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| CASE REPORT |
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| Year : 2014 | Volume
: 4
| Issue : 2 | Page : 75-77 |
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A case of fetal bradycardia following dexmedetomidine bolus
Menachem M Weiner, Robert Chow, Benjamin S Salter
Department of Anesthesiology, Icahn School of Medicine at Mount Sinai, New York, NY, USA
| Date of Web Publication | 1-Nov-2014 |
Correspondence Address:
Menachem M Weiner
Department of Anesthesiology, The Mount Sinai Medical Center, One Gustave L. Levy Place, Box 1010, New York, NY 10029-6574
USA
 Source of Support: Intramural Departmental Funding, Conflict of Interest: None  | Check |
DOI: 10.4103/2249-4472.143876
We report a case of fetal bradycardia immediately following the maternal administration of an intravenous bolus of dexmedetomidine for transesophageal echocardiography. Dexmedetomidine, a central acting selective alpha-2 agonist is increasingly being used for sedation. Little is known regarding placental transfer of dexmedetomide with most reports suggesting minimal transfer. A case of fetal bradycardia resulting from its administration has not been previously reported.
Keywords: Dexmedetomidine, mitral stenosis, placental transfer
How to cite this article:
Weiner MM, Chow R, Salter BS. A case of fetal bradycardia following dexmedetomidine bolus
. J Obstet Anaesth Crit Care 2014;4:75-7 |
How to cite this URL:
Weiner MM, Chow R, Salter BS. A case of fetal bradycardia following dexmedetomidine bolus
. J Obstet Anaesth Crit Care [serial online] 2014 [cited 2023 Feb 5];4:75-7. Available from: https://www.joacc.com/text.asp?2014/4/2/75/143876 |
| Introduction | |  |
Dexmedetomidine is a central acting selective alpha-2 agonist that is increasingly being used for sedation both in intensive care units as well as to facilitate procedures such as awake fiberoptic intubations. Little is known regarding the placental transfer of dexmedetomidine when administered to a parturient. The few case reports that have been published documenting its administration to pregnant women all suggest minimal fetal effects with conflicting data on placental transfer. [1],[2] We present a case where fetal bradycardia ensued immediately following the bolus administration of dexmedetomidine to a pregnant woman with mitral stenosis (MS).
| Case report | | |
A 33-year-old woman weighing 75 kg (gravida 2; para 1) at 27 weeks gestation with severe MS complicated by pulmonary hypertension (PHT) presented for percutaneous balloon mitral valvuloplasty (PBMV). The patient had complained of new onset shortness of breath, lower extremity edema, and palpitations. She was found to be in supraventricular tachycardia. The patient was immediately started on metoprolol and sent for a transthoracic echocardiogram, which revealed severe MS with a mean gradient of 18 mmHg and a valve area of 0.7 cm 2 . The decision was made to for her to undergo PBMV.
Prior to the procedure, the patient was positioned in the left uterine displacement position, a right radial arterial catheter was placed for hemodynamic monitoring, and continuous fetal heart rate (FHR) monitoring was placed. An obstetrical team was on standby for emergency cesarean section and a cardiac surgeon was available in case of maternal decompensation. An intravenous infusion of dexmedetomidine (0.7 mcg/kg/h) was started. Both maternal and fetal vital signs remained stable as the procedure started with maternal heart rate ranging from 90 to 100 bpm, maternal arterial blood pressure ranging from a systolic of 120 to 130 mmHg and diastolic from 70 to 80 mmHg and FHR ranging from 140 to 150 bpm with good variability. After initial transthoracic echocardiographic examination confirmed severe MS [Figure 1] it was determined that a transesophageal echocardiogram (TEE) was required for procedural guidance. The patient's oropharynx was topicalized with viscous lidocaine, and a bolus dose of dexmedetomidine (1 mcg/kg) was administered for deeper sedation to facilitate placement of the TEE probe. Immediately following its administration there was a fetal bradycardia with FHR dipping to 102 bpm [Figure 2] despite no significant change in maternal vital signs (maternal blood pressure remained the same and heart rate dropped slightly to 80 bpm). There was no other obvious cause for the reduction of FHR. The FHR slowly returned to baseline over the next few minutes, and no fetal intervention was deemed necessary. After successful PBMV, TEE showed a decrease in transmitral mean gradient from 18 to 4 mmHg [Figure 3] and [Figure 4] and much improved mitral valve (MV) opening [Figure 5]. | Figure 1: Transesophageal echocardiography: Midesophageal 4-chamber view demonstrating a stenotic MV. The LA is filled with spontaneous echocardiography contrast (or "smoke") due to stagnation of blood flow. LA: Left atrium, MV: Mitral valve, LV: Left ventricle
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 | Figure 2: Fetal heart tracing: Fetal bradycardia following the maternal intravenous administration of dexmedetomidine is seen
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 | Figure 3: Transthracic echocardiography: Continuous wave Doppler interrogation of transmitral flow demonstrating high gradient
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 | Figure 4: Transesophageal echocardiography: Continuous wave Doppler interrogation of transmitral flow demonstrating a much lower gradient following the valvuloplasty
