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304 Chapter 30 Mesenteric vein thrombosis
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30.3 Venogram example of the transjugular intrahepatic por-
tosystemic shunt (TIPS) procedure showing partially occlusive
mesenteric venous thrombus (large white arrow). The stented
communication (thin black arrows) with the inferior vena cava is
readily apparent.
30.2 Magnetic resonance imaging (MRI) example of mesen-
teric vein thrombus. Contrast-enhanced MRI of the abdomen demonstrates an acute occlusive venous thrombus (arrows) involving the superior mesenteric vein (SMV) in both cross-sec­tional
(a) and coronal (b) views. The SMV is distended with an
acute-appearing thrombus.
30.4.4 Venography
Although more invasive than the cross-sectional imaging modalities described, venography can include an assessment of mesenteric venous patency and ow direction, venous collaterals, and a comprehensive assessment of thrombus burden (Figure30.3). Pressure gradients can be measured directly, and endovascular therapies can be readily accom­plished. impaired lling of the accompanying veins, arterial spasm, and prolonged opacication of the arterial arcades, all of which provide indirect evidence supporting the diagnosis. The limitations of venography include the requirement of experienced personnel with appropriate imaging hard­ware. Additionally, the 2D image produced may overesti­mate or underestimate thrombus burden within the vessel, depending on angulation and view. The evaluation includes transfer of a potentially unstable patient to a uoroscopy suite for image acquisition, which is invasive and exposes the patient to both nephrotoxic contrast and ionizing radiation.
Selective mesenteric angiography demonstrates
In summary, there are several imaging studies to choose from in the evaluation of patients with suspected MVT. The choice involves a careful clinical assessment of the patient to determine the likelihood of MVT versus other diagnoses. For the stable patient with reasonable creati­nine clearance, contrast-enhanced CT imaging will provide considerable clinical information. For patients who are less stable, bedside duplex ultrasound will provide an assess­ment of mesenteric vascular patency; however, it requires an experienced tech comfortable with the imaging study. The ultimate choice of imaging will depend on the radiol­ogy expertise and machinery available at the institution that is caring for the patient. Discussion of the patient-spe­cic variables with the attending radiologist prior to deci­sion making is a very valuable and fruitful place to start.
30.4.5 Blood tests
Blood tests may be very helpful but are not very specic in the evaluation of patients with suspected MVT. The com­plete blood count with differentials is important for assess­ing both the hemoglobin and hematocrit to ensure that occult bleeding is not overlooked. Polycythemia rubra vera, essential thrombocythemia, leukemia, and other hemato­logic disorders that may predispose to venous thrombosis can also be screened for with this test. The white blood count will alert the physician to infections related to bowel
30.5 Treatment 305
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infarction or perforation. Elevated serum lactate levels and metabolic acidosis will help to identify those patients with a severely ischemic or infarcted bowel. Transaminase eleva­tion implies additional involvement of the portal or hepatic venous system. This is particularly relevant to the initiation of treatment with vitamin K antagonists. Fibrin D-dimer elevation may also be helpful in determining the timing of thrombosis. An acute thrombus is anticipated to be accom­panied by signicant D-dimer elevations. In the subacute or chronic setting, thrombosis evolution may no longer be associated with D-dimer abnormalities.
Thrombophilia laboratory assessment of MVT should be considered on all MVT patients. This assessment assists with choice of anticoagulant and guides duration of anti­coagulation. The timing of the laboratory prole may be a difcult decision to make. Ideally, one would obtain these types of tests once the thrombus has been appropriately treated and the patient is no longer taking warfarin or heparin. Typically, this type of testing would be performed more than 2 weeks after warfarin has been discontinued in order to maximize the test sensitivity and specicity. Even in the presence of a provoked factor such as abdominal surgery or pancreatitis, a panel should be considered, as thrombophilia is a known risk factor for MVT in these situations.
