Anaesthetic management of acute blunt thoracic trauma

Sunnybrook Health Science Centre is an adult regional trauma unit serving metropolitan Toronto and environs. We undertook a nvo-year retrospective review of patients admitted to our institution with blunt thoracic trauma. Three hundred and thirty-three patients with blunt trauma and an injury severity score (ISS) greater than 17 required emergency surgery. Of these, 208 had blunt thoracic injuries while 125 did not have chest injuries. Both groups were similar with respect to age but patients with thoracic trauma had a greater ISS. (P < 0.05) and greater intraoperative mortality (P < 0.01). The aetiology of the intraoperative deaths with one exception was exsanguination. Emergency thoracotomy or sternotomy indicated a poor prognosis with a mortality rate of 80%. The most common intraoperative problem was an elevated airway pressure. Awake intubation was undertaken in 77.5% of patients requiring anaesthesia and surgery because of the potentially compromised airways and difficult intubations due to the nature of the associated injuries. Finally, 74% of patients undergoing urgent surgery required mechanical postoperative ventilation. The presence of blunt chest trauma should be considered a marker of the severity of injury sustained by the patient.     

Insulin antibodies: methodology and clinical implications

Anti-insulin antibodies detection is based on the demonstration of a specific and saturable binding to insulin either radiolabelled with 125 I (Radiobinding assay or RBA) or coated on a solid phase (Enzyme linked immunosorbent assay or EIA). The 2 assays are remarkably different by their sensitivity to the affinity of the antigen antibody reaction. In addition, RBA may be biased by the presence of the iodine atom on the radioiodinated insulin whereas, at least on theoretical grounds. EIA could be biased because of denaturation or non availability of some epitopes when insulin is coated. Anti-insulin antibodies may be induced by insulin therapy. When they "spontaneously" appear, they are called autoantibodies. Insulin autoantibodies may be detected in the normal population, in type 1 diabetic patients before any administration of exogenous insulin and in patients suffering from the autoimmune hypoglycemic syndrome. In some patients, this syndrome may be associated with administration of a thiol containing drug. In some cases, insulin antibodies may appear several years after a transient insulin therapy, possibly as a consequence of a disturbance of the immunologic memory. The properties of antibodies and autoantibodies (concentration, affinity, number and nature of epitopes, heavy and light chain composition and ability to form aggregates) are relatively characteristic of the disease with which they are associated and determine their potential effects on insulin bioavailability and plasma glucose homeostasis.     

Katzenkratzkrankheit Eine wichtige Differentialdiagnose der Lymphadenopathie

Zusammenfassung Wir berichten über 2 F?lle von Katzenkratzkrankheit. Diese Erkrankung z?hlt zu den seltenen Ursachen einer Lymphadenopathie. Die Verdachtsdiagnose stützt sich auf Katzenkratzer in der Anamnese und die typischen Befunde mit Lymphknotenschwellung im Bereich der Prim?rl?sion.      

Immunohistochemical examination of the INK4 and Cip inhibitors in the rat neonatal cerebellum: cellular localization and the impact of protein calorie malnutrition

Expression of the cyclin-dependent kinase inhibitors (CKIs) has been linked to the inhibition of cellular proliferation and the induction of differentiation. Based on structure function analysis, two distinct families of CDKIs, the INK4 and the Cip/Kip family have been identified. The INK4 family member p16(Ink4), and the Cip/Kip protein p27(Kip1) have been implicated in normal development of the CNS and cerebellum. Recent studies have suggested a functional inter-dependence between the CKI and the abundance of cyclin D1 in orchestrating growth factor-induced cellular proliferation. The neonatal rat cerebellum undergoes proliferative growth and differentiation, localized to distinct topographical regions and cell types. The cell type and the temporal profile of CKI expression during postnatal cerebellar development had not been described. The current studies determined the specific cerebellar cell types in which the CKIs were expressed during post natal development by co-staining for cell-type specific markers. p16(Ink4a) and p27(Kip1) immunostaining was identified in both neurons and glial cells, increasing progressively between postnatal days 6 to 13 into adulthood. By contrast, neuronal and glial cell p21(Cip1) staining was prominent at days 6-11 and decreased thereafter. Cyclin D1 was expressed in the proliferating external granular cells, with occassional staining in the molecular, and internal granular layers. Dual immunostaining demonstrated cyclin D1 within cells expressing CKI (p16(Ink4a), p21(Cip1),p27(Kip1)). Cerebellar cellular growth arrest, induced by protein-calorie malnutrition, inhibited cyclin D1 protein levels without affecting CKI immunostaining suggesting CKI do not mediate the developmental arrest. These results demonstrate that the CKIs are induced by differentiation cues in specific cell types with distinct kinetics in the developing cerebellum in vivo.