Falls and Mobility

Falls Risk

Falls are commonly defined as an unexpected event in which a person comes to rest on the ground, floor, or lower level, excluding overwhelming external force or acute neurological events. In older adults they are best regarded as a multifactorial geriatric syndrome: risk rises non-linearly as intrinsic impairments, environmental hazards, medications, and acute illness interact. Approximately 30% of community-dwelling adults aged ≥65 years fall at least once annually, rising to 40–50% in those aged ≥80 years and in care-home residents. Around 5% of falls cause fracture, 1–2% hip fracture, and falls account for most injury-related hospital admissions in older people.

Risk stratification: who requires detailed assessment?

NICE guidance recommends asking all older people routinely whether they have fallen in the past year and about frequency, context, and injury. A multifactorial falls risk assessment is indicated after two or more falls in 12 months, a fall requiring medical attention, recurrent unexplained falls, or observed gait/balance abnormality. A single fall with clear, non-recurrent mechanical explanation still warrants screening for modifiable contributors, particularly medication and vision.

Clinical feature	Implication for risk	Exam-relevant action
Previous fall	Strongest single predictor; recurrence risk roughly doubles	Characterise prodrome, circumstances, injury, ability to rise, long lie
Fall with syncope, chest pain, palpitations, focal neurology	Suggests non-mechanical cause	Investigate arrhythmia, structural heart disease, TIA/stroke, seizure
Long lie >1 hour	Marker of frailty, poor reserve, rhabdomyolysis/pressure injury risk	Check CK, renal function, temperature, pressure areas, safeguarding
Fear of falling or activity restriction	Accelerates deconditioning and sarcopenia	Rehabilitation; confidence-building balance programme

Risk factors and mechanisms

Falls occur when postural control fails to match environmental or physiological demand. Postural control depends on visual, vestibular, proprioceptive, musculoskeletal, cognitive, and cardiovascular inputs. Ageing reduces reserve in each domain; pathology and drugs then lower the threshold for instability. The risk is cumulative: studies consistently show a steep increase from approximately 8% annual fall risk with no risk factors to >70% when four or more are present.

• Intrinsic factors: age ≥80 years, previous fall, frailty, sarcopenia, Parkinsonism, stroke, peripheral neuropathy, vestibular disease, arthritis, foot pain/deformity, urinary urgency/nocturia, cognitive impairment, delirium, depression, visual impairment, postural hypotension, anaemia, dehydration, acute infection.
• Medication-related factors: benzodiazepines, Z-drugs, antipsychotics, antidepressants, opioids, anticholinergics, antihypertensives, diuretics, antiarrhythmics, hypoglycaemic agents, and polypharmacy. Risk rises meaningfully with ≥4 regular medications, and particularly with centrally acting drugs.
• Extrinsic factors: poor lighting, loose rugs, trailing cables, lack of stair rails, inappropriate footwear, icy or uneven surfaces, unfamiliar environments, and poorly adjusted walking aids.
• Situational factors: rushing to the toilet, nocturnal falls, alcohol use, dual-task walking, transfers, and post-prandial periods.

Falls risk assessment tools

Risk scores are screening adjuncts, not substitutes for clinical assessment. Their performance varies by setting and case mix; MRCP questions often test inappropriate reliance on scores rather than identification of reversible pathology.

Tool	Threshold/interpretation	Limitations
Timed Up and Go	Time to rise from chair, walk 3 m, turn, return, sit. >12 seconds suggests increased fall risk; >20 seconds indicates impaired mobility; >30 seconds often indicates dependency.	Moderate predictive value; affected by cognition, pain, acute illness.
Berg Balance Scale	14 tasks, score 0–56. <45/56 associated with increased fall risk.	Ceiling effect in high-functioning patients; time-consuming.
Morse Fall Scale	Uses history, diagnoses, aid, IV therapy, gait, mental status; often ≥45 high risk.	Institutional screening tool; does not replace multifactorial assessment.
FRAT/STRATIFY	Used in some UK services/inpatients.	NICE cautions against using prediction tools alone for inpatients; all older inpatients require individualised assessment.

