Subarachnoid hemorrhage misdiagnosed as acute coronary syndrome leading to catastrophic neurologic injury: A case report

BACKGROUND Elevated levels of cardiac troponin and abnormal electrocardiogram changes are the primary basis for clinical diagnosis of acute coronary syndrome(ACS).Troponin levels in ACS patients can often be more than 50 times the upper reference limit.Some patients with subarachnoid hemorrhage(SAH)also show electrocardiogram abnormalities,myocardial damage,and elevated cardiac biomarkers.Unlike ACS patients,patients with SAH only have a slight increase in troponin,and the use of anticoagulants or antiplatelet drugs is prohibited.Because of the opposite treatment modalities,it is essential for clinicians to distinguish between SAH and ACS.CASE SUMMARY A 56-year-old female patient was admitted to the emergency department at night with a sudden onset of severe back pain.The final diagnosis was intraspinal hematoma in the thoracic spine.We performed an emergency thoracic spinal canal hematoma evacuation procedure with the assistance of a microscope.Intraoperatively,diffuse hematoma formation was found in the T7-T10 spinal canal,and no obvious spinal vascular malformation changes were observed.Postoperative head and spinal magnetic resonance imaging(MRI)showed a small amount of SAH in the skull,no obvious abnormalities in the cervical and thoracic spinal canals,and no abnormal signals in the lumbar spinal canal.Thoracoab-dominal aorta computed tomography angiography showed no vascular malfor-mation.Postoperative motor system examination showed Medical Research Council Scale grade 1/5 strength in both lower extremities,and the patient experienced decreased sensation below the T12 rib margin and reported a Visual Analog Scale score of 3.CONCLUSION Extremely elevated troponin levels(more than 50 times the normal range)are not unique to coronary artery disease.SAH can also result in extremely high troponin levels,and antiplatelet drugs are contraindicated in such cases.Emergency MRI can help in the early differential diagnosis,as a misdiagnosis of ACS can lead to catastrophic neurological damage in patients with spontaneous spinal SAH.

Mechanisms and Research Progress of Traditional Chinese Medicine Regulating NF-κB in the Treatment of Acute Lung Injury/Acute Respiratory Distress Syndrome

Acute lung injury(ALI)has multiple causes and can easily progress to acute respiratory distress syndrome(ARDS)if not properly treated.Nuclear factorκB(NF-κB)is a key pathway in the treatment of ALI/ARDS.By exploring the relevance of NF-κB and the pathogenesis of this disease,it was found that this disease was mainly associated with inflammation,dysfunction of the endothelial barrier,oxidative stress,impaired clearance of alveolar fluid,and coagulation disorders.Traditional Chinese medicine(TCM)has the characteristics of multitargeting,multipathway effects,and high safety,which can directly or indirectly affect the treatment of ALI/ARDS.This article summarizes the mechanism and treatment strategies of TCM in recent years through intervention in the NF-κB-related signaling pathways for treating ALI/ARDS.It provides an overview from the perspectives of Chinese herbal monomers,TCM couplet medicines,TCM injections,Chinese herbal compounds,and Chinese herbal preparations,offering insights into the prevention and treatment of ALI/ARDS with TCM.

Mirizzi syndrome:Problems and strategies

Mirizzi syndrome is a serious complication of gallstone disease.It is caused by the impacted stones in the gallbladder neck or cystic duct.One of the features of Mirizzi syndrome is severe inflammation or dense fibrosis at the Calot’s triangle.In our clinical practice,bile duct,branches of right hepatic artery and right portal vein clinging to gallbladder infundibulum are often observed due to gallbladder infundibulum adhered to right hepatic hilum.The intraoperative damage of branches of right hepatic artery occurs more easily than that of bile duct,all of which are hidden pitfalls for surgeons.Magnetic resonance cholangiopancreatography(MRCP)and endoscopic retrograde cholangiopancreatography(ERCP)are the preferable tools for the diagnosis of Mirizzi syndrome.Anterograde cholecystectomy in Mirizzi syndrome is easy to damage branches of right hepatic artery and bile duct due to gallbladder infundibulum adhered to right hepatic hilum.Subtotal cholecystectomy is an easy,safe and definitive approach to Mirizzi syndrome.When combined with the application of ERCP,a laparoscopic management of Mirizzi syndrome by well-trained surgeons is feasible and safe.The objective of this review was to highlight its existing problems:(1)low preoperative diagnostic rate,(2)easy to damage bile duct and branches of right hepatic artery,and(3)high concomitant gallbladder carcinoma.Meanwhile,the review aimed to discuss the possible therapeutic strategies:(1)to enhance its preoperative recognition by imaging findings,and(2)to avoid potential pitfalls during surgery.

