August 2019 Imaging Case of the Month: A 51-Year-Old Man with a Headache

Michael B. Gotway, MD

Department of Radiology

Mayo Clinic Arizona

Scottsdale, AZ USA

Clinical History: A 51-year-old previously healthy man presented with complaints of increasing headache frequency and severity. The patient noted headaches in the past, but that the frequency of these headaches, which he referred to as “migraines,” had been increasing in recent months. The patient does note some auras with the headaches.

The patient reported a history of pneumonia in the past, but denied recurrent pneumonias. The only medication the patient takes was ibuprofen, for his headaches; he denied allergies. The patient’s past surgical history was remarkable only for a right inguinal hernia repair, a right Achilles tendon injury repair, and surgical removal of a palpable left thigh mass, ultimately shown to represent scar tissue. The patient smoked 1-8 cigarettes / day for 35 years, quitting one year earlier.

The patient’s physical examination was remarkable for obesity (BMI= 30.4). His vital signs were within the normal range. A few reddish rounded spots were noted on his lower lip, but no other abnormalities were noted at physical examination.

Basic laboratory data, including a complete blood count, electrolyte panel, B12 and folate levels, a C-reactive protein level, and liver function studies were all within the normal range. Mild hypercholesterolemia was noted. An electrocardiogram revealed normal findings. As part of a routine office visit, frontal and lateral 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 ten pages)

1. The chest radiograph shows circumscribed nodular opacities
2. The chest radiograph shows multifocal nodular pulmonary consolidation
3. The chest radiograph shows multiple, bilateral cavitary nodules
4. The chest radiograph shows multiple, bilateral small circumscribed nodules
5. The chest radiograph shows nodular interstitial thickening

Cite as: Gotway MB. August 2019 imaging case of the month: a 52-year-old man with a headache. Southwest J Pulm Crit Care. 2019;19(2):52-64. doi: https://doi.org/10.13175/swjpcc052-19 PDF 

Medical Image of the Month: Reexpansion Pulmonary Edema

 

Figure 1. Large right hydrothorax with mild mediastinal shift to the left.

Figure 2. Status post right pleural pigtail drain placement with interval improvement of the now small right pleural effusion with re-expansion of the right lung and early edema.

Figure 3. Moderate right pleural effusion and worsening reexpansion pulmonary edema.

A 54-year-old woman with decompensated alcoholic liver cirrhosis presented to the emergency department with exertional dyspnea. She was afebrile, tachycardic (110), with oxygen saturation of 74% on 5 liters/minute (L/min), in moderate respiratory distress and was subsequently placed on a non-rebreather. On examination, she had absent breath sounds throughout her right lung with chest radiograph revealing large right-sided pleural effusion (Figure 1). A pigtail catheter was placed, draining approximately 4 liters of fluid (Figure 2), resulting in improved oxygenation to 93% on 3 L/min. On admission to internal medicine, the chest tube was clamped immediately. In the next 24 hours, patient developed increased oxygen requirements, with worsening tachypnea and tachycardia, requiring bilevel positive airway pressure and admission to the medical intensive care unit for reexpansion pulmonary edema (Figure 3).

Hepatic hydrothorax is a complication of cirrhosis and portal hypertension, defined as pleural effusion without any underlying pulmonary or cardiac etiologies. Though the pathophysiology is not completely understood, it is widely believed that the pleural effusion is caused by negative intrathoracic pressures allowing peritoneal fluid to enter the pleural cavity through diaphragmatic defects. Management of hepatic hydrothorax includes sodium restriction, diuresis, therapeutic thoracentesis, and transjugular intrahepatic portosystemic shunt. Repeated thoracentesis is the routine procedure to remove pleural fluid in refractory hepatic hydrothorax (1).

Though relatively safe, thoracentesis is associated with reexpansion pulmonary edema (RPE). RPE is believed to occur due to increased permeability of the pulmonary capillaries as a result of inflammation caused by ventilation and reperfusion of previously collapsed lung. Symptoms of RPE include chest discomfort and cough with onset typically within 24 hours of lung reexpansion. Signs of RPE include tachypnea, tachycardia, lung crackles, and hypoxemia refractory to oxygen therapy. Risk factors are young age (20-40 years), long duration of lung collapse, use of negative pressure during thoracentesis, large volume drainage, and rapid lung reexpansion. Management is largely supportive and ranges from diuresis to endotracheal intubation with mechanical ventilation (2).

Unfortunately, the amount of fluid that can be safely removed from the pleural effusion in order to prevent RPE has not been clearly defined. Feller-Kopman (3) reported that only one patient (0.5%) of 185 participants experienced clinical RPE, while four patients (2.2%) had radiographic RPE without symptoms. Our case demonstrates that removal of large volume from the pleural effusion via the chest tube resulted in clinical and radiographic RPE, thus, necessitating the need for clearly defined guidelines.

Chelsea Takamatsu BS, Aida Siyahian MS, Ella Starobinska MD, and Anthony Witten DO

University of Arizona College of Medicine- Tucson

Tucson, AZ USA

References

1. Garbuzenko DV, Arefyev NO. Hepatic hydrothorax: An update and review of the literature. World J Hepatol. 2017 Nov 8;9(31):1197-1204. [CrossRef] [PubMed]
2. Kasmani R, Irani F, Okoli K, Mahajan V. Re-expansion pulmonary edema following thoracentesis. CMAJ. 2010 Dec 14;182(18):2000-2. [CrossRef] [PubMed]
3. Feller-Kopman D, Berkowitz D, Boiselle P, Ernst A. Large-volume thoracentesis and the risk of reexpansion pulmonary edema. Ann Thorac Surg. 2007 Nov;84(5):1656-61. [CrossRef] [PubMed]

Cite as: Takamatsu C, Siyahian A, Starobinska E, Witten A. Medical image of the month: reexpansion pulmonary edema. Southwest J Pulm Crit Care. 2019;19(1):12-4. doi: https://doi.org/10.13175/swjpcc024-19 PDF

Medical Image of the Month: Bilateral Atrial Enlargement

Figure 1. Portable chest radiograph showing elevation of the left mainstem bronchus (red arrow).

Figure 2. Thoracic CT scan showing right atrial enlargement (blue circle) and left atrium (red circle).

Figure 3. Upper Image: Static image from echocardiogram showing right atrial enlargement (white circle). Lower image: video of echocardiogram.

A 97-year-old woman was repeatedly admitted for dyspnea, hypoxemia and treated with antibiotics for presumed left lower lobe pneumonia. She has a past medical history of atrial fibrillation, congestive heart failure and sick sinus syndrome with placement of a cardiac pacemaker. Notably on physical examination, she had heart rate of 110 beats/minute, temperature of 98.8°F, blood pressure of 122/72 mm Hg, and a respiratory rate of 27 breaths/minute. She had a sternal heave, a grade 4/6 "blowing" holosystolic murmur, a loud S2, jugular venous distension and an enlarged liver. Chest x-ray showed obscuration of the left lower lobe - the left heart border cannot be seen, and the L mainstem bronchus is straightened and lifted superiorly (Figure 1). An image of the heart is shown from a CT abdomen obtained 6 months previously, showing cardiomegaly, particularly massive atrial enlargement (Figure 2). An ultrasound showed bilateral atrial enlargement with moderate mitral regurgitation and severe tricuspid regurgitation (Figure 3). The left ventricular ejection fraction was 55%, but with abnormal septal motion. She was treated with gentle diuresis to help relieve volume overload, and isosorbide dinitrate for preload and afterload reduction. Pulmonary hypertension was attributed to chronic mitral regurgitation. The cause was unclear - the patient remembered that her brother had rheumatic fever as a young recruit in WWII, but didn't know whether she had ever experienced it.

