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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3080_Библиотеки_им_академика_М_И_Перельмана
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The Patient in Status Epilepticus
159
Metabolic, e.g. mitochondrial disorders, creatine disorders,
pyridoxine disorders
Immune, e.g. Rasmussen syndrome
Unknown
Would you give this patient antimicrobials?
Meningitis is a possible diagnosis so treat with antimicrobials until this has been
ruled out. There is also radiological evidence of lower respiratory tract infec-
tion (LRTI). Pre-
existing infection could have lowered his seizure threshold. In
this context, antimicrobial cover for bacterial and viral meningitis according
to local protocol would be reasonable, e.g. ceftriaxone 2
g IV bd with aciclovir
10 mg/kg IV tds.
Which organisms commonly cause meningitis?
Although meningitis can occur in anyone, certain pathogens are more common
in particular groups.
Neonates– the most common bacterial causes are Group B strep, E. coli,
S. pneumoniae, Listeria and Salmonella.
Children and younger adults (such as our patient)– the most common
bacterial causes are N. meningitidis (Men B is the most common strain in
the UK), S. pneumoniae and H. inuenzae type b. Common viral causes
include herpes viruses, enteroviruses, aviviruses and measles.
Immunocompromised– other causes such as TB and fungal infection
should always be considered, particularly in a patient like ours for whom
we have limited background history and who may be immunosuppressed.
Older adults (aged >60 years)– similar causes to those in younger adults
with the addition of Listeria. Susceptibility is increased due to a waning
immune system.
What are the causes of encephalopathy?
Infection– bacteria, viruses, fungi, parasites, prions
Hypoxia/anoxia– hypoxic ischaemic encephalopathy
You alert the team that this should be managed as a trauma scenario. You
intubate the patient with manual in-
line stabilisation. You elect to use thiopen-
tone as the induction agent for its antiseizure properties. On primary survey,
there do not appear to be any further life-
threatening injuries. You commence
loading the patient with phenytoin and transfer him to the CT scanner for CT
head and neck. There are no radiological abnormalities of the neck. The only
abnormalities noted on the CT head are an extracranial soft tissue swelling over
the occiput. Right basal consolidation is seen on plain chest radiograph. You
transfer the patient to intensive care for further management.
Some initial blood results are available: Hb 124
g/L, WBC 24×10
9
/L,
CRP106, platelets 134×10
9
/L, INR 1.4.
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Clinical Cases in Critical Care
160
Metabolic– e.g. derangement of calcium, glucose, sodium, etc.
Alcohol, drugs, poisons– e.g. cyanide, carbon monoxide and heavy metals
such as mercury and lead. Chemotherapy agents can induce encephalop-
athy which may present much like hypoxic ischaemic encephalopathy.
Hepatic– ammonia
Renal– urea
Tumour
Autoimmune– e.g. Hashimoto’ disease
Nutritional deciencies– e.g. lack of vitamin B1/Wernicke
Hypertension
Traumatic– chronic traumatic encephalopathy
Would you give steroids?
A Cochrane review in 2015 (Brouwer etal.) reviewed evidence on the eect of
corticosteroids in acute bacterial meningitis. After analysing 25 studies, there
is moderate-
quality evidence to support corticosteroids reducing hearing loss
and neurological sequelae in bacterial meningitis but there was no impact on
mortality.
This is not a classic presentation of bacterial meningitis. However, there is
sucient concern that it would be reasonable to start dexamethasone 10 mg
IV qds. If S. pneumoniae meningitis is conrmed, steroids should continue for
4
days. However, if an alternative cause is found or pneumococcal meningitis
is unlikely, dexamethasone can be stopped.
What is your plan in intensive care?
Provide appropriate organ support, investigate the cause, then try to wake the
patient up and assess neurology as soon as it is safe to do so.
Organ support
Invasive monitoring as required– intra- arterial monitoring as a minimum.
Lung- protective ventilation.
Manage pathology
Seizure control and neuro observations with regular frequent pupil
assessment.
