Part I - Birth Trauma: The Newborn Who Will Not Move a Limb
- Mechanisms and risk factors common to birth injury
Part II - Obstetric Brachial Plexus Palsy (OBPP)
Part III - Neonatal (Birth) Fractures
Part IV - Torticollis (Wry Neck)
- Congenital muscular torticollis (CMT)
- The differential diagnosis of the twisted neck
References

Part I - Birth Trauma: The Newborn Who Will Not Move a Limb

Passage through the birth canal is the most mechanically violent event most of us will ever survive. In the great majority of newborns it leaves no trace, but in a small minority the forces of a difficult delivery exceed what the soft, partly cartilaginous neonatal skeleton and its still-myelinating nerves can tolerate. The result is the family of conditions grouped under birth trauma (Bulg. родова травма): fractures of the clavicle, humerus and occasionally the femur; stretch injuries of the brachial plexus; haemorrhage into a neck muscle that later contracts into a torticollis; and the soft-tissue and cranial injuries (cephalhaematoma, facial-nerve palsy, fat necrosis) that complete the picture.

The three classic examination pillars of this topic, obstetric brachial plexus palsy, neonatal fracture, and torticollis, share a disarmingly simple presentation: a baby who does not move one arm, or who holds the head twisted to one side. The clinician’s task is to read that single sign correctly. The differential runs from the entirely benign, such as a clavicle fracture that needs nothing but reassurance, to conditions that demand urgent microsurgery, or that, if a non-muscular cause of torticollis is missed, can end in catastrophe.

A framing repeated across the paediatric literature holds that “lack of arm movement in the neonatal period is the most common clinical finding” for a whole group of shoulder problems: fracture of the clavicle, brachial plexus palsy, proximal humeral physeal separation, septic arthritis, osteomyelitis and non-accidental injury all share it.[1] The non-moving arm is therefore a syndrome, and the same discipline applies to the twisted neck.

Mechanisms and risk factors common to birth injury

The recurring obstetric risk factors are macrosomia (the large-for-gestational-age infant, classically of the diabetic mother), shoulder dystocia, breech delivery, prolonged or instrumented (forceps/vacuum) labour, multiparity, and a previous delivery already complicated by a birth injury.[2] The mechanical theme is shared: a large baby whose shoulders keep widening even as fetal head growth plateaus becomes wedged, and the traction or compression applied to free it is transmitted to clavicle, humerus and plexus alike.[3] Caesarean section reduces the risk of plexus injury without abolishing it, by roughly one hundred-fold in one estimate.[4]

Figure 1. Mechanism of shoulder dystocia: the fetal anterior shoulder is impacted behind the maternal pubic symphysis. Suprapubic pressure (a first-line manoeuvre) is shown; excessive lateral traction on the head in this situation is what overstretches the upper brachial plexus and may fracture the clavicle. Credit: Hariadhi, via Wikimedia Commons, CC BY-SA 4.0.

The rest of this summary takes each pillar in turn: the brachial plexus palsy (by far the largest examination topic), the neonatal fractures, and torticollis with its differential diagnosis.

Part II - Obstetric Brachial Plexus Palsy (OBPP)

Obstetric brachial plexus palsy, also written brachial plexus birth injury/palsy (BPBI/BPBP) and, in the Bulgarian tradition, акушерска пареза на брахиалния плексус, is a traction lesion of the C5-T1 nerve roots sustained during delivery. It has occupied surgeons since Smellie first mentioned it in 1764; Duchenne (1872) and Erb (1874) defined the upper-root lesion, and Augusta Déjerine-Klumpke (1885) the lower-root variant with its sympathetic involvement.[5]

Surgical anatomy of the brachial plexus

The plexus is formed by the ventral rami of C5 through T1. In about 22% of people a contribution from C4 makes the plexus prefixed; a T2 contribution (a postfixed plexus) is seen in roughly 1%.[6] From proximal to distal the organisation runs roots → trunks → divisions → cords → terminal branches: C5-C6 join as the upper trunk, C7 continues as the middle trunk, and C8-T1 form the lower trunk; each trunk splits into anterior and posterior divisions behind the clavicle; the posterior divisions of all three trunks become the posterior cord, the anterior divisions of the upper and middle trunks the lateral cord, and the anterior division of the lower trunk the medial cord.[7]

A handful of branch points carry localising value for the level of injury. The dorsal scapular nerve (to the rhomboids) and the long thoracic nerve (to serratus anterior, C5-C7) arise very proximally, so their loss, manifest as rhomboid weakness or scapular winging, points to a lesion at the root level. The suprascapular nerve leaves the upper trunk. The phrenic nerve (C3-C5, “3-4-5 keeps the diaphragm alive”) runs on anterior scalene and is a key surgical landmark traceable up to C5; an elevated hemidiaphragm therefore signals a high C5 (often preganglionic) injury.[8]

Figure 2. Schematic of the brachial plexus: roots (C5-T1), trunks, divisions, cords and the named terminal branches. Credit: Captain-n00dle / MissMJ, public domain, via Wikimedia Commons.

Epidemiology and risk factors

Reported incidence ranges from roughly 0.4 to 2.5 per 1000 live births. The spread reflects differences in obstetric care, average birthweight, and, not least, the thoroughness of the newborn neurological examination.[9] In the United States the incidence has been falling, from about 1.6/1000 in 2000 to 0.9/1000 by 2012, a trend echoed by DeFrancesco’s series (1.7 → 0.9/1000 over sixteen years) and one that contradicts the older assumption that rising fetal size was driving the rate up.[10]

The risk factors are those of birth trauma generally (macrosomia, maternal diabetes, multiparity, prolonged labour, shoulder dystocia, breech presentation, and assisted delivery), but two associations deserve emphasis. First, the lesion is not purely a failure of obstetric technique: shoulder dystocia is frequently unanticipated, intrauterine and even caesarean cases are recorded, and Gilbert estimated that between 58 and 1026 caesareans would be needed to prevent a single permanent injury even with perfect birthweight prediction.[11] Second, the side and presentation predict the pattern: in vertex deliveries the right side is affected about twice as often as the left (the left-occiput-anterior position places the right shoulder behind the symphysis), whereas breech delivery characteristically produces upper-root avulsions, which may be bilateral.[12]

Mechanism and pathoanatomy

The injury is a traction (stretch) lesion. Downward traction on the arm with lateral flexion of the neck maximally stretches the upper trunk (the commonest site), while traction on an abducted arm loads the lower roots; cadaveric work by Engelhard as early as 1906 displaced the old “compression at Erb’s point” theory in favour of overstretch.[13] Metaizeau’s measurements suggested a force of 20-40 kg is needed to produce a lesion.[14]

