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  • Understanding Eczema; More than just dry skin

    Understanding Eczema; More than just dry skin

    Eczema, or atopic dermatitis, is often brushed off as “just dry skin.” But for the millions affected globally, it’s a chronic inflammatory condition that disrupts sleep, self-esteem, and daily life. Its hallmark signs—itching, redness, and scaling—mask a complex interplay of genetics, environmental triggers, and immune dysregulation.

    What Exactly Is Eczema?

    Eczema is not a single disease, but a spectrum of conditions characterized by skin barrier dysfunction and immune hypersensitivity. It tends to run in families with a history of atopy—think asthma, allergic rhinitis, and food allergies. While children are more commonly affected, adults are by no means immune.

    At the heart of eczema is a compromised skin barrier. This makes the skin more permeable to allergens and irritants while losing moisture more easily—leading to dryness, inflammation, and that relentless itch.

    Triggers: More Than Meets the Eye

    Eczema flares can be provoked by a wide range of triggers:

    • Harsh soaps and detergents
    • Heat, sweating, or cold air
    • Stress and hormonal changes
    • Allergens like dust mites or certain foods

    Importantly, what triggers one patient may not affect another. That’s where personalized care becomes crucial.

    Management: Beyond Moisturizers

    Emollients are the foundation, but far from the whole story. Mild to moderate cases often respond well to topical corticosteroids or calcineurin inhibitors. In more severe or refractory cases, systemic therapies—including biologics like dupilumab—have significantly improved outcomes.

    General practitioners play a vital role in early recognition and long-term management. Dermatologists, meanwhile, bring value through advanced therapies and targeted interventions.

    But let’s not forget the patient. Education is empowering. Teaching patients to identify and avoid triggers, adhere to treatment, and care for their skin daily is as vital as any prescription.

    A Final Word

    Eczema is not simply a skin condition—it’s a quality-of-life issue. Its visibility and chronicity can be emotionally taxing. As clinicians, recognizing this holistic burden allows us to treat more than the skin—we treat the person.

  • Dementia types

    Dementia is an umbrella term for a variety of progressive neurological conditions that result in the decline of cognitive abilities. It affects memory, thinking, behavior, and the capacity to carry out everyday tasks. Rather than being a single illness, dementia represents a collection of symptoms caused by different diseases that lead to brain dysfunction, extending beyond the typical effects of aging. According to the National Institute for Health and Care Excellence, dementia involves a set of symptoms that impact intellectual and social functioning to the extent that they interfere with daily life.

    Alzheimer’s disease (AD) is the leading cause, accounting for 50–75% of dementia cases. It is characterized by cerebral cortex shrinkage, the build-up of amyloid plaques, and neurofibrillary tangles. Additionally, there is a decline in neurotransmitters—especially those involving the cholinergic system—as well as neuroinflammation. AD frequently coexists with other types, particularly vascular dementia, leading to mixed dementia. In some cases, AD has a genetic basis and tends to appear earlier in life. Neurological exams may appear normal, but brain imaging typically shows significant atrophy in the medial temporal lobes.

    Vascular dementia is the second most frequent cause. It results from various underlying vascular issues such as large strokes, multiple small infarcts, or microvascular disease seen post-mortem. Other causes include cerebral amyloid angiopathy and CADASIL (a hereditary condition involving subcortical infarcts and white matter changes). Cardiovascular risk factors like high blood pressure, diabetes, and smoking are often present. It’s commonly linked with strokes or transient ischemic attacks (TIAs) and tends to progress in a stepwise pattern. Like AD, early-onset cases may have genetic origins.

    Dementia with Lewy bodies (DLB) accounts for about 10–15% of dementia cases. It is marked by abnormal protein deposits called Lewy bodies in both the cortex and subcortical areas of the brain. DLB shares many features with Parkinson’s disease dementia (PDD). The key distinction lies in the timing of symptoms: if cognitive decline appears before or at least a year before motor symptoms, it is classified as DLB. If motor symptoms begin before or within a year of cognitive changes, it is considered Parkinson’s disease with dementia.

    Frontotemporal dementia (FTD) represents a group of conditions and makes up about 2% of all dementia cases. It often runs in families and involves the gradual deterioration of the frontal and/or temporal lobes. Common cognitive screening tools like the MMSE may not detect it, as they typically don’t assess frontal lobe function.

