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Antiplatelets: mechanism of action
(a)
(b)
(c)
(d)
https://t.me/med1917
Aspirin Inhibits
COX- 1
, suppressing prostaglandin and thromboxane synthesis.
Clopidogrel A thienopyridine that inhibits platelet aggregation by modifying
ADP
platelet
receptors, preventing further strokes and
Dipyridamole c
AMP
and thromboxane A2.
MI
S.
Fig 10.
formatted
with magnified axial
and coronal segments,
showing a left internal
carotid artery stenosis
65
% at the level of the
of
carotid bifurcation.
17
A digitally re-
CT
angio gram
© Iain McGurgan.
471
10 Neurology
Fig 10.
18
Categorization of pressure ulcers. (a) Stage 1: non- blanchable redness of intact skin, typically over a bony prominence. (b) Stage
open ulcer with a red/ pink wound bed, without slough. May also present as an intact or open/
ruptured serosanguinous blister. (c) Stage
Bone, tendon, or muscle are not exposed. (d) Stage
tendon, or muscle.
Images (a) to (d) reproduced from Gosney et al. Managing older people in primary care,
2
: partial- thickness loss of dermis presenting as a shallow
3
: full- thickness skin loss with visible subcutaneous fat.
4
: full- thickness tissue loss with exposed bone,
2009
permission from Oxford University Press.
, with
10 Neurology
Stroke: rehabilitation
https://t.me/med1917
472
A large majority of people with stroke will survive the initial illness. Living with the
long- term consequences of stroke exerts a great toll on survivors, their families,
and healthcare systems. It is our role to ensure that this is a life worth living.
Principles of eective stroke rehabilitation
• Coordinated multidisciplinary care on a specialized stroke unit.
• Early commencement of dedicated stroke rehabilitation, beyond just the preven-
tion of complications related to immobility.
• Input after discharge to consolidate inpatient gains and to help align the individual
with their previous capability (early supported discharge/ community rehab).
• The best outcomes are associated with high motivation among survivors and their
families; preserving optimism to cultivate motivation and involving the carer/
spouse with all aspects of care- giving is key.
• Identify and quantify the level of impairment, set achievable goals that replicate
the specific aims of the individual, and carefully monitor progress.
Prevention of complications
• Watch the patient swallow a small volume of water; if signs of aspiration (a cough
or voice change) make
fluids, then semi- solids (eg jelly; avoid soups and crumbly food). Avoid early
tube feeds; these may be needed to safeguard nutrition in those with swallowing
problems that persist beyond the first
sider benefits of enteral feeding tube placement (
in assessing swallowing diculties are invaluable here.
• Venous thromboembolism prophylaxis for all stroke patients with limited mo-
bility; thigh- length intermittent pneumatic compression at admission, plus
low- molecular- weight heparin (except within
anticoagulation use, or
• Avoid further injury: minimize falls risk and take care when lifting the patient not
to damage their shoulders.
• Ensure good bladder and bowel care through frequent toileting. Avoid early cath-
eterization which may prevent return to continence.
• Position to minimize spasticity (occurs in ~40%). Get prompt physiotherapy.
Splints and botulinum toxin injections are helpful for focal spasticity.
• Frequ ent mo nito rin g, hygi ene, and m oistu rizing for pressure ulcer prevention
fig
10.18
, p
471
(
• Monitor mood: in pseudo- emotionalism/ emotional lability (sobbing unprovoked by
sorrow, from failure of cortical inhibition of the limbic system), an
Screen for and treat
Rehabilitation interventions
• Motor rehabilitation. The majority of trials were neutral, but this could be a re-
sult of the challenges of delivering rehabilitation interventions in a standardized
and blinded manner in trials.
physiotherapy fun. Swimming (a hemiplegic arm may be supported on a special
float), music, and video games are all enjoyable and may recovery through promoting cerebral reorganization.
• Cognitive rehabilitation. Training can improve alertness and attention span for
those with attention deficit.
• Speech and language therapy. Frequently used for aphasia and dysarthria, but
there is a lack of supportive evidence.
• Visual, sensory, continence impairment. Interventions for improving sensory and
visual impairment (eg compensatory techniques and prisms for field defects) and
incontinence (eg bladder retraining, pelvic floor exercises) lack supportive evidence.
Tests. Asking to point to a named part of the body tests perceptual function.
