Medical Image of the Week: Kartagener Syndrome

Figure 1. Panel A: AP chest x-ray showing dextrocardia with left sided pneumothorax. Panel B: CT Chest lung windows showing diffuse bronchiectasis. Panel C: CT Abdomen consistent with situs inversus.

A 65-year-old woman presented with 7 days of productive cough and the new onset sharp central chest pain. She has a known history of chronic sinusitis and COPD after being a 50 pack-year smoker. On examination, her blood pressure was 116/70 with a heart rate of 86 (sinus rhythm) and oxygen saturations were 93% on 4L/min by nasal cannula. She had bilateral expiratory wheezes with reduced air entry on the left side.

An AP chest x-ray revealed dextrocardia with a left sided tension pneumothorax (Figure 1A). Our patient was stabilized with an urgent chest tube insertion and taken for a CT chest and abdomen. CT chest indicated diffuse bronchiectasis (Figure 1B, arrow) with a CT of the abdomen showing reversal of major abdominal organs (Figure 1C).

First described in 1933, the triad of chronic sinusitis, bronchiectasis, and situs inversus is classic for Kartagener syndrome (1). Otherwise known as primary ciliary dyskinesia, it is an autosomal recessive disorder affecting the dynein motor protein on microtubules. Ciliary dysfunction from an embryonic stage is the underlying cause for 50% of patients with situs inversus (2). Ongoing difficulties clearing mucous and secretions from abnormal ciliary movements accelerates the development of rhinosinusitis and bronchiectasis (3). Fertility is also a common concern with most males being infertile and females having a lower likelihood of successful pregnancy (4).

Confirmatory testing requires electron microscopy to determine ultrastructure and high-speed video microscopy to determine abnormal movement of cilia (4). Long-term management involves control of respiratory complications with regular spirometry and pulmonary follow up.

Debraj Das, MD

Department of Medicine

Faculty of Medicine and Dentistry

University of Alberta

Edmonton, AB, Canada

References 

1. Kartagener M. Zur pathogenese der bronchiectasien. I Mitteilung: bronchiectasien bei situs viscerum inversus. Betr Klin Tuberk. 1933; 83:498-501.
2. Noone PG, Leigh MW, Sannuti A, et al. Primary ciliary dyskinesia: diagnostic and phenotypic features. Am J Respir Crit Care Med. 2004; 169:459-467. [CrossRef] [PubMed]
3. Bush A, Cole P, Hariri M, et al. Primary ciliary dyskinesia: diagnosis and standards of care. Eur Respir J. 1998; 12:982-988. [CrossRef] [PubMed]
4. Knowles MR, Daniels LA, Davis SD, et al. Primary ciliary dyskinesia. Recent advances in diagnostics, genetics, and characterization of clinical disease. Am J Respir Crit Care Med. 2013; 188:913-22. [CrossRef] [PubMed] 

Reference as: Das D. Medical image of the week: Kartagener syndrome. Southwest J Pulm Crit Care. 2015;10(6):343-4. doi: http://dx.doi.org/10.13175/swjpcc057-15 PDF

Medical Image of the Week: Carcinoid at the Carina

Figure 1. Flow-volume loop showing flattening of expiratory loop suggesting variable intra-thoracic obstruction.

Figure 2. CT of the chest showing pedunculated tracheal lesion at the level of main carina.

Figure 3. Bronchoscopic view of endobronchial tumor before (Panel A) and after removal (Panel B).

A 74-year-old woman with history of 30 pack-year smoking, allergic rhinitis and asthma presented to pulmonary clinic with cough and dyspnea on exertion. She was placed on inhaled corticosteroids and long-acting beta-agonist. Pulmonary function test showed moderate obstructive ventilator defect and flow volume loop suggested variable intra-thoracic obstruction (Figure 1). In the meantime, she was hospitalized with complaint of dyspnea and possible COPD exacerbation. Het CT chest revealed an endobronchial 12 mm pedunculated lesion at anterior aspect of main carina (Figure 2). She underwent flexible bronchoscopy and lesion was removed using electro-surgical snare and cryoprobe (Figure 3). Her symptoms improved post-procedure. Pathologic examination of lesion revealed a carcinoid tumor.

Endobronchial tumors are masses confined within the bronchus, and may be associated with atelectasis or pneumonia of the distal parenchyma. These tracheobronchial tumors are classified as malignant or benign. Malignant tumors arising from surface epithelium include squamous cell carcinoma and neuro-endocrine tumors; and those arising from mesenchyme include sarcoma and malignant lymphoma. On the other hand, benign tumors arising from surface epithelium include squamous cell papilloma and mucus gland adenoma; and those arising from mesenchyme include hamartoma, lipoma, fibroma, leiomyoma, and neurogenic tumor. Hamartomas may present as a fatty mass, nodules with calcification, or as soft-tissue-density nodules on CT scans. The lipomas manifested as fat density on CT scans. The other benign tumors were low-attenuating, soft-tissue-density masses without characteristic findings on CT scans.

Tauseef Afaq Siddiqi, MD; Muhammad Alzoubaidi, MD; James Knepler, MD and Kenneth Knox, MD

Division of Pulmonary, Allergy, Critical Care and Sleep Medicine, The University of Arizona, Tucson, AZ

Reference

1. Ko JM, Jung JI, Park SH, Lee KY, Chung MH, Ahn MI, Kim KJ, Choi YW, Hahn ST. Benign tumors of the tracheobronchial tree: CT-pathologic correlation. AJR Am J Roentgenol. 2006;186(5):1304-13. [CrossRef] [PubMed] 

Reference as: Siddiqi TA, lzoubaidi M, Knepler J, Knox KS. Medical image of the week: carcinoid at the carina. Southwest J Pulm Crit Care. 2015;10(6):341-2. doi: http://dx.doi.org/10.13175/swjpcc052-15 PDF 

June 2015 Imaging Case of the Month

Michael B. Gotway, MD

Department of Radiology

Mayo Clinic Arizona

Scottsdale, AZ

Clinical History: A 58-year-old man presented for a pre-operative evaluation for surgery planned for resection of localized prostate malignancy. A frontal chest radiograph (Figure 1) was performed.

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

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

1. The frontal chest radiograph shows an abnormal mediastinal contour
2. The frontal chest radiograph shows basal predominant fibrotic abnormalities
3. The frontal chest radiograph shows large lung volumes with a cystic appearance
4. The frontal chest radiograph shows multifocal small pulmonary nodules
5. The frontal chest radiograph shows no abnormal findings

Reference as: Gotway MB. June 2015 imaging case of the month. Southwest J Pulm Crit Care. 2015;10(6):332-40. doi: http://dx.doi.org/10.13175/swjpcc078-15 PDF

Medical Image of the Week: Granulomatous Amoebic Encephalitis

Figure 1. Progressively worsened encephalitis with increasing T2/FLAIR hyperintensity, with restricted diffusion and increasing cortical enhancement in the left anterior/medial temporal lobe and inferior frontal lobe, multifocal areas of hemorrhage, mass effect and interval development of multiple progressive areas of rim enhancement with small areas of restricted diffusion suggested new abscess formation.

