Hydroxocobalamin-induced oxalate nephropathy in a patient with smoke inhalation

IntroductionIn the USA, Food and Drug Administration regulations prohibit the sale of flavoured cigarettes, with menthol being the exception. However, the manufacture, advertisement and sale of flavoured cigar products are permitted. Such flavourings influence positive perceptions of tobacco products and are linked to increased use. Flavourings may mask the taste of tobacco and enhance smoke inhalation, influencing toxicant exposure and abuse liability among novice tobacco users. Using clinical laboratory methods, this study investigates how flavour availability affects measures of abuse liability in young adult cigarette smokers. The specific aims are to evaluate the effect of cigar flavours on nicotine exposure, and behavioural and subjective measures of abuse liability.Methods and analysesParticipants (projected n=25) are healthy smokers of five or more cigarettes per day over the past 3 months, 18–25 years old, naive to cigar use (lifetime use of 50 or fewer cigar products and no more than 10 cigars smoked in the past 30 days) and without a desire to quit cigarette smoking in the next 30 days. Participants complete five laboratory sessions in a Latin square design with either their own brand cigarette or a session-specific Black & Mild cigar differing in flavour (apple, cream, original and wine). Participants are single-blinded to cigar flavours. Each session consists of two 10-puff smoking bouts (30 s interpuff interval) separated by 1 hour. Primary outcomes include saliva nicotine concentration, behavioural economic task performance and response to various questionnaire items assessing subjective effects predictive of abuse liability. Differences in outcomes across own brand cigarette and flavoured cigar conditions will be tested using linear mixed models.Ethics and disseminationThe Virginia Commonwealth University Institutional Review Board approved the study (VCU IRB: HM20007848). Dissemination channels for study findings include scientific journals, scientific meetings, and policy briefs.Trial registration numberNCT02937051.

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A novel large animal model of smoke inhalation-induced acute respiratory distress syndrome

Respiratory Research ◽

10.1186/s12931-021-01788-8 ◽

2021 ◽

Vol 22 (1) ◽

Author(s):

Premila D. Leiphrakpam ◽

Hannah R. Weber ◽

Andrea McCain ◽

Roser Romaguera Matas ◽

Ernesto Martinez Duarte ◽

...

Keyword(s):

Animal Model ◽

Acute Respiratory Distress Syndrome ◽

Respiratory Distress Syndrome ◽

Distress Syndrome ◽

Inhalation Injury ◽

Smoke Inhalation ◽

Large Animal Model ◽

Large Animal ◽

X Ray ◽

Chest X Ray

Abstract Background Acute respiratory distress syndrome (ARDS) is multifactorial and can result from sepsis, trauma, or pneumonia, amongst other primary pathologies. It is one of the major causes of death in critically ill patients with a reported mortality rate up to 45%. The present study focuses on the development of a large animal model of smoke inhalation-induced ARDS in an effort to provide the scientific community with a reliable, reproducible large animal model of isolated toxic inhalation injury-induced ARDS. Methods Animals (n = 21) were exposed to smoke under general anesthesia for 1 to 2 h (median smoke exposure = 0.5 to 1 L of oak wood smoke) after the ultrasound-guided placement of carotid, pulmonary, and femoral artery catheters. Peripheral oxygen saturation (SpO2), vital signs, and ventilator parameters were monitored throughout the procedure. Chest x-ray, carotid, femoral and pulmonary artery blood samples were collected before, during, and after smoke exposure. Animals were euthanized and lung tissue collected for analysis 48 h after smoke inhalation. Results Animals developed ARDS 48 h after smoke inhalation as reflected by a decrease in SpO2 by approximately 31%, PaO2/FiO2 ratio by approximately 208 (50%), and development of bilateral, diffuse infiltrates on chest x-ray. Study animals also demonstrated a significant increase in IL-6 level, lung tissue injury score and wet/dry ratio, as well as changes in other arterial blood gas (ABG) parameters. Conclusions This study reports, for the first time, a novel large animal model of isolated smoke inhalation-induced ARDS without confounding variables such as cutaneous burn injury. Use of this unique model may be of benefit in studying the pathophysiology of inhalation injury or for development of novel therapeutics.

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Bilateral Lobar Lung Transplantation after Smoke Inhalation Injury - A Case Report

The Journal of Heart and Lung Transplantation ◽

10.1016/j.healun.2021.01.2075 ◽

2021 ◽

Vol 40 (4) ◽

pp. S515

Author(s):

E. Olsson ◽

M. Silverborn ◽

U. Smedh ◽

G.C. Riise ◽

J.M. Magnusson ◽

...

Keyword(s):

Case Report ◽

Lung Transplantation ◽

Inhalation Injury ◽

Smoke Inhalation ◽

Smoke Inhalation Injury

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Peroxynitrite decomposition catalyst reduces vasopressin requirement in ovine MRSA sepsis

Intensive Care Medicine Experimental ◽

10.1186/s40635-019-0227-4 ◽

2019 ◽

Vol 7 (1) ◽

Cited By ~ 1

Author(s):

Osamu Fujiwara ◽

Satoshi Fukuda ◽

Ernesto Lopez ◽

Yaping Zeng ◽

Yosuke Niimi ◽

...

