MANAGEMENT OF ACUTE RENAL FAILURE IN ICU.ppt

ARF IN ICU

1. By:- Dr Sanjib Kumar Dhar
Guide-Asst Prof Dr S. S. Routroy
SCB MEDICAL
COLLEGE,CUTTACK
ACUTE RENAL FAILUREACUTE RENAL FAILURE
& &
POST DIALYSIS MANAGEMENT POST DIALYSIS MANAGEMENT

2. Def AKI:-
Abrupt↓ in function of kidneys
Accumulation of nitrogenous waste products &
Deranged fluid & electrolyte homeostasis.
Primary manifestration:
↓GFR
↑BUN
↑ creatinine
Oliguria(< 400 ml/day or <20ml/hr)

 .

3. RIFLE Criteria for classification ARF RIFLE Criteria for classification ARF (ADQI gr)(ADQI gr)

5. • History and Physical exam.
• Blood tests : CBC, BUN/creatinine, electrolytes, uric acid,
PT/PTT, CK, Ca, Phophate, ABG
• Urine analysis
• Renal Indices
• Renal ultrasound
• Doppler
 Nuclear Medicine Scans
◦ DMSA: anatomy
◦ DTPA and MAG3: renal function, urinary
◦ excretion and upper tract outflow
◦Renal Biopsy:
DiagnosisDiagnosis

6. Laboratory Evaluation:
◦S.cr : More reliable marker of GFR
small change reflects large change in GFR
◦BUN : generally follows S.cr
Elevation may be independent of GFR
Steroids, Catabolic state, hypovolemia, high protein diet
◦BUN/Cr : helpful in classifying cause of ARF
> 20:1  prerenal cause
10-15:1 intrinsic renal cause

7. Urinalysis
◦Differentiates ATN vs. AIN. vs. AGN
Muddy brown casts - ATN
WBC casts - AIN
RBC cast, Dysmorphic RBCs – AGN

8. Prenal Renal
BUN/Cr >20 <20
FeNa <1% >1%
RFI <1% >1%
UNa (mEq/L) <20 > 40
Specific gravity

FeUrea
High

<35%
Low

>50%


Urine and serum laboratory valuesUrine and serum laboratory values

9. Acute renal failure
Pre renal ARF (30-40%)
Intravascular volume depletion
Decreased effective blood volume
Altered intrarenal hemodynamics
       afferent vasoconstriction
      efferent vasodilation
Intrinsic ARF
Acute tubular necrosis
       ischemic
      nephrotoxic
acute interstitial nephritis
 acute glomerulonephritis
 acute vascular syndrome
Postrenal ARF
ARF sepsis =50%

10. Non ICU ICU Non ICU ICU

11. Prerenal ARFPrerenal ARF
↓effective circulating arterial volume……..inadequate
RBF & ↓GFR.
Reversible
Without injury to renal parenchyma.
Renal tubular and glomerular functions are intact.
sustained hypoperfusion  intrinsic renal parenchymal
damage develop.

13. ARF Associated with ACEI/ ARB & NSAIDARF Associated with ACEI/ ARB & NSAID

14. S.cr & electrolyte conc  measure 1 wk before & 1wk
after initiating or changing the dose of therapy
↑ Scr of >0.5 mg/dl if the initial Scr <2.0 mg/dl, or
↑ >1.0 mg/dl if the baseline Scr >2.0 mg/dl….
threshold for discontinuation of therapy.

15. •Mechanical limitations of abd. wall (tight surgical
closures or scarring after burn inj)
•Intraabdominal inflammation with fluid sequestration-
bowel obstruction, pancreatitis, & peritonitis
Oliguria -- intraabdominal pressure >15 mmHg,
anuria developing at pressures >30 mmHg
.
Abdominal Compartment SyndromeAbdominal Compartment Syndrome

16. Diagnosis
Suspect - tensely distended abdomen
progressive oliguria.
Measurement - U. bladder pressure.
Abdominal compartment syndrome, excluded when the
bladder pressure is <10 mmHg
virtually always present if the pressure is >20 mmHg
Treatment : Surgical decompression .
Paracentesis if massive ascites

17. 2)Postrenal ARF2)Postrenal ARF
Obstruction of urinary tract
In a patient with 2 functioning kidneys, obstruction must be
bilateral to result in ARF.
important to rule out quickly
potential for recovery of renal function is often inversely related
to duration of obstruction.

