Injuries and Polio

Fig. 39.1

(a, b). The typical appearance of foot drop following injection injuries. In these cases the deformities were mild and flexible on examination

../images/270913_2_En_39_Chapter/270913_2_En_39_Fig2_HTML.jpg — Fig. 39.2

Trophic ulcer in an insensate area of the foot in a patient with PIP

A surgical algorithm has been developed by the first author (JNP) for post-injection foot drop based on experience in Uganda (Table 39.1). Important pretreatment considerations include (1) degree and rigidity of heel varus, (2) presence of full passive range of motion, and (3) function of tibialis posterior.

Table 39.1

Treatment options for common foot deformities associated with post-injection paralysis and polio

Deformity	Causes	Treatment options
Equinus	1. Weak DF (TA, EHL, EDC, PB) 2. Strong PF (GS, FHL, FDL)	1. Gastrocsoleus lengthening
Equinovarus	1. Weak DF/EV (TA, EHL, EDC, peroneals) 2. Strong PF/IV (GS, FHL, FDL, TP)	1. TA transfer to middle cuneiform 2. TP transfer to third cuneiform 3. Subtalar stabilization
Equinovalgus	1. Weak DF/INV (TA) 2. Strong PF/EV (GS, TP, EHL, EDC, FHL,FDL, peroneals)	1. Gastrocsoleus lengthening 2. Transfer of peroneal tendons to dorsum of foot 3. Subtalar stabilization
Calcaneus or calcaneocavus	1. Weak PF [GS] 2. Strong DF/INV or EV	1. Ankle-foot orthosis 2. GS weak or absent: consider transferring all available muscles to calcaneus (PL, PB, TP, FHL) 3.Tenodesis of the tendoachilles to the fibula 4. Calcaneal osteotomy or triple arthrodesis
Cavovarus	1. Weak DF/EV [TA, peroneals] 2. Strong PF/INV (GS, TP, FHL, FDL ± EHL, EDC)	1. Percutaneous TAL, PF release 2. TP transfer to dorsum of foot 3. Subtalar stabilization 4. Transfer EHL to first metatarsal neck (Jones)

DF dorsiflexion, PF plantar flexion, INV inversion, EV eversion, TA tibialis anterior, TP tibialis posterior, GS gastrocsoleus, PL peroneus longus, PB peroneus brevis, EHL extensor hallucis longus, FHL flexor hallucis longus, EDC extensor digitorum communis, FDL flexor digitorum longus, PF plantar fascia

A flexible foot drop can be treated with an ankle-foot orthosis (AFO). Routine posterior tibial tendon transfer is recommended, if its strength is grade 4–5, to restore muscle balance and minimize or eliminate the need for an orthosis. We suggest the posterior tibialis be brought subcutaneously to the dorsum and into a tunnel in the third cuneiform (Fig. 39.3) or sutured to the peroneus tertius. Transfer through the interosseous membrane is vulnerable to adhesions and may function as a tenodesis. When fixed deformity is present, preliminary soft tissue release, osteotomy, or arthrodesis may be necessary before tendon transfer.

../images/270913_2_En_39_Chapter/270913_2_En_39_Fig3_HTML.jpg — Fig. 39.3

The tibialis posterior is transferred subcutaneously, inserted through a drill hole into the third cuneiform, and secured with a suture through a button on the plantar surface of the foot

Subtalar stabilization should be performed in all cases of tibialis posterior tendon transfer to prevent the foot from collapsing into planovalgus. In children under 10 years, we recommend an extra-articular technique (Grice-Green or Dennyson-Fulford). The Dennyson-Fulford, performed using corticocancellous graft with internal fixation, produces more predictable results in our experience. A full preoperative range of subtalar motion is needed; otherwise, a posteromedial soft tissue release is necessary. A triple arthrodesis should be performed in adolescents and adults, with the advantage of making medial soft tissue release unnecessary and allowing superior correction in very stiff cases. If a bony procedure is needed, some surgeons prefer to stage the tendon transfer, to minimize disuse atrophy from prolonged casting (see Chap. 35 for further discussion on correction of foot deformities).

With an isolated soft tissue release or tendon transfer, patients require 4–6-week cast immobilization followed by an AFO (ankle-foot orthosis) . Bony procedures require 8–12-week immobilization. Physiotherapy for tendon reeducation is necessary immediately after cast removal, and the AFO can often be discontinued when rehabilitation is completed, usually after 6 months.

Gluteal and Quadriceps Fibrosis

Fibrosis of the gluteal or quadriceps muscles is associated with injections into the muscles, often multiple. Numerous drugs have been implicated, but in malarial areas, quinine is the main culprit. It is thought that quinine is a potent producer of muscle necrosis with subsequent fibrotic contracture. In certain Asian countries, penicillin has been implicated. Gluteal fibrosis (GF) is thought to be caused by microabscesses in the setting of substerile technique, the intrinsic fibrosis-inducing effects of particular medications, mechanical disruption of the muscle tissue planes, or a combination of these and other factors that are not well understood.

