
 Ruptured Aneurysm
the intravascular to the interstitial space
o If the aneurysm ruptures  blood will ooze
decrease circulating blood volume 
 there is no space in the brain  Increase
decrease blood going to the kidney because
ICP
it is a secondary organ  cause injury to the
kidney
SEQUENCE OF EVENTS / PATHOPHYSIOLOGY
o Post traumatic pulmonary failure
Initial Organ injury  Activativation of resident macrophages (2)
/ neutrophils (1)  local systemic inflammation/stress response
SECONDARY MODS
 if further insult occurs  primary MODS
 It is the result of an excess inflammatory response in
1. Primed macrophages (mature WBC) release multiple
organs distant from the original injury.
mediators (SECONDARY MODS)
 Is an organ dysfunction that develops days after the
 TNF (Tumor necrosis factor alpha) and IL-1
admission.
(Interleukin 1)
 Endothelial damage throughout body (inner
RISK FACTOS
lining)
 Age 65 years old and above
o Immune system is decreased (they don’t
have thymus anymore)
o No more elastin and collagen
2. The macrophages release TNF and IL-1
 Renal Insufficiency
 Activation of the of the plasma cascades in
o Decreased blood supply going to the kidney
the response to endothelial damage
 Toxins will accumulate  uremia 
Anaphylatoxins C3a and C5a – cause
azotemia can go to the heart (pericarditis)
vasodilator by releasing histamine
 then it can go to the brain
Production of bradykinin (causes
(encephalopathy)
pain) causes vasodilation and
decrease systemic vascular
 Immunosuppressive Therapy
resistance (SVR)
o Decreases immune system
Coagulation Cascade – results in
o Cancer patient undergoing chemotherapy
microvascular thrombosis which
and radiation which destroys the bone
causes decrease microvascular
marrow.
circulation  ischemic damage to
 Coma on admission
organs  DIC with pooling clotting
o #1 Complication: Respiratory
factors in the micro vascular bed.
 Malnutrition
 oInjured tissue will produce  Bradypnea or tachypnea
plasminogen  converted  Crackles wheezes
into plasmin  and it will
dissolve the clotted blood 1. GIT DYSFUNCTION
 more BLEEDING  80% of the immunoglobulins (antibodies) synthesized
3. TNF is the cause of the exaggerated inflammatory in the body are secreted through the GI tract
response. o GIT is a secondary organ  there will be less
blood going to the GIT  increase
permeability in the intestines and E. Coli can
DIC PATHOPHYSIOLOGY: go out (which can be seen in the large
intestines)  bacterial translocation
Tissue injury  It is going to stimulate the SNS  It will trigger o GIT should have mucous to protect the
the release of norepinephrine  So the artery that is bleeding mucosa stomach  since GIT is a secondary
will immediately constrict/ vasoconstriction/vasospasm it is organ the mucous neck cells cannot produce
going to lessen the blood going out of the artery  Platelets adequate mucous  HCl and pepsin can
now will be attracted to that area  Platelets will go to the perforate the stomach and can cause
injured site then clamp to seal the wound  Proteins are being peritonitis and bacterial translocation.
release now by the liver  Prothrombin will be change to  Fasting states for the procedures or delays in the ____
thrombin  Fibrinogen to fibrin  The fibrin (fibers) are now  Record increase intestinal permeability
develop it was produced, it will now envelop the clotted blood  Hypo perfusion damage normal gastrointestinal
to be stable  After several hours, that clotted blood will not mucosa barrier
be there.  The injured tissue will be producing plasminogen  COLONIZATION
 Plasminogen will be converted to plasmin  Plasmin now o The oropharynx of the critically ill patient
will dissolve the clotted blood becomes colonized with pathogenic
organism from GIT.
HISTAMINE EFFECTS 2. STRESS HYPERGLYCEMIA
1. Vasodilation  Results from the release counter regulatory
2. Increase capillary permeability hormones such as:
o Cortisol – adrenal cortex
MASSIVE SYSTEMIC INFLAMMATORY RESPONSE o Glucagon – liver  glucogenolysis
 Release of the cytokines and other inflammatory  You are ill  there is an increase
mediators. metabolism of the cells  cells
 Release of highly active neutrophils that undergo needs glucose for food  since
oxidation  release oxygen free radicals you are sick, you cannot eat 
there will be two hormones that
PULMONARY will be secreted cortical (APG –
 ALI usually occurs 24-72 hours after initial insult Adrenal Cortex) and glucagon
 Intense mediator activity damages the pulmonary (alpha cells of the pancreas)  it
vascular endothelium and the alveolar epithelium will perform glucogenolysis
 SURFACTANT DEFICIENCY (glucagon from the liver to
