Literature Review

Contemporary Management of Increased Intraoperative Intracranial Pressure:

Evidence-Based Anesthetic and Surgical Review
Virendra R. Desai1, Saeed S. Sadrameli1, Szymon Hoppe1,2, Jonathan J. Lee1, Amanda Jenson1, William J. Steele III1,
Huong Nguyen3, David L. McDonagh3, Gavin W. Britz1

Key words Increased intracranial pressure (ICP) is frequently encountered in the neuro-
- Brain bulk surgical setting. A multitude of tactics exists to reduce ICP, ranging from patient
- Brain edema
- Brain swelling
position and medications to cerebrospinal fluid diversion and surgical decom-
- Cerebral edema pression. A vast amount of literature has been published regarding ICP man-
- Cerebral swelling agement in the critical care setting, but studies specifically tailored toward the
- Intracranial pressure
management of intraoperative acute increases in ICP or brain bulk are lacking.
Abbreviations and Acronyms Compartmentalizing the intracranial space into blood, brain tissue, and cere-
BP: Blood pressure brospinal fluid and understanding the numerous techniques available to affect
CBF: Cerebral blood flow these individual compartments can guide the surgical team to quickly identify
CBV: Cerebral blood volume
CMRO2: Cerebral metabolism
increased brain bulk and respond appropriately. Rapidly instituting measures for
CPP: Cerebral perfusion pressure brain relaxation in the operating room is essential in optimizing patient out-
CSF: Cerebrospinal fluid comes. Knowledge of the efficacy, rapidity, feasibility, and risks of the various
HoB: Head of the bed available interventions can aid the team to properly tailor their approach to each
HTS: Hypertonic saline
ICP: Intracranial pressure
individual patient. In this article, we present the first evidence-based review of
IV: Intravenous intraoperative management of ICP and brain bulk.
MAP: Mean arterial blood pressure
PEEP: Positive end-expiratory pressure
SAH: Subarachnoid hemorrhage
TBI: Traumatic brain injury increases in ICP.7-10 Intraoperatively, this intraoperative acute ICP increases
situation can lead to brain herniation out of (Figure 1). To the best of our knowledge,
From the 1Department of Neurosurgery, Houston Methodist the dural opening, rendering it vulnerable this is the first evidence-based review and
Hospital, Houston, Texas, USA; 2Medical University of to ischemia and injury; it can impede sur- systematic guideline for managing acute
Gdansk, Gdansk, Poland; and 3Departments of
Anesthesiology, Neurological Surgery, and Neurology,
gical access to deep lesions that require intraoperative ICP increases.
University of TexaseSouthwestern, Dallas, Texas, USA brain retraction; it can predispose to or
To whom correspondence should be addressed: aggravate brain retraction injury; or it can
Virendra R. Desai, M.D. complicate dural closure.11-15 Thus, prompt INTRAOPERATIVE SIGNS OF INCREASED
[E-mail: [email protected]] recognition and intervention are war- ICP
Citation: World Neurosurg. (2019) 129:120-129. ranted. Although management of The first step in managing ICP is recognizing
https://doi.org/10.1016/j.wneu.2019.05.224 increased ICP is well described in the crit- increases. ICP monitors, both parenchymal
Journal homepage: www.journals.elsevier.com/world- ical care setting, no guidelines exist for and ventricular (i.e., external ventricular
neurosurgery intraoperative management. The incidence drains), provide quantitative pressure read-
Available online: www.sciencedirect.com of acute intraoperative brain swelling ings that can help guide management.3,4
1878-8750/$ - see front matter ª 2019 Elsevier Inc. All ranges from 0.7% to 30% depending on the However, many intraoperative cases may
rights reserved. disease being treated.11 An important not have the benefit of such monitors. In
consideration during surgery is that these instances, qualitative subjective
INTRODUCTION increased ICP generally must be dealt with assessment by the surgeon based on clinical
Increased intracranial pressure (ICP) oc- rapidly, albeit with short-lasting tech- and physical signs can guide management.
curs commonly in patients with traumatic niques, whereas in the critical care setting, Before craniotomy, hemodynamic changes,
brain injury (TBI) and subarachnoid hem- typically slower, longer-lasting methods such as hypertension, bradycardia, and
orrhage (SAH) and is the most frequent may be preferred. Various options to reduce irregular respiratory pattern (Cushing reflex),
cause of mortality and morbidity in these ICP exist, ranging from patient position to can signify increased ICP.16 After
patients.1-6 Brain tumors, particularly ma- medications to surgical interventions. We craniotomy, physical signs such as tense
lignant ones, can also increase ICP. present these various options, describing dura, brain swelling out of the dural
Increased ICP can impair cerebral perfu- their usefulness and efficacy as ICP reduc- opening, or difficult brain retraction are
sion pressure (CPP), cerebral blood flow tion agents and the level of evidence sup- subjective tools to assess ICP.14
(CBF), and oxygenation, inciting a down- porting these. Based on this analysis, we When subjective data are unclear,
ward cycle of ischemia, edema, and further suggest a stepwise algorithm to manage measuring epidural or subdural ICP can

