Anesth Analg 2001;92:276-277
© 2001 International Anesthesia Research Society
CASE REPORTS
Indigo Carmine-Induced Bradycardia in a Patient During General Anesthesia
Ken-ichi Satoh, DDS, PhD,
Nozomu Sakamoto, DDS,
Yutaka Shinohe, DDS,
Maki Satoh, DDS, and
Shigeharu Joh, DDS, PhD
Department of Dental Anesthesiology, School of Dentistry, Iwate Medical University
Address correspondence and reprint requests to Ken-ichi Satoh, DDS, PhD, Department of Dental Anesthesiology, School of Dentistry, Iwate Medical University, 1–3-27 Chuohdohri, Morioka, Iwate 020-8505, Japan. Address e-mail to makeanu{at}dj.mbn.or.jp
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Abstract
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Implications: Indigo carmine is very often used to confirm if catheters for delivering anticancer drugs are placed in the appropriate vicinity of tumors. This report demonstrates that severe bradycardia can occur after intraarterial administration of indigo carmine.
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Introduction
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The blue dye indigo carmine (sodium indigotindisulfonate) is administered intravascularly in a variety of treatments: to locate ureteral orifices (1), to endoscopically examine gastric cancer (2), and to adjust the position of a catheter in the chemotherapy of hepatic tumors (3) and of oralmaxillo-facial tumors (4). Nevertheless, care must be taken when using indigo carmine because it occasionally induces adverse reactions, such as hypertension accompanied by bradycardia (5,6), bronchospasm, and urticaria (7). We report another adverse reaction, severe bradycardia without changes in blood pressure (BP), that was induced when indigo carmine was intraarterially administered to a patient during general anesthesia.
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Case Report
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A 62-yr-old woman, 54 kg, was admitted with an angiosarcoma in the cranial skin. Her medical history included old myocardial infarction and unstable angina pectoris. Her left ventricular function was normal with an ejection fraction of 73%. She was prescribed the vasodilator nicorandil (half-life 0.75 h) for 6 months. Her preoperative electrocardiogram showed a normal sinus rhythm, a low voltage, 0.3 mV, in all limb leads, a prolonged QT of 0.48 s, and inverted T waves and depressed ST confined to III, aVF, and V1–6 leads. All other laboratory values were within normal ranges. She had no drug allergies.
Anesthesia was induced with thiopental (250 mg) and vecuronium (6 mg) and then maintained with sevoflurane (1–2%) and fentanyl (100 µg) after endotracheal intubation. Her state of hemodynamics was stable for the subsequent 90 min: heart rate (HR) was 58–78 bpm, systolic BP 90–110 mm Hg, diastolic BP 48–68 mm Hg, and SpO2 99–100%. A catheter was placed in the right superior thyroid artery and 10 mL of 0.8% indigo carmine injected over a period of 30 s. Her HR decreased rapidly to 36 bpm, but her BP was approximately 96/54 mm Hg. Atropine (0.2 mg) was given IV and the HR was restored within 3 min to the level before indigo carmine injection. SpO2, end-tidal CO2, and ST-T segment were not changed. After we confirmed her stable hemodynamics in the subsequent 115 min (HR was 60–68 bpm, systolic BP 85–140 mm Hg, diastolic BP 46–80 mm Hg, and SpO2 99–100%), the left superior thyroid artery was catheterized and 10 mL of 0.8% indigo carmine injected over a 30-s period. Again her HR decreased rapidly to 50 bpm and BP remained around 126/75 mm Hg. This HR decrease was probably attributable to slowed sinus rhythm because her lead II electrocardiogram demonstrated regular heartbeats, normal forms of P wave and QRS complex, and P waves each followed by a QRS complex. Atropine, 0.2 mg, was given IV, but her HR continued to decrease to 32 bpm within a few s; even though a further 0.2 mg of atropine was given, signals on the electrocardiogram disappeared for approximately 10 s. The inhalation of sevoflurane was stopped, and 100% oxygen was administered. Her HR gradually increased to 72 bpm within approximately 30 s. The surgery was completed successfully approximately 45 min after this episode.
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Discussion
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The hemodynamic effects most often encountered on intravascular indigo carmine administration are increases in diastolic and systolic BP, which usually elicit reflex decreases in stroke volume and HR (5,6).
In contrast, severe bradycardia without changes in BP occurred in our patient who was administered indigo carmine intraarterially. We had previously experienced similar severe bradycardia in three other patients; on injection of 3 mL of 0.8% indigo carmine into the superficial temporal artery during IV sedation, HR rapidly decreased from 62–74 bpm to 45–52 bpm, but BP was not changed. After the HR was restored, 5 mL of saline was injected into the same artery, but no changes in hemodynamics were observed. Thus, bradycardia associated with indigo carmine does not always occur after hypertension. Though this patient took nicorandil preoperatively (but not on the day of surgery), we do not think nicorandil was implicated in the bradycardia, because it is confirmed in open-chest, generally anesthetized dogs that nicorandil does not affect HR as long as it is used at doses normally given for treating coronary arterial sclerosis (8,9).
Sudden severe hypotension also occurs in an otherwise stable surgery when indigo carmine is injected IV (10,11). Hence, the effects of intravascularly injected indigo carmine on hemodynamics are variable and difficult to anticipate. We do not have enough data to judge whether the effect of indigo carmine differs depending on the region of the body at which it is introduced. The pharmacological mechanism of action of indigo carmine needs to be clarified. It is prudent to consider the possibility of these adverse reactions when a bolus of indigo carmine is administered intravascularly.
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References
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Accepted for publication September 1, 2000.
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Abstract
Introduction
