Zoltan Bak

Acute kidney injury is common, parallels organ dysfunction or failure, and carries appreciable mortality in patients with major burns: a prospective exploratory cohort study

IntroductionThe purpose of this study was to determine the incidence, time course, and outcome of acute kidney injury after major burns and to evaluate the impact of possible predisposing factors (age, gender, and depth and extent of injury) and the relation to other dysfunctioning organs and sepsis.MethodWe performed an explorative cohort study on patients with a TBSA% (percentage burned of total body surface area) of 20% or more who were admitted to a national burn centre. Acute kidney injury was classified according to the international consensus classification of RIFLE (Risk, Injury, Failure, Loss of kidney function, and End-stage kidney disease). Prospectively collected clinical and laboratory data were used for assessing organ dysfunction, systemic inflammatory response, and sepsis.ResultsThe incidence of acute kidney injury among major burns was 0.11 per 100,000 people per year. Of 127 patients, 31 (24%) developed acute kidney injury (12% Risk, 8% Injury, and 5% Failure). Mean age was 40.6 years (95% confidence interval [CI] 36.7 to 44.5), TBSA% was 38.6% (95% CI 35.5% to 41.6%), and 25% were women. Mortality was 14% and increased with increasing RIFLE class (7% normal, 13% Risk, 40% Injury, and 83% Failure). Renal dysfunction occurred within 7 days in 55% of the patients and recovered among all survivors. Age, TBSA%, and extent of full thickness burns were higher among the patients who developed acute kidney injury. Pulmonary dysfunction and systemic inflammatory response syndrome were present in all of the patients with acute kidney injury and developed before the acute kidney injury. Sepsis was a possible aggravating factor in acute kidney injury in 48%. Extensive deep burns (25% or more full thickness burn) increased the risk for developing acute kidney injury early (risk ratio 2.25).ConclusionsAcute kidney injury is common, develops soon after the burn, and parallels other dysfunctioning organs. Although acute kidney injury recovered in all survivors, in higher acute kidney injury groups, together with cardiovascular dysfunction, it correlated with mortality.

Acute respiratory distress syndrome is as important as inhalation injury for the development of respiratory dysfunction in major burns

Respiratory dysfunction is common after major burns. The pathogenesis is, however, still under debate. The aim was to classify and examine underlying reasons for respiratory dysfunction after major burns. Consecutive adult patients (n=16) with a total burned body surface area of 20% or more who required mechanical ventilation were assessed for acute respiratory distress syndrome (ARDS), inhalation injury, sepsis, ventilator-associated pneumonia (VAP), ventilator-induced lung injury (VILI), using conventional criteria, together with measurements of cardiovascular variables and viscoelastic properties of the lung including extravascular lung water. Nine patients developed ARDS within 6 days of injury. ARDS was characterized by a large reduction in the PEEP-adjusted PaO(2):FiO(2) ratio, pulmonary compliance, and increased extra vascular lung water together with increased renal dysfunction rates. Seven patients fulfilled the criteria for inhalation injury. They also had decreased PaO(2):FiO(2) ratios. There was an increase in extra vascular lung water and a decrease in compliance measures though not to the same extent as in the ARDS group. White blood cell counts dropped from (mean) 21.4x10(9)l(-1) (95% CI 15.3-27.5) in day 1 to 4.3x10(9)l(-1) (2.2-6.5) on day 3, and lower values tended to correlate with the development of ARDS. Sepsis occurred before onset of ARDS in only three cases. One patient fulfilled the criteria for VAP, but none was thought to have VILI. We found that respiratory dysfunction after burns is multifactorial, and ARDS and inhalation injury are most important. The early onset of ARDS, together with the changes in white blood cell count and organ dysfunction, favours a syndrome in which respiratory distress is induced by an inflammatory process mediated by the effect of the burn rather than being secondary to sepsis. The power of these conclusions is, however, hampered by the small number of patients in this study.

Human cardiovascular dose-response to supplemental oxygen

Aim:  The aim of the study was to examine the central and peripheral cardiovascular adaptation and its coupling during increasing levels of hyperoxaemia. We hypothesized a dose‐related effect of hyperoxaemia on left ventricular performance and the vascular properties of the arterial tree.

