Maintaining the Internal Seas
in Harmony

What this article is: A concise practical approach and overview for nurses new to the Emergency Department setting who confront common presentations of dehydration and abnormal levels of sodium and potassium.

What this article does not do: It does not comprehensively examine pathophysiology, complex causation, metabolism, acid-base balance or their integration into practice. Nor does it discuss thoroughly discuss all useful data of drugs mentioned such as cautions, contraindications, interactions, and adverse reactions. One should always become familiar with drugs used and be in compliance with applicable policies, standards, and regulations.

Our disclaimer fully applies to all and every part of this article.

References & Useful Links [URLs] are provided.

         We’ve all heard that the body is 98% water in composition. Tears taste salty. Perspiration tastes salty. And, I have read in textbooks that urine tastes salty . . . ---Why? Have you ever held a penny or aluminum foil, or the wire hanger of an IV bottle in your mouth, and noticed a slight tingle of electric current? The salts or electrolytes in our bodily fluids make the conduction of current for our control circuits more efficient, and the gradient or concentration of them across membranes provides for an action potential for events to occur. When these concentrations are out of range, our ability to maintain homeostasis is impaired. The effects of disease, or consequences of some therapies, can adversely affect the proper concentration.

        While many specific problems can occur, such as arrhythmia or even paralysis, unless the patient is medically "savvy" he may not know what is wrong, but states it most commonly as "weakness", feeling "woozy" or dizzy, "tired", "don’t feel good", and may exhibit malaise or lassitude.

        Dehydration is a commonality of many ailments that we treat, the etiologies or differential diagnosis of which is too complex for the time that we have here. While we can readily replete fluid loss, we must not forget to consider the cause, nor to be especially wary when it afflicts the very young, the very old, or those with other disease, for upon them can dehydration fall disproportionately hard. Nor can we forget that world wide, ten million persons die annually of dehydration.

        While some patients or their parents will tell you that they are "dehydrated", others will not recognize that this has occurred. Some do not realize the insidious progression of dehydration in a febrile illness. They take to bed, sleep as much as they can, and do not undertake an active program of rehydration, or the necessity of drinking beyond thirst or desire when apathetic.

Dehydration may be suspected by the

How much fluid?:

        As a practical matter, adults who come to the ED with dehydration typically need at least 2 to usually 3 liters of intravenous replacement of Normal Saline (0.9% NaCl) in order to feel well enough to go home and continue hydrating orally. This amount may surprise them until you explain the diffusion from intravascular space to extracellular space to intracellular space and how the body has been "robbing Peter to pay Paul".

Patient Education:

        Another practical matter is to do as much teaching to the patient and his family throughout the episode of care. This not only remedies knowledge deficits, and empowers the patient with a plan to continue his self-care at home, but does much to lessen the need for a return visit on this or future illnesses. Do not, however, gloss over important caveats as to when to return if not improved.

        Telling the patient about anticipated side effects can beneficially enhance their effect and minimize complaints to you: "You may, or may not, notice some additional effects of the medicine. You might notice a little dryness in your mouth from the chemical, not a true thirst, just a little dryness to let you know that it’s there working for you. And, you might notice a little drowsiness, but it’s OK to enjoy that as much as you like.

Lab Studies:

        When drawing blood samples, expect needing CBC, "SMA-7" (electrolytes, creatinine, blood urea nitrogen, and glucose) as basic indicators of the level of disease. Additional chemistry studies may be indicated by the history. If the patient is very ill or critical, a prompt Arterial (or Venous) Blood Gas may be essential.

Infusion Rate & Potential Hypothermia:

        If the patient is significantly hypovolemic, and is a young and healthy adult without heart disease or other contra-indications, the first and sometimes second liter may be run in "wide open". Since this fluid is room temperature, (unless you have removed a warmed bag of saline from an approved fluid warming cabinet, or use an approved fluid warmer infusion system) the rapid flow will cause the IV site and limb to feel cool; in fact, by the end of 1 or 2 liters, the patient will feel chilled. Slow the infusion rate, provide warm blankets, and when possible, change to warm fluids (I tape a ChuxÒ around the bag to insulate against heat loss.)

