Incommensurate Oxygen Consumption in Response to Maximal Oxygen Availability Predicts Postinjury Multiple Organ Failure

Moore, Frederick A.; Haenel, James B.; Moore, Ernest E.; Whitehill, Thomas A.

doi:10.1097/00005373-199207000-00012

Cited by 207 publications

(63 citation statements)

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“…These results are consistent with recent findings on ischemia/reperfusion injury in rat organs (6) and human plasma from trauma activation and emergency department thoracotomies subjects (38). These results are consistent with incommensurate oxygen demands by trauma patients to sustain mitochondrial metabolism (35). Accumulation of TCA cycle intermediates, especially succinate, has been reported to occur in response to hypoxia following ischemia through reverse TCA fluxing of carbon backbones from aspartate (6).…”

Section: Discussionsupporting

confidence: 83%

Early hemorrhage triggers metabolic responses that build up during prolonged shock

D’Alessandro

Moore

et al. 2015

American Journal of Physiology-Regulatory, Integrative and Comp

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-Metabolic staging after trauma/hemorrhagic shock is a key driver of acidosis and directly relates to hypothermia and coagulopathy. Metabolic responses to trauma/hemorrhagic shock have been assayed through classic biochemical approaches or NMR, thereby lacking a comprehensive overview of the dynamic metabolic changes occurring after shock. Sprague-Dawley rats underwent progressive hemorrhage and shock. Baseline and postshock blood was collected, and late hyperfibrinolysis was assessed (LY30 Ͼ3%) in all of the tested rats. Extreme and intermediate time points were collected to assay the dynamic changes of the plasma metabolome via ultra-high performance liquid chromatography-mass spectrometry. Sham controls were used to determine whether metabolic changes could be primarily attributable to anesthesia and supine positioning. Early hemorrhage-triggered metabolic changes that built up progressively and became significant during sustained hemorrhagic shock. Metabolic phenotypes either resulted in immediate hypercatabolism, or late hypercatabolism, preceded by metabolic deregulation during early hemorrhage in a subset of rats. Hemorrhagic shock consistently promoted hyperglycemia, glycolysis, Krebs cycle, fatty acid, amino acid, and nitrogen metabolism (urate and polyamines), and impaired redox homeostasis. Early dynamic changes of the plasma metabolome are triggered by hemorrhage in rats. Future studies will determine whether metabolic subphenotypes observed in rats might be consistently observed in humans and pave the way for tailored resuscitative strategies. hemorrhagic shock; mass spectrometry; metabolomics; plasma; trauma DESPITE DECADES OF ADVANCES in prehospital care, trauma remains the leading cause of death for individuals under the age of 40 (36). As much as 40% of injury-related mortality is attributed to uncontrollable hemorrhage (36), which in both civilian and military settings is the leading preventable cause of death after injury (40). Conspicuous factors associated with early mortality in trauma patients include trauma-induced coagulopathy, hypothermia, and metabolic acidosis, a series of mechanisms referred to as the "bloody vicious cycle" and later renamed as the "lethal triad" (14). These concepts laid the foundation for "damage control surgery", an approach aimed at minimizing operating time as to control sources of significant bleeding and gastrointestinal contamination, while prioritizing early management of coagulopathy, hypothermia, and metabolic acidosis (46).Early descriptions of metabolic responses to trauma were documented by Cuthbertson, who characterized two distinct phases: the "ebb" and the "flow" (9). The former corresponds to an early hypometabolic state that may serve a protective role aimed at reducing posttraumatic energy depletion. The latter is accompanied by an increased metabolic rate (including increased energy expenditure and oxygen consumption) (14,18,24,29). Other overlapping stages have been described over the years, such as the "ischemia-reperfusion," "leukocytic," and ...

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Section: Discussionsupporting

confidence: 83%

Early hemorrhage triggers metabolic responses that build up during prolonged shock

D’Alessandro

Moore

et al. 2015

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Hypoperfusion, frequently resulting from a low cardiac output (compared with the required for that current physiological status) [42], causes cellular damage, activation of inflammatory response, and increases multiple organ dysfunction syndrome and death risks, if not corrected in a few hours [43][44][45][46][47][48].…”

Section: Recognizing a State Of Shockmentioning

confidence: 99%

Critical Care Issues in the Early Management of Severe Trauma

García

2006

Surgical Clinics of North America

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Violent trauma and road traffic injuries kill more than 2.5 million people in the world every year. It has been calculated by the World Health Organization that in 2002 there occurred 1.6 million violent deaths [1] and 1.2 million deaths from traffic injury [2], for a combined mortality of 48 deaths per 100,000 population per year.Most trauma deaths occur at the scene or in the first hour after trauma, with a proportion from 34% to 50% occurring in hospitals [3]. These deaths could be prevented by optimization of trauma care. Preventability of trauma deaths has been reported as high as 76% [4] and as low as 1% in mature trauma systems [5,6].Prehospitalization procedures, elapsed time to hospital arrival are, of course, vital to the whole trauma scenario, but errors made in the in-hospital phase of care are responsible for one third to two thirds of the reported by different authors [7,8]. Of these, intensive care unit (ICU) errors are among the most frequent and significant. Errors in the ICU management of trauma patients were studied by Duke and colleagues [9]. They reported 165 ICU trauma deaths. Two hundred fifty-eight errors occurred in 81 patients (52%), and 134 of them contributed to death in 52 patients (34%). ICU errors were classified as management errors (82%), diagnostic (9%), technique (5%), and system inadequacies (4%). Davis and colleagues [10] identified critical care errors in 30% of 125 trauma deaths with errors. These errors contributed to 48% of all preventable deaths.The most common critical care errors are related to airway and respiratory management, fluid resuscitation, neurotrauma diagnosis and support, and delayed diagnosis of critical lesions [9,10].It is imperative for the general surgeon who takes care of trauma patients to know how to deal with these critical aspects, to reduce preventable morbidity and mortality. In the next segment, the situations in which the participation of the surgeon is crucial, during the initial phases of reanimation and stabilization of the critically traumatized patient will be discussed. Airway and ventilation managementAirway and respiratory management errors are the most common of those identified by several authors [9][10][11] The cardinal manifestation is a sudden or a rapidly progressing desaturation, frequently accompanied by tachycardia and arrhytmias, and occasionally by agitation. Hypertension announces the cardiovascular collapse, and bradicardia appears immediately after the total collapse [12]. The symptoms should not be attributed to agitation when it is present, and other possible causes must be ruled out before. Diagnosing the complication involves a directed physical examination, the analysis of the airway pressures and ventilator volumes, chest radiographs, and sometimes the measurement of arterial blood gases (ABG), and the urinary bladder pressure ( Table 1).The emergency conditions in which the access to the airways must be gained, the displacement to diagnosis areas or operating room and the agitation, often present, make the critical...

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“…Initially, for old patients (cardiac index, 2.0 ± 0.2 L/min · m 2 ) and for young patients (cardiac index, 3.0 ± 0.2 L/min·m 2 ; 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 DO 2 IՆ600, and 11 (92%) survived 7 or more days and 5 (42%) 30 or more days.…”

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confidence: 99%