Medical Image of the Week: Chronic Bilateral Fibrocavitary Pulmonary Coccidioidomycosis

Figure 1. Chest x-ray showing bilateral upper lobe cavitation.

Figure 2. Thoracic computed tomography showed bilateral upper lobe, multiple thick-walled cavities with associated tree in bud opacities and consolidation in the right lower lobe.

Figure 3. Cytology of bronchoalveolar lavage fluid showing coccidioidomycosis spherules (arrows).

A 47-year-old Ethiopian immunocompetent male with no past medical history presented with cough and blood tinged sputum for 1 month with no fever, night sweats, or weight loss. Chest X-ray showed bilateral upper lobe cavitary lesions (Figure 1). Computed tomography of the chest showed bilateral upper lobe, multiple thick-walled cavities with associated tree-in-bud opacities and consolidation in the right lower lobe (Figure 2). TB was ruled out and a bronchoalveolar lavage (BAL) was performed. Cytology on the BAL showed the presence of Coccidioides immitis spherules (Figure 3). Serum coccidioidomycosis by complement fixation 1:64 with positive IgG by immunodiffusion; serum antigen by EIA 0.30; and urine antigen was negative. The patient was started on fluconazole and was discharged with pulmonology follow up. Bilateral cavitary lesions are rare and they can mimic the reactivation of M. tuberculosis, reinforcing the importance of including coccidioidomycosis in the differential diagnosis of bilateral cavitary lung lesions for patients in endemic areas.

Tarreq Noori MD*, Mohammed Al-Charakh MD*, and Andres Borja Alvarez MD**

Departments of Internal Medicine* and Pulmonology**

Maricopa Integrated Health System

Phoenix, AZ USA

Reference

1. Jude CM, Nayak NB, Patel MK, Deshmukh M, Batra P. Pulmonary coccidioidomycosis: pictorial review of chest radiographic and CT findings. Radiographics. 2014 Jul-Aug;34(4):912-25. [CrossRef] [PubMed]

Cite as: Noori T, Al-Charakh M, Alvarez AB. Medical image of the week: Chronic bilateral fibrocavitary pulmonary coccidioidomycosis. Southwest J Pulm Crit Care. 2018;16(3):168-9. doi: https://doi.org/10.13175/swjpcc043-18 PDF

Medical Image of the Week: Paget-Schroetter Syndrome

Figure 1. Venous contrast study demonstrating thrombosis and flow obstruction at the thoracic outlet (arrow). 

A 22-year-old right-handed man developed acute swelling of his right upper extremity following a weekend of vigorous physical military training. There was no associated pain or numbness. Physical examination demonstrated edema of the right arm. Radial and ulnar pulses were intact, and neurological exam was normal. Venous doppler examination demonstrated thrombus in the subclavian-axillary venous system. A confirmatory venous contrast study was performed (Figure 1), followed by catheter directed lysis.  Effort related thrombosis of the subclavian vein secondary to mechanical compression at the thoracic outlet is known as Paget-Schroetter Syndrome (1). Current treatment commonly includes catheter directed clot lysis and an arbitrary three-month period of systemic anticoagulation, followed by surgical resection of the first rib (2). Post-operative balloon angioplasty of the involved venous segment improves long-term results (3). This patient underwent successful lysis, was discharged on oral rivaroxaban, and has been referred to thoracic surgery for consideration of rib resection.

Charles Van Hook MD and Ken Hirasaki MD

Longmont United Hospital

Longmont, Colorado USA

References

1. Kucher N. Deep-vein thrombosis of the upper extremities. N Engl J Med. 2011;364:861-9.[CrossRef] [PubMed]
2. Engelberger RP, Kucher N. Management of deep vein thrombosis of the upper extremity. Circulation. 2012;126:768-73. [CrossRef] [PubMed]
3. Illif KA, Doyle AJ. A comprehensive review of Paget-Schroetter syndrome. J Vasc Surg. 2010;51:1538-47. [CrossRef] [PubMed]

Cite as: Van Hook C, Hirasaki K. Medical image of the week: Paget-Schroetter syndrome. Southwest J Pulm Crit Care. 2018;16(3):156. doi: https://doi.org/10.13175/swjpcc031-18 PDF 

A Finger-Like Projection in the Carotid Artery: A Rare Source of Embolic Stroke Requiring Carotid Endarterectomy

Neal S. Gerstein, MD FASE¹

Liem C. Nguyen, MD²

Omar S. Akbik, MD³

Howard Yonas, MD³

Andrew P. Carlson, MD MS-CR³

¹Department of Anesthesiology and Critical Care Medicine and ³Department of Neurosurgery

School of Medicine

University of New Mexico

Albuquerque, NM USA

²Department of Anesthesiology

University of California – San Diego Medical Center and Sulpizio Cardiovascular Center

San Diego, CA USA

Abstract

Atherosclerotic lesions of the extracranial carotid arteries are one of the most common cases of stroke. Rarely, a stroke may result from isolated non-stenotic carotid disease in the absence of systemic manifestations of cardiovascular disease or significant cardiovascular risk factors. We present an unusual case of multiple strokes resulting from a solitary finger-like projection within the posterior wall of the carotid artery in an otherwise healthy patient. This small finger-like projection has a propensity to act as a nidus for thrombus formation and a potential source of cerebral embolism.

Introduction

Atherosclerotic lesions of the extracranial carotid arteries are one of the most common causes of stroke. Intervention, whether it be via an open or endovascular technique, is typically reserved for symptomatic patients with moderate to severe carotid stenosis while intervention in asymptomatic patients is less clear (1,2). However, in rare cases, a cerebrovascular accident (CVA) may result from isolated non-stenotic carotid disease in healthy patients in the absence of systemic manifestations of cardiovascular disease or significant cardiovascular risk factors. CVA as a result from isolated carotid artery disease has not been previously described in the anesthesiology literature. We present an unusual case of CVA resulting from a solitary finger-like projection within the wall of the carotid artery in an otherwise healthy patient. The etiology associated with a CVA in this context relates to a small and minimal posterior carotid plaque that has a propensity to act as a nidus for thrombus formation and a potential source of cerebral embolism. Our case exemplifies this atypical cause of a CVA and heretofore minimally described entity involving the carotid artery system. 

Case

In April 2016, a 44-year-old non-smoking woman with a past medical history solely consisting of well-controlled hypertension and hyperlipidemia was exercising when she developed right-sided weakness. She was diagnosed with an ischemic right-sided CVA in the right middle cerebral artery territory. Her symptoms spontaneously resolved. She was managed with aspirin and warfarin for six months followed by aspirin monotherapy. In April 2017, she developed nearly identical symptoms, which again resolved with conservative therapy (aspirin and warfarin) and she was referred for neurosurgery consultation and further evaluation.     

During her most recent evaluation, aside from a body-mass index of 33 kg/m², her physical examination was completely normal including a complete neurologic and cardiac evaluation. Laboratory evaluation revealed no evidence of a hypercoagulable state or sickle-cell disease, autoimmune disease, abnormal erythrocyte sedimentation rate or C-reactive protein levels, and there was no evidence of an intracardiac shunt by transthoracic echocardiography.

