Mixed dementia and hyperactive delirium: a
diagnostic challenge
Louise Dunphy ‍ ‍,1 Tosin Akin-­Komolafe,2 Zac Etheridge2
1

Surgery, Royal Berkshire NHS
Foundation Trust, Reading, UK
2
Department of Acute Medicine,
Royal Berkshire NHS Foundation
Trust, Reading, UK
Correspondence to
Dr Louise Dunphy;
​Louise.​Dunphy@d​ octors.​org.u​ k
Accepted 17 April 2021

© BMJ Publishing Group
Limited 2021. No commercial
re-­use. See rights and
permissions. Published by BMJ.
To cite: Dunphy L,
Akin-K­ omolafe T,
Etheridge Z. BMJ Case
Rep 2021;14:e238542.
doi:10.1136/bcr-2020238542

SUMMARY
It is well recognised that acute confusion or delirium
complicates up to 10% of acute medical admissions.
Disorientation in time and place with an impaired short-­
term memory and conscious level are the hallmarks of
an acute confusion. In delirium, disorders of perception
may produce restlessness and agitation. A similar state
during the final days of life is termed ’terminal delirium’.
Less than 10% of affected individuals will have a
primary neurological disorder, for example, dementia,
a neurodegenerative disease with varying aetiologies.
Currently there are at least 50 million people globally
suffering from dementia rendering it a global healthcare
problem. Mixed dementia (MD) can be defined as
a cognitive decline sufficient to impair independent
functioning in daily life resulting from the coexistence of
Alzheimer’s disease (AD) and cerebrovascular pathology.
MD occurs in patients with a neurodegenerative disorder,
such as AD, Lewy body or Pick’s disease and additionally
cerebrovascular disease. The mechanistic synergisms
between the coexisting pathologies affecting dementia
risk, progression and the ultimate clinical manifestations
remain elusive. Although AD can be diagnosed with a
considerable degree of accuracy, the distinction between
isolated AD, vascular dementia and MD, when both
pathologies coexist in the same patient remains one of
the most difficult diagnostic challenges because their
clinical presentation can overlap. Neuropathological
studies indicate that mixed vascular Alzheimer’s
dementia (MD) has a prevalence of 22% in the elderly.
The authors present the case of a 78-­year-­old man
with a diagnosis of MD presenting to the emergency
department with delirium, a common but serious acute
neuropsychiatric syndrome with the core features of
inattention and global cognitive dysfunction. This case
demonstrates the challenges in establishing a diagnosis
in patients presenting with MD and shows that a
cognitive assessment at presentation in a delirious state
offers very little diagnostic information. It is therefore
suggested to conduct a routine cognitive function
examination on patients with dementia to anticipate new
neurological signs and/or symptoms thus allowing earlier
diagnosis and treatment. However, a baseline cognitive
assessment when the patient was well, duration and
nature of deterioration as well as collateral history will
help differentiate delirium from an underlying dementia.

BACKGROUND

Delirium is a common, multifactorial presentation
in the geriatric population, especially in those individuals with a diagnosis of dementia. Delirium is
generally classified as hyperactive, hypoactive and
a mixed type based on the level of activity, while

terminal delirium is a variant that occurs during the
final days of life. Most evidence-­
based medicine
focuses on Alzheimer’s disease (AD) and vascular
dementia (VaD) as separate, uncomplicated clinical
pathologies. It remains unclear on how to differentiate between these conditions as patients may
present with permutations of the aforementioned.
However, increasing evidence exists that demonstrates that in the older patient cohort, the brain
lesions associated with each pathological process
often occur together and that AD and VaD brain
lesions interact in important ways to increase
the likelihood of clinically significant cognitive
decline.1 2 The term mixed dementia (MD) is often
given to the coexistence of AD and VaD and its
prevalence is likely to increase as the population
ages. Admittedly, the differentiation between AD,
VaD and MD is complicated by symptom overlap
and the lack of well-­defined diagnostic criteria to
help establish the diagnosis. Despite advances in
neuroimaging, MD remains a challenging clinical
diagnosis to establish, however, controlling cardiovascular risk factors such as hypertension and hyperlipidaemia, likely represent important strategies for
preventing or slowing its progression. Admittedly,
the search for a single unifying diagnosis to explain
signs and symptoms, also known as the ‘Occam’s
razor rule’, likely does not apply to the geriatric
population, who are at risk of neurodegeneration
from both AD and cerebrovascular disease.3

