04.08 Nursing Care and Pathophysiology for Thrombophlebitis (clot)
Thrombus (clot) formation with associated inflammation in extremity.
Pathophysiology: Inflammation of the vein because of a blood clot. Venous status, damage to the vessel, and hypercoagulability cause the blood to pool so blood can not move the way that it should so more clots form.
- Thrombus v. Embolus
- Risk Factors
- Virchow’s Triad
- Venous stasis
- Damage to inner lining of vessel
- Hypercoagulability of blood
- Medical History
- History of thrombophlebitis
- Pelvic surgery
- HF, MI
- IV therapy
- Virchow’s Triad
- Unilateral findings on affected side
- Warm skin
- Febrile state
- Homan’s sign – pain on dorsiflexion of foot**
**Not reliable or specific. Only 33% of patients with DVT are positive. No longer recommended for standard practice. This maneuver can also dislodge the clot**
- Confirm clinical picture with diagnostics:
- D-Dimer (positive)
Therapeutic Management If patient has confirmed DVT:
- NO SCD/TED, NO massage, Bedrest.
- Could dislodge clot
- Initiate anticoagulant therapy
- Monitor PTT q6h
- Coumadin (warfarin)
- Monitor PT/INR
- IVC filter
- Sits in Inferior Vena Cava
- Collects clots before they reach the heart/lungs
- Monitor for s/s Emboli
- Heart – MI
- Chest Pain (CP)
- Lungs – Pulmonary Embolism
- ↑ HR
- ↑ RR
- Brain – Stroke
- Facial droop
- Arm Weakness
- Speech Difficulty
- Heart – MI
- Monitor distal pulses
- Elevate legs 10-20 minutes q2h
- Monitor for s/s Emboli
- Monitor circumference of limb BID
- SCD/TED + Lovenox
- Passive ROM
- Early ambulation
- Administer analgesics
- Smoking Cessation (↑ risk of clots, vasoconstriction)
- Avoid long periods of sitting
- S/S to report to HCP or RN
- Importance of early ambulation
Cornell Note-Taking System Instructions:
- Record: During the lecture, use the note-taking column to record the lecture using telegraphic sentences.
- Questions: As soon after class as possible, formulate questions based onthe notes in the right-hand column. Writing questions helps to clarifymeanings, reveal relationships, establish continuity, and strengthenmemory. Also, the writing of questions sets up a perfect stage for exam-studying later.
- Recite: Cover the note-taking column with a sheet of paper. Then, looking at the questions or cue-words in the question and cue column only, say aloud, in your own words, the answers to the questions, facts, or ideas indicated by the cue-words.
- Reflect: Reflect on the material by asking yourself questions, for example: “What’s the significance of these facts? What principle are they based on? How can I apply them? How do they fit in with what I already know? What’s beyond them?
- Review: Spend at least ten minutes every week reviewing all your previous notes. If you do, you’ll retain a great deal for current use, as well as, for the exam.
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Okay, let’s talk about Thrombophlebitis. But first, let’s break down this word – we know that ‘itis’ means inflammation, right? What about “phleb”? Think about ‘phlebotomy’ – it’s referring to the veins! Then “thrombo” refers to a “thrombus” or a blood clot. So this is inflammation of the veins because of a clot – make sense?
Now, we know in the blood we’ve got things in there like platelets and fibrin and clotting factors to help us clot when we need to, right? Sometimes, for reasons we’ll discuss in just a minute, a clot can form within the vessel that really shouldn’t be there. So in thrombophlebitis, a clot forms in the vein and causes inflammation. This causes more clotting and it just perpetuates itself. Now, what can happen is that this clot that has formed and gotten bigger here can actually break off from the vessel wall – even just pieces of it can break off. When that happens and the thrombus begins to travel through the circulatory system, it’s called an Embolus. The problem here is that it is heading for the heart – it can get lodged in the coronary arteries and cause an MI, it could go to the lungs and cause a Pulmonary Embolism or PE, or it could go to the brain and cause an ischemic stroke. So none of that is good, it’s important that we manage this issue.
