Imperial College London

DrSanoojSoni

Faculty of MedicineDepartment of Surgery & Cancer

Honorary Clinical Senior Lecturer
 
 
 
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s.soni

 
 
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Location

 

Chelsea and Westminster HospitalChelsea and Westminster Campus

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Summary

 

Publications

Publication Type
Year
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16 results found

Stephens J, Wong J, Broomhead R, Stumpfle R, Waheed U, Patel P, Brett S, Soni Set al., 2021, Raised serum amylase in patients with COVID-19 may not be associated with pancreatitis, British Journal of Surgery, Vol: 108, Pages: 152-153, ISSN: 0007-1323

Journal article

Chia G, Barrett H, Patel P, Soni Set al., 2021, One hundred eighteen days on a ventilator: a COVID-19 success story against all odds, BMJ Case Reports, Vol: 14, Pages: 1-4, ISSN: 1757-790X

Emerging data suggest that patients with certain comorbidities requiring intensive care unit (ICU) admission for COVID-19 have a poor prognosis. This report describes a case of a patient with multiple comorbidities who contracted COVID-19 pneumonitis but was successfully weaned off invasive mechanical ventilation after 118 days, despite his admission being complicated by recurrent septic episodes and requirement for advanced cardiovascular support and renal replacement therapy. Of note, our patient received three courses of steroids in total during his ICU stay,and current literature strongly supports the use of steroids in critically unwell patients with COVID-19. To the best of our knowledge, this is the longest reported ventilated time and intensive care/hospital stay for a surviving patient with COVID-19 and highlights the importance of allowing sufficient time for clinical interventions to take effect, even when the prognosis appears bleak.

Journal article

Chaggar RS, Shah SV, Berry M, Saini R, Soni S, Vaughan Det al., 2021, The Video Classification of Intubation (VCI) score: a new description tool for tracheal intubation using videolaryngoscopy, European Journal of Anaesthesiology, Vol: 38, Pages: 324-326, ISSN: 0265-0215

Journal article

Soni S, Garner J, O'Dea K, Kohn M, Finney L, Tirlapur N, Srikanthan K, aboelhassan A, Singh S, Wilson M, Wedzicha J, Kemp S, Usmani O, Shah P, Takata Met al., 2021, Intra-alveolar neutrophil-derived microvesicles are associated with disease severity in COPD, American Journal of Physiology: Lung Cellular and Molecular Physiology, Vol: 320, Pages: L73-L83, ISSN: 1040-0605

Despite advances in the pathophysiology of Chronic Obstructive Pulmonary Disease (COPD), there is a distinct lack of biochemical markers to aid clinical management. Microvesicles (MVs) have been implicated in the pathophysiology of inflammatory diseases including COPD but their association to COPD disease severity remains unknown. We analysed different MV populations in plasma and bronchoalveolar lavage fluid (BALF) taken from sixty-two patients with mild to very severe COPD (51% male; mean age: 65.9 years). These patients underwent comprehensive clinical evaluation (symptom scores, lung function, exercise testing) and the capacity of MVs to be clinical markers of disease severity was assessed. We successfully identified various MV subtype populations within BALF (leukocyte, PMN (polymorphonuclear leukocyte i.e. neutrophil), monocyte, epithelial and platelet MVs) and plasma (leukocyte, PMN, monocyte and endothelial MVs), and compared each MV population to disease severity. BALF neutrophil MVs were the only population to significantly correlate with the clinical evaluation scores including FEV1, mMRC dyspnoea score, 6-minute walk test, hyperinflation and gas transfer. BALF neutrophil MVs, but not neutrophil cell numbers, also strongly correlated with BODE index. We have undertaken, for the first time, a comprehensive evaluation of MV profiles within BALF/plasma of COPD patients. We demonstrate that BALF levels of neutrophil-derived MVs are unique in correlating with a number of key functional and clinically-relevant disease severity indices. Our results show the potential of BALF neutrophil MVs for a COPD biomarker that tightly links a key pathophysiological mechanism of COPD (intra-alveolar neutrophil activation) with clinical severity/outcome.

