Brachial Plexus

Foundations and mechanisms

Segmental architecture and organisational principles

The brachial plexus is a somatic nerve plexus formed classically by the anterior rami of C5–T1, supplying motor, sensory and sympathetic fibres to the upper limb. It is best conceptualised as a proximodistal re-sorting system: roots → trunks → divisions → cords → terminal branches. The arrangement allows fibres from multiple spinal segments to be redistributed to peripheral nerves according to limb compartment and function. For anaesthetic purposes, the plexus is not merely a list of nerves: it is a three-dimensional neurovascular structure whose relationship to fascial planes, the subclavian/axillary artery and the pleura determines block efficacy and complications.

Level	Constituents	Key anatomical relationship	Clinical relevance
Roots	C5, C6, C7, C8, T1 anterior rami	Between anterior and middle scalene muscles; prevertebral fascia	Interscalene block; high incidence of phrenic nerve block
Trunks	Upper C5–6, middle C7, lower C8–T1	Posterior triangle of neck; above clavicle	Supraclavicular block; compact plexus but close to pleura
Divisions	Each trunk divides into anterior and posterior divisions	Posterior to clavicle	Poorly accessible directly; transition zone for infraclavicular approaches
Cords	Lateral, posterior, medial	Named around second part of axillary artery	Infraclavicular and axillary block anatomy
Terminal branches	Musculocutaneous, axillary, radial, median, ulnar	Axilla and upper limb compartments	Selective distal nerve blockade and assessment of block failure

The cords are named by their relationship to the second part of the axillary artery, not by their eventual position in the arm. The lateral cord derives from anterior divisions of upper and middle trunks, the medial cord from the anterior division of the lower trunk, and the posterior cord from all three posterior divisions. Important variants include a prefixed plexus with substantial C4 contribution and reduced T1, or a postfixed plexus with greater T2 contribution. These variants explain incomplete anaesthesia despite apparently correct technique.

Functional anatomy: motor, sensory and autonomic components

Segmental innervation is clinically tested through myotomes and dermatomes but peripheral nerve lesions often produce mixed patterns because fascicles intermingle within the plexus. Key roots are: C5 shoulder abduction and elbow flexion; C6 wrist extension and thumb sensation; C7 elbow extension and middle finger sensation; C8 finger flexion; T1 intrinsic hand muscles. Sympathetic fibres to the upper limb arise predominantly from T2–T6, synapse in the stellate and upper thoracic ganglia, and travel with the plexus and vessels. Proximal blockade may therefore produce vasodilatation, anhidrosis and temperature rise in the blocked limb.

Fascial compartments and spread of local anaesthetic

The roots and trunks lie within an extension of the prevertebral fascia, often termed the brachial plexus sheath, although it is not a simple closed tube. Spread is determined by injection site, volume, connective tissue septa and pressure gradients rather than by a uniform sheath. Interscalene injection favours C5–C7 roots/trunks and may spare C8–T1, explaining ulnar-side sparing. Supraclavicular injection targets the plexus at its most compact point around the subclavian artery, typically producing dense upper limb anaesthesia with smaller volumes. Infraclavicular injection targets cords around the axillary artery, often giving more reliable blockade of musculocutaneous and axillary components than axillary approaches if spread is circumferential.

Approach	Typical target	Common effective volume	Characteristic limitation
Interscalene	C5–C7 roots/trunks	5–15 ml under ultrasound; historically 20–30 ml	Frequent phrenic nerve block; poor hand anaesthesia
Supraclavicular	Trunks/divisions lateral to subclavian artery	15–25 ml	Pneumothorax risk; possible ulnar sparing if lower trunk missed
Infraclavicular	Cords around axillary artery	20–30 ml	Deeper target; vascular puncture risk
Axillary	Terminal branches around axillary artery	20–40 ml divided	Requires separate musculocutaneous blockade

Mechanisms of neural blockade

Local anaesthetics block voltage-gated sodium channels from the intracellular side, stabilising the inactivated state and preventing action potential propagation. Clinically, blockade develops in the sequence sympathetic → pain → temperature → touch → motor, although this is modified by fibre diameter, myelination, firing frequency, drug pKa, lipid solubility and concentration. Small myelinated B fibres and Aδ fibres are blocked readily, while large myelinated Aα motor fibres generally require higher concentration or longer exposure. Unmyelinated C fibres are small but relatively resistant because multiple adjacent nodes do not exist; effective block requires sufficient longitudinal exposure.

