OCCASIONAL REVIEW
Acute presentation of
altered conscious state
Jonathon Holland
Richard Brown
Abstract
Children present to healthcare services with a range of disorders of
altered consciousness. Some are benign and self-resolving but others
will be rapidly fatal if untreated. Moreover, the most likely diagnosis is
not always obvious. Children and young people have a wider range of
causes than adults and the limited language skills of younger children
increase the diagnostic challenge. The clinician is faced with a number
of competing and overlapping priorities. They must be able to rapidly
assess the child, prioritise their management and investigations, whilst
also coordinating appropriate and timely specialist referrals. At the
same time, they need to be able to communicate these plans with
their teams, the child and often a very stressed or distressed family.
In order to do this effectively, it is necessary to have a toolkit in
place which includes knowledge, skills and a clear road-map. This
mini-review will equip the reader with a highly structured and practical
approach to the child or young person with altered consciousness and
it follows the recommendations set out by the Royal College of Paedi-
atrics and Child Health. It considers in detail some of the more impor-
tant differential diagnoses and outline the principles of management.
Keywords brain injuries; consciousness disorders; emergencies;
emergency medicine; pediatrics
Introduction
The clinician presented with a child in an acutely altered
conscious state must rapidly assess the situation e have they
fainted after a blood test? Is the child intoxicated? Could there be
raised intracranial pressure?
It is essential to have a general understanding of the reasons
why a child’s conscious state may change e and a strategy to
intervene. Failure to do so may be life-threatening. The impor-
tance of this problem within paediatric practice is recognized. It
is one of only a few presentations afforded its own Royal College
of Paediatrics and Child Health guideline e “The management of
children and young people with an acute decrease in conscious
level”.1
This mini-review provides the reader with a strategy to
approach the child with acute presentation of an altered
conscious state.
Jonathon Holland MB BChir MA(Cantab) MRCPCH, Paediatric Neurology
Registrar, Addenbrookes Hospital, Cambridge, UK. Conflicts of
interest: none declared.
Richard Brown BA (Hons, Oxon) MBBS (Hons) MRCPCH PCME, Consultant
Paediatrician, Addenbrookes Hospital and Cambridge University
Hospitals NHS Foundation Trust, Cambridge Biomedical Campus,
Cambridge, UK. Conflicts of interest: none declared.
PAEDIATRICS AND CHILD HEALTH 31:4
Background
The history of the RCPCH guideline’s development is an inter-
esting side note. Douglas Reye is credited as first describing and
characterising the ‘Reye Syndrome’ in 1963. By 1980 it was
recognised that aspirin use in children was significantly associ-
ated with risk of developing Reye Syndrome. In view of its pre-
sentation as a rapidly progressing encephalopathy e that is,
altered mental status arising from diffuse brain dysfunction e the
National Reye’s Syndrome Foundation UK funded a workshop on
the condition in 2002, which concluded that a formal evidence-
based guideline on management of altered consciousness was
required.
An initial guideline was then produced by a team in the
University of Nottingham in 2005, which evolved in to the cur-
rent RCPCH guidance, last updated in 2019. Incidentally 2002
was also the last year that a patient with ‘classical’ Reye Syn-
drome was diagnosed in the UK.
Definitions
How is conscious state defined? The question of “what is con-
sciousness” is perhaps best left to neuropsychologists and phi-
losophers. For our purposes, when describing the “acutely
altered conscious state” what we mean is a person is responding
differently to environmental stimuli than they normally would.
‘Scoring systems’ exist to assess levels of consciousness (see
Box 1) and so a practical definition for altered consciousness
would be a drop in such a score. For example, a child previously
alert only becomes responsive to pain (a drop from A to P on the
AVPU scale), or begins to appear disorientated or confused (a
drop in Glasgow Coma Scale (GCS) from 15 to 14).
The term ‘coma’ (deriving from ancient Greek for ‘deep
sleep’) should be reserved for those patients who cannot move or
respond to their environment, which will not apply to most
children presenting with acutely altered consciousness.
It is beyond the scope of this review to consider in detail a
deterioration in conscious level in a patient who has already had
a longstanding deficit in awareness. A child with longstanding
reduced GCS who has a further decline in consciousness should
generally be approached in the same way to avoid ‘diagnostic
bias’, however their pre-existing condition will likely have some
bearing on management. We will also not discuss primary psy-
chiatric illness presenting with altered consciousness.
Pathogenesis
From a neurological perspective, this means that normal brain
function has been impaired. Electroencephalography (EEG) can
often show non-specific features such as ‘diffuse slowing’ in this
patient group, indicative of cerebral dysfunction. The underlying
pathological mechanism will of course depend upon the specific
cause e of which there are very many.
Altered conscious state is thus in a general sense indicative of
an acquired brain injury (ABI). Not all ABI will give an acutely
altered conscious state but it is important to consider the po-
tential longer-term impact of ABI in all patients.
Epidemiology
Whilst ABI (particularly traumatic brain injury [TBI]) is relatively
well studied epidemiologically, there is much less information
available about presentations of decreased consciousness in
153 Ó 2021 Elsevier Ltd. All rights reserved.
 OCCASIONAL REVIEW

Glasgow Coma Scale and AVPU scale.2

Glasgow Coma Scale

Motor Voice Eyes

6 e obeys commands
5 e localises pain 5 e converses
4 e flexion withdrawal 4 e confused 4 e open
3 e abnormal flexion 3 e inappropriate words 3 e open to command
2 e abnormal extension 2 e incomprehensible 2 e open to pain
1 e no response 1 e no response 1 e no response

