Mystery Quiz

Mystery Quiz- The Answer

July 9, 2010

Vivian Hayashi MD and Robert Smith MD, Mystery Quiz Section Editors

The answer to the mystery quiz is pleural effusion that is loculated in both the horizontal and right oblique fissures. Pleural effusion is seen as blunting of the right costophrenic angle and tracking of fluid laterally (Image 3, arrowhead). The horizontal fissure thickens due to fluid which becomes an ovoid density more medially (Image 3, arrow). This ovoid density, representing loculated fluid in the horizontal fissure, is often referred to as a pseudotumor. It appears as a homogenous shadow suggesting fluid, rather than parenchymal disease which, when consolidated and airless, will appear denser. The second overlying shadow (Image 3, open arrows) represents loculated fluid in the oblique fissure. The opacity appears denser at its inferior margin where there is greater volume of fluid and fades as it tracks superiorly where there is less fluid. These fissural fluid collections and their relationship to each other can be further visualized in the transverse (Images 5-10) and coronal (Images 11-16) CT images.

In order to confirm that the opacification is fluid density, the region of interest can be quantified in Hounsfield units (HU) and compared to that of a soft tissue such as the liver (Image 17). The Hounsfield scale is a measure of the attenuation of radiation by different densities , wherein water is scaled at 0 HU, air at -1000 HU, fat at -120HU, bone at +400HU, and muscle at +40. Within an average transverse CT slice of 3mm thickness, a mixture of densities will yield a HU measure that will differ from these scaled values. Image 17 shows the density in the fissure as -16.59 HU while the liver is + 42.14HU indicating the presence of fissural fluid.

The most common reason for loculation of pleural fluid is inflammation of the pleural space with resulting fibrous stranding. In these cases, the pleura may appear thickened, diffusely or focally, and sometimes the area of thickening may be quite subtle. Alternatively, when the pleura appears normal and there is no history to suggest a past inflammatory process, loculation may be due to differing pressure gradients in the pleural space. In the latter instance, positional changes, such as the decubitus position, may shift the fluid and cause the typical appearance of layering pleural fluid.

Our patient had pleural effusions due to congestive heart failure related to severe mitral regurgitation and non-ischemic cardiomyopathy. His valvular heart disease had worsened considerably in the year prior to admission and was associated with a moderate reduction in left ventricular function. Twelve days after admission, the patient underwent a mitral valve repair and radiofrequency ablation of the atrial fibrillation.

This case illustrates how a common condition, pleural effusion, can present in an uncommon fashion, as a mass lesion. Knowing the fissural anatomy and the distinctive texture of pleural fluid can help identify the lesion.

 

Mystery Quiz

July 4, 2010

Vivian Hayashi MD and Robert Smith MD, Mystery Quiz Section Editors

The patient is a 61 year old man presenting with one month of worsening shortness of breath. The patient has a history of alcoholism and was diagnosed with atrial fibrillation during a hospital admission for detox three years earlier. Warfarin therapy was not begun due to a history of poor medication compliance. One year prior to admission an echocardiogram showed a normal global ejection fraction and mild mitral regurgitation. One month prior to admission, the patient noted the onset of worsening breathlessness and occasional palpitations. He denied hemoptysis, night sweats, sputum production, known exposure to tuberculosis, or changes in weight. Social history was noteworthy for current alcohol abuse and a remote history of IV drug abuse; the patient denies ever smoking. On admission, he was noted to be afebrile with labored respiration, an irregular pulse of 92 beats per minute, blood pressure of 150 systolic, O2 saturation of 93% on room air; chest exam revealed bibasilar rales and extremities were mildly edematous. WBC was 6.8K, hemoglobin 11.7gm, and platelet count 153K. Brain natriuretic peptide level was 630 (ref. range 0-100). Chest radiograph upon admission is shown below:


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Mystery Quiz- The Answer

March 28, 2010

Vivian Hayashi MD and Robert Smith MD, Mystery Quiz Section Editors

The answer to the mystery quiz is progressive massive fibrosis. This condition is a severe form of silicosis. The chest radiograph (Image 3) shows bullous disease of the right upper lobe, increased density of the right hilum, increased density and upward retraction of the left hilum (also seen in Image 4), increased density in peripheral areas of both lungs, and an air crescent sign in the left upper lobe (also seen in Image 5). The air crescent sign indicates the presence of a fungus ball (aspergilloma ) contained within a cavity. Image 6 shows conglomerate densities of both hila (block arrows) with calcification (thin arrows). Image 7 shows profuse small, irregular nodules throughout the lung.

