Epidemiological analysis of intramuscular hemorrhage of respiratory and accessory respiratory muscles in fatal drowning cases.

The postmortem diagnosis of drowning death and understanding the mechanisms leading to drowning require a comprehensive judgment based on numerous morphological findings in order to determine the pathogenesis and epidemiological characteristics of the findings. Effortful breathing during the drowning process can result in intramuscular hemorrhage in respiratory and accessory respiratory muscles. However, the characteristics of this phenomenon have not been investigated. We analyzed the epidemiological characteristics of 145 cases diagnosed as drowning, in which hemorrhage, not due to trauma, was found in the respiratory muscles and accessory respiratory muscles. Hemorrhage was observed in 31.7% of these cases, and the incidence did not differ by gender or drowning location. The frequency of hemorrhage was significantly higher in months with a mean temperature below 20°C than in months above 20°C, suggesting a relationship between the occurrence of hemorrhage and low environmental temperature. Moreover, the frequency of hemorrhage was significantly higher in the elderly (aged ≥65 years) compared to those <65 years old. In the elderly, the weakening of muscles due to aging may contribute to the susceptibility for intramuscular hemorrhage. Moreover, these intramuscular hemorrhages do not need to be considered in cases of a potential bleeding tendency due to disease such as cirrhosis or medication such as anticoagulants. Our results indicate that intramuscular hemorrhage in respiratory and accessory respiratory muscles can serve as an additional criterion to differentiate between fatal drowning and other causes of death, as long as no cutaneous or subcutaneous hematomas above the muscles with hemorrhages are observed. In addition, the epidemiological features that such intramuscular hemorrhage is more common in cold environments and in the elderly may provide useful information for the differentiation.

Respiratory Dysfunction in Becker Muscular Dystrophy Patients: A Case Series and Autopsy Report.

BACKGROUND: Few studies have examined respiratory dysfunction in patients with Becker muscular dystrophy (BMD). OBJECTIVE: This study aimed to examine the characteristics of respiratory dysfunction in patients with BMD. METHODS: The present retrospective study assessed respiratory parameters of adult BMD patients using medical records and compared these parameters with various patient characteristics to identify correlations. BMD patients aged 17 years and older who had been diagnosed genetically and/or pathologically were included in the analysis. RESULTS: Of the source population of 133 patients, respiratory function was assessed in 85. Two of these patients had no symptoms, and eight had died. Mean % forced vital capacity (% FVC) was 94.2+/-21.7% (median, 96.1%; range, 5.1-134.1%). In 16 (19%) of the 85 patients, % FVC was <80%. Of these, seven were non-ambulant. Age, ambulation, and cardiac function did not significantly differ between patients with or without respiratory dysfunction, whereas age at onset was significantly lower in patients with respiratory dysfunction (7.7+/-4.7 years vs. 14.4+/-11.9 years; p = 0.001). One non-ambulant patient was a continuous NPPV user, and one patient had been recommended NPPV use but refused. Autopsy of one patient revealed that the diaphragm and intercostal muscles were less affected than proximal skeletal muscles. CONCLUSION: BMD patients are at risk of developing respiratory dysfunction due to dystrophic changes in respiratory muscles. Respiratory function should be carefully and periodically monitored in these patients.

Pseudohernia intercostal tras un traumatismo torácico cerrado / Intercostal pseudohernia following blunt chest trauma

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Utilidad de la ecografía torácica en el diagnóstico de las hernias pulmonares intercostales / Usefulness of Thoracic Ultrasound in the Diagnosis of Intercostal Pulmonary Hernias

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Laparoscopic IPOM repair of an acquired abdominal intercostal hernia.

