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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 with Reduced Consciousness
189
infection, pregnancy, systemic lupus erythematosus (SLE) or drugs, and
can be treated eectively with prompt plasmapheresis. Haemolytic urae-
mic syndrome is clinically similar but the platelet microthrombi tend
to be conned to the kidneys and it is less likely to cause neurological
symptoms. If the platelet count is low, this should be investigated as a
potential cause of Debbie’s presentation (see Case 23).
Thrombus/obstruction to venous drainage of the brain– cerebral venous
sinus thrombosis accounts for less than 1% of all strokes. Thrombus
can form in the deep or supercial venous systems of the brain and,
depending upon location, can result in varying patterns of focal or
generalised neurological decit. Raised ICP results from several mech-
anisms including oedema formation due to mechanical obstruction of
venous drainage, vasogenic oedema from disruption of the blood–brain
barrier, and cytotoxic oedema generated as ischaemia develops with
falling cerebral perfusion.
Non- convulsive status epilepticus (NCSE) or a postictal state– it is relatively
common following subarachnoid haemorrhage (SAH) to see the GCS ‘arti-
cially’ worsened by NCSE or a postictal period. This often worsens the
WFNS (World Federation of Neurosurgical Societies) score and may lead
to surprise when these patients ‘do well’ despite having a WFNS score of 5.
What are your main concerns at this point?
Airway protection– Debbie’s GCS is 8 and she is tolerating an oropha-
ryngeal airway. She is at high risk of aspiration and airway obstruction.
Possible aspiration – there is a history of vomiting and, given Debbie has
a low GCS, she may already have aspirated. She is currently receiving
15
L/min oxygen via non- rebreathe mask with saturations of 98% but the
PaO
2
is unknown at this point. Aspiration pneumonitis or superadded
infection may develop over the next few hours or days.
Neuroprotection – Debbie’s presentation could be consistent with menin-
gism (look for the triad of nuchal rigidity, photophobia and headache,
often accompanied by nausea and vomiting). Intracranial pathology is
possible in this case. If ICP is rising, it is imperative to take control of
the situation to minimise further damage.
Diagnosis – the main differential diagnoses include several prob-
lems which could require urgent neurosurgical intervention. Identify
or rule these out rapidly to maximise Debbie’s chances of making a
good recovery.
Review this CT image (Figure 15.1). What is the
diagnosis?
This CT head demonstrates acute subarachnoid haemorrhage (SAH).
You decide to intubate Debbie and transfer her to the CT scanner. The CTA
head is shown in Figure15.1.
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Clinical Cases in Critical Care
190
What is the Monro–Kellie Doctrine?
The doctrine assumes that the sum of the volumes of non- compressible con-
tents within the cranium (brain, cerebrospinal uid (CSF) and intracranial
blood) is constant. Therefore, an increase in one should result in a decrease
in one or both of the other two. This pressure–volume relationship is partic-
ularly signicant because the cranium can be thought of as a rigid box with
one major opening (the foramen magnum) and limited capacity for accom-
modating changes in volume. Small increases in blood volume can be com-
pensated for without a resultant change in pressure through a decrease in CSF
volume. However, a sudden large increase in blood volume beyond this capacity
for compensation will lead to a rise in ICP. The increase in pressure leads to
the non- compressible contents expanding towards and possibly through the
foramen magnum. Initially, this causes false localising signs due to stretching
of the cranial nerves over the base of skull (i.e. sixth nerve palsy) and ultimately
tonsillar herniation and coning. This process can be exacerbated by cerebral
oedema development as perfusion of the brain is impaired.
The eects can be illustrated in the compliance curve (Figure15.2).
What is cerebral perfusion pressure (CPP)?
This equation reects the pressure gradient driving cerebral blood ow.
MAP, mean arterial pressure, ICP, intracranial pressure
Figure 15.1: CT head demonstrating SAH.
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The Patient with Reduced Consciousness
191
This is normally under autoregulatory control but can be disrupted when
either the mean arterial pressure (MAP) falls or ICP rises signicantly.
Note that normal ranges vary with age. In adults, ‘normal’ should be between
7–15 mmHg. Between 20 and 30 mmHg would constitute mild intracranial
hypertension. A pressure sustained above 40 mmHg would represent severe,
life- threatening intracranial hypertension.
What is secondary brain injury and how can you
minimise it?
This concept is used in trauma to describe the cellular processes which occur
following initial primary injury to the brain (e.g. diuse axonal injury or local
trauma) and includes problems such as the oedema and hypoxia which result
from raised ICP. These principles can also be applied in Debbie’s case as sudden
bleeding within the cranium exerts similar eects. The focus of clinicians is
to ameliorate the damage which occurs after the initial insult. Management
strategies include the following:
Conservative
Avoid impairing cerebral venous drainage– head in neutral position,
avoid tight endotracheal tube ties around the neck, 30–45° head up tilt.
