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Case 9: Intracranial Hypertension
andHydrocephalus
RitaBertuetti, NicolaZugni, MaurizioSaini,
DavideSavo, FrancescaSimonassi,
KartikaChandrapatham, andTarekSenussi
Fifty-nine-Year-old lady with a history of poorly
controlled arterial hypertension was taken to A&E
for sudden intense headache. Upon arrival at the
hospital she was in the state of unconsciousness
(GCS 3) associated with left anisocoria and arterial hypertension. She was then quickly sedated
and intubated for airway protection and was taken
to radiology for a head CT. Brain CT angio
showed subarachnoid haemorrhage Fisher 4 grade
with intraparenchymal haematoma from rupture
of a bilobate aneurysm of the left middle cerebral
artery (MCA) and initial hydrocephalus sings.
The patient was then admitted to ICU where a
TCCD was performed just after her arrival. The
brain ultrasound showed:
33
R. Bertuetti (*) · N. Zugni
Department of Anesthesiology, Critical Care
Medicine and Emergency, Division of Neurocritical
Care, ASST Spedali Civili di Brescia, University
Hospital, Brescia, Italy
M. Saini · D. Savo
Department of Emergency, Perioperative Medicine
and Intensive Care, Neuroanesthesia and
Neurointensive Care Unit, San Gerardo Hospital,
ASST-Monza, Monza, Italy
F. Simonassi · K. Chandrapatham
Anesthesia and Intensive Care, Ospedale Policlinico
San Martino– IRCCS for Oncology and
Neurosciences, Genoa, Italy
T. Senussi
Department of Surgical Sciences and Integrated
Diagnostics, University of Genoa, Genoa, Italy
© Springer Nature Switzerland AG 2021
C. Robba, G. Citerio (eds.), Echography and Doppler of the Brain,
https://doi.org/10.1007/978-3-030-48202-2_33
Fig. 33.1 Flow in left MCA
• A right midline shift of 3mm.
• Estimated ICP with the ow diastolic formula
of 21mmHg and an increased pulsatility index
of 1.5 (Fig.33.1).
• Third ventricle width of 7mm (Fig.33.2).
The following day, angiographic coiling of the
aneurysm was performed without complications,
and sedation was stopped: GCS E4 M6 Vt patient
was aphasic with a minor right motor weakness,
and the patient was extubated. 24 hours after,
319
320
Fig. 33.2 Third ventricle 7mm wide before the lumbar
puncture
GCS dropped to E4 M5 V2; a new brain CT
showed increased hydrocephalus with a patent
fourth ventricle, the reason why a lumbar punc-
R. Bertuetti et al.
Fig. 33.3 Third ventricle 5 mm wide after the lumbar
puncture
ture was carried out and 20ml of haematic CSF
(cerebrospinal uid) was subtracted. After the
procedure neurological status improved and brain
ultrasound showed a narrowed third ventricle
(5mm width) (Fig.33.3).
Case 10: Intracranial Hypertension
andDecompressive Craniectomy
RitaBertuetti, NicolaZugni, MaurizioSaini,
DavideSavo, FrancescaSimonassi,
KartikaChandrapatham, andTarekSenussi
34
Thirty-ve-Year-old young lady, found at the
bottom of a stair ight at home, transported by
ambulance to the emergency department of a
peripheral hospital where the rst neurological
evaluation is performed: GCS: E4 M5 V2 pupils
equal and reactive to light, and blood discharge
from the right ear meatus. The anaesthetist
decided at this point to intubate the patient before
taking the patient to have total body CT scan.
Brain CT showed post-traumatic subarachnoid
haemorrhage, left subdural haematoma, multiple
contusive lesions, temporal bone and petrous
bridge bilateral fracture, and left-to-right 5 mm
R. Bertuetti (*) · N. Zugni
Department of Anesthesiology, Critical Care
Medicine and Emergency, Division of Neurocritical
Care, ASST Spedali Civili di Brescia, University
Hospital, Brescia, Italy
M. Saini · D. Savo
Department of Emergency, Perioperative Medicine
and Intensive Care, Neuroanesthesia and
Neurointensive Care Unit, San Gerardo Hospital,
ASST-Monza, Monza, Italy
F. Simonassi · K. Chandrapatham
Anesthesia and Intensive Care, Ospedale Policlinico
San Martino- IRCCS for Oncology and
Neurosciences, Genoa, Italy
T. Senussi
Department of Surgical Sciences and Integrated
Diagnostics, University of Genoa, Genoa, Italy
midline shift (Fig.34.1). After the scan the patient
was transferred to a tertiary hospital.
