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Anesth Analg 2002;94:450-452
© 2002 International Anesthesia Research Society


REGIONAL ANESTHESIA

Interscalene and Infraclavicular Block for Bilateral Distal Radius Fracture

Konrad Maurer, MD*, Georgios Ekatodramis, MD*, Katharina Rentsch, MD{dagger}, and Alain Borgeat, MD*

Departments of *Anesthesiology and {dagger}Clinical Chemistry, University Hospital Zurich/Balgrist, Zurich, Switzerland

Address correspondence and reprint requests to Alain Borgeat, Chief of Staff Anesthesiology, Orthopedic University Clinic of Zurich/Balgrist, Forchstrasse 340, CH-8008 Zurich, Switzerland. Address e-mail to aborgeat{at}balgrist.unizh.ch


    Abstract
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 Abstract
 Case Report
 Discussion
 References
 
Brachial plexus blockade is a suitable technique for surgery of the forearm, because it provides good intraoperative anesthesia as well as prolonged postoperative analgesia when long-acting local anesthetics are used. However, simultaneous blockade of both upper extremities has rarely been performed (1), because local anesthetic toxicity caused by the amount of drug needed to achieve an efficient block on both sides may be a problem. We report a case of successful bilateral brachial plexus block with ropivacaine in a patient with bilateral distal radius fracture, with each fracture requiring an open osteosynthesis.

IMPLICATIONS: This case report presents the performance of a simultaneous blockade of both upper extremities in a patient who sustained a bilateral distal radius fracture. The patient was known to be difficult to intubate and to have a severe hypersensitivity to opioids.


    Case Report
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A 21-yr-old woman (58 kg, 160 cm, ASA physical status I) with bilateral distal fractures of the radius was admitted to our hospital 3 h after a snowboard accident. Immediately before the accident she consumed a complete meal. On arrival she complained of severe pain (visual analog scale score of 80 on a scale from 0 = no pain to 100 = worst pain imaginable). Her medical history was remarkable for smoking, asthma, symptomatic hiatal hernia, and hypersensitivity to opioids (vomiting). Two years before, she underwent an appendectomy. After the operation she was told that tracheal intubation was very difficult because of anatomic problems. Except for a Mallampati III airway, physical examination was unremarkable. Because of her past bad experience with morphine, the patient insisted on not receiving any opioids if possible. A regional anesthetic technique was therefore chosen. The patient was premedicated with 7.5 mg of midazolam orally 30 min before starting anesthesia. Monitoring included a continuous three-lead electrocardiogram, noninvasive blood pressure measurement, and pulse oximetry. IV access was established on the left foot. On the right side, an interscalene block (ISB) was performed with the use of a neurostimulator (Stimuplex, HNS 11; Braun Melsungen, Melsungen, Germany). The brachial plexus was localized on the first attempt, and a triceps contraction was obtained with a threshold of <0.32 mA and an impulse duration of 0.1 ms. On the left side, an infraclavicular block, according to the modified approach of the Raj technique (2), was performed 20 min later. Flexion of the fingers was obtained with a threshold of <0.28 mA and an impulse duration of 0.1 ms. The patient received 35 mL of ropivacaine 0.5% on each side (total volume, 70 mL ropivacaine 0.5% [350 mg]). Twenty minutes after receiving the second block, complete anesthesia (presence of paresthesias of the thumb and middle finger, inability to recognize cold in the five terminal nerves of the forearm—except of the ulnar nerve on the ISB side—associated with the disappearance of pain caused by the trauma) and motor blockade (inability to flex or extend the wrist and elbow) were present in both upper limbs. At this time, a targeted sedative concentration of 0.5 µg/mL propofol using the TCI (target-controlled infusion) technique (TCI Deltec Graseby 3500; Laubscher, Basel, Switzerland, and Diprifusor subsystem; AstraZeneca Ltd., Macclesfield, Cheshire, UK) was given to increase the threshold of central nervous system (CNS) toxicity. Venous plasma concentrations (high-pressure liquid chromatography/mass spectrometry) of total ropivacaine (free ropivacaine) measured 30, 60, and 90 min after the administration of the second block (Fig. 1) were 4.4 mg/L (0.27 mg/mL), 3.8 mg/L (0.24 mg/mL), and 3.3 mg/L (0.22 mg/mL) respectively. {alpha}1-Acid-glycoprotein was within normal range at all times (0.6, 0.58, and 0.6 g/L, respectively). No supplementary analgesics were needed during surgery, which lasted 100 min. The blocks wore off on both sides 7 h later, and postoperative pain could be controlled with nonsteroidal antiinflammatory drugs and propacetamol. Before leaving the hospital, 24 h after surgery, the patient reported her experience with anesthesia to be "as comfortable as can be expected in a similar situation."



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Figure 1. Venous plasma concentration of ropivacaine/{alpha}1-glycoprotein: time course evolution of total ({diamond}) and free ({blacktriangleup}) ropivacaine concentration. First arrow = time of application of 35 mL of ropivacaine 0.5% for the interscalene block on the right side; second arrow = time of application of 35 mL of ropivacaine 0.5% for the infraclavicular block on the left side

 

    Discussion
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 Abstract
 Case Report
 Discussion
 References
 
