Erratum to: Antimicrobials: a global alliance for optimizing their rational use in intra-abdominal infections (AGORA).

[This corrects the article DOI: 10.1186/s13017-016-0089-y.].

Emerging tropical diseases in Australia. Part 5. Hendra virus.

Hendra virus (HeV) was first isolated in 1994, from a disease outbreak involving at least 21 horses and two humans in the Brisbane suburb of Hendra, Australia. The affected horses and humans all developed a severe but unidentified respiratory disease that resulted in the deaths of one of the human cases and the deaths or putting down of 14 of the horses. The virus, isolated by culture from a horse and the kidney of the fatal human case, was initially characterised as a new member of the genus Morbillivirus in the family Paramyxoviridae. Comparative sequence analysis of part of the matrix protein gene of the virus and the discovery that the virus had an exceptionally large genome subsequently led to HeV being assigned to a new genus, Henipavirus, along with Nipah virus (a newly emergent virus in pigs). The regular outbreaks of HeV-related disease that have occurred in Australia since 1994 have all been characterised by acute respiratory and neurological manifestations, with high levels of morbidity and mortality in the affected horses and humans. The modes of transmission of HeV remain largely unknown. Although fruit bats have been identified as natural hosts of the virus, direct bat-horse, bat-human or human-human transmission has not been reported. Human infection can occur via exposure to infectious urine, saliva or nasopharyngeal fluid from horses. The treatment options and efficacy are very limited and no vaccine exists. Reports on the outbreaks of HeV in Australia are collated in this review and the available data on the biology, transmission and detection of the pathogen are summarized and discussed.

Differential induction of PPAR-gamma by luminal glutamine and iNOS by luminal arginine in the rodent postischemic small bowel.

Using a rodent model of gut ischemia-reperfusion (I/R), we have previously shown that the induction of inducible nitric oxide synthase (iNOS) is harmful, whereas the induction of heme oxygenase 1 (HO-1) and peroxisome proliferator-activated receptor-gamma (PPAR-gamma) is protective. In the present study, we hypothesized that the luminal nutrients arginine and glutamine differentially modulate these molecular events in the postischemic gut. Jejunal sacs were created in rats at laparotomy, filled with either 60 mM glutamine, arginine, or magnesium sulfate (osmotic control) followed by 60 min of superior mesenteric artery occlusion and 6 h of reperfusion, and compared with shams. The jejunum was harvested for histology or myeloperoxidase (MPO) activity (inflammation). Heat shock proteins and iNOS were quantitated by Western blot analysis and PPAR-gamma by DNA binding activity. In some experiments, rats were pretreated with the PPAR-gamma inhibitor G9662 or with the iNOS inhibitor N-[3(aminomethyl)benzyl]acetamidine (1400W). iNOS was significantly increased by arginine but not by glutamine following gut I/R and was associated with increased MPO activity and mucosal injury. On the other hand, PPAR-gamma was significantly increased by glutamine but decreased by arginine, whereas heat shock proteins were similarly increased in all experimental groups. The PPAR-gamma inhibitor G9662 abrogated the protective effects of glutamine, whereas the iNOS inhibitor 1400W attenuated the injurious effects of arginine. We concluded that luminal arginine and glutamine differentially modulate the molecular events that regulate injurious I/R-mediated gut inflammation and injury. The induction of PPAR-gamma by luminal glutamine is a novel protective mechanism, whereas luminal arginine appears harmful to the postischemic gut due to enhanced expression of iNOS.

Mortality from isolated civilian penetrating extremity injury.

