Elevated 18:0 lysophosphatidylcholine contributes to the development of pain in tissue injury.

ABSTRACT: Tissue injuries, including burns, are major causes of death and morbidity worldwide. These injuries result in the release of intracellular molecules and subsequent inflammatory reactions, changing the tissues' chemical milieu and leading to the development of persistent pain through activating pain-sensing primary sensory neurons. However, the majority of pain-inducing agents in injured tissues are unknown. Here, we report that, amongst other important metabolite changes, lysophosphatidylcholines (LPCs) including 18:0 LPC exhibit significant and consistent local burn injury-induced changes in concentration. 18:0 LPC induces immediate pain and the development of hypersensitivities to mechanical and heat stimuli through molecules including the transient receptor potential ion channel, vanilloid subfamily, member 1, and member 2 at least partly via increasing lateral pressure in the membrane. As levels of LPCs including 18:0 LPC increase in other tissue injuries, our data reveal a novel role for these lipids in injury-associated pain. These findings have high potential to improve patient care.

Near-fatal Panton-Valentine leukocidin-positive Staphylococcus aureus pneumonia, shock and complicated extracorporeal membrane oxygenation cannulation: A case report.

BACKGROUND: Panton-Valentine leukocidin (PVL) is an exotoxin secreted by Staphylococcus aureus (S. aureus), responsible for skin and soft tissue infections. As a cause of severe necrotising pneumonia, it is associated with a high mortality rate. A rare entity, the epidemiology of PVL S. aureus (PVL-SA) pneumonia as a complication of influenza coinfection, particularly in young adults, is incompletely understood. CASE SUMMARY: An adolescent girl presented with haemoptysis and respiratory distress, deteriorated rapidly, with acute respiratory distress syndrome (ARDS) and profound shock requiring extensive, prolonged resuscitation, emergency critical care and venovenous extracorporeal membrane oxygenation (ECMO). Cardiac arrest and a rare complication of ECMO cannulation necessitated intra-procedure extracorporeal cardiopulmonary resuscitation, i.e., venoarterial ECMO. Coordinated infectious disease, microbiology and Public Health England engagement identified causative agents as PVL-SA and influenza A/H3N2 from bronchial aspirates within hours. Despite further complications of critical illness, the patient made an excellent recovery with normal cognitive function. The coordinated approach of numerous multidisciplinary specialists, nursing staff, infection control, specialist cardiorespiratory support, hospital services, both adult and paediatric and Public Health are testimony to what can be achieved to save life against expectation, against the odds. The case serves as a reminder of the deadly nature of PVL-SA when associated with influenza and describes a rare complication of ECMO cannulation. CONCLUSION: PVL-SA can cause severe ARDS and profound shock, with influenza infection. A timely coordinated multispecialty approach can be lifesaving.

Lactate dehydrogenase activity staining demonstrates time-dependent immune cell infiltration in human ex-vivo burn-injured skin.

Burn injuries constitute one of the most serious accidental injuries. Increased metabolic rate is a hallmark feature of burn injury. Visualising lactate dehydrogenase (LDH) activity has been previously used to identify metabolic activity differences, hence cell viability and burn depth in burn skin. LDH activity was visualised in injured and uninjured skin from 38 sub-acute burn patients. LDH activity aided the identification of spatially correlating immunocompetent cells in a sub-group of six patients. Desorption Electrospray Ionisation Mass Spectrometry Imaging (DESI MSI) was used to describe relative lactate and pyruvate abundance in burned and uninjured tissue. LDH activity was significantly increased in the middle and deep regions of burnt skin compared with superficial areas in burnt skin and uninjured tissue and positively correlated with post-burn time. Regions of increased LDH activity showed high pyruvate and low lactate abundance when examined with DESI-MSI. Areas of increased LDH activity exhibited cellular infiltration, including CD3 + and CD4 + T-lymphocytes and CD68 + macrophages. Our data demonstrate a steady increase in functional LDH activity in sub-acute burn wounds linked to cellular infiltration. The cell types associated are related to tissue restructuring and inflammation. This region in burn wounds is likely the focus of dysregulated inflammation and hypermetabolism.

Colonic perforation following major burns: Experience from a burns center and a systematic review.

BACKGROUND: Major burns complicated by stress ulceration and perforation of the stomach or duodenum is a recognized clinical phenomenon. Colonic perforation in burns patients is not common, and the overall incidence, diagnosis, intervention undertaken and mortality is incompletely described in the literature. METHOD: We performed a systematic review of the literature on severe burns resulting in colonic perforation during the initial admission period. Relevant studies from January 1975 to June 2020 were retrieved from MEDLINE and EMBASE databases. Patient demographics, co-morbidities, total body surface area (TBSA) and anatomical region of burn, site of colonic perforation and management, nutrition, sepsis and microbiology, length of stay and overall outcome were extracted. We present a case series of five burns patients who had colonic perforations in our Specialist Burns Center. RESULTS: We identified 54 studies, of which nine (two case series and seven case reports) met the inclusion criteria. Colonic perforation following burns was most common in middle-aged male patients with a proportion of patients having a history of mental health issues. In most cases, the TBSA associated with a colonic perforation was ≥30% (11/16 patients, 69%). Perforations mainly affected the right side of the colon (12/16 patients, 75%), usually occurring after the second week of admission (13/16 patients, 81%). Right-sided colonic perforations were associated with an increased mortality rate compared to left-sided perforations (42% vs 25%). CONCLUSIONS: The current literature is mainly limited to case series and case reports and confirms that colonic perforations in burns patients are rare. Colonic perforations are related to the systemic effect of burn injuries including sepsis and gastrointestinal stasis. We have identified patients who are at higher risk of developing colonic perforations and have described the common findings in these patients. Through greater awareness early diagnosis and prompt intervention may be achieved to improve outcomes and reduce associated morbidity and mortality.