Medical Image of the Week: Polysomnogram Artifact

Figure 1. Thirty second polysomnogram epoch showing artifact in lead O1M2 (black arrow).

Figure 1. Ten second polysomnogram epoch showing artifact in lead O1M2 (black arrow).

A 54 year-old man with a past medical history of attention deficit hyperactivity disorder (ADHD), low back pain, and paroxysmal supraventricular tachycardia presented to the sleep laboratory for evaluation of sleep disordered breathing. Pertinent medications include fluoxetine, ambien, and clonazepam. His Epworth sleepiness score was 18. He had a total sleep time of 12 min. On the night of his sleep study, the patient was restless and repeatedly changed positions in bed. 

Figures 1 and 2 show the artifact determined to be lead displacement of O1M2 after the patient shifted in bed, inadvertently removing one of his scalp electrodes. The sine waves are 60 Hz in frequency. Once the problem was identified, the lead was quickly replaced to its proper position.

Jared Bartell¹, Safal Shetty, MD^1,2, and John D. Roehrs, MD^1,2

¹University of Arizona Medical Center

²Southern Arizona VA Health Care System

Tucson, AZ

Reference as: Bartell J, Shetty S, Roehrs JD. Medical image of the week: polysomnogram artifact. Southwest J Pulm Crit Care. 2015;10(2):95-6. doi: http://dx.doi.org/10.13175/swjpcc014-15 PDF

Medical Image of the Week: Bilateral Symmetrical Nephromegaly

Figure 1. Axial section from the CT scan through the abdomen. Also seen is the "misty mesenteric sign" (white arrow) and pancreatomegaly (black arrow).

Figure 2. Coronal section of the abdominal CT scan showing the diffuse symmetric nephromegaly.

A 70-year-old man was evaluated for symptoms of fatigue, abdominal pain and a 20 pound weight loss. Abdominal imaging was obtained as a part of work up and showed hepatomegaly, splenomegaly, nephromegaly, mesenteric infiltration and diffuse lymphadenopathy (Figures 1 and 2).

A liver biopsy was obtained and a diagnosis of diffuse large B-cell lymphoma was made. The patient opted for a palliative approach and was discharged to an inpatient hospice after a short hospital stay.

Bilateral symmetrical nephromegaly is an uncommon radiological finding in adults, and in the absence of infection, the differential includes HIV-associated nephropathy, amyloidosis, lymphoma, acute tubular necrosis and lupus nephritis.

Also seen in Figure 1 is the "misty mesenteric sign" (white arrow) which is a term used to describe the CT appearance of mesenteric fat with increased attenuation and stranding (1).  A number of processes can lead to the appearance including infiltration by inflammatory cells, edema, lymphatic accumulation, hemorrhage, tumor infiltration, and fibrosis.  

Tammer Elaini MD¹, Muna Omar MD² and Bhupinder Natt MD²

¹Department of Internal Medicine

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

University of Arizona Medical Center

Tucson, AZ

Reference

1. Corwin MT, Smith AJ, Karam AR, Sheiman RG. Incidentally detected misty mesentery on CT: risk of malignancy correlates with mesenteric lymph node size. J Comput Assist Tomogr. 2012 Jan-Feb;36(1):26-9. [CrossRef] [PubMed] 

Reference as: Elaini T, Omar M, Natt B. Medical image of the week: bilateral symmetrical nephromegaly. Southwest J Pulm Crit Care. 2015;10(2):93-4. doi: http://dx.doi.org/10.13175/swjpcc013-15 PDF

Medical Image of the Week: Ascaris Lumbricoides

Figure 1. 23 cm adult Ascaris lumbricodes recovered from patient's feces.

A 25 year-old man was admitted to the ICU with acute renal failure and acute respiratory failure from fluid overload after attempting to cross the border. The patient was successfully extubated after five days of mechanical ventilation and renal replacement therapy. Following extubation, the patient had a bowel movement and passed a 23cm adult Ascaris lumbricoides. He was treated with a single dose of albendazole 400 mg.

Ascariasis is a very common helminthic infection, particularly in pediatric populations, and affects mostly the gastrointestinal tract. When infective eggs are swallowed by the host, larvae hatch in the GI tract. The larvae invade the GI mucosa and then are brought into the lungs via portal circulation. The larvae can then move up the tracheobronchial tree and then are swallowed into the GI tract where the mature worms form (1).

While our patient had a simple gastrointestinal infection, several pulmonary complications of ascariasis have been reported (2). Adult worms can cause largyngospasm as well as mechanical obstruction of the airway which can result in cardiac arrest (3,4). This migration of worms from the stomach to the trachea may be related to the use of anesthetics and the subsequent relaxation of the lower esophageal sphincter. Ascaris larvae have been implicated in Loeffler’s syndrome, also described as simple pulmonary eosinophilia, characterized by transient pulmonary infiltrates and eosinophilia with a usually benign course.

Candy Wong¹; Aaron Fernandes², Jennifer Huang², and Sachin Chaudhary¹

¹Division of Pulmonary, Critical Care, Allergy, and Sleep Medicine.

² Department of Medicine

University of Arizona

Tucson, AZ

References

1. Centers for Disease Control and Prevention. Parasites – Ascariasis. Biology. Available at: http://www.cdc.gov/parasites/ascariasis/biology.html (accessed 1/13/2015).
2. Li QY, Zhao DH, Qu HY, Zhou CN. Life-threatening complications of ascariasis in trauma patients: a review of the literature. World J Emerg Med. 2014;5(3):165-70. [CrossRef] [PubMed]
3. Maletin M, Veselinović I, Stojiljkovic GB, Vapa D, Budakov B. Death due to an unrecognized ascariasis infestation: two medicolegal autopsy cases. Am J Forensic Med Pathol. 2009;30(3):292-4. [CrossRef] [PubMed]
4. Husain SJ, Zubairi AB, Sultan N, Beg MA, Mehraj V. Recurrent episodes of upper airway blockage associated with Ascaris lumbricoides causing cardiopulmonary arrest in a young patient. BMJ Case Rep. 2009;2009. pii: bcr01.2009.1415. [CrossRef] [PubMed]

Reference as: Wong C, Fernandes A, Huang J, Chaudhary S. Medical image of the week: ascaris lumbridoies. Souhtwest J Pulm Crit Care. 2015;10(2):81-2. doi: http://dx.doi.org/10.13175/swjpcc008-15 PDF

Medical Image of the Week: Wide Mediastinum Due to Lung Infiltrates

Figure 1. Panel A: Admission chest x-ray showing an apparent widened mediastinum. Panels B & C: CT scan showing consolidation in the posterior lungs bilaterally. Panel D: Chest x-ray showing resolution of his widened mediastinum with an increase in positive end-expiratory pressure.

