Medical Image of the Week: Right Middle Lobe Syndrome

Figure 1. Panel A: PA chest x-ray showing calcified mediastinal lymphadenopathy. Panel B:  Lateral view showing a triangle of increased density between the minor fissure and the lower half of the major fissure seen on the lateral view (blue arrow) .

Figure 2. Image from the thoracic CT scan in lung windows showing calcified mediastinal lymph notes (green arrows).

A 73 year-old woman, a lifetime non-smoker, presented to the pulmonary clinic with chronic dyspnea on exertion and cough. Physical exam was unremarkable and pulmonary function testing showed normal spirometry. A chest radiograph revealed calcified mediastinal adenopathy and increased density in the right middle lobe region (Figure 1).  A computed tomography scan of the chest revealed significant narrowing of the right middle lobe bronchus with partial atelectasis and prominent calcified mediastinal lymphadenopathy (Figure 2).  Bronchoscopy showed no endobronchial lesions but there was evidence of extrinsic compression surrounding the right middle lobe orifice.  An endobronchial biopsy revealed noncaseating granulomas. Bronchoscopy cultures and cytology were negative and this was presumed to be from a previous infection with histoplasmosis given the patient’s long-term residence in an endemic area. Given chronic narrowing of right middle lobe bronchus with persistent atelectasis of the right middle lobe, the patient was diagnosed with right middle lobe syndrome.  She was started on combination therapy with a long-acting beta agonist and inhaled corticosteroid with complete resolution of her symptoms.

Right middle lobe syndrome (RMLS) is defined as recurrent or chronic atelectasis of the right middle lobe.  Although more commonly described in children, it is becoming more prevalent in adults with a predilection for women.  There are two distinct types of pathophysiology- obstructive and non-obstructive.  Obstructive pathophysiology is defined when there is an endobronchial lesion or extrinsic compression of the middle lobe bronchus by lymphadenopathy (as in our case) or a tumor.  Non-obstructive pathophysiology occurs when there is recurrent infection or inflammation leading to bronchiectasis and scarring.  Certain anatomical characteristics, including the acute take-off angle of the right middle lobe bronchus create poor conditions for drainage and collateral ventilation (1).

Symptoms of RMLS include chronic or recurrent cough, dyspnea, wheezing and recurrent infections.  High resolution computed tomography of the chest is the gold standard for imaging, as this will show narrowing of the right middle lobe orifice along with etiologies of extrinsic compression (Figure 2).  Patients suspected of having RMLS warrant a bronchoscopy to evaluate for patency of right middle lobe bronchus, to exclude malignancy and for evaluation of infectious etiologies (1).  The treatment of RMLS includes bronchodilator therapy along with mucolytics, chest physiotherapy and antibiotics if bronchiectasis is problematic.  Lobectomy may be warranted if malignancy is diagnosed, aggressive medical management fails or hemoptysis occurs (2). 

Elaine A. Cristan, MD and Linda Snyder, MD

Department of Medicine

Division of Pulmonary, Critical Care, Sleep and Allergy Medicine

Banner University Medical Center

Tucson, AZ USA

References

1. Gudbjartsson T, Gudmundsson G. Middle lobe syndrome: a review of clinicopathological features, diagnosis and treatment. Respiration. 2012;84(1):80-6. [CrossRef] [PubMed]
2. Einarsson JT, Einarsson JG, Isaksson H, Gudbjartsson T, Gudmundsson G. Middle lobe syndrome: a nationwide study on clinicopathological features and surgical treatment. Clin Respir J. 2009 Apr;3(2):77-81. [CrossRef] [PubMed] 

Cite as: Cristan EA, Snyder L. Medical image of the week: right middle lobe syndrome. Southwest J Pulm Crit Care. 2016; May;12(5):199-200. doi: http://dx.doi.org/10.13175/swjpcc030-16 PDF 

Medical Image of the Week: Complex Arteriovenous Malformation

Figure 1. Initial chest radiograph demonstrating right mid lung field process.

Figure 2. Panel A: Contrast enhanced thoracic CT scan axial view demonstrating very large, complex AVM. Panel B: Sagittal view.

Figure 3. Chest radiograph after coil embolization.

A 62-year-old man presented to the emergency department complaining of shortness of breath with exertion and mild non-productive cough. The patient was afebrile and physical exam was remarkable only for scattered bilateral rhonchi. White blood cell count was 8,800 K/uL and hematocrit was 51.5%. Room air arterial blood gas (at 1520 meters altitude) was pH 7.41, pCO2 42 mm Hg, PO2 45 mm Hg, and O2 saturation 78%. D-dimer was normal at 0.36 ug/ml. Chest radiograph (Figure 1) demonstrated what was interpreted as a right-sided mid/lower lung field infiltrate. The patient was placed on high-flow supplemental oxygen and treatment was initiated with intravenous levofloxacin, methylprednisilone and nebulized beta-agonists. The patient’s oxygenation failed to improve over a period of several days, and a CAT of the chest (Figures 2) was obtained, which demonstrated a very large, right middle lobe, complex pulmonary arteriovenous malformation. The patient was referred to interventional radiology for catheter directed coil embolization (Figure 3). Following that procedure the patient’s oxygen requirement decreased from 15 l/m via nasal cannula to 3 l/m.

Pulmonary arteriovenous malformations (PAVM’s) are rare, with an incidence of 2-3 per 100,000, and are associated with hereditary hemorrhagic telangiectasia (HHT), in approximately 80% of cases (1). The intrapulmonary shunt associated with PAVM’s may result in significant hypoxemia, cerebrovascular accident or embolic brain abscess. The preferred screening tool is transthoracic contrast echocardiography, which demonstrates extra-cardiac shunt. Chest CT scan may be used to both confirm the diagnosis of PAVM and to define the vascular anatomy. Patients who meet three of the four Curacao criteria (epistaxis, family history, telangiectasia, and visceral lesions) are recognized as suffering from HHT (2). Catheter directed coil embolization is an effective and well-tolerated treatment method for PAVM; and generally results in reduced shunt fraction and improved oxygenation (3).

Kathleen Monahan and Charles J. VanHook MD

Longmont United Hospital

Longmont, Colorado USA

References

1. Cartin-Ceba R, Swanson KL, Krowka MJ. Pulmonary arteriovenous malformations. Chest. 2013 Sep;144(3):1033-44. [CrossRef] [PubMed]
2. Shovlin CL, Guttmacher AE, Buscarini E, Faughnan ME, Hyland RH, Westermann CJ, Kjeldsen AD, Plauchu H. Diagnostic criteria for hereditary hemorrhagic telangiectasia (Rendu-Osler-Weber syndrome). Am J Med Genet. 2000 Mar 6;91(1):66-7. [CrossRef] [PubMed]
3. Dutton JA, Jackson JE, Hughes JM, Whyte MK, Peters AM, Ussov W, Allison DJ.Pulmonary arteriovenous malformations: results of treatment with coil embolization in 53 patients. AJR Am J Roentgenol. 1995 Nov;165(5):1119-25. [CrossRef] [PubMed]

Cite as: Monahan K, VanHook CJ. Medical image of the week: complex arteriovenous malformation. Southwest J Pulm Crit Care. 2016 May;12(5):197-8. doi: http://dx.doi.org/10.13175/swjpcc027-16 PDF

Medical Image of the Week: Achalasia with Lung Abscess

Figure 1. CT coronal view showing a left lower lobe lung abscess measuring approximately 8 x 5 cm.