18. ETIOLOGY OF POSTRENAL ARFETIOLOGY OF POSTRENAL ARF
UPPER TRACT OBSTRUCTION
Intrinsic
 stone
 papillary necrosis
 blood clot
 TCC
Exstrinsic
 retroperitoneal fibrosis
 aortic aneurysm
 retroperitoneal/pelvic
malignanc
LOWER TRACT OBSTRUCTIO N
 urethral obstruction
 BHP
 prostrate cancer
 bladder stone
 fungus ball
 neurogenic bladder
 urethral catheter malposition

19. Etiology of Intrinsic ARFEtiology of Intrinsic ARF
Acute tubular necrosis
   Ischemic
      hypotension
      hypovolemic shock
      sepsis
      cardiopulmonary arrest
      cardiopulmonary bypass
   Nephrotoxic
      drug-induced
         aminoglycosides
         radiocontrast agents
         amphotericin
         cisplatinum
         acetaminophen
      pigment nephropathy
         intravascular hemolysis
         rhabdomyolysis
Acute interstitial nephritis
   Dug-induced
      penicillins
      cephalosporins
      sulfonamides
      rifampin
      furosemide
       NSAIDs
   Infection-related
      bacterial infection
      viral infections
      rickettsial disease
      tuberculosis

20. Systemic diseases
    SLE
      sarcoidosis
      Sjögren syndrome
      tubulointerstitial nephritis and
uveitis (TINU) syndrome
Malignancy
      malignant infiltration of

interstitium
      multiple myeloma
 Idiopathic
Acute glomerulonephritis
   PSGN
   postinfectious GN
   endocarditis-associated GN
   systemic vasculitis
   HUS/TTP
   RPGN
Acute vascular syndromes
   renal artery
thromboembolism
   renal artery dissection
   renal vein thrombosis
   atheroembolic disease

21. Most common form of intrinsic ARF (85 %)
Tubular injury
◦Nephrotoxic (35%)
◦Ischemic (50%)
◦Multifactorial.
Profound ischemic injury may result in bilateral cortical
necrosis
ATNATN

22. ISCHEMIC ISCHEMIC
ATNATN
Surgical
Cardiac
Vascular
Medical
Cardiogenic shock
Sepsis
Burns
Severe volume depletion
TOXIC ATNTOXIC ATN

23. CIN 3rd highest cause of hospital-acquired ARF.
Half of these cardiac diagnostic procedures(PCI).
Treatment
lower doses of contrast & avoidance of repetitive studies
(within 48 to 72 hours).
Avoidance of volume depletion or NSAIDs …
high-risk patient - low/iso-osmolar contrasts
IVF - Isotonic saline @1 mL/kg /hr, begun at least 2 hr prior,
continuing for 6 to 12 hrs after procedure.
Antioxidant Acetylcysteine- 600- 1200 mg po BD,
Therapies with Limited Evidence
Diuretics,Dopamine, fenoldopam, ANP,Theophylline
Radiocontratst NephropathyRadiocontratst Nephropathy

24. Heme pigment-induced ATN:RhabdomyolysisHeme pigment-induced ATN:Rhabdomyolysis
The majority of cases of rhabdomyolysis are The majority of cases of rhabdomyolysis are nontraumaticnontraumatic
Alcohol abuse
Massive muscle compression from immobilization in drug induced coma
Drug-induced
Seizures
Occlusive peripheral vascular disease
Combination therapy with itraconazole, simvastatin, and cyclosporine
Conversion from one fibric acid to another, or from one statin-fibrate combination to
another
Detergent ingestion

25. ABO incompatible.
G-6PD deficiency
Urine  low FENa despite tubular injury.
Heme-pigmented granular casts.
Plasma is normal color in myoglobinuria and red brown in
hemoglobinuria.
Positive dipstick test for heme pigment without RBC on
microscopic exam should suggest myoglobinuria.
Treatment: Isotonic saline @ 1 to 2 l/hr - titrated with UO of 200-
300mL/hr
Alkalinization of urine & Mannitol diuresis
Heme pigment-induced ATN: HemolysisHeme pigment-induced ATN: Hemolysis

26. Acute Interstitial NephritisAcute Interstitial Nephritis
Methicillin induced AIN
Symptoms- 2 to 3 wks after initiation of T/t
•Hematuria
•Pyuria with WBC casts
•Proteinuria < 1g/d
•Renal failure in 50% of patients
Extrarenal manifestations:
•Fever ,Eosinophilia, Rash, Arthralgias
Pathologic hallmark –inflam. Cells in interstitium.
Treatment Supportive t/t
Discontinue offending drug
Prednisone 1mg/kg/d for 4 weeks

27. MANAGEMENT OF ARFMANAGEMENT OF ARF
Prevention
Optimization vascular hemodynamics.
Discontinuation of offending drugs (NSAID & COX-2inhibitors).
Avoid nephrotoxic medications ( high-risk patients)
Using alternative imaging techniques such as MRI scanning.