Treat for meningitis until ruled out.
Consider treating for LRTI. Do not treat suspected aspiration pneumo-
nitis with antibiotics.
As soon as it is safe to do so, stop the sedative agents and assess the
patient’s neurology.
Although his cervical spine is radiologically clear, the patient needs to be
awake and co- operative to be fully assessed and cleared neurologically.
While he is sedated, he can be managed with inline C- spine stabilisation.
Clean the wound and request surgical review.
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The Patient in Status Epilepticus
161
Investigate underlying cause
Full septic screen including urinary antigen screen for S. pneumoniae
and Legionella, viral inuenza swab, wound swabs, sputum sample,
lumbar puncture with viral PCR.
Metabolic screen with LFTs, ammonia.
Drug levels– paracetamol, salicylate, alcohol, toxicology screen.
Collateral history focusing particularly upon drug history, history of sei-
zures and presence of other risk factors for seizures (e.g. exposure to
meningitis, etc.).
Complete secondary trauma survey.
Basic intensive care management
Venous thromboembolism prophylaxis following lumbar puncture.
Stress ulcer prophylaxis.
Replace vitamins B and C to prevent refeeding syndrome given this
patient looks unkempt and malnourished.
Insert an NG tube and start feed.
Temperature management.
Attempt to locate next of kin if possible.
What are your concerns regarding his slow
neurological progress?
This could be non- convulsive status epilepticus.
He might have sustained signicant brain injury which was not visible
on the initial CT head scan.
There could be unknown circulating toxins or an as yet unidentied
metabolic cause.
Bruce is homeless and has a history of drug misuse, making him vulner-
able to HIV and TB meningitis.
He may be non- compliant with medications or have taken an overdose
of his medication.
After 24 hours following sedation hold, the patient remains intubated and
has displayed no seizure activity but does not appear to be waking. His GCS is
3, his pupils are equal and reactive at 3
mm each. The initial lumbar puncture
results were as follows: WBC 4
cells/microlitre, RBC 1 cells/microlitre, no
organisms seen, no xanthochromia. He is breathing spontaneously on the
ventilator with a pressure support 10
cm H
2
O, PEEP6 cm H
2
O, FiO
2
0.30 to
achieve a PaO
2
8.4 kPa, PaCO
2
6.3 kPa. He has not required any cardiovas-
cular or renal support. His plasma WBC is 18 × 10
9
/L and his CRP is 64.
Temperature 37.1 °C.
The police tell you his name is Bruce. He is a 19-
year- old homeless man
with no next of kin. He is known to have problems with substance misuse
and epilepsy for which he takes phenytoin.
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Clinical Cases in Critical Care
162
What do you do about the antimicrobials?
The viral PCR results remain outstanding. Bruce’s white blood count is elevated.
He has not made signicant neurological recovery.
A viral cause of meningitis remains a possibility so continue aciclovir.
Although no organisms were seen on gram stain of the CSF, it would be rea-
sonable to continue antibiotics while the sample is processed and re-
discuss
the case with microbiology in 24
hours.
What are the next steps in management?
Neurological management
Neurology consultant review.
Remain without sedation with frequent neuro observations.
Add an additional anticonvulsant.
Investigations
Send blood sample to measure phenytoin level.
Request electroencephalogram (EEG).
Send blood for HIV.
Consider sending samples for acid- fast bacilli.
Safeguarding
Bruce has no next of kin so an IMCA (independent mental capacity
advocate) is required.
What is the role of EEG in intensive care and how
does it work?
Electroencephalographic data is essential for identifying non- convulsive status
epilepticus. Beyond this, EEG can help dierentiate types of epileptiform
activity and also assist in the diagnosis and investigation of encephalopathy.
Certain patterns within the EEG trace can suggest dierent causes of meta-
bolic encephalopathy.
Continuous EEG is not available in every centre but is often used in specialist
neuro-
intensive care units. EEG produces large volumes of data which require
expert interpretation. Many centres utilise modied EEG systems such as BIS
(Bispectral index) and E- entropy which are used for depth of anaesthesia mon-
itoring. These monitors use algorithms to integrate and interpret EEG data to
generate fewer, simplied variables.
