Department of Anesthesia and Critical Care Medicine, Childrens Hospital of Philadelphia, 34th and Civic Center Boulevard, Philadelphia, PA 19104-4399, USA
Corresponding author. E-mail: cucchiaro@email.chop.edu
Accepted for publication: February 26, 2003
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Abstract |
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Br J Anaesth 2003; 90: 8047
Keywords: anaesthetics local, bupivacaine; anaesthetic techniques, subarachnoid; children; complications, prolonged QT syndrome; sympathetic nervous system, epinephrine
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Introduction |
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We describe an episode of intraoperative cardiac arrest after accidental intravascular injection of bupivacaine with epinephrine via a misplaced epidural catheter, in a child with previously undiagnosed LQTS.
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Case report |
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The patient was then placed in the supine position. While the surgeons were preparing the abdomen, the patient received bupivacaine 0.25% 3 ml with epinephrine 1:200 000 epidurally, after negative aspiration for blood. We had planned to give boluses to a total dose of 10 ml of this local anaesthetic. One minute after the first dose of bupivacaine, dysrhythmias were noticed on the ECG. In particular, we observed the appearance of premature ventricular contractions, enlargement of the QRS complex and signs of occasional complete arteriovenous block. The patients heart rate remained stable (7478 beats min1), as did the arterial blood pressure (systolic 9095 mm Hg, diastolic 40 mm Hg). Because of these rhythm abnormalities, we decided to wait before administering the full dose of epidural bupivacaine. Approximately 3 min later and before surgical incision, the heart rhythm suddenly changed into ventricular tachycardia and a few seconds later into ventricular fibrillation and cardiac arrest. After a precordial thump, chest compressions were started. The desflurane was discontinued and the patient was ventilated with oxygen 100%. A single i.v. dose of epinephrine 1 mg was administered with immediate return to sinus rhythm, followed by sodium bicarbonate 30 mEq. The heart rate rose to 180 beats min1 and the arterial blood pressure to 150/100 mm Hg. A few seconds later, the patient had a second episode of ventricular fibrillation that resolved after brief chest compressions. The heart rate stabilized around 100 beats min1, and arterial pressure stabilized with systolic values around 90 mm Hg. Blood samples were taken for measurement of plasma bupivacaine concentration. Arterial blood gas was normal, with the exception of hypokalaemia (potassium 2.8 mmol litre1), probably because of the recent administration of bicarbonate. The patient was then extubated and taken to the cardiac intensive care unit. Before removal, we again aspirated the epidural catheter with a smaller syringe, and at this time we noticed a free return of blood. Repeated ECG in the first 24 h after the cardiac arrest revealed sinus rhythm and no evidence of WolffParkinsonWhite syndrome. The QT interval appeared borderline normal, but the corrected QT was constantly increased (Table 1). An exercise test performed 48 h later showed a QT that became increasingly prolonged to 516 ms without ectopies (Table 1). The echocardiogram showed normal anatomy and a shortening fraction of 32%. The patient was started on the ß-blocking agent nadolol, which decreased the resting heart rate from 88110 to 5870 beats min1.
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The direct family members (father, mother and one brother) were interviewed and asked to undergo exercise stress tests, which were all negative. There were no episodes of unexplained sudden death in the family, or events that could suggest a family history of LQTS.
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Discussion |
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Long QT syndrome is a congenital or acquired disorder characterized by abnormal prolongation of ventricular repolarization, measured as lengthening of the QT interval on any of the 12 ECG leads.13 Other ECG abnormalities include bradycardia, increased QT dispersion and T-wave alterations. These abnormalities cause predisposition to ventricular tachyarrhythmias, such as polymorphic ventricular tachycardia and ventricular fibrillation. Acquired QT prolongation is most often attributable to the administration of drugs or electrolyte imbalance. There are two known congenital forms of LQTS, the RomanoWard syndrome (autosomal dominant trait) and the Jervell and Lange-Nielsen syndrome (autosomal recessive inheritance, associated with congenital deafness). The pathophysiology of cardiac arrhythmias in these patients is related to impairment of outward potassium currents or to defective sodium channel activation. Both mechanisms result in reduced outward current during repolarization, with secondary prolongation of cardiac action potentials and lengthening of the QT interval. Our patient had been diagnosed with Pfeiffer syndrome in infancy because of craniosynostosis with minimal dysmorphic facial features. However, there are no reports of cardiac arrhythmias associated with Pfeiffer syndrome, and the patient did not have any of the other anomalies associated with this syndrome.
A screening ECG in every child undergoing general anaesthesia seems inappropriate, given the rarity of LQTS and the high incidence of a normal ECG at rest in patients with this congenital disorder. However, because of the potential for intravascular injection of the mixture of local anaesthetic and epinephrine during any regional anaesthesia technique, anaesthetists should consider the risks involved in performing central and peripheral nerve blocks in patients with known LQTS or a family history of LQTS. If it is decided to use a regional technique, anaesthetists should probably use a solution containing plain anaesthetic rather than a combination of local anaesthetic and epinephrine.
In conclusion, this case report confirms the difficulty of recognizing the intravascular migration of an epidural catheter. Other reasons besides local anaesthetic toxicity may be responsible for intraoperative cardiac arrest, and a full cardiac evaluation should be obtained in such cases.
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References |
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