Medical Image of the Week: Barium Aspiration

Figure 1: Upright X-Ray of the chest showing dense opacifications in the bilateral lower lobes consistent with Barium Aspiration.

An 88-year old man was referred for video fluoroscopic swallow study (VFSS) for concerns of aspiration as the cause of his chronic cough. As part of the study, he was given barium sulfate nectar which he aspirated and developed respiratory distress and hypoxia requiring hospital admission. Chest X-ray obtained at that time is shown (Figure 1).

Although inert, acute inflammation and even death attributed to barium aspiration has been described (1,2). Severe respiratory complications tend to occur in patients with extensive comorbidities (2,3). Treatment is mostly supportive and severe cases may require invasive ventilatory support. Bronchoscopy and suction clearance may be attempted although the success is variable. Recovery is usually complete although fibrosis is a known complication (4).

Bhupinder Natt, MD

Division of Pulmonary, Allergy, Critical Care and Sleep

Banner-University Medical Center

Tucson, AZ USA

References

1. Kaira K, Takise A, Goto T, Horie T, Mori M. Barium sulphate aspiration. Lancet 2004;364(9452):2220. [CrossRef] [PubMed]
2. Gray C, Sivaloganathan S, Simpkins KC. Aspiration of high density barium contrast medium causing acute pulmonary inflammation- report of two fatal cases in elderly women with disordered swallowing. Clinic Radiol. 1989;40(4):397-400. [CrossRef] [PubMed]
3. Fruchter O, Dragu R. Images in Clinical Medicine. A deadly examination. N Engl J Med. 2003;348(11):1016. [CrossRef] [PubMed]
4. Voloudaki A, Ergazakis N, Gourtsoyiannis N. Late changes in barium sulfate aspiration. HRCT Features. Eur Radiol. 2003;13(9):2226-9. [CrossRef] [PubMed]

Cite as: Natt B. Medical image of the week: barium aspiration. Southwest J Pulm Crit Care. 2017;15(6): . doi: https://doi.org/10.13175/swjpcc146-17 PDF 

December 2017 Imaging Case of the Month

Michael B. Gotway, MD

Department of Radiology

Mayo Clinic Arizona

Scottsdale, AZ USA

Imaging Case of the Month CME Information  

Completion of an evaluation form is required to receive credit and a link is provided on the last panel of the activity.

0.25 AMA PRA Category 1 Credit(s)™

Estimated time to complete this activity: 0.25 hours

Lead Author(s): Michael B. Gotway, MD. All Faculty, CME Planning Committee Members, and the CME Office Reviewers have disclosed that they do not have any relevant financial relationships with commercial interests that would constitute a conflict of interest concerning this CME activity. 

Learning Objectives: As a result of completing this activity, participants will be better able to:

1. Interpret and identify clinical practices supported by the highest quality available evidence.
2. Establish the optimal evaluation leading to a correct diagnosis for patients with pulmonary, critical care and sleep disorders.
3. Translate the most current clinical information into the delivery of high quality care for patients.
4. Integrate new treatment options for patients with pulmonary, critical care and sleep related disorders.

Learning Format: Case-based, interactive online course, including mandatory assessment questions (number of questions varies by case). Please also read the Technical Requirements.

CME Sponsor: University of Arizona College of Medicine at the Arizona Health Sciences Center.

Current Approval Period: January 1, 2017-December 31, 2018

Clinical History: A 57-year-old woman with a past medical history remarkable only for hyperlipidemia undergoing statin therapy presented with a history of slowly progressive dyspnea on exertion for at least months, possibly longer. The patient denied cough, hemoptysis, and chest pain.

Physical examination was largely unremarkable and the patient’s oxygen saturation was 96% on room air while resting. The patient’s vital signs were within normal limits.

Laboratory evaluation was unremarkable. Quantiferon testing for Mycobacterium tuberculosis was negative, and testing for coccidioidomycosis was unrevealing.

Frontal and lateral chest radiography (Figure 1) was performed.

Figure 1. Frontal chest radiography.

Which of the following statements regarding the chest radiograph is most accurate? (Click on the correct answer to proceed to the second of nine pages)

1. The chest radiograph appears normal
2. The chest radiograph shows bilateral, symmetric lower lobe reticulation suggesting fibrotic disease
3. The chest radiograph shows left upper lobe collapse
4. The chest radiograph shows linear right lower lobe opacity suggesting scarring
5. The chest radiograph shows numerous small miliary nodules

Cite as: Gotway MB. December 2017 imaging case of the month. Southwest J Pulm Crit Care. 2017;15(6):2563-66. doi: https://doi.org/10.13175/swjpcc149-17 PDF

Medical Image of the Week: Yellow Nail Syndrome

Figure 1. Photographs showing the patient’s discolored, yellowish nails.

Figure 2. Representative images from the thoracic CT scan in lung windows showing bronchiectasis most marked in the left upper lobe.

A 67-year-old woman with a previous history of yellow nail syndrome presented with a long history of cough, increased sputum production, recurrent swelling in her lower extremities and recurrent respiratory infections. Physical examination revealed non-pitting edema in the lower extremities and discolored nails (Figure 1). A thoracic CT scan showed bronchiectasis in the left upper lobe (Figure 2). She did not have a history of pleural effusions or chronic sinusitis.

Yellow nail syndrome is very rare disorder associating yellow nail discoloration, bronchiectasis and lymphedema (1). Other frequent manifestations include sinusitis and recurrent pleural effusions. The disease is most frequently isolated but may be associated with other diseases implicating the lymphatic system, autoimmune diseases or cancers. The symptoms result from lymphatic impairment but the cause of the impairment is unknown. Treatment is symptomatic for each component. Vitamin E, combined with fluconazole, is usually prescribed to treat yellow nails and achieves a partial or complete response. Spontaneous resolution is also possible. Although prognosis is usually considered to be good, a Kaplan–Meier survival curve estimated median survival at 132 months, shorter than that of a paired-control population (2).

Lewis J. Wesselius MD

Departments of Pulmonary Medicine

Mayo Clinic Arizona

Scottsdale, AZ USA

References

1. Vignes S, Baran R. Yellow nail syndrome: a review. Orphanet J Rare Dis. 2017 Feb 27;12(1):42. [CrossRef] [PubMed]
2. Maldonado F, Tazelaar HD, Wang CW, Ryu JH. Yellow nail syndrome: analysis of 41 consecutive patients. Chest. 2008;134:375–81. [CrossRef] [PubMed]

Cite as: Wesselius LJ. Medical image of the week: yellow nail syndrome. Southwest J Pulm Crit Care. 2017;15(4):230-1. doi: https://doi.org/10.13175/swjpcc142-17 PDF 

Medical Image of the Week: Moyamoya Disease

Figure 1. Cerebral angiogram of the brain demonstrating bilateral high-grade stenosis of the anterior and middle cerebral arteries, worse on the left.

Figure 2. Magnetic resonance imaging showing multiple punctate infarcts in the frontal and parietal lobes on the left side.

