After studying this note you will be able to differentiate dementia from delirium, list the common local aetiologies, perform a focused mental status exam, interpret basic investigations and outline immediate and definitive management plans – remembering to verify doses and local protocols against the Kenya MoH guideline and your hospital formulary.
Definition
Dementia – a progressive, usually irreversible decline in multiple cognitive domains (memory, language, executive function, visuospatial skills) that interferes with independence in daily activities and persists for ≥ 6 months.
Delirium – an acute, fluctuating disturbance of attention and awareness, with a change in cognition (e.g., memory, disorientation) that develops over a short period (hours–days) and tends to fluctuate during the day.
Anatomy and physiology you need
- Cerebral cortex – especially temporal (memory) and frontal (executive) lobes; loss of neuronal networks underlies dementia.
- Reticular activating system (RAS) – maintains arousal; disruption produces the inattention of delirium.
- Neurotransmitter balance – acetylcholine deficiency and dopaminergic excess are central to delirium; amyloid‑β deposition, tau tangles, and loss of cholinergic neurons are key in Alzheimer’s dementia.
- Blood‑brain barrier (BBB) – systemic inflammation or infection can increase permeability, precipitating delirium.
Causes and risk factors
| Category | Common local aetiologies | Key risk factors |
|---|---|---|
| Neurodegenerative | Alzheimer’s disease, vascular dementia, Lewy‑body dementia, frontotemporal dementia | Age > 65, family history, hypertension, diabetes |
| Infectious | HIV‑associated neurocognitive disorder, tuberculous meningitis, cerebral malaria, neurosyphilis, bacterial meningitis | HIV positivity, TB exposure, recent malaria, immunosuppression |
| Metabolic / Toxic | Vitamin B12 deficiency, folate deficiency, chronic alcohol, lead exposure, anticholinergic burden | Poor nutrition, alcoholism, occupational exposure |
| Vascular / Cardiac | Multi‑infarct dementia, cardio‑embolic stroke, hypertension, atrial fibrillation | Uncontrolled BP, AF, prior stroke |
| Hematologic / Genetic | Sickle‑cell disease (cerebral infarcts), sickle‑cell trait, hereditary ataxias | Sickle‑cell disease, consanguinity |
| Autoimmune / Inflammatory | Systemic lupus erythematosus, vasculitis, rheumatic fever (Sydenham chorea) | Autoimmune disease, recent streptococcal infection |
| Medication‑induced | Benzodiazepines, anticholinergics, opioids, corticosteroids | Polypharmacy, high‑risk drugs |
Pathophysiology
Dementia
Neuronal loss → synaptic dysfunction → cortical atrophy → progressive cognitive decline
Delirium
Systemic insult (infection, drugs, metabolic derangement) → inflammatory cytokines ↑ → BBB permeability ↑ → neurotransmitter imbalance (acetylcholine ↓, dopamine ↑) → impaired RAS function → fluctuating attention and cognition
The remainder of the clinical approach (assessment, investigations, severity grading, management, monitoring, safety and complications) will be covered in parts 2 and 3.
Clinical features
| Domain | Key questions / findings | Why it matters |
|---|---|---|
| Onset | “When did the problem start?” “Was the change sudden (hours‑days) or gradual (months‑years)?” | Sudden onset favours delirium; insidious onset points to dementia. |
| Course | Fluctuation of symptoms (better in the morning, worse at night)? | Fluctuating consciousness is classic for delirium; dementia is usually progressive but may have day‑to‑day variability in later stages. |
| Memory | Recent memory loss (forgetting recent conversations, appointments)? Remote memory intact? | Early episodic memory loss is typical of Alzheimer’s dementia; delirium may have global attention deficit with impaired recall of recent events. |
| Attention | Ability to follow a conversation, count backwards, spell “world” backwards? | Impaired sustained attention is a core feature of delirium; attention is relatively preserved early in most dementias. |
| Orientation | “What is the date? Where are you? Who are you?” | Disorientation to time/place is common in delirium; in dementia it appears later. |
| Behaviour / psychosis | Hallucinations, delusions, agitation, aggression, sleep‑wake reversal? | Visual hallucinations are frequent in Lewy body dementia and delirium; acute agitation suggests delirium. |
| Functional decline | Ability to perform ADLs (bathing, dressing, cooking) before and now? | Decline in instrumental ADLs precedes basic ADLs in dementia; delirium can cause abrupt loss of all functions. |
| Risk exposures | Recent infection, fever, new medication, surgery, electrolyte imbalance, alcohol withdrawal, substance use, HIV status, TB treatment, malaria, sickle‑cell crisis? | Identifiable precipitants point to delirium; chronic infections (TB, HIV) can also cause dementia‑type syndromes. |
| Past medical history | Vascular disease, hypertension, diabetes, stroke, head injury, rheumatic fever (carditis), neuro‑degenerative disease in family? | Vascular risk factors predispose to vascular dementia; rheumatic fever can cause Sydenham chorea and later cognitive issues. |
| Medication review | Anticholinergics, benzodiazepines, opioids, steroids, antipsychotics, HIV antiretrovirals, anti‑TB drugs? | Many drugs are delirium precipitants; some (e.g., cholinesterase inhibitors) are used in dementia. |
| Social / environmental | Recent relocation, sensory deprivation, lack of caregiver support? | Environmental stressors precipitate delirium; social isolation worsens dementia progression. |
| Physical symptoms | Fever, headache, neck stiffness, focal weakness, seizures? | Suggests infectious or metabolic cause of delirium; focal deficits hint at stroke or space‑occupying lesion. |
Examination findings
- General – fever, tachycardia, dehydration, signs of infection (e.g., pulmonary crackles, urinary tenderness). Fever or systemic illness supports delirium.
