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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5783_Библиотеки_им_академика_М_И_Перельмана.pdf
Intracranial
2 Neuro-ICU: Monitoring andManagement ofIntracranial Pressure. APractical Review
Table 2.1 Causes of
increased intracranial
pressure
Trauma
•Masslesion
• Depressed skull fracture
•Brain edema
•Hyperemia
•Hydrocephalus
•Extracranial causes
Nontraumatic intracranial hemorrhage
• Intracerebral
•Subarachnoid
Acute ischemic stroke
Hydrocephalus
• Communicating
•Obstructive
Brain tumor
Seizures
Cerebral vasospasm
Infection
Pseudotumor cerebri
Idiopathic intracranial hypertension
Extracranial (secondary)
Airway obstruction
Hypoventilation
•Hypoxia
•Hypercarbia
Hypertension
Head position or posture
Venous outflow obstruction
Hyperpyrexia
Agitationorpain
Increased intrathoracic or intra-abdominal pressure
Liver failure
Altered sodium balance
Hypoglycemia or hyperglycemia
High-altitude sickness
Drugs
17
Table 2.2 Predictors of intracranial hypertension
Major criteria
1. Compressed cisterns (Marshall diffuse injury III)
2. Midline shift >5 mm (Marshall diffuse injury IV)
3. Nonevacuated mass lesion (>25 cm3)
Minor criteria
4. Glasgow Coma Scale ≤ 4
5. Pupillary asymmetry
6. Abnormal pupillary reactivity
7. Marshall diffuse injury II (basal cisterns are present with midline shift of 0–5 mm
and/or high - or mixed-density lesion of ≥ 25 cm3)
Criteria and clinical decision rule were developed by consensus and approved by 97% of participants in
a working group of 43 neurosurgeons and intensivists. Increased ICP was considered in the presence of
one major or ≥2 minor criteria obtained at baseline following the resuscitation of severe TBI patients [8]
18
P. Le Roux
In this chapter, these issues will be briey reviewed and a pragmatic approach to
ICP management provided [20]. The focus is on ICP in adults. There are important
anatomic, physiologic, radiologic, and management differences in children, which
are beyond the scope of this chapter [21–24].
2.2 Which Patients Should Undergo ICP Monitoring?
ICP monitoring is best studied in TBI, although its uses have been described in
several other disorders, for example, SAH, ICH, meningitis, and liver encephalopathy, among others. Hence, the indications for ICP monitoring in neurocritical, in
large part, are based on TBI guidelines. Evidence-based guidelines from both
Europe and North America recommend use of ICP monitors to assess and manage
intracranial hypertension [10–14]. However, the most recent edition (4th edition)
[15] of The Brain Trauma Foundation’s (BTF) Guidelines indicated there was insufcient evidence to support a level I or IIA recommendation in TBI.In general, an
ICP monitor (ICPM) is indicated when clinical or imaging criteria suggest ICP is
likely to be—or become—elevated (Table2.2) [8, 9].
The 3rd edition of the BTF guidelines for TBI recommended ICP should be
monitored:
1. In all salvageable TBI patients with a postresuscitation Glasgow Coma Scale
(GCS) of 3–8 and an abnormal CT scan
2. In severe TBI patients with a normal CT scan, if two or more of the following
admission features are present: age>40years, unilateral or bilateral motor posturing, or systolic blood pressure (BP) <90mmHg [12]
In non-TBI patients (e.g., SAH or ICH), there is no dened consensus on indications for an ICPM.In these patients, TBI guidelines are applied and ICPMs recommended for: reduced GCS (≤8), cerebral edema or mass effect on imaging, and
neurological worsening.
