Spontaneous Pneumothorax in COVID-19 Patients Treated with High-Flow Nasal Cannula Outside the ICU: a Case Series
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The Child with Altered Respiratory Status
Path: K:/LWW-BOWDEN-09-0101/Application/LWW-BOWDEN-09-0101-016.3d Date: 3rd July 2009 Time: 16:31 User ID: muralir 1BlackLining Disabled CHAPTER 16 The Child With Altered Respiratory Status Do you remember the Diaz fam- Case History leave Lela, the baby sister, ily from Chapter 9, in which with Claudia’s mother, Selma, Jose has trouble taking his asthma medication, and head to the hospital. and in Chapter 4, in which Jose’s little sister, At the hospital the emergency department Lela, expresses her personality even as a new- nurse observes Jose sitting cross-legged and born? Jose is 4 years old and was diagnosed leaning forward on his hands. His mouth is with asthma this past fall, about 6 months ago. open and he is breathing hard with an easily Since that time Claudia, his mother, has audible inspiratory wheeze. He is using his noticed several factors that trigger his asthma subclavicular accessory muscles with each including getting sick, pollen, and cold air. breath. His respiratory rate is 32 breaths per One evening following a warm early-spring minute, his pulse is 112 beats per minutes, day, Jose is outside playing as the sun sets and and he is afebrile. Claudia explains that he the air cools. When he comes inside he was fine; he was outside running and playing, begins to cough. Claudia sets up his nebulizer and then came in and began coughing and and gives him a treatment of albuterol, which wheezing, and she gave him an albuterol lessens his coughing. Within an hour, Jose is treatment. -
Clinical Management of Severe Acute Respiratory Infections When Novel Coronavirus Is Suspected: What to Do and What Not to Do
INTERIM GUIDANCE DOCUMENT Clinical management of severe acute respiratory infections when novel coronavirus is suspected: What to do and what not to do Introduction 2 Section 1. Early recognition and management 3 Section 2. Management of severe respiratory distress, hypoxemia and ARDS 6 Section 3. Management of septic shock 8 Section 4. Prevention of complications 9 References 10 Acknowledgements 12 Introduction The emergence of novel coronavirus in 2012 (see http://www.who.int/csr/disease/coronavirus_infections/en/index. html for the latest updates) has presented challenges for clinical management. Pneumonia has been the most common clinical presentation; five patients developed Acute Respira- tory Distress Syndrome (ARDS). Renal failure, pericarditis and disseminated intravascular coagulation (DIC) have also occurred. Our knowledge of the clinical features of coronavirus infection is limited and no virus-specific preven- tion or treatment (e.g. vaccine or antiviral drugs) is available. Thus, this interim guidance document aims to help clinicians with supportive management of patients who have acute respiratory failure and septic shock as a consequence of severe infection. Because other complications have been seen (renal failure, pericarditis, DIC, as above) clinicians should monitor for the development of these and other complications of severe infection and treat them according to local management guidelines. As all confirmed cases reported to date have occurred in adults, this document focuses on the care of adolescents and adults. Paediatric considerations will be added later. This document will be updated as more information becomes available and after the revised Surviving Sepsis Campaign Guidelines are published later this year (1). This document is for clinicians taking care of critically ill patients with severe acute respiratory infec- tion (SARI). -
PALS Helpful Hints 2015 Guidelines - December 2016 Mandatory Precourse Assessment at Least 70% Pass
