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ERROR: type should be string, got "https://profreg.medscape.com/px/getpracticeprofile.do?method=getProfessionalProfile&urlCache=aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvMTE2ODQxNS1vdmVydmlldw==\nDrugs & Diseases > Neurology\nSubdural Empyema\nAuthor: Segun Toyin Dawodu, JD, MD, MS, MBA, LLM, FAAPMR, FAANEM; Chief Editor: Niranjan N Singh, MBBS, MD, DM, FAHS, FAANEM more...\nSections Subdural Empyema\nFurther Outpatient Care\nFurther Inpatient Care\nInpatient & Outpatient Medications\nSubdural empyema (ie, abscess) is an intracranial focal collection of purulent material located between the dura mater and the arachnoid mater. About 95% of subdural empyemas are located within the cranium; most involve the frontal lobe, and 5% involve the spinal neuraxis. This article focuses on the intracranial type, which causes clinical problems through extrinsic compression of the brain by an inflammatory mass and inflammation of the brain and meninges.\nSubdural empyema is a life-threatening infection that was first reported in the literature about 100 years ago. It accounts for about 15-22% of focal intracranial infections. The mortality rate approached 100% before the introduction of penicillin in 1944 and has declined since that time. Because the symptoms might be very mild initially, rapid recognition and treatment are important; the early institution of appropriate treatment gives the patient a good chance of recovery with little or no neurological deficit.\nSubdural empyema is a primarily intracranial infection located between the dura mater and the arachnoid mater. It has a tendency to spread rapidly through the subdural space until limited by specific boundaries (eg, falx cerebri, tentorium cerebelli, base of the brain, foramen magnum). The subdural space has no septations except in areas where arachnoid granulations are attached to the dura mater. Subdural empyema is usually unilateral.\nWith progression, subdural empyema has a tendency to behave like an expanding mass lesion with associated increased intracranial pressure and cerebral intraparenchymal penetration. Cerebral edema and hydrocephalus also may be present secondary to disruption of blood flow or cerebrospinal fluid (CSF) flow caused by the increased intracranial pressure. Cerebral infarction may be present from thrombosis of the cortical veins or cavernous sinuses or from septic venous thrombosis of contiguous veins in the area of the subdural empyema.\nIn infants and young children, subdural empyema most often occurs as a complication of meningitis. In such cases, subdural empyema should be differentiated from reactive subdural effusion (ie, sterile collection of fluid due to increased efflux of intravascular fluids from increased capillary wall fenestrations into the subdural space). In older children and adults, it occurs as a complication of paranasal sinusitis, otitis media, or mastoiditis.\nInfection usually enters through the frontal or ethmoid sinuses; less frequently, it enters through the middle ear, mastoid cells, or sphenoid sinus. This often occurs within 2 weeks of a sinusitis episode, with the infection spreading intracranially through thrombophlebitis in the venous sinuses. Infection also may extend directly through the cranium and dura from an erosion of the posterior wall of the mastoid bone or frontal sinus. Direct extension also could be from an intracerebral abscess. Rarely, infection spreads hematogenously from distant foci, most commonly from a pulmonary source or as a complication of trauma, surgery, or septicemia. The sphenoid sinus also could be a source of infection.\nSubdural empyema accounts for 15-22% of focal intracranial infections. Sinusitis is the most common predisposing factor in the developed world.\nFrequency is similar to that in the Unites States. However, otitis media and mastoiditis are the most common predisposing conditions.\nMortality/Morbidity\nIn the pre-antibiotic era, the mortality rate approached 100%; this still may be the case in developing countries.\nIn the developed world, the mortality rate has improved tremendously: it is about 6-35% (variance depending on areas and hospitals); however, about 55% of patients have neurological deficits at the time of hospital discharge.