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Hemorrhage, Shock, and Fluid Resuscitation

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Chapter 4

HEMORRHAGE, SHOCK, AND FLUIDRESUSCITATION

FREDERICK W. BURGESS, PH.D, M.D.*; MICHAEL J. SBOROV, M.D.; AND DEAN R. CALCAGNI, M.D.

INTRODUCTION

PHYSIOLOGICAL CONSEQUENCES OF HEMORRHAGE

Cardiovascular ResponseFluid Compartment ShiftsExtracellular Fluid LossOxygen Transport

HYPOVOLEMIAVenous AccessIntravenous Fluid-Delivery SystemsBlood-Salvage TechniquesIntraosseous Fluid Infusion

RESUSCITATION FLUID SELECTIONCrystalloid SolutionsColloid Solutions

Hypertonic Solutions

SUPPLEMENTAL THERAPEUTIC MEASURESPatient PositionPneumatic Antishock GarmentSupplemental OxygenTherapeutic HypothermiaIntraarterial InfusionVasopressorsVasodilators

CONDITIONS PECULIAR TO RESUSCITATING COMBAT CASUALTIESHyperthermia and DehydrationHypothermiaThermal BurnsHemorrhagic Shock and Head InjuryThe Chemically Contaminated Casualty

SUMMARY

*Formerly, Major, Medical Corps, U.S. Army Reserve; Director, Anesthesia Research, Madigan Army Medical Center, Tacoma, Washington98431-5000; currently, Department of Anesthesia, Rhode Island Hospital, 593 Eddy Street, Providence, Rhode Island 02903

Lieutenant Colonel, Medical Corps, U.S. Army Reserve; Chief, Anesthesia and Operative Services, Madigan Army Medical Center, Tacoma,Washington 98431-5000

Lieutenant Colonel, Medical Corps, U.S. Army; Staff Officer, Combat Casualty Care, U.S. Army Medical Research and Materiel Command,Fort Detrick, Frederick, Maryland 21702-5000


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INTRODUCTION

Victims of combat-related trauma may presentwith the classical manifestations of hemorrhagicshock following rapid exsanguination from a majorvascular structure. Hemorrhagic shock is the most

common cause of death among combat casualties.Early recognition, control of the hemorrhage sourceby effective first aid, and rapid volume restorationwith intravenous fluids are the ideal preparationfor definitive surgical repair of the injury. Unfortu-nately, most combat casualties manifesting evidenceof hypovolemia may not be rapidly transported,may not have an obvious bleeding source, may suffer

from sleep deprivation, may have occult injuries, and,depending on the climatic conditions, may sufferfrom hyperthermia, hypothermia, and dehydration.An understanding of the combat environment, the

climate, infectious epidemics, and the time of injuryare all important factors contributing to the delinea-tion of an appropriate diagnosis and treatment plan.This chapter focuses on the recognition and initialtreatment of hypovolemic shock in the combat ca-sualty, with an emphasis on associated medicalconditions that may accompany and confound thediagnosis and treatment of hypovolemia.

The adverse effects of hemorrhage on young andhealthy soldiers are directly related to two primary

factors: (1) decreased intravascular volume and (2)inadequate oxygen-carrying capacity. Reductionsin intravascular volume and the associated organhypoperfusion initiate a variety of autonomic andneurohumoral homeostatic responses, which aredesigned to maintain or restore the circulatingplasma volume and organ perfusion. The conse-quences of inadequate oxygen delivery are organdysfunction and possible death.

Cardiovascular Response

The response to rapid hemorrhage is complex

and time dependent. The sudden fall in venousreturn to the heart results in an immediate decreasein cardiac stroke volume. Because the aortic arch isless distended by blood, intraluminal pressure willfall. The immediate response to the fall in pressureis a diffuse activation of the sympathetic nervoussystem caused by reflexes that arise in the aorticand carotid baroreceptors. An additional compo-nent of this adrenergic response is caused by therelease of catecholamines from the adrenal me-dulla. The initial physiological effects are (a) in-creased heart rate and myocardial contractility; (b)increased systemic vascular resistance, which isdue primarily to vasoconstriction of arterioles inthe splanchnic viscera and skeletal muscle; and (c)decreased vascular capacitance, which arises pri-marily from constriction of the smaller veins andvenules. These responses tend to preserve perfu-sion of the critically important central organs suchas the heart and brain at the expense of the moreperipherally situated splanchnic viscera and skel-etal muscles.

Augmentation of the immediate vasoconstrictorresponse to hemorrhage occurs within minutes, with

the activation of the renin-angiotensin system (Table4-1). The formation of angiotensin II, an extremelypotent generalized vasoconstrictor, contributes tothe restoration of the arterial blood pressure andstimulates sodium conservation via the release ofaldosterone. Sodium conservation, together withwater conservation mediated via antidiuretic hor-mone secretion, also tends to restore the missingblood volume. The major mechanism that reestab-lishes an effective circulating blood volume in thefirst hours following a major hemorrhage istranscapillary transfer of plasma water from theintracellular fluid space to the intravascular fluid

space. Although this process begins within min-utes, it requires many hours for completion.

If the hemorrhage continues or if its magnitudeoverwhelms these compensatory mechanisms, avicious cycle may begin, arising from the profoundlyischemic splanchnic viscera and skeletal muscle(Figure 4-1). Ultimately, systemic hemostasis failsfor the following reasons:

the ability of ischemic cells to maintain anormal transmembrane ionic gradient islost,

precapillary sphincters in the ischemic vas-cular beds relax,

intravascular fluid leaves the circulationand collects in the ischemic tissues,

lactic and inorganic acids as well as pos-sible myocardial depressants enter the cir-culation, and

oxygen-derived free radicals are gener-atedespecially at the beginning of resus-citation when the ischemic beds are

PHYSIOLOGICAL CONSEQUENCES OF HEMORRHAGE


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Washout of Myocardial Depressants

From Ischemic Tissue

Loss of Fluid Into Extravascular Space

Blood Volume

Cardiac Output

Coronary Perfusion

Acidosis and Hypoxia

Perfusion of Extremitiesand Splanchnic Bed

Blood Pressure

Mean Aortic Pressure < 40 mm Hg(lower limits of coronary autoregulation)

Ischemia

Relaxation ofPrecapillary Sphincters

Cardiac Function

TABLE 4-1

COMPENSATORY RESPONSE TOHEMORRHAGIC SHOCK

Response Times Systemic Response

Few seconds Sympathetic nervous system

Vasoconstriction

Tachycardia

Few minutes Renin-angiotensin system

Vasoconstriction (Angiotensin II)

Sodium conservation

Aldosterone secretion

Glucocorticoid secretion

Water conservation

Vasopressin secretion (ADH)

Several minutes Fluid compartment shiftsTranscapillary refill

Thirst

reperfusedand add to the cellular dam-age already caused by ischemia.