28. PHARMACOLOGICAL TREATMENT
1)Dopamine: (0.5-2µg/kg/min)-- has shown no
evidence of benefit in pts with acute oliguric renal failure
MOA : RPF, GFR, Na excretion
2)Loop diuretics :
adv: urine flow wash out of obstructing intra luminal
cellular debris & caste.
-dosen’t converts oliguric RF to non oliguric RF
3)ANP:
MOA :dilate afferent arteriole &constrict efferent arteriole
4) FENOLDOPAM:
5) NAC (>1200mg/d bd, 48 hr)

29. No evidence of volume overload or cardiac failure
isotonic saline, 20 mL/kg over 30 min or more.

fails to void within 2 hrs
suspect intrinsic or postrenal ARF.

Furosemide (2–4 mg/kg) single IV dose

urine output not improved
continue diuretic infusion(lasix 40mg/hr,double the rate every 12hr to
achieve U/O 100ml/hr, max dose 169mg/hr).
no response to a diuretic challenge
Discontinue diuretics and restrict fluid

Fluid therapyFluid therapy

30. Euvolemic
vol replacement -
400 mL/m
2
/24 hr + U/O + extrarenal fluid loss

appropriate fluids
-insensible losses replaced by 5-10% dextrose
- urinary losses with N/2 saline
- preferable to give fluids by mouth
- potassium not given in oliguric patients
- daily weight, urine I/O, S.electrolytes should be monitored
fluid overloaded
- fluid restriction

31. Dilutional hyponatremia fluid restriction
 Symptomatic hyponatremia (seizures, lethargy) or
S. Na+ <120 mEq/L…Hypertonic(3%) saline.
Acute correction of S. Na+ to 125 mEq/L should be
accomplished using the following formula:
Nacl req. = 0.6 x weight x [125 – S. Na]
Severe hypernatremia (Na> 150 mEq/L): dialysis or
hemofiltration
sodiumsodium

32. Oliguric renal failure is often complicated by hyperkalemia, increasing the risk in cardiac arrhythmias
Treatment of hyperkalemia:
Restriction of dietary k+
Eliminate k+ supplement & k+ sparing diuretics
Loop diuretics
Calcium gluconate
insulin + hypertonic dextrose: 1 unit of insulin/4 g glucose
K+ binding resin
sodium bicarbonate (1-2 mEq/kg)
Inhaled ß agonist therapy
• sodium polystyrene (Kayexalate): 1 gm/kg . Can be repeated qh. (Hypernatremia and hypertension are potential
complications)
• dialysis
potassiumpotassium

33. Metabolic acidosis
Severe acidosis(pH <7.15; S.HCO3 <8 mEq/L) or assoc.
hyperkalemia treatment is required.
T/t- IV NaHCO3( pH > 7.2 or HCO3- >15 meq/l).
Nutrition
Provide adequate caloric intake( 50-60 Cal/kg/d)
Limit protein intake- (0.6-0.8 gms/kg/d in older children)
Minimize K+ & phosphorus intake(1 mEq/kg/d K+ & 20-25
mg/kg Phosphorus /d)
Limit fluid intake

34. Indications for RRT in ICUIndications for RRT in ICU
Renal
Uremia : azotemia(>30mmol/l,)
pericarditis, neuropathy, myopathy,
encephalopathy
Overload of fluids: pul edema,
oliguria/ anuria (u/o<200ml/12hr)
Electrolytes : hyperkalemia (K>6.5),
Na+(>160 or<115mmol/l)
Acid – base : metabolic acidosis
(pH<7.1)
Intoxications : with dialyzable
toxins

Non renal
Allowing administration of fluids
and nutrition
Hyperthermia
Severe hemodynamic instability
in severe sepsis
Elimination of inflammatory
mediators in sepsis

