Electrolyte Imbalances—Part 1: Sodium Balance Disorders

You respond to a local retirement center for a 76-year-old male patient seizing.

On arrival you find the patient supine in his bed in a postictal state. Nonmedical staff members describe a generalized tonic-clonic seizure and give you a history that includes agitation, headaches, apathy and a reduction in appetite. Further questioning reveals the onset of all the signs and symptoms occurred over the last 36 hours with the exception of the seizure, which had an acute onset, and staff immediately called for an ambulance. They also repeatedly state that the patient is allergic to water and has been "sneaking large amounts" of it over the last few days.

Your physical exam reveals normal development and nourishment. The patient's eyes are open, but he does not respond to verbal stimuli or follow commands. His airway is intact, and he is breathing rapidly in a crescendo-decrescendo pattern, followed by periods of apnea. He has no signs of dehydration or edema. As you continue your assessment, the patient seizes again. Although you treat it with a benzodiazepine, the seizure is poorly controlled. You later learn the patient died from his condition. What happened?

Overview

Electrolytes are substances that dissociate into electrically charged particles when dissolved in water. As a result, they are capable of conducting an electric current and are thus responsible for many of the activities of the body, including the automaticity of the heart, nervous impulse transmission and chemical reactions. There are many electrolytes in the body. Those that have positive charges are called cations, and those with negative charges are called anions. Cations of significant importance include sodium (Na⁺), potassium (K⁺), calcium (Ca²⁺) and magnesium (Mg²⁺). Anions include chloride (Cl^-), phosphate (PO₄^3-) and bicarbonate (HCO₃^-), among others. The primary function of anions is to offset the positive charges of the cations, and to function within various buffer systems.

As with all substances in the body, electrolytes are maintained within specific ranges by homeostatic processes. The kidneys are the primary regulators of electrolyte balance. In fact, as long as a person has functioning kidneys and adequate access to water, it is rare they will develop an electrolyte imbalance. The most common patients who develop these have varying stages of kidney dysfunction, lack of (or uncontrolled) access to water or a significant increase in total body water, or take medications that affect electrolyte excretion or retention.

Technology exists to evaluate electrolyte levels in the prehospital setting, but for a variety of reasons it is not commonly done. However, electrolyte imbalances can often be determined based on the patient's history and physical. It is important that prehospital professionals be able to recognize the presence of these disorders, as many have significant morbidity and mortality. Recognition not only allows appropriate treatment, but also aids in transport decisions and notification of receiving facilities.

This series of articles will examine four types of electrolyte disorders, beginning with sodium balance disorders.

Sodium Balance Disorders

Sodium is the most abundant extracellular electrolyte and therefore the primary extracellular cation. Normal Na⁺ extracellular concentration levels range from 135 to 145 mEq/L, and intracellular concentrations range from 10 to 12 mEq/L. The root pertaining to sodium is -natremia. Therefore, hyponatremia indicates extracellular sodium concentrations below 135 mEq/L, while hypernatremia indicates extracellular sodium concentrations above 145 mEq/L.

One primary role of sodium is in the transmission of electrical impulses in both the heart and nervous system. However, because it does not easily cross the cell membrane, sodium also plays a primary role in controlling water distribution throughout the body, and regulates the volume of the extracellular fluid (ECF). As a result, changes in sodium levels are normally accompanied by changes in water levels, and conversely, changes in total body water cause changes in sodium concentrations. Intracellular fluid (ICF) can also be affected by sodium levels. Hyponatremic states result in a diluted ECF in comparison to the ICF, causing water to move into the cells, leading to intracellular swelling and possible lysis. Hypernatremia will result in a concentrated ECF, causing water to move out of the cells, leading to cellular crenation.

Hyponatremia has many causes, which are listed in Figure 1. In addition to these, numerous medications can result in sodium loss. A partial listing can be found in Figure 2. The most common cause is the retention of water resulting in low sodium concentrations, called hypervolemic hyponatremia. In this situation, although the patient may have normal amounts of sodium in their body, the overall concentration is reduced due to the increase in total body water. Euvolemic hyponatremia results from the loss of sodium with a normal or slightly elevated level of total body water. Finally, the loss of sodium in excess of water is referred to as hyponatremic dehydration or hypovolemic hyponatremia. Patients who experience this condition have lost total body water, but their sodium loss exceeds their water loss, and as a result they have a sodium deficit associated with dehydration.