As the peripheral component of systemic hemostasisfails, the centrally circulating blood volume falls,leading to cardiac and respiratory dysfunction and

further reduction in cardiac output and blood pres-sure. Respiratory compensation for the increasingmetabolic acid load fails as the capacity of respira-tory muscles is impaired by hypoperfusion. Acido-sis, in conjunction with declining coronary perfu-sion pressure, impairs cardiac function; this leadsto a further fall in cardiac output and blood pres-sure. Even vigorous resuscitation instituted at thistime may not prevent death.

Fluid Compartment Shifts

After an untreated casualty sustains a major hem-orrhage, restoration of the intravascular fluid com-partment may require many hours as interstitialfluid is drawn into the intravascular compartmentthrough alterations in the normal balance betweenthe transcapillary hydrostatic and oncotic pressures.This phenomenon, transcapillary refill, depends on both adequate interstitial fluid reserves and theintegrity of the capillary bed. In the average adultmale, total body water accounts for approximately

Fig. 4-1. Positive feedback loops (a departure from the

normal steady state, which induces an ever-increasingdeparture) that may possibly develop and lead to deathfollowing massive hemorrhage can involve either theheart or the peripheral vascular beds of the soft tissues ofthe extremities and the splanchnic organs. The loops arenot independent because the magnitude of cardiac out-put is a component of both. The central role of cardiacoutput means that a decline in the hearts pumpingaction (if of sufficient duration and magnitude) can, byreducing peripheral perfusion, adversely affect myocar-dial function. This causes a further decline in the heartspumping action. The importance of myocardial depres-sants in hemorrhagic shock, in contrast to septic shock,remains controversial. Adapted with permission from

Bellamy RF, Pedersen DC, DeGuzman LR. Organ bloodflow and the cause of death following massive hemor-rhage. Circ Shock. 1984;14:115.

60% of total body weight.1 Two thirds of body wateris distributed within the intracellular compartment.The remaining one third is located in the extracellu-lar fluid compartment; 25% to 30% of this compart-ment comprises the intravascular plasma volume(approximately 5% of the total body water), withthe remainder making up the interstitial fluid space.Water freely distributes between each compartmentby passive diffusion; however, ionic equilibrium isprimarily determined by selective permeability, orion-selective active transport, or both, within eachcompartment. Water, ions, and, to a variable extent,proteins, are freely exchanged between the intra-vascular and much of the interstitial fluid compart-ments. The transmural exchange of fluid betweenthe intravascular compartment and the interstitiumcan be described by Starlings equation:


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fluid flux = K[(Pc P i) s (c i)]

where K represents the capillary filtration coeffi-cient; Pc and Pi represent the hydrostatic pressure ofthe intravascular (capillary) and interstitial com-partments, respectively; s , which is known as the

reflection coefficient, represents the impermeabil-ity of the membrane to a given substance; and c andirepresent the oncotic pressure of the intravascu-lar and interstitial fluid compartments, respectively.2

(See Chapter 25, Acute Respiratory Failure andVentilatory Management, for further discussion ofStarlings equation.)

In hemorrhagic shock, constriction of theprecapillary sphincter should decrease the net flowof fluid out of the intravascular space (decreased Pc)and promote the return of interstitial fluid into theintravascular compartment (transcapillary refill).Conversely, the loss of precapillary sphincter tone

in late shock is an important factor leading to de-compensation and death.

Extracellular Fluid Loss

Combat casualties presenting for care severalhours after being injured may suffer from (a) hem-orrhage-induced intravascular volume depletionand (b) preexisting depletion of the extracellularfluid compartment that is caused by concomitantdehydration secondary to environmental or nutri-tional factors. The importance of restoring theinterstitial fluid compartment, in addition to restor-

ing the circulating blood volume, was demonstratedin classic experiments performed during the 1950s.3

Using a dog hemorrhagic shock model, the research-ers found improved survival among the animalsthat were resuscitated with both lactated Ringerssolution and their shed blood, as opposed to resus-citation with shed blood alone or shed blood andadditional plasma. Because the crystalloid fluid isdistributed through the body water, it was soonafterwards determined that restoration of the in-travascular volume required the infusion of volumes3- to 4-fold greater than the putative missing volume;that is, after 1 L of lactated Ringers solution is infused,only 250 mL will remain in the intravascular space.

Trauma and severe hemorrhage frequently leadto a reduction in the functional extracellular fluidcompartment. The reduction in extracellular fluidis partly attributable to hemorrhage; transcapillaryrefill; and the sequestration of interstitial (isotonic)fluid, which represents the third-space loss. Rec-ommendations for replacing the third-space fluidsequestration include administering (a) a balanced

salt solution at 4, 6, and 8 mL/kg/h for minimal,moderate, and severe trauma, in addition to (b) theestimated hourly maintenance fluids.4

Oxygen Transport

Hemorrhage interferes with normal tissue oxy-genation by two mechanisms: (1) the anemic (ie,inadequate oxygen-carrying capacity) and (2) thehemodynamic (ie, inadequate tissue perfusion).Anemia is rarely appreciated immediately after ahemorrhage. This may be due to inadequate timefor equilibration or inadequate interstitial fluid re-serves. However, even in the setting of severehemorrhage, reduced hemoglobin content of the blood is rarely the cause of tissue hypoxia.5 Forexample, a healthy, 20-year-old, male soldier (with

body surface area of 1.73 m2) arrives at a combatsupport hospital within 1 hour of sustaining an

extremity wound. Medical personnel there esti-mate that he has experienced a 40% to 50% hemor-rhage from the femoral artery. Fortunately, thebleeding had been controlled at an aid station andhe had been resuscitated with 6% hetastarch andlactated Ringers solution. On arrival at the combatsupport hospital, his vital signs are stable and the bleeding has stopped. His hemoglobin is deter-mined to be 7 g/dL. Assuming a PaO2 (partialpressure of oxygen in the arteries) of 95 mm Hg, ahemoglobin saturation of 99%, and a normal car-diac output (C.O.) of 5 L/min, the arterial oxygencontent (CaO2) and oxygen delivery (DO2) of this

hypothetical casualty can easily be calculated:

CaO2 = 1.36 (hemoglobin concentration) (hemoglobin saturation) + 0.003 (PaO2)

CaO2 = 1.36 (7 g/dL) (.99) + 0.003 (95) = 9.71 mL O2/dL

C.O. CaO2 = DO25 L/min 9.71 mL/dL = 486 mL O2/min

Assuming a normal C.O. of 5 L/min, with a CaO2 of9.71 mL/dL, this hypothetical patient can deliver486 mL of O

2/min or 281 mL/m2. This value ex-

ceeds the predicted basal O2 consumption rate of250 mL/min. Under stress conditions, the basaloxygen requirement may increase 2- to 3-fold. How-ever, the cardiac output of most young, healthysoldiers can increase 2- to 3-fold to keep up withincreased metabolic demand, provided that an ad-equate cardiac preload has been maintained.

