1 Describe the functionally distinct compartments of body water, using a 70-kg patient for illustration

Accurate estimations are difficult because ordinarily ideal body weight (IBW) is used as a basis for calculation. Obesity is rampant in our society, making accurate estimations difficult. Figure 4-1 estimates body water compartments in a patient with an IBW of 70 kg.

Figure 4-1 Body water compartments in a patient with an ideal body weight of 70 kg. BV, Blood volume; ECF, extracellular fluid; ICF, intracellular fluid; ISF, interstitial fluid.

2 Describe the dynamics of fluid distribution between the intravascular and interstitial compartments

The intravascular and interstitial fluid spaces compose the extracellular fluid and are in dynamic equilibrium, governed by hydrostatic and oncotic forces. Under normal circumstances the capillary hydrostatic pressure produces an outward movement of fluid, whereas the capillary oncotic pressure results in resorption. The sum of the forces leads to an egress of fluids from arterioles; about 90% of the fluid returns into the venules. The remainder of the fluid is subsequently returned to the circulation via the lymphatic system.

3 How are body water and tonicity regulated?

Antidiuretic hormone (ADH) is a primary mechanism; it circulates unbound in plasma, has a half-life of roughly 20 minutes, and increases production of cyclic adenosine monophosphate in the distal collecting tubules of the kidney. Tubular permeability to water increases, resulting in conservation of water and sodium and production of concentrated urine. Stimuli for the release of ADH include the following:

Hypothalamic osmoreceptors have an osmotic threshold of about 289 mOsm/kg. Above this level ADH release is stimulated.

Hypothalamic thirst center neurons regulate conscious desire for water and are activated by an increase in plasma sodium of 2 mEq/L, an increase in plasma osmolality of 4 mOsm/L, and loss of potassium from thirst center neurons and angiotensin II.

Aortic baroreceptors and left atrial stretch receptors respond to volume depletion and stimulate hypothalamic neurons.

4 Discuss the synthesis of antidiuretic hormone

ADH, or vasopressin, is synthesized in the supraoptic and paraventricular nuclei of the hypothalamus. It is transported attached to carrier proteins down the pituitary stalk in secretory granules into the posterior pituitary gland (neurohypophysis). There it is stored and released into the capillaries of the neurohypophysis in response to stimuli from the hypothalamus. ADH-producing neurons receive efferent innervation from osmoreceptors and baroreceptors.

5 List conditions that stimulate and inhibit release of antidiuretic hormone

See Table 4-1.

TABLE 4-1 Conditions that Stimulate and Inhibit Release of Adrenocorticotropic Hormone

6 What is diabetes insipidus?

Diabetes insipidus (DI) is caused by a deficiency of ADH synthesis, impaired release of ADH from the neurohypophysis (neurogenic DI), or renal resistance to ADH (nephrogenic DI). The result is excretion of large volumes of dilute urine, which, if untreated, leads to dehydration, hypernatremia, and serum hyperosmolality. The usual test for DI is cautious fluid restriction. The inability to decrease and concentrate urine suggests the diagnosis, which may be confirmed by plasma ADH measurements. Administration of aqueous vasopressin tests the response of the renal tubule. If the osmolality of plasma exceeds that of urine after mild fluid restriction, the diagnosis of DI is suggested.

7 List causes of diabetes insipidus

See Table 4-2.

TABLE 4-2 Causes of Diabetes Insipidus

8 Discuss alternative treatments for diabetes insipidus

Available preparations of ADH include pitressin tannate in oil, administered every 24 to 48 hours; aqueous pitressin, 5 to 10 units intravenously or intramuscularly every 4 to 6 hours; desmopressin (DDAVP), 10 to 20 units intranasally every 12 to 24 hours; or aqueous vasopressin, 100 to 200 mU/hr. Incomplete DI may respond to thiazide diuretics or chlorpropamide (which potentiates endogenous ADH).

Because the patient is losing water, administration of isotonic solutions may cause hypernatremia; in addition, excessive vasopressin causes water intoxication. Measurement of plasma osmolality, urine output, and osmolality is indicated when vasopressin is infused.

9 Define the syndrome of inappropriate antidiuretic hormone release. What is the primary therapy?

Hypotonicity caused by the nonosmotic release of ADH, which inhibits renal excretion of water, typifies the syndrome of inappropriate antidiuretic hormone (SIADH) release. Three criteria must be met to establish the diagnosis of SIADH:

The patient must be euvolemic or hypervolemic.

The urine must be inappropriately concentrated (plasma osmolality <280 mOsm/kg, urine osmolality >100 mOsm/kg).

Renal, cardiac, hepatic, adrenal, and thyroid function must be normal.

The primary therapy for SIADH is water restriction. Postoperative SIADH is usually a temporary phenomenon and resolves spontaneously. Chronic SIADH may require the addition of demeclocycline, which blocks the ADH-mediated water resorption in the collecting ducts of the kidney.

