Lobar atelectasis

• Lobar atelectasis is usually caused by central bronchial obstruction (obstructive atelectasis), which may be secondary to mucus plugging or an obstructing neoplasm.
Left upper lobe atelectasis: The luftsichel (air-sickle in German) sign of left upper lobe collapse is a crescent of air seen on the frontal radiograph, which represents the interface between the aorta and the hyperexpanded superior segment of the left lower lobe.
Right upper lobe atelectasis: The reverse S sign of Golden is seen in right upper lobe collapse caused by an obstructing mass. The central convex margins of the mass form a reverse S. Although the sign describes a reverse S, it is also commonly known as Golden's S sign. Similar to left upper lobe collapse, a right upper lobe collapse should raise concern for an underlying malignancy, especially with a Golden's S sign present. The juxtaphrenic peak sign is a peridiaphragmatic triangular opacity caused by diaphragmatic traction from an an inferior accessory fissure or an inferior pulmonary ligament.
Left lower lobe atelectasis: In left lower lobe collapse, the heart slightly rotates and the left hilum is pulled down. The flat waist sign describes the flattening of the left heart border as a result of downward shift of hilar structures and resultant cardiac rotation.
Right lower lobe atelectasis: Right lower lobe atelectasis is the mirror-image of left lower lobe atelectasis. The collapsed lower lobe appears as a wedge-shaped retrocardiac opacity.
Right middle lobe atelectasis: The findings of right middle lobe atelectasis can be subtle on the frontal radiograph. Silhouetting of the right heart border by the collapsed medial segment of the middle lobe may be the only clue. The lateral radiograph shows a wedge-shaped opacity anteriorly.
Round atelectasis: is focal atelectasis with a round morphology that is always associated with an adjacent pleural abnormality (e.g., pleural effusion, pleural thickening or plaque, pleural neoplasm, etc.). All five of the following findings must be present to diagnose round atelectasis: 1) Adjacent pleura must be abnormal. 2) Opacity must be peripheral and in contact with the pleura. 3) Opacity must be round or elliptical. 4) Volume loss must be present in the affected lobe. 5) Pulmonary vessels and bronchi leading into the opacity must be curved this is the comet tail sign.

Abnormalities of the secondary pulmonary lobule

Consolidation and ground glass

• Consolidation and ground glass opacification are two very commonly seen patterns of lung disease caused by abnormal alveoli. The alveolar abnormality may represent either filling of the alveoli with fluid or incomplete alveolar aeration.
Consolidation can be described on either a chest radiograph or CT, while ground glass is generally reserved for CT.
Consolidation is histologically due to complete filling of affected alveoli with a liquidlike substance (commonly remembered as blood, pus, water, or cells).
Pulmonary vessels are not visible through the consolidation on an unenhanced CT.
Air bronchograms are often present if the airway is patent. An air bronchogram represents a lucent air-filled bronchus (or bronchiole) seen within a consolidation.
Acute consolidation is most commonly due to pneumonia, but the differential includes:
1. Pneumonia.
2. Acute respiratory distress syndrome (ARDS.
3. Pulmonary edema.

The differential diagnosis of chronic consolidation includes:

1. Bronchioloalveolar carcinoma mucinous subtype.
2. Organizing pneumonia,.
3. Chronic eosinophilic pneumonia.

Ground glass opacification (GGO): is histologically due to either partial filling of the alveoli (by blood, pus, water, or cells), alveolar wall thickening, or reduced aeration of alveoli (atelectasis).

• Acute ground glass opacification: causes include
  1. Pulmonary edema.
  2. Pulmonary hemorrhage. Acute respiratory distress syndrome (ARDS).
• Chronic ground glass opacification: causes include
  1. Bronchioloalveolar carcinoma.
  2. Idiopathic pneumonias.
  3. Hypersensitivity pneumonitis (HSP.
  4. Alveolar proteinosis.

The differential diagnosis for ground glass in a central distribution includes:

1. Pulmonary edema.
2. Alveolar hemorrhage.
3. Pneumocystis jiroveci pneumonia.
4. Alveolar proteinosis.

Peripheral ground glass or consolidation:

1. Organizing pneumonia.
2. Chronic eosinophilic pneumonia.
3. Atypical or viral pneumonia. Pulmonary edema.

Approach to multiple nodules

Centrilobular nodules:

Infectious causes of centrilobular nodules include:

1. Endobronchial spread of tuberculosis or atypical mycobacteria..
2. Bronchopneumonia.
3. Atypical pneumonia.

The two most common inflammatory causes of centrilobular nodules include

• hypersensitivity pneumonitis (HSP) and
• respiratory bronchiolitis interstitial lung disease (RB-ILD. HSP is a type III hypersensitivity reaction to an inhaled organic antigen. The subacute phase of HSP is primarily characterized by centrilobular nodules.
• Hot tub lung.
• Diffuse panbronchiolitis.

Perilymphatic nodules:

Causes of perilymphatic nodules include:

1. Sarcoidosis.
2. Pneumoconioses (silicosis and coal workers pneumoconiosis).
3. Lymphangitic carcinomatosis.

Random nodules:

Causes of random nodules:

1. Hematogenous metastases.
2. Septic emboli.
3. Embolic infection.
4. Pulmonary Langerhans's cell histiocytosis (PLCH).

A miliary pattern:

• is innumerable tiny random nodules disseminated hematogenously, suggestive of the appearance of millet seeds. The differential of miliary nodules includes:
  1. Disseminated tuberculosis.
  2. Disseminated fungal infection.
  3. Disseminated hematogenous metastases.
• Tree-in-bud nodules: Tree-in-bud nodules are multiple small nodules connected to linear branching structures, which resembles a budding tree branch in springtime as seen on CT.
• Tree-in-bud nodules are almost always associated with small airways infection, such as endobronchial spread of tuberculosis. The differential of tree-in-bud nodules includes:
  1. Mycobacteria tuberculosis and atypical mycobacteria.
  2. Bacterial pneumonia.
  3. Aspiration pneumonia.
  4. Airway-invasive aspergillus.

Cavitary and cystic lung disease

Solitary cavitary nodule/mass

• A solitary cavitary lesion is most likely cancer or infection.
• Primary bronchogenic carcinoma.
• Tuberculosis.

Multiple cavitary nodules

• Multiple cavitary lesions are typically vascular or spread through the vascular system:
• Septic emboli.
• Vasculitis.
• Metastases.

Cystic lung diseases

• A cyst is an air-containing lucency with a thin, nearly imperceptible wall.
• In general, cystic lung disease is usually due to a primary airway abnormality.
• The differential diagnosis for multiple lung cysts includes:
  1. Lymphangioleiomyomatosis (LAM).
  2. Emphysema.
  3. Pulmonary Langerhans cell histiocytosis.
  4. Diffuse cystic bronchiectasis.
  5. Pneumocystis jiroveci pneumonia.
  6. Lymphoid interstitial pneumonia (LIP).
• The differential for a single cyst includes:
  1. Bulla.
  2. Bleb.
  3. Pneumatocele.

Fibrotic changes

Lower lobe fibrotic changes

The differential diagnosis of basal-predominant fibrotic change includes:

1. Idiopathic pulmonary fibrosis (IPF).
2. End-stage asbestosis.
3. Nonspecific interstitial pneumonia (NSIP).

Upper lobe fibrotic changes

• Although IPF is the most common cause of pulmonary fibrosis, fibrosis primarily affecting the upper lobes should raise concern for an alternative diagnoses, such as:
  1. End-stage sarcoidosis..
  2. Chronic hypersensitivity pneumonitis.
  3. End-stage silicosis.

Pulmonary infection

Clinical classification of pneumonia

• S. pneumoniae is the most common cause of community-acquired pneumonia (CAP).
• Atypical pneumonia, including Mycoplasma, viral, and Chlamydia, typically infects young and otherwise healthy patients. Mycoplasma has a varied appearance and can produce consolidation, areas of ground glass attenuation, centrilobular nodules, and tree-in-bud nodules.
• Legionella most commonly occurs in elderly smokers.
• Infection by Klebsiella and other gram-negatives occurs in alcoholics and aspirators. Klebsiella classically leads to voluminous inflammatory exudates causing the bulging fissure sign.
• Hospital acquired pneumonia (HAP) Hospital acquired pneumonia (HAP) occurs in hospitalized patients and is due to aspiration of colonized secretions.
• the most important pathogens include MRSA and resistant gram-negatives including Pseudomonas.
• Health care associated pneumonia (HCAP)
  • Health care associated pneumonia is defined as pneumonia in a nursing home resident or in a patient with a>2 day hospitalization over the past 90 days.
  • Pathogens are similar to HAP. Ventilator associated pneumonia (VAP) Ventilator associated pneumonia is caused by infectious agents not present at the time mechanical ventilation was started.
  • Most infections are polymicrobial and primarily involve gram-negative rods such as Pseudomonas and Acinetobacter.
• Pneumonia in the immunocompromised patient : Any of the above pathogens, plus opportunistic infections including Pneumocystis, fungi such as Aspergillus, Nocardia, CMV, etc.

