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UHM 2018, Vol. 45, No. 1 – CCAD AND SCUBA: IS THERE A LINK?

Research Article
Cervicocranial artery dissection and scuba diving:
Is there a link or is it serendipity?
Gerald K. Walters, MS, PA-C.
Senior Physician Assistant, Johns Hopkins Bayview Medical Center,
Johns Hopkins School of Medicine, Baltimore, Maryland U.S.


Cervicocerebral artery dissection (CCAD) is a leading
Introduction: Numerous reports have documented cervico- cause of stroke in younger individuals. Carotid or verte-
cranial artery dissection (CCAD) associated with scuba diving. bral artery dissection occurs from a tear in the arterial
The question remains as to whether there are risk factors intima or disruption of the vaso vasorum, with resul-
unique to scuba diving related to the occurrence of CCAD. tant intramural hematoma. The results are narrowing or
Objectives: This article aims to perform an examination of occlusion of the affected vessel, with the possibility of
the reported cases to demonstrate any commonality among the embolization and cerebral infarction. Genetic, environ-
injured divers and association with known risk factors for CCAD. mental and traumatic factors have been identified as
Methods: A PubMed search was performed utilizing the key
etiologic variables.
words: carotid artery dissection, dissection, arterial dissection,
Recently, a correlation with cervicocerebral arte-
cranial artery dissection, scuba, diving, scuba diving.
rial dissection and scuba diving has been postulated. In
Articles including reports, reviews, trials, case series, and letters
were considered. Each report was critically dissected for 1995, Nelson first reported a case of carotid dissection in
information specific to the dive itself and the diver and analyzed a diver [1]. Since then, numerous others have presented
for similarities and consistency with known risks. carotid, vertebral and intracranial artery dissection
Results: Twelve (12) reports of CCAD associated with scuba occurring contemporary with scuba diving. Underwater
diving were identified. Activities involved with scuba diving appear diving unquestionably subjects an individual to a unique
to be consistent with CCAD risk factors. It is unclear if hyper- environment. Diving subjects individuals to minor
baric stress and physiological changes during a dive traumas: e.g., jumping from heights to enter the water,
present specific risk. Trauma – e.g., environmental protection constrictive environmental protection in the form of
and activities associated with diving – was identified as a wetsuit and drysuits as well as sustained head and neck
common risk factor in all cases. Ten (10) cases involved positions. Hyperbaric stress, submersion and water
arteries at anatomic sites commonly associated with dissections.
conditions all interact on human physiology while
Seven divers documented to have dive profiles suspicious of
using scuba. Since a possible link between diving and
decompression sickness were identified.
arterial dissection is proposed it then becomes reason-
Conclusion: There appears to be a correlation with minor
traumas that occur with diving and CCAD. The inconsistency able to explore what, if any, are the unique contributing
of the dive-related specific information reported makes it factors that are present in this activity.
impossible for investigation of hyperbaric stress-related risk The intent of this report is to critically review the doc-
factors for CCAD to be analyzed. umented cases of CCAD associated with scuba diving
to establish some commonality among the patients.
The role of trauma in the development of CCAD is well
___________________________________________________________________________ established. Are there any traumatic stressors that may
KEYWORDS: carotid artery dissection; dissection; be mitigated while diving to minimize the risk of
arterial dissection; cranial artery dissection; scuba; CCAD? Does hyperbaric stress in and of itself present
diving; scuba diving a risk for CCAD?

Copyright © 2018 Undersea & Hyperbaric Medical Society, Inc. 65

UHM 2018, Vol. 45, No. 1 – CCAD AND SCUBA: IS THERE A LINK?

