Although many disease processes and their imaging manifestations are quite similar between males and females, there are many instances when sex-specific considerations are necessary. Before image acquisition, pregnancy and lactation status should be ascertained to decide on the most appropriate imaging modality and use of intravenous contrast. Fetal developmental stage, pregnancy, and lactation status also need to be accounted for when prescribing imaging parameters and radiation dose reduction techniques. Familiarity with normal sex-based variations in anatomy and diseases prevalent or exclusively present in females is essential to accurately interpret imaging studies.
PERINATAL AND UNIQUE IMAGING CONSIDERATIONS IN FEMALES
Choice of Imaging Modality, Radiation Dose Consideration, and Contrast Agent Use
The potential of teratogenic and carcinogenic effects of ionizing radiation and adverse effects of intravenous (IV) contrast media require special consideration when imaging females in the perinatal period. The appropriateness of an imaging test, protocol modifications, and use of contrast material are essential. When feasible, ultrasound should be used as a first-line imaging investigation due to the absence of risks associated with ionizing radiation to both the mother and the fetus.1,2 If applicable, chest radiography (CXR) should be the modality of choice in the thoracic evaluation of acute conditions in pregnancy, with radiation dose to the fetus being negligible with modern technologies.1 Although thoracic computed tomography (CT) examinations do result in higher levels of radiation exposure compared with CXR, the dose to the fetus remains negligible when the fetus is outside of the scan field. For example, the estimated dose to the fetus for both a routine chest CT and computed tomography angiography (CTA) of the pulmonary arteries (PA CTA) is ~0.2 mGy, whereas the dose from a coronary CTA is ~0.1 mGy.1 Tube current modulation, available on most current CT scanners, also helps to reduce the radiation dose during image acquisition.1 Patient lead shielding is not recommended during the scanning since it can interfere with automatic exposure control and actually increase the fetal radiation dose, and obscure anatomic details.3 Overall, fetal risks from radiation doses of <50 mGy are considered negligible, and doses from thoracic CT are well below this threshold.2
No harm to the fetus from maternal IV iodinated CT contrast use is consistently reported, with most iodinated contrast agents classified as a category B by the FDA. As a result, the ACR does “not recommend withholding the use of iodinated contrast agents in pregnant women of potentially pregnant patients when it is needed for diagnostic purposes.4”
Pulmonary embolism (PE) and deep venous thrombosis (DVT) have special consideration in pregnancy. The risk of DVT in pregnancy is 5 times greater when compared with nonpregnant patients of the same age group.5 Lower extremity venous ultrasound (vUS) and CXR are considered the first-line tests, given their lowest radiation dose profile to the fetus. If lower extremity vUS is positive for DVT, no further imaging is required, as anticoagulation is usually warranted in this situation. If vUS is negative, PA CTA or lung scintigraphy (in the setting of a normal chest radiograph) is considered as the next test.2 Radiation doses for the perfusion portion of the ventilation/perfusion (V/Q) scan can be reduced in pregnant patients with a reduced dose of the radiotracer and compensatory increase in imaging time, and omission of the ventilation component if the perfusion portion is normal.2 Radiation dose to the fetus is higher with V/Q scanning compared with PA CTA during all trimesters6; however, the dose to the maternal breast is lower with scintigraphy.7 One of the major disadvantages of scintigraphy is the inability to suggest alternative diagnoses in comparison with CTA.2 Variations exist in the accuracy and nondiagnostic rates of each modality; however, a meta-analysis suggests that the 2 tests are comparable in terms of nondiagnostic rates and negative predictive value.7
Modifications to PA CTA, and other thoracic CT protocols can help to reduce the radiation dose further without compromising the quality of the study. Use of a standard 15-second delay after the start of contrast injection (instead of automatic triggering based on a set threshold and serial monitoring scans) has been shown to reduce dose while maintaining diagnostic image quality.8 Concomitant reduction of kVp, mAs, and z-axis coverage will also decrease the radiation dose. Exclusion of the lung apices on PA CTA is suggested, given the relatively low incidence of isolated apical pulmonary emboli and overall lower detection rate by CTA.9 Higher concentration and volume of contrast, faster rate of injection, and/or image acquisition during shallow inspiration may help to improve image quality and prevent “transient interruption of contrast,” and compensate for normal physiologic changes seen in pregnancy such as higher heart rate, cardiac output, and plasma volumes that may affect the quality of PA CTA.10,11
MRA plays a role in imaging females of reproductive age, including pregnancy, given its advantage of no ionizing radiation. However, noncontrast-enhanced MRA is rarely used in clinical practice, due to the wider availability, ease of acquisition and interpretation, and the relatively high negative predictive value and sensitivity of CTA for the detection of pulmonary emboli (median negative predictive value of 100% and median sensitivity of 83% in a Cochrane review of 11 studies12). At the same time, noncontrast-enhanced MRA with rapid sequences has demonstrated reasonable sensitivity (88.5%) and specificity (86.6%) for the detection of proximal PE in a small study.13 Slow infusion of IV ferumoxytol, an iron-based compound with prolonged blood pool time, off-label as a contrast agent, has shown good success in PE evaluation; however, it is considered a category C medication during pregnancy by the FDA.14,15
