Fluid and electrolyte management in the neurologically-impaired patient.
Fluid and electrolyte disturbances are a common occurrence in the patient with neurological impairment. Failure to correctly identify these various disorders may cause the patient's condition to worsen. Signs and .symptoms of some of these disorders may be vague and confusing. This article reviews principles of fluid and electrolyte balance in the body, discusses how and why these disorders can occur and offers guidelines for the management of disturbances in the patient with neurological impairment.
Overview of Water and Electrolytes
Water is a fundamental requirement for cellular function. The cell receives nutrition and excretes waste materials through a constant fluid exchange with extracellular fluid via a semipermeable membrane. Overall fluid volume in the body comprises about 60% of the total body weight. This fluid is distributed within two compartments: intracellular fluid (ICF) and extracellular fluid (ECF). The two are separated by a semipermeable membrane and the differences between them are very important. The ICF is primarily composed of potassium, phosphate and proteins, while ECF contains mainly sodium, chloride and bicarbonate. Each has its own different yet normative composition of water and electrolytes. The body expends energy to maintain these differences. The movement of water and electrolytes is critically important for the synthesis of protein and transmission of electrical impulses to nerve and muscle cells. The movement of two major electrolytes--sodium and potassium--is dependent upon three different mechanisms: osmosis, diffusion and active transport.
The movement of water across the cell membrane is termed osmosis. Water moves from a lower to higher concentration on either side of the membrane to achieve a balance. Osmolality, the concentration of solutes, is usually measured in milliosmoles (mOsm) per liter per volume. It is the index by which fluid needs to retain water or to draw it through the cell membrane.
Electrolyte balance is maintained through diffusion, the movement of particles from higher concentration to lower concentration. Diffusion is carried out via active transport to equalize particles, while osmosis occurs passively. Thus, water and electrolyte solutions are always in a state of flux.
Osmolality is controlled, in part, by osmo receptors in the hypothalamus. Within the hypothalamus is an area known as the thirst center which alerts the cerebral cortex for the need to drink fluids whenever osmolality begins to increase. In good health, our thirst reflex triggers responses to fluid needs, but an ill patient may not be able to sense thirst. To compensate for a lack of oral intake, ICF is pulled from the ECF to maintain the osmotic pressure.
The hypothalamus produces antidiuretic hormone (ADH) that also plays a primary role in water regulation. Also known as vasopressin, ADH is produced by the hypothalamus and stored in the posterior pituitary. Osmoreceptors in the hypothalamus are sensitive to overall fluid balance and release ADH accordingly. When released, ADH renders the renal tubules more permeable to water, thus retaining needed fluid. When body fluid volume decreases or solute concentration increases, osmolality likewise increases. This is sensed by osmoreceptors and then triggers the release of ADH. With hypotensive states, stretch receptors in the barocenters found in the right atrium or carotid artery bifurcation will release ADH to conserve volume. Pain or stress can also trigger ADH release.[6,14]
The regulation of sodium also influences water volume since water follows sodium. Another hormone, renin, is secreted when the distal tubules sense hypotension associated with low fluid volume.[11,15] is Renin produces angiotensin I and angiotensin II which in turn, stimulate the adrenal gland to secrete aldosterone to enable the renal tubules to retain sodium and water, while excreting potassium and hydrogen ions.
Sodium in Neurological Disease
Sodium is the main substance present in the ECF. Excess and deficits of sodium pose a serious risk since sodium profoundly influences renal regulation of water status. Since ECF is composed of water, sodium and its anions, regulation of these levels are critical to maintain osmolality and overall fluid volume. The serum sodium level is so very important because it is the primary electrolyte in ECF and as water follows sodium, hence, sodium's value reflects total body volume.[13,14]
Many patients with neurological disease exhibit dysfunction of sodium and water regulation. Both sodium and water are regulated by complex neural systems that integrate information regarding both extracellular and intravascular volumes as well as circulatory processes and osmolality. Sodium, the primary cation of ECF, has a number of important physiological functions such as maintaining osmotic pressure of ECF and regulating neuromuscular activity and water excretion by profoundly influencing the kidney's regulation of water status. Through this intricate feedback system, the patient that develops serum hyponatremia will have an automatic neural response which will result in increased water excretion. Hypernatremia will conversely result in water conservation.