Acquired abdominal intercostal hernia (AAIH) is an infrequent occurrence whereby intra-abdominal contents herniate into intercostal space directly from the peritoneal cavity through an acquired defect in the abdominal wall musculature and fascia. These hernias are difficult to diagnose and should always be suspected when a chest wall swelling occur after major or minor trauma. Surgical repair is warranted in symptomatic patients. The majority of AAIHs are repaired through an open approach using tension-free mesh, with significant recurrence risk. Recently, laparoscopic and robot-assisted repairs have been proposed. We discuss a 49-year-old man presented through outpatient setting with a 5-year history of ongoing left subcostal discomfort and a reducible lump. His history included a workplace accident 5 years ago. Contrast-enhanced abdominal CT confirmed AAIH with omentum herniation into the sac. A successful laparoscopic repair with intraperitoneal onlay mesh technique using composite mesh was performed.

Clinical importance of cross-sectional area of intercostal muscles in patients with chronic obstructive pulmonary disease.

INTRODUCTION: Limb muscle wasting is one of main systemic manifestation of chronic obstructive pulmonary disease (COPD). However, the change of respiratory muscle is unclear. OBJECTIVES: This study assessed the cross-sectional area (CSA) of the intercostal muscles (ICMs) in patients with COPD, using chest computed tomography (CT) and determined its association with the clinical characteristics of COPD. METHODS: They retrospectively reviewed 60 patients with stable COPD and compared them with 30 controls. CSA (mm2 ) of the ICM on chest CT was measured at the midline level of the lateral arch of the bilateral first rib with a 3-mm slice thickness by using CT histogram software. The association with the clinical characteristics of COPD and with the control groups was assessed. RESULTS: CSA of the ICM and the CSA/body mass index (BMI) were lower in the COPD group than in the control group. Patients with Global Initiative for Chronic Obstructive Lung Disease (GOLD) stage 4 had a significantly lower CSA of the ICM than patients with stage 1, 2, and 3. CSA of the ICM was positively associated with FEV1 , %FEV1 predicted, FEV1 /FVC ratio, and BMI and negatively associated with age. However, there were no associations with PaO2 , PaCO2 , smoking status, 6-minute walk test, frequency of acute exacerbation of COPD, and serum C-reactive protein level. CONCLUSION: Intercostal muscle atrophy occurs in COPD patients and is associated with severity of airway obstruction, BMI, and increasing age.

Complement activation at the motor end-plates in amyotrophic lateral sclerosis.

BACKGROUND: Amyotrophic lateral sclerosis (ALS) is a fatal progressive neurodegenerative disease with no available therapy. Components of the innate immune system are activated in the spinal cord and central nervous system of ALS patients. Studies in the SOD1(G93A) mouse show deposition of C1q and C3/C3b at the motor end-plate before neurological symptoms are apparent, suggesting that complement activation precedes neurodegeneration in this model. To obtain a better understanding of the role of complement at the motor end-plates in human ALS pathology, we analyzed post-mortem tissue of ALS donors for complement activation and its regulators. METHODS: Post-mortem intercostal muscle biopsies were collected at autopsy from ALS (n = 11) and control (n = 6) donors. The samples were analyzed for C1q, membrane attack complex (MAC), CD55, and CD59 on the motor end-plates, using immunofluorescence or immunohistochemistry. RESULTS: Here, we show that complement activation products and regulators are deposited on the motor end-plates of ALS patients. C1q co-localized with neurofilament in the intercostal muscle of ALS donors and was absent in controls (P = 0.001). In addition, C1q was found deposited on the motor end-plates in the intercostal muscle. MAC was also found deposited on motor end-plates that were innervated by nerves in the intercostal muscle of ALS donors but not in controls (P = 0.001). High levels of the regulators CD55 and CD59 were detected at the motor end-plates of ALS donors but not in controls, suggesting an attempt to counteract complement activation and prevent MAC deposition on the end-plates before they are lost. CONCLUSIONS: This study provides evidence that complement activation products are deposited on innervated motor end-plates in the intercostal muscle of ALS donors, indicating that complement activation may precede end-plate denervation in human ALS. This study adds to the understanding of ALS pathology in man and identifies complement as a potential modifier of the disease process.