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 LITERATURE REVIEW
VIRENDRA R. DESAI ET AL. INTRAOPERATIVE MANAGEMENT OF INTRACRANIAL PRESSURE

Figure 1. Stepwise algorithm for managing acute intraoperative intracranial cerebrospinal fluid; HoB, head of the bed; HTS, hypertonic saline; ICH,
pressure increases based on intracranial compartment affected. CSF, intracranial hemorrhage; PEEP, positive end-expiratory pressure.

provide objective data.15,17 A pressure blood pressure (BP) <90 mm Hg may also autoregulatory capacity, hypotension causing
transducer can be slid into the epidural be risk factors for acute brain swelling.19 cerebral hypoperfusion and reflex vasodila-
space from a burr hole or at the edge of a tion, venous hypertension from outflow
craniotomy.15,17 To measure subdural obstruction caused by head rotation or
ICP, a 22-gauge intravenous (IV) needle CAUSES OF INTRAOPERATIVE INCREASED increased thoracoabdominal pressure, or
connected to a pressure transducer can ICP certain medications such as volatile anes-
be inserted into the dura until typical thetics, nitroglycerin, or sodium nitroprus-
Intracranial volume consists of brain tissue
cardiac and respiratory waveforms side.9,25 During awake craniotomies,
(w88%), intravascular blood (2%e3%), and
appear.15 vomiting, pain/agitation, coughing, shiv-
cerebrospinal fluid (CSF) (w9%); as the
ering, and seizure activity during cortical
volume of one of these components in-
mapping can increase ICP and brain bulk,
creases, after initial compensation via
RISK FACTORS FOR INCREASED ICP leading to herniation through the dural
decrease in the volume of another compo-
opening.9,25
Independent risk factors for intraoperative nent, ICP increases at a nonlinear, nearly
brain swelling and subsequent high ICP are exponential rate, according to the Monro-
subdural ICP measured at the start of sur- Kellie hypothesis.3,4,6,8,9,20,21 More broadly, DATA COLLECTION
gery, regardless of the disease (tumor vs. ICP can be increased by intracranial or For the interventions mentioned earlier,
SAH), the degree of midline shift, and for extracranial/systemic disease.3,6,9 Intracranial an evidence-based review was conducted
tumor cases, a diagnosis of glioblastoma or causes include tumor, infarct, trauma, hem- via the following search terms in PubMed:
metastasis.15,18 Specifically, subdural ICP orrhage, hydrocephalus, abscess/infection,
>10 mm Hg suggests a strong possibility of parenchymal edema, or idiopathic.3,4,6,9,21-23 “intracranial pressure” AND agent (for
brain swelling after dural opening, whereas In addition, venous hypertension can in- instance, “hypertonic saline”)
<7 mm Hg indicates a low probability.15 crease brain bulk, when a cerebral vein with
The degree of peritumoral edema and no collateral flow is sacrificed, leading to “brain edema” AND agent
contralateral ventricular dilation correlate congestion of proximal vessels.24 “brain swelling” AND agent
with ICP as well.12 Mean arterial blood Extracranial causes include airway
“cerebral edema” AND agent
pressure (MAP) >140 mm Hg or obstruction, hypoxia/hypercarbia (hypo-
intraoperative hypotension with systolic ventilation), hypertension exceeding cerebral “cerebral swelling” AND agent

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 LITERATURE REVIEW
VIRENDRA R. DESAI ET AL. INTRAOPERATIVE MANAGEMENT OF INTRACRANIAL PRESSURE

