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Italian abstract
Raramente la lussazione anteriore di spalla, che rappresenta circa il
45% di tutte le lussazioni, provoca lesioni vascolari; infatti pochissimi
casi sono descritti in letteratura. La diagnosi è spesso tardiva
in quanto le strutture ossee e muscolari del torace e della spalla stessa
tendono a nascondere i segni della lesione e un efficiente circolo collaterale
può mantenere normosfigmico il polso radiale. Il comportamento
incostante e imprevedibile dei falsi aneurismi, i quali possono dare luogo
ad immediate e cospicue emorragie, a lente anemizzazioni, o rimanere silenti
per settimane o mesi manifestandosi in seguito sotto forma di ematomi
pulsanti, rende difficoltosa la compilazione di un protocollo di comportamento
standard che ne preveda e ne anticipi le pericolose conseguenze.
Gli autori descrivono con dovizia di particolari clinici un caso di pseudoaneurisma
dell’arteria ascellare conseguente ad un episodio di lussazione anteriore
di spalla ricercando eventuali fattori di rischio e soffermandosi sulle
difficoltà diagnostiche, considerata l’alta frequenza della
patologia potenzialmente determinante la lesione che nell’eventualità
di diagnosi mancata o tardiva può essere foriera di gravi conseguenze.
Parole chiave: Pseudoaneurisma, arteria ascellare.
Abstract
Rarely does anterior dislocation of the shoulder, which represents about
45% of all dislocations, cause vascular lesions; actually, there have
been very few cases described in literature. The diagnosis is often delayed
due to the bone and muscle structure in the chest and shoulder which tends
to disguise the signs of lesion; an efficient collateral circulation will
help maintain a normal radial pulse. The inconsistent and unpredictable
behavior of false aneurysms can lead to sudden and severe hemorrhaging,
to slowly developing anemia, or remaining hidden for weeks, even months
before manifesting themselves in the form of pulsating hematomas. Furthermore,
these factors render difficulties in compiling a standard protocol for
diagnosis and thus potentially create serious consequences for the patient.
The authors detail a clinical case of pseudoaneurysm involving the axillary
artery resulting from an anterior dislocation of the shoulder. The authors
also research eventual risk factors, investigate diagnostic difficulties
and considering the high frequency of this form of dislocation, the possibility
of a resulting vascular lesion and the consequences associated from late
or misdiagnosis.
Key words:
Pseudoaneurysm, axillary artery.
Anterior dislocation of the shoulder is a traumatic lesion, occurring
with high frequency, representing about 85% of all dislocations of the
glenohumeral joint and about 45% of all bodily dislocations[16]. Usually
this form of injury is benign, but in certain cases may be associated
with severe consequences; possibly involving bone structure, as well as
nervous and vascular systems.
Vascular complications resulting from anterior dislocation of the shoulder
are rare, lesions of the axillary artery, according to Fontaine, occur
in less than one case per 100 dislocations (7). Bertrand reports a frequency
of 0.3 per 100 dislocations (1). Sometimes lesions of the arterial wall
lead to the formation of a pseudoaneurysm that temporarily blocks or reduces
hemorrhaging and maintains open the lumen of the artery, thus disguising
symptoms of the vascular lesion and also delaying the diagnosis and eventual
treatment.
Case Report
A male aged 69 years, affected with, but not being treated for, hypertension
was struck by an automobile while walking resulting in a fracture of the
tibial plate and anterior dislocation of the left shoulder. The resultant
examination revealed the presence of bruising about the left shoulder,
no evidence of neurovascular damage (he retained normal mobility of the
elbow and hand, had no paresthesia sensation, and maintained a normal
radial pulse). Immediate reduction was performed under general anesthesia
and limb immobilized with a Dessault bandage. Routine laboratory examination
revealed hemoglobin of 13.60 gm The day following admission to the hospital,
after no longer being able to tolerate the Dessault bandage, the patient
autonomously removed it. X-rays were performed to verify the maintenance
of the reduction and a sling was utilized to maintain immobility while
casually allowing visibility of the bruising. On the seventh day of recovery
pre-scheduled surgery was performed on the fractured tibial (synthesis
with two cannulated screws). Post-surgery blood exam revealed a hemoglobin
value of 11.70 gm. Subsequent postoperative days progressed normally,
however bruising persisted about the anterior region of the left shoulder.
