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Goitre, thyroid disease and thyroid malignancy
Investigations
The following investigations are important in patients with
goitre/thyroid nodule:
• Thyroid function tests: hyperthyroidism or
hypothyroidism. Thyroid-stimulating hormone (TSH)
level is usually checked first; if it is abnormal, free
triiodothyronine (T3) and thyroxine (T4) levels are
measured.
• Calcitonin secretion: increased in medullary thyroid
cancer, and should be measured only in patients in
whom there is high clinical suspicion of medullary
thyroid cancer.
Imaging
• Thyroid size and nature: assessed by ultrasound,
CT or magnetic resonance imaging (MRI) scan.
Ultrasonography is quick to perform and can differentiate
between cystic and solid nodules. It cannot distinguish
benign from malignant lesions. CT or MRI is useful in
assessing compression or invasion of other structures.
• Respiratory function tests, including flow–volume
loop: if signs of upper airway obstruction are present.
• Radionuclide imaging (thyroid scintigraphy): can
distinguish ‘hot nodules’ (high uptake of radioisotope)
from ‘cold nodules’ (due to lack of concentration of
radioisotope). Unfortunately, there are no specific
features that indicate the benign or malignant nature
of a thyroid nodule. Malignant nodules are more likely
to be cold than hot, although most cold nodules are
benign. Even so, the presence of a hot nodule does not
exclude malignancy.
Further investigations
• Fine-needle aspiration cytology: performed on nodules
where there are suspicious features in the history or
examination findings. It can be performed in outpatients,
and is well tolerated; cytology is not completely reliable as
false-positive and false-negative results occur.
Differential diagnosis
• Nontoxic simple goitre: nonfunctioning nodules with
normal thyroid function test results (e.g. pregnancy,
puberty and menopause).
• Smooth toxic goitre associated with abnormal thyroid
function test results (e.g. Graves disease, Hashimoto
thyroiditis, de Quervain thyroiditis (neck pain,
fever and lethargy following viral illness)) or iodine
deficiency.
• Retrosternal goitre.
• Thyroid adenoma or cyst.
• Thyroid carcinoma.
• Nonthyroid lumps including thyroglossal cyst, brachial
cyst and pharyngeal pouch.
Thyroid disease
The control of thyroid hormone production and release is
outlined in Fig 33.4. Thyroid disorders are common, and
include both overactive and underactive thyroid, and thyroid cysts which may be benign or malignant. Some of these
disorders will present with an enlarged thyroid gland (i.e.
a goitre).
Hypothyroidism
Hypothyroidism results from deficiency of T4 or T3. The
prevalence is up to 2% in women; it is around five times less
common in men.
Aetiology
Primary thyroid failure may take the following forms:
• Chronic autoimmune (Hashimoto) thyroiditis: this is
around five to eight times more common in women
than in men, and tends to affect the middle-aged and
elderly. Patients may present with a firm, nontender
goitre, hypothyroidism, or both. It is associated with
vitiligo, pernicious anaemia, insulin-dependent
diabetes mellitus, Addison disease and premature
ovarian failure. Biopsy shows a lymphocytic infiltrate
with destruction of follicles and variable fibrosis.
• Idiopathic atrophic thyroiditis: this autoimmune
condition may represent progression or a different
presentation of chronic autoimmune thyroiditis. The
incidence increases with age, and it is more common in
women.
• Previous treatment for hyperthyroidism: operative or
radioiodine.
• Congenital hypothyroidism: the prevalence in the
United Kingdom is 1 in 3500–4000 infants, and
it is diagnosed in the first week of life by routine
screening, measuring TSH or T4. It is usually due
to thyroid agenesis, which is mostly sporadic, or
dyshormonogenesis, which is due to autosomal
recessively inherited enzyme defects.
• Iodine-deficient hypothyroidism: this is a major cause
of hypothyroidism and goitre worldwide, although
most iodine-deficient people are euthyroid even though
they have a goitre.
• Iatrogenic hypothyroidism: can occur with amiodarone
and lithium carbonate.
