Recommendations for Anticoagulated Patients Undergoing Image-Guided Spinal Procedures

Kennith F. Layton; David F. Kallmes; Terese T. Horlocker

Anticoagulated patients often need image-guided spinal procedures for CSF harvest, myelography, vertebroplasty, vertebral biopsies, or epidural injections. The risk of spinal hematoma is increased in anticoagulated patients who undergo lumbar puncture or neuraxial anesthesia. Any procedure involving needle manipulation or biopsy with potential transgression of the subarachnoid, subdural, or epidural vasculature, however, likely carries a similar risk. This risk is increased, often substantially, by the use of multiple anticoagulants and the intensity of anticoagulation. It is crucial that radiologists who perform spinal procedures be familiar with the common anticoagulant and antiplatelet medications.

Radiologists are increasingly being asked to provide fluoroscopically assisted access to the neuraxial system. Whether a routine lumbar puncture, epidural steroid injection, spinal biopsy, or the more unusual C1–2 cervical puncture, there is the potential for bleeding complications. Most of the case reports involving spinal hematomas following lumbar puncture, high cervical myelogram, and epidural injection (as well as those related to neuraxial anesthesia) are reported in the anesthesia and surgical literature.^1–4 Large series consistently note that the risk of spinal hematoma is potentiated by the concomitant administration of anticoagulant and/or antiplatelet therapy and difficult and/or traumatic spinal instrumentation.^5,6 Neurologic compromise typically presents as a sensory or motor deficit or bowel/bladder dysfunction, not severe radicular back pain. Because of delays in the diagnosis, neurologic recovery is poor in most cases. Thus, radiologists must be aware of the risk factors and diagnosis of spinal bleeding.

Much of the information related to postprocedure spinal hematomas in anticoagulated patients is derived from cases of spinal hematoma associated with neuraxial anesthesia and anesthesia. Formal recommendations have been put forth by the American Society of Regional Anesthesia and Pain Medicine, but correlative recommendations by the radiology community are currently not available.⁷ In hopes of facilitating the management of patients presenting to radiologists for spinal procedures in the setting of anticoagulant or antiplatelet therapy, we offer a focused, readily accessible set of guidelines for performing spinal procedures on anticoagulated patients.

Discussion

Literature is available regarding recommendations for managing patients with medication-induced coagulopathies and is reviewed below (Table). Patients typically receive these medications for chronic antithrombotic therapy in the prevention of stroke or myocardial ischemia, thromboprophylaxis following surgery, or treatment of acute thromboembolism or coronary syndrome. The intensity and duration of anticoagulation affect the risk of spontaneous, as well as procedural-related spinal bleeding.⁸ Although less common than needle placement for injection or biopsy, radiologists may also be requested to assist with placement of an indwelling neuraxial catheter, such as a spinal drainage catheter. In these cases, significant anticoagulant medications should not be administered until the catheter or drain is removed.

View this table:

Recommended guidelines for performing spinal procedures in anticoagulated patients

Anticoagulant Therapy

Warfarin.

Chronic warfarin therapy increases the risk of spinal hematoma following lumbar puncture. The addition of agents that affect different parts of the clotting mechanism likely increase the risk for spinal hematoma and do so without further elevation of the prothrombin time (PT) or international normalized ratio (INR).⁹ These medications include heparin, nonsteroidal anti-inflammatory drugs (NSAIDs), and antiplatelet agents. Warfarin should be discontinued in anticipation of the spinal procedure and normalization of the INR documented preprocedure. If a spinal procedure is performed on a patient with an INR >1.2, close neurologic testing of motor and sensory function should be performed for at least 24 hours to ensure prompt recognition and treatment of spinal hematoma. In emergent cases, the injection of vitamin K or transfusion of fresh frozen plasma may counteract the effects of warfarin.¹⁰

Heparin.

There is no contraindication to spinal puncture in patients receiving subcutaneous heparin as a prophylaxis for deep venous thrombosis providing the total dose is <10,000 U.¹¹ Higher dosing may result in sustained prolongation of the activated partial thromboplastin time (aPTT). These patients are managed similar to those who are systemically heparinized. Delaying the scheduled heparin injection until after the puncture may reduce the risk of spinal hematoma. The risk of bleeding is likely increased in debilitated patients on prolonged therapy. Patients receiving heparin for longer than 4 days need to have a platelet count assessment because of the potential for heparin-induced thrombocytopenia.¹²

Systemic heparinization represents an increased risk for spinal bleeding.⁸ Heparin infusion should be discontinued and aPTT normalized before the procedure. A subsequent dose of intravenous heparin should not be administered for at least an hour after the procedure.^11,13 The combined use of other anticoagulants with unfractionated heparin may increase the risk of spinal hematoma. These include antiplatelets, low-molecular-weight heparin (LMWH), and oral anticoagulants.