Drug	Usual brachial plexus concentration	Approximate maximum dose without adrenaline	Approximate maximum dose with adrenaline
Lidocaine	1–2%	3 mg kg-1	7 mg kg-1
Bupivacaine	0.25–0.5%	2 mg kg-1	3 mg kg-1
Levobupivacaine	0.25–0.5%	2 mg kg-1	3 mg kg-1
Ropivacaine	0.375–0.75%	3 mg kg-1	3–4 mg kg-1

Dose calculation must incorporate total milligrams: 20 ml of 0.5% bupivacaine contains 100 mg. Ultrasound guidance permits lower effective volumes but does not abolish systemic toxicity risk. The ASRA approach to local anaesthetic systemic toxicity emphasises early recognition, seizure control, airway management and 20% lipid emulsion: bolus 1.5 ml kg^-1, then infusion 0.25 ml kg^-1 min^-1, with repeat bolus and increased infusion for cardiovascular instability; recommended upper limit is approximately 12 ml kg^-1.

Injury mechanisms and classifications

Brachial plexus injury may result from traction, compression, ischaemia, needle trauma, intraneural injection, haematoma or inflammatory neuritis. Stretch injury classically affects the upper plexus when the shoulder is depressed and head turned contralaterally, whereas lower plexus injury follows arm hyperabduction. In anaesthesia, risk is increased by paraesthesia-seeking techniques, injection against high resistance, deep sedation preventing symptom reporting, anticoagulation and pre-existing neuropathy.

Classification	Pathology	Recovery expectation
Neuropraxia	Focal demyelination without axonal disruption	Days to weeks; usually complete
Axonotmesis	Axonal disruption with intact connective tissue scaffolding	Regeneration about 1 mm day-1; variable recovery
Neurotmesis	Complete nerve and sheath disruption	Poor without surgical repair

Seddon’s categories correspond broadly to Sunderland grades I–V, with grade I neuropraxia, grades II–IV increasing axonal/connective tissue injury, and grade V complete transection. Exam answers should distinguish root avulsion, a preganglionic lesion associated with severe neuropathic pain and poor spontaneous recovery, from postganglionic rupture, where reconstructive surgery may be feasible.

Clinical assessment and investigations

Clinical presentation and localisation

Assessment of brachial plexus pathology is anatomical pattern recognition: define whether the lesion is preganglionic (root avulsion proximal to dorsal root ganglion), postganglionic (trunk/division/cord/peripheral nerve), or a non-plexus mimic. Presentations include pain, paraesthesia, weakness, sensory loss, reflex loss, autonomic features and, in anaesthetic practice, delayed recovery after regional blockade or postoperative neurological symptoms.

Level	Typical motor deficit	Sensory/reflex clue	Clinical associations
C5–C6 roots / upper trunk	Shoulder abduction, external rotation, elbow flexion; “waiter’s tip” in severe lesions	Lateral arm/forearm; reduced biceps and supinator reflexes	Traction injury, interscalene block, obstetric Erb palsy
C7 root / middle trunk	Elbow, wrist and finger extension; triceps weakness	Middle finger sensory loss; reduced triceps reflex	Cervical disc disease common mimic
C8–T1 roots / lower trunk	Intrinsic hand weakness, finger abduction/adduction, grip	Medial forearm/ulnar hand; possible Horner syndrome if T1 sympathetic fibres involved	Klumpke palsy, thoracic outlet syndrome, Pancoast tumour
Posterior cord	Deltoid, triceps, wrist/finger extensors	Radial/axillary distribution	Axillary trauma, infraclavicular block complication
Lateral cord	Elbow flexion, forearm supination, median-innervated wrist flexion	Lateral forearm; median territory variable	Compression/haematoma below clavicle
Medial cord	Ulnar intrinsic hand function; medial median contribution	Medial arm/forearm and ulnar hand	Lower plexus compression, thoracic outlet pathology

Examination should document pain severity, onset relative to trauma, surgery, positioning, tourniquet use or block placement; motor power using the MRC 0–5 scale; dermatomal and named-nerve sensory territories; reflexes; pulses, capillary refill and limb temperature. Severe neuropathic pain, scapular winging, diaphragmatic symptoms, Horner syndrome, myelopathic signs or progressive deficit are red flags. After regional anaesthesia, compare deficit duration with expected local anaesthetic effect: plain lidocaine typically resolves within 2–4 h, mepivacaine 3–5 h, ropivacaine/bupivacaine 8–18 h; perineural dexamethasone may prolong analgesia by approximately 6–10 h.