BACKGROUND: Although studies have ascertained that ten percent of soldiers killed in battle bleed to death from extremity wounds, little data exists on exsanguination and mortality from extremity injuries in civilian trauma. This study examined the treatment course and outcomes of civilian patients who appear to have exsanguinated from isolated penetrating extremity injuries. METHODS: Five and 1/2 years' data (Aug 1994 to Dec 1999) were reviewed from two Level I trauma centers that receive 95% of trauma patients in metropolitan Houston, TX. Records (hospital trauma registries, emergency medical system (EMS) and medical examiner data) were reviewed on all patients with isolated extremity injuries who arrived dead at the trauma center or underwent cardiopulmonary resuscitation (CPR) or emergency center thoracotomy (ECT). RESULTS: Fourteen patients meeting inclusion criteria were identified from over 75,000 trauma emergency center (EC) visits. Average age was 31 years and 93% were males. Gunshot wounds accounted for 50% of the injuries. The exsanguinating wound was in the lower extremity in 10/14 (71%) patients and proximal to the elbow or knee in 12/14 (86%). Ten (71%) had both a major artery and vein injured; one had only a venous injury. Prehospital hemorrhage control was primarily by gauze dressings. Twelve (86%) had "signs of life" in the field, but none had a discernable blood pressure or pulse upon arrival at the EC. Prehospital intravenous access was not obtained in 10 patients (71%). Nine patients underwent ECT, and nine were initially resuscitated (eight with ECT and one with CPR). Those undergoing operative repair received an average of 26 +/- 14 units of packed red blood cells. All patients died, 93% succumbing within 12 hours. CONCLUSION: Although rare, death from isolated extremity injuries does occur in the civilian population. The majority of injuries that lead to immediate death are proximal injuries of the lower extremities. The cause of death in this series appears to have been exsanguination, although definitive etiology cannot be discerned. Intravenous access was not obtainable in the majority of patients. Eight patients (57%) had bleeding from a site that anatomically might have been amenable to tourniquet control. Patients presenting to the EC without any detectable blood pressure and who received either CPR or EC thoracotomy all died.

Inhibition of intestinal transit by resuscitation-induced gut edema is reversed by L-NIL.

BACKGROUND: Post-resuscitation gut edema and associated gut dysfunction is a common and significant clinical problem that occurs after traumatic injury and shock. We have shown previously that gut edema without ischemia/reperfusion injury delays intestinal transit [1]. We hypothesized that gut edema increases expression of inducible nitric oxide synthase (iNOS) protein, and that selective iNOS inhibition using L-NIL reverses the delayed intestinal transit associated with gut edema. MATERIALS AND METHODS: One hour prior to laparotomy, rats were pretreated with 10 mg/kg body weight of intraperitoneal L-NIL or saline vehicle and underwent 80 ml/kg body weight of 0.9% saline + superior mesenteric venous pressure elevation (Edema) or sham surgery (Sham). A duodenal catheter was placed to allow injection of a fluorescent dye for the measurement of intestinal transit. At 6 h, the small bowel was divided and the mean geometric center (MGC) of fluorescent dye was measured to determine transit. Ileum was harvested for histological assessment of mucosal injury, evaluation of iNOS protein expression by Western blotting, and MPO activity. Tissue water was determined using the wet-to-dry weight ratio to assess gut edema. Data are expressed as mean +/- SEM, n = 3-6 and * = P <0.05 using ANOVA. RESULTS: Gut edema, expressed as increased wet-to-dry ratio, was associated with decreased intestinal transit and elevated iNOS protein expression. Pretreatment with l-NIL improved intestinal transit and decreased expression of iNOS protein without decreasing intestinal tissue water compared to edema animals. There was no difference in mucosal injury or MPO activity among groups. CONCLUSION: Gut edema delays intestinal transit via an iNOS-mediated mechanism.

Heme oxygenase-1 induction by hemin protects against gut ischemia/reperfusion injury.

BACKGROUND: We have shown that both intraischemic hypothermia and hypertonic saline resuscitation provide dramatic protection against gut ischemia/reperfusion (I/R) injury that is in part mediated by heme oxygenase-1 (HO-1). We therefore hypothesized that induction of HO-1 by hemin would lessen damage and improve function after gut I/R. MATERIALS AND METHODS: Male Sprague-Dawley rats were treated with 50 micromol/kg hemin (HO-1 inducer ferric protoporphyrin IX chloride) sq or vehicle 2 h before superior mesenteric artery occlusion for 60 min or sham laparotomy. After 6 h of reperfusion, transit was determined by quantitation of percentage of tracer in 10 equal segments of small intestine 30 min following injection into the duodenum (expressed as mean geometric center). Ileum was harvested for assessment of mucosal histologic injury (Chiu score 0-5 by blinded observer), myeloperoxidase activity (MPO, index of inflammation), and HO-1 protein expression. RESULTS: Hemin treatment was associated with increased HO-1 protein expression, lessened mucosal injury, decreased MPO activity, and improved intestinal transit following gut I/R. CONCLUSION: These data corroborate that HO-1 plays an important role in protecting the gut against I/R-induced injury.