Since serum sodium levels determine ECF volume, any abnormalities of sodium are actually disorders of water metabolism. Either high or low levels of sodium can result in deleterious consequences for the patient. Either imbalance can present with altered mental status, exhibit unbalanced intake/output ratio and can prolong or exacerbate the underlying condition. Hyponatremia after subarachnoid hemorrhage (SAM) can lead to an increased risk of brain ischemia. The severity of the hyponatremic state is directly related to the rapidity of onset and the range of the abnormality.[2,10] Hypernatremia can indicate neurohypophyseal dysfunction as a result of diabetes insipidus (DI) and should serve as a warning that hypercalcemia may also develop, causing renal calculi that could result in renal tubular disease.[5,15]
Serial laboratory tests such as a complete blood count (CBC), electrolytes values and osmolality should be monitored. Changes in serum osmolality are usually synonymous with changes in sodium concentration, except with the use of mannitol or in cases where the patient is hyperglycemic or had recently ingested ethanol. An abnormal sodium level may be the result of either a disorder in sodium or water regulation or both together. In most neurologically-impaired patients, the causes of hypernatremia and hyponatremia are usually disturbances in water regulation.
The normative sodium values are important but it is equally important to know how quickly and by what margin the altered sodium level changed as this may affect treatment. The severity of the hyponatremic state is directly related to the rapidity of onset and the range of the abnormality.[2,10] Some patients can present with chronic hyponatremia in which their bodies have adapted with volume changes. If correction is attempted in this scenario, sodium replenishment must proceed as a gradual process to avoid brain swelling that may result. The following section discusses abnormalities of sodium content and respective treatment modalities along with the role of nursing management.
Syndrome of Inappropriate Antidiuretic Hormone
Syndrome of inappropriate antidiuretic hormone (SIADH) is a functional disorder of water regulation. The characteristics of the syndrome were first described in full by Schwartz et al in 1957 in two subjects with bronchogenic carcinoma. There are a variety of causes for SIADH including disorders of the nervous or endocrine systems, pulmonary dysfunction, intake of certain drugs or an idiopathic, ectopic production of ADH. There is no one specific cause. Most commonly, SIADH develops in patients with injury to the hypothalamic-neurobypophyseal system. Causes include brain tumor, abscess, head trauma, SAH, hydrocephalus, meningitis, encephalitis and Guillian-Barre syndrome.[2,7,16] Although the mechanism is not clearly understood, there is an abnormally high level of ADH in the blood stream in relation to the ratio of osmolality, thus altering the rate of renal excretion of water. In SIADH, serum sodium and osmolality are low in comparison to a high urine sodium and osmolality. Clinical symptoms usually develop when the serum sodium value drops near 120mEq/L and advance according to the severity of the hyponatremic state that develops.[11,16] Symptoms are usually slow to develop. The patient may be initially lethargic with complaints of headache. Mental status may decline further, with confusion and progress to significantly decreased levels of consciousness. Nausea and vomiting, diarrhea, anorexia, generalized muscle weakness and decreased tendon reflexes can also be present. There is concentrated low urine output. In a grossly severe state of water intoxication, seizures may develop which can lead to coma.
Serum laboratory tests reveal low blood urea nitrogen (BUN) and creatinine clearance (Table 1). Potassium is usually not affected but may be low. Hemoglobin and hematocrit are decreased due to the dilutional status that develops with increased ADH secretion.
[TABULAR DATA 1 OMITTED]
Current treatment modalities include strict fluid restriction, as little as 800cc/day. Intravenous solutions of 3% or 5% saline are given slowly with a potassium supplement often added. Oral sodium can be given via food or table salt if the patient is capable of oral intake. Medications which increase production of ADH of those which cause fluid retention should be avoided. Some drugs that counteract ADH production may also be given, such as lithium carbonate, naloxone and more commonly, demeclocycline. The goal of treatment is to increase serum sodium and decrease free water slowly to achieve a normal serum osmolality. The principle is not to increase serum sodium by more than 12mEq during the first twenty-four hours and no more than 20mEq in forty-eight hours. Lasix may also be given to induce diuresis. Potentiating factors related to the patients' medical diagnosis that may promote SIADH are evaluated on an individual basis.