The BTF guidelines were based on studies from the 1980s. Since then, image
quality has improved and neurocritical care has evolved. This has generated several
questions, for example, is an ICPM necessary in a comatose patient with only mild
traumatic SAH and open cisterns. This and other questions were addressed in the
Milan consensus conference on ICPM [25]. Comatose patients with compressed or
absent cisterns (in the absence of mass lesions) should undergo ICP monitoring,
whereas those with diffuse brain injury but open cisterns should have repeat CT
scanning and an ICPM be inserted in patients with evolving lesions or development
of cisternal compression. Other clinical circumstances were addressed in Milan
[25]. For example, an ICPM should be considered in select patients with multisystem injuries, severe respiratory issues, those who may require multiple anesthetic
procedures or prolonged sedation that preclude neurological assessment, or have
large bifrontal contusions even if they present with a GCS>8. Second, an ICPM
can be useful when the neurologic examination is not reliable, for example,
2 Neuro-ICU: Monitoring andManagement ofIntracranial Pressure. APractical Review
19
maxillofacial trauma or spinal cord injury. Third, an ICPM is useful in patients who
undergo a decompressive craniectomy (DC) or undergo a craniotomy for a mass
lesion particularly when there is hypoxia, hypotension, pupil abnormalities, midline
shift >5mm, or brain swelling.
Following surgery (i.e., a craniotomy for a mass lesion or a DCC), an ICPM is
pathology dependent. Following evacuation of an acute extradural hematoma
(AEDH), ICP increases are rare and, hence, an ICPM is not always needed [25]. By
contrast, following removal of an acute subdural hematoma (ASDH), ICP increases
associated with intraparenchymal contusions or hematomas or brain swelling are
common and can double mortality [26]. In these patients, an ICPM is necessary.
Similarly, after decompressive craniectomy, including primary DCC, increased ICP
and reduced CPP are common. This increase in ICP is associated with poor outcome
and, hence, an ICPM can help guide therapy after DCC [27]. Current DCC guidelines recommend ICPM placement after craniotomy for an ASDH including primary DCC [28].
2.3 How Should Intracranial Pressure BeMonitored?
Intracranial pressure can be monitored with invasive or noninvasive devices that
should be supplemented with the clinical examination and CT imaging. There are a
variety of signs and symptoms of increased ICP that depend in part on the severity
of the increase. However, initial signs are unreliable and nonspecic in the critically
ill patient or may be masked by medication, whereas denitive signs often are too
late. On CT, compressed or absent basal cisterns suggest increased ICP; when
absent, ICP values >30mmHg are observed in 74% of cases [29, 30].
Noninvasive technologies to measure and monitor ICP are evolving but currently
none are robust or accurate enough to allow accurate, continuous monitoring in
routine practice. However, these technologies can be used in specic patients when
invasive monitoring is contraindicated, for example, coagulopathy or is unavailable
[31]. Among the many described noninvasive technologies, transcranial Doppler
(including pulsatility index [PI]), optic nerve sheath diameter (ONSD), and automated pupillometry provide high sensitivity, diagnostic accuracy, and correlate well
with ICP measurements including over time [32–34].
A variety of invasive techniques can be used: Today, intraparenchymal strain
gauge or ber optic monitors or a ventricular catheter (external ventricular drain
[EVD]) are recommended [10, 11, 35]. Fluid-coupled or pneumatic devices placed
in the subarachnoid, subdural, or epidural space are less accurate and not recommended [10, 11, 35, 36]. EVDs were long considered the “gold standard” but this is
a matter of history (and perhaps cost) rather than merit. In Europe, surveys of neurotrauma centers enrolled in Collaborative European Neurotrauma Effectiveness
Research in Traumatic Brain Injury (CENTER-TBI) indicate that one-third use only
intraparenchymal monitors but <10% use only EVDs. In centers that use both,
EVDs tend to be placed when the ventricles are enlarged or for cerebrospinal uid
20
P. Le Roux
(CSF) diversion [16]. ICP measurements are equally accurate with EVDs or parenchymal monitors. However, EVD accuracy depends on setup and whether the device
is being used to drain CSF.Indeed, when CSF is drained, correlation between the
two methods can be lost and EVD measurements of ICP may be inaccurate [37, 38].
