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Revista Brasileira de Anestesiologia

Print version ISSN 0034-7094

Rev. Bras. Anestesiol. vol.54 no.6 Campinas Nov./Dec. 2004 



Accidental intravascular injection of 0.5% ropivacaine during thoracic epidural anesthesia. Case reports*


Inyección intravascular accidental de ropivacaína a 0,5% durante la realización de anestesia peridural torácica. Relato de casos



Fábio Geraldo Curtis, TSA, M.D.I; Robson Furlani, M.D.II; Yara Marcondes Machado Castiglia, TSA, M.D.III

IMestre em Anestesiologia/Membro do CET/SBA do Departamento de Anestesiologia da FMB UNESP; Anestesiologista do Hospital Santa Helena e da Clínica Pardo Oftalmologia  de São José do Rio Preto, SP
IIAnestesiologista do Hospital Santa Helena e da Clínica Pardo Oftalmologia de São José do Rio Preto, SP
IIIProfessora Titular do Departamento de Anestesiologia da FMB UNESP





BACKGROUND AND OBJECTIVES: Ropivacaine was introduced in the clinical practice a little more than 10 years ago, and has been associated to low risk for central nervous system and cardiovascular complications. These reports aimed at presenting a case of cardiac arrest and another one of neurological toxicity after accidental intravascular ropivacaine injection during epidural anesthesia.
CASE REPORTS: Two patients undergoing cosmetic plastic surgeries were submitted to  thoracic epidural anesthesia with 0.5% ropivacaine. After anesthetic injection, one has presented cardiac arrest in asystole and the other had signs of neurological toxicity. Patients were promptly treated and presented fast recovery, in a way that both surgical procedures could be performed.
CONCLUSIONS: The prompt Identification and treatment of the accidental intravascular injection, as well as ropivacaine pharmacological profile, were decisive in both cases for the satisfactory recovery of our patients.

Key Words: ANESTHETICS, Local: ropivacaine; ANESTHETIC TECHNIQUES, Regional: epidural; COMPLICATIONS: accidental injection


JUSTIFICATIVA Y OBJETIVOS: A ropivacaína fue introducida en la práctica clínica hace poco más de diez años, asociándose a bajo riesgo de complicaciones del sistema nervioso central y cardiovascular. Estos relatos tienen como objetivo presentar un caso de parada cardíaca y otro de toxicidad neurológica, después de inyección intravascular accidental de ropivacaína, durante la realización de anestesias peridurales.
RELATO DE LOS CASOS: Se trata de dos pacientes sometidas a cirugías plásticas estéticas bajo anestesia peridural torácica con ropivacaína a 0,5%. Durante la realización de la técnica, una de ellas presentó parada cardíaca en asistolia y la otra, toxicidad neurológica. Prontamente atendidas, ambas presentaron rápida recuperación, habiendo sido posible la realización de los respectivos actos quirúrgicos.
CONCLUSIONES: El reconocimiento y el tratamiento rápidos de la inyección intravascular accidental, bien como las características farmacológicas de la ropivacaína fueron decisivos, en ambos casos, con una buena recuperación de las pacientes.




Ropivacaine has been introduced in the clinical practice as potentially safer than bupivacaine 1. It is currently widely used in regional anesthesia because of its peculiarities, in particular the lower neuro and cardiotoxicity as compared to bupivacaine 2,3. Akerman et al. 4 have shown that bupivacaine produces a more intense block in Ad and C fibers (sensory fibers), while in other experimental models with dogs, motor block has been less intensive and shorter as compared to bupivacaine 5.

Thoracic epidural anesthesia is often employed in Brazil, especially for plastic surgeries 6, since it reduces operative bleeding by decreasing blood pressure. Systemic toxicity due to accidental intravascular injection, spinal injection and total spinal anesthesia, as well as neurological injuries are potential complications of this technique. Recent publications 7,8 have described ropivacaine-induced intoxication after peripheral nerve block, evolving to cardiac arrest which was promptly treated and reverted.

These reports aimed at presenting a case of cardiac arrest and another one of neurological toxicity after thoracic epidural anesthesia with 0.5% ropivacaine.



Case 1

A 49-year-old female patient, 83 kg, 170 cm, physical status ASA II, was scheduled to a  abdomen lipodystrophy correction. Her clinical history included arterial hypertension irregularly treated with propranolol (40 mg/day), spontaneously withdrawn 2 weeks before, ischemic encephalic stroke without neurological sequelae, morbid obesity and 3 surgeries to correct herniated lumbar disks.

Venoclysis of upper limb was performed in the operating room and lactated Ringer's solution infusion was started. After monitoring (noninvasive blood pressure, pulse oximetry and ECG at DII lead), patient was given 3 mg intravenous midazolam and then placed in the sitting position. Epidural puncture was performed with the Dogliotty technique at T10-T11 space. After a negative test dose with 60 mg of 2% lidocaine (3 mL) with epinephrine (1:200,000), 150 mg of 0.5% ropivacaine (30 mL) were administered and, even before the injection completion, patient referred ear hum and perioral paresthesia, immediately followed by loss of consciousness, tonoclonic seizures, bradycardia, hypotension and asystole.

