1.

Pneumothorax is defined as the presence of air or gas in the pleural cavity, that is, in the potential space between the visceral and parietal pleura of the lung. The result is collapse of the lung on the affected side. Air can enter the intrapleural space through a communication from the chest wall (ie, trauma) or through the lung parenchyma across the visceral pleura. 2. Primary and secondary spontaneous pneumothorax Primary spontaneous pneumothorax (PSP) occurs in people without underlying lung disease and in the absence of an inciting event. However, many patients whose condition is labeled as primary spontaneous pneumothorax have subclinical lung disease. Patients are typically between age 18 and 40 years. PSP is typically observed in tall, young people without parenchymal lung disease and is thought to be related to increased shear forces in the apex. Risks factors for primary spontaneous pneumothorax (PSP) include the following:Smoking, Tall, thin stature in a healthy person, Marfan syndrome, Pregnancy, Familial pneumothorax The pleural space has a negative pressure, If the pleural space is invaded by gas from a ruptured bleb, the lung collapses until equilibrium is achieved or the rupture is sealed. As the pneumothorax enlarges, the lung becomes smaller. The main physiologic consequence of this process is a decrease in vital capacity and partial pressure of oxygen. There is a growing body of evidence that indicates genetic factors may be important in the pathogenesis of many cases of PSP. Familial clustering of this condition has been reported. Genetic disorders that have been linked to PSP include Marfan syndrome, homocystinuria, and Birt-Hogg-Dube (BHD) syndrome. a) Birt-Hogg-Dube syndrome is an autosomal dominant disorder that is characterized by benign skin tumors (hair follicle hamartomas), renal and colon cancer, and spontaneous pneumothorax. The spontaneous pneumothorax occurs in about 22% of patients with this syndrome. b) Marfan syndrome is an inherited connective-tissue disorder transmitted as an autosomal dominant trait. Cardinal features of the disorder include major criteria in 2 different organ systems and involvement of a third organ system are required to make the diagnosis (organ system criteria described in Physical). Clinical presentations are as follows: Delayed achievement of gross and fine motor milestones secondary to ligamentous laxity of the hips, knees, ankles, arches, wrists, and fingers A decrescendo diastolic murmur from aortic regurgitation An ejection click at the apex followed by a holosystolic high-pitched murmur from mitral prolapse and regurgitation Dysrhythmia (a primary feature) Abrupt onset of thoracic pain, which occurs in more than 90% of patients with aortic dissection (Other signs include syncope, shock, pallor, pulselessness, and paresthesia or paralysis in the extremities. Onset of hypotension may indicate aortic rupture.) Low back pain near the tailbone, burning sensation and numbness or weakness in the legs in serious dural ectasia (Dural ectasia may cause headaches and even neurologic deficits.) Dural ectasia in the lumbosacral region. Joint pain in adult patients Dyspnea, severe palpitations, and substernal pain in severe pectus excavatum Breathlessness, often with chest pain, in spontaneous pneumothorax Visual problems, possibly loss of vision, from lens dislocation or retinal detachment (The most common refractory errors are myopia and amblyopia.). Secondary spontaneous pneumothorax (SSP) occurs in people with a wide variety of

