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3 Recognition and Treatment of Medical Emergencies in the Trauma Patient

Lucy Wibbenmeyer and Melhem J. Sharafuddin

L. A. Wibbenmeyer, MD

University of Iowa Hospitals and Clinics, Department of Radiology, 200 Hawkins Dr., Iowa City, IA 52242, USA M. Sharafuddin, MD

University of Iowa Hospitals and Clinics, Department of Radi- ology, 200 Hawkins Dr., 3957 JPP, Iowa City, IA 52242, USA

ist may occasionally be the only physician avail- able to provide timely recognition and prompt, sys- tematic treatment of life-threatening emergencies.

Adequate treatment of these emergencies is essential for optimizing the care of the trauma patient. This chapter will discuss recognition and treatment of two common life-threatening emergencies that the interventional radiologist may be the first physi- cian to encounter in the trauma patient. Definitive treatment will be presented for completeness and further study.

3.2

Airway Compromise

3.2.1 Recognition

The airway of an acutely unstable patient should be addressed first. The American College of Surgeons addresses the airway as the initial step of the primary survey in the Advance Trauma Life Support Protocol for evaluation of trauma patients (Table 3.1) [4]. The primary survey addresses all life-threatening inju- ries in an expedient manner by systematic review of all the systems. The primary survey protocol also works well to address any acutely decompensating patient. Airway emergencies in a previously stable patient can occur as a result of on-going cervical edema or hematoma from soft tissue injury or frac- tures. It can also accompany mental status deterio-

CONTENTS

3.1 Introduction 35 3.2 Airway Compromise 35 3.2.1 Recognition

35

3.2.2 Treatment Adjuncts 36 3.2.3 Definitive Control 37 3.3 Circulatory Shock 38 3.3.1 Recognition 38 3.3.2 Resuscitation 39

3.3.3 Pitfalls of Resuscitation 40

Cookbook: Recognition and Treatment of Medical Emergencies in the Trauma Patient 40

References 41

3.1

Introduction

The role of interventional radiology (IR) is expand- ing in the care of the acutely injured polytrauma patient. The interventional radiologist is often asked to perform therapeutic embolization of active bleed- ing from intraabdominal solid organ injuries and pelvic arterial injuries to provide initial control [1–3]. These patients are often accompanied by a traumatologist while in the interventional suite.

They are often ventilated and actively receiving blood products. When these patients are critically ill and potentially unstable, the interventionist can delegate their critical care to the traumatologist.

However, the challenge to the interventionist occurs in the setting of the “presumed stable” trauma patient with compensated shock. The intervention-

Table 3.1. The primary survey of the trauma patient. From [37], with permission

A Airway maintenance with cervical spine protection B Breathing and ventilation

C Circulation with hemorrhage control D Disability: Neurologic status E Exposure/environmental control:

Completely undress the patient, but prevent hypothermia

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36 L. Wibbenmeyer and M. Sharafuddin

ration, circulatory decompensation, or administra- tion of procedural conscious sedation medications.

It is therefore imperative that the interventionist be familiar with the signs and symptoms of impending respiratory collapse and the treatment.

Airway compromise may be insidious in onset.

Recognition of the signs and symptoms of airway obstruction can enable controlled airway access and prevent a respiratory arrest. Table 3.2 lists the signs of impending respiratory embarrassment sec- ondary to airway obstruction. Stridor or inspiratory wheezing heard over the cervical region is a sensi- tive marker for impending respiratory compromise.

Signs of increased labored breathing should also be observed. Flaring of the nasal alae, retraction of cervical soft tissues, and retraction of the ribs on inspiration all are signs of increased work of breath- ing. Paradoxical movement of the chest (abdominal distention on inspiration) is an ominous sign sug- gesting impending airway compromise.

Adequate oxygenation and ventilation should be assessed. The pulse oximeter data is readily avail- able to the interventionist during the procedure and can provide quantitative data reflecting the patient’s ability to oxygenate. Saturations above 95% are usually adequate to ensure sufficient oxy- genation [4]. However, due to the sigmoidal shape of the oxyhemoglobin desaturation curve, factors that shift the curve to the left such as hypothermia, alkalosis, and a decrease in 2,3-diphosphoglycer-

aldehyde (old banked blood) may impair sufficient oxygen unloading from oxyhemoglobin. Therefore, all trauma patients should receive supplemental oxygen by nasal cannula or mask. Unlike oxygen- ation, adequate ventilation can only be accurately accessed by arterial blood gas analysis demonstrat- ing normal carbia. Inadequate or marginal oxygen- ation or ventilation accompanied by increased signs of labored breathing should prompt consideration for intubation.