24,25
30.5 TREATMENT
30.5.1 Medical management
The appropriate treatment of patients with MVT involves multidisciplinary input from both medical and surgical ser­vices. Clinical observations suggest that immediate antico­agulation with heparin early in the course of the disease improves survival, reduces thrombus propagation, and reduces the risk of recurrence. ing is not necessarily a contraindication to anticoagulant therapy, but the risk of bleeding must be weighed against the risk of bowel infarction. This decision requires care­ful and thorough patient evaluation, including measures of bowel ischemia, thrombus burden and acuity, collateral circulation, and an assessment of bleeding risk. Although improved survival rates have been shown among patients receiving anticoagulant therapy, the need for chronic anti­coagulant therapy in these patients is less clear. Obser­vational studies suggest that chronic anticoagulant use reduces the incidence of recurrent venous thrombosis and promotes recanalization of the thrombosis and prevents its propagation. anticoagulant therapy, however, have not been dened by randomized trials. In general, anticoagulation should be continued until provoking factors have been eliminated, if possible. In those patients whose MVT can be attributed to temporary risk factors, 3–6 months of anticoagulants is likely reasonable. If genetic thrombophilia is uncovered
28
The efcacy and optimal duration of
18,26,27
Gastrointestinal bleed-
during the patient’s workup, indenite anticoagulation may be warranted.
Empiric antibiotics are often used during early treat­ment to prevent bacterial translocation. However, obser­vational data suggest there is no signicant benet in mortality with the use of empiric antibiotics. not been shown to reduce bacterial translocation, but there has been a reported increased rate of Clostridium difcile infection. Therefore, unless patients are suspected to have an intra-abdominal infection or sepsis, antibiotics should be used sparingly.
30
They have
30.5.2 Endovascular interventions
With the rise in endovascular techniques, various endo­vascular approaches to treating MVT have been reported. Endovascular therapies are generally pursued for very select patients with MVT that is early in the diagnosis, without any signs of bowel ischemia or sepsis. As such, potential candidates for these approaches are patients who do not have a surgical intervention planned and those at low risk for bleeding complications. This is generally suggested in noncirrhotic patients and patients without a malignancy, owing to the bleeding risk associated with
30
both.
Endovascular approaches have been described to be safe and effective in the available series. However, due to the relative rarity of MVT, the majority of these reports are single-center case series and are thus difcult to gen-
30,31
eralize. tion following in 75%–100% of patients and resolution of symptoms in 85%–100% of patients. However, bleed­ing complication rates vary and are poorly described. DiMunno et al. report that percutaneous treatment of MVT reduces the development of portal hypertension by 40%. randomized control trials into the benets of endovascular therapies for MVT is warranted.
treatment of MVT, there are multiple reported approaches. Access can be gained by cannulation of the portal venous system via a percutaneous transhepatic or transjugular approach. These approaches allow for mechanical throm­bectomy. Catheter-directed thrombolysis can also be performed through these routes, as well as others. Cath­eter-directed thrombolysis initiated through indirect can­nulation of the superior mesenteric artery has also been described. Additionally, if the patient is planned for sur­gical intervention and laparotomy, direct intraoperative catheterization can be achieved for thrombectomy. Pro­spective trials are needed to further investigate the safety proles of these approaches.
The available reports quote thrombus resolu-
32–34
34
Further investigation with comparative studies and
With regard to procedural technique to percutaneous
30.5.3 Surgical treatment
While the majority of patients with MVT can be treated safely with anticoagulation alone, there is a portion of
30
306 Chapter 30 Mesenteric vein thrombosis
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30.4 Computed tomography angiography shows (A) thrombus within the lumen of the superior mesenteric vein (SMV; circle) in a
patient without evidence of bowel ischemia and gestive of bowel ischemia (arrows).
(B) intraluminal thrombus in the SMV (circle) of a patient with dilated bowel, sug-
patients who require surgical exploration and bowel resec­tion. At our institution, we found that approximately 16% of patients presenting with MVT will require surgical intervention.
