 |
       |
|
|
REVIEWS ARTICLES
Current Concepts Review - Obstetric Palsy
Rujuta Mehta, Anirbaan Chatterjee, Kanti P Shetty, Mukund R Thatte
Obstetric brachial palsy needs to be treated with a definite plan in mind. A disappointing clinical and/or EMG recovery at 3 months is a good indication for exploration and if appropriate, microsurgical nerve reconstruction without further delay. Results are more encouraging than in the adult brachial palsy and secondary re-constructive procedures also offer rewarding results. Finally a close coordination between the surgeons the physiotherapist and the occupational therapist as well as continuous and realistic communication with parents go a long way in ensuring a favourable outcome.
INTRODUCTION
Obstetric Brachial Palsy has hitherto been a somewhat neglected problem in India. The standard advice was to wait and watch for ‘improvement’, which meant a combination of watchful expectancy and benign neglect. In the recent past however these views and attitudes are changing rapidly. This review hopes to briefly look at the current thinking and management strategies in this area. In 1991, Sir Sydney Sunderland29 ended his chapter on the repair of the Brachial Plexus by saying “Finally it is axiomatic that in the field of surgery, it is no longer a question of what can be done but of establishing “what should be done”.”
We present here a review of the changing face of treatment of obstetric brachial palsy over the years and the situation as it has evolved to its presently accepted norms - as regards ‘what should be done’!
Historical Background
The condition was probably first described clinically in 1779 by Smellie who cited a case of bilateral arm paralysis following a face presentation, which resolved in a few days.
Danyau9 gave the first anatomic description in 1851. He carried out an autopsy on a neonate who died shortly after traumatic forceps delivery. Duchenne in 187211 attributed the injury to traction on the arm and introduced the term obstetric paralysis. Erb12 in 1874, in his monograph on brachial plexus injuries in adults reported his experiments on electrical stimulation of the brachial plexus. He discovered that the characteristic paralysis of the deltoid, biceps, coracobrachialis and brachioradialis could be caused by disruption of C5 and C6 roots at the point where they emerge just between the scalene muscles, [which has therefore been named after him].
Klumpke20 in 1885 described the paralysis of the lower roots of the brachial plexus and highlighted the involvement of the sympathetic fibres in this paralysis.
AETIOLOGY AND PATHOGENESIS
The etiology of this peculiar condition has always aroused the interest of investigators world over, and hence extensive work has been done to analyse its aetiology. Theories proposed abound - almost as many exist as the number of investigators and they range from poliomyelitis, to speculations about it being a congenital lesion and even sequelae of sub-clinical systemic toxaemia. Some have proposed postural in-utero ischaemia during the course of a difficult labour as a causative factor. Trauma also has been postulated in the form of shoulder joint capsular damage causing a subluxation of the glenohumeral joint. However cadaver experiments have been carried out time and again and there is worldwide agreement on the risk factors as being- Shoulder dystocia, Maternal diabetes, Large foetus, Cephalo Pelvic Disproportion, Difficult labour: breech, face to pubis, transverse presentations etc.
Bentzon, in his thesis, “Clinical and experimental studies on obstetrical paralysis of the brachial plexus, with special respect to pathogenesis and orthopaedic treatment,” reviewed the earlier literature and established in convincing experiments that Erb - Duchenne paralysis always develops as a sequel to over-stretching of the plexus by simultaneous lateral flexion of the neck and contralateral depression of the opposite shoulder.
Recently, however some rethinking and studies have been carried out which raise the intriguing possibility of it being an ‘In Utero’ injury13 but these seem to be at least partly, medico-legally motivated. Contrary to popular belief it is more common in multiparous than in primiparous women.
CLASSIFICATION
Clinically there are three main types of lesions:
C5-6: the arm is adducted and internally rotated at the shoulder, elbow extended, forearm pronated, wrist and (sometimes) fingers flexed. (Classic waiter tip/Erb’s palsy/upper roots).