So what causes thrombophlebitis? Well there’s something called Virchow’s Triad. Virchow’s triad tells us the three main things that create ideal conditions for clot formation. The first one is venous stasis – that happens when the blood is pooling and isn’t returning to the heart like it should. This happens a lot with our patients who are bedbound and not ambulatory. The second is any damage to the inner lining or the intima of the blood vessel. Any time there’s damage here, a clot can form around it. And finally hypercoagulability which is caused by various conditions that make the patient much more prone to clotting. So things you might see in the patient’s medical history to tell you they’re at risk would be a previous DVT – obviously it has happened before so it can happen again. Obesity is a risk factor. Any cardiovascular disorders like Heart Failure or MI can cause damage to the vessels. Then A-Fib puts them at risk because when the atria are just quivering, that causes blood to pool in the atria. That stasis of blood can cause clots to form which can be ejected out of the heart and get lodged in an extremity – and we call that a DVT. Now, it can also go to the lungs or brain and cause a PE or Stroke as well. Immobility again causes venous stasis. Pregnancy because of some venous pooling but also they’re hypercoagulable. And then any patient receiving IV therapy because we have damaged the vessel by placing that IV. Okay – that’s, like, every patient in the hospital, right?? So that’s why when patients are admitted to the hospital, we put everyone on what we call DVT Prophylaxis. That’s SCDs or TED hose/compression stockings, and usually either SubQ heparin or SubQ lovenox (enoxaparin). We’re trying to prevent this from happening in the first place.
Now, if it does happen, what will we see in the patient? Symptoms will be unilateral meaning they’ll only be on the affected side. You can see here the patient’s right leg is affected. We see swelling, or edema, pain, the skin will be warm to the touch and probably red as well. Now…for years they’ve been teaching Homans Sign, which is pain with dorsiflexion of the foot, as an indicator of DVT. But the truth is that only 33% of people who have a DVT will have a positive Homans sign. Not only that but 20% of people without a DVT will have a positive Homan’s sign. So Evidence-Based Practice shows that it is actually unreliable and nonspecific and really shouldn’t be used as standard practice. Not to mention it can actually dislodge the clot if we aren’t careful. So, instead, we will confirm our other clinical findings with an ultrasound and/or a D-dimer assay – that’s a lab test that indicates clotting is present in the body.
Now, I did my research on this because the question I always get is “yeah, but will it be on the NCLEX?”. I checked on the NCSBN’s website and found this quote. Essentially they’re saying it’s not reliable and we need to be sure to use the whole clinical picture. So I want you guys to know about it and know that it exists, but understand that it cannot be your only sign, okay?
So – we’ve assessed the patient and now they have a confirmed DVT – what do we do? Well the first thing you need to do as the nurse is take off the SCDs or TED hose. Think about it – if this is their leg and they have a clot in here – and we squeeze it every 30 seconds – what could happen? It could break off, right? For the same reason we do not allow leg massages and we put the patients on bedrest until we can address the clot. The provider will likely order anticoagulants unless there’s a reason they can’t have them. For example, in the Neuro ICU we’ve seen patients develop DVTs who are recovering from a hemorrhagic stroke – we can’t give them an anticoagulant – they just had a brain bleed! Now, if we DO anticoagulate, it will usually start with a weight-based heparin drip and transition to PO warfarin. Remember with heparin we monitor PTT and with Warfarin we monitor PT/INR.
If we can’t anticoagulate, and even sometimes if we can we’ll do both, we’ll insert an IVC filter. IVC stands for inferior Vena Cava. An IVC filter looks like this, like a little claw with a filter. We’ll go in through the femoral vein and it will sit right up here in the inferior vena cava so it can catch any clots that may migrate towards the heart. Typically they’ll be removed after a few weeks, once the patient has adequate anticoagulation on board.
So when it comes to nursing care for these patients, the top priorities are going to be perfusion, clotting, and comfort. In terms of perfusion we want to assess distal pulses and monitor for any signs of embolus to the heart, lungs, or brain. To address clotting we’ll administer anticoagulants, monitor the circumference of their leg, and encourage mobilization. Then, of course, we’ll address their pain with analgesics. You can see more nursing interventions in the outline and the care plan attached to this lesson, but those are the big ones.
So remember that Virchow’s Triad tells us what puts patients at high risk for thrombophlebitis – it’s venous stasis, vascular damage, and hypercoagulability. If a patient does develop a DVT, you’ll see swelling, pain, warmth, redness, and tenderness on the affected side. You might also have a positive Homan’s sign, but remember that it’s not reliable. Our biggest goal is to prevent embolism, so if they do have a clot, we’ll put them on bedrest while we get them anticoagulated and place an IVC filter. Our nursing priorities are under the concepts of perfusion, clotting, and comfort. And finally, remember that prevention is key – identify patients who may be at risk and implement DVT prophylaxis – that’s SCD’s, TED hose, and usually SubQ Heparin or Lovenox.
This is a really common thing that affects nearly every patient in the hospital, so we want you to be confident knowing how to deal with it. Go out and be your best selves today! As always, happy nursing!