parenchymal lung diseases, that is, these individuals have underlying pulmonary structural pathology (see the image below). Air enters the pleural space via distended, damaged, or compromised alveoli. Patients may present with more serious clinical symptoms and sequelae due to comorbid conditions. Diseases and conditions associated with secondary spontaneous pneumothorax include the following: Chronic obstructive lung disease (COPD) or emphysema: Increased pulmonary pressure due to coughing with a bronchial plug of mucus or phlegm bronchial plug may play a role, Asthma, Human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS) with PCP infection, Necrotizing pneumonia, Tuberculosis, Sarcoidosis, Cystic fibrosis, Bronchogenic carcinoma or metastatic malignancy, Idiopathic pulmonary fibrosis, Inhalational and intravenous drug use (eg, marijuana, cocaine), Interstitial lung diseases associated with connective tissue diseases, Lymphangioleiomyomatosis, Langerhans cell histiocytosis, Severe acute respiratory syndrome (SARS): A reported 1.7% of SARS patients developed spontaneous pneumothorax, Thoracic endometriosis and catamenial pneumothorax, Collagen vascular disease, including Marfan syndrome Pneumocystis jiroveci pneumonia (previously known as Pneumocystis carinii pneumonia [PCP]) was a common cause of SSP in patients with AIDS during the last decade. In fact, 77% of AIDS patients with spontaneous pneumothorax had thin-walled cavities, cysts, and pneumothorax from PCP infection.[10] With the advent of highly active antiretroviral therapy (HAART) and widespread use of trimethoprimsulfamethoxazole (TMP-SMZ) prophylaxis, the incidence of PCP and associated SSP has significantly declined. SYMPTOMS:acute onset of chest pain and shortness of breath were present in all patients in one series; typically, both symptoms are present in 64-85% of patients. The chest pain is described as severe and/or stabbing, radiates to the ipsilateral shoulder and increases with inspiration (pleuritic). In PSP, chest often improves over the first 24 hours, even without resolution of the underlying air accumulation. Iatrogenic and traumatic pneumothorax Iatrogenic pneumothorax is a type of traumatic pneumothorax that results from incursion(serbuan) into the pleural space secondary to diagnostic or therapeutic medical intervention. Pulmonary TB remains a significant cause of secondary pneumothorax. Causes of iatrogenic pneumothorax include the following: Transthoracic needle aspiration biopsy of pulmonary nodules (most common cause, accounting for 32-37% of cases), Transbronchial or pleural biopsy, Thoracentesis, Central venous catheter insertion, usually subclavian or internal jugular, Intercostal nerve block, Tracheostomy, Cardiopulmonary resuscitation (CPR): Consider the possibility of a pneumothorax if ventilation becomes progressively more difficult, Acute respiratory distress syndrome (ARDS) and positive pressure ventilation in the ICU: High peak airway pressures can translate into barotrauma in up to 3% of patients on a ventilator and up to 5% of patients with ARDS, Nasogastric feeding tube placement. Causes of traumatic pneumothorax include the following: Trauma: Penetrating and nonpenetrating injury, Rib fracture, High-risk occupation (eg, diving, flying). Tension pneumothorax A tension pneumothorax is a life-threatening condition that develops when air is trapped in the pleural cavity under positive pressure, displacing mediastinal structures and compromising cardiopulmonary function. Promptly recognizing this condition saves lives, both outside the hospital and in a modern intensive care unit (ICU). Because tension pneumothorax occurs infrequently and has potentially devastating effects, a high index of suspicion and knowledge of basic emergency thoracic decompression are important for all healthcare personnel. This condition develops when injured tissue forms a 1-way valve, allowing air inflow into the pleural space and prohibiting air outflow. The volume of this nonabsorbable intrapleural air increases with each

