ARF II MAGDI AWAD SASI 2014

MANAGEMENT OF PRERENAL ARF-----PART TWO

REVERSALBE CAUSES OF ARF:

1. Hypovolemia2. Hypotension3. Hypercalemia4. Heart failure5. Accelerated phase OF hypertension6. Sepsis7. Urinary tract infection8. Urinary tract obstruction9. Nephrotoxic drug or poison

GENERAL LINES OF ARF MANAGEMENT

1. Fluid and electrolyte balance( I/O chart ,patients weight ,RFT and electrolytes)2. 500 ml fluid and asses the losses (( urine ,faeces ,vomitus ,aspirations ,ventilator ,

sweating ,increased temperature))3. Nutrition ( N/G ,parenteral ):

i. Protein 40gm/day (70 gm if H.D.)ii. Potassium restricted diets

iii. Fluid and fat for energyiv. Carbohydrate v. Vitamins and trace elements supplement

4. Treatment of complications of ARF5. Trial of frusemide ,mannitol ,dopamine ,dobutamine infusion after correction of fluid

loss ( using CVP line)6. If no dieresis or ARF complication-----early start of renal replacement therapy7. Renal replacement therapy:

CONTINOUS ARTERIOVENOUS(CAV), CONTINOUS VENOVENOUS(CVV)I. HAEMODIALYSIS OR PERITONEAL DIALYSIS

II. ULTRAFILTRATION ---REMOVAL OF FLUID 0—4KG /H.D. SESSION

III. HAEMOFILTRATION-----REMOVAL OF FLUID AND REPLACEMENT FLUID TREATMENT

IV. HAEMODIFILTRATION---- FLUID REMOVAL AND HEMODIALYSIS

8. Recovery ( polyuric phase) i. Accurate I/O , electrolyte balance

ii. Nutritioniii. Follow up (RFTs)

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ARF II MAGDI AWAD SASI 2014

SUMMARY OF CAUSES OF PRERENAL ARF:

1. Decrease of blood volume:

I. Hemorrhage –from orifices, internal bleeding ,hematemsis, delivery, surgeryII. Loss of plasma—burns , crush injuries

III. Na and Water depletion from :a. GIT---severe vomiting ,diarrhea , acute intestinal obstruction ,paralytic

ileus ,pancreatitis , fistulaeb. Urine ------excessive diuretics ,DKA

2. Decrease cardiac output and myocardial failure----cardiogenic shock

3. Increase in the size of vascular bed---septic shock

4. Intravascular hemolysis

5. Rhabdomyolysis-----release of globins----toxic effect on the kidney

6. Disease of the major renal vessels-----decrease of renal blood:

A. Thrombosis of arteriesB. Occlusive embolus of the aorta or renal arteriesC. Aortic dissecting aneurysm

MANAGEMENT:

1. Compatible history (risk factor for ARF )2. The clinical finding3. Progressive increase in blood urea and creatinine4. Examine for:

Fluid treatment chart (( input and output )) balance.Blood pressure ---hypotension (postural) in shock states.Look signs of dehydration----

Dry mucous membranes, inelastic skin ,decrease its turgor Postural hypotension and taccychardia ( worse in sitting) Collapsed superficial veins ,sunken eyes Cold cyanosed extremities Decrease JVP and CVP, sharp decrease in body weight

Changes in the body weight (( over hydration /dehydration)).

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ARF II MAGDI AWAD SASI 2014

Urine ----------decrease volume Effect of I.V. treatment (rehydration)Diuresis ----prerenal causeFluid over load and danger of pulmonary oedema.

Treatment :

1. Treat the cause.2. Treat hypovolemia:

A. Restore blood pressure( blood , plasma ,fluids)B. Use of inotropic drugs e.g. after correction of blood volume

Body weight x 15 = ----mg of dopamine to be used in 250ccN/S fluid. One drop = 1 micgm 5 –10 drops/min will increase renal perfusion.

c. Best treated by monitoring CVP or PCWP.

3. Treatment of septicemia---avoid nephrotoxic antibiotics

4. Aim of Early treatment---diuresis and improvement of RF

Otherwise, if not, pt is still oliguric ----- treat as ATN.