Radiographic patterns of infection

1. Lobar pneumonia.
2. Lobular pneumonia (bronchopneumonia).
3. Interstitial pneumonia.
4. Round pneumonia.

Complications of pneumonia

1. Pulmonary abscess.
2. Empyema.
3. Bronchopleural fistula (BPF).
4. Empyema necessitans.

Tuberculosis (TB)

• Initial exposure to TB can lead to two clinical outcomes:
  1. Contained disease (90%) results in calcified granulomas and/or calcified hilar lymph nodes.
  2. Primary tuberculosis results when the host cannot contain the organism.
• Reactivation (post-primary) TB is reactivation of a previously latent infection.
• Healed tuberculosis: is evident on radiography as apical scarring, usually with upper lobe volume loss and superior hilar retraction.
• Miliary tuberculosis: is a diffuse random distribution of tiny nodules seen in hematogenously disseminated TB.

Atypical mycobacteria

Atypical mycobacteria infection

"Hot-tub" lung

Endemic fungi

• Histoplasma capsulatum
• Coccidioides immitis and Blastomyces dermatitidis

Infections in the immunocompromised

• Pneumocystis jiroveci pneumonia
• Cryptococcus neoformans
• Aspergillus
  • Allergic bronchopulmonary aspergillosis (ABPA)
  • Saprophytic aspergillosis (aspergilloma)
  • Semi-invasive (chronic necrotizing) aspergillosis
  • Airway-invasive aspergillosis
  • Angioinvasive aspergillosis

Pulmonary edema and ICU Imaging

Pulmonary edema

The radiographic severity of pulmonary edema typically progresses through three stages:

1. Vascular redistribution
2. Interstitial edema
3. Alveolar edema

Vascular pedicle:

The vascular pedicle is the transverse width of the upper mediastinum. The right border of the vascular pedicle is the interface of the superior vena cava (SVC) and the right mainstem bronchus. The left border of the vascular pedicle is the lateral border of the takeoff of the subclavian from the aorta. The vascular pedicle width is normally 63 and >70 mm have been proposed as cutoffs) on sequential supine AP ICU-type chest radiographs generally correlates with increased pulmonary capillary wedge pressure (>18 mm Hg) and fluid overload.

Support devices

Endotracheal tube

The endotracheal tube tip should be approximately 4-6 cm above the carina with the neck in neutral alignment. However, in situations with low pulmonary compliance (e.g., ARDS), a tip position closer to the carina may reduce barotrauma.

Central venous catheters

The tip of a central venous catheter, including a PICC, should be in lower SVC or the cavoatrial junction. Azygos malposition is seen in approximately 1% of bedside-placed PICCs. Azygos malposition is associated with increased risk of venous perforation and catheter-associated thrombosis, and repositioning is recommended.

Pulmonary artery catheter

• The tip of a Swan–Ganz pulmonary artery catheter should be in either the main, right, or left pulmonary artery.

Lung cancer

Risk factors for lung cancer

• Tobacco smoking.
• Occupational and environmental exposures, including beryllium, radon, arsenic, etc., remain an important risk factor for lung cancer. Asbestos exposure increases the risk of lung cancer by a factor of five, synergistic with smoking.
• Pulmonary fibrosis.
• Pulmonary scarring.

Solitary benign pulmonary nodule

• Central, laminar, and diffuse calcification are almost always benign.
• Popcorn calcification, suggestive of a pulmonary hamartoma, is benign.
• Intra-lesional fat, suggestive of hamartoma or lipoid granuloma, is benign.
• Small <3 mm, any calcification, non-round shape, subpleural locatio9n and clustering are usually benign.

Nodule morphology suggesting malignancy

• Large size is the single most important risk factor for malignancy, regardless of morphology: 0.8 to 3 cm nodules have 18% risk of being lung cancer and masses >3 cm have a very high chance of being malignant.
• Irregular edge or spiculated margin is concerning.
• Round shape (as opposed to oblong) is suggestive of malignancy.
• A cavitary nodule or nodule containing small cystic spaces is suspicious for malignancy.

Follow-up of pulmonary nodule

• Follow-up is not recommended for a solitary pulmonary nodule if the nodule is small (4 and ≤6 mm
  • Low-risk: At least one follow-up at 12 months. If unchanged, no further follow-up.
  • High-risk: At least two follow-ups at 6m.
• Nodule >6 and ≤8 mm Low-risk: At least two follow-ups at 6–12 months and 18–24 months if no change.
• High-risk: At least three follow-ups at 3–6 months, 9–12, and 24 months if no change. Nodule >8 mm Regardless of risk, either PET, biopsy, or at least three follow-ups at 3, 9, and 24 months.

Histologic subtypes of lung cancer

• Adenocarcinoma
• Squamous cell carcinoma (SCC)
• Bronchioloalveolar carcinoma (BAC)
• Small cell carcinoma
• Large cell carcinoma
• Carcinoid tumor

Radiologic presentation of lung cancer

1. Solitary pulmonary nodule or lung mass. A nodule is defined as <3 cm and a mass >3 cm.
2. Segmental or lobar atelectasis
3. Consolidation
4. Hilar mass
5. Superior sulcus tumor: A superior sulcus tumor is a lung cancer occurring in the lung apex.
6. Lymphangitic carcinomatosis: Lymphangitic carcinomatosis represents diffuse spread of neoplasm through the pulmonary lymphatics, typically seen in late-stage disease. On imaging, carcinomatosis manifests as nodular interlobular septal thickening, which is usually asymmetric.
7. Pleural effusion
8. Pneumothorax

Staging of lung cancer

Treatment based on staging

• For early stages up to IIB and sometimes IIIA, surgery is usually performed. Neoadjuvant or adjuvant chemotherapy and radiotherapy can be used.
• Stage IIIB (N3 - contralateral or supraclavicular nodes; or T4/N2) is unresectable.
• Stage IV disease is generally not treated surgically unless there is a solitary adrenal or brain metastasis.
• T (tumor)
  1. T1: Tumor ≤3 cm surrounded by lung or visceral pleura. T1a: Tumor ≤2 cm; 5-year survival rate 77%; T1b: >2 and ≤3 cm; 5-year survival rate 71%.
  2. T2: Tumor >3 cm and ≤7 cm, or local invasion of the visceral pleura, or endobronchial lesions >2 cm from the carina. T2a: >3 and ≤5 cm; 5-year survival rate 58%; T2b: >5 and ≤7 cm; 5-year survival rate 49%.
  3. T3: Tumor >7 cm, or local invasion of chest wall, diaphragm, pleura, or superior sulcus tumor, or endobronchial lesion.
  4. T4: Separate tumor nodule in a different lobe in the ipsilateral lung, or tumor of any size with invasion of mediastinal structures including carina, heart, great vessels, or vertebral bodies. T4: 5-year survival rate 22%.
• M (metastasis)
  1. M0: No metastatic disease.
  2. M1a: Local thoracic metastatic disease. Separate tumor nodule in contralateral lung; 5-year survival rate 3%. Malignant pleural or pericardial effusion; 5-year survival rate 2%.
  3. M1b: Distant or extrathoracic metastatic disease. Median survival 6 months. 1-year survival rate 22%.

Pulmonary vascular disease

Pulmonary hypertension

Definition of pulmonary hypertension: Clinically, the term pulmonary hypertension is used to encompass both pulmonary arterial and pulmonary venous hypertension.

Overview of pulmonary hypertension classification: The classification in widest use in the radiology literature is the hemodynamic division of

1. precapillary and
2. postcapillary etiologies.

General imaging of pulmonary hypertension:

• A main pulmonary artery diameter ≥2.9 cm suggests the presence of pulmonary hypertension, although pulmonary hypertension may be present in a normal caliber pulmonary artery. A main pulmonary artery diameter larger than the aortic root diameter is also suggestive of pulmonary hypertension.

