Thoracic-Respiratory Disorders I - EMBR 2nd Edition

Educational Objectives

The Audio-Digest Emergency Medicine Board Review — Second Edition

The lecture you’ve selected is part of the Audio Digest Emergency Board Review Course. Our overall Board Review Course is designed to match the defined learning objectives of the American Board of Emergency Medicine, and it is intended to provide a source of review material for those who are preparing for the ABEM's Continuous Certification Examination and for those preparing for the ABEM’s Initial Certification Examination. The goal is to provide a comprehensive update in many aspects of emergency medicine practice that will enhance the lifelong learning experience.

Course Objectives

Upon completing this educational activity, participants will be able to:

1. Rapidly diagnose and medically respond to a wide variety of critical issues presenting in the emergency department.
2. Triage the need for medical care (as appropriate) and initiate therapeutic procedures where needed.
3. Manage patients who require continuing respiratory and cardiovascular support until stable or transitioned to other hospital care centers.
4. Determine circumstances in which hospital care beyond the emergency department is required, and initiate procedures to obtain such care.
5. Prescribe drugs as appropriate for the short term management of presenting medical problems.

After listening to this lecture and reading the accompanying summary, the clinician will be better able to:

1. Discuss the differential diagnosis and management of thoracic and respiratory disorders, including acute upper airway disorders and disorders of the pleura, mediastinum, and chest wall.

Summary

Infections of the upper airway

Bacterial tracheitis: membranous laryngotracheobronchitis or bacterial croup; uncommon but can be life threatening because it can cause upper airway obstruction; mean age of presentation is 5 to 8 years of age; can be secondary to a viral upper respiratory tract infection or can begin primarily; history of upper respiratory infection symptoms followed by sudden worsening with fever, stridor, and coughing; significant sputum production; patient is toxic in appearance; thick mucopurulent secretions can be seen in the posterior pharynx and in the trachea; there is tenderness on palpation of the trachea

Treatment: similar to epiglottitis; the patient requires antibiotics, intensive care, and aggressive airway management; for most patients intubation and ventilatory support would be the standard; bronchoscopy can be utilized to remove the purulent pseudomembranes that are located down the trachea

Associated pathogens: include predominantly Staphylococcus Aureus but also Streptococcus pneumoniae, Streptococcus pyogenes, Moraxella catarrhalis, Haemophilus influenza, and anaerobic bacteria

Treatment: an appropriate antibiotic choice would be to combine ampicillin and sulbactam with possibly a third-generation cephalosporin and clindamycin; consider adding vancomycin for methicillin resistant S aureus

Retropharyngeal abscess: the retropharyngeal space is an area between the posterior pharyngeal wall and the prevertebral fascia going from the base of the skull down to the level of the second thoracic vertebra; abscess begins with separation of lymph nodes located in the retropharyngeal area, which can be infected from a distant source or can be infected secondary to localized penetrating trauma (eg, when a child falls with a stick or other object in his or her mouth), traumatic esophageal instrumentation, or a ventral extension of a vertebral osteomyelitis

Presentation: evolves insidiously over a couple of days, usually after a minor upper respiratory infection; manifestations include neck pain, fever (in about 90% of patients), dysphagia, excessive drooling, and neck swelling; classically the child maintains his or her neck in an usual position in order to improve ventilation; there is associated stiffness, torticollis, and hyperextension; sometimes a bulging of the posterior oropharynx; progress of the abscess leads to stridor and respiratory distress; the complaint of pleuritic chest pain may signify extension of the infection into the mediastinum; if safe, obtain a soft tissue lateral of the neck taken during inspiration

Diagnosis: suggested when the retropharyngeal space at C2 is twice the diameter of the vertebral body or greater than one-half the width of the C4 vertebral body; there may be gas within soft tissues

Associated pathogens: S aureus, S pyogenes, Streptococcus viridans, and the beta lactamase-producing gram-negative rods; could also be oral anaerobic bacteria

Treatment: if the patient appears unstable, consider intubation; after the airway is stabilized, administer fluids and antibiotics and employ computed tomography (CT); most retropharyngeal abscesses are associated with mixed flora; single-agent antimicrobial therapy would include ampicillin, sulbactam, or clindamycin

Complications: airway obstruction, spontaneous abscess, perforation, mediastinitis, sepsis, aspiration, and jugular venous thrombosis

Peritonsillar abscess: deep oropharyngeal infection; most commonly in adolescents and young adults but can occur at any age; begins as a superficial infection but progresses to the accumulation of debris and pus in the space between the tonsillar capsule and the superior constrictor muscle; most commonly is unilateral, but in <10% of the cases is bilateral at the time of diagnosis

Symptoms: sore throat, fever, chills, trismus, and a “hot potato” voice; patients say they have never had a sore throat as bad as one presenting; obtaining CT or ultrasonography can help with the diagnosis

