13 Fluid Therapy in Acute Brain Injury

Gustavo Piñero ¹

¹ Neurological Intensive Care Coordinator. Intensive Therapy Service for Acute Municipal Hospital “Dr.Leonidas Lucero”, Bahía Blanca, Argentina

13.1 Introduction

The management of intravenous fluids in neurocritical patients plays an important role in the evolution and prognosis of acute brain injury. There is no clear consensus on what type of solution or at what stage of neurological disease fluid therapy should be initiated. Parameters extrapolated from studies on less neurocritical conditions provide only an approximation to the pathophysiology of acute brain injury.

This chapter develops general concepts in the management of water and electrolyte metabolism in the central nervous system, describes parenteral solutions commonly used in neurocritical care, and assesses their respective strengths and weaknesses.

The infusion of parenteral solutions may influence the development of cerebral edema [1], and the infusion of hypotonic fluids is reported to decrease plasma osmolarity, with the subsequent development of cerebral edema. Insofar as these observations may have been accurate, there was the widely held misconception that we should “restrict fluid intake” in the acute neurological patient to prevent intracranial hypertension [2]; however, fluid restriction also carries the risk of hypovolemia, hypotension and decreased cerebral perfusion pressure, a triad which favours the development of cerebral ischemia [3-6].

Water is the most abundant component of the body and accounts for 60-80% of body weight depending on age, sex, and body fat content. About half (50-60%) is distributed as intracellular water, the rest as extracellular water (38-45%), with the remaining small fraction as transcellular water.

With few exceptions, the cell membrane is permeable to the passage of water through an osmotic gradient. Osmolarity refers to the concentration of solutes in a solution; the osmotic gradient is the pressure difference between two solutions, wherein a solvent will move from a solution of lower to a solution of higher osmolar concentration, bringing it, the water in this example, to a higher osmolarity equal on both sides of the gradient.

Intracellular anions are macromolecules which do not diffuse across membranes; they attract large numbers of cations, the main one being potassium (K⁺). Conversely, extracellular anions are small, and the major cation is sodium (Na⁺). Cellular homeostasis is maintained by Na/K AT pumps that prevent cells from bursting. The other factor regulating cell volume is the osmolarity of the extracellular space [7].

The brain is highly sensitive to changes in homeostasis. A state of hyponatremia leads to an increase in cell volume, resulting in cerebral edema, whereas hypernatremia leads to cellular dehydration, with shrinkage of the brain parenchyma [8].

Importantly, some molecules are ineffective osmoles (ethanol, urea): they can increase the concentration of solutes in the extracellular space but do not cause water movement across a membrane. In contrast, effective osmoles such as hypertonic saline solutions attract water from the intracellular to the extracellular space by increasing the osmolarity [9]. For this reason, we use the term “tone” when referring to the effective osmolarity of a solution.

Tone is important in evaluating hyponatremic states which can be classified as: isotonic when the loss of Na⁺ equals that of water; hypotonic when the loss of Na⁺ is greater than that of water; and hypertonic when the loss of water is greater.

Control of osmoregulation is important because it involves the interaction between the kidney and the thirst mechanism through the antidiuretic hormone (ADH). This system is so sensitive that changes in serum osmolality of 1-2% can activate or inhibit it, while larger volume changes (8-10%) are required to activate the thirst mechanism and the release of ADH [10,11].

Fluid administration in neurocritical patients presents major challenges, including maintaining adequate cerebral perfusion pressure (CPP), while avoid hyperglycemia and controlling body temperature.

Preservation of CPP requires the maintenance of normovolemia without adversely affecting intracranial pressure [12]. Several physiological principles must be considered: in the peripheral tissues the capillaries of the membranes are highly permeable to water, ions and other low-molecular-weight molecules, but limit the movement of high-molecular-weight substances such as albumin. In these tissues, the distribution of fluid between plasma and interstitial fluid volume is regulated by oncotic pressure gradients. In contrast to the systemic capillary membranes, the brain capillary membranes constituting the brain blood-barrier (BBB) are impervious to most hydrophobic solutes, including sodium [13]. Acute changes in plasma sodium, however small, generate a significant osmotic pressure gradient of water movement that can bring about changes in the brain, with important clinical manifestations [14].

