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The Patient with Hyponatraemia
149
Concurrent use of diuretics may make interpreting urine sodium concen-
trations dicult, but diuretics should still be considered a contributing
factor to the hyponatraemia.
Describe the RASS
The RASS is one example of a scale that can be used to assess the level of alert-
ness and agitated behaviour in a critically ill patient. The scale ranges between
−5 and +4 (Table11.3). Even though the RASS can be used in all hospital-
ised patients, it is more frequently utilised in patients who are mechanically
ventilated to avoid over-
or undersedation. A RASS between −2 and 0in
mechanically ventilated patients:
Minimises sedation
Reduces mortality
Decreases the duration of mechanical ventilation
Shortens the length of stay in the ICU.
The RASS has been validated for use with the Confusion Assessment Method
for ICU (CAM- ICU) (discussed later).
Table 11.3: Richmond Agitation- Sedation Scale (RASS).
to staff
displays aggressive behaviour towards staff
patient–ventilator dyssynchrony
aggressive or vigorous
−1 Drowsy Not fully alert, but sustained (>10 s) awakening
to voice, with eye contact
−2 Light sedation Briey (<10 s) awakens with eye contact to voice
−3 Moderate
sedation
Any movement (but no eye contact) to voice
−4 Deep sedation No response to voice, but any movement to
physical stimulation
−5 Unarousable No response to voice or physical stimulation
On day 4 of admission, Gladys's serum sodium from the morning set of
bloods was reported as 136
mmol/L. You are asked to review her as she has
become acutely confused and agitated, and appears to be hallucinating. You
and the nursing sta consider that Gladys is now suering with delirium.
Her RASS (Richmond Agitation- Sedation Scale) is +3.
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Clinical Cases in Critical Care
150
What is delirium?
Delirium is dened as a disturbance in awareness, attention and cognition
that develops over a short period of time, is uctuating and is associated with
perceptual changes (e.g. hallucinations).
What are the different subtypes of delirium?
Clinically, three subtypes have been established:
Hypoactive delirium is probably the most common form as it is often
misdiagnosed and reportedly unrecognised in 66–84% of patients.
Typically, the patient appears co- operative and passive but will show
signs of inattention and decreased responsiveness and be unable to
organise thoughts.
Hyperactive delirium is the more familiar and recognisable form of
delirium but is much less common than the other types and in its pure
form is even rarer. Incidentally, this subtype has a better overall prog-
nosis. The patient can hallucinate and be agitated, combative, aggressive
and uncooperative, which can potentially put the patient and sta at
risk of physical harm.
Mixed delirium, as the name suggests, often presents as alternating
periods of aggressive behaviour and quiet confusion.
How common is delirium in critical care patients?
The incidence of delirium varies according to specic patient populations in
critical care but can aect up to 80% of patients in medical intensive care units.
Postoperative neurosurgical and trauma patients are also at increased risk.
Patients in critical care tend to have the highest incidence of delirium compared
to other clinical areas of a hospital. The incidence of delirium in ventilated
patients can approach 70%, with a mixed delirium presentation predominating,
followed by the hypoactive subtype.
Broadly speaking, what are the risk factors for delirium?
Modiable risk factors
Hypoxia
Hypercarbia
Acidosis
Infection
Dehydration or constipation
Polypharmacy (including use of opiates, benzodiazepines and anticho-
linergic medications)
Urinary catheter irritation
Urinary retention
Metabolic disturbances (e.g. hyponatraemia)
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The Patient with Hyponatraemia
151
Non- modiable risk factors
Age
Cognitive decline
Dementia
Depression
Liver impairment
What role do benzodiazepines have in the
development of delirium?
Benzodiazepines are considered an independent risk factor for delirium during
critical illness, with little variation in risk between the dierent classes. With
lorazepam, evidence suggests that the probability of transitioning to delirium
is great even at low doses.
How can we screen for delirium in critical care?
Two methods are available in critical care for delirium screening. These have
also been validated in intubated patients.
The CAM- ICU is a snapshot assessment of delirium and can be easily
carried out at the bedside by healthcare professionals (its specicity and
sensitivity are reported as 81% and 96% respectively). In critical care,
sedation must be assessed before carrying it out, and the assessment can
occur if the RASS is greater than or equal to −3. Features of delirium are
assessed sequentially in the following four stages:
Is there an acute onset and fluctuating course? This information
can be obtained from a family member or nurse by asking if there has
been any change in the patient’s baseline mental status and whether
the change has fluctuated throughout the day. If this has occurred
then proceed with the next step; if this is absent then the patient is
CAM- ICU negative.
