Otolaryngology resident experience with supraclavicular, submental and other regional flaps in the United States.

OBJECTIVE: Despite the resurgence in regional flap use, otolaryngology resident regional flap experience has been incompletely studied. We sought to characterize United States (US) otolaryngology resident exposure to, and perceptions of, supraclavicular flaps (SCFs), submental flaps (SMFs), and other regional flaps. METHODS: An online survey was disseminated every two weeks to 106 US otolaryngology residency program directors for distribution to residents within their programs between August and October 2016. 121 surveys were returned of which 106 were sufficiently completed and eligible for data analysis. RESULTS: Among residents with adequate responses, 52 were postgraduate year (PGY) 1-3 (junior) residents and 54 were PGY 4-7 (senior) residents. Senior residents participated in more pectoralis major flaps (mean: 8.1, 95%-CI: 6.5-9.8) compared to SCFs (mean: 1.5, 95%-CI: 1.0-2.0, p < 0.001) and SMFs (mean: 0.7; 95%-CI: 0.4-1.0, p < 0.001). Among senior residents exposed to SCFs, SMFs and pectoralis flaps, more individuals judged pectoralis major flaps as successful or very successful (96.2%, 95%-CI: 91.1-100%), compared to SCFs (64.3%, 95%-CI: 46.5-82.0%; p < 0.001) and SMFs (63.2%, 95%-CI: 41.5-84.8%; p = 0.001). CONCLUSIONS: Senior otolaryngology residents were exposed to fewer SCFs and SMFs compared to pectoralis major flaps. Resident perception that SCFs and SMFs were not as successful as pectoralis major flaps should be investigated further.

Induction of heme oxygenase-1 (HO-1) in glia after traumatic brain injury.

In this study we examined the induction of heme oxygenase-1 (HO-1) in glia in the traumatized rat brain. HO-1 was immunolocalized in fixed sections of brain 3 h to 5 days after injury. Induction of this enzyme in astrocytes, microglia/macrophages, and oligodendrocytes was evaluated using immunofluorescent double labeling with monoclonal antibodies to glial fibrillary acidic protein, complement C3bi receptor, and myelin basic protein. Induction of HO-1 was apparent in the injured hemisphere and cerebellum as early as 24 h postinjury. The protein was likewise noted in similar regions of the brain at 72 h postinjury but appeared to be more widespread in its distribution. At 5 days postinjury, there was a notable decline in the degree of immunostaining for HO-1. HO-1 was typically induced in astrocytes in the cerebral cortex at the site of impact, in the deep cortical layers adjacent to the hemorrhagic lesions, and in the hippocampus. HO-1 was induced in Bergmann glia in the vermis of cerebellum. In addition, HO-1 was also induced in microglia/macrophages scattered throughout the ipsilateral cerebral cortex, cerebellum and subarachnoid space. These findings demonstrate prolonged glial induction of HO-1 in the traumatized brain. Such a response may reflect a protective role of these cells against secondary insults including oxidative stress.

Induction of heme oxygenase-1 after hyperosmotic opening of the blood-brain barrier.

The induction of the stress protein heme oxygenase-1 (HO-1) was studied in the rat brain after intracarotid administration of hyperosmolar mannitol. HO-1 was immunolocalized in fixed sections of brain 24 h to 7 days after injection. Immunoglobulin G (IgG) was immunolocalized in adjacent sections to demonstrate areas of breakdown of the blood-brain barrier. Induction of HO-1 was also evaluated by Western immunoblots, performed at 24 h after the insult. Immunofluorescent double labelling with monoclonal antibodies to HO-1 and either glial fibrillary acidic protein or the complement C3bi receptor was used to determine if glia/macrophages expressed HO-1. There was pronounced, widespread induction of HO-1 in the ipsilateral hemisphere and cerebellum by 24 h both by immunocytochemistry and by Western blots. This induction was markedly attenuated at later times. HO-1 was induced in astrocytes and microglia/macrophages in the ipsilateral hemisphere. In addition, the protein was induced in Bergmann glia and scattered microglia/macrophages in the cerebellum. The mechanism of induction of HO-1 in glia after opening of the blood-brain barrier could include exposure to heme proteins, denatured proteins and other plasma constituents known to induce HO-1. This glial induction may reflect a protective response of these cells.

Induction of HSP-70 after hyperosmotic opening of the blood-brain barrier in the rat.

The cellular response resulting from breakdown of the blood-brain barrier was evaluated 24 h after hyperosomotic infusion of mannitol into the internal carotid artery in the rat. Heat shock protein (HSP-70), a marker of cellular stress and/or injury, was induced in scattered patches of neurons and glia in regions of barrier breakdown. These findings suggest that osmotically induced breakdown of the blood-brain barrier may result in cell injury.

Contemporary evaluation and management of parapharyngeal space neoplasms.

OBJECTIVE: This review summarises the contemporary, multidisciplinary approach to managing parapharyngeal space neoplasms. OVERVIEW: Parapharyngeal space neoplasms are uncommon head and neck tumours and are most often benign. Most tumours are of either salivary gland or neurogenic origin. Patients tend to be asymptomatic even when tumours reach large sizes. Patients may present with a mass in the pharynx or neck, although frequently the tumour is found incidentally on an imaging study. Due to the limitations of physical examination in this anatomical area, imaging studies are essential to the evaluation of parapharyngeal space neoplasms. Cytopathology may provide additional diagnostic information. Open biopsy is rarely necessary and can be hazardous. Treatment is primarily surgical, and various surgical approaches can be tailored for a given neoplasm. Recently, a trend toward observation of select patients with asymptomatic neurogenic tumours has been advocated. CONCLUSION: The evaluation and management of parapharyngeal space tumours is best done by a multidisciplinary team. Treatment should be individualised, and the risks and benefits of surgical intervention need to be carefully weighed. Complications are best avoided by careful surgical planning.