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Clinical Fluid Therapy in thePerioperative SettingSecond Edition

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Clinical Fluid Therapy in thePerioperative SettingSecond EditionEdited byRobert G. HahnResearch Director, Sodertalje Hospital, Sodertalje, Sweden






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Library of Congress Cataloging in Publication dataNames: Hahn, Robert G., editor.Title: Clinical fluid therapy in the perioperative setting / edited by Robert G. Hahn.Description: 2nd edition. | Cambridge ; New York : Cambridge University Press,2016. | Includes bibliographical references and index.Identifiers: LCCN 2015046421 | ISBN 9781107119550 (hardback : alk. paper)Subjects: | MESH: FluidTherapy | Perioperative Care | Rehydration Solutions –therapeutic useClassification: LCC RD51 | NLMWD 220 | DDC 617.9/6 – dc23LC record available at http://lccn.loc.gov/2015046421

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Contents

List of contributors page viiPreface xiOverview of chapter summaries xiii

Section 1 The fluids1 The essentials 1

Robert G. Hahn

2 Crystalloid fluids 3Robert G. Hahn

3 Colloid fluids 10Robert G. Hahn

4 Glucose solutions 20Robert G. Hahn

5 Hypertonic fluids 26Eileen M. Bulger

6 Fluids or blood products? 33Oliver Habler

Section 2 Basic science7 Body volumes and fluid kinetics 41

Robert G. Hahn

8 Acid–base issues in fluid therapy 52Niels Van Regenmortel and Paul W. G. Elbers

9 Fluids and coagulation 59Sibylle A. Kozek-Langenecker

10 Microvascular fluid exchange 67Per-Olof Grande and Johan Persson

11 The glycocalyx layer 73Anna Bertram, Klaus Stahl, Jan Hegermann, andHermann Haller

12 Monitoring of themicrocirculation 82Atilla Kara, Sakir Akin, and Can Ince

13 Pulmonary edema 92Goran Hedenstierna, Claes Frostell, and JoaoBatista Borges

Section 3 Techniques14 Invasive hemodynamic monitoring 100

Jonathan Aron and Maurizio Cecconi

15 Goal-directed fluid therapy 110Timothy E. Miller and Tong J. Gan

16 Non-invasive guidance of fluid therapy 120Maxime Cannesson

17 Hemodilution 127Philippe van der Linden

18 The ERAS concept 134Katie E. Rollins and Dileep N. Lobo

Section 4 The clinical setting19 Spinal anesthesia 141

Michael F. M. James and Robert A. Dyer

20 Day surgery 148Jan Jakobsson

21 Abdominal surgery 155Birgitte Brandstrup

22 Cardiac surgery 166Saqib H. Qureshi and Giovanni Mariscalco

23 Pediatrics 177Robert Sumpelmann and Nils Dennhardt

v






Contents

24 Obstetric, pulmonary, and geriatricsurgery 184Kathrine Holte

25 Transplantations 188Laurence Weinberg

26 Neurosurgery 202Hemanshu Prabhakar

27 Intensive care 206Alena Lira and Michael R. Pinsky

28 Severe sepsis and septic shock 215Palle Toft and Else Tønnesen

29 Hypovolemic shock 222Niels H. Secher and Johannes J. van Lieshout

30 Uncontrolled hemorrhage 231Robert G. Hahn

31 Burns 236Folke Sjoberg

32 Trauma 245Joshua D. Person and John B. Holcomb

33 Absorption of irrigating fluid 253Robert G. Hahn

34 Adverse effects of infusion fluids 262Robert G. Hahn

Index 270

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Contributors

Sakir Akin, MDDepartment of Intensive Care, Erasmus MCUniversity Hospital Rotterdam, Rotterdam,TheNetherlands

Jonathan Aron, MBBS BSc (Hons) MRCP (UK) FRCAFFICMIntensive Care, St George’s Healthcare Trust &Medical School, Tooting, London, United Kingdom

Joao Batista Borges, MD, PhD, Senior ResearcherSection of Anesthesia and Intensive Care,Department of Surgical Sciences, Uppsala University,Uppsala, Sweden

Anna Bertram, MDDepartment of Nephrology and Hypertension,Medizinische Hochschule Hannover, Hannover,Germany

Eileen M. Bulger, MD, FACS, ProfessorGeneral Surgery Clinic at Harborview, University ofWashington, Seattle, Washington, USA

Birgitte Brandstrup, MD, PhDDepartment of Surgery, Holbaek University Hospital,Smedelundsgade 60, 4300 Holbaek, Denmark

Maxime Cannesson, MD, PhD, ProfessorDepartment of Anesthesiology and PerioperativeCare, University of California, Irvine, School ofMedicine, Irvine, USA

Maurizio Cecconi, ProfessorIntensive Care, St George’s Healthcare Trust &Medical School, Tooting, London, United Kingdom

Nils Dennhardt, Dr. med.Klinik fur Anasthesiologie und Intensivmedizin,Medizinische Hochschule Hannover, Hannover,Germany

Robert A. Dyer, BSc (Hons), MBChB, PhD, FCA (SA)Department of Anaesthesia, University of Cape Townand Groote Schuur Hospital, Western Cape, SouthAfrica

Paul W.G. Elbers, MD, PhD, EDICDepartment of Intensive Care Medicine,VU University Medical Centre Amsterdam,Amsterdam, the Netherlands

Claes Frostell, MD, PhD, ProfessorDepartment of Anesthesia and Intensive Care,Karolinska Institutet at Danderyd Hospital,Danderyd, Sweden

Tong J. Gan, MD, MHS, FRCA, Professor andChairmanDepartment of Anesthesiology, Stony BrookMedicine, Stony Brook, NY, USA

Per-Olof Grande, MD, PhD, ProfessorDepartment of Anaesthesia and Intensive Care, LundUniversity Hospital, Lund, Sweden

Oliver Habler, ProfessorDepartment of Anesthesiology, Surgical IntensiveCare Medicine and PainTherapy, KrankenhausNordwest GmbH, Frankfurt amMain, Germany

Robert G. Hahn, MD, PhD, ProfessorSodertalje Hospital, Sodertalje, Sweden

Hermann Haller, ProfessorDepartment of Nephrology and Hypertension,Medizinische Hochschule Hannover, Hannover,Germany

Goran Hedenstierna, MD, PhD, ProfessorSection of Clinical Physiology, Department ofMedical Sciences, Uppsala University, Uppsala,Sweden

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List of contributors

Jan Hegermann, PhDDepartment of Anatomy, Medizinische HochschuleHannover, Hannover, Germany

John B. Holcomb, MD, ProfessorDepartment of Surgery, The University of Texas,Houston, Texas, USA

Kathrine Holte, MD, DMScDepartment of Surgical Gastroenterology, HvidovreUniversity Hospital, Hvidovre, Denmark

Can Ince, ProfessorDepartment of Intensive Care, Erasmus MCUniversity Hospital Rotterdam, Rotterdam,TheNetherlands

