The document discusses acute kidney injury (AKI) in critically ill patients. It covers definitions and criteria for AKI, common causes like sepsis and surgery, evaluation, management including fluid resuscitation and renal replacement therapy, and electrolyte disorders that can occur with AKI like hypernatremia, hypokalemia, hypomagnesemia, hypocalcemia, hypophosphatemia, and hyperphosphatemia. AKI is common in ICU patients, affecting 70% and requiring renal replacement in 5%, with mortality up to 70% in those requiring hemodialysis.

2. Renal disorders
Electrolytes disorder
Hypo and hypernatremia
Hypo and hyper kalemia
Hypo and hyper magnesimea
Hypo and hyper phosphatemia
Hypo and hyper calcemia
CONTENTS

4.  Renal dysfunction that occurs in critically ill patients
 Statistics of ICU patients:
 70% have some degree of renal dysfunction
 5% require renal replacement
 Mortality rate of patients who require hemodialysis 50–70%
 Diagnostic criteria :
 RIFLE criteria
 AKIN criteria
ACUTE KIDNEY INJURY

5. Acute Dialysis Quality
Initiative (ADQI) in 2002.
5 categories consist of:
 3 severity
 2 clinical outcome
Limitations:
i. No defined e period for change
in serum creatinine
ii. Minimum change in serum
creatinine required for the
diagnosis of AKI is considered
too large.
I. RIFLE CRITERIA

6. Revised criteria by Acute Kidney Injury Network (AKIN)
which have:
a smaller change in creatinine (≥0.3 mg/dL)
a time limit of 48 hours on the change in serum creatinine.
II. AKIN CRITERIA

7. Based on location of the
insult:
Prerenal disorders (30–40% )
 Decrease in renal blood flow
Renal disorders
 Acute Tubular Necrosis (50%)
 Result of renal hypoperfusion,
inflammatory injury in epithelial lining
tubules by tubuloglomerular feedback
 Severe sepsis and septic shock,
radiocontrast dye, nephrotoxic drugs
 Acute Interstitial Nephritis
 Inflammatory injury in the renal
interstitium
Postrenal obstruction(10% )
 Obstruction distal to the renal
parenchyma
 Distal portion of the renal collecting
ducts (papillary necrosis),
 The ureters (extraluminal obstruction
from a retroperitoneal mass),
 Urethra (strictures)
CATEGORIES OF ACUTE KIDNEY INJURY

8.  Sepsis (50%)
 Major surgery, particularly cardiopulmonary bypass
 Major trauma victims (30%)
 Rhabdomyolysis (30% )
 Nephrotoxic drugs and radiocontrast (20% )
 Increased abdominal pressure
COMMON CAUSES

9.  USG (postrenal obstruction)
 To determine prerenal disorder or renal disorder
EVALUATION

10. Volume infusion to promote
renal blood flow
Fluid challenge when prerenal
causes is ruled out
Discontinuing any
nephrotoxic drugs
LIST OF NEPHROTOXIC
DRUGS
Treating any conditions that
predispose to AKI
Examples:
 Contrast- induced renal injury: IV
hydration, high-dose N-
acetylcysteine
 AIN : re-solves spontaneously
after discontinueing offending
INITIAL MANAGEMENT

11.  70% of patients with acute renal failure will require some form of renal replacement
therapy (RRT).
 Indications :
a) Volume overload
b) Life threatening hyperkalemia or metabolic acidosis
c) Removal of toxins
RENAL REPLACEMENT THERAPY

12. Hemodialysis
 Diffusion
 Countercurrent exchange
technique
 Advantages:
 Rapid clearance of small solutes.
 Disavantages
 Limited removal of large molecules
 Risk of hypotension as need to maintain
a blood flow of 200–300 ml/min through
the dialysis chamber
Hemofiltration
TECHNIQUES
 Convection
 Continuous arteriovenous
hemofiltration (CAVH) or continuous
venovenous hemofiltration (CVVH)
 Advantages
 Allows more gradual fluid removal
 Removes larger molecules than
hemodialysis
 Disadvantage
 Slow solute removal

15.  25% of ICU patients.
 Can be due to :
 Loss of sodium and water ( hypotonic fluid loss)
 Free water loss
 Gain of sodium and free water (gain of hypertonic fluid)
 Causes increase in the effective osmolality of the extracellular fluid (hypertonicity)
 HYPERNATREMIC ENCEPHALOPATHY
 Mechanisms : shrinkage of neuronal cell bodies and osmotic demyelination
 Mortality rate as high as 50% (9)
1.HYPERNATREMIA

17.  <135 mEq/L
 in 40–50% of ICU patients.
 Condition can present as :
 Hypotonic
 Isotonic
 Eg.Pseudohyponatremia
(plasma lipid level > 1,500 mg/dL or the plasma protein levels >12–15 g/dL)
 Hypertonic
 Eg.Non ketotic hypergycemia
2.HYPONATREMIA

18. PREDISPOSING FACTORS

19. Pharmacotherapy to
be considered:
Demelocycline
Vasopressin antagonist
 Conivaptan
 Tolvaptan

20.  Distribution
 Sodium-potassium exchange pump 3:2 ratio
 Total body potassium: 50–55 meq per kg body weight
 98% intracellular (350meq)
 2% extracellular (70 meq)
 0.4% plasma (15meq)
 Excretion
 Stool (5–10 mEq/day)
 Sweat (0–10 mEq/day)
 Urine (40–120mEq/day)
POTASSIUM

21. Serum K+ <3.5 meq/L
Can be due to :
 Transcellular shift
 Β2 adrenergic receptors stimulation,
alkalosis, hypothermia, insulin.
 Potassium depletion
3. HYPOKALEMIA

