Medical Image of the Week: Tracheobronchopathia Osteochondroplastica

Figure 1: Panels (A and B) show the lumpy, bumpy nodules of tracheobronchopathia osteochondroplastica affecting the anterior tracheal wall with sparing of the posterior membrane. In this patient, copious amounts of white secretions can be seen in the distal trachea and the posterior membrane from her current MRSA pneumonia. 

Tracheobronchopathia osteochondroplastica (TO) is a rare, idiopathic tracheobronchial abnormality that is seen during 0.7% of bronchscopies. It is usually diagnosed in the 5th to 6th decades of life with a male preponderance (1,2)^. Here, we present the case of a 62-year-old woman with history of bronchial asthma with recurrent exacerbations who was admitted with pneumonia and a new mass-like consolidation on imaging. She underwent bronchoscopy for further work up and was found to have methicillin-resistant Staphylococcus aureus (MRSA) pneumonia. Incidental nodules were found in her trachea during the bronchoscopy (Figure 1). Most patients with TO are asymptomatic but can rarely present with cough, shortness of breath, and even non-massive hemoptysis due to ulceration of nodular mucosa. Secondary airway narrowing has also been reported. The lumpy, bumpy nodules typically are 3-8 mm in size, localize in the sub-mucosa of the trachea, and are difficult to biopsy due to their cartilaginous or osseous nature. Diagnosis can be made by chest CT or bronchoscopy. A very important distinctive feature is sparing of the posterior membranous wall of the trachea, differentiating it from other nodular airway diseases. TO is a benign disease that generally doesn’t need any specific treatment or intervention (1,2).

Huthayfa Ateeli, MBBS, Elaine Cristan, MD, and Afshin Sam, MD.

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

University of Arizona, Tucson, AZ USA

References

1. Lundgren R, Stjernberg NL. Tracheobronchopathia osteochondroplastica. A clinical bronchoscopic and spirometric study. Chest. 1981 Dec;80(6):706-9. [CrossRef] [PubMed]
2. Prince JS, Duhamel DR, Levin DL, Harrell JH, Friedman PJ. Nonneoplastic lesions of the tracheobronchial wall: radiologic findings with bronchoscopic correlation. Radiographics. 2002 Oct;22 Spec No:S215-30. [CrossRef] [PubMed] 

Cite as: Ateeli H, Cristan E, Sam A. Medical image of the week: tracheobronchopathia osteochondroplastica. Southwest J Pulm Crit Care. 2016;13(3):131-2. doi: http://dx.doi.org/10.13175/swjpcc067-16 PDF

Medical Image of the Week: Pneumothorax with Air Bronchograms

Figure 1. Panel (A) shows mild congestion with prominent bronchovascular markings. Panel (B) shows a large left pneumothorax with total collapse of the left lung marked by extensive airspace opacities and distinct air bronchograms. Panel (C) shows interval placement of a left-sided pigtail catheter with partial resolution of the left pneumothorax. There is persistent collapse of the medial aspect of the left upper lobe. Panel (D) shows complete resolution of the left pneumothorax and left lung atelectasis with continued bilateral airspace disease.

Development of pneumothoraces in critically ill patients is commonly encountered in the critical care unit (ICU). Incidence has been reported between 4-15% of patients. In most instances, pneumothorax in the ICU is considered a medical emergency especially when the patient is mechanically ventilated (1).  Here, we present a 61-year-old man with a past medical history of insulin dependent diabetes and paraplegia from prior spine injury who presented with acute respiratory distress after a pulseless electrical activity cardiac arrest. Cardiopulmonary resuscitation (CPR) was initiated by emergency medical services at home, and continued and the emergency department (ED) for a total of 30 minutes. The patient presented previously to the ED, one week prior, for a mild respiratory illness and tested positive for influenza B. He was sent home on oseltamivir. His family is unsure of compliance with medication but reported he was clinically stable up to the morning of presentation. The patient, as shown in the images, developed a left pneumothorax complicating an "adult respiratory distress syndrome (ARDS)- like" picture probably due to positive pressure ventilation with high positive end expiratory pressure, CPR, or both. The patient underwent immediate chest tube placement and with successful lung re-expansion. Unfortunately, his hemodynamic status/septic shock/multi-organ system failure continued to deteriorate within hours and he expired despite maximal support. Pneumothorax in patients with ARDS has higher morbidity and mortality compared to other critically ill patients due to the high-pressure needed during mechanical ventilation. This places patients at a high risk for the rapid progression to tension pneumothorax and even death. Therefore, in this high-risk population, a pneumothorax requires a high index of suspicion, prompt recognition, and immediate intervention (2).

Huthayfa Ateeli, MBBS and Steve Knoper, MD.

Department of Medicine, Division of Pulmonary, Critical Care, Sleep and Allergy Medicine. University of Arizona, Tucson, AZ USA

References

1. Yarmus L, Feller-Kopman D. Pneumothorax in the critically ill patient. Chest. 2012 Apr;141(4):1098-105. [CrossRef] [PubMed] 
2. Gattinoni L, Bombino M, Pelosi P, Lissoni A, Pesenti A, Fumagalli R, Tagliabue M. Lung structure and function in different stages of severe adult respiratory distress syndrome. JAMA. 1994 Jun 8;271(22):1772-9. [CrossRef] [PubMed] 

Cite as: Ateeli H, Knoper S. Medical image of the week: pneumothorax with air bronchograms. Southwest J Pulm Crit Care. 2016:13(3):129-30. doi: http://dx.doi.org/10.13175/swjpcc066-16 PDF

September 2016 Imaging Case of the Month

Michael B. Gotway, MD  

Department of Radiology

Mayo Clinic Arizona

Scottsdale, Arizona 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

Clinical History: A 64-year-old woman presents with a several month history of slowly worsening shortness of breath and dry cough, with worsening exercise limitation. Laboratory data, include white blood cell count and serum chemistries were within normal limits. Oxygen saturation on room air was 93%.

Frontal and lateral chest radiographs (Figure 1) were performed. Previous frontal and lateral chest radiographs, performed 7 years prior to presentation, are shown for comparison.

Figure 1. Frontal (A) and lateral (B) chest radiography. Frontal (C) and lateral (D) chest radiography performed 7 years prior are shown for comparison.

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

1. Frontal and lateral chest radiography appears normal
2. Frontal and lateral chest radiography bilateral linear and reticular abnormalities
3. Frontal and lateral chest radiography shows abnormally increased lung volumes
4. Frontal and lateral chest radiography shows bilateral hilar enlargement
5. Frontal and lateral chest radiography shows developing pleural thickening

Cite as: Gotway MB. September 2016 imaging case of the month. Southwest J Pulm Crit Care. 2016;13(3):114-22. doi: http://dx.doi.org/10.13175/swjpcc088-16 PDF

Medical Image of the Week: Superior Vena Cava Syndrome

Figure 1. Thoracic CT in soft tissue windows. Panels A, B, C and G show extensive collateral circulation along the right chest wall especially subcutaneous vessels and subcapsular hepatic vessels during contrast injection in the right arm (arrows). There are also prominent right hepatic and capsular enhancing vessels with vascular shunt within the posterior subcapsular right hepatic lobe. Panels D, E, F and I show extensive collateral circulation on the left side when the contrast is injected (on a different admission) in the left arm (arrows). Panel H shows absent blood flow in the totally thrombosed SVC stent.