Figure 2. Barium swallow study showed dilated esophagus with tapering off at the lower esophageal sphincter junction, demonstrating the classic bird-beak like appearance.

Figure 3. Upper endoscopy showing diffuse whitish plaque suggestive of candidiasis likely due to chronic stasis of food.

An 80-year old woman with past medical history of high grade serous fallopian tube carcinoma presented with 2 months history of productive cough. This was associated with shortness of breath and subjective fever, chills and weight loss of 5 pounds over 2 months. She was treated with outpatient antibiotics without improvement of symptoms. Patient was afebrile on presentation, hemodynamically stable, and saturating at 99% on room air. Lung examinations revealed dullness on percussion of left lower lung field and reduced breath sounds on the same area.

Computed tomographic imaging revealed a large lung abscess on left lower lobe (Figure 1) and moderately dilated esophagus and fluid filled to the level of gastro-esophagus junction. Barium swallow study showed a classic bird-beak like appearance (Figure 2). There was no contrast that passed through the gastro-esophagus junction during the entire course of the barium study. Upper endoscopy was performed to rule out intraluminal pathology that may contribute to the obstruction which revealed a large amount of barium and retained food in the entire esophagus with diffuse whitish plaque suggestive of candidiasis and a benign appearing intrinsic mild stenosis at lower third of esophagus (Figure 3). Pneumatic dilation and botulinum toxin injection were performed and she was started on pantoprazole. She was also started on broad-spectrum antibiotics (vancomycin, cefepime, metronidazole) for the lung abscess. A chest tube was inserted under computed tomography (CT) guidance. Subsequently, cultures from the chest tube drainage grew Streptococcus intermedius. She was discharged to a skilled nursing facility with additional 3-weeks of ampicillin-sulbactam. Repeat imaging at 3-weeks showed improvement of the lung abscess.

Achalasia is a rare primary esophageal motor disorder, with incidence of approximately 1 in 100,000 people annually and prevalence of 10 in 100,000 (1). Common presentations of achalasia includes gradual dysphagia to solid and liquids, heartburn symptoms unrelieved by adequate proton pump inhibitor therapy and weight loss. Achalasia presenting with respiratory symptoms without dysphagia is rare as this disease entity is gradual and patient will normally present with different degrees of dysphagia or regurgitation of food. This case report is a good reminder that aspiration should be considered as a cause for pneumonia in the elderly. Our patient could have been aspirating for a period of time, leading to the development of a large lung abscess. Kikuchi et al. (2) demonstrated the high incidence of silent aspiration in the elderly population. A more detailed assessment by trained swallowing therapist may aid in detecting dysphagia.

Kai Rou Tey MD¹ and Naser Mahmoud MD²

¹Department of Internal Medicine University of Arizona College of Medicine- South Campus

²Department of Pulmonary, Critical Care, Allergy and Sleep, University of Arizona College of Medicine

Tucson, AZ USA

References

1. Francis DL, Katzka DA. Achalasia: update on the disease and its treatment. Gastroenterology. 2010 Aug;139(2):369-74. [CrossRef] [PubMed]
2. Kikuchi R, Watabe N, Konno T, Mishina N, Sekizawa K, Sasaki H. High incidence of silent aspiration in elderly patients with community-acquired pneumonia. Am J Respir Crit Care Med. 1994 Jul;150(1):251-3. [CrossRef] [PubMed]

Cite as: Tey KR, Mahmoud N. Medical image of the week: achalasia with lung abscess. Southwest J Pulm Crit Care. 2016 May;12(5):194-6. doi: http://dx.doi.org/10.13175/swjpcc025-16 PDF

Medical Image of the Week: Saddle Pulmonary Embolism

Figure 1. Thoracic axial computed tomography angiogram (CTA) demonstrating saddle embolism within bilateral pulmonary arteries with extension into sub-segmental branches.

Figure 2. Coronal CTA.

A 66-year-old woman with recent history of left knee surgery and L2-L5 spinal fusion within the past month presented to the Emergency Department (ED) with pleuritic chest pain and shortness of breath for three days. On admission, reported crushing diffuse substernal chest pain worsened to 10/10 on the pain scale on the day of presentation. In the ED, physical examination was remarkable for tachycardia, tachypnea, diaphoresis and hypotension. Initial electrocardiogram was significant for sinus tachycardia with S1Q3T3 pattern. thoracic computed tomography angiogram (CTA) showed saddle pulmonary embolus (PE) with extension into segmental vasculature, right greater than left (Figures 1 and 2). A bedside echocardiogram demonstrated diastolic and systolic bowing of the intraventricular septum into the left ventricle. An emergent trans-thoracic echocardiogram confirmed flattened septum consistent with right ventricle pressure overload with right ventricular systolic pressure of 55 mmHg + central venous pressure (CVP) and reduced left ventricular ejection fraction of 38%. Her hemodynamic condition was stabilized by administering intravenous norepinephrine infusion. Interventional radiology was contacted for an emergent catheter directed thrombolysis. Ten milligrams of tissue plasminogen activator (tPA) was injected into the pulmonary artery with subsequent removable inferior vena cava filter placement. Vasoactive medications were titrated down and stopped four hours following tPA administration and anticoagulation with intravenous heparin was commenced. The patient was discharged from the hospital after initiation of rivaroxaban.

Saddle pulmonary embolism (SPE) is a form of large pulmonary thromboembolism that straddles the main pulmonary arterial branch at the bifurcation. The incidence of SPE is found in about 2.6% of the PE cases (1). The choice of diagnostic testing for PE is CTA based on multiple studies demonstrating CTA was both sensitive and specific for PE especially in moderate to high clinical probability PE (2,3). Suspicion for PE in our patient included sedentary status following knee replacement surgery, tachycardia, S1Q3T3 pattern on EKG, evidence for right ventricular strain on echocardiography, and no other diagnosis more likely thus lead to high clinical suspicion of pulmonary embolism with a Well’s score for PE of 6.

Faraz Jaffer, MD¹ See Wei Low, MD¹ and Sairam Parthasarathy, MD²

¹Department of Internal Medicine, Banner - University Medical Center

²Department of Allergy, Pulmonary, Critical Care and Sleep Medicine

Banner-University Medical Center

Tucson, AZ USA

References

1. Ryu JH, Pellikka PA, Froehling DA, Peters SG, Aughenbaugh GL. Saddle pulmonary embolism diagnosed by CT angiography: frequency, clinical features and outcome. Respir Med. 2007 Jul;101(7):1537-42. [CrossRef] [PubMed]
2. Van Belle A, Büller HR, Huisman MV, et al. Effectiveness of managing suspected pulmonary embolism using an algorithm combining clinical probability, D-dimer testing, and computed tomography. JAMA. 2006 Jan 11;295(2):172-9. [CrossRef] [PubMed]
3. Stein PD, Fowler SE, Goodman LR, et al. Multidetector computed tomography for acute pulmonary embolism. N Engl J Med. 2006 Jun 1;354(22):2317-27. [CrossRef] [PubMed] 

Cite as: Jaffer F, Low SW, Parthasarathy S. Medical image of the week: saddle pulmonary embolism. Southwest J Pulm Crit Care. 2016 May;12(5):192-3. doi: http://dx.doi.org/10.13175/swjpcc024-16 PDF

May 2016 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  

Members of the Arizona, New Mexico, Colorado and California Thoracic Societies and the Mayo Clinic are able to receive  0.25 AMA PRA Category 1 Credits™. 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 this activity I will be better able to:    

1. Correctly interpret and identify clinical practices supported by the highest quality available evidence.
2. Will be better able to establsh the optimal evaluation leading to a correct diagnosis for patients with pulmonary, critical care and sleep disorders.
3. Will improve the translation of the most current clinical information into the delivery of high quality care for patients.
4. Will integrate new treatment options in discussing available treatment alternatives 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, 2015-December 31, 2016

Financial Support Received: None.

