1 University of Pittsburgh Medical Center Susquehanna, Williamsport, PA, USA
2 University of Rochester, Rochester, NY, USA
Background
Fluid resuscitation is the medical practice of replenishing bodily fluid lost through sweating, bleeding, fluid shifts, or other pathologic processes.
When volume loss occurs, the body reacts by triggering a wide range of physiologic regulatory responses to maintain perfusion in the vascular beds of the vital organs, especially the heart, brain, and kidneys.
Fluid resuscitation is a crucial component in the management of critically ill patients.
Indications for fluid resuscitation
Hemorrhage.
Dehydration.
Sepsis and shock.
Insensible losses.
Fever.
Open wounds.
Unhumidified inspired respiratory gases.
Contraindications to fluid resuscitation
There are no known absolute contraindications, although fluid overload should be avoided because it can exacerbate pulmonary edema and lung injury.
Concerns exist that fluid resuscitation to a normal blood pressure before controlling bleeding may exacerbate hemorrhage by inhibiting or damaging the formation of clots in areas of vascular injury.
Additionally, some fears exist regarding replacing volume with fluids that lower the oxygen‐carrying capacity of circulating blood.
Factors affecting fluid balance
Three hormones control fluid balance:
Renin–angiotensin–aldosterone axis.
Antidiuretic hormone (ADH).
Natriuretic factors.
Renin–angiotensin–aldosterone axis
In hypovolemic states, the glomerular filtration rate (GFR) and sodium delivery rate to the distal tubules are relatively low, causing the release of renin as a homeostatic response.
Renin in turn activates angiotensin I via angiotensinogen which in turn converts to angiotensin II. Angiotensin II plays a key role in aldosterone and ADH release from the adrenal cortex and brain, respectively, which in turn act on the kidney to cause sodium and water retention.
Renin is a proteolytic enzyme that is released into the circulation primarily by the kidneys. Its release is stimulated by:
Sympathetic nerve activation, acting through β1‐adrenoceptors.
Renal artery hypotension, caused by systemic hypotension or renal artery stenosis. Decreased sodium delivery to the distal tubules of the kidney.
Renin cleaves angiotensinogen, to form the decapeptide angiotensin I.
Vascular endothelium, particularly in the lungs, has angiotensin‐converting enzyme (ACE), which cleaves off two amino acids to form the octapeptide, angiotensin II.
Angiotensin II has several very important functions:
Constricts resistance vessels, via angiotensin II (AT1) receptors, thereby increasing systemic vascular resistance and arterial pressure.
Stimulates sodium reabsorption at several renal tubular sites, thereby increasing sodium and water retention by the body.
Acts on the adrenal cortex to release aldosterone, which in turn acts on the kidneys to increase sodium and fluid retention.
Stimulates the release of vasopressin (ADH) from the posterior pituitary, which increases fluid retention by the kidneys.
Stimulates thirst centers within the brain.
Facilitates norepinephrine release from sympathetic nerve endings and inhibits norepinephrine reuptake by nerve endings, thereby enhancing sympathetic adrenergic function.
Stimulates cardiac hypertrophy and vascular hypertrophy.
Antidiuretic hormone
ADH is increased in most critically ill patients, especially those with surgical or traumatic stress. It is also known as arginine vasopressin, a 9‐amino‐acid peptide made in the supra‐ophthalmic nucleus of the hypothalamus.
The release of ADH is regulated by the osmotic pressure of the blood. Dehydration or increased osmotic pressure of the blood activates ADH release, and activates the V2 receptor, affecting the aquaporin‐2 pathway.
Natriuretic factors
These include atrial natriuretic peptide (ANP), brain natriuretic peptide, and a C‐type natriuretic peptide.
Atrial natriuretic peptide is released from cardiac atrial tissue in response to atrial hypertension (ECF volume overload, heart failure, renal disease, ascites) and primary hyperaldosteronism.
High levels of ANP increase sodium excretion and increase GFR even in the setting of systemic hypotension.
Distribution of body fluid
A total of 60% of body weight is composed of water in an average adult male (Figure 49.1).
The remainder is comprised of 7% minerals, 18% protein, and 15% fat.
An average adult woman has a total body water content of approximately 50% and slightly increased body fat content.
The amount of water in different compartments depends entirely on the quantity of solute present in that compartment.
The addition of solute to any compartment will increase the volume of that compartment by redistribution of water from compartments with lower solute concentrations (i.e. higher water) into the compartment to which the solute was added.