Superior vena cava (SVC) syndrome results from obstruction of blood flow in the SVC. Most cases are secondary to malignancy, the most common being lung cancer or non-Hodgkin lymphoma. Other less encountered etiologies include fibrosing mediastinitis and thrombosis associated with intravascular devices (1,2). Here, we present a case of advanced lung cancer undergoing chemo-radiation therapy who presented with typical symptoms of SVC syndrome including progressive shortness of breath and facial swelling/ fullness over weeks to months. His chest CT scan showed SVC obstruction due to his tumor mass (Figure 1). The patient underwent stenting and improved partially for sometime. However, he returned again with worsening symptoms over a few weeks with discovery of SVC in-stent thrombosis. He was started on therapeutic enoxaparin and his symptoms improved partially with time.

Huthayfa Ateeli, MBBS¹, Kawanjit Sekhon, MD² and Dena K. L'Heureux, MD³.

¹Department of Medicine, Division of Pulmonary, Critical Care, Sleep and Allergy Medicine; ²Department of Medicine, Internal Medicine Residency Program, Main Campus; and ³Department of Medicine, Division of Pulmonary, Critical Care, Sleep and Allergy Medicine, University of Arizona, Southern Arizona VA Health Care System, Tucson, AZ USA

References

1. Wilson LD, Detterbeck FC, Yahalom J. Clinical practice. Superior vena cava syndrome with malignant causes. N Engl J Med. 2007 May 3;356(18):1862-9. [CrossRef] [PubMed] 
2. Rice TW, Rodriguez RM, Light RW. The superior vena cava syndrome: clinical characteristics and evolving etiology. Medicine (Baltimore). 2006 Jan;85(1):37-42. [CrossRef] [PubMed] 

Cite as: Ateeli H, Sekhon K, L'Heureux DK. Medical image of the week: superior vena cava syndrome. Southwest J Pulm Crit Care. 2016;13(2):99-100. doi: http://dx.doi.org/10.13175/swjpcc065-16 PDF

Medical Image of the Week: MAC Infection

Figure 1. PA and lateral chest radiograph demonstrating left upper lobe air space disease with possible cavity (blue arrow).

Figure 2. Chest CT (axial image) demonstrating extensive LUL cavitary necrotizing pneumonia (red arrow).

A 61-year-old woman with history of severe COPD (FEV1 1.07L, 40%) complicated by chronic hypoxemic, hypercarbic respiratory failure, ongoing tobacco abuse, and allergic phenotype. Over the past month or so, she had developed progressively worsening dyspnea on exertion, fatigue, poor appetite, and weight loss. She denied fevers, chills, and night sweats. Thoracic CT did show LUL cavitary lesion and RLL sub segmental tiny pulmonary embolus. 

A PA and lateral chest radiograph was performed and revealed extensive areas of patchy airspace opacity in the left upper lobe. Lucent foci are noted within the patchy opacities of concern for potential cavitation (Figure 1). CT chest was performed and showed extensive cavitary, necrotizing left upper lobe pneumonia, Centrilobular and paraseptal emphysema. (Figure 2). Sputum AFB was positive for acid fast bacilli, culture was positive for Mycobacterium avium complex (MAC), and she was started on treatment.

The term Mycobacterium avium complex (MAC) encompasses several species including M. avium and M. intracellulare. These organisms are genetically similar and generally not differentiated in the clinical microbiology laboratory. Among non-tuberculosis mycobacterium, MAC is the most common cause of pulmonary disease worldwide. It is generally felt that these organisms are acquired from the environment. Mounting evidence suggests that municipal water sources may be an important source for MAC lung infections (1). Unlike M. tuberculosis, there are no convincing data demonstrating human-to-human or animal-to-human transmission of MAC.

Four major clinical presentations have been prescribed:

• Disease in those with known underlying lung disease, primarily white, middle-aged, or elderly men, often alcoholics and/or smokers with underlying chronic obstructive pulmonary disease.
• Disease in those without known underlying lung disease predominantly in nonsmoking women over age 50 who have interstitial patterns on chest radiography.
• One report noted an unexpectedly high frequency (78 of 244 patients) of MAC pulmonary infections presenting as solitary pulmonary nodules, which resembled lung cancer (2).
• MAC exposure in immunocompetent hosts without underlying lung disease has been linked to the development of hypersensitivity pneumonitis, particularly following hot tub use.

The American Thoracic Society and Infectious Disease Society of America's diagnostic criteria for nontuberculosis mycobacterial pulmonary infections include both imaging studies consistent with pulmonary disease and at least two separate expectorated sputum samples isolation of mycobacteria or isolated from at least one bronchial wash in a symptomatic patient.

The recommendation is to start a combination of two to four drugs (as tolerated) for treatment of MAC pulmonary infection in HIV-negative patients. treatment for MAC until sputum cultures are consecutively negative for at least one year.

The ATS/IDSA guidelines recommend a combination of clarithromycin (1000 mg three times per week) or azithromycin (500 mg three times per week) PLUS rifampin (600 mg three times per week) or rifabutin (300 mg three times per week) PLUS ethambutol (25 mg/kg three times per week).

For patients with fibrocavitary MAC lung disease or severe nodular or bronchiectatic disease, the ATS/IDSA guidelines recommend same therapy plus streptomycin or amikacin (both 10 to 15 mg/kg three times per week) as a fourth agent for the first eight weeks. Patients receiving MAC treatment should have monthly monitoring for drug toxicity and sputum cultures.

Muna Omar, MD and Cristine Berry, MD

Pulmonary, Critical Care, Sleep and Allergy Medicine

Banner University Medical Center-Tucson

Tucson, AZ USA

References

1. Mullis SN, Falkinham JO 3rd. Adherence and biofilm formation of Mycobacterium avium, Mycobacterium intracellulare and Mycobacterium abscessus to household plumbing materials. J Appl Microbiol. 2013 Sep;115(3):908-14. [CrossRef] [PubMed]
2. Teirstein AS, Damsker B, Kirschner PA, Krellenstein DJ, Robinson B, Chuang MT. Pulmonary infection with Mycobacterium avium-intracellulare: diagnosis, clinical patterns, treatment. Mt Sinai J Med. 1990 Sep;57(4):209-15. [PubMed]
3. An official ATS/IDSA statement: diagnosis, treatment, and prevention of nontuberculous mycobacterial diseases. Griffith DE, Aksamit T, Brown-Elliott BA, Catanzaro A, Daley C, Gordin F, Holland SM, Horsburgh R, Huitt G, Iademarco MF, Iseman M, Olivier K, Ruoss S, von Reyn CF, Wallace RJ Jr, Winthrop K; ATS Mycobacterial Diseases Subcommittee; American Thoracic Society; Infectious Disease Society of America. Am J Respir Crit Care Med. 2007 Feb 15;175(4):367-416. [CrossRef] [PubMed] 

Cite as: Omar M, Berry C. Medical image of the week: MAC infection. Southwest J Pulm Crit Care. 2016;13(2):92-4. doi: http://dx.doi.org/10.13175/swjpcc064-16 PDF 

Medical Image of the Week: Subarachnoid Hemorrhage

Figure 1. Axial CT of the head without contrast demonstrates a large subarachnoid hemorrhage in the basal cisterns and adjacent to the insular cortices (blue arrows).