Primary pulmonary hypertension (PPH) – WHO group 1, precapillary:

• The pathologic hallmark of primary pulmonary hypertension (PPH) is the plexiform lesion in the wall of the muscular arteries, which is a focal disruption of the elastic lamina by an obstructing plexus of endothelial channels. There is a relative paucity of prostacyclins and nitric oxide expressed by endothelial cells.

Pulmonary hypertension due to left-to-right cardiac shunts – WHO group 1, precapillary:

• Congenital left-to-right cardiac shunts, such as ventricular septal defect (VSD), atrial septal defect (ASD), and partial anomalous pulmonary venous return, cause increased flow through the pulmonary arterial bed. This chronically increased flow may eventually lead to irreversible vasculopathy characterized by pulmonary hypertension and reversal of the congenital shunt, known as Eisenmenger syndrome.

Pulmonary veno-occlusive disease – WHO group 1, postcapillary:

PAH secondary to pulmonary veno-occlusive disease is caused by fibrotic obliteration of the pulmonary veins and venules. Pulmonary veno-occlusive disease may be idiopathic but is associated with pregnancy, drugs (especially bleomycin), and bone marrow transplant.

Pulmonary venous hypertension – WHO group 2, postcapillary:

• COPD, sleep apnea, and interstitial lung disease can all lead to pulmonary hypertension.
• Chronic hypoxic vasoconstriction is thought to invoke vascular remodeling leading to hypertrophy of pulmonary arterial vascular smooth muscle and intimal thickening.
• Chronic lung disease can further contribute to obliteration of pulmonary microvasculature through emphysema and the perivascular fibrotic changes of pulmonary fibrosis.

Chronic thromboembolic pulmonary hypertension (CTEPH) – WHO group 4, precapillary:

• Chronic occlusion of the pulmonary arterial bed can lead to pulmonary arterial hypertension, which is a complication affecting 1–5% of patients who develope acute pulmonary embolism (PE). Due to the high prevalence of PE, a PE-protocol CT is typically the first step in workup of newly diagnosed pulmonary hypertension.
• Characteristic imaging features are peripheral, eccentric filling defects (in contrast to acute emboli which tend to be central) in the pulmonary arterial tree. Fibrous strands are sometimes visible on cross-sectional imaging. Mosaic perfusion may be present.
• CTEPH may cause secondary corkscrew bronchial arteries that are tortuous and dilated.
• Treatment of CTEPH is surgical thromboendarterectomy (similar to carotid endarterectomy).

Fibrosing mediastinitis – WHO group 5, postcapillary:

• Progressive proliferation of fibrous tissue within the mediastinum may lead to encasement and compression of mediastinal structures.
• The most common causes of fibrosing mediastinitis are histoplasmosis and tuberculosis.

Pulmonary embolism (PE)

Clinical diagnosis

• Diagnosis of pulmonary embolism (PE) can be challenging because the presenting symptoms are both common and nonspecific, including dyspnea, tachycardia, and pleuritic chest pain.
• Most pulmonary emboli originate in the deep veins of the thighs and pelvis. The risk factors for deep venous thrombosis are widely prevalent in a hospital environment.
• D-dimer is sensitive for thromboembolic disease.

Imaging of pulmonary embolism

• CT pulmonary angiogram is the most common method to image for PE.
• Plain film evaluation of pulmonary embolism: The Fleischner sign describes widening of the pulmonary arteries due to clot.

Cardiac evaluation

• Pulmonary embolism may cause acute right heart strain.

Diffuse lung disease

Idiopathic interstitial pneumonias

• Idiopathic pulmonary fibrosis (IPF)
• Nonspecific interstitial pneumonitis (NSIP)
• Cryptogenic organizing pneumonia (COP)
• Respiratory bronchiolitis–interstitial lung disease (RB-ILD)
• Desquamative interstitial pneumonia (DIP)
• Lymphoid interstitial pneumonia (LIP)
• Acute interstitial pneumonia (AIP)

Antigen and exposure-related lung disease

• Hypersensitivity pneumonitis (HSP)
• Pneumoconioses: A pneumoconiosis is a lung disease secondary to inorganic dust inhalation. In contrast, hypersensitivity pneumonitis is caused by organic dust inhalation.

Eosinophilic lung disease

• Simple pulmonary eosinophilia (Löffler syndrome),
• Chronic eosinophilic pneumonia.

Pulmonary vasculitis

• Churg–Strauss.
• Microscopic polyangiitis.
• Wegener granulomatosis (WG).

Iatrogenic lung disease

• Drug toxicity.
• Radiation lung injury.

Idiopathic systemic diseases affecting the lungs

• Sarcoidosis:
  1. Stage 0: Normal radiograph.
  2. Stage 1: Hilar or mediastinal adenopathy only, without lung changes.
  3. Stage 2: Adenopathy with lung changes.
  4. Stage 3: Diffuse lung disease without adenopathy.
  5. Stage 4: End-stage fibrosis
• Pulmonary Langerhans cell histiocytosis (PLCH)

Miscellaneous diffuse pulmonary disease

• Pulmonary alveolar proteinosis (PAP).
• Lymphangioleiomyomatosis (LAM).

Mediastinum

Anatomy of the mediastinum

Anterior mediastinum:

• The anterior mediastinum is the space between the sternum and the pericardium inferiorly and ascending aorta and brachiocephalic vessels superiorly.
• The contents of the prevascular anterior mediastinum include:
  1. Thymus.
  2. Lymph nodes.
  3. Enlarged thyroid gland, if it extends inferiorly into the mediastinum.

Middle mediastinum

• The anterior border of the middle mediastinum is the anterior pericardium and the posterior borders are the posterior pericardium and posterior tracheal wall.
• The contents of the middle mediastinum include:
  1. Heart and
  2. pericardium.

Posterior mediastinum

• The anterior border of the posterior mediastinum is the posterior trachea and posterior pericardium. The posterior border is somewhat loosely defined as the anterior aspect of the vertebral bodies; however, paraspinal masses are generally included in the differential of a posterior mediastinal mass.
• The contents of the posterior mediastinum include:
  1. Esophagus.
  2. Descending thoracic aorta.
  3. Azygos and hemiazygos veins.
  4. Thoracic duct.
  5. Vagus nerves.
  6. Lymph nodes.

Lines, stripes, and interfaces

• The anterior junction line is formed by four layers of pleura (parietal and visceral pleura of each lung) at the anterior junction of the right and left lungs.
• The posterior junction line is also formed by four layers of pleura (parietal and visceral pleura of each lung), but at the posterior junction of the right and left lungs.
• The right and left paratracheal stripes are formed by two layers of pleura where the medial aspect of each lung abuts the lateral wall of the trachea and intervening mediastinal fat.
• The posterior tracheal stripe is the only interface seen on the lateral radiograph, representing the interface of the posterior wall of the trachea with the two pleural layers of the medial right lung.
• The right and left paraspinal lines are actually interfaces but appear as lines due to Mach effect and are formed by 2 layers of pleura abutting the posterior mediastinum.
• The azygoesophageal recess is an interface formed by the contact of the posteromedial right lower lobe and the retrocardiac mediastinum.

Aortopulmonary (AP) window

• The aortopulmonary (AP) window is a mediastinal space nestled underneath the aortic arch (which forms the superior, anterior, and posterior boundaries) and the top of the pulmonary artery. The medial border of the AP window is formed by the esophagus, trachea, and left mainstem bronchus.
• e AP window, including:
  1. Lymph nodes: Adenopathy is the most common cause of an AP window abnormality.
  2. Left phrenic nerve: Injury may cause paralysis of the left hemidiaphragm.
  3. Recurrent laryngeal nerve: The AP window should be carefully evaluated in new-onset hoarseness, especially if associated with diaphragmatic paralysis.
  4. Left vagus nerve.
  5. Ligamentum arteriosum. Left bronchial arteries

Retrosternal clear space

• The retrosternal clear space is a normal area of lucency posterior to the sternum seen on the lateral radiograph only. It correlates to the prevascular space on CT

Left superior intercostal vein (LSIV)

• The left superior intercostal vein (LSIV) is a normal vein that is not often seen on radiography. When visible, the LSIV produces the aortic nipple, appearing as a small round shadow to the left of the aortic knob on the frontal radiograph.

Radiographic localization of a mediastinal mass

Detection of an anterior mediastinal mass

• Deformation of the anterior junction line suggests an anterior mediastinal mass.

