All India Institute of Medical Sciences, Bibinagar (AIIMS Bibinagar) is a public medical college and hospital based in Bibinagar, Yadadri Bhuvanagiri, Telangana, India, and one of the All India Institutes of Medical Sciences (AIIMSs). It is one of the six AIIMSs that started operation in 2019.
Background and Aims: del Nido cardioplegia (DC), initially developed for paediatric cardiac surgery, is increasingly used in adult procedures due to its ability to provide prolonged myocardial protection with a single dose. However, its superiority over blood cardioplegia (BC) remains unclear. This study compared the effects of DC and BC on acid–base balance, potassium levels, and metabolic profiles in adults undergoing elective cardiac surgery with cardiopulmonary bypass (CPB). Methods: A retrospective observational study was conducted at a tertiary care centre over a period of 6 months. Forty-seven patients were divided into Group BC (received blood cardioplegia) and Group DC (received del Nido cardioplegia). Arterial blood gases were recorded at four intraoperative time points. The four time points were T1, baseline before CPB; T2, immediately after cardioplegia administration; T3, post-rewarming just before separation from CPB; and T4, before transfer to the intensive care unit. Statistical analyses were performed using independent t-tests and Chi-square tests, or their equivalent non-parametric alternatives when appropriate. Results: Group DC exhibited a significantly higher potential of hydrogen (pH) (7.49 vs 7.43, P = 0.003) and base excess (0.15 vs − 1.80 mmol/L, P = 0.014) at post-rewarming (T3). Potassium was lower in group DC at baseline (T1). Blood glucose was significantly higher in group BC at T3 (275 vs 207 mg/dL, P < 0.001) and T4 (258 vs 217 mg/dL, P = 0.033). Five patients in the DC group required blood transfusion during CPB. Conclusion: DC and BC showed largely comparable intraoperative metabolic and physiological profiles, with most observed differences remaining within acceptable physiological ranges and of limited clinical significance. DC may be a practical alternative to BC; however, larger prospective studies evaluating direct myocardial injury markers and postoperative outcomes are needed.
BACKGROUND:Progressive supranuclear palsy (PSP) is a rare and devastating tauopathy with limited global data. Given India's large population, genetic diversity, and clinical heterogeneity, large multicenter datasets are crucial to enrich global understanding of PSP. OBJECTIVE:To characterize the demographic, clinical, and phenotypic profiles of a large multicenter Indian PSP cohort. METHODS:Subjects fulfilling MDS-PSP criteria were prospectively recruited across movement disorders centers (2021-2025). Standardized demographic and clinical data were collected. RESULTS:A total of 1035 subjects were enrolled (M:F = 709:326), with a median age of 65 years and a mean onset age of 62.2 ± 7.9 years. Regional distribution reflected pan-Indian recruitment (South 35%, North 26%, West 21%, East 18%). PSP-Richardson's syndrome was most common (41%), followed by PSP-Parkinsonism (18%) and PSP-CBS (11%); rarer phenotypes included PSP-PI (7%), PSP-F (7%), PSP-PGF (5%), PSP-OM (2%), PSP-SL (1%), and PSP-C (1%). Falls occurred earliest in PSP-PGF (13.7 months) and PSP-SL (16.3 months), while PSP-P showed delayed disability (falls at 31 months) indicating progression patterns. Cognitive onset was prominent in PSP-F (21%) and PSP-SL (57%). Levodopa was prescribed to 893 patients; 186 (21%) reported >25% subjective benefit, and 358 (40%) reported ≤25% benefit. Amantadine was used in 351 (34%) patients, with improvement in 177. CONCLUSION:This largest systematically profiled PSP cohort highlights both shared and distinctive features: high frequency of non-RS variants, aggressive course in PSP-RS/SL, better survival in PSP-P, and limited pharmacological benefit. These findings establish a foundation for longitudinal and genetic studies in diverse populations.
Extraoral cutaneous lesions of odontogenic origin are frequently misdiagnosed due to their asymptomatic dental causes and innocuous presentation. This literature review included 42 articles that highlight the diagnostic challenges of odontogenic cutaneous sinus tracts (OCSTs), which are often mistaken for skin infections, cysts, or neoplasms. As a result, patients typically consult dermatologists, general practitioners, or surgeons before reaching a dental specialist, with a diagnostic delay (Median = 12 months). Misdiagnosis can lead to unnecessary investigations, increasing patient distress and healthcare costs. IOPA radiographs with sinus-tract tracing OR cone-beam computed tomography (CBCT) are the investigation of choice to reach a correct diagnosis in such cases. A multidisciplinary approach involving timely referral to an endodontist/oral surgeon is essential for effective management. This paper presents two clinical cases from our institution that demonstrate successful diagnosis and resolution of OSCTs through appropriate dental intervention, emphasizing the importance of clinical awareness and interdisciplinary collaboration. Key Messages:Odontogenic cutaneous sinus tracts often mimic dermatologic lesions, leading to misdiagnosis. Early recognition, proper diagnosis, and timely referral to dental specialists are essential for effective management. Interdisciplinary collaboration is crucial to prevent unnecessary treatments and ensure complete healing.
Familial hypercholesterolaemia (FH) is an autosomal dominant genetic disorder of lipoprotein metabolism, characterised by highly elevated low-density lipoprotein cholesterol (LDL-C) from birth, leading to adverse cardiovascular effects at an early age. The prevalence of heterozygous FH is 1:200–250, while that of homozygous FH is 1:100,000–160,000 individuals. Patients with homozygous FH may have cholesterol levels of 25 mmol/L and develop cardiovascular diseases (CVDs) in their early twenties. In contrast, patients with heterozygous FH may have cholesterol levels of 5.2–10.4 mmol/L, with CVD manifesting around the age of 40 to 50 years. Familial hypercholesterolaemia is usually caused by inherited mutations in the APOB , LDLR and PCSK9 genes, and can be detected by routine lipid testing. Early recognition and aggressive management to lower the LDL-C level help to delay or prevent coronary atherosclerosis. This review summarises the epidemiology, genetic basis, screening and treatment options available for the management of FH.
