Brachial Plexus - Complete Anatomy & Regional Block Guide

PART 1: ANATOMY OF THE BRACHIAL PLEXUS

Overview

Roots → Trunks → Divisions → Cords → Terminal branches (Mnemonic: "Randy Travis Drinks Cold Beer")

Labelled Diagrams

Components in Detail

1. ROOTS (C5-T1)

• The anterior rami of C5, C6, C7, C8, and T1
• Emerge from their intervertebral foramina and travel in grooves between the anterior and posterior tubercles of the transverse processes
• Exit between the anterior scalene and middle scalene muscles, above and posterior to the subclavian artery
• Receive gray rami communicantes from the sympathetic trunk (carry postganglionic sympathetic fibres)
• Enclosed in the interscalene fascial sheath (an extension of prevertebral fascia)

2. TRUNKS (3)

• Superior trunk: Suprascapular nerve (C5, C6) - supplies supraspinatus and infraspinatus
• Superior trunk: Nerve to subclavius (C5, C6)

3. DIVISIONS (6 total - 2 per trunk)

• Anterior divisions supply flexor (anterior) compartment muscles
• Posterior divisions supply extensor (posterior) compartment muscles
• There are NO named branches from the divisions

4. CORDS (3) - Named for their relationship to the 2nd part of the axillary artery

• Lateral pectoral nerve (C5-C7) - pectoralis major
• Musculocutaneous nerve (C5-C7) - coracobrachialis, biceps, brachialis; lateral cutaneous nerve of forearm
• Lateral root of median nerve

• Medial pectoral nerve (C8, T1) - pectoralis minor and major
• Medial cutaneous nerve of arm (C8, T1)
• Medial cutaneous nerve of forearm (C8, T1)
• Ulnar nerve (C7, C8, T1)
• Medial root of median nerve

• Upper subscapular nerve (C5, C6) - subscapularis
• Thoracodorsal nerve (C6-C8) - latissimus dorsi
• Lower subscapular nerve (C5, C6) - subscapularis and teres major
• Axillary nerve (C5, C6) - deltoid and teres minor
• Radial nerve (C5-C8, T1) - all posterior compartment muscles of arm and forearm

5. TERMINAL BRANCHES (5 major)

Fascial Sheaths and Topography (Clinically Important)

1. Interscalene fascial sheath - between scalene muscles (target for interscalene block)
2. Axillary sheath - continuation in the axilla (target for axillary block)

• Subclavian/axillary artery - arteries are key landmarks for all blocks
• Phrenic nerve - runs anterior to scalenus anterior (vulnerable in interscalene and supraclavicular blocks)
• Pleural dome/lung apex - at risk in supraclavicular blocks
• Vertebral artery - at risk in deep interscalene injections
• Sympathetic chain - produces Horner syndrome if blocked

PART 2: APPROACHES TO BRACHIAL PLEXUS BLOCKS

Overview - Level of Block vs. Coverage

1. INTERSCALENE BLOCK (ISB)

• Shoulder surgery (rotator cuff repair, shoulder arthroplasty)
• Proximal humerus surgery, clavicle fracture fixation
• Acute shoulder dislocation reduction
• Postoperative analgesia following shoulder surgery
• AC joint procedures

• Contralateral phrenic nerve palsy (ABSOLUTE - bilateral phrenic block = respiratory failure)
• Contralateral hemidiaphragm paralysis
• Severe COPD or pulmonary insufficiency (phrenic palsy will worsen)
• Contralateral vocal cord paralysis
• Local infection, severe coagulopathy, patient refusal
• Bilateral ISB is ABSOLUTELY CONTRAINDICATED

• Patient supine, head rotated 30-45° away from the side to be blocked
• Ask patient to lift and rotate head against resistance to define the sternocleidomastoid (SCM)
• Identify the interscalene groove by rolling fingers posteriorly off the posterior border of the clavicular head of the SCM at the level of the cricoid cartilage (C6)
• The external jugular vein often crosses this groove at C6 level - useful landmark
• The groove lies between anterior scalene (anteriorly) and middle scalene (posteriorly)
• Insert needle at 45° caudally and slightly medially
• Endpoint: paresthesia to shoulder/arm OR motor response with nerve stimulator (deltoid twitch = axillary n., biceps = musculocutaneous n.)
• Inject 20-40 mL of local anesthetic