This example demonstrates that (a) blood re-placement is frequently unnecessary and (b) vol-


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ume restoration with asanguinous plasma expand-ers is, at least initially, the key element. If thecirculating plasma volume is maintained, then themetabolic consequences of severe hemorrhage canbe minimized. The critical point to be rememberedin this scenario is that the soldiers hemorrhage was

not ongoing but had been stopped by appropriatefirst aid. However, in the setting of unabated hem-orrhage and shock (as indicated by hypotension,tachycardia, mental-status changes, and diminishedor absent urinary output), the administration ofblood is essential and should not be withheld.

When combat casualties who are in shock arriveat a medical treatment facility with surgical capa-

bilities, medical officers should not underestimatethe amount of fluid required to reestablish a circu-lating blood volume compatible with survival. Forexample, during the Vietnam War, soldiers whorequired a blood transfusion received, on average,2.5 L of blood and 2 L of crystalloid fluid during

their initial resuscitation and surgery.6

Even combat casualties who are no longer bleedingwhohave normal hemodynamic indices and have re-ceived what should be adequate restoration of red blood cell mass on the basis of estimated bloodlossfrequently have a deficient red blood cellmass when this is measured several days after theresuscitative surgery.7

HYPOVOLEMIA

Vascular and visceral injuries secondary to mis-sile wounds, fractures of the long bones, and crush

injuries are frequently accompanied by visible andoccult hemorrhage. The amount of blood lost willnot always be evident, as blood loss tends to be overestimated with more-visible, superficialinjuries and underestimated with abdominal andorthopedic injuries (see Chapter 20, Abdominal In- juries, and Chapter 21, Extremity Injuries). Inter-vention in the field and mobilization of extracellu-lar fluid stores (transcapillary refill) may serve toconfuse the initial estimation of blood loss andresult in an underestimation of blood loss. Theclassic parameters for the estimating the severity ofhemorrhage are often a useful starting point for

determining the rapidity and types of fluid admin-istered, and for determining the response to resus-citation (Table 4-2). Supine hypotension in all com-

bat casualties should be recognized as hypovolemiathat requires rapid and immediate fluid resuscita-

tion.Trauma victims presenting with a suspected mild

hemorrhage (Class I: suspected blood loss in theabsence of tachycardia or hypotension) require ini-tial resuscitation with clear solutions, preferablyintravenous crystalloids. Resuscitation for moder-ate hemorrhage (Class II: tachycardia withouthypotension) should be initiated with crystalloidor colloid solutions or both; however, in the pres-ence of continued bleeding, early transfusiontherapy with packed red blood cells or whole bloodshould be initiated. The presence of hypotension(Class III or Class IV hemorrhage: tachycardia and

hypotension) requires immediate blood-volumereplacement with (a) packed red blood cells or wholeblood and (b) crystalloid solutions. Other causes of

TABLE 4-2

ESTIMATION OF HEMORRHAGE

Degree of Blood Loss Blood Vol. Heart Blood Pulse Respiratory Urinary Flow MentalHemorrhage (L) Lost (%) Rate Pressure Pressure Rate (mL/h) Status

Adapted with permission from Committee on Trauma, American College of Surgeons. Advanced Trauma Life Support Program for Physicians. Chicago,Ill: American College of Surgeons; 1989: 72.

Class I < 1 < 15% < 100 Normal Normal or 1420 > 30 Slightincreased anxiety

Class II 0.751.5 15%30% > 100 Normal Decreased 2030 2030 Mild anxiety

Class III 1.52.0 30%40% > 120 Decreased Decreased 3040 < 15 Anxious andconfused

Class IV > 2.0 > 40% > 140 Decreased Decreased Rapid and Negligible Confused andshallow lethargic


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hypotension (eg, tension pneumothorax, cardiactamponade) should be sought after fluid resuscita-tion has begun.

In the combat setting, tachycardia is a useful, butoften an insensitive, indicator of hypovolemia. Justhow insensitive was one of the more interesting

findings of the surgical research unit that workedduring World War II. Data on the effects of shock onheart rate were published in the seminal volume,The Physiologic Effects of Wounds, published as partof The Surgeon Generals official history of the U.S.Army Medical Department in World War II (Table4-3).8 The degree of shock in injured soldiers wasstratified not only by blood pressure but also bymeasurement of blood volume. The table demon-strates that the differences between the heart ratesin soldiers with varying degrees of shock are sosmall as to be useless for predictive purposes.

Subsequent studies on combat casualties have

confirmed that there may be no simple relationbetween magnitude of hemorrhage and heart rate. 9

Although the generalized discharge of the sympa-thetic component of the autonomic nervous systemfollowing a precipitous fall in blood pressure leadsto tachycardia, the decrease in venous return to theheart by unloading mechanoreceptors in the car-diac chambers, and especially the left ventricle,leads to reflex slowing of the heart through anefferent pathway that involves the parasympatheticnervous system. Thus, hemorrhage activates twodifferent components of the autonomic nervoussystem, and although tachycardia due to the sym-

pathetic component usually predominates, vagalslowing may also be seen.

In addition, other factors may confound anyrelation between the observed heart rate and themagnitude of blood loss. For example, atropineadministered in the field for chemical exposure,fear, and pain makes the use of heart rate unreliable.Trained athletes and infantry soldiers may tolerate

a substantial hemorrhage without manifestingtachycardia or hypotension until they are severelyhypovolemic. When possible, performance of a tilt-test will help to distinguish hypovolemia from othercauses of tachycardia.