METHODS In a letter to the editor from Chojdak-Lukasiewicz,

A PubMed search was performed utilizing the key the case of a 27-year-old male diver was presented
words: carotid artery dissection, dissection, arterial dis- [2]. The dive profile and specifics of the dive were not
section, cranial artery dissection, scuba, diving, scuba reported, only described as having been conducted
diving. All articles including reports, reviews, trials, in “cold water.” Vertigo and ataxia were present on
case series, and letters were considered. Articles were initial evaluation. MRI demonstrated a right medulla
not limited to only those in peer-reviewed journals. oblongata infarct. Right posterior inferior cerebellar
Each report was critically dissected for information artery (PICA) dissection was demonstrated on a subse-
specific to the dive itself and the diver and analyzed quent computerized tomography arteriogram (CTA).
for similarities and consistency with known risks. Kocigit discussed a 32-year-old diver who presented
for treatment after “diving at sea” three days earlier [3].
RESULTS Persistent drowsiness was the only chief complaint.
Twelve (12) articles were identified as reporting on Risk factors for arterial dissection were unremarkable
CCAD occurring contemporary with scuba diving by physical and laboratory examinations. A left PICA
(Table 1). Information regarding diver, type of dive, territory infarct was discovered, and angiography doc-
equipment used, dive profile and past personal and umented dissection of the posterior medullary segment
family history was harvested from the articles. Only of the left PICA.
those cases where the diagnosis was confirmed by Minutes after a scuba dive in the Mediterranean Sea,
imaging were considered. Presentation of symp- a 37-year-old female noted left-sided neck pain and
toms, treatment and outcomes varied throughout the left facial paresthesia accompanied by a feeling of
reports. Since the purpose of this paper is to search for pressure in the left ear, described by Hafner [4]. The
similarities in risk factors and inciting events, details water temperature was reported as approximately
about symptoms and treatment were not deemed 22° C, and the dive conducted with “adequate
necessary. weighting and a well-fitting scuba cylinder.” The
Nelson reported on a 52-year-old male with “mini- patient endorsed a history of multiple sclerosis (MS),
mal” diving experience [1]. On the day of presentation which was stable. There were no cardiovascular risk
to the emergency department complaining of headache, factors other than a 15 pack-year smoking history. A
the diver reported he had made three dives: color Doppler duplex of the cervical arteries revealed
• to 10 meters of seawater (msw) with a bottom time decreased flow velocities in the LICA without evidence
of 25 minutes; of stenosis or demonstrable lesions. MRI and magnetic
• 25 msw for 30 minutes; and resonance arteriography (MRA) of the brain and
• 30 msw for 25 minutes. cervical and intracranial arteries was performed. A
The surface intervals were not elucidated. The headache 2-cm subcranial LICA dissection was noted, along
worsened after making two subsequent freedives to with changes consistent with MS.
5 msw. Konno presented a case of an 18-year-old male diver
On the following day, the diver was noted to have with a right vertebral artery dissection [5]. The report
dysarthria and dysphasia. His past medical history was was void of information about the dive itself. The pre-
positive for hypertension only, and family history was viously healthy patient was evaluated at a local hospital
non-contributory. Expressive aphasia was documented for right occipital headache and neck pain associated
on examination. Magnetic resonance imaging (MRI) with vertigo and visual disturbance. Decompression
showed several small left parietal infarcts and a left sickness was suspected; medical treatment resulted in
internal carotid artery (LICA) occlusion. no improvement of symptoms. The authors did not
Progression of the aphasia and sudden right hemi- elaborate on the specific treatment or if it included
paresis prompted an emergency arteriogram, which recompression therapy.
confirmed an occlusion of the (LICA) and a near-total Two weeks later the patient was noted to have a left
occlusion of the right internal carotid artery (RICA) upper quadrant hemianopsia. MRI and cerebral angi-
at the skull base. Bilateral carotid artery dissection ography demonstrated infarction in the right cerebellar
was confirmed on MRI. hemisphere and medial occipital lobe and occlusion of

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Table 1. Reported cases of CAD and diving

author age/sex diving history missing data PMH/fam Hx risk factors vessel location