Atrial enlargement can be of prognostic significance. Left atrium size has been found to be a predictor of mortality due to both cardiovascular issues as well as all-cause mortality (1). Larger right atrium than left atrium has been associated with all-cause mortality in elderly patients with heart failure (2).

Robert A. Raschke, MD

University of Arizona College of Medicine-Phoenix

Phoenix, AZ USA

References

1. Patel DA, Lavie CJ, Milani RV, Shah S, Gilliland Y. Clinical implications of left atrial enlargement: a review. Ochsner J. 2009 Winter;9(4):191-6. [PubMed]
2. Almodares Q, Wallentin Guron C, Thurin A, Fu M, Kontogeorgos S, Thunstrom E, Johansson MC. Larger right atrium than left atrium is associated with all-cause mortality in elderly patients with heart failure. Echocardiography. 2017 May;34(5):662-7. [CrossRef] [PubMed]

Cite as: Raschke RA. Medical image of the month: bilateral atrial enlargement. Southwest J Pulm Crit Care. 2019;19(1):10-1. doi: https://doi.org/10.13175/swjpcc023-19 PDF

Medical Image of the Month: Thymolipoma

Figure 1. Chest radiograph PA view revealing subtle prominence of left upper heart border (white arrow).

Figure 2. CT Topogram: The prominence of left heart border is discretely seen suggesting pliability of the lesion (due to supine position).

Figure 3. CECT axial and coronal images revealing a fat containing anterior mediastinal mass with strands of soft tissues (HU values as depicted in image).

Figure 4. CECT of the thorax one year after resection: post contrast image revealing no mediastinal mass lesion.

A 20-year-old man presented with a continuous, mild, dull aching pain affecting the left chest pain for 15 days duration. There were no aggravating or relieving factors nor any history of fever, respiratory or cardiac symptoms. The patient’s vital signs were normal and examination of the respiratory and the cardiovascular systems revealed no abnormality. Electrocardiography and biochemical investigations, including cardiac enzymes, were normal. Chest radiography (Figure 1) revealed a subtle opacity causing fullness of the aorto-pulmonary window with subtle, smooth prominence of the left upper cardiac border; the left hilum was visualised discretely through the opacity (Figure 2). The patient underwent enhanced contrast chest CT (CECT, Figure 3) for further evaluation, revealing a large mass measuring 13 x 7.9 x 5 cm in the anterior mediastinum, extending from thoracic inlet to the left cardiophrenic angle. The mass consisted predominantly of fat density, with an average attenuation of - 84 Hounsfield units (HU). Non-enhancing strands of soft tissue foci (mean, 32 HU) were also seen within the lesion. No areas of calcification or cystic degeneration were present. Planes between the subjacent mediastinal structures were preserved (Figures 2 and 3). A radiological impression of thymolipoma was offered. The patient was transferred to a tertiary care center where he underwent thoracoscopic excision and histopathology confirmed thymolipoma. Following surgery, the patient recovered uneventfully and follow up chest radiography and enhanced contrast chest CT (Figure 4) showed no evidence of lesion recurrence.

Thymolipoma is a rare benign tumor originating in the anterior mediastinum, and comprises 2-9% of all thymic neoplasms (1). Cytogenetic analyses have demonstrated that thymolipoma is a neoplasm of thymic fat (2). There is no sex or age predilection and affected patients range in age from 3-76 years. Most patients remain asymptomatic until the size of the lesion produced local mass effects, resulting in symptoms such as cough, dyspnea, hemoptysis, chest pain and hoarseness (1,3). Autoimmune diseases, including myasthenia gravis, systemic lupus erythematosus, hypogammaglobulinemia, Graves’ disease, and erythroblastopenia, may coexist in 10% patients (1).

When thymolipomas are small, the lesion may not be detectable at chest radiography. When the lesion grows larger, it classically usually “drapes” around the heart and may simulate cardiomegaly (4). Extremely large thymolipomas have been described and can mimic pericardial effusion, pericardial cysts or pericardial tumors (5). Ultrasound can be used to differentiate fluid-containing lesions, such as pericardial effusion and cysts, from the echogenic fat typical of thymolipoma (4). Excessive epicardial fat, diaphragmatic elevation, sequestration or lobar collapse may also mimic this condition at chest radiography, whereas CT and/or MRI are diagnostic, revealing circumscribed anterior mediastinal fatty mass containing islands and strands of soft tissues with no invasion of adjacent structures (3-5).

Important differential diagnostic considerations for thymolipoma at cross sectional imaging include other fat-containing mediastinal masses such as mediastinal lipoma, mediastinal lipomatosis, liposarcoma and lipoblastoma. Lipomas are encapsulated whereas liopmatosis is an unencapsulated deposition of adipose tissues, and both lesions typically show homogeneous fat attenuation with no soft tissue strands. Liposarcoma frequently occurs in the posterior mediastinum and is usually symptomatic at the time of presentation, and often manifests with inhomogeneous appearance and invasion of subjacent mediastinal structures on CT/ or MRI (6). Lipoblastoma usually occurs under the age of 3, and shows intratumoral soft tissue stranding. Thymomas do not contain fatty tissue whereas some germ cell neoplasms contain cystic areas and calcification in addition to the fatty tissue (3,6). CT is considered the modality of choice for the evaluation of mediastinal masses in general, and thymolipoma in particular. For patients in whom CT findings are equivocal, or for patients with contraindications to enhanced CT (such as contrast media allergy) MRI may be utilized for further characterization of mediastinal lesions, such as thymolipoma. Encasement or invasion of the mediastinal vasculature, esophagus, and trachea as well as involvement of the pericardium, myocardium, and pleura are accurately detected with MRI. The primary disadvantages of using MRI for mediastinal lesion characterization include limited identification of calcifications, longer imaging time, and higher cost (3,6). Since thymolipomas are benign, and typically well encapsulated, with no invasion of surrounding structures, if detected incidentally, the lesion can be followed with imaging. However, when symptoms related to local mass effect develop, surgical resection is the treatment of choice which can be performed using a minimally invasive approach, such as thoracoscopic excision, with open resection reserved for larger lesions (7). Histopathological examination of thymolipoma reveals mature adipose tissue and hyperplastic thymic structures with Hassall’s corpuscles (2).

Amit Kumar Paliwal MD¹, Dr. Pradeep Jaiswal MCH (CTVS) AH

(R&R)², and Dr. Vivek Sharma MD³

¹Military Hospital Dehradun, Dehradun, Uttrakhand, India      

²Delhi Cantt, Delhi, India

³Command Hospital (CC), Lucknow, India

References

1. Dongel I, Imamoglu H, Şahin AF, Yıldırım S, Bayram M. A rare mediastinal tumor: thymolipoma. Eur J Gen Med. 2014;11:21-3. [CrossRef]
2. Hudacko R, Aviv H, Langenfeld J, Fyfe B. Thymolipoma: Clues to pathogenesis revealed by cytogenetics. Ann Diagn Pathol. 2009;13:185-8.[CrossRef] [PubMed]
3. Tomiyama N, Honda O, Tsubamoto M et al. Anterior mediastinal tumors: diagnostic accuracy of CT and MRI. Eur J Radiol. 2009;69(2):280-8. [CrossRef] [PubMed]
4. Yeh HC, Gordon A, Kirschner PA, Cohen BA. Computed tomography and sonography of thymolipoma. AJR Am J Roentgenol. 1983;140(6):1131-3. [CrossRef] [PubMed]
5. Gamanagatti S, Sharma R, Hatimota P, Guleria R, Arvind S. Giant thymolipoma. AJR Am J Roentgenol. 2005;185(1):283-4. [CrossRef] [PubMed]
6. Juanpere S, Canete N, Ortuno P, Martínez S, Sanchez, G, Bernado L. A diagnostic approach to the mediastinal masses. Insights Imaging. 2013;4(1):29-52. [CrossRef] [PubMed]
7. Carapinha CP, Wainwright L, Loveland JA. A giant thymolipoma. S Afr J Child Health. 2010;4(1):20-1.

