A hiatal hernia is a herniation of elements of the abdominal cavity through the esophageal hiatus of the diaphragm. On an upright chest radiograph, a gastric bubble containing an air fluid level can be seen above the diaphragm, usually in the mid-chest in the retrocardiac region. There are four types of hiatal hernia (I—IV). Type I, or sliding hiatal hernia, accounts for >95% of cases. This is caused by laxity of the phrenoesophageal membrane, allowing a portion of the gastric cardia to herniate upward. Most of these are asymptomatic. Types II—IV hiatal hernias are varieties of paraesophageal hernias where the GE junction remains fixed while a portion of the stomach herniates through the esophageal hiatus and lies beside the esophagus.
The majority of patients with hiatal hernia are asymptomatic. When symptoms do occur, the most common symptoms are intermittent epigastric or substernal pain, postprandial fullness, nausea, and vomiting. Shortness of breath can occur due to diaphragmatic irritation and palpitations can occur due to vagus nerve irritation. If a hiatal hernia is noted on plain radiographs and further characterization of the defect is needed, the best radiographic modality is a barium swallow.
Figure 5.1 ▪ Hiatal Hernia.
A, B: Frontal radiograph demonstrates a midline retrocardiac rounded mass with an air fluid level (arrows). The lateral view confirms a rounded and air-filled middle mediastinal mass. This is the typical appearance for a hiatal hernia. The patient has had shoulder replacement surgery.
The natural progression of a type II, III, or IV hernia is progressive enlargement. They never regress spontaneously. For this reason, these are referred for surgical treatment, even in the absence of symptoms. Complications of an enlarging hernia include gastric volvulus, torsion, bleeding, incarcerated hernia pouch, and respiratory complications from mechanical lung compression. Type I hernias rarely require any intervention.
Nipple shadows appear as hyperdense opacities in the lower lung fields on the PA view of the chest. The nipple of the male or female breast projects into the air and can create a radiographic shadow that resembles an intraparenchymal pulmonary nodule. Nipples tend to have fuzzy margins and are bordered by a radiolucent halo created by the projection of air from around the nipple. They are typically located at the level of the fifth or sixth anterior ribs or near the bottom of the breast shadow. On lateral chest radiograph, there is no orthogonal correlate within the lung parenchyma; however, a prominent nipple may be identified in a corresponding location outside the lung field.
If only an AP view of the chest is available, and there is a question whether the hyperdensity in the inferior chest represents a nipple shadow versus a pulmonary nodule, then repeat radiographs should be taken with nipple markers—1.5 mm lead objects that overlie the nipple—in order to determine if the opacity on imaging correlates with the location of the physiologic nipple.
Atelectasis means lung collapse or loss of lung volume. It appears as an opacity on plain radiographs that can obscure a lobe, part of a lobe, or an entire lung field. In the absence of any appreciable volume loss or fissural or mediastinal shift, atelectasis can be difficult to distinguish from a consolidation as both may appear as lung opacities. Pneumonia may result in signs of volume expansion due to mass effect. Atelectasis, however, is typically associated with signs of volume loss because alveoli have collapsed and lung volume has been lost. Signs of volume loss include elevation of the ipsilateral hemidiaphragm, graying of the ipsilateral lung base, migration of a fissure toward the atelectatic lung, and deviation of the trachea and mediastinum toward the affected side.
Figure 5.7 ▪ Complete Left Lung Atelectasis.
A-B: There is complete opacification of the left lung with shift of the trachea and heart to the left, consistent with volume loss from complete left lung atelectasis. This patient underwent emergent bronchoscopy where a mucous plug was discovered. The left lung is significantly better aerated on the post bronchoscopy images.