Glasgow Coma Scale modification for children under 5 years

Motor Voice Eyes

6 e normal spontaneous movements
5 e localises to supraorbital pain or 5 e alert, babbles, coos, words or sentences
withdraws from touch to usual ability
4 e withdraws from nailbed pain 4 e less than usual ability, irritable cry 4 e open
3 e abnormal flexion 3 e cries to pain 3 e open to command
2 e abnormal extension 2 e moans to pain 2 e open to pain
1 e no response 1 e no response 1 e no response

AVPU Scale
A ¼ alert; V ¼ responds to voice; P ¼ responds to pain; U ¼ unresponsive

Box 1

general. A UK 2001 study3 suggests an incidence of decreased
consciousness of 31 per 100 000 children under the age of 16
with non-traumatic related presentations of ‘coma’. They defined
this as a GCS less than 12 lasting for 6 hours. In contrast, a UK
study between 2001 and 2003 found a prevalence rate for chil-
dren admitted to paediatric intensive care units with traumatic
brain injury (TBI) of 5.6 per 100 000 population per year.4
Taking into account other milder presentations the true inci-
dence is likely to be far higher than both these figures. The latter
study also demonstrated socio-economic variation with children
from more deprived backgrounds being at higher risk of TBI
requiring intensive care support; one could extrapolate that this
may also be the case in minor injuries with altered
consciousness.
Acute presentation
It will usually be clear when a child is presenting with
moderately to severely altered consciousness, either from
parental/other report, or self-evident through the patient’s
behaviour. Principally this group will be patients presenting or
brought to hospital emergency departments. If such patients do
self-present to primary care or community teams then it will
usually be appropriate to urgently refer to the emergency
medical services. After formally confirming decreased con-
sciousness through either reduction in GCS from baseline, or
AVPU score less than ‘V’, patients should be assessed in a
systematic manner to identify any immediately life-threatening
problem, as per Advanced Paediatric Life Support or similar
protocols, e.g. ‘CABCDE’. We will identify some key points
from this below.
Mildly altered conscious state may be more difficult to elicit
but is less likely to present acutely (although it may then progress
rapidly). Personality change, developmental regression or
behavioural disturbance may be present but are not specific.
Tools such as the Mini Mental State Examination (MMSE) may
be useful for older children to objectify cognitive impairment.
Emergency assessment and management
C-Spine stabilisation and catastrophic bleeding: in the context
of trauma and injury, cervical spine stabilisation and control of
major haemorrhage will take priority for management. Major
trauma is discussed in most advanced life support courses and
will not be discussed in detail here other than to recognise that
trauma is a significant cause of reduced conscious level, either
through primary head/neck injury (e.g. diffuse axonal injury) or
complications of trauma such and hypovolaemic shock through
blood loss and raised intracranial pressure secondary to intra-
cranial haemorrhage.
Airway: any patient with altered consciousness has a potentially
at-risk airway and airway adjuncts should be considered e.g.
oropharyngeal airways.
In patients assessed as having GCS score lower than 8, or
being unresponsive to pain, intubation and ventilation should be
considered unless there is evidence to suggest that their

PAEDIATRICS AND CHILD HEALTH 31:4 154 Ó 2021 Elsevier Ltd. All rights reserved.
 OCCASIONAL REVIEW

Summary of approach to the altered conscious state

Paent presents In all presentaons, always consider non-accidental and self-inflicted injury.
with altered
consciousness Also consider presentaons such as simple faints, breath holding aacks, mild concussion, or with known
previous diagnosis of paroxysmal disorder with very similar presentaon – where no further invesgaon may
be required aer exclusion of serious illness and full recovery.

cABCDE assessment Always ask for senior support and consider whether paediatric intensive care input required.

Note this flowchart does not consider primary psychiatric disorders; such presentaons should be managed
jointly with local child and adolescent mental health services.

Glucose, blood gas, full blood count, electrolytes (including calcium and magnesium), liver enzyme profile,
Essenal invesgaons ammonia, coagulaon profile, blood culture. Consider paracetamol/salicylate levels, CRP, blood alcohol level
and serum save samples. Consider urine microscopy, toxicology and storage sample.

YES Cause for YES Acute management of

Major Follow major trauma
altered trauma
trauma? pathway consciousness?
Follow-up as required
NO NO

Iniate fluid resuscitaon Unless full recovery and

YES and targeted therapy. Cause for YES clear aeology e.g.
Shock? altered
anaphylaxis then connue
Consider sepsis and consciousness?
meningis assessment
NO NO

Paediatric endocrinology
Hypo- YES Perform hypoglycaemia Cause for YES or paediatric metabolic
altered
glycaemia? screen and treat consciousness? input. Support blood
glucose
NO
NO

YES YES Consider hyperosmolar Cause for YES Ongoing paediatric

Hyper- Ketones
state. See BSPED altered diabetes and
glycaemia? high? consciousness?
guideline endocrinology input
NO NO NO
Consider diabec
ketoacidosis. See BSPED
guideline

YES Cause for YES Paediatric neurology input

Suspected
Follow RCPCH stroke guideline altered Neurorehabilitaon and
stroke? consciousness? brain injury follow-up
NO NO

Consider observaon if
YES Follow APLS status epilepcus Known YES recovering, no focal
Seizure? algorithm
neurology and normal
epilepsy? glucose with paent’s
NO typical seizure paern
NO

YES Focal NO Consider observaon if

Neuroimaging if stable
neurology? normal glucose.