A 52-year-old, right-handed, Caucasian woman with a history of hypertension and morbid obesity presented with acute onset of word-finding difficulty and slurred speech. Her medical and family history was negative for cerebral vascular event, coronary artery disease or smoking. Computed tomography of the patient's brain showed narrow caliber middle cerebral artery vasculature bilaterally. This abnormal finding prompted further investigation with cerebral angiogram. The angiogram showed bilateral high-grade stenosis of the anterior and middle cerebral arteries, worse on the left (Figure 1). Magnetic resonance imaging revealed multiple left sided punctate infarcts in the frontal and parietal lobes (Figure 2). Diagnosis of ischemic stroke secondary to moyamoya disease was established. This patient was not a candidate for fibrinolytic therapy since it had been more than 4 hours from initial presentation. She was treated with aspirin, clopidogrel, and atorvastatin for secondary prevention of ischemic stroke. Two months after her discharge date, the patient had a middle cerebral artery to superior temporal artery bypass on the left side, followed by a middle cerebral artery to superior temporal artery bypass on the right two months after initial bypass. Patient progressed to an uneventful recovery. Discharge planning included the continuation of aspirin, clopidogrel, and atorvastatin indefinitely.

Moyamoya disease (MMD) is an uncommon vasculopathy of unknown origin associated with diverse risk factors (1). It was first discovered in a Japanese population, and reported more commonly in this sub-population. However, numerous cases were reported across the globe (2). Moyamoya disease associated with other systemic condition such as neurofibromatosis type 1, trisomy 21, thyroid cranial irradiation or thyroid disease is termed moyamoya syndrome (MMS) (1,2). Moyamoya syndrome is a cerebrovasculopathy originating from collateral flow that develops secondary to occlusion of the internal carotid artery and the proximal afferent vessels at the circle of Willis (3). MMS can have abrupt or insidious onset and may progress to diversifying cerebral ischemic stroke or to intracranial hemorrhage, which is a worse prognosis and the primary cause of death in patients with MMD (4). It has been shown that ischemic stroke associated with MDD or MMS usually occurs when compensatory collateral vessels are unable to supply sufficient blood to the brain after occlusion or stenosis of the internal carotid arteries or its tributary vessels (5,6). On the other hand, intracranial hemorrhage occurs secondary to the rupture of abnormal moyamoya vessels (7,8).

It is imperative to differentiate between non-hemorrhagic and hemorrhagic moyamoya. Neuroimaging is the preferred method of diagnosis after high clinical suspicion of MMD or MMS. Intracranial hemorrhage and cerebral infarction can be diagnosed with computed tomography and magnetic resonance imaging/ cerebral angiogram, respectively (8,9). Recent use of magnetic resonance perfusion imaging has been shown to be crucial in diagnostics and medical-surgical decision making. There is no common consensus when it comes to treatment of moyamoya at this time. Initial management is symptomatic with anticoagulants, antiplatelet and corticosteroids (10). Treatment options may also include direct or indirect surgical revascularization as optimal therapy (11,12).

Stella Pak MD, Kokou Adompreh-Fia MD, Damian Valencia MD, Adam Fershko MD, and Jody Short DO.

Department of Medicine

Kettering Medical Center

Kettering, OH USA

References

1. Phi JH, Wang KC, Lee JY, Kim SK. Moyamoya Syndrome: A window of moyamoya disease. J Korean Neurosurg Soc. 2015 Jun;57(6):408-14. [CrossRef] [PubMed]
2. Suzuki J, Takaku A. Cerebrovascular "moyamoya" disease. Disease showing abnormal net-like vessels in base of brain. Arch Neurol. 1969 Mar;20(3):288-99. [CrossRef] [PubMed]
3. Yamamoto, S, Koh M, Kashiwazaki D, Akioka N, Kuwayama N, Noguchi K, Kuroda S. Is Quasi-moyamoya disease a uniform disease entity? A three-dimensional constructive interference in steady state imaging study. J Stroke Cerebrovasc Dis. 2016 Jun;25(6):1509-16. [CrossRef] [PubMed]
4. Baba, T., Houkin, K. Kuroda. Novel epidemiological features of moyamoya disease. J Neurol Neurosurg Psychiatry. 2008 Aug;79(8):900-4. [CrossRef] [PubMed]
5. Miyamoto S, Kikuchi H, Karasawa J, Nagata I, Ihara I, Yamagata S. Study of the posterior circulation in moyamoya disease. Part 2: Visual disturbances and surgical treatment. J Neurosurg. 1986 Oct;65(4):454-60. [CrossRef] [PubMed]
6. Kuroda S, Ishikawa T, Houkin K, Iwasaki Y. Clinical significance of posterior cerebral artery stenosis/occlusion in moyamoya disease. No Shinkei Geka. 2002 Dec;30(12):1295-300. [PubMed]
7. Kang K, Lu J, Zhang D, Li Y, Wang D, Liu P, Li B, Ju Y, Zhao X. Difference in cerebral circulation time between subtypes of moyamoya disease and moyamoya syndrome. Sci Rep. 2017;7(1):2587. [CrossRef] [PubMed]
8. Lui, P, Han C, Li DS, Lv XL, Li YX, Duan L. Hemorrhagic moyamoya disease in children: Clinical, angiographic features, and long-term surgical outcome. Stroke. 2016 Jan;47(1):240-3. [CrossRef] [PubMed]
9. Kellner CP, McDowell MM, Phan MQ, Connolly ES, Lavine SD, Meyers PM, Sahlein D, Solomon RA, Feldstein NA, Anderson RC. Number and location of draining veins in pediatric arteriovenous malformations: association with hemorrhage. J Neurosurg Pediatr. 2014 Nov;14(5):538-45. [CrossRef] [PubMed]
10. Whitaker J. Management of moyamoya syndrome [comment]. Arch Neurol. 2001;58:132. [CrossRef] [PubMed]
11. Golby AJ, Marks MP, Thompson RC, Steinberg GK. Direct and combined revascularization in pediatric moyamoya disease. Neurosurg. 1999;45:50-8. [PubMed]
12. Mizoi K, Kayama T, Yoshimoto T, Nagamine Y. Indirect revascularization for moyamoya disease: is there a beneficial effect for adult patients? Surg Neurol. 1996;45:541-8. [CrossRef] [PubMed] 

Cite as: Pak S, Adompreh-Fia K, Valencia D, Fershko A, Short J. Medical image of the week: moyamoya disease. Southwest J Pulm Crit Care. 2017;15(5):227-9. doi: https://doi.org/10.13175/swjpcc136-17 PDF

Medical Image of the Week: Lemierre Syndrome

Figure 1. CT scan of chest (axial image) demonstrating peripheral cavitating lesion (arrow) with multifocal ground glass opacities and bilateral pleural effusions.

Figure 2. CT scan of neck, soft tissue (coronal [A], axial [B] image) demonstrating a partially occlusive thrombus in the left internal jugular vein (coronal red arrows, axial green arrow).