Treatment of atelectasis should be directed at the underlying cause of collapse. The most common cause of atelectasis is post-surgical collapse secondary to splinting and pain, which is treated with appropriate pain control, chest physiotherapy, positive pressure ventilation, and early ambulation. Other causes of atelectasis include bronchus or bronchiole obstruction from a mucus plug or aspirated foreign body. The bronchial cut-off sign, in which a bronchus suddenly disappears without visible tapering into smaller bronchioles, is usually due to large mucus plugging.
Atelectasis and consolidation may be difficult or impossible to distinguish radiographically, especially on portable AP radiographs.
Signs of volume loss (midline shift, fissure migration) favor atelectasis over consolidation.
Figure 5.8 ▪ Left Upper Lobe Atelectasis.
A, B: There is hazy opacification of the left lung compared to the right with a subtle crescent-shaped lucency adjacent to the aortic arch. On the lateral view, the left major fissure is displaced anteriorly (arrows) and the left lower lobe demonstrates compensatory hyperinflation.
Figure 5.9 ▪ Right Middle Lobe Atelectasis.
A, B: There is a hazy opacity in the right lung base obscuring the right heart border. There is only minimal associated volume loss with mild elevation of the right hemidiaphragm. On the lateral view, a wedge-shaped opacity can be seen projecting anteriorly, which represents the collapsed right middle lobe.
Figure 5.11 ▪ Right Upper Lobe Atelectasis.
There is an opacity in the right upper lung with elevation of the minor fissure and mild deviation of the trachea to the right, indicating volume loss. This appearance of the RUL and minor fissure is often referred to as the S sign of Golden” and underlying malignancy should be excluded. This patient had adenocarcinoma.
Dextrocardia refers to the position of the heart within the right hemithorax. Dextrocardia may take several forms: dextroposition, in which a normally configured heart points more to the right chest than normal; dextrocardia with situs inversus in which the heart is completely on the right side; and situs inversustotalis, in which all visceral organs are mirrored on the opposite side of their typical position.
When dextrocardia is suspected, first check that the radiograph is appropriately labeled. The apex of the normal heart sits in the left mid-clavicular line. In dextrocardia, the cardiac apex sits in the right mid-clavicular line. If the stomach bubble is located in the right upper quadrant under the cardiac apex, this suggests situs inversustotalis.
The majority of adult patients who have dextrocardia on chest radiograph are already aware of the diagnosis. Isolated dextrocardia without situs inversus is more likely to be associated with severe cardiac defects. One in twenty-five of these are associated with primary ciliary dyskinesia or Kartagener syndrome. These patients tend to present with recurrent sinus and bronchial infections secondary to poorly functioning ciliary clearance.
In patients with dextrocardia with situs inversus, there are typically no other associated abnormalities.
EKG changes in dextrocardia reflect the fact that the apex of the heart is in the right hemithorax instead of the left. There is a negative P wave and QRS complex in lead 1 since atrial and ventricular depolarization start on the left and spread toward the right. There is reverse R-wave progression across the precordium with the R wave tallest in V1 and getting progressively smaller through V6.
An enlarged cardiac silhouette is defined as a transverse diameter greater than or equal to 50% of the transverse diameter of the chest measured at the lung bases. On a portable AP radiograph, the heart can appear to be artificially enlarged. Since the heart is located within the anterior aspect of the thorax, its size is magnified as the image detector is placed further away from it, behind the patient’s back. On plain radiographs alone, it may be difficult to differentiate cardiomegaly from other causes of enlarged cardiac silhouette, including pericardial effusion, mass, left ventricular aneurysm, and pericardial fat pad. If there is cardiomegaly, it is usually possible to determine which cardiac chamber is enlarged. On a PA view, one can visualize the right atrium, left ventricle, and left atrium. The right ventricle can be visualized only on the lateral view.
With right ventricular enlargement, there is increased opacity filling the retrosternal clear space on the lateral view. Right atrial enlargement on the PA view appears as displacement of the right heart border to the right. Left ventricular enlargement appears as displacement of the left heart border laterally and to the left, inferiorly and posteriorly with rounding of the cardiac apex. Signs of left atrial enlargement on the PA view include splaying of the carina with an upward sweep due to the large left atrium. The “double density” sign occurs when the right side of the left atrium pushes into the adjacent lung. On the lateral view, the left atrium can be seen extending posteriorly towards or over the spine.