LMWH.

LMWH is the recommended thromboprophylactic agent following major orthopedic and general surgical procedures.¹⁴ It is important that there be a number of dosing regimens for LMWH, including low-dose (thromboprophylactic) and high-dose (therapeutic) applications. There are many pharmacologic differences between standard unfractionated heparin and LMWH, including prolonged half-life and irreversibility with protamine.^15,16 Early postoperative dosing, twice-daily dosing, and traumatic needle placement were identified as risk factors for spinal hematoma associated with neuraxial anesthesia. Because significant anticoagulant activity persists for 12 hours after low-dose injection (and 24 hours for a high-dose injection), these time intervals should be observed before a spinal procedure. Likewise, the first postprocedural LMWH dose should be administered 18–24 hours later, to allow for adequate hemostasis.

Thrombolytic Therapy

Data are not available to clearly define how long spinal puncture should be avoided following termination of thrombolytic/fibrinolytic therapy; however, significant defects in hemostasis are present for longer than 24 hours. Patients who have recently had or that are likely to receive thrombolytic/fibrinolytic therapy should be warned against receiving a spinal puncture except in very unusual circumstances. Likewise, patients should be questioned before starting thrombolytic/fibrinolytic therapy whether there has been a recent spinal procedure such as lumbar puncture. This will allow for appropriate monitoring in cases where the drug must be administered. Original guidelines recommended avoidance of thrombolytic drugs for 10 days following puncture of noncompressible vessels.¹⁷ In certain cases, measurement of fibrinogen level (one of the last clotting factors to recover) may be helpful in monitoring a patient who underwent or will undergo a spinal procedure.⁷

Antiplatelet Therapy

The antiplatelet medications include a diverse group of agents in terms of their effects on platelet function; therefore, it is not possible to extrapolate between the various groups of drugs regarding spinal procedures. These agents include NSAIDs, thienopyridine derivatives, and GP IIb/IIIa antagonists.

NSAIDs

The use of NSAIDs alone does not seem to increase the risk of spinal hematoma from spinal puncture. At this time, there do not seem to be specific concerns related to timing of spinal puncture in relation to the dosing of NSAIDs or postprocedure monitoring.^18,19

Thienopyridine Derivatives

This class of antiplatelet agents works by inhibiting adenosine diphosphate–induced platelet aggregation. These drugs affect both primary and secondary platelet aggregation as well as platelet-fibrinogen binding.²⁰ The agents in this class include clopidogrel (Plavix) and ticlopidine (Ticlid). The patient should be carefully assessed for other factors that might lead to bleeding such as easy bruising/bleeding, female sex, and increased age.⁷ The addition of other medications affecting different clotting mechanisms will likely increase the chance for spinal hematoma.

GP IIb/IIIa–Receptor Antagonists

These agents affect platelet-fibrinogen and platelet–von Willebrand factor binding to inhibit platelet aggregation. These medications are often given concomitantly with aspirin and heparin. This class of antiplatelet drugs includes abciximab (ReoPro), eptifibatide (Integrilin), and tirofiban (Aggrastat). Normal platelet aggregation is usually achieved 8 hours after discontinuation of tirofiban and eptifibatide and 24–48 hours after discontinuing abciximab.

The true risk of spinal hematoma in patients on thienopyridine derivatives or GP IIb/IIIa antagonists is unknown. Management is based on labeling precautions and prior experience. The concomitant use of aspirin with these agents may increase the risk for spinal hematoma. The GP IIa/IIIb antagonists have a profound effect on platelet aggregation and spinal puncture should be avoided until platelet function has recovered.²¹ Of note, these agents are contraindicated within 4 weeks of surgery. There is not a definitive test, including bleeding time, that can guide antiplatelet therapy.

Conclusion

The increased vigilance over venous thromboembolism and introduction of more efficacious antiplatelet agents has introduced a degree of complexity into the performance of spinal procedures. The presence and continued evolution of antiplatelet agents, various heparin derivatives and thrombolytic therapy requires a thorough investigation of a patient’s medication history. Continued surveillance of the literature will be necessary to stay abreast of the newer agents that are sure to appear, as well as any changes in the recommendations regarding agents currently in use. The guidelines referenced in the table and can be accessed on-line at www.asra.com.