The single most important distinction is preganglionic versus postganglionic injury, because it dictates whether spontaneous or surgical recovery is even possible:

A preganglionic lesion is a root avulsion from the spinal cord. Because the motor cell body sits in the cord and the dorsal root ganglion lies distal to the avulsion, the root cannot recover spontaneously and cannot be directly repaired; reconstruction is possible only by transferring axons from another nerve (neurotization).[15]
A postganglionic lesion is an extraforaminal rupture or a neuroma-in-continuity (neurotmesis). These are surgically reconstructable by interposition nerve grafts and, in their milder degrees, may recover on their own.[16]

A single traction event can produce different severities along the same plexus, from avulsion through extraforaminal rupture to a recoverable neurapraxia.[17] The classic gradings apply: Seddon’s neurapraxia/axonotmesis/neurotmesis map onto Sunderland types I-V. Type I (neurapraxia) is certain to recover, types II-IV (axonotmesis, recovering by axonal down-growth over up to two years) are intermediate, and type V (neurotmesis) carries a poor prognosis.[18]

Several findings flag an avulsion and therefore a poor prognosis: an elevated hemidiaphragm (phrenic, C5); rhomboid weakness (dorsal scapular); scapular winging (long thoracic); a pseudomeningocele on imaging (dural/arachnoid avulsion); and, above all, Horner syndrome, the tetrad of ptosis, miosis, enophthalmos and anhidrosis that betrays avulsion of the lower roots (T1, disrupting the sympathetic communication to the stellate ganglion).[19] Horner’s is so ominous that in Clarke’s series none of 48 total-palsy infants with a Horner sign recovered satisfactorily without surgery, and an unequivocal Horner sign is regarded as an absolute indication to operate.[20]

Figure 3. Brachial plexus MRI (with an explanatory diagram, panel a) demonstrating a right-sided traumatic pseudomeningocele at the C8-T1 level (arrows), the radiological marker of root avulsion. Credit: From Chaturvedi et al., Insights into Imaging 9 (2018), illustration by Gwendolyn Mack, via Wikimedia Commons, CC BY 4.0.

Classification

By root level (clinical type)

Erb-Duchenne palsy (C5-C6, upper trunk) is the commonest pattern and produces the classic “waiter’s tip” posture: the shoulder adducted and internally rotated, the elbow extended, the forearm pronated, and the wrist and fingers flexed, because abduction, external rotation, elbow flexion and forearm supination are lost while hand function is preserved. It carries the best prognosis.[21]
Extended Erb palsy (C5-C7) adds loss of wrist and finger extension (completing the “waiter’s tip” of the hand) and does worse than the pure upper-trunk lesion.[22]
Klumpke (Déjerine-Klumpke) palsy (C8-T1) affects the hand and is famously almost non-existent as an isolated obstetric lesion. Gilbert examined a thousand babies without seeing a single isolated distal-root palsy, and what is loosely called “Klumpke’s” is usually a total palsy.[23]
Total (global) palsy (C5-T1) is the least common but the most severe: a flail, atonic limb with sensory loss (the medial upper arm spared by the intercostobrachial nerve) and, by six months, an intrinsic-minus claw hand.[24]

Figure 4. Erb-Duchenne palsy of the right arm in the “waiter’s tip” posture: shoulder adducted and internally rotated, forearm pronated. Credit: Rdabhi, via Wikimedia Commons, CC BY-SA 4.0.

Figure 5. The intrinsic-minus “claw hand” posture (MCP hyperextension, IP flexion) seen with lower-plexus (C8-T1) involvement, here demonstrated by a healthy hand imitating the deformity. Credit: Mcstrother, via Wikimedia Commons, CC BY 3.0.

The Narakas classification - two schemes that must not be conflated

The name Narakas attaches to more than one scheme, and the examination favourite is the four-group clinical classification (as presented by Narakas and Slooff, and in Campbell’s):[25]

Group I: C5-C6 (classic Erb); ~46% of cases; best prognosis, with spontaneous recovery in as many as 90%.
Group II: C5-C7; ~30%; worse than group I.
Group III: total palsy, flail extremity, without Horner syndrome; ~20%.
Group IV: total/global palsy, flail extremity, with Horner syndrome (± phrenic palsy); the most severe, with little chance of meaningful spontaneous recovery.

Gilbert’s monograph instead presents a five-type scheme (Narakas 1986) based on the clinical course over the first eight weeks, and there is in addition a three-group recovery-timing formulation (Narakas 1985). These are distinct and should be cited specifically. The four-group “flail ± Horner” version is the one most often quoted clinically.[26]

Clinical assessment

The diagnosis is made clinically. The newborn lies with the affected arm motionless; the examiner observes spontaneous movement, the asymmetric Moro reflex, and the response to tactile stimulation, and it is serial examinations every one to three months through the first year that determine prognosis and the indication for surgery.[27] The first job is to exclude pseudoparalysis from a clavicle or humeral fracture (which declares itself with crepitus and a palpable callus by ten days to three weeks), and less commonly from infection or a congenital anomaly. As the aphorism has it, “the newborn whose arm remains immobile has either a brachial plexus palsy or a fracture,” and an X-ray with examination settles it “before the sun sets.”[28]

Several validated tools structure the follow-up:

The Active Movement Scale (Toronto / Hospital for Sick Children) grades 15 upper-limb movements on an 8-point (0-7) scale, with grades 0-4 assessed with gravity eliminated and 5-7 against gravity; full gravity-eliminated motion (grade 4) must be reached before antigravity grades are scored.[29]
The Toronto Test Score sums weighted grades for elbow flexion, elbow extension, and wrist, finger and thumb extension; a total ≤ 3.5 at three months indicates microsurgical exploration, while a higher score favours continued observation.[30]
The modified Mallet classification grades shoulder function from I (no function) to V (normal) across global abduction, external rotation, hand-to-neck, hand-to-spine and hand-to-mouth, the last accompanied by the “trumpet sign” (compensatory shoulder abduction to bring the hand to the mouth); Abzug added a sixth, internal-rotation, category.[31]
The “cookie test” (Clarke) is performed at nine months: with the arm held in adduction against the trunk, the child is offered a cookie; bringing it to the mouth with less than 45° of neck flexion passes, whereas failure, or marked neck flexion, corresponds to less than antigravity (AMS grade 6) elbow flexion and prompts consideration of surgery.[32]

