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Multiple Organ Dysfunction Syndrome (MODS)

Multiple Organ Dysfunction Syndrome (MODS). 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

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Multiple Organ Dysfunction Syndrome (MODS)

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  1. Multiple Organ Dysfunction Syndrome(MODS)

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

  3. Etiology • Infection: Gram positive/negative bacteria, fungal, Virus • Shock :hemorrhage, etc. • Allergy • Burns • Trauma • Severe acute pancreatitis

  4. Classification of MODS • Immediate Type (Primary)：Dysfunction are 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 type：Dysfunction leaded by chronic disease.

  5. Immediate Type Not related to SIRS Coup injury with chemical or physical factors No time interval from disease ARDS+ARF or ARDS+ARF+DIC+LF Delayed type Not the direct outcome from injury Relating to SIRS（systemic inflammatory response syndrome） Time interval existed from primary disease Attention Accumulation type • Accumulation • Irreversible

  6. Mechanism

  7. Injury factors Inflammatory mediators priming SIRS leading to MODS Vascular permeability↑＋ PMNchemotaxis Adhensive molecules PMN Mono / Macrophage elastase PLA2 oxygen free radicals TNF IL－8 IL－1 IL－6 Endothelium PAF DIC Tissue injury Liver： acute phase Remote organ injury PMN

  8. Common Manifestations of MODS

  9. Diagnosis of Criteria

  10. Organ/ system dysfunction and failure

  11. GLASGOW SCORE

  12. Treatments of MODS

  13. Combined therapy • Correction of ischemia: fluid resuscitation, mechanical ventilation • Prevention of infection：drainage, antibiotics • Interruption of pathological reaction：hemofiltration • Stabilization of internal enviroment：water, electrolyte, acid-base imbalance • Regulation of immunity：cellular and humor

  14. Support of organ function • Ventilator • Artificial kidney • Artificial liver • Protection of enteral mucosa • Drugs of protection of heart

  15. Thanks!

  16. Acute Renal Failure (ARF)

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

  18. Etiology and classification

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

  20. Postrenal • Distal to kidney. • Obstruction of urinary flow • Collecting system • Ureters: tumor, stone, etc. • Bladder outlet (strictures, prostatism)

  21. Intrinsic renal • Renal parenchyma injury (glomerular filtration ) • Renal tubular dysfunction • Both • Acute glomerulonephritis • ATN : renal ischemia（hemorrhage,septic,shock,serum anaphylaxis）; nephrotoxins (aminoglycosides, radiocontrast dye, pigments, biotoxins, polymyxin) • Acute interstitial nephritis

  22. Mechanism

  23. Oliguria and anuria stage（<400ml/24h or <100ml/24h） • Renal ischemia • Decrease in glomeruli filtration（systolic blood pressure < 8kpa; decrease in endothelia permeability after ischemia; constriction of renal artery. ) • ATN（stasis of blood in medulla）

  24. 3. Glomeruli-tubule feedback（ischemia → Na+ re-absorption decrease in medullary loop and distal convoluted tubule → Na+ increase in para-macula densa →renin release → afferent Arteriole of glomerulusspasm ）

  25. Reperfusion-ischemia injury: oxygen free radicals injure cells • Degeneration and necrosis of tubulus endothelium：ischemia→ATP →disorders of transport function →accumulation of sodium and calcium, loss of potassium→degeneration of endoplasmic reticulum, accumulation of matrix protein → renal tubular necrosis

  26. Obstruction of renal tubulus • mucousa and cells • filtration pressure • hemoglobin and myoglobin • Infection and drugs • Infection leading to decrease in renal blood flow • Drugs: amine, rifampicin, polymyxin • Non-oliguria acute renal failure • Discrepancy of renal tubulus and glomeruli of change • Normal blood flow in some renal unit

  27. Urorrhagia stage（>800ml/24h） • Glomerular filtrate not concentrated：un-recovery from resorption and concentrated function of renal tubulus re-epithelia • Osmotic diuresis: large amount of BUN accumulated in body during anuria stage. • Water diuresis：much electrolyte and water excess during anuria stage aggravate uresis.

  28. Clinical Manifestation

  29. Anuria stage：（7－14 days，the 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 intoxication：metabolic acidosis, water toxication

  30. Accumulation of metabolic products-uremia （azotemia, phenol, guanidine, etc.）： • Nausea , vomiting • Headache , restless, weakness, unconsciousness, coma • Hemorrhagic tendency（decrease in platelet function, increase in capillary fragility, hepatic dysfunction, DIC）： • Subcutaneous hemorrhage • Oral mucosa and gingiva bleeding • Gastrointestinal bleeding • Wounds bleeding

  31. Urorrhagia stage(14 days）： • Mode of urine recovery Increase Abruptly： usually in 5－7th day，urine output increases to 1500ml/24h abruptly. Increase gradually： Usually in 7－14th day， urine output increases to 200－500ml/24h Increase tardily： When urine output increases to 500－700ml/24h，stopping increasing. Prognosis is poor.

  32. Imbalance of water, electrolyte; and azotemia still exist. • Complicating with infection easily • Stage of recovery（several months）： • anemia • weakness • Wasting

  33. Diagnosis

  34. History and physical examination • Etiology • Whether prerenal factors exist • Whether postrenal factors exist

  35. 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 epithelia（cortex and medulla necrosis) • Lenity brown cast（renal failure cast） • Acidophilic cell increase（interstitial nephritis） • Red cell cast（glomerular nephritis） • Non apparent abnormality（early stage with prerenal or postrenal failure）

  36. 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 １.5 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

  37. Serum BUN, Cr：elevating for 3.8－9.4 mmol/L/d • Plasma/urine Cr>20 • Renal failure index (RFI) • RFI＝ U Na×（ P Cr / U Cr） • RFI＞１.5: ARF RFI＜１: Prerenal oliguria

  38. Renal and prerenal oliguria

  39. Renal and postrenal • Renal ultrasound（nephrauxe, ureter expansion） • Plain abdominal X-ray（calcification, stone or obstruction） • intravenously pyelography ( IVP) • Retrograde pyelography

  40. Treatment

  41. 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 daily＝dominance loss＋non-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）

  42. Antibiotics:harmful to kidney • Blood purification • hemodialysis：artificial kidney. High clearance rate for small molecules; hemodynamics unstable • peritonealdialysis：small molecular substances; infection; low clearance rate • hemofiltration：high clearance rate for middle molecules; hemodynamics stable

  43. Urorrhagia stage • Infuse optimal fluid，avoiding 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

  44. Prophylaxis

  45. 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

  46. Restrict inotropic agents • Norepinephrine • pressor agent • Treatments of DIC • Heparin

  47. Acute Respiratory Distress Syndrome (ARDS)

  48. 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

  49. Predisposing conditions • Injury • Lung injury：lung 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

  50. Mechanism

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