A Collection of Conditions of the Vasculature

Aberrant Ulnar Artery and Ulnar Artery Aneurysm With Nerve Entrapment

Nickul N. Shah, MD; David Roman, RPA-C; and Roland Purcell, MD
Interfaith Medical Center, Brooklyn, New York


A 73-year-old woman presented to a community hospital, accompanied by her daughter. The patient was Haitian and spoke very little English, so her daughter translated. The woman complained of numbness, pain, and weakness along her right arm, forearm, and wrist. She had been experiencing these symptoms for at least 2 years. She believed that she had unintentionally “bumped her hand on something.”

History. The patient had a significant past medical history of hypertension, arthritis of both hands, and bilateral cataracts, and she had undergone a lumpectomy of the right breast.

Physical examination. The woman appeared to be well nourished, in no apparent distress, and was alert and oriented. A 3-cm pulsatile mass with a palpable thrill was observed at the ulnar side of the right wrist. No obvious signs of trauma were observed. There were no signs of digital ischemia, cyanosis, or atrophic ulcerations. She described numbness and tingling along the fourth and fifth digits of her right hand, but strength was preserved.

Diagnostic tests. An Allen test was conducted, with no significant abnormalities observed. A Tinel test was also conducted and showed hyporeflexia. Pinprick sensation was diminished along the ulnar distribution of the hand. She underwent arteriovenous fistulography, the results of which demonstrated an aneurysm of the ulnar artery, along with an adjacent aberrant superficial branch of the ulnar artery (Figures 1-3). Contrast dye was used to isolate the aneurysm and observe the continuity of blood flow. It showed no disruption of flow proximal or distal to the aneurysm and no disruption of the adjacent artery.

Figures 1-3. Arteriovenous fistulogram demonstrated the flow of aberrant artery and aneurysm.

Treatment. A resection of the right wrist aneurysm was scheduled the same day. Under local anesthesia, a longitudinal incision was created to expose the aneurysm and its bifurcation points (Figure 4). The patient’s vital signs remained stable throughout the procedure. During the operation, an aberrant ulnar artery was noted medial to the aneurysm (Figure 5). Special care was taken to avoid damage to the artery or blood flow to the hand. Multiple microvascular connections were observed with the aneurysm, and again, special care was needed to isolate the aneurysm without excessive blood loss.

Figure 4. The ulnar artery aneurysm was identified and isolated.

Figure 5. The high origin and superficial course of the ulnar artery were identified.


Ring-handled bulldog clamps were placed in a tangential fashion to occlude flow of the aneurysm and its branch points. The microvascular connections were ligated throughout the procedure while still exposing the aneurysm and the artery of interest. Once the aneurysm was isolated both proximally and distally using additional clamps, it was resected for histopathologic evaluation (Figure 6). The isolated aberrant artery remained patent throughout the procedure with continuous flow as detected by Doppler ultrasonography.

Figure 6. The resected aneurysm, which was sent for histopathologic review.


Outcome of the case. After the procedure, an Allen test was again conducted to test for adequacy of blood flow to the hand, and no abnormalities were found. Pinprick sensation and Tinel test results had significantly improved.

She experienced no postoperative complications, and her pain was adequately controlled in the recovery room. She was discharged home the same day, and she was advised to follow up in the outpatient clinic a week later and to visit the hospital if any complications arose before that.

Discussion. Aneurysms of the ulnar artery and palmar arch arise from repetitive trauma involving the upper extremity or secondary to vasculitis. They are often found in young men and sometimes are related to anatomic vascular anomalies or infections. However, distal ulnar artery and palmar arch aneurysms are uncommon clinical findings that usually are associated with hypothenar hammer syndrome (HHS).1 HHS is a rare condition with an incidence of up to 14%, and it is considered a less common etiology of ischemia in the upper extremity from a repetitive or single trauma to the region of the hypothenar eminence.2 The pathogenesis is related to the anatomy of the ulnar artery as it enters the palm and exits the Guyon canal to form the superficial palmar branch.3 This arterial segment is susceptible to injury because of its limited protection from overlying tissues of the hypothenar muscles.

