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Atelectasis


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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sudarshana Datta, MD [2]

Synonyms and keywords: Pulmonary collapse, lung atelectasis

Overview

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ;Associate Editor(s)-in-Chief: Sudarshana Datta, MD [2]

Overview

Atelectasis is characterized by incomplete lung expansion leading to diminution of lung volume. It affects the whole lung or a part of it. Atelectasis may be classified based on etiology into obstructive and non-obstructive types. Obstructive atelectasis, which is the most common type of atelectasis may develop due to obstruction by foreign bodies, tumors and mucus plugs. Causes of non obstructive atelectasis include lung scarring caused by necrotizing pneumonia or granulomatous diseases, lung infiltration, extrinsic lung compression and diminished levels of surfactant. The most common cause of atelectasis is postoperative atelectasis, due to the effect of surgical manipulation or general anaesthesia on the patient. Chest trauma, general anaesthesia, thoracic surgery, cystic fibrosis, prematurity and respiratory distress syndrome are some of the common risk factors that predispose patients to developing atelectasis. Common symptoms of atelectasis include breathlessness, chest pain, and cyanosis. Symptoms in patients with atelectasis depend upon rapidity of bronchial occlusion, lung area affected and presence of any overlying infection. Physical examination of patients with atelectasis is usually remarkable for decreased chest expansion, mediastinal displacement towards the affected side and elevation of the diaphragm. Patients may develop dullness to percussion over the involved area, wheezing and diminished or absent breath sounds on auscultation. An x-ray may be helpful in the diagnosis of atelectasis. Findings on an x-ray suggestive of atelectasis include displacement of fissures, rib crowding, elevation of ipsilateral diaphragm, volume loss on ipsilateral hemithorax, hilar displacement and compensatory hyperlucency of the remaining lobes. CT scan of the chest without contrast is the gold standard diagnostic modality.The primary treatment for atelectasis is management of the underlying cause. Besides this, supportive therapy for atelectasis includes chest physiotherapy, breathing and coughing exercises, early ambulation, nasotracheal suctioning, humidifiers, nebulized bronchodilators and supplemental oxygen in order to maintain an arterial oxygen saturation of greater than 90 percent. Intubation, mechanical support, positive pressure ventilation and continous positive airway pressure (CPAP) help in the prevention of alveolar collapse, thereby assisting in lung inflation in patients with atelectasis.

Historical Perspective

The Greek words ateles and ektasis form the term atelectasis which translates into incomplete expansion.

Classification

Atelectasis may be classified based on etiology into obstructive and non-obstructive types. Obstructive atelectasis, which is the most common type of atelectasis may develop due to obstruction by foreign bodies, tumors and mucus plugs. Causes of non obstructive atelectasis include lung scarring caused by necrotizing pneumonia or granulomatous diseases, lung infiltration, extrinsic lung compression and diminished levels of surfactant. Atelectasis may also be classified based on duration into acute and chronic types. Acute atelectasis is associated with airlessness due to recent lung collapse while chronic atelectasis involves a combination of infection, bronchial destruction, and fibrosis, in adition to airlessness. If left untreated, atelectasis may be fatal in patients and progress to pneumonia, sepsis, and respiratory failure.

Pathophysiology

The pathophysiology of obstructive and non-obstructive atelectasis is determined by several factors. Obstructive atelectasis, the most common type of atelectasis and occurs due to obstruction from the trachea to the alveoli at any level. Foreign bodies, tumors, and mucus plugs are causes of obstructive atelectasis. Non obstructive atelectasis occurs due to severe lung scarring caused by necrotizing pneumonias or granulomatous diseases leading to cicatrisation atelectasis. Lung infiltration by a tumor (bronchoalveolar carcinoma) may cause replacement atelectasis, thoracic space occupying lesions can cause compression atelectasis, diminished levels of surfactant can lead to adhesive atelectasis presenting as ARDS. Passive atelectasis occurs due to absence of contact between the parietal and visceral pleurae due to fluid (pleural effusion), air (pneumothorax), blood (hemothorax) etc. Patients undergoing upper abdominal and thoracic procedures may develop postoperative atelectasis which may arise as a complication of surgery or anaesthesia leading to decreased surfactant activity and dysfunction of the diaphragm.

Causes

The most common cause of atelectasis is postoperative atelectasis, due to the effect of surgical manipulation or general anaesthesia on the patient. Obstructive atelectasis mostly develops due to blockage within the bronchiole or bronchus, which may be within the airway (foreign bodies, mucus plugs), arising from the wall (tumors such as squamous cell carcinoma) or space occupying lesions within the thoracic cavity (tumor, lymph node, tubercle). Causes of non-obstructive atelectasis include impaired surfactant formation or activation, leading to alveolar collapse due to increased surface tension.

Differentiating Hereditary pancreatitis from Other Diseases

Atelectasis must be differentiated from other diseases that cause acute dyspnea, fever, and chest pain, such as asthma, bronchitis, and interstitial lung disease.

Epidemiology and Demographics

The incidence and prevalence of atelectasis are not known. Patients of all age groups may develop atelectasis. Rounded atelectasis commonly affects individuals at sixty years of age. Atelectasis affects men and women equally.

Risk Factors

Chest trauma, general anaesthesia, thoracic surgery, cystic fibrosis, prematurity and respiratory distress syndrome are some of the common risk factors that predispose patients to developing atelectasis. Children less than three years of age and adults over sixty years of age are also at increased risk of alveolar collapse and impaired surfactant production in response to pulmonary stressors such as toxins, hyperoxia, hypoxia and ischemia. 

Screening

There is insufficient evidence to recommend routine screening for atelectasis.

Natural History, Complications, and Prognosis

If left untreated, atelectasis may be fatal in patients and progress to pneumonia, sepsis, and respiratory failure. Common complications of atelectasis include pneumonia, bronchiectasis, hypoxemia, respiratory failure, and sepsis. Depending on the extent of lung involvement at the time of diagnosis, the prognosis may vary. However, the prognosis is generally regarded as good. Involvement of a small portion of the lung is not associated with life threatening complications, as the remaining lung compensates for the hypoxemia. However, atelectasis is associated with poor prognosis if the surface area of lung involvement is very large, in the presence of pre-existing lung disease, in case of failure to remove obstruction and in case of atelectasis due to cancer.

Diagnosis

History and Symptoms

The majority of patients with atelectasis are asymptomatic. Common symptoms of atelectasis include breathlessness, chest pain, and cyanosis. Symptoms in patients with atelectasis depend upon rapidity of bronchial occlusion, lung area affected and presence of any overlying infection.

Physical Examination

Patients with atelectasis usually have non specific signs on physical examination. Physical examination of patients with atelectasis is usually remarkable for decreased chest expansion, mediastinal displacement towards the affected side and elevation of the diaphragm. Patients may develop dullness to percussion over the involved area, wheezing and diminished or absent breath sounds on auscultation.

Laboratory Findings

Patients with atelectasis have hypoxemia with low levels of PaO2 and normal/low PaCO2 levels on ABG analysis. Raised peak and end-inspiratory plateau pressures due to decreased lung compliance are also present in these patients.

X-ray

An x-ray may be helpful in the diagnosis of atelectasis. Findings on an x-ray suggestive of atelectasis include displacement of fissures, rib crowding, elevation of ipsilateral diaphragm, volume loss on ipsilateral hemithorax, hilar displacement and compensatory hyperlucency of the remaining lobes. Complete lung atelectasis and atelectasis involving different parts of the lung have their own characteristic appearance. While complete atelectasis of the lung may lead to opacification of the entire hemithorax and ipsilateral shift of the mediastinum, a right middle and lower lobe atelectasis may show subpulmonic effusions along with right hemidiaphragmatic elevation on X-ray.