10 What disorders are associated with SIADH?

Central nervous system events are frequent causes, including acute intracranial hypertension, trauma, tumors, meningitis, and subarachnoid hemorrhage. Pulmonary causes are also common, including tuberculosis, pneumonia, asthma, bronchiectasis, hypoxemia, hypercarbia, and positive-pressure ventilation. Malignancies may produce ADH-like compounds. Adrenal insufficiency and hypothyroidism also have been associated with SIADH.

11 What is aldosterone? What stimulates its release? What are its actions?

Aldosterone, a mineralocorticoid, is responsible for the precise control of sodium excretion. A decrease in systemic or renal arterial blood pressure, hypovolemia, or hyponatremia leads to release of renin from the juxtaglomerular cells of the kidney. Angiotensinogen, produced in the liver, is converted by renin to angiotensin I. In the bloodstream angiotensin I is converted to angiotensin II, and the zona glomerulosa of the adrenal cortex is then stimulated to release aldosterone. An additional effect of angiotensin II is vasoconstriction. Aldosterone acts on the distal renal tubules and cortical collecting ducts, promoting sodium retention. In addition to hyponatremia and hypovolemia, stimuli for aldosterone release include hyperkalemia, increased levels of adrenocorticotropic hormone, and surgical stimulation.

12 Discuss issues associated with estimating volume status in outpatients

For most outpatients the period of fasting would provide a rough estimate of volume deficit. A patient’s hourly metabolic requirement is roughly 4 ml/kg for the first 10 kg, 2 ml/kg for the second 10 kg, and 1 ml/kg for the remainder of his or her weight. The actual deficit may be less than calculated because of renal conservation of fluids. Factors that may result in volume depletion include chronic hypertension, diuretic use, diabetes mellitus, alcohol ingestion, and bowel preparations (2 to 4 L may be lost).

13 Discuss estimating volume status in acutely ill patients

Acutely ill patients are often hypovolemic as a result of conditions such as bleeding, peritonitis, pancreatitis, sepsis, gastrointestinal losses, traumatic injury, and inadequate fluid replacement.

Physical findings suggesting inadequate intravascular fluid include dry mucous membranes, loss of skin turgor, capillary refill greater than 2 seconds, postural hypotension, tachycardia, and oliguria (less than 0.5 ml/hr in adults, less than 1 ml/hr in children). If present, central venous or (rarely) pulmonary artery catheters may assist in the diagnosis of hypovolemia.

Useful laboratory values in the assessment of volume status include hemoglobin, hematocrit, electrolytes, blood urea nitrogen (BUN), creatinine, proteins, urine osmolality, specific gravity, and sodium concentration.

14 Are there distinct advantages to using colloids to resuscitate a patient?

Colloid advocates claim that, because these solutions have an intravascular space half-life of 3 to 6 hours (much greater than crystalloids), they are superior resuscitation fluids. When compared to crystalloids in a controlled fashion, they have not been shown to improve outcomes. Further, in cases in which capillary permeability increases (e.g., burns, sepsis, trauma), colloids accumulate extracellularly, pulling other fluids along because of the osmotic gradient, resulting in extracellular edema. Finally, colloid solutions are more expensive.

Although only a third to a fourth of a liter of crystalloid remains in the intravascular space, if given in sufficient quantities (replacing losses in a ratio of 3-4 to 1), crystalloids are excellent resuscitation fluids. It should be noted that dehydrated patients suffer from fluid losses in both intracellular and extracellular compartments and crystalloids will replete both compartments.

15 Review the composition of crystalloid solutions

Fluid resuscitation in the operating room is accomplished with isotonic fluids since intraoperative losses include both salts and water. Thus only relatively isotonic fluids are listed. Patients requiring replacement of maintenance fluids are usually treated with hypotonic fluids because their losses are predominantly free water, but this is uncommon intraoperatively. Although normal saline is the preferred crystalloid to dilute packed red blood cells, administering large quantities results in hyperchloremic metabolic acidosis caused by dilution of bicarbonate (Table 4-3).

16 Review the colloidal solutions that are available

There are two albumin preparations, 5% and 25%. Preparation methods eliminate the possibility of infection. The 5% solution has a colloid osmotic pressure of about 20 mm Hg, which is the approximate colloid osmotic pressure under normal circumstances. The 25% solution (also called salt-poor albumin) obviously has a colloid osmotic pressure of about five times the normal situation. If intravascular volume is depleted yet extracellular volume is greatly expanded, this excess colloid osmotic pressure will draw fluid from the interstitium into the vascular space.

Hydroxyethyl starch in a 6% solution (dissolved in either normal saline or lactated Ringer’s solution) is another colloid preparation. The heterogeneous preparation contains polymerized molecules with molecular weights of between 20,000 and 100,000 daltons. Metabolized by amylase, it accumulates in the reticuloendothelial system and is renally excreted. Partial thromboplastin time is increased. It has dilutional effects on clotting factors, and the hetastarch molecules can move into organizing fibrin clot. Thus coagulation can be impaired. It is recommended that not more than 20 ml/kg be administered. The preparation dissolved in lactated Ringer’s is thought to have lesser effects on coagulation, perhaps because it is less heterogeneous in molecular weight dispersion. There are no effects on crossmatching of blood.