Gadolinium-based IV contrast media use during pregnancy has not been well studied in humans and, therefore, the safety has not been well established. However, no adverse mutagenic effects to human fetuses were reported with the doses used for magnetic resonance imaging (MRI) examinations.4 On the basis of animal studies, the FDA has classified these agents as category class C. Similarly, the ACR (American College of Radiology) recommends that these agents be administered with caution in pregnancy and only if the potential benefits outweigh the unknown risk to the fetus, with no imaging alternative to answer the clinical question. If use is indicated, the ACR also recommends that informed consent be obtained from the patient.4
Imaging During Lactation
The safety of iodinated and gadolinium-based IV contrast agents and radiation dose are important to consider during lactation. Since only a very small amount of both iodinated and gadolinium-based contrast material is excreted in breast milk (<1%) and absorbed by the infant’s gastrointestinal system, the use of both classes of contrast agents with continuation of normal breast feeding is considered safe and recommended.4 Ultimately, the decision is left to the mother, with optional pumping and discarding milk from the time of, and up to 12 to 24 hours after, contrast administration.4 Before deciding to temporarily discontinue breast feeding after IV contrast administration, the mother should be counseled that even short periods of cessation could lead to weaning.16
In contrast to CT and MRI studies, the breast-fed infant will be exposed to radiation through radioactivity in the breast milk and by physical proximity to the mother after nuclear medicine examinations. The recommended length of temporary breast-feeding interruption depends on the physical and biologic half-life of an individual radiopharmaceutical; however, the resultant dose to the infant should be less than 1 mSv. After the administration of 67Gallium-citrate and 131I-sodium-iodide, complete cessation of breast feeding is advised.16
Although it is theorized that during pregnancy and lactation, mammary tissue may be more susceptible to the mutagenic effects of ionizing radiation, a study of both V/Q nuclear scans and thoracic CT examinations during the perinatal period did not show a statistically significant increase in early-onset breast cancer, although the long-term risk is uncertain.17 As a result, minimizing radiation dose to the breast tissue during this time, when possible, while maintaining diagnostic image quality is prudent.
PREGNANCY-RELATED PATHOLOGIC CONDITIONS
Acute Pulmonary Edema (APE) and Acute Respiratory Distress Syndrome (ARDS)
APE and ARDS result from both obstetric and non–obstetric-related conditions in pregnancy.18 Predisposing physiological changes leading to APE include increased cardiac output, anemia, and low colloid osmotic pressure.19 Nonphysiological risk factors include preexisting maternal cardiovascular disease, preeclampsia, and peripartum cardiomyopathy. On CXR, findings in APE are similar to edema in a nonpregnant patient (Fig. 1) and, depending on the severity, include upper lobe vascular redistribution, septal (Kerley B) lines, alveolar opacities, and pleural effusions.20 On CT, interlobular septal thickening, ground glass opacities (GGO), and pleural effusions are seen.
ARDS is associated with a maternal mortality rate of nearly 25% and linked to both nonobstetric (sepsis, pneumonitis, blood transfusions, and trauma) and obstetric (amniotic fluid embolism [AFE], preeclampsia, and retained products of conception) causes.18,21 The imaging appearance of ARDS on CXR and CT is similar to that in nonpregnant individuals and includes bilateral alveolar opacities (usually with extensive air-bronchograms) and pleural effusions.22
AFE is a rare but severe potential complication of pregnancy with a high mortality rate (up to 86%).23,24 The mechanism is linked to the immune and pro-thrombotic cascade that leads to anaphylaxis, septic shock, edema, disseminated intravascular coagulation, and cardiopulmonary collapse. This results from amniotic fluid entering the venous system through small tears in uterine veins after membrane rupture and labor.23,25,26 Findings on CXR are similar to other causes of noncardiogenic APE (Fig. 2). Microemboli are below the resolution of CT; however, ill-defined centrilobular ground glass nodules may be present. Neither of these findings are specific and may also be encountered in APE and pulmonary hemorrhage, among other entities.25,26 CT is usually considered to exclude other etiologies such as an acute PE.25
Ovarian Hyperstimulation Syndrome (OHSS)
OHSS is the result of iatrogenic changes due to ovarian induction, occurring during the luteal phase of the menstrual cycle or early pregnancy.27,28 The reported incidence varies depending on the classification scheme, clinical situation, and stimulation protocol used, but can reach up to 33%.27,28 Imaging manifestations include bilateral ovarian enlargement with multiple ovarian cysts or follicles and ascites (Fig. 3) due to increased vascular permeability. The diagnosis is established by ultrasound, CT, or MRI.27 Findings on CXR include pleural effusions and adjacent compressive atelectasis, with patients presenting with dyspnea and tachypnea.28 Pleural effusions are more common on the right side and may be accompanied by an elevated hemidiaphragm. Approximately 2% of patients with severe OHSS have PE and 2% develop ARDS.28,29