CASE PRESENTATION
A 78-­year-­old male UK resident with a diagnosis
of mixed AD and VaD presented to the emergency
department with a 5-­day history of increased confusion, agitation and aggression. His carer reported
his refusal to have personal care and a decreased
appetite. He was referred to the Memory Clinic
in 2011 when he developed cognitive problems.
An MRI showed small areas of vascular damage
with cerebral atrophy (figure 1). He commenced
treatment with donepezil. His dementia was now
severe with limited speech, comprehension and
the inability to have a conversation. He had a lack
of circadian rhythm impacting on the ability of
his live-­in carer and family to look after him. His
functional baseline included the ability to dress
himself and guidance required for a shower. He no
longer recognised his children. He was registered
blind due to hereditary retinal dystrophy. Three
months prior to this presentation, he experienced
a ‘black-­out’ of uncertain aetiology. A subsequent
24-­hour tape showed normal sinus rhythm. One
month later, he had an episode of atrial fibrillation

Dunphy L, et al. BMJ Case Rep 2021;14:e238542. doi:10.1136/bcr-2020-238542

1

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Case report

Table 1 Laboratory investigations showed an elevated white cell
count and CRP
Haematology

Figure 1 An MRI showed small areas of vascular damage with
cerebral atrophy.

Biochemistry

Haemoglobin 141 g/L (118–148)

Sodium 133 mmol/L (133–146)

White blood cell count 11.70×109/L
(3.5–11)

Potassium 4.9 mmol/L (3.5–5.3)

Platelet count 190×109/L (150–400)

Urea 12.1 mmol/L (1.0–7.8)

Mean cell volume 86 fl (80–100)

Creatinine 34 mmol/L (50–130)

Mean cell haemoglobin 30.9 pg (28–33)

Alkaline phosphatase 21 U/L (30–300)

Neutrophil count 359×109/L (2–7.5)

Alanine transaminase 88 U/L (<35)

Monocyte count 1.15×109/L (0.2–0.8)

Albumin 37 g/L (40–50)

Eosinophil count 0.05×109/L (0.0–0.4)

Calcium 2.32 mmol/L (2.2–2.6)

Basophil count 0.04×109/L (0.0–0.2)
Clotting

CRP 220 mg/L (<5)

Prothrombin time 15.5 s (9–12)

with a fast-­ventricular response requiring direct current cardioversion. Six weeks later, he developed acute onset of central and
epigastric pain. A 12 lead ECG showed sinus bradycardia with
no ischaemic change. His troponin was normal. His transthoracic
echocardiogram showed an ejection fraction of 55% with no
significant valve disease. The 24-­hour ECG showed sinus rhythm
with episodes of sinus bradycardia (predominantly nocturnal).
The heart rate profile was between 46 and 86 beats per minute
(mean 60 beats per minute) and all intervals were within normal
limits. He declined anticoagulation. His cardiac CT scan showed
an average amount of coronary calcification for a man of his
age (coronary calcification score 510, 50th percentile for age
and gender). There was potentially flow-­limiting stenosis within
the proximal and mid-­left anterior descending artery and also
the distal dominant left circumflex. Due to his chest pain which
likely represented angina, he commenced treatment with a low
dose of bisoprolol (1.25 mg), glyceryl trinitrate spray and atorvastatin (40 mg once daily). There was a decline in his cognitive function since donepezil was stopped due to concerns
about his chest pain. He developed complex partial seizures and
commenced treatment with Keppra 1000 mg two times per day.
As he could not tolerate this dose, it was reduced to 750 mg with
the addition of sodium valproate which caused a rash. Hence,
he was treated with carbamazepine titrated to 400 mg two times
per day while his Keppra was reduced to 250 mg two times
per day. One week later, he was admitted with confusion and
hyponatraemia (Na+ 112) with a plasma osmolality of 259. His
carbamazepine was discontinued and lamotrigine commenced.
His medications included levetiracetam liquid 500 mg mane and
750 mg nocte, flecainide 50 mg two times per day, lamotrigine
50 mg mane and 25 mg nocte, folic acid liquid 5 mg once daily,
memantine 20 mg nocte, aspirin 75 mg once daily and timolol
0.75% applied to both eyes. He was a non-­smoker and did not
consume alcohol. He was independently mobile. Classical music
helped to keep him calm. His observations were as follows:
temperature 37.2°C, blood pressure 107/83 mm Hg, heart rate
63, respiratory rate 16 and oxygen saturation (SpO2) 97% on
air. His pulse was regular and heart sounds were normal. Respiratory examination confirmed bibasal crackles. His abdomen
was soft and non-­tender. Rectal examination was unremarkable
with no evidence of faecal impaction. There was no peripheral
oedema. He appeared restless and agitated, therefore, physical
examination was challenging.

