Reminder of important clinical lesson

CASE REPORT

Blunt traumatic internal carotid artery dissection
with delayed stroke in a young skydiver
Michael Abbo,1 Kosar Hussain,2 Mohammad Baqer Mohammad Ali3
1

Department of Emergency
Medicine, Rashid Hospital
Trauma Center, Dubai Health
Authority, Dubai, UAE
2
Department of Internal
Medicine, Dubai Health
Authority, Dubai, UAE
3
Medical ICU, Rashid Hospital,
Dubai Health Authority, Dubai,
UAE
Correspondence to
Dr Kosar Hussain,
koshussain@dha.gov.ae

SUMMARY
We describe a case of a 33-year-old skydiver who
presented to the emergency department after a traumatic
landing following a parachuting episode. He initially
presented with right knee pain secondary to a tibial
plateau fracture. There were no neurological symptoms
or signs at the initial assessment. While he was still in
the emergency department, he suddenly developed
headache and left-sided hemiplegia. An urgent work-up
showed right middle cerebral artery thrombosis with
right internal carotid thrombosis and dissection. We have
discussed some possible mechanism of injury in
skydiving that may have predisposed to the occurrence
of cervical dissection in our patient.

BACKGROUND
To the best of our knowledge no previous cases of
internal cervical artery dissection causing stroke
after a skydiving episode has been previously
reported in the literature.
Internal carotid artery dissection is one of the
important causes of stroke in young adults, which
can lead to a potentially life-threatening condition.
Failure to consider, diagnose and treat this condition promptly may result in long-term neurological
disability or death.

CASE PRESENTATION

To cite: Abbo M,
Hussain K, Ali MBM. BMJ
Case Rep Published online:
[please include Day Month
Year] doi:10.1136/bcr-2012008412

A 32-year-old man presented to the emergency
department with right knee pain and swelling
that occurred after a traumatic landing following a
skydiving episode in a canopy-piloting tournament.
Gaining popularity with competitors, freestyle
canopy-piloting puts the skydiver in contact with
the water at high speeds, increasing the risk of a
unique deceleration injury. Following an uneventful
initial free-fall he landed on water surface and
tumbled many times prior to coming to a halt. The
patient, who was a professional skydiver, did not
recall any forced hyperextension, hyperflexion or
rotation of the neck during the take-off or free-fall.
There was no direct head trauma or loss of consciousness. Besides his right knee pain he was completely asymptomatic. There was no head or neck
pain. At initial assessment his Glasgow Coma Scale
(GCS) was 15/15 and his vitals signs were stable.
There was no sign of any neurological deficit (in
particular no clinical signs suggestive of a Horner
syndrome were noted). He had no phenotypic features of a connective tissue disease. He was
reviewed by the trauma team and his x-ray showed
a right tibial plateau fracture with minimal effusion.

Abbo M, et al. BMJ Case Rep 2013. doi:10.1136/bcr-2012-008412

After a time interval of 6 h, while the patient was
still in the emergency department, he suddenly
developed a generalised headache and left-sided
weakness. On examination he was found to have a
dense left-sided hemiplegia, an upper motor neuron
lesion of the left facial nerve, dysarthria and a leftsided neglect.

INVESTIGATIONS
An urgent brain CT showed a hyperdense right
middle cerebral artery (MCA) sign, which was suggestive of right MCA thrombosis (figure 1). Based
on the preceding history of trauma, an urgent cerebral and carotid CT angiography was carried out
which showed right MCA thrombosis and right
internal carotid (ICA) thrombosis and dissection
(figures 2–4).

TREATMENT
The neurological and neurosurgical teams were
consulted. They decided to manage the patient conservatively with aspirin. He was admitted to the
ICU for close observation of his vital signs and
neurological status.
Other therapeutic options that we considered for
this patient was thrombolysis with tissue plasminogen activator (t-PA); however, it was deemed
inappropriate as it was a massive stroke with a high
risk of haemorrhagic transformation and also due to
the recent history of trauma causing a fracture in the
right tibia. Therapeutic anticoagulation was also not
started because of the high risk of bleeding in this
patient.