Signs of YES Emergency treatment for raised Cause for YES Ongoing management
ICP. Urgent neuroimaging if altered
raised ICP? stable. PICU/neurosurgery input. consciousness? of underlying cause

NO NO

NO YES Consider hypertensive Urgent paediatric

Hyper-
encephalopathy. 4 limb nephrologist and PICU
tension?
(Beware
blood pressure. input.
Cushing triad)

Raised YES 2 ml/kg 10% glucose IV Cause for YES Ongoing metabolic
immediately. Repeat sample. altered
ammonia? Metabolic team input consciousness? specialist input
NO NO

Very high YES Consider hyper-viscosity Cause for YES Ongoing haematology
white cell syndrome . Oncology team altered and oncology specialist
input consciousness?
count? input
NO NO

YES Cause for YES Treatment of specific

Consult ToxBase® or Naonal
Poisoning? Poisons Informaon Service
altered poison/s. Input from
consciousness? mental health services
(including carbon
NO monoxide) NO

YES Treat underlying cause.

Other cause
Consider subspecialty
idenfied?
input.
NO

Seek senior input.

Consider neuroimaging
and specialist input.

Figure 1 Flowchart summarising approach to differential diagnosis in assessment of the altered

conscious state.

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 OCCASIONAL REVIEW
Initial investigations
Essential blood tests
C Point of care blood glucose (within 15 minutes of presentation)
C Blood gas (ideally including HbCO for CO poisoning)
C Full blood count
C Electrolyte profile (including sodium, potassium, calcium and
magnesium e always check a laboratory sample even if pre-
liminary results can be obtained from a blood gas)
C Liver profile (ALT, ALP, albumin)
C Ammonia (note laboratory may need advance notification and
have specific sampling and transport requirements)
C Coagulation profile
C Blood culture
Additional initial blood tests
C CRP
C Paracetamol/salicylate levels
C Blood alcohol level
C Viral serology/serum save samples
Urine tests
C Clean catch sample for dipstick then microscopy and culture
C Urine toxicology (consider chain of custody requirements)
C Storage sample (can be used to add specialist tests later)
Contraindications/cautions to lumbar puncture
C Signs of raised intracranial pressure (see Box 3) e cannot be
excluded by normal intracranial imaging!
C Focal neurological signs
C GCS less than 8
C GCS less than 12 after a prolonged (10 minutes) seizure
C Clinical evidence of circulatory shock
C Suspected meningococcal disease
C Imaging suggestive of CSF pathway obstruction (e.g. obstructive/
non-communicating hydrocephalus)
C Thrombocytopaenia (<50  109/L platelets, INR >1.4)
C Caution in where there is increased risk of cerebral herniation
(e.g. space occupying lesion, structural malformations)
C Caution if abnormal spinal anatomy (e.g. spina bifida, scoliosis)
CSF tests
C CSF microscopy, culture and sensitivity
C CSF viral PCR (including herpes simplex)
C CSF glucose (blood glucose taken before CSF)
C CSF protein
C CSF opening pressure (optional)
Box 2
condition is expected to improve (such as in a post-seizure post-
ictal period).
Breathing: prescribed supplementary oxygen therapy to main-
tain saturations >95% should be given. Outside the context of
PAEDIATRICS AND CHILD HEALTH 31:4
major trauma, hypoxaemia may give some clues towards aeti-
ology for altered consciousness e for example it might be sec-
ondary to local or systemic infection. Consider the pattern of
breathing as a possible marker of underlying cause e e.g. the
deep breathing of Kussmaul respiration in a metabolic acidosis.
Circulation: look for signs of impaired circulation e mottled
peripheries, weak peripheral pulses and cool extremities. In the
context of hypotension or oliguria (defined in the RCPCH guid-
ance as systolic blood pressure less than 5th centile for age, and
urine output less than 1 ml/kg/hour respectively1) this would
indicate (‘cold’) shock. Administer a 20 ml/kg isotonic fluid
bolus e unless there is a suspicion of raised intracranial pressure
(ICP) in which case 10 ml/kg should be given e with careful
reassessment. There should be improvement of tachycardia,
peripheral perfusion and conscious level, with blood pressure
normalisation for age, as shock is treated. Box 2 lists basic blood
investigations which should be taken whilst establishing venous
access.
If clinical examination and other signs (e.g. raised blood
lactate) suggest further fluid resuscitation is required then this
can be given; discussion with a paediatric intensive care unit
would be advised if giving beyond 40ml/kg in total.
Hypertension may be identified at this stage and can also be
relevant as a cause for altered consciousness, or secondary to the
underlying aetiology, which we will elaborate on during discus-
sion of differential diagnoses.
Alongside real-time cardiovascular monitoring, a formal 12
lead electrocardiogram should be obtained to look for rhythm
abnormalities and other cardiac pathology.
Disability: hypoglycaemia should be rapidly identified from
initial investigations e the RCPCH guidance defines this in the
context of reduced consciousness as less than 3 mM. Emergency
management consists of a 2 ml/kg 10% glucose IV/IO bolus with
a repeat blood sugar check soon after; oral glucose gel may be a
temporising measure and IM glucagon or repeat boluses may be
necessary if there is no improvement. We will discuss further on
hypoglycaemia (and hyperglycaemia) later.
Checking for ‘disability’ may identify focal neurological signs
and features raised intracranial pressure (ICP) as described in
Box 3. We discuss their potential causes later. Particular atten-
tion to posture, pupil light reaction and neck stiffness should be
paid. Abnormal posturing e extensor ‘decerebrate’ or flexor
‘decorticate’ e indicates significant neurological injury. Sus-
pected raised ICP should prompt immediate review for intuba-
tion. Treatment should be initiated, for example 20 head tilt and
intravenous bolus of 3 ml/kg of 3% sodium chloride. Urgent
neurosurgical referral is usually indicated. In a child who is
already intubated and ventilated where raised ICP is suspected,
the partial pressure of carbon dioxide (PaCO2) should be kept
between 4.5 and 5.0 kPa.1
Obtaining a urine sample early is recommended (especially
for toxicology, if poisoning seems likely) with testing as outlined
in Box 2.
Exposure: upon screening the patient for any other physical
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 OCCASIONAL REVIEW
Signs of possible raised intracranial pressure.
C Bradycardia (usually heart rate <60/min)
C Bradypnoea and/or abnormal breathing patten
C Hypertension (MAP >95th centile for age) with widened pulse
pressure
C Reduced or fluctuating level of consciousness (sudden or gradual)
C Abnormal posture e.g. decerebrate or decorticate e note may
only be elicited by a painful stimulus.
C Macrocephaly or elevated anterior fontanelle in a younger child
C Papilloedema
C Seizures
C Focal neurological signs, for example:
- Ophthalmoplegia, particularly abducent nerve palsy
- Unilateral or bilateral pupillary dilatation (i.e. ‘blown pupils’)
- Loss of or slow pupillary light reflex
- Abnormal oculocephalic (‘doll’s eye’) reflexes
- ‘Sunsetting eyes’ with loss of upwards gaze and the appearance