C5-7 : as above, although the elbow may be slightly flexed.
C5-T1 : the arm is totally flail with a claw hand. The arm has a marbled appearance due to vasomotor disturbances, Horner’s syndrome may or may not be present.
Narakas24 classified these lesions initially into five groups and then into four, based on the examination 2-3 weeks after birth:
1. Group I C5-6 : paralysis of shoulder and biceps.
2. Group II C5-7: paralysis of shoulder biceps and forearm extensors.
3. Group III C5-T1: complete paralysis of the limb
4. Group IV C5-T1: as above with Horner’s syndrome.
Prognostic Factors
Amongst the potential prognostic indicators are nature of injury (e.g. avulsion or rupture), extent of injury (e.g. upper, middle and lower plexus lesions) associated ipsilateral Horner’s syndrome, and associated fractures e.g. ribs, clavicle, humerus although the prognostic value of these additional injuries is questionable unlike in adult Brachial plexus injuries.
Brown2 stated that poor prognostic signs included lower paralysis, a global involvement, and persistence of pupillary signs of phrenic nerve palsy, as proposed by Sever27. Narakas24 noted that recovery in Group IV was especially poor, with 50% having little or no function.
Laurent et al21 stated that ruptures were more common in upper roots and avulsions more common in lower. This finding was reinforced by experimental work of Metaizeau et al23. This could explain why upper lesions carry a greater chance of recovery than the lower ones.
MANAGEMENT
Repeated Clinical Evaluation
Clinical testing of the newborn requires patience and should be performed in a calm atmosphere with the child relaxed. Simple aids should be used to stimulate the child and an attempt must be made to map out the area of affection not only by noting movements or the lack of it, but also palpating the muscle between the two examining fingers. Reaction on pinching, nail and hair growth, trophic changes give an approximate indication about sensations in the infant. Presence of Horner’s syndrome signifies T1 root injury.
It is crucial to examine the other extremities to exclude infantile tetraplegia, which has a poor prognosis, and also to look for other birth trauma.
Clinical examination is repeated at 3 weeks and the parents taught gentle exercises to maintain finger flexion and prevent
contractures.
Contrary to popular belief the splints used for maintaining external rotation and abduction at shoulder are not particularly helpful and sometimes dangerous as over enthusiastic use can cause abduction contractures. A baseline EMG should also be performed at this time.
ROLE OF ELECTRO PHYSIOLOGY
Electro Physiological studies are crucial in determining the level and type of injury and serial studies at right intervals can give important information regarding prognosis and aid therapeutic decisions. Essentially we need to decide if the palsy is likely to recover substantially or whether it will be better treated by surgical intervention.
These studies have 4 main components:
1. Electromyography (EMG)
2. Nerve conduction (NC) including CMAP and SNAP
3. Spinal evoked potentials (SEP)
4. Somato sensory evoked potentials (SSEP)
A combination of this information, preoperatively and sometimes intraoperatively, basically allows the surgeon to decide whether surgery is likely to be required and if so, what is the necessary operation. A case showing progressively improving EMG with clinical correlation will usually be conserved; on the other hand if denervation persists unchanged and SNAP and SSEP indicate a pregnanglionic injury then early operative intervention is perhaps the most optimum option.
SURGICAL MANAGEMENT
The history of treatment of obstetric palsy has come a full circle. Initially reports of improvement in function following after exploration of the plexus were published in the early 1900’s.14-17,30 Following Sever’s report in 1925 and Jepson’s report in 1930 describing disappointing results of surgery, surgeons had elected to treat these infants conservatively and then perform secondary reconstruction of their functional deficits with muscle transfers, corrective osteotomies, or joint fusion. Recent developments in paediatrics anaesthesia and microsurgery have revived the interest in early surgical treatment of obstetric palsy. The challenge now lies in deciding which children are likely to recover spontaneously and which children will require exploration and micro-surgical nerve grafting.