The patient is a 65-year-old man patient with a past medical history of poorly controlled hypertension and coronary artery disease who was admitted after a witnessed code arrest. He was found down, and paramedics arrived within 5 minutes and started chest compressions. His initial CXR showed a wide mediastinum (Figure 1A) that was concerning for possible aortic dissection especially with his history of poorly controlled hypertension. Due to his hemodynamic instability a chest CT scan couldn’t be done initially, but the patient underwent a trans-esophageal echo that was negative for aortic dissection.

When the patient became more stable a chest CT scan with contrast was done and showed consolidation of the medial parts of both lungs with 7 bilateral rib fractures (Figure 1 B & C). The impression was either lung contusion from the aggressive chest compression as evidenced by the bilateral 7 rib fractures or aspiration in the dependent parts of the lung. His apparent widened mediastinum resolved with increasing the positive end-expiratory pressure (PEEP) on the ventilator within 48 hours (Figure 1D).

Huthayfa Ateeli MBBS, Laila Abu Zaid MD

Department of Medicine

University of Arizona

Tucson, AZ.

References

1. Cohn SM. Pulmonary contusion: review of the clinical entity. J Trauma. 1997;42(5):973-9. [CrossRef] [PubMed]
2. Lai CC, Wang CY, Lin HI, Wang JY. Pulmonary contusion associated with chest compressions. Resuscitation. 2010;81(1):133. [CrossRef] [PubMed]

Reference as: Ateeli H, Zaid LA. Medical image of the week: widen mediastinum due to lung infiltrates. Southwest J Pulm Crit Care. 2015;10(2):77-8. doi: http://dx.doi.org/10.13175/swjpcc007-15 PDF 

February 2015 Imaging Case of the Month

Michael B. Gotway, MD

Department of Radiology

Mayo Clinic Arizona

Scottsdale, AZ

Clinical History: A 37-year-old man, a former smoker (quit 10 years ago) presented to his physician as an outpatient with complaints of intermittent chest pain, malaise, and intermittent fever. Stress ECG and upper endoscopy were negative. His previous medical history was otherwise unremarkable. Various physicians told the patient his symptoms were due to “stress”; presumptive antibiotic treatment had no effect.

Frontal chest radiography (Figure 1) was performed.

Figure 1. Frontal chest radiography.

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

1. The chest radiograph shows a circumscribed pulmonary mass
2. The chest radiograph shows asymmetric pulmonary vascularity
3. The chest radiograph shows bilateral linear and reticular opacities and diminished lung volumes suggesting fibrotic lung disease
4. The chest radiograph shows cardiomegaly and small pleural effusions
5. The chest radiograph shows numerous small nodules

Reference as: Gotway MB. February 2015 imaging case of the month. Soutwest J Pulm Crit Care. 2015:10(2):70-6. doi: http://dx.doi.org/10.13175/swjpcc018-15 PDF

Medical Image of the Week: Bilateral Atrial Appendage Thrombi

Figure 1. Panel A: Right atrial appendage (RAA) thrombus (red arrow) on chest computerized tomorgraphy angiogram (CTA). Panel B: Left atrial appendage (LAA) thrombus (yellow arrow) on chest CTA. Panel C: RAA thrombus (red arrow) on transesophageal echocardiography (TEE). Panel D: LAA thrombus (yellow arrow) on TEE.

A 63-year-old man with a past history significant for hypertension, low back pain and polysubstance abuse (tobacco and marijuana) presented with shortness of breath and hemoptysis for the last 8 days prior to admission. His initial exam showed elevated jugular venous pressure and bilateral basal crackles with reduced air entry on the right lower lung zone.

The patient was found to be in atrial fibrillation with a rapid ventricular response. His initial chest X-ray showed a moderate right-sided pleural effusion. Immediate bedside echo was concerning for bilateral ventricular dysfunction with concerns of right-sided heart pressure and volume overload. A chest CT angiogram was obtained and showed acute lower lobe pulmonary embolism, with possible distal infarct, moderate right sided pleural effusion, and filling defects in both atrial appendages concerning for thrombi (Figure 1, Panels A & B).

The patient was started on therapeutic anticoagulation and underwent therapeutic thoracentesis, gentle diuresis, and rate control for his atrial fibrillation. A few days later, a trans-esophageal echo confirmed the bilateral atrial thrombi (Figure 1, Panels C & D).

Huthayfa Ateeli MBBS¹, Andrew Kovoor MD¹, Hem Desai MBBS¹, Alana Stubbs MD², Tam Nguyen MD³

¹Department of Medicine, ²Radiology Department, and ³Cardiology Division

University of Arizona and Southern Arizona VA Health Care System

Tucson, AZ

References

1. Kim YY, Klein AL, Halliburton SS, Popovic ZB, Kuzmiak SA, Sola S, Garcia MJ, Schoenhagen P, Natale A, Desai MY. Left atrial appendage filling defects identified by multidetector computed tomography in patients undergoing radiofrequency pulmonary vein antral isolation: a comparison with transesophageal echocardiography. Am Heart J. 2007;154(6):1199-205. [CrossRef] [PubMed]
2. Shapiro MD, Neilan TG, Jassal DS, Samy B, Nasir K, Hoffmann U, Sarwar A, Butler J, Brady TJ, Cury RC. Multidetector computed tomography for the detection of left atrial appendage thrombus: a comparative study with transesophageal echocardiography. J Comput Assist Tomogr. 2007;31(6):905-9. [CrossRef] [PubMed] 

Reference as: Ateeli H, Kovoor A, Desai H, Stubbs A, Nguyen T. Medical image of the week: bilateral atrial appendange thrombi. Southwest J Pulm Crit Care. 2015;10(1):54-5. doi: http://dx.doi.org/10.13175/swjpcc006-15 PDF

Medical Image of the Week: Dobhoff Placement in a Patient with Hiatal Hernia

Figure 1. Arrows designate tip of Dobhoff feeding tube (DHT). Panel A: Chest radiograph. DHT appears to follow the left main bronchus into the left lower lobe. Panel B: Abdominal view of DHT placement. Panel C: Chest CT showing degree of hiatal hernia and DHT in the intra-thoracic hernia. Panel D: Follow-up fluoroscopy imaging showing appropriately placed DHT in the duodenum.