Detection of a middle mediastinal mass

• Distortion of the paratracheal stripes or convexity of the AP window suggests a middle mediastinal mass.

Detection of a posterior mediastinal mass

• Distortion of the azygoesophageal recess, distortion of the posterior junction line, or displacement of the paraspinal lines suggest paravertebral/posterior mediastinal disease.

Anterior mediastinal mass - prevascular (superior anterior mediastinum)

• An anterior mediastinal mass includes:
  1. Thymic epithelial neoplasm, such as thymoma.
  2. Germ cell tumor, including teratoma.
  3. Thyroid lesion, if there is extension of the mass above the thoracic inlet.
  4. Lymphoma.

Anterior mediastinal mass - precardiac (inferior anterior mediastinum)

1. Epicardial fat pad
2. Pericardial cyst
3. Morgagni hernia

Middle mediastinal mass

1. Lymphadenopathy.
2. Ascending aortic or aortic arch aneurysm.
3. Enlarged pulmonary artery (PA).
4. Foregut duplication cyst.

Posterior mediastinal mass

1. Neurogenic tumor:
2. Peripheral nerve tumors (more common in adults) include:
   1. Schwannoma (most common), neurofibroma, and malignant peripheral nerve sheath tumor.
3. Sympathetic ganglion tumors (more common in children/young adults) include:
   1. Ganglioneuroma (most common), a benign tumor of sympathetic ganglion cells.
   2. Neuroblastoma, a malignant tumor of ganglion cells seen in early childhood.
4. Ganglioneuroblastoma, intermediate in histology between ganglioneuroma and neuroblastoma, seen

Miscellaneous esophageal conditions

Esophageal anatomy

• The esophagus is a muscular tube that extends from the pharynx to the stomach.
• The adult esophagus measures approximately 25 to 30 cm in length.
• The esophagus is normally divided into three parts: cervical, thoracic, and abdominal.
• The cervical esophagus extends from the cricopharyngeus muscle to the thoracic inlet.
• The thoracic esophagus extends from the thoracic inlet to the diaphragmatic hiatus.
• The abdominal esophagus extends from the diaphragmatic hiatus to the gastroesophageal junction.
• The distal esophagus passes through the diaphragmatic hiatus at approximately T10.
• The three anatomic rings of the distal esophagus are the A (muscular), B (mucosal), and C (diaphragmatic impression) rings.

Esophageal rings and webs

• Esophageal web
• Schatzki ring

Esophagitis

• Reflux (peptic) esophagitis
• Barrett esophagus
• Infectious esophagitis
• Medication esophagitis
• Crohn esophagitis

Esophageal strictures

• Peptic stricture
• Barrett esophagus stricture
• Malignant stricture (due to esophageal carcinoma)
• Caustic stricture/nasogastric (NG) tube stricture
• Radiation stricture
• Extrinsic compression from mediastinal adenopathy

Benign esophageal masses

• Mesenchymal tumor
• Adenoma
• Inflammatory polyp
• Fibrovascular polyp
• Varices
• Foregut duplication cysts
• Esophageal foreign body

Malignant esophageal masses

• Esophageal carcinoma
• Metastasis
• Lymphoma
• Malignant GIST

Esophageal motility disorders

• Contraction waves
• Achalasia
• Diffuse esophageal spasm (corkscrew esophagus; shish kebab esophagus)

Esophageal diverticula

• Types of diverticula
  1. Pulsion diverticula
  2. Traction diverticula
• Zenker diverticulum
• Killian–Jamieson (KJ) diverticulum
• Pseudodiverticulosis

Miscellaneous esophageal disorders

Feline esophagus
Aberrant right subclavian artery
Scleroderma

Esophageal hernias

Hiatal hernia (HH)
Paraesophageal hernia

Stomach

Thickened gastric folds

• Helicobacter pylori gastritis
• Zollinger--Ellison (ZE)
• Eosinophilic gastritis
• Menetrier disease
• Crohn disease
• Other causes of thickened gastric folds
  1. Gastric varices
  2. Gastric lymphoma
  3. Submucosal carcinoma

Gastric polyps

• Hyperplastic polyp (inflammatory polyp)
• Adenomatous polyp
• Hamartomatous polyp

Benign gastric masses

• Lipoma (benign)
• Gastrointestinal stromal tumor (GIST)
• Ectopic pancreatic rest

Malignant gastric masses

• Gastric cancer
• GIST (malignant)
• Lymphoma
• Metastases: Commonest:
  • Breast
  • Lung
  • Melanoma

Gastric ulcers

• Benign gastric ulcer
• Gastric carcinoma

Complications of Roux-en-Y surgery

• Postoperative leak
• Gastrogastric fistula
• Small bowel obstruction (SBO)
• Internal hernia
• Stomal stenosis
• Marginal ulcers

Small bowel

Small bowel obstruction (SBO)

Radiographic evaluation of small bowel obstruction

• Radiographic findings of SBO include:
  1. Small bowel distention
  2. Multiple air--fluid levels
  3. Lack of gas in the colon
• CT imaging of small bowel obstruction
  1. Small bowel distention ≥3 cm with a transition point to collapsed bowel is highly specific for a small bowel obstruction
  2. CT can show the transition point
  3. The cause of obstruction
  4. Potential complications of obstruction such as ischemia or strangulation
  5. The small bowel feces sign
  6. Evaluate for signs of ischemia or impending ischemia
     • Engorged mesenteric vessels
     • Ascites surrounding the bowel
     • Wall thickening
     • Lack of bowel wall enhancement
     • Pneumatosis intestinalis

Closed loop obstruction

Obstruction due to adhesions

Obstruction due to external hernia

Obstruction due to internal hernia

1. Paraduodenal hernia
2. Foramen of Winslow hernia

Obstruction due to neoplasm

Obstruction due to intussusception

Obstruction due to Crohn disease

Obstruction due to gallstone

Enteritis

• Crohn disease
• Infectious enteritis
• Radiation enteritis
• Whipple disease
• Graft versus host disease (GVHD)
• Scleroderma
• Celiac disease (sprue, gluten-sensitive enteropathy)
• Complications of celiac disease include:
  1. Intussusception
  2. Pneumatosis intestinalis
  3. Splenic atrophy
  4. Venous thromboembolism
  5. Cavitating mesenteric lymph node syndrome (CMLNS)

Large bowel

Types

• Ischemic colitis
• Infectious colitis
• Pseudomembranous colitis
• Ulcerative colitis (UC)
• Typhlitis (neutropenic enterocolitis)

Polyposis syndromes affecting the bowel

• Familial adenomatous polyposis (FAP)
• Hereditary nonpolyposis colon cancer syndrome (HNPCC) = Lynch syndrome
• Peutz--Jeghers
• Cowden syndrome
• Cronkhite--Canada

Acute bowel

• Appendicitis
• Diverticulitis
• Epiploic appendagitis

Mesentery and peritoneum

Peritoneum: The peritoneum is a thin membrane consisting of a single layer of mesothelial cells that are supported by subserosal fat cells, lymphatic cells, and white blood cells.

Mesentery

1. Small bowel mesentery
2. Transverse mesocolon
3. Sigmoid mesentery

• greater and lesser omentum

"Misty" mesentery

• Mesenteric edema
• Mesenteric inflammation
• Intra-abdominal hemorrhage
• Neoplastic infiltration

Mesenteric masses

• Carcinoid
• Desmoid tumor
• Sclerosing mesenteritis
• Mesenteric metastases and lymphoma

Diffuse peritoneal disease

• Peritoneal carcinomatosis
• Pseudomyxoma peritonei

Genitourinary imaging

Retroperitoneum

Retroperitoneal disease

• Liposarcoma:
1. Liposarcomas are a diverse group of neoplasms that make up the most common primary retroperitoneal tumors. 10-15% of all liposarcomas arise from the retroperitoneum.
2. The most common type of liposarcoma is the well-differentiated group
• Retroperitoneal fibrosis:
Retroperitoneal fibrosis is a rare inflammatory disorder causing increased fibrotic deposition in the retroperitoneum, often leading to ureteral obstruction.

Adrenal glands

Anatomy

• Adrenal cortex:
The adrenal cortex synthesizes the steroid hormones aldosterone, glucocorticoids, and androgens, which are all biochemical derivatives of cholesterol.
• Adrenal medulla:
The adrenal medulla is the central portion of the adrenal gland and produces the catecholamines norepinephrine and epinephrine, which are derived from tyrosine.

