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Summary Table

Category	Details
Risk Factors	Macrosomia (birth weight >4 kg), shoulder dystocia, gestational diabetes, prolonged second stage of labor, assisted vaginal delivery (forceps or vacuum extraction), breech presentation
Etiology	Traction injury to the brachial plexus (C5-T1) during delivery. Erb's: lateral neck traction stretching the upper trunk (C5-C6). Klumpke's: upward arm traction stretching the lower trunk (C8-T1)
Patient Presentation	Neonate with a limp or immobile arm immediately after a difficult delivery. Parent or nurse notices the baby "does not move one arm"
Classic Physical Exam	Erb's: "Waiter's tip" posture (arm adducted, internally rotated, elbow extended, forearm pronated). Klumpke's: "Claw hand" deformity (loss of grip, MCP hyperextension, IP flexion), with or without ipsilateral Horner syndrome
Key Diagnostic Results	Clinical diagnosis confirmed by physical examination. X-ray to exclude clavicle or humerus fracture. EMG/NCS at 3-4 weeks to grade severity. MRI for nerve root avulsion if surgery is considered
Management	Early gentle passive range-of-motion exercises. Observation for spontaneous recovery over 3-6 months. Microsurgical nerve repair (grafting, transfer) if no biceps recovery by 3-6 months
Keywords	"Waiter's tip," "claw hand," shoulder dystocia, Horner syndrome, macrosomia, C5-C6, C8-T1, "arm hangs limp at birth," absent Moro reflex on affected side

1. Pathophysiology

The brachial plexus is a network of nerves formed by the ventral rami of spinal nerve roots C5 through T1. These roots merge into three trunks (upper, middle, lower), which then divide into anterior and posterior divisions, form three cords (lateral, medial, posterior), and finally branch into the terminal nerves of the upper limb. Understanding this anatomy is essential because the level of injury dictates the clinical picture, and exam questions are built around matching the injured root level to the expected motor and sensory deficit.

Erb's palsy results from excessive lateral traction on the head away from the shoulder during delivery. This mechanism stretches the upper trunk (C5-C6) and sometimes involves C7. The nerve roots most vulnerable to this force are C5 and C6 because the upper trunk is tethered superiorly and has less slack than the lower trunk. Loss of C5 and C6 function eliminates the muscles responsible for shoulder abduction (deltoid, supraspinatus), shoulder external rotation (infraspinatus, teres minor), elbow flexion (biceps, brachialis), and forearm supination (supinator, biceps). The resulting posture is the classic "waiter's tip" position: the arm hangs limply at the side, internally rotated, with the elbow straight and the forearm pronated. The hand and wrist are typically spared because C8 and T1 remain intact, so the baby can still grip your finger despite the arm hanging motionless.

Klumpke's palsy results from forceful upward traction on the arm, most classically during breech extraction when the arm is caught above the head or hyperabducted. This mechanism stretches the lower trunk (C8-T1). These roots supply the long finger flexors (flexor digitorum profundus via C8) and the intrinsic muscles of the hand (interossei, lumbricals, thenar, and hypothenar groups via T1). Loss of these muscles produces the "claw hand" deformity: the metacarpophalangeal joints hyperextend due to unopposed action of the extensor digitorum (radial nerve, C7), while the interphalangeal joints flex due to passive tension of the flexor tendons. Crucially, the T1 root runs in close proximity to the stellate (cervicothoracic) ganglion. If the T1 sympathetic fibers are disrupted, the baby will present with ipsilateral Horner syndrome: ptosis, miosis, and anhidrosis on the same side as the arm injury. The presence of Horner syndrome in Klumpke's palsy signals a more proximal, more severe injury (preganglionic root avulsion) and carries a worse prognosis.

The severity of the nerve damage itself follows the Seddon classification: neurapraxia (a conduction block from myelin disruption with the axon intact, carrying the best prognosis and full spontaneous recovery), axonotmesis (axonal disruption with intact endoneurium, allowing Wallerian degeneration and slow regeneration at roughly 1 mm/day), and neurotmesis (complete transection of the nerve, with no potential for spontaneous recovery and an absolute requirement for surgical repair). Most obstetric brachial plexus injuries fall into the neurapraxia category, which is why the majority recover without surgery.

2. Classification and Clinical Manifestation

Type	Nerve Roots	Mechanism	Frequency
Erb's Palsy (Upper)	C5-C6	Lateral neck traction; shoulder dystocia	Most common (~70-80% of cases)
Extended Erb's	C5-C6-C7	Same mechanism, greater force	~15-20%
Klumpke's Palsy (Lower)	C8-T1	Upward arm traction; breech delivery	Rare in isolation (~2-3%)
Total Plexus Palsy	C5-T1	Severe traction involving the entire plexus	~10-20%