A 79 year-old woman with a past medical history of obstructive sleep apnea, chronic obstructive pulmonary disease on home oxygen, obesity hypoventilation syndrome, hypertension, and anxiety presented with a 2 day history of altered mental status and symptoms consistent with a COPD exacerbation, including dyspnea and increased oxygen requirements. She was found to be hypercarbic and did not tolerate a trial of BiPAP due to her altered mentation. She was subsequently intubated. Due to an expected prolonged intubation period, plans for enteral access were made. A Dobhoff naso-duodenal feeding tube (DHT) was inserted. On chest radiograph and a concurrent abdominal radiograph, the DHT appeared to have been inserted into the left mainstem bronchus terminating in the left lower lobe (Figure 1A and 1B). The nursing staff removed and replaced the DHT resulting in a similar radiograph. A third placement was attempted with similar radiographic results. Therefore, a computed tomography (CT) scan of the chest was performed to evaluate tube placement. The CT of the chest showed a large hiatal hernia contained within thoracic cavity (Figure 1C). Upon chart review, previous radiographs mentioned hiatal hernia but it appeared that the degree of herniation had progressed. Fluoroscopy was used to confirm placement of the DHT beyond the herniated gastric contents into the duodenum (Figure 1D) and tube feeds were initiated.

Post-pyloric feeding tubes are often used in place of gastric feeding tubes under the assumption that the risk of aspiration in the intubated patient is reduced. Enteral nutrition is typically started within 36 hours of intubation as this has been shown to decrease mortality in intubated patients (1). There are contraindications to the use of nasogastric or nasoenteric feeding tubes, which include facial trauma, esophageal web, or recent esophagectomy. Hiatal hernias are not a contraindication to nasoenteric feeding tube placement, however, patients with unusual anatomy may benefit from placement under fluoroscopic or endoscopic visualization in order to ensure appropriate positioning (2).

Kawanjit K Sekhon, MD and Ryan Nahapetian, MD, MPH

Department of Internal Medicine

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

University of Arizona, Tucson, AZ

References

1. Marik PE, Zaloga GP. Gastric versus post-pyloric feeding: a systematic review. Crit Care. 2003;7(3):R46-51. [CrossRef] [PubMed]

2. Hodin RA, Bordeianou L. Nasogastric and nasoenteric tubes. Uptodate.com. Oct 17, 2013. Dec 20, 2013. Available at: http://www.uptodate.com/contents/nasogastric-and-nasoenteric-tubes?source=machineLearning&search=hiatal+hernia+feeding+tube&selectedTitle=1%7E150&sectionRank=3&anchor=H522922014#H522922014 (requires subscription).

Reference as: Sekhon KK, Nahapetian R. Medical image of the week: Dobhoff placement in a patient with hiatal hernia. Southwest J Pulm Crit Care. 2015;10(1):49-50. doi: http://dx.doi.org/10.13175/swjpcc005-15 PDF

Medical Image of the Week: Hepatic Hydrothorax

Figure 1. Panel A: Chest x-ray showing right pleural effusion. Panel B: Coronal view of the thoracic CT scan in soft tissue windows showing right pleural effusion.

Figure 2. Nuclear scan after intraperitoneal injection of technetium 99mTc albumin aggregated (99mTc-MAA). After less than one hour most of the tracer migrated into the right hemithorax consistent with hepatic hydrothorax.

A 63 year-old woman, with known alcoholic liver cirrhosis, esophageal varices with history of banding presented to an outside hospital with progressive shortness of breath, and was found to have a large right transudative pleural effusion. The patient underwent 2 diagnostic and therapeutic thoracenteses within 3 days, removing 1100 ml and 1500 ml respectively. No ascites was present. At the time of admission the patient had recurrent right effusion (Figure 1). Abdominal ultrasound showed minimal free intrabdominal fluid and she had signs of third spacing on her lower extremities. The patient underwent intraperitoneal injection of Technetium 99mTc albumin aggregated (99mTc-MAA). After less than one hour most of the tracer migrated into the right hemithorax consistent with hepatic hydrothorax (Figure 2).

While the exact mechanism involved in the development of hepatic hydrothorax is incompletely understood, it probably results from the passage of ascitic fluid from the peritoneal into the pleural cavity through small diaphragmatic defects. These are typically < 1 cm (and may be microscopic) and are generally located in the tendinous portion of the diaphragm. The negative intrathoracic pressure generated during inspiration favors the passage of the fluid into the pleural space. Thus, patients may have only mild or clinically undetectable ascites.

Once the diagnosis is made treatment follows algorithms for treatment of refractory ascites and include salt and water restriction, diuretics, and other validated options for portal hypertension. Repeated thoracentesis and chest tube placement is discouraged.

Huthayfa Ateeli, Justin Lee, Irbaz Riaz, Meenal Misal

Department of Internal Medicine

University of Arizona

Tucson, AZ

References

1. Huang PM, Chang YL,Yang CY,Lee YC.The morphology of diaphragmatic defects in hepatic hydrothorax: thoracoscopic finding. J Thorac Cardiovasc Surg. 2005;130:141-5. [CrossRef] [PubMed]
2. Lieberman FL, Hidemura R, Peters RL, Reynolds TB. Pathogenesis and treatment of hydrothorax complicating cirrhosis with ascites. Ann Intern Med. 1966;64:341-51. [CrossRef] [PubMed]
3. Emerson PA, Davies JH. Hydrothorax complicating ascites. Lancet. 1955; 268:487-8. [CrossRef] [PubMed]
4. Mouroux J, Perrin C, Venissac N, Blaive B, Richelme H. Management of pleural effusion of cirrhotic origin. Chest. 1996;109:1093-6. [CrossRef] [PubMed]
5. Chen A, Ho YS, Tu YC, Tang HS, Cheng TC. Diaphragmatic defect as a cause of massive hydrothorax in cirrhosis of liver. J Clin Gastroenterol. 1988;10:663-6. [CrossRef] [PubMed] 

Reference as: Ateeli H, Lee J, Riaz I, Misal M. Medical image of the week: hepatic hydrothorax. Southwest J Pulm Crit Care. 2015;10(1):47-8. doi: http://dx.doi.org/10.13175/swjpcc004-15 PDF

Medical Image of the Week: ECG in PE

Figure 1. ECG on presentation demonstrating sinus tachycardia, anterior precordial T wave inversions and S1Q3T3, classic ECG findings of pulmonary embolism.