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 | Figure 5: Transesophageal echocardiography: Midesophageal long-axis (left) and 4-chamber view (right) demonstrating greater opening of the MV following the valvuloplasty. LA: Left atrium, MV: Mitral valve, LV: Left ventricle
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| Discussion | | |
Severe MS is not well-tolerated in pregnancy. Normal pregnancy results in dramatic changes in the cardiovascular system including a 30-50% increase in blood volume and cardiac output and a decrease in systemic vascular resistance. [3],[4],[5],[6] In women with MS the gradient across the diseased MV increases as cardiac output increases during pregnancy causing an increase in left atrial pressure. The decrease in diastolic left ventricular filling time associated with pregnancy-induced tachycardia further increases left atrial pressures. [7] This increases the risk of pulmonary edema as this pressure increase is reflected back into the pulmonary venous circulation. Left untreated, PHT will result leading to increases in right ventricular pressures and if severe, to right ventricular failure. [7] PHT is associated with both extremely high maternal and fetal morbidity and mortality. [8]
Patients with MS in pregnancy will first be treated with medical therapy consisting primarily of heart rate control with beta-blockers as more time for diastolic filling is necessary to ensure adequate preload with the increase in transmitral gradient. The main hemodynamic goal in MS is to avoid tachycardia in order to optimize left ventricular diastolic filling time. [9] Other hemodynamic goals are the maintenance of normal to high preload, afterload, and contractility. Large decreases in systemic vascular resistance, resulting in reflex tachycardia, are poorly tolerated. If worsening or recurrent heart failure occurs despite medical therapy selected patients can be effectively managed with PBMV. [10]
Dexmedetomidine is a central acting selective alpha-2 agonist with minimal respiratory suppression that has been shown to have significant analgesic and sympatholytic properties. [11] It has been assigned to pregnancy category C due to the lack of well-controlled studies of its use during pregnancy and should only be used if the potential benefits justify the potential risk to the fetus. We believe that this was true in our patient with severe MS. It was chosen as the anesthetic for this procedure because of its unique properties allowing us to avoid tachycardia in order to optimize left ventricular diastolic filling time. Due to its greater alpha-2 selectivity than clonidine, which is known to cross the placenta and affect FHR and also have affects on uterine tone, [12] it has been used successfully during pregnancy and during labor. It has been reported to decrease opioid use, promote hemodynamic stability, and maintain placental blood flow during nonobstetric surgery in pregnant patients. [13] There are no in vivo human studies on placental transfer of dexmedetomidine or its effects on the neonate. One in vitro study did demonstrate much lower fetal maternal to fetal transfer with dexmedetomidine than with clonidine presumably due to its greater lipophilicity. [14]
Neumann et al. [1] report on the use of dexmedetomidine for awake fiberoptic intubation prior to cesarean section in a patient with spinal muscular atrophy. They found that there was significant fetal transfer, but minimal fetal effects with no resulting fetal bradycardia and normal umbilical cord blood gas analysis. Palanisamy et al. [2] report the successful use of dexmedetomidine as an adjunct for labor analgesia. No FHR irregularities occurred.
We believe that this is the first report of fetal effects from maternal administration of dexmedetomidine. Our dose of dexmedetomidine is similar to the doses used elsewhere and in the cited case reports. While specific pharmacokinetic data cannot be determined, this does seem to confirm previous reports of placental transfer of dexmedetomidine. Our case demonstrates that dexmedetomidine can have fetal effects. The multidisciplinary team caring for a pregnant patient who requires nonobstetrical care needs to be aware of this and treat the patient accordingly. Further studies are needed to determine maternal and fetal serum drug levels and fetal and neonatal effects.
| References | | |
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| 2. | Palanisamy A, Klickovich RJ, Ramsay M, Ouyang DW, Tsen LC. Intravenous dexmedetomidine as an adjunct for labor analgesia and cesarean delivery anesthesia in a parturient with a tethered spinal cord. Int J Obstet Anesth 2009;18:258-61. |
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| 11. | Coursin DB, Coursin DB, Maccioli GA. Dexmedetomidine. Curr Opin Crit Care 2001;7:221-6. |
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| 13. | Souza KM, Anzoategui LC, Pedroso WC, Gemperli WA. Dexmedetomidine in general anesthesia for surgical treatment of cerebral aneurysm in pregnant patient with specific hypertensive disease of pregnancy: Case report. Rev Bras Anestesiol 2005;55:212-6. |
| 14. | Ala-Kokko TI, Pienimäki P, Lampela E, Hollmén AI, Pelkonen O, Vähäkangas K. Transfer of clonidine and dexmedetomidine across the isolated perfused human placenta. Acta Anaesthesiol Scand 1997;41:313-9. |
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]
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