Differential diagnosis

• Cervical radiculopathy: neck pain, dermatomal symptoms, reflex change; Spurling test may reproduce pain. Sensory nerve action potentials are usually preserved because the lesion is proximal to the dorsal root ganglion.
• Peripheral mononeuropathy: ulnar neuropathy at elbow, median neuropathy/carpal tunnel, radial neuropathy; distribution respects a named nerve rather than plexus element.
• Central lesion: stroke, cord compression, demyelination; look for upper motor neurone signs, facial involvement or sensory level.
• Neuralgic amyotrophy: Parsonage–Turner syndrome; abrupt severe shoulder/arm pain followed days later by patchy weakness, often involving suprascapular, long thoracic or anterior interosseous nerves.
• Mass/infiltration: Pancoast tumour, lymphoma, radiation plexopathy, metastatic disease; progressive pain, weight loss, Horner syndrome or history of radiotherapy.
• Vascular/compartment pathology: expanding haematoma, pseudoaneurysm, ischaemia; particularly relevant after central venous access, axillary surgery, clavicular trauma or anticoagulation.

Investigations and interpretation

Investigation is guided by urgency. Immediate imaging is indicated for suspected root avulsion, spinal cord lesion, expanding haematoma, vascular compromise, infection, severe progressive deficit or complete motor deficit persisting beyond expected block duration. In postoperative/regional anaesthesia practice, early senior review and neurology referral are recommended when motor deficit is dense, progressive, painful or persists beyond 24–48 h; isolated resolving sensory symptoms can often be reviewed serially.

Investigation	Best timing	Key interpretation
MRI cervical spine and brachial plexus with contrast	Acute if red flags; otherwise early elective	Root avulsion, pseudomeningocele, haematoma, tumour, inflammatory plexitis, radiation fibrosis; MR neurography demonstrates nerve oedema, enlargement and signal change.
CT myelography	Often after acute phase; useful when MRI equivocal/contraindicated	High spatial resolution for preganglionic root avulsion; pseudomeningocele supports but is not pathognomonic.
Ultrasound	Bedside/early	Dynamic evaluation of compressive haematoma, nerve continuity, neuroma, vascular pseudoaneurysm; operator dependent.
Nerve conduction studies	Baseline after 7–10 days; most informative at 3–4 weeks	Reduced compound muscle action potential suggests axonal loss; preserved sensory nerve action potentials with sensory loss implies preganglionic radiculopathy.
Needle EMG	Denervation usually evident after 10–21 days; repeat at 6–12 weeks	Fibrillation potentials/positive sharp waves indicate axonal denervation; large polyphasic motor units indicate reinnervation.

Classification and prognostic thresholds

Classification	Pathology	Prognosis
Seddon neurapraxia / Sunderland I	Focal demyelination, axon intact	Recovery days to weeks; conduction block without denervation.
Axonotmesis / Sunderland II–IV	Axonal disruption with variable endoneurial/perineurial injury	Wallerian degeneration; regeneration approximately 1 mm/day after latency, outcome depends on distance and fascicular architecture.
Neurotmesis / Sunderland V	Complete nerve transection	No meaningful recovery without repair; early surgical referral.

Preganglionic avulsion has a poor spontaneous prognosis because the motor neuron connection is lost; reconstructive options include nerve transfer rather than direct grafting. Postganglionic lesions may be graftable if referred early. Persistent complete plexus palsy, absent clinical recovery by approximately 3 months, or EMG evidence of severe axonal loss warrants specialist peripheral nerve surgical assessment, as outcomes deteriorate when reinnervation is delayed beyond 6–9 months.