35. Post dialysis management Post dialysis management

36. Complication after Haemodialysis Complication after Haemodialysis
Hypotension — 25 to 55 %
Cramps — 5 to 20 %
Nausea and vomiting — 5 to 15 %
Headache — 5%
Chest pain — 2 to 5 %
Back pain — 2 to 5 %
Itching — 5 %
Fever and chills — Less than 1 %

37. 1) Hypotension 1) Hypotension
Usual manifestation of hemodynamic instability
patients with hemodialysis-associated hypotension
appear to have increased mortality.
Two clinical patterns
Episodic hypotension,
- occurs during latter stages of dialysis;
- associated with vomiting, muscle cramps, and
other vagal symptoms (such as yawning).
Chronic persistent hypotension
- patients with predialysis SBP<100 mmHg.

38. EtiologyEtiology
Rapid reduction in plasma osmolality, ECF  ICF
Rapid fluid removal in an attempt to attain "dry weight"
Autonomic neuropathy
Diminished cardiac reserve.
Use of acetate rather bicarbonate as a dialysate buffer.
Intake of antihypertensive medications
Lower Na+ conc. in the dialysate
Arrhythmias/pericardial effusion/tamponade,
Reactions to the dialyzer membrane
Inc synthesis of endogenous vasodilators(NO).
Sudden release of adenosine during organ ischemia
High magnesium concentrations in the dialysate.
Failure to inc plasma vasopressin levels.

39. Diagnosis and treatmentDiagnosis and treatment
Although occasionally asymptomatic, but
hypotension -
◦light-headedness.
◦muscle cramps.
◦Nausea & vomiting.
◦dyspnea.
Management :
- Trendelenburg position.
- IVF- mannitol or saline.
- temp controle
Currently use of an IV bolus of saline is the first-line
therapy for hypotension.

40. Cont…Cont…
Midodrine (selective α₁-adr agonist): patients with
autonomic neuropathy & hypotension not responsive
to other measures.
Carnitine .
Adenosine receptor antagonist. 
Vasopressin infusion. 

41. 2) 2) Muscle CrampsMuscle Cramps
common complication
Muscle of lower extremities
Low PTH Values and high serum Creatin
phosphokinase is frequent finding
Etiology
Plasma volume contraction.
Tissue hypoxia
Hyponatremia.
Hypomagnesemia.
Carnitine deficiency.

42. Managenent of Muscle crampManagenent of Muscle cramp
◦Prevention of dialysis-associated hypotension.
◦High conc. of sodium in the dialysate.
◦Carnitine supplementation
◦Administration of quinine ↓excitability of the motor
end-plate to nerve stimulation & inc. muscle refractory
period, thereby preventing prolonged involuntary
muscle contraction.
◦Other t/t- benzodiazepines (eg, oxazepam), nifidepine,
phynetoin, creatine monohydrate, carbamezapine,
amitryptalyin, and gabapentin.

43. 3) Headach, Nausea & Vomiting3) Headach, Nausea & Vomiting
Longer dialysis times & large degree of urea removal -
4) 4) Dialysis disequilibrium Syndrome(DDS)Dialysis disequilibrium Syndrome(DDS)
Neurological symptoms- d/t to cerebral edema.
New patient started on HD especially with high BUN.
Other risk factor - sever metabolic acidosis , extremes of
age , presence of CNS diseases like seizure disorders.

44. Clinical ManifestationClinical Manifestation
The classic DDS develops during or immediately after
hemodialysis. Early findings include
◦Headache
◦Nausea
◦Disorientation
◦Restlessness
◦Blurred vision
◦Asterixis
More severely affected patients progress to
confusion, seizures, coma, and even death.
t/t - self-limited & Symptomatic t/t

45. HemolysisHemolysis
May present as chest pain & tightness, or back pain &
If it is not recognized early, severe hyperkalemia
prepare to treat hyperkalemia & potentially severe
anemia
observation since life-threatening hyperkalemia may
develop after dialysis has been terminated.

46. CHEST PAINCHEST PAIN
could be associated with
hypotension
DDS
Angina
Hemolysis
Air or pulmonary embolism (rare).

47. 1.MILLER’S ANESTHESIA
2.MORGAN’CLINICAL ANESTHESIOLOGY
3.HARRISON’S INTERNAL MEDICINE
4.ICU BOOK PAUL L MARINO
5.ACUTE DIALYSIS QUALITY INTIATIVE GROUP CONCENSUS
6.IRWIN & RIPPE’ ICM
ReferencesReferences

48. THANK YOUTHANK YOU