Silicosis results from the inhalation of crystalline silica which is silicon dioxide (SiO2). This compound is abundantly present in rocks, such as sandstone, granite and slate. Occupations which involve blasting, mining, or tunneling in rock may expose workers to inhalation of silica. Workers in ceramics and glass manufacturing can also be exposed to inhalable silica. Silicosis is categorized as simple silicosis when pulmonary nodules are less than 10mm in size. This condition usually affects the upper lung zones and often manifests as innumerable nodules. Patients may be asymptomatic at this stage. Usually, the disease appears 10 to 30 years after exposure. When present before this time, as in our case, the disease is called accelerated silicosis as opposed to chronic silicosis. When the nodules of simple silicosis coalesce to form large conglomerate densities on imaging (Image 6), the disease is classified as progressive massive fibrosis. This condition, which is more frequently associated with accelerated silicosis, distorts the lung and results in areas of emphysema which are adjacent to areas of dense conglomerate fibrosis. The conglomerate densities may cavitate, sometimes spontaneously but often due to mycobacterial infection. Our patient was infected with Mycobacterium avium complex. Silicosis is believed to arise from injury due to oxygen free radicals, and ongoing toxicity may persist even after an individual is no longer exposed to silica.

Our case illustrates the multiple complications of progressive massive fibrosis, including emphysema and pulmonary cavitation associated with aspergilloma and atypical mycobacterial infection. Although these complications were listed as individual entries in the differential diagnosis of the mystery quiz, progressive massive fibrosis best explains all of the findings in the case. The treatment of our patient included frequent courses of antibiotics, anti-mycobacterial medications, supplemental oxygen, and bronchodilator therapy with occasional courses of prednisone. Other than lung transplantation, treatment options are limited.

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Mystery Quiz

March 17, 2010

Vivian Hayashi MD and Robert Smith MD, Mystery Quiz Section Editors

The patient is a 39yo male followed in pulmonary clinic for chronic breathlessness and intermittent sputum production, sometimes blood tinged. Symptoms were first noted eleven years earlier at which time pulmonary function testing revealed mixed obstructive and restrictive defects. The patient experienced some improvement with bronchodilators, occasional courses of oral steroids and antibiotics, but was never entirely free of his symptoms. Over an interval of ten years, the patient required several hospitalizations for treatment of breathlessness, pneumonia, and a spontaneous left-sided pneumothorax that required chest tube placement. He smoked half a pack per day for four years and quit seven years earlier. The patient worked from the ages of 20 to 24 in a quarry. Family history was non-revealing.

Current imaging is shown below.

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Mystery Quiz- The Answer

October 27, 2009

Vivian Hayashi MD and Robert Smith MD, Mystery Quiz Section Editors

The answer to the mystery quiz is thoracic splenosis. The key to the solution is the past medical history of a gunshot wound. Shrapnel is seen on the plain CXR (Image 1) as well as in the soft tissue of the back (Image 5). The CXR also shows a lateral diaphragmatic abnormality (Image 1, arrow) likely due to adhesions. The left upper quadrant is notable for colonic gas where one might expect a soft tissue density due to the spleen. The lateral film (Image 2) shows abdominal wall sutures. Presumably, the patient’s gunshot wound resulted in trauma to the upper abdomen and diaphragm necessitating a splenectomy (the left upper quadrant on Image 5 is noteworthy for the absence of a spleen).