Figure 2. Panel A: CT angiogram demonstrating bilateral pulmonary embolism involving nearly every segmental and subsegmental pulmonary artery. Panel B: Echocardiogram, apical 4-chamber view, with dilated right ventricle and poor function. Panel C: Right leg ultrasound showing acute, non-occlusive thrombus; the right side of the image demonstrates incompressibility of the right femoral vein.

A 44-year-old male long distance truck driver with no known medical history presented with intermittent episodes of dyspnea for the past 24 hours, and an episode of exertional syncope just prior to hospitalization. The patient complained of sharp severe chest pain and reports several week history of right leg swelling. Initial Electrocardiogram (ECG, Figure 1) shows sinus tachycardia and signs of right ventricular strain with an associated troponin elevation. CT pulmonary angiography confirmed bilateral, extensive pulmonary emboli (PE) (Figure 2A, arrow at left pulmonary artery embolus). An echocardiogram showed severe right ventricular systolic dysfunction (Figure 2B, arrow indicated RV). Duplex ultrasound of the right leg showed extensive, acute, non-occlusive thrombus (Figure 2C, arrow indicates clot failing to compress). The patient received an IVC filter due to substantial clot burden. A hypercoagulability workup was negative.

The ECG is part of the typical evaluation for syncope, chest pain and shortness of breath. Multiple studies evaluating the utility of the ECG in the diagnosis of PE have been conducted (1-3). One study in patients with suspected PE undergoing diagnostic testing found that only tachycardia and incomplete right bundle branch block were significantly more prevalent in patients with PE than those without. Another study found a 39% rate of sinus tachycardia in those ultimately found to have PE compared to 24% in those who had negative studies. The S1Q3T3 phenomenon was present in 12% of those with PE vs 3% in those without. One or more traditional findings of right ventricular strain: S1Q3T3, right bundle branch block, or right axis deviation was present in only 13% of patients with PE who had RV dilation on echocardiography, however these findings were also present in 8.8% of patients with PE without evidence of RV dysfunction. Non-specific ECG findings such as sinus tachycardia and ST-T changes are the most commonly identified ECG abnormalities in patients with PE. Overall the ECG as a test for PE exhibits poor test characteristics and thus has little clinical utility for its diagnosis, despite the frequent emphasis on these findings in medical education.

Our patient’s ECG demonstrates several classic findings suggestive of PE including sinus tachycardia, S1Q3T3, and T-wave inversions in the anterior precordial leads. While certain ECG findings do correlate with the presence of PE they are frequently present in patients without PE and absent in those with the disease. ECG may have some utility in risk stratification by identifying signs of right heart strain, however echocardiography is the preferred modality.

Taylor Shekell MD², Cameron Hypes MD MPH^1,2, Yuval Raz MD¹

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

² Department of Emergency Medicine

University of Arizona Medical Center

Tucson, AZ

References

1. Rodger M, Makropoulos D, Turek M, Quevillon J, Raymond F, Rasuli P, Wells PS. Diagnostic value of the electrocardiogram in suspected pulmonary embolism. Am J Cardiol. 2000;86:807-9. [CrossRef] [PubMed]
2. Sinha N, Yalamanchili K, Sukhija R, Aronow WS, Fleisher AG, Maguire GP, Lehrman SG. Role of the 12-lead electrocardiogram in diagnosing pulmonary embolism. Cardiol Rev. 2005;13:46-9. [PubMed]
3. Stein P, Matta F, Sabra M, et al. Relation of electrocardiographic changes in pulmonary embolism to right ventricular enlargement. Am J Cardiol. 2013;112:1958-61. [CrossRef] [PubMed] 

Reference as: Shekell T, Hypes C, Raz Y. Medical image of the week: ECG in PE. Southwest J Pulm Crit Care. 2015;10(1):44-6. doi: http://dx.doi.org/10.13175/swjpcc162-14 PDF

January 2015 Imaging Case of the Month

Michael B. Gotway, MD

Department of Radiology

Mayo Clinic Arizona

Scottsdale, AZ

Clinical History: A 68-year-old woman with a history of myelodysplastic syndrome associated with transfusion-dependent anemia and thrombocytopenia presented with recent onset left chest pain and fever. The patient had a remote history of total right knee arthroplasty, hypertension, asthma, and schizoaffective disorder. Several months earlier the patient was hospitalized with methicillin-sensitive Staphylococcus aureus infection involving the right knee arthroplasty, associated with bacteremia and a septic right elbow. This infection was treated with incision and drainage of the elbow, antibiotic bead placement about the right knee arthroplasty with an antibiotic-impregnated spacer, and antibiotics (6 weeks intravenous cefazolin followed by chronic doxycycline suppression therapy, the former later switched to nafcillin and rifampin). The patient had been discharged from the hospital with only compression hose for deep venous thrombosis prophylaxis, owing to her episodes of epistaxis in the setting of transfusion-dependent anemia.

Upon presentation, the patient was hypotensive, tachycardic, and hypotensive. Laboratory data showed a white cell count of 3.9 cells x 10⁹ / L, a platelet count of 7000 x 10⁹ / L, and a hemoglobin level of 7 g/dL.

Frontal chest radiography (Figure 1A) was performed (a baseline chest radiograph- Figure 1B- is presented for comparison).

Figure 1. Panel A: Frontal chest radiography Panel B: Frontal chest radiograph obtained 3 months to presentation.