Cite as: Paliwal AK, Jaiswal P, Sharma V. Medical image of the month: thymolipoma. Southwest J Pulm Crit Care. 2019;18(6):152-4. doi: https://doi.org/10.13175/swjpcc018-19 PDF

Medical Image of the Month: Double Aortic Arch

Figure 1. A chest radiograph performed after endotracheal intubation of the patient demonstrated prominence of the upper mediastinum in the region of the right paratracheal strip (red arrow).

Figure 2. A non-contrasted CT of the chest demonstrates a complete vascular ring secondary to the patient’s double aortic arch (outlined in red) surrounding the trachea (T) and esophagus (E).

Case Presentation: A 78-year-old gentleman presented to the hospital via EMS with altered mental status. An urgent CT of the head performed in the emergency room demonstrated a large, right intraparenchymal hemorrhage with intraventricular extension into the right lateral ventricle. His Glascow Coma Scale score was 6, and he was intubated for airway protection.  A chest radiograph performed to verify placement of the endotracheal tube demonstrated prominence of the upper mediastinum in the region of the right paratracheal strip (Figure 1). A CT of the chest (Figure 2) demonstrated a double aortic arch corresponding to the upper mediastinal abnormality noted on the chest radiograph. In speaking with the patient’s family after acquiring the CT of the chest, they stated that the patient had long-term issues with dysphagia – specifically choking with solid foods. Unfortunately, the patient passed away from complications of his large intraparenchymal hemorrhage.

A double aortic arch results from persistence of both the right and left embryonic arches with each arch giving rise to the ipsilateral, separate carotid and subclavian arteries (1). A double aortic arch is the most common cause of a symptomatic vascular ring with the trachea and esophagus being compressed by the two arches (1). Symptoms usually arise in childhood with good outcomes with surgical repair of this abnormality in pediatric populations. A few case series exist describing repair of this anomaly in adult populations (2).

Kelly Wickstrom DO, Steven P. Sears DO, and Laura Meinke MD

Division of Pulmonary, Critical Care, Allergy and Sleep Medicine

University of Arizona College of Medicine

Tucson, AZ USA

References

1. Hanneman K, Newman B, Chan F. Congenital variants and anomalies of the aortic arch. Radiographics. 2017 Jan-Feb;37(1):32-51. [CrossRef] [PubMed]
2. Noguchi K, Hori D, Nomura Y, Tanaka H. Double aortic arch in an adult. Interact Cardiovasc Thorac Surg. 2012 Jun;14(6):900-2. [CrossRef] [PubMed]

Cite as: Wickstrom K, Sears SP, Meinke L. Medical image of the month: Double aortic arch. Southwest J Pulm Crit Care. 2019;18(5):120-1. doi: https://doi.org/10.13175/swjpcc019-19 PDF 

May 2019 Imaging Case of the Month: Asymptomatic Pulmonary Nodules and Cysts in a 47-Year-Old Woman

Michael B. Gotway, MD

Department of Radiology

Mayo Clinic Arizona

Scottsdale, AZ USA

Clinical History: A 47-year-old previously healthy woman presented to her new physician for a routine physical examination. The patient had no complaints. The patient’s physical examination showed normal vital signs and clear lungs; the physical examination was essentially unremarkable. The patient’s past medical history included a brief smoking history, having quit over 20 years earlier, as well as seasonal allergies. Her past surgical history included an appendectomy nearly 20 years earlier and a hysterectomy for bleeding related to uterine leiomyomas approximately 12 years prior to presentation. The patient was not taking any prescription medications.

Basic laboratory data, including a complete blood count, electrolyte panel, and liver function studies were all within the normal range. An electrocardiogram revealed normal findings. 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 be directed to the second of eleven pages)

1. The chest radiograph shows mediastinal and hilar lymph node enlargement
2. The chest radiograph shows multifocal nodular pulmonary consolidation
3. The chest radiograph shows multiple, bilateral cavitary nodules
4. The chest radiograph shows multiple, bilateral circumscribed nodules
5. The chest radiograph shows nodular interstitial thickening

Cite as: Gotway MB. May 2019 imaging case of the month: Asymptomatic pulmonary nodules and cysts in a 47-year-old woman. Southwest J Pulm Crit Care. 2019;18(5):106-19. doi: https://doi.org/10.13175/swjpcc022-19 PDF 

Medical Image of the Month: Ludwig’s Angina

Figure 1.  A coronal reconstruction of the patient’s initial post-contrast maxillofacial CT demonstrates swelling of the soft tissues of the floor of the mouth consistent with phlegmonous changes and early abscess formation (blue arrows).  There is also swelling in the region of the vallecula and epiglottis (red arrow).

Figure 2.  A coronal reconstruction of the patient’s follow-up post-contrast maxillofacial CT after placement of a tracheostomy tube demonstrates marked progression of the swelling of the soft tissues of the floor of the mouth with development of a large, ill-defined abscess in the floor of the mouth (blue circle). Note the marked, progressive narrowing of the oropharynx (red arrow) over a period of approximately 24 hours.

Case Presentation: A 65-year-old gentleman with a history of insulin-dependent diabetes mellitus presented to the emergency room with a chief complaint of two days of difficulty swallowing and jaw pain.  Four days prior to presentation, he had extensive dental work performed to address multiple dental caries.  On arrival to the emergency room, he was noted to be tachycardic with difficulty swallowing his saliva and liquids.  On physical examination, he had difficulty opening his mouth with marked swelling of his tongue.  He also had marked swelling of the soft tissues of the floor of the mouth with palpable adenopathy.  A maxillofacial CT with contrast (Figure 1) was performed which demonstrated extensive edema and early abscess formation in the floor of the mouth.  He was initially admitted to the general medicine floor and started on broad-spectrum antibiotics.  Over the course of the next 12 hours, he began to have increased difficulty breathing and was unable to swallow his own secretions.  He was promptly transferred to the ICU where a fiberoptic nasotracheal intubation was attempted at bedside but was unable to be performed given the extensive soft tissue swelling in the posterior oropharynx.  An emergent awake tracheostomy was subsequently performed by ENT.  A repeat maxillofacial CT with contrast (Figure 2) demonstrated marked progression of the inflammatory changes and abscess formation in the floor of the mouth consistent with progressive Ludwig's angina.  The combination of prompt surgical drainage and broad-spectrum antibiotics resulted in marked clinical improvement over the next 72 hours. The patient's final tissue cultures grew Streptococcus viridans.

Ludwig's angina is a potentially life-threatening gangrenous cellulitis of the neck and floor of the mouth which is characterized by progressive submandibular swelling with elevation and posterior displacement of the tongue. Odontogenic infections are the cause for most cases. Pre-existing medical conditions which predispose patients to the development of Ludwig's angina include diabetes mellitus, malnutrition, alcoholism, and immunocompromised states (i.e. AIDS and organ transplantation).

In the early stages of the disease, patients may be managed with observation and intravenous antibiotics to cover for β-hemolytic streptococcus and anaerobic organisms. The most life-threatening complication of Ludwig's angina is airway obstruction.  Immediate involvement of an anesthesiologist and ENT are crucial in the management of this condition.  Blind nasotracheal intubation should not be attempted in these patients given the potential for bleeding and abscess rupture.  Flexible nasotracheal intubation requires skill and experience.  If flexible nasotracheal intubation is not possible, a cricothyrotomy and tracheostomy under local anesthesia can be performed in the emergent setting.  An elective awake tracheostomy is a safer and more logical method of airway management in patients with fully developed Ludwig's angina.