A previously healthy 18-year-old girl was evaluated at an urgent care center for a three day history of sore throat, fever, nausea, vomiting, diarrhea, and myalgias; the diagnosis of influenza was made at that time. Four days later, she presented to our Emergency Department with sore throat, left sided neck pain and swelling, productive cough, fever, worsening dyspnea, and pleuritic chest pain. On examination her temperature was 36.9 °C, heart rate was 142 beats per minute, and respiratory rate was 18 breaths per minute. She had enlarged tonsils without exudates, cervical and submandibular lymphadenopathy, and tenderness of her left lateral neck. Lung examination showed increased work of breathing with decreased breath sounds at the bases. Laboratory evaluation revealed an elevated white count (17,000 cells/µL) with 91% neutrophils, elevated blood urea nitrogen (21 mg/dL), creatinine (1.6 mg/dL), and venous lactate (4.0 mMol/L). Initial chest radiograph showed no evidence for acute cardiopulmonary process.  She was admitted, blood cultures were drawn, and treatment for sepsis with vancomycin, xeftriaxone, and azithromycin was initiated. Subsequent chest radiograph demonstrated an ill-defined airspace opacification in the right lower lobe.

Computed tomographic (CT) imaging of the chest showed multifocal ground glass opacities and areas of consolidation with cavitation, consistent with septic embolic disease (Figure 1). Blood cultures grew Streptococcus anginosus and Fusobacterium necrophorum. CT imaging of the neck showed a partially occlusive thrombus in the left internal jugular vein (Figure 2).  The diagnosis of Lemierre’s syndrome was made. The patient required chest tube drainage for bilateral empyema and was treated with 3 weeks of ampicillin followed by 3 weeks of high dose amoxicillin-clavulanate; she recovered completely.

Lemierre's syndrome, or anaerobic postanginal sepsis, was first described by Andre Lemierre in 1936. It is characterized by thrombophlebitis of the internal jugular vein and bacteremia caused by organisms of the normal oropharyngeal bacterial flora, classically Fusobacterium necrophorum. Lemierre’s syndrome is most commonly preceded by pharyngitis or tonsillitis, but can also be associated with odontogenic infections or otitis media. The primary infection progresses from the oropharynx and invades the lateral pharyngeal space, eventually leading to thrombophlebitis of the internal jugular vein. A majority of patients develop septic emboli, as seen in our patient, with the lungs and large joints being the most common sites of metastasis. Lemierre’s syndrome predominantly affects previously healthy children, adolescents, and young adults with most cases presenting in the second decade of life. Common physical findings include severe pharyngitis, cough/hemoptysis, dyspnea, and tenderness and swelling over the internal jugular vein. Diagnosis is confirmed by the presence of thrombophlebitis of the internal jugular vein and anaerobic organisms such as F. necrophorum in the bloodstream.

Elisa Phillips BA, BS*, Ziad Shehab MD**, and Daniela Lax MD***

*The University of Arizona College of Medicine; **Department of Pediatrics, Division of Infectious Disease; and ***Banner – University Medical Group, Pediatric Cardiology

University of Arizona

Tucson, AZ USA

References

1. Bliss SJ, Flanders SA, Saint S. Clinical problem-solving. A pain in the neck. N Engl J Med. 2004 Mar 4;350(10):1037-42. [CrossRef] [PubMed]
2. Kuppalli K, Livorsi D, Talati NJ, Osborn M. Lemierre's syndrome due to Fusobacterium necrophorum. Lancet Infect Dis. 2012 Oct;12(10):808-15. [CrossRef] [PubMed]
3. Eilbert W, Singla N. Lemierre's syndrome. Int J Emerg Med. 2013 Oct 23;6(1):40. [CrossRef] [PubMed]

Cite as: Phillips E, Shehab Z, Lax D. Medical image of the week: Lemierre syndrome. Southwest J Pulm Crit Care. 2017;15(5):223-4. doi: https://doi.org/10.13175/swjpcc135-17 PDF 

Medical Image of the Week: Chemotherapy-Induced Diffuse Alveolar Hemorrhage

Figure 1. Panel A: Chest X-ray on admission consistent showing some pulmonary edema and effusions at the bases. Panel B: Chest X-ray after initiation of chemotherapy showing diffuse bilateral infiltrates and consolidation.

Figure 2. CT scan of the chest after initiation of chemotherapy showing patchy ground glass consolidation throughout the lung fields bilaterally. Large bilateral pleural effusions can also be seen.

A 65-year-old man presented with relapse of his acute myeloid leukemia (AML). On admission he was seen to have a reduced ejection fraction at 40-50%. His chest X-ray showing pulmonary edema and bilateral pleural effusions (Figure 1A). He was diuresed to his dry weight to improve his clinical status. The decision was made to re-induce him for his AML with fludarabine and cytarabine without idarubicin (due to his reduced ejection fraction). After 2 doses of each the fludarabine and cytarabine the patient showed worsening respiratory distress, had increasing oxygen requirements and started having hemoptysis. Repeat imaging of his chest showed bilateral infiltrates in his lungs on both chest x-ray (Figure 1B) and chest CT (Figure 2). Infectious causes for the changes were sought and ruled out. He was transferred to the ICU where he was put on high flow oxygen and received methylprednisolone 1000 mg IV daily for 3 days. During this period his blood hemoglobin also dropped from 8.2 g/dl to 6.8 g/dl requiring transfusion of 1 unit of packed red blood cells. After 3 days of supportive care he was transferred back out of the ICU on oxygen by nasal cannula with progressive improvement in his lung function. Pulmonary toxicity is a known side effect resulting from both fludarabine and cytarabine and can present in a variety of forms. Their prompt recognition is important due to the steroid responsive nature of many of these once infectious causes have been ruled out.

Saud Khan, MD and Huzaifa A. Jaliawala, MD

Department of Internal Medicine

University of Oklahoma Health Sciences Center

Oklahoma City, OK USA

References

1. Helman DL Jr, Byrd JC, Ales NC, Shorr AF. Fludarabine-related pulmonary toxicity: a distinct clinical entity in chronic lymphoproliferative syndromes. Chest. 2002 Sep;122(3):785-90. [CrossRef] [PubMed]
2. Rudzianskiene M, Griniute R, Juozaityte E, Inciura A, Rudzianskas V, Emilia Kiavialaitis G. Corticosteroid-responsive pulmonary toxicity associated with fludarabine monophosphate: a case report. Turk J Haematol. 2012 Dec;29(4):392-6. [CrossRef] [PubMed]
3. Forghieri F, Luppi M, Morselli M, Potenza L.Cytarabine-related lung infiltrates on high resolution computerized tomography: a possible complication with benign outcome in leukemic patients. Haematologica. 2007 Sep;92(9):e85-90. [CrossRef] [PubMed]

Cite as: Khan S, Jaliawala HA. Medical image of the week: chemotherapy-induced diffuse alveolar hemorrhage. Southwest J Pulm Crit Care. 2017;15(5):219-20. doi: https://doi.org/10.13175/swjpcc131-17 PDF

November 2017 Imaging Case of the Month

Michael B. Gotway, MD¹

Isabel Mira-Avendano, MD²

¹Mayo Clinic Arizona, Scottsdale AZ USA

²Mayo Clinic Jacksonville, FL USA

Clinical History: A 70-year-old white woman with a remote history of smoking and mild gastroesophageal reflux disease presented with complaints of a dry cough and shortness of breath, present for some time but worsening over the previous 8 months. No hemoptysis was noted and the patient did not complain of chest pain. No history of syncope was noted.

