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Risk Factors for Acute Mesenteric Ischemia in Critically Ill Burns Patients—A Matched Case–Control Study

Soussi, Sabri*; Taccori, Marina*; De Tymowski, Christian*; Depret, François*,¶,**; Chaussard, Maïté*; Fratani, Alexandre*; Jully, Marion*; Cupaciu, Alexandru*; Ferry, Axelle*; Benyamina, Mourad*; Serror, Kevin; Boccara, David; Chaouat, Marc; Mimoun, Maurice; Cattan, Pierre; Zagdanski, Anne-Marie§; Anstey, James||; Mebazaa, Alexandre*,¶,**; Legrand, Matthieu*,¶,** for the PRONOBURN group

doi: 10.1097/SHK.0000000000001140
Clinical Science Aspects
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Objective: Burn-induced shock can lead to tissue hypoperfusion, including the gut. We performed this study to describe burn patients at risk of acute mesenteric ischemia (AMI) with the aim to identify potential modifiable risk factors.

Methods: Retrospective case–control study including adult severely burned patients between August 2012 and March 2017. Patients who developed AMI were matched to severely burned patients without AMI at a ratio of 1:3 (same year of admission, Abbreviated Burn Severity Index [ABSI], and Simplified Acute Physiology Score II [SAPSII]). Univariate and multiple regression analyses were performed.

Results: Of 282 severely burned patients, 15 (5%) were diagnosed with AMI. In the AMI group, patients had a median (interquartile range) total body surface area (TBSA), SAPSII, and ABSI of 55 (25–63)%, 53 (39–70), and 11 (8–13), respectively. The AMI mechanism in all patients was nonocclusive. Decreased cardiac index within the first 24 h (H24 CI), higher sequential organ failure assessment score on day 1 (D1 SOFA), and hydroxocobalamin use were associated with AMI. Odds ratios were 0.18 (95% confidence interval [CI], 0.03–0.94), 1.6 (95% CI, 1.2–2.1), and 4.6 (95% CI, 1.3–15.9), respectively, after matching. Multiple regression analysis showed that only decreased H24 CI and higher D1 SOFA were independently associated with AMI. Ninety-day mortality was higher in the AMI group (93% vs. 46% [P = 0.001]).

Conclusions: Burns patients with initial low cardiac output and early multiple organ dysfunction are at high risk of nonocclusive AMI.

*AP-HP, Hôpital Saint-Louis, Department of Anesthesiology and Critical Care and Burn Unit, Paris, France

AP-HP, Hôpital Saint-Louis, Plastic Surgery and Burn Unit, Paris, France

AP-HP, Hôpital Saint-Louis, Department of Digestive Surgery, Paris, France

§AP-HP, Hôpital Saint-Louis, Department of Radiology, Paris, France

||Intensive Care Unit, Royal Melbourne Hospital, Parkville, Melbourne, Australia

Hôpital Lariboisière, Institut National de la Santé et de la Recherche Médicale (INSERM), Paris, France

**Université Paris Diderot, Paris, France

Address reprint requests to Sabri Soussi, MD, Department of Anesthesiology and Critical Care and Burn Unit, St-Louis Hospital, 1 Avenue Claude Vellefaux, 75010 Paris, France. E-mail:

Received 20 December, 2017

Revised 23 January, 2018

Accepted 15 March, 2018

This study was partially supported by a grant from “la fondation des gueules cassées,” a nonprofit organization.

The authors report no conflicts of interest.

Supplemental digital content is available for this article. Direct URL citation appears in the printed text and is provided in the HTML and PDF versions of this article on the journal's Web site (

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Acute mesenteric ischemia (AMI) is a rare but severe complication in critically ill patients, with a high mortality rate (1, 2). This condition is even more frequent among severely ill patients with multiple organ failure (MOF) (3). In most studies including burn patients, the reported incidence of AMI is about 1% to 2% (4, 5). In this population, the main reported cause of AMI was nonocclusive which is consistent with the hypothesis of poor gut perfusion in the early phase of shock (6). Burn-induced shock still remains associated with poor outcome despite significant improvement over recent years. Reasons for this poor outcome are likely related to poor organs perfusion including the gut (7). A limited number of clinical studies have investigated risk factors of AMI in severely burned patients (6, 7). Identification of high-risk patients in this population is critical for early diagnosis and timely intervention to decrease the high morbidity and mortality rates of AMI. Therefore, the aim of this retrospective study was to describe episodes of AMI in burn patients and identify potential modifiable risk factors.