inspiration because of the 1-way valve effect. As the pressure increases, the ipsilateral lung collapses and causes hypoxia. Further pressure build-up causes the mediastinum to shift toward the contralateral side and impinge on and compress both the contralateral lung and the vasculature entering the right atrium of the heart. Symptoms of tension pneumothorax may include chest pain (90%), dyspnea (80%), anxiety, fatigue, or acute epigastric pain (a rare finding). Pneumomediastinum Pneumomediastinum is the presence of gas in the mediastinal structures occurring spontaneously or following procedures or trauma.A pneumothorax may occur secondary to pneumomediastinum. excessive intra-alveolar pressures lead to rupture of perivascular alveoli. Air escapes into the surrounding connective tissue and dissects into the mediastinum. Air may then travel superiorly into the visceral, retropharyngeal, and subcutaneous spaces of the neck. The following are factors that may result in pneumomediastinum: Acute production of high intrathoracic pressures (often as a result of inhalational drug use, such smoking marijuana or inhalation of cocaine), Asthma, Respiratory tract infection, Parturition, Emesis, Severe cough, Mechanical ventilation,Trauma or surgical disruption of the oropharyngeal, esophageal, or respiratory mucosa,Athletic competition. SYMPTOMS:67% of identified patients had chest pain; 42% had persistent cough; 25% had sore throat; and 8% had dysphagia, shortness of breath, or nausea/vomiting. Other symptoms may include substernal chest pain, usually radiating to the neck, back, or shoulders and exacerbated by deep inspiration, coughing, or supine positioning; dyspnea; neck or jaw pain; dysphagia, dysphonia, and/or abdominal pain (unusual symptoms). Catamenial pneumothorax Women aged 30-40 years who present with onset of symptoms within 48 hours of menstruation, rightsided pneumothorax, and recurrence raise suspicion for catamenial pneumothorax. The general appearance of the patient with pneumothorax may vary from asymptomatic to respiratory distress. It may include diaphoresis, splinting chest wall to relieve pleuritic pain, and cyanosis (in the case of tension pneumothorax). Affected patients may also reveal altered mental status changes, including decreased alertness and/or consciousness (a rare finding). Respiratory findings may include the following: Respiratory distress (considered a universal finding) or respiratory arrest, Tachypnea (or bradypnea as a preterminal event), Asymmetric lung expansion: A mediastinal and tracheal shift to the contralateral side can occur with a large tension pneumothorax, Distant or absent breath sounds: Unilaterally decreased or absent lung sounds is a common finding, but decreased air entry may be absent even in an advanced state of the disease, Lung sounds transmitted from the unaffected hemithorax are minimal with auscultation at the midaxillary line, Hyperresonance on percussion: This is a rare finding and may be absent even in an advanced state of the disease, Decreased tactile fremitus, Adventitious lung sounds (crackles, wheeze; an ipsilateral finding) Cardiovascular findings may include the following: Tachycardia: This is the most common finding. If the heart rate is faster than 135 beats per minute (bpm), tension pneumothorax is likely, Pulsus paradoxus, Hypotension: This should be considered as an inconsistently present finding; although hypotension is typically considered a key sign of a tension pneumothorax, studies suggest that hypotension can be delayed until its appearance immediately precedes cardiovascular collapse, Jugular

venous distention: This is generally seen in tension pneumothorax, although it may be absent if hypotension is severe,Cardiac apical displacement: This is a rare finding. DIAGNOSIS: Chest Computed tomography (CT) scanning is the most reliable imaging study for the diagnosis of pneumothorax, but it is not recommended for routine use in pneumothorax. This imaging modality can help to accomplish the following: Distinguish between a large bulla and a pneumothorax Indicate underlying emphysema or emphysemalike changes (ELCs) Determine the exact size of the pneumothorax, especially if it is small Confirm the diagnosis of pneumothorax in patients with head trauma who are mechanically ventilated Detect occult/small pneumothoraces and pneumomediastinum (although the clinical significance of these occult pneumothoraces is unclear, particularly in the stable nonintubated patient). Some Causes of Dyspnea Cause Acute (within minutes) Pulmonary causes Pneumothorax

Suggestive Findings

Diagnostic Approach* Chest x-ray

Pulmonary embolism

Asthma, bronchospasm, or reactive airway disease

Foreign body inhalation

Abrupt onset of sharp chest pain, tachypnea, diminished breath sounds, and hyperresonance to percussion May follow injury or occur spontaneously (especially in tall, thin patients and in patients with COPD) Abrupt onset of sharp chest pain, tachypnea, and tachycardia Often risk factors for pulmonary embolism (eg, cancer, immobilization, DVT, pregnancy, use of oral contraceptives or other estrogen-containing drugs, recent surgery or hospitalization, family history) Wheezing and poor air exchange that arise spontaneously or after exposure to specific stimuli (eg, allergen, URI, cold, exercise) Possibly pulsus paradoxus Often a preexisting history of reactive airway disease Sudden onset of cough or stridor in a patient (typically an infant or young child) without URI or constitutional symptoms Sudden onset after occupational exposure or inappropriate use of cleaning agents

Toxic airway damage (eg, inhalation of chlorine or hydrogen sulfide)

CT angiography or V/Q scanning Doppler or duplex studies of extremities showing positive findings of DVT Clinical evaluation Sometimes pulmonary function testing or bedside peak flow measurement Inspiratory and expiratory chest xrays Sometimes bronchoscopy Inhalation usually obvious by history Chest x-ray Sometimes ABGs and observation to determine severity ECG Cardiac enzyme testing Auscultation

