严重脑损伤后早期肠内营养支持的合理应用

目的：传统的鼻饲营养方法因脑损伤胃动力下降早期难以安全实施。本研究对４１例严重脑损伤病人实施改良后的早期鼻饲喂养计划,观察其应用的合理性和临床效果。方法：实验组采用了早期鼻饲要素膳,对照组按常规方法实施鼻饲营养支持;实验组开始时间为伤后４８ｈ,对照组为伤后６－８天。     

Influence of inhalation injury on energy expenditure in severely burned children

ObjectiveDetermine the effect of inhalation injury on burn-induced hypermetabolism in children.DesignProspective study comparing hypermetabolism (i.e., resting energy expenditure and oxygen consumption) in burned children with and without inhalation injury during acute hospitalization.SettingSingle pediatric burn center.PatientsEighty-six children (1–18 years) with ≥40% total body surface area burns were stratified to two groups: no inhalation injury and inhalation injury.InterventionsNone.Main measurements and resultsInhalation injury was diagnosed based on bronchoscopic evaluation. At admission, PaO₂:FiO₂ ratios (an index of respiratory distress) were significantly higher in patients with no inhalation injury than in patients with inhalation injury. No differences were detected in resting energy expenditure or percent of the predicted basal metabolic rate between groups. Additionally, oxygen consumption did not significantly differ between groups.ConclusionsInhalation injury does not augment the burn-induced hypermetabolic stress response in children, as reflected by resting energy expenditure and oxygen consumption.     

Nutritional state and energy balance in cirrhotic patients with or without hypermetabolism: Multicentre prospective study by the ‘Nutritional Problems in Gastroenterology’ Section of the Italian Society of Gastroenterology (SIGE)

BACKGROUND AND AIMS: A total of 334 stable, compensated cirrhotic patients admitted to 10 Italian Gastroenterology Units were included in a prospective study to evaluate nutritional state and energy balance in liver cirrhosis. MATERIALS AND METHODS: Nutritional state and calorie intake were examined in the total population, while adequacy of calorie intake versus measured total energy expenditure was evaluated in a comparable subpopulation and in 40 matched controls, by computing the energy balance. RESULTS: Our data demonstrated that: (i) malnutrition was present in 25% of the total patients and significantly correlated with the Child's group (A=16%; B=25%; C=44%); (ii) the type of malnutrition is influenced by mBEE: normometabolic patients exhibit a significant (p<0.005) reduction of mid-arm fat area while both hypermetabolic and hypometabolic patients show a significant (p<0.005) decline in kg of free fat mass; (iii) normometabolic and hypometabolic patients have a negative energy balance, due to a high level of physical activity (127+/-14 kJ) in the first group and a reduced energy intake/kg body weight (102+/-12 kJ) in the second; (iv) hypermetabolic patients have a positive energy balance due to decreased daily physical activity/kg body weight (108+/-28 kJ); (v) malnourished and normometabolic patients eat a significantly (p<0.05) reduced percentage of protein whereas malnourished and hypermetabolic patients eat a significantly increased percentage of fat (p<0.05). CONCLUSION: Although multivariate regression analysis confirms that the Child-Pugh's score is a better independent predictor of malnutrition, the measure of REE, TEE, calorie intake and energy balance need to be routinely performed in cirrhotic patients, in order to recognise hypermetabolic and hypometabolic patients (approximately 30%) in whom the nutritional and metabolic parameters are indispensable as a basis for designing and prescribing personalised nutritional strategies that can treat muscle malnutrition and thus improve the morbidity and mortality rates.     

Brown adipose tissue recruitment in a rodent model of severe burns

BackgroundSevere burns results in a prolonged hypermetabolic response. Brown adipose tissue (BAT), abundant in uncoupling protein 1 (UCP1), plays a key role in non-shivering thermogenesis. We set out to determine if BAT is recruited in response to severe burns.MethodsMale balb-c mice underwent scald burns on approximately 20–25% of their total body surface. BAT was harvested from the interscapular fat pad of sham and burned mice at 3 h, 24 h, 4 days, and 10 days after injury. High-resolution respirometry was used to determine mitochondrial respiratory function in BAT. BAT protein concentration, and mitochondrial enzyme activity were also determined.ResultsRespiration increased in BAT of burned mice, peaking at 24 h after injury (after injury, P < 0.001). While UCP1 independent respiration was not significantly altered by burn, UCP1 dependent respiration increased >2-fold at 24 h after injury when compared to the 3 h and sham group (P < 0.01). Normalized to citrate synthase activity, total uncoupled (P < 0.05) and UCP1 dependent (P < 0.01) respiration remained elevated at 24 h after injury.ConclusionsWe show a time-dependent recruitment of rodent BAT in response to severe burns. Given recent reports that humans, including patients with severe burns, have functional BAT, these data support a role for BAT in the hypermetabolic response to severe burns.     