Copying matchstick patterns tests spatial ability. Copying a clock face tests for
constructional apraxia (
apraxia, picking out and naming easy objects from a pile tests for agnosia.
End of life decisions. See p12.
).
NBM
until formal assessment by a speech therapist. Use IV
2– 3
d. If swallowing fails to recover, con-
p
743
). Speech therapists skilled
24
ICH
).
post- stroke depression early.
h of thrombolysis, existing
SSRI
may help.
8 Engage the patient in their own recovery by making
p70), miming actions such as brushing teeth for ideomotor
NG
Assessing dependence in daily life
https://t.me/med1917
Handicap entails inability to carry out social functions. ‘A disadvantage for a
given individual, resulting from an impairment or disability, that limits or prevents
the fulfilment of a role.’ Two people with the same
arm) may have dierent
disabilities (Barthel’s Index of activities of daily living;
impairment (eg paralysed
eg one may be able to dress but the other cannot). Disabilities are likely to determine quality of future life. Treatment is often best aimed at reducing disability,
not curing disease. For example, Velcro® fasteners in place of buttons may enable
a person to dress.
Barthel’s paradox
The more we contemplate Barthel’s eulogy of independence, the more we see
it as a mirage reflecting a greater truth about human aairs:
there is no such
thing as independence— only interdependence— and in fostering this interdependence lies our true vocation:
No man is an Island, intire of it selfe; every man is a peece of the Continent, a
part of the maine; if a Clod bee washed away by the Sea, Europe is the lesse,
as well as if a promontorie were, as well as if a Mannor of thy friends or of
thine owne were. Any man’s death diminishes me, because I am involved in
mankinde; And therefore never send to know for whom the bell tolls: It tolls
for thee.’
John Donne
1572–
1631
; Meditation
XVII
473
10 Neurology
.
10 Neurology
Subarachnoid haemorrhage (
https://t.me/med1917
474
Non- traumatic
catastrophic (
Incidence 8/
SAH
is spontaneous bleeding into the subarachnoid space, often
table
10.8
100 000
/ yr (far higher in Japan and Finland); typical age: 35– 65.
) and accounts for 5– 6% of stroke.
SAH
)
Symptoms Sudden- onset excruciating headache, typically occipital— like a ‘thun-
derclap’. Vomiting, collapse, seizures, and coma often follow. Coma/ drowsiness may
last for days. Some patients report a preceding, ‘sentinel’ headache, perhaps due to
a small warning leak from the oending aneurysm (~
6
%).
Signs Neck stiness; Kernig’s sign (takes 6h to develop); retinal, subhyaloid, and vit-
5
reous bleeds (= Terson’s syndrome; mortality ×
may suggest site of aneurysm (eg pupil changes indicating a
). Focal neurology at presentation
III
rd nerve palsy with
a posterior communicating artery aneurysm) or intracerebral haematoma. Later
deficits suggest complications (see later in topic).
Causes • Berry aneurysm rupture (80%). Common sites: junctions of posterior
fig
10.3
, p
447
communicating with the internal carotid (see
municating with the anterior cerebral artery, or bifurcation of the middle cerebral
fig
10.19
artery (
causes:
Risk factors Previous aneurysmal
smoking, alcohol misuse,
tory (
Ehlers– Danlos syndrome (
Dierentials Meningitis (p
thrombosis (
). 15% are multiple. • Arteriovenous malformations (15%). • Other
encephalitis, vasculitis, tumour, amyloid angiopathy, idiopathic.
SAH
(new aneurysms form, old ones get bigger),
) are all associated with berry aneurysms.
), migraine (p
454
3– 5
× risk of
BP
, bleeding disorders,
SAH
in close relatives). Polycystic kidneys, aortic coarctation, and
p
143
806
p
478
), dissection of a carotid or vertebral artery, benign thunderclap
) or of the anterior com-
SBE
(mycotic aneurysm), family his-
), intracerebral bleed, cortical vein
headache (triggered by Valsalva manoeuvre, eg cough, coitus).
Tests • Urgent CT Detects >95% of
drops rapidly with elapsed time thereafter.
SAH
(and no
CI:
gestive of
allow breakdown of
p
RBC
s so that a positive sample is xanthochromic (yellow, due to
bilirubin: dierentiates between old blood from
Management Refer all proven
• Re- examine
CNS
often; chart BP, pupils, and
and monitor for vasospasm with
ultrasound.