A CHRNE frameshift mutation causes congenital myasthenic syndrome in young Jack Russell Terriers.

Congenital myasthenic syndromes (CMSs) are a group of rare genetic disorders of the neuromuscular junction resulting in structural or functional causes of fatigable weakness that usually begins early in life. Mutations in pre-synaptic, synaptic and post-synaptic proteins have been demonstrated in human cases, with more than half involving aberrations in nicotinic acetylcholine receptor (AChR) subunits. CMS was first recognized in dogs in 1974 as an autosomal recessive trait in Jack Russell Terriers (JRTs). A deficiency of junctional AChRs was demonstrated. Here we characterize a CMS in 2 contemporary cases of JRT littermates with classic clinical and electromyographic findings, and immunochemical confirmation of an approximately 90% reduction in AChR protein content. Loci encoding the 5 AChR subunits were evaluated using microsatellite markers, and CHRNB1 and CHRNE were identified as candidate genes. Sequences of the splice sites and exons of both genes revealed a single base insertion in exon 7 of CHRNE that predicts a frameshift mutation and a premature stop codon. We further demonstrated this pathogenic mutation in CHRNE in archival tissues from unrelated JRTs studied 34 years ago.

Embolization biomaterial reinforced with nanotechnology for an in-situ release of anti-angiogenic agent in the treatment of hyper-vascularized tumors and arteriovenous malformations.

A polymer based material was developed to act as an embolic agent and drug reservoir for the treatment of arteriovenous malformations (AVM) and hyper vascularized solid tumors. The aim was to combine the blocking of blood supply to the target region and the inhibition of the embolization-stimulated angiogenesis. The material is composed of an ethanolic solution of a linear acrylate based copolymer and acrylate calibrated microparticles containing nanospheres loaded with sunitinib, an anti-angiogenic agent. The precipitation of the linear copolymer in aqueous environment after injection through microcatheter results in the formation of an in-situ embolization gel whereas the microparticles serve to increase the cohesive properties of the embolization agent and to form a reservoir from which the sunitinib-loaded nanospheres are released post-embolization. The swollen state of the microparticles in contact with aqueous medium results in the release of the nanospheres out of microparticles macromolecular structure. After the synthesis, the formulation and the characterization of the different components of the material, anti-angiogenic activity was evaluated in vitro using endothelial cells and in vivo using corneal neovascularization model in rabbit. The efficiency of the arterial embolization was tested in vivo in a sheep model. Results proved the feasibility of this new system for vascular embolization in association with an in situ delivery of anti-angiogenic drug. This combination is a promising strategy for the management of arteriovenous malformations and solid tumors.

Mass and fat infiltration of intercostal muscles measured by CT histogram analysis and their correlations with COPD severity.

RATIONALE AND OBJECTIVES: Chronic obstructive pulmonary disease (COPD) is characterized by progressive respiratory function impairment and respiratory muscle dysfunction. We hypothesized that the mass and fat infiltration of respiratory muscles correlates with COPD severity and emphysema extent. MATERIALS AND METHODS: Ninety-eight male patients with COPD underwent chest computed tomography (CT) and spirometry. The mass and fat infiltrations of intercostal and latissimus muscles were quantified as the cross-sectional area (CSA) and attenuation of these muscles using CT histogram analysis. Intercostal index and latissimus index were defined as intercostal CSAs and latissimus CSAs divided by body mass index. The emphysema extent was measured as the ratio of the emphysematous lung volume to the total lung volume using a density-mask technique. Pearson correlation analyses were performed to evaluate the relationships between these parameters. Multiple regression analysis was performed using forced expiratory volume in 1 second (FEV1) as the dependent parameter and the clinical and CT data as the independent parameters. RESULTS: FEV1 was significantly correlated with intercostal index (r = 0.57), latissimus index (r = 0.34), intercostal attenuation (r = 0.62), and latissimus attenuation (r = 0.38). Emphysema extent was significantly correlated with intercostal index (r = -0.36) and intercostal attenuation (r = -0.50). Multiple regression analysis showed that FEV1 was predicted by intercostal attenuation (B = 0.40), intercostal CSA (B = 0.23), emphysema extent (B = -0.23), and age (B = -0.21, R(2) = 0.64, P < .001). CONCLUSIONS: A decrease in intercostal mass and an increase in intercostal fat are associated with worsening of COPD severity.

