FLUID, ELECTROLYTES AND ACID-BASE DISTURBANCES IN SURGERY

Body water accounts for 50%-70% of body weight. There is a higher percentage of water in young people, thin people, and men and a lower percentage of water in older people, obese people, and women.

Compartments
Intracellular

Intravascular
Interstitial

Intracellular
This compartment accounts for 30% - 40% of body weight (65% of total body water). Most of the bodys intracellular water is contained in skeletal muscle cells; very little water is contained in adipose cells, which accounts for the lower percentage of water in obese and older people.

Intravascular
This compartment accounts for approximately 5% of body weight (10% of total body water). The body water in this compartment supplies the blood. Maintenance of the intravascular compartment is essential to survival and should be the primary consideration in fluid and electrolyte management.

Interstitial
This compartment accounts for approximately 15 % of body weight (approximately 25 % of total body water). This compartment is equilibrated rapidly with the intravascular compartment to maintain the intravascular compartment close to or within normal parameters.

NB!
The interstitial compartment increases in size and accounts for third-space fluid that accumulates after an operation, burn, trauma, or severe illness.

Electrolyte composition
Electrolytes

determine the amount of water that exists in any one space at any time. Electrolyte concentrations in the intracellular space differ compared with the extravascular spaces. Water follows electrolytes across cell membranes to equilibrate osmolality.

Compartments
Intracellular Intravascular Interstitial

Intracellular
This compartment contains approximately 200 mEq/L of osmotically active particles. This compartment has the highest osmotic pressure, which accounts for cell turgidity.

Intravascular
This compartment contains approximately 154 mEq/L of osmotically active particles. The intravascular compartment has a slightly higher osmotic pressure than the interstitial compartment, so that the contents of the intravascular compartment do not diffuse into the interstitial space.

Interstitial
This compartment is similar to the intravascular compartment and contains approximately 153 mEq/L of osmotically active particles.

NB!
Change in osmotic pressure in one compartment causes water to redistribute from the other compartments until equilibrium is returned.

Knowing how to calculate the approximate blood volume for a patient is important. Using the two-thirds rule, approximately 7 % of body weight is blood volume. This calculation is based on lean body mass for a 70-kg man, and it varies widely depending on the patients age, gender, and body

Blood volume

Water
The amount of water required by a person depends on the persons weight, age, gender, and illness. Most healthy adults are able to compensate for most inappropriately administered fluids. Therefore, any of the frequently used methods of calculating water requirements are usually satisfactory.

Methods of calculating water requirements

The utilization of the body water can be used as a guide for the amount of water maintenance needed. The amount of water required for maintenance can be based on the patients weight. A given amount of water per kg of body weight. A given amount of fluid can be used, regardless of body weight.

The major water loss from the body is through urine production. Generally, 0.5 mI/kg/hr is sufficient urine output to excrete the daily solute load. The next highest daily water loss is insensible loss (i.e., sweat, respiration, stool), which is estimated as 500 ml/24 hr. In a 70-kg man, water maintenance would be: (70 kg x 0.5 mI/kg/hr X 24 hr) + 500 ml/24 hr

This method usually is used for pediatric patients, because their body weights vary widely. Estimations are 100 mI/kg for the first 10 kg of body weight, 50 mI/kg for the second 10 kg of body weight, and 20 mI/kg for each additional kg of body weight (i.e., a 35-kg child would require 75 mI/hr).

A given amount of water per kg of body weight can be used to determine water maintenance requirements. The value used for this method is generally 35 ml/kg/24 hr.

Adults frequently have fluids administered at 125 ml/hr. This amount may be well tolerated by a healthy 70-kg man but may lead to water excess in a small, elderly patient.

Because water requirements vary, the most important aspect of water maintenance administration is evaluating the adequacy for the patient in question. Fever, environmental temperature, and respiratory rate can increase water requirements. The important factors are urine output, blood urea nitroge, and creatinine levels, heart rate, blood pressure, skin turgor, and peripheral edema.

Urine output variations

If urine output is high (> 0.5 ml/kg/hr), then less water may be required. If urine output is low, more water may be required or another action may be necessary.

As people age, muscle mass and the number of glomeruli decrease. The elderly should not be expected to produce as much urine as younger people. Elderly patients can be pushed into congestive heart failure by continued water administration for a low urine output, when the urine output is already adequate for their size.

The natural response in patients stressed by injury, illness, or surgery is to retain sodium and water. The physician must consider the urine output variations . If the patients overall condition and creatinine are stable, low urine output (< 0.5 ml/kg/hr) can be accepted and monitored closely.

Patients receiving total parenteral nutrition generally do not require additional water. A patient on total parenteral nutrition who does not have ongoing abnormal water losses rarely requires additional fluids. Patients who require diuresis already are overloaded with fluid, and intravenous fluids should be held. However, there may be electrolyte or nutritional aspects of fluid administration that require water as a carrier for other substances during diuresis.

Sodium.
Normally, approximately 75 mEq/day (4.5 g/day) of sodium is sufficient to replace the obligate losses of the body. During severe sodium restriction, the kidneys can reduce sodium loss to 1 mEq/day, so that almost no replacement sodium is required. It is best to provide patients with the minimum sodium requirements.