Table 1. Agents Reducing Intracranial Pressure Level of Evidence

Level of Evidence

Categories Agent I II III IV V Comments

Pulmonary management PEEP control 0 1 26 0 2 All had lower ICP at lower PEEP values except 1 level 2 and 14 level 3
articles that showed no ICP change when PEEP was increased. Only 1
level 3 article increased ICP when PEEP was decreased
Hyperventilation 2 5 18 1 6 All had positive results except 3 level 3 articles that had equivocal
results
Medications Propofol 4 6 26 1 2 Level 1: 1 was equivocal level 2: 5 were equivocal level 3: 11 were
equivocal. All others were positive. The equivocal ones were mostly
when propofol was compared with other agents and had lower ICP
values, but no direct effect of propofol on ICP was studied. Or multiple
agents were used so effect of propofol was unclear. Or propofol had no
effect
Benzodiazepines 0 2 4 1 0 One level 2, 1 level 3, and 1 level 4 equivocal. One level 3 negative.
(midazolam, remimazolam) Overall is positive because the equivocal ones had positive results but
were used in combination with another agent or did not specifically
study whether ICP was decreased but rather, the article noted that ICP
was the same as that with propofol
Etomidate 0 0 11 1 0 All positive
Hypertonic saline 26 27 40 2 24 All had positive results except 1 level 2, 2 level 3, and 2 level 5 that
were equivocal
Mannitol 13 20 32 9 5 All with positive results except 1 level 3 was equivocal
Surgical options Lobectomy/parenchymal resection 0 0 5 3 3 All had positive results except one that was questionably positive and
one that was negative, because stroke/infarct tissue in their study long-
term had functionality so the authors recommended against it. This is
more of a brain resection that could or could not be infarct and thereby
leaves out many articles related to infarct resection. Only 2 of these 7
were concerning normal brain resection whereas others were infarcted
or injured brain
Decompressive craniectomy 14 17 110 27 48 One level 1, 5 level 3, and 1 level 5 articles with equivocal results.
Many studies had concurrent brain or infarct resection and duraplasty in
addition to craniectomy; these articles were included in this analysis. In
addition, many articles reported long-term clinical outcomes rather than
ICP values; these were included under the presumption that long-term
outcome serves as a surrogate for ICP control
Hinge craniotomy 0 0 4 1 1 All were positive, but one was a cadaveric study
Dural expansion 1 0 4 0 5 32 total articles found but most were equivocal given concurrent
with duraplasty decompressive craniectomy and/or other intervention(s). The only
articles included here specified that dural opening or expansion alone
reduces ICP
Lumbar drain 0 5 9 3 6 All had positive results
Laparotomy 0 0 4 1 6 Two of the level 5 articles and one of the level 4 articles had equivocal
results whereas all others were positive

PEEP, positive end-expiratory pressure; ICP, intracranial pressure.

Inclusion criteria included articles that PubMed. Although systematic reviews and reducing ICP), equivocal (uninterpretable
directly or indirectly evaluated the efficacy meta-analyses were included, literature re- results or no effect on ICP), or negative
of the agent in ICP reduction and human views were not. Results of each study were (increase ICP). Table 1 includes agents that
studies only with abstracts accessible via classified as positive (efficacious in were positive, whereas Table 2 includes

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 LITERATURE REVIEW
VIRENDRA R. DESAI ET AL. INTRAOPERATIVE MANAGEMENT OF INTRACRANIAL PRESSURE

