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264 Chapter 25 Prevention of deep venous thrombosis
https://t.me/med1917
derive a composite score. Once the assessment is complete, the patient is assigned to a specic risk level (Table25.2) that recommends risk-commensurate prophylaxis.
Electronic order sets can be created to mandate (with “hard stops”) that a Caprini score be completed before admission or preoperative orders are nalized, and this step can also be required after the operation and upon discharge. Order sets can be customized to automatically
display the recommended course of prophylaxis. To be clear, this sort of system mandates the calculation of scores for each patient, although it does not mandate the selection of prophylaxis. Clinicians may still opt out of pharmaco­logical prophylaxis if contraindications exist, and the sys­tem can prompt documentation for declining. This design allows electronic monitoring of protocol compliance and reasons for nonadherence to guidelines.
TABLE 25.2 Risk assessment and prophylaxis based on Caprini Risk Score
Caprini score Risk category Recommended prophylaxis Recommended duration
0 Lowest Early frequent ambulation only OR at discretion of surgical team:
compression boots OR low-dose heparin OR low-molecular-weight heparin
1–2 Low Compression boots OR low-dose heparin OR low-molecular-weight
heparin (choose 1 item)
3–4 Moderate Compression boots AND low-dose heparin OR low-molecular-weight
heparin (choose 1 medication)
5–8 High Compression boots AND low-dose heparin OR low-molecular-weight
heparin (choose 1 medication)
≥9 Highest Compression boots AND low-dose heparin OR low-molecular-weight
heparin (choose 1 medication)
of chemoprophylaxis
During hospitalization
During hospitalization
During hospitalization
7–10 days total
30 days total
Guidelines 25.0 of the American Venous Forum on prevention of deep venous thrombosis*
No. Guideline Grade
25.1 We recommend a thorough assessment of VTE risk factors among patients undergo­ing operations, upon hospital admission, and throughout the perioperative phases.
25.2 We recommend VTE risk stratication of patients prior to outpatient operations. 1
25.3 We recommend VTE risk assessment upon hospital admission for medical patients. 1
25.4 We recommend mechanical prophylaxis, including early ambulation, for the patients at lowest risk for VTE.
25.5 We recommend mechanical prophylaxis in addition to pharmacological prophylaxis for patients who have at least a moderate risk for VTE.
25.6 We suggest against extended courses of pharmacological prophylaxis beyond hospi­tal discharge for most nonsurgical patients.
25.7 We recommend extended courses of pharmacological prophylaxis for high- and highest-risk surgical patients.
25.8 We recommend against routine IVC lter placement for VTE prophylaxis. 1
* Based on guidelines of the ACCP
3,4,8
and the ACH.
34
of recommendation
1 (strong)
(strong)
(strong) 1
(strong) 1
(strong) 2
(weak) 1
(strong)
(strong)
REFERENCES
Systematic reviewGuidelines
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Quality of evidence
A (high)
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B (moderate)
B (moderate)
B (moderate)
B (moderate)
B (moderate)
B (moderate)
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P, Gani J, Smith S. Efcacy of intermittent compression devices for thromboembolic prophylaxis in major abdominal surgery: Asystematic review and meta-analysis. ANZ J Surg. 2022 Nov;92(11):2926–34.
23. Siracuse JJ, Al Bazroon A, Gill HL, Meltzer AJ, Schneider DB, Parrack I, etal. Risk factors of nonretrieval of retrievable inferior vena cava lters. Ann Vasc Surg. 2015 Feb;29(2):318–21. doi: 10.1016/j. avsg.2014.08.008. Epub 2014 Oct 13. PMID: 25308241.
24. Charalel RA, Durack JC, Mao J, Ross JS, Meltzer AJ, Sedrakyan A. Statewide inferior vena cava lter placement, complications, and retrievals: Epide­miology and recent trends. Med Care. 2018 Mar;56(3):260–5. doi: 10.1097/ MLR.0000000000000867. PMID:
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Cuschieri J, Eberhardt RT, Johnson MS, etal. Society of interventional radiology clinical practice guideline for inferior vena cava lters in the treatment of patients with venous thromboembolic disease: Developed in collaboration with the American college of cardiology, American college of Chest physicians, American college of surgeons committee on trauma, American Heart Association, society for vascular surgery, and society for vascular medicine. J Vasc Interv Radiol. 2020 Oct;31(10):1529–44.
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27. CRISTAL Study Group; Sidhu VS, Kelly TL, Pratt N, Graves SE, Buchbinder R, Adie S, Cashman K, Ackerman I, Bastiras D, Brighton R, Burns AWR, Chong BH, Clavisi O, Cripps M, Dekkers M, de Steiger R, Dixon M, Ellis A, Grifth EC, Hale D, Hansen A, Harris A, Hau R, Horsley M, James D, Khorshid O, Kuo L, Lewis P, Lieu D, Lorimer M, MacDessi S, McCombe P, McDougall C, Mulford J, Naylor JM, Page RS, Radovanovic J, Solomon M, Sorial R, Summersell P, Tran P, Walter WL, Webb S, Wilson C, Wysocki D, Harris IA. Effect of aspirin vs enoxapa­rin on symptomatic venous thromboem­bolism in patients undergoing hip or knee arthroplasty: The CRISTAL randomized trial. JAMA. 2022 Aug 23;328(8):719–27. doi: 10.1001/jama.2022.13416. PMID: 35997730; PMCID: PMC9399863.mcan
28. Droege ME, Droege CA, Philpott CD, Webb ML, Ernst NE, Athota K, Wakeeld D, Dowd JR, Gomaa D, Robinson BHR, Hanseman D, Elterman J, Mueller EW. Impact of antithrombin III and enoxapa­rin dosage adjustment on prophylactic anti-Xa concentrations in trauma patients at high risk for venous thromboembo­lism: Arandomized pilot trial. J Thromb Thrombolysis. 2021 Nov;52(4):1117–28.
