Dorsal penile nerve block complicated by local anaesthetic systemic toxicity

Abstract

A 39-year-old man presented with priapism. To facilitate corporal cavernosal aspiration, a dorsal penile nerve block was performed. A dose of 2000mg lignocaine was administered, instead of the intended 200mg. The patient developed local anaesthetic systemic toxicity, including hallucinations, loss of vision and agitation. This was treated with sedation, intubation, intravenous 20 % lipid emulsion, corporal aspiration and intensive care admission. The following day the patient was extubated and discharged. Clinical governance processes identified four potential causes for drug error. This is the third reported case of local anaesthetic systemic toxicity due to penile block in an adult.

Highlights

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To facilitate treatment for priapism in a man in his 30s, a penile block was performed.
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A x10 intended lidocaine dose was given (2000mg), leading to hallucinations, loss of vision and agitation.
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After sedation, intubation and intravenous lipid, the patient was discharged the next day.
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Local anaesthetic systemic toxicity from urogenital instillation is rare but can be fatal.

1 Introduction

Local anaesthetic agents are ubiquitous in healthcare, with worldwide annual consumption in excess of one billion ampoules per annum. They are administered by health professional with diverse qualifications and experience, including doctors, nurses and dentists. Within urology, dorsal penile nerve blocks are commonly used in adults to facilitate procedures, including aspiration of the corporal caverosa to treat priapism.

Local anaesthetic systemic toxicity (LAST) is a rare and potentially fatal complication of both short- and long-acting local anaesthetics. We present the case of a male who presented with priapism, received an iatrogenic lidocaine overdose and developed LAST. This is the third report of LAST in an adult secondary to penile dorsal nerve block.

2 Case presentation

A man is his 30s presented with both painful priapism of 4 hours’ duration, and also a traumatic right ankle soft tissue injury. The patient had a history of two prior closely spaced episodes of ischaemic priapism ten months prior, associated with quetiapine and sildenafil use. These had both been successfully treated with penile dorsal nerve block, corporal aspiration of 80–140mL blood and on the first occasion 1mg intra-corporal phenylephrine. The patient’s past medical history included multiple limb fractures from dirtbike riding. He took no regular medications. The patient habituated with his parents. He daily consumed 5–10 cigarettes, 1–2 standard drinks of alcohol and recreational inhaled marijuana.

Two days prior to presentation, the patient’s right ankle had been trapped briefly between a car and a concrete gutter. The joint had developed pain, ecchymosis and oedema. He had remained able to walk with difficulty. On the day of presentation, the patient fell asleep at 0100am, and woke at 1100am to find both that his lower limb symptoms had progressed, and a painful erection. When the latter failed to subside, he attended our hospital. On examination, the patient was alert, orientated and able to walk with right foot touch weight bear. His vital signs were heart rate 69 beats/min, blood pressure 146/101 mmHg, temperature 36.1 °C, respiratory rate 18 and peripheral oxygen saturation 98 % on room air. Genital examination revealed a rigid, tender erection, without ecchymosis of the phallus, scrotum or perineum. His right ankle and dorsal mid foot displayed significant oedema and ecchymosis. There was a mildly tender superficial 60mm transverse laceration on the posterior right heel, with surrounding erythema.

Initial investigations revealed serum haemoglobin 140g/L (NR 135–175), white cell count 11.4 x109/L (NR 4–11), platelets 391 x109/L (NR 150–450) and Creatinine 75 μmol/L (NR 60–110). Right lower limb xrays revealed soft tissue swelling but no fracture.

The patient was assessed as having ischaemic priapism without clear precipitant, as well as a right lower limb soft tissue injury, with superimposed cellulitis. He received analgesia, intramuscular tetanus vaccine booster, intravenous (IV) flucloxacillin and a dressing to his right ankle. Urology staff verbally consented the patient for penile dorsal nerve block and cavernosal aspiration ± intra-cavernosal phenylephrine. Four 5mL vials were selected, assumed to contain 1 % lidocaine with total dose 200mg, and administered with standard technique of antiseptic solution, test aspiration then delivery of half to the dorsal penile nerve and half for a subcutaneous ring block. Post administration, rechecking the vials revealed actual contents of 10 % lidocaine, with total dose 2000mg. Immediately, this information was given to the patient and emergency department staff. The patient was moved to the close observation ‘Resuscitation Bay’, where he was commenced on continuous vital sign monitoring, 6L/min supplemental oxygen, 1000mL IV saline stat and 840mL IV 20 % lipid emulsion over 60mins. Despite this, he soon developed severe neurological manifestations of LAST. These included hallucinations that the curtains were undulating, then visual loss and agitation. No seizures or arrhythmias occurred. Assistance was requested from both anaesthetic and security staff, with a ‘Code Black’ initiated. The patient received 5mg IV midazolam without effect, followed by rapid sequency endotracheal intubation utilising 100mg IV propofol and 100mg IV rocuronium. At this time, urology staff performed corporal aspiration of 160mL blood, and detumescence was achieved. The patient was transferred to the intensive care unit, where his sedation was continued with dexmedetomidine and fentanyl IV infusions.

