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Hala Kilany, MD.

TREATMENT OF AKI

EVALUATE AND TREAT ACCORDING TO ETIOLOGY

PRERENAL:
-correct hypovolemia
-assess risk factors
-avoid: nephrotoxic drugs, contrast
media, ACEis, ARBs
POSTRENAL:
-refer to a urologist
-immediate relief of the obstruction

ATN

The most common cause of AKI.


The treatment is largely supportive,
related to complications of AKI.

FLUID AND ELECTROLYTES

Fluid balance can be maintained by


replacing insensible losses (400-600
ml\d), and replace measured losses:
-urine
-gastric drainage
-diarrhea
liter for liter with 0.45% saline.

Fluid management in nonoliguric AKI


tends to be easier.
These patients should receive a volume
of fluid= urine volume + insensible
losses.

OLIGURIA

Loop diuretics: high doses IV.


-no role for diuretics if in hypovolemia.
-consider loop diuretics only if
hypervolemia or edema.

DIURETICS

Several theoretical benefits:


- in case of intratubular obstruction, the
increase in tubular flow will flush out
obstructed tubules.
-loop diuretics could increase flow and
by inhibiting: Na+-K+-2Cl- transporter
in the TALH, decrease medullary O2
demand.

DIURETICS

Conversion from oliguric to non-oliguric


AKI has not been shown to decrease
mortality, but it may facilitate fluid and
electrolytes management.

METABOLIC COMPLICATIONS

Hyponatremia.(Nl: 136-145meq\l)
Hyperkalemia.(Nl:3.5-5.1 meq\l)
Hypocalcemia.(Nl:8.6-10.2mg\dl)
Hyperphosphatemia. (Nl:2.2 - 4.8
mg/dl)
Hypermagnesemia.(Nl:1.7-2.5mg\dl)
Hyperuricemia.(Nl:2.5-5.6mg\dl)
Metabolic acidosis.( Nl HCO3:22-29
meq\l)

NORMAL EKG

HYPERKALEMIA

HYPERKALEMIA

Restriction of dietary potassium


Discontinue K+ supplements or K+-sparing
diuretics
K+-binding resin
Loop diuretic
Glucose (50 mls of 50%) +
insulin (1015 U regular) IV
Sodium bicarbonate (50100 meq IV)
Calcium gluconate (10 mLs of 10% solution
over 5min)
Dialysis.

METABOLIC ACIDOSIS

Bicarbonte IV.
Dose: 0.5 x body weight x HC03Attention:
volume overload

HYPONATREMIA

Water restriction +/- diuretics: loop


diuretics.

Dialysis

CARDIOVASCULAR

Pulmonary edema: -loop diuretics


-dialysis
Hypertension: -salt restriction
-loop diuretics
-avoid: ACEis and ARBs
Pericarditis: -absolute indication for
dialysis
-anticoagulation is
contraindicated
Arrhythmias.

NEUROLOGIC

Asterixis.
Neuromuscular irritability.
Myoclonus.
Somnolence.
Seizures.
Coma.
Treatment: dialysis

HEMATOLOGIC

Anemia:
-Target: Hgb: 11-12g/dl
-causes:erythropoietin deficiency is the primary cause
of anaemia associated with renal failure.
Erythropoietin is predominantly produced by
peritubular cells in the kidney and is the hormone
responsible for maintaining the proliferation and
differentiation of erythroid progenitor cells in the bone
marrow.
Loss of peritubular cells leads to an inappropriately
low level of circulating erythropoietin in the face of
anemia.

OTHER CAUSES OF ANEMIA:

Iron deficiency
Blood loss/ hemorrhage
Hemolysis
Malignancy: multiple myeloma
Infection/inflammation
Vitamin B12 and folate deficiency
Pure red cell aplasia

TREATMENT OF ANEMIA

Treat the cause.


Erythropoietin

GASTRO-INTESTINAL

Nausea.
Vomiting.
Bleeding.
Treatment: Dialysis

INFECTIOUS

Pneumonia.
Bacteremia, e.g., secondary to dialysiscatheter infection.
Wound infection.

NUTRITIONAL SUPPORT

AKI is a state of metabolic stress.


Catabolism of protein stores to support
gluconeogenesis can result in marked
muscle and visceral protein wasting
and is associated with excess morbidity
and mortality.

THE FOLLOWING RECOMMENDATIONS

Protein and non-protein calories should


be provided to meet calculated energy
expenditure, at a rate not to exceed:
1.5g\kg\d protein intake.
Total parenteral nutrition should be given
only to patients:
-severely malnourished
-expected not to be able to eat > 14 days
Enteral feeding is preferred to TPN.

