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A=Cardiac index (L/min/m 2 ); B=Intrathoracic blood volume index (ml/m2); C= Extravascular lung water index (ml/kg); and D= Systemic vascular resistance index (dyn s cm-5 m 2 ), measured on days 1-14 after injury (n=17). Squares indicate the median, boxes extend from 25 th to 75 th centile, and error bars show the 10 th and 90 th centiles.
Source publication
Organ dysfunction and failure are important for burned patients as they increase morbidity and mortality. Recent evidence has suggested that organ injuries are occurring earlier after burns, and are more common than previously thought. In this study we have assessed the extent to which liver function, assessed by the plasma disappearance rate of in...
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Citations
... Burn injury causes hepatic injury due to hypoperfusion, inflammatory cytokines, edema, and fatty changes in the liver. 91 Fatty liver and hepatomegaly are seen in severely burned patients. [92][93][94] Fatty infiltration was found in 82% of patients undergoing liver biopsies and in 18% of patients with hepatic necrosis. ...
Immune responses that occur following burn injury comprise a series of reactions that are activated in response to damaged autologous tissues, followed by removal of damaged tissues and foreign pathogens such as invading bacteria, and tissue repair. These immune responses are considered to be programmed in living organisms. Developments of modern medicine have led to the saving of burned patients who could not be cured previously; however, the programmed response is no longer able to keep up, and various problems have arisen. This paper describes the mechanism of immune response specific to burn injury and the emerging concept of persistent inflammation, immunosuppression, and catabolism syndrome.
... Patients were treated according to a previously well-described protocol [4,18]. This included resuscitation using the Parkland formula with the following endpoints: urinary output ≥ 0.5 ml/kg per hour, MAP ≥ 65 mm Hg, and plasma lactate within the reference range (0.6-2.4 mmol/L). ...
Introduction:
Previous investigations have shown that fluid resuscitation of burns using the Parkland formula results in controlled hypovolaemia and that kidney injury is a common complication. Enhancing monitoring of tissue perfusion might reduce complications. Plasma renin has recently been suggested to be a promising marker for tissue hypoperfusion in intensive care patients. The aim of this study was to explore plasma renin levels during the first 48 hours after major burns in patients resuscitated using the Parkland formula.
Materials and methods:
Patients 18 years or older of age with 10% or more total body surface area (TBSA) burned, admitted to Linköping Burn Intensive Care Unit, and resuscitated using the Parkland formula were included. Samples for plasma renin were drawn at admission and eight-hourly thereafter for 48 hours.
Results:
Fifteen patients were included. Median TBSA burned was 36% and age 53 years. The fluid volumes provided were in accordance with the Parkland formula. Mean arterial pressure, urinary output, and lactate remained within reference ranges during the first 48 hours. At eight hours after burn median plasma renin was elevated to more than 25 times the upper reference value, decreasing to about four times the upper reference at 48 hours. Renin concentration was associated with lactate levels and TBSA burned.
Conclusion:
During Parkland fluid resuscitation of severe burns, plasma renin levels were extremely elevated. The fact that the traditionally used endpoints for Parkland fluid resuscitation remained within the reference range raises concerns about whether the increased renin concentrations may signal a relative renal hypoperfusion.
... Notwithstanding this, emerging literature stresses the importance of the hepatic response to thermal burn injury as a key predictor of clinical outcomes [126]. Indeed, early transient liver dysfunction is a common finding, with persistent and advanced hepatic impairment being associated with greater mortality [127]. In such circumstances, the PK of agents that are extensively metabolised by the liver may be deranged. ...
Patients suffering major burn injury represent a unique population of critically ill patients. Widespread skin and tissue damage causes release of systemic inflammatory mediators that promote endothelial leak, extravascular fluid shifts, and cardiovascular derangement. This phase is characterized by relative intra-vascular hypovolaemia and poor peripheral perfusion. Large volume intravenous fluid resuscitation is generally required. The patients clinical course is then typically complicated by ongoing inflammation, protein catabolism, and marked haemodynamic perturbation. At all times, drug distribution, metabolism, and elimination are grossly distorted. For hydrophilic agents, changes in volume of distribution and clearance are marked, resulting in potentially sub-optimal drug exposure. In the case of antibiotics, this may then promote treatment failure, or the development of bacterial drug resistance. As such, empirical dose selection and pharmaceutical development must consider these features, with the application of strategies that attempt to counter the unique pharmacokinetic changes encountered in this setting.
... The patients were treated according to our standard protocol, which includes early excision and grafting, standard ventilation with 8-10ml/kg tidal volumes, fluid management using the Parkland formula, early enteral feeding, and laboratory assessment (also according to a standard protocol). TBSA % and percentage full thickness burn (FTB %) were recorded on admission on a detailed Lund & Browder chart and all data are entered into a database [13][14][15][16]. ...
Introduction:
The Baux score - the sum of age and total body surface area burned (TBSA %) - is a good predictor of mortality has a high specificity but low sensitivity. Our aim was to examine the causes of death in patients who die with Baux scores of <100, which may explain the lower sensitivity and possibly affect the prediction of mortality.