The single most quoted prognostic milestone is recovery of the biceps: in Gilbert and Tassin’s data, if biceps contraction has not begun by three months the functional outcome is poor and exploration is warranted. The biceps is chosen because the deltoid’s recovery is mimicked by other muscles.[33] The caveat, stressed by every modern source, is that biceps recovery alone over-selects for surgery: roughly half of infants with no elbow flexion at three months still achieve good function, and 12-55% of those lacking biceps at three months do as well as nerve-grafted children. For this reason centres now wait to five or six months for an isolated upper-trunk lesion while operating earlier on a total palsy with Horner’s.[34]

Associated injuries to look for include clavicle and humeral fractures, an ipsilateral torticollis (the child turns away from the painful side, sometimes with a sternocleidomastoid pseudotumour), phrenic palsy (commoner after breech), and a posterior shoulder subluxation or radial-head dislocation appearing later as muscle imbalance takes hold.[35]

Imaging and electrodiagnostics

Plain radiographs exclude a clavicle or humeral fracture. For distinguishing avulsion from extraforaminal rupture, CT myelography and MRI are the workhorses, the radiological marker of avulsion being a pseudomeningocele; Kawai’s accuracy data give myelography ~84% true-positive, rising to ~94% with CT myelography, with frank meningoceles essentially always diagnostic but small diverticula only ~60% reliable.[36] The crucial proviso is that final determination of avulsion is made at surgery: imaging refines planning but is not definitive.[37]

Electrodiagnostics (EMG, nerve conduction) are notoriously misleading in infants: they tend to underestimate severity and give false optimism, because the plastic infant nervous system can show near-normal findings despite severe lesions, and substantial discrepancies exist between EMG, intraoperative evoked potentials and surgical reality.[38] About 20-25% of infants ultimately require microsurgery.[39]

Natural history and prognosis

The honest summary is that the true natural history can never be fully known, since it would require withholding beneficial treatment. Older teaching held that ~95% recover spontaneously; modern, more critical series put the residual deficit at 20-30%, and as high as 40% in some.[40] Reported “complete recovery” rates vary enormously, from 13% (Wickstrom) through 70-95% (Sharrard’s review) to ~73% (Hoeksma) and “92% did not need surgery” (Clarke). That spread reflects how recovery is defined and the referral bias by which orthopaedic surgeons see the worst cases.[41] The level-dependent gradient is consistent: upper (Erb) palsies do best and total palsies worst, partly because of the long distance axons must travel to reach the intrinsic hand muscles, and lower-plexus or Horner-positive injuries do badly.[42] Recovery generally plateaus by about six months, but motor improvement can continue to two-and-a-half years and sensory recovery beyond three.[43] Untreated, muscle imbalance produces a rapid fixed internal-rotation/adduction contracture of the shoulder, later posterior dislocation, forearm and elbow deformity, and some shortening and wasting of the limb.[44]

Conservative management

Reinnervation is sequential and asymmetric, the adductors and internal rotators recovering before the abductors and external rotators, so the central aim of conservative care is to prevent contracture while awaiting nerve recovery, above all preserving full passive external rotation of the shoulder with the arm adducted.[45] A gentle range-of-motion programme, taught to the parents (who, performing it after every feed, are “the best physiotherapists”), is begun early; Sharrard’s classical advice was to rest the limb for the first week to let haemorrhage and oedema settle before starting passive movement, and to avoid full abduction lest a previously subluxed shoulder redislocate.[46] Old rigid abduction-splinting is condemned because it produces its own fixed deformity; selective splinting (a night cock-up splint for the wrist, serial casting for an early elbow-flexion contracture) is used judiciously.[47] Botulinum toxin, investigational at the time of Gilbert’s monograph, has become an established adjunct for the muscle imbalance and co-contraction that follow misdirected reinnervation.[48] There is, notably, no role for neurolysis alone, whose results do not exceed natural history.[49]

Surgical management - primary microsurgery

Indications and timing

The classic indication, after Tassin and Gilbert, is failure of biceps recovery by three months; an unequivocal Horner sign, or a total palsy with Horner’s, justifies earlier exploration (around 2-3 months), while an isolated upper-trunk lesion is generally given to five or six months.[50] Waters’ explicit criteria are an avulsion injury, a Toronto score below 3.5 by six months, failure of antigravity biceps recovery by six months, or a failed cookie test at nine months.[51] Campbell’s allows a somewhat wider window: exploration if there is no deltoid or biceps recovery by three to six months, with most authors operating if antigravity elbow flexion is absent by three to nine months.[52] In complete palsies the goal shifts from the biceps to the hand, and one may even operate while the biceps is recovering, sometimes sacrificing already-recovered proximal function to gain a useful hand.[53]

Operative technique

Surgery is usually done between three and eight months, through a transverse supraclavicular incision, with a partial or complete clavicular osteotomy when the retroclavicular trunks or the C8-T1 roots need exposure.[54] The spinal accessory nerve is identified and tagged for possible neurotization. Two decisions dominate the operation. First, neuroma resection with grafting is preferred over neurolysis alone, whose results are discouraging. Second, the proximal root stump must be judged a suitable source of axons; Gilbert used routine frozen-section histology, in which the presence of ganglion cells signifies avulsion and the root, however normal it looks distally, must not be used.[55] The sural nerve is the workhorse graft (about 10-12 cm available per leg in a 6-8 kg infant), its cables secured with fibrin glue and a single 9-0/10-0 microsuture.[56]

Where a proximal stump is unavailable (avulsion), axons are imported by neurotization (nerve transfer): extraplexual donors include the spinal accessory nerve to the suprascapular nerve (the commonest, restoring shoulder external rotation), intercostal nerves to the musculocutaneous nerve, the medial pectoral nerve, the phrenic and hypoglossal nerves, and the contralateral C7; intraplexual transfers and the Oberlin transfer (a redundant ulnar-nerve fascicle to the biceps motor branch) are used to restore elbow flexion.[57]

Figure 6. Intra-operative Oberlin nerve transfer: a fascicle of the ulnar nerve (on the forceps) is coapted to the motor branch (MB) of the biceps muscle (BM) to restore elbow flexion. Credit: From Shigematsu et al. (2006), J Brachial Plex Peripher Nerve Inj, PMC1636634, Fig. 2, CC BY 2.0.