    Other less frequent causes of dementia include conditions such as progressive supranuclear palsy, Huntington’s disease, normal pressure hydrocephalus, benign brain tumors, chronic subdural hematomas, and metabolic disorders (e.g., hypothyroidism, Addison’s disease, hypopituitarism). Nutritional deficiencies like low vitamin B12 or thiamine, infections such as HIV and syphilis, autoimmune or inflammatory diseases, and transient epileptic amnesia can also lead to dementia symptoms.

    References

    NICE (2018) ‘Dementia: assessment, management and support for people living with dementia and their carers’, NG97. Available at: https://www.nice.org.uk/guidance/NG97/ (Accessed: 28 July 2025).

    Ladecola, C., et al (2019) ‘Vascular Cognitive Impairment and Dementia’ Journal of the American College of Cardiology, 73(25), pp. 3326-3344.

  • Understanding Osteoporosis: Causes and Risks

    Osteoporosis is a skeletal disorder characterised by weakened bone strength—due to reductions in bone mineral density, deterioration of the bone’s microarchitecture and impaired mineralisation—which dramatically raises the risk of fractures. Often silent until a low-impact injury occurs, it most commonly manifests as wrist, vertebral, hip, proximal humerus or pelvic fractures.

    Throughout life, bone tissue undergoes continuous remodelling: old bone is removed by osteoclasts and new bone is laid down by osteoblasts. When resorption outpaces formation, the microstructural and mineral changes that define osteoporosis ensue. This delicate balance is influenced by hormones, growth factors and genetic predisposition—indeed, having a parent who suffered a hip fracture increases fracture risk independently of bone density.

    Sex steroids are particularly important regulators: oestrogen deficiency after the menopause accelerates bone loss in women, while in men, rising levels of sex hormone–binding globulin with age diminish the availability of testosterone and oestrogen, similarly compromising bone strength. These age‑related changes underlie primary osteoporosis.

    Secondary osteoporosis arises from other diseases and drugs. Excess glucocorticoids—whether from long‑term corticosteroid therapy or Cushing’s syndrome—are the most frequent culprits, doubling the risk of hip fractures in women and raising it 2.6‑fold in men. In men, hypogonadism and heavy alcohol use (more than four units per day) can also halve bone density. Lifestyle factors such as smoking, which further suppresses bone formation, inadequate dietary calcium and vitamin D, and long‑term proton pump inhibitor use (which impairs calcium absorption) compound fracture risk. Low body weight and rapid weight loss—seen for example in some female athletes with hypothalamic amenorrhoea—similarly predispose to early bone loss.

    Clinically, one low‑trauma fracture vastly increases the likelihood of subsequent fractures in the following five to ten years. Even modest annual height loss—more than 0.5 cm—signals elevated risk of hip and other fractures in middle‑aged and older adults.

    A wide range of medical conditions may provoke secondary bone loss: endocrine disorders such as hyperthyroidism, hyperparathyroidism, hyperprolactinaemia and diabetes mellitus; malabsorption syndromes like coeliac disease and chronic pancreatitis; inflammatory diseases such as rheumatoid arthritis; haematological illnesses including multiple myeloma and haemoglobinopathies; chronic organ diseases affecting the liver, kidneys or lungs; and prolonged immobility. In women, roughly one‑third of osteoporosis cases stem from secondary causes, most often disturbances in calcium metabolism (for example hyperparathyroidism or vitamin D deficiency).

    At the cellular level, bone remodelling is orchestrated by the RANK–RANKL pathway: osteoblasts produce RANK ligand, which binds to RANK on osteoclast precursors, driving their activation and bone‑resorbing activity. Parathyroid hormone (PTH) exerts a dual effect—intermittent PTH stimulates osteoblast proliferation and increases bone mass, whereas chronically elevated levels promote resorption. Conversely, calcitonin suppresses osteoclastic activity via specific G‑protein–coupled receptors, reducing cytosolic calcium and inhibiting bone breakdown.

    Calcium, phosphate and vitamin D homeostasis is maintained through a feedback loop involving PTH, calcitonin and 1,25‑dihydroxyvitamin D. Low serum calcium triggers PTH secretion, enhancing renal calcium reabsorption, activating osteoclasts via RANKL to liberate skeletal calcium, and upregulating renal 1α‑hydroxylase to convert vitamin D into its active form, thereby increasing intestinal calcium uptake. Vitamin D itself is first hydroxylated in the liver to 25‑hydroxyvitamin D and then converted in the kidney to 1,25‑dihydroxyvitamin D—completing the cycle that sustains bone health.

