http://surgerybook.net/

septic shock in adults: a systemic review. JAMA 2009;301(22):2362–2375.

153. Minneci PC, Deans KJ, Eichacker PQ, et al. The effects of steroids during sepsis depend on dose and

severity of illness: an updated meta-analysis. Clin Microbiol Infect 2009;15(4):308–318.

154. Gordon AC, Mason AJ, Perkins GD, et al. The interaction of vasopressin and corticosteroids in

septic shock: a pilot randomized controlled trial. Crit Care Med 2014;42(6):1325–1333.

155. Malerba G, Romano-Girard F, Cravoisy A, et al. Risk factors of relative adrenocortical deficiency in

intensive care patients needing mechanical ventilation. Intensive Care Med 2005;31(3):388–392.

156. Rivers E, Nguyen B, Havsted S, et al. Early goal-directed therapy in the treatment of severe sepsis

and septic shock. N Engl J Med 2001;345:1368–1377.

157. Kopterides P, Siempos II, Tsangaris I, et al. Procalcitonin-guided algorithms of antibiotic therapy in

the intensive care unit: a systematic review and meta-analysis of randomized controlled trials. Crit

Care Med 2010;38(11):2229–2241.

158. Heyland DK, Johnson AP, Reynolds SC, et al. Procalcitonin for reduced antibiotic exposure in the

critical care setting: a systemic review and an economic evaluation. Crit Care Med 2011;39(7):1792–

1799.

159. Stolz D, Smyrnios N, Eggimann P, et al. Procalcitonin for reduced antibiotic exposure in ventilatorassociated pneumonia: a randomized study. Eur Respir J 2009;34(6):1364–1375.

160. Bouadma L, Luyt CE, Tubach F, et al. Use of procalcitonin to reduce patients’ exposure to

antibiotics in intensive care units (PRORATA trial): a multicenter randomized controlled trial.

Lancet 2010;375(9713):463–474.

161. Tang HJ, Lin HL, Lin YH, et al. The impact of central line insertion bundle on central lineassociated bloodstream infection. BMC Infectious Diseases 2014;14:356.

162. Safdar N, O’Horo JC, Ghufran A, et al. Chlorhexidine-impregnated dressing for prevention of

catheter-related bloodstream infection: a meta-analysis. Crit Care Med 2014;42(7):1703–1713.

163. Lam TB, Omar MI, Fisher E, et al. Types of indwelling urethral catheters for short term

catherisation in hospitalized adults. Cochrane Database Syst Rev 2014;9:CD004013.

164. Srinivasan A, Karchmer T, Richards A, et al. A prospective trial of a novel, silicone-based, silver

ion-impregnated urinary catheters in the prevention of nosocomial urinary tract infections (NUTIs).

Infect Control Hosp Epidemiol 2006;27(1):38–43.

165. Liberati A, D’Amico R, Pifferi S, et al. Antibiotic prophylaxis to reduce respiratory tract infections

and mortality in adults receiving intensive care. Cochrane Database Syst Rev 2009;(4):CD000022.

166. Silvestri L, Weir I, Gregori D, et al. Effectiveness of oral chlorhexidine on nosocomial pneumonia,

causative micro-organisms and mortality in critically ill patients: a systemic review and metaanalysis. Minerva Anestesiol 2014;80(7):805–820.

167. De Smet AM, Kluytmans JA, Cooper BS, et al. Decontamination of the digestive tract and

oropharynx in ICU patients. N Engl J Med 2009;360:20–31.

168. Oostdijk EA, Kesecioglu J, Schultz MJ, et al. Effects of decontamination of the oropharynx and

intestinal tract on antibiotic resistance in ICUs: a randomized clinical trial. JAMA

2014;312(14):1429–1437.

169. Jain R, Kralovic SM, Evans ME, et al. Veterans’ affairs initiative to prevent methicillin-resistant

staphylococcus aureus infections. N Engl J Med 2011;364(15):1419–1430.

