Neuromuscular sequelae of critical illness

PURPOSE OF REVIEW: To investigate the impact of critical illness polyneuropathy and critical illness myopathy on short-term and long-term patient outcome. RECENT FINDINGS: In the acute-care setting, critical illness polyneuropathy and critical illness myopathy are important causes of acute paralysis in critically ill comatose patients, and may cause inappropriately pessimistic prognoses. Duration of weaning from artificial ventilation is 2 to 7 times greater in patients with critical illness polyneuropathy than in patients without critical illness polyneuropathy. After intensive care unit and hospital discharge, many patients diagnosed with critical illness polyneuropathy or critical illness myopathy are reported to complain of profound muscle weakness. Chronic disability was a common finding among them. Complete functional recovery with patients regaining the ability to breathe spontaneously and to walk independently was reported in 180 of 263 patients (68.4%); severe disability with tetraparesis, tetraplegia, or paraplegia was reported in 74 patients (28.1%). Persisting milder disabilities were common even in patients with complete functional recovery, and included reduced or absent deep tendon reflexes, stocking and glove sensory loss, muscle atrophy, painful hyperesthesia, and foot drop. An association of critical illness polyneuropathy and critical illness myopathy with increased intensive care unit and hospital mortality has been demonstrated only in selected intensive care unit populations; data are insufficient to demonstrate any association with long-term mortality. SUMMARY: Intensive care unit-acquired critical illness polyneuropathy and critical illness myopathy influence the evaluation of acutely ill comatose patients and may instigate unreasonably pessimistic prognosis. Critical illness polyneuropathy and critical illness myopathy are an important cause of difficult weaning of patients from the ventilator and of persisting muscle weakness and disability after intensive care unit discharge.     

Polyneuropathy in intensive care patients

Critical illness polyneuropathy is an acquired critical illness syndrome of neuromuscular problems as polyneuropathy and/or myopathy that is caused by long-term immobilization, clinically manifested by general muscle weakness and a main reason for difficulty weaning from the ventilator. The review gives an update on the history, epidemiology, etiology, pathogenesis, clinical picture, diagnosis, differential diagnosis, course, outcome, prevention, and treatment of critical illness care polyneuropathy.     

Critical illness polyneuromyopathy: the electrophysiological components of a complex entity

Objective To evaluate the spectrum and time profile of electrophysiological parameters in the detection of neuromuscular involvement in critically ill patients and establish their correlation with biopsy findings.Design Prospective clinical and neurophysiological study.Setting One general and one neurological intensive care unit in a university hospital.Patients Forty-six critically ill patients with failure of at least two organ systems were enrolled and completed the 1-month follow up.Interventions Detailed clinical and electrophysiological evaluation including direct muscle stimulation was performed in all cases on entry and at the end of the follow-up. Muscle biopsy was performed in 11, and sural nerve biopsy in 5, cases.Measurements and results Electrophysiological signs of new or progressing neuromuscular involvement at the end of the first month were detected in 26 patients (56%) and could be classified into three groups: "pure motor syndrome" (12 cases), combined motor syndrome and sensory polyneuropathy (13 cases) and isolated sensory polyneuropathy (1 case). Direct muscle stimulation showed decreased muscle membrane excitability in 11 of these abnormal cases. Muscle biopsy disclosed various myopathic abnormalities in all 11 cases examined with motor syndrome, in 7 of them in association with denervation/re-innervation changes.Conclusions Electrophysiological and histological examinations showed significant overlapping of several pathogenic components of neuromuscular involvement in critically ill patients, namely decreased muscle excitability, myopathy, axonal motor neuropathy and sensory neuropathy. The characterisation of the electrophysiological components of a complex polyneuromyopathy is preferred to the strict categorisation of abnormalities into critical illness myopathy and polyneuropathy.The study was supported by the Internal Grant Agency of the Ministry of Health of The Czech Republic-Grant No NF/5980-3An editorial regarding this article can be found in the same issue ()     

