Skip Navigation LinksHome > Summer 2009 - Volume 4 - Issue 2 > Regional Anesthesia Emergencies
Simulation in Healthcare: The Journal of the Society for Simulation in Healthcare:
doi: 10.1097/SIH.0b013e3181925219
Case Report/Simulation Scenario

Regional Anesthesia Emergencies

Torsher, Laurence C. MD; Craigo, Paula MD; Lynch, James J. MD; Smith, Hugh M. MD, PhD

Free Access
Article Outline
Collapse Box

Author Information

From the Department of Anesthesiology, Mayo Clinic College of Medicine, Rochester, Minnesota.

Reprints: Laurence C. Torsher, MD, Department of Anesthesiology, Mayo Clinic, 200 First Street, S.W., Rochester, MN 55905 (e-mail: torsher.laurence@mayo.edu).

Back to Top | Article Outline

DEMOGRAPHICS

Module title: Regional Anesthesia Emergencies

Patient name: Standard Man Awake

Scenario name: CNS_toxicity, CV_toxicity, Oversedation, CV_ischemia

Simulator: METI HPS/ECS, Laerdal SimMan

Learner groups: Anesthesia residents, PGY-2, 3, 4

Back to Top | Article Outline

CURRICULAR INFORMATION

Educational Rationale

Large doses of local anesthetics during regional anesthetics can produce complications including seizure, cardiac toxicity, or high spinal. Symptoms associated with toxicity must be recognized immediately and differentiated from other etiologies. This lesson acquaints providers with presentations of local anesthetic toxicity, to emphasize the importance of a broad differential diagnosis and a systematic approach to therapy. Scenarios encourage teamwork and development of crisis resource management (CRM) skills as trainees work with team members with varying degrees of experience.

This lesson has been used at our institution for approximately 18 months. In that time, we have seen and reported on its effectiveness in successful resuscitation of a patient with cardiovascular collapse from local anesthetic toxicity.1

Back to Top | Article Outline
Learning Objectives

Using Accreditation Council for Graduate Medical Education General Competencies:

1. Medical knowledge: Trainees will describe the progression of clinical changes with increasing serum levels of local anesthetic. Trainees will describe central nervous system (CNS) toxicity and contrast this with an epileptic seizure (Table 1). Trainees will describe cardiac toxicity and the role of lipid infusions in management.2–4 Trainees will compare the resuscitation of cardiac collapse due to local anesthetic toxicity with cardiovascular collapse from other etiologies.

Table 1
Table 1
Image Tools

2. Patient care: Trainee will recognize changing physiologic status, develop a differential diagnosis and initiate treatment, calling for help and using a team when necessary. They will demonstrate emergency life support skills required to resuscitate a patient with local anesthetic toxicity. Trainee will not administer lipid infusion when there is no evidence supporting local anesthetic toxicity.

3. Practice-based learning and improvement: Trainee will participate in debriefing sessions, reflecting upon and discussing both the individual's and the team's performance.

4. Interpersonal and communication skills: Using CRM techniques, trainees will coordinate a team, assign clear roles, use closed-loop format during critical communications, and maintain open discussions during resuscitation.

5. Professionalism: Trainee will demonstrate cooperation with the simulation, communication, and respect for facilitators and fellow trainees in both scenarios and debriefings.

6. System-based practice: Trainees will determine whether to proceed with surgery and discuss events with the surgeon. They will decide upon disposition including investigations, monitoring, and further medical management. Trainees will list systems issues affecting response to the crisis and patient outcome.

Back to Top | Article Outline
Guided Study Questions

1. What early clinical signs and symptoms are seen with intravascular local anesthetic? How do these evolve with progressively larger doses of local anesthetic?

2. How can we detect intravascular local anesthetic before toxicity occurs?

3. How is CNS toxicity managed? Contrast this with management of seizure of unknown etiology.

4. What is the differential diagnosis for hemodynamic instability in a patient receiving a regional anesthetic?

5. How is cardiac toxicity from intravascular local anesthetic managed? In what way, if any, is the management of cardiac toxicity from local anesthetics different from standard Advanced Cardiac Life Support (ACLS) management?5

6. After stabilization, in what circumstances would you proceed with the planned surgery? Are other investigations or an intensive care unit stay warranted? If the patient goes to the intensive care unit, what plan would you expect there?