Potassium
The average daily intake of potassium is approximately 50-100 mEq/day, with a basal requirement of approximately 40 mEq/day. The vast majority of potassium in the body is intracellular. However, potassium can become extracellular, which can lead to severely depleted potassium stores that require large amounts of replacement potassium.

Deficits and excesses primarily refer to the volume of fluids in the extravascular space.

Deficits of water (hypovolemia) Signs of acute volume loss include tachycardia, hypotension, and decreased urine output. Signs of gradual volume loss include loss of skin turgor, thirst, alterations in body temperature, and changes in mental status. Replacing water deficits. A reasonable method of restoring water in a patient is by replacing half of the estimated deficit in the first 8 hours and reevaluating the patient. Then, in the next 8 hours, half of the deficit again is replaced; this is continued until the proper fluid replacement is achieved.

Excess of water (hypervolemia) leads to only high urine output in most people. Complications can arise in the elderly and those who are retaining fluids. If fluid excess occurs more slowly, pulmonary or peripheral edema may occur. Acute peripheral edema generally causes little harm. Edema also breaks down the tight junctions between cells, which decreases the interstitial pressure and leads to further edema .
(ii)

Deficit of sodium (hyponatremia)

Hyponatremia is defined as a serum sodium level of 1 30 m[q/L or less. Symptoms generally are irritability, increased deep tendon reflexes, muscle twitching, and, in addition, seizures if hyponatremia becomes severe.

In patients with hyponatremia caused by a total body sodium deficit, there often is a water deficit. These patients may manifest hypotension and decreased renal function, which must be managed before treatment for hyponatremia.

Hyponatremia can occur in patients with a normal level of sodium if the patient is unable to voluntarily control sodium and water intake (e.g., comatose patients), and a hypotonic solution is administered for a prolonged period of time. Patients with the syndrome of inappropriate secretion of antidiuretic hormone do not excrete excess free water appropriately and can become hyponatremic if their total body sodium level is normal.

These patients usually have an inability to excrete sodium and water appropriately, which occurs with renal failure, cirrhosis, and stress. There is evidence of fluid overload, such as pulmonary and pitting edema.

Treatment should be directed at determining the underlying cause of hypona tremia. Hyponatremia in hospitalized patients usually has an iatrogenic cause. It the patient is not symptomatic, correcting the underlying cause and allowing the body to correct itself is the most appropriate course. If the patient is symptomatic, a more rapid correction is necessary and is usually accomplished with hypertonic saline. However, when hypertonic saline is used, hypervolemia and pulmonary body water.

Excess of sodium (hypernatremia)

Hypernatremia is defined as a serum sodium level greater than 145mEq/L. Symptoms include those of volume depletion (e.g., tachycardia, hypotension, lethargy, agitation) as well as other signs of dehydration (e.g., dry mucous membranes, decreased skin turgor).

In hospitalized patients, it is more likely that a patient with an increased serum sodium level actually has an increased total body sodium, which can stem from administration of large amounts of sodiumcontaining fluids (e.g., normal saline). If there is a loss of water without an equivalent loss of sodium, hypernatremia results. Loss of water can occur from nasogastric tube drainage, sweating, tracheostomy, diarrhea, and diuresis.

When hypernatremia needs to be corrected, several factors must be considered. If the patients total body water status is decreased, hypernatremia can be treated with free water infusions. Signs of volume deficit should be monitored as a guide to proper free water administration. If the patients total body water is increased, the first step is to decrease the amount of sodium that is being administered. If sodium intake (e.g., antibiotics, drips in normal saline) cannot be decreased, free water can be infused to lower the serum sodium level, but this does not decrease the total body sodium content.

Calculating free water deficit: water deficit = 0.6 x body weight [1 (140/Nat)]

hypokalemia

Severe hypokalemia is defined as a serum potassium level of 3 mEq/L or less. Symptoms of hypokalemia are those of depression of neural, cardiac, and muscle function. The most serious of these are cardiac arrhythmias caused by hypokalemia, which begin as flattened or inverted T waves. Then, U waves appear, ST segments become depressed, the PR interval elongates, and the QRS complex widens. Neuromuscularly, the patient becomes weak, and the gastrointestinal tract may develop an ileus.

Hypokalemia in patients outside of the hospital usually occurs in those who have been severely depleted of potassium for a prolonged time (e.g., from starvation, anorexia, or diuretics without adequate replacement). Hospitalized patients may experience prolonged potassium depletion as well as nasogastric drainage, fistulas, diuretic therapy, and diarrhea, all of which lead to a loss of potassium from the body. Patients who are unable to eat are unable to replace potassium normally.

First, the potassium deficit should be corrected enough to resolve the major symptoms, then to correct the underlying cause of the hypokalemia and provide appropriate potassium replacement. In cases of severe hypokalemia with symptoms, an infusion of potassium is appropriate. If more than 10 mEq/L is infused hourly, a central line should be used to help prevent the irritation that potassium can cause. If potassium is being infused because of cardiac arrhythmias, the patient should have continuous electrocardiogram monitoring.