INVESTIGATIONS

His ECG showed sinus rhythm with a degree of ventricular
conduction delay (QRS duration
2

APTT 28.9 s (30–45)
APTT, Activated partial thromboplastin time; CRP, C-­reactive protein.

121 ms) but with no specific abnormality. His chest radiograph showed left-­sided consolidation. Laboratory investigations
including a full blood count, C-­reactive protein (CRP), renal and
liver function tests were requested (table 1). His blood cultures,
urinalysis and point of care influenza swab were negative. His
venous blood gas was unremarkable. A bladder scan showed
that he was in urinary retention and a catheter was inserted. His
glucose was in the normal range.

DIFFERENTIAL DIAGNOSIS

He was diagnosed with hyperactive delirium on a background
of mixed AD and VaD. Laboratory investigations showed an
elevated white cell count (11.7×109/L) and CRP (220 ng/L) as
well as an acute kidney injury (urea 12.1 mmol/L, creatinine
34 mmol/L) (table 1). His liver function tests and clotting were
normal. A bladder scan confirmed the diagnosis of acute urinary
retention and a catheter was inserted. As his physical examination revealed bibasal crackles and left-­
sided consolidation
was evident on his chest radiograph, he was diagnosed with a
community-­acquired pneumonia, CURB-65 score of 3. He also
developed fast atrial fibrillation, at a rate of 130 beats per minute
and remained normotensive. He remained restless and agitated.

TREATMENT

As per the Trust’s antimicrobial guidelines, he commenced treatment with Amoxicillin 1 g three times a day intravenously. His
fast atrial fibrillation was rate controlled with digoxin and bisoprolol. His agitation was treated with haloperidol and lorazepam.
He developed a maculopapular rash over 48–72 hours in the
context of recent antimicrobial therapy on his trunk, limbs and
his scalp (figures 2 and 3). There were no blisters or excoriation,
or evidence of oral, ocular or genital involvement. The clinical
diagnosis was of a drug exanthem and it remained unknown
which antibiotic was the cause. Diprobase cream was applied
two times per day to his skin. Elocon ointment was prescribed as
required if his skin became itchy as it recovered and dried out.
He was washed with dermol 500.

OUTCOME AND FOLLOW-UP

His bloods were monitored twice weekly. He became very
agitated, confused and physically aggressive towards the nursing
staff. He was pacing up and down the ward in a combative
manner. He was reviewed by the old age psychiatry team. He
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Case report

Figure 3 Image showing there were no blisters or excoriation. The
clinical diagnosis was of a drug exanthem.

