Intensive care nephrology

1. Intensive Care Nephrology
Dr. Osama El-Shahat
Head of Nephrology Department
New Mansoura General Hospital (international)
ISN Educational Ambassador

2. Objectives
Acute Kidney Injury
Indications of Acute Dialysis
Complications of Dialysis
Overview of certain drug overdoses and
acute management

3.  By AKI we actually mean “loss of small solute
clearance” (urea/creatinine increase in
blood)
 This implies loss of GFR
 So…clinically we actually mean
“acute decrease in GFR”
What do we mean by AKI?

4. Lameire N, Van BW, Vanholder R. Nat Clin Pract Nephrol 2006; 2: 364–377.
Can we do staging for AKI?

5. What is the advantages of RIFLE Criteria?
 Applying the RIFLE criteria revealed new insights.
 Firstly, the RIFLE classification is feasible and
fairly straightforward.
 Secondly, the patients categorized as RIFLE-F had a
far higher mortality than RIFLE-I and -R patients.
Max Bell et al; Nephrol Dial Transplant 2005 20:354 –360

6. Number of ARF Hospitalizations: 1979 to 2002
Rates per 1,000 persons
0.0
0.5
1.0
1.5
2.0
2.5
1980 1982 1984 1986 1988 1990 1992 1994 1996 1998 2000 2002
Source: National Center for Health Statistics, National Hospital Discharge Survey

7. Kidney International advance online publication , 1
May 2013
Mortality in AKI

8. Causes of AKI
Pre renal Intrinsic renal Post renal
Decrease in
effective
blood volume.
Arterial
occlusion
Or
stenosis.
Homodynamic
Form.
Vascular
Vasculitis.
Malignant
hypertension
Acute
Glomerulo
nephritis
Acute
Interstitial
nephritis
Acute
Tubular
necrosis
Ischemic. Nephrotoxic.
Obstruction
Of
Collecting
System
Or
Extra renal
drainage
Exogenous
Antibiotic
Radio contrast
cisplatin
Endogenous
Intra tubular pigment
Intra tubular protein.
Intra tubular crystal.

9. Causes of AKI
Post-OP, sepsis,
shock,multi-organ
failure 70%
Obstructive
uropathy 15%
Glomerulonephritis 5%
Nephrotoxic agents 10%
reduced blood flow
ischemia
acute tubular necrosis

10. Timing nephrology consultation
(Mehta, Am J Med 2002)
In-hospital mortality
Early
consult
Delayed
consult
P
40% 67% <0,001
 Early nephrologist involvement in patients with AKI
may reduce the risk of a further decrease in kidney
function.
Am J Kidney Dis. 2011;57(2):228-234

11. Kidney International (2013) 83, 901–908
Early Referral

12. Biomarkers are foot prints of actual organ
damage
 Creatinine Not A Biomarker
 The creatinine level is influenced by multiple non-
renal factors, such as age, gender, muscle mass, muscle
metabolism, diet, medications, and hydration status
 In AKI, the serum creatinine level can take several
hours or days to reach a new steady state and thus does
not reflect the actual decrease in GFR in the acute
setting
 Because of renal reserve, the serum creatinine level
may not rise until more than half of the kidney
function has been lost

13. New urinary biomarkers for the early detection of acute
kidney disease
Han, Bonventre,Current Opin Crit Care 2004, 10:476–482
Neutrophil gelatinase associated lipocalin

14. Early detection of AKI by Cystatin C
Definition of AF
Area under the ROC
Day - 2 Day - 1 Day 0
≥ 50 % increase 0.82 0.97 0.99
≥ 100 % increase 0.92 0.98 0.98
≥ 200 % increase 0.97 0.99 0.99
•Changes in cystatin C were able to detect the onset of AKI
one to two days earlier than comparable changes in serum creatinine
1. RIFLE- R ( ≥ 50 % increase ): 1.5 ± 0.6 days earlier
2. RIFLE- I ( ≥ 100 % increase): 1.2 ± 0.9 days earlier
3. RIFLE- F ( ≥ 200 % increase): 1.0 ± 0.6 days earlier
Herget-Rosenthal et al, Kidney Int 2004, 66: 1115- 1122