Ischemia/reperfusion-induced disruption of rat small intestine transit is reversed by total enteral nutrition.

OBJECTIVES: A reduced blood flow to the gut is a consistent event after traumatic shock. Enteral nutrition support has been shown to reduce the septic morbidity after major trauma. We evaluated the effects of a transient ischemia followed by reperfusion (I/R) and an enteral nutrition support regimen on the motility of the small intestine of the rat. METHODS: A catheter was placed in the upper duodenum and the small intestine was then made ischemic by clamping the superior mesenteric artery for 45 min; the arteries of sham rats were isolated but not clamped. Intestinal transit was evaluated by measuring the amount of fluorescein isothiocyanate-dextran (12 000 MW) in each of 10 intestinal sections at 30 min after injection through the duodenal catheter. The mean geometric center of marker distribution (MGC) was calculated for each group and compared. In a second study, I/R was followed by infusion of saline or a complete nutrient solution overnight, and transit was determined. RESULTS: Intestinal transit (as the MGC) of I/R rats at 24 h after the beginning of reperfusion (3.5 +/- 0.2) and 48 h after the beginning of reperfusion (4.5 +/- 1.1) was significantly lower than that in the respective sham controls (5.1 +/- 0.3 and 5.9 +/- 0.5). The MGC for rats receiving a nutrient solution overnight during the reperfusion phase (6.0 +/- 1.1) was significantly increased compared with the MGC of 4.8 +/- 0.3 for rats receiving saline during the same period. CONCLUSIONS: These results demonstrate a long-term deleterious effect of a non-lethal ischemia on intestinal transit and may be one explanation for many of the sequelae occurring after ischemia. In addition, these results demonstrate that a nutrient infusion will prevent the delayed transit. This may provide a partial explanation for the beneficial effects of total enteral nutrition in the clinical situation of posttraumatic injury.

Migrating motility complexes persist after severe traumatic shock in patients who tolerate enteral nutrition.

BACKGROUND: Postinjury small bowel ileus is poorly characterized and may be an important factor in intolerance to enteral nutrition (EN). We, therefore, placed jejunal manometry catheters in high-risk trauma patients. Our hypothesis was that the presence of "fasting migrating motility complex (MMC)" activity and conversion to a "fed pattern" at goal rate of EN would be present in those patients who tolerate jejunal feeding. METHODS: After obtaining baseline fasting manometry pressure tracings, jejunal feeding was advanced stepwise to a set goal while tolerance was monitored and intolerance was treated by a standard approach. RESULTS: Of the 10 study patients, 7 were able to be maintained on EN. Five (50%) had "fasting MMCs" and had good tolerance to early advancement of EN. The remaining five patients did not exhibit "fasting MMCs" and four had poor tolerance to early advancement of EN. Overall, nine patients reached goal rate of EN of which four converted to a "fed pattern." This, however, was not associated with later tolerance to EN. CONCLUSION: EN is feasible following severe traumatic shock. Surprisingly, half of the patients had fasting MMCs. This requires intact neural and motor function and was associated with good tolerance of early EN.

Inducible nitric oxide synthase mediates gut ischemia/reperfusion-induced ileus only after severe insults.

Inducible nitric oxide synthase (NOS 2) is thought to play a role in gut motility disorders that occur under proinflammatory conditions. Clinically, ileus occurs after sepsis and shock-induced gut ischemia/reperfusion (I/R). The purpose of this study was to determine if NOS 2 mediates impaired intestinal transit in well-established models of both moderate and severe gut ischemia/reperfusion. At laparotomy, Sprague-Dawley rats had duodenal catheters placed. Small intestinal transit was determined by quantitating the percentage tracer (FITC-dextran) in 10 equal segments of intestine 30 min after catheter injection [expressed as the mean geometric center (MGC) of distribution]. Transit was assessed at 6 and 24 h after gut ischemia [45 or 75 min of superior mesenteric artery occlusion (SMAO) with sham laparotomy as control]. In a separate set of experiments, N(6)-(iminoethyl)-L-lysine (L-NIL), a selective NOS 2 antagonist, was administered 1 h prior to laparotomy and transit was determined after 6 h as described above. Ileal NOS 2 expression was assessed by Western immunoblot and quantitative "real-time" RT-PCR. We observed that both 45 and 75 min of SMAO decreased intestinal transit at 6 h of reperfusion compared to sham. Ileal NOS 2 mRNA and protein were increased after 75, but not 45, min of SMAO. In addition, L-NIL improved transit after 75, but not 45, min of SMAO. We conclude that (1) NOS 2 is upregulated in the gut only after more severe ischemic insults, and (2) ileus is mediated, at least in part, by NOS 2 under these conditions.