Figure 2. Coronal CT angiogram of the head demonstrates a saccular outpouching of the anterior communicating artery (blue arrow) consistent with an aneurysm.

A 70-year-old lady with a past medical history of hypertension and dyslipidemia was brought in by her family members for evaluation of confusion and headache for 1 week. There was no history of recent trauma or falls. There was no known family history of aneurysm or sudden death. On examination, her blood pressure was 139/99 mmHg, heart rate 92 bpm, afebrile and respiratory rate was 13 breaths per minute. She was alert but only oriented to self. Pupils were symmetric and reactive to light. She was able to follow commands and power was symmetric in all limbs.

CT of the head without contrast showed diffuse subarachnoid and intraventricular hemorrhage with signs of raised intracranial pressure (Figure 1). Neurosurgery was consulted and she underwent emergent insertion of an external ventricular drain. Head CT post-ventriculostomy showed improvement in her ventricular dilatation. CT angiography was performed later and showed an anterior communicating artery aneurysm (Figure 2), thought to be culprit of her subarachnoid hemorrhage. Craniotomy with surgical clipping was performed. This was followed by improvement in her mental status.

The common presenting symptom of patients with subarachnoid hemorrhage is headache. They will classically describe it as "worst headache of my life". This can be accompanied by altered mental status, nausea, vomiting, or meningeal signs. Head CT without contrast should be obtained immediately if there is suspicion of subarachnoid hemorrhage. Studies have shown that head CT is extremely sensitive if obtained within 6 hours of clinical presentation but its sensitivity declines over time (1). Lumbar puncture should be performed if head CT is negative but there is strong suspicion of subarachnoid hemorrhage. A combination of negative head CT and lumbar puncture is sufficient to rule out subarachnoid hemorrhage in a patient presented with headache (2).

Kai Rou Tey¹, MD; Tammer Elaini², MD

¹Department of Internal Medicine, University of Arizona College of Medicine- South Campus and ²Department of Pulmonary, Critical Care, Allergy and Sleep University of Arizona College of Medicine

Tucson, AZ USA

References

1. Perry JJ, Stiell IG, Sivilotti ML, et al. Sensitivity of computed tomography performed within six hours of onset of headache for diagnosis of subarachnoid haemorrhage: prospective cohort study. BMJ. 2011;343:d4277. [CrossRef] [PubMed]
2. Perry JJ, Spacek A, Forbes M, et al. Is the combination of negative computed tomography result and negative lumbar puncture result sufficient to rule out subarachnoid hemorrhage? Ann Emerg Med. 2008 Jun;51(6):707-13. [CrossRef] [PubMed] 

Cite as: Tey KR, Elaini T. Medical image of the week: subarachnoid hemorrhage. Southwest J Pulm Crit Care. 2016;13(2):88-9. doi: http://dx.doi.org/10.13175/swjpcc063-16 PDF

Medical Image of the Week: Catheter-Induced Right Atrial Thrombus

  

Figure 1. Panel A: Apical 4 chamber view showing intra cardiac mass (arrow) in the right atrium located above the closed tricuspid valve in systole (left). Panel B: The mass moves into the right ventricle through the open tricuspid valve in diastole.

Figure 2. Axial TRUFISP MRI images through the mediastinum demonstrate a central venous catheter (yellow arrow) within the distal superior vena cava (a-b) and proximal right atrium (c).  A hypointense lesion (red arrow) is seen extending from and in close approximation of the catheter tip (d-e).  Axial T1 post-contrast MRI image through the heart demonstrates no associated enhancement (f) in this lesion. These findings are most consistent with a catheter-related thrombus. 

A 71-year-old woman with a history of renal amyloidosis complicated by end stage renal disease on long term hemodialysis through a permacath presented with complaints of recurrent syncope during hemodialysis. When propped up at 45 degrees, her examination showed an early systolic murmur located over her right upper sternal border and a crescendo systolic murmur located over left axillary region. The murmurs were grade 2/6 in intensity but increased to 4/6 when propped up at 90 degrees. A transthoracic echocardiogram revealed a 2.5 x 2.7 cm echogenic mass arising from the right atrial side of AV groove and prolapsing through the open tricuspic valve into the right ventricle during diastole (Figure 1). On contrast enhanced cardiac magnetic resonance imaging, the mass was identified as a thrombus measuring 2.9 x 2.7 x 2.2 cm and connected to the distal tip of the dialysis catheter (Figure 2).

It is difficult to confidently determine the best catheter tip position to avoid thrombosis.  Although placement of the catheter tip in the right atrium may decrease thrombosis, this location is debatable and subject to controversy (1). The optimal treatment for catheter-induced right atrial thrombus is also an area of controversy (2).  

Anticoagulation therapy is preferred over surgery by most physicians. For our patient, we treated her with warfarin to a target INR (International Normalized Ratio) of 2 to 3.  We were concerned about the possibility of thrombus detachment and catastrophic embolism. We retained the internal jugular catheter in place and obtained a new femoral access site for future hemodialysis.

Manjinder Kaur DO, Hem Desai MBBS, Emily S Nia MD, and Imo Ebong MD

Department of Medicine

University of Arizona

Tucson, AZ USA

References

1. Vesely TM. Central venous catheter tip position: a continuing controversy. J Vasc Interv Radiol. 2003 May;14(5):527-34. [CrossRef] [PubMed]
2. Lalor PF, Sutter F. Surgical management of a hemodialysis catheter-induced right atrial thrombus. Curr Surg. 2006 May-Jun;63(3):186-9. [CrossRef] [PubMed] 

Cite as: Kaur M, Desai H, Nia ES, Ebong I. Medical image of the week: catheter-induced right atrial thrombus. Southwest J Pulm Crit Care. 2016;13(2):82-3. doi: http://dx.doi.org/10.13175/swjpcc062-16 PDF

Medical Image of the Week: Splenic Infarction

Figure 1. Axial computed tomography demonstrating a wedge-shaped area of hypo-enhancement in the spleen in keeping with a splenic infarct.

Figure 2. Coronal computed tomography demonstrating a wedge-shaped area of hypo-enhancement in the spleen .

A 52-year-old Hispanic woman with a past medical history significant for Type 1 diabetes mellitus, hypertension, and rheumatoid arthritis presented with left upper quadrant pain for one day. Her review of systems was positive for bloating, severe epigastric and left upper quadrant tenderness that radiated to the back and left shoulder, nausea with non-bilious emesis, and diarrhea for one day prior to admission. Physical exam only revealed epigastric and left upper quadrant tenderness to light palpation without rebound or guarding.  Abdominal computed tomography of the abdomen demonstrated a new acute or subacute splenic infarct with no clear evidence of an embolic source in the abdomen or pelvis (Figures 1 and 2). Echocardiogram with bubble study and contrast did not demonstrate valve abnormalities, cardiac mass, vegetation, valve or wall motion abnormalities and no evidence of patent foramen ovale.