those that were equivocal or negative. The abdominal pressure can be managed with anesthetics. Although sevoflurane may not
level of evidence classification scheme is nasogastric or orogastric tubes, as indi- increase ICP in patients without intracra-
shown in Table 3, adapted from Ref.26 cated, or via laparotomy in cases of critical nial hypertension, in those with it, inha-
intra-abdominal pressure.30 Positive end- lational anesthetics should be used with
expiratory pressure (PEEP) contributes to extreme caution (i.e., close ICP moni-
MANAGEMENT OF ICP VIA NONINVASIVE intrathoracic pressure and decreasing this toring) or avoided altogether. Propofol
METHODS intuitively would be beneficial in ICP decreases CMRO2, with a concomitant
Intraoperatively, the anesthesiologist reduction.9,29 However, PEEP maintains reduction in CBF, resulting in decreased
wields significant power in ICP control. lung aeration (and hence oxygenation and CBV and ICP.4,8,32 Thus, especially in pa-
Communication between the surgeon and ventilation) and improves pulmonary tients with intracranial hypertension, pro-
anesthesiologist is vital to successful compliance. A PEEP of 5e10 cm H2O with pofol is considered the optimal anesthetic
recognition and management of brain 60% FiO2 (fraction of inspired oxygen) has agent.4
swelling. Basic principles of decreasing been proposed to maintain optimal brain Barbiturates, benzodiazepines, and eto-
ICP involve reducing the volume of blood, oxygenation levels in cases of increased midate can all decrease ICP by decreasing
brain, or CSF; removing a mass such as a ICP.8 However, in cases of acute lung or CBV, CBF, and CMRO2 without leading to
tumor or hemorrhage; or opening the thorax injury, higher PEEP levels of 10e15 anaerobic metabolism.8 A recent Cochrane
skull to increase the intracranial vol- cm H2O may be necessary, with some database review33 suggested that in the
ume.1,3,6,9,10,18,21,27,28 Regulating the studies suggesting no clinically relevant critical care setting, although barbiturate
different components of the Monro-Kellie ICP increase and 1 study even showing coma can reduce ICP, it does not decrease
doctrine allows the anesthesiologist to decreased ICP at these levels.4 mortality, and as many as 25% have issues
reduce ICP in a multifactorial manner. In Arterial inflow can be suppressed by with hypotension, which can counteract
the following sections, we outline the cerebral vasoconstriction. Hyperventila- the benefits of ICP reduction on CPP.
physical maneuvers and pharmacologic tion reduces the partial pressure of arterial Nevertheless, if ICP is refractory to other
treatment options available to the anes- carbon dioxide (PaCO2), alkalinizing CSF, measures in the operating room,
thesiologist and categorize them by the which vasoconstricts cerebral blood ves- barbiturate loading could be considered
intracranial compartment affected. Table 4 sels.31 However, this effect is transient as a rescue therapy.
lists the main ICP reductions agents along because choroid plexuses create Historically, ketamine has been avoided
with details of their onset time, magnitude ammonium ions, returning CSF pH back in neuroanesthesia because of older re-
and duration of effect, and side effects. In toward normal after several minutes to ports of ICP increases. However, more
awake craniotomies, the cause for hours of hyperventilation.3,4,8,21 recent studies have shown that ICP does
increased ICP (e.g., coughing, pain, or Moreover, this vasoconstriction can not change in sedated and ventilated pa-
seizurelike activity) should be addressed reduce CPP.27 tients.34,35 Intraoperatively, administration
first before instituting the measures Controlling BP is important in man- of low-dose boluses or infusion, while
discussed in the following sections. aging ICP.9 The autoregulatory capacity of watching the brain bulk, can be useful,
cerebral vessels determines ICP responses especially in patients with significant
Cerebral Blood Volume to BP control. When intact, decreased BP opioid tolerance.
Stated simply, cerebral blood volume below the autoregulatory plateau leads to Some opioids, particularly morphine,
(CBV) can be reduced by increasing cerebral vasodilatation to maintain CBF, can cause systemic histamine release with
venous drainage or decreasing arterial increasing ICP; however, increases in BP hypotension and cerebral vasodilation,
inflow. Standard practice to increase do not further increase ICP, because the subsequently increasing ICP.4,8 Large
venous drainage involves elevating the cerebral blood vessels vasoconstrict to sufentanil, alfentanil, and fentanyl boluses
head of the bed (HoB) and placing the avoid hyperperfusion.20 When have been shown to increase ICP, with a
head in a neutral position to avoid kinking autoregulation is not intact, as in some concomitant decrease in MAP and
the internal jugular vein.1,9,18,21,29 patients with TBI, CBF changes directly CPP.36,37 On the contrary, remifentanil
Although several studies have found that with BP, with increases increasing CBV bolus followed by infusion reportedly has
elevating HoB to 10
e30
reduces ICP and possibly resulting in cerebral edema, no adverse effects on cerebral hemody-
with no change in CPP,9,18 this is contro- whereas decreases can impair CBF.20 namics, CPP, or ICP.4,38
versial, and a Cochrane literature review1 Maintaining a CPP (¼MAPeICP) of 60e Nitrous oxide is a cerebral vasodilator,
suggests limited conclusive evidence of 80 mm Hg maintains adequate CBF.8 and thus, intuitively, it should be avoided
the benefit of HoB increase. Anesthetic agents have variable effects in patients with increased ICP.39 However,
Venous outflow obstruction, via on ICP by their effect on cerebral meta- in anesthetized hyperventilated patients,
increased intra-abdominal or intrathoracic bolism (CMRO2) and CBF. Volatile anes- nitrous oxide does not increase CBF
pressure, can increase CBV and ICP. Intra- thetics depress CMRO2 but are cerebral because, like sevoflurane, desflurane, and
operatively, this increase most commonly vasodilators.4,8 Halothane causes the most isoflurane, nitrous oxide does not blunt
occurs in the setting of patient arousal and vasodilation, whereas desflurane and iso- the cerebral vasoconstrictive response to
can be treated by deepening the anesthetic flurane cause more vasodilation than do hypocapnia.40
and adding neuromuscular blockade. Pa- sevoflurane.4,25 This effect is exacerbated Benzodiazepines are used in the inten-
tients with increased baseline intra- by the hypotension caused by inhalational sive care unit setting but rarely in the