Treatment: a trial of oral antibiotics, typically penicillin, in nontoxic patients; most cases require aspiration or incision of the peritonsillar area; if the patient is not toxic, they can be treated as outpatients; if the patient is too young or uncooperative, intervention in the operating room suite is more beneficial and safer; needle aspiration or incision and drainage (IND) of the area can cause hemorrhage, puncture the carotid artery, and result in airway aspiration of purulent material; if the patient appears toxic, consider polymicrobial infections

Predominant organisms: include the anaerobes, Group A beta-hemolytic streptococcus, S aureus, and H influenza

Treatment: send purulent material obtained with an IND or needle aspiration for Gram stain and culture; begin ampicillin, sulbactam, or clindamycin; otherwise penicillin, clindamycin, or amoxicillin clavulanate; may also consider administering single, high-dose steroid

Ludwig angina: potentially life threatening, expanding infection of the submandibular space; usually arises from an odontogenic source; typically spread from a periapical abscess from the mandibular molars; begins as a mild infection and then progresses to severe mouth pain, drooling, trismus, tongue protrusion, and brawny neck swelling; the child tries to position their head and neck in order to maximize airway diameter; stridor could signal progressive airway obstruction; control the airway early because it may be difficult to intubate a patient with significant pharyngeal swelling; one case series reported that 11 of 20 patients who had Ludwig angina underwent unsuccessful attempts at intubation and required an emergency tracheotomy

Treatment: antibiotics and oral surgery to remove the dental abscess; antibiotics to cover beta-lactamase producing aerobic or anaerobic gram-positive cocci and gram-negative bacilli

Diphtheria: acute, toxin-mediating disease caused by Corynebacterium diphtheriae; rarely seen in the United States because of the widespread use of vaccines (although there are individuals who believe that vaccination is inappropriate and unsafe); disease is transmitted person to person through respiratory secretions or skin lesions

Symptoms: pharyngeal diphtheria — sore throat, malaise, dysphagia, and a low-grade fever; thick, grey membrane over the tonsils and soft palate (pseudomembrane); laryngeal diphtheria — classic barking cough, stridor, hoarseness, and difficulty breathing; marked edema of the neck (“bull neck”) associated with the infection

Complications: myocarditis and neuritis that can lead to diaphragmatic paralysis and death secondary to respiratory failure; treatment includes antitoxin and antibiotics (eg, erythromycin, penicillin G), as well as intense respiratory support

Croup: most common cause of stridor once past the neonatal period; another name is viral laryngotracheobronchitis; commonly affects children between 6 months and 3 years; peak age is the second year of life; most common viruses include parainfluenza viruses, rhinoviruses, enteroviruses, respiratory syncytial virus, and influenza viruses

Clinical features: 1- to 3-day history of stuffy nose, runny nose, coughing, and a low-grade fever, followed by harsh, “barking” cough; voice becomes hoarse, and then stridor may be audible; symptoms are usually worse at night; parents usually bring their child into the emergency department in the middle of the night; many times after the drive in the car symptoms abate; severity of the condition is usually related to the amount of edema and inflammation of the airways; look for tachypnea, stridor at rest, nasal flaring, intercostal, subcostal, or supraclavicular retractions, and evidence of any mental status changes (eg, lethargy, agitation), and oxygen desaturation; usually symptoms last up to 7 days but improve on the third or fourth day

Diagnosis: it is a clinical diagnosis; obtain laboratory studies or x-rays if the differential diagnosis has to be broadened to consider epiglottitis, retropharyngeal abscess, or aspiration of a foreign body; x-rays may show subglottic narrowing (ie, “steeple sign”), but it is absent from 50% of children who have croup

Management: keep the child comfortable, preferably in the lap of the caretaker, in order to improve the child’s sense of well-being; avoid agitating the child, because this increases oxygen use and could compromise the airway

Therapy: if child has evidence of mild croup with mild or no retractions, no agitation, and no signs of distress, do not use nebulized epinephrine and corticosteroids; for the others, it is reasonable to begin racemic epinephrine, 0.05 cc/kg dosed via nebulization; observe the child for 3 hours before considering discharge; can also use 2 mg nebulized budesonide or 0.15 to 0.6 mg/kg dexamethasone per os or intramuscularly, but that is usually reserved for patients considered for discharge; alpha effects of epinephrine decrease airway edema and effect are seen as quickly as 10 minutes after nebulization and can last for over an hour; the use of epinephrine or racemic epinephrine decreases the intubation rate, the amount of time in ICU and admission into the hospital; there is no real difference in the studies with regards to racemic epinephrine vs levo-epinephrine at least initially; some data suggest that the levo-epinephrine can lead to lower croup scores after 2 hours; once epinephrine is given, observe for 3 hours prior to considering discharge; steroids are important whether the condition is mild, moderate, or severe; if mild, a one-time dose of oral steroids is appropriate; a single dose of dexamethasone (0.6 mg/kg per os) is reasonable; onset of action is 4 to 6 hours; other modalities include heliox (mixture of 70% helium and 30% oxygen); it is thought that the helium decreases airway resistance and the work of breathing; validated studies do not corroborate its theoretical benefit but anecdotally it has worked