8
MVT accompanied by evidence of perito­nitis or bowel infarction warrants surgical intervention and resection of the involved bowel (Figure30.4). Other clinical ndings that may suggest bowel ischemia include leukocytosis, lactic acidosis, or signs of sepsis. The key to successful surgery is to resect sufcient bowel to ensure proper anastomotic healing while preserving as much viable intestine as possible. The decision-making process may be complex and may require the technical skill and expertise of a surgeon who has familiarity with operations of this type. Management is dictated by the intraoperative ndings, which range from segmental bowel ischemia to widespread mesenteric necrosis. Bowel perforation may or may not be present. Often, the surgical procedure is staged with a repeat (“second-look”) laparotomy performed 1 day later. Postoperatively, anticoagulants should be initi­ated as soon as hemostasis is adequately achieved. Throm­bectomy remains a potential treatment option for selected patients but does add to the operative time, so a multidisci­plinary approach may be helpful with this complex clinical decision making.
30.6 OUTCOMES
Mortality rates have been reported to be as high as 32% in MVT. to be less than 12%, with no signicant difference when bowel resection is required. mortality rates of MVT as high as 25%; however, these are usually in systemically ill patients who do not pres­ent in the acute setting.
28,35
One-year mortality rates have been reported
8
Some studies have reported
36–38
When patients present acutely
and there is prompt treatment, mortality rates have been reported to be as low as 1.25%. yielded improved outcomes over time results with declin­ing mortality rates.
39
Delay of diagnosis and intervention,
2
Recent reports have
postsurgical complications, and underlying malignancy carry worse prognoses. The recurrence rate of venous thrombosis in these patients is not completely clear. Although the rates are said to be increased, Kumar and Kamath reported only two recurrences among 30 patients with MVT limited to the superior mesenteric vein over a median follow-up of 18 months.
40
Recurrent throm­bosis was noted in 5 out of 39 patients with combined porto-mesenteric-splenic thrombosis during a median follow-up period of 27 months. These data suggest recur­rence rates of 5%–6% per year. Morasch etal. reported that all 22 long-term survivors of MVT (19 treated with warfarin) were thrombosis free at the last follow-up visit (mean 57.7-month period).
37
Anticoagulant treatment has been associated with an essentially unchanged rate of major bleeding, at 3.9 per 100 patient-years, but a lower rate of thrombotic events, at 5.6 per 100 patient-years. When anticoagulation was discontinued, rates were 1.0 per 100 patient-years for bleeding and 10.5 per 100 patient-years for thrombo­sis recurrence.
37
The highest rates of major bleeding and thrombotic events are reported to be cirrhotics, while the lowest rates of bleeding are observed in patients with thrombosis secondary to transient risk factors.
8,41
30.7 CONCLUSION
MVT, although less common than arterial thrombosis, remains an important cause of mesenteric ischemia. The incidence of MVT is increased in patients with underlying
References 307
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thrombophilia, malignancy, and abdominal infection or surgery. There can be considerable delay in the diagnosis of MVT because of a low degree of clinical suspicion and the nonspecic clinical presentation. CT angiography and mag­netic resonance angiography are the preferred methods for MVT diagnosis, although other imaging techniques such as duplex ultrasonography can be utilized as well. Immediate
use of anticoagulation is recommended as rst-line therapy and can improve outcomes. Surgery should be limited to patients with peritonitis or perforation, with the objective of conserving as much bowel as possible yet ensuring viable margins. The safety and efcacy of endovascular techniques for the treatment of MVT remain unknown. MVT has lower morbidity and mortality than arterial mesenteric ischemia.
Guidelines 30.0 of the American Venous Forum on mesenteric vein thrombosis
No. Guideline Grade of
30.1 For evaluation of patients with suspected mesenteric vein thrombosis (MVT), we recommend computed tomography angiography and magnetic resonance angiography.