\nThe mortality rate has continued to decline because of early diagnosis and treatment, more accurate localization with head CT scan, early sinus drainage, and recognition of the prominent role of anaerobes in the disease.\nThe high incidence of morbidity (ie, neurological deficits) is attributed to the short follow-up period and low mortality rate. Very ill patients who would have died in the past now survive with deficits.\nSex- and age-related demographics\nSubdural empyema is more common in males, who can account for up to 80% of cases. The reason for this predominance is unknown. One theory is that the normal development of the paranasal sinuses in males results in anatomic differences that predispose them to recurrent sinusitis.\nSubdural empyema can occur at any age, but about two thirds of patients are aged 10-40 years.\nCarr TF. Complications of sinusitis. Am J Rhinol Allergy. 2016 Jul. 30 (4):241-5. [Medline].\nDabdoub CB, Adorno JO, Urbano J, Silveira EN, Orlandi BM. Review of the Management of Infected Subdural Hematoma. World Neurosurg. 2016 Mar. 87:663.e1-8. [Medline].\nZimmerman RD, Leeds NE, Danziger A. Subdural empyema: CT findings. Radiology. 1984 Feb. 150(2):417-22. [Medline].\nChen CY, Huang CC, Chang YC. Subdural empyema in 10 infants: US characteristics and clinical correlates. Radiology. 1998 Jun. 207(3):609-17. [Medline].\nBrennan MR. Subdural empyema. Am Fam Physician. 1995 Jan. 51(1):157-62. [Medline].\nGreenlee JE. Subdural empyema. In: Mandell GL, ed. Principles and Practice of Infectious Diseases. Vol 1. 4th ed. New York: Churchill. 1994:900-903.\nBrouwer MC, van de Beek D. Management of bacterial central nervous system infections. Handb Clin Neurol. 2017. 140:349-364. [Medline].\nFeuerman T, Wackym PA, Gade GF. Craniotomy improves outcome in subdural empyema. Surg Neurol. 1989 Aug. 32(2):105-10. [Medline].\nFrench H, Schaefer N, Keijzers G, Barison D, Olson S. Intracranial subdural empyema: a 10-year case series. Ochsner J. 2014 Summer. 14 (2):188-94. [Medline].\nSanford JP. Guide to antimicrobial therapy. Bethseda MD: Uniformed Services University Health Sciences. 1993. 3:\nDelgado Tapia JA, Galera Lopez J, Santiago Martin J, et al. Subdural empyema due to Mycoplasma hominis after a cesarean section under spinal anesthesia. Rev Esp Anestesiol Reanim. 2005. 52(4):239-242. [Medline].\nDwarakanath S, Suri A, Mahapatra AK. Spontaneous subdural empyema in falciparum malaria: a case study. J Vector Borne Dis. 2004 Sep-Dec. 41(3-4):80-2. [Medline].\nFoerster BR, Thurnher MM, Malani PN, Petrou M, Carets-Zumelzu F, Sundgren PC. Intracranial infections: clinical and imaging characteristics. Acta Radiologica. October 2007. 48(8):875-93. [Medline].\nHall WA, Truwit CL. The surgical management of infections involving the cerebrum. Neurosurgery. February 2008. 62 Supplement 2:519-30. [Medline].\nKrauss WE, McCormick PC. Infections of the dural spaces. Neurosurg Clin N Am. 1992 Apr. 3(2):421-33. [Medline].\nMauser HW, Van Houwelingen HC, Tulleken CA. Factors affecting the outcome in subdural empyema. J Neurol Neurosurg Psychiatry. 1987 Sep. 50(9):1136-41. [Medline].\nMigirov L, Eyal A, Kronenberg J. Intracranial complications following mastoidectomy. Pediatr Neurosurg. 2004 Sep-Oct. 40(5):226-9. [Medline].\nPlaceholder.\nMoorthy RK, Rajshekhar V. Intracranial Abscess. Neurosurg Focus. 2008. 24 (6):E3.\nMRI scan of a subdural empyema in the left parietal area.\nCT scan of a subdural empyema in the left temporal/parietal area.\nSegun Toyin Dawodu, JD, MD, MS, MBA, LLM, FAAPMR, FAANEM Attending Interventional Physiatrist, Wellspan Health\nSegun Toyin Dawodu, JD, MD, MS, MBA, LLM, FAAPMR, FAANEM is a member of the following medical societies: American College of Sports Medicine, American Academy of Physical Medicine and Rehabilitation, Royal College of Surgeons of England, American Association of Neuromuscular and Electrodiagnostic Medicine, American Medical Association, American Medical Informatics Association, Association of Academic Physiatrists, International Society of Physical and Rehabilitation Medicine\nNicholas Lorenzo, MD, MHA, CPE Co-Founder and Former Chief Publishing Officer, eMedicine and eMedicine Health, Founding Editor-in-Chief, eMedicine Neurology; Founder and Former Chairman and CEO, Pearlsreview; Founder