        With elder patients, it may be prudent to begin repletion at a slower rate, preferably controlled by an infusion pump, and to reassess cardiac and pulmonary status frequently. Check the infusion site frequently also as more fragile veins and connective tissue can easily lead to extravasation of fluid. If the patient is significantly dehydrated, has an electrolyte disturbance, or other issues, it may be necessary to admit the patient for gentle rehydration.

Pediatric Infusion & Reassessment:

        Mild cases can be offered Pedia-Lyte®, "PediPops", or the breast by Mom. If intravenous therapy is indicated, set up an infusion pump with Normal Saline as the resuscitation fluid, 10-20 ml/kg of body weight aliquots will be infused over ½ hour or at maximum rate. The child will then be reassessed, and another aliquot of 10-20 ml/kg ordered. If a third dose is given and the child is not vastly improved, it will probably be necessary to admit the child for continuing treatment.

        Very Ill and critical-appearing children should get a VBG (venous blood gas) drawn with their labs. Remember that Diabetic Keto-Acidosis can be the initial presentation of Juvenile Diabetes.

        If the child is shocky, it may be necessary to push the resuscitation fluid in with a syringe in order to deliver it rapidly. [Interposing a 3 or 4-way stopcock between the IV tubing and the T-set adapter at the cannula hub can make this easier. Alternatively, with a 60 ml syringe attached to gravity IV tubing, fluid can be pulled down from the bag, then injected via the cannula by pinching the tubing above the syringe if there is no anti-backflow valve.]

        When fluid resuscitation has improved the child’s perfusion, the infusate will be changed to "D5% in 0.2% Na Cl" for "maintenance fluid" (with Potassium 20 mEq/L added only after voiding of urine or renal function is known) for small children and infants or "D5% ½ NS for older children (with Potassium 20 mEq/L added only after voiding of urine or renal function is known).

        When a child has poor IV access, but it is desired to avoid a central IV line or Intraosseous infusion, it is sometimes possible to give oral rehydration therapy by nasogastric tube until the intravascular volume is sufficiently restored to "plump up" peripheral veins.

When To Begin PO Fluids:

        Defer permitting oral fluids, or using anti-emetic drugs, until after initial fluid replacement. IV rehydration, alone, will do much to reverse nausea and abdominal discomfort. [In pediatric practice, it is the AAP standard to use fluid replacement therapy alone.] When nausea has settled, the patient should begin sips of water, and advance as rapidly as tolerated. Being able to consume and tolerate oral fluids is a criterion for discharge; documented success of a "PO Challenge" is essential.

Anti-Emetic Therapy:

        If the patient clearly has active and intractable vomiting, anticipate or request an order for