Disposition: most children with croup can be discharged with steroids; observe those who receive epinephrine for 3 hours; those with persistent stridor at rest, tachypnea, retractions, and a low O2 saturation after treatment with epinephrine should be admitted; the use of aggressive airway management is possible, but the endotracheal tube should be smaller than recommended for size of the patient because of the inflammation of the mucosa; contacting anesthesiologist or pediatric intensivist is appropriate if not confident of ability of intubate

Epiglottitis: acute inflammation of the epiglottis and possibly the supraglottic structures that could lead to life-threatening airway obstruction; with the advent of the H influenzae type B vaccine, the number of cases in the pediatric population has decreased significantly; in the post vaccine era the usual causes of infectious epiglottitis include Streptococcus and Staphylococcus; immunocompromised children may be infected by candida; there could also be some noninfectious causes (eg, thermal injury, caustic burns)

Clinical features: abrupt onset of fever, drooling, and sore throat; can be evidence of stridor and respiratory distress; voice can sound muffled; child is often toxic appearing and anxious (eg, leaning forward in a tripod or sniffing position), with head hyperextended and the chin forward; child does this to protect the airway as much as possible; in many children, especially the older population, it is possible to directly visualize the epiglottis to rule in or out the possibility of epiglottitis; there have been concerns this particular maneuver might cause an abrupt closure of the airway (there have been no documented reports of this); diagnosis can be helped by obtaining a lateral neck x-ray for evidence of a swollen epiglottitis or the “thumb” sign but it is not 100% sensitive; performing that particular x-ray may require having the child go to the radiology department, which can put the child in peril if there is evidence of an acute airway compromise; portable lateral x-rays are not clear

Treatment: initial management is to keep the child upright, make sure the child is not upset, provide comfort (usually with the parents), and have blow-by oxygen if the child allows it; racemic epinephrine may be administered by nebulizer to reduce the airway edema; make sure that all experts are contacted as quickly as possible to facilitate securing the airway because it will probably have to be done; in the meantime make sure all of the equipment (eg, ventilation tubes, laryngoscopes) is at hand if complete obstruction occurs; keep in mind that the most skillful person should be the one who performs the intubation once a diagnosis is made; considering the use of sedations or paralytics can be problematic; if the child can maintain his or her airway, it is important to keep everything quiescent until the treatment team arrives; antibiotics are necessary; consider a second or third-generation cephalosporin (eg, cefuroxime, ceftriaxone); may also consider adding vancomycin if concerned about S aureus or highly resistant S pneumoniae; steroids can be considered

Acute airway obstruction in adults: there are a number of reasons why adults have an acute airway obstruction; should be considered a medical emergency; initial evaluation consists of determining the severity and suspected site of obstruction; look for stridor, poor airway movement, accessory muscle use, abnormal mentation or agitation, tachycardia, hypertension, and pulsus paradoxus

Foreign body aspiration: can be a major etiologic feature in adults although it is more common in children; syndrome consists of a sudden onset of choking and intractable coughing after aspiration of a foreign body; there may be vomiting, and if the obstruction is not complete, there may be persistent cough, fever, chest pain, shortness of breath and wheezing

Risk factors: diminished level of consciousness, impaired swallowing mechanism, or diminished upper airway sensation due to a neurologic syndrome; prior CVA; inability to chew food properly because of poor dentition; other possible etiologies include infections (eg, Ludwig angina), peritonsillar abscess, infections of the retropharyngeal spaces on the lateral aspects of the pharynx; bacterial infections of the larynx should be considered life threatening

Organisms: most commonly S aureus, S pneumoniae, H influenza, and C diphtheriae

Intervention: the Heimlich maneuver can be life-saving in acute situations; in subacute situations a flexible bronchoscope is usually successful in removing foreign bodies, but rigid bronchoscopy is an important backup

Acute upper airway obstruction in the pediatric population: upper airway obstruction is typically clinically apparent; there is inspiratory stridor; the child is obviously dyspneic and shows signs of respiratory distress (eg, tachypnea, nasal flaring, supraclavicular intracostal and/or subcostal retractions); can present with ventilation and oxygenation abnormalities; if the obstruction is severe, hypercapnia can be present, which is associated with changes in mental status, cyanosis, and diminished airway movement; apart from the foreign body etiology associated with upper airway obstruction, consider other possibilities (eg, croup, epiglottitis); less common conditions include bacterial tracheitis, retropharyngeal or peritonsillar abscess, trauma, caustic ingestion, neoplasm, or angioneurotic edema