SIADH usually takes 3-5 days to resolve. Nursing diagnoses may include actual fluid volume excess, altered mucus membranes and potential for skin breakdown due to the increased fluid volume. The short-term goals for the patient are prompt detection of signs and symptoms of SIADH and measures initiated to restore fluid and electrolyte balance. The long-term goal is to prevent permanent neurological deficit. Nursing activities include monitoring intake/output, serum osmolality, electrolytes (primarily sodium) and comparing findings with concurrent urine osmolalities and electrolytes, noting urine color and specific gravity. The patient should also be observed for generalized edema and daily weights. Adherence to the strict fluid restriction is of utmost importance; thorough patient and family teaching of the purpose of the fluid restriction will need to be done. Continued monitoring of neurological status with prompt reporting of any changes is necessary.
Cerebral Salt Wasting
Cerebral salt wasting (CSW) is a hyponatremic condition originally thought to cause all sodium losses in patients with cerebral disease. The theory of CSW eventually fell out of favor in the 1950s when Schwartz et al defined the syndrome of inappropriate ADH (SIADH) as the explanation for the onset of hyponatremia. Recent studies indicate that some cases of hyponatremia previously attributed to SIADH may actually be CSW. The concept of CSW has been reexamined and once again thought to be responsible for hyponatremia in some cases versus SIADH. These types of hyponatremia are similar in that patients exhibit low serum sodium and osmolality levels. However, CSW and SIADH differ significantly in terms of intravascular volume status, actual serum sodium concentration and vasopressin levels. Thus, treatment for CSW and SIADH differs.
CSW may be the more accurate definition for sodium loss since renal excretion of sodium may be the result of an extra-renal influence, atrial natriuretic factor (ANF), a fairly recent discovery. ANF cells have been located in both the hypothalamus and right atrium and may control fluid volume regulation, although its exact actions are yet unknown.
As water follows sodium, this renal excretion of sodium results in an overall decreased fluid volume. SIADH is a dilutional hyponatremia rather than a true loss of sodium; intravascular volume is increased because fluid is retained due to increased amounts of circulating vasopressin. Treatment for SIADH includes fluid restriction, especially free water, but also includes slow replacement of sodium with hypertonic intravenous solutions. Proposed treatment of CSW differs in that fluid volume as well as sodium replacement is necessary. Replenishing fluid volume status with an isotonic solution to expand intravascular volume will help diminish ADH secretion as well as rehydrate the patient.
Distinguishing between the two types of hyponatremia is important because therapies are different for each. Incorrect treatment may have a negative impact on the patient's outcome, such as restricting fluids in the patient with postoperative hyponatremia following SAH. Fluid restriction in this case could be ultimately fatal as we know that decreased fluid volume exacerbates vasospasm, and a hypervolemic state is preferred to decrease the risk of vasospasm. Recent studies have shown that CSW may be the primary cause of hyponatremia in SAH versus SIADH; therefore fluid replacement is advantageous in two ways in treating this patient.[3,10] Differentiation between CSW and SIADH is determined by serum vasopressin and ANF levels.
