Complications
Though septic complications are possible, they usually occur in upper extremity SVT due to intravenous catheterization and/or infusions. In the presence of signs of infection (e.g., fever, purulent discharge, lymphangitic streak), antibiotic treatment is indicated. Empiric antibiotic therapy for peripheral vein suppurative thrombosis should include an agent with activity against staphylococci plus an agent with activity against Enterobacteriaceae. Antibiotics should be tailored accordingly to culture and sensitivity data when available. If purulent discharge persists or an abscess is present, then surgical intervention may be needed.
The risk of anticoagulant bleeding varies according to type of anticoagulant, dose of anticoagulant, and patient risk factors. A thorough assessment of risk factors for bleeding (e.g., active peptic ulcer disease, thrombocytopenia, liver disease, other coagulopathy) must be done prior to any decision to prescribe anticoagulants.[61]
In general, unfractionated heparin (UFH) carries a higher risk of bleeding than low molecular weight heparin (LMWH); the rate of major hemorrhage with UFH ranges from 0% to 7%.[89] The risk of major bleeding is lower with direct oral anticoagulants compared with LMWH or vitamin K antagonists (e.g., warfarin).[61]
The management of heparin-associated bleeding depends upon the location and severity of bleeding, but usually necessitates prompt removal of heparin and may include urgent hospitalization for red blood cell transfusions and administration of an antidote in the case of UFH.
HIT is a rare but serious complication of patients who are receiving or who have recently received heparin. It usually manifests as a 50% platelet count drop 5-10 days after starting a course of heparin. It is more commonly associated with unfractionated heparin (UFH) than low molecular weight heparin (LMWH).
Thrombosis is an important complication of HIT. Routine platelet count monitoring for HIT is recommended for patients treated with therapeutic doses of UFH and may be appropriate for patients treated with LMWH. An urgent platelet count should be done if symptomatic thrombosis develops in a patient with SVT receiving heparin. If HIT is suspected, prompt cessation of heparin is critical, and referral to a hematologist or thrombosis specialist is recommended.
Nonsteroidal anti-inflammatory drugs (NSAIDs) can lead to salt and fluid retention and hypertension due to altered renal hemodynamics.
They can cause renal impairment, especially in combination with other nephrotoxic agents.
An assessment of concomitant medications and renal function should be done before prescribing NSAIDs for superficial vein thrombosis.
Common gastrointestinal adverse drug reactions associated with NSAID use include dyspepsia and gastric ulceration and bleeding.
Around 10% to 20% of patients experience dyspepsia with NSAIDs.[90] The effects are dose-dependent, and the risk of ulceration increases with duration of therapy and with higher doses. There are also some differences in the propensity of individual agents to cause gastrointestinal adverse effects. Indomethacin and piroxicam have the highest prevalence of gastric adverse effects; ibuprofen and diclofenac appear to have the lowest. It is prudent to use the lowest effective dose for the shortest period of time.
NSAIDs should not be given in combination with anticoagulants due to the increased risk of bleeding. In one cohort study, patients prescribed NSAIDs with oral anticoagulants had an increased risk of gastrointestinal bleeding, stroke, and major bleeding (hazard ratios 3.01, 2.71, and 2.77, respectively) compared with oral anticoagulants alone.[77]
Concomitant use of acid-suppressing medications may prevent or reduce gastrointestinal adverse effects (e.g., proton-pump inhibitors or misoprostol).
Superficial vein thrombosis (SVT) is a risk factor for venous thrombosis.[18] The risk for subsequent VTE within the first 3 months following SVT is about 1.5% to 6.2%.[61][87] A shorter duration of anticoagulation is associated with an increased risk of recurrent thromboembolic events.[87] A few studies report an incidence of subsequent VTE of 1.7% to 26.9% for patients who are not treated pharmacologically or surgically during a follow-up of 3 months.[50][68][76][79]
The long-term risk of VTE decreases over time, but the risk remains 5-fold higher than in the general population after 5 years and may remain elevated for 3 decades, according to one nationwide cohort study in Denmark.[88]
The risk of subsequent DVT or PE is dependent on factors such as a prior history of VTE.
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