EEG waves can be broadly described as follows:
Alpha, 8–15 Hz– these predominate in the normal resting state but are
also detected in comatose patients.
Beta, 16–31 Hz– these predominate where the patient is alert. They may
also be seen following administration of benzodiazepines.
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The Patient in Status Epilepticus
163
Theta, 4–7 Hz– these waves are often detected in those who are idle or
drowsy. Changes in theta waves can suggest specic forms of encepha-
lopathy or lesions in particular territories of the brain.
Delta, <4 Hz– these predominate in slow- wave sleep. Specic changes
can suggest encephalopathies or lesions in particular territories of
the brain.
Gamma, >32 Hz– originating in the somatosensory cortex, changes in
gamma wave patterns can be associated with cognitive decline.
Mu, 8–12 Hz– these originate in the sensorimotor cortex and are usually
most evident in a state of drowsiness.
In some countries such as the United States, EEG is one of the investigations
used in the diagnosis of brain death. In the UK, EEG may be used as part of
prognostication when dealing with patients with hypoxic ischaemic encepha-
lopathy. For further discussion on brain death, see Case 16.
What is an IMCA and why might you want one in
this case?
Independent mental capacity advocates were introduced in the Mental Capacity
Act 2005 to provide legal safeguarding for those people who are unable to make
specic important decisions for themselves. Bruce is unable to make decisions
for himself because he is unconscious. He does not have any relatives who
would be able to represent him, so an IMCA is required to full this role.
What is burst suppression and how do you do it?
This technique has been used in a variety of situations, including trying
to achieve neuroprotection during neurosurgery. It is most utilised to treat
refractory status epilepticus. There is limited strong supporting evidence
and no widely agreed protocol for carrying it out. Theoretically, burst
suppression allows resetting of the disordered neurotransmission within
the brain.
Generally, patients are sedated using an intravenous or inhalational agent,
e.g. thiopentone, propofol or a volatile anaesthetic. Continuous EEG is
mandatory, and depth of anaesthesia is titrated, aiming for a 1 : 10 burst sup-
pression ratio in EEG activity. Intra- arterial monitoring is required with careful
blood pressure control since deep anaesthesia may induce hypotension.
Phenytoin levels are within the normal range. The EEG ndings are consis-
tent with non- convulsive status epilepticus. You add another anticonvulsant,
levetiracetam. Microbiological investigations are, thus far, negative and the
HIV test is negative.
After a further 24 hours with drug levels within the therapeutic range and
o all sedation, Bruce is still not waking. You discuss with the neurology
consultant and decide to attempt burst suppression.
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Clinical Cases in Critical Care
164
Burst suppression is usually maintained for 24 hours (depending on
local practices). Following this, sedation is lightened and neurology can be
reassessed.
What outstanding issues do you need to highlight
for
follow- up on discharge to the ward?
This is a vulnerable young man who would benet from safeguarding
or social services input.
Compliance may remain an issue, particularly if he remains homeless
and without a resilient support network.
Neurology follow- up and medication review are warranted.
Viral PCR on lumbar puncture still not back, continue aciclovir until the
results are available and can be reviewed by the medical team.
Further reading
NICE Epilepsy: Diagnosis and Management. CG137 (2012) London: NICE.
Robinson, C. and Busl, K. (2019). Meningitis and encephalitis management in
the ICU. Curr. Opin. Crit. Care 25 (5): 423–429. Informative review article on ICU
management of meningitis.
Lapointe, S., Perry, A., and Butowski, N. (2018). Primary brain tumours in adults.
Lancet 392 (10145): 432–446. Excellent summary of primary brain tumour pathology
and management.
Your team successfully burst suppresses Bruce for 24 hours. On sedation
hold, he wakes up and gross neurological examination is normal, and you
are able to clinically clear his cervical spine. You extubate him on day 6 of
his admission and send him to the ward having had no further seizures.