The following morning the patient was extubated. Urology staff offered apologies and performed open disclosure with the patient and his family. He was transferred to the ward and discharged that afternoon. He represented the following day with symptoms of anxiety and re-experiencing LAST symptoms of hallucinations and loss of vision and inability to move during induction of anaesthesia. The patient was reassured and discharged. On review in clinic one month later, the patient’s priapism had not recurred, and he had been able to achieve normal erections.

The patient submitted their perspective; ‘After I came in with the sore foot and the erection. While treating the erection, the doctor gave me too much local anaesthetic. The curtains starting waving, then I couldn’t see, and I couldn’t move but for a time I could still hear. It shouldn’t have happened and it was the worst day of my life.’

3 Discussion

The earliest known use of local anaesthesia come from carvings in the ancient Egyptian tomb of Saqqara (2500BC), which depict peripheral nerve compression to numb limbs. Subsequent primitive techniques include topical bitterroot documented in Homer’s The Iliad in 800BC, electricity from a captured torpedo ray’s barb documented by Aristotle in 350BC and snow anaesthesia for limb amputation during Napoleon’s invasion of Russia in 1812. Major breakthroughs were the first hypodermic syringe in 1841 by American physician Zophar Jayne, the first routine procedural use of local anaesthesia, specifically topical cocaine for eye surgery in 1884 by Austrian ophthalmologist Carl (or Karl) Koller, and in 1943 the first synthesis of cocaine-derivative lidocaine, by Swedish chemist Nïls Lofgren.

Lidocaine would become the most widely used local anaesthetic globally. Local anaesthetic systemic toxicity (LAST) is a rare and potentially fatal complication of local anaesthetics. The most common cause is administration error, which may be due to dose error or inadvertent arterial or venous delivery of an intended subcutaneous dose. The principle toxic mechanism is the local anaesthetic reversibly binding to and inhibiting sodium channels within nerves separate from the intended site of action.

Onset of the neurological and cardiovascular manifestations is usually rapid. Severity corresponds to dose. Early and more mild symptoms include tinnitus, metallic taste, peri-oral numbness and light-headedness. More severe cases display visual impairment, hallucinations, agitation, reduced conscious state and seizures (central nervous system), hypotension from vasodilatation, arrhythmia or cardiac arrest (cardiovascular) or respiratory depression or apnoea (respiratory). Seizures or cardiac arrest may be the first manifestation.

Treatment of LAST consists of ceasing administration of local anaesthetic and calling for help. Patients in cardiac arrest should receive cardiopulmonary resuscitation, attachment of an automatic external defibrillator and commencement of IV 20 % lipid emulsion. Lipid emulsion guidelines from the Association of Anaesthetists of Great Britain and Ireland detail the combination bolus and infusion approach, with maximum total dose of 12mg/kg.

Patients not in cardiac arrest should receive supplemental oxygen, continuous monitoring, IV access. Lipid emulsion should also be considered in these patients, as it is difficult to predict which patients will progress to cardiovascular collapse, the potential benefit is high (prevention of deterioration) and the potential risk is low (rare complications include acute kidney injury, anaphylaxis, hypertriglyceridaemia with or without pancreatitis and fat embolism).

Penile dorsal nerve blocks are commonly used in adults to aid a range of interventions, including penile debridement, corporal aspiration in priapism, reduction of paraphimosis, prepucial dorsal slit, circumcision or penile biopsy. For awake patients, clinicians typically use the short-acting local anaesthetic lidocaine or articaine, either alone or in combination with longer-acting agents such as ropivacaine or bupivacaine. The latter agents are preferred for sedated patients, where the extended clinical effect (2–4 hours vs. <2 hours) is useful and the slightly longer onset of action (>5mins vs. <2mins) is unimportant. For the penis and other locations with end-arteries such as the digits and nose, supplementary adrenaline is never used.

This represents just the third case report of LAST in an adult secondary to penile dorsal nerve block. In 1996 Chiang et al. described a 65-year-old man undergoing circumcision who received 600mg lidocaine, complicated by hallucinations and agitation, managed conservatively. In 2018 Rao Kadam et al. reported a 29-year-old man undergoing circumcision who also received 600mg lidocaine, complicated by tinnitus, peri-oral numbness, hallucinations and agitation, requiring general anaesthesia. Neither patient received IV lipid emulsion.

For this patient, clinical governance processes in our institution were enacted, included case review by both a multi-disciplinary ‘Safety and Learning System’ team, and frank discussion in the urology departmental morbidity and mortality meeting. For this patient’s penile dorsal nerve block, four risk factors for potential dose error were identified, including after-hours timing, stocking without safeguards of a 10 % lignocaine vial with similar appearance to 1 % vials, absence of a second clinician to confirm dose and failure to inspect vials before administration. Whilst time of day cannot be altered for emergency presentations, we have taken steps to address the other modifiable risk factors. Urology trainees now discuss penile blocks pre-procedure with the on-call urologist via telephone, as well as display the vials in-person with a bedside nurse. Lastly, the 10 % lidocaine vials have been moved from the general imprest to the ‘Code Blue’ cardiac arrest trolley, to further restrict access. This followed an audit of our centre’s pharmaceutical imprests, which identified nineteen different local anaesthetic formulations ( Fig. 1 ). The 10 % lidocaine ampoule was nominally indicated in cardiac arrest due to ventricular tachycardia or fibrillation refractory to defibrillation, as well as continuous infusions for refractory chronic pain or migraine, but was in practice seldom used.