and CEO/CMO, PHLT Consultants; Chief Medical Officer, MeMD Inc\nNicholas Lorenzo, MD, MHA, CPE is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, American Association for Physician Leadership\nFlorian P Thomas, MD, PhD, MA, MS Chair, Neuroscience Institute and Department of Neurology, Director, National MS Society Multiple Sclerosis Center and Hereditary Neuropathy Foundation Center of Excellence, Hackensack University Medical Center; Founding Chair and Professor, Department of Neurology, Hackensack Meridian School of Medicine at Seton Hall University; Professor Emeritus, Department of Neurology, St Louis University School of Medicine; Editor-in-Chief, Journal of Spinal Cord Medicine\nFlorian P Thomas, MD, PhD, MA, MS is a member of the following medical societies: Academy of Spinal Cord Injury Professionals, American Academy of Neurology, American Neurological Association, Consortium of Multiple Sclerosis Centers, National Multiple Sclerosis Society, Sigma Xi\nNiranjan N Singh, MBBS, MD, DM, FAHS, FAANEM Adjunct Associate Professor of Neurology, University of Missouri-Columbia School of Medicine; Medical Director of St Mary's Stroke Program, SSM Neurosciences Institute, SSM Health\nNiranjan N Singh, MBBS, MD, DM, FAHS, FAANEM is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, American Headache Society\nEdward L Hogan, MD Professor, Department of Neurology, Medical College of Georgia; Emeritus Professor and Chair, Department of Neurology, Medical University of South Carolina\nEdward L Hogan, MD is a member of the following medical societies: Alpha Omega Alpha, Society for Neuroscience, American Society for Biochemistry and Molecular Biology, American Academy of Neurology, American Neurological Association, Phi Beta Kappa, Sigma Xi, Southern Clinical Neurological Society\nencoded search term (Subdural Empyema) and Subdural Empyema\nEpidural Infections (Spinal Epidural Abscess) and Subdural Infections (Subdural Empyema)\nPathology of Bacterial Infections\nBacterial Meningitis Imaging\nIntracranial Epidural Abscess\nSubdural Hematoma Surgery\nSpontaneous Intracranial Hypotension\nParietal Subdural Empyema as Complication of Acute Odontogenic Sinusitis: A Case Report\nImaging of Intracranial Infectious Diseases in Adults\nAccording to Neurologists\nMedical Cannabis Safe, Effective for Neurologic Symptoms in the Elderly\nTicagrelor: A New Antibiotic?\nNovel, 'Non-Habit Forming' Medication May Reduce Low Back Pain\nFDA Okays Smartphone-Controlled Wearable for Migraine Pain\nMonoclonals for Migraine: 'Probably the Best Option We've Ever Had'\nDiseases & Conditions Subdural Empyema\nDiseases & Conditions Epidural Infections (Spinal Epidural Abscess) and Subdural Infections (Subdural Empyema)\nDiseases & Conditions Pathology of Bacterial Infections\nDiseases & Conditions Brain Abscess"

ERROR: type should be string, got "https://profreg.medscape.com/px/getpracticeprofile.do?method=getProfessionalProfile&urlCache=aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvMzYzMjczLW92ZXJ2aWV3\nDrugs & Diseases > Radiology\nIdiopathic Pulmonary Fibrosis Imaging\nAuthor: Ali Nawaz Khan, MBBS, FRCS, FRCP, FRCR; Chief Editor: Eugene C Lin, MD more...\nSections Idiopathic Pulmonary Fibrosis Imaging\nNuclear Imaging\nIdiopathic pulmonary fibrosis (IPF) is defined as a specific form of chronic, progressive fibrosing interstitial pneumonia of unknown etiology, occurring primarily in older adults, limited to the lungs, and associated with the histopathologic and/or radiologic pattern of usual interstitial pneumonia (UIP). It is characterized by progressive worsening of dyspnea and lung function and is associated with a poor prognosis; most patients die of respiratory failure. [1] The mean survival is approximately 4 years.\nAccording to the American Thoracic Society (ATS), European Respiratory Society (ERS), Japanese Respiratory Society (JRS), and Latin American Thoracic Association (ALAT) evidence-based guidelines for diagnosis and management of IPF, the criteria for diagnosis are as follows [1] :\nAll known causes of interstitial lung disease (ILD) are excluded, including other idiopathic interstitial pneumonias and ILD associated with environmental exposure, medication, or systemic disease.\nA UIP pattern is present on high-resolution computed tomography (HRCT) in patients not subjected to surgical lung biopsy.