01OverviewDefinition, clinical context and the essential points that orientate the chapter.
Begin with the change, not the age. Ask the person and collateral witness for the last known well time, symptom sequence, falls or collapse, intake, urine and bowel change, medicines and baseline cognition and daily function. A relative's statement that they are not themselves can be high-value evidence even when initial observations appear normal.
Perform ABCDE, capillary glucose and a head-to-toe examination. Look for respiratory effort and oxygenation, pulse irregularity, perfusion, hydration, focal neurology, meningism, injury, pressure areas, abdominal distension and tenderness, retention, faecal loading and skin infection. Measure lying and standing blood pressure only when safe and relevant, without delaying resuscitation.
Delirium may be hyperactive, hypoactive or mixed. Use 4AT, obtain baseline cognition and search several simultaneous precipitants: infection, hypoxia, pain, constipation, retention, dehydration, metabolic disorder, medicine toxicity, withdrawal and environmental disruption. Do not stop after finding one plausible factor; older adults commonly have multiple interacting causes.
Infection assessment is source-led. Obtain cultures before antibiotics when this creates no harmful delay and use sepsis physiology and organ dysfunction to set urgency. Absence of fever is not reassuring, but neither is a positive urine dipstick proof of urinary infection. Asymptomatic bacteriuria is common; unnecessary antibiotics can cause adverse effects, resistance and Clostridioides difficile.
Falls require reconstruction. Determine trip, prodrome, loss of consciousness, seizure features, palpitations, post-event confusion, head strike and ability to rise. Examine gait, injuries, neurology and cardiovascular system and review postural and sedative or hypoglycaemic medicines. An unwitnessed fall in an anticoagulated person or new inability to weight bear lowers the threshold for imaging.
Cardiovascular and abdominal emergencies can be quiet. Consider ECG and serial troponin for compatible dyspnoea, nausea, sweating, syncope or unexplained decline. Bowel obstruction, ischaemia, perforation, cholecystitis and retention may produce delirium or anorexia with limited pain. Repeat abdominal examination and use lactate and imaging according to probability, recognising that normal early tests may not end the assessment.
Review every medicine, including recent starts, dose changes, adherence and non-prescription products. Link sedatives, opioids and anticholinergics to arousal and retention; insulin and sulfonylureas to hypoglycaemia; antihypertensives and diuretics to hypotension and renal injury; anticoagulants to occult bleeding. Adjust for current kidney and liver function and avoid abrupt withdrawal where dangerous.
Order tests to address explicit questions. Common early studies may include FBC, renal and liver profile, calcium, CRP, glucose, ECG and targeted imaging or microbiology, but presentation determines selection. Interpret modest abnormalities against baseline and medicines. Repeat observations and examination when trajectory and initial results disagree rather than escalating incidental findings.
Treat the cause and prevent the cascade simultaneously: oxygen when indicated, fluid with reassessment, analgesia, nutrition, glasses and hearing aids, orientation, sleep protection, early mobilisation, thrombosis and pressure prevention and removal of unnecessary catheters. Avoid sedating distress before pain, retention, constipation and fear are addressed.
Before discharge, explain the working diagnosis and residual uncertainty and compare cognition, intake, mobility and ADLs with baseline. Confirm medicine changes, rehabilitation, care support and safety-net triggers. Persistent unexplained functional loss warrants senior reassessment rather than being relabelled new frailty.
Key points
- Atypical presentation means the initial symptom does not localise the cause: common signals are delirium, falls, immobility, incontinence, anorexia, fatigue and functional decline.
- First-line action is ABCDE, observations, capillary glucose, pain and full examination while collateral establishes exact onset and stable baseline.
- Serious infection can occur without fever or leukocytosis; use physiology, organ dysfunction, source assessment and trajectory rather than one absent classic sign.
- Delirium is acute brain failure and demands a cause search. Known dementia increases risk but never explains a sudden fluctuation by itself.
- Acute coronary syndrome may present with dyspnoea, weakness, nausea, syncope or delirium; obtain ECG and troponin when the context supports it.
- A fall is an event, not a diagnosis. Ask what happened before, during and after and examine for syncope, stroke, infection, medicine harm and injury.
- Reconcile recent prescriptions, missed doses and renal function early; a medicine that was previously tolerated can become toxic during dehydration or acute kidney injury.
- Do not diagnose urinary infection from bacteriuria or a positive dipstick alone in an older adult without compatible urinary or systemic evidence.
- Use targeted testing from competing high-consequence hypotheses and repeat examination; indiscriminate panels create incidental findings and treatment harm.
- Track function and cognition as vital outcomes. Failure to regain expected mobility or intake should reopen the diagnosis before discharge.
02AetiologyUnderlying causes, associations and risk factors, with why each one matters.