Intramuscular myxoma in the chest wall.

Intramuscular myxomas are benign soft-tissue tumors that often develop in the thigh. A 66-year-old woman was referred with an abnormal shadow on chest roentgenogram. The tumor was well defined and smooth and originated from the second intercostal space. Positron emission tomography showed no accumulation of 18F-fluorodeoxyglucose in the tumor. The patient attended the outpatient department for follow-up care. Because the mass grew slightly after 52 months, the patient underwent complete removal by video-assisted thoracoscopic surgery. On histopathological examination, the tumor was diagnosed as an intramuscular myxoma in the chest wall. The patient has had no recurrence 3 years after surgery. A case of intramuscular myxoma in the chest wall, completely resected by video-assisted thoracoscopic surgery, is reported. A well-defined, smooth, homogeneous mass in the chest wall may therefore be intramuscular myxoma.

Characterization of intercostal muscle pathology in canine degenerative myelopathy: a disease model for amyotrophic lateral sclerosis.

Dogs homozygous for missense mutations in the SOD1 gene develop a late-onset neuromuscular disorder called degenerative myelopathy (DM) that has many similarities to amyotrophic lateral sclerosis (ALS). Both disorders are characterized by widespread progressive declines in motor functions, accompanied by atrophic changes in the descending spinal cord tracts. Some forms of ALS are also associated with SOD1 mutations. In end-stage ALS, death usually occurs as a result of respiratory failure from severe functional impairment of respiratory muscles. The mechanisms that lead to this loss of function are not known. Dogs with DM are euthanized at all stages of disease progression, providing an opportunity to characterize the onset and progression of any pathological changes in the respiratory muscles that may precede respiratory failure. To characterize such potential disease-related pathology, we evaluated intercostal muscles from Boxer and Pembroke Welsh Corgi dogs that were euthanized at various stages of DM disease progression. DM was found to result in intercostal muscle atrophy, fibrosis, increased variability in muscle fiber size and shape, and alteration in muscle fiber type composition. This pathology was not accompanied by retraction of the motor neuron terminals from the muscle acetylcholine receptor complexes, suggesting that the muscle atrophy did not result from physical denervation. These findings provide a better understanding of the mechanisms that likely lead to respiratory failure in at least some forms of ALS and will be useful in the development and evaluation of potential therapeutic interventions using the DM model.

Well-circumscribed type of intramuscular lipoma in the chest wall.

A tumor shadow was identified in the chest X-ray of a 40-year-old Korean man and he was referred to our hospital. The computed tomographic (CT) scan of his chest showed a 3-cm rounded pleural-based mass lesion with calcification, which was growing into the intercostal muscles. Thoracoscopic surgery was performed to resect the tumor. From the histological findings, the tumor was diagnosed as an intramuscular lipoma. The patient displayed no evidence of recurrence for more than 18 months. As well-circumscribed type of intramuscular lipoma is a rare tumor, we report this case with a literature review in this paper.

[Inflammation and oxidative stress in respiratory and limb muscles of patients with severe sepsis]. / Inflamación y estrés oxidativo en los músculos respiratorios y periféricos de pacientes con sepsis grave.

