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The Patient with Reduced Consciousness
199
What do you think is happening and why?
Debbie appears to be developing diabetes insipidus (DI). It usually develops
1–3
days following the initial insult to the brain and is often transient but can
persist for several months. Around 15% of SAH patients develop DI and it tends
to be associated with a worse prognosis.
Decreased production of arginine vasopressin results in reduced ability to
concentrate urine. The patient therefore passes large volumes (>200
mL/h)
of dilute urine (<300
mOsm/kg) and plasma sodium concentration increases.
How do you manage this?
Investigations include paired urine and serum osmolality and sodium
levels. In non- acute situations, a water deprivation test can be undertaken.
Where clinical suspicion is high and there is rapid loss of sodium and
water homeostasis, desmopressin (DDAVP) can be given in a divided dose
of 0.2–1.2 mg/d.
Of which other sodium regulation disorders
is
Debbie at risk?
Hyponatraemia after SAH is usually caused by the syndrome of inappro-
priate antidiuretic hormone (SIADH) but can also be caused by cerebral salt
wasting (CSW).
SIADH – due to central overproduction of arginine vasopressin follow-
ing stimulation of the hypothalamus. The result is low serum sodium
and relatively normal urine output. Treatment normally focuses on uid
restriction (<500 mL/d) but this can be challenging to maintain and can
predispose to cerebral vasospasm. Alternative therapies include hyper-
tonic saline, udrocortisone (0.1–0.2 mg/d) and vasopressin receptor
antagonists such as conivaptan.
CSW – this is a clinical picture of polyuria with loss of serum sodium.
The mechanism for this is unknown but may be related to release of
natriuretic peptides (Table15.1).
You manage Debbie's DI successfully and on day 15 she is well enough to
go to the ward. She is discharged home nearly 4 weeks after her initial SAH
and hopes to return to work after a period of recovery.
Your management improves Debbie's condition, and she settles over the
next 2
days. On day 8, as part of your daily assessment, you discover Debbie's
sodium has increased from 142 to 151
mmol/L. Her urine output has also
increased and is now over 500
mL per hour.
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Clinical Cases in Critical Care
200
What problems can SAH patients experience
during the recovery period?
Cognitive
Inattention
Memory deficits
Speech and language problems
Neurological
Seizures
Headaches
Psychological
Personality change
Physiological
Fatigue
Weakness
Further reading
Macdonald, R. and Schweizer, T. (2017). Spontaneous subarachnoid haemorrhage.
Lancet 389 (10069): 655–666.
Lawton, M. and Vates, G. (2017). Subarachnoid haemorrhage. N. Engl. J. Med. 377:
257–266. Two useful review articles on pathophysiology and management of sub-
arachnoid haemorrhage.
Stocchetti, N., Toccone, F., Citerio, G. etal. (2015). Neuroprotection in acute brain
injury: an up- to- date review. Crit. Care 19 (1): 186. Excellent review article on
neuroprotection in critical care.
Table 15.1: Sodium disorders with raised ICP.
Cerebral salt
wasting
Diabetes
Insipidus
Syndrome of
inappropriate
antidiuretic hormone
Fluid balance Decreased Decreased Normal or increased
Urine output Increased Increased Decreased
Serum sodium Decreased Increased Decreased
Urine sodium Increased Decreased Increased
Serum
osmolality
(mOsm/kg)
<280 >290 <280
Urine osmolality
(mOsm/kg)
>100 <300 >100
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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.
16
A
s the neurointensive care registrar, you receive a call from the neuroan-
aesthetist who requests a bed for Edward. He is a 63-
year- old managing
director who developed sudden-
onset dense right hemiparesis two hours ago
and is now being transferred to your hospital for thrombectomy.
What causes ischaemic stroke?
Ischaemic strokes are embolic or, more commonly, thrombotic:
Thrombotic strokes– usually result where chronic atheroma and plaque
development lead to stenosis in large or small cerebral arteries (larger
arteries include the carotid or middle cerebral), predisposing them to
obstruction with thrombus formation. Thrombus in smaller penetrating
arteries gives a pattern of ‘lacunar’ stroke.
Embolic strokes– secondary to clots that form elsewhere in the body
but lodge in the cerebral circulation, impairing distal blood ow. These
thrombi tend to develop within the heart secondary to the stagnation of
blood that accompanies atrial brillation.
What are the risk factors for ischaemic stroke?