In addition, there remains a debate on whether CSF should be drained intermittently
or continuously. When CSF is being drained, ICP is not measured, although newer
devices allow both to occur. Other variables that may be more important than the
numeric value of ICP also are not measured with an EVD.
One potential advantage of an EVD is CSF drainage, for example, ICP treatment.
This may be relevant in patients with hydrocephalus, but in others CSF drainage
inuences compliance and in some circumstances may have a deleterious effect on
other indices and even CBF.There are several disadvantages when using an EVD
and meta-analytic studies demonstrate a greater risk of complications with EVDs
[39, 40]. First, an EVD may be difcult to insert when there is brain swelling, small
ventricles, or if anatomy is distorted by mass effect. In these patients, a parenchymal
monitor that is easier to insert may be preferable. Second EVDs have a greater complication rate than parenchymal monitors. This includes misplacement or technical
errors (12% vs. <3%), infection (5–20% vs. <1%), and hemorrhage (5% vs. 1%)
[41–44]. However, the exact incidence of infection or hemorrhage depends on how
infection (vs. contamination or CSF colonization) is diagnosed or whether routine
head CT scans are obtained or not. On the other hand, parenchymal monitors share
a common disadvantage, that is, recalibration is not possible after placement and not
all devices are MRI compatible. The Spiegelberg catheter (which is pneumatic) is
an exception from this rule since it recalibrates itself every hour.
Use of standardized protocols or care bundles (when adhered to) and simulator
training can help to increase the safety of ICP monitoring [45, 46]. For example,
EVD-associated infection can be reduced with closed drainage systems, a longtunneled device, avoidance of ushing the system, and CSF sampling only if clinically indicated rather than routinely performed. Infection risk is less with a short
duration of CSF drainage (<4days), although there does not appear to be a role for
routine EVD replacement or long-term antibiotic use to prevent infections [43, 47–
49]. Today antibiotic impregnated EVDs are available and their use may help reduce
infection [50–52]. Technical complications such as catheter dislodgement, breakage, or malfunction can also occur but are easily recognized and usually of little
clinical consequence.
Does the type of ICPM (EVD or parenchymal) device make a difference? Several
studies including a meta-analysis have compared the two devices and, in general,
nd a greater risk of complications with EVDs. Kasotakis etal. [53] examined 377
adult TBI patients who required an ICPM, 253 received a parenchymal monitor, and
124 EVD.While outcome was similar, the use of EVD was associated with threefold—more device-related complications, longer duration of monitoring, and longer ICU stays. In the American College of Surgeons Trauma Quality Improvement
Program (ACS TQIP) database, 2562 patients who underwent ICP monitoring were
analyzed; 1358 (53%) had an EVD and 1204 (47%) a parenchymal monitor [54]. In
univariate analysis, 30-day mortality was signicantly higher in the EVD patients
2 Neuro-ICU: Monitoring andManagement ofIntracranial Pressure. APractical Review
21
than in patients with a parenchymal monitor. This relationship was lost in multivariate analysis. More recently, Bales etal. [55] retrospectively examined 224 severe
TBI patients included in the Citicoline Brain Injury Treatment trial (COBRIT); 45%
received an EVD, the rest an intraparenchymal device. Propensity scores were used
to reduce confounding by indication. Outcome, including in-hospital mortality and
6-month functional and neuropsychological outcomes, was better in the patients
who received intraparenchymal devices. Hence, it is recommended that unless CSF
drainage is needed (e.g., hydrocephalus) that a parenchymal ICPM be used.