Medication and falls

Medication review is high-yield and should be explicit. Psychotropics impair reaction time, vestibular compensation, attention, and proximal muscle control; cardiovascular drugs contribute via bradycardia, hypotension, electrolyte disturbance, and nocturia. Benzodiazepines and Z-drugs increase falls and fractures; risk is greatest after initiation or dose escalation and with long half-life agents such as diazepam, whose active metabolites may persist for 20–100 hours. Antipsychotics carry dose-related risks through sedation, extrapyramidal effects, and orthostatic hypotension. Antidepressants, especially tricyclics and SSRIs/SNRIs, increase falls through anticholinergic effects, hyponatraemia, sedation, and postural instability. Deprescribing should be planned rather than abrupt: for long-term benzodiazepines, typical tapering reduces total daily dose by about 10–25% every 1–2 weeks, individualised to dependence and withdrawal risk.

Interventions shown to reduce falls

The central principle is that multifactorial intervention follows multifactorial assessment. Components include strength and balance training, home hazard modification, vision optimisation, medication withdrawal, footwear advice, continence management, treatment of cardiovascular contributors, and assistive device review. Exercise has the most consistent evidence: Cochrane analyses show structured balance and functional exercise programmes reduce fall rate by approximately 20–30% in community-dwelling older adults, with greater benefit when delivered at sufficient intensity and duration, commonly ≥3 hours/week for ≥12 weeks. Tai Chi reduces falls in selected community populations but is less suitable for severe frailty or major cognitive impairment.

Vitamin D should not be used indiscriminately as a falls-prevention drug in replete community dwellers, but replacement is appropriate in deficiency, institutionalised patients, malabsorption, limited sunlight exposure, or osteoporosis risk. UK practice commonly uses colecalciferol 800–1000 IU daily for maintenance, with loading regimens for deficiency according to local protocols. Hip protectors may reduce hip fractures in care-home residents with adherence, but effectiveness is limited by poor tolerability. Importantly, restraints and routine sedatives worsen mobility, delirium, and injury risk and should not be used as falls-prevention strategies.

Gait Disorders

Gait disorders in older adults are rarely attributable to a single lesion; they usually reflect interaction between impaired motor programme generation, sensory integration, executive function, musculoskeletal reserve and fear of falling. Examination should therefore localise the dominant gait phenotype rather than merely label the patient as “unsteady”. Normal adult gait speed is approximately 1.2–1.4 m/s; in geriatric practice, <1.0 m/s predicts adverse outcomes, <0.8 m/s predicts frailty, hospitalisation and mortality, and <0.6 m/s implies high dependency risk. A gait speed change of 0.1 m/s is usually clinically meaningful.

Clinical classification and localisation

Phenotype	Key features	Likely localisation / causes	Exam discriminators
Parkinsonian	Short shuffling steps, reduced arm swing, stooped posture, festination, freezing, en bloc turning	Idiopathic Parkinson disease, drug-induced parkinsonism, vascular parkinsonism, atypical parkinsonism	Rest tremor and asymmetry favour idiopathic PD; early falls, gaze palsy or autonomic failure suggest atypical disease
Frontal / higher-level gait disorder	“Magnetic” feet, difficulty initiating gait, broad base, preserved leg movements when supine	Frontal-subcortical circuits: vascular cognitive impairment, normal pressure hydrocephalus, frontal tumours	Disproportionate start hesitation and turning difficulty; cognitive/executive dysfunction common
Cerebellar ataxic	Wide-based, irregular step timing and length, veering, impaired tandem gait	Cerebellar stroke, alcohol-related degeneration, paraneoplastic disease, spinocerebellar ataxias	Dysarthria, nystagmus, dysmetria; Romberg usually negative or only mildly worsens instability
Sensory ataxic	High-stepping, stomping gait, worsens in dark or eyes closed	Large-fibre neuropathy, dorsal column disease, B12 deficiency, tabes dorsalis	Positive Romberg, impaired vibration/joint position; reflexes often reduced
Spastic / upper motor neurone	Circumduction, scissoring, toe drag, hyperextension of knee	Stroke, cervical myelopathy, multiple sclerosis, hereditary spastic paraparesis	Hyperreflexia, extensor plantar responses, clonus; consider cervical cord compression in older patients
Antalgic / musculoskeletal	Short stance phase on painful side, limp, guarded posture	Hip/knee osteoarthritis, fracture, trochanteric pain syndrome, spinal stenosis	Pain reproduced by joint movement; Trendelenburg suggests hip abductor weakness or L5 lesion