- Neurological – level of consciousness (Glasgow), attention tests (e.g., digit span), orientation, language (naming, repetition), praxis, gait, reflexes, visual field testing. Fluctuating consciousness, impaired attention, disorganized thinking = delirium; focal deficits, extrapyramidal signs, primitive reflexes suggest specific dementias (vascular, Lewy body, Huntington).
- Cranial nerves – visual hallucinations may accompany preserved visual fields (Lewy body) vs. visual field loss (stroke).
- Motor – rigidity, tremor, myoclonus (possible Creutzfeldt‑Jakob, HIV‑associated neurocognitive disorder).
- Sensory – hearing/vision impairment can masquerade as cognitive decline; correcting deficits may improve performance.
Differential diagnosis
| Condition | Points to it | How it separates |
|---|---|---|
| Delirium | Acute onset, fluctuating course, impaired attention, recent precipitant (infection, drugs) | Reversible, altered consciousness, often hyperactive or hypoactive; improves with treatment of cause |
| Alzheimer’s disease | Insidious memory loss, preserved attention early, ApoE4 risk, no focal deficits | Progressive, no fluctuation, typical neuroimaging pattern (hippocampal atrophy) |
| Vascular dementia | Stepwise decline, focal neurological signs, hypertension, diabetes | Imaging shows multiple infarcts; abrupt step changes after strokes |
| Lewy body dementia | Visual hallucinations, parkinsonism, REM sleep behavior disorder, fluctuating cognition | Sensitivity to antipsychotics, prominent autonomic dysfunction |
| Frontotemporal dementia | Early personality/behaviour change, language impairment, relative memory preservation | Age <65 common, focal frontal/temporal atrophy |
| HIV‑associated neurocognitive disorder | HIV positive, CD4 low, opportunistic infections, subcortical slowing | Improves with ART; CSF may show pleocytosis |
| TB meningitis / CNS TB | Fever, neck stiffness, focal deficits, TB exposure, immunosuppression | CSF lymphocytic pleocytosis, basal meningeal enhancement on MRI |
| Cerebral malaria | Recent travel to endemic area, fever, seizures, anemia | Peripheral smear positive for Plasmodium falciparum |
| Sickle‑cell cerebral infarcts | Sickle‑cell disease, recurrent pain crises, focal deficits | MRI shows silent infarcts; history of vaso‑occlusive events |
| Metabolic encephalopathy (e.g., uremia, hepatic) | Organ failure, electrolyte disturbances, toxin exposure | Reversible with correction of metabolic derangement |
| Normal pressure hydrocephalus | Gait disturbance, urinary incontinence, dementia triad | Enlarged ventricles on imaging, CSF tap test improves gait |
Investigations
| Test | What it answers | Meaning of result |
|---|---|---|
| Full blood count, ESR/CRP | Infection, anemia, inflammation | Elevated CRP/ESR → possible infection precipitating delirium |
| Electrolytes, renal & liver panel, glucose | Metabolic derangements | Hyponatremia, hyperglycemia, hepatic failure → reversible delirium causes |
| Thyroid function (TSH, free T4) | Thyroid dysfunction | Hypo‑ or hyper‑thyroidism can mimic cognitive decline |
| HIV serology + CD4 count + viral load | HIV status, immune competence | Low CD4 with high viral load → risk for HIV‑associated dementia |
| TB work‑up (sputum GeneXpert, chest X‑ray) | Active TB | Positive GeneXpert → possible CNS TB contribution |
| Malaria rapid test / thick smear | Recent malaria infection | Positive → consider cerebral malaria if neurologic signs |
| Serum vitamin B12, folate, thiamine | Nutritional deficiencies | Low B12 → reversible cognitive impairment |
| Urinalysis & culture | Urinary infection | Significant bacteriuria → common delirium trigger |
| Brain CT (non‑contrast) | Structural lesions, bleed, hydrocephalus | Acute bleed → delirium; cortical atrophy → dementia |
| Brain MRI (if available) | Detailed parenchymal changes, infarcts, white‑matter disease | Multiple infarcts → vascular dementia; hippocampal atrophy → Alzheimer’s |
| EEG | Diffuse slowing vs. epileptiform activity | Diffuse slowing → metabolic or delirium; periodic sharp waves → CJD |
| CSF analysis (cell count, protein, glucose, cultures, PCR for TB, cryptococcus) | CNS infection, inflammatory disease | Lymphocytic pleocytosis + low glucose → TB meningitis |
| Neuropsychological testing (MMSE, MoCA) | Baseline cognitive profile, severity | Scores <24 suggest moderate‑severe dementia; rapid drop suggests delirium |
Diagnosis and severity
- Determine the primary syndrome
- Delirium: meets DSM‑5 criteria – acute onset, fluctuating course, impaired attention, and either disorganized thinking or altered level of consciousness, with evidence of a physiological trigger.