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Study design and eligibility

We performed a retrospective single-center case control study with 1:3 matching, in the Burns Unit of the Saint Louis Hospital, Paris, France. The study was approved by our local ethics committee (comité de protection des personnes IV, St-Louis hospital; Institutional review board 00003835, protocol 2013/17NICB). All medical records of the patients admitted to our Intensive Care Burns Unit (ICBU) between August 2012 and March 2017 were screened. During this time period, only severely burned patients of at least 18 years of age meeting at least one of the following criteria were included in the study: total body surface area (TBSA) burn-injured at least 20%, intubated mechanically ventilated patients within the first 24 h of admission and patients receiving vasopressors within the first 24 h of admission. Exclusion criteria were refusal to participate, patients moribund on admission or dead within 72 h from admission, and end-of-life patients with withdrawing life support in the first 7 days after admission (sustained MOF despite a maximal treatment for at least 72 h with other clinical conditions, e.g., high full thickness body surface area burned (>80%–90%) or in very old patients or in patients with severe underlying conditions (e.g., advanced respiratory or heart failure) or in patients presenting with severe neurological complications after out-of-hospital cardiac arrest).

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Matching procedure

The diagnosis of AMI was based on the analysis of abdominal computed tomography (CT) scans or digestive endoscopy or perioperative findings of bowel ischemia or histological intestinal examination after surgery or on postmortem examination (1, 8). The diagnosis of nonocclusive AMI (vs. occlusive AMI) was based on abdominal CT scans findings (absence of signs of thrombosis or occlusion, reduction in caliber and number of mesenteric vessels) and endoscopic and operative reports forms (presence of discontinuous segmental necrosis) (6, 8). A computer-generated list of potential controls was obtained during the same inclusion period. The patients who developed AMI were then matched to severely burned patients without AMI in a 1:3 ratio according to the following matching criteria: same year of admission, Abbreviated Burn Severity Index (ABSI) (±1 points) and Simplified Acute Physiology Score (SAPS) II (±5 points) (9, 10). Both ABSI and SAPS II were calculated within the first 24 h of ICBU admission. If more than three controls were eligible, we selected the controls with the closest admission date to the respective case admission date.

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Data collection

The data were retrospectively collected from patient records, either electronic or paper. Within the first 24 h after admission, we collected demographics, body mass index (BMI), TBSA, percentage of full thickness BSA burned, mechanism of injury, inhalation injury, patients’ characteristics and comorbidities, delay from the time of thermal injury to the time of ICBU, SAPS II, ABSI, lowest cardiac index (CI) and invasive mean arterial pressure (MAP), use and highest dose of vasopressors, prehospital and first 24-h administered fluid volume, use of hydroxocobalamin, cardiac dysfunction, use of dobutamine, highest plasma lactate levels, use of mechanical ventilation, renal replacement therapy (RRT), escharotomy, fasciotomy, and organ dysfunction evaluated using the sequential organ failure assessment score on day 1 (D1 SOFA) (11).

From admission to AMI diagnosis we collected the following data: time between ICBU admission and AMI diagnosis, use of RRT in the first 7 days, number of surgical procedures in the first 7 days (escharotomy, fasciotomy, and skin graft surgery), shock state within the 10 days preceding AMI diagnosis, number of surgical procedures within the 10 days preceding AMI diagnosis, de novo atrial fibrillation, and route of feeding (parenteral or enteral). On the day of AMI diagnosis, the following data were collected: the diagnosis procedure (abdominal CT scan, digestive endoscopy, abdominal surgery, autopsy), the mechanism of ischemia (nonocclusive vs. occlusive), the type of surgical procedure, the extent (massive infarction >50% of the bowel length) (6) and the localization of the necrotic bowel (large bowel, small bowel, and stomach), administration of antimicrobial treatment, use and highest dose of vasopressors in the first 24 h after AMI diagnosis, SOFA score and highest plasma lactate concentration in the first 24 h after AMI diagnosis, intraabdominal pressure, plasma white blood cell count, procalcitonin, and alkaline phosphatase levels.