Modiable
Hypertension
Smoking
Diabetes
Atrial brillation
Hypercholesterolaemia
Obesity and inactivity
Carotid artery disease
Alcohol excess
The Patient Who
had A Stroke
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Clinical Cases in Critical Care
202
Non-modiable
Increasing age
Female gender
Family history of stroke
African and Caribbean ethnicity
Previous strokes or transient ischaemic attacks (TIA)
What are the options for managing acute
thromboticstroke?
Refer to NICE guidance (NG 128, 2019). The pathway is dierent for those
with non-
disabling TIA.
Generalmeasures
Use FAST (Face, Arm, Speech, Test) prehospital to aid rapid diagnosis.
Use ROSIER (recognition of stroke in emergency room) or similar tool
to aid diagnosis in hospital.
Exclude hypoglycaemia.
Immediate non- enhanced CT brain where acute stroke is suspected and
any of the following apply:
Thrombolysis/thrombectomy could be used.
Patient is on anticoagulant therapy or has risk of bleeding.
Fluctuating symptoms.
Low GCS.
Severe headache, neck stiffness or papilloedema.
If thrombectomy might be an option, a contrast- enhanced CT scan
should be performed with CT angiography (CTA) following the initial
non-
enhanced scan.
Aspirin 300 mg unless contraindicated (if thrombolysis is to be given,
aspirin should be delayed for 24 hours post thrombolysis and should
only be administered once repeat CT head has excluded haemorrhagic
transformation).
Thrombolysiswithalteplase
Within 4.5 hours of onset of symptoms.
Haemorrhage must have been excluded.
This should be discussed with the on- call stroke consultant.
Thrombectomy
Within 6 hours of onset of symptoms.
Conrmed occlusion of proximal anterior circulation demonstrated on
CTA or magnetic resonance angiography (MRA).
There should be potential to salvage brain (as assessed by CT or MR imaging).
The patient was well between 6 and 24 hours prior to the event.
Pre- stroke modied Rankin score should be <3 and a score of >5 on the
National Institutes of Health Stroke Scale.
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The Patient Who had A Stroke
203
Where possible, patients should be considered for thrombectomy. In the UK,
thrombectomy is currently oered in a limited number of centres and transfer
time must be considered when assessing suitability for thrombectomy. Rapidity
of diagnosis and management is key to the successful treatment of acute stroke.
ReviewtheCTheadimage(Figure16.1).Whatisthe
diagnosis?
CT head demonstrates extensive left middle cerebral artery (MCA) infarction.
Whatpatternsofneurologicaldecitcanbeseen
in stroke?
There are subtle dierences in the patterns of neurological decit seen due to
the exact point of occlusion of the artery. Grossly, the changes are as follows:
Anterior cerebral artery (ACA)
Contralateral motor/sensory loss
Lower more than upper limb
Around 2 hours later, Edward arrives in your neurointensive care. He was
intubated for thrombectomy due to being agitated on arrival in the radiology
suite. He has now been extubated to facilitate neurological assessment. Fol-
lowing recovery from anaesthesia, he appears confused and has right-
sided
weakness. The radiologist informs you that it was a dicult procedure and,
due to anatomical issues, they could not remove all of the clot.
Figure 16.1: CTbraindemonstratingleftMCAinfarct.
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Clinical Cases in Critical Care
204
MCA
Contralateral motor/sensory loss
Greatest in face and upper limb
Contralateral homonymous hemianopia
Left MCA– aphasia
Right MCA– neglect to the left
Posterior inferior cerebellar artery (PICA) or vertebral artery
Wallenburg syndrome– vertigo, ipsilateral Horner syndrome, etc.
Various other eponymous syndromes may develop as a result of
brainstem lesions– Jackson, Raymond, Fouille, Millard-
Gubler,
Weber, Claude.
Whatdoyouthinkmayhavehappened?
Extension of ischaemic stroke
Haemorrhage into existing stroke
Oedema subsequent to original extensive MCA stroke
Seizure
Whatareyourmanagementpriorities?
Intubate and neuroprotect– Edward’s GCS is low, he has vomited and is
developing pathology for which he requires urgent radiological imaging.
Intubate him rapidly, control his gas exchange and haemodynamics, and
ensure neuroprotection. Examine Edward and consider treating him for
possible seizures but, given the potential dierential diagnoses, prioritise
urgent imaging of the brain.
