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Anesth Analg 2006;103:1586-1587
© 2006 International Anesthesia Research Society
doi: 10.1213/01.ane.0000246350.35872.0b


LETTER TO THE EDITOR

Editor-in-Chief Steven L. Shafer

Prolonged Activated Partial Thromboplastin Time in Patients with Antiphospholipid Antibody Syndrome

James R. Dyer, MD, and Tilak Raj, MD

Department of Anesthesiology; University of Oklahoma Health Sciences Center; Oklahoma City, Oklahoma; james-dyer{at}ouhsc.edu

To the Editor:

Harnett et al. (1) reported on a parturient with factor V Leiden mutation, antiphospholipid antibody syndrome (APLAS), and protein S deficiency, who suffered a deep venous thrombosis after cesarean delivery. We applaud their discussion of the factor V Leiden mutation. However, we question the decision to treat an APLAS patient with fresh frozen plasma (FFP) in response to a prolonged activated partial thromboplastin time (aPTT).

The patient’s aPTT remained prolonged at 38.4 s (normal 20–30 s), 18 h after she had received her last dose of unfractionated heparin. Although the unfractionated heparin dose was not disclosed, given the time interval, it is unlikely that the residual heparin effect caused her prolonged aPTT. The authors write "because of an unclear etiology of this prolonged level, 2 U of FFP were administered" before labor epidural catheter placement (1). Given the patient’s known diagnosis of APLAS, we believe it is more likely that her prolonged aPTT was caused by the presence of the lupus anticoagulant rather than residual heparin effect. Therefore we question the decision to administer FFP to a patient with known thrombophilia.

Lupus anticoagulant may interfere with phospholipid-dependent clotting tests, resulting in a prolonged aPTT (2). In Ralph’s review (3) of 27 cases of parturients with APLAS, 12 were positive for lupus anticoagulant and four had prolonged aPTT. In Ringrose’s review (4) of 20 parturients with APLAS, five patients had prolonged aPTT.

APLAS may rarely cause antibodies to clotting factors II, VII, VIII, and IX, antibodies that can also prolong the aPTT tests (5). A preoperative hematological evaluation including coagulation factor assays is warranted to investigate a prolonged aPTT in this setting. However, this information may not be available to the anesthesiologist at the time of labor and delivery. Thromboelastography (TEG®) has been used to assess coagulation status in obstetric patients. Unfortunately, the TEG® parameters at which it is safe to proceed with neuraxial techniques are unknown, and TEG® is not readily available to most anesthesiologists in the labor and delivery ward.

Prolonged aPTT from APLAS has not been associated with increased blood loss in patients undergoing surgery (6). The case series by Ralph (3) and Ringrose (4) describe successful neuraxial techniques without neurological sequelae in patients with APLAS and prolonged baseline aPTTs. However, given the small numbers of patients in these series and the rare occurrence of spinal and epidural hematomas, these studies do not prove that neuraxial techniques are safe in this setting.

Whether to proceed with a neuraxial technique in APLAS patients with prolonged aPTT is a challenging decision to make. We agree with Ringrose that "In the absence of coagulation defects secondary to clotting factor antibodies or platelet abnormalities, the in vitro phenomenon of prolonged aPTT alone should not, in theory, predispose to hemorrhage or be a contraindication to epidural anesthesia in patients with APLAS" (4).

In the absence of a hematological investigation that includes coagulation factor analysis, we assert that when presented with a patient with APLAS and an unexplained prolonged aPTT, the anesthesiologist must weigh the risks of epidural or spinal hematoma versus the risks of using alternatives to neuraxial techniques. In addition, such patients should not be treated with FFP, unless clinical or laboratory evidence of a coagulopathy supports this treatment and doing so increases the risk of life-threatening thrombosis in these patients.

REFERENCES

  1. Harnett MJ, Walsh ME, McElrath TF, Tsen LC. The use of central neuraxial techniques in parturients with factor V Leiden mutation. Anesth Analg 2005;101:1821–3.[Abstract/Free Full Text]
  2. Birdsall MA, Pattison NS. Antiphospholipid antibodies in pregnancy: clinical associations. Br J Hosp Med 1993;50:251–60.[Web of Science][Medline]
  3. Ralph CJ. Anaesthetic management of parturients with the antiphospholipid syndrome: a review of 27 cases. Int J Obstet Anesth 1999;8:249–52.[Web of Science][Medline]
  4. Ringrose DK. Anaesthesia and the antiphospholipid syndrome: a review of 20 obstetric patients. Int J Obstet Anesth 1997;6:107–11.[Web of Science][Medline]
  5. Espinoza LR, Hartmann RC. Significance of the lupus anticoagulant. Am J Hematol 1986;22:331–7.[Web of Science][Medline]
  6. Shapiro S, Thiagarajan P. Lupus anticoagulant. Prog Hemost Thromb 1982;6:263–85.[Web of Science][Medline]




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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins and Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press