JBJS | Dislocation of the Hip in Myelomeningocele. The McKay Hip Stabilization*

The Journal of Bone & Joint Surgery, Volume 78, Issue 5

Articles | May 01, 1996

Dislocation of the Hip in Myelomeningocele. The McKay Hip Stabilization*

LAURA L. TOSI, M.D.†; BRIAN D. BUCK, P.A.-C†; STEPHEN S. NASON, M.D.†; DOUGLAS W. MCKAY, M.D.†, WASHINGTON, D.C.

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Investigation performed at Children's National Medical Center, Washington, D.C.

The Journal of Bone & Joint Surgery. 1996; 78:664-73

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Abstract

We reviewed the clinical and radiographic results of varus osteotomy of the proximal aspect of the femur and transfer of the adductor and external oblique muscles (the McKay procedure) in thirty-four children (sixty-six hips) who had an unstable hip secondary to a myelomeningocele at the middle or caudad lumbar level. The average age at the time of the operation was twenty months (range, seven to forty-two months). The average duration of follow-up was 10.9 years (range, 0.7 to 20.0 years). An open reduction was performed in ten hips. None of the children had had any previous operative treatment.The index operation helped to maintain the stability of thirty-seven of the fifty-one hips in twenty-six children who remained neurologically stable: seventeen of nineteen hips that were at risk, two of three hips with acetabular dysplasia, fifteen of sixteen subluxated hips, one of three dislocated hips that had been previously reduced with a Pavlik harness, one of two dislocatable hips, and one of seven previously untreated dislocated hips. The index operation was not successful for one dislocated hip that had been treated with closed reduction and application of a spica cast. The operation was a success for eight of the fifteen hips in eight children who had a progressive loss of neurological function: three of five hips that were at risk, one hip with acetabular dysplasia, two of four subluxated hips, one of two hips that had been previously reduced with a Pavlik harness, and one dislocatable hip. Two dislocated hips redislocated.Initially the index operation was performed on all children who had a myelomeningocele at the third or fourth lumbar level. Recent data have shown that the hips in these children are not all at risk, and we now perform the operation only if there is documented instability of the hip.

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Introduction

Introduction | Materials and Methods | Results | Discussion | References

Extensive operations to stabilize or relocate a dysplastic hip in a child who has a myelomeningocele have been performed on the basis of the belief that the child will be able to walk more easily and less bracing will be needed if the hips are located^{5-7,9,13,20,24,26,33,34,36,43}. Some investigators^10,35 believe that all hips in children who have a myelomeningocele at the third or fourth lumbar level and most hips in children who have a lesion at the fifth lumbar level will eventually dislocate.

The senior one of us (D. W. McK.) believed that it was important to maintain a located hip in children who have a myelomeningocele, and he developed what is known as the McKay procedure²⁵. He performed this operation when the child was twelve to eighteen months old in order to maximize the probability of good acetabular development. He transferred the external oblique muscle to the greater trochanter (to provide active abduction and to strengthen the hip) and the adductors to the ischial tuberosity (to weaken flexion and perhaps to provide active extension). In addition, a varus osteotomy of the proximal aspect of the femur was performed simultaneously to relocate the dislocated femoral head, to stimulate acetabular development, and to increase the lever arm of the transferred external oblique muscle. Because of the young age of the children, prolonged supervised physical therapy was unnecessary and interference with school activities was not an issue. McKay hoped that the early intervention would avoid the need for additional procedures. He performed the procedure bilaterally, whether or not both hips were subluxated, on the basis of the belief that virtually all hips in children who have a lesion at the third or fourth lumbar level ultimately dislocate and also that unilateral transfer of major muscle groups could create a pelvic obliquity and lead to additional deformity. Since the index operations were bilateral, it was not possible to have a control group.

The results of the McKay procedure in thirty-four children (sixty-six hips) who had a lumbar myelomeningocele were retrospectively reviewed to determine whether the goals of the operation had been achieved.

*No benefits in any form have been received or will be received from a commercial party related directly or indirectly to the subject of this article. No funds were received in support of this study.

†Department of Orthopaedic Surgery, Children's National Medical Center, 111 Michigan Avenue, N.W., Washington, D.C. 20010.

*No benefits in any form have been received or will be received from a commercial party related directly or indirectly to the subject of this article. No funds were received in support of this study.

†Department of Orthopaedic Surgery, Children's National Medical Center, 111 Michigan Avenue, N.W., Washington, D.C. 20010.

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TABLE I DATA ON THE PATIENTS

* The number of months postoperatively at which the additional operation was performed is given in parentheses.† KAFO = knee-ankle-foot orthosis, AFO = ankle-foot orthosis, UCBL = University of California at Berkeley Laboratory foot orthosis, and HKAFO = hip-knee-ankle-foot orthosis.‡ NA = not available.§ The patient had a loss of neurological function postoperatively.¶ The diagnosis for one hip/the diagnosis for the other hip.