30.2 For patients with MVT, we recommend immediate anticoagulation to improve outcomes. 1
30.3 For patients with MVT and evidence of peritonitis or perforation, we recommend surgery. 1
30.4 For patients with MVT and high-risk inherited thrombotic disorders or other permanent risk for thrombosis, we recommend long-term anticoagulation.
recommendation
1 (strong)
(strong)
(strong) 1
(strong)
30
Quality of evidence
B (moderate)
B (moderate)
B (moderate)
B (moderate)
REFERENCES
Systematic reviewGuidelines
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13. Austin SK, Lambert JR. The JAK2 V617F mutation and thrombosis. Br J Haematol. 2008 Nov;143(3):307–20.
14. Colaizzo D, Amitrano L, Tiscia GL, Scenna G, Grandone E, Guardascione MA, etal. The JAK2 V617F mutation frequently occurs in patients with portal and mesenteric venous thrombosis. J Thromb Haemost. 2007 Jan;5(1):55–61.
15. Sutkowska E, McBane RD, Tafur AJ, Sutkowski K, Grill DE, Slusser JP, etal. Thrombophilia differences in splanchnic vein thrombosis and lower extremity deep venous thrombosis in North America. J Gastroenterol. 2013 Oct;48(10):1111–8.
16. Singal AK, Kamath PS, Tefferi A. Mesen­teric venous thrombosis. Mayo Clin Proc. 2013 Mar;88(3):285–94.
17. Klar E, Rahmanian PB, Bücker A, Hauenstein K, Jauch K-W, Luther B. Acute mesenteric ischemia: Avascular emergency. Dtsch Arztebl Int. 2012 Apr;109(14):249–56.
18. Maldonado TS, Blumberg SN, Sheth SU, Perreault G, Sadek M, Berland T, etal. Mesenteric vein thrombosis can be safely treated with anticoagulation but is associated with signicant sequelae of portal hypertension. J Vasc surgery Venous Lymphat Disord. 2016 Oct;4(4): 400–6.
19. Acosta S, Salim S. Management of acute mesenteric venous thrombosis: Asystematic review of contemporary studies. Scand J Surg SJS Off organ Finnish Surg Soc Scand Surg Soc. 2021 Jun;110(2):123–9.
20. Hall TC, Garcea G, Metcalfe M, Bilku D, Dennison AR. Management of acute non-cirrhotic and non-malignant portal vein thrombosis: Asystematic review. World J Surg. 2011 Nov;35(11): 2510–20.
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21. Feldman ZM, Wang LJ, Chou EL, Latz CA, Sumpio BJ, Eagleton MJ, etal. Venous mesenteric ischemia carries high procedural burden and elevated morta­lity in patients with severe presentation. J Vasc surgery Venous Lymphat Disord. 2021 Nov;9(6):1479–87.
22. Aschoff AJ, Stuber G, Becker BW, Hoffmann MHK, Schmitz BL, Schelzig H, etal. Evaluation of acute mesenteric ischemia: Accuracy of biphasic mesen­teric multi-detector CT angiography. Abdom Imag. 2009;34(3):345–57.
23. Bradbury MS, Kavanagh P V, Bechtold RE, Chen MY, Ott DJ, Regan JD, etal. Mesenteric venous thrombosis: Diagno­sis and noninvasive imaging. Radiogr Rev Publ Radiol Soc North Am Inc. 2002;22(3):527–41.
24. Parikh M, Adelsheimer A, Somoza E, Saunders JK, Ude Welcome A, Chui P, etal. Factor VIII elevation may contribute to portomesenteric vein thrombosis after laparoscopic sleeve gastrectomy: Amulticenter review of 40 patients. Surg Obes Relat Dis Off J Am Soc Bariatr Surg. 2017 Nov;13(11):1835–9.
25. Boiko JR, Srinath AI, Cooper JD. Portomesenteric venous thrombosis in previously healthy adolescents presenting with subacute abdominal pain. Clin Pediatr (Phila). 2016 Sep;55(10):975–8.