170. Harbath S, Fankhauser C, Schrenzel J, et al. Universal screening for methicillin-resistant

staphylococcus aureus at hospital admission and nosocomial infection in surgical patients. JAMA

2008;299(10):1149–1157.

171. Huskins WC, Huckabee CM, O’Grady NP, et al. Intervention to reduce transmission of resistant

bacteria in intensive care. N Engl J Med 2011;364(15):1407–1418.

172. Singh N, Squier C, Wannstedt C, et al. Impact of an aggressive infection control strategy on

endemic staphylococcus aureus infection in liver transplant recipients. Infect Control Hosp Epidemiol

2006;27(2):122–126.

173. Sandri AM, Dalarosa MG, Ruschel de AL, et al. Reduction in incidence of nosocomial methicillinresistant staphylococcus aureus (MRSA) infection in an intensive care unit: role of treatment with

mupirocin ointment and chlorhexidine baths for nasal carriers of MRSA. Infect Control Hosp

Epidemiol 2006;27(2):185–187.

174. Haung SS, Septimus E, Kleinman K, et al. Targeted versus universal decolonization to prevent ICU

335

http://surgerybook.net/

infection. N Engl J Med 2013;368(24):2255–2265.

336

http://surgerybook.net/

Chapter 11

Fluids, Electrolytes, and Acid–Base Balance

Richard B. Wait, M. George DeBusk, and Jeffry Nahmias

Key Points

1 The human body is conceptualized as being composed of two primary fluid compartments:

extracellular fluid (ECF) and intracellular fluid (ICF). The two compartments are separated by

cellular membranes.

2 The ECF can be further divided into smaller compartments: transcellular fluid, plasma, interstitial

fluid, and bone/connective tissue fluid. Blood is a composite compartment containing both ECF

(plasma) and ICF (red cell volume).

3 Sodium and potassium are the dominant cations of the ECF and ICF, respectively.

4 Extracellular tonicity is under tight regulation by osmoreceptors found in the hypothalamus. As

sodium accounts for the majority of ECF tonicity, these receptors function essentially as ECF

monitors.

5 Effective circulating volume is sensed by volume receptors (capacitance vessels, atria, hepatic, and

central nervous system [CNS]) and pressure receptors (aortic arch, carotid, and intrarenal) that alter

sodium and water balance mediated by renin–angiotensin, aldosterone, atrial natriuretic peptide

(ANP), dopamine, and renal prostaglandins.

6 Water losses are composed of both sensible (i.e., measurable) losses via urine, stool, and sweat and

insensible (i.e., immeasurable) via evaporative loss from the skin, respiratory tract, or open

abdomen.

7 Goals of fluid therapy are to normalize body fluid compartment volumes and electrolyte

concentrations. This can be achieved with crystalloid (preferable) or colloid infusion to correct

deficits and/or match ongoing and expected losses.

8 The major electrolytes (Na+, K+, Ca2+, Mg2+, Cl

-, HCO3

-, and HPO4

2-) should be monitored and

replaced, when possible, with respect to the pathophysiology of various disease states.

9 Acid–base balance is carefully buffered within very narrow limits. Acid–base disturbances are

frequently mixed, involving combined respiratory and metabolic derangements.

In this chapter, the normal physiologic mechanisms of fluid and electrolyte homeostasis, inclusive of

acid–base physiology, are reviewed. This will be the starting point for a discussion of fluid and

electrolyte pathophysiology and the management of specific clinical situations. With a thorough

understanding of disease- and injury-related alterations from normal fluid volume and electrolyte

physiology, one can effectively care for all surgical and critically ill patients.

