NOTES:
there will be a net movement of water from the intracellular to
Slide 4: Water constitutes approximately 50% to 60% of total
body weight. The relationship between total body weight and
TBW is relatively constant for an individual and is primarily a
reflection of body fat. In an average young adult male, TBW
accounts for 60% of total body weight, whereas in an average
young adult female, it is 50%.
The highest percentage of TBW is found in newborns, with
approximately 80%of their total body weight comprised of
water. This decreases to approximately 65% by 1 year of age
and thereafter remains fairly constant.
Total body weight and total body water (TBW) is relatively
constant for an individual
TBW is primarily a reflection of body fat.
Lean tissues such as muscle and solid organs have higher
water content than fat and bone
Young, lean males have a higher proportion of body weight as
water than elderly or obese individuals.
Slide 5: TBW is divided into three functional fluid
compartments: plasma, extravascular interstitial fluid, and
intracellular fluid. The extracellular fluids (ECF), plasma and
interstitial fluid, together compose about one third of the
TBW, and the intracellular compartment composes the
remaining two thirds. The extracellular water composes 20%
of the total body weight and is divided between plasma (5% of
body weight) and interstitial fluid (15% of body weight).
Intracellular water makes up approximately 40% of an
individual’s total body weight, with the largest proportion in
the skeletal muscle mass.
Slide 6: The normal chemical composition of the body fluid
compartments is shown in this figure.
The ECF compartment is balanced between sodium, the
principal cation, and chloride and bicarbonate, the principal
anions.
The intracellular fluid compartment is composed primarily of
the cations potassium and magnesium, and the anions
phosphate and sulfate, and proteins.
The concentration gradient between compartments is
maintained by adenosine triphosphate–driven
sodium-potassium pumps located with in the cell membranes.
Slide 7: The osmolality of the intracellular and extracellular
fluids is maintained between 290 and 310 mOsm in each
compartment.
Because cell membranes are permeable to water, any change
in osmotic pressure in one compartment is accompanied by a
redistribution of water until the effective osmotic pressure
between compartments is equal.
For example, if the ECF concentration of sodium increases,
the extracellular compartment.
Conversely, if the ECF concentration of sodium decreases,
water will move into the cells.
Slide 8: The healthy person consumes an average of 2000 mL
of water per day, approximately 75% from oral intake and the
rest extracted from solid foods. Daily water losses include 800
to 1200 mL in urine, 250 mL in stool, and 600 mL in
insensible losses.
Insensible losses of water occur through both the skin (75%)
and lungs (25%) and can be increased by such factors as fever,
hypermetabolism, and hyperventilation.
Sensible water losses such as sweating or pathologic loss of
gastrointestinal (GI) fluids vary widely, but these include the
loss of electrolytes as well as water
Slide 10: The most common cause of volume deficit in
surgical patients is a loss of GI fluids (Table 3-3) from
nasogastric suction, vomiting, diarrhea, or enterocutaneous
fistula.
Serum sodium concentration does not necessarily reflect
volume status and therefore may be high, normal, or low
when a volume deficit is present.
Slide 12: In fit patients, edema and hyperdynamic circulation
are common and well tolerated. However, the elderly and
patients with cardiac disease may quickly develop congestive
Slide 14: A low serum sodium level occurs when there is an
excess of extracellular water relative to sodium.
Extracellular volume can be high, normal, or low.
In most cases of hyponatremia, sodium concentration is
decreased as a consequence of either sodium depletion or
dilution
Mild: 130-134
Moderate: 125 – 129
Profound: less than 125
Slide 16: Hypernatremia results from either a loss of free
water or a gain of sodium in excess of water. Like
hyponatremia, iit can be associated with an increased, normal,
or decreased extracellular volume.
Urine sodium concentration is typically >20 mEq/L, and urine
osmolarity is >300 mOsm/L in hypervolemic hypernatremia.
When hypovolemia is present, the urine sodium concentration
is <20 mEq/L and urine osmolarity is <300 to 400 mOsm/L.
Slide 17: Symptomatic hypernatremia usually occurs only in
patients with impaired thirst or restricted access to fluid,
because thirst will result in increased water intake.
Symptoms are rare until the serum sodium concentration
exceeds 160 mEq/L but, once present, are associated with
significant morbidity and mortality.
Because symptoms are related to hyperosmolarity, central
nervous system effects predominate. Water shifts from the
