Anestezjologia. Intensywna Terapia 2/2016-Incidence and prognosis of intra-abdominal hypertension and abdominal compartment syndrome in severely burned patients: Pilot study and review of the literature

PRACE ORYGINALNE I KLINICZNE

Incidence and prognosis of intra-abdominal hypertension and abdominal compartment syndrome in severely burned patients: Pilot study and review of the literature

Robert Wise1, Jimmy Jacobs2, Sylvain Pilate2, Ann Jacobs2, Yannick Peeters2, Stefanie Vandervelden2, Niels Van Regenmortel2, Inneke De Iaet2, Karen Schoonheydt2, Hilde Dits2, Manu L.N.G. Malbrain2

1Head Clinical Unit Critical Care, Edendale Hospital, Pietermaritzburg, South Africa. Discipline of Anaesthesiology and Critical Care, Nelson R Mandela School of Medicine, University of KwaZulu-Natal

2ICU and High Care Burn Unit, ZiekenhuisNetwerk Antwerpen, ZNA Stuivenberg, Antwerpen, Belgium

Abstract

Background: Burn patients are at high risk for secondary intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS) due to capillary leak and large volume fluid resuscitation.

Our objective was to examine the incidence the incidence of IAH and ACS and their relation to outcome in mechanically ventilated (MV) burn patients.

Methods: This observational study included all MV burn patients admitted between April 2007 and December 2009. Various physiological parameters, intra-abdominal pressure (IAP) measurements and severity scoring indices were recorded on admission and/or each day in ICU. Transpulmonary thermodilution parameters were also obtained in 23 patients. The mean and maximum IAP during admission was calculated. The primary endpoint was ICU (burn unit) mortality.

Results: Fifty-six patients were included. The average Simplified Acute Physiology Score (SAPS II) and Sequential Organ Failure Assessment (SOFA) scores were 43.4 ± 15.1 and 6.4 ± 3.4, respectively. The average total body surface area (TBSA) affected by burns was 24.9% ( ± 24.9), with 33 patients suffering inhalational injuries. Forty-four (78.6%) patients developed IAH and 16 (28.6%) suffered ACS. Patients with ACS had higher TBSAs burned (35.8 ± 30 vs 20.6 ± 21.4%, P = 0.04) and higher cumulative fluid balances after 48 hours (13.6 ± 16L vs 7.6 ± 4.1L, P = 0.03). The TBSA burned correlated well with the mean IAP (R = 0.34, P = 0.01). Mortality was notably high (26.8%) and significantly higher in patients with IAH (34.1%, P = 0.014) and ACS (62.5%, P < 0.0001). Most patients received more fluids than calculated by the Parkland Consensus Formula while, interestingly, non-survivors received less. However, when patients with pure inhalation injury were excluded there were no differences. Non-surgical interventions (n = 24) were successful in removing body fluids and were related to a significant decrease in IAP, central venous pressure (CVP) and an improvement in oxygenation and urine output. Non-resolution of IAH was associated with a significantly worse outcome (P < 0.0001).

Conclusion: Based on our preliminary results we conclude that IAH and ACS have a relatively high incidence in MV burn patients compared to other groups of critically ill patients. The percentage of TBSA burned correlates with the mean IAP. The combination of high CLI, positive (daily and cumulative) fluid balance, high IAP, high EVLWI and low APP suggest a poor outcome. Non-surgical interventions appear to improve end-organ function. Non-resolution of IAH is related to a worse outcome.

 

Key words: abdominal pressure, abdominal hypertension, abdominal compartment syndrome, burns, incidence, fluid resuscitation, monitoring, treatment

 

Anestezjologia Intensywna Terapia 2016, tom 48, nr 2, 102–116

Należy cytować wersję:

Wise R, Jacobs J, Pilate S, Jacobs A et al.: Incidence and prognosis of intra-abdominal hypertension and abdominal compartment syndrome in severely burned patients: Pilot study and review of the literaturę. Anaesthesiol Intensive Ther 2016; 48: 95–109. doi 10.5603/AIT.a2015.0083.

Burn patients are at high risk of secondary intraabdominal hypertension (IAH) and abdominal compartment syndrome (ACS) due to capillary leak and large volume fluid resuscitation [1–3]. According to the recently revised consensus definitions of the World Society on Abdominal Compartment Syndrome (WSACS, www.wsacs.org), secondary ACS is defined as a sustained increase in intra-abdominal pressure (IAP) above 20 mm Hg with new onset organ dysfunction that does not originate from the abdominal-pelvic region [4, 5]. Secondary ACS is a common, and relatively under recognized, rapidly fatal condition in severely burned patients. The reported incidence varies from 30% to 80% [6]. The pathophysiological implications of IAH are numerous and can lead to acute renal failure, respiratory failure and splanchnic ischemia [7]. In addition, the physiological mayhem that ensues following a burn injury further complicates management. Urine output, often used as a marker of success in fluid resuscitation, may become an inadequate indicator during fluid management due to rising IAP, thus leading to overzealous administration and a large cumulative fluid balance. This will contribute to the development of secondary ACS. In previous studies, it was shown that peak inspiratory pressure correlates strongly with the IAP in patients with ACS [8]. However, with the advent of lung protective ventilation, these peak pressures are seldom seen. In contrast, a diminished chest wall compliance resulting in low tidal volumes and hypercapnia has become the hallmark of respiratory failure related to IAH and ACS [9].

While IAH may usually respond to conservative medical management (Table 1), surgical intervention with abdominal decompression is the only definitive treatment for ACS [10]. Although decompressive laparotomy aims to reverse worsening cardiovascular, respiratory and renal function, mortality remains high at 50%, despite this intervention [11]. A significant physiological improvement can, however, result following decompressive laparotomy, as reported by Hershberger et al., where mean urine output improved from 28 mL h-1 to 90 mL h-1 [12]. Latenser et al. [3] demonstrated that percutaneous drainage in burn patients is a safe and effective alternative to decompressive laparotomy when patients have less than 80% TBSA involved.

Table 1. Suggested medical interventions in burns patients suggested by the World Society on Abdominal Compartment Syndrome (WSACS) in the management of intra-abdominal hypertension [5]

Medical strategies in the management of intra-abdominal hypertension in burns

Improvement of abdominal wall compliance (sedation and paralysis, escharotomies, avoiding positive fluid balance)

Evacuation of intra-abdominal contents (percutaneous ascites drainage)

Evacuation of intraluminal contents (gastroprokinetics, stool softeners, enemas, adaptation of enteral nutrition speed)

Correction of capillary leak and fluid balance (hypertonic solutions, albumin 20%, colloids, diuretics, ultrafiltration)

Optimisation of organ perfusion

Of particular interest is the choice of fluids used to resuscitate burn patients. Colloid resuscitation has not shown improved outcomes [13]. Plasma-resuscitated patients maintained an IAP below the threshold associated with frequent complications, and urine output and kidney function remained unchanged [14]. Oda et al. demonstrated that in patients with severe burn injuries, hypertonic lactated saline resuscitation could reduce the risk of secondary ACS [2]. Further comparisons evaluating the difference in survival between crystalloid resuscitation and lower infusion volume regimens have not yet been conducted. In line with the results of recent large fluid trials, the use of starches can no longer be recommended in burn patients, as was summarized in a concise review [15]. Although goal-directed treatment has been advocated in septic patients in the past [16], recent data from the ProCESS study could not confirm this and, as such, this cannot be recommended in burn patients [17]. This is supported by previous reports showing that volumetric monitoring may lead to even higher resuscitation volumes and possible adverse effects [18].

The aim of this study was to examine the incidence of IAH and ACS in severely burned patients under mechanical ventilation (MV) and to study prognostic factors. Furthermore, we wanted to analyse the effects of medical management on IAH and how non-resolution of IAH may have an impact on outcome. Finally, we attempted to establish a control group before changing our fluid resuscitation from the classic Parkland formula to a more restricted regimen with balanced crystalloids and colloids.

METHODS

ETHICS

The study was conducted in accordance with the ICU protocol, the declaration of Helsinki and applicable regulatory requirements as approved by the institutional review board and the local institutional ethics committee (approval number 3852). In view of the nature of the study being purely observational and not demanding a deviation from standard clinical ICU care, informed consent from the patient or the next of kin was not deemed necessary. Retrospective data analysis of existing information based on the standard of care did not, therefore, influence management. Medical records were secure and only accessed by treating ICU physicians. All data were anonymized prior to the analysis.

STUDY POPULATION

All consecutive patients requiring mechanical ventilation (MV) that were admitted to our burns unit between April 2007 and December 2009 (32 months) were considered in the analysis. Inclusion criteria included the presence of an isolated inhalation injury for which MV was necessary, or patients with > 20% total body surface area (TBSA) burn area in adults, or >15% TBSA burns in children with or without inhalation that received fluid resuscitation. Patients were excluded if there was an “allow natural death order”, or an inability to measure IAP via the bladder or stomach. Fifty-six patients were included.

