scholarly journals Neutrophil chemokines and their role in IL-18-mediated increase in neutrophil O2− production and intestinal edema following alcohol intoxication and burn injury

2009 ◽  
Vol 297 (2) ◽  
pp. G340-G347 ◽  
Author(s):  
Suhail Akhtar ◽  
Xiaoling Li ◽  
Irshad H. Chaudry ◽  
Mashkoor A. Choudhry
Keyword(s):  
Neutrophil Elastase ◽  
Burn Injury ◽  
Alcohol Intoxication ◽  
Critical Role ◽  
Total Body Surface Area ◽  
Male Rats ◽  
Myeloperoxidase Activity ◽  
Neutrophil Accumulation ◽  
Total Body

We examined the role of interleukin (IL)-18 and cytokine-induced neutrophil chemokines (CINC)-1 and CINC-3 in the neutrophil release of superoxide anion (O2−) and elastase following alcohol/ethanol (EtOH) and burn injury. Male rats (∼250 g) were gavaged with EtOH to achieve a blood EtOH level of ∼100 mg/dl before ∼12.5% total body surface area burn or sham injury. Immediately after injury, rats were administered with anti-rat IL-18 antibody (80 μg/kg) or isotype control. After 20 min, anti-IL-18 antibody-treated rats were given either recombinant (r) rat CINC-1 or CINC-3. On day 1 after injury, the combined insult of EtOH and burn injury caused a significant increase in neutrophil elastase and O2− production as well as an increase in neutrophil accumulation, myeloperoxidase activity, and edema in the intestine. Treatment of rats with anti-IL-18 antibody normalized the above parameters. However, administration of rCINC-1 in anti-IL-18 antibody-treated rats increased the above parameters to levels similar to those observed following EtOH and burn injury. In contrast, administration of rCINC-3 did not influence the above parameters except neutrophil elastase. These findings indicate that IL-18 and CINC-1 may independently modulate neutrophil tissue-damaging actions following EtOH and burn injury. However, the finding that the treatment of rats with anti-IL-18 antibodies inhibits CINC-1 and CINC-3 supports the notion that IL-18 plays a critical role in increased neutrophil tissue-damaging action following a combined insult of EtOH intoxication and burn injury.

Acute alcohol intoxication increases interleukin-18-mediated neutrophil infiltration and lung inflammation following burn injury in rats

2007 ◽  
Vol 292 (5) ◽  
pp. L1193-L1201 ◽  
Author(s):  
Xiaoling Li ◽  
Elizabeth J. Kovacs ◽  
Martin G. Schwacha ◽  
Irshad H. Chaudry ◽  
Mashkoor A. Choudhry
Keyword(s):  
Lung Tissue ◽  
Lung Inflammation ◽  
Burn Injury ◽  
Alcohol Intoxication ◽  
Total Body Surface Area ◽  
Neutrophil Infiltration ◽  
Male Rats ◽  
Caspase 1 ◽  
Tissue Edema ◽  
Total Body

In this study, we examined whether IL-18 plays a role in lung inflammation following alcohol (EtOH) and burn injury. Male rats (∼250 g) were gavaged with EtOH to achieve a blood EtOH level of ∼100 mg/dl before burn or sham injury (∼12.5% total body surface area). Immediately after injury, rats were treated with vehicle, caspase-1 inhibitor AC-YVAD-CHO to block IL-18 production or with IL-18 neutralizing anti-IL-18 antibodies. In another group, rats were treated with anti-neutrophil antiserum ∼16 h before injury to deplete neutrophils. On day 1 after injury, lung tissue IL-18, neutrophil chemokines (CINC-1/CINC-3), ICAM-1, neutrophil infiltration, MPO activity, and water content (i.e., edema) were significantly increased in rats receiving a combined insult of EtOH and burn injury compared with rats receiving either EtOH intoxication or burn injury alone. Treatment of rats with caspase-1 inhibitor prevented the increase in lung tissue IL-18, CINC-1, CINC-3, ICAM-1, MPO activity, and edema following EtOH and burn injury. The increase in lung IL-18, MPO, and edema was also prevented in rats treated with anti-IL-18 antibodies. Furthermore, administration of anti-neutrophil antiserum also attenuated the increase in lung MPO activity and edema, but did not prevent the increase in IL-18 levels following EtOH and burn injury. These findings suggest that acute EtOH intoxication before burn injury upregulates IL-18, which in turn contributes to increased neutrophil infiltration. Furthermore, the presence of neutrophils appears to be critical for IL-18-meditaed increased lung tissue edema following a combined insult of EtOH and burn injury.

