Airway Trauma in a Patient on Dual Antiplatelets: When it Rains, It Pours

INTRODUCTION Intracranial atherosclerotic disease (ICAD) is the most common vascular lesion in patients with acute ischaemic stroke worldwide.1 Standard dual antiplatelet therapy (DAPT) is important in the treatment of patients with ICAD as a medical therapy and also in patients undergoing endovascular stent placement for the prevention of thromboembolic events. The most feared side effect of DAPTs is bleeding, with the gastrointestinal system being the most common site.2 During anaesthesia induction, even minor trauma during the laryngoscopy and intubation in such patients can lead to significant bleeding. Complications such as aspiration pneumonitis, acute lung injury, secondary infections and lung collapse can make even a small bleed in the respiratory tract fatal.3 We describe our experience in managing a patient who underwent ICAD stenting on dual antiplatelets and had a haemorrhagic event. CASE REPORT A 66-year-old male patient with a history of long-standing type-2 diabetes mellitus, hypertension and asthma well controlled on medications, presented with complaints of numbness in the right hand and both feet and unstable gait for 4 days. The patient had no history of any previous stroke/transient ischaemic attacks, facial weakness, slurring of speech, dysphagia, ischaemic heart disease, convulsions, visual disturbance and headaches. The patient was conscious, oriented to time, place and person, normal vitals and normal power in all four limbs (National Institutes of Health Stroke Scale-4). A non-contrast computed tomography head was done which revealed chronic lacunar infarcts seen in periventricular white matter and acute to subacute infarcts in right corona radiata, subcortical white matter of right precentral gyrus and adjacent periventricular white matter. The cerebral digital subtraction angiography (DSA) showed 90% stenosis in the right distal M1 segment of middle cerebral artery (MCA). The patient was planned to undergo endovascular stent placement in the M1 segment of MCA under general anaesthesia. Pre-operative blood investigations were within normal limits. The patient was kept Nil per Os for 8 h for solids and 2 h for water and was given a tablet of ticagrelor 180 mg, a tablet of Ecosprin 150 mg and a tablet of atorvastatin 80 mg. After obtaining the written informed consent, the patient was shifted to the DSA suite. Pre-operative standard American Society of Anaesthesiologists monitors such as electrocardiogram, non-invasive blood pressure, pulse oximetry, alongside neuromuscular monitoring (NMT) and bispectral index (BIS) were attached. The right radial artery was cannulated using a 20G cannula for invasive blood pressure monitoring. He was pre-oxygenated for 3 min and was induced using an injection of fentanyl 1.5 μg/kg and propofol bolus titrated to loss of verbal response and BIS value <60. After checking the ability to ventilate, the patient was administered an injection of rocuronium 50 mg intravenous and an injection of lidocaine 1.5 mg/kg was administered 90 s before intubation. On direct laryngoscopy, the patient was found to have the Cormack–Lehane grade of III-b. The patient was intubated with 8.0 mm internal diameter/polyvinyl chloride/cuffed endotracheal tube (ETT) using a Portex™ bougie (15 F) under the videolaryngoscopic view using a BPL videolaryngoscope VL 02 (manufactured by BPL Medical Technologies, Bangalore, India). The maintenance of anaesthesia was done using oxygen: air mixture, sevoflurane and atracurium boluses as per the NMT values and was ventilated using the volume-controlled mode of ventilation using dragger machine with settings of tidal volume 500 mL, respiratory rate (RR) 14 breaths/min and positive end-expiratory pressure (PEEP) 5 cm H2O. About ½ h into the procedure, it was noticed that the peak airway pressures of the patient increased from 22 cm H2O to 38 cm H2O and after a while, the patient could not be ventilated. Endotracheal suctioning was done, which revealed the presence of blood clots and fresh blood in the ETT. Even after repeated suctioning, the patient could not be ventilated, hence the the ETT was changed over a tube exchanger which enabled the authors to ventilate the patient and brought down the peak airway pressure to 26 cm H2O. There was a near-complete occlusion of the lumen of the old ETT due to the presence of blood clot while there was a continuous ooze of blood through the new ETT. The patient was given an injection of dexamethasone 8 mg and an injection of tranexamic acid 1-g infusion and epinephrine (1 mg in 20 mL