Managing Fluids & Brain Injury

In medical facilities across the country, the complexity of today’s patient continues to increase and the practicing intensive care nurse has an increasing potential to encounter a patient with some form of neurological injury in their day to day practice.

The bedside practitioner plays a vital role in the long-term outcome of their patients.

Neurological injuries have become wide spread and the administration of intravenous fluids (IVF) plays a vital role in the long-term outcomes of these patients, especially when the elements of cerebral edema and intracerebral hypertension are involved.

Managing Cerebral Edema

For nurses, our goal as the bedside practitioner, in conjunction with the medical staff, is to minimize the cerebral injury and preserve penumbral tissue. Penumbral tissue can be defined as, “ischemic tissue potentially destined for infarction but not yet irreversibly injured and the target of acute therapies.”1 It is the brain tissue that is damaged from decreased blood flow and cerebral edema but is not yet infarcted and with appropriate therapies can be salvaged.

One of the key components to managing cerebral edema is being mindful that the appropriate IVF are administered and that one does not inadvertently administer the wrong type of fluid and cause their patient’s cerebral edema to worsen.2,3 Salvaging this at risk tissue plays a key role in improving a patient’s long term morbidity and mortality especially when it pertains to their overall quality of life.4

Osmolarity and osmolality are two important terms to understand. Not all fluids are the same, and their effects on intravascular and intracellular water volume vary greatly. Distinguishing the difference between osmolarity and osmolality can be confusing, but it is important to understand when deciding whether a particular IVF is hypotonic, isotonic, or hypertonic in nature.

Osmolarity and osmolality are two terms that people use interchangeably but they are actually two separate units of measure. Osmolarity is defined as the number of milliosmoles/kg of solvent. It is the concentration of particles dissolved in a fluid where the osmolarity is the number of milliosmoles/L of solution.

In simple terms, these two units measure a solutions osmotic activity. Osmotic activity occurs when a solution of lower conductivity passes through a semi-permeable membrane barrier with the purpose of diluting the concentration of the solution on the opposing side of the membrane.2-3,5 In the human body, the osmolality of blood plasma is approximately 290mOsm/liter.

Fluids in the range of 240mOsm/liter to 340mOsm/liter are considered isotonic. Fluids with tonicities above 340mOsm/liter are considered to be hypertonic and those with tonicities below 240mOsm/liter are considered to be hypotonic.2-3,6&

The solute concentration of isotonic fluids is almost equal to that of plasma; therefore, it stays in the intravascular space, expanding it after administration.

The osmotic pressure remains constant inside and outside of the cells, so no fluid shift occurs and cells neither shrink nor swell. Subsequently, when isotonic fluids are administered they should increase the intravascular volume but not cause cerebral edema to worsen.

Types of isotonic solutions include: 0.9% sodium chloride (Normal Saline) and Lactate Ringers (LR). When caring for a patient with a neurological injury, it is important to note that Dextrose 5% in Water (D5W) is considered to be an isotonic fluid (chemically) while it is in the bag. When D5W is infused into the body, it transforms into a hypotonic solution when the glucose is metabolized by insulin, only free water is left behind.2-3,7

The solute concentration of hypotonic fluids is less than that of plasma, causing them to have low osmotic activity. Hypotonic fluids shift out of the intravascular compartment after being infused and into the cells and interstitial spaces. They are used to treat patients with conditions causing intracellular dehydration or when fluids specifically need to be shifted into the cells. It is important to be aware of how these fluid shifts will affect various body systems.

Hypotonic Solutions

Patients with neurological injury that have any potential for, or evidence of increased ICP’s should never receive hypotonic solutions. These solutions shift fluid into the brain tissue, which causes or worsens cerebral edema and may have life-threatening consequences. It is also important to be wary when administering hypotonic solutions to any patients with liver disease, trauma, or burns secondary to their potential for intravascular fluid depletion.

Types of hypotonic solutions include: 0.45% Sodium Chloride, 0.33% Sodium Chloride, 0.2% Sodium Chloride, and 2.5% Dextrose in water.2,4,7-9

Dextrose based fluids provide calories for energy and prevent ketosis, which occurs when the body burns fat. They also flush the kidneys with water, which helps them excrete solutes, and in some cases can improve liver function. When administering dextrose based solutions, be sure to watch for hypokalemia, hyponatremia, and water intoxication with prolonged treatment due to dilution of the body’s electrolytes.2,3,7

The solute concentration of hypertonic fluids is higher than plasma; therefore, they have a high osmotic activity. Hypertonic solutions draw fluid from the intracellular spaces and interstitial spaces and shift this fluid into the intravascular compartment. This fluid shifts out of the intracellular space is one of the key components to managing cerebral edema.