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Table 2. Agents Increasing Intracranial Pressure Level of Evidence

Level of Evidence

Agent I II III IV V Comments

Volatile anesthetics 0 8 20 0 2 About even split with studies showing volatile anesthetics increase ICP and
those showing no difference in ICP relative to propofol. Only a few studies
showed no change in ICP value, whereas none showed a decrease in ICP
Ketamine 0 5 9 0 2 Level 1, none; level 2, 3 no effect, 1 negative; level 3, 5 no effect, 1 negative;
level 4, none; level 5, both negative; overall, 1 level 2 and 1 level 3 decreased
ICP. Most of the others had no effect, with several showing increased ICP
Opioids (morphine, sufentanil, 1 7 17 2 3 Level 1, equivocal; level 2, 4 equivocal, 2 negative; level 3, 13 equivocal, 4
alfentanil, fentanyl, remifentanil) negative; level 4, 2 negative; level 5, 3 negative; overall, most were equivocal,
and the rest negative on reducing ICP. Only 1 study, which was level 2, showed
that fentanyl reduced ICP but not as much as hypertonic saline or pentobarbital,
and had the most frequent treatment failures
Nitrous oxide 0 4 6 0 0 One level 2 study had no effect on ICP, whereas other level 2 studies tended to
increase it. Three level 3 studies concluded that nitrous oxide increases ICP
whereas 3 had no effect or confounding results
Steroids 5 3 25 3 6 Level 1, 4 negative, 1 equivocal; level 2, 1 negative; for 2 positive ones, one
reduced ICP whereas the other reduced peritumoral edema; level 3, 1 reduced
ICP in head injury kids, 2 reduced ICP in patients with brain tumor, 1 reduced ICP
in patients with unknown disease, and 1 reduced edema in patients with
subdural grid; 20 reduced peritumoral edema; level 4, 1 reduced ICP in patients
with head injury, 1 reduced edema in patients with brain tumor, the other
reduced edema in patients with meningoencephalitis; level 5, reduced edema in
brain tumor, perilead, cerebellitis, schistosomiasis, and aspergillosis
Furosemide 0 2 7 2 5 7 of these 14 articles had equivocal findings because although overall findings
were positive, an additional agent was used concurrently, confounding the true
impact of furosemide (this includes both level 2, 1 level 3, 1 level 4, and 3 level
5 articles)

ICP, intracranial pressure.

operating room because of prolonged remain intravascular is essential for water mannitol causes diuresis, leading to
emergence times.41-43 Like propofol, extraction, and the reflection coefficient decreased systemic blood volume and
midazolam decreases CBF and CMRO2, quantifies this ability, with 1.0 being abso- CPP, which in turn causes autoregulatory
with similar effects on ICP, CPP, and ju- lutely impermeable and lower numbers cerebral vasodilation to maintain CBF;
gular bulb oxygen saturation in patients more permeable.21,47 Both mannitol and second, the diuresis, if not appropriately
with trauma.44 HTS have been extensively studied and used compensated for by IV fluids, can increase
Therapeutic hypothermia has been stud- for rapid ICP reduction, with both achieving the hematocrit level, opposing the initial
ied extensively in patients with TBI without this within several minutes and up to 10 mm hypoviscosity-mediated vasoconstriction;
proven benefit in long-term outcome.45 Hg within the first hour, as detailed in third, mannitol, unlike HTS, can cross an
However, therapeutic hypothermia does Table 4.9,27,30,48,49 Initial vasoconstriction intact bloodebrain barrier, with a reflec-
reduce CMRO2 and CBF, decreasing ICP.45 induced by blood hypoviscosity may tion coefficient of 0.9, slowly diffusing
The most feasible and rapid way to induce contribute to ICP reduction.8 Moreover, intraparenchymal; fourth, idiogenic os-
hypothermia in the operating room is with both mannitol and HTS increase moles form in response to plasma hyper-
isotonic refrigerated IV fluids.46 intravascular volume and cardiac output osmolality, increasing intracellular
and augment cerebral perfusion by osmolarity, which can increase brain vol-
Brain Tissue improving laminar flow and altering blood ume on discontinuation of mannitol.8,27,50
Brain volume can be decreased with hyper- viscosity by dehydrating endothelial cells Return to pretreatment increased ICP
osmolar therapy. Hypertonic saline (HTS) and red blood cells, although the clinical levels can be seen after rapid 5-minute
and mannitol achieve this decrease by benefit of this is speculative.8,27 mannitol infusions, whereas this situa-
extracting water from intracellular tissue With mannitol, a rebound delayed in- tion is usually not seen after 20-minute
into the intravascular compartment.5,21,27,47 crease in ICP can occur.5,8,27,50 This in- infusions.51 Purportedly, rapid infusion
The ability of hyperosmolar agents to crease can happen in 4 ways: first, may facilitate greater penetration of