Cardiac effects of burn injury complicated by aspiration pneumonia-induced sepsis

2003 ◽  
Vol 285 (1) ◽  
pp. H47-H58 ◽  
Author(s):  
Jean White ◽  
James Thomas ◽  
David L. Maass ◽  
Jureta W. Horton
Keyword(s):  
Burn Injury ◽  
Contractile Function ◽  
Total Body Surface Area ◽  
Multiple Organ ◽  
Male Rats ◽  
Intratracheal Administration ◽  
Degree Burn ◽  
The Subject ◽  
Total Body ◽  
Factor Α

Early fluid resuscitation, antimicrobials, early excision, and grafting have improved survival in the early postburn period; however, a significant incidence of pneumonia-related sepsis occurs after burn injury, often progressing to multiple organ failure. Recent studies have suggested that this initial injury (burn injury) primes the subject, producing an exaggerated response to a second insult, such as pneumonia-related sepsis. We developed an experimental animal model that included a third-degree burn over 40% of the total body surface area, followed by sepsis (intratracheal administration of Streptococcus pneumoniae, 4 × 106 colony-forming unit), which was produced either 48 or 72 h after burn injury in adult male rats. Hearts harvested after either burn alone, sepsis alone, or burn plus sepsis were used to assess either contractile function (Langendorff) or cardiomyocyte secretion of tumor necrosis factor-α, interleukin (IL)-1β, IL-6, and IL-10 (ELISA). Experimental groups included the following: 1) sham (sham burn and no sepsis); 2) burn injury alone studied either 24, 48, or 72 h postburn; 3) pneumonia-related sepsis in the absence of burn injury; and 4) pneumonia-induced sepsis studied either 48 or 72 h after an initial burn injury. Burn injury alone (24 h) or sepsis alone produced myocardial contractile defects and increases in pro- and anti-inflammatory cytokine secretion by cardiomyocytes. Sepsis that occurred 48 h postburn exacerbated the cardiac contractile defects seen with either burn alone or sepsis alone. Sepsis that occurred 72 h postburn produced contractile defects resembling those seen in either burn alone or sepsis alone. In conclusion, our data suggest that burn injury primes the subject such that a second insult early in the postburn period produces significantly greater cardiac abnormalities than those seen with either burn alone or sepsis alone.

Signaling mechanisms of elevated neutrophil O 2 − generation after burn injury

1998 ◽  
Vol 274 (2) ◽  
pp. R476-R485 ◽  
Author(s):  
Farideh Sabeh ◽  
Philip Hockberger ◽  
Mohammed M. Sayeed
Keyword(s):  
Burn Injury ◽  
Total Body Surface Area ◽  
Skin Thickness ◽  
Text Generation ◽  
Intracellular Ca ◽  
Effect Of Treatment ◽  
Peak Release ◽  
Total Body ◽  
Pkc Activation

A full skin thickness burn injury was produced in anesthetized rats by exposing 25% of total body surface area to 98°C water for 10 s. Sham (exposed to 37°C water) and burn rats were killed 1, 3, 7, or 10 days later. The role of Ca2+signaling and Ca2+-related protein kinase C (PKC) activation in neutrophil[Formula: see text] generation was ascertained by evaluating the effect of treatment of the rats with the Ca2+entry blocker, diltiazem. There was an overt enhancement of[Formula: see text] generation by polymorphonuclear leukocytes from burn rats on days 1, 3, and 7 postburn, with the peak release occurring on day 3 postburn.[Formula: see text] generation comparable to the sham was noted on day 10 after the burn.[Formula: see text] releases on days 1, 3, and 7 postburn were accompanied by marked elevation of [Formula: see text] and PKC responses. Like the [Formula: see text] release, intracellular Ca2+concentration ([Ca2+]i) response on day 10 after burn was suppressed to levels found in the sham group. The treatment of burn rats with diltiazem prevented the upregulation of both [Ca2+]iand PKC responses as well as [Formula: see text]generation in neutrophils in rats on days 1, 3, and 7 after the burn. Because previous studies have shown that increases in [Ca2+]iprecede [Formula: see text] generation and degranulation, our results suggest that neutrophil[Formula: see text] release enhancement in the early stages after burn injury (e.g., days 1- 7postburn) results from an overactivation of the[Formula: see text] and PKC signaling pathways. The heightened [Formula: see text] generation during the early burn injury phase might play a role in tissue damage in one or more of host organs.

scholarly journals Treatment of Anaemia in Patients with Acute Burn Injury: A Study of Blood Transfusion Practices

