Local Anesthetic Systemic Toxicity case

1. Morbidity & Mortality
December 2022
AROD: Dr. Georgie A. Martin Jr. (Level 1 Resident)
Consultant On-Deck: Dr. Christian Jeff Diego / Dr. Ted Kilayko

2. General Data
• F. C.
• 16 years old
• Male
• Single
• Filipino
• Brgy. Bagaygay, Sara, Iloilo
• Date of Admission: 11/25/2022
• CC: Multiple Injuries, Moderate Head Injury sec to MVA (Collision)

3. History of Present Illness
• NOI – MVA
• TOI – 6pm
• POI – Sara, Iloilo
• DOI – 11/24/22
• Px was accidentally hit by another vehicle sustaining multiple
injuries and also head injury (+) LOC, px was then rushed in this
institution for further management

4. Past Medical History
• Unremarkable
Personal, Social, Family History
• Non-alcoholic as claimed
• Non-smoker as claimed
• No food/drug allergies

5. Physical Examination
• GCS 15 (E4,V5,M6), (-) neuro deficits
• AS, PC, isocoric pupils
• AP, NCRRR, (-)murmurs
• SCE, CBS
• Flat abdomen, soft
• Full pulses
• (+) left arm/forearm with elastic bandage and splint
• (+) left frontotemporoparietal suture scars

6. Laboratories
• CBC 12.0/0.40/wbc 9.0/plt 757
• PT 13.7/92%/1.06
• S. Na 139, S. K 3.66, Crea 71.52
• ECG – normal sinus rhythm
• CXR – normal findings, clavicular fracture left

7. Admitting Diagnosis
 Fracture closed complete displaced middle 3rd clavicle left type 1,
fracture closed complete oblique displaced middle 3rd humerus left,
fracture closed complete comminuted displaced distal radius-ulna
left, avulsed wound elbow left sec to MVA
S/P Decompressive craniectomy, evacuation of hematoma (11/25/22)

8. Proposed Procedure:
• Debridement forearm left, application of elbow spanning external
fixator left, intramedullary pinning radius left, intramedullary pinning
clavicle left
Anesthetic Plan:
• General Endotracheal Anesthesia
• PNB: Supraclavicular Block (Post-op Analgesia)

9. Pre-op Meds:
• Omeprazole 40mg IV 1hr prior to OR
• Metoclopramide 10mg slow IV 1hr prior to OR

11. Post-Op Meds:
• Ketorolac 30mg IV q6h x 3 more doses
• Celecoxib 200mg/cap, 1 cap BID x 5 days
• Paracetamol 600mg IV q6h x 2 days
• Tramadol Drip, 200mg in 500cc D5W to run for 24hrs x 2 cycles
• Tramadol 25mg IV q6h PRN for breakthrough pain
• Ondansetron 4mg IV q8h PRN for nausea/vomiting

12. Post-Op Day 1 (PACU)
• Vital Signs: BP 100-110/70-80, CR 110s, RR 20s, O2sat 100%
• Fully awake, conscious, anisocoric pupils (reactive, slightly sluggish right
eye)
• Adynamic precordium, slightly tachy & regular rhythm, (-)murmur
• Symmetrical chest exp, clear breath sounds
• NRS 0/10, (-) nausea, vomiting, dizziness
• Norepinephrine discontinued, still on standby bedside
• Still on O2 support @ 4-5lpm via face mask
• Repeat CBC: 10.8/0.35/wbc 15/plt 486

14. Post-Op Day 2 (Padre Pio Ward)
• Vital Signs: BP 120/80, CR 90s, RR 20s, O2sat 98-99%
• Fully awake, conversant, comfortable, anisocoric pupils (both
reactive, right pupil slightly dilated compared to left pupil)
• Adynamic precordium, normal cardiac rate & rhythm, (-)murmur
• Symmetrical chest exp, clear breath sounds
• NRS 0-1/10, (-) nausea, vomiting, dizziness
• O2 support discontinued

15. DIFFERENTIALS
 Local Anesthetic Systemic Toxicity (LAST)
 Total Spinal Anesthesia following Peripheral Nerve Block
 Brachial Plexus Injury resulting to Horner’s Syndrome

16. DISCUSSION

17. Local Anesthetic Systemic Toxicity
• Local anesthetic systemic toxicity (LAST) is a life-threatening
adverse event associated with the increasingly prevalent
utilization of local anesthetic (LA) techniques throughout various
health care settings, with an incidence currently estimated to be
0.03%, or 0.27 episodes per 1,000 peripheral nerve blocks.

18. • Increasing plasma concentrations of LA initially compromises
cortical inhibitory pathways by blockade of NaV channels,
disrupting inhibitory neuron depolarization. Inhibiting these
pathways leads to excitatory clinical features of sensory and visual
changes, muscular activation, and subsequent seizure activity. As
the plasma concentrations of LA rise, excitatory pathways are
affected, producing a depressive phase of neurological toxicity,
with loss of consciousness, coma, and respiratory arrest.

20. • The multitude of aforementioned LA molecular targets produces
complex toxic features in the CVS, including conduction
disturbances, myocardial dysfunction, and lability of peripheral
vascular tone. The primary effects are likely to arise from rhythm
disturbance, with other CVS effects being secondary. Normal
conduction is disrupted by direct sodium channel blockade, chiefly
at the bundle of His. By driving the resting membrane potential to
a more negative level, action potential propagation is impaired,
leading to prolonged PR, QRS, and ST intervals. Re-entrant
tachyarrhythmias and bradyarrhythmias ensue, which may be
worsened by further potassium channel blockade, prolonging the
QT interval.