Biochemical approach to adrenal lesions

Adrenal hyperfunction

1. Cushing syndrome:
is excess cortisol production from non-pituitary disease, such as idiopathic adrenal hyperplasia, adrenal adenoma, or ectopic/paraneoplastic ACTH (e.g., from small cell lung cancer).
2. Cushing disease
is excess cortisol production driven by excessive pituitary ACTH.
3. Conn syndrome
is excess aldosterone production, most commonly from an adrenal adenoma, which causes hypertension and hypokalemia.
4. Adrenal cortical carcinoma
is a very rare adrenal malignancy that arises from the cortex and typically causes a disordered increase in all cortical adrenal hormones and precursors.
5. Pheochromocytoma
is a usually benign tumor of the adrenal medulla that causes an increase in catecholamines.

Adrenal hypofunction

• Significant destruction of the adrenals is required to produce adrenal insufficiency.

Imaging of adrenal adenoma and the indeterminate adrenal mass

• Adrenal adenoma is a benign tumor of the adrenal cortex.
• An adrenal nodule attenuating ≤10 Hounsfield units (HU) can be reliably diagnosed as an adenoma with no further imaging or follow-up needed.

MRI adrenal imaging: Chemical shift imaging = in- and out-of-phase imaging

• Adenomas contain intracytoplasmic lipid due to steroid production. MRI is able to detect even a small amount of intracytoplasmic lipid that may be undetectable on CT by taking advantage of the fact that protons resonate at different frequencies in fat and in water.
• Chemical shift imaging consists of images obtained both in-phase and out-of-phase. When fat and water are contained within the same voxel, out-of-phase images show fat drop-out of signal because fat protons are more shielded and resonate at a slower frequency. Chemical shift imaging is based on T1 images.
• Adenomas suppress on out-of-phase images, while metastases generally do not.
• A short list of malignancies do contain intracytoplasmic lipid and thus would also lose signal on out-of-phase images:
  1. Well-differentiated adrenocortical carcinoma (very rare).
  2. Clear cell renal cell carcinomas metastatic to the adrenal gland.
  3. Hepatocellular carcinoma metastatic to the adrenal gland.
  4. Liposarcoma (typically a predominantly fatty mass that is rarely confused with adrenal adenoma).

CT Imaging: Adrenal washout CT

• Adrenal adenomas demonstrate more rapid contrast washout than metastases do.

Myelolipoma

• An adrenal myelolipoma is a benign neoplasm consisting of myeloid cells (i.e., erythrocyte precursors -- not "myo" as in muscle) and fat cells.

Adrenal cyst

• Adrenal cysts are uncommon but have imaging characteristics typical of cysts elsewhere (thin, smooth, nonenhancing wall, and water-attenuation internal contents)

Malignant (or potentially malignant) adrenal masses

• Pheochromocytoma: Potentially malignant:
Pheochromocytoma is a neoplasm of chromaffin cells, usually arising from the adrenal medulla. Pheochromocytoma may cause hypertension and episodic headaches/diaphoresis.
• The "rule of 10's"
is a general rule characterizing the features of pheochromocytomas:
1. 10% are extra-adrenal.
2. 10% are bilateral.
3. 10% are malignant.
4. 10% are familial or syndromic.
• Pheochromocytoma
is associated with several syndromes:
1. Multiple endocrine neoplasia (MEN) 2A and 2B: Typically bilateral intra-adrenal pheochromocytomas.
2. von Hippel-Lindau.
3. Neurofibromatosis type 1.
4. Carney's triad (gastric leiomyosarcoma, pulmonary chondroma, and extra-adrenal pheochromocytoma).
• Adrenal cortical carcinoma:
Adrenal cortical carcinoma is a very rare malignancy
• Metastasis:
Autopsy studies show adrenal metastases are present in >25% of patients with a known primary. Lung cancer and melanoma are the most common adrenal metastases.
• Lymphoma:
Primary adrenal lymphoma is rare.

Diffuse adrenal disorders

• Adrenal hyperplasia
is caused by prolonged stress response or ectopic ACTH secretion.
• Adrenal hemorrhage:
can be spontaneous or due to anticoagulation. When secondary to anticoagulation, the hemorrhage typically occurs within the first few weeks of beginning anticoagulation. Hemorrhage involves the right adrenal gland more commonly than the left.
• Adrenal calcification:
rarely causes adrenal hypofunction. Adrenal calcification can be due to Wegener granulomatosis, tuberculosis, histoplasmosis, or old hemorrhage.

Kidneys

Diagnostic approach to a renal mass

• A renal mass protocol CT consists of at least three phases of data acquisition, with each phase providing important information to aid in the diagnosis of a renal mass.
  1. Unenhanced phase:
  Necessary as a baseline to quantify enhancement.
  2. Nephrographic phase (100 second delay):
  The nephrographic phase is the critical phase for evaluating for enhancement, comparing to the unenhanced images.
  3. Pyelographic phase (15 minute delay; also called the excretory phase):
  The pyelographic phase is helpful for problem solving and to diagnose potential mimics of cystic renal masses.

Evaluating enhancement (CT and MRI)

• The presence of enhancement is the most important characteristic to distinguish between a benign and malignant non-fat-containing renal mass (a lesion containing intralesional fat is almost always a benign angiomyolipoma, even if it enhances).
• On CT:
1. < 10 HU: No enhancement.
2. 10-19 HU equivocal enhancement.
3. >= 20 HU enhancement.
• On MRI:
1. < 15% no enhancement.
2. 15-15% equivocal enhancement.
3. >=20% enhancement.

Solid renal masses

• Renal cell carcinoma (RCC):
1. Clear cell
2. Papillary RCC
3. Chromophobe
4. Collecting duct carcinoma
5. Medullary carcinoma
• Staging of renal cell carcinoma
is based on the Robson system, which characterizes fascial extension and vascular/lymph node involvement. Stages I-III are usually resectable, although the surgical approach may need to be altered for venous invasion (stages IIIA and IIIC).
1. Stage I:
Tumor confined to within the renal capsule.
2. Stage II:
Tumor extends out of the renal capsule but remains confined within Gerota's fascia.
3. Stage III:
Vascular and/or lymph node involvement.
• IIIA:
Renal vein involvement or IVC involvement.
• IIIB:
Lymph node involvement.
• IIIC:
Venous and lymph node involvement.
4. Stage IVA:
Tumor growth through Gerota's fascia;
5. Stage IVB:
Distant metastasis.
• Angiomyolipoma (AML):
is the most common benign renal neoplasm
• Oncocytoma:
Oncocytoma is the most commonly resected benign renal mass and has overlapping imaging findings with renal cell carcinoma.
• Renal lymphoma:
1. Primary renal lymphoma is rare
2. Renal involvement of lymphoma has several patterns of disease: Multiple lymphomatous masses (most common pattern; seen in 50% of cases of renal lymphoma). Solitary renal mass. Diffuse lymphomatous infiltration, causing nephromegaly. Direct extension of retroperitoneal disease.
• Non-neoplastic solid renal masses:
When evaluating a potential renal mass, it's important to always consider that an apparent solid renal mass may represent a non-neoplastic lesion.
1. Renal arteriovenous malformation (AVM)
2. Renal pseudotumors

Syndromes with renal masses (all have increased risk of RCC)

• von Hippel-Lindau (VHL):
von Hippel-Lindau (VHL) is an autosomal dominant multiorgan syndrome caused by a mutation in the VHL tumor suppressor gene on chromosome 3, which leads to cysts and neoplasms in multiple organs.
• Birt-Hogg-Dube:
Tuberous sclerosis is an autosomal dominant neurocutaneous disease caused by a tumor suppressor gene mutation. It manifests clinically with seizures, developmental delay, and (mostly) benign tumors in multiple organ systems.

Approach to a cystic renal mass

• Neoplastic differential of a cystic renal mass
1. Cystic renal cell carcinoma.
Although renal cell carcinoma most commonly presents as a solid renal mass, it can also manifest as a cystic renal mass.
2. Multilocular cystic nephroma
is a benign cystic neoplasm with enhancing septa that occurs in a bimodal age distribution in baby boys and middle-aged women.
3. Mixed epithelial and stromal tumor (MEST)
is a benign neoplasm composed of epithelial and mesenchymal elements, typically found in middle-aged women. MEST may appear as either a solid or cystic mass.