Jan Jakobsson, ProfessorInstitution for Physiology and Pharmacology,Department of Anaesthesia and Intensive Care,Karolinska Institutet, Stockholm, Sweden

Michael F. M. James, MBChB, PhD, FRCA, FCA (SA)Department of Anaesthesia, University of Cape Townand Groote Schuur Hospital, Western Cape, SouthAfrica

Atilla Kara, MDDepartment of Intensive Care, Erasmus MCUniversity Hospital Rotterdam, Rotterdam,TheNetherlands, and Intensive Care Unit, HacettepeUniversity Medicine Faculty, Ankara, Turkey

Sibylle A. Kozek-Langenecker, MD, Professor, MBASigmund Freud Private University Vienna,Department of Anesthesia and Intensive Care,Evangelical Hospital Vienna, Vienna, Austria

Alena Lira, MDDepartment of Critical Care Medicine, University ofPittsburgh, PA, USA

Dileep N. Lobo, MS, DM, FRCS, FACS, FRCPEGastrointestinal Surgery, Nottingham DigestiveDiseases Centre, National Institute for HealthResearch Biomedical Research Unit, NottinghamUniversity Hospitals NHS Trust, Queen’s MedicalCentre, Nottingham, United Kingdom

Giovanni Mariscalco, MD, PhDUniversity of Leicester, Clinical Sciences Wing,Glenfield General Hospital, Leicester, UnitedKingdom

Timothy E. Miller, MBChB, FRCA, AssociateProfessorDivision of General, Vascular and TransplantAnesthesiology, Department of Anesthesiology, DukeUniversity Medical Center, Durham, NC, USA

Joshua D. Person, MDDepartment of Surgery, The University of Texas,Houston, Texas, USA

Johan Persson, MD, PhDDepartment of Anaesthesia and Intensive Care, LundUniversity Hospital, Lund, Sweden

Michael R. Pinsky, MD, Dr. h.c.Department of Critical Care Medicine, University ofPittsburgh, PA, USA

Hemanshu Prabhakar, ProfessorDepartment of Neuroanesthesiology, All IndiaInstitute of Medical Sciences, New Delhi, India

Saqib H. Qureshi, MDUniversity of Leicester, Clinical Sciences Wing,Glenfield General Hospital, Leicester, UnitedKingdom

Katie E. Rollins, BM BS, MRCSGastrointestinal Surgery, Nottingham DigestiveDiseases Centre, National Institute for HealthResearch Biomedical Research Unit, NottinghamUniversity Hospitals NHS Trust, Queen’s MedicalCentre, Nottingham, United Kingdom

Niels H. Secher, MD, PhDDepartment of Anaesthesia, Rigshospitalet,University of Copenhagen, Copenhagen,Denmark

Folke Sjoberg, MD, ProfessorBurn Center, Linkoping University Hospital andLinkoping University, Linkoping, Sweden

Klaus Stahl, Dr. med.Department of Nephrology and Hypertension,Medizinische Hochschule Hannover, Hannover,Germany

Robert Sumpelmann, Dr. med., ProfessorKlinik fur Anasthesiologie und Intensivmedizin,Medizinische Hochschule Hannover, Hannover,Germany

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List of contributors

Palle Toft, MD, ProfessorDepartment of Anaesthesiology and Intensive Care,Odense Universitetshospital, Odense, Denmark

Else Tønnesen, ProfessorDepartment of Anaesthesiology and Intensive Care,Aarhus University Hospital, Kommunehospitalet,Arhus, Denmark

Philippe van der Linden, MD, PhDDepartment of Anesthesiology, CHUBrugmann-HUDERF, Universite Libre de Bruxelles,Brussels, Belgium

Johannes J. van Lieshout, MD, PhD, ConsultantDepartment of Internal Medicine and the Laboratoryfor Clinical Cardiovascular Physiology, AMC Centrefor Heart Failure Research, University of Amsterdam,Amsterdam,The Netherlands

Niels Van Regenmortel, MDIntensive Care Unit and High Care Burn Unit,Ziekenhuis Netwerk Antwerpen, CampusStuivenberg, Department of Intensive CareMedicine, Antwerp University Hospital, Antwerp,Belgium

Laurence Weinberg, MD, BSc, MBBCh, MRCP,FANZCADepartment of Anesthesia, Austin Hospital,Department of Surgery and Anesthesia, PerioperativePain Medicine Unit, University of Melbourne,Australia

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Preface

Intravenous fluid is a cornerstone in the treatment ofthe surgical patient. Perioperative management withintravenous fluids is a responsibility of the anesthetist,but many others, including the surgeon, must be ori-ented in the principles that guide the therapy.

The clinical use of infusion fluids has long beenoverlooked as a science. One of the main reasons forthe neglect is that fluids have not been considered tobe drugs. Many of the usual requirements for registra-tion, such as the specification of a therapeutic windowand detailed pharmacokinetics, have been overlooked.On the other hand, the experience of the anesthetist isindeed that infusion fluids are drugs.Their appropriateuse can be life-saving, while inappropriate use mightjeopardize the clinical outcome and even be a threat tothe patient’s life.

The scattered scientific basis for perioperativefluid therapy has necessitated the development ofexperience-based “rules-of-thumb” which still play anenormously important role in daily practice. They areusually based on a summation of perceived and mea-sured losses and also include compensation for variousfactors, such as anesthesia-induced vasodilatation andprotein losses due to inflammation.

Alongside the trial-and-error approach and theo-retical calculations, scientific methods have been used

to find evidence-based guidelines. This has resulted ina marked change over the past decade. The amount offluid infused has been shown to affect the course ofthe postoperative follow-up greatly, at least after sometypes of operation. Another important insight is thatguiding fluid therapy by dynamic hemodynamic mea-sures reduces the risk of postoperative complications.A changeover from relying on the pulmonary arterycatheter to less invasive and even non-invasive toolsfor the monitoring of fluid administration is in fullswing.

I am extremely proud to welcome contributionsfrom colleagues around the world who are among thehighest-ranked researchers in the field of perioperativefluid therapy. I have taken great care to ask researchersand clinicians whom I respect and admire for out-standing contributions to our knowledge about howfluid therapy should be managed. They have writtenauthoritative chapters about subjects in which everyanesthetist should be updated when working withpatients subjected to common types of surgery.

Each chapter should be read as an independentessay, whichmeans that a topic discussed briefly by oneauthor is often explored in more detail by another. Asyou will see, the experts take you by the hand and tellyou not only what to do, but also why.

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Overview of chapter summaries

Section 1: The fluids

Chapter 2. Crystalloid fluidsRobert G. HahnCrystalloid electrolyte solutions include isotonicsaline, Ringer’s lactate, Ringer’s acetate, and Plasma-Lyte. In the perioperative period these fluids are usedto compensate for anesthesia-induced vasodilatation,small to moderate blood losses, and urinary excretion.Although evaporation consists of electrolyte-freewater, such fluid losses are relatively small duringshort-term surgery and may also be compensated by acrystalloid electrolyte solution.