Diabetes insipidus (DI) is a fluid imbalance resulting from either a deficiency of ADH or to renal unresponsiveness to the release of ADH. DI is classified in two different categories: central DI and nephrogenic DI. Nephrogenic DI is rare and occurs when the kidney is unable to utilize ADH. Thiazide diuretics may then be given to increase urinary concentration via a vasopressin-independent mechanism. Central DI is more common. Two-thirds of patients that develop central DI have damage to the supraoptic, hypophyseal-portal pathway from trauma, neurosurgery, or inflammatory or vascular lesions.[6,11] Central DI can develop quickly or appear up to fourteen days after surgery or insult and has been further subdivided into four types 16
* Type 1: Classical severe DI: the pituitary fails to produce or release ADH
* Type 2: Defective osmoreceptor DI the increased plasma osmolarity fails to release stored ADH
* Type 3: Reset osmoreceptor DI: the plasma osmolarity is abnormally high before ADH is released
* Type 4: Partial DI: there is not enough ADH secreted in response to serum osmolarity
ADH is normally released in response .o a 1%-2% increase in extracellular osmolality or with a decrease of 5%-10% of circulating blood volume.[11,13] Hypotension, stress, pain, anxiety and an upright position are causes for ADH to be released. If alert and conscious, the thirst mechanism is also activated in response to increased sodium or osmolarity. The most prevalent clinical symptoms of DI is a large volume of urine output. Urine color is very pale with a low specific gravity of 1.005 or less. Serum osmolality is concurrently elevated, greater than 295mOsm/ kg and serum sodium is greater than 145mEq/L (Table 1). The alert patient may complain of polydipsia, polyuria and nocturia. Complaints of generalized weakness are common. Loss of fluid can be extreme, up to fifteen liters within twenty-four hours. If untreated at onset, the patient quickly develops dehydration due to this extreme loss of fluid. Clinical signs of dehydration include dry mucus membranes, poor skin turgor and possible complaints of dysphagia. Neurologically, the patient can present as lethargic with a paradoxically increased anxiety level. Blood pressure may initially be normal or slightly elevated. Later stages may show tachycardia, a lack of thirst, hypotension and shock.
To assure early diagnosis of DI, urine output of greater than 200cc for two consecutive hours should be reported to the physician. Diagnosis can then be based on presenting clinical symptoms and lab work. If the patient has had pituitary surgery or head trauma, diagnosis may be made by simply ruling out other causes of polyuria. Another condition which may also produce polyuria is hyperglycemia, in which case the urine specific gravity would be elevated. Overhydration with IV fluids or excessive oral intake must be evaluated; in these cases, the serum osmolarity would tend to be low.
Keep in mind that although polyuria is the primary clinical symptom, patients with an already dehydrated state, especially the elderly, may have enuresis. Patients with trauma or surgical damage to the anterior pituitary may not exhibit polyuria until corticosteroid deficiency is corrected. However, clinical signs and symptoms of dehydration will be present and patient history should be suspicious for DI. On the other hand, alert patients who are able to keep a fair water balance by increased oral intake may not initially present with dehydration. Patients with decreased sensorium that have an impaired thirst center and cannot express their need for water, may progress to a dehydrated state very rapidly in which shock may occur from circulatory collapse.
Once the diagnosis of central DI is confirmed, the treatment is fluid replacement. Intravenous fluids, D5/W are typically administered along with careful replacement of electrolytes. If able, the patient may also be given oral fluids or fluids via nasogastric tube. If fluid replacement contains sodium, the polyuria may increase in severity in which case exagenous ADH (vasopressin) can then be given. The dose and frequency are determined by the severity of DI.
Usual dosage of vasopressin given for DI is 5-10u subcutaneously or intravenously. In cases of severe idiopathic DI, vasopressin tannate, an oil-based mixture which typically lasts up to 48 hours, may be given. The usual dosage of vasopressin tannate is Su-10u administered intramuscularly; injections can be painful. If DI is mild, the patient may be treated with fluid replacement alone or receive a nasal inhalation vasopressin solution, DDAVP. Duration of action of nasal inhalation of DDAVP is 18-24 hours with a typical dosage of 0.1-0.4cc. A newly released form of DDAVP is also available; doses range from 1-10u, once of twice a day. Note that nasal congestion or previous cocaine use (inhaled) has been found to interfere with drug absorption. When the patient with DI requires ongoing home treatment, assure that thorough patient teaching on the use of vasopressin and recognition of signs and symptoms associated with DI and water intoxication is carried out.
After start of therapy, patient response should be carefully monitored to prevent water intoxication. If the urine osmolality increases and then decreases, additional vasopressin is needed. If the urine output decreases significantly (less than 1000cc/24h) and specific gravity is greater than 1.015, then the dosage of vasopressin needs to be adjusted or discontinued if the problem is resolved.
Other treatment may include administration of drugs that increase release of ADH from the posterior pituitary and enhance action at the renal tubules. These drugs include morphine sulfate, barbiturates, cholinergics, caffeine, acetaminophen and beta-adrenergic agents, among others.