Clinical approach to the weak patient in the intensive care unit

Motor weakness in a patient in the intensive care unit (ICU) may be related to (1) pre-existing neuromuscular disorder that leads to ICU admission, (2) new-onset or previously undiagnosed neurological disorder, or (3) complications of non-neuromuscular critical illness. Neuromuscular syndromes related to ICU treatment consist of critical illness polyneuropathy, critical illness myopathy, and prolonged neuromuscular blockade, and are now recognized as a frequent cause of newly acquired weakness in ICU patients. Clinical features include quadriparesis, muscle wasting, and difficulty weaning from the ventilator. Evaluation of these patients is based on knowledge of clinical setting and predisposing factors, focused neurological examination, detailed electrophysiological investigation, serum creatine kinase level, other laboratory studies as needed, and histological examination of muscle biopsy. If a central nervous system (brain or spinal cord) lesion is suspected, neuroimaging studies are required. In addition to conventional nerve conduction and needle electromyography, phrenic nerve conduction, diaphragm electromyography, blink reflex, and (recently) the technique of direct muscle stimulation have been employed. Critical illness polyneuropathy is an axonal motor and sensory neuropathy that often follows sepsis and multiorgan failure. Risk factors for critical illness myopathy are corticosteroids and neuromuscular blocking drugs, acute respiratory illness, and organ transplant. Three subtypes (acute necrotizing myopathy, thick myosin filament loss myopathy, and type II fiber atrophy) are recognized. Major differential diagnoses of critical illness related paralysis are incidental Guillain-Barré syndrome and unmasked myasthenia gravis. Rarely, atypical presentation of amyotrophic lateral sclerosis, polymyositis or other myopathies, and precipitation of porphyria or rhabdomyolysis due to drugs used in the ICU have been described. Recently a poliomyelitis-like flaccid paralysis due to West Nile virus infection was reported. A subgroup of patients with myasthenia gravis with muscle-specific tyrosine kinase antibody is noted to present as respiratory crisis. Muscle biopsy in ICU paralysis syndromes may be helpful in arriving at a specific diagnosis or to classify the type of critical illness myopathy. Nerve biopsy is only rarely indicated.     

Critical illness myopathy and neuropathy

PURPOSE OF REVIEW: To present the major pathophysiological and diagnostic features of critical illness myopathy (CIM) and polyneuropathy (CIP), and to discuss problems concerning the risk factors for CIM and CIP. RECENT FINDINGS: The pathophysiology of critical illness myopathy and critical illness polyneuropathy is complex, involving metabolic, inflammatory, and bioenergetic alterations. This review cites new evidence supporting several pathogenetic mechanisms. These include microvascular changes in peripheral nerves (with increased endothelial expression of E-selectin), the possible role for an altered lipid serum profile in promoting organ dysfunction (including nerve dysfunction), the damage or inhibition of complex I of the respiratory chain as a cause of muscle ATP depletion and bioenergetic failure, and the activation of specific intracellular proteolytic systems causing myofilament loss and apoptosis in CIM. The diagnostic role of direct muscle stimulation and the rapid quantification of myosin/actin ratio based on electrophoresis are also presented. SUMMARY: Basic and clinical research is unraveling the pathophysiological mechanisms of critical illness myopathy and polyneuropathy, and methods for rapid diagnosis are actively investigated. Future studies should better define the population at risk of developing CIM and CIP. In fact, although sepsis, multi-organ failure and steroids are often cited as risk factors, uncertainty remains due to the poor methodological quality of studies, or because of inferences that are exclusively based on animal studies. New simplified diagnostic techniques and machines for electrophysiological investigations of peripheral nerves and muscles in the intensive-care unit (ICU) patient would also be welcome.     

Neuromuscular complications of sepsis

Sepsis and multiple organ failure are major problems in medical and surgical intensive care units. Critical illness polyneuropathy occurs in 70% of these patients. Difficulty in weaning from the ventilator is an early sign. Electrophysiological studies are necessary to establish the diagnosis; these studies show an axonal degeneration of peripheral nerve fibres. Recovery occurs in weeks or months, depending upon severity. Muscle biopsy reveals denervation atrophy. Sepsis itself does not induce a neuromuscular transmission defect, but neuromuscular blocking agents may increase the severity of critical illness polyneuropathy. If steroids are used in addition to neuromuscular blocking agents, a severe myopathy may result. Other effects on muscle are cachectic myopathy and panfascicular muscle fibre necrosis. A variety of combinations of these conditions may affect the same patient. Only well-designed prospective studies will determine the true effect of these medications on the neuromuscular system in septic patients.     

