TO MY WIFE WHO SUPPORT ME ALL THE WAY ,STOOD BESIDE ME ALL THE TIME , ENCOURAGE ME TO BE VALUABLE IN MY COUNTRY ......HOPPING ALLAH ACCEPT MY AIMS

1. ARF II MAGDI AWAD SASI 2014
1
DR MAGDI AWAD SASI
MANAGEMENT OF PRERENAL ARF-----PART TWO
REVERSALBE CAUSES OF ARF:
1. Hypovolemia
2. Hypotension
3. Hypercalemia
4. Heart failure
5. Accelerated phase OF hypertension
6. Sepsis
7. Urinary tract infection
8. Urinary tract obstruction
9. 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 energy
iv. Carbohydrate
v. Vitamins and trace elements supplement
4. Treatment of complications of ARF
5. 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 therapy
7. 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. Nutrition
iii. Follow up (RFTs)

2. ARF II MAGDI AWAD SASI 2014
2
DR MAGDI AWAD SASI
SUMMARY OF CAUSES OF PRERENAL ARF:
1. Decrease of blood volume:
I. Hemorrhage –from orifices, internal bleeding ,hematemsis, delivery, surgery
II. Loss of plasma—burns , crush injuries
III. Na and Water depletion from :
a. GIT---severe vomiting ,diarrhea , acute intestinal obstruction ,paralytic ileus
,pancreatitis , fistulae
b. 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 arteries
B. Occlusive embolus of the aorta or renal arteries
C. Aortic dissecting aneurysm
MANAGEMENT:
1. Compatible history (risk factor for ARF )
2. The clinical finding
3. Progressive increase in blood urea and creatinine
4. 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)).
Urine ----------decrease volume

3. ARF II MAGDI AWAD SASI 2014
3
DR MAGDI AWAD SASI
Effect of I.V. treatment (rehydration)
Diuresis ----prerenal cause
Fluid 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 used
Give 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.

4. ARF II MAGDI AWAD SASI 2014
4
DR MAGDI AWAD SASI
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 HTN
4. Arterial or venous occlusion(thrombosis , emboli)
5. Microangiopathic haemolysis (TTP,HUS,DIC)
II. Tubulo-interstitial diseases:
1. Acute interstitial nephritis—drug induced
2. Pyelonephritis
3. Hypercalcemia ,multiple myeloma ,acute uric acid nephropathy (tumor lysis)
B. Acute tubular necrosis((ATN)):
1. POST-ISCHEMIC INJURY:
i. Shock
ii. Major trauma ,burns ,crush injuries ,eclampsia
iii. Surgery ( cardiac ,aortic ,biliary)
iv. Pancreatitis
v. 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 media
iii. Anesthetics ---methoxyflurane
iv. Myoglobalinuria( rabdomylosis) ,Haemoglobulinuria (hemolysis)
v. Poisoning (paracetamol ,aspirin , methanol ,ethanol)
vi. Heavy meatals platinum ,amantide phalloides

5. ARF II MAGDI AWAD SASI 2014
5
DR MAGDI AWAD SASI
ATN
A. Very poor prognosis
1. Extensive burns
2. BY-pass surgery
3. Sepsis following abdominal surgery
4. Trauma to abdomen and thorax
5. Severe hepatic failure
6. Paraquat poisoning
7. Criminal abortion associated with clostridal infection
8. Any patient requiring ventilation for more than 48hr
B. Good prognosis
1. Obstetrical accident without Sepsis
2. Trauma to limbs
3. Mismatched blood transfusion
4. Viral infection( Coxsackie ,influenza ) causing myoglobinuria
5. 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 irreversible
3. 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 complication
3. TREATMENT---------Speed and efficiency of ARF treatment.