Bilateral neck ultrasound duplex scanning revealed normal flow in both the internal carotid and both vertebral arteries. Magnetic resonance angiography of her neck vessels at the time of the initial stroke demonstrated bilateral mild narrowing and a posterior irregularity along with enlargement of the proximal internal carotid artery (ICA) just beyond the bifurcation, which was deemed hemodynamically insignificant (Figure 1).

Figure 1. Preoperative magnetic resonance angiography with contrast; Red arrow indicating defect in posterior right internal carotid artery.

Computed tomographic angiography (CTA) of her neck vasculature performed at the time of the second stroke one year later revealed no significant stenosis of her common carotid, internal carotid, or vertebral arteries but did re-demonstrate a right-sided small finger-like extension in the posterior carotid wall at the level of the bifurcation (Figure 2).

Figure 2. Preoperative computed tomography angiogram. Red arrow indicating right posterior internal carotid artery abnormality.

Anticoagulation was continued for another 4 months and a follow-up CTA did not reveal any change in the previous noted finger-like lesion within the carotid artery.

After evaluation by our neurosurgical colleagues, the decision was made to prepare the patient for a right-sided carotid endarterectomy (CEA). In addition to the routine standard monitors, additional monitoring modalities included invasive arterial blood pressure monitoring, 16-lead electroencephalogram, and bilateral cerebral oximetry monitoring.  Her CEA consisted of a longitudinal arteriotomy from the distal common carotid artery into the proximal ICA. The ‘finger’ of firm, irregular plaque was seen on the posterior ICA wall and could be easily dissected off the wall, ruling out a congenital web. The plaque was neither soft nor ruptured at the time of surgery; it was an irregular finger-like extension from the underlying plaque that was presumably the focus of thrombus formation (Figure 3).

Figure 3. Panel A: blue arrow indicating finger-like abnormal projection from posterior wall of right internal carotid artery. Panel B: excised projection specimen.

Pathological examination of the plaque revealed no evidence of gross calcifications, no signs of microscopic ulceration, or intra-plaque hemorrhage that are associated with an unstable plaque. The ICA clamp was then released temporarily to allow backflow of blood and with it washout of plaque that might have migrated upstream. Once the arteriotomy closure was complete, vascular clamps were removed and satisfactory pulsations were noted in the common carotid artery and external carotid artery, as well as the ICA. Following an uneventful emergence from anesthesia, the patient was extubated and brought to ICU in stable condition. Postoperative CTA demonstrated a normal caliber and lumen in the surgically treated right carotid artery (Figure 4).

Figure 4. Postoperative computed tomography angiogram demonstrating normal right internal carotid artery lumen.

Discussion

Stroke is a leading cause of death in developed nations with a majority of those ischemic in nature. Extracranial carotid artery atherosclerotic disease is the third leading cause of ischemic stroke in the general population (3). While medical management including antiplatelet therapy, treatment of hypertension, hyperlipidemia, diabetes, and smoking cessation have been shown to decrease the risk of stroke, surgical intervention in the form of CEA has been widely investigated in several randomized control studies and has proven efficacy in the appropriate patient population. A 2017 Cochrane systematic review along with other robust reviews found CEA most effective in symptomatic patients with >70% and is of some benefit for patients with 50-69% symptomatic stenosis (4,5). Surgery plays a limited role in complete or near complete occlusion (6).

While the above trials deal primarily with symptomatic carotid stenosis, a different pathology known as free-floating thrombus (FFT) can exist with or without carotid stenosis. As in our case, these patients are typically younger patients without established peripheral vascular disease or other systemic cardiovascular diseases. They typically have underlying atherosclerotic disease that predisposes them to thromboembolic events and as such are at a high risk for recurrent ischemic strokes. Most studies show that patients with FFT who are treated medically with anticoagulation have complete dissolution of the FFT without any further neurologic progression (7,8).

In contrast to FFT, our case patient was found to have a finger-like projection from the posterior wall of the right ICA just distal to its bifurcation without evidence of luminal thrombus. Our patient had persistent ischemic CVAs despite therapeutic anticoagulation and antiplatelet therapy with warfarin and aspirin, respectively. She continued to have persistent imaging findings of a small finger like projection on repeat neck CTAs. Intraoperatively, no thrombus was identified but rather a small plaque was resected which appeared to be similarly shaped to the finger-like projection seen on her CTA with an irregular intraluminal surface thought to be the nidus for thrombus formation. Upon further examination of the plaque by pathology, no gross calcifications were identified. Histologically no signs of microscopic ulceration or intraplaque hemorrhage were identified to indicate an unstable plaque, which is more commonly seen in advanced atherosclerotic disease. Critical differences in plaque morphology have been found to highly correlate with whether a patient has symptomatic or asymptomatic carotid disease (9).

There is a single similar case from 2011 from our institution, describing a 48-year-old woman who presented with intermittent hand numbness, facial weakness, and dysarthria (10). CTA of her head and neck demonstrated a several millimeter protrusion from her posterior ICA just distal to the bifurcation.  The patient had recurrent neurologic symptoms attributed to ongoing cerebral emboli despite anticoagulation and antiplatelet requiring CEA, during which organized thrombus was found in continuity with her isolated thin (1 mm) posterior carotid artery atherosclerotic plaque. It was concluded that the development of significant neurologic symptoms in the context of minimal stenosis is due to carotid endothelial hyperplasia with organizing thrombus on top of a small preexisting carotid atherosclerotic plaque. Similarly, our case report illustrates a patient receiving maximal medical therapy in the form of warfarin anticoagulation and antiplatelet therapy with persistent ischemic CVAs and an intraluminal plaque. The previous case had evidence of organizing thrombus while our case demonstrated only irregular plaque. This could either be because any adherent thrombus was washed out during the opening or that the thrombus itself had resolved with prolonged anticoagulation, leaving the finger-like plaque in the lumen. This speaks to a different pathology than what is typically observed in patients with FFT in that this intraluminal plaque morphology itself likely places the patient at risk for recurrent thrombus formation.

In summary, our rare etiology of stroke is heretofore unreported in the perioperative medicine literature. This case illustrates that in an otherwise healthy patient without systemic cardiovascular disease, the possibility of significant but minimal isolated carotid disease may be a nidus for thrombus and ultimately an embolic etiology for a significant neurologic injury. This report, along with the similar case described by Tran and Yonas (10), do not indicate a clear causal relationship. However, it is plausible that the described recurrent ipsilateral strokes are related to these uncommon and characteristic carotid morphologic findings. These assertions are further substantiated by the lack of any new symptoms during all patient follow-up visits. Nonetheless, a detailed study to document morphology involving a large sample of similar plaques of otherwise similar size and composition would be needed in order to make a definitive conclusion regarding the association between this finger-like carotid projection and recurrent CVAs. Perioperative and critical care physicians need to be aware that advanced radiological imaging is required to identify this isolated carotid pathology. Its association with cerebral emboli should be considered when presented with recurrent CVA events in the context of minimal evidence of atherosclerotic disease on routine carotid screening studies.