29. Gates RS, Lollar DI, Collier BR, Smith J, Faulks ER, Gillen JR. Enoxaparin titrated by anti-Xa levels reduces venous throm­boembolism in trauma patients. J Trauma Acute Care Surg. 2022 Jan 1;92(1): 93–7.
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32. Van Thiel D, Kalodiki E, Wahi R, Litinas E, Haque W, Rao G. Interpretation of benet-risk of enoxaparin as comparator in the RECORD program: Rivaroxaban oral tablets (10 milligrams) for use in prophylaxis in deep vein thrombosis and pulmonary embolism in patients undergoing hip or knee replacement surgery. Clin Appl Thromb Hemost. 2009 Jul-Aug;15(4):389–94.
33. Raskob GE, Gallus AS, Pineo GF, Chen D, Ramirez LM, Wright RT, etal. Apixaban versus enoxaparin for thromboprophylaxis after hip or knee replacement: Pooled analysis of major venous thromboembolism and bleeding in 8464 patients from the ADVANCE-2 and ADVANCE-3 trials. J Bone Joint Surg Br. 2012 Feb;94(2):257–64.
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AE, Kahn SR, Beyer-Westendorf J, Spencer FA, Rezende SM, Zakai NA, Bauer KA, Dentali F, Lansing J, Balduzzi S, Darzi A, Morgano GP, Neumann I, Nieuwlaat R, Yepes-Nuñez JJ, Zhang Y, Wiercioch
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W. American society of hematology 2018 guidelines for management of venous thromboembolism: Prophylaxis for hospitalized and nonhospitalized medical patients. Blood Adv. 2018 Nov 27;2(22):3198–225. doi: 10.1182/ bloodadvances.2018022954. PMID: 30482763; PMCID: PMC6258910.
35. Krauss ES, Cronin M, Dengler N, Simon­son BG, Enker P, Segal A. Lessons learned: Using the caprini risk assessment model to provide safe and efcacious throm­boprophylaxis following hip and knee arthroplasty. Clin Appl Thromb Hemost. 2020;26:1076029620961450.
36. Pannucci CJ, Shanks A, Moote MJ, etal. Identifying patients at high risk for venous thromboembolism requiring treatment after outpatient surgery. Ann Surg. 2012;255(6). doi: 10.1097/SLA. 0b013e3182519ccf
37. Kim NE, Conway-Pearson L, Kavanah M, etal. Standardized risk assessment
and risk-stratied venous thromboembo­lism prophylaxis for patients under­going breast operation. J Am Coll Surg. 2020;230(6):947–55.
38. Macht R, Gardner I, Talutis S, Rosenkranz P, Doherty G, McAneny D. Evaluation of a standardized risk-based venous thromboembolism prophylaxis protocol in the setting of thyroid and parathyroid surgery. J Am Coll Surg. 2017;224(6):1029–35. doi: 10.1016/j. jamcollsurg.2016.12.054
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42. Razadeh R, Turgeon RD, Batterink J, Su V, Lau A. Characterization of venous thromboembolism risk in medical inpa­tients using different clinical risk assess­ment models. Can J Hosp Pharm. 2016 Nov-Dec;69(6):454–9. doi: 10.4212/cjhp. v69i6.1608.
43. Tsaplin S, Schastlivtsev I, Zhuravlev S, Barinov V, Lobastov K, Caprini JA. The original and modied Caprini score equally predicts venous thromboembolism in COVID-19 patients. J Vasc Surg Venous Lymphat Disord. 2021 Nov;9(6): 1371–81;e4.
CHAPTER
26
e
Subclavian ar
https://t.me/med1917
Management of venous thoracic
outlet syndrome
Chandu Vemuri
26.1 INTRODUCTION
Venous thoracic outlet syndrome (vTOS) is a clinical syn­drome caused by dynamic compression of the subclavian vein (SV) which can progress to deep venous thrombosis (DVT). It comprises approximately 2%–3% of all cases of TOS, which collectively include arterial, venous, or neuro­genic TOS [1].
The SV passes through the costoclavicular space, which is dened as the location where the rst rib and clavicle join the sternum and includes the costoclavicular liga­ment and subclavius tendon (Figure26.1). In patients with vTOS, as the upper extremity is progressively abducted, there is impingement on the SV. This dynamic, repetitive impingement causes trauma to the SV, resulting in chronic injury that leads to external scar tissue and intravascular scar formation with luminal loss and can progress to occlu­sion with DVT. Patients presenting with vTOS are usually 14–45years old and are otherwise healthy and physically active [2]. Clinical history often includes a history of repet­itive overhead arm use, and at times there is an inciting event of sustained overhead activity or trauma. While many patients may have the anatomic abnormality of a narrow
Anterior scalene muscl
Clavicle
First rib
tery
Subclavian vein
Costoclavicular ligament
26.1 Drawing of the anterior portion of the thoracic outlet (cos-
toclavicular junction) on the right, showing the vein at the ful­crum of the lever produced by the clavicle and rst rib. Note the proximities of the subclavian muscle and costoclavicular ligament.
(From Sanders, R.J., and Haug, C.E., Thoracic outlet syndrome: Acom­mon sequela of neck injuries. 1991, Philadelphia: JB Lippincott: 1991, page
237, with permission.)