22. Clinical features
 Asymptomatic
 Severe (<2.5 meq/L)
 Muscle weakness
 ECG abnormalities
 Prominent U waves ,
 Flattening and inversion of T waves,
 QT interval prolongation
Management
 Eliminate any condition that
promotes transcellular potassium
shifts
 If due to K+ depletion :
 20 mEq of K+ and 100 mL of
isotonic saline IV, infuse over 1 hour
at maximum rate of 20 mEq/hr

23.  Serum K+ >5.5 mEq/L,
Can be the result of :
 Potassium release from cells (transcellular shift)
 High urine K+ (>30 meq/L)
 Acidosis, rhabdomyolysis, tumor lysis syndrome,
 Impaired renal excretion of potassium
 Low urine K+ (<30 meq/L)
4.HYPERKALEMIA

24. Heart block and cardiac arrest.
ECG changes
Appear at 7 meq/L
Tall T wave , P wave amplitude
decreases, PR interval lengthens
P waves disappear and the QRS
complex widens.
Ventricular fibrillation
CLINICAL CONSEQUENCES

25.  Hemodialysis

26.  release of energy from ATP
 functioning of the Na+-K+
exchange pump
 regulates the movement of
calcium into smooth muscle
cells
MAGNESIUM

27.  67% ionized (active) form,
 19% bound to plasma proteins
 14% chelated with divalent anions such as phosphate and sulfate

28.  65% of patients in ICU’s
5.HYPOMAGNESIMEA

29.  b

30. 5% of hospitalized patients.
Predisposing factors :
 Renal insufficiency
 Hemolysis
 Other conditions like diabetic
ketoacidosis (transient), adrenal
insufficiency, hyperparathyroid-
ism
Clinical features
6. MAGNESIUM EXCESS

31.  Hemodialysis.
 Intravenous calcium gluconate (1 g IV over 2 to 3 minutes)
 to antagonize the cardiovascular effects of hypermagnesemia temporarily
MANAGEMENT

32.  In blood coagulation, neuromuscular
transmission, and smooth muscle
contraction
 Most abundant electrolyte in the
human body with 99% bone
 In the soft tissues, 10,000 times
more concentrated than in the
extracellular fluids
 Plasma calcium in:
 Ionized (biologically active)
 Complexed (biologically inactive)
 80% bound to albumin,
 20% to plasma anions such as proteins and
sulfates.
CALCIUM

33.  causes
7. HYPOCALCEMIA

34.  Major consequences :
 enhanced cardiac and neuromuscular excitability,
 reduced contractile force in cardiac muscle and vascular smooth muscle.
 Neuromuscular
 tetany ,hyperreflexia, paresthesias, and seizures
 Cardiovascular
 hypotension, decreased cardiac output, and ventricular ectopic activity.
CLINICAL MANIFESTATIONS

35.  Dosing Regimen
 bolus 200 mg elemental calcium (diluted in 100 mL isotonic saline and given over 5–10
minutes)
 continuous infusion at a rate of 1–2 mg/kg/hr (elemental calcium) for at least 6 hours.
 Maintenance Therapy
 Daily dose of calcium is 2–4 g in adults
 Oral calcium carbonate or calcium gluconate tablets
MANAGEMENT

36.  Clinical Manifestations
 Gastrointestinal: nausea, vomiting, constipation, ileus, and pancreatitis
 Cardiovascular: hypovolemia, hypotension, and shortened QT interval
 Renal: polyuria and nephrocalcinosis
 Neurologic: confusion and depressed consciousness, including coma
 evident when total serum calcium is >12 mg/dL and almost always present when
the serum calcium is >14 mg/dL
8.HYPERCALCEMIA

38.  serum PO4 <2.5 mg/dL or <0.8 mmol/L
 Can be the result of
 an intracellular shift of phosphorus
 an increase in the renal excretion of phosphorus
 a decrease in phosphorus absorption from the GI tract.
 Predisposing factors : Glucose loading, prolonged hyperglycemia, respiratory alkalosis,
beta-receptor agonist
9.HYPOPHOSPHATEMIA

39.  Energy Metabolism
 Cardiac Output: impair myocardial contractility and reduce cardiac output.
 Erythrocytes: hemolytic anemia
 Oxyhemoglobin Dissociation: shifts the oxyhemoglobin dissociation curve to the left
 Energy Availability: impeding the production of high-energy phosphate compounds (ATP).
 Muscle Weakness
CLINICAL MANIFESTATIONS

40.  Phosphate Replacement
 Recommended for all
patients with
 Severe hypophosphatemia
 Hypophosphatemia of any
degree who also have
cardiac dysfunction,
respiratory failure, muscle
weakness, or impaired
tissue oxygenation.
 Daily maintenance
therapy
 1,200 mg if given orally
 IV at 800 mg/day,
MANAGEMENT

41. Result of impaired PO4
excretion from renal
insufficiency, or PO 4
release from disrupted cells
(e.G., Rhabdomyolysis or
tumor lysis).
Clinical manifestations
The formation of insoluble
calcium–phosphate complexes
(with deposition into soft
tissues),
Acute hypocalcemia (with
Management
 There are two approaches to
hyperphosphatemia.
 promote PO4 binding in the upper
GI tract, which can lower serum
PO4 levels :
 Sucralfate or aluminum-containing
antacids can be used for this purpose.
 Enhance PO4 clearance with
hemodialysis.
 for patients with renal failure
10.HYPERPHOSPHATEMIA

42. REFERENCE