26. Björck M, Koelemay M, Acosta S, Bastos
Goncalves F, Kölbel T, Kolkman JJ, etal. Editor’s choice—Management of the diseases of mesenteric arteries and veins: Clinical practice guidelines of the Euro­pean Society of Vascular Surgery (ESVS). Eur J Vasc Endovasc Surg Off J Eur Soc Vasc Surg. 2017 Apr;53(4):460–510.
27. Hmoud B, Singal AK, Kamath PS. Mesenteric venous thrombosis. J Clin Exp Hepatol. 2014 Sep;4(3):257–63.
28. Russell CE, Wadhera RK, Piazza G. Mesenteric venous thrombo­sis. Circulation [Internet]. 2015 May5;131(18):1599–603. https:// doi.org/10.1161/CIRCULATIO­NAHA.114.012871
30. Lewcun JA, Khatun R, Allen S, Hazelton JP, Cooper A. Patient outcomes in mesenteric venous thrombosis treated with empiric antibiotics. Am Surg. 2021 Apr;87(4):658–63.
30. Oguslu U, Uyanik SA, Cenkeri HÇ, Atli E, Yilmaz B, Gümüş B. Transhepatic pharmacomechanical thrombectomy of symptomatic acute noncirrhotic, nonmalignant portomesenteric venous thrombosis: Midterm results. AJR Am J Roentgenol. 2021 Aug;217(2):418–25.
31. Rabuf P, Vagnarelli S, Bruni A, Anto­nuccio G, Ambrogi C. Percutaneous pharmaco-mechanical thrombectomy of acute symptomatic superior mesenteric vein thrombosis. Cardiovasc Intervent Radiol. 2020 Jan;43(1):46–54.
32. Hollingshead M, Burke CT, Mauro MA, Weeks SM, Dixon RG, Jaques PF. Transcatheter thrombolytic therapy for acute mesenteric and portal vein thrombosis. J Vasc Interv Radiol. 2005 May;16(5):651–61.
33. Cai W, Li X, Shu C, Qiu J, Fang K, Li M, etal. Comparison of clinical outcomes of endovascular versus open revasculari­zation for chronic mesenteric ischemia: Ameta-analysis. Ann Vasc Surg. 2015 Jul;30(5):934–40.
34. Di Minno MND, Milone F, Milone M, Iaccarino V, Venetucci P, Lupoli R, etal. Endovascular thrombolysis in acute
mesenteric vein thrombosis: A3-year follow-up with the rate of short and long-term sequaelae in 32 patients. Thromb Res. 2010 Oct;126(4):305–8.
35. Schoots IG, Koffeman GI, Legemate
DA, Levi M, van GulikTM. Systematic review of survival after acute mesenteric ischaemia according to disease aetiology. Br J Surg. 2004 Jan;91(1):17–27.
36. Dentali F, Ageno W, Witt D, Malato A, Clark N, Garcia D, etal. Natural history of mesenteric venous thrombo­sis in patients treated with vitamin K antagonists: Amulti-centre, retrospective cohort study. Thromb Haemost. 2009 Sep;102(3):501–4.
37. Morasch MD, Ebaugh JL, Chiou AC, Matsumura JS, Pearce WH, Yao JS. Mesenteric venous thrombosis: Achan­ging clinical entity. J Vasc Surg. 2001 Oct;34(4):680–4.
38. Hedayati N, Riha GM, Kougias P, Huynh TT, Cheng C, Bechara C, etal. Prognostic factors and treat­ment outcome in mesenteric vein thrombosis. Vasc Endovascular Surg. 2008;42(3):217–24.
39. Salim S, Zarrouk M, Elf J, Gottsäter A, Ekberg O, Acosta S. Improved prognosis and low failure rate with anticoagula­tion as rst-line therapy in mesenteric venous thrombosis. World J Surg. 2018 Nov;42(11):3803–11.
40. Kumar S, Sarr MG, Kamath PS. Mesen­teric venous thrombosis. N Engl J Med. 2001 Dec;345(23):1683–8.
41. Wang L, Guo X, Bai Z, Yin Y, Xu S, Pan J, etal. Impact of asymptomatic superior mesenteric vein thrombosis on the outcomes of patients with liver cirrhosis. Thromb Haemost. 2022 Dec;122(12):2019–30.