Figure 2. Necrotizing granulomas with acute inflammation and microorganisms with the morphologic features of amoeba (H & E stained slides: 500X and 1000X).

A 64-year-old woman with history of deceased donor kidney transplantation presented with altered mental status. MRI of the brain showed new region of T2/FLAIR hyperintensity with restricted diffusion and slight cortical enhancement in the left middle temporal lobe (Figure 1, Panel A). Her neurological exam was notable for expressive aphasia and right-sided weakness. Initial diagnosis of ischemic stroke was further evaluated due to immunosuppressive status. Her CSF showed a WBC of 12 cells/microL with 80% lymphocytes, glucose 61 mg/dL, and protein 53 mg/dL. Follow up MRI showed progression of T2/FLAIR hyperintensity, intraparenchymal hemorrhage, and peripheral patchy enhancement in the left anterior/medial temporal lobe and inferior frontal lobe suspicious for encephalitis (Figure 1, Panel B). Left temporal lobe biopsy revealed granulomatous encephalitis with microorganisms morphologically consistent with amoeba (Figure 2), and tissue cultures grew MRSA. Acanthamoeba species was confirmed by the Centers for Disease Control and Prevention (CDC) with antibody testing. Immunosuppression was tapered. She was treated with vancomycin and a CDC approved regimen of pentamidine, sulfadiazine, flucytosine, fluconazole, azithromycin, and miltefosine. Repeat MRI revealed continued progression of encephalitis with increased T2/FLAIR hyperintensity, mass effect, multifocal hemorrhage and new abscess formation (Figure 1, Panel C). Despite aggressive medical management, her neurologic status continued to deteriorate. Given her grim prognosis and failure to show clinical improvement, her family decided to pursue hospice care.

Granulomatous amebic encephalitis is a life-threatening central nervous system infection caused by the free-living amoebae Acanthamoeba spp., Balamuthia mandrillaris and Sappinia pedata. Onset is subacute to chronic affecting predominantly the immunocompromised population. The diagnosis requires high index of suspicion, and early diagnosis is crucial to survival. Radiological findings are nonspecific and can be seen in CNS tuberculosis, neurocysticercosis, disseminated encephalomyelitis, viral encephalitis etc. Multiple antibiotics targeting various proteins or receptors are required for successful treatment. A combination of surgical and medical interventions may be required to prevent morbidity and mortality.

Ateefa Chaudhury MD¹, Christopher Geffre MD², and Tauseef Afaq Siddiqi MD³

¹ Department of Medicine

² Department of Pathology

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

The University of Arizona, Tucson, AZ

Reference

1. Parija SC, Dinoop K, Venugopal H. Management of granulomatous amebic encephalitis: Laboratory diagnosis and treatment. Trop Parasitol. 2015;5(1):23-8. [CrossRef] [PubMed]

Reference as: Chaudhury A, Geffre C, Siddiqi TA. Medical image of the week: granulomatous amoebic encephalitis. Southwest J Pulm Crit Care. 2015;10(6):330-1. doi: http://dx.doi.org/10.13175/swjpcc051-15 PDF 

Medical Image of the Week: Actinomycosis

Figure 1. Thoracic CT scan showing right-sided necrotizing pneumonia, lung abscess and empyema (arrows).

Figure 2. Cytospin and cell block of right lower lobe bronchoalveolar lavage fluid stained with Grocott-Gomori's (or Gömöri) methenamine silver (GMS) stain showing positive filamentous organisms consistent with Actinomyces species within a background of inflammatory cells.

Figure 3. Low (Panel A) and high power view (Panel B) of the lung showing alveolar septa filled with predominantly acute (neutrophilic) infiltrate.

A 55-year-old man with history of tobacco and alcohol abuse, presented with unresolving pneumonia despite treatment with moxifloxacin. It was thought to be possible coccidioidomycosis and an azole was started. However, he returned with increasing dyspnea and hypoxemia. He had leukocytosis with a thoracic CT revealing a loculated empyema, multifocal necrotizing infection and a large intrapulmonary abscess (Figure 1). He was admitted to MICU, intubated and ventilated. He was in septic shock requiring fluid resuscitation, vasopressors, and broad antibiotics. Bronchoscopy revealed erythematous and edematous airways, with drainage of over one liter of purulent fluid. A chest tube was placed to drain pleural fluid with removal of around two liters of blood-tinged, purulent fluid. His condition worsened with development of disseminated intravascular coagulation leading to hemorrhagic shock. He arrested and died. Gram stain on bronchoalveolar lavage fluid showed mixed gram negative and gram variable rods, and cultures grew lactobacillus species. GMS stain revealed filamentous organisms consistent with Actinomyces (Figure 2).

Necrotizing pneumonia is usually secondary to aspiration of oral bacterial flora, and is usually associated with severe sepsis and acute respiratory failure. The obstruction of the bronchus and blood vessels corresponding to a lung segment leads to decreased perfusion that is often shown on contrast enhanced CT scan. Hence, systemic antibiotic treatment alone is usually not effective. The management of necrotizing pneumonia is multidisciplinary; including adequate antibiotic therapy, mechanical ventilation, closed pleural drainage and supportive care. Despite the serious morbidity, massive parenchymal damage and prolonged hospitalizations, long-term outcome following necrotizing pneumonia is good with multidisciplinary care. If initial medical therapy fails, surgery is a reasonable option. Resection of gangrenous lung parenchyma and drainage of pleural empyema can lead to recovery in up to 80% of patients. Rarely, lobectomy can be a salvage operation. Outcome is affected by the severity of disease and underlying comorbidities. It should be considered once operative risk is acceptable.

Tauseef Afaq Siddiqi MD^1,2, Tracy Lundberg MD³, Jennifer Thorn MD³, and Dena L’heureux MD^1,2

¹Division of Pulmonary, Allergy, Critical Care, and Sleep Medicine, The University of Arizona Medical Center, Tucson, AZ

²Department of Medicine, Southern Arizona Veterans Administration Health Sciences Center, Tucson, AZ

³Department of Pathology, The University of Arizona Medical Center, Tucson, AZ

References

1. Alifano M, Lorut C, Lefebvre A, Khattar L, Damotte D, Huchon G, Regnard JF, Rabbat A. Necrotizing pneumonia in adults: multidisciplinary management. Intensive Care Med. 2011;37(11):1888-9. [CrossRef] [PubMed]
2. Schweigert M, Dubecz A, Beron M, Ofner D, Stein HJ. Surgical Therapy for Necrotizing Pneumonia and Lung Gangrene. Thorac Cardiovasc Surg. 2013;61(7):636-41. [CrossRef] [PubMed]
3. Tsai YF, Ku YH. Necrotizing pneumonia: a rare complication of pneumonia requiring special consideration. Curr Opin Pulm Med. 2012;18(3):246-52. [CrossRef] [PubMed]

Reference as: Siddiqi TA, Lundberg T, Thorn J, L’heureux D. Medical image of the week: actinomycosis. Southwest J Pulm Crit Care. 2015;10(5):302-3. doi: http://dx.doi.org/10.13175/swjpcc050-15 PDF

Medical Image of the Week: Tumor-Induced Hypoglycemia

 

Figure 1. CT of the abdomen with IV contrast (axial image) demonstrating numerous large enhancing liver metastases (red oval) and tumor thrombus in the anterior segment branch of the right portal vein (arrow).