\nSpecific combinations of HRCT and surgical lung biopsy pattern in patients subjected to surgical lung biopsy.\nRadiologic characteristics of pulmonary fibrosis appear in the image below.\nHRCT of advanced stage of pulmonary fibrosis demonstrating reticular opacities with honeycombing, with predominant subpleural distribution.\nThe diagnosis is confirmed with a lung biopsy, but the histology shows striking variation from one region to the next (ie, the disease is characterized by histologic temporal and spatial heterogeneity). It is not unusual to find areas of normal lung next to areas with severe thickening of alveolar walls. Therefore, findings on bronchoscopic or percutaneous lung biopsy are difficult to interpret. Open lung biopsy and video-assisted thoracoscopic lung biopsy are the preferred methods.\nIPF usually affects patients 50-70 years of age. Most series report a male preponderance, with a male-to-female ratio of 2:1. Clinical features consist of progressive exertional dyspnea; the presence of interstitial infiltrates, as evidenced on chest radiographs; and physiologic evidence of restriction and impaired gas exchange on pulmonary function testing.\nPatients are generally treated with corticosteroids, other immunosuppressants, or both.\nPreferred examination\nThe diagnosis of IPF is made on the basis of the patient's history, clinical findings, pulmonary physiology, and imaging results. The diagnosis is one of exclusion. Nonidiopathic causes must be excluded first because of the important therapeutic implications. After nonidiopathic causes are excluded, further investigation of patients with IPF typically reveals radiographic abnormalities and restrictive lung physiology with decreased diffusion capacity. [2, 3, 4]\nPlain chest radiography is usually the first investigation performed for patients with suspected interstitial lung disease. However, the findings on conventional radiography are highly nonspecific.\nHigh-resolution computed tomography (HRCT) scanning defines the underlying lung parenchymal abnormalities better than plain radiography. [5, 6] Studies have shown that HRCT may obviate surgical lung biopsy in some patients. Raghu et al compared the diagnostic accuracy of clinical evaluation in combination with HRCT with the accuracy of histology of surgical lung-biopsy samples. [7] Clinical assessment in conjunction with careful review of HRCT scans was 60% sensitive and 97% specific for IPF. However, although HRCT may obviate the need for tissue diagnosis in 60% of patients, surgical lung biopsy is still needed in 40%.\nFor diagnoses other than IPF, a combination of clinical assessment and HRCT is neither sensitive nor specific enough to be relied on without surgical biopsy. Open lung biopsy remains the criterion standard. In immunocompetent patients, the benefit is relatively low because corticosteroid therapy is frequently administered after biopsy. In immunocompromised patients, approaches to therapy change substantially after tissue confirmation, but mortality is high. Therefore, open biopsy should be performed only in patients in whom the diagnosis is likely to change therapy and in patients who have a reasonable prognosis.\nRadionuclide scanning with gallium-67 may depict interstitial fibrosis and may show changes early. This feature may be of therapeutic benefit, but the changes are nonspecific and do not remove the need for lung biopsy.\nThe radiographic pattern differs with the stage of the disease. Early in the disease, the most common radiographic changes are an interstitial shadowing of small (1 to 2 mm), irregular opacities, which are seen in about 75% of patients. Less common are small, round opacities, which are seen in 20% of patients. This finding is generally known as reticulonodular opacities. Septal lines are occasionally observed. The distribution is predominantly basal. (See the image below.)\nBilateral lower lobe opacities and possible mild decrease in lung volumes. Courtesy of Sat Sharma, MD, FRCPC, FACP, FCCP, DABSM.\nPeripheral accentuation is also a common feature, but it is more easily appreciated on CT scans than on plain chest radiographs.