• Ipsilateral phrenic nerve palsy (virtually 100% incidence with nerve stimulator technique; ~27% with low-volume ultrasound): reduces ipsilateral hemidiaphragm function by ~25% - relevant in pulmonary compromise
• Horner syndrome (ptosis, miosis, anhidrosis): proximal tracking to cervicothoracic ganglion - requires reassurance only
• Recurrent laryngeal nerve block: hoarseness - especially concerning with contralateral vocal cord palsy
• Vertebral artery injection: immediate seizure activity (as little as 1 mL causes seizure)
• Spinal/epidural spread: possible; intrathecal injection/cervical syrinx reported
• Pneumothorax: less common than supraclavicular, but possible given proximity to apical pleura
• C8-T1 (ulnar) sparing: inferior trunk not well-blocked; interscalene NOT suitable for hand/forearm surgery

2. SUPRACLAVICULAR BLOCK

• Surgery at or distal to the elbow: forearm and hand procedures
• Upper arm surgery (with intercostobrachial nerve supplement for tourniquet)
• Dense, rapid-onset surgical anesthesia needed
• NOT ideal for isolated shoulder surgery (suprascapular nerve not reliably blocked)

• Patient supine, head turned 30° to contralateral side, arm adducted at side
• Identify the supraclavicular fossa (depression just above mid-clavicle)
• The subclavian artery is palpable at the lateral border of the anterior scalene
• Insert needle 1-2 cm above the clavicle at the posterior border of the SCM, directed caudally and medially at 45-60° to skin
• Endpoint: paresthesia to hand/forearm OR nerve stimulator response (finger/wrist movement)
• First rib acts as a natural barrier - needle should not penetrate beyond it
• Inject 25-40 mL of local anesthetic in divided doses

• Pneumothorax (0.5-6%): most feared; risk is reduced but not eliminated with ultrasound; peak incidence 6-12 hours post-block
• Phrenic nerve block (40-60%): similar precautions to ISB regarding pulmonary reserve
• Horner syndrome: sympathetic chain proximity
• Subclavian artery puncture/hematoma
• Ulnar nerve sparing (~10%): lower trunk can be missed; requires careful technique to identify inferior trunk
• Perineural catheters are inferior at this site compared to infraclavicular approach

3. INFRACLAVICULAR BLOCK

• Surgery at or distal to the elbow; elbow, forearm, wrist, and hand
• Best approach for continuous perineural catheter (most stable catheter position; no arm manipulation needed)
• Patients who cannot abduct the arm (e.g., painful shoulder, frozen shoulder)
• When supraclavicular block is undesirable (e.g., compromised pulmonary reserve)
• Upper arm surgery when combined with intercostobrachial nerve block

• Patient supine, arm slightly abducted; shoulder abduction to 90° facilitates visualization
• Identify the coracoid process (bony landmark just medial to glenohumeral joint) and the clavicle
• Insert needle 2 cm medial and 2 cm caudal to the coracoid process, directed perpendicular to the skin (or slightly caudal)
• Target is the posterior cord (posterior to axillary artery) - single injection here gives complete block
• Endpoint: nerve stimulator - hand extension/wrist extension (radial/posterior cord) OR paresthesia
• Inject 30-40 mL of local anesthetic posterior to the axillary artery

• Pneumothorax: lower risk than supraclavicular but not zero (deeper needle path)
• Axillary artery/vein puncture: hematoma; axillary vein is medial/inferior
• Deep nature of block: needle tip visualization is difficult; steep needle angle worsens this
• Musculocutaneous nerve sparing is rare (branches proximally, but captured within infraclavicular fascial space)
• Lower risk of phrenic nerve palsy compared to ISB or supraclavicular
• Lower risk of pneumothorax than supraclavicular approach
• No Horner syndrome typically

4. AXILLARY BLOCK

• Surgery distal to the elbow: forearm, wrist, hand procedures
• Safest approach - no risk of pneumothorax or phrenic nerve palsy
• Pediatric patients and outpatient procedures
• Patients with severe pulmonary disease (safe choice)
• Supplementation of incomplete proximal blocks

• Axillary lymphadenopathy, infection in axilla
• Inability to abduct and externally rotate the arm
• Note: axillary nerve, musculocutaneous nerve, and medial brachial cutaneous nerve branch proximal to the injection site and are NOT blocked by the axillary approach