Journal article

Gasparini M, Khan S, Patel JM, Parekh D, Bangash MN, Stumpfle R, Shah A, Baharlo B, Soni Set al., 2020, Renal impairment and its impact on clinical outcomes in patients who are critically ill with COVID-19: a multicentre observational study, ANAESTHESIA, Vol: 76, Pages: 320-326, ISSN: 0003-2409

Journal article

Soni S, Shah S, Chaggar R, Saini R, James E, Elliot J, Stephens J, McCormack T, Hartle Aet al., 2020, Surgical cancellation rates due to peri‐operative hypertension: implementation of multidisciplinary guidelines across primary and secondary care, Anaesthesia, Vol: 75, Pages: 1314-1320, ISSN: 0003-2409

Patients with uncontrolled hypertension are at increased risk of complications during general anaesthesia but the number of patients whose surgery is delayed or cancelled due to hypertension remains unknown. Prospective, regional multicentre service evaluations were performed on consecutive patients undergoing elective surgery before and after the publication of new guidelines from the Association of Anaesthetists and the British Hypertensive Society. The aim was to quantify the number of operations cancelled due to hypertension alone and to assess impact of the guidelines on cancellation rates. In October 2013 (before the publication of the guidelines), 1.37% (95%CI 0.69–2.11%) of patients listed for elective surgery were cancelled solely due to raised blood pressure. This reduced significantly to 0.54% (95%CI 0.20–0.92%, p < 0.001) in 2018. There was a significant reduction in inappropriate cancellations for stage 1 or 2 hypertension from 2013 to 2018 (72 vs. 14, respectively, p < 0.001) in keeping with the recommendations in the guidelines. Furthermore, the number of patients being referred back to primary care for the management of hypertension reduced from 2013 to 2018 (85 vs. 30, respectively, p < 0.001). Our data suggest achievement of three major outcomes: reduced surgical cancellations due to hypertension alone; improved detection of significant hypertension before elective surgery; and reduced referral back to primary care from hospital for hypertension management. To the best of our knowledge, this is the first time the successful implementation of guidelines from the Association of Anaesthetists has been assessed on such a broad scale. Our data indicate that these guidelines have been effectively implemented in both primary and secondary care, which is likely to have made a positive psychosocial, physical and economic impact on patients and the NHS.

Journal article

Stephens JR, Stümpfle R, Patel P, Brett SJ, Broomhead R, Baharlo B, Soni S, Stephens J, Stümpfle R, Patel P, Brett S, Broomhead R, Baharlo B, Soni Set al., 2020, Analysis of critical care severity of illness scoring systems in patients with coronavirus disease 2019: a retrospective analysis of three U.K. ICUs., Critical Care Medicine, Vol: 49, Pages: e105-e107, ISSN: 0090-3493

Journal article

O'Dea K, Tan YY, Shah S, Patel B, Tatham K, Wilson M, Soni S, Takata M, O'Dea KP, Tan YY, Shah S, Patel B, Tatham KC, Wilson MR, Soni S, Takata Met al., 2020, Monocytes mediate homing of circulating microvesicles to the pulmonaryvasculature during low-grade systemic inflammation, Journal of Extracellular Vesicles, Vol: 9, Pages: 1-16, ISSN: 2001-3078