Cardiac causes Acute myocardial ischemia or infarction Papillary muscle dysfunction or

Substernal chest pressure with or without radiation to the arm or jaw, particularly in patients with risk factors for CAD Sudden onset of chest pain, new or loud

rupture Heart failure

holosystolic murmur, and signs of heart failure, particularly in patients with recent MI Crackles, S3 gallop, and signs of central or peripheral volume overload (eg, elevated neck veins, peripheral edema) Dyspnea while lying flat (orthopnea) or appearing 12 h after falling asleep (paroxysmal nocturnal dyspnea) Sudden onset after trauma affecting the phrenic nerve Frequent orthopnea Situational dyspnea often accompanied by psychomotor agitation and paresthesias in the fingers or around the mouth Normal examination findings and pulse oximetry measurements

Echocardiography Auscultation Chest x-ray BNP measurement Echocardiography

Other causes Diaphragmatic paralysis Anxiety disorder hyperventilation

Chest x-ray Fluoroscopic sniff test Clinical evaluation Diagnosis of exclusion

Subacute (within hours or days) Pulmonary causes Pneumonia Fever, productive cough, dyspnea, sometimes pleuritic chest pain Focal lung findings, including crackles, decreased breath sounds, and egophony COPD exacerbation Cough, productive or nonproductive Poor air movement Accessory muscle use or pursed lip breathing Cardiac causes Angina or CAD Substernal chest pressure with or without radiation to the arm or jaw, often provoked by physical exertion, particularly in patients with risk factors for CAD Pericardial effusion or tamponade Muffled heart sounds or enlarged cardiac silhouette in patients with risk factors for pericardial effusion (eg, cancer, pericarditis, SLE) Possibly pulsus paradoxus Chronic (hours to years) Pulmonary causes Obstructive lung disease Extensive smoking history, barrel chest, and poor air entry and exit Restrictive lung disease Progressive dyspnea in patients with known occupational exposure or neurologic condition Fine crackles on auscultation Pleuritic chest pain and lung field that is dull to percussion with diminished breath sounds

Chest x-ray Sometimes blood and sputum cultures WBC count Clinical evaluation Sometimes chest xray and ABGs ECG Cardiac stress testing Cardiac catheterization Echocardiography

Interstitial lung disease Pleural effusion

Chest x-ray Pulmonary function testing (at initial evaluation) Chest x-ray Pulmonary function testing (at initial evaluation) High-resolution chest CT Chest x-ray Often chest CT and thoracentesis

Sometimes history of cancer, heart failure, RA, SLE, or acute pneumonia Cardiac causes Heart failure Crackles, S3 gallop, and signs of central or peripheral volume overload (eg, elevated neck veins, peripheral edema) Orthopnea or paroxysmal nocturnal dyspnea Substernal chest pressure with or without radiation to the arm or jaw, often provoked by physical exertion, particularly in patients with risk factors for CAD Auscultation Chest x-ray Echocardiography ECG Cardiac stress testing Sometimes cardiac catheterization

Stable angina or CAD

Other causes Anemia

Dyspnea on exertion progressing to CBC dyspnea at rest Normal lung examination and pulse oximetry measurement Sometimes systolic heart murmur due to increased flow Physical deconditioning Dyspnea only on exertion in patients with Clinical evaluation sedentary lifestyle *Most patients should have pulse oximetry and, unless symptoms are clearly a mild exacerbation of known chronic disease, chest x-ray. BNP = brain (B-type) natriuretic peptide; CAD = coronary artery disease; DVT = deep venous thrombosis; S3 = 3rd heart sound; V/Q = ventilation/perfusion. Review of systems should seek symptoms of possible causes, including chest pain or pressure (pulmonary embolism [PE], myocardial ischemia, pneumonia); dependent edema, orthopnea, and paroxysmal nocturnal dyspnea (heart failure); fever, chills, cough, and sputum production (pneumonia); black, tarry stools or heavy menses (occult bleeding possibly causing anemia); and weight loss or night sweats (cancer or chronic lung infection). Past medical history should cover disorders known to cause dyspnea, including asthma, COPD, and heart disease, as well as risk factors for the different etiologies: Smoking historyfor cancer, COPD, and heart disease Family history, hypertension, and high cholesterol levelsfor coronary artery disease Recent immobilization or surgery, recent long-distance travel, cancer or risk factors for or signs of occult cancer, prior or family history of clotting, pregnancy, oral contraceptive use, calf pain, leg swelling, and known deep venous thrombosisfor PE Occupational exposures (eg, gases, smoke, asbestos) should be investigated. Physical examination: Vital signs are reviewed for fever, tachycardia, and tachypnea. Neck veins should be inspected for distention, and the legs and presacral area should be palpated for pitting edema (both suggesting heart failure) Wheezing suggests asthma or COPD. Stridor suggests extrathoracic airway obstruction (eg, foreign body, epiglottitis, vocal cord dysfunction). Crackles suggest left heart failure, interstitial lung disease, or, if accompanied by signs of consolidation, pneumonia.