• Patient supine with arm abducted 90° and elbow flexed 90° (hand behind head)
• Palpate the axillary artery pulse as high in the axilla as possible
• The brachial plexus terminal nerves lie in specific positions around the artery:
  • Median nerve: anterosuperior to artery
  • Ulnar nerve: posteroinferior to artery
  • Radial nerve: posterior to artery
  • Musculocutaneous nerve: has already left the sheath, lies within coracobrachialis muscle
• Transarterial technique: Advance needle through the artery; inject 20 mL posterior (for radial/ulnar) and 20 mL anterior (for median) after withdrawing to skin
• Perivascular (fascial click) technique: Insert needle at 45° to skin alongside artery until fascial click is felt; inject 30-40 mL
• Multiple injection technique (most reliable): Use nerve stimulator or ultrasound to localize each nerve individually (5-10 mL per nerve)
• Musculocutaneous nerve must be blocked separately: inject 5-10 mL into the body of the coracobrachialis muscle

• Axillary artery/vein puncture: hematoma (most common)
• Local anesthetic systemic toxicity (LAST): axilla is highly vascular; small veins traumatized by needle placement increase absorption - aspirate frequently
• Infection: less common; axilla is not a sterile area
• Neuropathy: direct nerve trauma
• Incomplete block: most common problem - axillary, musculocutaneous, and intercostobrachial nerves require separate blocks
• No pneumothorax risk
• No phrenic nerve palsy risk
• No Horner syndrome

5. MIDHUMERAL BLOCK

Summary Comparison Table

General Complications of All Brachial Plexus Blocks

1. Local anesthetic systemic toxicity (LAST): seizures, cardiovascular collapse - have intralipid available
2. Peripheral nerve injury: incidence ~1.7-3% transient; ~0.04% persistent; from direct trauma, intraneural injection, ischemia
3. Infection: cellulitis, abscess, meningitis (epidural spread)
4. Hematoma: especially in anticoagulated patients
5. Allergic reaction: rare with amide local anesthetics
6. Failed block / incomplete anesthesia: requires supplementation or GA conversion

Local Anesthetic Systemic Toxicity (LAST) - Complete Guide

Definition

Incidence

• Overall incidence: ~0.03% for peripheral nerve blocks (higher with multiple/large volume blocks)
• Cardiac arrest from LAST: ~1 in 25,000 peripheral nerve blocks
• Incidence has declined with ultrasound guidance but has NOT been eliminated
• LAST is underreported, especially delayed presentations

Pharmacology Basis: Why LAST Occurs

1. Rate of absorption - highest to lowest vascularity of block site:
   • Intercostal > caudal > epidural > brachial plexus > sciatic/femoral > subcutaneous
2. Total dose administered (mg = concentration × volume)
3. Use of epinephrine - reduces peak plasma concentration by 10-20% via vasoconstriction
4. Drug metabolism - amide LAs (lidocaine, bupivacaine, ropivacaine) metabolized by liver; ester LAs (procaine, chloroprocaine) by plasma cholinesterase
5. Protein binding - only free (unbound) drug is active; hypoalbuminemia increases risk

Risk Factors for LAST

Toxic Dose Thresholds (Maximum Safe Doses)

Note: Bupivacaine 0.75% is NEVER used for epidural anesthesia in obstetrics (accidental IV injection = cardiac arrest)

Pathophysiology

CNS Mechanism

• Low concentrations → CNS depression (sedation, analgesia)
• Moderate concentrations → CNS excitation (inhibitory neurons blocked first, paradoxical excitation)
• High concentrations → Global CNS depression (coma, respiratory arrest)

Cardiovascular Mechanism

1. Na+ channel blockade in cardiomyocytes → slows conduction (prolonged PR interval, wide QRS)
2. K+ and Ca2+ channel blockade → impaired repolarization
3. Mitochondrial dysfunction → impaired fatty acid oxidation in cardiac muscle
4. Bupivacaine's unique danger: binds Na+ channels during the activated AND inactivated states with slow dissociation ("fast in, slow out") → accumulates with each cardiac cycle → refractory ventricular arrhythmias
5. Pulmonary vasoconstriction: rising LA concentrations cause pulmonary artery hypertension even before significant cardiac depression
6. CNS-mediated cardiovascular depression: bupivacaine disrupts brainstem baroreflex regulation

Clinical Presentation

Typical Sequential Progression

CNS PRODROME ──────────────────────────────► CVS COLLAPSE
   ↓                    ↓                        ↓
Early excitatory   CNS depression          Cardiovascular
(inhibition of        phase
inhibitory neurons)

CNS Manifestations (Dose-Dependent - Lidocaine Model)

CVS Manifestations

• Hypertension, tachycardia (adrenergic stimulation)
• ECG: PR prolongation, QRS widening

• Hypotension (vasodilation + myocardial depression)
• Bradycardia, heart block
• ECG: ST changes, bundle branch block

• Ventricular arrhythmias (VT, VF, torsades de pointes)
• Complete heart block
• Asystole
• Cardiovascular collapse and cardiac arrest

IMPORTANT Atypical Presentations

1. Pure CVS without CNS prodrome: Occurs when CNS signs are masked by concurrent sedation/GA. May be the first manifestation - especially dangerous.
2. Delayed onset LAST: Symptoms may appear 1-60 minutes after injection (peak absorption from tissue depot). Always monitor 30 min post-block.
3. Subtle CNS signs only: Agitation, confusion, or bizarre behavior in a sedated patient.
4. Bupivacaine cardiac arrest: Can occur without any preceding CNS signs, especially with accidental IV injection.