Neuromuscular complications of sepsis

Sepsis and multiple organ failure are major problems in medical and surgical intensive care units. Critical illness polyneuropathy occurs in 70% of these patients. Difficulty in weaning from the ventilator is an early sign. Electrophysiological studies are necessary to establish the diagnosis; these studies show an axonal degeneration of peripheral nerve fibres. Recovery occurs in weeks or months, depending upon severity. Muscle biopsy reveals denervation atrophy. Sepsis itself does not induce a neuromuscular transmission defect, but neuromuscular blocking agents may increase the severity of critical illness polyneuropathy. If steroids are used in addition to neuromuscular blocking agents, a severe myopathy may result. Other effects on muscle are cachectic myopathy and panfascicular muscle fibre necrosis. A variety of combinations of these conditions may affect the same patient. Only well-designed prospective studies will determine the true effect of these medications on the neuromuscular system in septic patients.     

Effect of critical illness polyneuropathy on the withdrawal from mechanical ventilation and the length of stay in septic patients

OBJECTIVES: No previous study has demonstrated whether critical illness polyneuropathy itself lengthens mechanical ventilation or whether this prolonged duration of ventilatory support is explained by concomitant risk factors for weaning failure. Our objectives were to evaluate the impact of critical illness polyneuropathy on the length of mechanical ventilation after controlling for coexisting risk factors for weaning failure and to assess the impact of critical illness polyneuropathy on the length of the stay in a cohort of septic patients. DESIGN: Prospective cohort study. SETTING: Intensive care unit of a tertiary hospital. PATIENTS: All patients with severe sepsis or septic shock who required mechanical ventilation for > or =7 days who were considered ready to discontinue mechanical ventilation. INTERVENTIONS: Patients underwent a neurophysiologic evaluation at onset of weaning from mechanical ventilation. MEASUREMENTS AND MAIN RESULTS: Sixty-four critically ill septic patients were enrolled, and 34 developed critical illness polyneuropathy (53.1%; 95% confidence interval, 40.2-65.7%). Length of mechanical ventilation was significantly higher in patients who had developed critical illness polyneuropathy (median 34 days vs. 14 days, p < .001). The duration of the weaning period was also significantly greater in patients with critical illness polyneuropathy (median 15 days vs. 2 days, p < .001) even though factors suspected to influence the weaning process did not differ between these two groups. Multiple logistic regression analysis indicated that critical illness polyneuropathy was the only risk factor independently associated with weaning failure (odds ratio, 15.4; 95% confidence interval, 4.55, 52.3; p < .001). Lengths of intensive care unit and hospital stays were significantly higher in patients with critical illness polyneuropathy. CONCLUSIONS: In critically ill septic patients, critical illness polyneuropathy significantly increases the duration of mechanical ventilation and prolongs the lengths of intensive care unit and hospital stays.     

A stronger approach to weakness in the intensive care unit

ICU-acquired limb and respiratory muscle weakness is a common, serious ICU syndrome, increasing in frequency with prolonged ICU stay and sepsis. A systematic approach facilitates precise localization of the problem within central or peripheral nervous system. Most cases relate to critical illness polyneuropathy or myopathy or a combination of both (critical illness neuromyopathy). Within the latter entity, the relative contribution of neuropathy versus myopathy varies considerably among affected patients. Muscle enzyme testing, electromyography-nerve conduction and muscle biopsy are valuable investigative tests. Nerve biopsy is less commonly needed, but is useful when vascultis is suspected.     

Clinical review: Critical illness polyneuropathy and myopathy

Critical illness polyneuropathy (CIP) and myopathy (CIM) are major complications of severe critical illness and its management. CIP/CIM prolongs weaning from mechanical ventilation and physical rehabilitation since both limb and respiratory muscles can be affected. Among many risk factors implicated, sepsis, systemic inflammatory response syndrome, and multiple organ failure appear to play a crucial role in CIP/CIM. This review focuses on epidemiology, diagnostic challenges, the current understanding of pathophysiology, risk factors, important clinical consequences, and potential interventions to reduce the incidence of CIP/CIM. CIP/CIM is associated with increased hospital and intensive care unit (ICU) stays and increased mortality rates. Recently, it was shown in a single centre that intensive insulin therapy significantly reduced the electrophysiological incidence of CIP/CIM and the need for prolonged mechanical ventilation in patients in a medical or surgical ICU for at least 1 week. The electrophysiological diagnosis was limited by the fact that muscle membrane inexcitability was not detected. These results have yet to be confirmed in a larger patient population. One of the main risks of this therapy is hypoglycemia. Also, conflicting evidence concerning the neuromuscular effects of corticosteroids exists. A systematic review of the available literature on the optimal approach for preventing CIP/CIM seems warranted.     

