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 

December 2017 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 57-year-old woman with a past medical history remarkable only for hyperlipidemia undergoing statin therapy presented with a history of slowly progressive dyspnea on exertion for at least months, possibly longer. The patient denied cough, hemoptysis, and chest pain.

Physical examination was largely unremarkable and the patient’s oxygen saturation was 96% on room air while resting. The patient’s vital signs were within normal limits.

Laboratory evaluation was unremarkable. Quantiferon testing for Mycobacterium tuberculosis was negative, and testing for coccidioidomycosis was unrevealing.

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

Figure 1. Frontal chest radiography.

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

1. The chest radiograph appears normal
2. The chest radiograph shows bilateral, symmetric lower lobe reticulation suggesting fibrotic disease
3. The chest radiograph shows left upper lobe collapse
4. The chest radiograph shows linear right lower lobe opacity suggesting scarring
5. The chest radiograph shows numerous small miliary nodules

Cite as: Gotway MB. December 2017 imaging case of the month. Southwest J Pulm Crit Care. 2017;15(6):2563-66. doi: https://doi.org/10.13175/swjpcc149-17 PDF

Medical Image of the Week: Moyamoya Disease

Figure 1. Cerebral angiogram of the brain demonstrating bilateral high-grade stenosis of the anterior and middle cerebral arteries, worse on the left.

Figure 2. Magnetic resonance imaging showing multiple punctate infarcts in the frontal and parietal lobes on the left side.

A 52-year-old, right-handed, Caucasian woman with a history of hypertension and morbid obesity presented with acute onset of word-finding difficulty and slurred speech. Her medical and family history was negative for cerebral vascular event, coronary artery disease or smoking. Computed tomography of the patient's brain showed narrow caliber middle cerebral artery vasculature bilaterally. This abnormal finding prompted further investigation with cerebral angiogram. The angiogram showed bilateral high-grade stenosis of the anterior and middle cerebral arteries, worse on the left (Figure 1). Magnetic resonance imaging revealed multiple left sided punctate infarcts in the frontal and parietal lobes (Figure 2). Diagnosis of ischemic stroke secondary to moyamoya disease was established. This patient was not a candidate for fibrinolytic therapy since it had been more than 4 hours from initial presentation. She was treated with aspirin, clopidogrel, and atorvastatin for secondary prevention of ischemic stroke. Two months after her discharge date, the patient had a middle cerebral artery to superior temporal artery bypass on the left side, followed by a middle cerebral artery to superior temporal artery bypass on the right two months after initial bypass. Patient progressed to an uneventful recovery. Discharge planning included the continuation of aspirin, clopidogrel, and atorvastatin indefinitely.

Moyamoya disease (MMD) is an uncommon vasculopathy of unknown origin associated with diverse risk factors (1). It was first discovered in a Japanese population, and reported more commonly in this sub-population. However, numerous cases were reported across the globe (2). Moyamoya disease associated with other systemic condition such as neurofibromatosis type 1, trisomy 21, thyroid cranial irradiation or thyroid disease is termed moyamoya syndrome (MMS) (1,2). Moyamoya syndrome is a cerebrovasculopathy originating from collateral flow that develops secondary to occlusion of the internal carotid artery and the proximal afferent vessels at the circle of Willis (3). MMS can have abrupt or insidious onset and may progress to diversifying cerebral ischemic stroke or to intracranial hemorrhage, which is a worse prognosis and the primary cause of death in patients with MMD (4). It has been shown that ischemic stroke associated with MDD or MMS usually occurs when compensatory collateral vessels are unable to supply sufficient blood to the brain after occlusion or stenosis of the internal carotid arteries or its tributary vessels (5,6). On the other hand, intracranial hemorrhage occurs secondary to the rupture of abnormal moyamoya vessels (7,8).

It is imperative to differentiate between non-hemorrhagic and hemorrhagic moyamoya. Neuroimaging is the preferred method of diagnosis after high clinical suspicion of MMD or MMS. Intracranial hemorrhage and cerebral infarction can be diagnosed with computed tomography and magnetic resonance imaging/ cerebral angiogram, respectively (8,9). Recent use of magnetic resonance perfusion imaging has been shown to be crucial in diagnostics and medical-surgical decision making. There is no common consensus when it comes to treatment of moyamoya at this time. Initial management is symptomatic with anticoagulants, antiplatelet and corticosteroids (10). Treatment options may also include direct or indirect surgical revascularization as optimal therapy (11,12).

Stella Pak MD, Kokou Adompreh-Fia MD, Damian Valencia MD, Adam Fershko MD, and Jody Short DO.