Assessment tools relevant to falls prediction

The Timed Up and Go test measures standing from a chair, walking 3 m, turning, returning and sitting. In community-dwelling older adults, >12–13.5 seconds is commonly used as an abnormal threshold; specificity is modest, so it should not be used alone to predict falls. The Tinetti Performance-Oriented Mobility Assessment scores balance and gait out of 28; <19 indicates high fall risk and 19–23 moderate risk. The Dynamic Gait Index is scored out of 24; ≤19 is associated with increased fall risk, particularly in vestibular and neurological disorders. Dual-task gait testing is valuable: disproportionate slowing while counting backwards or naming animals suggests impaired executive reserve and frontal-subcortical disease.

Key syndromes for MRCP

Parkinsonian gait

Idiopathic Parkinson disease reflects nigrostriatal dopaminergic loss with impaired basal ganglia scaling of internally generated movement. Gait becomes hypokinetic with reduced stride length; cadence may be relatively preserved until later disease. Freezing of gait is triggered by narrow spaces, doorways, stress and turning. NICE guidance supports levodopa as first-line when motor symptoms affect quality of life. Typical initiation is co-careldopa 62.5 mg three times daily, titrating to response; levodopa plasma half-life is approximately 60–90 minutes, explaining wearing-off. In older adults, dopamine agonists are less favoured because of hallucinations, somnolence, oedema and impulse-control disorders. Physiotherapy with external cueing, metronome rhythm, visual floor stripes and amplitude-based training can improve freezing and stride length.

Vascular parkinsonism

Vascular parkinsonism classically produces lower-body parkinsonism: gait initiation failure, short steps, postural instability and early falls, often with pyramidal signs, urinary symptoms and executive dysfunction. Tremor is less prominent and levodopa responsiveness is poor compared with idiopathic Parkinson disease. MRI typically shows confluent white-matter disease or strategic basal ganglia infarction, but radiology must be interpreted clinically because small-vessel disease is common in asymptomatic older adults.

Normal pressure hydrocephalus

Normal pressure hydrocephalus causes a frontal gait disorder with the triad of gait disturbance, cognitive impairment and urinary urgency/incontinence. Gait impairment is usually earliest and most reversible. Imaging shows ventriculomegaly disproportionate to sulcal atrophy; an Evans index >0.30 supports ventriculomegaly. Improvement after removal of 30–50 mL CSF by large-volume lumbar puncture predicts shunt responsiveness, although sensitivity is imperfect; extended lumbar drainage has higher predictive value but greater burden. Ventriculoperitoneal shunting improves selected patients, but complications include subdural haematoma, infection and over-drainage, so comorbidity and frailty are central to decision-making.

Cervical myelopathy

Degenerative cervical myelopathy is an important reversible cause of gait disturbance and falls. Patients develop spastic, broad-based gait, hand clumsiness, hyperreflexia and extensor plantars; neck pain may be absent. MRI cervical spine is the investigation of choice. Urgent referral is indicated with progressive neurological deficit, sphincter dysfunction or significant cord compression. Delay worsens outcome because established cord signal change reflects myelomalacia.

Practical examination approach

1. Observe rising from a chair, initiation, stride length, base width, arm swing, turning, tandem gait and response to distraction or dual task.
2. Look for localisation signs: parkinsonism, cerebellar signs, neuropathy, pyramidal signs, proximal weakness, joint pain and visual impairment.
3. Assess gait aids: incorrect stick height, absent rubber ferrules and inappropriate frames are common iatrogenic contributors to instability.
4. Correlate phenotype with medication exposure, especially antipsychotics and metoclopramide causing drug-induced parkinsonism.

In examination questions, the safest diagnostic strategy is to identify the dominant gait pattern and then choose the most anatomically coherent cause. “Unsteady gait” plus cognitive impairment is not automatically dementia: frontal gait disorder, normal pressure hydrocephalus, vascular parkinsonism and cervical myelopathy are high-yield, potentially treatable alternatives.