Non-neoplastic differential of a cystic renal mass

• Renal abscess
is a contained purulent collection within the kidney.
• Hemorrhagic renal cyst,
which will not have any enhancing component.

Role of MRI in evaluation of a complex cystic renal mass

• MRI has a limited role in the evaluation of a cystic renal mass. The key advantage of MRI is more accurate enhancement characterization, as MRI does not suffer from the CT phenomenon of pseudoenhancement due to beam hardening from adjacent, densely enhancing renal parenchyma.

Renal cysts and cystic renal masses

• Simple renal cyst:
are extremely common, found in approximately 50% of patients over age 50. A simple renal cyst is an incidental lesion that requires no follow-up, even when large.
• Renal sinus cyst:
Cysts in the renal sinus may be classified as parapelvic and peripelvic cysts. A parapelvic cyst is a renal cortical cyst that herniates into the renal sinus. These cysts are usually large but solitary. Peripelvic cysts, in contrast, are lymphatic in origin and usually small and multiple.
• Hyperdense cyst:
A homogeneous renal cyst with an attenuation of >70 Hounsfield units on noncontrast imaging represents a benign hyperdense cyst, likely secondary to prior hemorrhage.
• The Bosniak classification risk-stratifies cystic renal masses,
with increasing risk for cystic renal cell carcinoma with increasing Bosniak category. Classification is based on morphology, not size (except for hyperdense cysts in categories II and IIF).
• Category I and II:
No risk of malignancy. No follow-up necessary.
• Category I
Water-attenuation cyst, with a hairline wall and no areas of enhancement.
• Category II
Water-attenuation cyst containing a few (3 or fewer) hairline septa. May contain fine septal calcification. No enhancement.
• Category IIF:
Small risk of malignancy. Imaging follow-up is needed.
• Category IIF
Multiple septa, with minimal smooth thickening (3 mm or less). May have thick and nodular mural calcification.
• Category III and IV:
Surgical lesions, concerning for cystic renal cell carcinoma.
• Category III
Thickened, irregular walls or septa, with measurable enhancement.
• Category IV
Distinguishing feature is enhancing nodular component

Multicystic renal disease and risk for renal neoplasm

• Autosomal dominant polycystic kidney disease (ADPKD):
Autosomal dominant polycystic kidney disease (ADPKD) is responsible for 10% of patients on long-term dialysis. Patients typically present in their third to fourth decades, initially presenting with upper abdominal pain and a clinical course of progressive renal failure. The kidneys may become so enlarged as to be palpable.
• Acquired cystic kidney disease (due to end-stage kidney disease):
Dialysis-associated cystic renal disease does have an increased risk of renal cell carcinoma (~2-3% prevalence, compared to 1/10,000 prevalence in the general population).

Renal infection and inflammation

• Pyelonephritis:
Pyelonephritis is infection of renal parenchyma and is the most common bacterial infection of the kidney. The bacteria usually are ascending from the bladder. A striated nephrogram describes linear lucencies extending from the renal cortex to the medulla on a contrast-enhanced study. The differential diagnosis for a striated nephrogram is similar to that of a wedge-shaped perfusion defect and includes:
1. Pyelonephritis.
2. Renal infarct.
3. Renal vein thrombosis or vasculitis.
4. Renal contusion (typically focal).
5. Acute urinary obstruction.
6. Renal tumor (especially lymphoma if infiltrative).
7. Radiation nephritis.
• Pyonephrosis:
is the infection of an obstructed collecting system and is colloquially referred to as "pus under pressure." Treatment is emergent percutaneous nephrostomy.
• Renal abscess:
is a localized purulent collection within the kidney that most commonly results from coalescence of small microabscesses in the setting of acute bacterial pyelonephritis. An abscess may simulate a cystic renal mass.
• Emphysematous pyelonephritis:
is a severe renal infection characterized by gas replacing renal parenchyma, caused both by gas-forming organisms and renal infarction.
• Xanthogranulomatous pyelonephritis:
is a chronic renal infection due to obstructing calculi, leading to replacement of renal parenchyma with fibrofatty inflammatory tissue.
• Renal tuberculosis:
Mycobacterium tuberculosis infection of the renal parenchyma results from hematogenous dissemination. Active pulmonary TB is present in approximately 10%. Although initial renal TB infection typically involves both kidneys, chronic changes tend to be unilateral.
• Nephrolithiasis and ureterolithiasis:
Nephro/ureterolithiasis is a common problem that presents with renal colic. Hematuria is usually present, but may be absent if the stone is completely obstructing.
• Papillary necrosis:
is necrosis and sloughing of renal papillary tissue, which clinically can cause gross hematuria and may lead to chronic renal insufficiency. There are numerous causes of papillary necrosis, most commonly NSAIDs, sickle cell anemia, diabetes, and renal vein thrombosis. The commonly used POSTCARD mnemonic may be helpful to remember all causes: Pyelonephritis. Obstruction. Sickle cell disease. Tuberculosis. Cirrhosis. Analgesics (NSAIDS). Renal vein thrombosis. Diabetes mellitus.

Renal imaging patterns

• Delayed (prolonged) nephrogram:
A unilateral prolonged nephrogram can be due to acute ureteral obstruction, renal vein thrombosis, and renal artery stenosis. Bilateral prolonged nephrograms can be seen in bilateral obstruction, contrast nephropathy, systemic hypotension, and myeloma kidney.
• Medullary nephrocalcinosis:
represents calcification of the renal medullary pyramids, usually with preserved renal function. Medullary nephrocalcinosis can be caused by:
1. Hypercalcemic state (e.g., hyperparathyroidism, sarcoidosis, etc).
2. Medullary sponge kidney (cystic dilation of distal collecting ducts; may be unilateral or segmental).
3. Distal (type 1) renal tubular acidosis (RTA).
4. Furosemide therapy in a child.
• Cortical nephrocalcinosis:
Causes of cortical nephrocalcinosis include:
1. Acute cortical necrosis.
2. Chronic glomerulonephritis.
3. Chronic transplant rejection.
4. Hyperoxaluria.
5. Alport syndrome (hereditary nephropathy and deafness).
• Cortical necrosis:
Cortical necrosis is a rare form of renal injury from acute ischemic necrosis of the renal cortex. Cortical necrosis may lead to cortical nephrocalcinosis. Chronic renal failure develops in up to 50% of patients.
• Extracalyceal contrast medium:
Contrast shouldn't normally be seen beyond the calyces on excretory urogram.
1. Papillary necrosis,
2. tubular ectasia, and
3. calyceal diverticulum may cause this appearance.

Renal trauma

The OIS scale from the AAST is the most commonly used system for classifying renal trauma. It is a surgical classification but correlates well with the CT findings.

• Grade I injury
is by far the most common type of renal injury (95%) and describes a renal contusion or subcapsular hematoma. Treatment is conservative.
• Grade II injury
is a superficial laceration (<1 cm), without urinary extravasation. Treatment is typically conservative. A potential pitfall of a
• grade III injury
is that a clot at the collecting system may prevent urinary extravasation initially, but urinary extravasation may occur later as the clot is lysed by urinary urokinase.
• Grade IV
is a deep laceration that extends into the collecting system (causing urinary extravasation), or injury to the renal artery or vein with contained hemorrhage. Urinary extravasation is typically treated with surgical repair to prevent later development of urinoma or abscess formation. Vascular grade IV injury can be treated endovascularly.
• Grade V
is a shattered kidney, or avulsion of the renal hilum. Treatment is variable but typically surgical.
• Page kidney
(named after the doctor who performed experiments wrapping animal kidneys with cellophane) is a rare cause of secondary hypertension due to prior trauma.

Ureter

Overview of ureteral imaging

• CT urography (CTU) indications and protocol:
The goal of CT urography (CTU) is to evaluate the kidneys, ureters, and bladder. The key to successful imaging is to maximally distend and opacify the ureters and bladder. One of the most common indications for CTU is for the evaluation of microscopic or macroscopic hematuria. In adults ≥40 years of age, CTU is performed as a three-phase exam: Unenhanced CT of the abdomen and pelvis. Nephrographic phase through the kidneys (100 seconds after IV contrast administration). Excretory phase of the abdomen and pelvis (15 minutes after IV contrast). A split-bolus, dual-phase exam decreases radiation exposure in patients under age 40: Unenhanced CT of the abdomen and pelvis. Combined nephrographic/excretory phase (8 minutes delay after first IV contrast bolus and 100 seconds after the second bolus).