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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.
13
Y
ou attend a peri- arrest call on the ward. Joan is 86 years old and has been an
inpatient since yesterday morning. She was admitted following a collapse
at home and is being treated for a urinary tract infection (UTI). This afternoon,
she became unresponsive and was found to have a BP of 62/35 mmHg, HR
145 bpm and RR 35 breaths per minute.
What could be some of the potential causes
for Joan’s sudden deterioration?
Sepsis–since she was being treated for a UTI, the source would most
likely be urosepsis.
Cardiovascular event–acute myocardial infarction (AMI), arrhythmia
(e.g. atrial brillation).
Pulmonary embolus (PE) –massive PE can present with haemody-
namic collapse.
Intracranial event–acute stroke or intracerebral haemorrhage, seizures.
Metabolic or hypoglycaemic event–severe hyponatraemia may result in
a cardiac arrhythmia. Hypoglycaemia could precipitate a seizure.
Drug reaction –severe anaphylaxis occurring in response to her
medication.
Occult bleed–ensure the patient is adequately exposed to assess for
melaena/haematochezia (fresh PR bleed) in the initial evaluation.
How do we dene shock?
Shock is a generalised form of acute circulatory failure associated with inade-
quate cellular utilisation of oxygen that is life- threatening. Cellular dysfunction
occurs when the circulation is unable to deliver enough oxygen to meet the
metabolic demands of the tissues.
The Patient Who
is Hypotensive
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Clinical Cases in Critical Care
166
How can we classify the different types of shock?
Hypovolaemic–circulating volume loss that eectively leads to a decrease
in venous return to the heart (e.g. haemorrhage, persistent diarrhoea and
vomiting with inadequate uid intake).
Distributive –considered a relative hypovolaemia that has resulted
from maldistribution of the absolute intravascular volume (e.g. sepsis,
anaphylaxis or spinal injury).
Obstructive–occurs when elevated resistance to blood ow leads to
tissue hypoperfusion (e.g. pulmonary embolism, cardiac tamponade or
tension pneumothorax).
Cardiogenic–inadequate contractility of the myocardium (e.g. ischaemia,
infarction or major arrhythmia).
While the classication of shock can be invaluable for the clinician, a patient
may develop one or more of these types of shock at the same time or at dier-
ent times during their presentation (e.g. the septic shock patient who develops
cardiogenic shock due to a septic cardiomyopathy).
What do you now think is the most likely cause?
The most likely cause of her deterioration is sepsis and potentially
septic shock.
Dene sepsis
The Third International Consensus Denitions for Sepsis and Septic Shock
(Sepsis- 3) dened sepsis as life- threatening organ dysfunction caused by a
dysregulated host response to infection.
Dene septic shock
Sepsis- 3 denes septic shock as a subset of sepsis, where profound circulatory,
cellular and metabolic abnormalities are associated with an increased risk of
mortality compared with sepsis alone (hospital mortality rates greater than
40%). Clinically, these patients can be identied by a vasopressor require-
ment to maintain a mean arterial pressure of greater than 65 mmHg and the
presence of a serum lactate level greater than 7mmol/L in the absence of
hypovolaemia.
The medical team have given Joan 500 mL of fluid that resulted in her
becoming slightly more responsive but with confused speech. With the bed
positioned so her legs are raised, Joan's BP is now 83/40
mmHg. Her HR is
135
bpm, temperature 38.3 °C and blood sugar 6.7 mmol/L. Her respiratory rate
remains elevated at 30 breaths per minute with SpO
2
96% on 10 L/min oxygen.