Orthostatic Hypotension

Definition, classification and diagnostic technique

Orthostatic hypotension (OH) is a sustained fall in blood pressure on standing due to failure of cardiovascular compensation. The consensus definition is a fall in systolic BP ≥20 mmHg and/or diastolic BP ≥10 mmHg within 3 minutes of standing or head-up tilt to at least 60°. In patients with supine hypertension, a systolic fall of ≥30 mmHg is often used to improve specificity. OH is common in older adults, affecting approximately 10–30% of community-dwelling older people and up to 50–60% in frail institutionalised cohorts, and is strongly associated with falls, syncope, fractures, cognitive impairment and mortality.

Subtype	Timing	Typical mechanism	Clinical clue
Initial OH	Within 15 seconds of standing	Transient mismatch between venous pooling and sympathetic response	Immediate dizziness; often missed unless beat-to-beat BP is used
Classical OH	Within 3 minutes	Volume depletion, drugs or autonomic failure	Most relevant to falls assessment and routine bedside testing
Delayed OH	After 3 minutes of standing	Early autonomic failure or impaired vasoconstrictor reserve	Symptoms after prolonged standing; requires extended stand/tilt testing

Measurement should be standardised: after at least 5 minutes supine rest, record BP and pulse supine, then at 1 minute and 3 minutes after standing; extend to 5–10 minutes if symptoms are delayed. A fall may be absent if measured only sitting-to-standing. Reproduction of symptoms increases diagnostic relevance. Post-prandial hypotension should be considered where symptoms occur within 30–120 minutes after meals, especially after carbohydrate-rich meals.

Pathophysiology and differential diagnosis

Standing transfers approximately 500–1000 mL of blood to the splanchnic and lower-limb venous capacitance beds, reducing venous return and stroke volume. Normal compensation requires rapid baroreceptor-mediated sympathetic activation: increased heart rate, myocardial contractility and arteriolar/venous vasoconstriction. Ageing, arterial stiffness, impaired baroreflex sensitivity, reduced muscle pump activity and polypharmacy reduce reserve.

Category	Examples	Exam discriminator
Non-neurogenic	Dehydration, haemorrhage, sepsis, adrenal insufficiency, anaemia, venous pooling, prolonged bed rest	Appropriate tachycardia; reversible precipitant
Drug-induced	Diuretics, nitrates, alpha-blockers, antihypertensives, antipsychotics, tricyclics, opioids, dopaminergic therapy, alcohol	Temporal relation to initiation, titration or intercurrent illness
Neurogenic OH	Parkinson disease, multiple system atrophy, Lewy body dementia, diabetic autonomic neuropathy, amyloidosis, pure autonomic failure	Blunted heart-rate response, autonomic symptoms, supine hypertension

A useful bedside discriminator is the ΔHR/ΔSBP ratio: a rise in heart rate of <0.5 beats/min per mmHg fall in systolic BP supports neurogenic OH, whereas a robust tachycardic response suggests hypovolaemia or drug effect. However, beta-blockers, pacemakers, atrial fibrillation and intrinsic conduction disease limit interpretation.

Clinical significance and investigation

OH may present with dizziness, visual dimming, “coat-hanger” neck pain, weakness, falls, syncope or confusion, but many older patients are amnestic for prodrome. It should be actively sought in recurrent unexplained falls, Parkinsonism, diabetes, frailty, syncope, antihypertensive intensification and after hospitalisation. Baseline evaluation includes medication review, lying/standing BP, pulse, ECG, FBC, U&E, glucose/HbA1c and consideration of B12, thyroid function, cortisol or serum protein electrophoresis where clinically indicated. Tilt-table testing is reserved for unexplained syncope/falls, suspected delayed OH or autonomic failure when bedside testing is non-diagnostic.

Management

Management prioritises removal of reversible causes and prevention of falls rather than normalisation of standing BP. Current syncope and geriatric guidance emphasises medication rationalisation, hydration and physical countermeasures before pharmacotherapy.