21. • Although 40% of LAST presents atypically, CNS toxicity is the most common
feature of LAST (68%–77%), primarily in the form of seizures. Diverse early
manifestations have been described (although many are likely
underreported), and may include perioral paresthesia, confusion, audio–
visual disturbances, dysgeusia, agitation, or reduced level of consciousness.
One-third of the reported cases of LAST begin with CNS features that progress
to involve CVS signs, and one-fifth of LAST episodes present with isolated CVS
disturbances. Again, protean features of CVS toxicity are apparent, but
dysrhythmias, conduction deficits, hypotension, and eventually cardiac arrest
– most commonly of an asystolic nature – may be seen. LAST events most
frequently occur immediately following injection of LA, and recent data
demonstrate that delayed presentation may occur at various time points up to
several days following commencement of an infusion.

23. Total Spinal Anesthesia
• Total spinal anesthesia (TSA) results in respiratory depression,
cardiovascular compromise, and loss of consciousness. This may
or may not be preceded by numbness, paresthesia, or weakness of
the upper limb; shortness of breath; nausea; or anxiety.
• It can happen during epidural anesthesia, caudal anesthesia, spinal
anesthesia, paravertebral block, stellate ganglion block,
interscalene brachial blocks, and other regional anesthesia
techniques performed at or near to the vertebral column. The
clinical manifestations are often characterized by a sudden
decrease in blood pressure, rapidly increasing motor block,
temporary loss of breathing, loss of consciousness, dilated pupils,
apnea, and even cardiac arrest

24. • Before complete spinal block patients often complain and manifest
different clinical features, often depending on the level of spreads
of local anesthetics agents. Hypotension with or without
bradycardia is due to venous and arterial vasodilation resulting in
a reduced venous return, cardiac output, and systemic vascular
resistance, and due to direct blockage of the cardio accelerating
fibers (T1-T4). Patients often complain mild shortness of breath
secondary to blockade of abdominal and intercostal respiratory
accessory muscles (T1-T12) and numbness or weakness in the
arms, shoulders, and trunk (C5-T1), followed by nausea, with or
without vomiting secondary to cerebral hypotension, respiratory
arrest secondary to diaphragmatic paralysis (C3-C5), and loss of
consciousness (brainstem). Cardiac arrest may occur due to
hypotension and hypoxemia or unopposed vagal dominance

25. • Management comprises; reassurance, supplemental oxygen
(intubation if required to support oxygenation and ventilation or
for loss of airway reflexes), and IV fluid administration plus
vasopressors such as ephedrine or phenylephrine (adrenaline may
be required) to support maternal blood pressure. Early
recognition is vital, as block progression may be mitigated by
adjusting the patient’s position. If total spinal anesthesia occurs,
placing the patient in a Trendelenburg position will increase
venous return and improve cardiac output.

26. Brachial Plexus Injury
• The brachial plexus is a bundle of nerves that stems from nerve
roots in the cervical (neck) and upper trunk (torso) sections of the
spinal cord (C5-T1), creating a network that connects to the
nerves in the arm. These nerves control the motions of your
wrists, hands and arms, allowing you to raise your arm, type on
your keyboard or throw a baseball.

27. • From the roots, the brachial plexus nerves branch and fuse
through the shoulder and down the arm, classified into a few
different sections: trunks, divisions, cords and branches.
• The brachial plexus ends in five major nerve branches that extend
down the arm:
• Musculocutaneous nerve: Originates from nerve roots C5-C7 and flexes
muscles in the upper arm, at both the shoulder and elbow.
• Axillary nerve: Stems from nerve roots C5 and C6; it helps the shoulder
rotate and enables the arm to lift away from the body.
• Median nerve: Starts in nerve roots C6-T1 and enables movement in the
forearm and parts of the hand.
• Radial nerve: Begins in nerve roots C5-T1 and controls various muscles
in the upper arm, elbow, forearm and hand.
• Ulnar nerve: Rooted in C8-T1, it allows for fine motor control of the
fingers

28. • Common symptoms of brachial plexus injuries are:
• Numbness or loss of feeling in the hand or arm.
• Inability to control or move the shoulder, arm, wrist or hand.
• An arm that hangs limply.
• Burning, stinging or severe and sudden pain in the shoulder or
arm.
• Some brachial plexus injuries can result in Horner’s syndrome, a
disorder in which certain nerves of the sympathetic nervous
system are damaged. This syndrome can lead to a drooping eyelid,
overly constricted pupil and decreased facial sweating on one side
of the face. There is no specific treatment for Horner’s syndrome,
but sometimes treating its underlying cause may help to alleviate
symptoms.

30. • Horner's syndrome may correspond to a diffusion of local
anesthetics in prevertebral spaces ultimately involving the
sympathetic nerves and communicating with cervical nerve
trunks. It results from paralysis of the ipsilateral sympathetic
cervical chain (stellate ganglion) caused by surgery, drugs (mainly
high concentrations of local anesthetics), local compression
(hematoma or tumor), or inadequate perioperative positioning of
the patient
• Interscalene and supraclavicular blocks of the brachial plexus are
the main anesthetic techniques associated with this syndrome
• Causes of Horner's syndrome are large accumulation of local
anesthetic solution or the atypical proximal migration of the
solution above the clavicle toward the supraclavicular
paravertebral area.