Case	Side	Neurological Level at Diag.	Age at Op. (Mos.)	Indications for Op.	Preop. Treatment	Open Reduct.	Complications	Add. Op.*	Duration of Follow-up (Yrs.)	Neurological Level at Follow-up	Hip Contract. >15°	Amb. Status²¹	Brace or Walking Aids†	Radiographic Status	Center-Edge Angle⁴²‡ (Degrees)	Migration Index of Reimers‡ (Degrees)	Scoliosis >30°	Add. Data
At risk bilat.
1	R	L3	14	At risk	—	N	—	Varus osteot., shelf proc. (86)	8.5	L3	N	Commun.	KAFO, Lofstrands	Located	30	0	N	—
	L	L3	15	At risk	—	N	—	Varus osteot., shelf proc. (86)	8.4	L3	N			Located	20	0
2	R	L4	16	At risk	—	N	—	—	12.2	L4	N	Commun.	AFO, canes	Trace sublux.	12	37	N	—
	L	L4	16	At risk	—	N	—	12.2	L4	N			Located	16	36
3	R	L4	19	At risk	—	N	—	—	10.7	L4	N	Commun.	AFO, canes	Located	22	15	N	—
	L	L4	20	At risk	—	N	—	Varus osteot., shelf proc. (78)	10.6	L4	N			Located	24	8
4	R	L4	14	At risk	—	N	—	11.8	L4	N	Commun.	AFO, canes	Located	8	40	N	—
	L	L4	14	At risk	—	N	—	—	11.8	L4	N	Located	14	43
5	R	L4	22	At risk	—	N	—	—	7.3	L4	N	Commun.	Canes	Located	32	19	N	—
	L	L4	23	At risk	—	N	—	—	7.2	L4	N			Located	37	12
6§	R	L4	18	At risk	—	N	—	Release, hip capsule (103)	20.0	L2	N	Non-amb.	Wheelchair	Sublux.	-10	60	Y	Loss, motor func.; contract.; scoliosis
	L	L4	18	At risk	—	N	—	Release, hip capsule (103)	20.0	L2/L3	N			Located	26	24
At risk unilat.
7	R	L4	36	At risk	—	N	—	—	6.1	L4	N	Commun.	AFO, canes	Located	30	10	N	—
Acetab. dys. bilat.
8	R	L5	16	Acetab. dys.	—	N	Non-union	Repair of non-union (16)	7.0	L5	N	Commun.	UCBL, canes	Located	14	26	N	—
	L	L5	16	Acetab. dys.	—	N	Non-union	Repair of non-union (16)	7.0	L5	N			Located	12	21
Acetab. dys./at risk¶
9	L	L4	33	Acetab. dys.	—	N	—	—	17.4	L4	N	House.	Holds furniture, wheelchair	Sublux.	11	36	N	Could be commun. amb. but refuses
	R	L4	33	At risk	—	N	—	—	17.4	L4	N			Located	30	15
10§	L	L5	26	Acetab. dys.	—	N	Fract., osteot. site after cast removal	—	18.7	L3	Y	House. (prim. transfer & makes bed)	Wheelchair	Located	30	0	Y	Loss, motor func.; contract.; scoliosis
	R	L5	27	At risk	—	N	—	—	18.6	L3	N			Located	14	35
Sublux. bilat.
11	R	L3	37	Sublux.	—	N	—	—	0.7	L3	N	Commun.	AFO, walker	Located	14	17	N	—
	L	L3	37	Sublux.	—	N	Broken wire, fem. neck	—	0.7	L3	N			Located	14	0	N
12	R	L4	25	Sublux.	—	N	—	—	0.9	L4	N	House.	AFO, walker	Located	10	15	N	—
	L	L4	26	Sublux.	—	N	—	—	0.8	L4	N			Located	20	0	N
13	R	L4	12	Sublux.	—	N	—	—	6.8	L4	N	Commun.	AFO	Located	30	11	N	—
	L	L4	13	Sublux.	—	N	—	—	6.7	L4	N			Located	22	14
14	R	L4	9	Sublux.	—	N	—	Varus osteot., shelf proc. (91)	10.7	L4	N	Commun.	AFO, canes	Located	18	18	N	—
	L	L4	10	Sublux.	—	N	—	Varus osteot., shelf proc. (90)	10.6	L4	N			Located	0	0
15	R	L4	26	Sublux.	—	N	—	—	3.9	L4	N	Commun.	KAFO, canes	Located, very deficient acetab.	16	26	N	—
	L	L4	25	Sublux.	—	N	—	—	4.0	L4	N			Located very deficient acetab.	0	33
16	R	L4	39	Sublux.	—	N	—	Varus osteot., shelf proc. (90)	7.3	L4	N	Commun.	AFO, canes	Located	20	0	N	—
	L	L4	39	Sublux.	—	N	—	—	7.3	L4	N			Located	23	11
17§	R	L4	16	Sublux.	—	N	—	Varus osteot., shelf proc., tensor release (61)	11.7	L1	Y	Non-amb.	Wheelchair	Sublux.	0	44	Y	Loss, motor func.; contract.; scoliosis
	L	L4	17	Sublux.	—	N	—	Tensor release (61)	11.6	L1	Y			Sublux.	24	31
Sublux. unilat.
18§	L	L3	13	Sublux.	—	N	—	—	19.4	L2	Y	House.	KAFO, canes, wheelchair	Located	14	15;severely deficient L. acetab., not sublux.	Y	Loss, motor func.; contract.; scoliosis
Sublux./at risk¶
19	R	L3	14	Sublux.	—	N	—	—	3.9	L3	N	Commun.	KAFO, canes	Located	34	14	N	—
	L	L3	15	At risk	—	N	—	—	3.8	L3	N			Located	8	40
20	R	L5	14	Sublux.	—	N	—	Varus osteot. (144)	16.8	L5	N	Commun.	AFO	Located	19	4	N	—
	L	L5	15	At risk	—	N	—	—	16.8	L5	N			Located	21	17
21§	L	L5	15	Sublux.	—	N	—	—	10.7	L3	N	Non-func.	HKAFO, walker, wheelchair	located	40	0	Y	Loss, motor func.; contract.; scoliosis
	R	L5	14	At risk	—	N	Non-displaced fract., distal aspect of femur; superfic. wound infect.; ulcer, heel	—	10.8	L3	Y			Dislocated	NA	NA
Dislocated at birth bilat., treated with closed reduct.
22	R	L4	18	Dislocated	Pavlik harness (reduced)	N	—	—	9.3	L4	N	Commun.	AFO, canes	Located	15	31	N	—
	L	L4	18	Dislocated	Pavlik harness (reduced)	N	—	—	9.3	L4	N			Slightly sublux.	0	51
23§	R	L5	28	Dislocated	Pavlik harness (reduced)	N	Superfic, wound infect.	—	13.6	L3	Y	Non-func.	KAFO, canes, wheelchair	Dislocated	NA	100	Y	Loss, motor func.; contract.; scoliosis
	L	L5	28	Dislocated	Pavlik harness (reduced)	N	—	—	13.6	L3	Y			Located	42	0
Dislocated at birth, treated with closed reduct./at risk¶
24	R	L4	18	Dislocated	Closed reduct., hip-spica cast	N	—	Shelf proc. (45), fem. short., Chiari osteot. (101)	14.9	L3	N	Commun.	KAFO, canes	Severely sublux.	-12	58	N	—
	L	L4	18	At risk	—	N	—	—	14.9	L4	N			Located	30	0
Became dislocatable/at risk¶
25	L	L4	21	Dislocatable	—	N	—	Varus osteot., shelf proc. (56)	14.5	L4	N	House.	KAFO, canes	Slightly sublux.	10	31	N	—
	R	L4	21	At risk	—	N	—	—	14.5	L4	N			Located	30	0
26	L	L4	19	Dislocatable	—	N	—	Varus osteot., Chiari osteot. (84)	10.9	L4	N	Commun.	AFO, canes	Located	22	28	N	—
	R	L4	18	At risk	—	N	—	—	10.8	L4	N			Located	24	15
27§	R	L4	32	Dislocatable	—	N	—	Acetab. aug. (63)	11.7	T12-L1	Y	Non-amb.	Wheelchair	Fem. head located; non-union with high-riding greater trochant., fem. neck fract.	6	63	Y	Loss, motor func.; contract.; scoliosis
	L	L4	32	At risk	—	N	—	—	11.7	T12-L1	Y			Located	6	35
Dislocated bilat.
28	R	L4	42	Dislocated	—	Y	—	—	15.7	L4	Y	House.	Walker	Dislocated	NA	NA	N	—
	L	L4	42	Dislocated	—	Y	—	—	15.7	L4	Y			Dislocated	NA	NA
29	R	L5	15	Dislocated	—	Y	—	—	19.5	L5	N	Commun.	Canes	Dislocated	NA	100	N	—
	L	L5	15	Dislocated	—	Y	—	—	19.5	L4	N			Dislocated	NA	100
30§	R	L4	10	Dislocated	—	Y	—	—	10.5	L1-L2	Y	Non-func.	KAFO, wheelchair	Dislocated	NA	NA	N	Loss, motor func.; contract.
	L	L4	10	Dislocated	—	Y	—	—	10.5	L1-L2	Y			Dislocated	NA	NA
Dislocated/at risk¶
31	L	L3	7	Dislocated	—	Y	—	Varus osteot., open reduct., Pemberton osteot. (55)	18.7	L3	N	Commun.	AFO, canes wheelchair for distance	Dislocated	NA	100	N	—
	R	L4	18	At risk	—	N	—	—	17.8	L4	N			Dislocated	NA	NA
32	L	L4	15	Dislocated (init. reducible)	Pavlik harness (failed)	Y	Redislocated (immed. postop.)	Varus osteot., open reduct., psoas recess. (21)	7.4	L4	Y	Commun.	KAFO	Dislocated	NA	NA	N	—
	R	L4	16	At risk	—	N	—	—	7.3	L4	N		AFO	Located	22	3
Dislocated/sublux.¶
33	R	L4	12	Dislocated	—	Y	—	—	7.8	L4	N	Non-amb.	Wheelchair	Located; coxa vara, 78 degrees; premature growth plate arrest	24	0	N	Non-amb. due to chronic heel ulcer after revision of clubfoot
	L	L4	13	Sublux.	—	N	—	—	7.7	L4	N			Sublux	18	36
34	L	L4	11	Dislocated	—	Y	Rapid redislocation	Varus osteot., open reduct. (9)	7.3	L4	N	Commun.	AFO, canes	Slightly sublux., small fem. head	19	26	N	—
	R	L5	11	Sublux.	—	N	—	—	7.3	L5	N			Located	20	29

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TABLE I DATA ON THE PATIENTS