Department of Medicine

Kettering Medical Center

Kettering, OH USA

References

1. Phi JH, Wang KC, Lee JY, Kim SK. Moyamoya Syndrome: A window of moyamoya disease. J Korean Neurosurg Soc. 2015 Jun;57(6):408-14. [CrossRef] [PubMed]
2. Suzuki J, Takaku A. Cerebrovascular "moyamoya" disease. Disease showing abnormal net-like vessels in base of brain. Arch Neurol. 1969 Mar;20(3):288-99. [CrossRef] [PubMed]
3. Yamamoto, S, Koh M, Kashiwazaki D, Akioka N, Kuwayama N, Noguchi K, Kuroda S. Is Quasi-moyamoya disease a uniform disease entity? A three-dimensional constructive interference in steady state imaging study. J Stroke Cerebrovasc Dis. 2016 Jun;25(6):1509-16. [CrossRef] [PubMed]
4. Baba, T., Houkin, K. Kuroda. Novel epidemiological features of moyamoya disease. J Neurol Neurosurg Psychiatry. 2008 Aug;79(8):900-4. [CrossRef] [PubMed]
5. Miyamoto S, Kikuchi H, Karasawa J, Nagata I, Ihara I, Yamagata S. Study of the posterior circulation in moyamoya disease. Part 2: Visual disturbances and surgical treatment. J Neurosurg. 1986 Oct;65(4):454-60. [CrossRef] [PubMed]
6. Kuroda S, Ishikawa T, Houkin K, Iwasaki Y. Clinical significance of posterior cerebral artery stenosis/occlusion in moyamoya disease. No Shinkei Geka. 2002 Dec;30(12):1295-300. [PubMed]
7. Kang K, Lu J, Zhang D, Li Y, Wang D, Liu P, Li B, Ju Y, Zhao X. Difference in cerebral circulation time between subtypes of moyamoya disease and moyamoya syndrome. Sci Rep. 2017;7(1):2587. [CrossRef] [PubMed]
8. Lui, P, Han C, Li DS, Lv XL, Li YX, Duan L. Hemorrhagic moyamoya disease in children: Clinical, angiographic features, and long-term surgical outcome. Stroke. 2016 Jan;47(1):240-3. [CrossRef] [PubMed]
9. Kellner CP, McDowell MM, Phan MQ, Connolly ES, Lavine SD, Meyers PM, Sahlein D, Solomon RA, Feldstein NA, Anderson RC. Number and location of draining veins in pediatric arteriovenous malformations: association with hemorrhage. J Neurosurg Pediatr. 2014 Nov;14(5):538-45. [CrossRef] [PubMed]
10. Whitaker J. Management of moyamoya syndrome [comment]. Arch Neurol. 2001;58:132. [CrossRef] [PubMed]
11. Golby AJ, Marks MP, Thompson RC, Steinberg GK. Direct and combined revascularization in pediatric moyamoya disease. Neurosurg. 1999;45:50-8. [PubMed]
12. Mizoi K, Kayama T, Yoshimoto T, Nagamine Y. Indirect revascularization for moyamoya disease: is there a beneficial effect for adult patients? Surg Neurol. 1996;45:541-8. [CrossRef] [PubMed] 

Cite as: Pak S, Adompreh-Fia K, Valencia D, Fershko A, Short J. Medical image of the week: moyamoya disease. Southwest J Pulm Crit Care. 2017;15(5):227-9. doi: https://doi.org/10.13175/swjpcc136-17 PDF

Medical Image of the Week: Coronary Artery Ectasia

Figure 1. Coronary angiogram demonstrating ectatic right coronary artery (black arrow) with minimal laminar flow of contrast dye. 100% occlusion of distal RCA noted (white arrow), as well as sternotomy wires from prior CABG.

Figure 2. Intravascular ultrasound (IVUS) demonstrating dilated, ectatic right coronary artery with maximum dimension 9-10 mm (white line).

A 70-year-old man with a history of coronary artery disease and previous 3 vessel coronary artery bypass grafting (CABG) was admitted to the coronary care unit with acute chest pain and EKG concerning for ST elevations in II, III, aVF with first degree AV block. Troponins were negative on admission, and peaked at 35 ng/ml. The patient was taken immediately to the cardiac catherization lab for acute inferior ST elevation myocardial infarction (STEMI), and was found to have coronary artery ectasia throughout with diffuse atherosclerotic disease. 100% occlusion was noted in the distal RCA, but the wire was not able to be passed through the blockage due to tortuous and dilated vessels vessels. Left circumflex and left anterior descending arteries showing similar ectatic findings without acute blockage. No stents were able to be engaged in the RCA given the large diameter from the ectasia. The RCA notably had a diameter of 7-10 mm in width with minimal laminar flow of contrast dye (Figure1), and was confirmed with Intravascular Ultrasound (IVUS, Figure 2). Echocardiogram showed an ejection fraction of 55% with normal left ventricular function. Since stents were not able to be placed, the patient was medically optimized with aspirin, ticagrelor, and a high intensity statin. The patient felt improved following medical optimization, and was discharged home in stable condition with cardiology follow up.