  • Osteoporosis- key concepts

    Osteoporosis- key concepts

    Osteoporosis is often called a “silent thief” because bone loss proceeds painlessly and unnoticed—until a sudden low‑energy fracture unmasks the damage. For older adults, especially post‑menopausal women, this systemic skeletal disease threatens independence, mobility and longevity.

    Clinically, osteoporosis is defined in orthogeriatric practice as a systemic bone disorder marked by reduced bone mass and qualitative changes in bone micro‑architecture that together heighten fragility‑fracture risk. Diagnostic confirmation relies on dual‑energy X‑ray absorptiometry (DXA); a T‑score of –2.5 or lower at the hip or spine signals established disease.

    In the United Kingdom, the Royal Osteoporosis Society estimates that around 3.5 million people are living with osteoporosis today—roughly one in seven of all adults over fifty. Every year, more than half a million fragility fractures are linked to the condition, generating billions of pounds in healthcare and social‑care costs while eroding quality of life for patients and carers alike.

    Across the Atlantic, the public‑health burden is even larger. U.S. survey data show that about 10 million adults aged 50 and older meet DXA criteria for osteoporosis, and a further 43 million have low bone mass (osteopenia). Age‑adjusted analyses from NHANES 2017‑18 put overall osteoporosis prevalence in this age group at 12.6 %, rising to nearly one in five women.

    Taken together, these figures underscore why fracture prevention is a cornerstone of healthy ageing strategies on both sides of the Atlantic. Weight‑bearing exercise, adequate dietary calcium and vitamin D, fall‑prevention measures and timely DXA screening can all delay or blunt bone loss. For those already diagnosed, evidence‑based pharmacotherapies—ranging from bisphosphonates to newer anabolic agents—reduce fracture risk and preserve autonomy. Recognising the scale of osteoporosis is the first step toward tackling its hidden but profound human and economic costs.

    References

    Centers for Disease Control and Prevention (CDC) 2022, FastStats – Osteoporosis. Available at: https://www.cdc.gov/nchs/fastats/osteoporosis.htm (Accessed 22 July 2025).

    Falaschi, P. & Marsh, D. (eds) 2021, Orthogeriatrics: The Management of Older Patients with Fragility Fractures, 2nd edn, Springer, Cham.

    International Osteoporosis Foundation (IOF) 2021, SCOPE 2021 Country Profile: United Kingdom. IOF, Nyon.

  • Constipation in the Elderly: A Geriatrician’s Perspective

    Constipation in the Elderly: A Geriatrician’s Perspective

    Introduction

    Constipation is an extremely common issue in older adults – approximately one-third of people over 60 years old are affected, and more than half of nursing home residents struggle with it. Beyond discomfort, constipation can have serious consequences. In frail seniors, excessive straining on the toilet may trigger fainting or even cardiac ischemia, and severe cases can lead to complications like stercoral ulceration (where hard impacted stool causes pressure sores in the colon, risking perforation). As a geriatrician with years of experience, I have seen how chronic constipation can impair quality of life and how dangerous it can become if neglected. In this blog, I’ll share insights on why constipation is so prevalent in the elderly, how we manage it following British guidelines, and a few real-case examples – including an emergency where prompt intervention averted a life-threatening situation. The aim is to educate both fellow clinicians and caregivers or seniors themselves on managing this common yet often underestimated problem.

    Understanding the Problem in Older Adults

    What is constipation? In simple terms, constipation refers to bowel movements that are infrequent or difficult to pass. Stools are often hard, dry, and may be accompanied by a feeling of incomplete evacuation. Many people think you must have a bowel movement every day, but in fact there is no physiological necessity for daily bowel action. Normal frequency varies from person to person; for some older adults, going 2-3 times per week can be perfectly normal – as long as the stool is soft and passing without undue straining.

    Why are the elderly more prone to constipation? Constipation tends to increase with age due to a combination of factors. Older people are more likely to have diets low in fiber (for example, eating less fruits/vegetables due to reduced appetite or poor dentition) and may not drink enough fluids, leading to harder stools. Mobility often decreases with age – seniors who are less active or bedridden have slower gut transit. Many are on multiple medications (polypharmacy), and several common drugs can cause or worsen constipation. These include opioid painkillers (codeine, morphine), certain blood pressure pills like calcium-channel blockers, iron supplements, antacid therapies, and medications with anticholinergic effects such as some antidepressants or Parkinson’s disease drugs. Chronic medical conditions can play a role too: an underactive thyroid, high calcium levels, Parkinson’s disease, diabetes, stroke, or even early colorectal cancer can all lead to secondary constipation. Psychosocial issues like depression or dementia (where a person may ignore the urge or have toileting difficulties) further contribute. In hospital or care home settings, we also see factors like lack of privacy or having to use a bedpan hindering proper toileting. In short, constipation in the elderly is usually multifactorial – a combination of age-related changes, lifestyle, and medical factors.