Methods:
All patients admitted to our centre for burn care from 1993 to 2015 (n=1946) were included in this retrospective, descriptive, exploratory study. The study group comprised those patients who died with Baux scores of <100 (n=23), and their medical charts were examined for the cause of death and for coexisting diseases.
Results:
Crude mortality was 5% (93/1946) for the overall cohort, and a quarter of the patients who died (23/93) had Baux scores of less than 100 (range 64-99). In this latter group, flame burns were the most common (18/23), the median (10th-90th centile) age was 70 (46-86) years and for TBSA 21 (5.0-40.5) %, of which 7 (0-27.0) % of the area was full thickness. The main causes of death in 17 of the 23 were classified as "other than burn", being cerebral disease (n=9), cardiovascular disease (n=6), and respiratory failure (n=2). Among the remaining six (burn-related) deaths, multiple organ failure (predominantly renal failure) was responsible. When we excluded the cases in which the cause of death was not related to the burn, the Baux mortality prediction value improved (receiver operating characteristics area under the curve, AUC) from 0.9733 (95% CI 0.9633-0.9834) to 0.9888 (95% CI 0.9839-0.9936) and the sensitivity estimate increased from 45.2% to 53.9%.
Conclusion:
Patients with burns who died with a Baux score <100 were a quarter of all the patients who died. An important finding is that most of these deaths were caused by reasons other than the burn, usually cerebrovascular disease. This may be the explanation why the sensitivity of the Baux score is low, as factors other than age and TBSA % explain the fatal outcome.
... Тепловая травма приводит к повреждению печени несколькими путями: гипоперфузия, выделение провоспалительных цитокинов, отек, жировая дистрофия. В базе Американской ожоговой ассоциации повреждения печени находятся в списке топ-10 самых распространенных осложнений среди взрослых пациентов ожогового отделения [49]. Смертность от печеночной дисфункции составляет 3,5 % [24]. ...
Current information on the effects of extensive and deep burns upon the liver functions as well as some novel methods of its correction with succinic acid derivates are reviewed. The liver is the main target organ for extensive burn injuries. Manifestations of cytolytic and cholestatic syndrome were observed already on the first days of the disease. To correct these conditions a comprehensive layout of the infusion of intensive therapy is needed. In burn disease it is impossible to restore the circulating blood volume only by infusion of plasma-substituting solutions. Thus, these cocktails must contain drugs, stabilizing metabolic disorders and reducing the concentration of proinflammatory cytokines. Complex intensive therapy in case of burns should also include correction of energy production within the cells without increasing oxygen transport. Substrate antihypoxic drugs are used in order to reduce the need of tissues for oxygen, stabilization of cell membranes and reduction of lipid peroxidation. Succinic acid is a substrate antihypoxic drug capable of detoxification, antihypoxic, antioxidant and hepatoprotective effects. Its derivates modify cellular respiration, compensate for metabolic acidosis, reducing lactate, pyruvate and citrate concentration, normalize histamine and serotonin concentration, improve microcirculation without affecting systemic hemodynamics. All of these effects are pathogenetically substantiated in the treatment of patients with burns. Data regarding the use of drugs on the basis of succinic acid in the treatment of patients with extensive deep burns, critical and supercritical burns during various periods of burn disease, their influence on the severity of multiple organ dysfunction in these patients, the presence of hepatoprotective effect are reported in a few of publications and their conclusions are so far ambiguous enough.
... This cascade involves IL-1, IL-6 and PGE-2, with TNF-as the major trigger. [96][97] In one study, the levels of anti-thrombin (AT) and several cytokines were measured in the plasma and peritoneal fluids of people who developed abdominal compartment syndrome from severe burns. It was found that while AT levels were lowered, there was an increase in levels of INF-y, IL-10, IL-6, IL-4 and IL-2 in both fluids. ...
Severe burns trigger a wide range of responses in the victim. Initial vascular changes are followed by hypermeta-bolic, inflammatory and immunologic changes. The prolonged hypermetabolic response is associated with an elevated resting rate of energy consumption, tissue wasting and altered substrate kinetics. There is increased blood glucose though insulin levels are above normal. The cortisol level is raised and, together with catecholamine, drives the metabolic response. The immune system is typically weakened. There is elevation in blood levels of a wide range of cytokines from activated cells. These agents drive a prolonged inflammatory response which can lead to tissue damage and multiple organ failure. Dynamic fluid resuscitation regimens have cut down mortality from shock in the early post-burn period. However, unbalanced activity of pro-and anti-inflammatory cytokines can leave patients in an immuno-suppressed state that affects outcomes. So far, many treatments, such as pro-pranolol, a cardio-protector, and anabolic agents, such as oxandrolone and growth hormone, have been tried with mixed results. This review focuses on research that elucidated burn pathophysiology. Some clinical areas in which treatment centred on correcting altered physiology were also included. We have highlighted both the challenges and significant findings. Finally, this paper draws attention to the gaps between progress in basic research and clinical application and suggests areas where further research and funding could be focused. © 2015, Mediterranean Club for Burns and Fire Disasters. All rights reserved.
