CLINICAL DIFFERENTIATION OF CAUSE OF SHOCK What is the cause of the shoxk state?

Shock in a trauma patient is classified as hemorrhagic or nonhemorrhagic. A patient with injuries above the diaphragm may have evidence of inadequate organ perfusion due to puor cardiac performance from blunt myocardial injury cardiac temponade or a tension pneumothorax that produces inadequate venous return !preload". A high index os suspicion and careful observation of the patient#s response to initial treatment will enable the doctor to recogni$e and manage all forms of shock. %nitial determination of the cause of shock depends on taking an appropriate history and performing a careful physical examination. Selected additional tests such as monitoring central venouc pressure !&'(" and obtaining data from a pulmonary artery catheter chest and)or pelvic x*ray examinations and ultrasonography may provide confirmatory evidence for the cause of the shock state but should not delay aggressive volume restoration. BASIC CARDIAC PHYSIOLOGY &ardiac output which is defined as the volume of blood pumped by the heart per minute is determined by multiplying the heart rate by the stroke volume. Stroke volume the amount of blood pumped with each cardiac contraction is classically determined by the following+ (reload the volume of venous return to the heart is determined by venous capacitance volume status and the difference between mean venous systemic pressure and right atrial pressure. ,his pressure differential determines venous flow. ,he venous system can be considered are reservoir or capacitance system in which the volume of blood is divided into two components. -ne &omponent docs not contribute to the mean systemic venous pressure and represents the volume of blood that would remain in this capacity circuit if the pressure in the system were $ero. ,he second more important component represents the venous volume that contributes to the mean systemic venous pressure. .early /01 of the body2s total blood volume is estimated to be located in the venous circuit. ,he relationship between venous volume and venous pressure describes the compliance of the system. %t is this pressure gradient that drives venous now and therefore the volume of venous return to the heart. 3lood loss depletes this component of venous volume and reduces the pressure gradient4 as a consequence venous return is reduced. ,he volume of venous blood returned to the heart determines myocardial muscle fiber length after ventricular filling at the end of diastole. 5uscle fiber length is related to the contractile properties of myocardial muscle

according to Starling2s law. 5yocardial contractility is the pump that drives the system. Afterload is systemic !peripheral" vascular resistance or simply stated the resistance to the forward flow of blood.

BLOOD LOSS PATHOPHYSIOLOGY 6arly circulatory responses to blood loss are compensatory*progressive vasoconstriction of cutaneous. muscle and visceral circulation preserves blood now to the kidneys heart and brain. ,he response to acute circulating volume depletion associated with injury is an increase in heart rate in an attempt 70 preserve cardiac output. %n most cases tachycardia is the earliest measurable circulatory sign of shock. ,he release of endogenous catecholamine increases peripheral vascular resistance which in ,urn increases diastolic blood pressure and reduces pulse pressure but does little to increase -rgan perfusion. -ther hormones with vasoactive properties are released into the circulation during shock including histamine bradykinin 8*endorphins and a cascade of prostanoids and other cytokines. ,hese substances have profound effects on the microcirculation and vascular permeability. 'enous return in early hemorrhagic shock is preserved to some degree by the compensatory mechanism of contraction of the volume of blood in the venous system which does not contribute to systemic venous pressure. 9owever this compensatory mechanism is limited. ,he most effective method of restoring adequate cardiac output and end*organ perfusion is to

res tore venous return to normal by volume repletion. At the cellular level inadequately perfused and oxygenated cells are deprived of essential substrates for normal aerobic metabolism and energy production. %nitially cornpensation occurs by shifting to anaerobic metabolism which results in the formation of lactic acid and the development of metabolic acidosis. %f shock is prolonged and substrate delivery for the generation of adenosine triphos phate !A,(" is in adequate the cellular membrane loses the ability to maintain its integrity and the normal electrical gradient is lost. Swelling of the endoplasmic reticulum is the first ultra*structural evidence of cellular hypoxia. 5itochondrial damage soon follows. :ysosomes rupture and release en$ymes that digest t her in other cellular structural elements. Sodium and water enter the cell and cellular swelling occurs. %ntracellular calcium deposition also occurs. %f the process is not reversed progressive cellular damage additional tissue swelling and cellular death occur. ,his process compounds the impact of blood loss and hypoperfusion. ,he administration of a sufficient quantity of isotonic electrolyte solutions helps combat th is process. (atient treatment is directed toward reversing the shock state by providing adequate oxygenation ventilation and appropriate fluid resuscitation . ;esuscitation may be accompanied by marked increase in interstitial edema which is caused by reperfusion injury< to the capillary interstitial membrane. As a result larger volumes of fluid may be required for resuscitation than initially anticipated. ,he initial treatment of shock is directed toward restoring cellular and organ perfusion with adequately oxygenated blood. &ontrol of hemorrhage and restoration of adequate circulating volume are the goals of treatment of hemorrhagic shock. With the possible except ion of penetrating trauma of the torso without head injury euvolemia should be maintained. 'asopressors are contraindicated for the treatment of hemorrhagic shock because they organ tissue perfusion frequent monitoring of the patient2s indices of perfusion is necessary 70 evaluate the response 70 therapy and detect deterioration in the patient2s condition as early as possible.