Does the patient have difficulty focusing their attention? The
patient can be asked to squeeze your hand when they hear the letter
‘A’ upon spelling out the phrase ‘S A V E A H A A R T’ or ‘C A S A B L
A N C A’. If three or more errors occur (i.e. fails to squeeze your hand
on hearing the letter ‘A’ or squeezes your hand on another letter),
then the assessment is continued. If two or fewer errors occur, then
the patient is CAM-
ICU negative.
Does the patient have an altered level of consciousness? This is
essentially the RASS score taken from the first stage. If it is anything
except 0 (e.g. alert and calm) then the patient is considered CAM- ICU
positive, otherwise the next and last stage of assessment is undertaken.
Does the patient have disorganised thinking? This stage attempts
to determine if the patient has incoherent thoughts (e.g. rambling or
irrelevant conversation), disordered flow of ideas or unpredictable
switching from one idea to the next. If at this stage the patient has
more than one error, they are considered CAM- ICU positive.
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Clinical Cases in Critical Care
152
The Intensive Care Delirium Screening Checklist (ICDSC) assesses
eight features:
Altered level of consciousness
Inattention
Disorientation
Hallucinations
Psychomotor agitation/retardation
Inappropriate mood/speech
Sleep/wake cycle disturbance
Symptom fluctuation
The specicity and sensitivity for the ICDSC have been reported as 99%
and 66% respectively. It requires information to be gathered over a period and
therefore takes longer to complete than the CAM-
ICU.
How can we manage delirium?
Primary prevention remains the most eective strategy to reduce delirium and
its associated complications. However, some delirium is virtually inevitable
in many critical care patients. We can categorise the management of delirium
into non- pharmacological and pharmacological measures.
Non- pharmacological measures
It is important to apply basic patient management principles early and liberally.
Early mobilisation.
Reduce unnecessary noise and stimulation (especially at night).
Frequent reorientation.
Reducing the exposure of critical care patients to sedatives and analgesics (e.g.
propofol and fentanyl) through focused daily interruptions (‘sedation holds’) to
achieve a RASS score of 0 (alert and calm) to −1 (drowsy) and target- based seda-
tion have also been shown to improve patient outcomes. However, this needs to
be balanced against reducing pain, especially in postoperative patients, which
makes the use of regional anaesthetic techniques potentially useful although this
has yet to be fully validated. Involving family members in the care of the patient
while in hospital may also be of some benet, not only for the patient but for
the family members as well by teaching them to identify episodes of delirium.
Pharmacological measures
Drugs are used to treat the troublesome symptoms of delirium (usually the
hyperactive type). They do not treat the delirium itself. Ideally, medications
should only be employed when non- pharmacological measures have been
Gladys is becoming increasingly agitated and crying out for her husband.
She is CAM-
ICU positive. The result of the repeat urgent serum sodium
concentration that you requested is 136 mmol/L. This has remained stable
over the last 24
hours.
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The Patient with Hyponatraemia
153
exhausted or are considered inappropriate (e.g. the severely agitated patient
who poses a risk to themselves and others). A common choice in this context
is the butyrophenone haloperidol, which does not suppress respiratory drive
and works by partially blocking the dopamine D
2
receptor. As with all agents
used to treat delirium, there is little evidence for its safety and ecacy, and
it will potentially have psychoactive eects that will increase the duration
of cognitive impairment and potentially reduce the patient’s level of con-
sciousness.
What is the ICU Liberation Bundle?
This bundle has been shown to help reduce delirium, improve pain
management and reduce the long-
term consequences for adult critical care
patients. The components of this evidence-
based bundle are described using
the acronym ABCDEF:
Assess, Prevent and Manage Pain
Both Spontaneous Awakening Trials (SAT) and Spontaneous Breathing
Trials (SBT)
Choice of Analgesia and Sedation
Delirium: Assess, Prevent and Manage
Early Mobility and Exercise
Family Engagement and Empowerment
The use of this ABCDEF bundle (www.iculiberation.org) has been shown to
improve survival and increase the number of delirium-
free days after adjusting
for age, severity of illness and presence of mechanical ventilation. However,
strong evidence is still lacking on whether delirium prevention protocols can
prevent delirium in critical care patients.
Do patients who experience delirium in the ICU
have a poorer outcome?
Yes. In critical care patients, delirium has been shown to be an independent
predictor of mortality, increased length of stay, increased length of mechanical
ventilation and long-
term cognitive impairment. Critical care patients who
have a prolonged period of delirium are at highest risk for long- term cognitive
impairment.
The nursing staff suspect that Gladys was becoming delirious due to
disorientation and lack of family contact (as she keeps asking for her
husband of 55 years). Later that same day, her husband comes to visit.
With him sitting by her side, holding her hand and talking gently to her,
Gladys becomes much more relaxed and co- operative. Medication was
not required to treat her delirium and she is discharged to the ward the
following day.