Patient was ventilated with oxygen under facial mask, external cardiac massage was started and 1 mg intravenous epinephrine was administered, followed by cardiac function recovery with blood pressure = 160 x 95 mmHg, heart rate = 125 bpm and oximetry (SpO2) = 98%. Again patient presented seizures, now treated with sodium thiopental (375 mg), followed by tracheal intubation. Patient was then kept under general anesthesia and mechanical ventilation, with the aid of 30 µ alfentanil and 1% sevoflurane, monitored by the Dixtal gases analyzer. Neuromuscular block was obtained with 0.7 rocuronium.

Aiming at neurological protection, 10 mg dexamethasone and 20% mannitol (1 were infused. Since patient was hemodynamically stable, we decided to proceed with the proposed surgery, which lasted approximately 2 hours. At its completion, 1 mg atropine and 2 mg neostigmine were administered, in addition to 10 mg nalbuphine for postoperative analgesia. Patient had fast spontaneous breathing recovery and emergence, being extubated still in the operating room. In the post-anesthetic recovery unit (PACU), patient could not remember anything, would easily move limbs and did not refer pain, being discharged 2 hours later. No sequelae were observed during 6-month follow up.

Case 2

A 39-year-old female patient, 58 kg, 165 cm, physical status ASA I, was scheduled to mammary silicone prosthesis implant and abdominal liposuction. Venoclysis in upper limb was performed in the operating room and lactated Ringer's solution infusion was started. After monitoring with noninvasive blood pressure, pulse oximetry and ECG at DII lead, 2 mg intravenous midazolam was administered, followed by continuous propofol infusion by the Diprifusor® system (1 µg.mL-1 target-concentration). Patient was then placed in the sitting position.

Epidural puncture was performed with the Dogliotty technique at T8-T9. After a negative test-dose of 60 mg of 2% lidocaine (3 mL) with epinephrine (1:200,000), 150 mg of 0.5% ropivacaine was administered.

At the end of the initial 20 mL (100 mg) injection, blood reflux was observed thru the Tuohy needle (17G3½) when anesthetic syringe was being replaced. The needle was promptly removed and the patient immediately placed in the supine position. At this moment, she presented mental confusion followed by loss of consciousness and tonoclonic seizures. Propofol target concentration had to be increased to 2.5 µg.mL-1 to control neurological symptoms and ventilatory assistance was started with oxygen under facial mask.

Patient was intubated and general anesthesia was provided by 30 µ alfentanil and 2% sevoflurane, monitored by the Dixtal gases analyzer. Mechanical ventilation was facilitated by 0.7 rocuronium. There was no cardiovascular system involvement at any time: blood pressure was maintained at 115 x 80 mmHg, heart rate at 92 bpm and oximetry (SpO2) at 99%, what allowed the proposed surgical procedure to be performed. Surgery lasted approximately 2 hours, after what 1 mg atropine and 2 mg neostigmine were administered, in addition to 10 mg nalbuphine for postoperative analgesia. Patient presented fast spontaneous ventilation recovery and emergence, being extubated in the operating room. At PACU she referred bearable pain, could easily move limbs and did not remember the event. Discharged from PACU took place 90 minutes later. No sequelae have been observed during 6 months follow up.



The search for a new long lasting amide local anesthetic for clinical use is linked to the history of bupivacaine in the USA. Twenty-four years ago, George Albright published an editorial warning anesthesia practitioners about 6 almost simultaneous cases of seizures and cardiovascular collapse after accidental intravascular etidocaine and bupivacaine injections1. Resuscitation has failed for most those patients. Researches encouraged by this report have shown evidences that bupivacaine had lower therapeutic margin for heart conduction system block, as compared to current standards at that time (lidocaine) 9-11. Bupivacaine could rapidly block sodium channels during action potential, however with slower dissociation as compared to lidocaine 12. Resulting electric conduction depression would promote reentering ventricular arrhythmias. There has been also published that high bupivacaine concentrations could promote ventricular arrhythmias by a direct action on the brain stem 13.

Ropivacaine is an amino-amide local anesthetic differing from bupivacaine for presenting a shorter aliphatic chain (propyl and not butyl) bound to nitrogen of the piperidine group. This replacement, associated to lower lipid solubility, and the fact of being presented as pure isomer - enantiomer S(-) - provide bupivacaine with lower neurological and cardiac toxicity as compared to racemic bupivacaine in the same dosage 14,15. In different studies, high ropivacaine plasma concentrations after regional anesthesia (2 to 5.6 mg.L-1) were reached without neurological and cardiac toxicity 16,17. However, several ropivacaine-related accidents have been reported 18-25. These accidents were caused by direct intravascular injections (fast onset) or secondary to plasma absorption due to overdose (late clinical event).