Hemorrhagic Shock 9emorrhagic is the most common cause of shock after injury and virtually all patients with multiple injuries have an element of hipovolemia. %n addition most nonhemorraghic ashock states respond partially or briefly to volume resuscitation. ,herefore if signs of shock are present treatment ususally is instituted as if the patient is hypovolemic. 9owever as treatment is instituted it is important to identify the small number of patients whose shock has different cause !eg a secondary condition such as cardiac temponade

tension pneumothorax spinal cord injury or blunt cardiac injury which complicates hypovolemic)hemorrhagic shock". Specific information about the treatment of hemorrhagic shock is provided in the next section of this chapter. ,he primary focus in hemorrhagic shock is to identify and stop hemorrhagic promptly. Nonhemorrhagic Shock .onhemorrhagic shock includes cardiogenic shock cardiac tamponade tension pneumothorax neurogenic shock and septic shock. Car iogenic Shock 5yocardial dysfunction may be caused by blunt cardiac injury cardiac tamponade an air embolus or rarely a myocardial infarction associated with the patient2s injury. 3lunt cardiac injury should be suspected when the mechanism of injury to the thorax is rapid deceleration. All patients with blunt thoracic trauma need constant electrocardiographic !6&=" monitoring to detect injury patterns and dysrhythmias. 3lood creatine kinase !&>4 formerly creatine phosphokinase %&(>?" isoen$ymes and specific isotope studies of the rnyoc.7rdium rarely assist the doctor in diagnosing or treating patients in the emergency department !6@". 6chocardiography may be useful in the diagnosis of tamponade and valvular rupture but it is often not practical or immediately available in the 6@. Aocused assessmentsonography in trauma !AAS," in the 6@ can identify pericardial fluid and the likelihood of cardiac tamponade as the cause of shock. 3lunt cardiac injury may be an indication for early &'( monitoring to guide fluid resuscitation in this situation. Car iac !am"ona e is most commonly identified in penetrating thoracic trauma but it may occur as the result of blunt injury to the thorax. ,achycardia muffled heart sounds and dilated engorged neck veins with hypotension resistant to lluid therapy suggest cardiac tamponade. 9owever the absence of these classic findings does not exclude the presence of th is condition. ,ension pneumothorax may mimic cardiac tamponade but it is differentiated from the latter condition by the findings of absent breath sounds and a hyperresonant percussion note over the affected hemithorax. Appropriate placement of a needle into the pleural space in a case of tension pneumothorax temporarily relieves this life*threatening condition. &ardiac tamponade is best m2l%7aged by thoracotomy. (ericardiocentesis may be used as a tempori$ing maneuver when thoracotomy is not an available option.

Ten#ion Pne$mo!hora% is a true surgical emergency that requires immediate diagnosis and treatment. %t develops when air enters the pleural space but a flap*valve mechanism prevents its escape. lntrapleural pressure rises causing total lung collapse and a shift of the mediastinum to the opposite side with a subsequent impairment of venous return and fall in cardiac output. ,he presence of acute respir+ttory distress subcutaneous emphysema absent breath sounds hyperresonance to percussion and tracheal shift supports the diagnosis and warrants immediate thoracic decompression without waiting for x*ray confirmation of the diagnosis. Ne$rogenic Shock isolated intracranial injuries do not cause shock. ,he presence of shock in a patient with a head injury necessitates a search for a cause other than an intracranial injury. Spinal cord injury may produce hypotension due to loss of sympathetic tone. :oss of sympathetic tone compounds the physiologic effects of hypovolemia and hypovolemia compounds the physiologic effects of sympathetic denervation. ,he classic picture of neurogenic shock is hypotension without tachycardia or cutaneous vasoconstrict ion. A narrowed pulse pressure is not seen in neurogenic shock. (atients who have sustained a spinal injury often have concurrent torso trauma4 therefore patients with known or suspected neurogenic shock should be treated initiall y for hypovolemia. ,he failure of fluid resuscitation to restore organ perfusion suggests either continuing hemorrhage or neurogenic shock. &'( monitoring may he helpful in managing this sometimes complex problem. Se"!ic Shock due to infection immediately after injury is uncommon4 however if a patient2s arrival at an emergency facility is delayed for several hours it could occur. Septic shock may occur in patients with penetrating abdominal injuries and contamination of the peritoneal cavity by intestinal contents. (atients with sepsis who also have hypotension and are afebrile are clinically difficult to distinguish from those in hypovolemic shock as both groups may manifest tachycardia cutaneous vasoconstriction impaired urinary output decreased systolic pressure and narrow pulse pressure. (atients with early septic shock may have a normal circulating volume modest tachycardia warm pink skin systolic pressure near normal and a wide pulse pressure. HE&ORRHAGIC SHOCK IN IN'URED PATIENTS Direc! e((ec!# o( hemorrhage

