Chapter 25: Fluid and Electrolyte Therapy in the Critically III Obstetric Patient

The ultimate goal of fluid and electrolyte therapy is to maintain a balance between the intracellular and extracellular compartments. This means that often, in caring for the critically ill patient, fluid replacement and electrolyte balance become an afterthought of therapy instead of a goal. However, maintaining this balance is essential for an optimal outcome.¹

Many disease states in pregnancy can change the intracellular and extracellular compartments. Preeclampsia is a prime example of how changes in the dynamics of the intracellular and extracellular compartments can affect overall fluid physiology. Common therapies used during pregnancy such as intravenous tocolysis can change electrolyte balance. The purpose of this chapter is to explain basic fluid and electrolyte balance and to provide guidelines for initiating the therapy.

The human body is composed mostly of water. Approximately, 50% of total body weight in an average female is body water. (total body water [TBW] = 1/2 wt. [kg]). Given that, total blood volume increases by 50% during pregnancy with only 20% of that increase attributed to an increase in red cell mass, one can extrapolate that 60% to 65% of the total body weight in pregnancy can be attributed to TBW. The intracellular fluid compartment (ICF) contains 66% of TBW. The extracellular compartment is composed of 34% TBW. The extracellular fluid compartment (ECF) is composed of both intravascular and the interstitial components. Most of the ECF is interstitial (26%), plasma composes 8% (Fig. 25-1). Other examples of ECF include cerebrospinal fluid, synovial fluid, and secretions from the gastrointestinal tract. The fluid compartments are separated by semipermeable membranes. Water and smaller molecules may pass through the membranes; larger colloid substances and proteins are confined to the intravascular space. Hydrostatic pressure assists in maintaining an overall fluid balance as water moves by osmosis, from the area with the lowest concentration of plasma proteins (interstitial compartment) to the area with the highest concentration of plasma proteins (blood).

Osmotic activity is the expression of the concentration of solute or the density of solute particles in a fluid. In the ECF, osmotic activity can be defined as the sum of the individual osmotic activities of each solute in the fluid. Plasma osmolality can be calculated using the following formula:

Colloid osmotic pressure (COP) is produced by serum albumin (60%-80%) with fibrinogen and the globulins accounting for the remainder. Normal COP is decreased in pregnancy. While COP can be measured with electronic equipment, the equation in Table 25-1 below can estimate COP by using total protein (TP) in g/dL (Table 25-1).

In the obstetric patient, depletion of intravascular volume can occur in 2 ways: overall fluid loss, eg, vomiting, diarrhea, perspiration, or by shifting of the intravascular volume to the interstitial space. Overall fluid loss may be manifested by a clinical examination that reveals orthostasis, poor skin turgor, dry mucous membranes, and a thready pulse. These clinical findings respond to rehydration (Table 25-2).

Shifting of intravascular fluid occurs in disease states such as preeclampsia. Evaluation of volume status in this subset of patients may be much more difficult. In critically ill patients, the evaluation of volume status can be obtained by the judicious use of central pressure catheters (Table 25-3). The central venous pressure (CVP) may be used to evaluate long-term trends in fluid status; however, in patients with cardiac disease or preeclampsia, the CVP may not reflect left ventricular filling. For acute management of the disease states previously mentioned, a pulmonary artery catheter can be more useful in guiding therapy. The left ventricular end-diastolic pressure is best reflected by the pulmonary artery occlusion (wedge) pressure (PAOP). Numerous formulas have been used to evaluate the effect of volume replacement on ventricular filling pressures; we present the 7-3 rule as a handy guideline (Table 25-3).

The majority of intravenous fluid therapy is directed at expanding the plasma component of the ECF. Fluids used to optimize volume status are broadly classified as crystalloids and colloids. Some of the most common questions asked are: which fluid should I use, how much should I use, and when should I use it? Fluid therapy remains a controversial topic with variable recommendations for the volume and type of fluid given.² The goal of this section is to review the pharmacology of the available colloid and crystalloid therapies and discuss their pros and cons.

