Colchester Hospital is a district general hospital located in Colchester, Essex. It is managed by East Suffolk and North Essex NHS Foundation Trust.
BACKGROUND:Early mobilisation following total knee replacement (TKR) is a key component of Enhanced Recovery After Surgery (ERAS) pathways and is associated with improved functional recovery and reduced length of stay. An initial local audit (MAKE1) identified delays in mobilisation related to postoperative pain and lack of physiotherapy input on postoperative day (POD) 0. AIM:To assess compliance with early mobilisation standards following implementation of audit recommendations and to identify factors associated with delayed mobilisation and discharge after TKR. METHODS:A retrospective two-cycle clinical audit was conducted in the Orthopaedic Department at James Paget University Hospital. Patients undergoing primary TKR between June and July 2025 were included. Outcomes included time to first mobilisation, length of stay, documented barriers to mobilisation, timing of physiotherapy assessment, and recorded anaesthetic technique. Findings were compared with the initial audit cycle. The audit was registered with the hospital audit department. RESULTS:A total of 64 patients underwent TKR, and 63 were included in the final analysis due to incomplete documentation for one patient. Mobilisation within 24 hours was achieved in 57/63 patients (90.5%), compared with 35/53 (66%) in the first audit cycle. The median length of stay remained two days. Postoperative pain was the most frequently documented barrier to early mobilisation and was associated with prolonged admission (mean = 5.2 days). Other barriers included delirium, deep vein thrombosis or cellulitis, vasovagal episodes, and fatigue (mean = 4.8 days). No POD 0 physiotherapy assessments were documented; early mobilisation was supported by ward-based staff, with routine physiotherapy review occurring from POD 1. No clear differences in mobilisation timing or discharge were observed between spinal and general anaesthesia. CONCLUSION:The descriptive data show higher compliance with mobilisation within 24 hours in MAKE2 compared with MAKE1 following implementation of audit recommendations. Persistent barriers related to pain management and lack of POD 0 physiotherapy input remain key targets for ongoing quality improvement within ERAS pathways.
Summary: Background: Prior international studies indicate that 9–36% of people with cerebral palsy (CP) have a monogenic condition. However, the utility of whole genome sequencing (WGS) as a diagnostic tool for United Kingdom (UK) National Health Service (NHS) patients has not been evaluated. Methods: This prospective pilot study recruited 86 individuals with CP from specialist clinics in Bedford, Cambridge, Colchester, Newcastle, and Luton NHS Foundation Trusts. Gene-agnostic trio WGS was performed using AI-based variant prioritisation, with subsequent application of a CP gene list. Candidate diagnostic pathogenic (P) or likely pathogenic (LP) variants were reviewed at multidisciplinary meetings and confirmed in an NHS Genomic Laboratory Hub prior to issuing a clinical report. The use of human phenotype ontology (HPO) terms was evaluated to estimate probability of a diagnostic variant using a supervised linear discriminant analysis (PCA + LDA) model. Findings: 86/157 (54.7%) individuals approached consented to the study. Variants meeting P/LP diagnostic criteria were identified in 11/86 cases (12.8%). 8/86 participants (9.3%) carried variants strongly suggestive of disease causation. Variants of uncertain significance were identified in 27/86 cases (31.4%). In all cases with P/LP variants, findings informed patient prognosis, specialist care, clinical management, and familial recurrence risk. Machine learning approaches were used to segregate the probability of diagnosis for participants based on HPO terms. Interpretation: WGS is clinically useful for diagnosis and management of genetic conditions associated with CP in the UK. Validation of these findings in a larger cohort is warranted. Funding: Rosetrees Charitable Trust, Isaac Newton Trust, NIHR Cambridge Biomedical Research Centre, and the Wellcome Trust.