Back to Top | Article Outline

PREPARATION

Equipment

* Blood pressure cuff

* Electrocardiogram (ECG)

* Pulse oximeter

* Anesthesia machine

* Capnogram

* Airway equipment

* Standard anesthesia medications

* Code cart with ACLS resuscitation drugs and defibrillator

* Twenty percentage lipid emulsion

* Saline IV

* Peripheral nerve catheter fixed in place

* The 10-mL and 20-mL syringes labeled “0.50% bupivacaine with 1:200,000 epi”

* Time: (for each of the scenarios in the lesson)

Setup: 10 minutes

Simulation: 10 minutes

Debrief: 25 minutes

Back to Top | Article Outline

CASE STEM

You are called to the anesthesia procedure area where a psoas catheter (lumbar paravertebral block) has just been placed in Mr. Y. He is scheduled to undergo right-hip arthroplasty under general anesthesia. The psoas catheter was placed for postoperative analgesia. The attending anesthesiologist left report that placement of the block was unremarkable. A test dose of 3 mL of 0.5% bupivacaine with 1:200,000 epinephrine was given without changes in heart rate, blood pressure, or sensorium. There was no sign of spinal block at 3 minutes. The anesthesiologist has asked you to load the catheter with an additional 25 mL of the bupivacaine solution.

Back to Top | Article Outline

PATIENT DATA

Mr. Y is a 58-year-old man with a history of hypertension. He was previously fit and active, but hip pain over the last 4 months has made him difficult to assess functional capacity. He has had general anesthetics in the past without problems. No known allergies. Hydrochlorothiazide is his only medication. No other cardiac, respiratory, renal, or hepatic complaints. He has requested a general anesthetic.

Back to Top | Article Outline

FACILITATOR/COORDINATOR'S BACKGROUND INFORMATION

All four scenarios start with the same patient and same stem. Scenarios diverge after the trainee has begun loading the peripheral nerve block with local anesthetic solution.

The mannequin is positioned in a left lateral decubitus position. He has a single IV in place and all monitors have been applied. There is a nurse (confederate) who has assisted with the block in the room. The patient is anxious. He does not initiate conversation but answers questions when asked.

The peripheral nerve catheter is taped in place at L3/L4 level, 4 cm to the right of midline. The catheter is connected to a hidden one-way valve so that while the trainee aspirates the catheter nothing returns. Subsequent to this blood-colored fluid can be easily introduced to the circuit to simulate intravascular catheter location.

Back to Top | Article Outline
Part I (CNS Toxicity)

As the local anesthetic is injected, the patient becomes drowsy and then unresponsive. The trainee should recognize the changes in sensorium and apnea, and respond by moving the patient to his back. If using the ECS mannequin, the “seizure” condition is activated. On the HPS or SimMan, the confederate will gently shake one of the mannequin's limbs, saying “the patient is shaking.” The trainee should palpate a pulse before administering medication. The trainee should administer propofol or midazolam, and the seizure/shaking will stop after ∼45 seconds. The patient is apneic and the trainee should provide respiratory support, altering management when spontaneous ventilation returns. If intubation is attempted, the patient coughs.

Debrief discussion points:

* Patient monitoring while injecting local anesthetic.

* Epinephrine as intravascular marker; sensitivity, and specificity.

* Supine positioning during catheter loading, especially if resuscitative measures are required.

* Differential diagnosis for changes in level of consciousness.

* Differences between local anesthetic-induced seizure and epileptic seizure.

* Clinical changes associated with serum local anesthetic levels.

* Postresuscitation discussions with patient and surgeon.

* Decision to cancel or proceed with case.

* Follow-up management if canceled.