Crystalloids

As sodium is the major cation and determinant of osmotic pressure in the ECF, it is not surprising that most crystalloid preparations contain mixtures of sodium chloride and other physiologically active solutes. As crystalloid fluids are designed to expand the interstitial space, only about 20% remain in the vascular space. The remaining 80% enters the interstitial compartment over 25 to 30 minutes. Indications for the use of crystalloid include extracellular losses, as in dehydration, acute hemorrhage, and acute volume replacement.

Normal saline, 0.9%, is isotonic to normal body fluid, and, therefore, does not alter osmotic movement of water across the cell membrane. It is the most common fluid used for acute volume expansion. However, when administered in large amounts, normal saline can cause a normal anion gap metabolic acidosis.

There are variations of this fluid such as one-half normal saline, 0.45%; however, these hypotonic fluids have no place in acute volume expansion. Infusing normal saline may produce a hyperchloremic metabolic acidosis; however, this occurrence is rare.

Ringer lactate is an isotonic fluid that may be used interchangeably with normal saline in the treatment of hypovolemia or shock. Ringer lactate is a balanced electrolyte solution that substitutes potassium and calcium for some of the sodium. Lactate is added as a buffer. The concern that acidosis may be worsened by the installation of Ringer lactate during shock is unfounded; however, it is recommended that extreme caution should be taken while using the fluid in patients with diabetes or renal failure.

Hypertonic sodium-containing solutions (600-2400 mOsm/L) may be used in patients in whom a large volume load is contraindicated. Some studies have noted that the infusion of a hypertonic solution may reduce interstitial edema as well as create a positive inotropic effect. Care should be taken to use a slow infusion rate and to monitor sodium regularly to avoid hypernatremia.

Plasmalyte is a highly buffered fluid that has a pH equivalent to plasma. Although theoretically its adjusted pH may be preferential to saline or Ringer lactate, there are no definitive studies that show a great difference in its effects on vascular volume.³

Dextrose-Containing Solutions

Dextrose, 5% in water, is isotonic; but unlike normal saline, it penetrates the cell leaving behind the infused water. It provides a carbohydrate source during brief periods of fasting. One liter of a 5% solution contains approximately 170 kcal and a 10% solution contains 340 kcal. When dextrose is added to normal saline or to Ringer lactate, it raises the osmolality of the fluid to roughly twice that of plasma. This can promote significant changes in serum osmolality when large volumes of fluid are infused.

Colloid

Colloids are large molecular weight substances that do not pass readily across capillary walls. The rationale for the use of colloids is to expand the vascular volume and to decrease the amount of fluid that leaves the intravascular space. The duration of plasma expansion may last from 2 to 36 hours. A recent review in the Cochrane database does not support the routine use of colloid for volume resuscitation.⁴

Human Serum Albumin

Albumin, which is synthesized in the liver, is the major oncotic protein of plasma. Responsible for about 80% of the COP of plasma, it also serves as the major transport protein for drugs and ions. The preparation is available as 5% (50 g/L) and 25% solution (250 g/L) in isotonic saline. The 5% solution has a COP of 20 mm Hg, which is equivalent to plasma COP; the 25% solution has a COP of 70 mm Hg. An infusion of 100 mL of 25% albumin will expand the plasma volume to about 500 mL. The effect of the albumin infusion persists for 24 to 36 hours. Contrary to popular belief, albumin will eventually pass into the interstitial space. This may produce delayed pulmonary edema in patients at risk. Caution should also be exercised when using large volumes since dilutional coagulopathy can occur.