• Maintain cerebral perfusion by keeping well hydrated, but aim for
• Nimodipine (60mg/ 4h PO for 3wks, or 1mg/ h
vasospasm and consequent morbidity from cerebral ischaemia.
• Surgery: endovascular coiling vs surgical clipping (requiring craniotomy): the de-
cision depends on the accessibility and size of the aneurysm, though coiling is preferred where possible (fewer complications, better outcomes). Do catheter or
angiography to identify single vs multiple aneurysms before intervening. Newer
SAH
within the 1st 24h (fig
10.20
• LP If CT −ve but the history is very sug-
752
). This needs to be done >12h after headache onset to
SAH
SAH
to neurosurgery immediately.
CT/MR
vs a ‘bloody tap’).
GCS
(p
766
). Repeat CT if deteriorating
angiography or transcranial Doppler
2
IVI
+
) is a Ca
antagonist that reduces
techniques such as balloon remodelling, flow diversion, and new embolic materials
can be helpful in anatomically challenging aneurysms.
Complications Rebleeding is the commonest cause of death, and occurs in 10%,
1
often in the
manent
gery is not helpful at the time but may be so later.
of arachnoid granulations, requires a ventricular or lumbar drain.
is common, usually due to syndrome of inappropriate secretion of antidiuretic hormone (
st few days. Cerebral ischaemia due to vasospasm may cause a per-
CNS
deficit, and is the commonest cause of morbidity. If this happens, sur-
Hydrocephalus, due to blockage
SIADH,
p
235
), but should not be managed with fluid restriction as this can
prompt vasospasm. Seek expert help.
), but sensitivity
SBP
<
160
mmHg.
Hyponatraemia
CT
Table 10.
https://t.me/med1917
8
Mortality in subarachnoid haemorrhage, according to Hunt and Hess grade
Grade Signs Mortality: %
I
II
III
IV
V
Most mortality occurs in 1st month. 90% of survivors of the 1st month, survive >1 year.
None
Neck stiness and cranial nerve palsies
Drowsiness
Drowsy with hemiplegia
Prolonged coma
0
11
37
71
100
Unruptured aneurysms: ‘the time- bomb in my head’
Bear in mind the old adage: ‘if it ain’t broke, don’t fix it’— usually, risks of preventive intervention outweigh any benefits, except perhaps in
(more years at risk, and surgery is twice as hazardous if >
• aneurysms >7mm in diameter, especially if located at the • junction of the in-
ternal carotid and the posterior communicating cerebral artery, or at the
basilar artery bifurcation, and especially if there is
• past history of bleeds. Data from the
a
Intracranial Aneurysms (
7– 12
mm across is 3.3 compared with aneurysms <7mm across; if the diameter is
12
mm, the relative risk is 17.
>
ISUIA
) show that relative risk of rupture for an aneurysm
• uncontrolled hypertension or
2003
International Study of Unruptured
• young patients
45
yrs old) who have
• rostral
475
10 Neurology
Fig 10.
19
CT images can be manipulated to
show only high- density structures such as
bones and arteries containing contrast. Here is
a middle cerebral artery aneurysm.
© Prof Peter Scally.
Fig 10.
20
Blood from a ruptured aneurysm
occupies the interhemispheric fissure (top
arrow), a crescentic intracerebral area presumably near the aneurysm (
basal cisterns, the lateral ventricles (temporal horns), and the
arrow).
2
nd arrow), the
4
th ventricle (bottom
© Prof Peter Scally.
10 Neurology
Subdural haematoma
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476
Consider this very treatable condition in all whose conscious level fluctuates, and
also in those having an ‘evolving stroke’, especially if on anticoagulants. Bleeding
is from bridging veins between cortex and venous sinuses (vulnerable to deceleration injury), resulting in accumulating haematoma between dura and arachnoid.
This gradually raises
and, if untreated, leads to eventual tentorial herniation and coning. Most subdurals
are from trauma but the trauma is often forgotten as it was so minor or so long ago
9
months; chronic subdurals). It can also occur without trauma (eg
(up to
metastases). The elderly are most susceptible, as brain atrophy makes bridging
veins vulnerable. Other risk factors: falls (epileptics, alcoholics); anticoagulation.
Symptoms Fluctuating level of consciousness (seen in 35%) ± insidious physical
or intellectual slowing, sleepiness, headache, personality change, unsteadiness, and
occasionally seizures.