Coronary ectasia is a disease of the coronary arteries in which the vessel lumen is increased greater than 1.5 times in size (1). It is a very rare finding, with only 1.2-2% of coronary caths demonstrating ectasia. Clinical findings are believed to be due to increased wall stress and thinning of the arterial wall in the setting of atherosclerosis causing progressive dilation and remodeling (2). Ectasia is also commonly found in patients with connective tissue disease and vasculitis, classically Marfan syndrome and Kawasaki disease. Conventional stents are generally too small in diameter to be utilized. Treatment is largely devoted towards decreasing cardiac risk factors and avoiding medications that slow coronary blood flow such as nitrates (3).

Adam Berlinberg MD¹, Steven Stroud MD¹, Jaren Trost MD¹, Karl Kern MD²

¹Department of Internal Medicine and ²Department of Cardiology, Sarver Heart Center, Banner University Medical Center; Tucson, AZ

References

1. Lin CT, Chen CW, Lin TK, Lin CL. Coronary artery ectasia. Tzu Chi Med J 2008;20:270-4. [CrossRef]
2. Hsu PC, Su HM, Lee HC, Juo SH, Lin TH, Voon WC, Lai WT, Sheu SH. Coronary artery collateral circulation in patients of coronary ectasia with significant coronary artery disease. PLoS One. 2014;9(1): e87001. [CrossRef] [PubMed]
3. Eitan A, Roguin A. Coronary artery ectasia: new insights into pathophysiology, diagnosis, and treatment. Coron Artery Dis 2016;27(5):420-8. [CrossRef] [PubMed] 

Cite as: Berlinberg A, Stroud S, Trost J, Kern K. Medical image of the week: coronary artery ectasia. Southwest J Pulm Crit Care. 2017;14(5):253-4. doi: https://doi.org/10.13175/swjpcc049-17 PDF

Medical Image of the Week: Artery of Percheron Infarction

 

Figure 1. T2 weighted MRI demonstrating bilateral infarcts of the rostral midbrain (A, orange box) and thalami (B, orange box).

 

Figure 2. CT angiogram of posterior cerebral artery circulation demonstrating normal vascularization (A) and artery of Percheron (B, white arrow) (1).

A 55-year-old African-American man presented to the Emergency Department for acute altered mental status which started 4 hours ago. His medical history was significant for heart failure with reduced ejection fraction, diabetes mellitus, marijuana and opioid use. On admission, the patient appeared to be in a deep sleep, unarousable, with grimacing to noxious stimuli. He occasionally moved all extremities. He was intubated for airway protection. Initial CT head non-contrast demonstrated a previous right MCA infarct, with no new acute hemorrhage. MRI/MRA brain revealed complete infarction of the artery of Percheron (AOP), likely due to a left ventricular thrombus (Figure 1). The patient remained somnolent throughout hospitalization with minimal neurologic improvement, and was ultimately transferred to a long-term care facility after a tracheostomy and PEG placement.

The artery of Percheron is a rare, normal intracranial vascular variant in which a single arterial trunk originates from the posterior cerebral artery, giving rise to the vascular supply of both thalami and upper midbrain (Figure 2) (2). Acute occlusion of the artery results in posterior circulation infarction and is associated with impairment of consciousness, sleep and alertness. Diagnosis is usually based on magnetic resonance imaging demonstrating bilateral thalami and midbrain infarct. Management primarily consists of supportive measures, as reperfusion of cerebral microvascular carries significant surgical risk. Given the rarity of incidence, the prognosis of AOP infarct is unknown (3).

TC Ta¹, ET Vo¹, KS Goldlist², B Barcelo¹, JM Dicken³

¹Department of Internal Medicine

²Department of Internal Medicine at University of Arizona at South Campus

³University of Arizona College of Medicine.

University of Arizona

Tucson, AZ USA

References

1. Shetty A, Jones J. Artery of Percheron. Radiopedia. Available at: https://radiopaedia.org/articles/artery-of-percheron (accessed 3/24/17).
2. Lazzaro NA, Wright B, Castillo M, et al. Artery of Percheron infarction: imaging patterns and clinical spectrum. AJNR Am J Neuroradiol. 2010 Aug;31(7):1283-9. [CrossRef] [PubMed]
3. Amin OS, Shwani SS, Zangana HM, Hussein EM, Ameen NA. Bilateral infarction of paramedian thalami: a report of two cases of artery of Percheron occlusion and review of the literature. BMJ Case Rep. 2011 Mar 3;2011. [CrossRef] [PubMed] 

Cite as: Ta TT, Vo ET, Goldlist KS, Barcelo B, Dicken JM. Medical image of the week: artery of Percheron infarction. Southwest J Pulm Crit Care. 2017;14(3):127-8. doi: https://doi.org/10.13175/swjpcc037-17 PDF 

Medical Image of the Week: Abdominal Hematoma

 

Figure 1. Contrast-enhanced CT abdomen/pelvis showing A) coronal and B) sagittal views of a LLQ hematoma (blue braces) with active contrast extravasation (red arrow). Lines represent the level of respective axial images. C-F) Axial images demonstrating the hematoma within and expanding the rectus abdominis sheath (blue braces) as well as active contrast leak (red arrow).