Computerized decision support for mechanical ventilation of trauma induced ARDS: results of a randomized clinical trial.

BACKGROUND: Variability and logistic complexity of mechanical ventilatory support of acute respiratory distress syndrome, and need to standardize care among all clinicians and patients, led University of Utah/LDS Hospital physicians, nurses, and engineers to develop a comprehensive computerized protocol. This bedside decision support system was the basis of a multicenter clinical trial (1993-1998) that showed ability to export a computerized protocol to other sites and improved efficacy with computer- versus physician-directed ventilatory support. The Memorial Hermann Hospital Shock Trauma intensive care unit (ICU) (Houston, TX; a Level I trauma center and teaching affiliate of The University of Texas Houston Medical School) served as one of the 10 trial sites and recruited two thirds of the trauma patients. Results from the trauma patient subgroup at this site are reported to answer three questions: Can a computerized protocol be successfully exported to a trauma ICU? Was ventilator management different between study groups? Was patient outcome affected? METHODS: Sixty-seven trauma patients were randomized at the Memorial Hermann Shock Trauma ICU site. "Protocol" assigned patients had ventilatory support directed by the bedside respiratory therapist using the computerized protocol. "Nonprotocol" patients were managed by physician orders. RESULTS: Of the 67 trauma patients randomized, 33 were protocol (age 40 +/- 3; Injury Severity Score [ISS] 26 +/- 3; 73% blunt) and 34 were nonprotocol (age 38 +/- 2; ISS 25 +/- 2; 76% blunt). For the protocol group, the computerized protocol was used 96% of the time of ventilatory support and 95% of computer-generated instructions were followed by the bedside respiratory therapist. Outcome measures (i.e., survival, ICU length of stay, morbidity, and barotrauma) were not significantly different between groups. Fio2 > or = 0.6 and Pplateau > or = 35 cm H2O exposures were less for the protocol group. CONCLUSION: A computerized protocol for bedside decision support was successfully exported to a trauma center, and effectively standardized mechanical ventilatory support of trauma-induced acute respiratory distress syndrome without adverse effect on patient outcome.

Post-injury multiple organ failure: the role of the gut.

Despite intensive investigation, the pathogenesis of post-injury multiple organ failure (MOF) remains elusive. Laboratory and clinical research strongly suggests that the gastrointestinal tract (i.e., the gut) plays a pivotal pathogenic role. Since its inception in 1988, the Trauma Research Center (TRC) at the University of Texas-Houston Medical School (UTHMS) has focused its efforts on elucidating the role of the gut in post-injury MOF. On the basis of our observations and those of others, we believe that 1) shock with resulting gut hypoperfusion is an important inciting event, 2) the reperfused gut is a source of proinflammatory mediators that can amplify the early systemic inflammatory response syndrome (SIRS) and thus contribute to early MOF, 3) early gut hypoperfusion causes an ileus in both the stomach and small bowel that sets the stage for progressive gut dysfunction so that the proximal gut becomes a reservoir for pathogens and toxins that contribute to late sepsis-associated MOF, and 4) late infections cause further worsening of this gut dysfunction. Thus, the gut can be both an instigator and a victim of MOF. The purpose of this article is to provide the rationale behind these beliefs and to provide a brief overview of the ongoing research projects in the TRC at UTHMS.

[Enteral feeding of glucose increases intestinal mucosal blood flow during intestinal ischemia/reperfusion injury].