These fluids expand the plasma volume to a lesserdegree than colloid fluids as they hydrate both theplasma and the interstitial fluid space. However, thedistribution to the interstitial fluid space takes 25–30min to be completed, which is probably due to therestriction of fluid movement by the finer filaments inthe interstitial gel. The slow distribution gives crystal-loid electrolyte solutions a fairly good plasma volume-expanding effect as long as the infusion continues andshortly thereafter.

Isotonic saline is widely used, but has an electrolytecomposition that deviates from that of the extracellularfluid (“unbalanced”).This fluid is best reserved for spe-cial indications, such as hyponatremia, hypochloremicmetabolic alkalosis, and disease states associated withvomiting. Isotonic saline may also be considered intrauma and in children undergoing surgery. Hyper-tonic saline might be considered in neurosurgery and,possibly, in preoperative emergency care.

Ringer’s lactate, Ringer’s acetate, and Plasma-Lytehave been formulated to bemore similar to the com-position of the ECF (“balanced fluids”). They are themainstay of fluid administration in the perioperativeperiod and should be used in all situationswhere iso-tonic saline is not indicated.

Chapter 3. Colloid fluidsRobert G. HahnColloid fluids are crystalloid electrolyte solutions witha macromolecule added that binds water by its col-loid osmotic pressure. As macromolecules escape theplasma only with difficulty, the resulting plasma vol-ume expansion is strong and has a duration of manyhours. Clinically used colloid fluids include albumin,hydroxyethyl starch, gelatin, and dextran.

The plasma volume expansion shows one-compartment kinetics, which means that colloids, incontrast to crystalloids, have no detectable distribu-tion phase. Marketed fluids are usually composed sothat the infused volume expands the plasma volumeby the infused amount. Exceptions include rarely usedhyperoncotic variants and mixtures with hypertonicsaline.

The main indication for colloid fluids is assecondline treatment of hemorrhage. Because ofinherent allergenic properties, crystalloid electrolytefluids should be used when the hemorrhage is small.A changeover to a colloid should be performed onlywhen the crystalloid volume is so large that adverseeffects may ensue (mild effects at 3 liters, severe at6 liters). The only other clinical indication is that dex-tran can be prescribed to improve microcirculatoryflow.

There has been lively debate about clinical useof colloid fluids after studies in septic patients haveshown that hydroxyethyl starch increases the need forrenal replacement therapy. This problem has not beenfound in the perioperative setting but the use of starchhas still been restricted.

The colloids have defined maximum amounts thatcan be infused before adverse effects, usually arisingfrom the coagulation system, become a problem.

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Chapter 4. Glucose solutionsRobert G. HahnGlucose 5% is given after surgery to prevent starvationand to provide free water for hydration of the intracel-lular fluid space. Glucose is sometimes infused beforesurgery as well, in particular when surgery is startedlate during the day, and, in some hospitals, also as a2.5% solution during the surgical procedure. Glucoseinfusion has also been used together with insulin toimprove outcome in cardiac surgery and in intensivecare.

Because of the risk of hyperglycemia, intravenousglucose infusions need to bemanagedwith knowledge,attention, and responsibility. Hyperglycemia promoteswound infection and osmotic diuresis, by which thekidneys lose control of the urine composition. Theanesthetist has to consider a four-fold modification ininfusion rate of glucose to account for the periopera-tive change in glucose tolerance. The suitable rate ofinfusion when a glucose infusion is initiated can bepredicted by pharmacokinetic simulation. A controlplasma sample taken one hour later shows whether theprediction was correct, and also that plasma glucosewill only rise by another 25% if no adjustment of theinfusion rate is made.

Glucose solution is contraindicated in acute strokeand not recommended in operations associated witha high risk of perioperative cerebral ischemia, such ascarotid artery and cardiopulmonary bypass surgery.Subacute hyponatremia is a postoperative complica-tion that is promoted by infusing >1 liter of plain 5%glucose in the perioperative setting.

Chapter 5. Hypertonic fluids1Eileen M. BulgerHypertonic fluids have an osmotic content that ishigher than in the body fluids. When this contentremains in the extracellular fluid space, such as withsaline, the volume effect becomes very powerful owingto osmotic allocation of fluid from the intracellularto the extracellular fluid space. These fluids have alsobeen found to favorably modulate the inflammatoryresponse. The most studied preparations are saline7.5% with and without a colloid (dextran or hydrox-yethyl starch) added.

This chapter reviews the current clinical evidenceregarding the use of hypertonic fluids for the earlyresuscitation of injured patients and for perioperativeindications for a variety of procedures.While there is awealth of preclinical data suggesting potential benefitfrom this resuscitation strategy, the clinical trial datahave failed to show any clear benefit to the prehospitaladministration of these fluids in trauma patients, andthe data for perioperative use is limited. More study isneeded to define the best use of these fluids in a varietyof patient populations and surgical procedures.

1 For chapters 5, 12, 13, 15, 16, 20, 21, 25, 28, and 31, summary wascompiled by the Editor.

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Chapter 6. Fluids or blood products?Oliver HablerThanks to the impressive anemia tolerance of thehuman body, red blood cell (RBC) transfusion mayoften be avoided despite even important bloodlosses – provided that normovolemia is maintained.While a hemoglobin (Hb) concentration of 60–70 g/lcan be considered safe in young, healthy patients,older patients with preexisting cardiopulmonarymorbidity should be transfused at Hb 80–100 g/l.Physiological transfusion triggers (e.g. decrease ofVO2, ST-segment depression in the ECG, arrhythmia,continuous increase in catecholamine needs, echocar-diographic wall motion disturbancies, lactacidosis)appearing prior to the aforementioned Hb concen-trations necessitate immediate RBC transfusion. Inthe case of unexpected massive blood losses and/orlogistic difficulties impeding an immediate start oftransfusion, the anemia tolerance of the patient can beeffectively increased by several measures (e.g. hyper-oxic ventilation, muscular relaxation, or adequatedepth of anesthesia).

In cases of dilutional coagulopathy – often reflectedby an intraoperatively diffuse bleeding tendency –a differentiated coagulation therapy can either bedirected on the basis of viscoelastic coagulation tests(e.g. thromboelastometry/-graphy) or directed empir-ically by replacing the different components in theorder of their developing deficiency (i.e. starting withfibrinogen, followed by factors of the prothrombincomplex and platelets). The “global” stabilization ofcoagulation with fresh frozen plasma requires theapplication of high volumes and bears the risk of car-diac overload (TACO) and immunological alterations(TRIM).

Section 2: Basic science

Chapter 7. Body volumes and fluid kineticsRobert G. HahnBody fluid volumes can be measured and estimatedby using different methods. A key approach is to usea tracer by which the volume of distribution of aninjected substance is measured. Useful tracers occupya specific body fluid space only. Examples are radioac-tive albumin (plasma volume), iohexol (extracellularfluid space), and deuterium (total body water). Thetransit time from the site of injection to the site of elim-ination must be considered when using tracers with arapid elimination, such as the indocyanine green dye.The volume effect of an infusion fluid can be calcu-lated by applying a tracer method before and after theadministration.