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Clinical Cases in Critical Care
154
Further reading
Spasovski, G., Vanholder, R., Allolio, B. etal. (2014). Clinical practice guideline
on diagnosis and treatment of hyponatraemia. Eur. J. Endo. 170: G1–G47. Excel-
lent evidence- based guideline for the management of hyponatraemia developed in
conjunction with the European Society of Intensive Care Medicine.
Sessler, C., Gosnell, M., Grap, M. etal. (2002). The Richmond Agitation- Sedation
Scale. Am. J. Respir. Crit. Care Med. 166: 1338–1344. Seminal paper evaluating the
RASS in adult intensive care patients.
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Clinical Cases in Critical Care, First Edition. Alice Myers and Theophilus Samuels.
© 2023 John Wiley & Sons Ltd. Published 2023 by John Wiley & Sons Ltd.
12
Y
ou are called to review a young man in the resuscitation department. He
was found outside a pub earlier this evening having seizures. A bystander
placed him in the recovery position and an ambulance was called. He carried
no identication, appeared unkempt and had no friends with him. Paramedics
sited both a nasopharyngeal (NP) and an oropharyngeal (OP) airway and
administered two doses of lorazepam. He arrived with a GCS of 3without dem-
onstrating obvious seizure activity. However, he has now started seizing again.
The Patient in Status
Epilepticus
What could be causing his seizures?
Known epilepsy– approximately 60 million people throughout the world
have epilepsy, around 500 000in the UK. It is unknown whether this
man has epilepsy. He may suer regular breakthrough seizures or he
may be non-
compliant with medication. He may have a lowered seizure
threshold for an unknown reason such as infection or toxins.
Isolated seizure or new- onset epilepsy– approximately 1in 20 adults will
have a seizure at some point in their life. This may or may not progress
to epilepsy which may or may not continue throughout the individual’s
life. New-
onset epilepsy is most likely to develop in those under 20 or
over 65
years of age.
Pseudoseizures, factitious seizure disorder or non- epileptic seizures – it can
be extremely dicult to dierentiate factitious seizures from epilepti-
form seizures. Often, those patients who present with factitious seizures
also have co- existent epilepsy. Managing these cases is challenging
since overtreatment exposes patients to the risk of iatrogenic injury (e.g.
unnecessary treatment with benzodiazepines leading to airway compro-
mise and the need for intubation). However, avoiding treatment may
expose the patient to the risks of airway obstruction (i.e. where non-
epileptic seizures are suspected but the patient does in fact have reduced
GCS due to genuine seizure activity).
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Clinical Cases in Critical Care
156
Meningitis/encephalitis – meningitis is inammation of the meninges.
Encephalitis is inammation of the brain itself. Infective causes include
bacteria, viruses, fungi and parasites. Non-
infective causes include SLE
(systemic lupus erythematosus) and, rarely, drug reactions (such as with
NSAIDs). Meningococcal sepsis is a diagnosis not to be missed. Presen-
tation is most commonly with altered mental status, headache, neck
stiness, photophobia and seizures. Purpuric or petechial rash may be
a sign of the intradermal haemorrhage associated with sepsis secondary
to Neisseria meningitidis.
Intracranial haemorrhage– sudden spontaneous events such as sub-
arachnoid or intracerebral bleeding can occur secondary to aneurysm
(see Case 15).
Space- occupying lesion – seizure could be the manifestation of a progres-
sive pathology such as solid tumour (primary or secondary), lymphoma
or abscess. Small lesions may be tolerated with few or no symptoms. With
increasing size, the lesion itself, the surrounding oedema or resultant
mass eect can lead to symptoms. Examine the patient for focal neuro-
logical signs and perform imaging of the brain to look for tumour and
ring enhancing lesions.
The WHO reclassied CNS tumours in 2016, integrating molec-
ular data with histopathology. The 2007 grading system, based on
characteristics such as growth rate and likelihood of metastasis, is
still commonly used. In the UK
>4000 people are diagnosed annually
with lower grade tumours (I and II) and approximately 5000with the
more malignant grades III and IV. Glioblastoma multiforme, a grade
IV tumour, is the most common primary brain tumour accounting
for approximately 15% of all intracranial tumours with an incidence
of about 2 per 100
000. It has a median survival of 15 months and a
5- year survival rate of 4%.
Traumatic brain injury – the patient may have been involved in an
altercation or be the subject of assault. Inspect for signs of trauma and
examine the scalp as carefully as possible. Haematomas can be hidden
beneath hair. If there is reason to suspect trauma, state this clearly to
the attending team and re- call this incident as a trauma call, proceeding
according to ATLS
®
guidance.