Physical examination was largely unremarkable and the patient’s oxygen saturation was 86% on room air, 90% on 4 L/m by mask. The patient’s vital signs were within normal limits.

Laboratory evaluation was unremarkable.  Quantiferon testing for Mycobacterium tuberculosis was negative, and testing for coccidioidomycosis was unrevealing. Enhanced thoracic CT (Figure 1) was performed.

Figure 1. Panels A-D: Representative static images from the thoracic CT scan in lung windows. Lower panel: Video of thoracic CT scan in lung windows.

Which of the following statements regarding the thoracic CT is most accurate? (Click on the correct answer to proceed to the second of eight pages)

1. The thoracic CT shows advanced destructive emphysema
2. The thoracic CT shows bilateral, basal and subpleural predominant reticulation associated with ground-glass opacity, architectural distortion, and traction bronchiectasis
3. The thoracic CT shows multifocal lobular consolidation
4. The thoracic CT shows multifocal small pulmonary cysts
5. The thoracic CT shows small cavitary pulmonary nodules

Cite as: Gotway MB, Mira-Avendano I. November 2017 imaging case of the month. Southwest J Pulm Crit Care. 2017;15(5):199-208. doi: https://doi.org/10.13175/swjpcc134-17 PDF

Medical Image of the Week: Erythema Nodosum

Figure 1. Panel A: photograph of legs at initial presentation. Panel B: 2 weeks later.

A healthy 43-year-old woman presented to the emergency room with one day of diarrhea, vomiting and severe left-sided pleuritic chest pain. Chest radiography revealed an infiltrate in the left lower lobe with a small pleural effusion. White count was 14,000 cells/mcL. Eosinophil count was 2%. She was thought to have pneumonia and treated with azithromycin.

Two weeks later she returned to the emergency room with painful raised erythematous lesions on both lower extremities and generalized joint pain. A thoracic CT scan was performed showing left lower lobe pneumonia and small bilateral pleural effusions. Eosinophilia was 14%. She was diagnosed again as having pneumonia. There was no diagnosis made of the skin lesions. A cocci serology was drawn and sent to Davis California. She was given doxycycline.

Subsequently the cocci serology was found to be positive for IgG and IgM and negative for complement fixation antibodies. She was seen by her primary care physician who diagnosed acute coccidioidomycosis and started her on Diflucan 200 mg daily and referred her for consultation. At her first visit 6 weeks into her illness she was still complaining of arthralgias, fatigue and cough.

Physical examination was negative except for innumerable red raised lesions on her thighs and anterior surfaces of her legs with confluence at the ankles (Figure 1). One month after her initial visit her legs were much improved although there was some peeling of the skin and residual erythema of the lower extremities (Figure 2).

Erythema Nodosum (EN) is a panniculitis of subcutaneous fat which can be associated with a variety of conditions including streptococcal pharyngitis, tuberculosis, sarcoidosis, inflammatory bowel disease, cancer, or bacterial infections (1). The usual presentation of this disease is the presence of painful raised erythematous nodules symmetrically on the anterior surfaces of the lower extremities. These lesions do not represent sites of infection but are most likely a result of type IV delayed hypersensitivity.

EN was first described as a benign form of coccidioidomycosis in 1936, and was further characterized by Charles Smith in 1940 when he described acute coccidioidomycosis as an illness characterized by an “influenza like initial phase followed in 2 to 18 days by the eruptive phase of erythema nodosum lasting from six days to three weeks with pigmented areas lasting for months” (2). He noted that recovery was invariable. This was in a time where the frequent presentation of acute coccidioidomycosis as an inapparent infection was not known and the mortality of acute cocci was as high as 50%. Twenty years later, Smith and Pappagiannis made the observation that EN was 2 to 10 times more frequent in females than males (3). Braverman (4) in 1999 observed the protective effect of EN by reporting on 60 pregnant women with coccidioidomycosis. Thirty of these women with EN had no dissemination, and of the 30 without EN, 11 disseminated and one died. The mechanism of this protective effect has yet to be characterized.

Physicians living in the Southwest have learned that “the bumps” (EN), desert rheumatism (polyarthralgia), eosinophilia associated with a flulike illness, and acute knifelike pleuritic chest pain in an otherwise healthy person are all signs and symptoms which lead to a rapid diagnosis of coccidioidomycosis (5). Because of the time sequence of the appearance of EN in this illness this rash is often felt incorrectly to be an allergic reaction to antibiotics given for the previously diagnosed pneumonia. Even though EN is associated with many varied conditions, its presence in the Southwestern United States should lead the physician to consider coccidioidomycosis as the most likely diagnosis.

Gerald F. Schwartzberg, MD

HonorHealth Pulmonology

Phoenix, AZ USA

References

1. Blake T, Manahan M, Rodins K. Erythema nodosum - a review of an uncommon panniculitis. Dermatol Online J. 2014 Apr 16;20(4):22376. [PubMed]
2. Smith CE. Epidemiology of acute coccidioidomycosis with erythema nodosum ("San Joaquin" or "Valley Fever"). Am J Public Health Nations Health. 1940 Jun;30(6):600-11. [CrossRef] [PubMed]
3. Smith CE, Pappagianis D, Levine HB, Saito M. Human coccidioidomycosis. Bacteriol Rev. 1961 Sep;25:310-20. [PubMed]
4. Braverman IM. Protective effects of erythema nodosum in coccidioidomycosis. Lancet. 1999 Jan 16;353(9148):168. [CrossRef] [PubMed]
5. Stevens DA. Coccidioidomycosis. N Engl J Med. 1995 Apr 20;332(16):1077-82. [CrossRef] [PubMed]

Addendum: Another Erythema Nodosum

Figure 2. Another case of erythema nodosum.

While the above article was “in press”, another case of EN came into the office (Figure 2). Her history was similar to the first patient. Uncle Jun, the patriarch in the “Sopranos,” said in his heavy New York accent, “They come in threes.” Based on Uncle Jun, I am anticipating seeing another case of EN this week.

Gerald F. Schwartzberg, MD

HonorHealth Pulmonology

Phoenix, AZ USA

Cite as: Schwartzberg GF. Medical image of the week: erythema nodosum. Southwest J Pulm Crit Care. 2017;15(4):188-90. doi: https://doi.org/10.13175/swjpcc126-17 PDF 

Medical Image of the Week: Pulmonary Mycetoma

Figure 1. Thoracic CT scan showing mycetoma (arrow) in cavitary lesion in right upper lobe.

A 59 year-old woman presented with right sided chest pain and worsening shortness of breath. On CT of the chest she was found to have cavitary lesions in her right lung with one of them having a distinct opacity within the lesion concerning for a pulmonary mycetoma (Figure 1, arrow). Most literature describes pulmonary mycetomas occurring due to Aspergillus species. However, in our patient, neither the bronchoscopy with bronchoalveolar lavage (BAL) nor serological studies tested positive for Aspergillus. Cultures did however grow Candida albicans in 2 of the samples from the BAL. Mycetoma due to Candida has been described in the urinary tract in immunocompromised patients and, uncommonly, in the lung (1-3). Our patient had been treated for Stage III ovarian cancer with chemotherapy and at presentation her absolute neutrophil count was reduced at 860. In the hospital, she was treated for her shortness of breath with albuterol-ipratropium nebulizations to which she responded well. She was discharged once stable to follow up as outpatient for further treatment of her Candida albicans mycetoma.