Management of an incomplete foreign body obstruction: management should be careful and deliberate, obtaining all the necessary consultations at the bedside meanwhile and preparing a crash cart if a subacute obstruction become acute; keep the child as quiet as possible (preferably with the parents nearby), and be ready to intervene if necessary

Management of a complete foreign body obstruction in infants and children: if child is ≤1 year and conscious, 5 back blows with the infant prone in head-down position, then 5 chest thrusts with the infant supine in head-down position; repeat that process until the patient becomes unconscious; if patient loses consciousness, open the airway, perform tongue-jaw lift maneuver and remove the foreign body if visible; forceps could be the ideal instrument; if there are no spontaneous respirations, attempt rescue breathing; if unsuccessful, reposition the airway and try again; then cycle back to repeat back blows, chest thrusts, open airway, and attempt to ventilate; it is possible that with direct visualization and the use of an endotracheal tube, even the foreign body is not visible, you may be able to push it into the right main stem bronchus, thereby oxygenating and ventilating the left lung

Management of a complete foreign body obstruction in a child between the ages of 1 and 8: perform Heimlich maneuver with abdominal thrusts above the umbilicus standing behind the patient; continue thrusts until the foreign body is either expelled or the victim becomes unconscious; if the patient becomes unconscious, lower the victim to a supine position; open the airway with a tongue-jaw lift; remove any visible foreign bodies; if nothing is visible and there are no spontaneous respirations, attempt to ventilate; if unsuccessful and there is resistance, then (straddling or kneeling behind the patient) begin abdominal thrusts with the heel of the hand positioned above the umbilicus and below the xiphoid process; repeat the steps until the obstruction is relieved

Tracheostomy: surgical procedure that creates a surgical airway in the cervical trachea; not a common procedure for emergency physicians

Indications: congenital anomaly (eg, vascular web, laryngeal hypoplasia); an upper airway foreign body that cannot be dislodged via more traditional methods (eg, Heimlich maneuver); supraglottic or glottic pathologic condition (eg, neoplasm); neck trauma resulting in severe injuries to the thyroid or cricoid cartilage area or involving significant bleeding of the great vessels of the neck; subcutaneous emphysema; facial fractures that can lead to upper airway obstruction; upper airway edema secondary to trauma, burns or infection, and anaphylaxis and severe sleep apnea that is not amenable to more traditional methods

Contraindications: no absolute contraindications; a relative contraindication is the possibility that there is laryngeal carcinoma, and manipulation by means of the tracheostomy could lead to increased incidence of stomal recurrence; patients that may require a tracheostomy but can be recognized as being unfavorable candidates (eg, are obese, have abnormal or poorly palpable midline neck anatomy, require an emergency airway, have a coagulopathy, or pediatric patients and patients with thyromegaly)

Complications: pneumothorax, pneumomediastinum, drop in oxygen saturation, and bleeding, especially of the great vessels in and around the tracheostomy site; recommended that bedside ultrasonography could help survey the site to avoid specific vascular structures

Costochondritis: discerning the etiology of chest pain can be difficult; may be musculoskeletal or chest wall pain, as characterized by sharp, highly localized, and positional pain; pain from Tietze syndrome is usually sharp but can also be dull and is often increased with respirations

Examination: classically preferable to reproduce the pain with light to moderate palpation over the area of maximum discomfort or reproduce that pain with specific movements that can be exacerbated by inspiration or coughing; there is a significant differential diagnosis that must be considered; acute myocardial infarctions can mimic costochondritis; consider high-risk conditions (eg, acute coronary syndrome, acute aortic syndrome, pulmonary embolism, tension pneumothorax, pericarditis with tamponade, esophageal rupture) that can mimic acute costochondritis or Tietze syndrome

Treatment: essentially nonspecific; once everything that could be serious or life-threatening is ruled out, analgesia with anti-inflammatories should be sufficient in the majority of cases

Mediastinitis: the mediastinum is a potential space that is located between the 2 pleural cavities, and it communicates with the neck and the retroperitoneum; it is easy for air or infection to disseminate widely; composed basically of 3 compartments, anterior, middle, and posterior; the middle is commonly called the visceral compartment, and the posterior is commonly called the paravertebral sulcus

Acute mediastinitis: a life-threatening problem with significant morbidity and mortality; all 3 compartments can be affected; the anterior compartment is usually related to a sternotomy secondary to cardiac surgery; the middle compartment is usually related to esophageal perforation, and the posterior compartment is usually related to some process that has been initiated from the neck, the lung, or the spine; remember that the instrumental perforation of the esophagus is the most common cause of acute mediastinitis in the United States