Prognostic Factors in Cardiorenal Syndrome Type 1: Retrospective Observational and Analytical Study

Introduction: Type 1 cardiorenal syndrome (CRS 1) is characterized by acute impairment of cardiac function leading to acute renal dysfunction. CRS1 is present in 25% of patients admitted for heart failure. The objective of our study is to analyze the epidemiological, clinical, therapeutic profile and the risk and prognostic factors of these patients. Materials and Methods: We identified 120 patients with cardiorenal syndrome (CRS) over a one-year period to determine the prevalence and risk factors for developing CRS 1. We analyzed the clinical, biological, and evolutionary profiles of patients with CRS 1 and determined the risk factors for the occurrence of acute kidney injury (AKI) as well as the mortality factors in these patients. Résultats: The average age of our patients with CRS1 is 58 ± 9 years, with a sex ratio of 1.4. The average eGFR of our patients is 35 ± 6.5 ml/min/1.73m2. Diabetes was found in 17% of our patients and hypertension in 14%. The etiology of cardiac impairment is predominantly acute coronary syndrome (ACS), followed by rhythm disorders. Renally, all our patients have acute kidney injury (AKI), with 86% having functional acute renal failure and 14% having acute tubular necrosis. Therapeutically, 50% of our patients are on diuretics, 42% receive beta-blocker treatment, and RAAS blockers are used in 29% of cases. Renal replacement therapy (RRT) sessions were required in 13.8% of cases. In univariate analysis, male gender, tachyarrhythmia, and hypertension are associated with the early onset of acute kidney injury (AKI). The use of diuretics, anemia, and low left ventricular ejection fraction (LVEF) are linked to a higher risk of developing CRS 1 (p = 0.021, p = 0.037, p = 0.010 respectively). In multivariate analysis, advanced age is significantly associated with increased mortality risk in CRS 1 patients (p = 0.030), while beta-blocker use is considered a protective factor (p = 0.014). Conclusion: Our study identifies several key factors associated with outcomes in type 1 CRS. Male gender, tachyarrhythmia, and hypertension are linked to early-onset AKI. The use of diuretics and the presence of anemia increase the risk of developing CRS1. Advanced age is significantly associated with higher mortality rates. Conversely, the use of beta-blockers appears to be protective in this patient population. .

Outpatient insulin use in type 2 diabetes mellitus and acute respiratory distress syndrome outcomes:A retrospective cohort study

BACKGROUND The impact of type 2 diabetes mellitus(T2DM)on acute respiratory distress syndrome(ARDS)is debatable.T2DM was suspected to reduce the risk and complications of ARDS.However,during coronavirus disease 2019(COVID-19),T2DM predisposed patients to ARDS,especially those who were on insulin at home.AIMTo evaluate the impact of outpatient insulin use in T2DM patients on non-COVID-19 ARDS outcomes.METHODS We conducted a retrospective cohort analysis using the Nationwide Inpatient Sample database.Adult patients diagnosed with ARDS were stratified into insulin-dependent diabetes mellitus(DM)(IDDM)and non-insulindependent DM(NIDDM)groups.After applying exclusion criteria and matching over 20 variables,we compared cohorts for mortality,duration of mechanical ventilation,incidence of acute kidney injury(AKI),length of stay(LOS),hospitalization costs,and other clinical outcomes.RESULTS Following 1:1 propensity score matching,the analysis included 274 patients in each group.Notably,no statistically significant differences emerged between the IDDM and NIDDM groups in terms of mortality rates(32.8%vs 31.0%,P=0.520),median hospital LOS(10 d,P=0.537),requirement for mechanical ventilation,incidence rates of sepsis,pneumonia or AKI,median total hospitalization costs,or patient disposition upon discharge.CONCLUSION Compared to alternative anti-diabetic medications,outpatient insulin treatment does not appear to exert an independent influence on in-hospital morbidity or mortality in diabetic patients with non-COVID-19 ARDS.