Lauren Estep, MD and Tammer El-Aini, MD

Department of Pulmonary, Critical Care, Allergy and Sleep

University of Arizona College of Medicine

Tucson, AZ USA

References

1. Hasan W, Leonard D, Russell J. Ludwig's Angina-A Controversial Surgical Emergency: How We Do It. Int J Otolaryngol. 2011;2011:231816. [CrossRef] [PubMed]
2. Candamourty R, Venkatachalam S, Babu MR, Kumar GS. Ludwig's Angina - An emergency: A case report with literature review. J Nat Sci Biol Med. 2012 Jul;3(2):206-8. [CrossRef] [PubMed]

Cite as: Estep L, El-Aini T. Medical image of the month: Ludwig’s angina. Southwest J Pulm Crit Care. 2019:18(4):74-5. doi: https://doi.org/10.13175/swjpcc013-19 PDF 

Medical Image of the Month: Incarcerated Morgagni Hernia

Figure 1. Lateral view of abdominal-thoracic CT in soft tissue windows.

Figure 2. Coronal view of thoracic CT scan in lung windows.

A Morgagni hernia is a congenital diaphragmatic hernia in which abdominal viscera herniate into the thorax via a defect within an anterior attachment of the diaphragm. As with any bowel-containing hernia, the most feared complication is strangulation with subsequent bowel necrosis. In the present case, a 67-year-old woman presented with a five-day history of acute onset and progressively worsening upper abdominal pain and inability to tolerate oral intake, associated with nausea, vomiting, and mild shortness of breath. A CT revealed a large defect in the right hemidiaphragm consistent with a Morgagni hernia with herniation of the omentum, vessels, and a segment of transverse colon (Figure 1). Findings of bowel ischemia were observed, including (a) pneumatosis intestinalis, seen as cystic foci of air lining the bowel wall, and (b) fluid and fat-stranding adjacent to the affected bowel (Figure 2). Evidence of bowel wall perforation include large volume free air adjacent to the bowel in the right hemithorax and within the abdomen (Figures 1 and 2). Bowel ischemia and necrosis can occur with any hernia and requires prompt diagnosis and management.

Samandip Hothi MD¹ and Viral Patel MD²

¹Department of Medicine, Division of Internal Medicine and ²Department of Medical Imaging

University of Arizona College of Medicine-Tucson

Tucson, AZ USA

References

1. Arora S, Haji A, Ng P. Adult Morgagni Hernia: The Need for Clinical Awareness, Early Diagnosis and Prompt Surgical Intervention. Ann R Coll Surg Engl. 2008 Nov;90(8):694-5. [CrossRef] [PubMed]
2. Ly JQ. The Rigler Sign. Radiology. 2003;228(3):706-7. [CrossRef] [PubMed]
3. Morgan TB, Nguyen DN, Tran CD, Maheshwary RK, Mickus TJ. Morgagni Hernia Causing Incarcerated Bowel and Contributing to Cardiac Arrest. Curr Probl Diagn Radiol. 2018 Jul 31. pii: S0363-0188(18)30181-6. [CrossRef]

Cite as: Hothi S, Patel V. Medical image of the month: Incarcerated Morgagni hernia. Southwest J Pulm Crit Care. 2019;18:59-60. doi: https://doi.org/10.13175/swjpcc001-19 PDF 

Medical Image of the Month: Pectus Excavatum

Figure 1. A) PA chest radiograph at 38 years old demonstrates rib cage growth arrest at the time of pectus repair. B) and C) demonstrate the coronal and sagittal CT chest views.

Figure 2: Pulmonary function tests demonstrate severe restrictive ventilatory defect.

Clinical History

A 38-year-old man with obesity and history of pectus excavatum post-operative surgical repair at age 4 presented to the general pulmonary clinic with symptoms of severe dyspnea on exertion after walking one block. Chest x-ray and thoracic CT scan demonstrate anterior chest wall depression. (Figure 1). Pulmonary function testing demonstrated a severe restrictive lung disease (Figure 2).  High resolution CT demonstrated anterior chest wall depression. The Haller index was 2.5—mild excavatum—with associated scarring in the anterior right lung. Expiratory air-trapping was seen consistent with small airways disease.

Haller Index

The Haller index is calculated by dividing the transverse diameter of the chest by the anterior-posterior distance on the CT of the chest on the axial slice that demonstrates the smallest distance between the anterior surface of the vertebral body and the posterior surface of the sternum (1). Normal chest < 2.0; mild excavatum 2.0 – 3.2; moderate excavatum 3.2 – 3.5; severe excavatum > 3.5. Corrective surgery is considered for a Haller index of greater than or equal to 3.25.  Secondary thoracic dystrophy is a known consequence of too early repair of pectus excavatum (1).  Cases like our patient have changed when surgical repair is attempted until after puberty.

Michael Insel, MD and Janet Campion, MD

Division of Pulmonary, Allergy, Critical Care and Sleep Medicine

Banner University Medical Center-Tucson

Tucson, AZ USA

Reference

1. Haller JA Jr, Colombani PM, Humphries CT, Azizkhan RG, Loughlin GM. Chest wall constriction after too extensive and too early operations for pectus excavatum. Ann Thorac Surg. 1996 Jun;61(6):1618-24. [CrossRef] [PubMed]

Cite as: Insel M, Campion J. Medical image of the month: pectus excavatum. Southwest J Pulm Crit Care. 2019;18(2):50-1. doi: https://doi.org/10.13175/swjpcc124-18 PDF

February 2019 Imaging Case of the Month: Recurrent Bronchitis and Pneumonia in a 66-Year-Old Woman

Michael B. Gotway, MD

Department of Radiology

Mayo Clinic Arizona

Scottsdale, AZ

Clinical History: A 66–year old woman presented with complaints of a non-productive cough worsening over the previous several weeks. She complained that her cough had also occurred several months earlier, but resolved, and then subsequently returned.

The patient indicated that she has had bouts of bronchitis off and on for many years. Her smoking history included only 3 cigarettes / day for two years, quitting 20 years earlier. She did not note any allergies and her list of medications included only vitamin supplements, baby aspirin, omeprazole, and lisinopril. Her surgical history was remarkable only for remote tonsillectomy and hysterectomy.

Her physical examination was largely unremarkable, although some course breath sounds were detected over the medial right base. Her vital signs showed normal pulse rate and blood pressure, breathing at 12 breaths / minute. Her room air oxygen saturation was 97%.

Frontal chest radiography (Figure 1) was performed.

Figure 1. Initial frontal chest x-ray.

Which of the following represents the most accurate assessment of the chest radiographic findings? (Click on the correct answer to be directed to the second of sixteen pages)

1. Chest radiography shows a vague solitary pulmonary opacity
2. Chest radiography shows basilar fibrotic opacities
3. Chest radiography shows cavitary pulmonary lesions
4. Chest radiography shows marked cardiomegaly
5. Chest radiography shows numerous small nodular opacities

Cite as: Gotway MB. February 2016 imaging case of the month: Recurrent bronchitis and pneumonia in a 66-year-old woman. Southwest J Pulm Crit Care. 2019;18(2):31-49. doi: https://doi.org/10.13175/swjpcc006-19 PDF

Medical Image of the Month: Massive Right Atrial Dilation After Mitral Valve Replacement

Figure 1. Chest radiograph demonstrating massive cardiomegaly with pulmonary congestion and markedly dilated right atrium.

Figure 2. Transthoracic echocardiogram demonstrating marked dilation of the right atrium to 9.6 cm in its greatest dimension.