References

↵
Reitman CA, Watters W. Subdural hematoma after cervical epidural steroid injection. Spine 2002;27:E174–76
CrossRef PubMed
Aghi M, Valery-Coumans J, Brisman JL. Subarachnoid hematoma, hydrocephalus, and aseptic meningitis resulting from a high cervical myelogram. J Spinal Disord Tech 2004;17:348–51
PubMed
Stoll A, Sanchez M. Epidural hematoma after epidural block: implications for its use in pain management. Surg Neuro 2002;57:235–40
↵
Diaz FG, Yock DH Jr, Rockswold GL. Spinal subarachnoid hematoma after lumbar puncture producing acute thoracic myelopathy: case report. Neurosurgery 1978;3:404–06
PubMed
↵
Vandermeulen EP, Van Aken H, Vermylen J. Anticoagulants and spinal-epidural anesthesia. Anesth Analg 1994;79:1165–77
PubMed
↵
Horlocker TT, Wedel DJ. Neuraxial block and low molecular weight heparin: balancing perioperative analgesia and thromboprophylaxis. Reg Anesth Pain Med 1998;23:164–77
CrossRef PubMed
↵
Horlocker TT, Wedel DJ, Benzon H, et al. Regional anesthesia in the anticoagulated patient: Defining the risks: the second ASRA consensus conference on neuraxial anesthesia and anticoagulation. Reg Anesth Pain Med 2003;28:172–97
CrossRef PubMed
↵
Stafford-Smith M. Impaired haemostasis and regional anaesthesia. Can J Anaesth 1996;43:R129–41
CrossRef PubMed
↵
Harder S, Thurmann P. Clinically important drug interactions with anticoagulants: an update. Clin Pharmacokinet 1996;30:416–44
PubMed
↵
Shields RC, McBane RD, Kuiper JD, et al. Efficacy and safety of intravenous phytonadione (vitamin K1) in patients on long-term oral anticoagulant therapy. Mayo Clin Proc 2001;76:260–66
CrossRef PubMed
↵
Liu SS, Mulroy MF. Neuraxial anesthesia and analgesia in the presence of standard heparin. Reg Anesth Pain Med 1998;23:157–63
CrossRef PubMed
↵
Hirsh J, Raschke R, Warkentin TE, et al. Heparin: mechanism of action, pharmacokinetics, dosing considerations, monitoring, efficacy, and safety. Chest 1995;108:258S–75S
CrossRef PubMed
↵
Ruff RL, Dougherty JH Jr. Complications of lumbar puncture followed by anticoagulation. Stroke 1981;12:879–81
Abstract/FREE Full Text
↵
Geerts WH, Pineo GF, Heit JA, et al. Prevention of venous thromboembolism: the seventh ACCP conference on antithrombotic and thrombolytic therapy. Chest 2004;126(3 suppl):338S–400S
↵
Cosmi B, Hirsh J. Low molecular weight heparins. Curr Opin Cardiol 1994;9:612–18
PubMed
↵
Holst J, Lindblad B, Bergqvist D, et al. Protamine neutralization of intravenous and subcutaneous low-molecular-weight heparin (tinzaparin, Logiparin): an experimental investigation in healthy volunteers. Blood Coagul Fibrinolysis 1994;5:795–803
PubMed
↵
Majerus PW, Broze GJ, Miletich JP, et al. Goodman and Gilman’s the phamacological basis of therapeutics. 8th ed. New York: McGraw-Hill;1993 :1322–31
↵
CLASP (Collaborative Low-Dose Aspirin Study in Pregnancy) Collaborative Group. CLASP: a randomized trial of low-dose aspirin for the prevention and treatment of preeclampsia among 9364 pregnant women. Lancet 1994;343:619–29
CrossRef PubMed
↵
Horlocker TT, Bajwa ZH, Ashraft Z, et al. Risk assessment of hemorrhagic complications associated with nonsteroidal antiinflammatory medications in ambulatory pain clinic patients undergoing epidural steroid injection. Anesth Analg 2002;95:1691–97
CrossRef PubMed
↵
Taniuchi M, Kurz HI, Lasala JM. Randomized comparison of ticlopidine and clopidogrel after intracoronary stent implantation in a broad patient population. Circulation 2001;104:539–43
Abstract/FREE Full Text
↵
Shlansky-Goldberg R. Platelet aggregation inhibitors for use in peripheral vascular interventions: what can we learn from the experience in the coronary arteries? J Vasc Interv Radiol 2002;13:229–46
PubMed

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Periprocedural antithrombotic management for lumbar puncture: Association of British Neurologists clinical guideline

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[1] ↵
Reitman CA, Watters W. Subdural hematoma after cervical epidural steroid injection. Spine 2002;27:E174–76
CrossRef PubMed