Nursing goals for the patient with DI include early recognition and correction of fluid deficits. As patients can become volume depleted quickly, urine output greater than 200cc for two consecutive hours should be reported to the physician. Intake and output should be monitored hourly. Daily weights should be obtained and a 2-5 pound weight loss within 24 hours reported. The patient must be monitored for fluid retention as fluids and medications are administered. Measures of renal function including BUN, serum osmolarity and electrolytes must also be closely monitored. Prudent skin care should be carried out each shift. The long-term goal is to achieve a urinary output of 1000-1500cc per 24 hour period with urine specific gravity of 1.0101-1.015.
Finally, DI is usually transient as a result of the edema from cranial insult. Resolution can take days to a few weeks. A condition of permanent DI will develop only if 80% or greater destruction occurs to the ADH-producing nuclei of the hypothalamus or the proximal end of the pituitary
Hyperosmolar Hyperglycemic Nonketotic State
A hyperosmolar hyperglycemic nonketotic (HHNK) state is a metabolic complication of illness or disease characterized by fluid and sodium imbalances with concurrent severe hyperglycemia (600-1400mg/dl). It is not common and its onset is insidious. HHNK occurs most often in the non-insulin dependent diabetic, the elderly, the septic patient or in individuals with underlying renal or cardiovascular disorders.[6,19] In general, loss of body water is usually accompanied by a loss of electrolytes. This does not occur in HHNK and results in a state of true dehydration, the definition of which is loss of body water without loss of electrolytes.
Loss of free water can occur with prolonged hyperventilation, increased tracheal secretions, diarrhea, high fever or in the urine when the kidney fails to concentrate solutes. Solute accumulation can occur in patients with diets high in protein or dextrose, ie, tube feedings that result in nitrogenous waste products. Endogenous solute accumulation also occurs in diabetes mellitus with elevated glucose and ketone levels. Either mechanism results in an osmotic-induced diuresis, the body's attempt to excrete a solute load through the kidneys by excreting a large volume of urine. Formation of the urine in this process requires the use of a great deal of water, further expecditing the water deficit. This true state of dehydration is characterized by elevated serum sodium, BUN and osmolality (>290mg dl). Clinically, the patient presents with some degree of neurological impairment due to the hyperglycemic osmotic-reduced diuresis. Mental status often deteriorates and the patient's presentation may mimic that of a stroke with hemiparesis, visual field deficits and/or hemisensory deficits. Seizures may occur and mental status can progress to stupor and coma.
Because it is so uncommon, diagnosis of HHNK may be delayed, especially in elderly patients without a history of DM and who exhibit neurological deficits. Differential diagnosis to rule out diabetic ketoacidosis (DKA) versus HHNK is determined by the absence of ketones (thought to be the result of circulating endogenous insulin), an acetone odor to the breath and the absence of Kussmaul respirations. Because untreated cases of severe dehydration can lead to circulatory collapse, HHNK is potentially lethal. Studies have indicated a 40-60% mortality rate with approximately 50% of the deaths occurring within the first 2-3 days after onset.16 It is not a "self-correcting" disease, thus, timely medical intervention is required.
The goals of treatment are to correct the life-threatening fluid and electrolyte imbalances and to remove the underlying cause of HHNK. Medications that have been known to exacerbate HHNK should be reconsidered and deleted if possible. Such medications include thiazide diuretics, steroids, mannitol or phenytoin. As phenytoin has been known to inhibit ADH secretion and antagonize the hyperosmolar state, alternate antiepileptic medication may be given to avoid this.
Immediate treatment measures for HHNK include slow and cautious fluid replacement. Isotonic or hypotonic IV fluids such as sodium chloride or half normal saline are administered usually over a period of several days. Too rapid fluid administration can result in sudden intercompartmental water shifts and result in pulmonary edema.
Concurrent low-dose insulin infusion is often necessary due to the severe hyperglycemia. Electrolytes are typically not administered until the body has received a certain percentage of isotonic fluid, thus optimizing renal function. For patients with renal impairment, treatment modalities are similar, only correction is approached less aggressively.