If cardiomegaly is suspected based on a chest radiograph, echocardiography is recommended. An echocardiogram can be used to identify the presence of pericardial effusion, pericardial fat, mass, aneurysm, wall motion abnormalities, chamber dilation, chamber hypertrophy, and valve insufficiency.
Left ventricular hypertrophy is most commonly caused by chronic hypertension, with left ventricular muscle mass increasing in order to compensate for the high resistance that it needs to work against to maintain cardiac output. Common etiologies of chamber dilation include aortic and mitral regurgitation, and the various cardiomyopathies.
An enlarged cardiac silhouette is not synonymous with cardiomegaly. Echocardiography is the modality of choice to differentiate the underlying cause.
A lateral view of the chest may be able to diagnose a pericardial effusion: if the effusion is large enough it becomes visible as a radiodense layer sandwiched between the two relatively radiolucent layers of the epicardial and pericardial fat (the “oreo cookie sign”).
Suspected pathology can be determined based on the chamber/chambers that are enlarged.
Figure 5.15 ▪ Enlarged Cardiac Silhouette.
A, B: On the frontal view, the heart is significantly enlarged with prominence of the right heart border, suggesting right atrial enlargement. On the lateral view, there is filling of the retro-sternal clear space and the left atrium projects over the spine, suggesting right ventricular and left atrial enlargement, respectively. This patient had tricuspid and mitral regurgitation with subsequent valvuloplasty.
Figure 5.16 ▪ Enlarged Cardiac Silhouette.
A, B: On the frontal view, the right heart border is prominent indicating right atrial enlargement. The left atrial appendage is also prominent suggesting left atrial enlargement. On the lateral view, there is filling of the retrosternal clear space, consistent with right ventricular enlargement. This patient had significant right heart enlargement from tricuspid regurgitation and left atrial enlargement from mitral stenosis.
Radiographically, a pulmonary nodule is defined as a lesion less than 3 cm in diameter that is both within and surrounded by lung parenchyma. If greater than 3 cm, the lesion is called a mass. Pulmonary nodules are categorized as benign or malignant. The most common causes of a malignant nodule are primary lung cancer, carcinoid tumors, and lung metastases. Malignant nodules, whether primary or metastatic, are rarely calcified. Calcified nodules are usually benign. The most common causes of benign nodules are infectious granulomas (80%) and hamartomas (10%).
Figure 5.17 ▪ Pulmonary Nodule.
A-C: On the frontal view, there is a rounded density in the left upper lung (arrow). On the lateral view, the nodule can be seen posteriorly below the major fissure, suggesting that it is located in the superior segment of the left lower lobe. A CT was ordered, which showed a 1.0 cm pleural-based nodule that remained stable on follow-up and was a presumed granuloma.
When a pulmonary nodule is identified on chest radiograph, every attempt must be made to secure old imaging studies because size comparisons can be used to determine stability versus growth. A nodule that has not grown over 2 years may be considered benign.
Clinical features associated with an increased probability of malignancy include advanced age, history of smoking, and prior history of malignancy. Discovery of a new nodule requires that the patient be informed of the nodule, and appropriate follow-up arranged. The Fleischner Society guidelines advocate different frequencies of CT scans based upon the size of the nodule and the patient’s risk for lung cancer. Patients are considered low risk if they have no history or minimal history of smoking and no other risk factors (such as known carcinogen exposures); otherwise, patients are considered high risk. For a newly diagnosed pulmonary nodule found as an incidental finding on chest radiograph in the ED, these general guidelines may be followed: If nodules are ≤4 mm and the patient is low risk, no further imaging is required. If the patient is high risk, they should have a follow-up CT in 12 months. For nodules 4 to 6 mm, a CT scan should be performed at 12 months if the patient is low risk and at 6-12 months if the patient is high risk. For nodules 6 to 8 mm, a CT scan should be performed at 6-12 months if the patient is low risk, and at 3-6 months if the patient is high risk. For nodules greater than 8 mm, a CT scan should be performed at 3 months whether the patient is low or high risk.
