Malposition of central lines

Central venous access is a core skill in Critical care, useful for when peripheral access is impossible, to infuse phlebitic drugs or for rapid correction of electrolytes. Sites of access are the internal jugular veins, subclavian veins and femoral veins.

Ultrasound has helped make the procedure safer by reducing the incidence of arterial puncture and failed insertion than the traditional landmark technique. However a frustrating and potentially dangerous complication of central line insertion is malposition of the catheter which is not necessarily prevented by ultrasound. The ideal position for the catheter tip is within the superior vena cava, above its junction with the right atrium and lying parallel with the vessel walls. On a chest radiograph catheter tip placement over 10mm below the carina has a high risk of intracardiac placement. Despite the optimum placement being common knowledge there is a large variation in catheter tip placement¹.

Internal jugular vein

The commonest malposition associated with internal jugular vein cannulation is the catheter ending up in the ipsilateral subclavian vein. This can be detected with a post-insertion chest x-ray. The incidence of this is felt to be higher with a left sided cannulation (4.9% in one study² compared to 1.1% on the right). The incidence of vessel wall perforation is also felt to be higher with a left sided approach. Other potential routes of malposition are the azygous vein, thymic vein, contralateral subclavian vein and even the contralateral internal jugular vein.

Malposition of an IJV central venous catheter into the ipsilateral subclavian vein

Malposition of an IJV central venous catheter into the ipsilateral subclavian vein

Subclavian vein

The most common malposition associated with subclavian vein cannulation is malposition into the ipsilateral internal jugular vein. This is more common when a right sided approach is undertaken. Redirecting the central line into the superior vena cava requires interventional radiology assistance and the use of fluoroscopy. On chest x-ray a catheter that enters the left side of the heart should immediately raise concerns about inadvertent arterial cannulation.

Femoral vein

Aside from inadvertent arterial puncture, malposition of femoral lines are uncommon. The use of large bore haemodialysis lines presents the problem if vessel wall injury as described in a case report where a retroperitoneal haematoma occurred due to iliac artery perforation.

But does this cause a problem?

The problems associated with malposition of a CVC are theoretically increased risk of local thrombosis, risk of vessel wall perforation and inaccurate measurement of the central venous pressure (for whatever that’s worth).

However these risks might be a lot lower than expected. In one cohort study of 1619 patients over three years (Pikwer et al, 2008) a malposition rate of 3.3% was recorded. The right subclavian vein had the highest rate of malposition (9.1%) and the right internal jugular vein had the lowest (1.4%), and only 6 of the 53 malpositioned catheters were removed or adjusted. No case of malposition was associated with localised thrombosis, vessel wall perforation or cerebral complications.

Personally I would argue that catheter malposition can be divided into three categories, all of which have very different implications.

  1. Venous malposition: Probably not as a big a deal as we think, unless the line is being used for high volume fluid administration or large amounts of phlebitic drugs. The inadvertently cannulated vein should have it’s area of venous drainage (e.g. the arm for subclavian vein) monitored closely for signs of swelling and there should be a good reason not to re-site the central line when possible.
  2. Arterial malposition: A very serious complication with potentially debilitating or fatal consequences. Arterial puncture should be recognised immediately from pressure of blood flow, and ideally the guidewire should be confirmed within the target vein with ultrasound prior to dilatation.
    In one particularly terrifying case series the importance of not simply pulling out an arterial central venous catheter manually is highlighted. In the case series, of the patients who had the catheter immediately removed and manual pressure applied 47% had a serious complication including neurological injury and 2 out of 17 patients died. The patients who underwent immediate surgical exploration with removal by a vascular surgeon in the operating theatre had much better outcomes, with no serious complications or deaths.
  3. Extravascular malposition: Potentially serious complication depending where the catheter tip ends up. This should be recognised by inability to aspirate blood from all lumens and the lack of a CVP trace, and if not then by chest x-ray. Administering through these lines can have disastrous complications.

