Anesth Analg 2000;90:892-893
© 2000 International Anesthesia Research Society
OBSTETRIC ANESTHESIA
Severe Hypoglycemia After Labor Epidural Analgesia
Jeffrey S. Jacobs, MD,
Ricardo Vallejo, MD,
Gerard J. DeSouza, MD, and
Menno F. TerRiet, MD
Miami VAMC Department of Anesthesiology/University of Miami School of Medicine, Miami, Florida
Address correspondence to Jeffrey S. Jacobs, MD, 5334 SW 32nd Terrace, Ft. Lauderdale, FL 33312. Address e-mail to jjgasman{at}att.net
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Introduction
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Severe hypoglycemia in nondiabetic parturients is a rare but potentially dangerous event. We describe such a case, which occurred after initiation of epidural analgesia.
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Case Report
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A healthy, 30-yr-old, 154-cm, 54-kg primigravida taking only prenatal vitamins presented for the induction of labor at 38.5 wk of gestation. The induction began with a dinoprostone vaginal insert followed by oxytocin infusion titrated to produce contractions every 5 min. Per obstetric protocol, she received 1 L of D5NS over 4 h and then lactated Ringer’s solution at 125 mL/hr. Approximately 6 h after admission, the patient complained of severe pain at a cervical dilation of 3 cm and requested epidural analgesia. An IV bolus of 500 mL of normal saline was given, and the patient was placed in the sitting position. A 17-gauge Tuohy epidural needle was inserted at the L3-4 interspace after 1% lidocaine skin infiltration. When loss of resistance was felt, a multi-orifice catheter was threaded 3 cm. Aspiration for blood or cerebrospinal fluid was negative, and a test dose using 3 mL of 1.5% lidocaine with 5 µg epinephrine/mL was negative for signs of intrathecal or IV administration. Five milliliters of 0.25% bupivacaine was injected, and within 15 min, the patient had a sensory dermatomal level of T4 and was pain free. She did not exhibit a motor block, but because of the high sensory level, a continuous epidural infusion was not started. Approximately 75 min after the initial bolus, the patient’s pain returned and examination revealed a sensory level of T12. After negative aspiration for blood or cerebrospinal fluid and another negative test dose, 5 mL of bupivacaine 0.25% was injected. Approximately 10 min later, she complained of lightheadedness, facial tingling, and lethargy and stated "this is how I feel when I’m very hungry." Her heart rate and blood pressure were unchanged, and her sensory level was T6. Suddenly, she became stuporous and responded only to loud verbal commands. An immediate fingerstick (Surestix; Johnson & Johnson, Milpitas, CA) revealed a glucose of 18 mg/dL, and a repeat fingerstick was 16 mg/dL. Fifty milliliters of 50% dextrose was administered IV with almost immediate improvement of her mental status. A fingerstick (240 mg/dL) and blood glucose (223 mg/dL) at that time reflected her clinical improvement. Pelvic examination revealed a completely dilated and effaced cervix, and uneventful delivery of a newborn male with Apgar scores of 9 and 10 (1 and 5 min, respectively) occurred 30 min later. Approximately 60 min postpartum, a repeat blood glucose was 40 mg/dL, however the patient remained asymptomatic at that time. Her sensory level of anesthesia subsided by 90 min after delivery. The infant’s glucose was monitored for the first 24 h, remained normal, and he is healthy at 1 yr.
Postpartum follow-up for the parturient included normal results of oral glucose-tolerance test, adrenocorticotropic hormone, cortisol, glucagon, insulin, and thyroid function tests. By exclusion, she was diagnosed with "reactive hypoglycemia" and advised to have her blood glucose closely monitored during subsequent pregnancies.
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Discussion
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Pregnant women tend to develop hypoglycemia more readily than nonpregnant women because they are in a state of "accelerated starvation" (1). Prolonged labor, work of delivery, and fasting are contributing causes. Additionally, epidural analgesia inhibits the hyperglycemic response to pain and surgical stress, blocks sympathetic tone, and removes the autonomic control of both the adrenal medulla and the hepatic glycogenolytic systems (2).