Etiologies: esophageal perforation — instrumental perforation of the esophagus accounts for one-half of all esophageal perforations (usually related to the use of a rigid esophagoscopy, dilation of a stricture, or other interventions [eg, esophageal tube placement like the Sengstaken-Blakemore tube]); Boerhaave syndrome or postemetic rupture is classically associated with acute mediastinitis; patients usually present with an abrupt onset of severe substernal chest pain; many times it is pleuritic in nature and classically associated with forceful vomiting or retching; despite the fact that one of the principal complaints is acute shortness of breath, many times a pneumothorax is not seen; hemodynamic compromise can occur quickly; patient goes into shock and looks ill with significant tachypnea, tachycardia, fever, low blood pressure, splitting of the chest and abdominal cavities, and evidence of cervical emphysema; chest x-ray may show cervical or mediastinal emphysema, a pneumothorax, and a pleural effusion; contrast esophagram using water soluble contrast material can confirm the diagnosis but has a false-negative rate of 10%; another diagnostic modality is chest CT, especially in those who have a negative esophagram with a significantly high index of suspicion; the differential diagnosis for Boerhaave syndrome is significantly diffuse; other etiologies of chest pain include perforated ulcer, acute pancreatitis, acute MI, pneumonia, aortic dissection, and pulmonary embolism

Treatment: surgery as well as broad-spectrum antibiotics; mortality is <10% if the perforation is diagnosed rapidly and repair takes place within 24 hours of presentation; if that is not the case mortality can increase to 30% to 40%

Tracheobronchial perforation: usually associated with trauma or instrumentation; severe mediastinitis is less common than with tracheobronchial disruption probably because the contents that enter into the mediastinum are less noxious and better contained; intubation is now the most frequent cause of tracheobronchial injury

Acute descending necrotizing mediastinitis: occurs when there is severe deep head and neck infections originating from the oropharynx and hypopharynx; mixed aerobic and anaerobic organisms are associated with this; mortality can be as high as 40%; there is extension of infection from the neck area that descends down the fascial planes from the cervical region into mediastinum; criteria for making the diagnosis include (1) severe head and/or neck infection, (2) radiographic evidence of mediastinitis, (3) evidence of a necrotizing infection, and (4) the establishment of a relationship between the cervical infection and the necrotizing mediastinitis

Presentation: in descending order of frequency, odynophagia, neck swelling, neck pain, acute shortness of breath, and chest pain; also fever, swelling, and redness of the oropharynx; approximately 66% of patients are immunosuppressed or have multiple chronic illnesses; common causes include tooth abscess, pharyngitis, peritonsillar abscess, epiglottitis, and perforation of the pharynx

Diagnosis: if mediastinitis is suspected, the patient needs CT with IV contrast material

Predominant organisms: Streptococcus and Bacteroides

Treatment: antibiotics as early as possible; potentially surgical intervention

Acute mediastinitis from direct extension: necrotizing pneumonias precipitate direct extension into the mediastinum, especially in immunocompromised patients; Aspergillosis is reported with increased frequency in posterior mediastinitis; pancreatitis is another cause of mediastinitis secondary to direct extension; extends from the retroperitoneal area into the mediastinum; treatment is antibiotic therapy and surgical drainage/debridement

Sternal wound infection associated with cardiac surgery: incidence is low, about 0.5% to 1% of all sternotomies; mortality rate can be significant, up to 30% (the mean is 15%); most common organism is S aureus

Anthrax mediastinitis: inhaled anthrax spores germinate within the airways and spread into the mediastinum creating a hemorrhagic mediastinitis; pathology is the entry of the spores into the lungs and then transport into the mediastinal lymph nodes by alveolar macrophages; spores germinate releasing anthrax toxins; toxins are called edema factor and lethal factor; therapy includes antibiotics, specifically ciprofloxacin or doxycycline, plus 1 or 2 other antimicrobial agents

Pleural effusion: abnormal collection of fluid between the parietal and visceral pleura; related to a local disease or inflammatory process; usually there is 5 to 15 CCs of fluid within the pleural; effusion is much more extensive

Exudative pleural effusion: pleural fluid protein to serum protein ratio >0.5; pleural fluid lactate dehydrogenase to serum lactate dehydrogenase ratio of >0.6 and a pleural fluid lactate dehydrogenase (LDH) more than two-thirds of the upper limit of normal serum LDH; if those characteristics are not present, it is a transudate; exudate seen with a pleural effusion is related to a direct disease of the pleura itself, which can come from an infection and inflammation or a cancer

