Central Venous Access via Subclavian Approach to the Subclavian Vein

Overview

First described in 1952, central venous catheterization, or central line placement, is a time-honored and tested technique of quickly accessing the major venous system. Its benefits over peripheral access include greater longevity without infection, line security in situ, avoidance of phlebitis, larger lumens, multiple lumens for rapid administration of combinations of drugs, a route for nutritional support, fluid administration, and central venous pressure monitoring.

Central line equipment is depicted in the image below.

Central venous catheter equipment. Image courtesy of Wikimedia Commons.

Overall complication rates range up to 15%,[1, 2, 3, 4] with mechanical complications reported in 5-19% of patients,[5, 6, 7] infectious complications in 5-26%,[1, 2, 4] and thrombotic complications in 2-26%.[1] These complications are all potentially life-threatening and, invariably, consume significant resources to treat. Placement of a central vein catheter is a common procedure, and house staff require substantial training and supervision to become facile with this technique. A physician should have a thorough foreknowledge of the procedure and its complications before placing a central vein catheter.

Compared to femoral site access, internal jugular or subclavian access has been associated with a lower risk of catheter-related bloodstream infections in earlier studies, but newer studies (2008-2010) indicate that there is no difference in the rate of catheter-related bloodstream infections between these three sites.[8]

The advent of bedside ultrasonography has changed the overall technique of the placement of central venous catheters in both the internal jugular and femoral veins, but the subclavian approach remains the most commonly used blind approach. Its advantages include consistent landmarks, increased patient comfort, and lower potential for infection or arterial injury compared with other sites of access. The physician’s experience and comfort level with the procedure, however, are the main determinants as to the success of the line placement in cases with no other patient-related factors that may increase the incidence of complications.