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 LITERATURE REVIEW
VIRENDRA R. DESAI ET AL. INTRAOPERATIVE MANAGEMENT OF INTRACRANIAL PRESSURE

normal noneloquent brain tissue such as

Table 3. Level of Evidence Classification Scheme portions of the frontal lobe, anterior
Level of Evidence Type of Evidence temporal lobe, or cerebellum.8,62 Com-
plete frontal lobectomies performed the
I Randomized controlled trials; meta-analysis of randomized controlled trials traditional way incur several risks: CSF
II Prospective, comparative trials; heterogenous meta-analysis accumulation with hydrocephalus, as the
frontal horn is traversed as a guide; sup-
III Retrospective reviews; case-control studies
plementary motor area syndrome with
IV Case series transient postoperative weakness and
V Case reports; expert opinion; personal observation neglect; or injury to the insula or basal
ganglia if the resection deviates posteri-
orly. Thus, a more standardized approach,
mannitol into brain tissue and/or faster Corticosteroids can decrease peritu- with sparing of the frontal horn and sup-
renal elimination.52 However, it is moral edema, thereby reducing ICP; plementary motor area, has been sug-
unclear if a slower infusion merely delays however, they do not affect other causes of gested.63 Although this technique focuses
the rebound ICP increase or prevents it. edema.21 on gray matter resection for epilepsy, the
Overadministration of mannitol can be same steps can be applied for frontal
harmful; it should be used with caution in CSF lobectomy for increased ICP.
patients with preexisting renal dysfunction Decreased CSF volume via reduced pro- More limited resections can be performed
and serum osmolarity should be targeted duction can help decrease ICP. Acetazol- depending on the approach and disease. For
<320 mOsm/L to avoid renal injury, amide and topiramate are the typical instance, gyrus rectus resection is frequently
although some experts use a limit of 340 agents to achieve this decrease, whereas in used, with low risk of complication, to reduce
mOsm/L.5,27 With HTS, most practitioners animal models, furosemide can suppress frontal lobe retraction and improve visuali-
titrate serum sodium to an upper limit of CSF production.56-58 However, these zation, especially in approaching anterior
approximately 160 mEq/L. medications have a limited role intra- communicating artery aneurysms.64,65
Many studies suggest the superiority of operatively during acute ICP increases. Anterior temporal lobectomy is
HTS over mannitol; whereas both reduce commonly performed for epilepsy with
ICP within 5 minutes, HTS leads to a low risk for complication and can also be
longer duration and greater magnitude of MANAGEMENT OF ICP VIA INVASIVE performed for ICP control.66 Traditionally,
ICP reduction when comparing isovolemic METHODS this technique allows for the posterior
or equimolar dosages (although this is In conjunction with medical therapies, extent of resection to be 4.5 cm in the
controversial) and it has no rebound ICP several surgical options can help relax the dominant hemisphere and 5.5 cm in the
increase although it is better toler- brain, decreasing the need for brain nondominant.67
ated.7,27,50,51,53 A recent meta-analysis of retraction and improving visualization, Cerebellar tissue can be resected also,
randomized controlled trials comparing especially for deep-seated lesions. These especially for decompression after infarct,
HTS and mannitol in patients with TBI options can be categorized as follows: taking care to avoid deep nuclei and
showed no ICP difference at 30 minutes, intracranial (resecting intra-axial or extra- medial parenchyma, because this may
but significantly greater decrease with axial lesion or brain parenchyma), extra- incur a risk of cerebellar mutism.62,68
HTS at 60 and 120 minutes.5 In theory, no cranial (removal of skull and dura), and CSF If one is operating near venous sinuses,
ICP rebound increase occurs because HTS drainage. If the cause for acutely increased compression of these may predispose to
has a reflection coefficient of 1.0 and thus brain bulk is unknown, a reasonable option venous hypertension and induce acute
no diffusion across an intact bloodebrain is to place an ICP monitor or external ven- brain swelling. Releasing pressure on the
barrier.7,8 Moreover, HTS may be superior tricular drain, close the scalp with bone flap sinuses can alleviate this situation.
in achieving adequate brain relaxation off, and obtain an immediate computed
during elective supratentorial surgery.14,47 tomography scan.59 Extracranial
HTS may be preferred in patients with If the brain appears so swollen that the de-
hypovolemia or hyponatremia, whereas Intracranial cision to abort is made before dural open-
mannitol may be better in cases of cerebral If the culprit for increased ICP is a mass ing, one can consider dural expansion with
hypoperfusion, because it is safer and (tumor or hematoma), resecting this mass duraplasty, scarifying the dura to decrease
more effective in increasing CBF, and both should be the primary goal to reduce ICP.8 its rigidity, sectioning the falx, not replacing
are similar in terms of CPP increase.7,27,51 Rapid ICP increase may be suspicious for the bone flap, increasing the craniectomy
Given the increase in BP seen with HTS, acute hemorrhage. In this case, size, or performing bilateral craniec-
and the opposite with mannitol, HTS may ultrasonography can aid in identifying and tomies.6,10,28 Decompressive craniectomy
be preferred in aneurysmal SAH, because evacuating intraparenchymal hematomas may decrease mortality and improve func-
euvolemia and hypertension are generally by locating where the hematoma tional outcome in the setting of ischemic
recommended in this setting.54 In approaches the cortical surface.60,61 stroke, subdural hematoma, and
addition, mannitol may adversely affect If there is no such mass, another sur- SAH.10,69-71 In TBI, the results are mixed,
coagulation more than HTS.55 gical option is resecting damaged tissue or with the DECRA (Decompressive

