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 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 type：Dysfunction leaded by chronic disease. Mechanism Common Manifestations of MODS Diagnosis of Criteria Organ/ system dysfunction and failure GLASGOW SCORE Treatments of MODS  Combined therapy  Correction of ischemia: fluid resuscitation, mechanical ventilation  Prevention of infection：drainage, antibiotics  Interruption of pathological reaction：hemofiltration  Stabilization of internal environment：water, electrolyte, acid-base imbalance  Regulation of immunity：cellular and humor  Support of organ function  Ventilator     Artificial kidney Artificial liver Protection of enteral mucosa Drugs of protection of heart 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 ischemia（hemorrhage,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 filtration（systolic blood pressure < 8kpa; decrease in endothelia permeability after ischemia; constriction of renal artery. ) 2. ATN（stasis of blood in medulla） 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 glomerulus spasm ）  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  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 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. Clinical manifestation  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  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 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.  Imbalance of water, electrolyte; and azotemia still exist.  Complicating with infection easily  Stage of recovery（several 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  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） 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  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  Renal and prerenal oliguria  Renal and postrenal 1. Renal ultrasound（nephrauxe, ureter expansion） 2. Plain abdominal X-ray（calcification, 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 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）  Antibiotics:harmful to kidney  Blood purification 1. hemodialysis ： artificial kidney. High clearance rate for hemodynamics unstable • － small molecules; 1. peritonealdialysis：small molecular substances; infection; low clearance rate 1. hemofiltration：high clearance rate for middle molecules; hemodynamics stable 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 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 infiltration 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 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 Mechanism  Initial stage  Pulmonary capillary permeability lung parenchyma edema. Erythrocytes exudates Leukocytes infiltrate to 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 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 Diagnosis • Predisposing conditions  Acute injury      Systemic infection RR>30 Dyspnea Transplantation Exclude other conditions Diagnostic Criteria 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 inhibitor：Ibuprofen, 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 •