A 39 year-old man with a history of widely metastatic (brain, liver and lung) nonseminomatous germ cell tumor was admitted to the hospital with severe abdominal pain and altered mental status. A CT of the abdomen and pelvis with IV contrast revealed a marked increase in the size of the liver metastases, portal vein tumor thrombus and changes of pseudocirrhosis. There were numerous large heterogeneously enhancing masses within the liver parenchyma with central necrosis (Figure 1).

The patient had significant and sustained hypoglycemia, with the lowest glucose recorded of 30 mg/dl. He required multiple IV doses of 50% dextrose and an infusion of 10% dextrose to maintain a serum glucose level greater than 55 mg/dl. His mental status improved with treatment of the hypoglycemia. The patient decided to pursue a palliative approach to care and was discharged with home hospice services.

Tumor-induced hypoglycemia (TIH) is a paraneoplastic syndrome that is uncommon in clinical practice (1). The more common cause of TIH is insulin hypersecretion in the setting of pancreatic beta-cell tumors. Mechanisms that may lead to TIH without insulin hypersecretion include the hypersecretion by tumors of insulin-like growth factor 2 (IGF2) and it’s precursors, insulin-like growth factor 1 (IGF1), somatostatin, and glucagon-like peptide 1. Other pathogenic causes of hypoglycemia include tumor autoimmune hypoglycemia, massive tumor burden, massive tumor liver infiltration, and pituitary or adrenal gland destruction by the tumor. TIH unrelated to pancreatic tumors is called non-islet-cell tumor hypoglycemia (NICTH). The most common cause of NICTH is the hypersecretion of IGF2 and IGF2 precursors by the tumor. This results in increased glucose consumption peripherally and decreased production of glucose in the liver. We did not measure levels of IGF2 in our patient. It was felt the most likely cause of his hypoglycemia was extensive tumor invasion and destruction of the liver due to his advanced disease.

Pavan Parashar MD¹, Meghan Bullock BSN, RN, OCN, Linda Snyder MD²

¹Department of Medicine, Geriatrics, Palliative and General Medicine, Banner University Medical Center-Tucson

²Department of Medicine, Pulmonary, Critical Care and Palliative Medicine, Banner University Medical Center-Tucson

Reference

1. Iglesias P, Díez JJ. Management of endocrine disease: a clinical update on tumor-induced hypoglycemia. Eur J Endocrinol. 2014;170(4):R147-57. [CrossRef] [PubMed] 

Reference as: Parashar P, Bullock M, Snyder L. Medical image of the week: tumor-induced hypoglycemia. Southwest J Pulm Crit Care. 2015;10(5):300-1. doi: http://dx.doi.org/10.13175/swjpcc049-15 PDF

Medical Image of the Week: Leukemic Infiltrates

Figure 1. AP portable chest x-ray demonstrating diffuse bilateral infiltrates.

Figure 2. Histology showing extensive interstitial and perivascular lymphocytic infiltrates.

Figure 3. Immunohistochemical staining for CD8 positive T-cell immunophenotype.

A 50 year-old white man with newly diagnosed, acute T-cell prolymphocytic leukemia presented with progressive exertional dyspnea and non-productive cough. The patient was due to meet with his hematologist that day to discuss initiation of treatment. The patient had not noted fever, chills, night sweats, chest pain, or lower extremity swelling. Blood pressure was 112/60 mm Hg, respiratory rate was 36/minute and labored, pulse was 110/minute and temperature was 37 degrees Celsius. Oxygen saturation measured by pulse oximetry was 62% on room air at rest, and rose to 90% after the application of a 100% non-rebreather mask. Diffuse rales were present on chest auscultation. Marked splenomegaly was present on abdominal examination. Peripheral white blood count was 112.2 K/ul with 99% lymphocytes. Smudge cells were noted. Hemoglobin was 12.9 g/dl and platelet count was 93K/ul. Procalcitonin level was 0.3 pg/ml. The chest radiograph demonstrated diffuse bilateral infiltrates (Figure 1). The patient developed rapidly progressive hypoxemia, was intubated orally, and mechanical ventilation was initiated. Lung biopsies were performed via a video-assisted thoracic surgical approach of the right middle and right lower lobes. Microscopic examination demonstrated extensive leukemic infiltration of the pulmonary interstitium and perivascular space (Figure 2). Immunohistochemical staining showed that the infiltrating cells expressed a CD8 positive T-cell immunophenotype (Figure 3) pattern similar to the patient’s peripheral blood flow cytometry study. Therapy began with an escalating dose of alemtuzumab and intermittent pentostatin, but the patient developed progressive multi-organ failure and expired.

Acute T-cell prolymphocytic leukemia is an aggressive mature T-cell leukemia usually characterized by peripheral blood lymphocytosis and splenomegaly (1). Extramedullary involvement most commonly affects the skin (2). Diffuse interstitial and perivascular pulmonary involvement with respiratory failure has not been previously reported. Pathological involvement of the pulmonary interstitial space should be considered in patients with acute T-cell prolymphocytic leukemia and respiratory insufficiency.

Charles J. VanHook1, Carlyne Cool2, Todd DeBoom3, Robert Fisher4, and

Douglas J. Tangel1

1Department of Intensive Care Medicine

Longmont United Hospital

Longmont, CO

2Department of Pathology and Department of Medicine

University of Colorado and National Jewish Health

Denver, CO

3Department of Pathology

Longmont United Hospital

Longmont, CO

4Department of Oncology

Longmont United Hospital

Longmont, CO

References

1. Dearden CE. T-cell prolymphocytic leukemia. Med Oncol. 2006;23(1):17-22. [CrossRef] [PubMed]
2. Valbuena JR, Herling M, Admirand JH, Padula A, Jones D, Medeiros LJ. T-cell prolymphocytic leukemia involving extramedullary sites. Am J Clin Pathol. 2005;123(3):456-64. [CrossRef] [PubMed]

Reference as: VanHook CJ, Cool C, DeBoom T, Fisher R, Tangel DJ. Medical image of the week: leukemic infiltrates. Southwest J Pulm Crit Care. 2015;10(5):235-7. doi: http://dx.doi.org/10.13175/swjpcc043-15 PDF

May 2015 Imaging Case of the Month

Michael B. Gotway, MD 

Department of Radiology

Mayo Clinic Arizona

Scottsdale, AZ

Clinical History: A 66 year-old woman presented with a history of hypothyroidism on replacement therapy, and a past medical history of pancreatitis, presented to her gastroenterologist with complaints of abdominal pain and loose stools. The episodes of pancreatitis began over a decade earlier with epigastric pain that was ultimately attributed to cholecystitis, for which endoscopic retrograde cholangiopancreatography (ERCP) was performed; this procedure precipitated her first episode of pancreatitis. During the ERCP procedure, her common bile duct was noted to be narrowed and several stones were removed, with placement of a stent, after which her epigastric pain resolved. A second stent placement procedure was required for recurrent epigastric pain approximately three weeks later, with good result.