2.4 When Should ICP BeTreated?
The mechanisms that underlie increased ICP are multifactorial and complex. In
addition, what denes intracranial hypertension is uncertain [56] and several
numeric thresholds at which to initiate ICP treatment have been used. These are best
dened in TBI and then extrapolated to other pathologies. The 2007 BTF Guidelines
recommend treatment when ICP is >20mmHg [12]. The 4th edition of the BTF
guidelines recommended a new ICP threshold (22mmHg) [15]. The rational for this
is based on one single-center retrospective observational study [57]. In this study,
the association between mean ICP and outcome was examined, with a nadir threshold of 22 mmHg. However, the mean ICP is entirely different from a treatment
threshold. Hence, this new threshold and the rationale for it have been questioned
[58–60]. In addition, compliance with guidelines even in level I centers is low and
there remains wide variation in the treatment for elevated ICP despite these guidelines [16, 61].
It seems reasonable to initiate therapy when ICP is >20–25mmHg [10–15, 62].
These thresholds are lower in children [22, 23]. Consistent with this, physiologic
studies demonstrate cerebral circulation disturbance (i.e., cerebral blood ow [CBF]
decreases) at ICP values >20mmHg [63]. It is important to recognize that a single
numeric ICP threshold may be an oversimplication of complex physiology and not
applicable in all patients. For example, herniation (prevention of which is a reason
to treat ICP) can occur even when ICP is normal [64], and physiologic dysfunction,
for example, cellular hypoxia or cell energy dysfunction, also may be present when
ICP is normal [65, 66]. Similarly, metabolic failure often occurs before an ICP spike
[67] and even ICP insults at lower levels (15–20mmHg) aggravate outcome [68]. In
addition, rather than treat the ICP number per se, it may be more important to regard
this value as a marker of altered physiology and instead nd the reason why ICP is
elevated and treat that rather than the numeric value [69, 70].
Today the concept of a simple numeric treatment threshold is questioned. Instead,
total “ICP dose”, “area under the ICP curve”, and temporal evolution of ICP, how
ICP responds to treatment, or individualized ICP thresholds may be more important
parameters associated with outcome [4, 5, 71–73]. Rather than apply a “one size ts
all” threshold derived from population-based data, it appears that it may be preferable to individualize thresholds based on patient characteristics, pathology, other
22
P. Le Roux
physiologic parameters, and on a risk-benet analysis of treating the specic ICP,
that is, the threshold may vary from patient to patient and in the same patient
depending on time and other variables [69, 70]. For example, when ICP is
>20mmHg, most insults in adults are deleterious after >35–40min but when ICP is
>25mmHg, aggravate outcome within 10–15min [68]. To best individualize targets
requires multimodality monitoring (MMM) and interpretation of the ICP value
based on clinical and imaging characteristics. Further research is required to validate this approach and at present it still is being elucidated whether treating patients
to keep them below the given threshold or dose, based on either population-dened
thresholds or individualized thresholds, improves outcome.
Guidelines for ICP management in non-TBI patients (SAH, ICH IVH, and cardiac arrest) have evolved but there remains no clear consensus on when to treat ICP
in these patients [74, 75]. Intracranial hypertension (>20mmHg) is common after
SAH, including in good grade patients [5, 76] and, in particular, during the early
phase after poor grade SAH.Episodes of elevated ICP>5min can aggravate outcome and control of ICP can improve circulation [77]. However, cerebral metabolic
compromise may also be observed when ICP and CPP are normal [78–80]. In
hypoxic ischemic brain injury (HIBI), for example, cardiac arrest, small clinical
studies suggest compliance rather than ICP alone may be of greater importance
[81]. Further study is required in non-TBI patients. Perhaps data from SYNAPSE,
an ongoing observational study of ICP, will provide guidance [82].
2.5 How toManage Increased ICP?
The mechanisms that underlie and consequences of increased ICP are multifactorial
and complex, as is the interplay between injury and intervention. Therapy for
increased ICP is in large part empiric and phenomological and based on population
targets. However, in recent years, with a better understanding of pathophysiology,
introduction of neurointensivists, and advances in neuromonitoring, there is a growing trend to use precision medicine where treatment and therapy targets are individualized to patient’s need, rather than used on a “one size ts all” in ICP
management [17, 83, 84].