2021 ◽  
Vol 10 (3) ◽  
pp. 476
Author(s):  
Ioana Tichil ◽  
Samara Rosenblum ◽  
Eldho Paul ◽  
Heather Cleland
Keyword(s):  
Blood Transfusion ◽  
Surgical Management ◽  
Burn Injury ◽  
Total Body Surface Area ◽  
Perioperative Period ◽  
Hospital Length ◽  
Hospital Length Of Stay ◽  
Burn Care ◽  
Transfusion Requirements ◽  
Total Body

Objective: To determine blood transfusion practices, risk factors, and outcomes associated with the use of blood products in the setting of the acute management of burn patients at the Victorian Adult Burn Service. Background: Patients with burn injuries have variable transfusion requirements, based on a multitude of factors. We reviewed all acute admissions to the Victorian Adult Burns Service (VABS) between 2011 and 2017: 1636 patients in total, of whom 948 had surgery and were the focus of our analysis. Method and results: Patient demographics, surgical management, transfusion details, and outcome parameters were collected and analyzed. A total of 175 patients out of the 948 who had surgery also had a blood transfusion, while 52% of transfusions occurred in the perioperative period. The median trigger haemoglobin in perioperative was 80mg/dL (IQR = 76–84.9 mg/dL), and in the non-perioperative setting was 77 mg/dL (IQR = 71.61–80.84 mg/dL). Age, gender, % total body surface area (TBSA) burn, number of surgeries, and intensive care unit and hospital length of stay were associated with transfusion. Conclusions: The use of blood transfusions is an essential component of the surgical management of major burns. As observed in our study, half of these transfusions are related to surgical procedures and may be influenced by the employment of blood conserving strategies. Furthermore, transfusion trigger levels in stable patients may be amenable to review and reduction. Risk adjusted analysis can support the implementation of blood transfusion as a useful quality indicator in burn care.

scholarly journals Pediatric burn resuscitation: past, present, and future

2017 ◽  
Vol 5 ◽  
Author(s):  
Kathleen S. Romanowski ◽  
Tina L. Palmieri
Keyword(s):  
Fluid Resuscitation ◽  
Burn Injury ◽  
Total Body Surface Area ◽  
Burn Shock ◽  
Basic Principles ◽  
Future Directions ◽  
Number Of Children ◽  
History Of ◽  
Adults And Children ◽  
Total Body

Abstract Burn injury is a leading cause of unintentional death and injury in children, with the majority being minor (less than 10%). However, a significant number of children sustain burns greater than 15% total body surface area (TBSA), leading to the initiation of the systemic inflammatory response syndrome. These patients require IV fluid resuscitation to prevent burn shock and death. Prompt resuscitation is critical in pediatric patients due to their small circulating blood volumes. Delays in resuscitation can result in increased complications and increased mortality. The basic principles of resuscitation are the same in adults and children, with several key differences. The unique physiologic needs of children must be adequately addressed during resuscitation to optimize outcomes. In this review, we will discuss the history of fluid resuscitation, current resuscitation practices, and future directions of resuscitation for the pediatric burn population.

scholarly journals Restrictive Transfusion Strategy Is More Effective in Massive Burns: Results of the TRIBE Multicenter Prospective Randomized Trial

2019 ◽  
Vol 184 (Supplement_1) ◽  
pp. 11-15 ◽  
Author(s):  
Tina L Palmieri ◽  
James H Holmes ◽  
Brett Arnoldo ◽  
Michael Peck ◽  
Amalia Cochran ◽  
...  
Keyword(s):  
Wound Healing ◽  
Burn Injury ◽  
Total Body Surface Area ◽  
Inhalation Injury ◽  
Transfusion Strategy ◽  
Restrictive Transfusion ◽  
Blood Utilization ◽  
Outcome Differences ◽  
Total Body ◽  
Restrictive Transfusion Strategy

Abstract Objectives Studies suggest that a restrictive transfusion strategy is safe in burns, yet the efficacy of a restrictive transfusion policy in massive burn injury is uncertain. Our objective: compare outcomes between massive burn (≥60% total body surface area (TBSA) burn) and major (20–59% TBSA) burn using a restrictive or a liberal blood transfusion strategy. Methods Patients with burns ≥20% were block randomized by age and TBSA to a restrictive (transfuse hemoglobin <7 g/dL) or liberal (transfuse hemoglobin <10 g/dL) strategy throughout hospitalization. Data collected included demographics, infections, transfusions, and outcomes. Results Three hundred and forty-five patients received 7,054 units blood, 2,886 in massive and 4,168 in restrictive. Patients were similar in age, TBSA, and inhalation injury. The restrictive group received less blood (45.57 ± 47.63 vs. 77.16 ± 55.0, p < 0.03 massive; 11.0 ± 16.70 vs. 16.78 ± 17.39, p < 0.001) major). In massive burn, the restrictive group had fewer ventilator days (p < 0.05). Median ICU days and LOS were lower in the restrictive group; wound healing, mortality, and infection did not differ. No significant outcome differences occurred in the major (20–59%) group (p > 0.05). Conclusions: A restrictive transfusion strategy may be beneficial in massive burns in reducing ventilator days, ICU days and blood utilization, but does not decrease infection, mortality, hospital LOS or wound healing.