,he classilification of hemorrhage into four cbsses based on clinical signs is %% llseful tool for estimating the percentage of acute blood loss. ,hese changes represent a continuum of ongoing hemorrhage and guide initial therapy. 'olume replacement is guided by the patient2s response to initial therapy not solely by the initial classification. ,his classification system is useful in emphasi$ing the early signs and pathophysiology of the shock state. &lass % hemorrhage is exemplified by the condition of an individual who has donated a unit of blood. &lass %% is uncomplicated hemorrhage for which crystalloid fluid resuscitation is required. &lass %%% is a complicated hemorrhagic state in which at least crystalloid infusion is required and perhaps also blood replacement. &lass %' hemorrhage is considered a preterminal event and unless very aggressive measures are taken the patient will die with in minutes. Several confounding factors profoundly alter the classic hemodynamic response to an acute loss of circulating blood volume and these must be promptly recogni$ed by all individuals involved in the initial assessment and resuscitation of injured patients who are at risk for hemorrhagic shock. ,hese factors include+

B (atient2s age B Severity of injury with special attention to type and anatomic loca tion of injury B ,ime lapse between injury and initiation of treatment B (rehospital fluid therapy and application of a pneumatic antishock garment !(AS=" B 5edications used for chronic conditions %t is dangerous to wait until the trauma patient fits a precise physiologic classification of shock before initiating aggressive volume restoration. Aluid resuscitation must be initiated when early signs and symptoms of blood loss are apparent or suspected not when the blood pressure is falling or absent.

&lass % 9emorrhage Cp to 7D1 3lood 'olume :oss ,he clinical symptoms of volume loss with class % hemorrhage are minimal. %n uncomplicated situati ons minimal tachycardia occurs. .o measurable changes occur in blood pressure pulse pressure or respiratory rate. Aor otherwise healthy patients this amount of blood loss does not require replacement. ,ranscapillary refill and other compensatory mechanisms restore blood volume within EF hours. 9owever in the presence of other fluid changes this amount of blood loss may produce clinical symptoms in which case replacement of the primary fluid losses corrects the circulatory state. usually without the need for blood transfusion. &lass %% 9emorrhage*7D1 to G01 3lood 'olume :oss %n a /0*kg male volume loss with class %% hemorrhage represents /D0 to 7D00 m: of blood. &linical signs include tachycardia !heart rate above 700 in an adult" tachypnea and decreased pulse pressure4 the latler sign is related primarily to a rise in the diastolic component due to an increase in circulating catecho lamines. ,hese agents produce an increase in peripheral vascular tone and resistance. Systolic pressure changes minimally in early hemorrhagic shock4 therefore it is important to evaluate pulse pressure rather than

systolic pressure. -ther pertinent clinical findings with this amount of blood loss include subtle &.S changes such as anxiety fright and hostility. @espite the significant blood loss and cardiovascular changes urinary output is only mildly affected. ,he measured urine flow is usually E0 to G0 m:)hour in an adult. Accompanying fluid losses can exaggerate the clinical manifestations of class %% hemorrhage. Some of these patients may eventually require blood transfusion but may be stabili$ed initially with crystalloid solutions. &lass %%% 9emorrhage*G00)0 to F01 3lood 'olume loss ,he blood loss with class %%% hemorrhage !approximately E000 m: in an adult " may be devastating. (atients almost always present with the classic signs of inadequate perfusion including marked tachycardia and tachypnea significant changes in mental status and a measurable fall in systolic pressure. %n an uncomplicated case. this is the least amount of blood loss that consistently causes a drop in systolic pressure. (atients with this degree of blood loss almost always require transfusion. 9owever the priority of man agement is to stop the hemorrhage by emergency operation. if necessary in order to decrease the need for transfusion. ,he decision to transfuse blood is based on the patient2s response to initial fluid resuscitation and the adequacy of endorgan perfusion and oxygenation as described later in this chapter. &lass %' 9emorrhage*5ore than F01 3lood 'olume :oss ,he degree of exsanguination with class %' hemorrhage is immediately life threatening. Symptoms include marked tachycardia a significant decrease in systolic blood pressure and a very narrow pulse pressure !or an unobtainable diastolic pressure". Crinary output is negligible and mental status is markedly depressed. ,he skin is cold and pale. (atients with closs %' hemorrhage frequently require rapid transfusion and immediate surgical intervention. ,hese decisions are based on the patient2s response to the initial management techniques described in this chapter. :oss of more than D01 of blood volume results in loss of consciousness and decreased pulse and blood pressure.