\nThe pattern is usually symmetrical. Another common pattern is hazy, ground-glass opacification, which is either diffuse or patchy. Volume loss and a raised diaphragm are seen in up to 60% of patients. This may be accompanied by basal discoid atelectasis.\nPleural disease is not typical of IPF. Its presence should raise the possibility of other conditions, such as asbestosis, rheumatoid pulmonary disease, or systemic lupus. Pneumothorax, pneumomediastinum, or both have been reported in a few patients; these conditions have been associated with bullae in the lung parenchyma.\nWith progression of alveolitis to fibrosis, the initial fine lines become coarse, and small (2 mm) cysts appear. These cysts coalesce and increase to 5-7 mm in diameter; they appear as ring opacities within the honeycomb lung. As fibrosis worsens, the honeycombing becomes coarser with larger honeycomb cysts, and further volume loss occurs. In advanced stages, there is radiographic evidence of pulmonary arterial hypertension.\nDegree of confidence\nThe radiographic findings are not correlated with the stage of the disease, the histology, the respiratory symptoms, the respiratory function tests, or the prognosis.\nIn the majority of patients with IPF, the chest radiograph is abnormal at presentation; previous radiographs often will have shown reticular shadowing, even before symptom development. [8] Chest radiography is frequently the first investigation employed for patients with IPF; physiologic testing and HRCT scanning follow.\nFor symptomatic patients in whom the diffusion capacity is abnormal, results of chest radiography may be normal. For other patients, the radiographic appearances are abnormal before clinical symptoms appear. Results of HRCT scanning are abnormal for most patients with IPF.\nFor patients with IPF, HRCT scan findings may be used to predict outcomes and to guide the treatment, because the findings are well correlated with the histologic pattern of IPF (see the images below). The accuracy of the diagnosis of IPF is significantly increased with HRCT, as compared with chest radiography. When a trained observer performs HRCT, the accuracy of the diagnosis is reported to be about 90%. [9] ​ One third of all cases of IPF are missed on HRCT; a confident diagnosis of IPF is made in about two thirds of cases. [9] On HRCT, end-stage lung disease is characterized by honeycombing without ground-glass attenuation in typical distribution; with such findings on HRCT, the diagnosis may be made with confidence. This spares patients the risk of invasive diagnostic processes, such as a lung biopsy. In the active stage, scans demonstrate ground-glass attenuations. The active stage of the disease, which is characterized by active alveolitis, is potentially reversible and potentially amenable to treatment, unlike end-stage disease, which is irreversible. [10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21]\nHigh-resolution CT (HRCT) shows increased pulmonary attenuation with distortion of the pulmonary architecture. Courtesy of Sat Sharma, MD, FRCPC, FACP, FCCP, DABSM.\nHigh-resolution CT (HRCT) shows distortion of the pulmonary architecture with thickening of pulmonary interstitium and some areas of ground-glass attenuation. No obvious honeycombing is present. Courtesy of Sat Sharma, MD, FRCPC, FACP, FCCP, DABSM.\nOn HRCT, IPF is commonly characterized by patchy and predominantly peripheral, subpleural, and bibasilar reticular opacities. The distribution is predominantly posterior. It is often associated with traction bronchiectasis and subpleural honeycombing.\nEvidence has been found to suggest that alveolar collapse may precede lung fibrosis in IPF, potentially aiding in earlier diagnosis. [22, 23]\nGround-glass attenuations are relatively uncommon; they usually progress to the more common reticular attenuations and honeycombing. HRCT scans have been reported to show honeycombing in 90% of patients with IPF. In the absence of honeycombing, the extent of reticular and ground-glass densities can predict a diagnosis of IPF. The probability of IPF exceeds 80% in patients older than 60 years, with one third having reticular densities. [24]\nIn cases of suspected IPF in which lung HRCT shows more than 30% ground-glass attenuation, consideration should be given to other diagnoses; alternative diagnoses include desquamative interstitial pneumonitis, idiopathic bronchiolitis obliterans organizing pneumonia, respiratory bronchiolitis–associated interstitial lung disease, hypersensitivity pneumonitis, and nonspecific interstitial pneumonia.