Check: 3 branches of Trigeminal, EOM, Bones, Teeth
Injuries to cheek between tragus and midcheek have injured parotid or facial nerve until proven otherwise
1. How is your vision (inquire about bilateral diplopia, unilateral, usually from cornea/lens)
2. Is your face numb
3. Are your teeth meeting normally
Test muscles of facial expression
Feel entire face, especially infraorbital rim, zygomatic frontal-junction (lateral portion of orbit.)
Pull on upper palate for Lefort. Palpate zygoma inside bucal mucosa
Water’s View-orbital rims, infraorbital floor, maxilla, and maxillary sinuses
For mid-facial fractures, one view 30-degree occipitomental (Water’s) is sufficient, do not need 3 view series. If positive, get CT scan. (J Trauma 52:688 2002)
Jug Handle-zygomatic arches and skull base
Caldwell-AP for frontal bones and sinuses
Normal series is Water’s,
Extra-Townes for the zygoma and mandibular rami or
Panorex for mandibular condyles or base of skull
Orbital outline
Sinus outline
Elephant’s trunk (as it looks like one) made up of zygomatic line laterally, which extends along the superior margin of the zygomatic arch and body, and the maxillary line medially, which extends along the inferior margin of the arch, body, and buttress of the zygoma and along the lateral wall of the maxillary sinus.
Coronoid process—the tip of which should be equidistant from maxillary line on each side.
Lefort I-Maxilla and palate
II-Above and nasal pyramid
III-Above and severe craniofacial
Get waters view, can be safely discharged
Eye will be pulled down, needs
blowout fx, herniation of orbit into maxillary sinus
observe eye for enophthalmos, sunken globe, or proptosis
Check EOM
To differentiate between muscular damage and true entrapment, do duction test. Anesthetize eye, then push sclera upwards to see if you can move eye
Test sensation over maxillary lip and teeth
Palpate nasal bridge
Drain Septal hematomas Incise along inferior aspect after anesthesia
Inspect floor of mouth for ecchymoses or hematoma, if present get CT c neg x-rays
Tongue blade test-if you can
to reduce push down on third molars, then push slightly posterior
Ellis I-enamel, II-dentin, III-pulp, IV-Ridge
Forehead sensation
Ocular exam
If depressed, open or c posterior table involvement get ENT
or Neurosurgery consultation
High energy blows to bridge of nose
Pain with EOM or epiphora
Measure distances between medial canthi, normal is 35 to 40
mm. Any increase (telecanthus) appears
as
Tenderness over medial canthi, perform the intranasal palpation test. Anesthetize nasal passage on side of injury insert hemostat into the nari and press laterally along the medial orbital rim while simultaneously palpating the medial canthus. Movement of the bone=NEO injury
Need facial CT
Need
The solution to any facial bleeding should be angio, not surgery
First pack then go to the rads department
Review Article (Injury 1998;29(4):253-256)
origin of bleeding is often the internal maxillary artery and especially its intraosseous branches
brances of the internal carotid artery such as the lacrimal, zygomatic, as well as the anterior and posterior ethmoidal arteries
angiography can be very helpful, though there are "dangerous" arteries--vessels which contact the external and internal circulation
temporary reduction of the fractures will go a long way to stopping the bleeding
The American Journal of Emergency Medicine
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Copyright © 2007 Elsevier Inc. All rights reserved.
Case Report
Angioembolization as an effective alternative for hemostasis in intractable
life-threatening maxillofacial trauma hemorrhage: case study
Shih-Chi Wua, b, E-mail The Corresponding Author, Ray-Jade Chenb, E-mail The
Corresponding Author, Kwo-Whei Leec, E-mail The Corresponding Author,
Cheng-Cheng Tunga, E-mail The Corresponding Author, Wen-Pei Lina, E-mail The
Corresponding Author and Poon Yia, E-mail The Corresponding Author
aDivision of Trauma, Changhua Christian Hospital, Changhua, 500 Taiwan, ROC
bTrauma and Emergency Center, China Medical University Hospital, Taichung 404,
Taiwan, ROC
cDivision of Radiology, Changhua Christian Hospital, Changhua, 500 Taiwan, ROC
Available online 5 October 2007.
Article Outline
References
Life-threatening maxillofacial trauma hemorrhage is not common; oronasal
hemorrhage from maxillofacial trauma can often be managed with manual
compression or efficient tight packing. Surgery is reserved for cases where
failure of tight packing occurs. However, the use of angioembolization might
decrease the need for blood transfusion and provide an effective alternative for
early hemostasis after packing failure. We report 7 cases wherein
angioembolization was successfully performed for hemostasis of life-threatening
maxillofacial trauma hemorrhage.
