The Experts below are selected from a list of 249 Experts worldwide ranked by ideXlab platform
Michael J. Silka - One of the best experts on this subject based on the ideXlab platform.
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Bronchospasm AFTER INTRAVENOUS ADMINISTRATION OF ADENOSINE IN A PATIENT WITH ASTHMA
The Journal of Pediatrics, 1994Co-Authors: Curt G. Degroff, Michael J. SilkaAbstract:Abstract We describe a 13-year-old patient with asthma in whom severe Bronchospasm developed immediately after the intravenous administration of 12 mg of adenosine. The risk of Bronchospasm in patients with reactive airway disease may favor the use of alternative methods for the termination of supraventricular tachycardia. (J P EDIATR 1994;125:822-3)
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Bronchospasm after intravenous administration of adenosine in a patient with asthma.
The Journal of pediatrics, 1994Co-Authors: Curt G. Degroff, Michael J. SilkaAbstract:We describe a 13-year-old patient with asthma in whom severe Bronchospasm developed immediately after the intravenous administration of 12 mg of adenosine. The risk of Bronchospasm in patients with reactive airway disease may favor the use of alternative methods for the termination of supraventricular tachycardia.
Matthias Eikermann - One of the best experts on this subject based on the ideXlab platform.
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Negative pressure pulmonary edema following Bronchospasm.
Chest, 2011Co-Authors: David J. Krodel, Robert H. Brown, Edward A. Bittner, Raja-elie E. Abdulnour, Matthias EikermannAbstract:Negative pressure pulmonary edema (NPPE) is an important cause of noncardiogenic pulmonary edema but is rarely reported in the setting of Bronchospasm. A 43-year-old woman with severe reactive airway disease suffered an episode of severe Bronchospasm after endotracheal extubation following an otherwise uneventful general anesthetic. Subsequently, she developed clinical and radiographic signs of pulmonary edema in the absence of other symptoms of acute left-sided heart failure, leading to the diagnosis of noncardiogenic pulmonary edema. She received noninvasive positive pressure ventilation for a few hours, after which her clinical and radiologic signs and symptoms of pulmonary edema were greatly improved. This clinical scenario strongly suggests NPPE. We submit that it is possible to create NPPE by generating highly negative intrathoracic pressures in the setting of severe Bronchospasm.
Alfonso López-pérez - One of the best experts on this subject based on the ideXlab platform.
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Bronchospasm triggered by spinal anaesthesia. Case report and review of the literature
Colombian Journal of Anesthesiology, 2016Co-Authors: Ana María Rodilla-fiz, Marta Gómez-garrido, Fernando Martínez-lópez, José Ángel Monsalve-naharro, María Girón-la Casa, Alfonso López-pérezAbstract:Bronchospasm is a clinical condition that can occur unexpectedly during general anaesthesia, but is extremely rare after spinal anaesthesia. The following is a case presentation of a patient who developed Bronchospasm after undergoing spinal anaesthesia not attributable to other causes, and that adds another case to the limited literature. Most publications allude to asthmatic patients, and this is probably the first description about a patient with emphysema-type COPD. Our case shows that although spinal anaesthesia is considered safe for patients with respiratory disease, specifically in asthmatic patients there is a possibility of Bronchospasm in susceptible patients.
Hae Jin Lee - One of the best experts on this subject based on the ideXlab platform.
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Anticholinergic Relieves Bronchospasm Occurring during Spinal Anesthesia in a Asthmatic Patient - A case report -
Korean Journal of Anesthesiology, 2007Co-Authors: Chang Hoon Choi, Hae Jin LeeAbstract:Placement of the endotracheal tube is a potent airway irritant that may trigger Bronchospasm in asthmatic patients. But Bronchospasm has been reported in association with regional anesthesia, but no clear understanding of the mechanism involved. This case describes acute Bronchospasm during spinal anesthesia in lower limb surgery. In this case, Bronchospasm was relieved by intravenous injection of glycopyrrolate, not by β-agonist inhaler. We experienced repeated Bronchospasm which was also very effectively treated by intravenous injection of glycopyrrolate. (Korean J Anesthesiol 2007; 53: 259~61)
Hae Keum Kil - One of the best experts on this subject based on the ideXlab platform.
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Negative pressure pulmonary edema related to Bronchospasm during anesthetic recovery.