A 92-year-old woman with a history of mechanical mitral valve replacement (+25 years prior to presentation), coronary artery bypass grafting, pacemaker placement and heart failure (EF 25%) presented from a nursing facility for dyspnea of 1 day’s duration. Recently, the patient had experienced a bowel perforation s/p surgical repair 3 weeks prior.

Admission chest radiograph was significant for massive cardiomegaly with pulmonary congestion and markedly dilated right atrium (Figure 1). Formal echocardiography was ordered, which re-demonstrated the patient’s known heart failure with reduced ejection fraction. Additionally, all 4 chambers of the heart were noted to be dilated, but the right atrium was revealed to be severely enlarged to >9 cm (Figure 2). On review of outside records, the patient’s cardiac history was notable for chronic dilation of the RA, RV and LA for several years with low, but stable, LV ejection fraction. Ultimately, the patient was noted to have worsening abdominal distension concerning for acute abdomen. However rather than pursue additional aggressive work up after her recent surgery, comfort measures were preferred.

This case illustrates some of the possible long-term effects of mitral valve replacement. In recent years mitral valve repair has become the preferred method over replacement for degenerative valve disease in western countries (1). While there are documented short term benefits to both mitral valve replacement and mitral valve repair long term data is less available (2). Long-term survival in most studies is reported in 5,10, and 15-year intervals. As was the case with our patient, patients with mitral valve replacement greater than 20 years in age have significantly less information associated with them. Although at this time longitudinal studies suggest benefits for both mitral valve replacement and repair, further investigation into long term complications is warranted (3). As our society continues to age, understanding the risks and complications associated with previous valve repair will help guide therapeutic interventions in the geriatric patient.

Richard Young, MD* and Alexander Ravajy, BS**

*University of Arizona Department of Internal Medicine

**University of Oklahoma Department of Microbiology

Banner University Medical Center

Tucson, AZ USA

References

1. Gammie JS, Sheng S, Griffith BP, Peterson ED, Rankin JS, O'Brien SM, Brown JM. Trends in mitral valve surgery in the United States: results from the Society of Thoracic Surgeons Adult Cardiac Surgery Database. Ann Thorac Surg. 2009 May;87(5):1431-7. [CrossRef] [PubMed]
2. McNeely CA, Vassileva CM. Long-term outcomes of mitral valve repair versus replacement for degenerative disease: a systematic review. Curr Cardiol Rev. 2015;11(2):157-62. [CrossRef] [PubMed]
3. Christina MV, Gregory M, Christian M, Theresa B, Stephen M, Steven S, Stephen H. Long term survival of patients undergoing mitral valve repair and replacement a longitudinal analysis of Medicare fee-for-service beneficiaries. Circulation. 2013;127(18):1870–6. [CrossRef] [PubMed]

Cite as: Young R, Ravajy A. Medical image of the month: Massive right atrial dilation after mitral valve replacement. Southwest J Pulm Crit Care. 2018;18(1):8-9. doi: https://doi.org/10.13175/swjpcc111-18 PDF 

Medical Image of the Month: Chronic Ogilvie’s Syndrome

Figure 1. Coronal view of abdominal CT scan showing a massively dilated colon.

Figure 2. Sagittal view of abdominal CT scan.

Figure 3. Axial view of abdominal CT scan.

A 42-year-old man with chronic encephalopathy secondary to traumatic brain injury (TBI), craniotomy, seizure disorder, chronic alcohol abuse, and chronic Ogilvie syndrome presented to the Banner University Medical Center-South Campus emergency department (ED) after being found in his driveway with altered mental status. He complained of multiple episodes of non-bloody diarrhea for the last day but otherwise altered & unhelpful. He was noted to have to be hypotensive with a blood pressure of 70-90/35-56 mm Hg, afebrile with a temperature of 36  C, an elevated white cell count of 13.3 X 10⁹ cells/L, a hemoglobin of 4.4 g/dL, a creatinine of 2.6 mg/dL, a BUN of 30 mg/dL, and an elevated lactic acid to 5.4 mmol/L. Physical exam showed a massively dilated tympanic abdomen. Resuscitation and broad-spectrum antibiotics were initiated, a CT scan ordered (Figures 1-3) and he was admitted to the medical intensive care unit (MICU) for further work up and management.

On chart review, it was shown that he had presented to the same ED twice in the past with episodes of chronic constipation. Gastroenterology and general surgery consults concluded that he had developed a chronic pseudo-obstruction pattern due to likely decreased gastrointestinal motility presumed secondary to TBI and immobility. He was evaluated and deemed to not qualify for neostigmine treatment due to finding of stool acting as a mechanical obstruction. During this MICU visit, he was treated for septic shock but unfortunately did not survive the hospital stay.

Learning Points/Take Home Message:

1. Ogilvie syndrome is an acquired dilation of the colon in the absence of any mechanical obstruction in severely ill patients characterized by abnormalities affecting the involuntary, rhythmic muscular contractions within the colon. The symptoms of Ogilvie syndrome mimic those of mechanical obstruction of the colon, but no physical obstruction is present.
2. Studies have shown that intravenous administration of neostigmine has led to rapid decompression of the colon in individuals with Ogilvie syndrome who did not respond to conservative management. 
3. Colonoscopic decompression, in which a thin, flexible tube is inserted into the anal passage and threaded up to the colon, may be used in refractory cases. Although colonoscopic decompression has not undergone clinical study, numerous reports in the medical literature cite it as an effective method for removing air from the colon and, potentially, reducing the risk of perforation. 
4. Surgery is used when affected individuals have signs of perforation or ischemia or have failed to respond to other treatment options. Surgery can be associated with significant morbidity and mortality.

Michael Bernaba MD, Emilio Power MD, Sidra Raoof MD, Babitha Bijin MD, Yuet-Ming Chan MD

Department of Internal Medicine

University of Arizona College of Medicine at South Campus

Tucson, AZ USA

References

1. McNamara R, Mihalakis MJ. Acute colonic pseudo-obstruction: rapid correction with neostigmine in the emergency department. J Emerg Med. 2008;35:167-70. [CrossRef] [PubMed]
2. Saunders MD, Kimmey MB. Systemic review: acute colonic pseudo-obstruction. Aliment Pharmacol Ther. 2005;22:917-25. [CrossRef] [PubMed]
3. Maloney N, Vargas HD. Acute intestinal pseudo-obstruction (Ogilvie's syndrome). Clin Colon Rectal Surg. 2005;18:96-101. [CrossRef] [PubMed]
4. De Giorgio R, Knowles CH. Acute colonic pseudo-obstruction. Br J Surg. 2009;96:229-39. [CrossRef] [PubMed]

Cite as: Bernaba M, Power E, Raoof S, Bijin B, Chan Y-M. Medical image of the month: chronic Ogilivie's syndrome. Southwest J Pulm Crit Care. 2018;17(6):146-8. doi: https://doi.org/10.13175/swjpcc117-18 PDF

Medical Image of the Month: Malignant Pleural and Pericardial Effusions

Figure 1. CTA chest axial view showing moderate pericardial effusion, bilateral pleural effusions and an anterior mediastinal mass.

Figure 2. Echocardiography subcostal four-chambered view showing a large pericardial effusion with right ventricular collapse during diastole.

A 67-year-old woman with a history of presumed thymoma presented to the emergency department with four weeks of progressive shortness of breath and wheezing. CT imaging of the chest on arrival demonstrated a 13.1 x 8.6 x 8.2 cm anterior mediastinal mass with compression of the SVC, pulmonary veins, and right pulmonary artery (Figure 1). A moderate pericardial effusion was also seen. A transthoracic echocardiogram was performed to further evaluate the pericardial effusion, which revealed diastolic collapse of the right ventricle consistent with cardiac tamponade (Figure 2). The patient was taken for urgent pericardiocentesis, which drained 450cc of sanguineous fluid. Percutaneous biopsy of the mass revealed poorly differentiated carcinoma suspicious for a primary breast malignancy. Cytology of the pericardial fluid did not demonstrate malignancy, however. Cytology of subsequent pleural effusion also was not positive for malignancy, although, both effusions are believed to be related to the malignancy even if no malignant cells were present on analysis.