Thoracic splenosis (Images 3 and 4, arrows) is a condition that can follow traumatic injury to the spleen. During rupture, the splenic tissue disperses to distant sites including the peritoneal cavity, and possibly the thorax if the diaphragm is injured and tears. The splenic implants are often multiple. One study collected data over a twenty year period and identified five cases of splenosis: two were intraperitoneal and one each in intrahepatic, intrathoracic, and subcutaneous sites. In these five cases, there was an average interval of 29 years between the splenic injury and diagnosis, and most were incidental findings (Khosravi MR. Am Surg 2004 Nov; 70(11):967-70). The implants may mimic neoplasm or thoracic endometriosis.

Consideration of the diagnosis of thoracic splenosis may obviate surgical exploration. Radioisotope scanning, using either Tc99m sulfur colloid or labeled, heat-denatured red cells may confirm the diagnosis non-invasively as splenic tissue will take up these radioisotopes . Importantly, the splenic implants are functional and will keep the peripheral blood smear free of cells ordinarily observed in asplenic individuals (eg, Howell-Jolly bodies, Heinz bodies, and nucleated red cells).

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Mystery Quiz

October 23, 2009

Vivian Hayashi MD and Robert Smith MD, Mystery Quiz Section Editors

A 61 year old man was referred to the pulmonary service for an abnormal pulmonary function test (PFT). The patient was a lifelong smoker and had symptoms suggestive of obstructive sleep apnea. The PFT showed a mixed obstructive and restrictive defect. The latter abnormality was considered to be out of proportion to the patient’s obesity, hence a chest CT scan was obtained to evaluate for possible parenchymal lung disease (shown below). Past history was significant for hypertension, hyperlipidemia, GERD, and a remote gunshot wound to the back. Medications included irbesartan, simvastatin, omeprazole and combivent.

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Work-up revealed a negative bone scan, negative head CT, and a PET scan which showed no abnormal uptake in the thorax. Core needle biopsy of the lesion depicted in Image 3 revealed a chronic mixed inflammatory infiltrate with plasma cells, lymphocytes, endothelial cells and capillaries; tissue resembled parietal pleura with fibrous plaque and malignancy was not identified.


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Mystery Quiz- The Answer

July 23, 2009

Vivian Hayashi MD and Robert Smith MD, Mystery Quiz Section Editors

The answer to the mystery quiz is bland alveolar hemorrhage. The CXR (image 1) shows cardiomegaly with mild increase in opacification of the right middle and right lower lobes. The CT images show areas of multifocal ground glass opacification, that is, the underlying interstitium is visible through the opacification, and the variably sized opacities are widely distributed throughout the lungs (images 2, 3, and 4). Image 4 shows prominent interstitium through the ground glass. This pattern is sometimes referred to as “crazy paving” (arrow, image 5). “Crazy paving,” reflecting thickened interstitium along with ground glass attenuation, is often associated with alveolar proteinosis. The radiographic pattern, however, is non-specific and may be seen in any condition in which the interstitium is thickened, as in pulmonary venous congestion, and the alveoli are filled, as in pulmonary hemorrhage. Any alveolar process, such as edema, blood or lipid containing material, may be associated with a ground glass appearance on imaging, as long as the density of the alveolar material does not obscure the underlying lung architecture. Once obscured, the density is considered to be consolidation, as seen in the center of the ground glass opacification (image 5, arrowhead). Image 5 also shows small bilateral effusions.

Alveolar hemorrhage is a syndrome that spans pulmonary vasculitis, including Wegener’s, microscopic polyarteritis, Churg-Strauss, Goodpasture’s, glomerulonephritis with pulmonary hemorrhage, and pulmonary capillaritis. Patients usually present with evidence of systemic inflammation and appear acutely ill. Cases of alveolar hemorrhage may also be associated with drug toxicity that results in diffuse alveolar damage, such as penicillamine or crack cocaine. Other cases may be due to the effects of anticoagulation, possibly exacerbated by increased pulmonary venous pressure as seen in left ventricular failure or valvular disease, such as mitral stenosis. These latter cases are considered to be bland alveolar hemorrhage.