After admission in the ICU of a tertiary hospital, sedation was stopped and a new neurological evaluation revealed a GCS of E3 M6 Vt
with upper right limb weakness. After few
hours right over left anisocoria was noted and
brain ultrasound was then performed: TCCD
revealed increased PI in the left MCA with an
estimated ICP of 33 mmHg on the left and
22 mmHg on the right; ultrasound measurement of ONSDs showed signicantly enlarged
ONSD on the right (Fig.34.2a–d). Invasive ICP
monitoring was then positioned, sedation was
escalated and boluses of hypertonic saline 5%
were injected in order to keep ICP below
20–25mmHg (Fig.34.3a, b). Despite optimisation of medical treatment, ICP subsequently
spiked above threshold values in the following
hours; a new brain CT showed increase of both
the haemorrhagic component of the contusions
and the midline shift was undertaken. On such a
basis, the neurosurgeon on call decided to take
the patient to the operating room for decompressive craniectomy (DC). After DC ow
velocities in the MCAs and ONSD improved
proving normalisation of ICP and CPP.During
the following days she developed post-surgical
© Springer Nature Switzerland AG 2021
C. Robba, G. Citerio (eds.), Echography and Doppler of the Brain,
https://doi.org/10.1007/978-3-030-48202-2_34
321
322
ab
cd
Fig. 34.1 Brain CT scan at admission
R. Bertuetti et al.
Fig. 34.2 (a–d) Panels a and b showing left MCA ow velocity and ONSD, panels c and d showing right MCA and
ONSD before insertion of the invasive ICP monitoring system
infection complicated by convulsive episodes
treated with antibiotics (vancomycin and
cefepime) and levetiracetam. On day 7in ICU
she was tracheostomised and quickly weaned
from the ventilator.
Her neurological status gradually improved
becoming awake with uctuating levels of
attention, intermittently being able to obey commands as for aphasia; after 11days in ICU, the
patient was moved to the neurosurgical ward.
ab
34 Case 10: Intracranial Hypertension andDecompressive Craniectomy
Fig. 34.3 TCCD after DC points out complete normalization of ow in left MCA (left panel), while in right MCA
(right panel) PI, despite a decreasing trend, is still above normal limit (PI = 1.55)
323
Case 11: Hydrocephalus
withVentricular Vegetations
RitaBertuetti, MaurizioSaini, DavideSavo,
FrancescaSimonassi, KartikaChandrapatham,
andTarekSenussi
A 19-year-old man was admitted to ICU for polytrauma secondary to a car accident. He reported a
severe traumatic brain injury with bilateral interhemispheric and periencephalic hemorrhagic soffusion and frontal contusions. Three days after
admission he underwent a right temporoparietal
decompressive craniectomy and external ventricular drainage (EVD) placement for uncontrolled
intracranial hypertension. In the following months
the patients developed multiple hygromas and
concomitant Klebsiella pneumonia carbapenemasi producer infection (due to gastrointestinal
tract colonization) treated with EVD and antibiotic therapy, respectively. Tracheostomy was performed. Three months after trauma, cranioplasty
with autologous bone was performed. During the
R. Bertuetti (*)
Department of Anesthesiology, Critical Care
Medicine and Emergency, Division of Neurocritical
Care, ASST Spedali Civili di Brescia, University
Hospital, Brescia, Italy
M. Saini · D. Savo
Department of Emergency, Perioperative Medicine
and Intensive Care, Neuroanesthesia and
Neurointensive Care Unit, San Gerardo Hospital,
ASST-Monza, Monza, Italy
F. Simonassi · K. Chandrapatham
Anesthesia and Intensive Care, Ospedale Policlinico
San Martino- IRCCS for Oncology and
Neurosciences, Genoa, Italy
T. Senussi
Department of Surgical Sciences and Integrated
Diagnostics, University of Genoa, Genoa, Italy
35
Fig. 35.1 Brain ultrasound (transtemporal window)
shows enlarged lateral ventricles, on the top right, in the
occipital horn of the ventricle, presence of neoformation
can be appreciated
following weeks, the patient showed a neurological deterioration: an increase of brain ventricle
volumes and a hydroaerial level with alteration of
cerebrospinal uid (CFS) signal were observed on
CT scan. Similarly brain ultrasound showed
remarkably enlarged ventricles (Fig.35.1). Highquality images obtained with brain ultrasound
allowed us to monitor the evolution of hydrocephalus without performing multiple CTs (also given
the patient’s unstable clinical conditions)
(Figs.35.2a, b and 35.3), but also allowed us to
identify two different intraventricular neoformations (Figs. 35.2b and 35.4) consistent with
infected vegetations (Fig.35.3).