Which of the following statements regarding the chest radiograph is most accurate? (Click on the correct answer to proceed to the 2nd of 7 panels)

1. The frontal chest radiograph shows bilateral hilar and mediastinal lymph node enlargement
2. The frontal chest radiograph shows enlarged lung volumes with numerous cystic foci
3. The frontal chest radiograph shows linear and reticular abnormalities with architectural distortion associated with fibrotic lung disease
4. The frontal chest radiograph shows lingular and left lower lobe consolidation and left pleural effusion
5. The frontal chest radiograph shows multiple poorly defined bilateral pulmonary nodules

Reference as: Gotway MB. January 2015 imaging case of the month. Southwest J Pulm Crit Care. 2015;10(1):21-31. doi: http://dx.doi.org/10.13175/swjpcc003-15 PDF

Medical Image of the Week: Metastatic Collecting Duct Carcinoma

C

Figure 1. Transverse section of CT chest and abdomen shows enhancing pleural nodularity (yellow arrows) with a pleural effusion.

Figure 2.  Transverse section of CT abdomen shows heterogeneous enhancing mass in the right kidney (red arrow).

Figure 3. Coronal section of CT chest and abdomen showing a large right pleural effusion (yellow arrow) and atelectatic lung with mediastinal shift to the left. Red arrow points to the heterogeneous mass in the right kidney.

A 40-year-old woman home health nurse presented to the ED with intermittent right sided sharp chest pain and progressive dyspnea for 2 weeks. On admission she was found to be in respiratory distress. Chest x-ray revealed a massive right sided pleural effusion. Thoracic CT scan with contrast confirmed a large right pleural effusion with associated enhancing pleural nodularity also involving the diaphragmatic surface (Figure 1).  The visualized part of the abdomen revealed a mass in the midpole of right kidney (Figure 2). Subsequent CT scan of the abdomen with contrast revealed a heterogeneous enhancing mass in the right kidney suspicious for malignancy (Figure 3) and multiple paracaval lymph nodes. Thoracentesis revealed a hemorrhagic pleural effusion and during subsequent right video-assisted thoracoscopy showed disseminated tumorlets along the diaphragm and pleura. Pleural biopsy and fluid cytology was consistent with metastatic poorly differentiated collecting duct carcinoma of the kidney. The patient is currently getting outpatient chemotherapy. Collecting duct carcinoma of the kidney is an unusual variant of renal cell carcinoma and accounts for about 1% of all renal cell carcinomas (1). This variant has a poor prognosis and frequently metastasizes to the lung and liver.

Chandramohan Meenakshisundaram, MD

Nanditha Malakkla, MD

St. Francis Hospital.

Evanston, IL

Reference

1. Wang X, Hao J, Zhou R, Zhang X, Yan T, Ding D, Shan L, Liu Z. Collecting duct carcinoma of the kidney: a clinicopathological study of five cases. Diagn Pathol. 2013;8:96. [CrossRef] [PubMed]

Reference as: Meenakshisundaram C, Malakkla N. Medical image of the week: metastatic collecting duct carcinoma. Southwest J Pulm Crit Care. 2014;9(6):348-9. doi: http://dx.doi.org/10.13175/swjpcc160-14 PDF

Medical Image of the Week: CMV Cytopathic Effect

Figure 1. Cluster of 3 large cells, most likely infected type II pneumocytes, with a single prominent red stained nuclear inclusion surrounded by a clear halo. This appearance is the “cytopathic effect” needed to definitively diagnose active CMV infection.

Figure 2. Electron microscopy (8800x) of an infected cell showing  cytomegalovirus (CMV) virions within the nuclear inclusion (small black dots encircled).

Bronchoalveolar lavage (BAL) was performed on a 45-year old man with a history of treated mycosis fungoides and Sézary syndrome, who presented with fever and pulmonary infiltrates. BAL Papanicolaou stain (Figure 1, 400x) showed single cells (lymphocytes, arrows and alveolar macrophages, stars) and a small cluster of 3 large cells, most likely infected type II pneumocytes, with a single prominent red stained nuclear inclusion surrounded by a clear halo. Nuclear chromatin was marginated on the nuclear membrane creating this “owl’s eye” appearance. In vitro, infected cells show cytomegalovirus (CMV) virions within the nuclear inclusion (Figure 2, small black dots encircled, 8,800x)

The "owl's eye" appearance (Figure 1) is the “cytopathic effect” needed to definitively diagnose active CMV infection. While cells infected with adenovirus or herpesvirus may have nuclear inclusions, the cells typically are much smaller. CMV was cultured from the BAL, and no other pathogen was identified by cytology or culture. Quantitative PCR on blood for CMV was 144359 IU/ml.

Afshin Sam, MD; Felicia Goodrum, PhD; Robert Ricciotti, MD; Ken Knox, MD and Richard Sobonya, MD

Departments of Medicine, Immunobiology, and Pathology

University of Arizona Health Sciences Center

Tucson, AZ

Reference as: Sam A, Goodrum F, Ricciotti R, Knox KS, Sobonya R. Medical image of the week: CMV cytopathic effect. Southwest J Pulm Crit Care. 2014;9(6):341-2. doi: http://dx.doi.org/10.13175/swjpcc161-14 PDF

Medical Image of the Week: Tracheal Perforation

Figure 1. Axial thoracic CT scan showing air in the mediastinum (red arrow).

Figure 2. Coronal thoracic CT scan showing air in the mediastinum (orange arrow).

Figure 3. Axial thoracic CT scan showing air in the mediastinum (yellow arrow).

Figure 4. Axial thoracic CT scan showing pneumopericardium (blue arrow).

A 45 year old Caucasian man with a history of HIV/AIDS was admitted for septic shock secondary to right lower lobe community acquired pneumonia. The patient’s respiratory status continued to decline requiring emergency intubation in a non-ICU setting. Four laryngoscope intubation attempts were made including an inadvertent esophageal intubation. Subsequent CT imaging revealed a tracheal defect (Figure 1, red arrow) with communication to the mediastinum and air around the trachea consistent with pneumomediastinum (Figure 2, orange arrow and figure 3, yellow arrow). Pneumopericardium (figure 4, blue arrow) was also evident post-intubation. The patient’s hemodynamic status remained stable. Two days following respiratory intubation subsequent chest imaging revealed resolution of the pneumomediastinum and pneumopericardium and patient continued to do well without hemodynamic compromise or presence of subcutaneous emphysema. Post-intubation tracheal perforation is a rare complication of traumatic intubation and may be managed with surgical intervention or conservative treatment (1).