Malignant ureteral disease

• Transitional cell carcinoma (TCC):
Although upper-tract malignancy is rare, transitional cell carcinoma is the most common ureteral neoplasm. The typical imaging appearance is a single filling defect on CT urography; however, multiple filling defects may be seen in 40%. Less commonly, there may be focal thickening of the ureteral wall. Given the propensity of transitional cell carcinoma for multifocality, the bladder should be evaluated for a synchronous mass.

Benign ureteral masses

• Fibroepithelial polyp
• Urothelial papilloma
• Inverted papilloma

Inflammatory and infectious ureteral disease

• Ureteritis cystica
is a benign response to chronic urinary tract inflammation, such as chronic infection or stone disease. Several small subepithelial cysts are found unilaterally in the proximal third of the ureter and renal pelvis. Ureteritis cystica does not have any malignant potential.
• Leukoplakia (squamous metaplasia)
also known as squamous metaplasia, is a rare urothelial inflammatory condition named for the characteristic white patch that is produced. Leukoplakia is not thought to be premalignant when the renal collecting system is involved, although there is an association between squamous cell carcinoma and bladder leukoplakia.
• Malacoplakia
is an inflammatory condition associated with chronic urinary tract infection (usually Escherichia coli) that is typically seen in middle-aged women. It is not premalignant.
• Ureteral tuberculosis
Multifocal ureteral stenoses are suggestive of ureteral tuberculosis, even more so if there is also evidence of renal tuberculosis (parenchymal calcification and scarring) and/or bladder tuberculosis (small capacity bladder with a thickened wall).

Differential diagnosis of a ureteral filling defect

• The primary concern of a ureteral filling defect on CT urography is ureteral malignancy.
  1. Ureteral malignancy, of which transitional cell carcinoma is by far the most common.
  2. Ureteral calculus, which is almost always visible on pre-contrast images.
  3. Blood clot.
  4. Malacoplakia (multiple flat defects).
  5. Leukoplakia.
  6. Infectious debris (e.g., a mycetoma).
  7. Sloughed renal papilla.
  8. Benign ureteral mass (e.g., fibroepithelial polyp).

Structural ureteral lesions

• Ureteropelvic junction obstruction (UPJ obstruction)
Obstruction of the ureteropelvic junction (UPJ) can be either primary or secondary to infection, stones, or prior surgery. Primary UPJ obstruction may be due to a congenital aperistaltic segment of ureter, high insertion of the ureter on the renal pelvis, or crossing vessels causing extrinsic compression. The key imaging finding is a dilated renal pelvis with a normal caliber ureter.

Bladder

• Bladder stones.
• Bladder transitional cell carcinoma (TCC):
is by far the most common bladder cancer.
• Bladder adenocarcinoma:
is rare but is associated with a urachal remnant.

Bladder trauma

• CT cystography
is the standard test to evaluate for suspected bladder rupture.
• Extraperitoneal bladder rupture:
is defined as rupture of the bladder outside of the peritoneal space. Extraperitoneal bladder rupture is at least twice as common as intraperitoneal rupture.
• Intraperitoneal bladder rupture:
occurs with disruption of the bladder dome and peritoneum, causing resultant extravasation of urine into the peritoneal space.

Urethra

Male urethral anatomy

• Prostatic urethra (posterior urethra):
courses within the prostate and is lined with transitional epithelium.
• Membranous urethra (posterior urethra):
is the shortest, least mobile urethral segment.
• Bulbous urethra (anterior urethra):
is the site of drainage of Cowper's glands.
• Penile urethra (anterior urethra):
is the longest urethral segment. It is lined with squamous epithelium.

Imaging of the male urethra

• Retrograde urethrogram (RUG):
provides excellent evaluation of the anterior urethra and may be performed to evaluate for suspected urethral injury, stricture, or fistula.
• Voiding cystourethrogram (VCUG):
best evaluates the posterior urethra and is typically performed for evaluation of bladder and voiding function.
• Urethral stricture:
secondary to sexually transmitted disease (most commonly chronic urethritis from Neisseria gonorrhoea) occur most commonly in the bulbous urethra. A complication of chronic urethral infection is a periurethral abscess, which may result in a urethroperineal fistula. Post-traumatic saddle injury strictures also tend to occur in the bulbous urethra.
• Urethral trauma:
In the setting of trauma, if there is blood at the meatus, painful urination, or inability to void, a RUG should be performed emergently. If the RUG shows evidence of urethral injury, a suprapubic catheter is typically placed.

Female urethra

• Anatomy of the female urethra:
is much shorter than the male urethra. Unlike the male urethra, the female urethra is not divided into discrete segments.
• Urethral diverticulum:
Urethral diverticulum presents clinically with postvoid dribbling, urethral pain, and dyspareunia. Often, however, the symptoms may be vague and nonspecific.

MRI of the prostate

• From an imaging standpoint, there are two components to the prostate that can be resolved on MRI: The peripheral zone and the central gland. The central gland refers to both the central zone and the transition zone, as they cannot be distinguished on MRI.
• Prostate cancer:
MRI is able to clearly delineate the prostatic zonal anatomy (central gland versus peripheral zone) with T2-weighted sequences. Imaging is enhanced with an endorectal coil. The typical MRI appearance of prostate cancer is a T2 hypointense region within the T2 hyperintense peripheral zone.

T-staging

1. T1:
Tumor apparent by biopsy only.
2. T2:
Tumor confined within the prostate.
• T2a: <50% of one lobe;
• T2b: >50% of one lobe;
• T2c: Tumor involves both lobes.
3. T3:
Tumor extends through the prostate capsule. May involve seminal vesicles.
4. T4:
Tumor invades adjacent structures other than seminal vesicles.

N-staging

• Any regional lymph node metastasis is N1; however, extra-pelvic nodes are M1a.

M-staging

1. M0:
No metastases.
2. M1a:
Nonregional lymph nodes;
3. M1b:
Bone metastasis;
4. M1c:
Other metastasis.

MRI of the uterus and adnexa

Uterine anatomy

• T2-weighted MRI can distinguish the three layers of the uterus.
  1. Endometrial stripe:
  Hyperintense on T2.
  2. Junctional zone (first zone of myometrium):
  T2 hypointense. The hypointense T2 signal is due to the extremely compact smooth muscle. The junctional zone should measure ≤12 mm: Thickening of the junctional zone is seen in adenomyosis.
  3. Outer myometrium:
  Relatively T2 hypointense, although less so than junctional zone.

Benign uterine disease

• Adenomyosis
represents ectopic endometrial glands within the myometrium. In contrast to endometriosis, the ectopic endometrial tissue seen in adenomyosis is nonfunctioning.
• Leiomyoma (fibroid):
A leiomyoma, commonly known as a fibroid, is an extremely common benign tumor of smooth muscle, which affects up to 40% of reproductive-age women.

Malignant uterine disease

• Endometrial carcinoma
is the most common female gynecologic malignancy and is thought to be caused by prolonged estrogen exposure. Specific risk factors include nulliparity, hormone replacement, and Tamoxifen therapy.

The FIGO (International Federation of Gynecology and Obstetrics) staging of endometrial carcinoma

was revised in 2010.

1. Stage I:
Tumor confined to the uterus.
• IA: <50% myometrial invasion;
• IB: >50% myometrial invasion.
2. Stage II:
Spread to the cervical stroma, but tumor still contained within the uterus. Involvement of the endocervical glands only is stage I.
3. Stage III:
Spread to adnexa or uterine serosa (IIIA), vagina (IIIB), pelvic lymph nodes (IIIC1), or para-aortic lymph nodes (IIIC2). Prognosis is worse with para-aortic nodes, even in the absence of pelvic adenopathy.
4. Stage IVA:
Spread to bladder or bowel mucosa.
5. Stage IVB:
Distant metastases or inguinal lymph node spread.

MRI of the cervix

Normal cervical T2 zonal anatomy

1. Endocervical canal:
T2 hyperintense due to mucin, analogous to uterine endometrium.
2. Cervical mucosa:
Intermediate T2 signal intensity.
3. Inner cervical stroma:
Very hypointense on T2, analogous to the uterine junctional zone. Unlike the uterine junctional zone, however, the decreased T2 signal is due to compact fibrous tissue, not smooth muscle. The superior aspect of the inner cervical stroma is continuous with junctional zone of the uterus.