Figure 1 The initial brain CT showed a hyperdense
right middle cerebral artery sign.
1

Reminder of important clinical lesson

Figure 2 Carotid and cerebral CT angiogram showed a filling defect in right internal carotid artery and right middle cerebral artery.
While in the ICU the patient continued to have dense leftsided hemiplegia. He was occasionally drowsy, however
responding to verbal stimuli. GCS was fluctuating between 12
and 15. Throughout the course of his stay in the ICU he was
haemodynamically stable and did not require any ventilator
support. Brain CT scan was repeated after 2 days and it showed
a large hypodense lesion in the frontotemporoparietal region
with a mild mass effect on the right lateral ventricle with a
midline shift (figure 5). He was reviewed by the neurosurgical
team and they advised conservative management with close
observation and administration of intravenous mannitol.
A repeat brain CT after a week did not show any gross interval changes. His GCS improved to 15 and his vitals remained
stable. He was then started on prophylactic dose of
low-molecular-weight heparin and physiotherapy with assisted
out-of-bed mobilisation.

OUTCOME AND FOLLOW-UP
The patient was discharged after 3 weeks. GCS at discharge
was 15. His dysarthria had improved significantly; however, the
power on his left side continued to be 0/5.

Figure 3 Three-dimensional reconstruction of carotid CT angiogram
images showed a complete obliteration of blood flow in right internal
carotid artery.
2

He was discharged on an antiplatelet agent with a recommendation to follow-up with the neurologist.

DISCUSSION
Cervicocerebral dissection is a potentially life-threatening condition, that is, increasingly being recognised as one of the main
causes of ischaemic strokes among young adults.1 This condition
may involve both the intracranial and extracranial segments of
ICA and vertebral artery. However, the extracranial segments
are more likely to be injured due to their mobility and proximity
to surrounding bony structures.2 Patients who have had a stroke
secondary to ICA dissection are generally younger and have a
worst prognosis compared to those who have had stroke secondary to atherothrombotic occlusions.3
Dissection starts as an intimal tear which causes blood to
enter the arterial wall to form an intramural haematoma. This
can progress to either stenosis or an aneurysmal dilation of the
artery. Damage of the endothelial lining can activate platelets
and the coagulation pathway, which eventually leads to a thrombus formation.4 The signs and symptoms of ICA dissection are
either due to localised mass effect due to compression of surrounding structures or cerebral ischaemia. A dissection may lead
to cerebral ischaemia either by haemodynamic insufficiency or
by distal embolisation.5 6
In cases of ICA dissection, the lesion frequently involves the
distal parts of the ICA.7 However in our case the dissection was
more proximally located in the right ICA.

Figure 4 Three-dimensional reconstruction of cerebral CT angiogram
images showed a complete obliteration of blood flow in right middle
cerebral artery.
Abbo M, et al. BMJ Case Rep 2013. doi:10.1136/bcr-2012-008412

Reminder of important clinical lesson

Figure 5 Repeat brain CT showed a large hypodense lesion in the
frontotemporoparietal region with a mild mass effect on the right
lateral ventricle and a midline shift.

Cervicocerebral artery dissection can be either traumatic or
spontaneous. Spontaneous dissection is more often seen in
persons with underlying structural weakness in the vessel wall.
In traumatic dissections, the severity of the trauma can range
from a mild impact such as a forceful cough to severe impacts
such as blunt head and neck injuries in polytrauma victims.8 9
The availability of improved imaging modalities has led to
increased recognition of sport-related cervicocerebral artery
dissection. A prospective study by Schneidereit et al evaluated
the role of CT angiography-based screening protocols in
patients with blunt trauma. They found the incidence of blunt
vascular neck injuries to be 1.1%, which was significantly
higher than the 0.17% incidence before radiological screening
of the cases.10
In addition to the direct impact of trauma, the pathogenesis
of ICA dissection in sport-related activities is postulated to be
related to a number of other causes. This includes structural
aberrations in the vessel wall and weaknesses in the connective
tissue.11 Zhou et al have described a case of a young man who
presented with stroke symptoms that occurred 2 h after a
bungee-jumping event. The impact from sudden deceleration
involved in this activity was postulated to have caused carotid
artery dissection, which subsequently led to stroke.12 Other
sports that are reported to be implicated in causing cervicocerebral artery dissection include scuba diving, basketball, wakeboarding, diving and martial arts.13–17 Several cases that
reported the occurrence of cervicocerebral dissection after
roller coaster rides have been described in literature.18–20
Interestingly, Schneck et al19 described a case of bilateral vertebral artery dissection that was diagnosed months after a bumpy
roller coaster ride.
Skydiving is a form of extreme sports which carries with it
inherent risks of traumatic injuries. However after reviewing
medical literature, we could not find any reported case of ICA
dissection after parachuting. Unedited internet blogs have
described this phenomenon. This is perhaps due to underreporting of such cases and thus calls for increasing awareness
about such an association.
Abbo M, et al. BMJ Case Rep 2013. doi:10.1136/bcr-2012-008412