Keyword(s):

Septic Shock ◽

Fluid Resuscitation ◽

Conscious State ◽

Smoke Inhalation ◽

Post Injury ◽

Adjunct Treatment ◽

Aggressive Fluid Resuscitation ◽

Severe Hypotension ◽

Bolus Intravenous Injection

Abstract Background Sepsis is one of the most frequent causes of death in the intensive care unit. Host vascular hypo-responsiveness to vasopressors during septic shock is one of the challenging problems. This study tested the hypothesis that adjunct therapy with peroxynitrite decomposition catalyst (WW-85) would reduce arginine vasopressin (AVP) requirements during sepsis resuscitation, using ovine sepsis model. Methods Thirteen adult female Merino sheep, previously instrumented with multiple vascular catheters, were subjected to “two-hit” (cotton smoke inhalation and intrapulmonary instillation of live methicillin-resistant Staphylococcus aureus; 3.5 × 1011 colony-forming units) injury. Post injury, animals were awakened and randomly allocated to the following groups: (1) AVP: injured, fluid resuscitated, and titrated with AVP, n = 6 or (2) WW-85 + AVP: injured, fluid resuscitated, treated with WW-85, and titrated with AVP, n = 7. One-hour post injury, a bolus intravenous injection of WW-85 (0.1 mg/kg) was followed by a 23-h continuous infusion (0.02 mg/kg/h). Titration of AVP started at a dose of 0.01 unit/min, when mean arterial pressure (MAP) decreased by 10 mmHg from baseline, despite aggressive fluid resuscitation, and the rate was further adjusted to maintain MAP. After the injury, all animals were placed on a mechanical ventilator and monitored in the conscious state for 24 h. Results The injury induced severe hypotension refractory to aggressive fluid resuscitation. High doses of AVP were required to partially attenuate the sepsis-induced hypotension. However, the cumulative AVP requirement was significantly reduced by adjunct treatment with WW-85 at 17–24 h after the injury (p < 0.05). Total AVP dose and the highest AVP rate were significantly lower in the WW-85 + AVP group compared to the AVP group (p = 0.02 and 0.04, respectively). Treatment with WW-85 had no adverse effects. In addition, the in vitro effects of AVP on isolated artery diameter changes were abolished with peroxynitrite co-incubation. Conclusions The modulation of reactive nitrogen species, such as peroxynitrite, may be considered as a novel adjunct treatment option for septic shock associated with vascular hypo-responsiveness to vasopressors.

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Rat model of smoke inhalation-induced acute lung injury

BMJ Open Respiratory Research ◽

10.1136/bmjresp-2021-000879 ◽

2021 ◽

Vol 8 (1) ◽

pp. e000879

Author(s):

Premila Devi Leiphrakpam ◽

Hannah R Weber ◽

Tobi Ogun ◽

Keely L Buesing

Keyword(s):

Animal Model ◽

Acute Lung Injury ◽

Lung Injury ◽

Caspase 3 ◽

Small Animal ◽

Therapeutic Options ◽

Smoke Inhalation ◽

Small Animal Model ◽

Injury Score ◽

Confounding Variables

BackgroundAcute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is a lethal disease with limited therapeutic options and an unacceptably high mortality rate. Understanding the complex pathophysiological processes involved in the development of ALI/ARDS is critical for developing novel therapeutic strategies. Smoke inhalation (SI) injury is the leading cause of morbidity and mortality in patients with burn-associated ALI/ARDS; however, to our knowledge few reliable, reproducible models are available for pure SI animal model to investigate therapeutic options for ALI/ARDS without the confounding variables introduced by cutaneous burn or other pathology.ObjectiveTo develop a small animal model of pure SI-induced ALI and to use this model for eventual testing of novel therapeutics for ALI.MethodsRats were exposed to smoke using a custom-made smoke generator. Peripheral oxygen saturation (SpO2), heart rate, arterial blood gas, and chest X-ray (CXR) were measured before and after SI. Wet/dry weight (W/D) ratio, lung injury score and immunohistochemical staining of cleaved caspase 3 were performed on harvested lung tissues of healthy and SI animals.ResultsThe current study demonstrates the induction of ALI in rats after SI as reflected by a significant, sustained decrease in SpO2 and the development of diffuse bilateral pulmonary infiltrates on CXR. Lung tissue of animals exposed to SI showed increased inflammation, oedema and apoptosis as reflected by the increase in W/D ratio, injury score and cleaved caspase 3 level of the harvested tissues compared with healthy animals.ConclusionWe have successfully developed a small animal model of pure SI-induced ALI. This model is offered to the scientific community as a reliable model of isolated pulmonary SI-induced injury without the confounding variables of cutaneous injury or other systemic pathology to be used for study of novel therapeutics or other investigation.