Spectrum of delayed post-hypoxic leukoencephalopathy syndrome:A systematic review

BACKGROUND Delayed post hypoxic leukoencephalopathy syndrome(DPHLS),also known as Grinker’s myelinopathy,is a rare but significant neurological condition that manifests days to weeks after a hypoxic event.Characterized by delayed onset of neurological and cognitive deficits,DPHLS presents substantial diagnostic and therapeutic challenges.AIM To consolidate current knowledge on pathophysiology,clinical features,diagnostic approaches,and management strategies for DPHLS,providing a comprehensive overview and highlighting gaps for future research.METHODS Following the Preferred Reporting Items for Systematic Reviews and Meta-Analyzes guidelines,we systematically searched PubMed,ScienceDirect and Hinari databases using terms related to delayed post-hypoxic leukoencephalopathy.Inclusion criteria were original research articles,case reports,and case series involving human subjects with detailed clinical,neuroimaging,or pathological data on DPHLS.Data were extracted on study characteristics,participant demographics,clinical features,neuroimaging findings,pathological findings,treatment,and outcomes.The quality assessment was performed using the Joanna Briggs Institute critical appraisal checklist.RESULTS A total of 73 cases were reviewed.Common comorbidities included schizoaffective disorder,bipolar disorder,hypertension,and substance use disorder.The primary causes of hypoxia were benzodiazepine overdose,opioid overdose,polysubstance overdose,and carbon monoxide(CO)poisoning.Symptoms frequently include decreased level of consciousness,psychomotor agitation,cognitive decline,parkinsonism,and encephalopathy.Neuroimaging commonly revealed diffuse T2 hyperintensities in cerebral white matter,sometimes involving the basal ganglia and the globus pallidus.Magnetic resonance spectroscopy often showed decreased N-acetylaspartate,elevated choline,choline-to-creatinine ratio,and normal or elevated lactate.Treatment is often supportive,including amantadine,an antioxidant cocktail,and steroids.Hyperbaric oxygen therapy may be beneficial in those with CO poisoning.Parkinsonism was often treated with levodopa.Most of the patients had substantial recovery over the course of months and many cases had some residual neurocognitive deficits.CONCLUSION DPHLS remains a complex and multifaceted condition with various etiologies and clinical manifestations.Early recognition and appropriate management are crucial to improving patient outcomes.Future research should focus on standardizing diagnostic criteria,using advanced imaging techniques,and exploring therapeutic interventions to improve understanding and treatment of DPHLS.Conducting prospective cohort studies and developing biomarkers for early diagnosis and monitoring will be essential to advance patient care.

Finger compartment syndrome due to a high-pressure washer injury:A case report

BACKGROUND Although the finger compartment syndrome is not common,it compresses the neurovascular bundles in a limited space and blocks blood flow to the fingers,causing necrosis of the fingertips.Finger fasciotomy through unilateral or bilateral midline release of the finger can achieve decompression of the finger compartment.Herein,we report a case of the compartment syndrome in a finger injury caused by a high-pressure water flow which is commonly used in car washing stations.CASE SUMMARY A 60-year-old man injured his right middle finger while using a high-pressure washer at a car washing station.The patient complained of severe pain in his middle finger and a 0.2 cm punctured open wound on the volar side of the distal phalangeal joint of the middle finger.The fingertip was pale,numb,and characterized by severe swelling and a limited range of motion.Finger radiography showed that there was no fracture in the finger.Digital decompression was performed through finger fasciotomy by bilateral midline incision.On the second day after surgery,the color of the fingertip returned to pink,swelling was resolved,and the range of motion returned to normal.The sensation of the fingertip was completely restored,and the capillary refill test and pinprick test were positive.CONCLUSION The fingertip compartment syndrome can be caused by a high-pressure water flow damage to the fingers when using high-pressure washers at a car washing station.To avoid finger necrosis,rapid diagnosis of the finger compartment syndrome and appropriate digital decompression are essential to better outcome.