OBJECTIVE: To explore the relationship between enteral nutrition and the change in intestinal mucosal blood flow during intestinal ischemia/reperfusion injury. METHODS: Thirty-six Sprague-Dawley rats were randomly divided into alanine (12 rats), glucose (14 rats) and mannitol control (10 rats) groups. Jejunal sac was prepared with the filling of either 10 mM alanine, glucose or mannitol in the three groups. The laser doppler probe and intestinal mucosal tonometry were placed at the both ends of the sac. The superior mesenteric artery was occluded by arterial clamp for 60 mins and released thereafter for another 60 mins. Intestinal mucosal blood flow and regional pressure of CO(2) (PrCO(2)) were determined every 30 mins. RESULTS: During the process of ischemia/reperfusion, the intestinal mucosal blood flow in glucose group increased evidently and the PrCO(2) in glucose group decreased obviously (P < 0.01) when comparcd with those in mannitol group. CONCLUSION: During the process of ischemia/reperfusion, enteral feeding of glucose could increase intestinal mucosal blood flow, which provided guarding effects on the intestine suffering from ischemic/reperfusion injury.

Vacuum-assisted wound closure provides early fascial reapproximation in trauma patients with open abdomens.

BACKGROUND: Damage control and decompressive laparotomies salvage severely injured patients who would have previously died. Unfortunately, many of these patients develop open abdomens. A variety of management strategies exist. The end result in many cases, however, is a large ventral hernia that requires a complex repair 6 to 12 months after discharge. We instituted vacuum-assisted wound closure (VAWC) to achieve early fascial closure and eliminate the need for delayed procedures. METHODS: For 12 months ending June 2000, 14 of 698 trauma intensive care unit admissions developed open abdomens and were managed with VAWC dressing. This was changed every 48 hours in the operating room with serial fascial approximation until complete closure. RESULTS: Fascial closure was achieved in 13 patients (92%) in 9.9 +/- 1.9 days, and 2.8 +/- 0.6 VAWC dressing changes were performed. There were 2 wound infections, no eviscerations, and no enteric fistulas. CONCLUSIONS: Use of VAWC can safely achieve early fascial closure in more than 90% of trauma patients with open abdomens.

Nitroprusside in resuscitation of major torso trauma.

OBJECTIVE: Patients with thoracic aortic injury (TAI) usually have sustained other major trauma, and may require aggressive shock resuscitation. In the 24 hours after aortic repair and during resuscitation, our cardiothoracic surgeons request intravenous nitroprusside to maintain mean arterial pressure (MAP) less than 90 mm Hg to minimize bleeding at the repair. We compared the resuscitation response of patients who sustained major torso trauma (MTT) and TAI with that of patients who had MTT with no TAI to determine whether nitroprusside can effectively control MAP during resuscitation and whether use of nitroprusside, because of its peripheral vasodilatory effects, is associated with a favorable resuscitation response. METHODS: During the 9-month study period, 11 patients who sustained TAI and 38 patients who sustained MTT with no TAI met multiple organ failure risk/shock criteria and were resuscitated by a standardized protocol emphasizing volume loading and hemoglobin replacement to maintain systemic oxygen delivery index (DO2I) > or = 600 mL O2/min-m2 for the first 24 intensive care unit hours. For TAI patients, postoperative management included intravenous nitroprusside infusion titrated by the bedside nurse to maintain mean arterial pressure (MAP) less than 90 mm Hg during the same 24 hours. Data were obtained prospectively during resuscitation. Retrospectively, the resuscitation response of TAI and non-TAI patients was compared. RESULTS: For the TAI group, nitroprusside effectively controlled MAP (range, 77-87 mm Hg); for the non-TAI group, mean MAP exceeded 95 mm Hg within 5 hours. During the first 8 hours, MAP, pulmonary capillary wedge pressure, and systemic vascular resistance index were less, and DO2I was greater for the TAI than for the non-TAI group. The resuscitation goal of DO2I > or = 600 mL O2/ min-m2 was attained at 4 hours for the TAI group, and was attained at 12 hours for the non-TAI group. No revisions of aortic repairs were required during or as a result of resuscitation. CONCLUSION: During aggressive shock resuscitation, control of MAP using nitroprusside is feasible and is associated with a favorable resuscitation response. Nitroprusside may be a useful adjunct during shock resuscitation of MTT as a vasoactive agent that promotes peripheral tissue perfusion.