DATA COLLECTION

PATIENT DEMOGRAPHICS

Data collected on admission included the patients’ age, gender, weight, height, body mass index, body surface area, and their date of enrolment. The origin of burns was recorded: flame, scald, or toxic, together with the presence of an inhalation injury, if applicable. The percentage of TBSA that was burned was recorded together with the presence of full thickness burns (3rd degree) and/or deep and superficial 2nd degree burns (all expressed as a %). Information pertaining to clinical and physiological parameters was recorded from admission to hospital discharge, death, or for a maximum of 28 days. This was done irrespective of whether they remained in the burn unit, or were transferred to another ward within the department (within the same hospital). Patients that were discharged to another hospital during the study were not followed after this transfer, but if possible a 28-day outcome was recorded. Secondary endpoints were the duration of ICU and hospital stay, and the use of resources: duration of MV, hemodynamic monitoring and renal replacement therapy (RRT).

SEVERITY SCORES

Several measurements were made pertaining to severity scoring, fluids administered, IAP, and transpulmonary thermodilution techniques. During the first 24 hours of admission to the burn unit, acute physiology and chronic health evaluation (APACHE II) and simplified acute physiology score (SAPS II) scores were calculated. Daily sequential organ failure assessment (SOFA) scores were recorded for the duration of the admission. For each patient the worst value for each organ system (respiratory, cardiovascular, renal, coagulation, liver and neurologic) in each 24-hour period was considered.

FLUID BALANCE

Although the daily fluid balance was recorded by subtracting the total losses from the total daily intake, insensible losses were not included in these calculations. Daily fluid intake was expressed as mL kg-1 %TBSA and as mL kg-1. Cumulative intake at 48 hours (end of resuscitation period) was calculated. Daily enteral nutrition intake was recorded. Urine output was expressed as millilitres per day and as mL kg-1h-1. When available, losses from nasogastric and percutaneous abdominal drains were noted. The cumulative fluid balance within the first 7 days of stay was calculated. The capillary leak index (CLI) was also calculated as a ratio, defined as the serum C-reactive protein (CRP (mg dL-1)) divided by the serum albumin (g L-1) levels.

IAP MEASUREMENT

IAP measurements were made with the Foley Manometer (Holtech Medical, Charlottenlund, Denmark) via a Foley bladder catheter. This measurement followed a standardized protocol in the unit as published before [19], and was measured in a stable, supine position, at least four times a day with the zero reference at the level where the mid-axillary line crosses the iliac crest [5]. Patients identified as having a sustained IAP ≥ 12 mm Hg were monitored continuously via a balloon-tipped nasogastric probe connected to the Ci-MON monitor (Pulsion Medical Systems, Munich, Germany). Using the above techniques, daily records of the lowest (IAPlow) and highest (IAPhigh) intra-abdominal pressure, and the lowest abdominal perfusion pressure (APP) were made. Abdominal perfusion pressure (APP) was defined as the mean arterial pressure (MAP) minus the corresponding IAP. The mean IAP (IAPmean) and maximal IAP (IAPmax) were also calculated from the daily measurements during the first week of admission.

DEFINITIONS

According to the revised WSACS consensus definitions, IAH was defined as a sustained IAP equal to or higher than 12 mm Hg, while ACS was defined as a sustained IAP higher than 20 mm Hg with at least one new organ failure (as defined by a SOFA sub-score above 3) [5].

HEMODYNAMIC MONITORING

A central venous catheter was inserted in all the patients and a thermistor-tipped arterial thermodilution catheter (Pulsiocath 5F) was placed in the femoral artery in 23 patients. This was attached to a PiCCOplus or PiCCO2 monitoring system (Pulsion Medical Systems, Munich, Germany). Transpulmonary thermodilution measurements were obtained by injection of three 20 mL boluses of cooled saline (< 8°C) into the central venous catheter. For each set of thermodilution determinants, the mean value was used for statistical analysis [20]. Cardiac output (CO), global end diastolic volume (GEDV), extravascular lung water (EVLW), global ejection fraction (GEF), pulmonary vascular permeability index (PVPI), stroke volume variation (SVV) and pulse pressure variation (PPV) were calculated. Further calculations were made by correlating EVLW to predicted body weight (EVLWI), and CO and GEDV to body surface area (CI, GEDVI).

STATISTICAL ANALYSIS

Only the data obtained during the first week, or less if discharge or death occurred before day 7, were used for statistical purposes. Continuous variables are presented as the mean ( ± standard deviation, SD) or median in the case of skewed distribution. Categorical variables are expressed as numbers and percentages for the group from which they were derived. Continuous variables were compared with the Student’s t-test for normally distributed variables and the Mann Whitney test for non-normally distributed variables. The χ2 test or Fisher’s exact test were used to compare ordinal variables. All p-values are two-tailed and a P value lower than 0.05 was considered statistically significant. Statistical analysis was done with SPSS (Windows version 16.0, Chicago, IL, USA). The primary endpoint of the population studied was mortality. Secondary endpoints included the incidence of IAH and ACS, and the prognostic value of non-resolution of IAH after medical management together with the use of ICU resources (MV, hemodynamic monitoring, RRT).

FLUID RESUSCITATION AND STANDARD TREATMENT

Over the first 24–48 hours, the burn patients were resuscitated according to the Consensus Formula as suggested by Parkland. A balanced crystalloid (Plasmalyte) at 4 mL kg-1%TBSA burned was administered, together with a maintenance fluid of glucose 5% in 0.45% NaCl at 84 mL h-1. Urine output was used to help titrate the volume of fluid resuscitation, with a goal directed urine output between 0.5 and 1.0 mL kg-1 h-1. Enteral nutrition, following a unit specific standard protocol, was commenced from day 2 at 10 mL h-1 and gradually increased. Colloids were allowed from day 2 and included mainly hyperoncotic albumin 20% (if serum levels were < 25 g L-1) or balanced starches (Volulyte®, Fresenius-Kabi, Melsungen, Germany). Standard patient care was carried out in all individuals according to the protocols of the burn unit. Medical management for increased IAP was instituted to alleviate this problem (see Table 1) [21]. Abdominal decompression by laparotomy was used as the definitive treatment of ACS if the medical management implemented had failed to decrease the IAP.

RESULTS

PATIENT DEMOGRAPHICS

Table 2 summarizes the patient demographics and severity data for the whole group and in survivors vs nonsurvivors. Fifty-six patients were included in the study, with an average age of 43.1 ± 25.9 years, mean weight of 68.5 ± 28.3 kg, and a BMI of 24.5 ± 6.3. Data pertaining to demographics and biometric measurements are shown in Table 2. The male to female ratio was 2:1 and 10 children were included. The majority (n = 42) typically suffered flame burns, with a relatively high number (n = 33) also incurring inhalational injuries, while scald (n = 9) and toxic burns (n = 5) occurred less frequently.

Table 2. Patient demographics

Variable Total Survivors (n = 41) Nonsurvivors (n = 15) P value
Age (years) 43.1 ± 25.9 38.4 ± 24.9 55.9 ± 24.8 0.023
Weight (kg) 68.5 ± 28.3 66.2 ± 27.9 74.7 ± 29.3 0.324
Height (cm) 162 ± 30.9 160.3 ± 33.4 166.5 ± 23.4 0.512
Body mass index (kg m-2) 24.5 ± 6.3 24.1 ± 6.2 25.6 ± 6.8 0.460
Males/Females 2.1 2.4 1.5 NS
Origin Burn injury
Flame (n) 42 32 10 NS
Scald (n) 9 7 2 NS
Toxic (n) 5 2 3 NS
Inhalation (n) 33 25 8 NS
SAPS II 43.5 ± 15.1 39 ± 12.5 55.6 ± 15.1 < 0.0001
APACHE II 15.8 ± 6.8 13.9 ± 5.7 20.8 ± 6.9 < 0.0001
Probability mortality 34.6 ± 25.1 27.2 ± 21.2 54.9 ± 24.1 < 0.0001
SOFA 6.4 ± 3.5 5.9 ± 3.1 7.8 ± 4 0.062
SOFA respiratory 1.3 ± 1.1 1.3 ± 1 1.5 ± 1.2 0.508
SOFA coagulation 0.3 ± 0.7 0.1 ± 0.3 0.8 ± 1.1 < 0.0001
SOFA liver 0.3 ± 0.6 0.2 ± 0.5 0.7 ± 0.8 0.013
SOFA cardiovascular 1.7 ± 1.4 1.4 ± 1.2 2.4 ± 1.5 0.015
SOFA neurologic 2.3 ± 1.8 2.5 ± 1.8 1.9 ± 1.8 0.254
SOFA renal 0.5 ± 1.2 0.5 ± 1.1 0.6 ± 1.4 0.704
Organ failures (n) 1.2 ± 1 1.2 ± 0.9 1.4 ± 1.2 0.464
Body surface area (m2) 1.7 ± 0.5 1.7 ± 0.5 1.8 ± 0.5 0.402
%TBSA 24.9 ± 24.9 16 ± 15.1 49.1 ± 30.4 < 0.0001
3rd degree (%) 12 ± 23.6 5.1 ± 9.5 30.8 ± 37.5 < 0.0001
2nd degree deep (%) 5 ± 8.1 5.3 ± 6.7 4.3 ± 11.4 0.680
2nd degree superficial (%) 7.7 ± 14 5.4 ± 5.3 14.1 ± 25 0.038
IAP high (mm Hg) 9.9 ± 3 9.4 ± 3.1 11.3 ± 2.4 0.033
IAP mean (mm Hg) 10.3 ± 2.7 9.5 ± 2.2 12.6 ± 2.7 < 0.0001
IAP max (mm Hg) 16.4 ± 4.9 15.2 ± 4.6 19.6 ± 4.2 0.002
IAH 44 29 15 0.014
IAH treatment 24 17 7 NS
IAH resolution 25 24 1 < 0.0001
ACS 16 6 10 < 0.0001