Malignant pericardial effusions account for 18-23% of cases, and are one of the most common causes of hemorrhagic effusions. Multiple types of cancers can involve the pericardium; lung cancer is the most common but lymphoma, leukemia, melanoma, and breast cancer are other potentially causative malignancies. Presence of a symptomatic malignant effusion is a poor prognostic indicator with median survival on the order of 2-4 months after diagnosis, although certain malignancies (e.g. hematologic rather than solid) may have better results (1).

Nathan Coffman MD and Jessica Vondrak MD

Department of Internal Medicine

Banner University Medical Center

University of Arizona

Tucson, AZ USA

Reference

1. Dequanter D, Lothaire P, Berghmans T, Sculier JP. Severe pericardial effusion in patients with concurrent malignancy: a retrospective analysis of prognostic factors influencing survival. Ann Surg Oncol. 2008 Nov;15(11):3268-71. [CrossRef] [PubMed] 

Cite as: Coffman N, Vondrak J. Medical image of the month: Malignant pleural and pericardial effusions. Southwest J Pulm Crit Care. 2018;17(5): . doi: https://doi.org/10.13175/swjpcc107-18 PDF 

November 2018 Imaging Case of the Month: Respiratory Failure in a 36-Year-Old Woman

Michael B. Gotway, MD

Department of Radiology

Mayo Clinic Arizona

Scottsdale, AZ USA

Clinical History: A 36–year old woman presented with complaints of shortness of breath and worsening dyspnea on exertion. She had a reported history of central nervous system vasculitis of uncertain etiology, treated with azathioprine and prednisone currently, and cyclophosphamide in the past. Her symptoms reportedly responded well to this regimen. Her diagnosis of central nervous system vasculitis was established 6 months earlier when the patient presented with upper extremity paresthesia, headache, left arm weakness, diplopia, and a right eye visual field deficit, evidently with brain imaging showing some pathologic changes, although those records were not available at her presentation. Reportedly she responded well to her immunosuppressive therapy and her steroid and azathioprine doses had been tapered accordingly. Her past medical history was otherwise remarkable for a history of migraine headaches, depression, childhood asthma, hemorrhagic cystitis due to cyclophosphamide (which prompted discounting this drug in favor of azathioprine for the purported central nervous system vasculitis) in the past, and endometriosis.

The patient is a former smoker for a total of 5 pack-years, quitting years previously. She is the mother of a 3-year-old child. The patient denied alcohol and drug use. A history of penicillin allergy was elicited. In addition to azathioprine and prednisone, her medications included inhaled budesonide, Bactrim, escitalopram, topiramate, and sumatriptan/naproxen sodium as well as a multivitamin. There was some history of fenfluramine/phentermine (“Fen-Fen”) use years earlier.

Her physical examination was largely unremarkable. The patient complained of head pain and was visibly mildly dyspneic, but her lungs were clear and no abnormal heart sounds were detected. Her extremities appeared normal- no ecchymosis, cyanosis, or clubbing was detected. She did have some prior history suggesting the presence of erythema nodosum, now presenting as an erythematous region on the right lower extremity, which underwent biopsy, although changes characteristic of erythema nodosum were not present at her current examination. Reportedly this region had been injured when she bumped the right lower extremity on a chair, and this injury evidently became infected, requiring drainage, yielding cultures positive for Staphylococcus aureus and, about 1 month later, Actinomyces israelii. Her vital signs should normal pulse rate and blood pressure, breathing at 26 breaths / minute. Her room air oxygen saturation was 93%.

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

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

Which of the following represents the most accurate assessment of the chest radiographic findings? (Click on the correct answer to be directed to the second of twelve pages)

1. Chest radiography shows basilar fibrotic opacities
2. Chest radiography shows bilateral pleural effusions
3. Chest radiography shows cavitary pulmonary lesions
4. Chest radiography shows marked cardiomegaly
5. Chest radiography shows numerous small nodular opacities

Cite as: Gotway MB. November 2018 imaging case of the month: Respiratory failure in a 36-year-old woman. Southwest J Pulm Crit Care. 2018;17(5):119-33. doi: https://doi.org/10.13175/swjpcc114-18 PDF

Medical Image of the Month: Superior Vena Cava Syndrome

Figure 1. Coronal CT thorax with contrast showing a large apical mass with near complete atelectasis of the right upper lobe, mediastinal extension and effacement of the superior vena cava (arrow).

Figure 2. Caval-superficial-umbilical-portal pathway.  EMV = external mammary vein, EV = epigastric vein, IEV = inferior epigastric vein, IMV = internal mammary vein, SEV= superior epigastric vein (2).

Figure 3. Axial CT thorax with contrast showing avid arterial enhancement of hepatic segment IV (arrow, hot quadrate sign), consistent with superior vena cava syndrome.

Although superior vena cava syndrome (SVCS) may result from internal or external occlusion of the superior vena cava, 60-90% of cases are caused by external compression from malignant tumors, predominately lung cancer and lymphoma (1). Additional causes of SVCS via external occlusion include fibrosing mediastinitis, while internal occlusion may result from pacemaker lead or indwelling central venous catheter thrombosis (1). Symptoms of SVCS, such as facial and neck swelling, dyspnea and cough, typically develop over 2-4 weeks prior to diagnosis, during which collateral vessels develop (2). More severe symptoms of disease include laryngeal edema, cerebral edema, orthostatic syncope secondary to decreased venous return and altered mental status (3). In the presence of SVCS, cavoportal collaterals that may develop include caval-superficial-umbilical-portal pathways and caval-mammary-phrenic-hepatic capsule-portal pathways (3). Figure 2 demonstrates the anastomosis of inferior and superficial epigastric veins with internal and external mammary veins, allowing for recanalization of the paraumbilical vein and drainage into left portal vein. The presence of a caval-superficial-umbilical-portal pathway may be detected as a wedge-shaped area of increased enhancement in segment IV of the liver on CT or MRI, a radiographic finding known as the hot quadrate sign (Figure 3). Following diagnosis of SVCS in the setting of malignancy, goals of management may be palliative or curative and should take into account life expectancy. Endovascular stenting can provide near immediate symptomatic relief of SVCS, but requires the addition of chemotherapy, radiotherapy or combined-therapy if the goals of treatment are curative (1). Although the median life expectancy of a patient with SVCS due to underlying malignancy is often reported as 6 months, the prognosis is dependent on tumor type and the presence or absence of poor prognostic factors, including age >50 years old, history of tobacco use and treatment with corticosteroids (3).

Elliot Breshears MS IV, Lev Korovin MD, and Veronica Arteaga MD.

Department of Medical Imaging

The University of Arizona

Tucson, AZ, USA

References

1. Wan JF, Bezjak A. Superior vena cava syndrome. Hematol Oncol Clin North Am. 2010;24(3):501-13. [CrossRef] [PubMed]
2. Kapur S, Paik E, Rezaei A, Vu DN. Where there is blood, there is a way: unusual collateral vessels in superior and inferior vena cava obstruction. RadioGraphics. 2010;30(1):67-78. [CrossRef] [PubMed]
3. Manthey DE, Ellis LR. Superior vena cava syndrome (SVCS). In: Todd KH, Thomas CR Jr. Oncologic Emergency Medicine: Principles and Practice. Switzerland: Springer; 2016:211-222. Available at: https://books.google.com/books?id=_qQqDAAAQBAJ&pg=PA211&lpg=PA211&dq=Manthey+DE,+Ellis+LR.&source=bl&ots=MWH6bcbHSf&sig=L7Ul5sfS1sSGBTF5cnK7MvKF9eA&hl=en&sa=X&ved=2ahUKEwjGkoTC9LrdAhUEEHwKHbV2CF4Q6AEwAHoECAEQAQ#v=onepage&q=Manthey%20DE%2C%20Ellis%20LR.&f=false (accessed 9/14/18).