scholarly journals Role of Amygdala-Infralimbic Cortex Circuitry in Glucocorticoid-Induced Facilitation of Auditory Fear Memory Extinction

2021 ◽  
pp. 1-22
Author(s):  
Masoomeh Dadkhah ◽  
◽  
Abbas Ali Vafaei ◽  
Ali Rashidy-Pour ◽  
Parnia Trahomi ◽  
...  
Keyword(s):  
Critical Role ◽  
Fear Memory ◽  
Fear Extinction ◽  
Freezing Behavior ◽  
Extinction Training ◽  
Male Rats ◽  
Memory Extinction ◽  
The Right ◽  
Fear Expression

Purpose: The basolateral amygdala (BLA) and infralimbic area (IL) of medial prefrontal cortex (mPFC) are two inter-connected brain structures that mediate both fear memory expression and extinction. Besides the well-known role of the BLA in the acquisition and expression of fear memory, projections from IL to BLA inhibit fear expression and have a critical role in fear extinction. However, the details of IL-BLA interaction remain unclear. Here, we aimed to investigate the role of functional reciprocal interactions between BLA and IL in mediating fear memory extinction. Methods: Using lidocaine (LID), male rats underwent unilateral or bilateral inactivation of the BLA and then unilateral intra-IL infusion of CORT, prior to extinction training of auditory fear conditioning paradigm. Freezing behavior was reported as an index for the measurement of conditioned fear. Infusions were performed before the extinction training, allowing to examine the effects on fear expression and also further extinction memory. Experiments 1-3 investigated the effects of left or right infusion of CORT into IL, and LID unilaterally into BLA on fear memory extinction. Results: Results showed that intra-IL infusion of CORT in the right hemisphere reduced freezing behavior when administrated before the extinction training. Auditory fear memory extinction was impaired by asymmetric inactivation of BLA and CORT infusion in the right IL; however, the same effect was not observed with symmetric inactivation of BLA. Conclusion: It is concluded that that the IL-BLA neural circuit may provide additional evidence to contribution of this circuit in auditory fear extinction. This study demonstrate dissociable roles for right or left BLA in subserving the auditory fear extinction. Our finding also raise the possibility that left BLA-IL circuitry may contribute in mediating auditory fear memory extinction via underlying mechanisms, however further research is required.

scholarly journals A Comparative Study between C-Reactive Protein and Procalcitonin in Iraqi Burn Patients

2017 ◽  
Vol 28 (1) ◽  
pp. 41
Author(s):  
Alia E. Al-Ubadi
Keyword(s):  
Burn Injury ◽  
Total Body Surface Area ◽  
Latex Agglutination ◽  
Burn Patients ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Survivor Group ◽  
Significant Difference ◽  
The Mean ◽  
Total Body

Association between Procalcitonin (PCT) and C-reactive protein (CRP) and burn injury was evaluated in 80 burned patients from Al-Kindy and Imam Ali hospitals in Baghdad-Iraq. Patients were divided into two groups, survivor group 56 (70%) and non-survivor group 24 (30%). PCT was estimated using (Human Procalcitonin ELISA kit) provided by RayBio/USA while CRP was performed using a latex agglutination kit from Chromatest (Spain). Our results declared that the mean of Total Body Surface Area (TBSA %) affected were 63.5% range (36%–95%) in non-survivor patients, while 26.5% range (10%–70%) in survivor patients. There is a significant difference between the two groups (P = 0.00), the higher mean percentage of TBSA has a significant association with mortality. Serum PCT and CRP were measured at the three times of sampling (within the first 48hr following admission, after 5thdays and after 10th days). The mean of PCT serum concentrations in non-survivor group (2638 ± 3013pg/ml) were higher than that of survivor group (588 ± 364pg/ml). Significantly high levels of CRP were found between the survivor and non-survivor groups especially in the 10th day of admission P=0.000, present study show that significant differences is found within the non-survivor group through the three times P= 0.01, while results were near to significant differences within survivor group through the three times (P= 0.05).

