Sub‐mammary injection of ropivacaine resulting in severe toxicity with seizures

Dear Editor, Local anaesthetic toxicity can result in neurotoxicity such as seizures and although uncommon, they are a recognised complication of regional anaesthesia. We are reporting two cases that developed seizures, 1 h post bilateral sub-mammary ropivacaine administration for breast augmentation surgery. Case 1 involved a 37 year old (54 kg) woman, who presented to the ED with recurrent seizures following breast augmentation surgery, under sedation and local anaesthetic infiltration at a plastic-day surgery. She was otherwise well, on no regular medications. At the start of the procedure 20 mL of 1% ropivacaine (200 mg; 3.7 mg/ kg) and adrenaline (1 mg) was diluted in 200 mL of normal saline and infiltrated in the sub-mammary region bilaterally. She also received sedation that included midazolam 3 mg preprocedure and during the procedure a total of 320 μg intravenous fentanyl, propofol, midazolam and dexmedetomidine. Other medications received during the procedure were paracetamol 1 g intravenous, cephazolin, dexamethasone 8 mg intravenous and ondanestron. The procedure was completed with no haemodynamic instability or complications. One hour following ropivacaine infiltration, while in recovery, she felt unwell, anxious and reported perioral pins and needles. She subsequently had a tonic-clonic seizure lasting less than 1 min and was given 2 mg of intravenous diazepam. Over the next 15 min, she had two further seizures and was given 8 mg in total of intravenous diazepam. An ambulance was called, and during transport, the patient had a further two tonic-clonic seizures lasting less than a minute; no further treatment was given. On arrival to hospital, shewas awake and alert, with no focal neurology; electrolytes, electrocardiogram and head computed tomography were unremarkable. Shewas discharged after 24 h observation, following a normal electroencephalography. On followed up 2 weeks later, she had had no further seizures. The second case involved a 23 year old (52 kg) woman, who presented to another hospital, with seizures and decreased level of consciousness, again following breast augmentation surgery under sedation and local anaesthesia. She was 5 months post-partum and was on no regular medication. Similarly, at the start of the procedure, 20 mL of 1% ropivacaine (200 mg, 3.85 mg/kg) and adrenaline (1 mg) was diluted in normal saline (200 mL) and infiltrated into the sub-mammary region bilaterally. She received for sedation, midazolam, dexmedetomidine, propofol and fentanyl boluses during the procedure. She had no documented surgical or anaesthetic issues during the surgery. In recovery, she did not regain consciousness, and 1 h post-ropivacaine infiltration had a 5 min tonic-clonic seizure, followed by 40 min of focal seizures. She was given 10 mg of intravenous diazepam in 2.5 mg increments during this time by the recovery nurses. An ambulance was called, and a further 5 mg of intravenous midazolam was given by the paramedics. The patient remained Glasgow Coma Scale 3 throughout. On arrival to ED, she remained unresponsive and was intubated. She was noted to have generalised increased tone. Electrolytes, electrocardiogram and computed tomography brain were unremarkable. She was transferred to the intensive care unit where she had a large vaginal bleed, requiring one unit of packed cells and was confirmed to be pregnant. She was extubated the following day, had no further seizures and was neurologically normal. Total venous ropivacaine levels taken 2.5 and 4 h after local anaesthetic infiltration were 0.44 and 0.38 mcg/mL, respectively. Local anaesthetic toxicity is uncommon and can result in neurotoxicity and cardiotoxicity. Ropivacaine is a long-acting amide local anaesthetic. It is similar to bupivacaine in chemical structure, but with less cardiovascular and central nervous system toxicity. Local anaesthetic toxicity is not only based on the dose administered, but factors such as agent used, route, site of administration and patient comorbidities are important. The recommended safe dose of ropivacaine varies widely from 3 mg/kg to doses up to 5–6 mg/kg for infiltration around the hip. Many believe the maximum dose should be abandoned for a dosing range depending on the site and purpose of the injection. For example, injection into a highly vascular region will increase systemic absorption, while single injection versus an infusion will alter the absorption profile. In both these cases, the patients developed seizures 1 h post bilateral sub-mammary ropivacaine administration. These patients received 3.7 mg/kg and 3.85 mg/kg respectively of ropivacaine. The first case clearly had symptoms of local anaesthetic toxicity, describing perioral tingling and numbness, then becoming quite agitated, before having a generalised tonic-clonic seizure. While the second case did not regain consciousness after receiving procedural sedation and like the first case developed seizures 1 h after infiltration of ropivacaine. The likely cause of both of their seizures was local anaesthetic toxicity. The delay in onset of symptoms in the first case and seizures in both shows that toxicity was related to ropivacaine absorption and not inadvertent injection into a vessel, which is confirmed by the