Guiding estimates of the sizes of the body volumescan be obtained by bioimpedance measurements andanthropometric equations.

The blood hemoglobin (Hb) concentration is a fre-quently used endogenous tracer of changes in bloodvolume. Hb is the inverse of the blood water con-centration, and changes in Hb indicate the volumeof distribution of the infused fluid volume. Certainassumptions have to be made to convert the Hb dilu-tion to a change in blood volume. Volume kinetics isbased on mathematical modeling of Hb changes overtime which, together with measurements of the uri-nary excretion, can be used to analyze and simulate thedistribution and elimination of infusion fluids.

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Chapter 8. Acid–base issues in fluid therapyNiels Van Regenmortel and Paul W. G. ElbersSolutions such as NaCl 0.9% are an established causeof metabolic acidosis. The underlying mechanism, areduction in plasma strong ion difference, [SID], iscomprehensibly explained by the principles of theStewart approach. Fluid-induced metabolic acidosiscan be avoided by the use of so-called balanced solu-tions that do not cause alterations in plasma [SID].Many balanced solutions are commercially available,their only drawback being their higher cost. SinceNaCl 0.9% remains the first choice of resuscitationfluid in large parts of the world, there remains animportant question overwhether a large-scale upgradeto balanced solutions should be at hand. There is alack of high-quality data at the time of writing, butthere is increasing evidence that hyperchloremia hasa detrimental effect on renal function and has an eco-nomic impact of its own.Therefore, until we havemoredefinitive data, the use of balanced solutions in patientswho need a relevant amount of fluid therapy seems tobe a pragmatic choice.

Chapter 9. Fluids and coagulationSibylle A. Kozek-LangeneckerInfusion therapy is essential in intravascular hypo-volemia and extravascular fluid deficits. Crystalloidfluids and colloidal volume replacement affect bloodcoagulation when infused intravenously. Questionsremain over whether unspecific dilution and specificside effects of infusion therapy are clinically relevantin patients with and without bleeding manifestations,and whether fluid-induced coagulopathy is a riskfactor for anemia, blood transfusion, mortality, and adriver for resource use and costs. In this chapter, path-omechanisms of dilutional coagulopathy and evidencefor its clinical relevance in perioperative and criticallyill patients are reviewed. Furthermore, medico-legal aspects are discussed. The dose-dependentrisk of dilutional coagulopathy differs betweencolloids (dextran > hetastarch > pentastarch >

tetrastarch > gelatins > albumin). Risk awarenessincludesmonitoring for early signs of side effects.Withrotational thromboelastometry/thromboelastographynot only the deterioration in clot strength can beassessed but also in clot formation and platelet inter-action. Fibrinogen concentrate administration maybe considered in severe bleeding as well as relevantdilutional coagulopathy. Targeted doses of gelatinsand tetrastarches seem to have no proven adverseeffect on anemia and allogeneic blood transfusions.Further studies implementing goal-directed volumemanagement and careful definition of triggers fortransfusions and alternative therapies are needed.

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Chapter 10. Microvascular fluid exchangePer-Olof Grande and Johan PerssonThere is always a continuous leakage of plasma fluidand proteins to the interstitium, called the transcap-illary escape rate (TER). The transcapillary escaperate of albumin (TERalb) corresponds to 5–6% oftotal plasma albumin per hour. Plasma volume is pre-served mainly because of recirculation via the lym-phatic system and transcapillary absorption. Duringinflammation and after trauma, TER may increaseup to 2–3 times and exceed the recirculation capac-ity, resulting in hypovolemia, low plasma concen-tration of proteins, and tissue edema. The presentchapter discusses mechanisms controlling microvas-cular fluid exchange under physiological and patho-physiological conditions, including possible passiveand activemechanisms controlling transcapillary fluidexchange. Options to reduce the need for plasma vol-ume expanders while still maintaining an adequateplasma volume are presented. Consequently, this maysimultaneously reduce accumulation of fluid and pro-teins in the interstitium. The effectiveness of availableplasma volume expanders is also discussed.

Chapter 11. The glycocalyx layerAnna Bertram, Klaus Stahl, Jan Hegermann, andHermann HallerEndothelial cells cover the inner surface of the vas-culature and are essential for vascular homeosta-sis with regulation of vasodilation and vasoconstric-tion, permeability, inflammation, and coagulation.Theendothelium is not a barren surface but is covered bya thick layer of so-called glycocalyx. The glycocalyx isbuilt of heavily glycosylated proteins such as syndecanswhich are anchored in the cell membrane, freely asso-ciating proteoglycans such as hyaluronidase, and alsoamultitude of plasmamolecules that bind and interactwith the proteoglycans.

The glycoproteins collectively organize into theglycocalyx, which plays a vital role in several impor-tant vascular functions. It serves as a mechanotrans-ductor mediating information on blood flow andcellular movement to the endothelium, it regulatespermeability via its physical properties, it regulatesbinding of vascular factors to the endothelium, andit is the “habitat” of the resident components of thecomplement system and the coagulation cascade. Inaddition, the glycocalyx serves as a sink for smallmolecules and electrolytes in the plasma and gener-ates chemokine gradients to guide leukocytes to sitesof inflammation. The delicate structures of the glyco-calyx can be easily disturbed and damaged by acutedisease such as sepsis or ischemia, as well as chronicdisease such as diabetes or hypertension. The proteo-glycans and/or its sugar moieties can be shed by spe-cific enzymes. Novel tools have been developed to bet-ter visualize the glycocalyx both in vitro and in vivo.An understanding and, possibly, a molecular manipu-lation of the glycocalyx will be important to improveour therapeutic strategies in patients.

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Chapter 12. Monitoring of themicrocirculationAtilla Kara, Sakir Akin, and Can IncePerioperative fluid management requires comprehen-sive training and an understanding of the physiologyof oxygen transport to tissue. Administration of fluidshas a limitedwindowof efficacy. Too little fluid reducesorgan perfusion and too much fluid causes organ dys-function from edema. In addition, isotonic saline car-ries the danger of hyperchloremia, whereas balancedcrystalloid solutions are pragmatic choices of fluid inthe majority of perioperative resuscitation settings.

The prime aim of fluid therapy is to improve tis-sue perfusion so as to provide adequate oxygen to thetissues. Macrohemodynamical parameters and/or sur-rogates of tissue perfusion do not always correspondto microcirculatory functional states, and especiallynot in states of inflammation. Even when targets formacrohemodynamics are reached, the microcircula-tion may still remain damaged and dysfunctional.

Observation of the microcirculation in the periop-erative setting provides a more physiologically basedapproach for fluid therapy by possibly avoiding theunnecessary and inappropriate administration of largevolumes of fluids.