PART
Management of chronic venous disorders
https://t.me/med1917
SUB-PART A: General considerations
Edited by Michael C. Dalsing
31 Clinical presentation and assessment of patients with venous disease
Sarah Onida, Tristan R. A. Lane, and Alun H. Davies
32 Diagnostic algorithm for chronic venous disorders
Amani D. Politano and Robert B. McLafferty
33 Compression therapy for chronic venous disease and venous ulceration
Sergio Gianesini, Leo J. Daab, Erica Menegatti, Yung-Wei Chi, Hugo Partsch, and Gregory L. Moneta
34 Drug treatment for chronic venous disease
Monika L. Gloviczki and Joseph D. Raffetto
4
https://t.me/med1917
CHAPTER
31
https://t.me/med1917
Clinical presentation and assessment
of patients with venous disease
Sarah Onida, Tristan R. A. Lane, and Alun H. Davies
31.1 INTRODUCTION
Venous presentations are among the most common com­plaints in patients seeking assessment in primary and sec­ondary care vascular clinics. signs may be nonspecic and difcult to assess. It is there­fore important to have a comprehensive understanding of the presentations of venous disease to ensure patients are diagnosed and managed appropriately.
1
Patient symptoms and clinical
31.2 THE UPPER LIMB
Vascular disorders of the upper extremity are less common than in the lower limb, affecting approximately 10% of the population. importance in day-to-day activities. Furthermore, the vas­cular tree of the upper limb plays an important role in individuals with chronic disease, for example, with respect to the formation of arteriovenous stulae for dialysis or for the administration of long-term intravenous therapy. Venous pathology affecting the dominant arm can be life changing for an individual and can potentially cause con­siderable disability.
31.2.1 Trauma
Acute trauma and repetitive micro-trauma can both result in vascular disorders of the upper limb. This is particularly prevalent in middle-aged males employed in manual labor or young males involved in acute traumatic injury. Individ­uals working with handheld vibrating tools may be subject to chronic micro-trauma.
31.2.2 Intermittent subclavian/upper
Although uncommon, compression of the subclavian vein can result in intermittent symptomatology, including intermittent swelling, discomfort, and tightness (relieved by rest) and abnormally prominent supercial veins. These symptoms are aggravated in the erect position or when the arm is raised (e.g., when typing, driving, or painting a ceiling).
2
The upper limb is clearly of paramount
extremity vein obstruction
Thoracic outlet syndrome (TOS) may present in this
3
manner, rib, a congenital brous band compressing neurovascular structures, or compression at the costoclavicular junction. TOS may be neurological or vascular in nature accord­ing to the structure compressed: the brachial plexus and subclavian artery in the interscalene triangle or the sub­clavian vein in the costoclavicular space. Patients with these symptoms should be evaluated with their shoulders in the neutral position and in specic stress tests to elicit signs and symptoms. These include braced in the military position (Figure 31.1) or with arms hyperabducted and externally rotated at the shoulder (Figure 31.2), as this will result in the subclavian vein being compressed by the scissor-like closure of the costoclavicular space. Arm dis­comfort, swelling, and venous distension in this position suggest intermittent venous outow obstruction. However, as with arterial thoracic outlet obstruction, these ndings can be reproduced in approximately 50% of asymptomatic individuals at the extremes of movement. vers are useful in assessing patients but have been reported to have low sensitivity and specicity. thrombosis is a likely outcome of intermittent obstruction, active investigations with a view to surgical decompression are indicated.
usually secondary to the presence of a cervical
4
These maneu-
5
As subclavian vein
31.2.3 Subclavian/upper vein thrombosis
31.2.3.1 Primary upper extremity deep venous thrombosis
Deep venous thrombosis (DVT) can arise as a result of hypercoagulable disorders or acute or recurrent trauma to a blood vessel.