Ultrasound

There are no significant ultrasound findings associated with atelectasis.

CT scan

CT findings suggestive of atelectasis include hilar displacement, elevation of ipsilateral diaphragm, rib crowding, displacement of fissures, and compensatory hyperlucency of the remaining lobes. CT findings associated with complete atelectasis of an entire lung include opacification of the entire hemithorax and ipsilateral shift of the mediastinum. Collapse of different parts of the lung have their own characteristic appearance. For example, a collapsed right middle lobe has a tilted icecream sign which appears as a triangular opacity against the border of the right heart with a laterally pointed apex. On the other hand, RUL collapse appears as a right paratracheal opacity, with a concave lateral appearance of the minor lung fissure.

MRI

MRI may be helpful in distinguishing obstructive causes of atelectasis from non-obstructive causes. MRI does not play a significant role in the diagnosis of atelectasis.

Other Imaging Findings

There are no other imaging findings associated with atelectasis.

Other Diagnostic Studies

Flexible fibreoptic bronchoscopy may be helpful in the diagnosis of atelectasis. This technique assists in determining the cause of obstruction and removal of mucus plugs. Biopsies taken during fiberoptic bronchoscopy helps in the diagnosis of malignancy and allergic bronchopulmonary aspergillosis.

Treatment

Medical Therapy

The primary treatment for atelectasis is management of the underlying cause. Besides this, supportive therapy for atelectasis includes chest physiotherapy, breathing and coughing exercises, early ambulation, nasotracheal suctioning, humidifiers, nebulized bronchodilators and supplemental oxygen in order to maintain an arterial oxygen saturation of greater than 90 percent. Intubation, mechanical support, positive pressure ventilation and continous positive airway pressure (CPAP) help in the prevention of alveolar collapse, thereby assisting in lung inflation in patients with atelectasis.

Surgery

Surgical intervention is not recommended for the management of atelectasis.

Primary Prevention

Judicious use of anaesthetic agents known to cause narcosis, use of epidural analgesia in patients with underlying pulmonary disease, incentive spirometry, early ambulation, humidifiers, breathing exercises, coughing exercises and supplemental oxygen are effective measures of primary prevention in patients undergoing operative procedures, in order to prevent post operative atelectasis.

Secondary Prevention

Effective measures for the secondary prevention of atelectasis include incentive spirometry, deep breathing exercises, coughing exercises and early ambulation. These measures help prevent complications in patients such as post obstructive infection, bronchiectasis and fibrosis.

References

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Historical Perspective

Historical Perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sudarshana Datta, MD [2]

Overview

The Greek words ateles and ektasis form the term atelectasis which translates into incomplete expansion.

Historical Perspective

The Greek words ateles and ektasis form the term atelectasis which translates into incomplete expansion. 

References

Classification

Classification

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sudarshana Datta, MD [2]

Overview

Atelectasis may be classified based on etiology into obstructive and non-obstructive types. Obstructive atelectasis, is the most common type of atelectasis which may develop due to obstruction by foreign bodies, tumors and mucus plugs. Atelectasis may also be classified based on duration of symptoms into acute and chronic types. Acute atelectasis is associated with airlessness due to recent lung collapse while chronic atelectasis involves a combination of infection, bronchial destruction, and fibrosis, in adition to airlessness.

Classification

Atelectasis may be classified based on etiology into obstructive and non-obstructive types.

Based on Etiology

Obstructive atelectasis

  • Obstructive atelectasis, which is the most common type of atelectasis may develop due to obstruction by foreign bodies, tumors and mucus plugs.
  • In case of obstruction from the trachea to the alveoli at any level, alveolar gas reabsorption may occur leading to subsequent atelectasis.[1]
  • Middle lobe syndrome (fixed or recurrent atelectasis of the lingula/ right middle lobe) may occur due to Sjogren’s syndrome. Intraluminal or extraluminal obstruction (compression of the bronchi by adjacent structures) may result in middle lobe syndrome.[2][3]

Non-obstructive atelectasis

Based on Duration

Atelectasis may also be classified based on duration of symptoms into acute and chronic types.

Acute Atelectasis

  • Acute atelectasis is associated with airlessness due to recent lung collapse.
  • Acute atelectasis includes postoperative atelectasis, after thoracic or abdominal surgery, chest trauma, and rib fractures. Surfactant deficiency, excessive oxygen therapy and mechanical ventilation may lead to acute atelectasis.

Chronic Atelectasis

  • Chronic atelectasis is not only associated with airlessness, but a combination of infection, bronchial destruction, widening and fibrosis leading to scarring.
  • Middle lobe syndrome and rounded atelectasis are causes of chronic atelectasis.
  • Middle lobe syndrome (fixed or recurrent atelectasis of the lingula/ right middle lobe) may occur due to Sjogren’s syndrome. Intraluminal or extraluminal obstruction (compression of the bronchi by adjacent structures) may result in middle lobe syndrome.[5][6]
  • Rounded atelectasis is characterized by the formation of fibrous bands which adhere the lung to the pleura in patients with asbestosis.

References

  1. ↑ 1.0 1.1 “Atelectasis – Symptoms and causes – Mayo Clinic”.
  2. ↑ Chen HA, Lai SL, Kwang WK, Liu JC, Chen CH, Huang DF (2006). “Middle lobe syndrome as the pulmonary manifestation of primary Sjögren’s syndrome”. Med. J. Aust. 184 (6): 294–5. PMID 16548837.
  3. ↑ Rosenbloom SA, Ravin CE, Putman CE, Sealy WC, Vock P, Clark TJ, Godwin JD, Chen JT, Baber C (1983). “Peripheral middle lobe syndrome”. Radiology. 149 (1): 17–21. doi:10.1148/radiology.149.1.6611925. PMID 6611925.
  4. ↑ “Atelectasis | Causes, Symptoms, Treatment & Prevention”.
  5. ↑ Chen HA, Lai SL, Kwang WK, Liu JC, Chen CH, Huang DF (2006). “Middle lobe syndrome as the pulmonary manifestation of primary Sjögren’s syndrome”. Med. J. Aust. 184 (6): 294–5. PMID 16548837.
  6. ↑ Rosenbloom SA, Ravin CE, Putman CE, Sealy WC, Vock P, Clark TJ, Godwin JD, Chen JT, Baber C (1983). “Peripheral middle lobe syndrome”. Radiology. 149 (1): 17–21. doi:10.1148/radiology.149.1.6611925. PMID 6611925.

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Pathophysiology

Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sudarshana Datta, MD [2]

Overview

The pathophysiology of obstructive and non-obstructive atelectasis can be better explained by understading underlying pathology. Obstructive atelectasis, the most common type of atelectasis, occurs due to obstruction at any level from the trachea to the alveoli. Foreign bodies, tumors, and mucus plugs are the most common causes of obstructive atelectasis. Non obstructive atelectasis occurs due to severe lung scarring caused by necrotizing pneumonias or granulomatous diseases leading to cicatrisation atelectasis. Lung infiltration by a tumor (bronchoalveolar carcinoma) may cause replacement atelectasis, thoracic space occupying lesions can cause compression atelectasis, diminished levels of surfactant can lead to adhesive atelectasis presenting as ARDS. Passive atelectasis occurs due to absence of contact between the parietal and visceral pleurae due to fluid (pleural effusion), air (pneumothorax), blood (hemothorax) etc. Patients undergoing upper abdominal and thoracic procedures may develop postoperative atelectasis which may arise as a complication of surgery or anaesthesia leading to decreased surfactant activity and dysfunction of the diaphragm.

