Fractures in the Paralytic Extremity

Gürsel , Egemen Ayhan, Tüzün Fırat

Abstract

Muscle function is an important part of preserving bone structure and function. Many studies suggest bone loss in different paralytic conditions including spinal cord injury, stroke, peripheral nerve injuries, and even botulinum toxin injections. Paralysis leads bone mineral loss and fractures in addition to the systemic adverse effects of the pathological condition. Even minor loadings may result with fractures in paralytic disorders. The preceding long-lasting limited mobility contributes to higher morbidity and mortality following fractures in paralytic patients. Therefore, knowledge of paralytic bone mineral loss and fractures may help to prevent bone mineral loss–related fractures and morbidities. This chapter provides extensive knowledge on the causes of bone mineral loss and fracture in different paralysis models. Also, prevention and management methods in fractures are mentioned. Nevertheless, this field requires more research especially in lower motor neuron lesions.

Keywords: paralysis, fracture, spinal cord injury, stroke, botulinum toxin

11.1 Introduction

Loss of musculoskeletal functions secondary to dysfunction of the central and peripheral nervous system is mostly a devastating injury. Many patients are young, and treatment possibilities are usually limited to improve their quality of life, to regain self-ambulation, and to prolong survival. Neural involvement, as well as its secondary consequences such as decreased mobility and diminished sensation related to primary disease can be excruciating. Treatment of primary neural problems and prevention of secondary complications may help improve the quality of life.

Patients with central and peripheral nervous system disorders may have an increased risk of sustaining serious fractures of spine and extremities. Fractures may develop at the time of the neural injury, such as fractures of clavicle at birth in babies with brachial plexus birth palsy, or later in the course of the disease such as hip fractures in patients with paraplegia.

Loss of bone mineral density (BMD) which can be related to muscle paralysis and metabolic changes decreases mechanical resistance of bone. Consequently, fractures are possible even under physiological loads or during physical therapy. Depending on neural involvement, limbs may have different levels of muscle paralysis and loss of sensation. Pattern of muscle weakness and dystonia, duration of immobilization, altered metabolic and hormonal conditions, and duration of the disease affect the bone density in various ways.1 The risk of fracture may vary depending on the underlying condition and duration. The majority of these fractures occurs during chronic conditions. Fracture in a paralytic extremity causes severe functional limitation, even if it was not used functionally before the fracture.

The most common sites of fracture in paralytic disorders are the diaphysis and supracondylar region of femur. The involvement of upper extremity and hand are relatively rare. In this section, etiology, pathogenesis, diagnosis, and possible treatment modalities in the fractures of paralytic upper extremity are reviewed.

11.2 Basic Science

11.2.1 Changes in Bone

Spinal Cord Injury

Complete spinal cord injury (SCI) causes an instant paralysis of muscles and disuse atrophy of the paralyzed extremities. This is followed by connective tissue invasion, vascular system disruption, cartilage degeneration, and bone mass loss.2–5 Osteoporosis is also a common finding in individuals with SCI.^6,7 This is due to unloading of extremity similar to those observed with aging, bed rest, or disuse atrophy.^8,9 Loss of bone mass is associated with deterioration of trabecular microarchitecture.^7,10,11 The imbalance of bone turnover favoring resorption occurs after injury, peaks at third to fifth months, reaches to a steady state at 2 years, and possibly continues beyond that.^12–20 Bone loss occurs more rapidly in trabecular bone, and continues steadily in cortical bone.¹⁹ In the study by Garland et al,¹⁵ the rapid decline in bone mass for the first 4 months was attributed to metabolic changes after SCI. The exact etiology of bone weakening is not known.^7,17 It is suggested that, besides the loss of normal biomechanical stress and the neurotrophic failure, insufficient nutritional support, disordered vasoregulation, hypercorticoidism, alterations in gonadal function, and other endocrine disorders are other possible causes of the changes in the bone.^7,15–17,21