Nearly a decade later, the patient presented with loose stools and fecal urgency associated with abdominal pain. Upper endoscopy showed mild gastric erosions (the patient was taking non-steroidal anti-inflammatory agents for intermittent back pain) and colonoscopy showed mild, non-specific colitis. The paint was diagnosed with pancreatic insufficiency and enzyme replacement therapy was begun, with symptomatic improvement.

During the course of her gastrointestinal consult, a frontal chest radiograph (Figure 1) was performed.

 

Figure 1. Frontal chest radiograph.

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

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

Reference as: Gotway MB. May 2015 imaging case of the month. Southwest J Pulm Crit Care. 2015;10(5):223-34. doi: http://dx.doi.org/10.13175/swjpcc070-15 PDF

Medical Image of the Week: Nocardiosis

Figure 1. Panel A: Thoracic CT scan showing enlarged left upper lobe mass. Panel B: CT scan from one month earlier showing a smaller lesion.

Figure 2. Panel A: GMS Silver stain showing Nocardia (200X magnification). Panel B: GMS silver stain showing Nocardia (400X magnification).

Figure 3. MRI Brain with arrows pointing to the lesion.

A 67 year-old man with advanced adenocarcinoma of the lung on chemotherapy and severe steroid dependent chronic obstructive pulmonary disease (COPD) was admitted for treatment of acute on chronic respiratory failure. He was admitted to the intensive care unit and required non-invasive positive pressure ventilation. He had a chest computed tomography scan (Figure 1A), with a left upper lobe mass, which was significantly larger than noted on a previous PET/CT scan (Figure 1B) from one month ago. He was placed on empiric broad-spectrum antibiotics and clinically improved. He underwent a transthoracic lung biopsy (Figure 2), which revealed the presence of organisms consistent with Nocardia on silver stain.  A brain MRI (Figure 3) showed the presence of a 4 mm enhancing lesion likely consistent with Nocardia.

Nocardiosis is a gram-positive bacterial infection caused by aerobic actinomycetes and is an important opportunistic pulmonary infection. It should be considered in the differential diagnosis of pulmonary infiltrates in immunosuppressed patients, including those with neoplasms, after organ transplantation, advanced HIV disease and those receiving chronic corticosteroid therapy or chemotherapy (1). Of importance to pulmonologists, in two reviews, COPD was a common underlying condition, representing over 20% of patients with Nocardiosis in these reports (2,3). Nocardia species are found in soil and infection is generally acquired through inhalation. The most common symptoms are fever, cough, pleuritic chest pain and headache. Common chest radiographic findings include consolidation, nodules, cavities and pleural effusions. Nocardia infections can disseminate to any organ but it has a predilection for spread to the central nervous system and patients with pulmonary Nocardia infections should have brain imaging to evaluate for cerebral dissemination. Antibiotics that are typically effective in Nocardia infections include trimethoprim-sulfamethoxazole (TMP-SMX), imipenim, amikacin, ceftriaxone and cefotaxime. However, antibiotic susceptibilities should be obtained and treatment tailored accordingly. It is recommended to treat severe systemic infections with two or three intravenous agents while awaiting susceptibility results. Treatment is usually prolonged because of the tendency of Nocardia infections to relapse or progress.  For patients with serious pulmonary infections and immunocompromised patients, duration of therapy is often at least 6 to 12 months or longer. Our patient was treated with TMP-SMX and meropenem and clinically improved. His steroids were rapidly tapered. Sputum cultures grew Nocardia farcinica.

Aarthi Ganesh MD, Muna Omar MD, James Knepler MD, and Linda Snyder MD

Department of Pulmonary and Critical Care

Banner University Medical Center

Tucson, AZ

References

1. Grigor LM, Hoover SE. Nocardiosis at a university medical center in the American southwest. Infect Dis Clin Pract 2014:22:279-82. [CrossRef]
2. Minero MV, Marín M, Cercenado E, Rabadán PM, Bouza E, Mu-oz P. Nocardiosis at the turn of the century. Medicine (Baltimore). 2009;88(4):250-61. [CrossRef] [PubMed]
3. Martínez Tomás R, Menéndez Villanueva R, Reyes Calzada S, Santos Durantez M, Vallés Tarazona JM, Modesto Alapont M, Gobernado Serrano M. Pulmonary nocardio-sis: risk factors and outcomes. Respirology. 2007;12(3):394-400. [CrossRef] [PubMed]

Reference as: Ganesh A, Omar M, Knepler J, Snyder L. Medical image of the week: nocardiosis. Southwest J Pulm Crit Care. 2015;10(5):220-2. doi: http://dx.doi.org/10.13175/swjpcc046-15 PDF

Medical Image of the Week: Esophageal Perforation

Figure 1. Axial, non-contrast CT of chest demonstrates wall thickening of the mid-thoracic esophagus with an extra-luminal focus of gas (blue arrow) in the mediastinum in addition to a small amount of right peri-esophageal fluid (red arrow).

Figure 2. Sagittal, non-contrast CT of chest demonstrates extra-luminal air posterior to the mid-thoracic esophagus (blue arrows).

A 74 year old man with a past medical history of esophageal strictures status post dilatation, coronary artery disease status post CABG, and atrial fibrillation presented to hospital with complaints of severe chest pain that began after the consumption of tortilla chips one hour prior to presentation. Electrocardiogram and cardiac enzymes were not consistent with acute coronary syndrome. Chest X-ray was consistent with a widened mediastinal silhouette. Contrast esophogram was negative for extra luminal extravasation. CT scan of the chest with oral contrast demonstrated thickening of the mid-thoracic esophagus with an extra-luminal focus of gas in the mediastinum along with fluid along the inferior aspect of the esophagus (Figures 1 and 2). These findings were concerning for esophageal perforation. The patient was taken to the operating room for endoscopy which showed micro perforation in mid-esophagus.

Esophageal perforation remains a highly morbid condition. Mortality rates are based predominantly on time of presentation and the etiology of perforation. Symptoms of esophageal perforation are non-specific and include neck or chest pain, dysphagia, odynophagia, difficulty breathing, vomiting, drooling, hematemesis, and abdominal rigidity (1) Initial diagnostic assessment includes conventional radiography, which can be normal in up to 10% of patients. Follow-up contrast esophograms are used to determine the presence and precise location of an esophageal perforation. However, false negative rates of 10% have been reported (2). CT scan of the chest or abdomen is indicated when contrast esophogram cannot be performed or all other diagnostic modalities have not been helpful in diagnosing esophageal perforation despite high clinical suspicion. Extra-luminal air in the mediastinum or surrounding the esophagus is the most reliable sign and when taken in conjunction with the clinical presentation, has 92% accuracy. Other common findings include obliteration of fat planes in the mediastinum resulting from inflammation, peri-esophageal or mediastinal fluid (92% accuracy), esophageal thickening, pleural effusions, extravasation of oral contrast material into the peri-esophageal tissues, and a tract at the site of the tear (3).