Case	Side	Neurological Level at Diag.	Age at Op. (Mos.)	Indications for Op.	Preop. Treatment	Open Reduct.	Complications	Add. Op.*	Duration of Follow-up (Yrs.)	Neurological Level at Follow-up	Hip Contract. >15°	Amb. Status²¹	Brace or Walking Aids†	Radiographic Status	Center-Edge Angle⁴²‡ (Degrees)	Migration Index of Reimers‡ (Degrees)	Scoliosis >30°	Add. Data
At risk bilat.
1	R	L3	14	At risk	—	N	—	Varus osteot., shelf proc. (86)	8.5	L3	N	Commun.	KAFO, Lofstrands	Located	30	0	N	—
	L	L3	15	At risk	—	N	—	Varus osteot., shelf proc. (86)	8.4	L3	N			Located	20	0
2	R	L4	16	At risk	—	N	—	—	12.2	L4	N	Commun.	AFO, canes	Trace sublux.	12	37	N	—
	L	L4	16	At risk	—	N	—	12.2	L4	N			Located	16	36
3	R	L4	19	At risk	—	N	—	—	10.7	L4	N	Commun.	AFO, canes	Located	22	15	N	—
	L	L4	20	At risk	—	N	—	Varus osteot., shelf proc. (78)	10.6	L4	N			Located	24	8
4	R	L4	14	At risk	—	N	—	11.8	L4	N	Commun.	AFO, canes	Located	8	40	N	—
	L	L4	14	At risk	—	N	—	—	11.8	L4	N	Located	14	43
5	R	L4	22	At risk	—	N	—	—	7.3	L4	N	Commun.	Canes	Located	32	19	N	—
	L	L4	23	At risk	—	N	—	—	7.2	L4	N			Located	37	12
6§	R	L4	18	At risk	—	N	—	Release, hip capsule (103)	20.0	L2	N	Non-amb.	Wheelchair	Sublux.	-10	60	Y	Loss, motor func.; contract.; scoliosis
	L	L4	18	At risk	—	N	—	Release, hip capsule (103)	20.0	L2/L3	N			Located	26	24
At risk unilat.
7	R	L4	36	At risk	—	N	—	—	6.1	L4	N	Commun.	AFO, canes	Located	30	10	N	—
Acetab. dys. bilat.
8	R	L5	16	Acetab. dys.	—	N	Non-union	Repair of non-union (16)	7.0	L5	N	Commun.	UCBL, canes	Located	14	26	N	—
	L	L5	16	Acetab. dys.	—	N	Non-union	Repair of non-union (16)	7.0	L5	N			Located	12	21
Acetab. dys./at risk¶
9	L	L4	33	Acetab. dys.	—	N	—	—	17.4	L4	N	House.	Holds furniture, wheelchair	Sublux.	11	36	N	Could be commun. amb. but refuses
	R	L4	33	At risk	—	N	—	—	17.4	L4	N			Located	30	15
10§	L	L5	26	Acetab. dys.	—	N	Fract., osteot. site after cast removal	—	18.7	L3	Y	House. (prim. transfer & makes bed)	Wheelchair	Located	30	0	Y	Loss, motor func.; contract.; scoliosis
	R	L5	27	At risk	—	N	—	—	18.6	L3	N			Located	14	35
Sublux. bilat.
11	R	L3	37	Sublux.	—	N	—	—	0.7	L3	N	Commun.	AFO, walker	Located	14	17	N	—
	L	L3	37	Sublux.	—	N	Broken wire, fem. neck	—	0.7	L3	N			Located	14	0	N
12	R	L4	25	Sublux.	—	N	—	—	0.9	L4	N	House.	AFO, walker	Located	10	15	N	—
	L	L4	26	Sublux.	—	N	—	—	0.8	L4	N			Located	20	0	N
13	R	L4	12	Sublux.	—	N	—	—	6.8	L4	N	Commun.	AFO	Located	30	11	N	—
	L	L4	13	Sublux.	—	N	—	—	6.7	L4	N			Located	22	14
14	R	L4	9	Sublux.	—	N	—	Varus osteot., shelf proc. (91)	10.7	L4	N	Commun.	AFO, canes	Located	18	18	N	—
	L	L4	10	Sublux.	—	N	—	Varus osteot., shelf proc. (90)	10.6	L4	N			Located	0	0
15	R	L4	26	Sublux.	—	N	—	—	3.9	L4	N	Commun.	KAFO, canes	Located, very deficient acetab.	16	26	N	—
	L	L4	25	Sublux.	—	N	—	—	4.0	L4	N			Located very deficient acetab.	0	33
16	R	L4	39	Sublux.	—	N	—	Varus osteot., shelf proc. (90)	7.3	L4	N	Commun.	AFO, canes	Located	20	0	N	—
	L	L4	39	Sublux.	—	N	—	—	7.3	L4	N			Located	23	11
17§	R	L4	16	Sublux.	—	N	—	Varus osteot., shelf proc., tensor release (61)	11.7	L1	Y	Non-amb.	Wheelchair	Sublux.	0	44	Y	Loss, motor func.; contract.; scoliosis
	L	L4	17	Sublux.	—	N	—	Tensor release (61)	11.6	L1	Y			Sublux.	24	31
Sublux. unilat.
18§	L	L3	13	Sublux.	—	N	—	—	19.4	L2	Y	House.	KAFO, canes, wheelchair	Located	14	15;severely deficient L. acetab., not sublux.	Y	Loss, motor func.; contract.; scoliosis
Sublux./at risk¶
19	R	L3	14	Sublux.	—	N	—	—	3.9	L3	N	Commun.	KAFO, canes	Located	34	14	N	—
	L	L3	15	At risk	—	N	—	—	3.8	L3	N			Located	8	40
20	R	L5	14	Sublux.	—	N	—	Varus osteot. (144)	16.8	L5	N	Commun.	AFO	Located	19	4	N	—
	L	L5	15	At risk	—	N	—	—	16.8	L5	N			Located	21	17
21§	L	L5	15	Sublux.	—	N	—	—	10.7	L3	N	Non-func.	HKAFO, walker, wheelchair	located	40	0	Y	Loss, motor func.; contract.; scoliosis
	R	L5	14	At risk	—	N	Non-displaced fract., distal aspect of femur; superfic. wound infect.; ulcer, heel	—	10.8	L3	Y			Dislocated	NA	NA
Dislocated at birth bilat., treated with closed reduct.
22	R	L4	18	Dislocated	Pavlik harness (reduced)	N	—	—	9.3	L4	N	Commun.	AFO, canes	Located	15	31	N	—
	L	L4	18	Dislocated	Pavlik harness (reduced)	N	—	—	9.3	L4	N			Slightly sublux.	0	51
23§	R	L5	28	Dislocated	Pavlik harness (reduced)	N	Superfic, wound infect.	—	13.6	L3	Y	Non-func.	KAFO, canes, wheelchair	Dislocated	NA	100	Y	Loss, motor func.; contract.; scoliosis
	L	L5	28	Dislocated	Pavlik harness (reduced)	N	—	—	13.6	L3	Y			Located	42	0
Dislocated at birth, treated with closed reduct./at risk¶
24	R	L4	18	Dislocated	Closed reduct., hip-spica cast	N	—	Shelf proc. (45), fem. short., Chiari osteot. (101)	14.9	L3	N	Commun.	KAFO, canes	Severely sublux.	-12	58	N	—
	L	L4	18	At risk	—	N	—	—	14.9	L4	N			Located	30	0
Became dislocatable/at risk¶
25	L	L4	21	Dislocatable	—	N	—	Varus osteot., shelf proc. (56)	14.5	L4	N	House.	KAFO, canes	Slightly sublux.	10	31	N	—
	R	L4	21	At risk	—	N	—	—	14.5	L4	N			Located	30	0
26	L	L4	19	Dislocatable	—	N	—	Varus osteot., Chiari osteot. (84)	10.9	L4	N	Commun.	AFO, canes	Located	22	28	N	—
	R	L4	18	At risk	—	N	—	—	10.8	L4	N			Located	24	15
27§	R	L4	32	Dislocatable	—	N	—	Acetab. aug. (63)	11.7	T12-L1	Y	Non-amb.	Wheelchair	Fem. head located; non-union with high-riding greater trochant., fem. neck fract.	6	63	Y	Loss, motor func.; contract.; scoliosis
	L	L4	32	At risk	—	N	—	—	11.7	T12-L1	Y			Located	6	35
Dislocated bilat.
28	R	L4	42	Dislocated	—	Y	—	—	15.7	L4	Y	House.	Walker	Dislocated	NA	NA	N	—
	L	L4	42	Dislocated	—	Y	—	—	15.7	L4	Y			Dislocated	NA	NA
29	R	L5	15	Dislocated	—	Y	—	—	19.5	L5	N	Commun.	Canes	Dislocated	NA	100	N	—
	L	L5	15	Dislocated	—	Y	—	—	19.5	L4	N			Dislocated	NA	100
30§	R	L4	10	Dislocated	—	Y	—	—	10.5	L1-L2	Y	Non-func.	KAFO, wheelchair	Dislocated	NA	NA	N	Loss, motor func.; contract.
	L	L4	10	Dislocated	—	Y	—	—	10.5	L1-L2	Y			Dislocated	NA	NA
Dislocated/at risk¶
31	L	L3	7	Dislocated	—	Y	—	Varus osteot., open reduct., Pemberton osteot. (55)	18.7	L3	N	Commun.	AFO, canes wheelchair for distance	Dislocated	NA	100	N	—
	R	L4	18	At risk	—	N	—	—	17.8	L4	N			Dislocated	NA	NA
32	L	L4	15	Dislocated (init. reducible)	Pavlik harness (failed)	Y	Redislocated (immed. postop.)	Varus osteot., open reduct., psoas recess. (21)	7.4	L4	Y	Commun.	KAFO	Dislocated	NA	NA	N	—
	R	L4	16	At risk	—	N	—	—	7.3	L4	N		AFO	Located	22	3
Dislocated/sublux.¶
33	R	L4	12	Dislocated	—	Y	—	—	7.8	L4	N	Non-amb.	Wheelchair	Located; coxa vara, 78 degrees; premature growth plate arrest	24	0	N	Non-amb. due to chronic heel ulcer after revision of clubfoot
	L	L4	13	Sublux.	—	N	—	—	7.7	L4	N			Sublux	18	36
34	L	L4	11	Dislocated	—	Y	Rapid redislocation	Varus osteot., open reduct. (9)	7.3	L4	N	Commun.	AFO, canes	Slightly sublux., small fem. head	19	26	N	—
	R	L5	11	Sublux.	—	N	—	—	7.3	L5	N			Located	20	29

Materials and Methods

Introduction | Materials and Methods | Results | Discussion | References

We reviewed the records of forty-two children with a myelomeningocele who had been followed at Children's National Medical Center since infancy and had had the index operation performed between 1972 and 1993. Six patients had left the area and two had died; therefore, thirty-four children (sixty-six hips), sixteen boys and eighteen girls, formed the study cohort. Only children who had a lesion at the third or fourth lumbar level and children who had a lesion at the fifth lumbar level with evidence of acetabular dysplasia, subluxation, or dislocation of the hip were included. The average age at the time of the operation was twenty months (range, seven to forty-two months).

The demographic data obtained from the medical records included the age at the time of the operation, neurological function, details of any previous treatment, indications for the operation, additional operations, and complications. Each patient was examined by one of us (L. L. T.) to determine the range of motion of the hip, the current neurological and functional status, the presence of scoliosis, the ability to walk, and any need for braces or a wheelchair. Grade-3 strength of the quadriceps and the medial aspect of the hamstrings characterized a lesion at the third lumbar level, and grade-4 strength of those muscles characterized a lesion at the fourth lumbar level²⁵. The ambulatory status was determined according to the criteria of Hoffer et al.²¹. Stability of the hip was evaluated clinically and on radiographs made with the child in the supine position; the position of the hip was described with the migration index of Reimers and the center-edge angle of Wiberg⁴². (The migration index of Reimers measures the degree of lateral acetabular deficiency and is obtained by dividing the distance from the lateral border of the femoral head to the Perkins line by the width of the femoral head parallel to the Hilgenreiner line and multiplying the result by 100.)

Indications for the Index Operation

The indications for the McKay procedure were a risk of dislocation in a child who had a lesion at the third or fourth lumbar level or in whom one hip was unstable (twenty-four hips); acetabular dysplasia without subluxation of the hip but with an acetabular index of more than 30 (four hips); definite evidence of subluxation, such as a break in the Shenton line, widening of the distance between the teardrops, and early migration of the hip out of the joint (twenty hips); a dislocated hip that was noted at birth and had been successfully treated with a Pavlik harness or closed reduction and application of a spica cast but in which, it was assumed, the acetabulum would never develop normally given the muscle function (five hips); a dislocatable hip (three hips); and a dislocated hip that could not be reduced or that had dislocated within the first two years of life (ten hips).

