Ocular Lichen Planus: A clinicopathologic review.

Lichen planus is a chronic inflammatory dermatosis that can affect the skin, mucous membranes and nails. Cutaneous lichen planus lesions are best described by the "six Ps" - purple pruritic polygonal planar papules and plaques. Mucous membrane lesions are commonly associated with cutaneous lichen planus. Ocular involvement with lichen planus is rare and conjunctival involvement usually predominates, it can however be visually devastating. Ocular lichen planus often progresses to extensive conjunctival scarring which can be impossible to distinguish clinically from other cicatrising conjunctivitis, requiring histopathological confirmation. Here we review the ocular pathology of this condition.

Novel Map Biopsy Technique to Define the Extent of Infection Before Penetrating Keratoplasty for Acanthamoeba Keratitis.

PURPOSE: The purpose of this study was to report a novel approach of prepenetrating keratoplasty (PKP) corneal map biopsies to define the extent of Acanthamoeba cyst infiltration in recalcitrant Acanthamoeba keratitis. METHODS: Corneal map biopsies were performed 1 week before PKP. Four biopsies, 1 from each peripheral corneal quadrant, were obtained to delineate the extent of microscopic infection. Histological results of these map biopsies were used to determine the size and location of the subsequent PKP. RESULTS: In our first case, map biopsies revealed Acanthamoeba cysts in 2 of the 4 biopsies. This led to an inferotemporally eccentric 8.5-mm PKP. The final histology report indicated that the closest resection margin was 0.08 mm. In our second case, the peripheral map biopsies were clear and an inferiorly eccentric 8.25-mm PKP was performed. The final histology report indicated that the closest resection margin was 2.3 mm. Both grafts have remained clear at 6 months postoperatively. CONCLUSIONS: Map biopsies of the cornea can achieve total removal of the corneal tissues infested with Acanthamoeba cysts and prevent reinfection of the donor graft.

Novel application of Deep Anterior Lamellar Keratoplasty for retinal detachment repair in totally opaque cornea secondary to aniridia.

PURPOSE: We present a novel approach for managing retinal detachment in a patient with aniridia related corneal scarring precluding fundal view via a deep anterior lamellar keratoplasty. METHODS: A 30-year-old female patient who had bilaterally opaque cornea, due to advanced aniridia related keratopathy presented with, experiencing flashing of light in her right eye. Examination of the retinal fundus was not possible due to the dense corneal scarring and underlying cataract. A superior bullous macula off retinal detachment was diagnosed on ultrasonography. Visual acuity at presentation was hand motions. The corneal scarring extended to the mid to deep stroma. We performed a deep anterior lamellar dissection of the opacified corneal stroma, that allowed clear visualisation of a dense cataract. The cataract was removed by phacoemulsification and IOL inserted. This allowed to proceed with repair of retinal detachment, through pars plana approach. The surgery was completed by a donor deep lamellar keratoplasty. RESULTS: This achieved a good fundal view to proceed with phacovitrectomy visualised through the residual corneal layers. Uneventful pars plana vitrectomy, cryotherapy and SF6 gas were performed to reattach the retina. Post-operatively the graft remains clear at 6 months with a visual acuity of 20/160 in the right eye, a level of vision the patient had not experienced for decades. CONCLUSION: Deep anterior lamellar keratoplasty offered an alternative to temporary keratoprosthesis to achieve a clear view of the retinal fundus and perform pars plana vitrectomy and repair of the retinal detachment.

A Survey of Orthopedic Surgical Management of Pressure Ulcer-Related Pelvic Osteomyelitis.

Pressure-ulcer related pelvic osteomyelitis is managed with little high-quality evidence. We undertook an international survey of orthopedic surgical management, covering diagnostic parameters, multidisciplinary input, and surgical approaches (indications, timing, wound closure, and adjunctive therapies). This identified areas of consensus and disagreement, representing a starting point for future discussion and research.

Comorbidity and survival after admission to the intensive care unit: A population-based study of 41,230 patients.