Jawad Bilal MD, David Testa MD, Irbaz bin Riaz MD and Ryan Nahapetian MD MPH

University of Arizona

Tucson, AZ

References

1. Aronberg RM, Punekar SR, Adam SI, Judson BL, Mehra S, Yarbrough WG. Esophageal perforation caused by edible foreign bodies: A systematic review of the literature. Laryngoscope. 2015;125(2):371-8. [CrossRef] [PubMed]
2. Bladergroen MR, Lowe JE, Postlethwait RW. Diagnosis and recommended management of esophageal perforation and rupture. Ann Thorac Surg. 1986;42(3):235-9. [CrossRef] [PubMed]
3. Lee S, Mergo PJ, Ros PR. The leaking esophagus: CT patterns of esophageal rupture, perforation, and fistulization. Crit Rev Diagn Imaging. 1996;37(6):461-90. [PubMed] 

Reference as: Bilal J, Testa D, Riaz I, Nahapetian R. Medical image of the week: eosphageal perforation. Southwest J Pulm Crit Care. 2015;10(4):201-2. doi: http://dx.doi.org/10.13175/swjpcc033-15 PDF

Medical Image of the Week: Scleroderma

Figure 1. Frontal view of the chest shows shallow lung volumes with reticulation and bronchiolar dilatation, including slightly asymmetric basilar opacity, left greater than right most suggestive of interstitial lung disease.

Figure 2. X-ray of the right hand performed 2 years prior to the chest x-ray reveals distal tuft resorption and erosions in addition to distal subcutaneous calcifications. The finger tips also appear atrophied and tapered.

A 56-year-old man presents with cough and dyspnea. Pertinent history is significant for scleroderma. A complete blood count and differential count were unremarkable. A chest radiograph was obtained (Figure 1). Based on overall imaging and clinical history, the chest x-ray findings are highly suggest interstitial lung disease likely related to scleroderma and a recommendation for high resolution chest CT was made.

Progressive systemic sclerosis (scleroderma) is an autoimmune connective tissue disease that affects 30-50 year old women more often than men and is characterized by the overproduction of collagen which can lead to fibrosis which includes the lungs, skin, and may also affect visceral organs (1). In the hands, vasculitis and Raynaud's phenomenon may lead to distal tapering (2). Although acro-osteolysis or distal tuft resorption can be seen in a wide variety of disorders, it may be present in up to 80% of patients with scleroderma. High-resolution chest CT is helpful to characterize the degree of involvement and fibrosis which tends to be basilar and peripherally predominant and may include both usual interstitial pneumonia or nonspecific interstitial pneumonitis as common patterns.

Veronica A. Arteaga MD and Kenneth S. Knox MD

Departments of Medical Imaging and Pulmonary and Critical Care

University of Arizona Medical Center

Tucson, Arizona

References

1. Mayberry JP, Primack SL, Müller NL. Thoracic manifestations of systemic autoimmune diseases: radiographic and high-resolution CT findings. Radiographics. 2000;20(6):1623-35. [CrossRef] [PubMed]
2. Manaster BJ, May DA, Disler DG. Musculoskeletal Imaging, The Requisites, 4^th edition. Mosby, Elsevier. Chapter 20: Connective Tissue Disorders, pages 288-293.

Reference as: Arteaga VA, Knox KS. Medical image of the week: scleroderma. Southwest J Pulm Crit Care. 2015;10(4):199-200. doi: http://dx.doi.org/10.13175/swjpcc034-15 PDF

Medical Image of the Week: Renal Infarction

Figure 1. Contrast enhanced CT of the abdomen showing the majority of the right kidney infarcted with some preservation of the superior pole. 

A 79-year-old woman with past medical history of persistent atrial fibrillation not on anticoagulation, coronary artery disease, hypertension, diabetes, and hyperlipidemia presented with right flank pain accompanied by nausea and vomiting for two days. Laboratory studies showed leukocytosis with creatinine of 1.2. Urinalysis was negative for signs of infection and red blood cells. However, despite being on analgesic, she continued to have flank pain. The patient subsequent underwent CT scan of the abdomen and pelvis the next day, which showed that the majority of the right kidney was infarcted. Interestingly, there were two right-sided renal arteries and a thrombus was seen in the inferior main right renal artery. The superior pole of the right kidney was preserved as a result of the patent accessory renal artery. Due to delayed presentation of more than 48 hours after onset of pain, the tissue could not be re-vascularized by vascular surgery. Her renal function remained intact and her flank pain gradually improved. 

Acute renal infarction is difficult to diagnose as it is mimicked by more commonly seen causes such as pyelonephritis and nephrolithiasis. Pain in the unilateral flank and/or abdomen is the hallmark presenting feature, however nausea, vomiting, and fever are also common. New or increasingly severe hypertension is found in approximately half of acute renal infarction diagnosis, a sign that should raise clinical suspicion in similar clinical scenario. Proteinuria is another feature that may be present on urinalysis. Creatinine elevation consistent with acute kidney injury (AKI) occurs in approximately 30-40% of cases (1). Leukocytosis is commonly seen in as many as three-quarters of patients with renal infarct. The most common laboratory finding in renal infarction is elevation of LDH, although this is nonspecific and does not necessarily aid in specific diagnosis (2). Diagnosis is usually made through contrast enhanced CT abdomen, however angiography may also be used.

Our patient also had two renal arteries supplying her right kidney, allowing for the superior pole of her renal parenchyma to be spared and thus her kidney function. The kidney tolerates ischemia for approximately 12 hours, making early diagnosis paramount. In patient’s such as the one described here that involves all or majority of one kidney, embolectomy is recommended because of favorable outcomes in prior studies (3). In summary, the challenge of early diagnosis of renal infarction lies in the recognition of nonspecific clinical symptoms and signs in an already rare occurrence. Recognizing these signs within hours of presentation may be the difference between viable renal tissue and death of a kidney. Keeping a high suspicion in patients with atrial fibrillation will also aid in early diagnosis.

Jessica August MD and Jennifer J Huang DO

Department of Internal Medicine

University of Arizona

Tucson, AZ

References

1. Bae EJ, Hwang K, Jang HN, Kim MJ, Jeon DH, Kim HJ, Cho HS, Chang SH, Park DJ. A retrospective study of short- and long-term effects on renal function after acute renal infarction. Ren Fail. 2014;36(9):1385-9. [CrossRef] [PubMed]
2. Antopolsky M, Simanovsky N, Stalnikowicz R, Salameh S, Hiller N. Renal infarction in the ED: 10-year experience and review of the literature. Am J Emerg Med. 2012;30(7):1055-60. [CrossRef] [PubMed]
3. Tsai SH, Chu SJ, Chen SJ, Fan YM, Chang WC, Wu CP, Hsu CW. Acute renal infarction: a 10-year experience. Int J Clin Pract. 2007;61(1):62-7. [CrossRef] [PubMed]

Reference as: August J, Huang JJ. Medical image of the week: renal infarction. Southwest J Pulm Crit Care. 2015;10(4):195-6. doi: http://dx.doi.org/10.13175/swjpcc023-15 PDF

Medical Image of the Week: Fungus Ball

Figure 1. Panel A: Coronal view of thoracic CT scan shows a fungus ball (mycetoma) within a 4.7cm thin walled cavity, Panel B: Axial image of fungus ball and thin walled cavity.