NextIndicationsVolume resuscitationEmergent venous accessNutritional supportAdministration of caustic medications (eg, vasopressors)Central venous pressure monitoringTransvenous pacing wire introductionHemodialysisPulmonary artery catheterizationPreviousNextContraindicationsAbsolute contraindications to central venous access Distorted local anatomy (eg, vascular injury, prior surgery, radiation history)Infection at insertion siteRelative contraindications to central venous access Presence of anticoagulation or bleeding disorderPatient who is excessively underweight or overweightUncooperative patientCurrent or possible thrombolysisAbsolute contraindications to the subclavian approach Trauma to the ipsilateral clavicle, anterior proximal rib, or subclavian vesselsCoagulopathy (Direct pressure to stop bleeding cannot be applied to the subclavian vein or artery due to their location beneath the clavicle.) Relative contraindications to the subclavian approach Chest wall deformityChronic obstructive pulmonary disease (COPD)PreviousNextAnesthesiaLocal anesthesia using 1% lidocaine is required.For more information, see Local Anesthetic Agents, Infiltrative Administration.PreviousNextEquipmentCentral venous catheter tray (line kit)Sterile glovesAntiseptic solution with skin swabSterile drapes or towelsSterile gownSterile saline flush, approximately 30 mLLidocaine 1% (obtain additional vial of lidocaine 1% if needed)GauzeDressingScalpel, No. 11PreviousNextPositioningPlace the patient in the supine position.If possible, the bed should be raised to a comfortable height for the operator so bending over is unnecessary.Do not place towels between the shoulder blades or turn the head, as this has been shown to decrease the size of the subclavian vein.[5] Place the patient in 15 º of Trendelenburg position to reduce the risk of air embolism. Increasing this angle does not improve vessel distention as the subclavian vein is fixed within surrounding tissue. Needle insertion site options include the following: One centimeter inferior to the junctions of the middle and medial third of the clavicleInferior to the clavicle at the deltopectoral grooveJust lateral to the midclavicular line, with the needle perpendicular along the inferior lateral clavicleOne fingerbreadth lateral to the angle of the clavicleSternal notch: Direct the insertion needle toward this target in the coronal plane.PreviousNextTechniqueExplain the procedure, benefits, risks, and complications and obtain a signed informed consent.Position the patient.Identify landmarks.Open the line kit, and position the equipment so it is easy to reach. One may want to retract the curved J-tip wire into the plastic loop sheath for easy directing into the introducer needle. Also, uncap the distal lumen, which is commonly the brown lumen. Prepare the insertion site with the iodine or alcohol solution provided in the kit. This amount of preparation is often inadequate, and a wide area around the insertion site should be liberally prepared with 4 x 4 cm gauze soaked in a povidone iodine solution (e.g., Betadine). Prepare the neck as well, in case the subclavian approach fails and another approach must be attempted. Put on sterile mask, gown, and gloves.Drape the patient in a sterile fashion, with the insertion site exposed.Using a generous amount of lidocaine 1%, infiltrate the skin, subcutaneous tissue, and, possibly, the clavicular periosteum.Position the bevel of the introducer needle in line with the numbers on the syringe. Upon insertion, orient the bevel to open caudally, which facilitates smooth caudal progression of the guide wire down the vein toward the right atrium. Insert the introducer needle at the desired landmark while gently withdrawing the plunger of the syringe. Advance the needle under and along the inferior border of the clavicle, making sure the needle is virtually horizontal to the chest wall. Once under the clavicle, the needle should be advanced toward the suprasternal notch until the vein is entered. If the vein is difficult to locate, remove the introducer needle, flush it clean of clots, and try again. Change insertion sites after 3 unsuccessful passes with the introducer needle. When venous blood is freely aspirated, disconnect the syringe from the needle, immediately occlude the lumen to prevent air embolism, and reach for the guide wire. Insert the guide wire through the needle into the vein with the J-tip directed caudally to improve successful placement into the subclavian vein. If using a kit that allows for the wire to be placed directly through a port on the syringe, then it is not necessary to disconnect the syringe. Beware that disconnecting the syringe gives the added benefit of allowing verification of nonpulsatile flow of venous blood. Advance the wire until it is mostly in the vein or until ectopy is seen on the cardiac monitor. Then, retract the wire 3-4 centimeters. Holding the wire in place, withdraw the introducer needle and set aside.Use the tip of the scalpel to make a small stab just against the wire to enlarge the catheter entry site.Thread the dilator over the wire and into the vein with a firm and gentle twisting motion while maintaining constant control of the wire. After the introducer is inserted, hold the wire in place and remove the dilator. Thread the catheter over the wire until it exits the distal (brown) lumen and grasp the wire as it exist the catheter. Continue to thread the catheter into the vein to the desired length. Hold the catheter in place and remove the wire. After the wire is removed, occlude the open lumen.Attach a syringe with some saline in it to the hub and aspirate blood. Take needed samples and then flush the line with saline and recap. Repeat this step with all lumens. Verify line placement with chest radiograph. The tip of the line should end in the vena cava at the manubriosternal angle, not in the right atrium. Suture the catheter in place. For patient comfort, the clinician may need to infiltrate this area prior to suturing.Apply a clean dressing.PreviousNextPearlsThe key to a successful line placement is meticulous preparation and setup before starting or donning sterile garb.Prepare a sterile site from the jaw to several fingerbreadths below the clavicle.The amount of lidocaine provided in most kits is often inadequate. The authors recommend supplementing the kit with a 10-mL syringe and a bottle of 1% lidocaine. If the wire does not pass easily through the needle down the vein, remove the wire, reattach the syringe, and confirm that the needle is still in the lumen of the vein before reattempting. Beware a return of red pulsatile blood. If this occurs, the wire is in an artery.Beware aspirating air bubbles through the probing introducer needle. This indicates a pneumothorax. (For details, see Medscape Reference article Tube Thoracostomy.) Anesthetize the suture site as well as the insertion site.Some clinicians find it useful to remove the contents of the line kit and lay them out in the order and configuration that they will be used. Never place equipment on a patient.Antibiotic ointments are contraindicated. Transparent dressings are not beneficial.Choose the central line with the fewest number of lumens required; increasing the number of lumens has been shown to increase infection rates.[9] To date, ultrasonographic guidance has mainly been used in a "mark & go" fashion to identify points of insertion and in this usage may not improve the overall success rate of placement as it does for both the femoral and internal jugular vessels. However, a ICU-based prospective, randomized study suggested that real-time ultrasonographic guidance in sedated and ventilated patients was useful for the subclavian approach in the hands of experienced operators.[10] Further studies are needed to confirm these results and to evaluate the success of educational methods for learning this technique. PreviousNextComplications

The table below shows complication rates for the various approaches.