• Medication review: reduce or stop nitrates, alpha-blockers, unnecessary diuretics, sedatives and vasodilators; consider less aggressive BP targets in frail older adults.
• Fluid and salt: aim for 2–2.5 L/day fluid if not contraindicated; salt intake up to 6–10 g/day may help but is inappropriate in decompensated heart failure or advanced CKD.
• Water bolus: 500 mL rapidly can raise BP within 5–10 minutes for approximately 30–60 minutes via sympathetic activation.
• Mechanical measures: waist-high compression stockings or abdominal binders are more effective than knee-length stockings; teach leg crossing, squatting and gluteal contraction.
• Behavioural measures: rise slowly, elevate head of bed by 10–20°, avoid large carbohydrate meals, alcohol, hot environments and prolonged standing.

Drug	Typical dose	Mechanism	Key cautions
Midodrine	2.5 mg three times daily, titrate to 10 mg three times daily; avoid within 4 hours of bedtime	Peripheral alpha-1 agonist; active metabolite half-life about 3–4 h	Supine hypertension, urinary retention, piloerection, pruritus; caution in severe cardiac disease
Fludrocortisone	50–100 micrograms daily, titrate cautiously to 200 micrograms daily	Mineralocorticoid-mediated sodium and water retention	Hypokalaemia, oedema, heart failure, supine hypertension; monitor U&E and BP
Droxidopa	100 mg three times daily, titrate to 600 mg three times daily	Norepinephrine prodrug	Supine hypertension, headache; availability varies by country

Supine hypertension complicates neurogenic OH and is not benign. Avoid evening pressor doses, elevate the head of bed, and consider short-acting night-time antihypertensives only under specialist supervision. In MRCP-style questions, the highest-yield approach is to identify OH with correctly timed lying/standing BP, distinguish neurogenic from volume/drug-related causes using pulse response and context, then prioritise deprescribing and non-pharmacological measures before midodrine or fludrocortisone.

Immobility Complications

Immobility in older adults is not a benign consequence of acute illness; it is a pathophysiological state causing rapid multisystem decline. In hospitalised older patients, bed rest accelerates sarcopenia, insulin resistance, endothelial dysfunction, venous stasis, atelectasis, bone resorption, delirium and pressure injury. The clinical principle for MRCP is that immobility is both a marker of frailty and a modifiable iatrogenic risk; “mobilise early” is a therapeutic intervention, not merely rehabilitation.

Musculoskeletal Deconditioning, Sarcopenia and Contractures

Skeletal muscle loss begins within days of bed rest. Healthy older adults may lose approximately 1–1.5% muscle strength per day during strict bed rest, with preferential loss of antigravity lower-limb muscle. Mechanisms include reduced anabolic signalling, increased ubiquitin–proteasome-mediated proteolysis, inflammatory cytokines, reduced neuromuscular activation and impaired protein synthesis. Functional consequences include reduced gait speed, impaired transfers, falls, prolonged length of stay and institutionalisation.

• Frailty markers: gait speed <0.8 m/s, unintentional weight loss, exhaustion, low grip strength and reduced physical activity; Clinical Frailty Scale 5–9 indicates increasing vulnerability.
• Contractures: arise from prolonged shortened positioning, capsular fibrosis, altered collagen cross-linking and spasticity or pain-avoidance. Common sites are hip flexors, knees, ankles and shoulders.
• Bone loss: immobilisation increases osteoclastic resorption and urinary calcium excretion, worsening osteoporosis and fracture risk. Hypercalcaemia of immobilisation is uncommon in general geriatrics but may occur after spinal cord injury or prolonged profound immobility.

Prevention requires daily mobilisation targets, resistance exercise, adequate analgesia, nutrition and physiotherapy. Protein intake of approximately 1.0–1.2 g/kg/day is commonly recommended for older adults, rising to 1.2–1.5 g/kg/day during acute illness or rehabilitation if renal status permits.

Pressure Ulcers

Pressure ulcers result from sustained pressure, shear and microclimate-related tissue deformation causing capillary occlusion, lymphatic failure, ischaemia–reperfusion injury and inflammatory necrosis. Risk is greatest over sacrum, heels, trochanters, malleoli and occiput. Important contributors include immobility, malnutrition, moisture, anaemia, peripheral vascular disease, diabetes, reduced sensation and vasopressor use.