scholarly journals The predisposing factors of AKI for prophylactic strategies in burn care

PeerJ ◽  
2020 ◽  
Vol 8 ◽  
pp. e9984
Author(s):  
Shin-Yi Tsai ◽  
Chon-Fu Lio ◽  
Shou-Chuan Shih ◽  
Cheng-Jui Lin ◽  
Yu-Tien Chen ◽  
...  
Keyword(s):  
Burn Injury ◽  
Laboratory Data ◽  
Total Body Surface Area ◽  
Kidney Injury ◽  
Inhalation Injury ◽  
Predisposing Factors ◽  
Dust Explosion ◽  
Burn Care ◽  
Hospital Patients ◽  
Total Body

Background Acute kidney injury (AKI) is one of the most severe complications of burn injury. AKI with severe burn injury causes high mortality. This study aims to investigate the incidence of and predisposing factors for AKI in burn patients. Methods This is a single-center, retrospective, descriptive criterion standard study conducted from June 27, 2015, to March 8, 2016. We used Kidney Disease Improving Global Outcomes criteria to define and select patients with AKI. The study was conducted by recruiting in hospital patients who suffered from the flammable cornstarch-based powder explosion and were treated under primary care procedures. A total of 49 patients who suffered from flammable dust explosion-related burn injury were enrolled and admitted on June 27, 2015. The patients with more than 20% total body surface area of burn were transferred to the intensive care unit. Patients received fluid resuscitation in the first 24 hours based on the Parkland formula. The primary measurements were the incidence of and predisposing factors for AKI in these patients. Demographic characteristics, laboratory data, and inpatient outcomes were also evaluated. The incidence of AKI in this cohort was 61.2% (n = 30). The mortality rate was 2.0% (n = 1) during a 59-day follow-up period. The multivariate analysis revealed inhalation injury (adjusted OR = 22.0; 95% CI [1.4–358.2]) and meeting ≥3 American Burn Association (ABA) sepsis criteria (adjusted OR = 13.7; 95% CI [1.7–110.5]) as independent risk factors for early advanced AKI. Conclusions The incidence rate of AKI was higher in this cohort than in previous studies, possibly due to the flammable dust explosion-related burn injury. However, the mortality was lower than that expected. In clinical practice, indicators of inflammation, including ABA sepsis criteria may help in predicting the risk of AKI in patients with burn injury.

521 Incidence of Bone Fracture Rate Post-Burn and Trauma in Role 2 and 3 Treatment Centers

2021 ◽  
Vol 42 (Supplement_1) ◽  
pp. S107-S108
Author(s):  
Linda E Sousse ◽  
Amanda Staudt ◽  
Christopher VanFosson
Keyword(s):  
Bone Fracture ◽  
Injury Severity ◽  
Burn Injury ◽  
Bone Fractures ◽  
Total Body Surface Area ◽  
Anatomical Location ◽  
Fracture Rate ◽  
Initial Correlation ◽  
Total Body ◽  
Markers Of Bone Resorption

Abstract Introduction One of the hallmarks of critical illness and trauma is that it triggers resorptive bone loss, as well as an increase in bone fractures and a reduction in bone density. Sustained markers of bone resorption, bone formation, and regulators of bone signaling pathways are linked to prolonged inflammatory activities and the prolonged deterioration of bone microstructure. The objective of this study is to evaluate the bone fracture rate of the U.S Military, non-U.S. Military, North Atlantic Treaty Organization (NATO) Military, local civilian, and Coalition Forces population in Operation Enduring Freedom and Operation Freedom’s Sentinel with burns from 2005 to 2018 using the Department of Defense Trauma Registry (DoDTR; n=28,707). Our hypothesis is that there is a direct relationship between burn injury severity and bone fracture rates. Methods Pearson’s correlation coefficient and scatterplots were used in this retrospective, observational study to demonstrate the correlation between total body surface area (TBSA) burn and number of fractures by anatomical location. Results Approximately 15,195 patients (age: 26 ± 10 years) in Role 2 and Role 3 treatment centers reported fractures. Of those patients, 351 suffered from burns with 632 anatomical fracture locations. Facial fractures were most prominent (16%), followed by foot (12%), skull (12%), tibia/fibula (11%), hand (11%), and ulna/radius (10%). There was no initial correlation between n increasing severity of TBSA burn and count of fracture locations (ρ=-0.03, p=0.8572). Conclusions There was no acute correlation between burn severity and bone fracture rates; however, further analyses are required to assess chronic post-burn fracture rates.

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