Microvesicles (MVs), a plasma membrane-derived subclass of extracellular vesicles, are produced and released into the circulation during systemic inflammation, yet little is known of cell/tissue-specific uptake of MVs under these conditions. We hypothesized that monocytes contribute to uptake of circulating MVs and that their increased margination to the pulmonary circulation and functional priming during systemic inflammation produces substantive changes to the systemic MV homing profile. Cellular uptake of i.v.-injected, fluorescently labelled MVs (J774.1 macrophage-derived) in vivo was quantified by flow cytometry in vascular cell populations of the lungs, liver and spleen of C57BL6 mice. Under normal conditions, both Ly6Chigh and Ly6Clow monocytes contributed to MV uptake but liver Kupffer cells were the dominant target cell population. Following induction of sub-clinical endotoxemia with low-dose i.v. LPS, MV uptake by lung-marginated Ly6Chigh monocytes increased markedly, both at the individual cell level (~2.5-fold) and through substantive expansion of their numbers (~8-fold), whereas uptake by splenic macrophages was unchanged and uptake by Kupffer cells actually decreased (~50%). Further analysis of MV uptake within the pulmonary vasculature using a combined model approach of in vivo macrophage depletion, ex vivo isolated perfused lungs and in vitro lung perfusate cell-based assays, indicated that Ly6Chigh monocytes possess a high MV uptake capacity (equivalent to Kupffer cells), that is enhanced directly by endotoxemia and ablated in the presence of phosphatidylserine (PS)-enriched liposomes and β3 integrin receptor blocking peptide. Accordingly, i.v.-injected PS-enriched liposomes underwent a redistribution of cellular uptake during endotoxemia similar to MVs, with enhanced uptake by Ly6Chigh monocytes and reduced uptake by Kupffer cells. These findings indicate that monocytes, particularly lung-marginated Ly6Chigh subset monocytes, become a dominant

Journal article

Oakley C, Koh M, Baldi R, Soni S, O'Dea K, Takata M, Wilson Met al., 2019, Ventilation following established ARDS: a preclinical model framework to improve predictive power, Thorax, Vol: 74, Pages: 1120-1129, ISSN: 1468-3296

Background Despite advances in understanding the pathophysiology of acute respiratory distress syndrome, effective pharmacological interventions have proven elusive. We believe this is a consequence of existing preclinical models being designed primarily to explore biological pathways, rather than predict treatment effects. Here, we describe a mouse model in which both therapeutic intervention and ventilation were superimposed onto existing injury and explored the impact of β-agonist treatment, which is effective in simple models but not clinically.Methods Mice had lung injury induced by intranasal lipopolysaccharide (LPS), which peaked at 48 hours post-LPS based on clinically relevant parameters including hypoxaemia and impaired mechanics. At this peak of injury, mice were treated intratracheally with either terbutaline or tumour necrosis factor (TNF) receptor 1-targeting domain antibody, and ventilated with moderate tidal volume (20 mL/kg) to induce secondary ventilator-induced lung injury (VILI).Results Ventilation of LPS-injured mice at 20 mL/kg exacerbated injury compared with low tidal volume (8 mL/kg). While terbutaline attenuated VILI within non-LPS-treated animals, it was ineffective to reduce VILI in pre-injured mice, mimicking its lack of clinical efficacy. In contrast, anti-TNF receptor 1 antibody attenuated secondary VILI within pre-injured lungs, indicating that the model was treatable.Conclusions We propose adoption of a practical framework like that described here to reduce the number of ultimately ineffective drugs reaching clinical trials. Novel targets should be evaluated alongside interventions which have been previously tested clinically, using models that recapitulate the (lack of) clinical efficacy. Within such a framework, outperforming a failed pharmacologic should be a prerequisite for drugs entering trials.

Journal article

Soni S, Tirlapur N, O'Dea KP, Takata M, Wilson MRet al., 2019, Microvesicles as new therapeutic targets for the treatment of the acute respiratory distress syndrome (ARDS), EXPERT OPINION ON THERAPEUTIC TARGETS, Vol: 23, Pages: 931-941, ISSN: 1472-8222

Journal article

Soni S, O'Dea K, Tan YY, Cho K, Abe E, Romano R, Cui J, Ma D, Sarathchandra P, Wilson MR, Takata Met al., 2019, ATP redirects cytokine trafficking and promotes novel membrane TNF signalling via microvesicles, FASEB Journal, ISSN: 0892-6638