Role of sodium
Water balance and sodium balance are interdependent.
Extracellular volume is determined primarily by the sodium content of the body.
The average serum concentration is 140 mEq/L; intracellular sodium concentration is 12 mEq/L.
Fluid overload and edema are characterized by excess sodium and water content, whereas hypovolemia is characterized by inadequate sodium content (Figure 49.2).
A decrease in ECF volume is physiologically different compared with a decrease in effective circulating plasma volume.
Decreased effective circulating plasma volume may occur with decreased ECF (i.e. hypovolemia) or in the setting of an increased ECF and decreased intravascular oncotic pressure, such as in cases of heart failure, hypoalbuminemia, and inflammatory capillary leak syndromes.
The combined concentration of solutes in water determines the osmolarity of the fluid, which is the pressure gradient that drives fluid shifts towards equilibration.
Serum osmolarity (mOsm/kg) = total solute (mOsm)/total body water (kg).
Different fluid compositions have different effects on plasma and ECF volume.
Impact of 1 L IV fluid on body fluid compartments
Fluid
ICF
ECF
Interstitial
Intravascular
D5W
660 mL
340 mL
226 mL
114 mL
0.95 NaCl
0 mL
1000 mL
660 mL
330 mL
Concept of the third space
Plasma volume represents the ‘first’ ECF space; the interstitial fluid space is the ‘second’ ECF space.
The pathologically expanded interstitial fluid space is a ‘third’ ECF space and is expanded primarily at the expense of plasma volume.
The fluid in the third space is edema fluid and cannot be mobilized by diuresis, dialysis, or fluid restriction.
This fluid mobilizes spontaneously when inflammation subsides.
Role of water balance
Water intake is regulated by thirst, triggered by receptors in the anterolateral hypothalamus.
Critically ill patients cannot communicate thirst, and the thirst mechanism may be dysfunctional in conditions of hypothalamic impairment.
Assessment of fluid status
Physical examination
Signs of hypovolemia include:
Skin: the skin is cool and clammy, except in the cases of septic shock or ‘warm shock’ in which patients may be febrile. Skin tenting (loss of skin turgor) and dry mucous membranes may be present.
Cardiac: tachycardia becomes more pronounced with increasing volume loss. Central venous pressure may be low (<5 mmHg). Jugular veins in the neck may not be visible.
Renal: acute renal failure with decreased urine output.
Extremities: weak and faint pulses, slow capillary refill, and muscle weakness may be present.
Neurologic: early findings include altered mental status exhibited by restlessness, agitation, or general CNS depression. Later findings include more severe CNS depression, seizure, or coma.
Ultrasound: two possible sonographic markers that may be measured at the bedside as surrogates for hypovolemia are the diameters of the inferior vena cava (IVC) and the right ventricle. Complete collapse of the IVC on inspiration in patients with shock is usually an indication of hypovolemia that would respond to fluid resuscitation.
Measurement of cumulative fluid balance
There is no perfectly accurate way to measure daily fluid shifts.
Nursing daily in/out tallies are helpful but are not always accurate.
Weight changes reflect total body water changes and not intravascular volume changes.
Management
Rationale for use of fluids
Correction of reduced circulating ECF volume
Maintenance of cardiac output and organ perfusion
Correction of intracellular water deficits
Treatment of electrolyte abnormalities
Nutrition
Since hypovolemia is depletion of the volume of the intravascular space, replacement fluid should predominantly fill and remain in the intravascular space.
Repletion of the total extracellular volume is essential in patients with ECF depletion and intravascular volume will be corrected along with correction of extracellular volume.
The choice of intravenous fluids should be based on individual patients’ needs.
In clinical practice, the choice of fluid is determined largely by clinician preference, with marked regional variation. No ideal resuscitation fluid exists.
Colloids versus crystalloids
Colloids
Colloids consist of water, electrolytes, and higher molecular weight proteins or polymers.
This includes albumin and hydroxyethyl starch.
Fresh frozen plasma is an expensive and inefficient volume expander and should be reserved for correction of coagulation factor deficiencies.
Colloids do not offer advantages over crystalloid solutions with respect to hemodynamic effects.
Albumin is regarded as the reference colloid solution, but its cost limits its use. Although albumin has been determined to be safe for use as a resuscitation fluid in most critically ill patients and may have a role in early sepsis, its use is associated with increased mortality in patients with traumatic brain injury.