Increased oxygen consumption after cardiac surgery is associated with the inflammatory response to endotoxemia

Objective The aim of this study was to determine whether the increase in post-operative oxygen consumption (VO₂) in cardiac surgery patients in related to endotoxemia and subsequent cytokine release and whether VO₂ can be used as a parameter of post-perfusion syndrome.Design Prospective study.Setting Operating room and intensive care unit of a university hospital.Patients Twenty-one consecutive male patients undergoing elective coronary artery bypass surgery without major organ dysfunction and not receiving corticosteroids.Measurements and results Plasma levels of endotoxin, tumor necrosis factor (TNF) and interleukin-6 (IL-6) were measured before, during and for 18 h after cardiac surgery. Oxygen consumption, haemodynamics, the use of IV fluids and dopamine, body temperature and the time of extubation were also measured. Measurements from patients with high VO₂ (median value of the entire group) were compared with measurements from patients with low VO₂ (2 had higher levels of circulating endotoxin (P=0.004), TNF (P=0.04) and IL-6 (P=0.009) received more IV fluids and dopamine while in the ICU, and were extubated later than patients with low VO₂. Several hours after VO₂ the patient's body temperature rose, Forward stepwise regression analysis showed that circulating endotoxin and TNF explained 50% of the variability of VO₂.Conclusions This study demonstrates that patients with high post operative oxygen comsumption after elective cardiac surgery have higher circulating levels of endotoxin, TNF and IL-6 and also have more symptoms of post-perfusion syndrome. Early detection of high VO₂ might be used as a clinical signal to improve circulation in order to meet the high oxygen demand of inflammation. In addition, continuous measurement of VO₂ provides us with a clinical parameter of inflammation in interventional studies aiming at a reduction of endotoxemia or circulating cytokines.Part of this study was supported financially by Jaussen Pharmaceutica B.V. (Tilburg, The Netherlands)     

肿瘤患者高代谢及其机制的研究进展

恶性肿瘤发生中重度营养不良的发生率非常高,中国肿瘤患者的中度和重度营养不良发生率为58%,营养不良明显 影响肿瘤患者的临床结局,近25%的肿瘤患者直接死于营养不良。许多营养不良的肿瘤患者常常表现高静息态能量消耗和高 分解代谢。引发这些变化的因素主要包括两个方面：①肿瘤负荷;②由肿瘤引起的相关因素,包括炎症、神经内分泌紊乱、放化 疗、肠道微生态紊乱以及食欲下降和摄入减少等。这些因素交杂在一起并通过尚未完全阐明的复杂机制而激活不同组织器官 系统的能量消耗增加、分解代谢增强和合成代谢降低等,从而引起肿瘤患者的营养不良,甚至恶液质。由于引起肿瘤患者营养 不良的因素和机制是复杂多样的,因此,肿瘤患者营养治疗也应该是针对性的综合治疗,即在营养不良综合评估和诊断基础上, 进行有效综合营养干预和阻断高代谢的药物干预等。本文就肿瘤患者高能耗代谢及其相关机制进行综述。     

The impact of catecholamines on skeletal muscle following massive burns: Friend or foe?

Profound skeletal muscle wasting in the setting of total body hypermetabolism is a defining characteristic of massive burns, compromising the patient’s recovery and necessitating a protracted period of rehabilitation. In recent years, the prolonged use of the non-selective beta-blocker, propranolol, has gained prominence as an effective tool to assist with suppressing epinephrine-dependent burn-induced hypermetabolism and by extension, blunting muscle catabolism. However, synthetic β-adrenergic agonists, such as clenbuterol, are widely associated with the promotion of muscle growth in both animals and humans. Moreover, experimental adrenodemedullation is known to result in muscle catabolism. Therefore, the blunting of muscle β-adrenergic signaling via the use of propranolol would be expected to negatively impair muscle protein homeostasis. This review explores these paradoxical observations and identifies the manner by which propranolol is thought to exert its anti-catabolic effects in burn patients. Moreover, we identify potential avenues by which the use of beta-blocker therapy in the treatment of massive burns could potentially be further refined to promote the recovery of muscle mass in these critically ill patients while continuing to ameliorate total body hypermetabolism.     

Dynamic changes in local cerebral glucose utilization following cerebral concussion in rats: evidence of a hyper- and subsequent hypometabolic state

Following cerebral concussion, in which there is no evidence of direct morphological damage, cells are exposed to an increase in extracellular potassium as well as an accumulation of calcium. This concussion-induced ionic flux most likely alters the cellular energy demands thereby modifying metabolic processes. To investigate the metabolic changes after cerebral concussion, local cerebral metabolic rates for glucose (lCMRglc) utilizing [¹⁴C]2-deoxy-d-glucose were studied in rats(n=98; 250–300g) immediately, 30 min, 6 h, 1, 2, 3, 5 and 10 days following a unilateral fronttoparietal fluid percussion (F-P) injury (3.7–4.3 atm). Compared to sham controls, animals exhibited bilateral hypermetabolism immediately following brain injury. However, this effect was more pronounced in structures ipsilateral to the site of F-P and was especially marked for the cerebral cortex (46.6–30.1% higher than control) and hippocampus (90.1–84.4% higher than control). By 30 min post-trauma many ipsilateral regions still showed evidence of hypermetabolism, although their lCMRglc had subsided. Beginning as early as 6 h following injury many regions within the ipsilateral cortex and hippocampus went into a state of metabolic depression (16.4–33.7% of control) which lasted for as long as 5 days. These results indicate that, although not mechanically damaged from the insult, cells exposed to concussive injury dramatically alter their metabolic functioning. This period of post-concussive metabolic dysfunction may delineate a period of time, following injury, during which cells are functionally compromised.