Subclavius
muscle
costoclavicular space with dynamic venous compression, vTOS is diagnosed at the time of thrombosis of the SV. At the time of diagnosis, many patients undergo lysis, with follow-up venography demonstrating compression of the SV within the thoracic outlet. Adetailed history may reveal chronic symptoms of venous hypertension such as exer­tional heaviness and fatigue. Surgical correction focuses on decompression of the costoclavicular space through rst rib resection with or without excision of the anterior and middle scalene muscles. Surgical approaches to rst rib resection include para-clavicular, infra-clavicular, or transaxillary. Venous reconstruction may be appropriate in select patients, particularly for patients with symptom­atic venous hypertension and an anatomic abnormality of the SV not corrected by decompression alone [3]. Follow­ing surgery, systemic anticoagulation is recommended for a minimum of 3 months and may need to be extended if venoplasty becomes necessary to maintain venous patency and/or relieve venous hypertension.
26.2 DIAGNOSIS
While high suspicion for vTOS can be made based on clin­ical history and physical exam alone, the gold standard for diagnosis is a dynamic venogram (Figure26.2). Diagnostic workup can include a chest X-ray to identify bony anom­alies that may be leading to venous compression such as rst rib or clavicle fracture. Oftentimes patients will have had a CT venogram, which can reveal static compression of the SV with luminal compromise and collateral forma­tion (Figure26.3). Physical exam should include assessing for symptoms of venous hypertension, focusing on arm swelling and visible collateral veins on the arm, shoulder girdle, or chest. While patients with vTOS often present acutely with DVT, they will often recall a history of venous hypertension with progressive worsening of arm swelling and collateral vein formation that may span many years. It should be noted that ultrasound alone is often not spe­cic enough to diagnose vTOS, especially in a patient with­out any thrombotic event such as DVT or swelling. In the asymptomatic patient, isolated venous ultrasound is an unreliable indicator of vTOS, and therefore it is important to conduct a thorough history and physical examination to accurately diagnose this condition.
DOI: 10.1201/9781003328971-29
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268 Chapter 26 Management of venous thoracic outlet syndrome
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Acute thrombus is most successfully treated and cleared, while thrombus that has been present for 14 days or more is less likely to lyse due to the chronic nature of the mature clot, which may also have brotic changes [5]. Chun etal. examined the role of thrombolysis on acute thrombosis in vTOS and found improved patency (98%) in patients who underwent thrombolysis before decompression compared to those who received anticoagulation alone (74%) [6]. In this analysis, all patients underwent thrombolysis within 2
26.2 Venogram in a 20 year old baseball player showing some
recanalization of an occluded subclavian vein after 24 hours of catheter-directed thrombolysis. He underwent first rib resection 2 days later after heparin was discontinued.
26.3 3D reconstruction highlighting compression of the subcla-
vian vein in the costoclavicular space.
26.2.1 Indications for treatment
Surgical decompression is recommended for all patients with vTOS, as it offers an improved quality of life and, for most patients, freedom from lifelong anticoagula­tion. The clearest indications are for patients who pres­ent with an upper extremity DVT. Those patients should be started on systemic anticoagulation and undergo thrombolysis to restore venous patency. Following clot resolution, a dynamic venogram to conrm the diagno­sis, identify collaterals, and quantify the pressure gradi­ent is an essential next step. Some patients may present without a DVT but with chronic symptoms of venous hypertension with conrmed dynamic compression of the SV, and some of these patients may benet from sur­gical decompression [4].
26.3 THROMBOLYSIS
Axillosubclavian thrombosis is the most common clinical manifestation of vTOS. Most commonly, acute thrombo­sis requires aggressive treatment with thrombolysis, which includes instillation of a thrombolytic agent, most often tissue plasminogen activator (tPA), within the thrombus.
weeks of the thrombotic event. Therefore, a short interval from symptom onset to time of thrombolysis (recommend within 1 week) is an important determinant of treatment success and patency. The standard of care for acute DVT includes thrombolysis; however, in patients presenting with symptoms long after thrombosis occurs, thrombolysis pro­vides little benet due to the chronic nature of the clot. In these patients, decompression surgery and postoper­ative anticoagulation alone may be sufcient for patency [7]. In a series of 608 patients with axillosubclavian vein thrombosis, most of whom were treated within 6 weeks of thrombosis with thrombolysis and immediate decompres­sion, 97% had satisfactory results. However, in patients who were only treated with anticoagulation alone (no surgery), only 44% had satisfactory results, and 72% ulti­mately required surgical decompression due to symptoms. Finally, only 57% of patients presenting after 6 weeks who were treated with thrombolysis and surgery had satisfac­tory results, again highlighting the importance of immedi­ate thrombolysis and decompression after thrombosis [8].
thrombolysis begins with wire passage through the throm­bus. Conventional thrombolysis is performed using tPA at 1 mg/hr in combination with infusion of low-dose heparin. Venogram is usually performed 24hours after initiation of tPA to evaluate the effectiveness of thrombolysis. Alterna­tively, pharmacomechanical thrombolysis can be used and entails infusing the thrombus with tPA and then suction to remove the obstruction. After successful thrombolysis, sur­gical decompression should be performed within 2 weeks, as improved patency rates have been obtained after per­forming rib resection soon after thrombolysis [9, 10].