It is important to recognize that heart rate andblood pressure may normalize with initial resusci-tation efforts, but this may not be indicative ofnormal peripheral perfusion. Mixed venous bloodoxygen saturation may be the best single index forassessing the adequacy of systemic perfusion.10

However, this determination requires a blood gasanalyzer, a device not usually available in forward

surgical hospitals (this subject is discussed morefully in Chapter 5, Physiological Monitoring). Fur-thermore, a central venous line is required. Unfor-tunately, invasive arterial and central venous moni-toring, although often desirable for fluid manage-ment, may not be easily managed in the combattheater.

Traditionally, restoration of urinary output hasbeen used as a monitor of organ perfusion and as aguide to fluid therapy. An indwelling urinary blad-der catheter should be considered an essential moni-tor in all trauma victims. There may be no changein hematocrit immediately following hemorrhage,

because only when transcapillary fluid refill occurs(or when fluid resuscitation is initiated) does dilu-

TABLE 4-3

RELATIONSHIP OF DEGREE OF SHOCK TO HEART RATE (106 CASES)

Degree of Shock

None (n=13) Slight (n=24) Moderate (n=34) Severe (n=35)

Reduction of Blood Volume (%) 14.1 4.9 20.7 4.1 34.3 3.1 45.9 4.6

Blood Pressure (m SD)Systole 126 11.9 109 3.0 95 4.9 49 7.6

Diastole 75 1.5 66 2.7 58 3.5 25 5.8

Heart Rate (m SD) 103 7.2 111 3.4 113 3.6 116 3.3

(Range) (70140) (88150) (80160) (60144)

Data source: The Board for the Study of the Severely Wounded, North AfricanMediterranean Theater of Operations . The PhysiologicEffects of Wounds. In: Beecher, HK, ed. Surgery in World War II. Washington, DC: US Army Medical Department, Office of The SurgeonGeneral; 1952: 34, 35, 56.


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tion of the remaining red blood cell mass occur.Thus, acute changes in hematocrit and hemoglobinare not necessarily useful in evaluating ongoingblood loss.

Venous Access

The initial management of all combat traumacasualties must involve a team effort focusing oncombined assessment and intervention as indicatedby the immediacy of the situation. Casualties pre-senting with evidence of shock must quickly beinspected for evidence of external hemorrhage. If asite of major bleeding is found, appropriate first-aidmaneuvers designed to stop the bleeding (eg, directpressure) must be instituted immediately. Two ormore large-bore (preferably 14-gauge) intravenousfluid cannulae must be established early in all casu-alties in shock, or those suspected of having injuries

that might lead to shock. Venous access can beextremely difficult to obtain in the presence ofhypovolemia and dehydration. Additionally, ac-cess sites may be limited by the location and natureof the traumatic injuries. Optimal sites for venouscannulation in trauma victims include the ante-cubital, subclavian, saphenous, and femoral veins.

Surgical access (cutdown) may be required inpatients with severe hemorrhagic shock. The saphe-nous and antecubital vessels are convenient loca-tions for cutdown cannulation. This approach al-lows the sterile intravenous extension tubing to beinserted directly into the vessel to maximize deliv-

ery. A major disadvantage of the surgical approachis the risk of infection.

Central venous access may be obtained via theinternal and external jugular veins, the subclavianvein, and the femoral veins. Femoral access elimi-nates the risk of a pneumothorax (a recognizedcomplication of gaining venous access via the neckand chest); however, the femoral site is remote fromthe anesthesiologist during most surgical proce-dures. Also, penetrating intraabdominal injuriesmay involve the inferior vena cava. In such cases,resuscitation via the femoral vessels may contributeto intraabdominal bleeding or be rendered ineffec-tive by cross-clamping of the femoral vessel. Thesubclavian vein is a useful site for trauma access;however, this location carries a significant risk of apneumothorax. Both the subclavian and internaljugular sites carry a significant risk of unintentionalarterial injury or cannulation.11 Major blood losshas occurred following arterial injuries at both sites,and the potential exists for an expanding hematomain the neck to compromise the airway. Techniques

for obtaining peripheral, central, and cutdownvenous access are well taught in the AmericanCollege of Surgeons Advanced Trauma Life Sup-port course, which should be taken by all medicalofficers.12

Intravenous Fluid-Delivery Systems

Some consideration must be given to ensuringthe availability of large-bore, fluid-administrationsets. The ideal set contains a large-surface-areacombination drip chamber and blood filter (170 ),dual vessel-access ports, and a hand-operated pump-ing chamber.

Large-caliber, high-efficiency, blood-warmingunits are essential for large-volume resuscitation.The Level 1 infusion system (manufactured by Level1 Technologies, Inc., Rockland, Mass.) is a func-tional unit that provides rapid warming of intrave-

nous infusions, through a counter-current warmingsystem, at high rates of flow (500 mL/min) (Figure4-2). This system allows quick and effortless prim-ing, and has an in-line air vent to prevent accidentalair emboli when used in conjunction with a pres-

Fig. 4-2. The Level 1 blood warming system is manufac-tured by Level 1 Technologies, Inc., Rockland, Mass.


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sure infuser. These devices are being evaluated bythe U.S. Army Medical Department for use in itsfield hospitals. The space required for the warmingunit and the disposable components, and the ex-pense of the disposable components are disadvan-tages of the Level 1 fluid warmer.

Alternative methods for rapid warming of crys-talloid solutions include using microwave ovens orstoring the solutions in warming ovens. The use ofmicrowave ovens for blood components is pres-ently not recommended. Under no circumstancesshould the fluid be infused at a temperature exceed-ing 40C.

Pressure-assist, fluid-administration devices(pressure bags) are helpful in speeding fluid deliv-ery. Most of these are manually operated bladderdevices. Pneumatic infusers are currently mar-keted; however, under field conditions, the avail-ability of compressed gas may limit their use. The

Biomed Spring Activated Infusion Pressor (manu-factured by Migada, Inc., Burbank, Calif.) offers auseful mechanical alternative. This spring-oper-ated system provides a constant pressure and thusa more stable rate of delivery. Complications sec-ondary to pressure-assisted fluid administrationcan occur (eg, venous air emboli, which may occurwith compression of the residual air in an exhaustedintravenous fluid bag). Air traps in blood-warmingsets and air vents (eg, Level 1 system) can help tominimize this risk. Also, inverting the containerand venting the air prior to administration will alsoreduce this risk. Some concern has been raised over

the potential for damage to cellular elements withpressurized delivery systems, but the significanceof this concern remains to be clarified.