PURPOSE: To describe the relationship between comorbidities and survival following admission to the intensive care unit. METHODS: Retrospective observational study using several linked routinely collected databases from 16 general intensive care units between 2002 and 2011. Comorbidities identified from hospitalisation in the five years prior to intensive care unit admission. Odds ratios for survival in intensive care unit, hospital and at 30 days, 180 days and 12 months after intensive care unit admission derived from multiple logistic regression models. RESULTS: There were 41,230 admissions to intensive care units between 2002 and 2011. Forty-one percent had at least one comorbidity - 24% had one, 17% had more than one. Patients with comorbidities were significantly older, had higher Acute Physiology and Chronic Health Evaluation II scores and were more likely to have received elective rather than emergency surgery compared with those without comorbidities. After excluding elective hospitalisations, intensive care unit and hospital mortality for the cohort were 24% and 29%, respectively. Asthma (odds ratio 0.79, 95% confidence interval 0.63-0.99) and solid tumours (odds ratio 0.74, 0.67-0.83) were associated with lower odds of intensive care unit mortality than no comorbidity. Intensive care unit mortality was raised for liver disease (odds ratio 2.98, 2.43-3.65), cirrhosis (odds ratio 2.61, 1.9-3.61), haematological malignancy (odds ratio 2.29, 1.85-2.83), chronic ischaemic heart disease (odds ratio 1.53, 1.19-1.98), heart failure (odds ratio 1.79, 1.35-2.39) and rheumatological disease (odds ratio 1.53, 1.18-1.98). CONCLUSIONS: Comorbidities affect two-fifths of intensive care unit admission and have highly variable effects on subsequent outcomes. Information on the differential effects of comorbidities will be helpful in making better decisions about intensive care unit support and understanding outcomes beyond surviving intensive care unit.

Outcomes, Microbiology and Antimicrobial Usage in Pressure Ulcer-Related Pelvic Osteomyelitis: Messages for Clinical Practice.

Introduction: Pressure ulcer-related pelvic osteomyelitis is a relatively under-studied entity in the field of bone infection. We sought to add to the limited evidence base for managing this challenging syndrome. Methods: Cases were identified retrospectively from a surgical database and hospital discharge codes at a U.K. tertiary centre (2009-2018). Risk factors associated with outcomes were analysed by logistic regression. Results: We identified 35 patients (mean age 57.4 years), 69% managed with a combined medical and surgical approach, with mean follow-up of 3.7 years from index admission. Treatment failure (requiring further surgery or intravenous antimicrobials) occurred in 71% and eventual ulcer healing in 36%. One-year mortality was 23%. Lack of formal care support on discharge, post-traumatic (asensate) neurological deficit and index CRP (>184mg/L) were associated with treatment failure (p=0.001). Age (>59.5 years), lack of attempted soft tissue coverage, haemoglobin (<111g/L) and albumin (<25g/L) were associated with non-healing ulcers (p=0.003). Superficial wound swabs had low sensitivity and specificity compared to deep bone microbiology. Infection (based on deep bone microbiology from 46 infection episodes) was usually polymicrobial (87%), commonly involving S. aureus, Enterococci, GNB and anaerobes. Antimicrobial duration ranged from 0-103 days (mean 54) and was not associated with subsequent treatment failure. Conclusions: Attempted soft tissue coverage after surgical debridement, ensuring appropriate support for personal care after discharge and nutritional optimisation could improve outcomes. Superficial wound swabs are uninformative and deep bone sampling should be pursued. Long antimicrobial courses do not improve outcomes. Clinicians should engage patients in anticipatory care planning.

Ca2+-stimulated adenylyl cyclase isoform AC1 is preferentially expressed in guinea-pig sino-atrial node cells and modulates the I(f) pacemaker current.

Ca(2+)-stimulated adenylyl cyclases (AC) are known to play important roles in neurons but have not previously been reported in the heart. Here we present the first evidence for selective expression of Ca(2+)-stimulated AC in the sino-atrial node (SAN) but not in ventricular muscle of the guinea-pig heart. The AC1 isoform of Ca(2+)-stimulated AC was shown to be present in SAN, both as mRNA using RT-PCR and as protein using immuno-blotting with a specific antibody. Confocal immuno-fluorescence studies detected membrane localization of AC1 in SAN cells, but no AC1 in ventricular muscle. Ca(2+)-stimulated AC8 may also be present in SAN. The functional importance of AC activity was investigated by monitoring activation of I(f) (gated by hyperpolarization and regulated by cAMP, which shifts activation to more depolarized voltages). Basal activity of AC in isolated SAN myocytes was demonstrated by the observations that an inhibitor of AC activity (MDL 12330A, 10 microm) shifted activation in the hyperpolarizing direction, while inhibition of phosphodiesterases (IBMX, 100 microm) shifted I(f) activation in the depolarizing direction. Buffering cytosolic Ca(2+) with the Ca(2+) chelator BAPTA (by exposure to BAPTA-AM) shifted activation of I(f) in the hyperpolarizing direction, and under these conditions the AC inhibitor MDL had little or no further effect. The actions of BAPTA were overcome by exposure to forskolin (10 microm), a direct stimulator of all AC isoforms, to restore cAMP levels. These effects are consistent with the functional importance of Ca(2+)-stimulated AC, which is expected to be fundamental to initiation and regulation of the heartbeat.