Multiple Organ Dysfunction

Syndrome (MODS)
Inayatur Rosyidah., S.Kep.Ns
Definition


Dysfunction or failure of multiple organ or system
happened simultaneously or sequentially due to
various etiological factors.


Etiology
Infection: Gram positive/negative bacteria, fungal, Virus
Shock :hemorrhage, etc.
Allergy
Burns
Trauma
Severe acute pancreatitis
Classification of MODS
Immediate Type (Primary)Dysfunction are
happened simultaneously in two or more organs due to
primary disease.
Delayed type (SecondaryDysfunction happened in
a organ, other organs sequentially happened dysfunction or
failure.
Accumulation typeDysfunction leaded by chronic
disease.

Attention
Immediate Type

Not related to
SIRS
Coup injury with
chemical or
physical factors
No time interval
from disease
ARDS+ARF or
ARDS+ARF+DI
C+LF
Delayed type

Not the direct
outcome from
injury
Relating to SIRS
systemic inflammatory
response syndrome
Time interval
existed from
primary disease
Accumulation type

Accumulation
Irreversible
Mechanism

Inflammatory mediators priming SIRS leading to MODS
Vascular permeability PMN chemotaxis
Mono / Macrophage
PMN
elastase PLA2 oxygen free radicals

TNF IL8
IL1
IL6
Liver
acute phase
Remote organ injury
Tissue injury
Endothelium
Injury
factors
PMN
PAF
Adhensive
molecules
DIC
Common Manifestations of MODS

Organ Symptoms
Heart Acute heart failure
Peripheral circulation Shock
Lung ALI /ARDS
Kidney ARF
Gastro-intestine Stress ulcer/enteroparalysis
Liver Acute hepatic failure
Brain CNS failure
Coagulation DIC
Diagnosis of Criteria
Organ or
systems
Dysfunction Function Failure
Lung Hypoxia,ventilator support at
least 3-5 days
ARDSPEEP>10cmH
2
Oand
FiO
2
0.5
Liver Bile2-3mg/dL
And AST/ALTdouble normal
values
Bilirubin 8-10mg/dL
Jaundice
Kidney Oliguria
Or Cr 2-3mg/dL
hemodialysis
Intestine Intolerance of enteral nutrition at
least 5 days
Blood infusion due to stress ulcer
Severe enteroparalysis
Blood PT or APTT prolonged;PLT<5-
810
9
/L or hypercoagulation
DIC
CNS Insanity; mild disorientation Progressive coma
Cardia-
vascular
EF decreased or CLS No response to inotropic agent
Deitch EA . Ann Surg 1992; 216(2): 117-134


Organ/ system dysfunction and failure
GLASGOW SCORE
Treatments of MODS
Combined therapy

Correction of ischemia: fluid resuscitation, mechanical
ventilation
Prevention of infectiondrainage, antibiotics
Interruption of pathological reactionhemofiltration
Stabilization of internal enviromentwater, electrolyte,
acid-base imbalance
Regulation of immunitycellular and humor


Support of organ function

Ventilator
Artificial kidney
Artificial liver
Protection of enteral mucosa
Drugs of protection of heart
Thanks!
Acute Renal Failure (ARF)
Definition

Characterized by ineffective filtration across
glomeruli in short time. Such as azotemia,
imbalance of water, electrolyte and acid-base.
Etiology and classification
Prerenal

Proximal to kidney
Decrease in renovascular flow
1. Hypovolemia, severe cardiac dysfunction, loss of
vascular tone, drugs (renal vasoconstriction), renal
artery occlusion
2. Abdominal Compartment Syndrome (ACS)
3. 50% of the ARF
Postrenal

Distal to kidney.
Obstruction of urinary flow
1. Collecting system
2. Ureters: tumor, stone, etc.
3. Bladder outlet (strictures, prostatism)
Intrinsic renal

Renal parenchyma injury (glomerular
filtration )
Renal tubular dysfunction
Both
1. Acute glomerulonephritis
2. ATN : renal ischemiahemorrhage,septic,shock,serum
anaphylaxis; nephrotoxins (aminoglycosides, radiocontrast dye,
pigments, biotoxins, polymyxin)
3. Acute interstitial nephritis