• Proclorperazine Edisylate (if injection) or Maleate (if oral) (CompazineÒ ); 5-10 mgms Q6Hours, IV/IM/(PO in mild cases); PR suppositories are available in different strengths [N.B.: The adult suppository is 25 mgms intended to be used Q12Hours. Combined dosage of all routes in adults is Not To Exceed 50 mgms. (usual daily total is 40 mgms by routes other than rectal) The risk of side effects considerably increases.]
• Metoclopramide (Reglan®) 10 mgms IV/PO has the added property of enhancing intestinal motility.
• Droperidol (InapsineÒ ) is a powerful anti-emetic that also does much to lessen non-specific abdominal pain and cramping. It has little effect on blood pressure. It tends to produce more drowsiness than others. Adult doses are typically 625 mcgs, possibly repeated, or a single dose of 1.25 mgms. N.B. Unfortunately, this very useful and effective anti-emetic has received a "Black-Box Warning" to its labeling from the FDA. Essentially, the warning is of cardiac arrhythmia and death from even usual and low doses and urges EKGs, and cardiac monitoring for a number of hours. This labeling has made usage of the drug unacceptably difficult to defend if an adverse effect occurred, it is no longer listed to be used at our institution.
• Promethazine (PhenerganÒ ) is a "classic" anti-emetic given IV/IM; typically, in managing active nausea and vomiting, it is given intravenously 12.5 mgms-25mgms Q4hours.
• Hydroxyzine Hcl (VistarilÒ ), an injectable form of the antihistamine also known as AtaraxÒ , is labeled as IM only.
• Lorazepam (AtivanÒ ) is a useful adjuvant anti-emetic that eases anxiety and distress of the patient’s symptoms. It can be given IV/IM/PO but significantly can be dissolved sub-lingually in 30-60 seconds without taste but with rapid effect. This may then make it possible to look for an IV site in calmer fashion.
• Additional anti-emetics available from the pharmacy which are not stocked in our institution's ED Pyxis MedStation™ are:

        Disorders of Sodium and Potassium, the two principle electrolytes, are the most common problems. Hypokalemia [¯ K+] is the most prevalent. Hyperkalemia [­ K+ ] occurs in special instances, primarily in renal patients. Hyponatremia [¯ Na+] and Hypernatremia [­ Na+] generally occur in elderly and neurological patients.

        Serum Potassium levels below 3.5 mEq/L leads to weakness, fatigue, cardiac arrhythmia and irritability. It typically occurs in older patients with excessive diuresis and inadequate dietary or supplementary potassium sources. If a potassium disorder ("hypo" or "hyper") is suspected, immediately do a stat. electrocardiogram and begin cardiac monitoring (checking for EKG changes is faster than the laboratory). How symptomatic a patient may depend more on the rate of change in serum level and the chronicity of it, than the absolute level.

• Ongoing or severe fluid losses from the GI tract by vomiting, diarrhea, or nasogastric suction, are a major cause; chronic laxative abuse in the elderly; malnutrition may cause an inadequate dietary supply.
• Diuretics; b -adrenergic agonists e.g., Albuterol; Steroids; Theophylline; Aminoglycosides; are all implicated in lowering potassium levels.
• Renally mediated losses from Renal Tubular Acidosis or hyperaldosteronism, Magnesium depletion, and Leukemia.
• Insulin and alkalosis shift potassium out of circulation and into cells.

        The patient may complain of palpitations due to arrhythmia; muscle weakness, cramps, fasiculations, or tetany; nausea and vomiting; constipation, ileus; paresthesias and paralysis; polyuria and polydipsia, altered mental status.

        Mild hypokalemia can be treated with oral potassium (if tolerated), education upon dietary sources, possible change by the physician of medications to spare potassium, and follow-up to recheck the level.

        Symptomatic patients and more severe deficits will need careful and cautious intravenous replenishment of potassium.

Lab Studies:

        Electrolytes, Serum Creatinine, Blood Urea Nitrogen, Glucose are basic; Calcium, Magnesium, Phosphate may be needed. Digoxin level is very important (whether hypokalemic or hyperkalemic) if patient is taking Digoxin due to enhancement of proarrhythmic or toxic properties. Alkalosis can shift K⁺ into cells; an ABG may be needed.

EKG Changes:

Essential Points for Treatment:

1. Verify hypokalemia before giving Potassium.
2. Verify renal status before giving Potassium.
3. Do not use matrix tablets for acute replacement; they dissolve slowly and are for maintenance therapy. Use liquid or soluble potassium in chilled juice.
4. Always use an infusion pump when giving intravenously.
5. Always dilute potassium; never inject potassium by push!
6. Peripheral Veins: use small cannula in large vein.
7. Central Veins: preferable to peripheral infusion; higher concentrations better tolerated. Do not use Distal port of Pulmonary Artery Catheter (Swan-Ganz).
8. Infusion may be painful and phlebitic. Lidocaine may be given and warm packs may help. Infusion may need to be diluted further or slowed.
9. Cardiac Monitoring is desirable.
10. Be familiar with policy.