• Cervical carcinoma:
is the third most common gynecologic malignancy, with a steep decline in prevalence over the past 50 years due to screening with Pap smears.

The FIGO (International Federation of Gynecology and Obstetrics) staging of cervical cancer

was revised in 2010. The new staging takes into account lymph node involvement.

1. Stage I:
Confined to cervix or uterus.
• IA: Microscopic lesion.
• IB: Clinically visible lesion.
2. Stage IIA:
Spread to upper 2/3 vagina, without parametrial invasion. Typically treated surgically.
3. Stage IIB:
Parametrial invasion. Typically treated non-surgically (e.g., brachytherapy).
4. Stage IIIA:
Spread to lower vagina. Stage IIIB: Pelvic sidewall extension, hydronephrosis, or pelvic nodal involvement.
5. Stage IVA:
Spread to bladder or rectum;
6. Stage IVB:
Distant metastasis.

Congenital uterine anomalies

• Septate uterus:
is caused by incomplete resorption of the septum of fused Müllerian ducts. A septate uterus has a single external fundus but a fibrous or muscular septation dividing two endometrial canals. Infertility is more common in women with septate uterus compared to bicornuate uterus. Metroplasty (resection of the septum) can be performed hysteroscopically if the septum is fibrous, or via an open approach if the septum is muscular.
• Bicornuate uterus:
Bicornuate uterus is due to incomplete fusion of the Müllerian ducts. A bicornuate uterus describes a partially split uterus with two separate uterine fundi. In contrast to a septate uterus, the fundus of a bicornuate uterus pinches inwards >15 mm. If treated, metroplasty must be performed transabdominally, which is a more invasive procedure compared to hysteroscopic metroplasty.

MRI of the adnexa

• Endometriosis
represents ectopic foci of endometrial tissue that are hormonally responsive and therefore may be composed of blood products of varying ages.
• Mature cystic teratoma:
Also known as a dermoid cyst, mature cystic teratoma is the most common benign ovarian neoplasm in young women. It is composed of differentiated tissue from at least two embryonic cell layers. A mature cystic teratoma is typically a unilocular cystic structure filled with sebaceous material, hair follicles, and other tissues. Less commonly, a mature teratoma may appear as a heterogeneous mass or may be a solid fat-containing mass.
• Ovarian cancer:
Ovarian cancer is the second most common female pelvic malignancy but is one of the most lethal malignancies as 65% of patients present with advanced disease.

Neuroimaging

Cerebrospinal fluid (CSF)

The ventricular system consists of two lateral ventricles and midline third and fourth ventricles.

The foramen of Monro connects the lateral ventricles with the third ventricle.

The cerebral aqueduct (of Sylvius) connects the third ventricle with the fourth ventricle.

The fourth ventricle continues inferiorly as the central canal of the spinal cord. The fourth ventricle also drains into the subarachnoid space and basal cisterns via three foramina:

Paired foramina of Luschka (Luschka is lateral).

Single foramen of Magendie (Magendie is medial).

CSF dynamics

Cerebrospinal fluid is produced by the choroid plexus, which is located in specific locations throughout the ventricular system: Body and temporal horn of each lateral ventricle. Roof of third ventricle. Roof of fourth ventricle. There is NO choroid plexus in the cerebral aqueduct or occipital or frontal horns of the lateral ventricles.

CSF is absorbed primarily by the arachnoid granulations (leptomeningeal evaginations extending into the dural venous sinuses) and to a lesser extent by the lymphatic system and cerebral veins.

Cerebral edema

Edema within the brain can be caused by cell death, altered capillary permeability, or hemodynamic forces.

Cytotoxic edema: Cytotoxic edema is caused by cell death, most commonly due to infarct. Water ions trapped inside swollen cells feature reduced diffusivity.

Vasogenic edema: Vasogenic edema is caused most commonly by neoplasm, infection, or infarct.

Interstitial edema: Interstitial edema presents on imaging as periventricular fluid, often called “transependymal flow of CSF,” even though it is unlikely that the CSF actually flows across the ependymal cells lining the ventricles.

Herniation

Herniation may be due to a mass lesion (such as a neoplasm or hematoma) or may be due to edema secondary to a large stroke. Because the volume of the posterior fossa is especially limited, cerebellar infarcts are prone to herniation.

Subfalcine herniation: Subfalcine herniation is seen when the cingulate gyrus slides underneath the falx.

Subfalcine herniation may rarely cause compression of the anterior cerebral artery (ACA) against the falx, resulting in infarction.

Contralateral hydrocephalus may result from foramen of Monro obstruction, resulting in ventricular entrapment.

 

Transtentorial (uncal) herniation: Downward transtentorial herniation results in inferomedial displacement of the medial temporal lobe (uncus) through the tentorial notch, causing compression on the brainstem and adjacent structures.

Upward transtentorial herniation is superior transtentorial herniation of the cerebellar vermis due to posterior fossa mass effect. The main complication of upward transtentorial herniation is obstructive hydrocephalus from aqueductal compression.

Cerebellar tonsillar herniation: Downward displacement of the cerebellar tonsils through foramen magnum causes compression of the medulla.

Compression of medullary respiratory centers is often fatal.

 

Hydrocephalus

Communicating hydrocephalus is ventricular enlargement without an obstructing lesion.

Causes:

Subarachnoid hemorrhage

Normal pressure hydrocephalus

Noncommunicating hydrocephalus is hydrocephalus due to an obstructing lesion, such as a third ventricular colloid cyst or a posterior fossa mass obstructing the fourth ventricle.

MRI in neuroradiology

• Conventional spin-echo T1: Most brain lesions are hypointense on T1-weighted images.
• Causes of T1 shortening (hyperintensity) include: Most commonly: Gadolinium, fat, and proteinaceous substance. Some paramagnetic stages of blood (both intra- and extracellular methemoglobin). Melanin. Mineralization (copper, iron, manganese). Slowly-flowing blood. Calcium (rarely; when dispersed, not in bone). It is much more common for calcium to be hypointense.
• Conventional spin-echo T2: Most brain lesions are hyperintense on T2-weighted images.
• Causes of hypointensity on T2-weighted images include: Most paramagnetic stages of blood (except hyperacute blood and extracellular methemoglobin). Calcification. Fibrous lesion. Highly cellular tumors with a high nucleus:cytoplasm ratio producing low lesional water content (for instance, lymphoma and medulloblastoma). Vascular flow-void. Mucin. Desiccated mucin, as seen in desiccated sinus secretions, is hypointense on T2-weighted images. Conversely, mucinous lesions in the pelvis tend to be hydrated and thus hyperintense.
• Fluid attenuation inversion recovery (FLAIR): A normal FLAIR image may appear similar to a T1-weighted image since the CSF is dark on both. However, the signal intensities of the gray and white matter are different. T1: Normal white matter is brighter than gray matter because the fatty myelinated white matter has a shorter T1 time. FLAIR: White matter is darker than gray matter.
• Conventional spin-echo proton density (PD): Proton density (PD) images are not used in many neuroradiology MRI protocols.
• Diffusion weighted images and apparent diffusion coefficient (DWI and ADC): Diffusion weighted images and apparent diffusion coefficient (DWI and ADC). Signal is lost with increasing Brownian motion. Free water (CSF) experiences the most signal attenuation, while many pathologic processes (primarily ischemia) cause reduced diffusivity and less signal loss.
• Although diffusion MRI is most commonly used to evaluate for infarct, the differential diagnosis for reduced diffusion includes: Acute stroke. Bacterial abscess. Cellular tumors, such as lymphoma and medulloblastoma. Epidermoid cyst. Herpes encephalitis. Creutzfeldt–Jakob disease.
• Gradient recall echo (GRE): Hemosiderin and calcium produce inhomogeneities in the magnetic field, which creates blooming artifacts on GRE and makes even small lesions conspicuous.
• The differential diagnosis of multiple dark spots on GRE includes: Hypertensive microbleeds (dark spots are primarily in the basal ganglia, thalami, cerebellum, and pons). Cerebral amyloid angiopathy (dark spots are in the subcortical white matter, most commonly the parietal and occipital lobes). Familial cerebral cavernous malformations (an inherited form of multiple cavernous malformations). Axonal shear injury. Multiple hemorrhagic metastases.
• Magnetic resonance spectroscopy: MR spectroscopy describes the chemical composition of a brain region.
• Perfusion: Perfusion MR is an advanced technique where the brain is imaged repeatedly as a bolus of gadolinium contrast is injected.

Brain tumors

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