References

1. Kernan WN, Ovbiagele B, Black HR, et al. Guidelines for the prevention of stroke in patients with stroke and transient ischemic attack: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2014;45(7):2160-236. [CrossRef] [PubMed]
2. Meschia JF, Bushnell C, Boden-Albala B, et al. Guidelines for the primary prevention of stroke: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2014;45(12):3754-832. [CrossRef] [PubMed]
3. Ooi YC, Gonzalez NR. Management of extracranial carotid artery disease. Cardiol Clin. 2015;33(1):1-35. [CrossRef] [PubMed]
4. Orrapin S, Rerkasem K. Carotid endarterectomy for symptomatic carotid stenosis. Cochrane Database Syst Rev. 2017;6:CD001081. [CrossRef] [PubMed]
5. Meschia JF, Klaas JP, Brown RD, et al. Evaluation and Management of Atherosclerotic Carotid Stenosis. Mayo Clin Proc. 2017;92(7):1144-57. [CrossRef] [PubMed]
6. Rothwell PM, Eliasziw M, Gutnikov SA, et al. Endarterectomy for symptomatic carotid stenosis in relation to clinical subgroups and timing of surgery. Lancet. 2004;363(9413):915-24. [CrossRef] [PubMed]
7. Vellimana AK, Kadkhodayan Y, Rich KM, et al. Symptomatic patients with intraluminal carotid artery thrombus: outcome with a strategy of initial anticoagulation. J Neurosurg. 2013;118(1):34-41. [CrossRef] [PubMed]
8. Bhatti AF, Leon LR, Jr., Labropoulos N, et al. Free-floating thrombus of the carotid artery: literature review and case reports. J Vasc Surg 2007;45(1):199-205. [CrossRef] [PubMed]
9. Virmani R, Ladich ER, Burke AP, et al. Histopathology of carotid atherosclerotic disease. Neurosurgery. 2006;59(5 Suppl 3):S219-27; discussion S3-13. [CrossRef] [PubMed]
10. Tran H, Yonas H. Small carotid thrombus and minimal stenosis causing repeated embolic strokes. J Neuroimaging. 2011;21:266-8. [CrossRef] [PubMed]

Cite as: Gerstein NS, Nguyen LC, Akbik OS, Yonas H, Carlson AP. A finger-like projection in the carotid artery: A rare source of embolic stroke requiring carotid endarterectomy. Southwest J Pulm Crit Care. 2018;16(3):150-5. doi: https://doi.org/10.13175/swjpcc022-18 PDF 

Medical Image of the Week: Post-Traumatic Diaphragmatic Rupture

Figure 1. A: Admission portable chest radiograph, demonstrates elevation of the right hemidiaphragm of uncertain chronicity (large arrow, also shown in B and C). B: Study after 20 min, shows a moderate hemothorax (*). Mildly displaced fractures are evident, involving at least the3^rd and 5^th right ribs (small arrows). C: Follow up exam. A right chest tube (thin arrow in c) has been inserted, and the hemothorax is drained. Immediately after, a CT chest abdomen and pelvis is performed.

Figure 2. A-C: A large anterolateral diaphragmatic defect is diagnosed, as shown in the coronal images, from anterior to posterior (A-C), with displacement of the liver (L) and loops of bowel (B) into the chest. Note the discontinuity of the diaphragm (arrows in A, B and D). A small liver laceration is noted in the gallbladder bed (arrows in C). D:  Image, near the midline, showing atelectasis (A) in the posterior right lung base. Additional injuries (not shown), included, right ribs 2-11 fractures, gallbladder fossa liver, right adrenal hemorrhage, mesenteric root contusion and multiple pelvic fractures.

A 67-year-old woman was admitted after being struck by a vehicle, at high speed. She has a diaphragmatic rupture (Figures 1 and 2).

Diaphragmatic injuries occur in approximately 0.8%–8% of blunt trauma patients, largely from motor vehicle accidents (1). The mechanism of injury includes distortion of the chest wall with resulting shearing forces, or direct frontal impact with acute increased intraabdominal pressure (2).

Rupture of the left diaphragm is more common, presumably due to a protective mechanism by the liver, but also in part due to underdiagnoses (3). Most ruptures are large, posterolateral, between the lumbar and intercostal attachments (4).  Associated liver injuries are seen mostly with right diaphragmatic injuries (93 % vs. 24% with left injuries). Multiorgan abdominal injury and pelvic fractures are common (2).

In cases of associated hemothorax, pulmonary laceration/contusion, atelectasis, and phrenic nerve palsy, a diaphragmatic injury, may be masked on chest radiographs. Also, the positive pressure of ventilatory support may delay herniation of abdominal contents through the ruptured diaphragm (5).

Up to 12% to 66% cases of diaphragmatic rupture cases, are missed on chest radiograph. Suggestive findings include elevation of the hemidiaphragm, distortion or obliteration of the outline of the hemidiaphragm, and contralateral shift of the mediastinum (6,7).

On CT visualization of a diaphragmatic defect has most sensitivity and specificity for diaphragmatic injury (73% and 90%) respectively) (8). Intrathoracic herniation of abdominal contents has a sensitivity of 55% and a specificity of 100% (8). The “collar sign”, a waist-like constriction of the herniating hollow viscus at the site of the diaphragmatic tear, is usually seen sagittal and coronal multiplanar reformatted images (2,8). The “dependent viscera sign” (1), consists of bowel or solid organs fallen to a dependent position against the posterior ribs, due to lack of supported by the intact diaphragm. This may be an early sign of diaphragmatic tear on axial images, before visceral herniation is clearly seen on multiplanar reformatted images.

Diana Palacio MD, Veronica Arteaga MD, Berndt Schmidt MD

Department of Medical Imaging

The University of Arizona-Banner Medical Center

Tucson, AZ USA

References

1. Bergin D, Ennis R, Keogh C, et al. The "dependent viscera" sign in CT diagnosis of blunt traumatic diaphragmatic rupture. AJR Am J Roentgenol. 2001;177:1137-40. [CrossRef] [PubMed]
2. Shanmuganathan K, Killeen K, Mirvis SE, et al. Imaging of diaphragmatic injuries. J Thorac Imaging. 2000;15:104-11. [CrossRef] [PubMed]
3. Killeen KL, Mirvis SE, Shanmuganathan K. Helical CT of diaphragmatic rupture caused by blunt trauma. AJR Am J Roentgenol.1999;173:1611-6. [CrossRef] [PubMed]
4. Boulanger BR, Milzman DP, Rosati C, et al. A comparison of right and left blunt traumatic diaphragmatic rupture. J Trauma. 1993;35:255-60. [CrossRef] [PubMed]
5. Kuhlman JE, Pozniak MA, Collins J, Knisely BL. Radiographic and CT findings of blunt chest trauma: aortic injuries and looking beyond them. RadioGraphics. 1998;18:1085-1106. [CrossRef] [PubMed]
6. Iochum S, Ludig T, Walter F, et al. Imaging of Diaphragmatic Injury: A Diagnostic Challenge RadioGraphics 2002; 22:suppl. 1,S103-16. [CrossRef] [PubMed]
7. Gelman R, Mirvis SE, Gens D. Diaphragmatic rupture due to blunt trauma: sensitivity of plain chest radiographs. AJR Am J Roentgenol. 1991;156:51-7. [CrossRef] [PubMed]
8. Murray JG, Caoili E, Gruden JF, et al. Acute rupture of the diaphragm due to blunt trauma: diagnostic sensitivity and specificity of CT. AJR Am J Roentgenol. 1996;166:10. [CrossRef] [PubMed]

Cite as: Palacio D, Arteaga V, Schmidt B. Medical image of the week: post-trumatic diaphragmatic rupture. Southwest J Pulm Crit Care. 2018;16(3):143-5. doi: https://doi.org/10.13175/swjpcc030-18 PDF 

Medical Image of the Week: Bronchogenic Cysts

Figure 1. Posterior-anterior (A) and lateral (B) chest radiographs showing a large cyst with an air-fluid level in the right lung.