The radial artery and ulnar artery provide most of the blood supply to the hand, and additional circulation arises from the median artery or the interosseous arterial system.4 The deep palmar arch and superficial palmar arch are the most significant circuits in that they supply blood to each finger.3,4 The superficial palmar arch supplies all the fingers and the ulnar side of the thumb. The deep palmar arch has a connection with the deep palmar branch of the ulnar artery above the level of the hamulus. Repetitive blunt trauma can damage the intima of the ulnar artery as it passes adjacent to the hook of hamate. Subsequently, the artery becomes aneurysmal or thrombotic, affecting digital arteries.5,6

HHS arises because of the anatomic relationship of the sensory branch of the ulnar nerve and the superficial branch of the ulnar artery in association with the hamulus.4 A fibromuscular dysplasia etiology also has been suggested in which the intimal and medial hyperplasia results in a disruption of the internal elastic lamina with areas of stenosis and dilatation.7

Ulnar neuropathy, also known as Guyon canal syndrome, should also be considered in the differential diagnosis of neurologic symptoms such as those of our patient. Ulnar neuropathy affects cyclist athletes (handlebar palsy), in which repetitive and continuous pressure on the wrist compresses the ulnar nerve.4 The condition may also affect workers who are exposed to frequent vibrations.

Adjacent masses such as lipomas, anomalous muscles, ulnar artery aneurysms, and hamulus fractures can entrap the nerve. Nerve entrapment caused by an ulnar artery aneurysm can affect the superficial or sensory branch of the nerve and cause sensory loss to the hypothenar eminence, including the fourth and fifth digits. There is tenderness to palpation, and patients may complain of paresthesias, weakness, and tingling that radiates to the fourth and fifth digits.

Our case is unique in that the patient was a 73-year-old woman who did not injure herself through an occupational or sports activity that caused repetitive microtrauma on the heel of the hand. However, she did experience neurologic symptoms such as paresthesia, given that the sensory branches of the ulnar nerves coursed in close proximity to the ulnar artery aneurysm. In addition, a pulsatile hypothenar mass was present after the formation of the aneurysm.

Initially, the patient was evaluated using the Allen test to assess the patency of the superficial palmar arch. Positive Allen test results suggest occlusion, stenosis, or incomplete development of the superficial palmar arch or distal ulnar artery.3 In addition, a fistulogram was used to check for the presence of a proximal stenosis.8

Upon reviewing the literature, we determined that a Doppler ultrasonography examination of the extremity and serial arteriograms would be useful to evaluate the aneurysm and differentiate it from other vascular anomalies—for example, to rule out fibromuscular dysplasia with the absence of a corkscrew sign demonstrating areas of stenosis and ectasia.9 Given the results, we subsequently decided to surgically resect the aneurysm. Reasons to repair an aneurysm include skin changes such as thinning or erosion; inflammation; pain; and thrombosis with flow impediment. If left untreated, local compression, emboli, distal ischemia, or rupture can develop.10,11

The resected aneurysm was sent for pathologic evaluation, the results of which demonstrated wall thickening and abnormality of the vessel wall architecture due to thrombosis (Figures 7 and 8). Intraoperatively, an anatomical variation in the vascular bundle was noted, which was isolated and evaluated using Doppler ultrasonography. The presence of an ulnar artery of high origin is considered a rare anatomic variation.12 Pulakunta and colleagues reported a variation of a superficial ulnar artery and a coexisting adjacent aneurysm of the deep palmar arch in the hand.13

Figure 7. Low magnification view of the excised aneurysm showing significant wall thickening.

Figure 8. Higher magnification view of the excised aneurysm showing wall thickening, collagen infiltration, and marked derangement of wall architecture.