Table 1. Complication Rates of Central Venous Catheterization Approaches[6, 11, 7] (Open Table in a new window)

Internal Jugular Subclavian Femoral Arterial puncture6.3-9.13.1-4.99.0-15.0Hematoma1.2-2.13.8-4.4HemothoraxN/A0.1-0.6N/APneumothorax1.5-3.1N/AThrombosis7.61.921.5Total6.3-11.86.2-10.712.8-19.4Local site or systemic infection: Multiple studies have shown lower infection rates with the use of maximal sterile-barrier precautions, including mask, cap, sterile gown, sterile gloves, and large sterile drape. This approach has been shown to reduce the rate of catheter-related bloodstream infections and to save an estimated $167 per catheter inserted.[6] Arterial puncture: Lacerating the subclavian artery is theoretically possible, but the risk of this complication is higher with other approaches. The subclavian artery cannot be compressed; so, the subclavian approach should be avoided in anticoagulated patients. Hematoma: A hematoma usually requires monitoring only.Hemothorax: Check the chest radiograph for evidence of a hemothorax. If evidence is found, consult a surgeon immediately.Pneumothorax: Check a chest radiograph when finished or before switching to the contralateral side after failed insertion on one side. Catheter-related thrombosis: This complication may lead to pulmonary embolism.Air embolism: An air embolism may be caused by negative intrathoracic pressure, with inspiration by the patient drawing air into an open line hub. Be sure the line hubs are always occluded. Placing the patient in the Trendelenburg position lowers the risk of this complication. If air embolism occurs, the patient should be placed in Trendelenburg position with a left lateral decubitus tilt, which may prevent the movement of air into the right ventricle and onward into the left side of the heart. One hundred percent oxygen should be administered to speed the resorption of the air. If a catheter is located in the heart, aspiration of the air should be attempted. Dysrhythmias: Dysrhythmia is due to cardiac irritation by the wire or catheter tip. This can usually be terminated by simply withdrawing the line into the superior vena cava. Placing a central venous catheter without a cardiac monitor is unwise. Atrial wall puncture: This complication leads to pericardial tamponade.Lost guide wire: If the clinician is not conscientious about maintaining control of the guide wire, it may be lost into the vein and require retrieval by interventional radiology. Anaphylaxis: Patients who are allergic to antibiotics may experience anaphylaxis upon insertion of an antibiotic-impregnated catheter. Catheter tip too deep: Check for this complication on the postprocedure chest radiograph, and pull the line back if the tip disappears into the cardiac silhouette. Catheter in the wrong vessel: When the subclavian catheter is not in the correct position, it most often deviates cranially up the internal jugular instead of down the subclavian vein. Flushing 10 mL of saline through the distal port and palpating the neck for a thrill can help to detect misplaced subclavian venous catheters into the ipsilateral internal jugular.[12] Chylothorax: This complication is possible on the left side.PreviousNextCommon Errors in Technique

Kilbourne and colleagues analyzed failed subclavian catheter placement attempts by resident physicians in an effort to describe common technical errors and to direct future teaching strategies. Subclavian cannulations were videotaped. Analysis of 86 patients revealed 6 common errors in technique that occurred in the following frequencies over 277 attempts.[13]

Table 2. Common Errors in Technique (Open Table in a new window)

Error Percent of Failures (n = 277) Inadequate landmark identification14.7Improper insertion position32.3Insertion of needle through periosteum21.9Taking too shallow a trajectory with needle16.1Aiming the needle too cephalad7.5Failure to keep needle in place for wire passage7.5Previous, Central Venous Access via Subclavian Approach to the Subclavian Vein

Read More

Subclavian Vein Thrombosis

Background

Sir James Paget first described thrombosis of the subclavian veins in 1875.[1] He coined the name gouty phlebitis to describe the spontaneous thrombosis of the veins draining the upper extremity. He observed that the syndrome was accompanied by pain and swelling of the affected extremity. However, he incorrectly attributed the syndrome to vasospasm. In 1884, von Schrötter postulated that this syndrome resulted from occlusive thrombosis of the subclavian and axillary veins.[2] In recognition of the work of these pioneers, in 1949, Hughes coined the term Paget-von Schrötter syndrome.[3] A related condition is thrombosis of the subclavian vein that is induced by the presence of indwelling catheters. The incidence of this condition has increased remarkably over the past two decades because of the extensive use of catheters in patients with cancer and other chronic medical conditions.