Splenic infarction should be suspected when patients present with sharp, acute left upper quadrant pain radiating to the left shoulder (Kehr sign). Splenic friction rub may be auscultated but CT is diagnostic (1). Splenic infarction is an uncommon condition, with compiled reports from a 10-year retrospective study of an academic center showing only 32 cases (0.016% of admission). Causes included cardiogenic emboli (62.5%), autoimmune disease (12.5%), associated infection (12.5%), or hematological malignancy (6%) (2). Active malignancy, embolic events from atrial fibrillation or infective endocarditis, and inflammatory disorders appear to be consistent causes for splenic infarct as demonstrated in a compilation study of 123 case reports of non-traumatic splenic infarction (3). Management includes supportive care and treating the underlying cause, embolic (e.g. endocarditis), vasculitis, or in situ occlusion from predisposing conditions (e.g. sickle cell, polycythemia vera, chronic myeloid leukemia, or myelofibrosis) (1).  

Given her stable condition and improving clinical course, she was discharged to follow up with her outpatient provider with recommendation for an anti-phospholipid and hypercoagulability workup.

Daniel J Casey, MSIV. Faraz Jaffer, MD. and Don Leo Pepito, MD.

University of Arizona College of Medicine at South Campus

Tucson, Arizona USA

References

1. LeBlond R, Brown D, DeGowin R. The abdomen, perineum, anus, and rectosigmoid. In: Degowin's Diagnostic Examination. New York, NY: McGraw Hill Medical; 2009: 445-527.
2. Schattner A, Adi M, Kitroser E, Klepfish A. Acute Splenic Infarction at an Academic General Hospital Over 10 Years: Presentation, Etiology, and Outcome. Medicine (Baltimore). 2015 Sep;94(36):e1363. [CrossRef] [PubMed]
3. Cox M, Li Z, Desai V, Brown L, Deshmukh S, Roth CG, Needleman L. Acute nontraumatic splenic infarctions at a tertiary-care center: causes and predisposing factors in 123 patients. Emerg Radiol. 2016 Apr;23(2):155-60. [CrossRef] [PubMed]

Cite as: Casey DJ, Jaffer F, Pepito DL. Medical image of the week: splenic infarction. Southwest J Pulm Crit Care. 2016;13(2):63-4. doi: http://dx.doi.org/10.13175/swjpcc060-16 PDF

August 2016 Imaging Case of the Month

Michael B. Gotway, MD  

Department of Radiology

Mayo Clinic Arizona

Scottsdale, Arizona 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

Clinical History: A 47 year-old white man presented with a history of worsening shortness of breath over the past few months. When questioned, the patient indicated that his activity tolerance had probably been slow decreasing over a relatively long period of time, but had become more pronounced recently.

Laboratory data, include white blood cell count and serum chemistries were within normal limits. Oxygen saturation on room air was 93%.

Frontal chest radiography (Figure 1) was performed.

Figure 1. Frontal and lateral 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 seven panels)

1. The frontal chest radiograph appears normal
2. The frontal chest radiograph shows abnormal mediastinal contours
3. The frontal chest radiograph shows abnormally increased lung volumes
4. The frontal chest radiograph shows bilateral linear and reticular abnormalities
5. The frontal chest radiograph shows pneumothorax

Cite as: Gotway MB. August 2016 imaging case of the month. Southwest J Pulm Crit Care. 2016;13(2):54-62. doi: http://dx.doi.org/10.13175/swjpcc072-16 PDF

Medical Image of the Week: Lung Entrapment

Figure 1. Pleural Fluid (a) and the collapsed left lung within the hemi-thorax (b).

Figure 2. Malignant involvement of the visceral pleura (arrows).

Figure 3.  Persistent pneumothorax (white arrows) after several days of pleural catheter (black arrow) drainage.

A 74-year-old woman with a history of breast cancer 10 years ago treated with lumpectomy and radiation presented for evaluation of shortness of breath. She was diagnosed with left sided pleural effusion which was recurrent requiring multiple thoracenteses. There was increased pleural fludeoxyglucose (FDG) uptake on PET-CT indicative of recurrent metastatic disease. She underwent a medical pleuroscopy since the pleural effusion analysis did not reveal malignant cells although the suspicion was high and tunneled pleural catheter placement as adjuvant chemotherapy was initiated.

Figure 1 shows a pleurscopic view of the collapsed left lung and the effusion in the left hemi thorax. Figure 2 shows extensive involvement of the visceral pleura with metastatic disease preventing complete lung inflation. Figure 3 shows persistent pneumothorax-ex-vacuo despite pleural catheter placement confirming the diagnosis of entrapment.

Incomplete lung inflation can be due to pleural disease, endobronchial lesions or chronic telecasts.

Lung entrapment and trapped lung are related but distinct clinical entities (1). A trapped lung is a proper diagnosis when there is no active pleural disease however a fibrous peel has been formed due to a remote process and the mechanical effects of the pleura are the primary problem. Lung entrapment is used when incomplete lung inflation is secondary to visceral pleural peel secondary to active infection, inflammation or malignancy and the underlying process then becomes the primary problem.

The parietal pleural biopsies obtained during the pleuroscopy confirmed recurrent metastatic disease and the patient is currently undergoing chemotherapy.

Bhupinder Natt MD and James Knepler MD

Division of Pulmonary, Allergy, Critical Care and Sleep

University of Arizona Health Sciences,

Tucson, AZ USA

Reference

1. Huggins JT, Doelken P, Sahn SA. The unexpandable lung. F1000 Med Rep. 2010 Oct 21;2:77. [CrossRef] [PubMed]

Cite as: Natt B, Knepler J. Medical image of the week: lung entrapment. Southwest J Pulm Crit Care. 2016;13(1):36-7. doi: http://dx.doi.org/10.13175/swjpcc059-16 PDF

Medical Image of the week: Endobronchial Valves

Figure 1. Bronchoscopic view of the endobronchial valves in the right upper lobe sub-segments.

Figure 2. Post procedural chest x-ray shows the valves (encircled). Other findings on this chest x-ray include a tracheostomy tube, right sided chest tube, left sided PICC line. Bilateral pneumatoceles are also seen (arrows).

A 39 year-old woman was referred to our hospital for evaluation of persistent broncho-pleural fistula after severe necrotizing streptococcal pneumonia. She had undergone a segmentectomy for the necrosis resulting in the broncho-pleural fistula. Her overall medical condition and malnutrition precluded another major surgery such as a muscle flap for the persistent air leak. Endobronchial valve placement was attempted to minimize the gradient and leak across the parenchymal defect to promote healing.

A sequential balloon occlusion technique was used to localize the leak to the right upper lobe, which was the site of the previous surgery. The sub-segments were measured and three endobronchial valves (Spiration®, Olympus Respiratory, USA) (1). Valves of 5 mm, 6 mm and 7 mm – were placed in the three sub-segments of the right upper lobe (Figure 1) with a flexible bronchoscope. Near elimination of the air leak was seen post procedure. Figure 2 shows post procedure chest x-ray showing the three valves.

Removable endobronchial valves have been shown to be safe and effective in cases of persistent post-operative air leaks (2).

Bhupinder Natt MD and James Knepler MD

Division of Pulmonary, Allergy, Critical Care and Sleep

Banner University Medical Center-Tucson

Tucson, AZ USA

References

1. Olympus Corporation. Spiration® valve system. Available at: http://www.spiration.com/us/product-overview (accessed 6/21/16).
2. Gillespie CT, Sterman DH, Cerfolio RJ, Nader D, Mulligan MS, Mularski RA, Musani AI, Kucharczuk JC, Gonzalez HX, Springmeyer SC. Endobronchial valve treatment for prolonged air leaks of the lung: a case series. Ann Thorac Surg. 2011 Jan;91(1):270-3. [CrossRef] [PubMed]

Cite as: Natt B, Knepler J. Medical image of the week: endobronchial valves. Southwest J Pulm Crit Care. 2016;13(1):34-5. doi: http://dx.doi.org/10.13175/swjpcc057-16 PDF

Medical Image of the Week: Bronchial Artery Embolization

Figure 1. Thoracic CT with contrast demonstrating right upper and lower lobe tree-in-bud and ground glass opacities (arrows) consistent with progressing pulmonary coccidioidomycosis.