Saud Khan, MD and Huzaifa A. Jaliawala, MD

Internal Medicine

University of Oklahoma Health Sciences Center

Oklahoma City, OK USA

References

1. Praz V, Burruni R, Meid F, Wisard M, Jichlinski P, Tawadros T. Fungus ball in the urinary tract: A rare entity. Can Urol Assoc J. 2014 Jan-Feb;8(1-2):E118-20. [CrossRef] [PubMed]
2. Song Z, Papanicolaou N, Dean S, Bing Z. Localized candidiasis in kidney presented as a mass mimicking renal cell carcinoma. Case Rep Infect Dis. 2012;2012:953590. [CrossRef] [PubMed]
3. Bachh AA, Haq I, Gupta R, Varudkar H, Ram MB. Pulmonary candidiasis presenting as mycetoma. Lung India. 2008 Oct;25(4):165-7. [CrossRef] [PubMed]

Cite as: Khan S, Jaliawala HA. Medical image of the week: pulmonary mycetoma. Southwest J Pulm Crit Care. 2017;15(4):169-70. doi: https://doi.org/10.13175/swjpcc123-17 PDF

Medical Image of the Week: Pulmonary Infarction- the “Reverse Halo Sign”

Figure 1. CT Chest with contrast. Two different levels in the same patient displayed on mediastinal windows. Several triangular shaped subpleural lesions with annular peripheral solid appearance are depicted, better characterized in the lung windows below (yellow arrows). Note the partial filling defect (red arrow on B), indicating a non-occlusive thrombus(arrow). Bilateral pleural effusions are also identified.

Figure 2. CT Chest with contrast, lung window corresponding to the levels in Figure 1 above. Note the triangular shaped subpleural lesions with peripheral solid appearance and ground glass center, characteristic of the atoll sign (arrows). As above, bilateral pleural effusions are present.

Pulmonary infarction is a known complication of pulmonary embolism (PE), a common disorder that results in 100,000-200,000 deaths annually in the United States. Computed tomography (CT) is the first-line modality to assess the pulmonary circulation with the ability to directly the visualize pulmonary emboli as well as pleuro-parenchymal abnormalities.

The appearance of a pulmonary infarct varies depending on the degree of ischemic injury in the setting of a dual blood supply to the lung. Infarcts occur more commonly in the periphery of the lung, given, the alternate blood supply by the bronchial arteries, is not as efficient as it is centrally. This location is also favored by the more common occurrence after occlusion of small peripheral arteries of 3 mm or less in caliber.

On CT lung infarcts can take the can take the “reverse halo” sign, also known as the “atoll” sign configuration, representing a focal area of decreased enhancement, and surrounding solid appearance. In the case of lung infarcts, the lesions typically have a broad pleural base triangular form with apex toward the hilum (1). Pathologically this corresponds to a hemorrhagic consolidation. The center of the lesion appears to correspond to aerated non-infarcted lung coexisting side by side with infarcted lung in the same lobule. The broad-based configuration is explained by the fan shaped distribution of the arteries as they extend out into the periphery. The convex border reflects the extravasated blood within the infarcted lung. Once the hemorrhage reabsorbs, the infarct heals completely or may leave behind a linear band of scarring.

From the imaging stand point, the reverse halo sign initially described in cryptogenic organizing pneumonia, has also been noted in patients with fungal disease, granulomatosis with polyangiitis, sarcoidosis and neoplastic disease among others (2).

George R Wu MS IV¹, Berndt Schmit MD², Veronica Arteaga MD², and Diana Palacio MD²

¹Arizona College of Osteopathic Medicine, Midwestern University, Glendale, AZ USA

²Division of Thoracic Imaging, University of Arizona, Tucson, AZ USA

References

1. He H, Stein MW, Zalta B, Haramati LB. Pulmonary infarction: spectrum of findings on multidetector helical CT. J Thorac Imaging. 2006;21(1):1-7. [CrossRef] [PubMed]
2. Godoy MC, Viswanathan C, Marchiori E, et al. The reversed halo sign: update and differential diagnosis. Br J Radiol. 2012;85(1017):1226-35. [CrossRef] [PubMed]

Cite as: Wu GR, Schmit B, Arteaga V, Palacio D. Medical image of the week: pulmonary infarction- the “reverse halo sign”. Southwest J Pulm Crit Care. 2017;15(4):162-3. doi: https://doi.org/10.13175/swjpcc124-17 PDF 

Medical Image of the Week: Pulmonary Artery Sling

Figure 1. Computerized tomography (CT) of the chest showing the aberrant origin of the left pulmonary artery from the right pulmonary artery creating a pulmonary artery sling with mild tracheal narrowing (arrow).

Figure 2. Cardiac magnetic resonance imaging (MRI) confirming the presence of a pulmonary artery sling with aberrant origin of the left pulmonary artery from the right pulmonary artery.

A 42-year-old year woman with asthma was admitted to the hospital with an asthma exacerbation. The patient complained of dyspnea on exertion, two-pillow orthopnea and bipedal edema. An echocardiogram showed a severely dilated right ventricle (RV) with elevated right ventricular systolic pressure of 71 mmHg. The systolic left ventricular (LV) function was also reduced with an ejection fraction of 45%. Computerized tomography (CT) of the chest showed an aberrant origin of the left pulmonary artery (PA) creating a pulmonary artery sling with mild tracheal narrowing (Figure 1, arrow). Cardiac magnetic resonance imaging (MRI) confirmed the presence of a pulmonary artery sling with the aberrant origin of the left PA from the right PA (Figure 2). Cardiac catheterization showed a mean PA pressure of 46mmHg with LV end diastolic pressure of 12mm Hg. The patient was diagnosed with WHO Group I pulmonary hypertension and started on treatment with sildenafil with a stable outpatient course.

Pulmonary artery sling is an uncommon form of vascular ring. The anomaly is a result of formation of the left PA from the right sixth vascular arch (rather than the left), leading to the left PA arising from the posterior aspect of the right PA (1). Pulmonary artery slings may produce symptoms of airway compression and esophageal compression and usually presents in childhood (2). In asymptomatic cases, a PA sling may mimic a mediastinal mass on chest radiographs and CT and MRI may be used to establish the diagnosis (3).