Understanding, recognizing, and managing chronic critical illness syndrome

Purpose: No evidence-based guidelines exist for the care of patients with chronic critical illness syndrome (CCIS), a growing population of patients being cared for by nurse practitioners (NPs). The purpose of this article is to provide NPs with a beginning physiological framework, allostasis, to guide their understanding and management of patients with CCIS.
Data sources: Scientific publications, related clinical guidelines.
Conclusions: Patients with CCIS are a distinct group of critically ill patients whose care needs are different from those of patients who are acutely critically ill. These patients demonstrate widespread tissue and organ damage. The widespread tissue and organ damage results in a syndrome of interrelated elements, which include neuroendocrine problems, severe malnutrition, wounds, infections, bone loss, polyneuropathy and myopathy, delirium and depression, and suffering.
Implications for practice: In caring for patients with CCIS, NPs need to focus on treating the elements of the syndrome as a cohort of interrelated elements and on re-establishing normalcy for the patient.     

Rehabilitation after critical illness: could a ward‐based generic rehabilitation assistant promote recovery?

Aim: The aim of this paper is to explore issues surrounding the implementation of a generic rehabilitation assistant (GRA) to provide ward‐based rehabilitation after critical illness. Background: Following critical illness a range of both physical and psychological problems can occur that include muscle wasting and weakness, fatigue, reduced appetite, post‐traumatic stress, anxiety and depression. Limited research exists evaluating the provision of rehabilitation to this patient group. This paper explores one possible service delivery model providing ward‐based rehabilitation after critical illness. The model explored is a GRA working in conjunction with ward‐based staff. Results: We describe how a GRA worked effectively with ward‐based teams to provide additional rehabilitation in the period after discharge from intensive care. Benefits included greater continuity of care that was flexible to the individual needs of patients. Some aspects of the role were challenging for the GRA and highlighted the need for good communication skills. A need for comprehensive training of the GRA was demonstrated. Conclusions: Our experience demonstrates that it is feasible to deliver ward‐based rehabilitation after critical illness using the GRA service delivery model. Relevance to clinical practice: This model of service delivery offers the potential to improve outcomes for patients after a critical illness. Further research evaluating this model of care is required before implementation into clinical practice.     

新生儿危重病与胃肠功能障碍关系的探讨

目的探讨新生儿危重病与胃肠功能障碍的关系。方法评估 73例危重新生儿危重程度、多器官功能衰竭与胃肠功能障碍的关系。结果 73例危重新生儿中单项危重病 12例 ,多项危重病 6 1例 (其中危重 33例、极危重 2 8例 ) ;6 1例中 12例为单器官功能衰竭 ,余 4 9例为伴多器官功能衰竭。胃肠功能障碍发生率在危重病组与极危重病组分别为39.4 % (13/ 33)、71.4 % (2 0 / 2 8) ,两组比较具有显著性差异 (P <0 .0 5 )。单项危重病组与伴多器官功能衰竭组胃肠功能障碍发生率分别为 16 .7% (2 / 12 )、5 9.2 % (2 9/ 4 9) ,两组比较有非常显著性差异 (P <0 .0 1)。胃肠功能障碍的危重新生儿平均伴有器官衰竭的数目为 1.83个。结论新生儿病情越重 ,受损器官越多 ,胃肠功能障碍发生率越高 ,因此 ,要高度警惕 ,早期发现 ,早期治疗。     