Category	Definition	Exam-relevant points
Category 1	Non-blanchable erythema of intact skin	May be hard to identify in darkly pigmented skin; warmth, induration or pain may help
Category 2	Partial-thickness skin loss or blister	Superficial ulcer involving epidermis/dermis
Category 3	Full-thickness skin loss	Subcutaneous fat may be visible; bone/tendon not exposed
Category 4	Full-thickness tissue loss with exposed bone, tendon or muscle	High risk of osteomyelitis and sepsis
Unstageable	Base obscured by slough or eschar	Depth cannot be assessed until debrided, except stable dry heel eschar may be left intact

Risk assessment tools include the Waterlow score and Braden scale, but they supplement rather than replace clinical judgement. NICE guidance supports risk assessment on admission, pressure redistribution surfaces, heel off-loading, repositioning, continence care and nutritional optimisation. Repositioning frequency is individualised; “2-hourly turns” is not mandatory for every patient but remains a common practical standard in high-risk immobile patients.

Venous Thromboembolism

Immobility promotes venous thrombosis through Virchow’s triad: venous stasis from reduced calf-muscle pump activity, endothelial dysfunction and acute illness-related hypercoagulability. Older patients frequently have additive risks: malignancy, infection, heart failure, stroke, dehydration, previous VTE and oestrogen therapy. Hospital-associated VTE remains a major preventable cause of morbidity and mortality.

Agent	Typical prophylactic dose	Key cautions
Enoxaparin	40 mg subcutaneously once daily	Reduce to 20 mg once daily if eGFR <30 mL/min/1.73 m2; avoid/monitor in high bleeding risk
Dalteparin	5000 units subcutaneously once daily	Renal impairment and low body weight require caution
Unfractionated heparin	5000 units subcutaneously 8–12 hourly	Useful in severe renal impairment; higher HIT risk than LMWH
Mechanical prophylaxis	Intermittent pneumatic compression	Use when anticoagulation contraindicated; avoid in severe peripheral arterial disease or acute limb ischaemia

NICE recommends VTE risk assessment for hospitalised adults and pharmacological prophylaxis when VTE risk outweighs bleeding risk. LMWH is generally continued until mobility is no longer significantly reduced, commonly at least 7 days in medical inpatients depending on ongoing risk.

Cardiorespiratory, Metabolic and Neuropsychiatric Consequences

Bed rest reduces plasma volume and baroreflex responsiveness, worsening postural intolerance and promoting tachycardia on mobilisation. Reduced diaphragmatic excursion and dependent airway closure cause basal atelectasis, impaired cough, mucus retention and pneumonia, particularly in patients with COPD, stroke, sedation or dysphagia. Immobility also worsens insulin resistance within days, promotes negative nitrogen balance and contributes to constipation through reduced colonic transit, dehydration, opioids and anticholinergics.

• Urinary complications: urinary retention, functional incontinence, catheter-associated urinary tract infection and delirium. Avoid indwelling catheters unless strict indications exist.
• Constipation/faecal impaction: can precipitate urinary retention, overflow diarrhoea, delirium and stercoral colitis. Regular aperients are appropriate with opioids; e.g. senna 7.5–15 mg nocte plus macrogol 1–3 sachets daily, titrated.
• Delirium: immobility contributes via sleep disruption, pain, sensory deprivation, infection, hypoxia, constipation and polypharmacy. Multicomponent prevention programmes, such as HELP, reduce incident delirium by targeting mobilisation, orientation, hydration, sleep and sensory impairment.
• Rhabdomyolysis after a long lie: suspect after prolonged floor time following a fall. Check creatine kinase, potassium, phosphate, calcium and renal function. CK >5000 IU/L is associated with increased acute kidney injury risk; treatment is cautious isotonic fluid resuscitation balanced against heart failure risk.

Practical Examination Synthesis

In MRCP-style questions, immobility complications cluster: an older patient admitted after a fall develops delirium, sacral erythema, constipation, urinary retention, hypostatic pneumonia and calf swelling. The correct answer is rarely a single disease label; it is recognition of hospital-associated deconditioning requiring comprehensive geriatric assessment, early mobilisation, pressure-area prevention, VTE prophylaxis, medication review, hydration, nutrition, bowel care and discharge rehabilitation planning. The most effective intervention is often anticipatory prevention before irreversible loss of function occurs.