NS – non significant

SEVERITY SCORES

The average SOFA score was 6.4 ± 3.5, with a trend towards a higher score in non-survivors (7.8 ± 4 vs 5.9 ± 3.1 and a P-value of 0.062). The organ systems SOFA subscores which differed most between survivors and non-survivors were the cardiovascular (1.4 ± 1.2 vs 2.4 ± 1.5 with P = 0.015), and the liver subscores (0.2 ± 0.5 vs 0.7 ± 0.8 with P = 0.013). Figure 1 (Panel A) represents the divergence of SOFA scores from day 2 in the non-survivor group. The SAPS scores were significantly higher in non-survivors (55.6 ± 15.1 vs 39 ± 12.5 with P < 0.0001).

Figure 1. Day-by-day evolution of SOFA score, albumin and capillary leak index in survivors (open circles) vs non-survivors (closed circles) during the first week of stay, indicates P < 0.05. Panel A. Evolution of SOFA score; Panel B. Evolution of albumine levels (g L-1); Panel C. Evolution of capillary leak index in 33 patients with inhalation injury

MORTALITY AND OUTCOME PREDICTORS

The mortality rate was high at 26.8% (n = 15) and significantly higher in patients with IAH (34.1%, P = 0.014) and ACS (62.5%, P < 0.0001). In univariate analysis SAPS II, APACHE II, the TBSA burned, percentage of full-thickness third degree burns, IAP (low, high, mean and max), CLI, EVLWI (mean and max), PEEP, Pplat, total fluid intake, daily and cumulative fluid balance were all significantly higher in non-survivors, while APP and albumin were significantly lower (Table 3). In parallel to the severity scoring, albumin was noted to be significantly lower in the non-survivors, with a divergence from the survivor group occurring on day 2, possibly also demonstrating the severity of their injuries (Fig. 1, Panel B).

Table 3. Fluid intake and output

Variable Total Survivors (n = 41) Nonsurvivors (n = 15) P value
Intake (mL) 6582.4 ± 8301 4888.1 ± 3079.8 11213.5 ± 14567.7 0.01
Enteral Nutrition (mL) 226.5 ± 380.2 244.6 ± 396.8 179.8 ± 345.4 0.622
Consensus (mL kg-1%TBSA) 7.2 ± 7.5 8.4 ± 8.1 4.1 ± 4.2 0.056
Total intake (mL kg-1, 48 hrs) 196.1 ± 125 178.1 ± 95.9 244.1 ± 176.9 0.081
Gastric output (mL) 200.7 ± 197.3 166.8 ± 191.9 302.4 ± 196.6 0.19
Urine output (mL) 1368.4 ± 980.1 1317.7 ± 851.6 1506.9 ± 1293.7 0.527
Urine output (mL kg-1 h-1) 0.9 ± 0.7 1 ± 0.7 0.9 ± 0.6 0.639
Fluid Balance (mL) 4932.2 ± 7824.1 3289.3 ± 2555.4 9422.8 ± 13868.3 0.008
Cumulative FB (mL,48 hrs) 5682.4 ± 7989.4 3954.9 ± 2953.2 10404.3 ± 13900.1 0.006

On day 3 post injury, non-survivors were shown to have a higher capillary leak index, which once again may reflect a more significant initial injury, or alternatively, a greater injury to the vascular endothelium and glycocalyx (Fig. 1, Panel C). With regards to the fluid resuscitation in relation to Parkland Formula, Figure 2 (Panel A) shows non-survivors received a smaller volume of resuscitation fluid when comparing all patients. Most patients received more fluid than calculated by the Consensus Formula (7.2 ± 7.5 mL kg-1%TBSA). Although non-survivors received volumes in keeping with the Consensus Formula (4.1 ± 4.2 mL kg-1%TBSA), this was significantly less than survivors (8.4 ± 8.1 mL kg-1%TBSA). However, when comparing survivors and non-survivors with a TBSA involvement of 15–90% (and excluding pure inhalation injury), in Figure 2 (Panel B), similar volumes were given in each group. The evolution in daily and cumulative fluid balance is shown in Figure 3. Table 3 provides information on fluid intake and output. Non-survivors had more fluid intake, as well as a more positive daily and cumulative fluid balance at 48 hours (end of resuscitation period).

Figure 2. Daily fluid intake according to Parkland Consensus Formula. Panel A. Daily fluid intake according to Parkland formula (mL kg-1%TBSA) in all patients survivors (open circles) and nonsurvivors (closed circles), * indicates P < 0.05; Panel B. Daily fluid intake according to Parkland formula (mL kg-1%TBSA) in subgroup of adult patients with %TBSA between 15 and 90% (excluding isolated inhalation injury), survivors (open circles) and nonsurvivors (closed circles), * indicates P < 0.05

Figure 3. Day-by-day evolution of fluid management In survivors (open circles) and nonsurvivors (closed circles), * Indicates P < 0.05. Panel A. Dally fluid balance (mL); Panel B. Cumulative fluid balance (mL); Panel C. Dally enteral nutrition amount (mL); Panel D. Daily urine output

HEMODYNAMIC VARIABLES

Table 4 lists the hemodynamic and respiratory variables. In terms of assessing fluid resuscitation targets, transpulmonary thermodilution measurements (performed in 23 patients) confirmed a higher EVLWI in the non-survivors (for both the mean and maximum readings). Figure 4 (Panel A) shows the evolution of EVLWI in survivors vs non-survivors. The global ejection fraction (GEF) was lower in non-survivors (Figure 4, Panel B). The GEDVI was significantly higher in non-survivors on day 2 (830 ± 161 vs 678 ± 116 mL m-2 with P = 0.021) and day 5 (891 ± 242 vs 713 ± 96 mL m-2 with P = 0.046), suggesting that fluid overload may be associated with worse outcomes. The other PiCCO variables, including CI, and SVV were not significantly different. The average dose was 4.5 ± 3.9 μg kg-1 min-1 for dobutamine and 0.1 ± 0.1 μg kg-1 min-1 for norepinephrine.

Table 4. Cardiovascular and respiratory parameters

Variable Total Survivors (n = 41) Nonsurvivors (n = 15) P value
Cardiovascular drugs
Dobutamine (μg kg-1 min-1) 4.5 ± 3.9 2.7 ± 0.6 5.9 ± 4.9 0.323
Noradrenaline (μg kg-1 min-1) 0.1 ± 0.1 0.1 ± 0.1 0.2 ±0.1 0.082
Capillary leak
EVLWI mean (mL kg-1 PBW) 9.6 ± 3.3 8.1 ±1.8 11.2 ±3.8 0.017
EVLWI max (mL kg-1 PBW) 14.6 ±8.2 10.9 ±2.2 18.8 ±10.4 0.017
Day Max 4.6 ± 3.3 4.3 ± 2.3 5 ±4.3 0.599
CRP (mg dL-1) 3.4 ± 6.6 2.7 ±6.1 5.3 ± 7.7 0.197
Albumin (g L-1) 29.2 ± 9.7 31.9 ± 9 22 ± 7.7 < 0.0001
Capillary leak index (CLI) 23.3 ± 52.7 15.1 ±43.6 45.6 ± 68.8 0.053
Elaemodynamic parameters
HR (bpm) 106.9 ±30.8 107.4 ±31.8 105.4 ±28.6 0.841
CVP (mm Hg) 13.6 ±4.5 13.4 ±4.8 14.3 ±3.5 0.584
MAP low (mm Hg) 61.1 ±8.8 63 ± 8.5 56.1 ± 7.9 0.008
APP low (mm Hg) 51.0 ±9.4 53.4 ± 8.6 44.5 ± 8.5 0.001
Respiratory variables
RR 17.4 ± 5.6 17.2 ± 5.6 18.2 ±6 0.541
TV (mL) 480.5 ±183.8 483.2 ±189.4 471.5 ±171.9 0.849
Pplat(cm H2O) 22.4 ±5.2 21.2 ±4.3 26.3 ± 6.1 0.002
PEEP (cm H2O) 6.7 ±2.2 6.2 ±1.9 8.1 ± 2.5 0.008
MV (L min-1) 7.6 ± 2.6 7.4 ± 2.3 8.4 ± 3.5 0.255
Cdyn (mLcm H2O-1) 31.8 ±12.9 33.5 ±13 26.2 ±11.6 0.091