PALSPALS Helpful Helpful Hints Courtesy Hints are of CourtesyKey Medical of Resources, Key Medical Inc. Resources, www.cprclassroom.com Inc. PALS Helpful Hints 2015 Guidelines - December 2016 Mandatory precourse assessment at least 70% pass. Bring proof of completion to class. The PALS exam is 50 questions. Passing score is 84% or you may miss 8 questions. All AHA exams are now open resource, so you may use your books and/or handouts for the exam. For those persons taking PALS for the first time or updating/renewing with a current card, exam remediation is permitted should you miss more than 8 questions on the exam. Viewing the PALS book ahead of time with the online resources is very helpful. The American Heart Association link is www.heart.org/eccstudent has a pre-course self- assessment, supplementary written materials and videos. The code for these online resources is in the PALS Provider manual page ii. The code is PALS15. Basic Dysrhythmia knowledge is required. The exam has at least 5 strips to interpret. The course is a series of video segments then skills. The course materials well prepare you for the exam. Basic Dysrhythmias knowledge is required in relation to asystole, ventricular fibrillation, tachycardias in general and bradycardias in general. You do not need to know the ins and outs of each and every one. Tachycardias need to differentiate wide complex (ventricular tachycardia) and narrow complex (supraventricular tachycardia or SVT). Airway - child is grunting - immediate intervention. Airway - deteriorates after oral airway, next provide bag-mask ventilation. Airway - snoring with poor air entry bilaterally - reposition, oral airway. -
Allergic Bronchopulmonary Aspergillosis: a Perplexing Clinical Entity Ashok Shah,1* Chandramani Panjabi2
Review Allergy Asthma Immunol Res. 2016 July;8(4):282-297. http://dx.doi.org/10.4168/aair.2016.8.4.282 pISSN 2092-7355 • eISSN 2092-7363 Allergic Bronchopulmonary Aspergillosis: A Perplexing Clinical Entity Ashok Shah,1* Chandramani Panjabi2 1Department of Pulmonary Medicine, Vallabhbhai Patel Chest Institute, University of Delhi, Delhi, India 2Department of Respiratory Medicine, Mata Chanan Devi Hospital, New Delhi, India This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. In susceptible individuals, inhalation of Aspergillus spores can affect the respiratory tract in many ways. These spores get trapped in the viscid spu- tum of asthmatic subjects which triggers a cascade of inflammatory reactions that can result in Aspergillus-induced asthma, allergic bronchopulmo- nary aspergillosis (ABPA), and allergic Aspergillus sinusitis (AAS). An immunologically mediated disease, ABPA, occurs predominantly in patients with asthma and cystic fibrosis (CF). A set of criteria, which is still evolving, is required for diagnosis. Imaging plays a compelling role in the diagno- sis and monitoring of the disease. Demonstration of central bronchiectasis with normal tapering bronchi is still considered pathognomonic in pa- tients without CF. Elevated serum IgE levels and Aspergillus-specific IgE and/or IgG are also vital for the diagnosis. Mucoid impaction occurring in the paranasal sinuses results in AAS, which also requires a set of diagnostic criteria. Demonstration of fungal elements in sinus material is the hall- mark of AAS. -
Pneumothorax in Patients with Idiopathic Pulmonary Fibrosis
Yamazaki et al. BMC Pulm Med (2021) 21:5 https://doi.org/10.1186/s12890-020-01370-w RESEARCH ARTICLE Open Access Pneumothorax in patients with idiopathic pulmonary fbrosis: a real-world experience Ryo Yamazaki, Osamu Nishiyama* , Kyuya Gose, Sho Saeki, Hiroyuki Sano, Takashi Iwanaga and Yuji Tohda Abstract Background: Some patients with idiopathic pulmonary fbrosis (IPF) develop pneumothorax. However, the charac- teristics of pneumothorax in patients with IPF have not been elucidated. The purpose of this study was to clarify the clinical course, actual management, and treatment outcomes of pneumothorax in patients with IPF. Methods: Consecutive patients with IPF who were admitted for pneumothorax between January 2008 and Decem- ber 2018 were included. The success rates of treatment for pneumothorax, hospital mortality, and recurrence rate after discharge were examined. Results: During the study period, 36 patients with IPF were admitted with pneumothorax a total of 58 times. During the frst admission, 15 patients (41.7%) did not receive chest tube drainage, but 21 (58.3%) did. Of the 21 patients, 8 (38.1%) received additional therapy after chest drainage. The respective treatment success rates were 86.6% and 66.7% in patients who underwent observation only vs chest tube drainage. The respective hospital mortality rates were 13.3% and 38.0%. The total pneumothorax recurrence rate after hospital discharge was 34.6% (n 9). = Conclusions: Pneumothorax in patients with IPF was difcult to treat successfully, had a relatively poor prognosis, and showed a high recurrence rate. Keywords: Idiopathic pulmonary fbrosis, Hospitalization, Pneumothorax, Recurrence, Treatment Background pneumothorax was signifcantly associated with poor Idiopathic pulmonary fbrosis (IPF) is a specifc form survival in patients with IPF [11]. -