5. Frusemide and dopamine for pre renal failure is questionable.They are used if unresponsive to fluid challenge.Frusemide:

Don’t give until you are sure that the pt is fully hydrated.Don’t give if aminoglycoside have been usedGive 250mg I.V. over one hour by syringe pump.If the urine output remains ˂ 40 ml/hr over the next hours, give further 500mg I.V. over 2 hours by syringe pump.If the urine output increases ,further doses can be given as required up to maximum daily dose of 2 gm or continuous infusion can be used (30---60mg/hr)

Dopamine :

200---6000microgm/min (has a beneficial effect on renal output.). 400mg in 250ml ( 1600 micrigm/ml) give 1—2 micgm/kg/min (4mg). If dieresis occur , keep dopamine for 24—72hr and taper it.

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ARF II MAGDI AWAD SASI 2014

MANAGEMENT OF RENAL ARF

SUMMARY OF CAUSES:

A. Acute parenchymal disorders:I. Glomerular and vascular diseases:

1. Acute glomerular nephritis (primary or part of systemic disease)2. Vasculitis (including drug induced)3. Malignant HTN4. Arterial or venous occlusion(thrombosis , emboli)5. Microangiopathic haemolysis (TTP,HUS,DIC)

II. Tubulo-interstitial diseases:1. Acute interstitial nephritis—drug induced2. Pyelonephritis3. Hypercalcemia ,multiple myeloma ,acute uric acid nephropathy (tumor lysis)

B. Acute tubular necrosis((ATN)):1. POST-ISCHEMIC INJURY:

i. Shockii. Major trauma ,burns ,crush injuries ,eclampsia

iii. Surgery ( cardiac ,aortic ,biliary)iv. Pancreatitisv. Prolonged use of vasopressors

vi. Obstetric--- eclampsia ,abruption placenta vii. Prolonged pre-renal failure

2. NEPHROTOXIC INJURY:i. Antibiotic( aminoglycoside ,amphotericin ,rifampicin ,sulphonamide)

ii. Radioactive contrast mediaiii. Anesthetics ---methoxyfluraneiv. Myoglobalinuria( rabdomylosis) ,Haemoglobulinuria (hemolysis)v. Poisoning (paracetamol ,aspirin , methanol ,ethanol)

vi. Heavy meatals platinum ,amantide phalloides

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ARF II MAGDI AWAD SASI 2014

ATN

A. Very poor prognosis1. Extensive burns2. BY-pass surgery3. Sepsis following abdominal surgery4. Trauma to abdomen and thorax5. Severe hepatic failure6. Paraquat poisoning7. Criminal abortion associated with clostridal infection8. Any patient requiring ventilation for more than 48hr

B. Good prognosis1. Obstetrical accident without Sepsis2. Trauma to limbs3. Mismatched blood transfusion4. Viral infection( Coxsackie ,influenza ) causing myoglobinuria5. Some nephrotoxin

CLINICAL POINTS TO BE REMMEBERED:1. ATN is the commonest histology in ARF secondary to pre-renal causes or nephrotoxic drugs.2. A urine output ˂25-30ml/hour in adult should be investigated and urgently corrected. If oliguria persists ˃2-3 hour, it may be irreversible3. The simplest screening test for RF in ICU patients are : I. Hourly urine output ( at least 0.5ml/kg/hour) II. Accurate I/O fluid chart III.Daily serum creatinine assessment

Prognosis of ARF : DEPENDS ON

1. CAUSE-----------------Nature and severity of precipitating factor 2. DIAGNOSIS----------Early diagnosis and treatment of ARF complication3. TREATMENT---------Speed and efficiency of ARF treatment.

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ARF II MAGDI AWAD SASI 2014

Clinical presentation: Symptoms and signs of causative disease. Urine----oliguric

Pre renal normal kidney Established ARF CVP ˂ 2CM OF H2O N or high ≥ 12cmResponse to

1) Hydration2) Mannitol or lasix

Dieresis ± Dieresis ±

No effect or risk of pulmonary Edema

URINE volume Specific gravity Sediment Na + Urea Osmolality FE Na%

Small ˃ 1020

normal˂ 10mmol/l˃ 250 moml/l ˃600 ˂ 1

Small ˂ 1020 Casts ,depris , cells ˃ 20 ˃ 40(ATN) ˂ 150 moml/l 300-400mosm/l ˃ 3

Urine / plasma Urea ratio Creat ratio 0smolality

˃ 10 ˃ 10 ˃ 2

˂ 10 ˂3(ATN) ˂ 10 ˂ 1.1

Fractional excretion of Na FE Na= (U/P Na) / (U/P CR) X 100

Increase blood urea ,creatinine (if blood urea ˃ 50—100mg/d= hypercatabolic state—trauma ,infection , surgery ,drugs

Electrolytes :Hyperkalemia , dilutional hyponatremia (over load + oliguria), ca low

Metabolic acidosis: not so marked if excessive vomiting or aspiration of gastric content.