After such ndings, a lumbar puncture conrming the presence of turbid CFS was performed
© Springer Nature Switzerland AG 2021
C. Robba, G. Citerio (eds.), Echography and Doppler of the Brain,
https://doi.org/10.1007/978-3-030-48202-2_35
325
326
R. Bertuetti et al.
ab
Fig. 35.2 (a, b) In panel (a), on the left, measurement of ventricles size on a TC head image frame. In panel (b), on the
right, meaurement of ventricle width through using brain ultrasound
Fig. 35.3 Infectious vegetation in the occipital horn of
the left ventricles
Fig. 35.4 Measurement of the lateral ventricles and third
ventricle size through the use of brain ultrasound
Fig. 35.5 TCCD of right MCA: evaluation of cerebral
blood ow and estimation of intracranial pressure in the
follow up of hydrocephalus progression. The spectrogram
shows increased PI and a diastolic ow velocity at lower
limits
and antibiotic therapy was then restored and a new
EVD catheter was replaced. Fig.35.5 shows blood
ow velocities evaluated with TCCD in the right
middle cerebral artery during the phase of intracranial hypertension secondary to hydrocephalus.
Unfortunately, given the serious neurological and
infective situation, the patient developed several
uncontrolled intracranial hypertension episodes
associated with neurovegetative disorders; he died
after 6months from the initial injury.
Case 12: Intracranial Hypertension after Ischemic Stroke
RitaBertuetti, MaurizioSaini, DavideSavo,
FrancescaSimonassi, KartikaChandrapatham,
andTarekSenussi
36
A 40-year-old patient admitted to a trauma center
hospital after a workplace accident was diagnosed with a neck injury caused by direct impact
with a grinder and complicated with right internal carotid artery laceration. The Glasgow Come
Scale at the admission was 13/15. Urgent surgical
intervention was needed to repair the damaged
vessel and subsequently the patient was admitted
to intensive care unit. The day after the trauma,
because of neurological deterioration, the patient
was intubated and a brain CT was undertaken: it
showed a large area of ischemia at the level of the
right frontal-temporal-parietal areas with disappearance of the interhemispheric grooves and
midline shift. On the basis of brain CT ndings
decision was taken to insert an intracranial pres-
R. Bertuetti (*)
Department of Anesthesiology, Critical Care
Medicine and Emergency, Division of Neurocritical
Care, ASST Spedali Civili di Brescia, University
Hospital, Brescia, Italy
M. Saini · D. Savo
Department of Emergency, Perioperative Medicine
and Intensive Care, Neuroanesthesia and
Neurointensive Care Unit, San Gerardo Hospital,
ASST-Monza, Monza, Italy
F. Simonassi · K. Chandrapatham
Anesthesia and Intensive Care, Ospedale Policlinico
San Martino– IRCCS for Oncology and
Neurosciences, Genoa, Italy
T. Senussi
Department of Surgical Sciences and Integrated
Diagnostics, University of Genoa, Genoa, Italy
sure (ICP) probe to monitor the evolving intracranial hypertension. The invasive monitoring
system immediately conrmed a condition of
intracranial hypertension (ICP = 34 mmHg);
alongside TCD sessions were performed in order
to evaluate cerebral blood ow (Fig. 36.1).
Despite treatment escalation to deep sedation and
systemic blood pressure support with noradrenaline, intracranial hypertension worsened causing
severe hypoperfusion as showed by a signicant
reduction in diastolic ow (almost to zero) at the
TCCD.Figures 36.2 and 36.3 show the ow in
right middle cerebral artery at ICP of 50mmHg
and 57mmHg, respectively. Mannitol and hypertonic solution boluses were started and support
with vasoconstrictors was increased. The efcacy
of the treatment was monitored with TCCD and a
clear improvement in cranial hypertensive status
and cerebral perfusion was observed. Figure36.4
shows increasing of the diastolic ow with a clear
Fig. 36.1 TCCD of right MCA performed in order to
assess cerebral blood ow
© Springer Nature Switzerland AG 2021
C. Robba, G. Citerio (eds.), Echography and Doppler of the Brain,
https://doi.org/10.1007/978-3-030-48202-2_36
327
328
R. Bertuetti et al.
Fig. 36.2 TCCD of right MCA shows almost absent diastolic ow velocity at ICP of 50 mmHg
Fig. 36.3 TCCD of right MCA shows almost absent diastolic ow velocity at ICP of 57 mmHg
Fig. 36.5 TCCD of righr MCA shows further imprvement of ow after administration of a bolus of
hypertonic saline
reduction of the pulsatility index (ICP values=13mmHg) after administration of mannitol, and Fig.36.5 shows a further improvement of
the diastolic and systolic ow after administration of a hypertonic solution (values of
ICP=2mmHg). Despite the medical therapy, in
the following days the patient had further intracranial hypertensive crises so, in agreement with
the neurosurgeons, it was decided to proceed
with a decompressive craniectomy. Subsequently
to the decompression, ICP values remained well
controlled and the patient was extubated after
4days and transferred a week later to a neurorehabilitation center due to the neurological
sequelae reported (upper and lower left limb
motor decits and partial expressive aphasia).
After 1month cranioplasty with autologous bone
was performed.
Fig. 36.4 TCCD of right MCA after mannitol bolus and
initiation of vasopressors