Gestational Trophoblastic Neoplasms (GTN)
GTN are a group of malignant neoplasms within the larger category of gestational trophoblastic diseases. GTN include invasive moles, choriocarcinoma, and placental and epithelioid trophoblastic tumors.30 CXR and CT are the primary modalities for the evaluation of thoracic metastases in the setting of GTN, which are associated with an unfavorable prognosis.31 Thoracic metastatic disease most commonly presents with multiple well-defined round, solid noncalcified pulmonary nodules (Fig. 4). A halo of ground glass attenuation, due to neoplastic vascularity and tumorous infiltration, may surround the nodule (Fig. 5).30 Cavitation of the nodules may result in pneumothorax in the setting of subpleural location and rupture.30 Pulmonary arterial tumor embolization is less common, although classically presents with irregular beaded appearance of the distal pulmonary artery branches and occasionally results in pulmonary infarction (with classic peripheral wedge-shaped consolidative and/or GGO).30 Calcification of treated pulmonary metastases can occur.30 Pulmonary arteriovenous malformations (AVMs) after chemotherapeutic treatment of metastatic choriocarcinoma should be considered if one or several pulmonary nodules persist after other nodules have resolved posttreatment. As in pulmonary AVMs due to other etiologies, CT may reveal a feeding pulmonary artery and draining pulmonary vein. Larger AVMs are linked to hemoptysis and/or dyspnea, and cerebral complications from paradoxical emboli.30
LAM is a multisystem neoplastic disorder of smooth muscle cell proliferation with both thoracic and abdominal manifestations. LAM may be sporadic or associated with tuberous sclerosis complex (TSC), with the sporadic form almost exclusively affecting females of reproductive age. In contrast, LAM in males is nearly all associated with TSC.32 The most common presenting symptoms of LAM include dyspnea, pneumothorax, and cough.32,33 The course and symptoms of LAM in females may be exacerbated during pregnancy and menstruation.32
On CT, multiple, well-circumscribed, bilateral thin-walled air cysts throughout both lungs, diffusely distributed in axial and craniocaudal directions, are encountered (Figs. 6A, B).32,34 The size of the cysts correlates with the disease severity.32,33 Cyst shape is most commonly round.33 Lung parenchyma between the cysts is usually normal. Occasionally, ground glass may be present due to hemorrhage, edema, or smooth muscle cell proliferation in the alveolar walls.33 Air trapping within the intervening normal lung parenchyma is uncommon.33 Additional findings include solid, noncalcified pulmonary nodules, smooth thickening of the bronchovascular bundles and interlobular septa, and mediastinal lymphadenopathy.34 On CXR, lung volumes are preserved or increased, with the appearance of reticular opacities due to summation of cysts. Pleural effusions are not uncommon, reported in approximately one-third of the patients on CXR and up to two-thirds of the patients on CT.32,33,35 The chylous content of the pleural effusion often has a CT attenuation similar to that of pleural transudate.32 Chylous effusions often recur and pleurodesis may be necessary. However, pleurodesis may lead to the formation of pleural adhesions and chylous fluid buildup elsewhere in the body.32,33 Mediastinal ganglia and thoracic duct enlargement have also been reported.33
In the abdomen, manifestations include renal and hepatic angioleiomyomas, usually identifiable by the presence of macroscopic fat (Figs. 6C, D), and retroperitoneal leiomyomas, and chylous ascites.32–34
The classic clinical triad of TSC is epilepsy, intellectual disability, and cutaneous angiofibromas.32 Imaging findings in TSC also include pulmonary and extrapulmonary manifestations. Extrapulmonary findings are subependymal giant cell tumors of the brain, retinal hamartomas, cardiac rhabdomyomas, myocardial fatty foci (Fig. 6C), and renal cysts.32,36 In the lungs, in addition to the cysts, scattered small pulmonary nodules may be encountered, reflecting multifocal micronodular pneumocyte hyperplasia.32
Lung transplantation is reserved for the end-stage disease, with the recurrent disease occurring in rare posttransplantation, with only 10 case reports in the literature in 2017.32,37 For less severe cases, sirolimus (rapamycin), an FDA-approved mTOR inhibitor, is reported to decrease the level of serum vascular endothelial factor D and rate of lymphangiogenesis, thus stabilizing lung function and improving the quality of life.38
CONNECTIVE TISSUE DISEASES
Systemic Lupus Erythematosus (SLE)
SLE is a systemic autoimmune disorder characterized by the production of antibodies to components of the cell nucleus, which results in inflammation, immune complex deposition, and vasculopathy involving multiple organs.39 In adults, SLE is nine times more common in females than males, typically presenting during the reproductive years.40 SLE is associated with antiphospholipid antibody syndrome (APLAS), manifesting with arterial and venous occlusions, thromboses, pregnancy complications (spontaneous abortions and preeclampsia), and thromobocytopenia.41,42 In the thorax, SLE involves pleura, pericardium, lung parenchyma, respiratory muscles, and the cardiovascular system.