Secondary thyroid failure is rare and can be caused by
hypothalamus or pituitary disease resulting in reduced levels of thyrotropin-releasing hormone or TSH.
Clinical features
The onset is insidious, and the symptoms are often nonspecific. Common presenting symptoms include tiredness, lethargy, weight gain, cold intolerance, constipation,
hoarseness and dryness of the skin. However, virtually any
organ system can be affected. Very rarely it presents as myxoedema coma (see Chapter33).
108
Introduction
1717
Investigations
Blood tests
• Thyroid function tests: these include tests for TSH. If
the level of TSH is abnormal, then tests for T4 and T3
are performed.
• Antibodies to thyroglobulin or thyroid peroxidase
(microsomal antibodies): typically strongly positive in
Hashimoto thyroiditis.
• Cholesterol level is often raised.
• Full blood count: anaemia is often present, possibly
with a mild macrocytosis.
• Urea and electrolytes; hyponatraemia is a feature of
hypothyroidism.
Other
• ECG: sinus bradycardia, low-voltage complexes.
Imaging
• Ultrasonography, CT, MRI or radionuclide imaging
(thyroid scintigraphy) may be performed if nodules are
present.
CLINICAL NOTES
• In primary disease, the free and total T4 levels
are reduced and serum TSH level is high.
• In subclinical hypothyroidism, T4 level may be
normal, with a high serum TSH level.
• In secondary hypothyroidism, the free and
total T4 levels are reduced and the TSH level
is usually also low. This picture is also seen in
unwell people without thyroid disease (‘sick
euthyroid’) and in patients taking steroids and
anticonvulsants.
Hyperthyroidism
Thyrotoxicosis is the condition resulting from raised levels
of circulating free T4 and free T3. It affects approximately
10 in 1000 women and 1 in 1000 men. ‘Hyperthyroidism’
indicates thyroid gland overactivity, which may cause thyrotoxicosis. However, the terms ‘thyrotoxicosis’ and ‘hyperthyroidism’ are often used interchangeably.
Aetiology
Primary hyperthyroidism
Graves disease—This accounts for up to 80% of cases
of hyperthyroidism. It is caused by the production of autoantibodies that stimulate the TSH receptor. There is a
painless diffuse goitre in more than 90% of patients. In
addition to the general features of thyrotoxicosis (see
later), features specific to Graves disease may occur, including ophthalmopathy, pretibial myxoedema and thyroid acropachy.
The ophthalmopathy includes periorbital oedema, conjunctival oedema (chemosis), proptosis, diplopia, impaired
visual acuity and corneal ulceration due to exposure. It
is clinically obvious in up to 50% of patients with Graves
disease but subclinical ophthalmopathy can be detected in
more than 90% of patients by CT scan or MRI, revealing
enlargement of the extraocular muscles caused by lymphocytic infiltration, oedema and later fibrosis.
Pretibial myxoedema occurs in 1%–5% of patients with
Graves disease, and consists of painless thickening of the
skin in nodules or plaques, generally over the shin.
Thyroid acropachy occurs in less than 1% of patients,
and resembles finger clubbing.
Other causes of primary hyperthyroidism—Toxic multinodular goitre and toxic adenoma account for most of the
remaining causes. Less common causes include metastatic
thyroid cancer, genetic causes such as McCune–Albright
syndrome and TSH receptor mutations, ectopic thyroid
tissue (e.g. struma ovarii) and high iodine load (e.g. in contrast medium or amiodarone).
Secondary hyperthyroidism—This is very uncommon.
Causes include TSH-secreting pituitary adenoma and trophoblast or germ cell tumours secreting large amounts
of human chorionic gonadotrophin, which has mild
thyroid-stimulating effects.
Thyrotoxicosis without hyperthyroidism—This
may occur with destructive thyroiditis such as in postpartum thyroiditis, autoimmune thyroiditis, subacute/
de Quervain thyroiditis and amiodarone-induced thyroiditis, or with excessive T4 administration or selfadministered T4.