UREA is increased in:

Steroids , tetracycline, catabolic state ,high protein diet, dehydration ,GIT hemorrhage.

CREATININE is increased in:

Large muscle bulk, acute rhabdomylsis , high protein meal ,trimethoprium ,low GFR

UREA IS DECREASED IN :

Liver disease , anabolic state, starvation ,low protein diet ,pregnancy ,increase ADH

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ARF II MAGDI AWAD SASI 2014

ON EXAMINATION:

1) First feels well----after days ----uremic S&S2) c/o anorexia ,nauseas ,vomiting ,hiccough3) Apathy , mental confusion4) Muscles twitches ,fits ,drowsiness ,coma5) Bleeding episodes6) GIT bleeding ( may be serious)7) Respiratory rate—increase – infection , metabolic acidosis8) Pulmonary edema S&S

A. I.V. fluids and oliguria (over treatment)B. Increase PCWP in uremia – ARDS

9) Anemia -----increased hemolysis ,repeated sampling ,bleeding ----- decrease erythropoiesis

10) Infection –septicemia and shock due to -----( decrease cellular and humoral immunity)

11) Phases -- oliguric then diuretic

12) Diuretic phase: 7 –10 days ( 4 weeks ) of the onset of S&S Urine increase 3 – 5 l/day persist 4 days Urea is usually increased and creatinine slowly decrease Needs accurate supplement of fluid and electrolytes Few days later----normal chemistry and urine volume and pts can eats normal diet13) PROGNOSIS DEPENDS ON :

1. Speed and efficiency of treatment2. Early recognition and treatment of complication3. Nature and severity of causal disorder e.g.

I. Simple hemorrhageII. Drugs

III. Severe infectionsIV. Multiorgan failure mortality rate 50n--70%

4. Untreated cases----- MR ˃ 90%

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ARF II MAGDI AWAD SASI 2014

GENERAL TREATMENT OF THE OLIGURIC PHASE:

1. Get drug history and alter prescriptions appropriately.

2. Fluid and electrolyte balance (( daily weight ,fluid chart )).3. 500 ml fluid and asses the losses

(( urine ,faeces ,vomitus ,aspirations ,ventilator , sweating ,increased temperature—add 500ml for each increase ˃ 37.5))

4. Skilled nursing care (( mouth , skin )) and senior trained specialists.5. Establish under lying causes and start prompt medical action6. Exclude obstruction of the urinary tract.7. Assess and correct any respiratory or circulatory impairment.8. Nutrition ( NGT, Parenteral)

Protein—40mg/d (( increase to 70gm/d if on dialysis )K restriction dietFat and carbohydrate for energyVitamins supplement

9. Treatment of anemia, hypocalcemia ,DIC ,infections .10.Manage life threatening complications of ARF .

I. HYPERKALEMIAII. SEVERE ACODOSIS

III. SALT AND WATER OVERLOADIV. SEVERE UREMIA

11.Dialysis investigations and accurate I/O .12.Trial of :

I. Furosemide – 1 -2 mg/d and increase to 500-2000mg in 1 hr infusion or ethacryme acid 0.5mg/kg----If urine output is initiated, it can be maintained by lasix 40—80mg4 -8 hourlyDopamine drip (200—600microgm/min)

13.If all fail-----------DIALYSIS .

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ARF II MAGDI AWAD SASI 2014

MANAGEMENT OF POST --RENAL ARF

Obstructive nephropathy may be 2ry to upper or lower urinary tract obstruction.

Early diagnosis and relief of obstruction are essential to prevent renal damage by ultrasound abdomen and urologist consultation.

CLINICAL FEATURES:

1. H/O urinary symptoms—renal colic ,hematuria , difficulty of micturation.2. May be clinically silent and discovered on investigation3. Anuria--------suggestive of obstructive lesion.