Serositis in SLE is common, affecting both pleura and pericardium. Pleuritis is the most common intrathoracic system finding in SLE, with an incidence of 45% to 83%.43,44 Pleuritis can be classified as either “dry” or “wet.” “Dry” pleuritis presents with painful respirations and few, if any, imaging findings, whereas the “wet” variant presents with bilateral exudative pleural effusions.45 The latter needs to be differentiated from empyema or transudates due to heart failure.45 Long-standing inflammation produces pleural thickening and fibrosis involving visceral and parietal pleural layers and may be associated with rounded atelectasis.41,45 SLE pericarditis (Fig. 7) has an incidence of 40% to 50% and can be adhesive or exudative.44,46 When present, pericardial effusions are usually small and cardiac tamponade is rare.46
Other cardiovascular manifestations also include myocarditis, corticosteroid-induced cardiomyopathy, vasculopathy (due to increased incidence of vasculitis and atherosclerosis), and endocarditis.44 The latter ranges from thickened valves to a more severe form as Libman-Sacks (sterile) endocarditis, which is linked to complement deposition.44 Cardiac MRI is used for functional, morphologic, and tissue evaluation of the heart along and pericardium, with echocardiography often added for valve assessment.47
Pulmonary abnormalities in SLE include pneumonia, pulmonary hemorrhage, lupus pneumonitis, and chronic interstitial pneumonitis.41 Infectious pneumonia is the most common cause of pulmonary opacities in the setting of SLE45 due to underlying immune dysregulation and immunosuppressive medications.41,45 Pulmonary interstitial pneumonitis in SLE is less common than in the other connective tissue diseases, with the most common histopathologic patterns of organizing or nonspecific interstitial pneumonia (NSIP).44 On CT, it presents with irregular linear subpleural opacities, interlobular septal thickening, GGO, reticulation, and architectural distortion.42 These findings are more common in the setting of SLE associated with APLAS.42 Another pulmonary imaging manifestation in SLE is related to complement deposition and small-vessel vasculitis, resulting in diffuse alveolar hemorrhage48 that presents with bilateral GGO and consolidative opacities on CT (Fig. 8) and acute chest pain and dyspnea clinically.45
Respiratory muscle dysfunction may lead to elevated hemidiaphragms with adjacent atelectasis on imaging and restrictive changes on pulmonary function tests.41 The severe manifestation of this finding is referred to as “shrinking lung syndrome.” Shrinking lung syndrome is a rare complication of lupus, with an incidence of 0.5% to 1.1%, with a female to male ratio of 17:1.49 Its pathophysiology is largely unclear, with suggested theories ranging from microatelectatic changes due to the lack of a surfactant and increased surface tension, pleural adhesions, and diaphragm dysfunction from phrenic nerve palsy and SLE-induced myopathy.50 On imaging, decreased lung volumes, pleural effusions, pleural thickening, atelectasis, and diaphragmatic elevation are present (Fig. 9).48
Pulmonary arterial hypertension (PAH) in individuals with SLE occurs with an incidence of 1% to 18%, with 95% of patients being women.51 Raynaud’s phenomenon, renal involvement, and vasculitis with digital gangrene and skin changes are among the predictive factors of PAH.51 In addition, associations with APLAS, recurrent thromboemboli, and chronic interstitial lung disease (ILD) are reported.41 On CT, enlarged central pulmonary arteries with or without pruning of distal branches are observed. Mosaic attenuation of the lung parenchyma and an enlarged and hypertrophied RV may be present in cases of chronic thromboembolic PAH.
Sjogren Syndrome (SS)
SS is an autoimmune disorder related to the production of antibodies against cytoplasmic peptides.52 SS is more prevalent in females than males.52 Glandular involvement with sicca symptoms, usually involving the eyes and salivary glands, is common.52 Thoracic manifestations include airway abnormalities, interstitial pneumonias, and lymphoproliferative disorders. Airways involvement may result in bronchiectasis, bronchial wall thickening, mosaic attenuation of the lung parenchyma, and centrilobular nodules.52 These changes are considered to result from destruction of exocrine glands or cell infiltration.52 ILD manifestations include NSIP, usual interstitial pneumonia, organizing pneumonia, and lymphocytic interstitial pneumonia.53 The most common radiologic and histologic pattern in SS is NSIP, seen in 45% of the cases.53,54 Lymphocytic interstitial pneumonia results from diffuse lymphoid hyperplasia and is most often reported in association with SS, affecting twice as many women as men.55,56 It presents on CT with poorly defined centrilobular nodules, subpleural nodules, bronchovascular thickening, septal thickening, diffuse ground glass attenuation, randomly distributed cysts, and lymph node enlargement55,56 (Fig. 10). Another systemic disorder, pulmonary amyloidosis, in association with SS is uncommon, with most cases due to nodular AL amyloidosis.57 A review of the literature found 37 cases, nearly all of which occurred in women, with the most common CT findings of multiple nodules and cysts. In addition to pulmonary amyloidosis, SS is associated with an 3% to 5% increased risk of non-Hodgkin lymphoma, particularly marginal zone B cell and mucosa-associated lymphoid tissue lymphomas.44 On thoracic CT, these most commonly present with new or enlarging nodules or masses, consolidative or mixed opacities, mediastinal lymphadenopathy, and pleural effusions.52
Systemic sclerosis is an autoimmune disease that results in fibrosis of the skin and internal organs and small-vessel vasculopathy. It affects reproductive-age women more often than men.58 Pulmonary involvement occurs in >80% of the patients, with ILD being the most common manifestation.44,59 Other sequelae include PAH, pleural effusions, respiratory muscle weakness, and aspiration due to esophageal dysmotility.44