26.4 SURGICAL DECOMPRESSION
26.4.1 Para-clavicular approach
This approach allows for a complete thoracic outlet decompression and allows for concomitant venous repair if needed [11, 12]. An incision is made one ngerbreadth superior to the clavicle beginning just lateral to the ster­nocleidomastoid and ending at the medial edge of the tra­pezius muscles. The rst phase of the operation is aimed at achieving a critical view of safety. To accomplish this, the scalene fat pad is mobilized from the lateral border of the internal jugular (IJ) vein. As the dissection continues, the omohyoid muscle is divided. Then the phrenic nerve is identied running lateral to medial over the anterior sca­lene muscle. Using blunt dissection, the fat pad can be mobilized medial to lateral to the rst rib. The critical view of safety includes the IJ, the anterior scalene muscle, the phrenic nerve, the middle scalene muscle, the long thoracic
Once thrombosis has been conrmed with a venogram,
26.5 Follow-Up 269
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nerve, the brachial plexus, and the rst rib. The anterior and middle scalene muscles are then excised. Intercostal muscles are divided off of the lateral aspect of the rst rib. Then the posterior rst rib is divided with the plexus pro­tected. For the second part of the operation, an infraclavic­ular incision is made extending from the lateral edge of the sternum for 3–5cm. The pectoralis major muscle is identi­ed and then a vascular plane created between the clavic­ular and sternal components. In this space the rst rib is found, intercostal muscles removed, and then the anterior rib is divided. Then subclavius muscle tendon and costocla­vicular ligament are removed. For the third portion of the operation, an external venolysis is performed through both incisions and then a venogram done to assess for venous patency. If the vein is patent without signicant compres­sion, then the incisions are closed. However, if the patient has symptoms of venous hypertension and the vein has a high-grade stenosis or occlusion, then direct venous repair can be done with either a bovine pericardial patch angio­plasty or a venous bypass as dictated by the type of lesion.
26.4.2 Infraclavicular approach
Another operation strategy with comparable patency and complication rates when done by high-volume surgeons is the infraclavicular approach [13]. In the infraclavicular approach, only the anterior half of the rst rib is partially resected through an infraclavicular incision [14]. This is accompanied by resection of the subclavius tendon and anterior and middle scalene muscle division. For long sub­clavian vein stenoses (>2 cm), the infraclavicular incision may need to be extended medially to the midline. Optimal timing of surgical intervention relative to thrombolysis was determined by Molina etal., who compared thrombolysis followed by immediate decompression (within 2 weeks) ver­sus decompression 2 weeks to 3 months after thromboly­sis [9]. Patients in this second group received an additional round of thrombolysis in the time period leading up to sur­gery, and all patients underwent decompression through the infraclavicular approach. Strikingly, 100% of patients who underwent immediate surgery after thrombolysis had suc­cessful restoration of inow, in contrast to a 29% success rate in patients who had delayed decompression. All patients were managed postoperatively with 8 weeks of anticoagula­tion. In this series, 80% of patients also underwent venous reconstruction with vein patch at the time of decompression, which may contribute to the comparable patency rates of the infraclavicular approach with the supraclavicular approach.
26.4.3 Transaxillary approach
The transaxillary approach for vTOS is associated with low complication rates and high SV patency rates [15]. In this approach, the patient is placed in a lateral decubitus position with the affected side up. The arm and axillary are prepped and then the arm is placed in an impervious stock­inette. At our institution, we make use of an arm retractor, but an assistant can also be used. In either case, the arm should be rested every 20 minutes to prevent hyperabduc­tion injury on the nerves. Atransverse incision between the latissimus dorsi and the pectoralis major muscles is made. The incision is carried down through the clavipectoral
fascia until the edge of the chest wall is reached. In cases of vTOS, there can be signicantly large collaterals running through the axillary space. Typically, these can be preserved but may require ligation if their presence will hinder full visualization of deeper structures. Once dissection is carried down the chest wall, blunt dissection can often be carried up to the level of the rst rib. The subclavian vein can usu­ally be identied and followed to where it runs near the rst rib. The visualization is aided by narrow long retractors, but care should be taken to avoid placing this directly on the brachial plexus. At this point, the subclavian vein, ante­rior scalene muscle, and subclavian artery should be clearly visualized. The phrenic nerve will course lateral to medial and is often above the cephalad portion of the dissection, though care should be taken to identify any abnormal courses within the surgical eld. ACobb elevator is then used to separate the intercostal muscles from the anterior border of the rst rib. Once this is completed both medi­ally and laterally, the parietal pleural can also be bluntly separated from the underside of the rib, often with the backside of the Cobb elevator. Aright angle is then placed around the anterior scalene to isolate it, ensuring there are no branches of the subclavian artery, vein, or phrenic nerve within the anticipated area of dividing. The anterior scalene is then sharply divided. The Cobb or periosteal elevator can be used to divide the middle scalene off the rib, taking care not to injure the long thoracic nerve, which may be a sin­gle nerve or three separate nerves at this point. An angled long-handled rib cutter is then inserted, and the rst rib is divided rst anteriorly medial to the subclavian artery. The subclavius muscle or costoclavicular ligament may require division to allow for medial placement of the rib cutter. Once completed, the bone can be divided posteriorly with the rib cutter. Arongeur can then be used to ensure there is a smooth bone edge without impingement on the lower nerve root of the brachial plexus. Afocused venolysis of the subclavian vein can be performed with Metzenbaum scis­sors to ensure any remaining bands or compressive scars are removed to allow for full venous expansion. Once all dissection is completed and the rib is removed, the wound is lled with normal saline and the anesthesiologists are asked to perform a Valsalva maneuver to evaluate for violation of the pleura. This may be apparent if a large volume of the instilled saline is lost in the wound or if there are air bub­bles with Valsalva. If a violation is noticed, there are several mechanisms for treating, which involve placing a suction catheter through the pleural defect and evacuating the uid in the chest. Postoperatively, the timeline for restarting anti­coagulation is not well studied. In our practice, patients are maintained on aspirin for 5 days and then restart their oral anticoagulation on postoperative day 6.