Figure 2 Panel A. Prominent eosinophilic infiltration with epithelial-lined cavity containing fungus ball (orange arrow). Panel B: Higher magnification.

A 69 year-old Asian woman living in Arizona with a past medical history of nephrotic syndrome on high-dose steroids had worsening pulmonary symptoms. A computed tomography (CT) of the chest (Figure 1) showed a 4.7 cm thin walled cavitary lesion in the right middle lobe compatible with mycetoma. She underwent thoracotomy for mycetoma resection. Surgical pathology confirmed an epithelial-lined cavity containing dense mycelia (Figure 2). Given the patient lived in an endemic area; the cavity was thought to be likely due to coccidioidomycosis. However, the mycetoma was of unclear etiology. No spherules were noted on GMS stain and tissue culture was negative. While of unclear clinical significance which fungus colonizes a pre-existing cavity, a Coccidioides PCR was performed and no Coccidioides genes were amplified making a Coccidioides mycetoma very unlikely.

Pulmonary mycetoma or “fungus ball” consists of dense fungal elements and amorphous cellular material within a pre-existing pulmonary cavity. Classically presenting as an aspergilloma, other fungi can cause similar lesions. Patients with mycetoma rarely develop symptoms. When present, symptoms can include chest pain, cough, hemoptysis, fatigue, fever, or unintentional weight loss. If asymptomatic, no treatment is required. Surgical resection and/or embolization may be required in cases of severe symptoms including hemoptysis.

Scott Rosen MD, Bridget Barker PhD, Branden Larsen MD PhD, and Ishna Poojary MD

Department of Medicine and Pathology

University of Arizona Medical Center

Tucson, AZ

and

Tgen North

Flagstaff, AZ

References

1. Winn RE, Johnson R, Galgiani JN, Butler C, Pluss J. Cavitary coccidioidomycosis with fungus ball formation. Diagnosis by fiberoptic bronchoscopy with coexistence of hyphae and spherules. Chest. 1994;105(2):412-6. [CrossRef] [PubMed]
2. Sobonya RE, Yanes J, Klotz SA. Cavitary pulmonary coccidioidomycosis: pathologic and clinical correlates of disease. Hum Pathol. 2014;45(1):153-9. [CrossRef] [PubMed]
3. Sheff KW, York ER, Driebe EM, Barker BM, Rounsley SD, Waddell VG, Beckstrom-Sternberg SM, Beckstrom-Sternberg JS, Keim PS, Engelthaler DM. Development of a rapid, cost-effective TaqMan Real-Time PCR Assay for identification and differentiation of Coccidioides immitis and Coccidioides posadasii. Med Mycol. 2010;48(3):466-9. [CrossRef] [PubMed]

Reference as: Rosen S, Barker B, Larsen B, Poojary I. Medical image of the week: fungus ball. Southwest J Pulm Crit Care. 2015;10(4):182-3. doi: http://dx.doi.org/10.13175/swjpcc025-15 PDF

April 2015 Imaging Case of the Month

Michael B. Gotway, MD

Department of Radiology

Mayo Clinic Arizona

Scottsdale, AZ

Clinical History: A 73-year-old woman with a history of ovarian malignancy in remission for several years and treated with hysterectomy and oopherectomy, hypothyroidism, and hypertension, presented with rather abrupt onset cough, chest pain, dyspnea and low-grade fever (99.6°F). Her past medical history was otherwise unremarkable. Her medications included thyroid replacement, amlodipine, benazepril, and, recently, calcium and magnesium supplementation. Chest radiography was performed (Figure 1).

Figure 1. Frontal (panel A) and lateral (panel B) chest radiographs.

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

1. Chest radiography shows a large right pleural effusion
2. Chest radiography shows focal lung opacity
3. Chest radiography shows mediastinal widening
4. Chest radiography shows pneumomediastinum
5. Chest radiography shows pneumothorax

Reference as: Gotway MB. April 2015 imaging case of the month. Southwest J Pulm Crit Care. 2015;10(4):171-81. doi: http://dx.doi.org/10.13175/swjpcc048-15 PDF

Medical Image of the week: ECHO findings of Apical Ballooning Syndrome

  Figure 1. Panel A: Four chamber view of the heart at the end of diastole with a dilated left ventricle. Panel B: Same four chamber view of the heart at the end of systole with a dilation and akinesis of the apical portion (arrow) of the heart consistent with apical ballooning/stress cardiomyopathy

A 79 year old man with a history of lung cancer. bladder cancer, chronic obstructive pulmonary disease, and coronary artery disease with two previous myocardial infarctions, presented to the emergency department with respiratory failure secondary to pulmonary edema. Further evaluation was significant for non-ST segment elevation myocardial infarction. Cardiac catheterization was remarkable for a focal, eccentric 95% stenosis of the proximal to mid left anterior descending artery that failed stenting due to extensive calcifications. An echocardiogram (ECHO, Figure 1) revealed an ejection fraction of 47% with akinesis of the mid to distal anterior, lateral, inferior, septal and apical segments consistent with takotsubo cardiomyopathy.

Takotsubo cardiomyopathy, aka apical ballooning syndrome or stress induced cardiomyopathy, is a subtype of heart failure typically defined by proposed criteria from the Mayo Clinic that includes: 1. transient hypokinesis, akinesis, or dyskinesis in the left ventricular mid segments with or without apical involvement frequently occurring, but not always, in context to a stressful trigger; 2. the absence of angiographic evidence of obstructive coronary disease or plaque rupture; 3. new ECG abnormalities (ST-segment elevation and/or T-wave inversion) or modest elevation in cardiac troponin; and 4. the absence of pheochromocytoma and myocarditis (1). It predominantly occurs in post-menopausal women in relation to unexpected emotional or physical stress. Characteristic ECHO findings demonstrate a symmetrical regional wall motion abnormalities extending equally into the apical inferior and lateral wall with overall global hypokinesia (Figure 1) (2).

Sachin Kalarn MSIV; Sophie Galson MD; Kristina Skinner DO; Ryan Nahapetian MD, MPH

University of Arizona

Tucson, AZ

References

1. Akashi YJ, Goldstein DS, Barbaro G, Ueyama T. Takotsubo cardiomyopathy: a new form of acute, reversible heart failure. Circulation. 2008;118(25):2754-62. [CrossRef] [PubMed]
2. Chockalingam A, Xie GY, Dellsperger KC. Echocardiography in stress cardiomyopathy and acute LVOT obstruction. Int J Cardiovasc Imaging. 2010;26(5):527-35. [CrossRef] [PubMed]

Reference as: Kalarn S, Galson S, Skinner K, Nahapetian R. Medical image of the week: ECHO findings of aprical ballooning syndrome. Southwest J Pulm Crit Care. 2015;10(4):150-1. doi: http://dx.doi.org/10.13175/swjpcc024-15 PDF

Medical Image of the Week: REM without Atonia

Figure 1. Polysomnogram with thirty-second epoch showing leg movements and relative increase in chin tone during REM sleep.

