The impact of sensory neuropathy and inflammation on epithelial wound healing in diabetic corneas

Diabetic peripheral neuropathy (DPN) is the most common complication of diabetes, with several underlying pathophysiological mechanisms, some of which are still uncertain. The cornea is an avascular tissue and sensitive to hyperglycemia, resulting in several diabetic corneal complications including delayed epithelial wound healing, recurrent erosions, neuropathy, loss of sensitivity, and tear film changes. The manifestation of DPN in the cornea is referred to as diabetic neurotrophic keratopathy (DNK). Recent studies have revealed that disturbed epithelial-neural-immune cell interactions are a major cause of DNK. The epithelium is supplied by a dense network of sensory nerve endings and dendritic cell processes, and it secretes growth/neurotrophic factors and cytokines to nourish these neighboring cells. In turn, sensory nerve endings release neuropeptides to suppress inflammation and promote epithelial wound healing, while resident immune cells provide neurotrophic and growth factors to support neuronal and epithelial cells, respectively. Diabetes greatly perturbs these interdependencies, resulting in suppressed epithelial proliferation, sensory neuropathy, and a decreased density of dendritic cells. Clinically, this results in a markedly delayed wound healing and impaired sensory nerve regeneration in response to insult and injury. Current treatments for DPN and DNK largely focus on managing the severe complications of the disease. Cell-based therapies hold promise for providing more effective treatment for diabetic keratopathy and corneal ulcers.     

A case of sudden cardiac death due to mitochondrial disease

A 25-year-old, emaciated man without medical treatment was found to have died suddenly at home by his mother. At autopsy, there were no injuries to his body, but significant circulatory insufficiency was observed. Electron microscopy revealed abnormal mitochondria in cells of the cardiac conduction system. The conduction system was filled with mitochondrial size abnormalities and mitochondrial cristae abnormalities. No notable abnormal findings were observed in other organs. Genetic examination of the blood revealed the mitochondrial pathogenetic variant m.3243A>G. Epileptic seizures, diabetic ketoacidosis, and hyperosmolar hyperglycemic state were unlikely to be the cause of sudden death. The cause of death was diagnosed as arrhythmia possibly induced by the failure of the cardiac conduction system due to mitochondrial disease. This is a rare case of sudden death caused by an accumulation of abnormal mitochondria in the cardiac conduction system.     

A randomised controlled trial of intravenous dexmedetomidine added to dexamethasone for arthroscopic rotator cuff repair and duration of interscalene block

Prolongation of peripheral nerve blockade by intravenous dexamethasone may be extended by intravenous dexmedetomidine. We randomly allocated 122 participants who had intravenous dexamethasone 0.15 mg.kg⁻¹ before interscalene brachial plexus block for day-case arthroscopic rotator cuff repair to intravenous saline (62 participants) or intravenous dexmedetomidine 1 μg.kg⁻¹ (60 participants). The primary outcome was time from block to first oral morphine intake during the first 48 postoperative hours. Fifty-nine participants reported taking oral morphine, 25/62 after placebo and 34/60 after dexmedetomidine, p = 0.10. The time to morphine intake was shorter after dexmedetomidine, hazard ratio (95%CI) 1.68 (1.00–2.82), p = 0.049. Median (IQR [range]) morphine doses were 0 (0–12.5 [0–50]) mg after control vs. 10 (0–30 [0–50]) after dexmedetomidine, a difference (95%CI) of 7 (0–10) mg, p = 0.056. There was no effect of dexmedetomidine on pain at rest or on movement. Intra-operative hypotension was recorded for 27/62 and 50/60 participants after placebo vs. dexmedetomidine, respectively, p < 0.001. Other outcomes were similar, including durations of sensory and motor block. In conclusion, dexmedetomidine shortened the time to oral morphine consumption after interscalene block combined with dexamethasone and caused intra-operative hypotension.     

Surgical management of deep lobe parotid tumours with and without involvement of the parapharyngeal space

The diagnosis and treatment of deep lobe parotid tumours is challenging because of the complex surgical accessibility. There is a lack of studies describing the differences between deep lobe tumours that do and do not occupy the parapharyngeal space (PPS). Patients treated for deep lobe tumours occupying the PPS (PPS group) and not occupying the PPS (non-PPS group) were analysed retrospectively. A total of 227 patients were treated surgically for deep lobe parotid tumours between 1990 and 2019. Sixty patients (26.4%) presented with tumours that involved the PPS (PPS group), while 167 (73.6%) presented with tumours that did not occupy the PPS (non-PPS group). The majority of the PPS group tumours were removed using a transcervical or transcervical–transparotid approach. PPS group tumours were larger (P < 0.001), and tumour spill occurred more frequently in this group (benign tumours: P = 0.002; malignant tumours: P = 0.033). Complication rates did not differ between the PPS and non-PPS groups. A transcervical or transcervical–transparotid approach is the preferred method for the management of deep lobe parotid tumours that occupy the PPS in our practice. Tumour spill occurred more frequently in the PPS group, which is most probably due to the larger tumour size and more complex accessibility.