INITIAL &ANAGE&ENT OF HE&ORRHAGIC SHOCK ,he diagnosis and treatment of shock must occur almost simultaneously. Aor most trauma patients treatmcnt is instituted as if the patient has hypovolemicl ic shock unless there is clear evidence that the shock state has a different cause. ,he basic management principle is to stop the bleeding and replace the volume loss. (9HS%&A: 6IA5%.A,%-. ,he physical examination is directed towa rd the immediate diagnosis of life * threatening injuries a nd includes assessment of the A3&@6s. 3aseleline recordings are important to monitor the patient2s response to therapy. 'ital signs urinury output and level of consciousness are essential. A more detailed examination of the patient follows as the situation permits. Air)a* an Brea!hing 6stablishing a patent airway with adequate ventilation and xygenation is the first priority. Supplcmentary oxygen is supplied to maintain oxygen saturation at greater than JD1. Circ$+a!ion,Hemorrhage Con!ro+ (riorities for the circulation include controlling obvious hemorrhage obtaining adequate intravenous access and tissue perfusion. 3leeding from external wounds usually can be controlled by direct pressure to the bleeding site. A (AS= muy be used to control bleeding from pelvic or lower extremity fractures but its usc should not interfere with the rapid reestablishment of intravascular volume by intravenous flu id infusion. ,he adequacy of tissue perfusion dictates thc amount of fluid resuscitation required. Surgery may be required to control internal hemorrhage . Di#a-i+i!*,Ne$ro+ogic E%amina!ion A brief neurologic examination will determine the level of consciousness ere motion and pupi7lary response best motor function and degree of sensation . ,his information is useful in assessing cerebral perfusion following the evolution of neurologic disability and predicting future recovery. Alteration in &.S function in putients who have hypotension is result of hypovolemic shock do not necessarily imply direct intracranial injury and may

reflect inadequate brain perfusion. ;estoration of cerebral perfusion and oxygenation must be achieve before ascribing these findig to intracranial injury. E%"o#$re , Com"+e!e E%amina!ion After lifesaving priorities are addressed the patient must be completely und ressed and carefully examined from head o toe to search for associated injuries. When undressing the patient it is essential to prevent hypothermia. ,he use of fluid warmers as well as external pussive and active warming tedniques are essential to prevent hypothermia. Ga#!ric Di+a!ion,Decom"re##ion =astric dilation often occurs in trauma patients especilly In children. and may cause unexplained hypotension or cardic dysrhythmia usually bradycardia from excessive vagal stimulat ion. %n unconscious patients gastric distention increases he risk of aspiration of gastric contents which is a potentially fatal complication. =astric decompression is accomplished by intubating the stomach with a tube passed nasally or orally and attach ing it to suction to evacuate gastric contents. 9owever proper positioning of the tube does not completely obviate the risk of aspiration. Urinar* Ca!he!eri.a!ion 3%adder catheteri$ation allows for assessment of the urine for hematuria and continuous evaluation of renal perfusion by monitoring urinary output. 3lood at the urethral meatus or high*riding mobile or nonpalpaple prostate in males is an absolute contraindication to the insertion of a transurethral catheter prior to radiographic confirmation of an intact urethra. /ASCULAR ACCESS LINES Access to the vascular system must be obtained promptly. ,his is best done by inserting two large*caliber !minimum of 7K*gauge" peripheral intravenous catheters before placing a central venous line is considered. ,he rate of flow is proportional to the fourth power of the radius of the cannula and inversely related to its length !(oiseuille2s law". 9ence short large*caliber peripheral intravenous lines are preferred for the rapid infusion of large volumes of fluid. Aluid warmers and rapid infusion pumps are used in the presence of massive hemorrhage and severe hypotension.

,he most desirable sites for peripheral percutaneous intravenous lines in adults are the forearms and antecubital veins. %f circumstances prevent the use of peripheral veins large*caliber central venous !femoral jugular or subclavian vein" access using the Seldinger technique or saphenous vein cutdown is indicated depending on the skill and experience of the doctor. Arequently in an emergency situation central venous access is not accomplished under tightly controlled or completely sterile conditions. ,hese lines should be changed in a more controlled environment as soon as the patient2s condition permits. &onsideration also must be given to the potential for serious complications related to attempted central venous catheter placement such as pneumothorax or hemothorax in patients who may already be unstable. %n children younger than K years the placement of an intraosseous needle should be attempted before inserting a central line. ,he important determinant for selecting a procedure or route for establishing vascular access is the experience and skill of the doctor. %ntraosseous access with specially designed equipment also is possible in adults. As intravenous lines are started blood samples are drawn for type and crossmatch appropriate laboratory analyses toxicology studies and pregnancy testing for all females of childbearing age. Arterial blood gas !A3=" ana%ysis is performed at this time. A chest x*ray must be obtained after attempts at inserting a subclavian or internal jugular &'( monitoring line to document the position of the line and to evaluate for a pneumothorax or hemothorax. S"ecia+ Con#i era!ion# in !he Diagno#i# an Trea!men! o( Shock