The severity of injury, the extent of functional impairment, the duration of injury, and aging influence bone mass in SCI patients.¹⁷ Many studies have highlighted the osteoporosis below the level of injury.^15,16,22 Mechanical loading and active muscle forces may affect the composition of the bone.⁷ In their cross-sectional study, Tsuzuku et al²³ compared the BMD of 10 tetraplegic and 10 paraplegic patients. The authors found that lumbar spine, upper extremity, and trochanter region BMD of tetraplegic patients were significantly less than those of paraplegic patients. Similarly, other authors had reported more bone loss in arms of tetraplegic patients than those of paraplegic patients.^{15,19,24–26} The extent of SCI is also another important factor for bone metabolic response. In an early, but a still worthy, study of Comarr et al,27 the authors suggested that the more incomplete a lesion was, the more muscles preserved, the less atrophy would result and the less osteoporosis would develop. Supporting this, some authors reported greater BMD loss in their complete SCI patients than in incomplete SCI patients.^24,28–30 In complete SCI patients, it is postulated that the lack of reflex contractions possibly increases demineralization.³¹ Several authors reported that the bone mass reduce with increasing time postinjury and age in patients with SCI.^7,17,20,32

Lower motor lesion patients were found to be relatively more prone to fractures than the upper motor neuron lesion patients.²⁷ Lower motor neuron lesions result in flaccid paralysis and muscle atrophy, however, upper motor neuron lesions results with spastic paralysis and muscle spasms. The muscle atrophy causes reduced or absent mechanical forces on bone and may initiate osteoporosis. Supporting this theory, Demirel et al²⁴ reported lesser BMD loss in their patients with spasticity compared with their flaccid patients. Similarly, Eser et al³³ found that bone loss in the femur after SCI was reduced in subjects with stronger spasticity, compared with subjects with weaker or absent spasticity. However, Wilmet et al³⁴ claimed that spasticity and flaccidity had no effect on BMD loss. It is probable that spasticity is effective at preserving bone mass and reducing fracture risk.⁵ On the other hand, in a recent study of Kostovski et al,³⁰ the authors found that higher frequency and severity of spasticity correlated with lower BMD 12 months after the SCI. They reported that SCI men with incomplete injuries have less spasticity and are more ambulant, and hence spasticity correlates negatively with BMD. Although mild spasticity may have beneficial effects for preserving bone mass, the severe forms of spasticity would cause ambulation or rehabilitation problems that would make patients prone to fractures.

The most common site of SCI is the cervical region, causing upper extremity dysfunction and accounting for 50 to 64% of traumatic spinal cord injuries.³⁵ In regard to severity of permanent neurological dysfunction, SCI may be complete or incomplete. Since 2010, the most frequent neurological categories have been incomplete tetraplegia (41%), incomplete paraplegia (19%), complete paraplegia (18%), and complete tetraplegia (12%).³⁶

Tetraplegia occurs due to injury in one of cervical one to eight spinal cord segments. The area of injured spinal cord—which is called injured metamere—determines the type of paralysis.^36,37 The muscles that are innervated above the level of injury have normal strength (nerve function above the injured metamere is normal). The muscles in injured metamere will be flaccid but may improve by time (nerve function is absent). The muscles below the injured metamere may be flaccid or may have some spasticity. If the lower motor neuron is intact below the injured metamere, stimulation of the muscle is possible.

Other common causes of loss of neural functions are stroke, cerebral palsy, traumatic brain injury, infectious or metabolic diseases, genetic diseases, multiple sclerosis, Guillain–Barre syndrome, brain or spinal tumors. Whatever the cause, the bone is affected in a nonworking extremity.

Calcium homeostasis changes within the first months after injury in SCI. These changes involve hypercalcemia and hypercalciuria that lead renal calculi and changes in calciotropic hormonal profile. According to the histomorphometric data, the main cause of bone loss is increase in bone resorption due to increased number of eroded surfaces and osteoclasts.¹⁷ Bone resorption increases constantly from the first week after injury and peaks between weeks 10 and 16. In the first few months after SCI, BMD decreases 2 to 4% a month. This rate is 5 to 20 times greater than a metabolic factor. Bone mass loss is greater in trabecular than cortical regions.³⁸ After 1 year of injury, hydroxyproline and deoxyproline, the markers of bone resorption, remain elevated, while the bone markers show a minor rise. This imbalance begins immediately after injury and peaks between 3 and 5 months. Around 2 years after injury, bone metabolic process reaches steady-state level. However, depending on the lesion level, gender, age, and accompanying systemic problems, even after 2 years from injury, bone tissue turnover can be seen up to 8 years. Bone loss at the lower extremity is independent of the lesion level while loss at upper extremity is mostly seen tetraplegic patients. Trauma level determines the extent but not the degree of bone loss.^39,40