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Table 4. Medications to Reduce Intracranial Pressure

Duration Amount of Pressure
Agent Onset Time* of Effect* Reduction* Dose and Administration Deleterious Effects

Mannitol Effect starts 1e5 minutes 1.5e6 hours 5 mm Hg increasee10 mm Intravenous rapid infusion over 10 Rebound increase in ICP that can
after administration, Hg decrease over 1 hour; 7 e20 minutes of 0.25e1 g/kg body exceed the initial ICP level. Skin
with peak effect e12 mm Hg reduction over weight via peripheral or central sloughing from irritation,
after 15e60 minutes 2 hours venous catheter. Larger dose leads compartment syndrome from
to longer duration rather than larger forearm extravasation,
magnitude of ICP reduction hypokalemia and alkalosis from
diuresis, and a hyperglycemic
hyperosmolar state in diabetic and
elderly patients; extremely high
levels can damage kidneys via
acute tubular necrosis
Hypertonic saline Onset time within — 2e10 mm Hg reduction over 3% versus 23.4%. 3% NaCl is Hematologic and electrolyte
5 minutes 1 hour; 5e10 mm Hg approximately equiosmolar to 20% abnormalities, such as impaired
reduction over 2 hours mannitol platelet aggregation and
coagulation, hypokalemia, and
hyperchloremic acidosis; risk of
central pontine myelinolysis. With
significant hypernatremia (serum
Na >170 mol/L), higher incidence
of renal failure, thrombocytopenia,
neutropenia, and acute respiratory
distress syndrome. Venous
thrombosis if administered
through peripheral veins, although
2% hypertonic saline generally
safe for peripheral infusion
Propofol <1 minute Can last 1.5e7 mm Hg reduction 20e100 mg/kg/minute Hypotension, hypoventilation,
1e2 hours over 1e2 hours bradycardia, hyperlipidemia,
propofol infusion syndrome (high-
dose infusions can cause
metabolic acidosis,
rhabdomyolysis, dysrhythmias, and
cardiac arrest; higher risk with
sepsis, respiratory compromise
and severe brain injury)
Fentanyl <1 minute Can last 3e8 mm Hg reduction over 50e250 mg/hour Central nervous system and
2 hours 1e2 hours respiratory depression,
hypotension, constipation
Barbiturates Within minutes Can last 0e4 mm Hg reduction over Thiopental (125, 150, or 250 mg); Hypotension, decreased
2 hours 1 hour; 2e7 mm Hg methohexital (50, 70, 75, and 90 mg); peristalsis, central nervous system
reduction over 2 hours pentobarbital (50 and 100 mg or or respiratory depression,
intravenous loading dose 10 mg/kg myocardial depression
over 1 hour, then 5 mg/kg/hour for 3
hours, then 1e4 mg/kg/hour
intravenous drip)

ICP, intracranial pressure.

*All the variables (onset time, magnitude of ICP reduction, and duration of effect) are highly dependent on concentration and amount of agent used.