adverse physical, cognitive and psychological consequences and
is associated with an increased mortality and length of hospital
stay. Delirium represents a serious complication in patients
after anaesthesia and surgery and is predictive of mortality
at 6 months in patients in intensive care unit (ICU). Terminal
delirium, a form of the delirious state occurring during the final
days of life, is not a Diagnostic and Statistical Manual of Mental
Disorder’s diagnosis and is often unrecognised in patients with
multiple comorbidities or in those individuals requiring hospitalisation for exacerbation of a chronic condition. Dying is a
complex process but early recognition of the dying phase can
empower the patient and their families.
Dementia is a well-­recognised risk factor for delirium, occurring in 66% of the geriatric population. Indeed, the occurrence of delirium may alter the clinical course of an underlying
dementia with negative prognostic implications, including
further functional and cognitive decline, increased rehospitalisation and death. Patients with hyperactive delirium demonstrate features of restlessness, as described in our case, agitation,
hypervigilance, hallucinations and delusions. An alteration
in the patient’s behaviour is usually reported by a relative or
friend rather than by the patient. It is important to check for
disorientation and memory impairment with the mini-­mental
test, which is challenging in this patient cohort and not very
helpful. The drug chart should be reviewed as the risk of
drug-­induced delirium is high especially in elderly hospitalised
patients in whom polypharmacy, altered pharmaco kinetics and
underlying pathology all interact to cause delirium. Although
the pathophysiological mechanisms underlying delirium remain
to be fully elucidated, its aetiology is multifactorial. Medications acting on the cholinergic, γ-aminobutyric acid-­mediated
and monoaminergic neurotransmitter pathways are frequently
involved. The patient should be assessed for an acute illness.
Physical examination is required to exclude faecal impaction
and urinary retention. The differential diagnosis of delirium is
broad and includes a systemic disorder, drug toxicity, a central
nervous system disorder or a malignancy (table 2). The National
Institute of Neurological Disorders and Stroke-­
Association
Internationale pour la Recherche et l’Enseignement en Neurosciences (NINDS-­AIREN) diagnostic criteria for VaD does not
include a category for MD, recommending instead the term AD
with cerebrovascular disease.4 Admittedly, there is a significant
overlap between AD, VaD and synucleinopathies like Lewy
body dementia. Pathological Parkinson’s disease is present in
20% of patients with AD and 50% of cases of dementia with
Lewy bodies are associated with AD pathology.5 MD prevalence rates vary widely from 2% to 60%.6 The brain lesions
of AD include extracellular amyloid plaques and intracellular
neurofibrillary tangles. Neuropsychiatric signs of VaD include
apathy, emotional liability, lack of motivation and psychomotor
retardation. Memory, language and praxis have more variability
than AD. Individuals with a diagnosis of VaD present with more
agitation (40% vs 14%), sleep disturbance (57% vs 32%), higher
rates of depression (48% vs 20%) and aberrant motor behaviour
(31% vs 13%) than those with AD. VaD can be differentiated
from AD by the early onset of gait disturbance, falls, urinary
problems, a temporal association following a stroke and the
presence of ischaemic periventricular leukoencephalopathy. In
MD, both pathologies can occur together and interact in several
ways to increase the likelihood of a clinically significant cognitive decline. Indeed, autopsy series have suggested that a coexisting vascular pathology occurs in up to 8% of patients with
AD.7 Once the acute delirium has resolved, then the workup for
MD could be considered.

Dunphy L, et al. BMJ Case Rep 2021;14:e238542. doi:10.1136/bcr-2020-238542

3

Figure 2 A maculopapular rash developed on his trunk, limbs and his
scalp.
was prescribed haloperidol (0.5 mg doses not exceeding 3 mg/24
hours) as required (prn) for delirium and his memantine 20
mg once daily was continued. Long-­term use of antipsychotics
to manage the behavioural and psychological symptoms of
dementia were advised once he recovered from his delirium.
Occupation and distraction with music and tactile objects
including the ‘twiddle muff ’ were provided by the old age psychiatry team. He developed increased restlessness and refused to
eat. He pulled out his catheter causing urethral trauma. A Deprivation of Liberty Safeguards form was completed. He deteriorated clinically and it became apparent that he was in terminal
delirium. Following discussion with his family, he was reviewed
by the palliative care team and commenced a syringe driver with
morphine 5 mg, midazolam 5 mg, hyoscine butyl bromide 60
mg and haloperidol 1.5 mg. He died 5 days following his admission, with his family at his bedside. This case demonstrates the
inherent challenges in taking a history, performing a physical
examination and investigations in patients with a diagnosis of
MD presenting with acute onset of delirium. In addition, it
demonstrates the importance of performing a delirium workup
rather than diagnosing and treating dementia when in a state of
delirium. Teasing out the other characteristics of an underlying
dementia is nearly impossible unless the delirium resolves.

DISCUSSION

AD and VaD are the two most prevalent causes of dementia
and it remains a diagnostic challenge to differentiate them from
MD. Our patient also had delirium, a Latin term meaning ‘going
off the ploughed track’ presenting as a transient, reversible
syndrome that is acute, multifactorial and fluctuating, occurring in the setting of an acute medical condition or a medication
adverse effect. Indeed, it is well documented that delirium has

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Case report

Table 2

The differential diagnosis and investigation of delirium

Differential diagnosis

Investigations

Systemic disorder

Check urine
Blood cultures
Laboratory investigations—white cell
count, renal function, liver function,
glucose, calcium, CRP, troponin
Arterial blood gas
ECG
Chest radiograph

Sepsis is common
Alcohol withdrawal
Metabolic disorder
►► Hyperglycaemia or hypoglycaemia
►► Vitamin deficiency
►► Endocrine disease (thyroid/adrenal)
►► Uraemia
►► Hypercalcaemia is common

Consider magnesium, amylase, porphyrins,
thiamine, vitamin B12, folate, thyroid-­
stimulating hormone, free T4

Myocardial ischaemia
Organ failure
►► Renal
►► Respiratory
►► Liver
►► Cardiac
Drug toxicity