Clinical History:  A 58-year-old man with hypertension presents for a routine health examination. As part of his routine evaluation, frontal and lateral chest radiography (Figure 1) was performed.  

Figure 1. Frontal (panel A) and lateral (panel 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 panels)

1. The frontal chest radiograph shows a small lung nodule
2. The frontal chest radiograph shows a small metallic focus just posterior to the inferior sternum
3. The frontal chest radiograph shows an unusual right-sided mediastinal contour
4. The frontal chest radiograph shows asymmetrically increased attenuation of the left thorax compared with the right
5.  The frontal chest radiograph shows normal findings

Cite as: Gotway MB. May 2016 imaging case of the month. Southwes J Pulm Crit Care. 2016 May;12(5):180-91. doi: http://dx.doi.org/10.13175/swjpcc040-16 PDF 

Medical Image of the Week: Cheyne Stokes Breathing on Polysomnography

Figure 1. A 5-minute epoch showing Cheyne-Stokes breathing (arrow).

A 79-year-old man presented to the sleep lab for a split-night polysomnography (PSG) after a positive Berlin Questionnaire.  He was screened and directly referred to our sleep lab through his PCP.  Patient has a chart documented medical history of atrial fibrillation, idiopathic pulmonary fibrosis, obesity, and CHF. He did not have an echocardiogram available therefore the etiology of his CHF was unclear.  He was found to have severe obstructive sleep apnea and was split early in the night.  Prior to positive airway pressure, his apnea-hypopnea index (AHI) was 77 and were predominantly obstructive hypopneas.  Soon after initiation of positive airway pressure, his PSG revealed the breathing pattern seen in Figure 1.  His respirations exhibited a crescendo-decrescendo pattern (arrow) followed by a period of central apnea consistent with Cheyne Stokes breathing (CSB).  In this patient, CSB was likely due to heart failure, although systolic or diastolic remained unclear.  Of note, he was not on medications found to be responsible for CSB, and did not have a history of cerebral vascular accident. 

Cheyne-Stokes breathing (CSB) is a well-documented but poorly understood abnormal breathing pattern that is believed to be a type of central sleep apnea (CSA), meaning apneas without upper airway obstruction. This compensatory mechanism is characterized by a cyclic change from oscillating events of apnea and hyperpnea. The characteristic feature of CSA-CSB is a longer cycle length, typically 45-60 seconds, alternating with a respiratory phase exhibiting a crescendo-decrescendo pattern of flow. This result is thought to be due to a delay in correction centrally when an elevated arterial PCO2 is detected within the blood stream by chemoreceptors.  Co-morbid conditions often include cardiac disease (primarily heart failure independent of NYHA classification), neurologic disorders, prematurity, or sedation. Diagnosis is made by polysomnography.  Treatment often entails treating the underlying cause or associated disorder.  When all other strategies fail, remaining treatment includes the use of nocturnal continuous positive airway pressure (CPAP), supplemental oxygen, or adaptive servoventilation (ASV).  Although, systolic heart failure with LVEF <45% in patients with predominantly central sleep apnea currently precludes the use of ASV.

Tam Le, MD and Sekhon Kawanjit, MD

Banner University Medical Center Tucson

Tucson, AZ USA

References

1. Cherniack NS, Longobardo GS. Cheyne-Stokes breathing. An instability in physiologic control. N Engl J Med. 1973 May 3;288(18):952-7. [CrossRef] [PubMed]
2. Naughton M, Benard D, Tam A, Rutherford R, Bradley TD. Role of hyperventilation in the pathogenesis of central sleep apneas in patients with congestive heart failure. Am Rev Respir Dis. 1993 Aug;148(2):330-8. [CrossRef] [PubMed]
3. American Academy of Sleep Medicine. International classification of sleep disorders, 3rd ed. Darien, IL: American Academy of Sleep Medicine, 2014.

Reference as: Le T, Kawanjit S. Medical image of the week: Cheyne Stokes breathing on polysomnography. Southwest J Pulm Crit Care. 2016 Apr;12(4):163-4. doi: http://dx.doi.org/10.13175/swjpcc022-16 PDF 

Medical Image of the Week: A Positive Methacholine Challenge

Figure 1. Positive methacholine challenge. The patient had a 39% drop in FEV1 after inhalation of 0.0625 mg/dL of methacholine, the lowest concentration tested. The drop in FEV1 was reversed by a bronchodilator (Post BD).

A methacholine challenge test is one of the methods to assess bronchial hyperresponsiveness (BHR). BHR is one of the features that can contribute to the diagnosis of asthma. The test is reported as a PC-20 value; the inhaled provocative concentration causing a 20% drop or more in the pretest FEV1. This patient had a PC-20 of <0.1 mg/mL which is interpreted as a moderate to severe bronchial hyperresponsiveness by ATS guidelines (1). A normal bronchial response is a PC-20 > 16 mg/ml, 4-16 mg/mL is considered borderline and 1-4 mg/mL is mild BHR according to the ATS guidelines.

Mohammad Dalabih, MBBS and Linda Snyder, MD

University of Arizona

Tucson, AZ USA

Reference

1. Crapo RO, Casaburi R, Coates AL, Enright PL, Hankinson JL, Irvin CG, MacIntyre NR, McKay RT, Wanger JS, Anderson SD, Cockcroft DW, Fish JE, Sterk PJ. Guidelines for methacholine and exercise challenge testing-1999. Am J Respir Crit Care Med. 2000 Jan;161(1):309-29.

Cite as: Dalabih M, Snyder L. Medical image of the week: a positive methacholine challenge. Southwest J Pulm Crit Care. 2016 Apr;12(4):152. doi: http://dx.doi.org/10.13175/swjpcc017-16 PDF

Medical Image of the Week: Levamisole-Induced Vasculitis

Figure 1. Purpuric lesion on the auricle of the ear.

Figure 2. Diffuse purpuric lesions in retiform patterns of the trunk and extremities.

A 51-year-old Hispanic woman presented with a worsening, diffuse, painful purpuric rash over the last 3 months, involving both auricles of the ears, both lower extremities, and her trunk. She also reported purulent discharge drainage from one of the lesions on her right posterior thigh, associated with fever and chills for one day. She was a daily cocaine user for the last 30 years.

On examination, she was febrile and tachycardic. There were diffuse retiform like non-blanching purpuric lesions without necrosis on ears, her lower extremities, and trunk (Figure 1 and 2). There was an open wound on the posterior aspect of her right thigh that had purulent drainage.