15. Indications of Renal Biopsy
1
Urine
No cast
FENa<1%
Muddy
brown cast
FENa>1%
Red cell
cast
White cell
cast
eosinophil
Pre-renal
ATN Glomerular Interstitial
Biopsy
2. Unknown cause
3. Prolonged ATN

16. Loop diuretics in AKI
Diuretics, particularly high doses of loop diuretics, are frequently
administered to patients with acute renal failure. This is done in part
in an attempt to convert oliguric to nonoliguric acute renal failure.
However, a retrospective observational report found that the use of
diuretics in this setting may increase the risk of death and no
recovery of renal function.
3.4.1: We recommend not using diuretics to prevent AKI. (1B )
3.4.2: We suggest not using diuretics to treat AKI, except in the
management of volume overload. (2C )

17. There is insufficient evidence that the low-dose dopamine
improves survival or obviates the need for dialysis in persons with
acute renal failure. The routine use of low-dose dopamine should be
discouraged until a prospective, randomized, placebo-controlled trial
establishes its safety and efficacy.
Is the administration of dopamine associated with adverse or
favorable outcomes in acute renal failure? Auriculin Anaritide
Acute Renal Failure Study Group.
Low Dose Dopamine in AKI
3.5.1: We recommend not using low-dose dopamine to prevent or
treat AKI. (1A)

18. IV Fluids in AKI
3.1.1: In the absence of hemorrhagic shock, we
suggest using isotonic crystalloids rather than
colloids (albumin or starches) as initial
management for expansion of intravascular
volume in patients at risk for AKI or with AKI.
(2B)

19. Contrast Induced AKI
4.4.1: We recommend i.v. volume expansion with either isotonic sodium
chloride or sodium bicarbonate solutions, rather than no i.v. volume expansion,
in patients at increased risk for CI-AKI. (1A)
4.5.1: We suggest not using prophylactic intermittent hemodialysis (IHD) or
hemofiltration (HF) for contrast-media removal in patients at increased risk for
CI-AKI. (2C)
4.4.3: We suggest using oral NAC, together with i.v. isotonic crystalloids, in
patients at increased risk of CI-AKI. (2D)
4.3.2: We recommend using either iso-osmolar or low-osmolar iodinated
contrast media, rather than high-osmolar iodinated contrast media in patients
at increased risk of CI-AKI. (1B)

20. Bicarbonate or Saline
Among the large
randomized trials there
was no evidence of benefit
for hydration with sodium
bicarbonate compared
with sodium chloride for
the prevention of CI-AKI.
Contrast Induced AKI

21. Stage-based management
General Principles
Stage 1 (Risk)
Risk for more severe AKI
Monitor (prevent
progression)
Stage 2 (Injury)
Risk of AKI-related
mortality/morbidity high
Conservative therapy)
Stage 3 (Failure)
Highest risk of death
Consider RRT
Avoid subclavian catheters if possible
Discontinue all nephrotoxic agents when possible
Consider invasive diagnostic workup
Consider Renal Replacement Therapy
1 2 3
Non-invasive diagnostic workup
Ensure volume status and perfusion pressure
Check for changes in drug dosing
AKI Stage
Consider functional hemodynamic monitoring
Monitoring Serum creatinine and urine output
Consider ICU admission
Avoid hyperglycemia
Consider alternatives to radiocontrast procedures

22. Indications for RRT in critically ill AKI patients
Renal Indications
Life-threatening indications
Hyperkalemia
Metabolic Acidosis
Pulmonary edema
Uremic omplications

23. Dialysis Interventions for Treatment of AKI
 5.1.1: Initiate RRT emergently when life-threatening
changes in fluid, electrolyte, and acid-base balance
exist.(Not Graded)
 5.1.2: Consider the broader clinical context, the presence
of conditions that can be modified with RRT, and trends
of laboratory tests—rather than single BUN and
creatinine thresholds alone—when making the decision
to start RRT. (Not Graded)