Signs
ICP
(p
814
), seizures. Localizing neurological symptoms (eg unequal pupils,
hemiparesis) occur late, often >
Dierentials Stroke, dementia,
Imaging (fig
10.21
)
CT/ MRI
clots). Look for crescent- shaped collection of blood over one hemisphere. The sickle
shape dierentiates subdural blood from extradural haemorrhage.
Management Reverse clotting abnormalities urgently. Surgical management de-
pends on the size of the clot, its chronicity, and the clinical picture: generally those
10
mm or with midline shift >5mm need evacuating (via craniotomy or burr hole
>
washout). Address the cause of the trauma (eg falls, abuse).
Prognosis Often favourable, but mortality rates are as high as 50% in those re-
quiring surgery for acute subdurals.
Extradural (epidural) haematoma
Beware deteriorating consciousness after any head injury that initially produced
no loss of consciousness or after initial drowsiness post injury seems to have resolved. This lucid interval pattern is typical of extradural bleeds.
Cause Suspect after any traumatic skull fracture. Often due to a fractured temporal
or parietal bone causing laceration of the middle meningeal artery and vein, typically
after trauma to a temple just lateral to the eye. Any tear in a dural venous sinus will
also result in an extradural bleed. Blood accumulates between bone and dura.
Clinical features The lucid interval may last a few hours to a few days before a
bleed declares itself by
confusion, and seizures follow, ± hemiparesis with brisk reflexes and an upgoing
plantar. If bleeding continues, the ipsilateral pupil dilates, coma deepens, bilateral
limb weakness develops, and breathing becomes deep and irregular (brainstem
compression). Death follows a period of coma and is due to respiratory arrest.
Bradycardia and
Dierentials Epilepsy, carotid dissection, carbon monoxide poisoning.
Tests CT (fig
forms a more rounded shape compared with the sickle- shaped subdural haematoma as the tough dural attachments to the skull keep it more localized). Skull
may be normal or show fracture lines crossing the course of the middle meningeal
vessels.
Management Stabilize and transfer urgently (with skilled medical and nursing es-
corts) to a neurosurgical unit for clot evacuation ± ligation of the bleeding vessel.
Care of the airway in an unconscious patient and measures to
intubation and ventilation (+ mannitol
Prognosis Excellent if diagnosis and operation early. Poor if coma, pupil abnormal-
ities, or decerebrate rigidity are present pre- op.
BP
10.22
) shows a haematoma (often biconvex/ lens- shaped; the blood
Lumbar puncture is contraindicated.
ICP
, shifting midline structures away from the side of the clot
1
month after the injury.
CNS
masses (eg tumours, abscesses).
shows clot ± midline shift (but beware bilateral isodense
GCS
from rising
ICP
. Increasingly severe headache, vomiting,
are late signs.
ICP
IVI
, p
815
).
often require
ICP
; dural
X
- ray
Fig 10.
https://t.me/med1917
21
This image explains the cause
as well as the pathology. On the patient’s
left, cerebral sulci are prominent and prior
to this adverse event would have been
even larger. The brain had shrunk within
the skull as a result of atherosclerosis, and
poor perfusion, leaving large subarachnoid spaces. A simple, quick rotation of
the head is enough to tear a bridging vein,
causing this
Fig 10.
siform or biconvex collection) on the right
side is limited anteriorly by the coronal suture and posteriorly by the lambdoid suture.
This is th erefor e an
The low- attenuation
on the left is causing scalloping of the overlying bone. It is in the typical location of an
arachnoid cyst; an incidental finding of a
congenital abnormality.
acute subdural haematoma.
© Prof Peter Scally.
22
The blood (h igh attenu ation, fu -
extradural haemato ma.
CSF
density collection
© Prof Peter Scally.
477
10 Neurology
10 Neurology
Cerebral venous thrombosis (
https://t.me/med1917
478
Thrombosis of the cerebral sinuses or veins causes cerebral infarction, though
much less commonly than arterial disease. Seizures are common and focal; they
can complicate diagnosis and post- ictal drowsiness may impair
Although ~
80
% will make a good functional recovery, death is mainly due to
transtentorial herniation from mass eect or oedema.
Dural venous sinus thrombosis M ost co mmo nl y sa gi tt al s in us t hr omb os is ( figs
10.24; 47
% of all
CVT
) or transverse sinus thrombosis (35%). Sagittal sinus thrombosis
often coexists if other sinuses are thrombosed. Symptom onset is gradual (over days
or weeks). Features are dependent on the sinus aected:
• Sagittal sinus Headache, vomiting, seizures, vision, papilloedema.
