Case
Report - Stroke secondary to an unusual cause
.........................................................................................................................
Harsha
Bhatia*,
Ragab Hani Donkol**,
Shahid Aziz***,
Amer
Assiri***
Department of Neurology*,
Department of radiology**,
Department of internal medicine***
Aseer Central Hospital and King Khalid University,
Abha,
Kingdom of Saudi Arabia.
Correspondence:
Harsha Bhatia
Email: drharshabhatia@yahoo.co.in
|
ABSTRACT
A 34 year old man sustained blunt trauma
to his neck following repeated non-fatal
manual neck strangulation. After a few
hours he developed altered sensorium and
dysphasia and 6 hours later he deteriorated
further and was brought to the emergency
department. On examination he had a dense
right sided hemiplegia aphasia. Plain
CT scan of the head should a large hypodense
area in the vascular territory of the
left middle cerebral artery suggestive
of infarction. CT angiogram of the neck
and head showed thrombosis of the right
common carotid and internal carotid artery
with total occlusion of the left middle
cerebral artery stem. He was treated conservatively
and improved partially. Problems associated
with carotid artery thrombosis in the
setting of blunt head and neck trauma
are discussed.
Key Words: Bilateral Carotid Thrombosis,
Manual strangulation.
|
Thrombosis of the carotid
tree is caused by various diseases, resulting
in fatal and non-fatal outcomes. Bifurcation
of the common carotids in the neck leads to
the formation of internal and external carotids.
During their short course in the neck, the internal
carotid artery is vulnerable to both penetrating
and blunt trauma. The majority of extra-cranial
traumatic injuries to internal carotid artery
(ICA) are caused by direct trauma from penetrating
injuries, especially from gunshot wounds. There
is a small subset of injuries of extra-cranial
ICA injuries caused by blunt trauma and some
of these occur in the setting of head trauma.
The incidence of carotid injury in association
with blunt head and neck trauma is reported
to be less than 1%. We report a case of manual
strangulation leading to stroke after 6 hours
associated with bilateral carotid arterial tree
affection.
This 34 year old male was
brought by his brothers to the emergency department
with complaints of altered sensorium and inability
to speak for the past 6 hours. A day prior to
his presentation, the patient while eating food
felt that there was some abnormal sensation
in his throat. He went to one of the traditional
healers for indigenous treatment who started
manually pressing his neck repetitively and
vigorously. Six hours later, his relatives noticed
that he was drowsy and had difficulty in speaking,
and it took another 6 hours to bring him to
hospital, until he developed right sided hemiplegia.
His past history was notable of ill-defined
psychiatric illness for which he was indigenously
treated by religious healers and which used
to improve without visiting any psychiatrist.
There is no associated history of recurrent
oral ulcers, hair loss, fever, headache, rash,
or any symptoms suggesting connective tissue
disorders. He is single and works as a teacher.
Examination revealed that he was conscious but
drowsy, arousable to sounds, looked to direction
of sound, with gaze preference to the left side.
He was globally aphasic with few incomphrensible
sounds, and dense right sided hemiplegia. His
pupils were normal in size and reaction to light;
his fundi were also normal. There was neck swelling
on the right lateral aspect of the neck with
bruising on the right side of neck below the
angle of mandible. There was bruising also on
the anterior chest wall below the supra-sternal
notch and there was minimal swelling on the
left lateral aspect of the neck. The carotid
pulsations on the right side were feeble whereas
on the left side they were of good volume. His
vitals including his blood pressure (120/75
mmHg) and other systemic examination were unremarkable.
Immediately a non contrast CT scan of his head
was done on an emergency basis which showed
a large recent infarction in the vascular territory
of left middle cerebral artery (MCA) with significant
mass effect (Figures 1 and 2). CT angiogram
of his neck and head showed thrombosis of the
right common carotid and internal carotid artery
with total occlusion of the left middle cerebral
artery(MCA) stem (Figures 3 and 4). There was
no facility of an interventional thrombolysis
available, so the patient was started on anticoagulation
to inhibit the extension of right carotid thrombus,
along with other anti edema measures and anti
platelet therapy. His work up for the other
secondary causes of young stroke was done including
echocardiography, antinuclear and anticardiolipin
antibodies, and lupus anticoagulant, all of
which were negative. His work up for inherited
thrombophilia including proteins C and S, anti
thrombin III and factor V Leiden mutation were
done and were also negative.
Figure 1. Initial non contrast-CT scan of
the head shows ill-defined hypodense lesion
involving the cortical and subcortical of the
vascular territory of the left MCA. The arrow
points to the hyperdense MCA as a sign of recent
thrombosis.
Figure 2. Initial non-contrast CT scan of
the head shows the large left cerebral infarction
in the vascular territory of MCA with shift
of midline structures
Figure 3. Initial CT angiography (MIP in
axial plane) of the neck arteries shows partial
thrombosis of right ICA (arrow)
Figure 4: Initial CT angiography (MIP in
axial plane) of the intracranial arteries shows
total thrombosis of left MCA (arrow)
The patient started improving after 3 days,
became more alert, and started babbling a few
words and was started on physiotherapy and speech
therapy. He was initiated on antiplatelet therapy
with low dose aspirin (81 mg) and therapeutic
anticoagulation, initially, with unfractionated
heparin (target aPTT between 1.5 to 2.5) and
warfarin overlap and later on continued on warfarin
alone with his international normalized ratio
(INR) maintained between (2.5 to 3). He was
discharged in a relatively good condition with
residual right sided weakness and motor aphasia.
