Renal disorders

Electrolytes disorder

Hypo and hypernatremia

Hypo and hyper kalemia

Hypo and hyper magnesimea

Hypo and hyper phosphatemia

Hypo and hyper calcemia

CONTENTS

Renal dysfunction that occurs in critically i l l 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

Acute Dialysis QualityInitiative (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

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

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

Sepsis (50%)

Major surgery, particularly cardiopulmonary bypass

Major trauma victims (30%)

Rhabdomyolysis (30% )

Nephrotoxic drugs and radiocontrast (20% )

Increased abdominal pressure

COMMON CAUSES

USG (postrenal obstruction)

To determine prerenal disorder or renal disorder

EVALUATION

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

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

Hemodialysis

Diffusion

Countercurrent exchangetechnique

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

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

<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

PREDISPOSING FACTORS

Pharmacotherapy to

be considered:

Demelocycline

Vasopressin antagonist

Conivaptan

Tolvaptan

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

Serum K+ <3.5 meq/L

Can be due to : Transcellular shift

Β2 adrenergic receptors stimulation,

alkalosis, hypothermia, insulin.

Potassium depletion

3. HYPOKALEMIA

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

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

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

Hemodialysis

release of energy from ATP

functioning of the Na+-K+

exchange pump

regulates the movement of

calcium into smooth muscle

cells

MAGNESIUM

67% ionized (active) form,

19% bound to plasma proteins

14% chelated with divalent anions such as phosphate and sulfate

65% of patients in ICU’s

5.HYPOMAGNESIMEA

b

5% of hospitalized patients.

Predisposing factors :

Renal insufficiency

Hemolysis

Other conditions like diabetic

ketoacidosis (transient), adrenal

insufficiency, hyperparathyroid-

ism

Clinical features

6. MAGNESIUM EXCESS

Hemodialysis .

Intravenous calcium gluconate (1 g IV over 2 to 3 minutes)

to antagonize the cardiovascular effects of hypermagnesemia temporarily

MANAGEMENT

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

causes

7. HYPOCALCEMIA

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

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

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

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

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

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

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

tetany)

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

REFERENCE