Early in the study, we noticed a poor outcome in patients who had bilateral dislocation of the hip; therefore, after 1983 such patients were managed non-operatively. In addition, at the onset of this study, we performed this operation on all children who had a lesion at the third or fourth lumbar level on the basis of the belief that these hips would eventually dislocate.

The procedure was performed on both sides in thirty-two children and on one side in a child who had an asymmetrical neurological lesion and in another child who needed additional procedures. An open reduction was performed if the hip was dislocated.

Operative Technique

The origin of the adductor longus, adductor brevis, and gracilis was transferred posteriorly to the ischium with use of the technique originally described by Nickel et al.³¹. The external oblique muscle was identified (the Thomas-Thompson procedure⁴¹) through an oblique abdominal incision and was transferred subcutaneously to the greater trochanter. The varus osteotomy, performed through a lateral approach, was stabilized with a Roger Anderson device. The child was placed in a hip-spica cast immediately after the operation.

The second hip was operated on two to three weeks after the first. If the second operation was performed two weeks after, the Roger Anderson device was left in place and was then removed three weeks after the first operation through a window in the spica cast. The hip-spica cast was worn for six weeks after the second operation. Radiographs were made after the cast was removed.

Results

Introduction | Materials and Methods | Results | Discussion | References

The average duration of follow-up was 10.9 years (range, 0.7 to 20.0 years) (Table I). Of the two patients who had a unilateral procedure, one (Case 7) had a markedly asymmetrical lesion, which was believed to be at the first lumbar level on the left. On the basis of the assumption that one stable hip was better than none, the index procedure was performed on the right hip and a varus osteotomy was performed on the left hip, which dislocated six years later. The second patient (Case 18) had a lesion at the fifth lumbar level on the right and an adductor transfer was not performed on this side. The hip on this side, which was not included in this study, was still located and had a full range of motion at the latest follow-up examination.

After the operation, eight children had progressive loss of motor function. Contractures developed in all eight, and scoliosis also developed in seven. At the follow-up examination, the neurological status of these children had deteriorated so much that, if they had had similar findings at the time of the initial evaluation, they would not have been candidates for the operation.

Two factors influenced the need for additional procedures as well as the success of the index operation. The first was the severity of the instability of the hip before the operation. The greater the degree of initial subluxation or instability, the greater the probability that more than one procedure would be necessary to maintain stability. The results in the dislocated hips were dismal. The second factor was a history of deteriorating neurological function.

The center-edge angle⁴² was low and the migration index was high when the acetabulum was shallow and deficient. However, neither of these measurements were helpful in the prediction of clinical or radiographic stability. Stability of the hip did not determine the ability to walk or the need for bracing. All of the children walked during early childhood. The ability to walk was altered by a progressive loss of motor function. Twenty-one of the twenty-six children who did not lose neurological function were so-called community ambulators²¹. One child did not walk because of a chronic deep ulceration on the plantar aspect of the foot following unsuccessful revision of a clubfoot.

The transfer of the external oblique muscle did not alter the ability to abduct the hip. Hip flexion contractures of more than 15 degrees developed in seven of the eight children who lost neurological function; these contractures were the result of the loss of function and not of the operation. Such contractures also developed in two children who did not lose neurological function but in whom the hips dislocated. No hip contractures of more than 15 degrees developed in children in whom the hips were located or subluxated at the follow-up examination.

Hips at Risk for Dislocation

Twenty-four hips in eighteen children were thought to be at risk for dislocation (Table I). Six children (twelve hips) had a bilateral procedure because both hips were at risk. Five of the six remained neurologically stable. Two of the six children (three hips) needed additional procedures because of recurrent subluxation.

Eleven children who had one normal hip that was thought to be at risk for dislocation and an unstable hip had a bilateral procedure. Of the eight children (eight hips) who remained neurologically stable, none needed additional intervention but one child had redislocation of the hip. The remaining three children (three hips) lost neurological function and had no additional procedures. Two of these hips were located and one was dislocated at the latest follow-up examination.

One child (one hip) (Case 7) had the index procedure performed on the right hip, which was at risk, and had a varus osteotomy performed on the left. The right hip remained located and the left hip dislocated.

Hips with Acetabular Dysplasia

Four hips in three children had acetabular dysplasia (Table I). One child (Case 8), who was neurologically stable, had bilateral dysplasia. This child had bilateral corrective osteotomy to treat non-union at the osteotomy sites. Both hips remained located after the operation. One hip in a neurologically stable child (Case 9) remained subluxated. The remaining hip was in a child who had a loss of neurological function; this hip was located at the latest follow-up examination.

Subluxated Hips

Twenty hips in thirteen children were subluxated (Table I). Seven children (fourteen hips) had a bilateral procedure because both hips were subluxated. Six of these children remained neurologically stable; two (three hips) of the six needed additional procedures. All of the hips remained located. One child (two hips) (Case 17) had a loss of neurological function, and the hips remained subluxated even after additional procedures.

Three children (three hips) had one subluxated hip and one hip that was thought to be at risk. Of the two children (two hips) who remained neurologically stable, one needed an additional procedure; both hips remained located. The hip in the remaining child, who had a loss of neurological function, was still located at the follow-up examination, and the child had had no additional procedures. The contralateral hip, which was initially thought to be at risk, had dislocated, with an increasing loss of neurological function secondary to a tethered cord.

Two children (two hips) who had one subluxated hip and one dislocated hip remained neurologically stable and had no additional procedures. At the latest follow-up examination, one hip was located and the other was subluxated.

One child (one hip) who had unilateral subluxation had no additional procedures, and the hip remained located. She had a modified McKay procedure on the contralateral hip, but this was not included in the study. This patient had loss of neurological function.

Dislocated Hips Treated with a Pavlik Harness or Closed Reduction

Three children (five hips) had a dislocated hip at birth (Table I). Two of them (four hips) were treated with a Pavlik harness. Of these two children, one (two hips) remained neurologically stable with one located and one slightly subluxated hip. The other child (two hips) had a severe loss of neurological function. One hip was located and one was dislocated, but both were very stiff. This patient also had a spinal arthrodesis to the sacrum and could not sit in a wheelchair for several years because of the stiffness in the hips and spine.

One child (one hip) (Case 24) had unilateral dislocation that was treated with closed reduction and a hip-spica cast and, despite two additional operations, the hip remained severely subluxated.

Dislocatable Hips

Three dislocatable hips (three children) developed after birth (Table I). Two children (two hips) remained neurologically stable, but both needed additional procedures; at the latest follow-up examination, one hip was located and the other was slightly subluxated. The remaining child (one hip) had a loss of neurological function. One additional procedure was performed in this child. The hip remained located; however, the greater trochanter was very proximal secondary to treatment of a fracture of the femoral neck.

Hips with Primary Dislocation

Ten hips (seven children) had primary dislocation. Two of the three children who had bilateral dislocation at birth that was not initially treated remained neurologically stable. All four of the hips redislocated and no additional procedures were performed. One child (two hips), who had a loss of neurological function, had no additional procedures and both hips redislocated. Four children (four hips), two who had one dislocated hip and one hip that was considered at risk and two who had one dislocated hip and one subluxated hip, remained neurologically stable. Three hips needed additional procedures. Two of these hips redislocated and one was slightly subluxated.

Complications

Seven children had at least one complication. The hips of two children redislocated at the time of removal of the hip-spica cast; one was reduced successfully and the other was not. One child had fibrous non-union at the site of both osteotomies, and corrective osteotomies were performed. There was one superficial wound infection, one fracture at the site of the osteotomy, and one wire broke off within the femoral neck during placement and could not be retrieved. One child had a non-displaced fracture of the distal aspect of the femur, a superficial wound infection, and an ulcerated heel.

Discussion

Introduction | Materials and Methods | Results | Discussion | References

The premise that unopposed action of the psoas and adductors in children who have a myelomeningocele leads to subluxation and dislocation of the hip is based on a report by Carroll and Sharrard¹⁰, who suggested that the hips will ultimately dislocate in all children who have a lesion at the middle level of the lumbar spine. Operations to treat the expected dislocation of the hip have included release or transfer of the psoas tendon^{7,9,10,15,23,24,26,32,34,38,43}, varus osteotomy^13,22,30, and transfer of the adductor muscles^6,20,26,33. Other authors have maintained that a stable hip is not a prerequisite for walking by a child who has a myelomeningocele and have suggested that the rate of failure of operations performed to reduce dislocated hips is so high that they are not worthwhile^{2-4,11,12,15-17,19,21,22,35,38-40}. Findley et al.¹⁸ noted that, following a period of immobilization secondary to operative intervention, twenty of twenty-two adolescents had a decrease in the duration for which they could walk.

Recently, Broughton et al.⁸ questioned the assumption that all hips in children who have a lesion at the third or fourth lumbar level eventually dislocate. They reviewed the records of 802 children seen over a period of seventeen years and concluded that the rate of dislocation was much lower. They found that 42 per cent of hips in children who had a lesion at the third lumbar level, 67 per cent of hips in children who had a lesion at the fourth lumbar level, and 80 per cent of hips in children who had a lesion at the fifth lumbar level never dislocated or needed operative treatment. It should be mentioned that these percentages were estimated from graphs showing the rate of dislocation of the hip plotted against the age in years. There were two curves for each level, one for the observed rate of dislocation and the other for dislocations in hips that had been treated operatively. The rate of dislocation without the influence of an operation was estimated as being between the two curves. The authors then estimated the percentage of hips that would never dislocate from these graphs. They did not give the exact number of patients for each level of involvement, and it was difficult to estimate the denominator for each level.