AD/ANCE AGE 6lderly trauma patients require special consideration. ,he aging process produces a relative decrease in sympathetic activity with respect to the cardiovascular system. ,his is thought 70 results from a deficit in the receptor response to catecholamine rather than from a reduction in catecholamine production. &ardiac compliance decreases with age and older patients are unable to increase heart rate or the efficiency of myocardial contraction when stressed by blood volume loss as arc younger patients. Atherosclerotic vascular occlusive disease makes many vital organs extremely sensitive to even the slightest reduction in blood flow. 5any

elderly patients have preexisting volume depletion resulting from long*term diuretic use or subtle malnutrition. Aor these reasons hypotension secondary to blood loss is poorly tolerated by elderly trauma patients. is*adrenergic blockade may mask tachycardia as an early indicator of shock. -ther medications may adversely affect the stress response to injury or block it completely. 3ecause the therapeutic range for volume resuscitation is relatively narrow in elderly patients it is prudent to consider early invasive monitoring as a means to avoid excessive or inadequate volume restoration. ,he reduction in pulmonary compliance decrease in diffusion capacity and general weakness of the muscles of respiration limit the ability of elderly patients to meet the increased demands for gas exchange imposed by injury. ,his compounds the cellular hypoxia already produced by a reduction in local oxygen delivery. =lomerular and tubular senescence in the kidney reduces the ability of elderly patients to preserve volume in response to the release of stress hormones such as aldosterone catecholamine vasopressin and cortisol. ,he kidney also is more susceptible to the effects of reduced blood flow and nephrotoxic agents such GS drugs contrast agents and the toxic products of cellular destruction. Aor all of these reasons mortality and morbidity rates increase directly with age and long*term health status for mild and moderately severe injuries. @espite the adverse effects of the aging process comorbidities from preexisting disease and a general reduction in the <physiologic reserve< of geriatric patients the majority of these patients may recover and return to their pre injury status. ,reatment begins with prompt aggressive resuscitation and careful monitoring. ATHLETES ;igorous athletic training routines change the cardiovascular dynamics of this group of patients. 3lood volume may increase 7D1 to E01 cardiac output six fold and stroke volume D01 and the resting pulse can average D0. ,he ability of athletes2 bodies to compensate for blood loss is truly remarkable. ,he usual responses to hypovolemia may not be manifested in athletes even when significant blood loss has occurred. PREGNANCY (hysiologic maternal hypervolemia requires a greater blood loss to manifest perfusion abnormalities in the mother which also may be reflected in decreased fetal perfusion. &EDICATIONS

7G*adrenergic receptor blockers and calcium*channel blockers can significantly alter a patient2s hemodynamic response to hemorrhage. %nsulin overdosing may be responsible for hypoglycemia and may have contributed to the injury*producing event. :ong* term diuretic therapy may explain unexpected hypokalemia and .SAl@s may adversely affect platelet function. HYPOTHER&IA (atients suffering from hypothermia and hemorrhagic shock do not respond normally to the administration of blood and fluid resuscitition and coagulopathy often develops. 3ody temperature is an important vital sign to monitor during the initial assessment phase. 6sophageal or bladder temperature is an accurate clinical measurement of the core temperature. A trauma victim under the influence of alcohol and exposed to cold ternperature extremes is more likely to have hypothermia as a result of vasodilation. ;apid rewarming in a environment with appropriate external warming devices he+lt lamps thermal caps heated respiratory gases and warmed intravenous fluids and blood will generally correct hypotension and hypothermia. &ore rewarming !irrigation of the peritoneal or. thoracic cavity with crystalloid solutions warmed to GJ< & L70E.EM (% or extracorporeal bypass" occasionally be indicated. 9ypothermia is best treated by prevention PACE&AKER (atients with pacemakers are unable to respond to blood loss in the expected fashion because cardiac output is directly related to heart ratc. %n the significant number of patients with myocardial conduction defects who have such devices in place &'( monitoring is invaluable to guide fluid therapy.

INITIAL FLUID THERAPY Warmed isotonic electrolyte solutions such as lactated ;inger2s and normal saline are used for initial resuscitution. ,his type of fluid provides transient intravascular expansion and further stabili$es the vascular volume by replacing accompanying fluid losses into the