Patients diagnosed with GF present clinically with an awkward gait, especially with running and obligate external rotation and abduction of the hip on attempting hip flexion due to limitation of gluteal excursion. They show a combination of muscle wasting (Fig. 39.4) and fibrotic hypertrophy. They cannot sit comfortably or squat except with the legs externally rotated (Fig. 39.5). The condition is usually described as bilateral and frequently diagnosed in school age children. GF has been reported from throughout the world, with high rates noted particularly in China, Taiwan, and recently in areas of sub-Saharan Africa.

../images/270913_2_En_39_Chapter/270913_2_En_39_Fig4_HTML.jpg — Fig. 39.4

Patient with gluteal fibrosis and marked muscle atrophy of the gluteal muscles

../images/270913_2_En_39_Chapter/270913_2_En_39_Fig5_HTML.jpg — Fig. 39.5

Patient with gluteal fibrosis forced to squat in the “butterfly position” with lower extremities externally rotated due to the contracture

Surgical treatment of GF includes a variety of open surgical techniques in the lateral decubitus position with intraoperative identification and release of fibrous bands. Incision placement varies, ranging from just posterior to the greater trochanter to directly over the buttock. Full-thickness skin flaps are raised exposing the gluteus maximus and notable fibrotic bands. The gluteus maximus, gluteus medius, and gluteus minimus are sequentially released with diathermy while protecting the sciatic nerve (Fig. 39.6). Complete release is achieved when hip flexion greater than 90° and internal rotation beyond neutral are possible. Range of motion exercises, crutch walking, and gait training are started as soon as possible; rehabilitation takes 2–3 months.

../images/270913_2_En_39_Chapter/270913_2_En_39_Fig6_HTML.jpg — Fig. 39.6

The surgical scar following release of gluteal contracture

With quadriceps fibrosis and contracture, the child walks with a stiff knee gait. A modified Judet quadricepsplasty is recommended. Proximal release is a critical component, as distal release alone is less effective and has a higher incidence of weakness, extensor lag, or quadriceps rupture. A lateral incision extends proximally from the distal femoral metaphysis. The vasti are released extra-periosteally, and multiple transverse incisions may be necessary in the iliotibial band and vastus fascia. The rectus femoris is released from the anterior inferior iliac spine through a separate anterior incision.

The contracture can be limited to just the rectus femoris, as demonstrated in the Duncan-Ely test (with the patient prone, the knee is flexed, causing the pelvis to lift from the table). In this case the rectus femoris is released before considering quadricepsplasty. Postoperative therapy involves immediate passive range of motion and early active range of the knee.

Residua of Acute Poliomyelitis

Introduction

Besides the several hundred new cases of acute poliomyelitis each year, thousands of patients suffer from the residua of the disease. Polio is an enterovirus infected via the fecal-oral route. Most infected patients will have a self-limited diarrhea but can shed virus from the GI tract for up to 1 month. Approximately 50% of those infected will show no clinical illness. Another 48% will have an abortive illness consisting of muscle aches or headaches characteristic of an irritation of the meningeal linings of the brain and spinal cord. Only 2% will develop typical flaccid muscle paralysis.

In those with paralysis, the virus enters the central nervous system through peripheral nerve roots and migrates proximally to the anterior horn cells of the spinal cord, causing nerve cell injury and flaccid paralysis. Following the acute illness, characterized by high fevers, muscle pain, and varying degrees of paralysis, two-thirds of patients will recover, usually within the first 12 months, with a higher incidence of recovery in children compared to adults.

Polio presents as a nonprogressive, asymmetric flaccid motor paralysis or paraparesis. The diagnosis requires a history of a febrile illness, exam with normal sensation, no spasticity, and no bowel or bladder involvement. The differential diagnosis includes (1) post-cerebral malaria (spasticity, cognitive abnormalities); (2) Guillain-Barré or transverse myelitis (symmetric flaccid paralysis, sensory abnormalities); (3) konzo, lathyrism, and tropical myelopathy (spasticity, ataxia); (4) Burkitt’s lymphoma of spine, spinal tumors, and spinal tuberculosis (progressive, spasticity before flaccidity, bowel and bladder abnormalities, sensory involvement); and (5) post-injection paralysis.

Principles for polio treatment can be applied to other flaccid paralyses, remembering that the goal of surgery is functional restoration. Patient selection is critical, and surgical treatment must be complemented by rehabilitation and bracing.

Contractures are caused by muscle imbalance and positional or mechanical factors but also by interstitial fibrosis from the inflammatory myositis during the initial viremic infection. Contractures of the tensor fascia femoris and iliotibial band (ITB) are frequent and all but pathognomonic for polio confirmed with the Ober test. This test is performed with the patient lying on their uninvolved side, with the uninvolved knee and hip flexed. While stabilizing the pelvis, the leg to be tested is extended, internally rotated, and adducted toward the table (Fig. 39.7). The abduction contracture prevents the leg from reaching the Table.