    Impact on health: Aside from uncomfortable symptoms (bloating, abdominal pain, hard stools, straining), chronic constipation can significantly reduce an older person’s quality of life. It may cause loss of appetite, lethargy, and generally make people feel unwell. Importantly, severe constipation can present in atypical ways in seniors. For instance, an elderly person with confusion or delirium might actually be suffering from fecal impaction – in one hospital study, constipation was found to be a contributor to delirium in about 11% of older inpatients and even caused urinary retention in 5%. I’ve seen cases where resolving the constipation dramatically improved a patient’s alertness and comfort. This underlines why healthcare providers should always assess bowel habits in older patients, especially if there is a sudden change in mental or physical health.

    Warning signs (“red flags”): Whether you are a clinician or a concerned family member, it’s crucial to recognize when constipation might be a sign of something more serious. Red flag symptoms that warrant prompt medical evaluation include:

    • A marked, unexplained change in bowel habits (new-onset constipation or alternating with diarrhea out of the blue).
    • Any rectal bleeding that isn’t obviously from hemorrhoids (especially if blood is mixed with stool).
    • Persistent abdominal mass or new lump felt in the tummy.
    • Narrowed stool caliber (pencil-thin stools).
    • Unintended weight loss, iron-deficiency anemia, fever or generally feeling unwell.
    • Family history of colon cancer or inflammatory bowel disease in a patient with new constipation.
    • Severe constipation not responding to treatment.

    Such features could indicate an underlying colorectal cancer or other serious bowel disease. In line with NICE guidelines (NG12 in the UK), any older patient with suspicion of colon cancer should be referred urgently for further tests (often on a two-week cancer pathway). Fortunately, these are the minority of cases – most constipation in the elderly is benign and manageable – but vigilance is key.

    Case Study: A Chronic Constipation Turnaround

    To illustrate a typical scenario, let me share the story of Mrs. Edith, an 82-year-old retired teacher who came to my geriatric clinic with a long history of constipation. Edith lived alone and admitted she had been “bunged up” for years, relying on weekly doses of a stimulant laxative (senna) to force a bowel movement. Recently, her problem was worsening – she felt bloated, lost her appetite, and was only passing hard, pellety stool twice a week with much straining. She was worried and uncomfortable.

    On reviewing her case, several factors stood out. She had a habit of tea and toast for meals (low fiber intake), limited fluids (to avoid needing the loo at night), and painful arthritis in her knees which curtailed exercise. Her medications included calcium supplements and codeine for back pain – both notorious for causing constipation. On examination, her abdomen was soft but I could feel hard stool in the lower colon, and a rectal exam confirmed a lot of stool present but no masses or bleeding. There were no red flags suggesting cancer; this was a case of chronic idiopathic (functional) constipation likely exacerbated by lifestyle and medications.

    Management plan for Edith: We approached Edith’s constipation on two fronts – lifestyle modifications and judicious use of laxatives – following the stepwise strategy recommended by British guidelines:

    1. Lifestyle changes: I educated Edith that having a bowel movement every day isn’t necessary as long as she’s comfortable. We worked on diet first. Gradually, she increased her fiber intake – adding porridge or high-fiber cereal at breakfast, an extra piece of fruit (she discovered she quite likes prunes!), and more vegetables with meals. We discussed the importance of drinking enough fluids; she made an effort to drink water or herbal tea throughout the day to reach about 1.5–2 liters, as her heart and kidneys were healthy. I also encouraged gentle exercise – even a short daily walk or some chair exercises – to stimulate her digestion. Another useful tip was establishing a toilet routine: I advised her to sit on the toilet for a few minutes every morning after breakfast, taking advantage of the colon’s natural reflex after meals. Using a small footstool to elevate her feet and leaning forward (mimicking a squatting posture) can straighten the rectum and help stool pass more easily – she found this “modified squat” posture quite helpful. Importantly, we also reviewed her medications: I liaised with her GP to reduce her codeine use (switching to paracetamol and physiotherapy for her back pain) and to ensure calcium supplements were truly needed at the dose given – anything that could be deprescribed or swapped to a less constipating alternative, we adjusted.
    2. Laxatives (medical treatment): Despite improvements, lifestyle measures alone are often not enough for chronic constipation in the elderly. According to NICE guidance, the first-line laxatives for short-term constipation are usually bulk-forming fiber supplements like ispaghula husk (psyllium). However, these require adequate fluid intake to work well and can cause bloating. Given Edith’s already hard stools and long-standing issues, we opted to start with an osmotic laxative – in her case, polyethylene glycol (a macrogol powder) – which works by drawing water into the bowel to soften stool. After a week on a daily macrogol sachet, her stool consistency improved considerably. She was now stooling every other day with less straining. To further help her establish regularity, I added a gentle stimulant laxative (senna tablets at night, in a low dose) to stimulate the bowels if needed. Over about one month, Edith’s bowels “woke up” – she developed a routine of going every morning or second morning with soft, formed stools. Once she was consistently achieving at least three comfortable bowel movements per week, we discussed tapering off the laxatives. Abruptly stopping can cause rebound constipation, so we gradually reduced the senna and then the macrogol. With her new diet and habits, she was able to maintain regular bowel function on minimal medication. Edith reported feeling more energetic, her appetite returned, and she no longer dreaded the toilet.