Imaging– transfer Edward for urgent CT brain. Discuss with the radi-
ologist, neurosurgeon and intensive care consultant as to the specic
modality (i.e. with contrast/focusing on angiography/whether you
should perform MRI brain at this point).
Call neurosurgeons and ICU consultant– not only do you need advice
regarding the imaging required but you will need senior input as to
ongoing management since this could represent signicant deterioration.
Call next of kin– Edward’s next of kin need to know that he has deterio-
rated. You may wish to wait to review CT images before calling them in
the middle of the night since you are performing the scan urgently and
the outcome could be critical to Edward’s prognosis.
ReviewtheimagesinFigure16.2.Whatisthe
diagnosis?
Malignant MCA syndrome.
On day 2, Edward's nurse calls you to say that he has started vomiting and
his GCS has dropped to 7 (E1V2M4). On examining his pupils, the ICU nurse
also noted that his eyes are deviated to one side.
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The Patient Who had A Stroke
205
WhatisthepathophysiologyofEdward’sdeterioration?
Malignant MCA syndrome is a pattern of rapid neurological deterioration follow-
ing hemispheric infarction. Initially, ischaemic tissue induces cytotoxic oedema.
Subsequently, brain tissue
swells and vessels are occluded. As tissue necrosis
develops, there is a breakdown in the integrity of the blood–brain barrier. Pro-
teins and ischaemia-
induced mediators leak into the parenchyma and vasogenic
oedema further increases the volume of brain tissue. The oedema which develops
as a result can be dramatic, leading to mass eect and, eventually, brainstem
compression. Classically, this presents 2–4
days following the initial infarction.
The prognosis for MCA syndrome is generally poor. Up to 80% of patients
die within 1
week.
HowdoesinformationfromtheCTheadinuence
yourmanagementnow?
Urgent discussion with neurosurgeons regarding whether Edward would
be suitable for decompressive hemicraniectomy (DHC)– pooled analysis
has shown that DHC can reduce the risk of major disability in those
younger than 60 years of age (Rajwani etal. 2017). Similarly, analysis of
several studies shows improved survival for patients like Edward. DHC
is included in guidelines for management published in 2015 (Torbey
etal.). Removing a large bone ap allows for expansion of the brain
which would otherwise continue causing compression as explained by
the Monro–Kellie doctrine (see Case 15).
Temperature control – this is a controversial topic and local guide-
lines should be consulted. Maintaining a core temperature of 33 °C
(a) (b)
Figure 16.2: (a)PlainCTbraindemonstratingmalignantMCAwithmidlineshiftand
associatedACAterritoryinfarction(b)CTangiographyofbraindemonstratingabrupt
leftMCAcutoff.
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Clinical Cases in Critical Care
206
for 48–72 hours has been shown to reduce mortality in some studies
but is not universally accepted as benecial. In the UK, some centres
use evidence-
based guidelines recommending targeted temperature
management aiming for 36.5–37.5
°C or preventing hyperthermia.
Consider osmotic therapy with mannitol or hypertonic saline– discuss this
with your consultant and the neurosurgeons since benecial eects are
only transient. It is usually used as a ‘bridging’ therapy to other treatment
such as surgery. If the blood–brain barrier lacks integrity, this could
propagate further oedema so should not be administered without due
consideration.
HowwillyoumanageEdwardinneurocriticalcare
at this point?
Consider sedation– discuss with the team whether to wake Edward
immediately or to keep him sedated for a period of time. Many centres
would favour a period of sedation where others would immediately stop
sedation postoperatively and assess Edward’s neurology.
Neuroprotection– ensure positioning of head and neck to promote venous
drainage, optimise gas exchange for cerebral blood ow, optimise blood
pressure to improve cerebral perfusion pressure (see Case 15).
Monitoring – advanced monitoring should include invasive arterial blood
pressure monitoring. Neurosurgeons may also have inserted an intra-
cranial bolt or extraventricular drain (EVD) to help monitor intracranial
pressure (ICP) and allow drainage of CSF if required.
Blood tests– frequent measurement of sodium is vital. Rapid changes in
sodium, with the associated risks of cerebral oedema, must be avoided.
Monitor inammatory markers as Edward is susceptible to infection
following surgery.
Urine output monitoring– observe for disorders of sodium homeostasis
(see Table15.1).