\nPulmonary artery size measured on HRCT has been studied as an outcome predictor in IPF. In a study of 98 IPF patients, pulmonary artery and ascending aorta diameters were measured from chest HRCT with pulmonary artery:ascending aorta diameter (PA:A) ratio calculations. Patients with a PA:A ratio >1 had higher risk of death or transplant compared with patients with a PA:A ratio ≤1 (P< 0.001). A PA:A ratio >1 was also an independent predictor of outcomes in unadjusted and adjusted outcomes analyses (hazard ratio 3.99, P< 0.001, and hazard ratio 3.35, P=0.002, respectively). [25]\nIn cases of IPF, perfusion lung scintigraphy shows nonspecific, subsegmental mismatched perfusion defects. These are not correlated with clinical severity.\nGallium-67 imaging has not proven to be of value in cases of established IPF. [26]\nTechnetium-99m diethylenetriamine penta-acetic acid (DTPA) is cleared more rapidly when capillary permeability is increased than when it is not, and the findings may provide an index of lung inflammation. [27] Fluorodeoxyglucose (FDG) positron-emission tomography (PET) may show FDG accumulation in the lung bases; such findings correlate with the honeycomb fibrosis seen on high-resolution HRCT. [28, 29, 30, 31, 32]\nWin et al studied 13 patients with IPF recruited for 2 thoracic 18F FDG-PET studies performed within 2 weeks of each other. All patients were diagnosed with IPF in consensus at multidisciplinary meetings because of typical clinical, HRCT, and pulmonary function test features. The purpose of the study twas o investigate the reproducibility of pulmonary 18F FDG-PET in patients with IPF. This study demonstrated that there is excellent short-term reproducibility in pulmonary 18F FDG uptake in patients with IPF. [33]\nWhat is idiopathic pulmonary fibrosis (IPF)?\nWhat are the diagnostic criteria for idiopathic pulmonary fibrosis (IPF)?\nHow is the diagnosis of idiopathic pulmonary fibrosis (IPF) confirmed?\nWhich patient groups are at highest risk for idiopathic pulmonary fibrosis (IPF)?\nWhich medications are used to treat idiopathic pulmonary fibrosis (IPF)?\nHow is idiopathic pulmonary fibrosis (IPF) diagnosed?\nWhat is the role of radiography in the workup of idiopathic pulmonary fibrosis (IPF)?\nHow accurate are radiographic findings in the diagnosis of idiopathic pulmonary fibrosis (IPF)?\nWhat is the role of CT scan in the workup of idiopathic pulmonary fibrosis (IPF)?\nWhat is the role of nuclear imaging in the workup of idiopathic pulmonary fibrosis (IPF)?\n[Guideline] Raghu G, Collard HR, Egan JJ, et al. An official ATS/ERS/JRS/ALAT statement: idiopathic pulmonary fibrosis: evidence-based guidelines for diagnosis and management. Am J Respir Crit Care Med. 2011 Mar 15. 183 (6):788-824. [Medline]. [Full Text].\nPipavath S, Godwin JD. Imaging of the chest: idiopathic interstitial pneumonia. Clin Chest Med. 2004 Dec. 25(4):651-6, v-vi.\nStrollo DC. Imaging of idiopathic interstitial lung diseases. Concepts and conundrums. Am J Respir Cell Mol Biol. 2003 Sep. 29(3 Suppl):S10-8. [Medline].\nKatzenstein AL, Mukhopadhyay S, Myers JL. Diagnosis of usual interstitial pneumonia and distinction from other fibrosing interstitial lung diseases. Hum Pathol. 2008 Sep. 39(9):1275-94. [Medline].\nKishaba T. Practical management of Idiopathic Pulmonary Fibrosis. Sarcoidosis Vasc Diffuse Lung Dis. 2015 Jul 22. 32 (2):90-8. [Medline].\nOikonomou A. Role of imaging in the diagnosis of diffuse and interstitial lung diseases. Curr Opin Pulm Med. 2014 Sep. 20 (5):517-24. [Medline].\nRaghu G. Idiopathic pulmonary fibrosis. A rational clinical approach. Chest. 1987 Jul. 92(1):148-54. [Medline].\nJohnston ID, Prescott RJ, Chalmers JC, Rudd RM. British Thoracic Society study of cryptogenic fibrosing alveolitis: current presentation and initial management. Fibrosing Alveolitis Subcommittee of the Research Committee of the British Thoracic Society. Thorax. 1997 Jan. 52(1):38-44. [Medline].\nGrenier P, Valeyre D, Cluzel P, et al. Chronic diffuse interstitial lung disease: diagnostic value of chest radiography and high-resolution CT. Radiology. 1991 Apr. 179(1):123-32. [Medline].