interstitial and intracellular spaces. An alternative initial fluid is hypertonic saline although there is no evidence of survival advantage in the current literature. An initial warmed fluid bolus is given as rapidly as possible. ,he usual dose is 7 to E : for adults and E0 m:)kg for pediatric patients. ,his often requires application of pumping devices !mechanical or manual" to the fluid administration sets. ,he patient2s response is observed during this initial fluid administration and further therapeutic and diagnostic decisions are based on lhis response. ,he amount of fluid and blood required for resuscitation is difficult to predict on initial evaluation of the patient. ,able G*7 provides general guidelines for establishing the amount of fiuid and blood likely required. A rough guideline for the total amount of crystalloid volume required in the short term is to replace each 7 m: of blood loss with G m: of crystalloid fluid thus allowing for restitution of plasma volume lost into the interstitial and intracellular spaces. ,his is known as the G*for*7 rule. %t is most important to assess the patient2s response to fluid resuscitation and evidence of adequate end*organ perfusion and oxygenation !via urinary output level of consciousness and peripheral perfusion". %f during resuscitation the amount of fluid required to restore or maintain adequate organ perfusion greatly exceeds these estimates a careful reassessment of the situation and a search for unrecogni$ed injuries and other causes of shock are neccessary. ,he goal of resuscitation is to restore organ perfusion. ,his is accomplished by the use of resuscitation fluids to replace lost intravascular volume and guided by the goal of restoring a normal blood pressure. .ote however that if blood pressure is raised rapidly before the hemorrhage has been definitively controlled increased bleeding may occur. ,his can be seen in the small subset of patients in the transient or non responder category. (ersistent infusion of large volumes of fluids in an attempt to achieve a normal blood pressure is not a substitute for definitive control of bleeding. Aluid resuscitation and avoidance of hypotension are important principles in the initial management of blunt trauma patients particularly those with traumatic brain injury !,3%".ln penetrating trauma with hemorrhage delaying aggressive fluid resuscitation until definitive control may prevent additional bleeding. Although complications associated with resuscitationinjury are undesirable the alternative of exsanguination is even less so. A careful balanced approach with frequent reevaluation is required.

3alancing the goal of organ perfusion with the risks of rebleeding by accepting a lower*than*normal blood pressure has been termed <controlled resuscitation < <balanced resuscitation <<hypotensive resuscitation < and <permissive hypotension.< ,he goal is the balance not the hypotension. Such a resuscitation strategy may be a bridge to but is not a substitute for definitive surgical control of bleeding. 6valuation of Aluid ;esuscitation and -rgan (erfusion What is the patient's response? ,he same signs and symptoms of inadequate perfusion that are used to diagnose shock are useful determinants of patient response. ,he return of normal blood pressure pulse pressure and pulse rate are signs that suggest perfusion is returning to normal. 9owever these observations give no information regarding organ perfusion. %mprovements in the &'( status and skin circulation are important evidence of enhanced perfusion but are difficult to quantitate. ,he volume of urinary output is a reasonably sensitive indicator of renal perfusion4 normal urine volumes generally imply adequate renal blood flow if not modified by the administration of diuretic agents. Aor this reason urinary output is one of the prime monitors of resuscitation and patient response. &hanges in &'( can provide useful information and the risks incurred in the placement of a &'( line are justified for complex cases. 5easurement of &'( is adequate for most cases. C;%.A;H -C,(C, Within certain limits urinary output is used to monitor renal blood flow. Adequate resuscitation volume replacement should produce a urinary output of approximately 0.D m:)kg)hr in adults whereas 7 m:)kg)hr is an adequate urinary output for pediatric patients. Aor children under 7 year of age E m:)kg)hour should be maintained. ,he inability to obtain urinary output at these levels or a decreasing urinary output with an increasing specific gravity suggests inadequate resuscitation. ,his situation should stimulate further volume replacement and diagnostic endeavors. A&%@)3AS6 3A:A.&6 (atients in early hypovolemic shock have respiratory alkalosis due to tachypnea. ;espiratory alkalosis is frequently followed by mild metabolic acidosis in the early phases of shock and does not require treatment. Severe metabolic acidosis may develop from long*standing or

severe shock. 5etabolic acidosis is caused by anaerobic metabolism which results from inadequate tissue perfusion and the production of lactic acid. (ersistent acidosis is usually caused by inadequate resuscitation or ongoing blood loss and in the normothermic patient in shock it should be treated with fluids blood and consideration of operative intervention 70 control hemorrhage. 3ase deficit and)or lactate can be useful in determining the presence and severity of shock. Serial measurement of these parameters can be used to monitor the response to therapy. Sodium bicarbonate should not be used routinely to treat metabolic acidosis secondary to hypo*volemic shock. ,herapeutic @ecisions 3ased on ;esponse to %nitial Aluid ;esuscitation ,he patient2s response to initial fluid resuscitation is the key to determining subsequent therapy. 9aving established a preliminary diagnosis and treatment plan based on the initial evaluation the doctor now modifies the plan based on the patient2s response. -bserving the response to the initial resuscitation identifies patients whose blood loss was greater than estimated and those with ongoing bleeding who require operative control of internal hemorrhage. ;esuscitation in the operating room can accomplish simultaneously the direct control of bleeding by the surgeon and the restoration of intravascular volume. %n addition it limits the probability of overtransfusion or unnecessary transfusion of blood in patients whose initial status was disproportionate to the amount of blood loss. %t is particularly important to distinguish patients who are hemodynamically stableN from those who are <hemodynamically normal.< A hemodynamically stable patient may have persistent tachycardia tachypnea and oliguria clearly underresuscitated and still in shock. %n contrast a hemodynamically normal patient is one who exhibits no signs of inadequate tissue perfusion. ,he potential patterns of response to initial fluid administration can be divided into three groups+ rapid response transient response and minimal or no response. 'ital signs and management guidelines for patients in each of these categories are outlined in ,able G*E.