Neuromuscular disorders associated with failure to wean from the ventilator

Objective To determine, by retrospective chart analysis, the frequency, type and significance of neuromuscular disorders in patients whose clinical features suggested a neuromuscular cause of failure to wean.Background Failure to wean is a common and difficult problem in critical care units. While a neuromuscular cause may be suspected in some patients, the frequency and type has not been determined utilizing comprehensive electrophysiological studies of limbs and the respiratory system. Such knowledge may aid in patient management and prognosis.Methods The clinical setting was a critical care/trauma centre that admits 1500 patients per year, approximately 500 being on ventilators for longer than five days. We analyzed the hospital charts of 40 patients admitted to the unit during three years, whose respiratory assessment suggested a neuromuscular cause for failure to wean from the ventilator. To investigate this possibility, we performed electrophysiological studies of the limbs and also of the respiratory system by phrenic nerve conduction and needle electromyography of the chest wall and diaphragm. The results were compared to 25 healthy controls.Results 38 of 40 patients (95%) had a neuromuscular disorder: 25 — critical illness polyneuropathy, 2 — Guillain-Barré syndrome, 4 — diabetic and critical illness polyneuropathy, 2 — uremic and critical illness polyneuropathy, 10 — an abnormality of central drive, 5 — unilateral phrenic nerve palsy, 3 — a neuromuscular transmission defect, and 5 — a primary myopathy. Fifteen (38%) had a combination of disorders. Patients with more severe polyneuropathy took longer to wean, a mean of 136 versus 52 days (p=0.007).The severity of the polyneuropathy had no effect on mortality.Conclusions Electrophysiological studies of limbs and the respiratory system are together valuable in confirming the presence, and identifying the specific type of neuromuscular cause for difficulty in weaning from the ventilator. This information is important in patient management and prognosis.     

Critical illness polyneuropathy in multiple organ dysfunction syndrome and weaning from the ventilator

Background Acute axonal polyneuropathy has been found in patients with multiple organ dysfunction syndrome. This critical illness polyneuropathy (CIP) has been associated with difficult weaning from the ventilator in retrospective studies.Objective To test the hypothesis that CIP is related to the degree and number of organ dysfunctions, and to weaning problems.Design Prospective study of 18 months.Setting A multidisciplinary intensive care unit in a general hospital.Subjects Thirty-eight patients under 75 years of age who had been mechanically ventialted for more than 7 days, without previous signs of or risk factors for polyneuropathy.Measures Organ dysfunctions were quantified using a dynamic scoring system (0–12 points). Electromyography studies were performed during mechanical ventilation to identify patients with and without CIP.Results CIP was present in 18 out of 38 patients and associated with an increased organ dysfunction score (5.3±1.8 vs. 3.6±1.5;p=0.003) and number of organs involved [median (range): 4 (3–5) vs. 2 (1–4);p=0.009], in particular cardiovascular (p=0.003), renal (p=0.04), and hematopoietic failure (p=0.04). Patients with polyneuropathy were ventilated longer, but this was not clearly due to more difficult weaning [median: 16.5 (1–48) vs. 9.5 (1–38) days;p=0.26]. Polyneuropathy was present in 2 of 4 patients with normal weaning.Conclusions Axonal polyneuropathy is related to the severity of multiple-organ-dysfunction syndrome. Its presence does not necessarily implicate difficult weaning from artificial ventilation.Deceased     

胃肠功能状况与儿科危重症预后的相关性分析

[目的]研究胃肠功能状态对儿科危重病人预后的影响,为临床早期治疗提供依据.[方法]将本院ICU 2008~2009年收住院患者的临床资料进行回顾性研究,对出现胃肠功能障碍的及未出现胃肠功能障碍的危重症患者情况进行比较.同时对危重症中胃肠功能障碍的出现时间对预后的影响进行相关性分析.[结果]出现胃肠功能障碍患儿的休克及多脏器功能障碍综合征（MODS）发生率和病死率明显升高,与非胃肠功能障碍组比较差异有显著性（P〈0.05）.胃肠功能障碍出现的越早,患者发生休克,MODS的几率越大,同时亦可引起病死率增高.[结论]胃肠功能障碍出现越早,患者预后越差;同时胃肠功能状况对危重症预后的影响具有统计学意义.     