intracellular to the extracellular space in response to a
hyperosmolar extracellular space, which results in cellular
dehydration.
Slide 18: Hyperkalemia is defined as a serum potassium
concentration above the normal range of 3.5 to 5.0 mEq/L.
The intracellular and extracellular distribution of potassium is
influenced by a number of factors, including surgical stress,
injury, acidosis, and tissue catabolism.
Slide 19: Symptoms of hyperkalemia are primarily GI,
neuromuscular, and cardiovascular.
Early cardiovascular signs may be apparent from
electrocardiogram (ECG) changes and eventually lead to
hemodynamic symptoms of arrhythmia and cardiac arrest.
ECG changes that may be seen with hyperkalemia include
high peaked T waves (early), widened QRS complex,
flattened P wave, prolonged PR interval (first-degree block),
sine wave formation, and ventricular fibrillation
Slide 20: Hypokalemia is much more common than
hyperkalemia in the surgical patient.
Additionally, drugs such as amphotericin, aminoglycosides,
cisplatin, and ifosfamide that induce magnesium depletion
cause renal potassium wastage
Slide 21: The symptoms of hypokalemia, like those of
hyperkalemia, are primarily related to failure of normal
contractility of GI smooth muscle, skeletal muscle, and
cardiac muscle.
ECG changes suggestive of hypokalemia include U waves,
T-wave flattening, ST-segment changes, and arrhythmias
(with digitalis therapy).
Slide 22: Daily calcium intake is 1 to 3 g/d. Most of this is
excreted via the bowel, with urinary excretion relatively low.
Total body calcium balance is under complex hormonal
control, but disturbances in metabolism are relatively long
term and less important in the acute surgical setting. However,
attention to the critical role of ionized calcium in
neuromuscular function often is required.
Hypercalcemia is defined as a serum calcium level above the
normal range of 8.5 to 10.5 mEq/L or an increase in the
ionized calcium level above 4.2 to 4.8 mg/dL.
Primary hyperparathyroidism in the outpatient setting and
malignancy in hospitalized patients, from either bony
metastasis or secretion of parathyroid hormone–related
protein, account for most cases of symptomatic
hypercalcemia.
Symptoms of hypercalcemia, which vary with the degree of
severity, include neurologic impairment, musculoskeletal
weakness and pain, renal dysfunction, and GI symptoms of
nausea, vomiting, and abdominal pain. Cardiac symptoms can
be manifest as hypertension, cardiac arrhythmias, and a
worsening of digitalis toxicity.
ECG changes in hypercalcemia include shortened QT interval,
prolonged PR and QRS intervals, increased QRS voltage,
T-wave flattening and widening, and atrioventricular block
Slide 23: Hypocalcemia is defined as a serum calcium level
below 8.5 mEq/L or a decrease in the ionized calcium level
below 4.2 mg/dL.
The causes of hypocalcemia include pancreatitis, massive soft
tissue infections such as necrotizing fasciitis, renal failure,
pancreatic and small bowel fistulas, hypoparathyroidism,
toxic shock syndrome, abnormalities in magnesium levels,
and tumor lysis syndrome.
In addition, transient hypocalcemia commonly occurs after
removal of a parathyroid adenoma due to atrophy of the
remaining glands and avid bone remineralization, and
sometimes requires high-dose calcium supplementation
Asymptomatic hypocalcemia may occur when
hypoproteinemia results in a normal ionized calcium level.
In general, neuromuscular and cardiac symptoms do not occur
until the ionized fraction falls below 2.5 mg/dL.
ECG changes of hypocalcemia include prolonged QT interval,
T-wave inversion, heartblock, and ventricular fibrillation
Slide 24: Phosphorus is the primary intracellular divalent
anion and is abundant in metabolically active cells. Serum
phosphate levels are tightly controlled by renal excretion.
Hyperphosphatemia can be due to decreased urinary excretion,
increased intake, or endogenous mobilization of phosphorus.
Most cases of hyperphosphatemia
are seen in patients with impaired renal function.
Hypoparathyroidism or hyperthyroidism also can decrease
urinary excretion of phosphorus and thus lead to
hyperphosphatemia.
Most cases of hyperphosphatemia are asymptomatic, but
significant prolonged hyperphosphatemia can lead to
metastatic deposition of soft tissue calcium-phosphorus
complexes.
Slide 25: Clinical manifestations of hypophosphatemia
usually are absent until levels fall significantly.
In general, symptoms are related to adverse effects on the
oxygen availability of tissue and to a decrease in high-energy
phosphates, and can be manifested as cardiac dysfunction or
muscle weakness.
Slide 26: The normal dietary intake is approximately 20
mEq/d and is excreted in both the feces and urine.
Hypermagnesemia is rare but can be seen with severe renal
insufficiency and parallel changes in potassium excretion.