Management, pharmacology and procedures

Regional anaesthesia of the brachial plexus: procedural anatomy and block selection

Brachial plexus blockade is a core application of applied anatomy in anaesthesia. Choice of approach is dictated by the operative site, required tourniquet tolerance, respiratory reserve, anticoagulation status, and risk of neurological injury. Ultrasound guidance is now standard of care for most upper-limb blocks, improving block success and reducing vascular puncture and local anaesthetic dose, although it does not eliminate intraneural injection or systemic toxicity.

Approach	Anatomical target	Best surgical coverage	Typical volume	Important complications
Interscalene	Roots/trunks between anterior and middle scalene muscles, usually C5–C7	Shoulder, proximal humerus, lateral clavicle	5–15 ml ultrasound-guided; traditional 20 ml	Hemidiaphragmatic paresis, recurrent laryngeal nerve block, Horner syndrome, vertebral artery injection, epidural/spinal spread
Supraclavicular	Divisions clustered lateral and superficial to subclavian artery, above first rib	Arm below shoulder, elbow, forearm, hand	20–30 ml	Pneumothorax, phrenic nerve block, subclavian artery puncture
Infraclavicular	Cords around axillary artery, deep to pectoralis minor	Elbow, forearm, hand; catheter-friendly	20–30 ml	Vascular puncture, pneumothorax uncommon, incomplete medial cord block
Axillary	Terminal branches around axillary artery; musculocutaneous nerve often separate in coracobrachialis	Forearm and hand surgery	20–40 ml divided injections	Vascular puncture, tourniquet pain if intercostobrachial nerve not blocked

For shoulder surgery, interscalene block reliably anaesthetises the suprascapular, axillary and lateral pectoral contributions, but usually spares the inferior trunk; it is unsuitable as sole anaesthesia for distal hand surgery. The intercostobrachial nerve, derived from T2 and not part of the plexus, must be separately infiltrated for medial upper-arm tourniquet pain. Ulnar sparing is common with interscalene and occasionally supraclavicular approaches due to inferior trunk under-dosing.

Local anaesthetic pharmacology and dosing

Block onset and duration depend on pKa, lipid solubility, protein binding, concentration, dose, tissue vascularity and use of adjuncts. Lidocaine has faster onset but shorter duration; bupivacaine and ropivacaine provide prolonged analgesia through greater protein binding and lipid solubility. Ropivacaine is less cardiotoxic than racemic bupivacaine due to lower affinity for myocardial sodium channels and reduced lipid solubility.

Drug	Common concentration	Maximum dose without adrenaline	Approximate duration for plexus block	Notes
Lidocaine	1–2%	3 mg/kg; up to 7 mg/kg with adrenaline	2–4 h	Rapid onset; useful for short procedures
Prilocaine	1–2%	6 mg/kg	2–4 h	Risk of methaemoglobinaemia at high dose
Bupivacaine	0.25–0.5%	2 mg/kg	8–16 h	Highest cardiotoxicity among commonly used amides
Levobupivacaine	0.25–0.5%	2 mg/kg	8–16 h	S-enantiomer; less cardiotoxic than racemic bupivacaine
Ropivacaine	0.375–0.75%	3 mg/kg	6–14 h	Relative motor-sparing at lower concentrations

Adrenaline 1:200,000, equivalent to 5 micrograms/ml, reduces systemic absorption and acts as an intravascular marker, but should be used cautiously in severe peripheral vascular disease or where end-arterial perfusion is critical. Dexamethasone prolongs analgesia; typical perineural dose is 4 mg, although intravenous 4–8 mg provides a similar effect in many studies and avoids off-label perineural administration. Clonidine 0.5–1 microgram/kg and dexmedetomidine 0.5–1 microgram/kg prolong block but may cause sedation, bradycardia and hypotension.

Safety, complications and acute management

Pre-block assessment should document baseline neurological deficit, anticoagulant use, respiratory disease, contralateral diaphragmatic or recurrent laryngeal nerve dysfunction, infection at puncture site, allergy, and patient consent. Peripheral nerve block in anticoagulated patients follows risk stratification analogous to deep plexus/deep peripheral blocks; infraclavicular and supraclavicular blocks are generally treated more cautiously than compressible axillary blocks. Current ASRA/ESRA guidance should be applied for direct oral anticoagulants and neuraxial-equivalent deep blocks, commonly requiring interruption for 2–4 days depending on renal function and drug.