Fraser et al.¹⁹ were less optimistic and reported that twenty-five (86 per cent) of twenty-nine hips in children who had a lesion at the third lumbar level and eight of nineteen hips in children who had a lesion at the fourth lumbar level dislocated during the first year of life. This variability in rates of dislocation might be explained by the work of McDonald et al.^27,28, who reported that the patterns of neurological involvement in myelomeningocele are generally much more complex than those described by Sharrard³⁷. It is possible that certain patterns of muscle strength and function that are traditionally thought to characterize lesions at the third or fourth lumbar level may be associated with dislocation of the hip.

The McKay hip-stabilization procedure is based on the assumption that a located hip increases the ability to walk of children who have a myelomeningocele of the lumbar spine. However, several authors^{2-4,11-13,16,17,19-22,35,38-40} have pointed out that such children walk regardless of whether the hips are located. These authors have maintained that the most important predictors of walking ability are the level of neurological involvement and the degree of motor power. Most of the investigators did not evaluate whether children in whom the hips are located use less energy to walk, have greater endurance, or have a better chance of maintaining their ability to walk as adults. Alman et al.¹ reported that children who have a stable hip consume less oxygen while walking; however, they did not show a direct correlation between walking and oxygen consumption. Lee and Carroll²⁴ found that children who have similar neurological status are twice as likely to be community ambulators²¹ if the hips are stable.

Although children who have a lesion at the third or fourth lumbar level are at risk for dislocation, it is not inevitable, which weakens the argument for prophylactic operative intervention. However, the McKay procedure can stabilize unstable hips, and the earlier the operation is performed the more likely it is to have a successful result. It is difficult to compare the results of various studies, as some reports do not include the results of regular neurological examinations; this is an important issue because there may be a loss of neurological and muscle function as the child grows older.

At our latest follow-up evaluation, there was a dislocation of one of the eight hips in the children who had a lesion at the third lumbar level and six (13 per cent) of the forty-five hips in the children who had a lesion at the fourth lumbar level at the time of the operation. These results suggest that operative intervention may make a difference in the maintenance of stability of the hip in a child who has a lesion at the third or fourth lumbar level. Four of the thirteen hips in the children who had a lesion at the fifth lumbar level were dislocated. This group was difficult to assess because the children had had instability of one or both hips preoperatively. Four children who did not lose neurological function were household ambulators. One child did not walk because of a chronic ulceration of the heel following operative revision of a clubfoot. All of the other children who did not lose neurological function remained community ambulators. This finding may support the value of maintaining a located hip, as several authors have suggested that children with myelomeningocele at a caudad level may have a decrease in ambulatory function as they enter the teenage years^12,18,21.

McKay suggested that transfer of the external oblique muscle better stabilizes the hip in the stance phase of gait and eliminates Trendelenberg gait. We found this transferred muscle to be very weak, and the children could not actively abduct the extremity even in the supine position. Dias et al.¹⁴ demonstrated that the external oblique muscle fires during the swing phase of gait and may allow for better control of the lower extremity during that phase and may contribute to independent walking. Yngve and Lindseth⁴³ showed that improved development of the hip is most consistent when transfer of the external oblique or iliopsoas muscle is combined with transfer of the adductor muscles. We believe that the improved stability of the hips in the patients in the present study, in contrast to those in the study of Broughton et al.⁸, was due to better muscle balance about the hip.

Thirteen hips in eleven children who remained neurologically stable had an additional procedure to maintain stability an average of eight years after the index procedure. These included three of the nineteen hips at risk, four of the sixteen subluxated hips, both of the hips that became dislocatable, the dislocated hip that had been initially treated with a spica cast, and three of the four hips with a dislocation that had not been treated previously in a child who did not have a contralateral dislocation. This additional procedure failed to achieve stability in the dislocated hip that had been treated with a spica cast and in two of the three dislocated hips that had not been treated previously. Most of the additional procedures were performed to correct subluxation; only one hip was dislocated. Like all other procedures to stabilize hips, the index operation was not effective in children who had bilateral irreducible dislocation. Similarly, of the five hips (five children) that dislocated in a child who did not have a contralateral dislocation, four were treated with repeat operations. Two of these hips had redislocated, one was severely subluxated, and one was slightly subluxated at the time of follow-up.

It is difficult to compare our findings with those of Broughton et al.⁸ because they did not indicate how they classified children who had lost neurological function. We based our analysis and conclusions on the neurological level at the time of the index operation, not at the time of the follow-up evaluation. The outcome was poorest in children whose neurological status deteriorated. Broughton et al. may have categorized a child who had a lesion at the fourth lumbar level at birth but one at the first lumbar level at the time of follow-up as having a lesion at the first lumbar level, while we categorized such a child as having a lesion at the fourth lumbar level. Therefore, it is possible that operative intervention may have been more effective than our data suggests.

The patients who lost neurological function had the highest rate of failure of the McKay procedure. The loss of neurological function was accompanied by severe scoliosis or hip contractures, or both. There was no way to avoid operating on these children as it was impossible to predict at infancy which of them would have a loss of neurological function. Intervention for a so-called tethered cord has recently come into practice at our institution, and it is our hope that this intervention will prevent neurological deterioration.

We no longer automatically operate on hips that are considered to be at risk because the child has a lesion at the third or fourth lumbar level, as recent data⁸ have indicated that they will not all become unstable. As we are able to salvage hips once they begin to subluxate, we carefully follow all of these patients clinically and radiographically and we perform a McKay hip-stabilization procedure at the earliest sign of instability. However, in an effort to maintain mechanical balance, we do operate bilaterally if one hip begins to subluxate. We do not operate on children who have a bilateral dislocation. In addition, we watch closely for signs of neurological changes that may portend a loss of function.

References

Introduction | Materials and Methods | Results | Discussion | References

Alman, B. A.; Bhandari, M.; and |and |Wright, J. G.: The dislocated hip in lower lumbar level spina bifida: a comparison of function with and without surgical relocation [abstract]. European J. Pediat. Surg.,4(Supplement 1): 44-45, 1994.4(Supplement 1)44 1994

Asher, M., and |and |Oslen, J.: Factors affecting the ambulatory status of patients with spina bifida cystica. J. Bone and Joint Surg.,65-A: 350-356, March 1983.65-A350 1983

Barden, G. A.; Meyer, L. C.; and |and |Stelling, F. H., III: Myelodysplastics—fate of those followed for twenty years or more. J. Bone and Joint Surg.,57-A: 643-647, July 1975.57-A643 1975

Bazih, J., and |and |Gross, R. H.: Hip surgery in the lumbar level myelomeningocele patient. J. Pediat. Orthop.,1: 405-411, 1981.1405 1981 [CrossRef]

Beaty, J. H., and |and |Canale, S. T.: Current concepts review. Orthopaedic aspects of myelomeningocele. J. Bone and Joint Surg.,72-A: 626-630, April 1990.72-A626 1990

Benton, L. J.; Salvati, E. A.; and |and |Root, L.: Reconstructive surgery in the myelomeningocele hip. Clin. Orthop.,110: 261-268, 1975.110261 1975 [PubMed][CrossRef]

Breed, A. L., and |and |Healy, P. M.: The midlumbar myelomeningocele hip: mechanism of dislocation and treatment. J. Pediat. Orthop.,2: 15-24, 1982.215 1982 [CrossRef]

Broughton, N. S.; Menelaus, M. B.; Cole, W. G.; and |and |Shurtleff, D. B.: The natural history of hip deformity in myelomeningocele. J. Bone and Joint Surg.,75-B(5): 760-763, 1993.75-B(5)760 1993

Bunch, W. H., and |and |Hakala, M. W.: Iliopsoas transfers in children with myelomeningocele. J. Bone and Joint Surg.,66-A: 224-227, Feb. 1984.66-A224 1984

Carroll, N. C., and |and |Sharrard, W. J. W.: Long-term follow-up of posterior iliopsoas transplantation for paralytic dislocation of the hip. J. Bone and Joint Surg.,54-A: 551-560, April 1972.54-A551 1972

Crandall, R. C.; Birkebak, R. C.; and |and |Winter, R. B.: The role of hip location and dislocation in the functional status of the myelodysplastic patient. A review of 100 patients. Orthopedics,12: 675-684, 1989.12675 1989 [PubMed]

De Souza, L. J., and |and |Carroll, N.: Ambulation of the braced myelomeningocele patient. J. Bone and Joint Surg.,58-A: 1112-1118, Dec. 1976.58-A1112 1976

Dias, L. S., and |and |Hill, J. A.: Evaluation of treatment of hip subluxation in myelomenigocele by intertrochanteric varus derotation femoral osteotomy. Orthop. Clin. North America,11: 31-37, 1980.1131 1980

Dias, L. S.; Thomas, S. S.; Robinson, C.; Porcelli, R.; and |and |Sarwark, J.: Hip dislocation in spina bifida—the external oblique transfer: a gait analysis evaluation. Orthop. Trans.,16: 624-625, 1992-1993.16624 1992-1993