Respiratory Failure Diagnosis Coding
RESPIRATORY FAILURE DIAGNOSIS CODING Action Plans are designed to cover topic areas that impact coding, have been the frequent source of errors by coders and usually affect DRG assignments. They are meant to expand your learning, clinical and coding knowledge base. INTRODUCTION Please refer to the reading assignments below. You may wish to print this document. You can use your encoder to read the Coding Clinics and/or bookmark those you find helpful. Be sure to read all of the information provided in the links. You are required to take a quiz after reading the assigned documents, clinical information and the Coding Clinic information below. The quiz will test you on clinical information, coding scenarios and sequencing rules. Watch this video on basics of “What is respiration?” https://www.youtube.com/watch?v=hc1YtXc_84A (3:28) WHAT IS RESPIRATORY FAILURE? Acute respiratory failure (ARF) is a respiratory dysfunction resulting in abnormalities of tissue oxygenation or carbon dioxide elimination that is severe enough to threaten and impair vital organ functions. There are many causes of acute respiratory failure to include acute exacerbation of COPD, CHF, asthma, pneumonia, pneumothorax, pulmonary embolus, trauma to the chest, drug or alcohol overdose, myocardial infarction and neuromuscular disorders. The photo on the next page can be accessed at the link. This link also has complete information on respiratory failure. Please read the information contained on this website link by NIH. 1 http://www.nhlbi.nih.gov/health/health-topics/topics/rf/causes.html -
Approach to Type 2 Respiratory Failure Changing Nature of NIV
Approach to type 2 Respiratory Failure Changing Nature of NIV • Not longer just the traditional COPD patients • Increasingly – Obesity – Neuromuscular – Pneumonias • 3 fold increase in patients with Ph 7.25 and below Impact • Changing guidelines • Increased complexity • Increased number of patients • Decreased threshold for initiation • Lower capacity for ITU to help • Higher demands on nursing staff Resp Failure • Type 1 Failure of Oxygenation • Type 2 Failure of Ventilation • Hypoventilation • Po2 <8 • Pco2 >6 • PH low or bicarbonate high Ventilation • Adequate Ventilation – Breathe in deeply enough to hit a certain volume – Breathe out leaving a reasonable residual volume – Breath quick enough – Tidal volume and minute ventilation Response to demand • Increase depth of respiration • Use Reserve volume • Increase rate of breathing • General increase in minute ventilation • More gas exchange Failure to match demand • Hypoventilation • Multifactorial • Can't breathe to a high enough volume • Can't breath quick enough • Pco2 rises • Po2 falls Those at risk • COPD • Thoracic restriction • Central • Neuromuscular • Acute aspects – Over oxygenation – Pulmonary oedema Exhaustion • Complicates all forms of resp failure • Type one will become type two • Needs urgent action • Excessive demand • Unable to keep up • Resp muscle hypoxia Exhaustion • Muscles weaken • Depth of inspiration drops • Residual volume drops • Work to breath becomes harder • Spiral of exhaustion • Pco2 rises, Po2 drops Type 2 Respiratory Failure Management Identifying Those -
Secondary Spontaneous Pneumothorax in a Patient of Allergic Bronchopulmonary Aspergillosis: an Unusual Presentation
International Journal of Research in Medical Sciences Sandal S et al. Int J Res Med Sci. 2021 Apr;9(4):1205-1208 www.msjonline.org pISSN 2320-6071 | eISSN 2320-6012 DOI: https://dx.doi.org/10.18203/2320-6012.ijrms20211377 Case Report Secondary spontaneous pneumothorax in a patient of allergic bronchopulmonary aspergillosis: an unusual presentation Shivali Sandal1, Surender Kumar2* 1Department of Critical Care Medicine, Inderaprastha Apollo, New Delhi, India 2Department of Cardiology, UN Mehta Institute of Cardiology and Research Centre, Ahmedabad, Gujarat, India Received: 23 January 2021 Accepted: 01 March 2021 *Correspondence: Dr. Surender Kumar, E-mail: [email