Figure 2. Representative image from thoracic CT scan in lung windows showing large right lung cyst.

Bronchogenic cysts are congenital foregut malformations forming from abnormal budding of the bronchial tree between the 4^th and 6^th weeks of embryonic development. While identified primarily in children, the cysts are often asymptomatic and may not be identified until adulthood. Most (70%) are within the middle mediastinum and contain fluid or proteinaceous material. When involving the parenchyma, they generally do not communicate with the tracheobronchial tree. Communication with the airways may develop following infection, procedures, or trauma and may result in lesions with an air-fluid level (Figures 1 and 2). Bronchogenic cysts may be complicated by infection, bleeding, fistula formation, or most concerning, by malignant transformation. Unless the cyst contains air, it may manifest as a solitary pulmonary nodule on plain radiographs. Computed tomography or T2-weighted MRI images are used to confirm the diagnosis. 

Steven P. Sears DO¹ and Diana Maria Palacio MD²

¹Division of Pulmonary, Allergy, Critical Care and Sleep and ²Department of Medical Imaging

University of Arizona College of Medicine

Tucson, AZ USA

References

1. McAdams HP, Kirejczyk WM, Rosado-de-Christenson ML, et al. Bronchogenic cyst: Imaging features with clinical and histopathologic correlation. Radiology. 2000 Nov;217(2):441-6. [CrossRef] [PubMed]
2. St-Georges R. Deslauriers J, Duranceau A, et al. Clinical spectrum of bronchogenic cysts of the mediastinum and lung in the adult. Ann Thorac Surg. 1991;52:6-13. [CrossRef] [PubMed]
3. Cardinale L, Ardissone F, Cataldi A, et al. Bronchogenic cysts in the adult: Diagnostic criteria derived from the correct use of standard radiography and computed tomography. Radiol Med. 2008;113(3): 385-94. [CrossRef] [PubMed]

Cite as: Sears SP, Palacio DM. Medical image of the week: Bronchogenic cysts. Southwest J Pulm Crit Care. 2018;16(3):141-2. doi: https://doi.org/10.13175/swjpcc026-18 PDF 

March 2018 Imaging Case of the Month

Michael B. Gotway, MD

Department of Radiology

Mayo Clinic Arizona

Scottsdale, AZ USA

Imaging Case of the Month CME Information  

Completion of an evaluation form is required to receive credit and a link is provided on the last panel of the activity.

0.25 AMA PRA Category 1 Credit(s)™

Estimated time to complete this activity: 0.25 hours

Lead Author(s): Michael B. Gotway, MD. All Faculty, CME Planning Committee Members, and the CME Office Reviewers have disclosed that they do not have any relevant financial relationships with commercial interests that would constitute a conflict of interest concerning this CME activity. 

Learning Objectives: As a result of completing this activity, participants will be better able to:

1. Interpret and identify clinical practices supported by the highest quality available evidence.
2. Establish the optimal evaluation leading to a correct diagnosis for patients with pulmonary, critical care and sleep disorders.
3. Translate the most current clinical information into the delivery of high quality care for patients.
4. Integrate new treatment options for patients with pulmonary, critical care and sleep related disorders.

Learning Format: Case-based, interactive online course, including mandatory assessment questions (number of questions varies by case). Please also read the Technical Requirements.

CME Sponsor: University of Arizona College of Medicine at the Arizona Health Sciences Center.

Current Approval Period: January 1, 2017-December 31, 2018

Clinical History: A 56-year-old woman with no significant past medical history underwent routine breast imaging (MRI) which showed an abnormality outside the breast (images not shown). She has a sister with recently-diagnosed breast malignancy. The patient smoked for 30 years, quitting 10 years ago. Her surgical history is remarkable only for a tubal ligation and hysterectomy, and she is asymptomatic. Her medications consist only of vitamins and supplements.

Laboratory evaluation showed a normal complete blood count, electrolyte panel, and liver function tests. Frontal and lateral chest radiography (Figure 1) was performed.

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

Which of the following represents the most accurate assessment of the frontal chest imaging findings? (Click on the correct answer to proceed to the second of ten pages)

1. Chest frontal imaging shows a focal right lung nodule
2. Chest frontal imaging shows basilar fibrosis
3. Chest frontal imaging shows mediastinal and peribronchial lymphadenopathy
4. Chest frontal imaging shows multiple, bilateral small nodules
5. Chest frontal imaging shows normal findings

Cite as: Gotway MB. March 2018 imaging case of the month. Southwest J Pulm Crit Care. 2018;16(3):126-37. doi: https://doi.org/10.13175/swjpcc041-18 PDF 

Medical Image of the Week: Acute Pneumonitis Secondary to Boric Acid Exposure

Figure 1. Panel A: A normal baseline chest radiograph obtained a few months prior to the current presentation. Panel B: A chest radiograph obtained at the day of admission with respiratory distress post exposure to boric acid powder that shows diffuse hazy opacities of the lungs. Panel C: Representative image form thoracic computed tomography obtained on day of admission shows extensive diffuse central predominant ground glass opacification. Panel D: A chest radiograph obtained 3 days after large dose of systemic steroid given for a presumptive diagnosis of acute pneumonitis. Rapid improvement of the bilateral airspace disease is suggestive of resolving inflammation.

Figure 2. Video of thoracic computed tomorgraphy in lung windows obtained on the day of admission.

A 33-year-old man presented with acute severe dyspnea and pleuretic chest pain one day after accidental inhalational exposure to boric acid powder. The patient was spraying boric acid in his apartment to kill bugs and he got trapped in a poorly ventilated area with a cloud of the dusted boric acid for more than a minute. He did not feel any significant symptoms initially. Overnight he started to develop shortness of breath and chest tightness. The patient visited an urgent care where he was reassured due to normal chest radiograph and was given a course of oseltamivir empirically due to a widespread influenza epidemic. After a few hours the patient’s symptoms got much worse and he presented to the emergency department with severe pleuretic chest pain and respiratory distress. The patient required 5 liters of oxygen to keep his saturation above 90%. His chest images showed extensive bilateral airspace disease suggestive of either pulmonary edema, multifocal pneumonia or inflammatory pneumonitis. His microbiologic work up was negative including influenza PCR. Echocardiogram was normal. With his recent exposure to boric acid inhalation an acute chemical pneumonitis was suspected. The patient received systemic high dose prednisone for 3 days and he improved significantly clinically and on imaging. His oxygen saturation was 97% on room air 4 days post admission.