Abdominal USS should be done to R/O any obstructive lesion .If it showed pelvic or uretric dilatation ----urgent percutaneous nephrostomy is indicated to avoid need for dialysis treatment.

4. P.V.---palpable CA cervix P.R.----palpable recto-sigmoid junction carcinoma5. Management ---

I. Investigation aiming to diagnose and relief urinary bladder obstructionII. Supportive and palliative treatment may be needed

III. Accurate I.V. fluid treatment after relief of obstruction –postobstuctive dieresis

WHAT ARE THE INVESTIGATIONS TO BE DONE?

1. BLOOD----C.B.C. ,Blood glucose , Renal function test ,Na ,K ,Ca , CL , Bicarbonate ,osmolality ,Coagulation screen ,ESR ,Serum &urine electrophoresis , CPK

2. URINE---Na , Urea , Creatinine ,Osmolality . 3. Culture-------blood ,urine ,sputum , wound culture ,tracheostomy. 4. S .complement ,immunological studies –AGN5. Chest x ray , ABD USS , ECG , IVU ( ABDOMEN CAT OR MRI)6. Renal biopsy7. Daily pt weight ---input and out put

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ARF II MAGDI AWAD SASI 2014

TREATMENT OF ARF

1. Emergency measures :I. RX of hyperkalemia

II. Indication of dialysis

2. Determination of ARF cause .

3. General management of the oliguric phase:

I. Fluid and electrolyte balanceII. Nutrition

III. Nursing careIV. InfectionV. Anemia ,DIC, GIT hemorrhage

4. General management of recovery (diuretic ) phase :

Fluid electrolyte , nutrition.

INDICATIONS OF DIALYSIS IN AFR :

URGENT DIALYSIS---

1. Uraemic encephalopathy—impaired conscious level ,coma ,fits2. Fluid overload----- pulmonary edema3. Uraemic Pericarditis4. Uraemic gastritis5. Hyperkalemia(˃ 6.5)---- not responding to medical therapy6. Severe metabolic acidosis( HC03 ≤ 13 or PH ˂ 7.17. Severe hyeruricemia (tumor lysis syndrome8. Oxylate toxicity (ethylene glycol overdose)9. Severe uraemia----200mm0l/d

ROUTINE DIALYSIS :

1. Prevention of severe uremia and its complications ( when conservative TR failed)2. Maintenance of normal fluid ,electrolyte and acid base status ( TR medically failed)3. Space making for parenteral nutrition ,transfusion of blood and blood products 4. Prophylaxis before surgical procedures

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ARF II MAGDI AWAD SASI 2014

TREATMENT OF HYPERKALEMIA ( K ˃ 6mmol/L )

The first thing is to rule out pseudohyperkalemia:

1. Tourniquet application2. Haemolysis of drawn blood3. Increase WBC & platelets

Symptoms:

WeaknessLethargyMuscle crampsParesthesias Hypoactive DTRsDysrhythmias

ECG---

K > 5.5 -6Tall, peaked symmetrical T wavesWide QRSProlong PRDiminished /absent PDepressed STProlonged QTQRS- blends in T ((merge)) – classical sine wave of increase KVentricular fibrillationasystole

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ARF II MAGDI AWAD SASI 2014

I.V. access for:

Ca gluconate (10ml 10%)diluted over 10 minutes --AIM --protect heartGlucose 50ml 50%--with regular insulin 10 units , may be repeated.Na HCO3 8.4% 50cc for each 0.1 ▼ blood PH to correct metabolic acidosisCa or Na resonium (30mg) orally or rectallyB-agonist (IV /inhaler)-10-20mg albuterol decrease K in half hour for 2 hours

Once k ˂6mmol/l---dextrose 20% (30ml/hr) to prevent rebound hyperkalemiaDialysis---- definitive treatment if there is ECG changes

Summary of hyperkalemia TR:

TREATMENT OF BLOOD PRESSURE

Hypotension(shock)-----best under C.V.P.

1. I.V. fluids ,blood2. Dopamine ---IV drip

Hypertension:-

1. Ca channel blockers ,clonidine ,prazosine2. IV Na nitroprusside (may be needed in some cases)3. Dialysis TO BE CONTINUED

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