protected] Copyright: © the author(s), publisher and licensee Medip Academy. This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. ABSTRACT Allergic bronchopulmonary aspergillosis (ABPA) is a complex immunologic pulmonary disorder caused by hypersensitivity to fungus, Aspergillus fumigates. It clinically manifests with non-specific respiratory and systemic symptoms. ABPA is typically seen in patients with long-standing asthma or cystic fibrosis. Pleural involvement in ABPA is uncommon and secondary spontaneous pneumothorax is very rare. Herein, we report a case of 33 years old male patient presented with dyspnoea, low grade fever and productive cough. High Resolution Computed tomography (HRCT) scan of thorax was suggestive of ABPA with secondary pneumothorax. Keywords: Allergic bronchopulmonary aspergillosis, Aspergillus fumigates, High resolution computed tomography, Secondary spontaneous pneumothorax INTRODUCTION episodes of increasing dyspnea, cough with sputum production, pleuritic pain and fever. -
Cryptogenic Organizing Pneumonia
462 Cryptogenic Organizing Pneumonia Vincent Cottin, M.D., Ph.D. 1 Jean-François Cordier, M.D. 1 1 Hospices Civils de Lyon, Louis Pradel Hospital, National Reference Address for correspondence and reprint requests Vincent Cottin, Centre for Rare Pulmonary Diseases, Competence Centre for M.D., Ph.D., Hôpital Louis Pradel, 28 avenue Doyen Lépine, F-69677 Pulmonary Hypertension, Department of Respiratory Medicine, Lyon Cedex, France (e-mail: [email protected]). University Claude Bernard Lyon I, University of Lyon, Lyon, France Semin Respir Crit Care Med 2012;33:462–475. Abstract Organizing pneumonia (OP) is a pathological pattern defined by the characteristic presence of buds of granulation tissue within the lumen of distal pulmonary airspaces consisting of fibroblasts and myofibroblasts intermixed with loose connective matrix. This pattern is the hallmark of a clinical pathological entity, namely cryptogenic organizing pneumonia (COP) when no cause or etiologic context is found. The process of intraalveolar organization results from a sequence of alveolar injury, alveolar deposition of fibrin, and colonization of fibrin with proliferating fibroblasts. A tremen- dous challenge for research is represented by the analysis of features that differentiate the reversible process of OP from that of fibroblastic foci driving irreversible fibrosis in usual interstitial pneumonia because they may determine the different outcomes of COP and idiopathic pulmonary fibrosis (IPF), respectively. Three main imaging patterns of COP have been described: (1) multiple patchy alveolar opacities (typical pattern), (2) solitary focal nodule or mass (focal pattern), and (3) diffuse infiltrative opacities, although several other uncommon patterns have been reported, especially the reversed halo sign (atoll sign). -
Bronchiectasis and Cystic Fibrosis
Medical Services BRONCHIECTASIS AND CYSTIC FIBROSIS EBM – Bronchiectasis and Cystic Fibrosis Version: 2a (draft) MED/S2/CMEP~0053 (d) Page 1 Medical Services 1 Bronchiectasis 1.1 Description Bronchiectasis is a chronic disease characterised by irreversible dilatation of the bronchi due to bronchial wall damage from infection and inflammation. It is accompanied by chronic suppurative lung disease with productive cough and purulent sputum. The disease is caused by impairment of the mucociliary transport system, which normally protects the lungs from infection. This predisposes the lungs to bacterial infection, and hence an inflammatory response, increased mucus production and further impairment of mucociliary function. The walls of the bronchi become infiltrated by inflammatory tissue, losing their elastin content to become thin and dilated. 1.2 Aetiology Respiratory Infections cause the majority of cases. a) Infective and Aspiration Pneumonias (70% are bacterial and 30% are viral.) b) Tuberculosis (TB) (common in developing countries with increasing incidence in the UK.) c) Childhood Pertussis and Measles. Cystic Fibrosis – see Part 2. Bronchial Obstruction. a) Inhaled Foreign Body e.g. peanut. b) Bronchial Carcinoma. c) Lymph Node Enlargement e.g. TB. Immune Deficiency. a) HIV infection and AIDS.[1] b) Haematological Malignancies. c) Hypogammaglobulinaemia. Smoking (Impairs lung function and accelerates the progression of bronchiectasis.) [1] Allergic Bronchopulmonary Aspergillosis. Other Rare Causes. a) Inherited Ciliary Dyskinesias e.g. Kartagener’s Syndrome. b) Autoimmune Diseases e.g. ulcerative colitis, rheumatoid arthritis, vasculitis. Rarely, the cause of bronchiectasis cannot be determined. EBM – Bronchiectasis and Cystic Fibrosis Version: 2a (draft) MED/S2/CMEP~0053 (d) Page 2 Medical Services 1.3 Prevalence During the 20th century, severe and chronic respiratory infections declined in frequency due to the introduction of childhood vaccinations, the development of antibiotics, and improvements in socio-economic conditions. -