26.5 FOLLOW-UP
Postoperative care after vTOS decompression should focus on returning patients to full unrestricted activity. During the acute postoperative phase, it is important to assess for complications. These include but are not limited to postop­erative hematoma, injury to the brachial plexus, injury to the phrenic nerve, lymph leak, postoperative venous throm­bosis, pneumothorax, and pleural effusion. Postoperative
26
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protocols are specic to the type of surgical decompression and can include closed suction drains and pain infusion catheters. When safe from an operative standpoint, sys­temic anticoagulation should be resumed and maintained for a minimum of 3 months from the time of DVT. Early activity is important, and in that regard inpatient physical therapy is initiated the day after the operation. After dis­charge from the hospital, the patient should be seen on a scheduled basis to assess for complications, follow prog­ress with PT, and assess for venous patency. In patients with a patent vein, 3 months out from the initial DVT, anticoagulation can be safely stopped. However, if patients have persistent or recurrent symptomatic venous lesions, it is reasonable to extend anticoagulation and/or perform endovascular venoplasty.
26.6 CONCLUSION
vTOS is an uncommon condition that can have a signif­icant impact on young, healthy patients, and therefore timely anticoagulation, lysis, and decompression can allow patients to resume full activity and be free from lifelong anticoagulation. The standard of care for treating vTOS should begin with systemic anticoagulation and thrombol­ysis within 14 days, followed by surgical decompression. The surgical approach can be either para-clavicular, infra­clavicular, or transaxillary. Specic postoperative care algo­rithms are used to minimize complications after surgery, and routine postoperative care includes anticoagulation to ensure axillosubclavian patency, as well as appropriate follow-up.
Consensus Statements 26.0 of the American Venous Forum on the management of venous thoracic outlet syndrome
No. Consensus Statements
26.1 Patients with new upper extremity DVT without an indwelling catheter or alternative cause should undergo catheter-directed thrombolysis and venography to evaluate for venous thoracic outlet syndrome.
26.2 Stent placement to reduce subclavian vein narrowing should be avoided in patients with vTOS who have not yet had a surgi­cal decompression of the thoracic outlet.
26.3 Following thrombolysis and venography, patients with identied vTOS should undergo surgical decompression of the thorac­ic outlet within 2–6 weeks to reduce the risk of recurrence.
26.4 Surgical decompression through the supraclavicular, infraclavicular, or transaxillary approaches are equally effective for vTOS, and the surgeon should choose the method with which they are the most comfortable.
26.5 Following surgical decompression, patients should resume anticoagulation to complete a 3-month total treatment course from initial diagnosis.
26.6 A longer course (6 months) of anticoagulation can be considered for patients with persistent axillosubclavian vein occlusion to allow for recanalization.
26.7 Patients with chronic, partially occlusive thrombus in the axillosubclavian vein following rst rib resection should be evaluated for venography and balloon venoplasty to restore the normal vein contour.
REFERENCES
Systematic review
1. Skirven, T.M., etal., Rehabilitation of the hand and upper extremity. 7th ed. 2020,
Philadelphia: Elsevier.
2. Cook, J.R., and R.W. Thompson, Evalua-
tion and management of venous thoracic outlet syndrome. Thorac Surg Clin, 2021.
31(1): p.27–44.
3. Samoila, G., C.P. Twine, and I.M. Wil­liams, The infraclavicular approach for Paget–Schroetter Syndrome. Ann R Coll Surg Engl, 2018. 100(2): p.83–91.
4. Bozzay, J.D., etal., Infraclavicular tho-
racic outlet decompression compared to supraclavicular thoracic outlet decom­pression for the management of venous thoracic outlet syndrome. Ann Vasc Surg,
2020. 65: p.99.
5. Suresh, V., Venous clot lysis and sten- ting.Hematol Am Soc Hematol Educ Program, 2015. 2015(1): p.210–214.
6. Chun, T.T., etal., Preoperative throm-
bolysis is associated with improved
vein patency and functional outcomes after rst rib resection in acute Paget– Schroetter syndrome. J Vasc Surg, 2022.
76(3): p.806–813, e1.
7. de León, R., etal., First rib resection and
scalenectomy for chronically occluded subclavian veins: What does it really do?
Ann Vasc Surg, 2008. 22(3): p.395–401.
8. Urschel, H.C., and A.N. Patel, Surgery
remains the most effective treatment for Paget–Schroetter syndrome: 50years’ experience. Ann Thorac Surg, 2008.
86(1): p.254–260; discussion 260.
9. Molina, J.E., D.W. Hunter, and C.A. Dietz,
Paget–Schroetter syndrome treated with thrombolytics and immediate surgery. J
Vasc Surg, 2007. 45(2): p.328–334.
10. de Kleijn, R.J.C.M., etal., Timing of tho-
racic outlet decompression after throm­bolysis for primary upper extremity deep venous thrombosis: Asystematic review.
Ann Vasc Surg, 2020. 66: p.654–661.
11. Stanley, J.C., F.J. Veith, and T.W. Wake­eld, Current therapy in vascular and
endovascular surgery. 5th ed. 2014, Philadelphia, PA: Elsevier/Saunders. xxxi, 1008 pages.