Pathophysiology

Pathogenesis

  • It is understood that atelectasis is the result of obstructive and non-obstructive etiologies.
  • The pathophysiology of obstructive and non-obstructive atelectasis is determined by several factors.

Pathogenesis of Obstructive atelectasis

  • Obstructive atelectasis is the most common type of atelectasis
  • Obstructive atelectasis occurs due to obstruction at any level from the trachea to the alveoli.
  • Ventilation defect
  • Perfusion defect
    • Perfusion of under ventilated lung tissue leads to hypoxemia due to shunt formation. leading to obstruction
    • Following bronchial obstruction, complete collapse of the affected lung is prevented by secretions that fill up the spaces of the alveoli.
    • The adjacent lung distends to prevent collapse of the part of the lung undergoing atelectasis.
    • The mediastinum shifts towards the affected side.
    • Diaphragmatic elevation of the diaphragm leads to flattening of the chest wall.
  • The extent of atelectasis depends upon the level of obstruction.
    • Lobar atelectasis occurs due to lobar bronchus obstruction.
    • Segmental atelectasis arises from segmental bronchus obstruction.
  • The rate and pattern of development of atelectasis depends on collateral ventilation and gas composition of inspired air.

Pathogenesis of Non obstructive atelectasis

Middle lobe syndrome

Associated Conditions

Common conditions associated with atelectasis include:

Gross Pathology

  • On gross pathology, pleural folds with deep invaginations are characteristic findings of atelectasis.[4]

Microscopic Pathology

  • On microscopic histopathological analysis, fibrosis and pleural invaginations are characteristic findings of atelectasis.[4]
  • If there is an existing pathology leading to atelectasis, characteristic features of the underlying disease may also be seen on microscopic pathology.

References

  1. ↑ “Atelectasis – Symptoms and causes – Mayo Clinic”.
  2. ↑ Chen HA, Lai SL, Kwang WK, Liu JC, Chen CH, Huang DF (2006). “Middle lobe syndrome as the pulmonary manifestation of primary Sjögren’s syndrome”. Med. J. Aust. 184 (6): 294–5. PMID 16548837.
  3. ↑ Rosenbloom SA, Ravin CE, Putman CE, Sealy WC, Vock P, Clark TJ, Godwin JD, Chen JT, Baber C (1983). “Peripheral middle lobe syndrome”. Radiology. 149 (1): 17–21. doi:10.1148/radiology.149.1.6611925. PMID 6611925.
  4. ↑ 4.0 4.1 “Pathology Outlines – Round or rounded atelectasis”.

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Causes

Causes

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sudarshana Datta, MD [2]

Overview

The most common cause of atelectasis is postoperative atelectasis, due to the effect of surgical manipulation or general anaesthesia on the patient. Obstructive atelectasis mostly develops due to blockage within the bronchiole or bronchus, which may be within the airway (foreign bodies, mucus plugs), arising from the wall (tumors such as squamous cell carcinoma) or space occupying lesions within the thoracic cavity (tumor, lymph node, tubercle). Causes of non-obstructive atelectasis include impaired surfactant formation or activation, leading to alveolar collapse due to increased surface tension.

Causes

Atelectasis may arise due to obstructive and non-obstructive causes.

Obstructive atelectasis

Common causes of obstructive atelectasis include obstruction by:[1]

  • Foreign bodies
  • Tumors
  • Mucus plugs
  • Middle lobe syndrome[2][3]

Non-obstructive atelectasis

  • Non obstructive atelectasis may occur due to the following reasons:[1][4]
Type of non-obstructive atelectasis Pathophysiology behind atelectasis
Cicatrisation atelectasis Severe lung scarring caused by necrotizing pneumonia or granulomatous diseases
Replacement atelectasis Lung infiltration
Adhesive atelectasis Diminished levels of surfactant

Presents as ARDS

Passive atelectasis Absence of contact between the parietal and visceral pleurae due to
Rounded atelectasis Formation of fibrous bands which adhere the lung to the pleura in patients with asbestosis
Postoperative atelectasis Complication of surgery or anaesthesia leading to decreased surfactant activity and dysfunction of the diaphragm

Common Causes

The most common causes of atelectasis are:

Causes by Organ System

Cardiovascular No underlying causes
Chemical / poisoning No underlying causes
Dermatologic No underlying causes
Drug Side Effect Anesthesia, Acetaminophen, Follitropin beta, Urofollitropin
Ear Nose Throat Mucus Plug
Endocrine No underlying causes
Environmental No underlying causes
Gastroenterologic No underlying causes
Genetic No underlying causes
Hematologic Blood clot
Iatrogenic No underlying causes
Infectious Disease No underlying causes
Musculoskeletal / Ortho No underlying causes
Neurologic No underlying causes
Nutritional / Metabolic No underlying causes
Obstetric/Gynecologic No underlying causes
Oncologic Tumors
Opthalmologic No underlying causes
Overdose / Toxicity No underlying causes
Psychiatric No underlying causes
Pulmonary Lung Disease, Pleural effusion, Pneumonia, Pneumothorax, Scarring of lung tissue
Renal / Electrolyte No underlying causes
Rheum / Immune / Allergy No underlying causes
Sexual No underlying causes
Trauma Chest Trauma
Urologic No underlying causes
Dental No underlying causes
Miscellaneous Foreign object in the airway

Causes in Alphabetical Order

References

  1. ↑ 1.0 1.1 “Atelectasis – Symptoms and causes – Mayo Clinic”.
  2. ↑ Chen HA, Lai SL, Kwang WK, Liu JC, Chen CH, Huang DF (2006). “Middle lobe syndrome as the pulmonary manifestation of primary Sjögren’s syndrome”. Med. J. Aust. 184 (6): 294–5. PMID 16548837.
  3. ↑ Rosenbloom SA, Ravin CE, Putman CE, Sealy WC, Vock P, Clark TJ, Godwin JD, Chen JT, Baber C (1983). “Peripheral middle lobe syndrome”. Radiology. 149 (1): 17–21. doi:10.1148/radiology.149.1.6611925. PMID 6611925.
  4. ↑ “Atelectasis | Causes, Symptoms, Treatment & Prevention”.

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Differentiating Atelectasis from other Diseases

Differentiating Atelectasis from other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sudarshana Datta, MD [2]Eiman Ghaffarpasand, M.D. [3]

Overview

Atelectasis must be differentiated from other diseases that cause acute dyspnea, fever, and chest pain, such as asthma, bronchitis, and interstitial lung disease.