Hand-held videomicroscopy is able to visualizemicrocirculatory perfusion sublingually. It can be usedto monitor the functional state of the microcircula-tion by assessment and quantification of sublingualmicrovascular capillary density, and thus to guide fluidtherapy. The Cytocam-IDF device might provide theneeded clinical platformbecause of its improved imag-ing capacity in terms of density and perfusion param-eters as well as providing on-line quantification of themicrocirculation.

Chapter 13. Pulmonary edemaGoran Hedenstierna, Claes Frostell, andJoao Batista BorgesPulmonary edema can be either hydrostatic (cardiac)or high-permeability (non-cardiac). In the first type,therapy should focus on a reduction of hydrostaticpressure. Pain relief and anxiety relief reduces vascu-lar pressures by bringing down sympathetic nervoussystem drive. Treatment also consists in oxygen sup-plementation, furosemide, continuous positive airwaypressure (CPAP) on a tight-fitting face-mask, and pos-sibly venesection.

High-permeability pulmonary edema implies thatthe barrier function of the vasculature to largermolecules and cells is no longer intact.The permeabil-ity increase leads to a rapid and profound fluid leak-age, followed by inflammation and destruction of lungparenchymal structure. Treatment consists of fluidrestriction while maintaining adequate organ perfu-sion. Extracorporeal membrane oxygenation (ECMO)may be used in patients with severe non-cardiac pul-monary edema. Adequate treatment of the primaryetiology of the condition is essential.

Resolution of pulmonary edema might includelocal reabsorption, clearance through the lymphaticsystem, clearance via the pleural space, or clearancethrough the airway. Maintaining spontaneous breath-ing, whenever possible, cannot be over-emphasized.Spontaneous breathing with CPAP both counteractsatelectasis formation in the lung and facilitates theability to clear secretions with the re-emergence ofcough.

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Section 3: Techniques

Chapter 14. Invasive hemodynamicmonitoringJonathan Aron and Maurizio CecconiThe aim of hemodynamic monitoring is to enable theoptimization of cardiac output and therefore improveoxygen delivery to the tissues, avoiding the accumu-lation of oxygen debt, in the perioperative period.Instigating goal-directed therapy based on validatedoptimization algorithms has been shown to reducemortality in highrisk patients and complications inmoderate-to high-risk patients.

A number of devices are available to facilitatethis goal. The pulmonary artery catheter was thefirst hemodynamic monitor, but its invasive natureprecludes its routine use in today’s clinical practice.More recently, devices that continuously analyze thearterial pressure waveform to calculate various flowparameters have been developed and validated. Thesedevices have facilitated the introduction of hemo-dynamic monitoring to the wider surgical popula-tion, providing useful clinical information that enablesthe judicious use of fluid therapy whilst avoidinghypervolemia.

This chapter explores the role that hemodynamicoptimization plays in perioperative care, describessome of the commonly used invasive hemodynamicmonitors, and explains how to use the informationproduced effectively. Used correctly, any monitorcan be useful to improve outcome if applied to theright population, at the right time, and with the rightstrategy.

Chapter 15. Goal-directed fluid therapyTimothy E. Miller and Tong J. GanPerioperativemorbidity has been linked to the amountof fluid administered, with both insufficient and excessfluid leading to increased morbidity, resulting in acharacteristic U-shaped curve. The challenge for us asclinicians is to keep our patients in the optimal rangeat all times during the perioperative period. Goal-directed therapy (GDT) is a term that has been usedfor nearly 30 years to describe methods of optimizingfluid and hemodynamic status.The arrival of a numberof minimally invasive cardiac output monitors enablesclinicians to guide perioperative volume therapy andcardiocirculatory support.

The most widely used monitor is the esophagealDoppler. There are several others that are able to ana-lyze the arterial waveform to calculate stroke volumeand cardiac output, and therefore use the “10% algo-rithm” in response to a fluid challenge. There are anumber of studies that show improved outcomes withGDT-guided fluid optimization, as demonstrated by afaster return in gastrointestinal function, a reductionin postoperative complications, and reduced length ofstay. The underlying mechanisms for the success ofGDT are thought to relate to avoidance of episodesof hypovolemia, hypoxia, or decreased blood flowthat may cause mitochondrial damage and subsequentorgan dysfunction.

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Chapter 16. Non-invasive guidanceof fluid therapyMaxime CannessonOptimization of oxygen delivery to the tissues dur-ing surgery cannot be conducted by monitoringarterial pressure alone. Therefore, apart from cardiacoutput monitoring, functional hemodynamic param-eters have been developed. These parameters indicate“preload dependence,” which is defined as the abilityof the heart to increase stroke volume in response toan increase in preload. The Frank–Starling relation-ship links preload to stroke volume and presents twodistinct parts: a steep portion and a plateau. If thepatient is on the steep portion of the Frank–Starlingrelationship, then an increase in preload (induced byvolume expansion) is going to induce an importantincrease in stroke volume. If the patient is on theplateau of this relationship, then increasing preloadwill have no effect on stroke volume. The functionalhemodynamic parameters rely on cardiopulmonaryinteractions in patients under general anesthesia andmechanical ventilation and can be obtained inva-sively from the arterial pressure waveform or non-invasively from the plethysmographicwaveform.Here,the effects of positive-pressure ventilation on preloadand stroke volume are used to detect fluid respon-siveness. If mechanical ventilation induces impor-tant respiratory variations in stroke volume (SVV)or in pulse pressure (PPV) it is more likely that thepatient is preload-dependent. These dynamic param-eters, including passive leg raising, have consistentlybeen shown to be superior to static parameters, suchas central venous pressure, for the prediction of fluidresponsiveness.

Chapter 17. HemodilutionPhilippe van der LindenAcute normovolemic hemodilution entails theremoval of blood either immediately before or shortlyafter the induction of anesthesia and its simultaneousreplacement by an appropriate volume of crystalloidsand/or colloids to maintain “isovolemic” conditions.As a result, blood subsequently lost during surgerywill contain proportionally fewer red blood cells,thus reducing the loss of autologous erythrocytes.Although still frequently used in some surgicalprocedures, the real efficacy of acute normovolemichemodilution in reducing allogeneic blood transfu-sion remains discussed. The aim of this article is todescribe the physiology, limits, and efficacy of acutenormovolemic hemodilution.

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Chapter 18. The ERAS conceptKatie E. Rollins and Dileep N. LoboOptimum perioperative fluid administration as partof an Enhanced Recovery After Surgery (ERAS) pro-gram is dependent on a range of factors which arebecoming increasingly well documented. Followingprevious ambiguous terms and definitions for fluidmanagement strategies, appreciation of the impor-tance of “zero balance” (where amount infused equalsthe amount lost from the body) of both water andsalt is increasing, with both over- and underhydrationresulting in significantly worse clinical outcomes (ina U-shaped distribution). Excessive fluid loads have asignificant negative impact upon outcome. Electrolytebalance, from pre- to postoperative stages, is also nowunderstood to play a key role.