Figure 4. Evolution of transpulmonary thermodilution obtained parameters. Left panel. Day-by-day evolution of EVLWI in survivors (n = 12, open circles) vs non-survivors (n = 11, closed circles) in 23 patients with PiCCO monitoring, * P < 0.05; Right panel. evolution of global ejection fraction (GEF) in non-survivors (closed circles) and survivors (open circles). *P < 0.05

ABDOMINAL HYPERTENSION

Forty-four patients (78.6%) developed IAH and 16 (28.6%) suffered ACS based on the WSACS definitions. Seventeen patients had IAH on admission, while the others (n = 27) developed it during their ICU stay (on average day 2.6 ± 2). Patients with ACS (on average diagnosed after 5.6 ± 3.8 days) had higher TBSAs burned (39.6 ± 26.4 vs 21.7 ± 23.6%, P = 0.03) and higher cumulative fluid balances (11.4 ± 15.8 L vs 4.3 ± 3.6 L, P = 0.08). On admission, the APP was 50.5 ± 9.4 mm Hg and during the ICU stay the IAPmax was 15.7 ± 5.2. The again, happy with either maximum or maximal. Change to maximum as it is a finite value. IAP was reached after 4.7 ± 3.4 days. Non-survivors had higher IAPlow, IAPhigh, IAPhigh, IAPmean, and IAPmax recordings. Notably, the MAP|ow and APP|ow were all lower in the non-survivor group. Intra-abdominal pressure was uniformly higher in non-survivors, with a concomitant lower APP. The TBSA burned correlated well with the mean IAP (R = 0.34, P = 0.01) (Fig. 5). Patients with ACS had a significantly higher risk of death (Fig. 6, Panel A).

Figure 5. Correlation plot between mean IAP and %TBSA

Figure 6. Kaplan Meier curves. Panel A. Cumulative 28 day survival, solid line ACS, dotted line no ACS (P < 0.0001); Panel B. Cumulative 28 day survival, solid line no IAH resolution, dotted line IAH resolution (P < 0.0001). All patients in whom IAH resolved survived at 28 days; Panel C. Cumulative percentage of patients on mechanical ventilation (solid line = IAH, dotted line is no IAH) (P = 0.001 )

MEDICAL MANAGEMENT

Specific treatment for IAH was performed in 24 patients. In 8 patients with IAH this was done by sedation and the use of neuromuscular blockers. All 16 patients with ACS received treatment, and 3 underwent decompressive laparotomy. Two of these patients died despite the surgical intervention. The remaining 13 ACS patients were managed with medical therapies (paracenthesis in 5, diuretics In 3, gastric suctioning in 2, stool protocol in 8, renal replacement therapy with net ultrafiltration in 1). A total of 19 interventions were performed and were successful in removing 2.2 ± 1.3L of bodyfluids.This resulted in a substantial decrease in IAP and CVP measurements, together with improved oxygenation and urine output (Table 5). All patients in whom IAFH resolved survived to 28 days (P < 0.0001). The cumulative survival for those patients that did not have IAFH resolution was only 36.5% (Fig. 6, Panel B).

Table 5. Effect of medical management on organ function (19 interventions in 13 patients)

  Before After P value
IAP (mm Hg) 17.8 ± 3.4 11.1 ± 3.5 < 0.0001
APP (mm Hg) 62.3 ± 13.8 69.1 ± 12.7 NS
CVP (mm Hg) 16.6 ± 5.5 12.8 ± 4.3 0.005
paO2/FiO2 251 ± 110 303.2 ± 114.2 0.01
Urine output (mL h-1) 83.3 ± 75.3 208.4 ± 148.6 0.0003

NS – non significant

USE OF ICU RESOURCES

When comparing survivors and non-survivors, expectantly as expected, ICU (26.6 ± 28.1 vs 16.3 ± 16.2) and hospital length of stay (59.9 ± 81.2 vs 17.1 ± 15.9) was longer in survivors. The number of ventilator free days was also not significantly different in the non-survivor group. However, when comparing those that developed IAH with those that did not in the survivor group, the latter had significantly more ICU free days, hospital free days, and ventilator free days (Table 6). Moreover, patients without IAH were weaned off the ventilator much quicker (Fig. 6, Panel B).

Table 6. ICU and hospital free days in 40 survivors

  Total No IAH (n = 11) IAH (n = 29) P value
ICU free days 9.4 ± 8.3 16.4 ± 7.5 6.7 ± 7.1 < 0.0001
HOS free days 5.4 ± 7.2 10.6 ± 9.2 3.5 ± 5.7 0.006
MV free days 14.8 ± 8.5 20.8 ± 5.3 12.5 ± 8.4 0.004

DISCUSSION

INCIDENCE OF IAH/ACS

The treatment of physiological shock related to burn injuries is most often based on empirical fluid resuscitation formulae. This practice is still considered a reasonable initial approach and many formulae have been developed for this purpose.The Parkland Formula, now recognized as the Consensus Formula, has been the favoured technique since its introduction by Baxter and Shires in 1968 [22]. However, a correlation between IAP and total administered fluid volume has been reported [8, 23]. Patients with severe burns are at increased risk of developing (secondary) IAH and ACS due to the large volume of resuscitation fluid, decreased abdominal wall compliance,and increased capillary leakage, bowel oedema and other factors [24–33]. Oda et al. concluded that fluid resuscitation in excess of 300 mL kg-1 24 h-1 carries a high incidence of complications as a consequence of ACS [8]. Ivy et al. explored the relationship between the amount of fluid administered and IAP [34]. The correlation demonstrated an IAP of 24.4 mm Hg when resuscitation with 250 mL kg-1 was performed [34]. Interpreting these results, the Consensus Formulae requires a TBSA burn of 50% to achieve such amounts of fluid resuscitation. ACS complicates fluid resuscitation further since it causes urinary output to become an inaccurate guide to fluid administration [35–37]. Central venous pressure (CVP) is also nota suitable tool to guide fluid resuscitation during shock caused by burns [38]. The total circulating blood volume could be an ideal guide to resuscitation [39]. However, a previous study found goal-directed therapy by invasive monitoring, as compared to Baxter’s empiric resuscitation formula, caused a significant increase in the volume of fluid administration but did not improve preload or cardiac output parameters [18]. Thus, managing the appropriate volumes of resuscitation fluid is challenging. IAH/ACS is currently expected to be a life-threatening complication in severely burned patients.

There are a relatively small number of patients in previously conducted studies. In our study, intra-abdominal hypertension (IAH), defined as a sustained IAP > 12 mm Hg, was present in 44 (78.6%) patients and 16 (28.6%) patients developed ACS. To the best of our knowledge, we report the longest series of burn patients being evaluated for IAH and ACS.

Our study confirms that SAPS II, APACHE II, the TBSA burned, percentage of full-thickness 3rd degree burns, IAP (low, high, mean and max), CLI, EVLWI (mean and max), PEEP, Pplat, total fluid intake, daily and cumulative fluid balance were all significantly higher in non-survivors, while APP and albumin were significantly lower. The percentage of TBSA burned correlates with mean IAP. The combination of a high CLI, positive (daily and cumulative) fluid balance, high IAP, high EVLWI and low APP, correlate with a poor outcome. Most patients received more fluid than initially calculated by the Consensus Formula (7.0 ± 7.5 mL kg-1%TBSA) and remarkably, non-survivors received less (3.9 ± 4.1 vs 8.3 ± 8.2 mL kg-1%TBSA). This may be explained by a shortened time for fluid administration due to early death.

OUTCOME

The high mortality rate observed in the present study can probably be explained by the large number of inhalation injuries, advanced age and larger TBSA burned in nonsurvivors [40]. The comparison between survivors and nonsurvivors shows some remarkable findings. In addition, the burden of burn injuries on available critical care resources can be seen in the duration of ICU and hospital stays (23.9 ± 25.7 and 48.4 ± 72.3 respectively). These numbers, together with the SOFA scores demonstrating the need for organ support, highlight the resource and financial implications of burn injuries, and the need to identify ways in which to improve burn care management and shorten hospital stays. The mortality in those developing ACS was significantly higher (10 out of 16 patients, 62.5%) when compared to those that did not (5 out of 40 patients, 12.5%). The mortality in those developing IAH (15 out of 44 patients, 34.1%) was also significantly higher than those who did not suffer from IAH (0 out of 12 patients, P = 0.014). Burn patients are at a substantial risk to develop IAH and ACS and this influences mortality.

Medical interventions, as demonstrated in this study, significantly reduced both the IAP and the CVP, improving oxygenation and urine output [41–44]. Appropriate monitoring and early medical interventions may alleviate the consequences of IAH and ACS, as well as affect outcome [5].

Non-survivors showed a higher capillary leak index, which once again may reflect a more significant initial injury, or alternatively, a greater injury to the vascular endothelium and glycocalyx [45, 46]. This may account for the greater decrease in albumin with less control over the regulation of intravascular fluids due to the destruction of the glycocalyx. An ongoing inflammatory response, or one that is greater than that encountered in survivors may also account for the increased CLI and decrease in albumin.