    This case highlights the cornerstone of managing chronic constipation: start with lifestyle and address reversible factors, then use laxatives in a stepwise manner. Often a combination of agents is used (e.g. an osmotic to soften plus a stimulant to prompt bowel action), tailored to the patient’s response. It’s also crucial to prevent constipation proactively. For any older patient starting an opioid painkiller, I always prescribe a concurrent laxative regimen (typically a stool softener or osmotic and a stimulant) – in line with NHS recommendations to always offer laxatives when using opioids. This pre-empts the near-inevitable constipation that opioids cause.

    Management Strategies and Guidelines

    Lifestyle and toileting measures

    • Start with everyday habits: build a diet rich in fruit, vegetables and whole‑grains, introducing fibre gradually (aim for roughly 30 g daily) to limit bloating.
    • Encourage adequate fluid intake, as even mild dehydration can harden stools.
    • Promote regular physical activity suited to the person’s mobility; movement helps keep the gut moving.
    • Establish an unhurried, private toilet routine—ideally after meals or first thing in the morning, when the bowel is naturally more active.
    • A footstool that raises the knees above hip level (mimicking a squat) and responding promptly to the urge to defecate both aid easier evacuation.
    • Review current prescriptions for drugs that slow the bowel (e.g., opioids, certain calcium‑channel blockers, anticholinergics) and stop or substitute them wherever possible.

    Laxatives: a stepwise approach

    • If lifestyle adjustments are insufficient, introduce an oral laxative.
    • For short‑term or milder cases, begin with a bulk‑forming agent such as ispaghula husk, but remind patients to drink plenty of water.
    • When stools remain hard or infrequent, switch to—or add—an osmotic laxative (e.g., lactulose or macrogol). These draw water into the bowel; allow two to three days for full effect.
    • If softness improves yet emptying is still difficult or incomplete, add a stimulant laxative such as senna or bisacodyl to trigger colonic contractions.
    • Titrate doses so the person passes a soft, formed stool at least three times weekly with minimal straining. Once this pattern is stable, taper and stop laxatives gradually to check whether regularity can be maintained without them.

    When first‑line steps fail

    • Persistent constipation despite optimal use of a bulk‑former, an osmotic and (if needed) a stimulant calls for re‑evaluation and specialist input.
    • Further investigations might include colon imaging, anorectal physiology testing or screening for underlying disorders.
    • Advanced pharmacological options include prokinetics such as prucalopride (recommended for women with chronic constipation unresponsive to at least two laxative classes) and secretagogues such as lubiprostone or linaclotide, particularly where irritable bowel syndrome with constipation is suspected.
    • Biofeedback therapy can help if pelvic‑floor dysfunction impedes emptying.
    • Above all, avoid leaving an older patient on an ever‑expanding list of laxatives without improvement—timely referral prevents prolonged discomfort and uncovers treatable causes.

    Reference list

    National Institute for Health and Care Excellence (NICE) (2022) Constipation. Clinical Knowledge Summary. London: NICE. Available at: https://cks.nice.org.uk/topics/constipation/ (Accessed: 19 July 2025).

    Medway and Swale Medicines Optimisation Team (2023) Constipation: adult laxative guidance. Medway & Swale Formulary. Available at: https://medwayswaleformulary.co.uk (Accessed: 19 July 2025).