Differential Diagnosis

Prevention of LAST

1. Aspirate before injection and before each subsequent 5 mL aliquot
2. Incremental injection: inject in 5 mL aliquots, 15-30 seconds apart (allows CNS symptoms to manifest before full dose given)
3. Epinephrine marker dose: epinephrine 5 mcg/mL (1:200,000) added to LA - if accidentally intravascular, causes HR rise >20 bpm and systolic BP rise >15 mmHg within 1 minute
4. Adhere to maximum safe doses (calculate mg/kg before every block)
5. Ultrasound guidance: visualize needle tip and LA spread; reduce doses
6. Avoid highly vascular sites without aspiration
7. Choose safer agents: prefer ropivacaine over bupivacaine when equivalent efficacy expected
8. Pre-treatment: midazolam raises seizure threshold (but masks early CNS signs - two-edged sword)
9. Correct modifiable factors: avoid acidosis, hypoxia, hypercarbia which potentiate LAST

Management of LAST - Step-by-Step

IMMEDIATE ACTIONS (First 60 seconds)

STEP 1 - CALL FOR HELP

• Activate emergency response immediately at first sign of LAST
• Call for resuscitation cart, lipid emulsion, and defibrillator
• Call for cardiopulmonary bypass capability alert if available

STEP 2 - AIRWAY MANAGEMENT (Simultaneous)

• 100% oxygen via facemask or intubation
• Ventilate to normocapnia (avoid hypercarbia which potentiates toxicity)
• If seizures → may require intubation to protect airway
• Correct: hypoxia, hypercarbia, acidosis (all worsen LAST significantly)
• If intubating: succinylcholine preferred (short-acting) to minimize prolonged acidosis from fasciculations

STEP 3 - SEIZURE MANAGEMENT

• Benzodiazepines first-line: midazolam 0.05-0.1 mg/kg IV; lorazepam 0.05 mg/kg IV; diazepam 0.1 mg/kg IV
• Propofol (small doses: 0.5-1 mg/kg) - alternative but caution as it causes cardiovascular depression; avoid if haemodynamically unstable
• Thiopentone (1-2 mg/kg) for refractory seizures
• Small dose succinylcholine to stop motor activity if seizures are intractable (prevents rhabdomyolysis, acidosis, hypoxia) - NOTE: this terminates motor activity only, NOT cerebral electrical activity
• AVOID: phenytoin (sodium channel blocker - worsens cardiac toxicity)

STEP 4 - LIPID EMULSION THERAPY (Intralipid 20%) ⭐ KEY TREATMENT

1. "Lipid shuttle" / lipid sink effect: creates a lipid phase in blood that sequesters lipid-soluble local anesthetic molecules, reducing free drug available to target tissues ("scavenger" effect)
2. Direct metabolic support: provides fatty acid substrate to bupivacaine-poisoned myocardial mitochondria (rescues oxidative phosphorylation)
3. Direct positive inotropic effect: reverses LA-induced calcium channel blockade
4. Redistribution: carries LA from cardiac/CNS tissue back to peripheral depots (liver, adipose)

Intralipid 20% must be immediately available wherever local anesthetics are used.

STEP 5 - CARDIOVASCULAR RESUSCITATION (Modified ACLS)

• Epinephrine: LOW DOSE - initial bolus <1 mcg/kg (NOT standard ACLS 1 mg bolus)
  • Rationale: high-dose epinephrine triggers VF in a bupivacaine-poisoned heart by increasing automaticity in an already irritable myocardium
  • Small doses (10-100 mcg) correct hypotension without precipitating VF
• Phenylephrine or vasopressin for pure vasodilation without arrhythmia
• Calcium gluconate for direct inotropic support
• IV fluid bolus for volume resuscitation

• Amiodarone - drug of choice for ventricular arrhythmias in LAST
• AVOID the following (all worsen LAST):
  • Vasopressin (worsens cardiac depression)
  • Calcium channel blockers (worsen myocardial depression)
  • Beta blockers (worsen bradycardia and myocardial depression)
  • Local anesthetics as antiarrhythmics (lidocaine, mexiletine - obviously worsen Na+ channel blockade)
  • Class 1 antiarrhythmics (flecainide, procainamide - Na+ channel blockers)