12. Maxey, T.S., etal., Safety and efcacy of
the supraclavicular approach to thoracic outlet decompression. Ann Thorac Surg,
2003. 76(2): p.396–399; discussion 399–400.
13. Madden, N., etal., Evolving strategies for
the management of venous thoracic outlet syndrome. J Vasc Surg Venous Lymphat
Disord, 2019. 7(6): p.839–844.
14. Cronenwett, J.L., and K.W. Johnston, Rutherford’s vascular surgery. 8th ed. 2014, Philadelphia, PA: Saunders/Elsevier. 2 volumes (xxxviii, 2570, lxvi pages).
15. Faber, L.L., R.L. Geary, K.Z. Chang, M.P. Goldman, J. Freischlag, and G. Velazquez, Excellent results seen with
both transaxillary and infraclavicular approaches to rst rib resection in patients with subclavian vein thrombosis.
J Vasc Surg Venous Lymphat Disord, 2023 Jan. 11(1): p.156–160.
CHAPTER
27
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Acute central venous thrombosis in the
setting of central lines, pacemaker
wires, and dialysis catheters
Justin M. Robbins, Anil Hingorani, and Enrico Ascher
27.1 INTRODUCTION
Acute central venous thrombosis (CVT) is an important topic with a global effect. It can be divided into two causes: primary or secondary. Whereas primary causes are due to effort thrombosis or thoracic outlet syndrome, secondary causes are mostly due to either malignancy or indwelling catheters. Secondary causes of thrombosis have become the most likely source of this disease process.
Acute CVT lends itself to a signicant discussion because the use of central venous access, for the placement of catheters and treatment of cardiac arrhythmias with pacing wires and debrillators, has been rapidly increasing worldwide during the last few decades. The most recent data estimate approximately 5million central venous cath­eters (CVCs) are inserted yearly in the United States and that there are over 2 million patients with pacemakers worldwide. ids, medications, blood products, and antibiotics; perform hemodialysis; monitor hemodynamics; and provide paren­teral nutrition. All of these instruments carry signicant potential to cause central venous trauma, which can lead to CVT.
Upper extremity deep vein thrombosis (UEDVT) accounts for approximately 5% of all cases of DVT, with the majority being attributed to secondary causes such as cannulation and malignancy. large prospective registry of consecutive patients with acute symptomatic deep vein thrombosis (DVT), the Com­puterized Registry of Patients with Venous Thromboem­bolism (RIETE), the authors identied the prevalence of UEDVT as 512 among 11,564 DVT patients (4.4%). They also demonstrated that 228 of those 512 UEDVT patients (45%) had catheter-related UEDVT. has been associated with complications of pulmonary embolism (PE), post-thrombotic syndrome, and death.
As a consequence, our discussion in this chapter will focus on acute CVT in the setting of upper extremity cen­tral venous lines, dialysis catheters, and pacemaker wires. The diagnosis and treatment of lower extremity DVT (LEDVT) are discussed elsewhere.
1,2
They are utilized to administer various u-
3
In a study based on the
4
Furthermore, UEDVT
5
27.2 EPIDEMIOLOGY
27.2.1 Demographics
The RIETE registry comprises the largest amount of pro­spectively collected data on patients with DVT. Its review has demonstrated that patients with UEDVT compared to patients with LEDVT are younger (54 years ± 19 vs 66years ± 17), more often male (59% vs 52%), weigh less (71 kg ± 14 vs 74 kg ± 14), have less frequent recent history of DVT (7% vs 17%), and more commonly have cancer (38% vs 20%). Tohme etal. conducted a single-center ret­rospective study of 1009 upper extremity venous duplex studies with multinomial regression, nding hypertension, chronic kidney disease, malignancy, CVC, and peripherally inserted central venous catheters (PICCs) as independent predictors of UEDVT.
In a study by Hingorani etal. in 1997, 170 patients with UEDVT were analyzed. The average age of the patients was 64 (± 17) years, they were more often females (66%), and they had a history of cancer (22%). The overall mor­tality rate in this group was 29% at 2 months. Ascher et al. conducted a retrospective study evaluating 210 UEDVT identied on duplex. They were unable to nd a correlation between site of insertion and PE or mortal­ity. However, they did note that there was a high mortality rate associated with UEDVT, and APACHE III scores were calculated for the patients, which correlated for the high observed mortality, suggesting it was a result of underlying medical problems. evaluated 48 LEDVT and 35 UEDVT, nding that UEDVT had a signicantly higher proportion of comorbidities such as CAD (25.7% vs 13.1%, p=0.16), CHF (20% vs 6.6%, p=0.09), and malignancy (60% vs 42.6%, p=0.13). They also found that UEDVT had a signicantly higher all-cause mortality than LEDVT (33.3% vs 4.9%, p=0.0119).
27.2.2 CVC-related UEDVT
In the same study, Hingorani etal., utilizing duplex ultra­sonography as part of the workup for arm swelling or
6
5
In 2005,
7
Furthermore, in 2020, Rokosh et al.
8
DOI: 10.1201/9781003328971-30
271271
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PE, found 170 patients with UEDVT. This retrospective study demonstrated concurrent CVC or pacemakers in 110 (65%) of UEDVT patients. UEDVTs were associated with CVCs ranging from 32% to 70%.
9–10
Finally, a review by Kuter demonstrated that
5
Other studies have shown
patients with CVC-related infection had a greater likeli­hood of having thrombosis than those patients without CVC-related infection, with an odds ratio of 4.1 (95% CI
1.5–11.4).