Even low concentrations of this local anesthetic may determine toxicity, suggesting individual sensitivity, as observed in ropivacaine toxicity studies by Scott et al. 26 and Knudsen et al. 27. Many healthy volunteers have only tolerated low doses and there were neurological signs with plasma concentrations between 0.5 and 1 mg.L-1. One patient has tolerated 3.2 mg.L-1 plasma concentration. In our cases, it has not been possible to dose ropivacaine plasma concentrations.

Knudsen et al. 27 have also compared the incidence of central nervous system symptoms and changes in echo and electrocardiography during ropivacaine and bupivacaine infusion in volunteers. Reiz et al. 2 have experimentally shown in swine that there has been lower electrophysiological toxicity for ropivacaine as compared to bupivacaine. The incidence of ropivacaine-induced cardiovascular events and seizures is of approximately 6.1 and 8 cases per 1 million patients, respectively 28. In reported cases, cardiac complications were always preceded by neurological signs (confusion and seizures) and, in our first case, this has been confirmed. Recent studies 15,29 have also confirmed the significant cardiologic advantage of ropivacaine as compared to bupivacaine.

Experimental research has shown lower incidence of failed cardiopulmonary resuscitation after ropivacaine as compared to bupivacaine. In rats, Ohmura et al. 30 have emphasized that ropivacaine-induced cardiac arrest seems to respond better to treatment than that induced by bupivacaine or levobupivacaine, which is in line with what is seen in humans 1,7,8,11. Groban et al. 31 have reported lower incidence of epinephrine-induced ventricular fibrillation in dogs intoxicated with ropivacaine as compared to bupivacaine. In addition, plasma concentration during cardiovascular collapse was higher for ropivacaine (19.8 µg.mL-1) as compared to bupivacaine (5.7 µg.mL-1).

In healthy volunteers, ropivacaine may impair myocardial conduction and contraction, but this is only observed in much higher concentrations than those seen with bupivacaine, suggesting better tolerance and confirming animal results 26,27. In addition, these effects are more promptly reverted. As in the case reported by Ruetsch et al. 32, cardiac recovery in case 1 was immediate and successful with no ventricular arrhythmias. Although cardiopulmonary resuscitation was favored by early treatment, intrinsic ropivacaine low toxicity (as compared to bupivacaine) might have determined the outcome. In contrast with the difficult reverting cardiac arrests due to bupivacaine intoxication, where even cardiopulmonary bypass has been used 33,34, our case’s successful treatment - not exceeding one minute - has allowed the surgery to be performed, in line with previous publications 7,35.

Case 1 patient was in irregular use of b-blockers. The presence of neurological background, ischemic encephalic stroke without sequelae and three decompressive laminectomies has not interfered with early diagnosis of ropivacaine intoxication. Since spinal surgeries were performed in lumbar segments (L4-L5 and L5-S1), there was no counterindication for thoracic epidural puncture proposed for the patient. Thoracic epidural anesthesia in our service is based on the advantages of this technique 36,37. It may be used for anesthesia (plastic surgeries) or for postoperative analgesia (thoracotomies), among other indications.

The lack of pain after anesthetic recovery in the first case leads to the assumption that not all anesthetic solution was injected into the vessel, but even so, patient has evolved to cardiac arrest. On the other hand, case 2 patient presented only nervous system involvement with no cardiac rhythm, SpO2 (%) or blood pressure changes, which has already been observed in studies on individual sensitivity to ropivacaine 26,27. When administered in intravenous infusion to volunteers, Scott et al. 26 have observed seizures with plasma concentrations of 1 to 2 mg.L-1, while Knudsen et al. 27 have demonstrated a seizure threshold at 2.2 mg.L-1.

This 2 cases report stresses the possibility of intravascular local anesthetic injection during epidural anesthesia, even after test-dose administration. Techniques to detect intravascular injections may decrease, but not rule out catastrophic events. As a consequence, regional anesthesia with high local anesthetic doses should be performed in places where resuscitation equipment is available, and more importantly, by professionals trained to identify these complications and start early treatment 38.

Two cases of ropivacaine intoxication during epidural anesthesia were reported. In the first one, cardiopulmonary resuscitation was successful and allowed for the surgery to be performed, considering previous data attesting lower ropivacaine cardiotoxicity. In the second one, there has been central nervous system involvement not evolving to cardiac toxicity. There have been no sequelae, trauma or remembrances which could have impaired patients' physical and psychic integrity.



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Correspondence to
Dr. Fábio Geraldo Curtis
Address: Rua Coronel Spínola de Castro, 4061/83
ZIP: 15015-500 City: São José do Rio Preto, Brazil

Submitted for publication March 17,  2004
Accepted for publication July 21, 2004



* Received from Departamento de Anestesiologia da Faculdade de Medicina de Botucatu, FMB UNESP, Botucatu, SP

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