of the lower pupil/iris covered by the lower eyelid
Box 3
signs of injury, it is important to take note of whether there are
unusual patterns of bruising or skin marks, which may suggest
possible non-accidental injury as part of the overall presentation.
Patients who have reduced consciousness may be vulnerable
to hypothermia, or in some cases of drug intoxication may
develop hypo- or hyperthermia, which should be addressed.
Ongoing monitoring of ‘neurological observations’ must be
initiated including re-assessment of GCS and routine physiolog-
ical parameters. Cardiac monitoring should be considered.
History
A brief history, taken during emergency assessment as above,
can be invaluable. In the setting of trauma, a useful mnemonic is
‘AMPLE’ (Allergies, Medications, Past medical history, Last
meal, Events). Key points to include are listed in Box 4. A more
detailed full history should follow when possible.
Examination
Initial assessment as above may identify clues pointing towards a
cause for altered conscious state, including external injuries,
features of intoxication and signs of raised intracranial pressure.
A full systemic head-to-toe assessment should then be performed
and may reveal further relevant information such as signs of liver
or heart failure, previous surgical scars and neurocutaneous
signs. This should include a visual assessment of the perineal
area if possible. A normal examination may also be useful by
excluding other pathology. Be prepared for assessment to be
more challenging due to the patient’s altered conscious state and
document their mental state and behaviour, if relevant. Any skin
marks or rashes should be documented on a body map diagram
with measurements and if possible, photographs should be taken
early.
Further investigations
Initial investigations are outlined above and in Box 2. Further
tests may be indicated in specific presentations, for example
PAEDIATRICS AND CHILD HEALTH 31:4
plain radiographs of possible fractures or a computerised to-
mography (CT) ‘trauma series’ with major injury. NICE publish
guidelines on indication for CT head and neck in particular with
relevance to head trauma. Outside the setting of trauma, cranial
imaging will be required in many circumstances; for example, if
the child remains to have ongoing decreased conscious state
without cause or if there are focal neurological signs. CT will
usually be first line due to its relatively easy availability and
speed. It must be ensured patients are stable for transfer to CT
and appropriate emergency equipment available. Magnetic
resonance imaging (MRI) is unlikely to be indicated in the acute
setting with the significant exception of possible stroke, where
MR angiography of the head and neck must not be delayed.
Lumbar puncture is important in the diagnosis of infective
causes of altered conscious state (and more rarely in neuro-
metabolic conditions) however it will often be considered
appropriate to defer such investigation until a patient is more
stable e and pending review by an experienced paediatrician.
Contra-indications and CSF tests are outlined in Box 2.
Differential diagnoses
The causes for acute altered consciousness are so diverse that a
‘surgical sieve’ might seem intuitive, but this can take time. The
pragmatic clinician can begin by considering more common
presentations, an approach echoed in the RCPCH guidance which
specifically recommends to consider 12 specific groups of aeti-
ologies (but not necessarily diagnoses) in the first hour after
presentation. We will discuss these in turn below (some causes
grouped together for clarity), before considering some other
miscellaneous presentations. Figure 1 summarises a possible
approach.
Trauma
Possibly the most common cause of acute decreased conscious-
ness presenting to hospital, but usually only transient in nature,
is head trauma. Even mild head trauma may cause a brief loss of
consciousness and confusion, indicating the clinical syndrome of
concussion. In these circumstances it is important to be clear
Key points from a brief history (adapted from RCPCH
guidance1).
C Vomiting before or at presentation (?raised ICP ?metabolic/
endocrine cause)
C Headache before or at presentation (?raised ICP)
C Fever before or at presentation (?infection)
C Convulsions before or at presentation (and their phenomenology)
C Alternating periods of consciousness (?encephalopathy)
C Trauma
C Ingestion of medications, alcohol or recreational drugs
C Presence of any medications in the child’s home
C Any infant deaths in the family (?metabolic conditions)
C Duration of symptoms
C Travel history (infectious aetiologies)
C Vaccination history (but does not fully exclude vaccinated
conditions)
Box 4
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 OCCASIONAL REVIEW
whether there has been some precipitating event for the trauma
taking place, for example a syncopal episode or a seizure.
Furthermore, sometimes a history of mild trauma may be dis-
tracting as to the real cause of the presenting impairment e for
example, there is an association between mild head trauma and
paediatric stroke, whilst in vanishing white matter leukodystro-
phy, acute neurological deterioration can follow head injury.
More significant trauma can predispose a child to sequelae of
raised intracranial pressure or intrinsic brain injury, presenting
as diffuse axonal injury, which may only become apparent after
some time and not necessarily demonstrated on initial CT
imaging.
Although the initial recovery from concussion can be very
quick as alluded to above, patients should be advised about the
often much longer-term sequelae that can arise with any degree
of head injury.
As with all presentations, the possibility of non-accidental
injury should always be kept at the forefront of the clinician’s
mind, and may coexist with other accidental injuries. If in any
doubt consult a senior colleague. Self-inflicted injury may also
present as trauma, for example apparent strangulation, to major
polytrauma.
Shock (hypovolaemic, distributive and cardiogenic)
Circulatory shock, as discussed during the assessment of circu-
lation above, should prompt the clinician to consider an under-
lying cause. Older children may typically display a more
recognisable pattern of ‘warm’ shock with peripheral vasodila-
tation and tachycardia; this and ‘cold’ shock typically in the
setting of sepsis (see below). However, shock can arise many
other ways. Trauma or severe gastroenteritis could lead to
hypovolaemia. Anaphylaxis could produce a distributive shock.
Both trauma and heart failure could produce cardiogenic
shock. Other than acute fluid management with escalation to
paediatric intensive care support, management should attempt to
address the underlying cause.
Sepsis
Infection was the most common non-traumatic aetiology
identified in Wong et al. s 2001 study3 and as such any child
with features of paediatric systemic inflammatory response
syndrome e abnormal temperature, leucocyte count and heart
or breathing rate e should be investigated and treated for
sepsis. Less than 4  109/L and more than 12  109/L are
considered to be outside the normal range in this context but
bear in mind younger children often normally have higher