Maxillofacial injuries often result in airway compromise, hemorrhage, and bony
fracture [1], [2] and [3]. As the popularity of restraint-equipped automobiles
and airbags expanded, reports of maxillofacial injuries with airbag deployment
increased [4] and [5]. Most hemorrhages from maxillofacial injuries can be
managed with adequate nasal packing or direct pressure or even wiring of
mandibular fractures [6]. However, persistent life-threatening hemorrhage is not
common, the incidence rate ranges from 1.2% to 4.5% in maxillofacial injuries
[1], [2], [3] and [6]. Nonetheless, if persistent life-threatening hemorrhage
occurs, emergent life-saving surgery with open reduction and internal fixation
or ligation of focal vessels (eg, internal maxillary artery, external carotid
artery) might be necessary [6] and [7]. On the other hand, transcatheter
arterial embolization (TAE) has been applied in the management of intractable
posterior epistaxis and has achieved a high success rate with a low complication
rate [8], [9] and [10]. Therefore, it was also considered as an alternative in
the management of intractable hemorrhage in life-threatening maxillofacial
trauma [3], [11] and [12].
Herein, we report 7 cases where angioembolization was successfully performed in
hemostasis of life-threatening maxillofacial trauma hemorrhage.
Among 7 patients with life-threatening maxillofacial hemorrhage, we present 2
selected patients for discussion due to exemplary, vigorous hemorrhage.
The maxillofacial computed tomography (CT) scans were obtained using a GE Light
Speed Scanner (GE Medical Systems, Milwaukee, Wis). Patients received 100 mL of
intravenous bolus of nonionic contrast Ioversol (Optiray, Mallinckrodt Inc,
Hazelwood, Mo). Ten-millimeter cuts were obtained. All CT scans were initially
read by staff trauma surgeons and are later reviewed by staff radiologists.
Contrast extravasation/contrast blush is defined as a focus of high-attenuation
contrast material on CT film. The angioembolization was performed by
interventional radiologists. Arterial access was obtained via right femoral
artery, and a 6 Fr# right femoral sheath was used. A 5 Fr# RC1 catheter (Cook,
Bloomington, Indiana) was used for external carotid artery catheter. Patients
underwent embolization with coils (Cook, Bloomington, Indiana or Boston,
Scientific, Watertown, Mass) and/or Gelfoam (Pharmacia, Kalamazoo, Mich).
A 19-year-old back-seated male passenger was ejected from a vehicle after a
crash and was sent to our emergency department (ED) for resuscitation where
management followed the guidelines of Advanced Trauma Life Support. The
patient's blood pressure was 140/80 mm Hg, and heart rate 120 beats/min on
arrival. Emergent x-rays showed left zygomatic and orbital bony fracture, and a
helical CT revealed severe brain contusion with swelling and grade III liver
injury. However, vigorous active bleeding from the nares and oral cavity was
noted. The patient initially received direct pressure tight nasal packing, which
failed. Persistent hemorrhage would result in hypovolemic shock if the bleeder
was not arrested; therefore, an emergent angiography via the femoral route was
performed, which showed contrast extravasation of the left maxillary artery
(Fig. 1A). Embolization of the left maxillary artery was performed with 2
microcoils. A follow-up external carotid artery angiogram showed that the
bleeder had been embolized (Fig. 1B), and thus, no further oronasal bleeding was
detected. The patient was subsequently admitted to our intensive care unit for
further observation; however, on the sixth day, the patient died as a result of
severe brain injury.
Image Display Full Size version of this image (159K)
Fig. 1. A, Angiography shows left maxillary artery (large arrow) and active
contrast blush (small arrow). B, No more contrast blush after coil embolization
(small arrow). C, Right distal internal maxillary artery (large arrow) active
contrast blush and traumatic pseudoaneurysm formation (small arrow). D, Right
distal internal maxillary artery pseudoaneurysm was occluded after coil
embolization (small arrow).
A 39-year-old male patient had a motorcycle accident and was sent to the ED. On
arrival, the patient's blood pressure was 70/40 mm Hg, heart rate 145 beats/min;
he received vigorous resuscitation and became hemodynamically stable. X-rays
showed frontal bone fracture and right fourth to sixth rib fracture with a
hemothorax. Helical CT revealed intracranial and subarachnoid hemorrhage and a
grade III liver injury without contrast blush. After hemodynamics were
stabilized, the patient was admitted to our emergency intensive care unit for
further observation.