Abhinav Agrawal MD¹, Stuart L Cohen MD², Rakesh Shah MD², Arunabh Talwar MD FCCP¹

¹Division of Pulmonary, Critical Care & Sleep Medicine, Department of Medicine

²Division of Thoracic Radiology, Department of Radiology

Hofstra-Northwell School of Medicine

New Hyde Park, NY USA

References

1. Casta-er E, Gallardo X, Rimola J, Pallardó Y, Mata JM, Perendreu J, Martin C, Gil D. Congenital and acquired pulmonary artery anomalies in the adult: radiologic overview. Radiographics. 2006 Mar-Apr;26(2):349-71. [CrossRef] [PubMed]
2. Odell DD, Gangadharan SP, Majid A. Pulmonary artery sling: a rare cause of tracheomalacia in the adult. J Bronchology Interv Pulmonol. 2011 Jul;18(3):278-80. [CrossRef] [PubMed]
3. Ganesh V, Hoey ET, Gopalan D. Pulmonary artery sling: an unexpected finding on cardiac multidetector CT. Postgrad Med J. 2009 Mar;85(1001):128. [CrossRef] [PubMed] 

Cite as: Agrawal A, Cohen SL, Shah R, Talwar A. Medical image of the week: pulmonary artery sling. Southwest J Pulm Crit Care. 2017;15:160-61. doi: https://doi.org/10.13175/swjpcc116-17 PDF

Medical Image of the Week: Hypertensive Emergencies

Figure 1. Head CT scan showing basal ganglia hemorrhage (red arrow) and posterior reversible encephalopathy syndrome (green arrows).

A 39-year-old man had sudden onset of left sided hemiparesis, headache and nausea. He had a history of untreated hypertension and diabetes mellitus. On initial evaluation by emergency medical services, his blood pressure was 270/170 mm Hg. Shortly after admission, he suffered a generalized seizure treated with levetiracetam. His labs were remarkable for a creatinine of 4.4 mg/dL and microscopic hematuria. His head CT findings are consistent with two simultaneous neurological hypertensive emergencies – intracranial hemorrhage of the basal ganglia and posterior reversible encephalopathy syndrome (PRES) (Figure 1) (1). PRES is areas of edema seen as multiple cortico-subcortical areas of hyperintense (white) signal involving the occipital and parietal lobes bilaterally and pons. His renal failure likely represents a third hypertensive emergency. His blood pressure was lowered into the 140/90 range within 2 hours by nicardipine infusion and intravenous labetalol boluses. He subsequently suffered worsening mental status and unilateral pupillary dilation and underwent emergent craniotomy. He survived but is currently past 50 days in the hospital.

Robert A. Raschke MD

Critical Care Medicine

Banner University Medical Center at Phoenix

Phoenix, AZ USA

Reference

1. Vaughan CJ, Delanty N. Hypertensive emergencies. Lancet. 2000 Jul 29;356(9227):411-7. [CrossRef] [PubMed]

Cite as: Raschke RA. Medical image of the week: hypertensive emergencies. Southwest J Pulm Crit Care. 2017;15(4):147. doi: https://doi.org/10.13175/swjpcc111-17 PDF

October 2017 Imaging Case of the Month

Paul J. Conomos, MD¹

Michael B. Gotway, MD²

¹Arizona Pulmonary Specialists

Phoenix, AZ USA

²Mayo Clinic Arizona

Scottsdale, AZ USA

Clinical History: An 18-year-old man with no known previous medical history presented with complaints of intermittent cough persisting several months. No hemoptysis was noted.

Physical examination was largely unremarkable and the patient’s oxygen saturation was 99% on room air. The patient’s vital signs were within normal limits.

Laboratory evaluation was unremarkable.  Quantiferon testing for Mycobacterium tuberculosis was negative, and testing for coccidioidomycosis was unrevealing. Frontal and lateral chest radiography (Figure 1) was performed.

Figure 1. Figure 1. Frontal (A) and lateral (B) chest radiography.

Which of the following statements regarding the chest radiograph is most accurate? (Click on the correct answer to proceed to the second of eight pages)

1. The chest radiograph shows asymmetric reticulation and interlobular septal thickening
2. The chest radiograph shows bilateral reticulation associated with decreased lung volumes
3. The chest radiograph shows focal consolidation
4. The chest radiograph shows large lung volumes
5. The chest radiograph shows small cavitary pulmonary nodules

Cite as: Conomos PJ, Gotway MB. October 2017 imaging case of the month. Southwest J Pulm Crit Care. 2017;15(4):138-46. doi: https://doi.org/10.13175/swjpcc119-17 PDF

Medical Image of the Week: Typical Pulmonary CT Findings Following Radiotherapy

Figure 1. Panel A: CT chest, lung windows, demonstrating a spiculated nodule, biopsy proven adenocarcinoma in the right lower lobe (arrow). Panel B: Eight months post stereotactic radiation therapy, there has been development of focal consolidation, with air bronchograms, involving the right middle and lower lobes. Notice the volumetric appearance. The primary malignancy is no longer identified as such. Panel C: Thirteen months later the consolidation has evolved into an area of volume loss, containing bronchiectasis, and sharp contours as a result of organized fibrosis.

Radiation-induced lung disease (RILD) commonly develops in patients treated with radiation for intrathoracic and chest wall malignancies.

There are two distinct radiographic patterns:

1. Radiation pneumonitis which occurs within 4-12 weeks after completion of therapy, and is characterized by development ground-glass opacities and/or consolidation in and around the treated lesion. A somewhat nodular or patchy appearance may occur. Typically, the affected tissue conforms to the radiation ports and may cross fissures/lobes. There may be milder similar changes in the contralateral lung.
2. A chronic phase, known as radiation fibrosis, is noticeable about 6-12 months post treatment and may progress up to 2 years, after which the findings tend to stabilize. In this stage, the areas of consolidation undergo volume loss, architectural distortion and may contain traction bronchiectasis. Linear and band scarring may also be seen. In this phase, sharper demarcation between normal and irradiated lung parenchyma is commonly seen.

Special attention to the typical radiological characteristics and timeline, in most cases allows to distinguish RILD from potential superimposed infection, subacute inflammatory diseases, locally recurrent neoplasm and radiation-induced neoplasms.

Andrew Erickson MS IV¹, Berndt Schmidt MD², Veronica Arteaga MD², Diana Palacio MD²

¹Midwestern University – Arizona College of Osteopathic Medicine

²Division of Thoracic Radiology, Department of Medical Imaging. University of Arizona, Tucson (AZ)

Reference

1. Choi YW, Munden RF, Erasmus JJ, Joo Park K, Chung WK, Jeon SC, Park CK. Effects of radiation therapy on the lung: radiologic appearances and differential diagnosis. Radiographics. 2004 Jul;24(4):985-97. [CrossRef] [PubMed]

Cite as: Erickson A, Schmidt B, Arteaga V, Palacio D. Medical image of the week: typical pulmonary CT findings following radiotherapy. Southwest J Pulm Crit Care. 2017;15(3):120-1. doi: https://doi.org/10.13175/swjpcc112-17 PDF

Medical Image of the Week: Pembrolizumab-induced Pneumonitis

Figure 1. Thoracic CT showing multifocal, bilateral extensive lung opacities consistent with consolidation with a striking peribronchovascular distribution. Note the opacities are primarily distributed along the airways. Peripheral lung opacity, both ground-glass opacity and consolidation, is also present.

Figure 2. Axial thoracic CT performed several months after Figure 1 following discontinuation of the pembrolizumab and initiation, and subsequent tapering, of corticosteroid therapy, shows significant regression in the previously noted extensive peribronchovascular consolidation. Residual areas of consolidation and ground-glass opacity associated with architectural distortion are consistent with scarring.