3.2.2

Treatment Adjuncts

Several options are available for the initial man- agement of suspected airway obstruction. If neuro- logic deterioration secondary to closed head injury or administration of sedative agents is suspected, a soft plastic nasopharyngeal airway (trumpet) can be inserted (Fig. 3.1) [5–7]. Its counterpart the oropha- ryngeal should be avoided in the conscious patient because of excessive irritation of the upper airway.

The nasopharyngeal airway will lift the tongue and accompanying soft tissues off the back of the airway, enabling ventilation. In addition, a gentle chin lift or jaw thrust can alleviate upper airway obstruction (Fig. 3.2). These maneuvers alone may be sufficient if only upper airway obstruction is the problem. It should be remembered that extension of the neck

Table 3.2. Symptoms and signs of respiratory obstruction graded according to sever- ity. Modified from [38,39], with permission. First published in the British Medical Journal, 1964

Stage Signs and Symptoms

1. Mild or Potential Obstruction Hoarseness Cough

No stridor at rest

Stridor on moderate exertion 2. Moderate Obstruction Dyspnea

Rib retraction on inspiration

Use of accessory muscles of aspiration Stridor on slight exertion

3. Severe Obstruction Apprehension Restlessness Sweating and pallor

Increased blood pressure and heart rate Paradoxical movement of chest Stridor at rest

4. Total Obstruction Slowed respirations

Marked cyanosis

Impaired consciousness

Slowing heart rate

Hypotension

No longer stridorous

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should be avoided in all trauma patients until their cervical spine is radiographically and clinically cleared. These patients will almost invariably have hard cervical collars for neck immobilization, and these should never be removed without proper con- sultation with the trauma team.

3.2.3

Definitive Control

If the patient continues to show signs of airway obstruction or compromise, despite the insertion of a nasopharyngeal airway or manual airway opening procedure, a definitive airway needs to be estab- lished. Trauma patients have challenging airways due to the need to maintain manual in-line neck stabilization (MILS) and the presence of the cervical collar. Normally patients are placed in the sniff- ing position with the head and upper neck fully extended and the occiput slightly elevated. This position aligns the oral, pharyngeal, and laryngeal airways. MILS places the head in the neutral posi- tion, displacing the larynx anteriorly and impairing visualization [8,9]. The anterior faceplate of the cer- vical collar restricts mouth opening, further com- plicating access to the larynx [9]. Removal of the anterior faceplate as long as MILS is maintained is safe and will facilitate intubation. When available, an experienced provider should attempt definitive control of a the airway. However, as the intervention- ist may occasionally be the only one immediately

available, a systematic approach to the definitive airway will be presented.

A systematic approach to the airway consists of assessment of the level of airway difficulty, prepara- tion of the patient, collection of airway equipment and pharmacologic medication, and development of a back-up plan. A back-up plan is essential prior to any intubation attempt. Preparation is critical to avoid failed attempts resulting in airway trauma impairing subsequent laryngoscopies.

The first step, assessment of the level of airway difficulty, is critical. An unanticipated difficult airway can lead to a no intubation–no ventilation crisis where only a surgical airway can correct the situation. It is estimated that anywhere from 1.5%–

8.5% of airways are difficult [10]. Despite a number of scoring systems that rate airway difficulty, only 50% of these difficult airways can be accurately pre- dicted [11–13]. In general, patients who are difficult to intubate often have limited mouth opening, pro- truding teeth, receding chins, short necks, or lim- ited neck extension. The existing difficult airway scoring systems take into account these factors. If a difficult airway is anticipated, other options such as an awake intubation, Laryngeal Mask Airway, gum bougie, or a lighted stylet can be considered [7,14].

