Geriatrics- Delirium Flashcards
80 year old man. Presented to the Emergency Unit with a 3 day history of confusion, disorientation, urinary and faecal incontinence, falling and an inability to perform his basic activities of daily living.
Relatives reported that he had been a “bit forgetful” in the preceding year. Nevertheless he managed all basic and instrumental activities of daily living.
He had been treated about a year before for benign prostatic hypertrophy. On oxybutynin 5 mg twice daily for urinary frequency and nocturia.
In the past two days, his mental state had deteriorated markedly. He appeared to alternate between periods when he was quiet, sleepy and lethargic, to episodes where he became agitated, markedly disorientated, and paced up and down. The hyperactive symptoms were especially marked at night. His gait had become unsteady and he had fallen once on attempting to “escape” from the house. He had hardly eaten or taken fluids during this period.
In Emergency Unit: Unable to sustain attention for any length of time when an attempt was made to interview him. He was easily distracted by surrounding noises in the EU. His speech was incoherent and dysarthric. He kept picking at the bed clothes and attempted to catch imaginary objects in the air.
Examination: Temp. 38.5oC. Pulse 82/min and regular. BP 120/65 lying and 110/60 standing. Oxygen saturation 96% in room air. Normal praecordial & chest exam. Abdomen: mild suprapubic tenderness, no masses or visceromegaly. No obvious focal or lateralising signs on neurological examination. Power at least 4/5 in all limb muscle groups. Deep tendon jerks symmetrically present. Plantars equivocal bilaterally. Fundoscopic examination not possible because of poor co-operation.
What do you think the likely diagnosis is?
What are the main features of this condition on mental state examination?
What are the possible causes of this syndrome, and
How would you investigate it?
What is the difference between “dementia” and “delirium”?
What predisposes people to developing this acute confusional state?
What other conditions should you think of in a “confused” patient?
How would you manage this patient?
What is the prognosis?
- Likely Diagnosis:
The patient is likely suffering from delirium, specifically with mixed features (hypoactive and hyperactive). Delirium is characterized by an acute onset and fluctuating course of confusion, attention deficits, and changes in consciousness. This is consistent with the patient’s waxing and waning state of agitation and lethargy, along with disorientation and hallucinations (attempting to catch imaginary objects).
- Main Features of Delirium on Mental State Examination:
- Acute onset and fluctuating course: Sudden deterioration over a few days, with periods of agitation and lethargy.
- Impaired attention: Easily distracted, unable to sustain attention.
- Disorientation: To time, place, and often person.
- Perceptual disturbances: -Hallucinations or illusions (catching imaginary objects).
- Speech abnormalities: Dysarthria, incoherent speech.
- Sleep-wake cycle disturbances: Worse at night, alternating between agitation and sleepiness (sundowning).
- Possible Causes of Delirium (Delirium Precipitants):
Delirium can have multiple causes, including:
Infections: Urinary tract infection (likely given suprapubic tenderness and fever) or pneumonia.
Medications: Oxybutynin is an anticholinergic drug, which can precipitate delirium, particularly in older adults.
Metabolic imbalances: Electrolyte disturbances, dehydration (he has hardly eaten or taken fluids).
Hypoxia: Even though O₂ saturation is 96%, this should still be monitored.
Neurological events: Stroke or transient ischemic attack (though less likely given no obvious focal signs).
Urinary retention: Common in elderly males with benign prostatic hypertrophy.
Constipation: Could lead to delirium in the elderly.
Environmental changes: New environments, such as a hospital, can worsen confusion in elderly patients.
Investigations for Delirium:
Blood tests: Full blood count (FBC), electrolytes, renal function, liver function, glucose, and calcium to detect metabolic abnormalities.
Inflammatory markers: CRP or ESR to check for infection.
Urine dipstick and culture: To investigate a urinary tract infection.
Chest X-ray: To rule out pneumonia or other chest pathology.
ECG: Check for cardiac issues, arrhythmias.
Neuroimaging (CT or MRI brain): If a neurological event like stroke is suspected.
Blood cultures: If sepsis is suspected.
Arterial blood gas (ABG): To check for metabolic or respiratory causes of delirium.
Difference Between Dementia and Delirium:
Delirium:
Acute onset (hours to days).
Fluctuating course.
Impaired attention and awareness.
Reversible with treatment.
Dementia:
Chronic and progressive (months to years).
No fluctuation (usually steady decline).
Normal level of consciousness and attention until late stages.
Irreversible in most cases (e.g., Alzheimer’s).
Predisposing Factors for Delirium:
Age: The elderly are particularly vulnerable.
Cognitive impairment: A history of being “a bit forgetful” may indicate early dementia, increasing the risk for delirium.
Sensory impairment: Vision or hearing problems.
Polypharmacy: The use of anticholinergic drugs like oxybutynin.
Comorbidities: Benign prostatic hypertrophy, previous infections.
Dehydration or malnutrition: He has had little to eat or drink.