The arterial course can lead to a higher risk of damage during vascular surgery. Therefore, the use of Doppler ultrasonography was necessary to demonstrate the patency of both the ulnar artery and its superficial branch. After resection of the aneurysm, the aberrant artery remained, and an Allen test was conducted again to show perfusion of the deep palmar arch.

Conclusion. Most aneurysms in the forearm are found in the distal artery and often are associated with trauma.14 The resultant damage to the hypothenar eminence can cause entrapment within the Guyon canal and compress the sensory branch of the ulnar nerve. Surgical intervention was mandatory in our patient’s case to prevent irreversible consequences. The artery was assessed preoperatively with an Allen test, Doppler ultrasonography, and a fistulogram. Upon isolation and resection of the aneurysm, an aberrant superficial ulnar artery was identified. Careful evaluation of its persistent flow prevented its obliteration intraoperatively; its patency prevented complications such as ischemia and gangrene.


  1. Mazzaccaro D, Malacrida G, Stegher S, et al. Ulnar artery aneurysm: case report and review of the literature. G Chir. 2012;33(4):110-113.
  2. Nitecki S, Anekstein Y, Karram T, Peer A, Bass A. Hypothenar hammer syndrome: apropos of six cases and review of the literature. Vascular. 2008;​16(5):​279-282.
  3. Ablett TC, Hackett LA. Hypothenar hammer syndrome: case reports and brief review. Clin Med Res. 2008;6(1):3-8.
  4. Blum AG, Zabel J-P, Kohlmann R, et al. Pathologic conditions of the hypothenar eminence: evaluation with multidetector CT and MR imaging. Radiographics. 2006;26(4):1021-1044.
  5. Smith HE, Dirks M, Patterson RB. Hypothenar hammer syndrome: distal ulnar artery reconstruction with autologous inferior epigastric artery. J Vasc Surg. 2004;40(6):1238-1242.
  6. Monacelli G, Rizzo MI, Spagnoli AM, Monarca C, Scuderi N. Ulnar artery thrombosis and nerve entrapment at Guyon’s canal: our diagnostic and therapeutic algorithm. In Vivo. 2010;24(5):779-782.
  7. Ferris BL, Taylor LM Jr, Oyama K, et al. Hypothenar hammer syndrome: proposed etiology. J Vasc Surg. 2000;31(1 pt 1):104-113.
  8. Lo H-Y, Tan S-G: Arteriovenous fistula aneurysm—plicate, not ligate. Ann Acad Med Singapore. 2007;36(10):851-853.
  9. Cooke RA. Hypothenar hammer syndrome: a discrete syndrome to be distinguished from hand-arm vibration syndrome. Occup Med (London). 2003;​53(5):320-324.
  10. Pasklinsky G, Meisner RJ, Labropoulos N, et al. Management of true aneurysms of hemodialysis access fistulas. J Vasc Surg. 2011;53(5):1291-1297.
  11. Karatepe C, Yetim TD. Treatment of aneurysms of hemodialysis access arteriovenous fistulas. Turk J Thorac Cardiovasc Surg. 2011;19(4):566-569.
  12. Balla L, Syamala G, Prasad KSN. High origin and aberrant superficial course of ulnar artery: a case report. IOSR J Dental Med Sci. 2015;14(4):7-9.
  13. Pulakunta T, Potu BK, Vollala VR, Gorantla VR, Thomas H. Co-existence of superficial ulnar artery and aneurysm of the deep palmar arch in the hand. Bratis Lek Listy. 2009;110(11):738-739.
  14. Weinand C, Akbari C, O’Donnell S. A high bifurcation of the dorsal branch with dominant superficial palmar branch of the radial artery: a case report of an aberrant radial artery with traumatic aneurysm. J Hand Microsurg. 2011;​3(2):78-81.


The authors acknowledge Shamah Iqbal, MD, for providing histopathologic information from the biopsied specimen.