Boric acid is an odorless partially water-soluble antiseptic, insecticide, flame retardant, neutron absorber, and a precursor to other chemical compounds (1,2). The material safety data sheet for boric acid suggests that it may be also toxic to kidneys, cardiovascular system, central nervous system (CNS) (2). Repeated or prolonged exposure to the substance can produce target organ damage (1,2)

Huthayfa Ateeli, MBBS¹, Laila Abu Zaid, MD², Sachin Chaudhary, MD¹

¹Pulmonary and Critical Care Division, Department of Medicine, University of Arizona, Tucson, AZ USA

²Department of Medicine, University of Arizona, Tucson, AZ USA

References

1. Agency for Toxic Substances & Disease Registry. Toxicological profile of boron. November 2010. Available at: https://www.atsdr.cdc.gov/toxprofiles/tp26.pdf (accessed 2/27/18).
2. ScienceLab.com. Material Safety Data Sheet: Boric acid MSDS. October 10, 2005. May 21, 2013. Available at: http://www.sciencelab.com/msds.php?msdsId=9927105 (accessed 2/27/18).

Cite as: Ateeli H, Zaid LA, Chaudhary A. Medical image of the week: acute pneumonitis secondary to boric acid exposure. Southwest J Pulm Crit Care. 2018;16(2):108-9. doi: https://doi.org/10.13175/swjpcc025-18 PDF 

Medical Image of the Week: Traumatic Aortic Dissection

Figure 1. Chest x-ray demonstrating widened mediastinum with prominence of the aortic arch.

Figure 2. Contrast enhanced CT axial (A, left) and coronal (B, right) views demonstrate descending thoracic aortic dissection with mediastinal hematoma and intimal flap (arrow).

A 21-year-old gentleman with no significant past medical history presented to the emergency department following a highway speed motor vehicle collision. The patient was a restrained passenger in the back seat of the vehicle. On initial evaluation the patient was in stable condition and complaining of acute onset back pain. Physical exam was remarkable for facial contusions, tenderness to palpation about the thoracic and lumbar spine, and a normal neurologic exam.

Imaging with chest x-ray (CXR) revealed widening of the mediastinum with prominence of the aortic arch (Figure 1). Further investigation with contrast enhanced computed tomography (CT) of the chest, abdomen and pelvis showed descending thoracic aortic dissection with mediastinal hematoma (Figure 2). The patient underwent successful endovascular repair and was discharged in stable condition.

Acute traumatic aortic injury is a potentially life-threatening condition requiring prompt evaluation. Initial investigation in the trauma setting often includes CXR imaging (1). CXR findings which should raise suspicion for aortic injury in the appropriate clinical scenario include mediastinal widening, abnormality of the aortic silhouette, and right side tracheal deviation.

CT angiography (CTA) is considered the definitive diagnostic modality in most cases, with high sensitivity and specificity. Mediastinal, periaortic and retrocrural hematoma are findings suggestive of traumatic aortic injury. Definitive findings include contrast extravasation, irregularity of the aortic contour, contained rupture, intramural thrombus, and aortic dissection.

Justin S. Caskey, BS

University of Arizona

College of Medicine

Tucson, Arizona, USA

Reference

1. Nagpal P, Mullan BF, Sen I, Saboo SS, Khandelwal A. Advances in imaging and management trends of traumatic aortic injuries. Cardiovasc Intervent Radiol. 2017 May;40(5):643-54. [CrossRef] [PubMed]

Cite as: Caskey JS. Medical image of the week: traumatic aortic dissection. Southwest J Pulm Crit Care. 2018;16(2):94-5. doi: https://doi.org/10.13175/swjpcc016-18 PDF

Medical Image of the Week: Blue-Green Urine and the Serotonin Syndrome

Figure 1. Panel A: blue-green urine a few hours after parathyroid surgery. Panel B: normal urine color 72 hours post-surgery.

A 56-year-old woman was electively admitted for parathyroidectomy for primary hyperparathyroidism with osteoporosis. Five hours post operatively, she developed acute change in mental status. The neurological exam showed inducible clonus, agitation, diaphoresis, ocular clonus, rigidity and hyperreflexia. The patient met Hunter criteria for the diagnosis of serotonin syndrome by being on citalopram and tramadol with the neurological exam findings (1). The patient had been on the same doses of these medications for years with no recent change in kidney or liver functions. The blue-green urine color was strikingly strange. Reviewing the operation room event records showed that she received a high dose of methylene blue to help identify the parathyroid glands.

Serotonin syndrome has been reported with concomitant administration of methylene blue and serotonin reuptake inhibitors (e.g., SSRIs, SNRIs, tricyclic antidepressants). It is recommended to avoid concomitant use and allow a washout period of at least 4-5 half-lives of the serotonin reuptake inhibitor prior to intravenous methylene blue use (2). Within 72 hours of holding tramadol and citalopram the patient recovered completely.

Huthayfa Ateeli, MBBS and Laila Abu Zaid, MD.

Department of Medicine, University of Arizona, Tucson, AZ USA

References

1. Boyer EW, Shannon M. The serotonin syndrome. N Engl J Med. 2005 Mar 17;352(11):1112-20. [CrossRef] [PubMed]
2. Ng BK, Cameron AJ. The role of methylene blue in serotonin syndrome: a systematic review. Psychosomatics. 2010 May-Jun;51(3):194-200. [CrossRef] [PubMed] 

Cite as: Ateeli H, Azid LA. Medical image of the week: blue-green urine and the serotonin syndrome. Southwest J Pulm Crit Care. 2018;16(2):90. doi http://doi.org/10.13175/swjpcc024-18 PDF 

Medical Image of the Week: Acute Encephalopathy in a Multiple Myeloma Patient

Figure 1. Panels A, B & C: Skeletal survey with multiple well-defined "punched out" lytic lesions in the skull and pelvis bones. Panels D, E & F: Magnetic resonance images show infiltration and replacement of bone marrow in the skull with highly vascular lesions due to tightly packed plasma cells.

A 45-year-old man with new diagnosis of multiple myeloma waiting to start treatment presented with worsening dizziness, blurred vision that progressed to altered mental status over a week. His physical exam revealed confusion but no focal deficit. His extensive work up showed no abnormality except for mildly elevated serum viscosity. The patient was started immediately on plasmapheresis. He also received dexamethasone, thalidomide and cyclophosphamide. His symptoms resolved completely within a few days of therapy.

Serum viscosity measurements do not correlate well with symptoms or the clinical findings of hypervicosity syndrome. Plasmapheresis promptly relieves the symptoms and should be performed in symptomatic patients regardless of the viscosity level (1,2).