COMPLICATION
Intravascular Volume
Overload

Hyponatremia
Hyperkalemia

TREATMENT
Restriction of salt (<11.5 g/day) and
water (<1 L/day)
Consider diuretics (usually loops +/thiazide)
Ultrafiltration
Restriction of oral and intravenous free
water
Restriction of dietary potassium
Discontinue K+ supplements or K+sparing diuretics
K+-binding resin
Loop diuretic
Glucose (50 mls of 50%) + insulin (10
15 U regular) IV
Sodium bicarbonate (50100 meq IV)
Calcium gluconate (10 mLs of 10%
solution over 5 min)
Dialysis/hemofiltation

COMPLICATION

TREATMENT

Metabolic Acidosis

Restriction of dietary protein

Sodium bicarbonate (if HCO3- <15


mEq/L)
Dialysis/hemofiltation
Restriction of dietary phosphate
intake
Phosphate binding agents (calcium
carbonate, calcium acetate,
sevalemer)
Calcium carbonate (if symptomatic or
sodium bicarbonate to be
administered)
Discontinue magnesium containing
antacids
Restriction of dietary protein (<0.8
g/kg/day up to 1.5 g/kg/day on
CVVHD) 2530 kcal/day
Enteral route of nutrition preferred
Adjust all doses for GFR and renal
replacement modality
Clinical evidence of uremia

Hyperphosphatemia

Hypocalcemia
Hypermagnesemia
Nutrition

Drug Dosage
Absolute Indications for RRT

Intractable volume overload

CONSIDERATIONS WHEN STARTING DIALYSIS

Whether or not to provide dialysis, and if


so, when, are 2 fundamental questions
facing nephrologist in most cases of ARF.

Initiation of dialysis.
Dose of dialysis
Modality of dialysis
Type of dialysis membrane.

DILAYSIS

Guidelines for initiation of dialysis:


1. Oliguria (<400 ml\d)
2. Anuria
3. Serum creatinine > 6-7 mg\dl
4. Pulmonary edema unresponsive to
conservative therapy
5. Hyperkalemia
6. Symptomatic uremia: encephalopathy,
pericarditis
7. Metabolic acidosis.
8. Certain drugs and alcohol intoxication.

MODALITY OF DIALYSIS

Intermittent hemodialysis

Continuous dialysis

INTERMITTENT HD

IHD

Initially short: 2 hours, then alternate day: 3-4


hours.
Intermittent hemodialysis (IHD) is currently
the standard form of therapy worldwide for
treatment of ARF in both intensive care unit
(ICU) and non-ICU settings.
The vast majority of IHD is performed using
single-pass systems with moderate blood flow
rates (200 to 250 mL/min) and countercurrent
dialysate flow rates of 500 mL/min.

DRAWBACKS

Although this method is very efficient,


it is also associated with hemodynamic
instability resulting from the large shifts
of solutes and fluid over a short time.

MECHANISMS OF SOLUTE TRANSFER

Diffusion
Convection

DIFFUSIVE CLEARANCE

A result of random molecular motion


Influenced by concentration gradient of
the solute and its Molecular weight as
well as by the membrane permeability
to the solute

CONVECTIVE CLEARANCE

Water molecules passing through a


SPM carry with them the solutes. This is
called the solvent drag phenomenon
Water can be made to move across a
SPM by the application of either a
hydrostatic or an osmotic gradient

Principle:
Solute transfer across
semipermeable membranes
along concentration
gradients (diffusion)
Counter current flow for
optimized efficacy
Selectivity:
Low (dialysate composition)
Efficacy:
High for small molecular
weight substances (urea,
creatinine, electrolytes,
buffer...)
Low for higher molecular
weight substances (small
proteins, mediators, etc.)

Central venous catheter:

CATHETER INSERTION

CATHETER INSERTION

When choosing a vein for insertion of a dialysis


catheter in patients with AKI, consider these
preferences (Not Graded):
First choice: right jugular vein;
Second choice: femoral vein;
Third choice: left jugular vein;
Last choice: subclavian vein with preference
for the dominant side.
http://www.kidney-international.org chapter 5.4
& 2012 KDIGO
Kidney International Supplements (2012) 2, 89115 1

TYPES OF VASCULAR ACCESS

Native AVF

Synthetic graft:
-can be used earlier.
-more clotting
-more thrombosis