Cite as: Breshears E, Korovin L, Arteaga V. Medical image of the month: superior vena cava syndrome. Southwest J Pulm Crit Care. 2018;17(4):114-5. doi: https://doi.org/10.13175/swjpcc103-18 PDF 

Medical Image of the Month: Hot Tub Lung

Figure 1. Chest radiograph showing diffuse micronodular disease.

Figure 2. Representative images from the thoracic CT scan confirming diffuse micronodular disease with a centrilobular distribution.

Figure 3. Lung biopsy from VATS showing granulomas. Panel A: Low power view. Panels B & C: High power views.

The patient is a 65-year-old man with progressively worsening shortness of breath for 2 months. He had a past medical history of type 2 diabetes mellitus, hypertension, hypothyroidism and a 40 pack-year history of smoking. He suffered from chronic neck pain and sought relief by spending up to 6 hours daily in a hot tub. Chest x-ray (Figure 1) showed numerous small nodules which were confirmed on thoracic CT (Figure 2). The nodules spared the pleural space consistent with a centrilobular distribution. Bronchoscopy with bronchoalveolar lavage grew Mycobacterium avium intracellulare (MAC) and a lung biopsy obtained by video-assisted thorascopic surgery (VATS) showed non-caseating granulomas (Figure 3). Culture of the hot tub water also grew MAC.  He was advised to stop using the hot tub and was treated with prednisone, clarithromycin, rifampin and ethambutol. He rapidly improved though he stopped his therapy after about 3 weeks due to intolerance.  He continued to do well and was asymptomatic when last seen.

Hot tub lung may represent either an infectious process or a hypersensitivity pneumonitis to MAC inhaled from the hot tub. Improvement is usually seen with prednisone, anti-MAC therapy or both (1). The thoracic CT findings are consistent with subacute hypersensitivity pneumonitis including areas of ground-glass attenuation, centrilobular nodules, and air trapping on expiratory images (2). Granulomas, a compact collection of macrophages, are a nonspecific finding seen in both infectious (mycobacteria and fungi) and noninfectious lung diseases (sarcoidosis, hypersensitivity pneumonitis, hot tub lung, and several others) (3). In our patient’s case the clinical history, radiologic findings, lung histology and rapid improvement with removal of MAC exposure are all consistent with hot tub lung.

Allen R. Thomas, MD

Phoenix VA

Phoenix, AZ USA

References

1. Khoor A, Leslie KO, Tazelaar HD, Helmers RA, Colby TV. Diffuse pulmonary disease caused by nontuberculous mycobacteria in immunocompetent people (hot tub lung). Am J Clin Pathol. 2001 May;115(5):755-62. [CrossRef] [PubMed]
2. Hartman TE, Jensen E, Tazelaar HD, Hanak V, Ryu JH.CT findings of granulomatous pneumonitis secondary to Mycobacterium avium-intracellulare inhalation: "hot tub lung". AJR Am J Roentgenol. 2007 Apr;188(4):1050-3. [CrossRef] [PubMed]
3. Hutton Klein JR, Tazelaar HD, Leslie KO, Colby TV. One hundred consecutive granulomas in a pulmonary pathology consultation practice. Am J Surg Pathol. 2010 Oct;34(10):1456-64. [CrossRef] [PubMed]

Cite as: Thomas AR. Medical image of the month: hot tub lung. Southwest J Pulm Crit Care. 2018;17(3):93-4. doi: https://doi.org/10.13175/swjpcc077-18 PDF 

Medical Image of the Week: Chylothorax

Figure 1. A: CT of the chest (coronal image) demonstrating large right hilar and mediastinal adenopathy, leading to moderate to severe narrowing of the superior vena cava (SVC). B: CT of the chest (axial image) demonstrating moderate to severe narrowing of the pulmonary artery trunk due to compression from mediastinal adenopathy. A left pleural effusion is noted.

Figure 2. Pleural fluid sample demonstrating milky, pink fluid. The triglyceride level was 532 mg/dl and cholesterol level 63 mg/dl.

A 73-year-old man with untreated stage IV adenocarcinoma of the lung was admitted to the hospital with several days of progressively worsening dyspnea on exertion. The chest CT showed a large left pleural effusion with enlarging bilateral hilar and mediastinal lymphadenopathy, compression of the superior vena cava and right main pulmonary artery consistent with progressive lung cancer (Figure 1). Therapeutic and diagnostic left sided thoracentesis was performed, removing approximately 450 ml of milky, pink fluid suggestive of hemochylothorax (Figure 2). Analysis of the fluid was significant for 27,720 red blood cells, 476 total nucleated cells with lymphocyte predominance (87%), glucose 158 mg/dl, cholesterol 63 mg/dl, and amylase 28 U/L. The pleural fluid was exudative (protein 4.4 g/dl) with a significantly elevated triglyceride level of 532 mg/dl. No malignant cells were identified in the fluid.

This case illustrates a nontraumatic chylothorax secondary to metastatic adenocarcinoma of the lung. The leading cause of non-traumatic chylothorax is malignancy by compression and/or lymphangitic invasion (1). Thoracic duct invasion or leak can only be seen with nuclear medicine scintigraphy; however, this test was not performed on this patient. The appearance of the pleural fluid in chylothorax can be deceiving as less than half of pleural fluid samples will be milky in appearance (2). In addition, milky appearing pleural fluid is not specific for a chylothorax, as milky fluid can be seen in a cholesterol pleural effusion (pseudochylothorax) or an empyema. The detection of chylomicrons on pleural fluid lipoprotein electrophoresis is the definitive diagnostic criterion for chylothorax, however it is not widely available and is costly (3). The classic diagnostic criterion is a pleural fluid triglyceride level of >110 mg/dl in an appropriate clinical setting of mediastinal malignancy, lymphoma, recent thoracic surgery or penetrating trauma to the neck or thorax (4). A pleural fluid triglyceride level between 50 and 110 mg/dl does not exclude the diagnosis of chylothorax and clinicians should perform lipoprotein electrophoresis of the pleural fluid to detect chylomicrons. To distinguish a chylothorax from a pseudochylothorax (both have milky appearance), clinicians should obtain a cholesterol level on the fluid. The cholesterol level in a chylothorax is usually less than 200 mg/dl while a pseudochylothorax will have high levels, typically greater than 200 mg/dl.

The patient chose to undergo palliative radiation of the chest and symptomatic treatment of his dyspnea.  