Patients need to be preoxygenated prior to intu- bation. Preoxygenation washes out the nitrogen and ensures adequate oxygenation if prolonged laryn- goscopy is needed. In the spontaneously breathing trauma patient, this is done by giving them high flow oxygen via a non-rebreathing mask or a bag

Fig. 3.2. Manual in-line stabilization is provided as the patient’s airway is opened with the two-handed jaw thrust airway open- ing technique

Fig. 3.1. The mechanism of oropharyngeal obstruction in the

supine position and the proper placement of the nasopharyn-

geal airway. Modifi ed from [42], with permission. Copyright,

American Heart Association

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38 L. Wibbenmeyer and M. Sharafuddin

valve mask device. In the case of the non-ventilating patient, their ventilation must be provided through manual compression of a bag valve mask device.

This is best done using a two-person technique. The mask is placed over the bridge of the nose with the thumbs and then secured over the mouth and chin area with the index and middle fingers. The ring and little fingers support the jaw in the jaw thrust posi- tion. An additional person is needed to compress the ventilating bag.

Necessary equipment and pharmacologic medi- cation then needs to be made available to ensure smooth intubation. Essential equipment is listed in Table 3.3. Pharmacologic medications consist of hypnotic and paralytic agents and are listed in Table 3.4. All patients should have cardiopulmo- nary monitoring with cardiac, blood pressure, and pulse oximeter monitors. Intravenous lines should be checked for their patency. The choice of seda- tive or hypnotic agents will depend on the patient’s hemodynamic status, with etomidate and ketamine usually preferred in the hemodynamically unstable patient. The administration of a paralytic agent has

been demonstrated to help with successful intuba- tion [15,16]. However, the choice of a paralytic will depend on the difficulty of the airway and the abil- ity of the airway provider. A depolarizing paralytic (succinylcholine) is ideal as it results in rapid induc- tion and has the shortest half-life of all the paralyt- ics. However, its use should be restricted in patients with known neuromuscular disease, massive mus- cular trauma, burn injuries over 24 hours old, or suspected elevation in serum potassium. Non-depo- larizing paralytics should be reserved for patients with easy airways and experienced airway provid- ers, since paralysis can last up to 120 minutes.

Conscious trauma patients are intubated by the technique of rapid sequence intubation (RSI) with MILS. Unconscious patients can be intubated with- out medication. RSI calls for administration of a sed- ative or hypnotic agent followed by a paralytic agent.

Another team member provides MILS by cradling the trauma victim’s neck between their arms, effec- tively preventing neck extension (Fig 3.2). Exter- nal cricoid pressure (8 kg of pressure applied with three fingers over the cricoid ring) is applied prior to the administration of medication to decrease the risk of aspiration. The patient is then intubated, and verification of correct positioning of the tube is performed by physical exam and disposable cap- nography to assess for exhaled carbon dioxide. Fur- ther discussion of intubation techniques is beyond the scope of this chapter; the interested reader is referred to several references [14,17–19].

3.3

Circulatory Shock

3.3.1 Recognition

Once an adequate airway and breathing of the trauma patient is achieved, the primary survey of the trauma patient addresses the circulatory system.

A number of perfusion endpoints must be analyzed to determine whether the patient is adequately resuscitated or declining into circulatory shock. The predominate cause of shock in the trauma patient is under-perfusion secondary to bleeding. The treat- ment of shock is to replace the volume lost. By and large, the treatment of shock in the trauma patient has remained unchanged for the past few decades.

The recognition of shock, however, can be chal- lenging. Blood pressure and pulse are neither sensi-

Table 3.3. Essential airway management equipment. Modified from [40], p. 6, with permission

x Supply of 100% oxygen x Face mask

x Bag valve device x Suction equipment

 – Suction catheters

 – Large-bore tonsil suction apparatus (Yankauer) x Stylet

x Oral airways x Nasal airways

x Laryngoscope handle and blades (curved, straight, various sizes) x Endotracheal tubes (various sizes) x Tongue depressors

x Syringe for cuff inflation x Tape

x Tincture of benzoin

Table 3.4. Pharmacologic therapy for intubation. Modified from [41], with permission