Nelson 1 52/male 3 dives/ entry, HTN, non smoker, NS bilateral skull

35”at 10 msw, conditions, FMH-NC ICA base
30” at 25 msw, gear
25” at 30 msw
Chojdak- 27/male NS other than DP, entry, NS NS right IC
Lukasiewicz 2 cold water conditions, gear PICA

Kocigit 3 32/male “diving at sea” DP, entry, NC not left IC
conditions, present PICA
Hafner 4 37/female water-22°C, DP, entry, stable multiple NS left “sub-
adequate weighting conditions sclerosis, ICA cranial”
and well-fitting smoker
Konno 5 18/male NS, DCS DP, entry, NS NS right artery second
suspected conditions, vertebral segment
gear artery
Gibbs 6 38/male 36-m dive after entry, NS NS right skull
several hours of conditions, ICA base
diving, rapid direct gear
ascent, did undergo
Bartch 7 51/male 15” at 5 msw, entry, long smoking NS left skull
15” at 20 msw, conditions, history, ICA base
15” at 5 msw gear otherwise NC
Formento 8 32/male “deep scuba dive,” DP, entry smoker NS left NS
21°C water for conditions, ICA
3 hours, weight of gear
equipment “typical”
Brajkovic 9 52/male NS other than conditions, HTN, BPH, NS LICA skull
cold water gear tension headaches base
Fukuoka 10 51/male 60” at 20 msw entry, NS NS LACA IC
20 years’ diving conditions, except no PFO
experience gear or shunt
Mayer 11 35/female first scuba dive DP, entry, OI? OI bilateral C2 level,
conditions, vertebral, origin of
Shurnik 12 48/female 90” at 8 msw, DP, entry, NS NS LICA distal
carried heavy bag conditions, extracranial
after the dive gear

DP – dive profile; HTN – hypertension; FMH – family medical history; PMH – past medical history; NC – non-contributory,
NS – not stated; ICA – internal carotid artery; PICA – posterior inferior cerebellar artery; IC – intracranial; DCS – decompression sickness;
MCA – middle cerebral artery; HTN – hypertension; BPH – benign prostatic hypertrophy; PFO – patent foramen ovale