Clinical features
The general symptoms of hyperthyroidism include:
• weight loss
• increased appetite
• heat intolerance and sweating
• fatigue and weakness
• hyperactivity, irritability and sleep disruption
• tremor
Less common symptoms include:
• depression
• oligomenorrhoea
• pruritus
• diarrhoea and vomiting
• polyuria
Signs include:
• a goitre, possibly with a murmur over it
• tremor
• tachycardia and atrial fibrillation
• warm, moist skin
• lid retraction and lid lag (indicating Graves disease)
• muscle weakness
• proximal myopathy
• cardiac failure
109
Goitre, thyroid disease and thyroid malignancy
Investigations
• Thyroid function tests, including tests for TSH,
secretion of which is suppressed, and T4 and T3, the
levels of which are raised. In Graves disease, the levels
of TSH receptor antibodies are elevated.
• Thyroid imaging: if a toxic nodule or thyroiditis
is suspected, a radioisotope thyroid scan may be
performed. In the case of thyroiditis, a low level of
uptake is seen; a toxic nodule appears as a ‘hotspot’. In
Graves disease, there is diffusely increased uptake.
• ECG; may show tachycardia and atrial flutter/
fibrillation.
CLINICAL NOTES
• Thyroid function tests: secretion of TSH will
be suppressed in thyrotoxicosis because of
negative feedback (the exception to this being
secondary hyperthyroidism). It may also be
suppressed in euthyroid patients with Graves
ophthalmopathy, large goitres, recent treatment
for thyrotoxicosis or severe nonthyroid illness.
Subacute (de Quervain) thyroiditis
Various viruses (e.g. enterovirus or Coxsackie virus) can
cause subacute thyroiditis. Patients present with pain, a
small, tender goitre and initially thyrotoxicosis caused by
release of stored thyroid hormones. There may be a history
of preceding ‘influenza-like’ illness. Some weeks later, there
is a period of hypothyroidism followed by the recovery of
normal thyroid function 3–6months after onset.
The erythrocyte sedimentation rate is raised, and there
is low radioisotope uptake by the thyroid. Liver function
test results may be abnormal. Treatment is with NSAIDs for
mild symptoms and with high-dose prednisolone for moderate or severe thyroiditis. The dose is gradually tailed off in
subsequent weeks.
Treatment is by surgical excision, and the 5-year survival
rate is 95%.
Follicular thyroid carcinoma
HINTS AND TIPS
Papillary carcinoma is the most common thyroid
carcinoma, and has a tendency to spread to local
lymph nodes.
This occurs in older people (peak incidence at 40–60years)
and accounts for around 10% of thyroid cancers. Distant
metastases develop in around 15% of patients. Treatment
is by thyroidectomy and radioiodine ablation of the thyroid remnant. The 5-year survival rate is 80% in men and
almost 100% in women. Fine-needle aspiration biopsy may
not be able to distinguish between follicular adenoma and
carcinoma, and these patients often undergo surgery, with
the diagnosis being confirmed on pathology of the excised
specimen.
Anaplastic carcinoma
Anaplastic carcinoma is uncommon. The peak incidence is
at 60–70years. The malignant cells are atypical and undifferentiated, and the mean survival is only 6 months from
diagnosis.
Medullary thyroid carcinoma
This is rare, accounting for around 4% of thyroid cancer.
The cells secrete calcitonin and other hormones. The prognosis is poor. Family members should be screened as it is a
feature of multiple endocrine neoplasia.
Primary thyroid lymphoma
Lymphoma arising in the thyroid is almost always nonHodgkin lymphoma. There is an increased risk in patients
with autoimmune thyroiditis. Most are B-cell tumours,
which are treated with chemotherapy, often combined with
radiotherapy.
Thyroid malignancy
The incidence of thyroid cancer has risen greatly in the last
50years. This may be due to improved diagnosis of small
tumours. Prognosis is generally good, but worse in older age
groups, if metastases are present at presentation and with
anaplastic carcinoma.
Papillary thyroid carcinoma
This accounts for 80%–85% of thyroid malignancies,
and is more common in women; the peak age of onset
is 30–50 years. It may be locally invasive or multifocal.