Clinical and pathophysiological understanding of the hepatorenal syndrome:Still wrong or still not exactly right?

The hepatorenal syndrome(HRS)is one major extrahepatic complication of endstage liver diseases.While circulatory dysregulation is considered as primary etiology for HRS,cirrhosis-related(systemic)inflammation and/or cardial dysfunction may also play a key pathogenic role in HRS development.Exclusion of other causes of acute kidney injury(AKI)is required for diagnosis of HRS-AKI by the definition of the International Club of Ascites.However,the pathophysiology of HRS is not understood completely and there are still limited therapeutic options.Reversibility of renal dysfunction after liver transplantation indicates that HRS-AKI is a functional disorder caused by altered cellular function.The interplay between systemic inflammation and the onset of kidneyrelated hypometabolism may have a key role and needs to be studied in depth.This minireview challenges simplified views of the HRS in the context of diagnostics and therapy stressing the need for further evidence to advance the knowledge on this syndrome.

Review:Acute lung injury/acute respiratory distress syndrome (ALI/ARDS): the mechanism,present strategies and future perspectives of therapies

Acute lung injury/acute respiratory distress syndrome （ALI/ARDS）, which manifests as non-cardiogcnic pulmonary edema, respiratory distress and hypoxemia, could be resulted from various processes that directly or indirectly injure the lung. Extensive investigations in experimental models and humans with ALI/ARDS have revealed many molecular mechanisms that offer therapeutic opportunities for cell or gene therapy. Herein the present strategies and future perspectives of the treatment for ALI/ARDS, include the ventilatory, pharmacological, as well as cell therapies.

Ulinastatin for acute lung injury and acute respiratory distress syndrome: A systematic review and meta-analysis

AIM: To investigate the efficacy and safety of ulinastatin for patients with acute lung injury(ALI) and those with acute respiratory distress syndrome(ARDS).METHODS: A systematic review of randomized controlled trials(RCTs) of ulinastatin for ALI/ARDS was conducted. Oxygenation index, mortality rate [intensive care unit(ICU) mortality rate, 28-d mortality rate] and length of ICU stay were compared between ulinastatin group and conventional therapy group. Meta-analysis was performed by using Rev Man 5.1.RESULTS: Twenty-nine RCTs with 1726 participants were totally included, the basic conditions of which were similar. No studies discussed adverse effect. Oxygenation index was reported in twenty-six studies(1552 patients). Ulinastatin had a significant effect in improving oxygenation [standard mean difference(SMD) = 1.85, 95%CI: 1.42-2.29, P < 0.00001, I2 = 92%]. ICUmortality and 28-d mortality were respectively reported in eighteen studies(987 patients) and three studies(196 patients). We found that ulinastatin significantly decreased the ICU mortality [I2 = 0%, RR = 0.48, 95%CI: 0.38-0.59, number needed to treat(NNT) = 5.06, P < 0.00001], while the 28-d mortality was not significantly affected(I2 = 0%, RR = 0.78, 95%CI: 0.51-1.19, NNT = 12.66, P = 0.24). The length of ICU stay(six studies, 364 patients) in the ulinastatin group was significantly lower than that in the control group(SMD =-0.97, 95%CI:-1.20--0.75, P < 0.00001, I2 = 86%). CONCLUSION: Ulinastatin seems to be effective for ALI and ARDS though most trials included were of poor quality and no information on safety was provided.

