22 research outputs found

    Successful use of videolaryngoscopy in an adult patient with acute epiglottitis: A case report

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    Acute epiglottitis is a potentially life-threatening infection of the supraglottic structures, which can lead to sudden, fatal airway obstruction. Different techniques have been described to facilitate tracheal intubation in acute epiglottitis. We describe the successful intubation, with the help of the videolaryngoscope, of a 60-year-old female with acute epiglottitis. On admission the patient was ill and severely distressed, sitting in the upright position, drooling saliva, showing severe inspiratory stridor, hyperventilation, but no trismus. Intubation was performed in OR conditions with difficult intubation equipment including fiberoptic bronchoscope, videolaryngscope, laryngeal mask airway and surgical tracheostomy ready for use. After pre-oxygenation for three minutes with 100% oxygen with the patient still in the sitting position, induction was performed with 250 mg propofol I.V. The patient was subsequently positioned supine. Face mask ventilation was successful with capnographic tracing and 100 mg succinylcholine was administered. Videolaryngoscopy was performed and a red, swollen epiglottitis with pin point lumen was seen. Intubation with a 5 mm microlarynx tube was successful at the first attempt. This is the first case describing intubation using videolaryngoscopy in an adult patient with acute epiglottitis. Videolaryngoscopy has already proven to be an excellent intubation device in normal and difficult airways. Direct laryngoscopy in patients with epiglottitis may be difficult due to the swelling and distortion of the airway. This case report shows that videolaryngoscopy is a good alternative intubation device option in adults with acute epiglottitis. Nevertheless, all other precautions (difficult airway trolley, surgical tracheostomy) need to be ready for immediate use

    The DD genotype of the angiotensin converting enzyme gene is negatively associated with right ventricular hypertrophy in male patients with chronic obstructive pulmonary disease.

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    Departments of Pathology, Cardiology, Pulmonology and Asthmacentre, Cardiovascular Research Institute Maastricht, The Netherlands. The renin angiotensin system plays an important role in the development of pulmonary artery remodeling and right ventricular hypertrophy in hypoxia-induced pulmonary hypertension as may occur in patients with COPD. Several polymorphisms of genes encoding for components of the renin angiotensin system such as the M235T polymorphism in the angiotensinogen gene, the 287-base-pair insertion (I)/deletion (D) polymorphism at intron 16 of the ACE gene, and the A1166C polymorphism in the angiotensin II type 1 receptor gene have been associated with an increased risk of cardiovascular diseases. With respect to the pulmonary circulation, only limited data exist on possible associations between polymorphisms of these genes and pulmonary hypertension and/or right ventricular hypertrophy. The objective of the present study was to investigate a possible relationship between polymorphisms of the renin angiotensin system and electrocardiographic evidence of right ventricular hypertrophy in patients with COPD. We therefore determined the angiotensinogen (M235T), angiotensin converting enzyme (I/D), and angiotensin II type 1 receptor (A1166C) genotypes in 87 patients with severe COPD and correlated these data with electrocardiographic parameters of right ventricular hypertrophy. Thirty-one patients (36%) of 87 patients with COPD showed electrocardiographic evidence of right ventricular hypertrophy. In the male, but not in the female, subgroup, the angiotensin-converting enzyme DD genotype was negatively associated with electrocardiographic evidence of right ventricular hypertrophy (male: chi2 = 3.8, p = 0.05; female: chi2 = 0.05, p = 0.82). We found no associations between the investigated polymorphisms in the angiotensinogen and angiotensin II type 1 receptor genes and electrocardiographic evidence of right ventricular hypertrophy
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