Educomunicação, Transformação Social e Desenvolvimento Sustentável

Esta publicação apresenta os principais trabalhos dos GTs do II Congresso Internacional de Comunicação e Educação nos temas Transformação social, com os artigos que abordam principalmente Educomunicação e/ou Mídia-Educação, no contexto de políticas de diversidade, inclusão e equidade; e, em Desenvolvimento Sustentável os artigos que abordam os avanços da relação comunicação/educação no contexto da educação ambiental e desenvolvimento sustentável

Edema pulmonar neurogênico: relato de dois casos Neurogenic pulmonary edema: report of two cases

O edema pulmonar neurogênico é rara e grave complicação de pacientes com traumatismo craniencefálico (TCE). Pode ocorrer também em outras patologias do sistema nervoso central, tais como acidentes vasculares cerebrais (AVC), tumores ou após crises epilépticas, entre outras. Foram avaliados 36 casos com TCE grave e quatro pacientes com AVC, internados na UTI geral, no período de janeiro a setembro 1995. Nesse intervalo de tempo foram diagnosticados dois casos de edema pulmonar neurogênico, um ocorrendo em paciente com TCE grave e outro em paciente com AVC hemorrágico. O diagnóstico foi estabelecido pelo rápido desenvolvimento de edema pulmonar, com hipoxemia grave, queda da complacência pulmonar e infiltrados difusos bilaterais sem história prévia de aspiração traqueal ou outro fator de risco para o desenvolvimento de síndrome de angústia respiratória aguda. No primeiro paciente com trauma craniencefálico, o edema neurogênico foi diagnosticado na internação, uma hora após o trauma, com concomitante reação inflamatória grave e boa evolução em três dias. O outro caso, com AVC hemorrágico, desenvolveu edema neurogênico no quarto dia após drenagem de hematoma intraparenquimatoso, evoluindo para o óbito.Neurogenic pulmonary edema is a rare and serious complication in patients with head injury. It also may develop after a variety of cerebral insults such as subarachnoid hemorrhage, brain tumors and after epileptic seizures. Thirty six patients with severe head injury and four patients with cerebrovascular insults treated in Intensive Care Unit of HC-UNICAMP from January to September 1995 were evaluated. In this period there were two patients with neurogenic pulmonary edema, one with head injury and other with intracerebral hemorrhage. Diagnosis was made by rapid onset of pulmonary edema, severe hypoxemia, decrease of pulmonary complacence and diffuse pulmonary infiltrations, without previous history of tracheal aspiration or any other risk factor for developement of adult respiratory distress syndrom. In the first case, with severe head trauma, neurogenic pulmonary edema was diagnosed at admission one hour after trauma, associated with severe systemic inflammatory reaction, and good outcome in three days. The second case, with hemorragic vascular insult, developed neurogenic pulmonary edema the fourth day after drenage of intracerebral hematom and died

Neurogenic pulmonary edema: report of two cases

Neurogenic pulmonary edema is a rare and serious complication in patients with head injury. It also may develop after a variety of cerebral insults such as subarachnoid hemorrhage, brain tumors and after epileptic seizures. Thirty six patients with severe head injury and four patients with cerebrovascular insults treated in Intensive Care Unit of HC-UNICAMP from January to September 1995 were evaluated. In this period there were two patients with neurogenic pulmonary edema, one with head injury and other with intracerebral hemorrhage. Diagnosis was made by rapid onset of pulmonary edema, severe hypoxemia, decrease of pulmonary complacence and diffuse pulmonary infiltrations, without previous history of tracheal aspiration or any other risk factor for developement of adult respiratory distress syndrom. In the first case, with severe head trauma, neurogenic pulmonary edema was diagnosed at admission one hour after trauma, associated with severe systemic inflammatory reaction, and good outcome in three days. The second case, with hemorragic vascular insult, developed neurogenic pulmonary edema the fourth day after drenage of intracerebral hematom and died.O edema pulmonar neurogênico é rara e grave complicação de pacientes com traumatismo craniencefálico (TCE). Pode ocorrer também em outras patologias do sistema nervoso central, tais como acidentes vasculares cerebrais (AVC), tumores ou após crises epilépticas, entre outras. Foram avaliados 36 casos com TCE grave e quatro pacientes com AVC, internados na UTI geral, no período de janeiro a setembro 1995. Nesse intervalo de tempo foram diagnosticados dois casos de edema pulmonar neurogênico, um ocorrendo em paciente com TCE grave e outro em paciente com AVC hemorrágico. O diagnóstico foi estabelecido pelo rápido desenvolvimento de edema pulmonar, com hipoxemia grave, queda da complacência pulmonar e infiltrados difusos bilaterais sem história prévia de aspiração traqueal ou outro fator de risco para o desenvolvimento de síndrome de angústia respiratória aguda. No primeiro paciente com trauma craniencefálico, o edema neurogênico foi diagnosticado na internação, uma hora após o trauma, com concomitante reação inflamatória grave e boa evolução em três dias. O outro caso, com AVC hemorrágico, desenvolveu edema neurogênico no quarto dia após drenagem de hematoma intraparenquimatoso, evoluindo para o óbito.30530

[influence Of The Respiratory Physiotherapy On Intracranial Pressure In Severe Head Trauma Patients].