Huthayfa Ateeli, MBBS and Laila Abu Zaid, MD

Department of Medicine

University of Arizona

Tucson, AZ USA

References

1. Gertz MA, Kyle RA. Hyperviscosity syndrome. J Intensive Care Med. 1995 May-Jun;10(3):128-41. [CrossRef] [PubMed]
2. Palumbo A, Rajkumar SV, San Miguel JF, et al. International Myeloma Working Group consensus statement for the management, treatment, and supportive care of patients with myeloma not eligible for standard autologous stem-cell transplantation. J Clin Oncol. 2014 Feb 20;32(6):587-600. [CrossRef] [PubMed]

Cite as: Ateeli H, Zaid LA. Medical image of the week: acute encephalopathy in a multiple myeloma patient. Southwest J Pulm Crit Care. 2018;16(2):86-7. doi: https://doi.org/10.13175/swjpcc023-18 PDF

February 2018 Imaging Case of the Month

Michael B. Gotway, MD

Department of Radiology

Mayo Clinic Arizona

Scottsdale, AZ USA

Clinical History: An 18-year-old woman with a questionable history of asthma (one physician source claimed no clear history of asthma, whereas another source claimed severe asthma) presented to the emergency room with worsening shortness of breath and cough. The patient’s past medical history was otherwise largely unremarkable. She did have complaints of recurrent rhinorrhea and allergies, for which sinus CT (Figure 1) had been performed.

Figure 1. Unenhanced axial sinus CT shows multifocal sinus opacification (arrow = maxillary sinuses, arrowheads = ethmoid sinuses, double arrowhead= sphenoid sinus)

Physical examination was remarkable for coarse, right-greater-than-left basal rales and coarse breath sounds. The patient’s oxygen saturation was 98% on room air. Her nasal septum appeared deviated. The patient’s vital signs were within normal limits and she was afebrile.

Laboratory evaluation showed a normal complete blood count, electrolyte panel, and liver function tests. A digital frontal chest image (Figure 2) obtained at presentation is shown, with a comparison chest radiograph from 5 months earlier also shown.

Figure 2. A: Digital frontal chest image. B: Chest radiograph from 5 months earlier.

Which of the following represents the most accurate assessment of the frontal chest imaging findings? (Click on the correct answer to proceed to the second of seven pages)

1. Chest frontal imaging shows basilar fibrosis
2. Chest frontal imaging shows mediastinal and peribronchial lymphadenopathy
3. Chest frontal imaging shows multiple, bilateral small nodules
4. Chest frontal imaging shows normal findings
5. Chest frontal imaging shows patchy nodular opacities in the right lung

Cite as: Gotway MB. February 2018 imaging case of the month. Southwest J Pulm Crit Care. 2018;16(2):67-75. doi: https://doi.org/10.13175/swjpcc019-18 PDF

Medical Image of the Week: Stomach Rupture

Figure 1. Cross table view of patient showing massively dilated abdomen.

Figure 2. Chest x-ray showing air under diaphragm (arrow).

A 61-year-old man was transferred from another hospital for further care. He had a history of oxygen-dependent chronic obstructive pulmonary disease in addition to congestive heart failure, hypertension and diabetes mellitus. He had been seen earlier in the day at his primary care physician’s office for a routine visit. Although he was asymptomatic, emergency medical services (EMS) were called because of significant hypoxemia detected by pulse oximetry. EMS noted that the patient said he “feels OK”. However, a decision was made to intubate the patient. Multiple failed intubation attempts failed and he suffered a cardiopulmonary arrest. He was successfully resuscitated and underwent a cricotracheotomy with an uncuffed endotracheal tube. When transferred his mouth was taped shut and his nose clamped. His abdomen was markedly distended and tympanic (Figure 1). A supine chest x-ray showed air under the diaphragm. Abdominal exploration showed a ruptured stomach which was repaired. He made an uneventful recovery.

The difficult airway outside the operating room can be problematic. While preparation for airway control are made, preoxygenation should be performed (1). The patient should be placed in the “sniffing” position and mask ventilation performed. Appropriate positioning - with the tragus of the ear elevated parallel to the sternum - may require special preparation in obese patients. When adequate preoxygenation is accomplished endotracheal intubation can be attempted. However, when endotracheal intubation fails and/or mask ventilation is inadequate a variety of advanced intubation techniques can be considered including a laryngeal mask airway, fiberoptic intubation, cricothyroidotomy, or transtracheal jet ventilation (1).

Confirmation of proper endotracheal tube placement should be completed in all patients (2). Physical examination methods such as auscultation of chest and epigastrium, visualization of thoracic movement, and fogging in the tube are not sufficiently reliable to confirm endotracheal tube placement. During intubation, direct visualization of the endotracheal tube passing through the vocal cords into the trachea, especially with the use of a videolaryngoscope, constitutes firm evidence of correct tube placement. Use of an end-tidal carbon dioxide detector (i.e., continuous waveform capnography, colorimetric and non-waveform capnography) to evaluate and confirm endotracheal tube position should be performed.  For patients in cardiac arrest and for those with markedly decreased perfusion other methods of confirmation such as an esophageal detector device, ultrasound, or bronchoscopy should be used.

Robert A. Raschke, MD

University of Arizona College of Medicine Phoenix

Phoenix, AZ USA

References

1. Langeron O, Amour J, Vivien B, Aubrun F. Clinical review: management of difficult airways. Crit Care. 2006;10(6):243. [CrossRef] [PubMed]
2. American College of Emergency Physicians. Verification of endotracheal tube placement. January 2016. Available at: https://www.acep.org/Clinical---Practice-Management/Verification-of-Endotracheal-Tube-Placement/#sm.00004sk8v7vduedxxs618zbgnij0n (accessed 1/24/18).

Cite as: Raschke RA. Medical image of the week: stomach rupture. Southwest J Pulm Crit Care. 2018;16(1):53-4. doi: https://doi.org/10.13175/swjpcc008-18 PDF 

Medical Image of the Week: Methemoglobinemia

Figure 1. A: cyanotic lips and tongue. B: restoration of reddish color after methylene blue infusion.

Figure 2. Patient’s blood showing a chocolate brown color.

A 62-year-old man with a sternal infection post-coronary artery bypass grafting was transferred because of increasing oxygen requirements, decreased mental status and Candida paralopsis fungemia. He had been treated with multiple antibiotics including sulfonamides and had eventually undergone a tracheostomy. Cetacaine was used for complaints of a sore throat. Physical examination showed cyanotic lips and tongue (Figure 1A). Blood drawn was a chocolate brown color (Figure 2). His SpO2 was 88%, however, arterial blood gases showed his SaO2 was 100% and his PaO2 453 mmHg. Co-oximetry showed 26% methemoglobin. He was administered 0.2mL/kg of 1% solution of methylene blue and his cyanosis rapidly cleared (Figure 1B).

Methemoglobinemia is a condition characterized by increased quantities of hemoglobin with iron oxidized to the ferric (Fe3+) form (1). Methemoglobin is useless as an oxygen carrier and thus causes a varying degree of cyanosis and hypoxia. It can be genetic but is usually caused by exposure to drugs or toxins. Symptoms are proportional to the fraction of methemoglobin. A normal methemoglobin fraction is about 1%. Symptoms associated with higher levels of methemoglobin are: 3-15% - cyanosis; 25-50% - headache, dyspnea; 50-70% - cardiac arrhythmias, altered mental status, delirium, seizures, coma; >70% - death. Drugs most commonly associated with methemoglobinemia include topical and injected local anesthetics (benzocaine, lidocaine, cetacaine), sulfonamides (dapsone), and nitrates (nitroprusside).

Intravenous methylene blue, a reducing agent, is the traditional antidotal agent (1). Exchange transfusion and hyperbaric oxygen treatment are second-line options for patients with severe methemoglobinemia who do not respond to methylene blue or who cannot be treated with methylene blue (e.g., those with glucose-6-phosphate dehydrogenase [G6PD] deficiency).