Aetiology and mechanisms of injury in medial tibial stress syndrome: Current and future developments

Medial tibial stress syndrome(MTSS) is a debilitating overuse injury of the tibia sustained by individuals whoperform recurrent impact exercise such as athletes and military recruits. Characterised by diffuse tibial anteromedial or posteromedial surface subcutaneous periostitis, in most cases it is also an injury involving underlying cortical bone microtrauma, although it is not clear if the soft tissue or cortical bone reaction occurs first. Nuclear bone scans and magnetic resonance imaging(MRI) can both be used for the diagnosis of MTSS, but the patient's history and clinical symptoms need to be considered in conjunction with the imaging findings for a correct interpretation of the results, as both imaging modalities have demonstrated positive findings in the absence of injury. However, MRI is rapidly becoming the preferred imaging modality for the diagnosis of bone stress injuries. It can also be used for the early diagnosis of MTSS, as the developing periosteal oedema can be identified. Retrospective studies have demonstrated that MTSS patients have lower bone mineral density(BMD) at the injury site than exercising controls, and preliminary data indicates the BMD is lower in MTSS subjects than tibial stress fracture(TSF) subjects. The values of a number of tibial geometric parameters such as cross-sectional area and section modulus are also lower in MTSS subjects than exercising controls, but not as low as the values in TSF subjects. Thus, the balance between BMD and cortical bone geometry may predict an individual's likelihood of developing MTSS. However, prospective longitudinal studies are needed to determine how these factors alter during the development of the injury and to find the detailed structural cause, which is still unknown. Finite element analysis has recently been used to examine the mechanisms involved in tibial stress injuries and offer a promising future tool to understand the mechanisms involved in MTSS. Contemporary accurate diagnosis of either MTSS or a TSF includes a thorough clinical examination to identify signs of bone stress injury and to exclude other pathologies. This should be followed by an MRI study of the whole tibia. The cause of the injury should be established and addressed in order tofacilitate healing and prevent future re-occurrence.

Acute kidney injury and post-reperfusion syndrome in liver transplantation

In the past decades liver transplantation(LT) has become the treatment of choice for patients with end stage liver disease(ESLD). The chronic shortage of cadaveric organs for transplantation led to the utilization of a greater number of marginal donors such as older donors or donors after circulatory death(DCD). The improved survival of transplanted patients has increased the frequency of long-term complications, in particular chronic kidney disease(CKD). Acute kidney injury(AKI) post-LT has been recently recognized as an important risk factor for the occurrence of denovo CKD in the long-term outcome. The onset of AKI post-LT is multifactorial, with pre-LT risk factors involved, including higher Model for End-stage Liver Disease score, more sever ESLD and pre-existing renal dysfunction, either with intra-operative conditions, in particular ischaemia reperfusion injury responsible for post-reperfusion syndrome(PRS) that can influence recipient's morbidity and mortality. Post-reperfusion syndrome-induced AKI is an important complication post-LT that characterizes kidney involvement caused by PRS with mechanisms not clearly understood and implication on graft and patient survival. Since preLT risk factors may influence intra-operative events responsible for PRS-induced AKI, we aim to consider all the relevant aspects involved in PRS-induced AKI in the setting of LT and to identify all studies that better clarified the specific mechanisms linking PRS and AKI. A Pub Med search was conducted using the terms liver transplantation AND acute kidney injury; liver transplantation AND post-reperfusion syndrome; acute kidney injury AND post-reperfusion syndrome; acute kidney injury AND DCD AND liver transplantation. Five hundred seventy four articles were retrieved on Pub Med search. Results were limited to title/abstract of English-language articles published between 2000 and 2015. Twenty-three studies were identified that specifically evaluated incidence, risk factors and outcome for patients developing PRS-induced AKI in liver transplantation. In order to identify intra-operative risk factors/mechanisms specifically involved in PRSinduced AKI, avoiding confounding factors, we have limited our study to "acute kidney injury AND DCD AND liver transplantation". Accordingly, three out of five studies were selected for our purpose.