Hormonal responses (glucagon and epinephrine release) to hypoglycemia in the nonpregnant patient usually begin at a plasma glucose concentration of 64–68 mg/dL, inducing glycogenolysis and gluconeogenesis (3). In nonpregnant patients, autonomic symptoms start below a concentration of 55–60 mg/dL, and symptoms of cerebral hypoglycemia begin below 48–54 mg/dL (4). In the parturient, however, this hypoglycemic counter-regulatory hormone response is impaired (5). Hypoglycemia fails to stimulate glucagon and epinephrine release during pregnancy, and norepinephrine levels change minimally (4,6). Studies in pregnant rats suggest that these responses are more impaired during fasting because of an increase in ß-OH butyric acid (6). Additionally, arginine-stimulated glucagon release is reduced during pregnancy by increased levels of estrogen and progesterone (5). Growth hormone and cortisol normally prolong the effects of both glucagon and epinephrine, but they too are decreased during pregnancy, because of increases in placental hormones with somatostatin-like activity (5). Most hospitals have a fasting policy for laboring women to decrease the risk of aspiration. Although the American College of Obstetrics and Gynecology advocates this policy (7), fasting may predispose to maternal hypoglycemia.
Because this patient initially developed a relatively "high" sensory level from a low volume (8 mL) of local anesthetic, a continuous infusion was not used. Per routine, an epinephrine-containing local anesthetic test dose was before bolus drug administration through the labor epidural catheter. Because the catheter aspiration was negative (8) and she did not exhibit tachycardia or lower extremity motor block after a test dose, it was unlikely that her symptoms were caused by either intravascular or subarachnoid injection. Hypoglycemia was considered only because our patient stated that her symptoms were similar to what she experienced when she was hungry.
Blood glucose level was initially determined by fingerstick, which has been shown to correlate with laboratory blood glucose levels ±20% (9) (B. Ney, oral communication, September 3, 1999). Because of the emergent situation in this patient, a confirmatory blood sample was not sent to the laboratory until after treatment was started. After treatment, however, the fingerstick and laboratory values were similar. This information, when combined with her almost immediate response to treatment and her subsequent laboratory-confirmed hypoglycemia, strongly suggest that her initial fingerstick values were real.
This patient received lactated Ringer’s solution, which should not have precipitated profound hypoglycemia, because large amounts of nonglucose-containing crystalloids have been given to parturients without causing dilutional hypoglycemia (10). Additionally, she received dinoprostone and oxytocin, but neither is associated with hypoglycemia.
This is not the first report of hypoglycemia during labor (11), but this is the first report of a healthy parturient who suffered profound symptomatic hypoglycemia under epidural analgesia. Based on this case, hypoglycemia should be considered in the differential of a parturient who develops mental status changes after receiving epidural medications. The specific contribution of epidural analgesia to maternal hypoglycemia warrants further study.
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References
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Rosenn B, Miodovnik M, Khoury J, Siddiqi TA. Counterregulatory hormonal response to hypoglycemia during pregnancy. Obstet Gynecol 1996;87:568–74.[Web of Science][Medline]
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Luyckx AS, Gaspard U, Lefebvre PJ. Influence of elevated free fatty acids on the Glucagon response to hypoglycemia in normal and in pregnant women. Metabolism 1978;27:1033–40.[Medline]
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American Academy of Pediatrics and American College of Obstetrics and Gynecology. Guidelines for perinatal care, 4th ed. Washington, DC: , 1997.
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Norris MC, Ferrenbach D, Dalman H, et al. Does epinephrine improve the diagnostic accuracy of aspiration during labor epidural analgesia? Anesth Analg 1999;88:1073–6.[Abstract/Free Full Text]
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Clark WL, Cox D, Gonder-frederick LA, et al. Evaluating clinical accuracy of systems for self-monitoring of blood glucose. Care 1987;10:622–8.
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Chestnut DH, Bates JN, Choi WW. Effect of intravenous administration of Ringer’s lactate on maternal capillary blood glucose before elective Cesarean section. J Reprod Med 1987;32:191–3.[Medline]
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Smallridge RC, Corrigan DF, Thomason AM, Blue PW. Hypoglycemia in pregnancy: occurrence due to adrenocorticotropic hormone and growth hormone deficiency. Intern Med 1980; 40:564–5.
Accepted for publication December 16, 1999.
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Introduction
Case Report
