© Borgis - Postępy Nauk Medycznych 1/2017, s. 22-26
*Michał Wąsowski, Marek Tałałaj
Bone fractures after stroke
Złamania kości u osób po udarze mózgu
Department of Geriatrics, Internal Medicine and Metabolic Bone Diseases, Centre of Postgraduate Medical Education, Warsaw
Head of Department: Associate Professor Marek Tałałaj, MD, PhD
Udar mózgu jest jedną z głównych przyczyn niesprawności i śmierci. Pacjenci po udarze mózgu są podatni na przyspieszony ubytek masy kostnej, silniej zaznaczony po stronie niedowładu i w kończynach dolnych, oraz na złamania osteoporotyczne. Głównymi czynnikami, które wpływają na obniżanie się gęstości mineralnej kości (BMD), są: czas trwania unieruchomienia w następstwie niedowładu połowiczego, szybkość i stopień odzyskiwania sprawności ruchowej oraz zaawansowanie deficytów funkcjonalnych.
Strategia postępowania mająca na celu zapobieganie złamaniom u osób po udarze powinna być ukierunkowana na zahamowanie ubytku masy kostnej i zmniejszenie częstości upadków. Odpowiednio prowadzona rehabilitacja ruchowa może poprawić stan układu kostnego oraz mobilność osób po udarze. Ochraniacze bioder mogą być stosowane jako skuteczne amortyzatory ograniczające siłę urazu. Niedobór witaminy D musi zostać wyrównany. U pacjentów z niską wartością BMD i wysokim ryzykiem wystąpienia złamań należy wdrożyć leczenie z wykorzystaniem bisfosfonianów, takich jak: ryzedronian, alendronian, ibandronian lub kwas zoledronowy, a także suplementację witaminy B12 i kwasu foliowego.
Stroke is a major cause of disability and death. Patients after stroke are susceptible to accelerated bone loss, more evident at the paretic side and at lower extremities, as well as to osteoporotic fractures. Main factors that influence decrease in bone mineral density (BMD) are duration of hemiplegia-induced immobilization, time and degree of functional recovery, and severity of functional deficits.
Strategies for prevention of post-stroke fragility fractures should be focused on inhibition of bone mass loss and reduction of incidence of falls. Effective management, including physical exercise regimens, can improve bone health as well as patients’ mobility. Hip protectors can be used as effective shock absorbers. Vitamin D deficiency has to be corrected. In patients with low BMD and increased fracture risk antiresorptive treatment with bisphosphonates, such as risedronate, alendronate, ibandronate or zoledronic acid, as well as vitamin B12 and folate supplementation need to be used.
“I was looking forward to my 61st birthday in two days time. I enjoyed life-walks with the wind in my hair, driving to see loved ones, working in my garden for hours. Then my life stopped and I had to learn everything again. How to walk, how to dress and feed myself – everything I took for granted. But having to ask for help was hard – I’d been so independent all my life.
The stroke had wiped out all my left side. I walked with a frame with someone beside me and moving the log of wood that was my leg was exhausting. One doctor said it would be five years before my hand would move. I thought ‘never’ and worked on it hour after hour until I got one finger to move a fraction. The rest of my fingers came back in three months. I set myself targets and when I walked with a stick three months before the target month I was well chuffed. But last August, a freak fall broke my left hip. This has hit me harder than the stroke did...”.
(Letter to Stroke News, Volume 19.2, February 2001)
Stroke is a cause of long-term disability and leaves 90% of post-stroke patients with functional limitations such as muscle weakness, pain, spasticity, cognitive dysfunction, poor balance and frequent falls (1, 2).
The incidence of strokes increases with age. The association of age-related bone loss and sarcopenia together with functional deficits make the patients with stroke vulnerable to falls and osteoporotic fractures.
Bone fracture risk in stroke patients depends considerably on their tendency to falls (3). It was found that approximately 40% of patients experience at least one fall within the first year following stroke (4). Whether a fracture occurs when a person falls depends largely on the type and severity of falls (5, 6). As a result of impaired locomotor function, persons with stroke tend to fall towards the paretic side and demonstrate reduced ability to stretch the arm on the weak side in order to absorb the shock impact (3, 7).
Many factors are considered to be predictors of falls among stroke patients, such as: older age, male sex, right hemispheric stroke, post-stroke seizures, previous strokes, widespread white matter lesions, significant motor and mental dysfunctions, intercurrent infections and treatment with numerous drugs, especially analgesics, sedatives and antihypertensives (8). More than 7-fold increase in risk of falling has been described in stroke patients unaided while dressing (9).
Bone loss following stroke was found to contribute significantly to increased fracture risk. It starts within a few days following vascular brain injury and progresses until the 3rd-4th month after stroke. In the first year following stroke bone loss in the paretic arm can be the equivalent of more than 20 years of physiological bone loss in healthy individuals of comparable age (10).