Check prescribed medication
Serum alcohol
A drug screen

CNS disorder
►► Dementia—Alzheimer’s common
►► CVA
►► Intracranial bleed (SAH, subdural)
►► Infection (encephalitis, meningitis)
►► Trauma
►► Malignancy
►► Post-i­ ctal: non-­convulsive status
►► Cerebral vasculitis (SLE/PAN)

Consider a CT scan with contrast
Lumbar puncture
Electroencephalogram
Blood cultures
CRP
Syphilis and Lyme serology

Malignancy
►► Intracerebral tumour including
meningioma

Chest radiograph
CT head and chest
Serum calcium

CNS, Central nervous system; CRP, C-­reactive protein; CVA, cerebravascular accident; SLE,
systemic lupus erythematosus.

A criterion for the pathological diagnosis of mixed-­vascular-­
alzheimer-­
dementia (MVAD), including the combination of
autopsy-­
confirmed AD, with multiple lacunar infarcts in the
cortex, basal ganglia, thalamus, hippocampus and white matter,
with an infarcted volume of 30–50 mL has been proposed.8 The
MVAD, as well as other dementias, start several years before the
symptoms display. According to the vascular theory, cardiovascular disease such as hypertension and dyslipidaemia as well as
diabetes mellitus can produce several vascular changes resulting
in thickening of the capillary basal membrane and the accumulation of collagen in the vascular endothelium. These changes
affect the cerebral microvasculature reducing the cerebral blood
flow.9 Terminal delirium is a reliable predictor of impending
death within a few days. Agitation makes communication difficult and intensifies families’ frustrations and emotional stress.
Glaser and Strauss’ theories of ‘context of awareness and dying’
explain different patterns of onset and course of terminal
delirium in dying patients.10 11
The dementia workup should be completed for suspected VaD.
Comorbidities including cardiac or cerebrovascular risk factors,
diabetes and obstructive sleep apnoea raises the risk of VD.
Smoking, passive inhalation of smoke, obesity and alcohol excess
raises the VD risk. The association of the apolipoprotein E ε4
genotype with an increased risk for both AD and cardiovascular
4

disease further suggests a potential link.8 Amyloid deposition in
cerebral blood vessels due to AD increases the risk for haemorrhagic strokes and subsequent VaD. Several epidemiological
studies have suggested that age is the main risk factor followed
by hypertension, hyperhomocysteinaemia and leukoaraiosis that
are shown as hyperintensities on brain MRI.12 These factors
increase the risk of injury to cerebral blood vessels, leading
to cerebrovascular disease which can manifest with cognitive
defects exceeding those of normal ageing. There remains no
consensus for the diagnosis of MVAD. However, the Alzheimer’s Disease Diagnostic and Treatment Centres (ADDTC), the
NINDS-­AIREN have proposed diagnostic criteria.13 According
to the ADDTC criteria, the diagnosis of MVAD requires the existence of a typical AD and closely related cerebrovascular disease.
The International Society of Vascular Behavioural and Cognitive
Disorders (VASCOG) states that a near temporal relationship,
ideally 3 months, between a vascular event and the development
of cognitive symptoms and signs must be present to suspect
VD especially if previous imaging has been undertaken.14 Both
medial temporal atrophy and large vessel disease contribute to
global cognitive impairment and from a structural radiological
perspective, medial temporal atrophy is generally considered to
be the best surrogate marker of degenerative pathology in AD.
Idiopathic normal pressure hydrocephalus may mimic VaD with
its symptom triad of ataxia, urinary incontinence and dementia.
Delirium is diagnosed based on special tests such as 3D-­CAM
(Confusion Assessment Method) which can be completed in an
average of 3 min and performs very well compared with an expert
evaluation. In order to identify a CAM-­positive delirium, the
two essential features of ‘acute onset and fluctuating course’ and
‘inattention’ are required, in addition to ‘disorganised thinking’
or ‘altered level of consciousness’. Furthermore, the CAM for
Intensive Care Unit Patients Scale has been validated in medical
and coronary ICU patients. The 4 As test can also be used to
diagnose delirium in the geriatric cohort. It focuses on alertness,
AMT4, attention and an acute change or a fluctuating course. In
addition, a validated model of delirium prediction based on four
criteria evaluated using specific scales, include illness severity
(Acute Physiology and Chronic Health Evaluation Score), visual
impairment (Snellen test), cognitive impairment (Mini-­Mental
State Evaluation Score) and serum urea:creatinine ratio. CT
(CT) visualises established infarcts, whereas MRI enables its
degree, location and extent to be assessed.
Once the diagnosis has been established, the main goal of
delirium therapy is to identify important, potentially life-­
threatening, treatable, organic causes responsible for this
syndrome. Serious agitation with delirium requires emergency
pharmacological intervention. However, an organic cause must
first be eliminated before titrating to effect. Neuroleptics such
tolerated, easily titratable medication
as haloperidol, a well-­
can be used for sedation. It has been shown that management
of cognitive dysfunction, sleep deprivation, immobility, visual
and hearing impairment as well as multimodal physiotherapy
reduced the incidence of delirium in hospitalised elderly patients.
Death anxiety or an apprehension generated by an awareness of
oncoming death expressed by care workers, has an impact on a
patient’s emotional well-­being. Currently, therapeutic guidelines
suggest that treatment is symptomatic and offers only a modest
clinical benefit once a patient has developed MVAD, without
any modification of its evolution. Large trials focusing on the
pharmacological management of VaD are lacking. Acetylcholinesterase inhibitor drugs such as donepezil, galantamine and
rivastigmine as well as antidementia drugs such as memantine
can be used to treat patients with AD and VaD.15 Galantamine
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Case report