Magnesium-containing antacids and laxatives can produce
toxic levels in patients with renal failure. Excess intake in
conjunction with total parenteral nutrition (TPN), or rarely
massive trauma, thermal injury, and severe acidosis, may be
associated with symptomatic hypermagnesemia.
Clinical examination (see Table 3-6) may find nausea and
vomiting; neuromuscular dysfunction with weakness, lethargy,
and hyporeflexia; and impaired cardiac conduction leading to
hypotension and arrest.
ECG changes are similar to those seen with hyperkalemia and
include increased PR interval, widened QRS complex, and
elevated T waves
Slide 27: Magnesium depletion is a common problem in
hospitalized patients, particularly in the critically ill.
Depletion is characterized by neuromuscular and central
nervous system hyperactivity. Symptoms are similar to those
of calcium deficiency, including hyperactive
reflexes, muscle tremors, tetany, and positive Chvostek’s and
Trousseau’s signs.
Severe deficiencies can lead to delirium and seizures. A
number of ECG changes also can occur and include prolonged
QT and PR intervals, ST-segment depression, flattening or
inversion of P waves, torsades de pointes, and arrhythmias.
Hypomagnesemia is important not only because of its direct
effects on the nervous system but also because it can produce
hypocalcemia and lead to persistent
hypokalemia. When hypokalemia or hypocalcemia coexists
with hypomagnesemia, magnesium should be aggressively
replaced to assist in restoring potassium or calcium
homeostasis
Slide 29: The type of fluid administered depends on the
patient’s volume status and the type of concentration or
compositional abnormality present.
Both lactated Ringer’s solution and normal saline are
considered isotonic and are useful in replacing GI losses and
correcting extracellular volume deficits.
Slide 30: The type of fluid administered depends on the
patient’s volume status and the type of concentration or
compositional abnormality present.
Both lactated Ringer’s solution and normal saline are
considered isotonic and are useful in replacing GI losses and
correcting extracellular volume deficits.
Slide 31: Lactated Ringer’s is slightly hypotonic in that it
contains 130 mEq of lactate. Lactate is used rather than
bicarbonate because it is more stable in IV fluids during
storage. It is converted into bicarbonate by the liver after
infusion
Slide 32: The high chloride concentration imposes a
significant chloride load on the kidneys and may lead to a
hyperchloremic metabolic acidosis
Slide 33: This solution provides sufficient free water for
insensible losses and enough sodium to aid the kidneys in
adjustment of serum sodium levels.
The addition of potassium is useful once adequate renal
function and urine output are established.
Slide 34: Hypertonic saline (7.5%) has been used as a
treatment modality in patients with closed head injuries. It has
been shown to increase cerebral perfusion and decrease
intracranial pressure, thus decreasing brain edema.
Slide 35: Due to their molecular weight, they are confined to
the intravascular space, and their infusion results in more
efficient transient plasma volume expansion
In severe hemorrhagic shock, capillary membrane
permeability increases; this permits colloids to enter the
interstitial space
Slide 37: Albumin has been shown to induce renal failure and
impair pulmonary function when used for resuscitation in
hemorrhagic shock
Slide 38: They lead to initial volume expansion due to their
osmotic effect but are associated with alterations in blood
viscosity. Thus dextrans are used primarily to lower blood
viscosity rather than as volume expanders.

Slide 42: Treatment of hypernatremia usually consists of

treatment of the associated water deficit.

Once adequate volume has been achieved, the water deficit is

replaced using a hypotonic fluid such as 5% dextrose, 5%
dextrose in . normal saline, or enterally administered water.
The formula used to estimate the amount of water required to
correct hypernatremia is as follows.

The rate of fluid administration should be titrated to achieve a

decrease in serum sodium concentration of no more than 1
mEq/h and 12 mEq/d for the treatment of acute symptomatic
hypernatremia.

Slide 43: In patients with normal renal function, symptomatic

hyponatremia usually does not occur until the serum sodium
level is ≤120 mEq/L.

Slide 44: The goals of therapy include reducing the total body
potassium, shifting potassium from the extracellular to the
intracellular space, and protecting the cells from the effects of
increased potassium. For all patients, exogenous sources of
potassium should be removed, including potassium
supplementation in IV fluids and enteral and parenteral

solutions. Potassium can be removed from the body using a

cation-exchange resin such as Kayexalate that binds
potassium exchange for sodium.