13.2 Fluids Commonly Used in Neurocritical Care

Fluids commonly used in neurocritical care can be grouped into crystalloids (isotonic crystalloids, and hypertonic crystalloids) and colloids (natural colloids (albumin), and artificial colloids (gelatins, dextrans and starches).

13.2.1 Crystalloids

Isotonic crystalloid solutions (0.9% saline solution, Lactated Ringer) are inexpensive, nontoxic, safe and non-reactive (Table 13.1). Usually, in conditions where vascular permeability is involved, only one third of the administered volume remains in the intravascular space, significantly increasing the interstitial fluid; therefore, large volumes are required to overcome a particular hemodynamic situation, which can lead to a state of shock or poor progression of resuscitation [15,16]. In patients with impaired capillary permeability, a volume ratio from 1/7 to 1/10 per liter can be administered (of which only 100 ml remain in the intravascular space). Other negative effects associated with isotonic crystalloids are the development of tissue edema, acute renal failure and abdominal compartment syndrome (ACS), as may occur with aggressive resuscitation with large volumes [17-19].

Table 13.1. Isotonic crystalloid solutions.

Large volumes of saline (0.9% saline) may cause hyperchloremic acidosis; large volumes of Lactated Ringer’s solution can cause plasma hypotonicity, leading to hyperlactatemia without acidosis. Several studies have reported a pro-inflammatory effect of Lactated Ringer’s solution (caused by the structure of the D-isomer) [20,21].

Hypertonic crystalloid solutions (3%, 7.5%, 23%) have a high sodium concentration and exert a great effect as volume expanders. They expand the extracellular space very effectively, reducing the tissue water; they also have a slightly positive inotropic effect and decrease peripheral resistance [3,20,22,23]. The interest of these solutions in neurocritical care lies in their effects on cerebral hemodynamics by improving cerebral blood flow (CBF) and decreasing intracranial pressure (ICP). The mechanisms of action for these solutions are described in Table 13.2.

Table 13.2. Mechanisms of action of hypertonic crystalloid solutions.

CPP = Cerebral perfusion pressure; ICP = Intracranial pressure.

Their importance resides in their ability to expand with a small volume, but their effects are transient: increased diuresis and natriuresis, reduced cell swelling, including endothelial, and improved microcirculation [24].

However, their use can lead to hyperosmolarity, hyperchloremic acidosis, volume overload, renal failure, cerebral hemorrhage, pontine myelinolysis, hypernatremia and hypokalemia [25].

They can be given as a continuous infusion or bolus. A concentration of 2% can be given by the peripheral route; however, solutions with a concentration ≥3% may cause local irritation and local tissue damage.

Practical aspects in the administration of hypertonic crystalloids are the following:

• The rate of complications is low with close monitoring of serum sodium. (Keep Na⁺ 145-155 mEq/l, serum osmolarity <320 mOsm/l).
  
• They are given with an infusion pump. Caution is warranted since they are not compatible with all medications, including some that are compatible with 0.9% saline. Avoid administering medications and transfusions with hypertonic saline (SSH).
  
• General care: control the hydration status and assess the infusion according to age (greater risk of complications in the elderly).
  
• Laboratory monitoring: Check serum sodium every 6 h. In patients with Na⁺ levels <160 mmol/l there is a higher risk of renal failure, pulmonary edema and heart failure. The problem is greater if the levels remain elevated for more than 48 h. Levels >160 mmol/l increase the risk of seizures. Monitor plasma osmolarity.

Table 13.3. Mechanisms of action of hypertonic crystalloid solutions.

Discontinuation of therapy with SSH:

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