John Dicken MD¹, Madhav Chopra MD², Faraz Jaffer MD² and Linda Snyder MD²

¹Department of Internal Medicine and ²Division of Pulmonary, Allergy, Critical Care and Sleep

Banner University Medical Center-Tucson

Tucson, AZ USA

References

1. McGrath EE, Blades Z, Anderson PB. Chylothorax: aetiology, diagnosis and therapeutic options. Respir Med. 2010 Jan;104(1):1-8. [CrossRef] [PubMed]
2. Maldonado F, Hawkins FJ, Daniels CE, Doerr CH, Decker PA, Ryu JH. Pleural fluid characteristics of chylothorax. Mayo Clin Proc. 2009 Feb;84(2):129-33. [CrossRef] [PubMed]
3. Hooper C, Lee YC, Maskell N; BTS Pleural Guideline Group. Investigation of a unilateral pleural effusion in adults: British Thoracic Society Pleural Disease Guideline 2010. Thorax. 2010 Aug;65 Suppl 2:ii4-17. [CrossRef] [PubMed]
4. Staats BA, Ellefson RD, Budahn LL, Dines DE, Prakash UB, Offord K. The lipoprotein profile of chylous and nonchylous pleural effusions. Mayo Clin Proc. 1980 Nov;55(11):700-4. [PubMed]

Cite as: Dicken J, Chopra M, Jaffer F, Snyder L. Medical image of the week: Chylothorax. Southwest J Pulm Crit Care. 2018;17(2):70-1. doi: https://doi.org/10.13175/swjpcc100-18 PDF 

August 2018 Imaging Case of the Month: Dyspnea in a 55-Year-Old Smoker

Michael B. Gotway, MD

Department of Radiology

Mayo Clinic Arizona

Scottsdale, AZ USA

Clinical History: A 55–year old woman presented to the emergency room with complaints of shortness of breath and lower extremity swelling. The patient noted her shortness of breath had been worsening over the previous 6 months, especially in the last 3 months. The patient denies cough, fever, chills, and night sweats. The patient admits to some fatigue but has not lost weight recently.

The patient is a current smoker, averaging about 1 pack-per-day for the previous 40 years. Her allergies include penicillin and sulfa drugs, and her prior medical history was remarkable only for hypothyroidism and gastroesophageal reflux. Her only previous surgery was for an ectopic pregnancy. The patient’s mediation list included use of opiates for pain related to a herniated disc in the lower cervical spine following an automobile accident two years earlier.

Her physical examination was unremarkable aside from obesity and mild symmetric lower extremity edema. Her vital signs were within normal limits.

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

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

Which of the following represents the most accurate assessment of the chest radiographic findings? (Click on the correct answer to be directed to the second of ten pages)

1. Chest radiography shows a mediastinal mass
2. Chest radiography shows cavitary pulmonary lesions
3. Chest radiography shows miliary nodules
4. Chest radiography shows an interstitial abnormality consisting of reticular and nodular opacities
5. Chest radiography shows basilar fibrotic opacities

Cite as: Gotway MB. August 2018 imaging case of the month: Dyspnea in a 55-year-old smoker. Southwest J Pulm Crit Care. 2018;17(2):59-69. doi: https://doi.org/10.13175/swjpcc099-18 PDF

Medical Image of the Week: Tracheobronchopathia Osteochondroplastica

Figure 1. View of trachea during bronchoscopy showing submucosal nodules.

Figure 2. H & E staining of cartilage biopsy.

A 52-year-old asymptomatic woman underwent a low dose computed tomography (CT) of chest due to long-standing history of smoking. CT chest revealed a 4 mm right lower lobe pulmonary nodule. Also noted were several nodules throughout the trachea and in the left main-stem bronchus. Bronchoscopy revealed multiple non-obstructing submucosal nodules along the tracheal rings with sparing of the posterior membranous portion of the trachea (Figure 1).  Endotracheal biopsy showed benign cartilage and ciliated epithelium (Figure 2). The patient was diagnosed with tracheobronchopathia osteochondroplastica (TO). Clinical manifestations of TO are nonspecific and include cough, wheezing, hemoptysis, dyspnea, and recurrent lung infections (1). Therapy for TO includes alleviation of symptoms with bronchodilators, treatment of respiratory infections and tracheal dilation.  Therapeutic modalities for tracheal dilation includes surgical resection, laser ablation and vaporization.  CT chest was to be repeated at 12 months for follow-up of the pulmonary nodule. The patient was lost to follow-up.

Benjamin O. Lawson MD¹, Kelechi Abarikwu², and Aditya Gupta MD³

¹Internal Medicine and ³Pulmonary/Critical Care Medicine

HonorHealth Scottsdale Thompson Peak Medical Center

Scottsdale, AZ USA

²University of Arizona Tucson

Tucson, AZ USA

Reference

1. Simmons C, Vinh D, Donovan DT, Ongkasuwan J. Tracheobronchopathia osteochondroplastica. Laryngoscope. 2016 Sep;126(9):2006-9. [CrossRef] [PubMed]

Cite as: Lawson BO, Abarikwu K, Gupta A. Medical image of the week: Tracheobronchopathia osteochondroplastica. Southwest J Pulm Crit Care. 2018;17(2):45-6. doi: https://doi.org/10.13175/swjpcc094-18 PDF

Medical Image of the Week: Plastic Bronchitis in an Adult Lung Transplant Patient

Figure 1. Representative coronal (A) and axial (B) views of the thoracic CT scan in lung windows revealing bilateral dense consolidations and bronchial filling.

Figure 2. Photograph of bronchial gelatinous casts after bronchoscopic forceps removal.

Plastic Bronchitis is a rare condition characterized by the formation of branching gelatinous casts of the bronchial tree which lead to regional airway obstruction. There are thought to be two classifications of casts; type I being the formation of cellular inflammatory casts while type II are acellular. This entity is a well described complication of the Fontan procedure, a therapeutic intervention in pediatric patients with univentricular congenital heart disease (1). The condition is less well reported and thus recognized in adult populations (2).

Our patient is a 37-year-old man who is status post bilateral lung transplantation undertaken for severe workplace inhalation injury complicated by constrictive bronchiolitis-obliterans. Post-transplant, the patient suffered from refractory severe persistent asthma of the donor lung and therefore was scheduled for elective initial bronchial thermoplasty. Post-procedure the patient developed progressive respiratory distress and ultimately extremis requiring mechanical ventilation. Pulse-dose corticosteroids were initiated given a suspected etiology of acute rejection, although response to therapy was poor. Bronchoscopy was conducted which revealed diffuse fibrin casts of the right lung consistent with the development of plastic bronchitis. Symptoms significantly improved with removal of these casts, although a repeat bronchoscopy with cast removal was necessary shortly afterward. Our patient’s cast formation is unique given that it likely has components of both etiologies given his underlying bronchial hyper-secretory disorder and lymphatic disruption after lung transplant. For this reason, we consider this a unique case in its ability to highlight the overlap of these two pathologic processes in an otherwise unlikely demographic to develop bronchial casts. In our comprehensive literature search, we were unable to find significant description of this disorder in adult lung transplant. However, given the disruption in lymphatics, host vs graft inflammatory factors, and infectious inflammatory factors, it would seem to be a perfect setup pathologically. The underlying pathophysiologic mechanism of plastic bronchitis is believed to be cast formation via pulmonary lymphatic disruption by either surgical intervention or inflammatory processes. Gelatinous casts are formed by way of alveolar capillary leak of proteinaceous material, lymphatic seepage, and exudate accumulation from airway inflammation. The majority of literature regarding this disease processes has been described in pediatric thoracic surgery. Lung transplant, especially in the setting of acute rejection, seems to be a setup for this condition in adult populations.

Sarika Savajiyani DO, Nafis Shamsid-Deen MD, and  Raed Alalawi MD

University of Arizona, College of Medicine-Phoenix

Phoenix, AZ USA

References

1. Singhi AK, Vinoth B, Kuruvilla S, Sivakumar K. Plastic bronchitis. Ann Pediatr Cardiol. 2015 Sep-Dec;8(3):246-8. [CrossRef] [PubMed]
2. Eberlein M, Parekh K, Hansdottir S, Keech J, Klesney-Tait J. Plastic bronchitis complicating primary graft dysfunction after lung transplantation. Ann Thorac Surg. 2014 Nov;98(5):1849. [CrossRef]

Cite as: Savajiyani S, Shamsid-Deen N, Alalawi R. Medical image of the week: Plastic bronchitis in an adult lung transplant patient. Southwest J Pulm Crit Care. 2018;17(1):39-40. doi: https://doi.org/10.13175/swjpcc088-18 PDF