However, sudden onset of vigorous hemorrhage from the nares and oral cavity were
noted on day 10, and tight packing and compression were performed but failed and
persistent hemorrhage may induce hypovolemic shock. An emergent carotid artery
angiography via the femoral route showed right distal internal maxillary artery
active contrast leakage and traumatic pseudoaneurysm formation (Fig. 1C). Coil
embolization of the distal main trunk of the right internal maxillary artery
occluded the pseudoaneurysm (Fig. 1D), and no further oronasal bleeding was
detected. However, the patient underwent laparoscopic left lung wedge resection
due to iatrogenic lung injury and hemorrhage after removal of the chest tube on
the 20th day. The patient was discharged after careful management, and no facial
numbness or tissue necrosis or other symptoms were noted during outpatient
follow-up.
The characteristics of the 7 patients are listed in Table 1. The mean age of all
subjects (6 males and 1 female) was 32.9 ± 14.1 years. The mean injury severity
score was 41.7 ± 13.6, and all patients had blunt injuries. Time to embolization
after injury and the amount of blood transfused after embolization are shown in
Table 2. The average time to embolization was 11.6 ± 7.3 hours. Four patients
(57.1%) died of associated severe brain injury in spite of arresting
maxillofacial hemorrhage. Additional blood transfusions were not required after
facial TAE in all patients; however, some patients received a blood transfusion
due to other sources of hemorrhage (Table 2). There were 3 survivors, 1 patient
(patient 2) with persistent hemorrhage after failure of tight nasal packing for
19 hours, who received successful angioembolization. The remaining 2 patients
(patients 6 and 7) experienced delayed oronasal bleeding 10 and 11 days after
the initial crash, and angioembolization was performed after failure of
attempting hemostasis with tight nasal packing. There were no stroke, facial
numbness, tissue necrosis, or other symptoms that occurred in these 3 survivors
during outpatient follow-up.
Table 1.
Characteristics of maxillofacial injuries
Patient Age/Sex Injury mechanism Injury type ISS Vessel injured and embolized
Head injuries Lefort injury Associated injuries
1 19/male Blunt (MVC) Brain contusion Lefort II Liver grade III injury 35 Left
maxillary artery
2 22/male Blunt (MCC) ICH, Liver grade IV injury 48 Bilateral lingual artery,
perigingival branch
Skull bone fracture Lung injury
3 22/male Blunt (crush) Skull bone fracture Lefort II 26 Right accessory
maxillary artery
4 55/male Blunt (fall) ICH Pelvic fracture 59 Right maxillary artery
Skull bone fracture
5 26/female Blunt (MCC) Skull bone fracture, SAH Lefort II Liver grade V injury
57 Right facial artery, mandibular branch
6 39/male Blunt (MCC) ICH, SAH Lefort II Right hemothorax 50 Right distal
internal maxillary artery
Liver grade III injury
7 47/male Blunt (MCC) EDH Lefort II 29 Right distal internal maxillary artery,
sphenopalatine branch
MVC indicates motor vehicle crash; MCC, motorcycle crash; ISS, injury severity
score; ICH, intracranial hemorrhage; SAH, subarachnoid hemorrhage; EDH, epidural
hemorrhage.
Table 2.
Time to embolization after injury and amount of blood transfused post procedure
Patient no. Time to TAE after injury or delayed bleeding (h) BT before TAE (mL)
BT after TAE (mL) Local effect Systemic effect and outcome
1 17.7 2000 0 No more nasal bleeding after facial TAE Die of brain injury
2 19.2 1500 500 No further nasal bleeding after facial TAE Delayed liver
hemorrhage on the 12th day, received BT and liver TAE
Survived
3 5.8 2000 250 No further nasal bleeding after facial TAE Died of brain injury
4 4.0 1500 2000 No further nasal bleeding after facial TAE Died of brain injury
Associated pelvic fracture with bleeding, received BT and pelvic TAE
5 2.0 1000 12,000 No further nasal bleeding after facial TAE Died of brain
injury and severe liver injury induced hemorrhagic shock
6 17.0 5500 0 No further nasal bleeding after facial TAE Iatrogenic lung injury
and bleeding on the 20th day after removing chest tube, received laparoscopic
thoractomy, BT 1500 mL
Small groin hematoma Survived
7 15.2 1500 0 No further nasal bleeding after facial TAE Survived
BT indicates blood transfusion.
Life-threatening maxillofacial trauma bleeding is not common, the incidence rate
ranges from 1.2% to 4.5% in maxillofacial injuries [1], [2], [3] and [6], which
often results in airway compromise or hypovolemia [1], [2] and [3]. Management
should follow the guidelines of Advanced Trauma Life Support with protection of
the airway being the first priority [13].
