Antibiotic susceptibility of wound isolates in plastic surgery patients at a tertiary care centre

Context:Wound infection increases the hospital stay and adversely affects the recovery of patients. Culture and sensitivity of wound isolates help in proper diagnosis and management of these patients.Aim:To identify common bacteria causing wound infections and their antibiotic sensitivity pattern.Results:There were a total of 150 patients with infected wounds. Most common organism isolated was Pseudomonas followed by Klebsiella and Staphylococcus aureus. All of these organisms were resistant to most routine antibiotics.Conclusion:We suggest a multidisciplinary approach to wound management, rational drug use, routine microbiological surveillance of wounds and institution of hospital infection control policy.KEY WORDS: Bacteria, culture and sensitivity, wound infection     

Can postoperative renal dysfunction be predicted by measuring intraoperative glomerular filtration rate in patients undergoing coronary artery bypass grafting without cardiopulmonary bypass? A pilot study

Objective

Currently, there is no effective paradigm to identify patients who are at risk for renal dysfunction following cardiac surgery. The specific mechanisms of renal injury during surgery are incompletely understood. The aim of the study was to evaluate whether postoperative renal dysfunction can be predicted from intraoperative glomerular filtration rate (GFR).

Design

This is a prospective study.

Setting

The study was conducted in a tertiary care multi-specialty hospital.

Participants and interventions

GFR was measured in 24 patients (mean age 56.6 ± 11.09 years, 20 male) undergoing elective off-pump coronary artery bypass grafting during preoperative period, intraoperative period, 24 h after surgery (ICU GFR), and on the fifth postoperative day (final GFR ).

Measurements and main results

Patients were divided into two groups depending upon changes in intraoperative GFR. Group 1 (n = 10): who had a rise in intraoperative GFR in comparison with preoperative baseline measurement. All these 10 (41.7 %) patients with a rise in intraoperative GFR had an uneventful hospital course and achieved an improvement in final GFR. Group 2 (n = 14): 14 (58.3 %) patients had a fall in intraoperative GFR (mean 36.4 %) in comparison with preoperative baseline value. Of these 14 patients, 1 patient required dialysis support and 3 patients required ionotropic support. Among these 14 patients in group two, 7 had deterioration in final GFR (mean 28.7 %), when compared to preoperative baseline value.

Conclusion

Postoperative renal dysfunction can be predicted from intraoperative GFR. Patients who have a rise in intraoperative GFR do not develop postoperative renal dysfunction, and only patients with intraoperative fall in GFR are at risk of postoperative renal dysfunction.

     

Brachymetatarsia with accessory navicular in right foot: A rare coincidental finding

A 33 years old female patient presented with posttraumatic pain in the right foot for which radiographs of the right foot was advised. No fracture was detected on radiographs and patient was managed conservatively on medications and posterior splint immobilization. We found coincidentally a short fourth metatarsal and an accessory navicular bone in the right foot radiographs. After 3 weeks of immobilization, she underwent mobilization of the right foot, weight bearing and intensive physiotherapy for 6 weeks. After two months of injury she was still complaining of pain on the plantar aspect of right foot which was diagnosed as metatarsalgia and operated on by excision of the neuroma present in the 3rd web space of the right foot. After surgery she was completely relieved of pain and could do activities well related to the right foot.     

A hexanucleotide repeat upstream of eotaxin gene promoter is associated with asthma, serum total IgE and plasma eotaxin levels

Background

Eotaxin (CCL11) is a small protein produced in the lungs of patients with asthma, and is a potent chemoattractant for eosinophils.

Aim

To elucidate the role of eotaxin in asthma by an association study of functional and novel eotaxin polymorphisms in case–control and family‐based study designs.

Methods

Eotaxin +67G/A, –384A/G and –426C/T single‐nucleotide polymorphisms and a hexanucleotide (GAAGGA)_n repeat 10.9 kb upstream of the gene were genotyped in a cohort of age, sex and ethnically matched patients with asthma (n = 235) and healthy controls (n = 239), and also in a study population of 230 families with asthma recruited from north/northwest India. Total serum IgE (TsIgE) and plasma eotaxin levels were measured using ELISA.

Results

+67G/A polymorphism was found to be significantly associated with asthma in case–control (p = 0.009) and family‐based studies (p = 0.006). Its functional role, as it was correlated with plasma eotaxin levels (p = 0.006), was also demonstrated. Further, –384C/T single‐nucleotide polymorphism was found to be significantly associated with log₁₀ TsIgE (p = 0.016 in case–control and p = 0.018 in families) and eotaxin levels (p = 0.007). Most interestingly, for the first time, a highly significant association of the newly studied (GAAGGA)_n hexanucleotide repeat with asthma (p = 3×10⁻⁶), log₁₀TsIgE (p = 0.006) and eotaxin levels (p = 0.004) was observed. G_A_C_8 was also identified as an important risk haplotype associated with high TsIgE and plasma eotaxin levels.