• Transverse sinus Headache ± mastoid pain, focal
• Sigmoid sinus Cerebellar signs, lower cranial nerve palsies.
• Inferior petrosal sinus Vth and VIth cranial nerve palsies, with temporal and
retro- orbital pain (Gradenigo’s syndrome, suggesting otitis media is the cause).
• Cavernous sinus Often due to spread from facial pustules or folliculitis, causing
headache, chemosis, oedematous eyelids, proptosis, painful ophthalmoplegia, fever.
Cortical vein thrombosis Usually occurs with a sinus thrombus as it extends into
the cortical veins, causing infarction in a venous territory (
rise to stroke- like focal symptoms that develop over days. There are often seizures,
and an associated headache which may come on suddenly (thunderclap headache).
Causes Numerous, including anything that promotes a hypercoagulable state
p
370
). Common causes Pregnancy/ puerperium, combined
(
dration, blood dyscrasias, tumours (local invasion/ pressure), extracranial malignancy
(hypercoagulability), recent
cerebral malaria,
TB
). Drugs (eg antifibrinolytics, androgens),
Dierential diagnosis Subarachnoid haemorrhage, meningitis, encephalitis, intra-
cranial abscess, arterial infarction, idiopathic intracranial hypertension (
Investigations Exclude subarachnoid haemorrhage (if thunderclap headache,
p
474
) and meningitis (p
ography may show the absence of a sinus (
sinus can be a normal variant.
alize thrombus directly (
be normal early, but show a filling defect at ~
opening pressure.
CSF
Management Anticoagulation with heparin or
DOAC
tion with a
voked
or warfarin (
CVT
). If there is deterioration despite adequate anticoagulation, endovascular
thrombolysis or mechanical thrombectomy may provide limited benefit (but not in
those with large infarcts and impending herniation).
p
814
); decompressive hemicraniectomy may prevent impending herniation.
(
Idiopathic intracranial hypertension
Think of this in those presenting with symptoms of
papilloedema)— when no cause is found. Most commonly seen in obese females in
3
rd decade, who present with narrowed visual fields, blurred vision ± diplopia, VIth
nerve palsy, and an enlarged blind spot, if papilloedema is present (it usually is).
Opening pressure on
Associations En do cri ne abn or mal it ies (C us hin g’s s yn dro me , hy pop ar ath yro id ism ,
SLE, CKD, IDA, PRV
Management Weight loss, acetazolamide (avoid in pregnancy) or topiramate, loop
diuretics. Consider ventriculoperitoneal shunt or optic nerve sheath fenestration if
drugs fail and visual loss worsens. Venous sinus stenting is under investigation.
Prognosis can often b e tape red/ withdrawn. Permanent significant visual loss in 10%.
8
Predictors of poor prognosis include:
nancy, intracranial haemorrhage, mental status abnormality, age >
, drugs (tetracycline, steroids, nitrofurantoin, and oral contraceptives).
CVT
)
GCS
8
: ≥3:
1.
CNS
signs, seizures, papilloedema.
fig
10.25
). These infarcts give
OCP
, head injury, dehy-
LP.
Ot her c aus es Infection (meningitis, abscesses, otitis media,
806
). Bloods Thrombophilia screen. Imaging
MRI T2
fig
10.24
), and also identify haemorrhagic infarction. CT may
fig
- weighted gradient echo sequences can visu-
1
may be normal, or show
INR
2– 3) for 3– 6 months (up to 12 months if unpro-
LP
is usually >25cmH2O.
GCS
score on admission <9, deep
RBC
SLE
, vasculitis, Crohn’s or
10.23
), though an absent transverse
wk (delta sign). LP (If no CI): raised
S and xanthochromia.
LMWH
and then long- term preven-
ICP
requires prompt attention
ICP
(headache, vision loss,
CVT
location,
37
years, and .
CNS
assessment.
10.23
UC.
p
478
).
CT/ MRI
ven-
TSH
infection, malig-
,
),
Fig 10.
SV
https://t.me/med1917
24
MRI
LEFT
sinus is involved.
showing thrombus (arrows) in the sagittal sinus (sagittal T1- weighted image,
), and in the right transverse sinus (axial T2- weighted image,
Fig 10.