Differentiating X from other Diseases

  • Atelectasis must be differentiated from other diseases that cause acute dyspnea. This is depicted in the table below.
Organ system Diseases Clinical manifestations Diagnosis Other features
Symptoms Physical exam
Loss of consciousness Agitation Weight loss Fever Chest pain Cough Cyanosis Clubbing JVD Peripheral edema Auscultation CBC ABG Imaging Spirometry Gold standard
Acute Dyspnea Respiratory system Head and Neck,

Upper airway

Angioedema[1] – – – – – +/- – +/- – + Normal Normal ↓O2, ↑CO2 Normal N/A Physical exam Generalized edema
Anaphylaxis[2] +/- + – +/- – – +/- – – – Scattered wheezing Normal Normal Normal N/A Vital sign Type 1 hypersensitivity
Aspiration[3] – + – – +/- + + – – – Diminished breath sounds Normal Normal Atelectasis ↓Vt, ↑RV Bronchoscopy Choking
Croup[4] – + – +/- – + + – – – Stridor ↑WBC Normal Steeple sign Normal Physical exam Barking cough
Epiglottitis[5] – + – + – + – – – – Stridor ↑WBC Normal Thumb sign Normal Laryngoscopy Drooling
Rhinosinusitis[6] – – – + – +/- – – – – Normal ↑WBC Normal Air fluid level Normal Physical exam Headache
Vocal cord dysfunction[7] – – – – – +/- – – – – Stridor Normal Normal Normal ↓ FVC Laryngoscopy Choking sensation
Chest and Pleura,

Lower airway

Asthma attack[8] – + – – +/- + + – – – Wheeze ↑ Eosinophil Respiratory alkalosis Normal ↓ FEV1, PEF Physical exam and

Spirometry

Chest pain
Bronchitis[9] – – – + + + – – – – Rhonchi  ↑WBC Normal Normal Normal Physical exam Rhonchi relieved by cough
Bronchospasm[10] +/- + – – + +/- + – – – Wheeze Normal ↓O2, ↑CO2 Normal ↓Vt, ↑RV Physical exam Allergic reaction
Atelectasis – – – +/- +/- +/- +/- – – – Diminished breath sounds, Wheeze Normal ↓O2, Normal/↓CO2 Opacification of the collapsed lung lobe,

displacement of fissures

↓ FVC CT scan of chest without contrast History of surgical procedure, aspiration, mechanical ventilation
Bronchiolitis[11] – – – + +/- + – – – – Wheeze and Crackles ↑WBC Normal Bronchovascular markings ↓Vt Clinical assessment Respiratory syncytial virus (RSV)
COPD exacerbation[12] – + – + + + + +/- +/- +/- Wheeze, Rhonchi, and Crackles ↑WBC, ↑RBC Respiratory alkalosis Hyperexpansion ↓ FEV1/FVC Clinical assessment Acute exacerbations of chronic bronchitis (AECB)
Lung carcinoma[13] – – + – – + + + – – Wheeze and Crackles Normal Normal Mass lesion, hilar lymphadenopathy ↓Vt, ↑RV Bronchoscopy  Paraneoplastic syndromes, such as SIADH and lambert-Eaton
Pneumonia[14] – – – + + + – – – – Wheeze, Rhonchi, and Crackles ↑WBC, neutrophilia Normal Lobar consolidation Normal Chest X-ray and CT Scan productive cough
Pneumothorax[15] – – – – + – – – +/- – Diminished breath sounds Normal ↓O2, ↑CO2 Radiolucency without lung marking ↓Vt CXR and Chest CT scan Tracheal deviation
Pulmonary embolism[16] – – – – + – – – – – Normal Normal Respiratory alkalosis Normal Normal Pulmonary CT angiography Pleuritic chest pain
Rib fractures (flail chest)[17] – + – – + – – – – – Normal Normal Respiratory acidosis Fracture marks Normal Chest X-ray Pneumothorax
Cardiovascular system Acute myocardial ischemia[18] +/- + – +/- + – – – – – Normal Normal Normal Normal Normal Cardiac troponin I Nausea and vomiting, Positive pertinent risk factors, such as hypertension, diabetes, and smoking
Acute heart failure[19] +/- + – – +/- + + – + + S3 Normal Respiratory alkalosis ↑ Cardiothoracic ratio ↓Vt B-type natriuretic peptide (BNP) and N-terminal proBNP (NT-proBNP) Excessive sweating, high blood pressure
Pericardial tamponade[20] +/- – – – + – – – + – Muffled heart sounds Normal Normal Water bottle appearance enlarged heart Normal Echocardiography Fluid accumulation in pericardium
Tachyarrhythmia[18] +/- + – – +/- – – – – – High pulse rate Normal Normal Normal Normal ECG Palpitation
Pulmonary edema[21] +/- + – + + + + + + + Basal crackle Normal Respiratory alkalosis Bat wing pattern, air bronchograms ↓Vt, ↑RV Cardiac Catheterization Tachypnea
Central nervous system Stroke + – – +/- – – – – – – Normal Normal Normal Intracranial infarct or hemorrhage Normal Brain MRI Paralysis or paresthesia
Encephalitis[22] + + – + – – – – – – Normal ↑WBC, neutrophilia Normal Normal Normal CSF PCR Confusion
Traumatic brain injury[23] + +/- – – – – – – – – Normal Normal Respiratory acidosis Intracerebral hemorrhage Normal Brain CT scan Lucid interval
Toxic/Metabolic Organophosphate poisoning[24] + – – + – – – – – – Wheeze Normal ↓O2, ↑CO2 Normal Normal Blood test Salivation, Lacrimation, Emesis, Miosis
Salicylate poisoning[25] + – – – – – + – – – Normal Normal Metabolic acidosis, Respiratory alkalosis Normal Normal Blood test Vomiting, Tinnitus, Confusion, Hyperthermia
Carbon monoxide poisoning[26] + – – – + + + – – – Wheeze Carboxyhemoglobin ↓O2, ↑CO2 Normal N/A Carboxyhemoglobin (HbCO) level Headache, Dizziness, Weakness, Vomiting, Confusion
Diabetic ketoacidosis[27] + +/- – – – – – – – – Scattered wheeze, Kussmaul’s respiration ↑WBC Metabolic acidosis Normal Normal Blood test (acidosis, hyperglycemia, ketonemia) Vomiting, Abdominal pain, Weakness, Confusion
Systemic Panic attack[28] +/- + – – – – – – – – Normal Normal Normal Normal Normal Clinical assessment Severe anxiety
Pregnancy[29] – – – – +/- – – – – + Normal ↑WBC, RBC ↓O2, ↑CO2 Normal ↓Vt, ↑RV βhCG Missed period, Hyperemesis
Sepsis[30] +/- – – + – – – – – – Normal ↑WBC, neutrophilia ↓O2, ↑CO2 Normal Normal SIRS criteria Chills, Confusion
Organ system Diseases Clinical manifestations Diagnosis Other features
Symptoms Physical exam
Loss of consciousness Agitation Weight loss Fever Chest pain Cough Cyanosis Clubbing JVD Peripheral edema Auscultation CBC ABG Imaging Spirometry Gold standard
Chronic Dyspnea Respiratory system Head and Neck,

Upper airway

Goiter[31] – – – – – – – – – + Normal Normal Normal Normal Normal Blood test (TSH, T4) Weight gain
Laryngeal adenocarcinoma[32] – – + – – +/- – – – – Stridor Normal ↓O2, ↑CO2 Retropharyngeal tissue thickness Normal Laryngoscopy Choking sensation
Vocal cord paralysis[7] – – – – – +/- – – – – Stridor Normal Normal Pharyngeal constrictor muscles thinning, uvular deviation Normal Laryngoscopy Choking sensation
Tracheal stenosis[33] – – – – +/- +/- + + – – Stridor, Stertorous Normal ↓O2, ↑CO2 Soft tissue thickening internal to normal-appearing tracheal cartilage Normal Bronchoscopy Respiratory distress
Chest and Pleura,

Lower airway

Bronchial asthma[8] – + +/- – +/- + + + – – Wheeze ↑ Eosinophil Respiratory alkalosis, Metabolic acidosis Pulmonary hyperinflation,

Bronchial wall thickening

↓ FEV1/FVC Spirometry before and after bronchodilator Paroxysmal respiratory distress
Bronchiectasis[9] – – – + + + + + – – Rhonchi, Wheezing, Crackles ↑WBC, neutrophilia ↓O2, ↑CO2 Tram-track opacities ↑ FEV1/FVC High resolution computed tomography (HRCT) Chronic productive cough
COPD[12] – – +/- – – + + + + +/- Expiratory wheeze ↑ RBC Respiratory alkalosis, Metabolic acidosis ↑ Bronchovascular markings, Cardiomegaly ↓ FEV1/FVC Physical exam and

