Добавил:
kiopkiopkiop18@yandex.ru t.me/Prokururor I Вовсе не секретарь, но почту проверяю Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз: Предмет: Файл:

Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3896_Библиотеки_им_академика_М_И_Перельмана

.pdf
Скачиваний:
0
Добавлен:
10.10.2026
Размер:
9 Мб
Скачать
☆
Recognition and Treatment of Medical Emergencies in the Trauma Patient 33
Trauma and latrogenic Lesions
Recognition and Treatment of Medical Emergencies in the Trauma Patient 35
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 ai rway as the in itial step of the pri mary
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
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
Recognition and Treatment of Medical Emergencies in the Trauma Patient 37
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
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
Recognition and Treatment of Medical Emergencies in the Trauma Patient 39
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 hy potension
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 f luid. 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
wit h cr yst alloid, namely Lactated Ringers or nor mal
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
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 pit falls 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
Recognition and Treatment of Medical Emergencies in the Trauma Patient 41
References
1. Dondelinger RF, Trotteur G et al. (2002) Traumatic inju-
ries: radiological hemostatic intervention at admission. Eur
Radiol 12:979–993
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
4. American College of Surgeons (1997) Advanced trauma life
support manual, 6th edn. ACS, Chicago
5. Kaur S, Heard SO (1996) Airway management and endo-
tracheal intubation. In: Rippe JM, Irwin RS, Fink MP, Cera
FB (eds) Intensive care medicine, vol 1. Little Brown, New
York, pp 1–15
6. Hillman DR, Platt PR et al. (2003) The upper airway during
anaesthesia. Br J Anaesth 91:31–39
7. Nolan JP, Wilson ME (1993) Orotracheal intubation in
patients with potential cervical spine injuries. An indica-
tion for the gum elastic bougie (see comment). Anaesthesia
48:630–633
8. Heath KJ (1994) The effect of laryngoscopy of different
cervical spine immobilisation techniques (see comment).
Anaesthesia 49:843–845
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
17. Orebaugh SL (2002) Difficult airway management in the
emergency department. J Emerg Med 22:31–48
18. Butler KH, Clyne B (2003) Management of the difficult
airway: alternative airway techniques and adjuncts. Emerg
Med Clin North Am 21:259–289
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–
422
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–
774
25. Davis JW, Kaups KL et al. (1998) Base deficit is superior
to pH in evaluating clearance of acidosis after traumatic
shock. J Trauma Injury Infection & Crit Care 44:114–
118
26. Mullins R (2000) Management of shock. In: Mattox KL,
Feliciano DV, Moore EE (eds) Trauma. McGraw-Hill, New
York, pp 195–232
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
35. Reed RL 2nd, Johnson TD et al. (1992) The disparity
between hypothermic coagulopathy and clotting studies.
J Trauma Injury Infect Crit Care 33:465–470
36. Bell RM (2000) Initial assessment. In: Mattox KL, Feliciano
DV, Moore EE (eds) Trauma, 4th edn. McGraw-Hill, New
Yo r k
37. Mattox KL, Feliciano DV, Moore EE (eds) (2000) Trauma,
4th edn. McGraw-Hill, New York
38. Robinson RJS, Mulder DS, Forbes JA (1964) Airway control.
Br Med J 1:369
39. Rippe JM, Irwin RS, Fink MP, Cerra FB (1996) Intensive
care medicine, 3rd edn. Little Brown, Boston
40. Hartmannsbruber (2000) The traumatic airway: the anes-
thesiologist’s role in the emergency room. Int Anesthesiol
Clin 38:87–104
41. Cummins RO (ed) (1994) Textbook of advance cardiac life
support. American Heart Association, Dallas, Texas
Visceral and Abdominal Solid Organ Trauma 43
4 Visceral and Abdominal Solid Organ Trauma
Gary Siskin and Jafar Golzarian
G. Siskin, MD
Albany Medical College, Vascular Radiology, A113, 47 New
Scotland Avenue, Albany, NY 12208-3479, USA
J. Golzarian, MD
Professor of Radiology, Director, Vascular and Interventional
Radiology, University of Iowa, Department of Radiology,
200 Hawkins Drive, 3957 JPP, Iowa City, IA 52242, USA
patients after blunt injury to the spleen [1]. How-
ever, well-defined criteria are still not available to
apply to these patients in order to determine who is
best suited for nonoperative management and who
will ultimately require surgery. We do know that
hemodynamically unstable patients with multisys-
tem trauma and significant intraperitoneal bleeding
will likely not be successfully managed with obser-
vation and splenic salvage. All other hemodynami-
cally stable patients are now considered candidates
for nonoperative treatment consisting of observa-
tion with serial physical examination, frequent
hematocrit determinations, bed rest, and limited
oral intake [2].
The trend toward nonoperative management
after splenic injury has significant benefits for this
patient population. These include eliminating the
risks for immediate and late complications asso-
ciated with open surgery as well as preserving the
immunologic functions provided by the spleen [1,
3–5]. Immunologically, the spleen is best known for
its filtering function, which serves to remove partic-
ulate antigens, bacteria, and old erythrocytes from
circulation [6]. In addition to this, the spleen pro-
duces mediators such as immunoglobulin M, tuft-
sin, and properdin [6, 7]. The importance of these
functions manifests itself after splenectomy with
a significant post-surgical infection rate, which is
what initially prompted surgeons to increase their
interest in splenic salvage [6–9].
4.1.2
Patient Selection
With the benefits of splenic salvage rarely questioned,
it makes sense that this is most desirable option for
most, if not all, hemodynamically stable patients.