Craniectomy in Diffuse Traumatic Brain RESCUEicp (Randomized Evaluation of decompressive craniectomy as a last-resort
Injury) study suggesting no benefit from Surgery with Craniectomy for Uncontrolla- intervention.10,72,73 Some studies show that
decompressive craniectomy as an early ble Elevation of Intracranial Pressure) study decompressive craniectomy in patients with
intervention after failure of standard mea- suggested a mortality reduction and TBI can predispose to posttraumatic hydro-
sures to reduce ICP, whereas the improved functional outcome with cephalus requiring ventriculoperitoneal

126 www.SCIENCEDIRECT.com WORLD NEUROSURGERY, https://doi.org/10.1016/j.wneu.2019.05.224

 LITERATURE REVIEW
VIRENDRA R. DESAI ET AL. INTRAOPERATIVE MANAGEMENT OF INTRACRANIAL PRESSURE

Table 5. Ventriculostomy Entry Points and Trajectories

Eponym Entry Point Trajectory

Kocher point 1 cm anterior to coronal suture in midpupillary line 1) Ipsilateral medial canthus in sagittal plane and external auditory
meatus in coronal plane; 2) perpendicular to skull
Frazier point 6 cm above and 4 cm lateral to inion Aim toward point 4 cm above contralateral medial canthus
Dandy point 3 cm above and 2 cm lateral to inion Aim toward a point 2 cm above glabella
Keen point 3 cm above and 3 cm posterior to the superior border of pinna Perpendicular to skull to depth of 4e5 cm, then soft pass
Paine point Intersection of line 2.5 cm superiorly from floor of anterior cranial fossa Perpendicular to cortex
(lateral orbital roof) and another line 2.5e4.5 cm anterior to sylvian
fissure

shunting.74 These studies involved the points. The point chosen generally de- injury. Cochrane Database Syst Rev. 2017;12:
CD009986.
decision to decompress being made pends on several factors including patient
preoperatively. positioning, incision and craniotomy, and 2. Asehnoune K, Lasocki S, Seguin P, et al. Associ-
Another option is hinge craniotomy, in surgeon preference. One should be ation between continuous hyperosmolar therapy
which the bone flap is replaced loosely, familiar with all these points in the event and survival in patients with traumatic brain
injuryea multicentre prospective cohort study and
with one edge of the flap plated and of acute intraoperative ICP increase systematic review. Crit Care. 2017;21:328.
screwed to the bone across the craniotomy requiring ventriculostomy. In these situa-
edge, whereas the other edge has a plate tions, the route used relies on accessi- 3. Davanzo JR, Sieg EP, Timmons SD. Management
of traumatic brain injury. Surg Clin North Am. 2017;
screwed to the bone flap but not secured bility. In Table 5, we describe standard
97:1237-1253.
across the edge.75,76 This option allows the entry points and trajectories; some
craniotomy to hinge outward with variations of these techniques have been 4. Forster N, Engelhard K. Managing elevated
increased ICP but also prevents settling reported as well.13,23,81 intracranial pressure. Curr Opin Anaesthesiol. 2004;
17:371-376.
after the pressure has resolved.75,76 Arachnoid dissection with CSF drainage
can significantly relax the brain. The 5. Li M, Chen T, Chen SD, Cai J, Hu YH. Compari-
cisternal component fenestrated relies on son of equimolar doses of mannitol and hyper-
CSF Drainage tonic saline for the treatment of elevated
accessibility. In supratentorial surgeries,
intracranial pressure after traumatic brain injury: a
CSF drainage is an extremely valuable the basilar cisterns or lamina terminalis systematic review and meta-analysis. Medicine
adjunct in neurosurgery that can substan- can be fenestrated, whereas in the infra- (Baltimore). 2015;94:e736.
tially improve brain relaxation. This goal tentorial space, the cisterna magna or
can be achieved via catheter drainage, 6. Sahuquillo J, Arikan F. Decompressive craniec-
lateral cerebellar hemisphere/cer- tomy for the treatment of refractory high intra-
such as lumbar or external ventricular ebellopontine angle can be opened.78,82 cranial pressure in traumatic brain injury. Cochrane
drains, or by fenestration of cisternal Database Syst Rev. 2006:CD003983.
compartments.13,77-79
CONCLUSIONS 7. Alnemari AM, Krafcik BM, Mansour TR,
When brain retraction is necessary to ac- Gaudin D. A comparison of pharmacologic ther-
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drain can significantly reduce the amount of bulk is essential to optimize patient out- nial pressure after traumatic brain injury. World
Neurosurg. 2017;106:509-528.
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resection and cognitive impairment after surgery Boulos AS, German JW. Cranial decompression 1878-8750/$ - see front matter ª 2019 Elsevier Inc. All
for ruptured anterior communicating artery for the treatment of malignant intracranial rights reserved.

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