\nAntonio GE, Wong KT, Hui DS, et al. Thin-section CT in patients with severe acute respiratory syndrome following hospital discharge: preliminary experience. Radiology. 2003 Sep. 228(3):810-5. [Medline].\nMacDonald SL, Rubens MB, Hansell DM, et al. Nonspecific interstitial pneumonia and usual interstitial pneumonia: comparative appearances at and diagnostic accuracy of thin-section CT. Radiology. 2001 Dec. 221(3):600-5. [Medline].\nPotente G, Bellelli A, Nardis P. Specific diagnosis by CT and HRCT in six chronic lung diseases. Comput Med Imaging Graph. 1992 Jul-Aug. 16(4):277-82. [Medline].\nRaghu G. Interstitial lung disease: a diagnostic approach. Are CT scan and lung biopsy indicated in every patient?. Am J Respir Crit Care Med. 1995 Mar. 151(3 Pt 1):909-14. [Medline].\nShah RM, Miller W. Widespread ground-glass opacity of the lung in consecutive patients undergoing CT: Does lobular distribution assist diagnosis?. AJR Am J Roentgenol. 2003 Apr. 180(4):965-8. [Medline].\nWells A. Clinical usefulness of high resolution computed tomography in cryptogenic fibrosing alveolitis. Thorax. 1998 Dec. 53(12):1080-7. [Medline].\nWittram C, Mark EJ, McLoud TC. CT-histologic correlation of the ATS/ERS 2002 classification of idiopathic interstitial pneumonias. Radiographics. 2003 Sep-Oct. 23(5):1057-71. [Medline].\nZompatori M, Calabrò E, Chetta A, et al. [Chronic hypersensitivity pneumonitis or idiopathic pulmonary fibrosis? Diagnostic role of high resolution Computed Tomography (HRCT)]. Radiol Med (Torino). 2003 Sep. 106(3):135-46. [Medline].\nSong JW, Koh WJ, Lee KS, Lee JY, Chung MJ, Kim TS, et al. High-resolution CT findings of Mycobacterium avium-intracellulare complex pulmonary disease: correlation with pulmonary function test results. AJR Am J Roentgenol. 2008 Oct. 191(4):1070. [Medline].\nPiirilä P, Kivisaari L, Huuskonen O, Kaleva S, Sovijärvi A, Vehmas T. Association of findings in flow-volume spirometry with high-resolution computed tomography signs in asbestos-exposed male workers. Clin Physiol Funct Imaging. 2008 Sep 15. [Medline].\nRogliani P, Mura M, Mattia P, Ferlosio A, Farinelli G, Mariotta S, et al. HRCT and histopathological evaluation of fibrosis and tissue destruction in IPF associated with pulmonary emphysema. Respir Med. 2008 Aug 22. [Medline].\nVrielynck S, Mamou-Mani T, Emond S, Scheinmann P, Brunelle F, de Blic J. Diagnostic value of high-resolution CT in the evaluation of chronic infiltrative lung disease in children. AJR Am J Roentgenol. 2008 Sep. 191(3):914-20. [Medline].\nPetroulia V, Funke M, Zumstein P, Berezowska S, Ebner L, Geiser T, et al. Increased Expiratory Computed Tomography Density Reveals Possible Abnormalities in Radiologically Preserved Lung Parenchyma in Idiopathic Pulmonary Fibrosis. Invest Radiol. 2018 Jan. 53 (1):45-51. [Medline].\nMai C, Verleden SE, McDonough JE, Willems S, De Wever W, Coolen J, et al. Thin-Section CT Features of Idiopathic Pulmonary Fibrosis Correlated with Micro-CT and Histologic Analysis. Radiology. 2017 Apr. 283 (1):252-263. [Medline].\nSalisbury ML, Xia M, Murray S, Bartholmai BJ, Kazerooni EA, Meldrum CA, et al. Predictors of idiopathic pulmonary fibrosis in absence of radiologic honeycombing: A cross sectional analysis in ILD patients undergoing lung tissue sampling. Respir Med. 2016 Sep. 118:88-95. [Medline]. [Full Text].\nShin S, King CS, Puri N, Shlobin OA, Brown AW, Ahmad S, et al. Pulmonary artery size as a predictor of outcomes in idiopathic pulmonary fibrosis. Eur Respir J. 2016 May. 47 (5):1445-51. [Medline]. [Full Text].\nKataoka M, Kawamura M, Ueda N, et al. Diffuse gallium-67 uptake in radiation pneumonitis. Clin Nucl Med. 1990 Oct. 15(10):707-11. [Medline].\nLabrune S, Chinet T, Collignon MA, et al. Mechanisms of increased epithelial lung clearance of DTPA in diffuse fibrosing alveolitis. Eur Respir J. 1994 Apr. 7(4):651-6. [Medline].\nBaughman RP, Fernandez M. Radionuclide imaging in interstitial lung disease. Curr Opin Pulm Med. 1996 Sep. 2(5):376-9. [Medline].\nBourke SJ, Hawkins T, Keavey PM, et al. Ventilation perfusion radionuclide imaging in cryptogenic fibrosing alveolitis. Nucl Med Commun. 1993 Jun. 14(6):454-64. [Medline].\nJames JM, Lloyd JJ, Leahy BC, et al. 99Tcm-Technegas and krypton-81m ventilation scintigraphy: a comparison in known respiratory disease. Br J Radiol. 