The poor outcomes from burns patients who develop intra-abdominal hypertension and compartment syndrome is shown in Table 7. Including this study, the 42 publications show a marked variation in definitions of abdominal hypertension, compartment syndrome, inclusion criteria, and treatment methods. However, the outcomes remain poor. Only 8 of the studies are prospective, with the vast majority being observational, cohort studies, thus demonstrating the difficulty to design and run studies on this subject.

Table 7. Overview of studies reporting burns-related secondary abdominal hypertension and compartment syndrome

Author Year Study model Patients (n) Type of patients Inclusion TBSA
Greenhalgh [29] 1994 P 30 burns 56%
Ivy [57] 1999 CS 3 burns 70%
Ivy [23] 2000 P 10 burns 22%
Mayes [58] 2000 CS 6 burns 20%
Corcos [42] 2001 CS 3 burns 40%
Wilson [59] 2001 CR 1 burns 70%
Latenser [3] 2002 R 13 burns 40%
Hobson [43] 2002 R 10 burns 68%
Blinderman [60] 2002 CR 1 burns 80%
Tsoutsos [61] 2003 P 24 burns 35%
Pirson [62] 2004 CR 1 burns 53%
Rodas [30] 2005 CR 1 5 trauma (1 burn) 70%
Oda [63] 2005 P 36 burns 30%
O’mara [14] 2005 P 31 burns 25% +inhalation or 40%
Britt [64] 2005 CS 10 mixed Ṩ 40%
Oda [8] 2006 R 48 burns 30%
Kowal-Vern [33] 2006 R 29 burns 45.7%
Jensen [32] 2006 CS 4 3 burns, 1 TBI 65%
Parra [44] 2006 CR 1 burns 60%
Ball [31] 2006 CR 1 burns 52%
Kuntscher [39] 2006 R 16 burns 20%
Oda [2] 2006 R 36 burns 40%
Levis [65] 2006 CS 4 burns 20%
Hershberger [12] 2007 R 25 burns 65%
Oda [27] 2007 R 38 burns 40%
Klein [66] 2007 R 72 burns 44.5%
Muangman [67] 2007 CS 5 burns 40%
Keramati [68] 2008 CS 6 burns (5 thermal, 1 electrical) 78%
Ennis [69] 2008 P 118 burns 30%
Dulhunty [70] 2008 R 80 burns 15%
Markell [71] 2009 R 51 burns + trauma 48%
Sanchez [72] 2009 P 33 burns 20%
Poulakidas [73] 2009 CS 3 burns 92%
Thamm [74] 2009 CR 1 burns 11%
Cartotto [75] 2010 R 194 burns 15%
Lamb [76] 2010 CR 1 burns + trauma 33%
Rogers [77] 2010 CR 1 burns 57%
Mosier [78] 2011 R 153 burns 20%
Yenikomshian [79] 2011 R 50 burns 20%
Rocourt [80] 2011 R 2 burns 15%
Ruiz–Castilla [81] 2014 P 25 burns 20%
McBeth [82] 2014 R (175) burns ISS > 12
53 burns ISS > 12
Present study 2015 R 56 burns 20%
Total     1286   41.6%

Table legend: ACS – abdominal compartment syndrome; CR – case report; CS – case series; DL – decompressive laparotomy; IAH – intra-abdominal hypertension; IAP – intra-abdominal pressure; ISS – injury severity score; NA – not applicable; NR – not reported; P – prospective observational; PD – percutaneous drainage; R – retrospective cohort; TBI – traumatic brain injury; TBSA – total burned surface area; * converted from cmH2O to mm Hg (divided by 1.36); # direct peritoneal pressure was 29 ± 18 mm Hg (7–49); ° only suspected, not confirmed through measurement; Ṩ mixed: 4 burns, 3 extremity trauma, 1 lightening, 1 abdominal bleeding

Table 7 (cont.). Overview of studies reporting burns-related secondary abdominal hypertension and compartment syndrome

Author Year Mean TBSA (&/or range) IAH treshold (mm Hg) Mean IAP (range) IAH (n)
Greenhalgh [29] 1994 56.2 ± 3.6% 30 NR 12
Ivy [57] 1999 87.3% (74–98%) 25 45 3
Ivy [23] 2000 46% (22–80%) 25 30 (9–44) 7
Mayes [58] 2000 60% (20–91%) NR NR assumed to be 6
Corcos [42] 2001 60% (40–70%) 20 52 (36–82) 3
Wilson [59] 2001 NA Clinical NA NR
Latenser [3] 2002 58% 25 34 (26–42) 9
Hobson [43] 2002 71% 30 40 (30–50) 10
Blinderman [60] 2002 NA 50 NA 1
Tsoutsos [61] 2003 57.4% (37–85%) 14.7–18.3 17.1 10
Pirson [62] 2004 NA 22 NA 1
Rodas [30] 2005 NA Clinical NA NR
Oda [63] 2005 49% (30–99%) 22 52±9 8
O’mara [14] 2005 51 ±12% 25 24.2 (9–42) 26
Britt [64] 2005 NA clinical + IAP 40.6 (30–55) only 7 measured
Oda [8] 2006 45.9% (25.2–96.5%) 22 NR NR
Kowal-Vern [33] 2006 NR 25 NR 22
Jensen [32] 2006 70% 22 + Clinical NR NA
Parra [44] 2006 NA 34 NA NA
Ball [31] 2006 NA 20 38 1
Kuntscher [39] 2006 46% (26–67%) NR NR NR
Oda [2] 2006 65.2% (40–99%) 22 NR 13
Levis [65] 2006 20–50% 25 NR 4
Hershberger [12] 2007 46–84% 24 NR 25
Oda [27] 2007 NR 22* 14.6 ± 7.3* to 34.36 ± 8.2 14
Klein [66] 2007 20–90% NR NR NR
Muangman [67] 2007 61 ± 21% (40–90%) NA 36 ± 21 (10–60)# 5
Keramati [68] 2008 37% (65–85%) Clinical 39 6
Ennis [69] 2008 51% (33–69%) NR NR NR
Dulhunty [70] 2008 43% ± 19% 30 NR NR
Markell [71] 2009 48% ± 19% 30 NR NR
Sanchez [72] 2009 20–93% 12 NR 22
Poulakidas [73] 2009 92–95% 25 NR 3
Thamm [74] 2009 NA NR NA 1
Cartotto [75] 2010 31% (15–81%) NR NR NR
Lamb [76] 2010 NA NR NA
Rogers [77] 2010 NA 32 NA 1
Mosier [78] 2011 46% (28–64%) NR NR NR
Yenikomshian [79] 2011 41% (23–65%) NR NR NR
Rocourt [80] 2011 16.5% 25 NR NR
Ruiz–Castilla [81] 2014 33% (25–58%) 12 Only baseline IAP reported 18
McBeth [82] 2014 31.4 ± 20.9% (5–95%) 12 NR NR
35 ± 16% (11–70%) 20 12.1 ± 4.2(1–29) 12
Present study 2015 24.9 ± 24.9% 12 15.7 ± 5.2 44
Total   51.9% (32.9–81.5) 24 (12–30) 32.8 (18.1–47.4) 295

Table legend: ACS – abdominal compartment syndrome; CR – case report; CS – case series; DL – decompressive laparotomy; IAH – intra-abdominal hypertension; IAP – intra-abdominal pressure; ISS – injury severity score; NA – not applicable; NR – not reported; P – prospective observational; PD – percutaneous drainage; R – retrospective cohort; TBI – traumatic brain injury; TBSA – total burned surface area; * converted from cmH2O to mm Hg (divided by 1.36); # direct peritoneal pressure was 29 ± 18 mm Hg (7–49); ° only suspected, not confirmed through measurement; Ṩ mixed: 4 burns, 3 extremity trauma, 1 lightening, 1 abdominal bleeding

Table 7 (cont). Overview of studies reporting burns-related secondary abdominal hypertension and compartment syndrome