Local anaesthetic systemic toxicity presents with circumoral paraesthesia, tinnitus, agitation, seizures, then myocardial depression, conduction block and ventricular arrhythmias. Management is immediate cessation of injection, airway oxygenation, seizure control with benzodiazepines, avoidance of large-dose propofol in cardiovascular collapse, and lipid emulsion therapy. The standard regimen is 20% lipid emulsion 1.5 ml/kg bolus over 1 min, followed by 15 ml/kg/h infusion; repeat bolus up to two times for persistent instability and double infusion rate if necessary, with a usual maximum of 12 ml/kg in the first 30 min. Adrenaline doses should be small, preferably less than 1 microgram/kg boluses, and vasopressin, calcium-channel blockers and beta-blockers are avoided in established LAST.

Phrenic nerve block occurs in up to nearly 100% of conventional interscalene blocks and reduces forced vital capacity by approximately 20–30%. Low-volume ultrasound-guided interscalene injection, superior trunk block, or combined suprascapular and axillary nerve blocks may reduce but not abolish this risk. Pneumothorax after supraclavicular block is uncommon with ultrasound, generally less than 1%, but may present late; patients require discharge advice regarding dyspnoea, pleuritic pain and delayed presentation.

Brachial plexus injury: acute and longitudinal management

Traumatic plexus injury requires early classification into preganglionic root avulsion versus postganglionic rupture, stretch or compression injury. Severe pain, Horner syndrome, scapular winging, diaphragmatic paralysis, absent sensory nerve action potentials with preserved distal sensory symptoms, and MRI evidence of pseudomeningocoele suggest root avulsion. Initial management follows trauma priorities, cervical spine protection, vascular assessment of the subclavian/axillary vessels, splintage, analgesia and early referral to a peripheral nerve unit.

Electrodiagnostic testing is most informative after Wallerian degeneration, usually from 3 weeks post-injury; serial EMG identifies denervation and reinnervation. MRI neurography and CT myelography help define avulsion. Neurapraxic lesions are observed with physiotherapy and pain control; lack of recovery by 3 months, complete lesions, or avulsion features warrant surgical planning. Nerve grafting, neurolysis and nerve transfers, such as spinal accessory to suprascapular nerve or intercostal to musculocutaneous nerve, are ideally performed within 3–6 months; outcomes deteriorate after 9–12 months due to motor end-plate degeneration. Chronic management includes neuropathic analgesia, occupational therapy, contracture prevention, tendon transfer or free functional muscle transfer in late cases, and psychological support.

Exam controversies and advanced synthesis

Applied anatomy: where viva candidates lose marks

The brachial plexus is classically described as ventral rami C5–T1 forming roots, trunks, divisions, cords and terminal branches, but examination answers should acknowledge clinically important variation. A prefixed plexus receives a substantial C4 contribution with reduced T1 contribution; a postfixed plexus receives T2 with reduced C5. This is not trivia: postfixed plexuses may be more vulnerable to first rib compression and may explain incomplete anaesthesia if intercostobrachial territory is assumed to be blocked. The intercostobrachial nerve is T2, not a brachial plexus branch, and supplies medial upper arm sensation relevant to tourniquet pain.

At the interscalene level, the roots/trunks lie between anterior and middle scalene muscles; the vertebral artery lies anterior to C7 transverse process and the phrenic nerve descends on anterior scalene. At the supraclavicular level, the plexus is compact, superolateral to the subclavian artery and superior to the first rib/pleura. At the infraclavicular level, cords are named relative to the second part of the axillary artery, not their spatial orientation in every ultrasound image. At the axilla, the musculocutaneous nerve often leaves the sheath early and lies within coracobrachialis; failure to identify it is a common cause of lateral forearm sparing.