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the second segment of the right vertebral artery. non-contributory. A LICA dissection was subsequently
In a paper published by Gibbs, a 38-year-old experi- documented on MRI/MRA. There was no mention of
enced female diver was retrieved from the surface after cerebral infarction or other focal neurologic symptom
losing consciousness while making a rapid direct ascent. elucidated in the report.
She had made a 36-msw dive after several hours of Following a scuba dive in cold water, a 52-year-old
diving [6]. The diver suffered nausea, vomiting, neck male complained of persistent neck pain with pain ra-
pain and headache. She demonstrated a right gaze pref- diating behind the left eye. As reported by Brajkovic, the
erence, expressive aphasia and a left pronator drift. continuing headache – associated now with left-sided
Recompression utilizing the U.S. Navy Table 6 re- facial edema, left ptosis, myosis and neck pain – led the
sulted in resolution of the left-sided weakness. However, patient to seek evaluation [9]. Incomplete Horner
her expressive aphasia persisted. An acute right cortico- syndrome was discovered as well as dysesthesia of the
parietal stroke was seen on CT and MRI. MRA revealed left scalp and leftward deviation of the tongue.
a RICA narrowing at the skull base with a luminal hema- The patient’s past medical history was remarkable
toma. Right internal carotid artery dissection was sub- for hypertension, benign prostatic hypertrophy and
sequently confirmed on CTA. The authors did discuss tension headaches. Magnetic resonance imaging re-
a relationship between her recent diving experience but vealed dissection of the LICA near the skull base and
conceded the dissection was linked to scuba diving an incidental left MCA aneurysm.
coincidently. Fukuoka described a 51-year-old male with 20 years
Bartch described a 51-year-old male who suffered an of dive experience who suffered sudden right hemipa-
embolic stroke contemporary with scuba diving [7]. resis during a one-hour scuba dive to 20 msw [10]. On
The patient made an uneventful dive with the following presentation to the hospital he displayed a right hemi-
profile: 15 minutes at 5 msw; 15 minutes at 20 msw; paresis. A head CT did not demonstrate hemorrhage
and 15 minutes at 5 msw. Three hours after surfacing or infarcts. MRI/MRA revealed hyperdense areas in
he complained of slurred speech and problems with the left superior frontal and cingulate gyri and stenosis
word-finding, with symptoms lasting 15 minutes. of the left anterior cerebral artery (LACA). Additional
Two days later he noted difficulty in tongue movement, MRA imaging subsequently demonstrated a double
dysphagia and left-sided headache. Horner syndrome lumen finding consistent with dissection of the LACA.
was observed four days later. Patent foramen ovale or other right-to-left cardiac shunt
Examination revealed leftward tongue and uvula was ruled out.
deviation. The patient endorsed a long history of ciga- A genetic collagen disorder was reported by Mayer
rette use but had an otherwise unremarkable past or in this 35-year-old female who suffered multiple cere-
family history. MRI/MRA confirmed several small bral artery dissections following her first scuba dive [11].
embolic infarcts in the left middle cerebral artery Eight days after her uneventful scuba dive, she was
(MCA) territory and occlusion of the LICA below evaluated for vertigo, nausea and headache. Her symp-
the skull base. Carotid dissection was confirmed by toms intensified over several days, and she was ob-
the presence of an intramural hematoma on MRA. served to have nystagmus, right facial weakness and
Minutes following a “deep scuba dive,” a 32-year-old severe ataxia. She subsequently required intubation for
male diver experienced left neck pain and a full feeling severe dysphagia and respiratory compromise. Sub-
in his left ear, as reported by Formento [8]. This ex- sequently, she displayed bilateral brainstem deficits,
perienced diver had conducted an uneventful dive right Horner syndrome, left facial weakness, bilateral
in 21°C water for three hours. The other details of the palate and tongue weakness, nystagmus and ataxia.
dive were not reported except to state that the weight General physical examination revealed bluish sclerae.
of his equipment was typical for recreational diving. The past medical and family histories were non-contrib-
Six days later he was found to have Horner syndrome, utory. MRI and angiography demonstrated left superior
with ptosis and myosis. He did endorse cigarette use. cerebellum and right posterolateral medulla infarction.
Past medical history, detailed neurologic examination, Bilateral vertebral artery dissections were seen at the C-2
laboratory testing and CT of the neck and head were level along with dissection of the origin of the LICA.

