Cases reported "Bronchial Spasm"

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1/14. Bronchospasm induced by cardiopulmonary bypass.

    Severe bronchospasm during cardiopulmonary bypass (CPB) is an unusual event. A 16-year-old girl with pulmonary stenosis who underwent reconstruction of the right ventricle outflow tract experienced severe bronchospasm following CPB. Just after the initiation of the partial CPB, high inspiratory airway pressure was suddenly recognized. The lung had become too stiff for the anesthetic circuit bag to be squeezed by hand. Tracheobronchial obstruction was ruled out by investigation with a fiberoptic bronchoscope. A presumptive diagnosis of severe bronchospasm was made, and aggressive bronchodilator therapy was instituted. The attack was successfully treated with aggressive bronchodilator therapy. Although the exact causes for bronchospasm in our case are not clear, CPB factors, such as the release of complements and allergic reactions might have induced the attack under relatively light anesthetic state.
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2/14. Successful management of tracheotomized patients with chronic saliva aspiration by use of constant positive airway pressure.

    OBJECTIVE: Management of chronic aspiration of saliva is a challenge to clinicians. The purpose of this report is to review the clinical course of 3 patients with tracheotomy who we have followed for at least 1 year and who have received constant positive airway pressure (CPAP) as a primary treatment for ongoing aspiration of saliva. methods: Retrospective chart review. RESULTS: We present here 3 patients with chronic congestion and persistent hypoxemia in whom a diagnosis of chronic aspiration of saliva was established by use of radionuclide salivagram. Each of these children had tracheotomy for treatment of airway obstruction. In an attempt to decrease chronic aspiration of saliva, we instituted constant positive pressure via tracheotomy. Repeat radionuclide salivagram performed on CPAP demonstrated a marked decrease in saliva aspiration. All patients experienced improvement in clinical symptoms and required only rare subsequent hospitalizations for respiratory disease. CONCLUSION: We suggest, based on this case series, that CPAP administered via a tracheotomy is an acceptable means of managing chronic salivary aspiration and that it may decrease respiratory complications in such patients.
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3/14. Spontaneous negative pressure changes: an unusual cause of noncardiogenic pulmonary edema.

    The principal physiologic mechanism underlying the formation of negative pressure pulmonary edema (NPPE) is thought to be the creation of excessive negative intrathoracic force from inspiration against a critical obstruction of the upper airway. The increased subatmospheric transpulmonary pressures result in transudation of fluid from the pulmonary capillaries to the interstitium and alveoli. The clinical picture is that of pulmonary edema. Aggressive diagnostic and therapeutic intervention can be avoided if the syndrome is recognized early. This report highlights the clinical features of NPPE and serves as a reminder to the clinician that although NPPE can cause significant morbidity, conservative supportive therapy typically results in a good outcome.
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4/14. Vasopressin for treatment of shock following aprotinin administration.

    PURPOSE: To describe the utility of vasopressin in the treatment of acute distributive shock clinically compatible with the diagnosis of aprotinin anaphylaxis. CLINICAL FEATURES: A 57-yr-old female patient underwent repeat cardiac surgery to treat prosthetic valve endocarditis. She had received aprotinin during her first surgery 60 days ago. Despite a negative test dose of i.v. aprotinin 20,000 KIU, when aprotinin loading was initiated during the repeat surgery, the patient developed bronchospasm and hypotension secondary to acute distributive shock. Bronchospasm responded to inhaled salbutamol and ipatropium. The hypotension was refractory to high doses of phenylephrine. Two doses of i.v. vasopressin 5 U reversed the vasodilation and reestablished normal blood pressure. CONCLUSION: Vasopressin, in association with alpha-agonists, can reverse acute refractory distributive shock following aprotinin administration.
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5/14. The effect of sedation with propofol on postoperative bronchoconstriction in patients with hyperreactive airway disease.

    Two patients with chronic obstructive pulmonary disease developed postoperatively bronchospasm after insertion of a prostetic aortic valve. Continuous sedation with propofol infusion was associated with a significant decline in peak inspiratory pressure suggesting that propofol may have bronchodilating properties.
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6/14. troponin i elevation in a patient with acute severe bronchospasm.