Hospitalization: New environments can precipitate confusion.
Other Conditions to Consider in a Confused Patient:
Dementia: If confusion persists, it could indicate underlying dementia.
Stroke or TIA: Though no focal signs, should still be considered.
Sepsis: Fever and confusion might point to an infection leading to sepsis.
Electrolyte imbalances: Hypercalcemia, hyponatremia.
Hypoglycemia: Always check blood sugar.
Medication toxicity: Overdose or side effects from drugs like oxybutynin.
Alcohol withdrawal: If relevant to history.
Management of Delirium:
Treat the underlying cause: In this case, possible infection (e.g., UTI) and medication adjustment (reduce or stop oxybutynin).
Hydration and nutrition: Ensure adequate fluid intake and rehydration.
Monitor vitals: Regular checks of temperature, pulse, BP, oxygen saturation.
Avoid restraint and sedation if possible: Non-pharmacological approaches should be prioritized (e.g., reorienting the patient, ensuring a calm environment, regular reassurance).
Medications: Antipsychotics (e.g., haloperidol) may be used cautiously for agitation if non-pharmacological measures fail, but avoid sedating elderly patients where possible.
Prognosis:
Delirium is reversible, especially if the underlying cause (e.g., infection, dehydration, medication) is treated promptly.
If untreated, complications such as dehydration, aspiration pneumonia, or worsening confusion can occur.
Risk of recurrence: This patient may be at risk of further episodes of delirium, particularly in the context of illness or hospitalization, and may have underlying cognitive impairment (early dementia).
Long-term outcome: Recovery depends on the underlying condition, but even after resolution of delirium, some patients, particularly the elderly, may not return to their prior baseline cognitive function.
Delirium: definition (DSM IV)
(1) a disturbance of consciousness (i.e. reduced clarity of awareness of environment) with reduced ability to focus, sustain or shift attention
(2) a change in cognition (e. g. memory deficit, disorientation) or development of a perceptual disturbance that is not better accounted for by a pre-existing dementia
(3) the disturbance develops over a short period (usually hours to days) and tends to fluctuate during the course of the day.
(4) there is evidence from the history, physical exam or investigations that suggests the aetiology of the delirium
Delirium key features
- global cerebral dysfunction
= acute brain failure / acute generalised encephalopathy / “organic brain syndrome” - fluctuation
- circumstances of onset: acute, in context of a precipitating illness
- a serious condition. It indicates that there is an underlying pathological process severe enough to affect brain function acutely. Untreated, delirium can coma death
risk factors of delirium
old age
severe illness
dementia
physical frailty
admission with infection or dehydration
visual impairment
poly-pharmacy
surgery e.g. fractured neck of femur
alcohol excess
renal impairment
HIV infection
precipitating factors
immobility
use of physical restraints
use of bladder catheter
iatrogenic events
malnutrition
psycho-active meds
intercurrent illness
dehydration
prevalence
difficult to assess
common
average 20% in older people in general hospitals (7-61%) UK
GSH study: 20 % of admissions to acute general medical wards (incl. young)
Post neck of femur fracture: 10-50%
What is the role of the central cholinergic system in delirium?
The central cholinergic system is crucial for attention, arousal, and cognitive function. A disruption in acetylcholine transmission is one of the key mechanisms leading to delirium, particularly in older adults. Many medications with anticholinergic properties (e.g., oxybutynin) can trigger delirium by reducing acetylcholine activity in the brain.
How does a deficiency of acetylcholine contribute to delirium?
Acetylcholine deficiency impairs neuronal communication, which affects attention, memory, and learning. This deficiency is particularly prominent in delirium, where anticholinergic medications, metabolic derangements, and conditions like hypoxia or sepsis reduce acetylcholine availability in the brain.
What other neurotransmitters are implicated in the mechanism of delirium?
Besides acetylcholine, serotonin and dopamine imbalances are involved in delirium.
Serotonin: Low serotonin levels are associated with mood disturbances and cognitive dysfunction in delirium.
Dopamine: Excessive dopamine activity, especially in the frontal cortex, contributes to hallucinations, agitation, and disorganized thinking seen in delirium.
How does neuro-inflammation contribute to delirium?
Neuro-inflammation occurs when systemic infection or illness activates microglial cells in the brain. This activation is mediated by cytokines like IL-6 and TNF-alpha, which cross the blood-brain barrier or signal through neural pathways. The resulting inflammation disrupts neural circuits, impairing cognition and leading to delirium.
What role do hypothalamic-pituitary-adrenal (HPA) axis abnormalities play in delirium?
In delirium, the HPA axis may be dysregulated, leading to increased cortisol levels. Elevated cortisol affects brain regions like the hippocampus and prefrontal cortex, impairing memory, attention, and cognition. Prolonged stress and chronic illness can exacerbate HPA axis dysfunction, contributing to delirium.
What regional brain changes are seen on MRI or PET scans in patients with delirium?