Some Causes of Chest Pain Risk factors for coronary artery disease (CADeg, hypertension, hyperlipidemia, diabetes, cerebrovascular disease, tobacco use). Drug history should note use of drugs that can trigger coronary artery spasm (eg, cocaine, triptans, phosphodiesterase inhibitors) or GI disease (particularly alcohol, NSAIDs). Family history should note history of MI (particularly at an early age) and hyperlipidemia. Cause* Cardiovascular Myocardial ischemia (acute MI/unstable angina/angina) Suggestive Findings Acute, crushing pain radiating to the jaw or arm Exertional pain relieved by rest (angina pectoris) S4 gallop Sometimes late systolic murmur Often red flag findings Sudden, tearing pain radiating to the back Some patients have syncope, stroke, or leg ischemia Pulse or BP may be unequal in extremities Age > 55 Hypertension Red flag findings Constant or intermittent sharp pain often aggravated by breathing, swallowing food, or supine position and relieved by sitting leaning forward Pericardial friction rub Jugular venous distention Fever, dyspnea, fatigue, chest pain, recent viral or other infection Sometimes findings of heart failure, pericarditis, or both Diagnostic Approach Serial ECGs and cardiac markers; admit or observe Stress imaging test considered in patients with negative ECG findings and no cardiac marker elevation Often heart catheterization and coronary angiography if findings are positive Chest x-ray with findings suggesting diagnosis Enhanced CT scan of aorta for confirmation Transthoracic or transesophageal echocardiography

Thoracic aortic dissection

Pericarditis

ECG usually diagnostic Serum cardiac markers (showing elevated troponin with normal CK level)

Myocarditis

ECG Serum cardiac markers ESR C-reactive protein Usually echocardiography Chest x-ray findings suggest diagnosis Esophagography with water-soluble contrast for confirmation

GI 1 Esophageal rupture

Pancreatitis

Sudden, severe pain following vomiting or instrumentation (eg, esophagogastroscopy or transesophageal echocardiography) Subcutaneous crepitus on auscultation Multiple red flag findings Pain in the epigastrium or lower chest that is often worse when lying flat and is relieved by leaning forward Vomiting

Serum amylase and lipase Sometimes abdominal CT

Peptic ulcer

Esophageal reflux (GERD)

Biliary tract disease

Esophageal motility disorders

Upper abdominal tenderness Shock Often history of alcohol abuse or biliary tract disease Recurrent, vague epigastric or right upper quadrant discomfort in a patient who smokes or uses alcohol excessively that is relieved by food, antacids, or both No red flag findings Recurrent burning pain radiating from epigastrium to throat that is exacerbated by bending down or lying down and relieved by antacids Recurrent right upper quadrant or epigastric discomfort following meals (but not exertion) Pain, insidious onset, longstanding, may or may not accompany swallowing Usually also swallowing difficulty Often pleuritic pain, dyspnea, tachycardia Sometimes mild fever, hemoptysis, shock More likely with risk factors present (see Table 2: Symptoms of Cardiovascular Disorders: Clinical Prediction Rule for Diagnosing Pulmonary Embolism ) Significant dyspnea, hypotension, neck vein distention, unilateral diminished breath sounds and hyperresonance to percussion Sometimes subcutaneous air Fever, chills, cough, and purulent sputum Often dyspnea, tachycardia, signs of consolidation on examination Sometimes, unilateral diminished breath sounds, subcutaneous air May have preceding pneumonia, pulmonary embolism, or viral respiratory