However, it is still not known with certainty which
patients will be successfully managed with nonopera-
tive management and which will ultimately require
surgery despite initially being considered candi-
dates for observation. Patient age, injury severity
CONTENTS
4.1 Splenic Artery Embolization 43
4.1.1 Introduction 43
4.1.2 Patient Selection 43
4.1.3 Diagnosis 44
4.1.3.1 The Role of Abdominal CT 44
4.1.3.2 Diagnostic Angiography 44
4.1.4 Splenic Artery Embolization 45
4.1.4.1 Technique 45
4.1.4.2 Results 47
4.1.4.3 Post-Embolization Follow-up 48
4.2 Hepatic Artery Embolization 48
4.2.1 Patient Selection 48
4.2.2 Diagnosis 49
4.2.3 Hepatic Artery Embolization 49
4.2.3.1 Technique 49
4.2.3.2 Results 49
4.2.3.3 Post-Embolization Follow-up 51
4.3 Renal Artery Embolization 51
4.3.1 Patient Selection 51
4.3.2 Diagnosis of Renal Vascular Injury 52
4.3.3 Renal Artery Embolization 52
4.3.3.1 Technique 52
4.3.3.2 Results 52
4.3.3.3 Post-Embolization Follow-up 54
Cookbook 54
References 55
4.1
Splenic Artery Embolization
4.1.1
Introduction
During the past 10–15 years, there has been a clear
trend among trauma surgeons toward the use of bed
rest and observation for hemodynamically stable
44
G. Siskin and J. Golzarian
score, neurologic status, grade of injury on abdomi-
nal CT, and quantity of hemoperitoneum have all
been cited as factors that may affect the success of
nonoperative management [10–15]. Hemodynamic
stability as a reflection of injury severity is likely
the most important factor to consider; Peitzman et
al. found that nonoperative management was more
likely to be successful in patients with higher blood
pressure, higher hematocrit levels, less severe injury,
and smaller quantity of hemoperitoneum [15]. Early
on, it was recommended that patients older than age
55 be excluded from nonoperative management of
blunt splenic injuries [10, 16]. However, more recent
data suggest that the decision to pursue nonoperative
management should be based on clinical and hemo-
dynamic factors, and not necessarily on age [11, 17].
Despite the benefits of splenic salvage and the
trend towards nonoperative management for these
patients, there are those t hat advocate a more aggres-
sive approach to the treatment of splenic injuries.
These investigators cite the potential for delayed
rupture or progression of injury that may require
urgent transfusion or emergency splenectomy.
Federle et al. did note in the review of their insti-
tutional experience with splenic trauma patients
that 15% of patients selected for nonoperative man-
agement initially ultimately required surgery, most
commonly within 48 hours of presentation [18]. One
problem with managing patients with delayed rup-
ture or injury progression is the difficulty utilizing
techniques to preserve splenic tissue, such as par-
tial splenectomy and splenorrhaphy, depending on
clinical severity [19–22].
4.1.3
Diagnosis
4.1.3.1
The Role of Abdominal CT
Abdominal CT has become an integral part of the
evaluation of patients experiencing blunt traumatic
injury. For stable patients with splenic trauma,
CT is needed before a decision is made to proceed
with nonoperative therapy because it is important
to identify and characterize not only the degree of
splenic injury, but also any concomitant abdominal
injury [19, 23, 24]. There have been several CT-based
classi fication systems for splenic injury, based on the
morphologic grade of splenic injury and the amount
of intraperitoneal hemorrhage, to guide therapy and
predict success for nonoperative management [18,
25–29]. One example of a grading system for splenic
inj ur y i s the m od if ie d crite ri a of th e Americ an A ss o-
ciation for the Surgery of Trauma (AAST), which
grades splenic injuries from 1 to 5 on the basis of
increasing severity of parenchymal damage based
on radiologic assessment [18, 27] (Table 4.1). Despite
the widespread use of this and other classification
systems, their use remains controversial since sev-
eral studies have shown that they do not necessarily
correlate well with clinical outcome [26, 27, 30–32]
and may not provide sufficient information regard-
ing vascular injuries to be useful [23, 33]. However,
Federle et al. studied this issue and found that CT
can effectively recognize vascular injury and active
extravasation from splenic arterial branches [18].
In 2000, Shanmuganathan et al. evaluated the
potential role of contrast-enhanced spiral CT in pre-
dicting the need for splenic angiography and embo-
lization by correlating them with results from subse-
quent splenic angiograms [19]. In their study, contrast
extravasation at CT was highly predictive of the need
for embolization, regardless of the CT grade of injury.
The presence of a pseudoaneurysm or arteriovenous
fistulas on CT, both of which are seen as focal areas
of high attenuation, was a less sensitive finding, with
only 58% of patients with these CT findings requir-
ing embolization or splenectomy. The angiograms
of the remaining 42% of patients with CT findings
suggestive of a pseudoaneurysm or arteriovenous
fistula did not reveal any focal vascular abnormali-
ties. These false-positive CT findings were attributed
to islands of enhancing splenic parenchyma sur-
rounded by low-attenuating splenic lacerations or
contusions and intact intrasplenic vessels traversing
parenchymal lacerations simulating hemorrhage sur-
rounding a focal pseudoaneurysm [19]. The finding
of a splenic vascular lesion on contrast-enhanced
spiral CT was 83% sensitive in predicting the need
for splenic angiography and subsequent embolization
or surgery. Using this approach, 94% of patients were
successfully selected at presentation for conservative
management. This study demonstrated that the use of
contrast-enhanced spiral CT and splenic angiography
improves early diagnosis and potential ly increases the
number of patients with blunt splenic injuries who are
treated successfully without surgery.
4.1.3.2
Diagnostic Angiography
The role of diagnostic angiography in the evalua-
tion of patients experiencing blunt splenic trauma