CHAPTER 23. DEHYDRATION
Kim K. Kuebler and Valarie A. Pompey
The issues surrounding dehydration and the implementation of hydration in the palliative and end-of-life care setting to date have been somewhat controversial. The traditional standard of medical care has been to provide routine hydration, whereas the traditional hospice model has promoted the concept of not administering parenteral fluid during the dying or terminal phase of incurable illness, based on the experience that artificial hydration causes potentially uncomfortable symptoms in the dying patient (Walker, 2002). Evidence can be found to support both approaches of care. It is important, however, for the clinician to consider dehydration as a contributing factor in the exacerbation of patient symptoms (Walker, 2002). The use of hydration can be a simple and powerful intervention when combating various symptoms arising from the concomitant manifestations that result from dehydration. Symptoms such as delirium, agitation, somnolence, and dizziness can be resolved with simple, cost-effective hydration. At end-of-life, the benefits of artificial hydration must be balanced by the potential burdens of providing fluids, such as increased secretions, the discomfort of needle sticks, and the physical barrier between patient and family caused by adding tubes. The decision to provide or withhold artificial hydration is based on careful evaluation of the patient’s condition and goals. Artificial hydration should not be routinely administered or routinely denied.
DEFINITION AND INCIDENCE
A discussion of the definition and incidence of dehydration must include the symptoms that frequently accompany and are influenced by dehydration. Dehydration may cause a cluster of many symptoms, such as delirium, xerostomia, agitation, myoclonus, somnolence, dizziness, constipation, and fatigue (Huang & Ahronheim, 2002; Waller & Caroline, 2000). Many of these symptoms are discussed elsewhere in this text; the focus of this practice protocol is on briefly describing the role of dehydration in associated symptoms that ultimately influence patient-related quality of life.
Dehydration should be considered under the broader rubric of fluid deficit and defined as the overall reduction of water content within the human body, but particularly from within the intracellular space (Sarhill, Walsh, Nelson et al., 2001). Dehydration is always hypernatremic, while fluid depletion, which is loss of intravascular water and sodium deficit, may be isotonic, hypertonic/hypernatremic, or hypotonic/hyponatremic (Sarhill et al., 2001; Sarhill, Mahoud, Christie et al., 2003). Dehydration is a common condition that occurs in the dying and terminally ill patient as a result of diminished fluid intake, nausea/vomiting, cachexia, anorexia, and diaphoresis (Huang & Ahronheim, 2002). Dehydration may also be the result of drying medications such as opioids, anticholinergics, and diuretics. If not resolved, it can increase the incidence of pressure ulcers, confusion, and renal failure, resulting in an accumulation of active drug metabolites. Accumulation of drug metabolites can further prompt multiple symptoms, such as restlessness, myoclonus, seizures, and hyperalgesia (Walker, 2002).
When describing dehydration, the clinician should also consider the terms fluid deficit, hypovolemia, and volume depletion. Dehydration does not adequately describe, for example, fluid deficit, which is defined as the loss of water with or without accompanying electrolytes, particularly sodium (Beers & Berkow, 2000; Sarhill et al., 2001; Sarhill, 2003). Volume depletion occurs from loss of extracellular fluid (especially intravascular) and is accompanied by a normal, decreased, or increased plasma serum level (Beers & Berkow, 2000; Leaf, 1984; Sarhill et al., 2001). Dehydration occurs when intracellular water is lost. This leads to transmembrane water migration from the intravascular compartment under osmotic pressure and increased plasma sodium concentration (Sarhill et al., 2001; Sarhill et al., 2003).
ETIOLOGY AND PATHOPHYSIOLOGY
To dehydrate is to lose predominantly intracellular water (Feig & McCurdy, 1977; Sarhill et al., 2001). Total body water averages 60% of body weight in young adult males and 50% in young adult females (Sarhill et al., 2001). The total body water decreases with age and accounts for 50% in elder men and 45% in elder women (Sarhill et al., 2001). Because serum sodium and its associated anions account for more than 90% of the solute in extracellular fluid, the plasma sodium concentration is a good indicator of plasma osmolarity (Guyton & Hall, 2001).