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The presence of the blue sclerae prompted a work-up for genetic and environmental risk factors in 960 patients
a suspected genetic abnormality which demonstrated with CCAD and stroke and 658 ischemic stroke patients
findings consistent with osteogenesis imperfecta. without CCAD. One intriguing comparison was the
Skurnik reviewed a 48-year-old male who experienced relationship between time of year, autumn-winter vs.
severe pain on the left neck and face two days following spring-summer, and the occurrence of CCAD. A signifi-
a dive to 8 msw for 1.5 hours [12]. He also complained cant majority of patients suffered CCAD in the autumn-
of dysgeusia (all food tasted bitter) and anisocoria. winter months, (P=0.007). Additionally, more infec-
He could recall 10 minutes of some dizziness and stiff tions were noted in the autumn-winter group. This
neck immediately upon surfacing. He noted carrying connection could suggest that the presence of a
a heavy dive bag on his left shoulder after the dive. current or recent infection might be related to
Horner syndrome was confirmed on his initial exam- CCAD.
ination. A CT scan was normal, and the MRA demon-
strated dissection of the distal part of the extracranial Recent infections
LICA. Grau presented three cases of CCAD associated with
recent infection [18]. These patients suffered both
DISCUSSION carotid and vertebral artery dissection, with concurrent
Spontaneous vs. traumatic CCAD febrile respiratory infections. In fact, one patient experi-
Cervicocerebral artery dissection may be categorized enced a second dissection five years following a previous
as either spontaneous or traumatic. Spontaneous dissec- one, both associated with infection. All patients in this
tion implies a lack of trauma as a contributing factor. small series denied any recent trauma or congenital or
Controversy exists as to whether there are cases with a hereditary conditions known to be associated with
true absence of an instigating trauma or an injury that CCAD.
may be trivial and overlooked. A group of 24 non-diving Triggering mechanisms that may contribute to CCAD
patients who sustained a stroke related to a confirmed associated with a recent infection may include me-
carotid or vertebral artery dissection was compared chanical stress caused by vomiting or coughing,
with matched subjects who had stroke without dissec- injury to the arterial wall from antibiotic use, or
tion [13]. In the dissection group, 17 (71%) reported a increased inflammatory parameters [19].
history of trauma prior to presentation. Three categories
of trauma were described: intense physical efforts, jerky Altered vascular function
or abrupt neck movement, and sustained extreme neck The hyperbaric environment elicits many physiologic
positions. Suspected head movements included sporting changes on the human body, including altered vascular
activities that involved hyperextension or lateral devia- function and vasospasm [20]. A link between cerebral
tion of the neck. Intense physical effort, including the vasospasm and cervical artery dissection has been
lifting of heavy objects, has been identified as an incit- previously established by Mawet, et al. [21]. Their
ing event. Hyperextension of the neck has been cited as observations “strongly suggest that the association of
sufficient trauma in the development of CCAD [13-15]. reversible cerebral vasoconstriction (RCVS) and cer-
vical artery dissection is unlikely by chance.” RCVS
Risk factors associated with CCAD is associated with numerous conditions, including
Diving vs. non-diving events migraine and thunderclap headaches [22]. Certain
Additionally, events common to scuba diving have medication commonly used by divers – e.g., pseudo-
been implicated in CCAD. These include: prolonged ephedrine – may cause vasoconstriction.
neck hyperextension; falls from less than 3 meters; Cerebrovascular dysfunction occurring during scuba
lifting heavy objects; Valsalva maneuver; and external diving has been documented [23]. Sixteen (16) divers
vasocompression [13-16]. Data from the Cervical Artery were monitored for MCA and PCA blood flow follow-
Dissection and Ischemic Stroke consortium reported ing no-decompression dives in a water temperature
on a cohort of 1,618 patients with ischemic stroke not of 15°C and using air. Following the dives, increased
associated with diving [17]. The study compared velocities were observed in the anterior and posterior