Spirometry

Heavy smoking history
Emphysema[34] – – – – – +/- + + – – Expiratory wheeze, Hyperinflation Normal Respiratory alkalosis, Metabolic acidosis Flattening of diaphragm, vertical heart ↓ FEV1/FVC Physical exam and

Spirometry

Barrel chest
Pulmonary hypertension[35] – – – – +/- +/- +/- +/- + + Accentuated S2 Normal Hypoxia and acidosis Enlarged pulmonary arteries ↑Physiologic RV Cardiac catheterization Syncope,

Ascites, Pleural effusion

Interstitial lung disease[36] – – – – + + + + – – Rhonchi, Wheezing, Crackles Normal ↓O2, ↑CO2 Peripheral pulmonary infiltrative opacification ↑ FEV1/FVC High resolution computed tomography (HRCT) Pneumoconiosis
Sarcoidosis[37] – – +/- – +/- + + – – – Crackles Normal ↓O2, ↑CO2 Hilar adenopathy ↑ FEV1/FVC High resolution computed tomography (HRCT) Hypercalcemia, high ACE
Alveolitis[38] – – – + + + – – – – Basal crackle ↑WBC, neutrophilia Normal  Basal reticulonodular opacification   ↑ FEV1/FVC High resolution computed tomography (HRCT) Dry cough
Bronchiolitis obliterans[11] – – – + + + + + – – Expiratory wheeze ↑WBC ↓O2, ↑CO2 Hyperinflation, Reticulonodular opacities ↓ FEV1/FVC Lung biopsy Complication of allogeneic hematopoietic stem cell transplantation
Cystic fibrosis[39] – – + + – +/- + + – – Rhonchi, Wheezing, Crackles Normal Metabolic alkalosis Thick-walled bronchiectasis ↓ FEF75%/FVC Sweat test Absent vas deferens
Pleural effusion[40] – +/- + – + – – – +/- +/- Egophony (“E-to-A” change) Normal Normal Blunting of the costophrenic and cardiophrenic angle ↓Vt, ↑RV Light’s criteria ↓Tactile fremitus, Asymmetrical chest expansion
Pulmonary right-to-left shunt[41] – – – – +/- + + + – – Diminished breath sounds Normal ↓O2, ↑CO2, Respiratory acidosis Normal ↓Vt, ↑RV

(physiological)

Pulmonary CT angiography Chronic hypoxemia
Diaphragmatic paralysis[42] – – – +/- +/- +/- – – – – Normal Normal Normal Unilateral or bilateral diaphragmatic flattening ↓Vt, ↑RV

(anatomical)

CXR confirmed by fluoroscopic sniff test Respiratory insufficiency
Tuberculosis[43] – – + + + + +/- – – – Rhonchi, Wheezing, Crackles ↑WBC ↓O2, ↑CO2 Patchy consolidation or poorly defined linear and nodular opacities Restrictive, obstructive, or mixed IFN-γ release assay (IGRA)

Acid-fast staining

Night sweat
Cardiovascular system Constrictive pericarditis[20] – – – – + – – – + – Muffled heart sounds Normal Normal Calcifications  Normal Chest CT scan Syncope
Restrictive cardiomyopathy[44] – – – – + – – – – +/- Normal Normal Normal Dilatation of the inferior vena cava and right atrium Normal Right ventricular biopsy Weight gain,

Nausea

Valvular heart disease[18] – – – – + – – – – – Cardiac murmur Normal Normal Dilatation of heart chambers Normal Echocardiography Syncope, Palpitation
Bradyarrhythmia[45] – – – – – – – – – – Normal Normal Normal Normal Normal ECG Syncope, Palpitation
Pericardial effusion[46] – – – +/- + + – – + – Muffled heart sounds Normal Normal Fluid density around the heart Normal M-mode and 2-dimensional Doppler echocardiography Hoarseness, Palpitation
Coronary heart disease[18] – +/- – – + – – – – – Normal Normal ↓O2 Normal Normal Cardiac troponin I Nausea, Lightheadedness, Sweating
Intracardiac shunt[47] – – – – +/- – + + – – Cardiac continuous murmur Normal ↓O2 Dilatation of heart chambers Normal Echocardiography Syncope, Palpitation
Neuromuscular disease Amyotrophic lateral sclerosis[48] +/- – +/- – – – – – – – Normal ↑WBC Normal Normal ↓Vt, ↑RV Revised El Escorial criteria (clinical) Muscle weakness, Dysphagia
Polymyositis/dermatomyositis[49] – – +/- – + – – – – +/- Normal ↑WBC Normal Normal ↓Vt, ↑RV Muscle biopsy Muscle weakness, Heliotrope
Mitochondrial diseases[50] – – +/- – – – – – – – Wheeze ↓WBC, Plt Normal Normal ↓Vt, ↑RV Muscle biopsy Muscle pain
Glycolytic enzyme defects (e.g., McArdle)[51] +/- – – – – – – – – +/- Normal Normal Normal Normal ↓Vt, ↑RV Muscle biopsy (ragged red fibers) Myoglobinuria,

Muscle weakness

Toxic/Metabolic Metabolic acidosis[52] – – + – – – – – – – Normal Normal Metabolic acidosis, Respiratory alkalosis Normal Normal ABG Confusion, Vomiting
Renal failure[53] – – + – – – – – – + Normal ↓ RBC Metabolic acidosis Normal Normal Cr Nausea, Vomiting, Oliguria
Systemic Anemia[54] – – + – – – – – – – Normal ↓ RBC ↓O2 Normal Normal HGB, MCV Weakness, Fatigue
Anxiety[55] + + + – +/- +/- – – – – Normal Normal Normal Normal Normal Psychological interview Sweating, Palpitation
Ascites[56] – – – – – – – – – – Normal Normal Normal Peritoneal fluid accumulation ↓Vt, ↑RV Abdominal ultrasound Abdominal distention
Depression[57] – + + – – – – – – – Normal Normal Normal Normal Normal Psychological interview Depressed mood, Fatigue
Kyphoscoliosis[58] – – – – – – – – – – Wheeze Normal Normal Deviated vertebral column ↓Vt, ↑RV

(anatomical)

Standing lateral spine radiograph Low back pain
Obesity[59] – – – – – – – – – – Normal Normal ↓O2 Normal ↓Vt, ↑RV

(anatomical)

BMI Low stamina,

Sweating

Autoimmune Churg-Strauss syndrome[60] – – – – – + – – – – Scattered wheezing Normal Normal Areas of parenchymal opacification ↓Vt, ↑RV Biopsy  Fatigue,Numbness
Microscopic polyangiitis[61] – – +/- + + – – – – +/- Scattered wheezing ↑WBC ↓O2, ↑CO2 Normal ↓Vt, ↑RV Histological confirmation Skin lesions, Nerve damage
Wegener’s granulomatosis[62] – – +/- – – + – – – – Wheezing, Crackles ↓ RBC ↓O2, ↑CO2 Cavitate nodules, ground-glass opacity ↓ FEV1/FVC Biopsy demonstrating a granulomatous vasculitis Chronic rhinosinusitis
Goodpasture’s disease[63] – – – – – + – – – –  Bilateral coarse crepitations ↓ RBC, HGB, HCT Normal  Like pulmonary edema Normal Kidney biopsy Hematuria,