Blunt trauma resuscitation: the old can respond.

HYPOTHESIS: Old and young trauma patients are capable of hyperdynamic response during standardized shock resuscitation. DESIGN: The responses of old and young trauma patients resuscitated using a standardized protocol are compared in an inception cohort study. A standardized resuscitation protocol was used to attain and maintain an oxygen delivery index of 600 mL/min x m2 or greater (DO2I > or = 600) for the first 24 hours in the intensive care unit. Interventions, responses, and outcomes for old (> or = 65 years) and young (<65 years) patients are described. Data were analyzed using analysis of variance, the chi2 test, and the t test; P<.05 was considered significant. SETTING: A 20-bed shock trauma intensive care unit in a regional level I trauma center. PATIENTS: Patients at high risk of postinjury multiple organ failure, ie, major organ or vascular injury and/or skeletal fractures, initial base deficit of 6 mEq/L or greater, need for 6 units or more of packed red blood cells in the first 12 hours, or age of 65 years or older with any 2 previous criteria. INTERVENTIONS: Pulmonary artery catheter, crystalloid fluid infusion, packed red blood cell transfusion, and moderate inotrope support, as needed in that sequence, to attain DO2I > or = 600. MAIN OUTCOME MEASURES: Intensive care unit length of stay and survival. RESULTS: During 19 months ending June 1999, 12 old patients (58% male; age, 76 +/- 2 years [mean +/- SEM] [P<.0011; Injury Severity Score, 20 +/- 2 [P=.02]) and 54 young patients (61% male; age, 37 +/- 2 years; Injury Severity Score, 32 +/- 2) were resuscitated. Initially, for old patients (cardiac index, 2.0 +/- 0.2 L/min x m2) and for young patients (cardiac index, 3.0 +/- 0.2 L/min x m2; P=.01), 24-hour volumes were as follows: 16 +/- 3 L of crystalloid and 12 +/- 3 units of packed red blood cells for the old patients and 21 +/- 2 L of crystalloid and 19 +/- 2 units of packed red blood cells for the young patients. For old patients, 9 (75%) attained DO2I > or = 600, and 11 (92%) survived 7 or more days and 5 (42%) 30 or more days. For young patients, 45 (83%) attained the DO2I goal, and 48 (89%) survived 30 or more days. Intensive care unit length of stay was 25 +/- 9 days for the old patients and 23 +/- 2 days for the young patients. CONCLUSIONS: Elderly patients have initially depressed cardiac index but generate hyperdynamic response. Although ultimate outcome is poorer than in the younger cohort, resuscitation is not futile.

Age should not be a consideration for nonoperative management of blunt splenic injury.

BACKGROUND: Operative management of blunt splenic injury is recommended for adults > or = 55 years. Because this is not our practice, we did a retrospective review to compare outcomes of patients > or = 55 years old versus patients < 55 years old. METHODS: During a 5-year period ending in July of 1998, 461 patients (3%) admitted to our Level I trauma center had a blunt splenic injury. Eighty-six patients (19%) died within 24 hours of massive injuries, leaving 375 patients for evaluation. Data were obtained from our trauma registry and medical records. RESULTS: A total of 29 patients (8%) were > or = 55 years old (mean age, 67 +/- 2 years; mean injury severity score [ISS] 25 +/- 2). Of these, 18 patients (62%) underwent nonoperative management (NOM). A total of 346 patients (92%) were < 55 years old (mean age, 28 +/- 0.6; mean ISS, 20 +/- 1). Of these, 198 patients (57%) underwent NOM. The failure rate was not different between the two age groups (17% vs. 14%). However, the ISS and mortality rate were significantly higher in the older age group that failed (ISS, 29.3 +/- 2.6 vs. 19.5 +/- 2.1; mortality: 67% vs. 4%). None of the deaths could be attributed to splenic injury. CONCLUSION: Adults > or = 55 years old with blunt splenic injury are successfully treated by NOM. Although older adults had significantly greater injuries, they had similar failure rates of NOM when compared with younger adults. Older adults had significantly higher mortality, but this was not a result of their splenic injury. Therefore, age should not be a criteria for NOM of blunt splenic injury.

Tissue hemoglobin O2 saturation during resuscitation of traumatic shock monitored using near infrared spectrometry.