and memantine have shown therapeutic benefits for both cognitive and functional outcomes and randomised controlled trials
have shown that donepezil has treatment benefits for patients
with mild to moderate AD and VaD.16–19 Cholinesterase inhibitors have also shown reproducible beneficial effects on cognitive and functional outcomes in patients with MD.20 Secondary
prevention is necessary to prevent the development of acute
or recurrent stroke and to reduce the progression of cerebral
related changes. The Perindopril Protection Against
vascular-­
Recurrent Stroke Study showed that active treatment with an
ACE inhibitor, given alone or in combination with a diuretic,
was associated with a reduced dementia risk and cognitive
decline in patients with recurrent stroke.21 Lifestyle modification factors including regular exercise and a healthy diet with
a low consumption of red meat is advised to reduce the risk of
developing AD. Further prospective studies and randomised
controlled trials are required to further delineate and enhance
our understanding of MVAD.
Most individuals have some idea of how they want to live
their life, however, a large proportion have not communicated
of-­
life decision to family. The majority of family
their end-­
members do not recognise the terminal nature of dementia and
fail to conceptualise between dementia and impending death.
Shared communication with family may enhance their understanding of the dementia trajectory and the types of decisions
that need to be made. Treatment should be provided for reversible causes of delirium, as in our case, hyperactive delirium
was managed with intravenous antibiotics, while maintaining
a balance between somnolence and control of agitative symptoms. This case demonstrates the impact of terminal delirium
and the support that geriatricians and palliative care physicians
provide patients and their families during the advanced stages of
the disease. This case also highlights the importance of advance
care planning, addressing emotional distress and symptom

Learning points
►► This case demonstrates the challenges in establishing a

diagnosis in patients with a diagnosis of mixed dementia. It
highlights the importance of minimising cardiovascular risk
factors such as hypertension and hypercholesterolaemia. An
ECG should be performed to exclude cardiac pathology.
►► Individuals with dementia with Lewy bodies can present
with episodic reduced consciousness but this is not found in
Alzheimer’s. A trial of antiepileptic therapy may be required
even if the diagnosis is not confirmed (the long-­term
antiepileptic side effects are much less of a concern in this
patient cohort as their life expectancy is short).
►► A cognitive assessment at presentation in a delirious state
offers very little diagnostic information. A baseline cognitive
assessment when the patient was well, duration and nature
of deterioration and collateral history will help differentiate
delirium from an underlying dementia.

Dunphy L, et al. BMJ Case Rep 2021;14:e238542. doi:10.1136/bcr-2020-238542

burden as well as developing the appropriate treatment regimen
for a delirious patient.
Contributors LD wrote the case report. TA-­K was involved in the literature review.
ZE edited the paper.
Funding The authors have not declared a specific grant for this research from any
funding agency in the public, commercial or not-­for-­profit sectors.
Competing interests None declared.
Patient consent for publication Obtained.
Provenance and peer review Not commissioned; externally peer reviewed.
ORCID iD
Louise Dunphy http://​orcid.​org/​0000-​0001-​5499-​415X

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Dunphy L, et al. BMJ Case Rep 2021;14:e238542. doi:10.1136/bcr-2020-238542

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