Five days after surgery routine blood examination revealed the reduction
in hemoglobin level (10.10 gm). More frequent blood examinations were
scheduled, about every two days, these tests revealed a slow and steady
decrease in hemoglobin level until it reached a value of 8.00 gm. Excluding
other causes for the anemia, and taking into consideration a spreading
of the bruising onto the thorax, a decision was made to perform an angiogram
(fig. 1) of the axillary artery. This revealed a post-traumatic pseudoaneurysm
approximately 2 cm in diameter, probably caused by an avulsion to the
anterior circumflex artery. The middle and distal portion of the anterior
circumflex artery are clearly visible in the angiogram due to blood flow
from the collateral circulation (fig. 2). The angiogram reveals no evidence
of blood flow from the lesion. The patient was transferred to the operating
room, where under local anesthesia an incision was made to gain access
to the brachial artery. A Nitinol stent was inserted into the axillary
artery with fluoroscopic control to bypass the pseudoaneurysm (fig. 3).
The implantation, performed without complication, allowed a progressive
increase in the patient’s hemoglobin level and a return to general
well being.
Anatomy
The axillary artery is the continuation of the subclavian artery. It is
generally accepted that it initiates at the lateral border of the first
rib (16, 21) (according to Testut (20) it originates near the middle portion
of the clavicula) and ends at the inferior border of the pectoral major
muscle where it then becomes the brachial artery. At first the axillary
artery lies deep and later, distally, becomes more superficial where only
the skin and fascial sheath covers it. The pectoral minor muscle crosses
the vessel, dividing it into three sections; the proximal, middle, and
distal. The proximal portion gives rise to the superior thoracic artery.
The middle portion, posterior to the pectoral minor, gives rise to the
thoraco-acromial and lateral thoracic arteries. The distal portion gives
rise to the anterior and posterior circumflex arteries, as well as the
subscapular artery. The subscapular artery connects with the distal portion
of the axillary artery through anastomosis with the transverse cervical
(when present), dorsal scapular, branches of the subscapular, and soprascapular
arteries. Significant collateral circulation arises from anastomoses between
the lateral thoracic artery and the toracic scapular system; anastomoses
between the subscapular artery and the brachial system; and from the connections
between the anterior and posterior circumflex arteries. A common fascial
sheath encloses both the axillary artery and the brachial plexus together
(9). The medial, lateral and posterior cords of the brachial plexus surround
the proximal part of the axillary artery.
The median nerve lies on the anterior surface of, the ulnar nerve lies
medial to, and the radial and axillary nerves lie posterior, the axillary
artery.
Discussion
Lesions of the axillary artery originating from anterior dislocation of
the shoulder are rare due to the resiliency of this vessel. In addition
to atherosclerotic changes of the arterial wall, which reduces the vessel’s
resiliency (most cases occurring in the elderly), predisposing factors
leading to lesions of the axillary artery resulting from anterior dislocation
of the shoulder are: violent trauma yielding a large displacement of the
humeral head, recurring anterior dislocations (especially when scar tissue
is formed near the vessel), longstanding dislocation (the lesion occurring
at the moment of reduction), and reduction performed with excessive force
(due to insufficient muscle relaxation) (5,12,15).
Injuries to the axillary artery can be classified into three main groups.
Firstly, and most frequently occurring, lesions due to avulsion of a collateral
artery (full - thickness focal defects) (5). Secondly, subadventitial
lesions, which primarily involve the intima coat, could also be associated
with lesions of the middle coat, but never implicate the adventitia coat.
