1. Brachial Plexus Birth Palsy
Alireza Pahlevansabagh M.D.
T.U.M.S.

2. Etiology
Risk factors
Anatomy
Clinical Features
Classification
Prognosis and Natural History
Differential Diagnosis

3. Etiology
The mechanism of injury is stretch across the plexus. The causes of this stretch include the forces of labor, Especially in cases of shoulder dystocia. mechanical cause is the predominant theory
Fetal distress may contribute to muscle hypotonia and provide less protection of the plexus from stretch or compression injury during delivery

4. Whereas a mechanical basis for BPBP is well accepted, delivery by cesarean does not exclude the possibility of birth palsy.
Absence of shoulder dystocia. Posterior brachial plexus
injury can occur if there is impaction of the posterior
shoulder on the sacral promontoryAbnormal intrauterine pressures arising from uterine
anomalies, such as an anterior lower uterine segment
leiomyoma or an intrauterine septum, may be etiologic.
34 Dunn and Engle describe an infant with brachial
plexus and phrenic nerve palsy associated with a bicornuate
uterusRecent reports in the obstetric literature, however, have
suggested that in utero forces may underlie a significant portion of these injuries. Brachial plexus palsies
may therefore precede the delivery itself and may occur independent of the actions of the accoucheur.

5. Most stretch injuries of the brachial plexus involve a mixture of types of nerve lesions and may involve multiple sites of injury
incidence of these severe avulsion or axonal disruption injuries has been cited as being between 8% and 25 % of all brachial plexus birth palsies.

6. EPIDEMIOLOGY
Brachial plexus birth palsy has an incidence of 0.4 to 4 per 1000 live births.
Most common on the right side
because the most common delivery presentation is left occiput anterior vertex.
of less than 7 at 1 and 5 mins
The incidence of brachial plexus birth palsy (BPBP) is estimated to be between 0.4 and 4 per 1000 live births.
The range in reported incidence is postulated
to be a result of variance in clinical care and average
infant birth weights across regions.

7. RISK FACTORS large size for gestational age (macrosomia)
shoulder dystocia
maternal short stature
maternal diabetes
breech delivery
multiparous pregnancies
previous deliveries resulting in BPBP
prolonged labor
assisted (vacuum or forceps) deliveries
Only half of patients have 1 or more of these risk factors, which highlights the concept that the etiology of BPBP is not yet fully known.

8. Anatomy
Stronger connective tissue and a more oblique angle of traverse across the neck provided greater support to the upper plexus at the root level
A more transverse position and weaker proximal soft tissue support made the lower plexus more susceptible to disruption with less tensile force.

9. The anatomic variation of the so-called prefixed
plexus, with a greater contribution from the C4 root,
may predispose some infants to tolerate less stretch
across the upper plexus.

10. Prefixed cords (22%) receive a contribution from the C4
Postfixed cords (1%) receive a contribution from the T2

11. Clinical Features
Lack of movement of the affected arm usually leads to referral for orthopaedic opinion.

12. Tonic neck

13. Moro
asymmetry of infantile reflexes such as Moro's reflex or asymmetric tonic neck reflex

14. Palmar grasp
With involvement of the lower plexus, the grasp reflex may be absent.

15. An ipsilateral Horner syndrome consisting of ptosis, miosis, and enophthalmos or a small pupil with a droopy eyelid, indicates injury to the T1 cervical sympathetic nervesHorner's syndrome (ptosis, myosis, enophthalmos, anhidrosis)

16. Phrenic nerve involvement is said to occur in up to 5% of upper plexus lesionThis can be assessed by observation of the abdominal wall for symmetric diaphragmatic movement during respiration or by an expiratory chest radiograph,

17. FractureIpsilateral clavicle fracture is actually a favorable finding in birth-related plexopathy because the fracture allows the shoulder girdle to compress, thus decreasing the overall traction on the plexus.
s of the clavicle, humerus, and other long bones may also be seen

18. Classification Narakas et al.
Group I classic upper trunk lesion C5-6
Group II extended upper trunk lesion C5-7
Group III flail extremity
Group IV flail extremity + Horner’s syndrome
Group I refers to C5–C6 involvement, the classic Erb’s palsy. This represents 46% of all cases and is associated with the most favorable prognosis.
Group II occurs approximately 30% of the time and refers to C5–C7 involvement. Group II carries a worse prognosis than C5–C6 injury alone.
Group III denotes total plexopathy with flail extremity and occurs in only 20% of patients.
Isolated lower trunk injury is rare and may not even exist in birth palsies

19. spontaneous recovery 90%
Group I absence of shoulder abduction and external rotation, elbow flexion, and forearm supination.
spontaneous recovery %
The mildest clinical

20. Group II with the absence of wrist and digital extension added to the limitations noted in group I

21. classic "waiter's tip
These infants have the classic "waiter's tip" posture of their hand and wrist. The prognosis is poorer with C5-7 involvement.