Figure 2. A) Arteriogram demonstrating the large hematoma (solid arrow) with active extravasation of contrast from the inferior epigastric artery (arrowhead) arising from the external iliac artery (empty arrow). B) Coils in the inferior epigastric artery (arrow) block flow to the hematoma.

A 59 year-old man presented to clinic with acute-on-chronic non-productive cough along with sore throat and myalgias for 2 weeks and lower left quadrant (LLQ) abdominal pain for 2-3 days. He was a current smoker with history significant for COPD and mild “smoker’s cough” controlled with daily anticholinergic and as-needed beta-agonist, paroxysmal atrial fibrillation on dabigatran and diltiazem, hypertension controlled by diuretic, and a former alcoholic with hemochromatosis.

While getting an x-ray, he had a coughing fit resulting in abrupt worsening of his LLQ pain enough to inhibit ambulation. Due to his inability to walk, he came via ambulance to the emergency department, where he was mildly tachycardic with a 10cm firm, tender and ecchymotic LLQ mass.

Contrast-enhanced abdominal/pelvic CT demonstrated a large rectus abdominis hematoma. Figure 1 shows the hematoma within the rectus sheath measuring 16 cm with active contrast extravasation. The patient went directly to the interventional suite, where the left inferior epigastric artery was catheterized and subsequently embolized as shown in Figure 2.

The patient was noted to be in atrial fibrillation with rapid ventricular response (AFRVR), so was taken to the intensive care unit and placed on diltiazem drip, given digoxin and 1 unit of RBCs before his rhythm stabilized and he was transferred to the floor. His hemoglobin remained stable, and his cough and abdominal pain improved, so he was sent home off anticoagulation until follow-up with his cardiologist.

In the RE-LY trial, updated in 2010 (1), there was no difference in bleeding complications at this patient’s dosing of dabigatran compared to warfarin with INR of 2.0-3.0. However, this patient did not bleed into a critical area, require 2 units of RBCs, nor drop hemoglobin >2mg/dl, and would thus be considered having a minor bleeding event despite needing emergent embolization, losing enough blood to become tachycardic with resulting AFRVR, and getting 1 unit of RBC

Despite this particular bleeding complication, in a meta-analysis examining dabigatran vs warfarin, dabigatran uniformly was as good or better in preventing strokes with less devastating complications than warfarin (2). Additionally, although warfarin is touted as having vitamin K as its reversal agent, protein synthesis and secretion into the vasculature takes hours, similar in time to metabolically clear dabigatran (3).

In the end, after discussions about anticoagulants with the hospital team before discharge and his cardiologist thereafter, the patient elected to restart his dabigatran.

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

Banner-University Medical Center

University of Arizona

Medical Imaging Department

Tucson, AZ, USA

References

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Cite as: Larson M. Medical image of the week: abdominal hematoma. Southwest J Pulm Crit Care. 2016:13(4): 176-8. doi: http://dx.doi.org/10.13175/swjpcc083-16 PDF

Medical Image of the Week: Vascular Occlusion

Figure 1. Left arm angiogram showing complete occlusion of ulnar artery (red arrow).

Figure 2. Angiogram showing left radial artery complete occlusion (red arrow).

Figure 3. Left hand with necrotic fingers.

The patient is a 39 year-old woman with no significant past medical history presenting with progressive left hand pain for five days. The patient denied a history of Raynaud’s phenomenon or clotting disorders. She had no radial pulse on presentation and angiogram showed severe complete occlusion of the radial and ulnar arteries (Figures 1 and 2). She had an initial partial response with intra-arterial verapamil and nitroglycerin but her hand ischemia did not improve on heparin or with intra-arterial tissue plasminogen activator. Autoimmune and coagulation work-ups were negative. Her left hand finger necrosis at time of discharge is shown (Figure 3).  Further evaluation is ongoing for coagulation disorders.

Allison Shapiro MD, Carmen Luraschi-Monjagatta MD, Matthew Schreiber MD.

Department of Internal Medicine, Pulmonary and Critical Care, University of Nevada School of Medicine, Las Vegas, NV

Reference as: Shapiro A, Luraschi-Mongagatta C, Schreiber M. Medical image of the week: vascular occlusion. Southwest J Pulm Crit Care. 2014;9(1):36-7. doi: http://dx.doi.org/10.13175/swjpcc093-14 PDF