Hydroxyethyl Starch

Hetastarch is a synthetic colloid that closely resembles glycogen. It was introduced as a less expensive alternative to albumin. They are identified by 3 numbers corresponding to concentration, molecular weight, and molar substitution. The concentration influences the volume effect. A 6% solution is isotonic and has a COP of 30 mm Hg. The acute volume expansion is equivalent to that of albumin. A 10% solution is hyperoncotic with a volume expansion effect of 145%. Hetastarch has a longer half-life than albumin with 50% of the osmotic effect persisting for 24 hours. While hydroxyethyl starch (HES) products decrease circulating plasma concentrations of coagulation factor VIII and von Willebrand factor and impair platelet activity, coagulopathies are less common than albumin. The clinician should be aware that serum amylase may be elevated in patients receiving hetastarch as amylase is used to cleave polymers in order to facilitate renal excretion. This elevation usually persists 3 to 5 days after use.^5,6

HES should be used with caution in patient with renal insufficiency. While data are conflicting, a randomized controlled trial has suggested that the incidence of renal impairment was greater in patients resuscitated with HES than those receiving saline.⁵

Dextran

The dextrans are another group of synthetic colloids that are polysaccharides derived from the juice of sugar beets. The available preparations are dextran-40 (mean molecular weight—40,000) and dextran-70 (mean molecular weight—70,000). Dextran-40 is available as a 10% solution with a COP of 40 mm Hg. The acute volume expansion from dextran-40 is about twice the infused volume. However, more than 50% is cleared after 6 hours. While an effective artificial colloid, significant side effects limit its use. Dextrans may inhibit platelet aggregation, decrease platelet factor 3, and produce an anticoagulation effect. Anaphylactic reactions can occur in up to 1% of patients. Dextrans coat the surface of red blood cells and interfere with the ability to crosshatch blood. Dextran-induced renal failure or an osmotic diuresis may interfere with the overall fluid status (Tables 25-4 and 25-5).

Crystalloid or Colloid

Much debate has raged over the use of crystalloid versus colloid solution. Colloids are much more expensive and associated with an increased risk of side effects. Champions of colloid use maintain that the cost and the side effects are outweighed by the benefit of colloid use. Proponents of crystalloid use point out that the infusion of crystalloid increases intravascular volume and that the shift in interstitial fluid is a result of the underlying pathological process. Pulmonary edema may occur with both types of fluid, although the edema associated with colloid use may be delayed. While judicious use of colloid may be useful in some clinical situations, it is the opinion of the author based on current data that crystalloid resuscitation is preferred in the obstetric population.^3,4

Sodium

As the major cation of the ECF and the major determinant of osmolality, sodium maintains the concentration and volume of the ECF. Normal sodium ranges from 135 to 145 mg/dL in most laboratories. Sodium maintains irritability and conduction in nerve and muscle tissue and assists in the regulation of acid-base balance. Since most diets have an excess of sodium, the kidney maintains normal levels through excretion of sodium and retention of free water.

Hypernatremia

Shifts in fluid balance can lead to an increase in serum sodium and osmolality. This shift results in stimulation of thirst and an increase in antidiuretic hormone (ADH). In normal, alert individuals, hypernatremia is unlikely to occur.

Hypernatremia is defined as a sodium level greater than 145 mEq/L. It is a relative state of free water deficit and an increase in the solute concentration in all body fluids. The 3 major hypernatremic states result from loss of water, hypotonic fluid loss, and sodium retention.

Water Loss

Pure water loss usually occurs with increased insensible loss through the skin. Thermal burn injury is associated with the greatest risk of insensible water loss. Diabetes insipidus, which results in massive amounts of dilute urine output, can be seen in patients with severe preeclampsia.

Figure 25-2 offers a simple algorithm for the treatment of hypernatremia due to this cause.

Hypotonic Fluid Loss

Hypotonic fluid loss is the most common cause of hypernatremia. It is usually caused by dehydration due to gastroenteritis or an osmotic diuresis.

Signs of ECF depletion may be present. Oliguria will be present unless the osmotic diuresis has been induced. Treatment is outlined in Fig 25-3.