white cell counts. A non-blanching petechial or purpuric skin
rash is also recommended in the RCPCH guidance1 as sufficient
in the presence of abnormal consciousness, to treat as sepsis.
In addition to the initial investigations listed above, blood
bacterial PCR is recommended, alongside skin swabs of any
areas of inflammation, joint aspiration with suspected septic
arthritis and specific malaria blood film screen if there is
relevant travel history. Chest radiograph may help identify
‘silent’ atypical pneumonia. Treatment should usually involve
fluid resuscitation and broad-spectrum antibiotics following
local guidelines. The RCPCH has produced a series of podcasts
on the complexities of identifying and managing paediatric
sepsis.
PAEDIATRICS AND CHILD HEALTH 31:4
Poisoning and intoxication scenarios
C Alcohol intoxication e may be mixed with other overdose/inges-
tion e.g. MDMA and note use as an excipient in some medications
that may be inappropriate for most children e.g. phenobarbitone
elixir. Blood alcohol level may be possible.
C Opiate overdose e respiratory depression, dilated pupils,
naloxone reversal
C Tricyclic antidepressant overdose
C Serotonergic syndrome (e.g. SSRI overdose)
C Carbon monoxide poisoning (may be suggestion from history)
C ‘Street drugs’ e.g. cannabinoids, LSD, sympathomimetics
C Unintended overdose of prescribed medication e e.g. agitation
and confusion from antihistamine overdose.
C Intended overdose of prescribed medication with self-harm intent
e e.g. insulin overdose in a person with diabetes mellitus.
C Iatrogenic or improperly monitored medication e.g. anticonvul-
sant drugs.
Always consider co-existing injuries, specifically head trauma!
Box 5
Metabolic diseases
Hypoglycaemia: hypoglycaemia should be considered very early
in any patient presenting with altered conscious state e “neu-
roglycopaenia”. A point of care test can rapidly confirm or
exclude the diagnosis. The precise blood glucose threshold for
defining paediatric hypoglycaemia in the non-diabetic population
is debatable. Research studies suggest that cognitive function
begins to be impaired with blood glucose less than 2.8 mM; the
RCPCH guideline advises treating and investigating blood
glucose less than 3 mM in this context.1 Patients known to have
diabetes mellitus should still be given correction for hypo-
glycaemia less than 4.0 mM.
Hypoglycaemia in children without diabetes can arise from a
wide range of causes, for example from gastroenteritis with
prolonged poor oral intake. Beware: some patients with this
presentation may have relatively uncommon ketotic hypo-
glycaemia, which needs metabolic/endocrinology assessment e
ask about whether the child has had similar previous episodes.
There are also a number of much rarer conditions such medium
chain acyl Co-A dehydrogenase deficiency (MCADD). Known
patients in the latter category will often have very specific
management plans and as they can become unwell quickly, the
threshold to seek specialist advice from a metabolic expert
should be low. The British Inherited Metabolic Diseases Group
has published several relevant emergency guidelines on their
website, including a suggested panel of investigations to perform
as part of a ‘hypoglycaemia screen’.
If symptoms resolve as normoglycaemia is restored e and this
can usually be achieved quickly e then the conditions of
‘Whipple’s Triad’ are met and a diagnosis of symptomatic
hypoglycaemia can be made. If the underlying cause is unclear
consult with an endocrinologist.
A particularly important presentation which typically features
hypoglycaemia as part of a presentation with altered conscious-
ness is adrenal crisis. It may be difficult to ascertain clinical
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 OCCASIONAL REVIEW
features such as hyperpigmentation in the emergency setting and
other parameters such as hypothermia are not unique to the
presentation. If the patient is not known to be at risk, then
biochemical clues such as hyponatraemia and hyperkalaemia
may be useful in recognition. Blood investigation will show low
cortisol but the result will not be available quickly. There may be
a history of preceding courses of steroid therapy, or coexisting
infection precipitating the presentation. Alongside glucose
replacement, rescue treatment with hydrocortisone and fluid
resuscitation is vital and should be initiated if the diagnosis is
suspected.
Hyperglycaemia: diabetic ketoacidosis (DKA) and the hyper-
osmolar hyperglycaemic state can both present with hyper-
glycaemia and decreased consciousness. Checking blood ketones
can help differentiate between the two, usually being absent in
the latter (which is generally uncommon in children). It will
usually take some time to restore normoglycaemia and normal
conscious state. Management can be complex and should involve
senior clinicians e the British Society for Paediatric Endocri-
nology and Diabetes (BSPED) provide excellent management
guidelines for both presentations. Note that in 2020 BPSED have
made significant changes to the fluid management of patients
presenting with DKA in guidelines which supersede previous
practice.
Hyperammonaemia: a wide range of other primary and sec-
ondary metabolic disorders can present with raised ammonia
(and often lactate) e including Reye syndrome described above.
Our experience is that testing for ammonia is often omitted in the
early assessment of patients with reduced consciousness. Testing
for these parameters can aid in identification of this disease
group (for example urea cycle disorders) as an entity but not
necessarily specific conditions. There will usually be a preceding
history of progressive neurological decline, or possibly a family
history. The results of more specialist testing are unlikely to be
back quickly enough for diagnostic certainty. Hepatic encepha-
lopathy from acute or chronic liver failure (itself with many
causes) may similarly have elevated ammonia but there will also
be other biochemical markers such as deranged coagulation and
liver enzyme tests. Ammonia is neurotoxic and several presumed
mechanisms are proposed, for example disrupting glial cell po-
tassium transport. If ammonia levels are greater than 100 mM
then seek expert metabolic advice; intensive care support may be
required. Immediate treatment should include a 2 ml/kg 10%
glucose infusion. The British Inherited Metabolic Diseases Group
again provides a useful emergency management guideline.
Intracranial infection
Specifically consider the possibility of intracranial infection.
NICE publish comprehensive guidelines covering recognition and
management of bacterial meningitis. In patients with reduced
consciousness it may be more difficult to recognise typical clin-
ical signs, but shock, non-blanching rash, nuchal rigidity and
focal neurological signs such as pupil asymmetry may be helpful.
History can be very helpful e there may be travel history
PAEDIATRICS AND CHILD HEALTH 31:4
Miscellaneous presentations
Simple faints (syncope)
C Loss of or reduced consciousness for maximum 20 seconds.
C Vasovagal (neurocardiogenic) syncope most common in children.
C Usually a noxious stimulus e presumed to cause a sudden drop