From the day of AMI diagnosis to ICBU discharge or death, we reported the type and number of abdominal surgical procedures, duration of antimicrobial treatment and vasopressors use, type of anticoagulation (prophylactic vs. curative), organ support, ICBU length of stay, 90-day mortality, and in-hospital mortality.

Throughout the ICBU stay, hemodynamic parameters, fluid administration, and the dose of vasoactive drugs were determined at hourly intervals. Biochemical tests were conducted on admission and at least once a day thereafter.

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Patient management

Hemodynamic management (fluids and vasopressors) within 24 h of admission was defined by the Saint Louis Hospital ICBU resuscitation protocol (12). Cardiac function was routinely assessed in the first 24 h by echocardiography. Arterial pressure and CI were monitored continuously and checked hourly. CI was measured by transpulmonary thermodilution (TPTD) with a PiCCO monitor (PiCCO-2 Pulsion Medical Systems AG, Munich, Germany). The PiCCO monitor was calibrated every 2 h in the acute phase patients during the first 24 h.

Twenty percent albumin was administrated in patients with TBSA more than 30% after the 6th hour after thermal injury to reach a serum albumin concentration of 25 to 30 g/L. When mechanical ventilation was initiated, protective ventilation was applied (tidal volume = 6–7 mL/kg) while maintaining an inspiratory plateau pressure less than 30 cmH2O. Early enteral nutrition was initiated within 24 h. Glycemic control was adjusted to maintain glucose levels between 5 and 9 mmol/L. Surgical treatment included escharotomy or fasciotomy as needed and early coverage of excised burn wounds with allografts or autografts within the first 7 days of admission as permitted by the clinical condition of the patient.

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Statistical analysis

Using SOFA score as an indicator of early organ dysfunction, which have been reported as associated with the onset of AMI in critically ill patients (3, 13, 14), a power analysis was performed before commencing the study. It indicated that a total sample size of 36 patients (ratio 1:3) would be necessary (α = 0.05, power = 0.90) to detect a mean difference of 4 between D1 SOFA in the two groups (11). In a previous study including critically ill burns patients, mean D1 SOFA were 7 and 3, respectively, in patients with and without AMI, and the standard deviations were estimated at 3 (unpublished data) (12).

Patients with AMI and matched controls (1:3) were compared regarding demographic data, comorbidities, initial hemodynamic parameters, initial vasoactive drug support, D1 SOFA and organ support. Quantitative parameters are reported as median and interquartile range (IQR), and qualitative parameters are expressed as number and percentage. Categorical variables were compared using the chi-square test or Fisher's exact test as appropriate. Continuous variables were compared using the Mann–Whitney U test. Unadjusted odds ratios (ORs) and 95% confidence intervals (95% CI) for each outcome were calculated using logistic regression with generalized estimating equations to account for the matching. Variables associated with AMI in univariate analysis were entered in a multivariate logistic regression model to identify factors independently associated with this complication. Considering the rule of a minimum of 5 to 10 events for each predictor variable considered in the model (15), when several related variables were associated with the outcome in univariate analysis, only the most clinically relevant were included in the multivariate model. The final model expressed the adjusted ORs and 95% CIs. Patient survival was analyzed with the use of the Kaplan–Meier method and compared between groups (AMI group vs. matched controls group) with the use of the log-rank test. Differences at a level of P < 0.05 were considered statistically significant. The analyses were performed using SPSS 24.0 software (SPSS, Chicago, IL).

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Patients’ characteristics

During the study period, a total number of 982 adult burns patients were admitted, of whom 282 severely burned patients fulfilled the inclusion criteria. Because of lacking data, the final study population consisted of 272 individuals. At ICBU admission, severely burned patients were 47 (31–60) years of age, 44% female, with a median: TBSA of 30 (20–48)%, SAPS II of 30 (18–44), and ABSI of 8 (6–10). Inhalation injury was present in 107 patients (39%), 181 were mechanically ventilated (66%), and 102 received vasopressors in the first 24 h (37%). The in-hospital mortality rate was 27%. A total of 15 patients of the 272 severely burned patients presented an AMI as previously defined (5.5% of severely ill patients and 1.5% of the whole admissions). All the patients with AMI and the matched control patients had thermal injury. The construction of the study cohorts is described in the Supplemental Digital Content 1 (see Figure, The AMI and matched controls groups characteristics are summarized in Tables 1 and 2.

