Bilateral temporomandibular joint dislocations post-bronchoscopy in a case of paclitaxel-induced pneumonitis

Discussion

The TMJ is formed between the mandibular condyle and the mandibular fossa in the temporal bone of the skull. It is reinformed by surrounding muscles of mastication and its associated ligaments. Dislocation involves the condylar process being displaced from the mandibular fossa and the inability for it to reposition back to its usual position. Anterior dislocation is the most common form, with medial, lateral and superior dislocation as other possibilities.3 TMJ dislocation is a rare complication of transoral endoscopic procedures and few cases have been described.4 Other procedural causes include endotracheal intubation, transoesophageal echocardiogram, otolaryngology and dental procedures. Identified risk factors include previous dislocations, prolonged procedure time, increased age and relaxation of the masseter and temporalis muscles by sedation.5

TMJ dislocation is usually diagnosed on clinical examination. Patients often have inability to close their mouths, slurred speech and jaw pain and stiffness. Reduction should be performed promptly and a delay in treatment increases the risk of muscular spasms, pain and increasing difficulty in relocating the joint. No specific recommendations exist for the prevention of TMJ dislocations during bronchoscopy. Approapriate surveillance and investigations should be undertaken in patients with concerning symptoms to allow rapid relocation should such a complication occur. In this case, there were no obvious patient-related risk factors that predisposed to dislocation; it was likely that the prolonged procedure time and sedating medications were the main contributors. This risk could have been moderated by introduction of the bronchoscope via the nasal passage, thus avoiding the use of a mouth guard which held the jaw in an open position. Bronchoscopy under general anaesthesia usually reduces procedure time, but it does not appear to mitigate the risk of dislocation.6

Hypersensitivity pneumonitis is a respiratory syndrome usually caused by an offending agent that results in a delayed allergic reaction affecting the alveoli, terminal bronchi and alveolar interstitium of the lung. Usually it is caused by inhaled antigens that are less than 5 μm in diameter, reaching the distal airways. Type IV hypersensitivity reaction is one of the mechanisms behind this syndrome, characterised by bronchiolocentric interstitial mononuclear infiltration, poorly formed non-necrotising epithelioid cell granulomas and diffuse inflammation. This is mediated by T-lymphocytes with T-cell migration to the lung tissue. Th1-cytokines play a key role, with a gradual increase in CD 4+and the CD4+/CD8 +ratio,.7

Paclitaxel is a vinca-alkaloid cytotoxic antimicrotubule agent that is used to treat a variety of tumours, including locally advanced breast cancer. Type 1 (immediate) hypersensitivity reactions to paclitaxel are well recognised and usually characterised by dyspnoea, hypotension, wheeze and urticaria, mediated by immunoglobulin E. They usually occur within the first or second dose and are managed with premedication and desensitisation protocols.8

Type IV (delayed) hypersensitivity reactions are rare and present subacutely. It was first described by Fujimori et al 9 in a case of cell-mediated interstitial pneumonitis, supported by a positive leucocyte migration inhibitory test, lymphocytosis in the bronchoalveolar lavage and interstitial and alveolar mononuclear cell infiltration on lung biopsy.6 Paclitaxel induces a cell-mediated reaction with migration of the activated lymphocytes to the lungs. Clinically, paclitaxel-induced pneumonitis can present as a spectrum of disease severity. It usually responds well to drug cessation and tapering corticosteroids; however, mortality has been reported in up to 37% of patients of paclitaxel-induced pneumonitis, with most of these developing rapid respiratory failure requiring ventilation.8 Radiologically, the presence of bilateral interstitial ground glass opacities is consistent with drug-induced pneumonitis and has been described particularly in relation to paclitaxel in case reports.9

In conclusion, TMJ dislocations need to be considered in the evaluation of a patient with suggestive symptoms postbronchoscopy; particularly in transoral and protracted procedures with use of higher-level muscle relaxant medications. The increasing complexity of bronchoscopic procedures and increased duration of the procedures with the advent of new modalities such as endobronchial ultrasoundUS render a greater awareness of the risk for dislocation prudent. Pulmonary toxicity from paclitaxel and in particular, delayed hypersensitivity, needs to be considered in patients presenting with insidious onset dyspnoea and concerning radiological change. A low threshold for lung biopsy should be considered with cessation of the drug, until definitive diagnosis be made.