24. Indications for RRT
Renal Indications
Life-threatening indications
Hyperkalemia
Metabolic Acidosis
Pulmonary edema
Uremic complications
Non Renal Indications
Fluid removal in congestive heart
failure& Fluid management in
multiorgan failure
Cytokine manipulation in sepsis
Treatment of drug overdose
Nutrition support

25. Hyperkalemia
Renal failure is the most common cause of
Hyperkalemia in E.R.
Clinically significant Hyperkalemia occurs in
10–15% of patients requiring hemodialysis
(H.D.).
The rate of rise of serum K in ARF is usually
rapid and RX must be aggressive.

26. (Cont.)Hyperkalemia
 Mild ↑K : 5.5 - 6 mmol/l.
 Moderate ↑K : 6.1 - 6.9 mmol/l.
 Severe ↑K : > 7 mmol/l.

29. (Cont.)Hyperkalemia
The definitive management of severe
hyperkalemia in patients with CKD
HEMODIALYSIS**

30. (Cont.)Hyperkalemia
Initial management:
 Ca gluconate .
 Insulin with glucose.
 Salbutamole.
 Na HCO3.
 Na Polystyrene sulphate./Ca Resonium.

31. Management
Ca gluconate.
 Antagonizes cardiac membrane excitability
and does not affect the plasma K level.
 10% Ca gluconate IV over 5-10 min. and to
be repeated if necessary.
 Onset of action is immediate but its duration
is only a few min.

32. Management
Glucose-Insulin.
Insulin binds to specific membrane
receptors and via an unknown second
messenger stimulates (Na-K) ATP pump
resulting in intracellular uptake of K

33. Comparison of Clinical studies of
Insulin with Glucose
Reference
Sample
Size
Dose
of
Soluble
Insulin
Dose
Glucose
Mean
Initial
K(mmol)
Peak
Reduction
in K
(mmol)
Time of
Maximal
Action
(min)
Duration
of Effect
(min)
Hypogly
cemia
(%)
Kim HJ 8 5 40g 6.3 0.7 60 >60 0
Lens
XM
10 10U 40g 6.7 1.0 60 >360 20
Allon M 5 5* 60g 4.28 0.85 60 >60 0
Allon M 12 10U 25g 5.48 0.65 45 >60 75
Blombe
rg A
10 5* 5† 5.62 0.92 60 >60 50

34. Management (Cont)
Salbutamol:
Binds to β2 receptors in liver and muscle cells
stimulating adenylate cyclase that converts
ATP to 3,5 CAMP.
3,5 CAMP stimulates the Na-K ATP pump
resulting in intracellular K uptake.

35. Comparison of Clinical Studies of
salbutomol
Duration of
effect /min
Time of
Maximal
action/min
Peak
Reduction
K (mmol)
Mean
Initial K
(mmol/L)
Dose
Sample
Size
ReferenceRoute
>120401.486.74ug/kg13Kim HJIV
>360301.47.00.5mg24Lgutic DIV
>180300.925.530.5mg15Allon MIV
>120900.625.9310mg10Salem MMNeb
>120900.985.8120mg10Wrenn KDNeb
>180900.855.6610mg15Du-PLooyNeb

36. Comparison of studies of combined
Salbutamol and Insulin with Glucose
Size
Dose
Soluble
Insulin
Dose
Gluc
Route
Salb
Dose
Mean
Initial
K
(meq)
Peak
Reduct
K (meq)
Time of
Maximal
Action
(min)
Duration
of
Effect
(min)
Liou
HH
10 10U 40g IV 0.5mg 7.1 1.5 60 >360
Allon
M
10 10U 25g Neb 20mg 5.89 1.21 60 >60

37. Management (Cont)
Sodium Bicarbonate.
Na HCO3 has been recommended in
textbooks for many years.
It has no significant action on plasma K in
the first 60 min. after administration

38. Management (Cont)
Sodium polystyrene sulphonate (Kayexelate)
It may be indicated if HD is delayed (>2-3
Hs).
50 g kayexalate in 100-200 ml of 30%
sorbitol or 10% glucose at 37o C is given
rectally and left at least 60 min.
The onset of action is slow ( 1-2 hours ).