The constellation of a known difficult tracheal intubation, a symptomatic hiatal hernia, a full stomach, and the urgency to perform surgery (swelling of the injured members) led us to choose a bilateral regional anesthetic technique. On the right side, an ISB was performed because surgery did not involve the ulnar part of the forearm and the patient was not able to abduct her right arm (to permit an axillary block) because of pain. To prevent bilateral phrenic nerve paresis (3), an infraclavicular approach was chosen to block the left arm. Open surgery on both arms requires a large volume of local anesthetic to achieve adequate anesthesia, and therefore ropivacaine was chosen because it has a greater margin of safety (47). The second block was performed 20 minutes after the first one to limit the peak plasma concentration, which occurs, in our experience, 20 to 45 minutes after bolus administration (pilot study, unpublished data). The patient received a total dose of 350 mg of ropivacaine, which is superior to the recommended maximal dosage of 300 mg. In our experience, 40 mL is the most adequate volume to achieve a complete ISB or infraclavicular block. In this case we, therefore, compromised by giving 2 x 35 mL to ensure the success of the blocks and to minimize the potential risks of side effects. Our main concern was not the development of CNS toxicity, which can be easily and rapidly treated (8), but the appearance of cardiac toxicity. The constellation of a young, healthy, athletic patient and the known increased safety margin of ropivacaine (9,10) convinced us to slightly exceed the recommended dose. The measured venous blood concentrations of ropivacaine were larger than those tolerated by 12 unpremedicated healthy male subjects (total ropivacaine 0.5–3.2 mg/L, free ropivacaine 0.01–0.24 mg/L) (4). Propofol may increase the CNS threshold for local anesthetic toxicity because it has an agonist action on the {gamma}-aminobutyric acid-A receptor (11,12), has a global depression effect on the CNS (13), and inhibits the release of glutamate from the CNS (14). Propofol is very effective for treating either bupivacaine- or lidocaine-induced seizures (15,16), as well as refractory status epilepticus (17), in experimental studies. These interactions between propofol and epilepsy may explain the absence of any signs of CNS toxicity in this case despite the relatively large ropivacaine blood concentration. One of the characteristics of ropivacaine CNS toxicity—in the absence of direct IV administration—is the progressive appearance of premonitory signs (18), giving the clinician time to adjust the needed dose of propofol—or other drugs—accordingly and therefore to avoid the development of full seizure activity, which was particularly important in this case (full stomach and difficult airway).

In summary, we described a successful bilateral brachial plexus block performed with ropivacaine (350 mg) using a small concentration of propofol (TCI target of 0.5 µg/mL) in a very specific clinical situation without occurrence of signs of CNS or cardiac toxicity, despite a relatively high level of total and free ropivacaine venous plasma concentration. However, such a technique may be associated with complications caused by the relatively large drug dosage. Therefore, we reduced by 25 mg the usual amount of ropivacaine needed. Any further reduction would have jeopardized the success of the block. We questioned whether it would have been wiser to decrease the volume of drugs given, particularly for the infraclavicular block, but at the risk of an incomplete block. The appearance of signs of CNS toxicity can be treated in this context easily and very efficiently, but the development of cardiac toxicity may have severe consequences. We therefore recommend reserving this practice for particular indications in selected patients, such as the young and healthy.


    References
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 Abstract
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 References
 

  1. Lierz P, Schroegendorfer K, Choi S, et al. Continuous blockade of both brachial plexus with ropivacaine in phantom pain: a case report. Pain 1998; 78: 135–7.[ISI][Medline]
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  3. Urmey WF, Talts KH, Sharrock NE. One hundred percent incidence of hemidiaphragmatic paresis associated with interscalene brachial plexus anesthesia as diagnosed by ultrasonography. Anesth Analg 1991; 72: 498–503.[Abstract/Free Full Text]
  4. Knudsen K, Beckman M, Blomberg S, et al. Central nervous and cardiovascular effects of i.v. infusions of ropivacaine, bupivacaine and placebo in volunteers. Br J Anaesth 1997; 78: 507–14.[Abstract/Free Full Text]
  5. McClure JH. Review article: ropivacaine. Br J Anaesth 1996; 76: 300–7.[Free Full Text]
  6. Reiz S, Häggmark S, Johansson G, Nath S. Cardiotoxicity of ropivacaine: a new amide local anaesthetic agent. Acta Anaesthesiol Scand 1989; 33: 93–8.[ISI][Medline]
  7. Scott DB, Lee A, Fagan D, et al. Acute toxicity of ropivacaine compared with that of bupivacaine. Anesth Analg 1989; 69: 563–9.[Abstract/Free Full Text]
  8. Ruetsch YA, Fattinger KE, Borgeat A. Ropivacaine-induced convulsions and severe cardiac dysrhythmia after sciatic block. Anesthesiology 1999; 90: 1784–6.[ISI][Medline]
  9. Groban L, Deal DD, Vernon JC, et al. Cardiac resuscitation after incremental overdosage with lidocaine, bupivacaine, levobupivacaine, and ropivacaine in anesthetized dogs. Anesth Analg 2001; 92: 37–43.[Abstract/Free Full Text]
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  13. Cavazzuti M, Porro CA, Barbieri A, Galetti A. Brain and spinal cord metabolic activity during propofol anesthesia. Br J Anaesth 1991; 66: 490–5.[Abstract/Free Full Text]
  14. Collins GGS. Effects of the anesthetic 2,6-diisopropylphenol on synaptic transmission in the rat olfactory cortex slice. Br J Pharmacol 1988; 95: 939–49.[ISI][Medline]
  15. Heavner JE, Arthur J, Zou J, et al. Comparison of propofol with thiopentone for treatment of bupivacaine-induced seizures in rats. Br J Anaesth 1993; 71: 715–9.[Abstract/Free Full Text]
  16. Momota Y, Artru AA, Powers KM, et al. Posttreatment with propofol terminates lidocaine-induced epileptiform electroencephalogram activity in rabbits: effects on cerebrospinal fluid dynamics. Anesth Analg 1998; 87: 900–6.[Abstract/Free Full Text]
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Accepted for publication October 2, 2001.




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