Albumin results in a non‐sustainable rise in the colloid oncotic pressure because the plasma albumin level appears to dissipate rapidly. Lung capillary permeability correlates with the severity of acute lung injury or acute respiratory distress syndrome.
Albumin is a hyperoncotic volume expander and can be used to transiently increase the effects of diuretics, such as furosemide, to augment fluid mobilization. This is a common practice known as the ‘albumin–furosemide chaser.’ However, the utility of this practice is unproven and potentially dangerous.
The use of hydroxyethyl starch solutions is associated with increased rates of renal replacement therapy and adverse events among patients in the ICU. There is no evidence to recommend the use of other semisynthetic colloid solutions.
Antibiotics and intravenous albumin, 1.5 g/kg on day 1 and 1 g/kg on day 3, significantly reduced mortality and likelihood of renal failure in patients with cirrhosis and spontaneous bacterial peritonitis.
Albumin may also be helpful after large volume paracentesis and for correction of dialysis‐related hypotension.
Crystalloids
Crystalloids are made of water and small solutes.
This includes normal saline, lactated Ringer’s solution, and dextrose‐containing fluids (Table 49.1).
Normal saline solution is termed ‘normal’ because it is isotonic, and only slightly hypertonic at 308 mOsm/L with human ECF. It is acidic and unbuffered.
Lactated Ringer’s solution, or Hartmann’s solution, is a buffered or balanced salt solution with a composition that better approximates human ECF. Under normal conditions, the infused lactate is extracted, primarily in the liver, and converted to bicarbonate and water.
Lactated Ringer’s solution is no more effective than normal saline in most clinical situations.
Large volumes of sodium chloride‐containing fluids are likely to cause mild hyperchloremic acidosis. Therefore, some practitioners advocate crystalloid replacement with lactated Ringer’s solution, especially in hemorrhagic shock before blood replacement is available.
Solutions containing only dextrose and water (e.g. 5% dextrose in water) are poor volume replacement solutions because cells rapidly take up the glucose, with water subsequently distributed freely into both the intracellular and extracellular spaces.
Complications of fluid therapy
Volume overload
Weight gain and weakness are signs of ECF volume overload, which often occurs before edema formation.
Volume overload leads to pulmonary edema and impairs oxygen diffusion.
Volume overload can also give way to increased utilization of diuretics, electrolyte imbalances, renal replacement therapy, prolonged mechanical ventilation, and prolonged length of stay.
Hyperchloremic metabolic acidosis due to normal saline
The implementation of a chloride‐restrictive strategy in a tertiary ICU was associated with a significant decrease in the incidence of acute kidney injury and use of renal replacement therapy.
Renal failure
Patients with severe sepsis assigned to fluid resuscitation with hydroxyethyl starch had an increased risk of death at day 90 and were more likely to require renal replacement therapy, as compared with those receiving Ringer’s lactate.
Reading list
Caironi P. Albumin replacement in patients with severe sepsis or septic shock. N Engl J Med 2014; 370:1412–21.
Dellinger RP, Levy MM. Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock: 2012. Crit Care Med 2013; 41:e482–3.
Finfer S, Bellomo R, Boyce N, French J, Myburgh J, Norton R. A comparison of albumin and saline for fluid resuscitation in the intensive care unit. N Engl J Med 2004; 350(22):2247–56.
Goldflam K, Saul T, Lewiss R. Focus on: inferior vena cava ultrasound. ACEP News June 2011.
Perner A, Haase N. Hydroxyethyl starch 130/0.42 versus Ringer’s acetate in severe sepsis. N Engl J Med 2012; 367:124–34.
Roberts I, Blackhall K, Alderson P, Bunn F, Schierhout G. Human albumin solution for resuscitation and volume expansion in critically ill patients. Cochrane Database Syst Rev 2011;11:CD001208.
Yunos NM, Bellomo R, Hegarty C, Story D, Ho L, Bailey M. Association between a chloride‐liberal vs chloride‐restrictive intravenous fluid administration strategy and kidney injury in critically ill adults. JAMA 2012; 308(15):1566–72.
Zengin S, et al. Role of inferior vena cava and right ventricular diameter in assessment of volume status: a comparative study: ultrasound and hypovolemia. Am J Emerg Med 2013; 31(5):763–7.
Images
Figure 49.1 Body fluid compartments and distribution of body water.
Figure 49.2 Causes of increased or decreased sodium content.
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