Paget–Schroetter syndrome (effort vein thrombosis) describes a syndrome of axillosubclavian vein thrombosis associated with repetitive upper limb activities. The syn­drome is due to repeated trauma to the endothelium of the subclavian vein, which may be secondary to the presence of the anatomical abnormalities, leading to the development of venous TOS. This syndrome is more common in young, healthy men undertaking manual work, preferentially involving the dominant arm. Patients are usually symptom­atic, presenting with arm discomfort, pain, swelling, and dilated veins across the shoulder and upper arm (Urschel
DOI: 10.1201/9781003328971-35
311311
312 Chapter 31 Clinical presentation and assessment of patients with venous disease
retraction of shoulder
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Backward and downward
31.1 Compression of the subclavian vein in the military position. When the shoulder is retracted backward and downward, the sub-
clavian vein is narrowed by the scissoring action of the clavicle and the rst rib.
Source: (Adapted from Adams JT et al. Surgery 1968;63:147–65.)
31.2 Compression of the subclavian vein with hyperabduction of the arm. With hyperabduction and external rotation of the arm, the
clavicle rotates backward and downward and causes compression of the subclavian vein secondary to narrowing of the costocla­vicular space.
Source: (Adapted from Adams JT et al. Surgery 1968;63:147–65.)
sign).6 The arm may be pale, cyanotic, or red. Patients usually present acutely or subacutely, with sudden onset of symptoms. Often, patients can identify a precipitating event, such as a sports injury.
Pulmonary embolism (PE) following upper extremity DVT (UEDVT) has been reported to occur in 2%–35% of individuals.
7
Post-thrombotic syndrome, characterized by chronic pain, heaviness, and swelling, develops in up to 45% of individuals with UEDVT, while recurrent thrombosis is affects up to 9.8% at 3 years. of UEDVT in young men and its preferential involvement of the dominant arm, this can lead to considerable functional disability and a profound impact on quality of life.
Compression ultrasound with duplex assessment is a recommended initial investigation. Formal venography is the gold-standard diagnostic modality; however, due to its invasive nature, this is not usually performed as a
8
Considering the prevalence
9
rst investigation. Contrast computed tomography (CT) venography provides a noninvasive option to permit the assessment of venous anatomy. Further imaging modal­ities, including cervical spine radiography and magnetic resonance imaging (MRI), can reveal bony or soft tissue abnormalities that may have caused the DVT.
The initial management comprises anticoagulation. In highly symptomatic patients, thrombus removal strategies can be considered, including catheter-directed or pharma­comechanical catheter-directed thrombolysis (CDT and PCDT) with or without venoplasty followed by surgery for thoracic outlet decompression in selected cases.
10
31.2.3.2 Secondary UEDVT
DVT can result from direct trauma to the vessel—this can be iatrogenic or secondary to central venous cannulation, catheterization, or pacemaker insertion. Central venous
31.2 The upper limb 313
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catheters present a signicant risk of thrombosis, which is reported to occur in 14%–18% of cases. Recurrent intervention to the central veins can lead to stenosis and thrombosis. Unlike primary UEDVT, the onset of obstruc­tion is gradual with recurrent intervention. Patients, there­fore, have time to develop a collateral circulation and be asymptomatic. When present, the symptoms may be vague shoulder or neck discomfort or arm edema. Alternatively, patients can present with a nonfunctioning line; venous duplex imaging or a “linogram” (contrast injection) can reveal the thrombosis. Treatment involves thrombolysis if the thrombus is extensive, or simply removal of the line and anticoagulation. Lines should be placed, if possible, in the internal jugular, cephalic, or external jugular vein, as chronic venous scarring with narrowing (stenosis) is par­ticularly common following direct subclavian vein cannu­lation. A history of central venous cannulation is important in patients being considered for hemodialysis access and/or arterial reconstruction using an upper limb venous conduit due to the possibility of stenosis, especially in case of prior subclavian vein usage. If present, postoperative limb swell­ing may result in considerable patient morbidity.