See the images below.

This figure shows the area where the subclavian vein is obstructed in the neck area. The vein is usually compressed by the first rib, clavicle, and serratus anterior muscle. A venogram in a patient with subclavian vein obstruction. Long-standing obstruction causes development of collaterals. Recanalization after thrombolytic therapy and stent placement. Patient underwent first rib resection and scalenectomy later. NextHistory of the Procedure

Patients may describe a history of trauma or, more frequently, strenuous use of the arm (>50% of cases). Common precipitating activities involve repeated hyperabduction and external rotation of the arm or backward and downward rotation of the shoulder. Causative activities may include participating in cricket, tennis, wrestling, lifting weights, water polo, gymnastics, baseball, or chopping wood. Because the symptoms of subclavian stenosis are fairly dramatic, most patients present promptly to the emergency department, usually within 24 hours. They may report dull ache in the shoulder or axilla, and the pain often is worsened by activity. Conversely, rest and elevation often relieve the pain. Patients with catheter-associated axillary subclavian deep vein thrombosis (ASDVT) report similar symptoms of the ipsilateral arm or shoulder with the indwelling catheter.

PreviousNextEpidemiologyFrequency

Prior to 1967, thrombosis of the axillary or subclavian vein accounted for 1-2% of all cases of deep vein thrombosis. Since then, the incidence has risen due to the more frequent use of central venous access for multiple clinical conditions. Among patients with effort-induced thrombosis with subclavian vein stenosis, the thrombosis occurs in the dominant arm in 80% of cases.

PreviousNextEtiology

The primary etiology is referred to as effort-induced thrombosis or Paget-von Schrötter syndrome. It usually results from the excessive use of the involved arm by predisposed individuals.

The secondary etiology is subclavian vein catheterization, especially in patients with cancer. (For detailed descriptions of catheterization techniques, see Central Venous Access, Subclavian Vein, Subclavian Approach and Central Venous Access, Subclavian Vein, Supraclavicular Approach.) Other causes include transvenous pacemakers, factor V Leiden mutation, protein C deficiency, protein S deficiency, antithrombin III deficiency, and prothrombin 20210A mutation. Long-term parenteral nutrition and use of hemodialysis catheters account for some cases of subclavian vein thrombosis.[4] Trauma is only rarely associated with this syndrome.

In a few cases, the diagnosis remains unknown. However, routine follow-up with these patients has revealed the development of lung cancer within 1 year of follow-up. The most common lung malignancy associated with subclavian thrombosis has been the Pancoast tumor.

PreviousNextPathophysiology

During long term venous catheterization of the subclavian and internal jugular vein in cancer patients, the risk of complications appear to be similar. However, for short term catheterization, subclavian vein catheterization is recommended because of the decreased risks of thrombotic complications and catheter colonization by skin flora. For patients requiring hemodialysis, both the femoral and internal jugular veins appear to have similar thrombotic complications. However, the risk of mechanical complications via the internal jugular vein appear to be higher. The subclavian vein should be avoided for both long and short term hemodialysis as the risk of thrombosis is very high.[5]

Differentiating catheter-associated subclavian vein thrombosis and Paget-von Schrötter syndrome is important because they appear to have different natural histories.

Paget-von Schrötter syndrome

It sometimes is referred to as spontaneous axilla-subclavian vein thrombosis to express the usually dramatic unexpected presentation of the disorder in otherwise healthy, generally young individuals. Over the past 2 decades, recognition has grown that the disorder can occur equally in both sexes and can affect all age groups. In the 1960s, the term effort-induced thrombosis was used to describe this disease to acknowledge that it often follows unusually strenuous use of the arm or shoulder on the affected side.

The pathophysiology of effort-induced thrombosis is multifactorial. It involves compressive changes in the vessel wall, stasis of blood, and hypercoagulability. External compression of the axillary-subclavian vein has been suggested to contribute to the stasis of blood that engenders thrombosis.