Hemodynamic Changes During Resuscitation After Burns Using the Parkland Formula

BACKGROUND The Parkland formula (2-4 mL/kg/burned area of total body surface area %) with urine output and mean arterial pressure (MAP) as endpoints for the fluid resuscitation in burns is recommended all over the world. There has recently been a discussion on whether central circulatory endpoints should be used instead, and also whether volumes of fluid should be larger. Despite this, there are few central hemodynamic data available in the literature about the results when the formula is used correctly. METHODS Ten burned patients, admitted to our unit early, and with a burned area of >20% of total body surface area were investigated at 12, 24, and 36 hours after injury. Using transesophageal echocardiography, pulmonary artery catheterization, and transpulmonary thermodilution to monitor them, we evaluated the cardiovascular coupling when urinary output and MAP were used as endpoints. RESULTS Oxygen transport variables, heart rate, MAP, and left ventricular fractional area, did not change significantly during fluid resuscitation. Left ventricular end-systolic and end-diastolic area and global end-diastolic volume index increased from subnormal values at 12 hours to normal ranges at 24 hours after the burn. Extravascular lung water: intrathoracal blood volume ratio was increased 12 hours after the burn. CONCLUSIONS Preload variables, global systolic function, and oxygen transport recorded simultaneously by three separate methods showed no need to increase the total fluid volume within 36 hours of a major burn. Early (12 hours) signs of central circulatory hypovolemia, however, support more rapid infusion of fluid at the beginning of treatment.

Mortality After Thermal Injury: No Sex-Related Difference

BACKGROUND Young women have been reported to be more likely to survive than men after severe trauma. Girls also have less inflammation and hypermetabolism after major burns. Yet burned women have been found to have a twofold greater risk of death than men. Our aim was to find out if there is a sex-related difference in mortality after thermal injury, particularly in the age group between 16 years and 49 years, when hormonal differences would be most influential. METHODS All patients admitted to the Linköping University Hospital Burn Unit with thermal injuries during the years 1993-2008 were included and the variables percentage burned total body surface area (TBSA%), age, type of burn, mechanical ventilation, and year were included in a multiple regression (Poisson log) model. RESULTS Of 1,119 patients with thermal injury, 792 (71%) were men. Crude mortality was 5% among men, and 8% among women (p = 0.04). After adjustment for age and TBSA%, there was no correlation between mortality and sex, in any age group. Eight men and four women died in the group of young adults (16-49 years) in which TBSA% correlated with mortality (p < 0.01) but age did not. Mortality was 14% (32 of 221) among the men and 23% (23 of 102) of women in the group of older adults (50 years and older), and both age and TBSA% correlated with mortality (p < 0.001). CONCLUSIONS There is no relevant sex-related difference in survival after thermal injury. The conclusion is, however, tempered by the few deaths, particularly among younger adults.

Transesophageal Echocardiographic Hemodynamic Monitoring during Preoperative Acute Normovolemic Hemodilution

Background Preoperative acute normovolemic hemodilution may compromise oxygen transport. The aims of our study were to describe the hemodynamic effects of normovolemic hemodilution and to determine its effect on systolic and diastolic cardiac function by multiplane transesophageal echocardiography. Methods In eight anesthetized patients (aged 13–51 yr) without heart disease, hemoglobin was reduced in steps from 123 ± 8 (mean ± SD) to 98 ± 3 and to 79 ± 5 g/l. Hemodynamic measurements (intravascular pressures, thermodilution cardiac output, and echocardiographic recordings) were obtained during a stabilization period and at each level of hemodilution. Left ventricular wall motion was monitored continuously, and Doppler variables, annular motion, and changes in ejection fractional area were analyzed off-line. Results During hemodilution, cardiac output by thermodilution increased by 16 ± 7% and 26 ± 10%, corresponding well to the increase in cardiac output as measured by Doppler (difference, 0.32 ± 1.2 l/min). Systemic vascular resistance fell 16 ± 14% and 23 ± 9% and pulmonary capillary wedge pressure increased slightly (2 ± 2 mmHg), whereas other pressures, heart rate, wall motion, and diastolic Doppler variables remained unchanged. Ejection fractional area change increased from 44 ± 7% to 54 ± 10% and 60 ± 9% as a result of reduced end-systolic and increased end-diastolic left ventricular areas. Conclusions A reduction in hemoglobin to 80 g/l during acute normovolemic hemodilution does not normally compromise systolic or diastolic myocardial function as determined by transesophageal echocardiography. Preload, left ventricular ejection fraction, and cardiac output increase with a concomitant fall in systemic vascular resistance.