110
FURTHER READING
National Institute for Health and Care Excellence. NHS Clinical
Knowledge Summaries: Neck lump management. 2010. www.
cks.nhs.uk/neck_lump
British Thyroid Association, 2007. Guidelines for the Management
of Thyroid Cancer; Royal College of Physicians.
Mehanna HM, Jain A, Morton RP, et al.: Investigating the thyroid
nodule. BMJ, March 2009.
Loss of consciousness
18
INTRODUCTION
HISTORY AND EXAMINATION FINDINGS
Loss of consciousness may be transient (blackouts) or ongoing
(coma). The causes of blackouts are summarized in Table18.1.
In coma, the patient remains unconscious and is unarousable.
The causes of coma are summarized in Table18.2.
Many patients are admitted to hospital with ‘collapse
cause’. This term is rarely helpful as patients (and doctors)
use the word ‘collapse’ to describe a variety of situations,
and it is essential to determine whether or not the patient
has actually lost consciousness.
COMMUNICATION
Many people use the terms ‘dizziness’, ‘lightheadedness’, ‘fall’, ‘faint’, ‘loss of consciousness’
and ‘collapse’ interchangeably. Careful questioning
is needed to establish whether the patient had a
true loss of consciousness episode, as this is key
to making the correct diagnosis.
Table18.1 Differential diagnosis of blackouts
Causes Subgroups Examples and notes
Syncope (see Chapters27
and 32)
Epilepsy (see Chapter32) Focal onset seizure with
Hypoglycaemia (see
Chapter33)
AS, Aortic stenosis; HCM, hypertrophic cardiomyopathy; LOC, loss of consciousness; RAS, reticular activating system; TIA, transient
ischaemic attack.
Orthostatic (postural) syncope Old age, drugs (e.g. antihypertensives), autonomic
Neurocardiogenic (vasovagal)
syncope
Carotid sinus syndrome Syncope on minor stimulation of the carotid sinus
Situational syncope Cough, micturition, defecation
Cardiogenic syncope Arrhythmia (Stokes–Adams attack) or structural heart
TIA/vertebrobasilar insufficiency Transient ischaemia in posterior circulation causing
impaired awareness
Generalized onset seizure Generalized epileptic activity
Pseudoseizure Behaviour mimicking a seizure but no epileptic activity
Fasting See the list in Chapter33
Postprandial Dumping syndrome
History
COMMUNICATION
Always try to obtain a collateral history from
a witness, even if the patient has regained
consciousness. If a patient is unable to give
the history, attempts should be made to obtain
information from an eyewitness (e.g. the next of
kinor general practitioner).
Generally, the history in a patient presenting with loss of
consciousness should include the following:
neuropathy
Characterized by inappropriate vagal outflow in response
to stimulus (e.g. prolonged standing, fear, pain)
(e.g. head turning, shaving)
disease (e.g. AS, HCM)
LOC (i.e. needs to affect RAS in the brainstem; as
this is diffuse, TIAs rarely cause LOC alone – other
brainstem structures are affected), subclavian steal
Focal epileptic activity with altered consciousness
(e.g. temporal lobe epilepsy)
in brain
111
Loss of consciousness
Table18.2 Differential diagnosis of coma
Causes Examples
Neurological (see
Chapter32)
Metabolic Hypoglycaemia or hyperglycaemia
Trauma – especially closed head
injury
Cerebrovascular event – intracranial
haemorrhage or infarction
Epilepsy (postictal or nonconvulsive
status epilepticus)
Meningitis, encephalitis,
overwhelming septicaemia
Space-occupying lesion
Myxoedema or Addisonian crisis
(see Chapter33)
Hypothermia (see Chapter33)
Hypoxia or CO2 narcosis (see
Chapter28)
Severe electrolyte disturbance (see
Chapter31)
Uraemic encephalopathy
Hepatic encephalopathy (see
Chapter29)
Drugs and toxins (see Chapter38)
Before the event
• What was the patient doing at the time of the attack?
○ Was there a change in posture or position before the
event? Syncope due to postural hypotension often
occurs after standing up suddenly.
○ Exertional syncope is seen in aortic stenosis and
hypertrophic cardiomyopathy (HCM).