in blood pressure leading to cerebral hypoperfusion and loss of
consciousness.
C Consider whether other cause e.g. cardiac arrhythmia if history
atypical.
Breath-holding episodes
C Younger child voluntarily holds breath usually in context of being
upset and may lose consciousness with blue/grey or red skin
discolouration.
C Unconsciousness for 1e2 minutes maximum.
C Full blood count to exclude anaemia and ECG recommended.
Paroxysmal disorders
C Fully investigate unless well stereotyped repeated episodes.
C Migraine with brainstem aura can present with confusion or
decreased consciousness.
Box 6
exposure to tick-endemic areas (e.g. tick-borne encephalitidies)
or to malaria-endemic areas (cerebral malaria), or contact history
with an individual with a cold sore (herpesviruses).
Fluctuating consciousness, focal neurological signs and pro-
longed seizures are suggested in the RCPCH guidance to point
towards viral encephalitis as a possible aetiology.1 Treatment
with IV aciclovir as per the British National Formulary for Chil-
dren should be given if herpes simplex encephalitis is suspected.
Whilst MRI and EEG can be helpful in making this diagnosis,
they are unlikely to be practical acutely and ultimately CSF viral
PCR is the gold-standard diagnostic test e when safe to be taken.
Focal neurological signs should also prompt intracranial im-
aging, which may identify alternative infective pathology such as
an intracranial abscess. There may be a history of preceding
illness such as sinusitis or otitis media. Management may require
infectious diseases, otorhinolaryngology and neurosurgical
input. Be aware of less common causes of intracranial infection
such as TB meningitis (turbid, lymphocytic CSF, elevated pro-
tein, decreased CSF:blood glucose ratio) and meningitis affecting
immunocompromised patients and seek relevant history e.g.
cryptococcus and exposure to bird droppings etc. There are iso-
lated case reports of SARS-CoV-2 associated
meningoencephalitis.
Raised intracranial pressure and acute hydrocephalus
Raised ICP can arise from many causes, including (even minor)
trauma, infection, space-occupying lesions (e.g. brain tumour)
and congenital anomalies (e.g. Chiari malformation). Recogni-
tion of raised ICP can often be delayed with the ultimate outcome
159 Ó 2021 Elsevier Ltd. All rights reserved.
 OCCASIONAL REVIEW
cerebral tonsillar herniation (i.e. ‘coning’) which if untreated will
be fatal. Raised ICP can develop rapidly, causing acute decrease
in conscious level, hence the importance of reassessment and
‘neurological observations’ in patients at risk.
A clear history of features such as postural headache and
vomiting, progressive visual disturbance or pulsatile tinnitus is
unlikely to be available acutely and the clinician must rely on
clinical signs. There may be a history of perinatal difficulties e.g.
intraventricular haemorrhage. Box 3 summarises some of the
clinical signs of raised ICP, including the classical Cushing’s
Triad’ of systolic hypertension with widened pulse pressure,
bradycardia and bradypnoea which may be irregular in nature.
Supportive measures as described previously may provide
temporarily amelioration, however underlying cause must be
identified. Treatment without specialist help may be limited;
neurosurgical referral and if necessary, patient transfer, is time-
critical.
Special note should be made for patients already known to
have had previous neurosurgical intervention and devices such
as ventriculoperitoneal shunt, where any alteration in con-
sciousness should prompt immediate consideration for compli-
cations such as blockage, infection or bleeding. This could
present as acute-on-chronic hydrocephalus.
Hypertension
An important condition which may mimic some features of
raised intracranial pressure is hypertensive encephalopathy. The
main features of this clinical presentation are hypertension
(usually extreme), headache and disturbed consciousness. Sei-
zures, visual disturbance and focal neurological deficits are also
seen. The exact underlying mechanism is not known but it is
postulated that very high blood pressure exceeds the ability of
cerebral perfusion pressure autoregulatory mechanisms, leading
to failure of the bloodebrain barrier and resulted oedema. Blood
pressures are typically elevated and the RCPCH guidance sug-
gests to consider systolic blood pressure greater than 95th centile
for age and height on 2 separate readings as relevant.1 Any cause
for hypertension could lead to hypertensive encephalopathy (e.g.
primary renal or reno-vascular pathology, phaeochromocytoma
etc. e and hence a four-limb blood pressure check is recom-
mended), but other causes for altered consciousness that may be
associated with hypertension should also be reviewed e in
particular raised intracranial pressure. Papilloedema may be seen
in both situations. Symptoms are reversible with treatment e but
this should be guided by a paediatric nephrologist or intensive
care team.
Hypertensive encephalopathy is presumed to be one cause of
the posterior reversible encephalopathy syndrome (PRES), which
presents a similar clinical entity with symptoms as above, but
hypertension is not always present. Patients may have a history
of immunosuppression or autoimmune disease.
Stroke
Both ischaemic and haemorrhagic stroke may present with
altered conscious state, including through effects of raised ICP
(typically haemorrhagic strokes) or through the specific area of
PAEDIATRICS AND CHILD HEALTH 31:4
infarction (particularly infarct involving the thalamus). Stroke
typically features a rapid onset of sudden sometimes progressive
neurological signs. Alongside the well-known ‘Face, Arm,
Speech, Time’ (‘FAST’) mnemonic be aware stroke can present
with persistent change in conscious level, new onset seizures and
headache, other focal neurology such as ataxia, dizziness and
even transient focal neurological deficits. Patients with underly-
ing haematological disorders such as sickle cell disease and
hyperviscosity syndromes are at higher risk of stroke. CT imag-
ing should be performed initially and will identify or exclude
haemorrhage; if ischaemic stroke is still clinically suspected then
urgent MRI/MR angiography of the head and neck should be
performed. The window for intervention to improve outcome in
stroke (e.g. through thrombectomy or thrombolysis) is time-
critical. The RCPCH provides comprehensive guidance on the
management of suspected stroke in childhood.
Convulsions and recovering from a previous
convulsion
The term ‘convulsions’ is a non-specific broad term, which en-
compasses both epileptic and non-epileptic events. For example,
a febrile convulsion will acutely cause a child to have reduced
consciousness, but recovery would usually be expected relatively
quickly. Practitioners should be cautious that the child with fever
and a seizure does not have a more serious intracranial infection
or sepsis and for example use risk stratification tools to plan their
management further. The RCPCH guideline supports observation
of a post-ictal child with normal blood sugar without further
investigation during the first hour after the seizure, alongside a
careful history and examination.1
Epileptic seizures may cause a person to present with altered