In isotonic fluid deficit, there is a depletion of both sodium and water. The serum sodium level is within normal limits (135 to 148 mEq/L) despite a fluid volume deficit. Examples of this deficit can be seen in blood loss and loss of gastrointestinal fluids such as diarrhea, vomiting, or nasogastric suctioning (Sarhill et al., 2001). In hypernatremic dehydration, there is a water loss alone, and in fluid volume deficit, there is water loss in excess of serum sodium. Therefore, serum sodium is concentrated (≥145 mEq/L) as a result of lower fluid volume. Hyponatremic fluid deficit occurs with excessive loss of sodium along with some fluid volume loss, leading to a serum sodium level of less than 130 mEq/L (Guyton & Hall, 2001).
As disease becomes debilitating and the dying process approaches, patients lose their ability or desire to drink fluids. The lack of fluid intake may lead to an isotonic depletion of water and sodium or, possibly, a tendency toward hypernatremic dehydration. In studies of persons experiencing dehydration at end-of-life, more than half had normal or near-normal serum sodium concentrations (Burge, 1993; Ellershaw, Sutcliffe, & Saunders, 1995; Waller, Hershkowitz, & Adunsky, 1994). It must be noted, however, that the results of these studies cannot be generalized because of small sample sizes, potentially biased selection criteria, and missing data (Viola, Wells, & Peterson, 1997).
Patients with dehydration may demonstrate low blood pressure with dizziness and syncope, decreased skin turgor, dry mucous membranes, low-grade fever, decreased urine output, and weight loss. A complaint of thirst is common although not universal. Because the serum is more concentrated, laboratory data may show elevated hemoglobin, hematocrit, and blood urea nitrogen levels (Guyton & Hall, 2001).
Many of the patients in the studies noted did not have isotonic volume depletion but appeared to have a hypertonic/hypernatremic dehydration. Hypernatremia is possible with a prolonged decrease in fluid intake, as may be seen in the terminally ill; it also occurs in the presence of excessive diaphoresis and with diabetes insipidus. The signs and symptoms are the same as those of isotonic dehydration, except that thirst is almost universal, because even slight increases in sodium concentration (as little as 2 mEq/L above normal) activate the thirst mechanism (Guyton & Hall, 2001; Sarhill et al., 2001; Sarhill et al., 2003). As the sodium level increases, anxiety and restlessness may also be present.
The sensation of thirst is important to fluid balance. The presence of thirst or dry mouth has been reported in 25% to 64% of cancer patients initiated to a palliative care service (Morita, Tsunoda, Inoue et al., 1999; Ventafridda, DeConne, Ripamonti et al., 1990). The incidence of thirst is increased to 61% to 87% in the final week of life (Conill et al., 1997; Ellershaw et al., 1995). In dehydration, patients experience thirst due to either dry mucous membranes or increased serum sodium levels and are stimulated to drink to replace the fluid loss. It is important to note, however, that the presence of thirst does not necessarily indicate dehydration. Many medications, such as opioids, phenothiazines, antihistamines, antidepressants, and anticholinergics, can cause the sensation of thirst despite adequate hydration. Thus, thirst alone is not a good indicator of a patient’s hydration status.
The elderly are at an increased risk for dehydration, in part because of a decrease in the sense of thirst that accompanies the normal aging process. A lack of thirst may also be the result of a coexistent inability to respond physiologically to thirst from disease or disability (Morita, Tei, Tsunoda et al., 2001; West, 1993). In addition, the elderly are susceptible to the development of dehydration or hypovolemia as a result of chronic use of medications such as diuretic therapy, which can be responsible for significant water and vital electrolyte depletion (Sarhill et al., 2001).