Acute kidney injury and hepatorenal syndrome in cirrhosis

Acute kidney injury(AKI)in cirrhosis,including hepatorenal syndrome(HRS),is a common and serious complication in cirrhotic patients,leading to significant morbidity and mortality.AKI is separated into two categories,non-HRS AKI and HRS-AKI.The most recent definition and diagnostic criteria of AKI in cirrhosis and HRS have helped diagnose and prognosticate the disease.The pathophysiology behind non-HRS-AKI and HRS is more complicated than once theorized and involves more processes than just splanchnic vasodilation.The common biomarkers clinicians use to assess kidney injury have significant limitations in cirrhosis patients;novel biomarkers being studied have shown promise but require further studies in clinical settings and animal models.The overall management of non-HRS AKI and HRS-AKI requires a systematic approach.Although pharmacological treatments have shown mortality benefit,the ideal HRS treatment option is liver transplantation with or without simultaneous kidney transplantation.Further research is required to optimize pharmacologic and nonpharmacologic approaches to treatment.This article reviews the current guidelines and recommendations of AKI in cirrhosis.

Acute respiratory distress syndrome and lung injury: Pathogenetic mechanism and therapeutic implication

To review possible mechanisms and therapeutics for acute lung injury(ALI) and acute respiratory distress syndrome(ARDS). ALI/ARDS causes high mortality. The risk factors include head injury, intracranial disorders, sepsis, infections and others. Investigations have indicated the detrimental role of nitric oxide(NO) through the inducible NO synthase(i NOS). The possible therapeutic regimen includes extracorporeal membrane oxygenation, prone position, fluid and hemodynamic management and permissive hypercapnic acidosis etc. Other pharmacological treatments are anti-inflammatory and/or antimicrobial agents, inhalation of NO, glucocorticoids, surfactant therapy and agents facilitating lung water resolution and ion transports. β-adrenergic agonists are able to accelerate lung fluid and ion removal and to stimulate surfactant secretion. In con-scious rats, regular exercise training alleviates the endotoxin-induced ALI. Propofol and N-acetylcysteine exert protective effect on the ALI induced by endotoxin. Insulin possesses anti-inflammatory effect. Pentobarbital is capable of reducing the endotoxin-induced ALI. In addition, nicotinamide or niacinamide abrogates the ALI caused by ischemia/reperfusion or endotoxemia. This review includes historical retrospective of ALI/ARDS, the neurogenic pulmonary edema due to head injury, the detrimental role of NO, the risk factors, and the possible pathogenetic mechanisms as well as therapeutic regimen for ALI/ARDS.

Protective effect of nitric oxide on hepatopulmonary syndrome from ischemia-reperfusion injury