Dextrans are water-soluble, polymerized glucose molecules. Two preparations are available (dextran 40 and 70), and the molecular weights of the respective solutions are 40 and 70 kilodaltons. Anaphylactic and anaphylactoid reactions and inhibition of platelet adhesiveness have been noted. Crossmatching of blood may be difficult (Table 4-4).

TABLE 4-4 Commonly Administered Colloids

LR, Lactated Ringer’s solution; NS, normal saline.

17 What is the normal range for serum osmolality?

Different sources quote different ranges, but in general normal serum osmolality ranges between 285 and 305 mOsm/L. A quick rough estimate is to double the sodium concentration. A more accurate estimate of osmolality can be obtained using the following equation:

where the values in the brackets are the concentrations of the substances (sodium in mEq/L, glucose and BUN in g/L).

18 What situations might be appropriate for the use of hypertonic saline?

Hypertonic saline (usually 3%) has been used successfully during aortic reconstructions and extensive cancer resections; for hypovolemic shock, slow correction of symptomatic chronic hyponatremia, transurethral resection of the prostate syndrome, and increased intracranial pressure; and to reduce peripheral edema after major fluid resuscitations. It has been used in far forward combat situations and in trauma patients with prolonged transportation times (rural areas), but its use is still not extremely common.

19 How do you estimate fluid loss during a surgical procedure?

This is an inexact process. Gather as much information as you can. Estimating the volume found in suction canisters and subtracting whatever volume has been used for irrigation can assess blood loss. Surgical sponges can be weighed; a large laparotomy sponge can hold more than 100 ml of blood. Blood loss can also be occult, soaking into surgical drapes or running down onto the floor. Measure gastric aspirate. Significant peritoneal fluid collections may require replacement. Insensible losses are associated with intra-abdominal procedures in which the abdominal viscera are exposed, but estimating these can be problematic, and cookbook methods are not evidence based. For example, be smart when replacing urine output; if the patient has been given 5 L too much fluid, expect a vigorous urine output and do not replace this.

20 What is meant by third-space losses? What are the effects of such losses?

In certain clinical conditions such as major intra-abdominal operations, hemorrhagic shock, burns, and sepsis, patients develop fluid requirements that are not explained by externally measurable losses. Losses are internal, a temporary sequestration of intravascular fluid into a functionless third space, which may not readily participate in the dynamic fluid exchanges at the microcirculatory level. The volume of this internal loss is proportional to the degree of injury, and its composition is similar to plasma or interstitial fluid. The creation of the third space necessitates further fluid infusions to maintain intravascular volume, adequate cardiac output, and perfusion, and third-space fluids will persist until the patient’s primary problem has resolved.

21 How much fluid is appropriate to administer during a surgical procedure?

As has been previously mentioned, many cookbook recipes exist for administering intravenous fluids during surgical procedures. Many of these traditional recommendations have little evidence to support them. Clearly some fluid is better than none. For instance, nausea and vomiting and postural hypotension are reduced in patients having outpatient surgical procedures if the patient receives a liter or two of intravenous fluid perioperatively. But how much and for what procedure continue to be investigated. Every patient is different because each has differing periods of fasting, severity of illness, volume contraction, and coexisting disease.

There is good evidence that fluid restriction is beneficial in patients having thoracotomy and lung resections because of concern for postoperative pulmonary edema. Similarly, elective neurosurgical procedures and hepatic resections require judicious fluid administration. The viability of myocutaneous flaps is impaired in the setting of excess edema.

Recent investigations have compared liberal (consider this 12 to 15 ml/kg/hr or greater) to restrictive (consider this 4 to 8 ml/kg/hr) fluid administration protocols in patients having bowel resections. In the fluid-restricted group decreases in blood pressure of 20% of baseline or urine output of less than 0.5 ml/kg/hr were treated with repeated boluses of Ringer’s lactate, 250 ml. The restricted group had shorter hospitalizations, more rapid return of bowel function, and fewer surgical complications.

22 Is blood pressure a good sign of hypovolemia?

Blood pressure is not significantly affected until approximately 30% of blood volume is lost. Early compensatory mechanisms, including peripheral vasoconstriction and tachycardia, may mask significant volume loss.

23 What clinical findings support a diagnosis of hypervolemia?

The patient may have rales on lung auscultation, frothy secretions in the endotracheal tube, edematous mucous membranes and conjunctiva (although edematous conjunctiva by itself is not enough to make the diagnosis, especially when the patient has been in the prone position), polyuria, and peripheral edema. Like hypovolemia, hypervolemia is best diagnosed when a constellation of findings, and not just a single finding, is present.