Back to Top | Article Outline
Part II (Cardiovascular Toxicity)

As the local anesthetic is injected, the patient becomes drowsy and then unresponsive (Table 2). The trainee should notice the change in sensorium and apnea and move the patient supine. As he is being moved, the rhythm becomes pulseless ventricular tachycardia evolving into coarse ventricular fibrillation. The trainee should recognize the change, call for help, locate emergency equipment, institute ACLS measures, and initiate 20% lipid emulsion.

Table 2
Table 2
Image Tools

Debrief discussion points:

* Cardiovascular effects of toxic local anesthetic serum levels, including rhythm changes, hypotension, and cardiovascular collapse.

* Differential diagnosis of arrhythmias and how that affects choice of therapies.

* Lipid emulsion therapy: dosing, administration, efficacy, integration with ACLS interventions.

* CRM principles.

* Patient disposition and management after stabilization: surgery postponement, monitoring, ongoing lipid infusion, cardiac enzymes, ECG, etc.

Back to Top | Article Outline
Part III (Oversedation)

After 5 mL of the local anesthetic has been injected, the patient becomes drowsy and then unresponsive (Table 3). The trainee should notice the change in sensorium, move the patient supine, and recognize bradypnea. The trainee should stop injecting local anesthetic and assist ventilation.

Table 3
Table 3
Image Tools

Debrief discussion points:

* Differential diagnosis for decreased level of consciousness.

* Managing respiratory insufficiency.

* Physiologic and synergistic effects of sedative medications.

* Pharmacologic interventions: flumazenil, naloxone.

Back to Top | Article Outline
Part IV (Myocardial Ischemia)

After 5 mL of the local anesthetic has been injected, the patient complains of feeling unwell (Table 4). ECG monitor shows ST elevation that progresses to pulseless ventricular tachycardia. Trainee notes the changes, stops further injection, and moves the patient supine. The trainee calls for help and resuscitates according to ACLS recommendations. There is no need for lipid emulsion here.

Table 4
Table 4
Image Tools

Debrief discussion points:

* Performance of ACLS measures.

* CRM principles.

* Contrast myocardial ischemia and local anesthetic- induced toxicity: presentation, management, and prognosis.

Back to Top | Article Outline
Other Notes

We have developed additional scenarios including high spinal and anaphylaxis that we intersperse with these to continue to encourage the learners to broaden the differential diagnosis and to move them away from the “knee jerk” responses.

We frequently train with PACU nursing staff. They play the role of the nurse in the room. They are told only about the placement of block. We have a confederate in the room playing the role of orderly that can assist in the production of the scenario. The nursing staff is then an active participant in the scenario and debrief.

Back to Top | Article Outline

REFERENCES

1. Smith HM, Jacob AK, Segura LG, et al. Simulation education in anesthesia training: a case report of successful resuscitation of bupivacaine-induced cardiac arrest linked to recent simulation training. Anesth Analg 2008;106:1581–1584.

2. Rosenblatt MA, Abel M, Fischer GW, et al. Successful use of a 20% lipid emulsion to resuscitate a patient after a presumed bupivacaine-related cardiac arrest. Anesthesiology 2006;105:217–218.

3. Weinberg GL, Di Gregorio G, Ripper R, et al. Resuscitation with lipid versus epinephrine in a rat model of bupivacaine overdose. Anesthesiology 2008;108:907–913.

4. Weinberg GL, Ripper R, Murphy P, et al. Lipid infusion accelerates removal of bupivacaine and recovery from bupivacaine toxicity in the isolated rat heart. Reg Anesth Pain Med 2006;31:296–303.

5. ECC Committee, Subcommittees and Task Forces of the American Heart Association. 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2005;112:IV 1–IV 155.

Keywords:

Regional anesthesia; Local anesthetic toxicity; Lipid; Cardiac toxicity; CNS toxicity; Crew resource management

© 2009 Lippincott Williams & Wilkins, Inc.

Login

Article Tools

Images

Share

Search for Similar Articles
You may search for similar articles that contain these same keywords or you may modify the keyword list to augment your search.