Acute organ disease
Infection, vascular events, heart failure, arrhythmia, bleeding, fracture and abdominal or urinary emergencies commonly present through functional or cognitive change rather than a localising symptom.
Metabolic and endocrine disturbance
Hypoglycaemia, hyperglycaemia, sodium and calcium disorders, renal or hepatic failure, thyroid disease and dehydration can produce weakness, falls, reduced intake or delirium.
Medicine and substance effects
Sedatives, anticholinergics, opioids, antihypertensives, insulin, anticoagulants, withdrawal and recent dose changes can cause non-specific decline or amplify otherwise modest illness.
Environmental and social stress
Care disruption, sleep loss, unfamiliar surroundings, sensory deprivation, malnutrition and carer breakdown can precipitate decline but should be considered alongside, not instead of, medical disease.
03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.
- 1Reduced physiological reserve
Limited cardiovascular, renal, neurological and muscular reserve means a small stressor can cross functional thresholds and produce disproportionate dependency before organ-specific symptoms become prominent.
- 2Altered inflammatory response
Immunosenescence, frailty and medicines can blunt fever, tachycardia, leukocytosis and pain, so absence of classic inflammatory signs lowers sensitivity but never excludes serious infection.
- 3Brain as vulnerable organ
Systemic inflammation, hypoxia, metabolic change, pain and drugs disrupt attention and arousal, making delirium a frequent final common pathway of extracranial illness.
- 4Homeostatic cascade
Illness causes anorexia, dehydration, immobility and medication disruption, which then create kidney injury, constipation, pressure injury, thrombosis and further cognitive and functional loss.
- 5Communication and perception barriers
Cognitive, hearing, visual, language and neuropathic impairment can alter symptom recognition and reporting, while clinicians may unconsciously discount complaints because of age or disability.
04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.
Acute inattention, fluctuation or altered arousal may be the only visible sign of systemic infection, hypoxia, pain or metabolic disease.
A fall can follow syncope, arrhythmia, stroke, hypoglycaemia, infection, drug effect or fracture and requires event reconstruction.
New inability to cook, walk, toilet or take medicines can precede classic symptoms and quantifies physiological impact.
Serious infection may lack fever, tachycardia or leukocytosis, especially with frailty, immune suppression or rate-limiting medicines.
Dyspnoea, nausea, fatigue, collapse or confusion can replace chest pain in acute coronary, arrhythmic and thromboembolic disease.
A known dementia, frailty or care-home residence is used as the explanation before acute and reversible causes are assessed.
05InvestigationsWhat to request, why it matters and how to interpret it.
Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.
- 01
ABCDE, glucose and observationsFirst step - Why
- Detect immediate physiological and metabolic threat.
- Interpretation and limitations
- Treat abnormalities while repeating trends; normal temperature or one reassuring observation set does not exclude evolving disease.
- 02
Collateral timeline and baseline - Why
- Separate acute change from chronic vulnerability.
- Interpretation and limitations
- Record last known well, event sequence, baseline cognition, ADLs and IADLs, intake, continence, medicines and carer concern.
- 03
Full repeated examination - Why
- Localise disease that the history does not reveal.
- Interpretation and limitations
- Include neurology, cardiopulmonary, abdomen, bladder, injury, skin, hydration, pain, feet and pressure areas and repeat when trajectory changes.
- 04
Medication reconciliation - Why
- Identify toxicity, withdrawal and prescribing cascade.
- Interpretation and limitations
- Compare multiple sources, recent changes, missed doses and OTC products and interpret each against renal, hepatic, pressure and glucose status.
- 05
Targeted laboratory testing - Why
- Test several competing high-consequence clinical hypotheses.
- Interpretation and limitations
- Select blood count, renal, liver, calcium, glucose, inflammation, troponin, thyroid, cultures and urinalysis according to presentation and baseline.
- 06
ECG and presentation-led imaging - Why
- Find silent vascular, cardiac, pulmonary, abdominal and traumatic disease.
- Interpretation and limitations
- Choose CT, radiograph, ultrasound or other imaging from event, focal findings, anticoagulation, injury and failure to improve; avoid routine scanning without a question.
- 07
4AT and functional reassessment - Why
- Measure brain and whole-person response.
- Interpretation and limitations
- Screen delirium and repeatedly compare alertness, attention, mobility, intake and self-care with baseline after treatment.
06Differential diagnosisRealistic alternatives and the features that help distinguish them.
Primary neurological event
Stroke, seizure, subdural haemorrhage and neurodegeneration can cause falls or confusion; focal findings, headache, anticoagulation, trauma and time course guide urgent imaging.
Systemic infection or inflammation
Respiratory, urinary, skin, abdominal and device infection may be afebrile, but asymptomatic bacteriuria is common and must not become the default explanation for delirium.
Cardiopulmonary disease
Acute coronary syndrome, arrhythmia, heart failure, pulmonary embolism and respiratory failure can manifest as weakness, falls, nausea or confusion with little reported pain.