BACKGROUND: Near infrared (NIR) spectrometry offers a noninvasive monitor of tissue hemoglobin O2 saturation and has been developed to report a quantitative clinical variable, StO2 [= HbO2/(HbO2 + Hb)]. In this study, a prototype NIR oximeter was used to investigate the hypothesis that changes in systemic O2 delivery index (D(O2)I) would be reflected by changes in StO2 in skeletal muscle, subcutaneous tissue, or both, as reperfusion occurs during shock resuscitation. StO2 was also compared with other indices of severity of shock or adequacy of resuscitation, including arterial base deficit, lactate, gastric mucosal P(CO2) (PgCO2), and mixed venous hemoglobin O2 saturation (S(VO2)). METHODS: Skeletal muscle and subcutaneous tissue StO2 were monitored simultaneously in eight severely injured trauma patients (88% blunt mechanism; age, 42 +/- 6 years; Injury Severity Score, 27 +/- 3) during standardized shock resuscitation in the intensive care unit with the primary goal of D(O2)I > or = 600 mL O2/min/m2 for 24 hours, and for an additional 12 hours during transition from resuscitation to standard intensive care unit care. RESULTS: Skeletal muscle StO2 increased significantly from 15 +/- 2% (mean +/- SEM) at the start of resuscitation to 49 +/- 14% at 24 hours, and to approximately 55% from 25 to 36 hours. Subcutaneous tissue StO2 approximately 82% and was significantly greater than skeletal muscle StO2 throughout. D(O2)I increased significantly from 372 +/- 54 to 718 +/- 47 mL O2/min/m2 during resuscitation. Over 36 hours, mean D(O2)I and skeletal muscle StO2 were highly correlated (r = 0.95). Neither D(O2)I-PgCO2 nor D(O2)I-S(VO2) were significantly correlated; neither S(VO2) nor subcutaneous tissue StO2 changed significantly. CONCLUSION: Hemoglobin O2 saturation was monitored noninvasively and simultaneously in skeletal muscle and subcutaneous tissues as StO2 (%) by using a prototype NIR oximeter. Skeletal muscle StO2 tracked systemic O2 delivery during and after resuscitation. As a rapidly deployable, noninvasive monitor of peripheral tissue oxygenation and O2 delivery, skeletal muscle StO2 obtained using NIR spectrometry would be useful to guide resuscitation in the intensive care unit, to monitor resuscitation status in the operating room, and, potentially, in combination with indicators such as base deficit and lactate, to detect shock during initial assessment of the severe trauma patient in the emergency department.

Nonocclusive bowel necrosis occurring in critically ill trauma patients receiving enteral nutrition manifests no reliable clinical signs for early detection.

BACKGROUND: Nonocclusive bowel necrosis (NOBN) has been associated with early enteral nutrition (EN). The purpose of this study was to determine the incidence of this complication in our trauma intensive care unit population and to define a typical patient profile vulnerable to NOBN. METHODS: Thirteen cases of NOBN were identified among 4,311 patients (0.3%) over a 64-month period ending October 1998. Their charts were analyzed for a variety of clinical data, including prospective EN tolerance data in 4. RESULTS: Twelve (92%) patients were enterally fed prior to diagnosis for 10 +/- 8 days (range 3 to 21). Tachycardia (n = 12, 92%); fever/hypothermia, (n = 12, 92%), and an abnormal white blood cell count (n = 11, 85%) were consistently present. Abdominal distention was common but tended to be a late sign (n = 12). Seven (56%) survived. In 4 patients with tolerance data, 3 reached the goal rate of feeds prior to diagnosis. Two became distended at >12 hours from diagnosis. Gastric tonometry demonstrated a decreased NgpHi (<7.30) after starting EN in all 3 in whom it was monitored. CONCLUSIONS: NOBN developed in 0.3% of our trauma patients. Onset occurs in the second week in high-acuity patients who have had a period of EN tolerance. Clinical findings resemble bacterial sepsis with tachycardia, fever, and leukocytosis. Gastrointestinal specific signs are not consistent or occur late. Thus, we could not identify an early, useful clinical indicator. Gastric carbon dioxide tonometry may detect a vulnerable subgroup of patients.