Section 4: The clinical setting

Chapter 19. Spinal anesthesiaMichael F. M. James and Robert A. DyerFluid therapy is widely used in conjunction with spinalanesthesia to minimize hypotensive events. The use ofcrystalloids for this purpose seems to be only mini-mally effective, particularly when given prior to theadministration of the spinal anesthetic. To be effec-tive, substantial fluid boluses must be administered –of the order of 20ml/kg – and then preferably as a rapidcoload simultaneously with the induction of spinalanesthesia. Several studies and meta-analyses suggestthat colloids, either as preload or coload, are moreeffective than crystalloids andmay result in a smallervolume of fluid loading being required. However, flu-ids alone, whether crystalloid or colloid, are generallyinadequate to prevent or treat significant hypotensionassociated with spinal anesthesia, and the concomitantuse of a vasopressor will frequently be necessary, par-ticularly in obstetrics. The best that can be achievedwith optimal fluid therapy is an overall reduction inthe total dose of vasopressor required. The best avail-able management of spinal hypotension would appearto be optimal fluid therapy combined with carefullygraded administration of the appropriate vasopressor.It is possible that goal-directed fluid therapy, using anappropriate analysis of cardiac performance to assessthe response dynamic indices to a fluid challenge, mayimprove fluid therapy in the future, but, at present,the evidence for this is insufficient to make a firmrecommendation.

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Chapter 20. Day surgeryJan JakobssonRapid recovery and a minimum of residual effectsare factors of utmost importance when handling thedaycase patient. Prolonged preoperative fasting shouldbe avoided. Many countries have adopted revised fast-ing guidelines that allow patients without risk factorsto eat a light meal up to 6 hours and to ingest clear flu-ids up to 2 hours prior to the induction of anesthesia.Postoperative fatigue can be reduced by fluid intake upto 2–3 hours prior to surgery.

Perioperative intravenous fluid therapy should beinstituted on the basis of the case profile. In general,fluid infused during minor surgery may not exert amajor effect, but during intermediate surgery, such aslaparoscopic cholecystectomy, a liberal fluid programhas been shown to improve recovery and reduce post-operative fatigue. Administration of about 1 liter iso-tonic electrolyte solution to compensate for the fast-ing, and a further 1 liter during surgery, improves thepostoperative course. Liberal fluid administration alsoreduces the risk for postoperative nausea and the riskvs. benefit seems to be in favor for its routine use inASA 1–2 patients.The potential benefit in adding dex-trose to the intravenous fluid during the early postop-erative phase has been assessed, but the benefit seemsto be very minor.

Resumption of oral intake, drinking, and eating aretraditional variables for the assessment of eligibility fordischarge and thus an essential part of day surgery.However, there is no need for patients to drink beforedischarge; intake of fluid and food should be recom-mended but not pushed.

Chapter 21. Abdominal surgeryBirgitte BrandstrupNormal as well as pathological fluid losses should bereplaced with a fluid resembling the loss in quantityand quality (electrolyte composition). Elective surgi-cal patients can be allowed to eat until 6 hours anddrink up to 2 hours before surgery without increas-ing the risk of fluid aspiration. Preoperative admin-istration of sugarcontaining fluids, intravenous or bymouth, improves postoperative well-being andmusclestrength, and lessens the postoperative insulin resis-tance. It does not, however, reduce the number ofpatients with wound- or other complications, length ofstay, or mortality. Surgery does not increase the nor-mal fluid and electrolyte losses, but causes perspira-tion from the abdominal wound that approximatelyequals the decreased water loss from the lungs becauseof ventilation with moist air. It is not possible to treat adecrease in blood pressure caused by the use of epidu-ral analgesia with fluid.

The goal of zero fluid balance (formerly called“restrictive”) reduces postoperative complications andthe risk of death in major abdominal surgery.The goalof zero balance in combinationwith a goal of nearmax-imum stroke volume provides equally good outcome.During outpatient surgical procedures thewellbeing ofthe patient is improved by giving approximately 1 literof fluid. The role of glucose-containing fluid in thissetting may be beneficial, but the evidence is sparse.“Postoperative restricted fluid therapy,” allowing thepatients to drink nomore than 1,500ml/day, is not rec-ommended. To measure the body weight is the bestway to monitor the postoperative fluid balance. Fluidcharts are insufficient.

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Chapter 22. Cardiac surgerySaqib H. Qureshi and Giovanni MariscalcoCardiac surgical patients have altered vascular andimmunological factors that dictate short- and long-term clinical outcomes. So far, the evidence does notfavor any single choice of fluid therapy. In fact, vol-ume replacement is a determinant of “filling pressures”in isolation but requires a critical balance with otherdeterminants of tissue-oxygen debt such as vasomo-tor tone, fluid responsiveness, and cardiac contractil-ity. Lastly, none of the available fluid therapies havebeen assessed for their comparative endothelial home-ostatic potential. This leaves a significant knowledgegap and an incentive for researchers, clinicians, andindustry to design and test safer and more efficaciouschoices for clinical use.

Chapter 23. PediatricsRobert Sumpelmann and Nils DennhardtThe main aim of perioperative fluid therapy is to sta-bilize or normalize the child’s homeostasis. Younginfants have higher fluid volumes, metabolic rates, andfluid needs than adults. Therefore, short periopera-tive fasting periods are important to avoid iatrogenicdehydration, ketoacidosis, and misbehavior. Balancedelectrolyte solutions with 1–2.5% glucose are favoredfor intraoperative maintenance infusion. Glucose-freebalanced electrolyte solutions should then be addedas needed to replace intraoperative fluid deficits orminor blood loss. Hydroxyethyl starch or gelatin solu-tions are useful in hemodynamically instable patientsor those with major blood loss, especially when crys-talloids alone are not effective or the patient is at riskof interstitial fluid overload. The monitoring shouldfocus on the maintenance or restoration of a stable tis-sue perfusion. Also, in non-surgical or postoperativechildren, balanced electrolyte solutions should be usedinstead of hypotonic solutions, both with 5% glucose,as recent clinical studies and reviews showed a lowerincidence of hyponatremia.

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Chapter 24. Obstetric, pulmonary, andgeriatric surgeryKathrine HolteThis chapter focuses on fluid management in obstet-ric, pulmonary, and geriatric surgery. In obstetrics, thefluid administration debate largely centers on the rel-evance of fluid infusions to counteract hypotension inconjunction with regional anesthesia administered forpain relief during labor or as anesthesia for Cesareansection, where both colloids and sympathomimeticsreducematernal hypotension. Particular to pulmonarysurgery, a positive fluid balance is found to correlatewith postoperative lung injury and should be strictlycontrolled. Elderly patients, while being at increasedrisk for postoperative complications, may also bemoresusceptible to perioperative fluid disturbances includ-ing preoperative dehydration.

In summary, evidence suggests that fluid manage-ment should be individualized and integrated intoperioperative care programs. Both insufficient andexcessive fluid administration may increase complica-tions, and while determining fluid status is still a chal-lenge, individualized fluid therapy to obtain certainhemodynamic goals may be recommended.