Blood-Salvage Techniques

Salvaging blood for intraoperative autotransfu-sion is becoming an increasingly important part ofroutine anesthetic and surgical practice. Much ofthe recent emphasis on blood salvage has arisenover concerns about the safety of community au-tologous blood supplies, predominantly relatingto the transmission of the human immunodeficiencyvirus. Although blood-salvage techniques can re-duce the need for homologous transfusion, bloodsalvage usually does not completely eliminate theneed for transfusion of homologous blood productsin major trauma. Currently, there are two principalmethods for salvaging blood from the operativefield. The simplest method involves collecting theblood into sterile vacuum containers containing ananticoagulant (citrate-phosphate-dextrose or hep-

arin) and reinfusing the unwashed filtered blooddirectly into the patient. The advantages of thistechnique include low cost, simplicity, and minimalrequirements for storage or trained personnel. Thedisadvantages are that procoagulants, bacteria, andfree hemoglobin will also be infused into the pa-

tient.13

This approach appears to be ideally suitedfor use in field hospitals; unfortunately, the risksand benefits involved with transfusing unwashedblood have not yet been well delineated.

The alternative approach to blood salvage in-volves the collection of shed blood and processingit through a cell-washing device prior to reinfusion.These cell-washing devices, such as the Cell Saver 4(manufactured by Haemonetics, Boston, Mass.) havebecome increasingly efficient and automated (Fig-ure 4-3). The drawbacks include the need for per-sonnel training, equipment expense, the need forexpensive disposable plastic ware, and a time delay

during processing. Furthermore, the benefits of cellwashing, as opposed to the reinfusion of unwashedblood, have not been clearly demonstrated to im-prove patient outcome. With both techniques, co-agulation factors and platelets are lost, and there isa risk of trauma to the cellular elements. Althoughblood salvage is clearly beneficial in the manage-

Fig. 4-3. The Cell Saver 4 is manufactured by Haemonetics,Boston, Mass.


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ment of elective surgery, the advantages of intro-ducing this methodology into the care of the combatcasualty have yet to be demonstrated.

Intraosseous Fluid Infusion

Intraosseous fluid infusion has been advocatedin situations in which venous access is difficult orimpossible to obtain.14 This route of delivery isparticularly amenable in the pediatric population,and because pediatric casualties always occur inurban warfare, military anesthesiologists need tobe familiar with the technique. Intraosseous accessin adults is somewhat more difficult to obtain. Thisis partly related to the replacement of the marrowspace by fat and partly related to the density of theoverlying bone. Recent experimental animal stud-ies have demonstrated the benefits of intraosseousinfusion of a small-volume mixture of hypertonic

saline and dextran via the sternum. A sternal infu-sion device has been developed that could be placedin the field with minimal training of medics, and

then utilized for fluid access.15 This approach is stillin the early phase of development and testing.

At present, the intraosseous approach in adults isimpractical and inadequately tested. Special needlesare required for this technique (bone marrow sets)and the clinical utility in adults is unknown. Typi-

cally, the marrow space is entered by inserting a 15-or 18-gauge iliac bone marrow needle into the me-dial aspect of the proximal tibia. The distal femur,in the midline above the condyles, is an alternativesite. The medial malleolus has been used in patientsin cardiac arrest, in whom venous access is difficult.This approach may prove useful for the administra-tion of selected drugs. Unfortunately, the distaltibia provides inadequate flow rates for it to proveuseful in the management of hypovolemia. Com-plications with intraosseous infusions are uncom-mon.16 The most common complication is that oflocal extravasation. Local cellulitis and osteomyelitis

are fortunately rare (< 1%). Deaths have occurredwith the sternal approach secondary to unrecog-nized penetration of the thoracic cavity.17

RESUSCITATION FLUID SELECTION

Hypovolemia and hemorrhagic shock fall alonga continuum from mild to profound organhypoperfusion. As cardiac output falls, oxygentransport to less crucial end-organ cellular elements(eg, skin, muscle) may become progressively inad-equate, contributing to anaerobic metabolismand the accumulation of organic acids (eg, lac-

tate). Homeostatic efforts (vasoconstriction) to pre-serve perfusion to the heart and brain inevitablysacrifice perfusion to the kidneys, muscle, intestine,and skin, leading to the classic manifestations ofshock. The eventual lethality of the shock stateprobably results from the maintenance of this re-stricted perfusion pattern and progressive tissuehypoxia and acidosis.18 Some evidence suggeststhat blockade of the sympathetic nervous systemmay reverse the vasoconstriction-induced acidosisand improve survival after bleeding has beenstopped and blood volume restored.1921 However,a more effective and clinically relevant treatmentplan is to restore the circulating blood volume andorgan perfusion.

A variety of treatment regimens, including col-loids, crystalloid solutions, whole blood, and bloodcomponents, have been proposed (Table 4-4). Per-haps the best initial approach to the casualty withevidence of a mild-to-moderate hemorrhage (10%30% of the estimated blood volume) is to rapidlyadminister an intravenous fluid challenge of a

warmed, balanced, salt solution in 10- to 20-mL/kgincrements, depending on the severity of symp-toms and ongoing blood loss. Repeated fluid chal-lenges are administered until the desired hemody-namic response is obtained. Blood products shouldbe administered to keep pace with concurrent bloodloss and to maintain an acceptable hemoglobin level

(> 7 g/dL). When uncontrolled bleeding occurs,isovolumic transfusion with fresh whole blood orpacked red blood cells, in conjunction with a crys-talloid solution, is necessary.