AIM： To evaluate immunological protection of nitric ox- ide （NO） in hepatopulmonary syndrome and probable mechanisms of ischemia-reperfusion （IR） injury in rat liver transplantation, METHODS： Sixty-six healthy male Wistar rats were randomly divided into three groups （11 donor/recipi-ent pairs）. In group 11, organ preservation solution was lactated Ringer＇s solution with heparin 10 000/μL at 4℃. In groups I and 111, the pLeservation solution added, respectively, L-arginine or Ng-L-arginine methyl ester （L-NAME） （1 mmol/L） based on group 11, and recipients were injected with L-arginine or L-NAME （50 mg/kg） in the anhepatic phase. Grafted livers in each group were stored for 6 h and implanted into recipi- ents. Five rats were used for observation of postopera- tive survival in each group. The other six rats in each group were used to obtain tissue samples, and execut- ed at 3 h and 24 h after transplantation. The levels of alanine aminotransferase （ALT）, tumor necrosis factor （TNF）-a and NO metabolites （NOx） were detected, and expression of NO synthase, TNF-α and intercellular adhesion molecule 1 （ICAM-1） was examined by tri- phosphopyridine nucleotide diaphorase histochemical and immunohistochemical staining. RESULTS： By supplementing L-arginine to strengthen the NO pathway, a high survival rate was achieved and hepatic function was improved. One-week sur- viral rate of grafted liver recipients in group I was significantly increased （28.8 4±36.6 d ys 4 4±1.7 d, P 〈 0.01） as compared with groups 11 and Ill. Serum levels of ALT in group ] were 2-7 times less than those in groups 11 and 11I （P 〈 0.01）. The cyclic guanosine monophosphate （cGMP） levels in liver tissue and NOx in group I were 3-4 times higher than those of group 11 after 3 h and 24 h reperfusion, while in group ]]], they were significantly reduced as compared with those in group ]1 （P 〈 0.01）. The levels of TNF-（z in group I were significantly lower than in group Ⅱ after 3 h and 24 h reperfusion （P 〈 0.01）, while being sig- nificantly higher in group Ⅲ than group Ⅱ （P 〈 0.01）. Histopathology revealed more severe tissue damage in graft liver and lung tissues, and a more severe in- flammatory response of the recipient after using NO synthase inhibitor, while the pathological damage to grafted liver and the recipient＇s lung tissues was signifi-cantly reduced in group I after 3 h and 24 h reperfu- sion. A small amount of constitutive NO synthase （cNOS） was expressed in liver endothelial cells after 6 h cold storage, but there was no expression of inducible NO synthase （iNOS）. Expression of cNOS was particularly significant in vascular endothelial cells and liver cells at 3 h and 24 h after reperfusion in group Ⅱ but expres- sion of iNOS and ICAM-1 was low in group I. There was diffuse strong expression of ICAM-1 and TNF-α in group Ⅱ at 3 h after reperfusion. CONCLUSION： The NO/cGMP pathway may be critical in successful organ transplantation, especially in treat- ing hepatopulmonary syndrome during cold IR injury in rat orthotopic liver transplantation.

Acute lung injury and acute respiratory distress syndrome： experimental and clinical investigations

Acute lung injury （ALl） or acute respiratory distress syndrome （ARDS） can be associated with various disorders. Recent investigation has involved clinical studies in collaboration with clinical investigators and pathologists on the pathogenetic mechanisms of ALl or ARDS caused by various disorders. This literature review includes a brief historical retrospective of ALI/ARDS, the neurogenic pulmonary edema due to head injury, the long-term experimental studies and clinical investigations from our laboratory, the detrimental role of NO, the risk factors, and the possible pathogenetic mechanisms as well as therapeutic regimen for ALI/ARDS.

Effects of dynamic ventilatory factors on ventilatorinduced lung injury in acute respiratory distress syndrome dogs

BACKGROUND： Mechanical ventilation is a double-edged sword to acute respiratory distress syndrome （ARDS） including lung injury, and systemic inflammatory response high tidal volumes are thought to increase mortality. The objective of this study is to evaluate the effects of dynamic ventilatory factors on ventilator induced lung injury in a dog model of ARDS induced by hydrochloric acid instillation under volume controlled ventilation and to investigate the relationship between the dynamic factors and ventilator-induced lung injuries （VILI） and to explore its potential mechanisms.METHODS： Thirty-six healthy dogs were randomly divided into a control group and an experimental group. Subjects in the experimental group were then further divided into four groups by different inspiratory stages of flow. Two mL of alveolar fluid was aspirated for detection of IL-8 and TNF-α. Lung tissue specimens were also extracted for total RNA, IL-8 by western blot and observed under an electronic microscope.RESULTS： IL-8 protein expression was significantly higher in group B than in groups A and D. Although the IL-8 protein expression was decreased in group C compared with group B, the difference was not statistically significant. The TNF-a ray degree of group B was significantly higher than that in the other groups （P〈0.01）, especially in group C （P〉0.05）. The alveolar volume of subjects in group B was significantly smaller, and cavity infiltration and cell autolysis were marked with a significant thicker alveolar septa, disorder of interval structures, and blurring of collagenous and elastic fiber structures. A large number of necrotic debris tissue was observed in group B.CONCLUSION： Mechanical ventilation with a large tidal volume, a high inspiratory flow and a high ventilation frequency can cause significant damage to lung tissue structure. It can significantly increase the expression of TNF-α and IL-8 as well as their mRNA expression. Furthermore, the results of our study showed that small tidal ventilation significantly reduces the release of proinflammatory media. This finding suggests that greater deterioration in lung injury during ARDS is associated with high inspiratory flow and high ventilation rate.