Laboratory investigations revealed neutropenia, normal complete metabolic panel, high erythrocyte sedimentation rate (ESR) and high C-reactive protein. Further autoimmune work-up revealed positive perinuclear antineutrophil cytoplasmic antibodies (p-ANCA), high anti-myeloperoxidase antibodies (MPO) titer, elevated IgM anticardiolipin antibodies, negative antinuclear antibodies (ANA), and low complement levels. HIV, hepatitis viral panel and cryoglobulin were negative. Urine toxicology was positive for cocaine. Benzoylecgonine, m-OH-benzoylecgonine, and cocaethylene, which are cocaine metabolites were detected using qualitative liquid chromtaography-mass spectrography.

Her presentation is suggestive of drug-induced vasculitis, likely secondary to levamisole-adulterated cocaine, complicated by an abscess. We started intravenous (IV) vancomycin and performed a bedside incision and drainage for the abscess on her posterior thigh. On the third day of hospital admission, all her lesions improved remarkably with abstinence from cocaine.

Levamisole, an atihelminthic agent, is used as treatment for autoimmune disorders and cancer due to its immunomodulating effects. Association between levamisole and cutaneous vasculitis was first described in 1978 in a patient who has rheumatoid arthritis treated with levamisole (1). (Macfarlane, 1978 #19) In 2000, the Food and Drug Administration (FDA) banned the use of levamisole due to its side effects profile.  However, since 2009, reports of agranulocytosis and vasculitis associated with levamisole have been increasing. The emergence of these cases is attributed by the increased contamination of cocaine with levamisole. More than 70% of cocaine found in North America contains levamisole (2,3).

Clinical features of levamisole-induced vasculitis include retiform purpura or purpura that has an angulated or branched configuration. Some patients may develop bacterial superinfection of the purpuric lesions, which was seen in our patient. This requires more attention to prevent further complications as these patients are immune suppressed. Two classic pathologic findings of these rashes are leukocytoclastic vasculitis of small vessels with fibrinoid necrosis of the wall of the vessels and formation of fibrin thrombi in the small vessels of superficial and deep dermis (4). These individuals commonly have neutropenia, positive ANCA serology, and elevated anti-MPO antibody titers (5).

Treatment includes supportive measures and abstinence from cocaine. Due to its increasing incidence, physician should be made aware of this disease entity due to its life threatening complications – neutropenia.

Kai Rou Tey, MD¹; Enrique Villavicencio, MD²; and Don Leo Pepito, MD¹

¹Department of Internal Medicine,

²Department of Neurology

University of Arizona College of Medicine-South Campus

Tucson, AZ

References

1. Macfarlane DG, Bacon PA. Levamisole-induced vasculitis due to circulating immune complexes. Br Med J. 1978 Feb 18;1(6110):407-8. [CrossRef] [PubMed]
2. Centers for Disease Control and Prevention (CDC). Agranulocytosis associated with cocaine use - four States, March 2008-November 2009. MMWR Morb Mortal Wkly Rep. 2009 Dec 18;58(49):1381-5. [CrossRef] [PubMed]
3. Buchanan JA, Heard K, Burbach C, Wilson ML, Dart R. Prevalence of levamisole in urine toxicology screens positive for cocaine in an inner-city hospital. JAMA. 2011 Apr 27;305(16):1657-8. [CrossRef] [PubMed]
4. Roberts JA, Chévez-Barrios P. Levamisole-Induced Vasculitis: A characteristic cutaneous vasculitis associated with levamisole-adulterated cocaine. Arch Pathol Lab Med. 2015 Aug;139(8):1058-61. [CrossRef] [PubMed]
5. McGrath MM, Isakova T, Rennke HG, Mottola AM, Laliberte KA, Niles JL. Contaminated cocaine and antineutrophil cytoplasmic antibody-associated disease. Clin J Am Soc Nephrol. 2011 Dec;6(12):2799-805. [CrossRef] [PubMed] 

Cite as: Tey KR, Villavicencio E, Pepito DL. Medical image of the week: levamisole-induced vasclitis. Southwest J Pulm Crit Care. 2016 Mar;12(4):149-51. doi: http://dx.doi.org/10.13175/swjpcc013-16 PDF 

Medical Image of the Week: Bullous Emphysema

Figure 1. Chest radiograph showing hyperinflated lungs.

Figure 2. Panel A: Coronal view of chest computed tomography (CT) in  lung widows showing multiple large lucent spaces of lung parenchyma destruction interspersed normal lung tissue. Panel B: Axial view of chest CT showing coronal narrowing of the trachea with widening of the sagittal diameter (arrow). This is known as a saber sheath trachea which is pathognomonic of chronic obstructive pulmonary disease.

A 63-year-old gentleman, with a history of 90-pack-years of smoking and stage IV chronic obstructive pulmonary disease was receiving home oxygen at 2 L/min at baseline. He has had multiple prior hospital admissions for respiratory failure. Over the past 2 weeks he has had increased production of sputum, associated with worsening shortness of breath. He is on fluticasone-salmeterol inhaler, albuterol inhaler, and tiotropium as an outpatient.

On examination, he was hemodynamically stable, SpO2 was 92% on 4L/min of oxygen. He was in obvious respiratory distress, in a tripod position with tachypnea and using respiratory accessory muscles. Lung examination revealed diffuse expiratory wheezing.

Chest radiograph shows severe emphysema (Figure 1). Chest computed tomography showed diffuse centrilobular and bullous emphysema (Figure 2).  He was treated as an acute severe exacerbation of COPD and was eventually discharged to follow-up with the pulmonary clinic.

Emphysema is defined as alveolar destruction and airspace enlargement distal to the terminal bronchiole. There are subclassifications of emphysema based on its distribution within the secondary lobule (1). Bullae are defined as an air-filled space, greater than 1 cm in diameter, usually as a result of emphysematous destruction. Indications for bullectomy include patient symptoms, isolated bullae occupying > 30% of the hemithorax or complications arising from bullae (2).

Kai Rou Tey, MD¹; Akinbola Ajayi-Obe¹, MD; and Naser Mahmoud, MD²

¹Department of Internal Medicine, South Campus

²Department of Pulmonary, Critical Care, Allergy and Sleep

University of Arizona College of Medicine

Tucson, AZ

References

1. Terminology, Definitions, and Classification of Chronic Pulmonary Emphysema and Related Conditions: A Report of the Conclusions of a Ciba Guest Symposium. Thorax. 1959;14(4):286-299.
2. van Berkel V, Kuo E, Meyers BF. Pneumothorax, bullous disease, and emphysema. Surg Clin North Am. 2010 Oct;90(5):935-53. [CrossRef] [PubMed]

Cite as: Tey KR, Ajayi-Obe A, Mahmoud N. Medical image of the week: bullous emphysema. Souhwest J Pulm Crit Care. 2016 Apr;12(4):147-8. doi: http://dx.doi.org/10.13175/swjpcc157-15 PDF

April 2016 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  

Members of the Arizona, New Mexico, Colorado and California Thoracic Societies and the Mayo Clinic are able to receive  0.25 AMA PRA Category 1 Credits™. 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 this activity I will be better able to:    

1. Correctly interpret and identify clinical practices supported by the highest quality available evidence.
2. Will be better able to establsh the optimal evaluation leading to a correct diagnosis for patients with pulmonary, critical care and sleep disorders.
3. Will improve the translation of the most current clinical information into the delivery of high quality care for patients.
4. Will integrate new treatment options in discussing available treatment alternatives 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, 2015-December 31, 2016

Financial Support Received: None.