dilution) was instilled endotracheally. The bleeding was controlled and a fibre-optic bronchoscopy was done but it failed to show any mucosal rent causing the bleed. After the stabilisation of the patient, the procedure was continued. Post-operatively, it was decided to ventilate the patient given his chest status. A chest X-ray (CXR) done post-operatively Figure 1a revealed patchy, diffuse, homogenous opacities in the right upper and right lower zones along with blunting of the right costophrenic and cardiophrenic angles of the right lung. The arterial blood gas analysis showed type-2 respiratory failure. The patient was ventilated with right-up position using the pressure-controlled mode of ventilation with an inspiratory pressure of 20 cm H2O, RR = 20 breaths/min and PEEP = 10 cm H2O. Postural drainage was emphasised, closed-loop suction was attached and the patient was started on a broad-spectrum antibiotic and injection of dexamethasone 8 mg 8th hourly. The lung mechanics and the CXR Figure 1b of the patient improved and the patient was extubated after 2 days. After the active haemorrhage was controlled, DAPTs were continued because of the high thrombotic risk involved, and the patient was discharged with no residual deficits.Figure 1: (a) Diffuse, homogenous opacities in the right upper and right lower zones with blunting of the right costophrenic and cardiophrenic angles of the right lung. (b) Clearing up of lung fieldsDISCUSSION The patients undergoing ICAD stenting are usually started on DAPT to prevent recurrent stroke. Bleeding is a major complication of DAPT. Bleeding due to airway trauma although rare can be of clinical significance, especially in the patients on antiplatelets. The airway bleeding and endotracheal/endobronchial bleeding into the lungs can lead to aspiration pneumonitis progressing to acute lung injury or even adult respiratory distress syndrome. This also makes the lungs prone to develop secondary bacterial infections. The blockage of any bronchus can also lead to the collapse of the lung. The prior clinical trials done to study the major bleeding events due to DAPT found that the pulmonary system was 4th–7th most involved site.4 Although rare, airway bleeding can prove to be life-threatening. The bleeding can be triggered at the time of laryngoscopy and intubation. In cases of unanticipated difficult intubation, the traumatic complication rate can range from 0.5% to 7%.5 Hence, laryngoscopy in such patients should be done with the utmost care, preferably by the senior most anaesthesiologist as even trivial trauma in can lead to torrential bleeding. Furthermore, adequate preparation should be done to encounter any difficult airway as the goal should be to minimise the airway fiddling. The force used during the placement of the bougies has to kept as low as possible, the advancement of the bougie should be restricted to < 25 cm in average adults, withdrawing the bougie a couple of centimetres before railroading ETT and the railroading of ETT under the laryngoscopic view are the few tricks to avoid and minimise trauma.5 The literature available regarding airway trauma during intubation due to bougie suggests conservative management with endotracheal suctioning.6 In case of profuse bleeding not controlled by initial measures, fibre-optic bronchoscopy can be done to locate the trauma. The measures used to control the bleeding include the endobronchial instillation of tranexamic acid (500 mg in 20 mL) and epinephrine. To balance the risk of life-threatening bleeding and the neurologically threatening risk of stent thrombosis becomes very tricky in such cases. Hence, the antiplatelet therapy has to be started as soon as the airway/pulmonary bleeding has been adequately controlled. CONCLUSION The use of DAPT makes the upper and lower respiratory tract very assailable to trauma and bleeding. Hence, utmost care should be taken to avoid any such complications. Although very rare, even spontaneous pulmonary haemorrhage have been reported in patients using DAPT. A careful eye must be kept for detecting any such convolution and a multidisciplinary approach to be followed to expedite diagnosis and optimise treatment. Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understands that his name and initials will not be published and due efforts will be made to conceal his identity, but anonymity cannot be guaranteed. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest. Declaration of generative AI and AI-assisted technologies in the writing process During the preparation of this work, the authors did not use any Artificial intelligence tools/services.