Cases reported "Asthma"

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1/56. subarachnoid hemorrhage following permissive hypercapnia in a patient with severe acute asthma.

    In this article, we describe a case of a subarachnoid hemorrhage (SAH) in an acute severe asthma patient following mechanical hypoventilation. A 49-year-old man was admitted to an intensive care Unit with an acute exacerbation of asthma. After 3 days of mechanical ventilation (hypercapnia and normoxaemia), it was noted that his right pupil was fixed, dilated, and unreactive to light. Computed tomography (CT) scan showed localized SAH within the basilar cisterns and diffuse cerebral swelling. On the fourth day, a new CT scan showed hemorrhage resorption and a cerebral swelling decrease. In the following days, the patient's condition continued improving with no detectable neurological deficits. A review of similar published reports showed that all patients performed respiratory acidosis, normoxaemia, and hypercapnia. The most frequent neurological sign was mydriasis, and all subjects showed cerebral edema. Since normoxaemic hypercapnia has been associated with absence, or less cerebral edema, we considered additional factors to explain cerebral edema and intracranial hypertension causes. Thus, intrathoracic pressures due to patient's efforts by forcibly exhaling, or during mechanical ventilation, would further increase intracranial pressure by limiting cerebral venous drainage. This case emphasizes the fact that patients with acute severe asthma who have developed profoundly hypercarbic without hypoxia before or during mechanical ventilation, may have raised critical intracranial pressure.
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2/56. Too hot to handle: an unusual exposure of HDI in specialty painters.

    BACKGROUND: Hexamethylene Diisocyanate (HDI) is a color stable aliphatic isocyanate that is used in specialty paints as a hardener. Due to the lower vapor pressure of its commercial biuret form, it is considered a relatively "safe" isocyanate from an exposure standpoint. This case series reports on an unusual toxic exposure to HDI. Between November 1993 and May 1994, seven specialty painters and one boiler maker who were working at three different power plants were examined at the Institute of Occupational and environmental health at west virginia University. At their respective work sites, HDI was applied to the hot surfaces of boilers that were not shut down, and allowed sufficient time to cool. Consequently, these workers were exposed to volatile HDI and its thermal decomposition products. methods: All of these workers underwent a complete physical examination, spirometry, and methacholine challenge testing. RESULTS: All 8 workers complained of dyspnea, while 4 of the 8 also complained of rash. On examination 3 workers were methacholine challenge positive and 2 had persistent rash. At follow-up 4 years later, 5 workers still had to use inhalation medication and one had progressive asthma and dermatitis. All 8 workers, by the time of the follow-up, had gone through economic and occupational changes. CONCLUSIONS: This case series reports on an unusual exposure to HDI. It is unusual in that: 1) There were two simultaneous sentinel cases with two different material safety data sheets (MSDS) for the same product, 2) Exposure was to volatile HDI and its decomposition products and 3) Hazardous conditions of exposure occurred at three different sites.
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3/56. hyperthyroidism complicating asthma treatment.

    asthma is one of the most common chronic medical conditions. The usual treatment includes quick relief bronchodilator medications of the sympathomimetic class and controller medications that may include the long-acting inhaled bronchodilator salmeterol. Mild adverse cardiac and central nervous system effects are common with these medications, requiring modifications in dose or occasionally switching to a different medication. Both asthma and thyroid disease are common disorders that occasionally occur together. hyperthyroidism may exacerbate asthma. Many symptoms of hyperthyroidism are identical to the adverse effects of the commonly used inhaled bronchodilators and include tremor, nervousness, tachycardia, wide pulse pressure, palpitations, emotional lability, agitation, nightmares, aggressive behavior, and diarrhea. In this report we describe a patient with hyperthyroidism whose symptoms initially were thought to be adverse effects of the inhaled bronchodilator medications.
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4/56. churg-strauss syndrome complicated by eosinophilic endomyocarditis.

    A 34-year-old woman with asthma had increasing dyspnea on exertion for 9 months and new-onset mononeuritis multiplex. An examination demonstrated sinus tachycardia, elevated jugular venous pressure, and a tender nonpulsatile liver. The leukocyte count was 15.8 x 10(9)/L, with 23% eosinophils. echocardiography revealed a laminated thrombus obliterating much of the right ventricular cavity, with encasement of the tricuspid valve. Ultrafast computed tomography showed no evidence of pulmonary emboli. biopsy specimens of skin nodules revealed extravascular palisading granulomas. The thrombus was refractory to corticosteroids, and right ventricular thrombectomy was performed. To our knowledge, this is the third reported case of churg-strauss syndrome with thrombotic complications from coexistent eosinophilic endomyocarditis. In an asthmatic patient with chronic dyspnea, eosinophilic tissue infiltration, and neuropathy, churg-strauss syndrome should be considered; evaluation for cardiac involvement may be warranted.
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5/56. asthma mortality: an analysis of one years experience, review of the literature and assessment of current modes of therapy.