    Hull and East Riding Prescribing Committee (2019) Management of Constipation in Adults. Updated May 2019. Hull: Hull and East Riding Prescribing Committee. Available at: https://www.hey.nhs.uk/wp/wp-content/uploads/2019/08/GUIDELINE-Constipation-guidelines-updated-may-19.pdf (Accessed: 19 July 2025).

  • Understanding Delirium: Causes, Effects, and Management

    Key messages

    • Delirium is an acute, fluctuating disturbance of attention, awareness and cognition; it is a medical emergency with substantial morbidity and mortality.
    • Around 1 in 6 acute‑care in‑patients will be delirious at any one time and prevalence rises to >50 % in critical care. Early recognition halves downstream complications.
    • Multicomponent, non‑pharmacological prevention bundles are the single most effective intervention; drug therapy is reserved for severe distress or danger.
    • The 4AT is now the preferred bedside screening tool in the UK (2 minutes; no special training), and is embedded in NICE CG103 and national audit standards.

    1. Definition and clinical impact 

    The DSM‑5 and NICE guideline CG103 define delirium as an acute change in consciousness and cognition with a fluctuating course, precipitated by an underlying medical disorder. Delirium is independently associated with a two‑ to four‑fold rise in 30‑day mortality, longer length of stay, increased institutionalisation and a heightened long‑term risk of dementia

    2. Pathophysiology 

    Current models integrate neuro‑inflammation, impaired cortical connectivity and network dys‑synchrony triggered by systemic insults (sepsis, surgery, drug toxicity). Recent translational work implicates micro‑ and astro‑gliopathy as key amplifiers of the inflammatory cascade, opening avenues for disease‑modifying therapy 

    3. Predisposing and precipitating factors 

    Predisposing (baseline)

    • Age ≥ 65 y, dementia or mild cognitive impairment
    • Frailty, polypharmacy (>6 drugs), sensory impairment
    • Previous delirium, stroke or Parkinson’s disease

    Precipitating (acute)

    • Infection, surgery or trauma
    • Metabolic derangement (hypoxia, hypo‑/hyper‑glycaemia, electrolyte imbalance)
    • Psychoactive drugs (benzodiazepines, anticholinergics, opioids)
    • Environmental factors (sleep deprivation, restraints, transfer of care) 

    4. Clinical phenotypes 

    • Hyperactive (agitation, hallucinations) – easily recognised
    • Hypoactive (withdrawn, drowsy) – frequently missed; carries the worst prognosis
    • Mixed – oscillates between the two

    5.Screening

    As suggested by NICE guidelines, patient should be assessed using 4AT
    assessment tool. After this, an underlying cause must sought out and a calm and
    familiar environment should be ensured with adequate lighting. Orientation cues
    (clock, calender etc) should be encouraged and patient’s response to treatment
    should be monitored.

    6. Managment plan

    Take a full history and examine the patient carefully. Find out when the confusion started, how it has changed, how bad it is, and whether there were recent illnesses, new medicines, or changes in surroundings.

    Do basic blood and urine tests. Check a full blood count (infection, anaemia), electrolytes and kidney/liver tests (metabolic problems), and a urine test to look for infection.

    Order a brain scan when needed. A CT (or MRI if indicated) can help rule out stroke, bleeding, or other brain problems if the history or exam suggests it.

    Review every medicine. Include prescriptions, over-the-counter drugs, and “as needed” meds. Look for drugs that can cloud thinking—especially those with anticholinergic effects.

    Check the care environment. Is the patient getting their glasses/hearing aids? Are they sleeping at night? Are they over- or under-stimulated? Are restraints being used?

    Consider hidden dementia. Some people have undiagnosed memory problems; delirium may be the first sign something was already wrong.

    Look for simple physical triggers. Constipation with faecal impaction or not being able to pass urine (retention) can both cause or worsen delirium.

    Assess and treat pain. Uncontrolled pain is a common and often overlooked trigger for delirium.

    References

    NICE (2023) ‘Delirium: Prevention, diagnosis and management in hospital and
    long-term care. Available at http://www.nice.org.uk/guidance/cg103

    Azizi, Z., O’Regan, N., Dukelow, T. et al. (2024) ‘Informal judgement of delirium status underestimates delirium prevalence: World Delirium Awareness Day point prevalence results from Ireland’, Delirium Communications, 4 June.

    O’Connell, H. etal. (2025) ‘Outcomes associated with older patients who present or develop delirium in the emergency department: systematic review and meta‑analysis’, BMJ Open, 15(5):e095495.

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