Abstract Introduction DRESS is a severe hypersensitivity reaction characterized by fever, rash, facial oedema, lymphadenopathy, eosinophilia, and multi-organ involvement. Management typically involves prompt withdrawal of the causative drug and corticosteroid therapy. However, managing DRESS syndrome triggered with initial phase of anti-tuberculous medications is extremely challenging. A balancing decision needs to be made to control the potentially fatal hypersensitivity reaction which conflicts with the urgent need to continue effective treatment for tuberculosis. Management becomes even more complex in cases refractory to systemic corticosteroids. Case Presentation A 32-year-old woman developed DRESS syndrome two months after initiating treatment for cavitating pulmonary tuberculosis. She attended emergency department with seven day history of a widespread morbiliform rash, facial swelling and two days of fever, nausea with profound fatigue. On admission, she was febrile (39.2 °C), tachycardic (134 bpm), hypotensive (89/55 mmHg), and hypoxic, with diffuse erythematous rash and bilateral coarse crackles. Laboratory findings revealed leukocytosis (18.3 × 109/L), eosinophilia (peaking at 6.25 × 109/L), elevated IgE (5000 kU/L), and raised ALT (311 U/L). Infectious, autoimmune, and parasitic causes were excluded. Chest imaging demonstrated diffuse bilateral ground-glass opacities consistent with acute respiratory distress syndrome (ARDS). Given her recent drug history and clinical presentation, diagnosis of DRESS was made which was supported by a RegiSCAR score of 6. Anti-TB medications were stopped, and corticosteroid therapy initiated. However, the patient’s respiratory function deteriorated, necessitating mechanical ventilation. Treatment with high-dose intravenous methylprednisolone did not show sustained remission of the hypersensitivity reaction. Single dose of 30mg subcutaneous Benralizumab was administered. This resulted in rapid and sustained normalization of eosinophil count, resolution of rash, improvement in hepatic parameters, and significant recovery in pulmonary function, allowing successful extubation. Discussion This case highlights the pivotal role of IL-5 in eosinophil-driven inflammation in DRESS. It demonstrates the potential of IL-5 blockade with Benralizumab as an effective treatment in steroid-refractory DRESS. Importantly, the targeted mechanism of action allowed disease control without profound immunosuppression, minimising risk of infectious complications in a patient with partially treated tuberculosis. Conclusion IL-5 inhibition with benralizumab appears to be a promising therapeutic option for corticosteroid-resistant DRESS. This case highlights the potential role of targeted biologic therapy in managing severe and refractory cases. Further research and accumulation of clinical experience are needed to establish standardized treatment protocols. Reference Rubin et al. Front. Immunol. 14:1134178. doi: 10.3389/fimmu.2023.1134178 This abstract is funded by: None
Abstract Background and aims Midbrain infarctions produce characteristic syndromes depending on the anatomical structures involved. Weber syndrome results from involvement of the cerebral peduncle and oculomotor fascicles, producing ipsilateral third cranial nerve palsy with contralateral weakness. Claude syndrome arises from involvement of the midbrain tegmentum and oculomotor fascicles, typically sparing the cerebral peduncle. Reverse Claude syndrome represents a rare variation in which the pattern of crossed findings differs due to selective midbrain involvement. This report describes a paramedian midbrain infarction with overlapping Weber and reverse Claude syndrome. Methods A 71-year-old woman with vascular risk factors presented with acute dysarthria. Examination revealed pupil-sparing right 3rd nerve palsy, mild left facial and upper/lower limb weakness, and right unilateral(ipsilateral) ataxia. Results MRI demonstrated discrete acute infarctions involving the right paramedian midbrain and right cerebral peduncle, showing restricted diffusion on DWI /ADC.(figure) This accounted for the pattern of ipsilateral oculomotor nerve involvement and contralateral motor weakness due to cerebral peduncle involvement, alongside features consistent with reverse Claude syndrome arising from adjacent midbrain tegmental involvement. In reverse Claude’s syndrome, there is ipsilateral ataxia contrary to contralateral ataxia of Claude’s syndrome. This can be explained by the lesion involving ipsilateral cerebellar connections while sparing crossed cerebellar pathways. Conclusions This case demonstrates a rare midbrain stroke producing overlapping Weber and reverse Claude syndrome features. To our knowledge, this combination has not been previously reported. The case adds to the reported spectrum of complex presentations of midbrain stroke and emphasizes the importance of accurate clinical neurological examination. Conflict of interest Md Aziz Mazumdar: nothing to disclose. Ramachandran Sivakumar: nothing to disclose. Joseph Ngeh: nothing to disclose. Rajesh Saksena: nothing to disclose. Figure 1 - belongs to Results