Clinical History: A 19 year-old man with no previous medical history was vacationing when he was found down, intoxicated, surrounded by vomit. He went into cardiac arrest, and, after several minutes, cardiopulmonary resuscitation was initiated. He was intubated in the field, and epinephrine was administered.

Once at the hospital, frontal chest radiography (Figure 1) was performed.

Figure 1. Frontal chest radiograph.

Which of the following statements regarding the chest radiograph is most accurate?

1. The frontal chest radiograph shows central venous catheter malposition
2. The frontal chest radiograph shows focal consideration
3. The frontal chest radiograph shows pleural fluid loculated within the major fissures
4. The frontal chest radiograph shows pneumomediastinum
5. The frontal chest radiograph shows pneumothorax

Cite as: Gotway MB. April 2016 imaging case of the month. Southwest J Pulm Crit Care. 2016 Apr;12(4):137-46. doi: http://dx.doi.org/10.13175/swjpcc035-16 PDF

Medical Image of the Week: Spontaneous Pneumomediastinum

Figure 1. Upright chest radiograph showing pneumomediastinum tracking into neck and small right apical pneumothorax (arrows).

Figure 2. Coronal slice of CT chest showing extensive pneumomediastinum and subcutaneous emphysema (arrows).

Figure 3. CT scan of chest showing the Macklin effect with air tracking along the bronchovascular sheath in the left lower lobe.

A 24-year-old man with a past medical history significant for type I diabetes mellitus presented to the emergency department with complaints of nausea and vomiting for several days. He reported he had been on drinking alcohol heavily 4 days prior to presentation and subsequently had multiple episodes of vomiting. Initial laboratory evaluation was consistent with diabetic ketoacidosis (DKA). A routine chest x-ray was obtained to evaluate for an infectious etiology of his DKA and revealed pneumomediastinum and a small right apical pneumothorax (Figure 1). A CT scan of the chest was done and showed extensive pneumomediastinum as well as air tracking along the bronchovascular sheaths in the left lower lobe (Figure 2 and 3). It did not reveal evidence of esophageal injury.

Spontaneous pneumomediastinum (SPM) refers to pneumomediastinum that is not associated with noticeable cause such as esophageal rupture or trauma. It is typically a benign condition thought to be due to alveolar rupture and subsequent air tracking along the bronchial tree (1). It has been associated with a number of conditions including asthma, DKA, anorexia nervosa, and other conditions that lead to excessive coughing or vomiting. The radiographic appearance of air dissecting through the pulmonary intersitium along the bronchovascular sheath is known as the Macklin effect and can be seen in Figure 3.

Spontaneous pneumomediastinum typically resolves without complications but must be differentiated from the much more serious diagnosis of esophageal rupture, or Boerrhaave’s syndrome. Boerrhaave’s syndrome is more likely to present with fever, hemodynamic instability, and hydropneumothorax. All patients presenting with suspected SPM should be evaluated for esophageal perforation with a radiographic contrast swallow (2). In our case it was negative for evidence of esophageal disruption and the patient recovered completely.

Lucie Griffin DO and Erik Kraai MD

Division of Pulmonary, Critical Car, and Sleep Medicine

University of New Mexico Health Sciences Center

Albuquerque, NM USA

References

1. Murayama S, Gibo S. Spontaneous pneumomediastinum and Macklin effect: Overview and appearance on computed tomography. World J Radiol. 2014 Nov 28;6(11):850-4. [CrossRef] [PubMed]
2. Kelly S, Hughes S, Nixon S, Paterson-Brown S. Spontaneous pneumomediastinum (Hamman's syndrome). Surgeon. 2010 Apr;8(2):63-6. [CrossRef] [PubMed] 

Cite as: Griffin L, Kraai E. Medical image of the week: spontaneous pneumomediastinum. Southwest J Pulm Crit Care. 2016 Mar;12(3):115-6. doi: http://dx.doi.org/10.13175/swjpcc015-16 PDF

Medical Image of the Week: Pericardial Effusion in a Setting of Bacterial Endocarditis

Figure 1. Single portable semi-upright chest radiograph with findings of an enlarged cardiomediastinal silhouette, and indistinctness of the perihilar vasculature.

Figure 2. Axial contrast enhanced computed tomography—soft tissue windows. A large concentric rim (fluid density) surrounds all four chambers of the heart, consistent with a pericardial effusion. Notice how the right ventricle is normal, which can be collapsed in cardiac tamponade.

A 25-year-old man with an extensive history of intravenous drug abuse presents to the hospital with worsening shortness of breath and fevers for two weeks. In the emergency department, he was initially provided breathing treatments including ipratropium/albuterol and methylprednisolone. As the patient still required supplemental oxygen, a chest radiograph was performed to evaluate for an underlying infectious etiology.

However, the chest radiograph portrayed an enlarged cardiomediastinal silhouette in a “water-bottle” appearance and obscuration of the hilar vessels (Figure 1). Given these findings, there was a high concern for a pericardial effusion, and the physicians opted for further cross-sectional imaging. The contrast enhanced computed tomography (CT) images confirmed the aforementioned diagnosis (Figure 2). As blood cultures eventually grew Staphylococcus aureus, and given the patient’s extensive history of intravenous drug abuse, there was a high suspicion for bacterial endocarditis. A subsequent echocardiogram verified several valvular vegetations in keeping with endocarditis. The patient’s vitals remained stable throughout the hospital course, and he was continued on long-term antibiotic therapy.

Chest radiographs are often unreliable in depicting pericardial effusions, as they require at least 200 mL of pericardial fluid to portray an enlarged cardiomediastinal silhouette (1).  As fluid continues to accumulate in the pericardial space, the increase in pericardial pressure on the chambers can eventually lead to cardiac tamponade—a form of cardiogenic shock (2). Cardiac tamponade will result in a decrease in stroke volume, decreased blood pressure, and ultimately a diminished cardiac output; all of which require immediate intervention (2). Echocardiography remains the imaging modality of choice given its portability and high sensitivity in diagnosing pericardial fluid (3).

Amrit Hansra, MD

Department of Medical Imaging

University of Arizona

Tucson, AZ

References

1. Restrepo CS, Lemos DF, Lemos JA, et al. Imaging findings in cardiac tamponade with emphasis on CT. Radiographics. 2007 Nov-Dec;27(6):1595-610. [CrossRef] [PubMed]
2. Spodick DH. Acute cardiac tamponade. N Engl J Med. 2003 Aug 14;349(7):684-90. [CrossRef] [PubMed]
3. Chong HH, Plotnick GD. Pericardial effusion and tamponade: evaluation, imaging modalities, and management. Compr Ther. 1995 Jul;21(7):378-85. [PubMed] 

Cite as: Hansra A. Medical image of the week: pericardial effusion in a setting of bacterial endocarditis. Southwest J Pulm Crit Care. 2016 Mar;12(3):110-1. doi: http://dx.doi.org/10.13175/swjpcc009-16 PDF

Medical Image of the Week: Diffuse Gastric Bleeding and ALL

Figure 1. Technetium 99m tagged RBC scan showing abnormal radio tracer accumulation throughout the stomach (Panel A), and subsequently passing into the small bowel (Panel B).