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Secondary Oxalate Nephropathy: Causes and Clinicopathological Characteristics of a Case Series

Nephron ◽

10.1159/000517072 ◽

2021 ◽

pp. 1-8

Author(s):

Shaoshan Liang ◽

Lijuan Li ◽

Dacheng Chen ◽

Dandan Liang ◽

Feng Xu ◽

...

Keyword(s):

Renal Function ◽

Renal Replacement Therapy ◽

Renal Biopsy ◽

Replacement Therapy ◽

Case Series ◽

Common Cause ◽

Renal Function Recovery ◽

Function Recovery ◽

Renal Biopsies ◽

Oxalate Nephropathy

Introduction: Secondary oxalate nephropathy (OxN) is associated with a variety of causes and has not been well characterized in Chinese population. To investigate the etiology, clinicopathological features, and outcomes of secondary OxN, we report a case series from a single center in China. Methods: A retrospective analysis of 68 patients diagnosed with secondary OxN by renal biopsy from January 2013 to February 2019 in Jinling Hospital was performed. Results: Secondary OxN accounted for 0.23% of the renal biopsies and 2.31% of patients who received renal biopsies due to acute kidney injury (AKI). A total of 49 men and 19 women with an average age of 51.6 ± 11.8 years were enrolled. The most common cause was iatrogenic medication, followed by oxalate-rich diet and industry exposure. Stage 1, 2, and 3 AKI and AKI on chronic kidney disease (ACKD) were found in 4.4, 8.8, 69.1, and 17.6% of the patients, respectively. The peak serum creatinine during hospitalization was 8.62 ± 4.67 mg/dL. The median urinary oxalate excretion was 51.5 (23.2–147.1) mg/24 h. Kidney biopsy showed extensive calcium oxalate crystal deposits with acute tubulointerstitial nephritis. Thirty-four patients (50.0%) required renal replacement therapy. At the end of a follow-up that lasted 8.7 (0.1–72.1) months, 81.0% of patients achieved renal function recovery in 50 (14–432) days. Patients with renal function recovery had a lower rate of ACKD, a higher level of hemoglobin, a lower level of urine lysozyme, and a lower degree of interstitial fibrosis/tubular atrophy, interstitial inflammation, and global glomerulosclerosis than those in the nonrecovery group. Conclusions: In this case series of secondary OxN, the most common cause was iatrogenic medication, and it presented with AKI or ACKD. Half of the patients required renal replacement therapy, and in most of them, the renal function was reversible. Renal biopsy played an important role in diagnosis and prognosis evaluation.

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523 Retrospective Outcomes Analysis of Tracheostomy in Paediatric Burn Population

Journal of Burn Care & Research ◽

10.1093/jbcr/irab032.174 ◽

2021 ◽

Vol 42 (Supplement_1) ◽

pp. S108-S109

Author(s):

Nicholas Iglesias ◽

Anesh Prasai ◽

George Golovko ◽

Deepak K Ozhathil ◽

Steven E Wolf

Keyword(s):

Inhalation Injury ◽

Smoke Inhalation ◽

Research Network ◽

Burn Patients ◽

Pulmonary Injury ◽

Smoke Inhalation Injury ◽

Mortality And Morbidity ◽

Laryngeal Injury ◽

Icd 10 ◽

Potential Benefits

Abstract Introduction For decades, controversy has raged regarding the placement of tracheostomy in severe paediatric burns. Numerous variables including extent of smoke inhalation injury, % TBSA burned, age of the patient, and co-morbidities among others complicate reaching consensus. Furthermore, paediatric patients are particularly susceptible to complications including inadvertent loss of airway and long-term swallowing and other anatomic issues. Additionally, previous analysis of the efficacy of tracheostomy in paediatric burn patients appears to be hindered by a lack of nationwide analysis. The aim of this study was to explore the efficacy of tracheostomy in the general paediatric burn patient population. Methods De-identified patient data was obtained from the TriNetX Research Network database. Two cohorts were identified: paediatric burn patients with tracheostomy (cohort A) and paediatric burn patients without tracheostomy (cohort B). Burn patients were identified using the ICD-10 codes T20-T25 & T30-T32. Tracheostomy was identified using the ICD-10 codes 1005887, 1014613, 31600, 31601, 31603, 31604, 31610, and Z93.0. A total of 132 patients were identified in cohort A in 23 HCOs and 83,117 patients were identified in cohort B in 38 HCOs. Infection, hypovolemia, pulmonary injury, laryngeal injury, pneumonia, and death were compared between the cohorts. Results Cohort A had a mean age of 11 (SD=5) and Cohort B had a mean age of 9 (SD=5). Paediatric burn patients with tracheostomy had a higher risk for death, infection, hypovolemia, pulmonary injury, laryngeal injury, and pneumonia when compared to their non-tracheostomy counterparts. The risk ratios for these outcomes were 62.452, 4.713, 9.267, 26.483, 116.163, and 18.154, respectively. Conclusions The analysis of the longitudinal outcomes of pediatric burn patients with tracheostomy as compared to those without tracheostomy demonstrated the tracheostomy cohort suffered much worse mortality and morbidity across several metrics. The potential benefits of tracheostomy placement in pediatric burn patients should be weighed against these outcomes.

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