Crystalloid Solutions

Although a variety of crystalloid solutions isavailable, 0.9% sodium chloride or lactated Ringerssolution are reasonable first choices. Isotonic so-dium chloride (0.9%) may be readily mixed withblood products and is an excellent choice for vol-ume resuscitation. However, it has the minor dis-advantage of contributing to a hyperchloremic aci-dosis when large volumes of resuscitation fluidmust be used. Lactated Ringers solution has theadvantage of having a somewhat more physiologi-cal composition, providing elemental replacementof calcium and potassium, and more physiologicalconcentrations of sodium and chlorine ions. Adisadvantage of lactated Ringers solution is itsrelative incompatibility with blood products. The


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TABLE 4-4

RESUSCITATION FLUIDS

Solution Advantages Disadvantages

0.9% NaCl Inexpensive Nonphysiological Na+ and Cl concentrationsCompatible with blood Contributes to interstitial edemaReplenishes ECF space Large volumes required for replacement of Increases GRF blood loss (> 3-fold estimated blood loss)

Lactated Ringers Inexpensive Same as those for NaClPhysiological electrolyte concentrationsIncreases GFRReplenishes ECF space

5% Albumin Replaces plasma loss volume for volume Expensive(MW 6104) Provides rapid expansion of the intra- Redistributes into the interstitial fluid space

vascular space with less volume relatively quickly (compared to other colloids)May aggravate edema in leaky capillary states

6% Hetastarch Same as those for 5% albumin Expensive

(Hespan, Dupont) Provides a more persistent expansion May interfere with coagulation cascade if(MW 104107) of the intravascular space, relative to > 20 mL/kg is administered

albuminPlasma volume expansion may persist

> 24 h

5% Plasma Protein Resembles albumin Similar to albumin, somewhat less osmoticallyFraction (83% activealbumin) Contaminating plasma proteins may produce

hypotension with rapid administration

Dextran 40 (average Provides rapid expansion of the intra- Risk of anaphylaxis 0.5%5%MW 4104) vascular space with a small volume May contribute to renal failure

Reduces incidence of thromboembolism Interferes with platelet function and clottingRisk of bleeding with > 1.5 g/kg/d

Interferes with blood cross-matchingMay produce osmotic diuresis

Dextran 70 (average Same as those for dextran 40 Same as those for dextran 40MW 7104) Larger MW confers a greater duration

of plasma volume expansion

HDS Very rapid restoration of intravascular Same as those for dextran 40volume with a small volume Brief hypotension with rapid infusion

Small volume makes field use easier Hypernatremia, especially if used in dehydratedcasualties

calcium content of lactated Ringers solution mayactivate the coagulation cascade in blood products;however, slight dilution of packed red cells withlactated Ringers solution has not been shown tocause a problem.22 The lactate content of lactatedRingers solution may aggravate the correction ofthe ongoing metabolic acidosis in individuals suf-fering from profound acidosis or ketoacidosis.Under most circumstances, however, when organperfusion has been restored, the liver is quite ca-

pable of metabolizing the lactate load; the problemis, therefore, rarely of concern.23

Intravenous fluids containing dextrose (glucose)are rarely indicated and are potentially harmful inthe management of trauma casualties. The stressresponse induced by major trauma or surgeryfrequently contributes to a normal or an elevatedblood glucose level. Rapid administration of largevolumes of glucose solutions during resuscitationmay lead to an osmotic diuresis, confounding ef-

ECF: extracellular fluid; GRF: glomerular filtration rate; HDS: hypertonic saline (7.5%) and dextran 70 (6%); MW: molecular weight


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forts to restore the intravascular deficit. Hyper-glycemia has also been linked to a poorer neurologi-cal outcome among victims of trauma, cardiac ar-rest, and stroke.2325 Glucose may be included inmaintenance fluids during the postresuscitationphase.

Colloid Solutions

The use of colloid-containing intravenous solu-tions in the management of trauma and surgicalpatients remains a source of controversy and isthoroughly discussed in other textbooks26,27 and inChapter 24, The Syndromes of Septic InflammatoryResponse and Multiple Organ Dysfunction. His-torically, the only colloids that were available in themilitary for field use were albumin and plasma.More recently, the dextrans and hydroxyethyl starch(Hespan, manufactured by Du Pont Pharmaceuti-

cals, Wilmington, Del.) have become widely avail-able and are used by some civilian paramedic res-cue squads for field resuscitation of casualties inhemorrhagic shock. The most significant drawbackto these agents is their cost, which is excessiverelative to crystalloid solutions. The attractive fea-tures of the colloids include

rapid repletion of the intravascular com-partment with a smaller fluid volume,

a more-prolonged expansion of the plasmavolume, and

less peripheral edema.

Some have suggested a reduced risk of increasedintracranial pressure as another attractive featureof colloids. This may be true in comparison tolactated Ringers solution; however, the effects ofisotonic solutions (eg, normal saline) on intracra-nial pressure appear comparable to those of albu-min.28

Colloid solutions produce an increase in the in-travascular colloid oncotic pressure and may drawinterstitial water into the intravascular compart-ment.29,30 Thus, the plasma volume expands inexcess of the administered fluid volume. Con-versely, in leaky capillary states (eg, burns, sepsis,the adult respiratory distress syndrome), the col-loids can traverse the endothelial barrier and con-tribute to the formation of pulmonary and periph-eral edema. Although abnormal capillary mem-branes are not likely to be present during the initialtreatment of most combat casualties, other disad-vantages of colloid solutions that argue againsttheir use include the following:

the potential for impaired coagulation, interference with cross-matching of blood, increased viscosity, a transient fall in ionized calcium levels

(which albumin may produce), and the potential for a relative reduction in

glomerular filtration.

The reduction in glomerular filtration rate probablyreflects (a) the depletion of the interstitial fluidcompartment through third-space losses and (b) theinability of colloids to replace the loss.30 A rela-tively hyperoncotic state may result. Crystalloidsare better suited to improving glomerular filtration.Patients with compromised glomerular filtrationmay be placed at increased risk of renal failure ifresuscitated with a dextran solution.31 In hypo-volemic patients, renal tubular obstruction maydevelop due to precipitation of the dextran in the

tubules.In circumstances where blood loss is substantial

and continuing, dextran and hetastarch should beused cautiously. Dextran interferes with plateletadhesion and may aggravate blood loss.32 Heta-starch, when used in large cumulative volumes, hasbeen shown to produce a coagulopathy, probablyby interfering with Factor VIII activity.33 Clinicalcase reports have linked bleeding catastrophes tothe use of hetastarch in quantities greater than 20mL/kg.34 Life-threatening anaphylaxis can occurwith the dextrans and hetastarch. The overall riskof anaphylaxis appears to be on the order of 0.5% to

5% with the dextrans and 0.08% with hetastarch.33

Hypertonic Solutions

Hypertonic saline solutions, alone or in combina-tion with concentrated colloid solutions, have be-come the focus of intense interest over their pos-sible use as small-volume resuscitation fluids in thefield. The primary advantage of hypertonic solu-tions compared to conventional fluids for field re-suscitation is logistical: much less hypertonic fluidis required for an equivalent degree of resuscita-tionthus, the load of the combat medic is reduced.The U.S. Army Medical Research and Materiel Com-mand at Fort Detrick, Frederick, Maryland, has hadan ongoing research program into the developmentand clinical application of a hypertonic saline dex-tran solution (7.5% sodium chloride and 6% high-molecular-weight dextran 70). This solution, whenused in animal models for hemorrhagic shock, haseffected dramatic improvements in hemodynamicparameters and survival following a hemorrhage


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that would otherwise have been lethal.35 Limitedfield trials using human volunteers have docu-mented the beneficial hemodynamic effects whenhypertonic saline dextran is administered by para-medics; however, improved patient outcome hasnot yet been demonstrated convincingly.36,37 One

reason for this could be the rapidity with whichmost patients were transported to hospitals andreceived definitive care.