Rhabdomyolysis, compartment syndrome and thermal injury

Rhabdomyolysis(RML) after electrical burns and crush injuries is a well-known clinical entity, but its occurrence following thermal injury has not gained so much attention. Capillary leak syndrome and following polycompartmental syndrome are devastating end results of major thermal injuries. In the current review, polycompartment syndrome within the clinical picture of systemic oedema and its relationship to RML is discussed along with its management and prevention.

A novel mouse model of central cord syndrome

Patients with potential spinal stenosis are susceptible to central cord syndrome induced by blunt trauma.Suitable animal models are helpful for studying the pathogenesis and treatment of such injuries.In this study,we established a mouse model of acute blunt traumatic spinal cord injury by compressing the C6 spinal cord with 5 and 10 g/mm~2 compression weights to simulate cervical central cord syndrome.Behavioral testing confirmed that this model exhibited the characteristics of central cord syndrome because motor function in the front paws was impaired,whereas basic motor and sensory functions of the lower extremities were retained.Hematoxylin-eosin staining showed that the diseased region of the spinal cord in this mouse model was restricted to the gray matter of the central cord,whereas the white matter was rarely affected.Magnetic resonance imaging showed a hypointense signal in the lesion after mild and severe injury.In addition,immunofluorescence staining showed that the degree of nerve tract injury in the spinal cord white matter was mild,and that there was a chronic inflammation reaction.These findings suggest that this mouse model of central cord syndrome can be used as a model for preclinical research,and that gray matter is most vulnerable to injury in central cord syndrome,leading to impaired motor function.

Novel roles of lipopolysaccharide and TLR4/NF-κB signaling pathway in inflammatory response to liver injury in Budd-Chiari syndrome

BACKGROUND Budd-Chiari syndrome(BCS)is an uncommon disorder characterized by obstruction of hepatic venous outflow.To date,the exact mechanism underlying hepatic injury derived from the hepatic venous outflow obstruction in BCS remains largely unknown.AIM To assess the role of NF-κB-mediated inflammation in BCS-induced liver injury in humans and rats.METHODS A total of 180 rats were randomly assigned into nine groups,including four BCS model groups(1,3,6 and 12 wk),four sham-operated groups(1,3,6 and 12 wk),and a control group.Lipopolysaccharide(LPS)levels in each group were detected by the Tachypleus Amebocyte Lysate assay.The mRNA and protein levels of TLR4,NF-κB,tumor necrosis factor(TNF)-α,interleukin(IL)-2 and interferon(IFN)-γwere quantified.In addition,60 patients with BCS and 30 healthy controls were enrolled,and their blood samples were analyzed.RESULTS Hepatic and plasma LPS levels were significantly increased in rats.The mRNA and protein expression levels of TLR4,NF-κB and inflammatory cytokines(TNF-α,IL-2 and IFN-γ)in liver tissues were significantly higher in the BCS model groups compared with the other two groups.In addition,the model groups(1,3,6 and 12 wk after BCS induction)showed significant differences in the levels of LPS,TLR4,NF-κB,TNF-α,IL-2 and IFN-γ.Notably,there was a significant correlation between the LPS concentrations and mRNA and protein levels of TLR4,NF-κB and inflammatory cytokines.Importantly,it was revealed that the levels of LPS,TLR4,NF-κB and inflammatory cytokines were significantly greater in chronic BCS patients than healthy controls and acute BCS patients.CONCLUSION LPS level is markedly elevated in BCS,in turn activating the TLR4/NF-κB signaling pathway,leading to induction of inflammatory cytokines(TNF-α,IL-2 and IFN-γ)in response to BCS-induced liver injury.