Cellular stress or injury induces release of endogenous danger signals such as ATP, which plays a central role in activating immune cells. ATP is essential for the release of nonclassically secreted cytokines such as IL-1β but, paradoxically, has been reported to inhibit the release of classically secreted cytokines such as TNF. Here, we reveal that ATP does switch off soluble TNF (17 kDa) release from LPS-treated macrophages, but rather than inhibiting the entire TNF secretion, ATP packages membrane TNF (26 kDa) within microvesicles (MVs). Secretion of membrane TNF within MVs bypasses the conventional endoplasmic reticulum– and Golgi transport–dependent pathway and is mediated by acid sphingomyelinase. These membrane TNF–carrying MVs are biologically more potent than soluble TNF in vivo, producing significant lung inflammation in mice. Thus, ATP critically alters TNF trafficking and secretion from macrophages, inducing novel unconventional membrane TNF signaling via MVs without direct cell-to-cell contact. These data have crucial implications for this key cytokine, particularly when therapeutically targeting TNF in acute inflammatory diseases.—Soni, S., O’Dea, K. P., Tan, Y. Y., Cho, K., Abe, E., Romano, R., Cui, J., Ma, D., Sarathchandra, P., Wilson, M. R., Takata, M. ATP redirects cytokine trafficking and promotes novel membrane TNF signaling via microvesicles.

Journal article

Davies R, O'Dea KP, Soni S, Ward JK, O'Callaghan DJP, Takata M, Gordon ACet al., 2017, P362: Vasopressin alone and with noradrenaline attenuates TNF-α production in an in-vitro model of monocyte priming and deactivation, 37th International Symposium on Intensive Care and Emergency Medicine, Publisher: BioMed Central, ISSN: 1364-8535

Conference paper

Soni S, Wilson MR, O'Dea KP, Yoshida M, Katbeh U, Woods S, Takata Met al., 2016, Alveolar macrophage-derived microvesicles mediate acute lung injury, Thorax, Vol: 71, Pages: 1020-1029, ISSN: 1468-3296

Background Microvesicles (MVs) are important mediators of intercellular communication, packaging a variety of molecular cargo. They have been implicated in the pathophysiology of various inflammatory diseases; yet, their role in acute lung injury (ALI) remains unknown.Objectives We aimed to identify the biological activity and functional role of intra-alveolar MVs in ALI.Methods Lipopolysaccharide (LPS) was instilled intratracheally into C57BL/6 mice, and MV populations in bronchoalveolar lavage fluid (BALF) were evaluated. BALF MVs were isolated 1 hour post LPS, assessed for cytokine content and incubated with murine lung epithelial (MLE-12) cells. In separate experiments, primary alveolar macrophage-derived MVs were incubated with MLE-12 cells or instilled intratracheally into mice.Results Alveolar macrophages and epithelial cells rapidly released MVs into the alveoli following LPS. At 1 hour, the dominant population was alveolar macrophage-derived, and these MVs carried substantive amounts of tumour necrosis factor (TNF) but minimal amounts of IL-1β/IL-6. Incubation of these mixed MVs with MLE-12 cells induced epithelial intercellular adhesion molecule-1 (ICAM-1) expression and keratinocyte-derived cytokine release compared with MVs from untreated mice (p<0.001). MVs released in vitro from LPS-primed alveolar macrophages caused similar increases in MLE-12 ICAM-1 expression, which was mediated by TNF. When instilled intratracheally into mice, these MVs induced increases in BALF neutrophils, protein and epithelial cell ICAM-1 expression (p<0.05).Conclusions We demonstrate, for the first time, the sequential production of MVs from different intra-alveolar precursor cells during the early phase of ALI. Our findings suggest that alveolar macrophage-derived MVs, which carry biologically active TNF, may play an important role in initiating ALI.

Journal article

Soni S, Johannsson H, 2013, Does regional anaesthesia in trauma patients lead to delayed recognition of compartment syndrome?, British Journal of Hospital Medicine, Vol: 74, Pages: 358-358, ISSN: 1750-8460

Journal article

Soni S, Moss P, Jaiganesh T, 2011, Idiopathic adult intussusception, International Journal of Emergency Medicine, Vol: 4

Journal article

Soni S, Gandhi S, 2009, Flecainide overdose causing a Brugada-type pattern on electrocardiogram in a previously well patient, The American Journal of Emergency Medicine, Vol: 27, Pages: 375.e1-375.e3, ISSN: 0735-6757

Journal article

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