Hemoptysis

References

  1. ↑ Bernstein JA, Cremonesi P, Hoffmann TK, Hollingsworth J (2017). “Angioedema in the emergency department: a practical guide to differential diagnosis and management”. Int J Emerg Med. 10 (1): 15. doi:10.1186/s12245-017-0141-z. PMC 5389952. PMID 28405953.
  2. ↑ Bjornsson HM, Graffeo CS (2010). “Improving diagnostic accuracy of anaphylaxis in the acute care setting”. West J Emerg Med. 11 (5): 456–61. PMC 3027438. PMID 21293765.
  3. ↑ O’Horo JC, Rogus-Pulia N, Garcia-Arguello L, Robbins J, Safdar N (2015). “Bedside diagnosis of dysphagia: a systematic review”. J Hosp Med. 10 (4): 256–65. doi:10.1002/jhm.2313. PMC 4607509. PMID 25581840.
  4. ↑ Bjornson CL, Johnson DW (2013). “Croup in children”. CMAJ. 185 (15): 1317–23. doi:10.1503/cmaj.121645. PMC 3796596. PMID 23939212.
  5. ↑ Negus VE (1927). “The Function of the Epiglottis”. J Anat. 62 (Pt 1): 1–8. PMC 1250045. PMID 17104162.
  6. ↑ Meltzer EO, Hamilos DL (2011). “Rhinosinusitis diagnosis and management for the clinician: a synopsis of recent consensus guidelines”. Mayo Clin Proc. 86 (5): 427–43. doi:10.4065/mcp.2010.0392. PMC 3084646. PMID 21490181.
  7. ↑ 7.0 7.1 Wood RP, Milgrom H (September 1996). “Vocal cord dysfunction”. J. Allergy Clin. Immunol. 98 (3): 481–5. PMID 8828523.
  8. ↑ 8.0 8.1 Hodder R, Lougheed MD, Rowe BH, FitzGerald JM, Kaplan AG, McIvor RA (2010). “Management of acute asthma in adults in the emergency department: nonventilatory management”. CMAJ. 182 (2): E55–67. doi:10.1503/cmaj.080072. PMC 2817338. PMID 19858243.
  9. ↑ 9.0 9.1 Cantin, Luce; Bankier, Alexander A.; Eisenberg, Ronald L. (2009). “Bronchiectasis”. American Journal of Roentgenology. 193 (3): W158–W171. doi:10.2214/AJR.09.3053. ISSN 0361-803X.
  10. ↑ Molis MA, Molis WE (2010). “Exercise-induced bronchospasm”. Sports Health. 2 (4): 311–7. doi:10.1177/1941738110373735. PMC 3445098. PMID 23015953.
  11. ↑ 11.0 11.1 Holbro A, Lehmann T, Girsberger S, Stern M, Gambazzi F, Lardinois D, Heim D, Passweg JR, Tichelli A, Bubendorf L, Savic S, Hostettler K, Grendelmeier P, Halter JP, Tamm M (2013). “Lung histology predicts outcome of bronchiolitis obliterans syndrome after hematopoietic stem cell transplantation”. Biol. Blood Marrow Transplant. 19 (6): 973–80. doi:10.1016/j.bbmt.2013.03.017. PMID 23562737.
  12. ↑ 12.0 12.1 Qureshi H, Sharafkhaneh A, Hanania NA (2014). “Chronic obstructive pulmonary disease exacerbations: latest evidence and clinical implications”. Ther Adv Chronic Dis. 5 (5): 212–27. doi:10.1177/2040622314532862. PMC 4131503. PMID 25177479.
  13. ↑ Dela Cruz CS, Tanoue LT, Matthay RA (2011). “Lung cancer: epidemiology, etiology, and prevention”. Clin Chest Med. 32 (4): 605–44. doi:10.1016/j.ccm.2011.09.001. PMC 3864624. PMID 22054876.
  14. ↑ Simonetti AF, Viasus D, Garcia-Vidal C, Carratalà J (2014). “Management of community-acquired pneumonia in older adults”. Ther Adv Infect Dis. 2 (1): 3–16. doi:10.1177/2049936113518041. PMC 4072047. PMID 25165554.
  15. ↑ Currie GP, Alluri R, Christie GL, Legge JS (2007). “Pneumothorax: an update”. Postgrad Med J. 83 (981): 461–5. doi:10.1136/pgmj.2007.056978. PMC 2600088. PMID 17621614.
  16. ↑ Bĕlohlávek J, Dytrych V, Linhart A (2013). “Pulmonary embolism, part I: Epidemiology, risk factors and risk stratification, pathophysiology, clinical presentation, diagnosis and nonthrombotic pulmonary embolism”. Exp Clin Cardiol. 18 (2): 129–38. PMC 3718593. PMID 23940438.
  17. ↑ Swart E, Laratta J, Slobogean G, Mehta S (February 2017). “Operative Treatment of Rib Fractures in Flail Chest Injuries: A Meta-analysis and Cost-Effectiveness Analysis”. J Orthop Trauma. 31 (2): 64–70. doi:10.1097/BOT.0000000000000750. PMID 27984449.
  18. ↑ 18.0 18.1 18.2 18.3 Bruyninckx R, Aertgeerts B, Bruyninckx P, Buntinx F (2008). “Signs and symptoms in diagnosing acute myocardial infarction and acute coronary syndrome: a diagnostic meta-analysis”. Br J Gen Pract. 58 (547): 105–11. doi:10.3399/bjgp08X277014. PMC 2233977. PMID 18307844.
  19. ↑ Gaggin, Hanna K.; Januzzi, James L. (2013). “Biomarkers and diagnostics in heart failure”. Biochimica et Biophysica Acta (BBA) – Molecular Basis of Disease. 1832 (12): 2442–2450. doi:10.1016/j.bbadis.2012.12.014. ISSN 0925-4439.
  20. ↑ 20.0 20.1 van Steijn JH, Sleijfer DT, van der Graaf WT, van der Sluis A, Nieboer P (2002). “How to diagnose cardiac tamponade”. Neth J Med. 60 (8): 334–8. PMID 12481882.
  21. ↑ Martindale, Jennifer L.; Noble, Vicki E.; Liteplo, Andrew (2013). “Diagnosing pulmonary edema”. European Journal of Emergency Medicine. 20 (5): 356–360. doi:10.1097/MEJ.0b013e32835c2b88. ISSN 0969-9546.
  22. ↑ Debiasi RL, Tyler KL (2004). “Molecular methods for diagnosis of viral encephalitis”. Clin Microbiol Rev. 17 (4): 903–25, table of contents. doi:10.1128/CMR.17.4.903-925.2004. PMC 523566. PMID 15489354.
  23. ↑ McAllister TW (2011). “Neurobiological consequences of traumatic brain injury”. Dialogues Clin Neurosci. 13 (3): 287–300. PMC 3182015. PMID 22033563.
  24. ↑ Peter JV, Sudarsan TI, Moran JL (2014). “Clinical features of organophosphate poisoning: A review of different classification systems and approaches”. Indian J Crit Care Med. 18 (11): 735–45. doi:10.4103/0972-5229.144017. PMC 4238091. PMID 25425841.
  25. ↑ Chin RL, Olson KR, Dempsey D (2007). “Salicylate toxicity from ingestion and continued dermal absorption”. Cal J Emerg Med. 8 (1): 23–5. PMC 2859737. PMID 20440389.
  26. ↑ Lane TR, Williamson WJ, Brostoff JM (2008). “Carbon monoxide poisoning in a patient with carbon dioxide retention: a therapeutic challenge”. Cases J. 1 (1): 102. doi:10.1186/1757-1626-1-102. PMC 2533003. PMID 18710551.
  27. ↑ Westerberg DP (March 2013). “Diabetic ketoacidosis: evaluation and treatment”. Am Fam Physician. 87 (5): 337–46. PMID 23547550.
  28. ↑ Taylor CB (2006). “Panic disorder”. BMJ. 332 (7547): 951–5. doi:10.1136/bmj.332.7547.951. PMC 1444835. PMID 16627512.
  29. ↑ Lee SY, Chien DK, Huang CH, Shih SC, Lee WC, Chang WH (August 2017). “Dyspnea in pregnancy”. Taiwan J Obstet Gynecol. 56 (4): 432–436. doi:10.1016/j.tjog.2017.04.035. PMID 28805596.
  30. ↑ Askim Å, Mehl A, Paulsen J, DeWan AT, Vestrheim DF, Åsvold BO; et al. (2016). “Epidemiology and outcome of sepsis in adult patients with Streptococcus pneumoniae infection in a Norwegian county 1993-2011: an observational study”. BMC Infect Dis. 16: 223. doi:10.1186/s12879-016-1553-8. PMC 4877975. PMID 27216810.
  31. ↑ Stang MT, Armstrong MJ, Ogilvie JB, Yip L, McCoy KL, Faber CN, Carty SE (July 2012). “Positional dyspnea and tracheal compression as indications for goiter resection”. Arch Surg. 147 (7): 621–6. doi:10.1001/archsurg.2012.96. PMID 22430090.
  32. ↑ Schwenk NR, Schapira RM, Byrd JC (November 1994). “Laryngeal carcinoma presenting as platypnea”. Chest. 106 (5): 1609–11. PMID 7956433.