Mechanism
Oliguria and anuria stage<400ml/24h or
<100ml/24h
Renal ischemia
1. Decrease in glomeruli filtrationsystolic blood
pressure < 8kpa; decrease in endothelia
permeability after ischemia; constriction of renal
artery. )
2. ATNstasis of blood in medulla
3. Glomeruli-tubule feedbackischemia Na+
re-absorption decrease in medullary loop and
distal convoluted tubule Na+ increase in
para-macula densa renin release afferent
Arteriole of glomerulus spasm
Reperfusion-ischemia injury: oxygen free radicals injure
cells
Degeneration and necrosis of tubulus endothelium
ischemiaATP disorders of transport function
accumulation of sodium and calcium, loss of
potassiumdegeneration of endoplasmic reticulum,
accumulation of matrix protein renal tubular necrosis



Obstruction of renal tubulus
1. mucousa and cells
2. filtration pressure
3. hemoglobin and myoglobin

Infection and drugs
1. Infection leading to decrease in renal blood flow
2. Drugs: amine, rifampicin, polymyxin

Non-oliguria acute renal failure
1. Discrepancy of renal tubulus and glomeruli of change
2. Normal blood flow in some renal unit








Urorrhagia stage>800ml/24h

Glomerular filtrate not concentratedun-recovery
from resorption and concentrated function of renal tubulus
re-epithelia
Osmotic diuresis: large amount of BUN accumulated in
body during anuria stage.
Water diuresismuch electrolyte and water excess
during anuria stage aggravate uresis.
Clinical Manifestation
Anuria stage714 daysthe longest is more
than one month

Urine : hypobaric and fixed; albuminuria; red cells
and cast

Imbalance of water, electrolyte and acid-base.
Three increase blood phosphorus, potassium, magnesium
Three decrease: blood calcium, sodium, chloride
Two intoxicationmetabolic acidosis, water toxication
Accumulation of metabolic products-uremia
azotemia, phenol, guanidine, etc.
Nausea , vomiting
Headache , restless, weakness, unconsciousness, coma
Hemorrhagic tendencydecrease in platelet
function, increase in capillary fragility, hepatic
dysfunction, DIC
Subcutaneous hemorrhage
Oral mucosa and gingiva bleeding
Gastrointestinal bleeding
Wounds bleeding
Urorrhagia stage(14 days
Mode of urine recovery
Increase Abruptly
usually in 57th dayurine output increases to 1500ml/24h abruptly.
Increase gradually
Usually in 714th day urine output increases to 200500ml/24h
Increase tardily
When urine output increases to 500700ml/24hstopping increasing. Prognosis is poor.
Imbalance of water, electrolyte; and
azotemia still exist.
Complicating with infection easily

Stage of recoveryseveral months
anemia
weakness
Wasting
Diagnosis

History and physical examination

Etiology
Whether prerenal factors exist
Whether postrenal factors exist
Examination of urine
Record urine output per hour
Acid urine, specific gravity stabilizes at the range of
1.010-1.014
Microscopic examination
1. More red cells and renal tubulus epitheliacortex and medulla
necrosis)
2. Lenity brown castrenal failure cast
3. Acidophilic cell increaseinterstitial nephritis
4. Red cell castglomerular nephritis
5. Non apparent abnormalityearly stage with prerenal or postrenal
failure
Examination of renal function

Urine BUN decrease, less than 180mmol/24h usually.
Urine sodium increase, more than 175mmol/24h.
Fractional excretion of filtrated sodium is more
than .5
FE
Na
%=U
Na
/P
Na
P
Cr
/U
Cr
100
Urine osmolality
Less than 350 mOsm/L in ARF
More than 500mOsm/L in prerenal failure or glomerular
nephritis
Serum BUN, Crelevating for 3.89.4 mmol/L/d

Plasma/urine Cr>20

Renal failure index (RFI)
RFI U
Na
P
Cr
/ U
Cr

RFI.5: ARF
RFI: Prerenal oliguria

Renal and prerenal oliguria









Renal Prerenal
Fluid test No urine rise Urine rise
Urine specific gravity 1.010 >1.020
Urine sediments Casts and epithelia negative
Urine soudiummmol/L
>40 <20
Urine/plasma urea <3 >8
Urine/plasma Cr <20 >40
Serum K+ Elevate abruptly
Elevate gradually
HCT Decrease Increase
Serum BUN/ Cr <10 >15
*5GNS250500mlwithin 3060min dripping intravenously,
record urine output

Renal and postrenal
1. Renal ultrasoundnephrauxe, ureter
expansion
2. Plain abdominal X-raycalcification, stone
or obstruction
3. intravenously pyelography ( IVP)
4. Retrograde pyelography