A 76-year-old man with metastatic melanoma, undergoing treatment with pembrolizumab, an antibody against programmed cell death 1 (PD-1), beginning 8 months ago developed low-grade fever, non-productive cough, and shortness of breath. A thoracic CT scan showed multifocal, bilateral extensive lung opacities (Figure 1). The patient underwent bronchoscopy with bronchoalveolar lavage which showed non-specific inflammatory changes associated with foci of organizing pneumonia. Microbiologic studies, including Coccioides antibody enzyme immunoassay and Aspergillus antigen, were negative.

The patient was begun on corticosteroid therapy for presumed medication-induced pulmonary injury, manifestation as an organizing pneumonia pattern, due to pembrolizumab. Over the ensuing months, his symptoms abated and his CT scan abnormalities regressed (Figure 2).

Organizing pneumonia may occur as an idiopathic, primary pulmonary process, often referred to as “cryptogenic organizing pneumonia,” or may occur in the context of a number of systemic conditions, a situation often referred to as secondary organizing pneumonia. Among the various etiologies of secondary organizing pneumonia, medication-induced pulmonary injury is fairly common and when imaging features of organizing pneumonia are seen, careful correlation regarding the possibility of a medication-induced etiology should be undertaken. Recently, three cases of pembrolizumab-induced pneumonitis were described, two being consistent with organizing pneumonia (1).

The thoracic CT findings of organizing pneumonia include peripheral and peribronchovascular consolidation and ground-glass opacity, areas of consolidation surrounding ground-glass opacity (often referred to as the “atoll” or reverse ground-glass halo” sign- see Medical Image of the Week: The Atoll Sign in Cryptogenic Organizing Pneumonia), single and multiple nodules, and perilobular consolidation. The case illustrates a dramatically peribronchovascular distribution of pulmonary consolidation as a manifestation of medication-induced organizing pneumonia.

Michael B. Gotway, MD

Department of Radiology

Mayo Clinic Arizona

Scottsdale, AZ USA

Reference

1. Leroy V, Templier C, Faivre JB, Scherpereel A, Fournier C, Mortier L, Wemeau-Stervinou L. Pembrolizumab-induced pneumonitis. ERJ Open Res. 2017 May 2;3(2). pii: 00081-2016. [CrossRef] [PubMed]

Cite as: Gotway MB. Medical image of the week: pembrolizumab-induced pneumonitis. Southwest J Pulm Crit Care. 2017;15(3):118-9. doi: https://doi.org/10.13175/swjpcc110-17 PDF 

Medical Image of the Week: Asbestos Related Pleural Disease

Figure 1. Chest radiograph demonstrates bilateral coarse calcification, most elongated and vertically oriented in nature (white arrows). Also note coarse calcification outlining the hemidiaphragms (dark arrows). Editor's note: the patient's only chest x-ray was two different AP views which are merged above.

Figure 2.  Holly leaf. Its shape is similar to the irregular thickened nodular edges of pleural plaques on chest radiograph, referred to as “the holly leaf sign”.

Figure 3. Thoracic CT shown in soft tissue (A: top) and lung (B: bottom) windows clearly localizes the calcifications to the parietal pleura.

Pleural plaques are strongly associated with inhalational exposure to asbestos (1). The lesions may take up to thirty years to develop. Plaques are typically bilateral, involve the parietal pleura, commonly along the sixth through ninth ribs and are usually absent at the lung apices and costophrenic sulci (Figures 1 and 3). On chest radiograph, the “holly leaf sign” refers to the shape of the calcifications with thickened rolled and nodular edges (Figure 2). The plaques per se are benign in nature. However, they can potentially impair lung function, resulting in restriction.  They are also markers of the individual’s greater risk of developing a lung cancer or mesothelioma.

Wesley Hunter MS IV¹, Veronica Arteaga MD², and Diana Palacio MD²

¹College of Medicine and ²Department of Medical Imaging

University of Arizona

Tucson, AZ USA

Reference

1. Norbet C, Joseph A, Rossi SS, Bhalla S, Gutierrez FR. Asbestos-related lung disease: a pictorial review. Curr Probl Diagn Radiol. 2015 Jul-Aug;44(4):371-82. [CrossRef] [PubMed] 

Cite as: Hunter W, Arteaga V, Palacio D. Medical image of the week: asbestos related pleural disease. Southwest J Pulm Crit Care. 2017;15(3):116-7. doi: https://doi.org/10.13175/swjpcc104-17 PDF

Medical Image of the Week: Fast-growing Primary Malignant Mediastinal Mixed Germ Cell Tumor

Figure 1. A: Chest radiograph taken 3 months prior to presentation. B: Chest radiograph showing large mediastinal mass (arrows). C: Coronal view of thoracic CT in soft tissue windows showing the large mediastinal mass (arrows). D: Lateral view of thoracic CT showing large mediastinal mass.

A 28-year-old man presented with progressive hemoptysis for two weeks. He had fever, cough, and night sweats for one month prior to admission that was treated as inflenza, bronchitis and/or pneumonia. He had started to experience anorexia, dysphagia, fatigue, a 30-pound weight loss, panic attacks, and the new onset of hypertension during the 3 months prior to admission. He also had intermittent middle chest pain that was aggravated by coughing for 5 months, but a cardiac catherization two months prior failed to show an abnormality. The chest x-ray and CT scan on this admission demonstrated a 15 cm large anterior mediastinal mass exerting a mass effect on the heart and medistial lymphadenopathy (Figure 1-B,C,D) which were absent on a chest x-ray performed 3 months prior to admission (Figure 1A). Core biopsy and immunohistochemical staining revealed a mixed germ cell tumor with components of seminoma and yolk-sac tumor. He was started on chemotherapy, to which he responded well. The malignant mediastinal germ cell tumor in this case is fast-growing and most likely of extragonadal origin. The majority of tumors occ in men between 20 and 35 years (1). The symptoms of these tumor and nonspecific as described in our case, which may lead to a low index of suspicion of malignant tumor with resultant delayed diagnosis.

Yufei Tian, Stella Pak, and Qiang Nai

Department of Medicine

University of Toledo Medical Center

Toledo, Ohio USA

Reference

1. Carter BW, Marom EM, Detterbeck FC. Approaching the patient with an anterior mediastinal mass: a guide for clinicians. J Thorac Oncol. 2014 Sep;9(9 Suppl 2):S102-9. [CrossRef] [PubMed]

Cite as: Tian Y, Pak S, Nai Q. Medical image of the week: fast-growing primary malignant mediastinal mixed germ cell tumor. Southwest J Pulm Crit Care. 2017;15(3):114-5. doi: https://doi.org/10.13175/swjpcc103-17 PDF

September 2017 Imaging Case of the Month

Michael B. Gotway, MD

Department of Radiology

Mayo Clinic Arizona

Scottsdale, Arizona USA 

Clinical History: A 48-year-old woman with no previous medical history presented with complaints of intermittent cough persisting several months following a recent upper respiratory tract infection. No hemoptysis was noted.

Physical examination was largely unremarkable and the patient’s oxygen saturation was 98% on room air. Upon close inspection, the right thorax appeared slightly asymmetrically smaller than the left.