The recent Seattle international Severe Traumatic Brain Injury Consensus [20]
used a Delphi method-based consensus approach to address management of severe
TBI patients who have ICPMs. The recent Seattle international Severe Traumatic
Brain Injury Consensus [20] used an Intracranial pressure (ICP) delphi-methodbased consensus approach to address management of severe TBI patients who have
ICPMs. The resulting protocol was designed to assist ICP management in these
patients (Fig.2.1). In addition, several treatments that should not be used when only
ICP is monitored are described (Table2.3). With multimodality monitoring, however, some of these therapies may be feasible. Similarly, for severe TBI patients who
do not have ICPMs, the Imaging and Clinical Examination Protocol (ICE) has been
described to help guide care [85]. This protocol may be particularly useful in
2 Neuro-ICU: Monitoring andManagement ofIntracranial Pressure. APractical Review
23
Tier 1
• Maintain CPP 60–70 mmHg
• Increase analgesia to lower ICP
• Increase sedation to lower ICP
• Maintain P
(35–38 mmHg/4.7–5.1 kPa)
• Mannitol by intermittent bolus (0.25–1.0 g/kg)
Tier 2
• Mild hypocapnia range 32–35 mmHg/4.3–4.6 kPa)
• Neeuromusular paralysis in adequately sedated patients if efficacious**
• Perform MAP Challenge to assess cerebral autoregulation and guide MAP and CPP goals in
individual patients†
• Should be performed under direct supervision of a physician who can assess response and
ensure safety
• No other therapeutic adjustments (ie.sedation) should be performed during the MAP Challenge
• Initiate or titrate a vasopressor or inotrope to increase MAP by 10 mmHg for not more than 20
minutes
• Monitor and record key parameters (MAP,CPP,ICP and P
challenge
• Adjust vasopressorlinotrope dose based on study findings
• Raise CPP with fluid boluses, vasopressors and/or inotropes to lower ICP when autoregulation is intact
Tier 3
• Pentobarbital or Thiopentone coma
titrated to ICP control if efficacious‡
CO2 at low end of normal
a
• Hypertonic saline by intermittent bolus*
• CSF drainage if EVD in situ
• Consider placement of EVD to drain CSF
if parenchymal probe used initially
• Consider anti-seizure prophylaxis for 1 week
only (unless indication to continue)
• Consider EEG montoring
) before during and after the
tx O2
• Secondary decompressive craniectomy
• Mild hypothermia (35–36°C) using active cooling measures
Principles for Using Tiers:
• When possible, use lowest tier
treatment
• There is no rank order within a tier
• It is not necessary to use all
modalities in a lower tier before
moving to the next tier
• If considered advantageous, tier
can be skipped when advancing
treatment
• Re-examine the patient and
consider repeat CT to
re-evaluate intracranial
pathology
• Reconsider surgical options
for potentially surgical lesions
• Consider extracranial causes
of ICP elevation
• Review that basic physiologic
parameters are in desired
range (e.g. CPP, blood gas
values)
• Consider consuitation with
higher level of care if applicable
for your health care system
Fig. 2.1 Consensus-based algorithm for severe TBI management guided by ICP measurements
Upper right box presents the principles for navigating through the treatments and tiers. Lower tier
treatments are viewed as having a more favorable side effect prole than higher tiers and generally
should be employed rst. Inter-tier recommendations encourage patient reassessment for remediable causes of treatment resistance. CPP cerebral perfusion pressure, EEG electroencephalogram,
EVD external ventricular drain, ICP intracranial pressure, kPa kiloPascals, MAP mean arterial
pressure, PaCO
arterial partial pressure of carbon dioxide. (Courtesy: Hawryluk etal. [20])
2
Table 2.3 Treatment not
recommended for use in
severe traumatic brain
injury management
(when only ICP is
monitored)
Mannitol by non-bolus continuous intravenous infusion
Scheduled infusion of hyperosmolar therapy (e.g., every 4–6h)
Lumbar CSF drainage
Furosemide
Routine use of steroids
Routine use of therapeutic hypothermia to temperatures below
35°C
due to systemic complications
High-dose propofol to attempt burst suppression
Routinely decreasing P
below 30mmHg/4.0kPa
aCO2
Routinely raising CPP above 90mmHg
Courtesy: Hawryluk etal. [20]
CPP cerebral perfusion pressure, ICP intracranial pressure, kPa
kiloPascals, PaCO
arterial partial pressure of carbon dioxide
2
24
low- and middle-income countries (LMICs) where limited resources may limit
access to ICPMs [86, 87]. Neither protocol, however, can replace targeted, individualized care. The focus in this chapter will be on to manage patients who have an ICP
monitor.