Peri-Operative Respiratory Complications and the Post-Operative Consequences – Atelectasis and Risk Factors
Pelosi_edit_Layout 1 13/01/2010 10:15 Page 17 Respiratory and Airway Management Peri-operative Respiratory Complications and the Post-operative Consequences – Atelectasis and Risk Factors Paolo Pelosi1 and Cesare Gregoretti2 1. Associate Professor, Department of Environment, Health and Safety, University of Insubria, Varese; 2. Director, Anaesthesia and Intensive Care Services, Maria Adelaide Hospital, Turin Abstract Post-operative pulmonary complications (PPCs) play a significant role in the risks of surgery and anaesthesia. The definition of PPCs is not definitely established and may vary between different studies. Potential patient-related risk factors for PPCs are: age; chronic lung disease; cigarette use; congestive heart failure; functional dependence; American Society of Anesthesiologists (ASA) classification; obesity; asthma; obstructive sleep apnoea; impaired sensorium, abnormal findings on chest examination, alcohol use and weight loss; and exercise capacity, diabetes and HIV infection. Risk factors not related to the patient’s clinical characteristics are surgical site, duration of surgery, anaesthetic technique and emergency surgery. The most important and morbid PPCs are atelectasis, pneumonia and respiratory failure, which contribute to increased morbidity, mortality and hospital length of stay. An appropriate ventilation setting during mechanical ventilation for general anaesthesia may reduce intra-operative atelectasis, with beneficial effects in the post-operative period. Lung expansion modalities, mainly physiotherapy -
Non-Invasive Ventilation in Acute Respiratory Failure British Thoracic Society Standards of Care Committee
192 BTS GUIDELINE Thorax: first published as 10.1136/thorax.57.3.192 on 1 March 2002. Downloaded from Non-invasive ventilation in acute respiratory failure British Thoracic Society Standards of Care Committee ............................................................................................................................. Thorax 2002;57:192–211 INTRODUCTION A survey of acute admissions in Leeds has sug- Nomenclature gested that, if NIV was used in all patients with Non-invasive ventilation (NIV) refers to the chronic obstructive pulmonary disease (COPD) provision of ventilatory support through the with a pH of <7.35 (H+ >45 nmol/l) after initial patient’s upper airway using a mask or similar medical treatment, a typical district general device. This technique is distinguished from those hospital serving a population of 250 000 would which bypass the upper airway with a tracheal expect to treat around 70 patients per year.3 tube, laryngeal mask, or tracheostomy and are • Non-invasive ventilation has been shown to be an therefore considered invasive. In this document effective treatment for acute hypercapnic respiratory NIV refers to non-invasive positive pressure failure, particularly in chronic obstructive pulmo- ventilation, and other less commonly used tech- nary disease. Facilities for NIV should be available 24 niques such as external negative pressure or hours per day in all hospitals likely to admit such rocking beds will not be discussed. (NIPPV is an patients. [A] alternative abbreviation but it is more cumber- some and involves ambiguity as to whether “N” is NIV is not suitable for all patients with respira- for “non-invasive” or “nasal”.) tory failure. If used indiscriminately, patients who Continuous positive airway pressure (CPAP) in would be managed more appropriately by tra- this document refers to the non-invasive applica- cheal intubation will receive suboptimal treat- tion of positive airway pressure, again using a face ment.