39. Management (Cont)
Hemodialysis.
The definitive and most effective measure in
treatment of hyperkalemia.
Indicated in severe hyperkalemia.
K concentrations show a rebound after
dialysis has finished and this rebound may
require several hours to reach a plateau.

40. Fluid Overload
 Interventions that are useful in patients
with functioning kidneys also are useful in
patients with ESRD before dialysis can be
initiated.
 Patients on CAPD with volume overload are
managed differently.

41. Serious Complications Of Hemodialysis.
 Central line related complications.
 Disequilibrium syndrome.
 Dialyzer reaction type A (anaphylactic).
 Hemolysis.
 Air embolism.

42. Disequilibrium Syndrome
 During or immediately after dialysis.
 Acute increase in brain water or acute changes
in pH of CSF during dialysis.
 Minor symptoms: nausea, vomiting, dizziness,
headache, blurred vision, restlessness, cramps,
tremors.
 Major symptoms: confusion, psychosis, seizures,
coma.

43. Disequilibrium Syndrome (cont)
Management.
If seizures, obtundation or coma occur
during dialysis.
Stop dialysis.
Protect airway.
Blood work for Gluc, Ca, U&E.
Differential diagnosis?

44. Disequilibrium Syndrome (cont)
Management.
Treat hypoglycemia.
Seizures (valium – phenytoin).
Prevention is better
 short dialysis session
 small surface area dialyzer
 avoid low Na dialysate.

45. Pericarditis
Dialysis associated pericarditis
Etiological factors:
Infections. (bacterial , viral)
Hypercatabolic state
Volume overload
Hyperparathyroidism
Hyperuricemia
Malnutrition

46. Management of Pericarditis
Uremic Pericarditis
Stable Hemodynamics
Intensive Dialysis
Signs of Tamponade,
Enlarging effusion,
Unchanged effusion
Pericardiotomy
or
Pericardiectomy
Resolution
Unstable hemodynamics
Signs of Tamponade
Emergency
Pericardiocentesis
Pericardiotomy
Or
Pericardiectomy

47. Drug Overdose
 Recognition of poisoning and drug overdose
require high index of suspicion and careful
clinical evaluation.
 Multiple drugs overdose is common.

48. Role of Dialysis
in
Drug Overdose

49. Peritoneal Dialysis (P.D.)
Not very effective in removing drugs from the
blood.
It is 1/8 to 1/4 as effective as hemodialysis.
When HD is difficult to be used quickly as in
small children, P.D. can be used.

50. Hemodialysis
Great for water soluble drugs especially
those of low MW .
(Salicylates, Ethanol, Methanol, & Lithium)
Not very useful in removing lipid soluble
drugs or with drugs with extensive protein
binding

51. Serum Concentrations of Common Poisons in Excess of
Which hemodialysis or hemoperfusion Should Be
Considered
Drug
Serum Conc
mg/L
Method of
choice
Phenobarbital 100 HP>HD
Glutethimide 30-40 HP
Methaqualone 40 HP
Salicylates 80 HD
Theophylline 40 HP>HD
Paraquat 0.1 HP>HD
Methanol 500 HD
Trichloromethanol 500 HP>HD
Meprobamate 100 HP

52. Conclusions
 Early detection and treatment of AKI may improve outcomes.
 Even a minor acute reduction in kidney function has an
adverse prognosis.
 Hunting AKI in ICU….use a RIFLE .
 Early referral will improve outcome
 In emergency cases medical treatment must be initiated until
dialysis started.
 Dialysis therapy is invasive procedure with many
complications, some of them are very serious
 Renal replacement therapy has important role in
management of drug over dose.