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NOTES: For example, if the ECF concentration of sodium increases,

there will be a net movement of water from the intracellular to


Slide 4: Water constitutes approximately 50% to 60% of total the extracellular compartment.
body weight. The relationship between total body weight and
TBW is relatively constant for an individual and is primarily a Conversely, if the ECF concentration of sodium decreases,
reflection of body fat. In an average young adult male, TBW water will move into the cells.
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 Slide 8: The healthy person consumes an average of 2000 mL
approximately 80%of their total body weight comprised of of water per day, approximately 75% from oral intake and the
water. This decreases to approximately 65% by 1 year of age rest extracted from solid foods. Daily water losses include 800
and thereafter remains fairly constant. 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%)


Total body weight and total body water (TBW) is relatively and lungs (25%) and can be increased by such factors as fever,
constant for an individual hypermetabolism, and hyperventilation.

TBW is primarily a reflection of body fat. Sensible water losses such as sweating or pathologic loss of
gastrointestinal (GI) fluids vary widely, but these include the
Lean tissues such as muscle and solid organs have higher loss of electrolytes as well as water
water content than fat and bone

Young, lean males have a higher proportion of body weight as


water than elderly or obese individuals. 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
Slide 5: TBW is divided into three functional fluid fistula.
compartments: plasma, extravascular interstitial fluid, and Serum sodium concentration does not necessarily reflect
intracellular fluid. The extracellular fluids (ECF), plasma and volume status and therefore may be high, normal, or low
interstitial fluid, together compose about one third of the when a volume deficit is present.
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). Slide 12: In fit patients, edema and hyperdynamic circulation
Intracellular water makes up approximately 40% of an are common and well tolerated. However, the elderly and
individual’s total body weight, with the largest proportion in patients with cardiac disease may quickly develop congestive
the skeletal muscle mass.

Slide 14: A low serum sodium level occurs when there is an


Slide 6: The normal chemical composition of the body fluid excess of extracellular water relative to sodium.
compartments is shown in this figure. Extracellular volume can be high, normal, or low.
The ECF compartment is balanced between sodium, the In most cases of hyponatremia, sodium concentration is
principal cation, and chloride and bicarbonate, the principal decreased as a consequence of either sodium depletion or
anions. dilution
The intracellular fluid compartment is composed primarily of
the cations potassium and magnesium, and the anions
phosphate and sulfate, and proteins. Mild: 130-134

The concentration gradient between compartments is Moderate: 125 – 129


maintained by adenosine triphosphate–driven
Profound: less than 125
sodium-potassium pumps located with in the cell membranes.

Slide 16: Hypernatremia results from either a loss of free


Slide 7: The osmolality of the intracellular and extracellular
water or a gain of sodium in excess of water. Like
fluids is maintained between 290 and 310 mOsm in each
hyponatremia, iit can be associated with an increased, normal,
compartment.
or decreased extracellular volume.
Because cell membranes are permeable to water, any change
Urine sodium concentration is typically >20 mEq/L, and urine
in osmotic pressure in one compartment is accompanied by a
osmolarity is >300 mOsm/L in hypervolemic hypernatremia.
redistribution of water until the effective osmotic pressure
between compartments is equal.
When hypovolemia is present, the urine sodium concentration control, but disturbances in metabolism are relatively long
is <20 mEq/L and urine osmolarity is <300 to 400 mOsm/L. term and less important in the acute surgical setting. However,
attention to the critical role of ionized calcium in
neuromuscular function often is required.
Slide 17: Symptomatic hypernatremia usually occurs only in Hypercalcemia is defined as a serum calcium level above the
patients with impaired thirst or restricted access to fluid, normal range of 8.5 to 10.5 mEq/L or an increase in the
because thirst will result in increased water intake. ionized calcium level above 4.2 to 4.8 mg/dL.
Symptoms are rare until the serum sodium concentration Primary hyperparathyroidism in the outpatient setting and
exceeds 160 mEq/L but, once present, are associated with malignancy in hospitalized patients, from either bony
significant morbidity and mortality. metastasis or secretion of parathyroid hormone–related
Because symptoms are related to hyperosmolarity, central protein, account for most cases of symptomatic
nervous system effects predominate. Water shifts from the hypercalcemia.
intracellular to the extracellular space in response to a Symptoms of hypercalcemia, which vary with the degree of
hyperosmolar extracellular space, which results in cellular severity, include neurologic impairment, musculoskeletal
dehydration. 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
Slide 18: Hyperkalemia is defined as a serum potassium worsening of digitalis toxicity.
concentration above the normal range of 3.5 to 5.0 mEq/L.
ECG changes in hypercalcemia include shortened QT interval,
The intracellular and extracellular distribution of potassium is prolonged PR and QRS intervals, increased QRS voltage,
influenced by a number of factors, including surgical stress, T-wave flattening and widening, and atrioventricular block
injury, acidosis, and tissue catabolism.