A 26-year-old man with a medical history significant for acute lymphoblastic leukemia (ALL) presented with hypovolemic shock secondary to large volume hematemesis. The patient was diagnosed with ALL and treated with high dose chemotherapy followed by peripheral blood stem cell transplant from a matched unrelated donor one year prior to presentation. His treatment course was complicated by grade 4 acute graft versus host disease (GVHD) and CMV colitis. Blood work on admission showed hemoglobin of 6.4 g/dL and a leukocytosis. Patient was intubated for airway protection, transferred to ICU, and EGD was performed, which revealed diffusely friable mucosa, inflammation, and ulcerations throughout the gastric mucosa with only a few areas of normal appearing mucosa. Additionally, areas of spontaneous bleeding were seen. Selective arteriography within the right gastric and gastroduodenal arteries showed no active extravasation from the stomach or duodenum. However the gastroepiploic and right gastric arteries were prophylactically embolized. Subsequently, a technetium 99m tagged RBC scan demonstrated abnormal radio-tracer accumulation throughout the stomach with subsequent passage into the small bowel (Figure 1). The patient continued to have refractory gastric bleeding even with an increased dose of cyclosporine. Surgical measures including gastrectomy were discussed with the family. However, the family decided on comfort care. The patient died the following day.

Although gastric bleeding is rare in ALL patients in general, it is more commonly associated with certain condition such as GVHD and colitis following allogeneic stem cell transplantation (SCT). One of the retrospective studies with 447 SCT patients showed that 21.1% of study population experienced major GI bleeding, requiring transfusions or surgical intervention. Also, their mortality was shown to be twice higher than patients without bleeding complication, although most cases of bleeding were mild and occurred in the peri-transplant period with concurrent severe thrombocytopenia (1).

Hemorrhagic complications occur predominantly during the first month of post transplant, and bleeding is more commonly associated with allogeneic SCT compared to autologous SCT (2). This is mainly secondary to GVHD with gastrointestinal involvement, which leads to destruction and fragility of the epithelium as well as hyper-perfusion and proliferation of the blood vessels. As such, the risk of hemorrhage in patients with acute and chronic GVHD greater than grade I was 2.9 and 4.2 fold higher, respectively, and these patients had 10.8 fold higher risk of severe bleeding. The risk of bleeding is further increased by CMV infection, which infects vascular endothelial cells, narrows capillary lumens, and leads to ischemia and ulceration of gastric mucosa (3). The combination of GVHD and CMV infection could have synergistically damaged the gastric mucosa leading to severe refractory bleeding in our case.

Onyemaechi Okolo MD¹, Seongseok Yun MD PhD¹, Faiz Anwer MD, FACP²

¹Department of Medicine

²Department of Hematology & Oncology, Blood & Bone Marrow Transplantation Program

University of Arizona

Tucson, AZ, 85721

References

1. Pihusch R, Salat C, Schmidt E, Göhring P, Pihusch M, Hiller E, Holler E, Kolb HJ. Hemostatic complications in bone marrow transplantation: a retrospective analysis of 447 patients. Transplantation. 2002;74(9):1303-9. [CrossRef] [PubMed]
2. Törnebohm E, Lockner D, Paul C. A retrospective analysis of bleeding complications in 438 patients with acute leukaemia during the years 1972-1991. Eur J Haematol. 1993;50(3):160-7. [CrossRef] [PubMed]
3. Cheung AN, Ng IO. Cytomegalovirus infection of the gastrointestinal tract in non-AIDS patients. Am J Gastroenterol. 1993;88(11):1882-6. [PubMed]

Cite as: Okolo O, Yun S, Anwer F. Medical image of the week: diffuse gastric bleeding and ALL. Southwest J Pulm Crit Care. 2016;12(3):108-9. doi: http://dx.doi.org/10.13175/swjpcc010-16 PDF

Medical Image of the Week: Necrotizing Soft Tissue Infection

Figure 1. Axial view showing extensive gluteal and perineal soft tissue inflammation with gas formation (arrow).

Figure 2. Saggital view showing gas formation (arrow).

A 70-year-old man with a history of coronary artery disease, chronic back pain, and general debilitation presented to the emergency department with complaints of fever, weakness and right buttock discomfort. Physical exam was remarkable for a temperature of 101.7º F, and for moderate erythema of the skin of the right inguinal area and right buttock, with associated tenderness. Laboratory exam was significant for a WBC of 22.7 K/ɥL, erythrocyte sedimentation rate of 82 mm, and serum creatinine phosphokinase of 2856 U/L. CAT of the abdomen and pelvis demonstrated extensive gluteal and perineal soft tissue inflammation with gas formation, consistent with a necrotizing soft tissue infection (Figures 1 and 2).

Three basic subsets of necrotizing soft tissue infections (NSTIs) have been described. Type I infections are the most common form and are characterized by a polymicrobial process typically involving gram positive cocci, gram negative rods, and anaerobes. Type I infections occur most commonly in diabetics, in patients with severe peripheral vascular disease, or in the presence of other immune compromising conditions.  Type II infections involve Group A Streptococcus, either alone or in combination with Staphylococcus aureus. Type II NSTI’s occur most commonly in immunocompetent hosts. Type III NSTI’s, caused by Vibrio vulnoficus, are found in patients with exposure to warm sea water, with liver disease being the most common predisposing condition (1-3). Fournier’s gangrene is a NSTI that involves the perineum (2).

Physical examination often reveals fever and local erythema or tenderness. Gas formation may be present on imaging studies, with CAT scans more sensitive than plain films (1). Treatment relies on early antibiotic therapy with anaerobic coverage, fluid resuscitation, and aggressive debridement. Hyperbaric oxygen therapy may have a role as well (1). Mortality is high, in the range of 40%, and recovery is often prolonged (1,3).

Angela Taylor MD, Milena Beer PA, and Charles J. VanHook MD

Longmont United Hospital

Longmont, Colorado USA

References

1. Sarani B, Strong M, Pascual J, Schwab CW. Necrotizing fasciitis: current concepts and review of the literature. J Am Coll Surg. 2009 Feb;208(2):279-88. [CrossRef] [PubMed]
2. Pucket Y, Fisher B, Dissanaike S. Clinical comparison of Fournier's gangrene to other necrotizing soft tissue infections. Research Journal of Infectious Diseases. 2015;3:1. [CrossRef]
3. Khamnuan P, Chongruksut W, Jearwattanakanok K, Patumanond J, Yodluangfun S, Tantraworasin A. Necrotizing fasciitis: risk factors of mortality. Risk Manag Healthc Policy. 2015 Feb 16;8:1-7. [CrossRef] [PubMed] 

Cite as: Taylor A, Beer M, VanHook CJ. Medical image of the week: necrotizing soft tissue infection. Southwest J Pulm Crit Care. 2016 Mar;12(3):102-3. doi: http://dx.doi.org/10.13175/swjpcc005-16 PDF

March 2016 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  

Members of the Arizona, New Mexico, Colorado and California Thoracic Societies and the Mayo Clinic are able to receive  0.25 AMA PRA Category 1 Credits™. 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 this activity I will be better able to:    

1. Correctly interpret and identify clinical practices supported by the highest quality available evidence.
2. Will be better able to establsh the optimal evaluation leading to a correct diagnosis for patients with pulmonary, critical care and sleep disorders.
3. Will improve the translation of the most current clinical information into the delivery of high quality care for patients.
4. Will integrate new treatment options in discussing available treatment alternatives 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, 2015-December 31, 2016

Financial Support Received: None.