The factors that cause external compression include (1) anomalous subclavius or anterior scalene muscle, long transverse process of cervical spine, cervical rib, abnormal insertion of the first rib, congenital fibromuscular bands, or narrowing of the costoclavicular space from depression of the shoulder; (2) stress from exercise temporarily causing hypercoagulability; and (3) repetitive shoulder-arm motion causing microscopic intimal tears in the vessel wall. These factors, taken together, satisfy the classic Virchow triad for thrombosis. Furthermore, coexistent hematologic abnormalities that can contribute to thrombosis include protein C deficiency, antithrombin III deficiency, factor V Leiden mutation, and prothrombin 20210A mutation.

Catheter-induced subclavian vein thrombosis

Introducing catheters and transvenous pacemakers in to the subclavian vein alters the venous flow and increases turbulence. This results in platelet aggregation, release of procoagulants, and, ultimately, fibrin deposition. This causes a further reduction in the lumen of the vessel due to thrombus formation, which eventually culminates in total vessel occlusion. Intravenous medications and even parenteral nutrition have been known to cause thrombophlebitis. In patients with cancer, an additional contributing factor is that the tumor may generate procoagulant factors, predisposing to thrombosis at sites remote from the tumor.

PreviousNextPresentation

Not all patients with subclavian vein thrombosis are symptomatic. Those with symptoms may present with mild-to-moderate nonpitting edema and mild cyanosis of the hands and fingers on the affected side. Dilatation of subcutaneous collateral veins may be present over the upper arm and chest. This later sign may be the only clue to ASDVT in otherwise asymptomatic patients with catheter-related venous thrombosis. In a few cases, in which the diagnosis was missed or delayed or the patient presented late, the thrombus may have extended to the superior vena cava. These patients show most features of the superior vena cava syndrome, including face and neck swelling, periorbital edema, blurred vision, and some degree of facial cyanosis.[6]

PreviousNextIndications

In patients with effort-induced vein thrombosis of less than 2 weeks duration, thrombolytic therapy is recommended. Chronic ASDVT does not respond to thrombolytics and is better treated either conservatively with warfarin, or by surgical bypass, if symptoms are severe.

PreviousNextRelevant Anatomy

The subclavian vein courses over the first rib and posterior to the clavicle. The artery lies superior and posterior to the vein.

PreviousNextContraindications

Surgery is rarely indicated in ASDVT associated with central lines. Thrombolytic drug therapy is rarely recommended for patients who present with chronic subclavian vein thrombosis.

PreviousProceed to Workup , Subclavian Vein Thrombosis

Read More

Subclavian Artery Thrombosis

Background

Subclavian artery thrombosis is a condition in which the blood flow through the vessel is obstructed. The condition usually occurs secondary to some form of antecedent injury to the vessel, hypercoagulable state, or atherosclerotic changes. The condition is common in young athletic individuals who exert a significant amount of upper body activity.[1] Sudden occlusion from emboli followed by thrombosis of the artery is common in the population with signs of significant atherosclerotic disease.

The patient presenting with acute subclavian artery occlusion usually has a history of repetitive use and/or stress injury to the upper extremity on the affected side. A history of upper extremity claudication is common.

In situations in which the occlusion is secondary to atherosclerosis, acute thromboses of the artery are generally asymptomatic. In fact, in 9% of autopsy series, the left subclavian artery was either stenotic or occluded. If symptoms are present, upper extremity claudication on the affected side is most common. The patient may also present with dizziness, vertigo, imbalance, visual disturbances, or hemisensory dysfunction indicative of a subclavian steal syndrome. However, note that subclavian steal is observed on 2% of cerebral angiograms and causes no symptoms.

NextProblem

The occlusion arises secondary to damage to the intima of the artery. This damage can occur as a result of external muscular compression and repetitive stress to the artery or because of atherosclerotic changes to the vessel. Embolic phenomena and hypercoagulable states are also contributing factors.

Symptoms occur secondary to lack of blood flow to the affected extremity. To maintain blood supply to the extremity, blood is naturally rerouted from the vertebral, carotid, and internal mammary arteries, producing the various steal syndromes.