- Dementia: chronic progressive decline in two or more cognitive domains (memory, executive, language, visuospatial, praxis) that interferes with independence in daily life, not better explained by delirium.
- Classify type of dementia using history, exam, and imaging (Alzheimer’s, vascular, Lewy body, frontotemporal, HIV‑associated, etc.).
- Severity grading (use validated scales)
- Mild: MMSE 21‑26, able to perform most ADLs, some instrumental ADL loss.
- Moderate: MMSE 10‑20, needs assistance with instrumental ADLs, some basic ADL difficulty.
- Severe: MMSE <10, dependent for basic ADLs, possible incontinence, bedridden.
- Delirium severity can be staged with the Confusion Assessment Method (CAM) severity score or the Delirium Rating Scale – higher scores indicate more severe agitation, disorientation, and physiological disturbance.
- Document precipitating factors (infection, drugs, metabolic derangement) and underlying dementia subtype; this guides immediate versus long‑term management.
Management plans, monitoring, safety measures and complications are covered in part 3.
Management
Immediate stabilisation
- Airway, Breathing, Circulation – ensure patient is not hypoxic or hypotensive; treat fever, pain, dehydration promptly.
- Identify and treat precipitants – infection (urinary, respiratory, TB, malaria), metabolic derangements (electrolytes, glucose), drug toxicity or withdrawal (benzodiazepines, anticholinergics, opioids).
- Environment – quiet, well‑lit room, clocks/calendars, orientation cues; remove restraints if possible.
- Safety – low‑lying bed, padded rails, bedside commode, sitter if agitation threatens self‑harm or falls.
Definitive treatment
| Condition | First‑line pharmacologic class | Rationale | Non‑pharmacologic adjunct |
|---|---|---|---|
| Alzheimer’s disease | Acetylcholinesterase inhibitor (donepezil, rivastigmine, galantamine) | Improves cortical cholinergic transmission, modestly slows cognitive decline | Cognitive stimulation, regular exercise, caregiver education |
| Vascular dementia | Control of vascular risk (antihypertensives, statins, antiplatelets) | Prevents further infarcts | Physical therapy, gait training |
| Lewy‑body dementia | Antipsychotic avoidance; consider low‑dose atypical only if severe psychosis | High sensitivity to neuroleptics → severe parkinsonism | Structured routine, visual cues |
| Frontotemporal dementia | No disease‑modifying drugs; manage behaviour with selective serotonin reuptake inhibitors (SSRIs) for disinhibition | Targets serotonergic dysregulation | Speech therapy, occupational therapy |
| Delirium (hyperactive) | Low‑dose antipsychotic (haloperidol or atypical) only after non‑pharm measures fail | Reduces agitation, prevents injury | Reorientation, sleep‑wake cycle optimisation, early mobilisation |
| Delirium (hypoactive) | Treat underlying cause; consider low‑dose stimulant (e.g., methylphenidate) if severe lethargy | Improves alertness without excessive sedation | Mobilise, ensure adequate nutrition & hydration |
Monitoring & follow‑up
- Re‑assess mental status every 4–6 h in acute delirium (CAM or 4AT).
- Daily vitals, fluid balance, pain score, and review of medication list for anticholinergic load.
- After discharge, schedule outpatient review at 4–6 weeks, then 3‑monthly for progressive dementias.
- Use standardized scales (MMSE, MoCA, CDR) to track progression.
Contra‑indications & safety
- Avoid high‑potency anticholinergics, benzodiazepines (except for alcohol/benzodiazepine withdrawal), and typical antipsychotics in Lewy‑body disease.
- Do not use physical restraints as first resort; they increase mortality.
- Caution with haloperidol in patients with QT prolongation or Parkinsonian features.