Nour Parsa MD, Konstantin Mazursky DO, Sepehr Daheshpour MD, Naser Mahmoud MD

Department of Medicine

University of Arizona

Tucson, AZ

Reference

1. Fan CM, Ko PC, Tsai KC, Chiang WC, Chang YC, Chen WJ, Yuan A. Tracheal rupture complicating emergent endotracheal intubation. Am J Emerg Med. 2004;22(4):289-93. [CrossRef] [PubMed]

Reference as: Parsa N, Mazursky K, Daheshpour S, Mahmoud N. Medical image of the week: tracheal perforation. Southwest J Pulm Crit Care. 2014;9(6):335-6. doi: http://dx.doi.org/10.13175/swjpcc159-14 PDF

Medical Image of the Week: PE with Infarct and Pulmonary Cavitation

Figure 1. Panels A & B: thoracic CT scan showing multiple pulmonary emboli (arrows). Panel C: frontal chest radiograph showed extensive left lung opacification most dense in the left upper lobe. Panel D: frontal chest radiograph taken 3 weeks later showing mild volume loss of the left upper lobe with a large lucency suggestive of cavitation (arrow). Panel E: thoracic CT scan confirming the cavitation.

A 49 year old man with a history of COPD presented to the ER with the sudden onset of chest pain at 3:30 AM waking him from sleep. His pain was left sided, felt like broken ribs, and was worse with deep inspiration. He acknowledged some shortness of breath which was worse over baseline for the past couple days without cough or hemoptysis. The patient was tachycardic but comfortable with SpO2 saturation 98% on 2 liters. He had trace edema and pleurisy. Laboratory evaluation was unremarkable except for a WBC count 13,000 X 10⁶ cells/L. Chest x-ray was unremarkable but thoracic CT scan showed pulmonary emboli (PE) involving left upper and lower lobar arteries (Figure 1A and 1B, arrows). Anticoagulation was started and the patient experienced increasing shortness of breath, worsening oxygenation and fever to 102ºF. On Day 2, frontal chest radiograph showed extensive left lung opacification most dense in the left upper lobe (Figure 1C). Hemoglobin dropped from 12 to 9.8 g/dL suggesting alveolar hemorrhage. He improved over the next week but low grade fevers persisted and a chest x-ray taken 3 weeks later showed mild volume loss of the left upper lobe with a large lucency suggestive of cavitation (Figure 1D, Arrow). Thoracic CT confirmed a cavitary lesion in the left apex in the region of prior thrombus with adjacent consolidated atelectasis within a background of emphysema (Figure 1E).  The patient was lost to follow up after 6 months of anticoagulation.

Pulmonary infarction is relatively uncommon, occurring in less than 10% of PE, due to dual and collateral blood supply to the lung. Cavitary infarcts are even less common (4% in autopsy studies) and are more likely in those with pulmonary venous hypertension (1). Cavitary infarcts are more likely to occur when the infarct size in larger than 4 cm and most often occurs in the mid and upper lung zones. Despite alveolar hemorrhage, anticoagulation should be continued.

Kenneth S. Knox, MD and Veronica A. Arteaga, MD

Divisions of Pulmonary and Critical Care Medicine and Thoracic Imaging

University of Arizona

Tucson, AZ

Reference 

1. Libby LS, King TE, LaForce FM, Schwarz MI. Pulmonary cavitation following pulmonary infarction. Medicine (Baltimore). 1985;64(5):342-8. [CrossRef] [PubMed]

Reference as: Knox KS, Arteaga VA. Medical image of the week: PE with infarct and pulmonary cavitation. Southwest J Pulm Crit Care. 2014;9(6):333-4. doi: http://dx.doi.org/10.13175/swjpcc158-14 PDF 

December 2014 Imaging Case of the Month

Michael B. Gotway, MD

Department of Radiology

Mayo Clinic Arizona

Scottsdale, AZ

Clinical History: A 34-year-old non-smoking woman presented to her physician as an outpatient with complaints of intermittent chest pain and intermittent mild hemoptysis. Her previous medical history was otherwise unremarkable.

Frontal chest radiography (Figure 1) was performed.

Figure 1. Frontal chest radiography.

Which of the following statements regarding the chest radiograph is most accurate? (Click on the correct answer to proceed to the second of 6 panels)

1. The chest radiograph shows a circumscribed pulmonary mass
2. The chest radiograph shows asymmetric pulmonary vascularity
3. The chest radiograph shows bilateral linear and reticular opacities and diminished lung volumes suggesting fibrotic lung disease
4. The chest radiograph shows mild streaky central opacities, possibly reflecting airway thickening
5. The chest radiograph shows numerous small nodules

Reference as: Gotway MB. December 2014 imaging case of the month. Southwest J Pulm Crit Care. 2014;9(6):311-9. doi: http://dx.doi.org/10.13175/swjpcc157-14 PDF 

Medical Image of the Week: Asbestosis

Figure 1. Thoracic CT scan in soft tissue windows showing pleural plaques (arrows).

Figure 2. Thoracic CT scan in soft tissue windows showing subpleural curvilinear opacities (arrows).

Figure 3. Panel A: ground glass opacity (arrow). Panel B: parenchymal band (arrow).

A 76-year-old man with a past medical history of diabetes mellitus, hypertension, and an unspecified industrial-related asbestos exposure presented to the hospital after a syncopal episode and a ground level fall. A computed tomography (CT) of the chest was performed on admission which revealed several abnormalities including multiple bilateral calcified pleural plaques, pleural thickening, peripheral groundglass opacities (GGO) in the nondependent portion of the lungs and subpleural reticular and band like opacities. The patient unfortunately developed alcohol withdrawal and aspiration pneumonia requiring prolonged mechanical ventilation and was unable to provide additional details regarding his lung disease.