How to avoid central venous catheter malposition?

The safe use of ultrasound is now seen as standard of care. After vessel puncture and the guidewire is inserted the vessel should be scanned again with the ultrasound probe to ensure the guidewire is seen within the vessel. Using a longitudinal view you can also make sure the wire is passing down the vein and isn’t sticking in the posterior wall.

The J tip of the guidewire could theoretically be angled to ensure the guidewire passes down the vein and towards the right atrium. For subclavian vein cannulation the J tip should be angled so the tip faces caudad to encourage a turn towards the right atrium. Inserting the guidewire with the needle bevel facing down could also potentially encourage the guidewire to enter the brachiocephalic vein and subsequently the SVC. For internal jugular vein cannulation the J tip could be angled to the tip faces medially, to discourage the wire from turning into the ipsilateral subclavian vein. However in reality controlling the direction of the guidewire tip is almost impossible without fluoroscopic guidance.

For internal jugular vein cannulation one potential tip would be to use ultrasound to image the subclavian vein after insertion of the guidewire to ensure it is hasn’t entered there instead of the SVC. This is relatively simple to do and involves first imaging the subclavian vein in the short axis to distinguish it from the artery and then rotating the probe 90 degrees to see the vein in long axis and allowed guidewire visualisation.

Unfortunately the literature suggests that operator skill and patient position make no difference in the rates of venous malposition. The important aspect then becomes recognition, which is why post-insertion chest x-rays are important. Your institution may have a policy on the management of malpositioned central lines, ensure you are familiar with it and follow it’s advice.

Summary

Venous malposition may not be as bad as we think, however other types of malposition (arterial and extravascular) can be disastrous. Simple measures can reduce the risk and increase recognition of malposition:

  1. Use ultrasound and be competent in it’s use.
  2. Visualise the guidewire within the target vein prior to dilatation.
  3. Transduce the catheter to check a venous pressure waveform (or send a blood gas to ensure a venous sample).
  4. Get a post-insertion chest x-ray.
  5. Your institution may have a departmental policy on management of malpositioned central venous catheters.

 

References

  1. Tizard K, Welters I. Central venous catheter placement: where is the end of the line? Critical Care 2012, 16(Suppl 1):P208.
  2. Muhm M, Sunder-Plassmann G, Apsner R et al. Malposition of central venous catheters. Wien Klin Wochenschr. 6; 109(11):400-5, 1997.
  3. Malhotra D, Gupta S, Gupta S, Kapoor B. Malposition of internal jugular vein cannula into ipsilateral subclavian vein in reverse direction – Unusual case report. Intern J Anesthesiol. 2009;22:1
  4. Pikwer A, Bååth L, Davidson B, Perstoft I, Akeson J. The incidence and risk of central venous catheter malpositioning: a prospective cohort study in 1619 patients. Anaesth Intensive Care. 2008 Jan;36(1):30-7.
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Central Venous Pressure

A must read article on the subject of CVP is this systematic review by Paul Marik. Essentially static CVP readings are useless for predicting fluid responsiveness, you may as well flip a coin.


CVP

Central venous pressure is measured using a central venous catheter commonly placed in the subclavian or internal jugular veins, using fluid filled tubing and a strain gauge which converts pressure change into a change of resistance. Using a wheatstone bridge this can be used to calculate change in pressure.

Historically it has been used to guide fluid resuscitation, however this is falling out of favour.

CVP is used as a measure of right atrial pressure as there are no valves inbetween the large central valves and the right atrium.

High CVP

  • Increased intrathoracic pressure/PEEP
  • Cardiac failure
  • Vasoconstriction (increased stressed venous volume, more venous return)
  • Cardiac tamponade
  • Tension pneumothorax
  • Volume overload
  • SVC obstruction

Low CVP

  • Hypovolaemia
  • Vasodilation
  • Hypotension

The CVP trace

CVP

a wave – right atrial contraction
c wave – isovolumetric contraction of right ventricle causing tricuspid valve to bulge upwards into right atrium
x descent – contraction of right ventricle elongates the right atrium causing a pressure drop
v wave – right atrial filling
y descent – tricuspid valve opens, passive right ventricular filling

Abnormalities

Large (“cannon”) a waves –  atriventricular dissociation, the atrium contracts against a closed tricuspid valve causing pressure to be transmitted backwards into central veins.