P. Le Roux
2.5.1 Initial Care andGeneral Measures
If a mass lesion is identied on CT, it should be surgically evacuated. A tiered
approach then is recommended [20]. Such an approach has been used successfully
in BOOST-2, a phase II trial of multimodality monitoring in severe TBI [88]. Initial
care requires ICU admission and is largely preventative and directed at optimizing
normal physiology. This includes:
1. Appropriate head of bed elevation
2. Maintenance of the neck in a neutral position and avoidance of neck constriction
(e.g., loosening endotracheal tube ties) to optimize venous return from the head
3. Endotracheal intubation and mechanical ventilation
4. Prevention of hypercapnia and hypoxia
5. Adequate treatment of pain, agitation, fever, and seizures
6. Appropriate uid therapy to avoid hypotension (SBP <9–100mmHg) and main-
tain hemoglobin (>7–8g/dL)
7. Glucose control. Different physiologic targets are described in SEABICC [20]
and recent trials that have used a similar tiered and targeted approach, for example, BOOST-2 or ProTECT [88, 89].
These physiologic targets may also differ in conditions such as SAH and ICH
[90]. In addition, there are a paucity of studies on how individual components of this
care (e.g., head of bed position) and whether bundles of care inuence ICP [14].
Nevertheless, this goal-directed approach in critical care appears to be associated
with enhanced outcome [91].
2.5.2 Tiers ofCare
When ICP remains elevated (>20–22mmHg), then a series of tiered therapies [1–3]
can be used (Fig. 2.1). Items within a tier are not necessarily listed in order of
completion and many interventions may occur simultaneously or be difcult to
achieve (e.g., EVD insertion when there are slit ventricles). The tiers represent
increased levels of intensity for the treatment of elevated ICP and lower tiers are
considered to have less risk. Ideally, patients should be initiated in Tier I and then
staged through Tier 3 if no response is observed within a prespecied time (e.g., in
2 Neuro-ICU: Monitoring andManagement ofIntracranial Pressure. APractical Review
25
BOOST-2 and 120min in a tier). However, not all modalities in a tier need to be
used before moving to the next and a tier can be skipped if it appears to be mechanistically advantageous to do so. Within each tier, there are several components of
care (each briey discussed below) including sedation, osmotherapy and uid therapy, CSF diversion, ventilation, CPP augmentation, metabolic suppression including hypothermia, and decompressive craniectomy.
2.5.2.1 Sedation andAnalgesia
In initial care, sedation is directed at pain control or agitation. In Tier 1, it is directed
at ICP control. Robust evidence for a specic preferred opioid or sedative is lacking
but systemic reviews suggest that bolus administration should be avoided [92].