NEXT: Atypical Presentation of Vertebral Artery Dissection


Atypical Presentation of Vertebral Artery Dissection

Joseph Cruz, DO; Tessa Ndille, DO; Jennifer Chan, DO; James Espinosa, MD; and Alan Lucerna, DO
Rowan University School of Osteopathic Medicine, Stratford, New Jersey


A 23-year-old woman presented to the emergency department for evaluation of right leg pain and weakness and a loss of balance. The patient described a gradual onset of symptoms, and she denied any specific acute traumatic event. She also denied having had headaches, dizziness, visual changes, neck pain, numbness, or other paresthesias. Overall, the patient denied any other constitutional symptoms.

History. The patient’s medical history was significant only for renal calculi and attention-deficit/hyperactivity disorder. She had undergone a surgical procedure of the back for scoliosis but not on her cervical spine. She denied any pertinent family history. She denied any history of smoking, alcohol use, or drug use. She had not had any recent hospitalizations, recent illness, or recent travel outside the United States.

Physical examination. The patient was afebrile, with stable vital signs all within normal limits. Pertinent physical examination findings included pinpoint pupils bilaterally, decreased right lower extremity motor strength (3/5), and decreased sensation in the right lower extremity.

Diagnostic tests. Results of a complete blood cell count and basic metabolic panel were normal, as were the thyrotropin level and the results of a coagulation profile. Computed tomography (CT) of the head was performed, the results of which showed no intracranial hemorrhage or other acute findings. 

Considering the patient’s symptoms, CT angiography of the head and neck was also performed, the results of which demonstrated no positive findings. There was no evidence of occlusion, stenosis, dissection, or aneurysm of the major cervical or intracranial arteries. Considering the patient’s persistent and concerning neurologic complaints and findings, magnetic resonance angiography (MRA) of the head and neck was performed. The results showed high signal intensity surrounding the V4 segment of the left vertebral artery, suspicious for dissection (Figure).

Figure. Magnetic resonance angiography of the neck showed left vertebral artery tapering occlusion caused by vertebral artery dissection in the V4 segment.


The patient received a diagnosis of vertebral artery dissection, which resulted in infarction of the spinal cord, leading to quadriplegia.

Outcome of the case. She was admitted to the hospital with frequent neurologic checks, neurologist consultation, and management with intravenous corticosteroids. During the patient’s stay, she underwent physical therapy, and her dosing of corticosteroids was gradually tapered down. She was eventually discharged to a long-term acute care facility.

Discussion. The presentation of vertebral artery dissection is usually preceded by a clear history of trauma, specific neurologic symptoms, and findings on CT angiography of the head and neck.

Commonly, symptoms of vertebral artery dissection represent lateral medullary dysfunction (ie, Wallenberg syndrome), in which the patient abruptly develops ipsilateral facial pain and numbness, hoarseness, dysarthria, and contralateral loss of pain and temperature sensation. Reports in the literature also describe rare presentations of medial medullary syndrome (contralateral weakness, paralysis, or numbness) and even cerebral/cerebellar symptoms such as limb ataxia, nystagmus, absence of taste, and impairment of pain sensation.1-3

Cervical dissections are the underlying etiology in as many as 20% of the ischemic strokes presenting in younger patients aged 30 to 45 years.4-6 Carotid artery dissection is 3 to 5 times more common than vertebral artery dissection.4 The female to male ratio is 3 to 1.7 Also, in contrast with atherothrombotic disease, vertebral artery dissection occurs in a much younger population.7,8

Vertebral artery dissection has been associated with a 10% mortality rate in the acute phase.7 Nevertheless, most patients who survive the initial crisis of extracranial dissection do well, with as many as 88% recovering completely.7 However, a more severely affected subgroup is patients with intracranial vertebrobasilar dissection, which is associated with subarachnoid hemorrhage, brainstem infarctions, a high mortality rate, and vertebral artery pseudoaneurysm causing compressive cranial neuropathy.9