o SURFACTANT is in the alveoli  there is glucose) then gluconeogenesis
water molecules in the alveoli  the (proteins and fats converted into
tendency of the water molecule will be glucose)
attracted to each other  possible there o Adrenaline – epinephrine
will be pooling and alveoli can collapse  Adrenaline/Epinephrine is being
 surfactant lowers the surface tension produced by SNS  tachycardia 
(surfactant is being produced during 8th it will not allow the periphery to
month of pregnancy) use the glucose, it is reserving it for
 Pulmonary hypertension and increase pulmonary the most important part which is
capillary permeability  increase lung water. the brain.
 Can have respiratory acidosis  Which raise blood glucose by promoting the
breakdown of glucagon in the liver.
MANIFESTATION:
 Dyspnea with increase work of breathing
 Under STRESS, the liver produce and releases glucose in o Acidosis – decrease myocardial
response to: responsiveness to catecholamines.
o Glucocorticoid (cortisol)
o Epinephrine
o Growth hormone MANIFESTATION
o Cytokines  Tachycardia
The potent stress hormone CORTISOL impairs insulin o
receptors, making the patient more INSULIN RESISTANT  MAP < 70 mmHg
 glucose stays in the blood  since that the glucose o SBP + DBP (2) / 3
cannot go inside the cell  it will perform glucogenolysis  CVP < 8 mmHg
(glucagon to glucose)  then performs gluconeogenesis  Peripheral Edema
(fats and proteins converted into glucose)  it is being o Acidosis will decrease the response
catabolized and blood glucose surges.  to catecholamine (norepi) 
HYPERGLYCEMIA norepi causes vasoconstriction  it
If blood glucose to increase to over 200 mg/dL for 2 hours, will dilate  edema  and protein
the post-surgical risk for infection can increase tenfold. is being used by the cells and
The flood of inflammatory cytokines promotes neutrophil converts it in the glucose.
(first WBC to respond during acute infection) dysfunction.  Skin pale and warm initially (SNS is still
Adverse Outcome: associated with hyperglycemia. active); later pale, cool and clammy.
o Increase rates of healthcare associated
infections and sepsis. VASOACTIVE DRUGS
o Poor wound healing
o Increase risk of mortality/death
Low Dose Dopamine
 Increase SVR and improves renal and mesenteric
CARDIOVASCULAR
CAUSED BY: blood flow (blood supply to the GI).
 Ventricular dilation o DOBUTAMINE – Dobulex, Dobutrex
 Decreased diastolic compliance  Inotropic effects to the heart =
 Decreased systolic contractile function increase contractility of the
heart to increase blood supply.
CARDIAC FAILURE  Increase myocardial
- Inability of the heart to pump an adequate amount contractility, improving cardiac
of blood to different organ of the body. performance
N: 5L – 8L  Increase CO while decreasing
peripheral vascular resistance.
HTN  the lungs is being destroyed first  the blood
 AE:
from the lung will have less oxygen  hypoxemia 
heart will increase rate (PR) to give more oxygen   Tachycardia
AVV will immediately close  blood going to the  Headache, Tremors
ventricles are less  CO is less  stimulates SNS   Nausea and Vomiting
norepinephrine (vasoconstriction and increase BS)   Hypotension
increase workload of the heart.  Avoid in patient with ABP < 100 mmHg and signs
of shock.
CAUSED BY:
 Immune mediator
RENAL DYSFUNCTION
 TNF-IL-1 – has a myocardial depressant effect
and is associated with myocardial depression
 Oliguria or anuria resulting from decrease renal
during septic shock. perfusion and relative hypovolemia.
 Acidosis  Frequent use of nephrotoxic drug during critical
o Decrease blood  decrease O2 in illness.
the blood.  Prerenal Oliguria may progress to ATN
o Kidney  cannot produce
bicarbonates to maintain the acid GOALS OF THERAPY
base balance  Control infection
  Provide adequate tissue oxygenation
 Restore intravascular volume
 Support function of individual organs

MODS
 Control pf infection must be given a high priority

 Antibiotic and Culture

BUN - 7 to 20 mg/dL
CREATININE - 0.6 to 1.2 mg

ANTIBIOTICS

Levofloxacin – Floxel / Levocin

NURSING INTERVENTION:
 Maintain skin integrity
 Impeccable oral hygiene.
 Screening visitors with active infection
 Early enteral feeding to prevent bacterial
translocation.
 Assess skin every hours and reposition.
 Turn every hours.
 H2 blockers and antacids is essential for
complete GI stabilization.
o Ranitidine
o Esomeprazole
o Nizatidine
o Omeprazole
 Hand hygiene
 Aseptic technique during procedure
 Change central lines every 2 hours.
 Patients who are intubated should be
weaned and extubated.
 PEEP
 Aggressive pulmonary toilet for maximum air
exchange.
 Temperature and pain control
 Rest and sedation