FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W3149705488> ?p ?o ?g. }

• W3149705488 endingPage "e201" @default.
• W3149705488 startingPage "e197" @default.
• W3149705488 abstract "Case PresentationA 27-year-old man was hospitalized in the burn unit after sustaining an acute inhalational injury and facial burns after an accidental occupational exposure to an industrial disinfectant consisting of a mixture of hydrogen peroxide (15%-30%), acetic acid (5%-15%), and peracetic acid (5%-15%). He demonstrated cough, shortness of breath, and hoarseness of voice at presentation that had developed 6 h after exposure. In addition to the inhalational injury of the vocal cords and lower airways on bronchoscopy (Fig 1), the patient also was diagnosed with acute inhalational pneumonitis based on the findings of hypoxemic respiratory failure and bilateral perihilar airspace opacities on chest radiography (Fig 2). He required intubation and mechanical ventilation initially for 2 days for upper airway edema and was discharged 19 days after exposure with resolution of hypoxemia and reduction of airspace opacities on chest radiography. However, symptoms of productive cough and shortness of breath on exertion persisted, and he was rehospitalized 27 days after exposure. He was a nonsmoker with no prior history of atopy, asthma, or lung disease. His medical history was remarkable for hypertension and severe obesity with a BMI of 34.7 kg/m2. A 27-year-old man was hospitalized in the burn unit after sustaining an acute inhalational injury and facial burns after an accidental occupational exposure to an industrial disinfectant consisting of a mixture of hydrogen peroxide (15%-30%), acetic acid (5%-15%), and peracetic acid (5%-15%). He demonstrated cough, shortness of breath, and hoarseness of voice at presentation that had developed 6 h after exposure. In addition to the inhalational injury of the vocal cords and lower airways on bronchoscopy (Fig 1), the patient also was diagnosed with acute inhalational pneumonitis based on the findings of hypoxemic respiratory failure and bilateral perihilar airspace opacities on chest radiography (Fig 2). He required intubation and mechanical ventilation initially for 2 days for upper airway edema and was discharged 19 days after exposure with resolution of hypoxemia and reduction of airspace opacities on chest radiography. However, symptoms of productive cough and shortness of breath on exertion persisted, and he was rehospitalized 27 days after exposure. He was a nonsmoker with no prior history of atopy, asthma, or lung disease. His medical history was remarkable for hypertension and severe obesity with a BMI of 34.7 kg/m2. During the second hospitalization, the patient demonstrated a temperature of 35.8°C, BP of 158 mm Hg systolic and 100 mm Hg diastolic, pulse rate of 90 beats/min, and oxygen saturation of 95% on ambient air. He was not tachypneic. Breath sounds were equal and vesicular bilaterally on auscultation with no rhonchi. The remainder of the examination findings were unremarkable.Figure 2A, Chest radiograph obtained on admission showing bilateral perihilar airspace opacities. B, High-resolution CT scan showing ground-glass changes in the upper lobes of the lungs bilaterally in a peribronchovascular distribution.View Large Image Figure ViewerDownload Hi-res image Download (PPT) Laboratory studies revealed a hemoglobin level of 15.7 g/dL, WBC count of 9.21 × 109 cells/L, with a normal differential. Chest radiography showed near complete resolution of the airspace opacities that were present initially. Spirometry performed on day 30 showed severe airflow obstruction (FEV1, 1.03 L, 26% predicted) with no bronchodilator reversibility (Fig 3) and a reduction in diffusion capacity (41% predicted). Bronchoprovocation testing could not be performed because of the severe reduction in FEV1 and FVC. Bronchoscopy performed on day 34 showed no strictures of the trachea or bronchi. Aerobic culture from BAL showed positive results for Klebsiella pneumoniae. He was treated with inhaled ipratropium bromide 20 μg two puffs three times daily, a 1-week course of oral amoxicillin-clavulanic acid 625 mg three times daily, and oral prednisolone 30 mg once daily that was tapered gradually over 1 month. After discharge, he was seen in the outpatient clinic, and lung function testing showed persistent severe airflow obstructive pattern with near-normalization of diffusion capacity (Table 1). High-resolution CT scan performed at 16 weeks after exposure also showed complete resolution of ground-glass opacities.Table 1Serial Lung Function Test ResultsDuration After Exposure30 D18 Wk64 Wk32 MoPredictedActual% PredictedPredictedActual% PredictedPredictedActual% PredictedPredictedActual% PredictedSpirometry.................................... FEV1, L3.951.03263.921.42363.891.58413.851.8447 FVC, L4.972.27464.953.17644.933.16644.894.0181 FEV1/FVC, %844554834554835060834655Diffusion.................................... Dlcounc, mM/min/kPa11.074.694211.007.576910.938.8080——— Dlcocor, mM/min/kPa11.074.564111.007.106510.938.1875——— DL/VA, mM/min/kPa/L1.871.59851.861.63881.851.87101——— Hgb, gm/dL12-1815.7—12-1817.2—12-1817.6————DLCOcor = diffusing capacity of lungs for carbon monoxide, uncorrected for hemoglobin; DLCOunc = diffusing capacity of lungs for carbon monoxide, corrected for hemoglobin; DL/VA = diffusing capacity of the lung for carbon monoxide divided by alveolar volume; Hgb = blood hemoglobin; — = not measured. Open table in a new tab DLCOcor = diffusing capacity of lungs for carbon monoxide, uncorrected for hemoglobin; DLCOunc = diffusing capacity of lungs for carbon monoxide, corrected for hemoglobin; DL/VA = diffusing capacity of the lung for carbon monoxide divided by alveolar volume; Hgb = blood hemoglobin; — = not measured. What is the diagnosis? Diagnosis: Reactive airways dysfunction syndrome resulting from an industrial disinfectant mixture of hydrogen peroxide, acetic acid, and peracetic acid Reactive airways dysfunction syndrome (RADS) is the archetypal example of irritant-induced asthma that begins after a single, usually accidental, and often massive exposure to a very high level of a respiratory irritant without a latency period (usually severe enough to warrant immediate medical treatment at the time of exposure). It was first described in 1985 with the following diagnostic criteria: onset of asthma symptoms within 24 h of exposure to high levels of a respiratory irritant, persistence of symptoms for at least 12 weeks, objective evidence of asthma (positive methacholine or histamine bronchoprovocation test results or airway obstruction on spirometry with positive bronchodilator response), and absence of preceding history of asthma or chronic lung disease. These stringent criteria subsequently were expanded and modified to include multiple, but less extreme, exposures and delayed onset of symptoms after exposure (up to 7 days or longer) under the broader entity of irritant-induced occupational asthma. Documentation of airway hyperresponsiveness or reversible airflow obstruction, persistence of symptoms for at least 3 months, and absence of preceding asthma or chronic lung disease are not mandatory for the diagnosis under the modified (expanded) diagnostic criteria for RADS. The pathophysiologic features and factors that affect the initiation, severity, and persistence of RADS after irritant exposure remain poorly understood, but it is thought that airway epithelial injury and inflammation after exposure to high concentrations of an irritant agent results in airway remodelling, hyperresponsiveness, and chronic inflammation. Various respiratory irritants in the form of gases and fumes have been described, with inhalational exposure typically occurring as a result of spillage of volatile compounds, accidental release of chemicals under pressure, or accidental fire with the release of thermal combustion byproducts. Examples of respiratory irritants include sulfur dioxide, di-isocyanates, perchloroethylene, chlorine, acid spills (acetic and peracetic acid), welding fumes, and alkaline dust exposure from the World Trade Centre collapse. Pathologically, inhalational injury first leads to sloughing of the bronchial epithelium, airway inflammation, and edema. The release of inflammatory mediators, growth factors, and chemokines leads to recruitment of mast and other proinflammatory cells; myofibroblast activation, which causes chronic airway inflammation; subepithelial fibrosis; airway hyperresponsiveness; and asthma symptoms. These mechanisms, pathways, and responses resemble those involved in the pathogenesis of other forms of chronic asthma. No gold standard test exists to confirm a diagnosis of RADS. The diagnosis of RADS remains clinical and relies largely on circumstantial information such as exposure to a known respiratory irritant and onset and duration of symptoms. The typical presentation of RADS is the development of new asthmatic symptoms of cough, wheezing, and shortness of breath after acute exposure to a high level of respiratory irritant that persists for at least 3 months after the initial exposure. A detailed history about the nature of the exposure agent and level of exposure at the workplace, together with a review of previous medical records pertaining to the respiratory status of the patient before and after the implicated exposure and review of the safety data sheet are crucial in making the diagnosis of RADS. RADS has been associated individually with accidental exposures to acetic acid, peracetic acid, and hydrogen peroxide. The differential diagnoses of RADS are wide and include undiagnosed pre-existing asthma with mild symptoms aggravated by irritant exposure, induction of new-onset allergic occupational asthma by a high level of a respiratory irritant that also has the capacity to be a respiratory sensitizer (eg, di-isocyanates), and asthma mimes such as rhinitis, vocal cord dysfunction, sinusitis, and increased cough sensitivity. Investigations aimed at objectively demonstrating the presence of asthma with methacholine bronchoprovocation testing or bronchodilator reversibility testing with spirometry should be performed where possible. Specific inhalation challenges with the suspected respiratory irritants may be useful in distinguishing allergic occupational asthma from RADS. The diagnosis of RADS often is difficult to make in the initial setting because exposure to respiratory irritants can cause a range of occupational respiratory diseases that may be difficult symptomatically to differentiate from asthma. This can range from airway inhalational injury, vocal cord dysfunction, rhinitis, increased cough sensitivity, irritant- or sensitizer-induced occupational asthma, interstitial lung disease, and hypersensitivity pneumonitis. In addition, the concurrent occurrence of upper airway inhalational injury