Chapter 25. TransplantationsLaurence WeinbergPatients with end-stage liver disease have a hyper-dynamic resting circulation with high cardiac out-put states and low systemic vascular resistance andtachycardia. During liver transplantation, this state isamplified. The potential for massive bleeding is com-mon and can result in sudden and catastrophic hypo-volemia. Massive blood transfusion results in largevolumes of citrated blood being administered. Withlimited or no hepatic function to metabolize citrate,citrate intoxication can occur, and calcium chlorideshould be administered when appropriate. Mild tomoderate acidosis can be safely tolerated. Albuminis the most common colloid used, while the use oflactate-based crystalloid solutions can result in hyper-lactatemia as lactate anions are ineffectively metabo-lized. Acetate-buffered solutions should be preferred.The most common cause of death in fulminant liverfailure is intractable intracranial hypertension fromcerebral edema, present in approximately 50–80% ofpatients with fulminant liver failure. Therefore, per-missive hypernatremia and use of hypertonic salinesolutions are frequently treatment options in thissetting.

Crystalloids are the mainstay and first choice ofperioperative fluid intervention in renal transplanta-tion. Conventionally, 0.9% saline is widely advocatedbecause of concerns about hyperkalemia from the bal-anced/buffered solutions, which all contain potassium.However, this fear has not been confirmed in clinicaltrials. Hydroxyethyl starch should be avoided owing toincreased risk of a delayed graft function.

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Chapter 26. NeurosurgeryHemanshu PrabhakarFluid administration is one of the basic componentsin the management of neurosurgical patients. Despiteadvances and extensive research in the field of neuro-sciences, there is still a debate on the ideal fluid. Issuesrelated to adequate volume replacement and effects onthe intracranial pressure persist. Studies have demon-strated the harmful effects of colloids over crystal-loids. Normal saline has remained a fluid of choice,but there is now emerging evidence that it too is notfree from its harmful effects. Hypertonic saline hasalso been accepted by many practitioners, but its useand administration requires close monitoring and vig-ilance. There is now growing evidence on the use ofbalanced solutions for neurosurgical patients. How-ever, this evidence comes from a small number of stud-ies. This chapter tries to briefly cover various clini-cal situations in neurosciences with respect to fluidadministration.

Chapter 27. Intensive careAlena Lira and Michael R. PinskyFluid infusions are an essential part of the manage-ment of the critically ill, and include maintenance flu-ids to replace insensible loss and resuscitation effortsto restore blood volume.This chapter is on fluid resus-citation. Fluid administration is a vital component ofresuscitation therapy, with the aim being to restorecardiovascular sufficiency. Initial resuscitation aims torestore a minimal mean arterial pressure and cardiacoutput compatible with immediate survival. This isoften associated with emergency surgery and associ-ated lifesaving procedures. Then, optimization aimsto rapidly restore organ perfusion and oxygenationbefore irreversible ischemic damage occurs. Stabiliza-tion balances fluid infusion rate with risks of volumeoverload, and finally de-escalation promotes polyuriaas excess interstitial fluid is refilled into the circula-tion. There is no apparent survival benefit of colloidsover crystalloids. Hydroxyethyl starch solutions havedeleterious effects in certain patient populations, forexample in sepsis. Balanced salt solutions are superiorto normal saline. Further fluid resuscitation should beguided by the patient’s need for increased blood flowand by their volumeresponsiveness.

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Chapter 28. Severe sepsis and septic shockPalle Toft and Else TønnesenSepsis is a systemic disorderwith a protean clinical pic-ture and a complex pathogenesis characterized by therelease of both pro- and anti-inflammatory elements.The organ dysfunction and organ failure occurring inthe early phase of severe sepsis are believed to resultfrom an excessive inflammatory response. Degrada-tion or destruction of the glycocalyx layer causes tran-sudation of fluid from the vascular space into extravas-cular tissue. Such capillary leakage makes the patienthypovolemic and promotes a generalized edema inthe lungs, heart, gut, brain, and other tissues, whichimpairs organ function and sometimes causes exces-sive weight gain. Early, aggressive goal-directed ther-apy (EGDT) based on the protocol by Rivers et al.from 2001 stresses that adequate volume replacementis a cornerstone in management, as restoration of flowis a key component in avoiding tissue ischemia orreperfusion injury. It is the speed with which septicpatients are fluid resuscitated that makes the differ-ence. Deep general anesthesia should be avoided andnoradrenaline might be needed to prevent circulatoryshock before sufficient amounts of fluid have beenadministered.

Survival improves fromEGDTonly if optimizationis instituted before organ failure is manifested. Mostpatients require continuous aggressive fluid resuscita-tion during the first 24 hours of management. In thelater course of the disease, between 2 and 7 days, amore restricted fluid management strategy should beinstituted. Not all patients who are “fluid responders”should automatically receive fluids.

Chapter 29. Hypovolemic shockNiels H. Secher and Johannes J. van LieshoutHypovolemic shock is a response to a reduced cen-tral blood volume (CBV) whatever its cause – hemor-rhage, passive head-up tilt, or other cause – and fol-lows three phases. The first comprises a reduction ofCBV initially with reflex increase in heart rate (HR)to approximately 90 bpm and maintained blood pres-sure (BP) by increased vascular resistance. In the sec-ond phase, which corresponds to a reduction of theCBV by about 30%, a Bezold-Jarisch-like reflex ceasessympathetic activity, although plasma adrenaline con-tinues to increase, and together with vagal activa-tion enhances coagulation competence. At this stageof progressive CBV the HR decreases, eventually toextremely low values. In the third phase, BP remainslow while HR increases to more than 100 bpm.

To treat hypovolemia, volume substitution can bedirected to establishmaximal values for stroke volume,cardiac output, or venous oxygen saturation. Thesevariables do not increase when CBV is enhanced insupine healthy humans, and thereby define “normo-volemia.” The patient’s bed can be tilted head-down,and if the mentioned variables then increase signifi-cantly, the patient is in need of volume. If not, a vol-ume deficit does not explain the patient’s condition.Plasma atrial natriuretic peptide (ANP) also decreasesin response to a reduced CBV, and to maintain plasmaANP during major surgery requires a 2.5-liter surplusvolume of lactated Ringer’s solution. With recordingof deviations in central cardiovascular variables, theblood volume can be maintained within 100ml andprovide a comfortable margin to the deficit that affectsBP and regional blood flow.