Sodium Retention

Sodium retention is an uncommon phenomenon. It is usually seen only when hypertonic saline- or bicarbonate-containing solutions are being infused.

Central Diabetes Insipidus

Central diabetes insipidus (CDI) is a unique cause of hypernatremia. It is most often seen in the setting of acute head injury, pituitary injury, or cerebral hemorrhages. Early recognition is the key to treatment. The diagnosis of CDI should be suspected if the urine is not concentrated in the setting of the hypernatremia.⁷

Hyponatremia

Hyponatremia is defined as a serum sodium level of 135 mEq/L or less. Three major categories of hyponatremia exist: isotonic (pseudohyponatremia), hypertonic, and hypotonic. Severe hyponatremia (<120 mEq/L) is a serious life-threatening condition. Mortality rate may exceed 50%; however, rapid correction of sodium may produce central pontine myelinolysis and cerebral edema which can be fatal.

Isotonic

Isotonic hyponatremia is characterized by a low serum sodium level but a normal plasma osmolality. Common causes include hyperproteinemic states and hyperlipidemic states. The management requires evaluation and correction of the underlying cause. The following correction factors may be used to assist in correcting the sodium concentration:

Hypertonic

Hypertonic hyponatremia is diagnosed by a low serum sodium and a plasma osmolality of greater than 290 mOsm/kg H₂O. The most common cause of this disorder is hyperglycemia seen in association with diabetic ketoacidosis (see Chap 11). Correction of hyponatremia requires addressing the underlying disorder and replacing the free water deficit (Fig 25-3).

Hypotonic

Hypotonic hyponatremia is characterized by a low serum sodium and plasma osmolality. It can be divided into 3 subtypes: isovolemic, hypervolemic, and hypovolemic. The clinician should address 3 major concerns: The patient’s neurological status, volume status, and adrenal function.

Isovolemic hyponatremia is characterized by a small gain in free water. This may be related to inappropriate secretion of ADH or in rare instances psychogenic polydipsia. Numerous drugs have been implicated in this disorder and they are listed as follows:

• Morphine

• Nonsteroidal anti-inflammatory drugs (NSAIDs)

• Carbamazepine

• Oxytocin

Hypovolemic hyponatremia is characterized by the loss of fluid that is isotonic to plasma combined with volume replacement using a hypotonic fluid. This results in a net sodium loss. The most common causes of this disorder are diuretics, adrenal insufficiency, or diarrhea. A urine sodium can help to identify the etiology (ie, renal or extrarenal) of the hyponatremia.

Hypervolemic hyponatremia occurs in patients in which there is excess water and sodium gain. Edema is common in this population. Causes include heart, renal, and liver failure. The evaluation and management of hypotonic hyponatremia is presented in Fig. 25-4.

Potassium

Potassium is the major intracellular cation. The normal plasma potassium concentration is 3.5 to 5.0 mmol/L. Renal excretion is the major route of elimination of dietary or other sources of excess potassium. The clinician should keep in mind that serum potassium may be falsely elevated in the presence of hemolysis or factitiously decreased when processing of a lab sample is delayed.

Hypokalemia

Hypokalemia is defined as a serum potassium concentration below 3.5 mEq/L. The causes of hypokalemia may be classified as transcellular shift, as in the use of β agonist (ie, terbutaline), or from depletion. The major causes of the latter are renal loss, most commonly caused by diuretic therapy, or extrarenal, usually seen with excessive diarrhea. A number of drugs listed below are also associated with hypokalemia. Treatment is outlined in Fig 25-5.

• Laxatives

• Gentamycin-cephalexin combo

• Prostaglandin F2 α

• Steroids

• Furosemide

• Penicillins

• Lithium

• β agonists

Hyperkalemia

Hyperkalemia is defined as serum potassium above 5.5 mEq/L. It is caused by the release of potassium into the extracelluar fluid such as in myonecrosis, or by reduced renal excretion.⁸

Hyperkalemia can be associated with fatal cardiac arrythmias; therefore, it should be treated much more aggressively than hypokalemia (Fig 25-6).