An NSIP pattern of ILD is the most common, followed by usual interstitial pneumonia.59 Organizing pneumonia and obliterative bronchiolitis are less common.59 NSIP typically manifests on CT as bilateral lower lung predominant confluent GGO in the cellular subtype, with immediate subpleural sparing (Fig. 11). Peripheral reticular opacities, traction bronchiectasis, and honeycomb change are more common in the fibrotic subtype of NSIP.59,60
NONTUBERCULOUS MYCOBACTERIAL INFECTION
Mycobacterium avium intracellulare complex (MAC) is a chronic nontuberculous mycobacterial pulmonary infection. The nodular bronchiectatic subtype of MAC has a predilection for Caucasian women older than 50 years of age that most commonly presents with chronic cough.61–63 Subcentimeter pulmonary nodules, cylindrical bronchiectasis, and endobronchial mucous plugging, with predilection for the right middle lobe and lingula, are classic CT findings (Fig. 12).61–63 Cavitation, GGO, and lymphadenopathy are rarely seen in MAC in immunocompetent patients.61,62 The extent of the disease on CT has been shown to correlate with the severity of pulmonary functional impairment.64
THORACIC ENDOMETRIOSIS SYNDROME (TES)
Endometriosis is the abnormal growth of endometrial tissue in extrauterine sites, affecting 10% to 15% of reproductive-age women, most commonly occurring in the abdomen and pelvis.65 TES describes the clinical and radiological manifestations resulting from cyclical changes of functional endometrial tissue within the chest, affecting visceral or parietal pleura, lung parenchyma, airways, or diaphragm.65 On the basis of the region of involvement, TES is subdivided into the more common pleural form and the less common bronchopulmonary form.65 The proposed theories of pleural endometrial implants include retrograde menstruation, microembolization, and common embryological origins of the endometrium, pleural, and peritoneal mesothelium.66 The pleural form most often manifests with pneumothorax (73%) and hemothorax (14%).65 The bronchopulmonary presents with hemoptysis (7%) and pulmonary nodules (6%).66 In both forms, symptoms are temporally related to the onset of menstruation. Catamenial pneumothorax and recurrent pneumothoraces that occur within 24 hours before or 72 hours after the onset of menstruation are the most common manifestation.66 On cross-sectional imaging, endometrial implants are frequently located along the posterior and superior right hemidiaphragm (Fig. 13).65 On CT, the implants are usually small and hypo-attenuating to iso-attenuating. IV iodinated media increases conspicuity of the diaphragmatic deposits by improving the contrast between the enhancing liver parenchyma and the hypoenhancing endometrial implant.65 On MRI, the implants are typically hyperintense on T1-weighted imaging and have a low signal intensity on T2-weighted imaging due to hemorrhage.66
CHEST WALL AND OSSEOUS ABNORMALITIES
Elastofibroma Dorsi (ED)
ED is a benign hyperplastic fibroelastic lesion of the soft tissues, usually located between the thoracic wall and the lower third of the scapula, under the serratus anterior and latissimus dorsi musculature. ED can be bilateral and may be incidentally discovered on imaging performed for other indications.67,68 ED has a predilection for females in the fifth to sixth decades of life.69,70 On CT, the lesions present as a solid mass with ill-defined margins, indistinct to the deep costal plane and separate from the superficial soft tissues by a fat layer (Fig. 14). On MRI, the lesions have better defined margins with a fat plane on both the superficial and deep side without evidence of infiltration into the adjacent tissues or surrounding edema.69 They are typically isointense relative to skeletal muscle on both T1-weighted and T2-weighted images with interspersed streaks of fatty tissue with a high signal intensity on T1-weighted and T2-weighted images.68 Post-contrast enhancement is variable.68 On both CT and MRI, a fasciculated pattern can be helpful in differentiating ED from other tumors. Elastofibromas may show moderate FDG activity on PET/CT exams and should not be mistaken for malignancy when other characteristic imaging features are present.67
Osteoporosis (OS) and Insufficiency Fractures
OS, decreased bone mineralization, is influenced by many factors including age, sex, race, hormonal factors, medications, and dietary intake. OS is generally divided into primary and secondary etiologies, with primary OS further divided into postmenopausal and senile types. Postmenopausal OS affects women between the ages of 60 and 65 years, resulting from estrogen deficiency that leads to accelerated bone resorption, preferentially affecting the spine and wrist.71 Senile OS affects both trabecular and cortical bone, and may manifest as fractures of the hip, proximal humerus, tibia, and pelvis.71 On radiographs, OS presents with a thin cortex, endosteal resorption, and a decreased number of trabeculae. In the spine, cortical thinning may result in a well-demarcated outline of the vertebral body. Vertebral body compression fractures are the hallmark of OS.71 It has been estimated that more than one quarter of women aged 65 years and older have one or more vertebral compression fractures.72 Thoracic vertebral body compression fractures may lead to progressive kyphosis, which, in turn, can produce a deforming stress on the sternum, resulting in an insufficiency-type stress fracture.73 CT has a greater sensitivity for subtle fractures in comparison with radiographs. MRI is used when suspicion of spinal cord compression or presence of neurologic symptoms is present.74
Numerous pathologic cardiothoracic processes affect females exclusively, or with increased incidence, in comparison with males. Some of the diseases show distinct sex-based imaging features. In addition, unique female-specific conditions such as pregnancy and lactation require special considerations during the imaging. As such, sex-based differences must be taken into account across radiology, from the choice of imaging modality to the image interpretation.