There are no randomized, controlled studies of confirmed or suspected vertebral artery insufficiency, but the current consensus of management is anticoagulant therapy.9 This applies to patients who have no contraindications to anticoagulation, such as subarachnoid hemorrhage.9 This approach is intended to prevent embolic occlusion of the vertebrobasilar network, which could lead to subsequent infarction of posterior central nervous system structures, the brainstem, and the cerebellum. A number of published series show a good prognosis for patients who undergo anticoagulation.10

This case illustrates the importance of considering vertebral artery dissection in the presence of concerning neurologic symptoms on physical examination. While this patient did not present with the typical symptoms of vertebral artery dissection, and despite normal results of CT and CT angiography imaging studies, our patient went on to have MRA of the head and neck.11 The MRA results suggested the presence of vertebral artery dissection, a condition that ultimately resulted in infarction of her spine, leading to quadriplegia.

Especially considering the devastating implications of this condition, this case illustrates the importance of having a high clinical suspicion and to consider vertebral artery dissection in the differential diagnosis when presented with a similar ambiguous constellation of neurologic symptoms.


  1. Kim Y-K, Schulman S. Cervical artery dissection: pathology, epidemiology and management. Thromb Res. 2009;123(6):810-821.
  2. Raupp SF, Jellema K, Sluzewski M, de Kort PL, Visser LH. Sudden unilateral deafness due to a right vertebral artery dissection. Neurology. 2004;​62(8):1442.
  3. Stahmer SA, Raps EC, Mines DI. Carotid and vertebral artery dissections. Emerg Med Clin North Am. 1997;15(3):677-698.
  4. Beletsky V, Nadareishvili Z, Lynch J, Shuaib A, Woolfenden A, Norris JW; Canadian Stroke Consortium. Cervical arterial dissection: time for a therapeutic trial? Stroke. 2003;34(12):2856-2860.
  5. Norris JW, Beletsky V, Nadareishvili ZG; Canadian Stroke Consortium. Sudden neck movement and cervical artery dissection. CMAJ. 2000;163(1):38-40.
  6. Rubinstein SM, Peerdeman SM, van Tulder MW, Riphagen I, Haldeman S. A systematic review of the risk factors for cervical artery dissection. Stroke. 2005;​36(7):1575-1580.
  7. Lang ES. Vertebral artery dissection. Medscape. Updated November 7, 2015. Accessed August 9, 2016.
  8. Silbert PL, Mokri B, Schievink WI. Headache and neck pain in spontaneous internal carotid and vertebral artery dissections. Neurology. 1995;45(8):1517-1522.
  9. de Bray JM, Penisson-Besnier I, Dubas F, Emile J. Extracranial and intracranial vertebrobasilar dissections: diagnosis and prognosis. J Neurol Neurosurg Psychiatry. 1997;63(1):46-51.
  10. Lyrer P, Engelter S. Antithrombotic drugs for carotid artery dissection. Cochrane Database Syst Rev. 2003;(3):CD000255. doi:10.1002/14651858.CD000255.
  11. Provenzale JM, Sarikaya B. Comparison of test performance characteristics of MRI, MR angiography, and CT angiography in the diagnosis of carotid and vertebral artery dissection: a review of the medical literature. AJR Am J Roentgenol. 2009;193(4):1167-1174.

NEXT: Duplicated Inferior Vena Cava


Duplicated Inferior Vena Cava

Stephen Winfield, MD, and Kabir Ahmed, MS-III
Saba University School of Medicine, Saba, Dutch Caribbean

Andrew Rosenthal, MD
Memorial Regional Hospital, Hollywood, Florida


A 42-year-old male pedestrian was struck by an automobile and was brought to our trauma center. He had sustained numerous injuries, including an open left tibia and fibula fracture, an open left elbow fracture, and a closed right tibia and fibula fracture. A large right neck laceration with active hemorrhage required exploration and repair.