Drummond, D. S.; Moreau, M.; and |and |Cruess, R. L.: The results and complications of surgery for the paralytic hip and spine in myelomeningocele. J. Bone and Joint Surg.,62-B(1): 49-53, 1980.62-B(1)49 1980

Feiwell, E.: Surgery of the hip in myelomeningocele as related to adult goals. Clin. Orthop.,148: 87-93, 1980.14887 1980 [PubMed]

Feiwell, E.; Sakai, D.; and |and |Blatt, T.: The effect of hip reduction on function in patients with myelomeningocele. Potential gains and hazards of surgical treatment. J. Bone and Joint Surg.,60-A: 169-173, March 1978.60-A169 1978

Findley, T. W.; Agre, J. C.; Habeck, R. V.; Schmalz, R.; Birkebak, R. R.; and |and |McNally, M. C.: Ambulation in the adolescent with myelomeningocele. I: early childhood predictors. Arch. Phys. Med. and Rehab.,68: 518-522, 1987.68518 1987

Fraser, R. K.; Hoffman, E. B.; Sparks, L. T.; and |and |Buccimazza, S. S.: The unstable hip and mid-lumbar myelomeningocele. J. Bone and Joint Surg.,74-B(1): 143-146, 1992.74-B(1)143 1992

Gugenheim, J. J.; Rosenthal, R. K.; Dabrowski, S.; and |and |Hall, J. E.: The adductor transfer in the high-risk hip in myelodysplasia: a preliminary report. Clin. Orthop.,132: 108-114, 1978.132108 1978 [PubMed]

Hoffer, M. M.; Feiwell, E.; Perry, R.; Perry, J.; and |and |Bonnett, C.: Functional ambulation in patients with myelomeningocele. J. Bone and Joint Surg.,55-A: 137-148, Jan. 1973.55-A137 1973

Huff, C. W., and |and |Ramsey, P. L.: Myelodysplasia. The influence of the quadriceps and hip abductor muscles on ambulatory function and stability of the hip. J. Bone and Joint Surg.,60-A: 432-443, June 1978.60-A432 1978

Jackson, R. D.; Padgett, T. S.; and |and |Donovan, M. M.: Posterior iliopsoas muscle transfer in myelodysplasia. J. Bone and Joint Surg.,61-A: 40-45, Jan. 1979.61-A40 1979

Lee, E. H., and |and |Carroll, N. C.: Hip stability and ambulatory status in myelomeningocele. J. Pediat. Orthop.,5: 522-527, 1985.5522 1985 [CrossRef]

Lindseth, R. E.: Part IV. Treatment of the lower extremity in children paralyzed by myelomeningocele (birth to 18 months). In Instructional Course Lectures, The American Academy of Orthopaedic Surgeons. Vol. 25, pp. 76-82. St. Louis, C. V. Mosby, 1976.

London, J. T., and |and |Nicholas, O.: Paralytic dislocation of the hip in myelodysplasia. The role of the adductor transfer. J. Bone and Joint Surg.,57-A: 501-506, June 1975.57-A501 1975

McDonald, C. M.; Jaffe, K. M.; Mosca, V. S.; and |and |Shurtleff, D. B.: Ambulatory outcome of children with myelomeningocele: effect of lower-extremity muscle strength. Devel. Med. and Child Neurol.,33: 482-490, 1991.33482 1991 [CrossRef]

McDonald, C. M.; Jaffe, K. M.; Shurtleff, D. B.; and |and |Menelaus, M. B.: Modifications to the traditional description of neurosegmental innervation in myelomeningocele. Devel. Med. and Child Neurol.,33: 473-481, 1991.33473 1991 [CrossRef]

McKay, D. W.; Jackman, K. V.; Nason, S. S.; and |and |Eng, G. E.: McKay hip stabilization in myelomeningocele [abstract]. Devel. Med. and Child Neurol.,18 (Supplement 37): 168-169, 1976.18 (Supplement 37)168 1976

Menelaus, M. B.: Progress in the management of the paralytic hip in myelomeningocele. Orthop. Clin. North America,11: 17-30, 1980.1117 1980

Nickel, V. L.; Perry, J.; Garrett, A.; and |and |Feiwell, E. N.: Paralytic dislocation of the hip. In Proceedings of The American Academy of Orthopaedic Surgeons. J. Bone and Joint Surg.,48-A: 1021, July 1966.48-A1021 1966

Parker, B., and |and |Walker, G.: Posterior psoas transfer and hip instability in lumbar myelomeningocele. J. Bone and Joint Surg.,57-B(1): 53-58, 1975.57-B(1)53 1975

Phillips, D. P., and |and |Lindseth, R. E.: Ambulation after transfer of adductors, external oblique, and tensor fascia lata in myelomeningocele. J. Pediat. Orthop.,12: 712-717, 1992.12712 1992 [CrossRef]

Root, L.; Dhawlikar, S.; Weiner, L. S.; Smith, J. W.; and |and |Cheng, R. L.: Ambulation in myelomeningocele. Contemp. Orthop.,25: 237-244, 1992.25237 1992

Rueda, J., and |and |Carroll, N. C.: Hip instability in patients with myelomeningocele. J. Bone and Joint Surg.,54-B(3): 422-431, 1972.54-B(3)422 1972

Samuelsson, L., and |and |Skoog, M.: Ambulation in patients with myelomeningocele: a multivariate statistical analysis. J. Pediat. Orthop.,8: 569-575, 1988.8569 1988 [CrossRef]

Sharrard, W. J. W.: The segmental innervation of the lower limb muscles in man. Ann. Roy. Coll. Surg.,35: 106-122, 1964.35106 1964

Sharrard, W. J. W.: Posterior iliopsoas transplantation in the treatment of paralytic dislocation of the hip. J. Bone and Joint Surg.,46-B(3): 426-444, 1964.46-B(3)426 1964

Sherk, H. H.; Uppal, G. S.; Lane, G.; and |and |Melchionni, J.: Treatment versus non-treatment of hip dislocations in ambulatory patients with myelomeningocele. Devel. Med. and Child Neurol.,33: 491-494, 1991.33491 1991 [CrossRef]

Stillwell, A., and |and |Menelaus, M. B.: Walking ability in mature patients with spina bifida. J. Pediat. Orthop.,3: 184-190, 1983.3184 1983 [CrossRef]

Thomas, L. I.; Thompson, T. C.; and |and |Straub, L. R.: Transplantation of the external oblique muscle for abductor paralysis. J. Bone and Joint Surg.,32-A: 207-217, Jan. 1950.32-A207 1950

Wiberg, G.: Studies on dysplastic acetabula and congenital subluxation of the hip joint. With special reference to the complication of osteo-arthritis. Acta Chir. Scandinavica,Supplementum 58: 1939.Supplementum 58 1939

Yngve, D. A., and |and |Lindseth, R. E.: Effectiveness of muscle transfers in myelomeningocele hips measured by radiographic indices. J. Pediat. Orthop.,2: 121-125, 1982.2121 1982 [CrossRef]

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TABLE I DATA ON THE PATIENTS