Following the study of Tassin on patients treated non-operatively, Alain Gilbert,14-17 one of the foremost experts in the field has prescribed the following indications:
Total palsy at birth with a positive Horner’s syndrome.
We would like to reiterate that third month refers to 3 months of age and not three months from first presentation.
SURGICAL TECHNIQUES
Exploration of the brachial plexus:
This may reveal the following types of findings:clear ruptures avulsions of the entire plexus or avulsions of isolated roots or the most enigmatic of them all- the neuroma in continuity.
Neuroma in continuity still remains the big question at surgical exploration, the dictum in our minds is to err on the side of doing less, although there have been recent reports on the early resection and microsurgical repair of these,3,6,7 the results need to be looked at
Microsurgical repair
This may be in the form of a neurolysis, resection and anastomosis in ruptures or nerve grafting using sural nerves as interposition grafts. Broadly we divide treatment into repair using the proximal roots of the plexus itself if the injury is post ganglionic as in a rupture, or extra plexal neurotisation using other donor motor nerves to selectively aim at reinnervating the important muscle groups. Common donor nerves are:
Spinal accessory (XIth) nerve.
Intercostal nerves (commonly 3rd to 6th)
C4 motor root
Ansa hypoglossi
Opposite C7 (Chuang et al)4,5
The common recipient nerves are the Suprascapular, the Musculocutaneous, the Axillary and the Median. The actions to be restored are in order of priority:
Elbow flexion
Shoulder stability (rotator cuff via suprascapular nerve)
Shoulder abduction
Hand prehension
Results
The child should be periodically evaluated post-op at three monthly intervals for signs of nerve regeneration like Tinel’s sign, disappearance of trophic changes, maintenance of muscle mass and the ultimate contraction and return of movement, as well as EMG-NCV which would give documentary proof of nerve regeneration. Evaluation of results should be done using the Mallet22 scale of I-IV grades which is an easy to use practical and most important a functional scoring system or alternatively by the MRC grades for muscle power. Results are sufficiently encouraging to make surgical intervention a worthwhile and viable option in cases where the clinical and electro physiological recovery is not as per expectation in the early weeks after injury.
THE LATE OBSTETRIC PALSY
Despite an abundance of literature and advancements in available options the majority of referrals are still as late presentations largely due to lack of awareness about the management strategies. Stefanova28 in a unique and commendable study have clearly demonstrated that denervation at birth impairs normal development of muscle contractile properties.
Phenomena unique to the late presentation are ‘Cross-innervation’10 (caused by misdirection of regenerated axons), muscular imbalance and shoulder deformity due to growth, mainly rotational or subluxatory.
These have been satisfactorily dealt with secondary operations8 to restore a more functional muscle balance, viz. the L ‘Episcopo procedure of transferring the Teres major and Latissimus dorsi on the posterior side to the infraspinatus and then on to the Humerus anteriorly and the Chuang5,6 procedure of transferring the Teres major to the Infraspinatus and the clavicular head of the Pectoralis major to the area lateral to the long head of biceps anteriorly with gratifying results.
There are also indications for rotational osteotomy and capsulorraphy in select cases mainly for internal rotation deformity and gross subluxation.
REFERENCES
1. al-Qattan MM, et al. Klumpke’s birth palsy. Does it really exit? J Hand surg (Br) 1995; 20 (1) : 19-23.
2. Brown KL. Review of obstetrical palsies. Nonoperative treatment. Clin Plast Surg 1984; 11 (1) : 181-7.
3. Capek L, et al. Neuroma-in-continuity resection : early outcome in obstetrical brachial plexus palsy. Plast Reconstr Surg 1998; 102 (5) : 1555-64.
4. Chuang DC, et al. A new evaluation system to predict the sequelae of late obstetric brachial plexus palsy. Plast Reconstr Surg 1998; 101 (3) : 673-85.