[2] Aghi M, Valery-Coumans J, Brisman JL. Subarachnoid hematoma, hydrocephalus, and aseptic meningitis resulting from a high cervical myelogram. J Spinal Disord Tech 2004;17:348–51
PubMed

[3] Stoll A, Sanchez M. Epidural hematoma after epidural block: implications for its use in pain management. Surg Neuro 2002;57:235–40

[4] ↵
Diaz FG, Yock DH Jr, Rockswold GL. Spinal subarachnoid hematoma after lumbar puncture producing acute thoracic myelopathy: case report. Neurosurgery 1978;3:404–06
PubMed

[5] ↵
Vandermeulen EP, Van Aken H, Vermylen J. Anticoagulants and spinal-epidural anesthesia. Anesth Analg 1994;79:1165–77
PubMed

[6] ↵
Horlocker TT, Wedel DJ. Neuraxial block and low molecular weight heparin: balancing perioperative analgesia and thromboprophylaxis. Reg Anesth Pain Med 1998;23:164–77
CrossRef PubMed

[7] ↵
Horlocker TT, Wedel DJ, Benzon H, et al. Regional anesthesia in the anticoagulated patient: Defining the risks: the second ASRA consensus conference on neuraxial anesthesia and anticoagulation. Reg Anesth Pain Med 2003;28:172–97
CrossRef PubMed

[8] ↵
Stafford-Smith M. Impaired haemostasis and regional anaesthesia. Can J Anaesth 1996;43:R129–41
CrossRef PubMed

[9] ↵
Harder S, Thurmann P. Clinically important drug interactions with anticoagulants: an update. Clin Pharmacokinet 1996;30:416–44
PubMed

[10] ↵
Shields RC, McBane RD, Kuiper JD, et al. Efficacy and safety of intravenous phytonadione (vitamin K1) in patients on long-term oral anticoagulant therapy. Mayo Clin Proc 2001;76:260–66
CrossRef PubMed

[11] ↵
Liu SS, Mulroy MF. Neuraxial anesthesia and analgesia in the presence of standard heparin. Reg Anesth Pain Med 1998;23:157–63
CrossRef PubMed

[12] ↵
Hirsh J, Raschke R, Warkentin TE, et al. Heparin: mechanism of action, pharmacokinetics, dosing considerations, monitoring, efficacy, and safety. Chest 1995;108:258S–75S
CrossRef PubMed

[13] ↵
Ruff RL, Dougherty JH Jr. Complications of lumbar puncture followed by anticoagulation. Stroke 1981;12:879–81
Abstract/FREE Full Text

[14] ↵
Geerts WH, Pineo GF, Heit JA, et al. Prevention of venous thromboembolism: the seventh ACCP conference on antithrombotic and thrombolytic therapy. Chest 2004;126(3 suppl):338S–400S

[15] ↵
Cosmi B, Hirsh J. Low molecular weight heparins. Curr Opin Cardiol 1994;9:612–18
PubMed

[16] ↵
Holst J, Lindblad B, Bergqvist D, et al. Protamine neutralization of intravenous and subcutaneous low-molecular-weight heparin (tinzaparin, Logiparin): an experimental investigation in healthy volunteers. Blood Coagul Fibrinolysis 1994;5:795–803
PubMed

[17] ↵
Majerus PW, Broze GJ, Miletich JP, et al. Goodman and Gilman’s the phamacological basis of therapeutics. 8th ed. New York: McGraw-Hill;1993 :1322–31

[18] ↵
CLASP (Collaborative Low-Dose Aspirin Study in Pregnancy) Collaborative Group. CLASP: a randomized trial of low-dose aspirin for the prevention and treatment of preeclampsia among 9364 pregnant women. Lancet 1994;343:619–29
CrossRef PubMed

[19] ↵
Horlocker TT, Bajwa ZH, Ashraft Z, et al. Risk assessment of hemorrhagic complications associated with nonsteroidal antiinflammatory medications in ambulatory pain clinic patients undergoing epidural steroid injection. Anesth Analg 2002;95:1691–97
CrossRef PubMed

[20] ↵
Taniuchi M, Kurz HI, Lasala JM. Randomized comparison of ticlopidine and clopidogrel after intracoronary stent implantation in a broad patient population. Circulation 2001;104:539–43
Abstract/FREE Full Text

[21] ↵
Shlansky-Goldberg R. Platelet aggregation inhibitors for use in peripheral vascular interventions: what can we learn from the experience in the coronary arteries? J Vasc Interv Radiol 2002;13:229–46
PubMed

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American Journal of Neuroradiology

Recommendations for Anticoagulated Patients Undergoing Image-Guided Spinal Procedures