Complications and prognosis
- Falls & fractures – due to gait instability, orthostatic hypotension, or agitation.
- Pressure ulcers – especially in bedridden delirium.
- Infections – aspiration pneumonia, urinary tract infection from catheter use.
- Nutritional deficiency – poor intake, dysphagia.
- Accelerated cognitive decline – each episode of delirium adds to long‑term impairment.
- Institutionalisation – up to 50 % of moderate‑to‑severe dementia patients require nursing home care within 5 years.
- Mortality – delirium doubles in‑hospital mortality; advanced dementias carry a median survival of 3–7 years depending on aetiology (vascular < Alzheimer’s).
High‑yield exam points
- Look‑alike conditions: delirium vs. depression (pseudodementia), vs. normal ageing, vs. dementia with superimposed delirium.
- Commonest wrong first step: ordering a CT scan before treating reversible causes of delirium.
- Examiner bedside question: “What three environmental modifications would you implement right now for this confused patient?” (Answer: orienting clock, reduce noise, ensure adequate lighting).
- Key differentiator: fluctuating consciousness and inattention → delirium; insidious, progressive loss of memory → dementia.
- Drug safety: “Why is haloperidol preferred over olanzapine in a patient with Parkinsonism?” (Answer: lower anticholinergic burden, less worsening of motor symptoms).
Clinical case
Case: A 68‑year‑old man with known hypertension and type 2 diabetes is brought from the ward after a 2‑day history of increasing confusion, visual hallucinations, and a fever of 38.5 °C. He is disoriented to time, has a tremulous hand, and a urinary catheter in situ.
Questions
- What is the most likely diagnosis?
Answer: Hyperactive delirium secondary to a urinary tract infection.
- List the immediate three management steps.
Answer: (1) Obtain vitals, start IV fluids and treat fever; (2) Send urine for microscopy, culture and start empiric antibiotics covering Gram‑negative organisms; (3) Reorient the patient, provide a calm environment, and discontinue any anticholinergic drugs.
- Which long‑term medication should be reviewed to prevent recurrence?
Answer: Review and stop any anticholinergic or sedative agents (e.g., diphenhydramine, benzodiazepines) and assess the need for the urinary catheter.
Practice questions
Question 1
A 75‑year‑old woman with known Alzheimer’s disease is brought from her home because she has become increasingly agitated, pulling at her IV line and shouting. Her temperature is 37 °C, BP 130/80 mmHg, pulse 88 bpm. What is the most appropriate next step?
A. Give intramuscular haloperidol immediately
B. Remove the IV line and call a sitter
C. Perform a rapid bedside assessment for reversible causes (infection, pain, constipation)
D. Transfer to ICU for sedation
Answer: C. Perform a rapid bedside assessment for reversible causes (infection, pain, constipation)
Explanation: Delirium is often precipitated; treating the underlying trigger is priority before antipsychotics.
Question 2
A 60‑year‑old man with sickle cell disease presents with confusion, low grade fever, and a new focal seizure. MRI shows multiple small cortical infarcts. Which dementia subtype is most likely?
A. Alzheimer’s disease
B. Vascular dementia
C. Frontotemporal dementia
D. Lewy‑body dementia
Answer: B. Vascular dementia
Explanation: Recurrent cerebral infarcts in a young patient with sickle cell point to a vascular aetiology.
Question 3
A patient with known Parkinson’s disease develops visual hallucinations and fluctuating cognition. Which medication should be avoided?
A. Rivastigmine
B. Donepezil
C. Haloperidol
D. Memantine
Answer: C. Haloperidol
Explanation: Typical antipsychotics can precipitate severe parkinsonism and worsen cognition in Lewy‑body or Parkinson‑related dementia.
Question 4
During a ward round you encounter an elderly patient who is quiet, sleepy, and has a CAM score of 0 but a MMSE of 20/30. What is the most likely explanation?
A. Severe delirium
B. Pseudodementia
C. Normal ageing with mild cognitive impairment
D. Depression
Answer: C. Normal ageing with mild cognitive impairment
Explanation: CAM negative indicates no delirium; MMSE 20 suggests mild impairment, not severe dementia.
Question 5
A 45‑year‑old woman with HIV on antiretroviral therapy presents with progressive memory loss over 12 months, normal CT brain, and a CD4 count of 350 cells/µL. Which investigation is most useful next?
A. Lumbar puncture for cryptococcal antigen
B. Serum vitamin B12 level
C. Neuropsychological testing (MoCA)
D. Repeat MRI with contrast
Answer: C. Neuropsychological testing (MoCA)
Explanation: In the absence of opportunistic infection, formal cognitive testing helps stage HIV‑associated neurocognitive disorder.
Drafted with AI assistance from standard references and reviewed for structure. Check details against your lecture notes and the Kenya MoH guideline.