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cerebral arteries as recorded by transcranial Doppler. the lack of frequency of HCTD or other genetic risk
The proposed reasons for these findings were changes factors in the series of scuba-related dissections, it ap-
in arterial blood gases, cerebrovascular endovascular pears that this would not be a significant causal factor.
dysfunction and cerebral vasospasm.
Other evidence of the correlation between vascular Internal carotid arteries
changes with decompression stress has been shown to In the 12 cases presented, involvement of multiple ves-
be a result of microparticle shedding [24]. Lambrechts sels in the same patient was reported twice [1,11].
studied nine experienced divers who made a decom- A total of 15 arteries were affected in the reported cases.
pression dive in 15°C water [25]. After the experimental The ICA was affected in nine arteries, with seven on
dive, impairment of both cutaneous microcirculation the left side and two on the right. Intracranial arteries
as well as dysfunction in large conduit arteries was – two PICAs and an ACA – represented three of 15
observed. Intracardiac bubbles were also detected in all vessels with dissection. The vertebral artery was identi-
divers without any suspected cases of decompression fied in three of the affected arteries. In the seven divers
illness (DCI). There was no correlation between degree with ICA dissections, the location was described as at
of vascular function and bubble formation. It was the skull base in four, “sub-cranial” in one, distal part
therefore unclear how hyperbaric stress induced these of extracranial in one, and at the carotid origin in one.
changes. The results demonstrated that both macro- and One author did not report the location. The skull base
microvascular dysfunction resulted from the study is where the cervical carotid passes through the carotid
dives. Although it is evident hyperbaric stress alters foramen and courses through the petrous bone (Fig-
vascular function, it has yet to be proven these ures 1 and 2). This anatomical location leaves the artery
changes contribute to CCAD in divers. susceptible to trauma and is the most common location
for ICA dissections to occur [28,29].
Arterial abnormalities and hereditary disorders
Primary arterial abnormalities or anatomical varia- Diving-related vertebral dissection:
tions have been documented in patients with CCAD hyperextension, direct trauma, equipment
[13]. Anomalous arterial anatomy was documented in Regarding the vertebral dissections, the V2 portion,
several patients with CCAD as well as arterial fibro- defined as that part of the vertebral artery contained
muscular dysplasia. Genetic factors associated with within the foramina of the cervical vertebral transverse
connective tissue anomalies identified in patients with processes, is reported to be particularly vulnerable
CCAD include Ehlers-Danlos syndrome, Marfan’s syn- to stretching and tearing [28]. This observation is
drome and osteogenesis imperfecta (OI) [23]. OI was consistent with the location of the described diving-
diagnosed in a patient sustaining multivessel dissections related vertebral dissection. Caplan noted as well that
following a scuba dive [11]. In an interesting review of stretching movements are probably responsible for
84 patients with CCAD, none were identified with either contributing to intracranial dissections [28].
clinical or molecular finding meeting diagnostic criteria The location of arterial involvement and its relation-
for hereditary connective tissue disorder (HCTD) [27]. ship to stretching or movement suggests the physical
However, 96% displayed at least one historical, physical activities of scuba diving may be a common risk factor.
and/or symptomatic feature of 68 findings known to be First, entry to the water while diving occurs in several
associated with HCTD. This led the authors to conclude ways. Divers may simply walk into the water from the
that “systemic aberrations of connective tissue might be shore or make a shallow jump from a platform. One
implicated in the pathogenesis of the disease (CCAD).” common form of entry is the “giant stride.” The giant
Only one of the reported cases clearly displayed a stride is typically utilized when entry is gained from
hereditary disorder known to be a risk factor for an elevated platform or boat deck. Divers positions
CCAD: osteogenesis imperfecta [11]. The other reports themselves at the edge of the platform and take a
failed to provide any specific information regarding large step entering the water feet-first. Hypothetically,
hereditary or other genetic factors, except Kocigit, performing this entry may cause hyperextension or
who reported the absence of these factors [3]. Given direct trauma to the neck. Once in the water divers will

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Figure 1: Angiogram demonstrating carotid artery entering the petrous

bone. Solid line – base of the skull Arrow – point where the cervical
portion of the carotid artery enter the fixed bony structure.