Table 1

Table 1

Table 2

Table 2

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Variables associated with AMI

The lowest CI in the first 24 h was significantly lower in patients who developed AMI (1.50 [1.20–1.90] vs. 2.11 [1.44–2.7] L/min/m2 [P = 0.03]) and D1 SOFA was significantly higher in the AMI group (8 [5–9] vs. 3 [0–6] [P < 0.001]) (Fig. 1). Nonadjusted ORs were respectively 0.18 (95% CI, 0.03–0.94) and 1.6 (95% CI, 1.2–2.1) after matching.

Fig. 1

Fig. 1

AMI was also associated with hydroxocobalamin use (OR = 4.6 [95% CI, 1.3–15.9]) and RRT in the first 7 days (OR = 4.9 [95% CI, 1.2–19]) after matching. Furthermore, no statistical differences were observed between patients with and without AMI with regard to peripheral vascular disease, hypertension, diabetes, liver cirrhosis, inhalation injury, abdominal compartment syndrome in the first 72 h, the lowest MAP in the first 24 h, catecholamine use, and initial fluid administration (Table 1).

Using a multiple logistic regression analysis including the lowest CI in the first 24 h, D1 SOFA, and hydroxocobalamin use, only the two first parameters were independently associated with AMI (Table 3).

Table 3

Table 3

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Characteristics of the patients presenting with AMI

The characteristics and management of the patients presenting with AMI are summarized in Tables 1 and 2. In the AMI group, patients were mainly men (60%) with a median age of 56 (40–61) years. The median duration between the ICBU admission and AMI diagnosis was 15 (5–40) days. Abdominal CT scan was the main diagnostic procedure (66%). Representative CT scan findings of nonocclusive mesenteric ischemia are presented in Figure 2. The AMI mechanism in all patients (n = 15) was nonocclusive. In most cases, a laparotomy was performed (66%), and the main location of the infarction was the small bowel (46%).

Fig. 2

Fig. 2

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Outcome of AMI

In-hospital and 90-day mortality were significantly higher in the AMI group than in the control group: respectively 93% vs. 53% (P = 0.005) and 93% vs. 46% (P = 0.001). A comparison of the two survival curves (AMI vs. matched controls) is showed in Figure 3A. Kaplan–Meier estimates of cumulative probabilities of 90-day survival after AMI diagnosis is represented in Figure 3B. In all cases, death was due to sepsis-related multiple organ failure. ICU length of stay did not differ significantly between the two groups. The only patient who survived in the AMI group was a 57-year-old man who left the ICU after 107 days of hospitalization. His TBSA burned was 58%, SOFA score on admission was 8, and IGS II score was 72. This patient underwent laparotomy with bowel resection for a colic infarction.

Fig. 3

Fig. 3

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The main findings of this study are that the lowest CI in the first 24 h after admission and initial SOFA score were independently associated with the occurrence of AMI in critically ill burns patients. The use of hydroxocobalamin was associated with AMI only in univariate analysis. The AMI mechanism in all patients was nonocclusive, and the outcome was extremely poor (in-hospital mortality higher than 90%).

Only a few studies have investigated potential risk factors of AMI in severely burned patients and its incidence and outcome (4, 6, 7). Our study found a close incidence of AMI in burn patients (1.5%) to most of the previous studies in this patient group (respectively 2% and 1.7% in the studies of Muschitz et al. and Markell et al.) (6, 7). Our strategy is to have a systematic search of AMI using abdominal CT scan with intravenous contrast injection or endoscopy in patients with persistent shock state especially when associated with digestive symptom. Indeed, in a retrospective review of the medical and autopsy records of severely burned patients in the University of Texas Medical Branch, Desai et al. reported that 0.5% of their patients had this complication identified before death, and another 2% of children and 7% of adults who died were identified with necrotic bowel after death (5). These results suggest that AMI is under diagnosed in severely burned patients and that an aggressive diagnosis strategy could unmask this complication. The in-hospital mortality of severely burned patients with AMI in our study seems very high, and is concordant with the aforesaid studies (6, 7).