Some magnetic resonance imaging (MRI) studies showed that reduced bone volume and trabecular number resulting with increased trabecular space in long-standing complete SCI. Similar changes have also been shown with computed tomography (CT). After all process, BMD values of the patients with SCI are 50 to 60% lower than healthy peers.³⁸

Bone changes in SCI also have been supported in mouse studies. Increment in bone marrow cavity by 24% and thinning in cortical width by around 30% have been shown.³⁸ Moreover, SCI resulted in more severe BMD loss and disruption in trabecular microarchitecture and cortical bone geometry than hind limb cast immobilization (HCI) model in mouse.⁴¹

Hammond et al⁴² stated prevalence of osteoporosis in SCI as 34.9%. Duration of injury more than 1 year was associated with a threefold increased osteoporosis.^20,42 As a consequence, fractures are common in SCI. In chronic SCI, the most common fracture causes were falling from wheel chair (51%), twisting the lower extremity during transferring (14%), and hitting the lower extremity on doorframe during using wheelchair.⁴³ Bone impairments occur almost 75% of patients of SCI due to BMD decrease. Fracture rates were found 1.8% in men and 2.5 in women who had SCI over 5 years.⁴⁴ In the United States, fracture rate in 5 years after injury were given 14%. This rate increases to 28% after 10 years and 39% after 15 years. Besides, fracture rate increases with age and is higher in complete lesions, in paraplegics and in women.⁴¹ Additionally, rate of fractures other than the spine were 28% in SCI. Of those fractures, 52% were in chest, 25% were in lower extremity, 24% were in upper extremity, 17% were in head, and 9% were in pelvis.⁴⁵

Stroke

Osteoporosis is accepted as one of the major complications in stroke.46 Fractures in stroke are also common due to bone loss in paretic extremities. BMD loss, functional level, and risk of fall increase fracture risk in stroke. Disuse is defined as main causative factor BMD loss in stroke.⁴⁷ Ramnemark et al⁴⁸ stated that 1 year after stroke there was no significant BMD loss in head or spine. However, after 4 months from stroke, distal radius and proximal femur showed BMD loss compared to nonparetic side. Moreover, total arm showed BMD loss even 1 month after stroke. Similarly, de Brito et al⁴⁶ suggested lower BMD values in paretic forearms in proportion to unaffected forearms very recently to the stroke. Within the first year after stroke, BMD loss of femur neck in paretic extremity was 14% in nonambulatory patients, while it was 8% in ambulatory patients. Similarly, BMD loss in proximal humerus was higher than nonparetic arm 1 year after stroke.⁴⁶ The effect of immobilization duration on BMD loss also has been showed in SCI.⁴⁷

Cerebral Palsy

Fracture rates are relatively high in cerebral palsy (CP). In children with CP, diminished linear growth with defined risk factors, including weight bearing, muscle mass insufficiency, calcium and phosphate homeostasis, nutrition, medications, and immobilization lead to poor mineralization of bone and nontraumatic fractures. Additionally, severity of motor impairment was correlated with BMD loss.^49–52

In the study of Leet et al,⁵³ 50 of 418 children had fractures. Thirty-six patients were quadriplegic, 10 were diplegic, and 4 were hemiplegic. Mean age for fracture was 8.6 ± 4.0. Lower extremity rate was 70%, while upper was 25%. Most common fractures were in femur and in humerus. Children using standing equipment in physical therapy were more prone to having fracture.⁵³

Obstetrical Brachial Plexus Palsy

Obstetrical brachial plexus palsy (OBPP) is one of the lower motor neuron models that lead to paralysis. Several studies showed BMD loss in OBPP. The Z-score is a comparison with the bone density of people of the same age and gender as the patient and helpful in diagnosing secondary osteoporosis. Ibrahim et al⁵⁴ stated severe BMD loss in axonometric type brachial plexus injury and Z-scores in 30 of 45 children indicated increased risk in their study. BMD loss was associated with severity of paralysis. Lack of muscle contraction and mechanical loading were suggested as main causes of BMD loss.^54,55

In a series of 1,576 cases with OBPP, we observed three cases with fractures of the surgical neck of humerus ( Fig. 11.1). Two of these fractures developed during physical therapy, and one was after a fall during cycling. In two cases, fractures were observed in the middle third of radius at the level of the bone anchor, which was used in the supinator transfer of the brachioradialis muscle.