Case	Side	Neurological Level at Diag.	Age at Op. (Mos.)	Indications for Op.	Preop. Treatment	Open Reduct.	Complications	Add. Op.*	Duration of Follow-up (Yrs.)	Neurological Level at Follow-up	Hip Contract. >15°	Amb. Status²¹	Brace or Walking Aids†	Radiographic Status	Center-Edge Angle⁴²‡ (Degrees)	Migration Index of Reimers‡ (Degrees)	Scoliosis >30°	Add. Data
At risk bilat.
1	R	L3	14	At risk	—	N	—	Varus osteot., shelf proc. (86)	8.5	L3	N	Commun.	KAFO, Lofstrands	Located	30	0	N	—
	L	L3	15	At risk	—	N	—	Varus osteot., shelf proc. (86)	8.4	L3	N			Located	20	0
2	R	L4	16	At risk	—	N	—	—	12.2	L4	N	Commun.	AFO, canes	Trace sublux.	12	37	N	—
	L	L4	16	At risk	—	N	—	12.2	L4	N			Located	16	36
3	R	L4	19	At risk	—	N	—	—	10.7	L4	N	Commun.	AFO, canes	Located	22	15	N	—
	L	L4	20	At risk	—	N	—	Varus osteot., shelf proc. (78)	10.6	L4	N			Located	24	8
4	R	L4	14	At risk	—	N	—	11.8	L4	N	Commun.	AFO, canes	Located	8	40	N	—
	L	L4	14	At risk	—	N	—	—	11.8	L4	N	Located	14	43
5	R	L4	22	At risk	—	N	—	—	7.3	L4	N	Commun.	Canes	Located	32	19	N	—
	L	L4	23	At risk	—	N	—	—	7.2	L4	N			Located	37	12
6§	R	L4	18	At risk	—	N	—	Release, hip capsule (103)	20.0	L2	N	Non-amb.	Wheelchair	Sublux.	-10	60	Y	Loss, motor func.; contract.; scoliosis
	L	L4	18	At risk	—	N	—	Release, hip capsule (103)	20.0	L2/L3	N			Located	26	24
At risk unilat.
7	R	L4	36	At risk	—	N	—	—	6.1	L4	N	Commun.	AFO, canes	Located	30	10	N	—
Acetab. dys. bilat.
8	R	L5	16	Acetab. dys.	—	N	Non-union	Repair of non-union (16)	7.0	L5	N	Commun.	UCBL, canes	Located	14	26	N	—
	L	L5	16	Acetab. dys.	—	N	Non-union	Repair of non-union (16)	7.0	L5	N			Located	12	21
Acetab. dys./at risk¶
9	L	L4	33	Acetab. dys.	—	N	—	—	17.4	L4	N	House.	Holds furniture, wheelchair	Sublux.	11	36	N	Could be commun. amb. but refuses
	R	L4	33	At risk	—	N	—	—	17.4	L4	N			Located	30	15
10§	L	L5	26	Acetab. dys.	—	N	Fract., osteot. site after cast removal	—	18.7	L3	Y	House. (prim. transfer & makes bed)	Wheelchair	Located	30	0	Y	Loss, motor func.; contract.; scoliosis
	R	L5	27	At risk	—	N	—	—	18.6	L3	N			Located	14	35
Sublux. bilat.
11	R	L3	37	Sublux.	—	N	—	—	0.7	L3	N	Commun.	AFO, walker	Located	14	17	N	—
	L	L3	37	Sublux.	—	N	Broken wire, fem. neck	—	0.7	L3	N			Located	14	0	N
12	R	L4	25	Sublux.	—	N	—	—	0.9	L4	N	House.	AFO, walker	Located	10	15	N	—
	L	L4	26	Sublux.	—	N	—	—	0.8	L4	N			Located	20	0	N
13	R	L4	12	Sublux.	—	N	—	—	6.8	L4	N	Commun.	AFO	Located	30	11	N	—
	L	L4	13	Sublux.	—	N	—	—	6.7	L4	N			Located	22	14
14	R	L4	9	Sublux.	—	N	—	Varus osteot., shelf proc. (91)	10.7	L4	N	Commun.	AFO, canes	Located	18	18	N	—
	L	L4	10	Sublux.	—	N	—	Varus osteot., shelf proc. (90)	10.6	L4	N			Located	0	0
15	R	L4	26	Sublux.	—	N	—	—	3.9	L4	N	Commun.	KAFO, canes	Located, very deficient acetab.	16	26	N	—
	L	L4	25	Sublux.	—	N	—	—	4.0	L4	N			Located very deficient acetab.	0	33
16	R	L4	39	Sublux.	—	N	—	Varus osteot., shelf proc. (90)	7.3	L4	N	Commun.	AFO, canes	Located	20	0	N	—
	L	L4	39	Sublux.	—	N	—	—	7.3	L4	N			Located	23	11
17§	R	L4	16	Sublux.	—	N	—	Varus osteot., shelf proc., tensor release (61)	11.7	L1	Y	Non-amb.	Wheelchair	Sublux.	0	44	Y	Loss, motor func.; contract.; scoliosis
	L	L4	17	Sublux.	—	N	—	Tensor release (61)	11.6	L1	Y			Sublux.	24	31
Sublux. unilat.
18§	L	L3	13	Sublux.	—	N	—	—	19.4	L2	Y	House.	KAFO, canes, wheelchair	Located	14	15;severely deficient L. acetab., not sublux.	Y	Loss, motor func.; contract.; scoliosis
Sublux./at risk¶
19	R	L3	14	Sublux.	—	N	—	—	3.9	L3	N	Commun.	KAFO, canes	Located	34	14	N	—
	L	L3	15	At risk	—	N	—	—	3.8	L3	N			Located	8	40
20	R	L5	14	Sublux.	—	N	—	Varus osteot. (144)	16.8	L5	N	Commun.	AFO	Located	19	4	N	—
	L	L5	15	At risk	—	N	—	—	16.8	L5	N			Located	21	17
21§	L	L5	15	Sublux.	—	N	—	—	10.7	L3	N	Non-func.	HKAFO, walker, wheelchair	located	40	0	Y	Loss, motor func.; contract.; scoliosis
	R	L5	14	At risk	—	N	Non-displaced fract., distal aspect of femur; superfic. wound infect.; ulcer, heel	—	10.8	L3	Y			Dislocated	NA	NA
Dislocated at birth bilat., treated with closed reduct.
22	R	L4	18	Dislocated	Pavlik harness (reduced)	N	—	—	9.3	L4	N	Commun.	AFO, canes	Located	15	31	N	—
	L	L4	18	Dislocated	Pavlik harness (reduced)	N	—	—	9.3	L4	N			Slightly sublux.	0	51
23§	R	L5	28	Dislocated	Pavlik harness (reduced)	N	Superfic, wound infect.	—	13.6	L3	Y	Non-func.	KAFO, canes, wheelchair	Dislocated	NA	100	Y	Loss, motor func.; contract.; scoliosis
	L	L5	28	Dislocated	Pavlik harness (reduced)	N	—	—	13.6	L3	Y			Located	42	0
Dislocated at birth, treated with closed reduct./at risk¶
24	R	L4	18	Dislocated	Closed reduct., hip-spica cast	N	—	Shelf proc. (45), fem. short., Chiari osteot. (101)	14.9	L3	N	Commun.	KAFO, canes	Severely sublux.	-12	58	N	—
	L	L4	18	At risk	—	N	—	—	14.9	L4	N			Located	30	0
Became dislocatable/at risk¶
25	L	L4	21	Dislocatable	—	N	—	Varus osteot., shelf proc. (56)	14.5	L4	N	House.	KAFO, canes	Slightly sublux.	10	31	N	—
	R	L4	21	At risk	—	N	—	—	14.5	L4	N			Located	30	0
26	L	L4	19	Dislocatable	—	N	—	Varus osteot., Chiari osteot. (84)	10.9	L4	N	Commun.	AFO, canes	Located	22	28	N	—
	R	L4	18	At risk	—	N	—	—	10.8	L4	N			Located	24	15
27§	R	L4	32	Dislocatable	—	N	—	Acetab. aug. (63)	11.7	T12-L1	Y	Non-amb.	Wheelchair	Fem. head located; non-union with high-riding greater trochant., fem. neck fract.	6	63	Y	Loss, motor func.; contract.; scoliosis
	L	L4	32	At risk	—	N	—	—	11.7	T12-L1	Y			Located	6	35
Dislocated bilat.
28	R	L4	42	Dislocated	—	Y	—	—	15.7	L4	Y	House.	Walker	Dislocated	NA	NA	N	—
	L	L4	42	Dislocated	—	Y	—	—	15.7	L4	Y			Dislocated	NA	NA
29	R	L5	15	Dislocated	—	Y	—	—	19.5	L5	N	Commun.	Canes	Dislocated	NA	100	N	—
	L	L5	15	Dislocated	—	Y	—	—	19.5	L4	N			Dislocated	NA	100
30§	R	L4	10	Dislocated	—	Y	—	—	10.5	L1-L2	Y	Non-func.	KAFO, wheelchair	Dislocated	NA	NA	N	Loss, motor func.; contract.
	L	L4	10	Dislocated	—	Y	—	—	10.5	L1-L2	Y			Dislocated	NA	NA
Dislocated/at risk¶
31	L	L3	7	Dislocated	—	Y	—	Varus osteot., open reduct., Pemberton osteot. (55)	18.7	L3	N	Commun.	AFO, canes wheelchair for distance	Dislocated	NA	100	N	—
	R	L4	18	At risk	—	N	—	—	17.8	L4	N			Dislocated	NA	NA
32	L	L4	15	Dislocated (init. reducible)	Pavlik harness (failed)	Y	Redislocated (immed. postop.)	Varus osteot., open reduct., psoas recess. (21)	7.4	L4	Y	Commun.	KAFO	Dislocated	NA	NA	N	—
	R	L4	16	At risk	—	N	—	—	7.3	L4	N		AFO	Located	22	3
Dislocated/sublux.¶
33	R	L4	12	Dislocated	—	Y	—	—	7.8	L4	N	Non-amb.	Wheelchair	Located; coxa vara, 78 degrees; premature growth plate arrest	24	0	N	Non-amb. due to chronic heel ulcer after revision of clubfoot
	L	L4	13	Sublux.	—	N	—	—	7.7	L4	N			Sublux	18	36
34	L	L4	11	Dislocated	—	Y	Rapid redislocation	Varus osteot., open reduct. (9)	7.3	L4	N	Commun.	AFO, canes	Slightly sublux., small fem. head	19	26	N	—
	R	L5	11	Sublux.	—	N	—	—	7.3	L5	N			Located	20	29