Figure 5.18 ▪ Pulmonary Nodule.
A-C: On the frontal view, there is a rounded density in the right lower lung. On the lateral view, the nodule can be seen posteriorly below the major fissure, suggesting that it is located in the right lower lobe. A CT was ordered, which showed a 2.0 cm lobulated nodule with a small central calcification. This remained stable on follow-up and was a presumed hamartoma.
Nodules occurring in the lung apices may be particularly difficult to detect on radiographs. Ensuring the radiographic density of the left and right apices is similar is reassuring that there is no nodule.
Large nodules in the superior sulcus may result in shoulder and arm pain, Horner’s syndrome, and weakness and atrophy of the muscles of the hand, a constellation of symptoms referred to as Pancoast’s syndrome.
Figure 5.20 ▪ Pulmonary Nodule.
A-C: There is a subtle left lower lung density on the frontal view (the smaller more superior density represented a calcified granuloma). This density can be seen over the inferior heart on the lateral view. The CT showed a 1.5 cm nodule in the lingula and was subsequently biopsied. Pathology was consistent with metastatic renal cell carcinoma.
A cervical rib is a supernumerary rib that arises from the seventh cervical vertebra. It is a congenital abnormality located above the normal first rib, overlying the pulmonary apex. It is usually C-shaped and can be identified by noting that the rib arises from a vertebral body whose transverse processes point down, such as C7. In contrast, the transverse processes of T1 point up.
The majority of cervical ribs are of limited clinical significance. However, the presence of a cervical rib can cause a form of thoracic outlet syndrome due to compression of the lower trunk of the brachial plexus or subclavian artery or thoracic inlet syndrome due to compression of the subclavian vein. Clinical manifestations of brachial plexus involvement include pain in the neck and shoulder, which radiates into the upper extremities, paresthesias and sensory loss, and weakness of the muscles innervated by the brachial plexus. Subclavian vein compression can present with upper extremity edema and erythema while subclavian artery compression can result in limb ischemia with bluish discoloration and cold hands.
Aspiration pneumonia is an inflammation of the lung parenchyma precipitated by the abnormal entry of fluid, particulate exogenous substances, or endogenous secretions into the tracheobronchial tree. Radiographic findings are often delayed, with false-negative radiographs being common early in the disease course. Infiltrates can develop within 6-12 hours and frequently involve the posterior segments of the upper lobes (if aspiration occurred in the supine position) or the superior segments of the lower lobes, most commonly the right lower lobe (if aspiration occurred in the upright position). Later in the disease process, aspiration pneumonia tends to appear as patchy bilateral airspace opacities that are symmetric and somewhat nodular.
CT scanning provides a greater degree of sensitivity and specificity than radiographs alone, however, some of the same diseases that mimic plain radiographic findings of aspiration can also confound the diagnostic interpretation of CT scans. The differential includes: atypical pneumonia, varicella pneumonia, and ARDS.
Aspiration is a common event even in healthy individuals and usually resolves without detectable sequelae.
The diagnosis of aspiration pneumonia is usually presumptive based upon the clinical features and course. Treatment of patients with observed or suspected aspiration includes suctioning of the mouth and support of pulmonary function. The use of antibiotics early in the course of aspiration is controversial as damage is mostly due to a chemical pneumonitis. However, antibiotics are commonly given because of the difficulty in excluding bacterial infection as a primary or contributing factor in patients with aspiration.
False negative findings are common early in the course of the disease, as radiographic findings lag behind clinical findings.