Prospective studies determining biochemical markers of bone turnover revealed that bone resorption in hemiplegic patients increased as early as 7 days after stroke. It was accompanied by a decrease in bone formation suggesting significant remodeling imbalance at the bone multicellular unit level (11).
Increased bone resorption results in a rapid mobilization of bone calcium and immobilization-induced hypercalcemia, which is usually mild and can be detected by measurement of serum ionized calcium concentration. Significant positive correlation has been found between the degree of immobilization and serum ionized calcium concentration within the first and next years following stroke (10).
Several studies have reported a marked reduction in bone mineral density (BMD) of the paretic side after hemiplegic stroke (8). Measurements with dual-energy X-ray absorptiometry (DXA) scanning revealed that both upper and lower limbs appeared to be vulnerable to localized bone loss but a decrease in BMD of upper extremities was more evident than that of lower ones (8). It was found that within 1 year following stroke BMD in the paretic lower limb decreased by more than 10%, while BMD in the upper limb without paresis could actually increase, probably due to increased habitual use of the nonparetic hand (12) (fig. 1).
Fig. 1. Regional changes in bone density between 1 and 12 months after stroke in 18 individuals with pronounced paresis from unilateral stroke. Percentages are based on data from Ramnemark et al. (3) NS – non statistically significant
Immobility seems to be a major factor responsible for generalized bone loss. It was found that decrease in BMD correlated with the duration of hemiplegia-induced immobilization, time and degree of functional recovery, and severity of functional deficits (8, 13). Everyday capacity, muscle mass and strength as well as physical fitness of the paretic leg were found to influence BMD of the proximal femur (8, 10, 12).
Apart from reduced physical activity and immobilization the key mechanisms of bone loss in patients following stroke include: endocrine, nutritional, and pharmacological factors.
An important role in the development of osteoporosis seem to play disturbances in the vitamin D – parathyroid hormone (PTH) axis. In elderly individuals higher risk of stroke is often combined with vitamin D deficit, dramatically widespread in this population (14). It was shown that up to 83% of inpatients were vitamin D deficient and significant part of them had extremely low serum 25-hydroxyvitamin D concentrations, below 10 ng/mL (10, 15).
In most elderly patients with hemiplegic stroke even severe vitamin D deficiency is not accompanied by secondary hyperparathyroidism. It was suggested that elevated calcium serum levels, being the result of immobilization, reduced PTH secretion, and inhibited renal synthesis of 1,25-dihydroxyvitamin D. Consequently, stroke patients may show low serum concentrations of both 25OH vitamin D and 1,25(OH)2 vitamin D together with normal or low levels of PTH (10, 16-18).
Another factor that can be implied in post-stroke osteoporosis is vitamin K deficiency. It was found that vitamin K2 is essential for γ-carboxylation of bone Gla-protein, which is indispensable to set up bone matrix. In hemiplegic persons vitamin K deficiency was associated with low BMD and increased incidence of hip fractures on the paretic side (10).
Older age, mobility impairment, dysphagia, cognitive deficits and social isolation are important factors for poor nutrition frequently found in stroke patients. Apart from reduced vitamins D and K supply malnutrition may result in vitamin B12 and folate deficiency, and secondary hyperhomocysteinemia. It was shown that elevated serum homocysteine concentration influenced enzymatic collagen crosslinking in the posttranslational modification of collagen molecules, decreased bone tissue quality, and played important role in bone fragility associated with aging (10, 19, 20).
Treatment with oral anticoagulants is essential part of regimen in significant part of elderly stroke patients. It was found that warfarin, probably by inducing vitamin K deficiency, accelerated decrease of BMD in hemiplegic stroke patients compared with hemiplegic patients not given anticoagulants (10, 21).
Long-term therapy with heparin, often used as venous thromboembolism prophylaxis, leads to reduction in BMD and increased risk of bone fractures that may occur within 6 months of starting therapy. Heparin-induced bone loss is dose dependent and reversible upon discontinuation. It was suggested that low molecular weight heparins were associated with fewer fragility fractures while newer heparins, including fondaparinux, were predicted to be bone neutral for bone metabolism (10, 22).
Administration of antiepileptic drugs (AEDs) which attenuate liver 25-hydroxylation of vitamin D is another possible cause of accelerated bone loss in post-stroke patients (10). AEDs were suggested to exacerbate bone disease by increasing activity of cytochrome P-450 system and vitamin D catabolism. It was found that treatment with drugs being liver enzymes inductors, such as phenytoin, phenobarbital, carbamazepine and primidone resulted in greater bone loss compared to noninductors such as clonazepam, topiramate, valproic acid, ethosuximide and gabapentin (23).
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zaakceptowano do druku: 2016-12-28
Adres do korespondencji:
Department of Geriatrics, Internal Medicine and Metabolic Bone Diseases Centre of Postgraduate Medical Education
Czerniakowska 231, 00-416 Warsaw
tel. +48 (22) 584-11-47
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