Drugs/toxins/overdose/withdrawal – the patient was found outside a
pub. He has not necessarily been drinking alcohol, but this possibility
should be borne in mind. Severe alcohol withdrawal can be associated
with seizures, delirium tremens and hallucinations. Without careful
management, this can be fatal. Nearly 10% of cases of status epilepti-
cus are due to drugs and poisons including antidepressants, opioids,
recreational drugs, stimulants and insecticides. Neurotransmitters impli-
cated in the process can include GABA and glutamate. Drugs such as
amphetamine derivatives and cocaine can cause hyperpyrexia which
itself can also lead to seizures.
Metabolic causes – other occult causes of seizure should be considered,
including hyper- and hypoglycaemia, electrolyte imbalance and uraemia
secondary to renal failure. Many inborn errors of metabolism require
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The Patient in Status Epilepticus
157
careful management to avoid accumulation of neurotoxins. For instance,
phenylketonuria requires meticulous diet control due to deciency of phe-
nylalanine hydroxylase. In the absence of diet control, accumulation of
phenylalanine can result in intellectual impairment or even seizures. Fortu-
nately, this disease is rare (approximately 1in 10
000) and usually detected
in infancy, with careful management preventing symptom development.
What are your main concerns?
Life- threatening issues
Ongoing seizures with an unprotected airway.
Hypoxia and signs suggestive of aspiration.
Evidence of trauma to the head which could be the cause of his seizure
or sustained secondary to falling during a seizure.
Potential for occult injuries such as broken limbs or spinal injury.
Establishing the underlying cause(s) of seizures
No available collateral history.
Lactataemia with a mixed metabolic and respiratory acidosis.
Serum lactate can be raised subsequent to the sustained and excessive muscular
activity in tonic-
clonic seizures. If the lactate is raised due to seizures, this would
decrease rapidly following seizure control. If it does not, consider other causes.
What are your management priorities?
Take an ABCDE approach, give oxygen and call for help. This patient is likely
to need intubation and his airway may be dicult. Call for assistance early.
Management priorities are:
Airway management with cervical spine control
Terminate seizures
Investigate and treat the cause of his seizures (including traumatic
head injury)
Investigate and treat any problems resulting from his seizures.
On examination, the man has tonic- clonic movements of his upper and
lower limbs. There is vomitus around his mouth and a large boggy haema-
toma on the back of his head with some grazes around his elbows. His BP
before the current seizure was 135/89
mmHg, HR 110 bpm sinus rhythm,
RR 24 breaths per minute, temperature 35.8
°C, blood glucose 6.4 mmol/L,
lactate 6.5
mmol/L, pH 7.14, PaO
2
9.3 kPa on 15 L/min via non- rebreathe
mask, PaCO
2
7.6 kPa, base excess −7 mmol/L.
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Clinical Cases in Critical Care
158
What is the denition and pathophysiology of status
epilepticus?
Status epilepticus can be convulsive or non- convulsive. The International
League Against Epilepsy (ILAE) redened status epilepticus in 2017. Status
epilepticus is continuous seizure activity or repeated seizures without inter-
vening recovery of consciousness lasting 5 minutes or more.
Dysregulation of neurotransmission occurs, involving excitatory neurotrans-
mitters like aspartate, glutamate and acetylcholine, and inhibitory transmitters
such as GABA. Status epilepticus (convulsive and non- convulsive) is associated
with cognitive problems and even neuronal necrosis, possibly due to depletion
of ATP and lactate accumulation.
What is the pharmacological management
of refractory convulsive status epilepticus?
NICE guidance CG137 (updated 2021) species the use of oxygen, glucose and
IV thiamine, and refers users to the BNF regarding antiepileptic drugs. Appro-
priate antiseizure medications include IV lorazepam, IV diazepam, IV pheno-
barbital and rectal diazepam. At the time of writing, there is no evidence- based
preferred second therapy of choice, but options include IV levetiracetam, IV
valproic acid and IV phenytoin.
Classify epilepsy
The ILAE revised the classication of epilepsy in 2017 (terms such as ‘complex
partial’ and ‘secondarily generalised’ are no longer used).
Seizure types
Focal onset– aware vs impaired awareness, motor onset vs non-
motor onset
Generalised onset– motor (tonic- clonic) vs non- motor onset (absence)
Unknown onset– motor vs non- motor, unclassied
Epilepsy types
Focal
Generalised
Combined generalised and focal
Unknown
Aetiology
Structural, e.g. traumatic brain injury, post craniotomy, stroke
Genetic, e.g. point mutations, mosaicism, polymorphisms or syndromes
such as neurobromatosis
Infectious, e.g. HIV, malaria, TB
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