Be suspicious for aspiration pneumonitis in a patient who has risk factors such as altered mental status, impaired clearance mechanisms, dysphagia, GERD, and poor oral hygiene.
Aspiration pneumonia has a highly variable disease course, with up to 15% mortality.
Lobar pneumonia appears radiographically as a focal parenchymal consolidation of a portion or the entire lung lobe. Larger bronchi often remain patent with air, creating characteristic air bronchograms extending into the consolidated parenchyma.
Unlike atelectasis, where the predominant feature is volume loss within the affected segment or lobe of the lung, lobar pneumonia is characterized by mass effect within the involved portion of the lung. Fissures, a hemidiaphragm, or the mediastinal structures may be deviated away from the involved lung.
An obscured right heart border on AP view indicates a right middle lobe pneumonia. An obscured right hemidiaphragm on AP view indicates a right lower lobe pneumonia. Similarly, silhouetting of the left heart border on AP view suggests lingular pneumonia and silhouetting of the left hemidiaphragm is consistent with consolidation within the left lower lobe. On the lateral view, as you follow the spine inferiorly, the vertebral bodies get progressively darker on a normal chest radiograph. The “spine sign” is an interruption in the progressive increase in lucency of the vertebral bodies from superior to inferior and is suggestive of left lower lobe pneumonia in the correct clinical setting. Left lower lobe pneumonia can also be seen on AP view as an increased retrocardiac opacity.
Pneumonia is classically diagnosed by the presence of an area of consolidation on radiography with a supportive presentation. False negatives can occur early in the disease course. If clinical suspicion is high, it is reasonable to initiate antibiotic therapy based on the clinical picture alone.
The causes, treatment, and prognosis of hospital-acquired pneumonia are different from those of community-acquired pneumonia. Hospital-acquired microorganisms may include resistant bacteria such as MRSA, Pseudomonas, and Enterobacter sp. Broad-spectrum antibiotic coverage with a multidrug regimen is necessary to cover probable pathogens.
Figure 5.24 ▪ Lobar Pneumonia.
A, B: On the frontal view, there is a left mid-lung/peri-hilar opacity with obscuration of the superior left heart border. On the lateral view, an opacity can be seen projecting anterior to the major fissure. This patient had lobar pneumonia within the anterior segment of the left upper lobe with additional early consolidation within the lingula.
Clinical suspicion with a lobar consolidation on chest radiography is typical for lobar pneumonia.
Lobar consolidation may result in regional mass effect, as opposed to atelectasis that results in volume loss.
Subtle opacities from early pneumonia do not produce any appreciable mass effect and may be indistinguishable from subsegmental atelectaisis, especially on a portable chest radiograph.
Whenever possible, obtain PA and lateral chest radiographs rather than a portable AP radiograph. PA and lateral chest radiographs reveal much more information for half the cost. Portable chest radiographs obtained with the patient supine or recumbent almost always result in some component of atelectasis in the lung bases, which is indistinguishable from early pneumonia. A lateral view allows the evaluation of the retrosternal region, the lower lobes (which hide below the diaphragmatic domes on the AP view), and is much more sensitive for small pleural effusions. The assessment of the heart and mediastinum is also more accurate and complete on a PA and lateral study versus on a portable AP view.
Figure 5.26 ▪ Lobar Pneumonia.
A, B: On the frontal view, there is a right lower lung opacity obscuring the right heart border. On the lateral view, the opacity projects anteriorly and contains multiple small abscesses with air-fluid levels (arrows). This patient was diagnosed with necrotizing right middle lobe pneumonia from staphylococcus aureus.
Varicella pneumonia is a rare but rapidly progressive pneumonia with significant mortality. The findings on chest radiography in varicella pneumonia are due to diffuse alveolar damage initially with multiple ill-defined, 5—10 mm nodules that may be confluent and fleeting. These nodules usually resolve within one week after resolution of the skin lesions, but sometimes may persist for months. Sometimes the nodules calcify and persist indefinitely.