Clinical Manifestation by Type

Feature	Erb's Palsy (C5-C6)	Extended Erb's (C5-C7)	Klumpke's Palsy (C8-T1)	Total Plexus (C5-T1)
Posture	Waiter's tip	Waiter's tip with wrist drop	Claw hand	Completely flail limb
Shoulder	Cannot abduct or externally rotate	Same as Erb's	Normal	Flail
Elbow	Cannot flex	Cannot flex or extend	Normal	Flail
Wrist	Normal	Wrist drop (loss of extensors)	Normal	Flail
Hand/Grip	Preserved (key distinguishing feature)	Preserved	Lost (no grip, no fine motor)	Flail
Reflexes Lost	Biceps (C5-C6), brachioradialis (C6)	Biceps, brachioradialis, triceps (C7)	Finger flexor reflex	All upper limb reflexes
Moro Reflex	Asymmetric (absent on affected side)	Asymmetric	Present but with no hand component	Absent on affected side
Horner Syndrome	Absent	Absent	Present if T1 sympathetic chain involved	May be present
Sensory Loss	Lateral arm and forearm (axillary, musculocutaneous nerve territory)	Lateral arm, forearm, and dorsal hand	Medial forearm and hand (medial cutaneous nerve, ulnar nerve territory)	Entire limb

3. Diagnostic Workup

Test	Role	Timing	Key Findings
Physical Examination	Best initial test	At birth	Characteristic posture, asymmetric Moro, absent reflexes at the affected root level
Plain Radiograph (X-ray)	Rule out skeletal injury	At birth	Clavicle fracture, proximal humerus fracture, or epiphyseal separation
Ultrasound of Shoulder	Alternative to X-ray in neonates	At birth	Epiphyseal separation of proximal humerus (cartilaginous, not visible on X-ray)
EMG / Nerve Conduction Studies	Assess severity and prognosis	3-4 weeks of age	Denervation potentials, fibrillations; helps distinguish neurapraxia from axonotmesis/neurotmesis
MRI (or CT Myelography)	Most accurate test for nerve root avulsion	Before surgical planning (3-6 months)	Pseudomeningocele (CSF leak at avulsed root), absent nerve root shadow

Physical examination is the cornerstone of diagnosis and the best initial test. The examiner looks for asymmetric posture, tests the Moro reflex (which will be absent or incomplete on the affected side), evaluates passive and active range of motion, and checks deep tendon reflexes. In Erb's palsy, the biceps and brachioradialis reflexes are absent while the grasp reflex remains intact. In Klumpke's palsy, the grasp reflex is absent while the biceps reflex is preserved. This reflex pattern alone can localize the lesion, and exam questions frequently test this distinction.

Plain radiography of the clavicle and shoulder is ordered immediately after clinical assessment, not to diagnose the plexus injury itself, but to exclude a clavicle fracture or proximal humerus fracture, both of which can mimic a brachial plexus palsy by producing a "pseudoparalysis" of the arm. A clavicle fracture is actually more common than brachial plexus injury in difficult deliveries, so ruling it out is the mandatory first imaging step.

EMG and nerve conduction studies are not performed immediately at birth because Wallerian degeneration takes approximately 2-3 weeks to develop detectable electrical changes. These studies are best performed at 3-4 weeks of age and serve two purposes: they confirm the diagnosis and, more importantly, they grade the severity. The presence of fibrillation potentials and positive sharp waves on EMG indicates axonal damage (axonotmesis or neurotmesis), while preserved motor unit action potentials suggest neurapraxia with a favorable prognosis.

MRI of the brachial plexus (or CT myelography as an alternative) is the most accurate test and is reserved for cases being considered for surgical intervention, typically when no clinical recovery is observed by 3-6 months. The hallmark finding of a root avulsion is a pseudomeningocele, a CSF-filled outpouching where the nerve root has been torn from the spinal cord. Root avulsion is an important finding because it means the injury is preganglionic and the nerve cannot regenerate on its own, making surgical repair mandatory.

4. Management and Treatment

Phase	Intervention	Timing	Details
Acute (Birth-3 weeks)	Gentle positioning, avoid traction	Immediately	Protect the arm; pin the sleeve to the shirt to prevent further stretch
Early Rehabilitation	Passive range-of-motion exercises	Starting at 2-3 weeks	Gentle daily ROM to prevent joint contractures, especially shoulder external rotation and forearm supination
Observation Period	Serial clinical examinations	Monthly for 3-6 months	Track return of biceps function (most critical prognostic indicator for Erb's)
Surgical Intervention	Microsurgical nerve repair	3-6 months if no recovery	Nerve grafting (sural nerve graft), nerve transfer (Oberlin transfer), or neurolysis
Late Reconstruction	Secondary musculoskeletal procedures	2-4 years onward	Tendon transfers, humeral osteotomy for persistent internal rotation contracture
Ongoing	Occupational therapy	Throughout childhood	Functional training, strengthening, adaptive strategies

In the acute phase (birth to 2-3 weeks), the priority is protecting the injured limb from further traction. The arm is gently positioned across the abdomen and may be pinned to the infant's clothing. No aggressive manipulation is performed. Parents are counseled that most cases (roughly 70-90% of Erb's palsy) will recover spontaneously, which is an important point of reassurance.

Passive range-of-motion exercises are the first active intervention, beginning at 2-3 weeks of age. A physiotherapist or trained parent performs gentle stretching of the shoulder into abduction and external rotation, and the forearm into supination, to prevent the development of fixed contractures. These exercises are performed daily and represent the backbone of conservative management. Joint contracture prevention is critical because even if the nerve recovers, a stiff joint will limit functional outcome.