Transudative pleural effusion: commonly associated with congestive heart failure, cirrhosis of the liver with associated ascites, or nephrotic syndrome; findings associated with pleural effusion are pleuritic (or even nonpleuritic) chest pain and/or shortness of breath; chest examination may demonstrate dullness to percussion, decreased breath sounds, and decreased tactile fremitus on the involved side; if effusion is large enough, there may be hypoxea and evidence of respiratory compromise or even distress; upright posterior anterior (PA) and lateral chest x-ray can show pleural fluid; if seen there is more than likely 250 cc of fluid; obvious manifestation on x-ray is blunting of the costophrenic angles; a decubitus x-ray can help because it can show evidence of the fluid shifting if it is free flowing; CT can be helpful in detected underlying etiologies (eg, pneumonia, neoplasm, pulmonary emboli); treatment can consist of oxygen if the person is hypoxic; if the fluid accumulation is large enough and the patient is in respiratory distress or compromise, consider thoracentesis; watch for re-expansion pulmonary edema (rare but can happen even with pleural effusions); if etiology is unknown, obtain cell counts, protein, LDH, glucose, and pH; may also include pleural fluid cytology if an underlying malignancy is suspected; thoracentesis does not have to be done acutely in the ED unless the patient is experiencing respiratory compromise; can be done on the floor in a more stable situation; if fluid appears purulent it is empyema, and if so administer antibiotic therapy and chest tube drainage; fluid should be sent for a Gram stain and cultures; patient should be hospitalized for diagnosis and definitive therapy; if the cause is already known (eg, metastatic cancer, heart failure), the patient may be discharged after supportive therapy and amelioration of the condition

Pleuritis: acute pleural inflammation that can cause pain secondary to irritation of the parietal pleura; classically pain is localized and sharp and comes and goes with respiratory mechanics; is worsened by movement, coughing, sneezing, and taking deep breaths; if the inflammation of the pleura is associated with the diaphragm, pain can be referred to the ipsilateral shoulder; to diagnose pleuritis, attempt to diagnose the underlying cause; there are multiple causes; in the very young (typically healthy), the etiology is usually a viral respiratory infection or pneumonia; in other individuals, consider malignancy, pulmonary embolus, and other more serious conditions; if there is evidence of pleural effusion, pleural thickening, or air in the pleural space, further diagnostic and therapeutic measures are indicated; treatment of pleuritis is essentially to treat the underlying cause, but usually in a benign situation analgesics can include anti-inflammatory medications (eg, indomethacin, ibuprofen); may have to result to codeine or other opioids in more serious situations; the use of the opioids may also control coughing; a third possibility is intracostal nerve blocks (benefits are transient)

Pneumomediastinum: gas that is located in the mediastinum outside of the lumen of the esophagus or outside of the airways of the tracheobronchial tree; three main causes of pneumomediastinum are alveolar rupture causing dissection of the air from the alveoli into the mediastinum, perforation or rupture of the esophagus, trachea, or bronchi, and dissection of air from the neck or the abdomen into the mediastinum; the most common cause is the rupturing of the alveoli, which can be seen in asthmatics; can also occur with blunt trauma and forceful coughing; one unusual but classical way of developing pneumomediastinum is when a patient using crack cocaine attempts the valsalva maneuver while smoking the drug; by itself pneumomediastinum is a benign condition; the key for the physician is to find out the cause and to correct the underlying problem

Hamman sign: the classical “crunching” sound that is heard when one auscultates the chest specifically listening to the heart; it sounds like a crunch or a clicking sound and occurs with each heart beat; the key to the diagnosis is often x-ray, which can show streaks of gas outlining the mediastinal structures including the trachea, branches of the trachea, pulmonary artery, or even the aorta; literature indicates that the best way to locate pneumomediastinum is not on the frontal view of the chest but on the lateral view; it is possible on the frontal view that you may see mediastinal gas outlining the superior surface of the diaphragm separating the diaphragm from the heart

Boerhaave syndrome: rupture of the esophageal wall secondary to vomiting; the patient will develop severe retrosternal pain following a bout of retching and vomiting; it is possible to see pneumomediastinum on x-ray; in the setting of heavy alcohol use, retching and vomiting, and severe chest pain, it is Boerhaave syndrome with pneumomediastinum; treatment is to figure out the etiology of the condition; it could be related to trauma, asthma, or drug abuse; if the etiology is not determined, a condition may be missed that is emergent and if not recognized can be fatal; typically Boerhaave syndrome can have a fatal outcome without a prompt thoracotomy and esophageal repair

Pneumomediastinum associated with tracheobronchial rupture: can be fatal; if attempting to ventilate the lungs, there is danger of forcing air into the mediastinum, resulting in displacement of the other mediastinal structures thus causing a vascular catastrophe