Author Year IAH (%) ACS (n) ACS (%) Treatment
Greenhalgh [29] 1994 40.0% 7 23.3% PD/laparotomy
Ivy [57] 1999 NA 3 NA Escharotomy
Ivy [23] 2000 70.0% 2 20.0% Sedation/laparotomy
Mayes [58] 2000 assumed to be 100% 6 100.0% DL
Corcos [42] 2001 NA 3 NA PD/laparotomy
Wilson [59] 2001 NR 1 NA Escharotomy
Latenser [3] 2002 69.2% 4 30.8% PD/laparotomy
Hobson [43] 2002 100.0% 10 100.0% PD/laparotomy
Blinderman [60] 2002 NA 1 NA DL
Tsoutsos [61] 2003 41.7% 10 41.7% Escharotomy
Pirson [62] 2004 NA 1 NA laparotomy
Rodas [30] 2005 NR 1 burn + 4 others NA laparotomy
Oda [63] 2005 22.2% 8 22.2% Escharotomy
O’mara [14] 2005 83.9% 4 12.9% Sedation
Britt [64] 2005 70.0% 10 NA DL
Oda [8] 2006 NR 8 16.7% Escharotomy
Kowal-Vern [33] 2006 75.9% 9 31.0% PD/laparotomy
Jensen [32] 2006 NA 3 75.0% laparotomy
Parra [44] 2006 NA 1 NA PD/escharotomy
Ball [31] 2006 NA 1 NA Escharotomy/DL
Kuntscher [39] 2006 NR NR NR Escharotomy
Oda [2] 2006 36.1% 13 36.1% Sedation/paralysis/escharotomy
Levis [65] 2006 NA 4 NA 2 x DL
Hershberger [12] 2007 100.0% 25 100.0% Sedation/paralysis/escharotomy
Oda [27] 2007 36.8% 14 36.8% Sedation/paralysis/escharotomy
Klein [66] 2007 NR 3024 4.2% NR
Muangman [67] 2007 100.0% NA NA NA
Keramati [68] 2008 100.0% 6 100.0% laparotomy
Ennis [69] 2008 NR 12.98 11.0% NR
Dulhunty [70] 2008 NR 12.8 16.0% NR
Markell [71] 2009 NR 32 62.7% NR
Sanchez [72] 2009 66.7% 3 9.0% NR
Poulakidas [73] 2009 NA 3 NA Escharotomy + DL
Thamm [74] 2009 NA 1 NA DL
Cartotto [75] 2010 NR 7954 4.1% DL
Lamb [76] 2010 NA NA DL
Rogers [77] 2010 NA 1 NA DL
Mosier [78] 2011 NR 7038 4.6% NR
Yenikomshian [79] 2011 NR 4 8.0% NR
Rocourt [80] 2011 NR 2 16.6% PD
Ruiz–Castilla [81] 2014 72.0% 1 4.0% NR
McBeth [82] 2014 NR NR NR NR
22.6% 5 9.4% 3 x DL
Present study 2015 78.6% 16 28.6% Medical/3x DL
Total   59.1% (22.2–100) 272 26% (4.2–100)  

Table legend: ACS – abdominal compartment syndrome; CR – case report; CS – case series; DL – decompressive laparotomy; IAH – intra-abdominal hypertension; IAP – intra-abdominal pressure; ISS – injury severity score; NA – not applicable; NR – not reported; P – prospective observational; PD – percutaneous drainage; R – retrospective cohort; TBI – traumatic brain injury; TBSA – total burned surface area; * converted from cmH2O to mm Hg (divided by 1.36); # direct peritoneal pressure was 29 ± 18 mm Hg (7–49); ° only suspected, not confirmed through measurement; Ṩ mixed: 4 burns, 3 extremity trauma, 1 lightening, 1 abdominal bleeding

BURNS AND FLUIDS

Recent investigations, supported by our own preliminary results, have implied that the current practice in many burn centres is to infuse volumes greater than would be predicted by existing formulas. Until today, fluid restrictive regimes have not been shown to improve outcome in burn patients [47], although some have suggested a reduction in fluid volumes with restricted fluid regimens in burns [48, 49]. The data show that plasma-resuscitated patients maintained an IAP below the threshold of complications of intra-abdominal hypertension [14]. Oda et al. demonstrated that in patients with severe burn injury, hypertonic lactated saline resuscitation could reduce the risk of secondary ACS [2]. A further comparison evaluating the difference in survival between crystalloid resuscitation and fluid restrictive regimens has not yet been conducted. Unfortunately, future studies would need to be large, multi-centre trials that could enable the difference in survival on the basis of a bi-modal fluid resuscitation (early adequate followed by late conservative) to be evaluated [50]. To show a 10% difference in survival, with a power of 80% and expected P-value of 0.05, 900 patients would be required in each group, as previously stated [14].

PROGNOSIS

The results of this study support the hypothesis that (secondary) IAH and ACS are more prevalent in mechanically ventilated burn patients compared to other groups of critically ill patients [6, 24, 25]. Early implementation of medical interventions (as was performed in our study) is useful in improving IAP, oxygenation, and potentially venous return to the right side of the heart. Urine output improvement may reflect better renal perfusion. These interventions should become the standard of care, along with monitoring of IAP in all patients at risk of developing IAH and ACS. Failure to identify and manage IAH and ACS in burn patients will increase the risk of non-resolution of IAH/ACS and subsequent mortality.

INVASIVE CARDIOVASCULAR MONITORING

The CVP has proven to be a poor preload measurement in several studies on resuscitation of major burns [39]. The same holds true for urine output as a parameter to guide resuscitation. Pulmonary artery catheter (PAC) monitoring was considered the gold standard for assessment of cardiac output (CO), stroke volume (SV), systemic vascular resistance (SVR) and oxygen transport variables in the past. Recently, however, less invasive methods for the assessment of cardiac output and the measurement of intra-thoracic blood volumes have gained increasing acceptance in intensive care medicine [51, 52]. Although total circulating blood volume index (TBVI) guided burn resuscitation may be a superior method, its impact on outcome still needs to be demonstrated in future randomized studies [39]. In our study, PiCCO measured GEDVI was significantly higher in non-survivors on days 2 and 5. However, it is still unclear whether GEDVI is a useful outcome predictor or if it could be used as a resuscitation target.

PROPOSAL

Taking into account the findings of this study, we suggest an early, aggressive, goal-directed fluid resuscitation strategy. The results from this study support the idea that fluid restriction is not beneficial, and in fact more fluid than the Consensus Formula suggests is often administered. This phenomenon of fluid creep has emerged over the past few decades [53, 54], attributed by one author to an opioid creep [55]. It is yet to be established if the volume of fluid administered could be reduced by a combination of colloid and balanced salt solutions [56]. Once cardiovascular and perfusion parameters are achieved, the initial aggressive fluid strategy will need to be addressed and re-evaluated. Early monitoring of IAP in all burned patients, particularly those with TBSA burns of >20% (or > 15% in children) should become the standard of care. Early implementation of medical interventions to improve IAP should be attempted. Future research should also focus on evaluating the microcirculation and the effects of resuscitation on the glycocalyx.

LIMITATIONS

Firstly, the retrospective nature of the data analysis of this study may be regarded as a limitation. Secondly, there were no established protocols in the burn unit at the time the data was collected. Thirdly, there is no information on coagulation parameters, while an analysis on the possible role that blood products could have played in the outcome was not performed. Fourthly, the use of the PiCCO monitoring device was not standardized and, thus, not all patients have this cardiovascular data available which could have strengthened the findings regarding GEDVI. Moreover, no data was collected with regard to the strong ion difference (SID). Finally, albeit large in burns research publications, the total number of 56 patients included is still small.

CONCLUSION

Based on our preliminary results, we conclude that IAH and ACS has a relatively high prevalence in mechanically ventilated burn patients compared to other groups of critically ill patients. The percentage of TBSA burned correlates with the mean IAP. The combination of high CLI, positive (daily and cumulative) fluid balance, high IAP, high EVLWI and low APP, correlate with a poor outcome. Non-surgical interventions can lower IAP, CVP and can improve endorgan function. Non-resolution of IAH was related to a worse outcome. Future studies should focus on improved fluid resuscitation regimes, targeting microcirculation perfusion, with this group possibly benefitting from a bi-modal fluid model, favouring colloids rather than crystalloids.

ACKNOWLEDGEMENTS

  1. The authors declare no financial disclosure.
  2. Dr Wise declares that he has no financial or personal relationships that may have inappropriately influenced him in writing this paper. Dr De laet is member of the Executive Committee of the World Society on the Abdominal Compartment (WSACS) and current Secretary. Dr Malbrain is member of the Executive Committee of the World Society of the Abdominal Compartment (WSACS) and current Treasurer; he is member of the medical advisory board of Pulsion Medical Systems (Maquet Getinge group). The other authors have no possible conflicts of interest related to the content of this paper.