Hypertonic saline produces a rapid expansionof the intravascular space by drawing extracel-lular and intracellular water into the vascularcompartment. Hypertonic saline alone producesshort-lived improvements in hemodynamics, asthe sodium tends to redistribute rapidly. The ad-dition of a concentrated colloid solution (eg,dextran, hetastarch) increases the duration of theplasma volume expansion and improves survivalin animal models.35 However, two recent clinical

investigation studies involving traumatized hu-mans show no added benefit from dextran com-pared with 7.5% saline alone.38,39 Subsequent vol-ume replacement with isotonic, balanced salt solu-tions is essential to maintain organ perfusion asthe effects resolve, and to reverse the relative hyper-natremic/hyperoncotic state.40 Hypertonic salineresuscitation may offer additional advantages inthe management of head-injured, hypovolemic ca-sualties by minimizing elevations in intracranialpressure and by improving the cerebral-perfusionpressure.41 While the benefits are clearly evident inthe short term (hours), the long-term benefits or

disadvantages of hypertonic solutions on cerebralperfusion and neurological outcome need to bedemonstrated.

One important hazard associated with the use ofhypertonic-resuscitation measures in the field is therisk of promoting further exsanguination and dehy-

dration. Improvements in blood pressure and car-diac output in casualties with uncontrolled bleed-ing may increase the rate of blood loss, leading tofurther loss of oxygen-carrying capacity, progres-sive acidosis, and increased morbidity. Data fromstudies42 with experimental animals appear to sup-

port these conclusions. Thus, the administrationof hypertonic solutions in the presence of uncon-trolled hemorrhage, and in the absence of guaran-teed, short-term delivery of definitive supportiveand surgical treatment, may be contraindicated. Ofcourse, the same stricture applies to resuscitationwith any fluid that raises blood pressure, includinglactated Ringers solution. Further study is neededon this issue.

At present, and under most conditions, crystal-loid solutions appear to be the resuscitation fluid ofchoice. Perhaps some combination of colloid andcrystalloid solutions will prove to be the optimal

approach. Colloid solutions should probably beavoided during the initial resuscitation (ie, the first24 h) of victims with extensive burn injuries, casu-alties suffering from the adult respiratory distresssyndrome, and in casualties suffering from preex-isting dehydration. Hypertonic solutions may havea role in the immediate resuscitation of hypovolemictrauma casualties, provided continued volume sup-port with isotonic solutions is available. Colloidsolutions or hypertonic saline may prove particu-larly useful prior to the induction of anesthesia inconscious, hypovolemic casualties, or in hypo-volemic casualties with head injuries who require

immediate surgery. Of course, the development ofan oxygen-carrying solutionsuch as a stroma-freehemoglobin solutionwhich, in contrast to blood,could be taken into the field by the medic, would bean important step forward in our ability to treat thecombat casualty.

SUPPLEMENTAL THERAPEUTIC MEASURES

Although control of bleeding and rapid infusionof crystalloid fluids and blood are the essentialsteps that must be taken if the combat casualty inshock is to be salvaged, a variety of supplementaltherapeutic measures have been suggested in thepast; in some instances, they may play an importantrole. The use of other measures, such as steroidtheroid therapy in the management of head trauma,continues to be controversial and unresolved. How-ever, in the absence of Addisons disease, adreno-corticoids are unlikely to be beneficial in the man-agement of hypovolemic shock.

Patient Position

Conventional management of hypotensivetrauma victims frequently involves placing the pa-tient in the head-down (Trendelenburgs) positionto improve venous return to the heart (Figure 4-4).In otherwise normovolemic subjects experiencinghypotension (ie, those in neurogenic shock), lower-ing the head or elevating the legs may facilitatevenous return. However, studies43 of subjects withhemorrhagic shock have failed to demonstrateconsistent hemodynamic improvement from


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Fig. 4-4. The data shown in this phasic pressure and flow diagram were obtained in an anesthetized swineinstrumented with an aortic flow probe for measuring cardiac output (CO) and pressure transducers in the proximalaorta (AP) and left atrium (LAP). When the animals hind legs were raised abruptly, cardiac output, aortic pressure,and left atrial pressure were transiently elevated. Previously, 50% of the animals circulating blood volume had beenremoved. Cardiac output remained elevated when the legs were lowered, suggesting that the blood that transfusedinto the central circulation when the extremities were raised has not yet been redistributed back to the legs. The fallin aortic pressure caused by lowering the legs may mean that the hydrostatic pressure head above the site of the pressure

catheter is itself a factor in determining the magnitude of the measured pressure. If applicable to humans in shock, data suchas these suggest that Trendelenburgs position may be hemodynamically beneficial. Source: Medical Audio VisualAids Division, Letterman Army Institute of Research, Presidio of San Francisco, Calif. File Number 229-82-1, 1983.

kg) and the augmented cardiac output secondaryto the increased venous return is transient (Figure4-5). Maintenance of blood pressure with thisdevice probably is the result of a mechanical in-crease in resistance in the compressed tissue andtherefore is purchased at the cost of decreased per-fusion of already ischemic tissue. Clinical studies46

have demonstrated significantly reduced survivalin patients treated with the pneumatic anti-shock garment when the site of hemorrhage is in thechest and, therefore, is not compressed by the de-vice. This is not surprising given that any increasein blood pressure will simply increase the rate ofhemorrhage. If the pneumatic antishock garmenthas any utility in combat casualty care, it is instabilizing fractures of the pelvis and the long bonesof the legs. In this setting, the device may help toreduce ongoing blood loss and therefore permithemodynamic stabilization prior to definitive in-tervention.

Supplemental Oxygen

The routine administration of supplemental oxy-gen to trauma casualties may be beneficial in somevictims, in that multiple or massive injuries (eg,splinting, flail chest, fat emboli) are often associatedwith impaired oxygenation. However, expecta-

Trendelenburgs position, and this position mayhave an adverse impact on cardiac output and bloodpressure.44 Furthermore, Trendelenburgs positionmay produce adverse consequences in the hypo-volemic, head-injured victim by increasing intrac-ranial pressure and reducing the cerebral perfusionpressure. Most of these problems can be avoided

simply by elevating the legs to facilitate venousreturn, without placing the head in a dependentposition.