5. Chuang DC, et al. A new strategy of muscle transposition for treatment of shoulder deformity caused by obstetric brachial plexus palsy. Plast Reconstr Surg 1998; 101 (3) : 686-94.
6. Clarke HM, et al. An approach to obstetrical brachial plexus injuries. Hand Clin 1995; 11 (4) : 563-81.
7. Clarke HM, et al. Obstetrical brachial plexus palsy: results following neurolysis of conducting neuromas-in-continuity. Plast Reconstr Surg 1996; 97 (5) : 974-82; discussion 983-4.
8. Covey DC, et al. Modification of the L‘Episcopo procedure for brachial plexus birth palsies. J Bone Joint Surg Br 1992; 74 (6) : 897-901.
9. Danyau M. Paralysie du membre superieur, chez le nouveau-ne. Bull Soc Chir 1851; 2 : 148.
10. De Grandis D, et al. Anomalous reinnervation as a sequel to obstetric brachial plexus palsy. J Neurol Sci 1979; 43 (1) : 127-32.
11. Duchenne GBA. De l’ electrisation localise et de son Application a la pathologieet la therapeutique. Paris JB Balliere et fils 1872; 357-62.
12. Erb W Ueber eine eignethumliche localisation von Lahmun gen implexus brachialis. Verhandlungen des naturhisorischen veriens von Heidelberg. 1874; 2 : 130-7.
13. Gherman RB, et al. Brachial plexus palsy; an in utero injury? Am J Obstet Gynecol 1999; 180 (5) : 1303-7.
14. Gilbert A, et al. Indications and results of brachial plexus surgery in obstetrical palsy. Orthop Clin North Am 1988; 19 (1) :91-105.
15. Gilbert A, et al. Obstetrical brachial plexus lesions. J Hand Surg (Br) 1991; 16 (5) : 489-91.
16. Gilbert A, et al. Surgical treatment of brachial plexus birth palsy. Clin Orthop 1991; 264 : 39-47.
17. Gilbert A. Long-term evaluation of brachial plexus surgery in obstetrical palsy. Hand Clin 1995; 11 (4) : 583-95.
18. Laurent JP, Lee RT. Birth related upper brachial plexus injuries in infants: operative and non-operative approaches. J Child Neurolo 1994; 9 : 111-7.
19. Mallet J. Paralysie obstetricale du plexus brachial. Symposium sous la direction de J Mallet. Rev Chir Orthop Reparatrice Appar Mot 1972; 58 : 115-204.
20. Metaizieu JP, Gayet C, Planat F. (Brachial plexus birth injuries. An experimental study [author’s translation]). Chirurg Ped 1979; 20 : 159-63.
21. Narakas AO. The treatment of brachial plexus injuries. In Orthop 1985; 9 (1) : 29-36.
22. Ouzounian JG, et al. Permanent Erb palsy: a traction-related injury? Obstet Gynecol 1997; 89 (1) : 139-41.
23. Papazian O, et al. Neurophysiological assessment of children with obstetric brachial plexus palsy. Rev Neurol 1998; 27 (156) : 263-70.
24. Sever JW. Obstetric paralysis: report of 1100 cases. JAMA 1925; 1862-5.
25. Stefanova-Uzunova M, et al. Dynamic properties of partially denervated muscle in children with brachial plexus birth palsy. J Neurol Neurosurg Psychiatry 1981; 44 (6) : 497-502.
26. Sunderland S. Nerve injuries and their repair. Traction nerve injury. Edinburgh: Churchill Livingstone. 1991; 147-58.
27. White SJ, et al. Arthrography in evaluation of birth injuries of the shoulder. Can Assoc Radiol J 1987; 38 (2) : 113-5.
RESISTING RELAPSE
Treatment be continued for 4-6 months after stabilisation from an acute episode of illness. However, Geddes noted that for patients at appreciable risk of recurrence after 4-6 months of treatment, that another year, and probably more, of continuation treatment will approximtely halve their risk.
Lancet Oncol 2003; 4 : 653.
 |