There are many possible mechanisms that may predispose skydivers to carotid dissection. One possibility is ‘hard-opening’ of
the parachute may cause forced hyperextension of the neck,
which may attribute to traumatic ICA dissection. Another mechanism, which we believe caused the dissection in our patient, is
related to the increasing popularity of canopy-piloting. An
aspect of this sport is ‘pond swooping’ which typically uses a
body of water to touch or display a skill prior to landing on
solid ground on the other side. This type of canopy piloting is
increasingly gaining popularity among both skydivers and spectators. This manoeuvre involves trying to hit the surface at high
speeds and then decelerating, while dragging through the
surface of water. The smallest error in landing predisposes the
skydiver to various impact injuries and this is what had happened to our patient.
In cases of cervicocerebral artery dissection, the local signs
and symptoms often precede the cerebral ischaemic symptoms.
Classically ICA dissection presents with a triad of craniocervical
pain or Horner syndrome, that is, followed after a latency
period of hours-to-days by ischaemic manifestations. Although
such classic symptoms are seen in less than a third of the cases,
the presence of two of the above criteria are highly suggestive of
a diagnosis.2 However, our patient did not exhibit any of the
usual warning symptoms of ICA dissection prior to the onset of
stroke. In view of this latent period and the lack of warning
symptoms in the majority of patients who go on to stroke, clinicians should maintain a high suspicion and low threshold to
perform diagnostic studies based on mechanism of injury.
Currently MRI angiography is the preferred modality for
diagnosis of cervicocerebral artery dissection due to its high sensitivity and specificity. It also does not involve exposure to
harmful radiations. However in conditions where MRI is
inaccessible, CT angiography is considered the next best option.
Colour Doppler ultrasonography is another non-invasive modality; but it lacks sensitivity.21
There are no randomised control trials conducted to compare
the various treatment modalities in cases of cervicocerebral
artery dissection. A Cochrane systematic review by Lyrer et al
assessed the use of antiplatelet and anticoagulant medications in
cases of traumatic and spontaneous extracranial internal carotid
artery dissection. They reported that there was no significant difference between the antiplatelet and anticoagulant groups.22 It is
generally recommended to treat each patient on a case-by-case
basis.21 In our case, the patient was initially started on antiplatelet
agents. Anticoagulants were not initiated immediately due to the
recent history of trauma and high risk for haemorrhagic transformation of the infarct.

Learning points
▸ Traumatic carotid dissection may be silent until secondary
ischaemia occurs.
▸ Carotid dissection is described in ‘canopy-piloting’ which is
gaining in popularity.
▸ Physicians should be vigilant to pick up the early subtle
signs of cervicocerebral artery dissections.
▸ A diagnosis of traumatic cervicocerebral artery dissections
can be missed as there can be an asymptomatic ‘latent
period’ so diagnostic studies are advocated if the
mechanism is appropriate.
▸ Use of anticoagulants is controversial and need to be
considered on a case-by-case basis.
3

Reminder of important clinical lesson
Competing interests None.

10

Patient consent Obtained.
Provenance and peer review Not commissioned; externally peer reviewed.

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Abbo M, et al. BMJ Case Rep 2013. doi:10.1136/bcr-2012-008412