Treatment
Oliguria or anuria stage

Control fluid input: body weight is decreased
0.5kg daily.
Output is input, less input is better than the more
Fluid amount dailydominance lossnon-dominance loss
endogeny water
Nutrition
Less protein, high calorie, high vitamin diet
Protein synthesis hormone: GH, testosterone
Corection of electrolyte imbalance
(hyperkalemia, hyponatremia, hypocalcemia, acidosis

Antibiotics:harmful to kidney

Blood purification

1. hemodialysisartificial kidney. High clearance rate
for small molecules; hemodynamics unstable

2. peritonealdialysissmall molecular substances;
infection; low clearance rate

3. hemofiltrationhigh clearance rate for middle
molecules; hemodynamics stable

Urorrhagia stage
Infuse optimal fluidavoiding loss of extra cellular fluid
Fluid infusion is 1/3~1/2 fluid output equivalently.
Correction of electrolyte
Infuse sodium and potassium according to determination of
electrolyte daily.
Increase amount protein.
Treat infection actively
Prophylaxis
To diagnose volume deficient timely
Perform fluid test first when oliguria existed
To treat according to fluid deficient

To correct water and electrolyte imbalance in patients
with trauma and pre-operation

Management of xenotype blood infusion
To rise pH values in urine for alkali
Mannitol for diuresis

Restrict inotropic agents
Norepinephrine
pressor agent

Treatments of DIC
Heparin
Acute Respiratory Distress
Syndrome (ARDS)
Definition
Acute pulmonary dysfunction originating from diffuse
infiltrate and pulmonary compliance decreased leading to
severe hypoxia.

ARDS is an inflammatory process

Not a accumulation of edema fluid

Both lungs

Predisposing conditions
Injury
Lung injurylung contusion, smoke, aspiration of
gastric contents, toxic gas, drowning, oxygen
Extra-lung injury: fractures, trauma, burns,
massive transfusion, amniotic fluid thrombosis,
transplantation
Operation: cardiopulmonary bypass, major
operation
Infection: sepsis/septic shock
Shock and DIC
Mechanism
Initial stage

Pulmonary capillary permeability lung parenchyma edema.
Erythrocytes exudates
Leukocytes infiltrate deterioration of cellular damages
Pulmonary vasoconstriction, thrombosis, A-V shunt.
Alveoli
Edema
DPL
Hyaline and bloody fluid
Hyaline and bloody fluid in bronchia flake atelectasis
Advanced stage
Pulmonary parenchyma inflammation aggravated
Complicating with infection
Final stage
Pulmonary fibrosis
Capillary vessels occlusion
Afterload rise, hypoxia
Clinical Manifestation
1. Initial stage
Tachypnea, refractory to supplemental oxygen
Progressive hypoxemia
No rales
Unrevealing in chest X-ray

2. Advanced stage
Prominent dyspnea and cyanosis
Need mechanical ventilation
Rales; bronchi secretion rise
Chest X-ray: bilateral infiltrates
Conscious disturbance
Temperature and leukocytes rise

3. Final stage
Arrhythmia bradycardia cardiac arrest
Deep coma

Diagnosis
Predisposing conditions

Acute injury
Systemic infection
RR>30
Dyspnea
Transplantation
Exclude other conditions
Oxygenation
index


X-ray PAWP
ALI Acute
onset
PaO2/FiO2
?300mmHg
Bilateral
infiltrates
in P-A position
PAWP?18mmHg or
no left atrium
pressure rise
ARDS Acute
onset
PaO2/FiO2
?200mmHg
Bilateral
infiltrates
PAWP?18mmHg or
no left atrium
pressure rise


Diagnostic Criteria
FiO2(%)=4oxygen inflow(L/min) + 21
Therapy & Treatment
Correction of hypoxemia quickly
Mechanical ventilation earlier
Optimal PEEP, recovery of alveolar function and
functional residual capacity
Open lung

Recovery of circulation and prevention of
pulmonary interstitial edema
Optimal colloid and crystal fluid ratio
Optimal diuretics
Optimal negative fluid balance
To evaluate by CVP/PAWP, urine and rales
Treatment of infection:
-sputum drainage; antibiotics

Block SIRS
Glucocorticosteroid earlier
Inflammatory mediators inhibitorI buprofen,
oxpentifylline, TNF Ab.
Heparin
Hemofiltration

Mechanical ventilation

Ventilatory mode: positive ventilation
PEEP: the optimal
Prevention of hypovolemia: prevention of
imbalance of V/Q
Barotrauma: PIP 50cmH2O
Thanks