Korean journal of anesthesiology, 2013Co-Authors: Kwan Hyung Kim, Hae Keum KilAbstract:Negative pressure pulmonary edema (NPPE) related to upper airway obstruction is a well-described phenomenon [1], but NPPE related to Bronchospasm has only rarely been reported [2]. We experienced NPPE during recovery from anesthesia in 77-year-old male with gastric cancer patient who underwent robot-assisted total gastrectomy. The patient was 157 cm tall and weighed 47.5 kg, and was a non-smoker with no allergy or medico-surgical history except for antihypertensive medication (bisoprolol for 1 yr). Preoperative laboratory findings, including pulmonary function test, were within normal ranges. Anesthesia was induced with propofol, remifentanil, and rocuronium and the anesthetic procedure proceeded without incident. Although peak airway pressure and PetCO2 increased during CO2 insufflation for pneumoperitoneum, they normalized after intravenous patient controlled analgesia (PCA) (fentanyl 1,000 µg/100 ml normal saline, 2 ml/hr) connection during surgery. Surgery was completed uneventfully in 190 min, and fentanyl (35 µg) was administered for analgesia. The endotracheal tube was removed when the patient responded to verbal commands, and neuromuscular function was then ascertained by train-of-four stimulation. However, after several minutes of assisted ventilation with a mask, the patient became drowsy, unresponsive to verbal commands or physical stimulation, and his spontaneous respiration weakened. Because pupil constriction was noted, PCA was discontinued and naloxone (0.4 mg) was slowly administered. Manual ventilation was maintained for 2-3 min while waiting the patient's awakening, when the patient coughed severely and subsequently developed signs of Bronchospasm, such as, wheezing at forced exhalation and use of accessory muscles. Because ventilation was difficult via the oropharyngeal airway despite appropriate manipulations, tracheal intubation was performed with thiopental 50 mg and succinylcholine 50 mg. On auscultation, inspiratory and expiratory wheezing were apparent over the entire lung field. Arterial blood gas analysis (ABGA) immediately before intubation revealed pH 7.156, PCO2 75.8 mmHg, and PO2 84.4 mmHg. Controlled ventilation was maintained by isoflurane administration. Peak airway pressure was 48 mmHg at a tidal volume of 400 ml. Repeat ABGA revealed pH 7.283, PCO2 50.8 mmHg, and PO2 113.1 mmHg with a FiO2 of 1.0. Airway pressure was gradually decreased to 15 mmHg and signs of Bronchospasm resolved 3 min after epinephrine 0.05 mg i.v. was administered. After 3-4 min of controlled ventilation, a pink and frothy secretion was noted inside the endotracheal tube, and breathing sounds were coarse over the entire lung field on auscultation. Furosemide 20 mg was administered and 8 cmH2O positive endexpiratory pressure was applied for possible pulmonary edema. Plain chest radiography revealed bilateral perihilar interstitial and alveolar infiltrates (Fig. 1). The patient was transferred to the intensive care unit for ventilatory care. After applying synchronized intermittent mandatory ventilation and continuous positive airway pressure mode for 12 hr under sedation, symptoms and signs improved. He was then extubated and nasal oxygen was supplied. ABGA showed values within normal range and the patient's general condition was improved. The patient was transferred to a general ward on POD 2. Fig. 1 Chest AP just after the pulmonary edema was detected. In this patient, Bronchospasm, which occurred during recovery from anesthesia, is believed to have been a cause of the pulmonary edema. Negative intrathoracic pressure is generated in the chest when a patient attempts to inspire against constricted airways during Bronchospasm. Furthermore, this acute drop in intrathoracic pressure increases venous return to the right heart, and thus, increases pulmonary venous pressure. In addition, this increase in pressure in the venous circulation creates a transpulmonary hydrostatic pressure gradient and generates fluid movement. Allergic Bronchospasm is not a rare phenomenon in patients with a hypersensitive airway or asthma during anesthesia or recovery. However, our patient (a lifelong non-smoker) had no history of airway disease, and his preoperative pulmonary status was in the normal range. Non-allergic Bronchospasm may also occur immediately after nonspecific stimuli [3]. In a survey of perioperative Bronchospasm, non-allergic Bronchospasm was found to be more frequent (79%) than allergic Bronchospasm, and 20% of non-allergic Bronchospasms were found to occur during the emergence/recovery period [4]. An acute increase in airway responsiveness may result from irritation of the well-innervated airway by a foreign body, such as, an endotracheal tube or suction catheter, or by secretions. In a large cohort study conducted by Schwilk et al. [5], the incidence of perioperative Bronchospasm was 0.2% among 15,415 non-smoking patients without respiratory disease. In our patient, we believe that Bronchospasm resulted from irritation by aspirated oral secretions during manual ventilation during re-narcotization. Non-allergic Bronchospasm is usually not associated with cardiovascular symptom, but hypoxia following inadequate ventilation may lead to cardiovascular collapse, and may occasionally result in NPPE [3].