In our study, the AMI mechanism in all patients was nonocclusive. Muschitz et al. found similar results by identifying nonocclusive mesenteric ischemia (NOMI) as the main cause of the gastrointestinal infarction after severe burns (82%) (6). Concordant results were also found in studies including cardiac surgery patients in a low-flow state with a predominant nonocclusive etiology (3, 16). In other conditions (e.g., progressive atherosclerotic disease, thrombophilia, atrial fibrillation), an occlusive etiology (arterial or venous thrombosis and arterial emboli) was found as the main cause of AMI (2, 17).

Nonocclusive mesenteric ischemia is frequently associated with low-flow states related to severe hypovolemia or heart failure or shock-related microcirculatory hypoperfusion. This may be particularly true when the metabolic demands of the visceral organs are increased, mainly after major surgery and severe thermal injury (2, 18). In these conditions, the main cause of mesenteric dysoxia is related to a decrease in regional oxygen delivery to a level that is insufficient to meet the gut's metabolic needs. The initial response is splanchnic vasodilation, but prolonged ischemia leads to vasoconstriction, with redistribution of blood flow away from the splanchnic organs, which can persist even after intestinal blood flow normalization (2). Redistribution of blood flow may occur also at the microcirculatory level (18, 19). Furthermore, initial fluid overresuscitation in patients with thermal injury may be associated with splanchnic congestion. Venous congestion may result in intestinal dysoxia and hypoperfusion especially in the presence of right ventricular dysfunction (7, 20). This early injury may result in alteration of the intestinal integrity and induces bacterial translocation from the intestinal lumen with activation of systemic inflammatory pathways and MOF.

High D1 SOFA, low CI in the first 24 h, RRT in the first 7 days, and hydroxocobalamin use were associated with the risk of developing AMI in univariate analysis. All these risk factors are consistent with the pathophysiology of nonocclusive AMI. Nevertheless, only elevated D1 SOFA score and low CI in the first 24 h were independently associated with AMI. Indeed, elevated D1 SOFA and early RRT reflect MOF and global severity of the patient on admission which is related to poor outcome in critically ill burn patients (11, 21). The use of hydroxocobalamin as a cyanide antidote in the case of inhalation injury may compromise splanchnic and other organs perfusion by a potential vasoconstrictor effect (22–24). The role of hydroxocobalamin in gut microcirculatory disorders merits exploration in future studies. Furthermore, initial low cardiac output in severely burned patients is associated with high systemic vascular resistance (25). This hemodynamic profile is mainly related to initial hypovolemic shock which could generate a mesenteric low-flow state and nonocclusive AMI. In these conditions, the association with heart failure and high-dose vasopressors may worsen splanchnic perfusion (18). Our interest in this risk factor is that it is a potentially modifiable parameter, with avoidance of systemic and regional low-flow state potentially improving outcome. Previous studies focused on hemodynamic parameters on admission and found that cardiac output was independently associated with mortality in critically ill burns patients, suggesting early under-resuscitation in nonsurvivors (12, 26). The authors concluded that initial hemodynamic monitoring may allow earlier diagnosis of under-resuscitated severely burned patients and could allow tailored fluid resuscitation and inotropes to avoid organ hypoperfusion. In this study, despite patients with AMI received almost 1.5-fold higher fluid volume in the first 24 h than matched control patients without reaching statistical significance, the lowest CI in the first 24 h was significantly lower in the AMI group. This could be explained by a more important capillary leak syndrome in the AMI group and thus a more important fluid administration requirement leading to splanchnic congestion and dysoxia (7). Surprisingly, the lowest MAP, the use of norepinephrine, and inotropes in the first 24 h were not significantly different between the AMI group and the matched control group in this work as described in other studies including cardiac surgery patients (13, 14, 16). This may be explained by the matching procedure based on the SAPS II in which arterial pressure is one of the more weighted parameters. Furthermore, the use of low-dose norepinephrine in the first 24 h in the majority of our patients is unlikely to have altered gut perfusion (0.19 [0–0.98] vs. 0.09 [0–0.44] μg/kg/min [P = 0.43], respectively, in the AMI and the matched control group). Indeed, in an experimental study, Krejci et al. described the effects of vasopressors on regional and microcirculatory blood flow in multiple abdominal organs in sepsis. Higher norepinephrine mean doses at 0.7 ± 0.3 μg/kg/min significantly increased mean arterial pressure and induced a significant reduction in superior mesenteric artery flow and in microcirculatory blood flow in the jejunal and the pancreas mucosa evaluated by laser Doppler flowmetry (27). This is even more plausible because hypovolemia was ruled out in these conditions before norepinephrine use as described in our local standardized resuscitation protocol (12). Indeed, in our center norepinephrine is usually used secondarily in the hyperkinetic and vasoplegic phase (sepsis-like phase) of burn-related shock. Norepinephrine is used in patients with a low diastolic arterial pressure (<40 mmHg) and fluid unresponsiveness mainly in case of inhalation injury or early sepsis (hypotensive patients unresponsive to a fluid challenge).