The key prognostic milestone is the return of active elbow flexion (biceps function) by 3 months of age. This is the single most tested prognostic indicator. If the infant can actively flex the elbow against gravity by 3 months, the prognosis is excellent and continued observation is appropriate. If there is no biceps recovery by 3-6 months, the injury is unlikely to resolve spontaneously, and microsurgical nerve repair becomes the next best step. The exact timing varies by institution (some use 3 months, others 6 months as the cutoff), but this decision point is a high-yield concept.

Surgical options include nerve grafting (using the sural nerve from the leg as a donor graft to bridge the gap in the injured brachial plexus), nerve transfer (redirecting a functioning but expendable nerve to reinnervate a critical target, such as the Oberlin transfer where a fascicle of the ulnar nerve is transferred to the biceps motor branch), and neurolysis (freeing the nerve from scar tissue). For root avulsions, nerve grafting from the root is not possible because the root is detached from the spinal cord, so nerve transfers from extraplexal donors (spinal accessory nerve, intercostal nerves) are used instead.

Late reconstructive surgery is considered if residual deficits persist despite nerve recovery or repair. The most common problem is persistent internal rotation contracture of the shoulder due to muscular imbalance. Procedures include tendon transfers (subscapularis release, latissimus dorsi and teres major transfer to the rotator cuff) and external rotation osteotomy of the humerus.

Klumpke's palsy carries a worse prognosis than Erb's, particularly when Horner syndrome is present, as this indicates root avulsion at C8-T1. Intrinsic hand muscle function is difficult to restore surgically because the distance from the plexus to the hand muscles is long, and reinnervation may not reach the target before irreversible motor endplate degeneration occurs (typically by 12-18 months).

5. Differential Diagnosis and Distractors

Differential	Why It Is Similar	Key Discriminator
Clavicle Fracture	Newborn holds arm still after difficult delivery ("pseudoparalysis"); history of shoulder dystocia overlaps	Palpable crepitus or bony irregularity over the clavicle; X-ray shows fracture line; Moro reflex may return once pain resolves; no true neurological deficit on examination
Proximal Humerus Fracture / Epiphyseal Separation	Limp arm in a neonate with birth trauma; clinically indistinguishable from plexus injury at first glance	X-ray (or ultrasound if epiphysis is cartilaginous) shows fracture; arm swelling and point tenderness present; reflexes remain intact
Septic Arthritis of the Shoulder	Infant does not move the arm (pseudoparalysis); may present within the first few days of life	Fever, irritability, warmth, erythema over the joint; elevated CRP and WBC; joint aspiration yields purulent fluid
Cerebral Palsy (Hemiplegic type)	Unilateral upper limb weakness in an infant	Onset is noticed later (not immediately at birth); associated with increased tone (spasticity), hyperreflexia, and a positive Babinski; MRI brain shows periventricular leukomalacia or other CNS pathology
Cervical Spinal Cord Injury	Limp arm after traumatic delivery	Bilateral involvement (quadriparesis) is more typical; respiratory distress if high cervical; diaphragm paralysis (C3-C5); bowel/bladder dysfunction; MRI spine shows cord signal abnormality
Congenital Muscular Torticollis	Abnormal posture in a neonate after difficult delivery	Head tilted to one side with chin rotated to the opposite side; palpable sternocleidomastoid mass ("olive"); arm moves normally

6. Traps and High-Yield Pearls

The most common way students get questions about brachial plexus injury wrong is by confusing the level of injury with the clinical presentation. When a vignette describes a neonate in the "waiter's tip" position with preserved hand grip, many students are tempted to select a clavicle fracture or total plexus palsy instead of Erb's palsy. The key is recognizing that preserved hand function points to an upper trunk injury (C5-C6), not a lower trunk injury, and that the absence of bony crepitus or fracture on X-ray excludes a skeletal cause.

The second major trap involves Klumpke's palsy with Horner syndrome. Test-writers will describe a breech delivery followed by a claw hand deformity and then add ipsilateral ptosis and miosis. Students who do not connect the sympathetic chain to T1 may miss the Horner syndrome component entirely or, worse, interpret the ptosis and miosis as a separate neurological condition (such as third cranial nerve palsy or brainstem pathology). Remember: Horner syndrome in the context of a birth-related arm injury always points to a C8-T1 lower trunk lesion.

A third trap is the timing of EMG. A question may present a 2-day-old infant with a limp arm and ask what the next diagnostic step should be. Students who select EMG will get the question wrong because Wallerian degeneration has not yet occurred and the study will be falsely normal. The correct answer at this stage is plain radiography to rule out fracture, followed by clinical observation. EMG is appropriate only at 3-4 weeks.

Finally, remember the prognostic decision point: absence of active elbow flexion (biceps recovery) by 3 months is the trigger for surgical referral. If a vignette describes a 4-month-old with no biceps function despite physical therapy, the next best step is microsurgical consultation, not continued observation. This tests your ability to recognize when conservative management has reached its limit and intervention is required.

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