BACKGROUND AND OBJECTIVE: Oxidative stress and inflammation contribute to the diaphragm contractile dysfunction observed in animal models of sepsis and endotoxemia. In septic patients, molecular events have never been explored in their respiratory muscles. Levels of oxidative stress and inflammation were evaluated in a respiratory muscle, the external intercostal, and a limb muscle, the vastus lateralis, of patients with sepsis. PATIENTS AND METHODS: Levels of oxidized and nitrated proteins, protein adducts of malondialdehyde and hydroxinonenal, antioxidant enzymes catalase and Mn-superoxide dismutase, tumor necrosis factor (TNF)-α, TNF-α receptors i and ii, interleukin (IL)-1 and IL-6, the panleukocyte marker CD18, and fiber type composition were explored using immunoblotting, real time-polymerase chain reaction, and immunohistochemistry in the external intercostal and vastus lateralis of patients with severe sepsis and/or septic shock. RESULTS: Compared to the controls, in septic patients, levels of oxidized and nitrated proteins were increased in the vastus lateralis, but not in the external intercostal, while those of the antioxidant enzymes did not differ, and the proportions and sizes of the muscle fibers were not significantly different in any muscle between patients and controls. CONCLUSIONS: Differences in activity between the respiratory and limb muscles may account for the differential pattern of oxidative stress and inflammation observed among patients with severe sepsis. These findings may have relevant implications for the clinical and therapeutic management of these patients.

Resection of intercostal hemangioma with involved chest wall and ribs: in an 11-year-old girl.

We report a case of an 11-year-old girl who presented with a slowly enlarging mass in the right posterolateral chest wall. Computed tomography showed a soft-tissue mass 8.5 × 7.5 × 5.5 cm in size, arising from the right posterolateral 9th, 10th, and 11th intercostal spaces. Magnetic resonance imaging confirmed a vascular mass. The patient underwent complete resection of the tumor, together with the right 8th, 9th, 10th, 11th, and 12th ribs and their intercostal muscles. Reconstruction of the chest wall was performed with methyl methacrylate and Marlex mesh. Histopathologic examination of the tumor confirmed an intercostal cavernous hemangioma. At last examination, 6 months after the operation, the child was doing well, with no evidence of recurrence.

Muscle loss in elderly.

Aging is associated with loss of skeletal muscle mass, strength and endurance. The aim of this study was to determinate age related changes in human muscles with different function and location in the body (vastus lateralis muscle and intercostal internus muscle). Our results suggest that age related muscle atrophy affect both human skeletal muscles. Also, the results showed the increase in percentage of muscle fibers with high oxidative activity during aging.

Desmoid tumor of the chest wall in an elderly woman.

We report a case of desmoid tumor of the chest wall in a 79-year-old woman. The patient was referred to our hospital for management of a chest wall mass. Four months previously, the patient noted a small lump in the right lateral chest wall that had rapidly increased in size. Magnetic resonance imaging of the chest revealed a soft tissue tumor in the right lateral chest wall with unclear margins that extended into the intercostal muscles. Positron emission tomography with (18)F-fluorodeoxyglucose (FDG) showed slight FDG accumulation at the lesion. Because open biopsy suggested a desmoid tumor, full-thickness chest wall resection with reconstruction was performed. The final diagnosis was desmoid tumor of the chest wall. Wide surgical resection during the initial operation is an essential element in the treatment of this tumor.

Parálisis de la musculatura abdominal como complicación del herpes zóster / No disponible

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Citocinas inflamatorias y factores de reparaci¨®n en los m¨²sculos intercostales de pacientes con EPOC grave / Inflammatory Cytokines and Repair Factors in the Intercostal Muscles of Patients With Severe COPD