References:

  1. Oda J, Ivatury RR, Blocher CR, Malhotra AJ, Sugerman HJ: Amplified cytokine response and lung injury by sequential hemorrhagic shock and abdominal compartment syndrome in a laboratory model of ischemia-reperfusion. J Trauma 2002; 52: 625–631.
  2. Oda J, Ueyama M, Yamashita K et al.: Hypertonic lactated saline resuscitation reduces the risk of abdominal compartment syndrome in severely burned patients. J Trauma 2006; 60: 64–71.
  3. Latenser BA, Kowal-Vern A, Kimball D, Chakrin A, Dujovny N: A pilot study comparing percutaneous decompression with decompressive laparotomy for acute abdominal compartment syndrome in thermal injury. J Burn Care Rehabil 2002; 23: 190–195.
  4. Malbrain ML, Cheatham ML, Kirkpatrick A et al.: Results from the International Conference of Experts on Intra-abdominal Hypertension and Abdominal Compartment Syndrome. I. Definitions. Intensive Care Med 2006; 32: 1722–1732.
  5. Kirkpatrick AW, Roberts DJ, De Waele J et al.: Intra-abdominal hypertension and the abdominal compartment syndrome: updated consensus definitions and clinical practice guidelines from the World Society of the Abdominal Compartment Syndrome. Intensive Care Med 2013; 39: 1190–1206. doi: 10.1007/s00134–013–2906-z.
  6. Kirkpatrick AW, Ball CG, Nickerson D, D’Amours SK: Intraabdominal hypertension and the abdominal compartment syndrome in burn patients. World J Surg 2009; 33: 1142–1149. doi: 10.1007/s00268009–9995–4.
  7. Malbrain ML, De Iaet IE: Intra-abdominal hypertension: evolving concepts. Clin Chest Med 2009; 30: 45–70, viii. doi: 10.1016/j.ccm.2008.09.003.
  8. Oda J, Yamashita K, Inoue T et al: Resuscitation fluid volume and abdominal compartment syndrome in patients with major burns. Burns 2006; 32: 151–154.
  9. Pelosi P, Quintel M, Malbrain ML: Effect of intra-abdominal pressure on respiratory mechanics. Acta Clin Belg Suppl 2007; 62: 78–88. doi: 10.1179/acb.2007.62.s1.011.
  10. Cheatham ML, Malbrain ML, Kirkpatrick A et al.: Results from the International Conference of Experts on Intra-abdominal Hypertension and Abdominal Compartment Syndrome. II. Recommendations. Intensive Care Med 2007; 33: 951–962.
  11. De Waele JJ, Hoste EA, Malbrain ML: Decompressive laparotomy for abdominal compartment syndrome – a critical analysis. Crit Care 2006; 10: R51.
  12. Hershberger RC, Hunt JL, Arnoldo BD, Purdue GF: Abdominal compartment syndrome in the severely burned patient. J Burn Care Res 2007; 28: 708–714.
  13. Roberts I, Alderson P, Bunn F, Chinnock P, Ker K, Schierhout G: Colloids versus crystalloids for fluid resuscitation in critically ill patients. Cochrane Database Syst Rev 2004; 18: CD000567.
  14. O’Mara MS, Slater H, Goldfarb IW, Caushaj PF: A prospective, randomized evaluation of intra-abdominal pressures with crystalloid and colloid resuscitation in burn patients. J Trauma 2005; 58: 1011–1018.
  15. Malbrain MLNG:The great fluid debate: faith and evidence. Intensive Care Monit 2014; 21: 1.
  16. Rivers E, Nguyen B, Havstad S et al.: Early goal-directed therapy in the treatment of severe sepsis and septic shock. New Engl J Med 2001; 345: 1368–1377.
  17. The ProCESS Investigators. A Randomized Trial of Protocol-Based Care for Early Septic Shock. New Engl J Med 2014; 370: 1683–1693.
  18. Holm C, Mayr M, Tegeler J et al.: A clinical randomized study on the effects of invasive monitoring on burn shock resuscitation. Burns 2004; 30: 798–807.
  19. Desie N, Willems A, De Laet I et al.: Intra-abdominal pressure measurement using the FoleyManometer does not increase the risk for urinary tract infection in critically ill patients. Ann Intensive Care 2012; 2 (Suppl 1): S10. doi: 10.1186/2110–5820–2-S1-S23.
  20. Hofkens PJ, Verrijcken A, Merveille K et al.: Common pitfalls and tips and tricks to get the most out of your transpulmonary thermodilution device: results of a survey and state-of-the-art review. Anaesthesiol Intensive Ther 2015; 47: 89–116. doi: 10.5603/AIT.a2014.0068.
  21. De Iaet I, Malbrain ML: ICU management of the patient with intra-abdominal hypertension: what to do, when and to whom? Acta Clin Belg Suppl 2007: 190–199.
  22. Baxter CR, Shires T: Physiological response to crystalloid resuscitation of severe burns. Ann N Y Acad Sci 1968; 150: 874–894.
  23. Ivy ME, Atweh NA, Palmer J, Possenti PP, Pineau M, D’Aiuto M: Intra-abdominal hypertension and abdominal compartment syndrome in burn patients. J Trauma 2000; 49: 387–391.
  24. Strang SG, Van Lieshout EM, Breederveld RS, Van Waes OJ: A systematic review on intra-abdominal pressure in severely burned patients. Burns 2014; 40: 9–16. doi: 10.1016/j.burns.2013.07.001.
  25. Azzopardi EA, McWilliams B, Iyer S, Whitaker IS: Fluid resuscitation in adults with severe burns at risk of secondary abdominal compartment syndrome-an evidence based systematic review. Burns 2009; 35: 911–920. doi: 10.1016/j.burns.2009.03.001.
  26. Burke BA, Latenser BA: Defining intra-abdominal hypertension and abdominal compartment syndrome in acute thermal injury: a multicenter survey. J Burn Care Res 2008; 29: 580–584. doi: 10.1097/BCR.0b013e31817db84e.
  27. Oda J, Yamashita K, Inoue T et al.: Acute lung injury and multiple organ dysfunction syndrome secondary to intra-abdominal hypertension and abdominal decompression in extensively burned patients. J Trauma 2007; 62: 1365–1369.
  28. Tuggle D, Skinner S, Garza J, Vandijck D, Blot S: The abdominal compartment syndrome in patients with burn injury. Acta Clin Belg Suppl 2007; 62: 136–140. doi: 10.1179/acb.2007.62.s1.017.
  29. Greenhalgh DG, Warden GD: The importance of intra-abdominal pressure measurements in burned children. J Trauma 1994; 36: 685–690.
  30. Rodas EB, Malhotra AK, Chhitwal R, Aboutanos MB, Duane TM, Ivatury RR: Hyperacute abdominal compartment syndrome: an unrecognized complication of massive intraoperative resuscitation for extra-abdominal injuries. Am Surg 2005; 71: 977–981.
  31. Ball CG, Kirkpatrick AW, Karmali S et al.: Tertiary abdominal compartment syndrome in the burn injured patient. J Trauma 2006; 61: 1271–1273.
  32. Jensen AR, Hughes WB, Grewal H: Secondary abdominal compartment syndrome in children with burns and trauma: a potentially lethal complication. J Burn Care Res 2006; 27: 242–246.
  33. Kowal-Vern A, Ortegel J, Bourdon P et al.: Elevated cytokine levels in peritoneal fluid from burned patients with intra-abdominal hypertension and abdominal compartment syndrome. Burns 2006; 32: 563–569.
  34. Ivy ME, Atweh NA, Palmer J, Possenti PP, Pineau M, D’Aiuto M: Intra-abdominal hypertension and abdominal compartment syndrome in burn patients. J Trauma 2000; 49: 387–391.
  35. Johnson JM, Chang PK, Gagliardi RJ, Schwartz RW: Abdominal compartment syndrome. J Surg Educ 2007; 64: 208–211.
  36. De Iaet I, Malbrain ML, Jadoul JL, Rogiers P, Sugrue M: Renal implications of increased intra-abdominal pressure: are the kidneys the canary for abdominal hypertension? Acta Clin Belg Suppl 2007; 62: 119–130. doi: 10.1179/acb.2007.62.s1.015.
  37. Thorington JM, Schmidt CF: A study of urinary output and blood-pressure changes resulting in experimental ascites. Am J Med Sci 1923; 165: 880–890.
  38. Cheatham ML, Malbrain ML: Cardiovascular implications of abdominal compartment syndrome. Acta Clin Belg Suppl 2007; 62: 98–112. doi: 10.1179/acb.2007.62.s1.013.
  39. Kuntscher MV, Germann G, Hartmann B: Correlations between cardiac output, stroke volume, central venous pressure, intra-abdominal pressure and total circulating blood volume in resuscitation of major burns. Resuscitation 2006; 70: 37–43.
  40. Blot S, Brusselaers N, Monstrey S et al.: Development and validation of a model for prediction of mortality in patients with acute burn injury. Br J Surg 2009; 96: 111–117. doi: 10.1002/bjs.6329.
  41. De Iaet I, Malbrain ML: ICU management of the patient with intra-abdominal hypertension: what to do, when and to whom? Acta Clin Belg Suppl 2007; 62: 190–199. doi: 10.1179/acb.2007.62.s1.025.
  42. Corcos AC, Sherman HF: Percutaneous treatment of secondary abdominal compartment syndrome. J Trauma 2001; 51: 1062–1064.