Robert A. Raschke, MD, MS

University of Arizona College of Medicine-Phoenix and Banner University Medical Center

Phoenix, AZ USA

Reference

1. Denshaw-Burke M. Methemoglobinemia. Medscape. Nov 14, 2017. Available at: https://emedicine.medscape.com/article/204178-overview (accessed 1/11/18).

Cite as: Raschke RA. Medical image of the week: methemoglobinemia. Southwest J Pulm Crit Care. 2018;16(1):49-50. doi: https://doi.org/10.13175/swjpcc007-18 PDF 

Medical Image of the Week: Pulmonary Artery Dilation

Figure 1.  Axial section of the thoracic CT scan showing the massively dilated pulmonary trunk and artery.

The upper limit of the normal diameter of the main pulmonary artery on CT scan is 29 mm and of the right interlobar artery is 17 mm (1). A dilated pulmonary artery can arise from a variety of disease states. Most commonly from one of the many causes of pulmonary hypertension including idiopathic, previously termed primary, pulmonary artery hypertension (PAH). Other less common causes of pulmonary arterial dilation include pulmonary valvular stenosis, atrial septal defect, and idiopathic dilatation of the pulmonary artery.

Our patient is 66-year-old man with exertional dyspnea who was found to have a dilated pulmonary artery on thoracic CT scan during his work up (Figure 1).  His case is suspected to be idiopathic dilatation (1). This is a rare disease with estimates around 0.6% of patients with known congenital heart disease. The estimates in the general population are unknown. There have been a few different diagnostic criteria proposed, but most contain the following:

1. Dilation of the pulmonary trunk 
2. Absence of abnormal intracardiac or extracardiac shunts
3. Absence of chronic heart or lung disease
4. Absence of arterial diseases such as syphilis, arteriosclerosis or arteritis
5. Normal pressures in the right ventricle and pulmonary artery

Patients are usually asymptomatic or with minimal symptoms of dyspnea such as our patient. Rarely, it can present dramatically from compression of nearby structures. This includes constriction of the trachea or major branches or sudden cardiac death from compression of the left main coronary artery.

Tiffany Ynosencio MD and Swathy Puthalapattu MD

Division of Pulmonary, Allergy, Critical Care and Sleep

Banner-University Medical Center and Southern Arizona VA Health Care System

Tucson, AZ USA

Reference

1. Malviya A, Jha PK, Kalita JP, Saikia MK, Mishra A. Idiopathic dilatation of pulmonary artery: A review. Indian Heart J. 2017 Jan-Feb;69(1):119-24. [CrossRef] [PubMed]

Cite as: Ynosencio T, Puthalapattu S. Medical image of the week: pulmonary artery dilation. Southwest J Pulm Crit Care. 2018;16(1):46-7. doi: https://doi.org/10.13175/swjpcc012-18 PDF 

Medical Image of the Week: Plastic Bronchitis

Figure 1. Cast removed from the right main stem.

Figure 2. Casts removed from right lower lobe.

Plastic Bronchitis is a rare syndrome characterized with expectoration of bronchial casts.  Conditions associated with plastic bronchitis in adults include asthma, allergic bronchopulmonary aspergillosis, cystic fibrosis, bronchiectasis, tuberculosis, amyloidosis, sickle cell anemia and rheumatoid arthritis. In children, is its associated with congenital heart diseases (1).

Typical casts are large and branched. These can be expectorated or removed endoscopically as in our case of a 52-year old man with respiratory failure (Figures 1 and 2). The exact etiology of his plastic bronchitis remains obscure. These casts were removed using a bronchoscope with a cryotherapy probe. 

Lauren Estep MD and Bhupinder Natt MD FACP

Division of Pulmonary, Allergy, Critical Care and Sleep

Banner-University Medical Center, Tucson, AZ USA

Reference

1. Itkin MG, McCormack FX, Dori Y. Diagnosis and treatment of lymphatic plastic bronchitis in adults using advanced lymphatic imaging and percutaneous embolization. Ann Am Thorac Soc. 2016 Oct;13(10):1689-96. [CrossRef] [PubMed]

Cite as: Estep L, Natt B. Medical image of the week: plastic bronchitis. Southwest J Pulm Crit Care. 2018;16(1):28. doi: https://doi.org/10.13175/swjpcc005-18 PDF 

January 2018 Imaging Case of the Month

Michael B. Gotway, MD

Department of Radiology

Mayo Clinic Arizona

Scottsdale, AZ USA

Clinical History: An 81-year-old woman with little significant past medical history complained of a dry cough for the previous 1.5 years, but without hemoptysis or shortness of breath. The patient’s past medical history was remarkable only for hypothyroidism, for which she was taking levothyroxine. She smoked for 1 year only, at age 19. Her past surgical history was negative and she denied any alcohol use. Her only other medications included vitamin D3 supplementation and over-the-counter cough medicine.

Physical examination was remarkable only for coarse, left-greater-than-right basal rales. The patient’s oxygen saturation was 98% on room air. The patient’s vital signs were within normal limits and she was afebrile.

Laboratory evaluation showed a normal complete blood count, electrolyte panel, and liver function tests. Frontal chest radiography (Figure 1) was performed.

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

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

1. Chest radiography shows basilar fibrosis
2. Chest radiography shows left lower lobe consolidation
3. Chest radiography shows mediastinal and peribronchial lymphadenopathy
4. Chest radiography shows multiple small nodules
5. Chest radiography shows normal findings

Cite as: Gotway MB. January 2018 imaging case of the month. Southwest J Pulm Crit Care. 2018;16(1):16-27. doi: https://doi.org/10.13175/swjpcc001-18 PDF 

Medical Image of the Week: Pulmonary Alveolar Proteinosis

Figure 1. Representative image from an axial CT scan showing “crazy paving”.

Pulmonary alveolar proteinosis (PAP) is a rare pulmonary disease characterized by alveolar accumulation of surfactant (1). It usually results from mutations in surfactant proteins or granulocyte macrophage-colony stimulating factor (GM-CSF) receptor genes. Other causes include toxic inhalation or hematological disorders, or it may be auto-immune, with anti-GM-CSF antibodies blocking activation of alveolar macrophages.

Auto-immune alveolar proteinosis is the most frequent form of PAP, representing 90% of cases. Although not specific, high-resolution computed tomography shows a characteristic diffuse ground-glass attenuation with superimposed interlobular septal thickening and intralobular lines which is called “crazy paving” (Figure 1). In most cases, bronchoalveolar lavage findings establish the diagnosis. Whole lung lavage is the most effective therapy, especially for auto-immune disease. Novel therapies targeting alveolar macrophages (recombinant GM-CSF therapy) or anti-GM-CSF antibodies (rituximab and plasmapheresis) are considered investigational. 