Clinical History: A 66 year-old man with orthotopic heart transplantation 1 year previously presented with complaints of recent-onset small volume (<1 teaspoon) hemoptysis, post-nasal drip, and night sweats. The patient indicated he had recent contact with several young grandchildren who had upper respiratory tract symptoms. The patient’s past medical history was remarkable for recurrent constrictive pericarditis (surgically treated), hypertension, type II diabetes mellitus (treated with insulin), psoriasis, sleep-disordered breathing, and grade 2 cardiac transplant rejection diagnosed 6 months earlier. The patient’s medication list included insulin, Cellcept (mycophenolate mofetil), Prograf (tacrolimus), prednisone, among others. On physical examination, the patient was mildly tachycardic (heart rate = 104 beats/minute) with an oxygen saturation on room air of 92%. The white blood cell count was within the normal range, but C-reactive protein and B-type natriuretic peptide levels were reportedly elevated.

Frontal chest radiography (Figure 1) was performed, with a radiograph from one month other also shown for comparison.

Figure 1. Frontal (A) chest radiography shows interval development of a thick-walled left lower lobe cavity since a chest radiograph performed one month previously.

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

1. The frontal chest radiograph shows a new lung cavity
2. The frontal chest radiograph shows basal predominant fibrotic abnormalities
3. The frontal chest radiograph shows large lung volumes with a cystic appearance
4. The frontal chest radiograph shows new peribronchial lymph node enlargement
5. The frontal chest radiograph shows new poorly defined nodular opacities bilaterally

Cite as: Gotway MB. March 2016 imaging case of the month. Southwest J Pulm Crit Care. 2016(Mar);12(3):90-101. doi: http://dx.doi.org/10.13175/swjpcc023-16 PDF 

Medical Image of the Week: Lactate Threshold

Figure 1.  V slope method for lactate threshold is where the CO2 production (VCO) increases compared to oxygen consumption (VO2). This is indicated by the vertical line.

The lactate or anaerobic threshold in exercise physiology is the point at which lactic acid starts to accumulate as the anaerobic component of metabolism increases and has been used to assess cardiopulmonary fitness. The V-slope method is a non-invasive way of estimating the lactate or anaerobic threshold (1). As lactate accumulates the H+ is mainly buffered by HCO3- and produces CO2. A point can be seen in Figure 1 where CO2 production (VCO2) abruptly increases relative to O2 consumption (VO2). This represents the point at which the lactate threshold occurs.

Mohammad R. Dalabih, MBBS and Naser J. Mahmoud, MBBS

Division of Pulmonary, Allergy and Critical Care

The University of Arizona

Tucson, AZ USA

Reference

1. Beaver WL, Wasserman K, Whipp BJ. A new method for detecting anaerobic threshold by gas exchange. J Appl Physiol. 1986;60(6):2020-7. [PubMed]

Cite as: Dalabih MR, Mahmoud NJ. Medical image of the week: lactate threshold. Southwest J Pulm Crit Care. 2016;12(3):89. doi: http://dx.doi.org/10.13175/swjpcc006-16 PDF

Medical Image of the Week: Leriche Syndrome

Figure 1. Axial CT of the abdomen demonstrating complete occlusion of the abdominal aorta at the level of the renal arteries (black arrow). An extensive network of collateral arteries is noted throughout the abdomen (white arrow showing representative collateral in anterior abdominal wall). An atrophic left kidney is also noted.

Figure 2. CT runoff demonstrating extensive abdominal network of collateral arteries, with relatively maintained distal perfusion in the setting of complete abdominal aorta occlusion.

A 68-year-old man with GOLD stage 4 COPD was admitted to the Intensive Care Unit for worsening hypoxic and hypercarbic respiratory failure. The patient was treated with steroids for COPD exacerbation, and required continuous BIPAP. On hospital day 2 concern arose for possible pulmonary embolism given worsening oxygenation despite BIPAP, and a thoracic CT angiogram was performed. On imaging, an incidental finding was discovered that the patient had complete occlusion of his aortic artery at the level of the renal arteries with extensive collaterals throughout the abdomen (Figure 1). The patient had palpable pulses in both feet and extremities were warm to touch bilaterally with recovered circulation, as verified on CT runoff (Figure 2). Vascular surgery was consulted, and a decision was made for no surgical intervention given the extensive collateral system and likely chronic time course. On further questioning the patient had limited ability to ambulate due to claudication. The patient also had diminished femoral pulses bilaterally, as well as erectile dysfunction, constituting the triad associated with Leriche syndrome (1).

Adam Berlinberg MD¹, Tanner Elaini MD², and Cameron Hypes MD³

¹Department of Internal Medicine

²Department of Pulmonary and Critical Care Medicine

³Department of Emergency Medicine, Critical Care Medicine

Banner-University Medical Center Tucson

Tucson, AZ

Reference

1. Leriche R, Morel A. The syndrome of thrombotic obliteration of the aortic bifurcation. Ann Surg. 1948;127(2):193-206. [PubMed]

Cite as: Berlinberg A, Elaini T, Hypes C. Medical image of the week: Leriche syndrome. Southwest J Pulm Crit Care. 2016;12(2):72-3. doi: http://dx.doi.org/10.13175/swjpcc004-16 PDF

Medical Image of the Week: Sarcoidosis

Figure 1. The AP supine chest radiograph depicts bilateral hilar calcified lymphadenopathy with characteristic popcorn appearance of the lymph nodes (white arrows).  Incidentally noted are a tunneled dialysis catheter terminating in the right atrium and median sternotomy wires from a previous coronary artery bypass graft surgery.

We present a 58-year-old African American man with a complicated medical history including long-standing sarcoidosis that has caused him chronic, unrelenting pain for two decades.  He initially underwent placement of an intrathecal morphine pump, but recently began complaining of increasing pain.  Consequently, he was seen at our hospital for interrogation of his pain pump by the interventional radiologist, and was incidentally noted to have bilateral calcified hilar lymphadenopathy on fluoroscopic imaging.  A dedicated chest x-ray confirmed the abnormality, which was consistent with his known diagnosis of sarcoidosis.

Sarcoidosis is a complex disease process characterized by noncaseous granulomas that can affect various organ systems, with pulmonary involvement in up to 90% of cases (1).  Though sarcoidosis is a diagnosis of exclusion, clinicians should recognize that bilateral hilar lymphadenopathy is highly concerning for the underlying noncaseating granulomatous disease (2).  The most common pattern of lymphadenopathy is well-defined, bilateral, symmetric hilar and right paratracheal lymph node enlargement. Bilateral hilar lymph node enlargement, alone or in combination with mediastinal lymph node enlargement, occurs in an estimated 95% of patients affected with sarcoidosis (1). Although bilateral hilar adenopathy may be a feature of other disease processes including infections (especially fungal or mycobacterium) and malignancy (metastases or lymphoma), sarcoidosis is the most common cause of bilateral hilar lymphadenopathy in the absence of specific clinical features of these processes. The enlarged lymph nodes eventually calcify, and the chronicity of the disease process directly correlates to hilar lymphadenopathy calcification, occurring in up to 20% of patients after 10 years (3).  Of note are the popcorn like calcifications within perihilar lymph nodes silhouetting the normal vascular anatomy (Figure 1).