and chemical pneumonitis highlights the diagnostic challenges in making a timely diagnosis. Further investigations therefore may be required to assess the likelihood of nonasthmatic diagnoses. After emergency treatment for acute inhalational injury, patients can be considered for systemic or inhaled corticosteroid therapy, or both, with the intention of ameliorating airway inflammation, although the optimal dose and duration of treatment are uncertain. These patients then should be monitored closely for the development of bronchial hypersensitivity and persistent airflow obstruction as for RADS. Patients who demonstrate persistent respiratory impairment resulting from RADS should receive treatment as for occupational asthma, which consists of long-term treatment with inhaled bronchodilators and inhaled corticosteroids, in addition to environmental control measures. The patient continued to experience shortness of breath on exertion associated with persistent severe airflow limitation on spirometry after 32 months’ follow-up. He required stepwise escalation in asthma treatment to salmeterol 25 μg plus fluticasone propionate 250 μg combination inhaler two puffs twice daily, tiotropium 2.5 μg inhaler two inhalations every morning, and montelukast 10 mg every night. He also underwent 16 sessions of outpatient pulmonary rehabilitation over 3 months starting at 22 weeks after exposure with improvement in 6-min walk test distance of 380 m to 460 m. With treatment, symptoms eventually were controlled, with an asthma control test score of 21 at the last outpatient review, 39 months after exposure. 1.RADS is a form of irritant-induced asthma that begins after a single, usually accidental, high-level exposure to a very high level of a respiratory irritant without a latency period.2.RADS is diagnosed based on clinical and exposure features characterized by a strong causal relationship between irritant exposure and rapid onset of asthma symptoms (typically within 24 h or up to several days). Additional, although not mandatory, diagnostic features include persistence of symptoms for at least 12 weeks’ duration, objective evidence of asthma on spirometry with positive bronchoprovocation test results or bronchodilator response, and the absence of a preceding history of chronic lung disease.3.The differential diagnoses of persistent respiratory symptoms after inhalational injury are broad and include vocal cord dysfunction, rhinitis, increased cough sensitivity, irritant- or sensitizer-induced occupational asthma, interstitial lung disease, and hypersensitivity pneumonitis. Financial/nonfinancial disclosures: None declared. Other contributions: CHEST worked with the authors to ensure that the Journal policies on patient consent to report information were met." @default.
• W3149705488 created "2021-04-13" @default.
• W3149705488 creator A5007339295 @default.
• W3149705488 creator A5014775410 @default.
• W3149705488 creator A5078482449 @default.
• W3149705488 date "2021-04-01" @default.
• W3149705488 modified "2023-09-23" @default.
• W3149705488 title "A 27-Year-Old Man With Persistent Breathlessness After an Inhalational Injury" @default.
• W3149705488 cites W1992230297 @default.
• W3149705488 cites W2034552444 @default.
• W3149705488 cites W2045511520 @default.
• W3149705488 cites W2133359897 @default.
• W3149705488 cites W2163862598 @default.
• W3149705488 cites W4230897710 @default.
• W3149705488 cites W4232830084 @default.
• W3149705488 cites W4376999554 @default.
• W3149705488 doi "https://doi.org/10.1016/j.chest.2020.11.044" @default.
• W3149705488 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/34022018" @default.
• W3149705488 hasPublicationYear "2021" @default.
• W3149705488 type Work @default.
• W3149705488 sameAs 3149705488 @default.
• W3149705488 citedByCount "0" @default.
• W3149705488 crossrefType "journal-article" @default.
• W3149705488 hasAuthorship W3149705488A5007339295 @default.
• W3149705488 hasAuthorship W3149705488A5014775410 @default.
• W3149705488 hasAuthorship W3149705488A5078482449 @default.
• W3149705488 hasBestOaLocation W31497054881 @default.
• W3149705488 hasConcept C177713679 @default.
• W3149705488 hasConcept C187212893 @default.
• W3149705488 hasConcept C42219234 @default.
• W3149705488 hasConcept C71924100 @default.
• W3149705488 hasConceptScore W3149705488C177713679 @default.
• W3149705488 hasConceptScore W3149705488C187212893 @default.
• W3149705488 hasConceptScore W3149705488C42219234 @default.
• W3149705488 hasConceptScore W3149705488C71924100 @default.
• W3149705488 hasIssue "4" @default.
• W3149705488 hasLocation W31497054881 @default.
• W3149705488 hasOpenAccess W3149705488 @default.
• W3149705488 hasPrimaryLocation W31497054881 @default.
• W3149705488 hasRelatedWork W1995515455 @default.
• W3149705488 hasRelatedWork W2080531066 @default.
• W3149705488 hasRelatedWork W2170431845 @default.
• W3149705488 hasRelatedWork W2409957712 @default.
• W3149705488 hasRelatedWork W2410491650 @default.
• W3149705488 hasRelatedWork W2604682584 @default.
• W3149705488 hasRelatedWork W2748952813 @default.
• W3149705488 hasRelatedWork W2899084033 @default.
• W3149705488 hasRelatedWork W3032375762 @default.
• W3149705488 hasRelatedWork W4252371801 @default.
• W3149705488 hasVolume "159" @default.
• W3149705488 isParatext "false" @default.
• W3149705488 isRetracted "false" @default.
• W3149705488 magId "3149705488" @default.
• W3149705488 workType "article" @default.