Lastly, full-thickness circular wall rupture that occurs distally from
the collateral branches and yields a compressive hematoma or arterial
thrombosis (15). An extraordinary occurrence would be the imprisoning
of the axillary artery between the humeral head and the anterior edge
of the glenoid cavity (8).
Most lesions occur in the middle and distal portions of the axillary artery
due, respectively to, avulsion of the thoracoacromial trunk and of the
subscapular and circumflex arteries (5). Several hypothesis have been
suggested to explain the mechanisms of injury. According to Brown and
Navigato, the axillary artery which is fixed to the lateral border of
pectoralis minor muscle, is taut when the shoulder is at abduction and
external rotation. As the humeral head dislocates anteriorly it forces
the axillary artery forward and the pectoralis minor acts as a fulcrum
over which the artery is deformed and ruptured (2). The circumflex and
subscapular arteries originate from the posterior wall of the axillary
artery and serve to fix the axillary artery to posterior planes. According
to Bertrand, it is in those cases of traumatic displacement of the axillary
artery, in which the circumflex and subscapular arteries are unable follow,
that yield a tear at their origin (1).
Pseudoaneurysms normally arise from a full thickness focal defect in the
arterial wall, that lead to a saccular dilatation. In cases where the
hemorrhage is contained by surrounding tissues, the hematoma may continue
to communicate with the bloodstream through the arterial wall defect.
If this situation persists, the hematoma will transform into an aneurysm
sac by way of lysis or from compression of its contents by the pulsating
stream that communicates with it (10).
The difficulty in diagnosis is manly due to temporal variability in the
appearance of clinical signs relating to the traumatic event. Bone and
muscle structure can often hide an hematoma or a small pseudoaneurysm,
additionally the pain of injury and resulting muscular contraction renders
difficult the physical examination of axilla.
According to literature, early but aspecific signs of vascular lesion
secondary to anterior dislocation of the shoulder developing pseudoaneurysms
are: hematoma or bruise in the shoulder region, a week or absent radial
pulse prior to reduction or brachial plexus palsy (6,9,13).
Following normal progression, the pseudoaneurym can grow (up to 20x25cm)
and compress nervous and venous structures causing; respectively, neurological
deficit and venous obstruction, resulting emboluses, the limiting of gleno-humeral
joint range of motion, the stimulation of periosteal reactions, an eroding
clavicle, and to a slowly developing anemia. Sudden rupture ( which can
frequently occur before the restraining surrounding tissues have matured
into a definitive sac) can cause a massive hemorrhage and a large hematoma
to spread to limbs and chest causing shock (3,4,9,11,14,18).
In case presented, no pathognomic signs of arterial injury (distal circulatory
deficit, ischemia, diminished or absent pulses, bruiting, nor expanding
or pulsating hematoma) were apparent on admission (17). Additionally,
there were no signs of neurological deficit; according to many authors
(5,9,13,22) these deficits (which are sometime irreversible) are most
often reveled in cases involving an axillary artery lesion probably occurring
because of the close anatomical relationship between neural and vascular
structures.
The bruising ( which was visible after the Desault bandage was removed)
was believed to be secondary to trauma. Days following admission, however,
its color and size remained unchanged; not respecting the normal procedure
of reabsorption. Initially, the decrease in hemoglobin was associated
with the bruising and the operation. When the bruising suddenly spread
to the chest (two weeks after admission) it was then believed that a vascular
lesion was involved.
In conclusion, diagnosing pseudoaneurysms of the axillary artery can be
delayed by the causes we have reported and by the lack of suspicion for
axillary artery injury secondary to anterior shoulder dislocation. When
the risk factors are present, to avoid hemorrhage and permanent neurologic
deficit, we recommend careful study of the vessel by Doppler sonography
(or angiography if necessary) (19). Furthermore, high risk patients need
more frequent follow up (laboratory and clinical) and if necessary a longer
recovery period. These precautions should be integrate into the currently
adopted treatment for shoulder dislocation which usually consist of immobilizing
the shoulder in a Desault bandage and a follow up exam after two o tree
weeks.
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