Non-infective supraglottitis: two cases of unusual aetiology.

Supraglottitis is an ear, nose and throat emergency where swelling of the laryngeal structures can threaten to fatally obstruct the airway. Most cases of supraglottitis are of infective origin but other rarer causes have been documented. We present two patients who presented with stridor and were found to have supraglottic oedema on fibreoptic nasolaryngoscopy. Both patients presented with odynophagia and progressive dyspnoea and were initially medically managed to stabilise their airway. This included intravenous steroids, nebulised epinephrine and intravenous antibiotics. After this initial treatment they both required investigation and optimisation of their underlying medical conditions (rheumatoid arthritis with possible systemic lupus erythematosus and nephrotic syndrome) as more definitive management.

Osteoma arising from the middle turbinate-a case series.

This case series aims to highlight that although extremely rare, osteoma can arise from the middle turbinate. We discuss the condition and treatment options. We describe 2 cases of osteomas arising from the middle turbinate. One occurring in a 29-year-old gentleman who presented to the ENT clinic with left nasal obstruction, and the other in a 65-year-old lady admitted to hospital with headaches and hypotension. Both cases were further investigated with CT scan. Both patients were treated with endoscopic fusion navigation assisted excision. Due to the large size of the mass, the gentleman required the mass to be delivered after it was drilled through and requiring septal deflection and vomerine spur reduction. As for the lady, the mass also required drilling and a posterior septotomy to facilitate dissection and removal of the tumour. Both patients made good recoveries with resolution of symptoms. Although extremely rare, osteomas can arise from the middle turbinate causing symptoms such as headache, facial pain, nasal obstruction and visual problems. As they are slow growing, they can be of large size at presentation. Treatment usually involves surgical excision. Endoscopic excision is usually adequate and safe.

Granulomatosis with polyangiitis causing subglottic stenosis-two cases and their management.

Granulomatosis with polyangiitis (GPA) is characterised by vasculitis of small and medium sized blood vessels and granulomatous lesions of the respiratory tract. The aetiology is unclear, however it is thought to be due to an autoimmune process with about 92% of patients with the disease being antineutrophilic cytoplasmic antibodies (ANCA) positive. Patients normally present in early adulthood, more commonly in the winter months. Seventy percent of patients with GPA present with ear, nose or throat symptoms. These include nasal congestion, crusting, epistaxis, nasal septal perforation and nasal saddle deformity. Lesions in the airway can lead to subglottic stenosis with resultant airway obstruction. Treatment of the disease complicated by subglottic stenosis is not straightforward and the benefits and risks of options including medical and surgical management need to be weighed up and tailored to each individual case. We describe two cases of GPA complicated by airway obstruction due to subglottic stenosis and their management.

Loss of substance P and inflammation precede delayed neurodegeneration in the substantia nigra after cerebral ischemia.

Focal cerebral ischemia leads to delayed neurodegeneration in remote brain regions. The substantia nigra (SN) does not normally show primary neuronal death after ischemic events affecting the striatum, but can exhibit delayed neuronal loss after the ischemic injury through mechanisms that are unknown. No data are available in mice showing acute post-stroke inflammation and remote injury in the SN. Substance P (SP), a mediator of neurogenic inflammation, is a key element of the striato-nigral circuitry, but alterations of SP in the SN have not been studied after acute striatal injury. Inflammation, a key contributor to neuronal death, is found in the SN after striatal ischemia, but it is unknown whether it precedes or occurs concomitantly with neuronal death. We hypothesised that focal striatal ischemia induces changes in SP levels in the SN and that inflammation precedes neuronal death in the SN. Using the middle cerebral artery occlusion model, we found a significant loss of SP in the ipsilateral SN 24h after striatal ischemia in mice. In the same area where SP loss occurs, significant glial and vascular activation, but no neuronal death, were observed. In contrast, a marked neuronal loss was observed within six days in the area of SP loss and inflammation. Our data suggest that focal loss of SP and early inflammatory changes in the SN precede remote neuronal injury after striatal ischemic damage. These observations may have important implications for motor impairment in stroke patients and indicate that striatal ischemia might facilitate Parkinson's disease development.