Magnesium

Magnesium is not uniformly distributed in the body fluid compartments. Over half of the total body stores are located in the bone and less than 1% are distributed in plasma. This distribution creates a problem in diagnosing disturbances in magnesium balance. Magnesium levels are frequently overlooked in the critically ill patient and are not often replaced. For these reasons, magnesium may be the most common electrolyte abnormality in critically ill patients. In obstetrics, the use of magnesium for tocolysis and for neuroprophylaxis can further complicate the picture. The most common cause of magnesium depletion in our population is the use of diuretics.

The use of amnioglycosides can also lower magnesium levels. Alcoholism is a rare cause of magnesium depletion in obstetric patients. Low levels of magnesium may potentiate cardiac arrythmias.

Hypermagnesemia is almost always associated with renal insufficiency, with excess magnesium intake, or in cases of diabetic ketoacidosis. Infusion of magnesium in patients with preeclampsia or other diseases that may be associated with renal insufficiency should be done with care. Hypotension can be seen with magnesium levels of 3.0 to 5.0 mEq/L. A level greater than 12 mEq/L can be associated with respiratory depression. Levels greater than 14 mEq/L can be associated with cardiac arrest. Treatment protocols are outlined in Table 25-6.

Calcium and Phosphorus Balance

There are 3 fractions of calcium in the blood. About 50% of calcium is bound to serum proteins—with albumin accounting for 80% of protein binding. Anions like bicarbonate are bounded by 5% to 10% of calcium. The remainder of calcium is present as the free or “ionized” form of calcium. The interpretation of calcium levels must be adjusted for change in serum albumin.

A correction factor, that increases the total calcium by 0.8 mg/dL for each 1 mg/dL decrease in albumin, should be used. Obtaining an ionized calcium may avoid using the above correction factor; however, changes in pH or other factors may also alter calcium levels.

Hypocalcemia

The most common cause in an acute care setting is magnesium depletion. Other causes such as hypoparathyroidism are usually not a concern in an acute setting. Massive transfusion, pancreatitis, and burns are other causes of decreased calcium level in this patient population.

The clinical manifestations include neuromuscular excitability, which may vary, cardiovascular excitability including decreased myocardial contractility, and a prolonged QT interval. Treatment includes the infusion of calcium chloride or gluconate.⁹

Hypercalcemia

Hypercalcemia should be treated when the serum calcium level approaches 13 mg/dL or higher. Causes of hypercalcemia include malignancy and hyper-parathyroidism. Mental status changes are the most common clinical symptoms and warrant immediate therapy. The aim of the therapy is to facilitate the excretion of calcium in the urine (Table 25-7).

Phosphorous

Like magnesium and potassium, phosphorous is predominately an intracellular ion. While phosphorous levels may show diurnal variation, severe hypophosphotemia (serum level below 0.5 mg/dL) is uncommon. The most common causes of hypophosphotemia in the obstetric population are recovery from diabetic ketoacidosis, aluminum antacid use, or respiratory alkalosis. Phosphate deficiency reduces cardiac contractility, shifts the oxygen dissociation to the left, and may contribute to skeletal muscle weakness. Intravenous replacement is recommended (Table 25-8).

Hyperphosphatemia is seen in the face of renal failure or tissue destruction, such as rhabdomyolysis. Management is directed at correcting the underlying problem. Aluminum-containing antacids may also be administered (Table 25-8).

Caring for the critically ill obstetric patient requires a coordinated effort involving the maternal-fetal medicine specialist, internist, neonatologist, and other members of the critical care team. Meticulous attention to fluid and electrolyte balance will enable the clinician to restore the altered physiology that results from the underlying pathological process.