Figure 2. Chest radiograph demonstrates the ethylene vinyl alcohol polymer retained in the bronchial arteries after the embolization procedure (arrows).

A 25-year-old woman with a past medical history significant for pulmonary coccidioidomycosis and poorly controlled type I diabetes mellitus presented to the emergency department with a chief complaint of 4 days of progressively worsening shortness of breath and 3-4 days of intermittent hemoptysis. Initial CT scan demonstrated progressive tree-in-bud and ground glass opacities in the right upper and lower lung lobes suggesting worsening of her ongoing coccidiomycosis (Figure 1). On hospital day 3 she began to have worsening hypoxemia and hemoptysis requiring transfer to the intensive care unit. Interventional radiology was consulted who performed an emergent right sided bronchial artery embolization with the ethylene vinyl alcohol polymer, Onyx^tm. After embolization her chest radiographs demonstrated evidence of the embolization material in the pulmonary vasculature (Figure 2).

Ethylene vinyl alcohol polymer, Onyx^tm is a liquid embolic substance which solidifies after contact with ionic materials (1). This results in a rapid, irreversible and permanent embolization of the bleeding target vessel (2). It was initially approved for use in the embolization of cerebral arteriovenous malformations, however has been used for rapid embolization of other hemorrhagic conditions such has hemoptysis from bleeding bronchial arteries (3). The most common complication after embolization is chest pain that is self-limiting. Transverse myelitis from spinal cord ischemia is the most serious complication associated with bronchial artery embolization however the occurrence is significantly decreased by spinal arterial identification during initial angiography (4). This patient’s embolization was without complications. She was successfully extubated on hospital day 15 without evidence of ongoing hemoptysis and will continue to follow up in the pulmonary and infectious disease clinics for ongoing treatment of her Coccidiodes pulmonary disease.

Benjamin J. Jarrett MD, MPH and Sachin Chaudhary, MD

Department of Medicine

University of Arizona

Tucson, AZ USA

References

1. Lubarsky M, Ray C, Funaki B. Embolization agents-which one should be used when? Part 2: small-vessel embolization. Semin Intervent Radiol. 2010 Mar;27(1):99-104. [CrossRef] [PubMed]
2. Yamashita K, Taki W, Iwata H, Nakahara I, Nishi S, Sadato A, Matsumoto K, Kikuchi H. Characteristics of ethylene vinyl alcohol copolymer (EVAL) mixtures. AJNR Am J Neuroradiol. 1994 Jun;15(6):1103-5. [PubMed]
3. Guimaraes M, Wooster M. Onyx (Ethylene-vinyl Alcohol Copolymer) in Peripheral Applications. Semin Intervent Radiol. 2011 Sep;28(3):350-6. [CrossRef] [PubMed]
4. Sopko DR, Smith TP. Bronchial artery embolization for hemoptysis. Semin Intervent Radiol. 2011 Mar;28(1):48-62. [CrossRef] [PubMed]

Cite as: Jarrett BJ, Chaudhary S. Medical image of the week: bronchial artery embolization. Southwest J Pulm Crit Care. 2016;13(1):32-3. doi: http://dx.doi.org/10.13175/swjpcc053-16 PDF

Medical Image of the Week: Massive Abdominal Aortic Aneurysm

Figure 1. Non-contrast CT A) axial, B) sagittal, and C) coronal views demonstrate a massive abdominal aortic aneurysm measuring 12.5 cm wide at maximal diameter.

Figure 2. Representative images from a CT-angiogram shows A) upper and B) lower abdominal axial sections showing renal artery involvement (red arrow) and substantial intramural thrombus (light blue brace). C) Coronal view demonstrates fusiform dilation of the iliacs (green arrow) and D) sagittal view demonstrates involvement of the thoracoabdominal aorta (pink arrow) and all major arterial branches of the abdominal aorta (celiac trunk, superior and inferior mesenteric arteries; dark blue arrows).

An 88 year-old presented to the emergency department with left flank and lower back pain as well as lower abdominal fullness. The fullness had started 2 days prior, but the left flank pain acutely started in the early morning before presenting. He had a history of unmedicated hypertension, hyperlipidemia, and mild vertigo. His review of systems was positive for chills and difficulty urinating but no hematuria. He was a non-smoker, and had undergone orthopedic surgeries but had otherwise avoided emergent hospitalizations.

On exam, vitals were unremarkable; there was no flank nor costovertebral angle tenderness; however, a midline pulsatile mass was present. An initial non-contrast CT abdomen/pelvis revealed a massive abdominal aortic aneurysm (AAA, Figure 1). Follow-up CT angiogram of the AAA can be seen in Figure 2. Upon further questioning, he had undergone a research study some 30 years earlier involving ultrasound to screen for AAA and was told he did not have one at the time.

AAA’s occur in 4-9% of the population (1-3) because of the diminished elastin in the infrarenal aorta. Inciting or etiologic factors include inflammatory, genetic and biochemical mediators, with positive risk factors including white race, atherosclerosis, smoking, male gender, hypertension, personal history of other arterial aneurysms, family history of AAA’s, and advancing age. Screening all men aged 65-79 has been shown to reduce mortality (2) despite the non-trivial mortality associated with elective AAA repair (3). Only 1% of 65 year-old men with a negative ultrasound will go on to develop an AAA (2).

The feared and fatal complication of AAA is rupture, and occurs in 10,500 ± 1,500 patients yearly in the U.S.A., with larger AAA’s posing higher annual risk of rupture (1-3). Emergent surgical repair mortality in the 30-50% that survive a rupture long enough to go to the operating room is roughly 50%.

The extensive nature of this patient’s aneurysm would have made for a nearly-impossible surgery, with operative mortality estimates between 15% using the British Aneurysm Repair Score (3) to 50% based on clinical opinion. This dissuaded the patient, his family, and vascular surgery team from pursuing elective repair. The patient desired discharge with pain medications and stricter blood pressure control with outpatient follow-up.

Michael Larson, M.D., Ph.D.

Tucson Hospitals Medical Education Program

Tucson, AZ, USA

References

1. Lederle FA. Ultrasonographic screening for abdominal aortic aneurysms. Ann Intern Med. 2003 Sep 16;139(6):516-22. [CrossRef] [PubMed]
2. Cosford PA, Leng GC. Screening for abdominal aortic aneurysm. Cochrane Database Syst Rev. 2007 Apr 18;(2):CD002945. [CrossRef] [PubMed]
3. Grant SW, Hickey GL, Grayson AD, Mitchell DC, McCollum CN. National risk prediction model for elective abdominal aortic aneurysm repair. Br J Surg. 2013 Apr;100(5):645-53. [CrossRef] [PubMed]

Cite as: Larson M. Medical image of the week: massive abdominal aortic aneurysm. Southwest J Pulm Crit Care. 2016:13(1):30-1. doi: http://dx.doi.org/10.13175/swjpcc052-16 PDF

July 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: An 18-year-old non-smoking man with a previous diagnosis of Ehlers-Danlos syndrome presented with mild shortness of breath and new cough. Physical examination was normal. The patient was afebrile.

