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Thromboangiitis Obliterans Workup

  • Author: Naiem Nassiri, MD; Chief Editor: Vincent Lopez Rowe, MD  more...
 
Updated: Nov 19, 2015
 

Approach Considerations

No specific laboratory tests confirm or exclude the diagnosis of thromboangiitis obliterans (TAO), or Buerger disease.

Arteriographic abnormalities consistent with TAO are sometimes seen in limbs that are not yet clinically involved; therefore, arteriography of all four limbs may be required. Echocardiography and computed tomography angiography (CTA) should always be performed in patients thought to have TAO in order to exclude a proximal source of thromboemboli or atheroemboli as the cause of distal vessel occlusion.

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Laboratory Studies

The primary goal of a laboratory workup in patients thought to have the disease is to exclude other disease processes in the differential diagnosis. Tests often used as markers for the diagnosis of systemic vasculitis, such as the acute-phase reactants, yield negative results in patients with TAO. Tests commonly ordered include the following:

  • Complete blood count with differential
  • Liver function tests
  • Renal function tests
  • Urinalysis
  • Glucose (fasting)
  • Erythrocyte sedimentation rate
  • C-reactive protein
  • Antinuclear antibody
  • Rheumatoid factor
  • Complement
  • Anticentromere antibody
  • Scl-70 antibody
  • Antiphospholipid antibodies
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Arteriography

The hallmark angiographic findings in patients with TAO are nonatherosclerotic, segmental occlusive lesions of the small and medium-sized vessels (eg, digital, palmar, plantar, tibial, peroneal, radial, and ulnar arteries) with formation of distinctive small collateral vessels around areas of occlusion, known as corkscrew collaterals (see the image below). These corkscrew collaterals represent dilated vasa vasorum of the occluded arteries, which are now serving to provide distal perfusion, albeit at significantly higher resistance than the native vasculature.

Lower-extremity arteriogram of peroneal and tibial Lower-extremity arteriogram of peroneal and tibial arteries of patient with thromboangiitis obliterans (Buerger disease) demonstrates classic findings of multiple small and medium-sized arterial occlusions with formation of compensatory "corkscrew collaterals."

Such arteriographic findings suggest TAO but are not pathognomonic, because similar lesions can be observed in patients with scleroderma, CREST (calcinosis cutis, Raynaud phenomenon, esophageal motility disorder, sclerodactyly, and telangiectasia) syndrome, systemic lupus erythematosus, rheumatoid vasculitis, mixed connective-tissue disease, antiphospholipid-antibody syndrome, and even diabetes mellitus.

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Histologic Findings

In its acute phase, TAO is characterized by highly cellular, segmental, occlusive, inflammatory thrombi, with minimal inflammation in the walls of affected blood vessels. Secondary spread from the affected small and medium-sized arteries to contiguous veins and nerves is often observed. Microscopically, the polymorphonuclear leukocyte (PMN)-predominant inflammatory cellular aggregate may form microabscesses and multinucleated giant cells.

In the subacute phase, intraluminal thrombosis progressively organizes, but it may defer to vascular recanalization.[12] The end-stage phase of TAO is characterized by mature thrombus and vascular fibrosis.

In all three stages of the disease, the integrity of the normal structure of the vessel wall, including the internal elastic lamina, is maintained. This maintenance of structural integrity distinguishes TAO from arteriosclerosis and from other types of systemic vasculitis, in which disruption of the internal elastic lamina and the media can be extensive.

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Contributor Information and Disclosures
Author

Naiem Nassiri, MD RPVI, Instructor in Vascular Surgery, Rutgers Robert Wood Johnson Medical School; Founder and Director, Vascular Anomalies and Malformations Program, Vascular Center of New Jersey and Bristol Myers Squibb Children’s Hospital Center for Advanced Surgery

Naiem Nassiri, MD is a member of the following medical societies: American College of Surgeons, Society for Vascular Surgery, American Venous Forum, Society for Clinical Vascular Surgery, International Society for the Study of Vascular Anomalies

Disclosure: Nothing to disclose.