Asbestos is a naturally occurring mineral that historically was praised for its versatility. Its properties including heat and electrical resistance, tensile strength, and insulating capabilities made it a common component in materials used in both commercial and domestic settings.  Exposure to asbestos is linked to numerous respiratory diseases, including pleural and parenchymal disease, both malignant and nonmalignant. Pleural plaques are the most common manifestation of asbestos exposure (1,2). These are distinct areas of fibrosis that usually arise from the parietal pleura. Figure 1 shows bilateral pleural plaques located over the lateral and posterior chest walls as well as along the diaphragms, which is essentially pathognomonic for this disease. Asbestosis refers to lung fibrosis caused by asbestos dusts. Regional involvement of the lung parenchyma may be more pronounced in the subpleural and basilar locations.  An early finding of asbestosis is subpleural curvilinear opacities which are felt to represent peribronchial fibrosis (Figure 2). Additional features of asbestosis include ground glass opacities in the nondependent regions (Figure 3A), bilateral parenchymal bands (Figure  3B) and small nodular opacities, particularly suggestive when present with coexistent pleural disease. Honeycombing is a finding seen in more advanced disease.

Christopher Strawter MD¹, Veronica Arteaga MD², Jarrod Mosier MD^1,3

¹Pulmonary, Allergy, Critical Care, & Sleep Medicine; ²Radiology; ³Emergency Medicine

University of Arizona

Tucson, Arizona

References

1. Roach HD, Davies GJ, Attanoos R, Crane M, Adams H, Phillips S. Asbestos: when the dust settles an imaging review of asbestos-related disease. Radiographics. 2002;22(Spec No):S167–84. [CrossRef] [PubMed]
2. Peacock C, Copley SJ, Hansell DM. Asbestos-related benign pleural disease. Clin Radiol. 2000;55:422-32. [CrossRef] [PubMed]

Reference as: Strawter C, Arteaga V, Mosier J. Medical image of the week: asbestosis. Southwest J Pulm Crit Care. 2014;9(6):309-10. doi: http://dx.doi.org/10.13175/swjpcc156-14 PDF

Medical Image of the Week: Esophageal Cancer

Chandramohan Meenakshisundaram, MD 

Nanditha Malakkla, MD 

Saint Francis Hospital

Evanston, IL

Figure 1. Admission chest x-ray showing hyper-aerated lung fields and consolidation at the left lung base.

Figure 2. Video of selected images from thoracic CT scan in soft tissue windows showing large mediastinal mass with extravasation of contrast.

Figure 3. Views from endoscopy showing a large mass and the perforation site.

A 66-year-old Asian man with no significant past medical history was admitted with 1 week history of worsening retrosternal sharp chest pain, dyspnea on moderate exertion, and cough productive of brownish sputum. He also complained of some difficulty swallowing, decreased appetite and weight loss for the past 3 months. PPD was negative in the past. Vitals signs were significant for tachycardia and low grade fever. On physical exam he was cachectic and lung auscultation revealed bilateral scattered wheezes. Basic labs including complete blood count and comprehensive metabolic panel were unremarkable. EKG showed sinus tachycardia, serial troponin I was negative and chest x-ray revealed bilateral hyper-aerated lung fields and consolidation over the left lung base (Figure 1). He was started on antibiotics and bronchodilators. Since he continued to have chest pain and remained tachycardic, CT angiography of chest and abdomen (with IV and oral contrast) was done which revealed extravasation of contrast material into the mediastinum in the mid esophageal region representing rupture, a large mediastinal mass concerning for an abscess, and extensive infiltrates in the left lower lobe (Figure 2). During left thoracotomy, a large amount of necrotic material and phlegmon was seen in the mediastinum with adjacent area of lung necrosis which was drained and debrided. Upper GI endoscopy revealed a large mass in the mid-esophagus with perforation for which stenting was done (Figure 3). Pathology of phlegmon revealed squamous cell carcinoma with extensive necrosis. Culture of the fluid grew both viridians streptococci and anaerobes and he was started on broad spectrum antibiotics. His post-operative course was complicated and later he elected hospice care.

Reference as: Meenakshisundaram C, Malakkla N. Medical image of the week: eosphageal cancer. Southwest J Pulm Crit Care. 2014;9(5):295-6. doi: http://dx.doi.org/10.13175/swjpcc151-14 PDF

Medical Image of the Week: Killian-Jamieson Diverticulum

Figure 1. Chest x-ray showing worsening consolidation in both lungs.

Figure 2. Anterior (panel A) and lateral (panel B) fluoroscopic images showing retained contrast material in the anterior esophageal diverticulum in the hypopharynx.

An 89 year old female nursing home resident with a past medical history of hypertension and coronary artery disease was admitted with generalized weakness and vomiting for two days. Chest x-ray revealed consolidation in the left lung suggestive of pneumonia and she was started on broad spectrum antibiotics. Due to worsening consolidation in both lung fields (Figure 1) a video swallow was done for possible aspiration, which revealed contrast retained within the proximal esophagus within a diverticula in the anterior aspect (Figure 2). After excision of the diverticulum her pneumonia resolved and she was discharged back to the nursing home.

Killian-Jamieson diverticulum is a mucosal protrusion through a muscular gap in the anterolateral wall of the cervical esophagus; inferior to the cricopharyngeus and lateral to the longitudinal muscle of the esophagus just below its insertion on the posterior lamina of cricoid cartilage (gap also known as Killian-Jamieson space). This differentiates it from the Zenker’s diverticulum which arises from the muscular gap in the posterior portion of cricopharyngeus muscle (also known as Killian’s dehiscence). Killian-Jamieson diverticulum causes more non-specific symptoms than Zenker's diverticulum. Because these diverticula occur in close proximity to the recurrent laryngeal nerve, it should be carefully preserved during surgical resection.

Chandramohan Meenakshisundaram, MD and Nanditha Malakkla, MD

Medical Education

Saint Francis Hospital

Evanston, IL

References

1. Kim DC, Hwang JJ, Lee WS, Lee SA, Kim YH, Chee HK. Surgical treatment of killian-jamieson diverticulum. Korean J Thorac Cardiovasc Surg. 2012;45(4):272-4. [CrossRef] [PubMed]
2. Siddiq MA, Sood S, Strachan D. Pharyngeal pouch (Zenker's diverticulum). Postgrad Med J. 2001;77:506-11. [CrossRef] [PubMed]
3. Brant WE, Helms CA. Fundamentals of Diagnostic Radiology. Lippincott Williams & Wilkins. (2007) ISBN:0781765188

Reference as: Meenakshisundaram C, Malakkla N. Medical image of the week: killian-jamieson diverticulum. Southwest J Pulm Crit Care. 2014;9(5):287-8. doi: http://dx.doi.org/10.13175/swjpcc134-14 PDF

Medical Image of the Week: Abdominal Compartment Syndrome Due to Massive Upper Gastrointestinal Hemorrhage

Figure 1. Coronal section demonstrating a section of the Minnesota Tube within the stomach (yellow arrow), severe dilatation of the stomach (green arrow) and small bowel (blue arrow) due to intraluminal filling from blood. There is markedly reduced lungs volumes due to superior displacement of the diaphragm.