PreviousNextEpidemiologyFrequency

Symptomatic lesions occur in less than 1% of the population. In autopsy series, 9% of the population demonstrate stenosis or occlusion of one subclavian artery, usually on the left. Two percent of cerebral angiograms demonstrate asymptomatic subclavian steal.

PreviousNextEtiology

The occlusion arises secondary to damage to the intima of the artery. This damage can occur as a result of external muscular compression and repetitive stress to the artery, atherosclerotic changes to the vessel, or inflammatory processes.

Embolic or thrombotic occlusion of the artery occurs, particularly in the presence of atherosclerotic stenoses. Hypercoagulable states contribute to this scenario.

PreviousNextPathophysiology

The affected artery demonstrates detectable intimal damage, which is usually secondary to compressive forces exerted by the muscles of the shoulder girdle that compress the artery. Bony abnormalities in this area can also contribute to the process.[2] As these muscles enlarge secondary to physical activity, they exert pressure on the artery. This pressure, coupled with exertional activity of the upper extremity, can stretch and compress the intima, thus disrupting its natural integrity. This disruption precipitates platelet deposition in the area, with resulting thrombosis.

Atherosclerotic changes in the vessel occur secondary to the flow characteristics in the area. These depositions are accelerated by all of the dietary and sociological influences that affect the progression of atherosclerotic disease, including smoking, hypercholesterolemia, and hypertension. Occlusion secondary to atherosclerosis is more insidious and often causes no symptoms. At times, the symptom complex of claudication precedes the actual loss of blood flow.

Patients with hypercoagulable states, either intrinsic or secondary to dehydration complicated by concomitant cardiac arrhythmias and systemic inflammatory processes, comprise a small subset of individuals who may exhibit this pathology.

PreviousNextPresentation

A patient with an acute occlusion presents with a cold, painful, pulseless upper extremity. Axillary, brachial, and radial pulses are generally absent. When the occlusion is secondary to atherosclerotic changes, various prodromes and manifestations may be observed.

The patient may present with no symptoms or upper extremity claudication secondary to exertion. If the condition has precipitated a steal syndrome, no symptoms are typically present. The examining physician should be aware of the rare presentation of various neurological symptoms and findings that may be associated with the steal syndromes, including syncope, vertigo, ataxia, sensory loss, visual changes, and stroke, depending on the vessels involved in the steal. The affected upper extremity may or may not demonstrate diminished pulses. Blood pressure differences between the affected and unaffected sides may be noted.

PreviousNextIndications

Therapeutic intervention is indicated in any symptomatic patient once the etiology of the symptoms has been defined. For instances of upper extremity claudication or acute thrombosis in which the problem has been attributed to the subclavian artery, intervention should be planned and executed. For patients in whom cerebrovascular symptoms predominate, a careful neurological evaluation must be undertaken in order to isolate the problem. Once the anatomical aberration has been defined, intervention is indicated if the subclavian artery is involved.

PreviousNextRelevant Anatomy

In patients with subclavian artery occlusion secondary to variations in the thoracic outlet, 2 areas can undergo vascular compression during hyperabduction of the extremity. One site is where the axillary artery passes posterior to the pectoralis minor muscle and beneath the coracoid process. The other point is where the artery courses between the clavicle and the first rib. Fibrous tissue proliferation in this area can impose extrinsic compression on the vessel. The image below illustrates the relevant anatomy.

The anatomy of the subclavian artery in the thoracic outlet.

Aberrant origins of the subclavian artery off the aortic arch can be a cause of subclavian artery occlusion.[3]

In atherosclerotic disease, the carotid-subclavian junction or carotid-vertebral junctions are areas that appear to be predisposed to atheromata formation and calcification. Subsequently, this region is most likely to be involved in the occlusive process.[4]

Areas of the subclavian artery that are exposed to repeated forms of injury resulting in intimal damage are predisposed to occlusion.

PreviousNextContraindications

Contraindications to surgical intervention include inadequate distal runoff, inadequate vessel size, and marked collateralization of the occluded area. Concomitant medical problems that would endanger the patient during a surgical intervention are also contraindications to surgery. With the advent of stenting, patients with greater medical challenges can be treated successfully; however, the presence of appropriate arterial runoff and adequate artery size are imperative in order to ensure success of the procedure.

PreviousProceed to Workup , Subclavian Artery Thrombosis

Read More