conscious state. It is worth having at least basic familiarity with
the common childhood epilepsy syndromes in order to recognise
how they may present, as well as management of status epi-
lepticus. The National Institute for Health and Care Excellence
(NICE) has produced a comprehensive guideline. Electrolyte
disturbances (specifically sodium, calcium and magnesium)
should be checked for and treated, if seizures continue. They
may point towards an underlying cause if present (e.g. 22q11.2
deletion syndrome with hypocalcaemia, and Gitleman syndrome
with hypomagnesaemia).
When there has been a clear history of a recent seizure then a
patient may present in the ‘post-ictal’ phase with reduced or
altered consciousness that should self-resolve, usually over a
period of minutes to hours. If there is a history of previous
similar events with diagnosis or investigation for epilepsy then
clearly it may be acceptable not to investigate further at this
point. However in all cases it essential to consider possible
alternative diagnoses and the cause of the seizure itself. Todd
paresis following seizure e usually presenting as unilateral
weakness e is reported to persist for as long as 36 hours, how-
ever this or an apparently prolonged post-ictal period should
raise suspicion for an alternative neurological diagnosis such as
stroke.
A preceding history of insidious behavioural change may raise
the possibility of an encephalitis (acute inflammation of the
160 Ó 2021 Elsevier Ltd. All rights reserved.
 OCCASIONAL REVIEW
brain) or encephalopathy (disordered function of the brain).
Demyelinating conditions can very rarely present with seizure
and altered consciousness, such as acute disseminated enceph-
alomyelitis which may follow on from minor illness. There are
also many uncommon disorders, such as anti-NMDA receptor
encephalitis and encephalopathy associated with autoimmune
thyroid disease (i.e. Hashimoto encephalopathy) which can
present in this way. A paediatric neurologist may need to be
involved to guide further investigation and management.
If alternative diagnoses are excluded, or with the judgement of
a senior clinician, in some children presenting altered conscious
state, the diagnosis of a functional neurological disorder can also
be considered. Such patients may present with dissociative
symptoms (i.e. strange feelings of the body not belonging to
oneself, or sensation of being separated from the world around),
or have more typical events that may resemble seizures with a
postictal period but which lack any biological correlates e.g. EEG
changes, which are more typically called non-epileptic attacks.
Clinicians should gain experience of how to identify features of
non-epileptic episodes and how to explain such conditions to
patients and families.
Intoxication/poisoning
A wide range of legal and illegal drugs could cause a patient to
present with altered consciousness. Resources such as
ToxBaseÒ, the National Poisons Information Service and the
British National Formulary for Children may be consulted to
guide management. Box 5 lists scenarios where poisoning may
cause altered consciousness.
Miscellaneous
There are a number of e usually benign e presentations not
covered in the RCPCH guidance with which clinicians should be
familiar, summarised in Box 6.
Further management, outcomes and follow-up
With the exceptions of those children with a transient illness who
recover quickly, following emergency management as outlined
above most children with acutely altered consciousness will
subsequently need hospital admission and ongoing observation.
Subspecialist input to guide management as well as multi-
disciplinary involvement to help recovery is essential. Patients
may need care outside of an acute hospital setting in a specialist
neuro-rehabilitation unit, and sadly some children may not
recover. Wong et al. 20013 reported an overall mortality rate of
around 46% for their cohort, but varying widely depending upon
specific aetiology. Of the surviving children who had follow-up,
more positively, around 66% had no neurological, cognitive,
special sensory or behavioural impairment.
Nonetheless, most children should be offered longer-term
follow-up. Any child considered to have sustained an ABI is at
risk for later cognitive or behavioural difficulties and conse-
quently it is important to plan ahead e even when by discharge a
child seems to have recovered. Serial neuropsychology assess-
ment with an assessment interval of several years can help
PAEDIATRICS AND CHILD HEALTH 31:4
identify which areas a child may need support in. Various
community-based brain injury services also exist and can pro-
vide support for children and their families in both the short and
longer-term.
Prevention
As can be seen, a number of the above aetiologies may be pre-
ventable in some way. These are largely however interventions
at a population level directed by government and public health e
for example legislation to limit the exposure of children to toxic
chemicals such as lead (high-dose may present with acute en-
cephalopathy) and stringent laws regarding carrying children in
motor vehicles to reduce risk of physical injury in collisions.
Individual choices have an additional impact, for example uptake
of vaccination programmes, wearing a bicycle helmet and drug
mis-use. Referral to drug and alcohol support services should be
made available where relevant.
Summary
Clinicians should be vigilant to recognise children presenting
with an acutely altered conscious state. Rapid assessment and
management should be initiated with a systematic approach.
There are a wide range of possible causes for such presentations,
ranging from those easily reversed, to life-threatening ones.
Awareness of local policies and services is important in order to
ensure this can progress quickly. Specialist input and longer-term
follow-up will be often be required. Having an efficient approach
to such patients is critical. A
REFERENCES
1 The Royal College of Paediatrics and Child Health and The Uni-
versity of Nottingham. The management of children and young
people with an acute decrease in conscious level e a nationally
developed evidence-based guideline for practitioners. 2015. up-
date revised 2019, https://www.rcpch.ac.uk/resources/
management-children-young-people-acute-decrease-conscious-
level-clinical-guideline.
2 The Royal College of Paediatrics and Child Health. The manage-
ment of children and young people with acute decrease in
conscious level (DECON). 2016. updated April 2019, https://www.
rcpch.ac.uk/resources/management-children-young-people-
acute-decrease-conscious-level-clinical-guideline.
3 Wong CP, Forsyth RJ, Kelly TP, Eyre JA. Incidence, aetiology, and
outcome of non-traumatic coma: a population based study. Arch
Dis Child 2001; 84: 193e9.
4 Parslow RC, Morris KP, Tasker RC, Forsyth RJ, Hawley CA.
Epidemiology of traumatic brain injury receiving intensive care in
the UK. Arch Dis Child 2005; 90: 1182e7.
FURTHER READING
BIMDG: British Inherited Metabolic Diseases Group. BIMDG; 2020.
Emergency guidelines. 2020, http://www.bimdg.org.uk/site/
guidelines.asp.
161 Ó 2021 Elsevier Ltd. All rights reserved.
 OCCASIONAL REVIEW