○ Occasionally, syncope can occur following cough,
micturition, swallowing or straining during
defecation.
○ Syncope on head turning may suggest carotid
sinus hypersensitivity or rotational vertebrobasilar
insufficiency.
○ Very rarely, subclavian steal may cause syncope
during exercise of an arm.
• Did any symptoms occur before the event?
○ Was there any aura? Aura often precedes an
epileptic seizure.
○ Were there any chest symptoms (e.g. palpitations,
chest pain or dyspnoea)? Note, episodes of
bradycardia may cause collapse without any
warning (Stokes–Adams attacks).
The event itself
• Try to obtain an eyewitness account of the event if
available.
• Duration of loss of consciousness.
• Prolonged seizure activity associated with tongue
biting, particularly the side of the tongue, is suggestive
of epilepsy. Any cause of cerebral hypoxia may result
in brief anoxic seizures, which may be more prolonged
if the patient is upright. Urinary incontinence can
be a feature of both syncope and epilepsy; faecal
incontinence is usually not a feature of syncope.
• In Stokes–Adams attacks, the patient typically becomes
very pale, with flushing on recovery.
• If available, the pulse rate during the episode can help
(e.g. bradycardia or absent pulse in Stokes–Adams
attack). If the attack occurs in hospital, the blood
pressure and blood glucose level should be recorded
during the episode.
After the event
• How quickly did the patient recover? Syncope is
generally followed by rapid recovery. In epilepsy there
is usually postictal sleepiness or disorientation.
• Focal neurological impairment after recovery of
consciousness may suggest a stroke or Todd paresis
following a seizure (see Chapter32).
Risk factors
• A history of similar episodes, epilepsy, cardiac disease,
cerebrovascular disease, obstructive airway disease,
diabetes (especially if the patient is taking medication
known to cause hypoglycaemia, such as insulin,
sulphonylureas and sodium–glucose cotransporter 2
inhibitors).
• Cardiovascular risk factors or a relevant family history
(e.g. HCM, early cardiac death).
• History of drug abuse or depression.
• Previous head trauma.
Examination
Fig.18.1 summarizes the examination approach. The em-
phasis of the examination differs between the sick comatose
patient and one with recurrent blackouts. The different approaches are outlined below.
Comatose patient
• Start with the ABCDE approach. Calculating the
patient’s Glasgow Coma Scale score (Table18.3) is a
part of D – disability.
• Survey for injuries: especially closed head injury
and evidence of skull fracture such as blood or
cerebrospinal fluid in ears, or Battle sign (bruising over
the mastoid process).
• Check for evidence of liver disease, diabetes mellitus,
intravenous drug use (e.g. signs of chronic liver disease
or injection sites). Consider hepatic encephalopathy,
diabetic coma and opiate or another overdose.
• Is there a characteristic smell: alcohol, ketones,
hepatic fetor?
112
History and examination findings
Head
Neurology
— Chronic liver disease/
1818
— Focal signs
— Incontinence
— Pupillary responses
— Papilloedema
Neck
— Carotid bruits
— Meningism
— Dizziness on
looking upwards
Blood pressure
— Shock
— Postural drop
General
— ABC
— Coma scale
— BM
— Needle marks
— Pinpoint pupils
— Injury
— Tongue biting
— Jaundice
— Alcohol fetor
Smell
— Ketones
— Alcohol
— Hepatic fetor
Heart
— Murmur
Abdomen
— Peritonism
— Evidence of GI bleed
ascites
Pulse
— Tachycardia
— Arrhythmia
— Bounding
Vaginal examination
— Retained tampon
Fig.18.1 Examining the patient with loss of consciousness. ABC, the airway–breathing–circulation first-aid mnemonic;
BM, stick test for blood glucose; GI, gastrointestinal.