Laboratory data were remarkable except for a mildly elevated white blood cell count of 11 x 10⁹ cells/L. Serum chemistries were within normal limits. Oxygen saturation on room air was 97%.

Frontal chest radiography (Figure 1) was performed.

Figure 1. Frontal chest radiography

A previous comparison chest radiograph from 3 years earlier (Figure 2) is shown as well.

Figure 2. Frontal and lateral chest radiography from 3 years earlier.

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

1. The frontal chest radiograph shows new bilateral small nodular opacities
2. The frontal chest radiograph shows new focal opacity in the lateral right base 
3. The frontal chest radiograph shows new mediastinal lymphadenopathy
4. The frontal chest radiograph shows no focal abnormalities or change from prior
5. The frontal chest radiograph shows pneumothorax

Cite as: Gotway MB. July 2016 imaging case of the month. Southwest J Pulm Crit Care. 2016:13(1):15-26. doi: http://dx.doi.org/10.13175/swjpcc061-16 PDF

Medical Image of the Week: Bronchiectasis

Figure 1. Video of thoracic axial computed tomography (CT) images in lung windows demonstrating dependent cystic bronchiectasis with air-fluid levels.

Figure 2. Video of thoracic coronal CT images.

A 49-year old Native American woman with chronic hypoxic and hypercarbic respiratory failure requiring 3 liters continuous via nasal cannula and nocturnal non-invasive bi-level ventilation presented with acute shortness of breath for 5 days. She has history of recurrent respiratory infections since early childhood, however over the past five years has been treated multiple times for presumed COPD exacerbation with last such treatment one month prior to admission.

Upon arrival, vitals displayed elevated blood pressure 183/96. Clinical examination demonstrated morbidly obese patient in mild somnolence and has diffuse expiratory wheezing, basal crackles with reduced air entry bilaterally. Laboratory examination showed leukocytosis (13,800 cells/uL) with neutrophilic predominance, thrombocytopenia (85,000 cells/uL), and elevated bicarbonate (31 mg/dL). Arterial blood gas showed pH=7.29, pCO2 756 mm Hg, and pO2 73 mm Hg. Thoracic computed tomography (CT) with contrast ruled out pulmonary embolism, however demonstrated extensive cystic bronchiectasis in left upper and lower lobes, right lower lobe along with findings consistent with chronic bronchitis and bronchiolitis. (Figures 1 and 2)

Bronchiectasis workup showed-low serum globulins (IgG 388 mg/dL, IgM 18 mg/dL , IgA 64 mg/dL, with low IgG-1 226 mg/dL, IgG-2 140 mg/dL). Alpha Antitrypsin level was high. Blood culture, sputum culture, urine Legionella, Streptococcus pneumoniae antigen, Coccidioidomycosis serology, quantiferon and AFB stain for TB were all negative. Aggressive nebulization therapy, intermittent Bi-level positive airway pressure and antibiotics allowed her to become stabilized to a baseline oxygen requirement. She was  discharged with diagnosis of acute on chronic hypoxic and hypercarbic respiratory failure secondary to flare up of severe bronchiectasis secondary to common variable immunodeficiency (CVID).

Common Variable Immunodeficiency (CVID), a subset of primary humoral immunodeficiency diseases, is a condition of inadequate immunoglobulin expression in response to antigen exposure. Prevalent equally amongst the sexes and ranges from 1 in 10,000 to 50,000 with bimodal incidence either within the first or third decade of life. Initial history is nonspecific, consisting of recurrent episodes of sinusitis and bronchitis with severity of illness dependent on level of immunoglobulin expression. The European Society for Immunodeficiency defines CVID as reduced (below 2 standard deviations of the mean) levels of IgG with reduced IgA and/or IgM, together with failure to mount a significant antibody response to vaccination, in the absence of a known cause. However, etiology of CVID is still incompletely understood and given the clinical heterogeneity in patient presentation, there is lack of consensus on clinical definition. Persistent sinus or respiratory complaints, in combination with finding of airway bronchiectasis lead a referral to an immunologist or pulmonologist in pursuit of diagnosis.

Bronchiectasis, a syndrome characterized by irreversible destruction, abnormal dilatation impairing clearance and leading to mucous pooling, is a common development in this impaired immune condition. Management of disease is multifactorial with symptom control, administration of appropriate immunizations and immunoglobulin replacement in agammaglobulinemia in order to curb recurrence of infections. Pulmonary morbidity due to bronchiectasis is common, however role of lung transplant in this patient population is unknown.

Practitioners should remain cognizant of considering CVID in patients with history of recurrent pneumonias and imaging findings of bronchiectasis to hasten specialty referral early and minimize pulmonary morbidity.

Faraz Jaffer, MD. Nirmal Singh, MD. and Jennifer Huang-Tsang, MD.

Department of Internal Medicine

University of Arizona at South Campus

Tucson, Arizona USA

References

1. Panigrahi MK. Common variable immunodeficiency disorder - An uncommon cause for bronchiectasis. Lung India. 2014 Oct;31(4):394-6. [CrossRef] [PubMed]
2. Tarzi MD, Grigoriadou S, Carr SB, Kuitert LM, Longhurst HJ.Clinical immunology review series: An approach to the management of pulmonary disease in primary antibody deficiency. Clin Exp Immunol. 2009 Feb;155(2):147-55. [CrossRef] [PubMed]
3. Cunningham-Rundles C. How I treat common variable immune deficiency. Blood. 2010 Jul 8;116(1):7-15. [CrossRef] [PubMed]

Cite as: Jaffer F, Singh N, Huang-Tsang J. Medical image of the week: bronchiectasis. Southwest J Pulm Crit Care. 2016;12(6):258-60. doi: http://dx.doi.org/10.13175/swjpcc045-16 PDF

Medical Image Of The Week: Tricuspid Valve Vegetation with Septic Pulmonary Emboli

Figure 1. Chest radiograph on presentation consistent with septic pulmonary embolic and cavitation.

Figure 2. Echocardiogram demonstrating a highly mobile echo-dense vegetation attached to the atrial side of the tricuspid valve.

A 28-year-old woman with a history of extensive intravenous heroin use presented to the hospital with generalized chest and abdominal pain. Vital signs were remarkable for hypotension, tachypnea, and tachycardia. Laboratory studies revealed leukocytosis, hyponatremia, acute kidney injury, and lactic acidosis. A radiograph of the chest demonstrated multiple airspace opacities throughout the bilateral lungs with associated cavitary lesions and a small right-sided pleural effusion (Figure 1). A transthoracic echocardiogram was obtained, which demonstrated a 3.6 cm x 2.0 cm tricuspid valve vegetation (Figure 2). Blood cultures identified methicillin-sensitive Staphylococcus aureus.

Infective endocarditis, valvular vegetation, and septic pulmonary emboli are common complications of intravenous drug use. Staphylococcus aureus is the most common bacterial cause of infective endocarditis among intravenous drug users (1). Like endocarditis, patients with septic pulmonary emboli often present with non-specific clinical manifestations such as fever (86%), dyspnea (48%), and chest pain (49%) (2). Management may be surgical or medical, and determining the best course is complicated by social and psychiatric factors affecting adherence to treatment. Cardiac valve surgery has been advocated early for large right-sided vegetations but carries high morbidity and expense, as well as risk of compromised recovery, in the setting of ongoing IV drug use. Even for patients with valvular vegetations ≥ 1cm, medical therapy alone may be a safe option under some circumstances in the absence of other surgical indications (3).