Figure 2: ICA dissection originating at the skull base. ➠ FIGURE 2

attempt to maintain neutral buoyancy. Their attitude of that size can weigh approximately 15 kg. Larger-
in the water column ideally will be horizontal. In this capacity cylinders obviously weigh more, and some
position the diver is more streamlined and requires divers utilize more than one at a time. In addition
less energy. The neck will be hyperextended and to other equipment required, the total weight bur-
frequently rotated to allow the diver to observe the sur- den could be a risk factor for CCAD. External com-
rounding environment. Thomas has listed sustained pression of the neck may occur as well from various
extreme positions of the neck and abrupt head move- straps securing the tank. Interestingly, there were no
ment as potential sources of trauma in CCAD [13]. reports of CCAD associated with the use of rebreather
Another common feature in several reported scuba- units. Typically, these units are heavier than open-circuit
related dissections is the environmental protection equipment and are utilized often on technical dives.
required. To prevent hypothermia and remain comfort-
able in the water, divers may employ either a wetsuit or DCI and CCAD
drysuit. Both garments employ tight seals or neoprene The role of decompression illness (DCI) in the etiology
around the neck. Sufficient external compression, which of CCAD is unknown. Analysis of known dive profiles
is possible with various dive suits, has been implicated and presenting symptoms in the reported cases could
in CCAD [14,30]. Diving in cold water, which neces- bring a suspicion of DCI in these divers. In fact, two of
sitates use of environmental protection, was reported the 12 divers discussed were treated with recompression
in three cases. therapy [5,6]. In the case presented by Gibbs, the diver
Scuba diving is an equipment-dependent sport, and made a rapid ascent from depth and lost consciousness
the scuba cylinder is obviously an essential component. immediately, which would be consistent with an arterial
The cylinder, manufactured from aluminum or steel, gas embolism [6]. Additionally, this diver was reported
is worn on the diver’s back and secured there by straps to have made a 36-msw dive after several hours of
or a buoyancy compensation device. An empty cylinder diving, which would have increased to risk for DCS.

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Nelson reported the diver as making three dives. Per CONCLUSION

the U.S. Navy dive tables, none of the dives exceeded The typical locations of reported scuba-related CCAD
the no-decompression limits but would have violated suggest the physical activities of scuba, trivial trauma,
their directive of no more than two dives within a and equipment represent a common feature. Trauma
12-hour period [31]. Since these were repetitive dives, associated with the prolonged extension and rotation
however, the surface intervals would dictate the overall of the neck as well as the eternal compression from
nitrogen load and the risk of DCS. environmental protection garments could be a sufficient
Alonso Formento and Fukuoka similarly presented trigger for CCAD. The giant-stride entry may induce
dive profiles that could be suspicious for DCS [8,10]. significant traction on the carotid and vertebral arteries
One dive was described as a “deep scuba dive” in cold sufficient to cause a dissection. Vasoconstriction that
water for three hours. The other was a one-hour dive occurs from hyperbaric stress has yet to be correlated
at 20 msw, which is the no-decompression limit for with CCAD, as it has in the non-diving population.
depth. One subject’s presentation was inconsistent with A standardized approach in the reporting of these
CCAD and cerebral infarction. That diver’s only cases should include a description of the presence or
symptom was persistent drowsiness, which has been absence of known risk factors for CCAD. Similarly,
described with DCS [32]. factors such as composition of the dive gas, water
Whether CCAD is yet another manifestation of DCI temperature, decompression versus no-decompression
remains a question. An interesting hypothesis could dive, specific details of the dive itself and dive pro-
involve the role of microbubbles in disruption of the file, body habitus, and past personal and family history
vaso vasorum. Commercially available microbubble so- should be consistently reported. Vague descriptions
lutions have been used to image the vaso vasorum of of dives, such as in Alonso Formento’s report, leave
the coronary arteries to identify unstable plaques [33]. details unavailable for analysis [8]. A report of a “deep”
Filling of the vaso vasorum with microbubbles is ac- dive for three hours, which would be an atypical recre-
complished by intra-arterial injection of the contrast ational dive, lacks details required for thorough review.
solution. Intravascular ultrasound can then provide Future standardized and detailed reports of CCAD
diagnostic images of the vaso vasorum. It could there- and scuba diving, would aid the dive medicine com-
fore be feasible that nitrogen bubbles arising from munity in the analysis of these cases. Subsequently, a
decompression might enter the vaso vasorum. risk factor unique to scuba diving may be identified
While bubbles in the vaso vasorum have never been and a possible mitigation of risk offered.
documented in DCS, their presence can conceivably n
lead to intramural hemorrhage and CCAD. The author declares that no conflicts of interest exist
with this submission.

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