Bhupinder Natt MD FACP

Division of Pulmonary, Allergy, Critical Care and Sleep

Banner University Medical Center, Tucson (AZ) USA

Reference

1. Borie R, Danel C, Debray MP, Taille C, Dombret MC, Aubier M, Epaud R, Crestani B. Pulmonary alveolar proteinosis. Eur Respir Rev. 2011 Jun;20(120):98-107. [CrossRef] [PubMed]

Cite as: Natt B. Medical image of the week: pulmonary alveolar proteinosis. Southwest J Pulm Crit Care. 2018;16(1):14. doi: https://doi.org/10.13175/swjpcc002-18 PDF 

Medical Image of the Week: Fat Embolism

Figure 1. A CT with IV contrast at the pelvic level showing a filling defect (red arrow) in left external iliac vein extending from left common iliac vein in axial (A), sagittal (B), and coronal (C) sections. Its attenuation coefficient (Hounsfield Unit) suggests fat embolus mixed with thrombus.

A 74-year-old woman presented to the hospital with a left femoral neck fracture after a fall. The next day she underwent an uneventful left hip hemiarthroplasty. About 3 hours postoperatively, she became lethargic, tachycardic, tachypneic, febrile, and hypotensive. An arterial blood gas analysis revealed mild hypoxemia with PaO2 / FiO2 ratio of 270. Hemoglobin decreased from 9.4g/dL to 7.7g/dL postoperatively. A chest x-ray showed only bibasilar opacities. Sepsis, acute postoperative blood loss anemia, and pulmonary embolism (PE) were entertained as a differential diagnosis. The patient was resuscitated with intravenous fluids and packed red blood cells, and was started on broad-spectrum antibiotics. Her hemodynamic status stabilized shortly thereafter. A CT chest with PE protocol and abdomen/pelvis down to thigh level was performed; no PE was identified. It did not show any intraabdominal pathology or signs of hemorrhage. However, it incidentally revealed fat embolus mixed with thrombus in the left common and external iliac veins (Figure 1). All microbiologic studies were negative. Therefore, she was thought to have fat embolism syndrome (FES) with transient systemic inflammatory syndrome (SIRS). An IVC filter was placed and anticoagulation was also started.

FES is a collection of symptoms and signs including respiratory insufficiency, petechial rash, and neurologic impairment associated with fat in the circulation (1). Fat emboli cause an intense inflammation (2), and FES shares many features characteristic of systemic inflammatory response syndrome (SIRS) (1). It is a diagnostic challenge as many of the manifestations are common to other critical illnesses (1). It is most commonly associated with long bone fractures and orthopedic procedures. Literature on radiographic finding of fat emboli in the venous system is rare (3); although neither necessary nor sufficient, its radiographic demonstration in the venous system can substantially aid in diagnosis of FES, as demonstrated in our case.

Hyeong J. Kim MD¹, Michael Jesinger MD², and Medhi Khosravi MD²

¹ Division of Pulmonary, Critical Care, and Sleep Medicine, East Carolina University, Greenville, NC, USA

² Internal Medicine, University of Kentucky, Lexington, KY, USA

³ Division of Pulmonary, Critical Care, and Sleep Medicine, Division of Pulmonary, Critical Care, and Sleep Medicine, Lexington, KY, USA

References

1. Mellor A, Soni N. Fat embolism. Anaesthesia. 2001 Feb;56(2):145-54. [CrossRef] [PubMed]
2. Kwiatt ME, Seamon MJ. Fat embolism syndrome. Int J Crit Illn Inj Sci. 2013 Jan;3(1):64-8. [CrossRef] [PubMed]
3. Harris AC, Torreggiani WC, Lyburn ID, Zwirewich CV, Ho SG, Munk PL. CT and sonography of traumatic fat embolism in the common femoral vein. AJR Am J Roentgenol. 2000 Dec;175(6):1741-2. [CrossRef] [PubMed]

Cite as: Kim HJ, Jesinger M, Khosravi M. Medical image of the week: fat embolism. Southwest J Pulm Crit Care. 2017;15(6):297-8. doi: https://doi.org/10.13175/swjpcc138-17 PDF

Medical Image of the Week: Central Venous Access with Dextrocardia

Figure 1. Post CVC placement chest X-ray. Catheter traced with arrows.

An 88-year old man, with known dextrocardia, was admitted with a diagnosis of septic shock. A right sided internal jugular central venous catheter was placed uneventfully using ultrasound guidance. Chest X-ray obtained after the catheter placement is shown (Figure 1). Although the utility of a chest X-ray after every ultrasound guided central line placement is questionable, it continues to be “routine practice” in many centers. In dextrocardia, a right sided central line is expected to cross the midline as in this patient. When in doubt, the catheter may not be used unless venous placement is confirmed.

Venous placement of the catheter can be confirmed by:

1. Transducing the catheter and confirming venous waveform;
2. Blood gas analysis consistent with venous gas;
3. Imaging X-ray or cross sectional (1).

Bhupinder Natt MD

Division of Pulmonary, Allergy, Critical Care and Sleep

Banner-University Medical Center, Tucson, AZ USA

Reference

1. Morton PG. Arterial puncture during central venous catheter insertion. Crit Care Med. 1999 May;27(5):878-9. [CrossRef] [PubMed] 

Cite as: Natt B. Medical image of the week: central venous access with dextrocardia. Southwest J Pulm Crit Care. 2017;15(6):296. doi: https://doi.org/10.13175/swjpcc148-17 PDF 

Medical Image of the Week: Mucous Plugs Forming Airway Casts

Figure 1. Bronchoscopic view of the mucous plug.

Figure 2. Cast removed with cryo-adhesion probe.

A 64 -year-old man with a recent diagnosis of acute lymphocytic leukemia (ALL) on chemotherapy presented with acute hypoxic respiratory failure, multifocal pneumonia, neutropenic fever and septic shock. The patient was intubated and required vasopressors for septic shock. His blood and sputum cultures grew Pseudomonas aeruginosa. Chest computed tomography demonstrated extensive consolidation of the left lung mainly the left lower lobe with extensive endobronchial mucus plugs. The patient underwent bronchoscopy after noninvasive measures failed to resolve the left lung atelectasis. After multiple attempts to retrieve the mucus plugs (Figure 1) with suction failed, a cryo-adhesion probe was used to freeze and retrieve the mucus plug. The plug formed a cast taking the shape of the airway (Figure 2).

Flexible bronchoscopy is warranted in patients who have persistent atelectasis or pneumonia that is either of unknown cause or suspected of being due to airway obstruction (1). The use of cryo-adhesion and extraction has been particularly useful in the management of airway obstruction caused by foreign bodies especially mucus plugs and blood clots that are not easily extracted by more standard means such as suction or forceps (2).

Huthayfa Ateeli, MBBS and Cameron Hypes MD, MPH

Division of Pulmonary, Critical Care, Sleep and Allergy Medicine

University of Arizona, Tucson, AZ USA

References

1. Feinsilver SH, Fein AM, Niederman MS, Schultz DE, Faegenburg DH. Utility of fiberoptic bronchoscopy in nonresolving pneumonia. Chest. 1990 Dec;98(6):1322-6. [CrossRef] [PubMed]
2. Strausz J, Bolliger CT. Interventional pulmonology. Sheffield: European Respiratory Society; 2010: 165.

Cite as: Ateeli H, Hypes C. Medical image of the week: mucous plugs forming ariway casts. Southwest J Pulm Crit Care. 2017;15(6):278-9. doi: https://doi.org/10.13175/swjpcc147-17 PDF