6. ARF II MAGDI AWAD SASI 2014
6
DR MAGDI AWAD SASI
Clinical presentation:
 Symptoms and signs of causative disease.
 Urine----oliguric
Pre renal normal kidney Established ARF
CVP ˂ 2CM OF H2O N or high ≥ 12cm
Response to
1) Hydration
2) 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

7. ARF II MAGDI AWAD SASI 2014
7
DR MAGDI AWAD SASI
ON EXAMINATION:
1) First feels well----after days ----uremic S&S
2) c/o anorexia ,nauseas ,vomiting ,hiccough
3) Apathy , mental confusion
4) Muscles twitches ,fits ,drowsiness ,coma
5) Bleeding episodes
6) GIT bleeding ( may be serious)
7) Respiratory rate—increase – infection , metabolic acidosis
8) 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 diet
13) PROGNOSIS DEPENDS ON :
1. Speed and efficiency of treatment
2. Early recognition and treatment of complication
3. Nature and severity of causal disorder e.g.
I. Simple hemorrhage
II. Drugs
III. Severe infections
IV. Multiorgan failure mortality rate 50n--70%
4. Untreated cases----- MR ˃ 90%

8. ARF II MAGDI AWAD SASI 2014
8
DR MAGDI AWAD SASI
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 action
6. 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 diet
Fat and carbohydrate for energy
Vitamins supplement
9. Treatment of anemia, hypocalcemia ,DIC ,infections .
10.Manage life threatening complications of ARF .
I. HYPERKALEMIA
II. SEVERE ACODOSIS
III. SALT AND WATER OVERLOAD
IV. 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—80mg
4 -8 hourly
Dopamine drip (200—600microgm/min)
13.If all fail-----------DIALYSIS .

9. ARF II MAGDI AWAD SASI 2014
9
DR MAGDI AWAD SASI
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 investigation
3. 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 carcinoma
5. Management ---
I. Investigation aiming to diagnose and relief urinary bladder obstruction
II. 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 –AGN
5. Chest x ray , ABD USS , ECG , IVU ( ABDOMEN CAT OR MRI)
6. Renal biopsy
7. Daily pt weight ---input and out put

10. ARF II MAGDI AWAD SASI 2014
10
DR MAGDI AWAD SASI
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 balance
II. Nutrition
III. Nursing care
IV. Infection
V. 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 ,fits
2. Fluid overload----- pulmonary edema
3. Uraemic Pericarditis
4. Uraemic gastritis
5. Hyperkalemia(˃ 6.5)---- not responding to medical therapy
6. Severe metabolic acidosis( HC03 ≤ 13 or PH ˂ 7.1
7. Severe hyeruricemia (tumor lysis syndrome
8. 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

11. ARF II MAGDI AWAD SASI 2014
11
DR MAGDI AWAD SASI
TREATMENT OF HYPERKALEMIA( K ˃ 6mmol/L )
The first thing is to rule out pseudohyperkalemia:
1. Tourniquet application
2. Haemolysis of drawn blood
3. Increase WBC & platelets
Symptoms:
Weakness
Lethargy
Muscle cramps
Paresthesias
Hypoactive DTRs
Dysrhythmias
ECG---
K > 5.5 -6
Tall, peaked symmetrical T waves
Wide QRS
Prolong PR
Diminished /absent P
Depressed ST
Prolonged QT
QRS- blends in T ((merge)) – classical sine wave of increase K
Ventricular fibrillation
asystole

12. ARF II MAGDI AWAD SASI 2014
12
DR MAGDI AWAD SASI
I.V. access for:
Ca gluconate (10ml 10%)diluted over 10 minutes --AIM --protect heart
Glucose 50ml 50%--with regular insulin 10 units , may be repeated.
Na HCO3 8.4% 50cc for each 0.1 ▼ blood PH to correct metabolic acidosis
Ca or Na resonium (30mg) orally or rectally
B-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 hyperkalemia
Dialysis---- 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 ,blood
2. Dopamine ---IV drip
Hypertension:-
1. Ca channel blockers ,clonidine ,prazosine
2. IV Na nitroprusside (may be needed in some cases)
3. Dialysis TO BE CONTINUED