  33. ↑ Conti V, Calia N, Pasquini C, Zardi S, Finetti C, Stomeo F, Ravenna F (April 2013). “[Chronic cough and worsening dyspnea: a case of idiopathic tracheal stenosis]”. Recenti Prog Med (in Italian). 104 (4): 156–8. doi:10.1701/1271.14026. PMID 23748638.
  34. ↑ Sharafkhaneh A, Hanania NA, Kim V (2008). “Pathogenesis of emphysema: from the bench to the bedside”. Proc Am Thorac Soc. 5 (4): 475–7. doi:10.1513/pats.200708-126ET. PMC 2645322. PMID 18453358.
  35. ↑ Sajkov D, Petrovsky N, Palange P (June 2010). “Management of dyspnea in advanced pulmonary arterial hypertension”. Curr Opin Support Palliat Care. 4 (2): 76–84. doi:10.1097/SPC.0b013e328338c1e0. PMID 20407377.
  36. ↑ Baughman RP, Shipley RT, Loudon RG, Lower EE (1991). “Crackles in interstitial lung disease. Comparison of sarcoidosis and fibrosing alveolitis”. Chest. 100 (1): 96–101. PMID 2060395.
  37. ↑ Moher D, Cole CW, Hill GB (November 1992). “Epidemiology of abdominal aortic aneurysm: the effect of differing definitions”. Eur J Vasc Surg. 6 (6): 647–50. PMID 1451823.
  38. ↑ Khanna D, Clements PJ, Furst DE, Chon Y, Elashoff R, Roth MD, Sterz MG, Chung J, FitzGerald JD, Seibold JR, Varga J, Theodore A, Wigley FM, Silver RM, Steen VD, Mayes MD, Connolly MK, Fessler BJ, Rothfield NF, Mubarak K, Molitor J, Tashkin DP (February 2005). “Correlation of the degree of dyspnea with health-related quality of life, functional abilities, and diffusing capacity for carbon monoxide in patients with systemic sclerosis and active alveolitis: results from the Scleroderma Lung Study”. Arthritis Rheum. 52 (2): 592–600. doi:10.1002/art.20787. PMID 15692967.
  39. ↑ Ziegler, Bruna; Rovedder, Paula Maria Eidt; Dalcin, Paulo de Tarso Roth; Menna-Barreto, Sérgio Saldanha (2009). “Padrões ventilatórios na espirometria em pacientes adolescentes e adultos com fibrose cística”. Jornal Brasileiro de Pneumologia. 35 (9): 854–859. doi:10.1590/S1806-37132009000900006. ISSN 1806-3713.
  40. ↑ Thomas R, Jenkins S, Eastwood PR, Lee YC, Singh B (July 2015). “Physiology of breathlessness associated with pleural effusions”. Curr Opin Pulm Med. 21 (4): 338–45. doi:10.1097/MCP.0000000000000174. PMC 5633324. PMID 25978627.
  41. ↑ Vodoz JF, Cottin V, Glérant JC, Derumeaux G, Khouatra C, Blanchet AS; et al. (2009). “Right-to-left shunt with hypoxemia in pulmonary hypertension”. BMC Cardiovasc Disord. 9: 15. doi:10.1186/1471-2261-9-15. PMC 2671488. PMID 19335916.
  42. ↑ Dubé BP, Dres M (2016). “Diaphragm Dysfunction: Diagnostic Approaches and Management Strategies”. J Clin Med. 5 (12). doi:10.3390/jcm5120113. PMC 5184786. PMID 27929389.
  43. ↑ Campbell IA, Bah-Sow O (2006). “Pulmonary tuberculosis: diagnosis and treatment”. BMJ. 332 (7551): 1194–7. doi:10.1136/bmj.332.7551.1194. PMC 1463969. PMID 16709993.
  44. ↑ Nakamura M, Satoh M, Kowada S, Satoh H, Tashiro A, Sato F, Masuda T, Hiramori K (February 2002). “Reversible restrictive cardiomyopathy due to light-chain deposition disease”. Mayo Clin. Proc. 77 (2): 193–6. doi:10.4065/77.2.193. PMID 11838655.
  45. ↑ Barstow C, McDivitt JD (March 2017). “Cardiovascular Disease Update: Bradyarrhythmias”. FP Essent. 454: 18–23. PMID 28266824.
  46. ↑ Jung HO (2012). “Pericardial effusion and pericardiocentesis: role of echocardiography”. Korean Circ J. 42 (11): 725–34. doi:10.4070/kcj.2012.42.11.725. PMC 3518705. PMID 23236323.
  47. ↑ Vodoz JF, Cottin V, Glérant JC, Derumeaux G, Khouatra C, Blanchet AS; et al. (2009). “Right-to-left shunt with hypoxemia in pulmonary hypertension”. BMC Cardiovasc Disord. 9: 15. doi:10.1186/1471-2261-9-15. PMC 2671488. PMID 19335916.
  48. ↑ Lechtzin N, Lange DJ, Davey C, Becker B, Mitsumoto H (January 2007). “Measures of dyspnea in patients with amyotrophic lateral sclerosis”. Muscle Nerve. 35 (1): 98–102. doi:10.1002/mus.20669. PMID 17029274.
  49. ↑ Schwarz MI, Matthay RA, Sahn SA, Stanford RE, Marmorstein BL, Scheinhorn DJ (January 1976). “Interstitial lung disease in polymyositis and dermatomyositis: analysis of six cases and review of the literature”. Medicine (Baltimore). 55 (1): 89–104. PMID 1246203.
  50. ↑ Heinicke K, Taivassalo T, Wyrick P, Wood H, Babb TG, Haller RG (2011). “Exertional dyspnea in mitochondrial myopathy: clinical features and physiological mechanisms”. Am J Physiol Regul Integr Comp Physiol. 301 (4): R873–84. doi:10.1152/ajpregu.00001.2011. PMC 3197343. PMID 21813873.
  51. ↑ Tarui S (1995). “Glycolytic defects in muscle: aspects of collaboration between basic science and clinical medicine”. Muscle Nerve Suppl. 3: S2–9. PMID 7603522.
  52. ↑ Lane R, Adams L (1993). “Metabolic acidosis and breathlessness during exercise and hypercapnia in man”. J Physiol. 461: 47–61. PMC 1175244. PMID 8350272.
  53. ↑ DePalo LR (May 2002). “Fatal dyspnea in a patient with renal failure”. Mt. Sinai J. Med. 69 (3): 113–20. PMID 12035070.
  54. ↑ Sengupta A, Saha K, Jash D, Banerjee SN (2013). “Dyspnea with anemia turned out to be a case of hereditary hemorrhagic telangiectasia”. Asian J Transfus Sci. 7 (1): 75–8. doi:10.4103/0973-6247.106745. PMC 3613670. PMID 23559772.
  55. ↑ Bailey PH (July 2004). “The dyspnea-anxiety-dyspnea cycle–COPD patients’ stories of breathlessness: “It’s scary /when you can’t breathe““. Qual Health Res. 14 (6): 760–78. doi:10.1177/1049732304265973. PMID 15200799.
  56. ↑ Perri GA (2013). “Ascites in patients with cirrhosis”. Can Fam Physician. 59 (12): 1297–9, e538–40. PMC 3860926. PMID 24336542.
  57. ↑ Neuman A, Gunnbjörnsdottir M, Tunsäter A, Nyström L, Franklin KA, Norrman E, Janson C (October 2006). “Dyspnea in relation to symptoms of anxiety and depression: A prospective population study”. Respir Med. 100 (10): 1843–9. doi:10.1016/j.rmed.2006.01.016. PMID 16516455.
  58. ↑ Qiabi M, Chagnon K, Beaupré A, Hercun J, Rakovich G (2015). “Scoliosis and bronchial obstruction”. Can Respir J. 22 (4): 206–8. PMC 4530852. PMID 26083538.
  59. ↑ Sin DD, Jones RL, Man SF (July 2002). “Obesity is a risk factor for dyspnea but not for airflow obstruction”. Arch. Intern. Med. 162 (13): 1477–81. PMID 12090884.
  60. ↑ Uyar M, Elbek O, Bakır K, Kibar Y, Bayram N, Dikensoy Ö (2012). “Churg-Strauss syndrome related to montelukast”. Tuberk Toraks. 60 (1): 56–8. PMID 22554368.
  61. ↑ Tilanus A, Van der Niepen P, Geers C, Wissing KM (2015). “Pulmonary Limited MPO-ANCA Microscopic Polyangiitis and Idiopathic Lung Fibrosis in a Patient with a Diagnosis of IgA Nephropathy”. Case Rep Nephrol. 2015: 378170. doi:10.1155/2015/378170. PMC 4525752. PMID 26266064.
  62. ↑ Cardenas-Garcia J, Farmakiotis D, Baldovino BP, Kim P (2012). “Wegener’s granulomatosis in a middle-aged woman presenting with dyspnea, rash, hemoptysis and recurrent eye complaints: a case report”. J Med Case Rep. 6: 335. doi:10.1186/1752-1947-6-335. PMC 3492078. PMID 23034218.
  63. ↑ Bal, Amanjit; Das, Ashim; Gupta, Dheeraj; Garg, Mandeep (2014). “Goodpasture’s Syndrome and p-ANCA Associated Vasculitis in a Patient of Silicosiderosis: An Unusual Association”. Case Reports in Pulmonology. 2014: 1–7. doi:10.1155/2014/398238. ISSN 2090-6846.