MRI and PET studies show regional brain changes in delirium, such as:
Reduced perfusion in the frontal and parietal lobes, areas involved in attention and executive function.
Decreased metabolism in the posterior cingulate cortex and precuneus, critical regions for consciousness and cognitive integration.
Widespread atrophy may also be seen in patients with underlying dementia who develop delirium.
What electroencephalographic (EEG) changes are associated with delirium?
EEG in delirium typically shows diffuse slowing of background activity, reflecting global cortical dysfunction.
Generalized theta and delta wave slowing is common, indicating impaired cortical communication.
In hyperactive delirium, there may be intermittent fast activity, while in hypoactive delirium, the slowing is more pronounced and continuous.
Name the the 4 causes of delirium
(1) primary cerebral disease
(2) systemic disease
(3) intoxication with exogenous substances
(4) withdrawal states esp. alcohol, benzodiazepines
How can ischemia contribute to delirium, particularly in relation to cerebral infarcts?
Ischemia, particularly due to large cerebral infarcts, can lead to brain edema (swelling), which increases intracranial pressure and disrupts brain function. This can impair cognitive function and attention, leading to delirium, especially in the acute phase of stroke or after a large infarct.
What space-occupying lesions (SOLs) can cause delirium?
Space-occupying lesions (SOLs) can cause increased intracranial pressure, brain compression, and localized dysfunction, leading to delirium. These SOLs include:
Subdural haematoma: Often seen in elderly or post-trauma patients.
Extradural haematoma: Typically associated with head trauma and arterial bleeding.
Subarachnoid haemorrhage: Sudden onset with severe headache and confusion.
Intracerebral haematoma: Can cause mass effect and increase pressure on surrounding brain tissue.
Primary or secondary brain tumours: Tumour growth leads to compression and edema, causing cognitive disturbances.
Hydrocephalus: Accumulation of cerebrospinal fluid (CSF) causes pressure on brain structures.
Cerebral abscess: Infection within the brain can increase pressure and disrupt normal brain activity.
How do infections such as meningitis and encephalitis lead to delirium?
Meningitis and encephalitis cause inflammation of the brain and its surrounding membranes, which disrupts normal neural function, leading to cognitive impairment and delirium.
Meningitis: Inflammation of the meninges (outer coverings of the brain), often accompanied by fever, neck stiffness, and altered mental state.
Encephalitis: Inflammation of the brain parenchyma itself, commonly viral, resulting in confusion, seizures, and neurological deficits
How can epileptic activity cause delirium, especially post-generalized tonic-clonic seizures (GTCS)?
Following a generalized tonic-clonic seizure (GTCS), patients may enter a postictal state characterized by confusion, agitation, and disorientation, leading to delirium.
Non-convulsive status epilepticus or complex partial seizures can present as prolonged periods of confusion or altered mental state without obvious convulsive activity, contributing to the development of delirium.
How can hypoxia contribute to delirium, and what are its common causes?
Hypoxia reduces oxygen delivery to the brain, impairing cognitive function and leading to delirium. Common causes include:
Primary respiratory diseases: Pneumonia, pulmonary edema, and pulmonary embolism.
Secondary hypoxia: Severe anemia, carbon monoxide (CO) poisoning.
Poor cardiac output: Seen in conditions like severe congestive cardiac failure (CCF) or dysrhythmias.
What metabolic conditions can lead to delirium?
Metabolic disturbances affect brain function, contributing to delirium. Common causes include:
Renal or hepatic failure: Toxin accumulation (e.g., urea, ammonia) affects the brain.
Electrolyte disturbances: Hyponatremia, hypercalcemia, and hypocalcemia can disrupt neuronal activity.
Hypo- or hyper-glycemia: Impaired glucose regulation can lead to altered mental status.
Acidosis: Metabolic or respiratory acidosis can depress cognitive function.
Hypercapnia: Elevated carbon dioxide levels impair brain function.
What endocrine disorders can cause delirium?
Endocrine imbalances disrupt brain metabolism and lead to delirium. These include:
Myxoedema (hypothyroidism): Slows metabolism, causing cognitive impairment.
Thyrotoxicosis: Hypermetabolism leads to agitation and confusion.
Hypopituitarism: Reduced hormone production affects multiple body systems, leading to delirium.
Hypo- and hyperadrenalism: Adrenal hormone imbalances (e.g., Addison’s disease, Cushing’s syndrome) can impair cognition.
What vitamin and nutritional deficiencies are associated with delirium?
Deficiencies in essential vitamins affect neurological function, leading to delirium. These include:
Thiamine deficiency (Wernicke’s encephalopathy): Affects brain metabolism, leading to confusion, ataxia, and ocular disturbances.
Folic acid deficiency: Can lead to cognitive dysfunction and mental confusion.
Nicotinic acid deficiency (pellagra): Causes cognitive disturbances along with dermatitis and diarrhea.
Vitamin B12 deficiency: Causes neuropsychiatric symptoms, including confusion and memory impairment.
