Spasticity and dementia increase the risk of pressure ulcers

Abstract

The aim of this study was to identify and characterise the association between the prevalence of pressure ulcers, spasticity levels, and advanced dementia in disable elderly patients. Data were obtained from the patient medical files. Patients were hospitalised in the geriatric skilled nursing department. A total of 40 frail elderly patients, bedbound and suffering from advanced chronic diseases, advanced dementia, and high‐grade pressure ulcers, were examined. Pressure ulcer grades and spasticity in advanced dementia versus non‐dementia patients were evaluated. Logistic regression indicated that only advanced dementia and spasticity were significantly associated with the development of pressure ulcers versus those without dementia or without spasticity. Patients with advanced dementia displayed a significantly higher prevalence of severe spasticity. In multivariate logistic regression analyses, spasticity was significantly associated with pressure ulcers. The strong association of spasticity with the onset of pressure ulcers in advanced dementia should encourage clinicians to implement preventative measures to delay the onset of pressure ulcers.

1. INTRODUCTION

The development and onset of pressure ulcers (PUs) are a common soft tissue and skin injury pathophysiological condition in elderly bedridden patients.1, 2 The aetiology of PUs is multifactorial, and not all immobile patients are affected by PUs. Common extrinsic factors, such as physical direct pressure, shearing forces, friction, and humidity, contribute to the development of PUs. Intrinsic factors such as advanced chronic diseases, low level of albumin, haemoglobin, and low BMI appear to play a significant role in inducing the onset of PUs.3 Recent data suggested a link between dementia and PU and cardiovascular diseases and heart failure.2, 4, 5 In addition to immobilisation, the positioning of the body or body posture may also significantly affect the onset or prevention of PUs.6 Correspondingly, the clinical consequences of severe spasticity, which are directly associated with body positioning, should be further investigated as a possible risk factor in the development of PU.

Spasticity is a clinical movement disorder frequently observed in bedridden patients who are immobile for a long duration. Spasticity is mainly demonstrated by increased muscle tone (hypertonia) because of overactive stretch reflex, which means that an excess of muscle contraction occurs in response to reflex onset. Spasticity is manifested in upper‐motor neuron (UMN) syndrome, appearing after lesions within UMN pathways.7 Additional symptoms caused by UMN lesions are clonus, extensor, and flexor spasms; Babinski sign; cocontraction; and spastic dystonia. Any insult to the central nerve system (CNS), such as cerebral infraction, traumatic brain injury, spinal cord lesion, and anoxic encephalopathy, can lead to severe spasticity. In relevance, progressive CNS disorders such as advanced dementia and disorders of consciousness (eg, permanent vegetative state) may serve as an aetiological precursor of spasticity.8 The most frequent types of spasticity in these high‐risk populations are expressed by the flexor muscles of the upper limb (fingers, wrist, and elbow) and by the extensor muscles of the lower limbs (knee and ankle). Usually, this debilitating clinical condition prevents the range of movement of hands and legs, which is associated with muscle tone severity, resulting in significant functional impairment and comorbid systemic complications.7

In a cohort study in the skilled geriatric nursing department, a total of 174 patients comprised a 32‐bed ward.9 We studied aspects of acquired PUs for 3.5 years. Of 166 total acquired PUs, 35 (21%) developed in an atypical location. The largest group of acquired PUs in an atypical location was the group with severe spasticity, causing approximately half of the atypical wounds in locations around the medial aspects of knees, elbows, and palms. Medical devices caused the second largest atypical wounds at the neck, nape areas, penis, and on the nostrils. Bone deformity was the third largest group, with atypical wounds around the shoulders blades and upper spine. The spastic group of patients was the most difficult group to treat.9

Importantly, spasticity and its role in PU development have not been assessed systematically in the scientific literature. In the current investigation, we examined the relationships between severe spasticity, advanced dementia, and PU development. In light of recent research perspectives highlighting the inter‐relations between CNS pathophysiology and PU development,2 we hypothesised that, among demographic and clinical factors, severe spasticity will be significantly associated with PU development. Furthermore, advanced dementia was hypothesised to significantly contribute to the onset of PUs; however, we intended to inquire which clinical risk factors, including spasticity and advanced dementia, were more significantly associated with PUs. As PU onset represents a final pathway leading to a higher rate of suffering and mortality in elderly bedridden patients, identifying these relationships before the advanced stages of dementia may facilitate early treatment interventions to suppress PU onset and substantially alleviate end‐of‐life suffering.

