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Vol. 47. Issue 7.
Pages 411-413 (July 2023)
Vol. 47. Issue 7.
Pages 411-413 (July 2023)
Scientific Letter
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Vascular injury of the supra-aortic trunks in patients with traumatic brain injury
Lesión vascular de los troncos supraaórticos en pacientes con traumatismo craneoencefálico
Ana María Ferrete-Araujoa,b,
Corresponding author

Corresponding author.
, Daniel A. Godoyc,d, Francisco Murillo-Cabezasb
a Unidad de Neurocríticos, Servicio de Medicina Intensiva, Hospital Universitario Virgen del Rocío, Seville, Spain
b Departamento de Medicina, Facultad de Medicina, Instituto de Biomedicina de Sevilla (IBiS)/Centro de Investigaciones Científicas (CSIC)/Universidad de Sevilla, Seville, Spain
c Unidad de Cuidados Neurointensivos, Sanatorio Pasteur, San Fernando del Valle de Catamarca, Catamarca, Argentina
d Unidad de Terapia Intensiva, Hospital San Juan Bautista, San Fernando del Valle de Catamarca, Catamarca, Argentina
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Although infrequent, traumatic dissection of the internal carotid and vertebral arteries over their cervical trajectory is one of the leading causes of ischemic cerebral infarction (ICI) in young individuals. In this age group, the condition usually manifests in the absence of known risk factors, in the context of sports activities or secondary to cervical trauma, and the clinical manifestations (headache or neck pain, Horner’s syndrome, neurological deficits, etc.), while known, do not always manifest as such. In this context, the diagnosis is often not established or is established late – with the resulting ominous consequences for the patient.1 Ischemic cerebral infarction and its sequelae fundamentally result from the false lumen produced by endothelial or middle layer tearing, giving rise to stenosis, occlusion, pseudoaneurysms or embolization of the middle cerebral artery (MCA) from the thrombus formed at the dissection site.2,3 The concurrence of supra-aortic trunk dissection (SATD) with severe or moderate traumatic brain injury (S-MTBI) has received little attention in the medical literature, due to the diagnostic difficulties involved (the clinical manifestations tending to overlap or be confused) or to the inherent seriousness of traumatic brain injury (TBI), demanding immediate intervention. In this context, diagnostic omission or delay is even more common.4,5 Although the incidence of supra-aortic trunk dissection in the context of S-MTBI has not been clearly established, some publications estimate an incidence of 1%–9%, with a mortality rate of 20%–30%.6,7 The early diagnosis of SATD is crucial, since surgical or endovascular treatment (thrombectomy or stent placement) and anticoagulation or antiplatelet therapy,4 improve the prognosis. Digital subtraction angiography is the diagnostic technique of choice,8 though other tools such as CT angiography or MRI angiography are initially more often used in situations where dissection is suspected. The use of transcranial Doppler ultrasound (TCD) in the management of S-MTBI has become consolidated in Neurocritical Care Units, given the hemodynamic information it provides through calculation of the flow velocity (FV) in the arteries of the circle of Willis.5 However, very little has been mentioned on the screening capacity of TCD in detecting possible SATD in S-MTBI, even in recent publications,9 though some authors have already demonstrated that asymmetries of the FV and pulsatility index (PI) between both MCAs are valid suspicion criteria.10 We present a series of 15 patients with S-MTBI and SATD out of a total of 213 individuals with S-MTBI admitted to the Neurocritical Care Unit during the period 2017–2019, of which 50 had died at 6 months, underscoring the potential screening usefulness of TCD.

The main patient data are reported in Tables 1 and 2. In our series, all the patients were males with a mean age of 34 ± 13 years, and with no risk factors except for one case of Ehlers-Danlos syndrome. Traffic accidents predominated. Based on the Glasgow Coma Score (GCS), 11 patients were classified as presenting severe TBI (GCS ≤ 8 points) and four as presenting moderate TBI (GCS ≤ 14 points), with a predominance of diffuse lesions in the CAT exploration. Dissection mainly affected the internal carotid arteries, and in only two cases did dissection affect the vertebral arteries alone. Except for case 13, which manifested with Horner’s syndrome, the clinical manifestations in the rest of the cases were indistinguishable from those possibly attributable to TBI. The TCD study evidenced asymmetry, expressed as a mean 22% decrease in the FV and PI of the MCA corresponding to the damaged homolateral vessel, in all but two cases – one due to patient circulatory arrest. With the exception of case 4, where suspicion was delayed for 13 days, the mean time from suspicion to the diagnosis of dissection was 10 h. Computed tomography angiography was the technique most often used to establish the diagnosis, while anticoagulation or antiplatelet therapy was the most commonly used treatment – only 5 cases being subjected to stent placement. As a consequence of dissection (Table 2), 11 patients suffered cerebral infarction, fundamentally in the territory of the MCA. The exception was case 1, where the territory corresponding to the occluded vessel of the posterior circulation was affected. The mortality rate at 6 months was 20% (3 cases). According to the modified Rankin score, at 6 months only four patients had a good outcome; three suffered moderate disability; and 5 patients suffered a severe disability.