,A3:6 G*E ;esponses to initial Aluid ;esuscitation ;A(%@ ,;A.S%6., 'ital Signs ;6S(-.S6 ;eturn to normal ;6S(-.S6 ,ransient improvement recurrence or decreased blood pressure and increased heart rate

5%.%5A: -; .;6S(-.S6 ;emain abnormal

6stimated 3lood :oss .eed for more crystalloids .eed for blood 3lood preparation .eed for operative intervention 6arly presence of

5inimal !701* E01" :ow :ow ,ype and crossmatch (ossibly Hes

5oderate and ongoing !E01*F01" 9igh 5oderate to high ,ype*specific :ikely Hes

Severe !OF01" 9igh %mmediate 6mergency blood release 9ighly like Hes

surgeon PE000m: of isotonic solution in adults4 E0m:)kg bolus of ;inger#s lactate in children.

;A(%@ ;6S(-.S6 (atients in this group termed <rapid responders < respond rapidly to the initial fluid bolus and remain hemodynamically normal after the initial fluid bolus has been given and the fluids are slowed to maintenance rates. Such patients usually have lost minima7 !less than E01" blood volume. .o further fluid bolus or immediate blood administration is indicated for this group. ,yped and crossmatched blood should be kept available. Surgical consultation and evaluation are necessary during initial assessment and treatment as operative intervention may still be necessary.

,;A.S%6., ;6S(-.S6 (atients in the second group termed <transient responders< respond to the initial fluid bolus. 9owever they begin to show deterioration of perfusion indices as the initial fluids are slowed to maintenance levels indicating either an ongoing blood loss or inadequate resuscitation. 5ost of these patients initially have lost an estimated E01 to F01 of their blood volume. &ontinued fluid administration and initiation of blood transfusion are indicated. A transient response to blood administration should identify patients who are still bleeding and require rapid surgical intervention. 5%.%5A: -; .- ;6S(-.S6 Aailure to respond to crystalloid and blood administration in the 6@ dictates the need for immediate definitive intervention !eg operation or angioemboli$ation" to control

exsanguinating hemorrhage. -n very rare occasions failure to respond may be due to pump failure as a result of blunt cardiac injury cardiac tamponade or tension pneumothorax. .onhemorrhagic shock always should be considered as a diagnosis in this group of patients. &'( monitoring or cardiac ultrasonography helps to differentiate between the various causes of shock.

B+oo Re"+acemen! ,he decision to initiate blood transfusion is based on the patient2s response as described in the previous section. CROSSMATCHED, T !E"S!ECI#IC, A$D T !E % &'OOD ,he main purpose of blood transfusion is to restore the oxygen*carrying capacity of the intravascular volume. 'olume resusitation itself can be accomplished with crystalloid with the added advantage that restitution. Aully crossmatched blood is preferable. 9owever the complete crossmatching process requires approximately 7 hour in most blood banks. Aor patients who stabili$e rapidly cross matched blood should be obtained and made available for transfusion when indicated. ,ype*specific blood can be provided by most blood banks within 70 minutes. Such blood is compatible with A3- and ;h blood types but incompatibilities of other antibodies may exist. ,ype*specific blood is preferred for patients who are transient responders as described in the previous section. %f type*specific blood is required complete crossmatching should be performed by the blood bank. %f type*specific blood is unnvailable type - packed cells are indicated for patients with exsanguinating hemorrhage. ,o avoid sensiti$ation and future complications ;h* negative cells are preferred for females of childbearing age. Aor life*threatening blood loss the use of unmatched. type*specific blood is preferred over type - blood. ,his is true unless multiple unidentified casualties are being treated simultaneously and the risk of inadvertently administering the wrong unit of blood to a patients are great. WARMI$( #')IDS" !'ASMA A$D CR STA''OID it contributes to interstitial and intracellular volume