Pneumothorax: entry of free air into the potential space between the visceral and parietal pleura; primary — no evidence of clinically apparent lung disease that can occur spontaneously or as the result of trauma as external forces penetrate the intrapleural space; secondary — occur when there is underlying lung disease; primary spontaneous pneumothorax is predominantly seen in men and associated factors include cigarette smoking, mitral valve prolapse, Marfan syndrome and changes in ambient pressure; physical activity or exertion can also precipitate a pneumothorax, but it is relatively rare; causes of secondary spontaneous pneumothorax include COPD, asthma, cystic fibrosis, sarcoidosis, pulmonary fibrosis, tubular sclerosis, HIV, tuberculosis, lung abscess, Marfan syndrome, scleroderma, cancer, and catamenial pneumothorax; the parietal and visceral pleura are in close approximation, which is maintained with a negative pressure of -5 mm Hg on average; there is an inherent tendency of the chest wall to expand and at the same time the inherent tendency of the lungs to collapse from recoil; when there is loss of normal negative pressure, the lung collapses, leading to a pneumothorax; the pneumothorax can be simple in which case the collapse of the lung essentially stays the same; this must be differentiated from tension pneumothorax, in which the inhaled air accumulates and keeps accumulating in the pleural space; inhaled air does not exit because of a check valve system leading to increasing intrathoracic pressure, usually more than 20 mm Hg; the great vessels in the heart are compressed and shift contralaterally; there is severe restriction of the venous return to the heart and diastolic filling, and decrease in cardiac output as well as ventilation perfusion mismatch, all of which will result in hypoxia, hypoxemia, and shock

Classic symptoms: primary spontaneous pneumothorax — sudden onset of dyspnea, ipsilateral pleuritic chest pain, and can resolve within 24 hours; profound symptomatology is rare; there is not profound shortness of breath; there is sinus tachycardia but typically not to extreme limits; typically the simple pneumothoraces are small so often it is difficult to appreciate ipsilateral decreased breath sounds, hyperresonance to percussion, and tactile fremitus; tension pneumothorax — tracheal deviation to the uninvolved side, hyperresonance of the affected side, shock, and significant dyspnea and tachycardia

Imaging: chest x-ray is the typical imaging modality; there may be loss of lung markings in the periphery; the lateral chest x-ray identifies pneumothorax in an additional 14% of cases; sensitivity of an anterior posterior chest x-ray is about 75.5% with a specificity of 100%; CT is more sensitive; if the patient is too ill and there is a need to obtain radiography of the patient in a supine position, the pneumothorax is not seen; one indication is the deep sulcus sign, which is a deep, lateral costophrenic angle in the affected lung field; in COPD patients large bullae can mimic pneumothoraces; if time permits obtain a chest x-ray (this can differentiate between the 2); challenge to estimate the pneumothorax size or at least communicate the size to consultants; the American College of Chest Physicians use a modality of measuring from the apex of the lung to the cupula of the thoracic cavity on an upright PA x-ray; a measurement of <3 cm of radiolucency is considered a small pneumothorax; another method is to measure the interpleural distance at the level of the hilum; a distance of 2 cm correlates to a pneumothorax of about 50% by volume; ultrasonography is increasingly more important for the bedside diagnosis of a traumatic pneumothorax and has reported sensitivity of 98.1% and specificity of 99.2%; it visualizes the movement of the lung (the “ocean”) against a stationery chest wall (the “sea shore”); apart from the ultrasonography, chest CT will detect 25% to 40% of pneumothoraces that are not visualized on a routine chest x-ray; if there is clinical suspicion of a pneumothorax but it cannot be proven on chest x-ray, obtain CT (if patient is stable enough)

Treatment: depends on the size of the pneumothorax and the stability of the patient; options include oxygen, observation, needle or catheter aspiration, or tube thoracostomy; simple oxygen alone (>28% FiO₂) increases the pleural air resorption 3- to 4-fold over the baseline; if patient is discharged without oxygen or treatment and they have a simple pneumothorax of 25%, it resolves on its own in about 20 days; nevertheless, observation is appropriate with a small, stable pneumothorax; if observing the person without intervention, keep them on supplemental oxygen for approximately 4 hours and then repeat the chest x-ray; if the symptoms and the x-ray improve, the patient can be discharged with follow-up within 24 hours; typically a first-time spontaneous pneumothorax that involves <20% of the lung volume in an otherwise healthy person can be sent home with oxygen therapy; there are published criteria to determine a stable patient with a pneumothorax including respiratory rate of <24 breaths/minute, no dyspnea at rest, a patient who can speak in full sentences, a pulse rate that is 60 to 120 beats/minute, normal blood pressure for that particular patient, and an O₂ saturation that is >90% with no evidence of hemothorax; another option for people with small, primary pneumothoraces of <20% or whose apex to cupula distance is 3 cm or less and who are asymptomatic would be to use a small catheter aspiration to remove the intrapleural air, observe the patient for 3 hours, and discharge only if there are no symptoms, otherwise insert a small-sized catheter or small-sized chest tube, Heimlich valve, and admit the patient; for small secondary pneumothoraces, an option would be using a small catheter or small chest tube insertion plus a Heimlich valve or a water seal and admit patient; for a large pneumothorax (primary or secondary), especially if it is bilateral, it is recommended to insert at least a moderate sized chest tube and admit the patient; if there is evidence of a hemothorax or other fluid, insert a large chest tube plus water seal and admit the patient; for a tension pneumothorax there is no time to confirm a person who is hemodynamically unstable by means of a chest x-ray; the patient requires immediate needle decompression followed by moderate size or large chest tube insertion, water seal drainage, and admission to the hospital; an open pneumothorax results from an open wound of the chest wall with free communication between the pleural space and the atmosphere and is usually seen with major trauma; significantly impairs the ability to expand the lungs resulting in inadequate ventilation; with the expansion of the chest during a breath, air moves in and out of the chest wall instead of through the trachea producing hypoventilation and mismatch; this can ultimately lead to death if steps are not taken to correct it, including sealing the wound with an occlusive sterile dressing taped on three sides to act as a flutter valve; if there is no occlusive sterile dressing, any material (even if it is not sterile) is acceptable because the condition if not treated promptly can be life threatening; definitive treatment consists of a chest tube to re-expand the lung and surgical closure of the thoracic defect