Confusion, agitation, and restlessness are often associated with dehydration and may result from one of several of the following mechanisms. Dehydration directly affects the body’s blood volume and circulatory reserve and can cause confusion and restlessness in non–terminally ill patients as well as those with an advanced illness (Fainsinger, Mac Cachern, Miller et al., 1994; Fainsinger & Bruera, 1994; Pereira & Bruera, 1997; Sarhill et al., 2001). In addition, the decreased circulatory volume may lead to decreased renal perfusion and eventual renal failure. In persons receiving opioids, poor renal perfusion may cause accumulation of opioid metabolites, leading to confusion, myoclonus, and nausea (Bruera, Franco, Maltoni et al., 1995; Caraceni & Grassi, 2003). Constipation, pyrexia, and electrolyte imbalance result from dehydration and can further contribute to disorientation, agitation, and neuromuscular irritability (Fainsinger & Bruera, 1994; Steiner & Bruera, 1998).
Providing fluids to persons who are dehydrated may alleviate many of the symptoms of dehydration and assist in flushing waste products and medication metabolites from the circulation. Providing fluids to persons whose kidneys cannot eliminate the additional fluid may lead to discomfort from fluid overload, with symptoms of edema, ascites, pulmonary congestion, and nausea and vomiting.
ASSESSMENT AND MEASUREMENT
The determination of a patient’s hydration status is difficult in patients who have multiple problems associated with advanced diseases. Consideration of the following factors, as well as the signs and symptoms of dehydration identified in Box 23-1, may assist the clinician to discern an appropriate diagnosis for dehydration:
Box 23-1
Confusion
Restlessness
Delirium
Myoclonus
Seizures
Constipation
Nausea and vomiting
Decreased glomerular filtration rate (may also be the result of renal failure)
Presence of decubitus ulcers
Higher-than-normal systolic blood pressure
Tachycardia at rest
Thready pulse
Dry mouth, multiple tongue furrows
Delayed capillary refill
Orthostatic blood pressure changes
Increased body temperature
Weight loss
Hypoactive deep tendon reflexes
Flattened neck veins
Severely restricted oral intake
Decreased urine output in patients who do not have preexisting renal failure
Poor skin turgor, dry mouth, and postural hypotension, noting that dehydration is not the only cause of these symptoms
Changes in laboratory findings such as elevated urea, creatinine, hematocrit, sodium, and plasma protein levels
Confusion Restlessness Delirium Myoclonus Seizures Constipation Nausea and vomiting Decreased glomerular filtration rate (may also be the result of renal failure) Presence of decubitus ulcers Higher-than-normal systolic blood pressure Tachycardia at rest Thready pulse Dry mouth, multiple tongue furrows Delayed capillary refill Orthostatic blood pressure changes Increased body temperature Weight loss Hypoactive deep tendon reflexes Flattened neck veins Severely restricted oral intake Decreased urine output in patients who do not have preexisting renal failure Poor skin turgor, dry mouth, and postural hypotension, noting that dehydration is not the only cause of these symptoms Changes in laboratory findings such as elevated urea, creatinine, hematocrit, sodium, and plasma protein levelsIt is important to note that the presence of edema is not a good indicator of the patient’s hydration status. Edema in the advanced cancer population is often the result of low serum albumin level or tumor blockage of the venous or lymphatic systems. Patients taking corticosteroids may also experience edema. Despite excessive fluid in the interstitial spaces, there may be inadequate intravascular fluid.
HISTORY AND PHYSICAL EXAMINATION
History
Review history of the terminal illness and any coexisting medical conditions that may affect urinary elimination or the ability to ingest fluids. Review intake and output. An estimate from the patient or caregiver may provide sufficient information, or the clinician may instruct the patient and family caregivers to record intake and output. Review history of any recent infection causing fever. Review history of any condition causing fluid loss, such as nausea or vomiting, diarrhea, or fistulas or/draining wounds. Review patient reports of headache, fatigue, muscle weakness, or anorexia, noting onset and any correlation with decreased fluid intake. Assess for the onset and severity of any mental status changes, such as restlessness, confusion, or delirium. Assess the use of diuretics, including frequency of administration, last dose, and urine output after last dose.Physical Examination
Skin and mucous membranesBody temperature
Skin condition, noting skin turgor and any dryness or pruritus
Alterations in skin integrity, such as decubitus ulcers, draining wounds, or fistulas
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