1. McCollough CH, Schueler BA, Atwell TD, et al. Radiation exposure and pregnancy: when should we be concerned? Radiographics. 2007;27:909–917.
2. Pahade JK, Litmanovich D, Pedrosa I, et al. Quality initiatives: Imaging pregnant patients with suspected pulmonary embolism: what the radiologist needs to know. Radiographics. 2009;29:639–654.
3. American Association of Physicists in Medicine. AAPM Position Statement on the Use of Patient Gonadal and Fetal Shielding. 2019. Available at: https://www.aapm.org/org/policies/details.asp?id=468&type=PP
. Accessed September 7, 2020.
4. American College of Radiology. Manual on contrast media. Reston, VA: American College of Radiology; 2021. Available at: https://www.acr.org/Clinical-Resources/Contrast-Manual
. Accessed June 29, 2021.
5. Ring PA. Prevention of venous thrombosis and pulmonary embolism. JAMA. 1986;256:744–749.
6. Winer-Muram HT, Boone JM, Brown HL, et al. Pulmonary embolism in pregnant patients: fetal radiation dose with helical CT. Radiology. 2002;224:487–492.
7. Tromeur C, van der Pol LM, Le Roux P-Y, et al. Computed tomography pulmonary angiography versus ventilation-perfusion lung scanning for diagnosing pulmonary embolism during pregnancy: a systematic review and meta-analysis. Haematologica. 2019;104:176–188.
8. Litmanovich D, Boiselle PM, Bankier AA, et al. Dose reduction in computed tomographic angiography of pregnant patients with suspected acute pulmonary embolism. J Comput Assist Tomogr. 2009;33:961–966.
9. Halpern EJ. Triple-rule-out CT angiography for evaluation of acute chest pain and possible acute coronary syndrome. Radiology. 2009;252:332–345.
10. Ridge CA, Mhuircheartaigh JN, Dodd JD, et al. Pulmonary CT angiography protocol adapted to the hemodynamic effects of pregnancy. Am J Roentgenol. 2011;197:1058–1063.
11. Ridge CA, McDermott S, Freyne BJ, et al. Pulmonary embolism in pregnancy: comparison of pulmonary CT angiography and lung scintigraphy. Am J Roentgenol. 2009;193:1223–1227.
12. de Jong PG, van Mens TE, Leeflang MM, et al. Nijkeuter M. Imaging for the exclusion of pulmonary embolism in pregnancy. Cochrane Database of Systematic Reviews. Chichester, UK: John Wiley & Sons, Ltd; 2014:1–15.
13. Osman AM, Abdeldayem EH, Osman NM. MR pulmonary angiography: can it be used as an alternative for CT angiography in diagnosis of major pulmonary thrombosis? Egypt J Radiol Nucl Med. 2016;47:803–810.
14. Schiebler ML, Hamedani AG, Runo J, et al. CE-MRA in the primary diagnosis of pulmonary embolism: building a team to start a clinically relevant program. Appl Radiol. 2017;46:31–36.
15. US Food and Drug Administration. Feraheme (ferumoxytol) injection label. 2013. Available at: http://www.accessdata.fda.gov/drugsatfda_docs/label/2009/022180lbl.pdf
. Accessed September 7, 2020.
16. Tirada N, Dreizin D, Khati NJ, et al. Imaging pregnant and lactating patients. Radiographics. 2015;35:1751–1765.
17. Burton KR, Park AL, Fralick M, et al. Risk of early‐onset breast cancer among women exposed to thoracic computed tomography in pregnancy or early postpartum. J Thromb Haemost. 2018;16:876–885.
18. Duarte A. ARDS in pregnancy. Clin Obstet Gynecol. 2014;57:862–870.
19. Himoto Y, Kido A, Moribata Y, et al. CT and MR imaging findings of systemic complications occurring during pregnancy and puerperal period, adversely affected by natural changes. Eur J Radiol Open. 2015;2:101–110.