Maintain sodium >142 mmol/L, glucose 4.6–10 mmol/L.
Aim for normothermia.
Medical
Drugs such as mannitol and hypertonic saline can be used with caution
where the blood–brain barrier remains intact.
Intracranial volume
Intracranial pressure (mmHg)
0
10
20
30
40
Figure 15.2: Intracranial compliance (pressure–volume) curve. Compensatory
mechanisms maintain intracranial pressure (ICP) within normal range (green shaded
area). As increases in volume continue to occur, there is a steady decline in compliance,
causing a rise in ICP (yellow shaded area). Small increases in volume result in marked
increases in ICP, causing a fall in the perfusion pressure leading to cerebral ischaemia
(red shaded area).
Source: Theophilus Samuels.
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Clinical Cases in Critical Care
192
Where seizures are noted, rapid pharmacological control is indicated to
reduce cerebral metabolic rate and oxygen demand.
Anaesthetic
Optimise cerebral blood ow through careful ventilator management–
PaCO
2
4.5–6 kPa, systolic BP >90 mmHg but less than 160 mmHg to
avoid exacerbating bleeding from an unsecured aneurysm. Some cen-
tres advocate PaO
2
>10 kPa to avoid hypoxia though others would tol-
erate >8 kPa. Extreme hyperoxia (>40 kPa) is associated with poorer
outcome (Figure15.3).
Deep sedation can be used to reduce straining or agitation in intubated
patients, and to reduce cerebral metabolic rate and oxygen demand.
Surgical
Decompression– craniectomy.
Drainage of CSF.
What is the incidence and what are the causes
of subarachnoid haemorrhage (SAH)?
Incidence
SAH occurs in around 6–9 per 100 000 per year in the UK. Around 10% die
before reaching hospital and approximately only a third of patients have a
good outcome after treatment.
100
75
50
25
50
100 150
Pressure (mmHg)
CO
2
MAP
Cerebral blood flow (ml/100g/min)
Figure 15.3: Cerebral blood ow (mL/100 g/min) relationship with partial pressure of
oxygen and carbon dioxide, along with mean arterial blood pressure (MAP).
Source: Theophilus Samuels.
You promptly refer Debbie to the regional neurosurgical centre while
providing neuroprotection. She is accepted for transfer and neurosurgeons
request that you take her straight to the operating theatres on arrival.
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The Patient with Reduced Consciousness
193
Causes
Spontaneous SAH – usually caused by aneurysm rupture (85%). Approx-
imately 5% are due to other vascular anomalies such as arteriovenous
malformations. The remaining 10% are from non-
aneurysmal perimes-
encephalic bleeding. Mean age at presentation is 50
years and there is a
slight female preponderance (1.6:1). Risk factors include:
Hypertension
Smoking
Cocaine
Alcohol excess
Connective tissue disorders
Congenital syndromes including polycystic kidney disease and neu-
rofibromatosis type 1.
Saccular or ‘berry’ aneurysms occur in around 4% of the population
but only those greater than 7
mm will rupture. Approximately 80% occur
in the anterior circulation of the circle of Willis. Estimates of incidence
vary but the most common sites are at bifurcations of the anterior and
posterior communicating arteries (30–35% and 30–40% respectively).
Around 20% involve the middle cerebral artery and a small percentage
occur in the vertebrobasilar arteries.
A less common form of aneurysm is the fusiform aneurysm which
lacks the neck of the berry aneurysm.
Traumatic SAH – occurs in around 25–50% of patients with traumatic
brain injury.
Draw a diagram to represent the circle of Willis
See Figure15.4.
What scoring systems can be used to grade
the
severity of SAH?
Clinical
GCS– this was not developed specically in relation to SAH. However,
studies have shown that a GCS of 14 or 15 at presentation correlates with
good outcomes. Progressively lower GCS is associated with worse out-
comes, an impaired motor score being the most signicant component.
World Federation of Neurosurgical Societies (WFNS) – combines GCS
on presentation with focal neurological deficit to predict outcome.
Grades 1 and 2have no motor decit and favourable outcomes. Grades
3–5involve either motor decit or signicantly reduced GCS and result
in poorer outcomes.
Hunt and Hess– the oldest of the grading systems. Predicts percentage
survival based on signs and symptoms. From grade 1 (70% survival)
asymptomatic or minimal headache or neck stiness, to grade 5 (10%
survival) deep coma, decerebrate rigidity.