Our patient did not appear acutely ill and the clinical picture did not suggest a vasculitis or infectious disease. Although his INR was only 1.5 on admission, the patient was on enoxaparin and increased pulmonary venous pressures likely contributed to the bland pulmonary hemorrhage. A repeat CT two weeks later (image 6, 7, 8 ) showed resolution of the ground glass opacities and, coincidentally, increased bilateral effusions due to LV failure. An important clinical observation is that bland alveolar hemorrhage will clear quickly, often in just a few days, if the precipitating cause has been eliminated. In contrast, untreated inflammatory disease will usually persist or worsen.

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Mystery Quiz

July 18, 2009

Vivian Hayashi MD and Robert Smith MD, Mystery Quiz Section Editors

The patient is a 74 year old man complaining of hemoptysis for four days. The patient has a history of hypertension, but had not been followed medically for many years until two weeks earlier when he presented with leg swelling, breathlessness, and atrial flutter. He was admitted, diuresed, begun on antihypertensive medications including hydralazine, aspirin, and anti-coagulated with enoxaparin and warfarin. After discharge, the patient felt well for a few days before the onset of hemoptysis. There was no associated fever, chest pain, arthralgias, headaches, or visual changes. On this admission, the patient did not appear acutely ill. Resting pulse oximetry and vital signs were normal, except for a mildly elevated blood pressure. The chest was clear to auscultation; the lower extremities had mild pitting edema. Labs showed hemoglobin that was decreased nearly 3gm/dL from baseline; INR was 1.5; white blood cell count and serum creatinine were normal; the urinalysis was bland. post_image_1_question   post_image_2_question1                             

 

 

 

 

 

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Mystery Quiz- The Answer

May 1, 2009

Posted by Vivian Hayashi MD and Robert Smith MD, Mystery Quiz Section Editors

The answer to the mystery quiz is sarcoidosis. The CXR shows diffuse, bilateral infiltration with a predominantly nodular pattern. The pulmonary hila are also prominent. The CT image shows innumerable 2-3mm nodules, many of which have a perilymphatic distribution. The lymphatics, in parallel with the pulmonary vasculature, course through the interstitium. Hence, the perilymphatic nodularity has an interstitial distribution and appears as “studding” along the interstitium which is enhanced by vascular contrast (Image 2, short arrows). Additional nodules, however, have a random distribution (Image 2, arrowhead), while others appear to be centrilobular (Image 2, long arrow). As a granulomatous disease that involves activated CD4 lymphocytes, it is not surprising to find pathological involvement of perilymphatic tissue along with lymph nodes (Image 3, arrows). That said, sarcoidosis may involve any anatomical lung site: airways, interstitium or alveoli.

Perilymphatic nodularity also appears in the fissures and along the pleura where lymphatics are found (not shown). Other lung diseases included in the differential are also characterized by small nodules on chest imaging. Depending on their origin, the nodules have different distributions. Hematogenous spread of disease, such as miliary TB, will appear as interstitial disease because it is perivascular. Interstitial nodules due to miliary TB or metastatic disease, for example, appear to have sharp borders because they are enveloped by the interstitium which gives them a smooth edge on imaging. Nodules that arise from endobronchial spread of disease, such as aspiration or aerogenous spread of infection, often appear in a centrilobular distribution. The centrilobular location is where a bronchiole, filled with material conferring the appearance of a radiographic nodule, enters the lobule. The lobule appears as a polygonal structure (distal interstitium) on CT imaging. Beyond the bronchiole, nodules will manifest with a fuzzy border because they occupy airspace. Such nodules may also appear larger depending on how much neighboring airspace is involved.

Our patient was treated with prednisone to alleviate his cough. His cough improved after a few weeks and repeat imaging showed regression of the pulmonary nodules (Image 4) and mediastinal lymphadenopathy (Image 5). Our case illustrates how patients with sarcoidosis often have imaging that is worse than would be expected from their clinical presentation.