Daily review of venous thromboembolism (VTE) prophylaxis with a neu-
rosurgeon– Edward is high risk for devastating intracranial bleeding
following surgery. However, he is also high risk for developing deep
venous thrombosis and pulmonary embolus. The decision of whether
to give or withhold VTE prophylaxis is extremely important and should
be considered and documented daily.
Treat seizures to avoid increases in cerebral metabolic rate.
Document where the bone ap is kept, if it is being kept at all– tradition-
ally these have been surgically implanted subcutaneously (often on the
abdomen) or cryopreserved. Many centres now prefer to craft a titanium
plate as a replacement, should the patient survive.
Neurosurgeons decide to take Edward straight to theatre for decompressive
surgery. They perform a 15
cm craniectomy, leaving Edward with no bone
ap over the left temporoparietal region.
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The Patient Who had A Stroke
207
Whatarethecomplicationsofneurosurgery?
Bleeding
Infection– systemic, surgical site, intracerebral
Seizures
Hydrocephalus
CSF circulation derangement and hygroma development
Cognitive, neurological or psychological changes
WhyisitimportanttoexamineEdward’seyes
regularly?
Increased ICP can lead to expansion of the brain towards the foramen magnum
and consequent damage to soft tissue structures as they are compressed against
the bony base of skull. The observed pattern can reect the manner or extent
of that damage.
Rapid identication of ‘false localising signs’ can lead to earlier recognition
and management of raised ICP. The abducens (VI) nerve (due to its long course
and tendency to be stretched over the petrous temporal bone), the trigeminal
(V) and the oculomotor (III) nerves are particularly susceptible to early damage
from raised ICP.
Describetheclinicalpresentationsofdifferent
patternsofbrainherniationsecondarytoraisedICP
Uncal herniation (transtentorial herniation)
Temporal lobe compression leads to damage to the ipsilateral cranial
nerve III, resulting in a dilated pupil.
This is accompanied by hemiparesis, decerebrate posturing and coma.
Central tentorial herniation
Compression of the diencephalon can lead to small reactive pupils
or Parinaud syndrome (paralysis of vertical gaze).
The patient will also have decreased consciousness (eventually deep
coma) and decorticate rigidity, and may develop Cheyne–Stokes
breathing.
Transcalvarial herniation
This type of herniation can occur through a defect in the skull, e.g.
via craniotomy site or fractured skull. The eye signs here can be
unpredictable.
Cerebellar tonsil herniation (‘coning’)
Bilateral fixed and dilated pupils.
On day 4 you assess Edward's neurology. The sedation has been off for
24
hours. You are unable to elicit a response from Edward. He remains fully
ventilated and has shown no signs of coughing on suction. His pupils are
unreactive and 5
mm each.
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Clinical Cases in Critical Care
208
Herniation of the tonsils through the foramen magnum compresses
the medullary respiratory centre.
Death is inevitable.
Whatisyourmanagementplaninlightofyour
neurologyassessment?
Examination ndings could be consistent with damage to Edward’s brainstem.
Urgent imaging of the brain is indicated. MRI is a superior modality to CT for
visualising the posterior fossa.
Whatothersignsmightyouexpecttosee?
Cushing’s triad– bradycardia, widening pulse pressure, irregular respiration.
Papilloedema.
Headache and vomiting may be seen in early stages but sadly, Edward’s
case is too far advanced for this now.
Whatisyourassessmentoftheclinicalsituation
andhowwillyouproceed?
Edward has suered catastrophic, irreversible brain injury which is not com-
patible with life. The case must be discussed with the consultant intensivist and
the neurosurgeon. Given the information from the nurse (absence of cough
reex, pupils unresponsive to light, no attempt to initiate breaths in the absence
of sedation) in conjunction with his brain imaging, Edward may have suered
brainstem death.
Continue supportive measures and speak to his next of kin urgently to
explain the situation.
Whatpreconditionsmustbemetbefore
youcommencebrainstemtesting?
Evidence for irreversible brain damage of known aetiology.
Exclusion of reversible causes of apnoea and coma.
You take Edward to the MRI suite and imaging demonstrates that he has
‘coned’, i.e. he has suered cerebellar tonsil herniation and irreversible
damage to the brainstem.
You have a discussion with Edward's family about his neurological status
and the prognosis. You tell them that you would like to test him for brain-
stem death. In light of his clinical condition and his brain imaging, even if
he is not brainstem dead, he will not recover from this event. The family do
not object to brainstem death testing and choose not to be present for this.
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