Results of primary repair

Gilbert’s long-term data, followed to skeletal maturity because growth degrades the result, show that for C5-C6 lesions Grade IV-V shoulders rose from 52% at two years to 80% at four years (with secondary shoulder surgery in about a third); for C5-C6-C7 lesions, 61% reached Grade IV-V at four years; and even complete lesions achieved 77% Grade III-V shoulders and 81% good elbow flexion at eight years, with 76% useful hands after secondary wrist-extension transfers. These figures justify repair of the lower roots “at any cost.”[58] Breech palsy behaves as its own entity: birthweight is low, upper-root avulsions and bilateral meningoceles are “almost the rule,” roots are often found in situ (partial avulsions that recover spontaneously in about half), and contractures rarely develop. The strategy is therefore often to leave the roots, add transfers for shoulder and elbow, and reassess at six months.[59]

Secondary (palliative) reconstruction

The residual deformities of OBPP are predictable consequences of imbalance, and a large reconstructive armamentarium addresses them. The classical timing framework treats contractures at 8-24 months, a dislocating shoulder as soon as it is diagnosed, tendon transfers after 24 months, and bony procedures after about five years.[60]

The shoulder

The dominant problem is an internal-rotation/adduction contracture that progresses to posterior subluxation and then dislocation, with secondary flattening and retroversion of the glenoid (the biconcave “pseudoglenoid”) and of the humeral head, changes that can appear by age two.[61] MRI is the gold standard for assessing the glenohumeral deformity, with Waters’ glenoscapular (version) angle and the percentage of humeral head behind the scapular line used to grade it; affected glenoids in Waters’ series averaged −25.7° of retroversion versus −5.5° normal, and ~62% were posteriorly subluxed.[62] (Whether the bony deformity is a primary growth-plate injury or a secondary consequence of untreated contracture was long debated, Putti and Zancolli versus Gilbert and Birch, with Birch’s striking observation that twelve shoulders dislocated merely while awaiting admission supporting the “consequence of contracture” view.[63])

The reconstructive ladder runs:

Early release of the internal-rotation contracture on a still-congruent shoulder: a subscapularis release (Carlioz) or anterior release (Fairbank/Sever), after which active external rotation recovers spontaneously in 30-40%.[64]
Latissimus dorsi (± teres major) transfer to the rotator cuff, the Sever-L’Episcopo procedure with Hoffer’s modification, indicated for a shoulder with good abduction but weak external rotation and a strong latissimus; it improves abduction and active external rotation, though arthroscopic versions tend to cost some internal rotation.[65]
For the flail (Grade-0) shoulder, levator scapulae and trapezius transfers (the Saha principle) can convert a useless arm into a useful prop, though rarely beyond Gilbert grade III.[66]
For severe fixed bony deformity, an external-rotation (derotation) osteotomy of the humerus or, in older children with severe dysplasia, a glenoid anteversion osteotomy (Dodwell). Birch dissents sharply here, holding that shaft derotation “has no place” because it merely adds to the head-on-shaft retroversion, and favours open reduction into the true glenoid.[67]

The elbow and forearm

The commonest elbow problem is weak flexion progressing to a flexion contracture (clinically significant beyond ~30°), often resistant to splinting; options include axonal “supercharging” early (Oberlin and related transfers) and, later, flexorplasty: Steindler (flexor-pronator origin advancement, which requires intact wrist musculature), bipolar latissimus (Zancolli-Mitre), pectoralis major, or triceps transfer.[68] In the forearm, supination deformity is the most disabling, arising from an unopposed biceps with weak pronators; Zancolli’s staged algorithm corrects it by rerouting the biceps tendon to act as a pronator, combined with interosseous-membrane release and, in fixed or incongruent cases, distal radio-ulnar fusion, positioning the forearm in 20-30° of pronation.[69]

Co-contraction

Misdirected reinnervation makes antagonists fire together, most visibly the deltoid with the teres major (the trumpet sign) and the biceps with the triceps. Mild co-contraction needs no treatment; the moderate is managed with physiotherapy and biofeedback; the severe with botulinum toxin and, if necessary, tendon surgery. Hierner’s series of six young children with biceps-triceps co-contraction treated with botulinum toxin reached M4 elbow flexion and a positive cookie test by 24 months, with no recurrence and the early skeletal deformity resolving with growth.[70]

Part III - Neonatal (Birth) Fractures

Birth fractures are the second great cause of the non-moving newborn limb. They share a benign theme: the neonatal skeleton has thick, biologically active periosteum and a large capacity for remodelling, so the great majority heal rapidly and completely with minimal or no intervention. The diagnostic challenge is less the treatment than the recognition, and the differentiation from brachial plexus palsy, infection, non-accidental injury and rarer metabolic causes.

Clavicle - the most common birth fracture

The clavicle is the bone most often broken at birth, with an incidence of about 2-3 per 1000 live births; it arises from direct pressure or lateral compression of the shoulder girdle during a difficult delivery, and high birthweight, mid-forceps delivery and shoulder dystocia predispose to it.[71] A complete fracture displaces the distal fragment downward, forward and medially, and the displaced bone can press on the subclavian vessels; about one in nineteen birth clavicle fractures is associated with a brachial plexus injury.[72] Attention is usually drawn by limited spontaneous arm movement (a pseudoparalysis arising from the fracture itself, or signalling a coexisting plexus palsy), and the injury may escape notice for two or three weeks until the bump of healing callus appears in the mid-shaft.[73]

Treatment is essentially reassurance: a gauze pad in the axilla and a simple sling beneath the clothes for two weeks suffices, and even untreated the fracture unites and any malposition corrects with growth; only a fragment displaced enough to threaten the subclavian vessels is manipulated and held in a figure-of-eight bandage.[74] The important pitfall is congenital pseudarthrosis of the clavicle, distinguished by the absence of pain and callus, by its radiographic features, and by its characteristic right-sided location.[75]

Figure 7. Neonatal chest radiographs of bilateral diaphyseal clavicle fractures from shoulder dystocia: day 1 (displaced) and day 21 (consolidating with abundant callus). Credit: From Oliveira et al., Clinical Medical Reviews and Case Reports 3:119, via Wikimedia Commons, CC BY 4.0.

Humerus

Two distinct humeral birth injuries occur.