2. METHOD

This study examined 40 elderly patients (median age 73.5). All were hospitalised in the geriatric skilled nursing department. Inclusion criteria were as follows: hospitalised bed‐bound patients with advanced chronic diseases, such as lung, renal, heart, and liver failure; advanced dementia; and terminal cancer requiring palliative care.

The design of this observational study was cross sectional. Spasticity data were noted and collected by an occupational therapist who examined the spasticity levels of all patients according to the Modified Ashworth Scale. Modified Ashworth Scale severity scores are between 0 and 5, and the study included patients with spasticity at level 3 or higher.10 The nurse performed a weekly skin inspection for the presence of PUs. The staging of PUs was according to the recommendation of the National Pressure Ulcers Advisory Panel. Patients' PUs were of grade 3 or higher.11

Clinical care and prevention policy for each patient on admission involved the application of pressure relief devices, consisting of an air‐alternating pressure mattress overlay and foam cushion for sitting. The standard recommended nutritional support consisted of 30 kcal/kg/day, including 1 to 1.5 kg protein/day, given either orally or through tube feeding (nasogastric or percutaneous endoscopic gastrostomy). The rehabilitation team (OT and PT) routinely assessed every new admitted patient, and follow‐up exams were conducted to prevent and treat contractures and to permit sitting in wheel chairs.

Advanced dementia was defined as a Mini–Mental State Examination score of less than 18.12 Because of a lack of verbal cooperation in some of the patients, Functional Assessment Staging (FAST) was used to assess dementia as well.13 The FAST staging assessment indicates the degree of cognitive deterioration from normal at stage 1 and significant cognitive impairment at stage 7. The advanced dementia criterion for the study was a FAST score higher or equal to stage 6. Levels of consciousness were measured by the Glasgow Coma or Coma Recovery Revised scales.14, 15

Approval for the study was received from the Institutional Internal Review Board according to the declaration of Helsinki. Patient confidentiality was ensured by decoding all of the data with numerical codes without personal patient data.

Statistical methods: Descriptive statistics were used to examine PU prevalence (Yes/No) in the study. Independent t test and χ ² test of independence were used to compare socio‐demographics factors between the two groups. Logistic regression models were used to estimate the univariate and multivariate odds ratios (ORs) and 95% confidence intervals (CIs) for PUs. Variables entered into the multivariate logistic regression model included gender, polypharmacy, head injury, consciousness, dementia, and spasticity. All data were analysed with SPSS software (version 20, IBM, Armonk, NY). All statistical tests were two‐sided. A P value equal or below 0.05 was considered significant.

3. RESULTS

Forty patients were included in the study; 23(57.5%) were with PUs and 17 (42.5%) without PUs (NPUs). The mean age of the entire group was 73.63 + 14.27 (median age 73.5) years. There was no significant difference in the age group (t = 0.014[38], P = 0.989). Clinical and demographic variables (gender, polypharmacy, head injury, consciousness, dementia, and spasticity) were compared between the PU group and the non‐PU group using a χ ² test (Table 1). Of individuals with PU, 86% were diagnosed with dementia, compared with 17.4% who were not diagnosed with dementia (χ ² = 4.097, P < 0.05). 78.3% of individuals with PU, suffered from spasticity compared with 21.7% who did not suffer from spasticity (χ ² = 9.545, P < 0.01). The prevalence of other independent factors such as gender, head injury, low level of consciousness, and polypharmacy were not significantly different between the two groups (Table 1). In addition, 74.1% of patients with advanced dementia displayed spasticity, which was statistically different from the non‐demented patients, who showed only 25% of spasticity prevalence (Table 2). In univariate logistic regression, factors significantly associated with PUs were advanced dementia (OR: 4.222, 95% CI: 1.002–17.796; P = 0.05) and spasticity (OR: 8.640, 95% CI: 2.050–36.423; P = 0.003). Advanced dementia patients and spastic patients were significantly more likely to develop PUs than those without dementia or without spasticity (Table 3). In a multivariate logistic regression, only spasticity was significantly associated with higher risk for PU (adjusted OR = 11.033, 95% CI = 1.406‐86.597; P < 0.05). All the other factors (eg, polypharmacy) were not significantly different between the two groups (Table 4).

Table 1.