Hyponatremia is common in the hospital and nursing home settings, and recognizing it in the prehospital setting is critical to address cerebral edema and minimize brain stem herniation.

The signs and symptoms of hyponatremia are primarily related to the central nervous system (see Figure 3). As a result of the increased osmolarity of the ICF, water moves into the brain cells, causing cerebral edema. The number and severity of symptoms increase with the severity of the hyponatremia and its rate of onset. The brain can adapt to and minimize swelling by moving solutes and fluids to the extracellular space. This adaptation cannot occur in acute hyponatremia that develops in 48 hours or less and leads to brain stem herniation and death. This can happen before peripheral edema is apparent. Patients with chronic hyponatremia (developing over greater than 48 hours) have milder cerebral edema for their given sodium levels, and generally do not experience brain stem herniation. The key concept here is that although the actual sodium level is significant, it is the speed at which the patient develops that level that dictates its presentation and severity. For example, seizures and coma usually only occur with an acute reduction of serum sodium levels to less than 120 mEq/L. The mortality of acute hyponatremia can be up to 50%.

Treatment

Treatment is based on not only the serum levels of sodium, but also the rate at which it develops. In the hospital, patients with mild or chronic hypovolemia are treated for their underlying disorder. Severely symptomatic patients who have had an acute onset of hyponatremia are treated with 3% saline based on their sodium deficit and weight. However, the ability to measure sodium levels is not commonly available in the prehospital setting, and attempting to arbitrarily correct unknown levels can have serious complications, such as osmotic demyelination syndrome.

In general patients with sodium levels greater than 120 mEq/L do not require aggressive treatment; supportive care and evaluation of the underlying cause of the hyponatremia are often all that is indicated. Patients with levels below 120 mEq/L are most likely to present with severe signs and symptoms that manifest through the central nervous system and require immediate intervention.

As with any patient, life-threatening conditions must be addressed and supportive care initiated. Provide supplemental oxygen and ventilate the patient as needed. Monitor oxygen saturation, end-tidal carbon dioxide and cardiac rhythm. If allowed, obtain intravenous access, evaluate the blood glucose level and administer glucose if the patient is hypoglycemic. In the setting of hypervolemic hyponatremia, fluid restriction is indicated, and loop diuretics such as furosemide can be considered. This must be done with caution, as it will promote the excretion of sodium as well as water, and is often reserved for patients presenting with severe pulmonary edema.

If the patient is experiencing hypovolemic hyponatremia, isotonic saline can be administered to correct the volume loss. Seizures and other neurologic presentations, such as signs of increased intracranial pressure and brain stem herniation, are treated with standard therapy. Note, however, that hyponatremia-induced seizures respond poorly to benzodiazepines, and ultimately the serum sodium concentrations must be corrected.

Hypernatremia occurs when the sodium level is greater than 145 mEq/L. This condition is caused by either the gain of sodium in excess of water or the loss of water in excess of sodium. The latter, often referred to as hypernatremic dehydration, is the more common cause of hypernatremia. Hypernatremia is almost never found in an alert patient who has an intact thirst mechanism and access to water. Common causes of hypernatremia can be found in Figure 4.

The mortality rate for hypernatremia is high (reportedly 60% or greater), especially among the elderly. However, it is difficult to determine if this mortality rate is directly related to victims' hypernatremia. Many patients who develop this condition have several comorbid disease processes that may play a role in mortality.

Like hyponatremia, signs and symptoms of hypernatremia can develop acutely or chronically and are primarily related to the central nervous system (see Figure 5). Due to the hyperosmolarity of the ECF, water flows from the brain cells, leading to both crenation of the cells and a decrease in brain volume. As the brain shrinks in size, there can be enough traction on the bridging veins in the subdural space that their tensile strength is overcome and subdural hemorrhage occurs. This process may result in permanent neurologic deficits among survivors.