Pneumatic Antishock Garment

The use of the pneumatic antishock garment (acompression device first known as militaryantishock trousers [MAST]) was introduced by theU.S. Army during the Vietnam War. Until recently,use of this garment was considered to be a standardof practice but its use in the acute management ofhemorrhagic shock has now waned. The pneumaticantishock garment appears to support the bloodpressure by a combination of increased systemicvascular resistance and increased venous return.45

There seems little doubt that proper use of thepneumatic antishock garment results in anautotransfusion of blood from the compressed tis-sue in the lower half of the body into the centralcirculation, but the actual volume is small (23 mL/


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Fig. 4-5. The phasic pressure and flow data shown in this figure were obtained in an anesthetized swine instrumentedwith an aortic flow probe for measuring cardiac output (C.O.), a flowprobe inserted into the inferior vena cava (IVC),and pressure transducers in the proximal aorta (AP) and right atrium (RAP). A pneumatic antishock garmentespecially designed for application to a large swine was applied around the animals lower trunk and hind legs. Theupper panel shows pressure and flow transients associated with abrupt inflation and deflation of the pneumaticantishock garment. A bolus of blood is translocated through the inferior vena cava into the heart (equivalent to about2 mL/kg, or 100 mL total), but cardiac output actually falls. Possibly this is due to an increase in arterial impedancecaused by the external compression. The lower panel shows the effects of inflating the pneumatic antishock garmentafter 50% of the animals circulating blood volume is removed: both cardiac output and aortic pressure rise. Reprintedwith permission from Bellamy RF, DeGuzman LR, Pedersen DC. Immediate hemodynamic consequences of MASTinflation in normo- and hypovolemic anesthetized swine.J Trauma. 1984;24:892.

duced temperatures. Thus, hypothermia (< 37C)may be beneficial in reducing oxygen consumptionin individuals with reduced oxygen-carrying ca-pacity if blood transfusion cannot be provided, butthis approach to managing the seriously injuredcombat casualty can only be considered specula-tive.

Intraarterial Infusion

Intraarterial infusion was advocated during theKorean War because it appeared to provide thepotential for more-rapid volume replacement, com-pared with the intravenous routes then being used.However, clinical evidence failed to show any sig-nificant advantage of this route over more conven-tional intravenous approaches, and its complexityargues against its use today.

tions of improved tissue oxygenation in the pres-ence of hypovolemic shock are unrealistic: hemo-globin oxygen saturation in the typical youngcombat casualtywho is usually hyperventilating because of the injuryis already maximal.Furthemore, the added amount of dissolved oxy-gen in the plasma caused by breathing supplemen-tal oxygen is too small to be of importance. Until thecirculating blood volume is restored, supplementaloxygen is unlikely to reverse the anaerobic metabo-lism in poorly perfused tissues.

Therapeutic Hypothermia

Reductions in body temperature are associatedwith a reduced metabolic rate: approximately 13%for every 1C decrease in temperature.47 In addi-tion, oxygen solubility in plasma increases at re-


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Vasopressors

Efforts to support the arterial blood pressurethrough the administration of vasoconstrictors arementioned here only to be condemned. Intense vaso-constriction is the typical homeostatic response to

hemorrhagic shock and may be primarily responsiblefor the adverse consequences of hypovolemia (eg,acidosis, tissue hypoxia). Pharmacological supportof the blood pressure with vasoconstrictors willonly aggravate the reduction in tissue perfusion bydecreasing cardiac output, and will contribute to theprogressive acidosis. The benefits of transiently sup-porting the blood pressure with vasoconstrictors,until volume replacement or control of bleeding ispossible, have not been carefully evaluated.

Vasodilators

At face value, the administration of vasodilatorsto a hypovolemic patient would seem to be grossly

inappropriate. However, numerous animal stud-ies 1921using fixed-pressure shock models of theWiggers type, involving the use of epidural anes-thesia or the administration of adrenergic antago-nists in the presence of hemorrhagic shockhavedemonstrated both reductions in the severity of the

systemic acidosis and improved survival. The ben-eficial effects of sympathetic antagonism are re-lated to a reversal of the reflex vasoconstrictionassociated with hypovolemia. Tissue oxygenationand perfusion, albeit reduced, are maintained atlevels adequate to reduce the progression of theacidosis. However, the beneficial application ofcentral neuraxis anesthesia has not rigorously beenevaluated in the clinical setting. Case reports haveappeared in the literature; however, it is impos-sible to draw valid conclusions based on a limitednumber of uncontrolled reports. Conventionalwisdom has dictated the avoidance of spinal and

epidural anesthesia in hypovolemic and bleedingpatients. Further study clearly is needed.

CONDITIONS PECULIAR TO RESUSCITATING COMBAT CASUALTIES

The conditions of the battlefield, which are sounlike those encountered in civilian practice, can cre-ate unique problems for military anesthesiolo-gists. Not only are combat injuries quite differentfrom those encountered in civilian practice, but thepropensity for environmental hazards to become im-portant sources of comorbidity must also be kept inmind.

Hyperthermia and Dehydration

Military conflicts frequently occur under adverseclimatic conditions. Elevated ambient tempera-tures, physical exertion, and inadequate supplieson the battlefield can combine to contribute to thedevelopment of heat injury and dehydration. Coin-cident trauma and hemorrhage in the setting ofpreexisting dehydration and volume contractionwill adversely influence survival. Elevated bodytemperature and hypotension will accelerate theprogression to renal failure and contribute to thedevelopment of rhabdomyolysis. Rapid replace-ment of the intravascular and extracellular fluidspace with isotonic, balanced, salt solutions is keyto reversing this life-threatening process. Hyperoncoticcolloid or hypertonic saline solutions are relativelycontraindicated in casualties suffering from dehydra-tion. The hyperosmotic state will adversely impact on

glomerular filtration and further deplete the extracel-lular and intracellular fluid spaces.

Hypothermia

Hypothermia is a common problem afflictingtrauma victims. The pathophysiology of hypother-mia affects virtually all organ systems, and is dis-

cussed in detail in Chapter 28, Systemic Hypother-mia. Profound hypothermia (core temperature

h.shock and resucitation

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