For follow-up he was advised to come to the
neurology clinic after one month from the time
of discharge .A month later his CT Angiogram
was repeated which showed that the thrombus
had resolved in the right internal carotid artery,
and his middle cerebral artery was also patent
with a good flow. (Figure 5).
Figure 5: Follow up CT angiography (MIP in
axial plane) shows complete resolution of the
right ICA thrombosis
Traumatic thrombosis of internal carotid artery
is caused by four mechanisms; injury to the
intra- petrous part or cavernous part of internal
carotid artery during basal skull fracture;
injury to the point of emergence of internal
carotid artery from cavernous sinus as a result
of shearing strain; a direct blow to the neck
or trauma to the peri-tonsillar area by a
foreign object carried in the mouth; and stretching
of carotid artery by hyperextension and lateral
flexion of the neck. Secondary symptoms resulting
from thrombosis of the carotid artery develop
most commonly between 12 and 24 hours after
injury [1]. Blunt and penetrating trauma to
the neck and pharynx can both cause thrombosis
of the internal carotid artery [2, 3]. Manual
strangulation is also reported as a rare cause
of carotid thrombosis and it is possible that
excessive pressure to the neck may contribute
to thrombus formation and then traumatic occlusion
of middle cerebral artery [3] resulting in
infarction.
Incidence of carotid artery injury in the
setting of head injury is very low and can
be missed in the setting of cranio-cerebral
trauma. Yamada et al could collect only 52
cases in a review of literature [4]. Because
of this low incidence there is lack of awareness
that results in delay in the diagnosis. High
index of suspicion (hyperextension-hyperflexion
mechanism of injury, basilar skull fracture,
and cervical spine injury, mid-face fracture,
mandibular fracture, diffuse axonal injury
and neck seat belt sign) clinches early diagnosis
or directs efforts for early diagnosis and
treatment [5]. The suggested mechanism of
injury is hyper-extension and rotation of
the neck which results in stretching and compression
of ICA against lateral mass of C1 or C2 vertebra
that causes either tear in intima or hematoma
in the media of arterial wall and subsequent
thrombosis and occlusion [6, 7, 8]. Conventional
angiography was the gold standard for diagnosis
and CT scan and MRI will show the extent of
infarct. MR angiography and CT angiography
are useful non-invasive tests in showing the
stenosis, occlusion, tear of vascular intima
or hematoma in the wall of the carotid arteries
and their branches [9]. Positron Emission
Tomography scan of the brain will show the
area of hypo-perfusion which can be more than
the area of infarct. Anticoagulation is mandatory
for blunt carotid injuries to reduce the chances
of stroke, provided there is no contraindication
and patients are promptly diagnosed before
occlusion [10]. Once occlusion has occurred,
surgical intervention becomes imperative.
This report also highlights rare occurrence
of blunt carotid injury in the setting of
closed neck injury, which is usually missed
due to lack of awareness for early diagnosis
and treatment or arrives too late for any
worthwhile therapeutic intervention and results
in avoidable morbidity and mortality.
1. Tieulie N, Thi Humyxz, Hausfater. Forensic
Fatal and Nonfatal bilateral delayed carotid
artery dissection after manual strangulation.
Science Int. 2005; 149:143-50.
2. Hausfater P, Duhuat P, Fur A, Wehster B.
Internal Carotid Artery Thrombosis. Med Interna.
2003; 29:469-73.
3. Mackintosh RH. Unilateral Manual Strangulation.
Med Sci law. 1965; 5:117-18.
4. Yamada S, Kindt GW, Youmans JR. Carotid
occlusion due to non penetrating injury. J
Trauma. 1967; 7:333-42.
5. Mayberry JC, Brown CV, Mullins RJ. Blunt
Carotid Artery Injury: The futility of aggressive
screening and diagnosis. Arch Surg. 2004;
139:609-13.
6. Batzdorf U, Bentson JR, Machleder HL. Blunt
trauma to the high cervical carotid artery.
Neurosurgery. 1979; 5:195-201.
7. Boldrey E, Maass L, Miller E. The role
of atlantoid compression in the etiology of
internal carotid artery thrombosis. J Neurosurg.
1956; 13:127-39.
8. Sue DE, Brant-Zawadzki MN, Chance J. Dissection
of cranial arteries in the neck: correlation
of MRI and arteriography. Neuroradiology.
1992; 34:273-78.
9. Jernigan WR, Gardner WC. Carotid artery
injuries due to close cervical trauma.
J Trauma. 1971; 11:429-35.
10. Cothren CC, Moore EE, Biffl WL. Anticoagulation
is the Gold standard therapy for blunt carotid
injuries to reduce stroke rate. Arch Surg.
2004; 139:540-56.
|