Medication or metabolic toxicity
Hypoglycaemia, electrolyte disturbance, renal drug accumulation, anticholinergic load, opioid toxicity and withdrawal are rapidly testable causes that often coexist with acute disease.
Functional and psychosocial cause
Depression, pain, sensory loss, malnutrition and care failure can produce decline, but a new presentation requires medical exclusion before diagnostic closure.
07ManagementImmediate care, first-line treatment, alternatives and escalation.
01First-line acute sequenceStabilise, date the change and test serious hypothesesFirst stepFirst lineAn older adult presents with a fall, confusion, weakness, poor intake or functional loss.+
- 1Perform ABCDE, glucose, observations and immediate treatment while obtaining last-known-well and baseline collateral.
- 2Complete full examination and medicine reconciliation and investigate several plausible high-consequence causes in parallel.
- 3EscalationRepeat physiology, cognition and function and escalate when trajectory remains unexplained despite initially modest findings.
02Delirium routeTreat brain failure and its interacting causesAcute fluctuation, inattention or altered arousal is present.+
- 1Use 4AT, ensure safety and identify hypoxia, infection, pain, retention, constipation, metabolic and medicine precipitants.
- 2Treat causes and provide orientation, sensory support, hydration, sleep protection and mobilisation without unnecessary restraint or sedation.
- 3Monitor course and investigate persistent or focal change for neurological, malignant or other missed disease.
03Non-response routeReopen the diagnosis before accepting declineLaboratory values improve but function, intake or cognition does not.+
- 1Repeat history, examination, observations and medicine review and verify that treatment and rehabilitation were delivered.
- 2Reconsider occult injury, stroke, embolism, abdominal disease, depression, sensory loss, malnutrition and care factors.
- 3EscalationObtain senior and MDT review, update goals and support and communicate residual uncertainty and escalation triggers.
08ComplicationsImportant consequences, why they occur and why they matter clinically.
Delayed diagnosis and death
Attributing non-specific change to age, dementia or frailty can postpone antibiotics, reperfusion, surgery or treatment of metabolic and cardiopulmonary emergencies.
Delirium and persistent decline
Untreated illness and hospital stress can cause prolonged delirium, deconditioning and new care dependency even after the original physiology improves.
Iatrogenic cascade
Indiscriminate tests, catheters, bed rest, sedatives and treatment of colonisation can cause infection, adverse drug effects, immobility and further diagnostic confusion.
Falls and pressure harm
Weakness and immobility lead to recurrent falls, fracture, pressure injury, venous thromboembolism and aspiration unless prevention and mobilisation begin alongside diagnosis.
Unsafe transition
Discharge after laboratory improvement without recovery, explanation or support for new functional loss risks readmission, missed medicines and carer breakdown.
09Monitoring and follow-upTreatment response, safety checks and longer-term review.
- Trend observations, urine output and disease-specific tests together with 4AT, alertness, intake, mobility and ADL recovery.
- Repeat examination after analgesia, hydration and delirium change; evolving abdominal, neurological and injury signs may become clearer.
- Review medicines daily during renal, hepatic, pressure or glucose instability and document restart criteria for temporarily held treatment.
- Remove catheters and unnecessary monitoring promptly and track pressure, thrombosis, aspiration and deconditioning prevention.
- At transition compare with dated baseline, confirm the explanatory diagnosis and safety net any persistent or unexplained functional gap.
10Special situationsVariants, exceptions and circumstances that change the usual approach.
Collateral can be a vital sign
A reliable witness describing abrupt change may reveal severity before conventional observations become abnormal.
Afebrile is not uninfected
Older physiology and medicines may mute fever, but source evidence and organ dysfunction still determine treatment.
Bacteriuria can distract
Colonisation is common and may divert attention from pneumonia, retention, medicines or stroke.
A fall needs a verb before it
Tripped, fainted, collapsed, was pushed or lost balance generate different investigations.
Recovery tests the diagnosis
Failure of cognition or function to improve as predicted is evidence that the cause or intervention may be incomplete.
Frailty modifies, never explains
It predicts vulnerability to the stressor but does not identify which stressor occurred.
11Common pitfallsFrequent interpretation and management errors.
- 01
Writing mechanical fall without reconstructing prodrome, consciousness, injury and contributing illness.
- 02
Diagnosing urinary infection from a positive dipstick in delirium without compatible source evidence.
- 03
Using absent fever or normal leukocytes to exclude serious infection.
- 04
Attributing sudden decline to dementia or frailty before checking acute and reversible causes.
- 05
Ordering indiscriminate tests, then treating incidental abnormalities while the clinical trajectory worsens.
- 06
Discharging after biochemical recovery despite persistent unexplained immobility, anorexia or cognitive change.