1992 Dec. 65(780):1075-82. [Medline].\nRizzato G. Is nuclear imaging of any value in managing interstitial fibrosis?. Curr Opin Pulm Med. 1997 Sep. 3(5):372-7. [Medline].\nSimkin PH, Licho R, Brill AB. Pulmonary nuclear medicine. Curr Opin Radiol. 1991 Dec. 3(6):859-70. [Medline].\nWin T, Lambrou T, Hutton BF, Kayani I, Screaton NJ, Porter JC, et al. 18F-Fluorodeoxyglucose positron emission tomography pulmonary imaging in idiopathic pulmonary fibrosis is reproducible: implications for future clinical trials. Eur J Nucl Med Mol Imaging. 2012 Mar. 39(3):521-8. [Medline].\nCourtesy of Sat Sharma, MD, FRCPC, FACP, FCCP, DABSM. (Click Image to enlarge.)\nAli Nawaz Khan, MBBS, FRCS, FRCP, FRCR Consultant Radiologist and Honorary Professor, North Manchester General Hospital Pennine Acute NHS Trust, UK\nAli Nawaz Khan, MBBS, FRCS, FRCP, FRCR is a member of the following medical societies: American Association for the Advancement of Science, American Institute of Ultrasound in Medicine, British Medical Association, Royal College of Physicians and Surgeons of the United States, British Society of Interventional Radiology, Royal College of Physicians, Royal College of Radiologists, Royal College of Surgeons of England\nKlaus L Irion, MD, PhD Consulting Staff, The Cardiothoracic Centre Liverpool NHS Trust, The Royal Liverpool University Hospital, UK\nKlaus L Irion, MD, PhD is a member of the following medical societies: American Roentgen Ray Society, Radiological Society of North America\nAnitha James, MBBS, DMRD, FRCR Specialist Registrar, Manchester Radiology Training Scheme, Hospitals NHS Trust, UK\nBernard D Coombs, MB, ChB, PhD Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand\nEugene C Lin, MD Attending Radiologist, Teaching Coordinator for Cardiac Imaging, Radiology Residency Program, Virginia Mason Medical Center; Clinical Assistant Professor of Radiology, University of Washington School of Medicine\nEugene C Lin, MD is a member of the following medical societies: American College of Nuclear Medicine, American College of Radiology, Radiological Society of North America, Society of Nuclear Medicine and Molecular Imaging\nJeffrey A Miller, MD Associate Adjunct Professor of Clinical Radiology, University of Medicine and Dentistry of New Jersey-New Jersey Medical School; Faculty, Department of Radiology, Veterans Affairs of New Jersey Health Care System\nJeffrey A Miller, MD is a member of the following medical societies: American Roentgen Ray Society, Radiology Alliance for Health Services Research, Society of Thoracic Radiology\nAlberto Alonso, MD, MRCP Specialist Registrar in Radiology, Department of Radiology, Manchester Royal Infirmary, UK\nAlberto Alonso, MD, MRCP is a member of the following medical societies: Radiological Society of North America, Royal College of Physicians, and Royal College of Radiologists\nWilliam Musda, MBBS Specialist Registrar, Diagnostic Radiology, Manchester Radiology Training Sceme, UK\nVelauthan Rudralingam, MB, BCh, BAO, FRCS, FRCR Staff Physician, Gastrointestinal and Body Imaging Block, Hope Hospital and Wytenshawe Hospital, UK\nVelauthan Rudralingam, MB, BCh, BAO, FRCS, FRCR is a member of the following medical societies: British Medical Association and Radiological Society of North America\nencoded search term (Idiopathic Pulmonary Fibrosis Imaging) and Idiopathic Pulmonary Fibrosis Imaging\nIdiopathic Pulmonary Fibrosis\nFast Five Quiz: Diagnosing Idiopathic Pulmonary Fibrosis\nFast Five Quiz: Idiopathic Pulmonary Fibrosis Treatment\nHemosiderosis\nPathology of Usual Interstitial Pneumonia\nHunger for Air: Management Strategies in IPF: Living and Waiting\nIs Sooner Better? The Push to Use Antifibrotics Early in IPF\nMolecular Classifier Helps Spot Idiopathic Pulmonary Fibrosis\nAccording to Pulmonologists\nWomen Snore Too - and Just as Loudly\nDual Antibiotic Zerbaxa Gets FDA Nod for Bacterial Pneumonia\nAzithromycin May Reduce Treatment Failure for COPD Exacerbations\nInhaler Errors Common Among Kids Hospitalized for Asthma\nUndiagnosed Sleep Apnea Ups Risk for Postop CV Events\n2001 /viewarticle/913754\nDiseases & Conditions Idiopathic Pulmonary Fibrosis\nDiseases & Conditions Idiopathic Pulmonary Fibrosis Imaging\n2010 esbriet-pirfenidone-999972 Drugs\nDrugs pirfenidone"