2 resultados para INJURED CONSPECIFICS
Resumo:
Inhalation injuries are currently the factor most responsible for mortality in thermally injured patients. Inhalation injuries may occur independently, but generally occur together with skin burn. Smoke inhalation affects all levels of the respiratory system and the extent of the inhalation injury depends on the duration, exposure, amount and toxicity of the fume temperature, concentration and solubility of toxic gases, the occurrence of the accident in a closed space and pre-existing diseases. Smoke inhalation also induces changes in the systemic organs with the need for more fluid for resuscitation. Systemic vasoconstriction, with an elevation in systemic vascular resistance, a fall in myocardial contractility and a great increase in lymphatic flow in soft tissue are the most important changes in systemic organs. On admission of a burn patient there is a high suspicion of inhalation injury when there are signs and symptoms such as hoarseness, strides, dyspnea, carbonaceous sputum, anxiety or disorientation, with or without face burns. The patient with these findings has partial airway obstruction and there is substantial risk complete airway obstruction occurring of secondary to the edema. Patients with suspected inhalation injury should be intubated so as to maintain airway patency and avoid a total obstruction. This group of patients frequently develop respiratory failure with the need for mechanical ventilatory support. Nosocomial infections, sepsis and multiple organ system failure may occur. Late complications of inhalation injury are tracheitis, tracheal stenosis or tracheomalacia and chronic airway disease, which is relatively rare. Early diagnosis of inhalation injury and treatment in a Burn Unit by a group of highly motivated clinicians and a good team of nurses is essential in order to decrease the morbidity and mortality related to inhalation injury.
Resumo:
Background: Proteinuria (PT) with SRL appears not only after conversion from a calcineurin inhibitor (CI), but also in de novo patients. The PT may be related to a hemodynamic effect of CI withdrawal or to a direct effect of SRL in glomerulus (GL). Recently an association between PT in SRL patients and FSGS lesions has been described. It is also known that SRL decrease VEGF synthesis and experimental data suggest that VEGF is essential to podocyte survival and differentiation. Aim: To determine if glomerular lesions and PT in SRL patients could be related to altered glomerular VEGF expression. Material and methods: We evaluated glomerular VEGF expression in 10 biopsies: A-allograft kidney in backtable (n=3); B-native normal kidney (n=1); C-native kidney with FSGS lesions (n=2); D-allograft kidney with FSGS lesions from proteinuric patients under SRL after conversion from CI (n=3); E-allograft kidney in proteinuric patient under SRL with a membranous glomerulonephritis (n=1). We employed indirect immunohistochemistry in paraffin-embedded sections using a mouse monoclonal antibody against human VEGF-C1 (Santa Cruz). Results: The controls biopsies (A; B) showed normal global VEGF expression, with strong podocyte staining. The VEGF expression in the group C was similar to the controls, although no FSGS lesions were observed in the stained GL. The group D showed normal VEGF expression in the apparently normal GL, hypertrophied podocytes with reduction of VEGF in anomalous GL, and no staining in slcerotic lesions. We observed a gradual reduction of VEGF expression with progressive dedifferentiation of podocytes. In the group E the VEGF was globally reduced, with some hypertrophied podocytes expressing decreased VEGF. Conclusion: We confirmed the diminished VEGF expression in injured podocytes of SRL patients.This decreased expression may result from a direct effect of SRL and precede the appearance of FSGS lesions and PT. Further studies are needed with greater number of cases and controls, including early biopsies of patients under SRL.