9ypothermia must be prevented and reversed if a patient hals hypothermia on arrival at the hospital. ,he use of blood warmers in the 6@ is desirable even if cumbersome. ,he most efficient way to prevent hypothermia in any pntient receiving massive volumes of crystalloid is to heat the fluid to GJM & !70E.EM A" before using it. ,his can be accomplished by storing crystalloids in a warmer or with the use of a microwave oven. 3lood products cannot be warmed in a microwave oven but they can be heated by passage through intravenous fluid warmers. A)TOTRA$S#)SIO$ Adaptations of standard tube thoracostomy collection devices are commercially available4 these allow for sterille collection anticoagulation !generally with sodium citrate solutions not heparin" and retransfusion of shed blood. &ollection of shed blood for autotransfusion should be considered for any patient with a major hemothorax . COA()'O!ATH Severe injury and hemorrhage result in the consumption of coagulation factors and early coagulopathy. 5assive transfusion with the resultant dilution of platelets and clotting factors along with the adverse effect of hypothermia on platelets aggregation and the clotting cascade all contribute to coagulopathy in injured patients. (rothrombin time partial thromboplastin time and platelet count are valuable baseline studies to obtain in the first hour especially if the patient has a history of coagulation disorders takes medications that alter coagulation !eg. warfarin aspirin and nonsteroidal antiinflammntory agents L.SA%@sQ" or a reliable bleeding history cannot be obtained. ,ransfusion of platelets cryoprecipitate and fresh*fro$en plasma should be guided by these coagulation parameters including fibrinogen levels. ;outine use of such products is gener.tlly not warranted unless the patient has a known coagulation disorder or has undergone anticoagulation pharmacologically for management of a specific medical problem. %n such cases specific factor replacement therapy is immediately indicated when there is evidence of bleeding or the potential for occult blood loss exists !eg head abdominal or thoracic injury". 9owever consideration of early blood component therapy should be given to patients with class %' hemorrhage. (atients with major brain injury are particularly prone to coagulation abnormalities as a result of substances especially tissue thromboplastin that are released by damaged neural tissue. ,hese patients coagulation need to be closely monitored.

CA'CI)M ADMI$ISTRATIO$ 5ost patients receiving blood transfusions do not need calcium supplements. 6xcessive supplemental calcium may be harmful. Rea##e##ing Pa!ien! Re#"on#e an A0oi ing Com"+ica!ion# %nadequate volume replacement is the most common complication of hemorrhagic shock. %mmediate appropriate and aggressive therapy that restores organ perfusion minimi$es these problematic events. CO$TI$)ED HEMORRHA(E -bscure hemorrhage is the most common cause of poor response to fluid therapy. (atients with this condition are generally included in the transient response category as defined previously. %mmediate surgical intervention may be necessary. #')ID O*ER'OAD A$D C*! MO$ITORI$( After a patient2s initial assessment and treatment have been completed the risk of fluid overload is minimi$ed by careful monitoring. ;emember the goal of therapy is restoration of organ perfusion and adequate tissue oxygenation confirmed by appropriate urinary output &.S function skin color and return of pulse and blood pressure toward normal. 5onitoring the response to resuscitation is best accomplished for some patients in an environment in which sophisticated techniques are used. 6arly transfer of the patient to an intensive care unit should be considered for elderly patients and patients with non hemorrhagic causes of shock. &'( monitoring is a relatively simple procedure used as a standard guide for assessing the ability of the right side of the heart to accept a fluid load. (roperly interpreted the response of the &'( to fluid administration helps evaluate volume replacement. Several points to remember are+ 7. ,he precise measure of cardiac function is the relationship between ventricular end diastolic volume and stroke volume. ;ight atrial pressure !&'(" and cardiac output !as reflected by evidence of perfusion or blood pressure or even by direct

measurement" are indirect and at best insensitive estimates of this relationship. ;emembering these facts is important to avoid overdependency on &'( monitoring. E. ,he initial &'( level and actual blood volume are not necessarily related. ,he initial &'( is sometimes high even with a significant volume deficit especially in patients with chronic obstructive pulmonary disease generali$ed vasoconstriction and rapid fluid replacement. ,he initial venous pressure also may be high because of the application of "(AS= or the inappropriate use of exogenous vasopressors. G. A minimal rise in the initially low &'( with fluid therapy suggests the need for further volume expansion !minimal or no response to fluid resuscitation category". F. A declining &'( suggests ongoing fluid loss and the need for additional fluid or blood replacement !transient response to fluid resuscitation category". D. An abrupt or persistent elevation in &'( suggests that volume replacement is adequate or too rapid or that cardiac function is compromised. K. (ronounced elevations of &'( may be caused by hypervolemia as a result of overtransfusion cardiac dysfunction cardiac tamponade or increased intrathoracic pressure from a tension pneumothorax. &atheter malposition may produce erroneously high &'( measurements. Aseptic techniques must be used when central venous lines are placed. 5ultiple sites provide access to the central circulation and the decision regarding which route to use is determined by the skill and experience of the doctor. ,he ideal position for the tip of the catheter is in the superior vena cava just proximal to the right atrium. ,he placement of central venous lines carries the risk of potentially life threatening complications. %nfections vascular injury nerve injury emboli$ation thrombosis and pneumothorax may result. &'( monitoring reflects right heart function. %t may not be representative of left heart function in patients with primary myocardial dysfunction or abnormal pulmonary circulation.