The differential diagnosis for amicronodular pattern on plain radiograph includes: alveolar microlithiasis, pulmonary hemosiderosis, miliary tuberculosis, intravenous talc granulomatosis (seen in IV drug users who inject talc), calcified metastases, and early stages of pneumoconioses such as silicosis, talcosis, and coal worker’s pneumoconiosis.
Varicella pneumonia typically develops slowly within one to six days after the onset of skin lesions. Symptoms are similar to those of other pneumonias, including dry cough, fever, tachypnea, and dyspnea. Varicella pneumonia is the most serious complication of disseminated varicella-zoster virus infection with mortality rates of 10-50%. It is an uncommon complication of varicella in immunocompetent children. In adults, pneumonia accounts for the majority of the morbidity and mortality from varicella infection. More than 90% of cases of adult varicella pneumonia occur in immunocompromised patients and those with lymphoma. If the clinical presentation suggests varicella as the etiology, immediate treatment with IV acyclovir is recommended.
Immunosuppressed patients who present with varicella skin lesions, respiratory complaints, and suggestive radiography should be immediately treated with IV acyclovir.
The calcified nodules that form as sequelae to prior Varicella pneumonia are typically much more numerous and uniform in size and distribution within both lungs than the calcified granulomata resulting from prior granulomatous infection.
Acute Chest Syndrome is an acute pulmonary complication of sickle cell disease. Causes include pulmonary infarction, fat embolism, and infection. A chest radiograph typically demonstrates asymmetric opacities with other secondary signs of sickle cell disease, such as sclerosis of the humeral heads (secondary to bony infarcts), cardiomegaly, or Lincoln-log vertebrae.
Without secondary signs of sickle cell disease, it is difficult to diagnose acute chest based on a chest radiograph alone, as it can resemble atypical pneumonia, ARDS, or lobar pneumonia. It is only in conjunction with the clinical history or with secondary signs on the radiograph that the diagnosis of acute chest syndrome can be made.
Acute chest syndrome is the second most common cause of hospitalization and most common cause of death in patients with sickle cell disease. Triggers include vaso-occlusive crises and infections such S. pneumoniae, Mycoplasma, and Chlamydia.
The diagnosis of ACS requires a new pulmonary infiltrate on chest radiography that involves at least one complete lung segment. In addition, patients must have one or more of the following: chest pain; temperature >38.5°C; tachypnea, wheezing, or increased breathing; and hypoxemia relative to the patient’s baseline.
Respiratory complaint with a new opacity on chest radiography in a sickle cell patient is acute chest until proven otherwise. Pneumonia is in the differential.
Treatment of acute chest requires volume resuscitation, oxygenation, and pain control.
Figure 5.28 ▪ Acute Chest Syndrome.
A, B: The frontal radiograph demonstrates patchy opacities in the lower lungs bilaterally with cardiomegaly. Additionally, mild sclerotic changes are noted in the humeral heads representing osteonecrosis from the patient’s sickle cell disease. On the lateral view, classic changes of sickle cell disease can be seen in the spine with a “Lincoln log” appearance of the vertebral body endplates (arrows).
Figure 5.29 ▪ Acute Chest Syndrome.
A, B: The frontal radiograph demonstrates patchy opacities in the lower lungs bilaterally with cardiomegaly. On the lateral view, the opacities project in the perihilar region. This child had sickle cell disease and was admitted for management of acute chest syndrome. No osseous changes of sickle cell disease are noted in this patient.
Pneumocystis pneumonia is a common complication of AIDS resulting in severe pulmonary compromise. Chest radiographs may initially be normal in patients with PCP pneumonia. The most common radiographic findings are diffuse bilateral perihilar opacities. For immunosuppressed patients with suspected PCP pneumonia and equivocal chest radiograph, high-resolution CT scan is recommended and has been shown to be nearly 100% sensitive and nearly 90% specific for detecting PCP in HIV-positive patients. PCP pneumonia on CT appears as patchy or nodular ground-glass opacities.