Absent a waves – atrial fibrillation, no organised atrial contraction to cause an a wave.

Large v waves – tricuspid regurgitation.

 

Assays

Different assays are used to help show different components of haemostasis.

INTEM – Contact activation
Result influenced by coagulation factors, platelets, fibronogen and heparin. LMWH activity detected at high concentrations.

EXTEM – Tissue factor activation plus heparinase
Screening test primarily for extrinsic haemostasis system.
Not affected by heparin as reagent contains heparinase, therefore the result is only affected by coagulation factors, platelets and fibrinogen.

HEPTEM – Contact activation plus heparinase
Essentially INTEM without effects of heparin.
Allows detection of coagulation deficiencies even whilst on heparin. The difference between the INTEM CT and the HEPTEM CT can confirm the presence and effect of heparin.

FIBTEM – Tissue factor activation plus platelet inhibition
Essentially EXTEM without effects of platelets. Eliminates activation of platelets through cytochasin D which inhibits the action of actin forming the platelet cytoskeleton into a stellate shape.
Allows detection of fibrinogen deficiencies, but also fibrin polymerisation deficiencies which may not be reliably detected with normal clotting tests.

APTEM – Tissue factor activation plus aprotinin/tranexamic acid
Fibrinolysis inhibited, therefore a significant improvement of clot stability compared with EXTEM suggests a need for antifibrinolytics. If there is no significant improvement this would suggest a requirement for other clotting products.

Method and Interpretation

Rotational Thromboelastometry

A good background from Life in the Fast Lane (mainly describing TEG)

Clinical relevance and short literature review from St. Emlyn’s


Viscoelastic method for measuring haemostasis of whole blood

Method

300 microlitres of citrated blood placed in disposable cuvette.
A disposable pin is placed in the blood, this is attached to a thin shaft and spring which oscillates slowly. The change in tension as the blood clots is detected by optical sensors.
Different reagents are used depending on the test required.

TEG (thromboelastography) similar, but it is the cup that rotates. ROTEM is less sensitive to mechanical shocks and movement than TEG which is an advantage.

Interpretation

ROTEM
CT – Clotting time
Latency from time of adding reagents to start of clot formation.
Prolonged CT may be a result of coagulation factor deficiencies or heparin. The contribution of heparin can be assessed by comparing the INTEM CT with the EXTEM CT.

CFT – Clot Formation Time and Alpha angle
CFT is the time until a clot firmness of 20mm is reached. The alpha angle is the tangent between the CT and CFT points.
These parameters denote the speed of solid clot formation – primarily influenced by platelet function but also by fibrinogen and coagulation factors.
Prolonged CFT: Low platelets or poor function, low fibrinogen or fibrin polymerisation disorders
Shortened CFT: Hypercoaguability

MCF – Maximum Clot Firmness
The greatest vertical amplitude of the trace.
Reflects the absolute strength of the fibrin and platelet clot.
Low MCF indicates decreased platelet count or function, decreased fibrinogen or disorders of fibrin polymerisation, or low activity of factor XIII.

A5, 10, 15 or 20
Clot amplitude after a certain number of minutes. Allows projection of likely MCF.

LI30 (Lysis Index after 30 minutes) and ML (Maximum Lysis)
LI30 is the percentage or remaining clot stability in relation to the MCF after 30 minutes. Can also be calculated to give LI45 or LI60.
ML describes the percentage of lost clot stability relative to MCF at any selected point in time or when the test is stopped.
A low LIx or high ML is indicative of hyperfibrinolysis.