Drug Dose Onset Offset

Propofol 1–2 mg/kg 22–125 sec 5–10 min

Etomidate 0.25–0.5 mg/kg < 60 sec 5 min

Ketamine 1–3 mg/kg < 60 sec 10–15 min

Midazolam 0.1–0.3 mg/kg 30–60 sec 6–15 min

Succinylcholine 1–1.5 mg/kg 30–60 sec 5–10 min

Cisatracurium 0.4 mg/kg 60–90 sec 75–100 min

Vecuronium 0.3 mg/kg 60–90 sec > 120 min

Rocuronium 0.9–1.2 mg/kg 60 sec > 60 min

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tive nor specific markers for the diagnosis of early hemodynamic shock [20–22]. In fact, hypotension can be a late finding in shock after which circula- tory collapse can occur. In general, the signs and symptoms of shock are directly related to the blood volume lost [4]. The American College of Surgeons divides hemorrhage into four categories (Table 3.5).

Most patients tolerate class-1 hemorrhage or 10%

blood volume loss with little change in vital signs, due to a number of compensatory mechanisms, the earliest of which are tachycardia and narrowed pulse pressure (the difference between the sys- tolic and the diastolic pressures). If loss continues, the patient will demonstrate a decrease in cardiac output and blood pressure. As a result pallor, cool extremities, delayed capillary perfusion, decreased urine output, and mental status changes (agitation and anxiety) may develop. Although these signs may occur before, they are usually manifested in adults following around 20%–40% blood volume loss and therefore are late markers of shock. Children, on the other hand, may not manifest these signs until around 40% volume loss. Children with hypotension and tachycardia are significantly volume-depleted and can rapidly decompensate.

Biochemical markers may better quantify the initial and on-going magnitude of the shock state [22–26]). Both the base deficit and serum lactic acid level measure the acidosis produced by the anaerobic state during inadequate delivery of sub- strate to tissues [27]. Shock impairs nutritive blood flow to tissues, shifting cellular metabolism into the less efficient anaerobic glycolysis pathway. The formation of ATP from ADP is slowed, resulting in accumulation of hydrogen ion (H

+

) in the cytosol and extracellular fluid. This accumulation of the H

+

in the cytosol is quantified by the base deficit measured on the arterial blood gas. Base deficit

(the quantity of strong acid or base that would be required to titrate the patient to a normal pH assum- ing a PaCO

2

of 40 mmHg and a hemoglobin of 5 g/dl) reflects the metabolic component of shock. Initial and subsequent base deficit measurements provide markers to access the severity and recovery of the shock state. Initial base deficit < –6 has been asso- ciated with the need for transfusion [25]. Similar to the base deficit, lactic acid accumulates in the shock state. Under anaerobic conditions, pyruvate accumulates and is dehydrogenated in the cytosol to lactate. Lactate buffers H

+

, resulting in lactic acid.

Serial measurement of serum lactate can also help achieve a better follow-up of the compensated shock state and reduce the need for on-going resuscitation.

Persistent serum lactate elevation following resus- citation in trauma has been reported to portend a worse outcome [23].

3.3.2

Resuscitation

Once shock is identified, resuscitation needs to be instituted to prevent on-going perfusion mismatch, which can lead to multiple system organ failure and death. Although there is some controversy regard- ing resuscitating penetrating trauma victims to normal blood pressure before surgical control of their bleeding, resuscitation to normal volemia is the current paradigm in bluntly injured patients [28]. In penetrating trauma victims, normotension may lead to worsened hemorrhage, whereas blunt trauma patients often have accompanying head inju- ries that can be significantly worsened by hypoten- sion. Trauma patients in shock are first resuscitated with crystalloid, namely Lactated Ringers or normal saline. ATLS protocol dictates a 2-liter rapid bolus

Table 3.5. Estimated fluid and blood losses based on hemorrhagic shock severity class on patient’s initial presentation. From [42], with permission

Class I Class II Class III Class IV

Blood loss (ml) Up to 750 750-1500 1500-2000 > 2000

Blood loss (% blood volume) Up to 15% 15%–30% 30%–40% > 40%

Pulse rate < 100 > 100 > 120 > 140

Blood pressure Normal Normal Decreased Decreased

Pulse pressure (mmHg)

Normal or increased Decreased Decreased Decreased

Respiratory rate 14–20 20–30 30–40 > 35

Urine output (ml/h)

> 30 20–30 5-15 Negligible

CNS/mental status Slightly anxious Mildly anxious Anxious, confused Confused, lethargic

Fluid replacement (3:1 rule) Crystalloid Crystalloid Crystalloid and blood Crystalloid and blood

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40 L. Wibbenmeyer and M. Sharafuddin

in an adult and a 20 cc/kg bolus in a child. Non- responders or transient hemodynamic responders usually have lost > 25% of their blood volume or have on-going bleeding and need to receive blood.