If infusion of large amounts of potassium does not return the patients serum potassium level to normal, the patient should be assessed for ongoing losses. For all sources of loss (urine, nasogastric, stool) potassium levels must be determined. With this information, actual losses may be determined. The losses may be as great as several hundred mEq per day, much greater than normal replacement; without knowing the actual losses, it is likely that therapy will be inadequate.

hyperkalemia

Hyperkalemia is usually defined as a serum potassium level of 6 mEq/L or greater. Symptoms of hyperkalemia are those of hyperexcitability and are primarily manifested in the Cl tract as hypermotility (e.g., nausea, cramping, diarrhea, vomiting). In the heart, hyperkalemia causes peaking of the T waves and widening of the QRS complex on ECG. As hyperkalemia increases, heart block occurs, and eventually a diastolic cardiac arrest takes place.

Because the kidneys are very efficient at removing excess potassium from the serum, it is almost impossible for a person with normally functioning kidneys to become hyperkalemic. The primary cause of hyperkalemia in hospitalized patients is insufficient renal function and excess potassium, which can be iatrogenic or endogenous. Hyperkalemia also is associated with massive blood transfusionsand with Cl bleeding, in which the potassium from the shed blood is absorbed. Acidosis can cause acute, severe hyperkalemia.

Calcium can be administered intravenously to stabilize the membranes and to help the cardiac arrhythmias. The serum potassium level also can be lowered by administering bicarbonate (HCO3), insulin, or both, and both move potassium back into the cells. If the body is unable to remove excess potassium, ion exchange resins may be administered orally or rectally. These resins exchange the potassium for sodium ions, and when the resins are eliminated from the body in the stool, the potassium excess is lost. Dialysis is very effective.

hypochloremia
Hypochloremia is defined as a chloride level less than 90 mEq/L. Causes. Hypochloremia is unusual in most patients. Generally, it results from high Gl fluid losses (e.g., prolonged vomiting, nasogastric tube suction), in which large amounts of hydrogen and chloride ions are lost. Dilutional states, in which large amounts of hypotonic fluids have been administered, also may contribute to hypochloremia.

Symptoms. Loss of hydrogen ion and chloride, along with dehydration, can cause the kidneys to retain sodium, which leads to a loss of potassium and chloride and a retention of HCO3. Retention of HC03 can lead to a severe hypochloremic, hypokalemic metabolic alkalosis. Treatment for hypochloremia involves replacement of the chloride with sodium chloride solutions and, if the potassium also is low, replacement with potassium chloride.

hyperchloremia

Hyperchloremia is defined as a plasma chloride level greater than 110 mEq/L. Cause. The most common cause of hyperchloremia in hospitalized patients is the administration of large amounts of chloride in IV solutions. The chloride content in normal saline (1 54 mEq/L) is significantly higher than that in plasma (90110 mEq/L).

Symptoms. The pH of the plasma decreases, causing metabolic acidosis. This type of acidosis also can be caused by aggressive diuresis after administration of large amounts of saline solutions. Treatment. Terminating the administration of high chloride concentrations and allowing the kidneys to regulate the plasma back to normal is the primary treatment. Free water also may be necessary to return a hypertonic plasma to a more normal concentration, so that the kidneys can correct the electrolyte abnormalities.

The buffer systems

1) The bicarbonate system is the most important buffering system in the body, but it does not have the largest buffering capacity. The bicarbonate system is composed of H2C03 and sodium bicarbonate (NaHCO3). H2C03 is a weak acid. When it is in solution with its base, NaHCO3, a buffer system is created.

2) The phosphate system works in an identical manner as the bicarbonate system, except it uses phosphoric acid (H3P04) and its sodium salts [NaH2(P04) and Na2HPO4]. The phosphate system is important for buffering the renal tubular fluid because it is concentrated in the renal tubules.

3) The protein buffers. The proteins in the body are composed of amino acids joined by peptide bonds. Many of the amino acids have side branches with acid or base radicals. The side branches act as a buffer system much as the bicarbonate and phosphate systems do.

Acidosis
The bodys pH decreases when either the Pco2 increases or the concentration of HCO3 decreases, which leads to acidosis when a pH lower than 7.35 is reached. A loss of HCO3 results in metabolic acidosis; a rise in CO2 results in respiratory acidosis. A combination of both forms of acidosis is common.

Respiratory acidosis results from an increase in plasma CO2 levels, which can be produced either by increased production of CO2 or by decreased elimination of CO2 by the lungs. Metabolic acidosis results either from a loss of HCO3 or from an accumulation of acids, both of which can lead to a pH of 7,35 or less.

Alkalosis

Respiratory alkalosis is caused by an increase in alveolar ventilation and subsequent reduction in CO2 levels. This situation can be caused by any entity that causes hyperventilation, such as anxiety, pain, shock, toxic substances, or CNS dysfunction. Metabolic alkalosis occurs when the pH increases to over 7,45, and the HCO3 level is greater than 26 mEq/L.