Conclusions

This study provides further evidence that eotaxin polymorphisms are associated with the development of asthma by regulating eotaxin levels and reinforces towards the scanning of other chemokine genes present at 17q21 locus for their association with asthma and related phenotypes.Eosinophils play a major role in the pathogenesis of allergic diseases including asthma by releasing various granular proteins, reactive NO, cytokines and chemokines at the site of inflammation, thus causing tissue damage.¹ Interplay between chemokines and their receptors are considered to be crucial for the trafficking of eosinophil and other lymphocytes from the circulation to the bronchoalveolar spaces of the patients with asthma.² Eotaxin (chemokine, CC motif, ligand; CCL11) is a predominant eosinophil chemoattractant, which binds to chemokine receptor 3.^3,4 Chemokine receptor 3 is also present on the Th2 CD4⁺ lymphocytes, basophils, dendritic cells and mast cells.^5,6 Thus, the role of eotaxin in asthma is not confined to eosinophil migration and activation only, but extended to many other effector cells involved in disease pathogenesis. It has also been observed that along with interleukin 5, eotaxin prolongs the viability of eosinophils.⁷ Eotaxin mRNA and protein are found to be elevated in the induced sputum, bronchial epithelium and airways of the patients with moderate to severe asthma.^8,9,10 Bronchoalveolar lavage fluid of the patients with asthma also showed increased levels of eotaxin after allergen inhalation.¹¹ In addition, higher plasma eotaxin levels have been observed in subjects with symptoms of acute asthma and airflow obstruction than subjects with stable asthma. Plasma eotaxin levels have been correlated with severity of asthma even in the presence of steroid treatment.^12,13Eotaxin gene is present on chromosome 17q21.1, where linkage with asthma and related phenotypes has been previously reported in various ethnic populations.^14,15 Previous studies on eotaxin gene polymorphisms and asthma remain inconclusive as most of them failed to establish a strong association.^{16,17,18,19,20} However, in few other studies, eotaxin single‐nucleotide polymorphisms (SNPs) have been correlated significantly with asthma‐associated phenotypes including lung function, serum IgE, circulating blood eosinophils, eosinophil migration and activation, and plasma eotaxin levels.^{16,17,18,21,22} Studies have also been undertaken to demonstrate the functional implication of various promoter and exonic variants of the eotaxin.^20,22 Notably, the variant and the direction of association are inconsistent across different ethnic populations owing to some inherent reasons. However, no such studies have yet been undertaken in an ethnically divergent Indian population.Importantly, the 17q11–17q21 chromosomal region harbours many other important chemokines including RANTES, MCP1, MCP3 and so on, and also the gene for inducible nitric oxide synthase. Recently, we have reported the association of the gene for inducible nitric oxide synthase microsatellite repeats with asthma and related phenotypes in an Indian population, demonstrating the importance of 17q region in asthma predisposition.²³ The results of our previous study and the well‐documented role of eotaxin in asthma prompted us to undertake an association study of eotaxin gene with asthma and associated phenotypes in case–control and family‐based study designs. We have also measured the plasma eotaxin level and attempted to correlate it with eotaxin gene variants.     

Non‐peptide‐based new class of platelet aggregation inhibitors: Design,synthesis, bioevaluation,SAR, and in silico studies

A series of 2‐oxo‐2‐phenylethylidene linked 2‐oxo‐benzo[1,4]oxazine analogues 17a–x and 18a–o , incorporated with a variety of electron‐withdrawing as well as electron‐donating groups at ring A and ring C, were synthesized under greener conditions in excellent yields (up to 98%). These analogues 17a–x and 18a–o were evaluated for their arachidonic acid (AA)‐induced platelet aggregation inhibitory activities in comparison with the standard reference aspirin (IC₅₀ = 21.34 ± 1.09 µg/mL). Among all the screened compounds, eight analogues, 17i , 17x , 18f , 18g , 18h , 18i , 18l , and 18o , were identified as promising platelet aggregation inhibitors as compared to aspirin. In addition, cytotoxic studies in 3T₃ fibroblast cell lines by MTT assay of the promising compounds ( 17i , 17x , 18f–18i , 18l , and 18o ) were also performed and the compounds were found to be non‐toxic in nature. Furthermore, the results on the AA‐induced platelet aggregation inhibitory activities of these compounds ( 17i , 17x , 18f–18i , 18l , and 18o ) were validated via in silico molecular docking simulation studies. To the best of our knowledge, this is the first report of the identification of non‐peptide‐based functionalized 2‐oxo‐benzo[1,4]oxazines as platelet aggregation inhibitors.