        Acutely rising Serum Potassium threatens life. Symptoms are few and non-specific. A stat. electrocardiogram is essential for determining the effect of the hyperkalemia upon the heart. Most of our patients with hyperkalemia have renal failure (acute or chronic) and have been non-compliant with dialysis or have dietary indiscretions of food rich in potassium.

Symptoms:

        Fatigue, weakness, paresthesias, paralysis, palpitations.

Lab Studies:

        Electrolytes, Creatinine, Blood Urea Nitrogen, Glucose, Calcium, Digoxin level (if taking), Arterial Blood Gas (if acidosis), Urinanalysis (new renal problem?), Creatine Kinase [CK] (if rhabdomyolysis, e.g., "found on floor" or crush injury.

Treatment:

        In good health, sodium balance is finely regulated by the body to a range of 135 – 145 mEq/L and serum osmolarity of 290 (± 10) mOsm/kg through mechanisms of thirst, secretion of Anti Diuretic Hormone by the posterior pituitary gland, the renin-angiotensin-aldosterone system, and kidney responses to sodium. Changes in sodium and osmolarity can affect volume of intracellular fluid and the functioning of cells. This is especially so with rapid or acute changes, as slower chronic change may be better tolerated to a point. Cerebral cells are especially vulnerable to increases of intracellular volume as the skull provides no relief for edema and pressure increases until brain herniation occurs. The very young and the very old are more severely affected. Attempts to rapidly alter sodium level and osmolarity can have severe adverse effects such as fluid overload, or in chronic hyponatremia when compensatory changes have occurred too rapid correction can produce Central Pontine Myelinolysis (CPM) in which focal demyelination occurs in the pons and extrapontine areas.

Causes and Work-up:

        Not all hyponatremia is alike. Different causes and approaches to treatment exist due to acuity, volume status, total body water amount (TBW), and osmolarity. The full work-up may extend beyond the ED to inpatient or outpatient status, diagnostic studies, and consultations.

• Infants given only tap water during gastroenteritis.
• Hyperglycemia and Diabetic Ketoacidosis.
• Psychogenic polydipsia.
• Beer Alcoholism with malnutrition.
• Recreational use of MDMA "Ecstasy".
• Congestive Heart Failure.
• Malignancy.
• CNS disease.
• Pulmonary disease, Tuberculosis.
• Drug effects (good medication history is needed).
• Renal disorders.
• Hepatic Cirrhosis.
• Hypothyroidism.
• Adrenal Insufficiency.
• Syndrome of Inappropriate Antiduretic Hormone (SIADH).
• Iatrogenic replacement of fluid losses with hypotonic solutions.

Lab Studies:

        Electrolytes, Creatinine, BUN, Glucose (Hyperglycemia can cause a pseudohyponatremia by a factor of 1.6 mEq/L for each ­ 100 mg/dl of glucose, which is self-correcting as patient becomes normoglycemic.), Serum Osmolarity; Calcium, Magnesium, Phosphate may be requested; Urine Sodium and Osmolarity; additional tests may include lipids, thyroid function tests, serum cortisol and ACTH stimulation test.

        Chest X-Ray to look for malignancy. Head CT to check for cerebral edema, herniation, and possible tumor.

Presentation:

        The patient seems to have "failure to thrive" with anorexia, nausea, headache, cramps, or "altered mental status" ranging to confusion, status seizures, coma, and death. If sodium has declined gradually, compensatory changes will have occurred, the patient may have mild symptoms, and may tolerate serum sodium of 110 mEq/L. If change has occurred in 24-48 hours, then patients will be symptomatic at @ 120 mEq/L and risk of herniation increases with continued fall.