Amrit Hansra, MD and Unni Udayasankar, MD

Department of Medical Imaging

University of Arizona

Tucson, AZ

References

1. Criado E, Sánchez M, Ramírez J, Arguis P, de Caralt TM, Perea RJ, Xaubet A. Pulmonary sarcoidosis: typical and atypical manifestations at high-resolution CT with pathologic correlation. Radiographics. 2010;30(6):1567-86. [CrossRef] [PubMed]
2. Baughman RP, Culver DA, Judson MA. A concise review of pulmonary sarcoidosis. Am J Respir Crit Care Med. 2011;183(5):573-81. [CrossRef] [PubMed]
3. Miller BH, Rosado-de-Christenson ML, McAdams HP, Fishback NF. Thoracic sarcoidosis: radiologic-pathologic correlation. Radiographics. 1995;15(2):421-37. [CrossRef] [PubMed]

Cite as: Hansra A, Udayasankar U. Medical image of the week: sarcoidosis. Southwest J Pulm Crit Care. 2016;12(2):62-3. doi: http://dx.doi.org/10.13175/swjpcc003-16 PDF

Medical Image of the Week: Malignant Spinal Cord Compression

Figure 1. MRI lumbar spine (sagittal image) demonstrating increased signal in the L1 and L2 vertebral bodies with tumor erosion of the posterior cortices. Encroachment upon the spinal canal is noted at L2.

Figure 2. MRI lumbar spine (sagittal image, post gadolinium infusion) demonstrating heterogeneous enhancement of L1 and L2 consistent with metastatic disease; spinal cord compression is noted at L2 (blue arrows). 

An 81 year-old man with metastatic bladder cancer was admitted to the hospital with back pain. The pain progressed over several weeks and interfered with ambulation. He had severe pain with any movement. Physical exam revealed pain with palpation of the lower back but no weakness or sensory deficits in the lower extremities. An MRI of the lumbar spine (with and without gadolinium contrast) revealed metastatic disease involving the L1 and L2 vertebral bodies, right sacrum and left iliac wing. At L2, moderate spinal canal stenosis due to tumor encroachment was noted (Figures 1 and 2). The patient was urgently treated with IV dexamethasone. He declined surgical intervention but agreed to radiation therapy.

Malignant spinal cord compression (MSCC) is an oncologic emergency that affects approximately 5% of cancer patients. It is most commonly seen in lung, breast, and prostate cancers (1). Neurologic complications are relatively uncommon in patients with bladder cancer. In a review of 359 patients with bladder cancer, only 2% had metastatic spinal cord compression (2). In MSCC, patients most commonly present with back pain. Weakness, sensory deficits, ataxia, paralysis, bowel and bladder dysfunction are later symptoms. The devastating effects of MSCC for patients make it imperative that clinicians consider the diagnosis in an oncology patient with back pain. The description of back pain can be vague and clinicians may overlook the insidious progression of symptoms. A crucial point related to the return of neurologic function in MSCC is the pretreatment neurological status. If treatment is started promptly, before significant weakness or other neurologic deficits develop, outcomes are notably improved. MRI of the total spine should be performed in any patient suspected of having MSCC. If MRI cannot be performed, CT with myelography is an alternative (3).

Treatment for MSCC includes steroids, radiotherapy, and surgery. The steroid doses vary widely and high dose steroids (dexamethasone 96 mg IV bolus with 24 mg four times daily for three days and taper over 10 days) are often initiated in patients with severe neurologic deficits. Lower dose steroids (dexamethasone 10 mg IV bolus, followed by 16 mg daily in divided doses) are also effective but there are no randomized controlled trials to compare efficacy of different doses. Radiation therapy is an important component of MSCC management, particularly in patients who are not surgical candidates. Both single dose radiation and longer course radiation have shown benefit, so decisions about dosing and duration can be based on the patient’s expected survival. Surgical decompression in addition to radiation therapy may provide quality of life benefits to a cohort of patients with MSCC. This avenue is reserved for patients with reasonable functional status and prognosis. A widely cited study published in 2005 showed improved functional outcomes after decompression plus radiotherapy versus radiotherapy only (4). If surgical intervention is considered, emergent consultation is critical to ensure the best possible outcome.

Katie Hawbaker MD, Michael Debo DO and Linda Snyder MD

Division of General Internal Medicine, Geriatrics and Palliative Medicine and Pulmonary, Allergy, Critical Care, & Sleep Medicine

Banner University Medical Center-Tucson

References

1. McCurdy M, Shanholtz C. Oncologic emergencies. Crit Care Med. 2012;40:2212-2. [CrossRef] [PubMed]
2. Anderson TS, Regine WF, Kryscio R, Patchell RA. Neurologic complications of bladder carcinoma. Cancer. 2003;97(9):2267-72. [CrossRef] [PubMed]
3. Carter BW, Erasmus JJ. Acute thoracic findings in oncologic patients. J Thorac Imaging. 2015;30:233-46. [CrossRef] [PubMed]
4. Patchell RA, Tibbs PA, Regine WF, Payne R, Saris S, Kryscio RJ, Mohiuddin M, Young B. Direct decompressive surgical resection in the treatment of spinal cord compression caused by metastatic cancer: a randomized trial. Lancet. 2005; 366(9486):643-8. [CrossRef] [PubMed]

Cite as: Hawbaker K, Debo M, Snyder L. Medical image of the week: malignant spinal cord compression. Southwest J Pulm Crit Care. 2016;12(2):59-61. doi: http://dx.doi.org/10.13175/swjpcc160-15 PDF 

February 2016 Imaging Case of the Month

Michael B. Gotway, MD

Department of Radiology

Mayo Clinic Arizona

Scottsdale, AZ

Imaging Case of the Month CME Information  

Members of the Arizona, New Mexico, Colorado and California Thoracic Societies and the Mayo Clinic are able to receive  0.25 AMA PRA Category 1 Credits™. 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 this activity I will be better able to:    

1. Correctly interpret and identify clinical practices supported by the highest quality available evidence.
2. Will be better able to establsh the optimal evaluation leading to a correct diagnosis for patients with pulmonary, critical care and sleep disorders.
3. Will improve the translation of the most current clinical information into the delivery of high quality care for patients.
4. Will integrate new treatment options in discussing available treatment alternatives 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, 2015-December 31, 2016

Financial Support Received: None.

Clinical History: A 78 year-old woman presented to her physician for routine care. Her past medical history included hyperlipidemia, hypothyroidism, gout, hypertension, and arthritis.

Although she was asymptomatic, screening 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 panels)

1. The frontal chest radiograph shows a poorly defined nodular opacity in the left upper lung
2. The frontal chest radiograph shows abnormal mediastinal contours
3. The frontal chest radiograph shows basal predominant fibrotic abnormalities
4. The frontal chest radiograph shows large lung volumes with a cystic appearance
5. The frontal chest radiograph shows no abnormal findings

Cite as: Gotway MB. February 2016 imaging case of the month. Southwest J Pulm Crit Care. 2016;12(2):48-58. doi: http://dx.doi.org/10.13175/swjpcc014-16 PDF