Clinical evaluation Sometimes endoscopy Sometimes testing for Helicobacter pylori

Clinical evaluation Sometimes endoscopy Sometimes motility studies Ultrasonography of gallbladder

Barium swallow

Pulmonary 1 Pulmonary embolism

Varies with clinical suspicion (see Fig. 2: Pulmonary Embolism: Clinical Prediction Rule for Diagnosing Pulmonary Embolism )

Tension pneumothorax

Usually clinical Obvious on chest x-ray

Pneumonia

Chest x-ray

Pneumothorax

Chest x-ray Usually clinical evaluation

Pleuritis

infection Pain with breathing, cough Examination unremarkable Other 3 Musculoskeletal chest wall pain (including trauma, overuse, costochondritis) Often suggested by history Pain typically persistent (typically days or longer), worsened with passive and active motion Diffuse or focal tenderness Variable sometimes chronic cough, smoking history, signs of chronic illness (weight loss, fever), cervical lymphadenopathy Sharp, band-like pain midthorax unilaterally Classic linear, vesicular rash Pain may precede rash by several days Various features No red flag findings Clinical evaluation

Various thoracic cancers

Chest x-ray Chest CT if x-ray findings suggestive Bone scan considered for persistent, focal rib pain Clinical evaluation

Herpes zoster infection

Idiopathic

Diagnosis of exclusion

*Severity is categorized as follows: 1 Immediate life threats. 2 Potential life threats. 3 Uncomfortable but usually not dangerous. Most patients with chest pain should have pulse oximetry, ECG, and chest x-ray (basic tests). If there is suspicion of coronary ischemia, serum cardiac markers (troponin, CK) should also be checked. Red flag findings include abnormal vital signs (tachycardia, bradycardia, tachypnea, hypotension), signs of hypoperfusion (eg, confusion, ashen color, diaphoresis), shortness of breath, asymmetric breath sounds or pulses, new heart murmurs, or pulsus paradoxus > 10 mm Hg. S4 = 4th heart sound. Stridor is a high-pitched, predominantly inspiratory sound. It is most commonly associated with acute disorders, such as foreign body aspiration but can be due to more chronic disorders, such as tracheomalacia. Pathophysiology Stridor is produced by the rapid, turbulent flow of air through a narrowed or partially obstructed segment of the extrathoracic upper airway. Involved areas include the pharynx, epiglottis, larynx, and the extrathoracic trachea.

Some Causes of Stridor Cause Suggestive Findings Acute stridor Allergic reaction Sudden onset after exposure to allergen (severe) Usually accompanied by wheezing and sometimes orofacial edema; itching No fever or sore throat; cough rare

Diagnostic Approach Clinical evaluation

Croup

Age 636 mo, barking cough that is worse at night, URI symptoms, no difficulty swallowing, low-grade fever Mainly adults, as well as children who missed HiB vaccination Abrupt onset of high fever, sore throat, drooling+tripod position, and often respiratory distress and marked anxiety without cough Toxic appearance Sudden onset in a toddler or young child who has no URI or constitutional symptoms Foreign body in adult upper airway typically apparent by history Clinically apparent recent toxic inhalation

Epiglottitis

Clinical evaluation Sometimes anteroposterior neck x-ray showing subglottic narrowing (steeple sign) Lateral neck x-ray if the patient is stable Examination in operating room if any signs of distress

Foreign body

Direct or indirect laryngoscopy or bronchoscopy Clinical evaluation Sometimes bronchoscopy Clinical evaluation Sometimes direct laryngoscopy

Inhalation injury (eg, due to cleaning agents or smoke inhalation) Postextubation complications (eg, laryngeal edema, laryngospasm, arytenoid dislocation) Retropharyngeal abscess

Recent intubation and respiratory distress

Bacterial tracheitis (rare)