Nursing Approach:

1. Assess the patient. Get a sense of baseline. Determine the acuity and severity of change. Neurological abnormalities indicate the severest derangement and potential disaster.
2. Notify Attending Emergency Physician of Altered Mental Status stat.
3. ABCs Stat. SpO₂, Blood Glucose. Consider Naloxone (Narcan®); Dextrose; Thiamine. IV access and send lab studies.
4. Continue assessment of cardiopulmonary status and hydration status (hypovolemic, euvolemic, or hypervolemic and edematous).
5. The hypovolemic patient (continuing loss with replacement by free water or hypotonic solutions) with tachycardia, ¯ turgor, light-headedness, dry membranes, possible orthostasis, may need gentle hydration with Normal Saline as ordered by the physician.
6. The euvolemic patient without dehydration or edema will need fluid restriction and other actions as ordered by the physician.
7. The edematous and congested patient will need fluid and sodium restriction, other studies, and actions as ordered by the physician.
8. Anticipate admission.

Treatment Options:

        Hypernatremia (serum sodium >145 mEq/L) can be a significant electrolyte disturbance, especially in the elderly, with up to 50% mortality. Excessive sodium and hypertonicity or hyperosmolarity is ordinarily well regulated by thirst (given access to water) and ADH mechanism. When it occurs water extraction from brain cells can cause neurological change, and even protective compensatory transport of electrolytes and generation of solutes inside the cell to protect the cell structure impairs the functioning of the neuron. Brain shrinkage pulling on dural veins and sinuses can cause intracranial hemorrhage.

        Endogenous sodium gain as in Cushing’s Syndrome of mineralocorticoid excess, or exogenous sources such as Hypertonic Saline infusions, Salt or Sodium contaminated ingestants, or Sodium Bicarbonate administration may cause a problem.

        Water losses greater than sodium loss through diarrhea, vomiting or burns, or through renal disease or diuresis and osmotic diuresis may lead to hypernatremia.

        Disorders of thirst regulation by the hypothalamus, or of ADH regulation as in Central (neural) or Nephrogenic Diabetes Insipidus.

        Medication effects and other systemic diseases as causes mandate a thorough drug and medical history.

Signs & Symptoms:

        Thirst, dry membranes, apathy, confusion, restlessness, fever, decreased or absent urine output, hyperventilation, muscle twitching or spasticity, progressive decrease in mental status.

Lab Studies:

        Electrolytes, Creatinine, BUN, Glucose, Osmolarity; Urine Osmolarity and Electrolytes.

Other Studies:

        Head CT to rule out Intracranial Hemorrhage or tumor. CXR. Weight. Intake & Output.

Nursing Approach:

1. Assess the patient. Get a sense of baseline. Determine the acuity and severity of change. Neurological abnormalities indicate the severest derangement and potential disaster.
2. Notify Attending Emergency Physician of Altered Mental Status stat.
3. ABCs Stat. SpO₂, Blood Glucose (to consider and rule out Hyperglycemic Hyperosmolar Non-Ketotic Coma). IV access, and send lab studies.
4. Continue assessment of cardiopulmonary status and hydration status (hypovolemic, euvolemic, or hypervolemic and edematous).
5. The hypovolemic patient with tachycardia and hypotension may need hydration with Normal Saline or ½ Normal Saline to stabilize, until free fluid deficits can be corrected with D5%Water as ordered by the physician; dialysis may be needed in some cases.
6. The euvolemic patient may have free fluid deficits replaced by D5%Water as calculated and ordered by the physician.
7. Patients with Diabetes Insipidus (¯ ADH® inability to concentrate urine) will need hydration and correction with Vasopressin (Pitressin®) (given IV/IM/SC) which is synthetic ADH or with Desmopressin (DDAVP) (given IV/SC/IntraNasal Insufflation) to control the abnormality as ordered by the physician.
8. Anticipate admission.