Separation of the upper humeral epiphysis results from vigorous manipulation or traction on the arm and is, in effect, a Salter-Harris type-I physeal separation (occasionally a type-IV fracture-separation). Its diagnosis is treacherous because the humeral head is still cartilaginous and does not ossify until three to six months of age, so plain films at birth may look normal or be misread as a dislocation; the clue is extensive swelling and an apparent increase in the head-to-scapula distance, the confirmation a repeat film after a week (showing callus) or, best of all, ultrasonography, which directly demonstrates the step-off between the unossified epiphysis and the metaphysis.[76] Treatment is a collar-and-cuff sling for two to three weeks; abduction splintage is unwise.[77]

Fracture of the humeral shaft occurs typically in breech deliveries during attempts to free an extended arm, producing a transverse or spiral fracture; the limb dangles and is not moved, mimicking a plexus palsy, and a radial nerve palsy is often associated but usually recovers spontaneously.[78] A key teaching point for distinguishing a birth fracture from non-accidental injury is that the neonatal fracture shows callus by the tenth day.[79] Treatment is to strap the arm to the chest in neutral rotation; angulation corrects with growth (rotational deformity does not), and union is firm by three weeks.[80]

Femur

The femur is the long bone most often fractured at birth after the clavicle, again chiefly in breech deliveries, and an underlying osteogenesis imperfecta should be considered when a birth fracture seems disproportionate to the force. The diaphyseal fracture heals with exuberant callus and remodels readily; treatment in the neonate is simple splinting, a Pavlik harness, or gentle traction/spica, never operative.[81]

The pseudoparalysis differential - the essential synthesis

A newborn who will not move an arm must be worked through this differential:[82]

Clavicle (or humeral) fracture: crepitus, palpable mid-shaft callus, pain and swelling.
Obstetric brachial plexus palsy: the characteristic posture (waiter’s tip), asymmetric Moro, sensory changes; no bony crepitus.
Proximal humeral physeal separation: radiographically occult (unossified epiphysis); diagnosed by ultrasound, MRI or aspiration.
Neonatal septic arthritis of the shoulder / acute osteomyelitis: warmth, swelling, systemic upset, and the discriminating step of joint aspiration; malaise, pyrexia and a raised white-cell count with normal early films favour infection.[83]
Parrot pseudoparalysis of congenital syphilis: a painful pseudoparalysis from syphilitic osteochondritis/metaphysitis, classically bilateral and symmetrical with metaphyseal demineralisation and erosions (the Wimberger sign) in the first weeks of life; rare but a classic examination answer.[84]
Osteogenesis imperfecta: multiple fractures from trivial force, blue sclerae, family history.
Non-accidental injury: explicitly part of the differential; inconsistent history, fractures of differing ages.[85]

Other birth injuries

Beyond fractures and the plexus, three soft-tissue/cranial entities round out the picture, each generally benign:

Cephalhaematoma: a subperiosteal collection of blood over a cranial bone that, being subperiosteal, does not cross suture lines (distinguishing it from a caput succedaneum or a subgaleal haemorrhage); it resolves over weeks, occasionally calcifying at its rim.
Facial nerve palsy: usually a compression neurapraxia from the maternal sacral promontory or forceps; most resolve spontaneously.
Subcutaneous fat necrosis of the newborn: firm subcutaneous nodules after a traumatic or hypoxic delivery, generally self-limiting but warranting monitoring for hypercalcaemia.
Sternocleidomastoid haematoma: the link to torticollis, considered in Part IV.

(These soft-tissue entities are standard birth-trauma teaching and are summarised from general knowledge, as the supplied orthopaedic source extracts did not cover them in detail.)

Part IV - Torticollis (Wry Neck)

Torticollis (Lat. tortus + collum; Bulg. тортиколис / изкривен врат, the classical caput obstipum) is a combined head-tilt and rotational deformity of the neck. With a contracted sternocleidomastoid (SCM) the head tilts toward the affected side and the chin rotates toward the opposite shoulder, because the muscle, running from the sternum and clavicle to the mastoid process, both flexes the head toward its own side and turns the face away.[86] A purely rotatory deformity localises to C1-C2 (where about half of cervical rotation occurs), whereas a head tilt alone suggests a more generalised cervical problem.[87]

Figure 8. Anterior muscles of the neck with the sternocleidomastoid labelled. Credit: Henry Gray / H. V. Carter, Anatomy of the Human Body (1918), Plate 386, public domain, via Wikimedia Commons.

Figure 9. Infant with left congenital muscular torticollis, showing the characteristic “C-shape” posture of head tilt with contralateral chin rotation. Credit: From Płomiński et al. (2023), Healthcare (MDPI), PMC10778664, Fig. 1, CC BY 4.0.

Congenital muscular torticollis (CMT)

CMT is the commonest cause of torticollis in infancy and the commonest neck problem of childhood, presenting at a median age of about two months.[88] A soft-tissue abnormality of the SCM is detectable on ultrasound in roughly 4% of newborns, and the deformity is right-sided in about three of four cases.[89] A disproportionate number follow a primiparous, breech or difficult delivery, though CMT also occurs after normal birth and caesarean, a fact that argues for intrauterine crowding as much as birth trauma.[90]

Pathology

Several overlapping theories are advanced: intrauterine packing/positioning; an intrauterine or perinatal compartment syndrome of the SCM (the Davids-Wenger-Mubarak hypothesis, supported by MRI signal resembling limb compartment syndrome and by surgical histology suggesting venous occlusion, oedema and fibrosis); a neurogenic theory of accessory-nerve entrapment by the fibrosing muscle; and a mesenchymal/embryogenic theory.[91] What matters clinically is the ratio of fibrosis to functional muscle: where muscle predominates the SCM stretches with growth and no torticollis results, whereas dense fibrosis leaves little elastic potential.[92]

The sternocleidomastoid “tumour” (fibromatosis colli, the “olive”) is a non-tender fusiform mass within the muscle belly, usually near the clavicular attachment, which appears in the first two to four weeks, reaches maximal size by one to two months, then typically regresses and disappears within the first year; if it fails to resolve, permanent fibrotic contracture follows.[93] Cheng’s large series divided CMT into three subgroups, SCM tumour (43%), muscular torticollis (31%), and postural torticollis (22%), in descending order of severity and need for surgery.[94] Plain cervical films are normal apart from the tilt and rotation; the fibrotic nodule usually confirms the diagnosis, and ultrasound both differentiates CMT from other neck pathology and predicts the need for surgery.[95]

Figure 10. Ultrasound of fibromatosis colli: fusiform hypertrophy of the right sternocleidomastoid (arrow) compared with the normal left muscle. Credit: From Aljahdali et al. (2023), Cureus, PMC10657154, Fig. 1, CC BY 4.0.