    This analysis of asthma mortality has emphasized the roles played in its pathogenesis by different modes of therapy as reported in the literature. In addition attention was directed towards yet another potentially lethal therapeutic modality, IPPB, the efficacy and potential benefits of which are critically questioned. IPPB treatments were related to every fatal episode of asthma which made up the entire asthma mortality experience during a 12 month period at Morrisania Hospital. The adverse consequences of IPPB therapy were reviewed and it was further suggested that its use in acute asthma attacks was related to lethal episodes of hypoxia and pneumothorax. The patient must, in order to trigger an IPPB apparatus, create a pre-determined negative pressure to initiate inflation. The machine may, therefore, be ineffective in a patient with severe obstruction and greatly increased airway resistance either because of the inability to trigger it or with adequate triggering the subsequent delivery of an inadequate tidal volume at the pressure limitation set. Thus, severe hypercapnia and hypoxia may result especially if oxygen enriched gas mixtures are not used. This may occur even with the delivery of an adequate tidal volume since its distribution within the lungs is poor resulting in a worsening of ventilation-perfusion relationships as evidenced by an increase in the measured physiologic dead space. This experience and review of the literature suggests that IPPB treatment in asthma, especially during an acute attack, should always be administered with small doses of nebulized bronchodilators and oxygen with careful monitoring of arterial blood gases. This will allow for the detection of the adverse effects of this mode of therapy which may exceed the hoped for benefits, the most important being bronchodilatation and subsequent mobilization of secretions with continued treatment.
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6/56. Tension pneumoperitoneum aggravating respiratory failure. A case report.

    A case of tension pneumoperitoneum secondary to barotrauma is reported. Any patient needing high pressures for ventilation and oxygenation is prone to this complication. The important respiratory and haemodynamic implications are discussed. It is suggested that drainage of a tension pneumoperitoneum is easy and safe and has major beneficial effects on the respiratory and cardiovascular systems.
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7/56. Use of olprinone, a phosphodiesterase III inhibitor, in an asthmatic patient.

    Phosphodiesterase (PDE) III exists in airway smooth muscles. In addition, PDEIII inhibitors have been suggested to relax airway smooth muscle by increasing intracellular cAMP concentrations. We report a successful use of olprinone, a PDEIII inhibitor, for treatment of an asthmatic attack. A 15-year-old male patient treated with oral theophylline 400 mg x d(-1) was anesthetized with propofol, fentanyl and ketamine for knee joint surgery. Immediately after tracheal intubation, an asthma attack occurred with peak airway pressure (Paw)>40 cmH2O. Thus, propofol 20 mg was additionally given to increase anesthetic depth, and Paw gradually decreased to 30 cmH2O. In addition, we started monitoring bronchial cross-sectional area using a superfine fiberoptic bronchoscopic method previously reported. However, as Paw did not further decrease for 30 min, olprinone was intravenously infused (10 microg x kg(-1) x 10 min(-1) 0.3 microg x kg(-1) x min(-1), total 5 mg). Olprinone infusion rapidly decreased peak Paw from 30 cmH2O to 24 cmH2O and increased bronchial cross-sectional area by 50%. These findings suggest that olprinone produced bronchodilation.
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8/56. intraocular pressure elevation in a child due to the use of inhalation steroids--a case report.

    inhalation steroid therapy can cause ocular hypertension or open angle glaucoma. The authors describe the case of a young girl who presented with raised intraocular pressure and headaches due to the prolonged administration of nasal and inhalation steroids. The ophthalmologist should monitor the intraocular pressure in patients who use inhalation or nasal steroid therapy on a regular base. The physician or paediatrician should be aware of this complication in children with headaches or diminished visual acuity.
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9/56. The upper airway resistance syndrome masquerading as nocturnal asthma and successfully treated with an oral appliance.

    Over the past 10 years, our ability to recognize, treat, and identify the morbidity associated with the upper airway resistance syndrome (UARS) has improved vastly. The diagnosis of this syndrome is dependent on a high degree of clinical suspicion, and in the presence of an already known pulmonary disease such as asthma, the identification of UARS may be elusive. Treatment of this condition has received more recent attention in the literature, with oral appliance therapy as a viable treatment option in place of the usual positive-pressure ventilation devices.
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10/56. Case report and literature review of chlorine gas toxicity.

    chlorine gas exposure is uncommon in children and when it occurs usually results in mild ocular, oropharyngeal, or respiratory symptoms. Occasionally, however, chlorine gas poisoning may cause severe pulmonay toxicity. We report the case of a 14-y-old boy with a history of asthma who was exposed to chlorine gas as a result of an ill-advised science experiment. His clinical condition deteriorated over the course of several hours, and he required intubation and ventilatory support. During his hospitalization, he developed the acute respiratory distress syndrome. He was treated with positive pressure ventilation, beta-adrenergic agonists, and corticosteroids. After 19 d, he was extubated and subsequently made an excellent recovery. We discuss his case and review the etiology, pathophysiology, clinical presentation, laboratory findings, treatment and possible long-term sequelae of chlorine gas toxicity.
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