To evaluate influence of the respiratory physiotherapy on intracranial pressure (ICP) in patients with severe head trauma. Thirty five patients with severe head trauma were included in the study. The patients were divided into three groups: ICP 0-10, 11-20 and 21-30 mmHg. The following variables were measured: ICP and mean arterial pressure. Cerebral perfusion pressure was calculated as the difference between mean arterial and intracranial pressure. Endotracheal aspiration increased ICP in all patients. The mean arterial pressure didn't change and cerebral perfusion pressure decreased, but remaining normal value. Respiratory physiotherapy maneuvers can be safely applied in patients with severe head trauma with ICP below 30 mmHg. More attention should be taken during endotracheal aspiration.63110-

Flebotomíneos de Timóteo, Estado de Minas Gerais, Brasil (Diptera: Psychodidae) Sand flies in Timóteo, Minas Gerais, Brazil (Diptera: Psychodidae)

Casos esporádicos de leishmaniose tegumentar têm ocorrido no Município de Timóteo, Minas Gerais, basicamente na população rural. Para conhecer a fauna de flebotomíneos da região, foram instaladas sete armadilhas luminosas de New Jersey na cidade, em sete diferentes bairros. As coletas foram realizadas no período de junho a outubro de 1994, dezembro de 1994 e janeiro a março de 1995, com um total de 3.240 horas por armadilha. Foram capturados 4.396 flebotomíneos, distribuídos em dois gêneros e vinte espécies: Brumptomyia cunhai, Brumptomyia nitzulescui, Lutzomyia (Nyssomyia) whitmani, Lutzomyia (Nyssomyia) intermedia, Lutzomyia quinquefer, Lutzomyia lenti, Lutzomyia (Pintomyia) fischeri, Lutzomyia migonei, Lutzomyia sallesi, Lutzomyia termitophila, Lutzomyia aragaoi, Lutzomyia borgmeieri, Lutzomyia (Psathyromyia) lutziana, Lutzomyia (Sciopemyia) sordellii, Lutzomyia (Pintomyia) pessoai, Lutzomyia (Trichopygomyia) longispina, Lutzomyia misionensis, Lutzomyia (Psychodopygus) davisi, Lutzomyia lanei, Lutzomyia (Pressatia) sp. A espécie L. (N.) whitmani foi a mais freqüente com 52,12%, seguida de L. (N.) intermedia com 34,10%, e ambas podem estar participando da transmissão de leishmaniose cutânea na região.<br>Sporadic cases of tegumentary leishmaniasis have occurred in Timóteo, Minas Gerais State, basically among the rural population. In order to study the region's sand fly population, New Jersey light traps were set in seven different neighborhoods. Specimens were gathered from June through October 1994, December 1994, and January through March 1995, with a total of 3,240 hours per trap. A total of 4,396 sand flies were captured, distributed among two genera and twenty species: Brumptomyia cunhai, Brumptomyia nitzulescui, Lutzomyia (Nyssomyia) whitmani, Lutzomyia (Nyssomyia) intermedia, Lutzomyia quinquefer, Lutzomyia lenti, Lutzomyia (Pintomyia) fischeri, Lutzomyia migonei, Lutzomyia sallesi, Lutzomyia termitophila, Lutzomyia aragaoi, Lutzomyia borgmeieri, Lutzomyia (Psathyromyia) lutziana, Lutzomyia (Sciopemyia) sordellii, Lutzomyia (Pintomyia) pessoai, Lutzomyia (Trichopygomyia) longispina, Lutzomyia misionensis, Lutzomyia (Psychodopygus) davisi, Lutzomyia lanei, Lutzomyia (Pressatia) sp. The species L. (N.) whitmani was the most frequent, with 52.12% of the total, followed by L. (N.) intermedia with 34.10%, and both may be involved in transmission of tegumentary leishmaniasis in the region

Safety and Outcomes Associated with the Pharmacological Inhibition of the Kinin–Kallikrein System in Severe COVID-19

Background: Coronavirus disease 19 (COVID-19) can develop into a severe respiratory syndrome that results in up to 40% mortality. Acute lung inflammatory edema is a major pathological finding in autopsies explaining O2 diffusion failure and hypoxemia. Only dexamethasone has been shown to reduce mortality in severe cases, further supporting a role for inflammation in disease severity. SARS-CoV-2 enters cells employing angiotensin-converting enzyme 2 (ACE2) as a receptor, which is highly expressed in lung alveolar cells. ACE2 is one of the components of the cellular machinery that inactivates the potent inflammatory agent bradykinin, and SARS-CoV-2 infection could interfere with the catalytic activity of ACE2, leading to the accumulation of bradykinin. Methods: In this case control study, we tested two pharmacological inhibitors of the kinin–kallikrein system that are currently approved for the treatment of hereditary angioedema, icatibant, and inhibitor of C1 esterase/kallikrein, in a group of 30 patients with severe COVID-19. Results: Neither icatibant nor inhibitor of C1 esterase/kallikrein resulted in changes in time to clinical improvement. However, both compounds were safe and promoted the significant improvement of lung computed tomography scores and increased blood eosinophils, which are indicators of disease recovery. Conclusions: In this small cohort, we found evidence for safety and a beneficial role of pharmacological inhibition of the kinin–kallikrein system in two markers that indicate improved disease recovery