Bedside Monitoring of Cerebral Blood Flow in Traumatic Bilateral Internal Carotid Artery Injury
We report the possible application of a combined noninvasive monitoring of brain perfusion for the management of severe traumatic bilateral internal carotid artery (ICA) injury. A 15-y-old boy (body weight, 65 kg; height, 165 cm) was admitted to pediatric intensive care unit after a motorbike road accident: he suffered from a craniofacial trauma, having bilateral mandibular and right radius fractures. He was alert, somewhat confused (glasgow coma scale 13), whereas his cardiorespiratory status appeared stable, with no oxygen need nor signs of ongoing blood loss. Electroencephalography recording showed slight diffuse slowing, without lateralization. On admission, both brain and spine computed tomography (CT) showed the absence of injury, but revealed parapharingeal bleeding. Gaseous bullae were found in the lateral-cervical region, behind the mandibular angle. A CT-angiographic assessment (Fig. 1) revealed a pseudo-aneurysmatic lesion of the right ICA (21×9 mm). The left ICA showed a filling defect consistent with a dissection resulting in marked endoluminal stenosis. Internal jugular veins were compressed bilaterally. During the first few hours his condition progressively worsened due to a marked swelling of the lateral-cervical and submandibular regions, causing airway obstruction. Right othorragia and retroauricolar ecchymoses appeared. Because of impending respiratory failure, he underwent nasotracheal intubation and controlled ventilation under deep sedation with analgesics. Early transcranial doppler assessment was markedly abnormal bilaterally, whereas prolonged bifrontal near-infrared spectroscopy monitoring confirmed a normal cerebral oxygenation and permitted a noninvasive frontal cortex vascularization evaluation. At selective cerebral arteriography, a flow compensation was demonstrated from the right ICA through the anterior and posterior communicating arteries. Subsequently, the boy underwent a right ICA stenting, whereas left carotid artery flow was maintained by collateral circulation until spontaneous flow restoration was achieved. Transcranial doppler tracings improved substantially on day 15, having normal flow at M1 tract of middle cerebral artery bilaterally. Near-infrared spectroscopy monitoring was maintained until patient awakening. Low–molecular-weight heparin treatment was introduced early, together with antithrombin supplementation. A reactive thrombocytosis was evidenced, peaking on day 13 (plt 824×10E3/mcL); subsequently, he was given low-dose aspirin and clopidogrel. Assisted ventilation was needed for 15 days, and due to extubation failure and subsequent mandibular surgery, a percutaneous dilatative tracheostomy was made. Early postpyloric enteral nutrition was introduced. Blood pressure was controlled with clonidine and urapidil, to avoid both hypotension and hypertensive peaks. Clinical and radiologic evidence of pneumonia required antibiotic therapy. Bronchoalveolar lavage and blood cultures grew Pseudomonas aeruginosa and Klebsiella pneumoniae. One month postadmission the patient was alert, breathing spontaneously on room air and could be discharged from pediatric intensive care unit. The eventual clinical and neurological recovery was complete and tracheostomy was removed. Late brain CT demonstrated a minimal hemorrhagic postischemic lesion in the deep frontoparietal area, clinically negligible.
This report highlights the usefulness of combined noninvasive techniques of cerebral blood flow evaluation, mostly in critically ill patients under deep sedation. Continuous bedside monitoring can help clinicians to schedule further cerebral imaging as well as timely detection of complications.1,2 A correct cerebral perfusion pressure can also be addressed, based on side-by-side assessment. Noninvasive bedside cerebral monitoring may become a standard in critically ill neurointensive patients also in pediatric patients.