Table18.3 The Glasgow Coma Scale
Category Response Score
Eye opening Spontaneous 4
In response to voice 3
In response to pain 2
No eye opening 1
Best verbal response Orientated 5
Confused conversation 4
Inappropriate speech 3
Incomprehensible sounds 2
No response 1
Best motor response (i.e. best response
of any limb
Obeys commands 6
Localizes to pain 5
Withdraws to pain 4
Flexion to pain (decorticate) 3
Extension to pain (decerebrate) 2
No movements 1
The Glasgow Coma Scale is used in assessing loss of consciousness in a patient.
113
Loss of consciousness
Table18.4 Examination of the eyes in the comatose
patient
Test Findings Interpretation
Visual fields (by
visual threat –
normal response
is to blink)
Pupil reactions Normal direct and
Midposition,
Unilateral, fixed,
Small, reactive Pontine lesion,
Doll’s head
manoeuvre
to test
vestibuloocular
reflex (perform
only if cervical
spine intact)
Fundoscopy Papilloedema Raised ICP
ICP, intracranial pressure.
Hemianopia Suggests
consensual
unreactive to light,
irregular
dilated
Horner syndrome Ipsilateral lateral
Normal if pupils
fixed on same
point in space
when head moved
quickly
Subhyaloid
haemorrhage
Hypertensive
retinopathy
contralateral
hemisphere lesion
Intact midbrain
Midbrain lesion
Third nerve
compression (e.g.
due to tentorial
herniation)
opiate overdose
medullary or
hypothalamic lesion
Brainstem from third
to seventh nerve
nucleus intact
(occasionally CO2
narcosis)
Subarachnoid
haemorrhage
Hypertensive
encephalopathy
• Look for signs of meningism (e.g. meningitis,
subarachnoid haemorrhage) and rash
(meningococcal meningitis classically gives a
petechial or purpuric rash).
• Examine the pupils and eye movements
(Table18.4).
• Cardiovascular examination: arrhythmia
(including atrial fibrillation, which predisposes to
stroke), murmurs or other evidence of bacterial
endocarditis.
• Respiratory: focal consolidation, evidence of chronic
obstructive pulmonary disease and carbon dioxide
retention.
• Abdomen: gastrointestinal haemorrhage, ascites (which
may be infected), organomegaly, peritonism.
• Neurological examination: focal neurology suggests
intracranial cause.
HINTS AND TIPS
Remember to look for items hinting as to the
cause of loss of consciousness (e.g. MedicAlert
bracelets, neck tags or wallet cards).
Patient with blackouts
• Lying and standing blood pressure.
• Thorough cardiovascular and neurological
examination.
• Survey for any possible injuries sustained.
Investigations
HINTS AND TIPS
A blood glucose test should be performed
urgently in all unconscious patients to exclude
hypoglycaemia.
Investigation will be guided by findings in the history and
clinical examination.
• Full blood count: anaemia (e.g. severe haemorrhage or
haemolysis); leucocytosis (e.g. sepsis).
• Arterial blood gas: hypoxia, hypercapnia, acidosis (e.g.
in diabetic ketoacidosis).
• Urea and electrolytes: electrolyte disturbances, renal
failure.
• Calcium: hypocalcaemia.
• Glucose: hypoglycaemia/hyperglycaemia.
• Creatine kinase: rhabdomyolysis (if the patients has
been lying unconscious for a prolonged period).
• Liver function tests (biochemistry and synthetic
function): liver failure, hepatic encephalopathy.
• Thyroid function tests: hypothyroidism (myxoedema
coma).
• ECG: arrhythmia, left ventricular hypertrophy in aortic
stenosis and HCM.
• Chest X-ray: pulmonary disease, aspiration
pneumonia.
• Blood and urine drug screen.
• Brain imaging: head CT is usually more readily
available than MRI.
• Lumbar puncture: meningitis, subarachnoid
haemorrhage.
• Doppler studies of the carotid arteries: carotid artery
stenosis.
114
History and examination findings
1818
• Twenty-four-hour or 7-day ECG monitoring for
arrhythmia.
• Echocardiogram: heart rhythm, source of emboli,
aortic stenosis, HCM.
• Tilt-table testing: patients are moved from a
recumbent to an upright position while their pulse,
blood pressure, ECG and symptoms are monitored.