PCP pneumonia can also be associated with pleural effusions, lobar infiltrates, nodules, and pneumothorax. Those receiving pentamidine prophylaxis are more prone to developing predominantly apical infiltrates.
Diagnosis is made via a combination of clinical picture with radiographic findings. Treatment is based on disease severity. Patients with mild to moderate disease (A-a gradient less than 45 mmHg) can receive oral therapy with TMP-SMX, TMP-dapsone, or clindamycin—primaquine, all of which have excellent oral absorption and were found to have no difference in therapeutic failure rate. For patients with severe disease (A-a gradient greater than 45 mmHg), IV therapy combined with corticosteroids is recommended. Patients with PCP typically worsen after two to three days of therapy due to antibiotic-induced death of organisms and subsequent inflammation. Corticosteroids decrease this inflammation and have been shown to decrease the incidence of mortality and respiratory failure when given in patients if room air arterial blood gas reveals a partial pressure of oxygen less than or equal to 70 mmHg or an A-a gradient greater than or equal to 35.
PCP is still the most common opportunistic infection in HIV-positive patients.
Always check an ABG in patients with PCP, as the degree of hypoxemia measured by PaO2 and the A-a gradient determines the use of adjuvant corticosteroids.
Suspected PCP pneumonia warrants admission for observation as the condition can rapidly deteriorate even with appropriate antibiotics.
Chest radiographs may be normal or demonstrate perihilar opacities. High-resolution CT shows ground-glass opacities and interstitial prominence.
ARDS is a syndrome of rapidly developing respiratory insufficiency caused by leakage of protein-rich fluid into the alveolar spaces. Radiographically, ARDS appears as bilateral, symmetric air space opacities. The lung bases and costophrenic sulci may be relatively spared. This is a distinguishing feature from hydrostatic pulmonary edema, which is typically most severe in the lung bases. There are no associated pleural effusions or Kerley B lines or cardiomegaly. Typically, there is a 12 hour radiographic delay after the onset of clinical symptoms. After 12 hours, patchy alveolar infiltrates are seen in both lungs. After 24 hours, these infiltrates coalesce to form massive air-space consolidation. Sometimes, air bronchograms are observed.
The definition of Acute Respiratory Distress syndrome requires all four of the following features:
Acute onset of symptoms
Bilateral infiltrates on chest radiographs
No evidence of elevated left atrial pressure (pulmonary capillary wedge pressure less than or equal to 18 if measured)
A PaO2/FiO2 ratio less than or equal to 200 mmHg
Patients with ARDS typically present with tachycardia, tachypnea, dyspnea, hypoxemia, and with diffuse rales. Fever is often lacking or low-grade. Given the severity of lung injury, patients typically worsen rapidly, and mechanical ventilation is almost universally required. The most common causes are sepsis, aspiration, pneumonia, severe trauma, massive transfusion, transfusion-related acute lung injury (TRALI), post-op lung and hematopoietic stem cell transplantation, and drug overdose (salicylates and cocaine are commonly implicated). ARDS is a diagnosis of exclusion. Cardiogenic pulmonary edema and other causes of acute hypoxemic respiratory failure with bilateral infiltrates must be excluded prior to making a diagnosis of ARDS.
An ABG is necessary to determine the PaO2/FiO2 ratio, one of the criteria necessary to establish the definition of ARDS.
The lung bases and costophrenic sulci are usually spared, which is a distinguishing feature from hydrostatic pulmonary edema which is typically most severe in the lung bases.
The absence of pulmonary venous congestion, Kerley B lines, cardiomegaly, and pleural effusions also help distinguish ALI/ARDS from pulmonary edema.
Figure 5.33 ▪ ARDS.