Associations - and why you must screen the hips

The cardinal association is developmental dysplasia of the hip: every source mandates a hip examination, with quoted rates from about 8% up to 20% (Campbell’s gives “7-20%”). Even a normal hip examination should be backed by ultrasound in the neonate or a single AP pelvis radiograph after about ten weeks of age.[96] Other associations include metatarsus adductus, talipes equinovarus, and, developing secondarily, plagiocephaly and facial/cranial asymmetry: the face flattens on the side of the contracted muscle and, left for years, the eyes and ears come to lie at unequal levels, producing a permanent cosmetic deformity.[97]

Figure 11. Line diagram of cranial-shape deformities, including plagiocephaly, the asymmetric head shape that accompanies and complicates congenital muscular torticollis. Credit: E. Mendel / W. C. Krauss, “Types of Cranial Deformity,” public domain, via Wikimedia Commons.

Non-operative treatment

Conservative care is the first-line treatment throughout infancy and resolves the great majority of cases. A stretching programme positions the ear away from the contracted muscle and the chin toward it, reinforced by modifying the crib and toys so the infant stretches the neck while reaching; reported success rates are high, around 90-95% with stretching alone.[98] Outcome is strongly age-dependent: Petronic’s data show ~99% excellent results when treatment starts before one month, falling to ~19% when it starts after six months, and the SCM-tumour subgroup needs surgery in about 8% versus essentially none of the postural group.[99] Ultrasound also prognosticates: fibrosis confined to the lower third of the muscle responds to stretching in all cases, whereas whole-muscle involvement leads to surgery in about 35%.[100] Two thresholds predict failure of conservative care: more than 30° loss of rotation, or established facial asymmetry.[101] Botulinum toxin is a useful adjunct (improving in 60-90% in small series), and the key natural-history fact is that CMT does not resolve spontaneously once it persists beyond age one.[102]

Surgical treatment

Surgery is indicated when stretching fails (generally persistence beyond one year of age, or more than 30° loss of rotation or established facial flattening), and is best performed between about one and four years: early enough to leave growth for facial remodelling, late enough for the tissues to be large enough to dissect. Facial asymmetry can still improve when surgery is done before age five, and worthwhile gains are reported even in older children and adolescents.[103] The procedures are:

Unipolar release: a distal tenotomy at the sternoclavicular (or mastoid) pole, suitable for mild deformity, though open unipolar tenotomy risks scar tethering and is best postponed beyond age four.[104]
Bipolar release: division at both the mastoid and the clavicular/sternal ends, the most effective procedure for moderate-to-severe and recurrent cases. The Ferkel modification adds a Z-plasty of the sternal head to preserve the normal V-shaped neckline; the clavicular head is divided first (failure to do so gives a poor result), the muscle is freed from the investing fascia to prevent recurrence, the platysma is preserved as a separate layer, and the skin incision is kept off the clavicle itself to avoid a spreading scar.[105]

Figure 12. Intra-operative bipolar sternocleidomastoid release for neglected torticollis (panels i-k): the clavicular branch, sternal branch and upper end of the SCM are identified and divided. Credit: From Funao et al. (2023), J Clin Med (MDPI), PMC10780082, Fig. 3, CC BY 4.0.

The structures at risk are the spinal accessory nerve, the facial nerve (anteriorly, near the parotid), the external and anterior jugular veins, and the carotid sheath; postoperative care combines early physiotherapy with a collar or head-halter for the first 6-12 weeks.[106] Untreated, CMT worsens with growth into a fixed facial asymmetry that persists into adult life.[107]

The differential diagnosis of the twisted neck

This is the single most important safety lesson of the topic. A non-muscular cause is found in about 18-20% of children with torticollis, most often Klippel-Feil syndrome or a neurological disorder, and missing one (a posterior-fossa tumour, atlantoaxial instability) can be catastrophic.[108] Two bedside discriminators help: in true muscular torticollis the SCM “sticks out” and is palpably tight, and the absence of facial asymmetry argues against long-standing CMT (favouring an inflammatory or rotatory cause).[109]

Osseous and congenital causes

Klippel-Feil syndrome, congenital fusion of cervical vertebrae, presents with the classic but inconstant triad of a short neck, limited cervical motion and a low posterior hairline (all three present in fewer than half). Its associations are clinically vital: scoliosis (~60% have a curve >15°), Sprengel deformity (~42%), renal anomalies (~32%), deafness (~30%) and congenital heart disease (~14%), so a discovered fusion mandates flexion-extension films, renal imaging, a standing spine film and a cardiac examination.[110] Other osseous causes include congenital hemivertebra, basilar impression (suspect Langerhans cell histiocytosis when invagination is found), occipitocervical anomalies, and os odontoideum, an ossicle separate from the body of the axis, now regarded as an old traumatic non-union rather than congenital, which causes instability and is treated by C1-C2 fusion (to be distinguished from the harmless os terminale).[111]

Atlantoaxial rotatory subluxation / fixation

When the three joints linking C1 to C2 are rotated beyond their limit they can lock, producing the “cock-robin” posture (head tilted and rotated, “like a robin looking at a worm”). It may arise spontaneously, after minor trauma, or, as Grisel syndrome, following pharyngitis, otitis media or head-and-neck (e.g. adenotonsillar) surgery; Marfan patients are susceptible.[112] The Fielding & Hawkins classification has four types: type I, rotatory fixation without anterior displacement (intact transverse ligament); type II, 3-5 mm anterior displacement (one lateral mass as pivot); type III, >5 mm anterior displacement; type IV, posterior displacement. Diagnosis is by dynamic CT (plain films being hard to interpret through the twist), and treatment is graduated by duration: early cases reduce with a soft collar or head-halter traction, more established ones need 2-3 months in a Minerva cast, and resistant or recurrent cases come to manipulation, halo traction, or operative reduction with C1-C2 fusion.[113]

Neurogenic causes - the red flags

Although rare, neurogenic causes must be considered in any atypical, progressive or therapy-unresponsive torticollis. The list is led by posterior-fossa, brainstem and spinal-cord tumours (head tilt is a classic presenting sign of a posterior-fossa tumour), with syringomyelia, Arnold-Chiari malformation and, occasionally, leukaemia also implicated. The warning features are spasticity, clonus, bowel or bladder disturbance, and a child who protectively supports the chin with the hands; high cervical cord compression can, in the extreme, cause sudden death. A careful neurological examination is mandatory before any “muscular” torticollis is treated, and an MRI is indicated whenever the picture is atypical.[114]