Block choice: anatomy, efficacy and complication trade-offs

Approach	Best anatomical target	Strengths	Important limitations/controversies
Interscalene	C5–C7 roots/superior-middle trunks	Shoulder and proximal humerus analgesia	Ulnar sparing common; phrenic nerve block historically up to 100% with 20 ml; avoid or modify in severe respiratory disease
Supraclavicular	Trunks/divisions clustered lateral to subclavian artery	Dense anaesthesia for distal arm; rapid onset	Pneumothorax risk reduced but not abolished by ultrasound; haemidiaphragmatic paresis reported about 30–60% depending on volume and technique
Infraclavicular	Cords around axillary artery	Good catheter site; less phrenic involvement	Deeper target; vascular puncture and local anaesthetic systemic toxicity remain relevant
Axillary	Terminal branches around axillary artery	Compressible site; lower respiratory risk	Requires separate musculocutaneous block; unsuitable for upper arm/shoulder surgery without supplementation

Phrenic nerve controversy and “diaphragm-sparing” strategies

The major modern controversy is not whether interscalene block works, but whether its respiratory cost is acceptable. The phrenic nerve arises mainly from C4 with C3–C5 contributions and lies on anterior scalene, explaining spread from interscalene injection. Classic interscalene techniques using 20–40 ml local anaesthetic produced near-universal ipsilateral haemidiaphragmatic paresis and approximately 20–30% reductions in FVC and FEV₁. Ultrasound-guided low-volume techniques reduce but do not eliminate this risk.

In Riazi et al., ultrasound-guided interscalene block with 5 ml ropivacaine 0.5% markedly reduced diaphragmatic paralysis compared with 20 ml, with reported incidences around 45% versus 100%, while preserving early analgesia in selected patients. More recent work on superior trunk block, targeting C5–C6 distal to the interscalene groove, has shown substantially lower haemidiaphragmatic paresis; randomised data have reported incidences in the order of 5% versus over 70% for interscalene block, with non-inferior shoulder analgesia in selected arthroscopic populations. The exam-relevant synthesis is cautious: “diaphragm-sparing” does not mean “phrenic-proof”, and patient selection, volume, fascial plane, and definition of paresis vary between studies.

Guidelines and safety integration

For anticoagulation, contemporary ASRA/ESRA principles treat deep, non-compressible plexus blocks—particularly interscalene, supraclavicular and infraclavicular—as requiring neuraxial-style caution. Aspirin alone is generally not a contraindication. Prophylactic LMWH typically requires at least 12 h before needle placement; therapeutic LMWH 24 h. Direct oral anticoagulants are commonly withheld for approximately 72 h for higher-risk deep blocks, adjusted for renal function, dose and bleeding risk. Axillary block is more compressible but still requires documented risk assessment.

Local anaesthetic systemic toxicity is a viva favourite because brachial plexus blocks use relatively large doses near vascular structures. Typical maximum single doses are lidocaine 3 mg kg^-1 plain and 7 mg kg^-1 with adrenaline; bupivacaine 2 mg kg^-1 plain and 3 mg kg^-1 with adrenaline; ropivacaine about 3 mg kg^-1. These are ceilings, not targets, and should be reduced in frailty, pregnancy, hepatic impairment, low cardiac output and combined blocks. ASRA lipid rescue uses 20% lipid emulsion: 1.5 ml kg^-1 bolus, then 0.25 ml kg^-1 min^-1 infusion; repeat bolus and increase infusion to 0.5 ml kg^-1 min^-1 for persistent cardiovascular instability, with an approximate maximum of 12 ml kg^-1.

High-yield pitfalls for Primary FRCA answers

• Naming cords: cords are lateral, posterior and medial relative to the axillary artery; they are formed by divisions, not trunks.
• Shoulder innervation: glenohumeral analgesia requires C5–C6 contributions, especially suprascapular and axillary nerves; skin over the shoulder also receives supraclavicular nerves from the cervical plexus.
• Hand anaesthesia: ulnar distribution derives predominantly C8–T1 and is often spared by interscalene block.
• Horner syndrome: stellate ganglion spread causes ptosis, miosis and anhidrosis; usually benign but must be distinguished from intrathecal/epidural spread or evolving neurological injury.
• Pneumothorax: first rib is a protective backstop in supraclavicular ultrasound technique; the pleura remains medial/inferior and must be continuously visualised.
• Neurological injury: avoid intraneural injection; warning signs include high opening injection pressure, severe pain or paraesthesia on injection, and nerve swelling on ultrasound. Awake feedback is imperfect and not a substitute for imaging and pressure-aware technique.