Table 1.

Characteristics of the studied series.

Case  Age  RF  Cause of TBI  TCDB  Vascular injury  Initial clinical manifestations 
36  No  Motorcycle  RCA + PICA  No focality 
51  No  Motorcycle  RICA  Left hemiparesis 
15  E. Danlos  Swimming pool  LICA+  Right hemiparesis 
34  No  Motorcycle  LICA  Right hemiparesis 
29  No  Sports  LICA  No focality 
28  No  Fall  RCA  Profound coma 
15  No  Fall  RICA  Profound coma 
42  No  Run over  LICA  No focality 
23  No  Car collision  LICA  Right hemiparesis + aphasia 
10  57  No  Fall from height  RICA  Left hemiparesis 
11  29  No  Motorcycle  RICA  No focality 
12  50  No  Motorcycle  RICA + LICA  Right + left hemiparesis 
13  45  No  Motorcycle  LICA + RCA  Horner + 3rd cranial nerve paralysis 
14  46  No  Motorcycle  LICA  Right hemiparesis 
15  47  No  Car collision  RICA  Left hemiparesis 

RF: Risk factor; TBI: Traumatic brain injury; TCDB: Lesion type according to Traumatic Coma Data Bank; RCA: Right cerebral artery; PICA: Posteroinferior cerebellar artery; RICA: Right internal carotid artery; LICA: Left internal carotid artery; E. Danlos: Ehlers Danlos syndrome; Horner: Horner’s syndrome.

Table 2.

Diagnostic tests,treatment and evolution of patients.

Case  TCD MCA  Time from suspicion to diagnosis  Definitive diagnosis  Treatment  Dissection brain injury  GOSE at 6 months  mRankin at 6 months 
Asymmetry  48 h  CTangio  Antiplatelet  Infarction 
Asymmetry  2 h  CTangio  Antiplatelet  Infarction 
Asymmetry  24 h  DigitAngio  Stent  Infarction 
Asymmetry  13 days  DigitAngio  Stent  Infarction 
Asymmetry  20 min  CTangio  Antiplatelet  No 
Asymmetry  1 h  CTangio  Anticoagulation  No 
No  30 min  CTangio  No  Infarction  Death 
Circulatory arrest  15 min  CTangio  Anticoagulation  No 
Asymmetry  20 h  CTangio  Anticoagulation  Infarction 
10  Asymmetry  10 h  CTangio  Stent  Infarction  Death 
11  Asymmetry  30 min  DigitAngio  Antiplatelet  No 
12  Asymmetry  7 h  CTangio  Stent  Infarction 
13  Asymmetry  40 min  CTangio  Anticoagulation  Infarction 
14  Asymmetry  15 min  CTangio  Antiplatelet  Infarction 
15  Asymmetry  24 h  DigitAngio  Stent  Infarction  Death 

CTangio: computed tomography angiography; DigitAngio: digital subtraction angiography; Antiplatelet: antiplatelet medication. Anticoagulation: anticoagulant therapy; GOSE: Extended Glasgow Outcome Scale; mRankin: modified Rankin score 8290 min (187,209) 138 h mean 10 h.

Despite the few patients involved, our study describes one of the most extensive and homogeneous series in this field, since the majority of publications on SATD are set within the context of polytraumatisms or trauma limited to the cervical region. In coincidence with the observations of other authors, in our sample the incidence of SATD was low, associated with high-energy TBI, and with similar mortality figures fundamentally related to the severity of TBI. In contrast, the important disability was associated with the extent of the cerebral infarction caused by the vascular injury. Another observation of note is the usefulness of TCD for suspecting SATD in the context of TBI. Although a difference in the FV values between the cerebral hemispheres may be explained by the presence of space-occupying lesions or greater inflammation in one hemisphere, in this case the decrease in velocities was accompanied by an increase in PI secondary to the elevation of intracranial pressure. In contrast, a decrease in FV associated with a drop in PI is suggestive of an ischemic process, where the decrease in PI expresses the attempt to compensate the perfusion defect with a decrease in distal cerebrovascular resistance or through collateral circulation. Possibly, the routine use of TCD in our study can explain why the time elapsed from suspicion to the diagnosis of SATD was shorter than in other publications – with the exception of the single case characterized by an excessive diagnostic delay.

We are of the opinion that in all patients with S-MTBI, the possibility of SATD should be considered and either confirmed or discarded as soon as possible. Although CT angiography is the most accessible and reliable screening tool, the findings may sometimes prove negative if the technique is performed very early. Transcranial Doppler ultrasound, which can be repeated as often as needed, may be an option capable of securing earlier detection.1,2,10

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