Figure 2. Polysomnogram with thirty-second epoch demonstrating similar interval of REM without atonia with the addition of sleep-talking.

A 78 year-old man with a past medical history of Parkinson’s disease (PD) presented to the sleep medicine clinic for evaluation of obstructive sleep apnea (OSA). An overnight polysomnogram (PSG) study was consistent with sleep apnea and revealed frequent leg and arm movements and sleep-talking during rapid eye movement (REM) sleep.

REM sleep behavior disorder (RBD) is a parasomnia characterized by repeated episodes of abnormal behavior occurring during REM sleep (1,2). On PSG, REM sleep without atonia is seen while features of “normal REM” such as number of REM periods and REM cycling remain intact (2). RBD emerges most often in the context of alpha-synucleinopathies, and occurs in up to 60% of PD patients (3). The presence of RBD may be an important preclinical symptom prior to the onset of PD. Cases of PD with RBD are associated with a unique phenotype with an older age of onset, longer disease duration, more profound motor disability, and greater degrees of hallucinations and cognitive dysfunction (3). Establishing a safe sleep environment can be of primary importance in patients with RBD as REM without atonia is associated with injurious behavior. Melatonin is effective as a first-line agent in patients with dementia. In non-demented patients without OSA, low-dose clonazepam is the first line intervention and is rarely associated with withdrawal or need for dose escalation (1). Treating concomitant OSA is important adjunctive therapy.

Jared Bartell, Safal Shetty MD, and Kenneth S. Knox MD

University of Arizona Medical Center

Tucson, AZ

References

1. Aurora RN, Zak RS, Maganti RK, Auerbach SH, Casey KR, Chowdhuri S, Karippot A, Ramar K, Kristo DA, Morgenthaler TI; Standards of Practice Committee; American Academy of Sleep Medicine. Best practice guide for the treatment of REM sleep behavior disorder (RBD). J Clin Sleep Med. 2010;6(1):85-95. [PubMed]
2. Schenck CH, Mahowald MW. REM sleep behavior disorder: clinical, developmental, and neuroscience perspectives 16 years after its formal identification in SLEEP. Sleep. 2002;25(2):120-38. [PubMed]
3. Kim YE, Jeon BS. Clinical implication of REM sleep behavior disorder in Parkinson's disease. Parkinsons Dis. 2014;4(2):237-44. [CrossRef] [PubMed]

Reference as: Bartell J, Shetty S, Knox KS. Medical image of the week: REM without atonia. Southwest J Pulm Crit Care. 2015;10(3):147-8. doi: http://dx.doi.org/10.13175/swjpcc022-15 PDF

Medical Image of the Week: Cheyne-Stokes Respiration

Figure 1. Cheyne-Stokes Breathing pattern seen. The red arrow indicates the cycle time which is defined as the duration of the central apnea (or hypopnea) + the duration of a respiratory phase.

A 62 year-old male with a past medical history congestive heart failure, chronic obstructive pulmonary disease, and obesity with a body mass index of 38.02 kg/m² underwent an overnight polysomnogram for clinical suspicion for obstructive sleep apnea. He was found to have a periodic breathing as seen in the image above.

Cheyne-stokes respiration (CSR) is a type of periodic breathing characterized by crescendo-decrescendo pattern of respiration separated by central sleep apneas (CSA) or hypopneas (1). CSR-CSA may be seen in up to 15-37% of systolic heart failure patients (2,3). A longer cycle length, usually between 45-90 seconds, as well as the waxing and waning breathing pattern differentiate CSR from other forms of cyclic central apnea. CSA leads to chronically increased sympathetic activity and exerts multiple deleterious effects on the failing heart (2). The presence of CSR has been associated with higher mortality and rapid deterioration in cardiac function (4).

Jared Bartell and Safal Shetty, MD

University of Arizona Medical Center

Tucson, AZ

References

1. Berry RB, Budhiraja R, Gottlieb DJ, Gozal D, Iber C, Kapur VK, Marcus CL, Mehra R, Parthasarathy S, Quan SF, Redline S, Strohl KP, Davidson Ward SL, Tangredi MM; American Academy of Sleep Medicine. Rules for scoring respiratory events in sleep: update of the 2007 AASM Manual for the Scoring of Sleep and Associated Events. Deliberations of the Sleep Apnea Definitions Task Force of the American Academy of Sleep Medicine. J Clin Sleep Med. 2012;8(5):597-619. [CrossRef]  [PubMed]
2. Yumino D, Bradley TD. Central sleep apnea and Cheyne-Stokes respiration. Proc Am Thorac Soc. 2008;5(2):226-36. [CrossRef] [PubMed]
3. Garcia-Touchard A, Somers VK, Olson LJ, Caples SM. Central sleep apnea: implications for congestive heart failure. Chest. 2008;133(6):1495-504. [CrossRef] [PubMed]
4. Hanly PJ, Zuberi-Khokhar NS. Increased mortality associated with Cheyne-Stokes respiration in patients with congestive heart failure. Am J Respir Crit Care Med. 1996;153(1):272-6. [CrossRef] [PubMed] 

Reference as: Bartell J, Shetty S. Medical image of the week: Cheyne-Stokes respiration. Southwest J Pulm Crit Care. 2015;10(3):145-6. doi: http://dx.doi.org/10.13175/swjpcc017-15 PDF

Medical Image of the Week: Sleep Bruxism

Figure 1. Hypnogram and polysomnographic tracing showing an episode of rhythmic masticatory muscle activity (RMMA) during sleep. RMMA is defined when at least 3 consecutive EMG bursts (frequency 1 Hz) lasting greater than or equal to 0.25 seconds are scored on the masseter and temporalis channels.

Figure 2. Thirty second epoch of polysomnogram showing phasic sleep-bruxism during stage N2 sleep.

A 42 year-old man with a past medical history of insomnia, post-traumatic stress disorder, depression and both migraine and tension headaches was referred for an overnight sleep study. He had presented to the sleep clinic with  symptoms  of obstructive sleep apnea. Medications included sumatriptan, amitryptiline, sertraline, and trazodone. His sleep study showed: sleep efficiency of 58.2%, apnea-hypopnea index  of 33 events per hour, and arousal index of 14.5/hr. Periodic limb movement index was 29.2/hr. The time spent in the sleep stages included N1 (3.6%), N2 (72.5%), N3 (12.9%), and REM (10.9%). Figure 1 is representative of the several brief waveforms seen on his EEG and chin EMG. Sleep bruxism (SB) is a type of sleep-related movement disorder that is characterized by involuntary masticatory muscle contraction resulting in grinding and clenching of the teeth and typically associated with arousals from sleep (1,2).

The American academy of sleep medicine (AASM) criteria for sleep related bruxism diagnosis:

1. The patient reports or is aware of tooth-grinding sounds or tooth clenching during sleep.
2. One or more of the following is present: A. Abnormal wear of the teeth; B. Jaw muscle discomfort, fatigue, or pain and jaw lock upon awakening; and C. Masseter muscle hypertrophy upon voluntary forceful clenching.
3. The jaw muscle activity is not better explained by another current sleep disorder, medical or neurological disorder, medication use, or substance use disorder.