Chief Editor

Vincent Lopez Rowe, MD Professor of Surgery, Program Director, Vascular Surgery Residency, Department of Surgery, Division of Vascular Surgery, Keck School of Medicine of the University of Southern California

Vincent Lopez Rowe, MD is a member of the following medical societies: American College of Surgeons, American Heart Association, Society for Vascular Surgery, Vascular and Endovascular Surgery Society, Society for Clinical Vascular Surgery, Pacific Coast Surgical Association, Western Vascular Society

Disclosure: Nothing to disclose.

Acknowledgements

Matthew Carpenter, MD Program Director, Department of Internal Medicine, Department of Internal Medicine, Keesler Medical Center; Assistant Clinical Professor, Uniformed Services University of the Health Sciences, F Edward Hebert School of Medicine

Disclosure: Nothing to disclose.

E Jerry Cohn Jr, MD, FACS Vascular Surgeon, The Vein Center at Savannah Vascular Institute

E Jerry Cohn Jr, MD, FACS is a member of the following medical societies: American Medical Association

Disclosure: Nothing to disclose.

Eric J Hanly, MD Fellow, Department of Surgery, The Johns Hopkins University School of Medicine

Eric J Hanly, MD is a member of the following medical societies: American Medical Association, Association of Military Surgeons of the US, MedChi, Phi Beta Kappa, and Society of USAF Flight Surgeons

Disclosure: Nothing to disclose.

Ozanan R Meireles, MD Instructor in Surgery, Department of Surgery, Massachusetts General Hospital, Harvard Medical School

Ozanan R Meireles, MD is a member of the following medical societies: American College of Surgeons, American Society for Gastrointestinal Endoscopy, and Society of American Gastrointestinal and Endoscopic Surgeons

Disclosure: Nothing to disclose.

Brian D Peyton, MD Chief of Vascular and General Surgery, Keesler Medical Center; Assistant Professor, Department of Surgery, Associate Program Director, Department of General Surgery, Uniformed Services University of the Health Sciences, F Edward Hebert School of Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

References
  1. von Winiwarter F. Ueber eine eigenthumliche Form von Endarteriitis und Endophlebitis mit Gangran des Fusses. Arch Klin Chir. 1879. 23:202-26.

  2. Buerger L. Thrombo-angiitis obliterans: a study of the vascular lesions leading to presenile spontaneous gangrene. Am J Med Sci. 1908. 136:567-80.

  3. Espinoza LR. Buerger's disease: thromboangiitis obliterans 100 years after the initial description. Am J Med Sci. 2009 Apr. 337(4):285-6. [Medline].

  4. Malecki R, Zdrojowy K, Adamiec R. Thromboangiitis obliterans in the 21st century-A new face of disease. Atherosclerosis. 2009 Feb 12. [Medline].

  5. Salimi J, Tavakkoli H, Salimzadeh A, Ghadimi H, Habibi G, Masoumi AA. Clinical characteristics of Buerger's disease in Iran. J Coll Physicians Surg Pak. 2008 Aug. 18(8):502-5. [Medline].

  6. ICD10Data.com. 2014 ICD-10-CM Diagnosis Code I73.1. Available at http://www.icd10data.com/ICD10CM/Codes/I00-I99/I70-I79/I73-/I73.1. Accessed: May 2, 2014.

  7. Abyshov NS, Zakirdzhaev EA, Aliev ZM. [Modern aspects of diagnostics and treatment for thromboangiitis obliterans]. Khirurgiia (Mosk). 2009. 75-9. [Medline].

  8. Olin JW, Young JR, Graor RA, Ruschhaupt WF, Bartholomew JR. The changing clinical spectrum of thromboangiitis obliterans (Buerger's disease). Circulation. 1990 Nov. 82(5 Suppl):IV3-8. [Medline].

  9. Motukuru V, Suresh KR, Vivekanand V, Raj S, Girija KR. Therapeutic angiogenesis in Buerger's disease (thromboangiitis obliterans) patients with critical limb ischemia by autologous transplantation of bone marrow mononuclear cells. J Vasc Surg. 2008 Dec. 48(6 Suppl):53S-60S; discussion 60S. [Medline].