Figure 2. Saggital section demonstration the Minnesota Tube in place within the esophagus and stomach (yellow arrow) surrounded with intraluminal blood. There is intraluminal filling of the small intestine as well (green arrow).

A 29 year old woman with history of a Whipple procedure for pancreatic cancer and nonalcoholic steatohepatitis cirrhosis presented with a massive upper gastrointestinal bleeding (UGIB) likely from esophageal varices and developed hemorrhagic shock.

Emergent upper endoscopy could not be performed due to hemodynamic instability. Therefore, a Minnesota Tube was placed emergently for balloon tamponade of the bleeding. A transjugular intrahepatic portosystemic shunt was also placed emergently to decrease bleeding by reducing portal pressure. By this time, the patient had received 4 liters of normal saline, 14 units of packed red blood cells, 6 units of platelets, and 4 units of fresh frozen plasma.

The Minnesota tube did control the bleeding somewhat, however, there was continued bloody drainage from the stomach port of the Minnesota tube. The patient’s abdomen became remarkably distended and was dull to percussion throughout. A CT scan of the abdomen and pelvis revealed severe dilatation of the stomach and multiple loops of small bowel filled with mixed density blood (Figures 1 and 2). Intraabdominal bladder pressure was elevated to 34 mmHg. Given the radiographic findings, elevated bladder pressures, worsening lactic acid level and renal function, the patient was diagnosed with abdominal compartment syndrome. She was not a surgical candidate due to her grim prognosis. A large bore tube was placed into the abdominal cavity to drain ascitic fluid in effort to relieve the abdominal pressure.

Aggressive resuscitation including fluids, blood products, and four vasopressors was continued for the next several hours. However, due to patient’s poor prognosis, a decision was made to proceed with comfort care and the patient shortly passed away.

Acute upper gastrointestinal bleeding is a frequently encountered condition in the intensive care unit . Initial management generally consists of airway protection, intravascular resuscitation, correction of any coagulopathies, and acid-suppressive therapy (1). For UGIB with hemodynamic compromise, immediate upper endoscopic evaluation is indicated. The upper endoscopy allows for determination of the specific etiology of UGIB and for interventional therapy. If endoscopy cannot be done, bleeding cannot be controlled with endoscopic interventions or the patient is hemodynamically unstable, balloon tamponade should be considered (2). It is important to note that balloon tamponade is considered a bridge to more definitive therapy. Lastly, a multidisciplinary approach for management of massive UGIB should always be utilized especially in difficult cases.

VuAnh N. Truong, MD

Department of Medicine

Loma Linda University Medical Center

Loma Linda, CA

References

1. Conrad SA. Acute upper gastrointestinal bleeding in critically ill patients: causes and treatment modalities. Crit Care Med. 2002;30(6 Suppl):S365-8. [CrossRef] [PubMed]
2. Chen YI, Dorreen AP, Warshawsky PJ, Wyse JM. Sengstaken-Blakemore tube for non-variceal distal esophageal bleeding refractory to endoscopic treatment: a case report & review of the literature. Gastroenterol Rep (Oxf). 2014; Gastroenterol Rep (Oxf). 2014;2(4):313-5. [CrossRef] [PubMed] 

Reference as: Truong VN. Medical image of the week: abdominal compartment syndrome due to massive upper gastrointestinal hemorrhage. Southwest J Pulm Crit Care. 2014;9(5):284-6. doi: http://dx.doi.org/10.13175/swjpcc133-14 PDF

Medical Image of the Week: Paradoxical Stroke

Figure 1. Vegetation seen on the tricuspid valve on the transthoracic echocardiogram (arrow). RA=right atrium, RV=right ventricle.

Figure 2. Patent foramen ovale (PFO) with right to left shunt of the agitated saline contrast on the trans-esophageal echocardiogram (arrow). RA=right atrium, LA=left atrium.

Figure 3. Acute left cerebellar stroke, hyper-dense lesion on T2 weighted MRI of the brain. (encircled).

A 23-year-old man with a history of intravenous drug abuse (IVDA) was admitted to the intensive care unit (ICU) secondary to sepsis. His blood cultures were positive for methicillin sensitive Staphylococcus aureus. Transthoracic echocardiogram showed vegetation on the tricuspid valve (Figure 1). He had multiple systemic emboli leading to suspicion for right to left shunt, which was confirmed by the agitated saline test during the echocardiogram (Figure 2). Cerebellar strokes likely secondary to posterior circulation embolic phenomenon was also seen (Figure 3). Overall, after a protracted ICU course complicated by multi-organ failure, he improved and is continuing treatment and rehabilitation at this time.

Right-sided infective endocarditis (IE) incidence is low, accounting for 5-10% of all cases of IE (1). IVDA is a well-known cause of tricuspid valve endocarditis. Usual features of tricuspid endocarditis are fever, bacteremia and pulmonary septic emboli. Patent foramen ovale (PFO) is estimated in up to 25% of the general population. Management of PFO for secondary stroke prevention remains controversial. Closure can be achieved surgically or percutaneously. The efficacy of closure of a PFO on the rate of recurrent stroke has not been established.

Laila Abu Zaid MD¹, Evbu Enakpene MD² and Bhupinder Natt MD³

¹Department of Internal Medicine

²Division of Cardiovascular Diseases

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

University of Arizona Medical Center

Tucson, AZ.

Reference

1. Akinosoglou K, Apostolakis E, Marangos M, Pasvol G. Native valve right sided infective endocarditis. Eur J Intern Med. 2013;24(6):510-9. [CrossRef] [PubMed]

Reference as: Zaid LA, Enakpene E, Natt B. Medical image of the week: paradoxical stroke. Southwest J Pulm Crit Care. 2014;9(5):278-80. doi: http://dx.doi.org/10.13175/swjpcc135-14 PDF