2.5.2.2 Fluid Therapy andHemoglobin Management
Negative uid balance is associated with an adverse effect on outcome, independent
of its relationship to ICP, MAP, or CPP [93]. However, aggressive administration of
uid to induce hypervolemia or augment CPP can be harmful in both TBI and SAH
[94]. Hence, intravenous uid is a fundamental component of brain injury care. In
general, intravascular management should aim for euvolemia. Isotonic crystalloids
are preferred, whereas colloids, glucose-containing hypotonic solutions, other
hypotonic solutions, or albumin should be avoided [95–99]. Ideally, therapy should
be individualized rather than standardized [100] and there is some evidence that
hemodynamic goal, that is, what guides uid administration, may be more important than the amount of uid given [101]. Correcting volume status is complicated
further by frequent abnormalities of sodium homeostasis that become important in
osmotherapy. The role of anemia and transfusion is complex and beyond the scope
of this chapter. However, low Hgb can lead to vasodilatation and, hence, aggravate
ICP, whereas transfusion in some patients can correct brain hypoxia and so inuence outcome [102–104].
2.5.2.3 CSF Drainage
CSF drainage through an EVD should be considered particularly when there is
hydrocephalus. The optimal method of drainage (continuous vs. intermittent) has
not been established. In addition, while CSF drainage may reduce ICP, it can have
an adverse effect on compliance and CBF. In SAH, some studies demonstrate
improved microcirculation with CSF drainage [77]. This, however, depends on
the ICP.The role of external lumbar drainage (ELD) is limited but can be considered a therapeutic option if high ICP is due to communicating external
hydrocephalus.
26
P. Le Roux
2.5.2.4 Osmotherapy
Typically, mannitol or hypertonic saline (HTS) is administered but, despite clinical
use for >50years, there are still questions about optimal use. While both are effective, there are insufcient data to suggest superiority of one agent over the other
[104], and the optimal dose, mode of administration (e.g., bolus vs. continuous infusion), and concentration are still being elucidated. Some studies suggest HTS may
be more effective [105–107], particularly for refractory intracranial hypertension
[104], but to choose the appropriate hyperosmolar agent, patient characteristics,
such as volume status, renal function, hemodynamic status, and sodium levels,
among others, should be considered.
Mannitol treatment protocols vary from center to center, and the dose-response
relationship is not understood and often the ICP decrease depends more on the
administration protocol or the ICP level at the time the dose is given [108]. Initial
use for increased ICP is a single bolus (not infusion) of a 20–25% solution of
0.5–1g/kg, i.v., over 10–15min and repeated every 2–6h (although ideal dosing is
not well described). ICP decreases may be greatest shortly after the dose is given
because of its effect on viscosity and vessel caliber, that is, vasoconstriction.
Unnecessarily large doses or prophylactic doses could lead to more mannitol being
required later. In addition, when cerebral autoregulation (CA) or the blood brain
barrier (BBB) is impaired, aggressive mannitol use can increase ICP since it will
draw uid into brain. Hence, it is important to measure serum osmolarity or osmolar
gap (measured—calculated serum osmolarity) before infusing mannitol. Mannitol
should not be given if serum osmolarity is >320mOsm/kg H2O or osmolar gap >10
or in patients with acute kidney injury (AKI) or renal failure. Side effects of mannitol include hypotension, hypovolemia, hypokalemia, hyperkalemia, and AKI.
Hypertonic saline (HTS) increases serum osmolarity directly rather than by
inducing osmotic diuresis. Hence, it can reduce ICP and simultaneously maintain or
even expand intravascular volume. Therefore, HTS may be preferable when mean
arterial blood pressure (MABP) is reduced or patient volume status dictates caution
with large infusions. There are several different concentrations that range from 3%
++
to 23.4% NaCl solutions. Hypertonic saline should not be given if serum Na
is
>160mmol/L.To administer HTS (>3%), central venous access is required and a
50% chloride/50% acetate mix is recommended to reduce the risk of hyperchloremia. There are a variety of protocols for HTS administration but therapy can be
initiated with 3% saline at 75cc/h (or greater if requiring uid resuscitation). Serum
sodium should be checked frequently and infusion continued to goal sodium of
150mmol/L or a maximum of 160mmol/L if ICP remains refractory. Once the goal
sodium or ICP is achieved or ICP controlled, HTS can be continued as a 0.9% saline
infusion or 2% if Na++ drifts downward.