As typing and cross-matching require time, type O negative blood is preferentially transfused. It is cru- cial to remember that the ability to provide adequate resuscitation is also dependent on catheter dynam- ics. ATLS protocol dictates the placement of two large-bore (14–16 gauge) peripheral catheters. With short intravenous tubing (< 3 feet) and 300 mmHg external compression, these catheters can provide flow rates of 249–500 cc/min [29]. Central access is required if peripheral access is inadequate. The loca- tion of the placement of catheters is also important.

The lower extremities should be avoided if intraab- dominal injury is suspected.

3.3.3

Pitfalls of Resuscitation

The two main pitfalls of rapid resuscitation and mas- sive transfusion are hypothermia and coagulopathy.

Along with acidosis of the shock state, hypothermia and coagulopathy compose the “triangle of death”

well known to the trauma surgeon [30,31]. When these three conditions are present in the emergency room or operating room, only stabilizing procedures are performed and the patient is transferred to the intensive care unit for resuscitation. With resolution of the triad, the patient is returned to the operating room if necessary.

Hypothermia in the trauma patient is multifacto- rial, resulting from exposure to cold environment, bleeding, and infusion of cold fluids. Mild to mod- erate hypothermia (34°C to 30°C) can be associated with coagulopathy that can impair the patient’s response to ongoing resuscitation and at times be refractory to treatment [32]. During massive resus- citation, hypothermia can be avoided by admin- istration of warmed fluids, either by means of an in-line warmer, or rapid infuser. The ambient room temperature should be maintained at 21°C. Addi- tionally, patients can also be actively warmed by one of the commercially available convective blankets.

Coagulopathy can also be multifactorial in the multiple injured trauma patients. In addition to hypothermia-related coagulopathy, massive resusci- tation and massive transfusion are other important causes. Massive resuscitation can lead to throm- bocytopenia, prolonged prothrombin times, and decreased fibrinogen [32,33]. The incidence of coag-

ulopathy during resuscitation is variable, and there- fore its treatment remains controversial. Although some formulas have been proposed for replacement of coagulation factors and platelets based on the number of units of blood received, several studies have failed to show their reliability [34,35]. Without obvious microvascular bleeding, many recommend that fresh frozen plasma and platelet replacement be guided by laboratory abnormalities [33,36].

Cookbook:

Recognition and Treatment of Medical Emergencies in the Trauma Patient

Suspect Airway Compromise x Perform Primary Survey x Assess Airway for Patency x Open Airway

– Airway Opening Procedure

– Insertion of Naso- or Oropharyngeal Airway x Prepare for Defi nitive Airway

– Assessment of Airway Diffi culty – Preoxygenation

– Collection of Equipment – Development of a Back-up Plan x Provide Defi nitive Airway-Intubation x Confi rm Placement of Airway – Auscultation

– Capnography – Chest Radiograph

Suspect Circulatory Compromise x Perform Primary Survey x Assess Circulation

– Look for signs of perfusion abnormalities – Hypotension, tachycardia, diaphoresis,

agitation, pallor

– Obtain biochemical markers of perfusion abnormalities (base defi cit and lactic acid) x Provide Resuscitation

– Crystalloid (Ringer lactate) bolus

– Packed red blood cells for non-responders x Avoid hypothermia

– Warm room to 20°C – Warm fl uids

– Warm patient with a convective blanket x Assess for secondary coagulopathy during

massive resuscitation

– Obtain blood for PT, INR, PTT, Fibrinogen

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References

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2. Velmahos GC, Toutouzas KG et al. (2002) A prospective study on the safety and efficacy of angiographic emboliza- tion for pelvic and visceral injuries. J Trauma Injury Infect Crit Care 53:303–308