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Mystery Quiz

April 28, 2009

Vivian Hayashi MD and Robert Smith MD, Mystery Quiz Section Editors

The patient is a 42 year old man with a history of non-productive cough for several weeks. Three weeks prior to evaluation by the pulmonary service, the patient presented to the ER with a presumed vasovagal syncopal event that occurred on a subway platform. The patient’s prior medical history included allergic sinusitis and nasal polypectomy. Other than cough, the patient denied constitutional symptoms. The patient was not taking any medications. His social history was negative for smoking, intravenous drug abuse, risk factors for HIV infection, significant occupational exposures and travel. The patient did not own any pets. PPD placed by the pulmonary service was negative. Physical exam revealed a thin man with normal vital signs including normal resting pulse oximetry, clear chest, and otherwise no focal findings.

 

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Mystery Quiz- The Answer

March 10, 2009

Posted by Vivian Hayashi MD and Robert Smith MD, Mystery Quiz Section Editors

The answer to the mystery quiz is allergic bronchopulmonary aspergillosis (ABPA). The CXR shows right upper lobe opacities, two of which appear round (Image 3, arrow) and another tubular (Image 3, arrowhead), and a left upper lobe opacity which has the characteristics of subsegmental atelectasis (Image 3, double arrows). The CT scan, performed ten days after the CXR, shows central bronchiectasis of the RUL (Image 4, arrows); tubular branching shadows (Image 6, arrow) as well as ring shadows (Image 5 and 6, arrowhead) all of which represent ectatic airways filled with mucoid material. A left upper lobe ectatic airway with thickening of the bronchial wall is also present (Image 7, arrow). The left upper lobe subsegmental atelectasis seen on the initial CXR was not visible on the CT image, indicating clearing of mucoid impaction.

ABPA is seen in a small percentage of patients with asthma and represents a complex hypersensitivity reaction to aspergillus antigens colonizing the airways. The diagnosis is established when multiple clinical findings are present. These include frequently refractory asthma, eosinophilia, serum IgE reactive to aspergillus antigen, and very elevated total serum IgE levels (>1000 IU). Characteristic imaging shows central bronchiectasis and mucoid impaction (“finger in glove” shadows, Image 6, arrow) that result in subsegmental atelectasis, often in an upper lobe distribution. The atelectasis can appear migratory as one area clears and another becomes impacted. In addition to patients with asthma, ABPA is associated with cystic fibrosis in a small percentage of cases. Treatment consists of high dose glucocorticoids followed by a slow taper. Serum IgE levels decline but typically do not normalize and recurrences of disease are associated with increasing serum IgE levels. There is some evidence that the addition of itraconazole to glucocorticoids may be helpful. The addition of the antifungal agent may decrease the burden of aspergillus colonization and lead to less hypersensitivity. Left untreated, ABPA may progress to irreversible fibrosis.

Our patient was initially treated as an asthma exacerbation due to pneumonia. However, this initial diagnosis gave way to a final diagnosis of ABPA when the serum IgE level returned at 1365 IU (reference range 0-158), serum IgE specific for Aspergillus fumigatus was elevated and the CT imaging showed characteristic findings.

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Mystery Quiz

March 6, 2009

Posted by Vivian Hayashi MD and Robert Smith MD, Mystery Quiz Section Editors

The patient is a 42 year old male non-smoker with history of poorly controlled asthma (first diagnosed in 1994, recurrent need for steroid treatments but never intubated), severe seasonal allergies with chronic sinusitis, hepatic steatosis, GERD and gout who presented with complaints of five to ten days of myalgias, productive cough, wheezing and chest tightness. His medications included albuterol, fluticasone and formoteral inhalers, montelukast, colchicine, indomethacin prn, and fexofenadine. Exam was significant for T 97.6, HR 100, BP 120/83, RR 22, O2Sat 95% on RA. The patient was moderately obese, appeared anxious and tachypneic but speaking in full sentences. Heart exam was within normal limits with no JVD. Lung exam with decreased breath sounds and scattered inspiratory and expiratory wheezing throughout. No rales nor rhonchi. Labs were significant for WBC 12.0 with 75% polys, 12.7% lymphs, 8.4% eos; mild transaminitis (ast/alt 48/89—patient’s baseline). Blood cultures pending x 2.

Admission CXR: Images 1 & 2

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