Radial head and neck fractures in children and adolescents

BackgroundRadial head and neck fractures are a rare entity in pediatric patients. Due to specific characteristics of the blood supply and remodeling potential, the correct diagnosis and initiation of appropriate therapy are crucial for the outcome. Therefore, the aim of this retrospective observational study was to present the outcome of a series of pediatric patients with radial head and neck fractures.MethodsIn total, 67 pediatric and adolescent patients with a fracture of the proximal radius admitted to a Level I Trauma Center (Germany) between 2005 and 2017 were included in this retrospective observational study. Patients were stratified in accordance with the classification of Judet modified by Metaizeau and with the AO Pediatric Comprehensive Classification of Long Bone Fractures (AO-PCCF).ResultsAO-PCCF fracture type of proximal radius was age-dependent. Epiphyseal axis angle and displacement angle correlated significantly. Fractures treated with a K-wire or embrochage centromedullaire elastique stable (ECMES) presented higher displacement angles. The duration of callus formation was dependent on both the reduction technique and fracture displacement. The range of motion after complete fracture consolidation was dependent on the Metaizeau type and reduction technique but independent of the duration of immobilization and physical therapy.Conclusion and clinical relevanceBoth the epiphyseal axis and displacement angle are suitable for measuring the initial fracture displacement in radiographs. Consolidation is dependent on the initial displacement and reduction technique. The mini-open approach leads to a worse reduction result, later callus formation, and a more restricted range of motion in terms of pronation. Furthermore, the range of motion at follow-up is independent of the duration of immobilization and physiotherapy

Lung injury after asphyxia and hemorrhagic shock in newborn piglets: Analysis of structural and inflammatory changes.

ObjectiveAsphyxia of newborns is a severe and frequent challenge of the peri- and postnatal period. The purpose of this study was to study early morphological, immunological and structural alterations in lung tissue after asphyxia and hemorrhage (AH).Methods44 neonatal piglets (age 32 hrs) underwent asphyxia and hemorrhage (AH) and were treated according to the international liaison committee of resuscitation (ILCOR) guidelines. For this study, 15 piglets (blood transfusion (RBC) n = 9; NaCl n = 6, mean age 31 hrs) were randomly picked. 4 hours after ROSC (return of spontaneous circulation), lung tissue and blood samples were collected.ResultsAn elevation of myeloperoxidase (MPO) activity was observed 4 hrs after AH accompanied by an increase of surfactant D after RBC treatment. After AH tight junction proteins Claudin 18 and junctional adhesion molecule 1 (JAM1) were down-regulated, whereas Occludin was increased. Furthermore, after AH and RBC treatment dephosphorylated active form of Connexin 43 was increased.ConclusionsAH in neonatal pigs is associated with early lung injury, inflammation and alterations of tight junctions (Claudin, Occludin, JAM-1) and gap junctions (Connexin 43) in lung tissue, which contributes to the development of lung edema and impaired function

Sensory contact to the stressor prevents recovery from structural and functional heart damage following psychosocial trauma

Cardiovascular disorders (CVD) and posttraumatic stress disorder (PTSD) are highly comorbid, but the underlying mechanisms are not fully understood. Chronic psychosocial stress was induced in male mice by chronic subordinate colony housing (CSC), a pre-clinically validated mouse model for PTSD. Cardiac structure and function were assessed on day 20 of the CSC paradigm. Following CSC, mice were kept in different sensory contact modalities to the last aggressor for 30 days, and development of cardiac function and behavioral aspects were determined. Here we show that psychosocial trauma affects heart structure by disturbing cell-to-cell integrity of cardiomyocytes, causes tachycardia, disturbance of diurnal heart rate rhythmicity and behavioral deficits in a mouse model for PTSD. Structural and functional alterations were also found in cardiomyocytes upon in vitro treatment with pro-inflammatory cytokines typically increased after psychosocial trauma. Interestingly, sensory contact to the aggressor subsequent to psychosocial trauma prohibits functional and structural heart recovery, while isolation was beneficial for cardiac but detrimental for mental health. These findings contribute to our understanding of potential mechanisms underlying the high comorbidity of CVD and PTSD

Experimental blunt chest trauma-induced myocardial inflammation and alteration of gap-junction protein connexin 43

<div><p>Objective</p><p>Severe blunt chest trauma in humans is associated with high mortality rates. Whereas lung tissue damage and lung inflammation after blunt chest trauma have extensively been investigated, the traumatic and posttraumatic effects on the heart remain poorly understood. Therefore, the purpose of this study was to define cardiac injury patterns in an experimental blunt chest trauma model in rats.</p><p>Methods</p><p>Experimental blunt chest trauma was induced by a blast wave in rats, with subsequent analysis of its effects on the heart. The animals were subjected either to a sham or trauma procedure. Systemic markers for cardiac injury were determined after 24 h and 5 days. Postmortem analysis of heart tissue addressed structural injury and inflammation 24 h and 5 days after trauma.</p><p>Results</p><p>Plasma levels of extracellular histones were elevated 24 h and 5 days after blunt chest trauma compared to sham-treated animals. In the heart, up-regulation of interleukin-1β 24 h after trauma and increased myeloperoxidase activity 24 h and 5 days after trauma were accompanied by reduced complement C5a receptor-1 expression 24 h after trauma. Histological analysis revealed extravasation of erythrocytes and immunohistochemical analysis alteration of the pattern of the gap-junction protein connexin 43. Furthermore, a slight reduction of α-actinin and desmin expression in cardiac tissue was found after trauma together with a minor increase in sarcoplasmatic/endoplasmatic reticlulum calcium-ATPase (SERCA) expression.</p><p>Conclusions</p><p>The clinically highly relevant rat model of blast wave-induced blunt chest trauma is associated with cardiac inflammation and structural alterations in cardiac tissue.</p></div

Structural alterations in the heart after blunt chest trauma.

<p>Alteration of gap junctional protein connexin 43 (Cx43) after blunt chest trauma in the heart. A. Representative distribution of Cx43 in cardiac tissue after sham procedure or 24 h or 5d after blunt chest trauma as indicated. B. Representative western blot for Cx43 of left ventricular tissue homogenates. Densitometry revealed no significant increase in protein expression in left ventricular homogenates 24 h and 5 d after blunt chest trauma compared to sham procedure. For all frames n = 4 for each bar.</p

Local inflammation in cardiac injury after blunt chest trauma.

<p>A. Increased myeloperoxidase (MOP) activity in left ventricular cardiac tissue 24 h and 5 d after blunt chest trauma compared to sham procedure. B. Elevation of proinflammatory cardiodepressive cytokine IL-1β expression in left ventricular homogenates 24 h after blunt chest trauma compared to sham procedure as assessed by qRT-PCR. C. Representative western blot for C5aR1 of left ventricular tissue homogenates. Densitometry revealed diminished C5aR1 protein expression in left ventricular homogenates 24 h after blunt chest trauma compared to sham procedure. D. C5aR expression in left ventricular homogenates 24 h and 5 d after blunt chest trauma and after sham procedure as assessed by qRT-PCR. p<0.05; *differences were significant to sham procedure, For all frames n = 8 for each bar.</p

Systemic and local effects of blunt chest trauma.

<p>Apparence of extracellular histones in plasma 24 h and 5 d after blunt chest trauma or sham, * differences to sham procedure were significant, p<0.05; n = 4 for each bar. B. Representative H.E staining of left ventricles 24 h or 5 d after blunt chest trauma or sham procedure as indicated.</p