20. Dennis AT, Solnordal CB. Acute pulmonary oedema in pregnant women. Anaesthesia. 2012;67:646–659.
21. Perry K, Martin R, Blake P, et al. Maternal mortality associated with adult respiratory distress syndrome. South Med J. 1998;91:441–444.
22. Fanelli V, Vlachou A, Ghannadian S, et al. Acute respiratory distress syndrome: new definition, current and future therapeutic options. J Thorac Dis. 2013;5:326–334.
23. Clark SL, Hankins GDV, Dudley DA, et al. Amniotic fluid embolism: analysis of the national registry. Am J Obstet Gynecol. 1995;172:1158–1169.
24. Morgan M. Amniotic fluid embolism. Anaesthesia. 1979;34:20–32.
25. Plowman RS, Javidan-Nejad C, Raptis CA, et al. Imaging of pregnancy-related vascular complications. Radiographics. 2017;37:1270–1289.
26. Unal E, Balci S, Atceken Z, et al. Nonthrombotic pulmonary artery embolism: imaging findings and review of the literature. Am J Roentgenol. 2017;208:505–516.
27. Baron KT, Babagbemi KT, Arleo EK, et al. Emergent complications of assisted reproduction: expecting the unexpected. Radiographics. 2013;33:229–244.
28. Delvigne A, Rozenberg S. Review of clinical course and treatment of ovarian hyperstimulation syndrome (OHSS). Hum Reprod Update. 2003;9:77–96.
29. Abramov Y, Elchalal U, Schenker JG. Pulmonary manifestations of severe ovarian hyperstimulation syndrome: a multicenter study. Fertil Steril. 1999;71:645–651.
30. Shaaban AM, Rezvani M, Haroun RR, et al. Gestational trophoblastic disease: clinical and imaging features. Radiographics. 2017;37:681–700.
31. Vree M, van Trommel N, Kenter G, et al. The influence of lung metastases on the clinical course of gestational trophoblastic neoplasia: a historical cohort study. BJOG An Int J Obstet Gynaecol. 2016;123:1839–1845.
32. Abbott GF, Rosado-De-Christenson ML, Frazier AA, et al. Lymphangioleiomyomatosis: radiologic-pathologic correlation. Radiographics. 2005;25:803–828.
33. Pallisa E, Sanz P, Roman A, et al. Lymphangioleiomyomatosis: pulmonary and abdominal findings with pathologic correlation. Radiographics. 2002;22:185–198.
34. Tobino K, Johkoh T, Fujimoto K, et al. Computed tomographic features of lymphangioleiomyomatosis: evaluation in 138 patients. Eur J Radiol. 2015;84:534–541.
35. Taylor JR, Ryu J, Colby TV, et al. Lymphangioleiomyomatosis. N Engl J Med. 1990;323:1254–1260.
36. Adriaensen M, Schaefer-Prokop CM, Duyndam DAC, et al. Fatty foci in the myocardium in patients with tuberous sclerosis complex: common finding at CT. Radiology. 2009;253:359–363.
37. Zaki KS, Aryan Z, Mehta AC, et al. Recurrence of lymphangioleiomyomatosis: nine years after a bilateral lung transplantation. World J Transplant. 2016;6:249. doi: 10.5500/wjt.v6.i1.249
38. McCormack FX, Inoue Y, Moss J, et al. Efficacy and safety of sirolimus in lymphangioleiomyomatosis. N Engl J Med. 2011;364:1595–1606.
39. Mok C, Lau C. Pathogenesis of systemic lupus erythematosus. J Clin Pathol. 2003;56:481–490.
40. Weckerle CE, Niewold TB. The unexplained female predominance of systemic lupus erythematosus: clues from genetic and cytokine studies. Clin Rev Allergy Immunol. 2011;40:42–49.
41. Lalani TA, Kanne JP, Hatfield GA, et al. Imaging findings in systemic lupus erythematosus. Radiographics. 2004;24:1069–1086.
42. Oki H, Aoki T, Saito K, et al. Thin-section chest CT findings in systemic lupus erythematosus with antiphospholipid syndrome: a comparison with systemic lupus erythematosus without antiphospholipid syndrome. Eur J Radiol. 2012;81:1335–1339.
43. Dubois EL, Tuffanelli DL. Clinical manifestations of systemic lupus erythematosus. JAMA. 1964;190:104–111.
44. Mira-Avendano I, Abril A, Burger CD, et al. Interstitial lung disease and other pulmonary manifestations in connective tissue diseases. Mayo Clin Proc. 2019;94:309–325.
45. Goh YP, Naidoo P, Ngian GS. Imaging of systemic lupus erythematosus. Part I: CNS, cardiovascular, and thoracic manifestations. Clin Radiol. 2013;68:181–191.
46. Tincani A, Rebaioli CB, Taglietti M, et al. Heart involvement in systemic lupus erythematosus, anti-phospholipid syndrome and neonatal lupus. Rheumatology. 2006;45(suppl_4):iv8–iv13.
47. Burkard T, Trendelenburg M, Daikeler T, et al. The heart in systemic lupus erythematosus—a comprehensive approach by cardiovascular magnetic resonance tomography. PLoS One. 2018;13:1–14.