BSPED: British Society for Paediatric Endocrinology and Diabetes. The Children’s Trust e for children with brain injury. 2020. Tadworth,
Bristol: bioscientifica; 2017-2020. Guidelines; 2017 [Internet]. 2020, Surrey: The Children’s Trust, https://www.thechildrenstrust.org.uk/.
https://www.bsped.org.uk/clinical-resources/guidelines/.
National Institute for Health and Care Excellence. Meningitis (bacterial)
and meningococcal septicaemia in under 16s: recognition, diag-
nosis and management. 2015, https://www.nice.org.uk/guidance/
Practice points
cg102.
C Always prioritise seeing children with reported acutely
Royal College of Paediatrics and Child Health and the Stroke Asso-
altered consciousness as soon as possible.
ciation. Stroke in childhood e clinical guideline for diagnosis,
C Differential diagnosis can be challenging e start basic
management and rehabilitation. 2017, https://www.rcpch.ac.uk/
management following a CABCDE approach and have a low
resources/stroke-childhood-clinical-guideline-diagnosis-
threshold to involve senior support.
management-rehabilitation.
C Be aware of important national guidelines to help man-
Smith SJM. EEG in neurological conditions other than epilepsy: when
agement of specific presentations such as sepsis, menin-
does it help, what does it add? J Neurol Neurosurg Psychiatry
gitis, DKA and stroke.
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PAEDIATRICS AND CHILD HEALTH 31:4 162 Ó 2021 Elsevier Ltd. All rights reserved.