  43. Hobson KG, Young KM, Ciraulo A, Palmieri TL, Greenhalgh DG: Release of abdominal compartment syndrome improves survival in patients with burn injury. J Trauma 2002; 53: 1129–1133.
  44. Parra MW, Al-Khayat H, Smith HG, Cheatham ML: Paracentesis for resuscitation-induced abdominal compartment syndrome: an alternative to decompressive laparotomy in the burn patient. J Trauma 2006; 60: 1119–1121.
  45. Cordemans C, De Iaet I, Van Regenmortel N et al.: Fluid management in critically ill patients: the role of extravascular lung water, abdominal hypertension, capillary leak and fluid balance. Annals Intensive Care 2012; 2 (Suppl 1): S1. doi: 10.1186/2110–5820–2-S1-S1.
  46. Malbrain ML, Marik PE, Witters I et al.: Fluid overload, de-resuscitation, and outcomes in critically ill or injured patients: a systematic review with suggestions for clinical practice. Anaesthesiol Intensive Ther 2014; 46: 361–380. doi: 10.5603/AIT.2014.0060.
  47. Perel P, Roberts I: Colloids versus crystalloids for fluid resuscitation in critically ill patients. Cochrane Database Syst Rev 2007; 17: CD000567.
  48. Arlati S, Storti E, Pradella V, Bucci L, Vitolo A, Pulici M: Decreased fluid volume to reduce organ damage: a new approach to burn shock resuscitation? A preliminary study. Resuscitation 2007; 72: 371–378.
  49. Walker TL, Rodriguez DU, Coy K, Hollen LI, Greenwood R, Young AE: Impact of reduced resuscitation fluid on outcomes of children with 10–20% body surface area scalds. Burns 2014; 40: 1581–1586. doi: 10.1016/j. burns.2014.02.013.
  50. Cordemans C, De Laet I, Van Regenmortel N et al.: Aiming for a negative fluid balance in patients with acute lung injury and increased intra-abdominal pressure: a pilot study looking at the effects of PAL-treatment. Ann Intensive Care 2012; 2 (Suppl 1): S15. doi: 10.1186/2110–5820–2S1-S15.
  51. Csontos C, Foldi V, Fischer T, Bogar L: Arterial thermodilution in burn patients suggests a more rapid fluid administration during early resuscitation. Acta Anaesthesiol Scand 2008; 52: 742–749. doi: 10.1111/j.1399–6576.2008.01658.x.
  52. Sanchez M, Garcia-de-Lorenzo A, Herrero E et al.: A protocol for resuscitation of severe burn patients guided by transpulmonary thermodilution and lactate levels: a 3-year prospective cohort study. Crit Care 2013; 17: R176. doi: 10.1186/cc12855.
  53. Faraklas I, Cochran A, Saffle J: Review of a fluid resuscitation protocol: “fluid creep”is not due to nursing error. J Burn Care Res 2012; 33: 74–83. doi: 10.1097/BCR.0b013e318234d949.
  54. Saffle JI: The phenomenon of “fluid creep” in acute burn resuscitation. J Burn Care Res 2007; 28: 382–395.
  55. Sullivan SR, Friedrich JB, Engrav LH et al.: “Opioid creep” is real and may be the cause of “fluid creep”. Burns 2004; 30: 583–590.
  56. Lawrence A, Faraklas I, Watkins H et al.: Colloid administration normalizes resuscitation ratio and ameliorates “fluid creep”. J Burn Care Res 2010; 31: 40–47. doi: 10.1097/BCR.0b013e3181cb8c72.
  57. Ivy ME, Possenti PP, Kepros J et al.: Abdominal compartment syndrome in patients with burns. J Burn Care Rehabil 1999; 20: 351–353.
  58. Mayes T, Gottschlich MM, Warden GD: Nutrition intervention in pediatric patients with thermal injuries who require laparotomy. J Burn Care Rehabil 2000; 21: 451–456.
  59. Wilson MD, Dziewulski P: Severe gastrointestinal haemorrhage and ischaemic necrosis of the small bowel in a child with 70% full-thickness burns: a case report. Burns 2001; 27: 763–766.
  60. Blinderman C, Lapid O, Shaked G: Abdominal compartment syndrome in a burn patient. Isr Med Assoc J 2002; 4: 833–834.
  61. Tsoutsos D, Rodopoulou S, Keramidas E, Lagios M, Stamatopoulos K, Ioannovich J: Early escharotomy as a measure to reduce intraabdominal hypertension in full-thickness burns of the thoracic and abdominal area. World J Surg 2003; 27: 1323–1328.
  62. Pirson J, Zizi M, Jacob E, Deleuze JP: Acute ischemic optic neuropathy associated with an abdominal compartment syndrome in a burn patient. Burns 2004; 30: 491–494.
  63. Oda J, Ueyama M, Yamashita K et al.: Effects of escharotomy as abdominal decompression on cardiopulmonary function and visceral perfusion in abdominal compartment syndrome with burn patients. J Trauma 2005; 59: 369–374.
  64. Britt RC, Gannon T, Collins JN, Cole FJ, Weireter LJ, Britt LD: Secondary abdominal compartment syndrome: risk factors and outcomes. Am Surg 2005; 71: 982–985.
  65. Levis C, Ali F: Significance of early diagnosis of abdominal compartment syndrome in major burns. Can J Plast Surg 2006; 14: 175–178.
  66. Klein MB, Hayden D, Elson C et al.: The association between fluid administration and outcome following major burn: a multicenter study. Ann Surg 2007; 245: 622–628.
  67. Muangman P, Muangman S, Suvanchote S, Benjathanung R: Abdominal compartment syndrome monitoring in major burn patients with Siriraj device catheter. J Med Assoc Thai 2007; 90: 384–390.
  68. Keramati M, Srivastava A, Sakabu S et al.: The Wittmann Patch s a temporary abdominal closure device after decompressive celiotomy for abdominal compartment syndrome following burn. Burns 2008; 34: 493–497.
  69. Ennis JL, Chung KK, Renz EM et al.: Joint Theater Trauma System implementation of burn resuscitation guidelines improves outcomes in severely burned military casualties. J Trauma 2008; 64 (2 Suppl): S14651; S51–2. doi: 10.1097/TA.0b013e318160b44c.
  70. Dulhunty JM, Boots RJ, Rudd MJ, Muller MJ, Lipman J: Increased fluid resuscitation can lead to adverse outcomes in major-burn injured patients, but low mortality is achievable. Burns 2008; 34: 1090–1097. doi: 10.1016/j.burns.2008.01.011.
  71. Markell KW, Renz EM, White CE et al.: Abdominal complications after severe burns. J Am Coll Surg 2009; 208: 940–947; discussion 7–9. doi: 10.1016/j.jamcollsurg.2008.12.023.
  72. Sanchez M, Herrero E, Asensio MJ, Araujo P, Galvan B, Denia R: Intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS) in critically burn patients. Burns 2009; 35: S46.
  73. Poulakidas S, Kowal-Vern A: Component separation technique for abdominal wall reconstruction in burn patients with decompressive laparotomies. J Trauma 2009; 67: 1435–1438. doi: 10.1097/TA.0b013e3181b5f346.
  74. Thamm OC, Leitsch S, Spanholtz TA, Perbix W, Spilker G: Complicated course of a burned patient with severe inhalation injury: a case report. Perioper Med 2009; 1: 224–227.
  75. Cartotto R, Zhou A: Fluid creep: the pendulum hasn’t swung back yet! J Burn Care Res 2010; 31: 551–558. doi: 10.1097/BCR.0b013e3181e4d732.
  76. Lamb CM, Berry JE, DeMello WF, Cox C: Secondary abdominal compartment syndrome after military wounding. J R Army Med Corps 2010; 156: 102–103.
  77. Rogers AD, Karpelowsky J, Millar AJ, Argent A, Rode H: Fluid creep in major pediatric burns. Eur J Pediatr Surg 2010; 20: 133–138. doi: 10.1055/s0029–1237355.
  78. Mosier MJ, Pham TN, Klein MB et al.: Early enteral nutrition in burns: compliance with guidelines and associated outcomes in a multicenter study. J Burn Care Res 2011; 32: 104–109. doi: 10.1097/BCR.0b013e318204b3be.
  79. Yenikomshian H, Reiss M, Nabavian R, Garner WL: Gastric feedings effectively prophylax against upper gastrointestinal hemorrhage in burn patients. J Burn Care Res 2011; 32: 263–268. doi: 10.1097/BCR.0b013e31820aafe7.
  80. Rocourt DV, Hall M, Kenney BD, Fabia R, Groner JI, Besner GE: Respiratory failure after pediatric scald injury. J Pediatr Surg 2011; 46: 1753–1758. doi: 10.1016/j.jpedsurg.2011.04.018.
  81. Ruiz-Castilla M, Barret JP, Sanz D et al.: Analysis of intra-abdominal hypertension in severe burned patients: the Vall d’Hebron experience. Burns 2014; 40: 719–724. doi: 10.1016/j.burns.2013.09.021.
  82. McBeth PB, Sass K, Nickerson D, Ball CG, Kirkpatrick AW: A necessary evil? Intra-abdominal hypertension complicating burn patient resuscitation. J Trauma Manag Outcomes 2014; 8: 12. doi: 10.1186/1752–2897–8-12.

Corresponding author:
Manu L.N.G. Malbrain, MD, PhD
Intensive Care Unit and High Care Burn Unit
Ziekenhuis Netwerk Antwerpen
ZNA Stuivenberg
Lange Beeldekensstraat 267
2060 Antwerpen, Belgium
e-mail: manu.malbrain@skynet.be

 

Received: 10.09.2015
Accepted: 16.11.2015

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