31.2.3.2.1 Superficial venous thrombophlebitis
Supercial venous thrombophlebitis (SVT) is characterized by localized pain, redness, and swelling over a segment of a supercial vein. Iatrogenic injury, secondary to venous cannulation, is the most common cause, and is usually self-limiting. In some cases, the disease can be recurrent and persistent. Spontaneous thrombophlebitis, especially if recurrent, may be associated with malignant disease or thrombophilia. Upon examination, palpation will reveal tenderness over an underlying thrombus in the vein, with surrounding induration and erythema. If the thrombus is localized and not infected, there may be considerable distal swelling. Thrombus propagation to the deep veins is rare. A history of thrombophlebitis is important, as it may have important consequences for venous access and the utility of an arm vein for arterial bypass.
31.2.3.2.2 Phlegmasia cerulea dolens
This affects the upper limb very rarely and tends to occur in patients with advanced malignancy, often being treated with chemotherapy via an indwelling central venous cath­eter. Phlegmasia is characterized by extensive thrombosis affecting not only the major veins but also the venules and the microcirculation. It is characterized by severe pain associated with intense swelling and discoloration of the affected limb. Development of compartment syndrome is a potential complication and may even progress to venous gangrene requiring amputation. Further complications include PE and death.
31.2.3.2.3 Post-thrombotic syndrome
Post-thrombotic syndrome (PTS) is reported in 30%–70% of patients following a primary subclavian vein thrombosis and consist of chronic discomfort, heaviness, and swell­ing, particularly in positions that compress collaterals in the costoclavicular space. However, the skin changes com­monly found in the lower limb are extremely rare. PTS in the upper limb is more commonly associated with unpro­voked primary DVT than secondary DVT.
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31.2.3.2.4 Arteriovenous malformations
These can be frequently misdiagnosed and are associated with localized limb hypertrophy. Examples include Klip­pel-Trenaunay syndrome (KTS) and Parkes Weber syn­drome (PWS); they usually affect the lower limb and are discussed in further detail in the next section.
31.2.4 Examination findings
31.2.4.1 Inspection
Simply inspecting the arm and comparing it with the con­tralateral limb can yield useful clinical information. The examination process can help eliminate arterial, lymphatic, orthopedic, or rheumatologic pathology from the differen­tial diagnoses.
Inspection should aim to identify the following: swell­ing, hypertrophy, discoloration, pallor, venous collaterals, prominent veins, scars and/or puncture sites, evidence of previous trauma, presence of indwelling catheters, and peripheral venous catheters.
31.2.4.2 Palpation
This can help determine:
1. Differences in temperature
2. Tenderness over an inamed supercial vein or in the
supraclavicular fossa
3. Evidence of obstructing pathology in the axilla and/or
supraclavicular fossa (e.g., enlarged lymph nodes or a palpable cervical rib)
4. Hard and “cordlike” veins suggesting previous throm-
bophlebitis
5. Presence of a full complement of pulses; presence of any
abnormal pulsations, either venous or arterial (arterio­venous stula or malformation)
6. Presence of a palpable thrill
7. Presence of pitting edema
8. Allen test to conrm the arterial inow to the hand and
completeness of the palmar arch
31.2.4.3 Percussion
The presence of incompetence can be grossly assessed by the “tap test” of Chevrier. This is performed with the patient standing. One hand is placed on the proximal thigh, tap­ping dilated veins, while the other feels for a transmitted impulse in the veins of the lower leg. Venous return should ow from the foot to the groin. A palpable thrill in the lower leg veins is suggestive of continuity in the column of blood, implying the presence of nonfunctional valves and, therefore, venous incompetence.
31.2.4.4 Auscultation
Listen for a continuous machinery murmur, which might indicate an arteriovenous malformation.
31.2.4.5 Additional steps
The blood pressure should be measured in each arm, and a full neurovascular examination should be performed. If the arm is swollen, the examination should include the axilla for lymphadenopathy and the breast to exclude
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