Empyema: frank pus accumulating in the pleural space; it develops as a consequence of a parapneumonic effusion (complicated or uncomplicated); S pneumoniae and S aureus are frequent etiologic factors, as well as Klebsiella, Pseudomonas, and the Haemophilus species; besides an infectious etiology empyema can also arise from an esophageal perforation, trauma, a surgical procedure in the pleural space, or septicemia, which could take 2 to 3 weeks to develop; it is estimated that 500,000 to 750,000 patients annually develop a parapneumonic infusion; there are no numbers to estimate how many develop empyema or frank pus in the pleural space; in one small series it was discovered that up to 10% of the patients required drainage or a surgical procedure

Risk factors: age — it occurs in both the pediatric and the elderly population; debilitation — pneumonia requiring hospitalization; comorbid diseases — eg, bronchiectasis, rheumatoid arthritis, alcoholism, diabetes, or GERD; one study identified 7 clinical factors that predicted the development of empyema including an albumin value of <30 g/L, a serum sodium value of <130 mmol/L, a platelet count of >$400,000, a C-reactive protein level >100 mg/L, and a history of alcohol or IV drug abuse

Mortality: reported to be from 11% to 50%; some authors believe that the lower value is based on current diagnostic imaging, antibiotics, and drainage options; complicating factors include cardiac disease, respiratory comorbidities, immunosuppressive states (eg, those related to medications or HIV), and age

Prognosis: most patients recover, but the mortality rate remains approximately 10% based upon appropriate antibiotic therapy and early antibiotic therapy as well as early drainage of the pleural fluid; up to 25% of the patients require surgical intervention

Presentation: patients will be febrile, have tachypnea and tachycardia, look toxic, and can fulfill the criteria for systemic inflammatory response syndrome; they will have decreased or absent breath sounds, dullness to percussion, decreased tactile fremitus, and possibly a contralateral tracheal shift

Differential diagnosis: pneumonia, hemothorax, lung abscess, non-small cell lung cancer, secondary lung tumors, and tuberculosis

Laboratory/imaging: there are no specific laboratory studies but clinician may get a chest x-ray, which can show presence of a significant amount of pleural fluid leading to the diagnosis of empyema once a thoracentesis is performed; ultrasonography can be useful to localize the fluid as well as CT of the chest

Main procedure: thoracentesis, especially when the evidence of the effusion or empyema is ≥10 mm thick on the lateral decubitus chest x-ray; return on the thoracentesis can look opaque and turbid or grossly thick, viscous, and foul smelling; send the pleural fluid for a white blood cell count, as well as a differential cell count, and obtain total protein, LDH, and glucose; exudates are defined by a pleural serum total protein ratio of >0.5 and a pleural serum LDH ratio of >0.6, and a pleural fluid pH of <7.2 is suggestive of a complicated pleural effusion or empyema; obtain a Gram stain and bacterial culture

Medical care: definitive pleural drainage and antibiotic therapy

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Disclosures

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Acknowledgements

CME/CE INFO

Accreditation:

The Audio- Digest Foundation is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.

The Audio- Digest Foundation designates this enduring material for a maximum of 0 AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

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Lecture ID:

EMBR170127

Expiration:

This CME course qualifies for AMA PRA Category 1 Credits™ for 3 years from the date of publication.

Instructions:

To earn CME/CE credit for this course, you must complete all the following components in the order recommended: (1) Review introductory course content, including Educational Objectives and Faculty/Planner Disclosures; (2) Listen to the audio program and review accompanying learning materials; (3) Complete posttest (only after completing Step 2) and earn a passing score of at least 80%. Taking the course Pretest and completing the Evaluation Survey are strongly recommended (but not mandatory) components of completing this CME/CE course.

Estimated time to complete this CME/CE course:

Approximately 2x the length of the recorded lecture to account for time spent studying accompanying learning materials and completing tests.