48. Hannah JR, D’Cruz DP. Pulmonary complications of systemic lupus erythematosus. Semin Respir Crit Care Med. 2019;40:227–234.
49. Borrell H, Narváez J, Alegre JJ, et al. Shrinking lung syndrome in systemic lupus erythematosus. Medicine (Baltimore). 2016;95:e4626.
50. Duron L, Cohen-Aubart F, Diot E, et al. Shrinking lung syndrome associated with systemic lupus erythematosus: a multicenter collaborative study of 15 new cases and a review of the 155 cases in the literature focusing on treatment response and long-term outcomes. Autoimmun Rev. 2016;15:994–1000.
51. Tselios K, Gladman D, Urowitz M. Systemic lupus erythematosus and pulmonary arterial hypertension: links, risks, and management strategies. Open Access Rheumatol Res Rev. 2016;9:1–9.
52. Flament T, Bigot A, Chaigne B, et al. Pulmonary manifestations of Sjögren’s syndrome. Eur Respir Rev. 2016;25:110–123.
53. Reina D, Roig Vilaseca D, Torrente-Segarra V, et al. Sjögren’s syndrome-associated interstitial lung disease: a multicenter study. Reumatol Clínica. 2016;12:201–205.
54. Wang Y, Hou Z, Qiu M, et al. Risk factors for primary Sjögren syndrome-associated interstitial lung disease. J Thorac Dis. 2018;10:2108–2117.
55. Swigris JJ, Berry GJ, Raffin TA, et al. Lymphoid interstitial pneumonia: a narrative review. Chest. 2002;122:2150–2164.
56. Johkoh T, Müller NL, Pickford HA, et al. Lymphocytic interstitial pneumonia: thin-section CT findings in 22 patients. Radiology. 1999;212:567–572.
57. Rajagopala S, Singh N, Gupta K, et al. Pulmonary amyloidosis in Sjogren’s syndrome: a case report and systematic review of the literature. Respirology. 2010;15:860–866.
58. Steen VD, Oddis CV, Conte CG, et al. Incidence of systemic sclerosis in Allegheny county, Pennsylvania. A twenty-year study of hospital-diagnosed cases, 1963–1982. Arthritis Rheum. 1997;40:441–445.
59. Ohno Y, Koyama H, Yoshikawa T, et al. State-of-the-art imaging of the lung for connective tissue disease (CTD). Curr Rheumatol Rep. 2015;17:1–12.
60. Kligerman SJ, Groshong S, Brown KK, et al. Nonspecific interstitial pneumonia: radiologic, clinical, and pathologic considerations. Radiographics. 2009;29:73–87.
61. Hartman TE, Swensen SJ, Williams DE. Mycobacterium avium
complex: evaluation with CT. Radiology. 1993;187:23–26.
62. Erasmus JJ, McAdams HP, Farrell MA, et al. Pulmonary nontuberculous mycobacterial infection: radiologic manifestations. Radiographics. 1999;19:1487–1503.
63. Miller WT. Spectrum of pulmonary nontuberculous mycobacterial infection. Radiology. 1994;191:343–350.
64. Jong WS, Koh WJ, Kyung SL, et al. High-resolution CT findings of Mycobacterium avium
complex pulmonary disease: correlation with pulmonary function test results. Am J Roentgenol. 2008;191:160–166.
65. Rousset P, Rousset-Jablonski C, Alifano M, et al. Thoracic endometriosis syndrome: CT and MRI features. Clin Radiol. 2014;69:323–330.
66. Chamié LP, Ribeiro DMFR, Tiferes DA, et al. Atypical sites of deeply infiltrative endometriosis: clinical characteristics and imaging findings. Radiographics. 2018;38:309–328.
67. Pierce JC, Henderson R. Hypermetabolism of elastofibroma dorsi on PET-CT. Am J Roentgenol. 2004;183:35–37.
68. Clinckemaillie G, Larbi A, Omoumi P, et al. Bilateral elastofibroma dorsi: typical CT and MRI features. JBR-BTR. 2014;97:45.
69. Battaglia M, Vanel D, Pollastri P, et al. Imaging patterns in elastofibroma dorsi. Eur J Radiol. 2009;72:16–21.
70. Tepe M, Polat MA, Calisir C, et al. Prevalence of elastofibroma dorsi on CT: is it really an uncommon entity? Acta Orthop Traumatol Turc. 2019;53:195–198.
71. Patel AA, Ramanathan R, Kuban J, et al. Imaging findings and evaluation of metabolic bone disease. Adv Radiol. 2015;2015:21.
72. Melton LJ, Kan SH, Frye MA, et al. Epidemiology of vertebral fractures in women. Am J Epidemiol. 1989;129:1000–1011.
73. Cooper KL. Insufficiency fractures of the sternum: a consequence of thoracic kyphosis? Radiology. 1988;167:471–472.
74. Old JL, Calvert M. Vertebral compression fractures in the elderly. Am Fam Physician. 2004;69:111–116.