Following repair of the neck laceration, he underwent multiple orthopedic procedures. He remained on prolonged bed rest and was considered at high risk for venous thromboembolism. Therefore, prophylactic inferior vena cava (IVC) filter placement was recommended.

On computed tomography (CT) scans, a second IVC was noted on the left, joining the right IVC above the renal veins (Figures 1 and 2). This anatomic duplication prompted placement of 2 IVC filters (Figure 3).

Figure 1. Abdominal CT, coronal view, showing duplicated IVCs and the left renal vein emptying into the left IVC.

Figure 2. Abdominal CT, coronal view, showing the left IVC emptying into the right IVC.

Figure 3. Abdominal radiograph, anteroposterior view, showing 2 IVC filters placed in duplicated IVCs.

Discussion. Embryologic duplication of the IVC is rare.1 The IVC develops from 3 paired veins: the posterior cardinal veins, the subcardinal veins, and the supracardinal veins. The posterior cardinal veins, through which blood from the lower extremities returns to the heart, are the first to develop. Subcardinal veins then develop anteromedial to the posterior cardinal veins. Anastomoses develop between the subcardinal veins (intersubcardinal) and between subcardinal veins and posterior cardinal veins on either side of the aorta. Subsequent connections form between the right subcardinal vein and the hepatic IVC segment. The posterior cardinal veins then begin to atrophy, causing blood to be shunted through the subcardinal veins, then through the subcardinal-hepatic anastomoses, and then through the hepatic segment of the IVC. Paired supracardinal veins then develop dorsomedial to posterior cardinal veins. Anastomoses form between the posterior and supracardinal veins, as well as suprasubcardinal anastomoses. Further degeneration of the posterior cardinal veins leads to further shunting of blood through supracardinal veins and then the suprasubcardinal anastomoses.

The IVC comprises 4 segments: hepatic, suprarenal, renal, and infrarenal. The hepatic segment derives from the vitelline veins, the suprarenal segment derives from the right subcardinal vein, the renal segment derives from the right suprasubcardinal and postsubcardinal anastomoses, and the infrarenal segment derives from the right supracardinal vein.

The double IVC anomaly is due to persistence of both supracardinal veins. Most commonly, the persistence of the left supracardinal vein leads to the formation of a double IVC. Duplicated IVC has a prevalence of 0.2% to 3.0%.1 The diagnosis should be considered in cases of recurrent pulmonary embolic episodes despite IVC filter placement.

In the majority of cases, double IVC is an incidental finding on radiologic imaging.2 However, this finding can become critical in determining the medical and surgical management of patients with it. The condition complicates retroperitoneal surgical procedures in that the double IVC may be injured or ligated during the operation. It can also increase the risk of thromboembolic events.

In patients with double IVC requiring mechanical prophylaxis against pulmonary emboli, the placement of 2 IVC filters is recommended.


  1. Ng WT, Ng SSM. Double inferior vena cava: a report of three cases. Singapore Med J. 2009;​50(6):e211-e213.
  2. Sartori MT, Zampieri P, Andres AL, Prandoni P, Motta R, Miotto D. Double vena cava filter insertion in congenital duplicated inferior vena cava: a case report and literature review. Haematologica. 2006;91(6 suppl):e85-e86.

NEXT: Mycotic Aneurysm of the Abdomical Aorta


Mycotic Aneurysm of the Abdominal Aorta

Bilal Rizvi, MD; Hebert Ip, MD; William Palmer, MD; and Joseph Perras, MD
Mt Ascutney Hospital and Health Center, Windsor, Vermont


An 87-year-old man presented to the emergency department with worsening pain in his right lower back and associated right upper quadrant pain. He had been recently discharged from our community hospital after extensive workup for severe sudden-onset back pain and bacteremia. He had a past medical history significant for coronary artery disease, abdominal aortic aneurysm, peripheral vascular disease, hypertension, and chronic pancreatic cystic mass.