Sarah Harris BA¹, Kady Goldlist MD², Maria Tumanik DO², Cameron Hypes MD MPH^3,4

¹ University of Arizona College of Medicine

² Department of Internal Medicine, Banner University Medical Center – South Campus

³ Department of Medicine, Division of Pulmonary, Allergy, Critical Care, and Sleep Medicine

 ⁴Department of Emergency Medicine

University of Arizona

Tucson, AZ USA

References

1. Ortiz-Bautista C, López J, García-Granja PE, et al. Current profile of infective endocarditis in intravenous drug users: The prognostic relevance of the valves involved. Int J Cardiol. 2015;187:472-4. [CrossRef] [PubMed]
2. Ye R, Zhao L, Wang C, Wu X, Yan H. Clinical characteristics of septic pulmonary embolism in adults: a systematic review. Respir Med. 2014 Jan;108(1):1-8. [CrossRef] [PubMed]
3. Otome O, Guy S, Tramontana A, Lane G, Karunajeewa H. A retrospective review: significance of vegetation size in injection drug users with right-sided infective endocarditis. Heart Lung Circ. 2016 May;25(5):466-70. [CrossRef] [PubMed] 

Cite as: Harris S, Goldlist K, Tumanik M, Hypes C. Medical image of the week: tricuspid valve vegetation with septic pulmonary emboli. Southwest J Pulm Crit Care. 2016:12(6):253-4. doi: http://dx.doi.org/10.13175/swjpcc042-16 PDF

Medical Image of the Week: Boerhaave Syndrome

Figure 1. Panel A: Coronal CT image with IV contrast showing a massively dilated esophagus with retained food particles.  Panel B: Coronal CT image depicting distal esophageal perforation (red arrow) rupturing into the lung parenchyma with resultant abscess formation (yellow arrow). Panel C: Axial image showing the dilated esophagus, ruptured into the lung (arrow). There is also mass effect on the mediastinum and heart. Panel D. After insertion of a nasogastric tube and chest tube in the lung abscess, computed tomography was performed after administration of oral contrast. There is extravasation of contrast into the lung cavity which now contains a drainage catheter. Arrow shows the rupture site.

A 41-year-old woman with a history of gastroesophageal reflux disease (GERD), asthma and iron deficiency anemia presented with complaints of right sided chest pain, nausea and emesis for several days prior to hospital presentation. She had also been experiencing progressive dysphagia to solids for a month preceding admission. CT chest imaging revealed mega-esophagus (Figure 1A) with rupture into the right lung parenchyma and resultant abscess formation (Figure 1B and 1C). A subsequent echocardiogram also confirmed mitral valve endocarditis. An image-guided chest tube was placed in the abscess for drainage. Endoscopy was attempted but visualization was difficult due to the presence of retained food. Given her low albumin and poor nutritional state, a jejunostomy tube was placed. Follow up CT imaging with contrast through a nasogastric tube confirmed extravasation of esophageal contrast into the right lung parenchyma (Figure 1D).  

Blood and sputum cultures grew Candida glabrata. She was initially started on broad spectrum antibiotics which were later tapered to Liposomal Amphotericin B and ampicillin-sulbactam. Following resolution of her fungemia and optimization of her nutritional status 2 months later, she underwent Ivor Lewis esophagectomy, pyloroplasty and serratus anterior muscle flap buttress to the remnant esophageal staple line. Pathology of the excised esophageal tissue revealed muscular hypertrophy and marked reduction of ganglion cells consistent with achalasia. There was also a segment of esophageal mucosal ulceration, acute inflammation and an area of perforation. Post-operative esophagram revealed no obstructions and contrast flowed without issue through the proximal esophagus into the gastroesophageal anastomosis and into the stomach. The patient did well and on discharge from the hospital was tolerating oral intake.

This case illustrates the multi-faceted approach sometimes required for successful treatment of Boerhaave syndrome, or rupture of the esophagus usually after emesis. Initial management included treating the patient’s sepsis with appropriate antifungal therapy in addition to placing a jejunostomy tube for nutrition—a conservative approach which has proven successful in other reported cases (1). Following resolution of the fungemia, she underwent surgical repair for permanent treatment of her esophageal disease.

While the patient had underlying achalasia predisposing her to spontaneous esophageal rupture, Candida glabrata has also been reported to compromise the esophageal lining through angio-invasive mechanisms (2). Given the pathology findings of mucosal ulceration and inflammation of excised esophageal tissue, it is likely that the patient’s Boerhaave syndrome was due to both a combination of achalasia and Candida glabrata esophageal infection.

Nour Parsa MD¹, Bhupesh Pokhrel MD², Arash Meshksar MD³, Mark Meyer MD⁴, and Samuel Kim MD⁴

Departments of ¹Medicine, ²Gastroenterology, ³Radiology, and ⁴Cardiothoracic Surgery, University of Arizona

Tucson, AZ USA

References

1. Shen G, Chai Y, Zhang GF. Successful surgical strategy in a late case of Boerhaave's syndrome. World J Gastroenterol. 2014 Sep 21;20(35):12696-700. [CrossRef] [PubMed]
2. Tran HA, Vincent JM, Slavin MA, Grigg A. Esophageal perforation secondary to angio-invasive Candida glabrata following hemopoietic stem cell transplantation. Clin Microbiol Infect. 2003 Dec;9(12):1215-8. [CrossRef] [PubMed] 

Cite as: Parsa N, Pokhrel B, Meshksar A, Meyer M, Kim S. Medical image of the week: Boerhaave syndrome. Southwest J Pulm Crit Care. 2016;12(6):233-5. doi: http://dx.doi.org/10.13175/swjpcc039-16 PDF

Medical Image of the Week: Left Ventricular Non-compaction

Figure 1. Cardiac MRI showing severely enlarged and remodeled left ventricle (LV) and moderately enlarged right ventricle (RV) with severe global hypokinesis and akinesis of the interventricular septum. Significant trabeculation was noted in the apical, antero-lateral and anterior segments of the LV (red arrows), consistent with LV non-compaction.

A 38-year-old woman with history of type 2diabetes mellitus and hypertension presented to emergency department with worsening exertional dyspnea and orthopnea for the past 2-3 months. She also reported a 14 pound weight gain within the 2 weeks prior to presentation. She denied any prior history of cardiac or pulmonary disease. Also, there was no family history of heart disease. She denies any recent sick contacts, smoking, alcohol drinking, or substance abuse.

Physical exam revealed jugular venous pressure of 10 cm H₂O and significant bilateral lower extremity pitting edema. Chest x-ray showed an enlarged cardiac silhouette. Brain naturetic peptide (BNP) was 2,917 pg/mL. A subsequent echocardiogram revealed a left ventricular (LV) ejection fraction of 23% with severe global LV hypokinesia with moderate mitral regurgitation. Thyroid panel as well as iron panel were within normal range. Other laboratories were unremarkable. For the new onset systolic heart failure, a coronary angiography was performed, which demonstrated normal coronary arteries. The patient was diagnosed with non-ischemic cardiomyopathy and underwent a cardiac MRI, which showed severely enlarged and remodeled LV and moderately enlarged right ventricle (RV) with severe global hypokinesis and akinesis of the intraventricular septum. Moreover, a significant trabeculation was noted in the apical, antero-lateral and anterior segments of the left ventricle (Figure 1), consistent with “LV non-compaction” without any evidence of LV thrombus. The patient was started on diuretics and safely discharged with significant symptoms improvement.  