Laboratory evaluation was unremarkable. Quantiferon testing for Mycobacterium tuberculosis was negative, and testing for coccidioidomycosis was unrevealing. Frontal and lateral chest radiography (Figure 1) was performed.

Figure 1. Frontal (A) and lateral (B) chest radiography

Which of the following statements regarding the chest radiograph is most accurate? (Click on the correct answer to proceed to the second of nine pages)

1. The chest radiograph shows asymmetric reticulation and interlobular septal thickening
2. The chest radiograph shows bilateral reticulation associated with decreased lung volumes
3. The chest radiograph shows large lung volumes
4. The chest radiograph shows multifocal consolidation and pleural effusion
5. The chest radiograph shows small cavitary pulmonary nodules

Cite as: Gotway MB. September 2017 imaging case of the month. Southwest J Pulm Crit Care. 2017;15(3):104-13. doi: https://doi.org/10.13175/swjpcc109-17 PDF 

Medical Image of the Week: The Atoll Sign in Cryptogenic Organizing Pneumonia

Figure 1. Portable chest X-ray shows bilateral airspace opacities (yellow arrows) and possible trace pleural effusion (blue arrow).

Figure 2. Computed tomography of the chest showing (A) patchy ground glass opacity in the upper lungs with additional scattered circular areas of opacity in a reverse halo configuration (blue arrows, atoll sign) and (B) extensive bibasilar consolidation with air bronchograms.

A 54-year-old woman presented to the emergency department with cough and worsening shortness of breath. Her cough began approximately 1 month prior to presentation, at which time she was diagnosed with pneumonia by her primary care physician based on a chest X-ray at an outside institution. She tried and failed courses of azithromycin, doxycycline, and levofloxacin.

The patient had an oxygen saturation of 55% and hyperpyrexia to 101.7 F in the emergency department. An initial chest X-ray was suggestive of moderate multifocal pneumonia with pleural effusion (Figure 1). Subsequent chest computed tomography (CT; Figure 2) revealed findings consistent with cryptogenic organizing pneumonia (COP) including multiple upper lobe atoll signs. Infectious and autoimmune workups were negative and the patient experienced a rapid recovery with pulse steroids, providing further evidence for the diagnosis of COP.

CT is the best imaging modality for evaluation of potential COP. Features include consolidations and nodules, bronchial wall thickening or dilatation, and ground glass opacities (1). The atoll sign, consisting of a central ground glass opacity and surrounding consolidation which may also be called a reverse halo sign, is highly specific but not sensitive for organizing pneumonia (2). Definitive diagnosis requires lung biopsy, although the disease is often managed based on a presumptive diagnosis (3).

Joseph Frankl, BS¹ and Veronica A. Arteaga, MD²

¹University of Arizona College of Medicine and ²Department of Medical Imaging

Banner University Medical Center Tucson

Tucson, AZ USA

References

1. Lee JW, Lee KS, Lee HY, Chung MP, Yi CA, Kim TS, Chung MJ. Cryptogenic organizing pneumonia: serial high-resolution CT findings in 22 patients. AJR Am J Roentgenol. 2010 Oct;195(4):916-22. [CrossRef] [PubMed]
2. Davidsen JR, Madsen HD, Laursen CB. Reversed halo sign in cryptogenic organising pneumonia. BMJ Case Rep. 2016 Feb 8;2016. pii: bcr2015213779. [CrossRef] [PubMed]
3. Bradley B, Branley HM, Egan JJ, et al. Interstitial lung disease guideline: the British Thoracic Society in collaboration with the Thoracic Society of Australia and New Zealand and the Irish Thoracic Society. Thorax. 2008 Sep;63 Suppl 5:v1-58. [CrossRef] [PubMed]

Cite as: Frankl J, Artega VA. Medical image of the week: the atoll sign in cryptogenic organizing pneumonia. Southwest J Pulm Crit Care. 2017;15(2):92-3. doi: https://doi.org/10.13175/swjpcc100-17 PDF

Medical Image of the Week: Cannon V Waves

Figure 1. Video showing jugular venous distention to earlobes with cannon V waves.

A 66-year-old man experienced recurrent ascites of unknown etiology over six months. He had previously undergone a renal transplant secondary to complications of diabetes and hypertension and had known severe coronary artery disease. His most recent paracentesis revealed an albumin 1.6 g/dL (serum albumin 2.1) and a total protein of 3.8 g/dL. His adenosine deaminase was 11.6 U/L (normal <7.6 U/L), but repeated bacterial and mycobacterial ascites cultures were negative, as were a carcinoembryonic antigen assay and ascites cytology. Computerized tomography of the abdomen showed findings consistent with cirrhosis, but an extensive workup for common causes of cirrhosis was negative.

Physical exam showed jugular venous distention with prominent V waves and a holosystolic murmur at the left lower sternal border (Figure 1). Echocardiography showed a dilated right ventricle, moderate pulmonary and tricuspid regurgitation and an estimated right ventricular systolic pressure of 87 mm Hg. Cardiac catherization confirmed the presence of an elevated right ventricular pressure of 72/10 (22) mm Hg, an elevated pulmonary artery pressure of 75/27 (45) mm Hg and a left ventricular ejection fraction of 20-25%. The right atrial pressure was 20 and the pulmonary artery occlusion pressure was 22 mmHg.  A diagnosis of pulmonary hypertension secondary to left ventricular heart disease (type 2 pulmonary hypertension) with congestive hepatopathy and cardiac ascites was made.

The patient’s physical examination provided an important clue to the etiology of the ascites – cardiac ascites is thought to be due to chronic venous congestion of the liver due to transmission of high central venous pressures. Tricuspid regurgitation can be associated with severe hepatic congestion because of retrograde transmission of right ventricular pressure directly into the hepatic veins. In some patients (although not in this patient), careful examination will reveal that the liver in such patients is palpably pulsatile.

Cardiac ascites is typically characterized by a serum albumin gradient (SAAG) >1.1 g/dL (indicative of portal hypertension) and ascites protein level of >2.5 g/dL (1). We cannot fully explain why this patient’s SAAG was low. A complete workup for infectious and oncological etiologies of low SAAG ascites was negative. It has been noted that in patients with known cirrhosis (as in this patient), the finding of a low SAAG has a low specificity for infectious and oncological etiologies of ascites (2). Serositis which can sometimes manifest as ascites can also be a complication of tacrolimus which the patient was receiving s/p renal transplant. It’s possible that tacrolimus might have changed the nature of the ascites fluid in this patient but this is conjectural. 

Robert A. Raschke, MD

College of Medicine-Phoenix

Phoenix, AZ USA

References

1. Sam AH, James THT. Rapid Medicine. Wiley-Blackwell; 2009: ISBN 1-4051-8323-3.
2. Khandwalla HE, Fasakin Y, El-Serag HB. The utility of evaluating low serum albumin gradient ascites in patients with cirrhosis. Am J Gastroenterol. 2009 Jun;104(6):1401-5. [CrossRef] [PubMed] 

Cite as: Raschke RA. Medical image of the week: cannon V waves. Southwest J Pulm Crit Care. 2017;15(2):90-1. doi: https://doi.org/10.13175/swjpcc095-17 PDF