Intra-abdominal hypertension due to heparin - induced retroperitoneal hematoma in patients with ventricle assist devices: report of four cases and review of the literature

<p>Abstract</p> <p>Introduction</p> <p>Elevated intra-abdominal pressure (IAP) has been identified as a cascade of pathophysiologic changes leading in end-organ failure due to decreasing compliance of the abdomen and the development of abdomen compartment syndrome (ACS). Spontaneous retroperitoneal hematoma (SRH) is a rare clinical entity seen almost exclusively in association with anticoagulation states, coagulopathies and hemodialysis; that may cause ACS among patients in the intensive care unit (ICU) and if treated inappropriately represents a high mortality rate.</p> <p>Case Presentation</p> <p>We report four patients (a 36-year-old Caucasian female, a 59-year-old White-Asian male, a 64-year-old Caucasian female and a 61-year-old Caucasian female) that developed an intra-abdominal hypertension due to heparin-induced retroperitoneal hematomas after implantation of ventricular assist devices because of heart failure. Three of the patients presented with dyspnea at rest, fatigue, pleura effusions in chest XR and increased heart rate although b-blocker therapy. A 36-year old female (the forth patient) presented with sudden, severe shortness of breath at rest, 10 days after an "acute bronchitis". At the time of the event in all cases international normalized ratio (INR) was <3.5 and partial thromboplastin time <65 sec. The patients were treated surgically, the large hematomas were evacuated and the systemic manifestations of the syndrome were reversed.</p> <p>Conclusion</p> <p>Identifying patients in the ICU at risk for developing ACS with constant surveillance can lead to prevention. ACS is the natural progression of pressure-induced end-organ changes and develops if IAP is not recognized and treated in a timely manner. Failure to recognize and appropriately treat ACS is fatal while timely intervention - if indicated - is associated with improvements in organ function and patient survival. Means for surgical decision making are based on clinical indicators of adverse physiology, rather than on a single measured parameter.</p

Lipoxin B4 promotes the resolution of allergic inflammation in the upper and lower airways of mice

Chronic mucosal inflammation is the hallmark of important and common airway diseases, such as allergic rhinitis and asthma. Lipoxin A4 (LXA4) is an endogenous pro-resolving mediator for mucosal inflammation that decreases allergic and asthmatic responses. Lipoxin B4 (LXB4) is a structurally distinct member of the lipoxin family that signals in a manner distinct from LXA4. LXB4 is generated by mucosal tissues, but its actions in allergic inflammation are unknown. Here, we used murine models of allergic rhinitis and asthma to investigate LXB4’s activity in mucosal inflammation. In the upper airway, LXB4 significantly decreased nasal mucosal leukocytes and degranulation of mast cells and eosinophils. In the lower airway, LXB4 significantly decreased airway inflammation, mucus metaplasia and hyper- responsiveness. Inhibition of mast cell degranulation in vivo by LXB4 was more potent than dexamethasone, and these agents displayed unique profiles for cytokine regulation; however, their overall anti-inflammatory actions were comparable. LXB4 decreased eotaxin-dependent eosinophil chemotaxis, IgE-mediated mast cell degranulation and expression of type 2 cytokine receptors. Together, these findings indicate that LXB4 carries cell type selective and mucosal protective actions that broaden the lipoxin family’s therapeutic potential for upper and lower airway catabasis

Effect of Near Work on Intraocular Pressure in Emmetropes

Objective. To determine whether accommodation induced by reading alters intraocular pressure (IOP) in healthy, young, emmetropic adults and to document the duration and magnitude of this effect. Design. Cross-sectional study. Participants. Fifteen healthy, emmetropic young adults. Methods. Subjects performed 20 minutes of near work (reading at 33 cm) followed by 20 minutes of far work (reading at 520 cm) while IOP was measured using an iCare tonometer at baseline and every 5 minutes thereafter. Statistical analysis was performed using repeated measures ANOVA. Main Outcome Measures. Intraocular pressure. Results. IOP decreased significantly compared to baseline IOP after 10 minutes of near work (average change of −1.60 ± 2.2 (SD) mm Hg, p<0.05). IOP remained lower than baseline IOP throughout all subsequent near and far work. The difference in IOP at the end of experimentation compared to baseline IOP was −1.87 ± 1.81 mm Hg (p<0.05). The minimum IOP reached during experimentation compared to baseline was on average −3.8 ± 2.2 (SD) mm Hg (range: 0 to −8.0 mm Hg). 13 of 15 subjects (87%) and 9 of 15 subjects (60%) had at least one IOP measurement of at least 2 mm Hg and 4 mm Hg less than their baseline IOPs, respectively. Conclusions. Near work decreases IOP in healthy emmetropes, and this effect is sustained for at least 20 minutes after discontinuing prolonged near work. Providers may need to consider this effect when measuring IOP in clinical practice

Localization of Usher syndrome type II to chromosome 1q

Usher syndrome is characterized by congenital hearing loss, progressive visual impairment due to retinitis pigmentosa, and variable vestibular problems. The two subtypes of Usher syndrome, types I and II, can be distinguished by the degree of hearing loss and by the presence or absence of vestibular dysfunction. Type I is characterized by a profound hearing loss and totally absent vestibular responses, while type II has a milder hearing loss and normal vestibular function. Fifty-five members of eight type II Usher syndrome families were typed for three DNA markers in the distal region of chromosome 1q: D1S65 (pEKH7.4), REN (pHRnES1.9), and D1S81 (pTHH33). Statistically significant linkage was observed for Usher syndrome type II with a maximum multipoint lod score of 6.37 at the position of the marker THH33, thus localizing the Usher type II (USH2) gene to 1q. Nine families with type I Usher syndrome failed to show linkage to the same three markers. The statistical test for heterogeneity of linkage between Usher syndrome types I and II was highly significant, thus demonstrating that they are due to mutations at different genetic loci