Introducci¨®nLas acciones locales de las citocinas en los m¨²sculos de los pacientes con enfermedad pulmonar obstructiva cr¨®nica (EPOC) se hallan sometidas a debate. El objetivo del presente estudio ha sido analizar las relaciones entre su expresi¨®n y la activaci¨®n gen¨¦tica de programas de reparaci¨®n muscular.Pacientes y m¨¦todosSe incluy¨® en el estudio a 25 pacientes con EPOC grave en situaci¨®n estable. Se les realiz¨® una biopsia del m¨²sculo intercostal externo, donde se evaluaron los signos de lesi¨®n muscular (morfometr¨ªa), la infiltraci¨®n de c¨¦lulas inflamatorias (inmunohistoqu¨ªmica) y la expresi¨®n de genes seleccionados (t¨¦cnica de reacci¨®n en cadena de la polimerasa en tiempo real) correspondientes a las propias citocinas ¡ªfactor de necrosis tumoral alfa (TNF-¦Á) y sus receptores 1 y 2 (TNFR1 y TNFR2), e interleucinas-1¦Â, 6 y 10¡ª, un marcador panleucocitario (CD18) y mol¨¦culas clave en las v¨ªas de reparaci¨®n-miog¨¦nesis (Pax7, M-Caderina y Mio-D).ResultadosLa expresi¨®n de TNFR2 se relacion¨® directamente con la funci¨®n muscular inspiratoria (representada por la presi¨®n inspiratoria m¨¢xima sostenible; r=0,496, p<0,05), mientras que la expresi¨®n de CD18 se relacion¨® inversamente con ella (r=−0,462, p<0,05). Por otra parte, la expresi¨®n de los 2 receptores del TNF-¦Á se relacion¨® directamente con la de las mol¨¦culas clave de las v¨ªas de reparaci¨®n analizadas (TNFR1 con Pax7, r=0,650, y M-Caderina, r=0,678, ambas con p<0,001; TNFR2 con Pax7, r=0,395, M-Caderina, r=0,409, y Mio-D, r=0,418, con p<0,05 en todas).ConclusionesLa expresi¨®n de los receptores del TNF-¦Á guarda una estrecha relaci¨®n tanto con la activaci¨®n de los programas de miog¨¦nesis como con la propia funci¨®n muscular inspiratoria. Este hecho refuerza nuestra hip¨®tesis de que algunas citocinas locales participan en la reparaci¨®n de los m¨²sculos respiratorios en los pacientes con EPOC(AU)

ObjectiveThere is disagreement regarding the local action of cytokines in the respiratory muscles of patients with chronic obstructive pulmonary disease (COPD). The objective of this study was to analyze the relationships between cytokine expression and genetic activation of the mechanisms of muscle repair.Patients and methodsTwenty-five patients with severe COPD and in stable condition were enrolled in the study. We performed a biopsy of the external intercostal muscle of the patients and analyzed the specimen for signs of muscle lesion (morphometry), infiltration of inflammatory cells (immunohistochemistry), and expression of selected genes (real-time polymerase chain reaction technique) corresponding to the cytokines (tumor necrosis factor ¦Á [TNF-¦Á] and its type 1 and 2 receptors [TNFR1 and TNFR2], and interleukin [IL] 1¦Â, IL-6, and IL-10), a pan-leukocyte marker (CD18), and key molecules in the repair-myogenesis pathways (Pax7, M-cadherin, and MyoD).ResultsExpression of TNFR2 is directly related to inspiratory muscle function (represented by maximum sustainable inspiratory pressure; r=0.496; P<.05), whereas expression of CD18 is inversely related (r=0.462; P<.05). Moreover, expression of the 2 TNF-¦Á receptors was directly related to that of the key molecules of the repair pathways analyzed (TNFR1 to Pax7 [r=0.650; P<.001] and M-cadherin [r=0.678; P<.001]; TNFR2 to Pax7 [r=0.395; P<.05], M-cadherin [r=0.409; P<.05], and MyoD [r=0.418; P<.05]).ConclusionsExpression of TNF-¦Á receptors bears a close relationship both to activation of the myogenesis programs and to inspiratory muscle function. This reinforces our hypothesis that some local cytokines take part in the repair of respiratory muscles in patients with COPD(AU)