• Begin CPR immediately - standard BLS/ACLS
• Lipid emulsion simultaneously (do not delay)
• Defibrillation for VF: standard energy (200 J biphasic)
• Reduce epinephrine dose to <1 mcg/kg per bolus (avoid standard 1 mg doses)
• Prolonged resuscitation may be needed - LA-poisoned hearts can recover with time + lipid therapy

STEP 6 - ESCALATION: CARDIOPULMONARY BYPASS (ECMO)

• If cardiac instability persists despite lipid emulsion + modified ACLS
• Alert the nearest facility with CPB/ECMO capability immediately - this is time-critical
• CPB allows the heart time to recover as plasma LA concentrations fall through redistribution and metabolism
• Extracorporeal membrane oxygenation (ECMO) is increasingly preferred (venoarterial ECMO for CVS collapse)
• Historical case reports of survival after 1+ hour of resuscitation via CPB

STEP 7 - POST-RESUSCITATION MONITORING

• Monitor in ICU/HDU for minimum 2-6 hours after resolution of symptoms
• Extended monitoring (up to 12 hours) for patients with significant cardiovascular morbidity
• Repeat ECG, ABG, electrolytes, CXR
• Reassess neurological status
• Watch for delayed recurrence of LAST (LA redistribution from tissues)

Management Summary - ASRA Algorithm

LAST SUSPECTED?
      │
      ▼
1. CALL FOR HELP + Stop further LA injection
      │
      ▼
2. AIRWAY → 100% O2, prevent hypercarbia/acidosis
      │
      ▼
3. SEIZURES? → Benzodiazepines (avoid phenytoin)
      │
      ▼
4. ★ LIPID EMULSION 20% (Intralipid)
   • Bolus: 1.5 mL/kg over 2-3 min
   • Infusion: 0.25 mL/kg/min
   • Repeat bolus + increase infusion if unstable
      │
      ▼
5. CARDIOVASCULAR:
   • Epinephrine <1 mcg/kg boluses (NOT 1 mg)
   • Amiodarone for VT/VF
   • AVOID: vasopressin, Ca-blockers, β-blockers, class 1 antiarrhythmics
   • CPR if arrest
      │
      ▼
6. ESCALATE → Alert CPB/ECMO facility
      │
      ▼
7. MONITOR 2-6 hours post-resolution

Special Populations

Paediatric LAST

• Calculate doses STRICTLY by weight (mg/kg); children at higher risk from overdose errors
• Lipid emulsion dose same: 1.5 mL/kg bolus; no specific neonatal dosing guidelines exist, but wide dose ranges appear safe
• Neonates: reduced protein binding and hepatic metabolism = lower threshold for toxicity

Obstetric LAST

• Bupivacaine 0.75% is CONTRAINDICATED for epidural in obstetrics
• Pregnant women: increased cardiac output + reduced protein binding → faster absorption
• Fetal acidosis can trap LA in fetus ("ion trapping")
• Lipid emulsion safe in pregnancy

Elderly LAST

• Reduced hepatic blood flow and protein binding
• Decreased cardiac reserve
• Use lower doses; careful monitoring

What to Have Ready (Before Every Block)

• Resuscitation cart with defibrillator
• 20% lipid emulsion (Intralipid) 500 mL - immediately at hand
• IV access established
• Pulse oximetry, ECG monitoring
• Airway equipment (facemask, laryngoscope, ETT)
• Benzodiazepine drawn up or available
• Printed ASRA LAST checklist (cognitive aid)

Key Take-Home Points

1. Early recognition is everything - CNS prodrome (tinnitus, metallic taste, circumoral numbness) precedes cardiac arrest by precious minutes
2. Lipid emulsion (Intralipid 20%) is the antidote - give early and boldly
3. Modified ACLS - epinephrine doses must be LOW (<1 mcg/kg); avoid vasopressin, beta-blockers, Ca-channel blockers, and Class 1 antiarrhythmics
4. Bupivacaine is the most dangerous - can cause cardiac arrest without CNS warning, especially if sedation masks CNS signs
5. Prolonged resuscitation is justified - LA-poisoned hearts can recover with time + lipid rescue; do not give up
6. Prevention: aspiration, incremental injection, epinephrine test dose, ultrasound guidance, dose limits
7. Ultrasound reduces but does not eliminate LAST - vigilance is always required