Slide 23: Hypocalcemia is defined as a serum calcium level


Slide 19: Symptoms of hyperkalemia are primarily GI, below 8.5 mEq/L or a decrease in the ionized calcium level
neuromuscular, and cardiovascular. below 4.2 mg/dL.
Early cardiovascular signs may be apparent from The causes of hypocalcemia include pancreatitis, massive soft
electrocardiogram (ECG) changes and eventually lead to tissue infections such as necrotizing fasciitis, renal failure,
hemodynamic symptoms of arrhythmia and cardiac arrest. pancreatic and small bowel fistulas, hypoparathyroidism,
toxic shock syndrome, abnormalities in magnesium levels,
ECG changes that may be seen with hyperkalemia include
and tumor lysis syndrome.
high peaked T waves (early), widened QRS complex,
flattened P wave, prolonged PR interval (first-degree block), In addition, transient hypocalcemia commonly occurs after
sine wave formation, and ventricular fibrillation 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


Slide 20: Hypokalemia is much more common than hypoproteinemia results in a normal ionized calcium level.
hyperkalemia in the surgical patient.
In general, neuromuscular and cardiac symptoms do not occur
Additionally, drugs such as amphotericin, aminoglycosides, until the ionized fraction falls below 2.5 mg/dL.
cisplatin, and ifosfamide that induce magnesium depletion
ECG changes of hypocalcemia include prolonged QT interval,
cause renal potassium wastage
T-wave inversion, heartblock, and ventricular fibrillation

Slide 21: The symptoms of hypokalemia, like those of


Slide 24: Phosphorus is the primary intracellular divalent
hyperkalemia, are primarily related to failure of normal
anion and is abundant in metabolically active cells. Serum
contractility of GI smooth muscle, skeletal muscle, and
phosphate levels are tightly controlled by renal excretion.
cardiac muscle.
Hyperphosphatemia can be due to decreased urinary excretion,
ECG changes suggestive of hypokalemia include U waves,
increased intake, or endogenous mobilization of phosphorus.
T-wave flattening, ST-segment changes, and arrhythmias
Most cases of hyperphosphatemia
(with digitalis therapy).
are seen in patients with impaired renal function.
Hypoparathyroidism or hyperthyroidism also can decrease
Slide 22: Daily calcium intake is 1 to 3 g/d. Most of this is urinary excretion of phosphorus and thus lead to
excreted via the bowel, with urinary excretion relatively low. hyperphosphatemia.
Total body calcium balance is under complex hormonal
Most cases of hyperphosphatemia are asymptomatic, but Slide 29: The type of fluid administered depends on the
significant prolonged hyperphosphatemia can lead to patient’s volume status and the type of concentration or
metastatic deposition of soft tissue calcium-phosphorus compositional abnormality present.
complexes.
Both lactated Ringer’s solution and normal saline are
considered isotonic and are useful in replacing GI losses and
correcting extracellular volume deficits.
Slide 25: Clinical manifestations of hypophosphatemia
usually are absent until levels fall significantly.

In general, symptoms are related to adverse effects on the Slide 30: The type of fluid administered depends on the
oxygen availability of tissue and to a decrease in high-energy patient’s volume status and the type of concentration or
phosphates, and can be manifested as cardiac dysfunction or compositional abnormality present.
muscle weakness.
Both lactated Ringer’s solution and normal saline are
considered isotonic and are useful in replacing GI losses and
correcting extracellular volume deficits.
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 Slide 31: Lactated Ringer’s is slightly hypotonic in that it
insufficiency and parallel changes in potassium excretion. contains 130 mEq of lactate. Lactate is used rather than
bicarbonate because it is more stable in IV fluids during
Magnesium-containing antacids and laxatives can produce storage. It is converted into bicarbonate by the liver after
toxic levels in patients with renal failure. Excess intake in infusion
conjunction with total parenteral nutrition (TPN), or rarely
massive trauma, thermal injury, and severe acidosis, may be
associated with symptomatic hypermagnesemia.
Slide 32: The high chloride concentration imposes a
Clinical examination (see Table 3-6) may find nausea and significant chloride load on the kidneys and may lead to a
vomiting; neuromuscular dysfunction with weakness, lethargy, hyperchloremic metabolic acidosis
and hyporeflexia; and impaired cardiac conduction leading to
hypotension and arrest.

ECG changes are similar to those seen with hyperkalemia and Slide 33: This solution provides sufficient free water for
include increased PR interval, widened QRS complex, and insensible losses and enough sodium to aid the kidneys in
elevated T waves adjustment of serum sodium levels.

The addition of potassium is useful once adequate renal


function and urine output are established.
Slide 27: Magnesium depletion is a common problem in
hospitalized patients, particularly in the critically ill.

Depletion is characterized by neuromuscular and central Slide 34: Hypertonic saline (7.5%) has been used as a
nervous system hyperactivity. Symptoms are similar to those treatment modality in patients with closed head injuries. It has
of calcium deficiency, including hyperactive been shown to increase cerebral perfusion and decrease
intracranial pressure, thus decreasing brain edema.
reflexes, muscle tremors, tetany, and positive Chvostek’s and
Trousseau’s signs.

Severe deficiencies can lead to delirium and seizures. A Slide 35: Due to their molecular weight, they are confined to
number of ECG changes also can occur and include prolonged the intravascular space, and their infusion results in more
QT and PR intervals, ST-segment depression, flattening or efficient transient plasma volume expansion
inversion of P waves, torsades de pointes, and arrhythmias. In severe hemorrhagic shock, capillary membrane
Hypomagnesemia is important not only because of its direct permeability increases; this permits colloids to enter the
effects on the nervous system but also because it can produce interstitial space
hypocalcemia and lead to persistent

hypokalemia. When hypokalemia or hypocalcemia coexists Slide 37: Albumin has been shown to induce renal failure and
with hypomagnesemia, magnesium should be aggressively impair pulmonary function when used for resuscitation in
replaced to assist in restoring potassium or calcium hemorrhagic shock
homeostasis

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.