Computed tomography – a possible aid in the diagnosis of smoke inhalation injury?

Inhalation injury is an important contributor to morbidity and mortality in burn victims and can trigger acute lung injury and acute respiratory distress syndrome (ARDS) ( 1–3 ). Early diagnosis and treatment of inhalation injury are important, but a major problem in planning treatment and evaluating the prognosis has been the lack of consensus about diagnostic criteria ( 4 ). Chest radiographs on admission are often non‐specific ( 5 , 6), but indicators include indoor fires, facial burns, bronchoscopic findings of soot in the airways, and detection of carbon monoxide or cyanide in the blood ( 7 ). Changes in the lungs may be detected by bronchoscopy with biopsy, xenon imaging, or measurement of pulmonary extracellular fluid ( 4, 5, 8 ). These methods have, however, been associated with low sensitivity and specificity, as exemplified by the 50% predictive value in the study of Masanes et al. ( 8 ). Computed tomographs (CTs) are better than normal chest radiographs in the detection of other pulmonary lesions such as pulmonary contusion ( 9, 10 ). The importance of CT scans in patients with ARDS has been reviewed recently ( 9 ), but unfortunately there has been no experience of CT in patients with smoke inhalation injury. To our knowledge, there are only two animal studies reporting that smoke inhalation injury can be detected by CT ( 4, 11 ); specific changes in human CT scans have not yet been described.

Cardiac dysfunction after burns

OBJECTIVES Using transoesophageal echocardiography (TEE) we investigated the occurrence, and the association of possible abnormalities of motion of the regional wall of the heart (WMA) or diastolic dysfunction with raised troponin concentrations, or both during fluid resuscitation in patients with severe burns. PATIENTS AND METHODS Ten consecutive adults (aged 36-89 years, two women) with burns exceeding 20% total burned body surface area who needed mechanical ventilation were studied. Their mean Baux index was 92.7, and they were resuscitated according to the Parkland formula. Thirty series of TEE examinations and simultaneous laboratory tests for myocyte damage were done 12, 24, and 36h after the burn. RESULTS Half (n=5) the patients had varying grades of leakage of the marker that correlated with changeable WMA at 12, 24 and 36h after the burn (p< or =0.001, 0.044 and 0.02, respectively). No patient had WMA and normal concentrations of biomarkers or vice versa. The mitral deceleration time was short, but left ventricular filling velocity increased together with stroke volume. CONCLUSION Acute myocardial damage recorded by both echocardiography and leakage of troponin was common, and there was a close correlation between them. This is true also when global systolic function is not deteriorated. The mitral flow Doppler pattern suggested restrictive left ventricular diastolic function.

Incidence of early burn-induced effects on liver function as reflected by the plasma disappearance rate of indocyanine green: a prospective descriptive cohort study.

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 indocyanine green (PDR(ICG)), is affected in patients with severe burns. This is a prospective, descriptive exploratory study at a national burn centre. Consecutive adult patients with a percent total body surface area burned (TBSA%) of 20% or more, were examined prospectively by dynamic (PDR(ICG)) and static liver function tests (plasma: bilirubin concentration, prothrombin complex, and alanine aminotransferase and alkaline phosphatase activities). Early liver dysfunction was common, as it is assessed by both dynamic (7 of 17) and static liver function tests (6-17 of 17). A regression model showed that changes in PDR(ICG) were associated with age, TBSA%, plasma bilirubin concentration, plasma C-reactive protein concentration, and cardiac index. Persistent and advanced hepatic dysfunction was associated with mortality. The PDR(ICG) seems to give a comprehensive assessment of liver function after major burns. Hepatic dysfunction seems to be as common as dysfunction in other organs. We interpret the recorded effects on liver function as part of a multiple organ dysfunction syndrome, primarily induced by the burn itself. However, this needs to be further investigated.