Initial hemodynamic parameters and catecholamine use were not evaluated as potential AMI risk factors in previous studies including severely burned patients (4, 6, 7). Only TBSA and sepsis were identified as potential risk factors in previous studies including severely burned patients with different study designs (4, 7).

The risk factors identified in this study are not in themselves conclusive predictive tools, but may allow early identification of patients at increased risk of AMI. These patients may benefit from an early hemodynamic monitoring to diagnose under-resuscitation situations with a low cardiac output, and an aggressive diagnosis and therapeutic strategy. Furthermore, splanchnic microcirculatory monitoring may also identify situations of gut microvascular hypoperfusion even when macrocirculation (MAP, cardiac output) seems adequate with administration of fluids and vasopressors (19, 26). In this line, potential therapies targeting splanchnic microcirculation (mainly vasodilators, e.g., Iloprost) should be investigated in burn shock resuscitation (28, 29).

A high index of clinical AMI suspicion (abdominal pain, vomiting, bloody diarrhea) among high-risk patients should trigger a systematic search of AMI using abdominal CT scan with intravenous contrast injection and early surgical treatment before gut damage and development of MOF.

In this work, the extent of the intestinal infarction was massive (>50% of the bowel length) in almost one half of the AMI cases. Among these patients (n = 8), six patients had such severe gut necrosis that resection could not be performed. These findings are in agreement with the series of Muschitz et al. in severely burn patients. Indeed, almost one half of the nonocclusive AMI had massive infarction. Inoperable bowel infarction was found in 6 patients among 14 with nonocclusive AMI (6). Furthermore, among our patients who did not undergo laparotomy, five had an extended intestinal infarction diagnosed on CT scan and severe MOF. For these patients, abdominal surgery was considered futile after a multidisciplinary meeting.

It is important to recognize potential limitations in this study. First, it was a retrospective single-center study, which limited the total number of cases of AMI. Second, we reported hemodynamic variables as a single measurement (the lowest CI in the first 24 h). In a shock state, potential rapid changes in hemodynamics can occur, and a more appropriate approach could be to take into account both the duration and severity of low cardiac output. Third, severely burned patients without a diagnosis of AMI did not routinely undergo abdominal CT scans or digestive endoscopy. Therefore, we cannot exclude missing lower grade cases of AMI among these patients. Fourth, the small sample size of patients limited the number of variables entered in the multivariate analysis to three. Nonetheless, the most clinically relevant risk factors that are potentially modifiable (lowest CI in the first 24 h and hydroxocobalamin use) were included in the model. Finally, the observational design prevents us from drawing any firm conclusions regarding the causal relationship between the identified risk factors and the onset of AMI.

This study has several strengths. First, to the best of our knowledge, this is one of the largest recent studies assessing risk factors for AMI in severely burned adult patients. Second, in contrast to previous studies, this study assessed risk factors in patients who developed AMI who were matched to severely burned patients without AMI at a ratio of 1:3 according to SAPS II and ABSI (30). The aforesaid scores were previously described as strongly associated with poor outcome (12, 31). Indeed, previous studies were exclusively descriptive without a control group (6, 7) or with a case–control design without a matching procedure (4). Finally, this work was the first to include initial hemodynamic parameters in the analysis as potentially modifiable risk factors.

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Initial low cardiac output and early multiple organ dysfunction were independently associated with nonocclusive AMI in critically ill burns patients. The potential role of hydroxocobalamin in gut microcirculatory disorders merits further exploration.

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The authors thank Claire Coutzac and Stéphanie Letaleur (medical secretaries) for technical support.

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Acute mesenteric ischemia; burns; critically ill; outcome; risk factors; surgery

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