神经危重症患者床旁肌电图检查的应用价值

目的探讨神经危重症患者床旁肌电图检查对患者诊断及预后判断的意义。 方法对2016年11月至2017年4月在南方医科大学南方医院神经危重症病房（NCU）住院、且住NCU时间超过3 d的58例神经危重症患者进行床旁肌电图检查。检查项目包括运动神经传导、感觉神经传导、直接肌肉刺激。对超过两个肢体共计3条及以上运动和/或感觉神经传导出现异常定义为多发神经传导异常,并进行分组后病因分析、临床特点和电生理特点的比较。 结果48.3%（28/58）患者呈多发神经传导异常,为多发神经传导异常组,其余30例患者为对照组。与对照组比较,多发神经传导异常组的急性病生理学和长期健康评价（APACHE）Ⅱ评分[（12 ± 5）分vs.（16 ± 6）分]、在院最高脓毒症相关器官衰竭评分（SOFA）分值[4（3,6）分vs. 7（4,11）分]、脓毒症[11/30 vs. 21/28]及多器官功能障碍综合征（MODS）发生率[2/30 vs. 10/28]均更高,预后情况中机械通气时间[0（0,4）d vs. 6（0,16）d]、ICU住院时间[8（5,13）d vs. 14（7,20）d]均更长,出院后30 d [4（3,4）分vs. 5（5,6）分]及90 d [3.0（2.0,4.0）分vs. 6.0（4.2,6.0）分]的改良Rankin评分（mRS）分值、30 d（2/30 vs. 12/28）及90 d（4/30 vs. 15/28）病死情况均更高（P均< 0.05）。多因素Logistic回归分析发现,多发神经传导异常是出院后30 d及90 d病死情况的独立危险因素（P均< 0.05）。多发神经传导异常患者电生理特点显示与其他病因组（14例）比较,危重病性神经肌病（CIPNM）组（14例）运动神经传导未引出复合肌肉动作电位（CMAP）波形的比例更高（6/90 vs. 15/87）,而感觉神经传导异常占比均更低（58/83 vs. 28/81、29/37 vs. 14/37、29/44 vs. 14/44;P均< 0.05）。 结论神经危重症患者常存在周围神经肌肉病变,且病因复杂多样,床旁肌电图检查对神经危重症患者的病因鉴别具有重要意义,且对神经危重症患者预后判断具有重要价值。     

Cardiac biomarkers in the critically ill

Cardiac biomarkers have well-established roles in acute coronary syndrome and congestive heart failure. In many instances, the detection of cardiac biomarkers may aid in the diagnosis and risk assessment of critically ill patients. Despite increasing interest in the use of cardiac biomarkers in noncardiac critical illness, no clear consensus exists on how and in which settings markers should be measured. This article briefly describes what constitutes an ideal biomarker and focuses on those that have been most well studied in critical illness, specifically troponin, the natriuretic peptides, and heart-type fatty acid-binding protein.     

Critical illness polyneuropathy: clinical aspects and long-term outcome]

Patients treated in intensive care units may develop a primary axonal form of polyneuropathy complicating sepsis and multiple organ failure more frequently than previously assumed. This critical illness polyneuropathy causes difficulty in weaning patients from the ventilator and delays further recovery and mobilisation. Over a period of two years we have treated five patients with flaccid tetra- or paraparesis. Recovery of motor function was largely satisfactory, but a long rehabilitation process was necessary. If attention were paid to detecting this disease in the early stages of intensive care neurorehabilitation might be facilitated. Hence, electrophysiological tests should be performed as soon as possible. The clinical outcome was markedly influenced by long-lasting neuropsychological disturbances in three of the five patients as well as by other complications such as joint contractures.     

血必净注射液对凝血功能障碍危重病患者的临床价值研究

目的 探讨血必净注射液在有凝血功能障碍危重病患者中的临床应用价值.方法 将67例入住ICU有凝血功能障碍的危重病患者随机分为治疗组34例,对照组33例.两组患者均给予常规综合治疗,治疗组同时给予血必净注射液治疗7 d.治疗前后分别取静脉血,检测凝血功能相关指标[凝血酶原时间(PT)、凝血酶时间(TT)、活化部分凝血活酶时间(APTT)、纤维蛋白原(FIB)和血小板计数(PLT)]及血浆降钙素原(PCT)、白细胞介素-6(IL-6)、C-反应蛋白(CRP)浓度.结果 治疗组治疗前后PLT、PT、APTT、TT、FIB及CRP、IL-6、PCT、急性生理及慢性健康状况评分Ⅱ(APACHEⅡ)比较差异均有统计学意义(P<0.05);治疗后两组PLT、PT、FIB及IL-6、PCT、APACHEⅡ评分比较差异均有统计学意义(P<0.05).结论 血必净注射液可以明显改善危重病患者的凝血功能障碍,减少炎症因子的生成,具有很高的临床应用价值.