  10. Kulkarni S, Kulkarni G, Shyam AK, Kulkarni M, Kulkarni R, Kulkarni V. Management of thromboangiitis obliterans using distraction osteogenesis: A retrospective study. Indian J Orthop. 2011 Sep. 45(5):459-64. [Medline]. [Full Text].

  11. Papa MZ, Rabi I, Adar R. A point scoring system for the clinical diagnosis of Buerger's disease. Eur J Vasc Endovasc Surg. 1996 Apr. 11(3):335-9. [Medline].

  12. Graziani L, Morelli L, Parini F, Franceschini L, Spano P, Calza S, et al. Clinical Outcome After Extended Endovascular Recanalization in Buerger's Disease in 20 Consecutive Cases. Ann Vasc Surg. 2012 Apr. 26(3):387-95. [Medline].

  13. Lawrence PF, Lund OI, Jimenez JC, Muttalib R. Substitution of smokeless tobacco for cigarettes in Buerger's disease does not prevent limb loss. J Vasc Surg. 2008 Jul. 48(1):210-2. [Medline].

  14. Melillo E, Grigoratos C, De Sanctis F, Spontoni P, Nuti M, Dell'Omodarme M, et al. Noninvasive Transcutaneous Monitoring in Long-Term Follow-Up of Patients With Thromboangiitis Obliterans Treated With Intravenous Iloprost. Angiology. 2014 Jul 8. [Medline].

  15. Tavakoli H, Salimi J, Rashidi A. Reply: "Treatment-of-choice for Buerger's disease (thromboangiitis obliterans): still an unresolved issue". Clin Rheumatol. 2008 Jun. 27(6):813. [Medline].

  16. Saito S, Nishikawa K, Obata H, Goto F. Autologous bone marrow transplantation and hyperbaric oxygen therapy for patients with thromboangiitis obliterans. Angiology. 2007 Aug-Sep. 58(4):429-34. [Medline].

 
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Feet of patient with thromboangiitis obliterans (Buerger disease). Note ischemic ulcers on distal portion of left great, second, and fifth toes. Although patient's right foot is normal in gross appearance, angiography demonstrated compromised arterial flow to both feet.
Superficial thrombophlebitis of great toe in patient with thromboangiitis obliterans (Buerger disease).
Tobacco smoke stains on male patient's fingers suggest diagnosis of thromboangiitis obliterans (Buerger disease). Patient presented with small, painful ulcers on tips of thumb and ring finger.
Lower-extremity arteriogram of peroneal and tibial arteries of patient with thromboangiitis obliterans (Buerger disease) demonstrates classic findings of multiple small and medium-sized arterial occlusions with formation of compensatory "corkscrew collaterals."
Table 1. Scoring System for Diagnosis of Thromboangiitis Obliterans [11]
Positive Criterion Positive Points
Age at onset < 30 y (+2)



30-40 y (+1)



Foot intermittent claudication Present (+2)



By history only (+1)



Upper extremity Symptomatic (+2)



Asymptomatic (+1)



Migrating superficial thrombophlebitis Present (+2)



By history only (+1)



Raynaud phenomenon Present (+2)



By history only (+1)



Angiography; biopsy If typical, both (+2)



Either(+1)



Negative Criterion Negative Points
Age at onset 45-50 y (−1)



>50 y (−2)



Sex; smoking Female (−1)



Nonsmoker (−2)



Location Single limb (−1)



No lower extremity involved (−2)



Absent pulses Brachial (−1)



Femoral (−2)



Arteriosclerosis, diabetes, hypertension, hyperlipidemia Discovered 5.1-10 y after diagnosis (−1)



Discovered 2.1-5 y later (−2)



Table 2. Numerical Scores Defining Probability of Diagnosis of Thromboangiitis Obliterans
No. of Points Probability of Diagnosis of Thromboangiitis Obliterans
0-1 Diagnosis excluded
2-3 Diagnosis suspected (low probability)
4-5 Diagnosis probable (medium probability)
≥6 Diagnosis definite (high probability)
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