Prevalence in the study population of individuals with pressure ulcers and without pressure ulcers

		Pressure ulcers (N = 23)		No pressure ulcers (N = 17)		χ 2	P‐value
		N	%	N	%
Gender	Female	10	43.5	6	35.3	0.273	0.601
	male	13	56.5	11	64.7
Head injury	No	16	69.6	13	76.5	0.234	0.629
	Yes	7	30.4	4	23.5
Consciousness	No	7	30.4	3	17.6	0.853	0.356
	Yes	16	69.6	14	82.4
Dementia	No	4	17.4	8	47.1	4.097	0.043
	Yes	19	82.6	9	52.9
Spasticity	No	5	21.7	12	70.6	9.545	0.002
	Yes	18	78.3	5	29.4
Polypharmacy	No	4	19	2	12.5	0.287	0.592
	Yes	17	81	14	87.5

Table 2.

Prevalence in the study population of individuals with dementia and without dementia

		No dementia (N = 12)		Dementia (N = 28)		χ2	P‐value
		N	%	N	%
Spasticity	No	9	75	8	28.6	7.410	0.006
	Yes	3	25	20	71.4

Table 3.

The odds ratios of pressure ulcers according to the logistic regression

Factors	OR	95% CI	P‐value
Gender	0.709	2.581–0.195	0.602
Head injury	1.4222	5.941–0.340	0.629
Consciousness	0.490	2.264–0.106	0.361
Dementia	4.222	17.196–1.002	0.050
Spasticity	8.640	36.423–2.050	0.003
Polypharmacy	0.607	3.819–0.097	0.595

Abbreviations: OR, odds ratio; CI, confidence interval.

Table 4.

The odds ratios of pressure ulcers according to multivariate logistic regression

Factors	OR	95% CI	P‐value
Gender	0.404	2.459–0.066	0.325
Head injury	0.729	5.845–0.091	0.766
Consciousness	2.625	35.843–0.192	0.469
Dementia	3.933	27.908–0.554	0.171
Spasticity	11.033	86.597–1.406	0.022
Polypharmacy	1.995	28.011–0.142	0.608

Abbreviations: OR, odds ratio; CI, confidence interval.

4. DISCUSSION

The main findings of the current study supported our main hypothesis and previous findings9, 16 that spasticity is significantly associated with the development PUs in atypical and even typical locations. Severe spastic conditions might facilitate PU onset in various ways; increased tonus of the limbs leads to immobility, reduced capacity to reposition the body, and abnormal pressure redistribution, and induced rigidity causes abnormal soft tissue (eg, skin cells) pressure. The soft tissue and the skin cells covering the tonic muscles are more prone to damage because of intense pressure as a result of abnormal spastic stretching of the muscles. The upper limb muscles promote increased direct pressure on the elbow joint and rib cage and cause PU development in the internal surface of the arms. The spastic muscles that underlie finger movements increase the risk of impaired hygiene, reduced dexterity, and functioning of the hands, ultimately predisposing an individual towards the development of PU and related soft tissue pathological conditions. PU development is also salient around the legs. The knee and ankle joints impede basic “sitting” or “standing” movements and force patients to lie passively in beds. The flexion of the knees, which creates abnormally excessive skin contact, impedes hygiene and leads to the development of PUs at the internal surface of the knees (ie, kissing knees). Spasticity has a direct impact on the posture and positioning of the patients lying in bed and increases the pressure on certain risk area points, particularly in areas with an underlying bone (eg, sacrum, heels, elbows, knees, and rib cage). Spasticity can trigger muscle spasms, leading to pain and reduced quality of life. Studies show that, during immobilisation and under‐nutrition, the muscles show a reduced number of sarcomeres (sarcopenia) and an increase of connective tissue in the muscles; these changes enhance muscle resistance (ie, sensitivity to stretch) facilitating PU development in elderly bedridden patients.17

In addition, an important outcome of this study was the identification of a possible non‐salient inter‐relation between the prevalence of PU and advanced dementia. Both spasticity and advanced dementia significantly impacted the prevalence of PUs in elderly bedridden patients. Although spasticity was found as the most significant risk factor for the onset of PUs, dementia had a significant effect on the prevalence of PU and spasticity, independently. Thus, advance dementia directly impacts the prevalence of spasticity and, indirectly, significantly increases the risk of PU development. This finding is clinically important as it directs clinicians' attention to recognising the onset of spasticity or changes in the demented behaviour of bedridden patients suffering from dementia. Clinical alertness to significant changes in spasticity and dementia symptom variation signalling rapid neurodegenerative progression18 could lead to the implementation of early (before the advanced dementia stages) preventative therapies to suppress or delay the onset of PUs. However, it is important to note that all patients in the current study were severely disabled, bedbound elderly frail patients and do not represent the general frail elderly clinical population in nursing departments and at home.