When administering hypertonic solutions watch for electrolyte imbalances, and also fluid overload in patients with a history of heart failure and hypertension. Types of hypertonic solutions include: 3% Saline, D5 NS, D10W, and D5 1/2NS. The solutions containing dextrose are chemically hypertonic until they are administered intravenously, when they become clinically hypotonic.

When caring for patients with neurological injuries, dextrose solutions (free water) should not be administered. Their administration decreases the body’s plasma osmolality and in turn increases the water content of the brain tissue. Additionally, literature pertaining to treatment of brain injury, clearly states that elevated blood glucose levels from the dextrose is associated with worsening of neurological injury.2,4,7-9

Managing Patients with Brain Injury

Now that we have reviewed the basic principles regarding the tonicities of various intravenous solutions, let’s apply these principles to the management of the brain injured patient.

When brain injury occurs, there is an area of infarction. Surrounding that infarcted tissue is the penumbral tissue, which becomes edematous and hypo-perfused causing it to lose its auto-regulatory abilities.

Cerebrovascular auto regulation is the brain’s ability to maintain a constant cerebral blood flow despite large changes in Cerebral Perfusion Pressures (CPP) and is accomplished by neuromyogenic modification of the diameter of precapillary arterioles.1,2,7. This causes the perfusion of the vital penumbral tissue to be directly linked to a patient’s Mean Arterial Pressure (MAP). Mean Arterial Pressure is the average blood pressure throughout the cardiac cycle.

Cerebral Perfusion Pressure (CPP) is a global measure of cerebral perfusion and it is calculated by performing the following calculation [MAP – ICP = CPP], [5].2 As mentioned earlier, both CPP and MAP are significantly influenced by shifts in fluid states. These fluid shifts can happen quickly in patients with elevated intracranial pressures and one must be hyper-vigilant in managing the IVF administered to these patients.6

As mentioned, 3% saline earlier in the hypertonic fluid section, it is often given as a bolus versus a continuous infusion when caring for patients with sustained intracranial hypertension (elevated ICP’s). The Monroe-Kellie Doctrine simply stated: The contents within the intracranial vault are a relatively fixed volume. The contents include: brain tissue (80%), cerebral spinal fluid (10%), and blood volume (10%).

While cerebral compliance is the brain’s ability to buffer an intracranial volume increases while avoiding an increase in intracranial pressures.2,7 Once cerebral compliance is challenged or lost, patients begin to experience sustained increases in their ICP’s. Cerebral edema usually begins to develop within hours of injury and peaks around two to five days.4,5

There are two additional Intravenous Therapies available to treat cerebral edema and Intracranial Hypertension. The first solution is Mannitol, which is an osmotic diuretic and is often administered in doses of 0.5-1gm/kg IVP. Conversely, hypertonic saline delivers a high osmotic load and is administered in concentrations ranging from 3% to 23.4%. These various solutions are given in either IV bolus form or IVP administration depending on the concentration of solution being delivered.

Serum Osmolarity is the key when considering administration of these two fluids. Both of these solutions cause an elevation in a patient’s serum sodium content, and the belief is that some degree of elevated sodium concentration is thought to be neuroprotective in nature. Hypertonic saline raises one’s serum sodium content by delivering high concentrations of intravenous sodium, while Mannitol raises ones sodium content though diuresis and depletion of one’s overall intravascular volume content (hem concentration).4,6

Complications related to elevated Sodium levels include: rebound cerebral edema, Congestive Heart Failure (CHF), decreased platelet aggregation, a hyper-chloremic metabolic acidosis, and Cerebral Pontine Myelinolysis (CPM) if elevated serum sodium levels are corrected too rapidly in a 12-24 hour period of time.4,6. The most current literature trends make the case that Hypertonic Saline is superior to Mannitol in the treatment of intracranial hypertension.6

Randomized studies have shown that Hypertonic Saline is free of many of Mannitol’s adverse effects, including: dehydration and oliguria which can lead to acute renal injury, electrolyte disturbances, and a resistance to Mannitol’s effects with repeated administrations secondary to a disruption in the Blood Brain Barrier and Mannitol crossing into the brain parenchyma and aggravating cerebral edema.9

Attention to Detail

Managing patients with neurological injury can be very rewarding for those practitioners involved in their daily care.

Understanding fluids and their effect on intravascular and intracellular volumes is one of the key steps in ensuring patient’s facing neurological injuries have good outcomes.

We have made leaps and bounds when it comes to improving long-term patient outcomes, and it is the attention to even small details that can have huge long term benefits for not only the patient but their families.

References for this article can be accessed here.

Aimee Brewer, Angeleath Daley, Consuelo Scoggins and Marya Searcy are critical care nurses on staff in the intensive care unit at Tampa General Hospital, Tampa, Fla.

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