22. Group III consists of a flail extremity but without Horner's syndrome.

23. Group IV is manifested as a flail extremity and Horner’s syndrome
Group IV is manifested as a flail extremity and Horner’s syndrome. These infants may have an associated phrenic nerve palsy
The most severe involvement

24. Prognosis and Natural History
it is important to determine whether the injury is preganglionic or postganglionic.
Preganglionic avulsion injuries cannot spontaneously recover motor function

25. Horner's syndrome (sympathetic chain)
elevated hemidiaphragm (phrenic nerve)
winged scapula (long thoracic nerve)
absence of rhomboid (dorsal scapular nerve)
lower plexus involvement
upper trunk lesion seen with a breech delivery
complete palsy
lower Iimb weakness or spasticity
For prognostic reasons, it is important to determine whether the level of injury is preganglionic or postganglionic.
Because of the proximity of the ganglion to the spinal cord and the fact that the motor cell body is in the spinal cord, preganglionic lesions are avulsions from the cord that will not spontaneously recover.
no child with full recovery of motor function had complete palsy and nerve root avulsion

26. Infants who recover partial antigravity upper-trunk muscle strength in the first 2 months of life should have a full and complete neurologic recovery over the first 1 to 2 years of life

27. Cases in which the return of biceps function occurs after 3 months rarely have complete recovery without some notable limitations in strength or range of motion.

28. Muscle imbalance develops rapidly, and soft tissue contracture contributes to deformity and joint incongruence early in the neonatal period.

29. natural history of the developing glenohumeral joint in children with BPBP The uninvolved shoulders’ glenoscapular version averaged
minus 8° (range, 16° to 2°), and the percentage
of humeral head anterior to the middle of the glenoid
fossa (PHHA) averaged 45% (range, 34% to 54%). The
involved shoulders’ glenoscapular version averaged minus
24° (range, 64° to 7°) and PHHA averaged
28% (range, 0% to 51%)
Both version and
subluxation were significantly different (P .001) between
uninvolved and involved shoulders. There was a
significant correlation between version and subluxation
(r 0.91, P .001). Humeral head size was significantly
less (P .001) on the involved side.
These deficits often lead to muscle imbalance about the upper extremity. Differences in the strength of muscles surrounding the shoulder joint can lead to soft tissue and joint contractures as well as glenohumeral joint deformity.

30. Glenohumeral external rotation exercise with
scapular stabilization is the mainstay to prevent joint deformity. Scapular stabilization and passive glenohumeral mobilization in all planes is necessary on a frequent basis. Progressive
loss of external rotation beyond neutral correlated with
increased angles of retroversion and increased posterior
subluxation of the humeral head, and should be regarded
as in indicator of shoulder malformation (Fig.
4). This research highlighted the necessity of preserving
passive glenohumeral joint motion with the scapula
stabilized and was a catalyst to a paradigm shift in our
treatment of the newborn with BPBP (Fig. 5).

31. lengths of the affected limbs were compared with the unaffected side
upper arm 95%,
forearm 94%
hand 97%
Girth of the affected side was also noted to be smaller. Over 37% of patients and families thought this difference was “very” or “extremely important” to them, which highlights the importance of factors outside of function alone.

32. These children participate in sports at the same rate as their peers.
There was no increased injury rate for these children
In addition, participation in physical activities was similar to that of the unaffected population; however, two-thirds of the study group experienced symptoms during the activities primarily attributed to the affected upper limb.

33. Differential Diagnosis
fracture of the clavicle or humerus
proximal humeral physeal separation
septic arthritis of the shoulder
acute osteomyelitis
congenital malformation of the plexus
tumors involving the spinal cord or plexus
manifest as diminished spontaneous movement. Fractures of the
clavicle and humeral shaft are relatively common;
proximal physeal separation is rare. Gilbert' has reported on four cases of aplasia of the cervical spinal roots, some associated with other malformations in the upper limb.
Loss of normal reflexes occurs in all of these conditions
Tumors involving the spinal cord or plexus are rare but should be considered if there is deterioration in function