LV non-compaction is a cardiomyopathy characterized by altered myocardial wall with prominent left ventricular trabeculae and deep intertrabecular recesses (1). Some authors believe that non-compaction of the ventricular myocardium results from abnormal persistence of the trabecular layer  while others believe that altered regulation in cell proliferation, differentiation, and maturation during ventricular wall formation, resulting in hyper-trabeculation (2). Its prevalence in the general population is unknown but among patients undergoing echocardiography is estimated at 0.014 to 1.3 percent. In patients with heart failure, its prevalence has been reported as 3 to 4 percent (3). Patients with LV non-compaction may present with heart failure, arrhythmias, sudden cardiac arrest, syncope, and thromboembolic events. The diagnosis is usually established by transthoracic echocardiography. When echocardiography is indeterminate, cardiac MRI, computed tomography, or left ventriculography could be an alternative diagnostic modality. Data on treatment of LV non-compaction are limited, and there is no standard therapy established for this condition. Medical management depends on the clinical manifestations, LV ejection fraction, presence of arrhythmias, and risk of thromboembolism.

Rostam Khoubyari MD^1,2 and Seongseok Yun MD PhD³

¹Department of Cardiology, ²Sarver Heart Center; and the ³Department of Medicine, University of Arizona

Tucson, AZ USA

References

1. Maron BJ, Towbin JA, Thiene G, et al. Contemporary definitions and classification of the cardiomyopathies: an American Heart Association Scientific Statement from the Council on Clinical Cardiology, Heart Failure and Transplantation Committee; Quality of Care and Outcomes Research and Functional Genomics and Translational Biology Interdisciplinary Working Groups; and Council on Epidemiology and Prevention. Circulation. 2006 Apr 11;113(14):1807-16. [CrossRef] [PubMed]
2. Henderson DJ, Anderson RH. The development and structure of the ventricles in the human heart. Pediatr Cardiol. 2009 Jul;30(5):588-96. [CrossRef] [PubMed]
3. Kovacevic-Preradovic T, Jenni R, Oechslin EN, Noll G, Seifert B, Attenhofer Jost CH. Isolated left ventricular noncompaction as a cause for heart failure and heart transplantation: a single center experience. Cardiology. 2009;112(2):158-64. [CrossRef] [PubMed]

Cite as: Khoubyari R, Yun S. Medical Image of the week: left ventricular non-compaction. Southwest J Pulm Crit Care. 2016;12(6):229-30. doi: http://dx.doi.org/10.13175/swjpcc036-16 PDF

June 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 65-year-old non-smoking man with a past medical history significant only for dyslipidemia and hypertension presented to the emergency room with a 2-week complaint of intermittent, diffuse, high back pain accompanied by sweating and nausea and non-bloody emesis. The back pain does not radiate. The patient also notes that recently he has suffered from pronounced fatigue and some shortness of breath; until recently he had been an endurance athlete.

Physical Examination: Physical examination was normal; in particular, the back pain was not reproducible on palpation. The patient was afebrile.

Laboratory: Laboratory data were remarkable for a mildly elevated white blood cell count of 11 x 10⁹ cells/L. Serum chemistries were within normal limits and cardiac troponins were negative. Oxygen saturation on room air was 94%.

Radiography: 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 eight panels)

1. The frontal chest radiograph shows a large left pleural effusion
2. The frontal chest radiograph shows an abnormally widened mediastinum
3. The frontal chest radiograph shows multifocal consolidation
4. The frontal chest radiograph shows no significant findings
5. The frontal chest radiograph shows numerous small lung nodules

Cite as: Gotway MB. June 2016 imaging case of the month. Southwest J Pulm Crit Care. 2016 Jun;12(6):216-28. doi: http://dx.doi.org/10.13175/swjpcc047-16 PDF 

Medical Image of the Week: Bochdalek Hernia

Figure 1. PA (A) and lateral (B) chest radiograph demonstrating a lobulated homogenous opacity in the  posterior left lung base-blue arrows.

Figure 2. Chest CT (axial image) demonstrating fat-containing opacity consistent with a Bochdalek hernia- red arrow.

A 61 year-old man presented for an evaluation of a nonproductive cough. He has a history of well-controlled asthma, allergic rhinitis and nasal polyposis, hypertension, gastro-esophageal reflux and obstructive sleep apnea. The ACE inhibitor used to treat hypertension was discontinued. The physical exam was unremarkable. Pulmonary function testing was normal.

A PA and lateral chest radiograph was performed and revealed an abnormal contour of the left hemidiaphragm with a large lobulated opacity (Figure 1- blue arrows). Computed chest tomography revealed the lobulated opacity in the left lower lobe contained fat and was consistent with a Bochdalek hernia (Figure 2).

Congenital diaphragmatic hernia is a major malformation in newborns and in the perinatal period. The diagnosis of congenital diaphragmatic hernia in adults is rare. There are three types of congenital diaphragmatic hernias: posterolateral (Bochdalek) diaphragmatic hernia, subcostosternal (Morgagni) hernia and esophageal hiatal hernia. The Bochdalek diaphragmatic hernia is the result of a congenital diaphragmatic defect in the posterior costal part of the diaphragm in the region of 10th and 11th ribs, which allows free communication between the thoracic and abdominal cavity. The defect is usually found at the left side (90%) but may occur on the right side, where the liver often prevents detection.

A review of 173 adult patients with Bochdalek hernias revealed several important features:  55% of patients were male with an average age of 40 years, the hernia defect was located on the left side in 78% of patients and most patients were symptomatic (1,2). The most common presenting symptoms were pain or pressure in the chest or abdomen and obstruction. Pulmonary symptoms occurred in 37% of patients in this review. Of note, patients with Bochdalek hernias can develop symptoms precipitated by factors that increase intra-abdominal pressure and failure to promptly treat a symptomatic Bochdalek hernia may lead to bowel strangulation. A chest CT is an excellent diagnostic study, as a Bochdalek hernia can be difficult to appreciate on a chest radiograph (3).

Management of a Bochdalek hernia includes reducing the abdominal contents and repairing the defect through a laparotomy or thoracotomy. Successful laparoscopic and thoracoscopic repairs of Bochdalek hernias have both been described.

Muna Omar, M.D. and Linda Snyder, M.D.

Pulmonary, Critical Care, Sleep and Allergy Medicine

Banner University Medical Center-Tucson

Tucson, AZ USA

References

1. Brown SR, Horton JD, Trivette E, Hofmann LJ, Johnson JM. Bochdalek hernia in the adult: demographics, presentation, and surgical management. Hernia. 2011 Feb;15(1):23-30. [CrossRef] [PubMed]
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Cite as: Omar M, Snyder L. Medical image of the week: Bochdalek hernia. Southwest J Pulm Crit Care. 2016 Jun;12(6):203-4. doi: http://dx.doi.org/10.13175/swjpcc031-16 PDF