11
27.2.3 Cancer population
In 2004, Kuter evaluated CVC-related thrombosis (CRT) in the cancer population based on 12 studies with 607 patients and demonstrated that CRT occurred in 41% (range = 12–74%) of all cancer patients. The authors demonstrated a higher incidence of asymptomatic thrombi as compared to symptomatic thrombi: 29% (range 5%–62%) and 12% (range 5%–54%), respec-
11
tively.
 The same paper referenced an article in which longitudinal analysis was performed on cancer patients to evaluate the timing of thrombosis. Serial venography was performed at 8, 30, and 105 days after catheter insertion on 95 patients. The authors found that by 8, 30, and 105 days, 64%, 65%, and 66% of all CVCs were found to have thrombosis, respectively. However, in 2015 Leung et al. performed a systematic review of patient-related risk factors to determine if malignancy was associated with CRT, where he identied eight studies with a total of 1999 patients, with no effect detected in six studies. In two of the studies there was a positive association between malignancy (OR 4.1 95% CI 1.9–8.9 P ≤ 0.001) and CRT on multivariate analysis (OR 1.953 95% CI
1.014–3.761 P=0.05). They also evaluated chemother­apy as a risk factor and identied 11 studies, with ndings of 3 studies showing it was a signicant risk factor for CRT with an OR ranging from 3.19 to 4.109. Six of the studies reported no association.
12
27.3 CLINICAL PRESENTATION
The most common presentation of patients with UEDVT is asymptomatic. The symptoms of UEDVT are usually reective of the local effects of the thrombosis or embo­lization. In symptomatic patients, one or more of the fol­lowing may be present: swelling of the extremity, face and neck; pain of the extremity or neck; numbness; headache; paresthesia; engorgement of chest wall, neck, and extrem­ity veins; jaw pain; and erythema. highly variable among patients and can range from mild to debilitating. In rare cases, phlegmasia cerulea dolens has also been reported.
20
27.3.1 Pulmonary embolism
The incidence of PE is lower in UEDVT compared to LEDVT. Joffe etal. performed a prospective studyevalu­ating 324 patients with UEDVTs with CVCs and found that PE was less frequently found in UEDVT vs LEDVT (3% vs 16%, p < 0.001). attributed the risk of PE to be 5% of all UEDVT and up to
16
In another study, the authors
13–19
Symptoms can be
20% in patients with CVC-associated UEDVT,while other studies have demonstrated the risk of PE ranging between 4% and 15%.
5,21–22
Additionally, ndings from the RIETE registry have demonstrated that patients with UEDVT are associated with less severe symptoms of PE as compared to those with LEDVT (9.0% vs 29%), OR 0.24 (95% CI
0.18–0.33).
4
27.3.2 Post-thrombotic syndrome
Post-thrombotic syndrome (PTS) has been dened in stud­ies as persistent signicant swelling with pitting edema and is a known complication of UEDVT. In 2018, Thiyagara­jah etal. conducted a systematic review and meta-analysis regarding PTS with UEDVT and identied 22 studies with a total of 944 patients. The pooled proportion of PTS using a random effects model was 19.4% (95% CI 11.3–27.6). They then analyzed the recurrence of UEDVT in 37 studies with a total of 2552 patients and found the overall propor­tion of recurrent DVT was 7.5% (95% CI 4.1–10.9), with a higher proportion in secondary vs primary UEDVT (15.9 vs 6.4%).
3
27.4 RISK FACTORS
27.4.1 Risk with CVC
Risk factors for CRT can be related to patient comorbid­ities, insertion, catheter, or a combination of any of these factors. In 1970, Tilney and Grifths documented the rst series of patients with indwelling catheter-related UEDVT. Their study included 48 patients over a 25-year period who were found to have UEDVT, with 31 of 48 UEDVT (64.6%) being associated with indwelling catheters. That study forewarned the increasing incidence of such occlusions as methods for long-term central venous access become more widely used. Valeriani et al. conducted a systematic review and analyzed 20 observational stud­ies including 1473 patients receiving anticoagulation for UEDVT, with the presence of CVC being the most com­mon risk factor found (855/1407 patients [60.8%]; 16 studies).
23
In 2015, Winters etal. performed a case-cohort study of hospital-acquired VTE evaluating 64,034 admis­sions with 299 cases of VTE identied. They found that UEDVT had an incidence of 1.4 per 1000 admissions and that CVC was associated with a 14-fold increased risk of UEDVT (OR 13; 95% CI 0.8–2.1).
24
Some studies have evaluated if there is any correlation between the type of the catheter and the procedure itself. In 1988, Horattas et al. retrospectively reviewed data of all patients who presented to their facility with the diagnosis of UEDVT during a period of six years.They demonstrated that the risk of UEDVT increased with multiple punctures, large­bore catheters, the type of catheter material, and duration of placement of the catheter.
25
In 2014, Geerts identied multiple studies that found increased rates of CRT with the use of larger, multilumen, and peripherally inserted catheters in patients with cancer receiving chemother-
26
apy.
The 2013 review article by Murray etal. demonstrated a
positive correlation with patient-related risk factors includ-
19
27.4 Risk factors 273
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ing previous history of venous thromboembolism, inher­ited thrombophilia, malignancy, and presence of an acute infection.
14
Furthermore, they cited a prospective study on hematological malignancy in which CRT increased in the presence of catheter-related infection. That study was per­formed using 105 consecutive patients undergoing inten­sive chemotherapy and addressed the risk of CVC-related infection and thrombosis. All patients with clinical exam of the upper extremity suspicious for DVT underwent duplex ultrasonography or venography. The authors demonstrated the risk of thrombosis increased markedly in those with catheter-related infection compared to those without cath­eter-related infection (relative risk 17.6, 95% CI 4.1–74.1). Thus, it is prudent to understand that catheter infection has a signicant role in CVC-related thrombosis.
