Fluid and Electrolyte Management

Question 1

Body water in term versus preterm….

Answer 1

Water constitutes 70% to 80% of body weight in term born and > 90% in extreme preterm babies

Question 2

Physiological postnatal changes in body water ..?

Answer 2

Soon after birth, there is a rapid weight loss (decrease in total body water),

this weight loss in the first few days of life of a newborn happens due to water loss from extracellular extravascular compartment (interstitial fluid)

Question 3

This physiological contraction of ECF is achieved by …?

Answer 3

physiologic diuresis,

insensible water loss (IWL), and

shift of fluid to intravascular compartment.

Question 4

IWL =

Answer 4

IWL = fluid intake − (urine output + weight loss)

Question 5

the reason for a smaller saline bolus (10 mL/kg) in neonates when compared to 20 to 60 mL/kg in sick children …?

Answer 5

In term born babies, immediately after birth the renal blood flow increases rapidly and GFR rapidly increases over the first 2 weeks.

Before this happens the newborn, in first week of life, cannot excrete a fluid load.

Question 6

the reason to administer electrolyte-free (no sodium or potassium) fluids on the first few days, till diuresis happens..?

Answer 6

The very low GFR (almost similar to end stage renal failure of adult)

Question 7

At what age of life preterm babies are at risk of hyponatremia and reason …?

Answer 7

Preterm babies after 2 weeks of life are at risk of hyponatremia and may need as much as 10 mEq/kg/day (in contrast to 2 to 3 mEq/kg/day in term babies)

Renal tubular function is very immature in preterm babies. This results in polyuria and excess sodium loss after the first 2 weeks of life (after GFR improves)

Question 8

IWL can range from..?

Answer 8

IWL can range from 50 to 200 mL/ kg/day

Question 9

Diagnosis of SIADH…?

Answer 9

Weight gain usually occurs even without edema

Euvolemic hyponatremia

decreased urine output and

increased urine osmolarity

Question 10

Sodium supplements in SIADH….?

Answer 10

Sodium supplementation is not required despite low sodium except if

(i) serum Na concentration is less than approximately 120 mEq/L or

(ii) neurologic signs such as obtundation or seizure activity develop

Question 11

Treatment for symptomatic hyponatremia in SIADH ….?

Answer 11

furosemide 1 mg/kg IV q6h can be initiated while replacing urinary Na excretion with hypertonic NaCl (3%) (1 to 3 mL/kg initial dose).

Fluid restriction alone can be utilized once serum Na concentration is >120 mEq/L and neurologic signs abate.

Question 12

Metabolic acidosis results from…?

Answer 12

1) excessive loss of buffer or

2) from an increase of volatile or nonvolatile acid in the extracellular space

Question 13

Normal source of acid ….?

Answer 13

acid production include the metabolism of amino acids containing sulfur and phosphate

as well as hydrogen ion released from bone mineralization

Question 14

Maintenance of normal pH depends on …?

Answer 14

excretion of volatile acid (e.g., carbonic acid) from the lungs, skeletal exchange of cations for hydrogen, and

renal regeneration and reclamation of bicarbonate

Question 15

Causes of metabolic acidosis in newborn …?

Answer 15

hypoxia and ischemia at cellular level (asphyxia),

cellular dysfunction (sepis),

severe cardiac dysfunction (ductus dependent left sided obstructive lesion), and

poor oxygen delivery due to severe anemia or poor venous return due to overdistension of lungs resulting from inappropriately high ventilator pressures.

Question 16

primary ions of the extracellular space..?

Answer 16

Na, Cl, and bicarbonate

Question 17

An increased anion gap indicates …?

Answer 17

An accumulation of organic acid

Question 18

A normal anion gap indicates ….?

Answer 18

A loss of buffer equivalents.

Anion gap in healthy neonates is higher (5-15 mEq/L) than that of adults.

Question 19

Metabolic acidosis associated with an increased anion gap (>15 mEq/L)…?

Answer 19

Disorders include
renal failure,
inborn errors of metabolism,
lactic acidosis, and
toxin exposure

Question 20

Metabolic acidosis associated with a normal anion gap (<15 mEq/L)…?

Answer 20

results from buffer loss through the renal or gastrointestinal system

Question 21

Normal Anion Gap (<15 mEq/L)

Answer 21

Renal bicarbonate loss
Renal tubular acidosis Acetazolamide
Renal dysplasia
Gastrointestinal bicarbonate loss
Diarrhea
Cholestyramine
Small bowel drainage
Dilutional acidosis
Hyperalimentation acidosis

Question 22

An increase of 0.1 pH unit in serum results in approximately—— mEq/L fall in serum K concentration

Answer 22

0.6

due to an intracellular shift of K ions.

Question 23

Hypokalemia features…?

Answer 23

arrhythmias,
ileus,
renal concentrating defects, and
obtundation in the newborn

Question 24

Predisposing factors for Hypokalemia ,….?

Answer 24

respiratory depression,
apnea,
nasogastric or ileostomy drainage,
chronic diuretic use, and
renal tubular defects.

Question 25

Predisposing factors Hyperkalemia …?

Answer 25

a. Decreased K clearance due to renal failure, oliguria, hyponatremia, and congenital adrenal hyperplasia

b. Up to 50% of VLBW infants born before 25 weeks’ gestation manifest serum K levels >6 mEq/L in the first 48 hours of life

c. The most common cause of sudden unexpected hyperkalemia in the neonatal intensive care unit (NICU) is medication error.

d. Increased K release secondary to tissue destruction, trauma, cephalhematoma, hypothermia, bleeding, intravascular or extravascular hemolysis, asphyxia/ischemia, and IVH

e. Miscellaneous associations including dehydration, birth weight <1,500 g, blood transfusion, inadvertent excess (KCl) administration, chronic liver disease with KCl supplementation, and exchange transfusion

Question 26

The ECG findings in hyperkelemia ..?

Answer 26

peaked T waves (increased rate of repolarization),

flattened P waves, and increasing PR interval (suppression of atrial conductivity)

QRS widening and slurring (conduction delay in ventricular conduction tissue as well as in the myocardium itself), and

finally, supraventricular/ventricular tachycardia, bradycardia, or ventricular fibrillation

Question 27

Rationale of using sodium bicarbonate in hyperkelemia …?

Answer 27

Alkalemia will promote intracellular K-for-hydrogen-ion exchange.

Na bicarbonate 1 to 2 mEq/kg/hour IV may be used

Question 28

Rationale of using insulin in hyperkelemia ..?

Answer 28

Insulin enhances intracellular K uptake by direct stimulation of the membrane-bound Na–K-ATPase.

Question 29

ECG in hyperkelemia signs of progressive severity..?

Answer 29

Severe hyperkalemia is a life-threatening medical emergency.
Signs of progressive hyperkalemia on the electrocardiogram, in order of severity, consist of tall peaked T waves, heart block with widened QRS complexes, U wave formation, the development of sine waves, and finally cardiac arrest