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The Patient Who is Hypotensive
167
Describe the qSOFA Score
The quick Sequential Organ Failure Assessment (qSOFA) score consists of the
following three easily measured and repeatable criteria (with a score of 2 or 3
being associated with a poor outcome due to sepsis, and the patient is consid-
ered qSOFA positive):
Low systolic blood pressure <100 mmHg
Respiratory rate >22 bpm
Altered mentation (GCS <15)
A patient outside of ICU with a positive qSOFA should alert the clinician to
the possibility of sepsis. While the score appears attractive and very simple to
use (e.g. does not rely on laboratory tests, but uses bedside measurements), it
should be considered a predictive rather than a diagnostic tool. It should also
not be used in patients once they are admitted to critical care, as it has been
shown to be inferior to other scoring systems for predicting outcome. qSOFA
had a key role in screening for sepsis in Sepsis- 3 (2016). However, updated
guidance (2021) no longer recommends it to be used as a single screening tool
for sepsis or septic shock.
Describe NEWS2
NEWS2 is an aggregate scoring system based upon the following six simple
physiological parameters (Table13.1).
Respiration rate
Oxygen saturation
Table 13.1: NEWS2 (Royal College of Physicians).
Score
Physiological parameter 3 2 1 0 1 2 3
Respiration rate (per
minute)
≤8 9–11 12–20 21–24
25
SpO
2
Scale 1 (%) ≤91 92–93 94–95 96
SpO
2
Scale 2 (%) ≤83 84–85 86–87 88–92
93 on air
93–94 on
oxygen
95–96 on
oxygen
97 on
oxygen
Air or oxygen? Oxygen Air
Systolic blood pressure
(mmHg)
≤90 91–100 101–
110
111–219 220
Pulse (per minute) ≤40 41–50 51–90 91–110 111–130 131
Consciousness Alert CVPU
Temperature (°C) ≤35.0 35.1–
36.0
36.1–38.0 38.1–39.0 39.1
CVPU, confusion, voice, pain, unresponsive.
SpO
2
Scale 2 is used when the target range is between 88% and 92% (e.g. in hypercapnic respiratory failure).
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Clinical Cases in Critical Care
168
Table 13.2: SOFA score.
Points
0 1 2 3 4
PaO
2
/FiO
2
(mmHg) 400 300–399 200–299 100–199 and
mechanically
ventilated
<100 and
mechanically
ventilated
Platelets (× 10
3
/μL) 150 100–150 50–99 20–49 <20
Glasgow Coma Scale 15 13–14 10–12 6–9 <6
Bilirubin (μmol/L) <20 20–32 33–101 102–204 >204
Mean arterial pressure
(MAP) or use of
vasoactive agents
(mcg/kg/min)
No
hypotension
MAP <70 mmHg Dopamine ≤5
or dobutamine
(any dose)
Dopamine >5,
adrenaline <0.1
or noradrenaline
≤0.1
Dopamine >15,
adrenaline >0.1 or
noradrenaline >0.1
Creatinine (μmol/L) or
urine output (UOP)
<110 110–170 171–299 300–440 or
UOP <500 mL/d
>440 or
UOP <200 mL/d
Systolic blood pressure
Pulse rate
Level of consciousness or new confusion
Temperature
The further away the parameter is from the normal value then the higher
the score allocated. In addition, if supplementary oxygen is being given then a
further two points are added to the aggregated score. Since 2017, NHS England
(NHSE) has recommended using NEWS2 as the early warning score to detect
clinical deterioration in patients with suspected sepsis. Evidence suggests that
it is superior to qSOFA in predicting adverse outcomes in both the emergency
department and general ward setting. A raised NEWS2 score of 5 or more in
a patient with signs and symptoms of infection, or in a patient at high risk of
infection who clinically deteriorates, should trigger urgent review. Currently,
Joan scores a total of 15 using this scoring system.
How can organ dysfunction be identied in sepsis?
This can be identied by an increase in the Sequential (Sepsis- related) Organ
Failure Assessment (SOFA) score of two points or more.
Describe the SOFA Score
The SOFA score is well recognised within the critical care community, with
increased risk of mortality being associated with higher scores. This score is
not diagnostic for sepsis but enables the clinician to identify patients with a
high risk of dying from infection. Calculating the total score requires time
and therefore potentially delays recognition of acute organ dysfunction
(Table13.2).
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