Tracheal necrosis post endotracheal intubation is a rare but well-documented condition. Published data is mostly from case reports with 182 reported cases from 1966 to 2007 [1]. Factors that may lead to tracheal necrosis include prolonged intubation, elevated cuff pressure, tracheal blood supply disruption [2], bacterial and fungal infection [3], immunocompromised state, diabetes mellitus, upper airway surgery, esophageal surgery [4] and thyroidectomy [5]. Patients present with dysphonia, cough, dyspnea and respiratory failure. Histopathology findings include severe tracheal inflammation, pseudomembrane formation [3], mucosal ulceration and ultimately tracheal cartilage destruction [5]. Tracheal necrosis may lead to upper airway obstruction and tracheal perforation. Its treatment involves securing the airway with tracheostomy, debridement of necrotic tissue, acute infection treatment, management of co-morbidities and airway reconstruction once the infection has resolved [3, 4]. An early low-dose systemic corticosteroid treatment should be considered to reduce the risk of tracheal stenosis needing airway resections [6]. Tracheal necrosis poses a major challenge in airway management whereby ensuring a patent airway is the foremost step in any resuscitation attempts. We report the ultrasonographic (USG) upper airway findings of a patient with a tracheal necrosis post endotracheal intubation.

A middle-aged active smoker presented with productive cough with greenish sputum, reduced effort tolerance and noisy breathing for 2 weeks. He had no fever, throat discomfort or dysphagia.

One month prior, he was intubated for 4 days after a traumatic brain injury following a motor vehicle accident. He was extubated and discharged well after 2 weeks of admission. He was also treated for Streptococcus mitis bacteremia with 2 weeks of IV amoxycillin clavulanate and benzyl penicillin.

He had hypertension and type 2 diabetes mellitus (DM) which were not under any treatment as the patient opted for dietary control and observation. His hemoglobin A1C (HbA1C) upon admission was 10.5%.

On examination, he was conscious, alert, mildly tachypnoeic at rest with respiratory rate of 24 breaths per minute and saturating between 90 and 95% on room air. There was an audible stridor. Vital signs were otherwise normal. There was no recorded fever. Capillary blood sugar was 9.0 mmol/L. The rest of the physical examination was unremarkable. There were no evident micro- or macrovascular complications of DM.

Blood investigation showed a normal total white cell count (7.4 × 109/L). C-reactive protein (CRP) was elevated (6 mg/dL). His renal and liver profile were normal. Arterial blood gas showed no hypoxia or acidosis.

A flexible laryngoscopy showed thick mucopus inferior to the vocal cords which was difficult to remove with suction. There were parts of necrotic tracheal cartilage embedded in mucopus and debris obstructing the airway. A tracheal long segment upper airway obstruction with impending airway emergency was suspected. A bedside upper airway USG using the handheld Vscan Extend machine (GE Healthcare, Chicago, IL 60,661, USA) showed an irregular, jagged air-mucosal interface (AMI) at the level of the 1st (T1) and 2nd (T2) tracheal ring (Fig. 1). Comet tail artefacts were also seen beneath the abnormal AMI. Flexible bronchoscopy using a large-bore scope was not attempted due to fear of tracheal collapse.

(a) Axial USG view of T1. Note the jagged appearance (arrowhead) of the AMI. (b) Sagittal view of the trachea. Note the comet tail artefact (arrow) beneath T1 (asterix)

Computed tomography (CT) of the neck and thorax was showed a focal, short-segment endoluminal mucous secretion within the trachea at the subglottic region at the level of the 6th and 7th cervical vertebrae, 8 cm above the carina, along a length of 3.5 cm (Fig. 2). Tracheal wall irregularity was seen in this region with minimal wall thickening. There was also a poor fat plane. No goiter or lymphadenopathy were found. The lungs and mediastinum were normal.

(a-d) Contrast enhanced CT of the neck and thorax in axial and sagittal view at thyroid level. Lung window (a and b) demonstrates a focal, short-segment endoluminal mucous secretion within the trachea (arrow) at the subglottic region, along a length of 3.5 cm (double arrow). The tracheal wall is irregular with circumferential thickening (arrowhead) and luminal narrowing on soft tissue window (c and d)

A direct laryngoscopy under general anaesthesia (GA) was done. Removal of slough and necrotic tissue with tracheostomy was done to secure the airway (Fig. 3). Intraoperatively, a necrotic segment of the trachea was seen 2 cm from the free edge of the vocal cord, involving the 1st and 2nd tracheal cartilage. The inferior edge of the necrotic part was 5.5 cm from the carina. The bronchoscopy finding after the surgery was unremarkable.

(a-b) Direct laryngoscopy. Note the irregular tracheal mucosa (arrowhead) with pus dan debris adhering to the tracheal wall (short arrow). Necrotic tracheal cartilage (asterix) is seen in the trachea, causing obstruction. The posterior tracheal wall is covered with slough (long arrow)

Histopathology samples showed a fragment of benign hyaline cartilage displaying areas of dystrophic calcification. There was mild superficial infiltration by neutrophils admixed with fibrin. Parts of the superficial cartilage appeared pale and unhealthy with loss of chondrocytes within the lacunae. There was no granuloma and no evidence of malignancy. Cultures for fungus, mycobacteria and bacteria showed no growth.

The patient was discharged 1 week after the surgery. He had completed a 1-week course of amoxycillin clavulanate and nebulised ciprofloxacin.

His condition was complicated with tracheal stenosis, requiring multiple surgical procedures. Subsequent intraoperative cultures from the tracheal tissue grew Streptococcus mitis and Pseudomonas aeruginosa, both were sensitive strains and adequately treated with suitable antibiotics.