    Right ventricular strain is a source of troponin elevation in some patients with acute pulmonary embolism. Acute and/or severe obstructive airway disease could lead to a sudden increase in pulmonary arterial pressure and right ventricular afterload. We report a case of troponin i elevation in a 40-year-old woman who presented with acute severe bronchospasm and had a negative evaluation for coronary artery disease.
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7/14. Severe bronchospasm during laryngeal mask airway placement in an infant.

    A 35-day-old male infant was scheduled for bilateral inguinal herniorrhaphy. No history of recent upper airway infection or other reactive respiratory disease was noted before anesthesia. breath holding was noted immediately after laryngeal mask airway (LMA) insertion. Removal of the LMA and positive pressure ventilation via face mask did not solve the problem. On suspicion of laryngospasm, tracheal intubation facilitated by muscule relaxant was performed. However, when the patient was ventilated, high airway pressure, absence of chest wall movement and elevated end-tidal CO2 were noted. Despite visual confirmation of correct placement of tracheal tube, oxygen desaturation and bradycardia developed rapidly. After deepening the inhalational anesthesia of sevoflurane and concomitant administration of intravenous lidocaine, the patient's respiratory condition turned for the better and became compliable. Respiratory dysfunction may be caused by severe bronchospasm induced by placement of the LMA. The pathophysiology and risk factors of bronchospasm related to the LMA placement are discussed in the text.
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8/14. Utilization of pressure-volume curves in the pediatric patient.

    Seven patients treated with continuous mechanical ventialtion were monitored with static and dynamic pressure-volume curves. Three patients developed no pulmonary complications, and mechanical ventilation was discontinued within 96 hr. In four patients, pressure-volume curves were used as a diagnostic aid in the detection of the physiologic defect resulting from bronchoconstriction, atelectasis, loculated pleural fluid, pulmonary edema, and mucous plugging. These measurements were also utilized to evaluate the effectivess of therapeutic modalities such as treatment of bronchoconstriction with bronchodilators, mucous plugging with adequate suctioning, and drainage of loculated pleural effusion. Pressure-v-lume measurements are simple, noninvasive, and require the smae equipment used in continuous mechanical ventilation. Pressure-volume monitoring of pediatric patients with curves warrants further investigation to evaluate its value.
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9/14. Bronchospasm and hypotension during cardiopulmonary bypass after preoperative cimetidine and labetalol therapy.

    A 64-yr-old asthmatic patient underwent a two-vessel aortocoronary vein grafting. Before surgery, the patient received cimetidine 400 mg and labetalol 650 mg. During the first 60 min of bypass, hypotension (40-45 mm Hg) was observed in spite of phenylephrine 14 mg. This initial hypotension was followed, during rewarming, by a slow increase in arterial pressure to 150 mm Hg. On cessation of bypass, bronchospasm was observed and was protracted. It is assumed that labetalol clearance and metabolism were reduced by cimetidine, that labetalol alpha-antagonism was responsible for the vasodilatation withstanding the phenylephrine, and that a combination of labetalol beta-antagonism and phenylephrine alpha-agonism initiated the bronchospasm. These observations indicate that, after labetalol therapy, higher doses of vasopressor agents such as phenylephrine may be necessary, but that such therapy may lead to bronchospasm in asthmatic patients.
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10/14. Near-fatal bronchospasm in an asthmatic patient following ingestion of flurbiprofen. A case report.

    aspirin and other inhibitors of prostaglandin synthetase are known to precipitate bronchospasm in sensitive individuals. We describe a 42-year-old patient with mild asthma who had a near-fatal attack of bronchospasm and required intermittent positive pressure ventilation and resuscitation following ingestion of a single tablet of flurbiprofen (Froben; Boots). When prescribing such agents, an appropriate history should be taken, and when asthma or hypersensitivity to related drugs is suspected, oral challenge with a small test dose and administration of the first dose under supervision are essential.
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