The exact etiology of SB is unknown. It is associated with sleep arousals, genetic factors, stress, anxiety and behavioral factors and medications like selective serotonin receptor inhibitors, tobacco, alcohol and recreational drug use and sleep disordered breathing (2).

The electromyogram (EMG) activity pattern in patients with SB is known as rhythmic masticatory muscle activity (RMMA) and involves the masseter and temporalis muscles in patterns of phasic and/or tonic contractions, most typically during stages N1 and N2 of sleep (2,3). Clinically, bruxism can result in abnormal tooth wear, masseter muscle hypertrophy, reduced salivation, and morning headaches (1,2).

Sleep bruxism has been shown to be strongly associated with tension and migraine headaches (4). Treatment of the underlying sleep disordered breathing with positive airway pressure may eliminate bruxism during sleep (5). Treatment involves oral appliances such as occlusal splints or mandibular advancement devices (2). There is insufficient evidence to support pharmacotherapy in the treatment of sleep bruxism (1).

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

¹University of Arizona Medical Center, Tucson, AZ

²Southern Arizona VA Health Care System, Tucson, AZ

References

1. Macedo CR, Macedo EC, Torloni MR, Silva AB, Prado GF. Pharmacotherapy for sleep bruxism. Cochrane Database Syst Rev. 2014;10:CD005578. [CrossRef] [PubMed] 
2. Carra MC, Huynh N, Lavigne G. Sleep bruxism: a comprehensive overview for the dental clinician interested in sleep medicine. Dent Clin North Am. 2012;56(2):387-413. [CrossRef] [PubMed]
3. Valiente López M, van Selms MK, van der Zaag J, Hamburger HL, Lobbezoo F. Do sleep hygiene measures and progressive muscle relaxation influence sleep bruxism? Report of a randomised controlled trial. J Oral Rehabil. 2014 Nov 21. [CrossRef] [PubMed]
4. De Luca Canto G, Singh V, Bigal ME, Major PW, Flores-Mir C. Association between tension-type headache and migraine with sleep bruxism: a systematic review. Headache. 2014;54(9):1460-9. [CrossRef] [PubMed]
5. Oksenberg A, Arons E. Sleep bruxism related to obstructive sleep apnea: the effect of continuous positive airway pressure. Sleep Med. 2002;3(6):513-5. [CrossRef] [PubMed]

Reference as: Bartell J, Shetty S, Roehrs J. Medical image of the week: sleep bruxism. Southwest J Pulm Crit Care. 2015;10(3):140-2. doi: http://dx.doi.org/10.13175/swjpcc016-15 PDF 

Medical Image Of The Week: Westermark Sign

Figure 1. Chest x-ray showing decrease pulmonary vasculature on the right upper lobe (red circle, Westermark sign).

Figure 2. Coronal section of the CT angiogram showing occlusive thrombosis on the right pulmonary artery. 

A 71 year old man was evaluated in the Emergency Department for acute onset of dyspnea. On exam he was tachypneic, tachycardic and hypoxemic requiring 6 L/min of oxygen. He had recently underwent prostatectomy for prostate cancer. Past medical history was also significant for coronary artery disease treated with coronary bypass.

The chest x-ray (Figure 1) shows unilateral oligemia concerning for a pulmonary embolus and the CT angiogram of the chest (Figure 2) confirms the diagnosis.

While the chest radiograph is normal in the majority of pulmonary emboli, the ‘Westermark sign’ may be seen in up to 2% of the cases (1). It represents a focus of oligemia seen distal to a pulmonary embolism. The finding is a result of a combination of dilation of the pulmonary artery proximal to the thrombus and the collapse of the distal vasculature. 

Muna Omar MD¹, Tammer Elaini MD² and Bhupinder Natt MD¹

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

²Department of Internal Medicine

University of Arizona Medical Center

Tucson, AZ

Reference

1. Worsley DF, Alavi A, Aronchick JM, Chen JT, Greenspan RH, Ravin CE. Chest radiographic findings in patients with acute pulmonary embolism: observations from the PIOPED Study. Radiology. 1993;189(1):133-6. [CrossRef] [PubMed] 

Reference as: Omar M, Elaini T, Natt B. Medical image of the week: Westermark sign. Southwest J Pulm Crit Care. 2015;10(3):125-6. doi: http://dx.doi.org/10.13175/swjpcc015-15 PDF

March 2015 Imaging Case of the Month

Michael B. Gotway, MD

Department of Radiology

Mayo Clinic Arizona

Scottsdale, AZ

Clinical History: A 35-year-old man presented with a history of Von Hippel-Lindau syndrome, including prior right-sided renal cell carcinomas, cerebellar hemangioblastomas, and retinal hemangiomas. The patient’s renal malignancies were treated with laparoscopic radiofrequency ablations 6 and 8 years prior to presentation, and subsequently with percutaneous microwave ablations in the interim between 2008 and presentation. The latest percutaneous microwave ablation procedure (Figure 1) was performed to address two nodular enhancing foci in the posterior superior pole of the right kidney and one interpolar enhancing, septated lesion that were noted to have enlarged slightly on a recent MRI examination (Figure 2) of the abdomen compared with one year earlier.

 Figure 1. Percutaneous microwave of three right-sided renal lesions, 2 posterior-superior pole, the other lateral interpolar in location, shows two NeuWave microwave antennas inserted into suspicious lesions in the right kidney.

 

Figure 2. MRI of abdomen (A and B, axial steady-state free precession fat saturation images and, C and D, coronal subtraction contrast-enhanced images) shows three potentially solid, enhancing foci, two in the posterior and superior pole of the right kidney (arrowheads), and one in the lateral interpolar kidney, the latter with thick septations (arrow) that have shown slight enlargement from MR. performed one year previously.

A CT of the abdomen (Figure 3), performed 2 years earlier, is shown as a baseline comparison.

Figure 3.  Upper panel: selected image from the CT of the abdomen performed 2 years prior to presentation shows enlargement of the bilateral kidneys with numerous, bilateral renal cystic lesions. No pleural or lung base abnormality is evident. Lower panel: movie of CT scan performed 2 years prior to presentation.

Several days following the percutaneous microwave ablation procedure, the patient complained of right-sided chest pain, and frontal chest radiography was performed (Figure 4). 

Figure 4. Frontal and lateral chest radiography performed several days following the right-sided percutaneous microwave ablation procedure.

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

1. The frontal chest radiograph shows a large right pleural effusion
2. The frontal chest radiograph shows diffuse lung opacities suggesting diffuse alveolar damage
3. The frontal chest radiograph shows mediastinal widening
4. The frontal chest radiograph shows pneumomediastinum
5. The frontal chest radiograph shows pneumothorax 

Reference as: Gotway MB. March 2015 imaging case of the month. Southwest J Pulm Crit Care. 2015;10(3):112-24. doi: http://dx.doi.org/10.13175/swjpcc031-15 PDF