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Clinical Cases in Critical Care
194
Radiological
Fischer – based on appearance of haemorrhage on CT head. Grades:
1– none evident
2– less than 1 mm thick
3– more than 1 mm thick
4– diffuse or intraventricular haemorrhage, or parenchymal
extension.
Claassen – Claassen modified the Fisher scale to incorporate the
impact of intraventricular haemorrhage. This gives patients a score
from 0 to 4.
Ogilvy and Carter– this is a combined score based on the presence or
absence of each of the following factors:
Age over 50 years
Hunt and Hess grade 4 or 5
Fisher scale 3 or 4
Aneurysm size more than 10 mm
Posterior circulation aneurysm more than 25 mm
What are the treatment options for aneurysmal SAH?
Options for management depend upon the cause of the haemorrhage, the
condition of the patient on presentation as a reection of the severity of their
condition, and the previous performance status of the patient.
Conservative management– where the cause is an aneurysm which is not
amenable to intervention (usually through its anatomical position), or
Anterior
cerebral
artery
Anterior
communicating
artery
Middle
cerebral
artery
Ophthalmic
artery
Anterior
choroidal
artery
Posterior
cerebral
artery
Posterior
cerebellar
artery
Basilar
artery
Posterior
communicating
artery
Internal
carotid
artery
TS
Figure 15.4: Circle of Willis (green dashed line).
Source: Theophilus Samuels.
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The Patient with Reduced Consciousness
195
where attempting to perform the intervention is deemed too high risk,
conservative management is undertaken by optimising medical therapy.
Medical treatment
Nimodipine– a dihydropyridine which prevents calcium influx
through L-
type calcium channels. It is used to treat cerebral vaso-
spasm and is given in a dose of 60 mg 4 hourly for 14–21 days post
SAH (divided doses of 30 mg 2 hourly can reduce large fluctuations
in blood pressure).
Analgesia– the headache of SAH can be severe. This is usually
managed with paracetamol and codeine or morphine.
Antiemetics.
Antiseizure medication.
Surgical intervention
Clipping– craniotomy allows direct visualisation and placement of
a metal clip across the neck of the aneurysm.
Craniectomy– used less commonly in SAH but is employed where
ICP is high and cannot be managed. The patient can be left with no
bone flap to allow expansion of the brain without further damage to
parenchyma from compression against the wall of the cranium.
Interventional radiological approach
Coiling– usual approach via radial or femoral arteries. Under anaes-
thetic, platinum wires are coiled into the aneurysmal sac.
ISAT (International Subarachnoid Aneurysm Trial 2002) compared the out-
comes of patients undergoing endovascular coiling compared with neurosur-
gical clipping following SAH. They found that coiling resulted in better 1- year
disability-
free survival. A Cochrane review published in 2018 (Lindgren etal.,
Cochrane Database Syst Rev) found that where patients were in good condition
and the aneurysm was amenable to both management options, those patients
undergoing coiling were more likely than those undergoing clipping to survive
and return to independent living.
Apart from the issues already explored, how else
will you manage Debbie in critical care?
Physiological optimisation
Fluids – intravenous fluid of choice is usually 0.9% saline. Fluid
management strategy is contentious. Although dehydration is to be
avoided, studies have shown an association between excessive positive
uid balance and poorer functional outcomes.
Electrolyte and glucose management.
On arrival at the neurosurgical centre, Debbie is rushed to the interventional
radiology suite where she undergoes coiling of an anterior communicating
artery aneurysm. Following the procedure, she is moved to the neurointen-
sive care where sedation is stopped so she can be assessed neurologically.
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Clinical Cases in Critical Care
196
Temperature control– fever is common after SAH and is associated with
worse outcomes.
Careful ventilation and oxygenation– Debbie may have aspirated so her
lungs should be protected as much as possible.
Follow- up investigations
12- lead ECG – brain injury leads to massive catecholamine release.
Cardiac complications occur in over 50% of patients. Myocardial
ischaemia and cardiac failure can develop. Common ECG changes
include large U waves, T-
wave changes, prolonged QTc, high R waves
and ST depression.
Echocardiography– to assess for development of cardiac complications
including Takotsubo cardiomyopathy.
Lumbar puncture– Debbie’s SAH has been demonstrated on CT and
cerebral infection appears unlikely, so lumbar puncture (LP) is not
neurosurgeons if required.
Prophylactic medication
Ulcer prophylaxis– neurocritical care patients are at high risk of stress
ulcer development and upper gastrointestinal bleeding. Histamine-
2 antagonist or a proton pump inhibitor (selective inhibitor of H
+
/K
+
ATPase in gastric parietal cells) are commonly used agents.