Spasticity is defined as a condition involving an involuntary increase in muscle tone that leads to resistance in initiating normal movements of the body. Because of the increase in the muscle tone in the limbs, there is an increase in pressure applied between soft tissue—generally over a bony prominence—and the surface on which the patient is applying pressure. Spasticity pathophysiology is mainly a reflection of motor control system damage related to disruptions in supraspinal or spinal mechanisms.19 An imbalance in the inhibitory/excitatory circuits within supraspinal UMN pathways most likely contributes to spasticity.7, 20 Significant damage (eg, white matter lesions) to the dorsal reticulo‐spinal tract (DRT) and the cortico‐spinal tract are considered the main pathophysiological conditions mediating severe spasticity in the upper and lower limbs. The DRT is biased towards the extension of axial musculature mainly from trigeminal and somatosensory networks. The corticospinal pathway originates at the primary motor cortex, sending its motor commands via the basal ganglia, thalamus, red nucleus, and pontine nuclei, where its projections continue all the way down the spinal cord to the contralateral ventral horns to activate extensor/flexor muscles. This pathway runs in parallel to the DRT, and they can both activate upper motor neurons in the brain stem. The clinical features of the UMN syndrome appear to be directly related to damage to non‐pyramidal motor circuits within the brain stem, leading to a state of hyper‐excitability probably because of a loss of inhibition within these pathways. Reduced inhibition could be related to impaired circuitry within the DRT or as a result of damage to cortico‐reticular fibres associated with supratentorial lesions.20 In addition, lesions at the premotor area or internal capsule reduce control over medullary motor nuclei centres (eg, solitary tract nucleus, reticular formation nuclei), which generates hypertonicity. Axonal transport defects may serve as a pre‐existing condition causing rapid progression in a variety of neurodegenerative diseases (eg, Alzheimer's disease, Huntington's disease). Human motor protein mutations (eg, dynein and kinesin mutations) and pathogenic proteins (eg, APP, tau, synucleins) that are involved in the regulation of axonal transport are likely to increase the progression of neurodegenerative diseases.21 The role of axonal transport in the aetiology of neurodegenerative disease onset and progression appears to support direct damage to white matter within the cortico‐spinal pathway and is likely to be increased in advanced dementia patients versus non‐demented patients. These underlying mechanisms can explain the observed higher spasticity prevalence in advanced dementia patients versus non‐demented patients. Accordingly, we suggest that future studies focus on treatment interventions than can modulate axonal transport or maintain the activity of motor proteins in order to suppress the onset of spasticity and the following onset of PUs.

Currently, in the clinical setting, the prevention and treatment of spasticity can be achieved in several ways: (a) tendon‐release surgical procedures, (b) muscle relaxant drugs such as Baclofen and intrathecal baclofen, (c) use of botulinum toxin injection, and (d) preventive approaches utilising a passive range of motion exercises and the use of splints.6, 22 Thus, spasticity is treated medicinally and surgically, as well as with physiotherapy and occupational therapy. These treatments are essential in the prevention of painful and movement‐limiting range of motion in the knees, ankles, shoulders, and elbows, which can cause severe disability. Accordingly, we observed that elderly patients with spasticity suffer from PU wounds that are the most difficult to treat and are less likely to heal.9 The main treatment interventions in the elderly include physical and occupational therapy for passive range‐of‐motion exercises (3‐5 days per week) and splints to decrease muscle tone. The goal is to prevent or reduce the risk of joint contractures and onset of PUs. This “proactive” treatment intervention will improve motion and function and reduce rigidity and spasticity. Physical and occupational therapy also implements motion exercises, such as flexing and extension of patients' hands, arms, legs, and feet, through the use of splits. These treatment intervention approaches will increase patient flexibility and improve motor functioning (improving activities of daily living). Maintaining a set of motor‐recovery interventions can also be helpful in reducing falls, which may prevent immobility and, by doing so, will reduce the risk for PU.

To conclude, spasticity directly impacts the patient's quality of life and increases the development of PUs. Spasticity leads to immobility, reduced capacity to reposition the body, and increased abnormal pressure redistribution. In advanced dementia patients, spasticity onset would require more ongoing daily skin inspections to avoid poor hygiene, increase quality of life and function, and delay the onset of PUs.

Jaul E, Factor H, Karni S, Schiffmiller T, Meiron O. Spasticity and dementia increase the risk of pressure ulcers. Int Wound J. 2019;16:847–851. 10.1111/iwj.13110