Add to My JBJS

TABLE I DATA ON THE PATIENTS

Case	Side	Neurological Level at Diag.	Age at Op. (Mos.)	Indications for Op.	Preop. Treatment	Open Reduct.	Complications	Add. Op.*	Duration of Follow-up (Yrs.)	Neurological Level at Follow-up	Hip Contract. >15°	Amb. Status²¹	Brace or Walking Aids†	Radiographic Status	Center-Edge Angle⁴²‡ (Degrees)	Migration Index of Reimers‡ (Degrees)	Scoliosis >30°	Add. Data
At risk bilat.
1	R	L3	14	At risk	—	N	—	Varus osteot., shelf proc. (86)	8.5	L3	N	Commun.	KAFO, Lofstrands	Located	30	0	N	—
	L	L3	15	At risk	—	N	—	Varus osteot., shelf proc. (86)	8.4	L3	N			Located	20	0
2	R	L4	16	At risk	—	N	—	—	12.2	L4	N	Commun.	AFO, canes	Trace sublux.	12	37	N	—
	L	L4	16	At risk	—	N	—	12.2	L4	N			Located	16	36
3	R	L4	19	At risk	—	N	—	—	10.7	L4	N	Commun.	AFO, canes	Located	22	15	N	—
	L	L4	20	At risk	—	N	—	Varus osteot., shelf proc. (78)	10.6	L4	N			Located	24	8
4	R	L4	14	At risk	—	N	—	11.8	L4	N	Commun.	AFO, canes	Located	8	40	N	—
	L	L4	14	At risk	—	N	—	—	11.8	L4	N	Located	14	43
5	R	L4	22	At risk	—	N	—	—	7.3	L4	N	Commun.	Canes	Located	32	19	N	—
	L	L4	23	At risk	—	N	—	—	7.2	L4	N			Located	37	12
6§	R	L4	18	At risk	—	N	—	Release, hip capsule (103)	20.0	L2	N	Non-amb.	Wheelchair	Sublux.	-10	60	Y	Loss, motor func.; contract.; scoliosis
	L	L4	18	At risk	—	N	—	Release, hip capsule (103)	20.0	L2/L3	N			Located	26	24
At risk unilat.
7	R	L4	36	At risk	—	N	—	—	6.1	L4	N	Commun.	AFO, canes	Located	30	10	N	—
Acetab. dys. bilat.
8	R	L5	16	Acetab. dys.	—	N	Non-union	Repair of non-union (16)	7.0	L5	N	Commun.	UCBL, canes	Located	14	26	N	—
	L	L5	16	Acetab. dys.	—	N	Non-union	Repair of non-union (16)	7.0	L5	N			Located	12	21
Acetab. dys./at risk¶
9	L	L4	33	Acetab. dys.	—	N	—	—	17.4	L4	N	House.	Holds furniture, wheelchair	Sublux.	11	36	N	Could be commun. amb. but refuses
	R	L4	33	At risk	—	N	—	—	17.4	L4	N			Located	30	15
10§	L	L5	26	Acetab. dys.	—	N	Fract., osteot. site after cast removal	—	18.7	L3	Y	House. (prim. transfer & makes bed)	Wheelchair	Located	30	0	Y	Loss, motor func.; contract.; scoliosis
	R	L5	27	At risk	—	N	—	—	18.6	L3	N			Located	14	35
Sublux. bilat.
11	R	L3	37	Sublux.	—	N	—	—	0.7	L3	N	Commun.	AFO, walker	Located	14	17	N	—
	L	L3	37	Sublux.	—	N	Broken wire, fem. neck	—	0.7	L3	N			Located	14	0	N
12	R	L4	25	Sublux.	—	N	—	—	0.9	L4	N	House.	AFO, walker	Located	10	15	N	—
	L	L4	26	Sublux.	—	N	—	—	0.8	L4	N			Located	20	0	N
13	R	L4	12	Sublux.	—	N	—	—	6.8	L4	N	Commun.	AFO	Located	30	11	N	—
	L	L4	13	Sublux.	—	N	—	—	6.7	L4	N			Located	22	14
14	R	L4	9	Sublux.	—	N	—	Varus osteot., shelf proc. (91)	10.7	L4	N	Commun.	AFO, canes	Located	18	18	N	—
	L	L4	10	Sublux.	—	N	—	Varus osteot., shelf proc. (90)	10.6	L4	N			Located	0	0
15	R	L4	26	Sublux.	—	N	—	—	3.9	L4	N	Commun.	KAFO, canes	Located, very deficient acetab.	16	26	N	—
	L	L4	25	Sublux.	—	N	—	—	4.0	L4	N			Located very deficient acetab.	0	33
16	R	L4	39	Sublux.	—	N	—	Varus osteot., shelf proc. (90)	7.3	L4	N	Commun.	AFO, canes	Located	20	0	N	—
	L	L4	39	Sublux.	—	N	—	—	7.3	L4	N			Located	23	11
17§	R	L4	16	Sublux.	—	N	—	Varus osteot., shelf proc., tensor release (61)	11.7	L1	Y	Non-amb.	Wheelchair	Sublux.	0	44	Y	Loss, motor func.; contract.; scoliosis
	L	L4	17	Sublux.	—	N	—	Tensor release (61)	11.6	L1	Y			Sublux.	24	31
Sublux. unilat.
18§	L	L3	13	Sublux.	—	N	—	—	19.4	L2	Y	House.	KAFO, canes, wheelchair	Located	14	15;severely deficient L. acetab., not sublux.	Y	Loss, motor func.; contract.; scoliosis
Sublux./at risk¶
19	R	L3	14	Sublux.	—	N	—	—	3.9	L3	N	Commun.	KAFO, canes	Located	34	14	N	—
	L	L3	15	At risk	—	N	—	—	3.8	L3	N			Located	8	40
20	R	L5	14	Sublux.	—	N	—	Varus osteot. (144)	16.8	L5	N	Commun.	AFO	Located	19	4	N	—
	L	L5	15	At risk	—	N	—	—	16.8	L5	N			Located	21	17
21§	L	L5	15	Sublux.	—	N	—	—	10.7	L3	N	Non-func.	HKAFO, walker, wheelchair	located	40	0	Y	Loss, motor func.; contract.; scoliosis
	R	L5	14	At risk	—	N	Non-displaced fract., distal aspect of femur; superfic. wound infect.; ulcer, heel	—	10.8	L3	Y			Dislocated	NA	NA
Dislocated at birth bilat., treated with closed reduct.
22	R	L4	18	Dislocated	Pavlik harness (reduced)	N	—	—	9.3	L4	N	Commun.	AFO, canes	Located	15	31	N	—
	L	L4	18	Dislocated	Pavlik harness (reduced)	N	—	—	9.3	L4	N			Slightly sublux.	0	51
23§	R	L5	28	Dislocated	Pavlik harness (reduced)	N	Superfic, wound infect.	—	13.6	L3	Y	Non-func.	KAFO, canes, wheelchair	Dislocated	NA	100	Y	Loss, motor func.; contract.; scoliosis
	L	L5	28	Dislocated	Pavlik harness (reduced)	N	—	—	13.6	L3	Y			Located	42	0
Dislocated at birth, treated with closed reduct./at risk¶
24	R	L4	18	Dislocated	Closed reduct., hip-spica cast	N	—	Shelf proc. (45), fem. short., Chiari osteot. (101)	14.9	L3	N	Commun.	KAFO, canes	Severely sublux.	-12	58	N	—
	L	L4	18	At risk	—	N	—	—	14.9	L4	N			Located	30	0
Became dislocatable/at risk¶
25	L	L4	21	Dislocatable	—	N	—	Varus osteot., shelf proc. (56)	14.5	L4	N	House.	KAFO, canes	Slightly sublux.	10	31	N	—
	R	L4	21	At risk	—	N	—	—	14.5	L4	N			Located	30	0
26	L	L4	19	Dislocatable	—	N	—	Varus osteot., Chiari osteot. (84)	10.9	L4	N	Commun.	AFO, canes	Located	22	28	N	—
	R	L4	18	At risk	—	N	—	—	10.8	L4	N			Located	24	15
27§	R	L4	32	Dislocatable	—	N	—	Acetab. aug. (63)	11.7	T12-L1	Y	Non-amb.	Wheelchair	Fem. head located; non-union with high-riding greater trochant., fem. neck fract.	6	63	Y	Loss, motor func.; contract.; scoliosis
	L	L4	32	At risk	—	N	—	—	11.7	T12-L1	Y			Located	6	35
Dislocated bilat.
28	R	L4	42	Dislocated	—	Y	—	—	15.7	L4	Y	House.	Walker	Dislocated	NA	NA	N	—
	L	L4	42	Dislocated	—	Y	—	—	15.7	L4	Y			Dislocated	NA	NA
29	R	L5	15	Dislocated	—	Y	—	—	19.5	L5	N	Commun.	Canes	Dislocated	NA	100	N	—
	L	L5	15	Dislocated	—	Y	—	—	19.5	L4	N			Dislocated	NA	100
30§	R	L4	10	Dislocated	—	Y	—	—	10.5	L1-L2	Y	Non-func.	KAFO, wheelchair	Dislocated	NA	NA	N	Loss, motor func.; contract.
	L	L4	10	Dislocated	—	Y	—	—	10.5	L1-L2	Y			Dislocated	NA	NA
Dislocated/at risk¶
31	L	L3	7	Dislocated	—	Y	—	Varus osteot., open reduct., Pemberton osteot. (55)	18.7	L3	N	Commun.	AFO, canes wheelchair for distance	Dislocated	NA	100	N	—
	R	L4	18	At risk	—	N	—	—	17.8	L4	N			Dislocated	NA	NA
32	L	L4	15	Dislocated (init. reducible)	Pavlik harness (failed)	Y	Redislocated (immed. postop.)	Varus osteot., open reduct., psoas recess. (21)	7.4	L4	Y	Commun.	KAFO	Dislocated	NA	NA	N	—
	R	L4	16	At risk	—	N	—	—	7.3	L4	N		AFO	Located	22	3
Dislocated/sublux.¶
33	R	L4	12	Dislocated	—	Y	—	—	7.8	L4	N	Non-amb.	Wheelchair	Located; coxa vara, 78 degrees; premature growth plate arrest	24	0	N	Non-amb. due to chronic heel ulcer after revision of clubfoot
	L	L4	13	Sublux.	—	N	—	—	7.7	L4	N			Sublux	18	36
34	L	L4	11	Dislocated	—	Y	Rapid redislocation	Varus osteot., open reduct. (9)	7.3	L4	N	Commun.	AFO, canes	Slightly sublux., small fem. head	19	26	N	—
	R	L5	11	Sublux.	—	N	—	—	7.3	L5	N			Located	20	29