Thromboprophylaxis– this should be reviewed daily, ideally with the
input of a neurosurgeon, and the daily decision documented in the
patient’s notes. The risk of devastating intracranial bleeding must be
weighed up against the risk of deep vein thrombosis and life- threatening
pulmonary embolus. These patients are at high risk of both bleeding
and thrombus.
What do you think might have occurred?
Rebleeding– occurs in up to 25% of patients with SAH within the rst
72 hours. Mortality associated with rebleeding is up to 60%.
Vasospasm– most commonly 5–10 days post SAH. The mechanism is
not clearly understood but the breakdown of erythrocytes appears to
increase oxidative stress via activation of calcium channels in smooth
muscle and release of vasoactive proteins. This depletes ATP, causing
ischaemia and eventually cortical necrosis.
Initially, Debbie appeared to make a good recovery. On day 2 following her
procedure, she had a GCS 13 (E3V4M6) and she appeared to be progress-
ing well. However, on day 5 her motor score suddenly dropped from 6 to
4, with no sign of a seizure. You call the neurosurgeon and neurointensive
care consultant to discuss the case.
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The Patient with Reduced Consciousness
197
Hydrocephalus– estimated to occur in around 20–30% of patients with
SAH. It is classified as acute within 3
days, subacute 4–14 days and
chronic beyond 14
days. It can be obstructive or communicating.
What is the signicance of the TCD and CT
head report?
The TCD suggests cerebral vasospasm (normal range for MCA blood ow is
50–75cm/s). The CT head report suggests raised ICP. Raised ICP is often seen
alongside cerebral vasospasm. Manage both these problems urgently to pre-
vent cerebral ischaemia.
What other methods are used to diagnose cerebral
vasospasm?
Digital subtraction angiography (DSA) is the standard for detecting cerebral
vasospasm after SAH. CT angiography is also widely used.
What methods can be used for intracranial pressure
monitoring and how do they work?
Clinical signs can be used as an indication of raised ICP. GCS should be
assessed regularly and examine for papilloedema. Don’t wait to see the Cush-
ing reex as it is a late sign (bradycardia, widened pulse pressure and abnormal
respiratory pattern).
Invasive monitors are more precise but risk infection and haemorrhage:
ICP bolt/subdural screw/intraparenchymal microsensor (e.g. Codman)– a
strain gauge sensor is inserted into the parenchyma or CSF. This allows
analysis of pressure waveforms (A waves suggest raised ICP, B waves
suggest poor compliance and C waves are a normal nding; Figure15.5).
Extraventricular drain (EVD)– a catheter is inserted surgically into the
ventricle, facilitating manometry with CSF. This has the added benets
of facilitating sampling of CSF if needed, allowing drainage of CSF if
ICP is high, and intrathecal drug administration if required.
Epidural sensor– a sensor is sited between the skull and dura via a burr
hole drilled through the skull.
How do you manage cerebral vasospasm?
The mainstay of treatment is nimodipine. This is usually given orally but
adjusted doses can be given intravenously (or intra- arterially under radiological
The neurointensive care consultant performs transcranial Doppler (TCD)
which shows increased mean velocity in both middle cerebral arteries
(approximately 180
cm/s). You also take Debbie for a CT head which reveals
loss of sulci and reduction in ventricular space.
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Clinical Cases in Critical Care
198
guidance). Careful uid balance to ensure normal circulating volume is indi-
cated. Other treatments such as magnesium and statins have been trialled but
there is no good evidence to support routine use.
How do you manage Debbie’s blood pressure?
When vasospasm occurs, the patient’s blood pressure normally rises in response.
Where the aneurysm is secure, many centres aim to maintain hypertension in
such cases to promote cerebral circulation against high ICP and increased resis-
tance to ow. Vasopressors may be needed to induce systolic BP >180 mmHg.
Aims may be set higher on an individual basis if GCS is seen to improve with
higher systemic blood pressure.
0
100
0
40 80
120
Time (min)
A waves
30
10
B waves
1234 5
Time (min)
ICP (mmHg)
C waves
10 20 30 40 50
Time (min)
10
20
Figure 15.5: Lundberg waves. A waves – last around 5–20 minutes and are described
as plateau or vasogenic waves between 50 and 100
mmHg. They compromise cerebral
perfusion pressure (CPP). B waves
– short- duration elevations in ICP that are smaller in
amplitude occurring at a frequency between 1 and 2
minutes. They may be associated
with changes in partial pressure of carbon dioxide and oxygen due to respiration.
C waves – occur at a frequency of 4–8 minutes and are also of low amplitude. They are
products of cardiac and respiratory cycle interactions.
Source: Theophilus Samuels.
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