Treatment of hypernatremia in the prehospital setting is symptomatic and must first address any life-threatening conditions. Perform standard monitoring and glucose evaluations. Provide standard therapy for any presenting conditions (e.g., seizures). The primary treatment for hypernatremia is volume restoration using isotonic saline. As with hyponatremia, chronic hypernatremia should not be treated aggressively. In this setting the brain is able to adapt to the hypernatremia by producing substances that retain water in the cells. Aggressive fluid administration can lead to cerebral edema, an increased risk of seizures and permanent neurological damage. Hypernatremia that is acute in onset does not pose this risk, as the brain has not yet made these adaptations.

Conclusion

In the opening case, it was determined that the patient had an obsessive-compulsive disorder in which he would ingest large amounts of water if it was available. Upon arrival at the emergency department, his sodium level was 117 mEq/L and had developed over the previous 36 hours secondary to water ingestion.

In coming months, the remainder of this series will examine potassium, magnesium and calcium balance disorders and their treatment, and conclude with general recommendations for the treatment of electrolyte-based problems.

Next month: Potassium Disorders

Figure 1: Causes of Hyponatremia

Hypervolemic hyponatremia
•  Primary renal disease
•  Congestive heart failure
•  Decreased renal blood flow
•  Hepatic cirrhosis

Euvolemic hyponatremia
•  Inappropriate secretion of antidiuretic hormone
•  Excessive water intake (e.g., psychogenic polydipsia)
•  Uncorrected hypothyroidism
•  Cortisol deficiency

Hypovolemic hyponatremia
•  Excessive diaphoresis
•  Diarrhea
•  Vomiting
•  GI losses
•  Third spacing
•  Osmotic diuresis
•  Aldosterone deficiency
•  Salt-wasting nephropathy
•  Cerebral salt-wasting syndrome

Other causes
•  Hyperglycemia
•  Mannitol administration
•  Increased plasma proteins
•  Increased plasma lipids
•  Ecstasy use
•  Consumption of large amounts of beer

Figure 3: Signs and Symptoms of Hyponatremia

Anorexia
Nausea
Vomiting
Lethargy
Apathy
Difficulty concentrating
Confusion
Agitation
Headache
Disorientation
Muscle cramps
Weakness
Seizures
Focal neurologic deficits

Signs of brain stem herniation:
•  Coma
•  Unilateral fixed, dilated pupil
•  Posturing
•  Respiratory pattern changes
•  Bradycardia
•  Hypertension

Signs and symptoms of fluid retention:
•  Peripheral and pulmonary edema
•  Ascites
•  Acute weight gain

Signs and symptoms of dehydration if hypovolemic

Figure 4: Causes of Hypernatremia

Gain of sodium in excess of water
•  Excessive sodium bicarbonate infusions
•  Excessive hypertonic saline infusions
•  Antacid abuse
•  Excessive salt ingestion
•  Mineralocorticoid excess
•  Salt water ingestion
•  Cushing's syndrome

Loss of water in excess of sodium
•  Renal losses
•  Excessive use or misuse of diuretics
•  Intrinsic renal disease
•  Diabetes insipidus
•  Osmotic diuresis
•  Extrarenal losses
•  Diarrhea
•  Vomiting
•  GI losses
•  Burns
•  Third spacing

Reduced water intake
•  Decreased thirst mechanism
•  Water not available

References

Braunwald E, Fauci AS, Kasper DL, et al. Harrison's Principles of Internal Medicine, 15th ed. New York, NY: McGraw-Hill, 2001.

Marx JM, Hockberger RS, Walls RM, et al. Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed. Philadelphia, PA: Mosby, 2006.

Tintinalli JE, Kelen GD, Stapczynski JS. Emergency Medicine: A Comprehensive Study Guide, 6th ed. New York, NY: McGraw-Hill, 2004.

Robert Vroman, BS, NREMT-P, has been involved in all levels of EMS for almost 20 years, working with both rural and urban services as a provider and educator. He has a Bachelor's degree in Emergency Medical Care from Western Carolina University, and is currently pursuing a Master's of Education, specializing in Adult Education and Training at Colorado State University.