Other causes

Ocular torticollis: a squint (classically a superior-oblique, CN IV, palsy) makes the child tilt the head to level the horizon; suspect it when films are negative and the SCM is not contracted, and refer to ophthalmology.[115]
Sandifer syndrome: paroxysmal dystonic head/neck posturing associated with gastro-oesophageal reflux in infants (a standard differential, summarised from general paediatric knowledge as it was not in the source extracts).
Benign paroxysmal torticollis of infancy: recurrent, self-limited episodes of head tilt, on the migraine spectrum.[116]
Inflammatory / infectious: acute torticollis after an upper respiratory infection or cervical lymphadenitis (resolving within 24-48 h with a soft collar and rest), retropharyngeal abscess, juvenile idiopathic arthritis, intervertebral disc calcification, and, where endemic, tuberculous cervical osteomyelitis; osteoid osteoma is the commonest neoplasm to cause childhood torticollis.[117]
Drug-induced (acute dystonic reaction to neuroleptics/antiemetics) and idiopathic spasmodic (adult cervical dystonia) torticollis, completing the list, again from general knowledge as these were not page-cited in the source extracts.

When imaging is mandatory

Before embarking on a vigorous stretching programme, obtain cervical radiographs to exclude a congenital anomaly such as Klippel-Feil. Add ultrasound to confirm CMT and predict the need for surgery, dynamic CT for a suspected rotatory subluxation, and MRI for any atypical, progressive or neurologically abnormal case. The governing principle is simple: a full neurological examination, a hip screen, and a low threshold for advanced imaging protect against the 18-20% of childhood torticollis that is not muscular.[118]