Nursing responsibilities for the patient with HHNK include obtaining an accurate nursing history and evaluate any precipitating factors. If the patient is unable to be interviewed, family members can be quite helpful in providing information, such as whether the patient complained of extreme thirst, fatigue, and polyuria prior to admission. The nurse can also inquire if the patient was taking any of the medications implicated in an increased risk for HHNK. Nursing interventions include hourly neurological assessment, and monitoring intake and output with assessment of vital signs. Administering the ordered IV fluids and monitoring blood glucose hourly while insulin drip is infusing is crucial. Of utmost important is to watch for cardiac dysrrhythmias that may result from electrolyte imbalances and observe for signs of impending congestive heart failure. The nurse may need to assist with the insertion of a pulmonary artery catheter or central venous line if the physician wishes to more precisely observe the patient's fluid balance. Obtaining the patient's weight on a daily basis assists with the evaluation of fluid retention and diuresis. An indwelling urinary catheter is recommended to observe hourly output. Urine may initially be concentrated but will eventually clear as fluid equilibrium is restored. Frequent serial laboratory tests should include a complete blood count, sodium electrolytes and osmolality. Frequent mouth care and the initiation of safety measures are also requisite nursing interventions along with meticulous skin care to prevent skin breakdown from prolonged bedrest and immobility which often accompany such a serious, electrolyte and fluid imbalance.
Fluid and electrolyte imbalances are a common complication in the patient with intracranial injury or insult. Correct identification of these imbalances and familiarity with the different forms of intervention are important nursing functions. The neuroscience nurse must have an understanding of the basic principles of fluid homeostasis in the human body in order to grasp the importance of the potential each imbalance has for serious complications. Inappropriate ADH secretion, cerebral salt wasting, diabetes insipidus and hyperosmolar hyperglycemic nonketotic state each have the potential to become life threatening and/or render the patient with irreversible neurological deficits.
[1.] Bradley W, Baroff R, Fenichel G et al: Principles of diagnosis and management. Pages 620-622 in: Neurology in Clinical Practice, Cooper P (contributing editor). Butterworth-Heinmann, 1991. [2.] Green BA, Marshall LF, Gallagher TJ: Pages 298 299 in: Intensive Care for Neurological Trauma and Disease. Acadence Press, 1982. [3.] Hickey JV: The Clinical Practice of Neurological and Neurosurgical Nursing, 3rd ed. JB Lippincott, 1992. [4.] Ignatavicius D, Bayne M: Medical-Surgical Nursing: A Nursing Process Approach. WB Saunders Company, 1991. [5.] Leahy NM: Quick Reference to Neurological Critical Care Nursing Aspen Publishers, 1990. [6.] O'Brien MT, Pal]ett PJ: Total Care of the Stroke Patient. Little, Brown and Co., 1978. [7.] Patterson L, Noroian E: Diabetes insipidus versus syndrome of inappropriate antidiuretic hormone. Dimen Crit Care Nurs 1989; (4):226-233. [8.] Popper A, Kennedy S: Neurological and Neurosurgical Intensive Care, 2nd ed. Aspen Publishers Inc, 1988. [9.] Segatore M: Hyponatremia after aneurysmal subarachnoid hemorrhage. J Neurosci Nurs 1993; 25(2):92-97. [10.] Synder M: A Guide to Neurological and Neurosurgical Nursing Wiley Medical Publications, 1983. [11.] Veldhaus J: Endocrinology and Metabolism Clinics of North America. WB Saunders Co, 1992. [12.] Victor M, Adams R: Principles of Neurology, 5th ed. McGraw-Hill, Inc, 1993.
Questions or comments about this article may be directed to: Virginia M. Parobek RN, CNRN, Neuro Intensive Care Unit, staff nurse, Mount Carmel Medical Center, 793 W. State Street, Columbus, Ohio 43222.
Irene Alaimo RN, is a staff nurse in the Neuro Intensive Care Unit a Lakewood Hospital in Lakewood, Ohio.
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|Author:||Parobek, Virginia; Alaimo, Irene|
|Publication:||Journal of Neuroscience Nursing|
|Date:||Oct 1, 1996|
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