Those with orthostatic (postural) hypotension
show an early drop in blood pressure (within 2–3
minutes), whereas those with vasovagal syndrome
show a delayed response (up to 45 minutes)
in which the blood pressure alone may drop
(vasodepressor response), bradycardia may occur,
causing hypotension (cardioinhibitory response) or a
mixture of the two.
• EEG: epilepsy (including nonconvulsive status
epilepticus), viral encephalitis.
Chapter Summary
• In all patients presenting with loss of consciousness, the cause of the episode should be
investigated. Circumstances surrounding the episode will often guide the clinician as to
the cause.
• In an emergency, when a patient presents with loss of consciousness, follow the ABCDE
approach. Once the patient has been stabilized and initial interventions have been
performed, brain imaging is an important investigation in a patient who remains
unconscious despite appropriate treatment.
• The Glasgow Coma Scale is a useful score that enables assessment of consciousness. It
also allows monitoring of patients for deterioration/improvement.
115
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Confusion and delirium
19
INTRODUCTION
Confusion can be acute, subacute or chronic; reversible or
progressive. It is often divided into delirium (acute or subacute onset, often fluctuating, disturbance of consciousness,
perception or cognitive function) and dementia (progressive disease of the brain causing impairment of higher cortical function without impairment of consciousness). Any
cause of delirium can precipitate an acute exacerbation of
dementia – ‘acute-on-chronic confusion’. Confusional states
are very common, particularly in the elderly, and are often
worsened by admission to hospital. The most common
causes of delirium are summarized in Table19.1, whereas
causes of dementia are described in Table19.2.
Table19.1 Differential diagnosis of delirium.
Causes Examples
Infection Any – commonly urinary
tract, pneumonia, cellulitis,
meningitis, encephalitis
Drug intoxication Opiates, anxiolytics, steroids,
tricyclics, anticonvulsants,
drugs of abuse (see
Chapter38)
Drug withdrawal Alcohol, benzodiazepines
Metabolic Liver, kidney, cardiorespiratory
failure (hypoxia and
hypercapnia), hypernatraemia
or hyponatraemia,
hypoglycaemia,
hypercalcaemia
Endocrine Thyroid disorders, electrolyte
and glucose abnormalities
may be caused by Addison
disease, diabetes and
parathyroid disorders
Vitamin deficiency Wernicke–Korsakoff syndrome
(thiamine deficiency)
Cerebral disease Abscess, tumour,
haemorrhage, infarction,
trauma, epilepsy/postictal,
encephalitis (both infectious
and autoimmune) (see
Chapter32)
Pain Any cause
New surroundings Hospital ward, possibly
without hearing (hearing aid?)
or vision (spectacles?)
Table19.2 Differential diagnosis of dementia (see Crash
Course: Psychiatry)
Categories Causes
Common
causes
Rarer causes Long-term alcohol abuse, Huntington
Treatable causes
(which must
therefore be
excluded)
COMMUNICATION
In confused patients a good account from relatives,
carers or friends is almost always the only way of
getting a true picture of the pattern of disease. It
is important to try to establish what the patient’s
baseline level of cognitive function is, and whether
this presentation is a new problem or a part of a
long-standing problem.
HINTS AND TIPS
Depression can sometimes mimic dementia
(‘pseudodementia’). Other psychiatric illnesses,
causing psychosis and severe anxiety, can present
in a similar manner to acute confusional state.
Alzheimer disease, vascular dementia,
Lewy body dementia, frontotemporal
dementias
chorea, Creutzfeldt–Jakob
disease, Parkinson disease, Pick
disease, HIV, subacute sclerosing
panencephalitis, progressive multifocal
leucoencephalopathy, pellagra (niacin
deficiency)
Vitamin B12/folate deficiency,
hypothyroidism, thiamine deficiency,
subdural haematoma, normal pressure
hydrocephalus, neurosyphilis, resectable
tumour, depression (pseudodementia)
HISTORY AND EXAMINATION FINDINGS
History
Establish whether the patient is newly confused or if there
is a history of dementia, and if so whether the confusion is
worse than normal. The history taking should then focus on
possible underlying causes.
117