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Epidemiology and Demographics

Epidemiology and Demographics

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sudarshana Datta, MD [2]

Overview

The incidence and prevalence of atelectasis are not known. Patients of all age groups may develop atelectasis. Rounded atelectasis commonly affects individuals at sixty years of age. Atelectasis affects men and women equally.

Epidemiology and demographics

Incidence

  • The incidence of atelectasis is approximately 79 per 100,000 individuals worldwide.[1]

Prevalence

  • The prevalence of atelectasis is not known.
  • Postoperative atelectasis is the most common type of atelectasis.

Age

  • Patients of all age groups may develop atelectasis.
  • Rounded atelectasis commonly affects individuals at sixty years of age.

Race

  • There is no racial predilection to atelectasis.

Gender

  • Atelectasis affects men and women equally.

References

  1. ↑ Dembinski R, Mielck F (February 2018). “[ARDS – An Update – Part 1: Epidemiology, Pathophysiology and Diagnosis]”. Anasthesiol Intensivmed Notfallmed Schmerzther (in German). 53 (2): 102–111. doi:10.1055/s-0043-107166. PMID 29426049.

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Risk Factors

Risk Factors

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sudarshana Datta, MD [2]

Overview

Chest trauma, general anaesthesia, thoracic surgery, cystic fibrosis, prematurity and respiratory distress syndrome are some of the common risk factors that predispose patients to developing atelectasis. Children less than three years of age and adults over sixty years of age are also at increased risk of alveolar collapse and impaired surfactant production in response to pulmonary stressors such as toxins, hyperoxia, hypoxia and ischemia. 

Risk Factors

Common Risk Factors

Less Common Risk Factors

References

  1. ↑ 1.0 1.1 “Atelectasis | Causes, Symptoms, Treatment & Prevention”.
  2. ↑ “Atelectasis – Symptoms and causes – Mayo Clinic”.

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Screening

Screening

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sudarshana Datta, MD [2]

Overview

There is insufficient evidence to recommend routine screening for atelectasis.

Screening

There is insufficient evidence to recommend routine screening for atelectasis.

References

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Natural History, Complications and Prognosis

Natural History, Complications and Prognosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

Overview

If left untreated, atelectasis may be fatal in patients and progress to pneumonia, sepsis, and respiratory failure. Common complications of atelectasis include pneumonia, bronchiectasis, hypoxemia, respiratory failure, and sepsis. Depending on the extent of lung involvement at the time of diagnosis, the prognosis may vary. However, the prognosis is generally regarded as good. Involvement of a small portion of the lung is not associated with life threatening complications, as the remaining lung compensates for the hypoxemia. However, atelectasis is associated with poor prognosis if the surface area of lung involvement is very large, in the presence of pre-existing lung disease, in case of failure to remove obstruction and in case of atelectasis due to cancer.

Natural History, Complications, and Prognosis

Natural History

Complications

Prognosis

  • Depending on the extent of lung involvement at the time of diagnosis, the prognosis may vary. However, the prognosis is generally regarded as good.[3]
  • Involvement of a small portion of the lung is not associated with life threatening complications, as the remaining lung compensates for the hypoxemia.
  • The presence of atelectasis is associated with a particularly good prognosis among patients who develop symptoms postoperatively.
  • Atelectasis is associated with poor prognosis in the following scenarios:[3]
    • Surface area of lung involvement is very large
    • In the presence of pre-existing lung disease
    • Failure to remove obstruction in case of obstructive atelectasis
    • Atelectasis due to cancer

References

  1. ↑ Halvorsen T, Skadberg BT, Eide GE, Røksund OD, Carlsen KH, Bakke P (2004). “Pulmonary outcome in adolescents of extreme preterm birth: a regional cohort study”. Acta Paediatr. 93 (10): 1294–300. PMID 15499947.
  2. ↑ 2.0 2.1 “Atelectasis – Symptoms and causes – Mayo Clinic”.
  3. ↑ 3.0 3.1 “Atelectasis – Scripps Health”.

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Diagnosis

Diagnosis

History and Symptoms | Physical Examination | Laboratory Findings | Chest X Ray | CT | MRI | Ultrasound | Other Imaging Findings | Other Diagnostic Studies

Treatment

Treatment

Medical Therapy | Surgery | Primary Prevention | Secondary Prevention | Future or Investigational Therapies

Case Studies

Case Studies

Case #1


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