History. Workup during his recent stay had included an extensive physical examination; laboratory workup; magnetic resonance imaging of the thoracolumbar spine; a hepatobiliary iminodiacetic acid scan; computed tomographic angiography (CTA) of the chest, abdomen, and pelvis with iliofemoral runoff; abdominal ultrasonography; and infectious disease and surgical consultations. No source for the man’s bacteremia or back pain had been identified.

The patient’s initial blood cultures at the earlier visit had grown Bacteroides fragilis, Empedobacter brevis, Acinetobacter lwoffii, and Micrococcus species. Surveillance cultures at 48 hours were positive for B fragilis alone, which responded to meropenem. Repeated cultures were negative, and he had been discharged awaiting outpatient colonoscopy, incidental noninflammatory lung mass biopsy, and endoscopic ultrasonography.

Physical examination and diagnostic tests. At the current visit, initial workup showed recurrent gram-negative anaerobic bacteremia. On physical examination, the patient did not have a cardiac murmur, abdominal tenderness, or signs of radiculopathy or myelopathy. Due to new mild elevation in lipase and history of stable pancreatic mass, we ordered magnetic resonance cholangiopancreatography, the results of which showed a noninflammatory pancreatic mass measuring 6.2 × 4.5 cm (Figure 1, arrow B), and a new abdominal aortic saccular mycotic aneurysm with enlargement of crura and an associated 3.6 × 2.4-cm abscess in the crus of the right hemidiaphragm (Figure 1, arrow A, and Figure 2) that not been previously visualized on imaging studies. The patient received a diagnosis of mycotic aneurysm of the abdominal aorta.

Outcome of the case. A vascular surgeon was consulted and deemed the patient at extremely high risk for open surgery or endovascular repair as a result of aneurysmal involvement just proximal to the renal arteries. His lung and pancreatic mass would have required further invasive tests to rule out cancer, but the patient opted for a palliative approach.

Discussion. The majority of patients with symptomatic aortic abdominal aneurysm present with abdominal and/or back pain.1 Mycotic aneurysm may also present with similar or nonspecific symptoms, which can delay the diagnosis; therefore, a high index of suspicion is necessary.

Risk factors include arterial trauma, infection, immunosuppression, atherosclerosis, and preexisting aneurysm.2 Mycotic aneurysm should be considered in patients with bacteremia and a history of aortic aneurysm, especially in the elderly with no other etiology of back pain. Blood cultures can be negative for bacteria in as many as 54% of patients.3,4 Given our patient’s polymicrobial bacteremia, a gastrointestinal tract source was considered, but no imaging evidence supported the suspicion.

CTA is the most commonly used initial test, but magnetic resonance angiography, fluorodeoxyglucose positron emission tomography, and gallium scanning are important alternative imaging modalities in complex cases.5


  1. Cambria RA, Gloviczki P, Stanson AW, et al. Symptomatic, nonruptured abdominal aortic aneurysms: are emergent operations necessary? Ann Vasc Surg. 1994;8(2):121-126.
  2. Hsu R-B, Lin F-Y. Surgical pathology of infected aortic aneurysm and its clinical correlation. Ann Vasc Surg. 2007;21(6):742-748.
  3. Johnson JR, Ledgerwood AM, Lucas CE. Mycotic aneurysm: new concepts in therapy. Arch Surg. 1983;118(5):577-582.
  4. Kim MG, Jeon JW, Ryu IH, et al. Mycotic abdominal aortic aneurysm caused by Bacteroides thetaiotaomicron and Acinetobacter lwoffii: the first case in Korea. Infect Chemother. 2014;46(1):54-58.
  5. Fukuchi K, Ishida Y, Higashi M, et al. Detection of aortic graft infection by fluorodeoxyglucose positron emission tomography: comparison with computed tomographic findings. J Vasc Surg. 2005;42(5):919-925.