Indocyanine green angiography (ICGA) has been widely employed for quantitative evaluation of the rat comb burn model, but the imaging equipment, imaging protocol, and fluorescence data interpretation of ICGA remain unsatisfactory. The aim of this study is to provide better solutions for the application of ICGA on perfusion analysis. The rat comb burn model was established under a series of different comb contact durations including 10, 20, 25, 30, 35, and 40 s. ICGA was used to analyze wound perfusion. Sixteen rats were divided into ibuprofen and control groups for the burn model, and their perfusion was compared. Sixteen identical models were divided into standard and high-dose ICG groups, and ICGA was conducted to investigate the dynamic change in wound fluorescence. Escharectomy was performed under real-time fluorescence mapping and navigation. The results showed that a comb contact duration of 30 s was optimum for the burn model. ICGA could accurately evaluate the histologically determined depth of thermal injury and wound perfusion in the rat comb model. Digital subtraction of residual fluorescence was necessary for multiple comparisons of perfusion. Dynamic changes in fluorescence and necrotic tissues were observed more clearly by high-dose (0.5 mg/kg) ICG in angiography. In conclusion, perfusion analysis by ICGA can be used to assess the histologically determined depth of thermal injury and the impact of a specific treatment on wound perfusion. ICGA can help to identify necrotic tissue. Above findings and related imaging protocols lay the foundation for future research.
Anesthesia care for severely burned patients requires a thorough understanding of the alterations incurred by burn on every organ system, as well as an appreciation for the pharmacodynamic and pharmacokinetic changes that occur with severe burns. Attention to this pathophysiology informs the anesthesia clinician in planning each element of the anesthetic—including managing the airway, obtaining adequate vascular access, selecting the most favorable anesthetic agents, and establishing a multimodal analgesic regimen. Close communication and coordination among anesthesia clinicians, surgeons, and nurses improve teamwork and enhance patient safety in this often-critically ill population.KeywordsAnesthesiaNeuromuscular relaxantPharmacologyPharmacokineticsPharmacodynamicsAirwayAnalgesia
Introduction
Severe burns are devastating injuries affecting multiple organ systems. Little is known about the influence on the hepatic system and its physiology. This systematic review aimed to assess the current state of research on morphologic liver damage following severe burns.
Methods
A search was conducted in Pubmed, Web of Science and Cochrane databases using PRISMA guidelines. Outcomes included serum levels of transaminases, fatty infiltration and necrosis. Weighted individual study estimates were used to calculate pooled transaminase levels and necrosis/fatty infiltration rates using a random-effects approach. Risk ratios (RRs) or Odds ratios (ORs) and 95% confidence intervals (CIs) were used to describe pooled estimates for risk factors.
Results
The literature search retrieved 2548 hits, of which 59 studies were included into qualitative synthesis, and finally ten studies were included into meta-analysis. Studies were divided into those reporting autopsies and those reporting changes of serum transaminase levels. The majority of liver autopsies showed fatty infiltration 82% (95% CI39%-97%) or necrosis of the liver 18% (95% CI13%-24%).
Discussion
Heterogeneity in studies on hepatic functional damage following severe burns was high. Only few were well-designed and published in recent years. Many studies could not be included because of insufficient numerical data. There is a high number of patients deceasing from burns that present with fatty infiltration or necrosis of hepatic tissue. Transaminases were elevated during the first days after burn. Further research on how severe burns affect the hepatic function and outcome, especially long-term, is necessary.
Introduction: Management of benign positional vertigo (BPV) in the emergency department (ED) includes performing specific maneuvers at the bedside which relieve symptoms in a large proportion of cases. The aim of this study was to evaluate the effectiveness of therapeutic maneuvers in relieving BPV symptoms in the ED.
Materials and Methods: A convenience sample of patients who presented to our ED with vertiginous symptoms during an 80-day period were evaluated for the study. Patients were examined by a single physician using Dix-Hallpike and lateral canal testing to determine the character of each patient’s nystagmus, if present. Those with chronic disease or already taking anti-vertigo medications were excluded. According to their test findings, patients were subjected to one of the following maneuvers: the modified Epley, the modified Semont, or the Brandt-Daroff maneuver. Before the maneuver, and 15 and 30 minutes after the maneuver, patients rated their vertigo symptoms on a 0-10 verbal rating scale. Using SPSS 12 for Windows®, before and after ratings were compared using chi-squared and Kruskal Wallis testing.
Results: During the study period, 72 patients presented with vertiginous symptoms, and 40 were enrolled in the study. In the modified Epley (n=26) and modified Semont (n=11) maneuver groups, mean patient symptom scores decreased significantly between baseline and 15 minutes (p=0.0001 for both groups), and between baseline and 30 minutes (p=0.0001 and p=0.001, respectively). The number of patients (n=3) in the group subjected to the Brandt-Daroff maneuver was not sufficient for statistical testing.
Conclusions: All three performed therapeutic maneuvers are effective for the treatment of patients with BPV in the ED.
Key words: Benign positional vertigo, maneu vers, emergency department.