23
This magnetic resonance
MRV
venogram (
first glance: the hardest thing to see in
imaging is often that which is not there.
Much of the superior sagittal sinus is
not seen because it is filled with clot—
a superior sagittal sinus thrombosis.
The arrows point to where it should be
seen. Posteriorly, the irregularity of the
vessel indicates non- occlusive clot.
) could look normal at
© Prof P. Scally.
RIGHT
). Often more than one
© Prof David Werring.
479
10 Neurology
Fig 10.
25
Venous territories (compare with arterial territories on p
TS
— transverse sinus; SV— Sylvian veins;
sinus;
There is much greater variation in venous anatomy between individuals than there is in arterial
anatomy, so this diagram is only a rough guide. The key point is to realize that infarction that
crosses boundaries between arterial territories may be venous in origin.
SSS
ICV
ICV
— internal cortical veins.
447
).
SSS
TS
— superior sagittal
10 Neurology
Delirium (acute confusional state)
https://t.me/med1917
480
Delirium9 aects up to 50% of inpatients >65yrs, and is associated with a longer
admission, more complications, and higher mortality.
cause in any acute fluctuating, baing behaviour change; it may be an early indication of treatable pathology (eg
UTI
).
Look for an underlying
Clinical features Globally impaired cognition, perception, and consciousness which
develops over hours/ days, characterized by a marked memory deficit, disordered
or disorientated thinking, and reversal of the sleep– wake cycle. Some patients experience tactile or visual hallucinations. Delirium can be:
lessness, mood lability, agitation, or aggression
becomes slow and withdrawn or
much harder to recognize: it is crucial to compare current behaviour to the patient’s
baseline (see
BOX
).
• mixed. Hypoactive and mixed delirium are
• hyperactive, with rest-
• hypoactive in which the patient
Risk factors >65yrs, dementia/ previous cognitive impairment, hip fracture, acute
illness, psychological agitation (eg pain).
Causes
• Surgery/ post- GA.
• Systemic infection: pneumonia,
• Intracranial infection or head injury.
• Drugs/ drug withdrawal: opiates, levodopa, sedatives, recreational.
• Alcohol withdrawal (2– 5d post- admission;
• Metabolic: uraemia, liver failure, Na
• Hypoxia: respiratory or cardiac failure.
• Vascular: stroke, myocardial infarction.
• Nutritional: thiamine, nicotinic acid, or
Dierentials Dementia (see
ticus is an underdiagnosed cause of impaired cognition and odd behaviour: consider
EEG
. Primary mental illness (eg schizophrenia) can also mimic delirium, but this is
an
rare on the wards (especially if no past history).
Tests Look for the cause (eg
ABG
, septic screen (urine dipstick,
LP, EEG, CT
films,
.
UTI
, malaria, wounds, IV lines.
LFT
S,
MCV
+
or glucose, Hb, malnutrition (beriberi, p
B
deficiency.
BOX
12
), anxiety, epilepsy: non- convulsive status epilep-
UTI
, pneumonia, MI): do
CXR
, blood cultures); also consider
; history of alcohol abuse).
FBC, U&E, LFT
Management As well as identifying and treating the underlying cause, aim to:
• Reorientate the patient: explain where they are and who you are at each en-
counter. Hunt down hearing aids/ glasses. Visible clocks/ calendars may help.
• Encourage visits from friends and family.
• Monitor fluid balance and encourage oral intake. Be vigilant for constipation.
• Mobilize and encourage physical activity.
• Practise sleep hygiene: restrict daytime napping, minimize night- time disturbance.
• Avoid or remove catheters, IV cannulae, monitoring leads and other devices (they
increase infection risk and may get pulled out).
• Watch out for infection and physical discomfort/ distress.
• Review medication and discontinue any unnecessary agents. Only use sedation
if the patient is a risk to their own/ other patients’ safety (never use physical restraints). Consider short- term haloperidol
p15). Wait 20min to judge eect— further doses can be given if needed.
(
NB
: avoid in those with Parkinson’s disease or Lewy body dementia.
0.5– 2
mg PO if they will take it, IM if not
Be aware that delirium may persist beyond the duration of the original illness by
several weeks in the elderly. Do not assume this must be dementia— provide support and reassess
1– 2
months later.
240
).
, blood glucose,
ECG
, malaria
9
Delirium, from the Latin de (from) and lira (ridge between furrows), meaning ‘out of one’s furrow’.
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