27.4.2 Risk with PICC
PICCs have been able to provide convenient long-term intravenous access for patients. In a retrospective analysis, the authors reviewed all upper extremity venous duplex ultrasonography examinations completed over a 1-year period at their vascular lab to identify patients with newly diagnosed UEDVT and a PICC placement ≤30 days from the examination. scans, 154 (18.5%, 138 patients) scans were positive for UEDVT. PICC-associated DVT occurred in 54 of the 154 (35%) patients with UEDVT. These 54 PICC-associated DVTs occurred among the 1862 (2.6%) patients with PICC line placement during that time period. Previous large ret­rospective studies have also demonstrated the incidence of UEDVT ranges from 1.6% to 3.5% among all PICC place­ments. This study also found that large PICC diameter (≥5 Fr) had an odds ratio of 3.9 (95% CI 1.1–13.9; P=0.037) and concurrent malignancy had an odds ratio of 4.1 (95% CI 1.9–8.9; P ≤0.001) to develop UEDVT. The authors concluded that although the percentage of PICC-associ­ated UEDVT is low, the increasing number of PICC place­ments lends itself to the overall increase in the number of patients who experience PICC-associated UEDVT. Other authors have addressed the risk of UEDVT associated with PICC as compared to other CVCs. Chopra et al. com­pleted a systematic review and documented that from the meta-analysis of 11 studies with 3788 patients, PICC lines were associated with an increased risk of DVT compared to other CVCs (OR 2.55, 95% CI 1.54–4.23; P ≤ 0.0001). The number needed to harm for PICC compared to CVC was 26 (95% CI 13–71).
In another study, PICC line diameters and ow rates were analyzed. The authors demonstrated in a uid anal­ysis model that the risk of thrombosis increased as a func­tion of catheter size. This study documented that venous ow may be reduced by up to 80% with a 6 Fr catheter. Additionally, recent prospective studies have also shown an increased rate of symptomatic DVT with increasing PICC size from 4 Fr (1.0%–2.9%) to 6 Fr (8.8%–9.8%). Recently, Walusimbi etal. performed a retrospective study evaluating 6607 trauma patients at a level 1 trauma center to identify risk factors for UEDVT in trauma patients. They found there was a higher association of UEDVT in patients who had a higher mean injury severity score (22.06 +/–
8.84 vs 18.81 +/– 9.99; p=0.014), a TBI (83% vs 54.1%;
27
They found that of the 831 completed
28
29
p ≤ 0.001), or a PICC line during their hospitalization (94.3% vs 52.5%; p ≤ 0.001).
30
While PICCs are useful in the setting of long-term IV access for patients who may require medication or nutri­tion support for weeks in the home or community setting, the risk of UEDVT should be considered. The decision for placement of PICC lines should be considered on a case-by­case basis. However, the benets of a PICC line in patients who need long-term IV access, such as decreased rate of infection, compared to central lines likely outweigh the risk of UEDVT formation. Patients with PICC lines should be monitored closely for signs and symptoms of UEDVT and treated promptly upon diagnosis.
27.4.3 Risk factors in pediatrics
A large retrospective cohort study to examine the incidence of CVC thrombosis in pediatric patients found 3.2% of CVCs were associated with thrombosis (2.8% DVT and
0.4% supercial vein thrombosis). This review examined 24 studies with 11,479 children. The study reported an incidence of 50% of all venous thromboses in children occur in those patients with CVC.They demonstrated in 815 patients with catheters that increasing age (OR 1.08, 95% CI 1.03–1.13; P=0.002), renal dialysis (OR 3.2, 95% CI 1.09–9.66; P=0.035), and diagnosis of inammatory bowel disease (IBD) or short bowel syndrome (OR 4.3, 95% CI 1.2–15.0; P=0.02) increased the risk of thrombo-
31
In addition, they found that the risk of CVC-related
sis. venous thrombosis ranges from 1.7% to 81.0% in various subgroups (such as patients with cancer, hemophilia, criti­cally ill, children with IBD, and hospitalized and outpatient settings).
27.4.4 Risk with pacemaker wires
Patients with cardiac devices such as wires for pacing or debrillation are also at signicant risk for UEDVT. The rst study to document symptomatic UEDVT asso­ciated with transvenous pacing documented 5 patients with symptomatic UEDVT of the 212 patients with pace­makers (2%). These patients were treated with anticoag­ulation and arm elevation. performed a study to document the interval of time between pacemaker placement and UEDVT by perform­ing routine duplex ultrasonography before placement and then at 3, 6, and 12 months after placement. The study demonstrated that UEDVT was seen in 34 of 145 patients (23%). Most patients were found to have UEDVT within the rst 3 months of lead implantation (20/34, 59%).
33
The study also demonstrated a relative risk of 3.8 (95% CI 1.0–15.0) for risk of thrombosis in patients with multiple leads (27.4%) as compared with a single lead (7.2%).
The study by Korkeila et al. found that pacemaker implantation induced a transient hypercoagulable state, but the patient’s degree of hypercoagulability did not pre­dict subsequent venous thromboembolism. The authors concluded that thrombosis formation with pacemaker leads was likely to involve the three components of the Virchow triad: stasis, hypercoagulability, and endothelial damage, which has been echoed by other studies.
32
More recently, van Rooden
34
27