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Chapter 30. Uncontrolled hemorrhageRobert G. HahnFluid therapy in hemorrhage strives to restore hemo-dynamic function and tissue perfusion. However,these goals are not appropriate when there is an injuryto a large blood vessel and the hemorrhage has notbeen stopped surgically (uncontrolled hemorrhage).Clinical situations inwhich this is the case include pen-etrating trauma, ruptured aortic aneurysm, and gastricbleeding. Numerous animal experiments in pigs andrats have shown that the low-flow, low-pressure statecharacterizing serious hemorrhage promotes coagula-tion, even if a large blood vessel is injured. An imma-ture blood clot is easilywashedaway if the blood flowrate and the arterial pressure is normalized by infu-sion fluids. Vigorous fluid therapy then increases boththe blood loss and the mortality. The road to optimalsurvival is to infuse less fluid at lower speed (half vol-ume at half speed is suggested) and aim at a systolicarterial pressure of 90mmHg. In this situation, thestrategy is only to prevent progressive acidosis andirreversible shock. A deviation from normal hemo-dynamics should be accepted until the source ofbleeding has been treated surgically. A sudden dropin arterial pressure during ongoing fluid resuscitationsuggests that rebleeding is occurring, and the infu-sion rate should then be further reduced. There is anunfortunate lack of clinical studies showing that thefluid strategy that has been successful in animal exper-iments pertains also to humans. However, it is widelyaccepted in emergency departments and trauma hos-pitals to resuscitate trauma patients to a lower-than-usual systolic pressure (hypotensive resuscitation).

Chapter 31. BurnsFolke SjobergThe purpose of fluid treatment for burn-injuredpatients is to maintain organ perfusion despite majorleakage of fluid from the intravascular space.The leak-age is due to a sharp reduction of the pressure in theinterstitial fluid space (negative imbibition pressure)and an increase of the vascular permeability. Most ofthe fluid loss due to the first factor takes place withinthe first 3–4 hours and the bulk of loss from the secondfactor within 12 hours after the burn.

The formula for plasma volume support mostwidely used today is the “Parkland” strategy, in which2–4ml of buffered Ringer’s solution is administeredper total body surface area % per kilogram bodyweight. Half of the calculated volume is given duringthe first 8 hours after the burn and the other half dur-ing the subsequent 16 hours. A colloid rescue strategyshould come into play when the fluid volumes pro-vided are very large, and is adequate after 8–12 hourspost-burn.

The patient should be in a state of controlledhypovolemia. The combined use of urine output (aim30–50ml/h), mean arterial pressure, and the mentalstate of the patient is gold standard when guiding thefluid therapy. The use of central circulatory param-eters increases the risk of fluid overload and doesnot improve the outcome. The maximal tissue edemareaches a maximum between the first 24 and 48 hourspost-burn, and thereafter the added fluid volume isexcreted as an ongoing process over 7–10 days.

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Chapter 32. TraumaJoshua D. Person and John B. HolcombIn the United States, injury is the leading cause ofdeath among individuals between the ages of 1 and44 years, and the third leading cause of death overall.Approximately 20% to 40% of trauma deaths occur-ring after hospital admission are related to massivehemorrhage and are therefore potentially preventablewith rapid hemorrhage control and improved resus-citation techniques. Over the past decade, the treat-ment of this population has transitioned into a damagecontrol strategy with the development of resuscitationstrategies that emphasize permissive hypotension, lim-ited crystalloid administration, early balanced bloodproduct transfusion, and rapid hemorrhage control.This resuscitation approach initially attempts to repli-cate whole blood transfusion, utilizing an empiric1:1:1 ratio of plasma:platelets:red blood cells, and thentransitions, when bleeding slows, to a goal-directedapproach to reverse coagulopathy based on viscoelas-tic assays. Traditional resuscitation strategies withcrystalloid fluids are appropriate for the minimallyinjured patient who presents without shock or ongo-ing bleeding.This chapter will focus on the assessmentand resuscitation of seriously injured trauma patientswho present with ongoing blood loss and hemorrhagicshock.

Chapter 33. Absorption of irrigating fluidRobert G. HahnAbsorption of irrigating fluid can occur in endo-scopic surgeries. The complication is best knownfrom transurethral prostatic resection and transcer-vical endometrial resection. When monopolar elec-trocautery is used, the irrigation is performed withelectrolytefree fluid containing glycine, or mannitolor sorbitol. With bipolar electrocautery the irrigat-ing fluid is usually isotonic saline. Incidence data onfluid absorption and associated adverse effects showgreat variation, but absorption in excess of 1 liter usu-ally occurs in 5% to 10% of the operations and causessymptoms in 2–3 patients per 100 operations.

The pathophysiology of the complications arisingfrom absorption of electrolyte-free irrigating fluids iscomplex. Symptoms can be related to metabolic toxi-city, cerebral edema, and circulatory effects caused byrapidmassive fluid overload. Available data on absorp-tion of isotonic saline suggest that symptoms are likelywhen the volume exceeds 2 liters.

Ethanol monitoring is the most viable of the meth-ods suggested for monitoring of fluid absorption inclinical practice. By using an irrigating fluid that con-tains 1% of ethanol, updated information about fluidabsorption can be obtained at any time periopera-tively by letting the patient breathe into a hand-heldalcolmeter.

Treatment of massive fluid absorption is sup-portive with regard to ventilation, hemodynamics,and well-being. Hypertonic saline is indicated whenelectrolyte-free fluids are used, while diuretics shouldbe withheld until the hemodynamic situation has beenstabilized. In contrast, absorption of isotonic salineshould (logically) be treated with diuretics as salinedoes not cause osmotic diuresis and is not distributedto the intracellular space.

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Chapter 34. Adverse effects of infusionfluidsRobert G. HahnAdverse effects may arise if an infusion fluid divergesfrom the body fluids with respect to osmolality ortemperature. Coagulation becomes impairedwhen thefluid induced hemodilution is approximately 40%.Infusion of 2–3 liters of crystalloid fluid prolongs thegastrointestinal recovery time, while 6–7 liters pro-motes poor wound healing, pulmonary edema, andpneumonia. In abdominal surgery, suture insuffi-ciency and sepsis become more common. However, aliberal fluid program in the postoperative period prob-ably does not increase the number of complications.

Isotonic saline probably shares these adverse effectswith the balanced crystalloid fluids, but adds on atendency to metabolic acidosis and slight impair-ment of the kidney function (−10%). Glucose solu-tions may induce hyperglycemia and post-infusionrebound hypoglycemia. Glucose 5% without elec-trolytes increases the risk of postoperative subacutehyponatremia.

Adverse effects associated with colloid fluidsinclude anaphylactic reactions, which occur in approx-imately 1 out of 500 infusions. To reduce this prob-lem when dextran is used, pretreatment with a hapteninhibitor (dextran 1 kDa) should be employed. Hyper-oncotic colloid solutionsmay cause pre-renal anuria indehydrated patients. The indications for hydroxyethylstarch have been limited, owing to impairment of kid-ney function in severely ill patients.

Edema from a colloid is most clearly associatedwith inflammation-induced acceleration of the capil-lary escape rate. A factor promoting peripheral edemafrom crystalloid fluids is that volume expansion neg-atively affects the viscoelastic properties of the inter-stitial fluid gel. The slow excretion of crystalloid fluidduring anesthesia and surgery also contributes to thedevelopment of edema.

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