FLUID BALANCE
The placenta, the fetal and maternal kidenys, fetal skin, fetal membranes, and the fetal
lung and intestine all play roles on maintaining the volume and composition of fetal
fluids. During the first half of pregnancy, the amniotic fluid is consiered an extension of
the fetal extracellular fluid space. The fetal skin is freely permeable to water and sodium
early in gestation, and through midgestation, abortion can be induced by injection of
hypertonic saline into the amniotic fluid. Removal of amniotic fluid at mid-pregnancy
results in death of the fetus; however, removal near term still allows fetal survival. Late
in gestation, amniotic fluid is a composite of secretions from lungs and kidneys. Urea,
creatinine, and uric acid concentrations increase steadily towards the end of gestation;
concentrations at term are much higher than in fetal plasma. The primary source for
formation of amniotic fluid is the fetal kidney, while the primary source of disposal is the
fetal digestive tract. Failure of fetal swallowing often leads to hydramnios, compromising
fetal viability.
Fluid Changes During Growth
Both the water and chloride content of the body decrease with increasing growth and
development. These changes are a consequence of decreasing extracellular fluid and
increasing fat and protein. The brain of the newborn contains about 11% of the total
bodywater, while that of the adult contains only 2%. The chloride content of the newborn
is also proportionately higher than that of the adult. Muscle contains more extracellular
wwater and less intracellular water earlier in development, and altricial species have these
same differences when compared to precocial species. Heart muscle, by contrast, matures
earlier and shows none of the changes seen in striated muscle. Bone water content
decreases, while sodium content increases, during growth. The decrease in extracellular
water during developmentresults from two processes: 1) the decreasing proportion of
body weight accounted for by tissues high in extracellular water, and 2) the decrease in
the percentage of extracellular water in skeletal muscle.
In summary, the primary changes in fluid balance during maturation include decreases in
total body water, extracellular water, and chloride, with a concomitant increase in
potassium, protein, and fat content. Disturbances in the volume and composition of body
fluids are far more common in the perinatal period than at any other age.
Renal Function
The regulation of extracellular fluid osmolality and volume is an important function of
the renal system. Even with highly varied fluid intakes, the volume and composition of
body fluids remains almost constant. The ability of the body to conserve water is related
to the effective osmotic pressure of the extracellular fluid. Sodium plays an important
role in the level and regulation of extracellular fluid effective osmotic pressure
(osmoregulation) and volume (volume regulation). Osmoregulation is accomplished
through the regulation of the ratio of sodium to water, while volume regulation occurs
through control of sodium and water quantities. Plasma regulation is closely controlled
by adjusting water intake and excretion. These adjustments are controlled by the
hypothalamus which regulates the secretion of both antidiuretic hormone (ADH) and the
thirst mechanism. If water intake exceeds water excretion, ADH secretion is inhibited
and water excretion is enhanced. Conversely, if water loss exceeds intake, then ADH
secretion is stimulated and the thirst mechanism stimulates water intake.
Administratration of excess sodium tends to expand extracellular fluid volume which
stimulates renal excretion of sodium to normalize volume. Similarly, sodium is
conserved by the kidney in response to decreases in extracellular fluid volume. Changes
in extracellular fluid volume are detected by pressure receptors in the heart atria, carotid
sinuses, aortic arch, and afferent arterioles of the glomeruli. In the kidney, these receptors
are found in the juxtaglomerular cells of the afferent arterioles and the macula densa cells
of the distal tubules. These receptors stimulate the renin-angiotensin-aldosterone system
in response to decreased extracellular fluid volume. Renin is a proteolytic enzyme which
catalyzes the conversion of angiotensinogen (an inactive globulin) to angiotensin I (also
inactive). Angiotensin I is then converted to angiotensin II (active form) by angiotensin
converting enzyme. Angiotensin II directly enhances sodium reabsorption and water
conservation, while indirectly causing the adrenal cortex to secrete aldosterone, which
also enhances water reabsorption.
Another improtant function of the kidney is to regulate ion concentrations in the
extracellular fluid of the body. Although sodium reabsorption is affected by aldosterone,
aldosterone is not considered a regulator of sodium concentration in the extracellular
fluid. Regulation of potassium concentration of the extracellular fluid is accomplished by
increasing reabsorption or excretion in the distal nephron. This occurs by release of
aldosterone in response to an increase in plasma potassium concentration. Aldosterone
increases transport of potassium into tubular cells, enhances sodium reabsorption, and
increases luminal permeability to potassium, all of which enhance potassium movement
from the tubular cells to the lumen for excretion in the urine.
Renal regulation of acid-base balance is regulated through excretion or reabsorption of
strong ions. Changes in strong ion concentration cause changes in the concentrations of
bicarbonate and H+ across the renal tubule. The renal regulation of strong ion difference
is slow in comparison to the respiratory control of pCO2. The kidneys regulate plasma
strong ion difference by balancing sodium and chloride excretion rates. The response to
acidosis is increased chloride excretion, which raises strong ion difference and results in
the excretion of excess H+ and reabsorption of bicarbonate. Likewise, increased sodium
or decreased chloride concentrations produce an above normal strong ion difference
indicative of alkalosis. The renal response is to decrease excretion rates of chloride,
decreasing strong ion difference, resulting in a secretion of excess bicarbonate and
reabsorption of H+ following the chloride.
Most neonatal mammals are more susceptible to fluid and electrolyte disorders than are
adult animals. Newborns of most species have a limited capacity to excrete a water or
electrolyte load, a limited capacity to produce a concentrated urine or to react to antidiuretic hormones or aldosterone, and a limited glomerular filtration rate. The capacity of
newborn infants to excrete a water load is only about 10% of that of adults, although
mature function is reached by one month of age. The ability to produce a concentrated
urine does not appear until nearly 3 months of age, while the glomerular filtration rate is
limited until nearly 18 months of age.
These limitations are especially important in association with neonatal diarrhea. Neonatal
limitations in renal clearance and reabsorption quickly lead to dehydration. Species
differences complicate estimates of fluid and electrolyte replacement in newborns.
Neonatal calves, for example, are unique in that their renal system is highly developed at
birth. By 2-3 days postpartum, their renal function is similar to that of adult cattle.
Neonatal calves are able to produce a highly concentrated urine during dehydration as
early as 2 days of age. Calves may lose as much as 5% of their body weight during
starvation and up to 15% by 96 hours. Urine output during this period may decrease as
much as 90%, whereas urine osmolalaity may increase by up to 400%. In contrast,
human infants need approximately 2.5 L of water to produce 1000 mOsm urinary solute,
while a neonatal calf or adult human requires less than 1 L of water to produce such a
response.
Calves also have a unique ability to dilute urine and excrete large volume loads similar to
adults.. Calves given large volumes of milk water or hypotonic electrolyte solutions
respond by increasing urine output up to 10-fold. This diuretic response occurs very
quickly; calves produced peak urine output by 60-90 minutes after loading, with 70-100%
of the volume being excreted within 4 hours. Calves can easily handle a volume load of
50% of their body weight during the first day of life, while neonatal rats given 4.5% of
their body weight show no difference in urine output after 5 hours. This rapid response in
calves is due to their mature glomerular filtration rate and ability to dilute urine up to ~35
mOsm/L after volume loading. The diuretic response in calves is closer to adult humans
or dogs than to adult cows, whose response is slower in onset, slower to peak urine
output, and longer in duration than the calf.