3. Santucci RA, Wessells H et al. (2004) Evaluation and man- agement of renal injuries: consensus statement of the renal trauma subcommittee. BJU Int 93:937–954

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9. Crosby ET, Cooper RM et al. (1998) The unanticipated dif- ficult airway with recommendations for management (see comment). Can J Anaesth 45:757–776

10. Oates JD, Macleod AD et al. (1991) Comparison of two methods for predicting difficult intubation (see comment).

Br J Anaesth 66:305–309

11. Savva D (1994) Prediction of difficult tracheal intubation (see comment). Br J Anaesth 73:149–153

12. Rosenblatt WH (2004) Preoperative planning of airway management in critical care patients (see comment). Crit Care Med 32 [Suppl 4]

13. Blanda M, Gallo UE (2003) Emergency airway manage- ment. Emerg Med Clin North Am 21:1–26

14. Criswell JC, Parr MJ et al. (1994) Emergency airway man- agement in patients with cervical spine injuries (see com- ment). Anaesthesia 49:900–903

15. Li J, Murphy-Lavoie H et al. (1999) Complications of emer- gency intubation with and without paralysis. Am J Emerg Med 17:141–143

16. Behringer EC (2002) Approaches to managing the upper airway. Anesthesiol Clin North Am 20:813–832

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19. Luna GK, Eddy AC et al. (1989) The sensitivity of vital signs in identifying major thoracoabdominal hemorrhage. Am J Surg 157:512–515

20. Thompson D, Adams SL et al. (1990) Relative bradycardia in patients with isolated penetrating abdominal trauma and isolated extremity trauma. Ann Emerg Med 19:268–275 21. Wilson M, Davis DP et al. (2003) Diagnosis and monitoring

of hemorrhagic shock during the initial resuscitation of multiple trauma patients: a review. J Emerg Med 24:413–

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22. Abramson D, Scalea TM et al. (1993) Lactate clearance and survival following injury. J Trauma Injury Infect Crit Care 35:584–588

23. Manikis P, Jankowski S et al. (1995) Correlation of serial blood lactate levels to organ failure and mortality after trauma. Am J Emerg Med 13:619–22

24. Davis JW, Parks SN et al. (1996) Admission base deficit pre- dicts transfusion requirements and risk of complications (see comment). J Trauma Injury Infect Crit Care 41:769–

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27. Bickell WH, Wall MJ Jr et al. (1994) Immediate versus delayed fluid resuscitation for hypotensive patients with penetrating torso injuries (see comment). N Engl J Med 331:1105–1109

28. Millikan JS, Cain TL et al. (1984) Rapid volume replace- ment for hypovolemic shock: a comparison of techniques and equipment. J Trauma Injury Infect Crit Care 24:428–

431

29. Stone HH, Strom PR et al. (1983) Management of the major coagulopathy with onset during laparotomy. Ann Surg 197:532–535

30. Danks RR (2002) Triangle of death. How hypothermia acidosis and coagulopathy can adversely impact trauma patients. J Emerg Med Serv 27:61–66

31. Ferrara A, MacArthur JD et al. (1990) Hypothermia and acidosis worsen coagulopathy in the patient requiring mas- sive transfusion. Am J Surg 160:515–518

32. Faringer PD, Mullins RJ et al. (1993) Blood component supplementation during massive transfusion of AS-1 red cells in trauma patients. J Trauma Injury Infect Crit Care 34:481–485

33. Harrigan C, Lucas CE et al. (1985) Serial changes in primary hemostasis after massive transfusion. Surgery 98:836–844

34. Wudel JH, Morris JA Jr et al. (1991) Massive transfusion:

outcome in blunt trauma patients. J Trauma Injury Infect Crit Care 31:1–7

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36. Bell RM (2000) Initial assessment. In: Mattox KL, Feliciano DV, Moore EE (eds) Trauma, 4th edn. McGraw-Hill, New York

37. Mattox KL, Feliciano DV, Moore EE (eds) (2000) Trauma, 4th edn. McGraw-Hill, New York

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39. Rippe JM, Irwin RS, Fink MP, Cerra FB (1996) Intensive care medicine, 3rd edn. Little Brown, Boston

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