References

Lovell & Winter’s Pediatric Orthopaedics, ch. 32, p. 5232. The non-moving newborn arm is best regarded as a syndrome with a defined differential, not a single diagnosis.
Green’s OHS p. 1793; Waters & Bae p. 193. Rising maternal BMI and gestational diabetes in the developed world increase both fetal size and the risk.
Wenger & Rang p. 518.
Green’s OHS p. 1793; Campbell’s p. 1631 quotes a fall from ~0.2% to ~0.02% with caesarean delivery.
Gilbert pp. 160-161, p. 248; Sharrard p. 643. Kennedy performed the first surgical repair in 1903 and was also the first to propose exploring a plexus that had not recovered by three months.
Green’s OHS p. 1792; Waters & Bae p. 191 give identical figures.
Green’s OHS pp. 1792-1793.
Waters & Bae p. 191; Green’s OHS p. 1794-1795 (Table 40.1).
Green’s OHS p. 1793 (0.38-1.56/1000); Sharrard p. 643 (0.4-2.5/1000); Waters & Bae p. 193; Wenger & Rang p. 518 quote “1 in 500”.
Green’s OHS p. 1793; Campbell’s p. 1631.
Gilbert p. 165, citing Sacks & Chen 2000; Green’s OHS p. 1793.
Gilbert pp. 163-165; Green’s OHS p. 1793. In Gilbert’s operated cohort, breech cases averaged ~3050 g versus ~4334 g for cephalic cases; the breech injury is a different mechanism, not simply a bigger baby.
Sharrard p. 643; Gilbert pp. 160-161.
Gilbert p. 248.
Green’s OHS pp. 1794-1795; Waters & Bae p. 193.
Green’s OHS p. 1794.
Green’s OHS p. 1794, Fig. 40.2.
Sharrard p. 645; Waters & Bae p. 193.
Green’s OHS pp. 1794-1795 (Table 40.1); Gilbert pp. 160, 169, 174.
Gilbert pp. 178-179, citing Al-Qattan 2000.
Green’s OHS p. 1794; Gilbert p. 168.
Green’s OHS pp. 1794-1795.
Gilbert pp. 161, 174, citing Al-Qattan’s pointed paper “Klumpke’s birth palsy: does it really exist?”.
Sharrard p. 644; Gilbert p. 169.
Green’s OHS p. 1794; Campbell’s p. 1631.
Gilbert pp. 174, 177; the disagreement is flagged in Green’s OHS p. 1794. Narakas also described an S0-S3 sensory grade.
Green’s OHS p. 1794; Waters & Bae p. 194; Gilbert pp. 171-172.
Wenger & Rang p. 518; Waters & Bae p. 193.
Green’s OHS p. 1797 (Table 40.2); Gilbert p. 170. Inter-rater reliability is high (weighted κ ≈ 0.89).
Green’s OHS p. 1797 (Table 40.3); Gilbert pp. 177-178; Campbell’s pp. 1633-1634. Michelow showed that combining these five movements cuts the prediction error from ~12.8% (elbow flexion alone) to ~5.2%.
Green’s OHS p. 1796 (Fig. 40.4); Gilbert p. 173; Campbell’s p. 1632.
Gilbert pp. 177-179; Green’s OHS pp. 1795, 1799.
Gilbert pp. 177, 183, 214-215; Green’s OHS p. 1795.
Green’s OHS pp. 1797-1799; Gilbert p. 177; Waters & Bae p. 195. Wenger & Rang frame the same milestone around the deltoid rather than the biceps (p. 519), a minor source disagreement.
Green’s OHS p. 1794; Gilbert pp. 164-165, 168-169, 184-185; Sharrard pp. 643-645.
Green’s OHS p. 1796. MRI matches CT myelography and needs only sedation rather than the general anaesthetic an infant myelogram requires.
Green’s OHS p. 1796; Waters & Bae p. 194.
Green’s OHS p. 1797; Gilbert pp. 214, 273. The surgical decision should rest on clinical examination, not EMG.
Green’s OHS p. 1797.
Green’s OHS p. 1797; Wenger & Rang p. 519.
Sharrard p. 645; Gilbert pp. 175, 182-183.
Sharrard p. 645; Green’s OHS p. 1794.
Gilbert pp. 182, 184.
Sharrard p. 645; Gilbert pp. 184-186.
Waters & Bae p. 196; Gilbert pp. 184-185.
Gilbert p. 185; Sharrard p. 647 (Adler & Patterson).
Gilbert p. 185.
Gilbert pp. 185-186; later evidence (Buchanan; Duijnisveld) cited via Campbell’s reference list, p. 1644.
Green’s OHS p. 1798; Waters & Bae p. 195.
Gilbert pp. 214-216; Green’s OHS p. 1799; Waters & Bae p. 195.
Waters & Bae p. 195.
Campbell’s pp. 1632, 1634.
Gilbert pp. 215-216.
Gilbert pp. 198-202.
Gilbert pp. 204-205.
Gilbert pp. 205-206.
Gilbert pp. 206-207; the order of reconstruction priority is hand, then elbow flexion, then shoulder.
Gilbert pp. 221-224.
Gilbert pp. 217, 226-232.
Gilbert p. 251 (Table 6).
Campbell’s p. 1632; Gilbert pp. 258-260.
Campbell’s pp. 1632, 1635; Gilbert p. 251.
Gilbert pp. 259-260.
Gilbert pp. 235-236, 250; Campbell’s p. 1636.
Campbell’s pp. 1638-1641; Gilbert pp. 239-245. Gilbert prefers transferring the latissimus alone, by a posterior approach, citing the different excursion of the two muscles.
Gilbert pp. 234-239, 245-246.
Campbell’s pp. 1635-1638; Gilbert pp. 252, 264-267. The derotation-osteotomy question is a genuine source-versus-source conflict.
Gilbert pp. 270-281; Campbell’s p. 1629.
Gilbert pp. 284-298; Campbell’s p. 1635.
Gilbert pp. 312-318; Campbell’s p. 1632.
Sharrard p. 679 (Truesdell 1917); Lovell ch. 32 p. 5232.
Sharrard p. 679, citing Oppenheim 1990.
Sharrard p. 679; Lovell p. 5232.
Sharrard p. 679; Lovell p. 5232: “parental reassurance and gentle handling are all that are required.”
Lovell pp. 5232-5233; Sharrard p. 679 (Fig. 20.30).
Sharrard pp. 682-683 (Broker & Burbach 1990); Lovell pp. 5232-5233, which also lists MRI and joint aspiration.
Sharrard p. 683; Lovell p. 5233.
Sharrard pp. 686-687.
Sharrard p. 687.
Sharrard p. 687.
General paediatric teaching; the supplied source extracts (Sharrard, Lovell) addressed femoral birth fracture only incidentally, so this entity is summarised from established knowledge rather than a single page citation.
Lovell p. 5232 supplies the core list (fracture, plexus palsy, proximal humeral physeal separation, septic arthritis, osteomyelitis, non-accidental injury); the syphilis and osteogenesis-imperfecta entities are standard additions from the wider paediatric literature.
Sharrard p. 675 makes exactly this point: bone or joint infection “may present in the same way and with similar physical signs at first.”
Summarised from established paediatric-orthopaedic teaching; not present in the supplied source extracts and therefore not page-cited.
Lovell p. 5232.
Lovell pp. 2640, 2651; Campbell’s pp. 1396-1397.
Lovell p. 2640.
Lovell pp. 2640, 2642; Staheli p. 970.
Lovell pp. 2640-2641; Campbell’s p. 1394 (3.92% of neonates).
Lovell pp. 2640-2641; Wenger & Rang pp. 508-509.
Lovell pp. 2640-2641; Campbell’s pp. 1395-1396.
Lovell pp. 2640-2641.
Campbell’s p. 1394; Lovell p. 2642. The mass is palpable but goes unrecognised up to 80% of the time.
Lovell pp. 2641-2642.
Lovell p. 2642; Campbell’s p. 1396.
Lovell pp. 2641-2642; Campbell’s p. 1394; Staheli p. 971; Wenger & Rang p. 508. The wide spread in the DDH figure is a genuine inter-source disagreement, but all agree: screen the hips.
Campbell’s pp. 1394, 1396; Lovell p. 2642; Wenger & Rang p. 509.
Lovell p. 2643; Campbell’s p. 1396.
Campbell’s pp. 1396-1397; Lovell p. 2643.
Lovell p. 2643; Campbell’s p. 1396.
Campbell’s p. 1396; Lovell p. 2643.
Lovell p. 2643; Campbell’s pp. 1396-1397; Canale’s 19-year follow-up.
Lovell pp. 2643-2644; Campbell’s pp. 1396-1397; Staheli p. 972; Wenger & Rang p. 508.
Lovell p. 2643; Campbell’s p. 1397.
Campbell’s pp. 1397-1399; Lovell pp. 2645-2652. Bipolar release with Z-plasty achieved ~92% satisfactory results versus ~15% for other procedures in one series.
Lovell pp. 2643-2652; Campbell’s pp. 1397-1399.
Lovell p. 2642; Wenger & Rang p. 509.
Lovell p. 2640 (Ballock & Song); Staheli p. 969.
Wenger & Rang p. 510.
Wenger & Rang pp. 515-516 (Hensinger).
Lovell pp. 2640, 2814; Wenger & Rang p. 513; Staheli p. 969.
Wenger & Rang p. 510; Staheli pp. 967-968; Lovell p. 2826.
Fielding & Hawkins (JBJS 1977), via Lovell p. 2826 and Wenger & Rang p. 524; treatment per Staheli pp. 968-969 and Wenger & Rang p. 510. Staheli notes the reliability of dynamic CT is debated, a minor source disagreement.
Lovell pp. 2644, 2819-2820; Staheli pp. 968-969; Wenger & Rang pp. 511-514. In Down syndrome, atlantoaxial instability affects ~12%; screen before athletics.
Wenger & Rang p. 510; Staheli p. 969; Lovell p. 2644.
Lovell pp. 2644, 2820.
Staheli pp. 966-967; Wenger & Rang p. 510; Lovell pp. 2806-2814.
Wenger & Rang p. 510; Lovell pp. 2642, 2644; Campbell’s p. 1396; Staheli pp. 968-969.
Lovell p. 5232; Sharrard p. 675.
Green’s OHS p. 1794.
Gilbert pp. 169, 178-179; Green’s OHS p. 1794.
Green’s OHS pp. 1794-1795.
Campbell’s p. 1631; Green’s OHS p. 1794.
Gilbert pp. 214-216; Green’s OHS pp. 1797-1799; Waters & Bae p. 195.
Gilbert pp. 198-298; Campbell’s pp. 1636-1641.
Sharrard p. 679; Lovell pp. 5232-5233.
Sharrard pp. 682-683; Lovell p. 5233.
Lovell pp. 2640-2644; Campbell’s pp. 1394-1399.
Lovell pp. 2640, 2644; Wenger & Rang pp. 510-516; Staheli pp. 966-969.
Staheli pp. 966-969; Wenger & Rang p. 510.

Birth (obstetric) trauma. Obstetric [brachial plexus] palsy. Torticollis.

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