BODY FLUIDS

Total Body Water and Body Fluid Compartments

Total body water (TBW) is defined as the total amount of water contained within the body. The

relationship between TBW and body weight varies according to the percentage of body fat.1 The

average TBW in adult men is 60% of total body weight and 55% in adult women. In infants, water

makes up approximately 75% to 80% of body weight. This figure decreases to approximately 65% by 1

year of age and continues to decrease slowly throughout life, primarily related to decreases in lean body

mass. Estimates of TBW can be empirically adjusted for the obese and thin body habitus. In obesity,

estimates of TBW can be decreased by 10% to 20%. In very thin individuals, estimates can be increased

by up to 10%.1

1 TBW is principally distributed into the intracellular and extracellular compartments which are in

337

http://surgerybook.net/

dynamic equilibrium (Table 11-1). ICF makes up approximately two-thirds of the TBW, and the

remaining one-third is composed of ECF. Using these techniques, ECF volume estimates range from 30%

to 33% of TBW, or approximately 20% of body weight.2

2 The ECF compartment is subdivided into the interstitial and intravascular spaces. The interstitial

space extends from the blood vessels to the cells. It includes the complex ground substance making up

the acellular tissue matrix. The water in this space exists in free and bound phases. The free phase

contains water that is freely exchangeable with intravascular, lymphatic, and intracellular water. It is in

a constant state of flux. The bound phase is much less freely exchangeable. It is composed of water that

hydrates matrix materials such as glycosaminoglycans and mucopolysaccharides. Interstitial water

volume can be calculated as ECF–intravascular space volume and constitutes approximately 25% of

TBW, or 15% of body weight. The intravascular space accounts for 25% of the ECF and contains the

plasma volume, which is approximately 8% of the TBW or 5% of body weight.

The transcellular space, a third and smaller component of ECF, consists of water that is separated

from other compartments by endothelial and epithelial barriers, including cerebrospinal, ocular, and

synovial fluids, as well as fluid in the gastrointestinal (GI) tract. Under normal circumstances, fluid in

the transcellular space is not easily exchangeable with that in other compartments.3

Composition of Body Fluids

3 Sodium and potassium are the dominant cations in the body. As mentioned above, sodium is restricted

primarily to the ECF. Sodium content in an average adult is approximately 60 mEq/kg. Approximately

25% is confined to bone and is nonexchangeable. Of the exchangeable fraction, approximately 85% is in

the ECF. Potassium, calcium, and magnesium make up the remainder, smaller fraction, of the cations

present in the ECF (Table 11-2).

Table 11-1 Body Fluid Compartments

In the ICF, potassium is the dominant cation. Total body potassium is normally approximately 42

mEq/kg, and most of this potassium is intracellular and freely exchangeable. Magnesium and sodium

ions also contribute to a lesser extent to the cationic component of the ICF. Phosphate, sulfate anions,

bicarbonate, and intracellular proteins balance these cations.

The Gibbs–Donnan equilibrium describes the relationship between charged particles in a solution that

are unevenly distributed across a semipermeable membrane.4 This special type of equilibrium exists

between the ICF and ECF because of the high concentration of protein and nondiffusible phosphates in

the cell. ECF cations are in electrochemical balance with chloride, bicarbonate, phosphate, and sulfate

anions, although chloride is the major contributor to this balance. In addition, anionic proteins

contribute to ion balance in plasma but not in interstitial fluid, which is essentially an ultrafiltrate of

plasma that normally contains little protein. As a result, the content of both cations and anions in

interstitial fluid is slightly higher than in plasma (Table 11-2).

Interstitial fluid, in comparison, contains little protein. These impermeable intracellular negative

charges tend to favor diffusion of permeable anions into the ECF. The Gibbs–Donnan equilibrium also

exists across the capillary endothelial membrane because the concentration of protein is higher on the

blood side of the capillary than on the interstitial fluid side. Thus, the concentrations of diffusible ions

are not necessarily equal across these membranes because of the presence of these complex anions.

Table 11-2 Electrolyte Concentrations of Intracellular and Extracellular Fluid

Compartments

338