Mainly in children < 4 yr High fevers, severe throat pain, drooling, trouble swallowing, sometimes respiratory distress Swelling that may or may not be visible in the pharynx, neck stiffness and inability to extend the neck. Barking cough that is worse at night, high fever, and respiratory distress Toxic appearance Recurrent episodes, associated with gastroesophageal reflux or recent drug use or occurring after endotracheal intubation Usually in neonates or infants Sometimes other congenital anomalies present Sometimes infants have trouble feeding or sleeping Sometimes worse with URI History of head and neck cancer or obvious mass, night sweats, and weight loss Inspiratory or biphasic stridor that may progressively worsen as tumor enlarges

Lateral neck x-ray Sometimes neck CT with contrast

Laryngospasm

Neck x-rays Sometimes direct or indirect laryngoscopy with visualization and culture of purulent tracheal secretions Direct or indirect laryngoscopy

Chronic stridor Congenital anomalies (numerous; laryngomalacia most common)

CT of neck and chest Direct laryngoscopy Spirometry with flow-volume loops X-ray of neck and chest CT of neck and chest Direct or indirect laryngoscopy Direct or indirect laryngoscopy Spirometry with flow-volume loops

External compression Laryngeal tumors (eg, squamous cell carcinoma, hemangiomas, small cell carcinoma)

10

Congenital tracheomalacia

Chronic symptoms during coughing, crying, or feeding May worsen in the supine position Bilateral vocal cord paralysis or Recent trauma (eg, during dysfunction birth, thyroid or other neck surgery, intubation, deep airway suctioning) Various neurodegenerative or neuromuscular disorders present Good voice quality but limited intensity HiB = Haemophilus influenzae type B.

CT or MRI Spirometry with flow-volume loops Sometimes bronchoscopy Direct or indirect laryngoscopy

Wheezing is a relatively high-pitched whistling noise produced by movement of air through narrowed or compressed small airways Some Causes of Wheezing Cause Suggestive Findings Acute bronchitis URI symptoms No known history of lung disease Allergic reaction Sudden onset, usually within 30 min of exposure to known or potential allergen Often accompanied by nasal congestion, urticaria, itchy eyes, and sneezing Asthma Often known history of asthma Wheezing arising spontaneously or after exposure to specific stimuli (eg, allergen, URI, cold, exercise) Bronchiolitis In children < 18 mo (usually from November to April in the Northern Hemisphere) Usually URI symptoms and tachypnea Middle-aged or elderly patient Often known history of COPD Extensive smoking history Poor breath sounds Dyspnea Pursed lip breathing Use of accessory muscles Recent initiation of a new drug, most often in a patient with a history of reactive airway disease

Diagnostic Approach* Clinical evaluation Clinical evaluation

Clinical evaluation Sometimes pulmonary function testing, bedside peak flow measurement, methacholine challenge, or observation of response to empiric bronchodilators Clinical evaluation

COPD exacerbation

Clinical evaluation Sometimes chest x-ray and ABG measurement

Drugs (eg, ACE inhibitors, aspirin BUFFERIN ECOTRIN GENACOTE , -blockers, NSAIDs) Endobronchial

Clinical evaluation

Fixed and constant inspiratory and

Chest x-ray or CT

11

tumors

expiratory wheezes, especially in a patient Bronchoscopy with risk factors for or signs of cancer (eg, smoking history, night sweats, weight loss, hemoptysis) May be focal rather than diffuse Foreign body Sudden onset in a young child who has no Chest x-ray or CT URI or constitutional symptoms Bronchoscopy GERD with Chronic or recurrent wheezing, often with Trial of acid-suppressing drugs chronic heartburn and nocturnal cough Sometimes esophageal pH aspiration No URI or allergic symptoms monitoring Inhaled irritants Sudden onset after occupational exposure Clinical evaluation or inappropriate use of cleaning agents Left-sided heart Crackles and signs of central or peripheral Chest x-ray failure with volume overload (eg, distended neck ECG pulmonary veins, peripheral edema) BNP measurement edema (cardiac Dyspnea while lying flat (orthopnea) or Echocardiography asthma) appearing 12 h after falling asleep (paroxysmal nocturnal dyspnea) *Most patients should have pulse oximetry. Unless symptoms are very mild or are clearly an exacerbation of a known chronic disease, chest x-ray should be done. BNP = brain natriuretic peptide; GERD = gastroesophageal reflux disease.

12