Oronasal hemorrhage from venous origin or minor arterial vessels due to
maxillofacial trauma can often be managed efficiently with manual compression or
tight packing [3] and [6]. Some cases with serious maxillofacial trauma
hemorrhage can result in hemorrhagic shock and can often require emergent open
reduction and internal fixation for hemostasis [1] and [6]. Occasionally,
complicated techniques with ligation of focal vessels (eg, internal maxillary
artery, external carotid artery) are necessary for arresting hemorrhage [7],
however, this manipulation procedure could be laborious and might impinge on the
stability of the cervical spine and may cause further damage.
An alternative method for controlling hemorrhage is TAE [3], [11], [12] and
[14], which has been widely used in severe nontraumatic epistaxis for many years
[9] and [10]. Although the wide application of TAE in traumatic torso or
intra-abdominal solid organ hemorrhage or pelvic fracture had been reported
[15], knowledge of TAE usage for maxillofacial hemorrhage was mostly gained from
otolaryngology literature concerning patients with severe epistaxis [8], [9] and
[10]. However, TAE has been recently reported as the primary choice for
life-threatening maxillofacial trauma bleeding [2], [3], [11] and [12].
In this series, 7 patients experienced life-threatening maxillofacial trauma
hemorrhage and received TAE; no further nasal bleeding were detected after the
procedure. Additional blood transfusions were necessary in 4 patients due to
other sources of hemorrhage (Table 2). Four patients died of brain injuries. No
facial numbness, tissue necrosis, or other symptoms were detected in the 3
survivors during outpatient follow-up. Arresting nasal hemorrhage shows that TAE
may serve as an efficient alternative for hemostasis in life-threatening
maxillofacial hemorrhage.
Associated cerebral trauma and severe brain injuries are common in maxillofacial
trauma. To our knowledge, persistent maxillofacial hemorrhage might result in
brain hypoperfusion as well as secondary brain injuries, which often result in
adverse outcomes [16] and [17]. However, it has been reported that early
treatment of cerebral hypoperfusion status may reduce secondary brain injury and
decrease mortality [18]. We believe that in cases where failure of tight packing
occurs, early hemostasis for maxillofacial hemorrhage with TAE might be helpful
in shortening the hypoperfusion status and preventing the brain from further
damage.
Additional blood transfusions were not required after facial TAE in all
patients; however, some patients received a blood transfusion due to other
sources of hemorrhage (Table 2). The decreased amount of blood transfusion was
inclined to reduce the possibilities of blood-borne diseases [19].
In our series, there were no stroke, facial numbness, tissue necrosis, or other
symptoms that occurred in the 3 survivors. Although angioembolization is quite
safe for hemorrhage from branches of external carotid artery, it is not without
hazard when embolizing internal maxillary artery. The possibilities of embolus
migrating into the brain and causing cerebrovascular accident or stroke should
be noted. However, the reported risk of dislodging the embolizing agent is about
1.9% in experienced hands [20].
The oronasal status of patients 6 and 7 were normal initially; however, both
patients experienced delayed oronasal bleeding 10 and 11 days after the initial
crash. Tight packing of the nares was performed but failed; thus, embolization
was performed within 24 hours, and the bleeding was stopped. Although the exact
reason for the delayed hemorrhage is unclear, as we know, a higher injury
severity score often predicts nonoperative management failure in blunt splenic
injuries [21], it is to be elucidated whether a higher injury severity score is
of predictive value in delayed maxillofacial hemorrhage. On the other hand,
there were organized thrombus and blood clots after vessel injuries in normal
subjects [22] and [23]. In this series, both patients were with severe head and
brain injuries (head abbreviated injury score = 5) (Table 1) and were under
bedridden resting state within the first week of hospital stay. It is of
interest whether regaining activities after recovery might result in breakdown
of the stabilized blood clots and induce delayed hemorrhage. However,
possibilities of delayed life-threatening hemorrhage after maxillofacial trauma
should be considered.
Life-threatening maxillofacial trauma hemorrhage is not common; the oronasal
hemorrhage from maxillofacial trauma can often be managed with manual
compression or efficient tight packing. Emergency surgery is reserved for cases
where failure of tight packing occurs. In this series, TAE decreases the need
for blood transfusion and provides an effective alternative for early hemostasis
after packing failure, which might shorten hypoperfusion status and prevent
secondary brain injury. However, the possibilities of delayed life-threatening
maxillofacial hemorrhage have to be considered, and we suggest transarterial
embolization to be considered as the primary choice of treatment. Further
prospective studies elucidating the role of early transarterial embolization in
life-threatening maxillofacial trauma hemorrhage and determining the
relationship between higher injury severity score and delayed maxillofacial
hemorrhage are necessary.
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