A, B: Bilateral patchy airspace opacities are seen throughout both lungs in this patient with acute respiratory failure. The accompanying CT image demonstrates nodular and confluent ground-glass opacities in both lungs. This trauma patient was subsequently diagnosed with ARDS. Notice the relative sparing of the lung bases and costophrenic sulci and the normal heart size and vascular pedicle width; these are distinguishing features from hydrostatic pulmonary edema.
Atypical pneumonia is not caused by traditional pathogens, the most common being Mycoplasma, Chlamydia, and viruses such as RSV, influenza, parainfluenza, and adenoviruses. Radiographs typically show diffuse, poorly aerated, hazy opacities throughout the lung parenchyma. Opacities tend to be interstitial and linear and less alveolar.
The diagnosis of atypical pneumonia is based on the clinical presentation in conjunction with radiographic findings. The clinical features include the insidious onset of headache, myalgias, moderate fever, and nonproductive cough. Lab findings include a normal or mildly elevated WBC.
Patients with atypical pneumonias can also appear toxic. Exotic pathogens seen with Q fever (Coxiella burnetii), Tularemia (Francisella tularensis), and Psittacosis (Chlamydia psittaci) can cause a more virulent clinical course.
Mycoplasma and Chlamydia are more common causes of atypical pneumonia in younger patients while Legionella is more common in older patients.
CMV should be considered in transplant recipients and patients with AIDS.
Hantavirus should be considered in residents of or recent travelers to the southwestern United States.
Q fever pneumonia, due to Coxiella burnetii, should be considered in patients who work closely with animals, especially farm livestock. Patients tend to present looking ill, diaphoretic, and febrile.
Typical radiographic findings are increased interstitial markings and perihilar linear opacities (rather than focal parenchymal consolidation, as seen in lobar pneumonia).
An empyema is a collection of pus in the pleural space or fissures. The initial radiographic study is a standard 2-view chest radiograph, looking for the presence of a pleural effusion.
Thickening of the pleural space on a chest radiograph in the correct clinical setting is suggestive of empyema. Other causes of pleural space thickening include pleural fat, hemothorax, mesothelioma, and benign fibrous tumor of the pleura. Chest CT ideally should be performed with IV contrast because contrast enhances the pleural layers and nonenhancing fluid collection becomes more conspicuous. Ultrasound is superior to CT in differentiating between free or loculated effusions and can guide thoracentesis.
An empyema is defined by the presence of bacterial organisms on Gram stain of the pleural fluid or frank pus with pleural fluid aspiration.
Most empyemas are caused by bacterial pneumonia. Indications for thoracentesis in the presence of an effusion include: free-flowing and thicker than 10 mm on decubitus radiograph, presence of loculations, thickened parietal pleura on IV contrast CT scan, or clear delineation by ultrasound. Pleural fluid should be sent for cell count with differential, Gram stain, culture, total protein, lactate dehydrogenase, glucose, and pH. Early intervention decreases the mortality rate associated with empyema. Interventions include tube thoracostomy, intrapleural administration of fibrinolytic agents, thoracoscopic debridement with VATS (video-assisted thoracoscopic surgery), or decortication.
A lateral radiograph is much more sensitive and specific in detecting small pleural effusions than a portable AP chest radiograph. If the patient can tolerate it, always obtain PA and lateral views of the chest (more information for approximately half the cost). The additional radiation exposure is negligible.
Parapneumonic effusions that are free flowing and layer greater than 10 mm on a lateral decubitus radiograph should be sampled by thoracentesis.
Figure 5.36 ▪ Empyema.
A, B: There is a pleural-based density in the left lower lung. Upon closer inspection, a subtle crescent of air can be seen medially within the opacity (partially obscured by the overlying lead). An empyema was suspected and a CT scan was ordered. The CT image demonstrates a left pleural fluid collection that contains air. The visceral and parietal layers of the pleura are markedly thickened and show some enhancement. Notice the “split pleural sign;” the findings are consistent with an empyema. A simple left pleural effusion is also seen.
Figure 5.37 ▪ Empyema.
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