Multiple Organ Dysfunction Syndrome (MODS)

By Tiffany Olson,2014-05-05 08:42
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Multiple Organ Dysfunction Syndrome (MODS)

    Multiple Organ Dysfunction Syndrome (MODS)


    Dysfunction or failure of multiple organ or system happened simultaneously or sequentially due

    to various etiological factors.


    ; Infection: Gram positive/negative bacteria, fungal, Virus

    ; Shock, hemorrhage, etc.

    ; Allergy

    ; Burns

    ; Trauma

    ; Severe acute pancreatitis

Classification of MODS

    ; Immediate Type (Primary)Dysfunction is happened simultaneously in two or more

    organs due to primary disease.

    ; Delayed type (Secondary,,Dysfunction happened in a organ, other organs

    sequentially happened dysfunction or failure.

    ; Accumulation typeDysfunction leaded by chronic disease.


Common Manifestations of MODS

Diagnosis of Criteria

    Organ/ system dysfunction and failure


Treatments of MODS

    ; Combined therapy

     Correction of ischemia: fluid resuscitation, mechanical


     Prevention of infectiondrainage, antibiotics

     Interruption of pathological reactionhemofiltration

     Stabilization of internal environmentwater, electrolyte,

     acid-base imbalance

     Regulation of immunitycellular and humor

    ; Support of organ function


Artificial kidney

     Artificial liver

     Protection of enteral mucosa

     Drugs of protection of heart

    Acute Renal Failure (ARF)


    Characterized by ineffective filtration across glomeruli in short time. Such as azotemia,

    imbalance of water, electrolyte and acid-base.

    Etiology and classification


     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


     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


    1. Acute glomerulonephritis

    2. ATN : renal ischemiahemorrhage,septic,shock,serum anaphylaxis;

    nephrotoxins (aminoglycosides, radiocontrast dye, pigments, biotoxins,


    3. Acute interstitial nephritis


     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 endotheliumischemia?ATP ?disorders of

    transport function ?accumulation of sodium and calcium, loss of potassium?

    degeneration 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


    Clinical manifestation

    ; Anuria stage,?7(14 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-uremiaazotemia, phenol, guanidine,


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 5(7th dayurine output increases to 1500ml/24h abruptly.

    Increase graduallyUsually in 7(14th dayurine output increases to 200(500ml/24h

    Increase tardilyWhen urine output increases to 500(700ml/24hstopping increasing.

    Prognosis is poor.

     Imbalance of water, electrolyte; and azotemia still exist.

     Complicating with infection easily

; Stage of recoveryseveral months,,





    ; History and physical examination


     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

     More red cells and renal tubulus epitheliacortex and medulla


     Lenity brown castrenal failure cast

     Acidophilic cell increaseinterstitial nephritis

     Red cell castglomerular nephritis

     Non apparent abnormalityearly stage with prerenal or postrenal


    ; 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 3.8(9.4 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 and postrenal

    1. Renal ultrasoundnephrauxe, ureter expansion

    2. Plain abdominal X-raycalcification, stone or obstruction

    3. intravenously pyelography ( IVP)

    4. Retrograde pyelography


     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


    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

    1. peritonealdialysissmall molecular substances; infection; low clearance rate

    1. 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


     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


Management of xenotype blood infusion

     To rise pH values in urine for alkali

     Mannitol for diuresis

Restrict inotropic agents


     pressor agent

Treatments of DIC


    Acute Respiratory Distress Syndrome (ARDS)


    Acute pulmonary dysfunction originating from diffuse infiltration and pulmonary compliance

    decreased leading to severe hypoxia.

     ARDS is an inflammatory process

Not a accumulation of edema fluid

Both lungs

Predisposing conditions


     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


    ; Initial stage

     Pulmonary capillary permeability lung parenchyma edema.

     Erythrocytes exudates

     Leukocytes infiltrate to deterioration of cellular damages

     Pulmonary vasoconstriction, thrombosis, A-V shunt.




     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 manifestations

    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


     Predisposing conditions

     Acute injury

Systemic infection




     Exclude other conditions

    Diagnostic Criteria

    Therapy & Treatment

     Correction of hypoxemia quickly

     Mechanical ventilation earlier

     Optimal PEEP, recovery of alveolar function and functional residual


     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 inhibitorIbuprofen, oxpentifylline, TNF Ab.



     Mechanical ventilation

     Ventilatory mode: positive ventilation PEEP: the optimal

     Prevention of hypovolemia: prevention of imbalance of V/Q

     Barotrauma: PIP ?50cmH2O

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